Upon completion of surgery, the cardiac patient is transported to the intensive care unit (ICU) for postoperative management. The role of the anesthesiologist or the anesthesiology department in postoperative care depends on institutional policies and procedures. Anesthesiologists trained in intensive care, non-anesthesiologist intensivists or surgical physician assistants, and nurse practitioners in consultation with the patient’s attending cardiac surgeon might manage the ICU care. In other settings, the patient’s anesthesiologist will manage some elements of postoperative care (eg, ventilation) while the surgeon attends to issues regarding chest tube management. What must be emphasized for the practitioner new to cardiac anesthesiology is the need to be aware of the operating paradigm used in one’s individual institution. Moreover, it is critically important that the anesthesiologist carefully documents their report and the time of transfer of care to the ICU team. Unfortunately, sometimes patients survive the intraoperative period only to succumb minutes, hours, or days following arrival in the intensive care unit.

This chapter reviews common problems encountered in the postoperative care of the cardiac surgery patient. It is by no means a comprehensive text on critical care but rather highlights some of the particular problems that appear in routine postoperative cardiac surgery recovery and ICU.

ROUTINE TRANSPORT AND REPORT

Following cardiac surgery patients are transported fully monitored (ECG, arterial pressure, oxygen saturation) from the operating room to the ICU. As the transport of an unstable patient to the ICU carries in itself significant morbidity, every effort toward hemodynamic stability should be undertaken in the operating room prior to moving the patient. Anesthesiologists must be aware of the possibility of inadvertent extubation of the patient or the loss of a central venous line that can occur during routine patient transport and be prepared accordingly. Similarly, they must be prepared to treat hemodynamic instability. Blood pressure variations are common as patients begin to regain sympathetic tone once anesthetics are withdrawn. Propofol infusions, when hemodynamically tolerated, can be used to mitigate the increases in blood pressure often seen in postoperative patients. In particular, patients with a noncompliant vasculature (common among cardiac surgery patients) will frequently develop severe hypertension during emergence requiring the administration of propofol, narcotics, and vasodilators postoperatively. At the same time, because these patients may be hypovolemic, when hypertension is treated there is often a tendency to overshoot transforming hypertension into severe hypotension. Avoidance of hypertension is particularly desirous in the peri-operative period to avoid ensuing pressure-related postoperative bleeding. Efforts are likewise undertaken to avoid hypotension during patient transport and transfer to ICU care.

Patients are routinely brought from the operating room to the ICU with any one of many vasoactive infusions running. Care must be taken to be sure that during transport all expected infusions are flowing at the desired rate and that these can be adjusted. At times, as patients awaken and their vascular tone increases, there is less need for vasoconstrictors such as vasopressin and norepinephrine. Inotropic medications are continued and hemodynamic measurements as described in Chapter 2 are obtained to adjust vasoconstrictors, vasodilators, and volume administration to achieve a relatively normal blood pressure and cardiac index.

Patients upon transport to the ICU may continue to require pacing used after separation from CPB. Should the patient arrive in the ICU in normal sinus rhythm, the DDD pacemaker can be set for a slow backup rate (eg, 60 bpm) or be in the off position while continually attached to the patient in the event of unexpected brady-cardia. Many patients develop varying degrees of heart block following cardiac surgery and some patients require placement of a permanent pacemaker thereafter. Should patients have complete heart block and be totally pacemaker dependent, the ICU team must be specifically informed to be sure that a secondary temporary pulse generator is available and that pacemaker battery reserves are sufficient.

Upon arrival in the ICU, the majority of patients are placed on a mechanical ventilator. Ventilator settings are dependent upon local policies regarding “preferred” modes of postoperative ventilation. Usually a volume-controlled mode is employed in adult patients with a tidal volume from 400 to 800 mL (6-8 mL/kg) delivered at a rate of 8 to 12 breaths per minute depending upon patient size. Positive end-expiratory pressure (PEEP) is also used as indicated (customary PEEP is 5 mm Hg). The anesthesiologist confirms that the ventilator is actually delivering oxygen through observation of the rise and fall of the chest, auscultation, oxygen saturation, and/or respiratory gas analysis before leaving the patient’s bedside.

