Coronary circulation
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  • The left and right coronary arteries originate at the base of the aorta from openings called the coronary ostia located behind the aortic valve leaflets.

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  • 1. Coronary CirculationPhysiology Seminar18/04/2013©Dr. Anwar Siddiqui
  • 2. CORONARY CIRCULATION• CONSIST OF1) Arterial supply2) Venous drainage3) Lymphatic drainage
  • 3. ARTERIAL SUPPLY• The cardiac muscle is supplied bytwo coronary arteries the right andleft coronary arteries.• Both arteries arises from the sinusesbehind the cusps of the aortic valvesat the root of the aorta.
  • 4. RT. CORONARY ARTERY• Smaller than left coronaryartery.• Arises from anteriorcoronary sinus.
  • 5. COURSE:• Emerges from the surface of heartbetween pulmonary trunk and rightauricle.• Winds round the inferior border toreach the diaphragmatic surface toreach the posterior inter-ventriculargroove.• Terminates by anastomising with leftcoronary artery
  • 6. BRANCHES• Large Branches– marginal– Post-interventricular• Small branches:– Right atrial– Infundibular– Nodal – in 60% cases– Terminal
  • 7. Anterior schematic diagram of heart shows course of dominant rightcoronary artery and its tributaries. AV = atrioventricular, PDA =posterior descending artery, RCA = right coronary artery, RV = rightventricular, SA = sinoatrial
  • 8. AREAS OF DISTRIBUTION• Right atrium• Ventricles– Greater part of right ventricle, exceptthe area adjoining the anterior inter-ventricular groove.– A small part of the left ventricleadjoining the posteriorinterventricular groove.• Posterior part or the inter-ventricularseptum• Whole of the conducting system of theheart except a part of the left branch ofAV bundle. The SA node is supplied byleft coronary artery in 40% cases
  • 9. LEFT CORONARY ARTERY• Larger than the rightcoronary artery.• Arises from leftposterior aorticsinus.
  • 10. COURSE• Runs forward and to the left and emergesbetween the pulmonary trunk and the leftauricle.• Here the anterior inter-ventricular branch isgiven .• The further continuation of the left coronaryartery is sometimes called the circumflexartery.• After giving off the anterior interventricularbranch it runs into the left anterior coronarysulcus.• It winds around the left border and nearposterior interventriular groove it terminatesby anastomosing with the right coronaryartery.
  • 11. BRANCHES:• Large Branches:– Anterior interventricular– Branch to the diaphragmatic surface of theleft ventricle• Small Branches:― Left atrial― Pulmonary― Terminal
  • 12. Dominant left coronary artery anatomy. Left anterior oblique schematicdiagram of dominant left coronary artery anatomy, including leftanterior descending artery and left circumflex artery tributaries, isshown. AVGA = atrioventricular groove artery, PDA = posteriordescending artery.
  • 13. Areas of distribution• Left atrium• Ventricles:− Greater part of left ventricle, except thearea adjoing the posterior interventriculargroove.− A small part of right ventricle adjoining theanterior interventricular groove.• Anterior part of interventricular septum.• Part of left branch of AV bundle
  • 14. COLLATERAL CIRCULATION• Cardiac anatomosis: The two coronaryarteries anastomose in the myocardium.• Extra cardiac anastomosis: The coronaryarteries anastomose with the• Vasa vasorum of the aorta,• Vasa vasorum of pulmonary arteries,• Internal thoracic arteries• The bronchial arteries• Phrenic arteries.• These channels open up in the emergencieswhen the coronary arteries are blocked.
  • 15. CORONARY ARTERY DOMINANCE• The artery that gives the posteriorinterventricular artery determines the coronarydominance.• If the posterior interventricular artery is suppliedby the right coronary artery (RCA), then thecoronary circulation can be classified as "right-dominant".• If the posterior interventricular artery is suppliedby the circumflex artery (CX), a branch of the leftartery, then the coronary circulation can beclassified as "left-dominant".• If the posterior interventricular artery is suppliedby both the right coronary artery (RCA) and thecircumflex artery, then the coronary circulationcan be classified as "co-dominant".
