HAEMODYNAMIC MONITORING ( IABP, CVP, CO )

HAEMODYNAMIC MONITORING( IABP, CVP, CO )

Al jadidi Sulaiman Moderator: Dr Nik Azman

It is the measurement of haemodynamic

status

Haemodynamic status is an index of pressure

& flow within cardiovascular system –

pulmonary & systemic circulations

Haemodynamic monitoring..

Haemodynamic measurement are important

to establish – precise diagnosis - determine appropriate therapy - monitor response to therapy Extent of monitoring depends on how much

data is required to optimise pt’s condition, & how precisely data is to be recorded

Introduction

Early detection, identification, and treatment

of life-threatening conditions such as heart failure and cardiac tamponade

Evaluate the patient’s immediate response to treatment such as drugs and mechanical support

Evaluate the effectiveness of cardiovascular function such as cardiac output and index

Purpose of monitoring..

Previous experience using similar monitoring

technique was shown to be beneficial Next level – understanding the

pathophysiology of process being treated, such as heart failure or hypovolemic shock

Rationale for haemodynamic monitoring

(1)Diagnostic

causes of patient’s pathophysiological condition

(2)Therapeutic base on the index & clinical situation, specific

therapy & treatments are prescribed

(3)Research assess efficacy of new therapy

Indication

Any deficit or loss of cardiac function: such

as AMI,CHF,Cardiomyopathy

All types of shock;cardiogenic,neurogenic,or anaphylactic

Decreased urine output from dehydration, hemorrhage,G.I. bleed,burns,or surgery

Type of monitoring..

Invasive Arterial pressure

monitoring

Central venous pressure monitoring

Pulmonary artery pressure monitoring

cardiac output

pulse contour cardiac output

Non-invasive ECG Non-invasive blood

pressure Pulse oximetry Tissue perfusion

temperature mentation

Urine output Echocardiogram &

Doppler

Access to an artery or vein

catheter connected to fluid filled pressure tubing & pressure transducer

connected to bedside monitor

continuous & accurate

fluctuation: positional

calibration drift

leveling

different sites

Invasive pressure monitor

For accurate Haemodynamic pressure

readings, two baseline measurements are

necessary:

1. Calibration of the system to atmospheric pressure

2. Determination of the phlebostatic axis for

transducer height placement

Calibration of equipment

To zero the equipment, turn 3-way stopcock

open to air (atmospheric pressure), close to patient and flush system. The monitor is adjusted so that “0” is displayed, which equals atmospheric pressure.

Return the stopcock to original position to visualize the waveform and haemodynamic pressures.

zero once every 8 hours.

Zeroing the equipment

Left atrium - reference point on the chest Used as a baseline for consistent transducer

height placement. Obtaining the axis involves drawing a line

from the fourth intercostal space, where it joins the sternum, to a mid-axillary line.

The intersection of these lines approximates the level of the atria.

Phlebostatic Axis

The transducer air-reference stopcock is

leveled with this reference point to obtain accurate patient haemodynamic pressure.

Leveling..

Cannulation of an artery & attaching the

catheter to a fluid-filled transducer system

Continuous assessment of arterial perfusion to

the major organ systems of the body.

Arterial Pressure Monitoring

Direct arterial blood pressure monitoring

enables accurate continuous pressure

measurement.

Allow easy blood sampling for acid-base and

other measurements.

Indication

Usually the radial artery cannulation is used.

Other most common sites are dorsalis pedis,

brachial, femoral arteries.

Allen’s test should be performed before a

catheter is inserted into the radial artery to

ensure the presence of adequate collateral

circulation to the hand by the ulnar artery.

Arterial Line Insertion And Sites

Both the ulnar and radial arteries are

occluded.

Ask the patient to clench and unclench

the fist until the hand is blanched.

Release pressure on the ulnar artery only

and observe for color return to the hand.

Allen’s Test

If colour returns within 5-7 seconds, the

ulnar circulation is adequate.

Ulnar circulation is considered inadequate if

the hand remains blanched for longer than

15 seconds. The radial artery should not be

cannulated.

Allen’s Test

Insertion should be performed under sterile

technique.

The connecting tubing should be assembled and

flushed and the transducer zeroed and calibrated

before the catheter is inserted.

Secured the catheter once it is in place.

