Hypotension

Hypotension

Hypotension is common in the immediate postoperative period. Contributing

factors include hypovolemia, vasodilatation (relative hypovolemia), anemia,

pneumothorax, hemothorax, cardiac tamponade, electrolyte imbalance, hemorrhage,

metabolic alterations, and arrhythmias. Effective treatment of hypotension depends upon

quickly identifying the causes and initiating the appropriate treatment. Detrimental

complications can occur even with brief periods of hypotension, thus aggressive and

expedient treatment is needed.

When hypotension is accompanied by low CVP and PAWP volumes resuscitation

is needed to correct hypovolemia. A combination of crystalloids, colloids, and blood

products may be used. If anemic, packed red cells should be used, as hypotension is

commonly resolved when the hemoglobin is normalized. Large volumes of fluid are often

required due to fluid shifts, postoperative bleeding, and increased urine output in the

immediate postoperative period.

If hypotension persists after volume resuscitation, there may be a significant

vasodilatation requiring vasopressors to normalize blood pressure (relative hypovolemia).

This can be due to a loss of vascular tone that occurs as a result of the inflammatory

process after blood is exposed to foreign surfaces during extracorpeal bypass resulting in

vasoplegia syndrome (Raja and Dreyfuss 2004). Vasoplegia syndrome is characterized by

hypotension, tachycardia, increased cardiac output, decreased systemic vascular

resistance, and low filling pressures. It is poorly responsive or unresponsive to fluid alone

(Raja and Dreyfuss 2004).

Vasoplegia can also be resistant to vasopressor therapy and may be treated along

with steroids and vasopressin to help normalize blood pressure. Vasodilatation can be so

severe that high doses of vasopressors are often required to maintain blood pressure.

Any patient not responsive to fluids and vasopressors should be screened for

secondary (relative) adrenal insufficiency. Relative adrenal insufficiency occurs during

inflammation when the body becomes desensitized to glucocorticoid responsiveness at

the cellular level. Symptoms include eosinophilia, unexplained hypothermia,

hyperpigmentation, hyperkalemia, hyponatremia, nausea, vomiting, and abdominal pain

(Shenker and Skatrud 2001).

Use of steroids remains controversial in cardiac surgery (Shenker and Skatrud

2004) but more institutions are utilizing protocols to identify secondary adrenal

insufficiency. Secondary (relative) adrenal insufficiency is responsive to steroids and

raises cortisol levels. Cortisol is vital in regulating blood pressure by increasing the

sensitivity of the vasculature to epinephrine and norepinephrine. In the absence of normal

amounts of cortisol, widespread vasodilation occurs.

Hypotension can occur from compression of the heart or large vessels by

pneumothorax, hemothorax, and cardiac tamponade. Careful assessment, radiographs,

and echocardiography can help quickly identify a mechanical compression. Correction of

these life-threatening conditions should result in quick resolution of associated

hypotension, then vasoactive medications can usually be weaned rapidly.

Muscle, including the heart, depends on readily available amounts of vital

electrolytes to function normally. Electrolytes should be checked regularly and replaced

aggressively. Potassium, magnesium, and ionized calcium levels should be assessed

within one hour of admission to the cardiac recovery unit. A great deal of time is spent

normalizing electrolyte levels especially in the first eight hours postoperatively. Recheck

these levels at frequent intervals.

Hypokalemia and hypomagnesemia can contribute to cardiac arrhythmias, which

lead to or exacerbate hypotensive states. Fluid shifts, cardioplegia, diuresis, and exposure

to large doses of intravenous insulin can cause dramatic drops in potassium and

magnesium. Serum levels should be checked and replaced as often as needed to maintain

normal levels.

Magnesium levels must be replaced before potassium deficiencies can be

corrected. Administering potassium and not correcting magnesium will result in

increased excretion of potassium by the kidneys and further hypokalemia. Magnesium is

more slowly absorbed by the cells so prompt replacement is important (Smetana 1997).

Consider replacing magnesium first, or simultaneously replacing both magnesium and

potassium if potassium levels are dangerously low and intravenous access permits.

Calcium levels should be assessed utilizing an ionized calcium test. The ionized

calcium is the amount active in the bloodstream and available for use by the body.

Adequate calcium is necessary for muscle contraction. Ionized calcium levels drop in

response to citrate, which binds to calcium, and is added to blood as an anticoagulant.

