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Background Noninvasive ventilation (NIV) requires a close “partnership” between a conscious patient and the patient’s caregivers. Specific perceptions of NIV stakeholders and their impact have been poorly described to date. The objectives of this study were to compare the perceptions of NIV by intensive care unit (ICU) physicians, nurses, patients, and their relatives and to explore factors associated with caregivers’ willingness to administer NIV and patients’ and relatives’ anxiety in relation to NIV. Methods This is a prospective, multicenter questionnaire-based study. Results Three hundred and eleven ICU physicians, 752 nurses, 396 patients, and 145 relatives from 32 ICUs answered the questionnaire. Nurses generally reported more negative feelings and more frequent regrets about providing NIV (median score, 3; interquartile range, [1 to 5] vs. 1 [1 to 5]; P < 0.0001) compared to ICU physicians. Sixty-four percent of ICU physicians and only 32% of nurses reported a high level of willingness to administer NIV, which was independently associated with NIV case-volume and workload. A high NIV session–related level of anxiety was observed in 37% of patients and 45% of relatives. “Dyspnea during NIV,” “long NIV session,” and “the need to have someone at the bedside” were identified as independent risk factors of high anxiety in patients. Conclusions Lack of willingness of caregivers to administer NIV and a high level of anxiety of patients and relatives in relation to NIV are frequent in the ICU. Most factors associated with low willingness to administer NIV by nurses or anxiety in patients and relatives may be amenable to change. Interventional studies are now warranted to evaluate how to reduce these risk factors and therefore contribute to better management of a potentially traumatic experience. (Anesthesiology 2016; 124:1347-59)

Noninvasive ventilation (NIV) requires a close "partnership" between a conscious patient and the patient's caregivers. Specific perceptions of NIV stakeholders and their impact have been poorly described to date. The objectives of this study were to compare the perceptions of NIV by intensive care unit (ICU) physicians, nurses, patients, and their relatives and to explore factors associated with caregivers' willingness to administer NIV and patients' and relatives' anxiety in relation to NIV.This is a prospective, multicenter questionnaire-based study.Three hundred and eleven ICU physicians, 752 nurses, 396 patients, and 145 relatives from 32 ICUs answered the questionnaire. Nurses generally reported more negative feelings and more frequent regrets about providing NIV (median score, 3; interquartile range, [1 to 5] vs. 1 [1 to 5]; P0.0001) compared to ICU physicians. Sixty-four percent of ICU physicians and only 32% of nurses reported a high level of willingness to administer NIV, which was independently associated with NIV case-volume and workload. A high NIV session-related level of anxiety was observed in 37% of patients and 45% of relatives. "Dyspnea during NIV," "long NIV session," and "the need to have someone at the bedside" were identified as independent risk factors of high anxiety in patients.Lack of willingness of caregivers to administer NIV and a high level of anxiety of patients and relatives in relation to NIV are frequent in the ICU. Most factors associated with low willingness to administer NIV by nurses or anxiety in patients and relatives may be amenable to change. Interventional studies are now warranted to evaluate how to reduce these risk factors and therefore contribute to better management of a potentially traumatic experience. (Anesthesiology 2016; 124:1347-59).

