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Page 2
Hypoeffective heart resulting from negative inotropic effect decreases the stroke volume, increases the EDP, gradually increases the LVP and reduces the ejection phase.
Positive inotropic agents often promote Ca2+ inflow during impulses in cardiac muscle fibres. They include stimulation of the sympathetic division of the autonomic nervous system (ANS), hormones such as glucagon and the catecholamines (epinephrine and norepinephrine), increased Ca2+ level in the extracellular fluid, and the drug digitalis. Both glucagon and calcium chloride solution are on a hospital "crash cart" (for emergency treatment of heart attack victims) because they have potent positive inotropic effects and may stimulate a failing heart to contract more forcefully. Digitalis is a drug often used to treat people who have congestive heart failure. Negative inotropic agents include inhibition of the sympathetic division of the ANS, anoxia and acidosis, some anesthetics (e.g. halothane), and increased K+ level in the extracellular fluid.
Another mechanism of control of the work of the heart is by controlling the afterload (pressure that must be exceeded before ejection from the ventricles can begin). For example, if aortic pressure (thus blood pressure) increases, the stroke volume would decrease because more work has to be done by the left ventricle to force the aortic valve open. For a given EDV (end-diastolic volume), the residual volume in the left ventricle would increase. However, since the right ventricle is unaffected by the pressure rise in the systemic circulation, the right ventricular stroke volume would remain normal and increase the diastolic filling of the next beat by the same normal amount. Consequently, a larger EDV is attained in the left ventricle and the stroke volume from the left ventricle is gradually restored to normal.
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