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Basics

Basics

Definition

Failure of the left side of the heart to advance blood at a sufficient rate to meet the metabolic needs of the patient or to prevent blood from pooling within the pulmonary venous circulation.

Pathophysiology

  • Low cardiac output causes lethargy, exercise intolerance, syncope, and prerenal azotemia.
  • High hydrostatic pulmonary venous pressure causes leakage of fluid from pulmonary venous circulation into pulmonary interstitium and alveoli. When fluid leakage exceeds ability of lymphatics to drain the affected areas, pulmonary edema develops.

Systems Affected

  • All organ systems can be affected by poor perfusion.
  • Respiratory increased rate and effort because of edema.
  • Cardiovascular.

Genetics

Some congenital heart defects, cardiomyopathies, and valvular heart disease have a genetic basis in some breeds.

Incidence/Prevalence

Common

Geographic Distribution

Seen everywhere, but prevalence of causes varies with location.

Signalment

Species

Dog and cat

Breed Predilections

Varies with cause

Mean Age and Range

Varies with cause

Predominant Sex

Varies with cause

Signs

General Comments

Signs vary with underlying cause and species.

Historical Findings

  • Weakness, lethargy, exercise intolerance.
  • Coughing (dogs) and dyspnea (increased respiratory rate and effort); respiratory signs often worsen at night and can be partially relieved by assuming a standing, sternal, or “elbows abducted” position (orthopnea).
  • Cats rarely cough from heart failure, and a client complaint of coughing should prompt a search for primary airway disease.

Physical Examination Findings

  • Tachypnea.
  • Coughing, often soft in conjunction with tachypnea (dogs).
  • Dyspnea and tachypnea.
  • Pulmonary crackles and wheezes.
  • Pale/gray/cyanotic mucous membranes.
  • Prolonged capillary refill time.
  • Possible murmur or gallop.
  • Weak femoral pulses.

Causes

Pump (Muscle) Failure of Left Ventricle

  • DCM
  • Trypanosomiasis (rare)
  • Doxorubicin cardiotoxicity (dogs)
  • Hypothyroidism (rare)
  • Hyperthyroidism (rarely causes pump failure; more commonly causes high output failure)
  • Pacing-induced cardiomyopathy (muscle failure caused by persistent pathologic supraventricular or ventricular tachyarrhythmia)

Pressure Overload of Left Heart

  • Systemic hypertension (uncommon cause of heart failure in animals)
  • Subaortic stenosis
  • Coarctation of the aorta (rare; Airedales predisposed)
  • Left ventricular tumors (rare)

Volume Overload of Left Heart

  • Mitral valve endocardiosis (dogs)
  • Mitral valve dysplasia (cats and dogs)
  • PDA (dogs)
  • Ventricular septal defect
  • Aortic valve insufficiency secondary to endocarditis (dogs)

Impediment to Filling of Left Heart

  • Pericardial effusion with tamponade
  • Restrictive pericarditis
  • Restrictive cardiomyopathy
  • Hypertrophic cardiomyopathy
  • Left atrial masses (e.g., tumors and thrombus)
  • Pulmonary thromboembolism
  • Mitral stenosis (rare)
  • Cor triatriatum sinister (cats, rare)

Rhythm Disturbances

  • Bradycardia (high-grade AV block)
  • Tachycardia (e.g., atrial fibrillation, sustained supraventricular tachycardia, and ventricular tachycardia; see pacing-induced cardiomyopathy under pump failure)

Risk Factors

Conditions causing chronic high cardiac output (e.g., hyperthyroidism and anemia).

Diagnosis

Diagnosis

Differential Diagnosis

Must differentiate from other causes of coughing, dyspnea, and weakness.

CBC/Biochemistry/Urinalysis

  • CBC usually normal; maybe stress leukogram.
  • Mild-to-moderate liver enzyme elevation; bilirubin generally normal.
  • Prerenal azotemia in some animals.

Other Laboratory Tests

  • Thyroid disorders may be detected.
  • Serum NT-proBNP and troponin I concentrations are higher in animals with L-CHF than in normal animals.

Imaging

Radiographic Findings

  • Left heart and pulmonary veins enlarged.
  • Pulmonary edema, often hilar, especially involving the right caudal lung lobe in acute edema of dog, but may be patchy, especially in cats; acute pulmonary edema may begin in right caudal lung lobe.

Echocardiography

  • Findings vary markedly with cause, but left atrial enlargement a relatively consistent finding in cardiogenic pulmonary edema.
  • Diagnostic test of choice for documenting congenital defects, cardiac masses, and pericardial effusion.

