Subclinical right heart failure may contribute to the development of liver disease in feedlot cattle during the finishing phase

The objectives of this study were twofold: first, to evaluate the relationship between mean pulmonary arterial pressure and mean central venous pressure, and determine if they increase through the finishing period; and second, to determine if mean central venous pressure is associated with liver disease. A cohort of crossbred yearling steers (n = 22; initial BW = 364 ± 52 kg) was studied at an altitude of 975m. Steers were fed for 171 d. Vascular pressures were measured twice: 6 and 54 d before slaughter. Serum biochemistry and liver histology were performed on steers that had the greatest (n = 5) and lowest (n = 5) mean central venous pressure at 54 d before slaughter. Biochemistry included total bilirubin, AST, GGT, and albumin; blood samples obtained 6 and 54 d before slaughter were evaluated. Liver samples were collected from the caudate lobe and lesions scored semiquantitatively. Both central venous and pulmonary arterial pressures increased from 54 d to 6 d before slaughter: 24 ± 1 mmHg to 28 ± 1 mmHg (P = 0.03) and 47 ± 2 mmHg to 54 ± 2 (P < 0.01), respectively. There was a positive association between mean pulmonary arterial and central venous pressures at 6 d (P < 0.01) but not 54 d before slaughter (P = 0.41) indicating that increased pulmonary arterial pressure contributed to right heart failure in cattle closest to slaughter weight. Serum biochemistry was within normal limits even though all steers showed histological evidence of liver damage centered on the centrilobular region (zone 3). All steers showed hydropic degeneration and sinusoid dilation. Lesion severity was greatest in the high mean central venous pressure group: One liver had cirrhosis; another had multifocal necrosis. Congestion was moderate to severe and centered on zones 1 and 2. The findings of this study indicate that subclinical right heart failure secondary to pulmonary hypertension may contribute to hepatic congestion and disease in feedlot cattle during the finishing phase. Serum biochemistry analyses may not represent the insidious liver damage of cattle close to slaughter. Right heart failure secondary to pulmonary hypertension, or cor pulmonale, may contribute to the development of liver disease in feedlot cattle during the finishing phase.