The achievement of satisfactory hemodynamic performance is the primary objective of postoperative cardiac surgical management. Optimal cardiac function ensures adequate perfusion and oxygenation of other organ systems and improves the chances for an uneventful recovery from surgery. Even brief periods of cardiac dysfunction can lead to impairment of organ system function, leading to potentially life‐threatening complications. This chapter presents the basic concepts in cardiovascular management and then reviews the evaluation and management of low cardiac output syndrome, hypertension, perioperative myocardial infarction, coronary spasm, cardiac arrest, and rhythm disturbances that can contribute to compromised cardiovascular function.
I. Basic Principles
The important concepts of postoperative cardiac care are those of cardiac output, tissue oxygenation, and the ratio of myocardial oxygen supply and demand. Ideally, one should strive to obtain a cardiac index greater than 2.2 L/min/m2 with a normal mixed venous oxygen saturation, reflecting adequate oxygen delivery to meet metabolic needs, while optimizing the myocardial oxygen supply:demand ratio.1–4
Cardiac output is determined by the stroke volume and heart rate (CO = SV × HR). The stroke volume is equal to the left ventricular end‐diastolic volume (LVEDV) minus the left ventricular end‐systolic volume (LVESV) and is calculated by dividing the cardiac output by the heart rate. The three major determinants of stroke volume are preload, afterload, and contractility.
Preload refers to the LV end‐diastolic fiber length and is generally considered to reflect the LVEDV. Although this can be estimated best by echocardiography, preload in the postoperative patient is more commonly assessed by a measurement of left‐sided filling pressures using a Swan‐Ganz pulmonary artery catheter. These include the pulmonary artery diastolic (PAD) pressure and pulmonary capillary wedge pressure (PCWP). Thus, these pressure measurements acts as surrogates for the assessment of preload. The left atrial pressure (LAP) provides a more precise approximation of the left ventricular end‐diastolic pressure (LVEDP), but requires placement of a catheter directly into the left atrium at the time of surgery. The relationship between filling pressures and volumes is determined by ventricular compliance.
The PAD and PCW pressures generally correlate with each other, and in most patients “wedging” of the catheter is unnecessary. However, the PAD may be higher than the PCW pressure in patients with preexisting precapillary pulmonary hypertension (PH) or intrinsic pulmonary disease, in whom there is an increased transpulmonary gradient (equal to the PA mean pressure minus the PCW pressure). In these patients, the PAD pressure will underestimate the LV volume status, yet wedging of the catheter is not recommended because of an increased risk of PA rupture.
Filling pressures must be interpreted cautiously in the early postoperative period.5–7 The PAD and PCW pressures often correlate poorly with the LVEDV early after surgery and tend to be elevated relative to the intracardiac volume status due to altered ventricular compliance from myocardial edema resulting from cardiopulmonary bypass (CPB) and the use of cardioplegia solutions. Furthermore, the release of various inflammatory substances during bypass and the administration of blood products may increase the pulmonary vascular resistance (PVR), increasing the PAD out of proportion to actual left‐sided filling. A stiff, hypertrophied left ventricle noted in patients with hypertension or aortic stenosis has reduced ventricular compliance and frequently manifests diastolic dysfunction coming off bypass. These patients usually require high filling pressures to achieve adequate ventricular filling. In contrast, the dilated, volume‐overloaded heart may be highly compliant, with an elevated LVEDV at lower pressures.
Elevated filling pressures measured by a Swan‐Ganz catheter are somewhat insensitive to the status of intracardiac volume and in predicting fluid responsiveness.7–9 Numerous studies have shown that goal‐directed therapy (GDT) using alternative monitoring techniques, such as pulse pressure and stroke volume variation, is more accurate in predicting fluid responsiveness. GDT is designed to optimize fluid administration with subsequent use of inotropic medications to improve the cardiac output. GDT may increase volume administration, but it reduces vasopressor use, the duration of ventilation, and complications, producing a shorter hospital length of stay, but with no impact on mortality.4,10–14
For patients with relatively normal ventricular function, many centers do not use Swan‐Ganz catheters, and they rely upon central venous pressure (CVP) measurements to assess preload. Although this is a less accurate means of assessing preload in the diseased heart, it gives a fairly good approximation of left‐heart filling in the normal heart.15,16 One study showed that use of a Swan‐Ganz catheter provided no mortality benefit in low‐risk patients and, in fact, increased mortality in high‐risk patients, although patient selection for use of the catheter had to be taken into consideration.17 Generally, if the CVP exceeds 15–18 mm Hg, inotropic support is indicated. If the patient has other signs of low cardiac output (poor oxygenation, tapering urine output, acidosis), additional monitoring, whether it be by transpulmonary thermodilution (PiCCO, Pulsion Medical Systems), pulse contour analysis (FloTrac/Vigileo, Edwards Lifesciences),18 or insertion of a Swan‐Ganz catheter, will allow for a more objective evaluation of the problem.
Despite the invasiveness of the Swan‐Ganz catheter and concerns about its precise value in most patients, most anesthesiologists and cardiac surgeons still use it for perioperative management, since it is a less‐expensive, time‐proven means of providing scientific information about trends in hemodynamic management to those managing the patient in the critical early postoperative period.19 Its use actually supports the theory that GDT is beneficial, especially for the patient with tenuous hemodynamics after surgery.
Afterload refers to the left ventricular systolic wall tension, which is related to the intraventricular systolic pressure and wall thickness. It is determined by both the preload (Laplace’s law relating radius to wall tension) and the systemic vascular resistance (SVR) against which the heart must eject after the period of isovolumic contraction. The SVR can be calculated from measurements obtained from the Swan‐Ganz catheter (Table 11.1) and should be indexed to the patient’s size. The use of vasodilators to lower the SVR may improve the stroke volume, often in combination with volume infusions and inotropic agents.
Contractility is the intrinsic strength of myocardial contraction at constant preload and afterload. However, it can be improved by increasing preload or heart rate, decreasing the afterload, or using inotropic medications.
Contractility generally reflects systolic function as assessed by the ejection fraction (EF), but it is only indirectly related to the cardiac output. For example, the cardiac output generated by a dysfunctional dilated ventricle with a poor EF may be comparable to or greater than that generated by a normal sized heart with a normal EF, especially if a significant tachycardia is present. Furthermore, a low cardiac output does not necessarily imply that ventricular function is impaired. It may be noted with slow heart rates, hypovolemia, and with a small, hypertrophied ventricle.
Nonetheless, the state of contractility is usually inferred from an analysis of the cardiac output and filling pressures, based upon which steps can be taken to optimize hemodynamic performance. In cardiac surgery patients, the cardiac output is usually obtained by thermodilution technology using a Swan‐Ganz catheter and bedside computer. A measured aliquot of volume is infused into the CVP port of the catheter and the thermistor near the tip measures the pattern of temperature change from which the computer calculates the cardiac output. A continuous cardiac output catheter is frequently used during off‐pump surgery and can provide frequent in‐line assessments of the cardiac output. The FloTrac device calculates the cardiac output from the energy of the arterial pressure waveform and is helpful when thermodilution assessment appears inaccurate or the Swan‐Ganz PA catheter has been removed.18 There are numerous other less‐invasive hemodynamic monitoring system available, many of which have been used in the GDT studies.
Oxygen delivery to tissues is the basic principle upon which hemodynamic support should be based. It is determined by the cardiac output (CO), the hemoglobin (Hb) level, and the arterial oxygen saturation (SaO2). This is represented by the equation:
where 1.39 is the mL of oxygen transported per gram of Hb and 0.0031 is the solubility coefficient of oxygen dissolved in solution (mL/torr of PaO2).
It should be noted in this equation that the majority of oxygen transported to the tissues is in the form of oxygen bound to Hb, not that dissolved in solution. Thus, one of the major factors lowering O2 delivery in the postoperative period is a low hemoglobin (Hb) or hematocrit (HCT). Increasing the Hb level by 1 g/dL can increase blood oxygen content by 1.39 vol%, whereas an increase in PaO2 of 100 torr will only transport an additional 0.3 vol% of oxygen. However, in the profoundly anemic patient, dissolved oxygen represents a greater proportion of the oxygen delivered to tissues. Therefore, it is important to maintain the arterial oxygen saturation as close to 100% and to normalize the cardiac output to achieve adequate O2 delivery. However, trying to achieve supranormal cardiac outputs with excessive volume infusions and inotropes is probably more harmful than beneficial to myocardial metabolism.
Due to concerns that blood transfusions are not benign, numerous studies have attempted to identify the safe lower limit for hematocrit to establish an appropriate transfusion trigger. Transfused blood contains proinflammatory cytokines and low levels of 2,3‐DPG with increased Hb affinity for oxygen, which reduces tissue oxygen delivery. Transfusions are associated with an increased risk of myocardial infarction (MI), respiratory complications, stroke, renal failure, infections, and mortality.20–22 Thus, the transfusion trigger should be based on evidence of impaired oxygen delivery to tissues or hemodynamic issues. Numerous studies have demonstrated comparable outcomes using either a restrictive (transfuse if Hb <7–7.5 g/dL) and liberal (transfuse if Hb <9 g/dL) strategy.23,24 Thus, it is reasonable to accept a hematocrit of 21% in the stable postoperative patient and to prescribe iron supplements or, on occasion, even erythropoietin. However, it is also reasonable to transfuse patients to a hematocrit over 25% when they are elderly, frail and deconditioned, have poor ventricular function, borderline respiratory function, hypotension, tachycardia, ischemic ECG changes, oliguria, or a metabolic acidosis.
Mixed venous oxygen saturation (SvO2) can be used to assess the adequacy of tissue perfusion and oxygenation, aiming for an SvO2 >60%. Swan‐Ganz PA catheters using reflective fiberoptic oximetry are available to monitor the SvO2 in the pulmonary artery on a continuous basis. Intermittent SvO2 measurements can be obtained from blood samples from the distal PA port of the Swan‐Ganz catheter. A change of 10% in the SvO2 can occur before any change is noted in hemodynamic parameters. Despite its theoretical benefit, several studies have suggested that the SvO2 is an unreliable and insensitive predictor of the cardiac output since it is really measuring the balance between oxygen delivery and consumption.25,26 However, since it does reflect the adequacy of tissue oxygenation, it should indicate whether the cardiac output is sufficient to meet tissue needs. When analyzed in conjunction with other hemodynamic parameters, trends in the SvO2 offer insight into both cardiac performance and tissue oxygen delivery.
In the postoperative cardiac surgical patient, a fall in SvO2 generally reflects decreased oxygen delivery or increased oxygen extraction by tissues and is suggestive of a reduction in cardiac output. However, other constantly changing factors that affect oxygen supply and demand may also influence SvO2 and must be taken into consideration. These include shivering, pain, agitation, temperature, anemia, alteration in FiO2, and the efficiency of alveolar gas exchange. The Fick equation, which uses the arteriovenous oxygen content difference to determine cardiac output, can be rearranged as follows:
This equation indicates that a decrease in SvO2 may result from a decrease in SaO2, cardiac output, or hemoglobin level, or an increase in oxygen consumption.
When the arterial O2 saturation is normal (SaO2 >95%), an SvO2 <60% suggests the presence of a decreased cardiac output and the need for further assessment and therapeutic intervention. Conversely, a high SvO2 may reflect less oxygen extraction, as seen with hypothermia, sepsis, or intracardiac or significant peripheral arteriovenous shunting. When this is noted, oxygen delivery or utilization may be impaired and an otherwise “normal” cardiac output may be insufficient to provide adequate tissue oxygenation.
Studies have also analyzed whether the central venous oxygen saturation (ScvO2) has value in perioperative management. Many GDT protocols do utilize this parameter and have found that its use improved outcomes. Although a very low ScvO2 is most likely associated with a low cardiac output, the ScvO2 is not as accurate as the SvO2 in assessing either tissue oxygenation or cardiac output.26,27
When the cardiac index exceeds 2.2 L/min/m2 and the arterial oxygen saturation is adequate (>95%), it may be inferred that oxygen delivery to the tissues is satisfactory. Thus, SvO2 measurements to assess oxygen delivery are not necessary. However, there are a few situations in which calculation of tissue oxygenation may be valuable in assessing cardiac function:
When the thermodilution cardiac output is unreliable (tricuspid regurgitation, improperly positioned Swan‐Ganz catheter) or cannot be obtained (Swan‐Ganz catheter has not been placed or cannot be placed, such as in the patient with a mechanical tricuspid valve or central venous thrombosis, or has been removed).28
When the thermodilution cardiac output may seem spuriously low and inconsistent with the clinical scenario (malfunctioning Swan‐Ganz catheter or incorrect calibration of computer). A normal SvO2 indicates that the cardiac output is sufficient to meet tissue metabolic demands.
When the cardiac output is marginal, in‐line assessment of trends in the mixed venous oxygen saturation can provide up‐to‐date information on the relative status of cardiac function.
Myocardial oxygen supply and demand
Myocardial O2demand (mvO2) is influenced by factors similar to those that determine the cardiac output (afterload, preload, heart rate, contractility). Reducing afterload will generally improve cardiac output with a decrease in mvO2, whereas an increase in any of the other three factors will improve cardiac output at the expense of an increase in mvO2. Preoperative management of the patient with ischemic heart disease is primarily directed towards minimizing O2 demand.29
Myocardial O2supply is determined by coronary blood flow, the duration of diastole, coronary perfusion pressure, the Hb level, and the arterial oxygen saturation When complete revascularization has been achieved, postoperative management is directed towards optimizing factors that improve O2 supply and, to a lesser degree, minimize an increase in O2 demand.
A heart rate of 80–90 bpm should be achieved and excessive tachycardia and arrhythmias must be avoided.
An adequate perfusion pressure (mean arterial pressure [MAP] >70 mm Hg) should be maintained, taking care to avoid both hypotension and hypertension.
Ventricular distention and wall stress (i.e. afterload) should be minimized by avoiding excessive preload, reducing the SVR, and using inotropic medications to improve contractility.
The hematocrit should be maintained at a safe level. Although an increased level of Hb should improve oxygen delivery, transfusions carry inherent risks. In general, myocardial ischemia should not occur in the well‐protected, revascularized heart unless the hematocrit drops into the low 20s.
Ischemic ECG changes suggest that coronary blood flow may not be adequate. This may result from stenosis, thrombus, or spasm in a native vessel, anastomotic stenosis, kinking, thrombus or spasm in a bypass graft, or incomplete revascularization. If ECG changes are noted, immediate attention and possible reevaluation by catheterization are indicated.
Cardiac output (CO) and index (CI) CO = SV × HR CI = CO/BSA
4–8 L/min 2.2–4.0 L/min/m2
Stroke volume (SV)
60–100 mL/beat (1 mL/kg/beat)
Stroke volume index (SVI) SVI = SV/BSA
Mean arterial pressure (MAP)
70–100 mm Hg
Systemic vascular resistance (SVR)
Pulmonary vascular resistance (PVR)
Left ventricular stroke work index (LVSWI) LVSWI = SVI × (MAP − PCWP) × 0.0136
BSA, body surface area; HR, heart rate; DP, diastolic pressure; SP, systolic pressure; CVP, central venous pressure; PAP, mean pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure
II. Low Cardiac Output Syndrome
The achievement of a satisfactory cardiac output to achieve adequate tissue oxygenation is the primary objective of postoperative cardiovascular management. Hemodynamic norms for the patient recovering uneventfully from cardiac surgery are a cardiac index (CI) greater than 2.0 L/min/m2, a PAD or PCW pressure below 20 mm Hg, and a heart rate below 100 bpm with an SvO2 >65%. The patient should have warm, well‐perfused extremities with an excellent urine output.
Risk factors for low cardiac output states include:4,16,30,31
Preoperative clinical factors: advanced age, malnutrition, diabetes with chronic kidney disease, LV systolic dysfunction, (e.g. low EF or cardiac output), and diastolic dysfunction (e.g. low cardiac output often with a hyperdynamic ventricle and an LVEDP >20 mm Hg).
