Discontinuing Cardiopulmonary Bypass

Published on 07/02/2015 by admin

Last modified 22/04/2025

Print this page

This article have been viewed 1713 times

Chapter 25 Discontinuing Cardiopulmonary Bypass

Jack S. Shanewise, MD, Roberta Hines, MD, Joel A. Kaplan, MD

Cardiopulmonary bypass (CPB) has been used since the 1950s to facilitate surgery on the heart and great vessels, and even with the increased interest in off-pump coronary artery bypass grafting (CABG) CPB remains a critical part of most cardiac operations. Managing patients with CPB remains one of the defining characteristics of cardiac surgery and cardiac anesthesiology. Discontinuing CPB is a necessary part of every operation involving extracorporeal circulation. Through this process, the support of the circulation by the bypass pump and oxygenator is transferred back to the patient’s heart and lungs. In this chapter we review important considerations involved with discontinuing CPB and present an approach to managing this critical component of a cardiac operation, which may be routine and easy or extremely complex and difficult. The key to success in discontinuing CPB is proper preparation. The period during and immediately after weaning from CPB is usually very busy for the anesthesiologist, and having to do things that could have been accomplished earlier in the operation is not helpful. The preparations for bringing a patient off CPB may be organized into several parts: general preparations, preparing the lungs, preparing the heart, and final preparations.

GENERAL PREPARATIONS

Temperature

Because at least moderate hypothermia is used during CPB in most cardiac surgery cases, it is important that the patient is sufficiently rewarmed before attempting to wean from CPB (Table 25-1). Initiation of rewarming is a good time to consider whether additional drugs need to be given to keep the patient anesthetized. Anesthetic vaporizers need to be off for 10 to 20 minutes before coming off CPB to clear the agent from the patient if so desired. Monitoring the temperature of a highly perfused tissue such as the nasopharynx is useful to help prevent overheating the brain during rewarming, but these temperatures may rise more rapidly than others, such as bladder, rectum, or axilla temperatures, leading to inadequate rewarming and temperature dropoff after CPB as the heat continues to distribute throughout the body. Different institutions have various protocols for rewarming, but the important point is to warm gradually, avoiding hyperthermia of the central nervous system while getting enough heat into the patient to prevent significant dropoff after CPB.¹ After CPB, there is a tendency for the patient to lose heat, and measures to keep the patient warm such as fluid warmers, a circuit heater-humidifier, and forced-air warmers should be set up and turned on before weaning from CPB. The temperature of the operating room may need to be increased as well; this is probably an effective measure to keep a patient warm after CPB, but it may make the scrubbed and gowned personnel uncomfortable.

Table 25-1 General Preparations for Discontinuing Cardiopulmonary Bypass

Temperature	Laboratory Results
Adequately rewarm before weaning from CPB	Correct metabolic acidosis
Avoid overheating the brain	Optimize hematocrit
Start measures to keep patient warm after CPB	Normalize K⁺
Use fluid warmer, forced air warmer	Consider giving Mg²⁺ or checking Mg²⁺ level
Warm operating room	Check Ca²⁺ level and correct deficiencies

Laboratory Results

Arterial blood gas analysis should be obtained before weaning from CPB and any abnormalities corrected. Severe metabolic acidosis depresses the myocardium and should be treated with sodium bicarbonate or tromethamine (Tham). The optimal hematocrit for weaning from CPB is controversial and probably varies from patient to patient.² It makes sense that sicker patients with lower cardiovascular reserve may benefit from a higher hematocrit, but the risks and adverse consequences of transfusion need to be considered as well. Suffice it to say that the hematocrit should be measured and optimized before weaning from CPB. The serum potassium level should be measured before weaning from CPB and may be high due to cardioplegia or low, especially in patients receiving loop diuretics. Hyperkalemia may make establishing an effective cardiac rhythm difficult and can be treated with sodium bicarbonate, calcium chloride, or insulin, but the levels usually decrease quickly after cardioplegia has been stopped. Low serum potassium levels should probably be corrected before coming off CPB, especially if arrhythmias are present. Administration of magnesium to patients on CPB decreases postoperative arrhythmias and may improve cardiac function, and many centers routinely give all CPB patients magnesium sulfate. Theoretical disadvantages include aggravation of vasodilation and inhibition of platelet function.^3,⁴ If magnesium is not given routinely, the level should be checked before weaning from CPB and deficiencies corrected. The ionized calcium level should be measured, and significant deficiencies corrected before discontinuing CPB. Many centers give all patients a bolus of calcium chloride just before coming off CPB because it transiently increases contractility and systemic vascular resistance. However, it has been argued that this practice is to be avoided because calcium may interfere with catecholamine action and aggravate reperfusion injury.

PREPARING THE LUNGS

As the patient is weaned from CPB and the patient’s heart starts to support the circulation, the lungs again become the site of gas exchange, delivering oxygen and eliminating carbon dioxide. Before weaning from CPB, the lung function must be restored (Table 25-2). The lungs are reinflated by hand gently and gradually, with sighs using up to 30 cmH₂O pressure, and then mechanically ventilated with 100% oxygen. Care should be taken not to allow the left lung to injure an in situ internal mammary artery graft as the lung is reinflated. The compliance of the lungs can be judged by their feel with hand ventilation, with stiff lungs suggesting more difficulty with oxygenation or ventilation after CPB. If visible, both lungs should be inspected for residual atelectasis, and they should be rising and falling with each breath. Ventilation alarms and monitors should be activated. If prolonged expiration or wheezing is detected, bronchodilators should be given. The surgeon should inspect both pleural spaces for pneumothorax, which should be treated with chest tubes. Any fluid present in the pleural spaces should be removed before attempting to wean the patient from CPB.

Table 25-2 Preparing the Lungs for Discontinuing Cardiopulmonary Bypass

1. Suction trachea and endotracheal tube, if needed.

2. Inflate lungs gently by hand.

3. Ventilate with 100% oxygen.

4. Treat bronchospasm with bronchodilators.

5. Check for pneumothorax and pleural fluid.

6. Consider need for positive end-expiratory pressure, intensive care unit ventilator, and nitric oxide.

PREPARING THE HEART

Preparing the heart to resume its function pumping blood involves optimizing the five hemodynamic parameters that can be controlled: rhythm, rate, contractility, afterload, and preload (Table 25-3).

