Technique

Open heart surgery with cardiopulmonary bypass requires cannulation of the ascending aorta and vena cava or right atrium with drainage of venous blood to a reservoir. The venous blood is pumped through a membrane oxygenator and routed via an arterial filter to a cannula in the aortic arch ( Fig. 3-1 ). Clamping the aorta and insertion of the aortic cannula can dislodge atheromatous material in a severely diseased aorta, thereby leading to cerebral embolization. High-velocity or turbulent blood flow from the end of the cannula may also dislodge emboli. Intraoperative identification of aortic atheroma is possible with transesophageal echocardiography or the more sensitive epiaortic ultrasound technique ( Fig. 3-2 ). Such imaging demonstrates atherosclerotic plaque in 25 to 50 percent of patients undergoing CABG and may alter surgical management. The frequency of such aortic disease increases with age and is particularly prominent in patients older than 70 years.

Schematic of an extracorporeal circulation circuit used in cardiopulmonary bypass surgery.

(Modified from Machin D, Allsage C: Principles of cardiopulmonary bypass. Contin Educ Anaesth Crit Care Pain 6:176, 2006 with permission from Oxford University Press.)

Transesophageal echocardiography of the aorta. A , Normal aorta (Ao), also illustrating the aortic valve (AV) and the takeoff of the right coronary artery ( arrow ). B , Atherosclerotic plaque protruding into the aorta ( arrow ). C , Two large thrombi ( arrows ) associated with atherosclerotic plaque.

(Modified from Di Tullio MR, Homma S. Atherosclerotic disease of the proximal aorta. p. 741. In Mohr JP, Wolf PA, Grotta JC, et al (eds): Stroke. 5th Ed. Elsevier, Philadelphia, 2011, with permission from Elsevier.)

A secondary venous-to-arterial circuit is initiated by blood suctioned from the pericardial surgical field ( Fig. 3-1 ). This cardiotomy suction blood contains fat and debris that could form cerebral emboli if directly reinfused into the arterial circulation. Therefore, the blood is directed to a cardiotomy reservoir where it is filtered and processed in order to remove embolic material before being reintroduced to the circulation.

Extracorporeal circulation is used in association with systemic heparinization and hemodilution. When blood is exposed to the nonbiocompatible surfaces of the bypass circuits, a prothrombotic system inflammatory response is induced. Anticoagulation is used to prevent thrombus formation. Hemodilution is thought to improve microcirculatory flow by reducing blood viscosity. Excessive hemodilution is avoided because it reduces the oxygen-carrying capacity of blood and increases postoperative adverse outcomes.

The optimal mean arterial pressure and body temperature for cardiac surgery remain unclear. In many centers, an attempt is made to maintain the mean arterial pressure above 50 mmHg; others aim it above 70 mmHg in patients with prominent risk factors for cerebrovascular disease. The majority of cardiac bypass procedures use hypothermia for neuroprotection of the brain, but a meta-analysis of 19 randomized controlled trials comparing hypothermic cardiac surgery with normothermic surgery did not identify a clear advantage of either approach. It is still recommended, however, to use slow rewarming rates and to avoid temperatures above 37°C in order to reduce postoperative neurocognitive impairment.

Acute Brain Disorders

Stroke, encephalopathy, coma, and seizures are the major acute brain disorders complicating cardiac surgery. Stroke has decreased in frequency over the past two decades to less than 2 percent of patients undergoing CABG. Clinically silent stroke detected by magnetic resonance imaging (MRI) is probably more frequent. Stroke incidence increases with the number of preoperative stroke risk factors. Stroke after cardiac surgery leads to an approximately five- to sixfold increase in hospital mortality, prolongs length of stay in the intensive care unit, and typically requires inpatient rehabilitation or nursing home placement. The majority of stroke patients who survive to hospital discharge are substantially disabled. Stroke occurs more frequently when valvular heart surgery is combined with coronary artery bypass graft operations due to the additional risk of cerebral macroemboli with operations that require opening a heart chamber and removal or repair of diseased heart valves.

Ischemic stroke after cardiac surgery is most often the result of emboli or hypoperfusion. Diffusion-weighted brain MRI has identified watershed infarction as the cause of stroke after cardiac surgery and cardiopulmonary bypass in approximately half of stroke patients. Watershed infarction occurs at border zones between the major cerebral arteries and typically is associated with arterial hypoperfusion. More prolonged cardiopulmonary bypass time increases the risk of watershed stroke, and bilateral watershed stroke has a particularly poor outcome.