Ionized calcium levels should always be rechecked if hypotension is present after

transfusion.

Ionized calcium levels rise quickly in response to calcium chloride, which has a

high bioavailability as compared to calcium gluconate. Intravenous replacement can lead

to quick resolution of hypotension and necessitate rapid weaning or a decrease in

dependence on vasopressors. Calcium chloride should always be given through a central

line due to the intense burning sensation that can occur if given peripherally. Calcium

gluconate may be given slowly via peripheral line but larger doses are needed due to the

decreased bioavailability of the calcium in this form.

If vasopressors appear to become ineffective acidosis should be considered and

can occur from either metabolic or respiratory sources.

Respiratory acidosis can usually be contributed to hypoventilation. In the absence

of pneumothorax, increasing the minute volume (minute volume is the respiratory rate

times the tidal volume) will usually correct the hypercarbia that leads to acidosis. In

extubated patients this may mean increasing deep breathing through incentive spirometry

and coughing. If patients are sleepy and hypoventilate post-extubation, consider the need

for reintubation or bi-level positive airway pressure therapy (BiPAP).

Naloxone (Narcan®) may be indicated if hypoventilation is present after having

received narcotics. When this occurs, small doses of naloxone should be enough to

stimulate respiration. Care should be taken to closely monitor for continued

hypoventilation due to the relatively short half-life of naloxone when compared to some

narcotics.

Metabolic acidosis may be multifactorial and can be treated with bicarbonate

when there is an associated low bicarb level. If acidosis is due to low cardiac output

states, correcting cardiogenic shock should resolve the acidosis.

Vasopressors are used to normalize blood pressure when all known causative

factors are corrected and hypotension persists. Any patient receiving a vasopressor should

be continuously assessed for hypovolemia, which can occur even after adequate volume

resuscitation.

Vasopressors are commonly started in the operating room and can be weaned

rapidly after recovery from anesthesia in most cases. They are titrated to maintain blood

pressure within ordered parameters, usually mean arterial pressure over 65mm/hg or a

systolic pressure over 90mm/hg. Higher pressures may be required to perfuse organs

when patients have a history of extreme hypertension, carotid artery disease, peripheral

vascular disease, or renal dysfunction. Always use the least amount of drug necessary to

maintain the ordered parameters. Avoid any disruption in infusion, even brief disruptions

can result in severe hypotension.

The starting dose will be dictated by the severity of hypotension and should be

ordered by the health care provider. Too large of a starting dose may result in sudden

hypertension and the need to stop the medicine, leading to hypotension once again. This

labile effect is seen commonly in post-operative patients. Reflex bradycardia can occur

when the blood pressure is quickly raised with vasopressors. Starting at a moderate dose

and titrating up rapidly to achieve set parameters will reduce the chance of reflex

bradycardia and will help to avoid labile blood pressures.

The health care provider should be updated regularly if escalating doses of

vasopressors are required to maintain the ordered blood pressure parameter. Other

causative factors will need to be ruled out time and again.

Vasopressors cause vasoconstriction and significant tissue damage can occur if

extravasation into the subcutaneous tissue occurs. Decreased blood flow to tissue from

vasoconstriction may lead to tissue death. All vasopressors should be administered

through a central line. Adequate access to central veins should be assured prior to

releasing the operative team from the bedside.

Immediate treatment with an appropriate agent should be utilized promptly after

extravasation of a vasopressor is identified. Nurses administering vasopressors should be

familiar with their institutions policy for treating extravasations and the required

medications should be readily available on the unit.

There are four main vasopressors used after cardiac surgery: phenylephrine,

norepinephrine, epinephrine and vasopressin. Dopamine and Dobutamine are sometimes

used to treat hypotension when there is an associated decrease in cardiac output. They

will be discussed with other inotropes later in this chapter.

Phenylephrine is a common vasoconstrictor used after cardiac surgery to manage

mild to moderate hypotension. Phenylephrine offers little effect other than

vasoconstriction and is shunned by some practitioners for its tendency to cause decreased

tissue perfusion. The patient should receive adequate volume resuscitation prior to using

or significantly increasing the dose.

Phenylephrine should be started at a dose relative to the clinical situation. Effects

are often seen immediately at 20-50mcg/min. When dosages over 100-150mcg/min are

needed, a different medicine may be considered as an alternative. The lowest dosage to

meet set blood pressure parameters should be used.

