cardio vascular physiology anesthesiasia

cvs physiology ,anesthesia , cardio

1. CARDIOVASCULAR PHYSIOLOGY

2. The circulatory system consists of the heart, the blood vessel and blood. Heart ,a muscular organ, situated in the middle mediastinum just behind & left of the sternum. The heart consists of two atria and two ventricles . INTRODUCTION

3. Transport and distribute essential substances to the tissues. Remove metabolic byproducts. Adjustment of oxygen and nutrient supply in different physiologic states. Regulation of body temperature. Distribution of hormones to target tissues. FUNCTIONS

4. CORONARY CIRCULATION

5. Venous supply

6. Coronary perfusion is intermittent compared to continuous in other organs .+ CPP = Arterial diastolic pressure – LVEDP LV is perfused entirely during diastole. RV is perfused during both systole & diastole. Control of coronary blood flow CBF - 250ml/min at rest. Myocardium regulates its own blood flow between 50-120mmHg. Beyond this, flow becomes increasingly pressure dependent. Under normal conditions, changes in blood flow occur in response to metabolic demand. Hypoxia either directly or indirectly causes coronary vasodilatation by the release of adenosine. Sympathetic stimulation increases myocardial blood flow through β 2 effect Parasympathetic stimulation effects are minor & weakly vasodilatory .

7. Myocardial oxygen balance Myocardium extracts 65% 02 in arterial blood compared to 25% in most other tissues. Coronary sinus O2sat is usually 30%.Therefore the myocardium cannot compensate for reductions in BF by extracting more O2 from Hb . Factors effecting myocardial o2 supply & demand Supply – HR (diastolic filling time ) - coronary perfusion pressure -arterial 02 content -coronary vessel diameter Demand - basal requirement -HR - wall tension -contractility

8. Most volatile anaesthetic agents are coronary vasodilators . Halothane & isoflurane have the greatest effects, the former affects large coronary vessels ,the latter affects mostly smaller vessels. Vasodilatation due to desflurane is primarily autonomically mediated, whereas sevo lacks coronary vasodilatory properties. They reduce O2 req & also protective against reperfusion injury , enhance recovery of stunned myocardium. Volatile anaesthetics are benificial in heart failure patients because most of them decrease preload & afterload . ANAESTHETIC IMPLICATION

9. Heart valves ensure unidirectional blood flow through the heart. Atrioventricular (AV) valves lie between the atria and the ventricles. AV valves prevent backflow into the atria when ventricles contract. Chordae tendineae anchor AV valves to papillary muscles. Aortic semilunar valve lies between the left ventricle and the aorta. Pulmonary semilunar valve lies between the right ventricle and pulmonary trunk. Semi lunar valves prevent backflow of blood into the ventricles. HEART VALVE

10. CELLULAR PHYSIOLOGY At the cellular level heart consists of 3 major components :- 1) cardiac muscle tissue (contracting cardiomyosites ) 2) conduction tissue ( conducting cell) 3) extra cellular connective tissue :- a) mainly made up of collagen which determines cardiac stiffness. b) other major matrix proteins like elastin , proteoglycans etc.

11. Cardiac muscle is striated, short, fat, branched, and interconnected. The cardiac myocytes are interconnected to act as a functional syncytium . The connections are of two types : Mechanical:Intercalated discs & desmosomes Electrical: Gap junctions. Myocardium consists of two types of cells: Working myocardial cells Cells forming the junctional tissues. MICROSCOPIC STRUCTURE OF THE HEART

12. Properties of Cardiac Muscle Mechanical Electrical -Excitation contraction coupling - Autorhythmicit -Force of contraction Conductivity -Excitability

13. Sino- atrial node (SAN) -known as pacemaker of heart ,a small, flattened, ellipsoid strip of specialised tissue. -superior lateral wall of right atrium, below & lateral to opening of superior  venacava . - cardiac action potential spreads immediately from SA node to atria . Internodal pathway -Connects SA node to AV node. -Has faster rate of conduction than atrial muscles. -Anterior tract- Bachman’s bundle -Middle tract- Wenkebach’s bundle -Posterior tract- Thorel’s bundle CONDUCTION SYSTEM

14. AV node (AVN) - Only conducting pathway between atria & ventricles normally. - posterior septal wall of Rt. Atria, behind tricuspid valve. - has thinner fibres with more – ve RMP causing conduction delay. - the conduction velocity slows down in AV Node which is known as AV Nodal delay. This delay is important as it gives time for proper ventricular filling. Bundle of His -It begins from AV Node, passes downwards in the interventricular septum for 5-15mm. -Divides into right & left bundle branches. -Left branch divides into anterior & posterior fasciculus

15. Purkinje fibers -Takes origin from terminal divisions of bundle branches -Fastest conducting -It is 1-2mm thick- largest conducting fiber. Passes impulses to ventricular myocytes . Rates of impulse generation SAN- 70 to 80/min AVN- 40 to 60/min Purkinje fibers- 15 to 40/min  

16. Tissue Conduction rate (m/s) SA node .05 Atrial pathways 1 AV node .05 Bundle of His 1 Purkinje 4 Ventricular muscle 1 CONDUCTION SPEED

