bathmotropic

{{Short description|Agent affecting the excitability of the heart}}

Bathmotropic often refers to modifying the degree of excitability specifically of the heart; in general, it refers to modification of the degree of excitability (threshold of excitation) of musculature in general, including the heart. It especially is used to describe the effects of the cardiac nerves on cardiac excitability.Miriam Webster's Medical Dictionary and Online Medical Dictionary Positive bathmotropic effects increase the response of muscle to stimulation, whereas negative bathmotropic effects decrease the response of muscle to stimulation.{{Cite web |url=http://www.thekanjifoundrypress.com/b.html |title=The Kanji Foundry Press - b |access-date=2008-05-14 |archive-url=https://web.archive.org/web/20080312073454/http://www.thekanjifoundrypress.com/b.html |archive-date=2008-03-12 |url-status=dead }} In a whole, it is the heart's reaction to catecholamines (norepinephrine, epinephrine, dopamine). Conditions that decrease bathmotropy (i.e. hypercarbia) cause the heart to be less responsive to catecholaminergic drugs. A substance that has a bathmotropic effect is known as a bathmotrope.

While bathmotropic, as used herein, has been defined as pertaining to modification of the excitability of the heart, it can also refer to modification of the irritability of heart muscle, and the two terms are frequently used interchangeably.{{Cite web | url=http://medical-dictionary.thefreedictionary.com/bathmotropy |title = Bathmotropy}}

History

In 1897 Engelmann introduced four Greek terms to describe key physiological properties of the heart: inotropy,{{cite journal |last1=Engelmann |first1=Th. W. |title=Ueber den myogenen Ursprung der Herzthätigkeit und über automatische Erregbarkeit als normale Eigenschaft peripherischer Nervenfasern |journal=Pflügers Archiv |date=January 1897 |volume=65 |issue=11–12 |pages=535–578 |doi=10.1007/BF01795562 |s2cid=31891993 |language=de |issn=1432-2013}} the ability to contract; chronotropy, the ability to initiate an electrical impulse; dromotropy, the ability to conduct an electrical impulse; and bathmotropy, the ability to respond to direct mechanical stimulation. A fifth term, lusitropy, was introduced in 1982 when relaxation was recognized to be an active process, and not simply dissipation of the contractile event.{{cite journal|last=Katz AM|author2=Smith VE|title=Inotropic and lusitropic abnormalities in the genesis of heart failure|journal=Eur Heart J|year=1982|volume=3 (Suppl D)|pages=11–18|doi=10.1093/eurheartj/4.suppl_a.7|pmid=6220901}} In an article in the American Journal of the Medical Sciences, these five terms were described as the five fundamental properties of the heart.{{cite book|title=The American Journal of the Medical Sciences|url=https://archive.org/details/americanjournal20usgoog|year=1908|publisher=J.B. Lippincott, Company|pages=[https://archive.org/details/americanjournal20usgoog/page/n61 46]–}}

Physiological explanation

As various drugs and other factors act on the resting potential and bring it closer to the threshold potential, an action potential is more easily and rapidly obtained. Likewise, when the sodium channels are in a state of greater activation, then the influx of sodium ions that allows the membrane to reach threshold potential occurs more readily. In both instances, the excitability of the myocardium is increased.Scientific American Medical; Dale and Federman Vol 1; 2003 Edition p. 1907 chapter 160; Disorders of Acid-Base and Potassium Balance

Drugs, ions and conditions

= Increasing bathmotropy =

  • Hypocalcemia{{cite journal |author= Armstrong, C.M. |author2=Cota, Gabriel. |title=Calcium block of Na+ channels and its effect on closing rate |journal=Proceedings of the National Academy of Sciences of the United States of America |volume=96 |issue=7 |pages=4154–4157 |year=1999 |pmid=10097179 |pmc=22436 |doi=10.1073/pnas.96.7.4154|bibcode=1999PNAS...96.4154A |doi-access=free }} - calcium blocks sodium channels which prevents depolarization, so decreases in calcium allow increased sodium passage and which lowers the threshold for depolarization.
  • Mild to moderate hyperkalemia{{cite journal|last=Kahloon|first=Mansha U.|author2=Aslam, Ahmad K.|author3= Aslam, Ahmed F.|author4= Wilbur, Sabrina L.|author5= Vasavada, Balendu C.|author6= Khan, Ijaz A.|title=Hyperkalemia induced failure of atrial and ventricular pacemaker capture|journal=International Journal of Cardiology|date=November 2005|volume=105|issue=2|pages=224–226|doi=10.1016/j.ijcard.2004.11.028|pmid=16243117}} - causes a partial depolarization of the resting membrane potential
  • Norepinephrine{{cite journal|last=Veldkamp|first=M|title=Norepinephrine induces action potential prolongation and early afterdepolarizations in ventricular myocytes isolated from human end-stage failing hearts|journal=European Heart Journal|date=1 June 2001|volume=22|issue=11|pages=955–963|doi=10.1053/euhj.2000.2499|pmid=11428819|doi-access=free}} and sympathetic stimulation in general - raises the resting membrane potential
  • Digitalis - Converts the normal Purkinje action potential of heart muscle to the automaticity type, which increases myocardial irritability
  • Epinephrine - Also known as adrenaline, effects are similar to sympathetic stimulation
  • Mild hypoxia - causes a partial depolarization of the muscle membrane
  • Ischaemia - causes a partial depolarization of the muscle membrane

= Decreasing bathmotropy =

  • Hypercalcemia - decreases permeability to sodium, hyperpolarizes membrane.
  • Propranolol{{cite journal|last=Ebner|first=F|author2=Reiter, M|title=The alteration by propranolol of the inotropic and bathmotropic effects of dihydro-ouabain on guinea-pig papillary muscle.|journal=Naunyn-Schmiedeberg's Archives of Pharmacology|date=June 1979|volume=307|issue=2|pages=99–104|doi=10.1007/BF00498450|pmid=481617|s2cid=26706163}}
  • Quinidine and other Class A Antiarrhythmic agents - block the voltage gated sodium channels
  • Calcium channel blockers - in general have negative bathmotropic effects
  • Parasympathetic stimulation - decreases excitability only of atrial muscle cells
  • Hyponatremia - decreases external sodium concentration
  • HypokalemiaHypokalemia - hyper polarization of the resting membrane potential
  • Acetylcholine - same as parasympathetic stimulation
  • Marked hypoxia - causes a marked depolarization of the resting membrane potential

See also

References

{{reflist|2}}

{{wiktionary|βαθμός}}

{{Cardiovascular physiology}}

Category:Electrophysiology

Category:Cardiovascular physiology