Assuming the patient is hemodynamically stable and ventilation acceptable, the anesthesiologist provides report to whomever will be primarily responsible for the patient in the ICU (physician assistant, nurse, intensivist). Report includes a brief summary of the patient’s preexistent medical conditions, intraoperative course, the surgery completed, the results of the last intraoperative laboratory values, and any special concerns that the anesthesiologist might have (eg, difficult blood glucose control intraoperatively). Efforts to control postoperative bleeding are reviewed including a summary of any and all blood products administered in the operating room.

Once report is completed, the anesthesiologist’s duties are predicated upon the operative policy of the ICU.

Many patients following routine cardiac surgery will simply awaken from anesthesia and can be rapidly weaned from ventilatory support. So-called “fast track” approaches to ICU ventilator management permit ventilatory weaning within 2 to 4 hours of ICU arrival. Selected cardiac surgery patients can be extubated in the operating room. Appropriate consideration should be given to the potential for hemodynamic instability and airway compromise during patient transport when performing “in the OR” extubations of heart surgery patients.

Ventilatory weaning of the “routine” cardiac surgery patient in the ICU can be advanced when the patient is awake and responsive and maintains adequate respiratory parameters (tidal volume 300-500 mL, acceptable oxygen saturation, and arterial blood gas on 0.4 fraction of inspired oxygen (FiO₂), with a respiratory rate <30 breaths per minute). The patient should have a normal breathing pattern and the postoperative chest radiograph (CXR) should be acceptable.

Following extubation, the patient is ambulated as soon as possible, invasive monitors are discontinued, and hopefully the patient is discharged from the hospital on postoperative day 3 or 4. Simply put, the patient with an uneventful operation, an uneventful anesthetic, and an uneventful medical history can have an uneventful ICU experience. Unfortunately, nowadays cardiac surgery patients have complicated medical histories and their surgical procedures are more often than not complicated. Consequently, many patients do not experience the uneventful recovery described above. Rather, they can experience lengthy ICU stays with single or multiorgan systems failure.

INFLAMMATION AND THE CARDIAC SURGERY PATIENT

Much of the morbidity and mortality associated with prolonged ICU stays following cardiac surgery has been associated with the inflammatory process.¹ Inflammatory markers (eg, C-reactive protein, IL-6, IL-8) increase during and after cardiac surgery. Proposed mechanisms for the inflammatory state associated with cardiac surgery include: contact activation of the inflammatory system through interaction of blood with the cardiopulmonary bypass machine, ischemia-reperfusion injury secondary to aortic cross clamping, and endotoxemia.² Endotoxin is considered a major initiator of the inflammatory response associated with cardiac surgery. During cardiac surgery it is possible that impaired gut perfusion leads to endotoxin release. Once present, endotoxin can activate the complement cascade and neutrophils leading to a systemic inflammatory response including coagulopathy and microvascular thrombosis leading to organ dysfunction. Moretti et al have demonstrated an association between low preoperative endotoxin antibody levels and patient mortality.² Consequently, those patients with a reduced baseline immunity to endotoxin may be at increased risk for morbidity secondary to endotoxin release during cardiac surgery. Efforts are ongoing to identify therapies which would antagonize the contribution of endotoxin to systemic inflammation in the cardiac surgery patient.¹

Similarly, efforts have been undertaken to mitigate the inflammatory response to CPB (Chapter 17). Complement activation is associated with CPB and with multiorgan injury. The inhibition of complement component 5 (C5) during CPB has been studied and shown to decrease the production of terminal complement cascade components and reduce inflammation tissue injury.³ Complement mediated activation of leukocytes results in tissue injury. Complement activation also promotes neutrophil accumulation in the lungs resulting in perioperative respiratory failure.⁴ Activated neutrophils generate oxygen-free radicals and proteases producing inflammation-mediated tissue injury in many organ systems.

