Overview of Heart Disease

While most animals with heart disease do not develop heart failure, disease progression can result in significant morbidity and mortality in affected animals. The distinction between heart disease and heart failure is important and is often challenging to reconcile.

Heart failure is a syndrome and therefore is not a single disease. As such, heart failure can be associated with a wide range of structural or functional disorders with neurohormonal, hemodynamic, renal, and clinical outcomes.

Terminology is important and can help distinguish between stages or states of disease.

1.  Congestive heart failure refers to patients who have developed lung congestion (pulmonary edema), effusions (ascites, pericardial effusion, pleural effusion), or both, from cardiac disease.

2.  Acute heart failure defines the onset of clinical signs in a patient with no prior history of heart failure.

3.  Acute decompensated heart failure represents new or worsening clinical signs of dyspnea, shortness of breath, or edema.

4.  Diastolic heart failure refers to development of pulmonary edema associated with left ventricular diastolic dysfunction (as occurs commonly in cats with hypertrophic cardiomyopathy).

5.  Preserved left ventricular systolic function is usually inferred unless otherwise specified (as with dilated cardiomyopathy).

6.  Compensated heart failure refers to patients with substantial heart disease whose congestive signs have been controlled or abolished by cardiac therapy.

Several classification schemes have been proposed to characterize progressive cardiac severity, and rely upon a combination of clinical signs or disease characteristics. These schemes help frame a clinical context for managing heart disease.

The modified New York Heart Association functional classification of heart failure describes four classes: Class I included dogs with asymptomatic heart disease without clinical signs. Class II includes dogs with heart disease who show clinical signs with marked physical exertion. Class III includes heart disease patients who have clinical signs with routine activity, and Class IV includes patients with severe heart disease resulting in clinical signs at rest. A more recently developed system, the ISACHC (International Small Animal Cardiac Health Council) characterizes heart failure using three stages. Stage I refer to the patient without signs (Ia, heart disease is detected, but no cardiac enlargement is present; Ib, cardiac enlargement is present but without clinical signs). Stage II refers to advanced heart disease with either mild heart failure, or where heart failure has been controlled with cardiac therapy. Stage III refers to advanced heart failure with clinical signs including respiratory distress, marked ascites, and profound exercise intolerance. A newer classification scheme has been adapted from guidelines from the American College of Cardiology/American Heart Association, and modified for use in dogs (see: Guidelines for the diagnosis and treatment of canine chronic valvular heart disease. Atkins C, Bonagura J, Ettinger S, Fox P, Gordon S, Haggstrom J, Hamlin R, Keene B, Luis-Fuentes V, Stepien R. J Vet Intern Med. 2009 Nov–Dec;23(6):1142–1150). This relates the severity of clinical signs, stage of heart disease, and treatments, using four stages of heart disease and failure: Stage A includes dogs at high risk to develop heart disease, but without structural disease. Stage B includes dogs with structural abnormalities who have not progressed to CHF (B1 includes asymptomatic dogs without structural changes, and B2 includes asymptomatic dogs with radiographic or echocardiographic evidence of cardiomegaly). Stage C refers to dogs with past or current clinical signs of CHF, while Stage D denotes patients with end-stage CHF, refractory to therapy.

Acute CHF

Clinical signs are ultimately associated with acute pulmonary edema due to mitral regurgitation and associated elevated left ventricular filling pressures. Goals of therapy include rapid resolution of pulmonary edema through preload and afterload reduction. Intravenous furosemide boluses (2 to 4 mg per kg) produce brisk and rapid diuresis and natriuresis. Repeated boluses are given, or furosemide is changed to continuous infusion (0.35 to 0.75 mg/kg/h) as needed. Nonresponsiveness associated with escalating diuretic dose is usually associated with poor outcome. Aggressive use of loop diuretics can decrease renal perfusion and promote renal dysfunction (acute kidney injury) and electrolyte abnormalities including hypokalemia and hypochloremia. Addition of vasodilators to reduce afterload may be critically important in advanced cases. Constant infusion of sodium nitroprusside (2–15 mcg/kg/min IV) can act to reduce preload and afterload, thereby promoting forward cardiac flow and reducing myocardial oxygen demand. Alternatively, hydralazine can be used as an afterload reducer (1 to 2 mg per kilogram orally q12h). In some patients who cannot be hospitalized, hydralazine can be given using 0.5 mg per kilogram doses administered every hour for 3 to 4 hours, coupled with hourly IV furosemide bolus. Pimobendan should be administered, 0.2 to 0.3 mg per kilogram q12h. Short-term inotropic infusion using dobutamine (5–15 mcg/kg/min) may be necessary in dogs with severe systolic dysfunction in order to improve hemodynamics. Administration of an ACE inhibitor (enalapril, 0.5 mg/kg q12h) may help blunt neurohumoral activation, but should be used with caution if renal failure is present.

