Chapter 45 – Cardiovascular Monitoring - Fundanest

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Cardiovascular MonitoringBECKY SCHROEDER • ATILIO BARBEITO • SHAHAR BAR-YOSEF • JONATHAN B. MARK

K e y P o i n t s

• Most automated noninvasive arterial blood pressure measuring devices use an oscillometric measurement technique and rarely cause complications. Caution should be exercised in patients who cannot complain of arm pain, those with irregular rhythms that force repeated cuff inflation, and those receiving anticoagulant therapy.

• The Allen test for palmar arch collateral arterial flow is not a reliable method to predict complications from radial artery cannulation. Despite the absence of anatomic collateral flow at the elbow, brachial artery catheterization for perioperative blood pressure monitoring is a safe alternative to radial or femoral arterial catheterization.

• The accuracy of a directly recorded arterial pressure waveform is determined by the natural frequency and damping coefficient of the pressure monitoring system. Optimal dynamic response of the system will be achieved when the natural frequency is frequent, thereby allowing accurate pressure recording across a wide range of damping coefficients.

• Rather than the common placement at the midaxillary line, the preferred position for alignment (or “leveling”) of external pressure transducers is approximately 5 cm posterior to the sternomanubrial junction. When using external transducers and fluid-filled monitoring systems, this transducer location will eliminate confounding hydrostatic pressure measurement artifacts.

• Because of wave reflection and other physical phenomena, the arterial blood pressure recorded from peripheral sites has a wider pulse pressure than when measured more centrally.

• Dynamic measures of cardiac preload, such as stroke volume and pulse pressure variation, are better predictors of intravascular volume responsiveness than static indicators, such as central venous pressure (CVP) and pulmonary capillary wedge pressure.

• Selecting the best site, catheter, and method for safe and effective central venous cannulation requires that the physician consider the purpose of catheterization, the patient’s underlying medical condition, the intended operation, and the skill and experience of the physician performing the procedure. Right internal jugular vein cannulation is preferred due to its consistent, predictable anatomic location and its relative ease of access intraoperatively.

• Mechanical complications from central venous catheters can be decreased by the use of ultrasound vessel localization, venous pressure measurement before large catheter insertion, and radiographic confirmation that the catheter tip lies outside the pericardium and parallel to the walls of the superior vena cava.

• CVP is the result of a complex and diverse interplay among many different physiologic variables, the main ones being venous return and cardiac function. No simple relationship exists between CVP and circulating blood volume. Despite this, important pathophysiologic information can be obtained by careful assessment of the CVP waveform morphology.

• Catheter misuse and data misinterpretation are among the most common complications of central venous and pulmonary artery catheters.

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PART IV: Anesthesia Management1346

K e y P o i n t s — c o n t ’ d

• Pulmonary artery wedge pressure is a delayed and damped reflection of left atrial pressure. The wedge pressure provides a close estimate for pulmonary capillary pressure in many cases, but it may underestimate capillary pressure when postcapillary pulmonary vascular resistance is increased, as in patients with sepsis.

• Use of central venous, pulmonary artery diastolic, or pulmonary artery wedge pressures as estimates of left ventricular preload is subject to many confounding factors, including changes in diastolic ventricular compliance and juxtacardiac pressure.

• Pulmonary artery catheter monitoring has not been shown to improve patient outcome. Reasons cited for these results include misinterpretation of catheter-derived data and failure of hemodynamic therapies that are guided by specific hemodynamic indices.

• Thermodilution cardiac output monitoring, the most widely used clinical technique, is subject to measurement errors introduced by rapid intravenous fluid administration, intracardiac shunts, and tricuspid valve regurgitation.

• Mixed venous hemoglobin oxygen saturation is a measure of the adequacy of cardiac output relative to bodily oxygen requirements. This measurement is also dependent on the arterial hemoglobin oxygen saturation and hemoglobin concentration.

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INTRODUCTION TO CARDIOVASCULAR MONITORING: FOCUSED PHYSICAL EXAMINATION

Although electronic devices constitute crucially impor-tant cardiovascular monitors, the physician’s senses offer an integrated, panoramic view of the patient’s condition, enhanced further by an understanding of the specific clinical context. Whereas electronic instruments accu-rately and reliably collect massive volumes of data, the clinician plays a vital role by evaluating, and interpret-ing these data.1 Just as inspection, palpation, and aus-cultation are the cornerstones of physical examination, they are also fundamental to perioperative cardiovascular monitoring. For example, direct palpation of a pulse can differentiate true asystole from monitoring artifact more efficiently than troubleshooting an electrocardiogram (ECG) monitor, and direct observation of a beating heart during cardiac surgery or palpation of the aorta by the surgeon provide immediate and invaluable information about the potential causes of hemodynamic instability. However, the strengths and limitations of all monitoring techniques must be understood.

Given that the cardiovascular system is responsible for the transport of substrates and by-products to and from all organ systems, end-organ function is routinely substituted for cardiovascular performance. Inspection of mucous membranes, skin color, and skin turgor often yields important information about hydration, oxygen-ation, and perfusion. Empiric estimation of intravascular fluid deficits and blood loss, urine output, and changes in mental status is also helpful. Unfortunately, inter-pretation of these clinical signs and symptoms is often confounded by anesthetic drugs and preexisting organ dysfunction.

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STETHOSCOPY

Although Laennec is credited with introducing the stethoscope into general medical practice in 1818, nearly a century elapsed before Harvey Cushing proposed its routine use during surgery.2 Stethoscopy provides a sim-ple and reliable means of continuous monitoring of heart and breath sounds. Precordial stethoscopy consists of a heavy metal bell or accumulator attached to a length of rubber or plastic extension tubing and a custom-molded monaural plastic earpiece. The esophageal stethoscope facilitates temperature, clear breath, and heart sound monitoring, but it is only practical during general anes-thesia.3 Although generally considered very low risk, rare cases of pharyngeal or esophageal trauma or hypoxemia from tracheobronchial compression can occur.

Despite its purported value, widespread use of continu-ous stethoscopy has decreased in recent years, possibly related to routine use of pulse oximetry or capnogra-phy.4-6 As a practical matter, clinicians may no longer be as adept at recognizing changes in heart or breath sounds owing to the increasing reliance on electronic monitoring devices, distraction, or operating room noise. As a result, intraoperative stethoscopy has primarily become limited to specialized clinical settings (e.g., pediatric anesthesia, remote locations).

HEART RATE MONITORING

The ability to estimate the heart rate quickly with a “finger on the pulse” is a skill as important as this expression is common, even though electronic devices are most often used to continuously monitor this crucial vital sign as an important guide to anesthetic depth and surgical stimula-tion. The ECG is the most common method used in the operating room, even though any device measuring the

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Chapter 45: Cardiovascular Monitoring 1347

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Figure 45-1. Digital heart rate (HR) displays may fail to warn of dangerous bradyarrhythmias. Direct observation of the electrocardiogram (ECG) and the arterial blood pressure traces reveals complete heart block and a 4-second period of asystole, whereas the digital display reports a HR of 49 beats/min. Note that the ECG filter (arrow) corrects the baseline drift so that the trace remains on the recording screen. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)

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period of the cardiac cycle will suffice. Accurate detection of the R wave and measurement of the R wave–R wave interval serve as the basis from which digitally displayed values are derived and periodically updated (e.g., at 5- to 15-second intervals)7 (Fig. 45-1).

Electrical interference in the ECG trace most often arises from the electrosurgical unit but other sources may also be problematic. Power line noise appears as a 60-Hz artifact and may be eliminated by selecting narrower-bandpass ECG filters, including a 60-Hz notch filter. Problems can also be caused by random twitching and fasciculations, as well as by medical devices such as lithotripsy machines, cardiopulmonary bypass equipment, and fluid warmers.8 High-amplitude pacing spikes may be misinterpreted as R waves and confound heart rate measurement, as can tall T waves. Decreasing the ECG gain, adjusting R-wave detection sensitivity, changing the ECG lead to one with a smaller pacing spike or T-wave amplitude, or selecting pacing detection modes may improve R-wave detection and heart rate measurement.

PULSE RATE MONITORING

The distinction between heart rate and pulse rate is the difference between electrical depolarization with sys-tolic contraction of the heart (heart rate) and a detect-able peripheral arterial pulsation (pulse rate). Pulse deficit describes the extent to which the pulse rate is less than the heart rate and may arise in conditions such as atrial fibril-lation in which, intermittently, a very short R wave–to–R wave interval compromises the stroke volume to such an extent that no corresponding arterial pulse is detectable for that systolic ejection. The most extreme example of a pulse deficit is electrical-mechanical dissociation or pulse-less electrical activity, seen in patients with cardiac tam-ponade, extreme hypovolemia, and other conditions in which cardiac contraction does not generate a palpable peripheral pulse.

Many monitors report heart rate and pulse rate sepa-rately, the former from the ECG trace and the latter from the pulse oximeter plethysmograph or arterial blood pres-sure monitor. In addition to indicating the pulse rate, this waveform may also provide supplementary diagnostic clues to cardiovascular function.9,10 Although monitor-ing both heart rate and pulse rate may seem redundant,

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such redundancy is intentional, improves accuracy, and reduces measurement errors and false alarms.11

ARTERIAL BLOOD PRESSURE MONITORING

Like heart rate, arterial blood pressure is a fundamental cardiovascular vital sign included in the mandated stan-dards for basic anesthetic monitoring.12 Blood pressure is usually measured either by indirect cuff devices or direct arterial cannulation with pressure transduction. These techniques measure different physical signals and differ in their degree of invasiveness. However, both are sub-ject to numerous confounding factors that often result in significantly discrepant results, even with simultaneous measurements.13

INDIRECT MEASUREMENT OF ARTERIAL BLOOD PRESSURE

Manual Intermittent TechniquesMost indirect methods of arterial blood pressure measure-ment use a sphygmomanometer, first described by Riva-Rocci in 1896.14 Using an arm-encircling inflatable elastic cuff, a rubber bulb to inflate the cuff, and a mercury manometer to measure cuff pressure, the radial arterial pulse was palpated as the pressure in the cuff was increased (or later on rapid cuff deflation), identifying the systolic blood pressure (SBP). Detecting both systolic and diastolic pressure became possible with the description of the aus-cultatory method of blood pressure measurement by Korotkoff in 1905.15 The Korotkoff sounds are a complex series of audible frequencies produced by turbulent flow beyond the partially occluding cuff. The pressure at which the first Korotkoff sound is heard is considered the sys-tolic pressure (phase I). The sound character progressively changes (phases II and III), becomes muffled (phase IV), and is finally absent (phase V). Diastolic blood pressure (DBP) is recorded at phase IV or V (i.e., significant muf-fling or disappearance of the sounds altogether).

A fundamental shortcoming of the auscultatory method is its reliance on blood flow to generate Korot-koff sounds. Decreased peripheral blood flow from any

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etiology, including shock or intense vasoconstriction, can attenuate or obscure sound generation or detec-tion.16 In contrast, changes in vessel or tissue compliance underlying the cuff (such as in severe edema, shivering, or calcific arteriosclerosis) require excessively high cuff-occluding pressures and may yield completely inaccurate readings.17

Other common sources of error during intermittent manual blood pressure measurement include selection of an inappropriate cuff size and excessively rapid cuff deflation. A well-fitted cuff has a bladder that extends to 40% of arm circumference and 80% of length of the upper arm.17 The cuff should be applied snugly and con-tain no residual air, with the bladder centered over the artery. Although too large a cuff often provides acceptable results, the use of a cuff that is too small usually results in falsely high readings.17 The cuff pressure should decrease slowly enough for the changes in Korotkoff sounds to be detected and properly interpreted. An excessively rapid deflation would cause changes in the sounds to be missed and yield a falsely low pressure reading.

Automated Intermittent TechniquesAutomated noninvasive blood pressure (NIBP) devices are standard equipment in most critical care settings because they provide frequent, regular pressure measure-ments, free the operator to perform other vital clinical duties, provide audible alarms, and can transfer data to a computerized information system. Most NIBP devices are based on oscillometry, a technique first described by Marey in 1876.17 In this method, small changes in cuff pressure with arterial pulsation during cuff deflation are used to estimate mean arterial blood pressure (MAP). In contrast to the auscultatory method, in this case, the maximal degree of detectable pulsation is determined to be the MAP. SBP and DBP pressures are calculated accord-ing to proprietary algorithms that vary by manufacturer; they are thus less reliable than the values for MAP.17-19 Systolic pressure is typically identified as the pressure at which escalating pulsations reach 25% to 50% of maxi-mum. Diastolic pressure is the most unreliable oscillo-metric measurement and is commonly recorded when the pulse amplitude has declined to a small fraction of its peak value. In clinical practice, oscillometric automated NIBP measurement is from the upper arm.

In general, automated NIBP measurements closely approximate directly measured arterial pressure, espe-cially at mean pressures of 75 mm Hg and lower.17,20 However, significant shortcomings have been identified in clinical studies and are important to recognize. Stan-dards for performance of automated NIBP devices have been established by the Association for the Advance-ment of Medical Instrumentation (AAMI) and the Brit-ish Hypertension Society (BHS); however, given the ethical conflict that is posed by a requirement for valida-tion of noninvasive devices against invasive direct arte-rial measurements, auscultation remains the standard against which all devices are evaluated. Consequently, the minimum performance standards that all NIPB devices are required to meet are significantly affected by the fundamental nature of the auscultatory method and the specific protocols used during each validation

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procedure.21 At present, in a pool of 85 subjects, new automatic devices must demonstrate average differences no more than ± 5 mm Hg, with standard deviations no greater than 8 mm Hg. This implies that some values may deviate up to 20 mm Hg from the true pressure and still achieve “acceptable performance” as defined by the AAMI.22 However, attempts to reproduce these valida-tion procedures in clinical situations indicate that with at least one very commonly used device, only 74% of diastolic and 60% of mean and systolic measurements were within 10% of direct measured values. Although the device did meet the minimum performance stan-dards, (MAP ≤ 5 mm Hg difference from the standard), the variances were large.23

Clinical studies comparing NIPB with direct arte-rial pressure measurements also reflect the problematic nature of NIBP monitoring. Oscillometric methods often underestimate systolic and overestimate diastolic mea-surements, significantly underestimating pulse pressure calculations.24 These devices also tend to underestimate mean values during periods of hypertension and overes-timate during hypotension, potentially biasing clinical decisions in unstable patients.25 Ankle, calf, and thigh cuffs have never been validated at all, although there is sometimes no choice but to use a cuff in such a manner. Several well-conducted studies in critically ill patients have shown that NIBP measurements show acceptable agreement when a well-fitted cuff is used on the upper arm. The devices can also be reliably used in unstable patients or in alternative locations to identify patients who are hypotensive (MAP ≤ 65 mm Hg), and to differ-entiate those who have responded to a therapeutic inter-vention from those who have not (e.g., MAP ≤ 65 mm Hg versus MAP > 65 mm Hg). However, they cannot be reliably used to titrate therapy outside of these variables, and averaging of several measurements is necessary for a measurement to be considered reliable.20,26

NIBP devices are validated against a technique that measures something slightly different—and in a funda-mentally different manner. The auscultatory method measures the systolic and diastolic pressures, estimating the mean, whereas oscillometric devices measure the mean and calculate (in different ways) the systolic and diastolic. Furthermore, directly measured arterial pressure measurements use another technique altogether. It has been stated that “current protocols for validating blood pressure monitors give no guarantee of accuracy in clini-cal practice.”21 Perhaps expecting these techniques to yield identical or even similar values is unrealistic, espe-cially in complex and unstable clinical situations.

Complications of Noninvasive Blood Pressure MeasurementAlthough automated, noninvasive blood pressure mea-surement is generally safe, severe complications, though rare, do occur27 (Box 45-1). Compartment syndromes have developed after prolonged periods of frequent cuff cycling, likely related to trauma or impaired distal limb perfusion. Other contributing factors include cuff place-ment over a joint or other vulnerable tissue, or repeated use in the face of a significant confounding factor such as muscle tremors, significant dysrhythmias, or a kinked

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cable. Also, patients with peripheral neuropathies, arterial or venous insufficiency, severe coagulopathies, or recent use of thrombolytic therapy may be vulnerable to compli-cations from a noninvasive blood pressure monitor.

Automated Continuous TechniquesAdvances in microprocessor and servomechanical control technology have enabled noninvasive techniques to pro-vide a reasonable representation of the arterial pressure waveform and a nearly continuous assessment of blood pressure without resorting to direct arterial cannulation. One such device measures finger blood pressure with an arterial volume-clamp method designed and first reported by Penaz in 1973.28 Although reasonable accuracy of fin-ger blood pressure as a surrogate for intraarterial pressure measurements are possible, many factors have precluded more widespread application of this technology.29 Under many circumstances, finger blood pressure monitoring will not reflect brachial arterial pressure. In addition, finger arteries are prone to spasm with the potential for distal ischemia, hand position will influence pressure val-ues, and blood sampling cannot be performed without indwelling catheters. Changes in finger physiology also influence noninvasive hemoglobin (SpHb) monitoring (also see Chapter 61).

Other automatic continuous noninvasive techniques are available to measure arterial blood pressure, using technologies based on arterial wall displacement, pulse transit time, arterial tonometry, and other methods. All techniques have limitations, including need for calibra-tion, sensitivity to motion artifact, and limited applicabil-ity in critically ill patients.17,30,31 It is not clear whether any noninvasive technique will reduce the need for direct arterial pressure monitoring or whether these methods will replace automated intermittent oscillometry as the standard NIBP monitoring method in anesthesia and critical care.

DIRECT MEASUREMENT OF ARTERIAL BLOOD PRESSURE

Arterial cannulation with continuous pressure transduc-tion remains the accepted reference standard for arterial blood pressure monitoring. Despite its increased risk, cost, and need for technical expertise for placement and man-agement, its utility in providing crucial and timely infor-mation outweighs its risks in many cases (Box 45-2). The Australian Incident Monitoring Study of 1993 confirmed the superiority of direct arterial pressure monitoring over indirect monitoring techniques for the early detection of intraoperative hypotension.26,32

PainPetechiae and ecchymosesLimb edemaVenous stasis and thrombophlebitisPeripheral neuropathyCompartment syndrome

BOX 45-1 Complications of Noninvasive Blood Pressure (NIBP) Measurement

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Perhaps the most underemphasized value of direct arterial pressure monitoring is the potential for arterial pressure waveform analysis to provide diagnostic infor-mation regarding changes in the patient’s condition. This was directly proposed more than a half century ago by Eather and associates, who advocated monitoring of “arterial pressure and pressure pulse contours” in anes-thetized patients.33 Some aspects are readily apparent and routinely used, such as identification of the dicrotic notch to guide proper timing for intraaortic balloon counterpulsation. Others, such as recognition of exces-sive variation in arterial blood pressure variables as a sign of preload reserve, have only gained significant attention more recently.34

Percutaneous Radial Artery CannulationThe radial artery is the most common site for invasive blood pressure monitoring because it is technically easy to cannulate and complications are uncommon.35,36 Slog-off and coauthors described 1700 cardiovascular surgical patients who underwent radial artery cannulation with-out ischemic complications despite evidence of radial artery occlusion after decannulation in more than 25% of patients.37 Furthermore, most investigations of hand per-fusion, in both the early and late postoperative periods following radial artery harvest for coronary artery bypass and flap transfer procedures, have reported no significant decrease relative to the contralateral hand.38-43

Before attempting radial artery cannulation, many cli-nicians assess the adequacy of collateral flow to the hand by performing a modified Allen test. This bedside exami-nation is a variation on a technique originally described in 1929 to assess arterial stenosis in the hands of patients with thromboangiitis obliterans.44 The examiner com-presses both the radial and ulnar arteries and asks the patient to make a tight fist, exsanguinating the palm. The patient then opens the hand, avoiding hyperextension of the wrist or fingers. As occlusion of the ulnar artery is released, the color of the open palm is observed. Nor-mally, the color will return to the palm within several seconds; severely reduced ulnar collateral flow is pres-ent when the palm remains pale for more than 6 to 10 seconds.

Although the Allen test is often used to identify patients at increased risk for ischemic complications from radial artery cannulation, the predictive value of this test is poor. Numerous reports of permanent ischemic sequelae note that a normal Allen test result was present before vessel cannulation.38,45 In contrast, there are many descriptions of uncomplicated radial artery monitoring in the face of a

Continuous, real-time blood pressure monitoringPlanned pharmacologic or mechanical cardiovascular

manipulationRepeated blood samplingFailure of indirect arterial blood pressure measurementSupplementary diagnostic information from the arterial

waveform

BOX 45-2 Indications for Arterial Cannulation

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documented abnormal Allen test.37,46 In recent years, the radial artery has been used safely as an access site for coro-nary catheterization and stenting or harvested for use in coronary bypass grafting, even in individuals who have an abnormal Allen test.46,47 Although most patients show radial artery dominance with respect to overall hand per-fusion, total radial artery occlusion does not compromise distal perfusion, perhaps as the result of collateral recruit-ment.47 Overall, the diagnostic accuracy of the modified Allen test with a 5-second threshold is only 80% with 76% sensitivity and 82% specificity. It appears that the test is unable to provide a cutoff point below which per-fusion can be deemed vulnerable.48 Unfortunately, use of pulse oximetry, plethysmography, or Doppler ultrasound as adjuncts to visual inspection of the palm for return of circulation does not seem to improve its accuracy. Oxim-etry is able to detect blood flow at extremely low flows, leading to poor specificity, whereas no established ultra-sound criteria are available by which to evaluate radial or ulnar blood flow and identify abnormalities.38,49,50 In general, although a normal modified Allen test may be useful in identifying patients acceptable for radial artery harvest or use for coronary angiography, it does not pre-dict clinical outcomes following cannulation for arterial blood pressure monitoring as currently practiced.38

In preparation for cannulation of the radial artery, the wrist and hand are immobilized and secured with the wrist resting across a soft pad. Dorsiflexion of the wrist should be mild at most to avoid attenuating the pulse by stretch or extrinsic tissue pressure. The course of the radial artery proximal to the wrist is identified by gentle palpation, the skin is prepared with an antiseptic, and a local anesthetic is injected intradermally and subcutane-ously beside the artery. Arterial catheterization can be performed with a standard IV catheter or an integrated guidewire-catheter assembly designed for this purpose. A recent educational video provides great detail about this standard procedure.50-52

Once the catheter is fully advanced into the vessel lumen, the radial artery is occluded by applying proximal pressure, the needle is removed, the monitoring system pressure tubing is fastened to the catheter, an appropri-ate sterile dressing is applied, and the apparatus is taped and secured to the wrist. Although a soft arm board can be used to maintain the wrist in an anatomically neu-tral position during arterial pressure monitoring, extreme wrist dorsiflexion should be avoided to prevent injury to the median nerve.53,54

Some clinicians choose the “transfixion” technique for arterial cannulation, in which the front and back walls of the artery are punctured intentionally, the needle is removed from the catheter, the catheter is withdrawn until pulsatile blood flow appears, and then advanced into the vessel lumen either directly or over a wire using the Seldinger technique. Although it is unnecessary to place an additional hole in the back wall of the radial artery for successful cannulation, the technique per se is not associated with a more frequent rate of complications or failure.55

Other aids to arterial cannulation include the use of ultrasound imaging to guide catheter insertion, especially as a rescue method following a failed attempt.56 Although

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ultrasound techniques improve first-pass cannulation success rates, improved clinical outcomes and shorter times required to place have not been documented as a justification for routine use.57-60

Alternative Arterial Pressure Monitoring SitesIf the radial arteries are unsuitable or unavailable, mul-tiple alternatives exist. The ulnar artery is cannulated in a manner similar to that for the radial and has been used safely even following failed attempts to access the ipsilateral radial artery.37,61 Similarly, the brachial artery, although lacking collateral branches to protect the hand, has a long track record of safe use. Bazaral and associ-ates reported more than 3000 brachial artery catheters in patients undergoing cardiac surgery, with only one significant thrombotic complication and no long-term sequelae.62 The axillary artery has the advantages of patient comfort, mobility, and access to a central arterial pressure waveform, and complications are similar in inci-dence to those for use of radial and femoral arteries.36 A slightly longer catheter is preferred for the brachial or axil-lary sites because of their relatively deeper location and position with respect to the shoulder and elbow joints. However, the risk of cerebral embolization is significantly increased when more centrally located vessels are used.

The femoral artery is the largest vessel in common use for monitoring, but its safety appears to be comparable to those for other sites.36 As with axillary artery pressure monitoring, the femoral artery waveform more closely resembles aortic pressure than do waveforms recorded from peripheral sites. The risk of distal ischemia may be reduced because of the large diameter of the artery, but risk of atherosclerotic plaque embolization is significant during initial vessel manipulation. Catheterization of the femoral artery is best achieved with a guidewire tech-nique, and the point of vessel entry must be distal to the inguinal ligament to minimize the risk of arterial injury, hidden hematoma formation, or even uncontrolled hem-orrhage into the pelvis or peritoneum.63

Less commonly used alternatives include the dorsalis pedis, posterior tibial, and superficial temporal arteries, with the pedal vessels being more popular for pediatric patients.

