Bainbridge reflex and hypovolemia

Daniel Weil, M.D. discusses the role of the Bainbridge reflex in hypovolemia.  Cardiac reflexes are reflex loops between cardiovascular structures and the CNS that regulate and modulate cardiac function and vascular tone. In 1915, Francis Arthur Bainbridge published an observation, which bears his name that intravenous volume administration produces tachycardia in anesthetized dogs.  The increase in venous return detected by stretch receptors in either atrium sends signals along vagal afferents to the cardiovascular center in the medulla. These afferent signals inhibit parasympathetic activity, i.e. vagus efferents, thus increasing the heart rate. The response is absent following bilateral vagotomy or heart transplant. This reflex caused by increased preload increases cardiac output by increasing the heart rate. The magnitude of the change in heart rate is dependent on the underlying heart rate before stimulation and baseline vagal tone. This reflex competes with the baroreceptor-mediated decrease in heart rate produced by volume expansion and is diminished or absent when the initial heart rate is high. Its physiologic role and clinical significance remains unsettled.

            The baroreceptor reflex is the dominant cardiovascular mechanism responsible for control of blood pressure.  Stretch receptors located in the carotid sinus and aortic arch send afferent impulses via the glossopharyngeal and the vagus nerves to the nucleus solitarius located in the cardiovascular center of the medulla. The baroreceptor reflex plays a dominant role during acute blood loss and shock. It is unlikely that one would observe a further increase in heart rate with volume administration during acute hemorrhage.  References: Bainbridge FA, The influence of venous filling upon the rate of the heart, J Physiol 1915;50:65-84; Secher NH, Jacobsen J, Friedman DB, Matzen S: Bradycardia during reversible hypovolaemic shock:   Associated neural reflex mechanisms and clinical implications. Clin Exp Pharmacol Physiol 1992;19, 733-743

Dr. Weil has completed his anesthesia residency and is now a fellow in Cardiac Anesthesia.