Search PubMed⌕ Search

Biomedical subjects

F Lemaire

Publications and source records attributed to F Lemaire.

At least 127 records · Page 7Linked to original sources
PubMed1988

Acute left ventricular dysfunction during unsuccessful weaning from mechanical ventilation.

The authors studied the hemodynamic effects of rapidly weaning from mechanical ventilation (MV) 15 patients with severe chronic obstructive pulmonary disease (COPD) and cardiovascular disease who were recovering from acute cardiopulmonary decompensation. In each patient, 10 min of spontaneous ventilation (SV) with supplemental oxygen resulted in reducing the mean esophageal pressure (X +/- SD, + 5 +/- 3 to -2 +/- 2.5 mmHg, P less than .01) and increasing cardiac index (CI) 3.2 +/- 0.9 to 4.3 +/- 1.3 1/min/M2, P less than .001), systemic blood pressure (BP 77 +/- 12 to 90 +/- 11 mmHg, P less than .001), heart rate (HR 97 +/- 12 to 112 +/- 16 beats/min, P less than .001), and, most importantly, transmural pulmonary artery occlusion pressure markedly increased (PAOPtm 8 +/- 5 to 25 +/- 13 mmHg, P less than .001), mandating a reinstitution of MV. In four patients with left ventricular (LV) catheters, the PAOP correlated with the LV end-diastolic pressure during both MV and SV. Gated blood pool imaging showed SV increased the LV end-diastolic volume index (65 +/- 24 to 83 +/- 32/M2, P less than .002) with LV ejection fraction unchanged. Patients were treated for a mean of 10 days with diuretics, resulting in a reduction of blood volume (4.55 +/- 0.9 1 to 3.56 +/- 0.55 1) and body weight (-5 kg, P less than .001). Subsequently, nine of the 15 patients were weaned successfully from mechanical ventilation with unchanged PAOP.

Adult↗
PubMed1988

Low VA/Q areas: arterial-alveolar N2 difference and multiple inert gas elimination technique.

In 16 critically ill patients the arterial-alveolar N2 difference and data from the multiple inert gas elimination technique (MIGET) were compared in the evaluation of the contribution of low alveolar ventilation-perfusion ratio (VA/Q) lung regions (0.005 less than VA/Q less than 0.1) to venous admixture (Qva/QT). The arterial-alveolar N2 difference was determined using a manometric technique for the measurement of the arterial N2 partial pressure (PN2). We adopted a two-compartment model of the lung, one compartment having a VA/Q of approximately 1, the other being open, gas filled, unventilated (VA/Q = 0), and in equilibrium with the mixed venous blood. This theoretical single compartment represents all lung regions responsible for the arterial-alveolar N2 difference. The fractional blood flow to this compartment was calculated using an appropriate mixing equation (Q0/QT). There was a weak but significant relationship between Q0/QT and the perfusion fraction to lung regions with low VA/Q (0.005 less than VA/Q less than 0.1) (r = 0.542, P less than 0.05) and a close relationship between Q0/QT and the perfusion fraction to lung regions with VA/Q ratios less than 0.9 (r = 0.862, P less than 0.001) as obtained from MIGET. The difference Qva/QT-Q0/QT yielded a close estimation of the MIGET right-to-left shunt (Qs/QT) (r = 0.962, P less than 0.001). We conclude that the assessment of the arterial-alveolar N2 difference and Q0/QT does not yield a quantitative estimation of the contribution of pathologically low VA/Q areas to QVa/QT because these parameters reflect an unknown combination of pathological and normal (0.1 less than VA/Q less than 0.9) gas exchange units.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Gas Analysis↗
PubMed1988

Involvement of ANF in the acute antidiuresis during PEEP ventilation.

