Getting to the heart of the matter: Heart disease and heart failure (Proceedings)
The most common causes are defective heart muscle, valvular disease, cardiac tamponade, electrical malfunction, heartworms or administration of drugs with profound cardiac effects. In any case, when heart failure results in circulatory collapse and inadequate tissue oxygenation, the patient is said to be in cardiogenic shock. The term "cardiogenic shock" describes a shock syndrome where cardiac output is reduced as a direct result of heart failure.
The most common causes are defective heart muscle, valvular disease, cardiac tamponade, electrical malfunction, heartworms or administration of drugs with profound cardiac effects. In any case, when heart failure results in circulatory collapse and inadequate tissue oxygenation, the patient is said to be in cardiogenic shock. The term "cardiogenic shock" describes a shock syndrome where cardiac output is reduced as a direct result of heart failure. Cardiac output is a function of heart rate and stroke volume. Stroke volume is determined by preload (circulating blood volume), afterload (the forces that impede ventricular ejection such as arterial vascular resistance and blood viscosity) and contractility. Therefore, abnormalities in any of these factors can result in diminished cardiac output. Understanding the specific processes of the common causes of heart failure is essential to successful management of ensuing cardiogenic shock.
Heart failure can result from a number of diseases/disorders. However, there are only two types of heart failure. Low output (forward) failure and left or right sided congestive (backward) heart failure (CHF). Low output failure results from an inability to pump blood forward from the left ventricle to the systemic circulation. This results in weak pulses, low blood pressure, depressed mentation, cold periphery, prolonged CRT, oliguria, muscle weakness, syncope and inadequate perfusion. Left sided CHF results in pulmonary edema, crackles, rales, hypoxemia, cough, dyspnea while right sided CHF results in hepatomegaly, jugular distention, ascites, body cavity effusions. Each of the following disorders causes one or more type of heart failure:
Dilated cardiomyopathy (DCM)
DCM is associated with generalized heart enlargement (cardiomegaly) and dilation of all cardiac chambers. Poor left ventricular contractility leads to reduced ejection of blood and subsequent low output failure. Atrial fibrillation or ventricular tachycardia with DCM is a common finding
DCM is common in large breed dogs especially Doberman pinchers and boxers and most commonly in young to middle aged dogs. DCM also occurs in cats but with much less frequently due to improved, taurine regulated diets. Any process that disturbs myocardial function and structure can result in DCM. Infection, toxins, metabolic and nutritional abnormalities, genetic and immunological mechanisms have all been implicated as possible causes.
Clinical signs include, pale mucous membranes, tachypnea, dyspnea, syncope, weakness and collapse. ECG shows atrial fibrillation or ventricular premature contractions. Pulse deficits are often present. Generalized cardiomegaly is apparent on radiographs. Echocardiography is useful in determining the extent of impaired contractility.
Therapy is aimed at improving cardiac contractility and stroke volume. It may include diuretics, positive inotropic drugs (dobutamine) or vasodilators (nitroprusside). Antiarrhythmic drugs may be indicated in some animals.
Hypertrophic cardiomyopathy (HCM)
HCM is associated with ventricular thickening and stiffening. Diastolic ventricular filling is impaired. Poor filling capacity results in CHF and forward failure. The left atrium becomes dilated in response and stagnation of blood occurs in the chamber.
HCM is most commonly found in cats. Hyperthyroidism is a common underlying disease. Cats with HCM often present with aortic saddle thrombus as a result of persistent atrial torture and the unique hyperactivity of feline platelets. Embolization of a left atrial thrombus results in occlusion at the aortic bifurcation causing ischemic injury to distal tissues.
Clinical signs include tachypnea, dyspnea, weakness, syncope, anorexia, depression and emesis.
Auscultation reveals a gallop rhythm, systolic murmur, pronounced heartbeat and tachycardia. Weak arterial pulses are evident on palpation.
Treatment involves administration of positive inotropes (Diltiazem in cats, dobutamine in dogs) to improve cardiac contractility. Diuretics are administered to reduce pulmonary edema. Cats with saddle thrombus may also be treated with anticoagulants (heparin).
Valvular disease is the most common cause of heart failure in dogs. It is rare in cats. Mitral disease is more common than tricuspid disease. Middle aged, small breed, male dogs show predisposition.
