Postoperative Care of Cardiac Surgery Patients

	THE EVOLUTION OF CARE

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	CARDIOVASCULAR CARE

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Hemodynamic Assessment

Assessment and optimization of hemodynamics generally are the principal focuses of care following cardiac surgery. Appropriate management requires knowledge of preoperative cardiac function and an appreciation of the impact of intraoperative events. The goal of postoperative hemodynamic management is the maintenance of adequate oxygen delivery to vital tissues in a way that avoids unnecessary demands on a heart recovering from the stress of cardiopulmonary bypass, ischemia, and surgery.

A basic initial hemodynamic assessment includes a review of current medications, heart rate and rhythm, mean arterial pressure, central venous pressure, and electrocardiogram (ECG) to exclude ischemia and conduction abnormalities. The presence of a pulmonary artery catheter enables the measurement of pulmonary artery pressures, left-sided filling pressures [e.g., pulmonary capillary wedge pressure (PCWP)], and mixed venous oxygen saturation (MVO₂). Cardiac output, as well as pulmonary and systemic vascular resistances, also can be calculated when a pulmonary artery catheter is present. Cardiac output is determined using thermodilution or the Fick equation. Cardiac output (CO), blood pressure (BP), and systemic vascular resistance (SVR) are related to each other using Ohm’s law (Table 16-1). Reasonable minimum goals for most patients include an MVO₂ of about 60%, a mean arterial pressure (MAP) of more than 65 mm Hg, and a cardiac index (CI) of more than 2 L/m² per minute. Goals should be individualized. Patients with a history of hypertension or significant peripheral vascular disease probably will benefit from higher blood pressure; patients who are bleeding or who have suture lines in fragile tissue are best served with tighter control. Strategies designed to produce a supranormal cardiac index or MVO₂ have failed to demostrate a survival advantage.¹

Volume status is determined readily by invasive monitoring. Central venous pressure (CVP), unless it is very low, is an unreliable indicator of left ventricular end-diastolic volume (LVEDV). (An elevated CVP can be seen in volume overload, right-sided heart failure, tricuspid and mitral regurgitation, pulmonary hypertension, tamponade, tension pneumothorax, and pulmonary embolism.) Plumonary artery diastolic pressure correlates with left-sided filling pressures when pulmonary vascular resistance (PVR) is normal (low). PCWP (or left atrial pressure if this is being measured directly) provides the most accurate assessment of left-sided filling pressures, and its correlation with pulmonary artery diastolic pressure should be noted to enable a more continuous assessment of left-sided pressures. Determination of optimal filling pressures generally is empirical; a wedge pressure of 15 mm Hg generally is adequate, but many patients require significantly higher pressures. Most patients arrive from the operating room with a significant net fluid gain, but much of this excess volume is extravascular owing to third space and pleural cavity accumulation. Vasoplegia often is created by a systemic inflammatory response to cardiopulmonary bypass (CPB), and it is common to have a significant ongoing volume requirement in the immediate postoperative period. Urine output and bleeding are common sources of ongoing fluid loss. Hypothermia promotes vasoconstriction. As patients rewarm, changes in peripheral vascular tone contribute to labile hemodynamics, which often are best treated with volume.

Peripheral vascular tone needs to be sufficient to provide the patient with adequate blood pressure; excess vasoconstriction can create dangerous levels of hypertension and decrease cardiac output. Decreased afterload can be caused, in part, by medications (e.g., anesthetic agents and preoperative angiotensin-converting enzyme inhibitors), increased temperature, and a systemic inflammatory response to CPB. Increases in afterload can be caused by medications, hypothermia, and increased sympathetic output (including pain and anxiety) or may be secondary to hypovolemia or pump failure.

Pump function can be influenced by levels of exogenous or endogenous inotropes, postoperative stunning, ischemia or infarction, valve function, acidosis, electrolyte abnormalities, hypoxia, or tamponade. Bradycardia, arrhythmias, and conduction defects also can adversely affect cardiac output. The oxygen-carrying capacity of blood is a function of hematocrit and oxygenation. A hematocrit of 21% and a oxygen saturation of greater than 92% usually are adequate for a stable postoperative patient.

It is important not to allow evaluation of the patient to become obscured by too many numbers or theories, and an overall assessment of the patient is always more important than any single parameter. Trends in hemodynamic parameters usually are more important than isolated values. Patients generally do well if they have warm, well-perfused extremities, normal mental status, and good urine output (>0.5 mL/kg per minute). Acute changes in hemodynamic status are common postoperatively, and vigilant monitoring enables care to be more preemptive than reactive.

Hemodynamic Management

Fluid management

As emphasized previously, the goal of postoperative hemodynamic management is the maintenance of adequate end-organ perfusion without unnecessarily taxing the heart. Assessment and optimization of intravascular volume status generally are the first steps in this process. Most patients have ongoing fluid requirements in the immediate postoperative period that can be caused by persistent third spacing, warming, diuresis, vasodilation, and bleeding. Careful monitoring of fluid balances and filling pressures should guide volume resuscitation. Starling curves are highly variable; it is helpful to correlate cardiac output and MVO₂ with changes in volume status. Patients with ventricular hypertrophy (e.g., those with a history of hypertension or aortic stenosis) or diastolic dysfunction usually need higher filling pressures. Patients with persistently low filling pressures despite aggressive fluid administration usually are either bleeding or vasodilated. Calculation of CO and SVR often can help to sort this out. In the case of significant vasodilation, judicious use of a pressor agent can help to decrease fluid requirements. Inotropes should not be administered for the treatment of hypovolemia. Fluid requirements often can be reduced following extubation; decreased intrathoracic pressure improves venous return.

The choice of an optimal resuscitation fluid is unresolved. In the acute setting, colloid infusions achieve comparable hemodynamic effects with less volume than crystalloid solutions. After 1 hour, 80% of 1000 mL of 5% albumin solution is retained intravascularly. In situations characterized by loss of vascular endothelial integrity (e.g., following CPB), albumin may redistribute into the interstitial space and increase third-space fluid accumulation.^2,3 One study has shown that the accumulation of extravascular pulmonary water is unaffected by the prime type or the type of fluid administered postoperatively.⁴ The largest prospective, randomized, controlled study comparing colloid with crystalloid has been unable to demonstrate a difference in outcomes.⁵ Albumin and hetastarch provide comparable hemodynamic benefits, although hetastarch should be avoided in bleeding or coagulopathic patients and in those with renal impairment.^6,7

Although unusual in the immediate postoperative period, volume overload is a common problem in the days following surgery. If patients have normal cardiac function, they often diurese appropriately without intervention. Conversely, volume overload is a common cause of postoperative heart failure. Diuretics and vasodilators are required frequently in patients with impaired pump function before or following surgery or in those who received large volumes of fluid perioperatively. Patients with impaired renal function may require renal replacement therapy (e.g., ultrafiltration, continuous venovenous hemofiltration, or hemodialysis) to become euvolemic. Rapid diuresis accompanied by inadequate electrolyte repletion frequently is arrhythmogenic.

Pharmacologic support

Medications are used perioperatively to provide vasoconstriction, venous and arterial vasodilation, and inotropic support as well as to treat arrhythmias. As summarized in Table 16-2, many of the commonly used medications have multiple actions. Selection of appropriate agents depends on accurate hemodynamic assessment.

Vasodilators are indicated for hypertensive patients and for patients who are normotensive with poor pump function. Nitroglycerin and sodium nitroprusside are used commonly in the immediate postoperative period. Both have the advantage of being short acting and easy to titrate. Both can cause hypoxia by inhibiting pulmonary arterial hypoxic vasoconstriction and increasing blood flow through poorly oxygenated lung. Nitroglycerin is a stronger venodilator than an arterial dilator and can increase intercoronary collateral blood flow,¹⁰ but patients quickly can become tachyphylactic. Prolonged nitroprusside use can lead to cyanide toxicity, and methemoglobin levels must be monitored. Nicardipine is a calcium channel blocker with minimal effects on contractility or atrioventricular (AV) nodal conduction; it appears to have the efficacy of nipride without its toxicity. Nesiritide, or brain naturetic peptide, promotes diuresis in addition to vasodilation and may have beneficial lusitropic effects in patients with diastolic dysfunction.

