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Salenger R, Gammie JS, Vander Salm TJ. Postoperative Care of Cardiac Surgical Patients.
In: Cohn LH, Edmunds LH Jr, eds. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2003:439469.

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Chapter 15

Postoperative Care of Cardiac Surgical Patients

Rawn Salenger/ James S. Gammie/ Thomas J. Vander Salm

OVERVIEW OF MAJOR DERANGEMENTS
INFLAMMATORY RESPONSE TO CARDIOPULMONARY BYPASS
COMPLICATIONS: ANTICIPATION AND TREATMENT
HEART
????Minimal Requirements
????Determinants of Cardiac Output
PERIOPERATIVE VENTRICULAR DYSFUNCTION
????Causes
????????PERICARDIAL TAMPONADE
SUPPORT OF CARDIAC PERFORMANCE
????Pharmacologic Support
????????THYROID HORMONE
????Mechanical Circulatory Support
????????INTRA-AORTIC BALLOON COUNTERPULSATION
????????VENTRICULAR ASSIST DEVICES
BLEEDING
????Causes
????????PREDISPOSITION TO BLEEDING
????????MECHANICAL, ANATOMIC, OR SURGICAL CAUSES
????????BLEEDING DIATHESIS
????Diagnosis
????Treatment
????????INTRAOPERATIVE PREVENTION
????????PHARMACOLOGIC PREVENTION
????????REINFUSION OF SHED BLOOD
????????VOLUME REPLACEMENT
????????BLOOD FACTOR REPLACEMENT
????????OTHER METHODS OF CONTROLLING BLEEDING
????Reexploration for Bleeding
????ICU Emergency Sternotomy
LUNG
????Initial Assessment
????Pulmonary Dysfunction
????????PULMONARY EFFECTS OF CARDIOPULMONARY BYPASS
????????PHRENIC NERVE PALSY
????????OTHER CAUSES
????Ventilation
????????INITIAL MANAGEMENT: VENTILATOR SETTINGS
????????MAINTENANCE
????????VENTILATOR WEANING
????????WEANING CRITERIA
????????POSTEXTUBATION SUPPORT
????????REINTUBATION
????????COMPLICATIONS
????Long-Term Ventilator Support
????????CAUSES OF FAILURE TO WEAN FROM MECHANICAL VENTILATION
????????WEANING AFTER PROLONGED MECHANICAL VENTILATION
????????WEANING TECHNIQUES
????Tracheostomy
????General Care
KIDNEY
????Postoperative Renal Function
????Causes of Oliguria
????Pre-renal Oliguria
????Renal Failure
????????DIAGNOSIS
????????TREATMENT
????????PROGNOSIS
NERVOUS SYSTEM
????Central Neurologic Complications
????Neuropsychologic Complications
????Peripheral Deficits
GASTROINTESTINAL SYSTEM
PROPHYLACTIC ANTIBIOTICS
REFERENCES

?? OVERVIEW OF MAJOR DERANGEMENTS
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Major physiological derangements must be treated in patients recovering from a cardiac surgical operation. These fall into two types: those existing preoperatively and those that occur as a consequence of the operation and cardiopulmonary bypass (CPB). The goal is to restore normal homeostasis. The most important factor contributing to this restoration, of course, is the proper conduct of a well-conceived operation.

Because so many systems may be deranged, a systems-oriented approach is necessary to deal with problems in an orderly fashion.1 The cardiac system, usually the most perturbed, is the primary determinant of recovery, and consequently requires the greatest effort to restore normal function. Measured cardiac output, clinical signs of cardiac adequacy, and blood pressure must be maintained, and cardiac distension and ischemia must be avoided. A low cardiac index during the early postoperative period markedly increases the probability of death.2,3 With the physiological trauma of recent cardiopulmonary bypass, hearts are susceptible to ventricular arrhythmias early after operation and to atrial arrhythmias later.

Fluid accumulation in the perioperative period and interstitial edema cause pulmonary dysfunction. The goal is to wean the patient from mechanical ventilation and high oxygen concentrations as quickly as is commensurate with adequate spontaneous ventilation, ability to protect the airway, and satisfactory oxygenation.

High urine output usually results from operations performed on cardiopulmonary bypass; anything less raises the alarm of renal insufficiency and requires immediate evaluation and treatment. Renal dysfunction occurs commonly after heart operations, and early and aggressive treatment reduces the otherwise high mortality accompanying this complication.4

Neurologic complications occur more commonly after heart operations than after most other types of surgery. Early, careful assessment and documentation of the return of mental and central and peripheral neurologic function are required. Although many central deficits occurring in the perioperative period cannot be treated, others can be, and early diagnosis allows treatment before changes become irreversible.

Excessive bleeding complicates heart operations more often than other operations. Consistent, systematic intraoperative control of bleeding contributes more than any other factor to tolerable postoperative blood loss. Even then, excessive bleeding occurs with a frequency higher than with most other operations. Bleeding may be from surgical bleeding sites or caused by the temporary coagulation disorder that accompanies nearly all heart surgery.


?? INFLAMMATORY RESPONSE TO CARDIOPULMONARY BYPASS
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CPB harms patients, even while it enables life-preserving operations. In a time-dependent fashion, CPB activates plasma proteins and blood and endothelial cells.512 These complex reactions activate the complement, clotting, and fibrinolytic cascades and cause a bleeding tendency, microemboli, fluid retention, and perturbation of the hormonal milieu.1316 A detailed description of these events is provided in Chapter 11.


?? COMPLICATIONS: ANTICIPATION AND TREATMENT
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A protocol for postoperative care is useful if it anticipates and prevents complications while minimizing utilization of hospital resources. Many complications that occur from cardiac operations, such as renal failure, pulmonary dysfunction, and bleeding, may be anticipated. Accordingly, early and aggressive treatment mitigates morbidity and shortens convalescence.

Hemodynamic malfunction may be caused by the underlying heart disease, but to assume so precludes correcting mechanical complications of the operation at a time when damage may be minimized. Postcardiac surgical units routinely monitor the electrocardiogram (ECG), arterial blood pressure, and filling pressures (right atrial, left atrial, and/or pulmonary artery pressure) and also utilize continuous displays of arterial and mixed venous oxygen saturations (via pulse oximetry and oxymetric pulmonary artery catheters, respectively). These indices allow minute-to-minute assessment of cardiopulmonary physiology. Deviations from expected normal ranges prompt immediate reevaluation of heart and lung function (Table 15-1).


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TABLE 15-1 Expected values following cardiac surgery

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As a working policy, therefore, all hemodynamic malfunctionslow cardiac output, low blood pressure, elevated left or right atrial pressuresare first considered a direct mechanical complication of the operation performed or a result of mechanical ventilation or drug administration. Reparable maladies such as coronary artery graft occlusion or spasm, prosthetic paravalvular leak, mechanical valve leaflet immobility, pericardial tamponade, pneumothorax, hemothorax, endotracheal tube malposition, and incorrect doses of intravenous infusions are considered first.

Commonly used medications are listed in Table 15-2. Examples of standard postoperative orders are included in Table 15-3. Details of patient care are included in the following sections.


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TABLE 15-2 Commonly Used Postoperative Medications

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TABLE 15-3 Routine Postoperative Orders

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?? HEART
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Minimal Requirements

Adequate cardiac function is an absolute requirement for successful recovery from any operation, including one on the heart itself. During the immediate postoperative period, minimum requirements of systemic and pulmonary blood flow must be met to avoid organ dysfunction. Normal renal, gastrointestinal, and neurologic functions are the best indices of adequate systemic circulation, but other parameters, including measurements of cardiac output and oxygen utilization (VO2), are also useful.

Under basal conditions, oxygen consumption can be measured directly; taken from tables that correct for age, sex, and size; or estimated utilizing calculations based on the patient's size (125 mL O2 per minute per m2).17 A value for oxygen consumption provides a means of estimating cardiac output from measurements of mixed venous and arterial oxygen content using the Fick equation (Table 15-4). Frequently, measurements of mixed venous oxygen saturation (SvO2) are used to determine whether the cardiac output meets systemic demands. An SvO2 greater than 60% is acceptable for an awake normothermic patient. Following cardiac surgery, a number of factors may affect the oxygen content of blood, the ability of blood to release oxygen where it is needed, and the body's demand for oxygen (Table 15-5). The essence of postoperative critical care is to ensure the adequacy of systemic oxygen supply relative to demand.18,19


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TABLE 15-4 Fick equation of cardiac output*

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TABLE 15-5 Factors affecting systemic oxygen supply and demand after cardiac surgery

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Determinants of Cardiac Output

The cardiac output, expressed as liters per minute per square meter (cardiac index; CI), is the most commonly used measure of cardiac performance in the immediate postoperative period. Although other methods are possible, the thermodilution technique using a pulmonary artery catheter and room temperature injectate is simple and sufficiently precise.20 A normal value for CI after surgery is between 2.0 and 4.4 L/min/m2.21

Dietzman et al3 first reported the association between low cardiac output and mortality after cardiac surgery, and this observation was confirmed subsequently by others.2226 A normal recovery from cardiac surgery can be expected when the CI is maintained above 2.0 to 2.2 L/min/m2.27 Treatment of low cardiac output is predicated on manipulation of its primary determinants (Table 15-6).


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TABLE 15-6 Treatment of low cardiac output (CI 2)

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The determinants of cardiac output are heart rate and stroke volume. The latter is influenced by the cardiac rhythm, ventricular preload and afterload, and myocardial contractility. Although the heart rate is usually slightly increased immediately after surgery, patients using large amounts of beta blockers preoperatively or with an intrinsic rhythm disturbance may have a slow heart rate. Conversely, some patients, particularly younger ones or those with profound left ventricular dysfunction, may be tachycardic. The optimal heart rate balances coronary blood flow (which takes place mainly during diastole) with cardiac output and is usually between 80 and 100 beats per minute.28 Normal sinus rhythm ensures atrioventricular synchrony and maximizes cardiac efficiency.29 Loss of sinus rhythm (junctional rhythm or atrial fibrillation) usually reduces cardiac output by 10% to 25%.30 Patients with slow sinus rhythm (less than 70 beats per minute) or junctional (AV nodal) rhythm usually can be paced via atrial pacing wires placed at the time of surgery to improve cardiac output.31 Slowing a rapid rhythm (>110 bpm) is important to reduce the likelihood of developing myocardial ischemia in the immediate postoperative period when coronary flow reserve is limited. Reduction of exogenous catecholamines; administration of narcotics, sedatives, antipyretics, or intravenous fluids; and the use of antiadrenergics such as beta blockers are employed to slow a rapid heart rate.

Ventricular preload refers to sarcomere length at end-diastole when both passive filling and the contribution of atrial contraction are complete. Sarcomere length cannot be measured directly, and therefore, a number of surrogate measurements are used. These include left ventricular end-diastolic volume (LVEDV), which is related to left ventricular end-diastolic pressure (LVEDP). The relationship LVEDV/ LVEDP is referred to as ventricular compliance, a combination of active relaxation of the actin-myosin complex and the passive viscoelastic properties of the myocardium.32,33 Hearts with reduced ventricular compliance (a frequent finding after heart surgery34) exhibit diastolic dysfunction and therefore require a higher LVEDP to achieve a given preload. For example, patients with left ventricular hypertrophy secondary to aortic stenosis have poor left ventricular compliance. Left atrial pressure closely approximates LVEDP and its direct measurement is especially helpful in patients undergoing complex operations or with preexisting left ventricular dysfunction. Pulmonary capillary wedge pressure or pulmonary artery diastolic pressure provide good estimates of the left atrial pressure when pulmonary congestion, edema, and inflammation are absentconditions rarely met immediately after cardiac surgery.35

To maintain adequate preload, volume replacement frequently is necessary immediately after heart surgery due to loss of arterial and venous vasomotor tone, increased capillary permeability, bleeding, and high volumes of urine.36 Often, judicious fluid administration is all that is required to maintain hemodynamic stability or to treat low cardiac output accompanied by vasoconstriction. Lactated Ringer's solution is appropriate initially, but infusion of hydroxyethyl starch (hetastarch) or blood products may be indicated. Limited animal and retrospective data have raised concern regarding coagulation abnormalities associated with the use of hetastarch after cardiac surgery.3739 The preponderance of evidence, however, suggests that when administered in quantities under 20cc/kg/24h hetastarch does not cause increased bleeding, and is at least as effective as albumin solutions for volume expansion,37,3950 at half the cost. Transfusion of packed red blood cells should be governed by logical protocols and good clinical judgment with regard to the rate of blood loss. In general, blood is not necessary unless the hematocrit is less than 25%. Strategy based on recent data suggests that the mortality rate rises sharply if the intraoperative hematocrit is allowed to drop below 23%.51

Ventricular afterload refers to systolic wall stress, which is determined by intraventricular systolic pressure and ventricular wall thickness.52 Ventricular wall thickness changes minimally during heart surgery, and therefore changes in ventricular systolic pressure have the most impact on afterload. In the absence of left ventricular outflow obstruction, systolic blood pressure determines afterload and thereby influences both stroke volume and myocardial oxygen demand.53,54 Manipulations of systemic vascular resistance can improve cardiac output and the adequacy of coronary blood flow.55,56

Hypertension, or at least systemic vasoconstriction, is common after cardiac surgery.57 Increased arterial resistance has been associated with low PO2 in skeletal muscle and secondary metabolic acidosis despite adequate cardiac output and oxygen content of arterial blood.58 The microcirculatory changes that produce inadequate tissue perfusion appear to resolve after a period of 6 to 8 hours, but this interval does not correlate with rewarming following moderately hypothermic cardiopulmonary bypass.59 Humoral factors may play a role, since a number of circulating mediators are present and produce the whole-body inflammatory response to CPB.8,60 Regardless of etiology, sodium nitroprusside is an effective means to reduce afterload during and after cardiac surgery.57,61,62 The administration of this and other drugs via computer-controlled systems offers several advantages6365 but cannot substitute for a competent bedside clinician.

Some patients have a lowered systemic vascular resistance (SVR) during and immediately after cardiopulmonary bypass. The accompanying hypotension sometimes requires treatment with vasoconstrictors that are usually agents with pronounced alpha-adrenergic effects such as phenylephrine or norepinephrine. Christakis et al66 reported the incidence of low SVR to be more common in patients undergoing normothermic perfusion and in those with longer cardiopulmonary bypass times.66 Diabetics, patients with peripheral vascular disease, and those with a left ventricular ejection fraction of less than 0.40 are less likely to develop low systemic vascular resistance and associated hypotension. Phenylephrine has been shown to decrease flow in internal mammary grafts but not in saphenous vein grafts, whereas norepinephrine does not change and epinephrine increases flow in the internal mammary artery. 67

Most surgeons assess myocardial contractility before, during, and after a cardiac operation by indirect methods. Measurements of ejection fraction, ventricular wall motion, and cardiac output all depend on loading conditions present at the time, as well as intrinsic myocardial contractility. In the research laboratory, changes in the ventricular pressure/volume relationship during a cardiac cycle can be used to generate a load-independent assessment of contractility,68 but this methodology is impractical for routine clinical use. Thus appropriate assumptions regarding contractility are made when changes in cardiac output are not explained by the other determinants.

Following heart surgery, dysfunction of either ventricle may limit overall cardiac performance. Measurement and comparison of right and left atrial pressures (reflective of respective ventricular end-diastolic pressures) provide important information.69 When the atrioventricular valves are normal, the ventricle with the highest corresponding atrial pressure is the one limiting cardiac performance. Therapeutic interventions, including but not limited to the use of inotropes, are aimed at supporting that ventricle.


?? PERIOPERATIVE VENTRICULAR DYSFUNCTION
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Causes

The factor that contributes the most to depressed postoperative cardiac function is the pathology that existed immediately prior to operation. Even when reconstructive surgery is successful, it is unusual to see an immediate improvement in contractile function (without the administration of inotropes). Thus adequate cardiac reserve must be present to withstand the demands of heart surgery. Preoperative cardiac abnormalities are not limited to systolic function but may involve diastolic, valvular, electrophysiologic, and vascular function. Optimal perioperative care is aimed at compensating for this impaired preoperative function.

The operation itself may cause left ventricular dysfunction and low cardiac output. Contributors to cardiac dysfunction include inadequate protection of the myocardium during periods of aortic cross-clamping, myocardial and pulmonary edema, acute left ventricular distension or other trauma, uncorrected valvular lesions, and reduced coronary blood flow. The investigation as to whether the operation has been adequate to correct preexisting pathology begins as soon as the aortic cross-clamp is removed. Search for graft occlusion, valvular incompetence, cardiac compression, or intracardiac shunting continues throughout the postoperative period. Useful tools include assessment of wall motion abnormalities by direct visualization or echocardiography (usually transesophageal), the electrocardiogram, cardiac enzymes, blood gases obtained from the pulmonary and systemic vasculature, and right and left atrial pressure measurements. Discovery of an inadequate operation usually demands immediate reoperation.

PERICARDIAL TAMPONADE

Pericardial tamponade can occur either when the heart is too large for the available space (after sternum closure) because of the myocardial, lung, and mediastinal edema resulting from a long operation or when postoperative fluid collection compresses a heart that previously fit comfortably in the pericardial space. Compression of the heart, especially of the right atrium and ventricle, can reduce overall cardiac function dramatically. Increased right-sided heart pressures impair venous return and consequently diminish left ventricular preload.

Sternal closure tamponade This will be evident as soon as sternal closure is attempted. Delayed sternal closure is an accepted technique for avoiding compression of the seriously impaired or markedly edematous heart in the immediate postoperative period.7072 Infectious complications are minimized by covering the wound with an occlusive water-tight dressing70 and instituting continuous irrigation of the mediastinum with a diluted povidone-iodine solution.73,74 Because of the concern for possible iodine toxicity, antibiotic solutions may also be used. Closure of the sternum is usually possible in 2 to 4 days after achieving a negative fluid balance of several liters.71

Fluid accumulation tamponade This occurs in the early postoperative period from an accumulation of undrained blood and clot in patients who initially demonstrate adequate ventricular performance but have copious bleeding in the initial hours after surgery. Coagulopathy correction results in formation of a pericardial clot, with consequent inability of the mediastinal tubes to evacuate the accumulating blood. Tamponade results. Acute tamponade is usually associated with a rapid increase in right and left atrial pressures, which tend to equalize. Tamponade is almost invariably associated with widening of the mediastinal silhouette on the chest radiograph. The association of rising atrial pressures, diminished cardiac output, and a widening mediastinum is sufficient to prompt surgical exploration.

Although the majority of patients develop some degree of pericardial effusion in the days following heart surgery, only a minority develop signs and symptoms of tamponade.75 Delayed pericardial tamponade may develop insidiously. It can occur as late as several weeks after operation and is more common in patients receiving anticoagulants.76,77 Delayed tamponade is not associated with the postpericardiotomy syndrome (fever, pain, friction rub)78 but rarely may be caused by chylopericardium.79,80 Prolonged drainage of the pericardial space does not prevent subsequent development of delayed tamponade.81

The use of echocardiography to diagnose early or delayed tamponade has been well described,8284 and this test is indicated in patients with unexplained poor cardiac performance following heart surgery.85 Measurement of an exaggerated pulsus paradoxus (a decrease in systolic blood pressure during inspiration) remains a reliable clinical indicator and, together with adequate radiologic examination, indicates the need for drainage. Although percutaneous catheter drainage is useful for effusions unassociated with heart surgery, the safest treatment for delayed tamponade after median sternotomy is surgical, usually by a simple subxyphoid approach.86


?? SUPPORT OF CARDIAC PERFORMANCE
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Pharmacologic Support

If ventricular function is depressed following a cardiac operation, treatment with vasodilators and volume loading may not be sufficient to ensure adequate circulation. Ventricular contractility should be augmented, usually with inotropic agents. There are excellent reviews on this subject,8789 and a thorough understanding of the pharmacology involved is required to care for postoperative cardiac patients. Inotropic agents may be divided into catecholamines and noncatecholamines. The former include natural or synthetic adrenergic agents that stimulate alpha and beta receptors in the heart, lungs, and peripheral vasculature (Table 15-7). Noncatecholamines include calcium, digoxin, amrinone, and milrinone.


