L20 Heart Rate & Regulation PDF

1 L 20 Heart Rate And Its Regulation ILOs By the end of this lecture, students will be able to 1- Realize the importance of cardiovascular regulation. 2- Describe the location & function of the central areas controlling the cardiovascular system. 3- Mention the normal range of the heart rate (HR) &...

1 L 20 Heart Rate And Its Regulation ILOs By the end of this lecture, students will be able to 1- Realize the importance of cardiovascular regulation. 2- Describe the location & function of the central areas controlling the cardiovascular system. 3- Mention the normal range of the heart rate (HR) & list its possible physiological variations. 4- Describe the mechanisms involved in HR regulation (including nervous, chemical & thermal mechanisms). Cardio-vascular regulatory mechanisms They can cause rapid adjustment of the cardiovascular system (CVS) activity which is needed to maintain homeostasis. Aims: 1- Increase the blood supply to active tissues. 2- Increase or decrease heat loss from the body. 3- Maintain the blood flow to the vital organs i.e., heart & brain (as in hemorrhage). General mechanisms of control of CVS 1- By changing the cardiac output (COP) (by changing the heart rate & cardiac contraction) 2- By changing the diameter of blood vessels: - Arterioles: controlling the blood flow to the tissues. - Veins: controlling the amount of blood in them. Central nervous control of CVS [The Vasomotor center; Medullary CVCs] There are diffuse areas of neurons located bilaterally mainly in M.O & lower ⅓ of pons which control the autonomic discharge to CVS. Their total organization is still unclear, but they include: a) Vasoconstrictor area b) Vasodilator area c) Sensory area a) Vasoconstrictor (V.C) area in upper Ventrolateral part of M.O. (Rostral Ventro-Lateral Medulla; RVLM): This area sends descending fibers to LHCs of thoraco-lumber segments of the spinal cord from which preganglionic sympathetic fibers arise to reach the sympathetic ganglia. Activity in the postganglionic sympathetic fibers leads to generalized vasoconstriction elevating the arterial blood pressure (ABP) “Pressor effect”. Dr. Youssef Hatem 2 b) Vasodilator (V.D) area in lower ventrolateral part of M.O. (Caudal Ventro-Lateral Medulla; CVLM): This area receives impulses from medullary sensory neurons and it is not connected to any vasodilator fibers. When it is stimulated, it inhibits the V.C. area causing generalized vasodilation which leads to lowering of ABP “Depressor effect”. c) Sensory area: This area is located in the posterolateral part of M.O. & lower pons (in the Nucleus Tractus Solitarius; NTS). It receives input signals from different parts of the body and sends output signals to the other areas To adjust their activities. According to the effect on the heart: - The Lateral Portion: Transmits excitatory impulses through the sympathetic nerve fibers to the heart. - The Medial Portion: Sends signals to the adjacent Nucleus ambiguous in M.O (& Dorsal motor nucleus of the vagus) from which the preganglionic vagal fibers arise that relay in terminal ganglia (in nodal tissues in right atrium). Short postganglionic fibers supply the Atria, A.V bundle & coronary vessels [With the right vagus supplying mainly the SA node, and the left vagus supplying the AV node] leading to inhibition. Function of autonomic fibers to the heart: A) Vagal fibers: 1) Negative chronotropic effect. 2) Decrease excitability (especially of AVN). 3) Negative inotropic effect. 4) Decrease the release of the norepinephrine from the nearby sympathetic nerve endings. Dr. Youssef Hatem 3 5) Negative dromotropic effect (decreased conduction at AVN). Strong vagal activity may lead to complete AV Block, where the ventricles stop beating. Then they may regain their function by the Idioventricular rhythm. This is called the Vagal (Ventricular) escape phenomenon”. * Vagal Tone: “The continuous inhibitory impulses transmitted by the vagi which check the inherently high rhythm of S.A.N. at the basal level of ABP”. - It is reflexly produced through the baroreceptors. B) Sympathetic fibers: 1) Positive chronotropic effect “Sympathetic tone”. 