Page 85 - Small Animal Internal Medicine, 6th Edition

CHAPTER 3 Management of Heart Failure 57

Cellular signaling and biochemical abnormalities,
Heart disease local NH activation, and cytokine release
VetBooks.ir Cardiac remodeling Progressive cardiac dysfunction

ONSET OF HF

↓ Cardiac output
↓ Blood pressure Signals to
and baroreceptor unloading brain

↑ Adrenergic nerve traffic
↓ Renal perfusion and circulating NE

↑ Heart rate,
contractility, and
↑ Renin remodeling
secretion
↑ Adrenal
EPI release
↑ Endothelin
production
↑ AT I ↑ Vasopressin/
ACE ADH release
Constriction of
efferent arterioles
↑ Cardiac remodeling
↑ AT II

↑ Filtration
fraction ↑ Aldosterone
↑ Thirst
↓ Baroreceptor
sensitivity
Vasoconstriction

↑ H O resorption
2

↑ Na resorption

↑ Venous pressure

↑ Preload ↑ Afterload and
edema and effusions blood redistribution

FIG 3.1
Important neurohormonal mechanisms leading to volume retention and increased afterload
in congestive heart failure (CHF). Note: Additional mechanisms and interactions also
contribute. Endogenous vasodilatory and natriuretic mechanisms also become activated
during the evolution of CHF. ACE, Angiotensin-converting enzyme; ADH, antidiuretic
hormone (vasopressin); AT, angiotensin; EPI, epinephrine; HF, heart failure; NE,
norepinephrine.

catecholamines by blocking NE reuptake. Aldosterone recep- Arginine vasopressin (ADH) is released from the poste-
tors also are found in the heart and vasculature; aldosterone rior pituitary gland. This hormone directly causes vasocon-
produced locally in the cardiovascular system mediates striction and promotes free water reabsorption in the distal
inflammation and fibrosis. Chronic exposure contributes to nephrons. Although increased plasma osmolality or reduced
pathologic remodeling and myocardial fibrosis. blood volume are the normal stimuli for ADH release,