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TABLE 15-7 Adrenergic receptor activity of commonly used catecholamines*

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Patients likely to benefit from catecholamine support are those with low cardiac output (CI 2), with optimized heart rate, rhythm, ventricular preload, and afterload, and without evidence of acute cardiac tamponade. Dopamine and dobutamine enhance heart rate and cardiac output equally, but dobutamine produces greater reductions in left ventricular preload and afterload.90 Dobutamine augments myocardial coronary blood flow more than dopamine.91 Dopamine works well in conjunction with vasodilators for low cardiac output after heart surgery.92,93 As with all adrenergic agents, the hemodynamic effects of these drugs depend on dosage. When dopamine is administered at less than 8 ?g/kg per minute, beta and dopaminergic receptor stimulation predominates and enhances cardiac output and renal blood flow.94 At doses greater than 10 ?g/kg per minute, alpha vasoconstrictor effects predominate, and tachycardia may ensue. The underlying pathophysiology and age of the patient may alter the expected response.

The effect of epinephrine on both alpha- and beta-adrenergic receptors makes it a useful agent following cardiac surgery. The effects of epinephrine vary by dosage. At low doses (?g/kg/min), epinephrine stimulates peripheral beta2 receptors and causes vasodilation. Higher doses cause increasing cardiac effects, and the highest doses can cause vasoconstriction via peripheral alpha receptor stimulation. The response of an individual patient's peripheral and pulmonary hemodynamics is somewhat unpredictable, especially after cardiopulmonary bypass. Steen et al95 investigated the effects of epinephrine after cardiac surgery and discovered a consistent increase in cardiac output but variable changes in mean arterial pressure. Stephenson et al96 demonstrated similar increases in cardiac output with epinephrine infusions after heart surgery and showed that hypertension and tachycardia occurred when higher doses were used.

Norepinephrine, another naturally occurring catecholamine, is used after heart surgery when blood pressure is low. In addition to pronounced effects on peripheral alpha receptors, norepinephrine is a potent beta1 agonist and therefore increases myocardial inotropy. The increased blood pressure that these two effects provide must be balanced against increased myocardial oxygen consumption and reduced renal, mesenteric, and peripheral perfusion that may ensue, especially at higher doses.

Isoproterenol stimulates beta1- and beta2-adrenergic receptors but has little alpha action. Isoproterenol increases heart rate and contractility and decreases systemic vascular resistance. Isoproterenol is potentially useful when reactive pulmonary hypertension and right-sided heart failure contribute to postoperative low cardiac output, as may occur following mitral valve surgery or cardiac transplantation. Its nonselective beta-adrenergic stimulation, which may cause tachyarrhythmias and systemic vasodilation, limits its utility in other situations.

Calcium, in its ionized form, is critical for excitation-contraction coupling in cardiac muscle.97 Low calcium ion concentrations depress ventricular function and peripheral resistance and contribute to hypotension and low cardiac output. In addition, adequate calcium is necessary for the action of many cardiovascular drugs, including catecholamines. Drop and Scheidegger98 demonstrated that a calcium bolus injection is associated with increased myocardial contractility, an effect that is directly related to the initial calcium level (Fig. 15-1). Shapira et al99 also showed that a bolus of calcium can cause transient hemodynamic improvement in patients after cardiopulmonary bypass but that a continuous infusion of calcium does not sustain the beneficial effect. Because of these and similar100,101 observations, many surgeons administer a bolus of calcium (500 to 1000 mg) immediately before weaning from cardiopulmonary bypass when serum ionized calcium levels are generally low.



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FIGURE 15-1 Influence of initial calcium concentration on left ventricular response to calcium administration. (Reproduced with permission from Drop LJ: Ionized calcium, the heart, and hemodynamic function. Anesth Analg 1985; 64:432.)

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Inamrinone (initially named amrinone) is a noncatecholamine bypyridine derivative that inhibits phosphodiesterase to slow the hydrolysis of adenosine 3', 5'-cyclic monophosphate (cAMP).102 Because its congener, milrinone, causes less thrombocytopenia, milrinone has largely replaced inamrinone in clinical use.103106 Increased vascular (systemic and pulmonary) and myocardial cAMP augments cardiac output through pulmonary and systemic vasodilation and inotropic effects.107110 Milrinone also partially reverses the reduction in ventricular compliance induced by cardiopulmonary bypass.111 It is useful in cases of right ventricular and biventricular failure due to its ability to reduce right ventricular afterload. Milrinone clearly improves separation from cardiopulmonary bypass in patients who have preexisting left ventricular dysfunction.112 Since the mechanism of action complements that of catecholamines, which stimulate production of cAMP, these drugs can be used in combination with milrinone to achieve a synergistic effect.

Phosphodiesterase inhibitors appear to improve myocardial relaxation113 as well as coronary,114 skeletal muscle,115 and mesenteric blood flow.116 Their use is not associated with an increase in myocardial oxygen consumption,110,117 a finding that contrasts with all the catecholamines. Unfortunately, these agents cost substantially more than do traditional inotropes. They have a slight proarrhythmic effect.118

Once acute problems have subsided, some patients in sinus rhythm require chronic augmentation of contractile function. The use of digitalis in this setting has long been argued, but there is evidence that it increases contractility.119 Newer agents such as enoximone, another type III phosphodiesterase inhibitor, and vesnarinone, a quinalone with immunomodulatory properties, may be available for treatment of chronic heart failure, perhaps used in combination with beta-blocking agents.120122 Their role in the immediate postoperative period is not defined.

THYROID HORMONE

Several studies have demonstrated that cardiopulmonary bypass and hypothermic cardiac arrest result in low serum levels of thyroid hormone.13,123125 The pattern of thyroid hormone depletion after cardiopulmonary bypass is similar to that seen in other acute nonthyroid illnesses and the euthyroid sick syndrome. Traditionally, triiodothyronine replacement has not been administered to this group of patients. Several studies have challenged this view by demonstrating improved recovery of ischemic myocardium in animals126129 and improved hemodynamics with a lower incidence of atrial fibrillation in a small number of patients after cardiopulmonary bypass.125,130134 Thyroid supplementation to unstable organ donors may improve outcomes in cardiac transplantation.135138

Triiodothyronine (T3) augments cardiac output via nucleus-mediated mechanisms and direct stimulation of calcium-ATPase in the sarcolemma and sarcoplasmic reticulum.139 Enhancement of calcium transport reduces the cytoplasmic calcium concentration, which aids in myocardial relaxation. This action improves myocardial compliance and diastolic function in postischemic stunned myocardium.13,123,124,139 Triiodothyronine also decreases cardiac work postoperatively by acutely decreasing systemic vascular resistance.132,140,141

A number of studies, however, including a trial of over 200 patients, have failed to demonstrate any significant hemodynamic benefit from administering triiodothyronine to patients after cardiopulmonary bypass.141143 This may be related to intramyocardial T3 levels. Although serum levels of thyroid hormone are decreased for up to one week after cardiopulmonary bypass,13,124 the myocyte may not be depleted of thyroid hormone.144 Concerns regarding enhanced myocardial oxygen demand and conflicting data about atrial arrhythmias have further limited widespread use of this hormone.145,146 Further investigation will help elucidate the multiple cardiovascular effects of triiodothyronine and possibly define the subset of patients who will benefit from this therapy.

Mechanical Circulatory Support

Pharmacologic inotropic support is the first line of therapy for the patient who fails to separate from cardiopulmonary bypass or who experiences pump failure in the early postoperative period. The decision to add mechanical support (IABP or a ventricular assist device) to chemical support is frequently based on the presence of low cardiac output (CI 2) despite maximal inotropic support. Examination of levels of inotropic support at the time of separation from cardiopulmonary bypass in a group of adult patients undergoing cardiac surgery demonstrated a linear correlation between the level of pharmacologic inotropic support administered and hospital mortality. Patients requiring three high-dose inotropes at the time of weaning from cardiopulmonary bypass had a mortality of 80%.147 This series also showed greatly improved hospital discharge rates for patients who underwent ventricular assist device (VAD) insertion based on a defined formula (cardiogenic shock despite administration of two high-dose inotropes) that emphasized early insertion. It is clear that high-dose pharmacologic inotropic support alone may stabilize a patient's hemodynamics and permit transfer to the intensive care unit, but that a significant proportion of these patients will ultimately succumb to multisystem organ failure.

INTRA-AORTIC BALLOON COUNTERPULSATION

Intra-aortic balloon pumping (IABP) was first performed clinically by Kantrowitz et al in 1968.148 IABP uses the principle of diastolic counterpulsation, in which the balloon inflates in synchrony and out of phase with the cardiac cycle. Benefits of this technique include augmentation of diastolic coronary perfusion pressure, reduced systolic afterload, and increased cardiac output with an improvement in the myocardial oxygen supply/demand ratio. Major contraindications to IABP use include severe atherosclerotic disease of the aorta or iliofemoral arteries, descending aortic dissection, and aortic insufficiency. If indicated, insertion of the IABP can be accomplished bedside in the ICU. IABPs are used perioperatively in 8% to 12% of cardiac surgical operations. There are significant practice pattern variations in regards to timing of insertion, with the percentage of IABPs inserted preoperatively ranging from 20% to 70%.149151 Complications of femoral IABP placement include lower extremity ischemia and thrombocytopenia.152156

VENTRICULAR ASSIST DEVICES

The intra-aortic balloon pump is an attractive form of circulatory support for the patient undergoing cardiac surgery because of its ease of insertion and removal. However, the IABP only yields a modest increase in cardiac output and does not displace a significant volume. Failure of the IABP to improve hemodynamic performance of the failing heart should prompt consideration of rapid institution of mechanical circulatory support. An ideal circulatory support device would be rapidly and easily implanted and explanted, permit uni- or biventricular assist, have minimal anticoagulation requirements, provide maximal LV unloading, reliably provide intermediate length support (714 days), permit ambulation, have a low infection rate, and be easy to convert to a long-term device. Such a device does not exist. Currently available options include the centrifugal pump, extracorporeal life support (ECLS), the Abiomed BVS-5000, and the Thoratec system.


?? BLEEDING
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Causes

PREDISPOSITION TO BLEEDING

Although infrequent, preoperative disorders may cause postoperative bleeding. Acute myocardial infarction treated with thrombolytic therapy within hours before surgical revascularization causes a profound bleeding diathesis that can be controlled with fibrinogen replacement and/or aprotinin.157,158 Aspirin taken within 1 week before operation may increase the bleeding time but infrequently increases postoperative blood loss.159,160 A heart operation may be necessary after patients have had percutaneous coronary angioplasty or stent insertion. These patients will often be under the influence of platelet inhibitors such as the glycoprotein IIb/IIIa inhibitors eptifibatide, tirofiban, or abciximab; or the ADP binding inhibitor, clopidogrel. Platelet transfusion to counteract all these antiplatelet drugs and fresh frozen plasma or cryoprecipitate for the GP IIb/IIIa inhibitors will attenuate resultant coagulopathy.161

Other intrinsic clotting abnormalities are encountered occasionally; however, almost all can be ruled out in the absence of a history of unusual bleeding with lacerations, operations, or dental procedures. We do not recommend a routine preoperative bleeding time but do obtain a careful bleeding history.

MECHANICAL, ANATOMIC, OR SURGICAL CAUSES

In the presence of excessive bleeding (over 500 mL in the first hour), the first question is whether or not bleeding is coming from an anatomic source. Such sources include vascular anastomoses, side branches of saphenous veins or internal mammary arteries, cannulation sites, aortotomies or cardiotomies, left ventricular aneurysm resection lines, the distal transected end of an internal mammary artery, edges of pericardium, the coronary sinus and great coronary vein, sternal wire sites, and pleural or pericardial fat. If bleeding is exceptionally brisk or an anatomic source is suspected, the remedy is immediate operation.

BLEEDING DIATHESIS

Cardiac surgery causes a postoperative bleeding tendency.162167 The primary cause appears to be fibrinolysis caused by blood contact with the biomaterial components of the heart-lung machine and by blood suctioned from pericardial and pleural wells. (See Chapter 11 for a detailed discussion of the pathogenesis.) The degree of fibrinolysis correlates with the duration of cardiopulmonary bypass.163 Platelet dysfunction and heparin168 also contribute to postoperative bleeding. Hemodilution decreases platelet numbers. Most cardiac operations use moderate hypothermia, and persistent or recurrent hypothermia commonly occurs early after operation. Hypothermia-induced dysfunction of platelets and coagulation enzymes also causes a bleeding diathesis. Heparin reboundthe recurrence of measurable heparin activity after complete neutralization with protamineoccurs frequently and is probably caused by elution of heparin from plasma proteins.169 This problem is easily managed by protamine administration.170

Diagnosis

We define excessive bleeding as a chest tube effluent exceeding 500 mL/h in the first hour, 400 mL/h during the first 2 hours, 300 mL/h during the first 3 hours, or 200 mL/h during the first 6 hours. In addition, sudden increases in bleeding rate signify excessive bleeding and suggest a new arterial or intracardiac source. Massive bleeding is considerably in excess of these parameters and usually is accompanied by hemodynamic compromise.

At times, blood accumulates in the pericardial space but does not drain because clots fill the chest tubes. In these instances, the clot fills not only the chest tube but also the pericardium. Vigorous chest tube stripping can create high negative pressures but rarely succeeds in clearing clot from the tube. The clot cannot be removed in this manner because the tube is surrounded by a mediastinal clot that has the consistency of Jello. The high vacuum created by stripping can suck a saphenous vein graft into the chest tube and kink or occlude the graft. Chest tubes should not be stripped! Reexploration of the wound and manual removal of the clot are required.

Our routine postoperative laboratory test to screen for clotting disorders is an activated partial thromboplastin time (PTT). For patients with excessive bleeding or a markedly elevated PTT, other tests are performed. These include a prothrombin time (PT), thrombin time (TT), fibrinogen determination, and platelet count. Elevated fibrin degradation products (FDP) or d-dimer indicates fibrinolysis, but a low plasma fibrinogen concentration is sufficient to initiate antifibrinolytic therapy. If inadequate heparin neutralization exists, it may be identified by an elevated PTT or TT, and a normal reptilase test. An analysis of the causes of bleeding and recommended treatments are given in Table 15-8. In addition to these tests, a comparison of the blood hematocrit with one from a freshly drawn sample from the chest tube differentiates fresh bleeding and excessive serum reflux or lymphatic drainage. Finally, if pericardial tamponade is suspected, the chest x-ray taken immediately after operation should be compared with that taken several hours later; tamponade in the absence of widened mediastinum is rare.


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TABLE 15-8 Postoperative coagulopathy

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Treatment

INTRAOPERATIVE PREVENTION

The vast majority of excessive postoperative bleeding episodes can be prevented by a meticulous, systematic operation and sternal closure. At the completion of an orderly, carefully performed operation, and after neutralization of heparin with protamine, a compulsively thorough search for bleeding should be done. Beginning superficially, the skin and suprasternal tissues are inspected, followed by the sternum and periosteum. The internal mammary bed comes next, followed by reinsertion of the sternal retractor and examination of the pericardial and pleural fat and the veins in the region of the left innominate vein. Finally, all anastomoses, aortotomies, and cardiotomies and the lengths of all grafts are examined. Excessive bleeding during this inspection often precludes finding specific bleeding sites. Patience must be called upon to continue a systematic search for bleeding. Because some patients do not tolerate lifting the heart, the surgeon must be assured that the posterior surface is not bleeding before bypass is terminated. This routine was clearly advocated by Najafi, who stated, "The surgeon's determination to gain reliable hemostasis is the prerequisite for preventing reoperation for bleeding after cardiac operations."171

PHARMACOLOGIC PREVENTION

Regardless of efforts to prevent bleeding, a bleeding diathesis may still produce excessive blood loss after complex and long operations. Pharmacologic therapy of this nonsurgical clotting disorder is often helpful. Antifibrinolytic agents such as epsilon-aminocaproic acid and tranexamic acid and the protease inhibitor aprotinin reduce postoperative blood loss after heart operations.172176 However, aprotinin, the most effective of these agents, may contribute to renal dysfunction and early coronary artery graft thrombosis.177179 For this reason, and because of its considerable cost (about $1000 per patient), we reserve aprotinin for long operations with predictable excessive bleeding. We recommend, and routinely administer, epsilon-aminocaproic acid: 10 g with the skin incision, 10 g during the operation, and the final 10 g immediately before heparin reversal with protamine for other operations.

Desmopressin acetate (DDAVP) also has been given to reduce postoperative bleeding, but its effectiveness is unclear.180182 However, the drug appears to be effective in reducing postoperative bleeding in patients who receive preoperative aspirin.183185

REINFUSION OF SHED BLOOD

During cardiac operations, blood in the pericardium or pleural spaces is routinely aspirated back into the perfusion circuit. This admixture of circulating and shed blood probably contributes to some of the clotting disorders that occur after heart operations.186 Before heparin and after protamine, many centers reinfuse packed cells separated from washed blood aspirated from the field. After operation, chest tube effluent may be reinfused. This blood has already clotted in the mediastinum and hence contains high levels of fibrin degradation products and low levels of fibrinogen. Accordingly, fibrinolysis is detectable after reinfusion of shed blood, but this does not lead to a significant clotting disorder.187192 Nevertheless, we find that reinfusion is neither necessary nor cost-effective in most patients (in whom average postoperative blood loss over the first 24 hours is between 500 and 750 mL).

VOLUME REPLACEMENT

Volume replacement should satisfy two seemingly opposing goals: (1) maintenance of adequate intravascular volume for adequate blood circulation, (2) without increasing diffuse organ edema that accompanies heart operations. Blood oxygen-carrying capacity also must be adequate. If oxygenation and mixed venous O2 saturation are adequate, we do not transfuse patients unless the hematocrit falls below 25%.

BLOOD FACTOR REPLACEMENT

Component factor replacement is unnecessary unless bleeding is excessive and tests (Table 15-8) indicate a bleeding diathesis. For patients who require replacement, the usual clotting disorder demonstrates an elevated PT, PTT, and TT and a depressed fibrinogen concentration and platelet count. If the reptilase time is normal, heparin excess is present, and extra protamine should be given. If the reptilase test is elevated, fibrinogen deficiency and fibrinolysis are present in most cases. Continued bleeding and continued red cell replacement exacerbate this deficiency. Fibrinogen must be replaced after calculating the deficit. Although normal serum fibrinogen levels are between 200 and 400 mg/dL, a fibrinogen concentration of above 100 mg/dL should be sufficient to prevent bleeding due to hypofibrinogenemia. The deficit is calculated by subtracting the patient's serum fibrinogen concentration from 100 mg/dL and multiplying this by the patient's serum volume in deciliters. Volume replacement is calculated by dividing the deficit by the amount of fibrinogen in 1 unit of replacement. Fresh-frozen plasma contains about 500 mg per unit, and cryoprecipitate contains about 150 mg per unit. After replacing the deficit amount, serum fibrinogen should be remeasured. Continued bleeding further reduces the fibrinogen and must be treated with additional replacement.

In patients with excessive bleeding and a bleeding diathesis or a low platelet count, we replace platelets empirically and usually administer 6 to 10 units before assessing the response.

