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.

Cardiac performance depends on the heart rate, heart rhythm, myocardial contraction, and blood flow.

The heart's rate and rhythm are regulated by a specialized conducting system. They coordinate synchronized contractions through cardiomyocytes via voltage-sensitive channels.

Abnormalities in this system, like myocardial damage, conducting system defects, or increased sympathetic activity, can result in arrhythmias.

Within the cardiac muscles, the interaction of actin and myosin filaments triggers myocardial contraction, enabling the heart to pump blood.

The force of this contraction determines the cardiac output, which is the product of the heart rate and the mean ventricular stroke volume. It is influenced by the intrinsic contractility, preload —cardiac filling pressure, and afterload—the peripheral resistance during blood pumping.

Myocardial ischemia and cardiomyopathies can impair contractility, increasing cardiac workload and oxygen consumption.

Myocardial oxygen consumption relies on coronary blood flow, which is regulated by various physiological factors.

Conditions such as atherosclerosis and hormonal or metabolic responses to stress may reduce coronary flow, leading to ischemia or angina.