Presentation on theme: "Cardiac Cycle : Electrical and Mechanical Events"— Presentation transcript:
1Cardiac Cycle : Electrical and Mechanical Events Dr Manisha DesaiUniversity College of Medical Sciences & GTB Hospital, Delhi
2CARDIAC CYCLEThe cardiac events that occur from the beginning of one heart beat tothe beginning of the next.Events : ElectricalMechanicalElectrical and mechanical events occur in a co-ordinated manner togenerate effective contractionsDuration – 0.8 s
3ELECTRICAL EVENTSThe rhythmical activity of the heart is controlled by electrical impulsesA specialised conduction system generates and propagates impulsesCardiac muscle as a functional syncitium enables rapid and uniform passage of the impulsesEnsures : all parts of the ventricle contract simultaneously.atrial contraction → 1/6th sec before ventricular contraction
5SAN AVN LBB RBB LAF LPF PURKINJE SYSTEM BUNDLE OF HIS Myocardium ANT I/N TRACT OF BACHMANMIDDLE I/N TRACT OF WENCKEBACHPOST I/N TRACT OF THORELAVNBUNDLE OF HISLBBRBBLAFLPFPURKINJE SYSTEMMyocardium
6SINOATRIAL NODE Junction of SVC with right atrium Specialised neurocardiac tissue ; almost no contractile musclefilamentNormal pacemakerConnects directly with the surrounding atrial muscle fibres sothat action potential generated spreads immediately into the atrium.Properties of Self- excitation and Rhythmicity
7What causes the self excitation? Membrane in natural state permeable to Na and Ca ionsRMP in SA nodal fibre is less negative : -60 to -70 mvThis voltage closes fast Na channels but slow Na - Ca channels are openThe ions flow inward → membrane permeability further increased → Threshold reached → Action potential
8Half way through the action potential, slow Na-Ca channels begin to close. K channels open for a prolonged periodInside of the membrane becomes more negative = HYPERPOLARIZATIONThis persists for 0.5s after the Action potential endsThe K conductance weans off → RMP reached → Na –Ca opening overbalances K closure → threshold for Action potential→ Action potential
9SINO ATRIAL NODESelf–excitation & AP Recovery of APResting Memb Potential Hyperpolarisation
10Conduction through the other parts From SAN impulses through the 3 bands (1m/s) and atria (0.3m/s)Delay in the AVN – of 0.09 s. Due to reduced gap junction number. Allows time for the ventricles to fill completely before they contractRapid transmission through Purkinje fibres (4m/s) due to many gap junctionsTransmission in ventricular muscle- 0.3 – 0.5m/s
11AP in a ventricular muscle fibre 1234Phase 0 : rapid depolarization – opening of fast Na channelsPhase 1 : rapid repolarisation – closure of Na channelsPhase 2 : Plateau – slow prolonged opening of Ca channelsPhase 3 : final repolarisation – closure of Ca channelsPhase 4 : RMP (-85 to -90 mv) – opening of K channels
12REFRACTORY PERIOD :Refractory to re-stimulation during Action potentialAbsolute refractory period = 0.25 – 0.3 s. Phase 0 to 2 and half of phase 3Relative refractory period = phase 4Refractory period of the atria is shorter than that of ventricle
13Variation in length of action potential and associated phenomena with cardiac rate.1 Heart Rate 75/minHeart Rate 200/minDuration, each cardiaccycle0.800.30Duration of systole0.270.16Duration of actionpotential0.250.15Duration of absoluterefractory period0.200.13Duration of relative0.050.02Duration of diastole0.530.141 All values are in seconds.