17. Ion fluxes across the plasma membrane results in depolarization and repolarization . Can be divided in two types:- a) Fast response type- in His Purkinje system , & atrail or ventricular cardiomyocytes . b) Slow response type – in SA node & AV node RMP of cardiac muscle is -85 to - 95 mv . Causes Excitation contraction coupling . ACTION POTENTIAL (AP)

18. MEMBRANE POTENTIAL (mV) -90 1 2 3 4 TIME PHASE 0 = Rapid Depolarization (inward Na + current) 1 = Overshoot 2 = Plateau (inward Ca ++ current) 3 = Repolarization (outward K + current) 4 = Resting Potential Mechanical Response AP can be divided in to 4 phases :-

19. EXCITATION CONTRACTION COUPLING

20. Potent volatile anaesthetics depress SA node automaticity -increases conduction time and increases refractoriness. Opioids like fentanyl and sufentanyl depress cardiac conduction,increased AV node conduction and refractory period and prolonging the duration of the purkinje fibre AP. LA at high conc -systemic toxicity-depress conduction by binding to fast sodium channels.At very high conc ,it depresses SA node. But at low cocn,lidocaine is therapeutic. The most potent LA have great effects on heart particularly purkinje fibres and ventricular muscle. Bupivacaine binds open or inactivated sodium channels and dissociates from them slowly.It can cause profound sinus bradycardia and sinus node arrest as well as ventricular arrhytmias . CCBs block Ca influx through L type but not T type channel. ANAESTHETIC IMPLICATION

21. All volatile anaesthetics depress cardiac contractility by decreasing the entry of Ca into cells during depolarisation , altering its release and uptake into SR and decrease sensitivity of proteins to Ca. Halothane and enflurane depress contractility››››› isoflurane,sevoflurane and desflurane . Also potentiated by 1.hypocalcemia 2.B adrenergic blockade 3.CCBs. N2O also produce dose dependent decrease in contractility. Among all the major iv induction agents , ketamine has the least depressant effect on contractility. LA depress cardiac contractility by reducing Ca influx and release in a dose dependent manner.

22. HALO ISO SEVO DES HR  - -  BP     Cardiac Index  -  *  /  Conduction system slowing + Min - + Sensitization to Epi + Min - - Inhalational anaesthetics

23. Thio. Prop. Keta. Etom. HR  -/   - BP -/    - Preload    - Afterload -   - Intravenous Induction Agents

24. Cardiac cycle Systole Diastole Ventricle contracts Ventricle relaxes Events that occur from the beginning of one heartbeat to the beginning of next are called cardiac cycle. Duration- 0.833 secs /beat. HR l/t in cardiac cycle duration. Cardiodynamics

25. The Cardiac Cycle

26. JUGULAR VENOUS PRESSURE

27. Right atrial pressure. The normal JVP consists of 3 positive waves( a,c,v ) and 2 negative waves ( x,y ). ‘a’ wave - Rt atrial contraction. -absent in atrial fibrillation. Large giant ‘a’ waves -TS, PS, pulmonary hypertension. Cannon ‘a’ waves - complete heart block, ventricular tachycardia. JVP

28. ‘ c’ wave- Tricuspid valve bulging- Isovolumetric contn ‘X’ descent- Ventricular contn - ejection phase ‘X’ descent is obliterated –TR Prominent -constrictive pericarditis . ‘ V’ wave- Venous filling into Atria. Giant ‘V’ waves- TR. ‘ Y’ descent- opening of the tricuspid valve & subsequent rapid inflow of blood from rt atrium to the rt ventricle leading to sudden fall in pressure in the rt atrium. Rapid ‘Y’ descent - constrictive pericarditis , severe heart failure , TR. A short ‘Y’ descent - TS.

29. Heart sounds Early vent contn squeezes blood towards base making AV valve close HS-1 At the end of vent ejection vent relax fall in pressure below that in aorta HS-2 HS 3 & HS 4

30. Left ventricular volumes End Diastolic Volume (EDV)- Volume at the end of diastole (end of ventricular filling) End Systolic Volume (ESV)- Volume at the end of systole (end of ventricular contraction)

31. Cardiac output- amount of blood pumped by each ventricle in 1-min. CO= HR SV= 5 lts /m. Stroke volume - amount of blood pumped by each ventricle per beat/per contn . SV= EDV-ESV= 70ml. Preload : (EDV) volume of the left ventricle at the end of diastole (dependent on venous return & stretch of the cardiac muscle cells) Afterload : resistance to ventricular emptying during systole (the amount of pressure the left ventricle must generate to squeeze blood into the aorta)

32. Frank-Starling law “energy of contraction is proportional to the initial length of the cardiac muscle fiber” Force of cardiac contraction is proportional to EDV

