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physiology of coronary circulation.

physiology of coronary circulation.

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  • 1. DR JAYANT MAKWANA PROFESSOR & HEADDEPARTMENT OF PHYSIOLOGY, RDGMC
  • 2. WHILE CIRCULATORY SYSTEM IS PROVIDINGO2 & NOURISHMENT TO EVERY CELL OFTHE BODY‘LETS NOT FORGET THE HEART WHICHWORKS TIRELESSLY & HARDEST OF ALL,NEEDS NOURISHMENT TOO’.
  • 3. CORONARY CIRCULATION
  • 4. CORONARY CIRCULATION:• INTRODUCTION• PHYSIOLOGIC ANATOMY• MEASUREMENT• NORMAL CORONARY FLOW• FACTORS AFFECTING• APPLIED 4
  • 5. INTRODUCTION• 1/3rd Of All Deaths World Wide, 2/3rd Of Which Occur In The Developing Countries.• CAD Prevalence In India- 3.5% In 1960s To 11%In Late 1990s In Urban India.• Estimation - Doubling Of Deaths Due To CAD In India From 1985 To 2015. 5
  • 6. PHYSIOLOGIC ANATOMY;• ORIGIN OF CORONARY ARTERIES• BRANCH & TERRITORY• VENOUS DRAINAGE• ANASTOMOSIS 6
  • 7. ORIGIN OF CORONARY ARTERIES- CORONARY ARTERIAL TREEIS DIVIDED INTO 3 SEGMENTS;A) TWO (LEFT ANTERIOR DESCENDINGARTERY & CIRCUMFLEX ARTERY)ARISE FROM A COMMON STEM (LCA).B) THE THIRD SEGMENT IS THE RIGHTCORONARY ARTERY.
  • 8. • LEFT CORONARY ARTRY;• ORIGIN – LEFT CORONARY SINUS ( LEFT POSTERIOR AORTIC SINUS)• LARGER THAN RCA• MAIN BRANCHES -LEFT CIRCUMFLEX & LEFT ANTERIOR DESCENDING (LAD)? INTERMEDIATE ARTERY 8
  • 9. LEFT ANTERIOR DESCENDING ARTERY• CONTINUES FROM THE BIFURCATION OF THE LEFT MAIN STEM TO THE APEX OF THE HEART.• ITS BRANCHES AREDIAGONALS- Ant LV WALLSEPTAL PERFORATORS - Ant 2/3 IVSTERMINAL BR – APEX
  • 10. CIRCUMFLEX ARTERY (LCX)TERMINATES- NEAR OBTUSE MARGIN OF THE LV- TO THE CRUX OF THEHEART (PDA)- SUPPLIES - LATERAL AND POSTERIOR WALL OF LV THROUGH ITS OBTUSE MARGINAL BRANCH.
  • 11. RIGHT CORONARY ARTERY –ORIGIN- RIGHT ANTERIOR AORTIC SINUSNEAR THE CRUX RCABIFURCATES INTO- RIGHT MARGINAL (ACUTEMARGINAL) - Lat. & Ant. RV- POSTERIOR DESCENDINGARTERY(PDA) Post. 1/3 IVS, Post LV
  • 12. CAPILLARY DENSITY- In Human Heart > 3000/mm2.At Birth - 1 Cap./ 4 FibresAdult - 1 Cap / FibreVent. ˃ Atria - BETTER DIFFUSION*Smaller Diameter Of Cardiac Muscle Fibres (<20 mm)*Smaller Diffusion Distance (8μ)
  • 13. PATTERN OF DISTRIBUTN (Coronary Dominance) • CRUX OF THE VENTRICLE • THE ARTERY WHICH SUPPLY AV NODE
  • 14. RIGHT DOMINANCE;• SEEN IN 50% - 70%• PDA FROM RCA• SUPPLIES RV,POST. PART OF IVS& GREATER PART OFPOST. WALL OF LV• EXTREME RIGHT DOMINANCE
  • 15. LEFT DOMINANCE• SEEN IN 10% - 20%• PDA FROM LCA• SUPPLIES LV, ENTIRE IVS & PART OF RV
  • 16. • BALANCE DOMINANCE; - SEEN IN 20%-30% - CONTRIBUTION TO INFERIOR SURFACE IS EQUAL - RCA SUPPLIES RV, POSTERIOR PART OF IVS - LCA SUPPLIES ANTERIOR PART OF IVS, LV 18
  • 17. VENOUS DRAINAGE;• TO RIGHT SIDE OF THE HEART• DEEP VEINS – ARTERIOSINUSOIDAL VESSELS , ARTERIOLUMINAL VESSELS, THEBESIAN VEINS• SUPERFICIAL VEINS- CORONARY SINUS,- GREAT CARDIAC V.- SMALL CARDIAC V.• ANTERIOR CARDIAC V. 19
  • 18. CORONARY SINUS- IT IS IMPORTANT IN ELECTROPHYSIOLOGICAL STUDIES, FOR ABLATION OF WPW SYNDROME ACCESSORY PATHWAYS- IT MAY BE USED TO INFUSE CARDIOPLEGIC SOLUTIONS DURING CARDIAC SURGERY.- TO COLLECT BLOOD TO MEASURE CORONARY BLOOD FLOW
  • 19. ANASTOMOTIC CHANNELS;• BETWEEN CORONARY ARTERIES & EXTRACARDIAC ARTERIES• INTERCORONARY ANASTOMOSIS*IN NORMAL HEART THERE ARE NOCOMMUNICATIONS BETn LARGECORONARIES.* ANASTOMOSES DO EXIST AMONG THE SMALLER ARTERIES SIZED 20 TO 250 μm.
