The initial management of most patients after cardiac surgery occurs in specialized intensive care units (ICUs). The unique pathophysiologic alterations associated with hypothermia and cardiopulmonary bypass (CPB) mandate that a specialized environment, including sophisticated electrophysiologic and hemodynamic monitoring along with intensive attention and supervision by specially trained critical care nurses, be available. Although CPB is no longer universally applied in cardiac surgery, the multiple management problems posed by cardiac patients continue to demand specialized treatment.

The patient typically arrives in the ICU or postcardiac surgery recovery area from the operating room with the necessary apparatus for monitoring the following parameters: heart rate and rhythm; systemic arterial, central venous, pulmonary artery, and pulmonary artery occlusion pressures (PAOPs); cardiac output; urinary output; mediastinal drainage; body temperature; arterial oxygen saturation (SpO2); mixed venous oxygen saturation (SvO2); and end-tidal carbon dioxide (ETCO2) tension.

Most of the apparatus attached to the patient on arrival in the ICU serves multiple purposes. A pulmonary artery catheter allows monitoring of pulmonary artery pressures and can also be used to estimate the filling pressure of the left ventricle, cardiac output, and body core temperature. The pulmonary artery catheter allows for measurement of the SvO2, which is used as an indirect index of tissue oxygenation. The peripheral arterial cannula provides a continuous pulse-wave tracing of systemic blood pressure and ready access to arterial blood sampling for laboratory analysis. Regular periodic assessments of arterial blood gases, especially after a major change in ventilator settings, are essential unless continuous ETCO2 and SpO2 by pulse oximetry are being monitored. ETCO2 and SpO2 are reliable in guiding the weaning of mechanical ventilation and removal of the endotracheal tube. Monitoring of these parameters has been used very effectively in “fast-track” protocols, the notion that rapid extubation can lead to lower pulmonary complications from longer periods of mechanical ventilation. Assessment of volume loss is based on chest and mediastinal tube drainage plus urine output. The endotracheal tube secured in the correct position with an appropriately inflated cuff is essential for positive-pressure ventilation of the lungs. Confirmation of bilateral breath sounds and absence of tracheal air leak versus cuff inflation should be made upon the patient’s arrival in the ICU. The endotracheal tube’s position should be ascertained on the initial chest radiograph. The endotracheal tube also allows for suctioning of bronchial secretions and reduces (but does not completely eliminate) the risk of oropharyngeal and gastric reflux secretions entering the trachea and bronchi. The endotracheal tube can often be removed the evening of surgery if the patient is conscious, is able to protect the airway, has good ventilatory mechanics and muscle strength, and is able to take on the work of breathing. Most patients can have the pulmonary artery catheter removed within 12 to 24 hours if intravenous (IV) vasopressor and inotropic drug therapy is at minimum levels. The peripheral arterial cannula can be removed when cardiovascular function is satisfactory and the need for blood sampling is at a routine daily level. The urinary catheter is usually removed when the patient is ambulatory unless there is a vigorous diuresis or an increased risk of urinary retention. Chest tubes are generally removed when the total drainage is less than 100 mL per tube over 8 hours.

The primary factor that differentiates cardiac surgery from other forms of surgery is CPB. With such improvements in extracorporeal technology as membrane oxygenation, arterial blood filtration, and blood-sparing techniques, the noncardiac complications have been significantly reduced. Major improvements in myocardial protection coupled with changes in anesthetic and CPB techniques now frequently allow extubation within several hours of surgery.

The patient can often be safely and comfortably transferred from the ICU within the first 6 to 24 hours, a process that has been termed fast tracking.1 Individuals undergoing “off-pump” procedures also have the potential for rapid recovery and early extubation and removal of catheters and chest tubes; they can be sitting up in the chair the next morning ready for transfer.

Fast tracking requires that the patient’s status be characterized as follows: awake or easily aroused, neurologically intact, cooperative, and comfortable; stable, satisfactory hemodynamics; normothermia; satisfactory spontaneous ventilation; normal coagulation with minimal chest tube drainage; and satisfactory urine output, electrolyte, and acid–base balance.2

Pathophysiologic Consequences of Cardiopulmonary Bypass

The basic pathophysiology during the early postoperative period revolves around the following variables: transient left ventricular dysfunction, capillary leak, warming from hypothermia, mediastinal bleeding, and emergence from anesthesia.

