CORONARY
CIRCULATION
BY DR QAZI IMTIAZ RASOOL
1.
2.
3.
Describe the physiological anatomy of coronary circulation.
Identify the values for normal coronary blood flow.
Discuss control of coronary blood flow.
4.
Describe the physiological features of coronary circulation.
5.
Correlate knowledge to clinical conditions related to
myocardial ischemia.
IMPORTANCE
A) 1/3 rd Of All Deaths World Wide,
B) 2/3 rd of which occur in the developing countries.
C) 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.
1.
represent the enlarged vasavasorum of larger
vessels in the heart.
2.
R about the width of a drinking straw,1/8 inch
(4mm) .
3.
4.
Coronary comes from the latin ”Coronarius=
“Crown”.
Arises from the sinuses just superior to the aortic
valve behind cusps
has 3 cusps –left coronary (LC),
-right coronary (RC)
-posterior non-coronary(NC) cusps.
CHARACTERISTICS OF CORONARY CIRCULATION
1) Very short , rapid, and
phasic .
2) Blood flow mainly during cardiac diastole
3) No efficient anastomoses between the coronary vessels.
4) It is a rich circulation (5% of the CO ,as heart wt is 300gm)
5) Regulation is mainly by metabolites and not neural
6) Capillary permeability is high (the cardiac lymph is rich in
protein)
7) Vessels are susceptible to degeneration and atherosclerosis.
8) 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.
8) Eddy current keep the valves away from the orifices of
arteries it keeps the orifices patent throughout the cardiac
cycle.
10) As having highest O2 uptake achieved by a dense network of
capillaries, all is perfused at rest (no capillary reserve)
1.
2.
3.
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 2/3rd to IVS
3.A part of the left br. Of the AV bundle
4.Terminal Br.---apex
2. Left circumflex artery.
RIGHT CORONARY ARTERY
Origin R anterior coronary sinus
of Valsalva
Courses through the R AV groove
Branches;-Arteria coni arteriosis
1st Segment:
1.
2.
3.
4.
Anterior Atrial Brs
Artery to SA node
Anterior Ventricular Brs
Right Marginal Artery
1.
2.
3.
4.
5.
Posterior Ventricular Brs
Posterior Interventricular Brs
Posterior Interventricular (descending) Artery
Septal Brs
AV nodal Artery
2nd Segment
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.
CAPILLARY DENSITY
ANASTOMOTIC CHANNELS;
Between coronary arteries & extracardiac arteries
intercoronary anastomosis
*IN NORMAL HEART THERE ARE NO COMMUNICATIONS BET n
LARGE CORONARIES. *
ANASTOMOSES DO EXIST AMONG THE SMALLER ARTERIES
SIZED 20 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 n of small anastomoses( blood flow < ½)
-normal or almost normal coronary (within 1 month).
1.
5% of CO = +/- 250ml / 60-80ml/100gm/min pass through
coronary artery/min.
2.
RCA has > flow in 50-70% of individual.
3.
LCA > flow in 20% of individual.
4.
Equal distribution of flow in 30% of individual.
5.
At rest the heart extract 70-80% of O2 from each unit of
blood delivered to it.
NOTA;- Therefore, the most crucial factors for perfusing
coronary arteries are - aortic pressure / - duration of diastole
Why heart is extracting 60-70% of O2?
1. Muscle has 40% of cell is occupied by mitochondria
2. When more O2 is needed e.g. exercise, O2 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 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.
BLOOD FLOW DURING SYSTOLE &
DIASTOLE
1.
In systole as muscle contracts it
compresses arteries therefore CBF is
less -LV during systole and more
during diastole.
2.
Subendocardial portion of LV, occurs
only during diastole therefore, prone
to IHD+MI.
3.
CBF to 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
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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 norma
subendocardium receives slightly > blood flow than epicardium(1.1:1)
NOTE;- (LCA blood flow during systole is 15 - 16% of diastole)
2) Chemical factors(PRIMARY CONTROLLER) affecting
Coronary blood flow
a)Metabolic factors causing Coronary vasodilatation  CBF
1. -Lack of oxygen
2.
3.
4.
5.
-Increased local concentration of Co2
-Increased local concentration of H+ ion
-Increased local concentration of k + ion
-Increased local concentration of Lactate, Prostaglandin, Adenosine,
Adenine nucleotides.
6. NO
NOTE – Adenosine, which is formed from ATP during cardiac
metabolic activity,
b) Drugs: Nitrites,Aminophylline,Caffeine & Khellin are coronary
vasodilator   CBF.
3. Nervous Factors:
-
α (DOMANCE IN EPICARDIAL )ᵦ
The effect of the autonomic nerves to the heart on the coronary arteries is
indirect through their effect on cardiac metabolism I.e
a) Stimulation of sympathetic   cardiac metabolism 
 coronary
vasodilatation   CBF.
-Alpha Adrenergic receptors which mediate vasoconstriction
Beta Adrenergic receptors which mediate vasodilatation
b) Stimulation of parasymp   cardiac metasbolism  coronary
vasoconst.   CBF.
4. Neurohormonal factors
1. Thyroxin   cardiac metabolism  
  CBF.
coronary vasodilator
2.Vasopressin (antidiuretic hormone)  coronary vasoconst   CBF.
Applied Aspect
CORONARY ARTERY DISEASE
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is caused by myocardial ischemia due to
Imbalance between myocardial oxygen demand and supply from
coronary arteries.
Four types of Ischemic Heart Diseases:
1. Angina pectoris (Most common)
2. Acute Myocardial infarction (AMI)
3. 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
1.
Literally means chest pain
2.
Is intermittent chest pain caused by transient reversible
myocardial ischemia.
3.
4.
Ischemia insufficient to cause death of myocardium
3 Types:
1. Stable angina
2. 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
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1.
Within seconds: Switch to Anaerobic glycolysis for ATP
2.
Less than 2 min: loss of contractility
3.
1 - 10 min: Reversible injury
4.
20-40 minutes: irreversible damage
5.
Reperfusion within 40 min. saves muscle.
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26
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1.
Investigations:
1. ECG
2. Cardiac enzymes e.g. CK, LDH, Troponin etc.
3. Echocardiography
4. Treadmill exercise test
5. Thallium stress test
6. Coronary angiography
7. Note:
1. ECG changes in IHD:
1. St depression occurs in ECG in respective leads
2. ECG changes in MI:
1. St elevation occurs in ECG in respective leads
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TREATMENT:
1. CORONARY DILATORS E.g. NITRATES
2. BETA-BLOCKERS
3. ANGIOPLASTY (DILATE AREA OF CONSTRICTION)
4. STENT
5. BYPASS SURGERY
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