Norepinephrine is a powerful vasopressor that stimulates alpha and beta1

receptors causing vasoconstriction and cardiac stimulation (Micromedex 2008).

Norepinephrine is usually used in profound hypotension not responsive to phenylephrine.

Some health care providers use it as a first line vasopressor due to the positive inotropic

effect that is exerted by beta1 stimulation.

Initially started at 2-10mcg/min and titrated for desired response. High doses and

long term use cause decreased perfusion to the skin and can lead to tissue necrosis and

limb loss. Regularly assess for cyanosis and decreased capillary refill, which are signs of

decreased perfusion.

Epinephrine is a powerful catecholamine used after cardiac surgery as an

inotrope to improve cardiac function, as a vasopressor for refractory hypotension, and to

increase heart rate in bradycardia. Epinephrine is a sympathomimetic catecholamine that

acts on both alpha- and beta-adrenergic receptors. The drug effectively causes

vasoconstriction through its effect on alpha-adrenergic receptors and it induces relaxation

of the bronchial smooth muscle by acting on beta-adrenergic receptors (Micromedex).

While on Epi, the patient must be monitored closely for tachycardia and signs of

myocardial ischemia as it will increase myocardial oxygen demand. The higher the dose

the more likely you will see negative side effects such as atrial or ventricular ectopy and

tachyarrhythmias due to an increase in automaticity.

Sympathetic nervous system reflexes, such as piloerection, dilated pupils,

sweating, increased salivation, mucous production, tachycardia, decreased urine output,

decreased peristalsis, increased blood glucose levels, and tachypnea can be activated

when using epinephrine (Micromedex 2008).

Epinephrine can raise the blood sugar so profoundly that insulin drips have

become synonymous with its use and higher than normal doses may be needed to

maintain adequate glycemic control. Be prepared to quickly wean the dose of insulin if

the epinephrine drip is reduced or discontinued.

Vasopressin (antidiuretic hormone) is used in septic and vasodilatory shock along

with catecholamines to help raise blood pressure and reduce the duration and dose of

them (Raja and Dreyfuss 2004). Release of endogenous vasopressin is an important

vasoconstrictor mechanism in shock states and high concentrations of vasopressin cause

widespread constriction of arterioles leading to increased arterial pressure. Use extreme

caution in patients with vascular disease due to the extreme vasoconstriction that can

occur.

Vasopressin increases secretion of corticotropin, which is a hormone produced by

the anterior pituitary gland that stimulates the adrenal cortex. The adrenal cortex

produces cortisol, a major hormone responsible for blood pressure regulation.

Hypertension

Controlling hypertension is important after cardiac surgery to reduce bleeding

from surgical sites and enhance cardiac output. Blood pressure is primarily regulated by

the vascular system in the arterioles and is affected by many things including heart rate,

and circulating fluid volume.

Hypertension is commonly seen in cardiac surgery patients as an early sign of

hypovolemia. As the body becomes hypovolemic it attempts to increase blood pressure

shunting blood away from non-essential organs, increasing the volume in the chest and

great vessels. The kidneys are very sensitive to this shunting and respond by activating

the renin-angiotension-aldosterone system in an effort to and increase flow by raising

blood pressure. When the body is no longer able to compensate, hypotension ensues if

volume deficits are not replaced rapidly.

Care must be taken to correct hypovolemia in hypertensive patients prior to

administering a vasodilator. Abrupt, life-threatening hypotension can ensue when

vasodilators are used and there is an inadequate volume to fill the vasculature. Always be

prepared to give a rapid fluid bolus when starting any vasodilator should hypotension

occur. As with all vasoactive medications, use as small of a dose as necessary to

accomplish the desired effect. The risk of side effects rises with increased doses.

The most commonly used vasodilators are nitroglycerin, nitroprusside,

nicrardipine, and corlopam.

Nitroglycerine has many uses in the postoperative cardiac surgery patient. It

decreases preload and, to a lesser effect, afterload. Anytime ischemia is suspected

postoperatively, nitroglycerine may be ordered due to its ability to dilate coronary arteries

and increase coronary blood flow.

Nitroglycerine is also used short term (24-48 hours) to prevent spasm of internal

mammary arteries in the postoperative environment. Rates may be as low as 10mcg/min.

Cardizem is also used for this purpose and may be chosen when its other effects would be

beneficial in the specific patient situation. When the patient is able to take PO, an oral

nitrate is started and IV NTG is discontinued.

