cardiac cycle

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cardiac cycle

  1. 1. Dr.Praveen Nagula ,1st Year PG
  2. 2. Carl John Wiggers Otto Frank Sir Thomas Lewis Ernest H Starling
  3. 3. William Harvey Adolf Eugen Fick Willem Einthoven
  4. 4. 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.a low resistance pulmonary driven by right heart 2.a 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.
  5. 5. WIGGERS DIAGRAM EVENTS IN CARDIAC CYCLE DETERMINANTS OF MYOCARDIAL PERFORMANCE PRESSURE VOLUME LOOP PHYSIOLOGICAL VS PATHOLOGICAL HYPERTROPHY
  6. 6. Wiggers diagram The X axis is used to plot time, The Y axis contains all of the following on a single grid: Blood pressure Aortic pressure Ventricular pressure Atrial pressure Ventricular volume Electrocardiogram Arterial flow (optional) Heart sounds (optional) JVP Illustration of the coordinated events makes it easier to correlate the changes during the cardiac cycle.
  7. 7. WIGGERS DIAGRAM EVENTS IN CARDIAC CYCLE DETERMINANTS OF MYOCARDIAL PERFORMANCE PRESSURE VOLUME LOOP PHYSIOLOGICAL VS PATHOLOGICAL HYPERTROPHY
  8. 8. 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.
  9. 9. Mechanical events in Cardiac cycle • Systole • Isovolumic contraction • Maximal ejection • Reduced ejection • Diastole • Isovolumic relaxation • Rapid filling phase • Slow filling phase /diastasis • Atrial systole
  10. 10. 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.
  11. 11. LV contraction • Actin myosin contraction triggered by arrival of Calcium ions at • • • • • • • contractile proteins. ECG – peak of R wave LV pressure >LA pressure (10-15mm Hg) Followed approx. 50msec by M1. Delay of M1 – inertia of the blood flow – valve is kept open. Isovolumic contraction as volume is fixed. Increased pressure as more fibers enter contractile state. LV pressure >Aorta – Aortic valve opens – silent event clinically.
  12. 12. • Phase of rapid ejection: • Pressure gradient across the aortic valve • Elastic properties of aorta,arterial tree (systolic expansion) • LV pressure rises to peak and then falls.
  13. 13. LV relaxation • Activated phospholamban causes calcium transfer into SR. • Decreases contractile apparatus function – phase of reduced ejection – blood flow from LV to aorta decreases but maintained by aortic recoil – WINDKESSEL EFFECT*. • Aortic valve closes as LV pressure drops • Isovolumic relaxation • Mitral valve opens – clinically silent event. † Giovanni Borelli,Stephen Hales,Fick(mathematical foundation). †WINDKESSEL in german AIRCHAMBER or elastic resorvoir.
  14. 14. LV filling • Rapid filling phase – active diastolic relaxation of LV. • LA- LV pressures equalize - diastasis. • LA booster atrial systole – important in exercise and LVH. • First phase of diastole –isovolumic phase – no ventricular • • • • • filling. Most of ventricular filling –rapid filling phase. Diastasis -5% Final atrial booster phase -15%. The sucking effect of ventricle – myosin is pulled into the space between the two anchoring segments of titin. Dominant backward pressure wave –diastolic coronary filling.
  15. 15. Physiologic systole,diastole • It is related to the events occuring at the cellular level ,by change of pressure and the electrical events. • Physiological systole –start of isovolumic contraction to the peak of ejection phase. • Physiological diastole – commences as pressure falls. • Fits well in pressure volume curve .
  16. 16. Cardiological systole,diastole • It is related to the valve closures. • Systole – M1-A2 • Thereby starts later than physiological systole and ends later. • Diastole – A2-M1
  17. 17. Protodiastole • Proto –means original,first • The period of start of ventricular relaxation. • Lasts until the semilunar valves are closed. • It is 0.04 sec.
  18. 18. ECHO cardiac cycle Rapid filling phase of diastole Atrial systole
  19. 19. 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
  20. 20. Carotid Pulse Tracing (CPT) Reflects the pressure and possible small volume changes in a segment of the carotid artery with each cardiac cycle. P (percussion wave) is the first peak and is related to aortic ejection. 80 msec after the first heart sound. T (tidal wave) is the second wave and occurs late in systole. D (dicrotic notch) coincides with aortic closure (A2), plus the traveling time of the pulse to the neck (.01-.05 sec).
  21. 21. Causes of Abnormalities in the Carotid Pulse
  22. 22. Jugular Venous Pulse tracing
  23. 23. 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.
