Postoperative Management of the Cardiac Surgery Patient

Published on 07/03/2015 by admin

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Postoperative Management of the Cardiac Surgery Patient

This chapter will give the reader information on how to manage routine and complex cardiac surgery patients in the immediate and early postoperative period. The disproportionately small number of patients who undergo cardiac operations and have prolonged intensive care unit (ICU) stays often develop complications not unique to them but common to most ICU patients who have delayed recoveries or do not survive after a long ICU course. These ICU complications are covered elsewhere in this text. This chapter is divided by organ system into five broad areas (neurologic, cardiac, pulmonary, renal, transthoracic echocardiography) specific to these patients in this setting and includes a discussion of some miscellaneous topics.

Neurologic Care

Despite improvements in cardiac surgery techniques and perioperative critical care, postcardiotomy neurologic complications remain a major cause of morbidity and death following cardiac surgery. A spectrum of neurologic complications is seen in the postoperative period. Complications can be classified as generalized (global deficit) or focal. Generalized deficits can be manifested as delayed awakening from general anesthesia, coma, or new onset of seizure. Focal deficits may be transient or permanent. Except in their most severe form, neurologic complications cannot be completely assessed until the patient returns to consciousness and is weaned from the ventilator. Focal abnormalities are usually evaluated by a computed tomography (CT) scan. A CT for nonfocal, cognitive dysfunction rarely yields new information that is helpful for patient management, and imaging studies most often show old, chronic changes such as atrophy or lacunar infarcts. The patient must be stable enough to withstand transport to the CT (if the institution does not have a portable scanner), which is usually not the case in the early postoperative period.

The risk factors for neurologic injury after cardiac surgery have been well elucidated, but effective risk modification to reliably prevent neurologic complications has been elusive. In certain operations, measures to reduce risk have been implemented and have become incorporated in perioperative management.1,2 For example, patients with descending thoracic aortic operations are at significant intraoperative risk for spinal cord ischemia, as well as delayed injury (days postoperatively). These patients usually have a spinal drain placed preoperatively to reduce the risk of spinal cord injury. Spinal cord perfusion pressure (SCPP) is the difference between mean arterial pressure (MAP) and cerebrospinal fluid pressure (CSFP) (SCPP = MAP − CSFP); thus, lowering of CSFP will increase SCPP and potentially improve neurologic function as long as an adequate MAP is maintained.3

Neurologic complications are still considered one of the major risks associated with coronary artery grafting. The advanced age of bypass patients, high incidence of associated carotid occlusive disease, and increased aortic atheroembolic burden place older coronary artery bypass graft (CABG) patients at increased risk of central neurologic complications in the postoperative period.4

Other strategies for preoperative and intraoperative risk modification are becoming routine. They include selective use of preoperative carotid imaging, routine use of intraoperative transesophageal echocardiography (TEE) and epiaortic echocardiography, descending aortic cannulation with TEE guidance, aortic-no-touch technique, high-flow/high-pressure cardiopulmonary bypass (CPB), retrograde cerebral perfusion during circulatory arrest, carbon dioxide insufflation, intraoperative cerebral oxygen saturation monitoring, echocardiography de-airing, and maintenance of baseline perioperative blood pressure.5,6 Early neurologic complications vary in clinical presentation from focal to global neurologic deficit such as seizures, ischemic encephalopathy, and coma. Several authors have classified these complications as type I (focal injury, stupor, and coma) and type II (seizures, neurocognitive dysfunction, and delirium).7 This classification does not emphasize pathophysiologic mechanisms that could better inform preventive measures.5,7 Regardless of the classification system used, overlap often exists.

