Chapter 27 Postoperative Cardiovascular Management
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
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.
ASSESSMENT OF THE CIRCULATION
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
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).
THERAPEUTIC INTERVENTIONS
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.
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.
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 |