Cardiopulmonary response to exercise in patients with liver cirrhosis and impaired pulmonary gas exchange.

Maximal exercise capacity and pulmonary gas exchange are both commonly impaired in liver cirrhosis. Apart from rare cases of hepatopulmonary syndrome, it is still unknown whether these moderate pulmonary gas exchange abnormalities can alter aerobic capacity of cirrhotic patients. Resting pulmonary function tests and symptom-limited cardiopulmonary exercise testing were prospectively investigated in 30 patients with liver cirrhosis exhibiting a widened alveolar-arterial oxygen gradient (P(A-a)O(2) > 30 mm Hg at peak exercise) without pulmonary vascular dilatations at contrast-enhanced echocardiography. Data were compared with those of 30 normoxemic cirrhotic controls (matched for age, gender, body mass index, etiology and severity of liver disease, smoking habits, hemoglobin level, and beta-blocker therapy). Resting cardiopulmonary parameters were within normal range in both groups except carbon monoxide lung transfer (TLCO, 60.4 ± 2.9 vs 74.3 ± 2.8% in controls, p = 0.0004) and P(A-a)O(2) (28.8 ± 2 vs 15.3 ± 2 mm Hg in controls, p < 0.0001). Cirrhotics with impaired gas exchange during exercise exhibited a significant reduction in maximal oxygen uptake (VO(2)max, 1.18 ± 0.07 (53% predicted) vs 1.41 ± 0.07 L/min (62% predicted), p = 0.004), a higher ventilation level at ventilatory threshold (V(E)/VO(2), 39.2 ± 1.5 vs 35.3 ± 1.5, p = 0.01) without ventilatory limitation, and a greater dead space to tidal volume ratio (V(D)/V(T)max, 0.32 ± 0.01 vs 0.25 ± 0.01, p = 0.01). VO(2)max correlates negatively with V(D)/V(T)max (r(2) = 0.36; p < 0.0001). There were no differences in cardiac or metabolic response to exercise between groups. Taken together these findings suggest that clinically undetectable pulmonary vascular disorders can slightly contribute to further reduce exercise capacity of cirrhotic patients.

Determinants of dyspnea and alveolar hypoventilation during exercise in cystic fibrosis: impact of inspiratory muscle endurance.

UNLABELLED: Dyspnea is one of the main complaints of patients with cystic fibrosis (CF). Lung function at rest is not sufficient to explain dyspnea during exercise. Because inspiratory muscles are faced with an increased workload in advanced CF, we studied the impact of their strength and endurance on dyspnea and alveolar hypoventilation during exercise. METHODS: Eighteen stable CF patients performed a maximal exercise test on a cycloergometer. Level of exercise dyspnea was recorded by a Borg scale at exhaustion. Blood gases were analysed at rest and at maximal peak exercise. Inspiratory muscle endurance (IME), expressed as a percentage of maximal inspiratory pressure (PImax), was measured according to an incremental threshold loading technique (Martyn). RESULTS: Four men and fourteen women were included with a mean age of 32 years (20-67). Mean FEV(1) was 44% predicted (21-82%). Mean PImax was 78% predicted (24-148%). No significant correlation was found between dyspnea and age, body mass index, pulmonary function at rest, blood gases, inspiratory muscle strength (PImax) or exercise capacity. Dyspnea was correlated with IME (r=-0.72, p=0.0029) and plethysmographic airway resistance (r=0.64, p=0.009). When patients were grouped according to degree of exercise dyspnea, half expressed a dyspnea more than "severe" (above level 5 on Borg scale) and half reported a lower dyspnea (Borg score ≤5). Significant differences were observed between these two groups in inspiratory muscle endurance (46.8 versus 76.4% of PImax; p<0.001), PaCO2 at rest (40.3 versus 36.2 mmHg; p=0.03) and PaCO2 at peak exercise (47.7 versus 40.6 mmHg; p=0.04). CONCLUSION: Exertional dyspnea may be significantly influenced by inspiratory muscle function and alveolar hypoventilation in CF patients. Inspiratory muscle endurance could be of importance to analyse the impact of pulmonary rehabilitation in this specific disease.

Aerobic capacity in patients with chronic liver disease: Very modest effect of liver transplantation.