In comparison to the other complications, focal neurologic deficits from stroke carry a mortality rate of up to 20% in the first postoperative month and prolong ICU and hospital lengths of stay.8-10 In a mixed cardiac surgery patient population, the incidence of stroke varied among those patients having CABG, combined CABG and heart valve surgery, and ascending aorta repair.1113 The incidence of stroke depends on the surgical procedure (isolated CABG, 1.4-3.8%; combined CABG and valve, 7.4%; isolated valve, 4.8-8.8%; multiple valve, 9.7%; and aorta, 8.7%).12

Unfortunately, most of the known baseline patient variables associated with perioperative stroke are not modifiable. Despite the identification of many intraoperative variables that cause intraoperative stroke (macroembolism of debris, air embolism, hypoperfusion, hypoxemia, coagulation status), risk remains significant and continues in the early postoperative period. Although there was early enthusiasm for off-pump CABG as an operative technique to reduce stroke, in the most recent multicenter clinical trial the 30-day incidence of stroke was not significantly decreased compared with on-pump CABG.14

The majority of strokes are ischemic (62%); fewer are due to hypoperfusion (9%) or hemorrhage (<1%).12 Hemorrhagic strokes are rare after cardiac surgery and the clinical presentation is notable for delayed awakening and coma despite discontinuing sedation or progressive clinical deterioration as intracranial pressure (ICP) increases. Hemorrhagic transformation is recognized in 20% of ischemic strokes.10 Embolic strokes tend to present with acute hemiparesis and represent a compromise of specific cerebral artery area. Thrombotic or ischemic strokes are related to diminished blood flow with the most vulnerable areas being those between major cerebral artery perfusion territories (watershed areas).

Cardiac transplantation has a higher associated occurrence of neurologic complications than CABG.15,16 Symptom onset for focal motor deficits in these patients usually occur after the second postoperative day, especially in patients receiving mechanical circulatory support or experiencing major postsurgical complications such as tamponade, severe cardiac dysfunction, prolonged CPB, or postoperative hepatic failure.

Predictive models may enable implementation of earlier interventions.14 More than half of strokes are identified within the first day after CABG.10 Because of associated morbidity and death, an objective neurologic evaluation by minimizing sedation in the first 2 postoperative hours is desirable. Weaning sedation should be initiated only when the risk of doing so is minimal (i.e., a normothermic, nonacidemic, nonagitated patient with minimal chest tube output).

Once a new focal neurologic deficit, seizure, or delayed awakening is documented, a noncontrast brain CT scan should be obtained immediately. The most important tomographic findings include loss of insular ribbon, loss of gray-white interface, loss of sulci, acute hypodensity, mass effect, and dense mean cerebral artery sign. Owing to the relative insensitivity of CT scans for diagnosing ischemia, early CT scans may be normal, despite areas of brain infarction.17 Magnetic resonance imaging (MRI) may help identify these lesions.17 MRI usually cannot be obtained safely in the early postoperative period because of the need to move the patient off the unit to a usually remote location and because non-MRI compatible pericardial pacing wires are routinely placed in cardiac surgery patients. MRI will document a new lesion in 26% to 50% of cases, but there is often lack of correlation with the neurocognitive deficit.18,19 Brain CT scans are more sensitive in diagnosing large air embolism, which is often the cause of abnormal postoperative neurologic findings in these patients. In the patient with a focal deficit or persistent embolic events, transcranial Doppler, transthoracic echocardiography (TTE), or TEE can be used to help identify sources of recurrent cardiac or aortic embolization.

Stabilization of the patient who develops stroke after cardiac surgery is the most important initial intervention and includes continuation of cardiopulmonary support and tracheal intubation if the patient cannot protect the airway or has a Glasgow Coma Scale score less than 9. Secondary brain injury, which is additional brain injury due to the factors that initially caused an imbalance between oxygen supply and demand, should be prevented. The most important measures are prevention of hypoxemia, hypotension, hypercarbia, and hyperthermia.

