Page 230 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

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thus myocardial O 2 demand are raised. Should elevation or depression (depending on the
this continue over a long period, the ven- lead) of the ST segment as well as flattening
tricular myocardium will hypertrophy (→ or reversal of the T wave (similar to that in
p. 224ff.). This reduces wall tension, at least F4). If the resting ECG of a patient with angina
for a while (compensation). Decompensation is normal, these ECG changes can be provoked
occurs when the heart weight has reached the by controlled (heart rate, blood pressure)
critical value of 500 g, at which time the ventri- physical exercise.
cle dilates (→ p. 224ff.). The radius of the Stimulation of the nociceptors (by kinins?,
ventricular cavity and thus wall tension in- serotonin?, adenosine?) will lead not only to
creases, so that O 2 demand now suddenly rises – anginal pain (see above), but also to
to very high values. – generalized activation of the sympathetic
Consequences and symptoms of myocardial nervous system with tachycardia, sweating,
ischemia. The myocardium covers its energy Therapeutic attempts at restoring an even O 2
and nausea.
requirement by metabolizing free fatty acids,
Heart and Circulation for the O 2 -dependent formation of ATP (→ C, are: 2+
balance (→ p. 217 C) in patients with angina
glucose, and lactate. These substrates are used
! Lowering myocardial O 2 consumption (β-
normal). When blood supply is interrupted
adrenergic blockers; organic nitrates that re-
(ischemia), this aerobic energy gain stagnates,
duce the preload [and to some extent also the
so that ATP can only be formed nonaerobically.
Lactatic acid is now produced, dissociating
afterload] by generalized vasodilation; Ca
! Increasing the O 2 supply (organic nitrate
stances not only is lactate not used up, it is ac-
2+
and Ca
tually produced (→ C, early “ischemic anoxia”).
channel blockers that both function
7 into H + ions and lactate. In these circum- channel blockers), and
The ATP yield is thus quite meagre and, fur- to counteract spasm and to dilate coronary
+
thermore, the H ions accumulate because of vessels). In addition, the size and position of
the interrupted blood flow, both events being the atherosclerotically stenosed coronary ar-
responsible for abnormal ventricular contrac- teries make it possible to dilate them by bal-
tion (reversible cell damage; → C). If the ische- loon angioplasty or vascular stents or by revas-
mia persists, glycolysis is also inhibited by tis- cularization with a surgically created aortocor-
sue acidosis, and irreversible cell damage oc- onary bypass.
curs (infarct; see below) with release of intra-
cellular enzymes into the blood (→ C, left).
ATP deficiency leads to: Myocardial Infarction
! Impairment of the systolic pumping action
of the ventricle (forward failure; → p. 224ff.) Causes. If the myocardial ischemia lasts for
as well as some time (even at rest [unstable angina]; see
! Decreased compliance of the myocardium above), tissue necrosis, i.e., myocardial infarc-
during diastole (backward failure; → tion (MI), occurs within about an hour. In 85%
p. 224ff.), so that the diastolic atrial and of cases this is due to acute thrombus forma-
ventricular pressures are raised. tion in the region of the atherosclerotic coro-
! Congestion in the pulmonary circulation nary stenosis.
(dyspnea and tachypnea). Just before ventric- This development is promoted by
ular systole the lowered compliance in dia- – turbulence, and
stole produces a fourth heart sound that origi- – atheroma rupture with collagen exposure.
nates from the increased atrial contraction Both events
(“atrial gallop”). If the papillary muscles are af- – activate thrombocytes (aggregation, adhe-
fected by the ischemia, this may result in sion, and vasoconstriction by release of
! Mitral regurgitation (→ p.196). thromboxan). Thrombosis is also encour-
! Finally, disorder of myocardial excitation aged through
caused by the ischemia (→ E) may precipitate – abnormal functions of the endothelium, thus
220 dangerous arrhythmias (ECG; → p.186ff.). Dur- its vasodilators (NO, prostacyclin) and an-
ing the ischemia period the ECG will show an tithrombotic substances are not present
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Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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