Department of medical physiology 9 th week and 10 th week

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1 Department of medical physiology 9 th week and 10 th week Semester: winter Study program: Dental medicine Lecture: RNDr. Soňa Grešová, PhD. Department of medical physiology Faculty of Medicine PJŠU

2 1. Cardiac cycle Cardiovascular system 9th week and 10th week 2. Ventricular efficiency, cardiac output, cardiac work 3. The heart as a pump its control mechanism

3 1. Relationship of the electrocardiogram Systole = period of contraction Diastole = period of relaxation Phases of the cardiac cycle 1. Atrial Systole 2. Isovolumetric Ventricular Contraction Increased pressure in the ventricles causes the AV valves to close Creates the first heart sound (lub) 3. Ventricular Ejection the periods of rapid and slow ejection of the ventricles 4. Isovolumetric Ventricular Relaxation Intraventricular pressure drops below aortic pressure Semilunar valves close = second heart sound (dup) 5. Filling of the ventricles the periods of rapid and slow filling of the ventricles to the cardiac cycle Copyright: Hall, J. E., & Guyton, A. C. (2006). Guyton and Hall textbook of medical physiology. Philadelphia, PA: Saunders Elsevier.

4 1. Relationship of the electrocardiogram EDV =during diastole, normal filling of the ventricles increases the volume of each ventricle to about 110 to 120 milliliters. This volume is called the end-diastolic volume. to the cardiac cycle SV= then, as the ventricles empty during systole, the volume decreases about 70 milliliters, which is called the stroke volume output. ESV = the remaining volume in each ventricle, about 40 to 50 milliliters, is called the end-systolic volume. EDV= 120 ml SV= 70ml ESV= 50ml Copyright: Hall, J. E., & Guyton, A. C. (2006). Guyton and Hall textbook of medical physiology. Philadelphia, PA: Saunders Elsevier.

5 2. VENTRICULAR EFFICIENCY LV does not empty completely during systole ESV is around 50 ml EDV - ESV = SV (stroke volume) SV is the amount of blood transferred from LV to the arterial system during systole In healty person SV should be > 60 ml EF (ejection fraction) = SV / EDV (normally about 55% - 75%) EF is an important measurement of cardiac efficiency EF is used clinically to assess cardiac status in patients with heart failure

6 2. CARDIAC OUTPUT CO (L/min) = HR x SV HR is established on the SA node and is controlled by ANS SV is dependent on, LV preload LV afterload Contractility Preload: Muscle length before contraction begins - Preload is related with the volume of blood entering the chamber (EDV) - Depends from EDV, EDP, Left atrium pressure, Pulmonary veins pressure Afterload: The load against which a myocyte must shorten - The principal component of afterload is arterial pressure - depends from pressure in aorta, total peripheral resistance (TPR) Contractility: measure of a muscle s ability to shorten against a afterload - Contractility equates with the cytoplasmic free Ca concentration - depends from changes pressure/time, EF Preload and contractility are directly proporcional with stroke volume Afterload isinversely proportional with stroke volume

7 2. Measurement of cardiac output using the oxygen Fick principle CO L min = HR SV Fick principle CO L min CO = CO = 5040 ml min = O 2 absorbed per minute by the lungs ml min Arteriovenous O 2 difference mlτl of blood CO L min = 200 ml min 40 ml L CO = 5 L min Copyright: Hall, J. E., & Guyton, A. C. (2006). Guyton and Hall textbook of medical physiology. Philadelphia, PA: Saunders Elsevier.

8 2. CARDIAC WORK Minute Cardiac work = CO x Aortic pressure O 2 consumption is directly proportional to min. cardiac work Heart performs two kinds of work: I. Internal work II. External work Internal work (Aortic pressure = kinetic energy of blood flow): Expended in «isovolumic contraction» The force necessary to open the aortic and pulmonary valves Accounts for 90% of total cardiac workload External work (CO = volume-pressure work) : Expended in transferring blood to the arterial system against a resistance Accounts for 10% of total cardiac workload

9 Volume pressure diagram EW= External Work (CO = volume-pressure work) IW= Internal work (Aortic pressure = kinetic energy of blood flow) Copyright: Hall, J. E., & Guyton, A. C. (2006). Guyton and Hall textbook of medical physiology. Philadelphia, PA: Saunders Elsevier.

10 3. The heart as a pump its control mechanism

11 3. The heart as a pump its control mechanism factors affecting Heart Rate 1. Atrial reflex - Volumoreceptors (type B in RA): volume loading conditions Bainbridge response prevails (only HR is affected) - Atrial baroreceptors (type A-low pressure receptors)- stimulation: vasodilatation, 1. BP, HR - Ventricular baroreceptors (through unmyelinated vagal nerve fibers) stimulation: vasodilatation SY, HR

12 2. The heart as a pump its control mechanism factors affecting Heart Rate 2. Autonomic innervation Parasympathetic stimulation - a negative chronotropic factor Supplied by vagus nerve, decreases heart rate, acetylcholine is secreted and hyperpolarizes the heart Sympathetic stimulation - a positive chronotropic factor Supplied by cardiac nerves. Innervate the SA and AV nodes, and the atrial and ventricular myocardium. Increases heart rate and force of contraction. Epinephrine and norepinephrine released. Increased heart beat causes increased cardiac output. Increased force of contraction causes a lower end-systolic volume; heart empties to a greater extent. Limitations: heart has to have time to fill. 2.