Complications of Direct Arterial Pressure MonitoringLarge clinical investigations confirm the infrequent inci-dence of long-term complications after radial arterial monitoring.35-37 Although vascular complications from radial artery cannulation are uncommon, factors that may increase risk include vasospastic arterial disease, pre-vious arterial injury, thrombocytosis, protracted shock, high-dose vasopressor administration, prolonged cannu-lation, and infection.38,64,65 Catheter diameter and com-position as well as artery size and patient gender may be associated with arterial injury.38

Rare complications can occur after arterial cannulation at any location (Box 45-3). In most cases, catheter place-ment was technically difficult or there were contributory factors such as shock or coagulopathy. In a large obser-vational study of 2000 untoward clinical events resulting

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from vascular access of all kinds, only 13 were related to peripheral arterial cannulation, fewer than those associ-ated with central venous18 or peripheral venous can-nulation.33 Of these cases, 5 involved problems with equipment; in 3 cases the arterial line was used inadver-tently for drug injection, and in the remainder, the arte-rial line was either disrupted or kinked. In only 1 case did transient vasospasm follow radial artery cannulation.32,66 A second report from this study noted that direct pressure monitoring was problematic in 10 cases, resulting from incorrect calibration or interpretation of the pressure dis-play or unrecognized subclavian artery stenosis. Further-more, the anesthesia closed claims study reported claims related to arterial pressure monitoring at any site consti-tute only 8% of all claims related to any vascular access (2% of total claims). Of these, almost 54% were related to radial artery use (ischemic injury, median or radial nerve injury, or retained wire fragment), less than 8% were asso-ciated with use of the brachial artery, and the remainder followed severe thrombotic or hemorrhagic complications after femoral artery monitoring.67 Although patient physi-ology is important, equipment misuse, careful placement technique and catheter care, as well as improper data interpretation are primary issues in many complications related to arterial pressure monitoring.

Technical Aspects of Direct Blood Pressure MeasurementDirect measurement of arterial blood pressure requires that an accurate and appropriate pressure waveform be reproduced on the monitor. Unfortunately, several fac-tors, including extension tubing, stopcocks, flush devices, recorders, amplifiers, and transducers, influence this pro-cess and may introduce significant error.68

Most invasive blood pressure monitoring systems are underdamped second-order dynamic systems modeled after mass-spring systems that demonstrate simple har-monic motion dependent on elasticity, mass, and fric-tion.68-70 These three properties determine the system operating characteristics (i.e., frequency response or dynamic response), which in turn are characterized by critical system parameters, natural frequency (fn, ω) and damping coefficient (τ, Z, α, D). The natural frequency of a system determines how rapidly the system oscillates after a stimulus, whereas the damping coefficient reflects frictional forces acting on the system and determines how rapidly it returns to rest after a stimulus. Both vari-ables may be estimated or measured at the bedside and dramatically influence the appearance of the displayed pressure waveform.

Distal ischemia, pseudoaneurysm, arteriovenous fistulaHemorrhageArterial embolizationInfectionPeripheral neuropathyMisinterpretation of dataMisuse of equipment

BOX 45-3 Complications of Direct Arterial Pressure Monitoring

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Natural FrequeNcy, DampiNg coeFFicieNt, aND DyNamic respoNse oF pressure moNitoriNg systems. The displayed arterial blood pressure waveform is a periodic complex wave produced via Fourier analysis of a summation of a series of simpler but diverse propagated and reflected pressure waves. As such, it is a mathematic re-creation of the original complex pressure wave created by stroke vol-ume ejection.71,72 The original pressure wave is character-ized by its fundamental frequency, manifested clinically as the pulse rate. Although the pulse rate is measured in beats per minute, fundamental frequency is expressed as cycles per second or Hertz (Hz).

The sine waves that sum to produce the final complex wave have frequencies that are multiples or harmonics of the fundamental frequency. A crude arterial waveform depicting a systolic upstroke and peak, dicrotic notch, and so forth can be reconstructed with reasonable accuracy from only two sine waves, the fundamental frequency and the second harmonic (Fig. 45-2). If the original arte-rial pressure waveform contains high-frequency compo-nents such as a steep systolic upstroke, higher-frequency sine waves (and more harmonics) are needed to provide a faithful reconstruction of the original pressure wave-form. As a general rule, 6 to 10 harmonics are required to provide distortion-free reproductions of most arterial pressure waveforms.71,73 Hence, accurate arterial blood pressure measurement in a patient with a pulse rate of 120 beats/min (2 cycles/sec or 2 Hz) requires a monitor-ing system dynamic response of 12 to 20 Hz (i.e., 6 to 10 waveforms × 2 Hz). The faster the heart rate and the steeper the systolic pressure upstroke, the greater the dynamic response demands on the monitoring system.

All monitoring systems have an intrinsic natural fre-quency and damping coefficient. If the natural frequency is too low, frequencies in the monitored pressure wave-form will overlap that of the measurement system, the system will resonate, and pressure waveforms recorded on the monitor will be exaggerated or amplified versions

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Figure 45-2. Arterial blood pressure waveform produced by summa-tion of sine waves. The fundamental wave (top) added to 63% of the second harmonic wave (middle) results in a pressure wave (bottom) resembling a typical arterial blood pressure waveform (box). (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)



of true intraarterial pressure. An underdamped pressure waveform displays systolic pressure overshoot and may contain elements produced by the measurement system itself rather than the original propagated pressure wave (Fig. 45-3). In contrast, an overdamped waveform is rec-ognizable by its slurred upstroke, absent dicrotic notch, and loss of fine detail. Such waves display a falsely nar-rowed pulse pressure, although MAP may remain reason-ably accurate (Fig. 45-4).

Catheter-tubing transducer systems in routine clini-cal use tend to be underdamped but have an acceptable natural frequency that exceeds 12 Hz68 (Fig. 45-5). In general, the lower the natural frequency of the monitor-ing system, the more narrow the range of damping coef-ficients necessary to ensure faithful reproduction of the pressure wave. For example, if the monitoring system’s natural frequency is 10 Hz, the damping coefficient must be between 0.45 and 0.6 for accurate pressure waveform monitoring. If the damping coefficient is too low, the monitoring system will be underdamped, resonate, and display factitiously elevated systolic blood pressure; if the damping coefficient is too high, the system will be over-damped, systolic pressure will be falsely decreased, and fine detail in the pressure trace will be lost.

For any specific system, the most rapid possible natural frequency facilitates an optimal dynamic response.72 In theory, this is achieved best by using short lengths of stiff pressure tubing and limiting the number of stopcocks and other monitoring system appliances. Blood clots and air bubbles concealed in stopcocks and other connections have a similar impact on system dynamic response. As a general rule, adding air bubbles to a monitoring sys-tem will not improve its dynamic response because any

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Figure 45-3. Underdamped arterial pressure waveform. Systolic pressure overshoot and additional small, nonphysiologic pressure waves (arrows) distort the waveform and make it hard to discern the dicrotic notch (boxes). Digital values displayed for direct arterial blood pressure (ART 166/56, mean 82 mm Hg) and noninvasive blood pres-sure (NIBP 126/63, mean 84 mm Hg) show the characteristic relation-ship between the two measurement techniques in the presence of an underdamped system. (From Mark JB: Atlas of cardiovascular monitor-ing, New York, 1998, Churchill Livingstone.)


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Figure 45-4. Overdamped arterial pressure waveform. The over-damped pressure waveform (A) shows a diminished pulse pressure compared with the normal waveform (B). The slow-speed recording (bottom) demonstrates a 3-minute period of damped arterial pressure. Note that despite the damped system, mean arterial pressure remains unchanged. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)

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Figure 45-5. Interaction between damping coefficient and natural frequency. Depending on these two parameters, catheter tubing-transducer systems may be classified by their dynamic response range. Systems with an optimal or adequate dynamic response will record and display all or most pressure waveforms encountered in clinical practice. Overdamped and underdamped systems skew measure-ments in predictable ways, with those having a natural frequency <7 Hz proving unacceptable. The rectangular crosshatched box indicates the ranges of damping coefficients and natural frequencies commonly encountered in clinical pressure measurement systems. The red dot within the box marks the mean values of 30 such systems.74 (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)



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increase in system damping is necessarily accompanied by a decrease in natural frequency. Somewhat paradoxi-cally, monitoring system resonance may increase and cause even greater systolic pressure overshoot (Fig. 45-6).

The fast-flush test provides a convenient bedside method for determining dynamic response of the sys-tem and assessing signal distortion.68,70,72 The nature and duration of the flush artifact following a brief opening of the fast-flush valve are noted. Natural frequency is inversely proportional to the time between adjacent oscil-lation peaks, calculated as 1 cycle/1.7 mm × 25 mm/sec = 14.7 cycles/sec (14.7 Hz) (Fig. 45-7, A). Shorter oscillation cycles indicate a more rapid natural frequency.72 Alter-natively, the damping coefficient is related to the ampli-tudes of successive oscillation peaks. The amplitude ratio thus derived indicates how quickly the measuring system returns to a resting state. The damping coefficient can be

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Figure 45-6. Effect of small air bubbles within arterial pressure moni-toring systems. Arterial pressure waveforms are displayed, along with superimposed fast-flush square-wave artifacts. A, Original monitoring system has an adequate dynamic response (natural frequency 17 Hz, damping coefficient 0.2). B, A small 0.1-mL air bubble added to the monitoring system produces a paradoxical increase in arterial blood pressure. Note decreased natural frequency of the system. C, A larger 0.5-mL air bubble further degrades dynamic response and produces spurious arterial hypotension. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)

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calculated mathematically, but it is usually determined graphically from the amplitude ratio.68,72 For example, the amplitudes of two successive oscillation cycles are 24 and 17 mm, giving an amplitude ratio of 17/24 or 0.71. This corresponds to a damping coefficient of 0.11 based on the graphic solution (Fig. 45-7, B). Note that the monitoring system illustrated has an adequate natu-ral frequency (approximately 15 Hz) but is underdamped (damping coefficient 0.11, optimal range 0.45 to 0.6, see earlier). One would expect to find systolic pressure over-shoot in such a system.

Although the technical requirements for accurate arte-rial blood pressure measurement are well known, these

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Figure 45-7. Clinical measurement of natural frequency and damp-ing coefficient. A, Two square-wave fast-flush artifacts interrupt an arterial pressure waveform recorded on standard 1-mm grid paper at a speed of 25 mm/second. Natural frequency is determined by mea-suring the period of one cycle of adjacent oscillation peaks (1.7 mm). Damping coefficient is determined by measuring the heights of adja-cent oscillation peaks (17 and 24 mm). From these measurements, a natural frequency of 14.7 Hz and an amplitude ratio of 0.71 may be calculated. B, Relation between amplitude ratio and damping coef-ficient. The amplitude ratio determined in the fast-flush test in (A) corresponds to a damping coefficient of 0.11. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)

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conditions are often lacking in routine clinical practice. Examination of the frequency response of 30 radial artery catheter-transducer systems used in routine intensive care monitoring showed natural frequency (mean 14.7 ± 3.7 Hz) and damping coefficient (mean 0.24 ± 0.07) values that fell within the range of underdamped systems.68,74 Further-more, the range of frequency responses (10.2 to 25.3 Hz) and damping coefficients (0.15 to 0.44) measured in this setting suggests that distortion of the arterial waveform is common in clinical practice, particularly systolic arterial pressure overshoot resulting from underdamped systems (see Fig. 45-5).

pressure moNitoriNg system compoNeNts. Arterial pres-sure monitoring systems have a number of components, beginning with the intraarterial catheter and including extension tubing, stopcocks, inline blood sampling set, pressure transducer, continuous-flush device, and elec-tronic cable connecting the bedside monitor and wave-form display screen. The stopcocks in the system provide sites for blood sampling and allow the transducer to be exposed to atmospheric pressure to establish a zero refer-ence value. Needleless blood sampling ports and inline aspiration systems permit blood drawing without use of sharp needles and allow aspirated waste blood to be returned to the patient within a convenient closed sys-tem. Modifications such as these are intended to reduce the risk of needle injury and decrease waste of the patient’s blood during sampling. However, these addi-tional features may degrade the dynamic response of the monitoring system and further exacerbate systolic arterial pressure overshoot.

The flush device provides a continuous, slow (1 to 3 mL/hr) infusion of saline to purge the monitoring system and prevent thrombus formation within the arterial catheter. Dextrose solutions should not be used, because flush con-tamination of sampled blood may cause serious errors in blood glucose measurement.75 A dilute concentration of heparin (1 to 2 units heparin/mL saline) has been added to the flush solution to reduce further the incidence of catheter thrombosis, but this practice increases the risk of heparin-induced thrombocytopenia and should be avoided. The flush device not only ensures continuous slow flushing of the line and catheter but also includes a spring-loaded valve for periodic, high-pressure flush-ing. This rapid flushing is used to purge the extension line of blood after an arterial sample has been taken or to restore the dynamic response characteristics of the pres-sure monitoring system, which otherwise slowly deterio-rate over time.76

traNsDucer setup: ZeroiNg aND leveliNg. Before use, pressure transducers must be zeroed, calibrated, and lev-eled to the appropriate position relative to the patient. A zero pressure reference value must be established by opening the appropriate stopcock and exposing the trans-ducer to atmospheric pressure and executing the zero-command, a specific maneuver that may vary with each manufacturer. This underscores the fact that all pressures displayed on the monitor are referenced to local atmo-spheric pressure. To be precise, it is the air-fluid inter-face at the level of the stopcock that is the zero pressure


locus. This point must be specifically positioned relative to the patient to ensure correct transducer level. When a significant or unexpected change in pressure occurs, the zero reference value can be rechecked quickly by open-ing the stopcock and noting that the pressure value on the bedside monitor is still zero.72 Occasionally, a faulty transducer, cable, or monitor will cause the zero base-line to drift introducing significant error into all subse-quent pressure measurements until the zero reference is reestablished.77,78

Historically, transducer calibration closely followed zeroing. Calibration is an adjustment in system gain to ensure accurate transducer measurement relative to a known reference. Although traditionally calibrated against a mercury manometer, current disposable pres-sure transducers meet accuracy standards established by the AAMI and the American National Standards Insti-tute.77 As such, formal bedside transducer calibration is no longer performed. However, it is good practice to routinely compare pressures obtained via a newly placed arterial catheter with a blood pressure obtained via other means as a more informal but useful calibration. On occa-sion, despite successful transducer zeroing, the measured blood pressure values seem erroneous, and a malfunc-tioning pressure transducer, cable, or monitor is identi-fied and replaced.78

The final step in transducer setup is to adjust the pres-sure monitoring zero point to the appropriate level relative to the patient. Note that transducer zeroing and leveling are two distinct procedures. Zeroing established the zero reference point for the transducer system, whereas level-ing matches this reference point to a specific point on the patient’s body. That is, it determines where the value 0 will be and, hence, from where measurements will begin. Although the precise location for the zero reference level is important for accurate blood pressure monitoring, it is even more critical when the physiologic range of values is smaller, such as for cardiac filling pressures. In such cases, a small absolute error would have a large influence on the displayed pressures.

Arterial pressure transducers should be placed to best estimate aortic root pressure. Although the midchest position is often used in supine patients, several inves-tigators have shown that cardiac filling pressures are sig-nificantly overestimated when transducers are leveled to the midchest rather than a position approximately 5 cm posterior to the sternal border.79,80 This preferred (more anterior) transducer location obviates the confounding effect of hydrostatic pressure on cardiac filling pressure measurements.

The position of the pressure transducer relative to the patient must be considered in interpreting blood pressure measurements. In some circumstances, the clinician may choose to place the arterial transducer at a level differ-ent from the standard. In such a case, the displayed pres-sure is the pressure measured at that level and, important to note, is not the same at the aortic root. For example, when the arterial pressure transducer is elevated to the level of the patient’s ear to approximate the location of the circle of Willis during a sitting neurosurgical pro-cedure, arterial blood pressure at the level of the brain is being measured and displayed, and that at the aortic

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Figure 45-8. Effect of patient position on the relation between direct arterial blood pressure (ART) and indirect noninvasive blood pressure (NIBP) measurements. A, In the supine patient, pressures measured from the right (R) or left (L) arms by either technique will be the same. B, In the right lateral decubitus position, ART pressures recorded directly from the right and left radial arteries will remain unchanged so long as the respective pressure transducers remain at heart level. However, NIBP will be higher in the dependent right arm and lower in the nondependent left arm. Differences in NIBP are determined by the positions of the arms above and below the level of the heart and are equal to the hydrostatic pressure differences between the level of the heart and the respective arm. A 20-cm difference in height produces a 15-mm Hg difference in pres-sure. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)

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root is higher (by an amount equal to the vertical height difference between the two points). There is no need to re-zero the transducer when it is moved, as atmospheric pressure changes very little over the few inches of height adjustment. Errors are also common when pressure trans-ducers are fixed to an intravenous pole and the patient’s bed height is adjusted. Raising the height of the bed rela-tive to the transducer will cause overestimation of arterial blood pressure, whereas lowering the patient below the transducer will lead to underestimation.

For proper interpretation of blood pressure measure-ments from a patient in the lateral decubitus position, it is helpful to differentiate zeroing and leveling pressure transducers and to appreciate the differences between noninvasive and invasive blood pressure measurement. In this position, although the aortic root remains stationary, one arm is necessarily higher than the other. However, as long as the pressure transducer remains fixed at the level of the heart, the location of the arms or in which vessel the catheter resides has no influence on the measured arterial pressure. On the other hand, noninvasive cuff blood pres-sure measurements will be different in the two arms—higher in the dependent (down) arm and lower in the nondependent (up) arm (Fig. 45-8). As a result, to check the accuracy of a cuff measurement, it may be necessary to temporarily move the pressure transducer to the level of the blood pressure cuff in question.

Normal Arterial Pressure WaveformsIn the early era of arterial pressure monitoring, signifi-cant diagnostic information was gleaned from waveform analysis.33 Unfortunately, this practice declined, possibly because of increasing reliance on cuff sphygmomanom-etry, which provides “numbers which came to be linked in a simplistic way to cardiac strength (systolic pressure) and arteriolar tone (diastolic pressure). Pseudoscience had

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arrived with (these) numbers …”81 With the advent of automated graphic analysis and high-resolution, multi-colored displays, renewed interest in waveform analysis is attracting new attention.34 However, full apprecia-tion of the diagnostic clues provided by the direct arte-rial pressure waveform requires understanding of normal waveform components, their relationship to the cardiac cycle, and the implications of waveform variations when recorded from different arterial sites.

The systemic arterial pressure waveform results from ejection of blood from the left ventricle into the aorta during systole, followed by peripheral runoff during dias-tole. The systolic waveform components consist of a steep pressure upstroke, peak, and ensuing decline, and imme-diately follow the ECG R wave. The downslope of the arterial pressure waveform is interrupted by the dicrotic notch, continues its decline during diastole after the ECG T wave, and reaches its nadir at end-diastole (Fig. 45-9). The dicrotic notch, known as the incisura when recorded at the central aorta (from the Latin, meaning “a cutting into”) is sharply defined and thought to result from aortic valve closure.82 In contrast, more peripheral arterial waveforms generally display a later, more blunted dicrotic notch that is more dependent on properties of the arterial wall. Note that the systolic upstroke starts 120 to 180 milliseconds after beginning of the R wave (see Fig. 45-9). This interval reflects total time required for depo-larization of the ventricular myocardium, isovolumic left ventricular contraction, opening of the aortic valve, left ventricular ejection, propagation of the aortic pressure wave, and finally, transmission of the signal to the pres-sure transducer.

The bedside monitor displays values for the peak sys-tolic and end-diastolic nadir pressures. MAP is dependent on the algorithm used by the monitor. In simplest terms, MAP is equal to the area beneath the arterial pressure

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curve divided by the beat period, averaged over multiple cardiac cycles. Although MAP is often estimated as dia-stolic pressure plus one third times pulse pressure, this estimate is only valid at slower heart rates, because the proportion of the cardiac cycle spent in diastole decreases as the heart rate increases.83

An important feature of the arterial pressure wave-form is distal pulse amplification. Pressure waveforms recorded simultaneously from different sites have dif-ferent morphologies due to the physical characteristics of the vascular tree, namely, impedance and harmonic resonance31,81 (Fig. 45-10). As the pressure wave trav-els from the central aorta to the periphery, the arterial upstroke becomes steeper, the systolic peak increases, the dicrotic notch appears later, the diastolic wave becomes more prominent, and end-diastolic pressure decreases. As a result, compared with central aortic pressure, peripheral arterial waveforms have higher systolic, lower diastolic, and wider pulse pressures. Furthermore, as the signal is delayed in arriving at the peripheral site, the systolic pres-sure upstroke begins approximately 60 milliseconds later in the radial artery than in the aorta. MAP in the aorta is only slightly higher than that in the periphery.

Reflection of pressure waves within the arterial tree has a great impact on changes to the arterial pressure wave-form as it travels peripherally.81 As blood flows from the aorta to the radial artery, mean pressure decreases only slightly because there is little resistance to flow in the major conducting arteries. At the arteriolar level, though, mean blood pressure decreases markedly as a result of a dramatic increase in vascular resistance. This resistance to flow diminishes pressure pulsations in smaller down-stream vessels but augments upstream arterial pressure pulses by way of pressure wave reflection.84 The summa-tion of these antegrade and reflected waves determine

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Figure 45-9. Normal arterial blood pressure waveform and its rela-tion to the electrocardiographic R wave. (1) Systolic upstroke, (2) sys-tolic peak pressure, (3) systolic decline, (4) dicrotic notch, (5) diastolic runoff, and (6) end-diastolic pressure. (From Mark JB: Atlas of cardio-vascular monitoring, New York, 1998, Churchill Livingstone.)

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the shape of the arterial pulse wave recorded from dif-ferent arterial sites. For example, reduced arterial compli-ance causes premature return of reflected pressure waves, resulting in arterial pressure waveforms with increased pulse pressure, a late systolic pressure peak, attenuated diastolic pressure waves, and at times, an early systolic hump distorting the smooth upstroke (Fig. 45-11).

From these considerations, the morphology of the arterial waveform and the precise values of systolic and diastolic blood pressure vary throughout the arterial sys-tem under normal conditions in otherwise healthy indi-viduals. These variations are augmented and at times greatly exaggerated by various factors, including but not limited to age, pathologic processes, and pharmacologic interventions.

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Figure 45-10. Distal pulse wave amplification of the arterial pres-sure waveform. Compared with pressure in the aortic arch, the more peripherally recorded femoral artery pressure waveform demonstrates a wider pulse pressure (compare 1 and 2), a delayed start to the sys-tolic upstroke (3), a delayed, slurred dicrotic notch (compare arrows), and a more prominent diastolic wave. (From Mark JB: Atlas of cardio-vascular monitoring, New York, 1998, Churchill Livingstone.)

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Figure 45-11. Impact of pressure wave reflection on arterial pres-sure waveforms. In older individuals with reduced arterial compliance, early return of peripherally reflected waves increases pulse pressure, produces a late systolic pressure peak (arrow), attenuates the diastolic pressure wave, and at times, distorts the smooth upstroke with an early systolic hump.



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Figure 45-12. Arterial pressure gradients following cardiopulmonary bypass. A, Femoral and radial artery pressure traces recorded 2 minutes after bypass (2 min post-bypass), when radial artery pressure underestimates the more centrally measured femoral artery pressure and 30 minutes later (30-min post-bypass), when radial and femoral arterial pressures have equalized and radial pressure has resumed a more typical morphol-ogy. Note that dicrotic notch (arrows) is visible in the femoral pressure trace immediately after bypass, but is delayed in the radial pressure trace. B, Femoral and radial artery pressure traces recorded before cardiopulmonary bypass (pre-bypass), 2 minutes following bypass (2 min post-bypass), and 30 minutes following bypass (30 min post-bypass). Note changing relationship between femoral and radial artery pressure measure-ments at these different times.

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Arterial Blood Pressure GradientsA number of pathophysiologic conditions cause exag-gerated arterial pressure gradients between monitoring sites, be they real, iatrogenic, or artifactual. Frank and co-workers demonstrated that 21% of patients undergo-ing peripheral vascular surgery had a blood pressure dif-ference between the two arms that exceeded 20 mm Hg.85 Clearly, monitoring blood pressure in an arm that has yielded a lower NIBP measurement or has a weaker pal-pable pulse will likely lead to errors in measurement and perhaps management. Atherosclerosis or pathologic con-ditions such as arterial dissection, stenosis, or embolism may preclude accurate pressure monitoring from affected sites. In addition, unusual patient positions during sur-gery may produce regional arterial compression, whereas surgical retraction can compromise perfusion and moni-toring to a more localized area.86,87

The nature of the operative procedure is important when choosing the appropriate site for arterial pressure monitoring. Procedures requiring placement of a descend-ing thoracic aortic cross-clamp may interrupt arterial flow to the left subclavian artery, perfusion to the left arm, and


all vessels distal to the clamp unless some form of bypass is used. In such cases, blood pressure monitored in the right arm provides the best estimate of aortic root and carotid arterial pressure. Femoral artery pressure may be monitored simultaneously to estimate perfusion pressure distal to the aortic cross-clamp.

