Is it really heart failure I'm treating? (Proceedings)

Differentiating between congestive heart failure and respiratory disease as the cause of acute dyspnea in dogs and cats is one of the most difficult case scenarios facing veterinary clinicians. Clinical signs of the diseases affecting these systems often overlap with very minimal distinguishing characteristics; however, the diagnostic workups and therapy differ significantly. It is the goal of this presentation to review the approach to clinical cases with suspected cardiopulmonary disease and highlight relevant points that may help differentiate the two types of diseases.

History and Signalment:

Patients with cardiac and respiratory disease often have very similar histories. Episodes of coughing, dyspnea, tachypnea and/or exercise intolerance are frequently reported by owners. Also historically, bouts of cyanosis, collapse or syncopal episodes, lethargy, and a decreased appetite may be mentioned. These clinical signs, therefore, do not help distinguish between cardiac and pulmonary etiologies. However, the combination of clinical signs and the patient's signalment may help attribute the cause to one system versus the other. For example, a cat that presents with coughing is more likely to have a disease of the respiratory system rather than the cardiovascular system. Cardiovascular related dyspnea in cats often manifests as reclusive behavior along with signs of dyspnea such as assumption of an orthopnic position and/or a significant abdominal component to breathing (a restrictive breathing pattern). Certain canine breed predispositions may help distinguish between the respiratory and cardiovascular systems. For example, older Labrador retrievers with dyspnea should be assessed for laryngeal paralysis, toy breeds may often have tracheal collapse, bracheocephalic disease is seen in bulldogs, and dilated cardiomyopathy in Dobermans.

There may be other helpful hints when comparing the history of a patient with cardiovascular versus respiratory disease. In cardiac disease, a loss of body condition (cardiac cachexia) is often noted, compared to that of many respiratory disease patients where body condition is generally maintained (and often increased). Generally, with heart disease (failure), the onset of clinical signs may appear more acute compared with that of respiratory disease. For example some owners may complain of a sudden onset in abdominal distension in their pets, which might suggest ascites associated with right sided congestive heart failure.

Physical examination:

Nothing can replace a thorough and detailed general examination when dealing with a patient with suspected cardiopulmonary disease. However, physical examination of these patients should be carried out in a staged fashion. Stressing these patients by overzealous handling may be detrimental to their health status and lead to a rapid decline. Very subtle findings may help guide the next diagnostics that may save valuable time, stress on the patient and more importantly, especially in veterinary medicine, the owner's money.

Initially, observing the patient for respiratory rate, the apparent effort being expended, the phase of respiration during which the effort occurs, as well as for paradoxical movements of the abdomen is recommended prior to proceeding with the physical exam. In many cardiopulmonary cases the need for oxygen supplementation may be noted as flaring of the nostrils, open mouth breathing or orthopnea; indicating dyspnea. Noting patterns associated with respiratory effort may help localize the level of disease. In general, patients with upper airway disease of present with inspiratory dyspnea and patients with small airway disease show effort associated with expiratory phase of respiration. A restrictive breathing pattern is often seen with disease involving the pleural space. Thoracic auscultation is obviously very important in hearing abnormal lung sounds such as crackles and wheezes, as well as for cardiac murmurs and arrhythmias. However, the mere presence of abnormal lung sounds or heart murmurs will not necessarily help you distinguish between primary heart and primary lung disease.

Signs that might clue you into heart failure when most of the above clinical signs are present include increased heart rates with loss of heart rate variability related to breathing (especially in dogs). This is secondary to increased sympathetic output and decreased vagal output due the real or perceived decrease in arterial blood pressure by the baroreceptors. Weak and rapid femoral pulses or the presence of abnormalities such as pulsus paradoxus or pulsus alternans may also suggest primary cardiac disorders. Ascites with jugular venous distension suggest right-sided heart failure or pericardial disease.

Diagnostic Evaluation:

Complete systemic evaluation of patients suspected of cardiopulmonary disease is required by assessing minimally a complete blood count, biochemical profile, and urinalysis. However, thoracic radiographs are the most important diagnostic technique in evaluating the dyspneic patient - if they can be obtained without compromising your patient. High quality inspiratory films are very helpful in discriminating cardiac versus respiratory causes of dyspnea. Comparing inspiratory and expiratory films may also be helpful. Noting the pattern and distribution of any airway and parenchymal abnormalities, evaluating the heart size, and assessing pulmonary vasculature are essential when evaluating thoracic radiographs. The findings of distended pulmonary veins associated with parenchymal densities should indicate further evaluation of the cardiovascular system, or at least diuretic trial therapy.

