The regulation of heart rate is a complex process controlled by the autonomic nervous system (ANS), hormonal influences, and intrinsic cardiac mechanisms. The ANS has two main components: the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS).
The SNS increases heart rate through the release of norepinephrine and epinephrine, which act on beta-1 adrenergic receptors in the heart. This action increases the rate of depolarization in the sinoatrial (SA) node, the heart's primary pacemaker, and enhances the force of cardiac contractions.
Conversely, the PNS predominates at rest and decreases the heart rate by releasing acetylcholine, which acts on muscarinic receptors in the heart. This reduces the rate of depolarization in the SA node.
Intrinsic regulation involves the SA node, which sets the baseline heart rate (around 60-100 beats per minute). The atrioventricular (AV) node, the secondary pacemaker, delays the impulse, allowing the atria to contract before the ventricles.
Hormonal influences also play a role in heart rate regulation. Adrenaline (epinephrine) from the adrenal medulla increases heart rate, while thyroid hormones can enhance the sympathetic response, thus increasing heart rate.
Several reflexes contribute to heart rate regulation. The baroreceptors, located in the carotid sinus and aortic arch, adjust heart rate in response to blood pressure changes. The chemoreceptors, located in the carotid bodies and aortic bodies, respond to changes in blood chemistry, such as CO2, O2, and pH levels. The Bainbridge reflex (atrial reflex) increases heart rate in response to increased venous return. Additionally, body temperature affects heart rate, with higher temperatures increasing and lower temperatures decreasing the heart rate.
Understanding these mechanisms is crucial for managing cardiovascular conditions like arrhythmias, hypertension, and heart failure.
From Chapter 23:
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