The use of supplemental oxygen is recommended in patients with pulmonary edema and hypoxia. Addition of spironolactone (1 mg/kg q12–24h) has gained popularity for its action to block actions of aldosterone. Attention must be devoted to control important brady- and tachyarrhythmias. Patients with atrial fibrillation generally present with rapid ventricular heart rates. Resting ventricular response to atrial fibrillation > 160 beats per minute can substantially reduce cardiac filling and function, and efforts should be directed to reduce this heart rate. Calcium channel-blocking agents such as diltiazem hydrochloride (0.5–1.5 mg/kg q8h) or Dilacor (1.5–4 mg/kg q12h) are first-line agents to reduce the ventricular response to atrial fibrillation. Digoxin (0.0025–0.005 mg/kg q12h) with a target concentration 8 hours post pill of 0.8–1.5 ng/ml, may be added for cases of persistent rapid atrial fibrillation, if renal function is normal. Electrically or hemodynamically unstable ventricular arrhythmia is managed by lidocaine (2–8 mg/kg using 2 mg/kg IV boluses, followed by 40–80 mcg/kg/min CRI). It is important to monitor systemic blood pressure, renal function, electrolyte status, and ECG.

Refractory CHF

With recurrent heart failure, upward drug titration may be necessary. Amlodipine can be added for afterload reduction, 0.1–0.4 mg/kg q12h through judicious titration. Sildenafil (1–2 mg/kg q8–12h) is used to treat advanced CHF complicated by pulmonary hypertension. Addition of hydrochlorothiazide (0.5–1 mg/kg every 2nd or 3rd day) is reserved for refractory heart failure. Beta-blocker therapy should not generally be initiated during acute CHF, unless ultrashort acting agents (esmolol) are required to control tachycardia. Dietary management is important to reduce sources of excess sodium. It is prudent to assess BUN, creatinine, electrolytes and blood pressure during chronic therapy.

Cardiogenic Shock

Myocardial failure is most commonly associated with dilated cardiomyopathy. Less frequent etiologies include chronic volume overload (e.g., mitral regurgitation, left-to-right shunts) or sepsis. The principal hemodynamic feature of cardiogenic shock is systemic hypotension associated with reduced ventricular pumping (i.e., myocardial failure/systolic dysfunction). Pulmonary edema, systemic congestion, hypotension, and tissue hypoxia result. Acute management may require inotropes (dobutamine CRI), diuretics to reduce congestion, vasodilators such as sodium nitroprusside. ACEI, digoxin, pimobendan, and control of sepsis and arrhythmias.

Cardiac Tamponade (Ventricular Underfilling)

Conditions which interfere with return of blood to the heart may result in decreased cardiac preload, compensatory neuroendocrine activation, and a clinical condition known as cardiac tamponade. This is generally associated with pericardial disease (typically neoplasia in dogs; or FIP or idiopathic effusions in cats). Less common causes include space-occupying atrial or ventricular masses including blood clots or tumors. Initial management requires therapeutic pericardiocentesis. Avoid using drugs that decrease preload or cause vasodilation.

Hemodynamically Unstable Arrhythmias

Tachyarrhythmias may depress cardiac output, cause hemodynamic impairment or hypotension, and result in organ ischemia. Shortened diastolic filling decreases coronary blood flow, reduces myocardial oxygen supply, causes ischemia and results in more serious arrhythmias. Certain tachyarrhythmias may deteriorate by becoming electrically unstable.