Although improvements in surgical techniques, cardioplegia delivery, and other myocardial protection features achieved in the past 2 decades were expected to lessen the likelihood of developing transient left ventricular systolic dysfunction following CPB, the reported prevalence of this complication (90%) did not change between 1979 and 1990.3 This transient myocardial depression has been attributed by some authors to inadequate myocardial protection or the effects of cold cardioplegia, but the bulk of the evidence incriminates the inflammatory state induced by CPB as the primary causative factor.4

The inflammatory state induced by CPB involves platelet–endothelial cell interactions and vasospastic responses that result in low-flow states in the coronary circulation.5 This inflammatory reaction causes vascular endothelial adhesion molecules to attract inflammatory cells that subsequently adhere to the vascular endothelium. These inflammatory cells mediate much of the subsequent injury by the release of oxygen- free radicals or proteolytic enzymes. This release of oxygen-free radicals in response to reperfusion injury is now generally accepted as the explanation for the transient postoperative ventricular dysfunction.6,7 Whether the depressed ventricular function is caused by oxygen-free radicals or the myocardial ischemia associated with cardioplegia, the expectation would be that “off-pump” coronary artery bypass graft (CABG) would reduce myocardial injury in part by reducing the inflammatory response. A significant attenuation of the inflammatory response has been demonstrated with the “off-pump” approach. It must be emphasized, however, that the inflammatory response is not totally eliminated because other factors, such as surgical trauma and anesthetic agents, also contribute to this process. Better myocardial function in association with a reduction in systemic inflammation is substantiated by a reduced increase in creative kinase myocardial banding (CKMB) indicating less myocardial necrosis and better postoperative left ventricular function in the “off-pump” patients.8 Depressed myocardial function seems to be unrelated to CPB time, number of coronary artery grafts, preoperative medications, or postoperative core temperature. Ventricular function is generally depressed by 2 hours and is at its worst at 4 to 5 hours after CPB. Significant recovery of function usually occurs by 8 to 10 hours, and full recovery is reached by 24 to 48 hours.9 Systemic vascular resistance, although not rising immediately after surgery, increases as ventricular function worsens. This increase in systemic vascular resistance is likely secondary to reduced ventricular function and the need to maintain systemic blood pressure and is not per se a major causative factor of depressed cardiac contractility. The confounding effect of vasopressor drugs used in an attempt to increase systemic blood pressure must be recognized.

The inflammation-mediated production of oxygen-free radicals and release of proteolytic enzymes by neutrophils also damages the endothelial cells. The “gatekeeper” function of the endothelium is disturbed and capillary permeability increases, resulting in edema. The capillary leak syndrome may last from a few hours to 1 to 2 days, depending to a large degree on the duration of CPB. When the capillary leak ceases and interstitial edema fluid is mobilized, intravascular volume overload is a threat and must be recognized and treated appropriately with volume management, diuresis, or both.

Hypothermia predisposes the patient to cardiac arrhythmias, increases systemic vascular resistance, precipitates shivering (which increases O2 consumption and CO2 production), and impairs coagulation.9 Hypothermia with the patient’s core temperature below 95°F (35°C) frequently recurs after rewarming to 98.°F (37°C) at the end of CPB. This decrease in core temperature reflects the loss of heat from the surgical field after CPB; exposure of the patient to ambient temperature; and incomplete rewarming of peripheral tissues, especially fat and muscle. If the patient is hypothermic upon arrival in the ICU, monitoring the temperature of noncore body sites such as a finger or toe can ensure complete assessment of rewarming. Hypothermia causes peripheral vasoconstriction and contributes to the hypertension frequently seen after cardiac surgery. Furthermore, hypothermia causes a decrease in cardiac output by producing bradycardia along with the increase in vascular resistance. Most believe that the patient should be passively rewarmed by warm air (eg, Bear Hugger) and that shivering should be eliminated by the administration of meperidine (25-50 mg) and muscle relaxants. As the body temperature increases, the vasoconstriction and hypertension associated with hypothermia are replaced by vasodilatation, tachycardia, and hypotension. Volume loading during the rewarming process helps reduce the rapid swings in blood pressure. Vasopressors (eg, norepinephrine) may be required to maintain an adequate systemic blood pressure. As the patient is rewarmed, large increases in O2 consumption and CO2 production may occur, with a consequent increase in demand on cardiovascular and pulmonary functions.10

Hypercarbia causes catecholamine release, tachycardia, and pulmonary hypertension. If the patient cannot increase the cardiac output and O2 delivery, venous hemoglobin desaturation and metabolic acidosis result.

