Theory refresher

Chronic mitral valve insufficiency is usually the result of progressive valvular myxomatous degeneration and has a high prevalence in older dogs, especially of small to medium size. The most commonly affected breeds include the Cavalier King Charles spaniel, terrier breeds and poodles. The disease usually progresses over a period of years and is the most common cause of CHF in dogs.

In the long term, mitral regurgitation results in tachycardia, myocardial hypertrophy and reduced myocardial contractility; left atrial size and pressure increase, and pulmonary venous congestion and oedema may occur. Coughing may be the result of left main stem bronchus compression by the enlarged left atrium and/or pulmonary oedema.

Acute severe decompensated heart failure may occur in dogs with mitral valve insufficiency due to:

Major body system examination

On presentation the dog was alert but clearly in respiratory distress. Flow-by oxygen supplementation was commenced while a major body system examination was performed. Cardiovascular examination revealed a heart rate of 160 beats per minute with a grade VI/VI left apical systolic murmur that had wide radiation. Femoral and dorsal pedal pulses were very weak but pulse deficits were not detected. The jugular veins did not appear distended. Mucous membranes were hyperaemic with a fast capillary refill time.

Respiratory rate was 60 breaths per minute and there was a notable increase in effort. Lung sounds were diffusely harsh bilaterally and focal patches of crackles were audible. The dog’s abdomen was distended with a fluid thrill and rectal temperature was within normal limits. Blood pressure via Doppler sphygmomanometry was within normal limits at 130 mmHg.

Emergency database

As the dog remained tolerant and compliant with the flow-by oxygen supplementation, an intravenous catheter was placed in a cephalic vein and blood obtained via the catheter for an emergency database. This revealed mild hyponatraemia (137.0 mmol/l, reference range 140.0–153.0 mmol/l) and a mild increase in blood urea nitrogen (13.0 mmol/l, reference range 3.0–10.0 mmol/l) but was otherwise unremarkable.

Case management

Glyceryl trinitrate 2% paste (18 mm) was applied to the inner aspect of the dog’s right pinna and he was then placed into an oxygen cage with continuous electrocardiographic monitoring; this showed the dog to be in sinus tachycardia. Furosemide (4 mg/kg i.v.) and morphine (0.1 mg/kg slow i.v.) were administered via an extension line exiting the oxygen cage. Ad lib water was provided.

One hour later the dog’s respiration had improved to some extent and he had also urinated. As he was compliant, thoracic radiographs were performed with flow-by oxygen supplementation throughout (Figure 31.1). These findings were consistent with the suspected diagnosis of decompensated left-sided CHF secondary to probable mitral valve insufficiency but there was also evidence of right-sided heart failure.

Figure 31.1 (a) Right lateral and (b) dorsoventral thoracic radiographs of a dog with end-stage mitral valve disease showing cardiomegaly with left atrial enlargement and dorsal displacement of the caudal part of the trachea, an alveolar lung pattern affecting mainly the cranial lung lobes with air bronchograms, mild bilateral pleural effusion and hepatomegaly.

The dog was returned to the oxygen cage and continued to be treated with intermittent intravenous boluses of furosemide (2–6 mg/kg q 1–2 hr, prn) and morphine (0.1 mg/kg slow i.v. q 6 hr). Glyceryl trinitrate paste (18 mm q 8 hr) was also applied and the dog was continued on oral pimobendan and benazepril.

Although the dog showed some early improvement, his clinical condition deteriorated again. The owners were offered the option of an emergency referral to a hospital with a cardiologist and facilities to offer more intensive management but decided instead to have the dog euthanased which was therefore done in their presence as soon as possible.

Theory refresher

Dilated cardiomyopathy (DCM) is a primary myocardial disease characterized by enlargement of the heart, reduced systolic function and possible impaired diastolic function. The disease is seen most commonly in adult large and medium size dogs, with some breeds being over represented (e.g. the Great Dane, the Doberman Pinscher, the Irish Wolfhound, the Cocker Spaniel). There is significant variation between breeds with respect to both historical and clinical findings, and rate of disease progression.

DCM is definitively diagnosed by echocardiography that shows left (and perhaps bilateral) atrial and ventricular enlargement, and evidence of reduced left ventricular systolic function. Mitral regurgitation may be identified in association with the dilated left ventricle.

Major body system examination

On presentation the dog was ambulatory but quiet. Cardiovascular examination revealed an irregularly irregular heart rhythm with a left apical grade II/VI systolic heart murmur. Femoral pulses were weak and there were marked pulse deficits: heart rate 240 beats per minute, pulse rate 114 per minute. Mucous membranes were hyperaemic with a fast capillary refill time.

The dog was panting but it was decided not to stop this in order to auscultate the lung fields at initial presentation. Abdominal palpation was unremarkable but there was a mild increase in rectal temperature (39.5°C). Blood pressure via Doppler sphygmomanometry was within normal limits at 160 mmHg.

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