Significant physiologic disturbances, such as sepsis or shock, may produce generalized arterial pressure gradi-ents that can affect the choice of site for arterial pressure monitoring. In patients receiving vasopressor infusions for septic shock, the femoral arterial pressure was noted to exceed the radial pressure by more than 50 mm Hg.88 Such gradients, albeit less severe, have been noted with anesthetics, neuraxial blocks, and changes in patient tem-perature.31 During hypothermia, thermoregulatory vaso-constriction causes systolic pressure in the radial artery to exceed that in the femoral artery, whereas during rewarming, vasodilation reverses the gradient.89

Characteristic gradients between central and peripheral sites have been described in cardiac surgery patients under-going cardiopulmonary bypass (Fig. 45-12) (see Chapter 67). The mean radial artery pressure decreases on initiation



of bypass and remains less than mean femoral artery pres-sure throughout the bypass period.90 Notably, this pattern persists in the first few minutes following separation from bypass, often by more than 20 mm Hg.91 In most patients, this gradient resolves within the first hour, but occasion-ally, it remains well into the postoperative period.

Abnormal Arterial Pressure WaveformsDetailed examination of the morphologic features of indi-vidual arterial pressure waveforms can provide important diagnostic information (Table 45-1) (Fig. 45-13, A to D). Aortic stenosis produces a fixed obstruction to ejection

TABLE 45-1 ARTERIAL BLOOD PRESSURE WAVEFORM ABNORMALITIES

Condition Characteristics

Aortic stenosis Pulsus parvus (narrow pulse pressure)Pulsus tardus (delayed upstroke)

Aortic regurgitation Bisferiens pulse (double peak)Wide pulse pressure

Hypertrophic cardiomyopathy

Spike and dome (mid-systolic obstruction)

Systolic left ventricular failure

Pulsus alternans (alternating pulse pressure amplitude)

Cardiac tamponade Pulsus paradoxus (exaggerated decrease in systolic blood pressure during spontaneous inspiration)


resulting in reduced stroke volume and a slowed rate of ejection. As a result, the waveform is small in amplitude (pulsus parvus), and has a slowly rising systolic upstroke on the arterial pressure waveform and a delayed peak in systole (pulsus tardus) (see Fig. 45-13, B). A distinct shoul-der, termed the anacrotic notch, often distorts the pres-sure upstroke and even the dicrotic notch may not be discernible. These features may make the arterial pressure waveform appear overdamped.

In aortic regurgitation, the arterial pressure wave dis-plays a sharp increase, wide pulse pressure, and decreased diastolic pressure owing to the runoff of blood into both the left ventricle and the periphery during diastole. The arterial waveform may have two systolic peaks (bisferiens pulse), with the first peak resulting from antegrade ejec-tion and the second from a reflected wave originating in the periphery (see Fig. 45-13, C). In hypertrophic car-diomyopathy, the arterial pressure waveform assumes a peculiar bifid shape termed a spike-and-dome con-figuration. After an initial sharp blood pressure increase resulting from rapid, early systolic ejection, arterial pres-sure plummets as left ventricular outflow obstruction in mid-systole impedes ejection. This is finally followed by a second, late-systolic increase associated with arrival of reflected waves from the periphery (see Fig. 45-13, D).

Observation of how arterial waveform patterns change over time is another source of useful information. Pulsus alternans is a pattern of alternating beats of larger and

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Figure 45-13. Influence of pathologic conditions on arterial pressure (ART) waveform morphology. A, Normal ART and pulmonary artery pres-sure (PAP) waveform morphologies demonstrating the similar timing of these waveforms relative to the electrocardiographic R wave. B, In aortic stenosis, the ART waveform is distorted with a slurred upstroke and delayed systolic peak. These changes are particularly striking in comparison with the normal PAP waveform. Note the beat-to-beat respiratory variation in the PAP waveform. For A and B, the ART scale is on the left and the PAP scale is on the right. C, Aortic regurgitation produces a bisferiens pulse and a wide pulse pressure. D, Arterial pressure waveform in hyper-trophic cardiomyopathy shows a peculiar spike-and-dome configuration. The waveform assumes a more normal morphology following surgical correction of this condition. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)



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smaller pulse pressures that also vary with the respiratory cycle although its underlying mechanism remains poorly understood (Fig. 45-14, A). It may be a sign of severe left ventricular systolic dysfunction but can also be seen in patients with advanced aortic stenosis. Pulsus alternans should be distinguished from bigeminal rhythms, which are usually ventricular in origin. Although both appear as alternating pulse pressures in the arterial pressure wave-form, pulsus alternans presents a regular rhythm.

Pulsus paradoxus is exaggerated variation in arterial pressure (<10 to 12 mm Hg) during quiet breathing92,93 (Fig. 45-14, B). Pulsus paradoxus is not truly paradoxical, but rather an exaggeration of a normal variation in blood pressure that accompanies spontaneous ventilation. Pul-sus paradoxus is highly characteristic, almost universal, in patients with cardiac tamponade but may also develop with pericardial constriction, severe airway obstruction, bronchospasm, dyspnea, or any condition that involves large swings in intrathoracic pressure. It is important to note, though, that in cases of cardiac tamponade, the pulse pressure and left ventricular stroke volume decrease during inspiration, in contrast to the arterial blood pres-sure changes observed in patients with forced breathing patterns and exaggerated changes in intrathoracic pres-sure in which pulse pressure remains constant.94

ARTERIAL PRESSURE MONITORING AND WAVEFORM ANALYSIS FOR PREDICTION OF INTRAVASCULAR VOLUME RESPONSIVENESSS

The starting point for hemodynamic resuscitation begins with optimizing cardiac preload, or more precisely,

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determining whether a specific patient has sufficient residual preload reserve. The limitations of static indica-tors of preload such as central venous pressure are well documented, as are the array of factors that confound their interpretation.95 Newer dynamic markers of preload reserve and intravascular volume responsiveness have been studied for their ability to discriminate between those who would and those who would not benefit from volume expansion. Variations in arterial blood pressure observed during positive pressure ventilation, as well as a variety of derived indices, are the most widely studied of these dynamic indicators. Such changes in blood pressure may be visible on the bedside monitor in patients who are receiving direct arterial blood pressure monitoring, and they result from changes in intrathoracic pressure and lung volume that occur during the respiratory cycle.

During positive pressure ventilation, increases in lung volume compress lung tissue and displace blood con-tained within the pulmonary venous reservoir into the left heart chambers, thereby increasing left ventricular preload. Simultaneously, the increase in intrathoracic pressure reduces left ventricular afterload. The increase in left ventricular preload and decrease in afterload produce an increase in left ventricular stroke volume, an increase in cardiac output, and in the absence of changes in periph-eral resistance, an increase in systemic arterial pressure. In most patients the preload effects are more prominent, but in patients with severe left ventricular systolic failure, the reduction in afterload plays an important role in increas-ing ventricular ejection. Simultaneously with increasing left heart filling during early inspiration, rising intratho-racic pressure causes a decrease in systemic venous return and right ventricular preload. The increased lung volume

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Figure 45-14. Beat-to-beat variability in arterial pressure waveform morphologies. A, Pulsus alternans. B, Pulsus paradoxus. The marked decline in both systolic blood pressure and pulse pressure during spontaneous inspiration (arrows) is characteristic of cardiac tamponade. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)

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Figure 45-15. Systolic pressure variation. Compared with systolic blood pressure recorded at end expiration (1) a small increase occurs during positive-pressure inspiration (2, Δ Up) followed by a decrease (3, Δ Down). Normally, systolic pressure variation does not exceed 10 mm Hg. In this instance, the large Δ Down indicates hypovolemia even though systolic arterial pressure and heart rate are relatively normal. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)

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may also increase pulmonary vascular resistance slightly and thereby increase right ventricular afterload. These effects combine to reduce right ventricular ejection dur-ing early inspiration. During early expiration, the situ-ation is reversed. The smaller amount of blood ejected from the right ventricle during inspiration traverses the pulmonary vascular bed and enters the left heart, result-ing in reduced left ventricular filling. Left ventricular stroke volume falls, and systemic arterial blood pressure decreases. This cyclic variation in systemic arterial pres-sure is known as the systolic pressure variation (SPV).

SPV is often subdivided into inspiratory and expira-tory components by measuring the increase (Δ Up) and decrease (Δ Down) in systolic pressure relative to the end-expiratory, apneic baseline pressure (Fig. 45-15). In a mechanically ventilated patient, normal SPV is 7 to 10 mm Hg, with Δ Up being 2 to 4 mm Hg and Δ Down being 5 to 6 mm Hg.96 This observation has been used clinically in attempts to identify hypovolemic patients.97 Both in experimental animals and critically ill patients, hypovo-lemia causes a dramatic increase in SPV, particularly the Δ Down component. However, it may be more accurate to describe the patients identified by increased SPV as having residual preload reserve. Although not identical to hypovolemia, preload reserve describes a physiologic state in which intravascular volume expansion or fluid challenge shifts the patient upward on the Frank-Starling curve, resulting in increased stroke volume, and increased cardiac output as long as systemic vascular resistance remains unchanged.

In a heterogeneous group of intensive care patients, Marik demonstrated that a large SPV (>15 mm Hg) was highly predictive of a low pulmonary artery wedge pres-sure (PAWP) (<10 mm Hg).98 Using echocardiography to measure the left ventricular cross-sectional area as a sur-rogate for preload, Coriat and colleagues found Δ Down to be a better predictor of preload than wedge pressure.99 Using receiver-operator curve analysis, Tavernier and co-workers showed that compared with PAWP or left ventric-ular end-diastolic area, Δ Down was a far better indicator of volume responsiveness.100

Another dynamic marker of preload reserve is pulse pressure variation (PPV). Many automated devices are now available that provide real-time PPV, and although calculated according to slightly different and proprietary algorithms, PPV should not exceed 13% to 17%101-105

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(Fig. 45-16). In addition to SPV and PPV, more sophisti-cated pulse contour methods for measurement of cardiac output (see later) allow online measurement of variations in stroke volume variation (SVV). As with other dynamic indicators of preload reserve, normal SVV is approxi-mately 10% to 13%, whereas greater variability predicts a positive response to volume expansion.104,106 Although SVV may be theoretically superior to PPV, clinical studies have not borne this out.104

Devices based on respiratory cycle–induced varia-tion in the pulse plethysmogram have been developed as a less invasive but similar alternative. Measures such as photoplethysmography variation (ΔPOP) or the pleth-ysmography variability index (PVI) appear to be useful when conditions are good, but this particular physiologic signal is even more subject to confounding influences than arterial blood pressure waveform.103,107,108 Both numeric pulse oximetry and the photoplethysmogra-phy waveform are sensitive to sympathetic variations in regional circulation, especially in the skin and extremities in critically ill patients. Tidal volume, core and peripheral temperature, ambient light, and cardiac dysrhythmias pose significant impediments to valid and reproducible data collection and interpretation. There is no consen-sus regarding meaningful threshold values, and validity seems especially poor in children, under conditions of

PPMax =150−70=80PPMin =120−60=60PPV =(PPMax−PPMin)/([PPMax+PPMin]/2)PPV =80−60/([80+60]/2)=29%

Note: The arterial blood pressure tracing is not drawn to scale

PPMax

PPMin

Figure 45-16. Pulse pressure variation. Pulse pressure variation (PPV) is calculated as the difference between maximal (PPMax ) and minimal (PPMin ) pulse pressure values during a single mechanical respiratory cycle, divided by the average of these two values. (Note that the arte-rial blood pressure trace is drawn for illustrative purposes and not to scale.)



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mechanical ventilation in a sedated but not paralyzed patient, and in the setting of an open abdomen.108 Fur-thermore, there are sophisticated autogaining features incorporated in most commercially available monitoring systems to optimize signal display. As such, the degree of variation visible to the naked eye may not correlate with true signal variation, resulting in erroneous clinical decisions.

Dynamic measures are significantly superior to static indices of intravascular volume and are more valuable for making informed clinical decisions, especially in critically ill patients. Both PVV and SVV are accurate fol-lowing cardiac surgery (also see Chapter 67) in patients with normal and reduced ventricular function, whereas PPV was proved accurate in assessing intravascular fluid responsiveness in patients with septic shock.109,110 Intraoperative use has also been examined with similar results.111,112 Indeed, the ability of clinicians to “eye-ball” respiratory variation in the arterial blood pressure waveform as displayed on the monitor seems reasonably accurate. Subjective estimates of such pressure varia-tion were incorrect only 4.4% of the time, a rate that would have resulted in only 1% of treatments being erroneous.105

Newer automated monitors have obviated the need to interrupt mechanical ventilation and establish an apneic baseline in order to differentiate Δ Up from Δ Down and are able to continuously display PPV or SVV.96,113,114 How-ever, the automated nature of these monitors makes it important to recognize clinical conditions under which their use was validated. The magnitude of arterial blood pressure variation observed is influenced by positive-pressure ventilation variables, and most patients are no longer routinely ventilated in a manner similar to that in the supporting clinical studies. In general, mechanical ventilation with tidal volumes of 8 to 10 mL/kg, positive end-expiratory pressure of 5 mm Hg or greater, regular cardiac rhythm, normal intraabdominal pressure, and a closed chest are necessary to duplicate the experimental conditions. Also, effects of changes in patient position such as steep Trendelenberg or the lateral position are not clear.104 In addition, patients with pulmonary hyperten-sion or reduced right ventricular ejection fraction may not have reliable responses to changes in intrathoracic pressure, resulting in overhydration and worsening right heart failure.115 Increased respiratory rates, especially when coupled with respiratory failure or significant bra-dycardia, may disrupt the relationship between respira-tory cycle–induced changes in intrathoracic pressure and cardiac chamber volume, thus invalidating the theoretic basis for blood pressure variation analysis completely in these patients.104

As noted earlier, respiratory cycle–induced arterial pressure variations are not solely related to changes in left ventricular preload, but also depend in part on changes in afterload. Indeed, decreased arterial compliance and increased baseline pulse pressure seen with both normal and pathologic vascular aging results in an exaggerated PPV response to changes in stroke volume due to any stimulus. As such, PPV thresholds should be higher in such patients than in those with more elastance in their vascular tree.116,117

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There is disagreement on precise threshold values that differentiate responders from nonresponders, and the variety of techniques, devices, and approaches have not been standardized.103 In a recent systematic review, mean discriminatory thresholds for PVV and SVV were found to be 12.5% ± 1.6% and 11.6% ± 1.9%, respectively, with acceptable sensitivities and specificities (89%, 88% and 82%, 86%, respectively).118 However, simply differentiat-ing patients into responders and nonresponders does not take into account the nature of the clinical intervention at issue. Intravascular volume expansion does not result in a dichotomous outcome; it does not yield a simple posi-tive or negative result with an equivalent range of values on each side. The asymmetric nature of the Frank-Star-ling curve dictates that the cost-benefit ratio of acting in one direction will be different from acting in the other. Any particular change in preload will result in a differ-ent change in stroke volume in one direction than in the other, with the differential change being dependent on how close to the peak of the curve the patient begins. Consequently, the concept of the “gray zone” has been proposed, in which two cutoffs are identified, two values between which evidence-based decision making is not possible.119 For PPV, this zone has been described as 9% to 13%, such that those below 9% should receive intravascu-lar volume expansion, whereas those above 13% should not. For those between the two values, the measurement is not able to provide meaningful information and the decision should be made on other criteria.104,120

CENTRAL VENOUS PRESSURE MONITORING

Cannulation of a central vein and direct measurement of central venous pressure (CVP) are frequently performed in hemodynamically unstable patients and those under-going major operations. A central venous catheter may be inserted to provide secure vascular access for many reasons, including administration of vasoactive drugs or fluids, CVP monitoring, transvenous cardiac pacing, tem-porary hemodialysis, pulmonary artery catheterization, or aspiration of entrained air. A central venous catheter may also be inserted when no peripheral access can be obtained or when repeated blood sampling is required (Box 45-4).

CENTRAL VENOUS CANNULATION

When intraoperative cannulation is required, the deci-sion to perform central venous cannulation before or after induction of anesthesia is guided most often by indi-vidual patient and physician preferences or institutional practice. Preoperative central venous cannulation should be terminated in any patient who becomes overly sedated or uncooperative during the procedure. The need for cen-tral venous cannulation can be reevaluated after induc-tion of anesthesia and intubation of the trachea.

Choosing the Catheter, Site, and Method for Central Venous CannulationchoosiNg the catheter. Central venous catheters come in a variety of lengths, diameter, composition, and lumen

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configuration.121,122 Different catheters are chosen accord-ing to the purpose of catheterization, whether for CVP monitoring or other therapeutic indication, and whether intended for short- or long-term use. The most com-monly used catheter is a 7-Fr, 20-cm multiport catheter that allows simultaneous CVP monitoring and infusion of drugs and fluids.123 Rapid intravascular fluid resusci-tation is most efficient with short, large-bore, peripheral intravenous catheters, because central venous catheters are longer and have narrower individual lumina, signifi-cantly increasing resistance to flow. For example, accord-ing to the manufacturer’s product specifications, the maximal flow rate of the 16-gauge lumen of a standard 7-Fr 20-cm central venous catheter is one quarter that of a 16-gauge, 3-cm intravenous catheter.

A popular alternative method for multilumen cen-tral venous access uses a large introducer sheath with one or two integrated ports for multiple drug infusions, combined with a single-lumen catheter inserted through the hemostasis valve for continuous CVP monitoring. Although use of these larger introducer sheaths is not free from complications, they do allow rapid placement of a pacing wire or pulmonary artery catheter should the need arise.

choosiNg the iNsertioN site. Selecting the best site for central venous cannulation requires consideration of the indication for catheterization (pressure monitoring ver-sus drug or fluid administration), the patient’s underlying medical condition, the clinical setting, and the skill and experience of the clinician performing the procedure. In patients with severe bleeding diatheses, a puncture site should be selected where bleeding from the vein or adja-cent artery is easily detected and controlled with local compression. In such a patient, an internal or external jugular approach would be preferable to a subclavian site. Likewise, patients with severe emphysema or others who would be severely compromised by a pneumothorax would be better candidates for internal jugular than subclavian cannulation, owing to the more frequent pneumothorax risk with the latter approach. If transvenous cardiac pacing

Central venous pressure monitoringPulmonary artery catheterization and monitoringTransvenous cardiac pacingTemporary hemodialysisDrug administration • Concentrated vasoactive drugs • Hyperalimentation • Chemotherapy • Agents irritating to peripheral veins • Prolonged antibiotic therapy (e.g., endocarditis)Rapid infusion of fluids (via large cannulas) • Trauma • Major surgeryAspiration of air emboliInadequate peripheral intravenous accessSampling site for repeated blood testing

BOX 45-4 Indications for Central Venous Cannulation

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is required in an emergency situation, catheterization of the right internal jugular vein is recommended, because it provides the most direct route to the right ventricle. Trauma patients, with their necks immobilized in a hard cervical collar, are best resuscitated using a femoral or sub-clavian catheter; the latter may be placed even more safely if the risk of pneumothorax is obviated by prior placement of a thoracostomy tube. The physician must recognize that the length of catheter inserted to position the catheter tip properly in the superior vena cava will vary according to puncture site, being slightly (3 to 5 cm) greater when the left internal or external jugular veins are chosen, compared with the right internal jugular vein.124 Finally, a physi-cian’s personal experience undoubtedly plays a significant role in determining the safest site for central venous can-nulation, particularly when the procedure is performed under urgent or emergent circumstances.

Since its introduction into clinical practice in the late 1960s, percutaneous puncture of the right internal jugular vein has been the method preferred by anesthe-siologists for central venous cannulation.125-127 Reasons for this preference include the consistent, predictable anatomic location of the internal jugular vein, readily identifiable and palpable surface landmarks, and a short straight course to the superior vena cava. An internal jug-ular vein catheter is highly accessible during most surgi-cal procedures and has a high rate of successful placement (90% to 99%).126,128

Left internal jugular vein cannulation may be accom-plished reliably and safely, although several anatomic details make the left side less attractive than the right. The cupola of the pleura is higher on the left, theoreti-cally increasing the risk of pneumothorax. The thoracic duct may be injured during the procedure as it enters the venous system at the junction of the left internal jugular and subclavian veins.129 The left internal jugular vein is often smaller than the right and demonstrates a greater degree of overlap of the adjacent carotid artery.130 Most important, any catheter inserted from the left side of the patient must traverse the innominate (left brachio-cephalic) vein and enter the superior vena cava perpen-dicularly. As a result, the catheter tip may impinge on the right lateral wall of the superior vena cava, increas-ing the risk of vascular injury. This anatomic disadvan-tage pertains to all left-sided catheterization sites and highlights the need for radiographic confirmation of proper catheter tip location. Finally, most operators have less experience performing left internal jugular vein cannulation, which leads to more adverse events and morbidity.131,132

The subclavian vein is an important site for central venous cannulation and is particularly popular among surgeons and other physicians who place central venous catheters for emergency volume resuscitation and long-term intravenous therapy or dialysis, rather than for shorter-term monitoring purposes.133,134 Advantages of subclavian venous cannulation include a less frequent risk of infection compared with femoral sites, ease of insertion in trauma patients who may be immobilized in a cervical collar, and increased patient comfort, especially for long-term intravenous therapy, such as hyperalimen-tation and chemotherapy.135,136

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Both the right and left external jugular veins provide safe, albeit somewhat technically challenging, alternatives to internal jugular or subclavian vein cannulation. Because the external jugular veins are superficial, they allow central venous cannulation with essentially no risk of pneumo-thorax or unintended arterial puncture. In most instances, it is best to use an 18-gauge catheter rather than the thin-wall needle to introduce the guidewire (i.e., the modified Seldinger, as opposed to the Seldinger technique), because of the tortuous course of the external jugular vein and the frequent need to manipulate the guidewire repeatedly to guide it into the superior vena cava. A J-tip guidewire should always be used, because it may be advanced under the clavicle and into the central circulation more success-fully than a straight-tip wire.137,138 When the guidewire does not advance as desired and appears to be moving peripherally into the subclavian vein, abducting the ipsi-lateral shoulder beyond 90 degrees before advancing the wire may facilitate central venous passage. Alternatively, the patient’s ipsilateral arm is placed at the side, and an assistant applies mild caudad traction on the shoulder to straighten the course of the external jugular vein while the wire is advanced. Essentially, the only factors that pre-clude use of the external jugular veins for CVP monitoring are an inability to visualize and cannulate the vessel in the neck and to advance a catheter into the central cir-culation. Advancing catheters and stiff dilators into the external jugular vein requires extreme caution. The cath-eter needs to travel around the sharp angle in the vein as it enters the subclavian vein. This may be the site for venous injury if undue force is used during insertion of the cath-eter. Not surprisingly, approximately 20% of the problems occur in attempted external jugular central venous cath-eterizations, thus limiting more widespread application of this technique.139,140

Femoral vein cannulation is useful when the more common jugular and subclavian sites are not accessible, as is commonly the case in patients with burns, with trauma, during surgical procedures that involve the head, neck, and upper thorax, or during cardiopulmonary resuscita-tion (also see Chapters 85, 66, and 108). Use of the femo-ral vein obviates many of the common complications of central venous catheterization, particularly pneumotho-rax, but it also carries the risk of injury to the femoral artery and, more rarely, the femoral nerve. Femoral veni-puncture using the landmark technique is performed below the inguinal ligament just medial to the palpated femoral arterial pulse. Central venous pressure measure-ments may be made using longer (40 to 70 cm) catheters that reside in the inferior vena or with shorter (15 to 20 cm) catheters that terminate in the common iliac vein. Both provide CVP measurements that correlate with right atrial pressure, although the shorter more distally located catheters appear to provide wider variations in CVP val-ues.141,142 This holds true in both mechanically and spon-taneously ventilated patients.142,143 Disadvantages of the femoral venous route include increased risk of thrombo-embolic complications, as well as vascular injury that may lead to intraabdominal or retroperitoneal hemorrhage.144 In addition, patients with femoral vascular catheters are generally unable to ambulate, which can delay and com-plicate postoperative recovery.

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In patients with extensive, severe burn injuries, the axillary region is often spared and provides a useful site for either arterial or venous pressure monitoring.145 Stan-dard 20-cm CVP catheters placed in the axillary vein, approximately 1 cm medial to the palpated axillary artery, allow pressure measurement from the superior vena cava. Even more distal pressures measured from peripheral veins in the hand and forearm may provide a reasonably accurate estimate of CVP in selected surgical patients.146 Modified volumetric infusion pumps can even measure in-line peripheral venous pressures without the need for additional transducers and monitoring equipment.147 Although this method of measuring CVP incurs no risk beyond that associated with placing any standard periph-eral intravenous catheter, it has not been validated widely and cannot replace central venous cannulation in most circumstances.

