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Background: Weaning patients with heart failure who have required mechanical ventilation remains challenging. We evaluated echocardiographic indexes and N-terminal pro-brain natriuretic peptide (NT-proBNP) as markers of acute cardiac dysfunction before and after spontaneous breathing trials (SBT) in such patients to assess their ability to predict subsequent successful extubation., Methods: Forty-four patients who underwent their first SBT were prospectively included. Plasma levels of NT-proBNP and transthoracic echocardiography indices including cardiac index, E/A ratio and E/Ea ratio were recorded immediately before commencing and just before the end of SBT., Results: Ten patients (22.7%) failed their SBT. No significant difference was observed concerning baseline echocardiographic data and NT-proBNP level between the patients who succeeded the SBT or those that failed. Cardiac index increased significantly at end-SBT in patients who passed (3.3 [3.06-3.77] vs. 3 [2.68-3.3] L/min/m(2), P<0.001), whereas it remained unchanged in those that failed. E/Ea ratio (16.8 [8.5-27.3] vs. 10.7 [6.7-20.5], P=0.006) and NT-proBNP level (8199 [3106-10949] vs. 4200 [1855-7125] pg/mL, P=0.004) increased significantly in those who failed the SBT, in contrast to the weaning success group where they remained unchanged., Conclusion: Neither NT-proBNP level nor the studied echocardiographic indices before SBT were able to predict SBT outcome in patients presenting with severe heart failure. Failure to increase the cardiac index and increases in both E/Ea ratio and NT-proBNP levels were seen at end-SBT in patients who failed the SBT, and may reflect failure of myocardial reserve to cope with the stress of SBT.

Objective: Adverse respiratory and gasometrical effects have been described in patients with acute respiratory failure (ARF) undergoing noninvasive ventilation (NIV) with standard heat and moisture exchangers (HME). We decided to evaluate respiratory parameters and arterial blood gases (ABG) of patients during NIV with small dead space HME compared with heated humidifier (HH)., Design: Prospective randomized crossover study., Setting: A 16-bed medical intensive care unit (ICU)., Patients: Fifty patients receiving NIV for ARF., Measurements: The effects of HME and HH on respiratory rate, minute ventilation, EtCO(2), oxygen saturation, airway occlusion pressure at 0.1 s, ABG, and comfort perception were compared during two randomly determined NIV periods of 30 min. The relative impact of HME and HH on these parameters was successively compared with or without addition of a flex tube (40 and 10 patients, respectively)., Main Results: No difference was observed between HME and HH regarding any of the studied parameters, whether or not a flex tube was added., Conclusion: If one decides to humidify patients' airways during NIV, one may do so with small dead space HME or HH without altering respiratory parameters.

Purpose: Surgical treatment is crucial in the management of necrotizing soft tissue infections (NSTIs). The aim of this study was to determine the influence of surgical procedure timing on hospital mortality in severe NSTI., Methods: A retrospective study including 106 patients was conducted in a medical intensive care unit equipped with a hyperbaric chamber. Data regarding pre-existing conditions, intensive care and surgical management were included in a logistic regression model to determine independent factors associated with hospital mortality., Results: Overall hospital mortality was 40.6%. In multivariate analysis, underlying cardiovascular disease, SAPS II, abdominoperineal compared to limb localization, time from the first signs to diagnosis <72 h, and time from diagnosis to surgical treatment >14 h in patients with septic shock were independently associated with hospital mortality., Conclusion: In patients with NSTI and septic shock, hospital mortality is influenced by the timing of surgical treatment.

This study examined tap water as a source of Pseudomonas aeruginosa in a medical intensive care setting. We prospectively screened specimens of patients, tap water and hands of healthcare workers (HCWs) over a six-month period in a 16-bed medical intensive care unit. Molecular relatedness of P. aeruginosa strains was investigated by pulsed-field gel electrophoresis. A total of 657 tap water samples were collected from 39 faucets and 127 hands of HCWs were sampled. P. aeruginosa was found in 11.4% of 484 tap water samples taken from patients' rooms and in 5.3% of 189 other tap water samples (P<0.01). P. aeruginosa was isolated from 38 patients. Typing of 73 non-replicate isolates (water samples, hands of HCWs and patients) revealed 32 major DNA patterns. Eleven (52.4%) of the 21 faucets were contaminated with a patient strain, found before isolation from tap water in the corresponding room in nine cases, or from the neighbouring room in two cases. Among seven P. aeruginosa strains isolated from HCW hands, the genotype obtained was the same as that from the last patient they had touched in six cases, and in the seventh with the last tap water sample used. More than half of P. aeruginosa carriage in patients was acquired via tap water or cross-transmission. Carriage of P. aeruginosa by patients was both the source and the consequence of tap water colonisation. These results emphasise the need for studies on how to control tap water contamination.

