Download Determinants of Myocardial oxygen demands (MVO2)

pathophysiology
Lecture 24
Determinants of Myocardial oxygen demands (MVO2):
a-HR(increase demands because of the increase of Number of
contractions per minute).
b-contractility (as it increases, MVO2 will increase)
c- Intramyocardial wall tension during systole (most important)we
can represent myocardial wall tension by(tension time index TTI)
which is measured by :measuring the area under the curve of the left
ventricular pressure curve.
 Intramyocardial wall tension during systole is determined by 3
parameters:
1)intraventricular pressure (IVP)
2)Radius of ventricle (R)
3)Thickness of the wall
those parameters are linked with Laplace law
Laplace lowintramyocardial wall tension=(Radius* IVP)/(Thickness*2)
It states that: Intramyocardial wall tension is directly related to the
product of intraventricular pressure multiplied by radius( R) and
inversely related to the thickness multiplied by factor 2 .
 If systemic pressure increasedIntraventricular pressure
increaseincrease ventricular dilationincrease radius of the
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ventriclesincrease intramyocardial wall tensionincrease
MVO2
 Hypertrophyincrease thickness of the ventricular
walldecrease intramyocardial wall tension-decrease MVO2
 Hypertrophy, as process; was initiated due to chronic increasing in
hemodynamic load (not acute increase in hemodynamic laod), it is
a reversible process, it will increase the thickness of myocardial
wall , and by this it will reduce the tension on the walls (because
the tension will spread on larger area on the wall) and by this it
will reduce the MVO2again;here we are talking about reversible
process for short period of time (and the attempt to decrease
hemodynamic load will be initiated at the same time. e.g; ANF)
BUT when we talk about hypertrophy as chronic process (for long
period of time)we need to understand that it will increase the
myocardial oxygen demand MVO2 and it will aggravate ischemia
as well)
Regulation of coronary blood flow (regulation of supply):
How heart is supplied? By epicardial vessels then to the intramyocardial
ones then capillaries then to the myocytes.
 Parameters control blood flow:
A) Arteriolar resistance (inversely related)---most important factor
B) Coronary driving pressure(directly related)
If pressure increasesfilling increasesblood flow into these
epicardial vessels increases as a result.
 Epicardial vesselson the surface of the heart (bigger ones)
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 Intramyocardial vesselsinside myocardium(smaller ones)
 Resistanceit will be determined by intramyocardial
vessels(smaller) .If I want to calculate total resistance in the
coronary artery ,we will sum the resistance due to epicardial R1
and intramyocardial R2 vessels : Rt=R1+R2 (in normal situation
R2< R1)
 In case of atherosclerosis, the most common sites are epicardial
vessels.
 In case of IHD (the most common cause of atherosclerotic lesions
in the epicardial vessels) it will result in shift of resistance to the
epicardial vessel rather than intramyocardial ones R1<R2
 The distribution of blood between epicardial and intramyocardial
vessels is normally kept 1:1 even when we do exercise, because of
“Auto regulation”
 Autoregulation: when intramyocardial vessels sense a drop in
blood flow, they will vasodilate ,at the same time when they
sense an increase in blood flow they will vasoconstrict to
maintain normal perfusion .(So when we do exercise what will
keep blood distribution 1:1 between epicardial and
intramyocardial vessels is autoregulation, these intramyocardial
vessels will vasodilate)
 In case we have atherosclerotic lesion in epicardial vessels it will
result in decrease blood flow in intramyocardial vessels , and this
will initiate autoregulation (vasodilate) and they keep on doing
that until reaching a state where this vasodilation is no longer
sufficient to prevent Ischemia(to maintain normal perfusion to
myocytes)
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 As we said, the most important factor is Resistanceincreasing
diameter of the atherosclerotic lesion  decrease in the diameter
of the lumenincrease the resistanceas a result blood flow will
decrease
Notes: 1)When autoregulation occurs, vasodilation of intamyocardial
vessels occur, but when this vasodilation is insufficient to keep
perfusion we have what we call Coronary reserve. At severe stenosis
(<70%) ,coronary blood flow will decrease dramatically and this result
in ischemia and symptoms even at rest.
2)Remember the important determinant for resistance is Diameter of
the vessel.
3)if obstruction in epicardial vessels is huge this is called coronary steal.
 The anatomy of vascular bed will affect:
A) Oxygen supply
B) Myocardial metabolism
C) Mechanical function .
 Other factors also affect coronary blood flow and function of the
collateral circulation:
1)length of the lesion
2)the influence of the pressure drop across an area of stenosis
The resistance to flow in a vessel is directly related to length of the
obstructing lesion but resistance is inversely related to the diameter of
the vessel to the fourth power(the most important)
This relationship can dramatically affect collateral blood flow and its
response to exercise , resulting in what has been called coronary steal.
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A similar situation may also occur when the epicardial or subepicardial
vessel “steal” blood flow from the endocardium in the presence of a
stenotic lesion.
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