Is it Heart Failure?
Is Heart Failure Present?
This is not a trivial question by any means and may challenge an expert in the determination. It will be well worth your time to consider this question very carefully before trotting down the primrose path. Establishment of left-sided congestive heart failure (LCHF) is dependent upon a full complement of historical, physical, radiographic (and echocardiographic) findings. IF the patient is in LCHF, then MARKED cardiac disease should be present. It is a common mistake to diagnose LCHF based on the presence of dyspnea and one or more suggestive findings such as a murmur, typical breed, pulmonary infiltrates, etc. Diagnosis requires a thoracic radiographic pattern that is consistent with LCHF and suggests severe heart disease. Check for each and every of the following:
History consistent with severe heart disease and LCHF
While any animal can be in LCHF without obvious historical evidence, previous episodes of dyspnea in a dog (if present) are typically nocturnal or related to long periods of recumbency or exertion. Little dogs with mitral regurgitation and lots of heart disease may cough in the absence of LCHF due to compression of airways by a markedly enlarged heart. Clinical signs in cats differ in a number of important aspects. Cats usually do not cough from heart disease and may present with life-threatening disease where none was previously apparent. Clinical signs do not seem to vary in an obvious circadian pattern. For patients in which heart failure seems unlikely historically, it may be valuable to consider specific circumstances that can precipitate heart failure such as administration of intravenous fluids, steroids, or cardiac toxins (e.g. doxorubicin).
Evidence of severe heart disease on physical examination
Diagnosis of LCHF usually entails significant dyspnea/respiratory effort and tachypnea; there is the occasional dog (e.g. Dobermans) that can be walking around with fairly severe pulmonary infiltrates but little outward evidence of respiratory compromise. In most little dogs with mitral endocardiosis causing LCHF we expect to hear a readily audible murmur (grade III/VI or louder) but there are exceptions to this rule. A murmur may be relatively inaudible if dyspnea and respiratory sounds are so great as to obscure the murmur. Acute chordal rupture resulting in LCHF may not produce an obvious murmur. Large breed dogs with DCM may not have a loud murmur, or any; this, in fact, is one of the distinguishing features between DCM and mitral regurgitation (MR) due to endocardiosis. MR secondary to DCM is typically produced by a dilated, hypofunctional ventricle and murmurs may be subtle. LCHF in association with a soft murmur due to endocardiosis is unlikley (but possible). Listen carefully for a gallop sound in all cases. A reliable gallop (S3 or S4) is comparatively specific sign of significant heart disease in a small animal, i.e. consistent with LCHF. With great uniformity, a dog with LCHF is expected to have an “elevated” heart rate (e.g. 140/min or greater) and loss of sinus arrhythmia due to sympathetic activation. Exceptions to this rule include the presence of medications that artificially lower the heart rate (pimobendan, beta-blockers). If a dog's heart rate is 120/min or lower, you should be strongly aware of the possibility that LCHF is not present. Inspiratory crackles are supportive evidence of alveolar pulmonary edema due to LCHF. However, LCHF is not the only cause of crackles and any alveolar (pneumonia, noncardiogenic edema) or bronchial infiltrates (bronchopneumonia, collapsing airway syndromes, “pulmonary fibrosis”, reactive airway disease) may result in these sounds! Supportive evidence for LCHF in cats includes the presence of a murmur or gallop sound but there are many cats with severe heart disease and virtually no detectable physical abnormalities until the onset of LCHF. Tachycardia is not consistently present. Some cats actually present with bradycardia and this, in association with hypothermia, may be an ominous finding.
