Bainbridge Reflex

Bainbridge reflex was described first in 1915 by Francis Bainbridge (English physiologist, 1874–1921). He discovered and demonstrated that “saline or blood infusion into the jugular vein of the anesthetized dog” would result in reflex tachycardia.

This reflex is also called the “atrial reflex” and involves increased heart rate in response to dilation of “the main systemic veins, left and right atrium.” In response to dilation of the right atrium, stretch receptors located in the right atrium (i.e., venoatrial stretch receptors) are activated and send their impulse through the vagus nerve (tenth cranial nerve) to CNS; this is why the reflex is blocked if the patient is premedicated with atropine. Also, in animal studies, this reflex is blocked by “bilateral vagotomy or combined cholinergic and beta-adrenergic blockades.”
After being processed in the CNS, the response to the afferent impulse would result in increased sympathetic tone, which in turn would cause increased contractility and tachycardia which finally helps emptying of the heart. Simply saying, the “Bainbridge reflex” causes “hypervolemia-induced tachycardia.”The efferent limb of the reflex is mediated through the sympathetic pathways. In cardiovascular physiologic pathways, the Bainbridge reflex plays an important role and has control over heart rate and other hemodynamic variables; also, the effects of the Bainbridge reflex are in contrary to the effects of the “carotid baroreceptor reflex.” This reflex is sensed in the atria through the atrial type B mechanoreceptors; these receptors are located at the junction of venae cavae and the right atria and the junction of pulmonary veins and left atria, which in turn would trigger the neural pathway of the reflex

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CARDIAC REFLEXES