Preoperative abnormal lab values including anemia and elevated BNP levels
Operative factors: longer durations of aortic cross‐clamping or CPB, emergency surgery and reoperations, CABG with incomplete revascularization, concomitant CABG‐valve operations, mitral valve surgery.
Diastolic dysfunction. After weaning from CPB, this is a particularly difficult problem to treat and usually requires pharmacologic support for a low output state despite normal systolic function.32
Increased lactate release after five minutes of reperfusion is an independent predictor of a low cardiac output. It suggests that there is delayed recovery of aerobic metabolism, perhaps as a result of inadequate myocardial protection.33
Pathophysiology. A basic principle of cardiac surgery is to prevent myocardial damage while a corrective procedure is being performed. Although this has led to the concept of off‐pump bypass surgery or even beating heart surgery, the vast majority of open‐heart operations involve use of CPB with cardioplegic arrest. Despite adherence to basic principles and with improvements in cardioplegic solutions, including the more recent adoption of del Nido cardioplegia, myocardial protection is never perfect, and more myocardial injury tends to occur with longer cross‐clamp times. In general, myocardial function declines for about 6–8 hours following surgery, presumably from ischemia/reperfusion injury with use of cardioplegic arrest, and from the systemic inflammatory response. It then usually returns to baseline within 24 hours in the absence of significant myocardial injury (see section VIII, pages 586–589, on perioperative myocardial infarction).34
Temporary inotropic support is often required during this period to optimize hemodynamic performance. Drugs used at the conclusion of CPB should generally be continued for this brief period of time and can be weaned once the cardiac output is satisfactory. Although use of low‐dose inotropes for several hours is fairly common in most practices, even independent of LV function, studies do suggest that patients who receive inotropes after surgery have a higher mortality rate.35
When marginal ventricular function is present in the anesthetized or sedated patient, the compensatory mechanisms that can augment cardiac output in the awake patient are blunted. These include sympathetic autonomic stimulation and endogenous catecholamine production that can increase heart rate, contractility, and arterial and venous tone, elevating both preload and afterload. All of these factors may improve cardiac output or systemic blood pressure, but they may also increase myocardial oxygen demand at a time when asymptomatic ischemia may be present.
When these compensatory mechanisms are not present in the sedated patient, therapeutic intervention is necessary to improve the cardiac output. It is imperative to intervene before or at the first sign of clinical manifestations of a low cardiac output syndrome. These include:
Poor peripheral perfusion with pale, cool extremities, and diaphoresis
Pulmonary congestion and poor oxygenation
Impaired renal perfusion and oliguria
The use of invasive monitoring to continuously evaluate a patient’s hemodynamic status allows for appropriate therapeutic interventions to be undertaken before these clinical signs become apparent. Nonetheless, subtle findings, such as a progressive tachycardia or cool extremities, should alert the astute clinician to the fact that the patient needs more intensive management. Intervention is indicated for a low cardiac output state, defined as a cardiac index below 2.0 L/min/m2, usually associated with left‐sided filling pressures exceeding 20 mm Hg and an SVR exceeding 1500 dyn‐s/cm5. It cannot be overemphasized that observing trends in hemodynamic parameters, rather than absolute numbers, is important when evaluating a patient’s progress or deterioration.
A general scheme for the management of postoperative hemodynamic problems is presented in Table 11.2.
Etiology. A low cardiac output state is usually associated with impaired left or right systolic function and may result from abnormal preload, contractility, heart rate, or afterload. However, a variety of other factors may be contributory. It may also be noted in patients with satisfactory systolic function but marked left ventricular hypertrophy (LVH) and diastolic dysfunction.1–4,16,36
Decreased left ventricular preload
Hypovolemia (bleeding, vasodilation from warming, narcotics, or sedatives)
Positive‐pressure ventilation and PEEP
Right ventricular dysfunction (RV infarction, PH)
Low ejection fraction
Myocardial “stunning” from transient ischemia/reperfusion injury or myocardial ischemia; perioperative infarction
Poor intraoperative myocardial protection
Incomplete myocardial revascularization
Anastomotic complications/graft thrombosis
Native coronary artery or graft spasm
Evolving infarction at time of surgery
Hypoxia, hypercarbia, acidosis
Tachy‐ and bradyarrhythmias
Tachycardia with reduced cardiac filling time
Atrial arrhythmias with loss of atrial contraction
Second‐ or third‐degree heart block
Fluid overload and ventricular distention
Left ventricular outflow tract obstruction following mitral valve repair or replacement (from struts or retained leaflet tissue or uncorrected hypertrophic obstructive cardiomyopathy)
Diastolic dysfunction with impaired relaxation and high filling pressures37
Syndromes associated with cardiovascular instability and hypotension
Sepsis (hypotension from a reduction in SVR; hyperdynamic with a high cardiac output early and myocardial depression at a later stage)
Anaphylactic reactions (blood products, drugs)
Adrenal insufficiency (primary or in the patient on preoperative steroids)
Assessment (abnormalities of concern noted in parentheses)
Hemodynamic measurements: assess filling pressures and determine the cardiac output with a Swan‐Ganz catheter; calculate SVR; measure SvO2 (low cardiac output, high filling pressures, high SVR, low SvO2)
Arterial blood gases (hypoxia, hypercarbia, acidosis/alkalosis) hematocrit (anemia), and serum potassium (hypo‐ or hyperkalemia)
Chest x‐ray (pneumothorax, hemothorax, position of the endotracheal tube or intra‐aortic balloon)
Urinary output (oliguria)
Chest tube drainage (mediastinal bleeding)
Two‐dimensional echocardiography is very helpful when the cause of a low cardiac output syndrome is unclear. Along with hemodynamic measurements, it can help identify whether it is related to LV systolic or diastolic dysfunction, RV systolic dysfunction, or cardiac tamponade.
Transesophageal echocardiography (TEE) provides better and more complete information than a transthoracic study and can be readily performed in the intubated patient. It should always be considered when the clinical picture is consistent with tamponade but a transthoracic study is inconclusive.38
Ensure satisfactory oxygenation and ventilation (see Chapter 10).
Treat ischemia or coronary spasm if suspected to be present due to ECG changes. Myocardial ischemia often responds to intravenous nitroglycerin (IV NTG) but may require further investigation if it persists. Coronary spasm (see section IX, pages 589–591) can be difficult to diagnose but usually responds to IV NTG and/or a calcium channel blocker (CCB), such as sublingual nifedipine or IV diltiazem.
Optimize preload by raising filling pressures with volume infusion to a PAD or PCW pressure of about 18–20 mm Hg. Despite concerns that these pressures are insensitive measures of preload, their trends generally indicate when additional measures may be required to optimize cardiac output. Most times, a volume infusion that raises the PAD is all that is necessary to achieve a satisfactory cardiac output. This can initially be achieved using crystalloid or colloid solutions (see Chapter 12, page 678). Volume infusion is preferable to atrial pacing for improving cardiac output because it produces less metabolic demand on the recovering myocardium.39
Again, because left‐sided filling pressures are only surrogates for ventricular volume, the correlation between the two is best assessed from a review of pre‐ and intra‐operative hemodynamic data and an understanding of the patient’s cardiac pathophysiology. Filling pressures will differ once the patient is anesthetized due to alterations in loading conditions and autonomic tone. They will subsequently be affected by reduced ventricular compliance at the termination of CPB. Direct visual inspection of the heart, evaluation of TEE images to correlate ventricular end‐diastolic dimensions with filling pressures, and measurement of cardiac outputs at the same time will usually indicate the appropriate filling pressures for optimal ventricular filling and cardiac performance in the early postoperative period.
For example, a PAD or PCW pressure around 15–18 mm Hg is usually best for patients with preserved LV function. In contrast, a pressure in the low 20s may be necessary to achieve adequate preload in the patient with poor LV function, a stiff hypertrophied ventricle with diastolic dysfunction, a small LV chamber (mitral or aortic stenosis or after resection of a left ventricular aneurysm), or preexisting PH from mitral valve disease. Ventricular size and compliance should be kept in mind when deciding whether additional volume is the next appropriate step in the patient with marginal cardiac function.
The response to volume infusion may be variable (see the postoperative scenario described on pages 377–380). Failure of filling pressures to rise with volume may result from the capillary leak that is present during the early postoperative period. It may also result from vasodilation associated with rewarming or the use of medications with vasodilator properties, such as propofol or narcotics. It is more common in the volume‐overloaded compliant ventricle. However, it may also reflect the beneficial attenuation of peripheral vasoconstriction that is attributable to an improvement in cardiac output caused by the volume infusion. As the SVR and afterload gradually decrease, the cardiac output may improve further without an increase in preload.
A rise in filling pressures without improvement in cardiac output may adversely affect myocardial performance as well as the function of other organ systems. At this point, inotropic support is usually necessary. Thus, careful observation of the response to volume infusion is imperative.
Excessive preload increases left ventricular wall tension and may exacerbate ischemia by increasing myocardial oxygen demand and decreasing the transmyocardial gradient (aortic diastolic minus LV diastolic pressure) for coronary blood flow. It may also impair myocardial contractility.
Excessive preload may lead to interstitial edema of the lungs, resulting in increased extravascular lung water, ventilation/perfusion (V/Q) abnormalities, and hypoxemia.
Excessive preload in the patient with right ventricular dysfunction may impair myocardial blood flow to the RV, resulting in progressive ischemia. A distended RV may contribute to left ventricular dysfunction because of overdistention and septal shift that impairs LV distensibility and filling.
The presence of RV or biventricular dysfunction may also cause systemic venous hypertension which may reduce perfusion pressure to other organ systems. This may affect the kidneys (causing oliguria), the gastrointestinal (GI) tract (causing splanchnic congestion, jaundice, or ileus), or the brain (contributing to altered mental status).
Thus, the temptation must be resisted to administer additional volume to the failing heart with high filling pressures. Excessive preload must be avoided because it may lead to deterioration, rather than improvement, in hemodynamic performance. Once a satisfactory cardiac output has been achieved, volume infusions can be minimized.
Stabilize the heart rate and rhythm. All attempts should be made to achieve atrioventricular (AV) synchrony with a heart rate around 90 bpm. This may require atrial (AOO or AAI) or AV (DDD or DVI) pacing. These modalities take advantage of the 20–30% improvement in cardiac output provided by atrial contraction that will not be achieved with ventricular pacing alone. This is especially important in the hypertrophied ventricle. Temporary biventricular pacing may be beneficial in improving hemodynamics (both systolic and diastolic function) in patients with impaired ventricular function, especially with prolonged AV conduction (wide QRS complex).40–43 Antiarrhythmic drugs should be used as necessary to control ventricular ectopy or slow the response to atrial fibrillation (AF).
Improve contractility with inotropic agents.1–4,16,44 This should be based on an understanding of the α, β, or nonadrenergic hemodynamic effects of vasoactive medications and their anticipated effects on preload, afterload, heart rate, and contractility. These medications and a strategy for their selection are noted in section III, starting on page 535.
The use of inotropic agents in the early postoperative period may seem paradoxical in that augmented cardiac output is being achieved at the expense of an increase in oxygen demand (e.g. increased heart rate and contractility). However, the major determinant of oxygen demand is the pressure work that the left ventricle must perform. This is reflected by the afterload, which is determined by preload and SVR. Inotropic drugs that increase contractility do not necessarily increase oxygen demand in the failing heart, because they may reduce preload, afterload, and frequently the heart rate as a result of improved cardiac function.
If the cardiac output remains low despite pharmacologic support, physiologic support with an intra‐aortic balloon pump (IABP) should be strongly considered. If the patient cannot be weaned from bypass or has hemodynamic evidence of severe ventricular dysfunction despite maximal medical therapy and the IABP, use of a circulatory assist device should be considered.
Reduce afterload with vasodilators if the cardiac output is marginal while carefully monitoring systemic blood pressure to avoid hypotension. Vasodilators must be used cautiously when the cardiac index is very poor, because an elevated SVR from intense vasoconstriction is often a compensatory mechanism in low cardiac output states to maintain central perfusion. If the calculated SVR exceeds 1500 dyn‐s/cm5, vasodilators may be indicated either alone or in combination with inotropic medications.
It is essential to integrate all hemodynamic parameters when determining whether a patient is or is not doing well. For example, the blood pressure may be high when the heart is not performing well, the cardiac output may be acceptable when the heart is struggling, and the cardiac output can be low even when ventricular function is normal.
The presence of a satisfactory or elevated blood pressure is not necessarily a sign of good cardiac performance. Blood pressure is related directly to both the cardiac output and the systemic vascular resistance (BP = CO × SVR). In the early postoperative period, myocardial function may be marginal despite normal or elevated blood pressures because of an elevated SVR resulting from augmented sympathetic tone and peripheral vasoconstriction. Vasodilators can be used to reduce afterload in the presence of elevated filling pressures, thus reducing myocardial ischemia and improving myocardial function. However, withdrawal of inotropic support in the hypertensive patient should be considered only after a satisfactory cardiac output has been documented. Otherwise, acute deterioration may ensue.
One should not be deceived into concluding that myocardial function is satisfactory when the cardiac output is “adequate” but is being maintained by fast heart rates at low stroke volumes.
Although sinus tachycardia is often related to the use of catecholamines or even milrinone, it is often an ominous sign of acute myocardial ischemia or infarction, and it may render the borderline heart ischemic. The stroke volume index (SVI) is an excellent method of assessing myocardial function, because it assesses how much blood the heart is pumping each beat, indexed for the patient’s size. Once hypovolemia has been corrected, a low SVI (less than 30 mL/beat/m2) indicates poor myocardial function for which inotropic support is usually indicated. Although β‐blockers would theoretically be beneficial to control tachycardia in the injured or ischemic heart, they are poorly tolerated in the presence of LV or RV dysfunction and should be use cautiously, if at all. A potential role for ivabradine in this situation to lower the heart rate without affecting the inotropic effects of catecholamines is not clear.45
Sinus tachycardia may represent a beneficial compensatory mechanism for a small stroke volume in a patient with a small left ventricular chamber (following LV aneurysm resection or mitral valve replacement for mitral stenosis). In these situations, an attempt to slow the heart rate pharmacologically may compromise the cardiac output significantly. Not infrequently, sinus tachycardia is a means of compensating for hypovolemia and quickly resolves after fluid administration. It may also be present in the profoundly anemic patient.
Tachycardia may also be present in patients with marked LVH and diastolic dysfunction, especially after aortic valve replacement (AVR) for aortic stenosis. In these situations, the cardiac output may be low despite preserved ventricular function because of a small noncompliant LV chamber. β‐blockers or CCBs can be used to slow the heart rate after adequate volume replacement has been achieved, but they must be used with extreme caution. Use of a medication with lusitropic (relaxant) properties, such as milrinone, may be helpful.
Tachycardia accompanying a large stroke volume is often seen in young patients with preserved ventricular function. It can be treated safely with a β‐blocker, such as esmolol or IV metoprolol.
The cardiac output may be marginal despite normal LV systolic and diastolic function when the patient is hypovolemic but does not develop a compensatory tachycardia. This is noted in patients who were well β‐blocked prior to surgery, require pacing at the conclusion of the operation, or are receiving other medications that slow the heart rate, such as dexmedetomidine. Pacing up to a rate of 90 bpm and moderate volume infusion are invariably successful in improving the cardiac output in these situations. If the cardiac output is not acceptable once the filling pressures are satisfactory, an inotrope should be added. The common temptation to continue to administer fluid once the filling pressures are elevated may do more harm than good to the struggling heart.
Maintain blood pressure
Tissue perfusion may be impaired when the systemic pressure is low despite a satisfactory cardiac output. The mean arterial pressure is the average pressure during each cardiac cycle, and generally represents the perfusion pressure to organ systems. In addition to optimizing cardiac output and oxygenation, the mean arterial pressure should be maintained at a level exceeding at least 70 mm Hg to ensure adequate tissue perfusion.
