[Medical implantable devices and electromagnetic compatibility]. / Dispositifs médicaux implantables et compatibilité électromagnétique.

Continuing progress in medicine has led to a corresponding population growth among the elderly population resulting in an increase in the number of patients with active implanted medical devices. At the same time, there continues to be a proliferation of electromagnetic wave sources within our technological environment. The coexistence of implanted active medical devices and environmental electromagnetic waves requires particular attention in order to avoid electromagnetic interference. For this reason, experts are more and more involved in writing specific manufacturing standards.

Increased erythropoietin synthesis in patients with COLD or left heart failure is related to alterations in renal haemodynamics.

The mechanisms controlling erythropoietin (EPO) synthesis by the kidney in patients with chronic obstructive lung disease (COLD) or congestive left heart failure (CLHF) remain incompletely understood. Renal dysfunction occurs as a consequence of decreased renal blood flow (RBF) in these diseases. Because alterations in renal haemodynamics may affect EPO synthesis and red blood cell production, we investigated the potential relationships between renal function and plasma EPO synthesis in patients with COLD or CLHF. Thirty-two patients with COLD and 13 with CLHF underwent determination of renal physiology parameters, plasma EPO levels and haemoglobin levels. Plasma EPO concentrations were increased in patients with COLD or CLHF as compared to normal subjects, and were inversely correlated to haemoglobin concentrations. In patients with COLD or CLHF, plasma EPO was negatively correlated with both RBF and renal oxygen delivery (ROD) and positively correlated with filtration fraction. Plasma EPO was not correlated with glomerular filtration rate, fractional excretion of sodium, PO2 or PCO2. Among the patients with COLD, those with polycythemia (haemoglobin > 150 g L-1) had lower plasma EPO and higher RBF and ROD values than those with normocythemia (haemoglobin < or = 150 g L-1). Taken together, our data suggest that in patients with COLD or CLHF the critical determinant for EPO production is impairment of renal haemodynamics.

Polycythemia impairs vasodilator response to acetylcholine in patients with chronic hypoxemic lung disease.

To investigate whether polycythemia associated with chronic hypoxemic lung disease (CHLD) increases vascular resistance by altering endothelium-derived nitric oxide (NO), we examined the responses to acetylcholine (ACh) infusions (5, 10, and 15 mg/min) on hemodynamics and gas exchange in 21 patients with CHLD of varying severity. Patients were classified into two groups based on whether their hemoglobin (Hb) level was less or greater than 15.5 g/dl. In the normocythemic patients (Hb = 13.6 +/- 0.3 g/100 ml, n = 10), ACh decreased pulmonary artery pressure (Ppa) from 30 +/- 2 mm Hg 26 +/- 2 mm Hg (p < 0.01); pulmonary vascular resistance (PVR), from 5.1 +/- 0.4 U/m2 to 3.4 +/- 0.3 U/m2 (p < 0.001); systemic arterial pressure (Psa), from 111 +/- 4 mm Hg to 108 +/- 4 mm Hg (p < 0.05); and systemic vascular resistance (SVR), from 27 +/- 2 U/m2 to 22 +/- 2 U/m2 (p < 0.01); and also increased the cardiac index (CI), from 3.8 +/- 0.2 to 4.7 +/- 0.3 L/min/m2 (p < 0.001). PaO2 fell from 59 +/- 3 mm Hg to 48 +/- 3 mm Hg (p < 0.001) whereas venous admixture (Qs/Qt) rose from 32 +/- 4% to 44 +/- 4% (p < 0.01). In contrast, in patients with polycythemia (17.7 +/- 0.5 g/100 ml, n = 11) ACh failed to produce any changes in PaO2 (49 +/- 2 mm Hg versus 51 +/- 2 mm Hg, p = NS), Ppa (34 +/- 1 mm Hg versus 33 +/- 1 mm Hg, p = NS), PVR (6.7 +/- 0.9 U/m2 versus 6.9 +/- 0.8 U/m2, p = NS) or Psa, but slightly increased the CI, from 3.6 +/- 0.3 L/min/m2 to 3.9 +/- 0.3 L/min/m2 (p < 0.01), and Qs/Qt, from 40 +/- 4% to 45 +/- 3% (p < 0.05). In the 21 patients, negative correlations with Hb concentrations were found for ACh-induced changes in PVR (r = -0.57, p < 0.01), Ppa (r = -0.46, p < 0.01), CI (r = -0.5, p < 0.05), PaO2 (r = -0.79, p < 0.01), and Qs/Qt (r = -0.79, p < 0.01). In the six polycythemic patients who received isovolemic hemodilution, with a decrease in Hb concentration from 18.6 +/- 0.9 g/dl to 15.3 +/- 0.3 g/dl as a result, infusion of ACh, which was without effect before hemodilution, caused decreases in Ppa from 28 +/- 1 mm Hg to 23 +/- 1 mm Hg (p < 0.05) and in PVR from 5.7 +/- 0.8 U/m2 to 3.6 +/- 0.5 U/m2 (p < 0.02), as well as an increase in CI from 3.4 +/- 0.4 L/min/ m2 to 4.1 +/- 0.4 L/min/m2 (p < 0.05). In contrast to ACh, inhaled NO (40 ppm) induced pulmonary vasodilation in both the normocythemic and polycythemic groups. Our results show that high hematocrit (Hct) levels inhibit endothelium-dependent vasodilation in response to ACh in patients with CHLD, possibly through inactivation of endothelial-derived NO by Hb.