OTHER METHODS OF CONTROLLING BLEEDING

Increasing positive end-expiratory pressure (PEEP) may control excessive bleeding, but pressures approaching 20 cm H2O may cause hypotension and reduced cardiac output.193195

Other mechanical methods include placing a tamponading pack in the mediastinum, either with the chest closed or open. Sometimes the pack is covered with a rubber glove to reduce the possibility that bleeding will restart when the pack is removed. Lastly, high vacuum applied through a catheter to a specific bleeding area that cannot be controlled with sutures may cause local tamponade of the bleeding area.196,197

Reexploration for Bleeding

Excessive bleeding, as defined above, requires reexploration if clotting studies are normal. Delays in reexploration only increase morbidity by requiring more blood transfusions that further increase the bleeding tendency, increase organ edema, and exacerbate heart, lung, and renal dysfunction.

The decision to reexplore is more difficult if clotting studies are abnormal. If the bleeding rate does not produce hemodynamic compromise, and if pericardial tamponade is absent, replacement of clotting factors and protamine administration may be pursued aggressively. When clotting studies have returned to normal, or nearly so, the bleeding rate may be reassessed by criteria listed above to determine the need for reexploration.

When the clotting abnormality persists despite treatment, and if bleeding persists, reexploration should be performed. The likelihood of finding nonsurgical bleeding is high, but the likelihood of stopping the bleeding even without an anatomic source is also high. Evacuation of mediastinal clots seems to facilitate cessation of bleeding, even when no anatomically correctable site can be found.198

Massive bleeding demands immediate reexploration, as does pericardial tamponade.

ICU Emergency Sternotomy

Massive, sudden hemorrhage, and impending or actual cardiac arrest unresponsive to standard therapy usually require reopening the sternotomy in the ICU. The goals of reopening the chest are to release tamponade, prevent exsanguination, and facilitate better cardiac function. If the heart is still contracting, the act of releasing the sternum alone may result in hemodynamic improvement. Blood is aspirated while searching for sites of bleeding or kinked grafts. Massive bleeding can be controlled on the way to the operating room. Either pleura is opened if a pneumothorax is present. While this is being accomplished, an assistant should perform open heart massage. After these simple maneuvers are complete, the patient is transported to the operating room. Survival after emergently reopening the chest in the ICU varies from 20% to 70%.199204


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The goal of pulmonary management after heart surgery is a rapid transition from a patient who is anesthetized, intubated, and ventilated to one who is awake, extubated, and breathing spontaneously with adequate oxygenation.

Initial Assessment

In postcardiotomy patients who have extensive and invasive monitoring, there is a tendency to observe and treat the numbers rather than to rely on clinical assessment. On arrival to the ICU, most patients will be intubated and still asleep. Skin color and feel give early warning of poor cardiac output and poor oxygenation. Chest auscultation confirms adequate air exchange in both lungs.

Arterial blood gases (ABGs) should be obtained on admission to the ICU even though subsequent ventilator weaning may be monitored by pulse oximetry. A chest x-ray confirms proper endotracheal tube position and reveals pleural effusions, pulmonary edema, and atelectasis. The film also serves as a baseline for comparison of mediastinal width should a question of pericardial tamponade subsequently be raised.

Pulmonary Dysfunction

PULMONARY EFFECTS OF CARDIOPULMONARY BYPASS

Cardiopulmonary bypass (CPB) injures most organs, including the lung. Extracorporeal perfusion produces multiple emboli of gas, fibrin, fat, cells, and other biologic debris. Bypass activates coagulation, contact, complement and fibrinolytic systems, and leukocytes, monocytes, platelets, and endothelial cells (see Ch. 11).

The combination of microemboli and activated blood enzymes leads to increased functional residual capacity (FRC), pulmonary shunting with an increased alveolar-arterial oxygen gradient, ventilation/perfusion mismatch, microatelectasis, endothelial cell swelling, and increased total-body and lung fluid.205,206 The degree of damage increases with the time on CPB and is worse with bubble oxygenators than with membrane oxygenators.207,208 The pulmonary damage also correlates with the amount of pulmonary extracellular water and the degree of complement activation (as measured by C3a), and both these changes correlate with the duration of CPB.7,207,209

If patients sustain pulmonary insult from CPB, then performing coronary artery surgery off-pump would be expected to improve postoperative pulmonary function. Although some trials demonstrate that patients who undergo off-pump coronary artery bypass require less time on the ventilator,210212 numerous other trials demonstrate no difference in pulmonary function or time to extubation.213217 More investigation will be needed to understand if a pulmonary benefit exists with off-pump surgery.

Several methods to minimize this lung injury have been proposed. Intraoperative leukocyte depletion (by filtration) has produced inconsistent results.218220 Prostaglandin E1 (PGE1) or a synthetic analogue reduces the duration of ventilation and improves oxygenation postoperatively.221,222 Pharmacologic inhibition of platelet-activating factor decreases pulmonary vascular resistance, increases oxygenation, and decreases histologic lung damage.223

The use of PEEP postoperatively increases FRC but may not reduce intrapulmonary shunting.224 However, in our experience, increasing levels of PEEP usually improve oxygenation in patients with excessive shunting. Very high levels, above 10 to 15 cm H2O, may impair cardiac function.

PHRENIC NERVE PALSY

Left lower lobe atelectasis or infiltrates are quite common after heart operations.225 Reasons for this include wound pain, sedation, the supine position, hesitancy to cough, and general weakness of the patient. Partial palsy of one or both phrenic nerves may contribute.225227 More severe or complete phrenic palsy can be caused by topical cold or iced slush in the pericardium. Phrenic nerve palsy, particularly if bilateral, can lead to severe or even fatal pulmonary dysfunction.228230

OTHER CAUSES

Preoperative pulmonary dysfunction contributes to postoperative dysfunction.231 In patients with poor pulmonary function, both the incidence of pulmonary complications and the duration of intensive care increase. Patients with obstructive pulmonary disease fare less well than those with restrictive disease.

Persistent left ventricular failure after cardiac operations increases end-capillary hydrostatic pressure and favors fluid extravasation into alveoli. Interstitial and alveolar fluid inhibits oxygen transfer, increases shunting, decreases compliance, increases secretions, and facilitates atelectasis and pneumonia. Excessive pain, by inhibiting deep breathing, also leads to atelectasis and pneumonia. Epidural anesthesia effectively relieves severe pain and may be helpful in the uncommon patient who develops sternal fractures during operation.232

Ventilation

INITIAL MANAGEMENT: VENTILATOR SETTINGS

The ventilator is adjusted to achieve adequate oxygenation (PO2 of 80 to 100 mm Hg), carbon dioxide elimination (PCO2 of 35 to 45 mm Hg), and normal pH (7.3 to 7.5). Higher tidal volumes with lower rates help reduce atelectasis without hyperventilation. PEEP also helps to maintain lung volumes and prevent atelectasis. Low amounts of PEEP are tolerated well by all patients except those with emphysematous air trapping; in these patients, PEEP may be contraindicated. Typical initial ventilator settings are: minute volume, 120 mL/kg/min; tidal volume, 15 mL/kg; rate, 8 breaths per minute; and PEEP, 5 cm H2O. The inspired initial oxygen concentration (FIO2) is usually 0.9 but is quickly lowered to 0.5 or less as permitted by an initial ABG measurement. Subsequently, FIO2 is progressively reduced and monitored by transcutaneous O2 saturation.

MAINTENANCE

Intermittent mandatory ventilation (IMV) with PEEP of 5 mm Hg maintains alveolar expansion and facilitates weaning by gradual reduction in the ventilatory rate, but may not always prevent postoperative atelectasis.233 FIO2 is rapidly reduced as tolerated. Excessive secretions are removed by suction. An in-line suction catheter reduces airway contamination that may occur with repeated insertions of an independent suction catheter into the endotracheal tube. When the secretions are due to pulmonary edema, however, PEEP and addressing the cause constitute the best method of controlling them.

Shivering following hypothermic CPB increases systemic oxygen consumption and predisposes to respiratory and metabolic acidosis.234 Shivering is best treated by rewarming with radiant heat but may be arrested temporarily with narcotics or muscle relaxants.235,236

VENTILATOR WEANING

Whereas we once deferred extubation until the day after the operation, we now wean patients from the ventilator and extubate them as quickly as possible after (and occasionally before) leaving the operating room. This requires modification of the high-dose narcotic anesthesia protocol that is often used to blunt the sympathetic response in patients with ischemic heart disease.237,238 Perioperative myocardial infarctions increase if anesthesia is insufficient to prevent sympathetic discharge.237,238 However, other factors besides anesthesia also must be considered in a decision for early extubation. These include duration of cardiopulmonary bypass, extent of rewarming, preoperative pulmonary status, age, comorbidity, and adequacy of hemodynamics and hemostasis. The efficacy of the operation itself is a major factor in the decision for early extubation. Early extubation is safe and improves cardiac function by increasing preload as capacitance blood volume shifts into the chest.239241 Early extubation allows shorter stays in the ICU and decreased costs.

WEANING CRITERIA

If the initial ABGs are adequate, weaning the FIO2 to 0.5 or less may be performed by monitoring arterial O2 saturation (SaO2) by pulse oximetry. Weaning from controlled ventilation to spontaneous unassisted ventilation may be monitored similarly. However, adequate O2 saturation does not ensure absence of CO2 retention. Careful clinical assessment usually indicates satisfactory CO2 elimination. Rising blood pressure, rapid or shallow ventilation, and agitation suggest inadequate CO2 elimination; ABGs must be measured if there is any question of the adequacy of alveolar ventilation or CO2 removal. Even if ventilator weaning proceeds smoothly, ABGs should be remeasured prior to extubation to confirm the absence of CO2 retention and acidosis. Contraindications to extubation include inadequate ABG values, inadequate ventilatory mechanics, early pneumonia, unstable hemodynamics, and systemic complications.

For extubation, ABG criteria are:
PO2 >80 mm Hg with FIO2<=0.5
pH (on CPAP) >=7.35 (no respiratory acidosis)
PCO2 <= 45 mm Hg

Ventilatory criteria are:
Vital capacity (VC) >=15 mL/kg
Negative inspiratory force (NIF) >=20 cm H2O

Clinical requirements are:
Alert, awake
Absence of excessive bleeding, hemodynamic instability, or dangerous arrhythmia

When an intubated patient is breathing without assistance other than a positive airway pressure of 8 cm H2O or less, certain clinical parameters predict failure to extubate or the need for reinstitution of mechanical ventilatory support. These include tachycardia, tachypnea, excessive ventilatory effort, and sweating. The physiologic index most predictive of failure to wean and extubate is the minute frequency of spontaneous ventilation (f) divided by the tidal volume (Vt) in liters. When high, this index reflects a clinical picture of a patient with rapid, shallow breathing. When f/Vt is less than 105, 78% of patients can be weaned and extubated successfully.242 When greater than 105, 95% of patients cannot be weaned and extubated successfully. A Vt of 0.325 L is a good threshold value for predicting weaning success or failure.

Ventilator weaning, in uncomplicated cases, is quite simple. When the patient is fully awake and without excessive bleeding or hemodynamic instability, the ventilator is switched to spontaneous ventilation with CPAP of 5 mm Hg and FIO2 less than 0.5. If, after 30 minutes, the patient is comfortable, and without tachycardia, tachypnea, or dyspnea, the endotracheal tube is removed and replaced with humidified mask oxygen.

POSTEXTUBATION SUPPORT

Immediately after extubation, administer humidified oxygen at 10 L/min and at a concentration 10% greater than the patient received while intubated. Oxygen delivery may be decreased safely if the O2 saturation remains above 97% to 98%. Usually by the second postoperative day supplemental oxygen may be given via nasal prongs at progressively decreasing rates as long as the O2 saturation remains above 90%. SaO2 is maintained over 95% during the first 2 to 3 days after extubation and over 90% thereafter. Incentive spirometry helps the patient to visually assess and improve his or her ventilatory effort. Lobar collapse either before or after extubation may be treated by tracheal suctioning but usually requires bronchoscopy. Chest physiotherapy is particularly helpful in raising secretions and encouraging cough. During these first few postextubation days, several pulmonary complications may occur; anticipating problems allows earlier treatment and preempts an extended convalescence.

REINTUBATION

A few patients are too weak to sustain adequate ventilatory efforts despite having satisfied extubation criteria. They develop retained secretions and atelectasis and may progress to pneumonia. Treatment consists of chest physical therapy, nasotracheal suctioning, and occasionally bronchoscopy. Should these measures not restore adequate ventilatory mechanics, or should excessive weakness persist, reintubation is necessary.

This step must not be delayed to the point that more severe pulmonary complications ensue. The same clinical factors that predict failure to wean also predict the need for reintubation. Air hunger, feeble ventilatory effort, tachypnea, shallow breathing, or gross inability to clear secretions requires reintubation and mechanical ventilation. Other reintubation criteria include a rising PaCO2 from a normal value to 50 mm Hg over a few hours, hypoxia despite an increasing FIO2, and a falling cardiac output.243 A venous PCO2 can be measured in lieu of an arterial sample. Venous PCO2 is invariably 6 or 7 mm Hg higher than the simultaneous PaCO2.

COMPLICATIONS

Prolonged mechanical ventilation predisposes to pneumonia. The endotracheal tube not only bypasses defenses of the upper airway and tracheal cilia but also allows direct ingress of bacteria. The importance of strict asepsis during ventilator maintenance and endotracheal suctioning cannot be overemphasized. The drawbacks of endotracheal intubation and predisposition to pneumonia strengthen the argument for early extubation.

Noncardiogenic pulmonary edema develops from an allergic reaction, probably to blood or its products or to protamine.244,245 The edema presents as fulminating pulmonary edema with normal left atrial or pulmonary capillary wedge pressures and usually occurs either in the operating room or in the immediate postoperative period. The copious fluid bubbling from the endotracheal tube has a high protein content. When this edema occurs after cardiopulmonary bypass, the turgid, edematous lungs develop such severe air trapping that ventilation may cause the lungs to tamponade the heart, especially if sternal closure is attempted. Effective treatment consists of bronchodilators, corticosteroids, isoproterenol, and positive-pressure ventilation with high levels of PEEP. Because of tissue edema, sternal closure may effectively tamponade the heart and may need to be deferred. An intra-aortic balloon may be required to support cardiac function despite the absence of intrinsic cardiac abnormalities.

Barotrauma occurs most commonly in patients who require high levels of PEEP or high peak inspiratory pressure during mechanical ventilation. Sudden hypoxia suggests pneumothorax, either simple or tension, and demands immediate investigation. If present, prompt chest tube insertion is required. This complication is most common early after operation in elderly patients who cannot be extubated early and usually is due to rupture of apical blebs.

With an open pleural space, as often occurs from harvesting the internal mammary artery, postoperative bleeding may produce hemothorax rather than excessive blood drainage. An unexplained fall in hematocrit or hemodynamic instability suggests this possibility, and requires a chest x-ray for evaluation. Hemothorax requires chest tube insertion.

Late pleural effusions occur more commonly on the left than on the right, as does left lower lobe atelectasis. This predilection remains even without harvesting the left internal mammary artery. Effusions may require thoracentesis or occasionally a chest tube.

Pulmonary embolism occurs infrequently after heart operations (incidence 0.56%) but carries a high mortality of 34%.246 Risk factors include preoperative bed rest or hospitalization of more than 1 day, groin cardiac catheterization within 15 days of operation, and postoperative congestive heart failure or bed rest of more than 3 days.

Long-Term Ventilator Support

CAUSES OF FAILURE TO WEAN FROM MECHANICAL VENTILATION

Infrequently, a postoperative patient may require prolonged ventilator support for more than several days. Failure to wean has two causes: failure of gas exchange at the alveolar level and failure to ventilate adequately. The two most common reasons for deficiency in gas exchange are left-sided heart failure with pulmonary congestion and the adult respiratory distress syndrome (ARDS).

Predictable failure of ventilator weaning occurs in several circumstances. These include chronic illness with poor nutrition (cachexia) and ventilatory (diaphragm and chest wall) muscle weakness, central nervous system dysfunction, pain, mechanical disruption of the bony chest wall, chronic lung disease with stiff lung parenchyma, and sepsis. Muscle weakness also may be caused by hypothyroidism and deficiencies of magnesium, potassium, calcium, and phosphate.247,248

WEANING AFTER PROLONGED MECHANICAL VENTILATION

In patients who need prolonged ventilator support, weaning attempts must be preceded by elimination of the causes of ventilator dependence. When excessive lung water impedes weaning, negative fluid balance is required. In the patient with renal dysfunction, a compromise must be struck between the pulmonary and renal systems, usually in the favor of the lungs. During mild dehydration, the blood urea nitrogen (BUN) level may rise temporarily. Likewise, pneumonia must be resolved by appropriate antibiotics and airway toilet. When the disorders promoting ventilator dependence are corrected, the same weaning criteria as for the acute postoperative patient are used.

WEANING TECHNIQUES

The process of weaning from long-term ventilator support may be considered endurance training for the chest wall muscles and diaphragm. This consists of progressively increasing ventilatory load until mechanical ventilation can be discontinued. Spontaneous breathing trials (SBT) are performed once per day for durations of 30 to 120 minutes, or to the point of failure. Success criteria are stable arterial blood gases, stable hemodynamics, and a stable ventilatory pattern. Failure criteria consist of failing the above, or deterioration of mental status, worsening discomfort, diaphoresis, or signs of increased work of breathing.249 The SBT can be performed using a T-piece (giving no positive airway pressure), continuous positive airway pressure (CPAP) at a low pressure (5 cm H2O), or with low levels (5 to 7 cm H2O of pressure support ventilation (PSV). No convincing evidence suggests the superiority of one method over another. Using one method in a consistent protocol-driven fashion yields the most expeditious weaning, although in difficult weaning cases, it may be helpful to use an alternative method if the primary method continues to be unsuccessful. With all methods, weaning in an upright or sitting position optimizes the likelihood of success.

Tracheostomy

If, after 7 to 10 days of ventilation, weaning does not seem imminent, a tracheostomy should be performed. Tracheostomy offers several advantages over an endotracheal tube. The concern over possible laryngeal damage caused by an endotracheal tube may encourage premature weaning. With a tracheostomy, weaning can be managed independently of extubation. Tracheal toilet is more easily performed via tracheostomy. The dead space of a tracheostomy is less than that of an endotracheal tube, and this may facilitate weaning in a patient with marginal ventilation. A tracheostomy is more comfortable. Once established for a week or more, a tracheostomy offers greater security than an endotracheal tube in case of accidental extubation, because a tracheostomy tube is more easily inserted.

One serious complication of tracheostomy, whether performed by standard or percutaneous techniques, is accidental extubation during the first several days after initial placement. Hasty attempts to replace the tube easily lead to insertion outside the trachea; early accidental tracheostomy decannulation requires endotracheal intubation with subsequent elective reestablishment of the tracheostomy. Because of the possibility of contamination and infection of the median sternotomy incision from the proximity of a tracheostomy incision, the tracheal stoma should be established no lower than the second tracheal ring. With either a tracheostomy or endotracheal tube, obstruction of the tracheal end of the tube may occur from inspissated secretions. Adequate humidification helps prevent this complication. Difficulty passing a suction catheter through the tube suggests the problem, which may require changing the tube.

Percutaneous tracheostomies have replaced open (surgical) tracheostomies for many patients, although questions have been raised about the incidence of complications from the procedure with studies demonstrating both more and fewer complications with the percutaneous method.250253 Almost all of our elective tracheostomies are performed percutaneously and at the bedside. In 400 patients (not limited to cardiac surgical patients), there have been no procedure-related deaths, no false passages of dilators or tracheostomy tube, and two conversions to an open technique for bleeding (personal communication, Dr. Alan A. Conlan, May 22, 2002).

