Page 236 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

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left ventricular pressure (P LV ) is required (La- Myocardial remodelling. Remodelling of the
place’s law; → A). Forward HF with diminished myocardium occurs right at the beginning of
contractility develops (→ A2). An analogous HF (NYHA stage I) through mechanical and
situation exists regarding the right ventricle neurohormonal stimuli. This will decisively in-
in pulmonary hypertension. Compensatory hy- fluence the progression of HF. Causes of the re-
pertrophy will also develop when there is an modelling are: 1) increased wall tension (→ A)
increased pressure load, but it will be “concen- that, among other effects, raises cytosolic Ca 2+
tric” (→ A4), because in this case the ventric- concentration, and 2) systemic (catechol-
ular volume is not enlarged and may in some amines, ADH, angiotensin II; insulin in type II
circumstances actually be decreased. How- diabetes) and local growth signals (endothelin,
ever, even in concentric hypertrophy the end- TGF, platelet-derived growth factor [PDGF], fi-
diastolic volume will be reduced and thus also broblast GF [FGF]), and decrease in growth in-
the stroke volume (backward HF; → A3; see hibitors (NO and PGI 2 ). The myocardial cells
become enlarged (hypertrophy), but refractori-
also A5, orange arrows). When there is a high
Heart and Circulation low), and unfavorable capillary blood supply Ca -ATPase activity falls.
pressure load, myocardial remodeling (see be-
ness to catecholamines develops (down-regula-
tion of β 1 -adrenoreceptors, a rise in the antag-
onistic G i proteins, receptor decoupling), and
(relative coronary ischemia), a “critical heart
2+
weight” of ca. 500 g may be attained, at which
As a consequence, the myocardial action
the myocardial structure gives way, causing
decompensation.
potential is prolonged (due to decreased repo-
Neurohumoral consequences of HF. Next to
less negative. This can result in arrhythmias
(reentry, afterpotentials, ectopic pacemakers;
number of compensatory mechanisms that are
7 mechanical cardiac effects (→ A), HF induces a larization currents) and the resting potential is
primarily directed at restoring cardiac output → p.186ff.); in some circumstances even
and blood pressure (→ B) again. Most impor- ventricular fibrillation. (The latter occurs in
tant in this is an increased sympathetic tone to- about 50% of patients in HF, causing their sud-
gether with greater release of norepinephrine den cardiac death). Overall there will be weak
and epinephrine. Activation of cardiac β-adre- contractility (among other factors, due to part-
noreceptors will result in: ly functional decoupling between the dihydro-
! Heart rate being increased (the symptom pyridine and the ryanodine receptors;
being tachycardia); and → p.182) as well as reduced relaxation capacity
! Contractility being raised (positive ino- of the myocardium (cytosolic Ca 2+ concentra-
tropy), and thus the cardiac output slightly in- tion increased in diastole). Fibroblast activa-
creased. tion (FGF and others) is involved in this and re-
α 1 -adrenergic vasoconstriction will pro- sults in an increased deposition of collagen in
duce: the ventricular wall and fibrosis of myocar-
! Reduction in blood flow through skeletal dium and blood vesels.
muscle (the symptom being fatigue), skin (the The systemic consequences and symptoms
symptom being pallor), and kidneys, with the of chronic HF are mainly caused by water and
result that the decreased cardiac output is dis- salt retention (→ B, bottom). In left HF the pul-
tributed preferentially to the arteries supply- monary capillary pressure is increased. This
ing the heart and brain (centralization); can cause dyspnea and tachypnea via the J-re-
! Reduction in renal perfusion, now leading to ceptors in the lung and can lead to pulmonary
activation of the renin–angiotensin–aldoste- edema (cardiac asthma) with systemic hypoxia
rone system, to an increased filtration fraction, and hypercapnia. In right HF peripheral edemas
and to increased release of ADH; will occur (especially in the lower leg during
! All these mechanisms produce a rise in wa- the day; at night there is excretion of water
ter and salt absorption. Angiotensin II and ADH with nocturnal diuresis).
also have a vasoconstrictor effect.
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Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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