8-year-old 35 kg spayed female Weimaraner
with a history of mitral valve disease and congestive
heart failure was presented to the emergency
service for acute dyspnea. The dog had presented
to the emergency service one-and-a-half months
previously for acute dyspnea, and had been
hospitalized for 48 h. During that initial visit,
thoracic radiographs revealed cardiomegaly (VHS
11.8 [reference range, 8.5e10.7]), distended
pulmonary veins, a perihilar and caudodorsal
alveolar pulmonary pattern, and a trace of pleural
effusion. Echocardiography performed at that time
revealed left ventricular and atrial enlargement,
mild left ventricular systolic dysfunction, and
severe mitral regurgitation with an eccentricallydirected
jet towards the lateral wall of the left
atrium. The left ventricular end-diastolic and endsystolic
diameters were 6.6 cm and 5.4 cm,
respectively, and the left atrium to aortic root
diameter ratio was 1.9. A diagnosis of acute
pulmonary edema due to degenerative mitral
valve disease and secondary myocardial failure
was made. In between the initial hospitalization
and the current presentation to the emergency
service, the dog had visited the hospital as an
outpatient 2 additional times for recurrent mild
tachypnea and at both visits was found to have
radiographic evidence of pulmonary edema. The
first outpatient visit occurred 9 days after initial
hospitalization, and the second 14 days thereafter.
An additional 20 days had elapsed since the most
recent outpatient visit and the current presentation
to the emergency service. Since initial diagnosis,
the dog’s furosemide dose had been
increased from 1.4 mg/kg (50 mg) q12 h to 2.1 mg/
kg (75 mg) q12 h. The dog was also receiving
enalapril 0.43 mg/kg (15 mg) q12 h, hydrochlorothiazide
0.36 mg/kg (12.5 mg) q12 h, spironolactone
0.36 mg/kg (12.5 mg) q12 h,
amlodipine 0.11 mg/kg (3.75 mg) q12 h, digoxin
0.0054 mg/kg (0.1875 mg) q12 h, and pimobendan
0.21 mg/kg (7.5 mg) q12 h.
On presentation, the dog’s