Table 25-3 Preparing the Heart for Discontinuing Cardiopulmonary Bypass

Parameter	Preparation
Rhythm	Normal sinus rhythm is ideal. Defibrillate if necessary when temperature > 30°C. Consider antiarrhythmic drugs if ventricular fibrillation persists more than a few minutes. Try synchronized cardioversion for atrial fibrillation or flutter. Look at the heart to diagnose atrial rhythm. Try atrial pacing if AV conduction exists. Try AV pacing for heart block.

Heart rate

Rate should be between 75 and 95 beats per minute in most cases.

Treat slow rates with electrical pacing.

Treat underlying causes of fast heart rates.

Heart rate may decrease as the heart fills.

Control fast supraventricular rates with drugs and then pace as needed.

Always have pacing available during heart surgery.

Contractility

Inotropic support is more likely needed with depressed cardiac function before CPB, advanced age, long bypass or clamp time, poor preservation, or incomplete revascularization.

Look for the vigorous “snap” of a heartbeat with good contractility.

If depressed contractility is likely, begin inotropic drugs before weaning from CPB.

Severely impaired function may require mechanical support.

Afterload

Systemic vascular resistance is a major component of afterload.

Keep MAP between 60 and 80 mmHg at full CPB flow.

Consider a vasoconstrictor if the MAP is low and a vasodilator if the MAP is high.

Preload

End-diastolic volume is the best measure of preload and can be seen with TEE.

Filling pressures provide a less direct measure of preload.

Consider baseline filling pressures.

Assess RV volume and function with direct inspection.

Assess LV volume and function with TEE.

Cardiac distention may cause MR and TR.

AV = atrioventricular; CPB = cardiopulmonary bypass; LV = left ventricular; MAP = mean arterial pressure; MR = mitral regurgitation; RV = right ventricular; TEE = transesophageal echocardiography; TR, tricuspid regurgitation.

Rhythm

There must be an organized, effective, and stable cardiac rhythm before attempting to wean from CPB. This can occur spontaneously after removal of the aortic cross-clamp, but the heart may resume electrical activity with ventricular fibrillation. If the blood temperature is greater than 30°C, the heart may be defibrillated with internal paddles applied directly to the heart using 10 to 20 J. Defibrillation at lower temperatures may be unsuccessful because extreme hypothermia can cause ventricular fibrillation. If ventricular fibrillation persists or recurs repeatedly, antiarrhythmic drugs such as lidocaine or amiodarone may be administered to help achieve a stable rhythm. It is not unusual for the rhythm to remain unstable for several minutes immediately after cross-clamp removal, but persistent or recurrent ventricular fibrillation should prompt concern about impaired coronary blood flow. Because it provides an atrial contribution to ventricular filling and a normal, synchronized contraction of the ventricles, normal sinus rhythm is the ideal cardiac rhythm for weaning from CPB. Atrial flutter or fibrillation, even if present before CPB, can often be converted to normal sinus rhythm with synchronized cardioversion, especially if antiarrhythmic drugs are administered. It is often helpful to look directly at the heart when there is any question about the cardiac rhythm. Atrial contraction, flutter, and fibrillation are easily seen on CPB. Ventricular arrhythmias should be treated by correcting underlying causes such as potassium or magnesium deficits and, if necessary, with antiarrhythmic drugs such as amiodarone. If asystole or complete heart block occurs after cross-clamp removal, electrical pacing with temporary epicardial pacing wires may be needed to achieve an effective rhythm before weaning from CPB. If atrioventricular conduction is present, atrial pacing should be attempted because, as with normal sinus rhythm, it provides atrial augmentation to filling and synchronized ventricular contraction. Atrioventricular sequential pacing is used when there is heart block, which is frequently present for 30 to 60 minutes as the myocardium recovers after cross-clamp removal. Ventricular pacing remains the only option if no organized atrial rhythm is present, but this sacrifices the atrial “kick” to ventricular filling and the more efficient synchronized ventricular contraction of the normal conduction system.

Rate

In most situations for adult patients, the heart rate (HR) should be between 75 and 95 beats per minute for weaning from CPB. Lower rates may theoretically be desirable for hearts with residual ischemia or incomplete revascularization. Higher HRs may be needed for hearts with limited stroke volume, such as after ventricular aneurysmectomy. Slow HRs are best treated with electrical pacing, but β-agonist or vagolytic drugs also may be used to increase the HR. Tachycardia before weaning from CPB is more worrisome and difficult to deal with, and treatable causes such as inadequate anesthesia, hypercarbia, and ischemia should be identified and corrected. The HR often decreases as the heart is filled in the weaning process, and electrical pacing should always be immediately available during cardiac surgery. Supraventricular tachycardias should be electrically cardioverted if possible, but drugs such as β-antagonists or calcium channel antagonists may be needed to control the ventricular rate if they persist, most typically occurring in patients with chronic atrial fibrillation. If drug therapy lowers the rate too much, pacing may be used.

Contractility

The contractile state of the myocardium should be considered before attempting to wean from CPB. The likelihood of decreased contractility requiring inotropic support after CPB is greater with preexisting ventricular impairment (e.g., low ejection fraction, high left ventricular end-diastolic pressure [LVEDP] preoperatively or before CPB), advanced age, long CPB time, long aortic cross-clamp time, inadequate myocardial preservation, and incomplete revascularization. A heart with good contractility often has a vigorous snap with contraction that can be seen while on CPB, in contrast to the weak contractions of a heart with impaired contractility, but it may be difficult to assess global ventricular function while the heart is empty and on CPB. If significant depression of contractility is likely, inotropic support can be started before attempting to wean the patient from CPB. If depressed myocardial contractility becomes evident during weaning, the safest approach is to prevent cardiac distention by resuming CPB, resting the heart for 10 to 20 minutes while inotropic therapy with a catecholamine or phosphodiesterase inhibitor drug is started. Extreme depression of contractile function of the myocardium may require mechanical support with an intra-aortic balloon pump (IABP) or ventricular assist device (VAD).

Afterload

An important component of afterload in patients is the systemic vascular resistance (SVR). While on CPB at full flow, usually about 2.2 L/min/m², mean arterial pressure (MAP) is directly related to SVR and indicates whether the SVR is appropriate, too high, or too low. Low SVR after CPB can cause inadequate systemic arterial perfusion pressure, and high SVR can significantly impair cardiac performance, especially in patients with poor ventricular function. SVR is usually within a reasonable range when the arterial pressure is between 60 and 80 mmHg at full pump flow. If below that range, infusion of a vasopressor may be needed to increase SVR before attempting to wean from CPB. If the MAP is high while on CPB, vasodilator therapy may be needed.