Study Objectives: In the course of chronic obstructive pulmonary disease (COPD), pulmonary gas exchange deteriorates as a result of ventilation/perfusion inequalities and hypoxaemia. The aim of the present study was to evaluate the influence of cardiac output (CO) level observed at rest in COPD patients on interaction between central and peripheral O(2) exchange., Methods: One hundred and nine patients with advanced but stable COPD were analysed in a retrospective study by the multiple inert gas elimination technique. As a function of CO, simulations were conducted to evaluate the respective part of PvO(2) and VA/Q inequalities on the degree of hypoxaemia., Measurements and Results: PaO(2) was linked (i) to cardiac index (CI), (ii) to mean VA/Q ratio of blood flow distribution and (iii) to PvO(2), but PvO(2) was not correlated with CO. By comparing two groups with CI above and below the mean value of the series respectively, a significant difference was identified in PaO(2) (57 +/- 9 mmHg in the high CI group versus 63 +/- 10 mmHg in the low CI group, P<0.05) because of higher VA/Q inequalities in the high CI group. Comparing two other groups with values of PvO(2) above and below the mean value of the series respectively, a significant difference was identified in PaO(2): (mean +/- SD was 65 +/- 8 in high PvO(2) group versus 56 +/- 9 mmHg, P<0.001) but with no difference in either CI or perfusion distribution. Analysis of the cumulated effects of PvO(2) and CI values, indicated that high CI and low PvO(2) gave rise to the lowest PaO(2) (53 +/- 8 mmHg), with the highest PaO(2) (68 +/- 8 mmHg) being found in the low CI and normal PvO(2) group., Conclusions: We concluded that in COPD patients, PaO(2) appeared to be maintained better when peripheral gas exchange coped with tissue demand without an increase in CO. Conversely, when the physiological increase in CO could not maintain adequate tissue gas exchange, PaO(2) continued to fall due to the cumulative effects of increasing CO on VA/Q inequalities and low PvO(2).

Objectives: To measure the mass transfer and clearance of procalcitonin (PCT) in patients with septic shock during continuous venovenous hemofiltration (CVVH), and to assess the mechanisms of elimination of PCT., Setting: The medical department of intensive care., Design: A prospective, observational study., Patients: Thirteen critically ill patients with septic shock and oliguric acute renal failure requiring continuous venovenous postdilution hemofiltration with a high-flux membrane (AN69 or polyamide) and a 'conventional' substitution volume (< 2.5 l/hour)., Measurements and Main Results: PCT was measured with the Lumitest PCT Brahms(R) in the prefilter and postfilter plasma, in the ultrafiltrate at the beginning of CVVH (T0) and 15 min (T15'), 60 min (T60') and 6 hours (T6h) after setup of CVVH, and in the prefilter every 24 hours during 4 days. Mass transfer was determined and the clearance and the sieving coefficient were calculated according to the mass conservation principle. Plasma and ultrafiltrate clearances, respectively, at T15', T60' and T6h were 37 +/- 8.6 ml/min (not significant) and 1.8 +/- 1.7 ml/min (P < 0.01), 34.7 +/- 4.1 ml/min (not significant) and 2.3 +/- 1.8 ml/min (P < 0.01), and 31.5 +/- 7 ml/min (not significant) and 5 +/- 2.3 ml/min (P < 0.01). The sieving coefficient significantly increased from 0.07 at T15' to 0.19 at T6h, with no difference according to the nature of the membrane. PCT plasma levels were not significantly modified during the course of CCVH., Conclusions: We conclude that PCT is removed from the plasma of patients with septic shock during CCVH. Most of the mass is eliminated by convective flow, but adsorption also contributes to elimination during the first hours of CVVH. The effect of PCT removal with a conventional CVVH substitution fluid rate (<2.5 l/hour) on PCT plasma concentration seems to be limited, and PCT remains a useful diagnostic marker in these septic patients. The impact of high-volume hemofiltration on the PCT clearance, the mass transfer and the plasma concentration should be evaluated in further studies.