Patients with high preload (particularly high PA pressures) may benefit from IV

NTG. It will lower PA pressures and CVP via its vasodilatory action.

Abrupt discontinuation of NTG can cause coronary vasospasm, so close

monitoring of rhythm, blood pressure and hemodynamics are warranted when it is

stopped. Dose will be dependent upon blood pressure and hemodynamics, keeping in

mind that increasing coronary blood flow may improve cardiac function.

Potential side effects of nitroglycerine include headache, dizziness, weakness,

orthostatic hypotension, tachycardia, flushing, palpitations, nausea, vomiting, rash,

contact dermatitis, and/or hypersensitivity reactions (Micromedex 2008).

Nitroprusside is used to control hypertension and reduce afterload. It is a powerful

vasodilator that lowers blood pressure by increasing levels of nitrous oxide. It dilates the

arterial tree and to a lesser effect the venous vasculature. Nitroprusside can cause sudden,

life-threatening hypotension if not closely monitored. Initial doses as small as

0.2mcg.kg/min should be used and slowly titrated to keep the blood pressure within

specified limits. The smallest dose possible should be used to achieve the desired effect.

Care should be taken not to flush or initiate new medications in lines that contain

nitroprusside. This can result in abrupt hypotension. When nitroprusside is discontinued,

the line should be aspirated then flushed to avoid this from occurring.

Nitroprusside can cause a shunting of blood to atelectic areas of the lung,

resulting in lowered oxygen saturations and a need for higher concentrations of inspired

oxygen. This effect is usually seen immediately and can be dose dependent. If this

occurs, alert the ordering practitioner immediately, another therapy may be chosen.

Increasing positive end expiratory pressure (PEEP) to resolve atelectasis is useful in

helping decrease this effect.

Sodium nitroprusside rapidly reduces blood pressure and is converted in the body

to cyanide and then thiocyanate. Its adverse effects can be attributed mainly to excessive

hypotension and excessive cyanide accumulation; thiocyanate toxicity may also occur,

especially in patients with renal impairment. Intravenous infusion of sodium

nitroprusside may produce nausea and vomiting, apprehension, headache, dizziness,

restlessness, perspiration, palpitations, retrosternal discomfort, abdominal pain, and

muscle twitching, but these effects may be reduced by slowing the infusion rate

(Micromedex 2008).

An excessive amount of cyanide in plasma (more than 80 nanograms/mL),

because of overdosage or depletion of endogenous thiosulfate (which converts cyanide to

thiocyanate in vivo), may result in tachycardia, sweating, hyperventilation, arrhythmias,

tinnitus, miosis, hyperreflexia, confusion, hallucinations, convulsions and profound

metabolic acidosis. Metabolic acidosis may be the first sign of cyanide toxicity.

Thiocyanate can be removed by dialysis. Methaemoglobinaemia may also occur

(Micromedex 2008).

Cardene is an L-type selective calcium Channel Blocker that acts directly on

arterioles to cause vasodilatation and lowers blood pressure and is indicated for post-

surgical hypertension. It has also been shown to dilate the coronary vasculature (PDL

Biopharma 2008).

Dosage:

Initiate therapy at 5 mg/hr. The dose may be slowly increased by 2.5mg/hr to a maximum

of 15mg/hr. (PDL Biopharma 2008).

“Caution should be exercised when using CARDENE I.V., particularly in combination

with a ß-blocker in patients with CHF or significant left ventricular dysfunction. In vitro

and in some patients, a negative inotropic effect has been observed (PDL Biopharma).

Close monitoring of the blood pressure is required during therapy. CARDENE I.V. is

contraindicated in patients with known hypersensitivity to the drug and in patients with

advanced aortic stenosis. Reduction of diastolic pressure and reduced afterload may

worsen rather than improve myocardial oxygen balance. Caution is advised when

administering CARDENE I.V. to patients with impaired renal or hepatic function, in

combination with a beta-blocker in patients with congestive heart failure, or portal

hypertension. Observe caution in patients with significant left ventricular dysfunction due

to possible negative inotropic effect. CARDENE I.V. gives no protection against the

dangers of abrupt beta-blocker withdrawal; beta-blocker dosage should be gradually

reduced. Levels of cyclosporine should be closely monitored during therapy.

