Rapid-acting mechanisms for the regulation of systemic blood pressure involve nervous system responses as reflected by the baroreceptor reflexes, chemoreceptor reflexes, atrial reflexes, and central nervous system ischemic reflex. These reflex mechanisms respond almost immediately to changes in systemic blood pressure.
Baroreceptor Reflexes
Baroreceptors are nerve endings in the walls of large arteries in the neck and thorax, especially in the internal carotid arteries just above the carotid bifurcation and in the arch of the aorta.
These nerve endings respond rapidly to changes in systemic blood pressure and are crucial for maintaining normal blood pressure when an individual changes from the supine to standing position.
Chemoreceptor Reflexes
Chemoreceptors are cells that transduce chemical signals into nerve impulses. There are chemoreceptors located in the carotid bodies and aortic body. Each carotid or aortic body is supplied with an abundant blood flow through a nutrient artery so that the chemoreceptors are always exposed to oxygenated blood. When the systemic blood pressure, and thus the blood flow, decrease below a critical level, the chemoreceptors in the carotid body are stimulated by decreased availability of oxygen and also because of excess carbon dioxide and hydrogen ions that are not removed by the sluggish blood flow.
Chemoreceptors do not respond strongly until systemic blood pressure decreases below 80 mm Hg.
Chemoreceptors are more important in stimulating breathing when the Pao2 decreases below 60 mm Hg (ventilatory response to arterial hypoxemia). The ventilatory response to arterial hypoxemia is inhibited by subanesthetic concentrations of most of the volatile anesthetics (0.1 minimum alveolar concentration) as well as injected drugs such as barbiturates and opioids.
Central nervous system ischemic reflex occurs when blood flow to the medullary vasomotor center is decreased to the extent that ischemia of this vital center occurs. As a result of this ischemia, there is an intense outpouring of sympathetic nervous system activity, resulting in profound increases in systemic blood pressure. The central nervous system reflex response does not become highly active until mean arterial pressure decreases to less than 50 mm Hg and reaches its greatest degree of stimulation at systemic blood pressures of 15 to 20 mm Hg.
Cushing reflex is a central nervous system ischemic reflex response that results from increased intracranial pressure. When intracranial pressure increases to equal arterial pressure, the Cushing reflex acts to increase systemic blood pressure above intracranial pressure. Cushings triad is defined as having (a) hypertension, (b) bradycardia, and (c) irregular respirations (due to brainstem dysfunction). The latter is not often seen in this era, as most patients with severe intracranial hypertension are now mechanically ventilated.
Respiratory Variations in Systemic Blood Pressure
Systemic blood pressure normally varies by 4 to 6 mm Hg in a wavelike manner during quiet spontaneous breathing. This is due to increased venous return to the right heart during inspiration, which takes a few cardiac cycles to be transmitted to the left heart.
Positive pressure ventilation of the lungs produces a reversed sequence of blood pressure change because the initial positive airway pressure simultaneously pushes more blood toward the left ventricle.
Continuous or beat-to-beat monitoring of the changes in arterial blood pressure, pulse pressure, and stroke volume occurring during mechanical ventilation may provide an indication of the patients ability to respond to volume administration with an increase in cardiac output (fluid responsiveness). Respiratory variation in these parameters of more than 12% to 15% generally indicates fluid responsiveness.
Heart Rate Variability
Variations in heart rate occur during normal respiration, whereby inspiration increases heart rate and expiration decreases it. Analysis of heart rate variability provides information regarding the integrity of the autonomic nervous system.
Low heart rate variability can be a manifestation of disease (myocardial infarction, heart failure, neuropathy) and occurs universally following the denervation that occurs during cardiac transplantation.
Moderately Rapid-Acting Mechanisms for the Regulation of Systemic Blood Pressure. There are at least three hormonal mechanisms that provide either rapid or moderately rapid control of systemic blood pressure (catecholamine-induced vasoconstriction, renin-angiotensin-induced vasoconstriction, vasoconstriction induced by arginine vasopressin).
Long-term mechanisms for the regulation of systemic blood pressure, unlike the short-term regulatory mechanisms, have a delayed onset but do not adapt, providing a sustained regulatory effect on systemic blood pressure. The renal-body fluid system plays a predominant role in long-term control of systemic blood pressure because it controls both the cardiac output and systemic vascular resistance.