MODERATOR :- DR. ABRAHAM

Anatomy Of Coronary Circulation

AND

Factors Affecting It.

Myocardial Oxygen Supply & Demand.

Epicardial Vessel

Subepicardium

Subendocardium

Myocardium

Pericardium (Epicardium)

Coronary Vascular Resistance Epicardial conductance vessels

Only a small % of resistance normally

Stenotic lesions

Intramyocardial vessels (arterioles) Contribute most to total coronary vascular

resistance

Capillary Density in the Heart

CORONARY CIRCULATION

BLOOD SUPPLY OF THE HEART:

Arterial supply:

- The cardiac muscle is supplied by the first two branches of the aorta i.e. right & left coronary arteries.

- The coronary arteries branch freely to form a rich capillary network.

- There is about one capillary for each cardiac muscle fiber.

Coronary arteries are functional end arteries.

Anastomatic connections bet. the small branches of the two coronary arteries and bet. the coronary arterioles and extra cardiac arterioles.

These anatomizes are not sufficient to supply the cardiac muscle with blood if one of the coronary arteries is occluded.

Thus, occlusion of a large branch of the coronary artery e.g. by coronary thrombosis necrosis (=death) of the muscle supplied by that branch.

Venous Drainage:

Coronary venous drainage occurs through two systems:

1) Superficial system: It is formed of coronary sinus and anterior cardiac veins that open into the right atrium.

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.

CHARACTERISTICS OF THE

CORONARY CIRCULATION

1) It is very short and very rapid (so it is essential to the heart).

2) The blood flow in this circulation occurs mainly during cardiac diastole (75%)

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) Its regulation is mainly by metabolites and not neural

6) The capillary permeability is high (the cardiac lymph is rich in protein)

7) The coronary vessels are susceptible to degeneration and atherosclerosis.

CORONARY BLOOD FLOW

Under resting conditions coronary blood flow (CBF) in the human heart is about 250 ml/ minute (=5% of the cardiac output).

In severe muscular exercise, the work of the heart increased and the CBF may be increased up to 2 liters/ minute.

Coronary Inflow (arterial) occurs mainly during diastole, because during systole the coronary arteries are mechanically compressed by the contracting myocardium, i.e.

Systole of the heart coronary inflow

Diastole of the heart coronary inflow

Coronary Outflow (venous) occurs mainly during systolic due to compression of the coronary veins by the contracting myocardium. During diastole coronary outflow and veins are filled.

Normal diastolic blood pressure is important for coronary filling because filling of coronary arteries occurs mainly during ventricular diastolic.

Coronary Arterial System Right & Left

RIGHT CORONARY ARTERY

Arises from the ant. Coronary sinus of valsalva just above the ant. Cusp of aortic valve .

Passes bet. Pulmonay trunk & rt. Atrium.

Desends in the rt. Part of AV groove/sulcus.

In 80% continues as post. Inter-ventricular artery (PDA).

And anastamosis with ant. Inter-ventricular artery (br. Of LCA)

Branches:-

Before entering the AV groove gives SA nodal artery in 60%.

AV nodal branch in 90% (br. Of PDA)

Acute Marginal Branch – runs to the apex –ant. Wall of right ventricle

PDA gives of Septal branches– Post. 1/3 inter-ventricular septum

PDA gives off br. to post. Of right ventricle.

PDA gives off anastamotic br. with LCX & ant. Inter-ventricular A.

Brach to Post. Medial papillary muscle of left ventricle.

LEFT CORONARY ARTERY

Arises from the Post. Aortic sinus of valsalva.

Passes behind the Pulmonary trunk & left atrial appendage (1-2cm).

Divides in the space between Aorta & pulmonary artery into:-

1) Left ant. Inter-ventricular (LAD)

2) Circumflex Artery

LAD- Left Ant. Descending Artery :-----

Runs in Ant. Inter-Venticular Sulcus.

Turns sharply at the apex to anastomose with PDA.

Supplies apical portion of both ventricles.

Gives off Diagonal Braches – Left ventricular lateral wall.

