The Bainbridge reflexorBainbridge effect (also called the atrial reflex) is a cardiovascular reflex causing an increase in heart rate in response to increased stretching of the wall of the right atrium due to increased filling of the right atrium with venous blood. It is detected by stretch receptors embedded within the wall of the right atrium, and regulated by a center in the medulla oblongata of the brain.
The Bainbridge reflex is involved in matching heart rate to effective circulating blood volume which is signified to venous return to the right atrium.[1] Mechanistically, the increased heart rate evoked by the Bainbridge reflex acts to increase the transit rate of venous blood across the heart into the arterial side of the cardiovascular system, thereby decreasing blood pressure on the venous side to reach a homeostatic equilibrium.[citation needed]
Bainbridge reflex also mediates respiratory sinus arrhythmia as intrathoracic pressure decreases during inspiration, causing increased venous return.[2]
The Bainbridge reflex may raise heart rate by as much as 40% to 60%.[3] The Bainbridge reflex and the baroreceptor reflex together control heart rate: the Bainbridge reflex responds to increased blood volume, whereas the baroreceptor reflex responds to changes in arterial blood pressure. The reflex is most potent when heart rate is low; when heart rate is already high, additional venous return to the right atrium (i.e. additional increases in blood volume) will indirectly cause relatively greater stimulation of arterial baroreceptor reflex which will in fact reduce the heart rate. Thus, the effect of the Bainbridge reflex on heart rate may be counteracted by the baroreceptor reflex so that the net effect is determined by the balance of both reflexes, or, rather, the balance of factors determining their individual amplitude.[3][4]
The Bainbridge reflex is active only when atrial stretch is above normal; when atrial stretch (and therefore effective circulating volume) is below normal, changes in atrial stretch do not evoke any Bainbridge reflex response. Below normal effective circulating volume will lead to proportional increases in heart rate - mediated by the baroreceptor reflex alone - to ensure adequate perfusion of tissues as well to compensate for decreased pumping efficiency of the heart due to decreased filling in accordance with the Frank–Starling law.[1]
Increased blood volume in the right atrium leads to inflates the atrium, stretching of the atrial walls. This stretching is sensed by atrial stretch receptors[3] (which are located at the venoatrial junction[4]), causing an increased in the firing rate of group B nerve fibers (low pressure receptors).[1] The information about the degree of atrial stretch is then conveyed through afferent fibres of the vagus nerve (cranial nerve X) to the medulla oblongata; efferents controlling heart rate (chronotropy) and contraction strength (inotropy) are then conveyed back to the heart through sympathetic nerves as well as the vagus nerve itself.[3] Unusually, this tachycardia is mediated by increased sympathetic activity to the SAN with no fall in parasympathetic activity.[citation needed] Effects on cardiac contractility[4][1] and stroke volume are insignificant.[1] Bainbridge reflex is attenuated by both anticholinergics and beta-adrenergic receptor antagonists of innervated hearts (as one or the other afferent part of the reflex arc that mediating the Bainbridge reflex is destroyed),[5] and can be entirely abolished by bilateral vagotomy (as the afferent portion of the reflex arc is entirely destroyed).[4]
The Bainbridge reflex is the predominant but not the only mechanism mediating increases in heart rate in response to increased atrial stretch: stretching of the pacemaker cells of the sinoatrial node has a direct positive chronotropic effect on the rate of the SA node, and may by itself increase heart rate by as much as 15%. This local response involves stretch-activated ion channels, as was demonstrated by stretching single isolated pacemaker cells while recording their cellular electrical activity.[6]
In 1915, Francis Arthur Bainbridge reported that infusing fluid into the circulatory system of dogs leads to an increase in heart rate regardless of whether arterial blood pressure changed, but only when central venous pressure increases enough to cause distension of the righ atrium. He also found that bilateral vagotomy abolished this response.[4]
Subsequent work demonstrated a stretch-induced increase in heart rate in isolated hearts or even the fully separated sinoatrial node (SAN).[7][8][9] Thus, the positive chronotropic response of the heart to stretch must, at least in part, have been accomplished by mechanisms related to the SA node itself. This led to the suggestion to refer to the response discovered by Bainbrindge as an 'effect' rather than a 'reflex'.[10]