2) Increase excitability. 3) Positive dromotropic effect (increase conductivity). 4) Positive inotropic effect. 5) Decrease the effects of vagal stimulation. - The SA node is under the influence of both sympathetic & vagal fibers. - Normally, Vagal tone predominates at rest (mainly by inhibition of norepinephrin release from the sympathetic nerve endings by acetylcholine). - When both noradrenergic & cholinergic systems are blocked, H.R. is approximately 100 – 120 beats/min (bpm). HEART RATE (HR) Normal value under resting condition (for an adult man): - Average: 70 - 75 bpm. - Range: 50 – 100 bpm. - If the HR is < 50 bpm, the condition is called bradycardia, and if it is > 100 bpm, this is called tachycardia. Dr. Youssef Hatem 4 Physiological Variations: 1. Gender: HR in females is more than in males (due to lower ABP with a weaker vagal tone). 2. Age: HR in the young (due to high BMR) & in the elderly is more than in adults. - Fetus: 140-150 bpm. - Newborn: 130-140 bpm. - 1-3 years: 95-115 bpm. - Elderly: 75-80 bpm. 3. Circadian Rhythm: - Lowest in the early morning (65/min). - Highest in the evening (85/min). 4. Rest (Physical & Mental) & Sleep: Decrease HR (60 bpm). 5. Muscular Exercise (ME): - During ME, HR increases (up to ≈ 180 bpm). - Resting HR in athletes is less than in non-trained individuals (50 – 60 bpm, or even less). 6. Posture: - During standing → ↑ HR (by up to 25%) 7. Emotions: May increase or decrease HR. 8. High Metabolic Rate: increases HR 9. Increased respiration: is associated with accelerated HR. I] Nervous Regulation of HR A) Afferent impulses from CVS: 1- Arterial Baroreceptors: They are stretch receptors located in tunica adventitia in the wall of almost all arteries in the thorax & neck but extremely abundant in the Vasosensory Areas (which are supplied by “Buffer nerves”): a) The carotid sinus: It is supplied by the “carotid sinus nerve = Hering’s nerve” which is a branch of IX cranial nerve (Glossopharyngeal nerve). a) The aortic arch: It is supplied by the “aortic depressor nerve” which is a branch of X cranial nerve (Vagus nerve). Dr. Youssef Hatem 5 * Baroreceptors are stimulated by ABP above 60 mmHg, with maximal activity at 160 mmHg. They send impulses in the buffer nerves to the centers in M.O. producing the Baroreceptors reflexes: 1. Decreased HR & force of contraction. 2. Generalized peripheral vasodilation decreasing ABP back to normal. 3. Decreased ADH secretion. - (Marey’s Reflex): HR is inversely proportional with ABP (provided the other factors remain constant). - At normal mean ABP (≈ 100 mm Hg), a burst of action potentials stimulates the cardiac vagal neurons to decreased HR (vagal tone). N.B. - Baroreceptors reflexes respond very rapidly to changing ABP (by abrupt changes in posture, blood volume, C.O.P. or peripheral resistance) leading to rapid adjustments. - They adapt in 1 – 2 days to whatever pressure present “Baroreceptor resetting” as in chronic hypertension. 2- Cardiopulmonary Mechanoreceptors (Low pressure baroreceptors, Atrial stretch receptors): - They are present in the four cardiac chambers, SVC, IVC & pulmonary artery. - They are stimulated by distension due to increased venous return or blood volume. Type A: discharges during atrial systole. Type B: discharges during atrial diastole. Dr. Youssef Hatem 6 Response: a) Increased HR (by up to 75%). Mechanism: 1- Direct stretching of S.A.N. 2- “Bainbridge reflex”: Increased venous return stimulates type B receptors which discharge their impulses to the medullary centers through the vagi. Decreased vagal tone & increased sympathetic tone leads to increased HR. This prevents stasis of blood in veins, atria & pulmonary circulation. b) Inhibition of ADH secretion. c) Decreased sympathetic activity to renal arterioles causing their vasodilation. Both a & b lead to increased H2O excretion in urine which decreases the blood volume. d) Release of ANP, which caused potent diuresis & natriuresis & dilates the resistance & capacitance blood vessels to regulate the blood volume & ABP. 3- Peripheral Chemoreceptors: - They are present in aortic & carotid bodies. They have very high rates of blood flow. - Their sensory fibers run in IX & X cranial nerves. Peripheral Chemoreceptors are stimulated by: Decreased PaO2 , increased PaCO2 , increased H+ in blood, or decreased mean ABP < 80 mm Hg. Response: - Increased respiration. - Vasoconstriction B) Afferent impulses from other regions of the body: 1- Contracting voluntary muscles: They send impulses from proprioceptors to RVLM to increase ABP & to increase HR “Alam – Smirk reflex”. 