From a ventilator standpoint, higher levels of positive end-expiratory pressure (PEEP) to maintain optimal oxygenation might be required. If the patient has documented intracranial hypertension and requires PEEP 10 cm H2O or higher, ICP monitoring should be considered as high levels of PEEP and lung recruitment maneuvers may decrease cerebral perfusion. Increased PEEP may decrease cerebral perfusion pressure (CPP) by elevating ICP because CPP is the difference between MAP and ICP.

Although acute treatment of ischemic stroke is imperative, the traditional 3-hour time window for active stroke intervention and institution of thrombolytic therapy is often lost because the time of the last known normal is usually just before induction of anesthesia and duration of surgery usually exceeds 3 hours. Furthermore, intravenous administration of tissue plasminogen activator (tPA) is contraindicated in the immediate postoperative period because of the associated postoperative bleeding risk.

Intra-arterial administration of tPA is an alternative for acute treatment of ischemic stroke within 6 hours of clinical presentation. The safety and efficacy of intra-arterial urokinase and tPA in selected patients who presented ischemic stroke within 12 days after cardiac surgery have been demonstrated.20 The mean time from operation to stroke was 4.3 days. Thrombolytic therapy was commenced within 3.6 hours. No operative intervention for bleeding was necessary and 38% of the patients had neurologic improvement. Mechanical clot retrieval is another acute stroke therapy in the first 8 hours since neurologic deficit. Patients who will likely benefit from this therapy include those with significant neurologic deficit and large vessel occlusion with core ischemia approximately less than 30% of the middle cerebral artery territory.

Anticoagulation therapy has not proved beneficial in the cardiac surgery patient with ischemic stroke. However, it should be considered in cases of basilar stenosis, internal carotid dissection, and suspected cardiac embolism and specifically with concurrent atrial fibrillation and stroke. In this circumstance, the risk of ongoing embolism to cerebral circulation may be considered higher than active bleeding after cardiac surgery. A hematology consult is recommended in cases of suspected hypercoagulable state as the cause of this disorder demands a more comprehensive workup and potentially may require lifelong anticoagulation therapy. Antiplatelet therapy should be initiated in all cardiac surgery patients with acute stroke, especially if thrombolytic therapy is contraindicated. Aspirin is usually prescribed. The dose ranges between 160 mg and 1300 mg per day. Combined antiplatelet therapy with clopidogrel is not recommended because of the significant risk of bleeding.

In cases of suspected perioperative air embolism (i.e., opening of heart chambers for valve repair or replacement), the patient should remain in the supine position to avoid further embolic phenomena. If tolerable, the patient should be maintained in Trendelenburg position and mechanical ventilator support with FIO2 of 1.0 should be instituted. Measures to control intracranial hypertension (more common in intracranial hemorrhage) should be individualized after reassessment of brain CT imaging. Hyperventilation, as well as diuresis with mannitol or furosemide is recommended in the patient with intracranial hypertension.

In the cardiac surgery patient, coma is defined as prolonged unconsciousness after discontinuation of anesthetics, sedatives, and opioids and inability to show response to motor/verbal commands. A recent retrospective investigation found an incidence of delayed awakening in approximately 0.5% of all cardiac surgery patients.21 However, the period of time in the immediate postoperative phase can be challenging as the necessity of adequate neurologic examination must be weighed against the patient’s hemodynamic stability. If a specific diagnosis is not found, and there is concomitant severe heart failure, it portends a worse outcome.21 Moreover, up to 20% of patients with postcardiotomy stroke present with delayed awakening and coma-like symptoms.21

Evaluation with brain CT is mandatory in these cases and it should occur as soon as the coma state has been recognized and reversible metabolic causes have been treated. The identified risk factors for delayed awakening after cardiac surgery in the aforementioned investigation included urgent cardiac surgery, elevated serum creatinine (Cr), and lower postoperative hemoglobin level.21 Most of these patients had normal brain CT scan imaging and ultimately recovered consciousness after being comatose during the first 24 hours.21 Although some investigators have proposed a role for altered renal excretion of sedatives in patients with postoperative renal failure or decreased oxygen delivery to the brain with anemia, the specific underlying mechanisms in these cases remain unclear.

