Presentation on theme: "DR RAKESH JAIN SR Cardiology Govt. Medical College, Calicut."— Presentation transcript:
1DR RAKESH JAIN SR Cardiology Govt. Medical College, Calicut. CARDIAC CYCLEDR RAKESH JAINSR CardiologyGovt. Medical College, Calicut.
2Cardiac CycleDef: The cardiac events that occur from beginning of one heart beat to the beginning of the next.first assembled by Lewis in 1920 but first conceived by Wiggers in 1915
3Atria act as PRIMER PUMPS for ventricles & ventricles provide major source of power for moving the blood through the vascular system.Initiated by spontaneous generation of AP in SA node (located in the superior lateral wall of the right atrium near the opening of the superior vena cava)
4Electrical System: Brief Action potentials originatingin the sinus node travel toAV node (1m/s) in 0.03 sec.
5AV nodal delay of 0.09 sec before the impulse enters the penetrating portion of the A-V bundle2. A final delay of another 0.04 sec occurs mainly inthis penetrating A-V bundletotal delay in the A-V nodal and A-V bundlesystem is about 0.13 secA total delay of 0.16 sec occurs before the excitatorysignal finally reaches the contracting muscle of theventricles from its origin in sinus node.
6Delay in AV node (0.13sec) Why delay? Significance? Diminished numbers of gap junctions Between successive cells in the conducting pathways.Significance?Delay allows time for the atria to empty their blood into the ventricles before ventricular contraction begins
7Rapid Transmission in the Purkinje System (1.5 to 4.0 m/sec) i.e.• About 6x that in ventricular muscle• About 150x that in A-V nodal fibersallowing almost instantaneous transmission of the cardiac impulse throughout the ventricular muscle(B/c of very high level of permeability of the gap junctions)
14Physiologic Versus Cardiologic Systole and Diastole PHYSIOLOGIC SYSTOLECARDIOLOGICSYSTOLEIsovolumic contractionMaximal ejectionFrom M1 to A2,including: Major part of isovolumic contraction Maximal ejection Reduced ejectionPHYSIOLOGIC DIASTOLEDIASTOLEReduced ejection Isovolumic relaxation Filling phasesA2-M1 interval(filling phases included)20msecPhysiological systole
15cardiologic systole, demarcated by heart sounds rather than by physiologic events, starts fractionally later than physiologic systole and ends significantly later.Cardiologic systole> physiologic systole
17Atrial Systole A-V Valves Open; Semilunar Valves Closed Blood normally flows continually from great veins into atria80% flows directly thr atria into ventricle before the atria contracts.20% of filling of ventricles – atrial contractionAtrial contraction is completed before the ventricle begins to contract.
18Atrial 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
19Atrial Systole Pressures & Volumes ‘ a ‘ wave – atrial contraction, when atrial pressure rises.Atrial pressure drops when the atria stop contracting.
20After atrial contraction is complete LVEDV typically about 120 ml (preload)End-diastolic pressures ofLV = 8-12 mmHg andRV = 3-6 mmHgAV valves floats upward (pre-position)
21Abnormalities of “a” wave Elevated a waveTricuspid stenosisDecreased ventricular compliance (ventricular failure, pulmonic valve stenosis, or pulmonary hypertension)Cannon a wave Atrial-ventricular asynchrony (atria contract against a closed tricuspid valve)complete heart block, following premature ventricular contraction, during ventricular tachycardia, with ventricular pacemakerAbsent a wave Atrial fibrillation or atrial standstill Atrial flutter
22Why blood does not flow back in to SVC/PV while atria contracting, even though no valve in between? Wave of contraction through the atria moves toward the AV valve thereby having a "milking effect."Inertial effects of the venous return.
23Atrial 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.
24Atrial 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 sCaused by vibration of ventricular wall during rapid atrium emptying into non compliant ventricle
25Causes of S4 Physiological; >60yrs (Recordable, not audible) Pathological;All causes of concentric LV/RV hypertrophyCoronary artery diseaseAcute regurgitant lesionsAn easily audible S4 at any age is generally abnormal.
26Clinical Facts about S4 (This correlation is not applicable in HCM) In contrast to S3, which may mean ventricular failure, the presence of S4 does not indicates heart failure. It only signify “hardworking ventricle”.The presence of S4 correlate with a gradient of at least 50mmHg across LVOT in suspected LVOT obstruction.(This correlation is not applicable in HCM)
27In setting of MI, an audible S4 indicates that at least 10% of myocardium is at jeopardy. In presence of Shock, S4 indicates that hypovolemia is unlikely as PCWP will be >18mmHg.S4 can be heard when RVEDP >12mmHg on Rt or LVEDP > 15mmHg on Lt side. If EDP is very high i.e. >25 mmHg, S4 may be absent b/c of insufficient atrial functions.
