Acute heart failure (Decompensated heart failure, acute decompensation)

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• 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.

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

• Most are adult cats suffering from cardiomyopathy, either hypertrophic  or restrictive .
• Young cats with large left to right shunting lesions, (ie ventricular septal defects ) or with atrioventricular valve dysplasia  may present with decompensated heart failure.

• Hypertrophic cardiomyopathy (HCM) : certain breeds are predisposed including:
  • Maine Coon .
  • American Shorthairs .
  • Persians .
• In addition, many cats with DCM are domestic short or longhairs.
• No breed predilections have been recognized in cats with restrictive cardiomyopathy (RCM) .

• 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.

• 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 and stress.

• Etiologies behind development of feline HCM and RCM are not totally understood.
• A mutation in the myosin binding protein-C gene has been associated with HCM in a family of Maine Coons.
• Nutritional taurine deficiency  is well-described cause of feline myocardial failure (dilated cardiomyopathy). Adequate dietary taurine supplementation found in virtually all cat foods has greatly reduced the incidence this disease. Currently, the occasional cases of feline DCM that are detected are usually not taurine related, do not respond to supplementation, and are idiopathic with respect to etiology.

• Following the initial cardiac insult 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.
• Feline cardiomyopathies (HCM, RCM) are primarily diseases of diastolic dysfunction, in which concentric hypertrophy or myocardial fibrosis limits the ability of the heart to relax during diastole.
• Feline dilated cardiomyopathy (DCM ) is similar in pathophysiology to canine DCM, in which there is progressive loss of systolic function.
• Ultimately pulmonary capillary pressures rise promoting the development of pulmonary edema , pleural effusion , or ascites (rare in cats) while pronounced increase in afterload diminishes effective forward blood and increases myocardial oxygen demands.

• 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.
• Predisposing factors that may quickly shift a patient with compensated heart failure to a decompensated state include:
  • The development of arrhythmias , especially atrial fibrillation .
  • Abrupt discontinuation of prescribed medications.
  • Stress.
  • Corticosteroid administration.

• Sudden onset of respiratory distress.
• Restlessness often at night.
• Profound weakness and lethargy.
• Poor appetite.
• Hiding.
• Syncope.
• Coughing is extremely rare.
• May have undergone a recent stressful situation.
• May have history of cardiovascular disease.

• 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 :
    • Systolic, parasternal murmur common in cases of hypertrophic obstructive cardiomyopathy or right ventricular tract outflow obstruction.
  • Arrhythmias :
    • Sinus tachycardia.
    • Supraventricular premature complexes .
    • Ventricular arrhythmias.
    • Atrial fibrillation (rare as compared to dogs with advanced heart disease).
  • Gallops:
    • S4 gallop may be ausculted.

• May have decreased femoral pulse quality.
• 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.
• Ascites is relatively uncommon as compared to dogs with advanced heart disease.

• 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 :   
  • 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 may necessitate efforts to control the ventricular rate.
  • Significant ventricular arrhythmias (ie hemodynamically significant) may necessitate efforts to suppress them.
  • Continuous, telemetric ECG monitoring  is occasionally performed.
• Thoracic radiographs :   
  • 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:
  • Cardiac enlargement pattern.
  • Lateral: widened cardiac silhouette, dorsal displacement of the trachea .
  • DV: basilar widening of the cardiac silhouette representing atrial enlargement ("valentine" shaped heart) .
     The DV projection is typically more sensitive for cardiac enlargement than the lateral projection.

• The left atrial enlargement pattern that is commonly identified in dogs as loss of the caudal cardiac waist on the lateral projection is not a sensitive means to detect atrial enlargement in cats. Hence, the DV projection is preferred.
• Distribution of pulmonary edema is variable in the cat. Patchy, focal, diffuse, or unilateral pulmonary interstitial or alveolar patterns can be present.
• Hallmarks of pleural effusion  :
  • Fissure lines.
  • Severe cases may obscure pulmonary parenchyma and cardiac silhouette.
• Echocardiography :  
  • Abbreviated examination can be performed standing to identify underlying disease condition.
  • Assess myocardial wall thickness, systolic function, valvular integrity, and degree of atrial enlargement.
  • Identify pleural  or pericardial effusion .
  • Identify ascites and hepatic venous congestion if the abdomen is imaged.
• Thoracocentesis :  
  • High degree of suspicion for pleural effusion   thoracocentesis serves as a diagnostic and therapeutic modality.
  • Serum or plasma taurine level measurement in patients diagnosed with DCM.

• Left-sided congestive heart failure is documented radiographically, and in the cat, can present as pulmonary edema and/or pleural effusion.
• Not all alveolar or interstitial lung patterns represent cardiogenic pulmonary edema.
  • Hallmarks of cardiogenic pulmonary edema.
    • Left atrial enlargement.
    • Pulmonary venous congestion.
    • Variable distribution of alveolar or intersitial parenchymal pattern.
• Echocardiography can define the underlying cardiac disease process but cannot easily confirm the presence of pulmonary edema.
• Right-sided congestive heart failure:
  • Presence of pleural effusion or ascites (rare).
  • Positive hepato-jugular reflex.
  • Elevated systemic venous pressures measured by CVP  or cardiac catheterization.

• Severe heart failure:
  • Congestion:
    • Lungs: fulminant congestion with froth/edema extending into large airways.
    • Ascites or pleural effusion.
    • Hepatomegaly, hepatic congestion.
    • Caudal vena caval distension.
  • HCM: left ventricular concentric hypertrophy and left atrial enlargement, the anterior mitral valve leaflets may be thickened . 
  • RCM: left atrial enlargement, endomyocardial fibrosis.

• HCM: myocyte hypertrophy, myocardial fiber disarray, myocardial necrosis and fibrosis, dystrophic mineralization, coronary arteriosclerosis.
• RCM: endocardial fibrosis, myocyte necrosis and fibrosis.

• Respiratory distress:
  • Pneumonia .
  • Pulmonary thromboembolism .
  • Pneumothorax .
  • Non-cardiogenic pleural effusion or alveolar infiltration, eg hemothorax, chylothorax .
  • Diaphragmatic hernia .
  • Neoplasia .
  • Coagulopathies .

Emergency treatment of severe heart failure due to HCM or RCM  

• Furosemide .
  • Intravenous administration of 1-2 mg/kg, q1-4 h.
  • 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.
  • Oxygen cage.
  • Nasal insufflation.
  • Face mask.
     May promote agitation.
• Glyceryl trinitrate :
  • 4-6 mm applied topically to the skin q6-8 h.
  • Systemic vasodilator used in short term management of pulmonary edema (especially if acute) and to reduce ventricular filling pressures. 
     Unproven efficacy.
• Thoracocentesis /abdominocentesis  if large volumes of effusion are present.
• Specific treatment of severe (ie hemodynamically significant) arrhythmias is difficult in the cat. Many cases will respond favorably to resolution of heart failure and supplemental oxygen .
  • Lidocaine : 1 mg boluses IV, up to 1 mg/kg total dose. For life-threatening ventricular arrhythmias.
     May cause seizures.
  • Esmolol : 50-200 µg/kg/min IV for life-threatening ventricular or supraventricular arrhythmias.

Emergency treatment of severe heart failure due to DCM  

• Furosemide, oxygen therapy, and glyceryl trinitrate as above.
• Positive inotropic support:
  • Dobutamine : 2-10 µg/kg/min IV. Cats may develop seizures and require close monitoring and possible reduction of dosage.
  • Dopamine : 2-5 µg/kg/min IV. High doses may elicit unwanted vasoconstriction, tachycardia, and arrhythmias.

• Baseline complete blood count , biochemical profile , and urinalysis.
• Respiratory rate hourly.
• Attitude and activity hourly.
   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. Otherwise hourly.
• Assessment of urine production.
• Renal values and electrolytes daily during aggressive therapy.
• Appetite.
• Thoracic radiographs  prior to discharge.

• 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.
  • Vasodilator: ACE inhibitors .
  • Heart rate control: beta-blocker or calcium channel blocker.
  • Refractory heart failure requires tailored therapy with additional diuretics.
  • Antithrombotic agents: aspirin, warfarin, heparin, clopidogrel
  • Taurine supplementation (DCM) .

• Re-evaluate 5-7 days after discharge:
  • Renal profile including electrolytes.
  • Heart rate and rhythm.
  • Thoracic radiographs.
  • Owner assessment:
    • Respiratory rate and effort at rest.
    • Appetite.
    • Strength and activity.
    • 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 3-6 months.
  • Periodic re-evaluation of renal values, electrolyte status and serum digoxin level.

• Guarded at time of acute presentation but long-term prognosis depends on response to therapy. Aggressive therapy has potential to save cats that were only minutes from dying.
• Cats already intensively managed with numerous cardiovascular drugs that remain decompensated have a worse prognosis.

• As heart failure resolves patients often progress from orthopneic   resting sternally  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.

• Underlying cardiovascular disease was end stage.
• Therapy was not aggressive enough.
• Concurrent medical condition (ie renal failure).
• Respiratory distress was unrelated to cardiovascular disease.

• Recent references from PubMed.
• Schober K E, Maerz I (2006) Assessment of left atrial appendage flow velocity and its relation to spontaneous echocardiographic contrast in 89 cats with myocardial disease. J Vet Intern Med 20(1), 120-130.
• Cesta M F, Baty C J, Keene B W et al (2005) Pathology of end-stage remodeling in a family of cats with hypertrophic cardiomyopathy. Vet Pathol 42(4), 458-467 PubMed.
• Cote E, Manning A M, Emerson D et al (2004) Assessment of the prevalence of heart murmurs in overtly healthy cats. JAVMA 225(3), 384-388 PubMed.
• Pion P D (2004) Traditional and nontraditional effective and noneffective therapies for cardiac disease in dogs and cats. Vet Clin North Am Small Anim Pract 34(1), 187-216 PubMed.
• Baty C J (2004) Feline hypertrophic cardiomyopathy: an update. Vet Clin North Am Small Anim Pract 34(5), 1227-1234 PubMed.
• Rush J E, Freeman L M, Fenollosa N K, Brown D J (2002) Population and survival characteristics of cats with hypertrophic cardiomyopathy: 260 cases (1990-1999). JAVMA 220(2), 202-207 PubMed.

• Bryn Tennant Small Animal Formulary (2002) 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.

• Barret J Bulmer DVM DACVIM-Cardiology, Assistant Professor, Kansas State University College of Veterinary Medicine, Manhattan, Kansas, USA.
• Josephine Dandrieux BVM&S MRCVS, Department of Veterinary Clinical Studies, University of Glasgow Veterinary School, Bearsden Road, Bearsden, Glasgow, G61 1QH, UK.
• Mark A Oyama DVM DACVIM-Cardiology, Associate Professor, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.

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