Contributors: Barrett Bulmer, Dandrieux Josephine

 Species: Canine   |   Classification: Diseases

Introduction Pathogenesis Diagnosis Treatment Outcomes Further Reading

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.

Acute Presentation

  • Patients with decompensated heart failure often present with signs of congestive and/or low output heart failure.
  • Severe congestive heart failure:
    • Cough.
    • Profound increase in respiratory rate (tachypnea) and effort (dyspnea).
    • Orthopnea.
    • Anxiety/disorientation.
    • Weakness.
  • Cardiogenic shock (severe forward failure) Shock: cardiogenic :
    • Syncope/collapse.
    • Weakness and/or lethargy.
    • Cold extremities.

Age Predisposition

Breed Predisposition

Cost Considerations

  • Moderate costs involved with:
    • Diagnostics.
    • Hospitalization.
    • Oxygen therapy.
    • Intravenous drugs.
    • Intensive monitoring.
  • Intensely managed case of acute heart failure may cost around $700 to $1000 (UK: £400-600).
  • Inform owners that cardiovascular medications and periodic rechecks will be required throughout the remainder of the pet's life.

Special Risks

  • Any event contributing to stress and further decompensation.
    Patients with decompensated heart failure are very poor anesthetic candidates and every attempt should be performed to avoid anesthesia.

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 Acute heart failure: taurine supplementation.
  • 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:

Diagnosis

Client History

  • Coughing that may be productive.
  • Sudden onset of respiratory distress.
  • Restlessness and pacing often at night.
  • Rest standing up with head supported on furniture (orthopnea).
  • Significant abdominal distension.
  • Profound weakness and exercise intolerance.
  • Syncope.
  • May appear disoriented.
  • May have undergone a recent stressful situation, ie boarding.
  • May have history of cardiovascular disease.

Clinical Signs

  • Coughing.
  • Tachypnea and/or dyspnea.
  • Orthopnea.
  • Weakness and lethargy.
  • Tachycardia.
  • Prolonged capillary refill time.
  • Adventitious lung sounds in cases of fulminant pulmonary edema.
  • Cardiac auscultation.
    • Murmurs Murmur: overview.
      • Systolic, left apical murmur in cases of mitral insufficiency.
      • Systolic, left apical murmur may also be identified in dogs with DCM as the heart undergoes eccentric hypertrophy, causing stretching of the mitral valve annulus and regurgitation.
      • Systolic, right-sided murmur in cases of tricuspid insufficiency although mitral valve murmurs often radiate to the right.
    • Arrhythmias Heart: dysrhythmia.
      • Sinus tachycardia.
      • Atrial fibrillation Heart: atrial fibrillation.
      • Supraventricular premature complexes.
      • Ventricular arrhythmias are common in cases of DCM.
    • Gallops.
      • S3 gallop may be ausculted in cases of increased end diastolic pressures and/or stiffness (eg dogs with DCM or dogs with marked ventricular dilatation subsequent to CDVD).
  • May have decreased femoral pulse quality, particularly dogs with DCM; pulse deficit may be present (eg atrial fibrillation Heart: atrial fibrillation ).
  • May display jugular distension if right-sided heart failure is present (positive hepato-jugular reflex).
  • May have decreased lung sounds or an auscultable fluid line in cases of significant pleural effusion.
  • Significant ascites may be present.

Diagnostic Investigation

  • Most patients with acute, decompensated heart failure are extremely unstable and may require therapeutic decisions based solely on physical examination until their status improves.
  • Electrocardiogram ECG: overview
    • May be performed standing or in sternal recumbency in unstable patients since the primary goal is to determine the underlying cardiac rhythm and guide anti-arrhythmic therapy.
    • Atrial fibrillation Heart: atrial fibrillation may necessitate efforts to control the ventricular rate.
    • Significant ventricular arrhythmias (ie hemodynamically significant) may necessitate efforts to suppress them.
    • Continuous, telemetric ECG monitoring ECG: ambulatory monitoring is beneficial and well tolerated.
  • Thoracic radiographs Radiography: thorax
    • Patients may be too unstable for radiographs prior to therapeutic decisions.

    Dorsoventral (DV) radiograph may be better tolerated than a ventrodorsal or lateral view and may suffice during emergency situations.

