Cardiac physiology

Cardiac physiology
• The left ventricle (LV) is capable of tolerating large increases in arterial pressure without a substantial reduction in stroke volume, but the right ventricle may acutely decompensate with even modest increases in pulmonary vascular resistance.
• Atrial contraction establishes final ventricular stroke volume at end-diastole and normally contributes between 15 and20% of this volume.
• Diastolic dysfunction may independently cause heart failure, even in the presence of relatively normal contractile function. This “heart failure with normal systolic function” has been increasingly recognized as a major underlying cause for as many as 50% of patients admitted to the hospital with congestive heart failure.
• According to Starling's law, the force ofLV contraction and volume of blood ejected from the chamber during systole (stroke volume) is directly related to the end-diastolic myofilament length, and hence, the end-diastolic volume.
• The distensibility of the aorta, the resistance of the peripheral arterial vasculature, and the actions of reflected waves on the central aortic circulation are the principle determinants of afterload.Systemic vascular resistance (the ratio of pressure to cardiac output, P/Q) is the most commonly used nonparametric expression of peripheral resistance and is primarily affected by autonomic nervous system activity.
• The primary determinant of myocardial oxygen consumption is heart rate because the heart completes an entire cycle with each beat, and hence, the more frequently the heart performspressure-volume work, the more oxygen must be consumed.
• The fundamental contractile unit of cardiac muscle is the sarcomere. The myofilaments within each sarcomere are arranged in parallel cross-striated bundles of thin (containing actin, tropomyosin, and the troponin complex) and thick (primarily composed of myosin and its supporting proteins) fibers. Sarcomeres are connected in series,thereby producing characteristic shortening and thickening of the long and short axes of each myocyte, respectively, during contraction.
• Attachment of myosin to its binding site on the actin molecule releases the phosphate anion from the myosin head, thereby producing a molecular conformation within this cross-bridge structure that generates tension in both myofilaments. Release of adenosinediphosphate (ADP) and the stored potential energy from this activated conformation produce rotation of the cross-bridge (“power stroke”) at the hinge point separating the helix tail region from the globular myosin head and its associated light chain proteins.
• The QRS complex records potentials at the body surface when the wave of depolarization is distributed throughout ventricularmyocardium. The QRS complex is much larger in magnitude than the P wave because ventricular mass is greater than the atrial mass. Rapid conduction through the His-Purkinje system spreads the wave of depolarization quickly to the ventricles.
• Short-duration regulation of mean arterial pressure occurs through the arterial, and to a lesser extent, intracardiac baroreceptors. Arterial baroreceptors arelocated at the bifurcation of the common carotid arteries and in the aortic arch.
• Blood supply to the LV is directly dependent on the difference between the aortic pressure and LV end-diastolic pressure (coronary perfusion pressure) and inversely related to the vascular resistance to flow, which varies to the fourth power of the radius of the vessel (Poiseuille's law).
• Metabolicfactors are the major physiological determinants of coronary vascular tone and, hence, myocardial perfusion.
• Myocardial infarction may occur without evidence of major coronary thromboses, emboli, or stenosis. This form of infarction is caused by excessive metabolic demands resulting from severe LV hypertrophy (e.g., critical aortic stenosis) or vasoactive drug ingestion (e.g., amphetamines,...