Assessment and optimization of hemodynamics are generally the principal focus of care after 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 EKG analysis to exclude ischemia and conduction abnormalities. The presence of a pulmonary artery catheter enables the measurement of pulmonary artery pressures, left-sided filling pressures (pulmonary capillary wedge pressure, PCWP), and mixed venous oxygen saturation (MVO2). Cardiac output, as well as pulmonary and systemic vascular resistances can also be calculated when a PA catheter is present. Cardiac output is determined using thermodilution or by using 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%, mean arterial pressure (MAP) greater than 65 mm Hg, and a cardiac index (CI) greater than 2 L/min/m2. Goals should be individualized. Patients with a history of hypertension or significant peripheral vascular disease will probably benefit from higher blood pressure; patients who are bleeding or 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 demonstrate a survival advantage.1
Table 16-1 Common Intensive Care Values and Formulae ||Download (.pdf)
Table 16-1 Common Intensive Care Values and Formulae
Failure to achieve adequate cardiac output and end-organ oxygen delivery can be caused by many, often codependent factors. These include volume status (preload), peripheral vascular tone (afterload), cardiac pump function, heart rate and rhythm, and blood oxygen–carrying capacity.
Volume status is readily determined 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 central venous pressure can be seen in volume overload, right heart failure, tricuspid and mitral regurgitation, pulmonary hypertension, cardiac tamponade, tension pneumothorax, and pulmonary embolism.) Pulmonary 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 directly measured) 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 optimum filling pressures is generally empiric where a wedge pressure of 15 mm Hg is generally 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 is often created by a systemic inflammatory response to cardiopulmonary bypass (CPB), and it is common to have a significant continuous 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 are often best treated with volume replacement.
Peripheral vascular tone needs to be sufficient to provide the patient with adequate blood pressure; excess vasoconstriction can increase the systemic vascular resistance tremendously, therefore creating dangerous levels of hypertension and decrease cardiac output. Decreased afterload can be caused, in part, by medications (sedative, anesthetic agents, and preoperative ACE inhibitors), increased temperature, and a systemic inflammatory response to cardiopulmonary bypass, whereas increases in afterload can be caused by medications, hypothermia, or increased sympathetic output (including pain and anxiety), or may be secondary to hypovolemia or pump failure.
Left ventricular pump function can be influenced by levels of exogenous or endogenous inotropes, postoperative stunning, ischemia or infarction, valve function, acidosis, electrolyte abnormalities, hypoxia, or cardiac tamponade. Bradycardia, arrhythmias, and conduction defects can also adversely affect cardiac output.
The oxygen-carrying capacity of blood is a function of hematocrit and oxygenation. A hematocrit of 23% and oxygen saturation greater than 92% is usually adequate for a stable postoperative patient.
It is important not to allow the 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 are usually more important than isolated values. Patients generally do well if they have warm, well-perfused extremities, a normal mental status and good urine output (greater than 0.5 cc/kg/min). Acute changes in hemodynamic status are common postoperatively, and vigilant monitoring enables care to be more preemptive than reactive.
As emphasized, the goal of postoperative hemodynamic management is the maintenance of adequate end-organ perfusion without taxing the heart unnecessarily. Assessment and optimization of intravascular volume status are generally 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 (eg, 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 are usually either bleeding or vasodilated. Calculation of CO and SVR can often help sort this out. In the case of significant vasodilation, judicious use of a pressor agent can help to decrease fluid requirements. Inotropic agents should not be administered for the treatment of hypovolemia. Fluid requirements can often be reduced after 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 when compared with crystalloid solutions. After 1 hour, 80% of 1000 cc of 5% albumin solution is retained intravascularly. In situations characterized by loss of vascular endothelial integrity (ie, after CPB), albumin may redistribute into the interstitial space and increase third space fluid accumulation. One study has shown that the accumulation of extravascular pulmonary water is unaffected by the prime type or the type of fluid administered postoperatively.2 The largest prospective randomized controlled study comparing colloid with crystalloid has been unable to demonstrate a difference in outcomes.3 Albumin and hetastarch provide comparable hemodynamic benefits, although hetastarch should be avoided in bleeding or coagulopathic patients or in those with renal impairment.