INTRODUCTION: Aerobic capacity is commonly impaired in patients with liver cirrhosis, as demonstrated by their low oxygen consumption at peak exercise (peak VO(2)). This impairment is correlated with the severity of the liver disease. We investigated the effect of orthotopic liver transplantation (OLT) alone on exercise capacity in this prospective study of patients with liver cirrhosis. METHOD: Twenty liver transplant candidates, aged 27 to 61years, underwent resting pulmonary function tests, echocardiography, and incremental cardiopulmonary exercise testing (CPET) before OLT and 16.3 + or - 1.6months after OLT. RESULTS: Following OLT, peak VO(2) increased by a mean of only 7.7% (from 63.4 to 71.1% of predicted value), and decreased in one-quarter of the patients. Cardiac function was normal before OLT and no changes in respiratory indicators followed OLT. Change in peak VO(2) after OLT (Delta peak VO(2)) was related to changes in hemoglobin level (r(2)=0.45, p=0.04), the stopping of beta-blocker therapy, and muscle impairment, as suggested by the correlation between Delta peak VO(2) and peak lactate concentration before OLT (r(2)=0.64, p<0.01). DISCUSSION: Our study provides evidence of a very modest and inconsistent increase in aerobic capacity in liver transplant candidates after liver transplantation alone. This persistent impairment of exercise tolerance was principally of peripheral origin but anemia and beta-blocker treatment should be considered as major aggravating factors. Rehabilitation programs before and after transplantation may increase its benefits to these deconditioned liver transplant recipients in their daily lives.

Impact of impaired aerobic capacity on liver transplant candidates.

BACKGROUND: Oxygen consumption at peak exercise (peak VO2) is the most accurate index of aerobic capacity (AC), which reflects the physical condition of an individual and is currently considered the gold standard for cardiorespiratory fitness. Evaluation of peak VO2 to identify high-risk candidates for liver transplantation (LT) may represent an interesting approach. The aims of this study were (a) to describe AC and identify factors independently associated with peak VO2; (b) to analyze the prognostic value of peak VO2 in patients referred for preliminary evaluation of LT; and (c) to provide preliminary data on the influence of peak VO2 on length of hospitalization and the need for oxygen support after LT. RESULTS: Peak VO2 was determined in patients referred for preliminary evaluation for LT. One hundred thirty-five candidates were included. More than half had severe alterations in peak VO2. Age, gender, model-for-end-stage liver disease (MELD) score, tobacco use, and hemoglobin were independently associated with peak VO2. Candidates with severe alterations in peak VO2 had a lower 1-year survival than others. Model-for-end-stage liver disease score and peak VO2 were independently associated with survival. In patients with a MELD above 17, those with severe alterations of peak VO2 AC had lower 1-year survival than the others. Among patients who underwent LT, those with severe impairment of peak VO2 showed a trend toward a higher mean length of hospitalization after LT and had significantly longer need for oxygen support. CONCLUSIONS: Peak VO2 is severely impaired in candidates for LT and affects survival and post-LT course. Perioperative respiratory rehabilitation programs validated in lung and heart transplantation must be tested.

Dobutamine and gastric-to-arterial carbon dioxide gap in severe sepsis without shock.

OBJECTIVES: To evaluate the effect of an early dobutamine infusion on gastrointestinal perfusion in patients with severe sepsis. DESIGN: Prospective, randomized, controlled, multicenter clinical study. SETTING: Six medical and/or surgical intensive care units (ICU) of teaching hospitals. PATIENTS: Forty-two patients with severe sepsis. INTERVENTIONS: Patients were divided into two groups according to gastric-to-arterial CO2 gap (DeltaCO2) [normal DeltaCO2 group ( n=17): DeltaCO2 < or = 8 mmHg; increased DeltaCO2 group ( n=25): DeltaCO2 > 8 mmHg]. Patients within each group were then randomized to receive either dobutamine (5 microg/kg per min) or saline for 72 h. MEASUREMENTS AND MAIN RESULTS: SAPS II was similar in both groups [group 1: 44.0 (33.0-56.5); group 2: 48.5 (40.5-59.0), p=0.27]. At ICU admission, mean arterial pressure was lower in the high DeltaCO2 group [73.0 (67.0-79.5) mmHg, p=0.03] than in the normal DeltaCO2 group [84.0 (73.7-104.0) mmHg] while blood lactate [normal DeltaCO2 group: 1.6 (0.8-2.3); high DeltaCO2 group: 1.6 (1.1-1.9) mmol/l] was similar for the two groups. DeltaCO2 was significantly lower in the normal DeltaCO2 group [5.0 (2.0-6.0) mmHg)] than in the high DeltaCO2 group [11.0 (10.0-19.0) mmHg]. Dobutamine infusion did not significantly change hemodynamics, blood lactate concentration or tonometric parameters in any group within the first 72 h and had no particular beneficial effect in this population. CONCLUSIONS: An early infusion of dobutamine at a fixed dose of 5 microg/kg per min during the first 72 h of severe sepsis does not influence gastric DeltaCO2.