Page 715 - Small Animal Clinical Nutrition 5th Edition

742 Small Animal Clinical Nutrition

Table 36-3. Cardiovascular and neurohumoral adaptations that Crandall and DiGirolamo, 1990).
VetBooks.ir Increased perfusion requirements of expanding adipose tissue and plasma insulin, aldosterone and norepinephrine concentra-
occur during the transition from lean to obese body condition.
Obese people have increased plasma volume, cardiac output
Elevated cardiac output
Abnormal left ventricular function tions when compared with age-matched nonobese individuals
(Rocchini et al, 1989). These changes occur whether the indi-
Variable blood pressure response (normotensive to hypertensive) viduals eat high- or low-salt foods. Increases in blood pressure,
Increased retention of sodium and water by the kidney with
subsequent increase in plasma volume heart rate, cardiac output, left atrial pressure and extracellular
Increased plasma aldosterone and norepinephrine concentrations fluid volume also occur in dogs with experimentally induced
Increased left atrial pressure obesity (Hall et al, 1993; Mizelle et al, 1994). Blood pressure
Increased heart rate
Exercise intolerance always increases with increasing weight in dogs, regardless of
the initial blood pressure.
The tendency toward blood volume expansion and neurohu-
tem (Kivlighn et al, 1990). moral activation in obese animals parallels the compensatory
Although ANP is unable to normalize hemodynamics and changes that often occur in patients with cardiac disease.
natriuresis, it appears to provide an important modulating Obesity, therefore, may have profound adverse effects in pa-
effect on the pathogenesis of CHF. Elevated ANP concentra- tients with concomitant cardiovascular disease.
tions occur in dogs with spontaneous heart failure; furthermore, Body weight and blood pressure correlate strongly in people.
ANP concentration increases with increasing severity of heart Hypertension occurs more often in obese individuals than in
failure (Takemura et al, 1991; Vollmar et al, 1991; Haggstrom nonobese individuals (Alexander, 1986). The increase in blood
et al, 1994). pressure may be due to the combined effects of hyperinsuline-
mia, hyperaldosteronemia and increased sympathetic nervous
CHF-ASSOCIATED HYPONATREMIA system activity that characteristically occur in obesity (Rocchini
Although the precise pathogenesis of CHF-associated hypo- et al, 1989). Hyperinsulinemia and blood pressure elevation
natremia remains controversial, the important factors can be also occur in dogs that have become rapidly obese (Rocchini et
divided into two categories (Oster et al, 1994). First, the al, 1987). Hyperinsulinemia markedly reduces urinary sodium
increase in plasma angiotensin II concentration promotes thirst excretion (antinatriuresis) with resultant sodium and water
resulting in greater water intake. Second, renal diluting ability retention (Hall et al, 1990, 1990a; Brands et al, 1991), possibly
is impaired because the delivery of glomerular filtrate to the contributing to blood pressure changes. However, hyperinsu-
distal renal tubules is decreased (resulting from a reduced linemia for up to 28 days at levels comparable to those found in
glomerular filtration rate and enhanced reabsorption proximal- obese hypertensive people does not elevate mean arterial pres-
ly) and the plasma levels of AVP are increased. Both of these sure in dogs with reduced renal mass even when sodium intake
abnormalities might be mediated in part by angiotensin II.The is high (Hall et al, 1990). This finding suggests that chronic
osmotically inappropriate increase in plasma AVP concentra- hyperinsulinemia per se cannot account for obesity-associated
tion may be caused by a downward resetting of the osmostat hypertension. Further studies are needed to elucidate the path-
because of a reduction in the effective blood volume (Oster et ophysiology of blood pressure responses and hypertension in
al, 1994). Aggressive use of diuretics may also contribute to the obese patients.
pathogenesis of hyponatremia in some patients.
CHF-associated hyponatremia is an important marker of Cachexia
poor prognosis in people with heart failure; it is seen almost Cachexia is a syndrome of weight loss (defined generally as
exclusively in decompensated patients (Lee and Packer, 1986). unintentional loss of more than 10% body weight), lean tissue
People with heart failure and hyponatremia seem to have wasting and anorexia seen clinically in a variety of diseases,
decreased renal blood flow, higher serum urea nitrogen concen- including chronic heart failure.The loss of lean body mass seen
trations, lower blood pressure and higher plasma renin activity in cachexia is caused by a mismatch between food intake and
(Oster et al, 1994; Lee and Packer, 1986). Anecdotal reports nutritional requirements, resulting in negative nitrogen and
also suggest that hyponatremic patients in CHF have a poorer energy balances (Freeman and Roubenoff, 1994).These imbal-
prognosis. ances may be due to inadequate intake, excessive losses or
altered metabolism (Figure 36-4).
Obesity In patients with heart failure, anorexia may be due to the
Obesity has potentially profound cardiovascular consequences. clinical signs of heart failure itself (dyspnea, fatigue), the pres-
From a cardiovascular perspective, obesity is a disease of blood ence of concomitant disease (nausea associated with renal fail-
volume expansion with: 1) elevated cardiac output, 2) increased ure), use of drugs that cause nausea (e.g., toxic doses of cardiac
plasma and extracellular fluid volume, 3) increased neurohu- glycosides), the presence of elevated levels of inflammatory
moral activation, 4) reduced urinary sodium and water excre- cytokines or sudden nutritional changes.The rate of loss of lean
tion, 5) increased heart rate, 6) abnormal systolic and diastolic body mass with cardiac cachexia exceeds that attributable to
ventricular function, 7) exercise intolerance and 8) variable anorexia alone, and reflects in part the excessive caloric expen-
blood pressure response (Table 36-3) (Alexander, 1986; ditures of the increased work of respiration and elevated heart