The Bainbridge reflex or Bainbridge 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. However, below normal effective circulating volume will likewise 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]
The heart is a muscular organ found in most animals. This organ pumps blood through the blood vessels of the circulatory system. The pumped blood carries oxygen and nutrients to the body, while carrying metabolic waste such as carbon dioxide to the lungs. In humans, the heart is approximately the size of a closed fist and is located between the lungs, in the middle compartment of the chest, called the mediastinum.
Blood pressure (BP) is the pressure of circulating blood against the walls of blood vessels. Most of this pressure results from the heart pumping blood through the circulatory system. When used without qualification, the term "blood pressure" refers to the pressure in a brachial artery, where it is most commonly measured. Blood pressure is usually expressed in terms of the systolic pressure over diastolic pressure in the cardiac cycle. It is measured in millimeters of mercury (mmHg) above the surrounding atmospheric pressure, or in kilopascals (kPa). The difference between the systolic and diastolic pressures is known as pulse pressure, while the average pressure during a cardiac cycle is known as mean arterial pressure.
The parasympathetic nervous system (PSNS) is one of the three divisions of the autonomic nervous system, the others being the sympathetic nervous system and the enteric nervous system. The enteric nervous system is sometimes considered part of the autonomic nervous system, and sometimes considered an independent system.
Baroreceptors are sensors located in the carotid sinus and in the aortic arch. They sense the blood pressure and relay the information to the brain, so that a proper blood pressure can be maintained.
Systole is the part of the cardiac cycle during which some chambers of the heart contract after refilling with blood.
The renin–angiotensin system (RAS), or renin–angiotensin–aldosterone system (RAAS), is a hormone system that regulates blood pressure, fluid and electrolyte balance, and systemic vascular resistance.
A cardiac function curve is a graph showing the relationship between right atrial pressure (x-axis) and cardiac output (y-axis). Superimposition of the cardiac function curve and venous return curve is used in one hemodynamic model.
The sinoatrial node is an oval shaped region of special cardiac muscle in the upper back wall of the right atrium made up of cells known as pacemaker cells. The sinus node is approximately 15 mm long, 3 mm wide, and 1 mm thick, located directly below and to the side of the superior vena cava.
Cushing reflex is a physiological nervous system response to increased intracranial pressure (ICP) that results in Cushing's triad of increased blood pressure, irregular breathing, and bradycardia. It is usually seen in the terminal stages of acute head injury and may indicate imminent brain herniation. It can also be seen after the intravenous administration of epinephrine and similar drugs. It was first described in detail by American neurosurgeon Harvey Cushing in 1901.
The baroreflex or baroreceptor reflex is one of the body's homeostatic mechanisms that helps to maintain blood pressure at nearly constant levels. The baroreflex provides a rapid negative feedback loop in which an elevated blood pressure causes the heart rate to decrease. Decreased blood pressure decreases baroreflex activation and causes heart rate to increase and to restore blood pressure levels. Their function is to sense pressure changes by responding to change in the tension of the arterial wall. The baroreflex can begin to act in less than the duration of a cardiac cycle and thus baroreflex adjustments are key factors in dealing with postural hypotension, the tendency for blood pressure to decrease on standing due to gravity.
The atrium is one of the two upper chambers in the heart that receives blood from the circulatory system. The blood in the atria is pumped into the heart ventricles through the atrioventricular mitral and tricuspid heart valves.
The cardiac cycle is the performance of the human heart from the beginning of one heartbeat to the beginning of the next. It consists of two periods: one during which the heart muscle relaxes and refills with blood, called diastole, following a period of robust contraction and pumping of blood, called systole. After emptying, the heart relaxes and expands to receive another influx of blood returning from the lungs and other systems of the body, before again contracting to pump blood to the lungs and those systems.
Central venous pressure (CVP) is the blood pressure in the venae cavae, near the right atrium of the heart. CVP reflects the amount of blood returning to the heart and the ability of the heart to pump the blood back into the arterial system. CVP is often a good approximation of right atrial pressure (RAP), although the two terms are not identical, as a pressure differential can sometimes exist between the venae cavae and the right atrium. CVP and RAP can differ when arterial tone is altered. This can be graphically depicted as changes in the slope of the venous return plotted against right atrial pressure.
Atrial volume receptors are low pressure baroreceptors that are found in the atria of the heart. They are myelinated vagal fibres in the endocardium found at the junction between atria and the vena cava/pulmonary vein.
Venous return is the rate of blood flow back to the heart. It normally limits cardiac output.
Reflex bradycardia is a bradycardia in response to the baroreceptor reflex, one of the body's homeostatic mechanisms for preventing abnormal increases in blood pressure. In the presence of high mean arterial pressure, the baroreceptor reflex produces a reflex bradycardia as a method of decreasing blood pressure by decreasing cardiac output.
The Bezold–Jarisch reflex involves a variety of cardiovascular and neurological processes which cause hypopnea, hypotension and bradycardia in response to noxious stimuli detected in the cardiac ventricles. The reflex is named after Albert von Bezold and Adolf Jarisch Junior. The significance of the discovery is that it was the first recognition of a chemical (non-mechanical) reflex.
High pressure receptors or high pressure baroreceptors are the baroreceptors found within the aortic arch and carotid sinus. They are only sensitive to blood pressures above 60 mmHg.
Low pressure baroreceptors or low pressure receptors are baroreceptors that relay information derived from blood pressure within the autonomic nervous system. They are stimulated by stretching of the vessel wall. They are located in large systemic veins and in the walls of the atria of the heart, and pulmonary vasculature. Low pressure baroreceptors are also referred to as volume receptors and cardiopulmonary baroreceptors.
Cardiac physiology or heart function is the study of healthy, unimpaired function of the heart: involving blood flow; myocardium structure; the electrical conduction system of the heart; the cardiac cycle and cardiac output and how these interact and depend on one another.