physiology of coronary circulation.

1. DR JAYANT MAKWANA
PROFESSOR & HEAD
DEPARTMENT OF PHYSIOLOGY,
RDGMC

2. WHILE CIRCULATORY SYSTEM IS PROVIDING
O2 & NOURISHMENT TO EVERY CELL OF
THE BODY
‘LETS NOT FORGET THE HEART WHICH
WORKS 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 TREE
IS DIVIDED INTO 3 SEGMENTS;
A) TWO (LEFT ANTERIOR DESCENDING
ARTERY & CIRCUMFLEX ARTERY)
ARISE FROM A COMMON STEM (LCA).
B) THE THIRD SEGMENT IS THE RIGHT
CORONARY 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 ARE
DIAGONALS- Ant LV WALL
SEPTAL PERFORATORS -
Ant 2/3 IVS
TERMINAL BR – APEX

10. CIRCUMFLEX ARTERY (LCX)
TERMINATES
- NEAR OBTUSE MARGIN
OF THE LV
- TO THE CRUX OF THE
HEART (PDA)
- SUPPLIES - LATERAL AND POSTERIOR WALL OF
LV THROUGH ITS OBTUSE MARGINAL BRANCH.

11. RIGHT CORONARY ARTERY –
ORIGIN- RIGHT ANTERIOR AORTIC SINUS
NEAR THE CRUX RCA
BIFURCATES INTO
- RIGHT MARGINAL (ACUTE
MARGINAL) - Lat. & Ant. RV
- POSTERIOR DESCENDING
ARTERY(PDA) Post. 1/3 IVS, Post LV

14. CAPILLARY DENSITY
- In Human Heart > 3000/mm2.
At Birth - 1 Cap./ 4 Fibres
Adult - 1 Cap / Fibre
Vent. ˃ Atria
- BETTER DIFFUSION
*Smaller Diameter Of Cardiac Muscle Fibres (<20 mm)
*Smaller Diffusion Distance (8μ)

15. PATTERN OF DISTRIBUTN (Coronary Dominance)
• CRUX OF THE VENTRICLE
• THE ARTERY WHICH SUPPLY AV NODE

16. RIGHT DOMINANCE;
• SEEN IN 50% - 70%
• PDA FROM RCA
• SUPPLIES RV,
POST. PART OF IVS
& GREATER PART OF
POST. WALL OF LV
• EXTREME RIGHT DOMINANCE

17. LEFT DOMINANCE
• SEEN IN 10% - 20%
• PDA FROM LCA
• SUPPLIES LV, ENTIRE IVS & PART OF RV

18. • 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

19. 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

20. 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

21. ANASTOMOTIC CHANNELS;
• BETWEEN CORONARY ARTERIES &
EXTRACARDIAC ARTERIES
• INTERCORONARY ANASTOMOSIS
*IN NORMAL HEART THERE ARE NO
COMMUNICATIONS BETn LARGE
CORONARIES.
* ANASTOMOSES DO EXIST AMONG THE SMALLER
ARTERIES SIZED 20 TO 250 μm.

22. THERE ARE THREE AREAS OF ANASTOMOSES.
i) BETWEEN BRANCHES OF
LAD & PIV OF RCA
IN IV GROOVE
ii) BETWEEN LCX & RCA
IN AV GROOVE.
iii) SEPTAL BRANCHES OF
TWO CORONARY ARTERIES
IN THE IVS.

23. ANASTOMOSIS BETWN LCA & RCA
DOES IT HELP?

24. LIFESAVING VALUE OF COLLATERALS IN
HEART
OCCLUSION IN ONE OF THE LARGER CORONARY
WITHIN SECONDS
DILATATn OF SMALL ANASTOMOSES( BLOOD FLOW < ½)
NEXT 8-24 HRS NO DILATATN
INCREASE IN COLLATERAL FLOW (2ND/3RD DAY)
NORMAL OR ALMOST NORMAL CORONARY (WITHIN 1
MONTH).

25. 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

26. MEASUREMENT;
• OBJECTIVES;
TO FIND OUT
1. DETERMINANTS OF CORONARY FLOW
2. OXYGEN UPTAKE BY MYOCARDIUM
3. RELATION OF FLOW WITH WORK OF HEART
IN STATE OF NORMALCY, SED/ SED STRESS
4. CARDIAC ABNORMALITY
26

27. 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-99m
Stannous 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

28. NORMAL CORONARY FLOW
• 5 % OF CARDIAC OUTPUT
• 200 - 250 ml / min ( 0.7 TO 0.8 ml/gm/min)
• TIME - 5 – 8 seconds
28

29. FACTORS INFUENCING CORONARY BLOOD
FLOW;
1. PHYSICAL FACTORS
2. CARDIAC METABOLISM
3. NEURAL FACTORS
4. NEUROHORMONAL FACTORS
29

30. 1. PHYSICAL FACTORS;
A) CARDIAC CYCLE & MYOCARDIAL
PRESSURE
B) AORTIC PRESSURE
C) CORONARY VASCULAR RESISTANCE
D) HEART RATE
E) RIGHT ATRIAL PRESSURE
30

31. A. CARDIAC CYCLE & MYOCARDIAL PRESSURE
( THE PHASIC VARIATION)
- CORONARY BLOOD FLOW NOT ONLY VARIES IN
TIME DURING THE CARDIAC CYCLE, IT ALSO
VARIES WITH DEPTH IN THE WALL OF THE HEART

33. UNDER NORMAL CONDITION SUBENDOCARDIUM
RECEIVES SLIGHTLY HIGHER BLOOD FLOW THAN
EPICARDIUM (1.1:1)
LCA BLOOD FLOW DURING SYSTOLE IS 15 - 16%
OF DIASTOLE
33

34. Unmasking of the restricting effect of ventricular
systole on mean coronary blood flow by induction of
ventricular fibrillation during constant pressure
perfusion of the LCA

35. B) AORTIC PRESSURE
- PARADOXICAL CORONARY FLOW
- PROFILE OF BLOOD FLOW THROUGH THE
CORONARIES DEPEND ON BOTH
* THE PERFUSION PRESSURE IN AORTA
&
* THE EXTRAVASCULAR COMPRESSION

37. Pressure in Aorta and Left and Right Ventricles
in Systole and Diastole.
Press (mm Hg) in Press Diff (Hg)
Between Aorta &
AORTA LV RV LV RV
SYSTOLE 120 121 25 -1 95
DIASTOLE 80 0 0 80 80

39. C) CORONARY RESISTANCE:
P1- P2 P1- P2
Q = ------------ R = -------------
R Q
- WHEN AORTIC & LV PRESSURE IS HELD
CONSTANT CORONARY VASCULAR RESISTANCE
VARIES DIRECTLY WITH CORONARY PERFUSION
PRESSURE.

40. AUTOREGULATION
• HEART IS A STRONG AUTOREGULATOR OF
BLOOD FLOW AND MAINTAINS NORMAL FLOW
OVER A PERFUSION PRESSURE RANGE OF
• 60 -150 mm Hg.

41. Pressure-flow relationships in the coronary vascular bed. At constant aortic
pressure, cardiac output, and heart rate, coronary artery perfusion pressure
was abruptly increased or decreased from the control level.

42. - THE LOW-PRESSURE LIMIT FOR AUTOREGULATION
IN THE ENDOCARDIAL LAYER IS GREATER THAN IN
THE EPICARDIAL LAYER.
- ENDOCARDIAL ARTERIAL DILATION REACHES A
MAXIMUM WHEN ARTERIAL PRESSURE DROPS TO
~70 mm Hg, WHEREAS MAXIMUM DILATION IN THE
EPICARDIAL ARTERIES IS NOT REACHED UNTIL
PRESSURE IS ~40 mm Hg.

43. 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.

44. DURATION HEART RATE
65/min 75/min 200/min
CARDIAC CYCLE 0.89 0.80 0.30
SYSTOLE 0.27 0.27 0.16
DIASTOLE 0.62 0.53 0.14

45. 2. METABOLIC FACTORS
• MOST IMPORTANT
• LINEAR RELATION BETWN METABOLISM & CBF
• ALL OF THE HEART'S CAPILLARIES RECEIVE
BLOOD FLOW, EVEN AT NORMAL HEART RATE & CO.
• RESTING STATE - 70-80% OF O2 IS EXTRACTED
FROM EACH UNIT OF BLOOD DELIVERED.
• A V O2 DIFFERENCE - 12-15 ml%
- MAXIMUM IN BODY

46. Organ Mass Flow (ml / Total O2 USE Total O2
(kg) 100g / Flow (mL/100g USE
min) (mL/min) /min) (mL/min)
Heart 0.4 – 0.5
Rest 60-80 250 7-9 25-40
Exercise 200-300 1K-1.2K 25-40 65-85
Muscle 28
Rest 2-6 750-1K 0.2-0.4 60
Exercise 40-100 15K-20K 8-15 2400

47. HOW DOES HEART INCREASE ITS OWN
BLOOD FLOW
VASODILATION
OXYGEN LACK
MYOGENIC

48. VASODILATORS
• ADENOSINE, ADENINE NUCLEOTIDE
ADENOSINE FROM CARDIAC MYOCYTES
TO VASCULAR SMOOTH MUSCLE CELLS
ACTIVATES PURINOCEPTORS (A1 & A2A )
INCREASE cAMP
DECREASE ICF Ca++ VASODILATION

49. - ADENOSINE LOSS & CELLULAR HEALTH
ADENOSINE LOSS IS ONE OF THE MAJOR CAUSES
OF CARDIAC CELLULAR DEATH DURING
MYOCARDIAL ISCHEMIA.
- AFTER THE ISCHEMIA OF 30 Min OR MORE,
RELIEF OF THE ISCHEMIA MAY BE TOO LATE TO
SAVE THE LIVES OF THE CARDIAC CELLS.

50. ADENOSINE THE PRIME/ONLY VASODILATOR?
- BLOCKADE OF ACTIONS OF ADENOSINE FAILS TO PREVENT
CORONARY VASODILATN WHEN CARDIAC WORK IS
INCREASED / BLOOD FLOW IS SUPPRESSED / THE ARTERIAL
BLOOD IS DEPLETED OF OXYGEN.
- STUDIES IN SKELETAL MUSCLE HAVE SHOWN THAT
CONTINUED INFUSION OF ADENOSINE MAINTAINS
VASCULAR DILATION FOR ONLY 1 TO 3 HOURS, & YET
MUSCLE ACTIVITY STILL DILATES THE LOCAL BLOOD
VESSELS EVEN WHEN THE ADENOSINE CAN NO LONGER
DILATE THEM.

51. THE OTHER VASODILATOR
• K, NO, H, CO2, LACTATE, BRADYKININ, PGI2,
PGE2, CYANIDE

52. • K+
INTRACORONARY INFUSION OF KCl
ELEVATION OF CORONARY ARTERIAL PLASMA K+
FROM 4.23 TO 12.10 meq / L
INCREASES IN CBF AVERAGING (17.7%)
THE CHANGES IN CBF PRODUCED BY KCl INFUSION DOES
NOT PARALLEL THE CHANGES IN PLASMA K+
CONCENTRATION.

53. 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 The
Myocardium.
? K+ Release From Active Myocardium Is Responsible
For Adjustment In Coronary Resistance Which
Accompanies Changes In Metabolic Activity Of The
Myocardium.

54. •NITRIC OXIDE
• Nitric Oxide Causes Dilatation Of Epicardial
Coronary Arteries.
• Formation Of NO - By NOs
- Flow Dependent No Formation
- Receptor Stimulated No Formation

56. HOW DOES Nitric Oxide ACT
increases ICF activates k+ chan. increases ICF cGMP
cGMP
protein kinase
inhibition of K+ efflux activation of
Ca+ + entry
dec. ICF Ca+ + hyperpolarization MLC phosphatase
smooth muscle relaxation

57. • INHIBITION OF Nitric Oxide Synthesis
Results In Very Little Change In Coronary
Blood Flow.

58. • CORONARY FLOW RESERVE –
- It is the maximum increase in blood flow through
the Coronary Arteries above the normal resting
value.
- 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”

59. Effect of reducing LAD radius on
maximal distal blood flows. A 60%
reduction in LAD radius ( 40% of
maximum radius) decreases distal
flow capacity by more than 25%

60. • O2 LACK HYPOTHESIS
• MYOGENIC MECHANISMS

61. 3. NEUROHORMONAL FACTORS;
VASODILATOR – Ach, TH
VASOCONSTRICTOR - NE & E, VASOPRESSIN,
ANGIOTENSIN-II, PGH2 ,ERGONOVINE

62. 4. NEURAL FACTORS – ROLE OF ANS
- SYMPATHETIC
α1, β2, ? β1
- Effect;
* CORONARY VASODILATION
* MARKED INCREASE IN CBF
- ROLE OF α-ADRENERGIC RECEPTORS DURING
EXERCISE
DIRECT EFFECT –
VASOCONSTRICTION & REDUCED BLOOD FLOW

63. PARASYMPATHETIC
DIRECT-
VASODILATATION
INDIRECT –
VASOCONSTRICTION

64. - CHARACTERISTICS OF THE CORONARY
CIRCULATION
1) It is very short and very rapid.
2) The blood flow in this circulation occurs
mainly during cardiac diastole
3) 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

65. 6) Its regulation is mainly by metabolites and not
neural
7) 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 more
likely to cause mitral regurgitation.

66. THANK YOU…
HAPPY VALENTINE DAY
TAKE CARE
OF YOUR
CORONARIES

69. THE PAPILLARY MUSCLES OF LV
- THE ANTEROLATERAL PAPILLARY MUSCLE MORE
FREQUENTLY 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 MUSCLE
ARE SIGNIFICANTLY MORE SUSCEPTIBLE TO ISCHEMIA.
Myocardial infarction
CLINICAL SIGNIFICANCE;
involving the PDA is more likely to
cause mitral regurgitation.

70. 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

71. 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

72. LATEST :
CORELATION BETWEEN
ATHEROSCLEROSIS &
Lp(a), HOMOCYSTEINE, ANTIBODY TO CHLAMYDIA PNEMONAE

73. 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

74. 4. ECHOCARDIOGRAPHY & DOPPLER
ULTRASOUND
5. CARDIAC MRI
6. ELECTRON BEAM COMPUTED TOPOGRAPHY (
EBCT) - TO SEE Ca DEPOSITS IN CORONARY
VESSEL WALL
7. CARDIAC NUCLEAR MEDICINE STUDY
74

75. 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 STYLE
3) Vit B12, Folate
75

76. SURGICAL :
1. ANGIOPLASTY - BALLOON,
BALLOON WITH STENT, DRUG
ELUTING STENT
2. BYPASS
76

77. 77