Normocardia: defined as normal heart rate Range - 60 - 100 beats / min.

average 70/min Bradycardia: defined as decrease in heart rate to less than 60 beats / min-in athletes. Tachycardia: defined as increase in heart rate to more than 100 beats / min. in emotion, exercise, and fever.

Normal sinus rhythm refers to the heartbeat which originates from the SA node.

Physiological variations or Factors Affecting Heart Rate: 1.Age: As age increases HR decreases. In very old age HR is more than young adult. 2.Sex: HR is higher in females than males. HR w 1 Surface area When S.A increases, the HR decreases. 3. Surface area:

4. Muscular Exercise increases HR.

5. Sleep decreases the HR. 6.Respiration: Effect of respiration on H.R is called sinus arrhythmia. During inspiration the HR increases and during expiration HR decreases. 7. Effect of body temperature on HR. Fever. Every 10F rise in body temperature increase HR by 10 beats /min. Fall in body temperature decrease HR.

y Effect of posture on HR

HR increases in the standing posture. HR is lowest in supine posture.This is due to the activation of the baroreceptor (Sino.aortic) reflexes. Effect of BP on HR: Marey s law states that in a normal individual the HR varies inversely as the BP. that is HR E 1 BP when BP increases the HR decreases, when BP decreases the HR increases. Exception to Mareys law is muscular exercise where both BP and HR increase.

Regulation of Heart rate

y HR is one of the important factors which determine

CO and BP. tissue.

y So it determines the amount of blood flow to the y Eg.: HR increases during exercise to increase the

blood flow to the working muscle. demand for blood flow is less. homeostatic mechanisms.

y HR decreases during sleep or at rest because the y Regulation of heart rate is therefore one of the

Mechanisms Regulating Heart Rate: Role of Cardiac Nerves a. Sympathetic b. Parasympathetic Role of Cardiac Centers Role of cardiovascular reflexes in regulation of Heart rate a. Baroreceptor reflexes. b. Chemoreceptor Reflexes. Other Factors a. Role of cerebral and limbic cortex. b. Role of Hormones.

Role of Cardiac Nerves on HR a. Cardiac Sympathetic Nerves. The pre.ganglionic fibers arise from the lateral horn cells of T1 T5 spinal segments and end in the superior, middle and inferior cervical ganglia. The post ganglionic fibers arise from the ganglia and run in the superior, middle and inferior cardiac nerves to supply SAN, AVN, atria and the ventricles.

Effect of sympathetic stimulation This results in release of neurotransmitter nor- epinephrine at the sympathetic post ganglionic nerve endings. This acts on B1 adrenergic receptors on the heart to produce. 1.Increase in HR - + ve Chronotropic effect y 2.Increase in force of contraction - + ve inotropic effect. 3.Increase in excitability - +ve bathmotropic effect. 4.Increased conductivity through the conducting tissue. y + ve dromotropic effect

Mech. of increase Heart rate on sympathetic stimulation The neurotransmitter nor-epinephrine increases the rate of discharge of the SAN by increasing or steepening the slope of the pacemaker potential or (Prepotential)

Cardiac Parasympathetic Nerve is the Vagus Nerve: The preganglionic cardiac vagal fibers originate from three vagal nucleii in the medulla 1. Dorsal motor nucleus of the vagus 2. Nucleus of tractus solitarius 3. Nucleus Ambiguus Preganglionic vagal fibers run with the sympathetic nerves to end in parasympathetic ganglion cells in the wall of the atria, SAN, AVN.

HR decreases during vagal stimulation due to release of the neurotransmitter Acetylcholine from the parasympathetic post ganglionic endings. ACh decreases the conduction rate in SA node & AV node by decreasing the slope of prepotential Postganglionic vagal fibers are short and supply both atria. No vagal nerve supply to ventricles. The Right vagus supplies the sino atrial node (SAN) and the Left vagus supplies the A V Node.

In humans if a parasympatholytic (blocking) drug like atropine is given the HR rises from 70/min to 150 180 /min, due to unopposed action of sympathetic nerves. At rest there is a vagal inhibitory tone that keeps the resting HR at 70/min. If both sympathetic and parasympathetic nerves are blocked, then the HR is about 100/min. The resting HR is due to a balance between the sympathetic and parasympathetic nerve stimulation.

Causes of cardiac arrest due to vagal stimulation. Blow on eyeball Traction on abdominal viscera Effects of parasympathetic (vagal N) stimulation 1.Decrease in HR vely chronotropic effect. 2.Decrease in force of contraction vely inotropic effect 3.Decrease excitability of heart vely Bathmotropic effect 4.Decrease conductivity of heart vely dromotropic

Moderate vagal stimulation leads to slowing of HR. Intense vagal stimulation leads to cardiac arrest .

Definition of Vagal Tone: The tonic discharge of inhibitory impulses in the vagus nerve at rest is known as vagal tone. Experimental evidence for vagal tone. If both the vagi are cut in an experimental animal the HR is seen to go up.