Autoimmune inflammatory polyneuropathy (PN) can be triggered by vaccination. We report 3 such cases. A 36-year-old female nurse presented 15 days after a hepatitis B vaccination (HBV) with acute sensory disturbances in the lower limbs. She had severe ataxia but no weakness. Cerebrospinal fluid (CSF) protein level was 84 mg/100 mL, with 3 lymphocytes. A 66-year-old man presented 21 days after HBV with severe motor and sensory PN involving all 4 limbs. A 66-year-old man presented 15 days after a yellow fever vaccination with progressive motor and sensory PN involving all 4 limbs and bilateral facial paralysis. CSF protein level was 300 mg/100 mL, with 5 lymphocytes. Six weeks later, a tracheostomy was performed. In these 3 patients, the nerve deficits lasted for months. In each case, peripheral nerve biopsy showed KP1-positive histiocytes but no T-lymphocytes in the endoneurium. On ultrastructural examination, there was axonal degeneration in the first 2 cases; in case 2, a few myelinated fibers exhibited an intra-axonal macrophage but the myelin sheath was preserved. There was only 1 example of macrophage-associated demyelination in case 2, but these were numerous in case 3. It is likely that in the first 2 cases, an autoimmune reaction against some axonal or neuronal components was triggered by HBV. It induced an acute sensory ataxic PN in case 1 and an acute motor and sensory axonal neuropathy (AMSAN) in case 2. The third patient had a chronic inflammatory demyelinating PN, likely triggered by yellow fever vaccination.

Background: Bilateral adrenal hematoma is an uncommon cause of acute adrenal insufficiency. An association with thrombopenia induced by low-molecular-weight heparin even more so. Diagnosis is difficult as the clinical manifestations mimic septic shock., Case Report: A 63-year-old woman developed acute adrenal insufficiency due to bilateral adrenal hematoma following severe thrombopenia induced by low-molecular-weight heparin prescribed after an orthopedic operation. Outcome was favorable., Conclusion: Acute adrenal insufficiency must be entertained as a possible diagnosis in patients with heparin-induced thrombopenia.

beta-agonist bronchodilators are known to influence gas exchange and ventilation-perfusion relationships in asthmatic patients, where they induce hypoxaemia via hypoxic vasoconstriction. As this effect could have serious consequences in chronic obstructive pulmonary disease (COPD) patients with chronic hypoxaemia, alternative agents have been sought. It has been shown that inhaled anticholinergic drugs may be of value in this condition. In the present study, we compared the effects of salbutamol (Sb) and ipratropium bromide (IB) inhalation on gas exchange in 15 patients with stable COPD. All patients had a history of COPD (mean arterial oxygen tension (Pa,O2) = 8.2 +/- 1.0 kPa (61.8 +/- 7.3 mmHg) forced expiratory volume in one second (FEV1) = 39 +/- 12%; FEV1/vital capacity (VC) = 42 +/- 6%) and no evidence of acute respiratory failure. Haemodynamic and gas exchange data were recorded after right catheterization by the multiple inert gas elimination technique. Measurements were made under basal conditions, after two puffs of freon propellant (placebo) and after two puffs of either 200 micrograms Sb or 200 micrograms IB in a randomized design. Sb and IB reduced airway resistances to the same extent, but had no significant influence on the haemodynamic and ventilation parameters. There was a slight but significant decrease in arterial carbon dioxide tension (Pa,CO2) = 6.0 +/- 0.8 versus 6.4 +/- 0.8 kPa (45.4 +/- 5.9 versus 47.9 +/- 6.3 mmHg) p < 0.05 with an enhanced perfusion distribution heterogeneity and a slight improvement in ventilation homogeneity shown by a decrease of the decimal logarithm of SD of the ventilation distribution (LogSDV) after inhalation of IB relative to control. Since these alterations did not affect arterial oxygen tension we concluded that inhalation of these doses of salbutamol or ipratropium bromide do not affect gas exchange in patients with stable chronic obstructive pulmonary disease. The normal home treatment: inhalation of two puffs of these bronchodilating drugs thus appears to be safe. The choice of agent will depend on the extent of the bronchodilator effect in a given individual.

