Mortality and morbidity in cardiac surgery have continued to decline despite increases in patient age, comorbid conditions, and procedure complexity. Much of this success can be attributed to advances in critical care. This chapter will outline some strategies and principles of modern postoperative care.
Assessment and optimization of hemodynamics is a principle focus 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 (CPB), ischemia, and surgery.
A basic initial hemodynamic assessment includes a review of current medications, heart rate and rhythm, mean arterial pressure (MAP), central venous pressure (CVP), and an ECG 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 (CO), as well as pulmonary and systemic vascular resistances (SVRs) can also be calculated when a PA catheter is present. CO is determined utilizing thermodilution or by using the Fick equation. CO, blood pressure (BP), and SVR are related to each other using Ohm’s law (Table 17-1). Reasonable minimum goals for most patients include an MVO2 of about 60%, MAP > 65 mm Hg, and a cardiac index (CI) > 2 L/min/m2. Goals should be individualized. Patients with a history of hypertension or significant peripheral vascular disease will benefit from higher BP; patients who are bleeding or who have suture lines in fragile tissue are best served with tighter control. Strategies designed to produce a supra-normal CI or MVO2 have failed to demonstrate a survival advantage.1
Failure to achieve adequate CO and end-organ oxygen delivery can be caused by many co-dependent factors. These include volume status (preload), peripheral vascular tone (afterload), cardiac pump function, heart rate and rhythm, and blood oxygen carrying capacity.
Volume status can be estimated using invasive monitoring. CVP, unless it is very low, is an unreliable indicator of left ventricular end-diastolic volume. An elevated CVP 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 in the absence of significant mitral stenosis, 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. A wedge pressure of 15 mm Hg is generally adequate, but many patients can require higher pressures. Most patients arrive from the operating room with a significant net fluid gain, but much of this excess volume is extravascular due to third space and pleural cavity accumulation. Consequently, many patients are intravascularly underfilled and have on going volume requirements in the immediate postoperative period. Postoperative vasoplegia is common. Contributors include a systemic inflammatory response to CPB and the stress of surgery in addition to preoperative and perioperative medications including ACE inhibitors, calcium channel blockers, and sedatives. 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 BP; excess vasoconstriction can increase SVR and create dangerous levels of hypertension and decreased CO. Increases in afterload can be caused by medications, hypothermia, 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 ischemic stunning or infarction, valve function, acidosis, electrolyte abnormalities, hypoxia or cardiac tamponade. Bradycardia, arrhythmias, and conduction defects can also adversely affect CO.
The oxygen carrying capacity of blood is a function of hematocrit and oxygenation. A hematocrit of 21% and oxygen saturation greater than 90% is 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 (>0.5 cc/kg/min). Acute changes in hemodynamic status are common postoperatively, and vigilant monitoring should enable care to be more preemptive than reactive.
As emphasized previously, 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 balance and filling pressures should guide volume resuscitation. Starling curves are highly variable; it is helpful to correlate CO and MVO2 with changes in volume status. Patients with ventricular hypertrophy (eg, those with a history of hypertension or aortic stenosis) diastolic dysfunction or systolic anterior motion of the mitral valve 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. Monitoring devices that measure respiratory variation in the pulse arterial waveform have been shown to successfully predict the ability to improve CO with volume administration. 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 following extubation; as decreased intrathoracic pressures will improve venous return.
The choice of an optimal resuscitation fluid has been controversial. In the acute setting, colloid infusions achieve comparable hemodynamic effects with less volume when compared to crystalloid solutions. After one hour, 80% of 1000 cc of 5% albumin solution is retained intravascularly. In situations characterized by loss of vascular endothelial integrity (ie, following CPB) albumin will 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 to crystalloid has been unable to demonstrate a difference in outcomes, although a subsequent subgroup analysis found increased mortality in patients who suffered brain injury who were randomized to receive colloid.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 following surgery. If patients have normal cardiac function they often diuresis 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 following surgery, or in those who receive 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 17-2, many of the medications commonly used have multiple actions. Selection of appropriate agents depends on accurate hemodynamic assessment.