Although unusual in the immediate postoperative period, volume overload is a common problem in the days after 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 frequently required in patients with impaired pump function before or after surgery, or in those who received large volumes of fluid perioperatively. Patients with impaired renal function may require renal replacement therapy (ultrafiltration, continuous veno-venous hemofiltration, or hemodialysis) to become euvolemic. Rapid diuresis accompanied by inadequate electrolyte repletion is frequently arrhythmogenic.
Medications are used perioperatively to provide vasoconstriction, venous and arterial vasodilation, inotropic support, and treatment of arrhythmias. As summarized in Table 16-2, many of the medications commonly used have multiple actions. Selection of appropriate agents depends on accurate hemodynamic assessment.
Table 16-2 Common ICU Scenarios and Management Strategies ||Download (.pdf)
Table 16-2 Common ICU Scenarios and Management Strategies
|Cardiac output syndromes|
|NASPE/BPEG Pacemaker Identification Codes100|
|Chamber paced||Chamber sensed||Response to sensing||Programmable functions||Antitachyarrhythmia functions|
|D—dual (pacer and shock)|
|S—single chamber||S—single chamber||—||O—none||—|
|Postoperative Mediastinal Bleeding|
|<50 cc/h Stable BP, coagulopathy||Post-CPB||Observation|
Acute hypotension (MAP<50 mm Hg)
Diffuse bloody ooze
1. High PTT, PT
2. INR >1.4
3. Low fibrinogen
4. Platelets <105/μL
5. Platelets >105/μL
6. Bleeding >10 min
7. Bleeding >30 min (High d-dimers, evidence of fibrinolysis)
Hypothermia (see above)
Rebound heparin effect
Deficient clotting factors
Deficient clotting factors
Fluid resuscitation (aim MAP 60–65 mm Hg)
PEEP trial (5–10 cm H2O),
Heparin level; protamine
Tranexamic acid, ε-aminocaproic acid, aprotinin
>200 cc/h for 4 h
>300 cc/h for 2–3 h
>400 cc/h for 1 h
|Surgical bleeding||Surgical reexploration|
Pressors are indicated for vasodilated patients who have normal pump function and are unresponsive to volume. These agents include alpha agents (neosynephrine) and vasopressin. Methylene blue has demonstrated efficacy in vasopressor-resistant hypotension. Pressors can contribute to peripheral ischemia and vasospasm of coronary arteries and arterial conduits. Careful monitoring of extremity perfusion and electrocardiographic changes is required when using these agents.
Vasodilators are indicated for hypertensive patients and for patients who are normotensive with poor pump function. Nitroglycerin and sodium nitroprusside are commonly used 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, but patients can quickly become tachyphylactic. Prolonged nitroprusside use can lead to cyanide toxicity, and methemaglobin levels must be monitored. Nicardipine is a calcium channel blocker with minimal effects on contractility or 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 can also 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. Labetolol 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 (dobutamine) and cyclic nucleotide phosphodiesterase inhibitors (milrinone). Both of 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. 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. Because perioperative beta-blockade has been shown to improve mortality and morbidity after cardiac surgery, it seems reasonable to avoid the gratuitous use of inotropes, and efforts should be made to rapidly wean these agents 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 is frequently an effective way to improve hemodynamic status.
Within normal rate ranges, cardiac output increases linearly with heart rate, and pacing is often very helpful (see Table 16-2). However, it is important to carefully monitor the response to pacing. For example, sinus bradycardia is often more effective than ventricular pacing at a more normal rate. Ventricular pacing can cause ventricular dysfunction and dys-synchrony, 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 adversely affect cardiac performance by decreasing filling time or inducing ischemia. Internal pacemakers can often be reprogrammed to improve output.