Nitric oxide (NO) has been reported to be an endothelium-derived relaxing factor, and hypoxic pulmonary vasoconstriction seems to be enhanced by inhibitors of endothelially dependent vascular relaxation. We examined the circulatory effects of inhalation of 15 ppm NO in air in 14 hypoxic patients suffering from chronic obstructive pulmonary disease (COPD). Of these patients 4 breathed 100% O2 before NO. The effects of NO inhalation on pulmonary gas exchange were also studied in 12 of these patients using the multiple inert gas elimination technique, 3 of whom breathed air, 100% O2, and 15 ppm NO in air in succession. Under baseline conditions, both mean +/- SD pulmonary artery pressure and pulmonary vascular resistance were increased (Ppa = 24.3 +/- 10.4 mm Hg and PVR = 3.3 +/- 1.1 mm Hg/L/min, respectively). Although the pulmonary circulatory effects were not immediate, with no detectable changes after 1 min NO inhalation, Ppa and PVR fell significantly (-19.1 +/- 10.5%, p < 0.02 and -29.3 +/- 15.1%, p < 0.02, respectively) after 10 min NO inhalation. Moreover, the extent of the NO-induced reduction in Ppa was found to depend on the level of baseline pulmonary arterial hypertension. No systemic circulatory effects were observed. The mean VA/Q ratio and the dispersion of ventilation and blood flow distributions were not altered by NO inhalation, although there was a significantly higher percentage of ventilation (7.3 +/- 7.3%, p < 0.05) in poorly and unperfused areas (VA/Q > 10).(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of inspiratory flow rate (TI), without changing respiratory frequency, tidal volume, and FIO2, was investigated in 11 normal lungs in patients undergoing mechanical ventilation because of central respiratory failure due to stable coma. The patients were anesthetized and paralyzed. They first received a conventional ventilation (TI = 25 percent, pause = 10 percent) and then, were submitted to four different TI values, randomly administered without any end-inspiratory pause (EIP) (TI = 20 percent; TI = 33 percent; TI = 50 percent; TI = 67 percent). In the middle and at the end of the procedure, a return to basal conditions was introduced. At each ventilator setting, the following were obtained: respiratory flow (Pneumotachograph Fleish No. 2), airway pressure, FRC changes (inductive plethysmography), arterial and mixed venous blood gases, hemodynamic data, and VA/Q ratios distribution using multiple inert gases technique. EIP suppression provides a significant increase in VA/Q mismatch (until TI = 50 percent) and in shunt effect (between 3 and 9 percent of cardiac output [QT]). The absence of simultaneous PaO2 change is due to increasing PVO2 linked to a higher QT. The shorter the TI, the higher the PaCO2 connected with a relative alveolar hypoventilation. However, increasing TI without EIP significantly decreases ventilation distribution inequalities. This improvement is concomitant with a rise in FRC (FRC67-FRC20 = 0.340 +/- 0.450, p < 0.05) without any change in other variables or auto-PEEP production. In summary, in subjects with very slight mechanical lung impairment (peak inspiratory pressure = 20.5 +/- 5.3 cm H2O at TI = 20 percent and 15.2 +/- 3.3 cm H2O at TI = 67 percent), this study confirms the deleterious effect of EIP suppression and TI decrease. One can compensate for this effect of EIP absence by increasing TI as soon as it reaches TI = 67 percent, ie, inverse ratio ventilation.

Recent multi-centre studies have shown that high doses of Almitrine (100-200 mg per day), lead to a significant improvement in the hypoxaemia of patients presenting with chronic airflow obstruction, but that a high blood level (greater than 500 ng/ml) is often seen after 1 year, sometimes associated with signs of peripheral neuropathy. In order to maintain Almitrine blood levels in the range 200-300 ng/ml we have used an intermittent regime (with a "window" of 1 month every 3 months) and a dose limited to 100 mg per day. 102 hypoxic patients with chronic airflow obstruction, who were in a stable state were included. 65 patients were in the Almitrine group (A) and 37 patients in the placebo group (P). The treatment lasted for 1 year. In addition there was a 3 monthly follow up with arterial blood gases and spirometry, a clinical neurological examination and also electrophysiology, initially and after 6 and 12 months. 43% of patients in group A and 32% of patients in group P, left the study, most often due to poor cooperation, but sometimes as a result of side effects. After 12 months the PaO2 rose significantly in group A from 59.1 +/- 0.7 to 65.8 +/- 1.6 mmHg (p less than 0.001) whilst it was not changed in group P. The PaCO2 did not change in either group. On the other hand there was a significant fall in the subgroup of patients with hypercapnia in group A (p less than 0.001). The outcome of the neurological and electrophysiological assessments did not show any significant difference between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