Arterial Line Insertion And Sites

A normal arterial

waveform should has 3 components: a rapid upstroke –

systole a clear dicrotic

notch – closure of aortic valve

a definite end-diastole

Normal Arterial Waveform

Pattern of different waveform

Direct intra-arterial measurement may

overestimate systolic pressure dt systolic overshoot

This is result of fluid-pressure transducer monitoring system

Can be overcome by ↑ damping of system ( ie by using smaller gauge cannula-transducer tubing)

Arterial pressure..

However, ↑ damping reduces the resonant

frequency, thus the sensitivity of the sytem. >30Hz for HR up to 180bpm >20Hz for HR up to 120bpm The tubing should be non-compliant & < 1 m

in length

Rough approx of SV, therefore CO can be

obtained from area under systolic pressure curve

However, correlation with CO assessed by thermodilution is poor, & the method is not sufficiently reliable for clinical decision-making

Derived variables..

Systolic time intervals are an indirect index of ventricular contractility

Pre ejection period (PEP) = interval from ventricular electrical activity (Q wave) ejection of blood from ventricle.

It consists of electromechanical delay btw the AP & initiation of ventricular contraction, and the isovolumetric contraction

PEP is inversely proportional to ventricular activity

Adequacy of preload.. The variation in arterial pressure is exaggerated

in the presence of reduced preload Significant correlation has been demonstrated

between the systolic arterial pressure variation & end-diastolic area estimated with TOE.

1. Ischaemia distal to cannula

-major sequalae a/w low CO, shock, sepsis,

prolonged cannulation, vasculitis &

hyperlipidaemia

2. Exsanguination

-flow thru 18G cannula can cause blood loss

of 500ml/min

3. spurious result

4. Infection

5. Intra-arterial injection of drug

Complication

The morbidity associated with arterial

cannulation is less than that associated with 5 or more arterial punctures!!

Prevention of blood loss

Prevention of local obstruction

prevention of air embolism

Prevention of sepsis

Accuracies

Nursing responsibilities

Damped Waveforms

Pressure bag inflated to 300 mmHg

Reposition extremity or patient

Verify appropriate scale

Flush or aspirate line

Check or replace module or cable

Troubleshooting..

Directly reflects RA pressure

Indirectly reflects the preload of the right

ventricle(RV) or RV end-diastolic pressure.

Determined by the interaction of venous

tone, central venous volume (blood

returning to the heart), and the pumping

ability of the heart

Central Venous Pressure Monitoring

CVP is measured in the superior vena cava or

the RA.

Normal ranges 4 – 12 cmH2O

Central Venous Pressure

Common sites

Internal jugular

vein

Subclavian vein

Brachial vein

Femoral vein

The head is placed in a

dependent position (Trendelenburg),

which causes the internal jugular vein to

become more prominent, facilitating line

placement.

Position

A long intravenous catheter is inserted into the

large veins of the upper thorax (subclavian or

internal jugular) are most frequently used for

percutaneous CVP line insertion.

Catheter Placement

Threaded into position in the vena cava close

to the right atrium.

Correct placement confirmed by observing

pressure change with respiration, aspirating

blood freely thru catheter & CXR.

Catheter Placement

Measurement of central venous

pressure

Measurement of central venous

oxygenation

Parenteral nutrition

Administration of vasoactive and

inotropic agents

As a venous access when all IV sites

have been exhausted

Indication

CVP is used as guide to right ventricular filling However, right ventricular preload is determined

by EDV (not pressure) hence Isolated CVP reading is of limited value without

knowledge of ventricular compliance Compliance varies from patient to patient, & with

time in the same patient Thus dynamic changes in CVP are more useful

than absolute values.

If CVP ↑ <3mmHg in response to fluid challenge (eg 50-200ml of colloid over10min) more volume may be required

If CVP ↑ >7mmHg, fluid loading is then maximal If the CVP return to within 3mmHg of its original

value w/in 10min, risk of pulmonary oedema is moderate, no further filling is required

In most patients, adequate RV filling = LV filling,

except in lung disease with PHT, or in impaired RV fx (eg

severe sepsis & some patient with inferior MI)

CVP and PAOP are poor indicators for cardiac preload; they are the result of at least four components: Vascular filling Cardiac contractility Vascular compliance Intrathoracic pressure

They have wide normal ranges, large inter-individual scatter and low sensitivity for hypovolemia