Once thorough evaluation of the laboratory database and thoracic radiographs has been completed the clinician should have a good idea of the underlying disorder (respiratory, cardiac or both). Additional appropriate tests may then be performed, for example electrocardiogram and echocardiography with cardiac disorders. With respiratory disorders, tests such as an arterial blood gas analysis, laryngeal examination, a transtracheal wash, bronchoscopy or fluoroscopy may be performed.

Case scenario 1:

Although this seems straightforward we have all seen the middle aged, small breed coughing dog with chronic airway disease that presents with acute or chronic cor pulmonale. Signs of cyanosis, exercise intolerance and collapse may abound in these patients and a murmur and potentially crackles may be ausculted. Thoracic radiographs reveal significant cardiomegaly. However, close assessment of the pulmonary vasculature may clue you in as to the underlying pathophysiology. For example, enlarged pulmonary arteries with normal to small pulmonary veins may be more suggestive of pulmonary hypertension, heart worm disease or pulmonary thromboembolism with secondary cardiac change. Cardiac echocardiogram with spectral Döppler may help assess the presence and severity of pulmonary hypertension, or find heartworms in the pulmonary artery. In the absence of heartworm disease, a thorough assessment of the pulmonary system is in order to make appropriate recommendations and offer a prognosis.

Case scenario 2:

How about that patient with a restrictive breathing pattern and pleural effusion? They often present a diagnostic challenge. Thoracocentesis is required to stabilize this patient prior performing thoracic radiographs and the fluid obtained can be utilized to assess the origin of the effusion. Moreover, this also allows more information to be obtained from the thoracic radiographs since the cardiac silhouette can usually be more readily assessed. Identification of neoplastic cells or hemorrhage would decrease the likelihood of a cardiac etiology. Fluid analysis may be less helpful because cardiac, pulmonary or thoracic disease may all cause transudates, modified transudates and chylous effusions, and thus does not discern between the cardiovascular and respiratory system. An echocardiogram is very helpful in these circumstances in assessing for right heart failure or pericardial disease. However, assessment of the jugular veins on physical exam or measuring central venous pressures may give earlier and less expensive clues as to the presence of cardiac disease.

Case scenario 3:

We have all had that patient with the combination of mitral valve disease, large left atrium and chronic airway disease which poses the particular problem of which is causing the animal's clinical presentation for dyspnea. Loss of heart rate variability with an increased heart rate and the presence of weak, rapid femoral pulses may be more indicative of heart failure rather than respiratory disease. Close assessment of pulmonary vasculature on thoracic radiographs may be helpful. Dorsoventral radiographic projections in dogs may help in this endeavor.

Nevertheless we may not always be able to discern the primary etiology. Remember, you may have a combination of problems. Most importantly, we must remember that these systems are interdependent and that when one fails, the other will fail soon thereafter.

So what can be done in cases that cannot be completely evaluated (i.e. critical patient, owner restrictions) or that we just cannot figure out (IT HAPPENS!). In some cases a therapeutic trial may be indicated. Furosemide can be administered to clarify the nature of the clinical signs and distinguish pulmonary edema from other pulmonary diseases. The clinician should assess for clinical, as well as radiographic, improvement to suggest a diagnosis of cardiac failure. Sole reliance on clinical improvement may not by very accurate because animals with primary respiratory disease often show transient improvement following diuretic therapy. For example, obstructive pulmonary diseases frequently result in the development of some degree of edema and thus improve clinically with furosemide therapy. You may also see a temporary improvement in animals with lower airway disease. Thus it is important to document radiographic changes as well.

Future Direction:

The use of biochemical markers of heart failure is showing tremendous promise in helping to diagnose heart failure as the cause of acute dyspnea. In congestive heart failure natriuretic peptides, as well as other hormones, are released in response to atrial stretch (atrial natriuretic peptide - ANP) and ventricular stress (brain natriuretic peptide - BNP). In human medicine, plasma concentrations of these natriuretic peptides, especially BNP, can distinguish between cardiac and respiratory disease in patients presenting for dyspnea. A rapid bed-side test can be used to help diagnose the dyspneic patients. A similar, recent veterinary study had very promising results. Significant increases in ANP and BNP plasma concentration were found in congestive heart failure patients when compared with respiratory disease patients. Unfortunately, the test requires multiple steps and is limited to one or two university laboratories, and is therefore not clinically assessable. Research which develops a rapid test comparable to that available in human medicine may be very beneficial in saving the clinician, the patient and the owner valuable time, stress and money in distinguishing between cardiac and respiratory causes of dyspnea.

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