Gives off a branch to Antero-lateral papillary muscle of R ventricle

Gives off Septal Branches–Ant. 2/3 inter-ventricular septum

( In 1%Left coronary artery is absent – both branches originate from the aorta via separate Ostia)

LCX- Circumflex Artery:----

Arises at right angle to LCA near the base of left atrial appendage.

Runs in the left part of AV groove around the left border of heart.

Ends on the post surface of heart by anastamosing with RCA.

In Av groove lies close to the annulus of mirtal valve.

Gives off Atrial circumfles artery – Left atrium.

Gives off Obtuse Marginal Br. At left border –Post surface LV

In less than 40% SA Nodal br. Arises from LCX.

VENOUS DRAINAGE OF HEART

- Veins follow the arteries but different names.

- 2/3 of venous return via Coronary sinus & Ant. Cardiac Vein.

- Remaining by small veins – Venae Cordae Minimae- directly into the cavity of heart.

Coronary Sinus

2.25 cm wide channel – continuation of Great Cardiac Vein

Runs L-R in the Post. Portion of coronary groove on the Post. Surface of heart.

Opening located bet. Right AV orifice & IVC.

Receives blood from ---

Great cardiac vein, Oblique vein, Post. Vein of left ventricle from the left side.

Middle & Small cardiac vein on the right side.

Great Cardiac Vein

Begins at the apex

Ascends in Ant.inter-ventricular groove along with LAD artery

Drains areas supplied by LCA

Receives tributaries –Left ventricular surface via Ant. Inter-ventricular Vein

Left marginal vein (follows marginal branch of the circumflex artery)

Left posterior vein

Middle & Small Cardiac Vein

Middle cardiac vein :- begins at apex – Ascends in the post. Inter-ventricular groove along with PDA.

Empties into the right side of coronary sinus.

Small Cardiac Vein :- is a continuation of right marginal vein.

Runs along the lower border of heart.

Empties into coronary sinus but may drain directly into right atrium.

Both drain areas supplied by Right Coronary Artery

Oblique vein –

Descends on the back of left atrium.

Opens into the left side of coronary sinus.

Remnant of left superior vena cava.

Anterior Cardiac Vein –

Crosses the ant. Inter-venticular groove over RCA.

Opens directly into right atrium.

Drains most of ant. Surface of heart.

Venae Cordae Minimae / "lesser" venous system

Thebesian veins drain blood from the capillary bed into the ventricular cavity.

Arterioluminal vessels drain blood directly from the arteries into ventricles without traversing capillary beds.

Venoluminal vessels form direct communications with the coronary veins, shunting blood from these vessels into the ventricular cavities.

(this coronary venous blood draining directly into LV contributes to fixed shunt & to dilution of oxygenated blood)

Factors Affecting Coronary Blood Flow

The amount of blood passing through the coronary vessels (CBF) is directly proportional to the work done by the heart

i.e.

cardiac work CBF

and

cardiac work CBF.

The following factors modify the CBF:

1) Nervous Factors:

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.

b) Stimulation of parasymp cardiac metabolism coronary vasoconst. CBF.

2) Chemical Factors:

a) Metabolic factors: cardiac metabolism O2 tension (local hypoxia), CO2, K+, lactic acid & adenosine in the cardiac muscle coronary vasodilatation CBF.

cardiac metabolites active hyperemia during cardiac activity = auto regulation of CBF.

O2 lack (hypoxia) is the most effective coronary vasodilator. It produces coronary vasodilatation through:

• Direct action on coronary blood vessels and • Release of chemical substances such as adenosine (from ATP) which is a potent coronary vasodilator.

b) Drugs: Nitrites, aminophylline, caffeine & Khellin are coronary vasodilator coronary vasodilatation CBF.

c) Hormones Thyroxin cardiac metabolism coronary vasodilator CBF.

Vasopressin (antidiuretic hormone) coronary vasoconst CBF.

3) Mechanical factors (=effect of cardiac cycle):

-Ventricular systole of the intra-myocardial pressure compression of the coronary vessels CBF mainly in the left coronary artery (due to stronger cont of the left vent.)

-CBF during ventricular diastole (maximal at the end of isometric relaxation).

