Coronary circulation 14 10-14

Coronary circulation, anatomy, basic physiology and their clinical implications.

1. ANATOMY AND PHYSIOLOGY OF CORONARY CIRCULATION DR AFTAB HUSSAIN

2. ANATOMY OF CORONARY CIRCULATION As Throughout the body, the coronary system also comprises of arteries, arterioles, capillaries, venules and veins. The coronary arteries originate as the right and left main coronary arteries which exit the ascending aorta just above the aortic valve through the coronary ostia . These two branches subdivide and course over the surface of the heart ( epicardium ) progress inward to penetrate the epicardium and supply blood to the transmural myocardium.

3. An Overview of the Coronary Arteries Coronary Ostia giving rise to :- Left Main or left coronary artery (LCA) Left anterior descending (LAD) diagonal branches (D1, D2) septal branches Left Circumflex ( LCx ) Marginal branches (M1,M2) Right coronary artery Acute marginal branch (AM) AV node branch Posterior descending artery (PDA)

4. THE BIG PICTURE

5. The coronary arteries originate as the right and left main coronary arteries, which exit the ascending aorta just above the aortic valve ( coronary ostia ). The ostia of the left and right coronary arteries are located just above the aortic valve, as are the left and right sinuses of Valsalva .

6. THE CORONARY OSTIA (Origin of the coronary arteries)

7. Right Coronary Artery (RCA) The right coronary artery arises from the anterior sinus of Valsalva and courses through the right atrioventricular (AV) groove between the right artium and right ventricle to the inferior part of the septum. In 60% a sinus node artery arises as second branch of the RCA, that runs posteriorly to the SA-node (in 40% it originates from the LCx ).

8. The large acute marginal branch (AM) comes off with an acute angle and runs along the margin of the right ventricle. The RCA continues in the AV groove posteriorly and gives off a branch to the AV node. In 65% of cases the posterior descending artery (PDA) is a branch of the RCA (right dominant circulation). The PDA supplies the inferior wall of the left ventricle and inferior part of the septum.

9. THE LEFT MAIN CORONARY ARTERY(LMCA) The left coronary artery (left main coronary artery) emerges from the aorta through the ostia of the left aortic cusp. The left coronary artery travels from the aorta, and passes between the pulmonary trunk and the left atrial appendage. Under the appendage, the artery divides into the anterior interventricular (left anterior descending artery) and the left circumflex artery .

10. Branches of the left main coronary artery : Left anterior descending (LAD) artery (anterior interventricular artery) Left circumflex artery (LCX) R amus intermedius ( between the LAD and LCX )

11. THE LEFT ANTERIOR DESCENDING ARTERY(LAD) The left anterior descending ( interventricular ) artery is a direct continuation of the left coronary artery which descends into the anterior interventricular groove. Branches of this artery, anterior septal perforating arteries , enter the septal myocardium to supply the anterior two-thirds of the interventricular septum (in ~90% of hearts). most of the right and left bundle branches, and the anterior papillary muscle of the bicuspid valve.

12. THE LEFT CIRCUMFLEX ARTERY ( LCx ) The circumflex artery branches off of the left coronary artery and supplies most of the left atrium. Also, posterior and lateral free walls of the left ventricle, and part of the anterior papillary muscle. The circumflex artery may continue through the AV sulcus to supply the posterior wall of the left ventricle and (with the right coronary artery) the posterior papillary muscle of the bicuspid valve.

13. In 40-50% of hearts the circumflex artery supplies the artery to the SA node . Branches of the circumflex :- Obtuse marginal branches (OM): as it curves toward the posterior surface of the heart. 1-3 in numbers Supplies: - postero -lateral left ventricle -Inferior surface of left ventricle - anterolateral papillary muscle -Left atrium -SA node(40%)

14. THE CARDIAC VEINS From the innumerable cardiac capillaries, blood flows back to the cardiac chambers through venules , which in turn coalesce into the cardiac veins. Most cardiac veins collect and return blood to the right atrium through the coronary sinus. Cardiac veins contain valves preventing back flow; a Thebesian valve may or may not cover the ostium of the coronary sinus.

15. MAJOR VENOUS VESSELS OF THE HEART Coronary sinus The anterior inter ventricular veins Left marginal veins Posterior veins of the left ventricle 5. The Great Cardiac Vein

16. THE CORONARY SINUS The coronary sinus serves as the primary collector of cardiac venous blood, located in the right atrium. The coronary sinus receives drainage from most epicardial ventricular veins, including the oblique vein of the left atrium, the great cardiac vein, the posterior vein of the left ventricle, the left marginal vein, and the posterior interventricular vein. The coronary sinus empties directly into the right atrium.

17. THE GREAT CARDIAC VEIN It travels in the anterior interventricular groove beside the left anterior descending coronary artery and in the left atrioventricular groove beside the left circumflex artery. It opens into the left extremity of the coronary sinus. I t receives tributaries from the left atrium , from both ventricles and large left marginal vein.