Peripherally inserted central venous catheters (PICC) have become a popular alternative to centrally inserted catheters in patients requiring long-term intravenous therapy. Advantages of the PICC include bedside place-ment under local anesthesia, extremely low risk of major insertion-related complications, and safe placement by non-physicians (i.e., registered nurses and physician assistants). This technique may be particularly cost-effec-tive, because it eliminates the need for a minor opera-tive procedure in those patients who require a Hickman or Broviac central venous catheter.148 Venous access for a PICC is obtained through an antecubital vein, prefer-ably the basilic vein, which is generally more successfully catheterized than the cephalic vein due to its more lin-ear course. Early reports described only modest success with positioning PICCs in an appropriate central location as well as a considerable risk of venous thrombosis, but improvements in catheter design and insertion technique now result in successful placement with few complica-tions in most patients.148-150 Most PICCs are inserted for long-term therapeutic indications (chemotherapy or par-enteral nutrition), using very flexible, nonthrombogenic silicone catheters. Less commonly, a standard polyure-thane 40-cm intravenous catheter is inserted peripherally and advanced to a central location for short-term infu-sion of vasoactive drugs or monitoring CVP or PAP. Cen-tral venous pressure recorded via PICCs is slightly higher than the pressure measured using centrally inserted catheters, but this difference is clinically insignificant.151 When these standard long venous catheters are inserted from an antecubital vein, the catheter tip may advance into the heart as the arm is abducted, thereby increas-ing the risk of cardiac perforation or arrhythmias.152,153 Whenever a PICC line is in place, the clinician should cautiously place any additional central venous catheters because of the risk of shearing the PICC line within the central venous circulation.

choosiNg the ceNtral veNous caNNulatioN methoD. A central vein may be cannulated using either a landmark technique or ultrasound guidance. Ultrasound technol-ogy is rapidly gaining acceptance, and numerous specialty groups and governmental agencies have issued practice recommendations for its use during central line place-ment.154-156 See other sources for detailed descriptions

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A CB

Figure 45-17. A, Transverse plane ultrasound image showing the right internal jugular vein and its typical anatomic position anterior and lateral to the right common carotid artery. B, Needle entering the right internal jugular vein. It is essential that the operator directly visualize the needle entering the vessel lumen, as shown here, to avoid inadvertent puncture of the posterior wall of the vein. C, The wire is seen as an echodense structure within the vessel lumen. Confirmation of the location of the wire should always precede the use of the vessel dilator.

ber

and tutorials on the various insertion techniques for dif-ferent access sites using surface landmarks.123,157

Regardless of the insertion technique used or the can-nulation site chosen, certain general principles should be emphasized for all central line placements. Ideally, a protocol or checklist describing the basic procedural steps for central line insertion should be in place at every insti-tution, and all staff members should feel empowered to speak up when they witness a protocol violation. Stan-dardized equipment, routine use of an assistant, hand washing and maximal barrier precautions all contribute to the sterility of the procedure.154 The use of real-time ultrasound guidance for vessel localization and venipunc-ture should be strongly considered, especially when the internal jugular vein site is selected. Pressure manometry or waveform measurement should be used to confirm venous placement of the catheter before use. Finally, the position of the catheter tip should be verified as soon as clinically appropriate to avoid delayed complications (see later).

Ultrasound-Guided Central Venous CannulationFirst described in 1984, ultrasound-guided central venous catheter placement has proved beneficial in most set-tings, including the intensive care unit and the operating room156,158 (also see Chapter 58). Fewer needle passes are required for successful venous cannulation when real-time two-dimensional ultrasound guidance is used. In addition, ultrasound guidance reduces the time required for catheterization, increases overall success rates, and results in fewer immediate complications.159,160 The ben-efits of ultrasound-guided catheterization are clear for internal jugular vein catheters, when inexperienced oper-ators perform the procedure, and for adult rather than pediatric patients. Based on this evidence, the Agency for Healthcare Research and Quality has listed the use of real-time ultrasound guidance for central venous catheteriza-tion as one of 11 practices to improve health care.155 It is unknown whether the additional equipment and manip-ulation associated with real-time ultrasound guidance may increase the rate of catheter-related infections or whether the increased dependence on this technology by trainees will prove detrimental in those clinical settings.

As an alternative to real-time ultrasound-guided cath-eterization, ultrasound can be used to confirm vessel

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location and patency, provide a clear target to mark the skin, and then allow venipuncture to proceed in the usual fashion.154,161

Real-time, two-dimensional ultrasound guidance for internal jugular vein cannulation requires a 7.5- to 10-MHz transducer. A rapid ultrasound scan should be performed once the patient is placed in the Trendelen-burg position and before the skin is cleansed to identify the target vein location, confirm its patency, and rule out anatomic abnormalities. This simple step is aimed at avoiding futile insertion attempts when the patient has a thrombosed, narrowed, or anomalous central vein.

Once the site is prepped and draped, the operator holds the ultrasound probe protected by a sterile sheath with the nondominant hand to obtain a view of the tar-get vessel. The vein and artery appear as two circular black structures on the ultrasound image. The vein is identi-fied by anatomic location and by its compressibility. The artery appears mildly pulsatile, is generally smaller, and has a thicker wall (Fig. 45-17, A). When using ultrasound guidance, either the transverse (short axis) or longitudi-nal (long axis) view is adequate. In general, the transverse view is easier to learn and allows simultaneous identifi-cation of the artery and vein, whereas the longitudinal view allows visualization of the needle tip at all times, which may reduce perforation of the posterior wall of the vein.162 After positioning the vein in the center of the ultrasound screen, the vessel is punctured under direct vision using an 18-gauge needle (see Fig. 45-17, B) and then proceeds as a standard Seldinger (wire through needle) or modified Seldinger (wire through catheter) technique. An additional recommended safety stop is to confirm intravenous location of the guidewire before pro-ceeding with vessel dilation (see Fig. 45-17, C).

Ultrasound imaging of the subclavian vessels is more difficult and often hampered by the patient’s body hab-itus and ultrasound probe size and shape. When using ultrasound to guide subclavian vein cannulation, the transducer is placed in the infraclavicular groove at the level of the middle or lateral third of the clavicle and the axillary vein and artery are imaged as they exit the bony canal formed by the clavicle and the first rib.163 The artery is usually identified by its location cephalad to the vein, its noncompressibility, and its not varying size with res-pirations. Either a transverse or longitudinal view can be obtained and used to guide needle insertion.164 Another

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approach has been described for children in whom the probe is placed in the supraclavicular space to obtain a longitudinal view of the subclavian vein while cannula-tion is performed via the usual infraclavicular route165 (also see Chapter 93).

Confirming Catheter PositionCentral venous catheters placed in the operating room are commonly used for the duration of the surgical procedure without radiologic confirmation of the location of the catheter tip. Before monitoring or infusion commences, aspiration of blood should confirm intravenous location of each lumen of a multilumen catheter and remove any residual air from the catheter-tubing system. Following surgery, however, the position of the catheter tip must be confirmed radiographically. Catheter tips located within the heart or below the pericardial reflection of the supe-rior vena cava increase the risk of cardiac perforation and fatal cardiac tamponade. Ideally, the catheter tip should lie within the superior vena cava, parallel to the vessel walls, and be positioned below the inferior border of the clavicles and above the level of the third rib, the T4 to T5 interspace, the azygos vein, the tracheal carina, or the takeoff of the right mainstem bronchus.166,167 Using fresh human cadavers, Albrecht and colleagues confirmed that the tracheal carina was always more cephalad than the pericardial reflection on the superior vena cava, suggest-ing that a central venous catheter tip should always be located superior to this radiographic landmark.168

COMPLICATIONS OF CENTRAL VENOUS PRESSURE MONITORING

Complications of central venous cannulation are becom-ing increasingly recognized as major sources of morbid-ity, with more than 15% of patients experiencing some sort of related adverse event.144 Although serious immedi-ate complications are infrequent when these procedures are performed by well-trained, experienced clinicians, infectious complications are common, and use of central venous catheters continues to result in significant mor-bidity and mortality. Complications are often divided into mechanical, thromboembolic, and infectious etiolo-gies (Box 45-5).

Mechanical Complications of Central Venous CatheterizationThe incidence of complications depends on a number of factors, including the catheter insertion site and the patient’s medical condition. Large retrospective and observational studies provide the best estimates of inci-dence for these types of complications.

Vascular injuries from central venous catheterization have a range of clinical consequences. The most common minor complications are localized hematoma or injury to the venous valves.169 More serious complications include perforation into the pleural space or mediastinum, result-ing in hydrothorax, hemothorax, hydromediastinum, hemomediastinum, and/or chylothorax.129,170-173

In general, unintended arterial puncture is the most common acute mechanical complication, with incidence ranging from 1.9% to 15%.174 Many of these injuries

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result in localized hematoma formation, but in rare occa-sions even small-gauge needle punctures may lead to seri-ous complications such as arterial thromboembolism.175 If arterial puncture with a small needle occurs during cen-tral venous cannulation, the needle should be removed and external pressure applied for several minutes to pre-vent hematoma formation. When unintentional carotid artery cannulation with a dilator or large-bore catheter occurs, the dilator or catheter should be left in place and a vascular surgeon consulted promptly regarding removal. Immediate removal of the catheter has resulted in severe complications such as hemothorax, arteriovenous fistula, pseudoaneurysm, and cerebral infarction.176,177 Open or endovascular repair followed by careful neurologic moni-toring (and hence postponement of any elective surgical procedure) is usually required.176

Other catastrophic but rare vascular injuries have been reported, including aortic perforation and avulsion of the facial vein.178,179 Delayed vascular complications following central venous catheterization are uncommon but should be considered as consequences of this proce-dure. A number of these have been described in the litera-ture, including aortoatrial fistula, venobronchial fistula, carotid artery–internal jugular vein fistula, and pseudoa-neurysm formation.180-183

The most important life-threatening vascular compli-cation of central venous catheterization is cardiac tam-ponade resulting from perforation of the intrapericardial superior vena cava, right atrium, or right ventricle. These vascular injuries may cause hemopericardium or uninten-tional pericardial instillation of intravenous fluid leading to cardiac compression.184 This injury was the second-most common complication related to central catheters reported in the American Society of Anesthesiologists Closed Claims Project in 2004.185 Cardiac tamponade resulted in death in 81% of the cases in this report, and

MechanicalVascular injury

ArterialVenousCardiac tamponade

Respiratory compromiseAirway compression from hematomaPneumothorax

Nerve injuryArrhythmias

ThromboembolicVenous thrombosisPulmonary embolismArterial thrombosis and embolismCatheter or guidewire embolism

InfectiousInsertion site infectionCatheter infectionBloodstream infectionEndocarditis

Misinterpretation of dataMisuse of equipment

BOX 45-5 Complications of Central Venous Pressure Monitoring



D

often had a delayed presentation (1 to 5 days), indicating that this complication is related to catheter maintenance and use more often than to the vascular access procedure itself. Most reports document the avoidable nature of this catastrophic event and highlight that patients are predis-posed to this complication when central venous catheter tips are malpositioned within the heart chambers or abut-ting the wall of the superior vena cava at a steep angle. This latter position can be recognized radiographically as a gentle curvature of the catheter tip within the superior vena cava.186 These observations emphasize that objective confirmation of proper catheter tip location is manda-tory, regardless of whether the catheter is inserted from a central or peripheral site. In fact, many early reports of catheter-related cardiovascular perforation suggested that peripheral catheters may present an unusually high risk for this complication because arm abduction may cause the catheter tip to advance into a dangerous loca-tion within the heart.152,187 When cardiac tamponade is caused by catheter-induced cardiac perforation, symptoms develop suddenly, requiring a high index of suspicion if severe hypotension occurs in any patient with a central venous catheter in place. Cardiac arrhythmias may pro-vide an early clue to the intracardiac location of the cath-eter tip.153 Occasionally, both posteroanterior and lateral chest radiographs, as well as injection of radiopaque con-trast, are required to locate the catheter tip precisely.188

Pneumothorax is the most common complication of subclavian vein cannulation, although unintended arte-rial puncture may actually be more frequent.66,189 Mans-field and associates reported 821 patients who underwent attempted subclavian venous cannulation, with a 1.5% incidence of pneumothorax and a 3.7% incidence of arte-rial puncture when using the landmark technique.189 Pneumothorax is even less frequent with the internal jug-ular approach. Shah and colleagues reported an incidence of pneumothorax of 0.5% in their series of nearly 6000 internal jugular catheterizations.174 This is most likely a larger-than-expected estimate, because these patients had undergone sternotomy for cardiac surgery, a procedure that may have been responsible for the pneumothorax in many cases. Small pneumothoraces may be managed conservatively, whereas tube thoracostomy is the best treatment for larger air collections or for patients receiv-ing positive-pressure mechanical ventilation or scheduled for major surgery. The physician must always be pre-pared for the possibility of tension pneumothorax and its adverse hemodynamic sequelae. In addition to pneu-mothorax, other respiratory tract injuries occur following central venous catheterization, including subcutaneous and mediastinal emphysema, tracheal perforation, and rupture of an endotracheal tube cuff.190

Nerve injury is another potential complication of cen-tral venous cannulation. Damage may occur to the bra-chial plexus, stellate ganglion, phrenic nerve, or vocal cords.191,192 In addition, chronic pain syndromes have been attributed to this procedure.193

Thromboembolic Complications of Central Venous CatheterizationCatheter-related thrombosis varies according to the site of central venous catheterization, occurring in as many


as 21.5% of patients with femoral venous catheters and 1.9% of those with subclavian venous catheters.135 Cath-eters that are positioned low in the right atrium may be more prone to thrombus formation, possibly due to mechanical irritation of the right atrial endocardium by the catheter.194 Thrombi that form at the catheter tip or adhere to the endocardium have the potential to become a nidus for infection, cause superior vena cava syndrome, or embolize into the pulmonary circulation.195-197 Occa-sionally, surgical removal is required.198

In addition to thromboembolism, other reported embolic complications of central venous catheterization include embolism of portions of the catheter or guide-wire, and air embolism.199,200 Almost invariably, these are the result of equipment misuse, highlighting the need for proper education and training of nurses and physicians responsible for the use of these devices.

Infectious Complications of Central Venous CatheterizationBy far, the most common major late complication of cen-tral venous cannulation is infection. Central line–associ-ated bloodstream infections (CLABSI) have decreased in incidence, likely because of a focus on evidence-based best practices for catheter insertion and maintenance. Despite this, in 2009, CLABSI still represented 14% of all health care–related infections in the United States.201 Although most of these cases occurred in non-ICU patients (inpa-tient wards and outpatients receiving hemodialysis), many were diagnosed in ICU patients201-203 (also see Chapters 101 and 102).

As previously noted, the starting point for prevention of infection is meticulous attention to aseptic technique.204 A recent review showed, in addition to a declining CLABSI rate, equal rates of infection for internal jugular, femoral, and subclavian insertion sites.205 Multilumen catheters may create a more frequent risk of infection than single-lumen catheters, although the added clinical function-ality of such catheters often mandates their use.136,144 Catheters are made from a wide variety of materials, including silicone, polyvinyl chloride, Teflon, and poly-urethane. Furthermore, catheters of the same material may be manufactured differently, which influences their surfaces and the frequency of bacterial adherence to the surface.206 Heparin-bonded central venous catheters have been shown to reduce the incidence of catheter-related thrombosis and infection in children and adults.207,208 The incorporation of antimicrobial treatments such as silver (this metal has broad antimicrobial activity and is nontoxic), combinations of the antiseptics chlorhexidine and silver sulfadiazine, or the antibiotics monocycline and rifampin onto the catheter surfaces reduces rates of catheter colonization and in some cases bloodstream infection.208-210 The added expense has prevented more widespread adoption of these catheters, although an analysis has suggested their cost-effectiveness in settings in which the rate of catheter-related infections remains frequent, such as immunocompromised patients (more than 3.3/1000 catheter days).211

A chlorhexidine gluconate–impregnated sponge dress-ing reduces catheter colonization in infants and children, but it does not reduce the rate of catheter-associated



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bloodstream infections212,213 (also see Chapter 93). Cur-rent guidelines from the Centers for Disease Control and Prevention (CDC) do not support routine catheter site changes or scheduled changes over a guidewire. CDC guidelines provide other detailed recommendations for catheter management to reduce the risk of infectious complications.136

Other Complications of Central Venous CatheterizationMiscellaneous other adverse sequelae of central venous cannulation have been reported, and although their inci-dence is not clearly known, most appear to be uncom-mon (see Box 45-5). All physicians performing these procedures should be familiar with them, particularly since many of these complications are related to operator error.66,214

Use of guidewires, vessel dilators, and large-bore cath-eters carries certain additional risks that mandate metic-ulous attention to technique. The proximal tip of the guidewire must remain under the physician’s control at all times to avoid inserting the wire too far into the heart, thus causing arrhythmias, or potentially losing the guide-wire within the circulation.199,215 By design, vessel dilators are stiffer than catheters and may cause significant trauma if inserted forcefully or further than necessary to dilate the subcutaneous tissue tract from skin to vein.216 Large-bore introducer sheaths and multilumen catheters are popular because of their clinical utility, yet their size may increase the risk of cannulation-associated trauma, hemorrhage from unrecognized line disconnections, and major venous air embolism. Not only may air be entrained during initial cannulation, but improperly connected large-bore cannu-las may pose an additional risk because of the large site for air entry directly into the central venous circulation.200,217

Although many complications of CVP monitoring relate to equipment misuse, the impact of data misinter-pretation is unknown. It is extremely likely, though, that clinicians have a poor understanding of CVP monitoring and are thus more prone to misinterpretation of mea-sured values. A similar phenomenon has been repeatedly demonstrated for pulmonary artery catheter monitoring (see discussion later). Safe and effective use of CVP moni-toring requires a detailed understanding of cardiovascu-lar physiology, normal CVP waveforms, and common pathologic abnormalities in these measurements.

PHYSIOLOGIC CONSIDERATIONS FOR CENTRAL VENOUS PRESSURE MONITORING

Cardiac filling pressures are measured directly from a number of sites in the vascular system. Central venous pressure monitoring is the least invasive method, fol-lowed by pulmonary artery and left atrial pressure moni-toring. Proper interpretation of all cardiac filling pressures requires knowledge of normal values for pressures within the cardiac chambers, great vessels, and other measured and derived hemodynamic variables (Table 45-2).

CVP is the result of a complex interplay among a diverse array of physiologic variables, many of which are impos-sible to measure in the operating room or intensive care unit. Not surprisingly, CVP sometimes fails as a predictor

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of intravascular volume status or fluid responsiveness. There is, fundamentally, no simple relationship between CVP and circulating blood volume.95,218,219 Despite this, the CVP waveform is important, so its components and potential pitfalls must be understood.

NORMAL CENTRAL VENOUS PRESSURE WAVEFORMS

Mechanical events during the cardiac cycle are respon-sible for the sequence of waves seen in a typical CVP trace. The CVP waveform consists of five phasic events: three peaks (a, c, v) and two descents (x, y) (Table 45-3) (Fig. 45-18).220,221 The most prominent wave is the a wave of atrial contraction, which occurs at end-diastole following the ECG P wave. Atrial contraction increases atrial pressure and provides the atrial kick to fill the right ventricle through the open tricuspid valve. Atrial pressure decreases following the a wave, as the atrium relaxes. This smooth decline in pressure is interrupted by the c wave. This wave is a transient increase in atrial pressure produced by isovolumic ventricular contraction, which closes the tricuspid valve and displaces it toward the atrium. The c wave always follows the ECG R wave because it is generated during onset of ventricular sys-tole. Note that the c wave observed in a jugular venous pressure trace might have a slightly more complex ori-gin. This wave is due to early systolic pressure transmis-sion from the adjacent carotid artery and may be termed a carotid impact wave. 222 Because the jugular venous pressure also reflects right atrial pressure, however, this c wave likely represents both arterial (carotid impact) and venous (tricuspid motion) origins. Atrial pressure

TABLE 45-2 NORMAL CARDIOVASCULAR PRESSURES

Pressures Average (mm Hg) Range (mm Hg)

Right Atriuma wave 6 2-7v wave 5 2-7Mean 3 1-5Right VentriclePeak systolic 25 15-30End-diastolic 6 1-7Pulmonary ArteryPeak systolic 25 15-30End-diastolic 9 4-12Mean 15 9-19Pulmonary Artery WedgeMean 9 4-12Left Atriuma wave 10 4-16v wave 12 6-21Mean 8 2-12Left VentriclePeak systolic 130 90-140End-diastolic 8 5-12Central aortaPeak systolic 130 90-140End-diastolic 70 60-90Mean 90 70-105

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continues its decline during ventricular systole, owing to continued atrial relaxation and changes in atrial geom-etry produced by ventricular contraction and ejection. This is the x descent, or systolic collapse in atrial pressure. The x descent can be divided into two portions, x and x′, corresponding to the segments before and after the c wave. The last atrial pressure peak is the v wave, which is caused by venous filling of the atrium during late systole while the tricuspid valve remains closed. The v wave usu-ally peaks just after the ECG T wave. Atrial pressure then

TABLE 45-3 CENTRAL VENOUS PRESSURE WAVEFORM COMPONENTS

Waveform Component

Phase of Cardiac Cycle Mechanical Event

a wave End-diastole Atrial contractionc wave Early systole Isovolumic ventricular

contraction, tricuspid motion toward right atrium

v wave Late systole Systolic filling of atriumh wave Mid- to late diastole Diastolic plateaux descent Mid-systole Atrial relaxation, descent

of the base, systolic collapse

y descent Early diastole Early ventricular filling, diastolic collapse

150

0

15

0

ART

CVP

cv h

yx

a

R1 sec

Figure 45-18. Normal central venous pressure (CVP) waveform. The diastolic components (y descent, end-diastolic a wave) and the systolic components (c wave, x descent, end-systolic v wave) are all clearly delineated. A mid-diastolic plateau wave, the h wave, is also seen because heart rate is slow. Waveform identification is aided by timing the relation between individual waveform components and the electrocardiographic R wave. Waveform timing using the arterial (ART) pressure trace is more confusing, owing to the relative delay in the sys-tolic arterial pressure upstroke. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)


decreases, inscribing the y descent, or diastolic collapse, as the tricuspid valve opens and blood flows from atrium to ventricle. A final component of the CVP waveform, the h wave, occasionally appears as a pressure plateau in mid- to late diastole. The h wave is not normally seen unless the heart rate is slow and venous pressure is increased.222,223 In summary, the normal venous waveform components may be remembered as follows: the a wave results from atrial contraction; the c wave results from tricuspid valve closure and isovolumic right ventricular contraction; the x descent is the systolic decrease in atrial pressure due to atrial relaxation; the v wave results from ventricular ejec-tion, which drives venous filling of the atrium; and the y descent is the diastolic decrease in atrial pressure due to flow across the open tricuspid valve.

In relation to the cardiac cycle and ventricular mechanical actions, the CVP waveform can be considered to have three systolic components (c wave, x descent, v wave) and two diastolic components (y descent, a wave). By recalling the mechanical actions that generate the pressure peaks and troughs, these waveform components can be identified properly by aligning the CVP waveform and the ECG trace and using the ECG R wave to mark end-diastole and onset of systole. When the radial artery pressure trace is used for CVP waveform timing instead of the ECG, confusion may arise because the arterial pres-sure upstroke occurs nearly 200 milliseconds after the ECG R wave (see Fig. 45-18). This normal physiologic delay reflects the times required for the spread of the electrical depolarization through the ventricle (≈60 mil-liseconds), isovolumic left ventricular contraction (≈60 milliseconds), transmission of aortic pressure rise to the radial artery (≈50 milliseconds), and transmission of the radial artery pressure rise through fluid-filled tubing to the transducer (≈10 milliseconds).82,224

The normal CVP peaks are designated systolic (c, v) or diastolic (a) according to the phase of the cardiac cycle in which the wave begins. However, one generally identi-fies these waves not by their onset or upstroke, but rather by the location of their peaks. For instance, the a wave generally begins and peaks in end-diastole, but the peak may appear delayed to coincide with the ECG R wave, especially in a patient with a short PR interval. In this instance, a and c waves merge, and this composite wave is termed an a-c wave. Designation of the CVP v wave as a systolic event may be even more confusing. Although the ascent of the v wave begins during late systole, the peak of the v wave occurs during isovolumic ventricular relax-ation, immediately before atrioventricular valve open-ing and the y descent. Consequently, the most precise description would be that the v wave begins in late sys-tole, but peaks during isovolumic ventricular relaxation, the earliest portion of diastole. For clinical purposes, it is simplest to consider the v wave to be a systolic wave.

Although three distinct CVP peaks (a, c, v) and two troughs (x, y) are discernible in the normal venous pres-sure trace, heart rate changes and conduction abnor-malities alter this pattern. A short ECG PR interval causes fusion of a and c waves, and tachycardia reduces the length of diastole and the duration of the y descent, causing v and a waves to merge. In contrast, bradycardia causes each wave to become more distinct with separate

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Downl

x and x′ descents visible and a more prominent h wave. Although there are circumstances in which other patho-logic waves may be evident in the CVP trace, one should resist the temptation to assign physiologic significance to each small pressure peak, because many will arise as arti-facts of fluid-filled tubing-transducer monitoring systems. It is more useful to search for the expected waveform components, including those waveforms that are charac-teristic of the pathologic conditions suspected.

