Postoperative Cardiovascular Management

Chapter 30 

Postoperative Cardiovascular Management Jerrold H. Levy, MD, FAHA, FCCM  •  Kamrouz Ghadimi, MD  •  James M. Bailey, MD  •  James G. Ramsay, MD, PhD

Key Points 1. Maintaining oxygen transport and oxygen delivery appropriately to meet the tissue metabolic needs is the goal of postoperative circulatory control. 2. Cardiac function worsens after cardiac surgical procedures. Therapeutic approaches to reverse this dysfunction are important and often can be discontinued in the first few postoperative days. 3. Myocardial ischemia often occurs postoperatively, and it is associated with adverse cardiac outcomes. Multiple strategies have been studied to reduce this complication. 4. Postoperative biventricular dysfunction is common. It requires interventions to optimize the heart rate and rhythm, provide acceptable preload, and adjust afterload and contractility. In most patients, pharmacologic interventions can be rapidly weaned or stopped within the first 24 hours postoperatively. 5. Supraventricular tachyarrhythmias are common in the first postoperative days, with atrial fibrillation predominating. Preoperative and immediate postoperative pharmacotherapy can reduce the incidence and slow the ventricular response. 6. Postoperative hypertension has been a common complication of cardiac surgical procedures; newer vasodilator drugs are more arterial selective and allow greater circulatory stability than older, nonselective drugs. 7. Catecholamines, phosphodiesterase inhibitors, and the calcium sensitizer levosimendan have been studied for treating biventricular dysfunction. 8. Phosphodiesterase inhibitors and levosimendan are clinically effective inodilators that have important roles in patients with low cardiac output and biventricular dysfunction. 9. Long cardiopulmonary bypass times may cause a refractory vasodilated state (“vasoplegia”) requiring combinations of pressors such as norepinephrine and vasopressin. 10. Positive-pressure ventilation has multiple effects on the cardiovascular system, with complex interactions that should be considered in patients after cardiac surgical procedures. 11. Critical care management of patients undergoing transcatheter aortic valve replacement who have experienced intraoperative complications includes understanding and managing the postoperative consequences of iatrogenic vascular injuries, stroke, significant paravalvular leaks, and/or cardiac conduction abnormalities. 12. Hemodynamic management after cardiothoracic operations may benefit from the use of transesophageal echocardiography to determine myocardial function and assess cardiovascular structures. Echocardiography is particularly helpful in the diagnosis of causes of obstructive shock, including pericardial effusions leading to tamponade physiology.

758

Postoperative cardiovascular dysfunction is becoming more common as older and increasingly critically ill patients undergo cardiac surgical procedures. Biventricular dysfunction and circulatory changes occur after cardiopulmonary bypass (CPB), but they can also occur in patients undergoing off-pump procedures. Pharmacologic therapy with suitable monitoring and mechanical support may be needed for patients in the postoperative period until ventricular or circulatory dysfunction improves.

OXYGEN TRANSPORT Maintaining oxygen transport (ie, oxygen delivery [DO2]) satisfactory to meet the tissue metabolic needs is the goal of postoperative circulatory control. Oxygen transport is the product of cardiac output (CO) times arterial content of oxygen (CaO2) (ie, hemoglobin concentration × 1.34 mL of oxygen per 1 g of hemoglobin × oxygen saturation [SaO2]), and it can be affected in many ways by the cardiovascular and respiratory systems, as shown in Fig. 30.1. Low CO, anemia from blood loss, and pulmonary disease can decrease DO2. Before altering the determinants of CO, including the inotropic state of the ventricles, an acceptable hemoglobin concentration and adequate SaO2 should be provided, thus enabling increases in CO to supply the maximum available DO2. Hypoxemia from any cause reduces DO2, and acceptable arterial oxygenation (partial arterial pressure of oxygen [PaO2]) may be achieved with the use of an elevated inspired oxygen fraction (FIO2) or positive end-expiratory pressure (PEEP) in the ventilated patient. Use of PEEP or continuous positive airway pressure (CPAP) in the spontaneously breathing patient may improve PaO2 by reducing intrapulmonary shunt; however, venous return may be reduced, causing a decrease in CO, with DO2 decreased despite an increased PaO2. It is important to measure CO as PEEP is applied. Intravascular volume expansion may be used to offset this damaging effect of PEEP. Unexplained hypoxemia may be caused by right-to-left intracardiac shunting, most commonly by a patent foramen ovale. This situation is most likely to occur when right-sided pressures are abnormally increased; an example is the use of high

Rate Rhythm Preload Afterload Contractility

Oxygen Cardiac = transport output

Anemia

×

Hypoventilation · · V/Q mismatch Intrapulmonary shunt Low mixed venous saturation + shunt

Hemoglobin Oxygen × concentration saturation

Fig. 30.1  Important factors that contribute to abnormal oxygen transport. V̇ /Q̇ , Ventilation/ perfusion.

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Postoperative Cardiovascular Management

13. Echocardiography during the daily management of both venovenous and venoarterial extracorporeal membrane oxygenation (ECMO) may improve diagnosis of hemodynamic instability, troubleshoot common problems encountered during ECMO management, and aid in weaning the patient from mechanical support.

30

Postoperative Care

levels of PEEP. If this condition is suspected, echocardiography should be performed, and therapy to reduce right-sided pressures should be initiated. Patients with pulmonary disease may experience dramatic worsening of oxygenation when vasodilator therapy is started because of release of hypoxic vasoconstriction in areas of diseased lung. Although CO may be increased, the worsening in CaO2 results in a decrease in DO2. Reduced doses of direct-acting vasodilators or trials of different agents may be indicated. When DO2 cannot be increased to an acceptable level as judged by decreased organ function or development of lactic acidemia, measures to decrease oxygen consumption (V̇ O2) may be taken while awaiting improvement in cardiac or pulmonary function. For example, sedation and paralysis may buy time to allow reversible postoperative myocardial dysfunction to improve.

TEMPERATURE

T °C (nasopharyngeal)

Patients are often admitted to the intensive care unit (ICU) after cardiac operations with core temperatures lower than 35°C, especially after off-pump cardiac surgical procedures. The typical pattern of temperature change during and after cardiac operations and the hemodynamic outcomes are illustrated in Fig. 30.2. Decreases in temperature after CPB occur in part because of redistribution of heat within the body and in part because of heat loss. Monitoring of body sites other than the blood and brain (eg, urinary bladder, tympanic membrane temperatures) can help provide more complete rewarming, but the body temperature usually falls after CPB, especially when difficulties are encountered and the chest remains open for an extended period; in such cases, some degree of hypothermia is an almost unavoidable result. Intraoperative

VI

SVR ↑ · VCO2 ↓ · VO2 ↓

38

4

3 34

1

2

SVR ↓ · VCO2 ↑ · VO2 ↑

Maximum instability

30 0

5

10

15

Hours Event

OR

CPB

ICU

Fig. 30.2 Nasopharyngeal temperature during and after cardiac surgical procedures. (1) Core (ie, blood) cooling on cardiopulmonary bypass (CPB). (2) Core warming on CPB. (3) Afterdrop in temperature (T) after separation from CPB. (4) Rewarming after admission to the intensive care unit (ICU). Systemic vascular resistance (SVR) is increased, and carbon dioxide production (V̇ CO2) and oxygen consumption (V̇ O2) are decreased on admission to the ICU because of residual hypothermia. During rapid rewarming, SVR decreases and V̇ CO2 and V̇ O2 increase; these changes can cause marked cardiac and ventilatory instability. OR, Operating room. (From Sladen RN. Management of the adult cardiac patient in the intensive care unit. In: Ream AK, Fogdall RP, eds. Acute cardiovascular management: anesthesia and intensive care. Philadelphia: Lippincott; 1982:495.)

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Postoperative Cardiovascular Management

use of forced-air warming blankets or cutaneous gel pads can help reduce the temperature loss during and after surgical procedures. The normal thermoregulatory and metabolic responses to hypothermia remain intact after cardiac operations and result in peripheral vasoconstriction that contributes to the hypertension commonly seen early in the ICU. As temperature decreases, CO is decreased because of bradycardia, whereas oxygen consumed per beat is actually increased. Another adverse consequence of postoperative hypothermia is a large increase in V̇ O2 and carbon dioxide production during rewarming. When patients cannot increase CO (ie, DO2), the effects of this large increase in V̇ O2 include mixed venous desaturation and metabolic acidosis. Unless end-tidal carbon dioxide is monitored or arterial blood gases are analyzed often to show the increased carbon dioxide production and to guide increases in ventilation, hypercarbia will occur, causing catecholamine release, tachycardia, and pulmonary hypertension. The effects of rewarming are most intense when patients shiver. Shivering may be effectively treated with meperidine, which lowers the threshold for shivering. Muscle relaxation may provide more stable hemodynamic conditions than meperidine, but accompanying sedation must be administered to avoid having an awake and paralyzed patient. As the temperature rises, usually to approximately 36°C, vasoconstriction and hypertension are replaced by vasodilation, tachycardia, and hypotension, even without hypercarbia. Often, over minutes, a patient who needs vasodilators for hypertension then requires vasopressors or large volumes of fluid for hypotension. Volume loading during the rewarming period can help reduce the rapid swings in blood pressure (BP) that may occur. It is important to recognize when these changes result from changes in body temperature, to avoid attributing them to other processes that may call for different therapy.