33. The intrinsic ability of the myocardium to pump in the absence of changes in preload or afterload . Related to the rate of myocardial muscle shortening , which is in turn dependent on the intracellular Ca conc during systole. Can be altered by neural , humoral or pharmacological influences. Sympathetic fibres innervate atrial and ventricular muscle as well as nodal tissues. NE enhances contractility via B1 receptor activation in addition to chronotropic effects. Sympathomimetic drugs and secretion of Epinephrine from adrenal glands increase contractility via B 1 receptor activation. Contractility is depressed by hypoxia , acidosis , depletion of catecholamine store within the heart and loss of functioning muscle mass as a result of ischaemia or infarction. Most anaesthetics and antiarrhythmic agents at high doses are negative inotropes .(decrease contractility). CONTRACTILITY

34. INCREASING HEART RATE INCREASES CONTRACTILITY Normal Heart Rate Ca ++ Ca ++ Fast Heart Rate Ca ++ Ca ++ Ca ++ Ca ++

35. Ventricular systolic function ≡ CO ≡ volume of the blood pumped by the heart per minute. To compensate variations in body size, CO is often expressed in terms of TBSA. CI =CO\BSA (N) CI=2.5-4.2 L/min/sq m Abnormalities in CI reflect gross ventricular impairment. More accurate assessment is obtained by evaluating the response of the CO to exercise . Failure of the CO to increase & keep up with oxygen consumption is reflected by a falling mixed venous oxygen saturation. Determinants of ventricular performance

36. Cardiac output measurement Indirect methods- Fick’s principle - Dye dilution method - Thermodilution method Physical methods- Doppler echo - Ballistocardiography

37. Fick’s principle “the amount of a substance taken up by an organ or whole body per unit time is equal to arterial level of the substance(A) minus venous times the blood flow(F)” Q= (A-V) F F = Q/(A-V) Total body O2 consumptn 250ml/min CO= = (A-V) O2 difference 5ml/min = 5000ml/min.

38. Medulla oblongata VMC CVC venterolateral medulla Nucleus Ambigous NTS Symp . disch to Heart Parasymp . Disch toHeart REGULATION OF CVS

39. Lateral pressure exerted by the flowing blood on the walls of vessel. One of principal vital signs S ystolic pressure – maximum arterial pressure during systole, 120mmhg (105-135). D iastolic pressure – minimum arterial pressure during diastole, 80mmhg (60-90). - indicates the constant load against which heart has to work. Mean arterial pressure ( MAP )= DP + PP 1/3 MAP – CVP= SVR × CO Pulse pressure = Systolic BP – Diastolic BP. ARTERIAL BLOOD PRESSURE

40. Sex … M > F …due to hormones/ equal at menopause. Age … Elderly > children …due to atherosclerosis. Emotions …  due to secretion of adrenaline & noradrenaline . Exercise …  due to  venous return. Hormones …  ( e.g. Adrenaline, noradrenaline , thyroid H). Gravity …  Lower limbs > upper limbs. Race … Orientals > Westerns … ? dietry factors, or weather. Sleep …  due to  venous return. Pregnancy …  due to  metabolism FACTORS AFFECTING BP

41. CONTROL OF ARTERIAL BP

42. Immediate control Minute to minute control of BP- a function of ANS. Chemoreceptor Peripheral baroreceptor ( stretch receptors) aortic carotid After few minutes of sustained decrease in BP Renin angiotensin aldosteron system AVP Altered capillary permiability Intermediate control

43. Renin angiotensin aldosterone system

44. Arginine vesopressin Potent arteriolar vasoconstrictor . Immediate action is to increase the SVR. Mediates vasoconstriction via V1 receptor & antidiuretic effect via V2 receptors. After hours of sustained change in BP Sodium and water balance . Hypotension – Na retention , Hypertension – Na excretion . Long term control

45. Baroreceptor reflex ↑ BP  ↑ BR in carotid sinus & aortic arch  Sinus nerve & Aortic nerve  IX & X nerve  N. solitarius  ↑ vagal tone  ↓ HR CARDIAC REFLEXES

46. Chemoreceptor reflex ↓pO 2 ↑ pCO 2 & ↓pH  ↑ CR in carotid body & aortic arch  Sinus nerve & Aortic nerve  IX & X nerve  ↑ Respiratory centre  ↑ ventilatory drive

47. Bainbridge Reflex Venous engorgement of atria & great veins  Stimulation of stretch receptors  X nerve  CVS center medulla  ↓ Vagal tone  ↑ HR Bezold – Jarisch Reflex Ischemia  Receptors in LV  X nerve  Reflex bradycardia , Hypotension & coronary artery dilation

48. Valsalva maneuver Forced expiration against closed glottis ↑ Intrathoracic pressure → ↑ CVP → ↓ V.R → ↓ CO &BP → sensed by BR → ↑ HR & contractility When glottis opens ↑ VR → ↑ contractility → ↑ BP →sensed by BR → ↓ HR & BP Cushing Reflex ↑ Intracranial pressure  Cerebral ischemia  ↑ VMC  ↑SNS - ↑BP  ↑BR  ↑CIC  ↑ Vagal tone  reflex bradycardia ↓ HR

49. Occulocardiac Reflex Pressure on eye  long & short ciliary nvs  ciliary ganglion  gasserion ganglia  ↑ PNS → BRADYCARDIA

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