  • 20. THERE ARE THREE AREAS OF ANASTOMOSES.i) BETWEEN BRANCHES OFLAD & PIV OF RCAIN IV GROOVEii) BETWEEN LCX & RCAIN AV GROOVE.iii) SEPTAL BRANCHES OFTWO CORONARY ARTERIESIN THE IVS.
  • 21. ANASTOMOSIS BETWN LCA & RCA DOES IT HELP?
  • 22. LIFESAVING VALUE OF COLLATERALS INHEARTOCCLUSION IN ONE OF THE LARGER CORONARY WITHIN SECONDSDILATATn OF SMALL ANASTOMOSES( BLOOD FLOW < ½) NEXT 8-24 HRS NO DILATATNINCREASE IN COLLATERAL FLOW (2ND/3RD DAY)NORMAL OR ALMOST NORMAL CORONARY (WITHIN 1 MONTH).
  • 23. CORONARY ANOMALIES• ANOMALIES OF THE ORIGIN- ORIGIN OF CORONARIES FROM PULMONARY ARTERY- SINGLE CORONARY ARTERY- ORIGIN FROM NON CORONARY CUSP- ANOMALIES OF THE COURSE - MYOCARDIAL BRIDGING - DUPLICATION- ANOMALIES OF TERMINATION - CORONARY FISTULA- EXTRACARDIAC TERMINATION
  • 24. MEASUREMENT;• OBJECTIVES;TO FIND OUT1. DETERMINANTS OF CORONARY FLOW2. OXYGEN UPTAKE BY MYOCARDIUM3. RELATION OF FLOW WITH WORK OF HEARTIN STATE OF NORMALCY, SED/ SED STRESS4. CARDIAC ABNORMALITY 26
  • 25. METHODS;• FLOW METERS• N2O METHOD ( Kety’s method)• DYE DILUTION METHOD• RADIONUCLEIDE (201TI), RADIOACTIVE MATERIAL(REGIONAL FLOW, ISCHAEMIA & INFARCT, VENTRICULAR FUNCTN)RADIOPHARMACEUTICALS SUCH AS Technetium-99mStannous pyrophosphate (99mTc-PYP)- "HOT SPOTS• CATHETER TIP FLOW METER• PULSED DOPPLER TECHNIQUE - BL.FL. IN MAJOR A.• VIDEO DENSITOMETRY-• INTRACORONARY INJECTN OF MICROBUBBLES &TRACKING THEIR MOVEMENT BY ECHOCARDIOGRAPHY.• CINE CT & MRI-TOTAL & REGIONAL MYOCARDIAL BF.• CORONARY ANGIOGRAPHY WITH 133Xe WASHOUT – DETAILED ANALYSIS OF CORONARY BLOOD FLOW
  • 26. NORMAL CORONARY FLOW• 5 % OF CARDIAC OUTPUT• 200 - 250 ml / min ( 0.7 TO 0.8 ml/gm/min)• TIME - 5 – 8 seconds 28
  • 27. FACTORS INFUENCING CORONARY BLOODFLOW;1. PHYSICAL FACTORS2. CARDIAC METABOLISM3. NEURAL FACTORS4. NEUROHORMONAL FACTORS 29
  • 28. 1. PHYSICAL FACTORS;A) CARDIAC CYCLE & MYOCARDIAL PRESSUREB) AORTIC PRESSUREC) CORONARY VASCULAR RESISTANCED) HEART RATEE) RIGHT ATRIAL PRESSURE 30