Pressors are indicated for vasodilated patients who have normal pump function and are unresponsive to volume. These agents include α-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 atrioventricular (AV) nodal conduction; it appears to have the efficacy of nipride without its toxicity. Nicardipine has been shown to control BP with less variability than nitroglycerine or nitroprusside and this has been found to correlate with improved outcomes. 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 BP 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 CO persists despite optimization of fluid status (preload), vascular tone (afterload), and heart rate and rhythm. These agents include beta adrenergic agents (dobutamine) and cyclic nucleotide phosphodiesterase inhibitors (milrinone). Both of these agents increase CO by increasing myocardial contractility and by reducing afterload through peripheral vasodilation. Dobutamine is shorter acting and easier to titrate; milrinone achieves increases in CO with lower myocardial oxygen consumption. Both are arrhythmogenic and can exacerbate coronary ischemia. Both epinephrine and norepinephrine combine β and α adrenergic agonist effects; they are pressors in addition to positive inotropes. Relative α effects increase with dose. Dopamine in low doses causes splanchnic and renal vasodilation; α and β effects dominate at higher doses. 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 rapidly wean these agents when they are no longer required.
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, CO increases linearly with heart rate, and pacing is often very helpful (SEE TABLE 17-2). 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; ventricular pacing is often useful in acutely decreasing BP while waiting to initiate a vasodilator. 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, exacerbating ischemia or inducing heart block. Ensure that pacemakers in patients undergoing ventricular pacing can sense appropriately in order to avoid R on T and subsequent ventricular fibrillation. Internal pacemakers can often be reprogramed 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 (eg, digoxin, amiodarone, calcium channel blockers, and beta blockers). If a bi-atrial trans-septal approach to the mitral valve is employed, sinus rhythm can be lost due 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, pacing pulmonary artery catheter, or external pacing pads) if needed while waiting for placement of a permanent pacemaker.
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 (coronary angiography may be necessary), electrolytes should be replaced and inotropes should be minimized. Beta blockers, amiodarone, and lidocaine can be useful therapies. Electrocardioversion should be employed if sustained VT causes significant compromise.
The incidence of postoperative atrial fibrillation (POAF) following cardiothoracic surgery is 30 to 50%,5 and has been shown to be higher in the elderly and patients with renal impairment or chronic obstructive pulmonary disease (COPD).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 coronary artery bypass graft (CABG) patients but it is generally more common in patients undergoing valve and combined procedures. POAF is typically a transient phenomenon. Use of beta blockers for the prevention of POAF is supported by the highest level of evidence. Therefore, beta blockers should be started or resumed as soon as they can be safely tolerated following cardiac surgery. Inotropic support, hemodynamic compromise, and AV block (PR interval > 0.24 ms, 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 BP. Sotalol and amiodarone are also effective for prophylaxis but not superior. Sotalol, like other type II agents, can promote ventricular arrhythmias. Beta blockers also confer benefits other than atrial fibrillation prophylaxis, are easy to titrate, and do not have the toxicities associated with amiodarone. The postinflammatory milieu following cardiothoracic surgery may contribute to the pathogenesis of postoperative arrhythmias. For example, IL6 and C-reactive protein elevation postoperatively and atrial fibrillation (AF) have been linked. In the only randomized clinical trial in this arena atorvastatin started 7 days before cardiac surgery was associated with a >60% reduction in the incidence of postoperative AF among 200 patients undergoing CABG surgery. However, the high AF rate (~60%) in the control group of this study was not representative of the experience at most centers; this may reflect the fact that beta blockers were not administered routinely after surgery.
There are many treatment strategies for the management of atrial fibrillation. We have developed the guidelines outlined in Table 17-1. The principle premise of this strategy is the recognition that for most patients with new onset atrial fibrillation, the arrhythmia is well tolerated and 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 typically produces outcomes comparable to a rhythm control strategy. Our prophylactic regimen begins with metoprolol 12.5 to 25 mg orally (po) four times a day and is titrated upward as tolerated.
Initial assessment: The management of atrial fibrillation should be guided by the answers to the following three questions: (FIG. 17-1)
Is the patient symptomatic? Atrial fibrillation is generally well tolerated, and over 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, symptoms of coronary ischemia, and decreased CO 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 distension, increased sympathetic tone, electrolyte imbalances (particularly hypokalemia and hypomagnesemia precipitated by diuresis), acid-base disturbances (particularly alkalosis), 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 since 90% of patients with new onset atrial fibrillation following cardiac surgery will be in normal sinus rhythm within 6 weeks. In long-term studies of patients with chronic atrial fibrillation it has been difficult to show a benefit from rhythm control strategies.8 Optimal target heart rates depend on many patient-specific factors. A randomized study comparing strict control (heart rate less than 80) to lenient control (heart rate less than 110) in permanent atrial fibrillation found fewer adverse events in the lenient control group.9 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
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 typically less than 110 beats/minute at rest. The suggested treatment for new onset atrial fibrillation is 50 mg po. followed by 25 mg po every 2 to 3 hours until NSR or adequate rate control is achieved. Some patients may require oral doses over 400 mg/day.
Calcium channel blockers. Diltiazem is the agent of choice. It can be given orally starting at 30 mg po three time a day. It can also be initiated as a bolus of 0.25 mg/kg IV, followed by 0.35 mg/kg IV, followed by a continuous infusion at 5 to 15 mg/h.
Digoxin can be considered in patients with contraindications to beta blockers, in particular those with poor ejection fraction. There is 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.
Antiarrythmics
Metoprolol
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 torsade de pointes which may be increased if given in conjunction with amiodarone.
Amiodarone can cause myocardial depression, heart block, and acute pulmonary toxicity; 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 six weeks of surgery.
Adenosine is helpful in the treatment of supraventricular tachycardia. (It should be avoided in transplant recipients, partially revascularized patients and in patients with atrial flutter).
Dronedarone. Dronedarone is an amiodarone analog without iodine moiety in its structure, and is similar to amiodarone with regard to its structural and electrophysiological properties.10 It has been associated with increased mortality in patients with severely depressed left ventricular function.11,12 It appears to be less toxic but also less effective than amiodarone.13
Electrical cardioversion: Electrical cardioversion should be used emergently for the treatment of hemodynamically unstable atrial fibrillation. Synchronous cardioversion rather than defibrillation should be utilized to minimize the risk of precipitating ventricular fibrillation. Sedation should be used. In patients with atrial wires who are in atrial flutter, overdrive pacing can be attempted.
Anticoagulation: Patients who remain in atrial fibrillation for >24 hours or have multiple sustained episodes over this period should be started on coumadin in the absence of contraindications. Heparin (unfractionated IV or low molecular weight SQ) should be considered after 48 hours, particularly in patients with a history of stroke or TIAs or who have a low ejection fraction. Coumadin can be initiated in patients who may require permanent pacer placement as pacemakers can generally be safely placed with INR < 2. Postprocedure heparin bridging has been associated with significant rates of pocket hematoma formation.
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 following 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 be gained 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 significant myocardium appears at risk a timely trip to the operating room or the cardiac catheterization laboratory can dramatically improve outcomes. Ongoing ischemia should prompt consideration of standard treatment strategies including anticoagulation, beta blockade, and nitroglycerin as tolerated. Intra-aortic balloon pump placement should be considered to minimize inotrope requirements, decrease myocardial oxygen requirements and minimize infarct size.
Right ventricular failure can be a particularly difficult postoperative problem. It can be caused by perioperative ischemia or infarction or by acute increases in 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.14 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, CVP 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 RV has its own starling curve, and while the failing right ventricle (RV) 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 hypercapnia. Use of intravenous vasodilators to reduce PVR is frequently limited by systemic hypotension. Inotropes (typically milrinone which also provides vasodilation) can be beneficial. Vasopressin, unlike other pressors, appears to increase SVR more than PVR.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 NO and PGI2 have comparable efficacy. They can also improve oxygenation by shunting blood to ventilated lung.
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 (LV). For some patients, replacement of a stenotic valve allows a ventricle conditioned to pumping against abnormally high afterload to easily achieve supranormal levels of CO and BP postoperatively. Meticulous BP 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 ventricles). 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 LV 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.
Following 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 following surgery. Occasionally LV dysfunction can be the result of inadvertent suture placement compromising 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 PVR.
The incidence of cardiac arrest following cardiac surgery ranges between 0.7% and 2.9%. These patients represent a special case for application of advanced cardiac life support (ACLS) algorithms. The majority of these events happen in the immediate postoperative period when many patients are still intubated and monitored in the intensive care unit (ICU). In addition to ventricular arrhythmias, common etiologies for arrest in these patients include readily reversible causes: hypovolemia from hemorrhage, cardiac tamponade, acute hypoxia, electrolyte abnormalities, tension pneumothorax, pacing failure, and myocardial ischemia. Many of these patients develop clinical deterioration prior to the arrest which can provide clues to the mechanism of the arrest and guide therapy. Early recognition in a critical care environment, the presence of trained clinicians, patient-specific knowledge, and reversible etiologies combine to produce outcomes that are significantly better when compared to outcomes in the broader population of patients experiencing arrest. Cardiac surgery patients undergoing resuscitation in the 24 hours following surgery have survival rates up to 70%.16,17
The most important factors contributing to survival following cardiac arrest are prompt defibrillation and immediate, high quality, and uninterrupted chest compressions. There are special circumstances in cardiac surgery patients when chest compressions may be deferred. The European Resuscitation Council has recommended three successive (stacked) shocks for ventricular fibrillation or pulseless VT occurring in immediate postoperative cardiac surgery patients prior to chest compressions if defibrillation is immediately available.18 Minutes matter19 and patients at high risk for arrhythmias should have defibrillator pads placed postoperatively. Because chest compressions in the immediate postoperative period can cause myocardial injury, sternal and rib fractures, bypass graft injury, prosthetic valve dehiscence, lung injury, and hemorrhage,20 it would be preferable to avoid compressions if return of spontaneous circulation (ROSC) can be achieved with electrical cardioversion. For asystole or severe bradycardia, pacing wires should be utilized when available prior to initiating chest compressions. Adding a ground wire in the skin can sometimes improve the capture of poorly functioning temporary pacing wires. Patients with pulseless electrical activity may respond to volume administration or pressor administration; if these interventions are ineffective, chest compressions should be initiated. Finally, if tamponade is suspected and emergency resternotomy is immediately available in the ICU, it is reasonable to minimize chest compressions and open the chest.
The efficacy of chest compressions can be monitored with preexisting arterial lines or with end-tidal CO2 (ETCO2) monitoring (quantitative waveform capnography). These techniques can also minimize interruption of chest compressions and help to identify ROSC. Systolic pressures close to 80 mm Hg or ETCO2 > 10 mm Hg is considered to reflect adequate CPR. ETCO2 > 40 is associated with ROSC.
If patients are not ventilated, intubation should be deferred and mask ventilation utilized until experienced personnel are available. Chest compressions should be interrupted only to insert the endotracheal tube through the vocal cords once visualized. Postoperative cardiac surgery patients are often very sensitive to increases in intrathoracic pressure and respiratory rates should be approximately 10 breaths per minute and minimal tidal volumes should be used.
