摘要
BACKGROUND: Chronic anemia caused by different factors is a common complication in patients with portal hypertension, but attention has been rarely paid to its detrimental effect on hemodynamic status. This study was undertaken to investigate the effects of hemoglobin concentration on hyperdynamic disturbance associated with portal hypertension (PHT). METHODS: According to blood hemoglobin level of 120 g/L, 55 patients with portal hypertension were divided into two groups, anemic and nonanemic. Hemodynamic and clinical data of the patients were analyzed retrospectively. The data were analyzed separately according to the Child classification in an attempt to avoid the effects of differences on hepatic function. RESULTS: Compared with the nonanemic group, the anemic group had an increased cardiac output (7. 4 ± 1. 7 L/ min vs. 6.3+1.9 L/min, P =0. 028), free portal pressure (29. 1 ±3. 1 mmHg vs. 26.8 ±3.3 mmHg, P =0.012), a decreased mean arterial pressure (84.0 ± 10.7 mmHg vs. 97.1 ±12.0 mmHg, P<0.01), and systemic vascular resistance (866 ±215 dyn/s ·cm5 vs. 1207 ±317 dyn/s ·cm5, P <0.01). Similar results were obtained when Child A and Child B-C patients were analyzed separately. Multivariate logistic regression revealed that the concentrations of hemoglobin (standard coefficient =0.31, P=0.01) and albumin (standard coefficient =0.21, P=0.04) were independent factors influencing the systemic vascular resistance in PHT patients. CONCLUSIONS: Anemia aggravates the hyperdynamic circulation of portal hypertension. Hemoglobin concentration is an important variable for evaluating the degree of hemodynamic disturbance in PHT patients.
BACKGROUND: Chronic anemia caused by different factors is a common complication in patients with portal hypertension, but attention has been rarely paid to its detrimental effect on hemodynamic status. This study was undertaken to investigate the effects of hemoglobin concentration on hyperdynamic disturbance associated with portal hypertension (PHT). METHODS: According to blood hemoglobin level of 120 g/L, 55 patients with portal hypertension were divided into two groups, anemic and nonanemic. Hemodynamic and clinical data of the patients were analyzed retrospectively. The data were analyzed separately according to the Child classification in an attempt to avoid the effects of differences on hepatic function. RESULTS: Compared with the nonanemic group, the anemic group had an increased cardiac output (7. 4 ± 1. 7 L/ min vs. 6.3+1.9 L/min, P =0. 028), free portal pressure (29. 1 ±3. 1 mmHg vs. 26.8 ±3.3 mmHg, P =0.012), a decreased mean arterial pressure (84.0 ± 10.7 mmHg vs. 97.1 ±12.0 mmHg, P<0.01), and systemic vascular resistance (866 ±215 dyn/s ·cm5 vs. 1207 ±317 dyn/s ·cm5, P <0.01). Similar results were obtained when Child A and Child B-C patients were analyzed separately. Multivariate logistic regression revealed that the concentrations of hemoglobin (standard coefficient =0.31, P=0.01) and albumin (standard coefficient =0.21, P=0.04) were independent factors influencing the systemic vascular resistance in PHT patients. CONCLUSIONS: Anemia aggravates the hyperdynamic circulation of portal hypertension. Hemoglobin concentration is an important variable for evaluating the degree of hemodynamic disturbance in PHT patients.
