Regulation of Cardiac Function PDF

Regulation of Cardiac Function  Regulation of Heart Pumping When a person is at rest, the heart pumps only 4 to 6 liters of blood each minute During severe exercise, the heart may be required to pump four to seven times this amount.  Regulation of Heart Pumping The basic means by...

Regulation of Cardiac Function  Regulation of Heart Pumping When a person is at rest, the heart pumps only 4 to 6 liters of blood each minute During severe exercise, the heart may be required to pump four to seven times this amount.  Regulation of Heart Pumping The basic means by which the volume pumped by the heart is regulated are; 1. Intrinsic Regulation of Heart Pumping—The Frank-Starling Mechanism: each peripheral tissue of the body When an extra controls its own local blood flow amount of blood flows into all the local tissue flows combine and the ventricles, return by way of the veins to the the cardiac right atrium muscle itself is stretched to greater The heart, in turn, automatically length. pumps this incoming blood into the arteries, so that it can flow around the circuit again  Regulation of Heart Pumping 2. Control of heart rate and strength of heart pumping by the the Sympathetic and Parasympathetic Nerves: For given levels of input atrial pressure, the amount of blood pumped each minute (cardiac output) often can be increased more than 100 per cent by sympathetic stimulation By contrast, the output can be decreased to as low as zero or almost zero by vagal (parasympathetic) stimulation.  Cardiac Output The cardiac output is the volume of blood pumped per minute by each ventricle. The average resting cardiac rate in an adult is 70 beats per minute; the average stroke volume (volume of blood pumped per beat by each ventricle) is 70 to 80 ml per beat The product of these two variables gives an average cardiac output of 70 X 80 = 5600 ml (5.6 L) per minute An increase in cardiac output, as occurs during exercise, must thus be accompanied by an increased rate of blood flow through the circulation. This is accomplished by factors that regulate the 1. cardiac rate and 2. stroke volume.  1. Regulation of Cardiac Rate In the complete absence of neural influences, the heart will continue to beat according to the rhythm set by the SA node Normally, however, sympathetic and vagus (parasympathetic) nerve fibers are continuously active and modify the rate of spontaneous depolarization of the SA node Sympathetic effect Parasympathetic Norepinephrine, released primarily by effect released from Acetylcholine, sympathetic nerve endings, and parasympathetic endings, epinephrine, secreted by the adrenal promotes the opening of K+ medulla, stimulate the opening of Na+ channels in the pacemaker and Ca2+ channels in the plasma cells. membrane of pacemaker cells of the SA node This hyperpolarizes the SA stimulates an increased rate node and thus decreases the of firing of the SA node rate of its spontaneous firing CHRONOTROPIC EFFECTS (mechanisms affect rate) Regulation of Cardiac Rate The most important factors are: 1. Nervous factors 2. Chemical factors 3. Others 7  Regulation of Cardiac Rate In the complete absence of neural influences, the heart will continue to beat according to the rhythm set by the SA node Normally, however, sympathetic and vagus (parasympathetic) nerve fibers to the heart are continuously active and modify the rate of spontaneous depolarization of the SA node Norepinephrine, released primarily by Acetylcholine, released from sympathetic nerve endings, and parasympathetic endings, epinephrine, secreted by the adrenal promotes the opening of K+ medulla, stimulate the opening of Na+ channels in the pacemaker and Ca2+ channels in the plasma cells. membrane of pacemaker cells of the SA node This hyperpolarizes the SA stimulates an increased rate node and thus decreases the of firing of the SA node rate of its spontaneous firing CHRONOTROPIC EFFECTS (mechanisms affect rate) 8  Autonomic regulation of cardiac rate Sensory receptors > cardiovascular center in medulla oblongata > increase or decrease in frequency of nerve impulses in both sympathetic and parasympathetic branches of ANS. Sensory receptors: proprioceptors, chemoreceptors, and baroreceptors. Sympathetic