ASSESSMENT OF THE CIRCULATION Surgical dressings, chest tubes attached to suction, fluid in the mediastinum and pleural spaces, peripheral edema, and temperature gradients can distort or mask information obtained by the classic techniques of inspection, palpation, and auscultation in the postoperative period. However, the physician should not be deterred from applying these basic techniques in view of their potential benefit. Physical examination may be of great value in diagnosing gross or acute disease, such as pneumothorax, hemothorax, or acute valvular insufficiency, but it is of limited value in diagnosing and managing ventricular failure. For example, in the critical care setting, experienced clinicians (eg, internists) using only physical findings often misjudge cardiac filling pressures by a large margin. Low CO in particular is not consistently recognized by clinical signs, and systemic BP does not correlate with CO after cardiac surgical procedures. Oliguria and metabolic acidosis, classic indicators of a low CO, are not always reliable because of the polyuria induced by hypothermia, oxygen debts induced during CPB that cause acidosis, and medications or fluids given during or immediately after bypass. Although clinicians are taught that the adequacy of CO can be assessed by the quality of the pulses, capillary refill, and peripheral temperature, no relationship exists between these indicators of peripheral perfusion and CO or calculated systemic vascular resistance (SVR) in the postoperative period. Many patients arrive in the ICU in a hypothermic state, and residual anesthetic agents can decrease the threshold for peripheral vasoconstriction in response to this condition. A patient’s extremities may therefore remain warm despite a hypothermic core or a decreasing CO. Even after temperature stabilization on the first postoperative day, 761

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the relationship between peripheral perfusion and CO is too crude to be used for hemodynamic management. Despite the lack of a proven benefit with pulmonary artery catheter (PAC) use, many patients continue to have this monitor placed for cardiac surgical procedures. Cardiac anesthesiologists believe that the lack of evidence about the PAC may reflect the lack of a modern, well-designed randomized trial. That no such trials have been conducted in cardiac surgical patients probably attests to the reluctance of cardiac surgeons and anesthesiologists to manage their patients without what they consider to be important information. Postoperatively, many cardiac surgical centers do not have in-house physicians, and surgeons believe that the “objective” PAC data obtained over the telephone is valuable. As less invasive tools such as echocardiography or arterial waveform analysis devices become better known and more readily available, it seems likely that PAC use will diminish further in cardiac surgical patients. Echocardiography is the technique of choice for acute assessment of cardiac function. Just as transesophageal echocardiography (TEE) has become essential for intraoperative management in various conditions, several studies document its utility in the postoperative period in the presence and absence of the PAC. It provides information that may lead to urgent surgery or prevent unnecessary surgery, gives important information about cardiac preload, and can detect acute structural and functional abnormalities. Although transthoracic echocardiography (TTE) can be performed more rapidly in this setting, satisfactory images can be obtained only in about 50% of patients in the ICU. A small lumen single plane disposable echocardiography device, Imacor, has been developed for use up to 72 hours for ICU management.

POSTOPERATIVE MYOCARDIAL DYSFUNCTION

VI

Studies using hemodynamic, nuclear scanning, and metabolic techniques have documented worsening in cardiac function after coronary artery bypass grafting (CABG) procedures. All these studies showed significant declines in left ventricular (LV) or biventricular (when measured) function in the first postoperative hours, with a gradual return to preoperative values by 8 to 24 hours. Decreased ventricular performance at normal or elevated filling pressures occurs, suggesting decreased contractility. Similarly, “flattening” of the ventricular function curves is usually obvious; this finding suggests that preload expansion greater than 10 mm Hg for central venous pressure (CVP) or 12 mm Hg for pulmonary capillary wedge pressure (PCWP) is of little benefit. Satisfactory myocardial protection is important to prevent postoperative dysfunction. In off-pump surgical procedures, the idea is to preserve coronary perfusion, but during mechanical manipulation, changes in CO and BP occur. For CABG with CPB, most surgeons use some combination of hypothermia and crystalloid or blood cardioplegia to arrest the heart and reduce its metabolism. Although little consensus exists that any one technique is preferable in all circumstances, cold intermittent crystalloid cardioplegia with systemic hypothermia is the most widely used technique clinically. Other proposed factors that contribute to postoperative ventricular dysfunction include myocardial ischemia, residual hypothermia, preoperative medications such as β-adrenergic antagonists, and ischemia-reperfusion injury (Box 30.1).

POSTOPERATIVE MYOCARDIAL ISCHEMIA Although intraoperative myocardial ischemia has often been a focus, studies showed that ischemia frequently occurs postoperatively and is associated with adverse cardiac 762

Risk Factors for Low Cardiac Output Syndrome After Cardiopulmonary Bypass

Preoperative left ventricular dysfunction Valvular heart disease requiring repair or replacement Long aortic cross-clamp time and total cardiopulmonary bypass time Inadequate cardiac surgical repair Myocardial ischemia and reperfusion Residual effects of cardioplegia solution Poor myocardial preservation Reperfusion injury and inflammatory changes

outcomes. Electrocardiographic (ECG) and segmental wall motion abnormality (SWMA) evidence of ischemia occur early postoperatively in up to 40% of patients undergoing CABG procedures. Postbypass SWMAs were significantly associated with adverse outcomes (eg, myocardial infarction [MI], death). Surprisingly, these abnormalities most often appeared in the regions of the heart that had been revascularized. Hemodynamic changes rarely preceded ischemia; however, postoperative heart rates (HRs) were significantly higher than intraoperative or preoperative values. Whether such changes occur because of operation and reperfusion or as a result of events after CPB is not known. These findings do suggest that monitoring for ischemia must continue after revascularization. It may be that early recognition and treatment of ischemia or prophylactic medication can help prevent or reduce myocardial ischemia and dysfunction after CABG procedures.

Postoperative Cardiovascular Management

BOX 30.1

THERAPEUTIC INTERVENTIONS Therapeutic interventions for postoperative biventricular dysfunction include the standard concerns of managing low-CO states by controlling the HR and rhythm, providing an acceptable preload, and adjusting afterload and contractility. In most patients, pharmacologic interventions can be rapidly weaned or stopped within the first 24 hours postoperatively.

Postoperative Arrhythmias Patients with preoperative or newly acquired noncompliant ventricles need a correctly timed atrial contraction to provide satisfactory ventricular filling, especially when they are in sinus rhythm preoperatively. Although atrial contraction provides approximately 20% of ventricular filling, this may be more important in postoperative patients, when ventricular dysfunction and reduced compliance may be present. For example, in medical patients with acute MI, atrial systole contributed 35% of the stroke volume (SV). The SV is often relatively fixed in patients with ventricular dysfunction, and the HR is an important determinant of CO. Rate and rhythm disorders must be corrected when possible, using epicardial pacing wires. Approaches to postoperative rate and rhythm disturbances are shown in Table 30.1. Later in the postoperative period (days 1 through 3), supraventricular tachyarrhythmias become a major problem, with atrial fibrillation (AF) predominating. The 763

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Postoperative Care

Table 30.1  Postoperative Rate and Rhythm Disturbances Disturbance

Usual Causes

Treatments

Sinus bradycardia

Preoperative or intraoperative β-blockade Ischemia Surgical trauma

Atrial pacing, β-agonist, anticholinergic

Agitation or pain Hypovolemia Catecholamines Catecholamines Chamber distension Electrolyte disorder (hypokalemia, hypomagnesemia)

Sedation or analgesia Volume administration Change or discontinuance of drug Change or discontinuance of drug Treatment of underlying cause (eg, vasodilator, diuresis, potassium or magnesium administration) May require synchronized cardioversion or pharmacotherapy Cardioversion Treat ischemia, may require pharmacotherapy Change or discontinuance of drug

Heart block (first, second, and third degree) Sinus tachycardia Atrial tachyarrhythmias

Ventricular tachycardia or fibrillation

VI

Ischemia Catecholamines

Atrioventricular sequential pacing Catecholamines

overall incidence is between 30% and 40%, but with increasing age and valvular surgical procedures, the incidence may be in excess of 60%. Many reasons are recognized for this development, including inadequate intraoperative atrial protection, electrolyte abnormalities, change in atrial size with fluid shifts, epicardial inflammation, stress, irritation, and genetic factors. When AF or other supraventricular arrhythmias develop, treatment is often urgently needed for symptomatic relief or hemodynamic benefit. The longer a patient remains in AF, the more difficult it may be to convert the rhythm, and the greater is the risk for thrombus formation and embolization. Treatable underlying conditions such as electrolyte disturbances or pain should be corrected while specific pharmacologic therapy is being instituted. Paroxysmal supraventricular tachycardia (uncommon in this setting) can be abolished or converted to sinus rhythm by intravenous adenosine, and atrial flutter can sometimes be converted by overdrive atrial pacing with temporary wires placed at the time of operation. Electrical cardioversion may be needed if hypotension is caused by the rapid HR; however, atrial arrhythmias tend to recur in this setting. Rate control for AF or atrial flutter can be achieved with various atrioventricular (AV) nodal blocking drugs, and conversion is facilitated by many of these drugs as well. Table 30.2 summarizes the various treatment modalities for supraventricular arrhythmias. If conversion to sinus rhythm does not occur, electrical cardioversion in the presence of antiarrhythmic drug therapy should be attempted, or anticoagulation should be started.