2- Painful stimuli: - If mild or moderate, they increase ABP & HR. - If severe or if applied to Trigger areas (Eye balls, post-auricular, larynx, epigastrium & external genitalia), they decrease HR, cause vasodilation, decrease ABP which may lead to fainting. C) Afferent impulses from higher centers: 1- Cerebral cortex, Limbic system & Hypothalamus: - Conditioned reflexes. - Effect on ANS in reaction to emotions (e.g., stress & anger): Mild or moderate (e.g., anger) increase HR & ABP. Severe (especially fear or grief) decrease HR & cause vasodilation leading to decreased ABP. Dr. Youssef Hatem 7 2- Respiratory center: In “Respiratory sinus arrhythmia”, HR increases during inspiration & decreases during expiration. Found in healthy children & in adults after deep voluntary respiration. * Mechanism: a) Central irradiation from respiratory center to neighboring CVCs. b) Afferent impulses from the lungs during inspiration. c) Increased VR during inspiration. 3- CNS ischemic response: Decreased ABP ≤ 60 mmHg (maximal at 15- 20 mm Hg) results in ischemia of vasomotor centers (RVLM), with increased local CO2 & lactic acid which leads to strong stimulation with very strong activation of sympathetic nervous system. Accordingly, there is very strong peripheral vasoconstriction especially in the skin & kidneys with almost no urine. * It is an emergency ABP control system 4- Cushing’s reflex: Increased intracranial pressure leads to compression of cerebral vessels causing hypoxic state which activates RVLM neurons leading to systemic vasoconstriction elevating ABP. This maintains adequate blood flow to the brain. Reflexly, H.R decreases. II] Chemical Regulation of HR A) Changes in blood gases & H+: Decreased O2, increased CO2 & increased H+ Mechanism: 1- Direct action on CVCs. 2- Indirect action on peripheral chemoreceptors. Hypoxia, hypercapnia & acidosis: - Increase HR (Direct & indirect effects) as in heart failure, anemia & hemorrhage. - Severe premortal decrease HR (Effect on SAN & CVCs). B) Hormones: 1- Catecholamines: Dr. Youssef Hatem 8 2- Thyroxin: Increases HR. Mechanism: i- Direct stimulation of SAN. ii- Increased body metabolism. iii- Stimulating effect on sympathetic nervous system. III] Physical Regulation of HR Increased Body temperature (1˚C) increases HR (by ≈ 10 - 15 bpm). Mechanism: 1- Direct stimulation on SAN. 2- Stimulation of medullary CVCs. 3- Stimulation of hypothalamic heat regulating center by increased body metabolism. Some causes of increased HR: 1) Less stimulation of baroreceptors. 2) Stimulation of atrial stretch receptors. 3) During inspiration. 4) Muscular exercise. 5) Mild or moderate painful stimuli. 6) Mild or moderate emotions (e.g., stress & anger). 7) Moderate hypoxia (directly stimulates the RVLM or S.A. node). 8) Catecholamines. 9) Thyroxin. 10) Increased body temperature. Some causes of decreased HR: 1) More stimulation of baroreceptors. 2) Severe emotions (or fear & grief). 3) During expiration. 4) Increased intracranial pressure. 5) Severe premortal hypoxia & acidosis. 6) Hyperkalemia. 7) Severe pain or if applied to trigger areas. __________________________________________________________ References: 1- Hall JE. Guyton and Hall Textbook of Medical Physiology, 14th. Ed. Elsevier Saunders; 2021, Chapter 18. 2- Noble A, Johnson R, Thomas A, and Bass P. The Cardiovascular System, BASIC SCIENCE AND CLINICAL CONDITIONS, 2nd ED. Elsevier Limited; 2010, Chapters 4 & 10. Dr. Youssef Hatem