Radiographic evidence of LCHF and severe heart disease
While congestive heart failure is defined in terms of elevated venous pressure, requiring cardiac catheterization for determination, the practical clinical diagnosis of LCHF is most often determined radiographically. Dogs exhibit interstitial to alveolar infiltrates in the perihilar region, caudal-dorsal, or both. Early radiographic signs may consist of peribronchial cuffing that results from edema accumulation in the peribronchial interstitium. Look specifically to evaluate the pulmonary vasculature. Expect to see prominent to clearly dilated pulmonary veins with LCHF and keep your options open if you don't. Exceptions to this rule occur when the vasculature is obscured by the pulmonary infiltrates and when the patient has already received some measure of anti-congestive therapy (i.e. Lasix) prior to the radiograph. There is also the occasional patient that simply hasn't heard of this rule; there is individual variation in normal pulmonary vessels size and a particular patient with LCHF may overlap with normal expectations. However, don't forget to look for these vessels whether you were thinking of LCHF or not. For LCHF, there is a rough correlation between the severity of pulmonary infiltrates and the degree of clinical signs, i.e. dyspnea. If infiltrates are mild/moderate and the patient is in severe dyspnea, you will need to continue looking for causes of dyspnea. If LCHF is present, there should be evidence of severe left-sided cardiomegaly; LCHF is an end-stage condition and is not caused by mild heart disease. An exception to this rule occurs if cardiac disease has developed rapidly (e.g. myocarditis, acute chordal rupture), i.e. without sufficient time for cardiac remodeling and dilation. Cats with LCHF typically have patchy alveolar infiltrates (i.e. not specifically hilar or caudal dorsal) or may have pleural effusion. Mild pleural effusion alone does not cause severe dyspnea (but there may be alveolar infiltrates as well and these can be difficult to spot if there is pleural effusion). Cats with LCHF usually have cardiomegaly, best determined as an increase in cardiothoracic ratio on the dorsal-ventral radiograph; a lateral alone will commonly fail to depict cardiomegaly altogether. Abdominal effusion alone is rarely the result of heart disease in cats (one exception is heartworm disease).
There is an excellent tutorial on thoracic radiographic interpretation at the VetGo Cardiology site. You can also test your skills on some radiographic examples at this (Vermont Veterinary Cardiology) website.
Electrocardiography does not provide the diagnosis of LCHF. However supportive evidence may be apparent, e.g. if there is a clear pattern of left ventricular/left atrial enlargement, or it may suggest that other considerations are appropriate, e.g. right ventricular/right atrial enlargement pattern. Ventricular arrhythmias in a dog are nonspecific for primary heart disease. Common noncardiac associations for VPCs include splenic masses, gastric dilatation-volvulous syndrome, generalized trauma, circulatory shock, systemic infection/inflammation (e.g. pancreatitis), and a myriad of others. Sympathetic stimulation may be the common underlying pathway in many of these conditions. However there are circumstances in which ventricular tachyarrhythmias may be strongly supportive of a specific cardiac diagnosis, e.g. in a Doberman or boxer dog. While exceptions occur (so-called “lone atrial fibrillation”), atrial fibrillation in a dog is very suggestive of marked primary heart disease; the combination of atrial fibrillation and tachycardia is most likely the result of DCM or AV valve endocardiosis with severe atrial enlargement. I have never seen a cat with atrial fibrillation that did not have severe primary heart disease, most commonly in association with restrictive cardiomyopathy.
Echocardiography is very useful for definitive diagnosis of heart disease and establishing that the disease is severe enough to result in LCHF. However, this is not where the LCHF diagnosis comes from. Echocardiography is particularly valuable when pleural effusion or pulmonary infiltrates obscure the cardiac silhouette and vasculature on radiographs. The absence of obvious left atrial (LA) enlargement is cause for serious reconsideration of the LCHF diagnosis (potential exceptions - acute heart disease such as myocarditis or chordal rupture, iatrogenic LCHF from fluid loading, subsequent to marked Lasix administration). The LA should not appear small; this is inconsistent with LCHF (but can still occur with LCHF and pulmonary venous obstruction).
Recently there has been great interest in biomarkers for heart disease including the measurement of BNP, ANP, and cardiac troponin levels in the blood. These blood tests for heart disease hold great promise as diagnostic aids, particularly as “tie-breakers” when the LCHF diagnosis is in question. Recently there has been a great deal of clinical research on NT pro-BNP. This is a chemical (biomarker) that is released primarily in response to ventricular mechanical stress (stretch) and so is related to the severity of congestion. Blood levels are correlated with the severity of heart disease and the test has been touted as a means of differentiating cardiac and respiratory causes of dyspnea as well as determining the severity of heart disease. My personal integration of these investigations is that this test is not yet ready for prime time as a means of diagnosing or staging heart disease. Correlation of BNP levels with heart disease severity is one thing, but studies have often shown too much overlap of BNP levels between cases with and without heart disease. Once again, the LCHF diagnosis is based upon a constellation of findings and a preponderance of evidence. If the clinical picture deviates substantially from the above description, then the LCHF diagnosis is in question. You will have to weigh the risks and benefits of proceeding with LCHF therapy versus additional tests to solidify the diagnosis. Conditions commonly misdiagnosed as LCHF include pneumonia, feline asthma and reactive airway syndromes, pulmonary thromboembolism, noncardiogenic pulmonary edema, and a range of chronic respiratory conditions such as “pulmonary fibrosis”, pulmonary hypertension, and airway disease. The incidendal presence of a murmur in these cases often confounds accurate interpretation of the principal disease process.