Over the past 20 years, the cardiac surgery patient has become more acute, with sicker patients being operated upon. As an example, at Johns Hopkins, just in the past several years, the portion of elective cases for coronary artery disease (CAD) has decreased from 75 percent to approximately 40 percent, while urgent cases have increased from 25 percent to over 50 percent. Nevertheless, despite this increase in acuity of disease, the expected mortality for this same population has remained constant, at approximately 2 percent. It is more than possible that these similar outcomes in the face of sicker patients are the result of improvements in intra- and postoperative management strategies. It goes without saying that prevention of complications requires a thorough understanding of the pathophysiologic basis for the development of organ dysfunction after cardiac surgery, the ability to identify high-risk patients, and the ability to execute therapeutic strategies that prevent complications from developing. In many of those patients who develop complications, early diagnosis and treatment prevent further deterioration and limit subsequent morbidity and mortality.

The early management of the postoperative open heart surgery patient can be viewed as an extension of the intraoperative care the patient received, with a focus on recovery from hypothermia, restoring hemostatic capability, recognition and support during the inflammatory condition provoked by cardiopulmonary bypass (CPB) itself, and optimization of cardiac function as the heart recovers from the transient ischemic injury sustained while undergoing surgery. Our experience at Johns Hopkins suggests that roughly one-half of all open heart surgery patients have recovered sufficiently to be transferred out of the ICU to the step-down unit in a day and a half, and that for isolated coronary bypass procedures, the ICU recovery period lasts for less than 1 day. Nevertheless, 30 percent of patients remain in the ICU for more than 3 days, and more than 10 percent stay for more than 7 days, indicating that in those patients, at a time when the immediate recovery from intraoperative events peculiar to CPB should have been long over, persistent organ dysfunction requiring critical care continues. To a large degree, the disease processes associated with this latter group of patients are similar to those seen in noncardiac surgical intensive care. Nevertheless, whether in the acute recovery period or a more chronic phase of critical illness, effective postoperative management rests on early recognition of pathology and rapid institution of therapy to prevent further clinical deterioration or the development of overt morbidity. This chapter is designed to review those physiologic disturbances specifically related to postoperative cardiac surgery patients as well as the more common illnesses and conditions associated with critical care, in general.

Cardiac surgery involves a number of unique anatomic and physiologic stresses that tax the reserve of every organ system and increase the likelihood that clinical morbidity will develop. A list of these stressors and their pathophysiologic and clinical sequelae is shown in Table 26-1.

The early postoperative period is characterized by instability involving vascular tone, significant fluid shifts, pulmonary and cardiac function, hemostasis, and renal function. This instability is a direct result of the anatomic and physiologic disturbances that take place intraoperatively (see Table 26-1). In general, resolution is rapid because the primary stressors causing instability (i.e., insults related to CPB) are confined to the first 12 to 24 h postoperatively. Once removed from these intraoperative influences, patients recover rapidly, so long as organ systems were not hurt in a more severe fashion and that the insult of CPB was not too severe for the organ systems that may already have been dysfunctional. Intensive monitoring is needed during this initial recovery phase to determine if the patient has deviated beyond what one normally expects during this critical postoperative time period.

Transfer of Care and Monitoring

Transport of the patient and the transfer of care from the OR to the ICU is an inherently dangerous process. To reduce risk, hemodynamic stability should be assured prior to leaving the OR. Monitoring during transfer should be at a level comparable to that used intraoperatively and should include at a minimum the following: electrocardiogram (ECG), arterial blood pressure (BP), and pulse oximetry.

