Many clinical signs compatible with left-sided heart failure also may occur in respiratory diseases, making the distinction difficult in some cases.
What is the problem?
Many clinical signs compatible with left-sided heart failure also may occur in respiratory diseases, making the distinction difficult in some cases. For example, old dogs, particularly of small breeds, are commonly affected by chronic respiratory diseases and mitral regurgitation, both of which can result in coughing. Dyspnea may happen in patients with pulmonary edema or pleural effusion secondary to congestive heart failure (CHF) or in patients with primary respiratory disorders.
What are the Clinical Manifestations of Heart Failure?
Clinical signs in heart failure may result from accumulation of fluids, low cardiac output, or changes in skeletal muscles (Table 1). Dogs with CHF are usually brought to the clinics due to cough, dyspnea, exercise intolerance, abdominal enlargement, or syncopes. Compensatory mechanisms activated during heart failure cause sodium and water retention. Sodium and water retention increases circulating volume and venous pressure leading to transudation of fluids in body cavities (effusion) or interstitium (edema). These signs develop preferentially in the capillary beds drained by the failing ventricle. Thus, elevated pulmonary venous and capillary hydrostatic pressures lead to pulmonary edema and can be manifested as dyspnea, cough, pulmonary crackles, and exercise intolerance. Systemic venous hypertension causes jugular distention, hepatic congestion, ascites, and subcutaneous edema. In dogs, ascites always precedes subcutaneous edema in patients with right side CHF. Biventricular failure shows a combination of left and right side signs and is often associated with accumulation of pleural fluid.
Dyspnea may be caused by pulmonary edema or pleural effusion, but it may also occur before the patient develops severe fluid retention. Normal animals also became dyspneic during exercise in a manner similar to the one that occurs in CHF. The main difference between a normal fit animal, an untrained animal, and a patient with CHF, is the amount of exercise that will lead to dyspnea and fatigue. Cough is common sign of heart disease in dogs. Dogs with heart disease may cough due to left-sided CHF or due to compression of the left main stem bronchus without CHF. Dogs coughing from pulmonary edema are frequently thin, with severe weight loss and have a more subtle cough that tends to be worse at night, and may be accompanied by pink nasal discharge or sputum. Dogs coughing due to left main stem bronchus compression tend to be obese, have dry, hacking cough that is usually worse during the day. Dogs with left-sided CHF usually have fast heart rates caused by sympathetic activation, whereas dogs with left main stem bronchus compression have normal heart rates with pronounced sinus arrhythmia due to high parasympathetic tone.
Cardiac cachexia is a common finding during CHF it is usually more prominent during right-sided CHF and in giant breeds with dilated cardiomyopathy. It is very uncommon to an animal with overt CHF to be obese. Obesity is usually associated with respiratory problems. In situations in which CHF develops rapidly (e.g. rupture of a chordae tendineae, development of atrial fibrillation, a few Dobermans with dilated cadiomyopathy), time may not have been sufficient to cardiac cachexia to develop and the animal may show a reasonably normal body condition. During right-sided failure, interference with normal absorption of nutrients in the gastrointestinal tract caused by intestinal and hepatic congestion may also contribute to cachexia.
Clinical signs suggestive of heart disease, not necessarily with CHF, include: diastolic, continuous or a very loud systolic murmur, arrhythmias with pulse deficit, gallop rhythms, and ascites with jugular distention and presence of hepatojugular reflux. Right-sided CHF is a clinical diagnosis in dogs. It is likely to be present in patients with ascites and jugular vein distention, hepatomegaly, and abnormal cardiac auscultation. Diagnosis of left-sided heart failure however, requires a chest radiograph. Auscultatory pulmonary abnormalities during pulmonary edema are neither sensitive nor specific. A patient with dyspnea, cough or pulmonary crackles, even with abnormal heart auscultation, may have respiratory signs caused by a primary respiratory disease.
Is heart failure present?
Heart disease is not synonymous with heart failure. A patient may be presented with a heart murmur or gallop, and even have myocardial failure, and may not necessarily be in CHF. Presence of heart failure may be suspected during physical examination. Right-sided CHF is a clinical diagnosis based on jugular distention and pulsation, presence of ascites (dogs), pleural effusion, and peripheral edema. Diagnosis is confirmed by showing elevation of central venous pressure or more loosely by observing a large right heart on radiographs or echocardiography. Left-sided CHF is a radiographic diagnosis that can be suspected in patients with dyspnea and abnormal respiratory sounds. It can be confirmed by showing elevation of the pulmonary capillary wedge pressure, but identifying pulmonary edema in association with left-heart enlargement would suffice from a clinical stand point.
Some clinical findings may be helpful, providing indications of cardiovascular function. Gallop rhythms suggest the presence of ventricular dysfunction. The fourth heart sound (S4 gallop) occurs during late diastole and represents atrial contraction. An S4 gallop is associated with elevated ventricular end-diastolic pressure due to a decrease in ventricular compliance. An early diastolic filling sound (S3 gallop) may occur during ventricular dysfunction of any cause and is very sensitive indication of ventricular dysfunction. Increased in loudness and splitting of the second heart sound suggest the presence of pulmonary hypertension. A distended and sometimes pulsating jugular vein suggests that right atrial pressure is elevated and the patient is in right-sided heart failure.
What test should be selected?
