Page 259 - Feline Cardiology

266 Section G: Congestive Heart Failure

arterial baroreceptor dysfunction, which increases heart
rate due to increased sympathetic tone and decreased erythrocytes or hemosiderin (i.e., heart failure cells)
parasympathetic tone. Tachycardia and increased after- throughout the lungs.
load (from alpha receptor mediated vasoconstriction) • Pulmonary hemorrhage and infarction are commonly
lead to increased myocardial oxygen consumption, seen in cats with left heart failure.
which worsens myocardial hypoxia and mechanical dys- • Gross abnormalities of right heart failure include passive
hepatic congestion, where the liver is heavy, firm, and
function. High concentrations of norepinephrine at the has swollen rounded margins of the lobes. Chronic
level of the myocardium also cause toxic changes to the passive hepatic congestion leads to appearance of a
cardiomyocytes, including apoptosis, myofibrillar deg- nutmeg liver, characterized by red congested centers of
radation, and increased collagen synthesis. Chronic cat- the liver lobes and periacinar necrosis, surrounded by
echolamine stimulation may also induce malignant pale, slightly raised periportal regions containing fatty
ventricular arrhythmias. hepatocytes.
Chronic activation of the renin-angiotensin-aldoste- • Antemortem arterial thromboemboli are common in cats
rone system promote volume overload (ADH, aldoste- dying of heart failure. Thromboemboli may be found in
rone, increased thirst), excess vasoconstriction (ATII the distal abdominal aorta, renal arteries, iliac arteries,
carotid arteries, left and right atria, and pulmonary and
and endothelin I), and adverse myocardial remodeling • Acute or chronic renal infarctions are commonly seen in
hepatic vessels.
including hypertrophy and fibrosis. Overall, the deleteri-
Congestive Heart Failure myocardial oxygen consumption, increased preload, and Pulmonary pathology of left-sided congestive
ous effects of increased afterload, tachycardia, increased
cats dying of heart failure.
adverse myocardial remodeling leads to a vicious circle
of progressive systolic and diastolic failure, where heart
failure begets heart failure. Pharmacologic inhibitors
target the neurohormonal systems responsible for the
chronic deterioration of cardiac function and include
beta blockers, ACE inhibitors, angiotensin II receptor heart failure
Hydrostatic pulmonary edema (i.e., left-sided conges-
blockers, aldosterone receptor blockers, endothelin I tive heart failure) is caused by elevated pulmonary
antagonists, and antidiuretic hormone antagonists. venous and capillary pressures secondary to many heart
This sequence describes uncontrolled progression of diseases. The initial stage of heart failure consists of a
cardiac disease, producing heart failure. It is worth compensatory increase in lymphatic flow, which removes
remembering that a majority of cats with heart disease excess interstitial fluid, and the interstitial volume is
remain asymptomatic and never reach this end normal (Stage 1). Once the lymphatic drainage capacity
point, but rather live normal lives (Rush et al. 2002; is exceeded, fluid and colloid accumulate in the intersti-
Atkins et al. 1992; Paige et al. 2009). This compensated tial areas surrounding bronchioles, arterioles, and
state may be due to reaching a plateau in the above- venules. Early interstitial fluid often accumulates in the
mentioned mechanisms, or to a very slow rate of disease perihilar region, which has “looser” regions of the pul-
progression. monary interstitium. Interstitial fluid cuffs develop
around small airways and vessels (Stage 2). As the lung
Pathology fluid increases, lung compliance decreases and prema-
ture expiratory closure of small airways may occur (West
Key Points 1982). Once interstitial pressure exceeds alveolar pres-
sure, fluid enters into the alveoli and initially accumu-
• Pulmonary edema develops in several stages, starting lates in the corners (Stage 3A) and then progresses to
with excess interstitial fluid that is removed by a alveolar flooding (Stage 3B).
compensatory increase in lymphatic flow. Interstitial Edematous lungs are brown to dark brown, wet, heavy
pulmonary edema first develops around vessels and (∼50–70 grams), and sink when placed in water (SK Liu
small airways, and progresses to alveolar flooding once 1970). They do not collapse when the thorax is opened.
the interstitial pressure exceeds the alveolar pressure. Chronic pulmonary edema leads to fibrosis and thicken-
• Gross abnormalities of pulmonary edema include ing of alveolar walls, which leads to the gross appearance
dark, heavy lungs that exude fluid on cut surface and of firm and brown lungs (i.e., brown induration). Pink
sink when placed in water. Microscopic abnormalities to reddish, foamy edema fluid oozes from the cut surface.
include engorged tortuous pulmonary capillaries
and lymphatics, edema fluid within the interstitium In fulminant heart failure, the trachea may contain
and alveoli, and alveolar macrophages containing pinkish foamy fluid. In Stage 2 edema, interstitial fluid
may appear clear or slight yellow. Once alveolar flooding