The inflammatory response has also been shown to be modulated by the use of perioperative statin therapy.^5,6 Statins were initially employed to lower serum cholesterol concentrations through 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase inhibition. The overwhelming majority of patients presenting for cardiac anesthesia and surgery are on preoperative statin therapy. Although effective in lowering cholesterol, statins have also been shown to decrease inflammation, reduce thrombosis, and minimize ischemia-reperfusion injury. Patients on statins are at risk of increased morbidity if the statins are discontinued perioperatively. Statins inhibit generation of isoprenoids, which bind to Rho and Ras guanosine triphosphatases. Therefore, through the inhibition of Rho, statins have direct anti-inflammatory effects, and lead to a reduction in inflammatory cytokines, an increase in anti-inflammatory cytokines and an up-regulation of endothelial nitric oxide (NO) synthetase.⁵ Consequently, statins result in less inflammation but increased NO production. Moreover, statins increase thrombomodulin expression and reduce tissue factor expression on endothelial cells resulting in an antithrombotic effect. Since inflammatory and thrombotic effects can contribute to neural, cardiac, and renal injury perioperatively, preoperative statin therapy may reduce all these. Discontinuation of statin therapy results in down-regulation of endothelial nitric oxide synthetase reducing production of vasodilating nitric oxide.

Investigations of various agents to modulate the inflammatory response to cardiac surgery are ongoing and likely to become increasingly important in the management of the cardiac surgery patient.

GENETIC ASSOCIATIONS AND CARDIAC SURGERY OUTCOMES

Whereas inflammation and thrombosis may contribute to adverse outcomes secondary to organ failure following cardiac surgery, ultimately the degree of the inflammatory response and the propensity toward a thrombotic state are determined by the patient’s genotype. Gene association studies performed on cardiac surgery patients have attempted to identify the risk factors associated with perioperative organ injury.^7–10

These studies attempt to identify genotypes associated with adverse cardiac, renal, and neurological events perioperatively. Even though these studies may illustrate why and how certain patient populations respond to cardiac surgery, individualized anesthetic management based upon genotype may never become manifest. However, knowledge of the genotypes associated with adverse outcomes provides insight as to the disease mechanisms at work leading to poor outcomes. So far, genetic influences have been demonstrated to impact inflammation, response to endotoxin, perioperative dysrhythmias, neurocognitive dysfunction, renal failure, and thrombosis.^8,9

Although it is currently not possible to identify the propensity for an adverse outcome in routine patient management, it is increasingly likely that common allelic variations associated with poor outcomes will become at some point part of preoperative screening and may ultimately be factored into clinical decision making and risk/benefit discussions prior to undertaking surgery. At the same time, the fact that such analyses could be used to deny patients therapy based upon genotype certainly raises ethical questions well beyond the scope of this text.

PERIOPERATIVE NEUROLOGICAL INJURY

There is little as discouraging to cardiac anesthesiologists and surgeons as to conduct what is thought to be an “uneventful” case only to find that the patient emerges from anesthesia with a postoperative neurological deficit. The landmark study of Roach et al identified the problem of adverse cerebral outcomes following coronary bypass surgery.¹¹ They noted that 6.1% of patients experienced an adverse neurological outcome. These outcomes were identified as being either type I or type II injuries. Type I injuries (3.1% of the study population) were comprised of focal injuries, stupor, or coma at the time of hospital discharge. An additional 3% had a type II injury defined as deterioration in intellectual function, memory deficit, or seizures. Since 1996, numerous studies have been undertaken to better identify and reduce the incidence of type I and type II injury.