The most common side effects of CARDENE I.V. are headache, hypotension,

nausea/vomiting, and tachycardia. Less frequent adverse effects, in each case occurring

at, include ECG abnormalities, postural hypotension, ventricular extrasystoles, injection-

site reaction, dizziness, sweating and polyuria. Cardene is contraindicated in patients with

known hypersensitivity to the drug and in patients with advanced aortic stenosis.

Reduction of diastolic pressure and reduced afterload may worsen rather than improve

myocardial oxygen balance. (PDL Biopharma).

Fenoldopam mesylate is a dopamine D(1)-like receptor agonist and moderately

binds to alpha(2) adrenoreceptors. This results in lowered systemic and pulmonary

vascular resistances, resulting in enhanced cardiac output. It acts rapidly as a vasodilator

and increases renal blood flow (Micromedex 2008).

Doses range 0.05-1.7mcg/kg/min (some texts say 1.6mcg is a maximum rate)

(Nursing Drug Reference 2005). Corlopam should be started at the lower end of the dose

range, then titrated every 5-10 minutes to effect. It should not be used in excess of 48

hours.

Possible adverse effects include hypotension, tachyarrhythmias, flushing, nausea,

vomiting, dizziness, headache, angina, cardiac dysrhythmias, heart failure, myocardial

infarction, and serum creatinine elevation.

Inotropes

Inotropic support is required in many postoperative cardiac surgery patients even

when careful attention is paid to myocardial protection during the operation. Prolonged

surgeries, myocardial edema, advanced age, reperfusion injuries, and poor preoperative

cardiac function put the patient at higher risk for low cardiac outputs postoperatively.

Cardiac tamponade, pneumothorax, and hemothorax must always be considered when

cardiac output is low.

Cardiac index should be high enough to sustain end-organ perfusion and deliver

adequate amounts of oxygen to tissues. This should be judged subjectively with each

patient and evaluated by adequate urine output, normal capillary refill, normal mentation,

good blood pressure, warm skin, and the lack of acidosis. Objectively, cardiac index

should be over 2.0L/min/m2, however normal cardiac index in the non-diseased heart is

2.5 – 4.5L/min/m2.

There is a laundry list of things that can cause a low cardiac output after cardiac

surgery. After hypovolemia, hypertension, and arrhythmia have been corrected and

cardiac tamponade and hemo/pneumothorax have been ruled out, inotropes are used to

enhance cardiac output.

When preload is optimized and stroke volume remains low, poor contractility can

be assumed and inotropes are indicated. The left (or Right) ventricular stroke work index

(LVSWI/RVSWI) will be low. The stroke work index is the amount of work the right or

left ventricle does with each heartbeat. Adding inotropes will increase the amount of

contractile force and result in an improved stroke work index.

Right ventricular failure is apparent when CVP is elevated, PAWP is low and

RVSWI is low. The right side of the heart is unable to adequately pump blood into the

pulmonary vasculature and results in low left atrial pressure and low left ventricular end

diastolic volume (LVEDV). Blood backs up in the venous system raising CVP and

venous congestion occurs. The PA’s and PAWP fall due to lack of flow and the left heart

struggles to maintain blood pressure and cardiac output. Peripheral edema results from

increased venous congestion and eventually low cardiac output leads to decreased

myocardial perfusion and massive heart failure.

When left ventricular failure occurs, PA’s and PAWP will be elevated as blood is

pumped into the pulmonary circulation and the left heart is unable to adequately pump.

Blood pressure, cardiac index, and LVSWI will be depressed. If not corrected, pulmonary

edema results leading to respiratory distress. Then, progressing cardiogenic shock will

lead to rapid end-organ damage.

There are 5 main drugs used to treat low cardiac output after heart surgery:

Epinephrine, dopamine, Dobutrex, inamrinone, and milrinone. Each has its own side

effect profile and the drug used is typically chosen with this in mind. Epinephrine,

dopamine and Dobutrex may result in tachyarrhythmias or ectopi, where the direct

phosphodiesterase inhibitors inamrinone and milrinone may require vasopressors due to

the profound vasodilatation that occurs.

Dopamine is used to increase blood pressure, cardiac output and perfusion

through the renal vasculature. Systolic pressures are often elevated making it a poor

choice in patients with pulmonary hypertension. Dopamine stimulates the release of

endogenous norepinephrine.