  24. 24. Apex cardiogram
  25. 25. Apex cardiogram Records low-frequency vibrations over the apical impulse. Deflections not delayed. A –atrial contraction. C –onset of LV contraction. E – peak of the ascent (initial ejection from LV to aorta) O – opening of the mitral valve. RF –rapid filling wave SF – slow filling wave.
  26. 26. WIGGERS DIAGRAM EVENTS IN CARDIAC CYCLE DETERMINANTS OF MYOCARDIAL PERFORMANCE PRESSURE VOLUME LOOP PHYSIOLOGICAL VS PATHOLOGICAL HYPERTROPHY
  27. 27. Determinants of myocardial mechanical performance 3 main determinants Loading conditions (preload,afterload) Contractile state Heart rate
  28. 28. Preload • Wall stress at the end of diastole – maximum resting length of sarcomere. • Increasing LVEDV increases SV in ejecting beats,increases LV pressure in isovolumic beats. • Modulation of ventricular performance by changes in preload with constant afterload –heterometric autoregulation,operates on a beat –to beat basis.
  29. 29. Frank Starling mechanism • Starling – venous pressure in RA – heart volume • Within physiological limits – the larger the volume of the heart • • • • –greater the energy of its contraction – the greater the amount of chemical change at each contraction. LV volume – Cardiac Output Stroke volume related to LVEDV – modern version Real time 3D ECHO – global LV volume,endocardial function LV volume surrogate markers – LVEDP ,PCWP.
  30. 30. • Frank – greater the initial LV volume – more rapid rate of rise – • • • • • • • greater the peak pressure reached –faster the rate of relaxation. An important compensatory mechanism that maintains stroke volume,when there is myocardial dysfunction or excessive afterload. Atria also exhibit frank starling curve – exercise.(resistance to early diastolic filling). Passive P-V relationship is exponential. Chronic volume overload – EDPVR – rightward. Chronic pressure overload –EDPVR - leftward. Increased diastolic filling –Starling. Increased inotropic effect – Frank
  31. 31. Afterload Exact definition – wall stress during LV ejection. Tension in the LV wall that resists ventricular ejection or as the arterial input impedance. In clinical practice the arterial blood pressure is often taken as synonymous with afterload while ignoring aortic compliance (increase in stiff aorta).
  32. 32. Anrep effect • Homeometric autoregulation • Under experimental conditions sudden marked increase in aortic pressure is produced,LVEDP initially rises and the stroke volume then recovers. • Increased LV wall tension – increases Cytosolic Na - Calcium
  33. 33. Heart rate • Rate that would give maximal mechanical performance of an isolated muscle strip , also determined by the need for adequate time for diastolic filling. • Normally – pacing rates of 150/min –tolerated. • During exercise – 170/min • LVH – 100-130/min
  34. 34. Bowditch phenomenon Treppe effect Positive inotropic effect of activation Force freqeuncy relation • “increased heart rate – increases force of ventricular contraction” HR – negative staircase effect • More rapid stimulation – more sodium and calcium ions enter the myocardial cell that can be handled by sodium pump and the mechanisms for calcium exit - decreased force.  Clinical implications AF with varying interval. In HF – phenomenon is muted or lost. Post extrasystolic potentiation ,inotropic effect of paired pacing – increased contractile state. •
  35. 35. Contractility • It is the inherent capacity of the myocardium to contract independently of changes in the preload and afterload. • An increased contractile function –assosciated with greater degree of relaxation – LUSITROPIC effect • Important regulator of My02 uptake • Increased contractile function – exercise,adrenergic stimulation,digitalis,other inotropic agents.
  36. 36. Ventricular relaxation Four factors are of chief interest in influencing relaxation. 1.cytosolic calcium must fall to cause the relaxation phase(ATP,phospholamban). 2.the inherent viscoelastic properties of the myocardium.(hypertrophy) 3.increased phosphorylation of troponin I enhances the rate of relaxation. 4.systolic load influences relaxation(increased systolic load,increased lusitropic effect)(Brutsaert). Impaired relaxation is an early event of angina pectoris(decreased ATP –decreased early diastole filling). -dp/dt = (rate of isovolumetric relaxation)* *Glanz method P(t)= P0e-t⁄τE +Pα
  37. 37. Diastolic stiffness  Diastole is the summation of processes by which the heart loses its ability to generate force and shorten and returns to its precontractile state.  Chamber stiffness is quantified from the relationship between diastolic LV pressure and volume.  Volume dependent (slope of the tangent drawn to the PV curve)  Volume independent(intrinsic,extrinsic)  Diastolic LV stress( ) and strain( ).  Strain is the deformation of the muscle produced by an applied force and is expressed as percent change in length from unstressed length.