Hypertension also can be treated with beta blockers. These agents work by decreasing heart rate and contractility. Esmolol is useful in the presence of labile blood pressure because of its short half-life. Labetalol combines beta- and alpha-adrenergic blockade. Patients whose pump function is inotrope-dependent should not receive beta blockers.

Inotropic agents are indicated when low cardiac output persists despite optimization of fluid status (preload) and vascular tone (afterload). These agents include beta-adrenergic agents (e.g., dobutamine) and cyclic nucleotide phosphodiesterase inhibitors (e.g., milrinone). Both these agents increase cardiac output by increasing myocardial contractility and reducing afterload through peripheral vasodilation. Dobutamine is shorter acting and easier to titrate; milrinone achieves increases in cardiac output with lower myocardial oxygen consumption.¹¹ Both are arrhythmogenic and can exacerbate coronary ischemia. Both epinephrine and norepinephrine combine beta- and alpha-adrenergic agonist effects; they are pressors in addition to positive inotropes. Dopamine in low doses causes splanchnic and renal vasodilation. Since perioperative beta blockade has been shown to improve mortality and morbidity following cardiac surgery, it seems reasonable to avoid the gratuitous use of inotropes, and efforts should be made to wean these agents rapidly when they are no longer required.

Heart Rate and Rhythm Management

Deviations from normal sinus rhythm can cause significant clinical deterioration, and optimization of heart rate and rhythm frequently is an effective way to improve hemodynamic status.

Pacing (see Table 16-2)

Within normal rate ranges, cardiac output increases linearly with heart rate, and pacing often is very helpful. It is important to monitor the response to pacing carefully, however. For example, sinus bradycardia often is more effective than ventricular pacing at a more normal rate. Ventricular pacing can cause ventricular dysfunction and dyssynchrony, and the loss of consistent filling from atrial contraction can lead to clinical deterioration. If possible, atrial pacing is preferred to AV pacing, which is preferred to ventricular pacing. Pacing too rapidly can have an adverse effect on cardiac performance by decreasing filling time or inducing ischemia. Internal pacemakers often can be reprogrammed to improve output.

Heart block can occur following aortic, mitral, and tricuspid valve surgery. It is also associated with inferior myocardial infarction and can be secondary to medications (e.g., digoxin, amiodarone, calcium channel blockers, and beta blockers). If a biatrial transseptal approach to the mitral valve is employed, the sinus rhythm can be lost owing to divi-sion of the sinoatrial (SA) node.¹² Heart block frequently is transient. If the ventricular escape rate is absent or insufficient, pacing wire thresholds need to be monitored carefully and backup pacing methods employed (e.g., a transvenous wire or pacing pulmonary artery catheter or external pacing pads) if needed while waiting for placement of a permanent pacemaker.

Ventricular arrhythmias

Nonsustained ventricular tachycardia (VT) is common following cardiac surgery and typically a reflection of perioperative ischemia-reperfusion injury, electrolyte abnormalities (typically hypokalemia and hypomagnesemia), or an increase in exogenous or endogenous sympathetic stimulation. Generally, nonsustained VT is more important as a symptom of an underlying cause requiring diagnosis and correction than as a cause of hemodynamic instability.

Sustained VT (persisting for more than 30 seconds or associated with significant hemodynamic compromise) requires more aggressive treatment. Ongoing ischemia should be ruled out (with coronary angiography if necessary), electrolytes should be replaced, and inotrope should be minimized. Beta blockers, amiodarone, and lidocaine are useful therapies. Electrocardioversion should be employed if sustained VT causes significant compromise.

Atrial fibrillation and flutter

PROPHYLAXIS: Atrial fibrillation and flutter occur in 20 to 40% of patients undergoing coronary artery bypass grafting (CABG) and generally is more common in patients undergoing valve and combined procedures. Beta blockers are the most commonly used and effective prophylactic treatment and should be started or resumed as soon as they can be tolerated safely following surgery. Inotropic support, hemodynamic compromise, and AV block (e.g., PR interval > 0.24 ms or, second- or third-degree block) are contraindications. Beta blockers appear to provide more effective prophylaxis when they are dosed with high frequency and titrated to produce an effect on heart rate and blood pressure. Sotalol and amiodarone are also effective for prophylaxis but not superior. Beta blockers confer benefits other than atrial fibrillation prophylaxis, are easy to titrate, and do not have the toxicities associated with amiodarone.

TREATMENT: There are many treatment strategies for the management of atrial fibrillation.¹³ We have found that the use of a guideline reduces the incidence of atrial fibrillation and decreases the disruption and anxiety that it creates (Table 16-1). The principal premise of this strategy is recognition of the fact that for most patients with new-onset atrial fibrillation, the arrhythmia is self-limited (90% of patients are in sinus rhythm within 6 to 8 weeks independent of treatment approach). The pursuit of a rate control and anticoagulation strategy usually produces outcomes comparable with a rhythm-control strategy. Our prophylactic regimen begins with metoprolol 12.5 to 25 mg PO qid and is titrated upward as tolerated.

1. Initial assessment. The management of atrial fibrillation should be guided by the answers to the following three questions:
   1. Is the patient symptomatic? Atrial fibrillation generally is well tolerated, and overly aggressive management can cause significant morbidity. Nonetheless, the first step in the management of atrial fibrillation is an assessment of its hemodynamic significance. Significant symptoms may respond to rate control alone or may require chemical or electrical cardioversion. Evidence of compromise includes hypotension, changes in mental status, decreased urine output, impaired peripheral perfusion, anginal symptoms, and decreased cardiac output or increased filling pressures.
      
   2. What are the precipitating factors? Appropriate management of atrial fibrillation requires identification and treatment of potential risk factors. Atrial fibrillation can result from ischemia, atrial distension, increased sympathetic tone, electrolyte imbalances (particularly hypokalemia and hypomagnesemia precipitated by diuresis), acid-base disturbances, sympathomimetic medications (e.g., inotropes and bronchodilators), beta-blocker withdrawal, pneumonia, atelectasis, and pulmonary embolism.
      
   3. What are the goals of therapy? Hemodynamic stability is the primary goal. For most patients, rate control is sufficient because 90% of patients with new-onset atrial fibrillation following cardiac surgery will be in normal sinus rhythm in 6 weeks. Evidence of hemodynamic compromise or interference with recovery should prompt chemical or electrical cardioversion.
      
   
   
2. Drug therapy. Agents can be divided conveniently into rate-control and rhythm-control agents, although beta blockers are also effective in converting atrial fibrillation postoperatively. Monodrug therapy generally is better than polydrug therapy.
   1. Rate-control agents:
      1. Beta blockers. Metoprolol should be first-line therapy in most patients and can be given orally or intravenously. Metoprolol should be titrated to effect with a heart rate goal of less than 100 beats per minute at rest. The suggested treatment for new-onset atrial fibrillation is 50 mg PO, followed by 25 mg PO until normal sinus rhytum (NSR) or adequate rate control is achieved, up to eight doses. Some patients may require over 400 mg/d.
         
      2. Calcium channel blockers. Diltiazem is the agent of choice. It should be initiated as a bolus at 0.25 mg/kg IV, followed by 0.35 mg/kg IV, followed by a continuous infusion of 5 to 15 mg.
         