Moderate-to-severe proximal aortic atherosclerosis is associated with an incidence of type I adverse cerebral outcomes at least four times of that among patients without the condition.¹¹ Manipulation of the atheromatous aorta during cardiac surgery can produce multiple emboli leading to neurological injury. Consequently, many efforts to reduce neurological injury perioperatively are directed at minimizing embolic load during aortic manipulation. TEE and epiaortic ultrasound (EUA) as well as direct palpation have been employed to avoid manipulation of areas of the aorta with significant atheromatous disease. Manipulation of the atherosclerotic aorta can be avoided through the so-called “no-touch” approaches.¹² Also, selective aortic cannulation is used to avoid a “sandblast” effect of the aortic perfusion cannula. Other risk factors associated with type I neurological injury include prior neurological abnormality (stroke or transient ischemic abnormality), diabetes mellitus and the use of a left ventricular vent or an intra-aortic balloon pump. Patients undergoing “open chamber” cardiac procedures such as valve replacement are also at higher risk for type I neurologic injuries.¹³ Maintenance of a perfusion pressure of more than 70 mm Hg and avoidance of hypoperfusion during CPB may minimize areas of potential cerebral underperfusion and promote washout of microemboli from the cerebral vasculature. Off-pump techniques may reduce but do not eliminate the risk of perioperative focal neurological injury.¹⁴ Although reduction in the incidence of stroke with off-pump techniques has been suggested, studies remain inconclusive.¹³

Type II injury is more difficult to identify and often requires psychometric testing to detect.^15,16 Cognitive function is assessed through tests of verbal memory and language comprehension, abstraction, attention, concentration, and visual memory.¹⁵ At hospital discharge following cardiac surgery nearly 50% of patients show a decline from baseline in at least one of the domains of cognitive function.¹⁵ Risk factors associated with the development of type II neurologic injuries are a history of alcohol abuse, peripheral vascular disease, cerebral hypoperfusion during CPB and hyperthermia during rewarming from CPB.^11,15

Allelic variation has also been associated with an increased incidence of cognitive dysfunction.^17,18,9 Mathew et al examined gene candidates associated with inflammation, cell adhesion, thrombosis, lipid metabolism, and vascular reactivity and looked for associations with cognitive dysfunction at 6 weeks postoperatively. They identified allelic variations in the genes coding for P-selectin and C-reactive protein (CRP), which were associated with a reduced incidence of postoperative cognitive dysfunction. Similarly, Grocott et al¹⁷ showed that genetic variants coding for CRP and interleukin-6 (IL-6) may be associated with an increased incidence of type I injury through their effects on the inflammatory response.

Many patients present to surgery with preoperative cognitive impairment¹⁹ and cognitive impairment detected on postoperative analysis may merely reflect a preoperative condition.

Nonetheless, irrespective of a patient’s genetic predisposition toward an exaggerated inflammatory response or whatever their unknown preoperative condition, adverse neurological results have deleterious health, economic, and legal ramifications. Patients with focal neurological signs are generally evaluated by neurologists and receive supportive and rehabilitative care.

Type II injuries are often more subtle to detect and frequently it is a patient’s family and friends who detect that their loved one is not as “sharp” as they were prior to surgery. Unfortunately, cognitive deficit present at hospital discharge represents a predictor of cognitive dysfunction 5 years later.¹⁵

Patients that suffer a postoperative cardiac arrest are at obvious risk for neurological injury and require restoration of cardiac function. Most ICUs currently have a therapeutic hypothermia protocol to provide patient cooling in the setting of a survived, postoperative arrest in order to minimize neurological injury.^20,21 Such protocols attempt to cool the patient for 24 hours to 33°C. Midazolam or propofol and a muscle relaxant (eg, vecuronium) are administered for sedation and prevention of shivering, respectively. Close monitoring of arterial blood gases is required during hypothermia and blood glucose control with insulin may be necessary secondary to hypothermia-induced hyperglycemia.

RESPIRATORY FAILURE

Most patients following cardiac anesthesia and surgery can be readily separated from ventilatory support either in the operating room or within a few hours postoperatively.²² Although intraoperative extubation at the end of surgery can be performed in patients with relatively well-preserved ventricular function and limited pulmonary disease, such individuals are increasingly rare in cardiac anesthesia practice.

Nonetheless, many patients can be awakened fairly quickly following surgery and weaned from ventilatory support. Prior to weaning the patient from the ventilator, the ICU team confirms that the CXR is free of any overt pathology (eg, a collapsed lobe, pneumothorax, hemothorax) and any lung-related problem is corrected (bronchoscopy, chest tube, etc). The arterial blood gas should be adequate for extubation. Additionally, the patient should require a FiO₂ < 50% with minimal positive end-expiratory pressure (PEEP ≤ 5 cm H₂O) and adequate tidal volume (approximately 5 mL/kg) and respiratory rate (less than 30 breaths per minute). The chest is auscultated to rule out the presence of bronchospasm. The patient’s neurological examination should be intact with the patient capable of airway protection at the time of extubation. Lastly, the patient should be hemodynamically stable such that the probability for return to the operating room and hemodynamic collapse is considered low.