13 Key Properties of Myocardial Automaticity (Chronotropic effect) Can produce electrical activity without outside nerve stimulation Conductivity (Dromotropic effect) Ability to transmit an electrical stimulus from cell to cell throughout myocardium Excitability (Batmotropic effect) Ability to respond to an electrical stimulus Contractility (Inotropic effect) Ability of myocardial cells to contract when stimulated by an electrical impulse Cells Copyright: Hall, J. E., & Guyton, A. C. (2006). Guyton and Hall textbook of medical physiology. Philadelphia, PA: Saunders Elsevier.

14 3. The heart as a pump its control mechanism factors affecting Heart Rate 3. Hormones Epinephrine and norepinephrine from the adrenal medulla Occurs in response to increased physical activity, emotional excitement, stress increase heart rate 3. Glucagon Increases heart rate and force of contraction Thyroid hormones Increases heart rate and force of contraction

15 3. The heart as a pump its control mechanism Intrinsic factors affecting Stroke Volume Frank-Starling Law of the Heart 1. Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume; EDV leads to stretch of myocard. preload stretch of muscle force of contraction SV Unlike skeletal fibers, cardiac fibers contract MORE FORCEFULLY when stretched thus ejecting MORE BLOOD ( SV) If SV is increased, then ESV is decreased!! 1. Slow heartbeat and exercise increase venous return (VR) to the heart, increasing SV VR changes in response to blood volume, skeletal muscle activity, alterations in cardiac output VR EDV and in VR in EDV Any in EDV in SV Blood loss and extremely rapid heartbeat decrease SV

16 3. The heart as a pump its control mechanism Extrinsic Factors Influencing Stroke Volume 2. Contractility is the increase in contractile strength, independent of stretch and EDV Referred to as extrinsic since the influencing factor is from some external source Increase in contractility comes from: Increased sympathetic stimuli Certain hormones Ca 2+ and some drugs Agents/factors that decrease contractility include: Increased extracellular K + Calcium channel blockers 2.

17 3. The heart as a pump its control mechanism Extrinsic Factors Influencing Stroke Volume 2 a) Effects of Autonomic innervation on Contractility 2 a) Sympathetic stimulation Release norepinephrine from symp. postganglionic fiber Also, EP and NE from adrenal medulla Have positive ionotropic effect Ventricles contract more forcefully, increasing SV, increasing ejection fraction and decreasing ESV Parasympathetic stimulation via Vagus Nerve -CNX Releases ACh Has a negative inotropic effect Hyperpolarization and inhibition Force of contractions is reduced, ejection fraction decreased

18 3. The heart as a pump its control mechanism Extrinsic Factors Influencing Stroke Volume 2 b) Effects of Hormones on Contractility Epi, NE, and Thyroxine all have positive ionotropic effects and thus contractility Digitalis elevates intracellular Ca ++ concentrations by interfering with its removal from sarcoplasm of cardiac cells Beta-blockers (propanolol, timolol) block beta-receptors and prevent sympathetic stimulation of heart (neg. chronotropic effect) 2 b)

19 3. The heart as a pump its control mechanism Extrinsic Factors Influencing Stroke Volume 3. Afterload back pressure exerted by blood in the large arteries leaving the heart (or the load against which a myocyte must shorten) - the principal component of afterload is arterial pressure - depends from pressure in aorta, total peripheral resistance (TPR) 3.

20 3. The heart as a pump its control mechanism Extrinsic Factors Influencing Stroke Volume Effect of Potassium and Calcium Ions on Heart Function - the high potassium concentration in the extracellular fluids decreases the resting membrane potential in the cardiac muscle fibers - An excess of calcium ions causes effects almost exactly opposite to those of potassium ions, causing the heart to go toward spastic contraction Copyright: Hall, J. E., & Guyton, A. C. (2006). Guyton and Hall textbook of medical physiology. Philadelphia, PA: Saunders Elsevier.

21 3. The heart as a pump its control mechanism Extrinsic Factors Influencing Stroke Volume Effect of Temperature on Heart Function - the heat increases the permeability of the cardiac muscle membrane to ions that control heart rate, resulting in acceleration of the self- excitation process - Contractile strength of the heart often is enhanced temporarily by a moderate increase in temperature, as occurs during body exercise, but prolonged elevation of temperature exhausts the metabolic systems of the heart and eventually causes weakness