      3. Digoxin can be considered in patients with contraindications to beta blockers, in particular those with poor ejection fraction. There is some evidence that it increases atrial automaticity. It has a half-life of 38 to 48 hours in patients with normal renal function, significant potential toxicity, and a narrow therapeutic range. Levels must be monitored, particularly in patients with renal insufficiency. Many agents, including amiodarone, increase its serum level. Following chemical cardioversion, attempts should be made to minimize the number of rate-control agents used.
         
      
      
   2. Antiarrythmics:
      1. Metoprolol (diltiazem).
         
      2. Ibutilide. Ibutilide is given as a 1-mg intravenous bolus and repeated once if cardioversion fails to occur. Patients need to be monitored for a small but significant incidence of torsades de pointes that may be increased if given in conjunction with amiodarone.
         
      3. Amiodarone can cause myocardial depression and heart block; significant hypotension is associated most commonly with rapid bolus infusion. Significant toxicity can be associated with both short-term and prolonged use of amiodarone.
         
      4. Adenosine is helpful in the treatment of supraventricular tachycardia (SVT). (It should be avoided in transplant recipients, partially revascularized patients, and patients with atrial flutter.)
         
      
      
   
   
3. Electrical cardioversion. Electrical cardioversion should be used emergently for the treatment of hemodynamically unstable atrial fibrillation, starting at 200 J (synchronous). Sedation should be used. In patients with atrial wires who are in atrial flutter, overdrive pacing can be attempted.
   
4. Anticoagulation. Patients who remain in atrial fibrillation for more than 24 hours or have multiple sustained episodes over this period should be started on coumadin in the absence of contraindications. Heparin (intravenously, or low-molecular-weight heparin subcutaneously) should be considered after 48 hours in patients with a history of stroke or transient ischemic attacks (TIAs) or who have a low ejection fraction. Coumadin should not be initiated in patients who may require permanent pacer placement.
   

View larger version (38K): [in this window] [in a new window]   Figure 16-1 Postoperative atrial fibrillation guidelines. (Adapted from Maisel WH, Rawn JD, Stevenson WG: Atrial fibrillation after cardiac surgery. Ann Intern Med 2001; 135:1061.)

Postoperative ischemia and infarction can be caused by inadequate intraoperative myocardial protection; kinked, spasmed, or thrombosed conduits; thrombosed endarterectomized vessels; or embolization by air or atherosclerotic debris. It should be suspected in the presence of otherwise unexplained poor pump function, ST changes, new bundle-branch block or complete heart block, ventricular arrhythmias, or enzyme elevation. Electrocardiographic changes should be correlated with the anatomy of known atherosclerotic or revascularized territories. Air embolism preferentially involves the right coronary artery, and inferior ST-segment changes generally are present in the operating room. It typically resolves within hours. It is worth noting that nonspecific ST-segment changes are common postoperatively and usually benign. Pericarditic changes generally are characterized by diffuse concave ST-segment elevations, accompanied by a pericardial rub and delayed in onset by at least 12 hours following surgery.

New wall motion abnormalities or mitral regurgitation diagnosed echocardiographically can help to determine the hemodynamic significance of suspected ischemia or infarction. Knowledge of the quality of conduits, anastomoses, and target vessels is critical in planning management strategy (e.g., there may be little to be gained and much to lose in attempting to improve flow to a small, highly diseased posterior descending artery with poor runoff). If there appears to be significant myocardium at risk, on the other hand, a timely trip to the operating room or the cardiac catheterization laboratory can improve outcomes dramatically. Ongoing ischemia should prompt consideration of standard strategies, including anticoagulation, beta blockade, and nitroglycerin as tolerated. Intra-aortic balloon placement should be considered to minimize inotrope requirements, decrease myocardial oxygen requirements, and/or minimize infarct size.

Right Ventricular Failure and Pulmonary Hypertension

Right ventricular failure can be a particularly difficult postoperative problem. It can be caused by perioperative ischemia or infarction or by acute increases in pulmonary vascular resistance (PVR). Preexisting pulmonary hypertension is caused commonly by left-sided heart failure, aortic stenosis, mitral valve disease, and pulmonary disease. Chronic pulmonary hypertension is characterized by abnormal increased vasoconstriction and vascular remodeling.¹⁴ Acute increases in PVR are caused commonly by acute left ventricular dysfunction, mitral valve insufficiency or stenosis, volume overload, pulmonary edema, atelectasis, hypoxia, or acidosis. Pulmonary embolism also should be considered, but it is rare in the immediate postoperative period. As the right side of the heart fails, it becomes distended, central venous pressure increases, tricuspid regurgitation may develop, and pulmonary artery pressures and left-sided filling pressures become inadequate. Strategies for reversing this potentially fatal process begin with identifying potentially reversible etiologies. Volume status and left-sided function should be optimized. The right ventricle has its own Starling curve, and while the failing right ventricle often needs more volume to ensure adequate left-sided filling, overdistension will worsen function. Judicious use of positive end-expiratory pressure (PEEP) to recruit atelectatic lung and hyperventilation can decrease the impact of pulmonary vasoconstriction mediated by hypoxia and hypercarbia. Use of intravenous vasodilators [commonly, nitroprusside, nitroglycerin, tolazoline (PGI₂), hydralazine, prostacyclin, adenosine, and nicardipine] to reduce PVR frequently is limited by systemic hypotension. Inotropes (typically milrinone, which also provides vasodilatation) can be beneficial.¹⁵ Since no intravenous vasodilator is selective for the pulmonary vasculature, topical administration can be significantly more effective in reducing PVR without causing systemic hypotension. Inhaled nitric oxide (NO) and PGI₂ have comparable efficacy. They also can improve oxygenation by shunting blood to ventilated lung.

Valvular Disease: Special Postoperative Considerations

Aortic valve replacement

The different pathophysiologies associated with aortic stenosis (primarily a pressure-overload phenomenon) versus aortic insufficiency (volume overload) can result in significantly different postoperative courses.

AORTIC STENOSIS: Aortic stenosis can lead to the development of a hypertrophied, noncompliant left ventricle. For some patients, replacement of a stenotic valve allows a ventricle conditioned to pumping against abnormally high afterload to easily achieve supranormal levels of cardiac output and blood pressure postoperatively. Meticulous blood pressure control frequently is required to avoid disrupting fresh suture lines. In some patients, the degree of ventricular hypertrophy can lead to dynamic outflow obstruction; the condition is treated most effectively with volume, beta blockers, and afterload augmentation. Even without dynamic outflow obstruction, reduced compliance (diastolic dysfunction) can create significant hemodynamic compromise if the patient becomes hypovolemic or loses normal sinus rhythm. (Up to 30% of stroke volume can be dependent on synchrony between atria and ventricle.) The placement of atrial wires in addition to ventricular wires can provide significant advantages in the event that the patient is bradycardic or experiences heart block postoperatively.

AORTIC REGURGITATION: The left ventricle in a patient with aortic regurgitation frequently is dilated without significant hypertrophy and often functions poorly postoperatively. Optimization of volume, afterload, inotropy, and rhythm in these patients often is challenging.

Mitral valve repair/replacement

MITRAL REGURGITATION: Following repair or replacement of an incompetent mitral valve, increased afterload and consequent greater wall stress unmask left ventricular dysfunction. Frequently, inotropic support and systemic vasodilatation are required to reduce the afterload mismatch seen following surgery.¹⁶ Occasionally, left ventricular dysfunction can be the result of inadvertent suture placement over the circumflex coronary artery.

MITRAL STENOSIS: Unlike patients with mitral regurgitation, patients with mitral stenosis typically have preserved left ventricular function. Exacerbation of preexisting pulmonary hypertension is common, however. Postoperative strategies focus on optimizing right ventricular function and decreasing pulmonary vascular resistance.

	BLEEDING, THROMBOSIS, AND TRANSFUSION STRATEGIES

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One of the principal challenges of cardiac surgery is to achieve sufficient anticoagulation while the patient is supported on CPB without experiencing excessive bleeding postoperatively. Not surprisingly, patients undergoing off-pump CABG experience a significant reduction in postoperative bleeding and blood product transfusion requirements.^17,18 Excessive bleeding and its complications, including blood product transfusions, cause significant morbidity and mortality.

