When evaluating patients, it is important to distinguish heart disease from heart failure. Heart disease refers to a condition where there is an abnormality of the heart whereas heart failure exists when the heart is unable to meet the circulatory demands of the body. Most often, the development of clinical signs such as cough, edema, and tachypnea herald the presence of heart failure.
Signs of heart failure may be more pronounced in active animals as they have higher circulatory demands, likewise signs of heart failure may be delayed in sedentary animals as they rarely challenge their cardiovascular system. In general, heart failure may occur secondary to 1) decreases in stroke volume or 2) abnormal heart rates.

Decreases in stroke volume. Stroke volume (the amount of blood ejected each cycle from either ventricle) may decrease secondary to reductions in preload, impaired contractility, increased afterload, or inadequate valvular function. A significant reduction in preload (analogous to venous return) may result in a decreased stroke volume and consequent heart failure. Examples include shock secondary to hypovolemia or hemorrhage, excessive use of diuretics, pericardial effusion with tamponade, and hypertrophic cardiomyopathy. Impaired contractility decreases stroke volume and can precipitate congestive heart failure. Dilated cardiomyopathy of large breed dogs, and cardiomyopathy of overload (myocardial failure secondary to unligated PDA or chronic valvular disease) are disorders where contractility is decreased. In disorders where there is an increased afterload, a greater deterrent to ventricular emptying than usual exists. This may result in partial ventricular emptying and a decreased stroke volume. Examples include severe hypertension (pulmonary or systemic) and aortic or pulmonic stenosis. The atrioventricular valves (mitral and tricuspid valves) normally prevent blood from rushing back into the atria during the powerful contraction of the ventricles. When there is inadequate valve function, or insufficiency, blood is allowed to reenter the atria causing their dilation, reducing the amount of forward flow, and consequently decreasing stroke volume. The most common causes of valvular insufficiency are degenerative valve disease (endocardiosis) and infective endocarditis. With a basic understanding of blood flow through the heart. one can reliably predict the pathological changes that would occur. When there is insufficiency of the tricuspid valve due to infective endocarditis, then tricuspid valvular insufficiency would be expected, as well as right atrial enlargement, vena caval congestion, and ascites.

Abnormal rates. Abnormally slow rates (bradycardias) may result in decreased cardiac output . Animals with bradycardia (sick sinus syndrome, third degree AV block) often experience syncope as a result of decreased cerebral perfusion, which may occur when cardiac output drops. Abnormally fast rates (tachycardias) may also result in decreased cardiac output as there is insufficient time for ventricular filling. Animals with tachycardia (rapid atrial fibrillation, ventricular tachycardia) usually have reduced cardiac output, clinical signs of weakness and often syncope.

Regardless of the underlying cause of heart failure, the body reacts to a decrease in cardiac output in a consistent manner. Through a vast network of baroreceptors, there is constant neural input regarding blood flow and pressure. When decreased flow or pressure is sensed there is an immediate withdrawal of parasympathetic tone and activation of the sympathetic nervous system. These changes result in an immediate increase in heart rate and cardiac contractility, and constriction of arterioles and veins. Decreased blood pressure along with heightened sympathetic tone causes activation of the renin-angiotensin-aldosterone (RAA) axis. Renin is released by the juxtaglomerular apparatus of the kidney and converts angiotensinogen to angiotensin I, an inactive decapeptide. The two terminal amino acids of this peptide are cleaved by angiotensin converting enzyme (an enzyme found in high levels in pulmonary endothelial tissue) forming angiotensin II, a remarkably potent vasoconstrictor. Angiotensin II also increases thirst, promotes sodium retention by the kidneys, and stimulates secretion of aldosterone by the adrenal cortex, resulting in further sodium and water retention.

In the short-term, these compensatory mechanisms are beneficial and help to restore fluid volume and blood pressure. They are life-saving in cases with transient circulatory collapse, such as hemorrhage, but become maladaptive when stimulated by chronic conditions, such as heart disease. Sustained activation of the sympathetic nervous system increases myocardial oxygen demand, predisposes the heart to arrhythmias, and may cause myocardial damage (necrosis of myocytes). Persistent sodium and water retention hastens the development of pulmonary edema. Chronic vasoconstriction places a high strain on the heart through elevating afterload, or impeding ventricular emptying. As these compensatory mechanisms become deleterious, cardiac output declines, resulting in a further increase in these processes. Thus begets the "vicious cycle of heart failure."

In order to rationally select appropriate therapy and provide an accurate prognosis, it is advantageous to categorize the type and stage the degree of heart failure. A system for staging heart failure in animals was recently developed by the International Small Animal Cardiac Health Council. The three stages and their criteria are as follows: The asymptomatic patient - heart disease is detectable but there are no clinical signs . A cardiac murmur, arrhythmia and radiographic changes may be present. Mild to moderate heart failure - clinical signs of heart failure are evident at rest or with mild exercise. Advanced heart failure - there are critical clinical signs including respiratory distress, marked ascites, and profound exercise intolerance. With each advancing stage the prognosis worsens and the need for treatment increases. It is also important to determine whether there is left-sided, right-sided, or generalized heart failure present.

Left-sided CHF. Left atrial pressure rises whenever left ventricular emptying is encumbered or mitral insufficiency exists. The result is an impediment to pulmonary venous flow and an elevation of pulmonary venous pressure, which ultimately leads to the formation of pulmonary edema. Cough is a consistent feature of left-sided congestive failure and typically follows activity or is nocturnal. Cough is initially caused by edema-induced distortion of the pulmonary interstitium. As pulmonary edema worsens, fluid enters the alveoli and airways causing the cough to increase in intensity and frequency. At this point, rales are present on auscultation. Other signs of pulmonary edema secondary to left-sided congestive heart failure include tachypnea, orthopnea (labored breathing while recumbent), and dyspnea. Other clinical signs of left-sided congestive heart failure include exercise intolerance, tachycardia, and occasionally weight loss. Due to the dramatic impact of pulmonary edema, the development of left-sided congestive heart failure is almost always apparent.

Right-sided CHF. Elevation of right atrial pressure impedes venous flow from the cranial and caudal vena cava resulting in systemic venous congestion. Clinically, this is manifested as jugular venous distension, subcutaneous edema, and ascites. The pattern of subcutaneous edema is fairly species-specific - it is uncommon in dogs, and occurs generally, involves the submandibular and brisket area in cattle, and is seen in the preputial and mammary area in horses. Cats rarely have subcutaneous edema but often develop pleural effusion (hydrothorax). Systemic congestion also causes enlargement of the liver and spleen, and may result in pericardial effusion (hydropericardium). The presence of fluid within the pericardial sac muffles heart sounds. Ascites is detected by abdominal ballotment. Fluid from the pericardial sac, peritoneal cavity, and pleural space should be analyzed and is usually a modified transudate. Pericardial effusion and subcutaneous edema are both associated with low-amplitude ECG waveforms.

Generalized CHF. Diseases affecting one side of the heart often precipitate failure of the other side causing signs of both left and right-sided congestive heart failure. As congestion worsens, left-sided signs predominate due to the severe consequences of pulmonary edema.