Postoperative Cardiovascular Management

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Chapter 27 Postoperative Cardiovascular Management

Jerrold H. Levy, MD, Kenichi Tanaka, MD, James M. Bailey, MD, James G. Ramsay, MD

Oxygen Transport
Temperature
Assessment of the Circulation
Physical Examination
Invasive Monitoring
Echocardiography
Postoperative Myocardial Dysfunction
Postoperative Myocardial Ischemia
Therapeutic Interventions
Postoperative Arrhythmias
Preload
Afterload
Postoperative Hypertension
Postoperative Vasodilation
Coronary Artery Spasm
Decreased Contractility
Catecholamines
Phosphodiesterase Inhibitors
Levosimendan
Right-Sided Heart Failure
Diagnosis
Treatment
Effects of Mechanical Ventilation in Heart Failure
Effects of Ventilatory Weaning on Heart Failure
Cardiac Tamponade
Transplanted Heart
Summary
References

Biventricular dysfunction and circulatory changes occur after cardiopulmonary bypass (CPB) but can also occur in patients undergoing off-pump surgery. Pharmacologic therapy with appropriate monitoring and mechanical support may be needed for patients in the postoperative period until ventricular or circulatory dysfunction improves.

OXYGEN TRANSPORT

Maintaining oxygen transport (i.e., oxygen delivery [DO2]) satisfactory to meet the tissue metabolic requirements is the goal of postoperative circulatory control. Oxygen transport is the product of cardiac output (CO) times arterial content of oxygen (CaO2) (i.e., hemoglobin concentration × 1.34 mL of oxygen per 1 g of hemoglobin × oxygen saturation), and it can be affected in many ways by the cardiovascular and respiratory systems, as shown in Figure 27-1. 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 (9-10 g/dL) and adequate oxygen saturation (SaO2) should be provided, enabling increases in CO to provide the maximum available DO2.1

image

Figure 27-1 Important factors that contribute to abnormal oxygen transport.

Hypoxemia from any cause reduces DO2, and acceptable arterial oxygenation (PaO2) may be achieved with the use of an elevated inspired oxygen concentration (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.

Unexplained hypoxemia may be caused by right-to-left intracardiac shunting, most commonly by a patent foramen ovale. This is most likely to occur when right-sided pressures are abnormally elevated; an example is the use of high levels of PEEP. If suspected, echocardiography should be performed and therapy to reduce right-sided pressures should be initiated.

Patients with pulmonary disease may experience dramatic worsening of oxyge-nation 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 will result in a decrease in DO2. Reduced dosage 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 (imageO2) 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

Patients are often admitted to the intensive care unit (ICU) after cardiac surgery with core temperatures below 35°C (95°F), especially after off-pump cardiac surgery. The typical pattern of temperature change during and after cardiac surgery and the hemodynamic outcomes are illustrated in Figure 27-2. Decreases in temperature after CPB occur in part because of redistribution of heat within the body and because of heat loss.

image

Figure 27-2 Nasopharyngeal temperature during and after cardiac surgery: (1) core (i.e., 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 (imageCO2) and oxygen consumption (imageO2) are decreased on admission to the ICU because of residual hypothermia. During rapid rewarming, SVR decreases and imageCO2 and imageO2 increase, which 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, JB Lippincott, 1982, p 495.)

The normal thermoregulatory and metabolic responses to hypothermia remain intact after cardiac surgery, resulting 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. Other adverse outcomes of postoperative hypothermia during rewarming include large increases in imageO2 and CO2 production during this process. When patients cannot increase CO (i.e., O2 delivery), the effects of this large increase in imageO2 include mixed venous desaturation and metabolic acidosis. Unless end-tidal carbon dioxide is monitored or arterial blood gases are analyzed frequently to show the increased CO2 production and guide increases in ventilation, hypercarbia will occur, causing catecholamine release, tachycardia, and pulmonary hypertension. These effects of rewarming are most intense when patients shiver.

As the temperature rises, usually to about 36°C (96.8°F), the vasoconstriction and hypertension are replaced by vasodilation, tachycardia, and hypotension, even without hypercarbia. Often, over minutes, a patient who needs vasodilators for hypertension transforms into one requiring vasopressors or large volumes of fluid for hypotension. Volume loading during the rewarming period can help to 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

Physical Examination

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 the potential benefit. Physical examination may be of great value in diagnosing gross or acute pathology, 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 (e.g., 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 surgery. 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 causing 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, there is no relationship between these indicators of peripheral perfusion and CO or calculated systemic vascular resistance (SVR) in the postoperative period. By the first postoperative day, there is a crude correlation between peripheral temperature and cardiac index (CI) (r = −0.60). 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, the relationship between peripheral perfusion and CO is too crude to be used for hemodynamic management.