Preoperative Evaluation

Preoperative evaluation includes documenting a history of abnormal bleeding or thrombosis and obtaining basic coagulation studies, a hematocrit, and a platelet count. A history of recent heparin exposure associated with thrombocytopenia should suggest a diagnosis of heparin-induced thrombocytopenia (HIT). Confirmation of the presence of IgG directed against platelet factor 4 (the prevalence of these antibodies in patients with previous heparin exposure can be up to 35%¹⁹) requires either a delay in surgery until the assay is negative (usually 3 months) or, if surgery is urgently required, an alternative anticoagulation strategy. Recent experience with the direct thrombin inhibitor bivalirudin appears promising in this scenario.

Preoperative medications that can increase bleeding risk are common. Aspirin inhibits cyclooxygenase, reduces the synthesis of thromboxane A₂ (TXA₂), and decreases platelet aggregation.²⁰ Preoperative aspirin use modestly increases postoperative bleeding,^21,22 but preoperative and early postoperative use (i.e., within 6 hours) is beneficial to outcome and ultimate survival.²³ Other antiplatelet agents have more profound impacts on platelet function. The glycoprotein IIb/IIIa inhibitors eptifibitatide (Integrillin) and tirofiban (Aggrastat) are sufficiently short acting that surgery can be conducted safely despite recent exposure. Abciximab (Reopro) usually requires a 24- to 48-hour delay of surgery, if feasible, to avoid catastrophic bleeding.²⁴ Clopidogrel (Plavix) is a thienopyridine derivative that blocks platelet ADP P₂Y₁₂ receptors, inhibiting platelet activation by preventing ADP-mediated responses, decreasing alpha-granule release, and lowering TXA₂ and P-selectin expression with some anti-inflammatory effects.²⁵ Cessation of clopidogrel is preferred 5 days preoperatively but is not advisable in patients with drug-eluting coronary artery stents. Customarily, coumadin (which inhibits the vitamin K–dependent clotting factors II, VII, IX, and X) is discontinued 4 to 7 days preoperatively to allow gradual correction of the international normalization ratio (INR).

Intraoperative Strategies

Multiple intraoperative strategies have evolved to prevent unnecessary bleeding during blood product transfusion. Antithrombolytics -aminocaproic acid (Amicar) and tranexamic acid (Cyclokapron) inhibit plasminogen activation and limit fibrinolysis. Topical use of tranexamic acid intraoperatively prior to closure²⁶ may be a simple and effective way to reduce postoperative bleeding, particularly in patients with friable tissue who are having reoperations or have had previous exposure to chest irradiation. Aprotinin (Trasylol), a serine protease inhibitor, activates factor XII (Hageman factor), has antifibrinolytic properties (main hemostatic effect), and protects platelets. The drug is used primarily for patients who are at high risk for postoperative bleeding. A recent retrospective study has questioned aprotinin’s safety.²⁷

Retrograde autologous priming of the CPB circuit involves displacing circuit prime solution at the initiation of CPB with the patient’s blood draining both antegrade through the venous cannula and retrograde through the arterial cannula.²⁸ This strategy has been shown to decrease the requirement for blood transfusion significantly following CABG. The use of heparin-bonded circuitry has enabled the safe use of lower anticoagulation targets while on bypass. Careful attention to hemostasis intraoperatively and avoidance of excessive use of a blood salvage device (e.g, cell saver®) (which depletes platelets and clotting factors) pays dividends postoperatively.

Postoperative Bleeding

Strategies for avoiding postoperative hypothermia are also very important. Hypothermia (35°C) on arrival to the ICU is associated with delayed extubation,²⁹ shivering and increased peripheral O₂ consumption,³⁰ hemodynamic instability, atrial and ventricular arrhythmias, and increased systemic vascular resistance and coagulopathy.^31,32

Most patients are mildly coagulopathic postoperatively, but only a minority bleed excessively. Postoperative coagulopathy can be due to residual or rebound heparin effects following CPB, thrombocytopenia (qualitative and quantitative), clotting factor depletion, hypothermia, and hemodilution. Chest tube outputs persistently greater than 50 to 100 mL/h or other clinical evidence of bleeding demand attention.

The treatment of postoperative bleeding depends initially on making a judgment: Is bleeding surgical, coagulopathic, or both? Surgical bleeding is treated as soon as possible by reexploration; coagulopathies are corrected in the ICU. Coagulopathic patients rarely have significant clot formation in their chest tubes. Standard maneuvers include warming the patient, controlling blood pressure, extra PEEP, additional -aminocaproic acid, calcium gluconate, and blood products. In general, blood products should not be used to correct coagulation abnormalities unless the patient is bleeding significantly. All allogeneic blood products can contribute to transfusion-related lung injury and have other adverse effects. Protamine is indicated rarely and can increase bleeding. Desmopressin (DDAVP) is a synthetic vasopressin analogue that acts by increasing the concentration of von Willebrand factor, an important mediator of platelet adhesion. It is of benefit in patients with von Willebrand’s disease and in patients with severe platelet dysfunction secondary to uremia anitplatelet agents.³³

Recombinant factor VIIa (rFVIIa) is a drug approved for use in hemophiliacs that has been used successfully in arresting bleeding in patients with life-threatening hemorrhage after cardiac surgery. On combination with tissue factor, it activates the extrinsic coagulation system via factor X, resulting in thrombin generation and prompt correction of the prothrombin time (PT) with no evidence of systemic thrombosis.^34–36

Mediastinal Reexploration

Reexploration should be considered when CT outputs are greater than 400 mL/h for 1 hour, greater than 300 mL/h for 2 to 3 hours, and 200 mL/h for 4 hours³⁷ (see Table 16-2) or if signs of tamponade or hemodynamic instability develop. Tamponade should be considered in the presence of hypotension, tachycardia, elevated filling pressures, increasing inotrope requirements, pulsus paradoxus, and/or equalization of right and left atrial pressures.³⁸ An echocardiogram can be useful in this situation but cannot rule out tamponade. Chest x-rays are a necessary element of the evaluation for bleeding; look for a widening mediastinum or evidence of a hemothorax. Chest x-rays should be repeated on all patients with initial high chest tube output that later sub-sides to ensure that chest tubes have not clotted.

Autotransfusion

Autotransfusion of shed mediastinal blood remains controversial.³⁹ Red blood cell viability in unwashed shed mediastinal blood is comparable with that of autologous whole blood⁴⁰; additionally, there is evidence indicating no apparent clinical coagulopathy (e.g., low fibrinogen levels but normal coagulation times at 1 and 24 hours) following reinfusion of shed blood.^41–43 This method of blood salvage is without allogeneic transfusion risks and possibly is immunostimulatory.

Blood Transfusions

Despite meticulous preoperative planning, correcting drug-induced coagulopathies, and employing intraoperative "cell saving" techniques with "bloodless" fields, bleeding is inevitable postoperatively. The adverse effects of blood transfusions are well defined. The benefits are not. There is considerable evidence to suggest that blood transfusion increases the risk of postoperative infection and mortality following cardiac surgery.⁴⁴ The Canadian Critical Care Trials group in a randomized trial restricted transfusion for hemoglobin to less than 7.0 g/dL versus 10.8 g/dL, with no change in mortality rate.⁴⁵ These findings are consistent which are NIH consensus recommendation. A National Institutes of Health (NIH) consensus conference concluded that patients with a hemoglobin level of greater than 10.9 g/dL do not require blood, whereas those with less than 7.0 g/dL hemoglobin benefited from blood.⁴⁶ Tissue perfusion depends on cardiac output and hemoglobin level. A marginal MVO₂ or evidence of ischemia provides a rationale for increasing hematocrit.

