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CARDIAC CYCLE DR : SAIDALAVI Carl John Wiggers Otto Frank Sir Thomas Lewis Ernest H Starling Introduction Principal function of cardiovascular system is to deliver oxygen and nutrients to and remove carbon dioxide and wastes from metabolizing tissues. It is by two specialized circulations in series 1. low resistance pulmonary driven by right heart 2. high resistance systemic driven by left heart Systolic pressure in the vascular system refers to the peak pressure reached during the systole, not the mean pressure. The diastolic pressure refers to the lowest pressure during diastole. WIGGERS DIAGRAM EVENTS IN CARDIAC CYCLE PRESSURE VOLUME LOOP The Lewis or wiggers cycle, Guyton & Hall. Textbook of Medical Physiology, 11th Edition WIGGERS DIAGRAM EVENTS IN CARDIAC CYCLE PRESSURE VOLUME LOOP Cardiac cycle The cardiac cycle describes pressure, volume and flow phenomena in the ventricles as a function of time. Similar for both LV and RV except for the timing, levels of pressure. It yields important information on the temporal sequence of events in the cardiac cycle. The three basic events are (1)LV contraction (2) LV relaxation (3) LV filling Phases of cardiac cycle LV Contraction Isovolumetric contraction (b) Maximal ejection (c) LV Relaxation Start of relaxation and reduced ejection (d) Isovolumetric relaxation (e) LV Filling Rapid phase (f) Slow filling (diastasis) (g) Atrial systole or booster (a) Time Intervals Total ventricular systole 0.3 sec Isovolumic contraction (b) 0.05 sec (0.015sec for RV) Maximal ejection (c) 0.1 sec Reduced ejection (d) 0.15 sec Total ventricular diastole 0.5 sec Isovolumic relaxation (e) 0.1 sec Rapid filling phase (f) 0.1 sec Slow filling (diastasis) (g) 0.2 sec Atrial systole or booster (a) 0.1 sec GRAND TOTAL (Syst+Diast) = 0.8 sec Description of Cardiac cycle phases 1. Pressure & Volume events 2. ECG correlation 3. Heart sounds LV RELAXATION • Isovolumic contraction(b) • Maximal Ejection( c) LV CONTRACTION • Isovolumic relaxation(e) • Start of relaxation and reduced ejection (d) • Rapid phase(f) • Slow filling (diastasis)(g) • Atrial systole or booster(a) LV FILLING The letters are arbitrarily allocated so that atrial systole(a) coinicides with the a wave and (c ) with the c wave of JVP. LV contraction. LV pressure starts to build up when the arrival of calcium ions at the contractile proteins starts to trigger actin-myosin interaction. On the electrocardiogram (ECG), the advance of the wave of depolarization is indicated by the peak of the R wave . Soon after, LV pressure in the early contraction phase builds up and exceeds that in the left atrium . (normally, 10 to 15 mm Hg). about 20 milliseconds later M1, the mitral component of the first heart sound occurs. Mitral valve closure is often thought to coincide with the crossover point at which the LV pressure starts to exceed the left atrial pressure. In reality mitral valve closure is delayed because the valve is kept open by the inertia of the blood flow. Shortly thereafter, pressure changes in the right ventricle, similar in pattern but lesser in magnitude to those in the left ventricle, cause the tricuspid valve to close. there by creating T1, the second component of the first heart sound. When the pressure in the left ventricle exceeds that in the aorta, the aortic valve opens, usually a clinically silent event. Opening of the aortic valve is followed by the phase of rapid ejection. The rate of ejection is determined not only by the pressure gradient across the aortic valve, but also by the elastic properties of the aorta and the arterial tree, which undergoes systolic expansion. LV pressure rises to a peak and then starts to fall. Pressure & Volume Changes The AV valves close when the pressure in the ventricles (red) exceeds the pressure in the atria (yellow). As the ventricles contract isovolumetrically -- their volume does not change (white) -- the pressure inside increases, approaching the pressure in the aorta and pulmonary arteries (green). JVP: c wave- d/t Right ventricular contraction pushes the tricuspid valve into the atrium and increases atrial pressure, creating a small wave into the jugular vein. It is normally simultaneous with the carotid pulse. Ventricular chamber geometry changes considerably as the heart becomes more spheroid in shape; circumference increases and atrial baseto-apex length decreases. Early in this phase, the rate of pressure development becomes maximal. This is referred to as maximal dP/dt. Ventricular pressure increases rapidly LV ~10mmHg to ~ 80mmHg (~Aortic pressure) RV ~4 mmHg to ~15mmHg (~Pulmonary A pressure) At this point, semilunar (aortic and pulmonary) valves open against the