Invasive Monitoring

Despite the lack of a proven benefit with pulmonary artery (PA) catheterization, most patients in North America continue to have this monitor placed for cardiac surgery. This reflects a desire to have the information regarding myocardial performance readily at hand, and the potential difficulty in changing to PA catheterization in an emergency requiring resuscitation. Many cardiac anesthesiologists believe that the lack of evidence regarding the PA catheter may reflect the lack of a well-designed randomized trial. There can be little doubt that management of acute heart failure is facilitated by measures of filling pressures and CO. Postoperatively, many cardiac surgical centers do not have in-house physicians, and surgeons believe they can obtain more objective data over the telephone if a PA catheter is in place.

Use of the fiberoptic PA catheter to continuously monitor mixed venous oxygen saturation (SimageO2) helps evaluate the adequacy of DO2 and allows continuous assessment of the response to therapy, which may affect DO2 or imageO2 (e.g., PEEP therapy). The trend in the SimageO2 may function as an early warning signal of worsening in the oxygen supply-demand relationship as DO2 falls or imageO2 increases. Catheters that continuously measure the CO are also available. A wire coil on the catheter warms the blood passing by it at time intervals determined by an algorithm, and the measured changes in temperature at the tip of the catheter are used to provide a continuous display of the CO. Although the CO displayed needs gathering of information over several minutes and is therefore not as quick as conventional thermodilution, it avoids having to give injected volumes to the patient (which can add up to a significant amount every 24 hours) and provides trends that may give earlier warning than intermittent injections.

Echocardiography

There can be little doubt that echocardiography is the technique of choice for acute assessment of cardiac function. Just as transesophageal echocardiography (TEE) has become essential for intraoperative management in a variety of conditions, several studies document its utility in the postoperative period in the presence and absence of the PA catheter.2 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, adequate images can be obtained only in about 50% of patients in the ICU.

POSTOPERATIVE MYOCARDIAL DYSFUNCTION

Studies using hemodynamic, nuclear scanning, and metabolic techniques have documented worsening in cardiac function after coronary artery bypass grafting (CABG) surgery. All of these studies showed significant declines in left ventricular (LV) or biventricular (when measured) function in the first postoperative hours, with 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, suggesting that preload augmentation much above 10 mmHg for central venous pressure (CVP) or 12 mmHg for pulmonary capillary wedge pressure (PCWP) is of little benefit.

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 27-1).

BOX 27-1 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

POSTOPERATIVE MYOCARDIAL ISCHEMIA

Although intraoperative myocardial ischemia has often been a focus, studies have demonstrated that ischemia often occurs postoperatively and is associated with adverse cardiac outcomes. Electrocardiographic (ECG) and segmental wall motion abnormality (SWMA) evidence of ischemia occur early postoperatively in up to 40% of patients undergoing CABG surgery. Postbypass SWMAs are significantly associated with adverse outcomes (e.g., MI, death). Hemodynamic changes rarely preceded ischemia; however, postoperative heart rates (HRs) are significantly higher than intraoperative or preoperative values. Whether such changes occur because of surgery-reperfusion or events after CPB is not known. These findings do suggest that monitoring for ischemia must continue after revascularization.

THERAPEUTIC INTERVENTIONS

Therapeutic interventions for postoperative biventricular dysfunction include the standard concerns of managing low cardiac output states (LCOS) 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 after surgery.

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 15% to 20% of ventricular filling, this may be more important in postoperative patients, when ventricular dysfunction and reduced compliance may be present. Rate and rhythm disorders need to be corrected when possible, using epicardial pacing wires. Approaches to postoperative rate and rhythm disturbances are shown in Table 27-1.

Table 27-1 Postoperative Rate and Rhythm Disturbances

Disturbance Usual Causes Treatments
Sinus bradycardia Pre/intraoperative β-blockade Atrial pacing
β-Agonist
Anticholinergic
Heart block (first, second, and third degree) Ischemia Atrioventricular sequential pacing
Surgical trauma Catecholamines
Sinus tachycardia Agitation/pain Sedation/analgesia
Hypovolemia Volume administration
Catecholamines Change or stop drug
Atrial tachyarrhythmias Catecholamines Change or stop drug
Chamber distention Treat underlying cause (e.g., vasodilator, diuresis, give K+/Mg2+)
Electrolyte disorder (hypokalemia, hypomagnesemia) May require synchronized cardioversion or pharmacotherapy
Ventricular tachycardia or fibrillation Ischemia Cardioversion
Catecholamines Treat ischemia, may require pharmacotherapy

Later in the postoperative period (days 1 through 3), supraventricular tachyarrhythmias become a major problem, with atrial fibrillation (AF) predominating. The overall incidence is between 30% and 40%, but with increasing age and valvular surgery the incidence may be in excess of 60%. There are probably many reasons for this, including genetic factors, inadequate atrial protection during surgery, electrolyte abnormalities, change in atrial size with fluid shifts, epicardial inflammation, stress, and irritation. Randomized trials of off-pump coronary artery bypass grafting (OPCAB) have found a similar incidence of postoperative AF compared with on-pump CABG.3