Effects of ANF infusion on the renal responses to lower-body negative pressure in humans.

To investigate the role of atrial natriuretic factor (ANF) in renal responses to a decrease in central blood volume, we examined the effects of ANF infusion on renal function and hormones during prolonged lower-body negative pressure (LBNP). Ten healthy volunteers participated in two experimental sequences, each comprising a 120-min baseline period followed by the application of -20 mm Hg LBNP for 90 min. During one of the two sequences, ANF was infused throughout LBNP application at the constant rate of 2.5 ng/kg/min. Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured by using inulin and p-aminohippuric acid clearance techniques. LBNP induced a significant decrease in ERPF (534 +/- 28 to 457 +/- 26 ml/min; p < 0.05), GFR (120 +/- 2.5 to 112 +/- 2.5 ml/min; p < or = 0.01), in urine excretion (12 +/- 0.9 to 5.6 +/- 0.5 ml/min; p < 0.001), in sodium excretion (0.36 +/- 0.03 to 0.30 +/- 0.02 mmol/min; p < 0.05), and in plasma ANF (19 +/- 3 to 11 +/- 2 pg/ml; p = 0.001) concomitant with an increase in plasma renin activity (PRA; 0.48 +/- 0.09 to 0.87 +/- 0.16 ng/ml/h; p = 0.01) and of forearm vascular resistance (FVR; p < 0.05). The combination of ANF infusion with LBNP led to a slight increase in plasma ANF from baseline (from 20 +/- 2 to 28 +/- 3 pg/ml; p < 0.05). Compared with values obtained during LBNP with saline vehicle infusion, values obtained during LBNP with ANF infusion were similar for ERPF (463 +/- 23 vs. 457 +/- 26 ml/min), for GFR (111 +/- 2 vs. 112 +/- 2 ml/min), and for urine excretion (7 +/- 0.6 vs. 5.6 +/- 0.5 ml/min; p = 0.07), but greater for fractional excretion of sodium (2.38 +/- 0.25% vs. 1.91 +/- 0.11%; p < 0.05) and FVR (p < 0.05), and smaller for PRA (0.49 +/- 0.1 vs. 0.87 +/- 0.16 ng/ml/h; p < 0.01). These data show that ANF infusion attenuates the antinatriuretic effect of low-level LBNP and its PRA-increasing effects without altering renal hemodynamic responses to LBNP, although there is a decrease in the LBNP-induced forearm vasoconstriction. These results were obtained with plasma ANF levels slightly higher than those in baseline. They support the hypothesis that a decrease in ANF secretion might contribute to the antinatriuretic effect of LBNP.

Treatment of respiratory failure using minitracheotomy and intratracheal oxygenation in selected patients with chronic lung disease.