pressures in the aorta and pulmonary artery Isovolumetric Contraction ECG The QRS complex is due to ventricular depolarization, and it marks the beginning of ventricular systole. Isovolumetric Contraction Heart Sounds S1 is d/t closure and after vibrations of AV Valves. (M1 occurs with a definite albeit 20 msec delay after the LVLA pressure crossover.) S1 is normally split (~0.04 sec) because mitral valve closure precedes tricuspid closure. (Heard in only 40% of normal individuals) Ejection Aortic and Pulmonic Valves Open; AV Valves Remain Closed The Semilunar valves ( aortic , pulmonary ) open at the beginning of this phase. Two Phases • Rapid ejection - 70% of the blood ejected during the first 1/3 of ejection • Slow ejection - remaining 30% of the blood emptying occurs during the latter 2/3 of ejection Rapid Ejection Pressure & Volume Changes When ventricles continue to contract , pressure in ventricles exceed that of in aorta & pul arteries & then semilunar valves open, blood is pumped out of ventricles & Ventricular vol decreases rapidly. Slow Ejection Aortic and Pulmonic Valves Open; AV Valves Remain Closed Blood flow from the left ventricle to the aorta rapidly diminishes but is maintained by aortic recoil, the “Windkessel effect “ At the end of ejection, the semilunar valves close. This marks the end of ventricular systole mechanically. As the cytosolic calcium ion concentration starts to decline because of uptake of calcium into the SR under the influence of activated phospholamban, more and more myofibers enter the state of relaxation and the rate of ejection of blood from the left ventricle into the aorta falls. ( phase of reduced ejection) During this phase, blood flow from the left ventricle to the aorta rapidly diminishes but is maintained by aortic recoil—the Windkessel effect. †WINDKESSEL in German AIRCHAMBER or elastic reservoir Slow Ejection ECG & Heart Sounds T wave – slightly before the end of ventricular contraction it is d/t ventricular repolarization heart sounds : none LEFT VENTRICULAR RELAXATION. The pressure in the aorta exceeds the falling pressure in the left ventricle. The aortic valve closes, creating the first component of the second sound, A2 (the second component, P2, results from closure of the pulmonary valve as the pulmonary artery pressure exceeds that in the right ventricle). There after, the ventricle continues to relax. Because the mitral valve is closed during this phase, the LV volume cannot change (isovolumic relaxation). Beginning of Diastole Isovolumetric relaxation All Valves Closed At the end of systole, ventricular relaxation begins, allowing intraventricular pressures to decrease rapidly (LV from 100mmHg to 20mmHg & RV from 15mmHg to 0mmHg), aortic and pulmonic valves abruptly close (aortic precedes pulmonic) causing the second heart sound (S2) Valve closure is associated with a small backflow of blood into the ventricles and a characteristic notch (incisura or dicrotic notch) in the aortic and pulmonary artery pressure tracings After valve closure, the aortic and pulmonary artery pressures rise slightly (dicrotic wave) following by a slow decline in pressure Isovolumetric relaxation Throughout this and the previous two phases, the atrium in diastole has been filling with blood on top of the closed AV valve, causing atrial pressure to rise gradually JVP - "v" wave occurs toward end of ventricular contraction – results from slow flow of blood into atria from veins while AV valves are closed . LEFT VENTRICULAR RELAXATION. When the LV pressure falls to below that in the left atrium, the mitral valve opens (normally silent) and the filling phase of the cardiac cycle restarts. Isovolumetric relaxation ECG & Heart Sounds ECG : no deflections Heart Sounds : S2 is heard when the semilunar valves close. A2 is heard prior to P2 as Aortic valve closes prior to pulmonary valve. LEFT VENTRICULAR FILLING PHASES. As LV pressure drops below that in the left atrium, just after mitral valve opening, the phase of rapid or early filling occurs, which accounts for most of the ventricular filling. Active diastolic relaxation of the ventricle may also contribute to early filling ( “Ventricular Suction During Diastole”). Such rapid filling may cause the physiological third heart sound (S3), particularly when there is a hyperkinetic circulation. LV FILLING PHASES. As pressures in the atrium and ventricle equalize, LV filling virtually stops (diastasis). This is achieved by atrial systole (or the left atrial booster), which is especially important when a high cardiac output is required, as during exercise, or when the LV fails to relax normally, as in left ventricular hypertrophy. Diastasis A-V Valves Open blood which has accumulated in atria