When AF or other supraventricular arrhythmias develop, treatment is often urgently required for symptomatic relief or hemodynamic benefit. The longer a patient remains in AF, the more difficult it may be to convert, and the greater is the risk for thrombus formation and embolization.4 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 by intravenous adenosine, and atrial flutter can sometimes be converted by overdrive atrial pacing by temporary wires placed at the time of surgery. Electrical cardioversion may be required if hypotension is caused by the rapid rate; however, atrial arrhythmias tend to recur in this setting. Rate control for AF or flutter can be achieved with a variety of atrioventricular nodal blocking drugs, and conversion is facilitated by many of these drugs as well. Table 27-2 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 with warfarin (Coumadin) instituted.

Table 27-2 Treatment Modalities for Supraventricular Arrhythmias

Treatment Specifics* Indications
Overdrive pacing by atrial wires† Requires rapid pacer (up to 800/min); start above arrhythmia rate and slowly decrease PAT, atrial flutter
Adenosine Bolus dose of 6-12 mg; may cause 10 seconds of complete heart block AV nodal tachycardia
Bypass-tract arrhythmia
Atrial arrhythmia diagnosis
Amiodarone 150 mg IV over 10 min, followed by infusion Rate control/conversion to NSR in atrial fibrillation/flutter
β-Blockade Esmolol, up to 0.5 mg/kg load over 1 min, followed by infusion if tolerated Rate control/conversion to NSR in atrial fibrillation/flutter
Metoprolol, 0.5-5 mg; repeat effective dose q4-6h Rate control/conversion to NSR in atrial fibrillation/flutter
Propranolol, 0.25-1 mg; repeat effective dose q4h‡ Rate control/conversion to NSR in atrial fibrillation/flutter
Labetolol, 2.5-10 mg; repeat effective dose q4h‡ Conversion of atrial fibrillation/flutter to NSR
Sotalol, 40-80 mg PO q12h Conversion of PAT to NSR
Ibutilide 1 mg over 10 min; may repeat after 10 min Rate control/conversion to NSR in atrial fibrillation/flutter
Verapamil 2.5-5 mg IV, repeated PRN‡ Rate control/conversion to NSR in atrial fibrillation/flutter
Diltiazem 0.2 mg/kg over 2 min, followed by 10-15 mg/hr Rate control/conversion to NSR in atrial fibrillation/flutter
Procainamide 50 mg/min up to 1 g, followed by 1-4 mg/min Rate control/conversion to NSR in atrial fibrillation/flutter
Prevention of recurrence of arrhythmias
Treatment of wide-complex tachycardias
**Digoxin Load of 1 mg in divided doses over 4-24 hr§; may give additional 0.125-mg doses 2 hr apart (3-4 doses) Rate control/conversion to NSR in atrial fibrillation/flutter
Synchronized cardioversion 50-300 J (external); most effective with anterior-posterior patches Acute tachyarrhythmia with hemodynamic compromise (usually atrial fibrillation or flutter)

When diagnosis is unclear (ventricular vs. supraventricular) and there is no acute hemodynamic compromise (i.e., cardioversion not indicated).

AV = atrioventricular; NSR = normal sinus rhythm; PAT = paroxysmal atrial tachycardia; SVT = supraventricular tachycardia.

* See specific drug monographs for full description of indications, contraindications, and dosage. Doses are for intravenous administration; use lowest dose and administer slowly in patients with hemodynamic compromise.

† Verify pacer is not capturing ventricle.

‡ Infusion may provide better control. This drug is less useful than diltiazem owing to myocardial depression.

§ Rate of administration depending on urgency of rate control.

Limited experience; may cause less hypotension than verapamil.

** Less useful than other drugs owing to slow onset and modest effect.

Preload

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

Direct assessment of preload is clinically feasible using echocardiography. A fair-to-good correlation exists between echocardiographic and radionuclide measures of end-diastolic volume, and there is a good correlation between end-diastolic area by TEE and stroke volume. 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. Increased awareness of the value of TEE in the ICU and increased availability of echocardiography in general have made this modality a first choice in acute assessment of preload in the setting of unexplained or refractory hypotension. In the absence of echocardiography, pressure measurements are used as surrogates for volume measurements.

Afterload

Calculated SVR continues to be widely used in guiding therapy or drawing conclusions about the state of the circulation. This should only be done cautiously because 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, 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 27-3).