We investigated interactions between cardiac output, VA/Q distribution pattern, pulmonary gas exchange, O2 transport, and tissue oxygenation in 16 patients during the acute phase of pulmonary embolism (PE). The effects of breathing room air, O2 therapy (FIO2 = 0.40) (11 patients), and dobutamine (four patients) were studied after right catheterization using the multiple inert gas elimination technique. The pattern of VA/Q ratio distributions was found to depend essentially on cardiac output level. The individual blood flow perfusing ventilated areas was found to be inversely related to the mean VA/Q ratio of blood flow distribution. PVO2 was directly related to cardiac index (p less than 0.02), and negatively related to the mean VA/Q of blood flow distribution. In view of the influence of low VA/Q ratios and PVO2 on arterial hypoxemia, our results showed that the heart's response to PE conditioned the strategy of pulmonary gas exchange and O2 transport. Oxygen breathing led to a slight but consistent fall in cardiac output (-0.6 +/- 0.5 L/min, p less than 0.01). However, although PaO2 remained normal and PVO2 was slightly improved, we found no evidence for a role of hypoxic pulmonary vasoconstriction in the pulmonary hypertension observed during the acute phase of PE. Administration of dobutamine improved O2 transport and tissue oxygenation, although PaO2 remained constant or even fell in some cases because of increased VA/Q mismatch.

Peripheral nerve biopsies (PNB) from four children suffering from subacute or chronic inflammatory demyelinating polyneuropathy were studied by electron microscopy. Remyelinating features with onion bulb formations, inflammatory cell infiltrates and active demyelinating lesions were strongly suggestive of the disease. In the first case, a second PNB, performed after 7 months of severe subacute course, showed a striking evolution of the lesions. In the second case and in spite of severe neurological symptoms, the PNB was almost normal, suggesting that inflammatory lesions were mainly located in the proximal parts of the nerve. No signs of active demyelination could be seen in the third case but onion bulb formations and inflammatory cell infiltrates were present. In the fourth case, characteristic lesions of active demyelination were associated with a history of familial polyneuropathy; this association suggests an auto-immune process in certain kindreds with hereditary motor and sensory neuropathy.

In a series of 23 patients with COPD, Wagner et al showed three distinct patterns of VA/Q distributions and a correlation between Burrows' clinical classification and the observed distribution patterns. Using the inert gas method, we studied 51 patients suffering from severe but stable COPD (FEV1 = 0.84 +/- 0.38 L; PaO2 = 58.5 +/- 10.5 mm Hg; PaCo2 = 48 +/- 6 mmHg; Ppa = 22 +/- 8 mmHg) breathing room air in a steady state. The H pattern (high mode of VA in high VA/Q) was found in 24 cases. There was an L pattern (Q mode in low VA/Q units) in nine cases and an HL (high-low) pattern in 16 cases (two patients were assigned another group). The analysis of the distribution data confirmed that VA/Q heterogeneity was the main factor underlying gas exchange disturbances in COPD. The PaO2 of the H subjects was higher than that of both HL (p less than 0.02) and L subjects. The true shunt value in the L group was significantly lower than in the H and HL groups. However, the relationship between clinical or functional aspects and distribution was not direct. The fraction of patients of H, HL, or (H + HL) types was nearly identical in the three clinical groups. The H pattern was found to be predominant in cases of COPD.

Three serious cases of status asthmaticus with severe hypercapnic acidosis unresponsive to adequate conventional therapy were treated by halothane. The efficiency of this treatment was assessed by the clinical state of the patient, the blood gases and the changes in peak airway pressure. Two patients improved dramatically in less than 24 h. No signs of cardiac toxicity of this drug were noted in spite of acid-base disturbances. These three cases showed the beneficial effect of halothane's-beta 2 stimulation in the treatment of status asthmaticus.