Intracranial hemorrhage is an infrequent cause of stroke, but its rapid identification is important to allow for urgent medical or surgical treatment. Hematomas may be located in the brain parenchyma itself or in the subdural or epidural space. Intracranial hemorrhage during cardiopulmonary bypass may be related to reduced platelet adhesion and coagulation factors.

Repair of severe aortic stenosis causes a rapid increase in brain perfusion pressure and rarely can cause focal neurologic signs with MRI evidence of vasogenic brain edema without acute infarction. Both the focal neurologic deficits and brain edema may be reversible.

Encephalopathy, reflecting a diffuse brain disorder, occurs in greater than 8 percent of adults following heart surgery. Its prevalence is even greater in patients older than 65 to 70 years and in patients with known preexisting cerebrovascular disease. These encephalopathic patients may be slow to emerge from anesthesia, can be agitated, and may have fluctuating impairment of cognitive and perceptual function. Hallucinations may be present and occasionally there are bilateral Babinski signs. Improvement often occurs during the first postoperative week. Some of these encephalopathic patients have multiple, acute, small ischemic brain lesions detected with MRI, suggesting multiple emboli. However, in many patients the cause of encephalopathy cannot be defined clinically. CABG without the use of cardiopulmonary bypass results in less frequent postoperative delirium, whereas prolonged operating time increases its frequency.

Electrolyte dysfunction can also lead to neurologic compromise following cardiac surgery. Postoperative hyponatremic encephalopathy is important to recognize and reverse because it can lead to brain edema, particularly in younger women. A hypoglycemic encephalopathy is a risk in patients who are under “tight” insulin control for diabetes. A hypernatremic hyperosmolar state is a rare cause of encephalopathy after cardiac surgery.

Persistent coma after uncomplicated cardiac surgery is infrequent, occurring in less than 1 percent of patients. It may be due to global anoxia-ischemia, massive stroke, or multiple brain infarctions. When anoxia-ischemia is the cause of coma, myoclonus, at times accompanied by seizures, may be prominent and poorly responsive to anticonvulsant therapy. The outcome in these comatose patients is usually extremely poor, with only a rare patient making a meaningful recovery. The benefit of postoperative therapeutic hypothermia in patients who are comatose immediately after heart surgery is unknown.

Seizures may accompany coma, encephalopathy, or delirium, or they may occur independently after cardiac surgery. They occur in approximately 1 percent of patients, usually early in the postoperative period and often within the first 24 hours. Some early seizures have been associated temporally with high-dose tranexamic acid, a drug that decreases postoperative bleeding. Tonic-clonic or focal motor seizures are clinically apparent, but focal seizures with dyscognitive features in an encephalopathic patient may be difficult to recognize clinically and require electroencephalography to make the diagnosis. Choreoathetosis after heart surgery, a complication that occurs mainly in children, sometimes is mistaken for a seizure disorder. Nonconvulsive status epilepticus may occur with stroke complicating cardiac surgery and can contribute to a prolonged confusional state that is treatable with anticonvulsant drugs; therefore, electroencephalographic evaluation of patients with a persistent encephalopathy can be valuable.

Peripheral Nerve Disorders

The brachial plexus and phrenic nerves are the most frequent peripheral nerves injured during cardiac surgery. Brachial plexopathy after median sternotomy has been reported to occur in 1.5 to over 5 percent of patients. Most frequently, the lower trunk of the brachial plexus is involved, which may mimic an ulnar neuropathy. The intrinsic hand muscles are often most severely impaired, but—unlike an ulnar neuropathy—the triceps reflex may be decreased in the affected arm. Sensory loss in the hand is sometimes present, pain is prominent in some patients, and a minority of patients have a Horner syndrome. Injuries of the upper brachial plexus also occur but are less frequent. Although not life-threatening and usually reversible in 1 to 3 months, a brachial plexus injury may produce permanent disability in some cases, particularly if it affects the dominant hand or produces intractable causalgia.

These brachial plexus injuries may be due to torsional traction or compression during the open heart surgery. Intraoperative electrophysiologic monitoring of sensory nerve conduction in the upper extremity reveals significant disturbances during sternal retraction in many patients. This technique can detect disorders of the brachial plexus during surgery, predict postoperative nerve injury, and identify intraoperative factors that predispose to brachial plexus injury. Brachial plexus injuries may be reduced by minimizing the opening of the sternal retractor, placing the retractor in the most caudal location, and minimizing asymmetric traction.