Immunomodulation

It has become evident that blood transfusions have immunomodulating effects (by either alloimmunization or tolerance induction) that may increase the risk of nosocomial infections, transfusion-associated graft-versus-host disease (TAGVHD), transfusion-related lung injury (TRALI), cancer recurrence, and the possible development of autoimmune diseases later in life.⁴⁷ Furthermore, the risk of "newer" transfusion-transmitted diseases has become recognized. Proinflammatory mediators and cytokines have been associated with an increased risk of wound infection, sepsis, and pulmonary and renal insufficiency.⁴⁸

	RESPIRATORY CARE

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Postoperative Pulmonary Pathophysiology

Following the introduction of CPB nearly 50 years ago, pulmonary complications were recognized and attributed to pulmonary vascular overload.⁴⁹ Pump lung is pulmonary dysfunction secondary to an inflammatory response provoked by the bypass circuit. Increases are seen in the alveolar-arterial (A-a) gradient, pulmonary shunt fraction, and pulmonary edema, with a resulting decrease in compliance. Many inflammatory mediators have been implicated. Complement is activated (e.g., C3a and C5b–C9) and can damage pulmonary endothelium directly, as well as sequester neutrophils. When activated, these neutrophils release oxygen free radicals and proteases, furthering injury. Macrophage cytokine production and platelet degranulation also have been demonstrated in models of bypass-induced lung injury.^50,51 Transfusion-related lung injury also may exacerbate lung dysfunction.

Despite increased knowledge of the mechanisms of injury, to date, there have been no interventions with clear clinical benefit. To the contrary, administration of methyl-prednisolone in a randomized, double-blind study significantly increased A-a gradient and shunt fraction, decreased both static and dynamic compliance, and delayed early extubation in a dose-dependent manner.

Assessment on Arrival

On arrival to the ICU, auscultation of the lungs should be performed to ensure equal breath sounds and the absence of bronchospasm. Ventilator settings usually are a mandatory mode such as synchronized intermittent mandatory ventilation (SIMV) or assist-control (AC) with an FIO₂ of 100%, a rate of 12 to 18 breaths per minute, a tidal volume (TV) of 6 to 10 mL/kg, PEEP of 5 cm H₂O, and pressure support (PS) of 8 to 10 cm H₂O if on intermittent mandatory ventilation (IMV). A review of the initial postoperative chest x-ray (CXR) confirms proper endotracheal tube position 2 to 3 cm above the carina and proper nasogastric tube and intravenous line placement. Clinicians should be alert for pneumothoraces, hemothoraces, and a widened mediastinum. Arterial blood gas analysis should confirm adequate oxygenation and the absence of hypercapnea and metabolic acidosis. Arterial blood gas results should be correlated with pulse oximetry and minute ventilation.

Troubleshooting Hypoxia

As discussed earlier, oxygenation in all patients will be diminished compared with baseline. The inability to wean FIO₂ below 50% within the first few postoperative hours, however, should prompt a reevaluation because many causes can be treated. Sometimes simply replacing the pulse oximeter probe onto another finger or an earlobe will improve the reported oxygen saturation. This is particularly true in patients with peripheral vasoconstriction, and arterial blood gas analyses may be necessary for correlation. The use of vasodilators including nitroglycerin, milrinone, and particularly sodium nitroprusside can increase shunt fraction (by antagonizing hypoxic pulmonary vasoconstriction) enough to require a high FIO₂ to maintain adequate oxygenation. Increasing PEEP to improve alveolar recruitment may help,⁵² or changing agents may be necessary. Nebulizer treatments may be necessary for bronchospasm, and repeat CXR may demonstrate pneumothorax, hemothorax, mediastinal hematoma, atelectasis, or a new infiltrate representing aspiration.

Atelectasis, particularly in the left lower lobe, is present to some degree in nearly all patients. Bibasilar atelectasis is believed to be the combined product of prolonged supine position and intraoperative muscle relaxation allowing upward displacement of abdominal contents and the diaphragm. This reduces functional reserve capacity (FRC) by up to 1 L.⁵³ On the left, this is compounded by pleurotomy for internal mammary artery (IMA) takedown, compression of the left lung, and decreased ventilatory tidal volumes to clear the field for IMA dissection. Left lower lobar atelectasis owing to phrenic nerve injury is not likely to resolve acutely with bronchoscopic aspiration. Lobar atelectasis in general, however, especially when associated with mucus plugging, is improved by bronchoscopic aspiration in approximately 80% of patients.⁵⁴ A prospective study comparing bronchoscopy with aggressive chest physiotherapy found the two techniques to be equally effective,⁵⁵ but only if the chest physiotherapy regimen is adhered to.⁵⁶

Sedation

Sedation and pain relief in cardiac surgery "fast tracking" rely on short-acting agents, including propofol, fentanyl, and midazolam. Dexmedetomidine is a highly selective alpha₂-adrenoreceptor agonist that has anxiolytic, sympatholytic, and analgesic effects without contributing to respiratory depression, oversedation, or delirium. It may provide myocardial protection.⁵⁷ Hypotension and bradycardia can occur.

Early Extubation

Stable patients with a normal mental status often can be extubated either in the operating room or within a few hours following arrival in the ICU. Once an arterial blood gas analysis has confirmed adequate oxygenation and ventilation, pulse oximetry and monitoring of minute ventilation can guide extubation, often without the need for subsequent blood gas determinations.

Patients usually excluded from planning for early extubation include those with (1) preoperative pulmonary failure requiring intubation, (2) uncompensated congestive heart failure with pulmonary edema, (3) severe pulmonary hypertension or right-sided heart failure requiring hyperventilation or nitric oxide, (4) cardiogenic shock (including a requirement for intra-aortic balloon counterpulsion), (5) deep hypothermic circulatory arrest, (6) persistent hypothermia (<35.5(C), (7) persistent hypoxia (PaO₂:FIO₂ < 200), (8) persistent acidosis (pH less than 7.30), (9) persistent mediastinal bleeding, or (10) a cerebrovascular accident or reduced mental status (inability to follow commands or protect airway).

Ventilator Weaning and Extubation

For patients unable to wean from the ventilator immediately following surgery, a spontaneous breathing trial (30 minutes of spontaneous breathing with 5 cm H₂O of pressure support or unassisted breathing through a T-tube) has been shown to be the most accurate predictor of successful extubation. Breathing trials typically are discontinued for such signs of distress as respiratory frequency more than 35 breaths per minute, O₂ saturation less than 90%, heart rate greater than 140 beats per minute, systolic blood pressure greater than 180 mm Hg or less than 90 mm Hg, agitation, diaphoresis, or anxiety.^58,59 Yang et al. introduced the concept of a rapid-shallow breathing index (RSBI, f/VT, breaths per minute per liter). In their study of medical patients, the RSBI was calculated over 1 minute of unassisted spontaneous breathing through a T-tube. An RSBI of greater than 105 indicated a 95% likelihood that a subsequent weaning trial would not lead to successful extubation, and an RSBI of less than 105 indicated an 80% likelihood of subsequent success. The minute ventilation V_E and Mean Inspiratory Pressure (MIP) were significantly less predictive.

The strategy of daily or intermittent spontaneous breathing trials (SBTs) also was compared directly with weaning strategies based on stepwise reduction of the frequency of intermittent mandatory ventilation (IMV) or stepwise reduction of the level of pressure-support ventilation (PSV). Daily or intermittent SBTs lead to successful extubation two to three times earlier than either IMV or PSV weaning.⁵⁸

In a prospective series of ICU patients,⁶⁰ the 20% false-positive predictive value of an RSBI of less than 105 is overwhelmingly due to newly acquired problems, with only 7% of failures being referable to the process that initially required intubation. No direct study of the outcome of these strategies exists in the cardiac surgery population, but they are in broad clinical use, and we recommend at least daily SBTs, as quided by the SBI.