If the patient has a satisfactory cardiac output but a low systemic resistance and low blood pressure, the filling pressures are often low, and a moderate volume infusion should improve the blood pressure. This scenario is common in sedated patients receiving medications that have potent vasodilator properties. It is also common in patients who had been taking certain medications up to the time of surgery, including ACE inhibitors, angiotensin receptor blockers (ARBs), CCBs, and amiodarone (which blocks sympathetic stimulation by α and β blockade).
If hypotension persists after volume infusion, an α‐agent should be used to increase the SVR. Norepinephrine is the preferred drug when the cardiac output is marginal because it has β‐agonist properties, whereas phenylephrine is a pure α‐agonist and should be used only if the cardiac output is satisfactory. Some patients respond better to norepinephrine than phenylephrine, and others just the reverse.
Although norepinephrine does induce renal vasoconstriction, it generally has little adverse effect on renal function.46 Furthermore, unless used in high doses, norepinephrine is effective in raising the systemic pressure without adversely affecting intestinal mucosal perfusion or the splanchnic oxygen supply:demand ratio.47 Thus, unless the patient remains hypotensive in a low cardiac output state, concerns about impaired regional perfusion are mitigated.
When catecholamine‐resistant hypotension persists despite a satisfactory cardiac output, it may represent a condition of autonomic failure termed “vasoplegia”. This may be a consequence of the systemic inflammatory response (although it has been noted after off‐pump surgery as well) and may be related to vasodilation induced by nitric oxide. Levels of vasopressin are low in most normotensive patients after bypass but are inappropriately low in patients with “vasodilatory shock”. Arginine vasopressin acts on vasomotor V1 and renal V2 receptors and, given in a dose of 0.01–0.1 units/min, can restore blood pressure in these patients and may be preferable to use of norepinephrine.48,49 Such low doses may suffice because patients with vasodilatory shock tend to be hypersensitive to its effects. It induces intestinal and gastric mucosal vasoconstriction and also reduces renal blood flow while increasing renal oxygen consumption. Thus, if the cardiac output remains marginal, mesenteric and renal ischemia are more likely to occur.50,51
When there is a poor response to vasopressin, methylene blue 1.5 mg/kg should be considered. It inhibits guanylate cyclase activation by nitric oxide and has been reported to reduce morbidity and mortality in patients with postbypass vasoplegia, especially when given early.52 Another alternative is hydroxocobalamin (5 g IV), which can be used in patients taking serotonergic antidepressants (citalopram, sertraline, fluoxetine), in whom methylene blue is contraindicated.53
If the patient has a persistently low blood pressure and cardiac output despite volume infusions and adequate filling pressures, inotropic support should be initiated or increased, anticipating a rise in systemic blood pressure. If this does not occur, an IABP may be required to improve the cardiac output. Frequently, an α‐agent must also be added simultaneously to augment the blood pressure, and norepinephrine is preferable because it provides some β effects. Sometimes, use of an α‐agent to improve coronary perfusion pressure leads to an improvement in cardiac output. Vasopressin and phenylephrine are best avoided when the cardiac output is marginal because they are pure vasoconstrictors with no inotropic properties and may compromise renal and splanchnic blood flow.
Correct anemia with blood transfusions. The hematocrit is usually maintained above 21% in the postoperative period, but transfusions should be considered for persistent hypotension, ongoing bleeding, hemodynamic instability, metabolic acidosis, or evidence of myocardial ischemia.
Right ventricular failure and pulmonary hypertension (PH) (also see pages 382 and 396–397)14,16,54,55
Mechanisms. Right ventricular dysfunction results from decreased RV contractility and may be exacerbated by excessive RV preload, elevated RV afterload (PH), or right coronary ischemia or infarction.
Volume overload (elevated preload) may occur with tricuspid regurgitation or excessive fluid administration.
Pressure overload (elevated afterload) may result from any condition causing PH, whether pulmonary (ARDS, positive pressure ventilation, pulmonary embolism) or left‐sided cardiac disease (LV dysfunction, left‐sided valve disease).
The right ventricle functions in a low‐pressure circuit, so when any of the above factors is present, the RV will dilate, causing an increase in RV end‐diastolic pressure, which will reduce right coronary perfusion pressure. RV dilatation will also shift the interventricular septum leftward, impairing LV distensibility and filling, which will reduce the cardiac output. Progressive LV dysfunction will then create a vicious cycle by reducing systemic perfusion pressure, causing RV ischemia, and raising PA pressures and RV afterload, which will worsen RV function.
Preoperative risk factors
Proximal RCA occlusion with possible RV infarction
PH of any cause: most commonly, this is “postcapillary” and associated with mitral/aortic disease or severe LV dysfunction, but it may result from severe lung disease (cor pulmonale) or primary PH (“precapillary”).
Intraoperative and postoperative contributing factors:
Poor myocardial protection, usually due to poor collateral circulation with an occluded RCA or due to exclusive use of retrograde cardioplegia, which provides suboptimal RV protection
Prolonged ischemic times/myocardial stunning
Inadvertent RCA distribution ischemia (obstruction of a coronary ostium during AVR, kinking of the RCA ostial button in aortic root replacements)
Coronary embolism from air (usually in valve operations), thrombi, or particulate matter (in reoperative CABG or valve operations)
Systemic hypotension causing RV hypoperfusion
Acute PH (increased PVR and RV afterload) from:
Vasoactive substances associated with blood product transfusions and CPB
RV pressure overload from intrinsic pulmonary disease, ARDS, pulmonary embolism
Echocardiography is the best way to identify RV dysfunction, which is usually associated with RV dilatation. Markers of RV dysfunction include an RV fractional area change <35% or a tricuspid annular plane systolic excursion (TAPSE – the distance traveled between end‐diastole and end‐systole at the lateral corner of the tricuspid annulus) <16 mm.56 These findings may be identified by TEE during surgery, but are uncommonly assessed in the ICU.
Specially designed Swan‐Ganz catheters can measure RVEF and RVEDV, but the correlation with contractility is not that precise. The EF may increase with increased preload or decreased afterload without any change in contractility since, by definition, the EF only reflects contractility at constant preload and afterload. The presence of significant tricuspid regurgitation will render thermodilution cardiac outputs unreliable. Alternative means of assessing the cardiac output, directly by using the FloTrac system or indirectly by measuring the SvO2, may be helpful, although the former cannot be relied upon if atrial fibrillation is present.
CVP measurements alone often do not accurately reflect the RVEDV, but trends in the CVP with volume challenges along with cardiac output measurements are valuable in dictating the best course of action. If the CVP rises above 15–18 mm Hg without an improvement in cardiac output, further volume infusions should not be given, and steps to reduce RV afterload and increase contractility are indicated. Although isolated RV dysfunction is best characterized by a high RA/PCW pressure ratio, this is unreliable when LV dysfunction is also present.
RV afterload is generally assessed by the mean PA pressure and less commonly by the PVR, since the latter is not influenced by RV dilatation and will be higher when the cardiac output is lower (mean PA = PVR × CO). However, sometimes a low PA pressure is encountered when the RV is failing, because the RV is simply incapable of generating an adequate PA pressure, yet the PVR will remain unchanged.
Treatment. The goals of treatment are to optimize RV preload, ensure AV conduction, maintain systemic and coronary perfusion pressures, improve RV contractility, reduce RV afterload by reducing PVR, and optimize LV function (Table 11.4).
RV preload must be raised cautiously to avoid the adverse effects of RV dilatation on RV myocardial blood flow and LV function. It is generally taught that cardiac output can be improved by volume infusions in patients sustaining an RV infarction with compromised RV function. However, the CVP (RA pressure) should not be increased to more than 18–20 mm Hg, which indirectly indicates RV volume overload. If no improvement in cardiac output ensues when volume is given to reach this level, additional volume infusions should be avoided. Volume overload of the right ventricle contributes to progressive deterioration of RV function, impairment of LV filling, and systemic venous hypertension.
AV conduction is essential if it can be achieved.
Systemic perfusion pressure must be maintained while trying to avoid medications that can also increase PVR. Maintaining adequate perfusion of the RV might benefit from IABP support.
Correction of hypothermia, hypoxemia, and respiratory acidosis by hyperventilation will decrease the PVR (acidosis rather than hypercarbia is most deleterious).
Inotropic medications that can support RV and LV function and also reduce the pulmonary artery pressure should be selected, and they may be combined with a pulmonary vasodilator.
Milrinone is a phosphodiesterase (PDE) inhibitor that is very beneficial in improving RV contractility and reducing PA pressures, although it usually causes systemic hypotension that requires an α‐agent to support the SVR. Unfortunately, the use of α‐agents may also increase the PVR. The combination of IV milrinone with oral sildenafil produces a synergistic reduction in PVR.55
Isoproterenol may be the most effective drug to improve RV contractility. Its use must be tempered by the possibility of inducing a significant tachycardia.
Dobutamine is an effective inotrope that improves RV contractility in patients with RV failure, although it has little effect on pulmonary hemodynamics. It has fairly similar effects to milrinone and acts synergistically with it, but it does cause more tachycardia.
If RV function remains depressed, addition of epinephrine may be considered. Norepinephrine may be necessary to maintain SVR in the hypotensive patient, although it will also increase PVR.
Levosimendan (see section III.L.2, pages 544–545) exhibits similar inotropic effects to dobutamine but is more effective in reducing RV afterload.57
Pulmonary vasodilators should also be considered to reduce RV afterload.58
Intravenous nitroso dilators, including NTG and nitroprusside, may be effective in reducing PA pressures, but NTG is usually associated with a reduction in cardiac output, and nitroprusside primarily reduces the SVR. Thus, they may be beneficial in patients with moderate PH and RV dysfunction, but they have relatively limited application in patients with severe RV dysfunction. They have been supplanted by other more potent and selective pulmonary vasodilators.
Inhaled nitric oxide (iNO) is a selective pulmonary vasodilator that can decrease RV afterload and augment RV performance with minimal effect on SVR, thus maintaining systemic perfusion pressure. Despite these benefits, a meta‐analysis reported that iNO did not reduce the duration of mechanical ventilation or mortality when used for postoperative RV dysfunction.59
It does not increase intrapulmonary shunting and may reverse the hypoxic vasoconstriction that is frequently noted with other pulmonary vasodilators (such as nitroprusside) and may improve the PaO2/FiO2 ratio.60
The usual dose is 10–40 ppm administered via the ventilatory circuit. The circuit must be designed to optimally mix O2 and NO to generate a low level of NO2, which is toxic to lung tissue. Measurements of the concentration of iNO in the inhalation limb and NO2 in the exhalation limb of the ventilatory circuit by chemiluminescence are essential during delivery. Ideally, a scavenger system should be attached to the exhaust port of the ventilator. Once in the bloodstream, iNO is rapidly metabolized to methemoglobin, which rarely causes methemoglobinemia in adults but can be a significant problem in young children.
iNO should be weaned slowly to prevent a rebound increase in PVR. A general guideline is to decrease the dose no more than 20% every 30 minutes. Inhalation can be stopped once 6 ppm is reached.
Comparative studies in patients with postoperative PH have shown that iNO is comparable to inhaled epoprostenol, but not quite as effective as iloprost, in lowering PA pressures and improving RV function.61,62 In comparison with IV milrinone, iNO is associated with lower heart rates, better RVEF, and less requirement for vasopressor support.63
Prostaglandin and prostacyclin analogues are potent pulmonary vasodilators that have been used primarily to assess vascular reactivity in patients awaiting heart transplantation. However, they are also beneficial in reducing PA pressure and improving RV function in patients with severe PH during and after various types of cardiac surgery, including mitral valve surgery and heart transplantation. These medications can optimize the PVR/SVR ratio and maintain RV contractility without affecting systemic perfusion pressure.
Epoprostenol (prostacyclin, PGI2 [Flolan]) is both a pulmonary and very strong systemic vasodilator when administered intravenously because it is not inactivated by the lungs. However, inhaled PGI2 is a very effective short‐acting selective pulmonary vasodilator that can improve RV performance without affecting SVR. It may also improve oxygenation by decreasing V/Q mismatch. A single 60 μg inhalation in the operating room may initially be used, but a continuous inhalation setup in the ICU, using either a weight‐based protocol (up to 50 ng/kg/min, at which dose some systemic vasodilation may occur) or a concentration‐based protocol, giving 8 mL/h of a 20 μg/mL solution, can be recommended. There is complete reversal of effect about 25 minutes after inhaled PGI2 is stopped. It is as effective as iNO while being less expensive and less cumbersome to administer.61
Iloprost (Ventavis) is a synthetic prostacyclin analogue that also reduces PVR and increases cardiac output with little effect on blood pressure or SVR. It can be given in an aerosolized dose of 25–50 μg during and after surgery. Its hemodynamic effect lasts 1–2 hours after a single administration. Comparative studies have shown it to be more effective than iNO in reducing PVR,62,63 with the combination of iNO and iloprost having additive effects on the pulmonary vasculature.64
Inhaled milrinone has shown comparable effects to IV milrinone in reducing PA pressures while demonstrating more pulmonary selectivity by not influencing the SVR and mean arterial pressure.65 It also improves oxygenation by reducing intrapulmonary shunting and V/Q mismatch.66 Studies have found it to be less effective than iNO or inhaled iloprost,66,67 but to have an additive effect in reducing PA pressures and the requirement for vasoactive support when used with inhaled prostacyclin.68 The dose is 50 μg/kg when given as an inhalation, but a 5 mg bolus into the endotracheal tube might be just as effective in reducing PA pressures and improving RV function.69 Studies of preemptive pre‐CPB inhaled milrinone have shown some pulmonary vasodilatory effect without any effect on clinical outcome.70 Despite individual reports of efficacy, a meta‐analysis failed to show clinical benefits of inhaled milrinone.71
Sildenafil is a PDE type V inhibitor that prevents the degradation of cGMP and reduces pulmonary vascular tone without any effect on the systemic vasculature. Studies have shown a significant pulmonary vasodilatory effect postoperatively when given for 24 hours before surgery (25 mg q8h),72 10 minutes before induction (50 mg),73 and when given in the ICU through an NG tube (20 mg every eight hours in one study74 and 0.5 mg/kg in another).75 It is also beneficial when given along with iNO.76 It may be helpful in weaning patients off intravenous or inhaled pulmonary vasodilator support.
If RV dysfunction persists despite use of inotropic support, pulmonary vasodilators, and an IABP, implementation of mechanical assistance with a right ventricular assist device may be necessary. Commonly used systems are the Impella RP, the CentriMag device, TandemHeart RVAD, Protek Duo, or veno‐arterial ECMO (see pages 559–560).
Diastolic dysfunction is a common cause of congestive heart failure (HF) in hypertensive patients, and can pose hemodynamic problems after surgery when ventricular compliance is affected by the use of CPB and cardioplegia. It is most prominent after a prolonged period of cardioplegic arrest, especially with small hypertrophied hearts.
Diastolic dysfunction is caused by decreased diastolic compliance, often with an inappropriate tachycardia.77 The end result is a low cardiac output syndrome with low end‐diastolic volumes yet high left‐sided filling pressures. The stiffness of the heart is usually evident on echocardiogram, which may confirm normal systolic function even though the patient is in a low output state.
This problem can be difficult to manage and often results in end‐organ dysfunction, such as renal failure, that progresses until the diastolic dysfunction improves (see pages 381–382). Although inotropic drugs are frequently given, they are of little benefit. In contrast, ACE inhibitors may improve diastolic compliance; lusitropic drugs, such as the CCBs, magnesium, and milrinone, may improve ventricular relaxation; and bradycardic drugs, such as β‐blockers or CCBs, can be used for an inappropriate tachycardia. Aggressive diuresis may also be beneficial in reducing myocardial edema that might contribute to reduced compliance.
