CARDIAC PHYSIOLOGY.pptx..............................................................

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1. CARDIAC PHYSIOLOGY PRESENTOR: DR.DHARSHINI.K MODERATOR: DR.R.V.RANJAN

2. CORONARY CIRCULATION Right coronary artery supplies: Right atrium Right ventricle A small part of left ventricle near the posterior interventricular groove Posterior part of interventricular septum Major portion of the conducting system of the heart

3. Left coronary artery supplies: Left atrium Left ventricle A small part of right ventricle near anterior interventricular groove Anterior part of interventricular septum A part of left branch of bundle of his It has 2 branches: Anterior descending branch Left circumflex branch

4. Coronoary arteries are end artery Funtional anastomoses are present which become active under abnormal condition 2 types of anastomosis: Cardiac anastamosis Branches of one coronary artery with other Branches of coronary arteries and branches of deep system of veins Extracardiac anastamosis Vasa vasora of aorta Vasa vasora of pulmonary artery Intrathoracic arteries Bronchial arteries Phrenic arteries

5. VENOUS DRAINAGE OF HEART Coronary sinus Great cardiac vein Anterior cardiac vein Arterio sinusoidal vessel Arterio luminal vessel Thebesian vessel

6. MYOCARDIUM Involuntary, striated muscle tissue in the heart between the epicardium and the endocardium, its cells are called cardiomyocytes. Primary structural proteins are actin and myosin filaments Unlike skeletal muscles these filaments are branched, the cardiac T tubules are larger, broader and fewer in number

7. T tubules form dyads with the SR intercalated discs with permeable junction Thus cardiomyocytes are functionally interconnected

8. CARDIAC ACTION POTENTIAL

9. EXCITATION CONTRACTION COUPLING Occurs in both cardiac and skeletal muscle when the action potential spreads into the cell through transverse tubules Depolarisation of T tubule causes influx of calcium into the sarcoplasm  binds to troponin  activates contraction of actin and myosin filaments. It triggers an additional release of calcium from the SR into the sarcoplasm.

10. CARDIAC CYCLE Sequence of changes in the pressure and flow in the heart chambers and blood vessels between 2 subsequent cardiac contractions.

11. ELECTRICAL EVENTS AND ELECTROCARDIOGRAM ECG is the result of differences in electrical potential generated by the heart SA node  AV node  His bundle  Purkinje system  cardiomyocytes P wave  atrial systole PR interval  delay in atrial and ventricular contraction QRS complex  ventricular depolarization T wave  ventricular repolarization

12. MECHANICAL EVENTS Atrial systole – 0.1 sec Ventricular systole – 0.3 sec -isovolumetric ventricular contraction - ventricular systole proper Ventricular diastole – 0.5 sec - protodiastole, isovolumetric ventricular relaxation phase, ventricular diastole proper & rapid filling phase due to atrial systole Atrial systole – 0.7 sec

13. VR to right and left atria Increase in atrial pressure > ventricular pressure Opening of AV valves Blood flows passively into ventricular chamber Onset of atrial systole or kick

14. Closure of AV valve Isovolumetric contraction of ventricles Ventricular pressure > aortic & Pulmonary.A pressure Opening of pulmonary and aortic valve Ventricular ejection

15. Progressive fall in ventricular pressure Closure of aortic and pulmonary valve Isovolumetric relaxation Decreased ventricular pressure < atrial pressure Opening of AV valves

16. NORMAL VOLUMES OF BLOOD IN VENTRICLE Atrial systole pushes final 20-25 ml blood (20%) After atrial contraction, 110-120 ml in each ventricle (end-diastolic volume) Contraction ejects ~70 ml (stroke volume output) Thus, 40-50 ml remain in each ventricle (End‐ systolic volume) The fraction ejected is then ~60% (ejection fraction)

17. Blood pressure in aorta is 80-120 mm Hg Blood pressure in pulmonary trunk is 8-25 mm Hg Ventricular pressure usually not increases during diastole Right Atrial pressure changes reflected in Jugular vein

18. CENTRAL VENOUS WAVEFORM a wave- atrial contraction c wave- ventricular systole, tricuspid bulging v wave- systolic filling of right atria x descent- atrial relaxation y descent- early ventricular filling

19. “a- c” interval measures the time of conduction of the cardiac impulse from the right atrium to the ventricles “a- c” interval is prolonged in cases of delayed conductivity in the AV bundle which is an early sign of heart block In partial heart block, the number of “a” waves is greater than the number of the “c” or “v” waves. In atrial fibrillation, the “a” wave is absent.

20. PRELOAD Ventricular load at the end of diastole, before contraction has started Pulmonary wedge pressure or central venous pressure is used to measure preload When the HR & contractility remains constant , CO is directly proportional to preload

21. AFTERLOAD Systolic load on LV after contraction has begun Aortic compliance is a determinant of afterload Measurement of afterload done by echocardiography and SBP

22. LAPLACE’S LAW States that wall stress is the product of pressure and radius divided by wall thickness, Wall stress=PR/2h Preload and afterload is the wall stress that is present at the end of diastole and left ventricular ejection.