Measuring errors may result from: Incorrect zero calibration, damping of pressure curve Positioning of the patient Ventilation (PEEP, ventilation phase, lung zone) Positioning of the catheter

condition Pressure changes Waveform changes

Tricuspid regurgitation

Increased RA pressure

Prominent v wave, x descent

RV infarction RA & RV pressures elevated. RAP does not fall and may rise in inspiration

Prominent x and y descent

Constrictive pericarditis

RA, RV diastolic, PA diastolic and occlusion pressure elevated & equalised. RAP may rise in inspiration

Prominent x and y descent

Pericardial temponade

RA, RV diastolic, PA diastolic and occusion pressure elevated & equalised. RAP usually falls in inspiration

y descent damped or absent

Hypervolaemia: - volume overload

hepatic disease

depressed cardiac function

vasoconstriction

cardiac tamponade

chronic or acute pulmonary hypertension

PEEP with mechanical ventilation

Factors increase CVP reading

Hypovolaemia: venous return

haemorrhage

dehydration

loss of vascular tone (sepsis) venous pooling

Factors decrease CVP reading

1. Associated with insertion-pneumo/haemothorax-arterial puncture-air embolism-arrhythmias (especially with Seldinger method)-nerve injury (eg Horner’s syndrome)-mediastinal / pleural effusion-chylothorax (left IJV,subclavian)2. Associated with use-sepsis-disconnection, leading to bleeding / air embolus-pleural or pericardial effusion dt use of misplaced catheter

Complication

Cardiac Output

Monitoring..

Methods of estimating CO

Impedance cardiography – BioZ method CO2 rebreathing technique – NICO method Trans-esophageal Echo

Methods of measuring CO PA catheter thermodilution

Intermittent Continuous – Abbot, Baxter, TruCCO

Pulse contour analysis – LidCo, PiCCO

Cardiac output

Impedance Cardiography

CO2 Re-breathing Method

Trans-esophageal Echo

PA Thermodilution Method

Requires insertion of a pulmonary artery catheter with a thermistor attached to the tip.

A bolus of room temperature saline is injected in to the RA, and the corresponding temperature drop is measured by the thermistor in the PA.

Stewart-Hamilton formula is used to calculate the volume of blood in which the bolus was diluted.

Measurement of CO is intermittent, and requires injections of thermodilution bolus.

The heart is a series of 4 chambers.

The same volume of blood is transferred from chamber to chamber during the heart cycle.

If we measure the volume of blood ejected by any one of the chambers, it is equal to the amount ejected by LV in to the aorta (ie SV).

How CO is measured..

RA RV LA LV SV

The temperature drop is graphed and Stewart-Hamilton formula

is applied to the graph to calculate the SV.

Basis: if the temperature (t) and volume (v) of the injectate is known, and if the temperature of blood after dilution (tb) is also known, it is possible to calculate the volume of blood (vb):

v . t vb . vt

The calculation

Temp difference -t

Time

Tb x dt

(Tb - Ti) x Vi x

K

Tb

Injection

t

∫D=COTD a

Tb = Blood temperatureTi = Injectate temperatureVi = Injectate volume∫ ∆ Tb

. dt = Area under the thermodilution curve

K = Correction constant, made up of specific weight and specific heat of blood and injectate

The CO is calculated by analysis of the thermodilution curve using the modified Stewart-Hamilton algorithm

Calculation of the Cardiac Output

The area under the thermodilution curve is inversely proportional to the CO.

36,5

37

5 10

Thermodilution curves

Normal CO: 5.5l/min

36,5

37

36,5

37

Time

low CO: 1.9l/min

High CO: 19l/min

Time

Time

Temperature

Temperature

Temperature

Later adaptations of the PA thermodilution

method allowed automatic continuous cardiac output measurement without the need for injections: Abbot / Baxter CCO method – a heating element

proximal to the thermistor creates boluses of warmed blood.

TruCCO method – system measured the amount of energy necessary to keep a heating element at a constant temperature of 1 degree above the blood temperature. Very short response time.

Continuous Cardiac Output

The pulse contour method for determining

cardiac output is based on the following principles: The hemodynamic pressure in the aorta is a

product of: The volume of blood ejected to the aorta during

systole(stroke volume) Compliance of the walls of the aorta and central

arteries The three values exist in a proportional relationship

AoBP SV / Cp

Pulse Contour Analysis

The aortic compliance usually varies very

slowly. Vasoactive substances (adrenaline, dopamine etc) have no appreciable effect on the compliance of the aorta or the large arteries, as the walls of these vessels contain more fibrous tissue than muscle.