Laboratory examination is used to confirm the presence and cause of the heart disease, the presence and severity of the CHF and ventricular dysfunction, and presence of complications. Some tests are useful to diagnose specific conditions and may offer no information regarding cardiovascular function, whereas others may assess only function or offer a combination of functional and diagnostic information. In addition to physical examination, confirmation of the exact cause of CHF a combination of radiographic, electrocardiographic, echocardiographic, and laboratory examination is usually necessary. Echocardiography is very helpful in determining the disease leading to CHF.
Electrocardiogram can be used to evaluate heart rhythm, but provides only indirect information regarding cardiovascular function. Arrhythmias may be due to heart disease, but may also result from noncardiac causes. The electrocardiogram provides no definitive criteria for diagnosing of heart failure. It may however, contribute to diagnosis (e.g. decrease QRS voltage and electrical alternans in pericardial effusion). One should bear in mind that a normal electrocardiogram does not rule out CHF or heart disease.
Chest radiographs are a very important test in patients suspected to have heart d isease. Changes in cardiac size and shape may show the compensation effects in the heart (cardiomegaly) and be very helpful in determining the cause of CHF in dogs. Chest radiographs are of paramount importance to determine the presence of left-sided CHF (pulmonary venous congestion, pulmonary interstitial or alveolar edema). They are also useful to visualize pleural effusion in patients with CHF.
Echocardiographic examination is extremely helpful in determining the cause of CHF. There are no echocardiographic criteria to diagnose CHF, but is uncommon to see left-sided CHF without echocardiographic abnormalities such as left atrial enlargement in left-sided CHF, and right-atrial enlargement or pericardial effusion in right-sided CHF.
Measurement of biochemical markers that are increased during heart disease or CHF can provide information about the presence of heart disease and in some cases may have prognostic value. The most commonly used in small animals are cardiac troponin I, cardiac troponin T, ANP, and BNP. Cardiac troponins are leakage markers that are released in the circulation when cardiac cell membrane integrity is compromised and therefore indicate myocardial damage. Any myocardial injury, including CHF, can increase cardiac troponins and there is a correlation between the magnitude of myocardial damage and the degree of elevation of cardiac troponins only in acute states. ANP and BNP are functional markers that increase in presence of increased circulating volume (e.g. CHF) or during left ventricular hypertrophy. ANP and BNP tend to increase regardless of the underlying heart disease, but correlate well with the degree of left ventricular dysfunction. They can potentially be used to assess cardiac function, monitor therapy and to help determine prognosis. Unfortunately, there is a paucity of clinical studies highlighting indications usefulness, and limitations of different biochemical markers during heart disease in dogs and cats, which limits their use. As more information become available, however, clinical use of biochemical markers will likely increase.
References
Atkins, C. Diagnostic Approach to coughing dogs with heart murmurs. In: Proceedings of the 10th ACVIM Forum., 1992. pp 224-225.
Bauer, T. Clinical approach to cardiopulmonary disorders. In: Kirk, RW, Bonagura, JD. Current Veterinary Therapy X. 10.ed. Philadelphia, WB Saunders, pp. 188-194, 1989.
Boswood A. Editorial: The rise and fall of the cardiac biomarker. J. Vet Int Med, 18:797-799, 2004.
de Morais HSA and Faria MLE. Dyspnea: Stop, look and listen. In: Proceedings XXVII World Congress of the World Small Animal Veterinary Association. Granada, Spain. October 2002
de Morais HAS and Schwartz DS. Pathophysiology of heart failure. In: Ettinger SJ and Feldman EC (eds). Textbook of Veterinary Internal Medicine. 6th ed., Philadelphia, W.B. Saunders, 2005, pp: 914-940.
Mawby DL. Dyspnea and Tachypnea. In: Ettinger SJ and Feldman EC (eds). Textbook of Veterinary Internal Medicine. 6th ed., Philadelphia, W.B. Saunders, 2005, pp: 192-195.
Schober KE. Biochemical markers of cardiovascular disease. In: Ettinger SJ and Feldman EC (eds). Textbook of Veterinary Internal Medicine. 6th ed., Philadelphia, W.B. Saunders, 2005, pp: 940-949.
Sisson, D. D. and Ettinger, S. J. The physical examination. In: Fox, P. R.; Sisson, D. D.; Moïse, N. S. Textbook of Canine and Feline Cardiology. Philadelphia, WB Saunders. 1999. cap. 5. p: 46-64.
Table 1. Clinical Signs in CHF
Low output signs
Complaints => exercise intolerance, syncope
Clinical signs => weak arterial pulses, tachycardia, arrhythmias, cool extremities
Signs due to fluid retention
Left side (Pulmonary edema)
Complaints => dyspnea, orthopnea, exercise intolerance, cough
Clinical Signs => pulmonary crackles, tachypnea, gallop rhythm, functional mitral regurgitation, cyanosis caused by ventilation/perfusion inequality
Right side (systemic venous congestion)
Complaints => abdominal enlargement (ascites), subutaneous edema
Clinical signs => jugular distention and pulsation, ascites, hepatomegaly, splenomegaly, hepatojugular reflux, gallop rhythm
Bilateral
Complaints => left side + right side complaints, dyspnea due to pleural effusion
Clinical signs => left + right side clinical signs, muffled heart and lung sounds with fluid line in the chest (pleural effusion)
Adapted from: de Morais HSA and Schwartz DS: Pathophysiology of heart failure. In: Ettinger SJ and Feldman EC: Textbook of Veterinary Internal Medicine. 6th ed. Philadelphia, WB Saunders, 2005.
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