From a study conducted in 1981 in patients with chronic obstructive pulmonary disease breathing spontaneously, it was concluded that almitrine ensured a more even distribution of ventilation-perfusion ratios in the lung. Another study has recently been undertaken to suppress the effects of stimulated ventilation observed and to measure more accurately the pulmonary vascular effect of this new drug. This was a randomized double-blind drug versus placebo trial using the same doses of almitrine (1.5 mg/kg orally) in patients of the same type under stable artificial respiration controlled by repeated measurements of ventilation during the weaning period at the end of an episode of acute respiratory failure. The preliminary results obtained in one-half of the patients (4 under almitrine, 4 under placebo) are reported. There was little difference in haemodynamic values between the two groups. Improvement in PaO2 was maximum 90 min after almitrine was administered and varied from 0.7 to 1.4 kPa; there was no modification in the control group. In the absence of any change in ventilation and respiratory rate, perfusion was reduced in lung areas with low ventilation-perfusion ratio. These partial results seem to confirm that almitrine exerts a moderate, though real, effect on pulmonary vessels.

One case of severe acute hepatic failure happening after surgical treatment of large tuberculous ureteral stenosis is reported. The etiology was the association of isoniazide-rifampicin; the clinical, biological and histological data of these hepatitis cases are specified; their physiopathology, as well as their treatment is studied; prevention by plasmatic evaluation of isoniazide is especially important.

Several outbreaks of fatal opportunistic infections and tumors have recently been reported among homosexual men in the United States. Almost all patients had evidence of cellular immunodeficiency. We have studied a French homosexual man with fatal central nervous system toxoplasmosis. Morphological features (light and electron microscopy) of toxoplasma encephalitis are described.

In ten normal subjects, series dead space was determined for six intravenously infused inert gases (SF6, ethane, cyclopropane, fluothane, ether, acetone) from their expired and alveolar concentrations. The method for sampling alveolar gas was based on the criterion of identity of mean alveolar and expired gas exchange ratios. Inert gases were analysed chromatographically. Acetone, the most soluble gas, yielded the lowest dead space, the difference to the other gases being about 4.5%. This is probably due to the non-infinite value of the series dead space ventilation-perfusion ratio (VA/Q) which was estimated at about 2,000. The diffusivity, inversely related to the molecular weight, also played a role, the heaviest gas (fluothane) having a greater dead space than the lightest (ethane). The underestimation of the dead space from acetone is expected to be greater in subjects with low tidal volume and high bronchial blood flow, i. e. in some patients with respiratory disease.

Although the respiratory stimulant effects of almitrine bismesylate (AB) via an action on the peripheral chemoreceptors have been demonstrated, the mechanism of its intrapulmonary action has not yet been elucidated. In order to abolish the stimulation of ventilation, observed in studies on spontaneously breathing patients, an investigation of patients suffering from severe COPD under constant mechanical ventilation, with FIO2 = 0.21, during the weaning period was carried out. Eighteen patients were randomly divided into 2 groups (9 receiving 1.5 mg/kg AB and 9 receiving placebo). The ventilatory and hemodynamic variables, blood and alveolar gases, and the VA/Q ratio distributions using the multiple inert gas technique were collected before treatment with drug or placebo, as well as 90 and 180 min afterwards. The PaO2 was found to be raised 90 min after AB administration (+57 +/- 3.9 mm Hg, p less than 0.01) and remained above the baseline value at 180 min (+5.4 +/- 4.6 mm Hg, p less than 0.01). Compared with those in the placebo group, these increases were significant (p less than 0.01). A slight decrease in PaCO2 but similar in the 2 groups was observed despite constant ventilation. The hemodynamic data were the same for the 2 groups. The changes in overall criteria of the distributions (mean VA/Q and SD) were small. The main finding was a decrease in the percentage of the perfusion flowing through the true shunt and the underventilated areas after AB treatment. In the control group, the blood flow percentage in the true shunt and low VA/Q units was either stable or increased.(ABSTRACT TRUNCATED AT 250 WORDS)

A double blind study of effects of a low dose of almitrine has been performed in patients with severe chronic obstructive lung diseases. Besides hemodynamic and ventilation data, ventilation-perfusion ratio distribution was measured by the inert gas method in order to try to explain the improvement in blood gases caused by this drug. At the dose of 1.5 mg/kg almitrine produces : 1) an increase in ventilation and PaO2, 2) no change in pulmonary vascular resistances compared to a rise on placebo, 3) a drop of 4% in the percentage of cardiac output perfusing low VA/Q lung units with a concomitant increase in lung units with VA/Q ratio between 0.1 and 10, and 4) no significant change in the distribution of ventilation. The change in the distribution of blood flow is one of the causes of the rise in PaO2, but its mechanism is at yet not clear. The present results suggest arterial vasoconstriction in units with very low VA/Q accompanied by diversion of blood flow towards lung units with higher VA/Q ratio.

