Page 253 - Feline Cardiology

260 Section G: Congestive Heart Failure

PATHOPHYSIOLOGY AND GROSS PATHOLOGY
ventricular eccentric hypertrophy develops in response
to increased diastolic wall stress, which further worsens
myocardial failure.
Key Points
• Chronic deleterious effects of sympathetic stimulation
include tachycardia, increased afterload, increased
• Left heart failure is caused by elevated left ventricular myocardial oxygen demand, and potentially toxic
diastolic pressure and subsequent increased pulmonary myocardial effects such as apoptosis and fibrosis.
capillary pressure, typically over 25 mm Hg. • Chronic activation of the renin-angiotensin-aldosterone
• Radiographically, pulmonary edema initially develops as system promotes ventricular volume overload
patchy interstitial infiltrates and progresses to alveolar and progressive backward heart failure, excessive
flooding. vasoconstriction, and adverse myocardial remodeling
• Pleural effusion can develop in cats secondary to including hypertrophy and fibrosis.
elevated pulmonary capillary pressure in left heart • Pharmacologic antagonists of RAAS and the adrenergic
failure and may be due to increased hydrostatic nervous system may be used to lessen their chronic
pressure in the visceral pleural veins that drain into the deleterious effects on the circulatory system.
pulmonary veins.
• Right heart failure develops when the right ventricular Congestive Heart Failure
Congestive Heart Failure • Low output heart failure is caused by severely reduced Left heart failure
diastolic pressure, right atrial pressure, and central
venous pressure exceed 10–15 mm Hg. Right heart
failure consists of pleural effusion, jugular venous
distension, and often ascites or mild pericardial effusion
CHF develops when there is increased capillary hydro-
not severe enough to cause cardiac tamponade.
static pressure that overwhelms the lymphatic system’s
removal capability. Pulmonary edema develops due to
cardiac output. Clinical sequelae include signs of poor
tissue perfusion and arterial hypotension.
• Diastolic heart failure is caused by many cardiac
the capillaries and the interstitium. The Starling equa-
diseases that impair diastolic relaxation and increase an imbalance of hydrostatic and osmotic forces between
tion defines the factors of fluid filtration as follows:
left ventricular stiffness, which increase left ventricular
diastolic filling pressure. J =K [Π χ − Π Φι − δ( Π χ − Π Φι )]
f
V
• Systolic heart failure is caused by a decrease in
myocardial contractility, which decreases stroke volume where J v is the fluid filtration, K f is the membrane fluid
and cardiac output. The most important cause of filtration coefficient, Π χ is capillary pressure, Π ιΦ is inter-
myocardial failure in cats is idiopathic DCM. stitial pressure, δ is the membrane reflection coefficient
• Diseases that cause left ventricular volume overload to protein, Π χ is oncotic capillary pressure, and Π ιΦ is
include abnormalities of the mitral valve, left to right interstitial fluid oncotic pressure (Guyton and Lindsey
shunting congenital heart diseases, or aortic valve 1959). There is normally a slow fluid filtration (J v ) from
insufficiency. In response to decreased effective stroke the pulmonary capillaries into the interstitium, that is
volume, renin-angiotensin-aldosterone system (RAAS) removed by lymphatic drainage into the thoracic duct.
activation increases circulatory blood volume, which During left heart failure, the left ventricular diastolic
increases preload (i.e., diastolic wall stress) of the left pressure, left atrial pressure, pulmonary venous pressure,
ventricle.
• Activation of the sympathetic nervous system is an and pulmonary capillary pressure increase, which leads
acute compensatory mechanism in heart failure, which to increased accumulation of fluid in the pulmonary
increases heart rate and contractility via beta receptor interstitium (see Figure 19.1). Lymphatic drainage com-
stimulation, and increases blood pressure by alpha pensates to remove the excessive interstitial fluid, and
receptor stimulation and arteriolar vasoconstriction. This can increase lymphatic flow by tenfold above baseline.
response is short-lived (2–3 days) due to beta receptor Lymphatic flow increases over the first 4 hours of ele-
uncoupling and down-regulation. vated pulmonary capillary pressure to achieve a new
• Activation of RAAS is an important chronic steady state of fluid balance. This provides an “edema
compensatory mechanism in heart failure, which safety factor” so pulmonary edema does not occur until
increases sodium and water retention via aldosterone the pulmonary capillary pressure increases to ∼25 mm Hg.
and antidiuretic hormone, and causes arteriolar Pulmonary edema initially develops as interstitial fluid
vasoconstriction through increasing circulating levels accumulation that progresses to alveolar flooding and
of angiotensin II, antidiuretic hormone (vasopressin),
and endothelin-I. In animals with ventricular volume alveolar edema when there is severe fluid accumulation.
overload (e.g., as a result of mitral regurgitation), left When there is chronically elevated left atrial pressure
and chronic interstitial edema, connective tissue is