Postoperative Cardiovascular Management

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Chapter 27 Postoperative Cardiovascular Management

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

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.

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.

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

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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