65 biopsies of peripheral nerve from patients suffering from Guillain-Barré syndrome were studied by electron microscopy. In 48 cases there was macrophagic invasion of the Schwann cells of certain myelinated fibers, and in 32 of these cases some myelin sheaths were stripped away by an elongated macrophagic process. Vesicular disruption of the myelin sheath was observed in only 8 cases and in less than 1% of the myelinated fibers. Uncompacted myelin lamellae were observed in a few myelinated fibers. These ultrastructural lesions are analysed and commented on with a view to selecting patients who are to undergo plasma exchange.

The efficacy and tolerance of a nasal CPAP device marketed in France (Pression +, Sefam) for the treatment of obstructive sleep apnoea syndromes have been evaluated in a co-operative trial including 12 patients. This study confirmed the efficacy of nasal CPAP on sleep parameters: total sleep time was increased; light non-REM sleep was diminished; slow-wave sleep and REM sleep were augmented; sleep apnoeas were eliminated completely or almost completely; oxygen saturation was markedly improved. At one month follow-up, most clinical features were improved; daytime blood gases showed little change but the number of red cells was decreased. On the whole, the tolerance was good in this highly motivated group of patients: eleven patients (92%) were willing to continue their home treatment with the same device. Most difficulties were due to the making of a tailored molded nasal mask and its use during sleep.

The main results obtained, in healthy or unhealthy man, with the inert gas method are gathered together. The major factor at the source of hypoxemia is the uneven distribution of VA/Q ratios. The fall in the partial pressure of oxygen in mixed venous blood amplifies this effect. Only hypoxemia, during muscular exercise, in patients with interstitial lung diseases could be explained, in part, by a decrease in membrane diffusion and a reduction in the transit time of blood in pulmonary capillaries. The differences between the methods used to analyse pulmonary gas exchange are discussed.

Ventilation and perfusion distributions were measured in the patients with COPD breathing room air and normoxic helium-oxygen mixture (heliox) successively, using the multiple inert gas method. The D (A-a) O2 were calculated from ideal alveolar gas (Ai) and with West's gas mean model (A). Measured PaO2 and predicted PaO2 were compared during room air and heliox breathing. There were no change in overall distributions and in D (Ai-a) while D (A-a) O2 increase significantly during heliox breathing and the predicted PaO2 were significantly higher than the measured PaO2. Heliox breathing does not seem to change parallel heterogeneity in COPD. These results suggest an impairment of series heterogeneity and O2 diffusion during heliox breathing.

We report a case of severe pulmonary embolism in a 37 years old man admitted to the intensive care unit for severe acute respiratory failure. The presenting signs and symptoms were typical for severe pulmonary oedema. Chest radiograph shortly after admission showed local alveolar shadows. In the absence of sepsis, haemodynamic evidence of left ventricular failure on catheterization of the right heart and because of the history of the recent illness, a tentative diagnosis of pulmonary embolism was made. The diagnosis was confirmed by selective pulmonary angiography. The latter demonstrated that pulmonary oedema had been localized only in areas with patent pulmonary arteries and, in addition, confirmed that left ventricular function was normal. Such a pattern of local pulmonary oedema is uncommon in patients and is reminiscent of that observed in animal experiments with severe pulmonary arterial obstruction and overperfusion of unblocked territories. Possible mechanisms of overperfusion oedema are discussed and the hypothesis that humoral factors may increase the permeability of pulmonary microvasculature in cases of severe pulmonary embolism is put forward.