II. Role of cardiac centers and cardiovascular reflexes on HR regulation. The cardiac centers are present in the Medulla or Brain stem. They are 1. Vasomotor Center cell bodies are present in RVLM that is Rostral ventrolateral medulla. 2. Cardio Inhibitory center present in the medulla. CIC consists of the three vagal Nuclei. 3.Nucleus Ambiguus (NA) 4. Nucleus of the tractus solitarius (NTS) 5. Dorsal Motor Nucleus of vagus. Efferent nerve from CIC to heart is the vagus Nerve:

CARDIO VASCULAR reflexes that control vagal tone and Heart rate are 1.Baroreceptor reflexes are important for regulation of BP and HR. Sites are 1. Sino Aortic Baroreceptor reflex (Most Imp) 2. Atrial stretch receptor reflex 3. Left ventricular stretch receptor reflex. 4. Receptors present in pulmonary blood vessels. 5. Bainbridge reflex.

y Role of atrial stretch receptors in control of

HR and vagal tone:

Atrial stretch receptors are of 2 types. Type A receptors discharge during atrial systole and Type B Receptors which are stimulated by atrial distension due to increased venous return. Stimulation causes reflex vasodilation resulting in hypotension and Tachycardia.

c. Bainbridge Reflex: Bainbridge first described this in 1915. He observed that rapid infusion of saline in anesthetized animals produces an increase in heart rate if the intial heart rate is low. The receptors may be the tachycardia producing Atrial Type B receptors. Bainbridge reflex is a true reflex as it is abolished by bilateral vagotomy. It may be a protective reflex to prevent over stretching of atrium. Physiological significance not known.

Sino aortic baroreceptor reflex. Receptor: Stretch receptors located in the carotid sinus and aortic arch. Stimulus : increase BP causes stretch of the baroreceptor Afferent Nerve: from carotid sinus is the sinus nerve branch of glossopharyngeal N. From the aortic arch impulses are carried in the vagus nerves to the Center: CIC in the nucleus of the tractus solitarius Efferent N for S.A reflex is the vagus Nerve. Effector organ is the HEART

y Mechanism of Baroreceptor reflex when BP is high

Increase blood pressure (standing to supine) Increase stretch of carotid sinus Increase impulse traffic in sinus nerve Increase stimulation of the cardio inhibitory center Increased vagal stimulation or Increase in vagal tone Decrease Heart Rate

y Mechanism of Baroreceptor reflex when the BP is decreased:

Supine to standing the BP is decreased Decrease stretch of carotid sinus Decrease impulse traffic in sinus nerve Decrease stimulation of cardio inhibitory center Decrease impulses in vagal nerve Decrease vagal tone Increase in Heart Rate

Role of left ventricular receptors on HR Distension of L.V in experimental animals causes hypotension and bradycardia. Stretch of L.V Increase impulses in baroreceptor afferents Stimulate CIC or dorsal M.N of vagus Bradycardia (increase vagal tone)

II. Chemoreceptor reflexes.important for regulation of respiration, BP & HR.They are a. Peripheral chemoreceptors present in the carotid body and aortic body. b. Coronary chemoreflex or Bezold Jarisch reflex. c. Pulmonary chemoreflex. d. Cushing Ischemic reflex

The peripheral chemoreceptors Location: the carotid body (at the bifurcation of common carotid Art) and aortic body in the arch of aorta. Stimuli are hypoxia, hypercapnia and acidosis. Afferent nerve is Glossopharyngeal from Carotid body and vagus N from the aortic body. Center:It stimulates the vasomotor center to produce an increase in BP and decrease HR(Bradycardia). However hypoxia releases catecholamines from adrenal medulla, which produces Tachycardia (increase HR) and increase in BP.

Coronary Chemoreflex or Bezold Jarisch reflex:

y Injection of serotonin,& veratridine into the left

coronary artery which supplies the left ventricle produces apnea followed by rapid breath and reflex hypotension and Bradycardia. y Clinical implication: In myocardial infarction we get hypotension and bradycardia. It is thought that chemical substances liberated from infarcted tissue stimulate nerve fiber endings, which are the receptors. Afferent nerve is the vagus nerve

Pulmonary chemoreflex. Injection of serotonin, capsaicin, veratridine into the pulmonary artery produces apnea followed by rapid breathing, hypotension and bradycardia. This is mediated by vagal fibers present close to the lung capillaries.

Cushings Ischemic Reflex:

Patient with increase in intracranial pressure q Decrease blood supply to vasomotor center q Local hypoxia and hypercapnia q Stimulation of vasomotor center q Vasoconstriction and increase blood pressure q Increase discharge from baroreceptors q Increased stimulation of CIC q Increase in vagal tone and Bradycardia

y y

Effect of painful stimuli: Stimulation of C fibers causes tachycardia Stimulation of A delta fibers causes Bradycardia Effect of emotional stimuli on HR Emotions affect HR by acting via higher centers that is the limbic Cortex and hypothalamus They act on the Cardio inhibitory Center. Anger, excitation increase HR, Fear and grief decrease HR.

Effect of Hormones on HR.

1. 2. 3.

Thyroxine increases the sleeping pulse rate (HR) Epinephrine increase HR Nor epinephrine increases BP and decreases HR q Stimulates the Baroreceptors q Stimulate Cardioinhibitory Center q Reflex Bradycardia