Lecture 14: Cardiac Cycle and Heart Rate - PDF

About This Chapter 14.4 The Heart as a Pump 15.1 The Blood Vessels 15.2 Blood Pressure Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved 14.4 The Heart as Pump • Electrical signals coordinate contraction • Internodal pathway from sinoatrial node (SA node) to atrioventric...

About This Chapter 14.4 The Heart as a Pump 15.1 The Blood Vessels 15.2 Blood Pressure Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved 14.4 The Heart as Pump • Electrical signals coordinate contraction • Internodal pathway from sinoatrial node (SA node) to atrioventricular node starts at SA node (autorythmic cells in right atrium) —> specialized conducting system of non-contractile (AV node) Depolarization autorythmic fibres —> AV node (autorythmic cells near the floor of the right atrium) – Routes the direction of electrical signals so the heart contracts from apex to base conducting cells of centrioles • Purkinje fibers transmit electric signals down the atrioventricular bundle (AV branch fibres continue downward to bundle or bundle of His) to left and right bundle branches. Bundle apex, where they divide into smaller in ventricular septum • SA node sets the pace of the heartbeat at 70 bpm Purkinje fibers that spread outward among the contractile cells – AV node (50 bpm) and Purkinje fibers (25–40 bpm) can act as pacemakers under some conditions – AV node delay with slower conductional signals through nodal cells slow down transmission of AP slightly to allow the atria to complete their contraction before ventricular contraction begins • Pacemakers set the heart rate in SA node bc fastest Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.14 Electrical conduction in myocardial cells Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.15 The conducting system of the heart Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved The Electrocardiogram Reflects Electrical Activity • Electrocardiogram (ECG) – Show the summed electrical activity generated by all the cells of the heart – Not the same as an action potential • Waves of the ECG – Three waves ▪ P wave: depolarization of the atria ▪ QRS complex: wave of ventricular depolarization Q wave sometimes absent on normal ECGs –Atrial repolarization is part of QRS but not represented by a special wave ▪ T wave: repolarization of the ventricle – Two segments ▪ P-R segment: AV nodal delay ▪ T-P segment: ventricular and atrial relaxation Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved The Heart Contracts and Relaxes during a Cardiac Cycle (1 of 3) atria and ventricles do not contract and relax at the same time • Diastole: cardiac muscle relaxes • Systole: cardiac muscle contracts • Five phases of the cardiac cycle (1 – 2) ① The heart at rest: atrial and ventricular diastole ▪ The atria are filling with blood from the vein ▪ AV valves open → ventricles fill ② Completion of ventricular filling: atrial systole ▪ Atria contract ▪ Last 20% of blood volume driven to ventricles ▪ End-diastolic volume (EDV): volume in ventricle at the end of ventricular relaxation Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved The Heart Contracts and Relaxes during a Cardiac Cycle (2 of 3) • Five phases of the cardiac cycle (3 – 4) heart sound: vibrations following closure of AV ③ Early ventricular contraction First « lub » of « lub-dup » ▪ AV valves close ▪ No blood in or out (isovolumic ventricular contraction) ▪ Increasing pressure due to ventricular muscle contraction ▪ Concurrent atrial diastole –Atria relax and blood flows in the atria ④ The heart pumps: ventricular ejection ▪ Semilunar valves open ▪ Blood is ejected into arteries ▪ End-systolic volume (ESV): volume in ventricle at the end of ventricular contraction Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved The Heart Contracts and Relaxes during a Cardiac Cycle (3 of 3) • Five phases of the cardiac cycle (5) ⑤ Ventricular relaxation second heart sound: dup caused by vibrations created by semilunar valve closure ▪ Arterial blood flows back towards heart –Semilunar valves shut ▪ Ventricular muscles relax pressure drops (still higher than atrial pressure) ▪ No blood enters or exits (isovolumic ventricular relaxation) ▪ AV valves open when ventricular pressure drops below atrial pressure • Pressure-volume curves represent one cardiac cycle see figure 14.18b Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.18 Mechanical events of the cardiac cycle A: ventricle has completed a contraction and contains a minimum amount of blood that it will hold during cycle. It has relaxed, and its pressure is at its minimum value. Blood is flowing into atrium from pulmonary veins Once pressure in atrium > pressure in ventricle: mitral valve opens A —> B: atrial blood flows into ventricle, increasing volume As blood flows in, relaxing ventricle expands to accommodate blood entry, so volume of ventricle increases, but the pressure in the ventricle goes up very little A’ —> B: ventricular filling completed by atrial contraction B: ventricle contains maximum volume of blood that it will hold during cardiac cycle (EDV) (135 ml) B —> C: ventricular contraction begins, so mitral AV valve closes (AV and semilunar valve closed so blood in ventricle has nowhere to go), ventricle continues to contract, causing pressure to increase rapidly during isovolumic contraction C: Once ventricular pressure > aorta, aortic valve opens C —> D: pressure continues to increase as ventricle contracts further, but ventricular volume decreases as blood is pushed out into the aorta D: ESV is minimum volume of blood