OBJECTIVE: To evaluate the efficacy of minitracheotomy (MT) insertion for intratracheal oxygen insufflation (ITO2) on arterial blood gases and survival in patients with respiratory failure from chronic lung disease. DESIGN: Open, prospective clinical study. SETTING: A 12-bed medical intensive care unit in a non-university hospital. PATIENTS: 20 patients (14 males and 6 females, mean age 74.8 +/- 2.6 years), admitted for respiratory failure and denied mechanical ventilation. INTERVENTION: Percutaneous insertion of an MT for ITO2. Arterial blood gases were drawn just prior to, then 3, 24, 48 h and 1 week after MT insertion. Data are evaluated with a two-way analysis of variance for distribution-free data (Friedman's rank sums test). MEASUREMENTS AND RESULTS: Three hours after starting ITO2, the partial pressure of oxygen in arterial blood (PaO2) and the arterial oxygen saturation (SaO2) both increased from 51.7 +/- 2.8 to 85.4 +/- 5.6 mmHg and from 79.7 +/- 3.1 to 93.7 +/- 0.9%, respectively (p < 0.001 for both), along with a slight worsening in the partial pressure of carbon dioxide in arterial blood (PaCO2), from 59.6 +/- 2.5 to 63.5 +/- 3.0 mmHg (p < 0.05). At 1 week, improvements in PaO2 and SaO2 were maintained in all patients, while PaCO2 decreased in 14 patients (mean decrease 8.3 mmHg) and increased in the remaining patients (mean 12.5 mmHg), when compared to pre-ITO2 values. Seven patients died during follow-up, leading to a success rate of 65%. Eight and 4 patients were discharged home and to a nursing home, respectively, 9 still receiving ITO2 via MT as chronic oxygen therapy. CONCLUSION: Our results suggest that MT insertion for ITO2 may be a therapeutic option in selected patients with respiratory failure from CLD.

Spontaneous pneumothorax. Comparison of thoracic drainage vs immediate or delayed needle aspiration.

In the first part of this study, 61 patients admitted for the first episode or the first recurrence of a spontaneous pneumothorax (SP) were randomly treated with thoracic drainage (TD; 28 patients) or with simple needle aspiration (NA; 33 patients). Success rate of therapy was significantly higher with TD than with NA (93%, CI 84 to 100 vs 67%, CI 51 to 83; p = 0.01). Hospital stay was similar between the two groups (7 +/- 4.6 vs 7 +/- 5.6 days), mainly because NA was delayed by 72 h in 26 patients. Recurrence rates at 3 months were 29% (CI 11 to 47%) after TD, and 14% (CI 0 to 29%) after NA (p > 0.20, NS). In the second part of the study, an additional population of 35 patients was treated by immediate NA, with a success rate of 68.5% (CI 53.5 to 83.5%), and a recurrence rate at 3 months of 30% (CI 10 to 50%). Taken together, our results indicate that NA may be proposed as a first-line treatment of SP, with a successful result in two thirds of patients and recurrence in one fifth of patients. In patients who do not heal with NA, a combined risk of TD failure and short-term recurrence of 50% may be an incentive for undelayed surgical procedures.

Haemodynamics and gas exchange before and after coil embolization of pulmonary arteriovenous malformations.

A complete description of haemodynamics and gas exchange before and after percutaneous coil embolization of multiple pulmonary arteriovenous malformations is reported in a 45 year old woman with hereditary haemorrhagic telangiectasis (HHT). Before treatment, whilst the patient complained of severe dyspnoea during daily activities, an intrapulmonary shunt of 31% was measured (inert gas elimination technique), together with a cardiac output (thermodilution technique) of 12.4 L.min-1, resulting in a resting arterial oxygen tension (PaO2) of 8.53 kPa. Effective occlusion of all visible pulmonary malformations resulted in a rapid and major improvement in exercise tolerance, whilst resting PaO2 remained almost unchanged. A second investigation performed 4 months after treatment revealed a persistent intrapulmonary shunt of 19%, a cardiac output of 7.35 L.min-1, and a resting PaO2 of 10.53 kPa. We conclude that major increases in cardiac output largely contribute to the maintenance of PaO2 in patients with multiple pulmonary arteriovenous malformations and intrapulmonary shunt. The benefit of coil embolization is due both to an improvement in arterial oxygenation and a normalization of cardiac output.

[Nitric oxide, from vascular physiology to therapeutics]. / Le monoxyde d'azote, de la physiologie vasculaire à la thérapeutique.

