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Electrical Component Phases of the Cardiac Cycle Ventricular filling (mid-to-late diastole) Heart blood pressure is low as blood enters atria and flows into ventricles AV valves are open Atrial contraction - systole 2 1 Phases of the Cardiac Cycle Ventricular contraction Atria relaxation Rising ventricular pressure results in closing of AV valves Early phase of ventricular systole (isovolumic) phase Ventricular ejection phase opens semilunar valves – ventricular filling 3 Phases of the Cardiac Cycle Ventricular relaxation Backflow of blood in aorta and pulmonary trunk closes semilunar valves Dicrotic notch – brief rise in aortic pressure caused by backflow of blood rebounding off semilunar valves Isovolumetric relaxation – early diastole Pressure lower than atria and AV valves open 4 2 Ventricular, Aortic and Atrial Pressures 0 0 .1 Time ( sec) 0 .3 0 .4 0 .5 0 .6 0 .7 0 .8 Aortic valve closes Dichrotic notch 0 .2 Aortic valve opens mmHg 120 Aorta atrium Pressure 100 Aort ic 80 60 Mitral valve closes 40 Mitral valve opens 20 Atrial Vent ricular 0 a wave c wave v wave R T P (a) ECG 1 4 8 Q 0.1 sec Atrial systole 0.3 sec Ventricular systole 120 0.4 sec Relaxation period Atrial depolarization 2 Begin atrial systole 3 End (ventricular) diastolic volume 4 Ventricular depolarization 5 Isovolumetric contraction 6 Begin ventricular ejection 7 End (ventricular) systolic volume 8 Begin ventricular repolarization 9 Isovolumetric relaxation 9 Dicrotic wave 100 Aortic pressure 5 80 6 (b) Pressure (mmHg) 1 S Left ventricular pressure 60 40 Left atrial pressure 10 20 2 0 (c) Heart sounds S1 S2 S3 S4 3 End (ventricular) diastolic volume 130 10 Ventricular filling Stroke volume (d) Volume in ventricle (mL) 60 7 0 (e) Phases of the cardiac cycle Atrial contraction Isovolumetric contraction UniversityIsovolumetric of Jordan Ventricular ejection relaxation Ventricular filling Atrial contraction 6 3 Heart Sounds 7 Auscultation – listening to heart sound via stethoscope Four heart sounds S1 – “lubb” caused by the closing of the AV valves S2 – “dupp” caused by the closing of the semilunar valves S3 – a faint sound associated with blood flowing into the ventricles S4 – another faint sound associated with atrial contraction First Heart Sound (S1) • Sudden closing of the mitral and tricuspid valves during the onset of systole will cause echo as a result of blood oscillation and vibration of the valves and walls of the ventricles. • Loudest at the apex of the heart • "lubb" of "lubb-dub" 4 Second Heart Sound (S2) • Sudden closing of the semilunar valves at the end of systole caused the sudden block of arterial blood back into the ventricles. The elastic recoil of the arteries cause the blood to bounce forward which will vibrate the blood, valves and ventricle walls. •Best heard in the second thoracic interspace just left and right of the sternum (pulmonic area) • Shorter duration than S1 • “dub" of "lubb-dub" Heart Sounds 10 5 Aortic Pressure Curve o Aortic pressure starts increasing during systole after the aortic valve opens o Aortic pressure decreases toward the end of the ejection phase o After the aortic valve closes, an incisura occurs because of sudden cessation of back-flow toward left ventricle o Aortic pressure decreases slowly during diastole because of the elasticity of the aorta 11 Cardiac Cycle ECG - P - atrial wave QRS - Ventricular wave T - ventricular repolarization Systole - muscle stimulated by action potential and contracting Diastole - muscle reestablishing Na+/K+/Ca++ gradient and is relaxing 12 6 Atrial Pressure Atrial pressure waves (a-c-v waves) a-wave - atrial contraction c-wave – ventricular contraction (A-V valves bulge) v-wave - flow of blood into atria 13 Ventricular Pressure and Volume Curves Diastole Isovolumic relaxation A-V valves open (ventricular pressure < atrial pressure) Rapid filling (first 1/3) Diastasis - slow flow into ventricle Atrial systole - extra blood in and this just follows P wave (accounts for less than 25% of filling) 14 7 Ventricular Pressure and Volume Curves Systole Isovolumic contraction A-V valves close (ventricular pressure >atrial pressure) Aortic valve opens Rapid Ejection phase Slow ejection phase 15 Ventricular Filling (Diastole) Rapid filling phase mmHg Slow Filling Phase: Diastasis 120 100 80 Aort ic 120 ml 60 40 Ventricular volume 50 ml 20 0 Stroke