Page 254 - Feline Cardiology

Chapter 19: Congestive Heart Failure 261

deposited into the interstitial space. This connective and the mechanism may involve elevated TNF-α con-
tissue absorbs some of the excess fluid and reduces Π ιΦ , centration. Future areas of interest may involve investi-
which favors increased fluid filtration into the intersti- gating potential pathophysiologic mechanisms of TNF-α
tium. Lung mechanics are adversely affected by increased in feline heart failure, and the potential for pharmaco-
lung fluid weight as well as decreased compliance due to logic therapeutic intervention.
fibrosis (Drake and Doursout 2002). In response to
chronic left heart failure, the pulmonary venules, arteri- Low output heart failure
oles, and alveolar membrane hypertrophy, which reduces Low output heart failure (forward heart failure) occurs
diffusion capacity and impairs oxygenation (Guazzi when there is severely decreased cardiac output and
2000). poor tissue perfusion. Usually the diagnosis is made
Contrary to dogs, cats may develop pleural effusion once there is severe end-stage cardiac disease. Presenting
secondary to elevated left atrial pressure. Similar to man, complaints often include exercise intolerance, lethargy,
the visceral pleural veins in cats drain into the pulmo- and fatigue. Severe weakness, cold extremities, pale
nary veins, and the parietal pleural veins drain into the mucous membranes, delayed capillary refill time, hypo-
cranial vena cava (McLaughlin et al. 1961). Therefore, thermia, and hypotension are all clinical features of low
elevated pulmonary venous pressure from left heart output heart failure. Low cardiac output decreases tissue
failure may impair visceral pleural venous drainage and oxygen delivery, yet tissue extraction remains the same,
lead to accumulation of pleural effusion. Most often, leading to decreased venous oxygen tension (PvO 2 ).
there is accumulation of pulmonary edema as well as Anaerobic metabolism occurs when the PvO 2 is critically
pleural effusion in cats with left heart failure. Pulmonary low (<24 mm Hg), and results in hyperlactatemia and
arterial hypertension and right atrial hypertension are acidosis. Cardiogenic shock is rare, and consists of severe Congestive Heart Failure
not necessary for development of pleural effusion in arterial hypotension related to a dramatic reduction in
people, but elevated pulmonary capillary wedge pres- cardiac output, and is most often seen in cases of acute
sure is strongly associated with development of pleural heart failure such as infective endocarditis.
effusion (Wiener-Kronish et al. 1987). This is likely the
same in cats. Diastolic heart failure
Diastolic heart failure occurs when there is normal
Right heart failure systolic function and concurrently increased ventricu-
Ascites and pleural effusion are sequelae to increased lar diastolic filling pressure. It is diagnosed when there
right ventricular diastolic pressure, right atrial pressure are clinical signs of heart failure in the absence of sig-
and right heart failure (see Figure 19.1). Compared to nificant myocardial failure, diseases causing ventricular
the pulmonary capillaries, the hepatic sinusoids have volume overload such as valvular insufficiency or left to
larger gaps that promote fluid filtration at less severe right shunting congenital defects, or pericardial disease.
elevations in pressure. Right heart failure develops once Given the high prevalence of feline cardiomyopathies
the right atrial and central venous pressures exceed 10– that impair diastolic function (e.g., hypertrophic cardio-
15 mm Hg (Gookin and Atkins 1999). Hepatic venous myopathy and restrictive cardiomyopathy), diastolic
distension is a consistent abnormality seen in cats with heart failure is the most common cause of heart failure
ascites secondary to right heart failure, and may be visu- in cats.
alized on ultrasound of the liver. Isolated right heart Diastole is divided into an active phase of isovolumic
failure is uncommon in cats, since they often develop relaxation, early rapid filling, passive filling (diastasis),
concurrent left- and right-sided heart disease. In a large and atrial contraction (Figure 19.3). Rapid early filling
case series of cats with ascites, 29% had right heart accounts for approximately 80% of the end-diastolic left
failure as a cause of the effusion (Wright et al. 1999). ventricular volume. Impaired diastolic function can be
Concurrent pleural effusion is present in a majority of divided into two main categories: impaired active dia-
cats (89%) with ascites from right heart failure (Wright stolic relaxation and decreased ventricular compliance.
et al. 1999). Although discussed as two separate categories, there are
Tumor necrosis factor-α (TNF-α) is a proinflamma- interplays and links in the pathophysiologic processes
tory cytokine that may contribute to cardiac cachexia, that lead to global diastolic dysfunction and elevated
ventricular dysfunction, myocarditis, myocardial fibro- diastolic filling pressures.
sis, and heart failure. TNF-α concentration was elevated Active relaxation occurs when calcium dissociates
in nine of 20 cats with right heart failure, and one of six from troponin C and is sequestered by the sarcoplasmic
cats with left heart failure (Meurs et al. 2002). Right reticulum-calcium ATPase pump (SERCA) into the
heart failure often leads to significant cardiac cachexia, sarcoplasmic reticulum. Altered levels or activity of