Table 27-3 Hemodynamic Therapy Guidelines

Blood Pressure Cardiac Output Treatment
Low Low Inotrope
Normal Low Vasodilator ± inotrope
High Low Vasodilator
Low High Vasopressor

POSTOPERATIVE HYPERTENSION

Hypertension has been a common complication of cardiac surgery, reported to occur in 30% to 80% of patients.5 The current population of older, 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 or a prior history, any patient may develop hypertension. Multiple factors contribute to postoperative hypertension, including awakening from general anesthesia, increases in endogenous catecholamines, activation of the plasma renin-angiotensin system, neural reflexes (e.g., heart, coronary arteries, great vessels), and hypothermia. Arterial vasoconstriction with various degrees of intravascular hypovolemia is the hallmark.

The hazards of untreated postoperative hypertension include depressed LV performance, increased MimageO2, cerebrovascular accidents, suture line disruption, MI, rhythm disturbances, and increased bleeding. Historically, pharmacologic therapy for hypertension in this setting has often been with sodium nitroprusside because of its rapid onset and short duration of action. With the introduction of alternative vasodilators, sodium nitroprusside is no longer the drug of choice.

There are many alternative drugs to sodium nitroprusside for the treatment of hypertension after cardiac surgery, including nitroglycerin, adrenergic-blocking agents such as phentolamine, β-adrenergic blockers, and the mixed α- and β-adrenergic blocker labetalol. Direct-acting vasodilators, dihydropyridine calcium channel blockers (e.g., nicardipine, clevidipine), ACE inhibitors, and fenoldopam (a dopamine-1 [D1] receptor agonist) have also been used. Novel therapeutic approaches are listed in Table 27-4.

Table 27-4 Novel Vasodilators

Drug Mechanism of Action Half-Life
Nicardipine Calcium channel blocker Intermediate
Clevidipine Calcium channel blocker Ultra-short
Fenoldopam Dopamine1 agonist Ultra-short
Nesiritide β-Natriuretic agonist Short
Levosimendan K+-ATP channel modulator Intermediate

Dihydropyridine calcium channel blockers relax arterial resistance vessels without negative inotropic actions or effects on atrioventricular nodal conduction and are important therapeutic options. Dihydropyridines are artery-specific vasodilators of peripheral resistance arteries, resulting in a 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. 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 more rapid control is essential, a dosing strategy consisting of a loading bolus or 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, a new ultra-short-acting dihydropyridine, is in phase III studies, has a half-life of only minutes, and may represent a potential alternative to sodium nitroprusside in the future.6

POSTOPERATIVE VASODILATION

Vasodilation alone should be associated with a hyperdynamic circulatory state presenting as systemic hypotension in association with an increased CO (and a low calculated SVR). More commonly after cardiac surgery, a combination of vasodilation and myocardial dysfunction occurs, requiring vasoconstrictor and inotropic therapy. The vasoplegic syndrome requires very high doses of vasoconstrictors and occurs after off-pump and on-pump surgery.7

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

Coronary artery or internal mammary artery (IMA) vasospasm can occur postoperatively. Mechanical manipulation and underlying atherosclerosis of the native coronary circulation and the IMA have the potential to produce transient endothelial dysfunction. The endothelium is responsible for releasing endothelium-derived relaxing factor (EDRF), which is nitric oxide, a potent endogenous vasodilator substance that maintains normal endogenous vasodilation. Thromboxane can be liberated as a result of 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 additional factors that may put the cardiac surgical patient at risk for spasm of native coronary vessels and arterial grafts. The therapy of choice remains empirical. Nitroglycerin is a first-line drug, but nitrate tolerance can occur. Phosphodiesterase (PDE) inhibitors represent novel approaches to this problem and have been reported to be effective. Intravenous dihydropyridine calcium channel blockers are also important therapeutic considerations.

Successful use of the radial artery as a bypass conduit have rekindled interest in this vessel. In the early days of CABG surgery, this conduit was abandoned because of its propensity to spasm. In later reports, techniques developed in the use of the IMA have been applied to the radial artery, as well as prophylactic use of diltiazem infusions.

DECREASED CONTRACTILITY

Drugs that increase contractility all result in increased 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, causing an improvement in myocardial contraction. Inhibition of the breakdown of cAMP by PDE inhibitors increases intracellular cAMP independent of the β-receptor. The “calcium sensitizers” constitute a new class of inotropic agents (Box 27-2).8

BOX 27-2 Pharmacologic Approaches for Perioperative Ventricular Dysfunction

• Inotropic agents

• Catecholamines
• Phosphodiesterase inhibitors
• Levosimendan

• Vasodilator therapy
• Pulmonary vasodilators

• Phosphodiesterase inhibitors
• Inhaled nitric oxide
• Prostaglandins

Catecholamines

The catecholamines used postoperatively include dopamine, dobutamine, epinephrine, norepinephrine, and isoproterenol (Box 27-3). These drugs have various effects on α- and β-receptors and therefore various effects on HR, rhythm, and myocardial metabolism. Dosing recommendations for the catecholamines are provided in Table 27-5.