Preload

In the intact heart, the best measure of preload is end-diastolic volume. Less direct clinical measures of preload include left atrial pressure (LAP), pulmonary artery occlusion pressure (PAOP), and pulmonary artery diastolic pressure, but there may be a poor relationship between end-diastolic pressure and volume during cardiac surgery. Transesophageal echocardiography (TEE) is a useful tool for weaning from CPB because it provides direct visualization of the end-diastolic volume and contractility of the left ventricle.⁵ The process of weaning a patient from CPB involves increasing the preload (i.e., filling the heart from its empty state on CPB) until an appropriate end-diastolic volume is achieved. When preparing to discontinue CPB, some thought should be given to the appropriate range of preload for the particular patient. The filling pressures before CPB may indicate what they need to be after CPB; a heart with high filling pressures before CPB may require high filling pressures after CPB to achieve an adequate preload.

FINAL PREPARATIONS

The final preparations before discontinuing CPB include leveling the operating table, re-zeroing the pressure transducers, ensuring the proper function of all monitoring devices, confirming that the patient is receiving only intended drug infusions, ensuring the immediate availability of resuscitation drugs and appropriate fluid volume, and verifying that the lungs are being ventilated with 100% oxygen (Table 25-4).

Table 25-4 Final Preparations for Discontinuing Cardiopulmonary Bypass

Anesthesiologist’s Preparations	Surgeon’s Preparations
Level operating table	Remove macroscopic collections of air from the heart
Re-zero transducers	Control major sites of bleeding
Activate monitors	CABG lying nicely without kinks
Check drug infusions	Cardiac vents off or removed
Have resuscitation drugs and fluid volume on hand	Clamps off the heart and great vessels
Reestablish TEE/PA catheter monitoring	Tourniquets around caval cannulas loose

CABG = coronary artery bypass graft; TEE = transesophageal echocardiography; PA = pulmonary artery

The surgeon must confirm that he or she has completed the necessary preparations in the surgical field before discontinuing CPB. Macroscopic collections of air in the heart should be evacuated before starting to wean from CPB. These are most easily detected with TEE, which can also be helpful in monitoring and directing the de-airing process. Major sites of bleeding should be controlled, cardiac vent suction should be off, all clamps on the heart and great vessels should be removed, coronary artery bypass grafts should be checked for kinks and bleeding, and tourniquets around the caval cannulas should be loosened or removed before starting to wean a patient from CPB.

ROUTINE WEANING FROM CARDIOPULMONARY BYPASS

There should be close and clear communication among the perfusionist, the surgeon, and the anesthesiologist while weaning a patient from CPB, and the surgeon or the anesthesiologist should be in charge of the process. The anesthesiologist should be positioned at the head of the table, able to readily see the CPB pump and perfusionist, the heart and the surgeon, and the anesthesia monitor display. If present, the TEE display should also be easily in view. Weaning a patient from CPB is accomplished by diverting blood back into the patient’s heart by occluding the venous drainage to the CPB pump. The arterial pump flow is decreased simultaneously as the pump reservoir volume empties into the patient and the heart’s contribution to systemic flow increases. This can be accomplished most abruptly by simply clamping the venous return cannula and transfusing blood from the pump until the heart fills and the preload appears to be adequate. Some patients will tolerate this method of discontinuing CPB, but many will not, and a more gradual transfer from the pump to the heart is usually desirable. The worse the function of the heart, the slower the transition from full CPB to off CPB needs to be.

Before beginning to wean the patient from CPB, the perfusionist should communicate to the physicians involved three important parameters: the current flow rate of the pump, the volume in the pump reservoir, and the oxygen saturation of venous blood returning to the pump from the patient. The current flow rate of the pump indicates the stage of weaning as it is decreased. Weaning is just beginning at full flow, is well under way when down to 2 or 3 L/min in adults, and is almost finished at less than 2 L/min. The reservoir volume indicates how much blood is available for transfusion to fill the heart and lungs as CPB is discontinued. If the volume is low, less than 400 to 500 mL in adults, more fluid may need to be added to the reservoir before weaning from CPB. The oxygen saturation of the venous return () gives an indication of the adequacy of peripheral perfusion during CPB. If the is greater than 60%, oxygen delivery during CPB is adequate; if it is less than 50%, oxygen delivery is inadequate, and measures to improve delivery (e.g., increase pump flow or hematocrit) or decrease consumption (e.g., give more anesthetic agents or neuromuscular blocking drugs) need to be taken before coming off CPB. An between 50% and 60% is marginal and must be followed closely. As the patient is weaned from CPB, a rising suggests that the net flow to the body is increasing and that the heart and lungs will support the circulation; a falling indicates that tissue perfusion is decreasing and that further intervention to improve cardiac performance will be needed before coming off CPB.

The actual process of weaning from CPB begins with partially occluding the venous return cannula with a clamp. This may be done in the field by the surgeon or at the pump by the perfusionist. This causes blood to flow into the right ventricle. As the right ventricle fills and begins to pump blood through the lungs, the left side of the heart will begin to fill. When this occurs, the left ventricle will begin to eject, and the arterial waveform will become pulsatile. Next, the perfusionist will gradually decrease the pump flow rate. As more of the venous return goes through the heart and less to the pump reservoir, it becomes necessary to gradually decrease the pump flow to avoid emptying the pump reservoir. One approach to weaning from CPB is to bring the filling pressure being monitored (e.g., central venous pressure [CVP], PAOP, LAP) to a specific, predetermined level somewhat lower than may be necessary and then assess the hemodynamics. Volume (preload) of the heart may also be judged by direct observation of its size or with TEE. Further filling is done in small increments (50 to 100 mL) while closely monitoring the preload until the hemodynamics appear satisfactory as judged by the arterial pressure, the appearance of the heart, and the trend of the . It is typically easy to see the right-sided heart volume and function directly in the surgical field and the left side of the heart with TEE, and combining the two observations is a useful approach for weaning from CPB. Overfilling and distention of the heart should be avoided because it may stretch the myofibrils beyond the most efficient length and dilate the annuli of the mitral and tricuspid valves, rendering them incompetent, which is easily detected with TEE. If the patient has two venous cannulae, the smaller of the two may be removed when the pump flow is one half of the full flow rate to improve movement of blood from the great veins into the right atrium. When the pump flow has been decreased to 1 L/min or less in an adult and the hemodynamics are satisfactory, the venous cannula may be completely clamped and the pump flow turned off. At this point, the patient is “off bypass.”