28JVP: x descentProminent x descent 1 Cardiac tamponade 2 Constrictive pericarditis 3 Right ventricular ischemia with preservation of atrialcontractilityBlunted x descent 1 Atrial fibrillation 2 Right atrial ischemia
29Beginning of Ven.Systole Isovolumetric Contraction All Valves Closed
30Isovolumetric Contraction 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.
31Ventricular pressure increases rapidly Ventricular chamber geometry changes considerably as the heart becomes more spheroid in shape; circumference increases and atrial base-to-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 rapidlyLV ~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
32LV Torsion (J Am Coll Cardiol Img 2009;2:648–55) left-handed helix in subepicardiumright-handed helix in subendocardiumFigure: Schematic Drawing of LV TorsionThe 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 Cardiol Img 2009;2:648–55)
33Isovolumetric Contraction ECG The QRS complex is due to ventricular depolarization, and it marks the beginning of ventricular systole.
34Isovolumetric 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 LV-LA pressure crossover.)S1 is normally split (~0.04 sec) because mitral valve closure precedes tricuspid closure.(Heard in only 40% of normal individuals)
35S1 heart sound low pitch and relatively long-lasting lasts ~ secfrequency ~ Hzappears – 0.04 sec after the beginning of the QRS complex
36Some Clinical facts about S1 S1 is a relatively prolonged, low frequency sound, best heard at apex.Normally split of S1 (~40%)is heard only at tricuspid area.(As tricuspid component is heard only here.)If S1 is equal to or higher in intensity than S2 at base, S1 is considered accentuated.
37Variable intensity of S1 and jugular venous pulse are highly specific and sensitive in the diagnosis of ventriculoatrial dissociation during VT, and is helpful in distinguishing it from supraventricular tachycardia with aberration.Value of physical signs in the diagnosis of ventricular tachycardia. C J Garratt, M J Griffith, G Young, N Curzen, S Brecker, A F Rickards and A J Camm, Circulation. 1994;90:
39Ejection 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 bloodejected during the first 1/3 of ejection• Slow ejection - remaining 30% ofthe blood emptying occurs duringthe latter 2/3 of ejection
40Rapid 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.
42Rapid Ejection ECG & Heart Sounds In rapid ejection part of the ejection phase there no specific ECG changes / heart sounds heard.
43Slow 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.
44Slow Ejection ECG & Heart Sounds T wave – slightly before the end of ventricular contractionit is d/t ventricular repolarizationheart sounds : none
45Beginning 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 tracingsAfter valve closure, the aortic and pulmonary artery pressures rise slightly (dicrotic wave) following by a slow decline in pressure
46Isovolumetric relaxation Volumes remain constant because all valves are closedvolume of blood that remains in a ventricle is called the end-systolic volume (LV ~50ml).pressure & volume of ventricle are low in this phase .
47Isovolumetric 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 graduallyJVP - "v" wave occurs toward end of ventricular contraction – results from slow flow of blood into atria from veins while AV valves are closed .
48Isovolumetric relaxation ECG & Heart Sounds ECG : no deflectionsHeart Sounds : S2 is heard when the semilunar vlaves close.A2 is heard prior to P2 as Aortic valve closes prior to pulmonary valve.
49Why A2 occurs prior to P2 ?“Hangout interval” is longer for pulmonary side (~80msec),compared to aortic side (~30msec).Hangout interval is the time interval from crossover of pressures (ventricle with their respective vessel) to the actual occurrence of sound.Due to lower pressure and higher distensibility, pulmonary artery having longer hangout interval causing delayed PV closure and P2.
50S2 heart sound Appears in the terminal period of the T wave lasts 0.08 – 0.12s
51Some clinical facts about S2 Normal split: Two components heard during inspiration and is single sound during expiration.(A2-P2 ~ msec in inspiration)Clinically split is defined as wide, if it is heard well in standing position, in expiration (normally not heard as the split is 15 msec, which can not be heard by human ears)Single S2: absence of audible split in either phase of respiration.
52Fixed split: two components fails to move with respiration. Reverse split: Inaudible split during inspiration and audible split during expiration. (recognized by wider split in expiration)
53Common causes of wide split S2 RBBBSev PAHASDIdiopathic dilatation of pul arterySev right heart failureModerate to severe PSSevere MRNormal variant
54Common causes of wide fixed split S2 ASDAll causes of wide split with associated severe right ventricular failure.