Vasodilatation can occur due stimulation of dopamine receptors at doses of 0.5-

2.0mcg/kg/min. At 2-10mcg/kg/min beta1 stimulation is seen and cardiac output is

enhanced. Doses over 10mg/kg/min alpha stimulation occurs and effects trend toward

vasoconstrictive and the positive renal effect is lost (Global RPH.com 2008). Dopamine

should be started at a low dose and titrated upwards slowly to achieve the desired effect.

Dobutrex is a synthetic catecholamine and acts as a beta1 agonist. It will increase

CI while lowering systemic vascular resistance and increasing heart rate. Dobutrex is

useful when patients have low cardiac output with high systemic or pulmonary vascular

resistance and cannot tolerate vasodilators to decrease afterload. Dobutamine should not

be given to hypovolemic patients. Tachycardia and fluctuations in blood pressure can

occur. It has no effect on dopaminergic receptors so hypertension is less likely to be seen

that if dopamine was used.

Patients with high pulmonary pressures (mitral valve replacement) with or

without a history of pulmonary hypertension, and low heart rate may benefit from

dobutamine over dopamine.

The onset of dobutamine is rapid and it is rapidly cleared when discontinued

allowing for rapid titration of the drug.

Milrinone and inamrinone both enhance cardiac output by directly inhibiting

phosphodiesterase from metabolizing cyclic adenosine monophosphate (Cyclic AMP) in

myocardial cells (myocytes). An increase in Cyclic AMP causes an increase in the

amount calcium moving into cells through ion channels. This results in a more forceful

contraction.

Phosphodiesterase inhibitors also produce vasodilatation in vascular smooth

muscle by decreasing the intracellular concentration of calcium. This causes relaxation of

the vasculature and lowers resistance and blood pressure (Levy, Bailey & Deeb 2002)

resulting in lowered blood pressures on both sides of the heart. Vasopressors are

commonly needed when phosphodiesterase inhibitors are used due to the profound

hypotension that can occur.

Inamrinone may decrease platelet counts and has largely been replaced by

milrinone in some hospitals due to this effect. It has a long (4 hour) half-life making it

important to slowly wean the drug and monitor cardiac function hours after the drug is

discontinued. Platelet counts should be checked daily.

Milrinone has a shorter half-life (36 minutes) (Levy, Bailey & Deeb 2002) and

may be weaned more quickly than inamrinone, making it the drug of choice for some

practitioners. A loading dose should be followed by continuous infusion. Ventricular

tachycardia can occur when administering milrinone due to the proarrhythmic properties.

Aggressively replace potassium and magnesium when using milrinone and closely

monitor for ventricular ectopi during treatment.

Epinephrine is an alpha and beta agonist and has a direct effect on cardiac

function. Beta effects are seen at lower doses while higher doses yield a primarily alpha

effect. It is both a powerful catecholamine and vasopressor used to improve cardiac

function and raise blood pressure in refractory hypotension. While on Epinephrine, the

patient must be monitored closely for tachycardia, signs of myocardial ischemia and

increased oxygen demand. While raising the blood pressure and increasing cardiac index

are goals of therapy, vasodilators may be necessary to control elevated blood pressure

when epinephrine must be used at high doses to maintain cardiac output.

Sympathetic nervous system reflexes, such as piloerection, dilated pupils,

sweating, increased saliva and mucous production, tachycardia, decreased urine output,

decreased peristalsis, increased blood glucose levels, and tachypnea can be activated.

Epinephrine can raise the blood sugar so profoundly that insulin drips have

become synonymous with its use and higher than normal doses may be needed to

maintain adequate glycemic control. Be prepared to quickly wean the dose of insulin if

the Epinephrine drip is reduced or discontinued.

Epinephrine increases automaticity and the higher the dose the more likely you

will see atrial or ventricular ectopy and tachyarrhythmias. Adequate oxygenation should

be maintained and the pt monitored for signs of ischemia because epinephrine increases

myocardial oxygen demand.

Tissue necrosis secondary to epinephrine vasoconstriction has been reported. It

should only be given via central line to limit this risk in case of extravasation.

If aggressive treatment with inotropes fail intra-aortic balloon pump, ventricular

assist device or other mechanical circulatory support devices can be utilized.

