Key Points
- 1.
Maintaining oxygen transport and oxygen delivery appropriately to meet the tissue metabolic needs is the goal of postoperative circulatory control.
- 2.
Cardiac function worsens after cardiac surgical procedures. Therapeutic approaches to reverse this dysfunction are important and often can be discontinued in the first few postoperative days.
- 3.
Myocardial ischemia often occurs postoperatively, and it is associated with adverse cardiac outcomes. Multiple strategies have been studied to reduce this complication.
- 4.
Postoperative biventricular dysfunction is common. It requires interventions to optimize the heart rate and rhythm, provide acceptable preload, and adjust afterload and contractility. In most patients, pharmacologic interventions can be rapidly weaned or stopped within the first 24 hours postoperatively.
- 5.
Supraventricular tachyarrhythmias are common in the first postoperative days, with atrial fibrillation predominating. Preoperative and immediate postoperative pharmacotherapy can reduce the incidence and slow the ventricular response.
- 6.
Postoperative hypertension has been a common complication of cardiac surgical procedures; newer vasodilator drugs are more arterial selective and allow greater circulatory stability than older, nonselective drugs.
- 7.
Catecholamines, phosphodiesterase inhibitors, and the calcium sensitizer levosimendan have been studied for treating biventricular dysfunction.
- 8.
Phosphodiesterase inhibitors and levosimendan are clinically effective inodilators that have important roles in patients with low cardiac output and biventricular dysfunction.
- 9.
Long cardiopulmonary bypass times may cause a refractory vasodilated state (“vasoplegia”) requiring combinations of pressors such as norepinephrine and vasopressin.
- 10.
Positive-pressure ventilation has multiple effects on the cardiovascular system, with complex interactions that should be considered in patients after cardiac surgical procedures.
- 11.
Critical care management of patients undergoing transcatheter aortic valve replacement who have experienced intraoperative complications includes understanding and managing the postoperative consequences of iatrogenic vascular injuries, stroke, significant paravalvular leaks, and/or cardiac conduction abnormalities.
- 12.
Hemodynamic management after cardiothoracic operations may benefit from the use of transesophageal echocardiography to determine myocardial function and assess cardiovascular structures. Echocardiography is particularly helpful in the diagnosis of causes of obstructive shock, including pericardial effusions leading to tamponade physiology.
- 13.
Echocardiography during the daily management of both venovenous and venoarterial extracorporeal membrane oxygenation (ECMO) may improve diagnosis of hemodynamic instability, troubleshoot common problems encountered during ECMO management, and aid in weaning the patient from mechanical support.
Postoperative cardiovascular dysfunction is becoming more common as older and increasingly critically ill patients undergo cardiac surgical procedures. Biventricular dysfunction and circulatory changes occur after cardiopulmonary bypass (CPB), but they can also occur in patients undergoing off-pump procedures. Pharmacologic therapy with suitable monitoring and mechanical support may be needed for patients in the postoperative period until ventricular or circulatory dysfunction improves.
Oxygen Transport
Maintaining oxygen transport (ie, oxygen delivery [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.
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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.
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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.
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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.
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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 ).
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
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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.
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Therapeutic Interventions
Therapeutic interventions for postoperative biventricular dysfunction include the standard concerns of managing low-CO states by controlling the HR and rhythm, providing an acceptable preload, and adjusting afterload and contractility. In most patients, pharmacologic interventions can be rapidly weaned or stopped within the first 24 hours postoperatively.