The commonly reported prevalence of severe postoperative bleeding (>10 U of blood transfused) after cardiac surgery is between 3% and 5%. Although approximately 50% of the patients who undergo reoperation for excessive bleeding exhibit incomplete surgical hemostasis, the remainder bleed because of various acquired hemostatic defects, most often related to the platelet dysfunction that accompanies CPB.11 There is a reduced need for blood products in patients operated upon without CPB. The factors that predispose patients to bleeding after CPB are residual heparin effect, platelet dysfunction (which may be intensified by preoperative drug therapy, eg, aspirin, clopidogrel, and glycoprotein [GP] IIb/IIIa inhibitors), clotting factor depletion, inadequate surgical hemostasis, hypothermia, and postoperative hypertension. CPB decreases both platelet count and function. Hemodilution causes platelet counts to decrease rapidly to approximately 50% of preoperative values. Within minutes after instituting CPB, the bleeding time is prolonged, and platelet aggregation impaired. The bleeding time usually normalizes by 2 to 4 hours after CPB. The platelet count usually requires several days to return to normal levels. Although the exact mechanism responsible for the transient platelet dysfunction remains undefined, it appears to be related to contact of platelets with the synthetic surfaces of the extracorporeal oxygenator and to hypothermia. Reductions in the plasma concentrations of coagulation factors II, V, VII, IX, X, and XIII as a consequence of hemodilution occur during CPB, but these coagulation factors remain well above levels considered adequate for hemostasis and generally normalize within the first 12 hours after surgery. Moreover, although bleeding after CPB is often attributed to excessive fibrinolysis, the decrease in both plasminogen and fibrinogen levels during CPB is more a result of hemodilution and not consumption.11 Exploration for postoperative bleeding commonly identifies no localized site of bleeding but only diffuse oozing. Less frequently, a specific site such as an internal mammary pedicle is identified.

Recombinant activated factor VIIa (NovoSeven, Novo Nordisk Inc., Princeton, NJ) is a prohemostatic agent that may be considered in patients with life-threatening bleeding. Factor VIIa is thought to act locally at sites of vascular wall disruption. It binds to exposed tissue factor and generates thrombin sufficient to activate platelets. The agent is approved only for the management of patients with hemophilia A and B in the presence of inhibitors. It is not clear at what stage of intractable bleeding it should be used, but a reasonable approach is to administer after all other treatments (full-dose aprotinin, platelets, fresh-frozen plasma, and cryoprecipitate) have failed.12

Vasoconstriction with Hypertension and Borderline Cardiac Output

Increased arteriolar resistance as a consequence of hypothermia and increased levels of circulating catecholamines, plasma renin, or angiotensin II is present in most postoperative cardiac patients. The usual criterion for pharmacologic lowering of blood pressure in postoperative patients is a mean arterial blood pressure 10% above the upper level of normal (>90 mm Hg). Patients with a friable aorta or friable suture lines might be subjected to a lower mean arterial pressure (MAP) to prevent dehiscence. The mean arterial blood pressure is monitored because it is most reflective of systemic vascular resistance. As a hypothermic patient is rewarmed, a short-acting vasodilator (nitroprusside, nitroglycerin, or nicardipine) can be infused IV to maintain MAP at 80 to 90 mm Hg. Intravascular volume should be maintained at a relatively high level (PAOP, 14-16 mm Hg) in anticipation of vasodilation on rewarming and to enhance cardiac output and peripheral perfusion. If the cardiac index is marginal (2.0-2.2 L/min/m2), an inotropic drug should be administered in addition to the vasodilator.

Vasodilatation and Hypotension

This condition, which generally appears during rewarming, is most effectively prevented and best treated by fluid administration. There is a paucity of data indicating that any specific volume expander is better than another, although colloids remain in the intravascular space longer than crystalloid solutions. Fluid should be administered until cardiac output no longer increases or appropriate left ventricular filling pressures have been restored (PAOP, ~14-16 mm Hg for a normal ventricle or 18-22 mm Hg for a noncompliant ventricle).

