Contractility (syn.: inotropy) is a unique feature of cardiac muscle that provide cardiomyocytes with ability to generate force, which is independent of preload and afterload. In addition to force, contractility also influences velocity of sarcomere shortening during the phase of isovolumetric contraction. An increase in generated force and velocity of cardiomyocyte shortening will enhance the ejection velocity and, correspondingly, ejection fraction and stroke volume (with concomitant reduction in end systolic and end diastolic volume).
Factors enhancing contractility
- Sympathetic stimulation
- Catecholamines
- Inotropic drugs (see below)
Factors inhibiting contractility
- Physiologic
- Vagal (parasympathetic) stimulation
- Pathologic
- Advanced heart failure (unknown mechanism)
- Acute MI
- Chronic ischemic heart disease
Inotropic drugs
- Drugs used for cardiac failure treatment
- Beta-adrenoceptor agonists (dopamine, dobutamine, etc)
- + peripheral vasodilation with resoration of end-organ perfusion and reduction of afterload
- Phosphodiesterase inhibitors (milrinone)
- + veno and arterial vasodilation with a decrease in preload and afterload
- Digoxin
- Caffeine
- Theophylline
To be continued
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