The decision to extubate must take into account the combined factors of mechanics, as described earlier, as well as an estimation of the patient’s ability to manage secretions and protect his or her airway.⁶¹

Extubation Failure

Overall, approximately 5% of cardiothoracic patients require reintubation.^62,63 Patients with chronic obstructive pulmonary disease (COPD) have a 14% incidence,⁶⁴ whereas those with a past history of stroke have a 10% incidence.⁶⁵ Other risk factors include New York Heart Association (NYHA) class IV functional status, renal failure, need for intra-aortic balloon counterpulsion, reduced PaO₂:FIO₂, reduced vital capacity, longer operating room time, a longer CPB run, and longer initial ventilatory requirement.⁶³ Unfortunately, in ICU patients overall, reintubation is an ominous predictor of increased length of stay and increased mortality.

Chronic Ventilation and Tracheotomy

In the early 1960s, translaryngeal intubation was associated with a prohibitively high rate of tracheal stenosis. As a result, a consensus existed that tracheotomy should be performed on patients requiring mechanical ventilation for longer than 3 days.⁶⁶ Low-pressure cuffs and soft tubes since have muddled this question of timing. A consensus subsequently evolved in that patients who continue to require mechanical ventilation at 2 weeks should undergo tracheotomy. Data surrounding this practice have been soft.⁶⁷ Several trials suggest earlier discontinuation of mechanical ventilation and reduced complications associated with earlier tracheotomy.^67,68 Causation is not clear, but compelling arguments for reduced dead space and airway resistance, as well as facilitated pulmonary toilet, are made in favor of early tracheotomy. Additionally, less sedation is required. It is also strongly suggested that clinician behavior is positively affected by the presence of a tracheostomy tube. That is, more aggressive attempts at weaning and discontinuation of mechanical support are made because reconnecting the ventilator is easy.⁶⁸

Percutaneous dilatational tracheotomy (PDT) performed in the ICU is becoming recognized increasingly as a safe procedure.⁶⁸ A recent randomized, prospective study of medical patients projected to require more than 14 days of mechanical ventilation⁶⁹ compared two groups: PDT within 48 hours and PDT within 14 to 16 days. One hundred and twenty patients were enrolled. In the early PDT group, there was a strongly significant reduction in duration of mechanical ventilation (7.6 ± 4.0 versus 17.4 ± 5.3 days; p < .001), incidence of pneumonia (5% versus 25%; p < .005), and mortality (31.7% versus 61.7 %; p < .005). There was no difference in incidence or severity of tracheal stenosis identified in-hospital and at 10 weeks. With hope and with increasing evidence, early tracheotomy will come to be viewed more widely as beneficial to patient recovery rather than as an admission of defeat.

Pleural Effusion

Accumulation of fluid in the pleural space is common after cardiac surgery, particularly on the left side, and usually resolves with time and diuresis. The specific cause often is unknown, but a combination of factors can contribute, including fluid overload, hypoalbuminemia, pericardial and pleural inflammation (i.e., postpericardiotomy syndrome), atelectasis, pneumonia, and pulmonary embolism. Pleural effusion can cause chest pain or heaviness, shortness of breath, and hypoxia. Symptomatic effusions should be tapped, and usually thoracentesis does not have to be repeated. Nonsteroidal anti-inflammatory agents are used to treat postpericardotomy syndrome. Occasionally, tube thoracostomy drainage may be necessary until resolution of the inciting process. In contrast, retained hemothorax should be evacuated to avoid delayed development of fibrothorax requiring decortication.

Pneumonia

Nosocomial pneumonias have high associated mortality, and the incidence of ventilator-associated pneumonia increases approximately 1% per day.⁷⁰ Clinical diagnosis involves identification of a new or progressive infiltrate on CXR, change in character of sputum, leukocytosis, and fever.^71,72 Expectorated sputum cultures are considered to be very inaccurate, and directed bronchosopic sampling is preferred. Proper bronchoalveolar lavage requires large volumes of irrigant (>100 mL) and is performed infrequently. More commonly, tracheobronchial aspiration is performed using several milliliters of normal saline. Gram stain containing 25 or more squamous epithelial cells per low-power field indicates oral contamination. More than 25 neutrophils per low-power field suggests infection. Quantitative culture of 10⁵ to 10⁶ colony-forming units per milliliter (i.e., "moderate to numerous" or "3 to 4+") is indicative of infection, whereas 10⁴ or fewer colony-forming units per milliliter (i.e., "rare to few" or "1 to 2+") is more suggestive of colonization. Gram-negative organisms are seen most commonly and should be the target of first-line empiric antibiotic coverage. Specific patient factors and culture results and sensitivities will further refine antibiotic therapy.⁷³

The important role of pulmonary toilet in both the prevention and the treatment of nosocomial pneumonias cannot be overemphasized. All patients should be encouraged to get out of bed and ambulate (even if attached to the ventilator), turn, cough, and deep breathe with chest physiotherapy and bronchodilators. Sterile in-line suctioning should be performed in ventilated patients to aid in secretion clearance. Nasotracheal suctioning is extremely effective in unintubated patients in that the procedure stimulates very strong coughing and secretion clearance. Therapeutic fiberoptic bronchoscopy also can be performed.

Pulmonary Embolism

Deep venous thrombosis (DVT) and pulmonary thromboembolism (PE) are considered uncommon in the cardiac surgery population.⁷⁴ Reported incidence of PE ranges from 0.5 to 3.5%, accounting for only 0.3 to 1.7% of perioperative deaths. This is believed to be due to large intraoperative doses of heparin, both a quantitative and qualitative thrombocytopenia after CPB, and increased use of antiplatelet agents and anticoagulants, as well as early ambulation. A recent autopsy study⁷⁵ demonstrated a 52% incidence of DVT, that 20% of deceased patients have minor PE, and that PE is identified as the cause of death in 7%. Unfortunately, risks of bleeding and heparin-induced thrombocytopenia make the choice of heparin DVT prophylaxis problematic. Intermittent pneumatic compression devices are effective if patients and staff are compliant with their use.

The diagnosis of PE requires a high index of suspicion and should be considered in any patient who postoperatively acquires a newly increased PaO₂:FIO₂ gradient, shortness of breath, or reduced exercise tolerance, particularly in the setting of a clear or unchanged CXR. Diagnosis is fairly reliably obtained by PE-protocol thin-cut high-speed helical computed tomography of the chest,⁷⁶ although accuracy is still influenced by pretest probability.⁷⁷

	RENAL AND METABOLIC SUPPORT

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Perioperative Renal Dysfunction/Insufficiency

The new onset of renal dysfunction following cardiac surgery is correlated with significant morbidity and mortality. The incidence of acute renal failure (ARF) in CABG patients in the 1997 STS database was 3.14%, and 0.87% of these patients required dialysis.⁷⁸ Chertow⁷⁹ studied 43,642 Veterans Administration (VA) patients undergoing CABG or valve surgery. The overall risk of acute renal failure requiring dialysis was 1.1%. The mortality rate in this group was 63.7% versus 4.3% in patients without ARF. Decreased myocardial function and advanced atherosclerosis were independent risk factors for the development of dialysis-dependent renal failure.