General Care

Multiple problems may develop in the patient who requires long-term ventilation, and these are best prevented by prophylaxis.

In an immobile patient, skin breakdown may occur over pressure points. A mattress designed to eliminate constant pressure focused over these pressure points should be used. Pooling of body fluids may cause skin maceration and breakdown. Assiduous nursing care must be employed to prevent pooling of urine, stool, or other fluids.

Inadequate nutrition impairs the ability to wean from the ventilator. Nutritional maintenance is started if the patient has not been extubated by the second postoperative day. Most cardiac patients have an intact gut; enteral feeding has many advantages over parenteral feeding. In these patients, and especially in those receiving narcotics, stool impaction may easily occur. This possibility should be assessed frequently by rectal examination if necessary. Stool softeners are used routinely.

Physical therapy is started to maintain joint mobility through range-of-motion exercises and muscle mass through resistance exercises. Contractures in patients with neurologic dysfunction are prevented with stretching exercises and splinting.

Infection constantly threatens these patients. Assiduous, aseptic care must be given to intravenous lines and all catheters. Intravenous catheters are changed on a regular schedule, usually every 5 days, or immediately if abrupt fever develops. Pulmonary toilet is maintained with strict asepsis.


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Postoperative Renal Function

Urine volume, blood urea nitrogen (BUN) level, and plasma creatinine level are the primary measures of adequate renal function following cardiac surgery. Urine output in the early postoperative course is usually copious as the kidneys excrete the extra volume acquired during cardiopulmonary bypass, and should be a minimum of 0.5 to 1.0 mL/kg/h. When urine volume is less, the cause must be sought.

Causes of Oliguria

The causes of oliguria can be divided into three categories: pre-renal, renal, and postrenal. Following cardiac surgery, postrenal obstruction is usually the result of a kinked or otherwise blocked Foley catheter. This can be diagnosed and usually treated by repositioning and flushing the catheter. If the bladder is obstructed secondary to hematuria and clot formation, this will also often respond to flushing. Ongoing hematuria with obstruction, however, requires continuous bladder irrigation and urology consultation.

With postrenal oliguria ruled out, the task is to differentiate a pre-renal cause from intrinsic renal failure. Pre-renal causes of oliguria are common and include low cardiac output, bleeding, hypovolemia, hypothermia, and intense vasoconstriction. Pre-renal oliguria is a result of decreased renal blood flow, and is often the first sign of generalized inadequate tissue perfusion. An example is the patient with falling urine output secondary to cardiac tamponade. If allowed to persist, inadequate renal perfusion will eventually lead to renal failure from ischemia. When diagnosed early, most causes of pre-renal oliguria can be corrected.

Pre-renal Oliguria

If a pre-renal cause for oliguria exists, and remains untreated, renal parenchymal ischemia will cause acute tubular necrosis (ATN). Obversely, assuming oliguria to be established renal failure becomes self-fulfilling: if renal failure was not present, lack of treatment will cause it. That treatment starts with the elimination of causes of diminished renal perfusion as discussed above.

If, despite this treatment, oliguria persists, early pharmacologic treatment should be used. Many centers use mannitol in the priming solution for cardiopulmonary bypass, and it is the agent of choice for prevention of renal dysfunction when periods of decreased glomerular filtration are anticipated. Pretreatment with intravenous mannitol, continued throughout any ischemic episode, improves subsequent renal blood flow and glomerular filtration.254 A strong solute diuresis relieves tubular obstruction and reduces tubular cellular swelling.254,255 Mannitol increases renal blood flow in both dogs and humans during CPB.256,257

The renovascular and functional effects of loop diuretics are similar to those of mannitol. Furosemide increases renal blood flow and promotes solute excretion.258 The theoretical benefit of furosemide in the patient with incipient acute renal failure is to convert oliguric to nonoliguric renal failure. Although this may not improve chances of recovery,259,260 it avoids some of the complications associated with complete renal shutdown. Furosemide early in renal dysfunction, when only abnormalities in free water clearance are apparent, improves medullary blood flow and free water clearance and identifies patients who are likely to require dialysis by their failure to respond.261,262

Dopamine at low doses (35 mg/kg/min) enhances renal blood flow. Dopamine and furosemide act synergistically and are more effective than either drug alone.263 This drug combination prompts a brisk diuresis and reduces serum creatinine levels, possibly by enhancing vasodilatation to allow increased delivery of furosemide to the distal tubule.264 A continuous infusion of dopamine, furosemide, and mannitol immediately upon the appearance of oliguria is particularly effective in restoring renal function and decreasing the need for dialysis.265

Other drugs that have some protective effect in experimental models include calcium channel blockers266,267 and PGE1.268,269 None of these agents has found clinical application. The mainstay of early support is improvement in renal blood flow and maintenance of tubular patency by ensuring adequate cardiac output and blood pressure while promoting renal vasodilatation and glomerular filtration with dopamine, mannitol, and furosemide.

Renal Failure

DIAGNOSIS

Because of the frequent difficulty of distinguishing pre-renal and renal causes of oliguria in the early postoperative period, the first responsibility must be to treat as if pre-renal causes exist: optimize cardiac output, eliminate vasoconstrictors and hypothermia that cause splanchnic vasoconstriction, and assure adequate blood volume and the absence of significant bleeding.

In the early hours after surgery, BUN and creatinine elevation are neither sensitive nor specific for renal failure. Mild elevations of BUN and creatinine are common after cardiac surgery and may be associated with an adequate or even large urine volume.270 These changes are nearly always transient, with complete return of normal renal function. In cardiac surgical patients with normal preoperative renal function, 15% have an increase in serum creatinine above 1.5 mg/dL postoperatively. Only a fraction of these patients develop acute renal failure (oliguria, creatinine >2.5 mg/dL), a complication associated with a high mortality rate. New azotemia reflects hypoperfusion of the kidney, and its degree depends on the severity and duration of decreased glomerular filtration.

The insensitivity of BUN and plasma creatinine levels for predicting the onset of acute renal failure has led to other analyses of renal function that are related primarily to renal concentrating capacity.271,272 Free water clearance is a simple and accurate method of identifying early, subclinical renal dysfunction.261,262 Free water clearance (CH2O) can be determined according to the method of Smith273:

where Uosm and Posm are urine and plasma osmolality in mmoles per liter, and V is urine volume (mL/h). Free water clearance values range from 100 (or more negative) to 20 mL/h; pathologic values range from 20 to 0 mL/h or more positive. Abnormal free water clearance is a constant finding that precedes elevations of BUN or creatinine in patients who develop renal failure271 (Fig. 15-2). However, abnormal free water clearance is also detectable in patients with mild reversible renal insufficiency and therefore is not predictive of renal shutdown. Baek et al261 and Brown262 used free water clearance measurements and the response to furosemide to prospectively determine which patients would experience frank renal failure. A response to furosemide correlated with a better prognosis. Thus free water clearance measurements allow earlier detection and treatment of incipient renal failure.



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FIGURE 15-2 Representative profiles of serum urea, creatinine, urine volume, and free water clearance (CH2O) in a patient who developed irreversible acute renal failure following heart surgery. Note that changes in free water clearance preceded significant alterations in seurm urea nitrogen or creatinine.

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Other tests for renal dysfunction lag behind the free water clearance. These tests include the BUN/creatinine ratio, urine osmolality, and fractional excretion of sodium (FeNa) (see Table 15-9).


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TABLE 15-9 Distinguishing pre-renal from renal oliguria

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TREATMENT

In the absence of a pre-renal cause for oliguria, acute renal failure exists. Patients at highest risk for acute renal failure are those with preoperative renal dysfunction, diabetes, congestive heart failure, renal artery stenosis, long bypass runs, advanced age, and emergency operations.270,274278 Other contributory factors are hemolysis with the liberation of free hemoglobin during prolonged cardiopulmonary bypass,279,280 circulatory arrest,281,282 and perioperative sepsis.

Once renal failure is established, early and aggressive dialysis decreases mortality in surgical patients.283,284 The goals of dialysis include removal of excess fluid, reduction of serum potassium level, removal of toxic metabolites including nephrotoxins, and correction of metabolic acidosis. Intermittent hemodialysis has been largely replaced by either continuous hemofiltration or hemodialysis.285 The former refers to ultrafiltration of blood plasma driven across a semipermeable membrane by a pressure gradient, whereas the latter refers to ultrafiltration via osmotic differences between the blood and solute sides of the membrane. The former is primarily used to remove volume, and the latter to reduce levels of specific solutes.

Hemofiltration was first described as continuous arteriovenous hemofiltration (CAVH) and employed to correct the hemodilution following cardiopulmonary bypass.286288 The simpler method of continuous venovenous hemofiltration (CVVH) has replaced CAVH and is mainly used, in conjunction with continuous venovenous hemodialysis (CVVHD), in the treatment of acute renal failure.285,289,290 Arterial catheters are no longer required because CVVHD is performed via a double lumen dialysis catheter placed in a large vein. CVVH machines include a roller pump that allows hypotensive patients to continue therapy. This is in contrast to CAVH, which required a mean arterial pressure of 70 mm Hg to drive the hemofiltration.285

The benefit of early hemofiltration/hemodialysis of patients with postoperative renal failure and volume overload is noted above. This slow continuous process has a low risk of inducing hemodynamic instability when compared to conventional intermittent hemodialysis. Other advantages include improved filtration of middle-sized molecules and inflammatory mediators, virtually unlimited potential for fluid removal, and no requirement for a specialized dialysis nurse at the bedside.285 There is evidence that CVVH provides benefit to patients independent of fluid removal by filtering tumor necrosis factor, complement, and interleukin-6.289,291293 Instituting such therapy for patients with renal failure after cardiac surgery may also decrease time on the ventilator, shorten ICU stay, and possibly improve the rate of renal recovery.289,293

PROGNOSIS

Despite all supportive measures available today, the prognosis for patients with established acute renal failure after CPB remains poor. Survival is 90% in patients who maintain nonoliguric renal insufficiency,294 but those who progress to oliguric renal failure have a mortality over 50%.278,294296 Most patients who develop acute renal failure have sustained hypotension during the perioperative period and develop failure of several organ systems. Infection becomes a common terminal event in patients who die with renal failure. Age is a significant prognostic factor in determining survival from acute renal failure after heart surgery,294 although Lange et al296 did not find age, sex, preoperative renal dysfunction, severity of underlying heart disease, cardiopulmonary bypass time, or oliguria to be significant influences in a univariate analysis of patients who required hemodialysis after heart surgery. They did find that the number and types of complications were significant predictors of outcome; the highest mortality rate was associated with respiratory failure, central nervous system dysfunction, persistent hypotension, and infection. Bhat et al295 noted a marked increase in mortality in patients whose serum creatinine rose higher than 6 mg/dL.

The best survival occurs in patients who can be maintained in nonoliguric renal failure. Early dialysis and nutritional support in patients with oliguric failure minimize metabolic complications, but the prognosis remains poor because of late septic complications. Although many recover renal function after a brief period (days to weeks) of oliguria, the incidence of chronic dialysis dependency in these patients is significant.


?? NERVOUS SYSTEM
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Postoperative neurologic dysfunction occurs with disturbing frequency. This group of complications can be divided into three categories: central neurologic, neuropsychologic, and peripheral neurologic. Because of differences in definitions, in tests to measure deficits, and in the diligence of postoperative examinations and testing, the medical literature is confusing, especially with respect to the incidence of these complications.

Central Neurologic Complications

Cerebrovascular accidents (CVAs) that result in lasting deficits occur after heart operations in 2% to 5% of patients.297300 These may appear after recovery from anesthesia but usually are obvious when the patient awakens. Perioperative strokes kill one-eighth of all patients afflicted.301

After a CVA, a computed tomographic (CT) scan demonstrates the cerebral infarction within a day or two. Insofar as no treatment exists, there is little need to document cerebral damage early if the patient is too hemodynamically unstable to travel. However, in the comatose patient, treatable causes may exist and therefore a CT scan should be performed as soon as possible.

Carotid artery stenosis may be a risk factor for stroke in patients without preoperative neurologic symptoms only when the stenosis is greater than 80%, although the evidence is contradictory.298,299,302306 We are wary of performing cardiac operations in the presence of critical (>80%) stenosis on one or both sides without prior or concomitant carotid endarterectomy. Symptomatic carotid stenoses increase the risk of stroke and usually require prophylactic or concomitant carotid endarterectomy.

Perioperative strokes have multiple causes. Operations performed at normothermia have a higher incidence of CVA than those performed at moderate (28 to 32?C) hypothermia.307 Open heart operations may cause embolic cerebral infarction from air boluses, intracardiac clot, calcified debris, or foreign material (such as felt pledgets). However, the most probable cause of most strokes is atheromatous emboli from the ascending aorta and aortic arch. Increasing age, incidence of aortic atheroma, incidence of peripheral embolization (in autopsy series), and incidence of CVA are closely correlated.297,299,301,308 If aortic atheromas are documented by echocardiography in older patients, operation is tailored to reduce aortic manipulation and embolization.299 Some authors find a correlation between low perfusion pressure (50 to 60 mm Hg) during CPB and CVA and recommend higher perfusion pressures (between 80 and 100 mm Hg).309

Neuropsychologic Complications

A large number of symptoms fall into this category and range from alterations of mood to bizarre behavior to quantifiable deficits in intellectual function. Postoperative depression occurs commonly, may last 2 to 3 months, and may be sufficiently severe to disrupt families and, rarely, cause patients to become suicidal. Usually, mild symptoms of depression disappear spontaneously and require no treatment other than reassurance. Early postoperative delirium follows a lucid period and presents as paranoia or hallucinations. Together with depression, these disorders occur in about 40% of patients.310 The reported incidence of delirium varies widely from 7% to 57% of cardiac surgical patients.311,312 Delirium usually disappears within a week; patient management is facilitated by small doses of haloperidol.

In some studies, deficits in intellectual function such as memory and cognition occur in as many as 75% of patients in the early postoperative period, decline to half that number by 8 weeks, and decline minimally over the next year.313316 Others, however, report little change between preoperative and postoperative assessments of intellectual function.317,318 The changes seem to be caused by cerebral microemboli and correlate with the duration of CPB.298,313,316,318 Membrane oxygenators as compared with bubble oxygenators reduce the production of microemboli.319 The incidence of transcranially detected microemboli correlates with both stroke and behavioral change, as well as with cardiac and pulmonary complications and mortality.320 These neurologic changes also correlate with new cerebral abnormalities detected by magnetic resonance imaging.321 Increasing age also predicts neuropsychologic deficits.314,318

Debate continues regarding decreased neurologic morbidity for patients receiving coronary bypass without cardiopulmonary bypass. Despite the claims of a few investigators,322,323 off-pump surgery has failed to demonstrate a significant decrease in stroke rate or incidence of neurocognitive dysfunction after heart surgery.210,212,217,322,324330

Peripheral Deficits

Intraoperative femoral arterial bleeding (usually from a recent cardiac catheterization) can compress the femoral nerve. Foot drop can occur from pressure on the peroneal nerve as it wraps around the fibula. This complication of leg positioning for saphenous vein harvesting can be prevented by proper padding or use of a cushion designed to protect the nerve.

Upper extremity deficits are more common and are related to the median sternotomy.331334 The incidence increases with wide retraction or placement of the retractor.331,332 Upper extremity deficits produce sensory deficits in the fourth and fifth fingers and usually disappear within 2 to 3 months. In severe cases, deficits involve a wider area, result in permanent sensory and motor deficits, and can lead to sympathetic dystrophy. These injuries are not completely preventable. In mild forms, sensory deficits occur in as many as 24% of patients332 and are caused by brachial plexus injury from a first rib fracture or from the plexus stretching over an intact first rib. Nerves C8 and T1 are damaged most commonly.

Injuries of the nerves around the elbow, especially the ulnar nerve, may be confused with brachial plexus injuries. Proper padding prevents these cubital nerve injuries.


?? GASTROINTESTINAL SYSTEM
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Major gastrointestinal complications occur more frequently after cardiac operations than after noncardiac, nonintestinal surgery. The incidence reported is from 0.5% to 3%.335341 Decreased visceral blood flow occurring during episodes of hypotension contributes to such complications.342344 Pancreatitis, mesenteric ischemia, gastroduodenal ulceration and inflammation, cholecystitis, and hepatic failure have all been attributed to hypotension, shock, or cardiopulmonary bypass.342,345350

The most common major complications are upper gastrointestinal (GI) bleeding from gastritis or ulcer disease, pancreatitis, hollow viscus perforation, mesenteric ischemia, and cholecystitis.336338,342,350352 In aggregate, these complications have a frighteningly high mortality between 20% and 80%; mesenteric ischemia is nearly always fatal.338341,346,353355

Risk factors for these complications include older age, perioperative hypoperfusion, emergency operation, longer CPB times, need for high-dose vasopressors and intra-aortic balloons, and valve operations.335,338,342,350,354,355 More than 800 mg of calcium chloride per square meter of body surface area is an independent risk factor for pancreatitis.349

Treatment and diagnosis must be pursued vigorously for all these complications, without regard to the recent heart operation. Delayed diagnosis and therapy may initiate a chain reaction that culminates in multiorgan failure. An unexplained, persistent metabolic acidosis should raise the spectre of an intra-abdominal catastrophe.

Mesenteric ischemia can occur secondary to a superior mesenteric artery embolus or low mesenteric flow. An elevated lactate level supports the diagnosis but is nonspecific. Initial treatment for mesenteric ischemia secondary to low flow includes volume resuscitation and minimizing vasopressor therapy. An arteriogram can diagnose mesenteric vasospasm, low flow, or embolic occlusion, but is often impractical in an unstable postcardiac surgery patient. If the suspicion for mesenteric ischemia is high in an unstable patient, early laparotomy can be life saving. Necrotic bowel is resected and marginal bowel is reassessed at a second look operation in 24 hours. When an embolic cause is likely, a superior mesenteric artery embolectomy can restore mesenteric flow.353

An elevated amylase level postoperatively occurs far more often than does clinical pancreatitis. About 30% of patients develop an elevated amylase level postoperatively, but only 10% have an increased lipase or pancreatic amylase level; 20% have a nonpancreatic source for the increased amylase.356 The clinical setting of abdominal pain and tenderness usually helps distinguish those patients with true pancreatitis. CT scan can serve as an adjunct for the diagnosis. Only 0.04% to 1% of patients develop severe pancreatitis.349,351 Treatment includes withholding oral intake, nasogastric tube decompression, and possibly, antibiotics. Development of pancreatic abscess requires laparotomy and drainage.

Hollow viscus perforation usually produces free peritoneal air (which should not be confused with air introduced during a median sternotomy incision that extended too far caudally). This usually mandates laparotomy.

Calculous or acalculous cholecystitis can occur in the postcardiopulmonary bypass patient. Ultrasound or radionuclide scan with hepatobiliary iminodiacetic acid (HIDA) supports this diagnosis. Cholecystectomy is the treatment of choice. In the rare patient that cannot withstand cholecystectomy, cholecystostomy is a reasonable second choice.

