Cvs physio
- 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.
- 11. 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
- 12. 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
- 13. Ventricular Systole Mitral & tricuspid valves close Intraventricular pressure rises sharply as myocardium presses on blood in ventricle .
- 14. 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
- 15. 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
- 16. 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
- 17. 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.
- 18. 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
- 19. 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
- 20. 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
- 21. 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
- 22. 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
- 24. 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)
- 26. 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)
- 28. 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
- 30. 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)
- 31. 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
- 33. 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
- 34. 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
- 35. 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
- 36. 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
- 37. 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