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Bathmotropic, (derived from the Greek word "Bathmos," meaning step or threshold), refers to modification of the degree of excitability, (threshold of excitation), of musculature in general, and of heart musculature specifically. It is used especially 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] Bathmotropic is one of five adjectives used to describe various qualities of the cardiac cycle; the other four are: inotropic chronotropic dromotropic and lusiotropic. In an article in the American Journal of Medical Sciences these five terms were described as the five fundamental properties of the heart.[3] While Bathmotropic, as used herein has been defined as pertaining to modification of the excitability of the heart it can equally well refer to modification of the irritability of heart muscle, and the two terms are frequently used interchangeably.[4]

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Physiological Explanation of the Bathmotropic Effect

The bathmotropic effect modifies the heart muscle membrane excitability, and thus the ease of generating an action potential. The easiness of generating an action potential 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 membrane action potential please see the related Wikipedia article on the action potential.) During stage 4 of the action potential the inside of the 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 fast gated 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, the 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. [5]

Drugs, ions and conditions that have a positive bathmotropic effect

  • Hypocalcemia [6] -causes a partial depolarization of the resting membrane potential
  • Mild to Moderate Hyperkalemia [7] - causes a partial depolarization of the resting membrane potential
  • Norepinephrine[8] 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 increases myocardial irritability
  • 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

Drugs and conditions that have a negative bathmotropic effect

  • Propanolol[9]
  • Quinidine and other Class A Anti arrhythmic 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 - hyper polarization 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

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