31 Cardiovascular emergencies
Acute Decompensated Heart Failure
Progressive heart disease results in failure of the heart to pump adequately and this may manifest as low-output heart failure, where sufficient blood is not pumped into the aorta or pulmonary artery, or congestive heart failure (CHF). In CHF, there is inadequate emptying of blood from the venous system: left-sided CHF results in congestion of the pulmonary circulation with pulmonary oedema; right-sided CHF causes congestion of the systemic circulation with ascites and pleural effusion. Bilateral heart failure presents with a combination of both types of signs.
Failure of the heart to pump adequately may result from systolic dysfunction, i.e. the heart is physically unable to eject enough blood, or from diastolic dysfunction, i.e. the ventricles are unable to fill properly. Both mechanisms are often involved and the end result is reduced cardiac output and a lowering of arterial blood pressure. Systolic dysfunction may result from failure of the myocardium itself (e.g. dilated cardiomyopathy), from an increase in ventricular pressure (pressure overload; e.g. pulmonic stenosis, subaortic stenosis) or from volume overload (e.g. atrioventricular valve disease). Diastolic dysfunction (impaired ventricular filling) may result, for example, from ventricular hypertrophy, dilated cardiomyopathy, atrioventricular valve stenosis or pericardial effusion (cardiac tamponade).
Compensatory mechanisms during heart disease include mechanisms relating to the heart itself, such as tachycardia, increased inotropy (force of contraction) and myocardial hypertrophy, and peripheral compensation involving vasoconstriction and sodium and water retention. In time these compensatory mechanisms become detrimental.
Treatment
Although signalment and history may help to some small degree, emergency treatment of animals with acute decompensated heart failure often needs to be performed without a definitive diagnosis of the nature of the underlying heart disease. Management of such cases may involve:
Canine chronic mitral valve insufficiency
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:
Case example 1
Presenting Signs and Case History
An 11-year-old male neutered Norfolk terrier presented following an episode of collapse and onset of severe respiratory distress. The dog had had a number of similar episodes in the 2 weeks prior to emergency presentation but none had been as severe as the most recent one. He had a history of chronic mitral valve insufficiency and CHF for which he was receiving furosemide, pimobendan and benazepril. The owner reported a variable appetite recently and admitted that she had not managed to administer all of the dog’s medications as directed. No other significant preceding history was reported.
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.
Assessment
The dog’s cardiovascular examination revealed tachycardia and marked hypoperfusion as well as a maximal grade heart murmur. Putting this together with the respiratory findings and the dog’s history, a diagnosis of decompensated CHF was most likely. The possible pulmonary oedema suggested left-sided heart failure, and the fluid thrill may have suggested a degree of right-sided failure as well.
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.
Clinical Tip
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.
Clinical Tip
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.
Canine tricuspid valve insufficiency
Tricuspid valve insufficiency is often an incidental finding in dogs and cats. Clinically significant tricuspid valve insufficiency may be seen with:
Right atrial enlargement may result in supraventricular tachydysrhythmias, and increased right atrial pressure may result in ascites, pleural effusion, pericardial effusion, hepatomegaly and splenomegaly. From an emergency perspective, animals with tricuspid valve insufficiency are more likely to require treatment for a concurrent disorder than for primary right-sided heart failure.
Canine dilated cardiomyopathy
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.
Case example 2
Presenting Signs and Case History
A 6-year-old male neutered Great Dane presented with a 10-day history of inappetence and retching that was worse when the dog was lying down. There had been some noticeable exercise intolerance on daily walks and the owner had noticed that the dog had a very fast heart rate prompting emergency presentation. The dog had had surgical treatment of gastric dilatation/volvulus syndrome 2 years previously but no other significant history was reported.
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.
Assessment
The dog’s cardiovascular examination was highly suggestive of atrial fibrillation and the history of inappetence and exercise intolerance most likely suggested a degree of CHF. Given the dog’s breed, there was a high index of suspicion for DCM. The mild increase in rectal temperature was suspected to represent hyperthermia rather than pyrexia.
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