Preload Assessment of preload is probably the single most important clinical skill for managing hemodynamic instability. Preload rapidly changes in the postoperative period because of bleeding, spontaneous diuresis, vasodilation during warming, the effects of positivepressure ventilation and PEEP on venous return, capillary leak, and other causes. 764

Treatment

Specificsa

Indications

Overdrive pacing by atrial wiresb Adenosine

Requires rapid pacer (≤800/ min); start above arrhythmia rate and slowly decrease Bolus dose of 6–12 mg; may cause 10 s of complete heart block 150 mg IV over 10 min, followed by infusion

PAT, atrial flutter

Amiodarone β-Blockade

Ibutilide

Esmolol, up to 0.5 mg/kg load over 1 min, followed by infusion if tolerated Metoprolol, 0.5–5 mg, repeat effective dose q4–6h Propranolol, 0.25–1 mg; repeat effective dose q4hc Labetalol, 2.5–10 mg; repeat effective dose q4hc Sotalol, 40–80 mg PO q12h 1 mg over 10 min; may repeat after 10 min

Verapamil Diltiazem

2.5–5 mg IV, repeated PRNc 0.2 mg/kg over 2 min, followed by 10–15 mg/hd

Procainamide

50 mg/min up to 1 g, followed by 1–4 mg/min

Digoxinf

Load of 1 mg in divided doses over 4–24 hg; may give additional 0.125-mg doses 2 h apart (3–4 doses) 50–300 J (external); most effective with anteriorposterior patches

Synchronized cardioversion

AV nodal tachycardia, bypass-tract arrhythmia, atrial arrhythmia diagnosis Rate control or conversion to NSR in atrial fibrillation or flutter Rate control or conversion to NSR in atrial fibrillation or flutter Rate control or conversion to NSR in atrial fibrillation or/ flutter

Postoperative Cardiovascular Management

Table 30.2  Treatment Modalities for Supraventricular Arrhythmias

Conversion of atrial fibrillation or flutter to NSR Conversion of PAT to NSR Rate control or conversion to NSR in atrial fibrillation or flutter Rate control or conversion to NSR in atrial fibrillation or flutter Rate control or conversion to NSR in atrial fibrillation or flutter, prevention of recurrence of arrhythmias, treatment of wide-complex tachycardiase Rate control or conversion to NSR in atrial fibrillation or flutter Acute tachyarrhythmia with hemodynamic compromise (usually atrial fibrillation or flutter)

a See specific drug monographs for full descriptions of indications, contraindications, and dosages. Doses are for intravenous administration; use the lowest dose, and administer slowly in patients with hemodynamic compromise. b Verify that the pacer is not capturing the ventricle. c Infusion may provide better control. This drug is less useful than diltiazem because of myocardial depression. d Limited experience; may cause less hypotension than verapamil. e When diagnosis is unclear (ventricular versus supraventricular) and no acute hemodynamic compromise is present (ie, cardioversion not indicated). f Less useful than other drugs because of its slow onset and modest effect. g Rate of administration depends on the urgency of rate control. AV, Atrioventricular; IV, intravenously; NSR, normal sinus rhythm; PAT, paroxysmal atrial tachycardia; PO, orally; PRN, as needed.

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Direct assessment of preload is clinically feasible using echocardiography. A fairto-good correlation exists between echocardiographic and radionuclide measures of end-diastolic volume and a good correlation between end-diastolic area measured by TEE and SV. Although the use of echocardiography to assess preload must always be tempered by the realization that the clinician is viewing a two-dimensional image of a three-dimensional object, this is the most direct technique clinically available. Greater awareness of the value of TEE in the ICU and increased availability of echocardiography in general have made this modality a first choice for the assessment of preload in the setting of acute unexplained or refractory hypotension. Without echocardiography, pressure measurements are used as surrogates for volume measurements. For example, in the absence of mitral valve disease, left atrial pressure (LAP) is almost equal to LV end-diastolic pressure (LVEDP), and pulmonary artery occlusion pressure (PAOP) is almost equivalent to these two pressures. In patients without LAP catheters, the PAOP or the pulmonary artery diastolic pressure is used. When ventricular compliance is normal and the ventricle is not distended, small changes in end-diastolic volume are usually accompanied by small changes in enddiastolic pressure. In patients with noncompliant ventricles from preexisting congestive heart failure (HF), chronic hypertrophy resulting from hypertension or valvular disease, postoperative MI, or ventricular dysfunction, small increases in ventricular volume may produce rapid increases in end-diastolic pressure that require therapeutic intervention. Increased intraventricular pressure elevates myocardial oxygen demand (Mv̇ O2) and decreases subendocardial coronary artery blood flow. Myocardial ischemia may be the result. Elevations in LVEDP are transmitted to the pulmonary circulation, thus causing congestion and possibly hydrostatic pulmonary edema.

Contractility

VI

Quantifying the contractility of the intact heart has been complicated by the difficulty of finding a variable to measure contractility that is also independent of preload and afterload. Therapy for decreased contractility should be directed toward correcting any reversible causes, such as myocardial depressants, metabolic abnormalities, or myocardial ischemia. If the cause of depressed myocardial contractility is irreversible, positive inotropic agents may be necessary to keep CO satisfactory to support organ function.

Afterload Calculated SVR continues to be used in guiding therapy or drawing conclusions about the state of the circulation. This should be done only cautiously, if at all. SVR is not a complete indicator of afterload. Even if SVR were an accurate measure of impedance, the response to vasoactive agents depends on the coupling of ventricular-vascular function, not on impedance alone. Hemodynamic therapy should be guided based on the primary variables, BP and CO. If preload is appropriate, conditions of both low BP and low CO are treated with an inotropic drug. If BP is acceptable (and preload appropriate) but CO is low, a vasodilator alone or in combination with an inotropic drug is used. If the patient is hypertensive (with low CO), vasodilators are indicated; if the patient is vasodilated (low BP and high CO), vasoconstrictors are employed (Table 30.3).

POSTOPERATIVE HYPERTENSION Hypertension has been a common complication of cardiac surgical procedures, and it was reported to occur in 30% to 80% of patients. The current population of older, 766

Blood Pressure

Cardiac Output

Treatment

Low Normal High Low

Low Low Low High

Inotrope Vasodilator with or without inotrope Vasodilator Vasopressor

Table 30.4  Novel Vasodilators Drug

Mechanism of Action

Half-Life

Nicardipine Clevidipine Fenoldopam Nesiritide Levosimendan

Calcium channel blocker Calcium channel blocker Dopamine1-agonist Brain natriuretic agonist K+ATP channel modulator

Intermediate Ultrashort Ultrashort Short Intermediate

Postoperative Cardiovascular Management

Table 30.3  Hemodynamic Therapy Guidelines

K+ATP , Adenosine triphosphate–sensitive potassium channel.

sicker patients appears to have fewer problems with hypertension than with low-output syndromes or vasodilation. Although hypertension most commonly occurs in patients with normal preoperative ventricular function, following aortic valve replacement or with a previous history of increased BP, any patient may develop hypertension. Multiple reasons contribute to postoperative hypertension, including preoperative hypertension, preexisting atherosclerotic vascular disease, awakening from general anesthesia, increases in endogenous catecholamines, activation of the plasma renin-angiotensin system, neural reflexes (eg, heart, coronary arteries, great vessels), and hypothermia. Arterial vasoconstriction with various degrees of intravascular hypovolemia is the hallmark of perioperative hypertension. The hazards of untreated postoperative hypertension include depressed LV performance, increased Mv̇ O2, cerebrovascular accidents, suture line disruption, MI, rhythm disturbances, and increased bleeding. Historically, therapy for hypertension in cardiac surgery was sodium nitroprusside because of its rapid onset and short duration of action. With multiple vasodilators available in the current era, sodium nitroprusside is no longer the drug of choice. Many pharmaceutical alternatives to nitroprusside are available for treating hypertension after cardiac surgical procedures, including nitroglycerin, β-adrenergic blockers, and the mixed α- and β-adrenergic blocker labetalol. Direct-acting vasodilators, dihydropyridine calcium channel blockers (eg, nicardipine, isradipine, clevidipine), angiotensin-converting enzyme inhibitors, and fenoldopam (a dopamine1 [D1] receptor agonist) also have been used. Novel therapeutic approaches are listed in Table 30.4. Dihydropyridine calcium channel blockers are particularly effective in cardiac surgical patients because these drugs relax arterial resistance vessels without negative inotropic actions or effects on AV nodal conduction and provide important therapeutic options. Dihydropyridines are arterial-specific vasodilators of peripheral resistance arteries that cause generalized vasodilation, including the renal, cerebral, intestinal, and coronary vascular beds. In doses that effectively reduce BP, the dihydropyridines have little or no direct negative effect on cardiac contractility or conduction. Nicardipine 767

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Postoperative Care

is an important therapeutic agent to consider because of its lack of effects on vascular capacitance vessels and preload in patients after cardiac operations. The pharmacokinetic profile of nicardipine suggests that effective administration requires variable-rate infusions when trying to treat hypertension because of the half-life of 40 minutes. If even faster control of BP is essential, a dosing strategy consisting of a loading bolus or a rapid infusion dose with a constant-rate infusion may be more efficient. The effect of nicardipine may persist even though the infusion is stopped. Clevidipine, an ultrashort-acting dihydropyridine approved in 2008 in the United States for clinical use, has a half-life of only minutes; this drug represents an important alternative to nitroprusside.

POSTOPERATIVE VASODILATION Vasodilation and a need for vasoconstrictor support are relatively frequent complications of cardiac surgical procedures, with and without CPB. Vasodilation alone should be associated with a hyperdynamic circulatory state manifesting as systemic hypotension in association with an increased CO (and a low calculated SVR). More commonly after cardiac operations, a combination of vasodilation and myocardial dysfunction occurs, requiring vasoconstrictor and inotropic therapy. Vasoplegic syndrome requires high doses of vasoconstrictors, and occurs after off-pump and on-pump surgical procedures. While underlying causes are being sought and treated, the therapeutic approach to systemic vasodilation includes intravascular volume expansion, α-adrenergic agents, and vasopressin. Administration of vasoconstrictors for more than a brief period must be guided by measures of cardiac performance because restoration of BP may camouflage a low-output state.