4) Other Factors:

a) Heart Rate:

Excessive in the heart rate diastolic period coronary filling (as it occurs mainly during ventricular diastole) CBF.

b) Cardiac Output:

CBF is directly proportional to COP i.e.

COP CBF COP CBF

c) Blood Pressure:

CBF is directly proportional to aortic BP especially diastolic

diastolic pressure CBF

and

diastolic aortic pressure (as in aortic regurgitation) CBF

Determinants of coronary blood flow

- Coronary perfusion pressure

- Perfusion Time

- Vessel wall diameter

Coronary Perfusion Pressure

Pressure gradient that drives blood through the coronary circulation.

Coronary Perfusion Pressure =

Diastolic BP – LVEDP (or PCWP)

Perfusion Time

Increased heart rate ---

Decreases Diastole Time ---

Reduces Perfusion Time

Vessel wall diameterSubstances having DIRECT effect on coronary Vasculature…

Constriction Dilation

prostaglandin H2 prostacyclin (PGI2)

thromboxane A2 endothelium-derived relaxing factor (NO)

peptide endothelin protein C

Alpha-1 tissue-type plasminogen activator

Calcium channel blockers

ACE Inhibitors

Beta-2

H+, K+, Histamine

Adenosine

Factors affecting coronary vasomotor tone. α = alpha receptor, β = beta receptor, M = muscarinic receptor, AT = angiotensin receptor, ET = endothelin receptor, EDRF=endothelium

derived relaxant factor

Regulation of Coronary Blood Flow

Coronary Blood Flow

1) Metabolic control

2) Autoregulation

3) Endothelial control of coronary

vascular tone

4) Extravascular compressive forces

5) Neural control

Vascular Resistance

Coronary Blood Flow

Heart Rate

Contractility

Systolic Wall Tension

O2-Carrying Capacity

SUPPLY DEMAND

Diastolic Phase

Metabolic Control

Auto regulation

Extravascular Compressive

Forces

Neural Control

Endothelial Control

Regulation of Coronary Blood Flow

Metabolic Control

Coronary circulation is exquisitely sensitive to myocardial tissue oxygen tension

Increased oxygen demand results in a lower tissue oxygen tension. This causes vasodilation and increased blood flow via- Adenosine Nitric oxide Prostaglandins

K+ATP channels

Metabolic Control of Blood Flow

Lack of oxygen? Formation of vasodilators?

Combination of both??

Metarteriole

Precapillary Sphincter

Capillary

Relaxation of smooth muscle

Increased Blood Flow

Auto regulation Ability of a vascular network to maintain constant

blood flow over a range of arterial pressures.( 60–140 mm Hg)

Beyond this range flow becomes pressure- dependent

Autoregulation is an independent determinant of CBF

The set point at which CBF is maintained depends on MVO2

Coronary Perfusion Pressure

Flow

Auto regulation

Normal Autoregulation

Maximal Available Coronary Blood Flow

Autoregulation in Anemia or LVH

60 140

Endothelial Control of Coronary Vascular Tone

When Damage to Endothelium Occurs--

Damage to endothelial cells will lead to: Decreased Nitric Oxide and Prostacyclin

production Increased Endothelin production

This will lead to: Vasoconstriction Vasospasm Thrombosis

Neural Control

Coronary blood flow is controlled predominantly by local metabolic, autoregulatory, and endothelial factors

Neural control of the coronary circulation complements the above local effects

Neural Control

Sympathetic Control Alpha = constrict coronary vessels

Beta = dilate coronary vessels Beta1 in conduit arteries

Beta2 in resistance arterioles

Parasympathetic Control Acetylcholine

Vasodilation in healthy subjects

Vasoconstriction in patients with atherosclerosis

Extravascular Compressive Forces

The heart influences its blood supply by the squeezing effect of the contracting myocardium on the blood vessels coursing through the heart.

Extravascular Compressive Forces

Left Ventricle Early Systole > Initial Flow Reversal

Remainder of Systole > Flow follows aortic pressure curve, but at a much reduced pressure

Early Diastole > Abrupt pressure rise (80-90% of LV flow occurs in early diastole)

Remainder of Diastole > Pressure declines slowly as aortic pressure decreases

Extravascular Compressive Forces

Extravascular Compressive Forces

Right Ventricle Lower pressure generated by thin right

ventricle in systole.