Upper gastrointestinal bleeding in the postoperative patient is usually secondary to hemorrhagic stress gastritis or ulceration. Routine stress ulcer prophylaxis after cardiac surgery is widely practiced, but the benefit has not been studied in a randomized trial.357 Patients at highest risk for upper GI bleeding include those who require prolonged mechanical ventilation, anticoagulation, or steroid therapy.42,358 Long cardiopulmonary bypass and aortic cross-clamp times have also been associated with an increased risk of postoperative GI bleeding.358 When considering stress ulcer prophylaxis for high-risk patients, sucralfate may be preferable to ranitidine, which has been linked to increased infectious complications in ICU patients.359363 Infections in patients treated with H2 blockers are theoretically due to loss of gastric acidity and subsequent bacterial colonization of the stomach. Although gastric colonization does occur, it has not been demonstrated conclusively to cause higher rates of pneumonia or other infections in patients treated with H2 blockers.364369 Helicobacter pylori has not been shown to be a factor in postoperative stress ulceration for cardiac surgery patients.358,370

Endoscopy is used to evaluate and often treat upper GI bleeding. Anticoagulants are stopped temporarily. The severity of bleeding must be weighed against the danger of discontinuing anticoagulation. When the danger of prolonged stoppage is unacceptable, early operation is performed to arrest the bleeding. Tissue valves are preferred for patients at high risk for postoperative upper GI bleeding.

Minor GI complications are more frequent than major complications. Mild postoperative ileus is common and is best treated by extending the duration of nasogastric tube suction. Forcing oral intake while ileus persists only lengthens hospitalization. Diarrhea suggests Clostridium difficile enteritis. A stool swab for fecal leukocytes and enterotoxin secures the diagnosis. Treatment requires specific antibiotics (metronidazole or oral vancomycin) and, when necessary, nutritional support.


?? PROPHYLACTIC ANTIBIOTICS
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Operations performed using cardiopulmonary bypass cause major derangements of multiple body systems and of the mediators of inflammation. Immunocompromise seems to be one of the derangements; the incidence of infection without prophylactic antibiotics is as high as 50%. Prophylactic antibiotics reduce this rate substantially.371 To be effective, antibiotics must be circulating at the start of the operation and must be maintained in an adequate concentration during the entire operation.372375 In the immediate postoperative period, antibiotic treatment should be continued for 24 to 48 hours. Administration for longer periods of time affords no better protection against infection.372374,376 The choice of antibiotic generally varies with recommendations of hospital epidemiologists or infectious disease committees and varies among institutions.