CORONARY ARTERY SPASM

VI

Coronary artery or internal mammary artery vasospasm can occur postoperatively. Mechanical manipulation and underlying atherosclerosis of the native coronary circulation and the internal mammary artery have the potential to produce transient endothelial dysfunction. The endothelium is responsible for releasing endothelium-derived relaxing factor (EDRF), which is nitric oxide (NO), a potent endogenous vasodilator substance that preserves normal endogenous vasodilation. Thromboxane can be liberated by heparin-protamine interactions, CPB, platelet activation, or anaphylactic reactions to produce coronary vasoconstriction. Calcium administration, increased α-adrenergic tone from vasoconstrictor administration (especially in bolus doses), platelet thromboxane liberation, and calcium channel blocker withdrawal represent added reasons that may put the cardiac surgical patient at risk for spasm of native coronary vessels and arterial grafts. The therapy of choice remains empiric. Nitroglycerin is a first-line drug, but nitrate tolerance can occur. Phosphodiesterase (PDE) inhibitors represent newer approaches to this problem and have been reported to be effective. Intravenous dihydropyridine calcium channel blockers are also important therapeutic considerations. The radial artery is still used by some surgeons as a bypass conduit for revascularization. This conduit was abandoned by some groups because of its propensity to spasm. However, techniques developed in the use of the internal mammary artery have been applied to the radial artery, as well as prophylactic use of calcium channel blocker infusions. Which components of this approach are responsible for the reported success 768

DECREASED CONTRACTILITY Drugs that increase contractility all augment calcium mobilization from intracellular sites to and from the contractile proteins or sensitize these proteins to calcium. Catecholamines, through β1-receptor stimulation in the myocardium, increase intracellular cyclic adenosine monophosphate (cAMP). This second messenger increases intracellular calcium and thus improves myocardial contraction. Inhibition of the breakdown of cAMP by PDE inhibitors increases intracellular cAMP independent of the β-receptor. The “calcium sensitizers” constitute a newer class of inotropic agents. One drug in this class, levosimendan, is already available in certain countries and is currently being evaluated in the United States (Box 30.2).

Postoperative Cardiovascular Management

are not known, but use of a calcium channel blocking drug is recommended by many surgeons. The arterial selectivity of the dihydropyridine drugs (eg, nicardipine) should be an advantage in this setting.

Catecholamines The catecholamines used postoperatively include dopamine, dobutamine, epinephrine, norepinephrine, and isoproterenol (Box 30.3). These drugs have various effects on α- and β-receptors and therefore various effects on HR, rhythm, and myocardial

BOX 30.2

Pharmacologic Approaches for Perioperative Ventricular Dysfunction

Inotropic Agents • Catecholamines • Phosphodiesterase inhibitors • Levosimendan

30

Vasodilator Therapy • • • •

Pulmonary vasodilators Phosphodiesterase inhibitors (milrinone, sildenafil) Inhaled nitric oxide Prostaglandins (PGI2, PGE1, iloprost, and derivatives)

BOX 30.3 

Disadvantages of Catecholamines

Increased myocardial oxygen consumption Tachycardia Arrhythmias Excessive peripheral vasoconstriction Coronary vasoconstriction β-Receptor downregulation and decreased drug efficacy

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Postoperative Care

Table 30.5  Catecholamines Used Postoperatively Drug

Infusion Dose (µg/kg per min) a,b

Dopamine Dobutamineb Epinephrinec Norepinephrinec Isoproterenolc

2–10 2–10 0.03–0.20 0.03–0.20 0.02–0.10

a Less than 2 µg/kg per minute predominantly “dopaminergic” (renal and mesenteric artery dilatation). b If 10 µg/kg per minute is ineffective, change to epinephrine or norepinephrine. c Dose to effect; may require higher dose than indicated.

metabolism. Dosing recommendations for the catecholamines are provided in Table 30.5. Isoproterenol Isoproterenol is a potent β1-agonist in the heart and a β2-agonist in the periphery. Its positive inotropic effect is accompanied by an increase in HR and a propensity for arrhythmias. In patients with coronary artery disease, tachycardia and associated peripheral vasodilation increase Mv̇ O2 and decrease coronary perfusion pressure. In patients with bradycardias in whom pacing is not an immediate or practical option or in those in whom increased HR is desirable (eg, cardiac transplant recipients, patients with regurgitant valvular lesions), isoproterenol has long been used for this purpose, but increasingly dobutamine is used. Epinephrine

VI

Epinephrine is a potent adrenergic agonist with the desirable feature that, in low doses (<3 µg/min), β1 and β2 effects predominate. As the dose is increased, α effects (eg, vasoconstriction) and tachycardia occur. However, in the acutely failing heart postoperatively, only drugs such as epinephrine or norepinephrine provide positive inotropy and perfusion pressure. These features and its low cost make epinephrine a common first-line drug in the postoperative setting. Despite what is often stated in older literature, epinephrine causes less tachycardia than dopamine or dobutamine at equivalent inotropic doses. Because of the metabolic actions of α2 stimulation, epinephrine infusion can cause hyperglycemia and increased serum lactate levels. Norepinephrine Norepinephrine, which has potent β1- and α-receptor effects, preserves coronary perfusion pressure while not increasing HR, actions that are favorable to the ischemic, reperfused heart. When norepinephrine is used alone without a vasodilator or PDE inhibitor, the potent α1 effects may have variable effects on CO. Ventricular filling pressures usually increase when this drug is given because of constriction of the capacitance vessels. Administration of a vasodilator, including the PDE inhibitors, with norepinephrine may partially oppose the vasoconstriction. End-organ ischemia would appear to be unlikely if CO can be preserved at normal levels when norepinephrine is given. PDE inhibitors in combination with norepinephrine attenuate the arterial vasoconstrictive effects. 770

A precursor of norepinephrine, dopamine probably achieves its therapeutic effects by releasing myocardial norepinephrine or preventing its reuptake, especially in high doses. This indirect action may result in reduced effectiveness when dopamine is given to patients with chronic HF or shock states because the myocardium becomes depleted of norepinephrine stores. In contrast to dobutamine, the α-agonist properties of dopamine cause increases in pulmonary artery pressure (PAP), pulmonary vascular resistance (PVR), and LV filling pressure. At doses higher than 10 µg/kg per minute, tachycardia and vasoconstriction become the predominant actions of this drug. Tachycardia is a consistent side effect, and in patients with cardiogenic shock, dopamine has been shown to increase mortality rates. Dobutamine In contrast to dopamine, dobutamine shows mainly β1-agonist properties, with decreases in diastolic BP and sometimes systemic BP observed. Dobutamine is functionally similar to isoproterenol, with less tendency to induce tachycardia in the postoperative setting, although it is often infused at doses up to 40 µg/kg per minute to increase HR as part of a dobutamine stress echocardiographic evaluation. The favorable actions of dobutamine may be limited if tachycardia develops, and, as with dopamine, the inotropic potency of dobutamine is modest in comparison with that of epinephrine or norepinephrine.

Postoperative Cardiovascular Management

Dopamine

Phosphodiesterase Inhibitors The PDE inhibitors are nonglycosidic, nonsympathomimetic drugs that have positive inotropic effects independent of the β1-adrenergic receptor and unique vasodilatory actions independent of endothelial function or nitrovasodilators. Patients with HF have downregulation of the β1-receptor, with a decrease in receptor density and altered responses to catecholamine administration. Milrinone, amrinone, and enoximone bypass the β1-receptor and increase intracellular cAMP by selective inhibition of PDE fraction III (ie, fraction IV), a cAMP-specific PDE enzyme. In vascular smooth muscle, these agents cause vasodilation in the arterial and capacitance beds. PDE inhibitors increase CO, decrease PAOP, and decrease SVR and PVR in patients with biventricular dysfunction, and they are important therapeutic agents in postoperative cardiac surgical patients. Sildenafil and other PDE 5 inhibitors are also increasingly used for pulmonary hypertension. PDE III inhibitors have a clinical effect as inodilators; they produce dilation of arterial and venous beds and decrease the mean arterial pressure (MAP) and central filling pressures. Increases in CO are induced by multiple mechanisms, including afterload reduction and positive inotropy, but not by increasing HR. The net effect is a decrease in myocardial wall tension, representing an important contrast to most sympathomimetic agents. Catecholamine administration often needs the simultaneous administration of vasodilators to reduce ventricular wall tension. Milrinone and other PDE inhibitors also have unique mechanisms of vasodilation that may be favorable for coronary artery and internal mammary artery flow (Box 30.4). Milrinone is a bipyridine derivative with inotropic activity that is almost 20 times more potent than that of amrinone and a shorter half-life. Milrinone is an effective inodilator for patients with decompensated HF and low CO after cardiac surgical procedures. Suggested administration of milrinone is a loading dose of 50 µg/kg over 10 minutes, followed by an infusion of 0.5 µg/kg per minute (0.375–0.75 µg/kg per min). By using slower loading doses, high peak concentrations can be prevented, and the vasodilation that is observed with rapid loading can be attenuated. 771

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BOX 30.4 

Advantages of Preemptive Phosphodiesterase Inhibitor Administration

Increased myocardial contractility (left and right ventricles) Pulmonary vasodilation Resolution and prevention of ischemia Minimal drug side effects during cardiopulmonary bypass Dilation of internal mammary artery Avoidance of mechanical intervention Prevention of “failed weaning”

Levosimendan Levosimendan is a calcium-sensitizing drug that exerts positive inotropic effects by sensitization of myofilaments to calcium and vasodilation through opening of ATPdependent potassium channels on vascular smooth muscle. These effects occur without increasing intracellular cAMP or calcium and without an increase in Mv̇ O2 at therapeutic doses. As would be expected with an inodilator, the hemodynamic effects include a decrease in PAOP in association with an increase in CO. β-Blockade does not block the hemodynamic effects of this drug. Levosimendan itself has a short elimination half-life, but it has active metabolites with elimination half-lives up to 80 hours. A study in patients with decompensated HF found that hemodynamic improvements at 48 hours were similar whether patients received the drug for 24 hours or 48 hours. Increasing plasma levels of the active metabolite were found for 24 hours after the drug infusion was stopped. Levosimendan is approved in many European countries and is currently undergoing a cardiac surgical trial for use in the United States.