Heart block can occur after aortic, mitral, and tricuspid valve surgery. It is also associated with inferior myocardial infarction and can be secondary to medications (eg, digoxin, amiodarone, calcium channel blockers, and beta blockers). If a bi-atrial trans-septal approach to the mitral valve is employed, the sinus rhythm is can be lost owing to the division of the sinoatrial node.4 Heart block is frequently transient. If the ventricular escape rate is absent or insufficient, pacing wire thresholds need to be carefully monitored and backup pacing methods employed (by transvenous wire or pacing pulmonary artery catheter, external pacing pads) if needed while waiting for placement of a permanent pacemaker.
Nonsustained ventricular tachycardia (VT) is common after 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 (coronary angiography is necessary), electrolytes should be replaced, and inotropes 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
The incidence of postoperative atrial fibrillation (POAF) after cardiothoracic surgery is 30 to 50%,5 and has been shown to be higher in the elderly (age ≥ 75 years), renally impaired and COPD patients.6 This is associated with an increased risk of stroke, longer hospitalization, higher cost, and greater risk of long-term mortality.7
The incidence of POAF is 20 to 40% in CABG patients, but it is generally even more common in those undergoing valve and combined procedures. POAF is typically a transient reversible phenomenon that may develop in patients who possess an electrophysiologic substrate for the arrhythmia that is present before or as a result of surgery. Numerous studies support the efficacy of beta blockers in POAF prevention; they are currently the most common medication used in POAF prophylaxis. Therefore, beta blockers should be started or resumed as soon as they can be safely tolerated after cardiac surgery. Inotropic support, hemodynamic compromise, COPD, and AV block (PR interval greater than 0.24 millisecond, 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 also confer benefits other than atrial fibrillation prophylaxis, are easy to titrate, and do not have the toxicities associated with amiodarone. Although beta blockers and amiodarone are known to reduce the incidence of postoperative AF after cardiac surgery, the postinflammatory milieu after cardiothoracic surgery may also be involved in the pathogenesis of postoperative arrythmias. For example, IL6 and CRP elevation postoperatively and AF have been linked. Although statin treatment appeared to lower the risk of postoperative AF in some initial observational studies, no benefit was noted in a recent, well-conducted cohort study of more than 4000 patients. In the only randomized clinical trial in this arena Atorvastatin started 7 days before cardiac surgery was associated with a greater than 60% reduction in the incidence of postoperative AF among 200 patients undergoing coronary artery bypass graft (CABG) surgery. However, the extraordinarily high AF rate (approximately 60%) in the control group of this study was not representative of the experience at most centers. Furthermore, beta blockers, which unequivocally reduce postoperative AF, were not administered routinely after surgery and the number of patients undergoing concomitant valve surgery was small (n = 41). Although in patients treated with postoperative beta blockers, statin treatment reduces the incidence of POAF; when used at higher dosages, there is not enough evidence that statin treatment prevents AF among patients receiving postoperative beta blockers. Our group has shown that statin therapy in the elderly and renally impaired patients undergoing noncoronary cardiac surgery may be renoprotective. The recently started SPAR Trial (an international, prospective multicenter trial) will investigate perioperative high-dose use of statins (greater than 40 mg simvastatin, 3-hydroxy-3-methylglutaryl-coenzyme A [HMG-CoA] reductase inhibitors) to reduce the postinflammatory milieu after cardiac surgery and therefore might decrease the incidence of POAF.
There are many treatment strategies for the management of atrial fibrillation. We have found that the use of a guideline reduces the incidence of atrial fibrillation and decreases the disruption and anxiety that it creates (see Fig. 16-1). The principal premise of this strategy is the recognition 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 to a rhythm control strategy. Our prophylactic regimen begins with metoprolol 12.5 to 25 mg PO qid and is titrated upward as tolerated.
Postoperative atrial fibrillation guidelines. (Adapted with permission from Maisel WH, Rawn JD, Stevenson WG: Atrial fibrillation after cardiac surgery. Ann Intern Med 2001; 135:1061.)
