Bathmotropic
Bathmotropic is derived from the Greek word "Bathmos," meaning step or threshold, and refers to modifying the degree of excitability, (threshold of excitiation), of musculature in general, and of heart musculature specifically. It is used especially to describe the effects of cardiac nerves on cardiac excitability, (from Miriam Webster's Medical Dictionary and Online Medical Dictionary). Positive bathmotropic effects increase the response of muscle to stimuli, whereas negative bathmotropic effects decrease the response of muscle to stimulation.[1] Bathmotropic is one of five adjectives describing qualities of the cardiac cycle; the other four adjectives are: ionotropic chronotropic dromotropic and lusiotropic.
Physiological Explanation of the Bathmotropic Effect
The bathmotropic effect, or modification of the ease of generation of an action potential, (called membrane excitability), is related both to the magnitude of the resting potential and to the activation state of membrane sodium channels. (For a complete description of the action potential please view the related Wikapedia article on the action potential.) In the resting state, (stage 4 of the action potential), the inside of the cardiac muscle cell is 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 sodium ions, then the resting potential becomes progressively less negative, more and more fast gated sodium channels are opened, and the action potential is generated. The electrical potential at which the rapid sodium influx outruns the tonic sodium efflux is called the threshold potential. Various drugs and other factors can help to reset the initial resting potential. When this potential is closer to -60 mv, then the threshold potential is reached more easily. 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. [2]
Drugs, ions and conditions that have a positive bathmotropic effect
- Hypocalcemia [3] -causes a partial depolarization of the resting membrane potential
- Mild to Moderate Hyperkalemia [4] - causes a partial depolarization of the resting membrane potential
- Norepinephrine[5] and sympathetic stimulation in general - lowers the resting membrane potential,
- Digitalis - Converts the normal Purkinje action potential of heart muscle to the automaticity type, which increaes myocardial irritability
- Adrenaline - effects are similar to sympathetic stimulation
- Mild hypoxia - causes a partial depolarizatiion of the muscle membrane
- Ischaemia - causes a partial depolarization of the muscle membrane
Drugs and conditions that have a negative bathmotropic effect
- Propanolol[6]
- 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
- Marked Hyperkalemia - causes a marked depolarization of the resting membrane potnetial
- Hypokalemia - hyperpolarization of the resting membrane potential
- Hypercalcemia - decreases permeability to sodium
- Acetyl choline - same as parasympathetic stimulation
- Marked Hypoxia - causes a marked depolarization of the resting membrane potential
References
- ^ The Kanji Foundry Press - b
- ^ Scientific American Medical; Dale and Federman Vol 1; 2003 Edition p.1907 chapter 160; Disorders of Acid-Base and Potassium Balance
- ^ Calcium block of Na+ channels and its effect on closing rate
- ^ linkinghub.elsevier.com/retrieve/pii/S016752730500269X
- ^ Norepinephrine induces action potential prolongation and early afterdepolarizations in ventricular myocytes isolated from human end-stage failing hearts - Veldkamp et al. 22 (11): 955 - European Heart Journal
- ^ SpringerLink - Journal Article