On arrival in the ICU, all care providers should initially focus on assuring the adequacy of cardiopulmonary function. Although the anesthesia team who knows the patient well should provide guidance to the receiving care team, in general, mechanical ventilation is protocolized, for example, tidal volume set at 7 to 8 cm³/kg ideal body weight with a rate of 16, a positive end expiratory pressure set at 5 cm³ H₂O, and the FIO₂ at 1.0. At that point, successive blood gases dictate changes required in ventilation while the weaning of FIO₂ can be guided by the SpO₂. It should be noted that shivering in response to hypothermia increases O₂ consumption and CO₂ production, thus increasing the workload of the pulmonary system. As a sedated, postoperative patient may not produce adequate respiratory compensation for this increase in work, hypercapnia with significant respiratory acidosis may ensue unless mechanical ventilation is maintained at appropriate levels.

Hemodynamic monitoring should be reestablished at the intraoperative level. All patients should have arterial BP monitoring. In addition, continual ECG monitoring with ST-segment analysis is standard so as to allow for the early detection of arrhythmias and ischemia. The combination of leads allowing the most sensitive detection of ischemia is somewhat controversial. Some authors advocate monitoring leads II/V₅ while more recent data support the use of II/V₃ or V₄. Full 12-lead ECG analysis should occur on arrival to the ICU. At Hopkins, we have also decided to repeat the ECG at 4 and 8 h, as well as daily on POD 1 and 2.

A chest x-ray is mandatory in all patients to verify (1) the positioning of the endotracheal tube, which is generally halfway between the carina and the sternal notch, (2) that there is no undrained effusion, usually the result of inadequate evacuation in the operating room, (3) that there is no pneumothorax, (4) that there are no unexpected infiltrates, and (5) that the invasive tubes and central venous or pulmonary catheters are well positioned. Left lower lobe atelectasis with silhouetting of the left hemidiaphragm is the rule, although this may not be evident until positive pressure ventilation is discontinued. It should not be overinterpreted.

Routine postoperative laboratory tests should include hemoglobin or hematocrit, sodium and potassium, glucose, calcium, and arterial blood gas; these should be obtained every 4 to 8 h or more frequently when clinically indicated. Additional hematologic and chemistry tests need not be routine but should be obtained based on clinical signs/symptoms.

A central venous catheter is mandatory for the administration of vasoactive drugs. However, the need for a central venous catheter versus a pulmonary artery (PA) catheter remains controversial. Although the PA catheter can provide hemodynamic information about a patient’s status that might otherwise be difficult to determine, it has yet to be incontrovertibly demonstrated that this information improves patient outcome.

For example, one prospective randomized trial in critically ill patients failed to demonstrate the benefit of PA catheter–directed management compared with a central venous catheter alone¹; however, a prospective, randomized study in postoperative cardiac surgery patients in which goal-directed therapy was protocolized did show benefit.² In the face of this evidence, PA catheters probably need not be routinely used, but when hemodynamics are tenuous and incompletely understood, the information gained from better understanding the patient’s cardiac output, filling pressures, pulmonary arterial pressures, and oxygen delivery can significantly impact on therapeutic decision making.

Hypothermia

During cardiac surgery when cardiac arrest is anticipated, hypothermia is deliberately induced intraoperatively to protect organs from ischemic injury during periods of diminished blood flow. The ability of hypothermia to reduce ischemic organ damage, particularly in the brain, has been shown in a number of animal models and clinical settings. In a prospective randomized trial of hypothermic (28°C–32°C) versus normothermic (37°C) CPB for coronary revascularization, normothermia was associated with a worse neurologic outcome.³ The degree to which hypothermia should be induced has changed; however, temperatures less than 30°C are associated with higher mortality, increased cardiac dysfunction, more renal injury, coagulation factor and platelet dysfunction, an increased inflammatory response, and an increased incidence of wound infections (see Table 26-1). It now appears that although a few degrees of hypothermia are beneficial for brain preservation, more severe hypothermia than that appears to be deleterious.⁴

To mitigate the adverse effects of hypothermia in the postoperative period, active warming should be initiated postoperatively with a goal of restoring temperature between 36°C and 37°C. Although a number of warming methods are available, forced-air warming devices appear to be the most effective.

