Acute Collapse

Elisa M. Mazzaferro, MS, DVM, PhD, DACVECC, Cornell University Veterinary Specialists

ArticleLast Updated December 20064 min readPeer Reviewed
Black English mastiff in sternal recumbency, panting heavily with tongue hanging out of its mouth with head extended.

Sherman, a 6-year-old, 78-kg, intact male English mastiff presented to the veterinarian after a 15-kg weight loss and a history of decreased appetite, diarrhea, and sudden reluctance to stand or walk.

History

At the time of presentation, Sherman was mildly hyperthermic (103.2° F), weak, lethargic, and ambulatory only with assistance. His mucous membranes were pale pink and slightly cyanotic with a prolonged capillary refill time (> 2 seconds). Thoracic auscultation revealed irregular heart sounds with no murmurs present. Lung sounds were harsh but were attributed to increased salivation and upper airway noise. A small amount of blood and diarrhea were noted on rectal examination. The prostate was large, nonpainful, and symmetrical. There was an intermittent history of a dry, nonproductive cough. No prior episodes of exercise-induced collapse or collapse at rest were reported.

Initial Diagnostics

A complete blood count revealed mild leukocytosis (15,700 WBC with normal leukogram). Serum biochemistry values were normal. A free-catch urine sample was obtained; urinalysis revealed small numbers of cocci with no evidence of pyuria. Next, abdominal ultrasonography showed prostatomegaly. A presumptive diagnosis of prostatitis was made. Sherman was referred to a specialist for further medical care.

Physical Examination

At the time of presentation to the referral hospital, Sherman was weak and lethargic. He had a sporadically irregular heartbeat and pulse deficits, was thin (body condition score 2/5), and had a poor hair coat with generalized superficial pyoderma. Mucous membranes were pale pink and slightly cyanotic. Lung sounds were harsh with crackles in the mid to dorsal lung fields. He was ambulatory only with assistance. Cranial nerve examination was normal. The patient was weak but was able to stand and walk with assistance. Spinal reflexes, withdrawal, and conscious proprioception were all normal.

Further Diagnostics

Sherman was normotensive (148 mm Hg systolic/70 mm Hg diastolic; mean arterial pressure 107 mm Hg). ECG revealed the rhythm shown in Figure 1. Thoracic radiographs showed marked cardiomegaly without evidence of pulmonary edema. Echocardiography revealed biventricular and biatrial enlargement with decreased fractional shortening (19%) (Figure 2).

ECG tracing with sporadically irregular QRS complexes and fibrillation waves.

FIGURE 1 Lead II electrocardiogram (paper speed 25 mm/sec) performed at the time of presentation

M-mode echocardiogram revealing both decreased fractional shortening and changes in ventricular diameter.

FIGURE 2 M-mode echocardiogram denoting extremely poor fractional shortening. Note the relatively small change in ventricular internal diameter during systole and diastole.

Diagnosis: Dilated cardiomyopathy

Based on Sherman's signalment, history, presenting clinical signs, and echocardiogram findings, a diagnosis of dilated cardiomyopathy with systolic heart failure was made. A naso­pharyngeal oxygen catheter was placed, and supplemental oxygen was administered (100 ml/kg/min). The ideal treatment for dilated cardiomyopathy is directed at increasing cardiac contractility and decreasing heart rate. Rhythm control with biphasic electrocardioversion has also been described, but the owners declined this therapy.

Digoxin (0.325 mg PO Q 12 H) was prescribed as a positive inotrope and negative chronotrope and is considered one of the mainstays of therapy for DCM. More recently, the use of pimobendan, a positive inotrope and venoarteriolar dilating drug, has been associated with improved survival and quality of life in Doberman pinchers and cocker spaniels with DCM.1 Sherman's clinical condition improved over the next 2 days of therapy, and he was discharged from the hospital with the following oral medica-tions: enalapril maleate (20 mg PO Q 12 H), furo-semide (25 mg PO Q 12 H), digoxin (0.375 mg PO Q 12 H), and diltiazem (45 mg PO Q 8 H).2

Reevaluations of the ECG, digoxin levels, and echocardiogram were done 2 weeks after the initial presentation and revealed continued atrial fibrillation with slowing of the ventricular rate, normotension (BP 130 mm Hg SBP; 65 mmHg DBP), and improved fractional shortening (increased to 29%). Sherman's owner reported that he was active and alert and had a good appetite. He had gained 4 kg in the 2 weeks since the diagnosis and initiation of treatment. Sherman survived for 4 months after the initial diagnosis was made.

Treatment at a Glance

For acute care

  • Place a nasopharyngeal oxygen catheter with supplemental oxygen (100 ml/kg/min).

  • Digoxin (0.325 mg PO Q 12 H as a positive inotrope and negative chronotrope); pimobendan, a positive inotrope and venoarteriolar dilating drug, has been associated with improved survival and quality of life in Doberman pinchers and cocker spaniels with DCM.

  • Controlling rhythm with biphasic electrocardioversion has also been described.

Discharge with

  • Enalapril maleate (0.5 mg/kg PO Q 12 H)

  • Furosemide (2.2-4.4 mg/kg PO Q 12 H)

  • Digoxin (0.005-0.01 mg/kg PO Q 12 H, maximum dose 0.375 mg Q 12 H)

  • Diltiazem (10 mg/kg PO Q 12 H)