To investigate the potential role of natriuretic factor (ANF) on changes on renal excretory function in response to increased intrathoracic pressure, seven patients were studied during three successive 60-min periods of 1) mechanical ventilation (MV) and zero end-expiratory pressure (ZEEP), 2) MV with 12 cmH2O positive end-expiratory pressure (PEEP), and 3) MV with the same level of PEEP while lower-body positive pressure (LBPP) was applied to restore venous return and increase central blood volume without fluid loading. Hemodynamics, renal excretory function parameters, and plasma immunoreactive atrial natriuretic factor (irANF) levels were recorded at the end of each period. Compared with ZEEP, PEEP induced a significant reduction of diuresis (from 134 +/- 17 to 59 +/- 13 ml/h, P less than 0.01) and natriuresis (from 8.37 +/- 3.5 to 3.83 +/- 2 mmol/h, P less than 0.01), whereas plasma irANF fell from 520 +/- 292 to 155 +/- 40 pg/ml (P less than 0.01) and transmural right atrial pressure decreased from 3.9 +/- 0.5 to 2.4 +/- 0.3 mmHg (P less than 0.01). Opposite changes were observed during application of LBPP, which restored diuresis and plasma irANF to near control ZEEP values, despite continuation of PEEP. Changes in renal excretory function parameters thus paralleled changes in right atrial pressure and plasma irANF. We suggest that changes in plasma irANF in response to hemodynamic variations induced by changes in intrathoracic pressure may contribute to alterations of renal excretory function during PEEP.

Adult↗
PubMed1988

The effects of urapidil therapy on hemodynamics and gas exchange in exercising patients with chronic obstructive pulmonary disease and pulmonary hypertension.

To examine the hemodynamic changes induced by vasodilator therapy with urapidil during exercise in patients with chronic obstructive pulmonary disease (COPD) and their potential impact on symptom-limited maximal oxygen consumption, we studied 12 clinically stable patients using a randomized, crossover design. Placebo or urapidil (60 mg orally thrice a day) was given during 48 h preceding each incremental maximal exercise testing. Urapidil compared to placebo consistently lowered the pulmonary artery pressure either at rest from 29 +/- 2.5 to 24 +/- 1.5 mm Hg (p less than 0.001) or during exercise from 55 +/- 3 to 46 +/- 2 mm Hg (p less than 0.01). At rest, the systemic arterial pressure was reduced from 97.5 +/- 4 to 88.5 +/- 3 mm Hg (p less than 0.001) with no significant difference in heart rate or cardiac index. During exercise, systemic arterial pressure decreased from 135 +/- 4 to 119 +/- 3 mm Hg (p less than 0.001). As compared to placebo, urapidil tended to increase the cardiac index from 6.1 +/- 0.4 to 6.6 +/- 0.4 L/min.m2 (NS) and to decrease heart rate, from 122 to 116 beats/min (NS); the resulting stroke volume index increased with urapidil from 49 +/- 3 to 57 +/- 4 ml/m2 (p less than 0.01); at rest, urapidil did not induce alteration in gas exchange, while during exercise, C(a-v)O2 decreased from 8.6 +/- 0.5 to 7.7 +/- 0.4 vol% (p less than 0.01), SVO2 increased from 39.5 +/- 2 to 44.5 +/- 1.5% (p less than 0.01), and SaO2 from 82 +/- 2 to 85 +/- 2% (p less than 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Inspiratory work of breathing during spontaneous ventilation using demand valves and continuous flow systems.

To diminish the work of breathing, some demand valve systems are equipped with inspiratory pressure support (IPS). The purpose of this study was to evaluate the work performed during spontaneous breathing using the Siemens Servo 900C ventilator (SVC) at the minimal IPS level available, and comparing it with a demand valve ventilator without IPS, the Ohmeda CPU1 (CPU1), and with a home-built continuous flow system (CFS). We found a larger minute ventilation and inspiratory peak flow with the SVC and the CFS than with the CPU1 (p less than 0.05). When the work of breathing was measured at the airway opening, we found that the CFS led to the least amount of work (0.17 +/- 0.05 J.L-1, p less than 0.05). Additionally, this work was strikingly less for SVC than for CPU1 (0.22 +/- 0.06 versus 0.42 +/- 0.10 J.L-1, p less than 0.001) as a result of a higher flow supplied by the SVC. By contrast, the work measured using the esophageal pressure, i.e., including the work dissipated on the lung and airways, was significantly reduced with the CFS (1.34 +/- 0.45 J.L-1, p less than 0.05), but surprisingly not different between SVC and CPU1 (1.49 +/- 0.57 versus 1.54 +/- 0.51 J.L-1). We conclude that the absence of a demand valve in CFS involves the lowest work of breathing. Likewise, the high flow capability in SVC reduces the work necessary to overcome the circuit and demand valve resistances.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Improved efficacy of spontaneous breathing with inspiratory pressure support.