Failure to wean from the ventilator following cardiac surgery has many etiologies including:

• Impaired pulmonary compliance secondary to fluid overload or inflammatory lung disease

• Bronchospasm, airway compromise

• Ventricular failure

• Neuromuscular blockade, anesthetic effects

• Delirium, stroke

• Metabolic acidosis

• Pain

Each of these etiologies must be considered and corrected before weaning can be successful. Failure to wean is often heralded by tachypnea, desaturation, hypertension, and tachycardia.

Many patients who present for cardiac surgery have associated pulmonary disease following many years of smoking. Other patients have no pulmonary history but can develop respiratory failure nonetheless following heart surgery.⁴ Inflammation following heart surgery with CPB is secondary to activation of the complement cascade, ischemia-reperfusion injury, and endotoxemia from the potentially hypoperfused gut. The inflammatory response to CPB can lead to acute lung injury. Neutrophils accumulate in the lung and contribute to lung tissue injury producing an increasing alveolar-arterial oxygen gradient, lung edema, reduced pulmonary compliance, increased pulmonary vascular resistance, and right heart dysfunction. Although most patients tolerate CPB-induced inflammatory lung injury, up to 1% of cardiac surgery patients⁴ develop life-threatening acute respiratory distress syndrome (ARDS).

RENAL DYSFUNCTION

Patients with impaired preoperative renal function are at increased risk for worsened postoperative renal dysfunction.^23,24 More than 8% of the patients undergoing cardiac surgery experience renal injury and up to 1% develop renal failure requiring dialysis.^25–27 Glomerular filtration rate (GFR) can decrease from greater than 100 mL/min to less than 20 mL/min secondary to ischemic or nephrotoxic kidney injury. Emboli and hypoperfusion can injure the kidney during cardiac surgery. Indeed, patients with postoperative stroke have an increased peak of creati-nine levels postoperatively compared to patients with uneventful surgery.²⁵ Antifibrinolytic agents (ie, aprotinin and to a lesser extent epsilon aminocaproic acid) may contribute to perioperative renal injury. Contrast dyes, antibiotics, angiotensin-converting enzyme (ACE) inhibitors, and nonsteroidal anti-inflammatory agents can all contribute to toxic renal injury. Compound A, resulting from the degradation of sevoflurane, has also been described as a potential perioperative cause of renal dysfunction.

Low urine output should be addressed by correcting any pre- or post-renal causes. Hypovolemia, ventricular failure, and hypotension should be corrected. Kinked or occluded bladder catheters need to be managed accordingly. Patients manifesting a small increase in serum creatinine perioperatively may in reality have significant decreases in GFR.²⁴ Consequently, renal dysfunction should be suspected in the post-cardiac surgery patient with a rising creatinine and nephrology consultation obtained. Of course, most cardiac surgery patients demonstrate a mild creatinine increase on the second postoperative day.²⁵

Operative patients with preoperative serum creatinines greater than 2.5 mg/dL have a 30% chance of developing acute renal failure.²⁸ Additional factors that contribute to the development of perioperative acute renal failure include: duration of CPB, presence of diabetes mellitus, presence of a carotid bruit as a sign of the presence of atherosclerosis and peripheral vascular disease, reduced ejection fraction, and increased body weight.²⁸ These factors as well as genetic associations may permit anesthesiologists to better identify those patients at risk for perioperative renal dysfunction.

When ARF occurs, management is supportive in consultation with a nephrolo-gist. Renal replacement therapy may be required to correct acid/base and electrolyte concentrations in addition to removing excess fluid accumulated during cardiac surgery. Patients on dialysis taken to surgery often require immediate postoperative dialysis to remove excessive potassium following repeated administrations of potassium-rich cardioplegia solution during the bypass run. Unfortunately, hemodialysis can lead to hemodynamic instability perioperatively necessitating close attention by the ICU team.