ABNORMAL CENTRAL VENOUS PRESSURE WAVEFORMS

Various pathophysiologic conditions may be diagnosed or confirmed by examination of the CVP waveform (Table 45-4). One of the most common applications is the rapid diagnosis of cardiac arrhythmias.225 In atrial fibrilla-tion, the a wave disappears and the c wave becomes more prominent because atrial volume is larger at end-diastole and onset of systole, owing to the absence of effective atrial contraction (Fig. 45-19, A). Occasionally, atrial fibrillation or flutter waves may be seen in the CVP trace when the ventricular rate is slow. Isorhythmic atrioven-tricular dissociation or junctional (nodal) rhythm alters the normal sequence of atrial contraction before ven-tricular contraction (see Fig. 45-19, B). Instead, retrograde conduction of the nodal impulse throughout the atrium causes atrial contraction to occur during ventricular sys-tole while the tricuspid valve is closed, resulting in a tall “cannon” a wave in the CVP waveform. Absence of nor-mal atrioventricular synchrony during ventricular pacing can be identified in a similar fashion by searching for can-non waves in the venous pressure trace (see Fig. 45-19, C). In these instances, the CVP helps diagnose the cause of arterial hypotension; loss of the P wave may not be as evident in the ECG trace as are the changes in the CVP waveform.

Right-sided valvular heart diseases alter the CVP waveform in different ways.226 Tricuspid regurgitation

TABLE 45-4 CENTRAL VENOUS PRESSURE WAVEFORM ABNORMALITIES

Condition Characteristics

Atrial fibrillation Loss of a waveProminent c wave

Atrioventricular dissociation Cannon a waveTricuspid regurgitation Tall systolic c-v wave

Loss of x descentTricuspid stenosis Tall a wave

Attenuation of y descentRight ventricular ischemia Tall a and v waves

Steep x and y descentsM or W configuration

Pericardial constriction Tall a and v wavesSteep x and y descentsM or W configuration

Cardiac tamponade Dominant x descentAttenuated y descent

Respiratory variation during spontaneous or positive-pressure ventilation

Measure pressures at end-expiration

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produces abnormal systolic filling of the right atrium through the incompetent valve. This results in a broad, tall systolic c-v wave, beginning in early systole and oblit-erating the systolic x descent in atrial pressure (Fig. 45-20, A). The CVP trace is said to be ventricularized, resembling

0

135

0

15

0

150

0

10

20

0

150

0

45

A

B

C

CVP

ART

1 sec

CVP a

ART

1 secR R

CVP

ART

1 secR

cv

y

*

V A V

Figure 45-19. Central venous pressure (CVP) changes caused by car-diac arrhythmias. A, Atrial fibrillation. Note absence of the a wave, a prominent c wave, and a preserved v wave and y descent. This arrhythmia also causes variation in the electrocardiographic (ECG) R-R interval and left ventricular stroke volume, which can be seen in the ECG and arterial (ART) pressure traces. B, Isorhythmic atrioven-tricular dissociation. In contrast to the normal end-diastolic a wave in the CVP trace (left panel), an early systolic cannon wave is inscribed (*, right panel). Reduced ventricular filling accompanying this arrhyth-mia causes a decreased arterial blood pressure. C, Ventricular pacing. Systolic cannon waves are evident in the CVP trace during ventricu-lar pacing (left panel). Atrioventricular sequential pacing restores the normal venous waveform and increases arterial blood pressure (right panel). ART scale left, CVP scale right. (From Mark JB: Atlas of cardiovas-cular monitoring, New York, 1998, Churchill Livingstone.)



right ventricular pressure. Note that this regurgitant wave differs in onset, duration, and magnitude from a normal v wave caused by end-systolic atrial filling from the vena cavae. In patients with tricuspid regurgitation, right ven-tricular end-diastolic pressure is overestimated by the numeric display on the bedside monitor, which reports a single mean value for CVP. Instead, right ventricular end-diastolic pressure is estimated best by measuring the CVP value at the time of the ECG R wave, before the regurgitant systolic wave (see Fig. 45-20, A). Unlike tricuspid regurgitation, tricuspid stenosis produces a dia-stolic defect in atrial emptying and ventricular filling (see Fig. 45-20, B). Mean CVP is elevated, and a pressure

20

10

0

20

10

0

A

B

1 secR

cv

1 sec

a

v

y

Figure 45-20. Central venous pressure (CVP) changes in tricuspid valve disease. A, Tricuspid regurgitation increases mean CVP, and the waveform displays a tall systolic c-v wave that obliterates the x descent. In this example, the a wave is not seen because of atrial fibril-lation. Right ventricular end-diastolic pressure is estimated best at the time of the electrocardiographic R wave (arrows) and is lower than mean CVP. B, Tricuspid stenosis increases mean CVP, the diastolic y descent is attenuated, and the end-diastolic a wave is prominent. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)


gradient exists throughout diastole between right atrium and ventricle. The a wave is unusually prominent and the y descent is attenuated, owing to the impaired diastolic egress of blood from the atrium. Other conditions that reduce right ventricular compliance, such as right ven-tricular ischemia, pulmonary hypertension, or pulmonic valve stenosis, may produce a prominent end-diastolic a wave in the CVP trace but do not attenuate the early diastolic y descent. CVP waveform morphology changes in other characteristic ways in the presence of pericar-dial diseases and right ventricular infarction. These pat-terns are interpreted best in conjunction with pulmonary artery pressure monitoring, which is discussed later.

Perhaps the most important traditional application of CVP monitoring is to provide an estimate of the adequacy of the circulating blood volume. Several randomized tri-als and systematic reviews have demonstrated a very poor relationship between CVP and circulating blood volume, as well as the inability of a static CVP value to predict the hemodynamic response to a fluid challenge.227-229 This is not surprising given the complexity of the interactions among the many variables that affect CVP. Perhaps the important clinical question with regard to intravascular volume responsiveness should be phrased in the nega-tive—that is, whether a patient is unlikely to respond to an intravenous fluid challenge. The subset of patients that will suffer all the deleterious effects of fluid admin-istration (capillary leak and tissue edema) and no benefit (increased cardiac output) is in most instances the group of clinical interest.

PULMONARY ARTERY CATHETER MONITORING

In 1970, Swan, Ganz, and colleagues introduced pulmo-nary artery catheterization into clinical practice for the hemodynamic assessment of patients with acute myo-cardial infarction.230 These catheters allowed accurate measurement of important cardiovascular physiologic variables at the bedside, and their popularity soared. By the mid-1990s, estimated annual pulmonary artery cath-eter (PAC) sales in the United States approached 2 million catheters, with an estimated cost associated with their use in excess of 2 billion dollars each year.231

The PAC provides measurements of several hemody-namic variables that many clinicians, including experts in intensive care, cannot predict accurately from stan-dard clinical signs and symptoms.232 However, it remains uncertain whether PAC monitoring improves patient outcome.233

PULMONARY ARTERY CATHETERIZATION

The standard PAC has a 7.0- to 9.0-Fr circumference, is 110 cm in length marked at 10-cm intervals, and contains four internal lumina. The distal port at the catheter tip is used for pulmonary artery pressure monitoring, whereas the second port is 30 cm more proximal and is used for CVP monitoring. The third lumen leads to a balloon near the tip, and the fourth houses wires for a temperature therm-istor, the end of which lies just proximal to the balloon.



D

30

0

a-c vvca

WedgePulmonary arteryRight ventricleRight atrium

1 sec

R R R R

Figure 45-21. Characteristic waveforms recorded during passage of the pulmonary artery catheter. The right atrial pressure resembles a central venous pressure waveform and displays a, c, and v waves. Right ventricular pressure shows a higher systolic pressure than seen in the right atrium, although the end-diastolic pressures are equal in these two chambers. Pulmonary artery pressure shows a diastolic step-up compared with ven-tricular pressure. Note also that right ventricular pressure increases during diastole, whereas pulmonary artery pressure decreases during diastole (shaded boxes). Pulmonary artery wedge pressure has a similar morphology to right atrial pressure, although the a-c and v waves appear later in the cardiac cycle relative to the electrocardiogram. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)

ow

PACs can be inserted from any of the central venous cannulation sites described earlier, but the right internal jugular vein provides the most direct route to the right heart chambers. A large-bore introducer sheath with a hemostasis valve at its outer end is inserted in a manner similar to that for central venous cannulation. The PAC is passed through a sterile sheath to allow for later sterile manipulation of the PAC position, its distal lumen is con-nected to a pressure transducer, and then the catheter is inserted through the introducer’s hemostatic valve to a depth of 20 cm. The gentle curvature of the PAC should be oriented to point just leftward of the sagittal plane (the 11-o’clock position, as viewed from the patient’s head) to facilitate passage through the anteromedially located tricuspid valve. The balloon at the tip of the catheter is inflated with air, and the catheter is advanced into the right atrium, through the tricuspid valve, the right ventri-cle, the pulmonic valve, into the pulmonary artery, and finally into the wedge position. Characteristic waveforms from each of these locations confirm proper catheter pas-sage and placement (Fig. 45-21).

After the pulmonary artery wedge pressure is mea-sured, the balloon is deflated, and the pulmonary artery pressure waveform should reappear. Wedge pressure may be obtained as needed by reinflating the balloon and allowing the catheter to float distally until pulmonary artery occlusion again occurs.

Additional Guidelines for Pulmonary Artery Catheter InsertionFrom a right internal jugular vein puncture site, the right atrium should be reached when the PAC is inserted 20 to 25 cm, the right ventricle at 30 to 35 cm, the pulmonary artery at 40 to 45 cm, and the wedge position at 45 to 55 cm. When other sites are chosen for catheter placement, additional distance is required, typically an additional 5 to 10 cm from the left internal jugular and left and right external jugular veins, 15 cm from the femoral veins, and 30 to 35 cm from the antecubital veins.234 These distances serve only as a rough guide; waveform morphology must always be verified and catheter position confirmed with a chest radiograph as soon as practical. The tip of the PAC should be within 2 cm of the cardiac silhouette on a stan-dard anteroposterior chest film.235


Use of these typical distances helps avoid complica-tions caused by unintended catheter loops and knots within the heart. If a right ventricular waveform is not observed after inserting the catheter 40 cm, coiling in the right atrium is likely. Similarly, if a pulmonary artery waveform is not observed after inserting the catheter 50 cm, coiling in the right ventricle has probably occurred. The balloon should be deflated, the catheter withdrawn to 20 cm, and the PAC floating sequence repeated.

If repeated attempts to advance the PAC to the right ventricle prove difficult, an abnormal venous anatomy may exist. The most common abnormality of the systemic veins is persistence of the left superior vena cava (LSVC), which is present in approximately 0.1% to 0.2% of the general population and 2% to 9% of patients with other forms of congenital heart disease.236,237 The persistent LSVC descends along the left mediastinum and empties into a dilated coronary sinus. Because of the benign nature of LSVC, virtually all cases are asymptomatic and discov-ered incidentally at the time of failed central venous or pulmonary artery catheterization. Because a normal right superior vena cava is present in most of these patients, the anomaly is recognized only when attempted PAC placement proceeds from a left-sided vein. More rarely, difficult PAC placement is encountered during attempted right-sided venous cannulation because the right superior vena cava is absent as well. In these cases, the right inter-nal jugular vein joins the persistent left superior vena cava by a bridging innominate vein. A rare form of atrial septal defect, termed unroofed coronary sinus, may also be encountered in these patients providing coronary sinus–left atrial communication and the potential for a PAC to enter the left atrium and systemic circulation.237 With any of these venous anomalies, PAC advancement into the coronary sinus may disclose an unexpected pressure waveform, coronary sinus pressure.

A few additional points might aid successful position-ing of the PAC. The air-filled balloon tends to float to nondependent regions as it passes through the heart into the pulmonary vasculature. Consequently, positioning the patient head down will aid flotation past the tricuspid valve, and tilting the patient onto the right side and plac-ing the head up will encourage flotation out of the right ventricle, as well as reduce the incidence of arrhythmias



during insertion.238,239 Deep inspiration during sponta-neous ventilation will increase venous return and right ventricular output transiently and may facilitate catheter flotation in a patient with low cardiac output. On occa-sion, a catheter may be floated to proper position when stiffened by injecting 10 to 20 mL of ice-cold solution through the distal lumen. Finally, a catheter that is ini-tially difficult to place may be positioned easily when hemodynamic conditions change, as commonly occurs after induction of general anesthesia and initiation of positive-pressure ventilation.

COMPLICATIONS OF PULMONARY ARTERY CATHETER MONITORING

Complications of PAC use may be divided into those resulting from catheter placement, those associated with the in vivo presence of the catheter, and those resulting from catheter use and misuse. For the most part, prob-lems encountered during catheter placement are the same for both PAC and CVP monitoring (see Box 45-5). However, catheterization of the right ventricle and pul-monary artery causes complications uniquely associated with PACs (Box 45-6).240

When all adverse effects from PAC use are considered, including self-limited arrhythmias observed during cath-eter insertion, minor complications occur in more than 50% of catheterized patients.231 However, major morbid-ity specifically attributable to PAC use is uncommon.241 In 2003, the American Society of Anesthesiologists Task Force on Pulmonary Artery Catheterization emphasized that the reported incidence of complications from PAC monitoring varies widely, although serious complica-tions occur in 0.1% to 0.5% of PAC-monitored surgical patients.231 In 1984, Shah and colleagues reported use of PACs in 6245 patients undergoing cardiac and noncar-diac operations.174 Quite remarkably, only 10 patients (0.16%) had serious complications resulting in morbidity and only 1 patient (0.016%) died as a result of pulmonary artery catheterization. Furthermore, a 1998 European report of PAC use in 5306 patients undergoing cardiac surgery confirms this infrequent incidence of major mor-bidity, with injury of the right ventricle or PA occurring in only 4 patients (0.07%).242 Finally, only 1 of 2000 adverse events reported in the Australian Incident Moni-toring Study of 1993 involved use of a PAC, in contrast to 64 adverse events involving access to the arterial or venous systems.66 However, although these large studies indicate an infrequent incidence of serious complications attributable to the use of PACs, the frequency of com-plications in a particular clinical setting or patient group remains unknown.

Arrhythmias are the primary complication observed during pulmonary artery catheterization. In fact, self- limited atrial or ventricular arrhythmias are so common during PAC passage through the heart that most clini-cians do not consider them complications, but rather confirmation that the PAC is traversing the cardiac cham-bers appropriately. Shah and associates observed transient premature ventricular contractions in 68% and atrial dysrhythmias in 1.3% of their catheterized patients.174 Of more clinical significance, persistent ventricular


dysrhythmias requiring treatment occurred in only 3.1% of patients, none of whom suffered prolonged hemo-dynamic instability. Although the balloon-tipped PAC is less arrhythmogenic when it strikes the endocardium than a standard intravenous catheter or transvenous pac-ing wire, PACs have been reported to induce sustained atrial fibrillation, ventricular tachycardia, and even ven-tricular fibrillation.242-244

Prophylactic use of IV lidocaine before pulmonary artery catheterization is not effective in reducing ven-tricular ectopy.245 When such problems arise, the balloon should be deflated and the catheter withdrawn to the right atrium. When hemodynamically significant dys-rhythmias develop hours or even days after placement, it is unlikely that the PAC is responsible. However, the position of the catheter tip should always be checked by observation of the pressure waveform and chest radio-graph to identify catheters that have migrated back into the right ventricle.

As the PAC passes through the right ventricle and strikes the interventricular septum, transient right bun-dle branch block occurs in up to 5% of patients.246,247 This is important only in patients with preexisting left bundle branch block. In these patients, complete heart block may be precipitated, although this is rare. Shah and associates catheterized 113 patients with preexisting left bundle branch block; only 1 patient developing complete heart block (0.9%).174 In a different population of 47 high-risk patients with left bundle branch block, many of whom had acute myocardial infarction or heart failure, Morris and colleagues inserted 82 PACs without a single episode of complete heart block for the initial 24 hour period. 246 However, transcutaneous pacing equipment, an external pulse generator, and a temporary transvenous pacing wire or pacing PAC should be readily available as a precaution, especially as the onset of heart block in this setting may be delayed.

Many mechanical problems have been reported with PACs or introducer sheaths. In the setting of cardiac sur-gery, PACs may be damaged by surgical instruments or become entrapped in sutures or bypass cannulas.174,248-250 Whenever right heart structures are involved in surgery, free movement of the PAC should be ensured before chest closure. Sternal retraction during cardiac surgery

CatheterizationArrhythmias, ventricular fibrillationRight bundle branch block, complete heart block

Catheter residenceMechanical, catheter knotsThromboembolismPulmonary infarctionInfection, endocarditisEndocardial damage, cardiac valve injuryPulmonary artery rupturePulmonary artery pseudoaneurysm

Misinterpretation of dataMisuse of equipment

BOX 45-6 Complications of Pulmonary Artery Catheter Monitoring



Dow

may pose other problems, particularly when the PAC is inserted through the external jugular or subclavian route. The PAC may kink as it exits the introducer sheath and makes an acute angle between the sheath and vessel wall.251,252 These mechanical difficulties should be sus-pected whenever there is a damped appearance of the monitored pressure trace or difficulty in either infusing fluids or withdrawing blood through one of the catheter lumina.

Although gross structural defects in the catheter itself should be recognized by inspection of the catheter before insertion, more subtle manufacturing problems may escape detection. Some, such as communications between the PAP, CVP, and balloon inflation lumina may be suspected only when data are contradictory or inconsistent.253,254

PACs may dislodge temporary transvenous pacing wires, become entangled with other cardiac catheters, or form knots within the heart.255,256 Arnaout and colleagues reported a PAC knot around the tricuspid valve chordae tendinae, which resulted in severe tricuspid valve regur-gitation following catheter removal.255 Catheter knots should be suspected when there is difficulty withdraw-ing a PAC and the diagnosis may be confirmed by chest radiography. Knots may be untied by radiologists using intravascular snares and fluoroscopic guidance.257 If the knot has already been drawn tight, surgical exploration and removal are usually required.

Although both severe tricuspid regurgitation and severe pulmonic regurgitation have been reported, these are rare complications of PAC use.255,258,259 Using color flow Doppler echocardiography, Sherman and associates demonstrated that placement of a PAC caused a slight increase in the magnitude of tricuspid regurgitation, but in no instance did the PAC lead to severe right-sided val-vular insufficiency.260

Although the incidence of thromboembolic complica-tions is increased in patients who require PAC monitoring for longer periods of time, thrombi have been detected on PACs within hours of placement.261 When adminis-tration of drugs such as aprotinin and aminocaproic acid reduce perioperative bleeding, the risk of thrombus for-mation on the PAC may be increased.262,263 Although external surface heparin bonding unquestionably has reduced thrombogenicity of PACs, it does not entirely eliminate the possibility.261,264 Fortunately, major pulmo-nary embolism is a rare occurrence.265

The incidence of PAC-related infection increases after 3 days of continuous monitoring and in patients with preexisting sepsis.266 The most catastrophic of these infections is endocarditis, most often of the right-sided valves.259,267 Using sophisticated microbiologic tech-niques in 297 critically ill patients, Mermel and col-leagues demonstrated a 22% incidence of local infection of the introducer sheath, but only 0.7% incidence of bacteremia related to the PAC.268 Changes of PACs do not reduce the risk of bloodstream infection, particularly when the catheter is changed over a guidewire.269 How-ever, cannulation at a new site carries a significant risk of vascular complications. The specific risks and benefits must be weighed in each patient. Although heparin-bonded PACs carry an infection risk similar to central


venous catheters, non–heparin-bonded catheters have double the risk.136

Pulmonary artery rupture, the most deadly but also most preventable of complications, occurs in approxi-mately 0.02% to 0.2% of catheterized patients and car-ries a mortality rate of 50%.174,270 Several factors increase the risk of this catastrophic event, including hypother-mia, anticoagulation, and advanced age, although many reported cases involve heart transplant procedures.270-272 Pulmonary hypertension also may predispose patients to arterial injury during balloon inflation owing to the increased gradient between the proximal arterial and dis-tal wedge pressures or because pulmonary hypertension distends the pulmonary vasculature and causes the PAC to wedge in a distal, less compliant vessel.273

Several mechanisms exist for pulmonary artery injury. These include forceful inflation of the PAC balloon and chronic erosion by the catheter tip abutting the ves-sel wall or eccentric balloon inflation forcing the non-cushioned catheter tip through the vessel wall.272,274 Regardless of the precise mechanism by which pulmo-nary arterial injury occurs, case reports highlight that this complication often results from suboptimal catheter insertion and management techniques. Procedural errors include unnecessary catheter manipulation, excessive insertion depth, unrecognized persistent wedge pressure, prolonged balloon inflation, or improper balloon infla-tion with liquid rather than air.273-275 It is critical that the clinician recognize artifactual “over-wedged” pressure recordings that indicate peripheral migration of the PAC tip or impaction against the vessel wall and correct this problem immediately by withdrawing the catheter into the proximal pulmonary artery. This problem is more common during cardiopulmonary bypass, owing to the repeated cardiac manipulations and temperature changes that alter the stiffness of the catheter.276

The hallmark of catheter-induced pulmonary artery rupture is hemoptysis, which may cause life-threatening exsanguination or hypoxemia. Less commonly, occult hypotension or respiratory compromise may develop. If the visceral pleura fails to contain the bleeding, free rupture into the pleural space produces a large hemotho-rax. When time allows, a chest radiograph helps deter-mine the diagnosis by revealing the hemothorax or a new infiltrate near the tip of a distally positioned PAC. Although its initial appearance may be confused with catheter-related pulmonary infarction, the pattern of res-olution and clinical course differentiate these diagnoses. In confusing cases, the diagnosis may be confirmed by performing a wedge angiogram, in which radiopaque dye injected through the wedged PAC will extravasate into the pulmonary parenchyma to identify the site of arterial disruption.271

Treatment of pulmonary artery rupture focuses on resuscitation and immediate control of the hemorrhage. Specific therapeutic steps are highly individualized, depending on the setting. The first priority is ensuring adequate oxygenation and ventilation and may require endobronchial intubation with either a single- or dou-ble-lumen endotracheal tube to selectively ventilate and protect the unaffected lung. In addition, positive end-expiratory pressure applied to the affected lung may help



control hemorrhage.277 Any anticoagulation should be reversed unless the patient must remain on cardiopulmo-nary bypass and bronchoscopy is performed to localize and control the site of bleeding. A bronchial blocker may be guided into the involved bronchus to tamponade the bleeding and prevent contamination of the uninvolved lung.278 Management of the PAC itself is more contro-versial. Some experts recommend removing the catheter, but others suggest leaving the PAC in place to monitor pulmonary artery pressure and guide antihypertensive therapy targeted at decreasing this pressure and reducing bleeding.279,280 The PAC balloon may be carefully rein-flated and the catheter floated into the involved pulmo-nary artery to occlude the bleeding arterial segment as a temporizing measure.278 Although these measures may be effective in some cases, many patients will require defini-tive surgical therapy, such as oversewing the involved pulmonary artery or resecting the involved segment, lobe, or lung.271,278 In addition, angiography may be rec-ommended to rule out pseudoaneurysm formation in those managed conservatively due to the high morbidity associated with secondary hemorrhage.270,278,281,282

A more insidious but possibly more common com-plication of PAC use is misinterpretation of data.283,284 Although the magnitude of the problem is not clear, widespread knowledge deficits likely exist among prac-titioners who use PACs. In 1990, Iberti and colleagues reported the results of a 31-question multiple-choice examination given to 496 resident and staff physicians in medicine, surgery, and anesthesiology departments, who practiced in 13 North American medical centers. The authors found a poor overall level of knowledge of PACs, as evidenced by a mean score of only 67% cor-rect answers. Although higher scores were demonstrated by individuals with more training and more experience inserting and using PACs, none of these factors ensured a high level of knowledge.285 These results have been duplicated in a variety of other specialty care groups.286 It is especially concerning that pulmonary artery wedge pressure measurement was performed incorrectly by 30% to 50% of the clinicians in these studies and that edu-cational programs failed to improve performance.287,288

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Taken together, these observations highlight the fact that effective use of PACs requires a great deal of expertise and clinical experience, and even measuring the most funda-mental PAC-derived variable, namely wedge pressure, is a complicated endeavor.289

NORMAL PULMONARY ARTERY PRESSURES AND WAVEFORMS

As the balloon-tipped PAC is floated to its proper position in the pulmonary artery, characteristic pressure wave-forms are recorded (see Fig. 45-21). In the superior vena cava or right atrium, a CVP waveform with characteris-tic a, c, and v waves and low mean pressure should be observed. At this point, the PAC balloon is inflated, and the catheter is advanced until it crosses the tricuspid valve to record right ventricular pressure, characterized by a rapid systolic upstroke, a wide pulse pressure, and low dia-stolic pressure. Next, the PAC enters the right ventricular outflow tract and floats past the pulmonic valve into the main pulmonary artery. Premature ventricular beats are common during this period as the balloon-tipped cath-eter strikes the right ventricular infundibular wall. Entry into the pulmonary artery is heralded by a step-up in dia-stolic pressure and a change in waveform morphology.

On occasion, it may be difficult to distinguish right ventricular pressure from PAP, particularly if only the numeric values for these pressures are examined. How-ever, careful observation of the pressure waveforms, focusing on the diastolic pressure contours, allows dif-ferentiation. During diastole, the PAP will fall because of interruption of flow during pulmonic valve closure, whereas the pressure in the right ventricle will increase as a result of filling from the right atrium234 (see Fig. 45-21).

