4. Right coronary artery supply
• Right atrium
• Greater part of RV except area near ant. inter ventricular
groove
• Small part of LV near posterior inter ventricular groove
• Posterior part of inter ventricular septum
• Whole of conducting system of heart except a part of
left branch of AV bundle
5. Left coronary artery supply
• Left atrium
• Greater part of LV except area near post. inter ventricular
groove
• Small part of RV near anterior inter ventricular groove
• A part of left branch of the AV bundle
14. Phasic flow
• Intramural vessels are compressed in Iso Volumet. Contract.
• Aortic pressure will be very low during IVC
• So, no flow during IVC
• Variable flow during rest of systole
• Maximal flow occurs in diastole as vessels dilate→ 80%
15. Left coronary artery
• LV pressure is high, sharp fall in flow in IVC phase
• During rapid ejection phase→ aortic pressure rises → flow
increases rapidly
• During reduced ejection phase →aortic pressure falls →
flow decreases
• During diastole, maximum flow , remains high and falls
gradually
16. Right coronary artery
• Similar phasic changes occur
• RV systolic pressure is low : 25 mm Hg
• Reduction in flow during IVC
• Flow increases first and declines later in systole
• Flow increases during diastole
17.
18. Subendocardial region
• Pressure in sub-endocardial region higher than outer portions
of heart muscle during systole
• Sub-endocardial region of LV receives blood flow only
during diastole
• More prone for ischemia Physiological
basis
19. Other regions
• Pressure differential between aorta & RV, and also
between aorta & atria, are more during systole
• So coronary flow in those parts of the heart is not
appreciably reduced during systole
20. Heart rate and CBF
• Tachycardia reduces diastole
• Blood flow reduced especially to LV
21. • Blood flow to left ventricle is decreased in AS patients
• Pressure in left ventricle must be much higher than
that in aorta to eject the blood
• So coronary vessels are severely compressed during
systole
Aortic stenosis
22. • Patients with AS are particularly prone to develop symptoms
of myocardial ischemia because of
– Compression of coronary vessels
– Myocardium requires more O2 to work more to expel blood
through stenotic aortic valve
Aortic stenosis
23. What we will discuss today…
• Functional Anatomy
• Special features of CBF
• Measurement of CBF
• Regulation of CBF
• Insufficient CBF
24. What we will discuss today…
• Functional Anatomy
• Special features of CBF
• Measurement of CBF
• Regulation of CBF
• Insufficient CBF
26. Measurement of coronary blood flow
• Using Fick’s principle
– Kety’s method
• Using radioactive substances (Thallium-201 / 201Tl)
– Radioactivity detected with radiation detectors over the chest
– Used to study regional blood flow in heart
– To detect areas of ischemia and infarct
– To evaluate ventricular function
27. What we will discuss today…
• Functional Anatomy
• Special features of CBF
• Measurement of CBF
• Regulation of CBF
• Insufficient CBF
28. What we will discuss today…
• Functional Anatomy
• Special features of CBF
• Measurement of CBF
• Regulation of CBF
• Insufficient CBF
30. Autoregulation
• Local muscle metabolism is primary controller of coronary flow
• By local arteriolar vasodilation in response to nutritional needs of
cardiac muscle
• Whenever vigor of cardiac contraction is increased, the rate of
coronary blood flow also increases and vice versa
• It is regulated almost exactly in proportion to the need of the
cardiac musculature for oxygen
31. • At rest, heart extracts 70–80% of the O2 from each unit of blood
delivered to it
• So O2 consumption can only be increased significantly by
increasing blood flow
• Hypoxia in heart causes vasodilator substances to be released
from the muscle cells like adenosine
32. Chemical factors
• The products of metabolism cause coronary vasodilation
• Lack of O2
• Increased local concentrations of CO2, H+, K+, lactate,
prostaglandins, adenine nucleotides and adenosine
33. Reactive hyperemia
• If coronary artery is briefly occluded → release of obstruction
→ increase in blood flow
• Release of adenosine by hypoxia
34. Neural factors
• Coronary arterioles contain
– α-adrenergic receptors – mediate vasoconstriction
– β-adrenergic receptors – mediate vasodilation
• Direct effect of noradrenergic stimulation is constriction
• But activity in noradrenergic nerves to heart → coronary
vasodilation
35. • Norepinephrine increases the heart rate and the force of
contraction
• Vasodilation is due to production of vasodilator metabolites
in the myocardium secondary to the increase in its activity
• When BP falls, overall effect of reflex increase in noradrenergic
discharge is increased coronary blood flow
36. • Simultaneously cutaneous, renal, and splanchnic vessels are
constricted
• In this way circulation of the heart is preserved when flow to
other organs is compromised
• Direct effect of stimulation of vagal fibers to heart is coronary
vasodilation
37. What we will discuss today…
• Functional Anatomy
• Special features of CBF
• Measurement of CBF
• Regulation of CBF
• Insufficient CBF
38. What we will discuss today…
• Functional Anatomy
• Special features of CBF
• Measurement of CBF
• Regulation of CBF
• Insufficient CBF
40. Myocardial ischemia
• Commonest cause : atherosclerosis → reduced blood flow &
reduced O2
• Mild : symptomless
• Severe : angina pectoris & MI
41. Angina pectoris
• Periodic attacks of chest pain during muscular effort
• Severe and short duration
• Retrosternal region, referred to shoulder
• Coronary artery narrowing
42. Prinzmetal’s angina
• Refers to reversible myocardial ischemia that results from
coronary artery spasm
• During an episode of vasospasm, the patient develops ST
segment elevation in the affected territory
43. Role of Collateral Circulation in Heart
• Anastomoses exist among the smaller arteries sized 20 to 250
micrometers in diameter
• Damage to heart muscle is determined mainly by the degree
of collateral circulation
– that has already developed or
– that can open within minutes after the occlusion
44. Role of Collateral Circulation in Heart
• These developing collateral channels help in almost complete
recovery, when area of muscle involved is not too great
• Regular aerobic exercise promotes formation of collaterals
45. Myocardial infarction
• Rupture of an atheromatous plaque
• Coronary thrombosis → occlusion→ necrosis →death of
tissue
• Fibrosis and scar formation
49. Intensive coronary care unit
• Sedation : opioid analgesics
• Complete rest to prevent “coronary steal” syndrome
• If heart becomes excessively active, vessels of normal
musculature become greatly dilated
• This allows most of blood to flow through normal muscle
tissue
• So blood flow through collateral channels into ischemic area
decreases and ischemia worsens
50. • Nitrates like nitroglycerine
• Vasodilator used in the treatment of angina
• Acts by releasing NO
55. Role of low dose aspirin
• Aspirin inhibits thromboxane A2
• Inhibits platelet aggregation
• Useful in preventing MI
56. Role of beta blockers
• Block sympathetic beta-adrenergic receptors
• So prevents sympathetic enhancement of heart rate &
cardiac metabolism during exercise or emotional episodes
• Helps in reducing the number of anginal attacks, as well as
their severity