  • Findings:

    • Left ventricular enlargement pattern.
      • Lateral: dorsal deviation of the carina, tracheal elevation, straightened caudal cardiac border.
    • Left atrial enlargement pattern.
      • Lateral: loss of the waist of the caudal border of the cardiac silhouette.
      • DV: splaying of the caudal mainstem bronchi ('cowboy' leg sign), left auricular enlargement at the 2 to 3 o'clock position of the clock-face analogy.
    • Right ventricular and right atrial enlargement patterns.
      • Substantially less sensitive than the left-sided enlargement patterns (lateral: increased cardiac sternal contact; DV: reverse 'D' shape).
      • Often over-interpreted.
    • Hallmarks of pleural effusion.
      • Fissure lines.
      • Severe cases may obscure pulmonary parenchyma and cardiac silhouette.
  • Echocardiography Ultrasound: echocardiology
    • Abbreviated exam can be performed standing to identify underlying disease condition.
    • Assess valvular integrity, systolic function and degree of atrial enlargement.
    • Identify ruptured chordae tendinae and left atrial tears/pericardial effusion.
    • Identify pleural effusion.
    • Identify ascites and hepatic venous congestion if the abdomen is imaged.
  • Thoracocentesis Thoracocentesis
    • High degree of suspicion for pleural effusion → thoracocentesis serves as a diagnostic and therapeutic modality (safe method if effusion present).
  • Cardiac catheterization
  • Not standard practice especially as an emergency diagnostic tool (vs humans) unless specialized hospital. Could be used as part of follow-up treatment.
    • Swan-Ganz catheter Acute heart failure: Swan-Ganz catheter.
      • Flow-directed catheter inserted via the jugular vein.
      • Enables measurement of right atrial pressure, cardiac output and provides an estimation of left atrial pressure.
  • New information:
    • Measurement of serum biochemical markers, including:
      • Atrial natriuretic peptide.
      • Brain natriuretic peptide.
      • Troponin levels (at present mainly marker for myocardial infarction).
  • May hold promise in the near future for the diagnosis and management of canine cardiovascular disease.
  • Serum or plasma taurine level measurement in predisposed patients diagnosed with DCM Acute heart failure: taurine supplementation.

Definitive diagnostic features

  • Left-sided congestive heart failure is documented radiographically.
  • Not all alveolar lung patterns represent cardiogenic pulmonary edema.
    • Hallmarks of cardiogenic pulmonary edema.
      • Left atrial enlargement.
      • Pulmonary venous congestion.
      • Peri-hilar interstitial edema.
      • Interstitial edema ultimately coalesces to an alveolar pattern.
  • Echocardiography can define the underlying cardiac disease process but cannot easily confirm the presence of left-sided congestive heart failure.
  • Right-sided congestive heart failure.
    • Presence of ascites or pleural effusion.
    • Positive hepato-jugular reflex.
    • Elevated systemic venous pressures measured by CVP Central venous pressure or cardiac catheterization.

Gross Autopsy Findings

  • Severe left-sided heart failure.
    • Lungs: fulminant congestion with froth/edema extending into large airways.
    • DCM: marked left ventricular dilation, left atrial enlargement, papillary muscles may appear atrophied, biventricular disease often occurs.
    • Mitral insufficiency: left ventricular eccentric hypertrophy and left atrial enlargement, the mitral valve cusps are grossly distorted Acute heart failure: degenerative mitral valve , contracted and may curl, the chordae tendinae may be thickened, elongated or ruptured, jet lesions may be present in the left atrium.
  • Severe right-sided heart failure.
    • Ascites or pleural effusion.
    • Hepatomegaly, hepatic congestion.
    • Caudal vena caval distension.
    • Potentially subcutaneous edema.
    • DCM: usually display biventricular disease in cases of right-sided failure, right ventricular and atrial dilation.
    • Tricuspid insufficiency: right ventricular eccentric hypertrophy and right atrial enlargement, the tricuspid valve cusps are grossly distorted, contracted, and may curl, the chordae tendinae may be thickened, elongated, or ruptured.

Histopathology Findings

  • Dilated cardiomyopathy Heart: dilated cardiomyopathy (DCM) : myocardial degeneration, vacuolization and atrophy of myocytes.
  • CDVD: alterations within the spongiosa and fibrosa layers of the affected valve.

Differential Diagnosis

Treatment

Initial Symptomatic Treatment

Emergency treatment of severe DCM 

  • Furosemide Furosemide Therapeutics: cardiovascular.
    • Intravenous administration of 4-8 mg/kg, q 1-4h.
    • Life-threatening cases may require once hourly administration.
    • Monitor respiratory rate in effort to help guide dosing interval.
    • Promotes rapid diuresis → reduces preload and hence congestion.
    • Potentially lowers left atrial pressure via vasodilation.
  • Oxygen therapy.

May promote agitation.

  • Glyceryl trinitrate Glyceril trinitrate.
    • 6-50 mm applied topically to the skin q 6-8h.
    • Systemic vasodilator used in short term management of pulmonary edema (especially if acute) and to reduce ventricular filling pressures.
  • Nitroprusside Nitroprusside
    • Used if pulmonary edema not resolved with aggressive IV furosemide and glyceryl trinitrate treatment or in the first instance (depending on severity).
    • Constant rate IV administration of 2-5 micrograms/kg/min.
    • Mix high concentration of drug in IV fluids (ie 5% dextrose) so a low infusion rate (ie 15 mls/hr) may achieve desired rate of administration.
    • Potent balanced vasodilator.
    • Reduction in afterload.
      • Decrease volume of mitral regurgitation.
      • Decrease myocardial work/oxygen demands.
      • Increase effective forward stroke volume.
    • Systemic blood pressure must be monitored during infusion Central venous pressure.

Nitroprusside is light sensitive and should not be infused with another agent thereby necessitating placement of a second IV line. Prolonged administration (> 48 hours) may produce cyanide toxicity.

  • Dobutamine Dobutamine.
    • Constant rate intravenous administration of 5-15 micrograms/kg/min.
    • Mix high concentration of drug in IV fluids (ie 5% dextrose) so a low infusion rate (ie 15 mls/hr) may achieve desired rate of administration.
    • Positive inotrope.
      • Increases contractility via cAMP dependent mechanisms.

Dobutamine may increase the heart rate or exacerbate arrhythmias so continuous ECG monitoring is recommended. If profound tachycardias develop the infusion rate may need to be slowed or discontinued.

  • If constant monitoring or a constant rate of infusion are not available, an oral positive inotrope, such as pimobendan Pimobendan is recommended. If not available, digoxin Digoxin can be used, but is a weak positive inotrope.
  • Pimobendan Pimobendan.
    • 0.2-0.6 mg/kg po q12h one hour before food.
    • Calcium sensitizer and vasodilator-'inodilator'. Acts as a potent positive inotrope.
  • Thoracocentesis Thoracocentesis /abdominocentesis Abdominocentesis if large volumes of effusion are present.
  • Treatment of severe (ie hemodynamically significant) arrhythmias.

Use appropriate anti-arrhythmic therapy according to the type of arrhythmia, eg use digoxin Digoxin in atrial fibrillation (0.2 mg/m2 BSA q12h; diastolic function will improve due to its negative chronotropic effect).

Emergency treatment of severe mitral insufficiency/tricuspid insufficiency 

  • Furosemide Furosemide Therapeutics: cardiovascular.
    • Intravenous administration of 2-8 mg/kg, q 1-4h.
    • Life-threatening cases may require once hourly administration.
    • Monitor respiratory rate in effort to help guide dosing interval.
    • Promotes rapid diuresis → reduces preload and hence congestion.
    • Potentially lowers left atrial pressure via vasodilation.
  • Oxygen therapy.

May promote agitation.

  • Glyceryl trinitrate Glyceril trinitrate.
    • 6-50 mm applied topically to the skin q 6-8h.
    • Systemic vasodilator used in short term management of pulmonary edema (especially if acute) and to reduce ventricular filling pressures.
  • Nitroprusside Nitroprusside:
    • Used if pulmonary edema not resolved with aggressive IV furosemide and glyceryl trinitrate treatment or in the first instance (depending on severity).
    • Constant rate IV administration of 2-5 micrograms/kg/min.
    • Mix high concentration of drug in IV fluids (ie 5% dextrose) so a low infusion rate (ie 15 mls/hr) may achieve desired rate of administration.
    • Potent balanced vasodilator.
    • Reduction in afterload.
      • Decrease volume of mitral regurgitation.
      • Decrease myocardial work/oxygen demands.
      • Increase effective forward stroke volume.
    • Systemic blood pressure must be monitored during infusion Central venous pressure.

Nitroprusside is light sensitive and should not be infused with another agent thereby necessitating placement of a second IV line. Prolonged administration (> 48 h) may produce cyanide toxicity.

  • If nitroprusside unavailable, vasodilation may be attempted combining:
    • Arterial vasodilator: Hydralazine Hydralazine at 0.5 to 2.0 mg/kg PO BID to TID.
    • Venodilator: Isosorbide dinitrate Isosorbide at 0.5 to 2.0 mg/kg PO TID or 2% nitroglycerine ointment, 1/4 to 1 inch cutaneously every 6-8 h.

Despite the ease of administration it appears this combination does not promote vasodilation as effectively as the labor intensive nitroprusside protocol.

  • Most cases of mitral insufficiency can be managed without intravenous inotropic agents.
  • Thoracocentesis Thoracocentesis /abdominocentesis Abdominocentesis if large volumes of effusion are present.
  • Treatment of severe (ie hemodynamically significant) arrhythmias.

Use appropriate anti-arrhythmic therapy according to the type of arrhythmia, eg use digoxin Digoxin in atrial fibrillation (0.2 mg/m2 BSA q12h).

  • Acts on specialized conducting tissue and SA node, increasing the refractory period, while decreasing conduction velocity, thereby slowing the heart rate (also acts as a minor positive inotrope). This will improve diastolic filling.

Care: digoxin is contraindicated in other types of arrhythmias (eg ventricular premature complexes Ventricular premature contraction ).

