Myocardial contractility
Myocardial contractility refers to the heart's ability to contract and generate force. It is a key factor in the heart's ability to pump blood throughout the body. The level of myocardial contractility can be influenced by various factors, including the heart's intrinsic properties, neurohormonal activation, and the loading conditions of the heart.
Physiology
The heart's contractility is primarily determined by the amount of calcium that enters the myocytes during each heartbeat. This calcium binds to troponin, which initiates the process of myocardial contraction. The amount of calcium that enters the myocytes is regulated by various factors, including the heart's intrinsic properties, neurohormonal activation, and the loading conditions of the heart.
Factors affecting myocardial contractility
Several factors can affect myocardial contractility. These include:
- Preload: This is the volume of blood in the ventricles at the end of diastole, just before contraction. An increase in preload can increase contractility by stretching the myocardial fibers and allowing more cross-bridges to form between the actin and myosin filaments.
- Afterload: This is the pressure that the heart must overcome to eject blood during systole. An increase in afterload can decrease contractility by making it harder for the heart to eject blood.
- Heart rate: An increase in heart rate can increase contractility by increasing the amount of calcium that enters the myocytes.
- Neurohormonal activation: The sympathetic nervous system can increase contractility by releasing norepinephrine, which binds to beta-adrenergic receptors on the myocytes and increases the amount of calcium that enters the cells.
Clinical significance
Abnormal myocardial contractility can lead to various heart conditions, including heart failure, cardiomyopathy, and myocardial infarction. These conditions can result in symptoms such as shortness of breath, fatigue, and fluid retention.
See also
References
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