Page 226 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Coronary Circulation
The myocardial blood supply comes from the demand of the heart at maximal physical
two coronary arteries that arise from the aortic work (→ p. 219 A, normal).
root (→ B,D). Usually the right coronary artery 3. Q ˙ cor is closely linked to myocardial O 2 de-
supplies most of the right ventricle, the left mand. The myocardium works aerobically, i.e.,
one most of the left ventricle. The contribution there must be a rapid and close link between
of the two arteries to the supply of the inter- the momentary energy demand and Q ˙ cor . Sev-
ventricular septum and the posterior wall of eral factors are involved in this autoregulation:
the left ventricle varies. ! Metabolic factors. First of all, O 2 acts as a va-
Coronary blood flow, Q ˙ cor , has a few special soconstrictor, i.e., O 2 deficiency dilates the cor-
features: onary arteries. AMP, a metabolic breakdown
1. Phasic flow. Q ˙ cor changes markedly during product of ATP, cannot be sufficiently regener-
ated to ATP during hypoxia, and thus the con-
the cardiac cycle (→ A), especially due to the
Heart and Circulation areas close to the endocardial regions of the adenosine rises in the myocardium. Adenosine
centration of AMP and its breakdown product
high tissue pressure during systole that, in
acts as a vasodilator on the vascular muscula-
left ventricle, reaches ca. 120 mmHg (→ B).
While the main epicardial branches of the cor-
ture via A 2 receptors (cAMP increase). Finally,
+
the accumulation of lactate and H ions (both
onary arteries and the flow in the subepicar-
of them products of the anaerobic myocardial
dial regions are largely unaffected by this
left ventricle are “squeezed” during systole,
din I 2 will locally cause vasodilation.
because during this phase the extravascular
! Endothelium-mediated factors. ATP (e.g.,
7 (→ B), vessels near the endocardium of the metabolism; → p. 219 C) as well as prostaglan-
pressure (≈ left ventricular pressure) surpasses from thrombocytes), ADP, bradykinin, hista-
the pressure in the lumen of the coronary ar- mine, and acetylcholine are vasodilators. They
teries. Blood supply to the left ventricle is act indirectly by releasing nitric oxide (NO) that
therefore largely limited to the diastole (→ A). secondarily diffuses into the vascular muscle
Conversely, the high systolic tissue pressure cells, where it increases guanylylcyclase activ-
presses the blood out of the coronary sinus ity, and thus intracellularly raises the concen-
and other veins, so that most of it flows into tration of cyclic guanosine monophosphate
the right occurs during systole. (cGMP). Finally, cGMP activates protein kinase
2. Adaptation to O 2 demand is achieved G, which relaxes the vascular musculature.
largely by changes in vascular resistance. O 2 de- ! Neurohumoral factors. Epinephrine and nor-
mand of an organ can be calculated from the epinephrine, circulating and released from the
blood flow through it, Q ˙ , multiplied by the ar- sympathetic nerve fiber endings, respectively,
teriovenous O 2 concentration difference (C a – act as vasoconstrictors on the α 1 -adrenorecep-
C v ) O 2 . If O 2 demand rises, for example, through tors that prevail in epicardial vessels, and as va-
physical activity or hypertension (→ C, right sodilators at β-adrenoceptors that predomi-
and p. 218), both variables may in principle be nate in subendocardial vessels.
and thus oxygen ex- If O 2 supply can no longer keep in step with
increased, but (C a – C v ) O 2
) ≈ 60%) is very oxygen demand, for example, at a high heart
traction (= 100 · [(C a – C v )/C a ] O 2
rate with a long systole, or in atherosclerotic
high even at rest. During physical work, O 2
supply to the myocardium, and thus cardiac obstruction of the coronary arteries, coronary
work, can essentially only be increased by an isufficiency (hypoxia) results (→ C,D and
increase in Q ˙ cor (= aortic pressure P Ao /coronary p. 218ff.).
resistance R cor ). If P Ao remains unchanged, R cor
must be reduced (vasodilation; → C, left),
which is normally possible down to ca. 20–
25% of the resting value (coronary reserve). In
this way Q ˙ cor can be increased up to four to
216 five times the resting value, i.e., it will be able
to meet the ca. four to fivefold increase in O 2
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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