Under normal conditions, the PAP upstroke slightly precedes the radial artery pressure upstroke as a result of the longer duration of left ventricular isovolumic contrac-tion and the time required for pressure wave propagation to a distal monitoring site. As a practical matter, though, the pulmonary and systemic arterial pressure waveforms appear to overlap on the bedside monitor (Fig. 45-22). Understanding these temporal relations is critically

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Figure 45-22. Temporal relations between normal systemic arterial pressure (ART), pulmonary artery pressure (PAP), central venous pressure (CVP), and pulmonary artery wedge pressure (PAWP). Note that the PAWP a-c and v waves appear to occur later in the cardiac cycle compared with their counterparts on the right side of the heart seen in the CVP trace. ART pressure scale on the left; PAP, CVP, and PAWP pressure scales on the right. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)

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important if one is to properly interpret abnormal pulmo-nary artery and wedge pressure waveforms, particularly when tall v waves are present (see later).

As noted earlier, the wedge pressure is an indirect mea-surement of pulmonary venous pressure and left atrial pressure and should therefore resemble these venous waveforms with characteristic a and v waves and x and y descents. However, owing to the pulmonary vascular bed interposed between the PAC tip and left atrium, wedge pressure is a delayed and damped representation of left atrial pressure.290 On average, 160 milliseconds are required for the left atrial pressure pulse to traverse the pulmonary veins, capillaries, arterioles, and arteries. Additionally, atrial depolarization originates in the sino-atrial node located at the junction of the superior vena cava and the right atrium, and therefore the left-sided a wave appears slightly later than the right-sided a wave (Fig. 45-23). As a consequence of these two phenomena, the wedge pressure a wave appears to follow the ECG R wave in early ventricular systole, even though the a wave is an end-diastolic event (see Fig. 45-22). Although the a wave is the most prominent pressure peak in a normal CVP trace, the v wave is often taller than the a wave in a normal left atrial pressure waveform, suggesting that atrial contraction is stronger on the right than the left, and that the left atrium is less distensible than the right.82 Finally, the interval between atrial and ventricular con-traction is approximately 40 milliseconds longer on the right than on the left.82 Consequently, a and c waves are seen as separate waves in a right atrial pressure trace, whereas on the left they merge into a composite a-c wave (see Fig. 45-22).

To recognize prominent a or v waves in the wedge pressure trace, it is not always necessary to inflate the PAC balloon. Because the PAWP trace reflects pressure waves transmitted in retrograde fashion from the left atrium, these waves will not normally be visible within the ante-grade pulmonary artery pressure waves produced by right ventricular ejection. In the setting of prominent a or v waves, the PAP trace becomes a composite wave, reflect-ing both retrograde and antegrade components. Tall left atrial a or v waves will distort the normal pulmonary

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Figure 45-23. Normal temporal relations between the electrocardio-graphic, central venous pressure (CVP), and left atrial pressure (LAP) traces. The LAP and CVP waveforms have nearly identical morpholo-gies, although the CVP a wave slightly precedes the LAP a wave. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)

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artery pressure waveform appearance, with the a wave inscribed at the onset of the systolic upstroke and the v wave distorting the dicrotic notch290,291 (Fig. 45-24). Once these waves are identified by wedging the PAC and comparing the PAP and PAWP traces, it is wise to “follow” the wedge-pressure a and v waves in the unwedged PAP trace, rather than repeatedly inflating the balloon.

The terms pulmonary artery wedge pressure and pulmo-nary artery occlusion pressure are used interchangeably and refer to the same measurement obtained from the tip of a PAC following balloon inflation and flotation to the wedged position. However, pulmonary capillary pressure must not be confused with wedge pressure or left atrial pressure, nor should the term pulmonary capillary wedge pressure be used at all. The hydrostatic pressure in the pul-monary capillaries that causes edema formation accord-ing to the Starling equation is different from LAP. This is the pressure that must exceed left atrial pressure in order to maintain antegrade blood flow through the lungs. Although the magnitude of the difference between pul-monary capillary pressure and wedge pressure is generally small, it can increase markedly when resistance to flow in the pulmonary veins is elevated.292 In most situations, the major component of pulmonary vascular resistance occurs at the precapillary, pulmonary arteriolar level. However, rare conditions like pulmonary venoocclusive disease may cause a marked increase in postcapillary resis-tance to flow. Similar situations arise in conditions that disproportionately increase pulmonary venous resistance, such as central nervous system injury, acute lung injury, hypovolemic shock, endotoxemia, and norepinephrine infusion.291,293 Under these conditions, measurement of wedge pressure will underestimate pulmonary capillary pressure substantially and thereby underestimate the risk of hydrostatic pulmonary edema. Although pulmo-nary capillary pressure may be measured at the bedside by analyzing the decay in pulmonary artery pressure trace following PAC balloon inflation, these techniques have not been widely adopted in clinical practice.294,295 To avoid confusion, the term pulmonary capillary wedge pressure should be abandoned because it is imprecise and misleading.

ABNORMAL PULMONARY ARTERY AND WEDGE PRESSURE WAVEFORMS

PAC monitoring is subject to the same technical artifacts inherent in all invasive pressure monitoring techniques,

PAP LAP

Figure 45-24. Tall left atrial pressure (LAP) a and v waves transmitted in a retrograde direction through the pulmonary vasculature distort the antegrade pulmonary artery pressure (PAP) waveform. The LAP a wave distorts the systolic upstroke, and the v wave distorts the dicrotic notch. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)



as well as some additional problems unique to this method.274,296,297 Because the PAC is longer and passes through the cardiac chambers, it is more prone to distor-tions from clot or air bubbles, and motion-related arti-facts are more problematic. Artifactual pressure spikes may be distinguished from the underlying physiologic pressure waveform by their unique morphology and timing.

At the onset of systole, tricuspid valve closure accom-panied by right ventricular contraction and ejection result in excessive catheter motion, causing the most common PAC trace artifact.296,298 This pressure artifact is simulta-neous with the CVP c wave and may produce either an artificially low pressure or a pressure peak. If the moni-tor detects this inappropriate pressure nadir, it may be erroneously designated as the pulmonary artery diastolic pressure (Fig. 45-25). Repositioning the PAC often solves the problem.

Another common artifact in PAC pressure mea-surement occurs when the balloon is overinflated and occludes the lumen orifice. This phenomenon is termed overwedging and usually is caused by distal catheter migration and eccentric balloon inflation that forces the catheter tip against the vessel wall. The catheter now records a gradually rising pressure as the continuous flush system builds up pressure against the obstructed distal opening (Fig. 45-26). For a catheter that has migrated to a more distal position, it is possible for overwedging to occur without balloon inflation. Note that the over-wedged pressure is devoid of pulsatility, is higher than expected, and increases continuously because of the con-tinuous flush pressure. This should be corrected by cath-eter withdrawal.

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As emphasized earlier, with each PAC balloon infla-tion and wedge measurement, the catheter tip migrates distally. When a wedge pressure tracing appears during partial balloon inflation, it suggests that the PAC is inap-propriately located in a smaller, distal branch of the pul-monary artery. The catheter should be withdrawn before overwedging results in vascular injury or pulmonary infarction.

Pathophysiologic conditions involving the left-sided cardiac chambers or valves produce characteristic changes in the pulmonary artery and wedge pressure waveforms. One of the most easily recognized patterns is the tall v wave of mitral regurgitation. Unlike a normal wedge pres-sure v wave produced by late systolic pulmonary venous inflow, the prominent v wave of mitral regurgitation begins in early systole. Mitral regurgitation causes fusion of c and v waves and obliteration of the systolic x descent, as the isovolumic phase of left ventricular systole is elimi-nated owing to the retrograde ejection of blood into the left atrium.226 Because the prominent v wave of mitral regurgitation is generated during ventricular systole, the mean wedge pressure overestimates left ventricular end-diastolic filling pressure, which is better estimated by the pressure value before onset of the regurgitant v wave (Fig. 45-27). Although mean wedge pressure exceeds left ventricular end-diastolic pressure in patients with severe mitral regurgitation, it remains a good approximation for mean left atrial pressure and the subsequent risk of hydrostatic pulmonary edema.

When large v waves are present in the wedge pressure trace, it is critically important to recognize them and be able to distinguish the wedged from the unwedged pres-sure waveform. At first glance, a wedge trace with a tall

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Figure 45-25. Artifactual pressure peaks and troughs in the pulmonary artery pressure (PAP) waveform caused by catheter motion. The correct value for pulmonary artery end-diastolic pressure is 8 mm Hg (A), although the monitor digital display erroneously reports the PAP as 28/0 mm Hg (B). (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)

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Figure 45-26. Overwedging of the pulmonary artery (PA) catheter causes artifactual waveform recordings. The first two attempts to inflate the PA catheter balloon (first two arrows) produce a nonpulsatile increasing pressure caused by an occluded catheter tip. After the catheter is with-drawn slightly, balloon inflation allows proper wedge pressure measurement (third arrow). Before the third attempt at balloon inflation, the PA pressure lumen is flushed. This restores the appropriate pulsatile nature to the PA and wedge pressure waveforms on the right side of the trace. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)

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systolic v wave resembles a typical unwedged pulmonary artery pressure trace, but closer observation reveals a number of discriminating details. The pulmonary artery pressure upstroke is steeper and slightly precedes the sys-temic arterial pressure upstroke, whereas a wedge tracing with a prominent v wave has a more gradual upstroke that begins after the radial artery pressure upstroke. Fur-thermore, the wedge pressure v wave reaches its peak later in the cardiac cycle, after the ECG T wave as opposed to the simultaneous peaks of the systemic and pulmonary arterial peaks226,299 (see Fig. 45-27). Another distinguish-ing feature in patients with severe mitral regurgitation is the unusual morphology of the pulmonary artery wave-form itself. The larger the regurgitant v wave, the more it distorts the pulmonary artery waveform, giving it a bifid appearance and obscuring the normal end-systolic dicrotic notch291 (see Fig. 45-27).

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Figure 45-27. Severe mitral regurgitation. A tall systolic v wave (v) is inscribed in the pulmonary artery wedge pressure (PAWP) trace and also distorts the pulmonary artery pressure (PAP) trace, giving it a bifid appearance. The electrocardiogram (ECG) is abnormal owing to ventric-ular pacing. Left ventricular end-diastolic pressure is estimated best by measuring PAWP at the time of the electrocardiographic R wave, before onset of the regurgitant v wave. Note that mean PAWP exceeds left ventricular end-diastolic pressure in this condition. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)

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A close look at left atrial pressure-volume relations helps to explain the apparently paradoxical coexistence of severe mitral regurgitation and a normal pulmonary artery wedge pressure trace.300,301 Three factors determine whether mitral regurgitation produces a prominent v wave in the left atrial or wedge pressure traces: left atrial volume, left atrial compliance, and regurgitant volume (Fig. 45-28). Given that the left atrial pressure-volume relation is not linear, the same volume of regurgitation will result in a variable increment in systolic pressure, depending on the preexisting atrial volume at onset of systole. Furthermore, the nature of that relationship is dependent on the compliance (i.e., stiffness) of the left atrium. Although the total regurgitant volume of blood entering the left atrium will influence the height of the v wave, this clearly is not the only determinant of v wave magnitude. This may explain why patients with acute mitral regurgitation tend to have tall wedge pressure v waves—they have smaller, stiffer left atria with poorer compliance compared with those of patients with long-standing disease. It is not surprising that wedge pres-sure v waves are neither sensitive nor specific indicators of mitral regurgitation severity, and the height of these waves should not be used in such a manner.300 Promi-nent wedge pressure v waves may exist in the absence of mitral regurgitation when left atrial pressure is high, as might occur when the left atrium is compressed.302 Tall v waves are also seen commonly in patients with hyper-volemia, congestive heart failure, and ventricular septal defect.300 Note that the giant v waves observed in patients with ventricular septal defect are not caused by retrograde flow, but rather by excessive antegrade systolic flow into the left atrium due to the intracardiac shunt.303

In contrast to mitral regurgitation, which distorts the systolic portion of the wedge pressure waveform, mitral stenosis alters its diastolic aspect. In this condition, the holodiastolic pressure gradient across the mitral valve results in an increased mean wedge pressure, a slurred early diastolic y descent, and a tall end-diastolic a wave. Similar hemodynamic abnormalities are seen in patients with left atrial myxoma or whenever mitral flow is obstructed. Diseases that increase left ventricular stiffness

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Figure 45-28. V wave height as an indicator of mitral regurgitation severity. Left atrial pressure-volume curves describe the three factors that determine v wave height. A, Influence of left atrial volume. For the same regurgitant volume (x), the left atrial v wave will be taller if baseline atrial volume is greater (point B versus point A). B, Influence of left atrial compliance. For the same regurgitant volume (x), the left atrial v wave will be taller if baseline atrial compliance is reduced (point B versus point A). C, Influence of regurgitant volume. Beginning at the same baseline left atrial volume (points A and B), if regurgitant volume increases (X versus x), the left atrial pressure v wave will increase (V versus v). (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)



(e.g., left ventricular infarction, pericardial constriction, aortic stenosis, and systemic hypertension) produce changes in the wedge pressure that resemble in part those seen in mitral stenosis. In these conditions, mean wedge pressure is increased and the trace displays a prominent a wave, but the y descent remains steep, because there is no obstruction to flow across the mitral valve during dias-tole. Because patients with advanced mitral stenosis often have coexisting atrial fibrillation, the a wave will not be present in many of these cases226 (Fig. 45-29).

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Figure 45-29. Mitral stenosis. Mean pulmonary artery wedge pressure (PAWP) is increased (35 mm Hg), and the diastolic y descent is markedly attenuated. Compare the slope of the y descent in the PAWP trace with the y descent in the central venous pressure (CVP) trace. In addition, compare this PAWP y descent with the PAWP y descent in mitral regurgi-tation (see Fig. 45-27); a waves are not seen in the PAWP or CVP traces, owing to atrial fibrillation. Arterial blood pressure (ART). (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)

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Myocardial ischemia may be detected by PAC in several ways. Ischemia itself impairs left ventricular relaxation resulting in diastolic dysfunction, a pattern particularly characteristic of demand ischemia associated with tachy-cardia or induced by rapid atrial pacing.304-306 Impaired ventricular relaxation results in a stiffer, less compliant left ventricle, resulting in an increased left ventricular end-diastolic pressure. Not only does this, in turn, increases left atrial and wedge pressures, but the morphology of these waveforms changes as well, with the phasic a and v wave components becoming more prominent as diastolic filling pressure increases.307-309 Although myocardial isch-emia will often be detectable as a rise in pulmonary artery diastolic, mean, or systolic pressures, these changes are generally less striking than the accompanying change in wedge pressure and new appearance of tall a and v waves (Fig. 45-30). In patients with left ventricular ischemia, the tall wedge pressure a wave is produced by end-diastolic atrial contraction into a stiff, incompletely relaxed left ventricle.310 Although the diastolic dysfunction accom-panying myocardial ischemia leads to an increase in left ventricular end-diastolic pressure, this pressure elevation often coexists with a decreased left ventricular end-dia-stolic volume or preload.304 The dissociation between fill-ing pressure and filling volume in this condition must be appreciated to avoid diagnostic and therapeutic errors.

Myocardial ischemia also produces a characteristic pat-tern of left ventricular systolic dysfunction. Systolic dys-function is the hallmark of supply ischemia, caused by a sudden reduction or cessation of coronary blood flow to a region of the myocardium.306,311 With severe systolic dysfunction, changes in global left ventricular contractile performance may be detected with hemodynamic moni-toring. As ejection fraction falls significantly, left ventric-ular end-diastolic volume and pressure rise and systemic arterial hypotension and elevated pulmonary diastolic and wedge pressures develop.312 A more common hemo-dynamic manifestation of myocardial ischemia occurs when left ventricular geometry is distorted or when the region of ischemic myocardium underlies a papillary muscle, resulting in acute mitral regurgitation.313 This form of ischemic mitral regurgitation is often termed papillary muscle ischemia or functional mitral regurgita-tion. As noted earlier, PAC monitoring is particularly well suited to detect this event by revealing the onset of new regurgitant v waves in the pulmonary artery or wedge pressure traces (see Fig. 45-27).

Whether the PAC should be used in high-risk patients as a supplemental monitor for detection of myocardial ischemia remains controversial.309,314-316 None of the cur-rent methods for detecting perioperative myocardial isch-emia is perfectly sensitive or specific. Although patients with left ventricular ischemia are likely to have higher mean wedge pressures than those without ischemia, these differences are small and may be difficult to detect clini-cally.309 Furthermore, clear quantitative threshold values for mean wedge pressure or a and v wave peak pressures that are diagnostic of ischemia have not been identified, perhaps owing to the wide variations in normal patients. Consequently, when a PAC is used to diagnose myocar-dial ischemia, the best approach is to integrate the PAC data with other clinical and monitored information.317

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Figure 45-30. Myocardial ischemia. Pulmonary artery pressure (PAP) is relatively normal and mean pulmonary artery wedge pressure (PAWP) is only slightly elevated (15 mm Hg). However, PAWP morphology is markedly abnormal with tall a waves (21 mm Hg) resulting from the diastolic dysfunction seen in this condition. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)

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Right ventricular ischemia produces characteristic PAC waveform patterns that may be helpful in diagnosis and management. Just as left ventricular ischemia increases pulmonary artery wedge pressure, right ventricular isch-emia increases CVP. In fact, this is one of the few situa-tions in which CVP may be higher than wedge pressure. In addition, CVP waveforms may display a prominent a wave resulting from right ventricular diastolic dysfunc-tion, and a prominent v wave resulting from ischemia-induced tricuspid regurgitation.318,319 This particular CVP waveform is described as having an M or W configura-tion, referring to the tall a and v waves and interposed steep x and y descents. Severe pulmonary artery hyper-tension may also result in right ventricular ischemia and dysfunction as well as increased CVP, but this is distin-guished from primary right ventricular dysfunction in that the pulmonary artery pressure and calculated pul-monary vascular resistance are normal in primary right ventricular failure.

The CVP waveform in right ventricular infarction is similar to that from a patient with restrictive cardiomy-opathy or pericardial constriction, including elevated mean pressure, prominent a and v waves, and steep x and y descents.320 The cardinal feature common to these con-ditions is impaired right ventricular diastolic compliance, often termed restrictive physiology. In restrictive car-diomyopathy and right ventricular infarction, diastolic dysfunction impairs ventricular relaxation and decreases chamber compliance, whereas in constrictive pericarditis cardiac filling is limited by the rigid, often calcified peri-cardial shell. Impaired venous return decreases end-dia-stolic volume, stroke volume, and cardiac output. Despite reduced cardiac volumes, cardiac filling pressures are markedly elevated and equal in all four chambers of the heart at end-diastole (Fig. 45-31). Although PAC monitor-ing reveals this pressure equalization, the characteristic M or W configuration is more apparent in the CVP trace, most likely because of the damping effect of the pulmo-nary vasculature on the left-sided filling pressures.321-323

Another hallmark of pericardial constriction is observed in the right and left ventricular pressure traces. These demonstrate rapid but short-lived early diastolic ventric-ular filling, which produces a diastolic dip-and-plateau

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pattern or “square root sign.”93,324 In some cases, particu-larly when heart rate is slow, a similar waveform pattern may be noted in the CVP trace: a steep y descent (the diastolic dip) produced by rapid early diastolic flow from atrium to ventricle, followed by a mid-diastolic h wave (the plateau) from the interruption in flow imposed by the restrictive pericardial shell (see Fig. 45-31).

Like pericardial constriction, cardiac tamponade impairs cardiac filling, but in the case of tamponade, a

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Figure 45-31. Pericardial constriction. This condition causes eleva-tion and equalization of diastolic filling pressures in the pulmonary artery pressure (PAP), pulmonary artery wedge pressure (PAWP), and central venous pressure (CVP) traces. The CVP waveform reveals tall a and v waves with steep x and y descents and a mid-diastolic plateau wave (*) or h wave. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)



compressive pericardial fluid collection produces this effect. This results in a marked increase in CVP and a reduced diastolic volume, stroke volume, and cardiac output. Despite many similar hemodynamic features, tamponade and constriction may be distinguished by the different CVP waveforms seen in these two conditions. In tamponade, the venous pressure waveform appears more monophasic and is dominated by the systolic x pressure descent. The diastolic y pressure descent is attenuated or absent, because early diastolic flow from right atrium to right ventricle is impaired by the surrounding com-pressive pericardial fluid collection321,325,326 (Fig. 45-32). Clearly, other clinical and hemodynamic clues help dis-tinguish these diagnoses, such as the presence of pulsus paradoxus, an almost invariable finding in cardiac tam-ponade327 (see Fig. 45-14). Coexisting abnormalities such as tachycardia, arrhythmias, and atrial contractile failure may complicate interpretation of these waveforms. On occasion, localized pericardial constriction may simulate valvular stenosis, and hypovolemia may lower cardiac fill-ing pressures to within the normal range and confound the diagnosis.

Probably the single most important waveform abnormality or interpretive problem in PAC monitor-ing is discerning the correct pressure measurement in patients with large intrathoracic pressure swings like those receiving positive-pressure ventilation or those with labored spontaneous breathing. Just as in the case

30

15

0

1 sec

ac

x

v

Figure 45-32. Cardiac tamponade. The central venous pressure waveform shows an increased mean pressure (16 mm Hg) and attenu-ation of the y descent. Compare with Figure 45-31. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)

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of CVP monitoring, all transmural cardiac filling pres-sures are estimated best when end-expiratory pressure values are recorded. During positive-pressure ventila-tion, inspiration increases pulmonary artery and wedge pressures. By measuring these pressures at end-expira-tion, the confounding effect of this inspiratory increase in intrathoracic pressure is minimized328 (Fig. 45-33). Forceful inspiration during spontaneous ventilation has the opposite effect, but again, measurement of these pressures at end-expiration eliminates this confounding factor. Bedside monitors are designed with algorithms that aim to identify and report the numeric values for end-expiratory pressures but are often inaccurate.329,330 The most reliable method for measuring central vascu-lar pressures at end-expiration is examination of the waveforms on a calibrated monitor screen or paper recording.330,331

PHYSIOLOGIC CONSIDERATIONS FOR PULMONARY ARTERY CATHETER MONITORING: PREDICTION OF LEFT VENTRICULAR FILLING PRESSURE

One of the main reasons to measure pulmonary artery diastolic and wedge pressures is to be able to estimate left ventricular end-diastolic pressure, the closest surrogate to left ventricular end-diastolic volume, which is the true left ventricular preload (also see Chapter 46). When a PAC floats to the wedge position, the inflated balloon iso-lates the distal pressure-monitoring orifice from upstream pulmonary artery pressure. A continuous static column of blood now connects the wedged PAC tip to the junction of the pulmonary veins and left atrium. Thus, wedging the PAC, in effect, extends the catheter tip to measure the pressure at the point at which blood flow resumes on the venous side of the pulmonary circuit. Because resistance in the large pulmonary veins is negligible, pulmonary artery wedge pressure provides an indirect measure-ment of both pulmonary venous pressure and left atrial pressure.71,332

Pulmonary artery diastolic pressure (PAD) is often used as an alternative to PAWP to estimate left ventricu-lar filling pressure. This is acceptable under normal cir-cumstances because when pulmonary venous resistance is low, the pressure in the pulmonary artery at end of diastole will equilibrate with downstream pressure in the pulmonary veins and left atrium.333,334 From a monitor-ing standpoint, PAD has the added advantage of being

45

0

1

2

1 sec

Figure 45-33. Influence of positive-pressure mechanical ventilation on pulmonary artery pressure. Pulmonary artery pressure should be mea-sured at end expiration (1, 15 mm Hg) in order to obviate the artifact caused by positive-pressure inspiration (2, 22 mm Hg). (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)

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Down

available for continuous monitoring, whereas PAWP is only measured intermittently.

For both PAD and PAWP to be valid estimates of left ventricular filling pressure, the column of blood con-necting the tip of the wedged catheter and the draining pulmonary vein must be continuous and static. At the microcirculatory level, this channel consists of pulmo-nary capillaries that are subject to external compression by surrounding alveoli. West and associates described a three-zone model of the pulmonary vasculature based on the gravitationally determined relationships between relative pressures in the pulmonary arteries, pulmonary veins, and surrounding alveoli.335 In West zone 1, alve-olar pressure exceeds pressure in both the pulmonary artery and pulmonary veins, whereas in zone 2, it is intermediate between these two pressures (Fig. 45-34). A PAC positioned in both zone 1 and 2 will be highly susceptible to alveolar pressure, and measurements will reflect alveolar or airway pressure rather than left ventricular filling pressure. As such, the tip of the PAC must lie in zone 3 for PAWP measurements to be accu-rate. In most clinical settings, the supine position of the patient favors zone 3 conditions, a finding that has been confirmed by radiographic studies.336 However, when patients are placed in the lateral or semi-upright posi-tion, zone 2 may expand significantly. In general, zones 1 and 2 become more extensive when left atrial pressure is low, when the PAC tip is located vertically above the left atrium, or when alveolar pressure is high. Clues to an incorrectly positioned catheter include absence of nor-mal PAWP a and v waves, marked respiratory variation in PAWP, and a PAD that exceeds the PAWP measure-ment without excessively tall a or v waves visible on the trace.71

Assuming the PAC resides appropriately in West zone 3, the end-diastolic wedge pressure following atrial con-traction is generally the best predictor of left ventricular end-diastolic filling pressure as measured at the Z-point.