?? REFERENCES
 Top
?
  1. Kirklin JW: Systems analysis in surgical patients with particular attention to the cardiac and pulmonary subsystems. The Macewen Memorial Lectures, no.155. Glasgow, University of Glasgow, 1970.
  2. Appelbaum A, Kouchoukos NT, Blackstone EH, Kirklin JW: Early risks of open heart surgery for mitral valve disease. Am J Cardiol 1976; 37:201.[Medline]
  3. Dietzman RH, Ersek RA, Lillehei CW, et al: Low output syndrome: recognition and treatment. J Thorac Cardiovasc Surg 1969; 57:138.[Medline]
  4. Gailiunas P, Chawla R, Lazarus JM, et al: Acute renal failure following cardiac operations. J Thorac Cardiovasc Surg 1980; 79:241.[Abstract]
  5. Edmunds LH Jr: Blood-surface interactions during cardiopulmonary bypass. J Card Surg 1993; 8:404.[Medline]
  6. Edmunds LH Jr: Inflammatory response to cardiopulmonary bypass. Ann Thorac Surg 1998; 66 (5 suppl):S12.[Abstract/Free?Full?Text]
  7. Kirklin JK, Westaby S, Blackstone EH, et al: Complement and the damaging effects of cardiopulmonary bypass. J Thorac Cardiovasc Surg 1983; 86:845.[Abstract]
  8. Downing SW, Edmunds LH Jr: Release of vasoactive substances during cardiopulmonary bypass. Ann Thorac Surg 1992; 54:1236.[Abstract]
  9. Markewitz A, Faist E, Lang S, et al: Regulation of acute phase response after cardiopulmonary bypass by immunomodulation. Ann Thorac Surg 1993; 55:389.[Abstract]
  10. Kappelmayer J, Bernabli A, Gikakis N, et al: Upregulation of Mac-1 surface expression on neutrophils during simulated extracorporeal circulation. J Thorac Cardiovasc Surg 1993; 121:118.
  11. Chenoweth DE, Cooper SW, Hugli TE, et al: Complement activation during cardiopulmonary bypass. N Engl J Med 1981; 304:497.[Abstract]
  12. Aslan R, Tunerir B, Dernek S, et al: The factors effecting complement activation in open heart surgery. J Cardiovasc Surg (Torino) 1992; 33:754.[Medline]
  13. Chu SH, Huang TS, Hsu RB, et al: Thyroid hormone changes after cardiovascular surgery and clinical implications. Ann Thorac Surg 1991; 52:791.[Abstract]
  14. Tulla H, Takala J, Alhava E, et al: Hypermetabolism after coronary artery bypass. J Thorac Cardiovasc Surg 1991; 101:598.[Abstract]
  15. Chiara O, Giomarelli PP, Biagioli B, et al: Hypermetabolic response after hypothermic cardiopulmonary bypass. Crit Care Med 1987; 15:995.[Medline]
  16. Crock PA, Ley CJ, Martin IK, et al: Hormonal and metabolic changes during hypothermic coronary artery bypass surgery in diabetic and non-diabetic subjects. Diabet Med 1988; 5:47.[Medline]
  17. Braunwald AG: Cardiac catheterization, in Grossman W (ed): Heart Disease. Philadelphia, WB Saunders, 1992; p 180.
  18. Boyd O, Grounds RM, Bennett ED: A randomized clinical trial of the effect of deliberate perioperative increase of oxygen delivery on mortality in high-risk surgical patients. JAMA 1993; 270: 2699.[Abstract]
  19. Finch CA, Lenfant C: Oxygen transport in man. N Engl J Med 1972; 286:407.
  20. Chiolero R, Mavrocordatos P, Bracco D, Schutz Y, Cayeux C, Revelly JP: O2 consumption by the fick method: methodologic factors. Am J Respir Crit Care Med 1994; 149:1118.[Abstract]
  21. Kumon K, Tanaka K, Hirata T, et al: Organ failures due to low cardiac output syndrome following open heart surgery. Jpn Circ J 1986; 50:329.[Medline]
  22. Parr GV, Blackstone EH, Kirklin JW: Cardiac performance and mortality early after intracardiac surgery in infants and young children. Circulation 1975; 51:867.[Medline]
  23. Sadeghi N, Sadeghi S, Mood ZA, Karimi A: Determinants of operative mortality following primary coronary artery bypass surgery. Eur J Cardiothorac Surg 2002; 21:187.[Abstract/Free?Full?Text]
  24. Yau TM, Fedak PW, Weisel RD, et al: Predictors of operative risk for coronary bypass operations in patients with left ventricular dysfunction. J Thorac Cardiovasc Surg 1999; 118:1006.[Abstract/Free?Full?Text]
  25. Nemec P, Bedanova H, Necas J, et al: Coronary artery bypass grafting in patients with left ventricular ejection fraction of 30% or less. Bratisl Lek Listy 2001; 102:15.[Medline]
  26. Bech-Hanssen O, Caidahl K, Wall B, et al: Influence of aortic valve replacement, prosthesis type, and size on functional outcome and ventricular mass in patients with aortic stenosis. J Thorac Cardiovasc Surg 1999; 118:57.[Abstract/Free?Full?Text]
  27. Kirklin JK, Kirklin JW: Management of the cardiovascular subsystem after cardiac surgery. Ann Thorac Surg 1981; 32:311.[Medline]
  28. Kotter GS, Kotrly KJ, Kalbfleisch JH, et al: Myocardial ischemia during cardiovascular surgery as detected by an ST segment trend monitoring system. J Cardiothorac Anesth 1987; 1:190.[Medline]
  29. Gosselink AT, Crijns HJ, van den Berg MP, et al: Functional capacity before and after cardioversion of atrial fibrillation: a controlled study. Br Heart J 1994; 72:161.[Abstract/Free?Full?Text]
  30. Creswell LL, Schuessler RB, Rosenbloom M, Cox JL: Hazards of postoperative atrial arrhythmias. Ann Thorac Surg 1993; 56:539.[Abstract]
  31. Friesen WG, Woodson RD, Ames AW, et al: A hemodynamic comparison of atrial and ventricular pacing in postoperative cardiac surgical patients. J Thorac Cardiovasc Surg 1968; 55:271.[Medline]
  32. Fozzard HA: Relaxation and diastolic properties of the heart, in Smith VE, Weisfeldt ML, Katz AM (eds): The Heart and Cardiovascular System. New York, Raven Press, 1986; p 803.
  33. Rankin JS, Arentzen CE, McHale PA, et al: Viscoelastic properties of the diastolic left ventricle in the conscious dog. Circ Res 1977; 41:37.[Medline]
  34. McKenney PA, Apstein CS, Mendes LA, et al: Increased left ventricular diastolic chamber stiffness immediately after coronary artery bypass surgery. J Am Coll Cardiol 1994; 24:1189.[Abstract]
  35. Mammana RB, Hiro S, Levitsky S, et al: Inaccuracy of pulmonary capillary wedge pressure when compared to left atrial pressure in the early postsurgical period. J Thorac Cardiovasc Surg 1982; 84:420.[Abstract]
  36. Norris SO: Managing low cardiac output states: maintaining volume after cardiac surgery. AACN Clin Issues Crit Care Nurs 1993; 4:309.[Medline]
  37. Canver CC, Nichols RD: Use of intraoperative hetastarch priming during coronary bypass. Chest 2000; 118:1616.[Abstract/Free?Full?Text]
  38. Cope JT, Banks D, Mauney MC, et al: Intraoperative hetastarch infusion impairs hemostasis after cardiac operations. Ann Thorac Surg 1997; 63:78.[Abstract/Free?Full?Text]
  39. Strauss RG: Review of the effects of hydroxyethyl starch on the blood coagulation system. Transfusion 1981; 21:299.[Medline]
  40. Mastroianni L, Low HB, Rollman J, et al: A comparison of 10% pentastarch and 5% albumin in patients undergoing open-heart surgery. J Clin Pharmacol 1994; 34:34.[Abstract]
  41. Lacy JH, Wright CB: Use of plasma volume expanders in myocardial revascularisation. Drugs 1992; 44:720.[Medline]
  42. Moggio RA, Rha CC, Somberg ED, et al: Hemodynamic comparison of albumin and hydroxyethyl starch in postoperative cardiac surgery patients. Crit Care Med 1983; 11:943.[Medline]
  43. Shatney CH, Deepika K, Militello PR, et al: Efficacy of hetastarch in the resuscitation of patients with multisystem trauma and shock. Arch Surg 1983; 118:804.[Abstract]
  44. Rackow EC, Falk JL, Fein IA, et al: Fluid resuscitation in circulatory shock: a comparison of the cardiorespiratory effects of albumin, hetastarch, and saline solutions in patients with hypovolemic and septic shock. Crit Care Med 1983; 11:839.[Medline]
  45. Eising GP, Niemeyer M, Gunther T, et al: Does a hyperoncotic cardiopulmonary bypass prime affect extravascular lung water and cardiopulmonary function in patients undergoing coronary artery bypass surgery? Eur J Cardiothorac Surg 2001; 20:282.[Abstract/Free?Full?Text]
  46. Kasper SM, Giesecke T, Limpers P, et al: Failure of autologous fresh frozen plasma to reduce blood loss and transfusion requirements in coronary artery bypass surgery. Anesthesiology 2001; 95:81.[Medline]
  47. Diehl JT, Lester JL 3rd, Cosgrove DM: Clinical comparison of hetastarch and albumin in postoperative cardiac patients. Ann Thorac Surg 1982; 34:674.[Abstract]
  48. Kirklin JK, Lell WA, Kouchoukos NT: Hydroxyethyl starch versus albumin for colloid infusion following cardiopulmonary bypass in patients undergoing myocardial revascularization. Ann Thorac Surg 1984; 37:40.[Abstract]
  49. Palanzo DA, Parr GV, Bull AP, et al: Hetastarch as a prime for cardiopulmonary bypass. Ann Thorac Surg 1982; 34:680.[Abstract]
  50. Sade RM, Stroud MR, Crawford FA Jr, et al: A prospective randomized study of hydroxyethyl starch, albumin, and lactated Ringer's solution as priming fluid for cardiopulmonary bypass. J Thorac Cardiovasc Surg 1985; 89:713.[Abstract]
  51. DeFoe GR, Ross CS, Olmstead EM, et al: Lowest hematocrit on bypass and adverse outcomes associated with coronary artery bypass grafting. Northern New England Cardiovascular Disease Study Group. Ann Thorac Surg 2001; 71:769.[Abstract/Free?Full?Text]
  52. Yin FC: Ventricular wall stress. Circ Res 1981; 49:829.[Medline]
  53. Buckberg GD, Archie JP, Fixler DE, Hoffman JI: Experimental subendocardial ischemia during left ventricular hypertension. Surg Forum 1971; 22:124.[Medline]
  54. Franciosa JA, Guiha NH, Limas CJ, et al: Arterial pressure as a determinant of left ventricular filling pressure after acute myocardial infarction. Am J Cardiol 1974; 34:506.[Medline]
  55. Fremes SE, Weisel RD, Baird RJ, et al: Effects of postoperative hypertension and its treatment. J Thorac Cardiovasc Surg 1983; 86:47.[Abstract]
  56. Roberts AJ, Niarchos AP, Subramanian VA, et al: Systemic hypertension associated with coronary artery bypass surgery: predisposing factors, hemodynamic characteristics, humoral profile, and treatment. J Thorac Cardiovasc Surg 1977; 74:846.[Abstract]
  57. Estafanous FG, Tarazi RC: Systemic arterial hypertension associated with cardiac surgery. Am J Cardiol 1980; 46:685.[Medline]
  58. Beerthuizen GI, Goris RJ, Bredee JJ, et al: Muscle oxygen tension, hemodynamics, and oxygen transport after extracorporeal circulation. Crit Care Med 1988; 16:748.[Medline]
  59. Kuttila K, Niinikoski J: Peripheral perfusion after cardiac surgery. Crit Care Med 1989; 17:217.[Medline]
  60. Bailey DR, Miller ED Jr, Kaplan JA, Rogers PW: The renin-angiotensin-aldosterone system during cardiac surgery with morphinenitrous oxide anesthesia. Anesthesiology 1975; 42:538.[Medline]
  61. Lappas DG, Lowenstein E, Waller J, et al: Hemodynamic effects of nitroprusside infusion during coronary artery operation in man. Circulation 1976; 54:III4.
  62. Stinson EB, Holloway EL, Derby G, et al: Comparative hemodynamic responses to chlorpromazine, nitroprusside, nitroglycerin, and trimethaphan immediately after open-heart operations. Circulation 1975; 52:I26.
  63. Chitwood WR Jr, Cosgrove DM 3rd, Lust RM: Multicenter trial of automated nitroprusside infusion for postoperative hypertension. Titrator Multicenter Study Group. Ann Thorac Surg 1992; 54:517.[Abstract]
  64. Cosgrove DM 3rd, Petre JH, Waller JL, et al: Automated control of postoperative hypertension: a prospective, randomized multicenter study. Ann Thorac Surg 1989; 47:678.[Abstract]
  65. Ferrari HA, Robicsek F: Coronary surgery and computerized monitoring-patient care. Coll Works Cardiopulm Dis 1979; 22:98.[Medline]
  66. Christakis GT, Fremes SE, Koch JP, et al: Determinants of low systemic vascular resistance during cardiopulmonary bypass. Ann Thorac Surg 1994; 58:1040.[Abstract]
  67. DiNardo JA, Bert A, Schwartz MJ, et al: Effects of vasoactive drugs on flows through left internal mammary artery and saphenous vein grafts in man. J Thorac Cardiovasc Surg 1991; 102:730.[Abstract]
  68. Sagawa K: The ventricular pressure-volume diagram revisited. Circ Res 1978; 43:677.[Medline]
  69. Berglund E: Ventricular function, VI: Balance of left and right ventricular output: relation between left and right atrial pressures. Am J Physiol 1954; 178:381.[Free?Full?Text]
  70. Josa M, Khuri SF, Braunwald NS, et al: Delayed sternal closure: an improved method of dealing with complications after cardiopulmonary bypass. J Thorac Cardiovasc Surg 1986; 91:598.[Abstract]
  71. Furnary AP, Magovern JA, Simpson KA, Magovern GJ: Prolonged open sternotomy and delayed sternal closure after cardiac operations. Ann Thorac Surg 1992; 54:233.[Abstract]
  72. Fanning WJ, Vasko JS, Kilman JW: Delayed sternal closure after cardiac surgery. Ann Thorac Surg 1987; 44:169.[Abstract]
  73. Durandy Y, Batisse A, Bourel P, et al: Mediastinal infection after cardiac operation: a simple closed technique. J Thorac Cardiovasc Surg 1989; 97:282.[Abstract]
  74. Serry C, Bleck PC, Javid H, et al: Sternal wound complications: management and results. J Thorac Cardiovasc Surg 1983; 80:861.
  75. Weitzman LB, Tinker WP, Kronzon I, et al: The incidence and natural history of pericardial effusion after cardiac surgeryan echocardiographic study. Circulation 1984; 69:506.[Medline]
  76. Wickstrom PH, Monson BK, Helseth HK: Delayed postoperative bloody pericardial effusion. Minn Med 1985; 68:19.[Medline]
  77. Ofori-Krakye SK, Tyberg TI, Geha AS, et al: Late cardiac tamponade after open heart surgery: incidence, role of anticoagulants in its pathogenesis and its relationship to the postpericardiotomy syndrome. Circulation 1981; 63:1323.[Medline]
  78. Nishimura RA, Fuster V, Burgert SL, Puga FJ: Clinical features and long-term natural history of the postpericardiotomy syndrome. Int J Cardiol 1983; 4:443.[Medline]
  79. Pereira WM, Kalil RA, Prates PR, Nesralla IA: Cardiac tamponade due to chylopericardium after cardiac surgery. Ann Thorac Surg 1988; 46:572.[Abstract]
  80. Rose DM, Colvin SB, Danilowicz D, Isom OW: Cardiac tamponade secondary to chylopericardium following cardiac surgery: case report and review of the literature. Ann Thorac Surg 1982; 34:333.[Abstract]
  81. Smulders YM, Wiepking ME, Moulijn AC, et al: How soon should drainage tubes be removed after cardiac operations? Ann Thorac Surg 1989; 48:540.[Abstract]
  82. Hochberg MS, Merrill WH, Gruber M, et al: Delayed cardiac tamponade associated with prophylactic anticoagulation in patients undergoing coronary bypass grafting: early diagnosis with two-dimensional echocardiography. J Thorac Cardiovasc Surg 1978; 75:777.[Abstract]
  83. Spodick DH, Paladino D, Flessas AP: Respiratory effects on systolic time intervals during pericardial effusion. Am J Cardiol 1983; 51:1033.[Medline]
  84. Louie EK, Hariman RJ, Wang Y, et al: Effect of acute pericardial tamponade on the relative contributions of systolic and diastolic pulmonary venous return: a transesophageal pulsed Doppler study. Am Heart J 1995; 129:124.[Medline]
  85. Reichert CL, Visser CA, Koolen JJ, et al: Transesophageal echocardiography in hypotensive patients after cardiac operations: comparison with hemodynamic parameters. J Thorac Cardiovasc Surg 1992; 104:321.[Abstract]
  86. Borkon AM, Schaff HV, Gardner TJ, et al: Diagnosis and management of postoperative pericardial effusions and late cardiac tamponade following open-heart surgery. Ann Thorac Surg 1981; 31:512.[Abstract]
  87. DiSesa VJ: The rational selection of inotropic drugs in cardiac surgery. J Card Surg 1987; 2:385.[Medline]
  88. DiSesa VJ: Pharmacologic support for postoperative low cardiac output. Semin Thorac Cardiovasc Surg 1991; 3:13.[Medline]
  89. Lollgen H, Drexler H: Use of inotropes in the critical care setting. Crit Care Med 1990; 18:S56.[Medline]
  90. DiSesa VJ, Brown E, Mudge GH Jr, et al: Hemodynamic comparison of dopamine and dobutamine in the postoperative volume-loaded, pressure-loaded, and normal ventricle. J Thorac Cardiovasc Surg 1982; 83:256.[Medline]
  91. Fowler MB, Alderman EL, Oesterle SN, et al: Dobutamine and dopamine after cardiac surgery: greater augmentation of myocardial blood flow with dobutamine. Circulation 1984; 70: I103.
  92. Sturm JT, Fuhrman TM, Sterling R, et al: Combined use of dopamine and nitroprusside therapy in conjunction with intra-aortic balloon pumping for the treatment of postcardiotomy low-output syndrome. J Thorac Cardiovasc Surg 1981; 82:13.[Abstract]
  93. Loeb HS, Ostrenga JP, Gaul W, et al: Beneficial effects of dopamine combined with intravenous nitroglycerin on hemodynamics in patients with severe left ventricular failure. Circulation 1983; 68:813.[Medline]
  94. Goldberg LI, Rajfer SI: Dopamine receptors: applications in clinical cardiology. Circulation 1985; 72:245.[Medline]
  95. Steen PA, Tinker JH, Pluth JR, et al: Efficacy of dopamine, dobutamine, and epinephrine during emergence from cardiopulmonary bypass in man. Circulation 1978; 57:378.[Medline]
  96. Stephenson LW, Blackstone EH, Kouchoukos NT: Dopamine vs epinephrine in patients following cardiac surgery: randomized study. Surg Forum 1976; 27:272.[Medline]
  97. Drop LJ: Ionized calcium, the heart, and hemodynamic function. Anesth Analg 1985; 64:432.[Medline]
  98. Drop LJ, Scheidegger D: Plasma ionized calcium concentration: important determinant of the hemodynamic response to calcium infusion. J Thorac Cardiovasc Surg 1980; 79:425.[Medline]
  99. Shapira N, Schaff HV, White RD, Pluth JR: Hemodynamic effects of calcium chloride injection following cardiopulmonary bypass: response to bolus injection and continuous infusion. Ann Thorac Surg 1984; 37:133.[Abstract]
  100. Auffant RA, Downs JB, Amick R: Ionized calcium concentration and cardiovascular function after cardiopulmonary bypass. Arch Surg 1981; 116:1072.[Abstract]
  101. Gallagher JD, Geller EA, Moore RA, et al: Hemodynamic effects of calcium chloride in adults with regurgitant valve lesions. Anesth Analg 1984; 63:723.[Medline]
  102. Alousi AA, Johnson DC: Pharmacology of the bipyridines: amrinone and milrinone. Circulation 1986; 73:III10.
  103. Kikura M, Lee MK, Safon RA, et al: The effects of milrinone on platelets in patients undergoing cardiac surgery. Anesth Analg 1995; 81:44.[Abstract]
  104. Ansell J, Tiarks C, McCue J, et al: Amrinone-induced thrombocytopenia. Arch Intern Med 1994; 144:949
  105. Ross MP, Allen-Webb EM, Pappas JB, McGough EC: Amrinone-associated thrombocytopenia: pharmacokinetic analysis. Clin Pharmacol Ther 1993; 53:661.[Medline]
  106. Kikura M, Lee MK, Safon RA, et al: The effects of milrinone on platelets in patients undergoing cardiac surgery. Anesth Analg 1995; 81:44.
  107. Levy JH, Bailey JM, Deeb GM: Intravenous milrinone in cardiac surgery. Ann Thorac Surg 2002; 73:325.[Abstract/Free?Full?Text]
  108. Baim DS, McDowell AV, Cherniles J, et al: Evaluation of a new bipyridine inotropic agentmilrinonein patients with severe congestive heart failure. N Engl J Med 1983; 309:748.[Abstract]
  109. Borow KM, Come PC, Neumann A, et al: Physiologic assessment of the inotropic, vasodilator and afterload reducing effects of milrinone in subjects without cardiac disease. Am J Cardiol 1985; 55:1204.[Medline]
  110. Monrad ES, McKay RG, Baim DS, et al: Improvement in indexes of diastolic performance in patients with congestive heart failure treated with milrinone. Circulation 1984; 70:1030.[Medline]
  111. Lobato EB, Gravenstein N, Martin TD: Milrinone, not epinephrine, improves left ventricular compliance after cardiopulmonary bypass. J Cardiothorac Vasc Anesth 2000; 14:374.[Medline]
  112. Lobato EB, Florete O Jr, Bingham HL: A single dose of milrinone facilitates separation from cardiopulmonary bypass in patients with pre-existing left ventricular dysfunction. Br J Anaesth 1998; 81:782.[Abstract/Free?Full?Text]
  113. Monrad ES, McKay RG, Baim DS, et al: Improvement in indexes of diastolic performance in patients with congestive heart failure treated with milrinone. Circulation 1984; 70:1030.
  114. Monrad ES, Baim DS, Smith HS, et al: Effects of milrinone on coronary hemodynamics and myocardial energetics in patients with congestive heart failure. Circulation 1985; 71:972.[Medline]
  115. Drexler H, Faude F, Winterer H, et al: [Central and regional vascular hemodynamics of milrinone in experimental heart failure: comparison with captopril and dobutamine]. Z Kardiol 1987; 76:507.[Medline]
  116. Drexler H, Faude F, Hoing S, Just H: Blood flow distribution within skeletal muscle during exercise in the presence of chronic heart failure: effect of milrinone. Circulation 1987; 76:1344.[Medline]
  117. Martin JL, Likoff MJ, Janicki JS, et al: Myocardial energetics and clinical response to the cardiotonic agent MDL 17043 in advanced heart failure. J Am Coll Cardiol 1984; 4:875.[Abstract]
  118. Tisdale JE, Patel R, Webb CR, et al: Electrophysiologic and proarrhythmic effects of intravenous inotropic agents. Prog Cardiovasc Dis 1995; 38:167.[Medline]
  119. Cook LS, Toal KW, Elkins RC: Cardiovascular time course in patients with postoperative myocardial dysfunction requiring catecholamine administration. Curr Surg 1987; 44:124.[Medline]
  120. Gottlieb SS: New approaches to managing congestive heart failure. Curr Opin Cardiol 1995; 10:282.[Medline]
  121. Feldman AM, Bristow MR, Parmley WW, et al: Effects of vesnarinone on morbidity and mortality in patients with heart failure. Vesnarinone Study Group. N Engl J Med 1993; 329: 149.[Abstract/Free?Full?Text]
  122. Shakar SF, Abraham WT, Gilbert EM, et al: Combined oral positive inotropic and beta-blocker therapy for treatment of refractory class IV heart failure. J Am Coll Cardiol 1998; 31:1336.[Abstract/Free?Full?Text]
  123. Holland FW, Brown PS Jr, Weintraub BD, Clark RE: Cardiopulmonary bypass and thyroid function: a "euthyroid sick syndrome." Ann Thorac Surg 1991; 52:46.[Abstract]
  124. Murzi B, Iervasi G, Masini S, et al: Thyroid hormones homeostasis in pediatric patients during and after cardiopulmonary bypass. Ann Thorac Surg 1995; 59:481.[Abstract/Free?Full?Text]
  125. Klemperer JD, Klein I, Gomez M, et al: Thyroid hormone treatment after coronary-artery bypass surgery. N Engl J Med 1995; 333:1522.[Abstract/Free?Full?Text]
  126. Dyke CM, Yeh T Jr, Lehman JD, et al: Triiodothyronine-enhanced left ventricular function after ischemic injury. Ann Thorac Surg 1991; 52:14.[Abstract]
  127. Dyke CM, Ding M, Abd-Elfattah AS, et al: Effects of triiodothyronine supplementation after myocardial ischemia. Ann Thorac Surg 1993; 56:215.[Abstract]