Patients with preoperative renal dysfunction (serum creatine >1.5 mg/dL) have a higher incidence of stroke, bleeding complications, dialysis, prolonged mechanical ventilation, length of stay, and death.⁸⁰ Chertow found that preoperative renal function correlated with postoperative renal failure. The risk of ARF was 0.5, 0.8, 1.8, and 4.9% with baseline serum creatinine concentrations of less than 1, 1.0 to 1.4, 1.5 to 1.9, and 2.0 to 2.9 mg/dL, respectively. Chronic dialysis patients undergoing cardiac surgery have an 11.4% operative mortality rate, a 73% complication rate, and 32% 5-year actuarial survival rate.⁸¹ Cardiac surgery following renal transplantation has an associated operative mortality rate of 8.8%.⁸²

Patients with recent or long-standing hypertension should undergo renal angiography at the time of catheterization to assess renal artery stenosis, which, if significant, can be treated preoperatively in hope of improving postoperative renal function. To optimize preoperative renal function, contrast loads should be minimized, and patients should be well hydrated and receive renoprotective agents (e.g., N-acetylcysteine).⁸³

Effects of CPB on Renal Function

Operative considerations include limiting the duration of CPB and maintaining mean arterial pressures at greater than 60 mm Hg.^84,85 Additional effects of CPB include trauma to the blood constituents, especially erythrocytes, with increased free hemoglobin levels and microparticle embolic insults to the kidneys. Hypothermia (during rewarming, vasodilatation and hyperemia of tissue beds result in third spacing of fluid), hemodilution (reduces viscosity of blood and plasma oncotic pressure), and ischemia-reperfusion injury can influence renal function; additionally, CPB leads to an increased release of catecholamines, hormones (e.g., rennin, aldosterone, angiotensin II, vasopressin, atrial natriuretic peptide, and urodilan⁸⁶), and inflammatory cytokines (e.g., kallikrein and bradykinin) that also affect renal function adversely. These adverse stimuli cause decreased renal blood flow, a decreased glomerular filtration rate (GFR), and an increase in renal vascular resistance. Hypotension and pressor agents accentuate this response. Ultrafiltration is used in long pump runs to decrease volume overload in patients with renal dysfunction.

Independent of preoperative renal function, the primary postoperative goal is the maintenance of adequate renal perfusion pressure and a urine output greater than the 0.5 mL/kg per hour. Brisk diuresis (>200 to 300 mL/h) is common following CPB. Volume replacement and maintenance of adequate blood pressure and cardiac output are required for adequate renal perfusion. The best measure of kidney perfusion is adequate urine output independent of diuretics. Beyond optimizing hemodynamics and avoiding nephrotoxic medications, there is no convincing evidence that treatment with diuretics, mannitol, dopamine, fenoldapam, nesiritide, or any other agent is renoprotective. This is not to say, however, that these agents are of no benefit in promoting diuresis and avoiding renal replacement therapies in the event of renal dysfunction.

Electrolyte Disturbances

Calcium

Levels of ionized calcium (normal 1.1 to 1.3 mmol/L) are critical for myocardial performance and are involved in reperfusion injury. Hypocalcemia causes a prolonged QT interval. Hypocalcemia is common following CPB or an episode of hemodilution, sepsis, or citrated blood transfusions. The concentration of calcium ion is greatest in the intracellular space, with small amounts in the extracellular fluid (ECF). Calcium levels bound to albumin change with the levels of serum albumin, whereas ionized levels remain unchanged.⁸⁷

Potassium

Potassium fluxes during cardiac surgery can be significant and may affect cardiac automaticity and conduction. Cardioplegia, decreased urine output, decreased insulin levels, and red blood cell (RBC) hemolysis all contribute to hyperkalemia.⁸⁸ Brisk diuresis, insulin, and alkalosis can cause hypokalemia.⁸⁹ Aggressive treatment of hypokalemia decreases the incidence of perioperative arrhythmias. Serum potassium levels and replacement protocols are an integral part of the early postoperative management. Serum potassium rises logarithmically with replacement; larger quantities are required to treat significant hypokalemia.

Magnesium

Magnesium (normal 1.5 to 2 mEq/L) is the second most common intracellular cation after potassium. It is involved in endothelial cell homeostasis,⁹⁰ cardiac excitability, and muscle contraction through its role as an ATP cofactor and calcium antagonist; it is also closely involved in the regulation of intracellular potassium.⁹¹ Following hemodilution and CPB, hypomagnesemia is common (>70% of patients) and is associated with an increased risk of atrial fibrillation and torsades de pointes.^92–94

Endocrine Dysfunction

Diabetes mellitus

Up to 30% of patients have diabetes (type I or II) in the cardiac surgery population. Following CPB, the hormonal stress response (i.e., increased growth hormone, catecholamines, and cortisol) causes hyperglycemia (even in nondiabetics) with a decrease in insulin production; this may persist for up to 24 hours postoperatively and is exacerbated by exogenous catecholamine administration. Tight control of blood glucose levels with continuous insulin infusions has been shown to reduce the incidence of sternal wound infection by an order of magnitude.⁹⁵ Although a trial in critically ill ICU patients found a survival benefit in patients those blood sugars were kept below 110 mg/dL, only patients with an ICU length of stay greater than 3 days were shown to benefit, and hypoglycemia was shown to be an independent risk factor for mortality. It is not clear whether such aggressive control will benefit the majority of cardiac surgery patients. A recent study has shown an increase in stroke rate and mortality from intraoperative targets between 80 and 100 mg/dL.⁹⁶

Adrenal dysfunction

The stress of cardiac surgery activates the hypothalamic-pituitary-adrenal (HPA) axis and increases plasma adrenocorticotropic hormone (ACTH) and cortisol levels. Subclinical adrenal insufficiency is present in up to 20% of the elderly population and can be unmasked by the stress of surgery. Any patient taking exogenous steroids within 6 months of surgery should receive stress-dose steroids perioperatively. Any patient exhibiting prolonged, unexplained vasodilatory shock should be suspected of having adrenal insufficiency. In a stressed patient, a low or normal cortisol plasma level can be assumed to be associated with adrenal insufficiency. In a stressed patient, a low or normal plasma cortisol leval can be assumed to be associated with adrenal insufficiency. A cosyntropin stimulation test can also be performed for diagnosis. In the interim, dexamethasone may be administered intravenously without interfering with the test.

	RELEVANT POSTOPERATIVE COMPLICATIONS

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Neurologic

Central nervous system

The incidence of stroke following cardiac surgery is procedure-specific and varies between 1 and 4%. Ricotta and colleagues⁹⁷ showed that associated carotid stenosis (>50%), redo heart surgery, valve surgery, and prior stroke are associated with an increased postoperative risk of stroke. John and colleagues⁹⁸ reviewed 19,224 patients in New York State. The stroke rate was 1.4% following CABG, with a 24.8% mortality rate in that group. Multivariable logistic regression identified the following predictors: calcified aorta, prior stroke, age, carotid artery disease, duration of CPB, renal failure, peripheral vascular disease, smoking, and diabetes. Intraoperative factors that may cause postoperative neurologic deficits include particulate macroembolization of air, debris, or thrombus⁹⁹; microembolization of white blood cells, platelets, or fibrin¹⁰⁰;duration of CPB¹⁰¹; cerebral hypoperfusion during nonpulsatile CPB; and hypothermic circulatory arrest.¹⁰²

Up to 50% of cardiac surgery patients experience delirium, particularly those with preexisting organic mental disorders, significant prior alcohol consumption, advanced age, or intracranial cerebral artery disease.¹⁰⁷ Perioperative anesthetic and sedative administration are significant contributing factors. Causes of postoperative delirium in the cardiac intensive-care patient include sleep deprivation, renal failure, hepatic failure, and thyroid abnormalities. Electroencephalograms (EEGs) on these patients usually are abnormal, whereas in primary psychiatric diseases they are normal. Treatment involves correcting metabolic abnormalities, establishing a normal sleep-wake cycle, and minimizing medications likely to cause delirium.