neurons go from medulla oblongata > spinal cord (thoracic region) > SA (cardiac accelerator), AV, portions of 9 myocardium. Heart Regulation by Baroreceptors 10 Heart Rate - Determined by SA Node Firing Rate – SA node intrinsic firing rate = 100/min No extrinsic control on heart, HR = 100 – SA node under control of ANS and hormones Rest: parasympathetic dominates, HR = 75 Excitement: sympathetic takes over, HR increases Effects of Sympathetic Activity on Heart Rate Increased sympathetic activity (nerves or epinephrine) Beta 1 receptors in SA node Increase open state of If and calcium channels Increase rate of spontaneous depolarization Increase heart rate Effects of Parasympathetic Activity on Heart Rate Increased parasympathetic activity (vagus nerve) Muscarinic Cholinergic Receptors in SA Node Increase open state of K channels and closed state of calcium channels Decrease rate of spontaneous depolarization and hyperpolarize cell Decrease heart rate Sympathetic Effects: SA Potentials Chemical regulation of cardiac rate 1. Hormones: ▪ Norepinephrine and epinephrine (from adrenal medulla) lead to ▪ ↑HR & ↑ contractility ▪ Adrenal medulla stimulated by: ▪exercise ▪ stress ▪excitement ▪ Thyroid hormones result in ↑ HR & ↑Contractility ▪ Hyperthyroidism occurs tachycardia 2. Cations ↑ Na+ & K+ → ↓ HR & Contractility ↑Ca2+ → ↑ HR & ↑Contractility 15  Other factors in regulation of cardiac rate ❖ Age: Newborn HR ~120 beats/min Old people may also develop ↑ HR ❖ Gender: Adult females → higher HR than males ❖ Exercise: Athletic bradycardia (60 or under) (more efficient heart) ❖ Body temperature (BT): ↑ BT (fever or exercise) →↑ HR ↓BT→ ↓ HR & contractility 16  2. Regulation of Stroke Volume The stroke volume is regulated by three variables: (1) the end diastolic volume (EDV), which is the volume of blood in the ventricles at the end of diastole; (2) the total peripheral resistance, which is the frictional resistance, or impedance to blood flow, in the arteries; and (3) the contractility, or strength, of ventricular contraction.  End-diastolic volume The end-diastolic volume is the amount of blood in the ventricles immediately before they begin to contract This is a workload imposed on the ventricles prior to contraction, and thus is sometimes called a preload The stroke volume is directly proportional to the preload; an increase in EDV results in an increase in stroke volume. Frank–Starling Law of the Heart= when the ventricles contract more forcefully, they pump more blood. 18  Total peripheral resistance In order to eject blood, the pressure generated in a ventricle when it contracts must be greater than the pressure in the arteries The pressure in the arterial system before the ventricle contracts is, in turn, a function of the total peripheral resistance—the higher the peripheral resistance, the higher the pressure. In summary, the stroke volume is inversely proportional to the total peripheral resistance; the greater the peripheral resistance, the lower the stroke volume Thereafter, a healthy heart is able to compensate for the increased peripheral resistance by beating more strongly. 19  Contractility Contractility: strength of contraction at any given preload + inotropism: It means of increased contractility. It may result from sympathetic stimulation, - Hormones; Norepinephrine and epinephrine - inotropism: It means of decreased contractility. It may result from: - inhibition of the sympathetic system - anoxia - acidosis 20 21  Factors Affecting Cardiac Output: Stroke Volume Primary factors affecting stroke volume – Ventricular contractility – End-diastolic volume – Afterload  Stroke Volume – Ventricles never completely empty of blood More forceful contraction will expel more blood – Extrinsic controls of SV Sympathetic drive to ventricular muscle fibers Hormonal control – Intrinsic controls of SV Changes in EDV Extrinsic Control of Stroke Volume – Sympathetic innervation of contractile cells Cardiac nerves NE binds to β1 adrenergic receptors Increases cardiac contractility – Parasympathetic innervation of contractile cells Not significant – Hormones Thyroid hormones, insulin and glucagon increase force of contraction Sympathetic Effects on Contractility – Increased sympathetic