Nitric oxide (NO) synthesised by endothelial cells, plays a key role in the control of vascular tone. Its synthesis from L-arginine is assured by NO-synthase, the activity of which is dependent on intracellular calcium concentrations, which are themselves modulated by pharmacological (acetylcholine, serotonin, bradykinin...) or physical factors (shearing forces exerted by blood flow). NO acts by stimulating a soluble guanylate-cyclase of the smooth muscle cells in the vessel wall. Its vasodilator effect is therefore mediated by an increase in intracellular cyclic GMP concentration. The synthesis or liberation of NO by the endothelium may be decreased or abolished during many pathological processes (hypercholesterolaemia, atherosclerosis, systemic or pulmonary hypertension...). The significance of this abnormality of NO-mediated endothelium-dependent vasodilation in different pathological conditions has not been established. However, it is probably significant in view of the different properties of NO: vaso-relaxation, antiaggregant and inhibition of vascular smooth muscle growth. It is not yet known whether this abnormality is a cause or a consequence of the underlying disease. From the therapeutic point of view, NO is an active metabolite of nitrate derivatives, sodium nitroprussiate and molsidomine which therefore share the same mode of action as the so-called "endothelium-dependent" vasodilatoe agents. The inhalation of NO, which is increasingly used in neonatal and adult intensive care units, is an alternative therapeutic approach in many conditions associated with pulmonary hypertension.

A clinical study of amiodarone as a single oral dose in patients with recent-onset atrial tachyarrhythmia.

Forty-five patients with recent-onset sustained atrial tachyarrhythmia (mean heart rate at entry; 140.0 +/- 3.5 beats.min-1) associated with various cardiovascular diseases were treated by oral amiodarone, given as a single loading dose of 25.7 +/- 0.9 mg.kg-1 body weight. Conversion to sinus rhythm was observed in 29 patients during the first 24 h of treatment, leading to a success rate of 64.4%. Five additional patients converted to sinus rhythm with continuation of oral amiodarone, (10-15 mg.kg-1 by day) with a mean delay of 4.2 days. A similar population of 27 patients (mean heart rate at entry; 140 +/- 3 beats.min-1) was treated by intravenous amiodarone, given as a bolus infusion of 3-5 mg.kg-1 over 30 min (mean; 4.1 +/- 0.2 mg.kg-1), followed by a continuous infusion of 10-15 mg.kg-1 for 24 h (mean; 11.1 +/- 0.7 mg.kg-1). Eighteen patients converted to sinus rhythm during the first 24 h of therapy, leading to a success rate of 66.7%. Minor adverse effects of therapy were observed in two patients given oral amiodarone, and in seven given intravenous amiodarone. No major effect was observed. We suggest that amiodarone given as a single oral loading dose of 25-30 mg.kg-1 body weight is an effective, simple and well-tolerated therapy, suitable for most patients with recent-onset ATA.

Intravenously administered atrial natriuretic factor in patients with COPD. Effects on ventilation-perfusion relationships and pulmonary hemodynamics.

The potent pulmonary vasodilating property of atrial natriuretic factor (ANF) may alter gas exchange in patients with COPD. We examined the hemodynamic and gas exchange responses to intravenous infusion of ANF (0.01 and 0.03 ng/min/kg body weight) in eight stable patients with COPD studied during spontaneous breathing, using the inert gas elimination technique. When compared with baseline, ANF infusion was associated with a dose-dependent decrease in pulmonary artery pressure (from 27.3 +/- 2.5 to 23.9 +/- 1.8 and 20.2 +/- 1.7 mm Hg, respectively) and a dose-dependent increase in blood flow perfusing poorly ventilated and unventilated units (VA/Q < 0.1: from 5.80 +/- 2.05 to 7.25 +/- 2.5 and 12.0 +/- 5.4 percent of total blood flow, respectively; p = 0.02). However, PaO2 remained unchanged (70.2 +/- 3.6, 68.1 +/- 3.8 65.4 +/- 3.5 mm Hg, respectively) because of a significant increase in minute ventilation (VE) from 8.6 +/- 0.8 to 9.6 +/- 0.8 and 10.3 +/- 0.7 L/min (p < 0.002). Six additional COPD patients receiving intravenously administered ANF at the same dosages were studied during controlled mechanical ventilation using right heart catheterization. In these patients, pulmonary vasodilation was associated with a significant increase in venous admixture (from 12.7 +/- 2.4 to 14.4 +/- 2.9 and 17.5 +/- 3.5 percent of total blood flow, respectively; p < 0.02), and a dose-dependent reduction in arterial PO2 (from 117 +/- 17 to 110 +/- 15 and 96.4 +/- 8.8 mm Hg, respectively; p < 0.05). The present results show that ANF infusion is associated with alterations in the VA/Q relationship in patients with COPD. However, a decrease in arterial oxygenation may be prevented by an increase in VE.