This is a critical juncture in the operation. The anesthesiologist should pause a moment to make a brief scan of the patient and monitors to confirm that the lungs are being ventilated with oxygen, the hemodynamic status is acceptable and stable, the electrocardiogram shows no new signs of ischemia, the heart does not appear to be distending, and the drug infusions are functioning as desired. Further fine-tuning of the preload is accomplished by transfusing 50- to 100-mL boluses from the pump reservoir through the arterial cannula and observing the effect on hemodynamics. If there is acute failure of the circulation as evidenced by unstable rhythm, falling arterial and rising filling pressures, or visible distention of the heart, the patient is put back on CPB by unclamping the venous return cannula and turning on the arterial pump flow. Once back on CPB, an assessment of the cause of failure to wean is made and appropriate interventions undertaken before attempting to wean again. When the hemodynamics appear to be stable and adequate, the surgeon may remove the venous cannula from the heart.

The next step in discontinuing CPB is to transfuse as much as possible of the blood remaining in the pump reservoir into the patient before removal of the arterial cannula. This is usually easier and quicker than transfusing through the intravenous infusions after decannulation. The blood in the venous cannula and tubing (usually about 500 mL) may be drained into the reservoir for transfusion. The patient’s venous capacitance can be increased by raising the head of the bed (i.e., reverse Trendelenburg position) or giving nitroglycerin, being more cautious with these maneuvers in patients with impaired cardiac function. Filling the vascular space with the head up and while infusing nitroglycerin increases the ability to cope with volume loss after decannulation by allowing rapid augmentation of the central vascular volume by leveling the bed and decreasing the nitroglycerin infusion rate.

After discontinuing CPB, the anticoagulation by heparin is reversed with protamine. Depending on institutional preference, protamine may be administered before or after removal of the arterial cannula. Giving it before removal allows for continued transfusion from the pump and easier return to CPB if there is a severe protamine reaction. Giving protamine after removal of the arterial cannula probably decreases the risk of thrombus formation and systemic embolization. After the infusion of protamine is started, pump suction return to the reservoir should be stopped to keep protamine out of the pump circuit in case subsequent return to CPB becomes necessary. Protamine should be given slowly through a peripheral intravenous catheter over 7 to 15 minutes while watching for systemic hypotension and pulmonary hypertension, which may indicate that an untoward (allergic) reaction to protamine is occurring.⁶ Technically flawed coronary artery bypass grafts may thrombose after protamine administration, causing acute ischemia and mimicking a protamine reaction.

When transfusion of the pump reservoir blood is completed, a thorough assessment of the patient’s condition should be made before removing the arterial cannula, because after this is done returning to CPB becomes much more difficult. The cardiac rhythm should be stable. Cardiac function is assessed by evaluating pressures, cardiac output, and TEE. Hemodynamics should be satisfactory and stable. Adequate oxygenation and ventilation should be confirmed by arterial blood gas analysis or pulse oximetry and capnography. Bleeding from the heart should be at a manageable level before removal of the arterial cannula. The perfusionist should not have to transfuse significant amounts of blood through the arterial cannula before removing it, because it may be difficult to keep up with the blood loss through intravenous infusions alone. Bleeding sites behind the heart may have to be repaired on CPB if the patient cannot tolerate lifting the heart to expose the problem area. At the time of arterial decannulation, the systolic pressure should be between 85 and 105 mmHg to minimize the risk of dissection or tearing of the aorta. The head of the bed may be raised, or small boluses of a short-acting vasodilator (e.g., nitroglycerin, nitroprusside) may be given to lower the systemic blood pressure as necessary. Tight control of the arterial blood pressure may be needed for a few minutes until the cannulation site is secure.

When the arterial cannula has been removed, the heparin effects are reversed with protamine, and the hemodynamic status remains stable, the routine process of discontinuing CPB is complete. However, in patients with poor ventricular function after CPB, multiple drugs or even mechanical assist devices may be required throughout the rest of the operation and continued in the intensive care unit.

PHARMACOLOGIC MANAGEMENT OF VENTRICULAR DYSFUNCTION

Perioperative ventricular dysfunction is usually a transient state of contractile impairment that may require temporary support with positive inotropic agents. In a subset of patients, contractility may be significantly depressed such that combination therapy with positive inotropes and vasodilator agents is needed to effectively improve cardiac output and tissue perfusion. The use of mechanical assist devices is reserved for conditions of overt or evolving cardiogenic shock.

Severe ventricular dysfunction, specifically the low cardiac output syndrome (LCOS), occurring after CPB and cardiac surgery differs from chronic congestive heart failure (CHF) (Box 25-1). Patients emerging from CPB have hemodilution, moderate hypocalcemia, hypomagnesemia, and altered potassium levels. Depending on temperature and depth of anesthesia, these individuals may demonstrate low, normal, or high SVR. Increasing age, female sex, decreased LV ejection fraction, and increased duration of CPB are associated with a greater likelihood that inotropic support will be needed after CABG surgery (Table 25-5).

BOX 25-1 Risk Factors for the Low Cardiac Output Syndrome after Cardiopulmonary Bypass

• Preoperative ventricular dysfunction

• Myocardial ischemia

• Poor myocardial preservation

• Reperfusion injury

• Inadequate cardiac surgical repair or revascularization

Table 25-5 Patient Characteristics Associated with the Use of Inotropic Drug Support

Contractile dysfunction during or after cardiac surgery can result from preexisting impairment in contractility or be a new-onset condition. Abnormal contraction, especially in the setting of coronary artery disease (CAD), usually is caused by myocardial injury resulting in ischemia or infarction. The magnitude of contractile dysfunction corresponds to the extent and duration of injury. Brief periods of myocardial oxygen deprivation (<10 minutes) produce regional contractile dysfunction, which can be rapidly reversed by reperfusion. Extension of the ischemia to 15 to 20 minutes is also associated with restoration of cardiac function with reperfusion; however, this process is very slow and can take hours to days. This condition of postischemic reversible myocardial dysfunction in the presence of normal flow is referred to as myocardial stunning. Irreversible cell injury will occur with longer periods of ischemia, producing a myocardial infarction characterized by release of intracellular enzymes, disruption of cell membranes, influx of calcium, persistent contractile dysfunction, and eventual cellular swelling and necrosis.

In addition to the previously described factors, right ventricular (RV) dysfunction and failure are potential sources of morbidity and mortality after cardiac surgery. Numerous factors may predispose patients to the development of perioperative RV dysfunction, including CAD, RV hypertrophy, previous cardiac surgery, and operative considerations such as inadequate revascularization or hypothermic protection. Technical and operative difficulties are associated with various cardiac surgical procedures (e.g., right ventriculotomy), RV trauma, rhythm and conduction abnormalities, injury to the right ventricle during cessation of CPB, or protamine reaction.