During inspiratory pressure support (IPS) ventilation, first a negative airway pressure is produced by the patient to open a demand valve and then a constant positive airway pressure is maintained at a present level while the patient inhales. The aim of this study was to assess the ability of 10 cm H2O IPS to improve the efficacy of spontaneous ventilation. We studied 8 intubated patients recovering from acute respiratory failure, all were breathing spontaneously via 3 different systems: a Servo 900 C ventilator (SCV) without IPS, a Servo 900 C ventilator with 10 cm H2O IPS, and a continuous flow system (CFS). Compared with the CFS, breathing with the SVC without IPS resulted in an increased respiratory rate (RR), increased tidal Volume (VT), increased transdiaphragmatic pressure (Pdi), and no significant change in PaO2 or PaCO2. Ventilation with IPS resulted in significant improvements in VT, PaO2, and PaCO2 with a decreased RR and Pdi when compared with both the other modes of spontaneous ventilation. A significant decrease in the pressure-time index of the diaphragm (i.e., the product of the mean transdiaphragmatic pressure and the inspiratory duty cycle) occurred during IPS. In 2 patients, we recorded diaphragmatic electromyographic activity during both SVC and IPS. In both patients during IPS, an increased VT and a decreased Pdi coincided with a major reduction of electromyographic activity. We conclude that IPS at a level of 10 cm H2O markedly increases the efficacy of spontaneous breathing while reducing the activity of the inspiratory muscles.

Blood Gas Analysis↗
PubMed1987

Effects of indomethacin on pulmonary hemodynamics and gas exchange in patients with pulmonary artery hypertension, interference with hydralazine.

To assess the ability of indomethacin (Indo) to influence pulmonary vascular tone in patients with chronic lung disease, we studied the hemodynamic and gas exchange alterations induced by a 50-mg indomethacin infusion in 10 patients suffering from varying degrees of pulmonary artery hypertension and hypoxemia. The most pronounced effects were observed 3 h after Indo administration. Mean systemic arterial pressure (Psa) increased from 76 +/- 4 to 86 +/- 4 mm Hg (p less than 0.01), whereas mean pulmonary arterial pressure (Ppa) was unchanged. The cardiac index (CI) decreased from 3.1 +/- 0.2 to 2.8 +/- 0.2 L/min/m2 (p less than 0.02) because of the reduced heart rate, which decreased from 86 +/- 5 to 80 +/- 4 beats/min (p less than 0.05). Systemic and pulmonary vascular resistance indexes increased, respectively, from 22 +/- 2 to 27.5 +/- 2 U/m2 (p less than 0.001) and from 11.9 +/- 2 to 13.4 +/- 2 U/m2 (p less than 0.05). We measured an increase in PaO2, from 49.5 +/- 4 to 57.5 +/- 4 mm Hg (p less than 0.001) simultaneously with a reduced venous admixture, from 39.5 +/- 4 to 30.5 +/- 3% (p less than 0.001). The calculated PO2 uptake was unchanged, but mixed venous O2 tension increased from 30.5 to 33.5 mm Hg (p less than 0.01). Because Indo may interfere with the hypotensive effect of hydralazine and because hydralazine has been proposed in the treatment of patients with pulmonary hypertension, 7 of these patients also received 0.35 mg/kg hydralazine and Indo plus hydralazine (Indo + H) injected simultaneously.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Cardiopulmonary effects of ketanserin infusion in human pulmonary embolism.

The release of platelet-derived vasoactive substances, particularly serotonin (5-HT), have been implicated in the pulmonary vasoconstrictor response following acute pulmonary embolism. Therefore, we studied the effects of infusing ketanserin, a 5-HT blocking agent, upon pulmonary and systemic hemodynamics and gas exchange in 10 patients with severe acute pulmonary embolism. These patients evidenced 45 +/- 17% mean angiographic pulmonary vascular obstruction. Ketanserin significantly decreased the mean pulmonary arterial pressure from 26 +/- 6 to 23 +/- 5 mm Hg (p less than 0.001). The total pulmonary vascular resistance decreased from 9.1 +/- 3.2 to 8.3 +/- 2.5 mm Hg/L X min X m2 (p less than 0.001). However, the mean cardiac index was unchanged. The systemic arterial and right atrial pressures were significantly decreased after ketanserin. The PaO2 increased in all patients from 60.5 +/- 12.6 to 66.5 +/- 13.6 mm Hg (p less than 0.05), whereas the venous admixture was unchanged. This was attributed to an increased PVO2 (27 +/- 7 to 30 +/- 5 mmHg, p less than 0.01) secondary to a reduction of calculated peripheral oxygen consumption during ketanserin infusion. The results indicate ketanserin is a mild pulmonary vasodilator and can reduce the pulmonary hypertension and increase the PaO2 after pulmonary embolism.