BOX 27-3 Disadvantages of Catecholamines

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

Table 27-5 Catecholamines Used Postoperatively

Drug Infusion Dose (μg/kg/min)
Dopamine*,† 2-10
Dobutamine† 2-10
Epinephrine‡ 0.03-0.20
Norepinephrine‡ 0.03-0.20
Isoproterenol‡ 0.02-0.10

* Less than 2 μg/kg/min predominantly “dopaminergic” (renal and mesenteric artery dilatation).

† If 10 μg/kg/min is ineffective, change to epinephrine or norepinephrine.

‡ Dose to effect; may require higher dose than indicated.

Epinephrine

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 (e.g., vasoconstriction) and tachycardia occur. However, in the acutely failing heart postoperatively, drugs such as epinephrine or norepinephrine provide positive inotropy and perfusion pressure. These features and its low cost make it 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 β2 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 (CPP) 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 β1 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.

Dopamine

A precursor of norepinephrine, dopamine probably achieves its therapeutic effects by releasing myocardial norepinephrine or preventing its reuptake, especially when administered in high doses. This indirect action may result in reduced effectiveness when given to patients with chronic congestive heart failure 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), peripheral vascular resistance (PVR), and LV filling pressure. At low doses (<2 μg/kg/min), dopamine stimulates renal dopaminergic receptors to increase renal perfusion more than can be explained by an increase in CO. Despite this action, a multicenter study in New Zealand and Australia clearly demonstrated that use of low-dose dopamine in critically ill patients confers no protection from renal dysfunction.9 At doses higher than 10 μg/kg/min, tachycardia and vasoconstriction become the predominant actions of this drug.

Dobutamine

In contrast to dopamine, dobutamine exhibits mainly β1-agonist properties, with decreases in diastolic BP and sometimes systemic BP being observed. Dobutamine is functionally similar to isoproterenol, with less tendency to induce tachycardia in the postoperative setting. The favorable actions of dobutamine may be limited if a tachycardia develops, and, like dopamine, its inotropic potency is modest in comparison with that of epinephrine or norepinephrine.

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.10 Patients with CHF 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, causing increases in intracellular cAMP by selective inhibition of PDE fraction III (i.e., 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 PCWP, and decrease SVR and PVR in patients with biventricular dysfunction, and they are important therapeutic approaches in postoperative cardiac surgical patients.

PDE III inhibitors have a clinical effect as inodilators; they produce dilation of arterial and venous beds, decreasing the mean arterial pressure 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 IMA flow (Box 27-4).

BOX 27-4 Advantages of Preemptive Phosphodiesterase Inhibitor Administration

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

Milrinone is a bipyridine derivative with an inotropic activity that is almost 20 times more potent than that of amrinone, and it has a shorter half-life. Milrinone is an effective inodilator for patients with decompensated CHF and low CO after cardiac surgery. Suggested dosing for milrinone is a loading dose of 50 μg/kg over 10 minutes, followed by an infusion of 0.5 μg/kg/min (0.375 to 0.75 μg/kg/min). By loading the patient with milrinone over a longer period, high peak concentrations can be prevented, and the vasodilation that is observed with rapid loading can be attenuated. A milrinone loading dose of 50 μg/kg in conjunction with an infusion of 0.5 μg/kg/min consistently maintained plasma concentrations more than 100 ng/mL. Clearance was 3.8 ± 1.7mL/kg/min, volume of distribution was 465 ± 159 mL/kg, and terminal elimination half-time was 107 ± 77 minutes (values expressed as mean ± SD). The relationship between plasma concentration and pharmacodynamic effects produced about a 30% improvement in CI with plasma levels of 100 ng/mL, and there was a curvilinear relationship between plasma levels and improvement in CI.

Levosimendan

Levosimendan is a calcium-sensitizing drug that exerts positive inotropic effects through sensitization of myofilaments to calcium and vasodilation through opening of ATP-dependent potassium channels on vascular smooth muscle. These effects occur without increasing intracellular cAMP or calcium and without an increase in MimageO2 at therapeutic doses. As would be expected with an inodilator, the hemodynamic effects include a reduction in pulmonary artery occlusion pressure (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 congestive heart failure found 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.11 Levosimendan is in phase III clinical studies in the United States and Europe, and it has been granted fast-track status by the U.S. Food and Drug Administration (FDA).

In a study after cardiac surgery, patients were given levosimendan; of 11 patients with severely impaired CO and hemodynamic compromise, 8 patients (73%) showed evidence of hemodynamic improvement within 3 hours after the start of levosimendan infusion. Specifically, cardiac index and stroke volume were significantly increased, whereas the mean arterial pressure, indexed SVR, mean PAP, right atrial pressure, and PAOP were significantly lowered.12 Clinical studies continue to evaluate the potential role for this new positive inotropic agent in patients with heart failure.