Diagnostic Procedures

Electrocardiographic Findings

  • Atrial or ventricular arrhythmias.
  • Evidence of left heart enlargement (e.g., wide P waves, tall and wide QRS complexes, and left axis orientation).
  • May be normal.

Pathologic Findings

Cardiac findings vary with disease.

Treatment

Treatment

Appropriate Health Care

  • Usually treat as outpatient unless animal is dyspneic or severely hypotensive.
  • Identify and correct underlying cause whenever possible.
  • Minimize handling of critically dyspneic animals. Stress can kill&excl

Nursing Care

Oxygen in dyspneic patients.

Activity

Restrict activity when dyspneic or tachypneic.

Diet

Initiate moderately sodium-restricted diet. Severe sodium restriction is indicated in animals with advanced disease.

Client Education

With few exceptions (e.g., animals with thyroid disorders, arrhythmias, nutritionally responsive heart disease), left congestive heart failure is not curable.

Surgical Considerations

  • Surgical intervention, coil embolization, Amplatz occluder placement or balloon valvuloplasty may benefit selected patients with some forms of congenital and acquired valvular heart disease. Response to these interventions varies.
  • Pericardiocentesis in animals with pericardial effusion.

Medications

Medications

Drug(s) Of Choice

Diuretics

  • Furosemide (1–2 mg/kg q8–24h) or other loop diuretic is the initial diuretic of choice; diuretics are indicated to reduce preload and remove pulmonary edema. Critically dyspneic animals often require high doses (4–8 mg/kg) given IV to stabilize; this dose can be repeated in 1 hour if animal is still severely dyspneic. An IV bolus of 0.66 mg/kg followed by a CRI of 0.66–1 mg/kg/h for 1–4 hours causes greater diuresis than an equal dose divided into two IV boluses given 4 hours apart. Once edema resolves, taper to the lowest effective dosage.
  • Spironolactone (0.5–2 mg/kg PO q12–24h) increases survival in humans with CHF and is in current clinical trials in dogs. Use in combination with furosemide.
  • Thiazide diuretics can be added to furosemide and spironolactone in refractory heart failure cases.
  • Torsemide may be useful as a substitute for furosemide in animals requiring chronic furosemide dosing in excess of 12 mg/kg (total daily dose).

ACE Inhibitors

  • ACE inhibitor such as enalapril (0.5 mg/kg q12–24h) or benazepril (0.25–0.5 mg/kg q24h) indicated in most animals with L-CHF.
  • ACE inhibitors improve survival and quality of life in dogs with L-CHF secondary to degenerative valve disease and DCM.

Positive Inotropes

  • Pimobendan (0.25–0.3 mg/kg PO q12h) is a calcium channel sensitizer that dilates arteries and increases myocardial contractility. First-line agent in treating DCM or CHF due to chronic valve disease. Efficacy in cats with CHF is not known, but possibly beneficial.
  • Dobutamine (dogs, 2.5–10 µg/kg/minute; cats, 0.5–5 µg/kg/minute) is a potent positive inotropic agent that may provide valuable short-term support of a heart failure patient with poor cardiac contractility.
  • Positive inotropes in general are potentially arrhythmogenic, monitor carefully.

Venodilators

  • Nitroglycerin ointment (one-fourth inch/5 kg q6–8h) causes venodilation, lowering left atrial filling pressures.
  • Used for acute stabilization of patients with severe pulmonary edema and dyspnea.
  • May be useful in animals with chronic L-CHF; to avoid tolerance, use intermittently and with 12-hour dose-free interval between the last dose of 1 day and the first dose of the next.

Antiarrhythmic Agents

Treat arrhythmias if clinically indicated.

Contraindications

Avoid vasodilators in patients with pericardial effusion or fixed outflow obstruction.

Precautions

  • ACE inhibitor and arterial dilators must be used with caution in patients with possible outflow obstruction.
  • Pulmonary hypertension, hypothyroidism and hypoxia increase risk for digoxin toxicity; hyperthyroidism diminishes effects of digoxin.
  • ACE inhibitor and digoxin-use cautiously in patients with renal disease.
  • Dobutamine-use cautiously in cats.
  • Spironolactone-may cause facial pruritis in cats.

Possible Interactions

  • Combination of high-dose diuretics and ACE inhibitor may cause azotemia, especially in animals with severe sodium restriction.
  • Combination diuretic therapy adds to risk of dehydration and electrolyte disturbances.
  • Combination vasodilator therapy predisposes animal to hypotension.

Alternative Drug(s)

Arterial Dilators

  • Hydralazine (0.5–2 mg/kg PO q12h; 0.5 mg/kg PO to start when added to ACEI) or amlodipine (0.05–0.2 mg/kg PO q24h) can be substituted for an ACE inhibitor in patients that do not tolerate the drug or have advanced renal failure. Monitor for hypotension and tachycardia; can be cautiously added to an ACE inhibitor in animals with refractory L-CHF.
  • Nitroprusside (1–10 µg/kg/minute) is a potent arterial dilator that is usually reserved for short-term support of patients with life-threatening edema.

Digoxin

  • Digoxin (dogs, 0.22 mg/m2 q12h; cats, 0.01 mg/kg q48h) is used in animals with atrial fibrillation and myocardial failure (e.g., dilated cardiomyopathy). Commonly used in combination with diltiazem to control the rate of atrial fibrillation.
  • Digoxin is also indicated to treat dogs with refractory heart failure from either myocardial failure or volume loads. However, its use as a primary agent in myocardial failure has been replaced by pimobendan.
  • In humans, digoxin has no effect on mortality but decreases hospitalization due to heart failure.

Calcium Channel Blockers

  • Diltiazem (0.5–1.5 mg/kg PO q8h) is frequently used in L-CHF patients for rate control in animals with supraventricular arrhythmias not controlled by digoxin and in cats with hypertrophic cardiomyopathy.

Beta-Blockers

  • Atenolol and metoprolol are used for rate control in animals with supraventricular tachycardia, hypertrophic cardiomyopathy, and hyperthyroidism.
  • Used alone or with a class 1 antiarrhythmic drug for control of ventricular arrhythmias; these drugs depress contractility (negative inotropes), so use cautiously in patients with myocardial failure or active signs of CHF.
  • On basis of human studies, may enhance survival in animals with idiopathic DCM; treatment is best initiated under the guidance of a cardiologist, starting with very low dosage and gradually increasing the dosage. Carvedilol is sometimes used for this purpose, starting at 0.1 mg/kg q24h and titrating to 0.5 mg/kg q12h.

Nutritional Supplements

  • Potassium and magnesium supplementation if deficiency is documented; use potassium supplements cautiously in animals receiving an ACE inhibitor or spironolactone.
  • Taurine supplementation in cats with DCM and dogs with DCM and taurine deficiency (e.g., American cocker spaniels)
  • L-carnitine supplementation may help some dogs with DCM.
  • Coenzyme Q10 is of potential value based on the results in humans with DCM.

Follow-Up

Follow-Up

Patient Monitoring

  • Monitor renal status, electrolytes, hydration, respiratory rate and effort, heart rate, body weight, and abdominal girth (dogs).
  • If azotemia develops, reduce the dosage of diuretic. If azotemia persists and the animal is also on an ACE inhibitor, reduce or discontinue the ACE inhibitor. Use digoxin with caution if azotemia develops.
  • Monitor ECG if arrhythmias are suspected.
  • Check digoxin concentration periodically. Recommended range is 0.5–1.5 ng/mL, 8–10 hours after a dose.

Prevention/Avoidance

  • Minimize stress, exercise, and sodium intake in patients with heart disease.
  • Prescribing an ACE inhibitor early in the course of heart disease in patients with DCM may slow the progression of heart disease and delay onset of CHF. Their role in asymptomatic animals with mitral valve disease remains controversial. Pimobendan delays the onset of CHF in Doberman pinschers, and in dogs with hemodynamically significant mitral valve regurgitation.

Possible Complications

  • Syncope
  • Aortic thromboembolism (cats)
  • Arrhythmias
  • Electrolyte imbalances
  • Digoxin toxicity
  • Azotemia and renal failure

Expected Course and Prognosis

Prognosis varies with underlying cause; cats and dogs that survive their initial episode of pulmonary edema and can be reliably medicated often survive months to more than a year with a good quality of life.

Miscellaneous

Miscellaneous

Age-Related Factors

  • Congenital causes seen in young animals.
  • Degenerative heart conditions and neoplasia generally seen in old animals.

See Also

  • Pulmonary Edema, Non-cardiogenic

Abbreviations

  • ACE = angiotensin converting enzyme
  • AV = atrioventricular
  • DCM = dilated cardiomyopathy
  • ECG = electrocardiogram
  • L-CHF = left-sided congestive heart failure
  • PDA = patent ductus arteriosus

Authors Francis W.K. Smith, Jr. and Bruce W. Keene

Client Education Handout Available Online