RIGHT-SIDED HEART FAILURE VI

HF after cardiac surgical procedures usually results from LV impairment. Although an isolated right-sided MI can occur perioperatively, most perioperative inferior MIs show variable involvement of the right ventricle. The myocardial preservation techniques that are best for the left ventricle may not offer ideal right ventricular (RV) protection because the right ventricle is thin-walled and more exposed to body and atmospheric temperature. Cardioplegic solution given through the coronary sinus (retrograde) may not reach parts of the right ventricle because of positioning of the cardioplegia cannula in relation to the venous outflow from this chamber and because the thebesian veins do not drain into the coronary sinus. Impairment of RV function postoperatively is more severe and persistent when preoperative right coronary artery stenosis is present. Although depression of the ejection fraction (EF) is compensated by preload augmentation, right ventricular ejection fraction (RVEF) cannot be preserved if coronary perfusion pressure is reduced or impedance to ejection is increased. Certain aspects of the physiology of the right ventricle make it different from the left ventricle. Normally, the RV free wall receives its blood flow during systole and diastole; however, systemic hypotension or increased RV systolic and diastolic pressures may cause supply-dependent depression of contractility when Mv̇ O2 is increased while coronary perfusion pressure is decreased. The normal thin-walled right ventricle 772

Diagnosis

Postoperative Cardiovascular Management

is at least twice as sensitive to increases in afterload as is the left ventricle. Relatively modest increases in outflow impedance from multiple causes in the postoperative period can exhaust preload reserve and cause a decrease in RVEF with ventricular dilation. RV pressure overload may be complicated by volume overload caused by functional tricuspid regurgitation. Decreases in RV SV reduce LV filling, and dilation of the right ventricle can cause a leftward shift of the interventricular septum that interferes with diastolic filling of the left ventricle (ie, ventricular interaction) (Fig. 30.3). A distended right ventricle limited by the pericardial cavity further decreases LV filling. RV failure has the potential to affect LV performance by decreasing pulmonary venous blood flow, decreasing diastolic distending pressure, and reducing LV diastolic compliance. The resulting decrease in LV output further impairs RV pump function. The mechanical outcomes of RV failure in postoperative cardiac surgical patients are depicted in Fig. 30.4. It can therefore be appreciated how, once established, RV failure is self-propagating, and aggressive treatment interventions may be needed to interrupt the vicious cycle.

In the postoperative cardiac surgical patient, a low cardiac index with right atrial pressure (RAP) increased disproportionately compared with changes in left-sided filling pressures is highly suggestive of RV failure. The PAOP may also increase because of ventricular interaction, but the relationship of RAP with PAOP stays close to or higher than 1.0. The absence of a step-up in pressure in going from the right atrium

Pulmonary afterload

RV Poor RV RCA air perfusion protection embolism

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RV failure

Blood pressure

Septal shift

LV return

RV failure Fig. 30.3  Sequence inducing right ventricular failure and causing a downward spiral of events. LV, Left ventricular; RCA, right coronary artery; RV, right ventricular.

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Postoperative Care

Decreased systemic Increased intrapericardial pressure venous return Opening of PFO with R → L shunt LA

RA

Decreased PV return

Tricuspid regurgitation Displaced septum LV RV Dilated RV

Compressed LV

Fig. 30.4  Mechanical changes produced by acute right ventricular failure. LA, Left atrium; LV, left ventricle; PFO, patent foramen ovale; PV, pulmonary venous; R → L, right-to-left; RA, right atrium; RV, right ventricle.

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to the pulmonary artery (mean), provided PVR is low, suggests that RV failure is severe and the right side of the heart is acting only as a conduit. This hemodynamic presentation is typical of cardiogenic shock associated with RV infarction. The venous waveforms are accentuated with a prominent Y descent similar to findings in constrictive pericarditis, thus suggesting reduced RV compliance. Large V waves may also be discernible and may relate to tricuspid regurgitation. Echocardiography allows qualitative interpretation of RV size, contractility, and configuration of the interventricular septum, and it can enable the clinician to provide a definitive diagnosis of RV dysfunction or RV failure. Because of the crescent shape of the right ventricle, volume determination is not easy, but the qualitative examination and assessment for tricuspid regurgitation are very valuable. TEE is also useful to determine whether the increased RAP opens a patent foramen ovale, thus producing a right-to-left shunt. This is important because traditional methods to treat hypoxemia such as PEEP and larger tidal volumes in this setting will only increase the afterload of the right ventricle and potentially increase the shunt and hypoxemia.

Treatment Treatment approaches in postoperative RV failure may differ from those used in LV failure, and they are affected by the presence of pulmonary hypertension (Box 30.5). In all cases, preload should be increased to the upper range of normal; however, the Frank-Starling relationship is flat in RV failure and, to avoid ventricular dilation, the CO response to an increasing CVP should be determined. Volume loading should be stopped when the CVP exceeds 10 mm Hg and the CO does not increase despite increases in this pressure. The CVP should not be permitted to exceed the PAOP because, if these pressures equalize, any increase obtained in pulmonary blood flow will be offset by decreased diastolic filling of the left ventricle by ventricular interdependence. The atrial contribution to RV filling is important when the ventricle is dilated and noncompliant. Maintenance of sinus rhythm and use of atrial pacing are important components of treating postoperative RV failure. 774

Postoperative Cardiovascular Management

BOX 30.5 

Treatment Approaches in Postoperative Right-Sided Heart Failure

Preload Augmentation • Volume, vasopressors, or leg elevation (CVP/PCWP <1) • Decrease juxtacardiac pressures (pericardium and/or chest open) • Establishment of atrial kick and treatment of atrial arrhythmias (sinus rhythm, atrial pacing)

Afterload Reduction (Pulmonary Vasodilation) • • • • •

Nitroglycerin, isosorbide dinitrate nesiritide cAMP-specific phosphodiesterase inhibitors, α2-adrenergic agonists Inhaled nitric oxide Nebulized PGI2 Intravenous PGE1 (and left atrial norepinephrine)

Inotropic Support • cAMP-specific phosphodiesterase inhibitors, isoproterenol, dobutamine • Norepinephrine • Levosimendan

Ventilatory Management • Lower intrathoracic pressures (tidal volume <7 mL/kg, low PEEP) • Attenuation of hypoxic vasoconstriction (high FIO2) • Avoidance of respiratory acidosis (PaCO2 30–35 mm Hg, metabolic control with meperidine or relaxants)

Mechanical Support • Intraaortic counterpulsation • Pulmonary artery counterpulsation • Right ventricular assist devices cAMP, Cyclic adenosine monophosphate; CVP/PCWP, central venous pressure/pulmonary capillary wedge pressure; FIO2, fraction of inspired oxygen; PaCO2, partial pressure of arterial carbon dioxide; PEEP, positive end-expiratory pressure; PGI2, prostaglandin I2; PGE1, prostaglandin E1.

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Although vasodilators may lead to cardiovascular collapse in patients with RV infarction (as a result of decreases in RV filling and coronary perfusion), postoperative RV failure is often associated with increased PVR and pulmonary hypertension. In this context, attempts to decrease RV outflow impedance may be worthwhile. Intravenous vasodilators invariably reduce systemic BP and mandate the simultaneous administration of a vasoconstrictor. One way to reduce the pulmonary effects of the needed vasoconstrictor is to administer the vasoconstrictor through a left atrial (LA) catheter and treat RV dysfunction with intravenous prostaglandins and LA norepinephrine. The PDE inhibitors are commonly used for their effect on the pulmonary vasculature and RV function. Interest in and availability of aerosolized pulmonary vasodilators have increased. This route of administration reduces or even abolishes undesirable systemic vasodilation. Delivery of the drug directly to the alveoli improves pulmonary blood flow to these alveoli and potentially improves oxygenation by better matching blood flow to ventilation. Three drugs have been used: NO, PGI2 (ie, epoprostenol or prostacyclin), and milrinone. 775

Postoperative Care

NO is an important signaling molecule throughout the body. In the lung, it rapidly diffuses across the alveolar-capillary membrane and activates soluble guanylate cyclase, thereby leading to smooth muscle relaxation by several mechanisms. Inhaled NO is given through a specialized delivery system in a concentration of 5 to 80 parts/million. It is commercially available in the United States, but it is costly. NO has been used successfully to treat RV dysfunction associated with pulmonary hypertension after heart operations, mitral valve replacement, cardiac transplantation, and placement of LV assist devices (LVADs). An intraaortic balloon pump may be of great benefit, even in patients with a right ventricle that is mainly responsible for circulatory decompensation. This beneficial effect is mediated by increased coronary perfusion. Right-sided heart assist devices have a place as temporizing measures in severe intractable right-sided HF. Pulmonary artery counterpulsation is experimental, and its clinical role is uncertain. In cases of severe RV failure it may be necessary to leave the sternum open or to reopen the chest if it has been closed. This approach decreases the tamponadelike compression of the left ventricle by the distended right ventricle, right atrium, and edematous mediastinal tissues.