Postoperative Arrhythmias
Patients with preoperative or newly acquired noncompliant ventricles need a correctly timed atrial contraction to provide satisfactory ventricular filling, especially when they are in sinus rhythm preoperatively. Although atrial contraction provides approximately 20% of ventricular filling, this may be more important in postoperative patients, when ventricular dysfunction and reduced compliance may be present. For example, in medical patients with acute MI, atrial systole contributed 35% of the stroke volume (SV). The SV is often relatively fixed in patients with ventricular dysfunction, and the HR is an important determinant of CO. Rate and rhythm disorders must be corrected when possible, using epicardial pacing wires. Approaches to postoperative rate and rhythm disturbances are shown in Table 30.1 .
| Disturbance | Usual Causes | Treatments |
|---|---|---|
| Sinus bradycardia | Preoperative or 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 or pain | Sedation or analgesia |
| Hypovolemia | Volume administration | |
| Catecholamines | Change or discontinuance of drug | |
| Atrial tachyarrhythmias | Catecholamines | Change or discontinuance of drug |
| Chamber distension | Treatment of underlying cause (eg, vasodilator, diuresis, potassium or magnesium administration) May require synchronized cardioversion or pharmacotherapy | |
| Electrolyte disorder (hypokalemia, hypomagnesemia) | ||
| Ventricular tachycardia or fibrillation | Ischemia | Cardioversion |
| Catecholamines | Treat ischemia, may require pharmacotherapy | |
| Change or discontinuance of drug |
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 surgical procedures, the incidence may be in excess of 60%. Many reasons are recognized for this development, including inadequate intraoperative atrial protection, electrolyte abnormalities, change in atrial size with fluid shifts, epicardial inflammation, stress, irritation, and genetic factors. When AF or other supraventricular arrhythmias develop, treatment is often urgently needed for symptomatic relief or hemodynamic benefit. The longer a patient remains in AF, the more difficult it may be to convert the rhythm, and the greater is the risk for thrombus formation and embolization. Treatable underlying conditions such as electrolyte disturbances or pain should be corrected while specific pharmacologic therapy is being instituted. Paroxysmal supraventricular tachycardia (uncommon in this setting) can be abolished or converted to sinus rhythm by intravenous adenosine, and atrial flutter can sometimes be converted by overdrive atrial pacing with temporary wires placed at the time of operation. Electrical cardioversion may be needed if hypotension is caused by the rapid HR; however, atrial arrhythmias tend to recur in this setting. Rate control for AF or atrial flutter can be achieved with various atrioventricular (AV) nodal blocking drugs, and conversion is facilitated by many of these drugs as well. Table 30.2 summarizes the various treatment modalities for supraventricular arrhythmias. If conversion to sinus rhythm does not occur, electrical cardioversion in the presence of antiarrhythmic drug therapy should be attempted, or anticoagulation should be started.
| Treatment | Specifics a | Indications |
|---|---|---|
| Overdrive pacing by atrial wires b | Requires rapid pacer (≤800/min); start above arrhythmia rate and slowly decrease | PAT, atrial flutter |
| Adenosine | Bolus dose of 6–12 mg; may cause 10 s 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 or conversion to NSR in atrial fibrillation or flutter |
| β-Blockade | Esmolol, up to 0.5 mg/kg load over 1 min, followed by infusion if tolerated | Rate control or conversion to NSR in atrial fibrillation or flutter |
| Metoprolol, 0.5–5 mg, repeat effective dose q4–6h | Rate control or conversion to NSR in atrial fibrillation or/flutter | |
| Propranolol, 0.25–1 mg; repeat effective dose q4h c | ||
| Labetalol, 2.5–10 mg; repeat effective dose q4h c | Conversion of atrial fibrillation or 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 or conversion to NSR in atrial fibrillation or flutter |
| Verapamil | 2.5–5 mg IV, repeated PRN c | |
| Diltiazem | 0.2 mg/kg over 2 min, followed by 10–15 mg/h d | Rate control or conversion to NSR in atrial fibrillation or flutter |
| Procainamide | 50 mg/min up to 1 g, followed by 1–4 mg/min | Rate control or conversion to NSR in atrial fibrillation or flutter, prevention of recurrence of arrhythmias, treatment of wide-complex tachycardias e |
| Digoxin f | Load of 1 mg in divided doses over 4–24 h g ; may give additional 0.125-mg doses 2 h apart (3–4 doses) | Rate control or conversion to NSR in atrial fibrillation or flutter |
| Synchronized cardioversion | 50–300 J (external); most effective with anterior-posterior patches | Acute tachyarrhythmia with hemodynamic compromise (usually atrial fibrillation or flutter) |
a See specific drug monographs for full descriptions of indications, contraindications, and dosages. Doses are for intravenous administration; use the lowest dose, and administer slowly in patients with hemodynamic compromise.