No reversal of blood flow during early systole.

Systolic blood flow constitutes a much greater proportion of total blood flow.

Transmural Distribution of Myocardial Blood Flow Extravascular compressive forces are greater in the

subendocardium (inner) and least near the subepicardial layer (outer)

Under normal resting conditions this does not impair subendocardial blood flow as increased flow during diastole compensates

Subendocardial to subepicardial ratio: 1.25/1 Due to preferential dilatation of the subendocardial vessels secondary to increased wall stress and, therefore, increased MVO2 in the subendocardium

Transmural Distribution of Myocardial Blood Flow

The subendocardium is more susceptible to ischemia than the mid-myocardium or subepicardium.

Epicardial coronary stenoses are associated with reductions in the subendocardial to subepicardial flow ratio.

Coronary Flow Reserve Difference between baseline blood flow

and maximal flow Usually measured following pharmacologic

coronary vasodilation

In the absence of coronary artery disease, maximal flow is 4 – 5 times as great as at rest.

Coronary flow reserve decreases with increasing severity of coronary artery disease.

Myocardial Oxygen Supply

Determined by –

1) Coronary Perfusion Pressure.

2) Oxygen Carrying Capacity of Blood

3) Heart rate - diastolic time

4) Coronary artery diameter

Resting O2 Consumption of Various Organs

Liver 2.0 ml/100 g/min Kidneys 6.0 ml/100 g/min Brain 3.3 ml/100 g/min Skin 0.3 ml/100 g/min Skeletal muscle 0.2 ml/100 g/min Cardiac muscle 9.7 ml/100 g/min Whole body 0.4 ml/100 g/min

Myocardial Oxygen Supply Oxygen Content of Blood

O2 Content = (1.36 x Hb x % Saturation) + (pO2 x 0.003)

O2 delivered to myocardium = O2 content x coronary blood flow

Myocardial Oxygen Supply Oxygen Extraction

The heart extracts oxygen to a greater extent than any other organ

Coronary sinus pO2 value is normally in range of 20-22 mmHg (% sat = 32-38%)

Can only minimally increase O2 extraction

Increases in O2 demand must be met by increased coronary blood flow

Myocardial Oxygen Demand

Myocardial Oxygen Consumption Oxygen consumption is defined as the

volume of oxygen consumed per minute (usually expressed per 100 grams of tissue weight)

Myocardial Oxygen Demand is Related to Wall Stress

LaPlace’s Law

h

Pr

Wall Stress

P

r

Wall Stress

h

Factors Increasing Myocardial Oxygen Consumption

Increased Heart Rate

Increased Inotropy (Contractility)

Increased Afterload

Increased Preload Changes in preload affect myocardial oxygen

consumption less than do changes in the other factors

Oxygen Cost of Myocardial WorkPressure work is much more costly than

volume work for the heart Pressure work = increasing arterial pressure

at a constant cardiac output

Volume work = increasing cardiac output while maintaining a constant pressure

Volatile anaesthetics & coronary circulation

Volatile anesthetics cause direct coronary artery vasodilation in vitro.

myocardial oxygen consumption (MVO2 )--heart rate, preload, afterload, and inotropic state, cause coronary vasoconstriction in vivo via metabolic autoregulation

Direct and indirect actions ultimately determines the net effect.

Halothane produces coronary artery dilation in arteries larger than 2000 um.

Halothane – direct myocardial depression – dec.BPCoronary Blood flow dec. coz of low BPBut O2 demand also decreases so CPP maintained Isoflurane causes vasodilation of predominantly small (<900 um) canine epicardial coronary arteries.

Isoflurane, desflurane, and sevoflurane little cardiac depression.

Enflurane – same profile as Halothane.

Coronary Artery Steal

Absolute decrease in collateral dependent myocardial perfusion at the expense of an increase in blood flow to a normally perfused area of myocardium, as may follow the drug-induced vasodilation of coronary arterioles

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