RIGHT-SIDED HEART FAILURE

Heart failure after cardiac surgery 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.13 The myocardial preservation techniques that are best for the left ventricle may not offer ideal 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 (RCA) stenosis is present. Although depression of the ejection fraction is compensated by preload augmentation, right ventricular ejection fraction (RVEF) cannot be preserved if CPP is reduced or impedance to ejection is increased.

Certain aspects of the physiology of the right ventricle make it different from the left. 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 MimageO2 is increased while CPP is decreased. The normal thin-walled right ventricle 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, causing a decrease in RVEF with ventricular dilation. RV pressure overload may be complicated by volume overload caused by functional tricuspid regurgitation. Decreases in RV stroke volume will diminish LV filling, and dilation of the right ventricle can cause a leftward shift of the interventricular septum, interfering with diastolic filling of the left ventricle (i.e., ventricular interaction) (Fig. 27-3). 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 decreasing LV diastolic compliance. The resulting decrease in LV output will further impair RV pump function. The mechanical outcomes of RV failure in postoperative cardiac surgical patients are depicted in Figure 27-4. 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.

image

Figure 27-3 Sequence inducing right ventricular (RV) failure and causing a downward spiral of events. RCA = right coronary artery; LV = left ventricular.

image

Figure 27-4 Mechanical changes produced by acute right ventricular failure. LA = left atrium; LV = left ventricle; PFO = patent foramen ovale; PV = pulmonary veins; RA = right atrium; R→L = right to left; RV = right ventricle.

Diagnosis

In the postoperative cardiac surgical patient, a low cardiac index with right atrial pressure 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 right atrial pressure to PAOP stays close to or higher than 1.0. The absence of a step-up in pressure in going from the RA 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 constrictive pericarditis, suggesting reduced RV compliance. Large V waves may also be discernible and may relate to tricuspid regurgitation.

Echocardiography allows a qualitative interpretation of RV size, contractility, and configuration of the interventricular septum and can provide a definitive diagnosis of RV dysfunction or 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 if the increased right atrial pressures open a patent foramen ovale, producing a right-to-left shunt.

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 (Table 27-6). 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 mmHg and 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 means of 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.

Table 27-6 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)
Establish atrial kick (sinus rhythm, atrial pacing)
Afterload Reduction (Pulmonary Vasodilation)
Nitroglycerin, isosorbide dinitrate nesiritide
cAMP-specific phosphodiesterase inhibitors, β2-adrenergic agonists
Inhaled nitric oxide
Nebulized PGI2
Intravenous PGE1 (+ 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
Intra-aortic counterpulsation
Pulmonary artery counterpulsation
Right ventricular assist devices

CVP/PCWP = central venous pressure/pulmonary capillary wedge pressure; cAMP = cyclic adenosine monophosphate; PGI2 = prostaglandin I2; PGE1 = prostaglandin E1; PEEPs = positive end-expiratory pressures.

Although vasodilators may lead to cardiovascular collapse in 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, mandating the simultaneous administration of a vasoconstrictor. One way to reduce the pulmonary effects of the required vasoconstrictor is to administer the vasoconstrictor through a left atrial catheter. The PDE inhibitors are commonly used for their effect on the pulmonary vasculature and RV function, but this also usually requires systemic norepinephrine. In recent years, there has been an increased interest in and availability of aerosolized pulmonary vasodilators. This route of administration reduces or even abolishes the undesirable systemic vasodilation. Delivery of the drug directly to the alveoli improves pulmonary blood flow to these alveoli, potentially improving oxygenation by better matching blood flow to ventilation. Three drugs have been used: nitric oxide, prostaglandin I2 (i.e., epoprostenol or prostacyclin), and milrinone.14

The intra-aortic balloon pump (IABP) may be of substantial benefit, even in patients in whom the right ventricle 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 failure. 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 decreases the tamponade-like compression of the left ventricle by the distended right ventricle, right atrium, and edematous mediastinal tissues.

Effects of Mechanical Ventilation in Heart Failure

Congestive heart failure at the time of surgery is 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 inevitable rise in intrathoracic pressure caused by positive-pressure ventilation or PEEP is associated with a decreased CO. However, in the presence of congestive heart failure or myocardial ischemia, raised intrathoracic pressure has the potential to favorably affect the determinants of global cardiac performance. Understanding these heart-lung interactions is essential for the integrated management of the ventilated patient with congestive heart failure after cardiac surgery. The effects of ventilation on RV and LV failure need to receive independent consideration.

