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

1. 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 :-
1. Left Main or left coronary artery (LCA)
 Left anterior descending (LAD)
 diagonal branches (D1, D2)
 septal branches
 Left Circumflex (LCx)
 Marginal branches (M1,M2)
2. 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.

10. 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.

11. Branches of the left main coronary artery :
 Left anterior descending (LAD) artery (anterior
interventricular artery)
 Left circumflex artery (LCX)
 Ramus intermedius ( between the LAD and LCX )

13. 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.

15. 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.

16.  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%)

18. 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.

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

20. 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.

21. 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.
 It receives tributaries from the left atrium , from both
ventricles and large left marginal vein.

22. Venous drainage of heart

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

25. PHYSIOLOGY OF CORONARY
CIRCULATION

26. 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 .

27. 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 O2].
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28. CORONARY BLOOD FLOW
Why heart is extracting 60-70% of O2?
• 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 O2.
• When more oxygen is needed e.g. exercise, O2
can be increased to heart only by increasing
blood flow.
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29. 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
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30. Phasic changes in coronary blood flow
Effect of cardiac muscle contraction
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31.  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.
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32. 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 0 0 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.
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33.  CORONARY
BLOOD FLOW
DURING SYSTOLE
AND DIASTOLE
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34.  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.
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35.  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.
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36. 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

37.  Factors Affecting Blood Flow to CORONARY
ARTERIES
-Pressure in aorta
-Chemical factors
-Neural factors
-Autoregulation.
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38. • 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
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39. Chemical factors affecting Coronary blood flow
 Chemical factors causing Coronary vasodilatation
(Increased coronary blood flow)
 -Lack of oxygen
 -Increased local concentration of Co2
 -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.
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40. Neural factors affecting Coronary Blood Flow
1. -Effect of Sympathetic stimulation
2. -Effect of Parasympathetic stimulation
 Sympathetic stimulation
 Coronary arteries have
 Alpha Adrenergic receptors which mediate
vasoconstriction
 Beta Adrenergic receptors which mediate
vasodilatation
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41. 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
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42. 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.
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43. 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
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44.  Effect of Parasympathetic stimulation
 -Vagus nerve stimulation (Parasympathetic) causes
coronary vasodilatation.
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45. EFFECT OF ANAESTHESIA ON
MYOCARDIAL OXYGEN
CONSUMPTION AND
CORONARY CIRCULATION

46. 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

47. 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

48. 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

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

50. I.V AGENTS
AGENT HR PRELOA
D
CONTRACTILI
TY
MVo2 CBF
PROPOFOL - ↓ ? ↓ ↓
BARBITURATE
S
↑ ↓ ↓ ↑ ↑
KETAMINE ↑ - - ↑ ↑
ETOMIDATE - - - - ↑
DEXMEDITO
MIDINE
↓ - ↓ ↓ ↑

51. INHALATIONAL AGENTS
AGENT HR CONTRACTILI
TY
SVR MVo2 CBF
HALOTHAN
E
-/↓ ↓ ↓ ↓
ENFLURANE ↑ ↓ ↓ ↓ ↑
ISOFLURANE ↑ MINIMAL ↓ ↓ ↑
SEVOFLURA
NE
- ↓ ↓ ↓ ↑
DESFLURAN
E
↑ ↓ ↓ ↓ ↑
N2O ↓ ↓ ↑

52. OPIOIDS
OPIOIDS
HR/BP CONTRA
CTILITY
SVR
MORPHINE ↑/↓ SAME
MEPERIDINE ↑/↓ ↓
FENTANYL
AND
ANALOGUES
↓/↓ SAME ↓

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

54. 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

55. 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)

56. 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)

57. 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

58. 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

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

60. THANK YOU