Unilateral phrenic nerve injuries with hemidiaphragmatic paralysis occur in over 10 percent of patients during open heart surgery. The location of the phrenic nerve adjacent to the pericardium makes it particularly vulnerable to injury from manipulation and ischemia as well as from hypothermia associated with topical cold cardioplegia. Unilateral phrenic nerve injury causes atelectasis and inspiratory muscle weakness, predisposing to postoperative respiratory complications. Phrenic nerve involvement in patients with preoperative chronic obstructive pulmonary disease adds to postoperative morbidity. In most patients, however, morbidity is low and some recovery is usually evident by about 6 months. Occasionally, there may be a more protracted course consistent with axonal injury and regeneration. Severe, bilateral phrenic nerve injury is a rare complication of heart surgery and leads to prolonged mechanical ventilation.

Mononeuropathies resulting from compression or trauma during surgery may involve the spinal accessory, facial, lateral femoral cutaneous, fibular (peroneal), radial, recurrent laryngeal, saphenous, long thoracic, and ulnar nerves. Ischemia to the cochlea-auditory nerve can result in severe hearing loss. A recurrent laryngeal nerve injury with vocal cord paralysis may cause only hoarseness when mild, but aspiration when severe or bilateral. Injury to the saphenous nerve when a saphenous vein is harvested for CABG may cause hyperesthesia, decreased sensation and pain along the medial lower leg. A persistent fibular (peroneal) neuropathy causes a disabling foot drop and may be due to positioning in the operating room. Most mononeuropathies are transient. This reversibility, usually within 4 to 8 weeks, may reflect focal selective injury to myelin, with relative sparing of nerve axons. Awareness of possible intraoperative compression sites helps to prevent these complications.

Diffuse paralysis as a result of the Guillain–Barré syndrome may follow otherwise uncomplicated cardiac surgery as well as other surgical procedures. Persistent paralysis also occurs after cardiac surgery in critically ill patients who require days of vecuronium to facilitate mechanical respiration. If heart surgery is complicated by sepsis and multiorgan failure lasting for more than a week, a critical illness polyneuropathy and myopathy may develop, with difficulty in weaning from the ventilator.

Neuro-ophthalmologic Disorders

Visual disorders associated with cardiac surgery may involve the retina, optic nerves, or retrochiasmal visual systems. Retinal disorders include multifocal areas of retinal nonperfusion, which occur in 44 to 100 percent of patients. Cotton wool spots have been reported in 17.3 percent of patients and retinal emboli visualized in 2.6 percent. These retinal disorders are infrequently associated with reduced visual acuity.

An anterior ischemic optic neuropathy is an uncommon, disabling complication, occurring in 0.1 percent or fewer patients after heart surgery. There is infarction of the optic nerve head and optic disc swelling, with a painless and usually permanent decrease in visual acuity. On visual field testing, a monocular altitudinal, arcuate, or central scotoma may be seen. A retrobulbar or posterior ischemic optic neuropathy due to infarct of the intraorbital nerve is even less common, producing acute blindness without optic disc swelling, accompanied by impaired pupillary reactions. Both the anterior and posterior ischemic optic neuropathies may produce unilateral or bilateral blindness.

Homonymous visual field defects occur with focal ischemic injury to the visual cortex or retrochiasmal visual pathways. An occasional patient is found to be cortically blind after heart surgery, usually from bilateral ischemia of the occipital cortex. Retinal and pupillary examinations are both normal in such patients and some will deny any visual impairment. At least partial recovery from cortical blindness is possible.

Horner syndrome occurs in association with injuries to the lower brachial plexus and may result from concomitant injury to the preganglionic sympathetic fibers that travel through the eighth cervical and first thoracic ventral roots. It also develops in the postoperative period in hypertensive and diabetic patients, presumably due to ischemic injury to sympathetic fibers.

Gaze deviation, gaze paralysis, and dysconjugate gaze may occur in postoperative patients who have a brainstem or large hemispheric stroke involving eye movement systems. Intermittent gaze deviation with nystagmoid movements raises concern for postoperative focal seizures.

Pituitary apoplexy resulting from acute hemorrhage or infarction of a pituitary adenoma is a rare complication of cardiopulmonary bypass. The pituitary tumor is usually not recognized prior to surgery and is particularly susceptible to the ischemic and hemorrhagic risks associated with cardiopulmonary bypass. Patients awake from surgery with headache, ptosis, ophthalmoplegia, and visual impairment from compression of the adjacent cranial nerves and the anterior visual pathways. Transsphenoidal surgical decompression has been used safely in some patients. Infarction of a normal pituitary during CABG also may occur and leads to panhypopituitarism.

Visual hallucinations occurring solely on eye closure have been reported following cardiovascular surgery. Patients are otherwise fully alert and lucid and can stop the hallucinations simply by opening their eyes. Atropine or lidocaine toxicity as well as focal seizures with dyscognitive features have been associated with such hallucinations.