Flp(

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This is the point at which the slope of the left ventricu-lar pressure upstroke changes, approximately 50 millisec-onds after the ECG Q wave, and it generally coincides with the ECG R wave82 (Fig. 45-35).

However, in many cases, the left ventricular end-dia-stolic pressure is either underestimated or overestimated by the PAWP and/or PAD. These situations are summa-rized in Figure 45-36 and Tables 45-5 and 45-6 (also see several excellent references for further discussion of this topic).71,332,337

USE OF CENTRAL FILLING PRESSURES TO ESTIMATE LEFT VENTRICULAR PRELOAD

A detailed understanding of the relationship between left ventricular filling pressure and preload is important for clinically meaningful interpretation of PAC-derived data. Even when surrogate pressures such as pulmonary artery diastolic pressure and wedge pressure accurately estimate left ventricular end-diastolic pressure, many factors can influence the relationship between end-diastolic pressure and end-diastolic chamber volume, which is the true pre-load. For example, a pulmonary artery wedge pressure of 20 mm Hg is somewhat higher than normal, but depend-ing on its interpretation and the clinical setting, differ-ent treatments would be indicated. Proper interpretation of filling pressures requires assessment of juxtacardiac pressure and ventricular compliance. When juxtacardiac pressure and ventricular compliance are normal, a wedge pressure of 20 mm Hg is interpreted as hypervolemia, with an increased left ventricular end-diastolic volume causing the increased PAWP. However, different conclusions are reached if juxtacardiac pressure is increased, for example, as a result of cardiac tamponade, pericardial constriction, or positive-pressure ventilation. Furthermore, a wedge pressure of 20 mm Hg may mean that ventricular com-pliance is decreased, such as might occur with diastolic dysfunction from myocardial ischemia, hypertrophy, or

RA LA

Zone 1

Zone 2

Zone 3

Zone 1 PA > Pa > PV Zone 2 Pa > PA > PV Zone 3 Pa > PV > PA

LV

Pa

PV

PA

PA

RV

PA

PA

igure 45-34. The pulmonary artery catheter tip must be wedged in lung zone 3 to provide an accurate measure of pulmonary venous (Pv) or eft atrial (LA) pressure. When alveolar pressure (PA) rises above Pv in lung zone 2, or above pulmonary arterial pressure (Pa) in lung zone 1, wedge ressure will reflect alveolar pressure rather than intravascular pressure. LV, left ventricle; PA, pulmonary artery; RA, right atrium; RV, right ventricle. From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)



cardiomyopathy (Fig. 45-37). Under these two situations, a wedge pressure of 20 mm Hg can coexist with a small, hypovolemic left ventricle.

A fluid challenge may be useful in deciding whether hypovolemia exists. An intravenous bolus of crystal-loid or colloid solution (250 to 500 mL) is given over 15 minutes, and the change in wedge pressure is measured. Small increases in wedge pressure following the fluid challenge (e.g., less than 3 mm Hg) suggest that the ven-tricle is operating on the flat portion of its diastolic filling

80

40

0

P

Q S

T

R

LVP

LAP

ac

z(LVEDP)

v LAP

Figure 45-35. Relationship between left atrial pressure (LAP) and left ventricular end-diastolic pressure (LVEDP). LVEDP is measured at the Z-point on the left ventricular pressure (LVP) trace, at the time of the electrocardiographic R wave. Mean LAP (9 mm Hg) underestimates LVEDP (15 mm Hg), but the LAP a wave pressure peak closely esti-mates LVEDP.456 (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)


curve, whereas large increases in wedge pressure (e.g., 7 mm Hg or greater) suggest that the steep portion of the curve has been reached and that little further increase in stroke volume and cardiac output can be achieved with-out a substantial risk of producing hydrostatic pulmonary edema.71,330

The shared septum of the left and right ventricles as well as the presence of the pericardium lead to further interpretive problems in the use of CVP for assessing ventricular preload. Ventricular interdependence and pericardial constraint couple changes in right and left ventricular function, such that a primary change in right ventricular filling may produce a secondary and opposite change in left ventricular filling by altering its diastolic pressure-volume relation.338,339 For example, acute pul-monary artery hypertension increases right ventricular end-diastolic volume and pressure, shifts the ventricular septum leftward, and increases left ventricular end-dia-stolic pressure while simultaneously decreasing left ven-tricular end-diastolic volume, owing to a shift in the left ventricular pressure-volume relation to a steeper, stiffer curve. Conversely, primary changes on the left side can adversely affect the right heart structures in similar ways. Finally, numerous additional factors may alter the rela-tionship between CVP and left ventricular preload340 (see Fig. 45-37). With all these considerations in mind, both CVP and PAWP do not correlate with blood volume and do not predict the cardiac output response to an intrave-nous fluid challenge.227,341

PULMONARY ARTERY CATHETER–DERIVED HEMODYNAMIC VARIABLES

The cardiovascular system is often modeled as an electri-cal circuit, with the relationship between cardiac output, blood pressure, and resistance to flow related in a manner similar to Ohm’s law:

SVR = MAP − CVP

CO× 80

PVR = MPAP − PAWP

CO× 80

where SVR = systemic vascular resistance (dyne·sec/cm5)PVR = pulmonary vascular resistance (dyne·sec/cm5)MAP = mean arterial pressure (mm Hg)CVP = central venous pressure (mm Hg)MPAP = mean pulmonary artery pressure (mm Hg)PAWP = pulmonary artery wedge pressure (mm Hg)CO = cardiac output (L/min)Normal values for SVR and PVR are given in Table

45-7. When the numeric constant (80) in the above equations is not included, the units for SVR and PVR are termed Wood units rather than the derived metric unit values. Note that these calculations of systemic and pul-monary vascular resistance are based on a hydraulic fluid model that assumes continuous, laminar flow through a series of rigid pipes.342 Atrial pressures are used as the downstream pressure for systemic or pulmonary flow, with CVP used for right atrial pressure in the SVR calcu-lation and PAWP used for left atrial pressure in the PVR calculation.



D

RV

Pulmonary vascular resistanceHeart rate

CVP(A)

Diastolic RV P-V relationTricuspid disease

Diastolic LV P-V relationAlveolar pressurePulmonary venous disease

PADP(B)

PAWP(C)

LAP(D)

LVEDP(E)

LV volumeLV fiber lengthLV preload

Mitral valve diseaseHeart rate

PA

RA

Lung

D

LA

LV

A

B

C

E

Figure 45-36. Anatomic and physiologic factors that influence the relations between various measures of left ventricular (LV) filling and true LV preload. The further upstream the filling pressure is measured, the more confounding factors may influence the relation between this mea-surement and LV preload. CVP, Central venous pressure; LA, left atrium; LAP, left atrial pressure; LVEDP, left ventricular end-diastolic pressure; PA, pulmonary artery; PADP, pulmonary artery diastolic pressure; PAWP, pulmonary artery wedge pressure; P-V, pressure-volume; RA, right atrium; RV, right ventricle. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)

own

These formulas oversimplify the behavior of the car-diovascular system to a tremendous degree. A more phys-iologic model of the systemic circulation considers the vasculature to be a series of collapsible vessels with intrin-sic tone. This model, also called the vascular waterfall, describes a critical closing pressure in the downstream end of the circuit that exceeds right atrial pressure and serves to limit flow—an effective downstream pressure that is higher than the right atrial pressure used in the SVR formula. A detailed consideration of these issues is beyond the scope of this discussion and is available in other sources.343,344 The important point, though, for cli-nicians is that therapy focused on the fine adjustment of SVR may be very misleading and should be avoided.

TABLE 45-5 UNDERESTIMATION OF LEFT VENTRICULAR END-DIASTOLIC PRESSURE

ConditionSite of Discrepancy Cause of Discrepancy

Diastolic dysfunction Mean LAP <LVEDP

Increased end-diastolic a wave

Aortic regurgitation LAP a wave <LVEDP

Mitral valve closure before end-diastole

Pulmonic regurgitation

PADP <LVEDP

Bidirectional runoff for pulmonary artery flow

Right bundle branch block

PADP <LVEDP

Delayed pulmonic valve opening

Post-pneumonectomy PAWP <LAP or LVEDP

Obstruction of pulmonary blood flow

Modified from Mark JB: Predicting left ventricular end-diastolic pressure. In Mark JB, editor: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone, p 59.

LAP, Left atrial pressure; LVEDP, left ventricular end-diastolic pressure; PADP, pulmonary artery diastolic pressure; PAWP, pulmonary artery wedge pressure.

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Additional problems arise in considering the pulmo-nary vasculature and using the formulas as a measure of resistance to flow through the lung.345 The pulmonary vasculature is more compliant than the systemic vascula-ture, and marked increases in pulmonary blood flow may not produce any significant increase in pulmonary artery

TABLE 45-6 OVERESTIMATION OF LEFT VENTRICULAR END-DIASTOLIC PRESSURE

ConditionSite of Discrepancy Cause of Discrepancy

Positive end-expiratory pressure

Mean PAWP >Mean LAP

Creation of lung zone 1 or 2, or pericardial pressure changes

Pulmonary arterial hypertension

PADP >Mean PAWP

Increased pulmonary vascular resistance

Pulmonary venoocclusive disease

Mean PAWP >Mean LAP

Obstruction to flow in large pulmonary veins

Mitral stenosis Mean LAP >LVEDP Obstruction to flow across mitral valve

Mitral regurgitation

Mean LAP >LVEDP Retrograde systolic v wave raises mean atrial pressure

Ventricular septal defect

Mean LAP >LVEDP Antegrade systolic v wave raises mean atrial pressure

Tachycardia PADP >Mean LAP >LVEDP

Short diastole creates pulmonary vascular and mitral valve gradients

Modified from Mark JB: Predicting left ventricular end-diastolic pressure. In Mark JB, editor: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone, p 59.

LAP, Left atrial pressure; LVEDP, left ventricular end-diastolic pressure; PADP, pulmonary artery diastolic pressure; PAWP, pulmonary artery wedge pressure.



pressure. In addition, flow usually ceases at end-diastole in the low resistance pulmonary circuit. Thus, changes in pulmonary vascular resistance may result from intrinsic alterations in pulmonary vascular tone (constriction or dilation), vascular recruitment, or rheologic changes. For the pulmonary circuit, a better approach to evaluating the changes in pulmonary vascular resistance may be to examine the end-diastolic gradient between the pulmo-nary artery diastolic and wedge pressures (Fig. 45-38).

Another set of common calculations derived from stan-dard hemodynamic variables adjusts these measurements for the patient’s body surface area (BSA) in an attempt to normalize these measurements for patients of differ-ent sizes. The BSA is generally determined from a stan-dard nomogram based on height and weight. The most

20 20 20

25 10 25

+20 +20+10–5 –5

+20

A B C

LA LA LA

LVLV LV

TransducedPAWP

TransmuralPAWP

LV compliance Normal Normal Stiff

LV volume Increased Normal Normal (or reduced) (or reduced)

Figure 45-37. Influence of juxtacardiac pressure and ventricular compliance on left ventricular (LV) preload. Three interpretations of an increased transduced pulmonary artery wedge pressure (PAWP, 20 mm Hg) are possible. A, Juxtacardiac pressure (−5 mm Hg) and LV compliance are normal, transmural PAWP is increased (25 mm Hg), and LV volume is increased. B, Juxtacardiac pressure is increased (+10 mm Hg), LV compliance is normal, transmural PAWP is decreased (10 mm Hg), and LV volume is normal or decreased. C, Juxtacardiac pressure is normal, LV compliance is decreased, transmural PAWP is increased (25 mm Hg), and LV volume is normal or decreased. (From Mark JB: Atlas of cardiovascular monitoring, New York, 1998, Churchill Livingstone.)

TABLE 45-7 NORMAL HEMODYNAMIC VALUES

Average Range

Cardiac output (L/min) 5.0 4.0-6.5Stroke volume (mL) 75 60-90Systemic vascular resistance

(Wood units)15 10-20

(Dynes-sec-cm-5) 1200 800–1600Pulmonary vascular resistance

(Wood units)1 0.5–3

(Dynes-sec-cm-5) 80 40–180Arterial oxygen content (mL/dL) 18 16-20Mixed venous oxygen content

(mL/dL)14 13-15

Mixed venous oxygen saturation (%)

75 70-80

Arteriovenous oxygen difference (mL/dL)

4 3-4

Oxygen consumption (mL/min) 225 200-250


commonly indexed variables are the cardiac index (car-diac index = cardiac output/body surface area) and stroke volume index (stroke volume index = stroke volume/body surface area). On occasion, the systemic and pulmonary vascular resistances are indexed as well (systemic vascular resistance index = systemic vascular resistance × body sur-face area; pulmonary vascular resistance index = pulmo-nary vascular resistance × body surface area). In theory, normalizing hemodynamic values through “indexing” should help clinicians determine appropriate normal physiologic ranges to help guide therapy. Unfortunately, there is little evidence that these additional calculations provide valid normalizing adjustments. Body surface area is a biometric measurement with an obscure relation-ship to blood flow, and it does not adjust for variations between individuals based on age, sex, body habitus, or metabolic rate.346 The patient’s size and medical history is important in interpreting and treating changes in any of the measured or calculated hemodynamic variables. Therapy should not be solely directed towards achieving normal indexed values.

PULMONARY ARTERY CATHETERIZATION AND OUTCOME CONTROVERSIES

Pulmonary artery catheterization has stimulated much controversy. It is an expensive, invasive technique that is widely used but still not proven to improve patient out-come. The PAC controversy has been fueled in part by strongly worded editorials, written by prominent physi-cians, debating whether PAC use should be suspended pending scientific proof of its efficacy.347-349 Although similar controversies have surrounded the use of other widely adopted, highly technical, clinical monitor-ing techniques such as electronic fetal monitoring,350 physicians who use PACs should especially appreciate the uncertainties surrounding PAC monitoring and be fully informed of the evidence that must guide patient selection.351,352

The study published by Connors and colleagues in 1996 examining the association between PAC use dur-ing the first 24 hours of intensive care and subsequent survival marked a tipping point in the use of PACs for monitoring.353 This prospective multicenter cohort study included 5735 patients with predicted 6-month

45

0

1 sec

PAP

PAWP

Figure 45-38. Pulmonary hypertension. The increased gradient across the pulmonary vasculature causes pulmonary artery diastolic pressure to exceed pulmonary artery wedge pressure (PAWP). PAP, Pulmonary artery pressure. (From Mark JB: Atlas of cardiovascular mon-itoring, New York, 1998, Churchill Livingstone.)



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mortality in excess of 50%. Patients who were in the PAC-monitored group were judged to be sicker by every measurement recorded, although to the extent statisti-cally possible, authors used case-matching analyses and applied a propensity score to adjust for these confounding medical covariates. After all adjustments, PAC-monitored patients had increased lengths of hospital stay and 20% increased mortality, and they incurred increased costs. Moreover, no subgroup of patients appeared to benefit from PAC monitoring. The publication of this study was accompanied by a strongly worded editorial calling for a moratorium on PAC use or a randomized controlled trial to define its efficacy.347

In the years since the study by Connors and col-leagues, numerous studies have tried to determine whether patients are being helped or harmed by use of PACs. Many of these studies have been plagued by prob-lems in study design (lack of randomization, small sam-ple size), lack of standardization, and heterogeneity of both patients and clinical settings (medical versus surgi-cal, cardiac surgery patients versus patients in acute con-gestive heart failure). In addition, little consensus exists regarding which hemodynamic variables are the most relevant to be obtained from catheter use. Furthermore, appropriate therapeutic interventions in response to specific findings are not clear.283 Several large, random-ized, adequately powered studies have been published regarding the use of the PAC in various settings: general noncardiac surgery,233 vascular surgery,354 CABG sur-gery,338 nonsurgical patients with congestive heart fail-ure,355 patients with acute lung injury,356 and critically ill patients in the intensive care unit.357 Generally, these studies have shown no benefit to PAC use, but they also show no increase in mortality or in hospital or intensive care unit length of stay despite sometimes a more fre-quent incidence of adverse events, mainly infections or insertion-related events.

One common drawback to most of these large ran-domized studies is that they have necessarily examined the routine use of PAC and enrolled a sequential cohort of patients, most of them with a relatively moderate risk of death or complications. Also, not all of these studies have used a specific therapeutic intervention protocol.358

In especially high-risk patients, a clinical benefit from use of the PAC became evident. A review of 53,312 patients from the National Trauma Data Bank showed no mortality benefit to those treated with PACs in the group as a whole. However, in those with an injury severity scale greater than 25, those that arrived to the hospital in severe shock, or those older than 60 years of age, mortality was decreased significantly if PAC was used.359 In another cohort study of 7300 mixed medi-cal and surgical population, PAC use was associated with reduced mortality in patients with a high APACHE score (>31), but increased mortality in patients with a low APACHE score (<25).360 Last, in a cohort of 280 older patients undergoing colon surgery, preoperative optimi-zation with the use of PAC reduced mortality threefold in patients with a high Goldman’s cardiac risk index but was not beneficial in those at a low cardiac risk (also see Chapter 80).361

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PULMONARY ARTERY CATHETERIZATION: INDICATIONS

The most recent recommendation pertaining to the peri-operative use of PACs is the American Society of Anes-thesiologists practice guideline published in 2003.231 The task force considered PAC monitoring to be appropriate in high-risk surgical patients undergoing high-risk pro-cedures. Furthermore, the specific practice setting and the proficiency and experience of clinicians should be considered.

PAC use must be tailored to the degree of risk for the patient and the risk posed by the procedure itself. For example, a patient with advanced ischemic cardiomy-opathy who needs lower extremity amputation under regional anesthesia would not warrant PAC monitor-ing whereas a patient with stable ischemic heart disease scheduled for extensive abdominal cancer resection may benefit from perioperative use. Furthermore, the individual practice setting must be considered.231 Keats has termed this feature “the role of environment in the outcome of operation,” by which he means important unmeasurable aspects of the clinical setting, including, but not limited to, technical skill and experience.362 Clearly, all physicians and nurses using PAC must have the requisite knowledge and skills to use it safely and effectively.

The conclusion is that PAC use should be limited, although a moratorium on use is ill-advised. Indeed, data demonstrate a significant and continuing decrease in PAC usage.316 Use should be reserved to centers with sig-nificant experience and expertise. PAC generally should be used to monitor and guide therapy in patients at high risk for hemodynamic instability, those who are judged more critically ill by a variety of clinical means, and those who are in shock, especially if they are older and suffer from other systemic diseases.

Much uncertainty and controversy continue to sur-round PAC use. Among the many measurements and calculations possible from PAC, little consensus exists regarding the most meaningful or the most useful. Obvi-ously, PAC itself has no capacity to benefit unless it guides therapies that improve patient outcomes. Future research should focus on defining subgroups of patients who might benefit from the use of PAC, as well as defin-ing effective therapeutic interventions based on the hemodynamic information gained from PAC.351,358

SPECIAL TYPES OF PULMONARY ARTERY CATHETERS

The popularity of PACs is largely due to the fact that they are multipurpose and provide a wide range of supplemen-tary features for therapeutic and diagnostic applications. Some catheters have a third lumen, which is often used as an additional venous infusion line that opens 20 to 30 cm from the catheter tip. Specialized PACs allow temporary endocardial pacing or intracardiac ECG recording and may even have combinations of electrodes permanently implanted along its length to allow bipolar ventricu-lar, atrial, or atrioventricular pacing.363 These catheters can be especially useful for minimally invasive cardiac



surgery, where avoiding sternotomy hinders the place-ment of epicardial pacing leads.364 Other models have a special lumen that opens into the right ventricle, through which a thin bipolar wire may be introduced for endocar-dial ventricular pacing, or separate atrial and ventricular lumina for passage of two pacing wires for dual-chamber sequential pacing.365

Specific PAC modifications were designed to allow for continuous cardiac output measurement, mixed venous oxygen saturation monitoring, or right heart function evaluation, vastly expanding the types of physiologic information available to those caring for critically ill patients.

Mixed Venous Oximetry Pulmonary Artery CatheterAlthough the formal Fick cardiac output method is not widely applied in clinical practice outside the cardiac cath-eterization laboratory, the physiologic relations described by the Fick equation form the basis for another PAC-based monitoring technique termed continuous mixed venous oximetry. Rearrangement of the Fick equation reveals the four determinants of mixed venous hemoglobin satura-tion (Sv̇o2):

SvO2 = SaO2 − V̇O2

Q̇ × 1.36 × Hgb

where Svo2 = mixed venous hemoglobin saturation (%)Sao2 = arterial hemoglobin saturation (%)V̇o2 = oxygen consumption (mL O2/min)Q̇ = cardiac output (L/min)Hgb = hemoglobin concentration (g/dL)To the extent that arterial hemoglobin saturation,

oxygen consumption, and hemoglobin concentration remain stable, mixed venous hemoglobin saturation may be used as an indirect indicator of cardiac output. For example, when cardiac output falls, tissue oxygen extraction increases and the mixed venous blood will have a lower oxygen content and lower hemoglobin oxygen saturation. However, as noted in this equation, mixed venous hemoglobin saturation also varies directly with arterial hemoglobin concentration and saturation, and varies inversely with oxygen consumption. When any of these other variables change significantly, one cannot assume that a change in mixed venous hemo-globin saturation results solely from a change in cardiac output. Although these considerations may confound the use of mixed venous hemoglobin saturation as an indicator of cardiac output, monitoring this variable provides more comprehensive information about the balance of oxygen delivery and consumption by the body—not just the cardiac output value, but also the adequacy of that cardiac output compared with tissue oxygen requirements.366

Although mixed venous hemoglobin saturation may be determined by intermittent blood sampling from the distal port of PAC, a specially designed PAC can provide this information reliably and continuously. Fiberoptic bundles incorporated into PAC determine the hemoglo-bin oxygen saturation in pulmonary artery blood based on the principles of reflectance oximetry using either a


two- or three-wavelength system. A special computer con-nected to this PAC displays the mixed venous hemoglo-bin saturation continuously. The technology is typically incorporated into the standard PAC or the continuous cardiac output PAC (see later), in the latter case providing both continuous cardiac output and venous oximetry data.

Technical problems with continuous mixed venous oximetry are generally limited to improper PAC tip posi-tioning against the vessel wall or inaccurate calibration.367 Multi-wavelength fiberoptic technology and reflection intensity algorithms help to reduce wall artifacts caused by spurious reflections from a PAC thrombus or the pul-monary arterial walls. These catheters are calibrated at the bedside before use but may also be calibrated in vivo from a pulmonary artery blood gas sample. Recalibration every 24 hours is usually recommended because of a drift arti-fact. One note of caution is that a wedged PAC will read spuriously high oxygen saturation values corresponding to arterialized pulmonary blood. Most clinical trials com-paring PAC-derived continuous venous oximetry values with laboratory analysis of pulmonary artery blood sam-ples have shown good agreement between techniques.368 Mixed venous hemoglobin saturation values reflect global, whole-body measurement. Therefore, regionally inadequate blood flow and tissue oxygen delivery (such as with limb or intestinal ischemia) can coexist with a normal or high mixed venous hemoglobin saturation.

Recently, the technology to continuously measure oxygen saturation has been incorporated into central venous catheters as well. These catheters measure central venous saturation, measured in the superior vena cava. Normally, this saturation is around 70% versus 75% in the pulmonary artery.366 Low central venous saturation has been associated with increased complications both in trauma patients and in major surgery patients.369,370

The real value of measuring venous oxygen satura-tion lies in its ability to guide therapeutic interventions. Because one of the body’s physiologic compensations for anemia is increased oxygen extraction, low venous hemoglobin saturation has been used to guide the need for blood transfusion.371 Several studies have used venous hemoglobin saturation to guide interventions aimed at increasing cardiac output, a goal-directed approach. A recent randomized study in patients undergoing cardiac surgery has shown better outcome in patients random-ized to protocol-driven interventions aimed at achiev-ing mixed venous hemoglobin saturation above 70% (and blood lactate <2 mg/dL).372 Similarly, optimizing the central venous oxygen saturation has been shown to improve outcome in patients with early sepsis373 and in high-risk noncardiac and off-pump cardiac surgical patients.374,375

These studies have used strict protocol-driven thera-peutic interventions. In contrast, a large Veterans Affairs observational trial of 3265 cardiac surgical patients noted that 49% of patients received continuous mixed venous oximetry PACs, and use of this catheter was associated with increased cost but no better outcome than the stan-dard PAC group.376 In this study, however, no protocol was used to guide therapeutic interventions based on monitoring results.