Raised intrathoracic pressure may significantly improve LV performance as a result of the reduced transmural pressure required to generate an adequate systemic BP. This can be viewed as afterload reduction, a beneficial 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 surgery. 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 right and biventricular failure the increase in the airway pressure caused by ventilatory support should be kept at a minimum compatible with adequate 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 the use of positive-pressure ventilation with PEEP. In particular, patients with elevated LV filling pressures, mitral regurgitation, and reversible ischemic dysfunction may improve from afterload reduction related to increased airway and intrathoracic pressures.

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 CHF, the response of global hemodynamics to spontaneous respirations must also be considered. The changes of the loading conditions of the heart brought about by the resumption of 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. Consequently, large decreases in inspiratory intrathoracic pressure are needed to cause adequate lung inflation. These negative swings of intrathoracic pressure increase venous return. Increased diaphragmatic movements may increase intra-abdominal pressure, further increasing the pressure gradient for venous return. Decreased intrathoracic pressure also raises the ventricular transmural pressures, raising the impedance to ventricular emptying. The increased afterload causes further increases in preload, with these changes jeopardizing the myocardial oxygen balance. Accordingly, worsening of myocardial ischemia as evidenced by ST-segment deviations was demonstrated when ventilatory support was removed in patients ventilated after MI.

CARDIAC TAMPONADE

Cardiac tamponade is an important cause of the low cardiac output syndrome after cardiac surgery 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 surgery. Postoperative cardiac tamponade usually manifests acutely during the first 24 hours after surgery, but delayed tamponade may develop 10 to 14 days after surgery and has been associated with postpericardiotomy syndrome or postoperative anticoagulation.

The mechanism of hemodynamic deterioration during tamponade is primarily 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 surgery.15 As the end-diastolic volume and end-systolic volume decrease there is a concomitant decrease in stroke volume. In the most severe form of cardiac tamponade, ventricular filling occurs only during atrial systole. Intense sympathoadrenergic activation increases venous return by constricting venous capacitance vessels. Tachycardia helps to maintain CO in the presence of a reduced stroke volume. Adrenergic mechanisms may also 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 heart surgery is a clinical entity distinct from the 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 surgery in any patient with inadequate or deteriorating hemodynamics, as evidenced by hypotension, tachycardia, increased filling pressures, or low CO, especially when there has been excessive chest tube drainage. A more subtle presentation of postoperative tamponade is gradually increasing requirements for inotropic and pressor support. Many of the classic signs of tamponade may not be present in these patients, partly because they 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. There may be localized accumulations that affect one chamber more than another.16 The classic findings of elevated CVP or equalization of CVP, PAd, and PAOP may not occur.17,18 It may therefore be difficult in the presence of a declining CO and elevated filling pressures to distinguish tamponade from biventricular failure. A useful clue may be 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 positive-pressure ventilation may further impair the already compromised ventricular filling in the presence of tamponade.

Echocardiography may provide strong evidence for the diagnosis of tamponade. Echolucent crescents between the RV wall and the pericardium or the posterior LV wall and the pericardium are discernible with transthoracic imaging 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, 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 to the severity of the hemodynamic alteration, but such findings are frequently absent in the postcardiac surgery patient. In many cases, transthoracic imaging is difficult because of mechanical ventilation, and TEE is required for adequate visualization.

The definitive treatment of tamponade is surgical exploration with evacuation of hematoma. The chest may have to be opened in the ICU if tamponade proceeds to hemodynamic collapse. In the case of delayed tamponade, pericardiocentesis may be adequate. 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 permit chest closure at the initial operation and necessitate staged chest closure after the edema has subsided. Similarly, it was found that some patients with inadequate hemodynamics after cardiac surgery despite maximum support in the ICU improve with opening of the chest because of relief of this tamponade effect. Reclosure of the chest in the operating room is often possible after a few days of continued cardiovascular support and diuresis.

TRANSPLANTED HEART

Postoperative circulatory control in the heart transplant recipient differs from that of the nontransplant population in three major respects. The transplanted heart is noncompliant with a relatively fixed stroke volume, acute rejection must be considered when cardiac performance is poor or suddenly deteriorates, and these patients are at risk for acute RV failure if pulmonary hypertension develops.

The fixed stroke volume combined with denervation of the donor heart means that maintenance of CO is often dependent on therapy to maintain an elevated HR (110 to 120 beats per minute). 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 effect on the pulmonary vasculature may be of benefit if PVR is above 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 corticosteroids or azathioprine, or both. These drugs also suppress the patient’s response to infection, and corticosteroid therapy may induce elevations in the white blood cell count, 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 RV may acutely fail if presented with an elevated PAP in the recipient. However, patients may have progression of disease between the time of evaluation and surgery, 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 on multiple drug therapy, including the inhaled agents nitric oxide and prostacyclin, as described earlier. Gradual withdrawal of these drugs occurs in the first postoperative days, with close monitoring of PAPs and oxygenation.