Select inotropes with vasodilator properties (milrinone, low‐dose epinephrine, dobutamine, isoproterenol)
Use a pulmonary vasodilator
Inhaled nitric oxide (iNO)
Optimize LV function
Mechanical circulatory assist (RVAD or ECMO) if no response to the above
III. Inotropic and Vasoactive Drugs
A variety of vasoactive medications are available to provide hemodynamic support for the patient with marginal myocardial function.1–4,16,44 They should be chosen carefully to achieve a satisfactory cardiac index (>2.2 L/min/m2) and blood pressure (MAP >70 mm Hg) once adequate filling pressures have been achieved. The selection of a particular drug depends on an understanding of its mechanism of action and limitations to its use (see section M, page 545 for recommendations on drug selection). The catecholamines exert their effects on α‐ and β‐adrenergic receptors. They elevate levels of intracellular cyclic AMP (cAMP) by β‐adrenergic stimulation of adenylate cyclase. In contrast, the PDE inhibitors (milrinone) elevate cAMP levels by inhibiting cAMP hydrolysis. Elevation of cAMP augments calcium influx into myocardial cells and increases contractility.
α1 and α2 stimulation result in increased systemic and pulmonary vascular resistance. Cardiac α1‐receptors increase contractility and decrease the heart rate.
β1 stimulation results in increased contractility (inotropy), heart rate (chronotropy), and conduction (dromotropy).
β2 stimulation results in peripheral vasodilation and bronchodilation.
The net effects of medications that share α and β properties usually depend on the dosage level and are summarized in Table 11.5.
The concomitant use of several medications with selective effects may minimize the side effects of higher doses of individual medications. For example:
Inotropes with vasoconstrictive (α) properties can be combined with vasodilators to improve contractility while avoiding an increase in SVR (e.g. norepinephrine with clevidipine, propofol, or nitroprusside).
Inotropes with vasodilator properties can be combined with α‐agonists or other vasoconstrictors to maintain SVR (e.g. milrinone with phenylephrine, norepinephrine, or vasopressin).
Catecholamines can be combined with a PDE inhibitor to provide synergistic inotropic effects while achieving pulmonary and systemic vasodilation (e.g. epinephrine or dobutamine with milrinone).
α‐agents can be infused directly into the left atrium to maintain SVR while a pulmonary vasodilator is infused into the right heart.
The benefits of most vasoactive medications are noted when adequate blood levels are achieved in the systemic circulation. Thus, these medications should be given into the central circulation via controlled infusion pumps rather than peripherally. Although higher levels can be reached by drug infusion into the left atrium to avoid pulmonary vascular effects and reduce drug inactivation by the lungs, this is an uncommon practice.
The standard mixes and dosage ranges are listed in Table 11.6.
Inotropic drugs should be used to normalize the cardiac output after steps have been taken to improve preload, afterload, and rhythm issues. Although numerous studies have suggested that the use of inotropes is associated with increased morbidity and mortality after cardiac surgery, it is difficult to conclude that the patients who needed such support would have done better without hemodynamic support.78–80
Epinephrine is a potent β1‐inotropic agent that increases cardiac output by an increase in heart rate and contractility, generally increasing myocardial oxygen demand. At doses of less than 2 μg/min (<0.02–0.03 μg/kg/min), it has a β2 effect that produces mild peripheral vasodilation, but the blood pressure is usually maintained or elevated by the increase in cardiac output. At doses greater than 2 μg/min (>0.03 μg/kg/min), α effects will increase the SVR and raise the blood pressure. Metabolic acidosis may also be noted at low doses of epinephrine when α effects are not evident, but this is not related to reduced tissue perfusion.81
Epinephrine has strong β2 properties that produce bronchodilation.
Although epinephrine may contribute to arrhythmias or tachycardia, studies have shown that epinephrine given at a dose of 2 μg/min causes less tachycardia than dobutamine given at a dose of 5 μg/kg/min.82
Epinephrine may be considered a first‐line drug for a borderline cardiac output in the absence of tachycardia or ventricular ectopy. Some authors state that it should be considered a second‐line inotrope because of the risk of tachycardia and arrhythmias, an increase in myocardial oxygen consumption, a decrease in splanchnic blood flow, and the risk of lactic acidosis.16 It is very helpful in the hypertrophied heart that often takes a while to recover adequate systolic function after cardioplegic arrest. Epinephrine is extremely effective and has very low cost.
It is especially helpful in stimulating the sinus node mechanism when the intrinsic heart rate is slow. It is frequently beneficial in improving the atrium’s responsiveness to pacing at the conclusion of bypass.
Bronchospasm may respond well to epinephrine, especially when an inotrope is also required.
Anaphylaxis (protamine reaction)
Resuscitation from cardiac arrest
Starting dose is 1 μg/min (about 0.01 μg/kg/min) with a mix of 1 mg/250 mL. Dosage can be increased to 4 μg/min (about 0.05 μg/kg/min). Higher doses are rarely indicated in patients following cardiac surgery.
Dobutamine is a positive inotropic agent with a strong β1 effect that increases heart rate in a dose‐dependent manner and also increases contractility. Although it has a mild vasoconstrictive α1 effect, this is offset by its mild vasodilatory β2 effect, resulting in reduced filling pressures, a reduction in SVR, but maintenance of blood pressure due to improved cardiac performance. Although the increased heart rate may increase myocardial oxygen demand, this is mostly offset by augmented myocardial blood flow and a reduction in preload and afterload, reducing LV wall stress.83 This is particularly evident in volume‐overloaded hearts (valve replacement for mitral or aortic regurgitation).84
Dobutamine may cause more tachycardia than low‐dose epinephrine, so switching from one inotrope to another may be considered to minimize any increase in oxygen demand that could trigger ischemia.82
Dobutamine and the PDE inhibitors (milrinone) provide comparable hemodynamic support, although dobutamine is associated with more hypertension, tachycardia, and a greater chance of triggering atrial fibrillation.85
Dobutamine is most useful when the cardiac output is marginal and there is a mild elevation in SVR. Its use is usually restricted by development of a tachycardia. Some groups consider this the best first‐line drug for inotropic support.
It is a moderate pulmonary vasodilator and may be helpful in improving RV function and lowering RV afterload.
It has a synergistic effect in improving cardiac output when used with a PDE inhibitor (milrinone). This combination is commonly used in patients awaiting cardiac transplantation.
Starting dose is 5 μg/kg/min using a mix of 500 mg/250 mL. Dosage can be increased to 20 μg/kg/min.
Milrinone is a phosphodiesterase (PDE) III inhibitor best described as an “inodilator”.86 It improves cardiac output by reducing systemic and pulmonary vascular resistance, lowers coronary vascular resistance,87 and exerts a moderate positive inotropic effect. There is usually a modest increase in heart rate, a lowering of filling pressures, and a moderate reduction in systemic blood pressure despite the improvement in myocardial contractility. This is generally associated with a reduction in myocardial oxygen demand. Although the unloading effect produced by the decrease in SVR may contribute a great deal to its efficacy, an α‐agent (phenylephrine or norepinephrine) is frequently required to maintain systemic blood pressure.
Milrinone increases cyclic AMP levels, which causes relaxation of myofilaments. Although this lusitropic effect improves ventricular compliance after bypass, some studies suggest that milrinone has no effect on diastolic function and does not have lusitropic properties.88–92
Additive effects on ventricular performance are noted when milrinone is combined with one of the catecholamines, such as epinephrine or dobutamine, due to differing mechanisms of action.
Milrinone may produce a tachycardia, especially in the hypovolemic patient. However, in comparison with dobutamine, it generally produces a comparable increase in cardiac output with less increase in heart rate, suggesting strong inotropic properties, and is associated with a lower incidence of arrhythmias, although one study found that milrinone was an independent risk factor for atrial fibrillation.93 Since it is generally used in addition to a catecholamine in patients with poor RV or LV dysfunction, it is not clear if the risk of AF might still have been high without its use.
Although it would seem counterintuitive to use a β‐blocker (with its negative inotropic properties) with a PDE inhibitor, one study did show that β‐blockers could offset the tachycardia produced by a PDE inhibitor without compromising the beneficial inotropic effects.94
Prior to the availability of milrinone, inamrinone (known at the time as amrinone or Inocor) was the preferred PDE inhibitor. Both drugs had comparable effects, but inamrinone was associated with thrombocytopenia, so its use has declined.95
Several meta‐analyses have found that milrinone use in cardiac surgery is associated with similar or higher mortality rates than use of other or no inotropes at all.96,97 However, it is difficult to justify using no inotropic support in a low cardiac output state. Thus, when milrinone is added due to inadequate response to a catecholamine, it is most likely beneficial in reducing the need for an IABP, optimizing organ system function, and improving outcomes in the early postoperative period.
Inhaled milrinone has selective pulmonary vasodilator effects that can reduce PA pressures and improve RV function without any systemic effects. The literature provides conflicting evidence of its efficacy and benefits.66–71
Milrinone is generally the second medication selected for a persistent low cardiac output state despite use of one of the catecholamines or when their use is limited by tachycardia. However, a preemptive bolus of milrinone given on pump significantly reduces the need for any catecholamine in the immediate perioperative period.98
It is particularly valuable in patients with right ventricular dysfunction associated with an elevation in PVR, such as patients with PH from mitral valve disease or those awaiting and following cardiac transplantation. Use of inhaled or intratracheal milrinone shows selective pulmonary vasodilatory effects without influencing systemic hemodynamics, but is of unclear benefit.
The lusitropic (relaxant) property may be of value in patients with significant diastolic dysfunction that may contribute to a low output state, even with preserved systolic function.
Milrinone is effective in dilating arterial conduits and may be beneficial when there is suspected coronary or graft spasm and the need for inotropic support.87
Advantages and disadvantages
Milrinone has a long elimination half‐life of 1.5–2 hours that increases to 2.3 hours in patients with low cardiac output states or HF. Thus, an intraoperative bolus can be used to terminate bypass and provide a few hours of additional inotropic support without the need for a continuous infusion.
Because the hemodynamic effects persist for several hours after the drug infusion is discontinued (in contrast to the short duration of action of the catecholamines), the patient must be observed carefully for deteriorating myocardial function for several hours as the hemodynamic effects wear off. The dose is generally sequentially halved, and if hemodynamic performance remains adequate, it is then stopped.
Starting dose is a 50 μg/kg IV bolus over 10 minutes, followed by a continuous infusion of 0.25–0.75 μg/kg/min of a 20 mg/200 mL solution. Note that, because of its long half‐life, it takes up to six hours to reach a steady‐state level if not given with a loading dose. The inhalational dose is comparable to the IV bolus dose.
The hemodynamic effects of dopamine vary with increasing doses, but reports of adverse effects have significantly reduced its usage. It tends to cause a tachycardia and arrhythmias, accelerates AV conduction in atrial fibrillation,99 will depress ventilation due to inhibition of peripheral chemoreceptors causing V/Q mismatch, and may worsen renal function despite producing an improvement in urine output.16,100
Renal dose dopamine (2–3 μg/kg/min) is effective in improving urine output, but it has adverse effects on renal function if used during surgery and does not alter the natural history of acute kidney injury if it develops.101,102
At moderate doses of 3–8 μg/kg/min, dopamine exhibits a β1 inotropic effect that improves contractility, and, to a variable degree, a chronotropic effect that increases heart rate and the potential for arrhythmogenesis.
At doses greater than 8 μg/kg/min, there are increasing inotropic effects, but also a predominant α effect that occurs directly and by endogenous release of norepinephrine. This raises the SVR, systemic blood pressure, and filling pressures, and may adversely affect myocardial oxygen consumption and ventricular function. Concomitant use of a vasodilator, such as nitroprusside, to counteract these α effects allows for the best augmentation of cardiac output.
Dopamine may be considered for a low cardiac output state, especially when the SVR is low and the blood pressure is marginal, but its use is usually limited by the development of a profound tachycardia and other potential adverse effects, so the other inotropes listed above are preferable.
It does improve urine output in patients with or without preexisting renal dysfunction, but has no demonstrable benefit in preserving renal function, and may in fact worsen renal function if used intraoperatively.101
Isoproterenol has a strong β1 effect that increases cardiac output by a moderate increase in contractility and a marked increase in heart rate with a slight β2 effect that lowers SVR. The increased myocardial O2 demand caused by the tachycardia limits its usefulness in coronary bypass patients. Isoproterenol may produce ischemia out of proportion to its chronotropic effects, and it also predisposes to ventricular arrhythmias.
Isoproterenol’s β2 effect lowers PVR and reduces RV afterload.
There is a strong β2 bronchodilator effect.
Right ventricular dysfunction associated with an elevation in PVR. Isoproterenol is both an inotrope and a pulmonary vasodilator and thus is helpful in supporting RV function following mitral valve surgery in patients with PH. Because it causes a profound tachycardia, it has generally been replaced by the PDE inhibitors and dobutamine. However, it is still used following heart transplantation to reduce PVR, improve RV function, and produce ventricular relaxation.
Bronchospasm when an inotrope is required.
Bradycardia in the absence of functioning pacemaker wires. It may be used after heart transplantation to maintain a heart rate around 100 bpm.
Starting dose is 0.5 μg/min with a mix of 1 mg/250 mL. It can be increased to about 10 μg/min (usual dosage range is 0.0075–0.1 mg/kg/min).
Norepinephrine is a powerful catecholamine with both α‐ and β‐adrenergic properties. Its predominant α effect raises SVR and blood pressure, while the β1 effect increases both contractility and heart rate.
By increasing afterload and contractility, norepinephrine increases myocardial oxygen demand and may prove detrimental to the ischemic or marginal myocardium. Although it may also cause regional redistribution of blood flow, studies suggest that renal and intestinal perfusion are maintained if the systemic blood pressure improves. Furthermore, the addition of dobutamine has been shown to improve gastric mucosal perfusion in patients receiving norepinephrine.103
Note: there is a tendency to think that norepinephrine is providing only an α effect, but it does possess strong β properties. Thus, it should be anticipated that both the stroke volume and heart rate will fall when the drug is weaned.
Norepinephrine is primarily indicated when the patient has a marginally low cardiac output with a low blood pressure caused by a low SVR. This is often noted when the patient warms and vasodilates. Use of a pure α‐agent is feasible if the cardiac index exceeds 2.5 L/min/m2, but norepinephrine can provide some inotropic support if the cardiac index is borderline. If the cardiac index is below 2.0 L/min/m2, another inotrope should probably be used in addition to norepinephrine.
It is frequently effective in raising the blood pressure when little effect has been obtained from phenylephrine (and vice versa).
It has been used as an inotrope to improve cardiac output in conjunction with a vasodilator to counteract its α effects.
Starting dose is 1 μg/min (about 0.01 μg/kg/min) with a mix of 4 mg/250 mL. The dose may be increased as necessary to achieve a satisfactory blood pressure. Higher doses (probably >20 μg/min or >0.2 μg/kg/min) most likely will reduce visceral and peripheral blood flow and may produce a metabolic acidosis.
Phenylephrine is a pure α‐agent that increases SVR and may cause a reflex decrease in heart rate. Myocardial function may be compromised if an excessive increase in afterload results. However, it is frequently improved by an elevation in coronary perfusion pressure that resolves myocardial ischemia.
Phenylephrine has no direct cardiac effects.
Phenylephrine is indicated only to increase the SVR when hypotension coexists with a satisfactory cardiac output. This is commonly noted at the termination of bypass or in the ICU when the patient warms and vasodilates. If the blood pressure remains low after volume infusions yet the cardiac output is satisfactory, phenylephrine can be used to maintain a systolic blood pressure around 100–110 mm Hg. Significantly higher pressures should be avoided to minimize the adverse effects of an elevated SVR on myocardial function.