ventricle has during 1 cycle (65 ml) At the end of each ventricular contraction, they begin to relax, so ventricular pressure decreases and once pressure in ventricle < aortic pressure, semilunar valve closes and ventricle becomes a sealed chamber D —> A: Remainder of relaxation occurs without a change in blood volume = isovolumic relaxation When ventricular pressure < atrial pressure, mitral valve opens and cycle begins again Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Electrical and mechanical events of cardiac cycle Figure 14.19 The Wiggers diagram Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Stroke Volume is the Volume of Blood Pumped per Contraction • Stroke volume (SV) = EDV-ESV – Volume of blood before contraction minus volume of blood after contraction – Average = 70 mL (70-kg man at rest) • Cardiac output is a measure of cardiac performance – Volume of blood pumped by one ventricle in a given period of time – Cardiac output (CO) = heart rate  stroke volume – Average = 5 L/min Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved The Autonomic Division Modulates heart Rate • Parasympathetic control – Decrease heart rate + – K permeability increases ▪ Pacemaker potential begins at a lower value – Ca2+ permeability decreases ▪ Slows rate of pacemaker depolarization • Sympathetic control – Increase heart rate – β1-adrenergic receptors on the autorhythmic cells – Na+ & Ca2+ permeability increases ▪ Increases rate of pacemaker depolarization • Tonic control Spontaneous depolarization rate of SA when sympathetic and parasympathetic input is blocked: 90/100 times per minute —> tonic parasympathetic activity must slow the intrinsic rate down from 90 bpm to achieve a resting heart rate of 70 bpm – Normally dominated by parasympathetic activity Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.20c Autonomic control of heart rate Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.20(d)-(e) Autonomic control of heart rate Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Multiple factors Influence Stroke Volume • Contractility: intrinsic ability of a cardiac muscle fiber to contract at any given fiber length is a function of Ca2+ interaction with contractile filaments • Length-tension force created by a muscle fiber is directly related to the length of the sarcomere (initial length of muscle fiber) relationships the longer the muscle fiber and sarcomere when a contraction begin, the grater the tension developed up to a maximum – Determined by volume of blood at beginning of contraction – Degree of stretch is called preload stretch represents load placed on cardiac muscles before contraction • Frank-Starling law of the heart – Stroke volume is proportional to EDV – The heart pumps all the blood that is returned to it • Stroke volume and venous return – EDV is determined by venous return which is affected by skeletal muscle contractions that squeeze veins to push blood toward the heart during Increased pressure in abdominal veins + decreased pressure in thoracic enhances venous return during inspiration 1) skeletal muscle pump exercise When chest expands and diaphragm moves toward abdomen, thoracic cavity enlarges and 2) respiratory pumpdevelops a subatmospheric pressure (low pressure) —> decreases pressure in inferior vena cava as it passes through thorax, —> helps draw more blood into vena cava from veins from abdomen 3) sympathetic innervation of veins constriction of veins: volume decreases, which squeezes more blood ouf of them and into heart with larger ventricular volume at beginning of next contraction, ventricle contracts more, sending blood out into the arterial side of circulation Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.21 Length-tension relationships Longer the muscle fiber and sarcomere when a contraction begins, the greater the tension developed, up to a maximum A stretch of the ventricular wall increases, so does the stroke volume stroke volume changes with increased contractility due to norepinephrine Contractility is not the same thing as length-tension relationship —> a muscle can remain at one length, but show increased contractility bc calcium more available Increasing sarcomere length makes cardiac muscle more sensitive to calcium thus linking contractibility to muscle length Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Contractility Is Controlled by the Nervous and Endocrine Systems • Any chemical that affects contractility is an inotropic agent → inotropic effect • Positive inotropes – increase contractility medication – Epinephrine, norepinephrine, and digitalis neurotransmitters (E, NE) regulatory protein – Catecholamines increase Ca2+ storage with phospholamban • Negative inotropes – decrease contractility • EDV and arterial blood pressure determine afterload – Afterload: combined load of EDV and arterial resistance during ventricular contraction – Ejection fraction: percentage of EDV ejected with one contraction ▪ Stroke volume/EDV Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.22 Catecholamines increase cardiac contraction Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.23 Stroke volume and heart rate determine cardiac output Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved 15.1 The Blood Vessels • Walls of blood vessels contain smooth muscle and elastic and fibrous connective tissue • Wall thickness varies in different vessels • Inner layer is endothelium • – Secretes paracrine factors – Regulates blood pressure, blood vessel growth, and absorption Blood vessels contain vascular smooth muscle – Arranged in circular or spiral layers