18. Venous drainage of heart

19. Structure Usual Blood Supply Variant Interventricular Septum Anterior Interventricular septum Posterior Anterolateral Wall Left Posterior Wall Anterolateral Papillary Muscle Posteromedial Papillary Muscle Apex Inferior Wall LAD RCA ,Proximal 2/3 rd LAD ,Distal 1/3 rd LCx , Diagonals LCx , RCA LAD , LCx RCA LAD RCA RCA(Small Portions including the Apex), LCx LCx , LAD Distal 2/3 rd Ramus Intermedius LCx RCA , LCx LCx , Distal LAD

20. PHYSIOLOGY OF CORONARY CIRCULATION

21. Coronary Blood Flow Two-thirds of coronary blood flow occurs during diastole . Five percent of cardiac output goes to the coronary arteries . Seventy percent of oxygen is extracted by the myocardial tissues of the heart, in comparison to the rest of the body at twenty five percent. During times of extreme demand, the coronary arteries can dilate up to four times greater than normal .

22. CORONARY BLOOD FLOW Coronary blood flow in Humans at rest is about 225-250 ml/minute , about 5% of cardiac output. At rest, the heart extracts 60-70% of oxygen from each unit of blood delivered to heart [other tissue extract only 25% of O 2 ]. 27

23. CORONARY BLOOD FLOW Why heart is extracting 60-70% of O 2 ? Because heart muscle has more mitochondria, up to 40% of cell is occupied by mitochondria, which generate energy for contraction by aerobic metabolism, therefore, heart needs O 2 . When more oxygen is needed e.g. exercise, O 2 can be increased to heart only by increasing blood flow. 28

24. Blood flow to Heart during Systole & Diastole During systole when heart muscle contracts it compresses the coronary arteries therefore blood flow is less to the left ventricle during systole and more during diastole. Blood flows to the subendocardial portion of Left ventricle ,which occurs only during diastole 29

25. Phasic changes in coronary blood flow Effect of cardiac muscle contraction 30

26. Coronary blood flow to the right side is not much affected during systole. Reason ---Pressure difference between aorta and right ventricle is greater during systole than during diastole, therefore more blood flow to right ventricle occurs during systole. 31

27. Effect of pressure gradient of aorta &diff chambers of heart pressure (mm hg) in Pressure diffrential (mmhg) Between aorta & Aorta Left ventricle Rt ventricle Lt ventricle Rt ventricle Systole 120 121 25 -1 95 diastole 80 80 80 As in systole pressure in left ventricle is slightly higher than in aorta blood flow reduces. On the other hand press diff in aorta & rt ventricle & aorta & rt atrium is more during systole than diastole, coronary bld flow is not appreciably reduce during systole. 32

28. CORONARY BLOOD FLOW DURING SYSTOLE AND DIASTOLE 33

29. As we know during systole blood flow to subendocardial surface of left ventricle is almost not there, therefore, this region is prone to ischemic damage and most common site of Myocardial infarction. 34

30. Effect of Tachycardia on coronary blood flow: During increased heart rate, period of diastole is shorter therefore coronary blood flow is reduced to heart during tachycardia. 35

31. REGULATION OF CORONARY BLOOD FLOW RESTING CBF = 225 mL /min = 5% of total cardiac output Peak CBF – early diastole ( after isovolumic relaxation) According to Poiseuille Hegan formula – Blood flow (Q) = ∆P∏r4/8Lᶯ where ∆P = coronary perfusion pressure r = radius , L = length of vessel ᶯ = fluid viscosity

32. Factors Affecting Blood Flow to CORONARY ARTERIES -Pressure in aorta -Chemical factors -Neural factors - Autoregulation . 37

33. causes of decreased blood flow to left ventricle 1- Aortic stenosis Reason ---As left ventricle pressure is very high during systole, therefore, it compresses the coronary arteries more. 2-When diastolic pressure in aorta is low, coronary blood flow is decreased 38

34. Chemical factors affecting Coronary blood flow Chemical factors causing Coronary vasodilatation (Increased coronary blood flow) -Lack of oxygen -Increased local concentration of Co 2 -Increased local concentration of H + ion -Increased local concentration of k + ion -Increased local concentration of Lactate, Prostaglandin, Adenosine. NOTE – Adenosine, is formed from ATP during cardiac metabolic activity, causes coronary vasodilatation. 39

35. Neural factors affecting Coronary Blood Flow -Effect of Sympathetic stimulation -Effect of Parasympathetic stimulation Sympathetic stimulation Coronary arteries have Alpha Adrenergic receptors which mediate vasoconstriction Beta Adrenergic receptors which mediate vasodilatation 40

36. Indirect effect of sympathetic stimulation Stimulation of sympathetic nerves release of nor adrenaline Increase of H.R &force of contraction Release of vasodilator metabolites vasodilatation 41

37. Direct effect of sympathetic stimulation When the ionotropic & chronotropic effect of noradrenergic discharge are blocked by Beta adrenergic receptor blocking drugs, stimulation of noradrenergic nerves elicits coronary vasoconstriction. Thus direct effect of noradrenergic stimulation is Vaso -constriction . 42