  • 29. A. CARDIAC CYCLE & MYOCARDIAL PRESSURE( THE PHASIC VARIATION)- CORONARY BLOOD FLOW NOT ONLY VARIES INTIME DURING THE CARDIAC CYCLE, IT ALSOVARIES WITH DEPTH IN THE WALL OF THE HEART
  • 30. UNDER NORMAL CONDITION SUBENDOCARDIUMRECEIVES SLIGHTLY HIGHER BLOOD FLOW THANEPICARDIUM (1.1:1)LCA BLOOD FLOW DURING SYSTOLE IS 15 - 16%OF DIASTOLE 33
  • 31. Unmasking of the restricting effect of ventricularsystole on mean coronary blood flow by induction ofventricular fibrillation during constant pressureperfusion of the LCA
  • 32. B) AORTIC PRESSURE- PARADOXICAL CORONARY FLOW- PROFILE OF BLOOD FLOW THROUGH THE CORONARIES DEPEND ON BOTH * THE PERFUSION PRESSURE IN AORTA & * THE EXTRAVASCULAR COMPRESSION
  • 33. Pressure in Aorta and Left and Right Ventriclesin Systole and Diastole. Press (mm Hg) in Press Diff (Hg) Between Aorta & AORTA LV RV LV RVSYSTOLE 120 121 25 -1 95DIASTOLE 80 0 0 80 80
  • 34. C) CORONARY RESISTANCE: P1- P2 P1- P2 Q = ------------ R = ------------- R Q- WHEN AORTIC & LV PRESSURE IS HELDCONSTANT CORONARY VASCULAR RESISTANCEVARIES DIRECTLY WITH CORONARY PERFUSIONPRESSURE.
  • 35. AUTOREGULATION• HEART IS A STRONG AUTOREGULATOR OF BLOOD FLOW AND MAINTAINS NORMAL FLOW OVER A PERFUSION PRESSURE RANGE OF• 60 -150 mm Hg.
  • 36. Pressure-flow relationships in the coronary vascular bed. At constant aorticpressure, cardiac output, and heart rate, coronary artery perfusion pressurewas abruptly increased or decreased from the control level.
  • 37. - THE LOW-PRESSURE LIMIT FOR AUTOREGULATIONIN THE ENDOCARDIAL LAYER IS GREATER THAN INTHE EPICARDIAL LAYER.- ENDOCARDIAL ARTERIAL DILATION REACHES AMAXIMUM WHEN ARTERIAL PRESSURE DROPS TO~70 mm Hg, WHEREAS MAXIMUM DILATION IN THEEPICARDIAL ARTERIES IS NOT REACHED UNTILPRESSURE IS ~40 mm Hg.
  • 38. E) HEART RATE• CARDIAC MUSCLE HAS THE UNIQUE PROPERTY OF CONTRACTING AND REPOLARIZING FASTER WHEN THE HEART RATE IS HIGH.• INCREASE IN HEAR RATE DECREASES THE DURATION OF BOTH THE SYSTOLE AS WELL AS THAT OF DIASTOLE.• THE DURATION OF SYSTOLE IS MUCH MORE FIXED THAN THAT OF DIASTOLE.• TACHYCARDIA SHORTENS DIASTOLE MORE THAN SYSTOLE.
  • 39. DURATION HEART RATE 65/min 75/min 200/minCARDIAC CYCLE 0.89 0.80 0.30SYSTOLE 0.27 0.27 0.16DIASTOLE 0.62 0.53 0.14
  • 40. 2. METABOLIC FACTORS• MOST IMPORTANT• LINEAR RELATION BETWN METABOLISM & CBF• ALL OF THE HEARTS CAPILLARIES RECEIVEBLOOD FLOW, EVEN AT NORMAL HEART RATE & CO.• RESTING STATE - 70-80% OF O2 IS EXTRACTEDFROM EACH UNIT OF BLOOD DELIVERED.• A V O2 DIFFERENCE - 12-15 ml% - MAXIMUM IN BODY
  • 41. Organ Mass Flow (ml / Total O2 USE Total O2 (kg) 100g / Flow (mL/100g USE min) (mL/min) /min) (mL/min)Heart 0.4 – 0.5Rest 60-80 250 7-9 25-40Exercise 200-300 1K-1.2K 25-40 65-85Muscle 28Rest 2-6 750-1K 0.2-0.4 60Exercise 40-100 15K-20K 8-15 2400
  • 42. HOW DOES HEART INCREASE ITS OWNBLOOD FLOWVASODILATIONOXYGEN LACKMYOGENIC
  • 43. VASODILATORS• ADENOSINE, ADENINE NUCLEOTIDEADENOSINE FROM CARDIAC MYOCYTESTO VASCULAR SMOOTH MUSCLE CELLSACTIVATES PURINOCEPTORS (A1 & A2A )INCREASE cAMPDECREASE ICF Ca++ VASODILATION
  • 44. - ADENOSINE LOSS & CELLULAR HEALTHADENOSINE LOSS IS ONE OF THE MAJOR CAUSESOF CARDIAC CELLULAR DEATH DURINGMYOCARDIAL ISCHEMIA.- AFTER THE ISCHEMIA OF 30 Min OR MORE,RELIEF OF THE ISCHEMIA MAY BE TOO LATE TOSAVE THE LIVES OF THE CARDIAC CELLS.
  • 45. ADENOSINE THE PRIME/ONLY VASODILATOR?- BLOCKADE OF ACTIONS OF ADENOSINE FAILS TO PREVENTCORONARY VASODILATN WHEN CARDIAC WORK ISINCREASED / BLOOD FLOW IS SUPPRESSED / THE ARTERIALBLOOD IS DEPLETED OF OXYGEN.- STUDIES IN SKELETAL MUSCLE HAVE SHOWN THATCONTINUED INFUSION OF ADENOSINE MAINTAINSVASCULAR DILATION FOR ONLY 1 TO 3 HOURS, & YETMUSCLE ACTIVITY STILL DILATES THE LOCAL BLOODVESSELS EVEN WHEN THE ADENOSINE CAN NO LONGERDILATE THEM.
  • 46. THE OTHER VASODILATOR• K, NO, H, CO2, LACTATE, BRADYKININ, PGI2, PGE2, CYANIDE
  • 47. • K+INTRACORONARY INFUSION OF KClELEVATION OF CORONARY ARTERIAL PLASMA K+FROM 4.23 TO 12.10 meq / LINCREASES IN CBF AVERAGING (17.7%)THE CHANGES IN CBF PRODUCED BY KCl INFUSION DOESNOT PARALLEL THE CHANGES IN PLASMA K+CONCENTRATION.
  • 48. Infusion Of 2,4-dinitrophenol/Epinephrine, Asphyxia, Or Increased Aortic Pressure Increase Myocardial O2 Consumption & CBF Did Not Result In The Release Of K+ From TheMyocardium.? K+ Release From Active Myocardium Is ResponsibleFor Adjustment In Coronary Resistance WhichAccompanies Changes In Metabolic Activity Of TheMyocardium.
  • 49. •NITRIC OXIDE• Nitric Oxide Causes Dilatation Of Epicardial Coronary Arteries.• Formation Of NO - By NOs - Flow Dependent No Formation - Receptor Stimulated No Formation
  • 50. HOW DOES Nitric Oxide ACTincreases ICF activates k+ chan. increases ICF cGMPcGMP protein kinaseinhibition of K+ efflux activation of Ca+ + entrydec. ICF Ca+ + hyperpolarization MLC phosphatase smooth muscle relaxation
  • 51. • INHIBITION OF Nitric Oxide Synthesis Results In Very Little Change In Coronary Blood Flow.