narrows diameter widens diameter of vessel lumen – Vasoconstriction and vasodilation – Muscle tone is a state of partial contraction in most blood vessels Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 15.2 Blood vessel structure Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Arteries and Arterioles Carry Blood Away from the Heart • • • Arteries – Act as pressure reservoir – Thick layers of vascular smooth muscles – Lots of elastic and fibrous connective tissue Arterioles – Site of variable resistance – Part of the microcirculation – Less elastic and more muscular Metarterioles – Branches of arterioles – Partial smooth muscle layer – Precapillary sphincters open and close to direct blood flow to capillaries or venous circulation Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Exchange Takes Place in the Capillaries • Smallest vessels • Primary site of exchange between blood and interstitial fluid • Walls • – Lack smooth muscle – Flat layer of endothelium – Basal lamina Pericytes – Contractile cells associated with capillaries – Contribute to capillary impermeability – Secrete paracrine factors that promote vascular growth and differentiation Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 15.3 Capillary beds Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Blood Flow Converges in the Venules and Veins • • Venules – Receive blood from capillaries – Thin exchange epithelium – Little connective tissue – Convergent pattern of flow Veins take blood back to the heart – Act as volume reservoir – Thin walls of vascular smooth muscles – Contain one-way valves, prevent backward flow – More numerous than arteries – Lie closer to the body surface – Less elastic tissue Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 15.4 Valves ensure one-way flow in veins Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved 15.2 Blood Pressure decrease in pressure occurs bc energy is lost as a result of resistance to flow offered by vessels • Blood pressure is highest in arteries and lowest in veins – Pulse pressure measure of strength pressure wave produced by ventricular contraction ventricular systole ventricular diastole ▪ Pulsepressure = systolic pressure – diastolicpressure ▪ Decreases over distance due to friction – Venous return aided by valves, skeletal muscle pump, and respiratory pump by the pumping action of the heart ventricle pressure difficult to measure, so we assume that arterial blood pressure reflects it —> pulsatile • Arterial blood pressure reflects the driving pressure for blood flow – Mean Arterial Pressure (MAP) represents driving pressure ▪ MAP = diastolic pressure + 1 3 (systolic pressure – diastolic pressure) – Hypotension is lower than normal MAP, hypertension is higher than instrument consisting of inflatable cuff and pressure normal MAP gauge: cuff encircles upper arm and is inflated until • Blood pressure is estimated by sphygmomanometry – Korotkoff sounds as blood squeezes through the still-compressed artery, that sound can be head with each pressure wave bc of turbulent flow of blood through compression pressure higher than systolic pressure driving arterial blood, when cuff pressure > arterial pressure, blood flow into lower arm stops, now pressure on cuff gradually released and when cuff pressure < systolic arterial blood pressure, blood begins to flow again Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 15.5 Arteries are a pressure reservoir Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 15.6 Systemic circulation pressures Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Cardiac Output and Peripheral Resistance Determine Mean Arterial Pressure • MAP  CO × Rarterioles • Blood flow into aorta = cardiac output of left ventricle • If flow in exceeds flow out of aorta then blood volume increases and MAP increases • If flow out exceeds flow in of aorta then blood volume decreases and MAP decreases • Changes in blood volume affect blood pressure – Blood volume is relatively constant ▪ Some gain and loss throughout the day ▪ If blood volume increase, then pressure increases – Kidney is responsible for removing excess fluid volume ▪ If blood volume decrease, then pressure decreases – Lost fluid volume compensated through drinking or intravenous infusion – Vasoconstriction and sympathetic stimulation of heart Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 15.8(a) Mean Arterial Blood Pressure (a) Mean arterial pressure is a function of cardiac output and peripheral resistance Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 15.8(b) Mean Arterial Blood Pressure (b) Factors that influence mean arterial pressure Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 15.9 Compensation for increased blood volume Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Key words sinoatrial node (SA node), internodal pathway, atrioventricular node (AV node), atrioventricular (AV) bundle (bundle of His), Purkinje fibers, bundle branches, AV node delay, cardiac cycle, diastole, systole, end diastolic volume (EDV), isovolumic ventricular contraction, ventricular ejection, end-systolic volume (ESV), isovolumic ventricular relaxation, end-diastolic volume (EDV), cardiac output, Frank-Starling law of the heart, perfusion, elastic recoil, pressure reservoir, arterioles, volume reservoir, vascular smooth muscle, vasoconstriction, vasodilation, muscle tone, systolic pressure, diastolic pressure, pulse, pulse pressure, venous return, skeletal muscle pump, respiratory pump, mean arterial pressure (MAP), myogenic autoregulation, Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved