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.[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 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.[3]


The term "bathmotropic" is derived from the Ancient Greek word βαθμός (bathmós), meaning "step" or "threshold".


In 1897 Engelmann 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 the American Journal of the Medical Sciences, these five terms were described as the five fundamental properties of the heart.[6]

Physiological explanation

The bathmotropic effect modifies the heart muscle membrane excitability, and thus the ease of generating an action potential. The ease of generating an action potential is related both to the magnitude of the resting potential and to the activation state of membrane sodium channels.

During stage 4 of an action potential, the inside of a cardiac muscle cell rests at −90 mV. As the inner muscle cell potential rises towards −60 mV, electrochemical changes begin to take place in the voltage-gated rapid sodium channels, which permit the rapid influx of sodium ions. When enough sodium channels are opened, so that the rapid influx of sodium ions is greater than the tonic efflux of potassium ions, then the resting potential becomes progressively less negative, more and more sodium channels are opened, and an action potential is generated. The electrical potential at which this occurs is called the threshold potential.

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.[7]

Drugs, ions and conditions

Increasing bathmotropy

  • Hypocalcemia[8] - 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[9] - causes a partial depolarization of the resting membrane potential
  • Norepinephrine[10] 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

See also


  1. Miriam Webster's Medical Dictionary and Online Medical Dictionary
  2. The Kanji Foundry Press - b
  3. "Bathmotropy".
  4. 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. ISSN 1432-2013.
  5. 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. PMID 6220901.
  6. The American Journal of the Medical Sciences. J.B. Lippincott, Company. 1908. pp. 46–.
  7. Scientific American Medical; Dale and Federman Vol 1; 2003 Edition p. 1907 chapter 160; Disorders of Acid-Base and Potassium Balance
  8. Armstrong, C.M.; Cota, Gabriel. (1999). "Calcium block of Na+ channels and its effect on closing rate". Proceedings of the National Academy of Sciences of the United States of America. 96 (7): 4154–4157. Bibcode:1999PNAS...96.4154A. doi:10.1073/pnas.96.7.4154. PMC 22436. PMID 10097179.
  9. 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. PMID 16243117.
  10. Veldkamp, M (1 June 2001). "Norepinephrine induces action potential prolongation and early afterdepolarizations in ventricular myocytes isolated from human end-stage failing hearts". European Heart Journal. 22 (11): 955–963. doi:10.1053/euhj.2000.2499. PMID 11428819.
  11. 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. PMID 481617.
  12. Hypokalemia
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