  • 52. • CORONARY FLOW RESERVE –- It is the maximum increase in blood flow throughthe Coronary Arteries above the normal restingvalue.- Its measurement is often used in medicine to* assist in the treatment of conditions affecting the coronary arteries.* determine the efficacy of treatments used.• VASODILATOR DRUGS & "CORONARY STEAL”
  • 53. Effect of reducing LAD radius onmaximal distal blood flows. A 60%reduction in LAD radius ( 40% ofmaximum radius) decreases distalflow capacity by more than 25%
  • 54. • O2 LACK HYPOTHESIS• MYOGENIC MECHANISMS
  • 55. 3. NEUROHORMONAL FACTORS;VASODILATOR – Ach, THVASOCONSTRICTOR - NE & E, VASOPRESSIN, ANGIOTENSIN-II, PGH2 ,ERGONOVINE
  • 56. 4. NEURAL FACTORS – ROLE OF ANS- SYMPATHETIC α1, β2, ? β1- Effect;* CORONARY VASODILATION* MARKED INCREASE IN CBF- ROLE OF α-ADRENERGIC RECEPTORS DURINGEXERCISEDIRECT EFFECT –VASOCONSTRICTION & REDUCED BLOOD FLOW
  • 57. PARASYMPATHETICDIRECT-VASODILATATIONINDIRECT –VASOCONSTRICTION
  • 58. - CHARACTERISTICS OF THE CORONARY CIRCULATION1) It is very short and very rapid.2) The blood flow in this circulation occurs mainly during cardiac diastole3) There is no efficient anastomoses between the coronary vessels.4) It is a rich circulation (5% of the CO while the heart weight is 300gm).5) Efficient Autoregulation
  • 59. 6) Its regulation is mainly by metabolites and not neural7) The capillary permeability is high (the cardiac lymph is rich in protein)8) The coronary vessels are susceptible to degeneration and atherosclerosis.9) There is evident regional distribution: The subendocardial myocardial layer in the left ventricle receives less blood.10. Subendocardium is more liable to ischemia and infarction.11. Myocardial infarction involving the PDA is morelikely to cause mitral regurgitation.
  • 60. THANK YOU…HAPPY VALENTINE DAYTAKE CARE OF YOURCORONARIES
  • 61. THE PAPILLARY MUSCLES OF LV- THE ANTEROLATERAL PAPILLARY MUSCLE MOREFREQUENTLY RECEIVES TWO BLOOD SUPPLIES: LAD &THE LCX ARTERY.- IT IS THUS MORE RESISTANT TO CORONARY ISCHEMIA.• THE POSTEROMEDIAL PAPILLARY MUSCLE IS USUALLY SUPPLIED ONLY BY THE PDA.• THUS THE POSTEROMEDIAL PAPILLARY MUSCLEARE SIGNIFICANTLY MORE SUSCEPTIBLE TO ISCHEMIA. Myocardial infarctionCLINICAL SIGNIFICANCE; involving the PDA is more likely to cause mitral regurgitation.
  • 62. APPLIED:1. ANGINA PECTORIS - ISCHAEMIC PAIN- SHARP, ACUTE, SUBSTERNAL RADIATING TO BASE OF THE NECK, SHOULDER, INNER HALF OF ARM - CAUSE OF PAIN “ P” FACTOR 70
  • 63. 2. MYOCARDIAL INFARCTION;• PROLONGED & IRREVERSIBLE CHANGES IN MUSCLE• OBSTRUCTION MORE THAN 75%• CARDIAC MUSCLE REQUIRES 1.3 ml OF O2 / 100 gms / min TO REMAI ALIVE• CUASE OF DEATH - SHOCK, EDEMA, FIBRILLATION, RUPTURE OF INFARCTED AREA 71
  • 64. LATEST : CORELATION BETWEENATHEROSCLEROSIS &Lp(a), HOMOCYSTEINE, ANTIBODY TO CHLAMYDIA PNEMONAE
  • 65. INVESTIGATION:• BLOOD ENZYMES - CK-MB, LDH, TROPONIN T, I• C-Reactive Protein, PPARγ,• ECG - LEAD II, III, aVF - INFERIOR WALL INFARCTION LEAD I, aVL, - ANTERIOSEPTAL INF. V1,V2, - RV , V4 - INFERIOR WALL, V5,V6 - LV• ANGIOGRAPHY 73
  • 66. 4. ECHOCARDIOGRAPHY & DOPPLER ULTRASOUND5. CARDIAC MRI6. ELECTRON BEAM COMPUTED TOPOGRAPHY ( EBCT) - TO SEE Ca DEPOSITS IN CORONARY VESSEL WALL7. CARDIAC NUCLEAR MEDICINE STUDY 74
  • 67. TREATMENT:1. ANGINA PECTORIS REST, NITRATES, BYPASS (AORTOCORONARY)2. MI ACUTE – THROMBOLYTIC AGENTS- STREPTOKINASE, UROKINASE, TPA PREVENTION OF THROMBUS FORMATION - ASPIRIN, CLOPIDEGEROL BETA BLOCKERS, REST, CHANGE IN LIFE STYLE3) Vit B12, Folate 75
  • 68. SURGICAL :1. ANGIOPLASTY - BALLOON, BALLOON WITH STENT, DRUG ELUTING STENT2. BYPASS 76
  • 69. 77