The following discussion provides an overview of the pharmacologic approach to management of perioperative ventricular dysfunction in the setting of cardiac surgery. Management goals are described in Table 25-6. These are extensions of the routine preparations made for discontinuing CPB shown in Table 25-3.

Table 25-6 Management of Cardiac Dysfunction

Physiologic Variable	Management
Heart rate and rhythm	Maintain normal sinus rhythm, avoid tachycardia; for tachycardia or bradycardia, consider pacing or chronotropic agents (atropine, isoproterenol, epinephrine), correct acid-base disturbances and electrolytes, and review current medications.
Preload	Reduce increased preload with diuretics or venodilators (nitroglycerin or sodium nitroprusside); monitor CVP, PCWP, and SV; obtain echocardiogram to rule out ischemia, valvular lesions, tamponade, and intracardiac shunts; consider using inotropes, IABP, or both.
Afterload	Avoid increased afterload (increased wall tension); use vasodilators (sodium nitroprusside); avoid hypotension; maintain coronary perfusion pressure; consider IABP, inotropes devoid of α₁-adrenergic effects (dobutamine or milrinone), or both IABP and inotropes.
Contractility	Assess hemodynamics, rule out ischemia/infarction, assess rate/rhythm, preload, and afterload; use inotropes; if uncertain, obtain echocardiogram to assess cardiac function. Consider combination therapy with inotropes and vasodilators and/or assist devices (IABP/LVAD/RVAD).
Oxygen delivery	Increase FiO₂ and CO; check ABGs and chest radiograph; mechanical ventilation if indicated; correct acid-base disturbances.

FiO₂ = inspired oxygen concentration; ABGs = arterial blood gas; CO = cardiac output; CVP = central venous pressure; IABP = intra-aortic balloon pump; PCWP = pulmonary capillary wedge pressure; SV = stroke volume.

Sympathomimetic Amines

Sympathomimetic drugs (i.e., catecholamines) are pharmacologic agents capable of providing inotropic and vasoactive effects (Box 25-2). Catecholamines exert positive inotropic action by stimulation of the β₁-receptor. The predominant hemodynamic effect of a specific catecholamine depends on the degree to which the various α-, β-, and dopaminergic receptors are stimulated (Tables 25-7 and 25-8).

BOX 25-2 Pharmacologic Approaches to Ventricular Dysfunction

• Inotropic drugs

• Phosphodiesterase inhibitors

• Vasodilators

• Vasopressors

• Metabolic supplements

Table 25-7 Sympathomimetics

Table 25-8 Hemodynamic Effects of Catecholamines and Phosphodiesterase Inhibitors

The physiologic effect of an adrenergic agent is determined by the sum of its actions on α-, β-, and dopaminergic receptors. The effectiveness of any adrenergic agent will be influenced by the availability and responsiveness of adrenergic receptors. Chronically elevated levels of plasma catecholamines (e.g., chronic CHF and long CPB time) cause downregulation of the number and sensitivity of β-receptors. Maintenance of normal acid-base status, normothermia, and electrolytes also improve the responsiveness to adrenergic-receptor stimulation.

The selection of a drug to treat ventricular dysfunction is influenced by pathophysiologic abnormalities as well as by the physician’s preference. If LV performance is decreased primarily as a result of diminished contractility, the drug chosen should increase contractility. Although β-agonists improve contractility and tissue perfusion, their effects may increase myocardial oxygen consumption () and reduce coronary perfusion pressure (CPP). However, if the factor most responsible for decreased cardiac function is hypotension with concomitantly reduced CPP, use of an α-adrenergic agonist can increase blood pressure and improve diastolic coronary perfusion.

Catecholamines are also effective for treating primary RV contractile dysfunction, with all of the β₁-adrenergic agonists augmenting RV contractility. Studies have documented the efficacy of epinephrine, norepinephrine, dobutamine, isoproterenol, dopamine, and phosphodiesterase-III (PDE-III) inhibitors in managing RV contractile dysfunction. When decreased RV contractility is combined with increased afterload, agents that exert vasodilator and positive inotropic effects should be used, including epinephrine, isoproterenol, dobutamine, and the PDE-III inhibitors.

Epinephrine

Epinephrine stimulates α- and β-adrenergic receptors in a dose-dependent fashion. It is frequently the inotrope of choice after CPB (Box 25-3). Doses of 10, 20, and 40 ng/kg/min increased stroke volume by 2%, 12%, and 22%, respectively, and increased cardiac index (CI) by 0.1, 0.7, and 1.2 L/min/m². The HR also increased, but by no more than 10 beats per minute at any dose. Epinephrine is frequently used after cardiac surgery to support the function of the “stunned” reperfused heart. During emergence from CPB, Butterworth and colleagues showed epinephrine (30 ng/kg/min) increased CI and stroke volume by 14% without increasing HR.⁷ In cardiac surgical patients, epinephrine infusion (0.01 to 0.4 μg/kg/min) effectively increases cardiac output, minimally increases HR, and has acceptable side effects.

BOX 25-3 Inotropic Drugs

Phosphodiesterase Inhibitors

The PDE-III inhibitors amrinone (inamrinone) and milrinone increase cyclic adenosine monophosphate, calcium flux, and calcium sensitivity of contractile proteins. These drugs have a similar mode of action because they are noncatecholamine and nonadrenergic agents. They do not rely on β-receptor stimulation for their positive inotropic activity. As a result, the effectiveness of the PDE-III inhibitors is not altered by previous β-blockade nor is it reduced in patients who may experience β-receptor downregulation. In addition to their positive inotropic effects, these agents produce systemic and pulmonary vasodilation. As a result of this combination of hemodynamic effects (i.e., positive inotropic support and vasodilation), the term inodilator has been used to describe these drugs (Box 25-4).