Noninvasive ventilation (NIV) is a treatment option in patients with acute respiratory failure who are good candidates for intensive care but have declined tracheal intubation. The aim of our study was to report outcomes after NIV in patients with a do-not-intubate (DNI) order.Prospective observational cohort study in all patients who received NIV for acute respiratory failure in 54 ICUs in France and Belgium, in 2010/2011.Goals of care, comfort, and vital status were assessed daily. On day 90, a telephone interview with patients and relatives recorded health-related quality of life (HRQOL), posttraumatic stress disorder-related symptoms, and symptoms of anxiety and depression. Post-ICU burden was compared between DNI patients and patients receiving NIV with no treatment-limitation decisions (TLD). Of 780 NIV patients, 574 received NIV with no TLD, and 134 had DNI orders. Hospital mortality was 44 % in DNI patients and 12 % in the no-TLD group. Mortality in the DNI group was lowest in COPD patients compared to other patients in the DNI group (34 vs. 51 %, P = 0.01). In the DNI group, HRQOL showed no significant decline on day 90 compared to baseline; day-90 data of patients and relatives did not differ from those in the no-TLD group.Do-not-intubate status was present among one-fifth of ICU patients who received NIV. DNI patients who were alive on day 90 experienced no decrease in HRQOL compared to baseline. The prevalences of anxiety, depression, and PTSD-related symptoms in these patients and their relatives were similar to those seen after NIV was used as part of full-code management (clinicaltrial.govNCT01449331).

Resume Ce travail retrospectif presente l'experience du centre medical de Bligny dans la prise en charge du sevrage difficile et prolonge de la ventilation mecanique, sur une periode de dix ans (1989–1999). Cent-quarante-six patients, d'âge moyen 68,2 ± 8,5 ans, tous tracheotomises, ont ete transferes de 32 services de reanimation d'Ile-de-France apres une duree moyenne de ventilation mecanique de 57 ± 33 jours. Cent-un etaient porteurs d'une insuffisance respiratoire chronique (groupe 1), 45 en etaient exempts (groupe 2). Les patients du groupe 1 ont ete hospitalises 25 ± 24 jours en reanimation, et 48 ± 43 jours en pneumologie. Le taux de deces intra-hospitalier a ete de 27 %. Un sevrage complet a ete obtenu chez 65 % des survivants. La survie a un an a ete de 64 %. Les patients du groupe 2 ont ete hospitalises 24 ± 18 jours en reanimation, et 38 ± 31 jours en pneumologie. Le taux de deces intra-hospitalier a ete de 23 %. Un sevrage complet a ete obtenu chez 85 % des survivants. La survie a un an a ete de 74 %. Les auteurs concluent sur la necessite de developper les structures specialisees de prise en charge des patients de reanimation restant dependants de la ventilation mecanique.

THE INTERNAL MAMMARY ARTERY (IMA) is used as the conduit of choice in coronary artery bypass grafting (CABG) due to its superior long-term outcomes compared to venous grafts. The IMA collateralizes to the external iliac artery by anastomosis with the inferior epigastric artery. In patients with chronic aortoiliac occlusion, arterial perfusion of the lower limbs may be supplied mostly by this collateral pathway. In this case report, the authors describe the occurrence of acute bilateral lower limb ischemia following CABG using bilateral IMA grafts in a patient with severe aortoiliac occlusive disease.

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.

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. (CHEST 1995; 108:335-40)

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.

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 2 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 ( V . E ) from 8.6 ± 0.8 to 9.6 ±0.8 and 10.3 ±0.7 L/min (p 2 (from 117 ± 17 to 110 ± 15 and 96.4 ± 8.8 mm Hg, respectively; p

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.

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.

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.

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.