Phenylephrine can be used preoperatively to treat ischemia by maintaining perfusion pressure, while IV NTG is used to reduce preload. It is beneficial in maintaining the blood pressure in patients with hypertrophic obstructive cardiomyopathy in whom inotropes will accentuate the outflow tract gradient and is useful in patients who exhibit systolic anterior motion (SAM) after mitral valve repair.
Advantages and disadvantages
Patients often become refractory to the effects of phenylephrine after several hours, necessitating a change to norepinephrine. Conversely, some patients respond very poorly to norepinephrine and have an immediate blood pressure response to low‐dose phenylephrine.
By providing no cardiac support other than an increase in central perfusion pressures, phenylephrine has limited indications.
Note: be very careful when administering an α‐agent to the patient whose entire revascularization procedure is based on arterial grafts, as it may provoke spasm and causes profound ischemia, which can be fatal.
Starting dose is 5 μg/min with a mix of 40 mg/250 mL. The dosage can be increased as necessary to maintain a satisfactory blood pressure. The usual dosage range is 0.05–1.5 μg/kg/min.
Vasopressin acts on vasomotor V1 and renal V2 receptors to increase SVR. It has no direct cardiac effects, so any improvement in cardiac function is related to an improvement in perfusion pressure.
It may improve renal perfusion in that it constricts the efferent rather than the afferent arterioles, in contradistinction to the effects of α‐agents on renal perfusion. However, one study suggested that it reduced renal blood flow, increased renal oxygen extraction, and impaired renal oxygenation.50
It induces intestinal and gastric mucosal vasoconstriction; thus if the cardiac output remains marginal, mesenteric ischemia is more likely to occur.51
It is beneficial in patients with a low SVR and PH as it does not produce a significant alteration in PA pressures.
It may induce vasospasm in internal thoracic artery (ITA) and radial artery grafts.
Low blood pressure that is poorly responsive to phenylephrine or norepinephrine.
Vasodilatory shock (“vasoplegia”) after CPB associated with a satisfactory cardiac output that is not responsive to norepinephrine or phenylephrine. Norepinephrine is preferable in patients with a compromised cardiac output.
Dosage is an infusion of 0.01–0.1 units/min.
The primary effect of calcium chloride (CaCl2) is an increase in SVR that improves the mean arterial pressure.104 It has little effect on the heart rate. It produces a transient improvement in systolic function at the termination of CPB, although it may increase ventricular stiffness, suggesting it produces transient diastolic dysfunction.105
One study showed that CaCl2 produces a transient inotropic effect if hypocalcemia is present and a more sustained increase in SVR, independent of the calcium level.106
A study that compared epinephrine and calcium chloride upon emergence from CPB showed that both increased the mean arterial pressure, but only epinephrine increased the cardiac output, suggesting that calcium did not provide any inotropic support.107 Although this study did not find any beneficial or negative effects of combining these two medications, another one did suggest that calcium salts may attenuate the cardiotonic effects of catecholamines, such as dobutamine or epinephrine, but have little effect on the efficacy of inamrinone (and presumably milrinone).108
Frequently used at the termination of CPB to augment systemic blood pressure by either a vasoconstrictive or positive inotropic effect. This is a common practice despite concerns that calcium influx during reperfusion may contribute to myocardial dysfunction.109,110
To support myocardial function or blood pressure on an emergency basis until further assessment and intervention can be undertaken. Note: calcium is not recommended for routine use during a cardiac arrest.
Hyperkalemia (K+ >6.0 mEq/L).
Usual dose is 0.5–1 g slow IV bolus.
Thyroid hormone (triiodothyronine or T3) exerts a positive inotropic effect by increasing aerobic metabolism and synthesis of high‐energy phosphates. It causes a dose‐dependent increase in myocyte contractile performance that is independent of and additive to β‐adrenergic stimulation.111
A low T3 level preoperatively is associated with low cardiac output syndrome and increased mortality after CABG.112 Most patients have reduced levels of free T3 for up to three days following operations on CPB.113,114 Routine administration of T3 to maintain normal levels produces a transient improvement in cardiac output, lowers troponin release, reduces SVR, and may reduce the need for inotropes, but it does not appear to influence outcomes.115–117 However, a significant improvement in hemodynamics has been noted in patients with impaired ventricular function, many of whom could not be weaned from bypass on multiple inotropes until T3 was administered.118
Note: CCBs have been shown to interfere with the action of T3.
There is some evidence that postoperative atrial fibrillation is more common in patients with subclinical hypothyroidism and low T3 levels, and administration of T3 may reduce the incidence of postoperative AF.119,120
T3 may be indicated to provide inotropic support as a salvage step when CPB cannot be terminated with maximal inotropic support and an IABP.
T3 is helpful in improving donor heart function in brain‐dead patients when ventricular function is depressed.
Usual dose is 10–20 μg, although some studies have used a bolus of 0.8 μg/kg followed by an infusion of 0.12 μg/kg/h for six hours.116
Other modalities to treat low cardiac output
Glucose–insulin–potassium (GIK) has been demonstrated to have an inotropic effect on the failing myocardium after cardioplegic arrest. It provides metabolic support to the myocardium by increasing anaerobic glycolysis, lowering free fatty acid levels, preserving intracellular glycogen stores, and stabilizing membrane function. It has been shown to reduce myocardial injury and improve hemodynamic performance.121 The mixture contains 50% glucose, 80 units/L of regular insulin, and 100 mEq/L of potassium infused at a rate of 1 mL/kg/h.
Levosimendan is a calcium‐sensitizing “inodilator” that has been used for patients with decompensated HF and has been further evaluated in the management of cardiac surgical patients. There is vast literature suggesting that its administration before initiating CPB may improve myocardial function after revascularization, with a reduced requirement for additional inotropes, less IABP usage, and a reduction in mortality.122–124 However, several additional studies have not shown any survival benefit independent of the extent of LV dysfunction.125–129
Mechanisms and effects. Levosimendan improves cardiac function by both inotropic and vasodilatory effects. The positive inotropic effect results from sensitizing myofilaments to calcium without increasing intracellular calcium levels. It also has coronary, pulmonary, and systemic vasodilator effects by opening ATP‐dependent potassium channels in vascular smooth muscle. Thus, it improves cardiac output by increasing stroke volume with little increase in heart rate, by reducing afterload from its vasodilating effects, and to a slight degree by lusitropic effects. Given at high doses, it may require use of an α‐agent to counteract systemic vasodilation. The one major difference between levosimendan and other inotropes is the enhancement of contractility without an increase in myocardial oxygen demand. At low doses, it is not arrhythmogenic. The half‐life is 70–80 hours, so it has a long‐lasting effect after administration.
Indications. Levosimendan is useful in improving hemodynamics in patients with anticipated postcardiotomy RV and LV dysfunction and in facilitating weaning from bypass. In patients with RV dysfunction, it decreases PVR and improves RV contractility (better than dobutamine in one study).57 An infusion started prior to bypass (with or without a loading dose of 24 μg/kg) is very effective in reducing troponin leakage, suggesting a cardioprotective effect, and in maintaining an improved cardiac output without the need for additional inotropic support. In view of numerous studies suggesting no significant impact on outcomes, the role for levosimendan in cardiac surgical patients remains undefined.
Starting dose. It is given as a 12–24 μg/kg loading dose over 10 minutes, followed by a continuous infusion of 0.1 μg/kg/min.
Recommended strategy for selection of vasoactive medications
The selection of a vasoactive medication should be based on several factors:
An adequate understanding of the underlying cardiac pathophysiology derived from hemodynamic measurements and echocardiography.
Knowledge of the α, β, or nonadrenergic hemodynamic effects of the medications and their anticipated influence on preload, afterload, heart rate, and contractility.
Assessment of intravascular volume, since preload should be optimized before inotropic drugs are initiated. However, it is common practice to initiate low‐dose inotropic support at the termination of CPB, which may or may not need to be continued depending on volume status and cardiac performance.
Vasoactive medications are usually started in the operating room and maintained for about 6–12 hours while the heart recovers from the period of ischemia/reperfusion. The doses are adjusted as the patient’s hemodynamic parameters improve. Occasionally, when the heart demonstrates persistent “stunning” or has sustained a perioperative infarction, pharmacologic support and/or an IABP may be necessary for several days.
When the cardiac index is satisfactory (>2.2 L/min/m2) but the blood pressure is low, an α‐agent should be selected. Phenylephrine is commonly used in the operating room, but norepinephrine is probably a better drug to use in that it provides some β effects that are beneficial during the early phase of myocardial recovery. Systolic blood pressure need only be maintained around 100 mm Hg (mean pressure >70 mm Hg) to minimize the increase in afterload. If neither of these medications suffices, vasopressin should be utilized. Occasionally, a simple bolus of 1–2 units of vasopressin overcomes the initial vasoplegic state after pump and minimizes the subsequent need for an α‐agent.
When the cardiac index remains marginal (<2.0 L/min/m2) after optimizing volume status, heart rate, and rhythm, an inotropic agent should be selected. The first‐line drugs are usually epinephrine or dobutamine. The major limitation to their use is the development of tachycardia, which tends to be less prominent with low‐dose epinephrine. At inotropic levels, epinephrine tends to raise SVR, whereas dobutamine’s effect on SVR is variable but usually not significant. If a satisfactory cardiac output has been achieved and the blood pressure is elevated, addition of a vasodilator is beneficial. If the blood pressure is low, an α‐agent can be added.
If the cardiac output still remains suboptimal despite moderate doses of drugs (epinephrine 2–3 μg/min [0.03–0.04 μg/kg/min] or dobutamine 10 μg/kg/min), a second drug should be added. The PDE inhibitor milrinone exhibits additive effects to those of the catecholamines and should be selected. This will lower the SVR and may cause a modest tachycardia. It commonly requires the use of norepinephrine to maintain SVR, although blood pressure may be maintained by the improvement in cardiac function. If norepinephrine is used, its β effect may further improve contractility, but it can also increase the heart rate. Its α effect usually has minimal effect on organ system perfusion if a satisfactory cardiac output can be achieved, but it can compromise flow in arterial conduits (such as the ITA or radial artery). If the cardiac index remains marginal despite the use of two medications, an IABP should be inserted.
If the patient cannot be weaned from bypass and has hemodynamic evidence of persistent cardiogenic shock (CI <1.8 L/min/m2, PCWP >20 mm Hg) despite medications and the IABP, a circulatory assist device should be considered.
Note: it is not uncommon for the cardiac output to fall to below 1.8–2.0 L/min/m2 during the first 4–6 hours after surgery, which represents the time of maximal myocardial depression. After optimizing fluid status, the dose of an inotrope may need to be increased transiently or, less frequently, another one added if the cardiac output does not improve. Such goal‐directed hemodynamic management usually improves outcomes. However, it is the persistence of a low output state beyond this time that raises concerns, especially if there is any evidence of myocardial ischemia on ECG, a low SvO2, rising filling pressures out of proportion to fluid administration, oliguria, or a progressive metabolic acidosis. An IABP may need to be inserted in the ICU if these problems are present. However, in the absence of any specific identifiable problem, most patients will gradually improve, and one should not be overly alarmed by transient drops in cardiac output and respond too aggressively. If there is any concern, echocardiography is helpful in assessing whether ventricular dysfunction or cardiac tamponade is causing the low output state, and can direct management appropriately.
Note: use of α‐agents can be dangerous in patients receiving radial artery grafts or when multiple grafts are based on ITA inflow. It is preferable to reduce the dose of the vasodilating drug (diltiazem or IV NTG used to prevent spasm), rather than increase the dose of a vasoconstricting medication if hypotension is noted.
Vasoactive medications provide specific hemodynamic benefits, but their use may be limited by the development of adverse effects. Nearly all of the catecholamines will increase myocardial oxygen demand by increasing heart rate and contractility. Other side effects that may necessitate changing to or addition of another medication include:
Arrhythmogenesis and tachycardia (epinephrine, dobutamine, isoproterenol)
Vasoconstriction and poor renal, splanchnic, and peripheral perfusion (norepinephrine, phenylephrine, vasopressin)
Vasodilation requiring α‐agents to support systemic blood pressure (milrinone)
Excessive urine output (dopamine)
Cyanide and thiocyanate toxicity (nitroprusside)
Methemoglobinemia (IV NTG)
Weaning of vasoactive medications
Once the cardiac output and blood pressure have stabilized for a few hours, vasoactive medications should be weaned. α‐agents should generally be weaned first. Their use should ideally be restricted to increasing the SVR to support blood pressure when the cardiac output is satisfactory. However, there are circumstances when α‐agents are required to maintain cerebral and coronary perfusion in the face of a poor cardiac output. In these desperate life‐saving situations, the resultant intense peripheral vasoconstriction can compromise organ system and peripheral perfusion, causing renal, mesenteric, and peripheral ischemia, acidosis, and frequently death.
In the routine patient, SVR and blood pressure increase when myocardial function improves, narcotic effects abate, and sedatives, such as propofol or dexmedetomidine, have been discontinued. As the patient awakens and develops increased intrinsic sympathetic tone, α‐agents can be stopped.
When milrinone or an IABP is used to support myocardial function, an α‐agent is frequently required to counteract the unloading effect and decreased SVR that is achieved. It may not be possible to wean the α‐agent before the patient has been weaned from milrinone or the IABP, because the patient may become hypotensive despite an excellent cardiac output. It is usually necessary to wean the α‐agent in conjunction with the weaning of the other modalities.
An occasional patient who has sustained a small perioperative infarction will have an excellent cardiac output but a low SVR. This requires temporary vasoconstrictor support until the blood pressure improves spontaneously. Such support may be required for several days.
The stronger positive inotropes with the most potential detrimental effects on myocardial metabolism should be weaned next. Those that possess α properties should be decreased to doses at which these effects do not occur. If an IABP is present, it should not be removed until the patient is on a low dose of only one inotrope, unless complications of the IABP develop. Otherwise, weaning of the IABP should usually be deferred.
The catecholamines should be weaned first to low doses. If the patient is on multiple drugs, epinephrine should be weaned to a low dose (2 μg/min or less) to avoid any α effects. Dobutamine (which lacks a significant α effect) should be weaned to doses of less than 10 μg/kg/min.
Milrinone is usually weaned off with the patient still supported by low doses of catecholamines. However, since it has few deleterious effects on myocardial function, and catecholamines may cause a tachycardia, it is not unreasonable to continue the milrinone while the catecholamine is weaned off. Because of its long half‐life, it should be withdrawn slowly, usually halving the dose and then discontinuing it if the patient remains hemodynamically stable. Occasionally, deterioration in myocardial function may occur several hours later and require the reinstitution of inotropic support.
IABP removal may be performed once the patient is on low doses of inotropic support, such as epinephrine at 1 μg/min, dobutamine <10 μg/kg/min, or milrinone at ≤0.5 μg/kg/min.
The requirement for vasoactive medications in patients on circulatory assist devices depends on the extent of support provided and the function of the unsupported ventricle. In patients receiving univentricular support, inotropic medications may be necessary to improve the function of the unassisted ventricle. Patients with biventricular support are usually given only α‐agents or vasopressin to support systemic resistance. If the device is being used for temporary support, rather than as a bridge to transplantation, inotropes may be given to assess cardiac reserve when flows are transiently reduced. If ventricular function is recovering, an inotrope, such as milrinone, can be given to provide support after removal of the device, if necessary. With the use of ECMO, it is beneficial to support some LV contraction to minimize the risk of LV thrombus formation.
Vasodilators are commonly used during the early phase of postoperative recovery to reduce blood pressure when the patient is hypothermic, vasoconstricted, and hypertensive. They are weaned when the patient vasodilates to maintain a systolic blood pressure of 100–120 mm Hg.
Vasodilators may also be used alone or in conjunction with inotropic medications to improve myocardial function by lowering the SVR. In this situation, they are weaned concomitantly with the inotropes, depending on the cardiac output and the blood pressure. Sodium nitroprusside and clevidipine have half‐lives of only two and one minute, respectively, but nicardipine has a duration of action of 4–6 hours.