  38. 38. Time varying elastance concept Ventricular volume and loading are altered under conditions of unvarying contractility.(frank starling preparations are load independent). At any time t,following the onset of contraction,the P-V relation is linear P(t) = E(t)-{V(t)-Vo},E –time varying elastance,Vo is volume at zero pressure or dead volume. Ventricle behaves like a spring with a stiffness(elastance) that increases during contraction,decreases during relaxation. PVA area bounded by the LV P-V loop is a measure of the total mechanical energy of LV contraction.
  39. 39. Formulae Ejection fraction = (stroke volume/end diastolic volume 100). Wall tension = (P.r)/2h(P pressure,r radius,h wall thickness) EA = PES/SV , [E- effective arterial resistance,PES-end systolic pressure,SV- stroke volume}. EA/Ees ratio (index of ventriculo arterial coupling,pump performance). Fick equation VO2 = Q(AVO2)  V/ P = compliance. P/ V =stiffness Cardiac output = stroke volume HR PVA = PE+SW PE = PES(VES-V0)/2 – PED(VED-V0)/4 PVA MV02
  40. 40. PRESSURES (mm Hg) Right atrium mean 0-5 wave Normalavalues 1-7 Right ventricle peak systolic/end diastolic 17-32/1-7 Pulmonary artery peak systolic/end diastolic 17-32/1-7 v wave 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
  41. 41. WIGGERS DIAGRAM EVENTS IN CARDIAC CYCLE DETERMINANTS OF MYOCARDIAL PERFORMANCE PRESSURE VOLUME LOOP PHYSIOLOGICAL VS PATHOLOGICAL HYPERTROPHY
  42. 42. 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).
  43. 43. Atrial Pressure Volume Loop
  44. 44. Atrial function 1.Blood receiving reservoir chamber 2.contractile chamber (booster pump) 3.conduit 4.volume sensor of the heart (ANP) – diuresis. 5.mechanoreceptors (Bainbridge reflex – VR - HR). Rapid atrial repolarization – increased Ito ,I K Ach. During atrial pacing,the preload is increased and the atria are distended,so that the volume part of the loop is small and the pressure part of the loop is much enlarged.
  45. 45. Pressure volume loop diagram in various pathological scenarios
  46. 46. INCREASED AFTERLOAD EXERCISE INCREASED PRELOAD INOTROPIC EFFECT HEART RATE
  47. 47. WIGGERS DIAGRAM EVENTS IN CARDIAC CYCLE DETERMINANTS OF MYOCARDIAL PERFORMANCE PRESSURE VOLUME LOOP PHYSIOLOGICAL VS PATHOLOGICAL HYPERTROPHY
  48. 48. Physiologic ,pathological hypertrophy
  49. 49. Meerson,studied the cardiac hypertrophic response to experimental constriction of aorta.- compensatory hypertrophy.  Increased wall stretch,as a result of an increased intraventricular LV pressure (Systolic stress correction hypothesis,Grossman)- myocytes grow in width and thicken. Response to a sustained LV pressure overload Beneficial hypertrophy ERK,Akt(protein kinaseB) Pathological hypertrophy P38MAPkinase,JNK,TGF-B
  50. 50. Chronic elevation of the preload was associated with Akt activation without fibrosis,little apoptosis,better function,and lower mortality. Chronic elevation of afterload (AS) caused maladaptive hypertrophy,increased fibrosis,rapid failure,increased mortality. Increased release of angiotensin II from myocardium. TGF B maldaptive hypertrophy in AS (diastolic dysfunction) Cardiac steatosis in insulin resistance – increased TG
  51. 51. Isometric versus isotonic contraction An isometric exercise is a form of exercise involving the static contraction of a muscle without any visible movement in the angle of the joint. The term "isometric" combines the Greek words "isos" ("equal" or "same") and "metron" ("distance" or "measure"), meaning that in these exercises the length of the muscle and the angle of the joint do not change, though contraction strength may be varied.  This is in contrast to isotonic contractions, in which the contraction strength does not change, though the muscle length and joint angle do.
  52. 52. WIGGERS DIAGRAM EVENTS IN CARDIAC CYCLE DETERMINANTS OF MYOCARDIAL PERFORMANCE PRESSURE VOLUME LOOP PHYSIOLOGICAL VS PATHOLOGICAL HYPERTROPHY RV CARDIAC CYCLE
  53. 53. RV cycle
  54. 54. 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,9th edition 6.Circulation Journal. 7.European Heart Journal.
  55. 55. THE WONDERFUL DAY 11-12-13

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