Pulmonary artery occlusion pressure (Ppao) represents the pressure in a pulmonary vein (Ppv) and reflects left atrial pressure (Pla) provided alveolar pressure (Palv) does not exceed the pressure existing at the venous end of the collapsible alveolar vessels. Three major factors may influence the relationships between Palv and Ppv: mechanical ventilation with positive end-expiratory pressure (PEEP), vertical location of the pulmonary artery catheter (PAC) tip relative to the left atrium, and volemia. In an experimental and clinical study, we assessed a simple means to ensure meaningful measurements of Ppao during mechanical ventilation with PEEP, based on the following reasoning: if Ppao reflects Palv and not Ppv, it will increase during positive pressure inspiration by an amount (ΔPpao) similar to Palv; thus, ΔPpao will widely exceed the increase in pulmonary arterial pressure (ΔPpa), which approximates the increase in pleural pressure. Conversely, when Ppao actually reflects Ppv, ΔPpao will be close to ΔPpa. A preliminary experimental study in an animal with a left atrial catheter and PAC in place showed that Ppao widely exceeded Pla when ΔPpao/ΔPpa widely exceeded 1 during mechanical ventilation with PEEP. After fluid infusion, Pla and Ppao were almost identical and ΔPpao/ΔPpa was now close to 1. In 12 patients ventilated for adult respiratory distress syndrome and with a left ventricular catheter and PAC in place, we verified at four levels of PEEP (0, 10, 15, and 20 cm H 2 O) that a Ppao close to left ventricular end-diastolic pressure was always associated with a ΔPpao/ΔPpa ratio close to 1 (38 measurements). In 34 additional patients ventilated for noncardiogenic pulmonary edema, we also tested the ΔPpao/ΔPpa ratio during the same incremental PEEP protocol and found that ΔPpao/ΔPpa was close to 1 at each level of PEEP in 30 of the patients (108 measurements). In five measurements in four hypovolemic patients, ΔPpao/ΔPpa widely exceeded 1; only one of these four patients was found to have a PAC tip located above the left atrium level on a lateral chest x-ray film. We conclude that the bedside determination of the ΔPpao/ΔPpa ratio should identify the cases in which Ppao measurements are not valid more reliably than lateral chest x-ray film, thus avoiding misleading interpretations of Ppao during PEEP ventilation.

Background Rapid and accurate estimation of the glomerular filtation rate (GFR) is required for many major clinical decisions in patients with chronic nephropathies [1]. Direct GFR measurement is time-consuming and expensive, frequently requires urine collection and isotope use, and is routinely available in only a few medical centers [1]. In clinical practice, GFR is usually estimated from the serum creatinine concentration. However, this last is affected by factors other than creatinine glomerular filtration, such as diet, muscle mass, tubular secretion, unstable renal function, colorimetric interference, and day-to-day assay variability [1]. To circumvent these limitations, several equations have been developed to estimate GFR from the serum creatinine concentration adjusted for age, sex, body weight and demographic factors [1]. The equation proposed by Cockcroft and Gault in 1976 is widely used throughout the world [2,3]. Adjustment for body surface area has been shown to improve the accuracy of the original Cockcroft-Gault equation [4]. In recent years, the Modification of Diet in Renal Disease (MDRD) group developed three multiple regression models that improved the prediction of GFR from the plasma creatinine concentration [5]. The first includes urinary urea excretion and the second is derived from demographic factors combined with serum creatinine, urea and albumin; the third, which is slightly less accurate, uses demographic factors and serum creatinine (MDRD abbreviated equation) [5]. Finally, the Mayo Clinic team have developed a quadratic equation (MCQ) based on results of both healthy subjects and patients with chronic renal diseases [6]. The validity of these creatinine-based equations for the follow-up of renal function in patients with known renal disease is uncertain, notably during therapeutic interventions and data on this topic are scarce [7]. Indeed, five studies, all restricted to patients with diabetic nephropathy suggested that, in patients with normal renal function or hyperfiltration (microalbuminuric), prediction equations are not accurate enough to monitor kidney function, whereas in chronic kidney disease (CKD) stages 2 and 3 these equations may be valid [8-12]. The aim of this study was therefore to compare the accuracy of prediction equations (original Cockcroft and Gault equation, Cockcroft and Gault equation adjusted for body surface area, Abbreviated MDRD and Mayo Clinic Quadratic Equation) for the follow-up of non-diabetic nephropathies, by comparison with inulin clearance, the gold standard for GFR estimation. We analyzed data from a prospective cohort of 260 European patients with non-diabetic chronic kidney disease [4], 126 of whom had repeated measures of their GFR based on inulin clearance during their long-term follow-up.