In patients with preexisting hypertension, conversion from intravenous antihypertensives to oral agents can be tricky. Some patients require significant doses of multiple drugs to control their blood pressure, only to become hypotensive when the drugs take effect and sympathetic stimulation and the hormonal response to surgery abate. The initial drug is usually a β‐blocker (unless the patient is bradycardic), which is routinely used for prophylaxis of atrial fibrillation. An ACE inhibitor or ARB is then added, starting at a low dose if not used before or at a lower dose than used preoperatively. Amlodipine is another option, especially if the patient is bradycardic. Intravenous hydralazine can be used on a prn basis until higher doses of medications take effect.
Table 11.5 Hemodynamic Effects of Vasoactive Medications
↑ increased; ↓ decreased; ↔ no change; ↓↑ variable effect. The relative effect is indicated by the number of arrows.Note: the effect may vary with dosage level (particularly dopamine and epinephrine, in which case the effect seen at low dose is indicated by the first arrow). For some medications, an improvement in MAP may occur from the positive inotropic effect despite a reduction in SVR. The effects of milrinone and calcium are not mediated by α and β receptors.
Table 11.6 Mixes and Dosage Ranges for Vasoactive Medications
1 mg/250 mL
1–4 μg/min (0.01–0.05 μg/kg/min)
500 mg/250 mL
20 mg/200 mL
50 μg/kg bolus, then 0.25–0.75 μg/kg/min
400 mg/250 mL
1 mg/250 mL
0.5–10 μg/min (0.0075–0.1 μg/kg/min)
4 mg/250 mL
1–30 μg/min (0.01–0.3 μg/kg/min)
40 mg/250 mL
5–150 μg/min (0.05–1.5 μg/kg/min)
40 units/80 mL
Note: × milligrams placed in 250 mL gives an infusion rate of × micrograms (mg divided by 100) in 15 drops of solution. For example, a 200 mg/250 mL mix gives a drip of 200 μg in 15 drops. 60 microdrops = 1 mL. 15 drops/min = 15 mL/h.
IV. Intra‐aortic Balloon Counterpulsation
Intra‐aortic balloon counterpulsation provides hemodynamic support and/or control of ischemia both before and after surgery.130–132 In contrast to the inotropic drugs, the IABP provides physiologic assistance to the failing heart by decreasing myocardial oxygen demand and improving coronary perfusion. Although it is an invasive device with several potential complications, it has proven invaluable in improving the results of surgery in high‐risk patients and allowing for the survival of many patients with postcardiotomy ventricular dysfunction.
Ongoing ischemia refractory to medical therapy or hemodynamic compromise prior to urgent or emergent surgery.
Prophylactic placement prior to surgery for high‐risk patients with critical coronary disease (usually left main disease) or severe LV dysfunction – usually following cardiac catheterization, but occasionally at the beginning of surgery.133–136
Unloading for mechanical complications of myocardial infarction (acute mitral regurgitation, ventricular septal rupture) prior to emergent surgery.
High‐risk patients undergoing off‐pump surgery to maintain hemodynamic stability during lateral wall or posterior wall grafting.137
Acute myocardial infarction primarily with, but occasionally without, cardiogenic shock. This remains a common indication for use of an IABP, yet most studies have not demonstrated any mortality benefit even when percutaneous coronary intervention (PCI) is performed.138–143 In this situation, use of a mechanical circulatory assist device may be preferable.144
Postcardiotomy low cardiac output syndrome unresponsive to moderate doses of multiple inotropic agents. One study devised a clinical risk score to predict the need for an IABP after CABG. These factors included older age, poor LV function, redo and emergency procedures, left main disease, recent MI, and class 3–4 symptoms.146 Although this study reported a 19% mortality rate in this situation, others have reported mortality rates of 30–50%.147,148
Postoperative myocardial ischemia
Acute deterioration of myocardial function (refractory heart failure) to provide temporary support or serve as a bridge to transplantation.
Aortic regurgitation (unless mild)
Aortic dissection/extensive aneurysmal disease
Severe aortic and peripheral vascular atherosclerosis (balloon can be inserted via the ascending aorta during surgery)
The IABP reduces the impedance to LV ejection (“unloads the heart”) by rapid deflation just before ventricular systole.
It increases diastolic coronary perfusion pressure by rapid inflation just after aortic valve closure with improvement in native coronary, ITA, and graft diastolic flow.
This sequence reduces the time–tension index (systolic wall tension) and increases the diastolic pressure–time index, favorably altering the myocardial oxygen supply:demand ratio.
The IABP may also improve left ventricular diastolic function after surgery.149
In patients with RV failure, the IABP may improve RV function by improving right coronary perfusion pressure and reducing RV afterload by decreasing LV filling pressures. However, the benefit of an IABP for severe RV failure is limited and further mechanical circulatory assist may be necessary.54,150–153
The IABP is placed through the femoral artery with the balloon situated just distal to the left subclavian artery so as not to impair flow into the left internal thoracic artery (LITA) (Figure 11.1). Generally, a 50 mL balloon is selected for patients >162 cm (5’4″) tall, using smaller balloons with shorter lengths (the Datascope 25 mL or 34 mL or Arrow 40 mL balloons) for smaller patients.
Percutaneous insertion is performed by the Seldinger technique, placing the balloon over a guide wire and either through a sheath or without a sheath (“sheathless”). The catheter is usually 7.5 Fr in diameter. The sheath can be left in place or removed from the artery, especially if the femoral artery is small. Smaller‐caliber systems can minimize the reduction in flow that could cause distal ischemia, and are preferable in patients with peripheral vascular disease and diabetes. Sheathless insertion may cause shearing of the balloon during placement if significant iliofemoral disease is present. Although insertion of the IABP can be performed blindly in the OR or at the bedside, preoperative placement is usually performed in the cardiac cath lab using fluoroscopy to visualize the wire and the eventual location of the balloon. This may allow for placement through a tortuous ilio-femoral system, which otherwise might be fraught with danger. During surgery, the position of the balloon catheter can be identified by TEE.
Surgical insertion can be accomplished by exposing the femoral artery and placing the balloon through a sidearm graft or directly into the vessel through a pursestring suture. This is rarely required with current systems.
Alternative cannulation sites in patients with severe aortoiliac disease include the ascending aorta during surgery and the subclavian or brachial artery.154,155 For patients in whom long‐term IABP support is considered prior to transplantation, percutaneous insertion into the left axillary/subclavian artery can be used.156
IABP timing is performed from the ECG or the arterial waveform.
ECG: input to the balloon console is provided from skin leads or the bedside monitor. Inflation is set for the peak of the T wave at the end of systole with deflation set just before or on the R wave. The use of bipolar pacing eliminates the interpretation of pacing spikes as QRS complexes by the console.
Arterial waveform: inflation should occur at the dicrotic notch with deflation just before the onset of the aortic upstroke. This method is especially useful in the operating room, where electrocautery may interfere with the ECG signal.
A typical arterial waveform during a 1:2 ratio of IABP inflation is demonstrated in Figures 11.2 and 11.3. This shows the systolic unloading (decrease in the balloon‐assisted systolic pressure and end‐diastolic pressure) and the diastolic augmentation (increase in the balloon‐assisted diastolic pressure) that are achieved with the IABP.
Appropriate timing of inflation and deflation is essential. Proper timing should improve stroke volume and reduce LVESV and pressure. Early inflation may decrease stroke volume due to the abrupt increase in LV afterload during late systolic ejection. Late deflation will increase afterload during early ejection and decrease afterload during late ejection. This may increase stroke volume but also increase stroke work.
During a cardiac arrest, ballooning may be synchronized to cardiac contractions using the pressure trigger mode. Without cardiac massage, an internal trigger at 100 inflations/minute should be used.
IABP problems and complications
Inability to balloon. Once the balloon is situated properly and has unwrapped, satisfactory ballooning should be achieved by proper timing of inflation and deflation. However, unsatisfactory ballooning can occur in the following situations.
Unipolar atrial pacing. This produces a large atrial pacing spike that can be interpreted by the console as a QRS complex leading to inappropriate inflation. Use of bipolar pacing eliminates this problem. Most monitoring equipment suppresses pacing signals.
Rapid rates. Some balloon consoles are unable to inflate and deflate fast enough to accommodate heart rates over 150 (usually when there is a rapid ventricular response to atrial fibrillation). Augmentation can be performed with a 1:2 ratio.
Arrhythmias. Atrial and ventricular ectopy can disrupt normal inflation and deflation patterns and must be treated.
Volume loss from the balloon detected by the console monitor alarms. This indicates a leak in the system, either at the connectors or from the balloon itself. Volume loss may also indicate that the balloon has not unwrapped properly, preventing proper inflation.
Balloon rupture. When blood appears in the balloon tubing, the balloon has perforated. Escape of gas (usually helium) from the balloon into the bloodstream can occur. The balloon must be removed immediately. Difficulty with removal (balloon entrapment) may be encountered if thrombus has formed within the balloon, and this tends to occur extremely quickly. Most consoles have alarms that will call attention to this problem and prevent the device from inflating.
Catastrophic complications, such as aortic dissection, usually from inadvertent advancement of the guide wire into the vessel wall creating a false lumen, or rupture of the iliac artery or aorta, are very uncommon. Paraplegia can result from development of a periadventitial aortic hematoma or embolization of atherosclerotic debris.157 Bleeding around the balloon cable may occur if placed into a diseased vessel and can be problematic upon percutaneous removal.
Embolization to visceral vessels, especially the mesenteric and renal arteries, can occur in the presence of significant aortic atherosclerosis, although balloon placement usually does not affect mesenteric flow.158 Cerebral embolization can occur if there are mobile atheromas in the proximal descending thoracic aorta.159 Renal ischemia may occur if the balloon is situated too low and inflates below the level of the diaphragm.160
Distal ischemia is the most common complication of indwelling balloons, occurring in 8–18% of patients.161–163 It is more likely to occur with use of larger catheter sizes, so sheathless techniques are preferable. Ischemia is more likely when the IABP remains in place longer, and when the patient has impaired ventricular function, often requiring inotropic or vasopressor support.164 Additional risk factors include female gender (small femoral arteries), comorbidities (including diabetes, hypertension, obesity, and smoking), and peripheral vascular disease, especially involving the iliofemoral system. Thrombosis near the insertion site or distal thromboembolism can also occur and is related more to the duration of IABP usage. Use of intravenous heparin (maintaining a PTT of 1.5–2 times control) is advisable to minimize ischemic and thromboembolic problems if the balloon remains in place for more than a few days after surgery. Otherwise, patients have a low‐grade coagulopathy in the early postoperative period and anticoagulation is not necessary.
The presence of distal pulses or Doppler signals must be assessed frequently in all patients with an IABP. This should be compared with a preoperative peripheral pulse examination. Not infrequently, cool extremities with weak signals are noted in the early postoperative period from peripheral vasoconstriction that may be associated with a low cardiac output state, hypothermia, or use of vasopressors. This should resolve when the patient warms and myocardial function improves. However, persistent ischemia jeopardizes the viability of the distal leg and could also lead to a compartment syndrome. Options at this time include:
Removing the sheath from the femoral artery if the balloon has been placed percutaneously.
Removing the balloon if the patient appears to be hemodynamically stable. If adequate distal perfusion cannot be obtained, femoral exploration is indicated.
Removing the balloon and placing it in the contralateral femoral artery (if that leg has adequate perfusion) if the patient is IABP‐dependent. Using as small a caliber balloon as possible with sheath removal is essential.
Considering placement of the balloon through another site, such as the axillary/subclavian artery.156
Thrombocytopenia. Persistent inflation and deflation of the IABP will destroy circulating platelets, with thrombocytopenia being noted in about 50% of patients. It is not always clear whether progressive thrombocytopenia is caused by the IABP or by medications that the patient may be receiving, such as heparin. Platelet counts must be checked on a daily basis.
Sepsis may occur with longer duration of IABP usage.
Weaning of the IABP
IABP support can be withdrawn when the cardiac output is satisfactory on minimal inotropic support (usually 1 μg/min of epinephrine, 5 μg/kg/min of dobutamine, or ≤0.5 μg/kg/min of milrinone). However, earlier removal may be indicated if complications develop, such as leg ischemia, balloon malfunction, thrombocytopenia, or infection.
Weaning is initiated by decreasing the inflation ratio from 1:1 to 1:2 for about 2–4 hours, and then to 1:3 or 1:4 (depending on which console device is used) for 1–2 more hours. If the patient is not heparinized, the duration at a low inflation ratio should be minimized. Once it is determined that the patient can tolerate a low inflation ratio with stable hemodynamics, the IABP should be removed. Recovery of LV function is usually suggested when the arterial tracing suggests a good stroke volume with a systolic pressure that approaches or exceeds the diastolic augmentation pressure on the monitor. Remember that the IABP produces efficient unloading, and the blood pressure noted on the monitor is lower during balloon assistance than with an unassisted beat (actually the diastolic pressure is higher, but the true systolic pressure is lower). Thus, visual improvement in blood pressure with weaning of the IABP is not, by itself, a sensitive measure of the patient’s progress. If there is an anticipated delay in removal of more than a few hours for manpower reasons or because of the need to correct a coagulopathy, the ratio should be maintained at 1:1 or 1:2 to prevent thrombus formation on the balloon.
IABP removal techniques
Balloons inserted by the percutaneous technique can usually be removed percutaneously. This is performed by compressing the groin distal to the insertion site as the balloon is removed, allowing blood to flush out the skin wound for 1–2 heart beats, and then compressing just proximal to the skin hole where the arterial puncture site is located (Figure 11.4). Pressure must be maintained for at least 45 minutes to ensure satisfactory sealing at the puncture site. This may on occasion cause thrombosis of the vessel, so a distal pulse examination during and after compression is essential. Note: it is important to resist the temptation to remove manual pressure and peek to see if hemostasis is achieved. This can be counterproductive and flush away immature clot that is sealing the vessel. Improved hemostasis may be obtained using the D‐STAT Dry (Teleflex) or QuikClot (Z‐Medica) hemostatic pads.
Note: coagulation parameters must be checked and corrected before percutaneous removal or the patient may require groin exploration for persistent hemorrhage or a false aneurysm.
Surgical removal should be considered in patients with small or diseased vessels and in those with very weak pulses or Doppler signals with the balloon in place. The need for a thrombectomy and embolectomy may be anticipated in these patients. If the IABP has been in place for more than five days, percutaneous removal can be performed, but there is a greater chance that surgical repair of the femoral artery may be required.
Results of IABP usage
The indications for placement of an IABP are virtually all high‐risk situations with high mortality rates despite some benefits of the IABP. Preoperative placement for cardiogenic shock or active ischemia is associated with high operative mortality. Results are the best when an IABP is placed prophylactically in the cath lab or prior to surgery in “high risk” patients, specifically those with threatening anatomy and/or poor LV function who are hemodynamically stable. In these situations, use of an IABP has been shown to lower the likelihood of postoperative low cardiac output syndrome and operative mortality.133–136 Patients receiving an IABP for postcardiotomy support have already demonstrated failure of pharmacologic management to achieve satisfactory hemodynamics, and most studies have shown a 30–50% mortality in such patients, which is greatest if the IABP is placed postoperatively.146–148
One study showed that the most significant correlate of operative mortality in patients requiring an IABP was a serum lactate level >10 mmol/L during the first eight hours of support (100% mortality). Additional poor prognostic signs were a metabolic acidosis (base deficit >10 mmol/L), mean arterial pressure <60 mm Hg, urine output <30 mL/h for two hours, and the requirement for high doses of epinephrine or norepinephrine (>10 μg/min) during the early postoperative period.165
V. Mechanical Circulatory Support
If a patient cannot be weaned from CPB despite maximal pharmacologic support and use of an IABP, consideration should be given to use of extracorporeal membrane oxygenation (ECMO) or placement of a circulatory assist device for mechanical circulatory support (MCS). These devices provide flow to support the systemic and/or pulmonary circulation while resting the heart, allowing it to undergo metabolic and functional recovery. In some cases, weaning and removal of the device may be possible after several days of recovery. In others, weaning is not possible, and conversion to a long‐term device as a bridge to transplantation or for destination therapy must be considered.