If the aortic compliance could be measured, the equation could be solved to derive the stroke volume from the aortic blood pressure.

SV AoBP . Cp

Basic Principles Of The Method

There are no direct methods for measuring aortic

compliance. However the previous equation could be used to

calculate the aortic compliance, if the values for aortic blood pressure and stroke volume were known.

Cp SV / AoBP

Therefore, in order to measure SV using pulse contour analysis, SV must first be measured using some other method! ( = calibration)

The Practical Difficulties

Step 1: Continuous AoBP measurement Step 2: Calibration Step 3: Calculation of SV based on AoBP

SV AoBP . Cp

Pulse Contour Analysis

For all practical purposes, the pressure measured in a large artery (axillary or femoral) can be substituted for AoBP

The various methods of continuous cardiac

output derivation using pulse contour analysis differ by their calibration methods: Indicator dilution – LidCo method Thermodilution – PiCCO method

Methods Of Pulse Contour Analysis

Uses trans-pulmonary thermodilution to

calibrate the pulse contour analysis. A bolus of room-temperature saline is injected

in to the SVC through the triple lumen CVP line. The drop in blood temperature is measured at

the femoral artery using a thermistor attached to the tip of the femoral artery catheter.

After calibration, the cardiac output is calculated continuously using the femoral artery pressure waveform.

PiCCO Method

Preload

Filling Pressures

CVP / PCWP

Volume Responsiveness

SVV / PPV

Volumetric

Preload parameters

GEDV / ITBV

The global end-diastolic volume consists of the

end-diastolic volumes of all four cardiac chambers.

Even if this volume does not exist physiologically (diastole of all four cardiac chambers is not simultaneous), it does reflect the filling status of the heart and is a valid parameter of cardiac preload compared to the filling pressures.

GEDV

GEDV shows good correlation with the stroke

volume Better than CVP or PCWP

ITBV = GEDV + PULMONARY BLOOD VOLUME The intrathoracic blood volume is usually 25%

higher than the global end-diastolic blood volume. A linear association has been demonstrated for the two parameters.

The ITBV can therefore be calculated from the GEDV.

ITBV

Intrathoracic pressure

Venous return to left and right ventricle

Left ventricular preload

Left ventricular stroke volume

Systolic arterial blood pressure

Intrathoracic pressure

„Squeezing “ of the pulmonary blood

Left ventricular preload

Left ventricular stoke volume

Systolic arterial blood pressure

PPmax PPmin

PPmax

PPmin

Inspiration

Reuter et al., Anästhesist 2003;52: 1005-1013

Physiology of the dynamic parameters of volume responsiveness

Expiration Inspiration Expiration

Early Inspiration Late Inspiration

79

Fluctuations in blood pressure during the respiration cycle

SVmax

SVmin

SVmean

SVV = Stroke Volume Variation

• The variation in stroke volume over the respiratory cycle

• Correlates directly with the response of the cardiac ejection to preload increase (volume responsiveness)

mean

Role of the dynamic volume responsiveness parameters SVV / PPV

PPV = Pulse Pressure Variation

• The variation in pulse pressure amplitude over the respiration cycle • Correlates equally well as SVV for volume responsiveness

PPmax

PPmean

PPmin


A PPV threshold of 13% differentiates between responders and non-responders to volume administration

Michard et al, Am J Respir Crit Care Med 162, 2000

Respondersn = 16

Non – Respondersn = 24


respiratory changes in arterial pulse pressure (%)

- are good predictors of a potential increase in

CO due to volume administration

- are only valid with patients who are fully ventilated and who have no cardiac arrhythmias

SVV and PVV

- is useful for differentiating and quantifying

lung oedema

- is, for this purpose, the only parameter available at the bedside

- functions as a parameter for fluid overload

Extra Vascular Lung Water

• is calculated as the difference between MAP and CVP divided by CO

• as an afterload parameter it represents a further determinant of the cardiovascular situation

• is an important parameter for controlling volume and catecholamine therapies

(MAP – CVP) x 80SVR =

CO

Afterload parameter

SVR = Systemic Vascular Resistance

MAP = Mean Arterial PressureCVP = Central Venous PressureCO = Cardiac Output80 = Factor for correction of units