Cardiovascular System

Hemodynamics

Hemodynamic instability is common in the early postoperative phase of cardiac surgery. Intraoperative insults (see Table 26-1) frequently have an adverse impact on cardiovascular function. For example, preoperative ischemia, ischemia-reperfusion injury, and CPB-related inflammation all contribute to depressed myocardial contractility after cardiac surgery. In most patients, this dysfunction resolves within 24 h; however, inotropic support may be required until this transient dysfunction resolves. Patients with ventricular dysfunction prior to surgery are more likely to require more inotropic support than those with normal ventricular function.

Inadequate preload, the result of relative intravascular hypovolemia, occurs routinely and can be a major contributor to poor cardiac output and unstable hemodynamics. The causes of intravascular volume depletion are threefold: bleeding, which occurs to a variable degree but averages approximately 400 to 500 cm³ per case; warming and the temperature-dependent opening of vascular beds, most notable when patients return to the ICU cold (that is, less than 36°C); and third space losses, the sequelae of CPB-induced abnormalities that result in systemic inflammation. These three determinants of intravascular volume play an active role for the first 6 to 10 h postoperatively. Thereafter, volume resuscitation to maintain adequate preload should not be required. Should significant volume requirements persist to maintain adequate preload in the face of low cardiac output, other adverse clinical causes should be sought, for example, tension pneumothorax, tamponade, valvular dysfunction, or cardiac ischemia. Finally, despite adequate preload and cardiac function, vascular tone can be excessively high from adrenergic hyperactivation or low from CPB-induced systemic inflammatory response syndrome (SIRS). Thus, transient infusions of vasodilators or vasoconstrictors, separate and apart from inotropic agents, may be needed until vascular stability returns, again, almost always within 24 h of surgery.

The goal of hemodynamic management in the early postoperative phase is to maintain adequate oxygen delivery to the tissues by optimizing cardiac performance. In all cases, this relies on the caregiver to optimize preload and afterload, and thereafter, use inotropic agents or mechanical assist devices, most commonly the intra-aortic balloon pump and rarely a ventricular assist device.

Cardiac performance is reflected in the cardiac index, which normally ranges from 2.4 to 4.2 L/min/m². However, “normal” cardiac performance in patients after cardiac surgery is not clearly defined, and attempting to reach a specific “value,” for example, a cardiac index (CI) of 2.4 L/min/m² can be self-defeating. Ventricular dysfunction is ubiquitous in the early postoperative period; adequacy of perfusion, therefore, must be determined clinically, though frequently guided by a more quantitative assessment of myocardial performance. Clinical targets that reflect adequate cardiac output are (1) a mean arterial pressure (MAP) adequate for renal, splanchnic, and cerebral perfusion, usually 60 to 85 mm Hg; (2) warm extremities with palpable pedal pulses; (3) urine output of 0.5 mL/kg/h; and (4) the ability to mentate. As mentioned earlier, invasive monitors, such as a PA catheter, can be extremely useful to guide therapeutic decision making, but frequently ideal hemodynamics are not possible to obtain. A CI of 2.0 to 2.2 L/min/m² is generally adequate immediately following cardiac surgery. Monitoring of mixed venous oxygen saturation, from either intermittent blood sampling or continuous invasive cooximetry, can provide data to complement other information. As a general guideline, a mixed venous saturation of 60 to 70 percent, with an arteriovenous oxygen difference of less than 5 to 6 cm³/dL is adequate. Mixed venous oxygen saturations of less than 50 percent and larger A-VO₂ differences are markers of inadequate oxygen delivery. Invariably, poor oxygen delivery results in an increase in the base deficit with the development of a lactic acidosis, so a blood gas and serum lactate level can be used to help track the adequacy of hemodynamic resuscitation.

