Postoperative Cardiovascular Management

Oxygen Transport

Maintaining oxygen transport (ie, oxygen delivery [D o ₂ ]) 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 (Ca o ₂ ) (ie, hemoglobin concentration × 1.34 mL of oxygen per 1 g of hemoglobin × oxygen saturation [Sa o ₂ ]), 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 D o ₂ . Before altering the determinants of CO, including the inotropic state of the ventricles, an acceptable hemoglobin concentration and adequate Sa o ₂ should be provided, thus enabling increases in CO to supply the maximum available D o ₂ .

Hypoxemia from any cause reduces D o ₂ , and acceptable arterial oxygenation (partial arterial pressure of oxygen [Pa o ₂ ]) may be achieved with the use of an elevated inspired oxygen fraction (F io ₂ ) 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 Pa o ₂ by reducing intrapulmonary shunt; however, venous return may be reduced, causing a decrease in CO, with DO ₂ decreased despite an increased Pa o ₂ . 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 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 Ca o ₂ results in a decrease in D o ₂ . Reduced doses of direct-acting vasodilators or trials of different agents may be indicated.

When D o ₂ cannot be increased to an acceptable level as judged by decreased organ function or development of lactic acidemia, measures to decrease oxygen consumption (V̇O ₂ ) 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 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 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 V̇O ₂ and carbon dioxide production during rewarming. When patients cannot increase CO (ie, D o ₂ ), the effects of this large increase in V̇O ₂ 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, 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

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 ).

Box 30.1

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 showed that ischemia frequently 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 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.

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 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, 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 o ₂ , 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 dopamine ₁ [D ₁ ] 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 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

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 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.

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 β ₁ -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 ).

Box 30.2

Pharmacologic Approaches for Perioperative Ventricular Dysfunction

Inotropic Agents

• Catecholamines

• Phosphodiesterase inhibitors

• Levosimendan

Vasodilator Therapy

• Pulmonary vasodilators

• Phosphodiesterase inhibitors (milrinone, sildenafil)

• Inhaled nitric oxide

• Prostaglandins (PGI ₂ , PGE ₁ , iloprost, and derivatives)