PPT CORONARY CIRCULATION BY DR QAZI IMTIAZ RASOOL

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DR QAZI IMTIAZ RASOOL H.O.D GOVERNMENT MEDICAL COLLEGE BLA KASHMIR INDIA

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CORONARY CIRCULATION BY DR QAZI IMTIAZ RASOOL

OBJECTIVES:

OBJECTIVES Describe the physiological anatomy of coronary circulation. Identify the values for normal coronary blood flow. Discuss control of coronary blood flow. Describe the physiological features of coronary circulation. Correlate knowledge to clinical conditions related to myocardial ischemia.  Guyton & Hall Textbook of Physiology - 12 th ed. Ch 21

Ischaemic heart disease world map DALY – WHO 2016:

Ischaemic heart disease world map DALY – WHO 2016 A) 1/3rd Of All Deaths World Wide, B) 2/3rd of which occur in the developing countries. C) 15% of deaths in India were due to heart diseases in 1990; now up to 28% . IMPORTANCE

Coronary Circulation.:

Coronary Circulation . Coronary , latin ” Coronarius = “Crown”. Def: Blood flow to heart through coronary arteries is called coronary circulation. Normal value : -250 mL/min at rest. - 70 ml / 100 gm / min. - May increase to 2000 ml / min.

PHYSIOLOGICAL -ANATOMY:

PHYSIOLOGICAL -ANATOMY . width of a drinking straw,1/8 inch (4mm) . Arises from the sinuses just superior to the aortic valve behind 3 cusps 1.R 2.L. 3 POT. NC

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Origin R anterior coronary sinus of Valsalva Courses through the R AV groove RIGHT CORONARY ARTERY Branches ;- 1 st Segment: Anterior Atrial Brs Artery to SA node Anterior Ventricular Brs Right Marginal Artery (ACUTE) 2 nd Segment Posterior Ventricular Brs Posterior Interventricular Brs Posterior Interventricular (descending) Artery Septal Brs AV nodal Artery

LEFT CORONARY ARTERY:

LEFT CORONARY ARTERY Length – 10-15mm Arises from left coronary cusps Almost immediately bifurcate into 1. left anterior descending 1. Diagonal Br.--- Most of Ant LV wall, A small part of RV 2.Septal perforating Br –ant 2/3 rd to IVS 3. AV bundle 4.Terminal Br.--- apex 2. Left circumflex artery . (Obtuse) Marginal br.

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VENOUS DRAINAGE 2 systems: 1) Superficial system: which drains LV. It is formed of coronary sinus and anterior cardiac veins that open into the RA. 2) deep system: which drains the rest of the heart. It is formed of thebasian veins and arterio -sinusoidal vessels that open directly into the heart chamber . 3 WAYS 1.Coronary sinus. 2. Anterior cardiac veins 3. T hebasian veins .

CORONARY ARTERY DOMINANCE:

CORONARY ARTERY DOMINANCE P osterior interventricular artery determines the coronary dominance . If right coronary artery (RCA), "right- dominant ". If by the circumflex artery (CX), " left-dominant ". If by both than "co-dominant " .

1. In Human Heart > 3000/mm 2 . At Birth - 1 Cap/ 4 Fibres 3. Adult - 1 Cap / Fibre 4. Vent. ˃ Atria 5. Better diffusion *Smaller Diameter Of Cardiac Muscle Fibres (<20 mm ) * Smaller Diffusion Distance (8 μ ):

1. In Human Heart > 3000/mm 2 . At Birth - 1 Cap/ 4 Fibres 3. Adult - 1 Cap / Fibre 4 . Vent . ˃ Atria 5. Better diffusion * Smaller Diameter Of Cardiac Muscle Fibres (<20 mm ) * Smaller Diffusion Distance (8 μ ) CAPILLARY DENSITY SKELETON MUSCLE CARDIAC MUSCLE