Clinical conditions that may benefit from MCS include:
Postcardiotomy ventricular dysfunction refractory to maximal medical therapy and an IABP. Although left ventricular and right ventricular assist devices (LVADs and RVADs) may be used, biventricular failure is not uncommon and is often associated with hypoxemic respiratory failure from a long pump run. Therefore, short‐term ECMO is often the easiest way to provide initial support.166,167
Acute myocardial infarction with cardiogenic shock. Percutaneous LVADs can provide superior hemodynamic support to that which can be achieved with an IABP, but only the use of MCS prior to PCI improves results.142,168–171
Supporting high‐risk interventions in the cath lab. Studies comparing Impella‐ and IABP‐supported procedures showed improved event‐free survival with use of an Impella, but not with IABPs.172–174
Patients with class IV heart failure and deteriorating clinical status in INTERMACS classes 1–5. Bridging to transplantation or destination therapy with long‐term devices may be indicated for patients with HF from advanced cardiomyopathies, but temporary support may also be useful in patients with myocarditis, which may have a self‐limited course.
Basic principles of VADs
VADs are preload‐dependent, so their output is reduced with low filling pressures either from hypovolemia or cardiac tamponade, which restricts atrial filling and decreases cardiac output. The centrifugal and axial pumps are also afterload‐sensitive, such that an increase in blood pressure will decrease pump flow/output.
VADs decompress an overdistended ventricle to allow it to recover some function, although unloading of the left ventricle with an LVAD can precipitate RV failure. Unloading is comparable with nonpulsatile continuous flow devices and earlier pulsatile devices.176,177 ECMO does not unload the left ventricle or reduce oxygen demand as well as VADs and can exacerbate myocardial ischemia or precipitate pulmonary edema, but additional support with an IABP or LVAD can address that concern.178
VADs provide pulmonary (RVAD) or systemic (LVAD) flow, in contrast to the IABP, which supports ventricular function only by systolic unloading. The improvement in systolic flow, independent of pulsatility, usually allows organ system function to improve.179
VADs function independently of the ECG and can keep a patient alive during ventricular fibrillation (VF).
They require an energy source.
They require anticoagulation despite attempts at biocompatibility.
They are associated with multiple major complications, including infection, bleeding, stroke, and device malfunction.
Left ventricular assist devices (LVADs)
Technique and hemodynamics. Drainage of oxygenated blood from the left atrium or ventricle passes through the pump and is returned to the ascending aorta. This will provide systemic perfusion while decompressing the left ventricle. LV wall stress is reduced by about 80% with a 40% decrease in myocardial oxygen demand. LVAD flow is dependent on adequate intravascular volume and right ventricular function. Although volume unloading might be superior with the early generation pulsatile pumps, left ventricular pressure unloading is generally considered comparable with nonpulsatile (centrifugal or axial flow) pumps.176,177
Indications (Table 11.7). The general indications for LVAD insertion are the presence of a cardiac index <1.8 L/min/m2 with a systolic blood pressure <90 mm Hg and a PCW pressure or LAP >20 mm Hg on maximal medical support and an IABP. In the postcardiotomy patient, an extensive delay in initiating VAD support increases the risk of multisystem organ failure and death.180 Any of the clinical situations listed in section V.B with primarily LV failure may benefit from LVAD insertion.
Contraindications to the use of an LVAD vary depending on the access and drainage sites of the particular device.
General contraindications include aortic regurgitation, a mechanical aortic valve, aortic aneurysm/dissection, left heart thrombus (atrial or ventricular), iliofemoral disease for percutaneous systems, and sepsis.
When the indications for LVAD placement are present, critical elements of decision‐making include whether there is a reasonable chance of recovery, whether the patient is a candidate for transplantation or destination therapy if there is little chance for recovery, whether RVAD placement is also indicated, and whether placement is contraindicated based upon noncardiac comorbidities. Generally, one must consider the patient’s age and general medical condition, the status of RV function, noncardiac organ system function (neurologic, pulmonary, renal, hepatic), and other medical issues (infectious, vascular disease, diabetes), in making this critical decision, whether for postcardiotomy support or for heart failure patients. Risk models to assess survivability after LVAD implantation in heart failure patients are helpful in reaching the appropriate decision.181
Devices to provide LVAD support (see sections H and I, pages 565–571)
Postcardiotomy support is most readily achieved using systems that use central cannulation sites that are exposed during open‐heart surgery via a sternotomy. The CentriMag system (Abbott) can be used for LVAD support using left atrial (LA) or left ventricular (LV) and aortic cannulation, for RVAD support using right atrial and pulmonary artery cannulation, and for ECMO using right atrial and aortic cannulation with an oxygenator added to the circuit.182–184 An alternative is the Impella LD (Abiomed), which is inserted directly through the ascending aorta into the left ventricle.185
Percutaneous devices are used for procedures performed in the cath lab or hybrid operating room, and can be placed in a postcardiotomy patient. These include the Impella series and the TandemHeart (TandemLife, LivaNova).186 The Impella can also be inserted through the subclavian/axillary artery, either via a cutdown or percutaneously.
Long‐term devices for bridging and destination therapy include the second‐generation HeartMate II (HM II) and HeartWare, and the third‐generation HeartMate 3 (HM 3) (Abbott).
Management during LVAD support
LVAD flow is initiated to achieve a systemic flow of 2.2 L/min/m2 with an LA pressure of 10–15 mm Hg. The flow rate of centrifugal or axial flow devices can be preset on a console, with limitations to flow being hypovolemia, improper position of the drainage catheter, or RV failure. Adequacy of tissue perfusion can be assessed by mixed venous oxygen saturations.
To decrease myocardial oxygen demand and allow for ventricular recovery, vasoactive medications should be used only as necessary to support RV function or increase systemic resistance to maintain a MAP >75 mm Hg. α‐agents or vasopressin may be necessary because LVAD patients commonly manifest “vasodilatory shock”.187
Heparinization is recommended to achieve a PTT of 2–2.5 times normal or an ACT of 185–200 seconds for most short‐term assist devices once perioperative bleeding has ceased. An infusion of 500 units/h of heparin usually suffices, although most patients become heparin‐resistant. For pump flows <3 L/min or during weaning attempts, the PTT and ACT should be increased to 2.5–3 times normal and 250–300 seconds, respectively. Anticoagulation is also required in patients with bioprosthetic or mechanical valves.
When used for temporary postcardiotomy support, LV function is assessed by TEE after at least 48 hours of support. However, weaning is rarely possible before five days of support. Flow is reduced in 0.5 L/min intervals every five minutes to 2 L/min with careful observation of regional and global wall motion, filling pressures, and systemic pressure. Low‐dose inotropic support can be initiated during the weaning process. If adequate recovery has occurred, the device may be explanted.
Note that external compressions during VF are feasible with percutaneous and continuous flow devices, but generally are not recommended, because they can cause displacement of the devices.188
Overall results. The mortality rate associated with VAD usage for postcardiotomy support depends on how aggressively one manages a low output syndrome. Because of the high incidence of bleeding and other organ system problems associated with VADs, there is often a reluctance to insert the device “prematurely”, because in many cases, the heart will gradually improve with time on pharmacologic and IABP support without organ system sequelae. Although there are concerns that complications associated with premature VAD insertion could compromise outcomes, an early, aggressive approach to VAD insertion may lower mortality rates, not just because the patient might have survived without it, but because it might avoid the adverse sequelae of a prolonged low cardiac output syndrome in some patients.
In general, it has been estimated that about 50% of patients receiving LVADs for postcardiotomy support are discharged from the hospital.189 The RECOVER I study noted a 93% hospital survival with use of the Impella 5.0/LD for postcardiotomy circulatory support.185 Improved survival may be noted in patients with preserved RV function, no evidence of a perioperative MI, and recovery of LV function within 48–72 hours.
If ventricular function does not recover after a week of support with a short‐term device, a longer‐term device should be considered for destination therapy or as a bridge to transplantation. Survival following transplantation is similar to that of patients not requiring bridging with mechanical circulatory support.190
Right ventricular assist devices (RVADs)142,191–197
Technique and hemodynamics. Deoxygenated blood is drained from the right atrium and returned to the pulmonary artery, thus providing pulmonary blood flow while decompressing the right ventricle. Achieving satisfactory systemic flow rates depends on having adequate intravascular volume and satisfactory LV function. Although isolated RV failure may occur, it is more commonly associated with LV failure and often with oxygenation issues in the postcardiotomy period that might benefit preferentially from ECMO.
Indications (Table 11.7). RVAD insertion is indicated when there is evidence of severe RV dysfunction with a high CVP (usually >20mmHg) and inability to maintain a satisfactory cardiac output despite maximal pharmacologic therapy (usually epinephrine/milrinone and an IABP). RV failure may result from an RV infarction, worsening of preexisting RV dysfunction caused by PH or correction of severe tricuspid regurgitation, or poor intraoperative protection. RV dysfunction is exacerbated by an elevation in PVR, which can often be attributed to proinflammatory cytokines due to CPB, noncardiogenic or cardiogenic pulmonary edema, and microembolization from multiple blood product transfusions. Evidence of severe RV dysfunction with vasopressor‐refractory low cardiac output syndrome, hypotension, oliguria, and lactic acidosis is highly predictive of mortality; therefore, early RVAD placement should be considered in such a patient. LVAD placement may also lead to RV failure, for which RVAD support may also be required.
Available systems for RV assist
Postcardiotomy support is best provided by the CentriMag system using cannulas placed directly into the right atrium and pulmonary artery. The percutaneously placed systems can be used, but they require a hybrid OR with appropriate radiographic imaging for placement.
The Impella RP is an 11 Fr catheter with a 22 Fr pump motor (Figure 11.5) that is placed via the femoral vein and propels blood from the right atrium directly into the PA at a rate of up to 4 L/min, resulting in a reduction in RA pressure and an increase in mean PA pressure. The device will increase LV preload, so it can only be used when there is satisfactory LV function; otherwise, increased LV preload and afterload may result in pulmonary edema.191–195
The TandemHeart RVAD has been used to provide RV support by placing one 62 cm cannula into the RA through the femoral vein to drain blood into the pump, with blood return via a 72 cm cannula placed through the contralateral femoral vein and positioned in the PA. This produces similar hemodynamic benefits as the Impella RP, but it leaves the patient bedbound with femoral cannulas and has been replaced by the Tandem Protek Duo system.
The TandemLife Protek Duo system uses a dual lumen catheter placed via the right internal jugular vein that drains blood from the right atrium, passes it through the TandemHeart pump, and returns it to the pulmonary artery at a rate of up to 4.5 L/min (Figure 11.6). An oxygenator can also be placed in the circuit to improve systemic oxygenation.196,197
RV and LV support can also be achieved using a veno‐arterial ECMO circuit.
Management during RVAD support
RVAD flow is initiated to achieve a flow rate of 2.2 L/min/m2, increasing the LA pressure to 15 mm Hg while maintaining an RA pressure of 5–10 mm Hg. The flow rate of centrifugal or axial flow devices can be preset on a console. Inability to achieve satisfactory flow rates may indicate hypovolemia, improper position of the drainage catheter, or cardiac tamponade that compresses the right atrium. If intravascular volume is adequate and tamponade is not present, systemic hypotension may result from systemic vasodilation that requires use of an α‐agent or vasopressin. If impaired LV function is present, additional inotropic, IABP, LVAD, or ECMO support may be necessary. TEE is helpful in evaluating the status of LV function in patients on RVAD support.
Pulmonary vasodilators, including IV milrinone, inhaled NO, epoprostenol, iloprost, or milrinone, or oral sildenafil, may be beneficial in reducing pulmonary artery pressures and RV afterload, allowing for recovery of RV function.
The requirement for heparinization is similar to that for LVADs.
Assessment of myocardial recovery by TEE and weaning of the device are similar to LVADs.
Overall results. Patients receiving isolated RVADs for acute RV failure have about a 70% one‐month survival.191–193 However, patients requiring RVAD support for postcardiotomy support fair much worse, with limited data suggesting survival rates of only 25%.194
Biventricular assist devices (BiVADs)
Technique and hemodynamics. BiVADs incorporate the drainage sites of both RVAD and LVAD systems. They provide support of both the pulmonary and systemic circulations but do not provide oxygenation, and can function during periods of VF. In the postcardiotomy patient, ECMO is more readily accomplished using the cannulas already in place for CPB and is used for short‐term support.
In patients receiving continuous flow LVADs, RV failure is noted in about 15–20% of patients and can often be managed with pulmonary vasodilators and inotropic support. However, RVAD support will be necessary in about 4–5% of these patients. This is less than previously noted with pulsatile devices as complete LV unloading can be avoided, resulting in less septal shift with better preservation of RV mechanics.198 Generally, an acute increase in LV unloading with an increase in RV preload may distort RV geometry and unmask RV dysfunction.199
Numerous studies have evaluated predictors for RV failure and the necessity for additional RVAD assist in patients receiving LVADs.200–204 These predictors include:
A higher severity of global illness: patients in INTERMACS I‐II, preop ECMO or renal replacement therapy, severe tricuspid regurgitation, reoperative surgery, and concomitant procedures other than TV repair at the time of LVAD implantation.
Hemodynamic instability: high RA pressures (specifically an RA/PCW ratio >0.63), reduced pulmonary artery pulse pressure, stroke volume, stroke work index, and cardiac output, and the requirement for multiple vasoactive drugs to maintain flow.
End‐organ dysfunction: preoperative ventilatory support, hepatic or renal dysfunction.
One study proposed an echo score which was predictive of RV failure to identify patients who might benefit from RVAD support. These included a higher RA pressure, lower RV fractional area change, and lower LA volume.203 Another study designed an RV failure risk score based on vasopressor requirement, abnormal LFTs, and abnormal renal function.204
Postcardiotomy BiVAD support can be achieved using two CentriMag devices using RA/PA and LA/aortic cannulation through a median sternotomy. Percutaneous systems combining an Impella RP or Protek Duo with a left‐sided Impella device can also be used.205,206
If the patient requires longer‐term BiVAD support, the HM II, HM 3, or the HeartWare system (Medtronic) is implanted and is combined with either an Impella RP inserted via the axillary artery or the TandemHeart Protek Duo inserted via the internal jugular vein.
Management during BiVAD support
Sequential manipulations of RVAD and LVAD flow are used to achieve a systemic flow rate of 2.2 L/min/m2. The RVAD flow is increased to raise the LA pressure to 15–20 mm Hg, and then the LVAD flow is increased to reduce the LA pressure to 5–10 mm Hg. Inability to achieve satisfactory flow rates usually indicates hypovolemia, tamponade, or catheter malposition on either side. Left‐ and right‐sided flow rates may differ because of varying contributions of the native ventricles to pulmonary or systemic flow.
Heparin requirements are similar to those noted above for LVADs.
Assessment of recovery and weaning are similar to the methods described for RVAD and LVAD devices.
Overall results. The requirement for biventricular support has an adverse effect on survival. However, one report on BiVAD support for postcardiotomy low cardiac output syndrome with the CentriMag system showed a 56% 30‐day survival.182
ECMO is a form of extracorporeal life support (ECLS) that serves as an alternative to ventricular assist devices. The system employs a membrane oxygenator, centrifugal pump, heat exchanger, oxygen blender, and a heparin‐coated circuit. The latter provides a more biocompatible surface that minimizes platelet activation and the systemic inflammatory response, and reduces the heparin requirement. This allows the ECMO circuit to be used for several days.