Antiarrhythmics

Arrhythmia can be common after cardiac surgery. A wide range of rhythm

disturbances can be seen with atrial fibrillation (A-fib) being the most common,

occurring in up to 47% of all cases (Brantman & Howie 2006, p. 51). Onset can be seen

at any time but is most common between 24 and 48 hours post-operatively. The exact

mechanism that triggers a-fib after cardiac surgery is not known, but a combination of

inflammation that occurs from surgical trauma to the heart and exposure to catecholamine

surges are thought to be largely responsible. Advanced age and valve replacement also

put the patient at greater risk (Brantman & Howie 2006 p. 49).

Surgically, atrial fibrillation may be treated with the Maze procedure. During the

procedure, the surgeon attempts to ablate the pathways in the atria and stop conduction

through abnormal electrical conduits. This is accomplished with incisions made in a

maze-like pattern and can be performed utilizing surgical incision, radio frequency,

ultrasonic energy, or cryosurgery. The Maze procedure has become the standard surgical

treatment for atrial fibrillation.

Bradycardia is also commonly seen post-operatively. Cold cardioplgeia, valve

replacement, hypothermia, exposure to beta-blockers, and surgical trauma near the

sinoatrial and atrioventricular nodes can be causative factors of bradycardia and heart

blocks. Normal rate is typically restored within 24-48 hours with epicardial pacing used

in the interim. Some patients require permanent pacemaker placement after surgery to

maintain normal rate and rhythm. It is important to aggressively treat bradycardia or heart

blocks that depress cardiac function as they can quickly lead to cardiogenic shock.

Ventricular fibrillation, ventricular tachycardia, and tordades de pointes are rare

after heart surgery but can occur. Precautions must be taken to avoid an “r on t

phenomenon” when using pacemakers. Immediate defibrillation and treatment with

amiodarone is necessary to terminate these lethal arrhythmias. Tordades de pointes

should be treated by institutional orders and/or ACLS protocol and is commonly

terminated after correcting low magnesium levels or by removing the causative agent if

initiated in response to a medication.

Correcting electrolyte imbalances is paramount in preventing and correcting all

arrhythmias. The goal of treatment is to lower the rate to reduce the workload on the

heart and conversion back to sinus rhythm as soon as possible.

There is a wide array of oral medication used to treat atrial arrhythmias after heart

surgery and all help to re-establish normal sinus rhythm, maintain the rhythm after it has

been achieved, and/or reduce the heart rate druing atrial fibrillation. Medications are

separated in to four classes. These are not usually started in the immediate post-operative

period. The particular medication used will depend on its action, the suspected cause of

the arrhythmia, and the side effect profile of each drug.

Class I are sodium channel blockers and include quinidine, procainamide,

disopyramide, lidocaine, propafenone, flecanide, and encainde. Class II are beta blokers

and include propanolol, motoprolol, and sotalol. Class III are agents that delay

repolarixation and include amiodarone and bretylium. Class IV are the calcium channel

blockers diltiaxem and verapamil.

The most common medications used in the immediate post-operative phase are

reviewed below.

Metoprolol

Metoprolol is used widely to decrease the workload of the heart, protect against

endogenous catecholamines during surgical procedures, to reduce heart rate, and thus

workload during tachycardia, and as a prophylactic to prevent A-fib/flutter after cardiac

surgery. Metoprolol will be started prior to surgery when time allows and typically

continues for several months after discharge.

Valve replacement surgeries make the patient prone to heart blocks and

metoprolol is contraindicated in these patients. It should be used with caution in patients

with chronic obstructive pulmonary disease and asthma due to airway constriction that

can occur.

After adminastraion observe for signs of bradycardia, AV block, bluish discoloration

of the fingers and toes, numbness/tingling/swelling of the hands or feet, trouble

breathing, cough, and increased thirst. (Micromedex 2008).

Other side-effects include dizziness, lightheadedness, drowsiness, tiredness, diarrhea,

unusual dreams, ataxia, trouble sleeping, and vision problems. It may also reduce blood

flow to the hands and feet, causing them to feel numb and cold; smoking may worsen this

effect (Micromedex 2008).

Metoprolol is commonly used by patients with history of angina and heart attack.

Thre patients are at rick of beta blocker withdrawal, which can occur following abrupt

cessation of therapy. Withdrawal may result in tachycardia and myocardial ischemia.

Metoprolol dose should be gradually reduced over a period of 1–2 weeks prior to

stopping the drug. Metoprolol is sometimes prescribed for off-label use in performance

anxiety, and anxiety disorders. These patients are also at risk of beta blocer withdrawal

symptoms after cardiac surgery.