Effects of Mechanical Ventilation in Heart Failure

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HF at the time of a surgical procedure has been identified as a significant predictor of postoperative respiratory complications. Maintenance of gas exchange in these situations usually mandates prolonged ventilatory support. Besides improving PaO2, mechanical ventilation can influence DO2 through its effects on CO. Suppression of spontaneous respiratory efforts may substantially decrease the work of breathing and improve the oxygen supply-demand relationship. Traditionally, the influence of mechanical ventilation on hemodynamics has been viewed as negative. The unavoidable rise in intrathoracic pressure caused by positive-pressure ventilation or PEEP is associated with decreased CO. However, in the presence of HF or myocardial ischemia, raised intrathoracic pressure has the potential to affect the determinants of global cardiac performance favorably. Understanding these heart-lung interactions is essential for the integrated management of the ventilated patient with HF after cardiac operations. The effects of ventilation on RV and LV failure must receive independent consideration. Raised intrathoracic pressure may significantly improve LV performance as a result of the reduced transmural pressure needed to give an acceptable systemic BP. This pressure can be viewed as afterload reduction, a favorable effect separate from the resistance to venous return that may also help such patients. Clinically significant improvements in cardiac function have been documented in patients ventilated for cardiogenic respiratory failure produced by myocardial ischemia and after CABG operations. High LV filling pressures may help identify a subgroup benefiting from reduced afterload with increased intrathoracic pressure. The circulatory responses to changes in ventilation should always be assessed in patients with cardiac disease; the goal of improving or maintaining DO2 must be kept in mind. This usually requires measurement of arterial oxygenation and CO. In RV and biventricular failure the increase in the airway pressure caused by ventilatory support should be kept at a minimum compatible with acceptable gas exchange. This means avoidance of high levels of PEEP and trials of decreased inspiratory times, flow rates, and tidal volumes. Breathing modes that emphasize spontaneous efforts such as intermittent mandatory ventilation, pressure support, or CPAP should be considered. Alternatively, if isolated LV failure is the reason for ventilatory therapy, improvements in cardiac performance may be achieved by positive-pressure ventilation with PEEP. In particular, patients with increased LV filling pressures, mitral regurgitation, 776

Effects of Ventilatory Weaning on Heart Failure Traditional criteria for weaning of ventilatory support assess the adequacy of gas exchange and peak respiratory muscle strength. In the patient with HF, the response of global hemodynamics to spontaneous respirations must also be considered. The changes of the loading conditions of the heart brought about by resuming spontaneous ventilation can induce a vicious cycle resulting in hypoxemia and pulmonary edema. Pulmonary congestion, often present in patients with LV dysfunction, decreases pulmonary compliance. Thus large decreases in inspiratory intrathoracic pressure are needed to cause satisfactory lung inflation. These negative swings of intrathoracic pressure increase venous return. Increased diaphragmatic movements may raise intraabdominal pressure and further increase the pressure gradient for venous return. Decreased intrathoracic pressure also raises the ventricular transmural pressures and the impedance to ventricular emptying. The increased afterload causes further increases in preload, and these changes jeopardize the myocardial oxygen balance. Accordingly, worsening of myocardial ischemia as shown by ST-segment deviations was demonstrated when ventilatory support was removed in patients ventilated after MI.

Postoperative Cardiovascular Management

and reversible ischemic dysfunction may improve from afterload reduction related to increased airway and intrathoracic pressures.

CARDIAC TAMPONADE Cardiac tamponade is an important cause of the low-CO state after cardiac operations and occurs when the heart is compressed by an external agent, most commonly blood accumulated in the mediastinum. Hemodynamic compromise, to some degree attributable to the constraining effect of blood accumulating within the chest, is often observed in the 3% to 6% of patients needing multiple blood transfusions for hemorrhage after cardiac surgical procedures. Postoperative cardiac tamponade usually manifests acutely during the first 24 hours postoperatively, but delayed tamponade may develop 10 to 14 days after the operation, and it has been associated with postpericardiotomy syndrome or postoperative anticoagulation. The mechanism of hemodynamic deterioration during cardiac tamponade is the result of impaired filling of one or more of the cardiac chambers. As the external pressure on the heart increases, the distending or transmural pressure (external intracavitary pressure) is decreased. The intracavitary pressure increases in compensation lead to impaired venous return and elevation of the venous pressure. If the external pressure is high enough to exceed the ventricular pressure during diastole, diastolic ventricular collapse occurs. These changes have been documented in the right and the left sides of the heart after cardiac surgical procedures. As the end-diastolic volume and end-systolic volume decrease, a concomitant reduction in SV occurs. In the most severe form of cardiac tamponade, ventricular filling occurs only during atrial systole. Adrenergic and endocrine mechanisms are activated in an effort to maintain venous return and perfusion pressure. Intense sympathoadrenergic activation increases venous return by constricting venous capacitance vessels. Tachycardia helps maintain CO in the presence of reduced SV. Adrenergic mechanisms may explain decreased urinary output and sodium excretion, but these phenomena may also be caused by reduced CO or a reduction in atrial natriuretic factor from decreased distending pressure of the atria. The diagnosis of cardiac tamponade depends on a high degree of suspicion. Tamponade after cardiac surgical procedures is a clinical entity distinct from the 777

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tamponade typically seen in medical patients in whom the pericardium is intact and the heart is surrounded by a compressing fluid. In the setting of cardiac surgery, the pericardial space is often left open and in communication with one or both of the pleural spaces, and the compressing blood is at least in part in a clotted, nonfluid state and able to cause localized compression of the heart. Serious consideration should be given to the possibility of tamponade after cardiac surgical procedures in any patient with an inadequate or worsening hemodynamic status, as evidenced by hypotension, tachycardia, increased filling pressures, or low CO, especially when chest tube drainage has been excessive. A more subtle presentation of postoperative tamponade is characterized by gradually increasing needs for inotropic and pressor support. Many of the classic signs of cardiac tamponade may not be present in these patients, partly because the patients are usually sedated and ventilated, but also because the pericardium is usually left open, resulting in a more gradual increase in the restraining effects of blood accumulation. Patients may have localized accumulations that affect one chamber more than another. The classic findings of elevated CVP or equalization of CVP, pulmonary artery diastolic pressure, and PAOP may not occur. It may therefore be difficult in the presence of declining CO and elevated filling pressures to distinguish tamponade from biventricular failure. A useful clue may be the pronounced respiratory variation in BP with mechanical ventilation in association with high filling pressures and low CO because the additional external pressure applied to the heart by positivepressure ventilation may further impair the already compromised ventricular filling in the presence of tamponade. Echocardiography may provide strong evidence for the diagnosis of cardiac tamponade. Echolucent crescents between the RV wall and the pericardium or the posterior LV wall and the pericardium are visible with TTE or TEE. Echogenicity of grossly bloody pericardial effusions, especially when clots have been formed, may sometimes make delineation of the borders of the pericardium and the ventricular wall difficult, thus compromising the sensitivity of this technique. A classic echocardiographic sign of tamponade is diastolic collapse of the right atrium or right ventricle, with the duration of collapse bearing a relationship with the severity of the hemodynamic alteration, but such findings are often absent in patients after cardiac surgical procedures. Often, TTE is difficult because of mechanical ventilation, and TEE is required for satisfactory imaging. The definitive treatment of cardiac tamponade is surgical exploration with evacuation of hematoma. The chest may have to be opened in the ICU if tamponade proceeds to hemodynamic collapse. For delayed tamponade, pericardiocentesis may be acceptable. Medical palliation in anticipation of reexploration consists of reinforcing the physiologic responses that are already occurring while preparing for definitive treatment. Venous return can be increased by volume administration and leg elevation. The lowest tidal volume and PEEP compatible with adequate gas exchange should be used. Epinephrine in high doses gives the needed chronotropic and inotropic boost to the ventricle and increases systemic venous pressures. Sedatives and opioids should be given cautiously because they may interfere with adrenergic discharge and precipitate abrupt hemodynamic collapse. Occasionally, patients develop significant cardiac tamponade without accumulation of blood in the chest. Edema of the heart, lungs, and other tissues in the chest after CPB may not allow chest closure at the first operation, and staged chest closure may be required after the edema has subsided. Similarly, some patients with an inadequate hemodynamic status after cardiac surgical procedures despite maximum support in the ICU improve with opening of the chest because this tamponade effect is relieved. Reclosure of the chest in the operating room is often possible after a few days of continued cardiovascular support and diuresis. 778

Postoperative circulatory control in the heart transplant recipient differs in three major respects from that of the patient who has not received a heart transplant: (1) the transplanted heart is noncompliant, with a relatively fixed SV; (2) acute rejection must be considered when cardiac performance is poor or suddenly deteriorates; and (3) these patients are at risk for acute RV failure if pulmonary hypertension develops. The fixed SV combined with denervation of the donor heart means that maintenance of CO often depends on therapy to maintain an elevated HR (110–120 beats/min). The drug most commonly used is isoproterenol because it is a potent inotropic agent and because it causes a dose-related increase in HR. Its vasodilating β2-adrenergic effect on the pulmonary vasculature may be of benefit if PVR is greater than normal. Alternatively, atrial pacing may be used to maintain HR if contractility appears normal. Pacing is often used to allow the withdrawal of isoproterenol in the first postoperative days. Parasympatholytic drugs, such as atropine, do not have any effect on the transplanted heart. Major concerns in monitoring and therapy for the transplant recipient are the potential for infection and rejection. Immunosuppressive therapy regimens include cyclosporine and usually steroids or azathioprine, or both. These drugs also suppress the patient’s response to infection, and steroid therapy may induce elevations in the white blood cell count, thus further confusing the issue. Protocols for postoperative care stress strict aseptic technique and frequent careful clinical evaluations for infection. Preoperative evaluation helps screen patients with fixed pulmonary hypertension because the normal donor right ventricle may acutely fail if it is presented with an elevated PAP in the recipient. However, patients may have progression of disease between the time of evaluation and operation, or the right ventricle may be inadequately protected during harvest or transport. When separation from CPB is attempted, acute RV dilation and failure occur, and such patients may emerge from the operating room receiving multiple drug therapy, including the inhaled agents NO and prostacyclin, as described earlier, to focus on treating RV dysfunction and/or pulmonary hypertension. Gradual withdrawal of these drugs occurs in the first postoperative days, with close monitoring of PAPs and oxygenation.

ADVANCES IN CARDIOVASCULAR SURGERY AND POSTOPERATIVE MANAGEMENT Advances in cardiothoracic surgery include minimally invasive transcatheter aortic valve replacement (TAVR), the incorporation of echocardiography in the cardiothoracic ICU, and improved biotechnology and durability related to cardiopulmonary support by extracorporeal membrane oxygenation (ECMO). The following section explores these advances and highlights the major postoperative considerations for patients in the cardiothoracic ICU.

