Introduction

• Although many patients suffering from cardiovascular disease are identified during routine examination or present with mild clinical signs, a subset will present on an emergency basis with severe, life-threatening congestive heart failure.
• These patients often require aggressive therapy and intensive monitoring to achieve a successful outcome.
• Despite their critical status at presentation many will survive for prolonged periods if the acute episode is successfully managed.

Pathogenesis

Etiology

• Etiologies behind development of CDVD and DCM are not totally understood (genetic component plays a role, eg Cavalier King Charles Spaniels Cavalier King Charles Spaniel with CDVD).
• Ruptured chordae tendinae Heart: rupture of chordae tendinae.
• Some dogs, predominately American Cocker Spaniels American Cocker Spaniel , have been recognized to have taurine responsive dilated cardiomyopathy .
• Stressful events (eg provoking cardiogenic shock Shock and decompensation in a patient with DCM).

Pathophysiology

• Following the initial cardiac insult (induction of CDVD or DCM) and a reduction in cardiac output there are short-term compensatory mechanisms that become activated to facilitate circulatory homeostasis, including:
  • Sympathetic nervous system.
  • Renin-angiotensin-aldosterone system (RAAS).
  • Release of arginine-vasopressin.
  • Renal sodium and water retention.
  • Increased preload optimizing Frank-Starling mechanism in an attempt to increase stroke volume.
• The heart's ability to hypertrophy, eccentrically in the face of volume overload and concentrically in the face of pressure overload, normalizes the cardiac output and serves as long-term compensatory mechanism.
• Unfortunately cardiovascular disease in dogs is mostly progressive and in some instances the heart's capacity to hypertrophy is overwhelmed.
• This results in decline of cardiac output and reactivation of short-term compensatory mechanisms.
• Instead of augmenting the heart's capacity to deliver blood, the short-term compensatory mechanisms now prove deleterious by further increasing preload and afterload.
• Ultimately pulmonary capillary pressures rise promoting the development of pulmonary edema Lung: pulmonary edema while pronounced increase in afterload diminishes effective forward blood and increases myocardial oxygen demands.

Timecourse

• Time until development of decompensated heart failure is difficult to predict based on today's diagnostic modalities.
• Some patients live for years with significant cardiovascular disease but never develop nor require treatment for heart failure.
• Recognized predisposing factors that may quickly shift a patient with compensated heart failure to a decompensated state include:
  • The development of arrhythmias Heart: dysrhythmia , especially atrial fibrillation Heart: atrial fibrillation.
  • Ruptured chordae tendinae Heart: rupture of chordae tendinae.
  • Left atrial tear.
  • Abrupt discontinuation of prescribed medications.
  • Stress.

Diagnosis

Treatment

Prevention

Outcomes