  • 16. FUNCTIONAL DIVISION• Large coronary arteries(epicardial cortonaryarteries) - lies on epicardial surface,– conduct blood with little resistance.• Small coronary arteries – descends intomyocardium, are of two types:– subepicardial vessels and– subendocardial vessels.• Small coronary arteries are the principleresistance vessels of the heart, change intheir diameter regulate the coronary bloodflow
  • 17. VENOUS DRAINAGE OF THEHEART• The venous drainage ofthe heart is by threemeans:– Coronary sinus.– Anterior cardiac veins– Venae Cordis minimae.
  • 18. CORONARY SINUS• This is the largest of vein of heart situated inthe left posterior coronary sulcus. It is about3 cm long and ends by opening into theposterior wall of the right atrium.• Its tributaries are:−Great cardiac vein: It enters the left endof the coronary sinus.−Middle cardiac vein: It accompanies theposterior interventricular artery andjoins the right end of the coronary sinus.−Small cardiac vein: It accompanies theright coronary artery and joins the rightend of the coronary sinus.
  • 19. − Posterior vein of left ventricle: It runs on thediaphragmatic surface of the left ventricle andends in the middle of the coronary sinus.− Oblique vein of left atrium ( of Marshall): It runson the posterior surface of the left atrium, joinsthe left end of coronary sinus and develops fromthe left common cardinal vein.− The right marginal vein: It accompanies themarginal branch of the right coronary artery.
  • 20. ANTERIOR CARDIAC VEIN3 to 4 small veins run on the anterior wall ofthe right ventricle, open directly into the rightatrium.VENAE CORDIS MINIMAE(also called smallest cardiac veins, venae cardiacae minimae, orThebesian veins)• Numerous small veins present in all 4chambers of heart which open directly into thecavities.• The Thebesian venous network is consideredan alternative (secondary) pathway of venousdrainage of the myocardium. It is named afterGerman anatomist Adam Christian Thebesius,who described them in a 1708 treatise calledDisputatio medica inauguralis de circulosanguinis in corde.
  • 21. Lymphatics of heart• Lymphatics of the heart accompanythe coronary arteries and form 2trunks.• Right trunk ends in brachiocephalicnodes and the left trunk into thetracheobronchial lymph nodes at thebifurcation of the trachea.
  • 22. PECULIARITIES OF COR.CIRCULATION• BF during diastole• End arteries• High capillary density• High 02 extraction• Regulation is mainly by metabolites• Anatomical anastomosis• The coronary vessels are susceptible to degenerationand atherosclerosis.• There is evident regional distribution: Thesubendocardial myocardial layer in the left ventriclereceives less blood, due to more myocardialcompression (but this is normally compensated duringdiastoles by V.D). However, this renders this area moreliable to ischemia and infarction
  • 23. CORONARY BLOOD FLOW(CBF):• The resting coronary blood flow isabout 225 ml/min., which is about0.7 – 0.8 ml/gm of heart muscle, or 4-5 % of the total cardiac output.• In severe muscular exercise, the workof the heart increased and the CBFmay be increased up to 2 liters/minute
  • 24. FACTORS REGULATINGCORONARY BL.FLOW• Physical• Chemical• Neural• Hormonal• Reflex
  • 25. PHYSICAL FACTORAortic blood pressure:• CBF is directly proportional to aorticblood pressure, especially the diastolicaortic pressure , most of CBF occurduring diastole.• When diastolic pressure decreases e.g.aortic incompetence or when MAP isdecreased e.g. shock or aortic stenosis,the CBF decreases.• Blood flow to the endocardial regions ismore severely impaired than is that tothe epicardial regions of the ventricle
  • 26. Heart Rate:• Excessive in the heart rate e.g.paroxysmal tachycardia diastolic periodcoronary filling (as it occurs mainly duringventricular diastole) CBF.Cardiac Output:• CBF is directly proportional to COP i.e. COP CBFCOP CBF• Increased cardiac output BP in aorta + reflexinhibition of the vagal vasoconstrictor tone (a nrepisreflex) coronary vasodilatation CBF.
