Cardiac Performance, Dr. D. Penney
Control of Cardiac Performance: STROKE VOLUME:
Release of the following substances from the sympathetic and parasympathetic sympathetic branches of the autonomic nervous system, affect inotropicity:
norepinephrine (+) - neural
acetylcholine (-) - neural*
epinephrine (+) - blood borne
These actions are mediated through cardiopulmonary receptors, such as the carotid sinus (aortic) baroreceptors, carotid (aortic) body chemoreceptors, central chemo-receptors, venae cavae/atrial volume receptors (Bainbridge), and the ventricular volume receptors.
Attention: Inotropicity (ie. contractility) and strength of contraction are not synonomous. Increased / decreased strength of contraction can be achieved by changing preload
(ie. Frank-Starling) with no change in inotropicity. Inotropicity reflects the biochemical state within the muscle (eg. Ca, ATP), not simply the positioning of the thick and thin
myofilaments as determined by stretch.
Frank-Starling - through preload (heterometric autoregulation)
afterload - through increased / decreased arterial blood pressure acting on aortic valve.
Anrep effect - laboratory curiousity?
Bowditch effect } (homeometric autoregulation) (Treppe, Staircase)
environment - ischemia, O2, CO2
cardiac hypertrophy - longterm effect
* In actual fact, there are few parasympathetic fibers in the ventricular myocardium, so ACH has little practical effect physiologically on ventricular inotropicity (contractility).
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