Spontaneous idiopathic pneumothorax occurs frequently in young tall subjects with smoking habits, and is usually of good prognosis. Secondary pneumothorax is a life-threatening complication of an underlying lung disease, such as acute pneumonia. Pneumocystis carinii pneumonitis or chronic obstructive pulmonary disease. Short-term therapeutic options oppose non-traumatic needle aspiration, with a success rate of more than 50%, versus thoracic drainage, with a recurrence rate exceeding 35%. The existing literature also indicates that video-assisted surgery leads to a much better long-term prognosis than the standard drainage procedure, with a long-term recurrence rate of less than 2%, for equivalent hospital stays and complication rates. The widely accepted recommendation that surgery should be proposed only at the first or second pneumothorax recurrence may be challenged in the next decade.

International audience; 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.

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.Open, prospective clinical study.A 12-bed medical intensive care unit in a non-university hospital.20 patients (14 males and 6 females, mean age 74.8 +/- 2.6 years), admitted for respiratory failure and denied mechanical ventilation.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).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 (p0.001 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 (p0.05). 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.Our results suggest that MT insertion for ITO2 may be a therapeutic option in selected patients with respiratory failure from CLD.

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.

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 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.

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)

To investigate the influence of atrial natriuretic factor (ANF) on renal function during mechanical ventilation (MV), we examined the renal and hormonal responses to synthetic human ANF infusion in eight patients during MV with zero (ZEEP) or 10 cmH2O positive end-expiratory pressure (PEEP). Compared with ZEEP, MV with PEEP was associated with a reduction in diuresis (V) from 208 +/- 51 to 68 +/- 11 ml/h (P less than 0.02), in natriuresis (UNa) from 12.4 +/- 3.3 to 6.2 +/- 2.1 mmol/h (P less than 0.02), and in fractional excretion of sodium (FENa) from 1.07 +/- 0.02), 0.21 to 0.67 +/- 0.17% (P less than 0.02) and with an increase in plasma renin activity (PRA) from 4.83 +/- 1.53 to 7.85 +/- 3.02 ng.ml-1.h-1 (P less than 0.05). Plasma ANF levels markedly decreased during PEEP in four patients but showed only minor changes in the other four patients, and mean plasma ANF levels did not change (163 +/- 33 pg/ml during ZEEP and 126 +/- 30 pg/ml during PEEP). Glomerular filtration rate and renal plasma flow were unchanged. Infusion of ANF (5 ng.kg-1.min-1) during PEEP markedly increased V and UNa by 110 +/- 61 and 107 +/- 26%, respectively, whereas PRA decreased from 7.85 +/- 3.02 to 4.40 +/- 1.5 ng.ml-1.min-1 (P less than 0.05). In response to a 10 ng.kg-1.min-1 ANF infusion, V increased to 338 +/- 79 ml/h during ZEEP but only to 134 +/- 45 ml/h during PEEP (P less than 0.02), whereas UNa increased, respectively, to 23.8 +/- 5.3 and 11.3 +/- 3.3 mmol/h (P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

To examine the interrelations between humoral systems involved in the circulatory and body fluid volume homeostasis of patients with chronic obstructive pulmonary disease (COPD), we measured plasma levels of renin activity (PRA), aldosterone (Aldo), and atrial natriuretic factor (ANF) in 14 patients with stable COPD who used continuous O2 therapy. Hemodynamics, blood gases, and plasma hormone levels were measured (1) while patients received supplemental O2; (2) after 30 min O2 discontinuation; and (3) after a 30-min period of 96% O2 breathing. Plasma immunoreactive ANF concentrations were 196 +/- 50 pg/ml during O2 breathing and were positively related to transmural pulmonary arterial wedge pressure (tPpaw, r = 0.90, p less than 0.001) and to PaCO2 (r = 0.57, p less than 0.02). Compared to normal subjects matched for age and sex, patients had higher plasma ANF levels (196 +/- 52 versus 72 +/- 6 pg/ml, p less than 0.01), similar PRA (2.1 +/- 0.5 versus 1.3 +/- 0.3 ng/ml/h, NS), and slightly lower plasma Aldo (98 +/- 17 versus 156 +/- 19 pg/ml, p less than 0.05). Discontinuation of O2 while decreasing PaO2 from 70 +/- 3 to 50 +/- 3 mm Hg resulted in a significant increase in pulmonary arterial pressure (Ppa) from 29 +/- 2 to 32.5 +/- 3 mm Hg (p less than 0.01) and cardiac index (Cl) from 3.6 +/- 0.1 to 3.9 +/- 0.1 L/min/m2 (p less than 0.01) and a decrease in systemic arterial pressure (Psa) from 96 +/- 3 to 91 +/- 2 mm Hg (p less than 0.05); transmural cardiac filling pressures and pulmonary vascular resistance (PVR) were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