14Effect of autonomic nervous system on conduction
15Effect of parasympathetic system Vagal stimulation causes release of AchTwo effects:↓ rate of rhythm of SAN – RMP becomes more negative↓ excitability of A-V junctional fibresSlowing of heart rate, complete block in transmission may occurStrong vagal stimulus → ventricles stop beating for 5-20s →purkinje fibres take over → ventricles contract at beats perminute → VENTRICULAR ESCAPE
16Effect of sympathetic system Sympathetic stimulation → Noradrenaline releasedThree effects :↑ rate of SAN discharge – RMP more positive↑ rate of conduction and overall excitability↑ the force of contraction – increases Ca permeabilityHeart rate may increase 3 times and strength of contraction mayincrease 2 times the normal
17EXCITATION-CONTRACTION COUPLING Mechanism by which AP causes myofibrils to contractAP over cardiac muscle membraneReaches interior through T TubulesT tubule AP acts on longitudinal sarcoplasmic reticulumRelease of Ca ions into sarcoplasmCa ions catalyze sliding of actin-myosin filaments
18How is this different from the skeletal muscle contraction? T tubules also pump Ca ions into the sarcoplasmCa from sarcoplasmic reticulum + T tubules = effective contractionSarcoplasmic reticulum in cardiac muscle – less well developedT tubule diameter and volume in cardiac muscle >> skeletal muscleSince T tubules are in contact with ECF in the interstitium, the ECF Caconcentration determines the strength of the contraction
19MECHANICAL EVENTSThe heart contracts and relaxes alternately during every heart beat and this occurs in concordance with the electrical events. The mechanical events can be studied in various phases such as:
24…….. Atrial systoleJVP – ‘a’ waveECG – P wave preceeds the atrial systole. PR segment – depolarization proceeds to the AVN. The brief pause allows complete ventricular fillingHeart sounds - S 4 – pathological. Vibration of the ventricular wall during atrial contraction. Heard in ‘stiff’ ventricle like in hypertrophy and in elderly. Also heard in massive pulmonary embolism, cor pulmonale, TR
25ISOVOLUMETRIC CONTRACTION Increase in ventricular pressure > atrial pressure → AV valves closeAfter 0.02s, semilunar valves openPeriod between AV valve closure and semilunar valve opening → contraction occurs without emptyingTension develops without change in muscle length
27ECG – Interval between QRS complex and T wave (QT interval) ………… Isovolumetric contractionJVP – ‘c’ wave → due to the bulging of the Tricuspid valve into RA secondary to increased pressure in the ventricle.‘x’ descentECG – Interval between QRS complex and T wave (QT interval)Heart Sounds – S1 : closure of the AV valves. Normally split as mitral valve closure preceeds tricuspid valve closure.
28EJECTION When LV pres > 80 mm Hg RV pres > 8 mm Hg, The semilunar valves open.Rapid Ejection – 70% emptying in first 1/3Slow Ejection – 30% in last 2/3The pressure in the ventricle keeps decreasing until it becomes lower than that of the great vessels
30Aortic pressure - Rapid rise in the pressure = 120 mm Hg …………. ejectionJVP – no wavesECG – T waveHeart sounds – noneAortic pressure - Rapid rise in the pressure = 120 mm HgEven at the end of systole pressure in the aortais maintained at 90 mm Hg because of theelastic recoil
31ISOVOULUMETRIC RELAXATION When ventricle pressure < arterial pressure→ backflow of blood → forces semilunar valves to close.For s, ventricle relaxes despite no change in its volumeMeanwhile, atria fill up and atrial pressure gradually risesPressures in ventricle keep falling till it is < atrial pressure
33JVP – ‘v’ wave – due to venous return to the atria from SVC and IVC …………… isovolumetric relaxationJVP – ‘v’ wave – due to venous return to the atria from SVC and IVCECG- no deflectionsHeart sounds – S2 : closure of the semilunar valves. Normally split because aortic valve closes slightly earlier than the pulmonary valveAortic pressure curve – INCISURA - when the aortic valve closes. Caused by a short period of backflow before the valve closes followed by sudden cessation of the backflow when the valve closes.
34VENTRICULAR FILLING Begins with the opening of AV valves Rapid filling – first 1/3 of diastoleReduced filling (Diastasis) – middle 1/3 of diastoleAtrial contraction – last 1/3 of diastoleAs the atrial pressures fall, the AV valves close and left ventricular volume is now maximum → EDV (120 ml in LV)
36JVP – ‘y’ descent ECG – no deflections …………… ventricular fillingJVP – ‘y’ descentECG – no deflectionsHeart sounds - S3 - Pathological in adults. Seen in dilated congestive heart failure, MI, MR, severe hypertension. Normal in children.
39The filling phase moves along the end-diastolic pressure-volume relationship (EDPVR) The slope of the EDPVR is the reciprocal of Ventricular ComplianceThe maximal pressure that can be developed by the ventricle at any given left ventricular volume → end-systolic pressure-volume relationship (ESPVR), which represents the inotropic state.
40SYSTOLIC DYSFUNCTION Impaired ventricular contraction ↓ slope of ESPVR i.e. ↑ ESVCompensatory rise in preload i.e. ↑ EDV↓ SV↓ EF↓ Work↑ EDP
41FORCE- VELOCITY RELATIONSHIP At any given preload and afterload, a loss of inotropy results in decrease in shortening velocity of the cardiac fibres.
46AORTIC REGURGITATION No true isovolumetric relaxation Blood from aorta to ventricle throughout diastole↑ EDV↑ SV (if no failure)↑ ESV and ↓ SV in failure
47SUMMARYThe conduction system and the atrial and ventricular muscle in the normal heart work in an extremely well co- ordinated manner to ensure correct opening and closure of the atrio- ventricular and semilunar valves and movement of the blood through the heart in an appropriate direction with minimal regurgitation.
48REFERENCES1 . William F. Ganong. The heart as a Pump. Review of Medical Physiology, Lange, 2010: Guyton and Hall. Heart Muscle, the heart as a Pump and function of the heart valves. Textbook of Medical Physiology.Philadelphia, Mosby Elsevier, 2006: Ronald D. Miller. Cardiac Physiology.Miller’s Anaesthesia.Philadelphia, Mosby Elsevier, 2010: