1) Normal coronary blood flow is 60-80 ml/100 gm/min, with 80% occurring during diastole and 20% during systole to accommodate the heart's demand for blood when it is relaxed between contractions. 2) The heart has compensatory mechanisms for obtaining oxygen, including deeper capillary layers and higher myoglobin content in the deeper layers to facilitate diffusion during limited flow. 3) Coronary blood flow is regulated both locally, through mechanisms like autoregulation and metabolic factors, and neurogenically through the sympathetic and parasympathetic nervous systems. Increased demand is met by increased blood flow rather than solely by extracting more oxygen.

1. Coronary Blood Flow
 Normal resting CBF is 60-80ml/100 gm/min.
or 250ml/min.
 O2 consumption .
A – V O2 difference in myocardium is 19-6=13ml/dl
other parts of body 19-14=5ml/dl

2. Phasic Coronary Flow
 Phasic Coronary flow is 80% during diastole and 20%
during systole.
 All other parts of the body receives blood supply during
systole but heart receives blood supply during diastole.
Right coronary artery supplies right ventricle and atrium. Less
forceful contraction of right ventricle does not inhibit flow
from high pressure aorta.

3. systole

4. Sys. Sys.
Diast.
C
O
R
O
N
A
R
Y
F
L
O
w
NORMAL LEFT VENTRICULAR CORONARY FLOW IN SYSTOLE & DIASTOLE

5. L
Coronary
blood
flow
(ml/min)
Systole Diastole
0
100
200
300

6. Compensatory mechanism
DEEP MYOCARDIAL
(ENDO/SUBENDOCA
RDIAL) LAYER
SUPERFICIAL(EPICAR
DIAL) LAYER
CAPILLARY DENSITY 1100 capillaries/mm2 750 capillaries/mm2
DIFFUSION DISTANCE 16.5µm 20.5µm.
MYOGLOBIN
CONTENT
HIGHER LOWER
LACTATE PYRUVATE
RATIO
HIGHER LOWER

7. Regulation of Coronary Blood Flow
1. Local control mechanism
 Autoregulation
 Local metabolites
 Role of endothelial cells
 Coronary perfusion pressure
2.Nervous control mechanism.
 Sympathetic
 Parasympathetic
Myocardium extracts 70% o2 at rest , but during activities o2 demand
is compensated by increased CBF not by increased o2 extraction.

8.  Metabolic Theory
 CO2
H+
NO
Adenosine
Prostaglandins
K+
Bradykinin.
Myogenic Theory.
 Heart rate
Autoregulation
LOCAL CONTROL MECHANISMs

9. BERNE HYPOTHESIS
(ADENOSINE)
FALL IN ART.PO2 ↑MYOCARDIAL METABOLISM
ISCHEMIA/HYPOXIA
INTRACELLULAR
ADENOSINE
NUCLEOTIDE
ADENOSINE
CORONARY
VASODILATOR
↑ CORONARY BLOOD FLOW

10. coronary perfusion
pressure

11. HR-
75/min
HR-
200/min
%
CHANGE
DURATION OF
CARDIAC CYCLE
0.80 sec 0.30 sec 62.50
DURATION OF
SYSTOLE
0.27 sec 0.16 sec 40.70
DURATION OF
DIASTOLE
0.53 sec 0.14 sec 73.58
CORONARY BLOOD FLOW WILL BE MORE COMPROMISED AT
HIGHER HEART RATES DUE TO FALL IN DURATION OF DIASTOLE.
NEUROGENIC CONTROL OF CORONARY PERFUSION

12. Stimulation of Sympathetic
(Epinephrine & Norepinephrine)
 HR
 Cardiac metabolism
 Coronary vasodilatation
 CBF
Neural Regulation

13. SYMPATHETIC STIMULATION
METABOLIC
ADENOSINE,
H+, K+, PGE2, PGI2
ALPHA ACTIVITY
↑CONTRACTILITY-↑O2 DEMAND
VASOCONSTRICTION-↓O2 SUPPLY
BETA ACTIVITY
↑HEART RATE-↑O2 DEMAND
VASODILATATION-↑O2 SUPPLY
MVO2

14. Neural Regulation contd…
Stimulation of parasympathetic
 cardiac metabolism
coronary vasoconstriction
↓CBF
 HR

15. Factors affecting CBF
 Mean aortic pressure .
 Muscular exercise.
 Hypotension.
 Hormones
 Heart rate.
 Effect of ions.
 Temperature.

16. Rest
Exercise
O2 Supply O2 Demand
CAD
O2 Supply
O2 Demand
&
NORMAL

17. ↑OXYGEN DEMAND
CORONARY
BLOOD FLOW
↓DIASTOLIC
DURATION
EXCERCISE
SYMPATHETIC
STIMULATION
↑MYOCARDIAL
CONTACTILITY
HYPOXIA
↑HEART RATE
H+, K+, PGI2, PGE2
CORONARY
VASODILATATION
ATP→ADP→AMP→ADENOSINE
OXYGEN
SUPPLY

19. Measurement of CBF
1.Nitrous oxide method(kety method)
2.Radio nuclide utilization technique.
3.Coronary angiography
4.Electromagnetic flowmeter technique

20. CLINICAL ANALYSIS OF CBF
•ECG
•Stress ECG
•Ambulatory ECG (Holter monitor)
•Echocardiography.
• 2D
• Doppler
• Transoesophageal
•CT imaging
•MRI imaging
•Cardiac catheterization.
•Radionuclide imaging
•Myocardial perfusion imaging

21. Applied physiology
 Ischemic Heart Disease
 Atherosclerosis of coronary arteries
 Thrombus formation
 Embolus from other areas
 Spasm of coronary arteries

22.  Angina Pectoris means severe chest pain (usually
retrosternal i.e. behind the sternum) due to ischemia
of the cardiac muscle.
• The anginal pain may radiate to the left shoulder, left
arm or forearm (referred pain).
 Angina pectoris is usually due to narrowing of the
coronary arteries  ischemia.
 Anginal pain may be relieved by rest & coronary VD
drugs.
ANGINA PECTORIS

23. MYOCARDIAL INFARCTION
• Myocardial Infarction means necrosis of a part of
the myocardium due to
a) Severe & prolonged ischemia due to narrowing
of the coronary arteries.
b) Occlusion of one of the coronary arteries or its
branches by coronary thrombosis  severe
ischemia.
 Myocardial Infarction produces also chest pain
which is more severe than that of angina and it
cannot be relieved by rest or coronary VD drugs.
 It is frequently complicated by ventricular
fibrillation  death.

25. COMPLETE
OCCLUSION