Indications. ECMO is indicated for the short‐term treatment of severe postcardiotomy ventricular dysfunction with or without hypoxemia. Criteria for use are similar to those for left ventricular or biventricular assist. In many patients requiring VAD support, the duration of CPB is quite long due to the delay in deciding to proceed with VAD support, often resulting in both cardiogenic and noncardiogenic pulmonary edema that impairs oxygenation. ECMO can also be used emergently in patients sustaining a cardiac arrest and in patients with severe hypoxemic ARDS, while the lung recovers from the inciting pathologic insult. Veno‐venous ECMO is used for pulmonary support alone (see Figure 5.12, page 314).
Technique. At the conclusion of surgery, the same cannulation setup used for CPB is maintained (right atrium and aorta). If ECMO is considered subsequently, it may be established with venous drainage from the internal jugular vein or femoral vein with return of blood to the femoral, axillary, or carotid artery (Figure 11.7). Steps should be taken to ensure distal perfusion with the use of femoral arterial cannulation (see page 312). Because ECMO does not produce LV unloading, it may cause ventricular distention with rising filling pressures and will worsen myocardial oxygen demand. Therefore, either an IABP or preferably an Impella should be considered to unload the LV.178 Percutaneous femorofemoral bypass may be used to resuscitate a patient from cardiac arrest.
Management. Maximal medical support is essential to optimize the results of ECMO. Some of the essential elements are:
Optimizing preload to provide pulmonary perfusion.
Supporting SVR with α‐agents or vasopressin; however, elevated SVR and bronchial venous return to the left ventricle can elevate LV pressures and cause LV thrombus formation or pulmonary edema. Since the LV is not unloaded, additional support (IABP or Impella) may be indicated to prevent pulmonary edema and worsening of LV function.
Use of femoral artery–femoral vein ECMO may cause coronary or cerebral ischemia if there is any cardiac ejection.142
Aggressive use of pulmonary vasodilators for PH.
Early and aggressive use of renal replacement therapy.
Use of low tidal volume ventilation.
Minimizing bleeding by initiating anticoagulation after mediastinal bleeding is at a minimum and use of low ACTs in the heparin‐coated circuit.
If the patient has suffered a severe neurologic insult or is not considered a candidate for transplantation, ECMO is usually terminated after 48 hours. If the heart does not recover after up to one week of ECMO support, a clinical decision must be made about conversion to long‐term support. Detailed assessment of neurologic, pulmonary, hepatic, and renal status is essential. It is sometimes difficult to ascertain whether the patient has survivable or nonsurvivable organ system dysfunction that might contraindicate LVAD implantation.
Results. The results of ECMO depend on the indication for its use and the degree of organ system failure at the time it is initiated.
About one‐third of patients receiving ECMO for postcardiotomy support will survive for 30 days, but most would have died without support.166,167,209–212 A study of ECMO vs. VAD support for postcardiotomy cardiogenic shock found better survival in patients receiving VADs, and in that study only 16% of patients on ECMO support survived the hospital stay.213
A large multicenter study provided a postcardiotomy ECMO score to quantify the mortality risk. This included female gender (1 point), advanced age (60–69, 2 points, >70, 4 points), prior cardiac surgery (1 point), lactate >6 mmol/L prior to ECMO (2 points), aortic arch surgery (2 points), and preoperative stroke/coma (5 points). Mortality rate was 45–57% for 1–3 points, but increased to 70% or greater for ≥4 points.210 Another study confirmed that older age, an elevated lactate level (>4 mmol/L after 48 hours), and hepatic and renal failure were associated with higher mortality.211
One study reported a 31% survival in patients undergoing emergent ECMO for prolonged cardiac arrest.214
Complications are not insignificant with ECMO. A meta‐analysis reported a 47% need for dialysis, 43% reoperations for bleeding, 15% mediastinal wound infections, 11% neurologic events, and an 11% incidence of lower limb ischemia.212
Short‐term devices to provide ventricular assist
Short‐term support for high‐risk PCI or cardiogenic shock is best provided with percutaneous systems that require fluoroscopic imaging for their insertion. This is usually performed in the cath lab or hybrid operating room.
The Impella series includes LVAD devices, such as the Impella 2.5, CP, and 5.0 devices, which provide increasing amounts of systemic flow, and the Impella RP, which provides RV support.
The Impella 5.0 is a 9 Fr catheter with a 21 F pump motor that is inserted through the femoral artery and positioned across the aortic valve into the left ventricle (Figure 11.8). This axial‐flow device withdraws blood from the distal end of the catheter in the LV and pumps it into the ascending aorta. The Impella CP is a 9 Fr catheter with a 14 Fr pump motor that can provide 4L/min flow and is preferred during high‐risk PCI.
The Impella RP is designed for RVAD support.
The TandemHeart (PTVA) system (LivaNova) is a continuous‐flow centrifugal pump that can provide up to 5 L/min flow (Figure 11.9). It consists of a 21 Fr transseptal cannula placed percutaneously through the femoral vein and positioned across the atrial septum into the left atrium. Blood drains into a dual‐chamber pump which uses a magnetically driven impeller to pump the blood back to the patient through 15 or 17 Fr cannulas placed into one or both femoral arteries. Anticoagulation with heparin to achieve a PTT of 2.5–3 times normal (65–80 seconds) or an ACT >200 seconds is recommended. This device can also be used for postcardiotomy LVAD support with direct LA or LV and aortic cannulation, or as an RVAD for postcardiotomy support or cardiogenic shock from an RV infarct with percutaneous or direct placement of cannulas into the RA and PA. Use of the TandemLife Protek Duo allows for RV support through a cannula placed through the right internal jugular vein.196,197
Short‐term postcardiotomy support can be achieved using continuous‐flow (centrifugal, axial) devices that can implanted during surgery. These are the most readily available, easy‐to‐use systems for uni‐ or biventricular short‐term support. Their use is usually limited to several weeks, at which time conversion to long‐term devices may be necessary if recovery does not occur.
The CentriMag is a centrifugal pump that uses standard cannulation techniques and can provide RVAD, LVAD, or ECMO support by placing a membrane oxygenator in the circuit. This pump uses a magnetically levitated rotor to propel blood forward at a rate of up to 10L/min (Figure 11.10). This avoids friction to minimize blood trauma and hemolysis and can be used for several months of support, although the pump head and external circuit may need to be changed after six weeks. Heparinization to achieve a PTT of 60–100 seconds is recommended.
In the absence of an approved device, the Bio‐Medicus (Medtronic) centrifugal pump that is routinely used for CPB can be used successfully to provide a brief period of uni‐ or biventricular support until other devices can be implanted. These systems can also be used in ECMO circuits.
The Impella LD device is inserted directly through a graft in the ascending aorta.
The Impella 5.0 device can be inserted through an axillary/subclavian approach usually via a cutdown.215
ECMO can be established using the right atrial and aortic cannulas from CPB. Several systems, including the CentriMag device with a oxygenator spliced into the system (Quadrox, MAQUET), and the Cardiohelp system (Getinge), which uses the MAQUET Rotaflow magnetically levitated centrifugal pump that produces minimal hemolysis, can be used to provide ECMO support (Figure 11.7). The latter is a fairly compact system that allows for transport to tertiary care hospitals.216,217
If myocardial recovery does not occur, a clinical decision must be made as to whether a device capable of longer‐term support should be implanted either as a bridge to transplantation or destination therapy, based primarily upon the patient’s neurologic function and organ system recovery. Thus, these devices are implanted as a “bridge to decision”.218
Long‐term devices have evolved from bulky, paracorporeal, and intracorporeal pulsatile systems to smaller, intracorporeal, nonpulsatile, continuous flow devices that are more biocompatible and have improved durability with newer designs. These systems are valve‐less and designed with a permanent magnetic field that rapidly spins a simple impeller supported by mechanical bearings. They are preload‐ and afterload‐sensitive and can provide unloading comparable to that of pulsatile devices. However, the degree of unloading can be prescribed, such that excessive LV unloading that can lead to RV failure can be minimized. These devices are effective in maintaining organ system perfusion and can be used as long‐term bridges to transplantation or for destination therapy in patients who are not considered transplant candidates. Technologic advances in newer generation systems have resulted in smaller devices with improved biocompatibility, more durability, and fewer complications, including device thrombosis.
The Impella 5.0 can be used for long‐term support as a bridge to transplantation. It can flow up to 5 L/min. It is inserted through the axillary artery, thus enabling the patient to ambulate.215
The HeartMate II (HM II) is a continuous axial flow device with a rotary pump that can provide up to 10 L/min flow.219 The inflow cannula is placed through the LV apex, and the outflow cannula is sewn to the ascending aorta (Figure 11.11). The pump is inserted in a preperitoneal pocket with a drive line exiting the right upper quadrant. Early anticoagulation with heparin has been used, but it can contribute to bleeding and is probably not essential. The patient is then maintained on warfarin with a target INR of around 2.0. This device is an excellent bridge to transplantation and has also been used for destination therapy.
The HeartWare device (HVAD) (Medtronic) is a very small 160 g device implanted through the left ventricular apex which consists of a small centrifugal pump that relies on magnetic and hydrodynamic rotor levitation to generate up to 10 L/min of flow that is returned to the aorta through a 10 mm graft (Figure 11.12).220 It has one moving part and no mechanical bearings. It can be used as a bridge or for destination therapy.
The HeartMate 3 (HM 3) is a continuous flow centrifugal pump that is partially inserted into the left ventricular apex with return of up to 10 L/min of flow through a graft sewn to the ascending aorta (Figure 11.13). The technological advance is the use of “Full MagLev™” (magnetically levitated) technology that allows the device’s rotor to be suspended by magnetic forces. Since the parts “float”, there is no friction and therefore less wear and tear on the rotor. This contact‐free environment is designed to optimize hemocompatibility and reduce blood trauma through gentle blood handling. There is also “artificial pulse technology” designed to promote washing of the pump to prevent the formation of zones of recirculation and stasis.221 It can be used as a bridge to transplantation or for destination therapy.
Other axial/rotary flow pumps that have been used successfully as bridges to transplantation and for destination therapy include the Jarvik 2000 (Jarvik Heart) and Heart Assist 5 (Reliant Heart) devices.222,223
The HeartWare miniaturized VAD (MVAD) uses hydrodynamic levitation with a layer of blood to lift the rotor. Blood flow follows the axis of rotation of the impeller, but exits perpendicular to inflow. This lowers shear stress on the impeller and optimizes blood flow paths, which is expected to improve hemodynamic performance. The system also incorporates a pulsatility algorithm called the qPulse™ Cycle individualized for each patient to enhance aortic valve function and reduce chronic bleeding. This device was not approved as of mid‐2020.224
Total artificial hearts (TAHs) potentially hold promise for destination therapy, but are only approved as bridges to transplantation. The most commonly implanted TAH is the SynCardia system, which is an offshoot of the Jarvik 7 heart, first implanted in 1988 (Figure 11.14). It consists of two artificial ventricles with mechanical valves, and a pneumatic drive line that compresses a polyurethane diaphragm and can generate up to 9 L/min of flow.225–227
A number of other devices have been developed and evaluated for long‐term ventricular assist with the objective of minimizing complications and improving durability. Advances include technology to provide pulsatility, enable physiologic feedback to control flow, and reduce shear stress to improve biocompatibility, which should reduce platelet activation, hemolysis, and von Willebrand factor degradation, which contributes to bleeding. Some of these advances are present in the HM 3 and HeartWare MVAD devices. Improved transcutaneous energy transmission systems should reduce the risk of infection.
Complications.188,199 The evolution from early‐generation pulsatile pumps (Novacor, Thoratec, Abiomed BV, HeartMate XVE) to axial and continuous flow pumps has reduced but not eliminated the many complications associated with the use of MCS. The most common morbidities with use of short‐term assist devices are bleeding, stroke, and organ system failure, the latter usually due to hypoperfusion or hypotension before circulatory assist is initiated. Other complications associated with these devices include the following:
Bleeding. Despite reversal of anticoagulation, a substantial percentage of patients (up to 60%) require re‐exploration for evacuation of mediastinal clot that can cause tamponade (manifested by inadequate drainage into the device). Contributing factors include coagulopathies related to a long duration of CPB in postcardiotomy patients, the large amount of dead space around the catheters in the mediastinum, often an open chest, and the use of early postoperative anticoagulation to minimize thrombus formation within the devices. Although early anticoagulation is desirable, it must be withheld until bleeding is at minimum.
Gastrointestinal bleeding is noted in 15–30% of patients due to the use of anticoagulation, low pulsatility, development of AV malformations, and acquired von Willebrand factor (vWF) deficiency. The latter is caused by the high sheer stress that causes degradation of vWF high‐molecular‐weight multimers and may be less common with the HM 3 system because of lower sheer stress.228
Hemolysis, fibrinolysis, and platelet dysfunction are common with LVADs.229
Heparin‐induced thrombocytopenia (HIT) was noted in 26% of patients in one report.230 Use of warfarin for device thromboprophylaxis and an alternative anticoagulant at the time of transplantation may be necessary unless the time from the diagnosis of HIT to transplantation exceeds three months.
Mediastinitis and sepsis. With the use of implantable devices, infection is usually related to the drive lines for energy transmission, which exit through the skin. About 20% of patients will develop drive line infections and 15–20% will develop mediastinitis or sepsis.231,232 Because long‐term antibiotic usage is commonplace, resistant organisms are often identified. In addition, many patients are debilitated and malnourished and have numerous intravascular and other invasive catheters that can become colonized. The most common organisms are Staphylococcus aureus and coagulase‐negative staph, Candida, and Pseudomonas aeruginosa. Infection is associated with a significantly increased mortality, especially so in the case of fungal endocarditis, which occurs in about 20% of patients. If this develops, antifungal therapy along with either device removal and replacement or urgent transplantation may lead to a successful result. Generally, however, infections are controllable and do not influence the results of transplantation.
Neurologic complications are noted in 10–20% of patients and are more commonly ischemic than hemorrhagic in nature, although the latter is associated with higher mortality.233 Ischemic strokes are related to device/graft thrombosis, whereas hemorrhagic strokes are related to anticoagulation, acquired von Willebrand syndrome, endocarditis, hypertension, and hemorrhagic conversion of ischemic cerebral infarcts. The ENDURANCE trial found that the stroke rate was 2.5 times higher with the HeartWare device compared with the HM II (30% vs. 12%),220 but was comparable with both devices at around 12–15% at two years with good blood pressure control.234 The MOMENTUM trial showed a 50% reduction in stroke with the HM 3 compared with the HM II devices (19% vs 10%).221 Patients with mechanical aortic valves should have them covered with tissue or sewn shut to prevent thromboembolism.
Malignant ventricular arrhythmias may develop as a result of myocardial ischemia, infarction, or the use of catecholamines.235 BiVADs function during VF, as can LVADs as long as the PVR is not high. If LVAD flow cannot be maintained, the patient may require placement of an RVAD. VF may foster thrombus formation in the ventricles and should be treated aggressively. Early cardioversion should also be considered to prevent RV injury from prolonged VF. Chest compressions can be used for percutaneous and continuous flow devices, but are usually not necessary nor recommended.188
Renal failure is usually caused by prolonged episodes of hypotension or low cardiac output prior to insertion of a VAD. Serum creatinine generally returns to the patient’s baseline after VAD implantation, except when there is evidence of other organ system failure (especially hepatic) or infection. Early aggressive treatment with renal replacement therapy (usually continuous veno‐venous hemofiltration) should be considered. The mortality rate for patients with persistent renal failure on VAD support is very high.
Respiratory failure is usually attributable to a prolonged duration of CPB, sepsis, and use of multiple blood products.
Vasodilatory shock due to inappropriately low levels of vasopressin is not uncommon in patients requiring placement of VADs. In fact, vasopressin hypersensitivity may be noted. Use of arginine vasopressin in doses up to 0.1 units/min is effective in increasing the mean arterial pressure in these patients.187
Worsening heart failure may result from:
De novo aortic regurgitation
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