Introduction

• Cause: taurine deficiency; idiopathic.
• Signs: dyspnea, lethargy, reduced activity, inappetence.
• Diagnosis: radiography, ultrasound.
• Treatment: rest, diuretics, vasodilators, digoxin; taurine.
• Prognosis: good if taurine related; very poor if idiopathic.

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Pathogenesis

Etiology

Undefined

• Idiopathic.
• May be end-stage of hypertrophic cardiomyopathy Heart: hypertrophic cardiomyopathy, or other unclassified forms of cardiomyopathy Heart: restrictive cardiomyopathy.

Metabolic

• Taurine deficiency Taurine deficiency: canned/dried foods   →   destruction of taurine. Feeding an unfortified diet, eg dog food, can   →   low blood levels which have been associated with DCM, retinal degeneration Taurine.
• Need 1000-1500 mg/kg dry matter taurine in dry foods and 2000-2500 mg/kg dry matter taurine in canned foods.

Predisposing factors

General

Factors which worsen congestive failure

• Exertion.
• Stress.
• Sudden increase in salt intake.

Specific

• Age.

Pathophysiology

• Poorly understood or unknown.
• Metabolic or biochemical lesion affecting cardiac myocyte   →   failure of contractility/increased work for myocardium   →   chronic hypovolemic shock response Shock:
  • Right-sided failure due to myocardial involvement or secondary to the left backward failure   →   ascites, hepatomegaly, jugular pulse, pleural effusion, pericardial effusion.
  • Salt and water retention by kidney due to poor renal perfusion   →   sympathetic drive and RAAS (aldosterone) leads to increased venous return (preload) and venous pressure, further stretch of myocardium and predisposition to edema.
  • Increased end-diastolic left ventricular volume and pressure   →   dilation and non-compensatory hypertrophy (La Place relationship) of left ventricle   →   compromized papillary muscle function and passive dilation of atrioventricular annulus causing mitral regurgitation   →   increased left atrial pressures   →   left atrial enlargement   →   increased pulmonary venous (capillary wedge) pressure and pulmonary edema +/- pleural effusion   →   pleural effusion.
    Note pleural effusion will occur with left-sided as well as right-sided failure in cats.
  • Poor cardiac output (CO) due to decreased stroke volume (SV)   →   sympathetic drive   →   increased heart rate (HR).
  • Reduced cardiac output with arteriolar contraction to increase vascular resistance (mediated through sympathetic tone, active renin-angiotension-aldosterone system (RAAS) and increased vasopressin release); also venoconstriction   →   increased venous return   →   increased stretch of myocardium (preload).
  • Arteriolar constriction increases afterload (left ventricle wall stress) and myocardial workload   →   further myocardial dysfunction, further dilation.
• Signs of poor systolic function and vasoconstricted state: poor pulse, pale mucous membranes, delayed capillary refill time, cold extremities, etc.
• Left atrial stretch may   →   supraventricular dysrhythmias, eg atrial fibrillation.
• Increased myocardial wall stress, poor coronary perfusion of myocardium and diseased myocytes may result in ventricular dysrhythmias.

Timecourse

• Weeks-months from onset of signs.
• Usually weeks-months survival after diagnosis.

Diagnosis

Treatment

Prevention

Outcomes