Guidelines recommend strict rate control in patients with permanent atrial fibrillation (AF), but this is still not based on clinical evidence. RACE II (Rate Control Efficacy in Permanent Atrial Fibrillation: a Comparison between Lenient versus Strict Rate Control II) was a prospective, multicenter, randomized, open-label, noninferiority trial designed to compare two rate-control strategies in patients with permanent AF (Fig. 16-2). Six hundred fourteen patients were assigned to undergo a lenient rate-control strategy (resting heart rate 110 beats per minute) or a strict rate-control strategy (resting heart rate 80 beats per minute and heart rate during moderate exercise 110 beats per minute). The primary outcome was a composite of death from any cause, hospitalization for heart failure, stroke, systemic embolism, bleeding, and life-threatening arrhythmic events. To achieve the target heart rates patients were given beta blockers, calcium channel blockers, and/or digoxin. During follow-up ranging from 2 to 3 years, the primary outcome occurred in 12.9% of patients in the lenient-control group, as compared with 14.9% of patients in the strict-control group (p = .0001 for the prespecified noninferiority margin; see Fig. 16-1). More patients in the lenient-control group met the heart rate targets (97.7 versus 67.0% in the strict-control group; p = .001) with fewer total visits (75 versus 684; p = .001). In conclusion, lenient rate control was noninferior to strict rate control in the prevention of major cardiovascular events in patients with permanent AF. Furthermore, for both patients and health care providers, lenient rate control is more convenient, because fewer outpatient visits and examinations are needed. The clinical implications of RACE II are that lenient rate control may be adopted as a first-choice rate-control strategy in patients with permanent AF. Nevertheless, because the study was relatively small, large-scale studies have to reveal the long-term effect of lenient rate versus strict control in patients with AF in more detail.
RACE II. Kaplan-Meier estimates of the cumulative incidence of the primary outcome, according to treatment group. The numbers at the end of the Kaplan-Meier curves is the estimated cumulative incidence of the primary outcome at 3 years.
Initial assessment: The management of atrial fibrillation should be guided by the answers to the after three questions:
Is the patient symptomatic? Atrial fibrillation is generally 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 include hypotension, changes in mental status, decreased urine output, impaired peripheral perfusion, angina pectoris symptoms, and decreased cardiac output or increased filling pressures.
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 distention, increased sympathetic tone, electrolyte imbalances (particularly hypokalemia and hypomagnesemia precipitated by diuresis), acid-base disturbances, sympathomimetic medications (inotropes, bronchodilators), beta-blocker withdrawal, pneumonia, atelectasis, and pulmonary embolism.
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 after 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.
Drug therapy: Agents can be conveniently divided into rate control and rhythm control agents, although beta blockers are also effective in converting atrial fibrillation postoperatively. Mono drug therapy is generally better than poly drug therapy.
Rate control agents:
- (1) Beta blockers. Metoprolol should be first-line therapy in most patients and can be given per os (PO) or intravenously. Metoprolol should be titrated to effect with a heart rate goal less than 100 beats/min at rest. The suggested treatment for new-onset atrial fibrillation is 50 mg PO, followed by 25 mg PO until NSR or adequate rate control is achieved, up to 8 doses. Some patients may require over 400 mg/day PO.
- (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 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. After chemical cardioversion, attempts should be made to minimize the number of rate control agents used.
- (1) Metoprolol (± diltiazem)
- (2) 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, which may be increased if given in conjunction with amiodarone.
- (3) Amiodarone can cause myocardial depression and heart block; significant hypotension is most commonly associated with rapid bolus infusion. Significant toxicity is associated with prolonged use of amiodarone, and consideration should be given to discontinuing the drug within 6 weeks of surgery.
- (4) Adenosine is helpful in the treatment of supraventricular tachycardia (SVT). (It should be avoided in transplant recipients, partially revascularized patients and those with atrial flutter.)
