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Ann Fr Anesth Reanim ; 8(3): 267-72, 1989.
Article in French | MEDLINE | ID: mdl-2675691

ABSTRACT

During an acute decompensation of chronic obstructive pulmonary disease (COPD) associated with pulmonary arterial hypertension (PAHP), the right cardiac ventricle is unable to tolerate the increased workload required to overcome the increase in pulmonary arterial pressure (Ppa). As a result, the cardiac (CI) and systolic (SI) indices decrease much more than in those patients without PAHP. This study aimed to evaluate the effects of nifedipine on haemodynamic parameters and oxygen availability (QO2) when given to mechanically ventilated COPD patients with PAHP during an acute decompensation. The series included 14 patients aged 68 +/- 8 yr, admitted to an intensive care ward for an acute decompensation of COPD, with Ppa greater than 20 mmHg. They remained haemodynamically stable throughout the study period. The measurements were made 20 min after the Swan-Ganz and radial artery catheters were set up (t0), and one hour after administration of 10 mg sublingual nifedipine (t1). Thereafter this agent was given three times a day. A further set of measurements were carried out in seven patients, 24 h after the first dose of nifedipine (t2). At t1, there was a significant increase in CI (+12.3%) and QO2 (+14.1%), whereas Ppa, indexed pulmonary vascular resistances, indexed systemic vascular resistances (SVRI) and PaO2 decreased significantly (-9.2%; -20%; -12.8% and -6.4% respectively). At t2, QO2 was significantly higher (+18.4%), whereas Ppa and SVRI were significantly lower, than at t0. PaO2 and the shunt fraction (Qs/Qt) returned to basal values, with a significant decrease in Qs/Qt when compared with t1.(ABSTRACT TRUNCATED AT 250 WORDS)


Subject(s)
Hemodynamics/drug effects , Hypertension, Pulmonary/drug therapy , Lung Diseases, Obstructive/drug therapy , Nifedipine/pharmacology , Humans , Hypertension, Pulmonary/etiology , Hypertension, Pulmonary/physiopathology , Lung Diseases, Obstructive/complications , Lung Diseases, Obstructive/physiopathology , Oxygen/blood , Respiration, Artificial
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