Echocardiography in a Horse with Cor Pulmonale from Recurrent Airway Obstruction

Abstract

A 440-kg, 25-year-old Quarter horse mare presented to the University of Minnesota Veterinary Medical Center for assessment of recurrent airway obstruction. She had exhibited a seasonal (summer and fall) cough for the past 5 years. The latest cough began 4 months before presentation and did not respond to treatment with dexamethasone or prednisone. The mare was housed on pasture and fed alfalfa hay and sweet feed. Vaccinations and deworming were current. The mare was in good body condition and had a normal rectal temperature and heart rate. The facial pulse was weak, most likely because of dehydration, which was estimated at 5%. Tachypnea (40 breaths per minute) and marked dyspnea with a pronounced expiratory effort were present and auscultation disclosed wheezes in the caudoventral lung fields bilaterally. No other abnormalities were detected on physical examination. Endoscopy of the upper airway was unremarkable, but foam and mucus were present in the trachea.Tracheal wash fluid obtained through the endoscope contained mostly nondegenerate neutrophils with lesser numbers of macrophages. Actinobacillus suis, Klebsiella oxytoca, and Aspergillus spp. were grown from the tracheal wash fluid and deemed to be contaminants because of the low colony counts. A bronchointerstitial pattern, most prominent in the caudoventral lung fields was present on radiographic examination. Ultrasonography of the thorax exposed well-aerated peripheral pulmonary parenchyma with small hypoechoic areas of irregularity of the lung surface scattered bilaterally. Mild hypoxia was apparent in an arterial blood gas sample from the transverse facial artery (PaO 2 , PaCO 2 , and pH were 79.0 mm Hg, 45.5 mm Hg, and 7.449, respectively; normal values 95.6 6 11.43 and 40.53 6 4.14 mm Hg and 7.417 6 0.03, 1 respectively). A leukocytosis characterized by mature neutrophilia was suggestive of a stress leukogram because it was present on the day of admission only.Intravenous fluid therapy was initiated to correct dehydration. Furosemide (1.1 mg/kg IV), atropine (0.01 mg/kg IV), and intranasal oxygen initially were given with no improvement. Clenbuterol (1.7 mg/kg PO q12h), phenylbutazone (4.5 mg/kg IV once then 2.3 mg/ kg IV q24h), and dexamethasone (0.1 mg/kg IV q24h) were given for 4 days with no effect. Guafenesin (3 mg/ kg PO) was given once to help remove mucus from the airways. Inhaled albuterol (720 mg q6h) produced only mild improvement in respiratory effort and rate. a Echocardiography disclosed high-velocity end diastolic pulmonary insufficiency and enlargement of the pulmonary artery diameter compared with aortic diameter. Both findings were indicative of pulmonary hypertension. 2 All other variables obtained during echocardiography were normal (Table 1). Vascular pressures were recorded with a 160-cm balloon-tipped catheter placed in the right jugular vein. Right ventricular and pulmonary artery systolic pressures were 142 and 137 mm Hg, respectively (normal values 45.84 6 5.76 and 42.12 6 5.22 mm Hg). Mean right atrial, right ventricular, p...

Cor pulmonale secondary to pulmonary fibrosis in a 16‐year‐old mare

“…A few cases reported hypoxaemia from severe pulmonary diseases in horses as low as 79 mmHg (Sage et al . ), 71.4 mmHg (Schwarzwald et al . ) and 61 mmHg (Hanka et al .…”

Equine myocardial right ventricular ouflow tract function in horses with RAO

“…In früheren Studien konnte mittels konventioneller Echokardiographie nur bei hochgradig COB-kranken Pferden eine Hypertrophie des rechten Herzens oder eine Dilatation des rechten Ventrikels im Sinne eines Cor pulmonale nachgewiesen werden (Sage et al 2006, Johansson et al 2007). Demgegenüber zeigten invasive Herzkatheter-Druckmessungen Unterschiede zwischen COB und Kontrollpferden (Dixon 1978, Dixon et al 1982, Seiffert 1997.…”

Cor pulmonale and respiratory disease: unique features of the equine cardiopulmonary system

“…Horses, in contrast, rarely develop pulmonary vascular anatomical changes, even in the face of long-standing pulmonary hypertension and hypoxia (Dixon et al 1982). The most common chronic pulmonary disease of horses in Northern Europe is recurrent airway obstruction (heaves) and although affected horses almost universally develop pulmonary hypertension (Dixon 1978), cor pulmonale is seldom observed (Sage et al 2006). The lungs of horses suffering from recurrent airway obstruction (RAO) do not develop the vascular anatomical changes seen in other species (Dixon et al 1982).…”

“…Although the basis for the difference between horses and other species is not clear, it does appear that the ability of the equine pulmonary vascular system to respond to hypoxia with functional, rather than anatomical, changes may be a mechanism that protects against development of cor pulmonale. However, right ventricular hypertrophy does develop in a small proportion of RAO cases secondary to hypoxia-driven pulmonary hypertension (Dixon et al 1982;Sage et al 2006) and clinicians should be vigilant for this minority of RAO-affected horses with cor pulmonale. It has been suggested that it is the intermittent nature of RAO that prevents cor pulmonale and that it might be expected to occur more frequently in response to chronic, persistent pulmonary disease (Sage et al 2006).…”

“…However, right ventricular hypertrophy does develop in a small proportion of RAO cases secondary to hypoxia-driven pulmonary hypertension (Dixon et al 1982;Sage et al 2006) and clinicians should be vigilant for this minority of RAO-affected horses with cor pulmonale. It has been suggested that it is the intermittent nature of RAO that prevents cor pulmonale and that it might be expected to occur more frequently in response to chronic, persistent pulmonary disease (Sage et al 2006). The two cases discussed in this issue suggest that this is not the case as despite both horses having severe, progressive, irreversible pulmonary disease with hypoxia/hypoxaemia, both did not develop cor pulmonale.…”