  • 27. • C.B.F. occurs mainly during diastole dueto compression of coronary blood vesselsduring systole by the contracted musclefibers.During systolic phasesC.B.F. is less than that duringdiastole. With minimal bloodflow during iso volumetriccontraction phase. (due tocompression of coronary bloodvessels with low aortic pressure).During diastolic phasesC.B.F. is more than that duringsystole.With maximal blood flowduring iso volumetric relaxationphase. (due to dilated coronary bloodvessels with high aortic pressure).
  • 28. CHEMICAL FACTORS:Metabolic factors:cardiac metabolism O2tension (local hypoxia),CO2, K+, lactic acid & adenosine in the cardiacmuscle coronary vasodilatation CBF.O2 lack (hypoxia) is the most effective coronaryvasodilator. It produces coronary vasodilatationthrough:• Direct action on coronary blood vessels and• Release of chemical substances such as adenosine (fromATP) which is a potent coronary vasodilator.Drugs:• Nitrites, angised, aminophylline, caffeine &Khellin are coronary vasodilator coronaryvasodilatation CBF.
  • 29. NERVOUS FACTORS:Direct effect:• Parasympathetic: vagus has very slight distribution tocoronary, so its stimulation has slight dilator effect.• Sympathetic: Both alpha and Beta receptors exist in thecoronary vessels. Sympathetic stimulation causes slightdirect coronary constriction.Indirect effect:• Plays a far more important role in normal control ofcoronary blood flow than the direct. Sympatheticstimulation increase both heart rate and myocardialcontractility, as well as its rate of metabolism leading todilatation of coronary blood vessels. The blood flowincrease proportional to the metabolic need of heartmuscle
  • 30. HORMONAL FACTOR• Thyroxin cardiac metabolismcoronary vasodilator CBF.• Vasopressin (antidiuretic hormone)coronary vasoconst CBF.
  • 31. REFLEX CONTROL• Anrep’s reflex: Increased venous returncauses increased pressure in right atrium,leading to reflex increase in CBF e.g. duringmuscular exercise.• Gastro-coronary reflex: Distention of thestomach with heavy meal causes reflexvasoconstriction of coronary blood vesselsdecreasing CBF.
  • 32. Coronary Autoregulation• If there is sudden change in aortic pressure,coronary vascular resistance will adjustitself proportionally within few seconds; sothat a constant blood flow is maintained.• Range of autoregulation: 60 – 140 mmHg.Mechanism:• Myogenic response: an increase in passivestretch, caused by increased perfusionpressure, causes active smooth musclecontraction.
  • 33. • Chemical theory:• Decrease perfusion pressure leads toIncrease adenosine & Decreased oxygenwhich causes Vasodilatation andincrease CBF• Endothelium derived relaxation factor(EDRF):• Hypoxia, ADP, VIP, muscular exercise(increase distention force), stimulate vascularendothelium to secrete EDRF, which is apotent vasodilator, that causes coronarydilatation and increase CBF.
  • 34. Applied aspects
  • 35. CORONARY ARTERY DISEASEANGINA PECTORIS• Angina Pectoris means severe chest pain (usuallyretrosternal i.e. behind the sternum) due toischemia of the cardiac muscle.• Angina pectoris is usually due to narrowing of thecoronary arteries ischemia.• When the coronary artery is only partly obstructed(by spasm or atherosclerosis) and the coronaryblood flow is only moderately reduced, symptomsof ischemia appears only when cardiac work isincreased by effort, exercise, excitement, food orsevere cold, or anemia and relived by treatment.• Pain is due to accumulation of pain producingsubstances in the myocardium such as, P factor,lactic acid, histamine, K, and Kinins.
  • 36. • MYOCARDIAL INFARCTION• Myocardial Infarction means necrosis of a part of themyocardium due to− Severe & prolonged ischemia due to narrowing ofthe coronary arteries.− Occlusion of one of the coronary arteries or itsbranches by coronary thrombosis severeischemia.• Myocardial Infarction produces also chest painwhich is more severe than that of angina and itcannot be relieved by rest or coronary VD drugs.• It is usually complicated by fatal ventricularfibrillation.
  • 37. Coronary bypass operation
  • 38. Angioplasty
  • 39. A Presentation By DR ANWAR H SIDDIQUI, JR, Physiology