The determinants of hypoxemia were studied in 10 patients with acute pulmonary embolism demonstrated by pulmonary angiography. Two patients were mechanically ventilated, and in the 8 who breathed room air spontaneously, the mean arterial PO2 was 61.5 mmHg. Measurements of the distributions of ventilation (VA) and perfusion (Q) against VA/Q ratios by the multiple inert gas infusion technique demonstrated an increase in VA/Q inequality. The major part of pulmonary blood flow was distributed in a mode near to, or slightly above, a VA/Q ratio of 1. The cumulative fraction of blood in true shunt and low VA/Q mode (VA/Q less than 0.01) was 9.1%. For a small part of the AaDO2 (13%), an oxygen diffusional component was found. The remaining hypoxemia was due to the fall in the mixed venous PO2 (PVO2), irrespective of its cause: low cardiac output, low hemoglobin concentration, high oxygen consumption, low P50. The fall in PVO2 led to a fall in end-capillary blood PO2 in both shunt or ventilated and perfused units. We conclude that the major determinant of hypoxemia in these patients suffering from acute pulmonary embolism is the fall in PVO2. This is enhanced by a moderate increase in the fraction of blood flowing through low VA/Q units. Diffusion impairment plays only a minor role.

Arterial oxygen desaturation is commonly found in patients with cirrhosis of the liver, but severe hypoxemia is unusual. To investigate the mechanism of the impairment in gas exchange, six severely hypoxemic (mean PaO2, 55.9 +/- 5.9 mm Hg) cirrhotic patients (five confirmed by biopsy), without pulmonary or cardiovascular disease and in the absence of acute hepatic disease, were submitted to right heart catheterization. Inequalities of VA/Q were estimated in the respiratory steady state using the multiple inert gas technique. The mean pulmonary arterial pressure was low (7.2 +/- 2.3 mm Hg) and the cardiac output high (Q = 11.0 +/- 2.06 L/min), indicating a low PVR. The VA/Q mismatching of the ventilated and perfused units ranged from mild to moderate, but a large percentage of Q flowed through unventilated areas. Furthermore, there was a significant difference between predicted and measured PaO2 (9.27 +/- 5.9 mm Hg; p less than 0.01), which was attributed to either an unmeasured postpulmonary shunt (between portal and pulmonary vein) or a diffusion defect. The impairment in gas exchange in these patients is thus due primarily to an intrapulmonary, and possibly extrapulmonary, shunt. This was thought to be due mainly to an impaired regulatory mechanism of the microcirculation by the hepatic dysfunction.

The effectiveness of assisted ventilation at home, especially in the case of tracheostomized patients, has been nearly established at the present time. The experience of various centers in France, having or not the support of an independent structured organization, shows that the setting-up and supervision of such therapy can be effectively carried out. Nevertheless, difficult choices remain. Some indications are still questionable, such as the choice of the respirator if the patient has not been tracheostomized. The type of organization is not univocal and could perhaps depend on the number of patients to be cared for. In any case, in the years to come, the experience of the different teams and the technical progress made will lead to a solution to the problems raised: a decrease in the number of hospitalizations and more comfort for the patients can be hoped for.

Fourteen patients suffering from severe but stable chronic airway obstruction were studied while breathing room air and mildly hyperoxic mixture (26%). The data were collected at the end of each 30 min randomized breathing period. The multiple inert gas elimination technique was used to detect alterations in ventilation-perfusion (VA/Q) mismatching. Ventilatory, arterial and mixed venous blood gases, and hemodynamic measurements were made simultaneously. To show a possible effect of O2 on hypoxic pulmonary vasoconstriction (HPV), the fractional part of cardiac output perfusing low VA/Q areas was separated using as upper limit of VA/Q the compartments with PAO2 70, 60 and 50 mmHg while breathing oxygen, compared to the percentage of blood flow in the same areas limited by the same VA/Q unit in air breathing conditions. Only a few changes due to O2 are statistically significant: 1) a rise in PaO2 (+20.2 +/- 8.3 mmHg) and PvO2 (+4.2 +/- 2.18 mmHg) without any change in ventilation, respiratory frequency, pH, PaCO2, haemodynamics and overall criterion of distribution; 2) a moderate increase in inert gas dead space; 3) an increase in the percentage of blood flow under the limit when chosen at 50 mmHg (+3 +/- 2.8%). This change could be related to an inhibition of HPV response while breathing O2 in compartments previously placed above the limit in air. Consequently, their VA/Q decrease and their perfusions are summed with those under the limit in O2. These data suggest that mild hyperoxia has a slight but real deleterious effect on pulmonary gas exchange.