volume At rial 8 Stroke Volume • Stroke volume is the volume of blood pumped out by the right/left ventricle in one contraction. • SV = end diastolic volume (EDV) end systolic volume (ESV) – EDV = amount of blood collected in a ventricle at the end of diastolic phase – ESV = amount of blood remaining in a ventricle after contraction 17 Ejection fraction • Fraction of the end-diastolic volume that is ejected is called the ejection fraction (EF) - usually greater than 55 % • Ventricles empty during systole - the volume decreases about 70 ml which is called the stroke volume EF = SV÷EDV 9 Cardiac Output • Is volume of blood pumped per minute by each ventricle • CO = volume of blood ejected from left (or right) ventricle into aorta (or pulmonary trunk) each minute • CO = stroke volume (SV) x heart rate (HR) • In typical resting male 5.25L/min = 70mL/beat x 75 beats/min • Entire blood volume flows through pulmonary and systemic circuits each minute Ejection Fraction 20 End diastolic volume = 125 ml End systolic volume = 55 ml Ejection volume (stroke volume) = 70 ml Ejection fraction = 70ml/125ml = 56% (normally 60%) If heart rate (HR) is 70 beats/minute, what is cardiac output? Cardiac output = HR * stroke volume = 70/min * 70 ml = 4900ml/min 10 Maintain Flow (QIN = QOUT) QIN Vein HEART Aorta QOUT HEART NORMAL QIN Aorta Vein QOUT HEART Vein Aorta QOUT QIN To maintain QIN = QOUT the heart must rapidly adjust its force of contraction on a beat-to-beat basis. How does the heart do this? FRANK – STARLING LAW FRANK – STARLING LAW Maintain Flow (QIN = QOUT) QIN QOUT 11 Frank-Starling Mechanism Within physiological limits the heart pumps all the blood that comes to it without excessive collection in the veins. With increased stretch of cardiac muscle the heart muscle contracts with more force The actin and myosin filaments are brought to a more optimal degree of overlap for force generation Stretch of the right atrial wall directly increases the heart rate by 10 to 20% Frank-Starling Law of the Heart An increase in the end-diastolic volume ↑ sarcomere length ↑ increases the stroke volume ↑ ejection fraction Failing hearts use the Frank-Starling law 12 Preload : the degree of stretch in the heart before it contracts Contractility: the forcefulness of contraction of individual ventricular muscle fibers Afterload: the pressure that must be exceeded if ejection of blood from the ventricles is to occur 25 Factors Affecting Stroke Volume Preload – amount ventricles are stretched by contained blood =EDV Contractility – cardiac cell contractile force due to factors other than EDV Afterload – back pressure exerted by blood in the large arteries leaving the heart (Aortic pressure) 26 13 Frank-Starling Law of the Heart Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume Slow heartbeat and exercise increase venous return to the heart, increasing SV Blood loss and extremely rapid heartbeat decrease SV (↓Q) 27 Autonomic Effects on Heart Sympathetic stimulation causes increased HR and increased contractility with HR = 180-200 and CO = 15-20 L/min. Parasympathetic stimulation decreases HR markedly and decreases cardiac contractility slightly. Vagal fibers go mainly to atria (hyperpolarization) Fast heart rate (tachycardia) can decrease CO because there is not enough time for heart to fill during diastole 14 29 Changes during Cardiac Cycle Volume changes: End-diastolic volume, End-systolic volume, Stroke volume and Cardiac output. Aortic pressure: Diastolic pressure 80 mmHg, Systolic pressure 120 mmHg (most of systole ventricular pressure higher than aortic) Ventricular pressure 30 Diastolic 0 Systolic Lt. 120; Rt. 25 mmHg. Atrial pressure: A wave =atrial systole, C wave= ventricular contraction (AV closure), V wave= ventricular diastole (AV opening) Heart sounds: S1 = turbulence of blood around a closed AV valves, S2 = turbulence of blood around a closed semilunar valves. 15 Phases of the Cardiac Cycle 31 Factors that Increase Cardiac Output CO = SV x HR 16 Extrinsic Factors Influencing Stroke Volume Contractility is the contractile strength, at fixed preload and afterload Increase in contractility comes from: Increased sympathetic stimuli Certain hormones (epinephrine) Ca2+ and some drugs 33 Extrinsic Factors Influencing Stroke Volume Agents/factors that decrease contractility include: Acidosis (H+) Increased extracellular K+ Calcium channel blockers 34 17