Use of epinephrine should be limited and not follow standard algorithms in the resuscitation of cardiac surgery patients because of the potential for hypertension leading to suture line disruption and hemorrhage. Smaller doses may be cautiously titrated to effect. Amiodarone (300 mg IV) should be considered for persistent ventricular fibrillation or tachycardia resistant to electrical cardioversion.
Chest tubes should be placed in the mid-clavicular line in the second intercostal space if tension pneumothorax is suspected. Resternotomy should be considered if resuscitative efforts have failed to achieve ROSC within 5 to 10 minutes, particularly if tamponade is suspected. Ultrasonography can suggest, but not rule out, cardiac tamponade. Upon opening the chest, internal cardiac massage can be initiated. Clot should be evacuated, sources of bleeding identified, and bypass graft patency can be assessed.
Effective teamwork is a critical component of effective cardiopulmonary resuscitation. A call for additional help should be made if personnel resources are suboptimal. A team leader needs to be identified to manage the effort. If resources are adequate, the leader’s role should be restricted to coordinating care. The leader should assign tasks after assessing a practitioner’s competence to perform the assigned task. Communication should be closed loop; when team members are assigned a task they need to communicate that they understand the task and provide notification when they have completed it. The effective leader should rely on the collective knowledge of the team by actively soliciting information about the patient’s condition prior to the arrest and exploring potential diagnoses and courses of action. As mentioned previously, ACLS algorithms were not developed for cardiac surgery patients specifically, and cardiopulmonary resuscitation should be performed with awareness of the special problems facing these patients postoperatively and with awareness of the specific circumstances of the patient. Knowledge of the patient’s medical problems, operative details (including bleeding problems, hemodynamic instability coming off bypass, echocardiographic findings, and revascularization challenges) and postoperative course should guide strategy. Mobilization of personnel and equipment to open the chest should occur if resuscitation efforts are not immediately successful.
Training of practitioners in resuscitation is critical to optimization of outcomes. As important as knowing what to do in an emergency situation is to know how to do it. Mock codes should focus on teamwork and effective leadership in addition to focusing on issues specific to cardiac surgery patients. Required equipment should be dedicated and readily available and all members of the team should know how to access it.
One of the principle challenges of cardiac surgery is to achieve sufficient anticoagulation while 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.21 Excessive bleeding and its complications, including blood product transfusions, cause significant morbidity and mortality.
Preoperative evaluation includes documenting a history of abnormal bleeding or thrombosis, and obtaining basic coagulation studies, a hematocrit and 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%)22 requires either a delay in surgery until the assay is negative (usually 3 months), or if surgery is more urgently required, alternative anticoagulation strategies (bivalirudin23) can be considered. Preoperative medications that can increase bleeding risk are common. Aspirin inhibits cyclooxygenase, reduces the synthesis of thromboxane-A2, and decreases platelet aggregation. Preoperative aspirin use modestly increases postoperative bleeding, but preoperative and early postoperative use (ie, within 6 hours) is beneficial to outcome and ultimate survival.24 Other antiplatelet agents have more profound impacts on platelet function. The glycoprotein IIb/IIIa inhibitors eptifibatide (Integrillin) and tirofiban (Aggrastat) are sufficiently short acting that surgery can be safely conducted despite recent exposure. Abciximab (Reopro) usually requires a 24 to 48-hour delay of surgery, if feasible, to avoid catastrophic bleeding. Clopidogrel (Plavix), prasugrel (effient), and ticagrelor (brilinta) inhibit the P2Y12 component of platelet ADP receptors preventing ADP platelet activation. Discontinuing these agents 5 to 7 days before surgery will minimize bleeding, but they are often continued closer to the time of surgery because the risk of mortality is high from acute coronary stent occlusion, particularly in patients with recently placed drug-eluting stents. Customarily, warfarin (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 INR. Although patients undergoing an interruption in warfarin administration frequently receive bridging anticoagulation with heparin, increasing evidence suggests that this strategy increases bleeding without preventing thromboembolism.25,26
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