activity Increased epinephrine release Increases strength of contraction Increases rate of contraction Increases rate of relaxation Principle of Frank-Starling’s Law – Increased EDV stretches muscle fibers – Fibers closer to optimum length – Optimum length = greater strength of contraction – Result = Increased SV Intrinsic Control - Frank-Starling’s Law Increase venous return Increase strength of contraction Increase stroke volume Blood Pressure = Cardiac Output x Total Peripheral Resistance Cardiac Output = Stroke volume x cardiac rate  CHANGES IN CARDIOVASCULAR PERFORMANCE BY ALTERING THE CARDIAC FUNCTION - CHANGING CONTRACTILITY - CHANGING HEART RATE BY ALTERING THE VASCULAR FUNCTION - CHANGING MEAN CIRCULATORY PRESSURE Blood Volume Venous Capacity - CHANGING TOTAL PERIPHERAL RESISTANCE  MOTOR CORTEX HYPOTHALAMUS Sympathetic Chemosensitive Area Nervous System VASOMOTOR CENTER PRESSOR AREA Glossopharyngeal DEPRESSOR AREA Nerve CARDIOINHIBITORY AREA Vagus Baroreceptors Carotid Sinus Aortic Arch HEART Arterioles Veins Chemoreceptors Adrenal Carotid Bodies Aortic Bodies Medulla Bainbridge Reflex (↑ Heart Rate) Atrial Receptors Volume Reflex (↑ Urinary OUTPUT) a. ↓ Vascular Sympathetic Tone b. ↓ ADH Secretion c. ↓ Aldosterone Secretion Principles of hemodynamics and regulation of blood pressure  Blood pressure The arterial blood pressure carries blood from the heart to organs and tissues. The blood pressure is the highest in the aorta. The blood pressure is the lowest in the vena cava. During the cardiac cycle, the highest pressure is called systolic blood pressure, and the lowest pressure is called diastolic blood pressure. 33  Arterial pressure = Cardiac Output X Total Peripheral Resistance The Total Peripheral Resistance is generated by arterial system occuring pressure via vasodilatation or vasoconstruction, and blood volume. Normal values of the blood pressure: Systolic pressure 120 mm/Hg Diastolic pressure 80 mm/Hg 34  Blood Pressure The pressure of the arterial blood is regulated by the blood volume, total peripheral resistance, and the cardiac rate. Resistance to flow in the arterial system is greatest in the arterioles because these vessels have the smallest diameters Blood flow and pressure are thus reduced in the capillaries, which are located downstream of the high resistance imposed by the arterioles 35  Blood Volume Fluid in the extracellular environment of the body is distributed between the blood and the interstitial fluid compartments by filtration and osmotic forces acting across the walls of capillaries. The function of the kidneys influences blood volume because urine is derived from blood plasma. The hormones ADH and aldosterone act on the kidneys to help regulate the blood volume. The distribution of water between the tissue fluid and the blood plasma is determined by a balance between opposing forces acting at the capillaries. 36 Exchange of Fluid Between Capillaries and Tissues The distribution of extracellular fluid between the plasma and interstitial compartments is in a state of dynamic equilibrium. Glucose and various other solutes are passed to tissues as well; balance is achieved. Movement of plasma proteins is restricted (oncotic pressure). The osmotic pressure is higher in capillaries. Starling forces favor movement of water out of capillaries and back into venules exchange is continuous some of the fluid is returned to lymph (about 15%) and eventually to circulation. Tissue fluid is a continuously circulating medium, formed from and returning to the vascular system 38  Filtration results from blood pressure within the capillaries. hydrostatic pressure, which is exerted drops to against the inner about 17 capillary wall, is equal mmHg at the to about 37 mmHg at venular end of the arteriolar end the capillaries 39  Causes of Edema Excessive accumulation of tissue fluid is known as edema 1. high arterial blood pressure, which increases capillary pressure and causes excessive filtration 2. venous obstruction—or mechanical compression of veins (during pregnancy, for example)—which produces a congestive increase in capillary pressure 3. leakage of plasma proteins into interstitial fluid, which causes reduced osmotic flow of water into the capillaries. 40