Bathmotropic often refers to modifying the degree ofexcitability 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.[1] Positive bathmotropic effects increase the response of muscle to stimulation, whereas negative bathmotropic effects decrease the response of muscle to stimulation.[2] In a whole, it is the heart's reaction tocatecholamines (norepinephrine,epinephrine,dopamine). Conditions that decrease bathmotropy (i.e. hypercarbia) cause the heart to be less responsive tocatecholaminergic drugs. A substance that has a bathmotropic effect is known as abathmotrope.
While bathmotropic, as used herein, has been defined as pertaining to modification of theexcitability of the heart, it can also refer to modification of theirritability of heart muscle, and the two terms are frequently used interchangeably.[3]
In 1897Engelmann introduced four Greek terms to describe key physiological properties of the heart:inotropy,[4] 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.[5] In an article in theAmerican Journal of the Medical Sciences, these five terms were described as the five fundamental properties of the heart.[6]
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 themyocardium is increased.[7]
Hypocalcemia[8] - calcium blockssodium channels which prevents depolarization, so decreases in calcium allow increasedsodium passage and which lowers the threshold for depolarization.
Mild to moderatehyperkalemia[9] - causes a partial depolarization of the resting membrane potential
^Engelmann, Th. W. (January 1897). "Ueber den myogenen Ursprung der Herzthätigkeit und über automatische Erregbarkeit als normale Eigenschaft peripherischer Nervenfasern".Pflügers Archiv (in German).65 (11–12):535–578.doi:10.1007/BF01795562.ISSN1432-2013.S2CID31891993.
^Katz AM; Smith VE (1982). "Inotropic and lusitropic abnormalities in the genesis of heart failure".Eur Heart J. 3 (Suppl D):11–18.doi:10.1093/eurheartj/4.suppl_a.7.PMID6220901.
^Kahloon, Mansha U.; Aslam, Ahmad K.; Aslam, Ahmed F.; Wilbur, Sabrina L.; Vasavada, Balendu C.; Khan, Ijaz A. (November 2005). "Hyperkalemia induced failure of atrial and ventricular pacemaker capture".International Journal of Cardiology.105 (2):224–226.doi:10.1016/j.ijcard.2004.11.028.PMID16243117.
^Ebner, F; Reiter, M (June 1979). "The alteration by propranolol of the inotropic and bathmotropic effects of dihydro-ouabain on guinea-pig papillary muscle".Naunyn-Schmiedeberg's Archives of Pharmacology.307 (2):99–104.doi:10.1007/BF00498450.PMID481617.S2CID26706163.
