Page 353 - Feline Cardiology

368 Section L: Comorbidities

CONCURRENT HEART DISEASE AND example, which helps guide the dose and frequency of
KIDNEY DISEASE diuretic or fluid administration (Gouni et al. 2008;
Sharkey 1997). PCWP is a nearly exact measurement of
The fundamental problem a clinician faces when pulmonary venous pressure, which is an important
managing a feline patient with both heart disease and determinant of whether left-sided congestive heart
kidney disease is one of vascular volume. Increasing a failure (pulmonary edema and/or cardiogenic pleural
patient’s circulating vascular volume, such as with admin- effusion) occurs. The enormous clinical limitation that
istration of parenteral fluids, helps to maintain or increase hinders PCWP measurement in the cat is the required
glomerular filtration rate, but it also increases the risk of placement of a Swan-Ganz catheter, which is large in
iatrogenically triggering congestive heart failure. diameter (e.g., 6 or 8 Fr) and challenging to place,
Conversely, decreasing circulating volume, such as with although this can be done successfully in healthy, anes-
administration of diuretics, is appropriate for eliminat- thetized cats (Lamont et al. 2001). Noninvasive surro-
ing fluid retention such as pulmonary edema, but doing gates for PCWP have been explored in other species,
so may exacerbate underlying kidney dysfunction. including Doppler echocardiographic estimates of left
In concert, coexisting heart disease and kidney disease ventricular filling pressures (E/E’) (Oyama et al. 2004;
can produce cumulatively detrimental effects (Schriffren Schober et al. 2008a,b) but have not yet been validated
et al. 2007; Sica 2006; Bonagura et al. 2006), and any or for the cat. An alternative with limited uses is the mea-
all of the following mechanisms may explain the obser- surement of central venous pressure (CVP) (Gouni et al.
vation that cats with hypertrophic cardiomyopathy are 2008; de Madron 2007). Placement of a jugular intrave-
more likely to be azotemic than are normal cats (Gouni nous catheter is required for CVP measurement, which,
et al. 2008).
with appropriate technical skill, is feasible in most cats
barring severe dyspnea (Petrollini and Drobatz 2007).
• Decreased renal perfusion due to renal afferent arte- Measuring CVP provides information on the likelihood
riolar constriction in heart disease of right-sided congestive heart failure: CVP reflects the
• Direct autonomic cardiac-renal interactions, where a pressure of blood reaching the right ventricle (right
decrease in distending volume of chronically dis- ventricular end-diastolic pressure, barring tricuspid
tended atria may, via low-pressure cardiopulmonary stenosis) and therefore the propensity for transudation
baroreceptors, be perceived locally as “underfilling” of fluid through the walls of the systemic veins. The
and expressed through alterations in renal sympa- pulmonary capillary bed’s action as pressure diffuser
thetic tone (Weinfeld et al. 1999). means that CVP cannot reliably identify increases in
pulmonary venous pressure or the likelihood of left-
• Vasopressin/antidiuretic hormone release in advanced
Comorbidities • Decreased renal perfusion in heart disease (due to sided congestive heart failure, yet a majority of heart
heart disease, contributing to intravascular volume
diseases in cats are predominantly or exclusively left-
overload
sided. Therefore, jugular catheter placement and serial
decreased cardiac output, systemic hypotension, or
fluid therapy titration in hospitalized cats with echocar-
hypovolemia secondary to diuretics), leading to CVP measurements should be considered for optimal
sodium retention diographically confirmed heart disease that is predomi-
• Systemic hypertension from chronic kidney disease nantly or exclusively right-sided (uncommon). Normal
increasing afterload and consequently end-systolic CVP in the cat is 4.2 ± 1.1 mm Hg (Lamont et al. 2001).
ventricular wall stress In cats, pleural effusion (of any origin) increases the CVP
• Tense ascites causing abdominal compartment syn- independent of right heart filling pressures (Gookin and
drome, reducing renal perfusion Atkins 1999), and this important confounder is discussed
• Sympathetic and renin-angiotensin-aldosterone below (see “Cardiac Disease and Unrelated Pleural
system activation as compensatory cardiac mecha- Effusion”).
nisms worsening renal disease Certain basic principles are essential for the optimal
management of patients with concurrent cardiac and
renal disorders. These principles include the following:
Managing a patient with both disorders is challenging
in the cat, in part due to restrictions imposed by small • Which disorder is predominant?
body stature and logistical/financial limitations in veteri- • Chronic versus acute decompensation
nary medicine. Optimal fluid or diuretic administration • Identification and management of contributing/
may be achieved in human beings through serial mea- additional factors
surement of pulmonary capillary wedge pressure, for • Monitoring and treatment adjustments