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10.7: Pathophysiology of Cardiac Performance

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Pharmacology

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Pathophysiology of Cardiac Performance
 
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10.7: Pathophysiology of Cardiac Performance

Typical heart performance is influenced by heart rate, rhythm, myocardial contraction, and metabolism or blood flow. The cardiac muscle exhibits distinct electrophysiological features, including pacemaker activity and calcium channel control, which play a vital role in the heart's response to various drugs. The autonomic nervous system, comprising the sympathetic and parasympathetic branches, regulates heart rate. Sympathetic activation increases heart rate, while parasympathetic activation reduces it.

Stroke volume, which affects cardiac output, is determined by preload, afterload, and myocardial contractility factors. Preload represents the initial stretching of cardiomyocytes before contraction and is related to left ventricular filling pressure and end-diastolic fiber length. Afterload, or the resistance encountered during blood pumping, is represented by aortic impedance and systemic vascular resistance. The Frank-Starling law states that the stroke volume increases proportionally to the end-diastolic volume, assuming other factors remain constant. This relationship highlights the heart's ability to adjust its output according to the body's needs. Coronary blood flow, vital for providing oxygen and nutrients to the heart, is regulated by several physiological factors. Physical factors include arterial pressure, vascular resistance, and vessel diameter. Metabolite-driven vascular control involves adenosine, nitric oxide, and endothelin, which modulate coronary vasodilation and constriction. Neural and humoral control mechanisms involve neurotransmitters and hormones, further influencing coronary blood flow to maintain heart function. So, cardiovascular drugs can affect cardiac function via alteration of electrophysiology, contraction, oxygen consumption, and coronary blood flow or autonomic control and help treat disorders like heart failure.

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