Page 223 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003

Myocardial Oxygen Supply Arteriosclerosis (atherosclerosis) of the coronary
arteries leads to luminal narrowing and a resultant
Coronary arteries. The blood flow to the myo- decrease in poststenotic pressure. Dilatation of the
cardium is supplied by the two coronary arteries that distal vessels then occurs as an autoregulatory re-
arise from the aortic root. The right coronary artery sponse (see below). Depending on the extent of the
(approx. 1/7th of the blood) usually supplies the stenosis, it may be necessary to use a fraction of the
greater portion of the right ventricle, while the left coronary reserve, even during rest. As a result, lower
coronary artery (6/7th of the blood) supplies the left or insufficient quantities of O 2 will be available to
ventricle (! A). The contribution of both arteries to satisfy increased O 2 demand, and coronary insuffi-
blood flow in the septum and posterior wall of the ciency may occur (! D)
left ventricle varies. Myocardial O 2 demand increases with cardiac
. output (increased pressure–volume–work/time),
Coronary blood flow (Q cor) is phasic, i.e., the i.e., in response to increases in heart rate and/or con-
amount of blood in the coronary arteries fluc- tractility, e.g., during physical exercise (! D, right).
It also increases as a function of mural tension (T ventr)
tuates during the cardiac cycle due to ex-
Cardiovascular System sure during systole (! B, C). The blood flow in Since T ventr = P ventr · r ventr/2w (Laplace’s law ! Eq. 8.4b,
times the duration of systole (tension–time index).
tremely high rises in extravascular tissue pres-
p. 188), O 2 demand is greater when the ventricular
the epicardial coronary artery branches and
pressure (P ventr) is high and the stroke volume small
subepicardial vessels remains largely unaf-
than when P ventr is low and the stroke volume high,
these
by
pressure
fected
fluctuations.
even when the same amount of work (P ! V) is per-
However, the subendocardial vessels of the left
formed. In the first case, the efficiency of the heart
ventricle are compressed during systole when
vated, e.g., in hypertension, the myocardium there-
the extravascular pressure in that region (!
fore requires more O 2 to perform the same amount
8 pressure in left ventricle, P LV) exceeds the pres- is reduced. When the ventricular pressure P ventr is ele-
of work (! D, right).
sure in the lumen of the vessels (! C). Con-
sequently, the left ventricle is mainly supplied Since the myocardial metabolism is aerobic, an
during diastole (! B middle). The fluctuations increased O 2 demand quickly has to lead to va-
in right ventricular blood flow are much less sodilatation. The following factors are involved
distinct because right ventricular pressure in the coronary vasodilatation:
(P RV) is lower (! B, C). . ! Metabolic factors: (a) oxygen deficiency since O 2
Myocardial O 2 consumption (VO 2) is defined acts as a vasoconstrictor; (b) Adenosine; oxygen defi-
.
as Q cor times the arteriovenous O 2 concen- ciencies result in insufficient quantities of AMP being
tration difference, (C a–C v)O 2. The myocardial re-converted to ATP, leading to accumulation of ade-
nosine, a degradation product of AMP. This leads to
(C a–C v)O 2 is relatively high (0.12 L/L blood), and A 2 receptor-mediated vasodilatation; (c) Accumula-
oxygen extraction at rest ([C a–C v]O 2/CaO 2 = 0.12/ tion of lactate and H ions (from the anaerobic myo-
+
0.21) is almost 60% and, thus, not able to rise cardial metabolism); (d) prostaglandin I 2.
.
much further. Therefore, an increase in Q cor is ! Endothelial factors: ATP (e.g., from platelets),
practically the only way to increase myocardial bradykinin, histamine and acetylcholine are vasodila-
.
VO 2 when the O 2 demand rises (! D, right tors. They liberate nitric oxide (NO) from the en-
side). dothelium, which diffuses into vascular muscle cells
Adaptation of the myocardial O 2 supply ac- to stimulate vasodilatation (! p. 279 E).
! Neurohumoral factors: Norepinephrine released
cording to need is therefore primarily achieved from sympathetic nerve endings and adrenal epi-
by adjusting vascular resistance (! D, left side). nephrine have a vasodilatory effect on the distal
The (distal) coronary vessel resistance can nor- coronary vessels via ! 2 adrenoceptors.
mally be reduced to about /4 the resting value Myocardial energy sources. The myocardium can
1
(coronary reserve). The coronary blood flow use the available glucose, free fatty acids, lactate and
.
Q cor (approx. 250 mL/min at rest) can therefore other molecules for ATP production. The oxidation of
be increased as much as 4–5 fold. In other each of these three energy substrates consumes a
certain fraction of myocardial O 2 (O 2 extraction
words, approx. 4 to 5 times more O 2 can be coefficient); accordingly, each contributes approx.
supplied during maximum physical exertion. one-third of the produced ATP at rest. The myo-
cardium consumes increasing quantities of lactate
210 from the skeletal muscles during physical exercise
(! A, ! p. 72 and 282).
Despopoulos, Color Atlas of Physiology © 2003 Thieme
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