Complete sinus arrest during diltiazem therapy; clinical correlates and efficacy of intravenous calcium.

The occurrence of severe sinus node dysfunction in 10 patients (three males and seven females; mean age 78.5 +/- 3.4, range 57-92 years) receiving oral diltiazem therapy (mean 190 +/- 20 mg/24 h, range 90-300) is described. Six of them were concomitantly taking amiodarone and/or beta-blocking agents. On admission, seven patients exhibited systemic hypotension and nine complained of asthenia and/or dizziness or drowsiness. ECG findings showed in all a persistent sinus arrest with atrial, junctional or ventricular escape, leading to a mean heart rate of 40.2 +/- 3 beats.min-1 (range 25-56). All patients had chronic renal failure on biological tests, with a mean endogenous creatinine clearance of 25 +/- 3 ml.min-1 (range 12-36). Intravenous calcium hydrochloride (mean 1.4 +/- 0.2 g, range 1-2), given in nine patients, rapidly restored stable sinus activity in seven. We suggest that diltiazem should be given cautiously to ageing patients with chronic renal failure, and confirm the efficacy of intravenous calcium in reversing calcium channel blocker toxicity on sinus node.

Lack of clinical benefit from subcutaneous tunnel insertion of central venous catheters in immunocompromised patients.

To assess the efficacy of subcutaneous tunneling, we randomly designated 212 central venous catheters for tunneling (107 catheters) or for standard insertion (105 catheters) in 169 immunocompromised patients. The patients who received tunneled catheters (TCs) and the patients who received nontunneled catheters (NTCs) were similar with respect to age, gender, underlying disease, incidence of leukopenic episodes, receipt of blood product transfusions or parenteral nutrition, and medical care and attendants. The life span of catheters was 112.5 +/- 9.5 days in the TC group and 119 +/- 9 days in the NTC group (P = .5). Clinically relevant bacteremia occurred in 26 cases in the TC group (0.22 episode per 100 catheter-days), a rate not significantly different from that in the NTC group (25 episodes; 0.20 episode per 100 catheter-days). Catheter-related bacteremia was documented in seven cases and non-catheter-related bacteremia in five cases. In most instances, the precise origin of the septic episode could not be determined. Cutaneous infection and bacteremia were associated with the same microorganism in two cases in each group. Since the present study failed to demonstrate any clinical benefit of subcutaneous tunneling, such a procedure is no longer performed in our hospital.

Role of atrial natriuretic factor in impaired sodium excretion of normocapnic and hypercapnic patients with chronic obstructive lung disease.

To investigate the mechanisms of sodium retention in patients with chronic obstructive lung disease (COLD), we examined the renal and hormonal responses to volume expansion with isotonic saline and to infusion of atrial natriuretic factor (ANF) in 10 hypercapnic (PaCO2 52 +/- 2 mm Hg) and 12 normocapnic patients (PaCO2 39 +/- 1 mm Hg). Sodium excreted within 4 h of loading (expressed as % sodium load) was 23.5 +/- 2.5% (p < 0.05) in normocapnic and 8.5 +/- 1.5% (p < 0.001) in hypercapnic patients, compared with 32.5 +/- 3.0% in 11 age-matched control subjects. Sodium excretion and renal blood flow correlated negatively with arterial PCO2 and positively with FEV1. Basal plasma ANF concentrations were 72 +/- 5 pg/ml in controls, 100 +/- 14 pg/ml in normocapnic patients, and 230 +/- 52 pg/ml in hypercapnic patients (p < 0.001). Plasma renin activity and aldosterone did not differ between groups. In response to volume expansion, plasma ANF increased in both normocapnic and controls (with a greater increase in normocapnic patients) but remained unchanged in hypercapnic patients. Exogenous ANF increased glomerular filtration rate, renal plasma flow, natriuresis, and diuresis in both groups of patients. Patients with COLD have depressed renal function that appears unrelated to activation of the renin-angiotensin-aldosterone system. An increased secretory response of ANF to volume expansion may help to maintain volume homeostasis in normocapnic patients, while a blunted secretory response of ANF may contribute to sodium retention in hypercapnic patients.

Hemodynamic and gas exchange responses to infusion of acetylcholine and inhalation of nitric oxide in patients with chronic obstructive lung disease and pulmonary hypertension.