Hemodynamic impact of tachyarrhythmias are influenced by factors related to underlying cardiac disease and the particular type of arrhythmia - i.e., (a) loss of synchronized atrial systole, (b) altered ventricular activation sequence, (c) rapidity of ventricular rate, (d) timing of ectopic beats relative to preceding P-QRS-T complexes, (e) background vasomotor tone, (f) cardiac effects of antiarrhythmic drugs, and (g) underlying cardiac dysfunction or health. Because cardiac output = heart rate x stroke volume, sustained tachycardia may reduce cardiac output and atrial blood pressure.

In atrial fibrillation with rapid ventricular response, ventricular filling shortens due to loss of atrial contraction, variation in cycle length and high ventricular rate. This is worsened by concurrent myocardial dysfunction (e.g., dilated cardiomyopathy) or exercise. Impulses originating in the ventricle (e.g., ventricular tachycardia) alter patterns of electrical activation and reduce stroke volume. Rapid, sustained ventricular tachycardia decreases cardiac output, results in hypotension and organ ischemia. Ventricular flutter causes precipitous deterioration, and all circulation ceases with ventricular fibrillation. Short paroxysms of atrial tach with normal ventricular activation may not cause clinical consequences; multifocal atrial or ventricular tachycardia is more likely to compromise hemodynamics, especially if ventricular function is abnormal. Electrical instability is increased by rapid ventricular rates and multifocal impulse origination. Additional factors include timing of the ectopic impulse (i.e., the earlier the premature complex relative to the preceding T wave, the greater electrical liability). Depolarizations occurring within the preceding T wave are extremely dangerous. The underlying state of ventricular function, systemic and metabolic alterations, and concurrent drug or anesthetic agents influence electrical stability. Electrical instability is increased by rapid ventricular rates and multifocal impulse origination.

Additional factors include timing of the ectopic impulse (i.e., the earlier the premature complex relative to the preceding T wave, the greater electrical liability). Depolarizations occurring within the preceding T wave are dangerous. The underlying ventricular function, systemic and metabolic alterations, and concurrent drug or anesthetic agents influence electrical stability. Tachycardia = ventricular rate > 240 bpm in cats; > 180 bpm in small-breed dogs; > 160 bpm in large breeds, and > 220 bpm in puppies. With supraventricular tachycardias, vagal maneuvers may occasionally convert the arrhythmia. Supraventricular arrhythmias may be treated with digitalis glycosides, calcium channel blockers, beta blockers, and other agents. Acute management of ventricular tachycardia includes treatment of the underlying cause and lidocaine. Pacemaker implantation may be required to treat high grade AV block.

References

1.  Atkins C, Bonagura J, Ettinger S, et al. Guidelines for the diagnosis and treatment of canine chronic valvular heart disease. J Vet Intern Med. 2009;23(6):1142–1150.

2.  Kraus MS, Rassnick KM, Wakshlag JJ, Gelzer AR, Waxman AS, Struble AM, Refsal K. Relation of vitamin D status to congestive heart failure and cardiovascular events in dogs. J Vet Intern Med. 2014;28(1):109–115.

3.  Häggström J, Lord PF, Höglund K, Ljungvall I, Jöns O, Kvart C, Hansson K. Short-term hemodynamic and neuroendocrine effects of pimobendan and benazepril in dogs with myxomatous mitral valve disease and congestive heart failure. J Vet Intern Med. 2013;27(6):1452–1462.

4.  Cunningham SM, Rush JE, Freeman LM. Short-term effects of atorvastatin in normal dogs and dogs with congestive heart failure due to myxomatous mitral valve disease. J Vet Intern Med. 2013;27(4):985–989.

5.  Ferasin L, Crews L, Biller DS, Lamb KE, Borgarelli M. Risk factors for coughing in dogs with naturally acquired myxomatous mitral valve disease. J Vet Intern Med. 2013;27(2):286–292.

6.  Wolf J, Gerlach N, Weber K, Klima A, Wess G. Lowered N-terminal pro-B-type natriuretic peptide levels in response to treatment predict survival in dogs with symptomatic mitral valve disease. J Vet Cardiol. 2012;14(3):399–408.