Brachial plexus injury/peripheral nerve injury

Excessive sternal retraction during a median sternotomy may cause a brachial plexus injury because the first rib may impinge on the lower trunk and branches.^108,109 IMA harvesting also may cause damage to the brachial plexus.¹¹⁰ Malpositioning of the upper limbs during surgery may result in a neurapraxia owing to compression of the ulnar nerve.¹¹¹ Palsy or plegia of dorsiflexion and eversion of the foot can be caused by common peroneal nerve stretch or compression at the level of the head of the fibula.¹¹² Saphenous neuropathy (i.e., sensory changes on the medial side of the calf to the great toe) following open vein graft harvesting (less so with endoscopic harvest) is also a potential complication secondary to the avulsion of pretibial or infrapatellar branches of the nerve.¹¹³

Gastrointestinal

Mesenteric ischemia following cardiac surgery is infrequent but usually catastrophic.^114,115 Risk factors include duration of bypass (i.e., hypoperfusion), use of pressor support (i.e., sympathetic vasoconstriction), use of the intra-aortic balloon pump (IABP) or other sources of atherosclerotic embolism, atrial fibrillation, peripheral vascular disease, and heparin-induced thrombocytopenia. Early surgical intervention (<6 hours) is associated with a 48% mortality rate, and this rises to 99% with delays (>6 hours) in surgical intervention. Gastrointestinal bleeding is common and can cause significant morbidity. The incidence of gastrointestinal bleeding can be reduced with the use of H₂ inhibitors, proton pump inhibitors, and sucralfate.¹¹⁶ Other pertinent complications affecting the gastrointestinal system include pancreatitis (hyperamylasemia, 35 to 65% leads to 0.4 to 3% with overt pancreatitis)^117,118,119 acute acalculous cholecystitis (2 to 15% of all acute cholecystitis patients,¹²⁰ likely owing to hypoperfusion, narcotics, or parenteral nutrition that promote biliary stasis¹²¹), swallowing dysfunction or oropharyngeal dysphasia secondary to tracheal intubation or perioperative use of transesophageal echocardiography),¹²² and small or large bowel ileus (i.e., Olgilvie’s syndrome is associated with long-term ventilation).¹²³ Preoperative liver dysfunction (noncardiac cirrhosis) is associated with a high incidence of postoperative morbidity and mortality (Child class A cirrhosis: 20% morbidity, 0% mortality; Child class B cirrhosis: 80% morbidity, 100% mortality).¹²⁴ Although 20% of patients develop a transient hyperbilirubinemia, fewer than 1% have significant hepatocellular damage that progresses to chronic hepatitis or liver failure.¹²⁵

Infections

Nosocomial infections

Between 10 and 20% of cardiac surgery patients develop a nosocomial infection. Infections may be related to the surgical wound, lung, urinary tract, invasive lines or devices, or the gastrointestinal tract. Prolonged mechanical ventilation is associated with nosocomial pneumonia. These are second only to urinary tract infection in frequency and carry the highest mortality rate.¹²⁶ Smokers and COPD patients are most likely to be colonized preoperatively and have a higher incidence of pneumonia (15.3% versus 3.6% in controls).¹²⁷

Catheter-related infections (i.e., bladder and vascular-related) are common in the ICU. The most common pathogens are Staphylococcus aureus (12%), coagulase-negative staphylococci (11%), Candida albicans (11%), Pseudomonas aeruginosa (10%), and Enterococcus spp.^128,129

Fever

Fevers are common in the ICU setting but are an insensitive indicator of postoperative bacteremia (3.2% incidence in 835 febrile CABG patients).¹³⁰ The yield of true-positive bacteremia ranges from 4 to 5%, with a contamination rate ranging from 32 to 47%.¹³¹ Noninfectious causes of fever relative to cardiac surgery include myocardial infarction, postpericardiotomy syndrome, and drug fever. Infectious causes include wound infection, urinary tract infection, pneumonia, catheter sepsis, and loculated areas of contaminated blood accumulation (e.g., pericardial, pleural, retroperitoneal, and leg wound spaces).

Sepsis/septic shock

Septic shock following cardiac surgery can have devastating consequences. Pathophysiologic features of sepsis include systemic inflammation, coagulation changes, impaired fibrinolysis, and subsequent target-organ failure, with overall multiorgan failure, irreversible shock, and death (20 to 50%).^132,133 Mixed venous oxygen saturation can be abnormally high secondary to shunting and a failure to extract oxygen at the cellular level. In vasodilatory shock, the maintenance of end-organ tissue perfusion is critical; treatment includes aggressive fluid management and vasopressin.^134–137 Methylene blue (which inhibits NO synthesis)¹³⁸ has been used successfully in refractory hypotension. Bernard and colleagues¹³⁹ for the PROW/ESS study group showed a distinct survival advantage in the treatment of severe sepsis using drotrecogin alfa (activated) or recombinant human activated protein C (Zigris). The mechanism of action is a modulation of the systemic inflammatory, procoagulant, and fibrinolytic reaction to infection. In a randomized study of 1690 patients, the mortality rate was 30.8% in the placebo group versus 24.7% in the treatment group.

Wounds

DELAYED STERNAL CLOSURE/STERNAL INFECTION: Complicated operations with persistent bleeding and hemodynamic instability (owing to tissue edema) may preclude primary sternal closure. Delayed sternal closure allows hemodynamic stabilization and diuresis.¹⁴⁰ Anderson and colleagues¹⁴¹ outlined the recent BWH experience; 1.7% (87 of 5177) open chests were managed with a hospital survival rate of 76%. Complications included deep sternal infection (n =4), stroke (n =8), and dialysis (n =13). Multivariate analysis revealed mechanical ventricular assistance and reoperation for bleeding as independent predictors of in-hospital mortality.

SUPERFICIAL AND DEEP STERNAL WOUNDS: Superficial and deep sternal wound infections are significant complications of cardiac surgery. Deep sternal infection with associated mediastinitis occurs in 1 to 2% of cardiac operations, with a resulting mortality rate approaching 10%.¹⁴² Common organisms are Staphylococcus epidermidis, Staphylococcus [including methicillin-resistant S. aureus (MRSA)], Corynebacterium, and enteric gram-negative bacilli.¹⁴³ Patients predisposed to sternal infections include those with significant comorbidities (e.g., obesity, diabetes, COPD, renal dysfunction, and low serum albumin), prolonged CPB, reoperations, diabetics with bilateral IMA harvests,^144,145 and patients with hyperglycemia.¹⁴⁶ Simple preoperative measures such as clipping of chest hair,¹⁴⁷ using Hibiclens washes,¹⁴⁸ administering adequate prophylactic antibiotics prior to skin incision, ensuring good intraoperative hemostasis without the use of bone wax,¹⁴⁹ and closure with subcuticular sutures and a topical adhesive (e.g., DERMABOND®) rather than skin staples are helpful; additionally, tight glucose control during surgery and in the days following surgery results in a significantly lower sternal wound infection rate.⁹⁵

Minor infections frequently respond to intravenous antibiotics, opening of the wound, and local wound care. Deeper infections require intravenous antibiotics (6 weeks); initial empirical therapy should consist of broad coverage against gram-positive cocci and gram-negative bacilli, with the regimen adjusted when cultures (i.e., blood or mediastinal or deep sternal wound drainage) have been speciated. The mainstay of treatment is surgical exploration and extensive débridement, which may require removal of the sternum with primary or secondary closure with muscle or an omental flap.¹⁵⁰ Postoperative vacuum-assisted closure (VAC)¹⁵¹ of mediastinal wounds improves wound healing and reduces hospital length of stay.¹⁵²

Nutrition

Preoperative debilitated or cachectic patients (i.e., more than 10% weight loss over 6 months) with albumin levels of less than 3.5 g/dL¹⁵³ are exceptionally prone to complications, such as infections, following surgery. There is no evidence to support a role for preoperative hyperalimentation.¹⁵⁴ Body mass index (a good nutritional index) of less than 15 kg/m² is associated with increased morbidity.¹⁵⁵ Postoperative patients have accelerated catabolic protein loss, usually requiring 25 to 40 kcal/kg per day. Advances in immunonutritional pharmacology (i.e., arginine, glutamine and n-3 fatty acids) in complex postoperative cardiac surgery patients may have a defined role in the future.^156–158