Issues

Congestive Heart Failure, Left-Sided

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

 

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

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

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!

 

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

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.

 

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.

 

ABBREVIATIONS

ACE = angiotensin converting enzyme

AV = atrioventricular

DCM = dilated cardiomyopathy

ECG = electrocardiogram

L-CHF = left-sided congestive heart failure

PDA = patent ductus arteriosus