Many agents including renal dose dopamine and fenoldopam have been found ineffective for preventing postoperative renal dysfunction.²⁹ Nesiritide, a B-type natriuretic peptide was initially suggested to attenuate the decline in glomerular filtration rate associated with cardiac surgery. The physiologic mechanisms by which nesiritide supposedly attenuates renal impairment may be secondary to overall improved hemodynamic profile in acute heart failure patients resulting in peripheral vasodilation, natriuresis, inhibition of the renin-angiotensin-aldosterone system, and improved renal perfusion. Other reports have suggested that in patients with heart failure, nesiritide actually worsens renal function.³⁰

Postoperative kidney failure contributes to perioperative mortality especially when combined with other organ systems’ failures and the search for renoprotective strategies during cardiac surgery remains ongoing.

ICU HEMODYNAMICS

Hemodynamic principles whether in the operating room or the ICU remain essentially the same for the management of the cardiac surgery patient. Consequently, strategies used during surgery remain in effect when the patient is transferred to ICU care and as such will not be reviewed here. Nonetheless, postoperative hypertension can be particularly problematic following cardiac surgery. More than 50% of cardiac surgery patients require intravenous antihypertensive medications.³¹ Uncontrolled postoperative hypertension can lead to cerebral edema, stroke, bleeding around aortic suture lines, and aortic dissections. However, when treating hypertensive episodes consideration should be given to the fact that in patients with uncontrolled chronic hypertension the autoregulation of organ blood flow tends to shift toward higher pressures.³¹ Ideally, mean arterial pressure should be maintained within 20% of the patient’s baseline to prevent decreases in organ blood flow associated with shifted autoregulatory thresholds. However, in the postoperative cardiac surgery patient mean arterial pressure may need to be reduced by greater than 20% of the patient’s baseline should postoperative conditions (eg, aortic dissection, anastomotic bleeding at surgical suture lines) be of concern.

There are many agents available for blood pressure control postoperatively. Propofol can be administered along with narcotics when indicated in patients requiring ongoing ventilatory support.

Intravenous antihypertensive agents employed include:

1. Sodium nitroprusside (SNP) is well associated with the release of cyanide and cyanide toxicity. SNP produces both arterial and venous dilation and can lead to dramatic swings in blood pressure leading to potentially reduced organ perfusion.

2. Nicardipine is a calcium antagonist that provides more selective arterial vasodilation. Clevidipine,^32,33 a rapid-acting calcium antagonist, has recently been shown to be an effective, direct acting, arterial vasodilator. Unlike nicardipine, clevidipine has a very short half-life (1 min), which makes it useful for rapid titration to effect.

3. Fenoldopam a vasodilatory dopamine agonist was once thought to provide renal protection perioperatively; however, subsequently, like nesiritide, its ability to “protect” the kidney has been questioned.

4. As previously noted, nesiritide is a synthetic natriuretic peptide with vasodilatation and natriuretic properties. Unfortunately, it has been found to worsen renal function in heart failure patients.

5. Beta-blockers are generally administered to patients following cardiac surgery if tolerated to avoid dysrhythmias. However, in the immediate postoperative period there may be reluctance to administer intravenous beta-blockers in patients with limited ventricular function.

The management of heart failure and hypotension in the immediate postoperative period continues from the operating room. Inotropes, vasoconstrictors, and fluids are administered in response to the interpretation of hemodynamic monitors and perioperative echocardiography.