Patients who do not exhibit adequate perfusion need immediate resuscitation before end-organ compromise occurs. Frequently, direct cardiac output and intracardiac pressure monitoring using a PA catheter can be particularly useful to diagnose the patient’s condition and guide therapy. Furthermore, despite an initial ECG and chest x-ray that may have been acceptable, when inadequate perfusion is recalcitrant to what is perceived as adequate intervention, a repeat ECG and chest x-ray are always in order. Furthermore, a cardiac echocardiogram can be very useful, particularly when tamponade and ventricular dysfunction are part of the differential diagnosis.

When adequate perfusion is an issue, a large number of inotropic and vasoactive agents are available to support the circulation. Each of these agents has particular pharmacokinetic and pharmacodynamic properties that may be more or less advantageous in any single patient (Table 26-2). Although there is no evidence indicating a difference in patient outcome based on selection of vasoactive drug, an astute clinician should be familiar with the theoretic advantages of each agent so as to be able to select agents appropriate to the particular circumstance at hand. Regardless, if oxygen delivery is still marginal after optimization of preload and afterload and the addition of significant inotropic agents, strong consideration should be given to placement of an intra-aortic balloon pump. An intra-aortic balloon pump can be expected to increase coronary perfusion due to diastolic augmentation of pressure and to further diminish afterload as a result of active balloon emptying timed to systole. Although increased perfusion may be less than 500 cm³/min as a result of the balloon mechanics itself, clinically the change in the balance of myocardial oxygen supply and demand can be considerable, leading to vastly improved cardiac performance, with improvement in the CI by as much as 50 percent and mixed venous oxygen saturation by as much as 15 to 20 percent.^5,6

Furthermore, to the degree that the catecholamine requirements are diminished as a result of the balloon pump, adrenergic causes of cardiac arrhythmias can be mitigated and at times, intractable arrhythmias can resolve.

Myocardial Ischemia.

The presence of ECG and echocardiographic evidence of myocardial ischemia appears frequently in the first several hours after coronary revascularization and, if indicative of ongoing cardiac ischemia, is predictably associated with an adverse outcome.⁷ However, in the majority of patients who undergo cardiac surgery, early ECG changes are nonspecific and do not represent clinically or hemodynamically meaningful ischemia. However, poor cardiac indices, evidence of shock, high central filling pressures, and arrhythmias all suggest ongoing ischemia and poor ventricular function. In this setting, the presence of regional abnormalities on ECG or segmental wall motion abnormalities by echo support the diagnosis of significant myocardial ischemia. Beta-blockade and antiplatelet/anticoagulant therapy, the therapeutic mainstays for myocardial ischemia in other settings, are generally not useful immediately after cardiac surgery because of the invariable need for inotropes, not myocardial depressants, and the risk of exacerbating postoperative bleeding. Intravenous infusion of nitroglycerin or a calcium channel antagonist may be useful, particularly in cases of internal mammary artery (IMA) spasm⁸; however, hypotension often precludes their use as well.

Medical management of myocardial ischemia after cardiac surgery is limited to physiologic manipulations aimed at preventing shock by optimizing myocardial O₂ supply and demand. Improving cardiac output, as always, requires optimization of preload and afterload, and then the addition of inotropic agents. Although evidence supports transfusion of red blood cells to a hemoglobin of 10 to 11 g/dL in patients above 65 years of age with ongoing myocardial ischemia, the applicability of this to the postoperative cardiac surgery patients is questionable, as blood transfusions appear to be associated with a poorer outcome in this patient group.⁹ Nevertheless, it is hard to argue against the correction of anemia in the face of ongoing myocardial ischemia. Whether or not medical management is successful in the treatment of postoperative shock due to ongoing ischemia, consideration of invasive therapy is always warranted, including insertion of an intra-aortic balloon pump, percutaneous coronary intervention, or surgical reexploration and repeat coronary bypass grafting.⁵

Arrhythmias.