Metoprolol has a negative inotropic effect and decreases heart Rate, contractility,

cardiac output, and blood pressure. It is commonly given as an extended release tablet

prior to surgery and its negative inotropic and chronotropic effects will last well into the

immediate post-operative period. Dobutamine and dopamine can be used to stimulate

beta receptors to counter these effects. Cardiac pacing should treat low cardiac output and

blood pressure due to bradycardia when contactility is not effected.

Diltiazem hydrochloride is used in CVRU to lower heart rate in atrial fib and

flutter when the heart rate is over 100 beats per minute. Cardizem bolus is typically given

followed by an IV drip. The goal of therapy is to keep the heart rate under 100 (or other

ordered rate). Conversion to normal sinus rhythm is commonly seen after administration,

however the primary goal is rate control with diltiazem.

Diltiazem blocks calcium ion influx during depolarization of cardiac and vascular

smooth muscle. It decreases vascular resistance and causes relaxation of the vascular

smooth muscle resulting in a decrease in blood pressure (Micromedex 2008). This has a

negative inotropic effect since the strength of contraction is regulated by calcium flowing

in and out of the cell. The health care provider must weigh the risk versus benefit for

diltiazem when treating arrhythmias with a corresponding low cardiac output or

hypotension.

Diltiazem can be safely administered to patients with marginal blood pressures if

given slowly. Reduction of heart rate will improve diastolic filling, which will improve

cardiac output and reduce myocardial workload after rate control is achieved. If the

patient is on vasodilators to treat hypertension, consider lowering the dose or stopping

them prior to administering diltiazem. Co-administration may potentiate a hypotensive

effect. Alternately, anticipate an increased need for vasopressors or fluid bolus if

hypovolemia is suspected.

When administering Diltiazem and vasopressors, continuously monitor the heart

rate and blood pressure. An initial bolus is typically ordered. This should be given over 5-

10 minutes and can be slowed or stopped if a reduction in blood pressure is seen or if the

target heart rate is reached prior to completing the initial bolus. The total bolus dose is

usually, but not always required. More than one bolus dose may be required.

IV bolus should be followed by a continuous infusion. This may be titrated to

maintain the heart rate within the ordered parameters. Be cautious not to lower the heart

rate too much, 80-100 beats per minute will maximize cardiac output for the post-op

patient.

If an AV block is seen, diltiazem should be placed on hold and the MD updated

immediately with vital signs and patient presentation. AV block will be more common in

patients that have had valve operations, particularly the mitral valve.

Diltiazem may be used to prevent vasospasm in patients with internal mammary

grafts by relaxing vascular smooth muscle and stabilizing the vessel.

Cardizem can increase the effects of anesthetics. Patients may not awaken as

quickly or may be more difficult to arouse after receiving it during the first 24 hours post-

op (Micromedex 2008).

Cordarone

Cordarone is used in postoperative cardiac surgery patients to treat atrial

fibrillation and has been used in numbers of studies as a prophylactic measure. It creates

its antiarrhythmic effect by blocking potassium channels, which prolongs the action

potential and decreases membrane excitability. Cordarone also decreases impulse

conduction by indirectly blocking sodium channels, blocks beta-adrenergic receptors,

causing beta-blockade, and inhibits alpha-adrenergic receptors and calcium channels,

producing antianginal effects (Brantman & Howie 2006, p. 50).

Cordarone has been associated with a wide array of side effects in including

pulmonary and liver toxicity and is not typically our first line drug for postop

arrhythmias.

Typical dosing of Cordarone is 150mg IV over 10 minutes followed by a 24-hour

infusion. 1mg/min for the first 6 hours and 0.5mg/min for 18 hours. The patient should be

changed to PO or an order obtained to continue IV use after 24 hours.

Closely monitor for AV block, bradycardia, electrolyte imbalance, hypotension, left

ventricular dysfunction, and new or worsened arrhythmias. Use caution with concomitant

QTc-prolonging drugs and in the presence of electrolyte imbalance, pulmonary disease,

and hepatic disease.

Pulmonary toxicity may occur leading to adult respiratory distress syndrome

(ARDS) after exposure to Cordarone. Preoperative low-dose amiodarone is also

associated with various cardiac complications and an increased need for more intense

inotropic support after cardiac operations. These findings may be related to the drug's

depressant effect on the myocardium and its use has been shunned by many health care

providers for this reason.

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