55Common causes of single S2 Truncus arteriosusPulmonary atresiaAortic atresiaTGAAS, PSSingle loud P2 in extreme PAH
56Causes of reverse split S2 LBBBRV pacingRV ectopySevere ASAcute MIWPW type BSevere TRAneurysm of ascending aortaSevere systemic hypertension
57JVP: V waveElevated v wave 1 Tricuspid regurgitation 2 Right ventricular heart failure 3 Reduced atrial compliance (restrictive myopathy)a wave equal to v wave 1 Tamponade 2 Constrictive pericardial disease 3 Hypervolemia
58Rapid Inflow ( Rapid Ven. Filling) A-V Valves Open Once AV valves are open the blood that has accumulated in atria flows into the ventricle.
59Rapid Inflow Volume changes Despite the inflow of blood from the atria, intraventricular pressure continues to briefly fall because the ventricles are still undergoing relaxationJVP: Seen as y-descent.
60Rapid Inflow ( Rapid Ven. Filling) ECG & Heart Sounds ECG : no deflectionsHeart sounds : S3 is heard, lasts 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.
61Clinical facts about S3In presence of HF, S3 correlates well with ventricular end diastolic pressure and is usually >25mmHg on left side.Right sided S3 correlate well with rapid y descend in neck veins.Normal A2-S3 interval is between msec.
62Correlates of S3 Anatomical Functional Hemodynamics LVEDP Dilated ventricleFunctionalSystolic dysfunction(EF<40%)HemodynamicsLVEDPCardiac indexSymptomsDoppler flow across AVvalve>25 mmHg<2 L/min/m2Dyspnea, PND, OrthopneaTall E wave compare to A wave
63Gallop rhythmA gallop rhythm is a grouping of three heart sounds that together sound like hoofs of a galloping horse.Protodiastolic gallop or ventricular gallop or S3 gallopaddition of an S3 to the physiological S1 and S2 creates a three-sound sequence, S1-S2-S3.Presystolic gallop rhythm or atrial gallopaddition of an S4 to the physiological S1 and S2 creates a three-sound sequence, S4-S1-S2.(during tachycardia S4-S1 can fuse, producing a summation gallop )
64Causes of S3Physiological: Childrens & young adults <40 yrs (nearly 25%)(Not heard in normal infants & adult >40 yrs.)Pathological:Ventricular failureHyperkinetic state (anemia, thyrotoxicosis, beri-beri)MR, TRAR, PRSystemic AV fistula
65JVP: y descentProminent y descent 1 Constrictive pericarditis 2 Restrictive myopathies 3 Tricuspid regurgitationBlunted y descent 1 Tamponade 2 Right ventricular ischemia 3 Tricuspid stenosis
66Diastasis A-V Valves Open remaining blood which has accumulated in atria slowly flows into the ventricle.
67Diastasis Volume changes Ventricular volume increases more slowly now. The ventricles continue to fill with blood until they are nearly full.
69The Lewis or wiggers cycle, Guyton & Hall The Lewis or wiggers cycle, Guyton & Hall. Textbook of Medical Physiology, 11th Edition
70VolumesEnd diastolic vol : During diastole, filling of ventricle increases vol of each ventricle to~ mlStroke Vol : amount of blood pumped out of ventricle during systole. ~ 70 mlEnd systolic vol : the remaining amount of blood in ventricle after the systole. ~ ml
71Pressure-Volume Loop Pressure-volume loop of RV is same as that of LV, however the area is only 1/5thof LV because pressuresare so much lower on right
72RV v/s LV Rt Ventricular Pressure wave 1/5th dp/dt is less Isovolumic contraction &relaxation phases are short.
73Timing of Cardiac EVENTS RA start contracting before LALV start contracting before RVTV open before MV,so RV filling start before LV.RV peak pressure 1/5th of LV.RV outflow velocity smoothrise & fall, while Lt side initialpeak followed by quick fall.
74The First cardiac catheterization Cardiac catheterization was first attempted by Dr Werner Forssmann in 1929, at the age of 25 yrs only, when he was a resident in a hospital at Eberswalde, near Berlin. He was his own subject. A fellow resident who agreed to pass the catheter, got scared and abandoned the effort by the time the catheter reached the axilla. Forssmann completed the task himself with radiographer holding the mirror infront of screen. Forssmann catheterize his heart safely nine times till he had no more peripheral veins left to try. But this was not enough to convince the medical world about the safety of the procedure. After being banished from academics, frustrated Forssmann settled for medical practice in a small town.It was extensive studies with catheterization by Dr Andre Cournand & Dr Dickinson Richard Jr. and eventually the novel prize for physiology & medicine was awarded jointly to Forssmann, Cournand & Richard in 1956.The history of cardiac catheterization illustrates what reckless idealism of youth can achieve and the long time (here 27 yrs) might take the world to realize the value of even something of great significance.