Eg: PICCO technology

Central venous catheter

PULSIOCATHArterial thermodilution catheter (femoral, axillary, brachial)

Injectate temperature sensor housing

Patient with secondary myeloid leukemia due to non-Hodgkin’s lymphomaCurrently: aplasia as a result of ongoing chemotherapy.Transfer from the oncology ward to intensive care unit due to development of septic status

Clinical Case

Status on transfer to the Intensive Care Unit

Initial Therapy

Given 6500 ml crystalloids and 4 PBC

Hemodynamic BP 90/50mmHg, HR 150bpm SR, CVP 11mmHgRespiration SaO2 99% on 2L O2 via nasal prongsAbdomen Severe diarrhoea, probably associated with chemotherapyRenal Retention values already increasing, cumulative 24h diuresis 400mlLaboratory Hb 6.7g/dl, Leuco <0.2/nl, Thrombo 25/nl

High fluid loss because of severe diaphoresis

Haemodynamics • despite extensive volume therapy during the first 6 hours, catecholamines had to be commenced

• requirement for catecholamines steadily increased• echocardiography showed good pump function• CVP increased from 11 to 15mmHg

Respiration • respiratory deterioration with volume therapy: SaO2 90% on 15L O2/min, pO2 69mmHg, pCO2 39mmHg, RR 40/min

• radiological signs of pulmonary edema • started on intermittent non-invasive BIPAP ventilation

Renal • ongoing poor quantitative function despite the use of diuretics (frusemide)

Infection Status • evidence of E.Coli in the blood culture

Diagnosis: Septic Multiorgan Failure

Ongoing Development

Therapeutic Problems and Issues

Haemodynamics • further requirement for volume? (rising catecholamine needs despite good pump function)

• problematic assessment of volume status (CVP initially raised, patient diaphoretic / diarrhoea)

Respiration • evidence of lung edema (deterioration in pulmonary function) • danger of need for intubation and ventilation with high risk of ventilator-

associated pneumonia (VAP) because of immunosuppression

Renal • impending anuric renal failure

Application of the PiCCO system

- continuation of the noradrenaline infusion- careful GEDI guided volume therapy

Initial measurement

3.4

760

14

950

16

Normal values

3.0 – 5.0 l/min/m2

680 - 800 ml/m2

3.0 – 7.0 ml/kg 1700 - 2400 dyn*s*cm 5 m2

2 - 8 mmHg

Cardiac Index

GEDI

ELWI

SVRI

CVP

Other therapy

- stabilization of haemodynamics- steady noradrenaline requirement- start of negative fluid balance, guided by the PiCCO parameters

Further course

- non-invasive ventilation- targeted antibiotic therapy - administration of hydrocortisone / GCSF

PiCCO values the next day

Actual values

3.2

750

8

1810

14

Normal values

3.0 – 5.0 l/min/m2

680 - 800 ml/m2

3.0 – 7.0 ml/kg 1700 - 2400 dyn*s*cm 5 m2

2 - 8 mmHg

CI

GEDVI

EVLWI

SVRI

CVP

- stabilization of pulmonary function- cessation of catecholamines- good diuresis with frusemide

Actual values

3.5

780

14

990

16

Normal range

3.0 – 5.0 l/min/m2

680 - 800 ml/m2

3.0 – 7.0 ml/kg 1700 - 2400 dyn*s*cm 5 m2

2 - 8 mmHg

CI

GEDI

ELWI

SVRI

CVP

PiCCO values the following day

GEDI with volume therapy persistently within the high normal range, however no increase in ELWI

Pulmonary Artery / Swan Ganz Catheter

Information derived from PA catheter

Directly measured CVP PAOP Pulmonary

artery pressure SvO2 Cardiac output

Calculated Systemic

vascular resistance

Pulmonary vascular resistance

Stroke volume Oxygen delivery

Associated with cordis placement Ventricular arrhythmias requiring treatment 1.3 –

1.5% Right bundle branch block ~0.5 -5% Pulmonary artery rupture ~0.06 to 0.2% Pulmonary artery pseudoaneurysm formation Pulmonary infarction ~ 1.4% Thromboembolic events ~1.6% Mural thrombi Sterile cardiac valve vegetation Endocarditis esp of the pulmonic valve

Swan complications

Thank you for listening…

HAEMODYNAMIC MONITORING ( IABP, CVP, CO )

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