To investigate endothelium-dependent and endothelium-independent nitric oxide (NO) mediated pulmonary vasodilation in patients with chronic obstructive lung disease (COLD), we examined the responses to incremental infusion rates of acetylcholine (ACh) or inhaled NO on hemodynamic and gas exchange. In 13 patients, ACh (15 mg/min) decreased pulmonary artery pressure (Ppa) from 31 +/- 1 to 28 +/- 1 mm Hg (p < 0.01) and systemic arterial pressure while increasing cardiac index from 3.7 +/- 0.4 to 4.7 +/- 0.4 L/min/m2 (p < 0.01). Inhaling 40 parts per million (ppm) NO decreased Ppa from 32 +/- 1 to 26 +/- 1 mm Hg (p < 0.001) with no associated hemodynamic change. ACh reduced PaO2 from 57 +/- 3 to 48 +/- 2 mm Hg (p < 0.01) and increased venous admixture (QVA/QT) from 35 +/- 3 to 45 +/- 3% (p < 0.01). Inhaling 40 ppm NO increased PaO2 from 57 +/- 3 to 60 +/- 3 mm Hg (p < 0.01) and decreased QVA/QT from 36 +/- 3 to 32 +/- 3% (p < 0.01). Pulmonary vascular resistance changes were similar in response to 40 ppm NO or 15 mg/min ACh. In COLD patients, ACh produces both pulmonary and systemic vasodilation but impairs arterial oxygenation whereas inhaled NO induces selective pulmonary vasodilation while improving gas exchange. The resistance to ACh in some patients could be related to pulmonary endothelial dysfunction.

A clinical study of intravenous cibenzoline in selected patients with recent-onset atrial tachyarrhythmia.

Twenty-five adult patients with sustained atrial tachyarrhythmia (ATA) and without heart failure were treated by intravenous cibenzoline, 1 mg/kg, as a slow bolus infusion, followed by a 8 mg/kg/24 h continuous infusion. Sinus rhythm conversion was observed in 18 patients (72 percent success rate). Severe adverse cardiac events were observed in only one patient (4 percent occurrence rate), as a wide QRS complex tachycardia finally requiring a semiemergency direct-current cardioversion. Two minor side effects were additionally observed. A similar population of 21 patients was conventionally treated with amiodarone, either given intravenously, 15 to 20 mg/kg/24 h, or orally, 30 mg/kg/24 h as a single dose. An identical success rate (15/21; 71 percent) was observed. Our results indicate that in selected patients with ATA, cibenzoline and amiodarone are highly effective for producing sinus rhythm conversion. We suggest that the former drug may be used as a first-line treatment. In case of failure, the latter may constitute an alternative to transthoracic electrical countershock.

Mechanisms of impaired arterial oxygenation in patients with liver cirrhosis and severe respiratory insufficiency. Effects of indomethacin.

The mechanisms of impaired arterial oxygenation that occur in certain patients with chronic liver cirrhosis are still debated. In the present study, we investigated nine cirrhotic patients with severe respiratory disability (mean PaO2, 64 +/- 5 mm Hg), using the inert gas elimination technique to assess the distribution of ventilation-perfusion (VA/Q) ratios. We also determined shunt fraction during pure oxygen breathing, both in supine and sitting positions. To test the hypothesis that vasodilating prostaglandins could contribute to alter gas exchange in such patients with cirrhosis, we examined the hemodynamic and gasometric responses to indomethacin, 50 mg IV, in six of them. During baseline conditions, patients had high cardiac index (CI, 4.9 +/- 0.2 L/min/m2), and low pulmonary (PVR, 1.78 +/- 0.37 mm Hg/L/min/m2) or systemic (SVR, 17.7 +/- 1.15 mm Hg/L/min/m2) vascular resistances. Large intrapulmonary shunt fraction was documented in each patient with a mean value of 19.6 +/- 2.7 percent. Small perfusion in low VA/Q areas was associated with shunt in only three patients (2.5 to 5.3 percent of blood flow). Arterial PO2 was negatively related to shunt (p < 0.01) and to the dispersion of blood flow distribution (p < 0.02). There was no difference between measured and predicted PaO2. Shunt estimates from the inert gas and the 100 percent O2 breathing techniques were, respectively, 19.6 +/- 2.7 percent and 21.7 +/- 3.0 percent. During 100 percent oxygen breathing, changing from supine to sitting position decreased PaO2 from 401 +/- 50 to 333 +/- 64 mm Hg (p < 0.02), while O2 shunt remained unchanged, arteriovenous difference widened, and mixed venous PO2 decreased, from 61 +/- 3 to 47 +/- 4 mm Hg (p < 0.001). Indomethacin did not improve gas exchange or VA/Q distribution and did not affect systemic or pulmonary hemodynamics. The results show that in cirrhotic patients with severe respiratory disability, intrapulmonary shunting is the main determinant of impaired gas exchange, with no evidence of a defect in oxygen diffusion or an extrapulmonary shunt. Vasodilating prostaglandins do not appear to contribute to these alterations.

Severe hypoxemia-associated intrapulmonary shunt in a patient with chronic liver disease: improvement after medical treatment.

A 20-yr-old woman with chronic liver disease and angioimmunoblastic lymphadenopathy presented with marked hypoxemia caused by intrapulmonary shunt. Her respiratory tract showed her to be free of angioimmunoblastic lymphadenopathy manifestations. After 12 months of treatment with cyclophosphamide and corticosteroid, the immunologic disease disappeared. Unexpectedly, hypoxia-associated intrapulmonary shunt was no longer present either. To the best of our knowledge, this is the first case of dramatic improvement, with medical therapy, of severe hypoxemia related to noncirrhotic liver disease. However, the mechanism by which this treatment caused the regression of intrapulmonary shunt is unknown.

Bedside evaluation of the resistance of large and medium pulmonary veins in various lung diseases.

To evaluate the contribution of large and medium pulmonary veins to the total pulmonary vascular resistance in various human lung diseases, we compared in 64 patients the pulmonary arterial proximal wedge pressure (Ppw), obtained when the balloon of a 7F pulmonary artery catheter was inflated with 1.5 ml air, with the distal wedge pressure (Pdw), obtained after the tip of the catheter was advanced until wedged in a small artery without balloon inflation. Ppw, reflecting the pressure in a large pulmonary vein, approximates the left atrial pressure, whereas Pdw reflects the pressure in a smaller pulmonary vein. Pdw was greater than Ppw in all 64 patients. The Pdw-Ppw gradient was 1.1 +/- 0.5 mmHg in nine patients with normal lungs and was significantly higher in 13 patients with chronic congestive heart failure (3.8 +/- 0.8 mmHg, P less than 0.01) and in 22 patients with adult respiratory distress syndrome (3.8 +/- 0.8 mmHg; P less than 0.01), but not in 20 patients with chronic obstructive pulmonary disease (1.8 +/- 0.7 mmHg). The distribution of the pulmonary vascular resistance was clearly different among the four groups. The fraction of the total pulmonary vascular resistance attributable to large and medium pulmonary veins was significantly increased (P less than 0.01) in adult respiratory distress syndrome (27.5 +/- 12%) and cardiac patients (27.5 +/- 9%) compared with patients with chronic obstructive pulmonary disease (13 +/- 5%) and normal lungs (13.5 +/- 6%).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of sodium-nitroprusside and urapidil on gas exchange and ventilation-perfusion relationships in patients with congestive heart failure.

Vasodilators usually decrease arterial PO2 in patients with congestive heart failure (CHF) because of alteration in ventilation-perfusion (Va/Q) relationships. The effects of sodium nitroprusside (SNP) and urapidil (U), a new selective alpha 1-receptor antagonist, were investigated in seven patients with CHF. The distribution of ventilation and perfusion was examined using the multiple gas elimination technique. The haemodynamic responses to SNP and U were similar, cardiac index increasing by 25% with SNP and by 31% with U. Despite a similar increase of mixed venous oxygen tension, the arterial PO2 decreased from 11.3 +/- 0.8 to 9.6 +/- 0.6 kPa (p less than 0.01) with SNP but remained unchanged (11.0 +/- 0.9 vs 11.4 +/- 0.8 kPa, NS) with U. SNP and U both increased perfusion to lung units with Va/Q ratios of 0.1 or less with no change in shunt fraction. The fractional perfusion to total low Va/Q ratios (low Va/Q + shunt) was higher with SNP than with U (14.1 +/- 2.6 vs 9.5 +/- 2.3%, p less than 0.01). The results suggest that gas exchange and Va/Q relationships are altered less with U than with SNP in patients with CHF.