slowly flows into the ventricle. Rapid Inflow ( Rapid Ven. Filling) ECG & Heart Sounds ECG : no deflections Heart sounds : S3 is heard, lasts 0.02-0.04 sec (represent tensing of chordae tendineae and AV ring during ventricular relaxation and filling) Whatever the mechanism, a sudden inherent limitation in the long axis filling movement of the LV is consistently observed. Protodiastole Proto –means original, first The period of start of ventricular relaxation. Lasts until the semilunar valves are closed. It is 0.04 sec. Atrial Systole A-V Valves Open; Semilunar Valves Closed Blood normally flows continually from great veins into atria 80% flows directly thro atria into ventricle before the atria contracts. 20% of filling of ventricles – atrial contraction Atrial contraction is completed before the ventricle begins to contract. Atrial contraction normally accounts for about 10%-15% of LV filling at rest, however, At higher heart rates, atrial contraction may account for up to 40% of LV filling referred to as the "atrial kick” The atrial contribution to ventricular filling varies inversely with duration of ventricular diastole and directly with atrial contractility Atrial Systole Pressures & Volumes ‘ a ‘ wave – atrial contraction, when atrial pressure rises. Atrial pressure drops when the atria stop contracting. Atrial Systole ECG p wave – atrial depolarization impulse from SA node results in depolarization & contraction of atria ( Rt before Lt ) PR segment – isoelectric line as depolarization proceeds to AV node. This brief pause before contraction allows the ventricles to fill completely with blood. Atrial Systole ECG p wave – atrial depolarization impulse from SA node results in depolarization & contraction of atria ( Rt before Lt ) PR segment – isoelectric line as depolarization proceeds to AV node. This brief pause before contraction allows the ventricles to fill completely with blood. Atrial Systole Heart Sounds S4 (atrial or presystolic gallop) - atrial emptying after forcible atrial contraction. appears at 0.04 s after the P wave (late diastolic) lasts 0.04-0.10 s Caused by vibration of ventricular wall during rapid atrium emptying into non compliant ventricle Physiologic Versus Cardiologic Systole and Diastole cardiologic systole, demarcated by heart sounds rather than by physiologic events, starts fractionally later than physiologic systole and ends significantly later. Cardiologic systole> physiologic systole Physiological systole –start of isovolumic contraction to the peak of ejection phase. Physiological diastole – commences as pressure falls. Fits well in pressure volume curve ECHO cardiac cycle Rapid filling phase of diastole Atrial systole Left ventricular rotation: a neglected aspect of the cardiac cycle Rotation of the left ventricle around its longitudinal axis is an important but thus far neglected aspect of the cardiac cycle. LV rotation during systole maximizes intracavitary pressures, increases stroke volume, and minimizes myocardial oxygen demand. LV Torsion left-handed helix in subepicardium right-handed helix in sub endocardium Figure: Schematic Drawing of LV Torsion The image on the left shows the myofiber directions. Solid lines epicardial region; dashed lines endocardial region. The image on the right shows untwisting. ED end-diastole; ES end-systole; LV left ventricle. (J Am Coll Cardio Img 2009;2:648–55) Shearing and restoring forces accumulated during systolic twisting are released during early diastole and result in diastolic LV untwisting or recoil promoting early LV filling. LV twist and untwist are disturbed in a number of cardiac diseases and can be influenced by several therapeutic interventions by altering preload, afterload, contractility, heart rate, and/or sympathetic tone, Phonocardiogram A graphic recording of cardiac sound A specially designed microphone on the chest wall. Sound waves amplified, filtered and recorded. Doppler Echocardiography has replaced the phonocardiography Hemodynamic Correlates of S1 The first high-frequency component of M1 coincides with the downstroke of the left atrial c wave and is delayed from the LV–left atrial pressure crossover by 30 ms. Forward flow continues for a short period following LV–left atrial pressure crossover as a result of the inertia of mitral flow, with M1 occurring 20 to 40 ms later. An even greater delay between the occurrence of T1 and RV–right atrial pressure crossover has been shown. T1 coincides with the downstroke of the right atrial c wave. These hemodynamic data confirm the prime role played by the AV valves in the genesis of S1 The Second Heart Sound RV ejection begins prior to LV ejection, has a longer duration, and terminates after LV ejection, resulting in P2 