BOX 25-4 Inodilator Drugs

• Inamrinone

• Milrinone

• Dobutamine

• Epinephrine plus nitroprusside (“epipride”)

Because these agents exert their hemodynamic effects by a nonadrenergic mechanism of action, when used in combination with β-agonists they have an additive effect on myocardial performance. Investigators have demonstrated the clinical application of combination therapy using PDE-III inhibitors and dopamine, phenylephrine, epinephrine, and nitroglycerin.¹⁰

A second-generation PDE-III inhibitor, milrinone has a similar hemodynamic profile to amrinone; however, its positive inotropic action is 15 to 30 times that of amrinone. Thrombocytopenia has been a potential clinical concern with the administration of PDE-III inhibitors, particularly amrinone. However, no significant reduction in platelet count occurred after 48 hours of milrinone infusion in cardiac surgical patients. Intravenous milrinone has been studied extensively and demonstrates a favorable short-term effect in CHF and ventricular dysfunction after CPB.¹¹

Milrinone, like other PDE-III inhibitors, appears to increase cardiac output without increasing overall . Data also suggest that milrinone may improve myocardial diastolic relaxation (i.e., positive “lusitropic” effect) and augment coronary perfusion. The proposed mechanism for this effect on diastolic performance is that by decreasing LV wall tension, ventricular filling is enhanced and myocardial blood flow and oxygen delivery are optimized.

The ability of short-term administration of milrinone to augment ventricular performance in patients undergoing cardiac surgery was shown in the results from the European Milrinone Multicentre Trial Group.¹² In this prospective study, intravenous milrinone was studied in patients after CPB. All patients received a bolus infusion of milrinone at 50 μg/kg over 10 minutes, followed by a maintenance infusion of 0.375, 0.5, or 0.75 μg/kg/min for 12 hours. Significant increases in stroke volume and CI were observed. In addition, significant decreases in pulmonary capillary wedge pressure (PCWP), CVP, PAP, MAP, and SVR were seen. Eighteen patients (14%) had arrhythmias; most occurred in the group receiving 0.75 μg/kg/min. Two arrhythmic events were deemed serious; both were bouts of rapid atrial fibrillation occurring with the higher dose.

After CPB, a loading dose of milrinone at 50 μg/kg, followed by a continuous infusion of 0.5 μg/kg/min, resulted in a significant increase in cardiac output. Butterworth and colleagues ¹³ also studied the pharmacokinetics and pharmacodynamics of milrinone in adult patients undergoing cardiac surgery; milrinone (25, 50, or 75 μg/kg) was given if the CI was less than 3.0 L/min/m² after separation from CPB. All three doses of milrinone significantly increased CI. The 50- and 75-μg/kg doses produced significantly greater increases in CI than the 25-μg/kg dose. The 75-μg/kg dose produced increases in CI comparable with the 50-μg/kg dose, but it was associated with more hypotension, despite administration of intravenous fluid, blood, and a phenylephrine infusion. The initial redistribution half-lives were 4.6, 4.3, and 6.9 minutes, and the terminal elimination half-lives were 63, 82, and 99 minutes for the 25-, 50-, and 75-μg/kg doses, respectively. The results of these investigations suggest that for optimizing hemodynamic performance (while minimizing any potential for arrhythmias), the middle dose range (i.e., loading dose of 50 μg/kg) of milrinone may be most efficacious with a continuous infusion of 0.5 μg/kg/min, leading to a plasma concentration of more than 100 mg/mL. In patients with poor LV function, the loading dose should be given during CPB to avoid a decrease in MAP and to minimize the need for other inotropes on discontinuing CPB.

Vasodilators

The indications for using vasodilators such as nitroglycerin or nitroprusside in cardiac surgery include management of perioperative systemic or pulmonary hypertension, myocardial ischemia, and ventricular dysfunction complicated by excessive pressure or volume overload (Box 25-5). In most conditions, nitroglycerin or nitroprusside may be used. Both share common features such as rapid onset, ultra-short half-lives (several minutes), and easy titratability. Nevertheless, there are important pharmacologic differences between nitroglycerin and nitroprusside. In the setting of ischemia, nitroglycerin is preferred because it selectively vasodilates coronary arteries without producing a coronary “steal.” Likewise, in the management of ventricular volume overload or RV pressure overload, nitroglycerin may offer some advantage over nitroprusside. It has a predominant influence on the venous bed such that preload can be reduced without significantly compromising systemic arterial pressure. The benefits of nitroglycerin are improvement in stroke volume, reduction in wall tension and , increased perfusion to the subendocardium as a result of a lower LVEDP, and maintenance of CPP. Nitroprusside is a more potent arterial vasodilator and may potentiate myocardial ischemia due to a coronary steal phenomenon or a reduction in coronary perfusion pressure. Its greater potency, however, makes nitroprusside the vasodilator of choice for management of perioperative hypertensive disorders and for afterload reduction during or after surgery for regurgitant valvular lesions.

BOX 25-5 Vasodilator Mechanisms Helpful in Discontinuing Cardiopulmonary Bypass

• Decreased right and left ventricular wall stress (afterload)

• Decreased venous return (preload)

• Improved lusitropy

• Improved coronary blood flow

Additional uses of vasodilators include management of RV dysfunction. Sodium nitroprusside can augment cardiac output by decreasing RV afterload and PVR. Similarly, nitroglycerin has been shown to decrease PVR, transpulmonary pressure, and mean PAP and to increase cardiac output in patients with elevated PVR resulting from mitral valve disease. Although nitroglycerin and nitroprusside decrease the impedance to RV ejection and increase the RV ejection fraction by reducing afterload, they are nonspecific pulmonary vasodilators. As a result, new studies have focused on the ability of agents such as prostaglandins (particularly prostaglandin E₁), nitric oxide, and the PDE-III inhibitors to more specifically decrease PVR.

Despite proven benefits of vasodilator therapy in the management of CHF, they can be difficult drugs to use in treatment of perioperative ventricular dysfunction. This is most evident in cases of the LCOS when impaired pump function is complicated by inadequate perfusion pressure. In these situations, multidrug therapy with vasoactive and cardioactive agents is warranted (i.e., nitroglycerin or nitroprusside plus epinephrine or milrinone and norepinephrine). Combination therapy enables greater selectivity of effect. The unwanted side effects of one drug can be avoided while supplementing the desired effects with another agent.¹⁴ To maximize the desired effects of any particular combination of agents, frequent assessment of cardiac performance with a pulmonary artery catheter and TEE is needed. This allows the Starling curve and the pressure-volume loops to be visualized as they are shifted up and to the left with therapy.

Additional Pharmacologic Therapy

Following the steps outlined in Tables 25-3 and 25-6, most patients can be weaned off of CPB. However, a small percentage will be difficult to safely remove from CPB because of their chronic end-stage CHF or an acute insult during cardiac surgery producing cardiogenic shock. These patients will probably require mechanical circulatory support. However, while instituting these further steps, some clinicians try additional pharmacologic therapy.

Controversial Older Treatments

Some studies suggest that a reduction in plasma thyroid hormone concentration may be the cause of decreased myocardial function after CPB. Some patients exhibit signs of hypothyroidism, including decreases in HR, CI, and myocardial and systemic oxygen consumption and increases in arteriovenous oxygen difference and SVR. Multiple investigators have documented declines in the circulating triiodothyronine (T₃) concentration during and after CPB, and the most dramatic decreases in T₃ are seen at the end of CPB and during the first few hours after CPB. The reduced thyroid hormone concentrations after CPB may exacerbate myocardial stunning and the LCOS encountered in the post-CPB period. Thyroid hormone in the form of an intravenous T₃ infusion (2 μg/hr to a total dose of 0.5 μg/kg) has been used during cardiac surgery. This therapy has resulted in increases in the MAP and HR and reductions in LAP and CVP in patients who initially could not be weaned from CPB. Some of these patients have been successfully weaned from CPB and have required lower doses of dobutamine and other cardiac drug support after treatment with thyroid hormone.

The administration of glucose-insulin-potassium or just glucose and insulin has been found to be useful for metabolic support of the heart after CPB. The trauma of cardiac surgery produces insulin resistance, which restricts the availability of carbohydrates to the heart. The increased level of catecholamines during CPB may also put further strain on the energy metabolism of the heart, whereas insulin may improve this situation.¹⁵ The administration of high-dose insulin has been compared with dopamine in patients undergoing CABG surgery. The infusion of dopamine (7 μg/kg/min) alone induced metabolic changes unfavorable to the myocardium, whereas dopamine plus insulin increased carbohydrate use with cessation of cardiac uptake of free fatty acids.

New Treatments for Heart Failure and Cardiogenic Shock

Levosimendan is a new positive inotropic drug belonging to the class of calcium sensitizers. The drug stabilizes the calcium-induced conformational change in cardiac troponin C and prolongs the effective cross-bridging time. In contrast to other positive inotropic drugs, levosimendan does not increase intracellular calcium. The drug has vasodilating and anti-ischemic properties produced by opening K⁺-ATP channels ¹⁶ (Table 25-9).

Table 25-9 Emerging Drugs for Heart Failure and Cardiogenic Shock

Levosimendan is recommended by the European Society of Cardiology for treatment of acute worsening of heart failure and for acute heart failure after myocardial infarction.¹⁷ It has also been found to enhance contractile function of stunned myocardium in patients with acute coronary syndromes. It is available clinically in Europe and is undergoing evaluation in the United States. The use of levosimendan has been reported in cardiac surgical patients with high perioperative risk, compromised LV function, difficulties in weaning from CPB, and severe RV failure after mitral valve replacement. The doses used were 12 μg/kg as a 10-minute loading dose, followed by an infusion of 0.1 μg/kg/min. It has been used preoperatively, during emergence from CPB, and in the postoperative period for up to 28 days. The potential for levosimendan to produce increased contractility, decreased resistance, minimal metabolic cost, and no arrhythmias makes it a potentially useful addition to the treatments for patients with LCOS or RV failure.

Nesiritide is a recombinant human brain–type natriuretic peptide with vasodilatory and diuretic effects. In patients with heart failure, intravenous nesiritide acts as a vasodilator and reduces preload; SVR is decreased, and CI subsequently increases. The drug has no positive inotropic effects. Compared with nitroglycerin and dobutamine, nesiritide had a greater effect on decreasing preload than nitroglycerin, and it did not cause as many arrhythmias as dobutamine. Its ultimate role in the treatment of acute heart failure is uncertain, but it may augment the vasodilators or diuretics.

Numerous other drugs are being studied for their uses in patients with acute decompensated heart failure and cardiogenic shock. These drugs include positive inotropic agents such as toborinone (a PDE-III inhibitor), vasodilators such as tezosentan (a specific and potent dual endothelin-receptor antagonist), and vasopressors such as L-NAME (a nitric oxide inhibitor) (see Table 25-9). These various drugs may prove useful for certain types of cardiovascular problems in the future.

INTRA-AORTIC BALLOON PUMP COUNTERPULSATION

The IABP is a device that is designed to augment myocardial perfusion by increasing coronary blood flow during diastole and unloading the left ventricle during systole. This is accomplished by mass displacement of a volume of blood (usually 30 to 50 mL) by alternately inflating and deflating a balloon positioned in the proximal segment of the descending aorta. The gas used for this purpose is carbon dioxide (because of its great solubility in blood) or helium (because of its inertial properties and rapid diffusion coefficients). Inflation and deflation are synchronized to the cardiac cycle by the electronics of the balloon console producing counterpulsations. The results of effective use of the IABP are often quite dramatic. Improvements in cardiac output, ejection fraction, coronary blood flow, and MAP are frequently seen, as well as decreases in aortic and ventricular systolic pressures, LVEDP, PCWP, LAP, HR, frequency of premature ventricular contractions, and suppression of atrial arrhythmias.

Indications and Contraindications

Since its introduction, the indications for the IABP have grown (Table 25-10). The most common use of the IABP is for treatment of cardiogenic shock. This may occur after CPB or after cardiac surgery in patients with shock preoperatively with acute postinfarction ventricular septal defects or mitral regurgitation, those who require stabilization before surgery, or patients who decompensate hemodynamically during cardiac catheterization. Patients with myocardial ischemia refractory to coronary vasodilation and afterload reduction are stabilized with an IABP before cardiac catheterization, and some patients with severe CAD will prophylactically have an IABP inserted before undergoing CABG or off-pump coronary artery bypass surgery.¹⁸

Table 25-10 Intra-Aortic Balloon Pump Counterpulsation Indications and Contraindications

Indications	Contraindications
1. Cardiogenic shock a. Myocardial infarction b. Myocarditis c. Cardiomyopathy 2. Failure to separate from CPB 3. Stabilization of preoperative patient a. Ventricular septal defect b. Mitral regurgitation 4. Stabilization of noncardiac surgical preoperative patient 5. Procedural support during coronary angiography 6. Bridge to transplantation

1. Aortic valvular insufficiency

2. Aortic disease

a. Aortic dissection

b. Aortic aneurysm

3. Severe peripheral vascular disease

4. Severe noncardiac systemic disease

5. Massive trauma

6. Patients with “do not resuscitate” instructions

Contraindications to IABP use are relatively few. The presence of severe aortic regurgitation or aortic dissection is listed as an absolute contraindication for the IABP, although successful reports of its use in patients with aortic insufficiency or acute trauma to the descending thoracic aorta have appeared.

Insertion Techniques

In the initial development of the IABP, insertion was by surgical access to the femoral vessels. In the late 1970s, refinements in IABP design allowed the development of percutaneous insertion techniques. Now the technique most commonly used, percutaneous IABP insertion is rapidly performed with commercially available kits.