Monitoring

Often best measure of effectiveness of therapy is patient's respiratory rate, effort and attitude. Patients have likely not slept for many hours and as the pulmonary edema resolves they finally feel comfortable enough to lie down and sleep.

  • Ideally heart rate and rhythm are monitored continuously via telemetry Acute heart failure: telemetric ECG unit. Otherwise hourly.
  • Assessment of urine production Urinalysis.
  • Renal values and electrolytes daily during aggressive therapy.
  • Thoracic radiographs Radiography: thorax prior to discharge.

Subsequent Management

Treatment

  • Discharge when patients are:
    • Stable.
    • No longer require oxygen or intravenous drugs.
  • Patients usually require life-long management of their congestive heart failure.
    • Diuretic: furosemide Furosemide.
    • Vasodilator: ACE inhibitors ACE inhibitor: overview.
    • Inotrope: digoxin Digoxin.
    • Refractory heart failure requires tailored therapy with additional diuretics and vasodilators.

Monitoring

  • Re-evaluate 5 to 7 days after discharge:
    • Renal profile including electrolytes.
    • Serum digoxin level.
    • Heart rate and rhythm.
    • Thoracic radiographs.
    • Owner assessment:
      • Degree of coughing.
      • Respiratory rate and effort at rest.
      • Appetite.
      • Strength and exercise capacity.
      • Quality of life.

Long-term monitoring

  • Vigilant observation is required by pet owner.
  • Owners may record respiratory rate and effort at rest on a daily basis.
  • Recheck thoracic radiographs every 3 to 6 months.
  • Periodic re-evaluation of renal values, electrolyte status and serum digoxin level.

Outcomes

Prognosis

  • Guarded at time of acute presentation but long-term prognosis depends on response to therapy. Aggressive therapy has potential to save dogs that were only minutes from dying.
  • CDVD appears to carry a better prognosis than DCM.
  • Dogs already intensively managed with numerous cardiovascular drugs that remain decompensated have a worse prognosis.
  • Dogs with left atrial tears or rupture of primary chordae tendinae have a very poor prognosis.

Expected Response to Treatment

  • As heart failure resolves patients often progress from orthopneic → standing → resting sternally → resting laterally → sleeping.
  • Respiratory rate and effort improve quickly in response to oxygen supplementation and resolution of edema.
  • Thoracocentesis dramatically and immediately resolves respiratory distress if pleural effusion accounts for the respiratory impairment.
  • If no improvement in 24 hours, therapy should become more aggressive.

Reasons for Treatment Failure

  • Underlying cardiovascular disease was end stage.
  • Therapy was not aggressive enough.
  • Concurrent medical condition (ie renal failure, pulmonary hypertension Pulmonary Arterial Hypertension (PHT) ).
  • Respiratory distress was unrelated to cardiovascular disease.

Further Reading

Publications

Papeles arbitrados

  • Recent references from PubMed and VetMedResource.
  • Boswood A, Attree S & Page K (2003) Clinical validation of a proANP 31-67 fragment ELISA in the diagnosis of heart failure in the dog. J Small Anim Pract 44 (3), 104-108 PubMed.
  • Greco D S, Biller B & Van Liew C H (2003) Measurement of plasma atrial natriuretic peptide as an indicator of prognosis in dogs with cardiac disease. Can Vet J 44 (4), 293-297 PubMed.
  • Capomolla S, Pozzoli M, Opasich C, Febo O, Riccardi G, Salvucci F et al (1997) Dobutamine and nitroprusside infusion in patients with severe congestive heart failure: hemodynamic improvement by discordant effects on mitral regurgitation, left atrial function, and ventricular function. Am Heart J 134 (6), 1089-1098 PubMed.
  • Tidolm A, Svensson H & Sylven C (1997) Survival and prognostic factors in 189 dogs with dilated cardiomyopathy. J Am Anim Hosp Assoc 33 (4), 364-368 PubMed.
  • Monnet E, Orton E C, Salman M & Boon J (1995) Idiopathic dilated cardiomyopathy in dogs: survival and prognostic indicators.  Vet Intern Med (1), 12-17 PubMed.

Otras fuentes de información

  • Small Animal Formulary (2002) Bryn Tennant. 4th Edn BSAVA. pp 211-212.
  • Kittleson M (2000) Therapy of heart failure. In: Textbook of Veterinary Internal Medicine.5th edn. Ed S J F E Ettinger. Philadelphia: WB Saunders Company. pp 713-737.
  • Sisson D & Kittleson M (1999) Management of Heart Failure: Principles of Treatment, Therapeutic Strategies, and Pharmacology. In: Textbook of Canine and Feline Cardiology: Principles and Clinical Practice.2nd edn. Eds P R Fox, D Sisson and N S Moise. Philadelphia: WB Saunders. pp 216-250.

 

Other Sources of Information