38. Benefits of indirect effect of noradrenergic discharge When systemic B.P decreases very low reflex increase of noradrenergic discharge Increase c.b.f sec to metabolic changes in myocardium In this way circulation of heart is preserved while flow to other organs compromised 43

39. Effect of Parasympathetic stimulation - Vagus nerve stimulation (Parasympathetic) causes coronary vasodilatation . 44

40. EFFECT OF ANAESTHESIA ON MYOCARDIAL OXYGEN CONSUMPTION AND CORONARY CIRCULATION

41. EFFECT ON MYOCARDIAL OXYGEN CONSUMPTION AND CORONARY CIRCULATION General anaesthesia – intubation/ extubation intravenous agents inhalational agents opioids neuromuscular blockers Regional/local anaesthesia Positioning I V Fluids

42. EFFECT OF INTUBATION/LARYNGOSCOPY Noxious stimulus – hypertension and tachycardia occurs Response proportional to – - force - duration of laryngoscopy Increase in B.P starts in 5 sec peaks in 1-2 mins settles in 5 mins Can result in myocardial ischaemia

43. EFFECT OF INTUBATION/ LARYNGOSCOPY contd. Ways to reduce this response : Increase the depth of anaesthesia Narcotics ( like fentanyl ) Aerosol application of topical anaesthetic agents Labetalol / esmolol Direct arterial B.P monitoring in high risk patients

44. EFFECT OF EXTUBATION Increase in B.P , HR Increase myocardial oxygen consumption (MVo2) Narcotics , beta adrenergic agents , Ca channel blockers - protective

45. I.V AGENTS AGENT HR PRELOAD CONTRACTILITY MVo2 CBF PROPOFOL - ↓ ? ↓ ↓ BARBITURATES ↑ ↓ ↓ ↑ ↑ KETAMINE ↑ - - ↑ ↑ ETOMIDATE - - - - ↑ DEXMEDITOMIDINE ↓ - ↓ ↓ ↑

46. INHALATIONAL AGENTS AGENT HR CONTRACTILITY SVR MVo2 CBF HALOTHANE -/↓ ↓ ↓ ↓ ENFLURANE ↑ ↓ ↓ ↓ ↑ ISOFLURANE ↑ MINIMAL ↓ ↓ ↑ SEVOFLURANE - ↓ ↓ ↓ ↑ DESFLURANE ↑ ↓ ↓ ↓ ↑ N2O ↓ ↓ ↑

47. OPIOIDS OPIOIDS HR/BP CONTRACTILITY SVR MORPHINE ↑/↓ SAME MEPERIDINE ↑/↓ ↓ FENTANYL AND ANALOGUES ↓/↓ SAME ↓

48. NMBs NMBS HR CONTRACTILITY Sch ↓ ( vagal ) Pancuronium ↑ ↑ pipecurium No significant effect vecuronium ↓( vagal ) rocuronium ↑ Atracurium Cis atracurium ↑ (histamine release) - mivacurium ↑ (histamine release)

49. LOCAL ANAESTHETICS Decrease in action potential duration and relative refractory period Dose dependent negative inotropic effect (Ca influx and release from SR affected) ↓contractility α conduction blocking potency Bupivacaine > lidocaine CV Toxicity – slowing of conduction in myocardium, peripheral vasodilatation

50. NEURAXIAL BLOCKS- TECHNIQUES Spinal/epidural/caudal ↓ in HR and B.P Sympathectomy that accompanies the technique depends on height of block HR – Block of cardio accelerator fibres B.P – Vasodilatation ( veno > arteriolar)

51. EFFECT OF POSITIONING Supine - ↑ in venous return ↑ in preload , ↑ SV , ↑ C.O Reflex baroreceptor activation → compensatory decrease in HR/SV/CO Trendelenberg position - ↑ venous return→ baroreceptor reflex response→ vasodilatation and bradycardia . Lithotomy - ↑ preload Prone - ↓ preload ( venous return impeded)

52. INTRA OPERATIVE I.V FLUIDS Effect of anaesthesia – venodilatation and cardiac depression . Goal of fluid therapy – sustained adequate oxygen delivery in relation to oxygen consumption Fluids administered to expand blood volume (as a compensation for venodilatation )→ increase preload → increase stroke volume

53. LAPAROSCOPIC SURGERY EFFECT OF PNEUMOPERITONIUM ↓ C.O ( α to IAP) – due to decreased venous return ↑SVR,PVR (↑ arterial pressures) – mediated by mechanical and neurohumoral factors Deleterious in cardiac disease patients ↓ in venous return and C.O can be prevented by- Fluid loading Head down before peritoneal insufflation Intermittent sequential pneumatic compression devices

54. REFERENCES Wylie and Churchill-Davidson’s A Practice Of Anesthesia; 7 th edition Miller’s Anesthesia; Ronald D.Miller . 7 th edition Pharmacology and Physiology in Anesthesia Practice; Robert K.Stoelting , Simon C.Hillier . 4 th edition Kaplan’s Cardiac Anesthesia; 5 th edition Morgan’s anaesthesia;5 th edition Grays anatomy for students; 2 nd edition

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