Function
Since the heart operates solely under aerobic metabolism, myocardial mitochondria must maintain an abundance of oxygen to continue oxidative phosphorylation. Heart rate, contractility, and ventricular-wall tension are the three factors that determine myocardial oxygen demand. An increase in any of these variables requires the body to adapt to sustain adequate oxygen supply to the heart.
Heart rate is thought to be the most important factor affecting myocardial oxygen demand. With an increased heart rate, the myocardium must work harder to complete the cardiac cycle more efficiently. With a shortened cardiac cycle, the time spent in diastole decreases. Because diastole ends prematurely, the amount of blood that normally fills the ventricles decreases, and oxygen-saturated hemoglobin is not allowed to reach the subendocardium. Under optimal conditions, myocardial oxygen demand will equal myocardial oxygen supply; however, when there is structural damage from a plaque that impedes flow, there can be a mismatch between supply and demand that results in ischemia.
Bạn đang xem: Bookshelf
Contractility or inotropism is the rate of increase in the intraventricular pressure during contraction at a given muscle fiber length. Interestingly, myocytes have the innate ability to exert a contraction at any muscle length. This force is measured after the closure of the mitral valve and before the opening of the aortic valve during which time the intraventricular volume remains constant.
Xem thêm : Newborn Pulse Oximetry Screening to Detect Critical Congenital Heart Disease
Contractility is impacted by a variety of intrinsic and extrinsic forces including calcium concentration. Calcium is released by the sarcoplasmic reticulum of cardiac muscle and binds to troponin C. This bond stimulates a conformational change of tropomyosin that releases it from the binding sites on the actin filament. With the release of tropomyosin, the active sites on actin are free to bind myosin which causes adenosine triphosphate (ATP) to be broken down into adenosine diphosphate (ADP) and inorganic phosphate (P). Subsequently, there is a power stroke of the myosin head which forces the actin filament centrally towards the sarcomere, and ADP and P detach from the myosin head resulting in contraction. Once ATP re-attaches to myosin, actin is freed. This cycle continues until intracellular calcium supplies are depleted, there is no longer binding between troponin C and calcium, and tropomyosin can revert to its initial confirmation to cover the binding sites on actin. Therefore, the intracellular calcium concentration is directly proportional to the contraction force [2].
Ventricular wall tension is based on the thickness of the ventricular myocardium. The law of Laplace states that ventricular wall tension is proportional to ventricular radius and intraventricular pressure. Patients with coronary artery disease will have decreased blood and oxygen supply to the myocardium. In this case, contractility will be diminished. Because the ventricle can no longer achieve adequate contraction, the end-systolic volume will increase. The excess blood remaining in the ventricle will cause expansion of the ventricular radius and intraventricular pressure resulting in higher wall tension.
Nguồn: https://buycookiesonline.eu
Danh mục: Info
