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M04.03.02 Control of the heart rate
The control of heart rate is a crucial aspect of cardiovascular physiology, involving intricate mechanisms that maintain cardiac output and ensure efficient circulation. This detailed note explores the neural and hormonal regulation of heart rate, incorporating tables, side notes for key points, and a bibliography for further reading.
Overview
The heart rate (HR) is controlled by:
- Intrinsic Factors: Properties of the cardiac tissue itself.
- Extrinsic Factors: Neural and hormonal influences.
Intrinsic Control
Intrinsic Factors:
- Sinoatrial (SA) Node: The primary pacemaker of the heart, located in the right atrium.
- Generates spontaneous action potentials.
- Sets the baseline heart rate (typically 60-100 beats per minute).
Extrinsic Control
Extrinsic Factors involve the autonomic nervous system (ANS) and endocrine system, which modulate the heart rate in response to various physiological demands.
Autonomic Nervous System (ANS)
| Branch | Key Components | Effect on Heart Rate | Mechanism |
|---|---|---|---|
| Sympathetic NS | Norepinephrine (NE) | Increases heart rate (tachycardia) | Increases SA node activity via β1 receptors |
| Parasympathetic NS | Acetylcholine (ACh) | Decreases heart rate (bradycardia) | Decreases SA node activity via muscarinic receptors (M2) |
Sympathetic Stimulation:
- Norepinephrine (NE) binds to β1-adrenergic receptors on the SA node.
- Increases the rate of depolarization, leading to a higher heart rate.
Parasympathetic Stimulation:
- Acetylcholine (ACh) binds to muscarinic receptors (M2) on the SA node.
- Decreases the rate of depolarization, leading to a lower heart rate.
Side Note: The balance between sympathetic and parasympathetic activity is crucial for maintaining heart rate homeostasis.
Hormonal Control
| Hormone | Source | Effect on Heart Rate | Mechanism |
|---|---|---|---|
| Epinephrine | Adrenal Medulla | Increases heart rate | Binds to β1-adrenergic receptors |
| Thyroxine | Thyroid Gland | Increases heart rate | Increases overall metabolism and SA node activity |
Key Points to Memorize:
- Epinephrine enhances sympathetic effects, increasing heart rate.
- Thyroxine increases the basal metabolic rate, indirectly elevating heart rate.
Feedback Mechanisms
Baroreceptor Reflex:
- Location: Carotid sinuses and aortic arch.
- Function: Detects changes in blood pressure and modulates heart rate accordingly.
- High BP: Activates parasympathetic output, reducing heart rate.
- Low BP: Activates sympathetic output, increasing heart rate.
Chemoreceptor Reflex:
- Location: Carotid and aortic bodies.
- Function: Responds to changes in blood pH, CO2, and O2 levels.
- High CO2/Low pH: Increases heart rate via sympathetic activation to enhance blood flow and gas exchange.
- Low O2: Similar response to ensure adequate oxygen delivery.
Side Note: Understanding these reflexes is essential for managing conditions like hypertension and heart failure.
Clinical Implications
- Tachycardia: Abnormally high heart rate; can be caused by stress, fever, hyperthyroidism, or heart disease.
- Bradycardia: Abnormally low heart rate; may result from vagal stimulation, athletic conditioning, or pathologies like hypothyroidism.
Key Points to Memorize:
- Beta-blockers are commonly used to manage tachycardia by blocking β1-adrenergic receptors.
- Atropine is used to treat bradycardia by inhibiting parasympathetic (vagal) effects.
Bibliography
- Guyton, A.C., & Hall, J.E. (2016). Textbook of Medical Physiology (13th ed.). Elsevier.
- Berne, R.M., & Levy, M.N. (2018). Physiology (6th ed.). Mosby.
- Hall, M.E. (2015). Cardiovascular Physiology (10th ed.). McGraw-Hill Education.
- Levick, J.R. (2013). An Introduction to Cardiovascular Physiology (5th ed.). CRC Press.
- Lilly, L.S. (2016). Pathophysiology of Heart Disease (6th ed.). Lippincott Williams & Wilkins.