Page 532 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

520 FLUID THERAPY

peracute pulmonary edema. The second example is a
cat with hypertrophic cardiomyopathy and a noncompli-
ant left ventricle (see Figure 21-4, bottom left curve). It is
not uncommon for severe pulmonary edema to follow a
bout of protracted tachycardia (e.g., stress). Develop-
ment of pulmonary edema in these situations can be
explained by acute deterioration of left ventricular systolic
or diastolic performance that rapidly increases left atrial
and pulmonary venous pressure. Although diuresis is a
critical treatment in this situation, short-term success
may hinge on therapy that reduces mitral regurgitant frac-
tion (i.e., afterload reduction).
Another issue of relevance to CHF and fluid therapy of
the cardiac patient is the relative size of the vascular
compartments. The vascular compliance of the pulmo-
nary circulation is much smaller than that of the systemic
circulation, and sudden expansion of the plasma volume
Figure 21-4 Ventricular function curves in heart failure.
Ventricular function curves demonstrate the potential relationships usually increases pulmonary venous pressure more than
between venous pressure (a determinant of ventricular filling and systemic venous pressure. This is particularly true in the
end-diastolic volume), ventricular compliance or distensibility patient with left-sided heart disease and explains why
(which determines the venous and atrial pressures required to fill some dogs and cats develop pulmonary edema after intra-
the ventricle), and stroke volume (determined by ventricular end- venous administration of a so-called maintenance volume
diastolic volume, ventricular afterload, and myocardial contractility). of crystalloid solution. Furthermore, central venous pres-
The top of the graph demonstrates ventricular systolic function, and sure (CVP) cannot be used to gauge the effect of intrave-
nous fluid therapy on left-sided cardiac filling pressures,
the lower curves demonstrate ventricular filling dynamics.Top,
When inotropic (“contractile”) state and afterload are held especially in the setting of isolated left-sided CHF. 141
constant, the ventricular stroke volume depends on cardiac filling Owing to differences in vascular compliance and cardiac
(preload), although this relationship is depressed in patients with function, left-sided filling pressures may increase much
myocardial failure. Patients treated with excessive dosages of more rapidly than CVP, though both increase
diuretics may develop inadequate ventricular filling, leading to
decreased stroke volume and cardiac output and causing prerenal simultaneously.
azotemia. Reduction of diuretic dosage or fluid therapy is generally
required to reestablish cardiac output.Bottom, Ventricular RENAL FUNCTION IN
distensibility—the tangent of any point on the diastolic pressure- HEART FAILURE
volume curve—depends on the amount of ventricular hypertrophy,
myocardial fibrosis, and the volume of the ventricle. Animals with Remarkably, the kidney often is able to maintain glomer-
stiff ventricles resulting from ventricular hypertrophy or myocardial ular filtration in the setting of decreased blood pressure or
fibrosis require high ventricular filling pressures and are poorly cardiac output. Decreases in renal perfusion are coun-
tolerant of fluid infusions. Note that increased cardiac filling can tered by dilatation of the afferent arteriole mediated by
progress only at disproportionately higher venous pressures, a the release of prostaglandin E 2 , and constriction of the
situation that predisposes to pulmonary edema. Recognize that even
dilated ventricles can develop diastolic dysfunction (bottom right). efferent arteriole primarily by angiotensin II. Efferent
Once the grossly dilated ventricle reaches a certain point, arteriolar constriction also is augmented by arginine vaso-
distensibility decreases. Compare the slope at the extreme right of pressin (antidiuretic hormone [ADH]) and norepineph-
122
this diastolic filling curve with that of the smaller, hypertrophied rine. These microvascular responses increase
ventricle. The benefit of diuretic therapy in this setting can be glomerular filtration pressure, increase filtration fraction,
appreciated because even small reductions in plasma volume and and maintain glomerular filtration in the setting of
preload may permit the ventricle to fill at substantially lower venous reduced renal blood flow (see Chapter 2). 116,138,159
pressures. However, considering normal renal function demands
approximately 20% of a normal cardiac output, it is not
In contrast to right-sided or biventricular CHF, severe surprising to identify azotemia in advanced CHF, espe-
left-sided heart failure can develop without substantial cially during aggressive diuretic therapy. Progressive renal
sodium retention or weight gain. 69 Two common failure is common in dogs and cats with CHF, and the
examples in veterinary medicine can be cited. The first treatment of patients with both intrinsic renal disease
example is rupture of a mitral chorda tendinea in an older and heart failure is especially difficult. This situation also
dog with previously stable mitral regurgitation. The sud- occurs in human patients in whom worsening of renal
den increase in mitral regurgitant volume increases mean function is associated with a poorer prognosis and higher
left atrial and pulmonary capillary pressures, leading to mortality and often requires dialysis for control of both