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Myocardial contractility represents the innate ability of the heart muscle (cardiac muscle or myocardium) to contract. It is the maximum attainable value for the force of contraction of a given heart.
As a larger volume of blood flows into the ventricle, the blood stretches cardiac muscle, leading to an increase in the force of contraction. The Frank-Starling mechanism allows the cardiac output to be synchronized with the venous return, arterial blood supply and humoral length, [2] without depending upon external regulation to make ...
Cardiac physiology or heart function is the study of healthy, ... sex, contractility, duration of contraction, preload or EDV, and afterload or resistance. Normal ...
Cardiac contractility modulation device implantation was first successfully done in India in Royal Hospital, Trivandrum, Kerala, under the leadership of Dr. C. Bharath Chandran. Advocate Harishankar was the first person in India to get the cardiac contractility modulation device implanted.
The cardiac cycle is the performance of the human heart from the beginning of one heartbeat to the beginning of the next. [1] It consists of two periods: one during which the heart muscle relaxes and refills with blood, called diastole, following a period of robust contraction and pumping of blood, called systole. [1]
Rhythmicity and contractility of the heart may be normal, but the stiff walls of the heart chambers (atria and ventricles) keep them from adequately filling, reducing preload and end-diastolic volume. Thus, blood flow is reduced, and blood volume that would normally enter the heart is backed up in the circulatory system.
Afterload is the mean tension produced by a chamber of the heart in order to contract. It can also be considered as the ‘load’ that the heart must eject blood against. Afterload is, therefore, a consequence of aortic large vessel compliance, wave reflection, and small vessel resistance (LV afterload) or similar pulmonary artery parameters (RV afterload
In response, cardiac contractility increased, a phenomenon Anrep attributed to the release of adrenaline from the suprarenal glands, independent of preload changes. Later, Ernest Starling suggested that enhanced coronary flow, improving myocardial nourishment (a concept later termed the Gregg effect [ 9 ] ), might explain the increase in ...
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