1. Mitral insufficiency and/or chordae tendineae rupture results in left sided congestive heart failure.
2. Triscupid insufficiency results in right-sided congestive heart failure.
Pericardial effusion and cardiac tamponade
Excessive accumulation of fluid in the pericardial sac results in compression of the thin-walled cardiac chambers (right atrium and ventricle) with subsequent compromised cardiac filling, decreased stroke volume (cardiac tamponade) and decreased cardiac output. Traumatic atrial tears in small dogs may cause pericardial effusion. The most common cause is right atrial hemangiosarcoma.
Initial clinical signs are of right-sided heart failure and include tachycardia, jugular venous distension, hepatomegaly, ascites, weakness, collapse and hypotension. Muffled heart sounds and weak, rapid peripheral pulses are apparent on clinical exam. Ultimately left sided and forward failure also occurs. Thoracic radiographs and cardiac ultrasound are the diagnostic tests of choice. ECG findings include low amplitude QRS complexes and electrical alternans.
Treatment involves pericardiocentesis to relieve effusion. Surgery to remove all or part of the pericardium may be indicated as a palliative measure.
Life threatening cardiac arrhythmias
Ectopic impulses arising in the ventricles result in premature complexes (VPCs). V-tach is a result of repetitive VPCs with a ventricular rate of > 140 BPM. V-tach results in hemodynamic compromise due to reduced cardiac output. Signs of forward failure are apparent. Progression to ventricular fibrillation results in sudden death. ECG findings include wide aberrant QRS and rapid regular rhythm. Treatment is by chemical conversion with Lidocaine or Procainamide. Mechanical defibrillation is recommended for V-fib.
A-Fib is characterized by rapid, chaotic, irregular atrial activity stemming from multiple ectopic foci. There is a rapid but irregular ventricular rate due to varying AV nodal conduction of atrial impulses. Diastolic filling is compromised due to rapid rate and cardiac output is reduced. Low output and congestive heart failure are likely. ECG findings include rapid irregular rhythm, normal QRS and absent P waves. Treatment is aimed at slowing AV conduction to allow more time for filling. Digitalis and Diltiazem (calcium channel blocker) are often used.
Extremely slow heart rate results in decreased cardiac output. ECG findings include extremely slow rate of <70 BPM. Treatment is to increase heart rate with atropine or epinephrine. Some patients may require pacemaker implantation.
Hyperkalemic cardiotoxicity (usually cats)
Elevated serum potassium disturbs cardiac muscle function. Most commonly occurs in blocked cats or Addisonian dogs. ECG findings include spiked T waves, prolonged P-R interval, absent P waves and bradycardia. Treatment is aimed at correcting hyperkalemia with IV Sodium chloride administration. Regular insulin and IV glucose may be used to increase movement of potassium intracellularly.
Treatment for cardiac cases
Fluid therapy options are limited by the heart's inability to handle even normal fluid loads (see fluid therapy paper). Initial resuscitation from cardiovascular collapse may be best achieved by administration of hypertonic saline and/or colloids rather than crystalloids. This allows administration of minimal fluid volume while improving circulating blood volume by rescuing interstitial fluid. Sodium poor fluids (.45% NaCl) are often used for supportive therapy.
Treatment is geared towards identifying and correcting the specific cardiac abnormality. This often involves administration of inotropic, vasoactive, diuretic and/or antiarrhythmic drugs. Oxygen supplementation is provided in nearly all cases. Central venous pressure and arterial blood pressure are monitored continually. Assessments of perfusion and oxygenation are made at frequent intervals.
Oxygen Supplementation is often indicated to decrease the work of breathing until patients can be stabilized
Diuretics: Typically Lasix or Spironolactone are used to reduce preload and relieve pulmonary edema
Positive inotropes such as Dobutamine, Dopamine, Digoxin or Milrinone are used to improve myocardial contractility in diseases such as dilated cardiomyopathy
Negative inotropes such as betablockers (the "olols") and calcium channel blockers (the 'azems") are used to decrease myocardial contractility in diseases such as Hypertrophic Cardiomyopathy
Vasodilators can be used to effect the veins (nitroglycerine), arteries (hydralazine) or both (nitroprusside, the "prils") and function to decrease vascular resistance and systemic blood pressure.
Inodilators such as Pimopendan provide both vasodilation and positive inotropic activity and are used as adjunct therapy in many heart failure cases.