b Verify that the pacer is not capturing the ventricle.
c Infusion may provide better control. This drug is less useful than diltiazem because of myocardial depression.
d Limited experience; may cause less hypotension than verapamil.
e When diagnosis is unclear (ventricular versus supraventricular) and no acute hemodynamic compromise is present (ie, cardioversion not indicated).
f Less useful than other drugs because of its slow onset and modest effect.
g Rate of administration depends on the urgency of rate control.
Preload
Assessment of preload is probably the single most important clinical skill for managing hemodynamic instability. Preload rapidly changes in the postoperative period because of bleeding, spontaneous diuresis, vasodilation during warming, the effects of 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 a good correlation between end-diastolic area measured by TEE and SV. Although the use of echocardiography to assess preload must always be tempered by the realization that the clinician is viewing a two-dimensional image of a three-dimensional object, this is the most direct technique clinically available. Greater awareness of the value of TEE in the ICU and increased availability of echocardiography in general have made this modality a first choice for the assessment of preload in the setting of acute unexplained or refractory hypotension. Without echocardiography, pressure measurements are used as surrogates for volume measurements. For example, in the absence of mitral valve disease, left atrial pressure (LAP) is almost equal to LV end-diastolic pressure (LVEDP), and pulmonary artery occlusion pressure (PAOP) is almost equivalent to these two pressures. In patients without LAP catheters, the PAOP or the pulmonary artery diastolic pressure is used.
When ventricular compliance is normal and the ventricle is not distended, small changes in end-diastolic volume are usually accompanied by small changes in end-diastolic pressure. In patients with noncompliant ventricles from preexisting congestive heart failure (HF), chronic hypertrophy resulting from hypertension or valvular disease, postoperative MI, or ventricular dysfunction, small increases in ventricular volume may produce rapid increases in end-diastolic pressure that require therapeutic intervention. Increased intraventricular pressure elevates myocardial oxygen demand (Mv̇ o 2 ) and decreases subendocardial coronary artery blood flow. Myocardial ischemia may be the result. Elevations in LVEDP are transmitted to the pulmonary circulation, thus causing congestion and possibly hydrostatic pulmonary edema.
Contractility
Quantifying the contractility of the intact heart has been complicated by the difficulty of finding a variable to measure contractility that is also independent of preload and afterload. Therapy for decreased contractility should be directed toward correcting any reversible causes, such as myocardial depressants, metabolic abnormalities, or myocardial ischemia. If the cause of depressed myocardial contractility is irreversible, positive inotropic agents may be necessary to keep CO satisfactory to support organ function.
Afterload
Calculated SVR continues to be used in guiding therapy or drawing conclusions about the state of the circulation. This should be done only cautiously, if at all. SVR is not a complete indicator of afterload. Even if SVR were an accurate measure of impedance, the response to vasoactive agents depends on the coupling of ventricular-vascular function, not on impedance alone. Hemodynamic therapy should be guided based on the primary variables, BP and CO. If preload is appropriate, conditions of both low BP and low CO are treated with an inotropic drug. If BP is acceptable (and preload appropriate) but CO is low, a vasodilator alone or in combination with an inotropic drug is used. If the patient is hypertensive (with low CO), vasodilators are indicated; if the patient is vasodilated (low BP and high CO), vasoconstrictors are employed ( Table 30.3 ).
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