Adult↗
PubMed1987

Hemodynamic effects of urapidil in patients with pulmonary hypertension. A comparative study with hydralazine.

Vasodilator therapy for pulmonary hypertension ideally should cause a proportionately greater reduction of resistance in the pulmonary vascular bed than in the systemic circulation. This should limit the occurrence of systemic hypotension, which can complicate the use of most vasodilator drugs. Urapidil is a new vasodilator that acts by postsynaptic alpha 1-blockade while inhibiting the aortic pressure baroreceptor reflex and reducing central sympathetic tone. We investigated and compared the short-term effects of Urapidil and hydralazine in 10 patients suffering varying degrees of pulmonary hypertension. Each patient received either 0.35 mg/kg hydralazine or 0.75 mg/kg Urapidil intravenously on 2 sequential days in a randomized order. The main effect of Urapidil was to decrease the mean pulmonary artery pressure in all 10 patients from 44 +/- 4 to 37 +/- 3.5 mm Hg (p less than 0.001). After Urapidil infusion, the mean decrease of resistance in the pulmonary vascular bed (32%) exceeded that in the systemic circulation (25%). In contrast, pulmonary artery pressure remained unchanged with hydralazine, and predominant systemic vasodilation occurred: systemic vascular resistance decreased by 45%, whereas pulmonary vascular resistance decreased by 25%. Hydralazine markedly increased the cardiac index and induced tachycardia. Urapidil maintained the heart rate nearly constant and only slightly increased the cardiac index, thereby fostering the diastolic emptying of the pulmonary circulation. No significant change in arterial oxygenation occurred with either drug, although arterial oxygen partial pressure tended to increase with hydralazine. Urapidil may be a promising drug in the treatment of patients with pulmonary hypertension.

Aged↗
PubMed1987

[The value of respiratory function tests in the surveillance of asthmatic children].

The purpose of pulmonary function testing in children with asthma is to search for obstructive airway disease. We examined the charts of 169 asthmatic children during intervals between acute exacerbations. The severity of asthma was determined according to VIALATTE classification, with the Tiffeneau ration FEV1/VC (1) and the MMFR/VC ratio serving as obstructive indices. According to these data, children were classified into three groups: normal children (normal FEV1/VC and MMFR/VC), children with probable obstruction of the distal airways (normal FEV1/VC and decreased MMFR/VC), and children with both proximal and distal airway obstruction (decreased FEV1/VC and MMFR/VC). Since suggested normal values vary in the literature, we compared FEV1 and MMFR to determine as accurately as possible the number of children with obstructive disease. The relationship between the degree of clinical involvement and pulmonary function testing results was studied. Clinically, asymptomatic children with suspected normal respiratory function had evidence of obstructive disease in two out of three cases, and would benefit from drug therapy.

Adolescent↗
PubMed1985

Total respiratory compliance as a function of lung volume in patients with mechanical ventilation.

In normal subjects breathing spontaneously, compliance has been shown to be influenced by the lung volume from which deflation started. We wondered whether this would also be true for patients with acute respiratory failure who required mechanical ventilation and we accordingly studied 15 such patients. Chest inflation was performed using a continuous flow device (ATM-PV 102), and total compliance was measured as the slope of the pressure-volume relationship during deflation. As inflated lung volumes were increased by 10 to 15, 20 and 25 ml/kg body weight above FRC, mean compliance increased to 38.2, 45.5, 52.2 and 59.3 ml/cmH2O respectively. Each of these increases in mean compliance was statistically significant (p less than 0.001). Increasing the inflated lung volume to 30 ml/kg produced no further significant increase in mean compliance. This study showed that, in patients with acute respiratory failure requiring mechanical ventilation, compliance measured during deflation is a function of the inflated lung volume. We recommend that the compliance should be measured from a constant and high lung volume, equal to 25 ml/kg body weight above FRC.

Acute Disease↗