23. FRANK STARLING RELATIONSHIP Relationship between sarcomere length and myocardial force Stretching of myocardial sarcomere results in enhanced myocardial performance i.e force of contraction of ventricular muscle fibre is directly proportional to its initial length

24. CONTRACTILITY Defined as the work performed by cardiac muscle at any end- diastolic volume

25. Pressure volume loops, requiring catheterization of the left side of the heart , best way to determine the contractility in an intact heart. Pressure volume loop, an indirect measure of frank starling relationship between force and muscle strength. Noninvasive index of ventricular contractile function is ejection fraction. EF= [LVEDV- LVESV]/LVEDV

26. CARDIAC WORK External work is work done to eject blood under pressure Stroke work= SV x P or [LVEDV- LVESV] x P Internal work is the work done to change shape of heart for ejection Wall stress directly proportional to internal work of the heart Cardiac efficiency=external work/energy equivalent of O2 consumption

27. HEART RATE AND FORCE FREQUENCY RELATIONSHIP In isolated cardiac muscle, an increase in frequency of stimulation induces an increase in force of contraction However when a stimulation becomes extremely rapid, the force of contraction decreases. Pacing induced positive inotropic effect may be effective only upto a certain HR. In a failing heart, the force frequency relationship may be less effective in producing a positive inotropic effect

28. CARDIAC OUTPUT Amount of blood pumped by the heart per unit of time CO= SV x HR Determined by:- Intrinsic factor: HR & myocardial contractility Extrinsic factor: preload and afterload

29. Heart rate- no.of beats per min, influenced by ANS Enhanced vagal activity decrease HR Enhanced sympathetic activity increase HR Stroke volume: volume of blood pumped per contraction Determined by: preload, afterload & contractility

30. Methods to measure CO Thermodilution method Fick method Echocardiography Thermodilution method Cold saline  arm vein  right atrium Change in temperature is inversely related to the amount of blood flowing through the aorta

31. Direct Fick method FICK PRINCIPLE: amount of substance taken per min = [A- V] difference of the substance x blood flow/min Diasdvantage- Invasive procedure, risk of haemorrahge, infection Patient is conscious, so CO may be higher Ventricular fibrillation

32. CONTROL OF CARDIAC FUNCTION

33. NEURAL REGULATION OF CARDIAC FUNCTION SNS provide positive chronotropic, inotropic and lusitropic effects [during exercise or stress] PNS has direct inhibitory effect on the atria and has a negative modulatory effect on the ventricle [at rest] Parasympathetic innervation is by vagal nerve  activation of muscarinic receptor  reduce pacemaker activity, slows AV conduction, directly decrease atrial contractile force, inhibitory modulation of ventricular contractile force

34. Atria  innervated by both SNS & PNS Ventricles  principally by SNS SNS continually discharge at a slow rate maintaining a strength of ventricular contraction 20- 25% Maximal SNS stimulation  increase CO by 100% above normal Maximal PNS stimulation  decrease ventricular contractile strength only by about 30%

35. HORMONAL CONTROL Hormones produced by cardiomyocytes:- natriuretic peptide, adrenomedullin, aldosterone, angiotensin II ANP & BNP are released from atria and ventricle in response to stretch of the chamber wall Participate in homeostasis of body fluids, in regulation of BP and in growth and development of cardiac tissue

36. Adrenomedullin, a peptide hormone that increase level of c AMP and has positive inotropic and chronotropic effect on the heart and is a vasodilator. Angiotensin II stimulates AT1 receptors with positive inotropic and chronotropic effect It also stimulate AT2 receptor which mediates cell growth and proliferation of cardiomyocytes. Other hormones: growth hormone, thyroid hormone, sex steroid hormone

37. SEX STEROID HORMONES AND THE HEART Premenopausal women has more intense cardiac contractility, lower cardiovascular risk compared to men  estradiol 2 types of estrogen receptors in heart Estrogen has vasodilatory effect In men, aromatase mediated conversion of testosterone to estrogen maintains normal vascular tone

38. CARDIAC REFLEXES

39. BARORECEPTOR REFLEX Increase in BP Stimulation of BR in carotid sinus and aortic arch IX & X NERVE N.solitarius Increase in vagal tone

40. CHEMORECEPTOR REFLEX Pao2<50mmhg or acidosis Chemosensitive cells in carotid bodies and the aortic body Sinus nerve of hering and X cranial nerve Stimulates the respiratory centre Increase the ventilator drive

41. Activation of parasympathetic system  reduction in HR and myocardial contractility Persistent hypoxia  CNS directly stimulated

42. BAINBRIDGE REFLEX Increase in right side filling pressure Stretch receptors in right atrial wall and the cavoatrial junction Vagal afferent signals to medulla Inhibit parasympathetic activity  increase HR

43. BEZOLD- JARISCH REFLEX Ischemia or infarction, thrombolysis or revascularization and syncope Activation of chemoreceptors and mechanoreceptors within the LV wall Hypotension, bradycardia and coronary artery dilatation

44. VALSALVA MANEUVER Forced expiration against a closed glottis  increase intrathoracic pressure, CVP and decrease venous return Decrease in CO & BP Sensed by baroreceptor  sympathetic stimulation  increase in HR & myocardial contractility When glottis opens-  increase in VR & BP Increase in BP  sensed by baroreceptor  stimulate parasympathetic

45. CUSHING REFLEX Increase in ICP Cerebral ischemia at VMC Activation of SNS Increase in HR, ABP & myocardial contractility

46. OCULOCARDIAC REFLEX Pressure on eye or traction of surrounding structures Stretch receptors send afferent signals through short and long ciliary nerves Trigerminal.N carry impulse to gasserian ganglion Increase PNS  bradycardia

47. HEMODYNAMIC EQUATIONS CO= HR x SV [5- 7L/MIN] CI = CO/BSA [2.4L/MIN] SV = EDV-ESV [1ML/KG or 70-90 ML] MAP = CO x SVR MAP = 2/3 DBP + 1/3 SBP [60- 90MMHG]

48. REFERENCES Stoelting’s pharmacology and physiology in anesthesia practice , 6 th edition Millers Anesthesia, 10 th edition Barash, clinical anesthesia , 9 th edition

49. THANK YOU