Atrial fibrillation (AF) complicates the postoperative course in 10% to 65 % of the patients.³⁴ Risk factors associated with postoperative AF include advanced age, previous history of AF, male gender, decreased left-ventricular ejection fraction, left atrial enlargement, valvular heart surgery, chronic obstructive pulmonary disease, chronic renal failure, diabetes mellitus, and rheumatic heart disease.³⁵ Atrial fibrillation occurs most frequently within 2 to 4 days postoperatively.³⁴ Re-entrant atrial mechanisms are thought primarily responsible for the development of atrial fibrillation and may be associated with inflammation, ischemia, increased sympathetic tone, and atrial suture lines. Postoperative hypomagnesemia may also contribute to the development of atrial fibrillation supporting routine intravenous magnesium replacement. Numerous drugs have been studied regarding prophylaxis of atrial fibrillation. The present data suggest that beta-blockers are effective and safe and should not be discontinued before cardiac surgery. Intravenous amiodarone also reduces the incidence of postoperative atrial fibrillation and may be used in high-risk patients.

Patients who develop postoperative atrial fibrillation are generally treated with beta-blockers and often convert to sinus rhythm. Patients who are hemodynamically unstable require synchronized cardioversion. Intravenous amiodarone can be administered to convert atrial fibrillation to sinus rhythm and can be continued orally in patients who require antiarrhythmic prophylaxis following hospital discharge. Patients with persistent atrial fibrillation should be started on anticoagulant therapy after 48 hours of AF and should have TEE examination to rule out the presence of atrial clot prior to attempts at cardioversion.

Ventricular tachyarrhythmias also frequently complicate the immediate postoperative period. Ventricular fibrillation (VF) requires immediate defibrillation. Altered sympathetic tone, inflammation, embolic phenomena, electrolyte abnormalities, mechanical effects, pacemaker dysfunction, myocardial ischemia, ventricular scarring, and a legion of other possible etiologies can contribute to the development of postoperative ventricular fibrillation. Usually, it is impossible to identify the cause of VF in a particular patient when it occurs. Ventricular tachycardia occurs most frequently postoperatively in patients having both coronary bypass and concurrent valve surgery.³⁶ Low ventricular ejection fraction is considered the strongest risk factor for the development of sustained ventricular tachycardia and ventricular fibrillation. Nonetheless, ventricular tachycardia and ventricular fibrillation can occur in any cardiac surgery patient. Amiodarone also is useful in suppressing ventricular arrhythmias postoperatively.

Patients can also experience varying degrees of heart block after separation from CPB. Placement of epicardial pacemaker leads is routine in cardiac surgery and patients can require atrial or atrial-ventricular pacing depending upon the degree of heart block present. Temporary pacing as established in the operating room (Chapter 4) is continued to the ICU. Usually, a DDD mode (dual-chamber pacing, dual-chamber sensing, dual-chamber inhibition) is selected. If the patient has an appropriate intrinsic rhythm and rate, the pacemaker is set as a backup at a low heart rate (usually 60 bpm).

ANALGESIA, ELECTROLYTES, GLUCOSE

Postoperative pain is usually controlled with parenteral opioids. Nonsteroidal anti-inflammatory drugs (NSAIDs) have also been employed (eg, ketorolac). Obviously, there are potential complications from the use of NSAIDs related to gastrointestinal bleeding, platelet function, and renal function. Intrathecal morphine has been advocated to improve postoperative analgesia.^37,38 However, intrathecal morphine in combination with large doses of systemic narcotics may increase requirements for postoperative ventilatory support. Thoracic epidural analgesia has also been employed, however, the risk of epidural hematoma formation following catheter placement in patients who are to be administered large doses of heparin has retarded the use of neuraxial techniques in cardiac surgery patients.

Electrolyte disturbances are very common following cardiac surgery and arterial blood gas, serum electrolytes, and blood glucose should be closely monitored during the immediate postoperative period.

Hypokalemia is often secondary to diuresis and requires potassium replacement. Hyperkalemia also occurs perioperatively, particularly, in patients with renal dysfunction. Regular insulin and glucose can be given to shift potassium intracellularly. Increasing ventilation and/or administering sodium bicarbonate can correct acidosis. Hypocalcemia is usually self-correcting following cardiac surgery and is often associated with a decreased serum albumin concentration (if total calcium is measured) or blood product transfusions. Reduced ionized calcium if symptomatic can be treated with calcium chloride administration. Likewise, hypomagnesemia can be corrected through the administration of parenteral magnesium sulphate.