normally occurring after A2. the pulmonary artery incisura is delayed relative to the aortic incisura, primarily a result of a larger interval separating the pulmonary artery incisura from the RV pressure compared with the same left-sided event. This interval has been called the hangout interval, a purely descriptive term coined in Shaver et al more than 40 years ago. Its duration is felt to be a reflection of the impedance of the vascular bed into which the blood is being received. Normally, it is less than 15 ms in the systemic circulation and only slightly prolongs the LV ejection time. Circulation, Volume 51, January 1975 EDWARD I. CURTISS, M.D., ROBERT G. MATTHEWS, M.D., AND JAMES A. SHAVER, M.D. In the low-resistance, high-capacitance pulmonary bed, however, this interval is normally much greater than on the left, varying between 43 and 86 ms. Hangout interval contributes significantly to the duration of ejection. Normal Physiologic Splitting Normally during expiration, A2 and P2 are separated by an interval of less than 30 ms and are heard by the clinician as a single sound During inspiration, both components become distinctly audible as the splitting interval widens, primarily caused by a delayed P2, although an earlier A2 contributes to a lesser degree . Jugular Venous Pulse tracing JUGULAR VENOUS PULSE Reflects volume change in the internal jugular vein and closely resembles the pressure changes in the right atrium. A wave atrial contraction. C wave onset of ventricular contraction. X descent atrial diastole. V wave atrial filling before AV valves open. Y descent AV valves open filling of the ventricles. PRESSURES (mm Hg) Right atrium mean Normalavalues wave v wave 0-5 1-7 1-7 Right ventricle peak systolic/end diastolic 17-32/1-7 Pulmonary artery peak systolic/end diastolic 17-32/1-7 mean 9-19 PCWP 4-12 LA mean 4-12 a wave 4-15 v wave 4-15 LV peak systolic/end diastolic 90-140/5-12 Aorta peak systolic/end diastolic 90-140 /60-90 mean 70-105 Resistance (dynes/cm2) SVR 900-1400 PVR 40-120 Oxygen consumption index (L-min/m2) 115-140 Cardiac index (L-min/m2) 2.8-4.2 WIGGERS DIAGRAM EVENTS IN CARDIAC CYCLE PRESSURE VOLUME LOOP Pressure volume loop Best of the current approaches to the assessment of the contractile behaviour of the intact heart. Es,the pressure – volume relationship . Changes in the slope of this line joining the different Es points are generally good load independent index of the contractile performance of the heart. Enhanced inotropic effect, Es shifted upward and to the left. Lusitropic effect shifted Es downward and to right. The P-V relationship is linear in smooth muscle,curvilinear in cardiac muscle(exponential). Volumes End diastolic vol : During diastole, filling of ventricle increases vol of each ventricle to ~ 110 -120 ml Stroke Vol : amount of blood pumped out of ventricle during systole. ~ 70 ml End systolic vol : the remaining amount of blood in ventricle after the systole. ~40 -50 ml Pressure volume loop in cardiac cycle Atrial Pressure Volume Loop The atrium serves as a “conduit” for flow from the venous circulation to the ventricle, especially in early diastole when the atrium is not contracting. In addition, elevations in ventricular diastolic pressures will be reflected in elevated pressures in the atrium. Atrial Pressure Volume Loop A small reversal of flow following atrial contraction (a-wave) A systolic phase (which is effectively “diastole” for the atrium) when blood flows from the superior and inferior venacavae into the atrium A small reversal of flow at end-systole (v-wave) A diastolic filling phase when the atrium serves as a conduit for flow from the systemic venous return to the RV These filling phases are reflected in the patterns of jugular venous pulsation : a-wave following atrial contraction, x-descent corresponding to atrial filling during ventricular systole, v-wave at end-systole y-descent corresponding to atrial filling during ventricular diastole WIGGERS DIAGRAM EVENTS IN CARDIAC CYCLE PRESSURE VOLUME LOOP RV CARDIAC CYCLE RV cycle RV v/s LV Rt Ventricular • Pressure wave 1/5th • dp/dt is less • Isovolumic contraction & relaxation phases are short. Timing of Cardiac EVENTS 1. RA start contracting before LA 2. LV start contracting before RV 3. TV open before MV, so RV filling start before LV. 4. RV peak pressure 1/5th of LV. 5. RV outflow velocity smooth References 1.Ganong’s Review of Medical Physiology,24th Edition. 2.Guyton and Hall, Textbook of Medical Physiology. 3.Best and Taylor’s Physiological Basis of Medical Practice,13th edition. 4.HURST’S,THE HEART ,13th edition 5.Braunwald’s Heart Disease,10th edition 6.Circulation Journal. 7.European Heart Journal. Clinical Echo; Catherine . M. Otto, 5th edition