The femoral vessel with the greater pulse is sought by careful palpation. The length of the balloon to be inserted is estimated by laying the balloon tip on the patient’s chest at Louis’ angle and appropriately marking the distal point corresponding to the femoral artery. Care must be taken when removing the balloon from its package to follow the manufacturer’s procedures exactly so as not to cause perforation of the balloon before insertion. Available balloons come wrapped and need only be appropriately deflated before removal from the package. The femoral artery is entered with the supplied needle, a J-tipped guidewire is inserted to the level of the aortic arch, and the needle is removed. The arterial puncture site is enlarged with the successive placement of an 8-Fr dilator and then a 10.5- or 12-Fr dilator and sheath combination (Fig. 25-1). In the adult-sized (30- to 50-mL) balloons, only the dilator needs to be removed, leaving the sheath and guidewire in the artery. The balloon is threaded over the guidewire into the central aorta and into the previously estimated correct position in the proximal segment of the descending aorta. The sheath is gently pulled back to connect with the leakproof cuff on the balloon hub, ideally so that the entire sheath is out of the arterial lumen to minimize risk of ischemic complications to the distal extremity. Alternatively, the sheath may be stripped off the balloon shaft much like a peel-away pacemaker lead introducer, thereby entirely removing the sheath from the insertion site. At least one manufacturer offers a “sheathless” balloon for insertion.

Figure 25-1 Diagram of intra-aortic balloon pump (IABP) insertion. A, Cannulation and insertion of the balloon through the femoral artery. Notice the tightly wrapped balloon as it traverses the sheath. A guidewire is not visible in this drawing. B, Correct positioning of balloon in the proximal descending aorta. The J-tipped guidewire is seen exiting from the balloon’s central lumen.

(A, Courtesy of Datascope Corporation; B, Courtesy of Kontron, Inc.)

If fluoroscopy is available during the procedure, correct placement is verified before fixing the balloon securely to the skin. Position may also be checked by radiography or echocardiography after insertion. If an indwelling left radial arterial catheter is functioning at the time of insertion, a reasonable estimate of position may be made by watching balloon-mediated alteration of the arterial pulse waveform (Fig. 25-2). After appropriate positioning and timing of the balloon, 1:1 counterpulsation may be initiated. The entire external balloon assembly should be covered in sterile dressings.

Figure 25-2 Arterial waveforms seen during intra-aortic balloon pump (IABP) assist. The first two waveforms are unassisted, and the last is assisted. Notice the decreased end-systolic and end-diastolic pressures and augmented diastolic pressures caused by IABP augmentation and the (correct) point at which balloon inflation occurs. These are waveforms generated by a correctly positioned and timed balloon.

(Courtesy of Datascope Corporation.)

Removal of a percutaneously inserted IABP may be by the open (surgical removal) or closed technique. If a closed technique is chosen, the artery should be allowed to bleed for several seconds while pressure is maintained on the distal artery after balloon removal to flush any accumulated clot from the central lumen. This maneuver helps prevent distal embolization of clot. Pressure is then applied for 20 to 30 minutes on the puncture site for hemostasis. If surgical removal is chosen, embolectomy catheters may be passed antegrade and retrograde before suture closure of the artery.

Alternate routes of IABP insertion exist. The balloon may be placed surgically through the femoral artery. This is now performed without the use of an end-to-side vascular conduit, although this placement still requires a second surgical procedure for removal. In patients in whom extreme peripheral vascular disease exists or in pediatric patients in whom the peripheral vasculature is too small, the ascending aorta or aortic arch may be entered for balloon insertion. These approaches necessitate median sternotomy for insertion and usually require reexploration for removal. Other routes of access include the abdominal aorta and the subclavian, axillary, and iliac arteries. The iliac approach may be especially useful for pediatric cases.

Timing and Weaning

There are a number of different manufacturers of IABP systems commercially available. The basic console design includes electrocardiographic and arterial blood pressure waveform monitoring and printing, balloon volume monitoring, triggering selection switches, adjustments for inflation and deflation timing, battery backup power sources, and gas reservoir. Some of these systems have become quite sophisticated, with advanced computer microprocessor circuits allowing triggering based on pacemaker signals or detection of and compensation for aberrant rhythms such as atrial fibrillation. Portable models exist for transportation of patients by ground, helicopter, or air ambulances.

For optimal effect of the IABP, inflation and deflation need to be correctly timed to the cardiac cycle. Although a number of variables, including positioning of the balloon within the aorta, balloon volume, and the patient’s cardiac rhythm, can affect the performance of the IABP, basic principles regarding the function of the balloon must be followed. Balloon inflation should be timed to coincide with aortic valve closure, or aortic insufficiency and LV strain will result. Similarly, late inflation will result in a diminished perfusion pressure to the coronary arteries. Early deflation will cause inappropriate loss of afterload reduction, and late deflation will increase LV work by causing increased afterload, if only transiently. These errors and correct timing diagrams are illustrated in Figures 25-2 and 25-3.

Figure 25-3 Alterations in arterial waveform tracings caused by errors in timing of intra-aortic balloon pump (IABP). A, The balloon was deflated too early. B, The balloon was deflated too late. C, The balloon was inflated too early. D, The balloon was inflated too late.

(Courtesy of Datascope Corporation.)

As the patient’s cardiac performance improves, the IABP support must be removed in stages rather than abruptly. Judicious application and dosing of vasodilator and inotropic medications can assist this procedure. The balloon augmentation may be reduced in steps from 1:1 counterpulsation to 1:2 and then to 1:4, with appropriate intervals at each stage to assess hemodynamic and neurologic stability, cardiac output, and mixed venous oxygen saturation changes. After appropriate observation at 1:4 or 1:8 counterpulsation, balloon assistance can be safely discontinued, and the device can be removed by one of the methods discussed. If percutaneous removal is chosen, an appropriate interval for reversal of anticoagulation (if employed) before removal of the balloon should be allowed.

Complications

Several complications have been associated with IABP use (Table 25-11). The most frequently seen complications are vascular injuries, balloon malfunction, and infection.^19,²⁰

Table 25-11 Intra-Aortic Balloon Pump Counterpulsation Complications

Vascular	Miscellaneous	Balloon
Arterial injury (perforation, dissection) Aortic perforation Aortic dissection Femoral artery thrombosis Peripheral embolization Femoral vein cannulation Pseudoaneurysm of femoral vessels Lower extremity ischemia Compartment syndrome Visceral ischemia