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Characteristic of coronary circulation Very short , rapid, and phasic . Blood flow mainly during cardiac diastole No efficient anastomoses between the coronary vessels. It is a rich circulation (5% of CO,as heart wt is 300gm) Regulation is mainly by metabolites and not Nervous Capillary permeability is high (the cardiac lymph is rich in protein)

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Vessels are susceptible to degeneration and atherosclerosis. Evident regional distribution ( subendocardial layer in LV receives < blood, due to compression (but normally compensated during diastoles by V.D). NOTE;- Hence more prone to IHD+MI. Eddy current keep the valves away from the orifices of arteries it keeps the orifices patent throughout the cardiac cycle. 10) As having highest O 2 uptake achieved by a dense network of capillaries, all is perfused at rest (no capillary reserve)

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ANASTOMOTIC CHANNELS; * No communications between large coronaries. * but exist in smaller arteries20 to 250 μ m. 3 Common areas of anastomoses. 1. Between branches of LAD & PIV OF RCA in IV groove 2. Between LCX & RCA IN AV groove. 3. Septal branches of 2 coronary arteries in the IVS . NOTE; - Lifesaving value of collaterals in heart :  Occlusion-- within sec; dilatation of small anastomoses( blood flow < ½) -normal or almost normal coronary (within 1 month).

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Transmural variations in coronary autoregulation and myocardial metabolism 1. Arteries run from epicardium into endocardium almost perpendicularly between myocardial cells . 2. Coronary arteries  are functionally  end arteries   referred to as potential anastomoses, which lack  function , as opposed to true anastomoses like that in the palm of the hand .

Pathophysiology of the coronary circulation:

Pathophysiology of the coronary circulation

CORONARY BLOOD FLOW :

CORONARY BLOOD FLOW RCA has > flow in 50-70% of individual. LCA > flow in 20% of individual. Equal distribution of flow in 30% of individual. At rest the heart extract 70-80% of O 2 from each unit of blood delivered to it. NOTE;- Therefore, the most crucial factors for perfusing coronary arteries are - aortic pressure / - duration of diastole

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BLOOD FLOW DURING SYSTOLE & DIASTOLE In systole as muscle contracts it compresses arteries flow is less -LV during systole and more during diastole. Subendocardial portion of LV, occurs only during diastole therefore, prone to IHD+MI. R side is not much affected during systole. Reason;- Pressure difference between aorta and RV is greater during systole than during diastole, therefore more blood flow to RV occurs during systole 18

Coronary reserve:

Coronary reserve

CORONARY BLOOD FLOW END ARTERIAL CIRCULATION:

CORONARY BLOOD FLOW END ARTERIAL CIRCULATION Why heart is extracting 60-70% of O 2 ? 40 % of cell is occupied by mitochondria When more O 2 is needed e.g. exercise, O 2 can be increased to heart only by increasing blood flow. NOTE;- low-pressure limit for autoregulation in the endocardial layer is > in the epicardial layer. – endocardial arterial dilation maximum when < ~70 mm hg , - epicardial arteries when < ~40 mm hg.

Factors infuencing CBF 1.Physical factors 2. Chemical Factors (Cardiac metabolism) 3. Neural factors 4. Neurohormonal factors 5. Reflexs:

Factors infuencing CBF 1.Physical factors 2. Chemical Factors ( Cardiac metabolism) 3. Neural factors 4. Neurohormonal factors 5. Reflexs NOTE —Blood flow shows considerable Autoregulation . A.PHYSICAL FACTORS a. Cardiac cycle & myocardial pressure ( the phasic variation) – CBF not only varies in time during C.C also varies with depth in the wall of the heart normally subendocardium receives slightly > blood flow than epicardium( 1.1 : 1 )  NOTE; - (LCA blood flow during systole is 15 - 16% of diastole)

  b. Aortic pressure paradoxical coronary flow depend on both perfusion pressure in aorta & extravascular compression c.Coronary vascular resistance d. Heart rate;-    diastolic period   coronary filling (as it occurs mainly during ventricular diastole)   CBF. e. Right atrial pressure (cardiac output)  CO BP in aorta + reflex inhibition of the vagal vasoconstrictor tone (anrepis reflex) coronary VD. :

  b. Aortic pressure paradoxical coronary flow depend on both perfusion pressure in aorta & extravascular compression c . Coronary vascular resistance d. Heart rate;-    diastolic period   coronary filling (as it occurs mainly during ventricular diastole)   CBF. e. Right atrial pressure (cardiac output)  CO BP in aorta + reflex inhibition of the vagal vasoconstrictor tone ( anrepis reflex) coronary VD.