75ReferencesGuyton and Hall Textbook of Medical Physiology, 11th Ed. Arthur C. Guyton, John E. Hall.Cardiovascular Physiology Concepts Second Edition, Lippincott Williams & Wilkins, 2011Clinical Methods in Cardiology By Soma Raju, Second Edition, orient longmanBraunwald's Heart Disease: A Textbook of Cardiovascular Medicine, ninth editionHarrison's Principles of Internal Medicine, 19th edition, McGraw-Hill Book CoUnderstanding Medical Physiology: A Textbook for Medical Students: By R.L. Bijlani, M.D., RL Bijlani MD SM DSc (Hon Causa) FAMS, S. Manjunatha,4th edition
767. Medical Physiology E-Book: By Walter F. Boron, Emile L Medical Physiology E-Book: By Walter F. Boron, Emile L.Boulpaep, Second EditionValue of physical signs in the diagnosis of ventricular tachycardia. C J Garratt, M J Griffith, G Young, N Curzen, S Brecker, A F Rickards and A J Camm, Circulation. 1994;90:Color Atlas of Physiology. Stefan Silbernagel, Agamemnon Despopoulos. 6th Edition.10. Jacc: cardiovascular imaging, Vol.2 No. 5, May 2009:
77QUIZ1. Which letter indicates the point in the cardiac cycle that the mitral valve opens?A. A B. B C. C D. D
782. In a normal cardiac cycle , true is A. RA ejection precedes LA ejection B. RV contraction starts before LV contraction C. LV ejection starts before RV ejection D. Pulmonary valve closes before aortic valve
793. Which letter in the image represents the isovolumic contraction of the left ventricle in the heart?A. F B. B C. H D. D2.
804. Which of the following pairs is INCORRECT? A. P wave: atrial depolarization B. QRS complex: ventricular depolarization C. T wave: ventricular repolarization D. QT interval: Measure of duration of atrial actionpotential
815. Isovolumic contraction phase correspond to A 5. Isovolumic contraction phase correspond to A. AV opening to AV Closure B. MV closure to MV opening C. MV closure to AV opening D. AV opening to MV opening
826. Left ventricular end-diastolic volume is: A. 30-50 mls B 6. Left ventricular end-diastolic volume is: A mls B mls C mls D mls
837. Prominent y descent in JVP seen in all except A. Constrictive pericarditis B. Restrictive cardiomyopathies C. Tricuspid regurgitationD. Cardiac temponade
848. All are true about S3 except A. Right sided S3 correlate well with rapid y descendin neck veins.B. S3 normally heard in normal infantsC. S3 usually indicates systolic dysfunctionD. S3 correlates well with ventricular end diastolicpressure usually >25mmHg on left side
859. Cardiac apex is palpable during which phase of cardiac cycle A. Isovolumic contraction phaseB. Isovolumic relaxation phaseC. Rapid ejection phaseD. Atrial systole phase
8610. Sensitive & specific sign of ventricularterial dissociation in VT areA. Variable intensity of S1B. Variable jugular venous pulseC. Both A & BD. None of the above
87Answers1. Which letter indicates the point in the cardiac cycle that the mitral valve opens?A. A B. B C. C D. D
882. In a normal cardiac cycle , true is A. RA ejection precedes LA ejection B. RV contraction starts before LV contraction C. LV ejection starts before RV ejection D. Pulmonary valve closes before aortic valve
893. Which letter in the image represents the isovolumic contraction of the left ventricle in the heart?A. F B. B C. H D. D2.
904. Which of the following pairs is INCORRECT? A. P wave: atrial depolarization B. QRS complex: ventricular depolarization C. T wave: ventricular repolarization D. QT interval: Measure of duration of atrial actionpotential
915. Isovolumic contraction phase correspond to A 5. Isovolumic contraction phase correspond to A. AV opening to AV Closure B. MV closure to MV opening C. MV closure to AV opening D. AV opening to MV opening
926. Left ventricular end-diastolic volume is: A. 30-50 mls B 6. Left ventricular end-diastolic volume is: A mls B mls C mls D mls
937. Prominent y descent in JVP seen in all except A. Constrictive pericarditis B. Restrictive cardiomyopathies C. Tricuspid regurgitationD. Cardiac temponade
948. All are true about S3 except A. Right sided S3 correlate well with rapid y descendin neck veins.B. S3 normally heard in normal infantsC. S3 usually indicates systolic dysfunctionD. S3 correlates well with ventricular end diastolicpressure usually >25mmHg on left side
959. Cardiac apex is palpable during which phase of cardiac cycle A. Isovolumic contraction phaseB. Isovolumic relaxation phaseC. Rapid ejection phaseD. Atrial systole phase
9610. Sensitive & specific sign of ventricularterial dissociation in VT areA. Variable intensity of S1B. Variable jugular venous pulseC. Both A & BD. None of the above