Postoperative seizure is an independent predictor of permanent neurologic deficit and increased mortality risk.22,23 A recent study showed seizures were a strong predictor of permanent neurologic deficit and increased mortality risk. It is important to remember that any neurologic injury can present initially as a seizure. The independent risk factors for postoperative seizures included deep hypothermic circulatory arrest, aortic calcification or atheroma, and critical preoperative state. Other specific risk factors for early seizures include perioperative administration of the antifibrinolytic tranexamic acid administration and preexisting renal insufficiency.

Tranexamic acid has proconvulsant properties and it is reasonable to hold the infusion of this agent in the early postoperative period if the patient presents with seizures. The most common proposed mechanism of seizures after cardiac surgery is focal or global ischemia from hypoperfusion (air or atheroembolism) or metabolic disorders. Early brain CT scan is essential because it may detect potential reversible causes of neurologic injury such as cerebral edema, intracranial bleeding, or emboli in a major cerebral artery.10

Delirium is considered a subtle category of brain injury in the postcardiotomy patient. The intensivist should include perioperative stroke in the differential diagnosis of perioperative psychomotor agitation or delirium in the ICU. A common missed diagnosis is drug and alcohol withdrawal in patients with acute delirium in the ICU.

Cardiovascular Care

Mean Arterial Pressure

MAP is one of the most commonly measured and manipulated hemodynamic variables in the perioperative period. Although MAPs are routinely maintained in the 70 to 80 mm Hg range, target blood pressure may be altered based upon comorbid disease and the intraoperative course of events. Hypertensive patients with neurologic or renal disease may have altered autoregulatory curves, which require higher blood pressures for adequate end-organ function. Conversely, in patients with friable cardiac tissue, tenuous surgical repairs, or uncorrected aneurysmal disease lower MAPs may be desirable. Ideally, intraoperative manipulation of the blood pressure while observing the echocardiogram and changes in central venous (CVP) and pulmonary artery pressures (PAPs) will allow the practitioner to define optimal blood pressure.


Cardiac surgical patients presenting in the postoperative period with hypertension should be evaluated for routine causes of acute postoperative hypertension and treated accordingly. Pain, residual neuromuscular blockade, hypoxemia, hypercarbia, hypothermia, or bladder distention may provoke hypertension. If these precipitants are ruled out, pharmacologic lowering of blood pressure with an infusion of a vasodilator, sodium nitroprusside, or nitroglycerin can be initiated. The rapid titratability and short duration of action of these medications is desirable as hemodynamic lability is commonplace. Alternatively, short-acting or ultra-short-acting dihydropyridine calcium channel blockers (e.g., nicardipine or clevidipine) have been used as they exert maximal effect in the peripheral arterial system with minimal impact on cardiac function.24 While MAP is lowered, serial measurements of cardiac output and urine output should be recorded to assess the patient’s tolerance of a lower blood pressure.


With a reported incidence of 9% to 44%, hypotension is more common than hypertension following cardiac surgery.25 Studies of off-pump CABG surgery compared to on-pump CABG surgery have demonstrated a significant increase in the incidence of hypotension in those patients exposed to CPB.26 Some clinicians also associate the relatively common hypotensive response to more critically ill patients with prolonged medical management prior to surgery. Additionally, widespread use of angiotensin-converting enzyme inhibitors has been implicated as a potential contributor.27 Regardless of the predisposing factors, postoperative hypotension demands prompt investigation and treatment.

From a physiologic standpoint, MAP = central venous pressure (CVP, mm Hg) + cardiac output (CO, L/minute) × systemic vascular resistance (SVR, dyn⋅s⋅cm−5). A decrease in any of these parameters will reduce MAP. It is useful to consider the common causes of postoperative hypotension relative to these hemodynamic variables. Low CVP corresponds with hypovolemia. Decreased CO can occur as a consequence of cardiac insufficiency/cardiogenic shock or new-onset myocardial ischemia. Vasoplegia following CPB leads to a depressed SVR. Routine causes of hypotension in the acute postoperative period include hypovolemia, cardiac insufficiency/cardiogenic shock, vasoplegia following CPB, new-onset myocardial ischemia, and tamponade. Crucial to postoperative management is understanding the patient’s intraoperative hemodynamics and immediate postbypass cardiac function.

The most readily correctable cause of hypotension is hypovolemia. Commonly boluses of crystalloid (500 mL to 1 L of 0.9% normal saline or lactated Ringer’s solution) are administered and the patient’s hemodynamic responses (MAP, CVP, PAP, and cardiac index [CI]) are evaluated. Colloid solutions can be used, but some concern exists when administering hetastarch solutions because of its effects on the coagulation cascade and potential contribution to a bleeding diathesis.28

A low preoperative ejection fraction (<35%), advanced age (>70 years old), and prolonged CPB times (>120 minutes) correlate with an increased risk of decreased cardiac output in the postbypass period.29 Postoperatively, a depressed CI often manifests early, during separation from CPB in the operating room. The pattern observed on hemodynamic monitoring is a depressed CI (<2.2 L/minute/m2), hypotension, normal or elevated SVR, and elevated filling pressures. Echocardiography demonstrates global ventricular hypokinesia. Patients will frequently require exogenous pharmacologic support to maintain a CI of greater than 2.2 L/minute/m2. Epinephrine, dopamine, dobutamine, or milrinone may be initiated for inotropic support.30 It is not uncommon for cardiac insufficiency to persist for several days following CPB.

Even after successful coronary revascularization, the astute practitioner must be vigilant for postoperative myocardial ischemia. During weaning from CPB, air may become entrained within the heart that is not effectively evacuated by the atrioventricular (AV) bypass vents. Some of this air may enter the coronaries and lead to cardiac arrest or ischemia. In addition, during chest closure, bypass grafts may become kinked, obstructing flow. During aortic or valvular surgery, graft material or sutures may inadvertently obstruct coronary ostia or may occlude native coronary flow. Although multiple patient monitors—electrocardiogram (ECG), pulmonary artery catheter, and echocardiography—can identify ischemia, studies have demonstrated new-onset wall motion abnormalities on echocardiography as the most sensitive and earliest indicator of malperfusion.31,32 If ischemia is present, surgical revascularization or percutaneous coronary revascularization may be necessary for reestablishing flow.

For approximately 5% to 15% of patients, exposure to CPB will lead to a prolonged vasodilatory state or vasoplegia.33 The classical pattern is normal biventricular function, normovolemia, and decreased SVR. In these patients, infusing additional volume will not increase MAP and will frequently decrease systemic pressure secondary to activation of the atrial stretch receptors. In patients who are adequately volume resuscitated, the most effective treatment is infusion of a vasopressor, commonly norepinephrine, phenylephrine, or vasopressin.10 Patients requiring progressively increasing doses of vasopressors should be continually assessed for hypovolemia or anemia, as these problems might happen concurrently in the vasoplegic patient. Experimental evidence suggests that these patients may suffer from a relative vasopressin deficiency. As such, exogenous vasopressin added to one of the other aforementioned vasopressors has been used successfully to maintain an adequate MAP.34


Acute tamponade is a surgical emergency that demands immediate treatment. In the early postoperative period following cardiac surgery, tamponade may occur as a consequence of uncorrected coagulopathy or from chest tube obstruction. Classic signs of tamponade on physical examination include hypotension, pulsus paradoxus, diminished peripheral pulses, and oliguria. Invasive hemodynamic monitoring may demonstrate equalization of CVP, pulmonary artery (PA) diastolic, and PA systolic pressures as the pericardium fills and pericardial pressure exceeds intracardiac pressures. Echocardiographic signs include right atrial systolic collapse and right ventricular diastolic collapse.35

Unfortunately, although prompt recognition and treatment are crucial, many patients with tamponade fail to demonstrate classic physical examination findings. Depending upon the rate of accumulation, hypotension may be sudden and severe or may occur gradually over a period of hours. If decompensation is sudden and severe, emergent bedside reexploration is warranted. Otherwise, the patient may be taken to the operating room for emergent chest evacuation.


