Bainbridge reflex
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]
Physiology
[edit]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]
Mechanism
[edit]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]
History
[edit]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]
See also
[edit]- Low pressure receptor
- Atrial natriuretic peptide: When the atrium stretches, blood pressure is considered to be increased and sodium is excreted to lower blood pressure.
- Renin-angiotensin system: When the blood flow through the juxtaglomerular apparatus decreases, blood pressure is considered low, and the adrenal cortex secretes aldosterone to increase sodium reabsorption in the collecting duct, thereby increasing blood pressure.
- Baroreflex: When the stretch receptors in the aortic arch and carotid sinus increase, the blood pressure is considered to be elevated and the heart rate decreases to lower blood pressure.
- Antidiuretic hormone: The hypothalamus detects the extracellular fluid hyperosmolality and the posterior pituitary gland secretes antidiuretic hormone to increase water reabsorption in the collecting duct.
References
[edit]- ^ a b c d e Boron, Walter F.; Boulpaep, Emile L., eds. (2017). Medical Physiology (3rd ed.). Philadelphia, PA: Elsevier. pp. 547–548. ISBN 978-1-4557-4377-3.
- ^ Pakkam, Madona L.; Moore, Marlyn J. (2024), "Physiology, Bainbridge Reflex", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 31082061, retrieved 2024-06-22
- ^ a b c d Hall, John E.; Hall, Michael E.; Guyton, Arthur C. (2021). Guyton and Hall Textbook of Medical Physiology (14th ed.). Philadelphia, PA: Elsevier. pp. 224–225. ISBN 978-0-323-59712-8.
- ^ a b c d e Koeppen, Bruce M.; Stanton, Bruce A.; Swiatecka-Urban, Agnieszka, eds. (2024). Berne & Levy Physiology (8th ed.). Philadelphia, PA: Elsevier. ISBN 978-0-323-84790-2.
- ^ Reitz, Bruce A.; Dong, Eugene; Stinson, Edward B. (May 1971). "The Bainbridge Reflex in Canine Cardiac Autotransplants". Circulation. 43 (5s1). doi:10.1161/01.CIR.43.5S1.I-136. ISSN 0009-7322.
- ^ Cooper PJ, Lei M, Cheng LX, Kohl P. Axial stretch increases spontaneous pacemaker activity in rabbit isolated sinoatrial node cells. J Appl Physiol (1985). 2000 Nov;89(5):2099-104. doi: 10.1152/jappl.2000.89.5.2099. PMID 11053369.
- ^ BLINKS JR. Positive chronotropic effect of increasing right atrial pressure in the isolated mammalian heart. Am J Physiol. 1956 Aug;186(2):299-303. doi: 10.1152/ajplegacy.1956.186.2.299. PMID 13362527.
- ^ Deck, K.A. Dehnungseffekte am spontanschlagenden, isolierten Sinusknoten. Pflügers Archiv 280, 120–130 (1964). https://doi.org/10.1007/BF00363751
- ^ Lange G, Lu HH, Chang A, Brooks CM. Effect of stretch on the isolated cat sinoatrial node. Am J Physiol. 1966 Nov;211(5):1192-6. doi: 10.1152/ajplegacy.1966.211.5.1192. PMID 4380793.
- ^ Rossberg F. Der Bainbridge-Effekt [The Bainbridge effect]. Z Gesamte Inn Med. 1973 Sep 1;28(17):513-8. German. PMID 4588170.
- Berne, R., Levy, M., Koeppen, B., & Stanton, B. (2004) Physiology, Fifth Edition. Elsevier, Inc.