Cardiovascular Functions

The central neurons that control the circulatory system distribute diffusely in the pontine and medullary reticular core^[33] (see Chapter 18 ). Of these neurons, the vasomotor and cardioaccelerating neurons undergo negative-feedback control through the carotid and aortic sinus nerves, which relay at the nucleus tractus solitarius. Activation of these cells induces sympathetic nervous outflow, thereby increasing the heart rate and arterial blood pressure. Hypertension then suppresses these cells through the feedback mechanism, and circulation returns to preactivation levels.

During the process of brain death after head injury or intracranial bleeding, intracranial pressure increases, and compression of the brainstem leads to marked hypertension and bradycardia (i.e., the Cushing phenomenon). In an animal model of brain death, a precise mechanism of cardiovascular responses by the progression of CNS ischemia as a result of an expanding supratentorial mass was studied. When the entire cerebrum was ischemic, vagal activation with resultant decrease in heart rate, mean arterial pressure, and cardiac output was observed. As ischemia progresses rostrally to approach the pons, sympathetic stimulation was added to vagal stimulation, leading to bradycardia and hypertension (Cushing phenomenon). When the entire brainstem became ischemic,

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Some authorities think that myocardial damage may occur at this stage of autonomic storm, which may contribute to the early failure of some transplants and obscure or complicate the histologic manifestations of rejection in others.^[34] However, in humans, this stage of tachycardia and hypertension may be brief, and attempts to reduce blood pressure may not be necessary or even not be recommended. ^{[35] [36]} When intracranial pressure is elevated, arterial blood pressure suddenly decreases ( Fig. 79-1 ). This sudden decrease is the sign of tonsillar herniation (i.e., herniation of the cerebellar tonsils) through the foramen magnum on the cervical spinal cord, in which outflow of the cardioaccelerating and vasomotor neurons to the spinal cord suddenly ceases. This is one typical onset for brain death. Such dramatic changes in arterial blood pressure are not observed in other types of brain death such as that induced by hypoxia or those involving other intricate factors. Adequate volume replacement with balanced salt solution or colloid solution and, in some cases, blood transfusion is required. Inotropic agents, such as dopamine, epinephrine, and norepinephrine, are sometimes required to maintain an adequate blood pressure. The additional use of vasopressin or catecholamines may be beneficial for maintaining hemodynamic stability and renal function of brain-dead patients.^{[13] [37]}

The vasomotor and cardioaccelerating neurons of the spinal cord (located in the lateral horn) obtain automaticity within several days of disconnection from the supraspinal structures, and arterial blood pressure returns to normal without supplementation with vasopressors.^[38] This situation is familiar to anesthesiologists because background arterial blood pressure is usually normal in tetraplegic patients.

Figure 79-1 The representative time course of arterial blood pressure and heart rate before and after brain death. The 18-year-old male patient was involved in a traffic accident. Sustained hypertension was followed by a sudden and marked decrease in blood pressure. Dopamine was administered to increase blood pressure, which gradually became stable. Doses of dopamine were tapered and finally became unnecessary.

After the establishment of brain death, different types of autonomic spinal cord reflexes develop, such as elevation of arterial blood pressure because of bladder distention. Surgical stimulation-induced hypertension and tachycardia are well known by anesthesiologists in tetraplegic patients. A similar phenomenon has been observed in brain-dead patients.^[39] Vasodilators or general anesthesia, or both, may be used during the donation operation.^[40] Although the cardioaccelerating and vasomotor neurons are located in the brainstem, changes in arterial blood pressure are not used as an index of brainstem function.