Cvs physio

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  • 1. Moderator: Dr Shaila S. Kamath Presenter :Samiksha Khanooja
  • 2.  Cardiac cycle  JVP  Myocardial action potential  Coronary circulation
  • 3.  Modern concept of circulation & heart as generator of circulation was advanced by Harvey in 1628.  Field of cardiac physiology has developed to include • physiology of heart as pump • cellular & molecular biology of cardiomyocyte, & • regulation of cardiac function by neural & humoral factors
  • 4.  Basic anatomy of heart consists of 2 atria & 2 ventricles - provide 2 separate circulations in series.  Pulmonary circulation, low-resistance & high- capacitance vascular bed, receives output from right side heart, chief function - bidirectional gas exchange.  Systemic circulation, high resistance, receives output from left side heart & provides output for systemic circulation, delivers O2, nutrients & removes CO2 & metabolites from tissue beds.
  • 5. CARDIAC CYCLE  Sequence of electrical & mechanical events during course of single heart beat. 1. Electrical events represented by ECG 2. Mechanical events represented by left atrial & left ventricular pressure pulses correlated in time with aortic flow & ventricular volume
  • 6.  Electrical events of pacemaker & specialized conduction system are represented by ECG at body surface & is result of differences in electrical potential generated by heart at sites of surface recording.
  • 7.  P wave action potential initiated at SA node is propagated to both atria by specialized conduction tissue, it leads to atrial systole (contraction) & P wave of ECG  P-R interval.. PR interval can be used to measure delay between atrial & ventricular contraction at level of AV node
  • 8.  From distal His bundle, electrical impulse propagated through left & right bundle branches finally to Purkinje system fibers  Electrical signals are transmitted from Purkinje system to individual ventricular cardiomyocytes.
  • 9.  Spread of depolarization to ventricular myocardium is manifested as QRS complex on ECG.  Depolarization is followed by ventricular repolarization and appearance of T wave on ECG.
  • 10. LATE DIASTOLE  Mitral & tricuspid valves - open, aortic & pulmonary valves -closed  Blood flows into heart throughout diastole  Rate of filling declines as ventricles become distended, —especially when heart rate is low— cusps of AV valves drift toward closed position  Pressure in ventricles remains low
  • 11. Atrial Systole  It pumps additional blood into ventricles, but about 70% of ventricular filling occurs passively during diastole  Contraction of atrial muscle that surrounds the orifices of SVC,IVC & pulmonary veins narrows their orifices; however, there is some regurgitation of blood into veins during atrial systole
  • 12. Ventricular Systole  Mitral & tricuspid valves close  Intraventricular pressure rises sharply as myocardium presses on blood in ventricle .
  • 13.  This isovolumetric (isovolumic, isometric) ventricular contraction lasts about 0.05 s, until pressures in left & right ventricles exceed pressures in aorta (80 mm Hg ) & pulmonary artery (10 mm Hg) & aortic & pulmonary valves open  AV valves bulge into atria, causing a sharp rise in atrial pressure
  • 14.  When aortic pulmonary valves open, phase of ventricular ejection begins  Rapid at first, slowing down as systole progresses.  Intraventricular pressure rises to a maximum ,then declines before ventricular systole ends  Peak left ventricular pressure is about 120 mm Hg, & peak right ventricular pressure is 25 mm Hg or less
  • 15.  Late in systole, the aortic pressure actually exceeds the ventricular, but for a short period momentum keeps the blood moving forward  The AV valves are pulled down by the contractions of the ventricular muscle, and atrial pressure drops
  • 16.  Amount of blood ejected by each ventricle per stroke at rest is 70–90 mL.  End-diastolic ventricular volume is about 130 mL.  Thus, about 50 mL of blood remains in each ventricle at end of systole (end-systolic ventricular volume), the ejection fraction, percent of EDVV- that is ejected with each stroke, is about 65%.  Ejection fraction is a valuable index of ventricular function.