Postoperative Management of Complications After Transcatheter Aortic Valve Replacement TAVR is increasingly used in clinical practice and is also described elsewhere. Although the benefits and indications for TAVR are well established, four major clinical challenges have emerged: vascular complications, stroke, paravalvular leak (PVL), and cardiac 779

Postoperative Cardiovascular Management

TRANSPLANTED HEART

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conduction abnormalities. The mechanisms of these intraoperative complications have immediate postoperative consequences and require appropriate management in the ICU. Vascular Complications Major vascular complications are independent predictors of major bleeding, transfusion, end-organ failure, and death. Atherosclerotic disease of the femoral arteries and operator experience are other notable predictors of clinical outcomes. Strategies to minimize vascular injury involve designing smaller and sleeker delivery systems. Major vascular complications are defined as thoracic aortic dissection, distal extremity or noncerebral vascular embolization requiring surgical intervention, and amputation. In addition, irreversible end-organ injury and iatrogenic access-related vascular injuries resulting in death, unplanned intervention, blood transfusion of 4 units or more, or permanent end-organ injury are considered major vascular complications related to TAVR. Access-related vascular injuries included dissection, stenosis, perforation, pseudoaneurysm formation, arteriovenous fistula, hematoma, compartment syndrome, and irreversible nerve injury. Minor vascular complications include distal embolization not requiring surgical intervention or leading to irreversible end-organ damage. The incidence of major and minor vascular complications is 15.3% and 11.9%, respectively, within 30 days of TAVR. Furthermore, the most common major vascular complications were dissection, access-site hematoma, and arteriotomy of the posterior femoral arterial wall. Moreover, major vascular complications significantly increased the risks of major bleeding (and therefore blood transfusions), renal failure requiring continuous renal replacement therapy, and death at 30 days and again at 1 year. Postoperative cardiovascular management of the patient who has undergone TAVR complicated by intraoperative vascular injury includes assessment of the degree of vascular injury as well as continuous monitoring of peripheral arterial pulses (focus on access site), adequate perfusion, development and treatment of end-organ dysfunction, and hemodynamic and hemostatic resuscitation. Stroke

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Asymptomatic cerebral embolism is common during TAVR. Clinically silent cerebral embolism occurs in up to 70% of these patients. Major stroke, however, independently predicts prolonged recovery and increased mortality rates. Identified stroke predictors include history of previous stroke, functional disability, transapical approach, and AF. The long-term effects of asymptomatic cerebral embolism associated with TAVR are unknown. The predictors of stroke early after TAVR include previous stroke, severe arterial atheroma, and a smaller aortic valve area. Patients should be admitted to the ICU after undergoing TAVR and postoperatively monitored for immediate evidence of neurocognitive decline or focal neurologic deficit heralding a major stroke. Neurology consultation and activation of a stroke workup protocol native to the home institution should occur, and neuroimaging should be ordered to direct further clinical management. In the event of a stroke in the ICU, multidisciplinary decision making among physicians and patient care teams should be implemented regarding the initiation of permissive hypertension and procedural intervention. Paravalvular Leak PVL is common and significantly decreases survival. This undersizing is balanced against oversizing and aortic root trauma or rupture, which typically warrants emergency CPB and immediate repair. The formal grading of PVL severity in TAVR is based on its percentage of the circumferential extent of the aortic valve annulus. Further 780

Cardiac Conduction Abnormalities Cardiac conduction disturbances after TAVR are common and important. New-onset AF is defined as an arrhythmia within the hospital stay that has the ECG characteristics of AF and lasts longer than 30 seconds. The types of heart block associated with TAVR may occur anywhere along the cardiac conduction pathway, including first-degree AV block, second-degree AV block (Mobitz I or Mobitz II), third-degree AV block, bundle branch block, and AV block requiring pacemaker insertion. The native aortic valve lies in close proximity to the AV conduction system, a location that puts the ventricular septal conductive system at risk during aortic valve procedures. The basal attachments of the three aortic leaflets form an annulus that separates the aortic root from the LV outflow tract (LVOT). The noncoronary cusp lies adjacent to the membranous portion of the interventricular septum. The superior continuation of the membranous septum is an interleaflet triangle that separates the noncoronary from the right coronary cusp. Both structures, the membranous septum and the interleaflet triangle, are in fibrous continuity and overlie the bundle of His as it extends leftward from the AV node. The left bundle branch traverses below the membranous septum and penetrates superficially to traverse along the LV side of the interventricular septum. The circumferential forces of the bioprosthetic valve in TAVR on the adjacent, underlying cardiac conduction system are believed to be a cause of cardiac conduction disturbances after TAVR. Prompt recognition and proper management of AV blockade remain essential in the management of patients undergoing TAVR because hemodynamically significant heart block after TAVR may be common in selected patients and require permanent pacemaker implantation (PPM). Certainly, in the postoperative ICU setting in the patient who does not have a preoperative pacemaker, new heart block and resulting hemodynamic instability may require swift intervention with transvenous pacing. This temporary measure may be implemented as a bridge to PPM.

Echocardiography in the Cardiothoracic Intensive Care Unit Guidelines outlining basic TEE examinations have facilitated the adaptation of echocardiography in the ICU by intensivists without previous training in this modality. Outlining 11 TEE views that together comprise the full basic TEE perioperative examination: the midesophageal four-chamber view, the midesophageal two-chamber view, the midesophageal long-axis view, the midesophageal ascending aortic long-axis view, the midesophageal ascending aortic short-axis view, the midesophageal aortic valve short-axis view, the midesophageal RV inflow-outflow view, the midesophageal bicaval view, the transgastric midpapillary short-axis view, and the descending aortic long-axis and short-axis views. Additionally, TTE may be particularly useful in the ICU when determining the causes of hemodynamic instability after cardiothoracic operations. In the immediate postoperative period, TTE may yield poor visualization as a result of postoperative change and positioning of support devices. For this reason, TEE is advocated during this early point-of-care setting for definitive and accurate diagnoses of hemodynamic aberrancies. 781

Postoperative Cardiovascular Management

management strategies for PVL include a repositionable valve prosthesis and transcatheter plugging. The immediate postoperative importance of PVL after TAVR relates to the presence of aortic regurgitation in an otherwise noncompliant left ventricle with diastolic dysfunction, as commonly seen with severe aortic stenosis. The cardiothoracic ICU physician should be informed if a post-TAVR patient has moderate or higher degree of PVL because this finding may have consequences for clinical management.

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Miniaturized Transesophageal Echocardiography Probe The use of a miniaturized, monoplane TEE probe (ClariTEE; ImaCor, Uniondale, NY) may provide benefit in the assessment of hemodynamically unstable patients in the cardiothoracic ICU. This probe is capable of performing monoplane views of midesophageal four-chamber, midesophageal ascending aortic short-axis, and transgastric short-axis views. The probe is 5.5 mm in diameter and is approved by the Food and Drug Administration (FDA) to remain indwelling for up to 72 hours; it may connect to the portable ultrasound console. The probe may be disconnected when required from this portable ultrasound machine to facilitate evaluation of other patients with indwelling probes. The ultrasound machine (computer and monitor screen) is small and can be transported into patients’ rooms. The ClariTEE probe uses a relatively high frequency (7 MHz) combined with specialized signal processing software to enhance penetration and contrast resolution. The inability to rotate the ultrasound scan sector, however, makes it difficult to obtain a complete diagnostic ultrasound scan of the cardiovascular structures. Echocardiography During Postoperative Intensive Care Unit Management of Left Ventricular Assist Devices Echocardiography is particularly useful for the postoperative management of patients after LVAD implantation. Assessment of RV function is central to the hemodynamic management of these patients in the immediate postoperative period, and echocardiography may help visualize interventricular septal position, RV systolic function, degree of the tricuspid valve regurgitation, and LV chamber size. TTE typically provides poor visualization of the cardiac chambers postoperatively as a result of inflammation, thoracostomy and mediastinal tubes, and echogenic dropout from the LVAD hardware. RIGHT VENTRICULAR DYSFUNCTION AFTER LEFT VENTRICULAR ASSIST DEVICE PLACEMENT

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Classically, the patient may present to the ICU with central venous access, a PAC, and invasive arterial monitoring. These hemodynamic data alert the ICU physician to aberrancies that may suggest RV dysfunction, venous hypertension, and inadequate LVAD filling and ejection. The use of echocardiography together with these hemodynamic variables allows the immediate titration of pharmacologic support and LVAD speed to optimize CO, right-sided filling pressures, mixed venous oxygenation, RV systolic function, and LV filling. Akin to the TEE examination on separation from CPB in the operating room, the TEE examination in the ICU similarly focuses on the position of the interventricular septum. Equal filling and emptying of both the right ventricle and the left ventricle result in a midline position of the septum. When LVAD flows are relatively higher than the ability of the right ventricle to deliver CO to the left ventricle, the interventricular septum tends to bow toward the left ventricle, thus resulting in an LV “suckdown” effect, RV failure, and increased tricuspid regurgitation (Fig. 30.5A). Tricuspid regurgitation occurs as a result of tricuspid valve annular distortion (Fig. 30.5B). This effect may be somewhat offset by increasing SVR, increasing LV chamber size, and tempering the leftward interventricular septal shift. On occasion, titration of pharmacologic and mechanical support (LVAD settings) is ineffective, and a return to the operating room may be warranted for RV assist device (RVAD) placement. ECHOCARDIOGRAPHY TO RULE OUT OBSTRUCTIVE SHOCK AFTER LEFT VENTRICULAR ASSIST DEVICE PLACEMENT

Increasing right-sided filling pressures, reduced cardiac index, and low mixed venous oxygenation saturation may alert the intensivist to problems with intrinsic RV function, 782

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Fig. 30.5  Left ventricular assist device (LVAD) “suckdown” effect seen by transesophageal echocardiography (TEE) in the cardiothoracic intensive care unit. (A) Midesophageal four-chamber view using TEE to illustrate LVAD suckdown as a result of right ventricular failure and relatively increased and mismatched LVAD flows. (B) Midesophageal four-chamber view with color-flow Doppler illustrating severe tricuspid regurgitation during this suckdown event. LV, Left ventricle; RV, right ventricle. (Courtesy K. Ghadimi, MD.)

Postoperative Cardiovascular Management

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but causes of obstructive shock should be excluded. Invasive hemodynamic monitoring cannot always discern among different causes of poor RV function. However, TEE enables the clinician definitively to diagnose new pericardial effusions, large right-sided pleural effusions, or bleeding resulting in mass compression of the atria and/or ventricles. In the setting of cardiac tamponade physiology, immediate return to the operating room is warranted to relieve mass compression of the involved cardiac chambers. Echocardiography in Patients Requiring Extracorporeal Membrane Oxygenation ECMO is mechanical support of the lungs and/or heart for a period of days to weeks by a modified pulmonary or CPB machine; venovenous (VV) ECMO is primarily used for treating severe but potentially reversible respiratory failure, and venoarterial (VA) ECMO is primarily used for treating severe cardiac or cardiorespiratory failure. With VV ECMO, deoxygenated blood is drained from the inflow cannula placed in a large central vein, typically the inferior vena cava (IVC), and oxygenated blood is returned through a cannula whose tip lies in or close to the right atrium. Ideally, all or most of the blood from the outflow cannula passes through the tricuspid valve into the pulmonary circulation. One single-cannula technique uses a double-lumen single cannula (Avalon Elite Bicaval Dual-Lumen Catheter and Vascular Access Kit, Maquet Cardiopulmonary, Rastatt, Germany), and it is designed for placement in the right internal jugular vein. The tip of the (larger) inflow lumen is situated within the IVC, thus taking care to avoid insertion into a hepatic vein. The inflow lumen has an end hole and side fenestrations at the tip, as well as side holes proximal to the exit site of the inflow lumen that allow drainage from the both the superior vena cava (SVC) and the IVC. The outflow lumen of the single cannula opens 10 cm above the inflow cannula tip and is designed to return blood to the right atrium. Once inserted, the outflow cannula lumen should be positioned inward and toward the tricuspid valve to direct flow through the valve. TEE may be used to illustrate flow within the inflow and outflow cannula lumina and to illustrate position of each limb within the IVC and the right atrium, respectively. During VA ECMO, systemic venous blood drains into the circuit through a cannula placed in the right atrium through either the IVC (femoral approach) or SVC (internal 783

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jugular vein approach). This may be visualized by TEE to establish flow through the cannula and correct positioning. If TEE is contraindicated, TTE may provide utility in selected patients who allow adequate echocardiographic visualization through the chest wall. Akin to VV ECMO, blood passes through the inflow cannula of the VA ECMO circuit into the pump and the oxygenator/heat exchanger before returning to the patient through a cannula placed within or grafted to a large artery (femoral, axillary, or aorta, commonly). Systemic arterial blood flow is the sum of the VA ECMO circuit flow and any ejection from the left ventricle. Systemic BP is determined by flow and vascular tone. Using Echocardiography to Troubleshoot Common Complications of Venoarterial Extracorporeal Membrane Oxygenation

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• North-south syndrome: This syndrome occurs in the specific circumstance of severely impaired lung function in conjunction with femoral placement of the VA ECMO outflow cannula. In this situation, the potential exists for upper body hypoxemia (coronary arteries, cerebral blood vessels, and upper limbs) because proximal branches of the aorta receive predominantly deoxygenated blood ejected from the left heart. This phenomenon of north-south syndrome may be seen on echocardiography as stagnant, “swirling” flow in the descending thoracic aorta as a result of the interface created by blood ejected from the left ventricle and blood returning to the patient from the outflow limb. Even in the presence of significant LV ejection, this situation does not arise if pulmonary function is good or the outflow cannula is transitioned to central placement (proximal aorta or axillary artery). For this reason, institutional practice may dictate transition from peripheral (through the femoral artery) to central (through the aortic or axillary artery) cannulation as soon as the patient is clinically stable enough to handle this transition. Alternatively, after recovery of LV function is confirmed by echocardiography, but lung function continues to suffer, transition to VV ECMO may be initiated. • Hemodynamic instability: Hypotension during “full-flow” VA ECMO and complete circulatory support in the absence of native cardiac function suggests vasodilation or LV distension. LV distension may become particularly problematic in patients with aortic and mitral regurgitation. Clinically, the patient may present with pulmonary edema frothing from the endotracheal tube shortly after institution of VA ECMO and/or ventricular arrhythmia requiring defibrillation. The diagnosis may be confirmed by identifying a severely dilated left ventricle with TEE. Increasing pump flows reduce pulmonary blood flow and can ameliorate the issue. Failing this, the left side of the heart must be vented. Echocardiographic confirmation of LV vent placement is important to ensure that the left ventricle is decompressed and that the risk of developing LV thrombus has been significantly reduced. Weaning and Discontinuing Venoarterial Extracorporeal Membrane Oxygenation An early sign of recovery of myocardial function is the presence of pulsatility on the arterial waveform. Patients are usually weaned from VA ECMO onto moderate doses of inotropic support (eg, epinephrine 0.04–0.1 µg/kg per min). The planned inotropic regimen should be started several hours before weaning. Circuit flows are slowly reduced to 1 to 2 L/minute and cardiac function is assessed with TEE during hemodynamic monitoring. If the patient is hemodynamically stable and TEE imaging demonstrates preserved cardiac function on pharmacologic support, then decannulation and discontinuation of VA ECMO are planned. In summary, understanding the process of initiation, management, weaning, and discontinuation from both VV and VA ECMO represents an important skill set for 784

SUGGESTED READINGS Aronson S, Dyke CM, Stierer KA, et al. The ECLIPSE Trials: comparative studies of clevidipine to nitroglycerin, sodium nitroprusside, and nicardipine for acute hypertension treatment in cardiac surgery patients. Anesth Analg. 2008;107(4):1110–1121. Bellomo R, Chapman M, Finfer S, et al. Low-dose dopamine in patients with early renal dysfunction: a placebo-controlled randomized trial: Australian and New Zealand Intensive Care Society (ANZICS) Clinical Trials Group. Lancet. 2000;356:2139. Esper SA, Levy JH, Waters JH, et al. Extracorporeal membrane oxygenation in the adult. Anesth Analg. 2014;118(4):731. Feinman J, Weiss SJ. Hemodynamic transesophageal echocardiography in left ventricular assist device care: a complementary technology. J Cardiothorac Vasc Anesth. 2014;28:1181. Fischer GW, Levin MA. Vasoplegia during cardiac surgery: current concepts and management. Semin Thorac Cardiovasc Surg. 2010;22:140. Follath F, Cleland JG, Just H, et al. Efficacy and safety of intravenous levosimendan compared with dobutamine in severe low-output heart failure (the LIDO study): a randomized double-blind trial. Lancet. 2002;360:196. Genereux P, Webb JG, Svensson LG, et al. Vascular complications after transcatheter aortic valve replacement: insights from the PARTNER (Placement of AoRTic TraNscathetER Valve) trial. J Am Coll Cardiol. 2012;60:1043–1052. George I, Xydas S, Topkara VK, et al. Clinical indication for use and outcomes after inhaled nitric oxide therapy. Ann Thorac Surg. 2006;82(6):2161–2169. Gomez WJ, Erlichman MR, Batista-Filho ML, et al. Vasoplegic syndrome after off-pump coronary artery bypass surgery. Eur J Cardiothorac Surg. 2003;23:165. Hill LL, Kattapuram M, Hogue CW. Management of atrial fibrillation after cardiac surgery. Part 1. Pathophysiology and risks. J Cardiothorac Vasc Anesth. 2002;16:483. Ichinose F, Roberts JD, Zapol WM. Inhaled nitric oxide: a selective pulmonary vasodilator; current uses and therapeutic potential. Circulation. 2004;109:3106. Kodali SK, Williams MR, Smith CR, et al. Two-year outcomes after transcatheter or surgical aortic-valve replacement. N Engl J Med. 2012;366:1686–1695. Lehmann A, Boldt J. New pharmacologic approaches for the perioperative treatment of ischemic cardiogenic shock. J Cardiothorac Vasc Anesth. 2005;19:97. Levy JH. Treating shock: old drugs, new ideas. N Engl J Med. 2010;362:841. Levy JH, Bailey JM, Deeb M. Intravenous milrinone in cardiac surgery. Ann Thorac Surg. 2002;73:325. Lovich MA, Pezone MJ, Wakim MG, et al. Inhaled nitric oxide augments left ventricular assist device capacity by ameliorating secondary right ventricular failure. ASAIO J. 2015;61:379–385. Nardi P, Pelligrino A, Scaferi A, et al. Long term outcome of CABG in patients with left ventricular dysfunction. Ann Thorac Surg. 2009;87:1401. Puskas JD, Williams WH, Mahoney EM, et al. Off-pump versus conventional coronary artery bypass grafting: early and 1-year graft patency, cost, and quality of life outcomes. JAMA. 2004;291:1841. Vincent JL, Rhodes A, Perel A, et al. Clinical review: update on hemodynamic monitoring: a consensus of 16. Crit Care. 2011;15:229. Webb JG, Binder RK. Transcatheter aortic valve implantation: the evolution of prostheses, delivery systems and approaches. Arch Cardiovasc Dis. 2012;105:153–159. Wiener RS, Welch HG. Trends in the use of pulmonary artery catheters in the United States, 1993–2004. JAMA. 2007;298:423.

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today’s cardiothoracic intensivist. In particular, the utility of TEE in the care of these patients with complex conditions provides the intensive care physician with a tool that confirms the diagnosis of common complications or even routine management during VV and VA ECMO.

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