Perioperative glucose control with insulin is often required. Regular insulin infusions are maintained through to the ICU.

Postoperative bleeding and coagulopathy are discussed in detail in Chapter 16. Chest tube drainage of greater than 300 mL/h must be closely watched and may require surgical reexploration. Supplemental protamine can be given in the ICU to treat so called “residual heparin” or “heparin rebound” and blood products are administered as clinically indicated.

ECHOCARDIOGRAPHY IN THE ICU

The role of transthoracic echocardiography (TTE) and TEE in the ICU is primarily evaluation of hemodynamic instability. Causes of hemodynamic instability in the immediate postoperative period are numerous including graft thrombosis with resultant ischemia and right or left heart dysfunction, pericardial tamponade, valvular dehiscence, and hypovolemia. In all these instances, TEE/TTE can potentially identify the cause of instability in a matter of minutes.

Pericardial tamponade³⁹ often presents with nonspecific signs and symptoms. Tachycardia, increased pressor requirements, hypotension, rising central venous pressures, pulsus paradoxus can all herald its presence. Patients with chronic pericardial fluid accumulations often tolerate large amounts of fluid before clinical tamponade is overt. In the immediate postoperative period localized collections of clot compressing on cardiac chambers can impair cardiac function (Videos 14–1 and 14–2). Reopening of the sternum and removal of the clots restores the normal chamber geometry and hemodynamic stability.

Anesthetic management of the patient with postoperative pericardial tamponade depends on the time course of its development and the degree of hemodynamic compromise. Intubated patients with acute pericardial tamponade are brought emergently to the operating room. In this scenario the patient needs to be transported to the operating room for reexploration, removal of any compressing clots, and correction of any source of surgical bleeding. Transport to the operating room can be problematic as such patients often have increasing pressor requirements and are unstable. At times, the sternum must be opened in the intensive care unit if transport is not deemed feasible due to patient instability. Full monitoring, airway equipment, and resuscitative drugs must accompany the patient from the ICU to the operating room in the presence of the anesthesiology and surgery staff.

Patients with chronic effusions from either pericardial disease processes (malignancy, infection, uremia) may require creation of a pericardial window. Some of these patients might have had a pericardiocentesis prior to the presentation for the creation of pericardial window with subsequent amelioration in their symptoms. Such patients often can have general anesthesia induced uneventfully. Other patients will present with unrelieved, symptomatic tamponade and may become hemodynamically unstable following the induction of anesthesia and institution of positive pressure ventilation. Invasive arterial pressure monitoring and reliable venous access is necessary prior to induction of anesthesia. These patients may tolerate very poorly the institution of positive pressure ventilation and spontaneous breathing has to be maintained throughout induction and endotracheal intubation. The surgical staff should be present and ready to emergently open the chest and relieve the tamponade immediately following induction should severe, irreversible hemodynamic instability ensue. TEE is useful to guide therapy and to ensure that all areas of localized compression are free of clot and fluid. TEE can also demonstrate the presence of left and right pleural effusions (Video 14–3). The presence of fluid in the chest following surgery can decrease pulmonary compliance and make oxygenation difficult. Prior to chest closure in the operating room the pleural spaces should be examined and thoroughly suctioned of any residual fluid. TEE is also employed in the ICU for the examination of the atria prior to attempts at elective cardioversion for atrial fibrillation.

SUMMARY

This chapter provides an overview of many of the acute postoperative events, which can occur in the ICU following cardiac surgery. Patients with prolonged ICU stays may develop additional problems related to infections, skin breakdown, and nutritional concerns. Review of any ICU manual will touch on approaches to the management of ICU acquired infections and nutritional support. Patients with sternal wound infection often require return to the operating room for debridement and stabilization, days to weeks postoperatively. General anesthesia is required and invasive arterial pressure monitoring advised particularly if the patient manifests signs of systemic sepsis.

The involvement of cardiac anesthesiologists in the postoperative care of the cardiac surgery patient varies between institutions. Irrespective of the local operating paradigm, the cardiac anesthesiologist will find much reward in visiting all patients postoperatively.

REFERENCES

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