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Right Ventricular Ejection Fraction Pulmonary Artery CatheterAlthough cardiovascular monitoring has focused pre-dominantly on left ventricular performance, in some instances right ventricular dysfunction may be the more important factor limiting circulation. Patient populations at increased risk for right ventricular dysfunction include those with chronic obstructive pulmonary disease, adult respiratory distress syndrome, pulmonary hyperten-sion, and right ventricular ischemia and infarction.377 Pulmonary artery catheter monitoring in patients with right ventricular infarction often reveals the character-istic hemodynamic patterns described earlier. However, accurate evaluation of right ventricular performance has proved more complicated. In patients with severe respi-ratory failure, for example, the confounding effects of mechanical ventilation with high levels of positive end-expiratory pressure (PEEP) have made interpretation of cardiac filling pressures difficult and, in some cases, misleading.378

Measurement of right ventricular ejection fraction (RVEF) with a specially designed PAC offers another method for evaluating right ventricular function. This method uses a standard PAC equipped with a rapid response thermistor that detects and quantifies the small changes in pulmonary artery blood temperature that occur with each heartbeat, in a manner somewhat analo-gous to a standard continuous cardiac output PAC. The cardiac output computer measures the residual fraction of thermal signal following each heart beat and derives the RVEF.379 Clearly, all factors that confound standard thermodilution cardiac output measurement (described later) will also interfere with accurate determination of RVEF. In addition, because the temperature changes mea-sured by the RVEF PAC are small beat-to-beat changes, the method will not work if the ECG R waves cannot be detected accurately, when the R-R interval is short owing to tachycardia, or if the cardiac rhythm is irregular.367 Comparison of PAC-based RVEF measurements with angiographic or nuclear techniques has yielded mixed results in terms of accuracy, but this may reflect, in part, the absence of a widely accepted reference standard for this measurement.379,380 Intraoperative use of the RVEF PAC has focused primarily on detection of right ven-tricular dysfunction in patients with coronary artery disease undergoing surgical revascularization. Reduced RVEF has been noted following cardiopulmonary bypass, particularly in patients with preexisting right coronary artery obstruction.381 However, RVEF is an extremely load-dependent measurement of right ventricular per-formance, and the clinician must keep this fact in mind to interpret this measurement properly.367,382 Clinical use of the RVEF PAC appears to have found its greatest application to date in critically ill patients, especially in those with respiratory failure.382,383 In these applications, the measurement of greatest interest has been the right ventricular end-diastolic volume, which is derived math-ematically from RVEF:

RVEDV = SV

RVEF

nloaded for Ivan Groisman ([email protected]) at Federacion Argentina De Asoci 06, 2018. For personal use only. No other uses without permi

where RVEDV = right ventricular end-diastolic volume (mL)

SV = stroke volume (mL)RVEF = right ventricular ejection fractionThe right ventricular end-diastolic volume appears to

correlate better with volume status than standard preload measurements, such as CVP or PAWP.383,384 These find-ings are not surprising given all the interpretive problems associated with cardiac filling pressure monitoring pre-viously discussed. It should be kept in mind, however, that the better correlation between right ventricular end-diastolic volume and cardiac output may result from the mathematical coupling of measurements, because both are derivatives of stroke volume determined with PAC. Furthermore, as in the case of standard PAC monitoring, the benefit of RVEF PAC monitoring, in terms of patient outcomes, remains unproven.231

CARDIAC OUTPUT MONITORING

Cardiac output is the total blood flow generated by the heart, and in a normal adult at rest, it ranges from 4.0 to 6.5 L/min. Measurement of cardiac output provides a global assessment of the circulation, and in combina-tion with other hemodynamic measurements (heart rate, arterial blood pressure, CVP, pulmonary artery pressure, and wedge pressure), it allows calculation of additional important circulatory variables, such as systemic and pul-monary vascular resistance and ventricular stroke work (see Table 45-7).

Three factors have driven efforts to measure cardiac output in clinical practice. The first is the recognition that in many critically ill patients, low cardiac output leads to significant morbidity and mortality.385 Second, clinical assessment of cardiac output is often inaccurate; for example, seriously ill patients with decreased cardiac output might have normal systemic arterial blood pres-sures.386 Finally, newer techniques for cardiac output measurement are becoming less invasive and thus might provide benefit to many patients without the attendant risks of invasive monitoring.386,387 The advantages and disadvantages of each technique must be appreciated for proper clinical application.

THERMODILUTION CARDIAC OUTPUT MONITORING

The thermodilution technique has become the de facto clinical standard for measuring cardiac output because of its ease of implementation and the long clinical experi-ence with its use in various settings. It is a variant of the indicator dilution method, described in more detail in Chapter 44, in which a known amount of a tracer sub-stance is injected into the bloodstream and its concen-tration change is measured over time at a downstream site.388 For thermodilution, a known volume of iced or room-temperature fluid is injected as a bolus into the proximal (right atrium) lumen of the PAC, and the result-ing change in the pulmonary artery blood temperature is recorded by the thermistor at the catheter tip. As in all other forms of cardiovascular monitoring, it is important

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to have a real-time display of the thermodilution curve resulting from each cardiac output measurement.389 This allows the clinician to discern artifacts that would invali-date the cardiac output measurement, such as unstable blood temperature, recirculation, or incomplete indicator injection.

Because several groups have demonstrated equiva-lent accuracy in cardiac output determinations when either ice-cold or room-temperature injectates are used, it appears that room-temperature injectate is preferred for almost all clinical applications.390 In adults, an injectate volume of 10 mL should be used, whereas in children, an injectate volume of 0.15 mL/kg is recommended.389

Usually, three cardiac output measurements per-formed in rapid succession are averaged to provide a more reliable result. When only a single injection was used to determine cardiac output, a difference between sequen-tial cardiac output measurements of 22% was required to suggest a clinically significant change. In contrast, when three injections are averaged to determine the thermodi-lution measurement, a change greater than 13% indicates a clinically significant change in cardiac output.391

Even when carefully performed, some studies have found that thermodilution cardiac output measurements may not agree with other reference methods.392,393 How-ever, few complications are directly attributable to the technique itself, and following the trend in cardiac out-put is probably more clinically useful than emphasizing any absolute value.

Sources of Error in Thermodilution Cardiac Output MonitoringSeveral important technical issues and potential sources of error must be considered to interpret thermodilution cardiac output measurements properly388,389 (Box 45-7). The thermodilution technique measures right ventricu-lar output. With intracardiac shunt, right ventricular and left ventricular outputs will not be equal. In patients with a left-to-right shunt, early recirculation of the thermal indicator can be seen to distort the downward slope of the thermodilution curve, and in patients with right-to-left shunt, some of the injected indicator will bypass the thermistor, resulting in overestimation of the left ventric-ular cardiac output.

Patients with tricuspid or pulmonic valve regurgita-tion pose additional problems for thermodilution car-diac output measurement owing to recirculation of the indicator across the incompetent valve. In patients with severe tricuspid regurgitation, the thermodilution curves have an abnormally prolonged decay time and the mea-sured cardiac output is simply unreliable, either underes-timated or overestimated, depending on the severity of valvular regurgitation and the magnitude of the cardiac output.389,394

Other technical problems with thermodilution cardiac output measurement are caused by inadequate delivery of the thermal indicator. Mishandling of an iced injec-tate syringe can warm the solution and reduce the signal-to-noise ratio of the thermal indicator administered. In addition, fibrin or blood clot on the PAC tip may lead to thermistor malfunction and result in spurious car-diac output values. Unrecognized fluctuation in blood

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temperature may also influence cardiac output measure-ment. In most patients, pulmonary artery blood tem-perature falls rapidly in the initial minutes following cardiopulmonary bypass when the rewarmed body core redistributes the heat gained at the end of bypass. Owing to this progressive decline in central core and pulmonary artery blood temperature, the thermal baseline is unsta-ble. Thermodilution cardiac output measurements made in the minutes following bypass are notoriously unreli-able, most often leading to marked underestimation of the true cardiac output.395 Other inaccuracies in thermo-dilution cardiac output measurement occur when pulmo-nary artery blood temperature changes because of rapid fluid infusion.396 Either overestimation or underestima-tion of cardiac output occurs, depending on the timing of the additional fluid bolus.

One controversy surrounding bolus thermodilution cardiac output monitoring is the proper timing of mea-surement in relation to the respiratory cycle, particularly in patients receiving positive-pressure mechanical ventila-tion, because right ventricular stroke output varies as much as 50% during the respiratory cycle. Although reproduc-ibility of consecutive measurements improves markedly when the bolus injections are synchronized to the same phase of the respiratory cycle, an accurate measurement of average cardiac output is achieved more reliably by mak-ing multiple injections during the different phases of the respiratory cycle and then averaging the results.389,397 Last, the measured thermodilution cardiac output can overesti-mate true cardiac output during low-flow states because of significant heat loss from slow injectate transit.398

CONTINUOUS THERMODILUTION CARDIAC OUTPUT MONITORING

Newer technologies applied to PAC monitoring allow nearly continuous cardiac output (CCO) monitoring using a warm thermal indicator.388,399 In brief, small quan-tities of heat are released from a 10-cm thermal filament incorporated into the right ventricular portion of a PAC, approximately 15 to 25 cm from the catheter tip, and the resulting thermal signal is measured by the thermistor at the tip of the catheter in the pulmonary artery. The heating filament is cycled on and off in a pseudorandom binary sequence, and the cardiac output is derived from cross correlation of the measured pulmonary artery tem-perature with the known sequence of heating filament activation.399 Typically, the displayed value for cardiac

Intracardiac shuntsTricuspid or pulmonic valve regurgitationInadequate delivery of thermal indicator

Central venous injection site within catheter introducer sheathWarming of iced injectate

Thermistor malfunction from fibrin or clotPulmonary artery blood temperature fluctuations

Following cardiopulmonary bypassRapid intravenous fluid administration

Respiratory cycle influences

BOX 45-7 Factors Influencing Accuracy of Thermodilution Cardiac Output Measurement

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output is updated every 30 to 60 seconds and represents the average value for the cardiac output measured over the previous 3 to 6 minutes. In a laboratory investigation examining how CCO measurements responded to unsta-ble hemodynamic conditions, such as hemorrhage and fluid resuscitation, Siegel and associates showed that CCO changes were markedly slower than changes detected by ultrasonic flow probe, blood pressure, or mixed venous oxygen saturation.400 In view of these inherent time delays, the PAC CCO method should be considered a con-tinual rather than a continuous real-time monitor.

In general, the CCO method has good agreement with standard bolus thermodilution cardiac output measure-ments or electromagnetic flow probe techniques.388,401 The device performed well in patients with a wide range of cardiac outputs (1.6 to 10.6 L/min) and core tempera-tures (33.2° C to 39.8° C). Reproducibility and precision appear to be better with the CCO method compared with the standard bolus thermodilution technique, probably because the continuous method displays a time-weighted average cardiac output value, as opposed to a single instantaneous measurement.402,403

The CCO PAC has been widely accepted into clinical use for a number of practical reasons. Although these catheters are more expensive than standard PACs, obviat-ing the need for bolus injections reduces nursing work-load and the potential risk of fluid overload or infection. Furthermore, because the CCO PAC provides a cardiac output value that is an average derived over the previous several minutes, beat-to-beat variations in stroke volume that occur during a single respiratory cycle are all equally represented. As a result, a cardiac output measured by the CCO method may provide a more accurate measurement of global cardiac output for patients receiving positive-pressure mechanical ventilation.

However, like cold bolus thermodilution techniques, warm thermal CCO has certain methodologic pitfalls that must be recognized and avoided. The CCO computer and catheter require a significant amount of time to warm up and may work poorly in an environment with a great deal of thermal noise, such as the cardiac operating room. As already emphasized, CCO monitors have an inherent 5- to 15-minute delay in responding to abrupt changes in cardiac output, and the magnitude of this delay depends on the type of physiologic perturbation, as well as the CCO computer monitor algorithm.400 Although modifi-cations of CCO algorithms provide a “STAT mode” rapid response time, acute changes in cardiac output are still detected more slowly by CCO monitoring than by other methods, such as direct arterial pressure or mixed venous oximetry. In effect, the CCO technique involves a funda-mental tradeoff between rapid response time and overall accuracy of measurement. The standards for these perfor-mance characteristics have not been defined, but must balance the response time against the stability of the dis-played value and its immunity from thermal noise.402

TRANSPULMONARY THERMODILUTION CARDIAC OUTPUT

For transpulmonary thermodilution measurement, ice-cold saline is injected into a central venous line while the


change in temperature is measured in a large peripheral artery (femoral, axillary, or brachial artery) via a special arterial catheter equipped with a thermistor.404 Several studies have shown adequate agreement with standard thermodilution cardiac output.405,406 Because the mea-surement lasts over several cardiac cycles, respiratory effects on stroke volume are averaged and eliminated, in contrast to standard thermodilution.407

Mathematic derivation from the transpulmonary ther-modilution curve can produce several additional useful indices. Extravascular lung water is a measure of pul-monary edema and can be used to guide fluid therapy in patients with acute lung injury or sepsis.408-410 Other derived indices are the global end-diastolic volume and intrathoracic blood volume. These indices are a better measure of cardiac preload than traditional measurements such as CVP or pulmonary artery wedge pressure.411,412 However, these indices still cannot predict cardiac output response to intravenous fluid administration.413 The last parameter derived from the transpulmonary thermodilu-tion curve is called the cardiac function index, calculated using cardiac output and the intrathoracic blood volume. It correlates closely with echocardiography-derived left ventricular ejection fraction.414

LITHIUM DILUTION CARDIAC OUTPUT MONITORING

The lithium dilution technique is another cardiac out-put monitoring method that derives its fundamental basis from indicator dilution principles.415 In brief, fol-lowing an intravenous bolus injection of a small dose of lithium chloride, an ion-selective electrode attached to a peripheral arterial catheter measures the lithium dilution curve, from which the cardiac output is derived. This is an accurate technique compared with standard thermo-dilution or electromagnetic flowmetry.416,417 The lithium indicator can be injected through a peripheral intrave-nous catheter with similar measurement accuracy, thus eliminating the need for a central venous line.418 This technique can also be used in children.419 Lithium dilu-tion cannot be used in patients who are taking lithium or those who have just received nondepolarizing neuro-muscular blockers (because these blockers also alter the lithium sensor electrode measurement).

OTHER METHODS FOR MONITORING CARDIAC OUTPUT AND PERFUSION

ESOPHAGEAL DOPPLER CARDIAC OUTPUT MONITORING

All of the ultrasound-based methods for cardiac output monitoring employ the Doppler principle (also see Chap-ters 44 and 46). Cardiac output can be intermittently measured by the Doppler technique during transtho-racic or transesophageal echocardiography examinations (see Chapter 46). A special esophageal Doppler probe has been developed that could be positioned and left in place for continuous monitoring without the need for time- consuming measurements and calculations by the



D

physician or ultrasonographer. The transducer is incor-porated into the tip of a probe resembling a standard esophageal stethoscope and allows continuous monitor-ing of cardiac output by measuring the Doppler shift of the interrogated blood flow in the descending thoracic aorta. The Doppler probe is inserted into the esophagus to a depth of approximately 35 cm from the incisor teeth and is adjusted to optimize the audible Doppler flow sound from the descending aorta. In most patients, opti-mal probe tip position is at the T5-T6 vertebral interspace or the third sternocostal junction, because the esophagus and the descending aorta lie in close proximity and run essentially parallel to each other at this location.420 The ultrasound transducer is mounted at a fixed angle that is anatomically defined and known by the cardiac output computer. This angle is then used to correct the resulting Doppler shift frequency to provide an accurate velocity measurement.

Several limitations of the esophageal Doppler tech-nique must be recognized to avoid incorrect data interpre-tation. This monitoring method interrogates blood flow in the descending thoracic aorta and therefore measures only a fraction of total cardiac output. To report total cardiac output, either the esophageal Doppler measure-ment must be “calibrated” by some alternative method, or an empirically determined correction constant of 1.4 is used.421 This constant is accurate for most patients but does not apply universally, especially in the pres-ence of conditions that redistribute blood flow (such as pregnancy), in aortic cross-clamping, and following car-diopulmonary bypass.420,422 In addition, the descending thoracic aorta diameter is either measured using A-mode ultrasound or calculated from a nomogram based on the patient’s age, sex, height, and weight.423 When calculated, the aortic diameter is assumed not to change throughout the cardiac cycle.424 In addition, the technique is likely to be inaccurate in the presence of aortic valve stenosis or regurgitation and in patients with thoracic aortic dis-ease. It is not easily applied in nonintubated, nonsedated patients, and it cannot be used in individuals with esoph-ageal pathology. Finally, like all ultrasound techniques, the acoustic window needed to acquire the Doppler sig-nal may not be adequate in some individuals, thereby precluding use of this method.

Advantages of the esophageal Doppler monitoring technique include its ease of use, minimal invasiveness, and inherent safety. It appears that limited experience is needed for clinical success—as few as 10 to 12 cases for accurate application of the technique.420 A recent review described 25 clinical trials comparing esophageal Doppler cardiac output measurement with PAC thermodilution measurements and noted that the Doppler cardiac out-put values correlated well with thermodilution measure-ments, showed minimal overall bias, and resulted in good tracking of directional changes in thermodilution cardiac output with low intra- and interobserver measurement variability.420

Recently, the esophageal Doppler method has seen renewed popularity.425,426 Current devices provide a clear visual display of the spectral Doppler waveform and also calculate and display additional hemodynamic variables, including the peak blood flow velocity, flow acceleration,


and heart rate–corrected flow time (Fig. 45-39). Some studies have shown that these additional measures pro-vide useful information about left ventricular preload, fluid responsiveness, contractility, and systemic vascu-lar resistance.421,427,428 One of the more important ben-efits of this monitor may be focusing clinical attention on optimizing stroke volume rather than total cardiac output. Indeed, in critically ill patients, complications may be better predicted by low stroke volume than by low cardiac output.429 Several studies have shown that volume resuscitation, guided by maximizing esophageal Doppler-measured stroke volume in moderate risk surgi-cal patients, reduces perioperative morbidity and short-ens hospital stay.425,426

BIOIMPEDANCE CARDIAC OUTPUT MONITORING

The technique of bioimpedance cardiac output monitor-ing was first described by Kubicek and associates and is based on changes in electrical impedance of the thoracic cavity occurring with ejection of blood during cardiac

TimeFlow time

* Rounding of waveform

Meanacceleration(slope)

Peakvelocity

Predominant change in waveform

FTc SD PV

Strokedistance

(area undercurve)

Vel

ocity

Phy

siol

ogic

cha

nge

from

bas

elin

e st

ate

↓ Contractility

↑ Contractility ↔

↔

↑

↔ *

↑

↓

↓ Preload

↑ Preload ↑

↓

↑

↓

↔

↔

↓ Afterload

↑ Afterload ↓

↑

↓

↑

↓

↑

Figure 45-39. The velocity-time waveform displayed by esophageal Doppler cardiac output monitoring devices reflects alterations in con-tractility, preload, and afterload. Stroke distance (SD) is directly related to calculated stroke volume and provides a useful surrogate measure of cardiac output. FTc, Systolic flow time corrected for heart rate; PV, peak velocity.



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systole.430 Their original formula relates these bioimped-ance measurements to stroke volume:

SV = ρL2/Zo2 • VET • max

dZdt

where SV = stroke volumeρ = specific resistivity of bloodL = thoracic lengthZO = basal thoracic impedanceVET = ventricular ejection time

maxdZdt

= maximum rate of impedance change during

systolic upstroke

For performing the measurements, disposable elec-trodes are applied to the skin surface along the sides of the neck and lateral aspect of the lower thorax, and a con-tinuous small electrical current is applied across the chest. Patient height, weight, and gender are used to calculate the volume of the thoracic cavity. Bioimpedance cardiac output is computed for each cardiac cycle and continu-ously displayed as an average value over several heart beats.

Although the bioimpedance method is accurate in healthy volunteers, its reliability deteriorates in criti-cally ill patients, including those with sepsis, pulmonary edema, aortic regurgitation, and cardiac pacing431-433 (also see Chapters 47, 67, and 101). More recent changes in signal processing techniques have improved the accu-racy of thoracic bioimpedance measurements and might increase its clinical acceptance.434

PARTIAL CO2 REBREATHING CARDIAC OUTPUT MONITORING

Another method for cardiac output monitoring that does not require pulmonary artery catheterization is the partial CO2 rebreathing technique.435,436 Owing to the difficulty encountered in the standard Fick method involving mea-suring oxygen consumption and mixed venous hemoglo-bin saturation, this alternative technique is based on a restatement of the Fick equation for carbon dioxide elimi-nation rather than oxygen uptake.

Q̇ = V̇CO2/(CvCO2 − CaCO2)

where Q̇ = cardiac outputV̇co2 = rate of carbon dioxide eliminationCvco2 = carbon dioxide content of mixed venous bloodCaco2 = carbon dioxide content of arterial bloodThis method uses the change in CO2 production and

end-tidal CO2 concentration in response to a brief, sudden change in minute ventilation. With a specially designed breathing system and monitoring computer, this mea-surement is easily performed in any tracheally intubated patient. Every 3 minutes, a computer-controlled pneu-matic valve intermittently increases dead space for a 50-second period, thereby causing partial rebreathing of exhaled gases. Changes in end-tidal CO2 in response to the rebreathing maneuver are used to calculate cardiac output by a differential version of the Fick equation for carbon dioxide. This method is entirely noninvasive, it

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can be performed every few minutes, and the brief epi-sodes of rebreathing pose no substantial risk to most patients, with end-tidal CO2 measurements increasing by less than 3 mm Hg. Unfortunately, accurate measure-ments with this technique require tracheal intubation for precise measurement of exhaled gases. Furthermore, changing patterns of ventilation may have an unpredict-able influence on the measurement. As with all Fick-based techniques, the partial CO2 rebreathing method measures pulmonary capillary blood flow as an indicator of total cardiac output and thus requires correction for pulmo-nary shunt.

There is good agreement between the partial rebreath-ing CO2 cardiac output method and other techniques, such as thermodilution. However, the clinical trials were small (i.e., number of patients studied) and mainly focused on specific patient groups, particularly coronary artery bypass surgery patients.437 The clinical role for this technique is mainly focused on short-term intra-operative applications or mechanically ventilated post-operative patients. Because of the mandatory increase in Paco2, the technique is relatively contraindicated in patients with increased intracranial pressure.

PULSE CONTOUR CARDIAC OUTPUT MONITORING

Analysis of the arterial pulse pressure waveform is one of the most recent developments in the area of cardiac output monitoring. Basically continuous measurement of cardiac output is derived from the analysis of the arterial pulse pressure waveform. These methods, gen-erally termed pulse contour cardiac output, determine stroke volume from computerized analysis of the area under the arterial pressure waveform recorded from an arterial catheter or even a noninvasive finger blood pressure waveform.438-441 Pulse contour methods offer the potential for noninvasive, continuous, beat-to-beat cardiac output monitoring. Also, the change in stroke volume from beat to beat (termed stroke volume varia-tion) can be used to evaluate volume status in ventilated patients.118,442

However, several shortcomings need to be consid-ered.443 First, a baseline calibration with a known cardiac output is required to account for individual differences in vascular resistance, impedance, and wave reflectance. Additionally, recalibration is required every 8 to 12 hours to account for changes in vascular characteristics over time. This need for external calibration might require the use of a more invasive technique, negating the noninva-siveness advantage of pulse contour methods. Recently, several systems were developed with the capability for an autocalibration based on patient’s demographic variables. However, the accuracy of this autocalibration in various clinical situations is questionable.444 A reasonably well-defined arterial pressure waveform with a discernible dicrotic notch is required for accurate identification of systole and diastole, a condition that might not exist under severe tachycardia or dysrhythmia, or other very low output states. Last, for a meaningful use of beat-to-beat variation in stroke volume (as well as systolic pres-sure or pulse pressure variation), the patient needs to be



on controlled mechanical ventilation with a tidal volume of at least 8 mL/kg body weight.445

Still, clinical trials in surgical patients have shown that the pulse contour cardiac output methods provide an acceptable level of accuracy with a bias of less than 0.5 L/minute compared with thermodilution cardiac output.440,446,447 Stroke volume variation above 10% is a useful predictor of responsiveness to intravenous fluid administration.106 Finally, goal-directed therapy based either on maximizing pulse contour–derived cardiac output or minimizing stroke volume variation results in improved perioperative outcome.448,449

GASTRIC TONOMETRY

Gastric tonometry aims at monitoring gastric circulation as an early indication of splanchnic hypoperfusion.450 A balloon-tipped tube is inserted into the stomach, and the saline or air in the balloon is allowed to equilibrate with the CO2 in the gastric lumen. Intermittently, the saline or air is aspirated and the CO2 level is measured. With development of gastric hypoperfusion, CO2 clearance from the gastric mucosa decreases, whereas CO2 produc-tion increases from bicarbonate titration of acid released by anaerobic metabolism. The CO2 from the mucosa dif-fuses freely to the gastric lumen and is detected by the tonometry device.

Gastric mucosal CO2 and pH are predictors of post-trauma and perioperative complications or death.451-

453 Also, therapy guided by gastric tonometry can improve clinical outcome in critically ill or perioperative patients.454,455 However, this somewhat cumbersome and time-consuming method for monitoring tissue perfusion has not been widely adopted.

Complete references available online at expertconsult.com

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Chapter 45 – Cardiovascular Monitoring - Fundanest

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