If the systemic arterial pressure is inadequate despite fluid administration, vasoactive drugs become the mainstay of hemodynamic management. If the cardiac index is over 2.5 L/min/m2, either dopamine in high doses or norepinephrine is preferable. Although the safety and efficacy of vasopressin seems established and endogenous vasopressin levels are depressed after CPB, vasopressin is not currently recommended as first-line therapy. Epinephrine produces visceral hypoperfusion and lactic acid production and, consequently, is not recommended as first-line therapy. If the cardiac index is marginal (<2.0 L/min/m2), an inotropic agent—either a β1-adrenoceptor agonist (dobutamine) or a phosphodiesterase III inhibitor (milrinone)—is used to push the mixed venous or central venous oxygen saturation to greater than 70%. Each of these classes of inotropic agents increases myocardial oxygen demand and has the potential to cause arrhythmogenesis. Levosimendan offers favorable hemodynamic and neurohormonal effects but has not demonstrated a survival benefit over dobutamine. β-Blocker therapy may be used to attenuate the sympathetic hyperactivity and arrhythmogenic risks associated with this drug. Regardless of the inotrope used, norepinephrine should be added if the MAP remains below 60 mm Hg.

In critically ill patients, hemodynamic optimization is probably best achieved by measuring the SvO2 in conjunction with the cardiac output. The central venous oxygen saturation (ScvO2) can be used as a surrogate for the SvO2; although the absolute values of the ScvO2 and SvO2 differ, the values tend to change in parallel over a wide range of hemodynamic conditions.

Normal Ventricular Systolic Function and Low Cardiac Output

This set of circumstances is often noted in small body size women with systemic hypertension and in patients undergoing aortic valve replacement for aortic stenosis. The likely explanation is diastolic dysfunction. The problem should be managed by volume expansion with the intent to elevate PAOP to levels as high as 20 to 25 mm Hg if necessary as long as right ventricular function is adequate to fill the left ventricle. Sinus rhythm and atrioventricular (AV) synchrony are essential and, if not present, consideration should be given to restoration. In the absence of other reasons for diastolic dysfunction, the possibility of cardiac compression from clots in the mediastinum and pericardial space should be considered. If volume expansion does not lead to hemodynamic improvement, transesophageal echocardiography may be used to establish or exclude the presence of clots or other causes of low output.

Low Cardiac Output Syndrome

Satisfactory cardiac performance after cardiac surgery is usually indicated by a cardiac index greater than 2.2 L/min/m2 with a heart rate below 100 beats/min . Marginal cardiac function is present with a cardiac index between 2.0 and 2.2 L/min/m2. A cardiac index below 2.0 L/min/m2 is unacceptably low, and therapeutic intervention is indicated. Clinical signs of the adequacy or inadequacy of organ perfusion must be incorporated into any assessment of cardiac performance. It is also useful to measure the mixed venous oxygen saturation because a subset of patients who are hypothermic may have a low cardiac index but an acceptable mixed venous oxygen tension.

Assessment

The most common causes of low cardiac output after surgery are related to a decreased left ventricular preload. The decreased preload, in turn, can likely be attributed to hypovolemia (a result of bleeding or of vasodilatation as a consequence of warming or of drugs), cardiac tamponade, or right ventricular dysfunction. Alternative explanations for low cardiac output include decreased contractility caused by a preexisting low ejection fraction or to intra- or postoperative ischemia or infarction. Tachy- or bradyarrhythmias decrease cardiac output by reducing ventricular preload (eg, decreased diastolic filling time, loss of atrial contraction or AV synchrony) or by reducing the number of effective ventricular contractions per minute. Substantial increases in systemic vascular resistance (ie, vasoconstriction) impede ventricular ejection and lower cardiac output. Vasodilatation from sepsis or anaphylaxis resulting in systemic hypotension can lead to reduced coronary blood flow and myocardial ischemia. Vasopressin may be uniquely effective in anaphylactic shock secondary to its ability to reverse mediator-induced vasoplegia. Sepsis (an unlikely occurrence in the immediate postoperative period) is also associated with the production of myocardial depressant factors. Anemia may result in reduced blood viscosity (a major determinant of total peripheral resistance) leading to hypotension and decreased oxygen delivery to the heart. The hypotension associated with anemia, however, is most often caused by changes in effective blood volume rather than by the changes in viscosity.

Etiology and Management