  128. Holland FW, Brown PS Jr, Clark RE: Acute severe postischemic myocardial depression reversed by triiodothyronine. Ann Thorac Surg 1992; 54:301.[Abstract]
  129. Novitzky D, Matthews N, Shawley D, et al: Triiodothyronine in the recovery of stunned myocardium in dogs. Ann Thorac Surg 1991; 51:10.[Abstract]
  130. Novitzky D, Cooper DK, Swanepoel A: Inotropic effect of triiodothyronine (T3) in low cardiac output following cardioplegic arrest and cardiopulmonary bypass: an initial experience in patients undergoing open heart surgery. Eur J Cardiothorac Surg 1989; 3:140.[Abstract]
  131. Novitzky D, Cooper DK, Barton CI, et al: Triiodothyronine as an inotropic agent after open heart surgery. J Thorac Cardiovasc Surg 1989; 98:972.[Abstract]
  132. Novitzky D, Fontanet H, Snyder M, et al: Impact of triiodothyronine on the survival of high-risk patients undergoing open heart surgery. Cardiology 1996; 87:509.[Medline]
  133. Mullis-Jansson SL, Argenziano M, Corwin S, et al: A randomized double-blind study of the effect of triiodothyronine on cardiac function and morbidity after coronary bypass surgery. J Thorac Cardiovasc Surg 1999; 117:1128.[Abstract/Free?Full?Text]
  134. Klemperer JD, Klein IL, Ojamaa K, et al: Triiodothyronine therapy lowers the incidence of atrial fibrillation after cardiac operations. Ann Thorac Surg 1996; 61:1323.[Abstract/Free?Full?Text]
  135. Taniguchi S, Kitamura S, Kawachi K, et al: Effects of hormonal supplements on the maintenance of cardiac function in potential donor patients after cerebral death. Eur J Cardiothorac Surg 1992; 6:96.[Abstract]
  136. Orlowski JP, Spees EK: Improved cardiac transplant survival with thyroxine treatment of hemodynamically unstable donors: 95.2% graft survival at 6 and 30 months. Transplant Proc 1993; 25: 1535.[Medline]
  137. Novitzky D, Wicomb WN, Cooper DK, Tjaalgard MA: Improved cardiac function following hormonal therapy in brain dead pigs: relevance to organ donation. Cryobiology 1987; 24:1.[Medline]
  138. Novitzky D, Cooper DK, Chaffin JS, et al: Improved cardiac allograft function following triiodothyronine therapy to both donor and recipient. Transplantation 1990; 49:311.[Medline]
  139. Davis PJ, Davis FB: Acute cellular actions of thyroid hormone and myocardial function. Ann Thorac Surg 1993; 56:S16S23.
  140. Ojamaa K, Balkman C, Klein IL: Acute effects of triiodothyronine on arterial smooth muscle cells. Ann Thorac Surg 1993; 56: S61.
  141. Vavouranakis I, Sanoudos G, Manios A, et al: Triiodothyronine administration in coronary artery bypass surgery: effect on hemodynamics. J Cardiovasc Surg (Torino) 1994; 35:383.[Medline]
  142. Bennett-Guerrero E, Jimenez JL, White WD, et al: Cardiovascular effects of intravenous triiodothyronine in patients undergoing coronary artery bypass graft surgery: a randomized, double-blind, placebo-controlled trial. Duke T3 study group. JAMA 1996; 275:687.[Abstract]
  143. Teiger E, Menasche P, Mansier P, et al: Triiodothyronine therapy in open-heart surgery: from hope to disappointment. Eur Heart J 1993; 14:629.[Abstract/Free?Full?Text]
  144. Gotzsche LS, Weeke J: Changes in plasma free thyroid hormones during cardiopulmonary bypass do not indicate triiodothyronine substitution. J Thorac Cardiovasc Surg 1992; 104:273.[Abstract]
  145. Lowenstein E: Implications of triiodothyronine administration before cardiac and noncardiac operations. Ann Thorac Surg 1993; 56:S43.
  146. Clark RE: Triiodothyronine: to be or not to be, that is the question. Ann Thorac Surg 1991; 51:5.[Medline]
  147. Samuels LE, Kaufman MS, Thomas MP, et al: Pharmacological criteria for ventricular assist device insertion following postcardiotomy shock: experience with the Abiomed BVS system. J Card Surg 1999; 14:288.[Medline]
  148. Kantrowitz A, Tjonneland S, Freed PS, et al: Initial clinical experience with intraaortic balloon pumping in cardiogenic shock. JAMA 1968; 203:113.[Medline]
  149. Torchiana DF, Hirsch G, Buckley MJ, et al: Intraaortic balloon pumping for cardiac support: trends in practice and outcome, 1968 to 1995. J Thorac Cardiovasc Surg 1997; 113:758.[Abstract/Free?Full?Text]
  150. Creswell LL, Rosenbloom M, Cox JL, et al: Intraaortic balloon counterpulsation: patterns of usage and outcome in cardiac surgery patients. Ann Thorac Surg 1992; 54:11.[Abstract]
  151. Naunheim KS, Swartz MT, Pennington DG, et al: Intraaortic balloon pumping in patients requiring cardiac operations: risk analysis and long-term follow-up. J Thorac Cardiovasc Surg 1992; 104:1654.[Abstract]
  152. Gol MK, Bayazit M, Emir M, et al: Vascular complications related to percutaneous insertion of intraaortic balloon pumps. Ann Thorac Surg 1994; 58:1476.[Abstract]
  153. Perler BA, McCabe CJ, Abbott WM, Buckley MJ: Vascular complications of intra-aortic balloon counterpulsation. Arch Surg 1983; 118:957.[Abstract]
  154. Iverson LI, Herfindahl G, Ecker RR, et al: Vascular complications of intraaortic balloon counterpulsation. Am J Surg 1987; 154:99.[Medline]
  155. McCabe JC, Abel RM, Subramanian VA, Guy WA Jr: Complications of intra-aortic balloon insertion and counterpulsation. Circulation 1978; 57:769.[Medline]
  156. Vonderheide RH, Thadhani R, Kuter DJ: Association of thrombocytopenia with the use of intra-aortic balloon pumps. Am J Med 1998; 105:27.[Medline]
  157. Alajmo F, Calamai G: High-dose aprotinin in emergency coronary artery bypass after thrombolysis. Ann Thorac Surg 1992; 54:1022.[Medline]
  158. Skinner JR, Phillips SJ, Zeff RH, Kongtahworn C: Immediate coronary bypass following failed streptokinase infusion in evolving myocardial infarction. J Thorac Cardiovasc Surg 1984; 87:567.[Abstract]
  159. Rawitscher RE, Jones JW, McCoy TA, Lindsley DA: A prospective study of aspirin's effect on red blood cell loss in cardiac surgery. J Cardiovasc Surg (Torino) 1991; 32:1.
  160. Reich DL, Patel GC, Vela-Cantos F, et al: Aspirin does not increase homologous blood requirements in elective coronary bypass surgery. Anesth Analg 1994; 79:4.[Medline]
  161. Becker RM, Fintel DJ, Green D: Antithrombotic Therapy, 2d ed. West Islip, NY, Professional Communications, 2002.
  162. Kestin AS, Valeri CR, Khuri SF, et al: The platelet function defect of cardiopulmonary bypass. Blood 1993; 82:107.[Abstract/Free?Full?Text]
  163. Khuri SF, Wolfe JA, Josa M, et al: Hematologic changes during and after cardiopulmonary bypass and their relationship to the bleeding time and nonsurgical blood loss. J Thorac Cardiovasc Surg 1992; 104:94.[Abstract]
  164. Edmunds LH Jr: Why cardiopulmonary bypass makes patients sick: strategies to control the blood-synthetic surface interface. Adv Card Surg 1995; 6:131.[Medline]
  165. Taylor KM: Perioperative approaches to coagulation defects. Ann Thorac Surg 1993; 56:S78.
  166. John LC, Rees GM, Kovacs IB: Inhibition of platelet function by heparin: an etiologic factor in postbypass hemorrhage. J Thorac Cardiovasc Surg 1993; 105:816.[Abstract]
  167. Michelson AD: Bleeding associated with cardiopulmonary bypass in children. Int J Pediatr Hematol Oncol 1994; 1:147.
  168. Walls JT, Curtis JJ, Silver D, et al: Heparin-induced thrombocytopenia in open heart surgical patients: sequelae of late recognition. Ann Thorac Surg 1992; 53:787.[Abstract]
  169. Teoh KH, Young E, Bradley CA, Hirsh J: Heparin binding proteins: contribution to heparin rebound after cardiopulmonary bypass. Circulation 1993; 88:II420.
  170. Martin P, Horkay F, Gupta NK, et al: Heparin rebound phenomenonmuch ado about nothing? Blood Coagul Fibrinolysis 1992; 3:187.[Medline]
  171. Najafi H: Reoperation for excessive bleeding after cardiac operations. J Thorac Cardiovasc Surg 1992; 103:814.[Medline]
  172. Vander Salm TJ, Ansell JE, Okike ON, et al: The role of epsilon-aminocaproic acid in reducing bleeding after cardiac operation: a double-blind randomized study. J Thorac Cardiovasc Surg 1988; 95:538.[Abstract]
  173. Daily PO, Lamphere JA, Dembitsky WP, et al: Effect of prophylactic epsilon-aminocaproic acid on blood loss and transfusion requirements in patients undergoing first-time coronary artery bypass grafting: a randomized, prospective, double-blind study. J Thorac Cardiovasc Surg 1994; 108:99.[Abstract/Free?Full?Text]
  174. Arom KV, Emery RW: Decreased postoperative drainage with addition of epsilon-aminocaproic acid before cardiopulmonary bypass. Ann Thorac Surg 1994; 57:1108.[Abstract]
  175. Royston D: High-dose aprotinin therapy: a review of the first five years' experience. J Cardiothorac Vasc Anesth 1992; 6:76.[Medline]
  176. Royston D: The serine antiprotease aprotinin (Trasylol): a novel approach to reducing postoperative bleeding. Blood Coagul Fibrinolysis 1990; 1:55.[Medline]
  177. Cosgrove DM 3rd, Heric B, Lytle BW, et al: Aprotinin therapy for reoperative myocardial revascularization: a placebo-controlled study. Ann Thorac Surg 1992; 54:1031.[Abstract]
  178. Sundt TM 3rd, Kouchoukos NT, Saffitz JE, et al: Renal dysfunction and intravascular coagulation with aprotinin and hypothermic circulatory arrest. Ann Thorac Surg 1993; 55:1418.[Abstract]
  179. Laub GW, Riebman JB, Chen C, et al: The impact of aprotinin on coronary artery bypass graft patency. Chest 1994; 106: 1370.[Abstract/Free?Full?Text]
  180. Salzman EW, Weinstein MJ, Reilly D, Ware JA: Adventures in hemostasis: desmopressin in cardiac surgery. Arch Surg 1993; 128:212.[Abstract]
  181. Temeck BK, Bachenheimer LC, Katz NM, et al: Desmopressin acetate in cardiac surgery: a double-blind, randomized study. South Med J 1994; 87:611.[Medline]
  182. Ansell J, Klassen V, Lew R, et al: Does desmopressin acetate prophylaxis reduce blood loss after valvular heart operations? A randomized, double-blind study. J Thorac Cardiovasc Surg 1992; 104:117.[Abstract]
  183. Dilthey G, Dietrich W, Spannal M, Richter JA: Influence of desmopressin acetate on homologous blood requirements in cardiac surgical patients pretreated with aspirin. Anesthesiology 1993; 7:425.
  184. Sheridan DP, Card RT, Pinilla JC, et al: Use of desmopressin acetate to reduce blood transfusion requirements during cardiac surgery in patients with acetylsalicylic-acid-induced platelet dysfunction. Can J Surg 1994; 37:33.[Medline]
  185. Shirvani R: An evaluation of clinical aspects of post-operative autotransfusion, either alone or in conjunction with pre-operative aspirin, in cardiac surgery. Br J Clin Pract 1991; 45:105.[Medline]
  186. de Haan J, Boonstra PW, Monnink SH, et al: Retransfusion of suctioned blood during cardiopulmonary bypass impairs hemostasis. Ann Thorac Surg 1995; 59:901.[Abstract/Free?Full?Text]
  187. Ovrum E, Holen EA, Lindstein Ringdal MA: Elective coronary artery bypass surgery without homologous blood transfusion: early results with an inexpensive blood conservation program. Scand J Thorac Cardiovasc Surg 1991; 25:13.[Medline]
  188. Schaff HV, Hauer JM, Bell WR, et al: Autotransfusion of shed mediastinal blood after cardiac surgery: a prospective study. J Thorac Cardiovasc Surg 1978; 75:632.[Abstract]
  189. Hartz RS, Smith JA, Green D: Autotransfusion after cardiac operation: assessment of hemostatic factors. J Thorac Cardiovasc Surg 1988; 96:178.[Abstract]
  190. Breyer RH, Engelman RM, Rousou JA, Lemeshow S: Blood conservation for myocardial revascularization: is it cost effective? J Thorac Cardiovasc Surg 1987; 93:512.[Abstract]
  191. Griffith LD, Billman GF, Daily PO, Lane TA: Apparent coagulopathy caused by infusion of shed mediastinal blood and its prevention by washing of the infusate. Ann Thorac Surg 1989; 47:400.[Abstract]
  192. Axford TC, Dearani JA, Ragno G, et al: Safety and therapeutic effectiveness of reinfused shed blood after open heart surgery. Ann Thorac Surg 1994; 57:615.[Abstract]
  193. Hoffman WS, Tomasello DN, MacVaugh H: Control of postcardiotomy bleeding with PEEP. Ann Thorac Surg 1982; 34:71.[Abstract]
  194. Ilabaca PA, Ochsner JL, Mills NL: Positive end-expiratory pressure in the management of the patient with a postoperative bleeding heart. Ann Thorac Surg 1980; 30:281.[Abstract]
  195. Zurick AM, Urzua J, Ghattas M, et al: Failure of positive end-expiratory pressure to decrease postoperative bleeding after cardiac surgery. Ann Thorac Surg 1982; 34:608.[Abstract]
  196. Bouboulis N, Rivas LF, Kuo J, et al: Packing the chest: a useful technique for intractable bleeding after open heart operation. Ann Thorac Surg 1994; 57:856.[Abstract]
  197. Vander Salm TJ: Two techniques for the control of cardiac bleeding. Ann Thorac Surg 1994; 57:762.[Abstract]
  198. Pelletier MP, Solymoss S, Lee A, Chiu RC: Negative reexploration for cardiac postoperative bleeding: can it be therapeutic? Ann Thorac Surg 1998; 65:999.[Abstract/Free?Full?Text]
  199. Fairman RM, Edmunds LH Jr: Emergency thoracotomy in the surgical intensive care unit after open cardiac operation. Ann Thorac Surg 1981; 32:386.[Abstract]
  200. Anthi A, Tzelepis GE, Alivizatos P, et al: Unexpected cardiac arrest after cardiac surgery: incidence, predisposing causes, and outcome of open chest cardiopulmonary resuscitation. Chest 1998; 113:15.[Abstract/Free?Full?Text]
  201. Feng WC, Bert AA, Browning RA, Singh AK: Open cardiac massage and periresuscitative cardiopulmonary bypass for cardiac arrest following cardiac surgery. J Cardiovasc Surg (Torino) 1995; 36:319.[Medline]
  202. Hill RC: Open-chest resuscitation and postcardiac surgery arrest. Chest 1998; 113:3.
  203. Pottle A, Bullock I, Thomas J, Scott L: Survival to discharge following open chest cardiac compression (OCCC): a 4year retrospective audit in a cardiothoracic specialist centerRoyal Brompton and Harefield NHS Trust, United Kingdom. Resuscitation 2002; 52:269.[Medline]
  204. Wahba A, Gotz W, Birnbaum DE: Outcome of cardiopulmonary resuscitation following open heart surgery. Scand Cardiovasc J 1997; 31:147.[Medline]
  205. Ratliff NB, Young WG Jr, Hackel DB, et al: Pulmonary injury secondary to extracorporeal circulation: an ultrastructural study. J Thorac Cardiovasc Surg 1973; 65:425.[Medline]
  206. Gillespie DJ, Didier EP, Rehder K: Ventilation-perfusion distribution after aortic valve replacement. Crit Care Med 1990; 18:136.[Medline]
  207. Pacifico AD, Digerness S, Kirklin JW: Acute alterations of body composition after open intracardiac operations. Circulation 1970; 41:331.[Medline]
  208. Hill DG, de Lanerolle P, Kosek JC, et al: The pulomary pathophysiology of membrane and bubble oxygenators. Trans Am Soc Artif Intern Organs 1975; 21:165.[Medline]
  209. Cohn LH, Angell WW, Shumway NE: Body fluid shifts after cardiopulmonary bypass, I: effects of congestive heart failure and hemodilution. J Thorac Cardiovasc Surg 1971; 62:423.[Medline]
  210. Lancey RA SBVT: Off-pump versus on-pump coronary artery bypass surgery: a case-matched comparison of clinical outcomes and costs. Heart Surg Forum 2000; 4:277.
  211. Magee MJ, Dewey TM, Acuff T, et al: Influence of diabetes on mortality and morbidity: off-pump coronary artery bypass grafting versus coronary artery bypass grafting with cardiopulmonary bypass. Ann Thorac Surg 2001; 72:776.[Abstract/Free?Full?Text]
  212. Arom KV, Flavin TF, Emery RW, et al: Safety and efficacy of off-pump coronary artery bypass grafting. Ann Thorac Surg 2000; 69:704.[Abstract/Free?Full?Text]
  213. Yokoyama T, Baumgartner FJ, Gheissari A, et al: Off-pump versus on-pump coronary bypass in high-risk subgroups. Ann Thorac Surg 2000; 70:1546.[Abstract/Free?Full?Text]
  214. Bowles BJ, Lee JD, Dang CR, et al: Coronary artery bypass performed without the use of cardiopulmonary bypass is associated with reduced cerebral microemboli and improved clinical results. Chest 2001; 119:25.[Abstract/Free?Full?Text]
  215. Hernandez F, Clough RA, Klemperer JD, Blum JM: Off-pump coronary artery bypass grafting: initial experience at one community hospital. Ann Thorac Surg 2000; 70:1070.[Abstract/Free?Full?Text]
  216. Kshettry VR, Flavin TF, Emery RW, et al: Does multivessel, off-pump coronary artery bypass reduce postoperative morbidity? Ann Thorac Surg 2000; 69:1725.[Abstract/Free?Full?Text]
  217. van Dijk D, Nierich AP, Jansen EW, et al: Early outcome after off-pump versus on-pump coronary bypass surgery: results from a randomized study. Circulation 2001; 104:1761.[Abstract/Free?Full?Text]
  218. Coleman SM, Demastrice L: Leukocyte depletion reduces postoperative oxygen requirements. Ann Thorac Surg 1994; 58:1567.
  219. Mihaljevic T, Tonz M, von Segesser LK, et al: The influence of leukocyte filtration during cardiopulmonary bypass on postoperative lung function: a clinical study. J Thorac Cardiovasc Surg 1995; 109:1138.
  220. Connell RS, Page US, Bartley TD, et al: The effect on pulmonary ultrastructure of dacron-wool filtration during cardiopulmonary bypass. Ann Thorac Surg 1973; 15:217.[Medline]
  221. el Gatit A, al Khaja N, Belboul A, et al: Influence of alprostadil on pulmonary dysfunction after a cardiac operation. Ann Thorac Surg 1992; 53:1018.[Abstract]
  222. Mayumi H, Tokunaga K: Prostaglandin E1 for patients who have both heart and lung failure after cardiotomy. J Thorac Cardiovasc Surg 1993; 105:1120.[Medline]
  223. Zehr KJ, Poston RS, Lee PC, et al: Platelet activating factor inhibition reduces lung injury after cardiopulmonary bypass. Ann Thorac Surg 1995; 59:328.[Abstract/Free?Full?Text]
  224. Downs JB, Mitchell LA: Pulmonary effects of ventilatory pattern following cardiopulmonary bypass. Crit Care Med 1976; 4:295.[Medline]
  225. Markand ON, Moorthy SS, Mahomed Y, et al: Postoperative phrenic nerve palsy in patients with open-heart surgery. Ann Thorac Surg 1985; 39:68.[Abstract]
  226. Large SR, Heywood LJ, Flower CD, et al: Incidence and aetiology of a raised hemidiaphragm after cardiopulmonary bypass. Thorax 1985; 40:444.[Abstract]
  227. Estenne M, Yernault JC, De Smet JM, De Troyer A: Phrenic and diaphragm function after coronary artery bypass grafting. Thorax 1985; 40:293.[Abstract]
  228. Benjamin JJ, Cascade PN, Rubenfire M, et al: Left lower lobe atelectasis and consolidation following cardiac surgery: the effect of topical cooling on the phrenic nerve. Radiology 1982; 142:11.[Abstract]
  229. Dajee A, Pellegrini J, Cooper G, Karlson K: Phrenic nerve palsy after topical cardiac hypothermia. Int Surg 1983; 68:345.[Medline]
  230. Diehl JL, Lofaso F, Deleuze P, et al: Clinically relevant diaphragmatic dysfunction after cardiac operations. J Thorac Cardiovasc Surg 1994; 107:487.[Abstract/Free?Full?Text]
  231. Bevelaqua F, Garritan S, Haas F, et al: Complications after cardiac operations in patients with severe pulmonary impairment. Ann Thorac Surg 1990; 50:602.[Abstract]
  232. Moore R, Follette DM, Berkoff HA: Poststernotomy fractures and pain management in open cardiac surgery. Chest 1994; 106:1339.[Abstract/Free?Full?Text]
  233. Good JT Jr, Wolz JF, Anderson JT, et al: The routine use of positive end-expiratory pressure after open heart surgery. Chest 1979; 76:397.[Abstract/Free?Full?Text]
  234. Zwischenberger JB, Kirsh MM, Dechert RE, et al: Suppression of shivering decreases oxygen consumption and improves hemodynamic stability during postoperative rewarming. Ann Thorac Surg 1987; 43:428.[Abstract]
  235. Sharkey A, Lipton JM, Murphy MT, Giesecke AH: Inhibition of postanesthetic shivering with radiant heat. Anesthesiology 1987; 66:249.[Medline]
  236. Rodriguez JL, Weissman C, Damask MC, et al: Physiologic requirements during rewarming: suppression of the shivering response. Crit Care Med 1983; 11:490.[Medline]
  237. Slogoff S, Keats AS: Does perioperative myocardial ischemia lead to postoperative myocardial infarction? Anesthesiology 1985; 62:107.[Medline]
  238. Hall RI: Anaesthesia for coronary artery surgerya plea for a goal-directed approach. Can J Anaesth 1993; 40:1178.[Abstract/Free?Full?Text]
  239. Gall SA Jr, Olsen CO, Reves JG, et al: Beneficial effects of endotracheal extubation on ventricular performance: implications for early extubation after cardiac operations. J Thorac Cardiovasc Surg 1988; 95:819.[Abstract]
  240. Chong JL, Grebenik C, Sinclair M, et al: The effect of a cardiac surgical recovery area on the timing of extubation. J Cardiothorac Vasc Anesth 1993; 7:137.[Medline]
  241. Butler J, Chong GL, Pillai R, et al: Early extubation after coronary artery bypass surgery: effects on oxygen flux and haemodynamic variables. J Cardiovasc Surg (Torino) 1992; 33:276.[Medline]
  242. Yang KL, Tobin MJ: A prospective study of indexes predicting the outcome of trials of weaning from mechanical ventilation. N Engl J Med 1991; 324:1445.[Abstract]
  243. Postoperative care, in Kirklin JW, Barratt-Boyes BG (eds): Cardiac Surgery. New York, Churchill-Livingston, 1993; p 195.
  244. Culliford AT, Thomas S, Spencer FC: Fulminating noncardiogenic pulmonary edema: a newly recognized hazard during cardiac operations. J Thorac Cardiovasc Surg 1980; 80:868.[Abstract]
  245. Olinger GN, Becker RM, Bonchek LI: Noncardiogenic pulmonary edema and peripheral vascular collapse following cardiopulmonary bypass: rare protamine reaction? Ann Thorac Surg 1980; 29:20.[Abstract]
  246. Gillinov AM, Davis EA, Alberg AJ, et al: Pulmonary embolism in the cardiac surgical patient. Ann Thorac Surg 1992; 53:988.[Abstract]
  247. Dhingra S, Solven F, Wilson A, McCarthy DS: Hypomagnesemia and respiratory muscle power. Am Rev Respir Dis 1984; 129:497.[Medline]
  248. Martinez FJ, Bermudez-Gomez M, Celli BR: Hypothyroidism: a reversible cause of diaphragmatic dysfunction. Chest 1989; 96:1059.[Abstract/Free?Full?Text]
  249. MacIntyre NR, Cook DJ, Ely EW Jr, et al: Evidence-based guidelines for weaning and discontinuing ventilatory support: a collective task force facilitated by the American College of Chest Physicians; the American Association for Respiratory Care; and the American College of Critical Care Medicine. Chest 2001; 120:375S.[Free?Full?Text]
  250. Massick DD, Yao S, Powell DM, et al: Bedside tracheostomy in the intensive care unit: a prospective randomized trial comparing open surgical tracheostomy with endoscopically guided percutaneous dilational tracheotomy. Laryngoscope 2001; 111:494.[Medline]
  251. Dulguerov P, Gysin C, Perneger TV, Chevrolet JC: Percutaneous or surgical tracheostomy: a meta-analysis. Crit Care Med 1999; 27:1617.[Medline]
  252. Cheng E, Fee WE Jr: Dilatational versus standard tracheostomy: a meta-analysis. Ann Otol Rhinol Laryngol 2000; 109:803.[Medline]