Postoperative arrhythmias are the most common complication after cardiac surgery with an overall reported incidence of 5% to 63%.36 The most frequent arrhythmia is atrial fibrillation, which occurs in up to 40% of patients following bypass graft surgery and 60% of patients following combined CABG valve surgery.36 Inflammation of the myocardium and mechanical disruption of the cardiac conduction system during surgery predispose cardiac surgical patients to bradyarrhythmias and heart block during the postoperative period. Accordingly, placement of temporary epicardial pacing wires in the ventricles and atria is routine.37 Atrial wires will allow for AV synchrony during contraction, but removal of these wires from the more fragile atrial tissue may place the patient at an increased risk of atrial damage and tamponade.

Given the association of supraventricular arrhythmias with increased morbidity and length of stay, considerable research effort has focused on prevention and treatment.38 In the postoperative period, 60% of arrhythmias manifest within the first 3 postoperative days.38 For the patient with new-onset atrial fibrillation or flutter, the first step is to decide whether any hemodynamic instability is present. In the unstable patient, preparations should be made for immediate cardioversion according to Advanced Cardiac Life Support (ACLS) guidelines. In the hemodynamically stable patient, examination of the serum metabolic panel should be done for evidence of hypokalemia or hypomagnesemia with repletion of potassium or magnesium as necessary. If atrial fibrillation persists, the clinician must decide whether rate or rhythm control is preferred. Although rate control will limit tachycardia and myocardial oxygen consumption, it will not provide the benefit of atrial contraction and requires long-term anticoagulation.

If rate control is deemed appropriate for the patient, the most common agents used include beta blockers (e.g., atenolol or metoprolol), calcium channel blockers (e.g., diltiazem or verapamil), and digoxin.38 Care should be avoided when administering beta blockers to patients with severe chronic obstructive pulmonary disease (COPD) or reduced ejection fraction.

In patients with atrial fibrillation or flutter for less than 48 hours or with an echocardiogram devoid of intracardiac thrombus, rhythm control can be attempted. Prior to initiation of antiarrhythmic therapy, a 12-lead ECG should be examined for evidence of QT interval prolongation. The most common medications used for rhythm control include amiodarone, sotalol, procainamide, and ibutilide. In patients with decreased ejection fraction, amiodarone is the agent of choice. ECG monitoring should be performed during initiation and maintenance of rhythm control agents because any of these medications may provoke malignant arrhythmias. If medications fail to restore sinus rhythm and atrial fibrillation or flutter is less than 48 hours in duration, synchronized cardioversion with a biphasic defibrillator can be performed.


If left untreated, hemorrhage and uncorrected coagulopathy can lead to devastating complications in the cardiac surgery patient. Excess bleeding occurs in 20% of cardiac surgical patients with approximately 5% requiring surgical reexploration.39,40 Many factors contribute to this increased risk of hemorrhage. Preoperatively, patients are routinely on antiplatelet therapy and anticoagulant medications. Intraoperative exposure to CPB initiates contact activation of platelets with resultant thrombocytopathy and thrombocyopenia. In addition, the extracorporeal circuit exacerbates inflammation and amplifies fibrinolysis.41

Thromboelastography (TEG) and point-of-care (POC) testing are useful to guide blood product administration as the rapid rate of bleeding in the cardiac surgery patient outpaces the results obtained with standard laboratory testing.42,43

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