  • 17. Early Diastole  Once ventricular muscle is fully contracted,already falling ventricular pressures drop more rapidly  This is the period of protodiastole ,lasts about 0.04sec, ends when aortic & pulmonary valves close  After the valves close, pressure continues to drop rapidly during isovolumetric ventricular relaxation
  • 18.  Isovolumetric relaxation ends when ventricular pressure falls below atrial pressure & AV valves open, permitting ventricles to fill  Filling -rapid at first, then slows as next cardiac contraction approaches  Atrial pressure continues to rise after the end of ventricular systole until AV valves open, then drops and slowly rises again until next atrial systole
  • 19. Length of Systole & Diastole  Cardiac muscle has unique property of contracting & repolarizing faster when heart rate is high  Duration of systole decreases from 0.27 s at a heart rate of 65 to 0.16 s, diastole from 0.62sec to 0.14 sec at a rate of 200 beats/min  THUS, duration of systole is much more fixed than diastole, & when heart rate is increased, diastole is shortened to much greater degree
  • 20.  This fact has important physiologic and clinical implications  It is during diastole that heart muscle rests, and coronary blood flow to the subendocardial portions of the left ventricle and most of the ventricular filling occurs
  • 21.  At heart rates up to about 180, filling is adequate as long as there is ample venous return, and cardiac output per minute is increased by an increase in rate  At very high heart rates, filling may be compromised such that cardiac output per minute falls and symptoms of heart failure develop
  • 22.  JVP is a vertical height from sternal angle to zone of transition of distended & collapsed IJV’s  Patient reclining at 45 degree,it is normally 4-5cm  It is an indicator of right mean atrial pressure.  It is the reflection of phasic pressure changes in right atrium  Consists of three positive waves (a,c,v) and two negative troughs(x,y)
  • 23.  a wave depicts atrial contraction(atrial systole)  c wave depicts bulging of tricuspid valve into the atria (isovolumetric contraction)  x descent shows atrial relaxation(ventricular systole)  v wave venous filling,(isovolumetric relaxation)  y descent indicates atrial emptying(ventricular filling)
  • 24. The types of action potential in the heart can be separated into two categories:  fast-response action potentials, which are found in the His-Purkinje system and atrial or ventricular cardiomyocytes, and  Slow response action potentials, which are found in the pacemaker cells in the SA and AV nodes
  • 25.  Phase 0 – Depolarization ( Na influx)  Phase 1 -Transient repolarization(activation of transient outward K+ current)  Phase 2 -Plateau phase(net influx of Ca2+ through L- type calcium channels efflux of K+ through K+ channels  Phase 3 -Repolarization(when efflux of K+ from 3 outward K+ currents exceeds the influx of Ca2+)  Phase 4 -Diastole(little ionic changes)
  • 26.  Action potentials in SA & AV nodes are largely due to Ca+, with little contribution by Na influx  So there is no sharp rapid depolarization spike before plateau,as in other parts of conduction system  When compared with fast-response action potential, phase 0 is much less steep, phase 1 is absent, phase 2 is indistinct from phase 3
  • 27. ANATOMY  RCA and LCA  RCA - rt atrium, most of rt ventricle & inferior wall of left ventricle  In 85% cases,RCA gives rise to posterior descending artery(superior posterior IVS & inferior wall)-Rt Dominant Circulation
  • 28.  LCA –left atrium, most of interventricular septum, left ventricle  Bifurcates into left anterior descending(septum &anterior wall) and circumflex artery(lateral wall)  SA node-RCA(60%), LAD(40%)  AV node-RCA(85%),circumflex(15%)  Bundle of His-PDA,LAD
  • 29.  Difference between aortic & ventricular pressure  CPP= arterial diastolic pressure – LVEDP  Decrease in aortic pressure ,increase in VEDP reduces CPP  Increase in heart rate also decrease CPP(because of reduction in diastolic time)  Endocardium-most vulnerable to ischemia
  • 30.  Parallels myocardial metabolic demand  Approx 250ml/min at rest  Myocardium regulates its own blood flow between perfusion pressures 50 &120mm Hg  Changes in blood flow mainly due to coronary arterial tone  Hypoxia cause vasodilation(directly or by adenosine release)  Sympathetic stimulation increases myocardial blood flow
  • 31.  Most important determinant of myocardial blood flow  Myocardium extracts 65% of oxygen in arterial blood, compared with 25% in other tissues  Coronary sinus saturation -30%  Myocardium cannot compensate for blood flow reductions by extracting more O2 from Hb  Increase in demand must be met by increase in CBF