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)

To define the relationship between plasma levels of immunoreactive atrial natriuretic peptide (IR-ANP) and hemodynamic parameters in patients with chronic pulmonary artery hypertension, we measured plasma concentrations of the peptide in 15 patients during right heart catheterization. Eleven patients had chronic obstructive pulmonary disease and 4 had pulmonary vascular disease of diverse etiology. At rest, plasma concentrations of IR-ANP positively correlated with mean pulmonary artery pressure (r = 0.70, p less than 0.01) and pulmonary vascular resistance (r = 0.88, p less than 0.001), but not with right atrial pressure. Nine of these patients, all with chronic obstructive pulmonary disease, were also evaluated during exercise. Plasma concentrations of IR-ANP increased from 131 +/- 22 to 191 +/- 30 pg/ml (p less than 0.003) at maximal exercise, whereas pulmonary artery pressure increased from 29 +/- 1.5 to 56 +/- 2.5 mm Hg and right atrial pressure from 5 +/- 1 to 13 +/- 2 mm Hg. Increases of plasma IR-ANP concentrations correlated with changes in pulmonary artery pressure and right atrial pressure but not with changes in pulmonary capillary wedge pressure. These findings suggest that ANP is released in response to an increase in pulmonary artery pressure and are consistent with the hypothesis that ANP could modulate the pulmonary vascular tone in patients with pulmonary artery hypertension.

To investigate the physiological role of atrial natriuretic factor (ANF) in patients with hypoxic pulmonary hypertension secondary to chronic obstructive lung disease (COLD), we infused synthetic alpha-human ANF in seven such patients, and investigated the physiological correlates to circulating peptide levels in 24 patients with COLD. ANF infusion, at incremental rates of 0.01, 0.03, and 0.1 micrograms/kg.min, increased basal plasma immunoreactive (ir) ANF (136 +/- 38 pg/ml) by 3-, 10-, and 26-fold, respectively, and reduced pulmonary artery pressure (from 33 +/- 3 to 25 +/- 2 mmHg, P less than 0.001) and systemic arterial pressure (from 88 +/- 4 to 79 +/- 4 mmHg, P less than 0.001) in a dose-related fashion. Cardiac index increased by 13.5% (P less than 0.01) while heart rate was unchanged. Cardiac filling pressures decreased at 0.1 micrograms/kg.min ANF. Pulmonary and systemic vascular resistance fell by 37% (P less than 0.001) and 19% (P less than 0.001), respectively. Arterial oxygenation was impaired during ANF infusion, suggesting partial reversal of hypoxic pulmonary vasoconstriction. Plasma renin activity remained unchanged but aldosterone fell by 44% (P less than 0.01). The levels of plasma irANF in 24 patients correlated directly with the degree of hemoconcentration (r = 0.67, P less than 0.001), respiratory acidosis (r = -0.65, P less than 0.001), and pulmonary hypertension (r = 0.52, P less than 0.01). The results suggest that ANF may serve as a potent pulmonary vasodilator involved in the circulatory homeostasis of patients with COLD.

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.