Supraventricular and ventricular arrhythmias occur commonly after cardiac surgery. A number of factors associated with an increased risk of postoperative arrhythmias have been identified: advanced age, preoperative history of arrhythmia, history of congestive heart failure, use of bicaval venous cannulation, and longer duration of CPB. In addition to arrhythmogenic intraoperative events (see Table 26-1), a number of postoperative conditions can incite arrhythmias as well, for example, sympathetic hyperactivity, myocardial ischemia, electrolyte disturbances, atrial distention, mechanical irritation from an indwelling central venous line, and drug therapies. As in all clinical settings, hemodynamically unstable arrhythmias require immediate attention and treatment, often including cardioversion/defibrillation.

Bradycardia: Sinus bradycardia, junctional rhythm, and atrioventricular (AV) conduction disturbances comprise the majority of bradycardic rhythms after cardiac surgery. Perioperative drug therapies (β-blockers, digoxin, or amiodarone), hypothermia, electrolyte disturbances, and direct trauma to conductive tissue may all contribute to the development of bradycardia. High-grade conduction blockade (i.e., new bifascicular or trifascicular block and complete heart block) is the most serious of these as it is frequently associated with significant hemodynamic compromise and reflects an intraoperative injury to the conduction system that may be permanent. Infusion of β₁-agonists (see Table 26-2) frequently can increase heart rate and perfusion, but pacing is the simplest method of treating any postoperative, symptomatic bradycardia. In this circumstance, whenever possible, AV synchrony should be preserved by simple atrial pacing as stroke volume is greater when the electrical impulse is generated at or above the AV node, with the resultant coincident synchrony of ventricular systole.¹⁰ In patients who require pacing, the rule of thumb is that atrial pacing is favored over AV sequential pacing, which is favored over ventricular pacing. Most patients who have significant AV conduction block that persists 5 to 7 days after surgery require permanent pacemaker placement.

Supraventricular arrhythmia: Without prophylaxis, supraventricular tachycardia occurs in 30 to 40 percent of patients undergoing cardiac surgery, more frequent after valve surgery than coronary artery bypass grafting (CABG). The vast majority of supraventricular tachycardia after cardiac surgery is atrial fibrillation (AF) or flutter, which most commonly develops between postoperative days 1 and 4, with peak incidence on days 2 and 3. These two rhythm disturbances are associated with an increased length of hospital stay, higher cost, and increased risk of stroke. In poorly contractile ventricles, it can lead to hemodynamic compromise. The incidence of AF can be reduced by approximately 50 percent by the initiation of prophylactic treatment with β-blockers, amiodarone, or sotalol.¹¹ Preoperative loading with amiodarone is more effective than postoperative loading; however, both methods reduce the incidence of AF. Daily magnesium started preoperatively and continued for 4 days postoperatively has also been shown to reduce the incidence of AF after CABG. When AF does develop, initial therapy should be directed at assuring hemodynamic stability and rate control. Cardioversion should be used in patients who are hemodynamically unstable. A rapid ventricular response can usually be controlled with intravenous β- or calcium channel blockers, although β-blockers may be superior in the perioperative period. Intravenous amiodarone may be preferable for rate control in patients with reduced LV function (ejection fraction below 40 percent) because it is less negatively inotropic than β- or calcium channel blockers. At Johns Hopkins, currently amiodarone is the drug of choice for postoperative AF, both for rate control and conversion to sinus rhythm.

Ventricular arrhythmias: Unexpected, prolonged postoperative ventricular ectopy is unusual and ischemia as a cause should be ruled out. In the face of ischemia, antiarrhythmic therapy may be indicated. It goes without saying that patients who develop sustained ventricular tachycardia or ventricular fibrillation should be cardioverted and/or defibrillated and treated with an antiarrhythmic agent. Amiodarone is the pharmacologic agent of choice according to present American Heart Association (AHA) guidelines. Patients who do experience significant ectopy and/or sudden cardiac death (i.e., in-hospital cardiac arrest) without a reversible cause should be considered for an electrophysiologic study. Particularly in the setting of poor ventricular function, implantation of an automatic internal cardioverter defibrillator (AICD) may improve survival.¹²

Antiplatelet Therapy and Saphenous Vein Graft Patency