- (5) Dronedarone is an amiodarone analog without iodine moiety in its structure, and is similar to amiodarone with regard to its structural and electrophysiologic properties.8 Dronedarone is largely denuded of the potentially life-threatening adverse effects of antiarrhythmics. Major clinical studies have demonstrated both rhythm and rate-controlling efficacy of dronedarone compared to placebo without any serious adverse effects in patients with AF. However, the ANDROMEDA trial (The Antiarrhythmic- Trial with Dronedarone in Moderate-to-Severe Congestive Heart Failure Evaluating Morbidity Decrease),9 a large-scale study, including patients hospitalized for symptomatic congestive heart failure (with severely depressed left ventricular systolic functions), was prematurely terminated because of the increased mortality in the dronedarone arm compared with placebo, indicating a lack of safety in this group of patients. Conversely, the recently published ATHENA study (including more than 4600 high-risk patients, but excluding those with severe heart failure)10 demonstrated a significant reduction in cardiovascular hospitalizations and cardiovascular mortality with dronedarone compared with placebo. In contrast, the DIONYSOS study, comparing dronedarone with amiodarone, demonstrated better safety but lower efficacy of dronedarone for the maintenance of sinus rhythm in patients with AF.11
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. Overdrive pacing can be attempted in patients with atrial wires who are in atrial flutter.
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 (IV or low molecular weight SQ) should be considered after 48 hours in patients with a history of stroke or TIAs or who have a low ejection fraction. Coumadin should not be initiated in patients who may require permanent pacer placement.
Postoperative Ischemia and Infarction
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 changes are generally present in the operating room. It typically resolves within hours. It is worth noting that nonspecific ST changes are common postoperatively and usually benign. Pericardial changes are generally characterized by diffuse concave ST elevations, accompanied by a pericardial rub and delayed in onset by at least 12 hours after surgery.
New wall motion abnormalities or mitral regurgitation diagnosed echocardiographically can help determine the hemodynamic significance of suspected ischemia or infarction. Knowledge of the quality of conduits, anastamoses, and target vessels is critical in planning management strategy (eg, there may be little to gain and much to lose in attempting to improve flow to a small, highly diseased posterior descending artery with poor run-off). On the other hand, if the patient appears to be at risk for significant myocardium, a timely trip to the operating room or cardiac catheterization laboratory can dramatically improve outcomes. 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 acute increases in pulmonary vascular resistance (PVR). Preexisting pulmonary hypertension is commonly caused 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.12 Acute increases in PVR are commonly caused by acute left ventricular dysfunction, mitral valve insufficiency or stenosis, volume overload, pulmonary edema, atelectasis, hypoxia, or acidosis. Pulmonary embolism should also be considered, but it is rare in the immediate postoperative period. As the right 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 although the failing RV often needs more volume to ensure adequate left-sided filling, overdistention will worsen function. Judicious use of PEEP to recruit atelectatic lung and hyperventilation can decrease the impact of pulmonary vasoconstriction mediated by hypoxia and hypercapnia. Use of intravenous vasodilators (commonly nitroprusside, nitroglycerin, tolazoline [PGI2 ], hydralazine, prostacyclin, adenosine, and nicardipine) to reduce PVR is frequently limited by systemic hypotension. Inotropes (typically milrinone, which also provides vasodilation) can be beneficial. Because no intravenous vasodilator is selective for the pulmonary vasculature, topical administration can be significantly more effective in reducing PVR without causing systemic hypotension. Inhaled NO and PGI2 have comparable efficacy. They can also improve oxygenation by shunting blood to ventilated lung.
Valve Diseases: Special Postoperative Considerations
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 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 is frequently required to avoid disrupting fresh suture lines. In some patients, the degree of ventricular hypertrophy can lead to dynamic outflow obstruction; the condition is most effectively treated 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.
The left ventricle in a patient with aortic regurgitation is frequently dilated without significant hypertrophy and often functions poorly postoperatively. Optimization of volume, afterload, inotropy, and rhythm in these patients is often challenging.
Mitral Valve Repair/Replacement
After repair or replacement of an incompetent mitral valve, increased afterload and consequent greater wall stress unmask LV dysfunction. Frequently inotropic support and systemic vasodilation is required to reduce the afterload mismatch seen after surgery. Occasionally LV dysfunction can be the result of inadvertent suture placement over the circumflex coronary artery.
Unlike patients with mitral regurgitation, patients with mitral stenosis typically have preserved LV function. Exacerbation of preexisting pulmonary hypertension is common, however. Postoperative strategies focus on optimizing right ventricular function and decreasing pulmonary vascular resistance.