SUMMARY

• Maintaining oxygen transport and oxygen delivery appropriately to meet the tissue metabolic requirements is the goal of postoperative circulatory control.
• Multiple parameters of cardiac function worsen after cardiac surgery.
• Myocardial ischemia often occurs postoperatively, and it is associated with adverse cardiac outcomes.
• Therapeutic interventions for postoperative biventricular dysfunction include controlling the heart rate 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 after surgery.
• In the postoperative period, supraventricular tachyarrhythmias become a major problem, with atrial fibrillation predominating.
• Postoperative hypertension has been a common complication of cardiac surgery, and newer therapeutic interventions, including the dihydropyridine calcium channel blockers, have an expanding role in the treatment.
• Multiple drugs that increase contractility, including catecholamines, phosphodiesterase inhibitors, and levosimendan, have been studied for treating biventricular dysfunction.
• Many drugs are important for producing vasodilation in systemic, pulmonary, and other vascular beds. Phosphodiesterase inhibitors and levosimendan have clinical effects as inodilators. Vasoactive therapies often are required after cardiac surgery and are useful in understanding vasodilatory shock. Vasopressin has an expanding role.
• Right ventricular dysfunction is an important complication of cardiac surgery that warrants specific vasodilator therapy for reducing right ventricular afterload.
• Mechanical positive-pressure ventilation has multiple effects on the cardiovascular system, with complex interactions that should be considered in patients after cardiac surgery.

REFERENCES

1. Wu W.C., Rathore S.S., Wang Y., et al. Blood transfusions in elderly patients with acute myocardial infarction. N Engl J Med. 2001;345:1230.

2. Costachescu T., Denault A., Guimond J.G., et al. The hemodynamically unstable patient in the intensive care unit: Hemodynamic vs TEE monitoring. Crit Care Med. 2002;30:1214.

3. Puskas J.D., Williams W.H., Mahoney E.M., et al. Off-pump versus conventional coronary artery bypass grafting: Early and 1-year graft patency, cost, and quality of life outcomes. JAMA. 1841;291:2004.

4. Hill L.L., De Wet C., Hogue C.W. Management of atrial fibrillation after cardiac surgery: II. Prevention and treatment. J Cardiothorac Vasc Anesth. 2002;16:626.

5. Vuylsteke A., Feneck R.O., Jolin-Mellgard A., et al. Perioperative blood pressure control: A prospective survey of patient management in cardiac surgery. J Cardiothorac Vasc Anesth. 2000;14:269.

6. Bailey J.M., Lu W., Levy J.H., et al. Clevidipine in adult cardiac surgical patients: A dose-finding study. Anesthesiology. 2002;96:1086.

7. Gomez W.J., Erlichman M.R., Batista-Filho M.L., et al. Vasoplegic syndrome after off-pump coronary artery bypass surgery. Eur J Cardiothorac Surg. 2003;23:165.

8. Lehmann A., Boldt J. New pharmacologic approaches for the perioperative treatment of ischemic cardiogenic shock. J Cardiothorac Vasc Anesth. 2005;19:97.

9. 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.

10. Levy J.H., Bailey J.M., Deeb M. Intravenous milrinone in cardiac surgery. Ann Thorac Surg. 2002;73:325.

11. Kivikko M., Lehtonen L., Colucci W.S., et al. Sustained hemodynamic effects of intravenous levosimendan. Circulation. 2003;107:81.

12. Labriola C., Siro-Brigiani M., Carrata F., et al. Hemodynamic effects of levosimendan in patients with low-output heart failure after cardiac surgery. Int J Clin Pharmacol Ther. 2004;42:204.

13. Jacobs A., Leopold J., Bates E., et al. Cardiogenic shock caused by right ventricular infarction: A report from the SHOCK registry. J Am Coll Cardiol. 2003;41:1273.

14. Meade M.O., Granton J.T., Matte-Martyn A., et al. A randomized trial of inhaled nitric oxide to prevent ischemia-reperfusion injury after lung transplantation. Am J Respir Crit Care Med. 2003;167:1483.

15. Chuttani K., Pandian N.G., Mohanty P.K., et al. Left ventricular diastolic collapse: An echocardiographic sign of regional cardiac tamponade. Circulation. 1999;83:1991.

16. Kochar G.S., Jacobs L.E., Kotler M.N. Right atrial compression in postoperative cardiac patients: Detection by transesophageal echocardiography. J Am Coll Cardiol. 1990;16:511.

17. Bommer W.J., Follette D., Pollock M., et al. Tamponade in patients undergoing cardiac surgery: A clinical-echocardiographic diagnosis. Am Heart J. 1995;130:1216.

18. Chuttani K., Tischler M.D., Pandian N.G., et al. Diagnosis of cardiac tamponade after cardiac surgery: Relative value of clinical, echocardiographic, and hemodynamic signs. Am Heart J. 1994;127:913.

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