  253. Freeman BD, Isabella K, Lin N, Buchman TG: A meta-analysis of prospective trials comparing percutaneous and surgical tracheostomy in critically ill patients. Chest 2000; 118:1412.[Abstract/Free?Full?Text]
  254. Frega NS, Dibona DR, Guertler B, Leaf A: Ischemic renal injury. Kidney Int Suppl 1976; 10:525.
  255. Levinsky NG, Bernard DB, Johnston PA: Mannitol and loop diuretics in acute renal failure, in Brenner BM, Lazarus JM (eds): Acute Renal Failure. Philadelphia, WB Saunders, 1983; p 712.
  256. Kahn DR, Cerny JC, Lee RS, Sloan H: The effect of mannitol on renal function during open-heart surgery. Surgery 1965; 57:676.[Medline]
  257. Schuster SR, Kak M van, Vawter GF, Narter N: An experimental study of the effect of mannitol during cardiopulmonary bypass. Circulation 1964; 29:72.
  258. Patak RV, Fadem SZ, Lifschitz MD, Stein JH: Study of factors which modify the development of norepinephrine-induced acute renal failure in the dog. Kidney Int 1979; 15:227.[Medline]
  259. Kleinknecht D, Ganeval D, Gonzalez-Duque LA, Fermanian J: Furosemide in acute oliguric renal failure: a controlled trial. Nephron 1976; 17:51.[Medline]
  260. Nierenberg DW: Furosemide and ethacrynic acid in acute tubular necrosis. West J Med 1980; 133:163.[Medline]
  261. Baek SM, Brown RS, Shoemaker WC: Early prediction of acute renal failure and recovery, II: renal function response to furosemide. Ann Surg 1973; 178:605.[Medline]
  262. Brown RS: Renal dysfunction in the surgical patient: maintenance of high output state with furosemide. Crit Care Med 1979; 7:63.[Medline]
  263. Lindner A, Cutler RE, Goodman G: Synergism of dopamine plus furosemide in preventing acute renal failure in the dog. Kidney Int 1979; 16:158.[Medline]
  264. Lindner A: Synergism of dopamine and furosemide in diuretic-resistant, oliguric acute renal failure. Nephron 1983; 33:121.[Medline]
  265. Sirivella S, Gielchinsky I, Parsonnet V: Mannitol, furosemide, and dopamine infusion in postoperative renal failure complicating cardiac surgery. Ann Thorac Surg 2000; 69:501.[Abstract/Free?Full?Text]
  266. Hashimoto K, Nomura K, Nakano M, et al: Pharmacological intervention for renal protection during cardiopulmonary bypass. Heart Vessels 1993; 8:203.[Medline]
  267. Zanardo G, Michielon P, Rosi P, et al: Effects of a continuous diltiazem infusion on renal function during cardiac surgery. J Cardiothorac Vasc Anesth 1993; 7:711.[Medline]
  268. Abe K, Fujino Y, Sakakibara T: The effect of prostaglandin E1 during cardiopulmonary bypass on renal function after cardiac surgery. Eur J Clin Pharmacol 1993; 45:217.[Medline]
  269. Mauk RH, Patak RV, Fadem SZ, et al: Effect of prostaglandin E administration in a nephrotoxic and a vasoconstrictor model of acute renal failure. Kidney Int 1977; 12:122.[Medline]
  270. Zanardo G, Michielon P, Paccagnella A, et al: Acute renal failure in the patient undergoing cardiac operation: prevalence, mortality rate, and main risk factors. J Thorac Cardiovasc Surg 1994; 107:1489.[Abstract/Free?Full?Text]
  271. Holper K, Struck E, Sebening F: The diagnosis of acute renal failure (ARF) following cardiac surgery with cardio-pulmonary bypass. Thorac Cardiovasc Surg 1979; 27:231.[Medline]
  272. Kron IL, Joob AW, Van Meter C: Acute renal failure in the cardiovascular surgical patient. Ann Thorac Surg 1985; 39:590.[Abstract]
  273. Smith HW: Principles of Renal Physiology. Baltimore, University Park Press, 1956.
  274. Abel RM, Buckley MJ, Austen WG, et al: Etiology, incidence, and prognosis of renal failure following cardiac operations: results of a prospective analysis of 500 consecutive patients. J Thorac Cardiovasc Surg 1976; 71:323.[Abstract]
  275. Corwin HL, Sprague SM, DeLaria GA, Norusis MJ: Acute renal failure associated with cardiac operations: a case-control study. J Thorac Cardiovasc Surg 1989; 98:1107.[Abstract]
  276. Andersson LG, Ekroth R, Bratteby LE, et al: Acute renal failure after coronary surgerya study of incidence and risk factors in 2009 consecutive patients. Thorac Cardiovasc Surg 1993; 41:237.[Medline]
  277. Corwin HL, Sprague SM, DeLaria GA, Norusis MJ: Acute renal failure associated with cardiac operations: a case-control study. J Thorac Cardiovasc Surg 1989; 98:1107.
  278. Zanardo G, Michielon P, Paccagnella A, et al: Acute renal failure in the patient undergoing cardiac operation: prevalence, mortality rate, and main risk factors. J Thorac Cardiovasc Surg 1994; 107:1489.
  279. Osborn JJ, Cohn K, Hart M: Hemolysis during perfusion. J Thorac Cardiovasc Surg 1962; 43:459.
  280. Savitsky JP, Doczi J, Black J, Arnold JD: A clinical safety trial of stroma-free hemoglobin. Clin Pharmacol Ther 1978; 23:73.[Medline]
  281. Carlson DE, Karp RB, Kouchoukos NT: Surgical treatment of aneurysms of the descending thoracic aorta: an analysis of 85 patients. Ann Thorac Surg 1983; 35:58.[Abstract]
  282. Roberts AJ, Nora JD, Hughes WA, et al: Cardiac and renal responses to cross-clamping of the descending thoracic aorta. J Thorac Cardiovasc Surg 1983; 86:732.[Abstract]
  283. Kleinknecht D, Jungers P, Chanard J, et al: Uremic and non-uremic complications in acute renal failure: evaluation of early and frequent dialysis on prognosis. Kidney Int 1972; 1:190.[Medline]
  284. Norman JC, McDonald HP, Sloan H: The early and aggressive treatment of acute renal failure following cardiopulmonary bypass with continuous peritoneal dialysis. Surgery 1964; 56:240.[Medline]
  285. Meyer MM: Renal replacement therapies. Crit Care Clin 2000; 16:29.[Medline]
  286. Walpoth B, Geroulanos S, Turina M, Senning A: [Reducing hemodilution through ultrafiltration following cardiopulmonary bypass]. Helv Chir Acta 1980; 47:231.[Medline]
  287. Darup J, Bleese N, Kalmar P, et al: Hemofiltration during extracorporeal circulation (ECC). Thorac Cardiovasc Surg 1979; 27:227.[Medline]
  288. Walpoth BH, Amport T, Schmid R, et al: Hemofiltration during cardiopulmonary bypass: quality assessment of hemoconcentrated blood. Thorac Cardiovasc Surg 1994; 42:162.[Medline]
  289. Lamer C, Valleaux T, Plaisance P, et al: Continuous arteriovenous hemodialysis for acute renal failure after cardiac operations. J Thorac Cardiovasc Surg 1990; 99:175.[Medline]
  290. Morgan JM, Morgan C, Evans TW: Clinical experience of pumped arteriovenous haemofiltration in the management of patients in oliguric renal failure following cardiothoracic surgery. Int J Cardiol 1988; 21:259.[Medline]
  291. Baudouin SV, Wiggins J, Keogh BF, et al: Continuous veno-venous haemofiltration following cardio-pulmonary bypass: indications and outcome in 35 patients. Intensive Care Med 1993; 19:290.[Medline]
  292. Cole L, Bellomo R, Journois D, et al: High-volume haemofiltration in human septic shock. Intensive Care Med 2001; 27:978.[Medline]
  293. Journois D, Israel-Biet D, Pouard P, et al: High-volume, zero-balanced hemofiltration to reduce delayed inflammatory response to cardiopulmonary bypass in children. Anesthesiology 1996; 85:965.[Medline]
  294. McLeish KR, Luft FC, Kleit SA: Factors affecting prognosis in acute renal failure following cardiac operations. Surg Gynecol Obstet 1977; 145:28.[Medline]
  295. Bhat JG, Gluck MC, Lowenstein J, Baldwin DS: Renal failure after open heart surgery. Ann Intern Med 1976; 84:677.
  296. Lange HW, Aeppli DM, Brown DC: Survival of patients with acute renal failure requiring dialysis after open heart surgery: early prognostic indicators. Am Heart J 1987; 113:1138.[Medline]
  297. Katz ES, Tunick PA, Rusinek H, et al: Protruding aortic atheromas predict stroke in elderly patients undergoing cardiopulmonary bypass: experience with intraoperative transesophageal echocardiography. J Am Coll Cardiol 1992; 20:70.[Abstract]
  298. Smith PL, Treasure T, Newman SP, et al: Cerebral consequences of cardiopulmonary bypass. Lancet 1986; 1:823.[Medline]
  299. Wareing TH, Davila-Roman VG, Daily BB, et al: Strategy for the reduction of stroke incidence in cardiac surgical patients. Ann Thorac Surg 1993; 55:1400.[Abstract]
  300. Roach GW, Kanchuger M, Mangano CM, et al: Adverse cerebral outcomes after coronary bypass surgery. Multicenter Study of Perioperative Ischemia Research Group and the Ischemia Research and Education Foundation Investigators. N Engl J Med 1996; 335:1857.[Abstract/Free?Full?Text]
  301. Gardner TJ, Horneffer PJ, Manolio TA, et al: Stroke following coronary artery bypass grafting: a ten-year study. Ann Thorac Surg 1985; 40:574.[Abstract]
  302. Furlan AJ, Sila CA, Chimowitz MI, Jones SC: Neurologic complications related to cardiac surgery. Neurol Clin 1992; 10:145.[Medline]
  303. Harrison MJ, Schneidau A, Ho R, et al: Cerebrovascular disease and functional outcome after coronary artery bypass surgery. Stroke 1989; 20:235.[Abstract]
  304. Hogue CW Jr, Murphy SF, Schechtman KB, Davila-Roman VG: Risk factors for early or delayed stroke after cardiac surgery. Circulation 1999; 100:642.[Medline]
  305. Ali IM, Cummings B, Sullivan J, Francis S: The risk of cerebrovascular accident in patients with asymptomatic critical carotid artery stenosis who undergo open-heart surgery. Can J Surg 1998; 41:374.[Medline]
  306. Yoon BW, Bae HJ, Kang DW, et al: Intracranial cerebral artery disease as a risk factor for central nervous system complications of coronary artery bypass graft surgery. Stroke 2001; 32:94.[Abstract/Free?Full?Text]
  307. Martin TD, Craver JM, Gott JP, et al: Prospective, randomized trial of retrograde warm blood cardioplegia: myocardial benefit and neurologic threat. Ann Thorac Surg 1994; 57:298.[Abstract]
  308. Blauth CI, Cosgrove DM, Webb BW, et al: Atheroembolism from the ascending aorta: an emerging problem in cardiac surgery. J Thorac Cardiovasc Surg 1992; 103:1104.[Abstract]
  309. Gold JP, Charlson ME, Williams-Russo P, et al: Improvement of outcomes after coronary artery bypass: a randomized trial comparing intraoperative high versus low mean arterial pressure. J Thorac Cardiovasc Surg 1995; 110:1302.[Abstract/Free?Full?Text]
  310. Huse-Kleinstoll G, Dahme B, Flemming B, et al: Open-heart surgery: somatic predictors of postoperative psychopathology. Thorac Cardiovasc Surg 1979; 27:271.[Medline]
  311. Calabrese JR, Skwerer RG, Gulledge AD, et al: Incidence of postoperative delirium following myocardial revascularization: a prospective study. Cleve Clin J Med 1987; 54:29.[Medline]
  312. Dubin WR, Field HL, Gastfriend DR: Postcardiotomy delirium: a critical review. J Thorac Cardiovasc Surg 1979; 77:586.[Abstract]
  313. Blauth C, Griffin S, Harrison M, et al: Neuropsychologic alterations after cardiac operation. J Thorac Cardiovasc Surg 1989; 98:454.[Medline]
  314. Newman S, Smith P, Treasure T: Acute neuropsychological consequences of coronary artery bypass surgery. Cur Psychiatr Res Rev 1987; 6:115.
  315. Sotaniemi KA, Mononen H, Hokkanen TE: Long-term cerebral outcome after open-heart surgery: a five-year neuropsychological follow-up study. Stroke 1986; 17:410.[Abstract]
  316. Shaw PJ, Bates D, Cartlidge NE, et al: Neurologic and neuropsychological morbidity following major surgery: comparison of coronary artery bypass and peripheral vascular surgery. Stroke 1987; 18:700.[Abstract]
  317. O'Brien DJ, Bauer RM, Yarandi H, et al: Patient memory before and after cardiac operations. J Thorac Cardiovasc Surg 1992; 104:1116.[Abstract]
  318. Townes BD, Bashein G, Hornbein TF, et al: Neurobehavioral outcomes in cardiac operations: a prospective controlled study. J Thorac Cardiovasc Surg 1989; 98:774.[Abstract]
  319. Johnston WE, Stump DA, DeWitt DS, et al: Significance of gaseous microemboli in the cerebral circulation during cardiopulmonary bypass in dogs. Circulation 1993; 88:II319.
  320. Clark RE, Brillman J, Davis DA, et al: Microemboli during coronary artery bypass grafting: genesis and effect on outcome. J Thorac Cardiovasc Surg 1995; 109:249.[Abstract/Free?Full?Text]
  321. Toner I, Peden CJ, Hamid SK, et al: Magnetic resonance imaging and neuropsychological changes after coronary artery bypass graft surgery: preliminary findings. J Neurosurg Anesthesiol 1994; 6:163.[Medline]
  322. Diegeler A, Hirsch R, Schneider F, et al: Neuromonitoring and neurocognitive outcome in off-pump versus conventional coronary bypass operation. Ann Thorac Surg 2000; 69:1162.[Abstract/Free?Full?Text]
  323. Ricci M, Karamanoukian HL, Abraham R, et al: Stroke in octogenarians undergoing coronary artery surgery with and without cardiopulmonary bypass. Ann Thorac Surg 2000; 69:1471.[Abstract/Free?Full?Text]
  324. Koutlas TC, Elbeery JR, Williams JM, et al: Myocardial revascularization in the elderly using beating heart coronary artery bypass surgery. Ann Thorac Surg 2000; 69:1042.[Abstract/Free?Full?Text]
  325. Hernandez F, Cohn WE, Baribeau YR, et al: In-hospital outcomes of off-pump versus on-pump coronary artery bypass procedures: a multicenter experience. Ann Thorac Surg 2001; 72:1528.[Abstract/Free?Full?Text]
  326. Puskas JD, Thourani VH, Marshall JJ, et al: Clinical outcomes, angiographic patency, and resource utilization in 200 consecutive off-pump coronary bypass patients. Ann Thorac Surg 2001; 71:1477.[Abstract/Free?Full?Text]
  327. Taggart DP, Browne SM, Halligan PW, Wade DT: Is cardiopulmonary bypass still the cause of cognitive dysfunction after cardiac operations? J Thorac Cardiovasc Surg 1999; 118:414.[Abstract/Free?Full?Text]
  328. Murkin JM: Neurological outcomes after OPCAB: how much better is it? Heart Surg Forum 2000; 3:207.[Medline]
  329. Angelini GD, Taylor FC, Reeves BC, Ascione R: Early and midterm outcome after off-pump and on-pump surgery in Beating Heart Against Cardioplegic Arrest Studies (BHACAS 1 and 2): a pooled analysis of two randomised controlled trials. Lancet 2002; 359:1194.[Medline]
  330. van Dijk D, Jansen EW, Hijman R, et al: Cognitive outcome after off-pump and on-pump coronary artery bypass graft surgery: a randomized trial. JAMA 2002; 287:1405.[Abstract/Free?Full?Text]
  331. Vander Salm TJ, Cutler BS, Okike ON: Brachial plexus injury following median sternotomy: part II. J Thorac Cardiovasc Surg 1982; 83:914.[Abstract]
  332. Vander Salm TJ, Cereda JM, Cutler BS: Brachial plexus injury following median sternotomy. J Thorac Cardiovasc Surg 1980; 80:447.[Abstract]
  333. Kirsh MM, Magee KR, Gago O, et al: Brachial plexus injury following median sternotomy incision. Ann Thorac Surg 1971; 11:315.[Medline]
  334. Treasure T, Garnett R, O'Connor J, Treasure JL: Injury of the lower trunk of the brachial plexus as a complication of median sternotomy for cardiac surgery. Ann R Coll Surg Engl 1980; 62:37.
  335. Leitman IM, Paull DE, Barie PS, et al: Intra-abdominal complications of cardiopulmonary bypass operations. Surg Gynecol Obstet 1987; 165:251.[Medline]
  336. Eustace S, Connolly B, Egleston C, O'Connell D: Imaging of abdominal complications following cardiac surgery. Abdom Imaging 1994; 19:405.[Medline]
  337. Tsiotos GG, Mullany CJ, Zietlow S, van Heerden JA: Abdominal complications following cardiac surgery. Am J Surg 1994; 167:553.[Medline]
  338. Johnston G, Vitikainen K, Knight R, et al: Changing perspective on gastrointestinal complications in patients undergoing cardiac surgery. Am J Surg 1992; 163:525.[Medline]
  339. Zacharias A, Schwann TA, Parenteau GL, et al: Predictors of gastrointestinal complications in cardiac surgery. Tex Heart Inst J 2000; 27:93.[Medline]
  340. Sakorafas GH, Tsiotos GG: Intra-abdominal complications after cardiac surgery. Eur J Surg 1999; 165:820.[Medline]
  341. Mierdl S, Meininger D, Dogan S, et al: Abdominal complications after cardiac surgery. Ann Acad Med Singapore 2001; 30:245.[Medline]
  342. Christenson JT, Schmuziger M, Maurice J, et al: Postoperative visceral hypotension the common cause for gastrointestinal complications after cardiac surgery. Thorac Cardiovasc Surg 1994; 42:152.[Medline]
  343. Fiddian-Green RG: Studies in splanchnic ischemia and multiple organ failure, in Marston A, Buckley GB, Fiddian-Green RG: Splanchnic Ischemia and Multiple Organ Failure. London, Edward Arnold, 1989; p 349.
  344. Bailey RW, Bulkley GB, Hamilton SR, et al: The fundamental hemodynamic mechanism underlying gastric "stress ulceration" in cardiogenic shock. Ann Surg 1987; 205:597.[Medline]
  345. Albes JM, Schistek R, Baier R, Unger F: Intestinal ischemia associated with cardio-pulmonary-bypass surgery: a life threatening complication. J Cardiovasc Surg (Torino) 1991; 32:527.[Medline]
  346. Allen KB, Salam AA, Lumsden AB: Acute mesenteric ischemia after cardiopulmonary bypass. J Vasc Surg 1992; 16:391.[Medline]
  347. Chu CM, Chang CH, Liaw YF, Hsieh MJ: Jaundice after open heart surgery: a prospective study. Thorax 1984; 39:52.[Abstract]
  348. Svensson LG, Decker G, Kinsley RB: A prospective study of hyperamylasemia and pancreatitis after cardiopulmonary bypass. Ann Thorac Surg 1985; 39:409.[Abstract]
  349. Fernandez-del Castillo C, Harringer W, et al: Risk factors for pancreatic cellular injury after cardiopulmonary bypass. N Engl J Med 1991; 325:382.[Abstract]
  350. Rosen HR, Vlahakes GJ, Rattner DW: Fulminant peptic ulcer disease in cardiac surgical patients: pathogenesis, prevention, and management. Crit Care Med 1992; 20:354.[Medline]
  351. Egleston CV, Wood AE, Gorey TF, McGovern EM: Gastrointestinal complications after cardiac surgery. Ann R Coll Surg Engl 1993; 75:52.[Medline]
  352. Krasna MJ, Flancbaum L, Trooskin SZ, et al: Gastrointestinal complications after cardiac surgery. Surgery 1988; 104:773.[Medline]
  353. Mansour MA: Management of acute mesenteric ischemia. Arch Surg 1999; 134:328.[Abstract/Free?Full?Text]
  354. DePriest JL: Stress ulcer prophylaxis: do critically ill patients need it? Postgrad Med 1995; 98:159.
  355. Simic O, Strathausen S, Hess W, Ostermeyer J: Incidence and prognosis of abdominal complications after cardiopulmonary bypass. Cardiovasc Surg 1999; 7:419.[Medline]
  356. Rattner DW, Gu ZY, Vlahakes GJ, Warshaw AL: Hyperamylasemia after cardiac surgery: incidence, significance, and management. Ann Surg 1989; 209:279.[Medline]
  357. van der Voort PH, Zandstra DF: Pathogenesis, risk factors, and incidence of upper gastrointestinal bleeding after cardiac surgery: is specific prophylaxis in routine bypass procedures needed? J Cardiothorac Vasc Anesth 2000; 14:293.[Medline]
  358. Halm U, Halm F, Thein D, et al: Helicobacter pylori infection: a risk factor for upper gastrointestinal bleeding after cardiac surgery? Crit Care Med 2000; 28:110.[Medline]
  359. O'Keefe GE, Gentilello LM, Maier RV: Incidence of infectious complications associated with the use of histamine2receptor antagonists in critically ill trauma patients. Ann Surg 1998; 227:120.[Medline]
  360. Messori A, Trippoli S, Vaiani M, et al: Bleeding and pneumonia in intensive care patients given ranitidine and sucralfate for prevention of stress ulcer: meta-analysis of randomised controlled trials. BMJ 2000; 321:1103.[Abstract/Free?Full?Text]
  361. O'Keefe GE, Gentilello LM, Maier RV: Incidence of infectious complications associated with the use of histamine2receptor antagonists in critically ill trauma patients. Ann Surg 1998; 227:120.
  362. Maier RV, Mitchell D, Gentilello L: Optimal therapy for stress gastritis. Ann Surg 1994; 220:353.[Medline]
  363. Prod'hom G, Leuenberger P, Koerfer J, et al: Nosocomial pneumonia in mechanically ventilated patients receiving antacid, ranitidine, or sucralfate as prophylaxis for stress ulcer: a randomized controlled trial. Ann Intern Med 1994; 120:653.[Abstract/Free?Full?Text]
  364. Hanisch EW, Encke A, Naujoks F, Windolf J: A randomized, double-blind trial for stress ulcer prophylaxis shows no evidence of increased pneumonia. Am J Surg 1998; 176:453.[Medline]
  365. Cook D, Guyatt G, Marshall J, et al: A comparison of sucralfate and ranitidine for the prevention of upper gastrointestinal bleeding in patients requiring mechanical ventilation. Canadian Critical Care Trials Group. N Engl J Med 1998; 338:791.[Abstract/Free?Full?Text]
  366. Moesgaard F, Jensen LS, Christiansen PM, et al: The effect of ranitidine on postoperative infectious complications following emergency colorectal surgery: a randomized, placebo-controlled, double-blind trial. Inflamm Res 1998; 47:12.[Medline]
  367. Thomason MH, Payseur ES, Hakenewerth AM, et al: Nosocomial pneumonia in ventilated trauma patients during stress ulcer prophylaxis with sucralfate, antacid, and ranitidine. J Trauma 1996; 41:503.[Medline]
  368. Sirvent JM, Verdaguer R, Ferrer MJ, et al: [Mechanical ventilation-associated pneumonia and the prevention of stress ulcer: a randomized clinical trial of antacids and ranitidine versus sucralfate]. Med Clin (Barc) 1994; 102:407.
  369. Pickworth KK, Falcone RE, Hoogeboom JE, Santanello SA: Occurrence of nosocomial pneumonia in mechanically ventilated trauma patients: a comparison of sucralfate and ranitidine. Crit Care Med 1993; 21:1856.[Medline]
  370. Schilling D, Haisch G, Sloot N, et al: Low seroprevalence of Helicobacter pylori infection in patients with stress ulcer bleedinga prospective evaluation of patients on a cardiosurgical intensive care unit. Intensive Care Med 2000; 26:1832.[Medline]
  371. Fong IW, Baker CB, McKee DC: The value of prophylactic antibiotics in aorat-coronary bypass operations: a double-blind randomized trial. J Thorac Cardiovasc Surg 1979; 78:908.[Abstract]
  372. Burke JF: Use of preventive antibiotics in clinical surgery. Am Surg 1973; 39:6.[Medline]
  373. Burke JF: The effective period of preventive antibiotic action in experimental incisions and dermal lesions. Surgery 1961; 50:161.[Medline]
  374. Goldmann DA, Hopkins CC, Karchmer AW, et al: Cephalothin prophylaxis in cardiac valve surgery: a prospective, double-blind comparison of two-day and six-day regimens. J Thorac Cardiovasc Surg 1977; 73:470.[Abstract]
  375. Stone HH, Haney BB, Kolb LD, et al: Prophylactic and preventive antibiotic therapy: timing, duration and economics. Ann Surg 1979; 189:691.[Medline]
  376. Nelson CL, Green TG, Porter RA, Warren RD: One day versus seven days of preventive antibiotic therapy in orthopedic surgery. Clin Orthop 1983; 176:258.




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