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C.B.F. occurs mainly during diastole due to compression of coronary blood vessels during systole by the contracted muscle fibers. During systolic phases C.B.F. is less than that during diastole. With minimal blood flow during iso volumetric contraction phase. (due to compression of coronary blood vessels with low aortic pressure). During diastolic phases C.B.F. is more than that during systole.With maximal blood flow during iso volumetric relaxation phase. (due to dilated coronary blood vessels with high aortic pressure).

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2) CHEMICAL FACTORS ( PRIMARY CONTROLLER ) a) Metabolic factors --- VD 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 , Adenine nucleotides. NO NOTE – Adenosine, which is formed from ATP during cardiac metabolic activity, b ) Drugs : Nitrites,Aminophylline,Caffeine are VD   CBF.

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3. Nervous Factors: α (DOMANCE IN EPICARDIAL ) ᵦ Effect of ANS is indirect through their effect on cardiac metabolism a ) Stimulation of sympathetic   cardiac metabolism   VD   CBF α vasoconstriction ᵦ vasodilatation b ) Stimulation of parasymp   cardiac metasbolism  VC.   CBF. 4. Neurohormonal factors 1. Thyroxin   cardiac metabolism   coronary vasodilator   CBF. 2.Vasopressin (antidiuretic hormone)  coronary vasoconst   CBF.

5. REFLEXS:

5. REFLEX S Anrep’s reflex : sudden increase in  afterload   on the heart causes an increase in ventricular  inotropy . Gastro-coronary reflex : constrict with "functional cardiovascular symptoms" similar to chest-pain on the left side and radiation to the left shoulder, dyspnea, sweating, up to angina pectoris -like attacks with extrasystoles , drop of blood pressure, and tachycardia .

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Applied Aspect CORONARY ARTERY DISEASE 28

IHD:

IHD is caused by myocardial ischemia due to Imbalance between myocardial oxygen demand and supply from coronary arteries. Four types : Angina pectoris (Most common) Acute Myocardial infarction (AMI) Chronic IHD 4.Sudden cardiac death (SCD) Unexpected death within 1 hour due to cardiac causes In many patients SCD is the first clinical manifestation of IHD

Angina pectoris:

Angina pectoris Literally means chest pain Is intermittent chest pain caused by transient reversible myocardial ischemia. Ischemia insufficient to cause death of myocardium 3 Types: Stable angina Prinzmetal’s angina (Variant angina) occuring at rest due to coronary artery spasm. Stress ECG reveals ST elevation representing transmural ischemia 3. Unstable (crescendo) angina Frequent bouts of chest pain at rest or with minimal exertion. May progress to acute MI

Myocardial Response to Ischemia:

Myocardial Response to Ischemia Within seconds: Switch to Anaerobic glycolysis for ATP Less than 2 min : loss of contractility 1 - 10 min : Reversible injury 20-40 minutes : irreversible damage Reperfusion within 40 min. saves muscle. 31

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ECG --exercise test. :

ECG --exercise test. 33

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INVESTIGATIONS : ECG Cardiac enzymes e.g. CK, LDH, Troponin etc. Echocardiography Treadmill exercise test Thallium stress test Coronary angiography (CORONARY LUMINAL PLASTY) Before going for stent Coronary physiology FFR, iFR , IMR: 34

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TREATMENT : CORONARY DILATORS E.g. NITRATES BETA-BLOCKERS ANGIOPLASTY (DILATE AREA OF CONSTRICTION) STENT BYPASS SURGERY 35

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