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Lung-protective ventilation strategies in acute lung injury.

OBJECTIVES: To review the challenges of providing mechanical ventilatory support for respiratory failure while avoiding ventilator-associated lung injury in patients with acute lung injury. To review the results of several randomized clinical trials of lung-protective ventilation strategies using conventional mechanical ventilators. DATA SOURCES: Published reports of clinical trials comparing clinical outcomes of patients with acute lung injury, randomized to mechanical ventilation with either a lung-protective or a control, conventional, standard, or traditional approach. DATA EXTRACTION AND SYNTHESIS: Lung-protective mechanical ventilation strategies are designed to prevent injury from overdistention by using lower tidal volumes and lower inspiratory pressures (volume- and pressure-limited ventilation) or injury from ventilation with atelectasis and alveolar flooding at end-expiration (open-lung ventilation). In one trial, clinical outcomes were better in the study group that received combined volume- and pressure-limited and open-lung strategies compared with the study group that received a conventional approach. Of four trials focusing on volume- and pressure-limited ventilation alone, three did not demonstrate improvements in clinical outcomes, whereas one demonstrated a substantial reduction in mortality and an increase in ventilator-free days. The different results in these four trials may be attributable to differences in tidal volumes between the study groups, chance variation, or differences in the management of respiratory acidosis. CONCLUSIONS: Evidence supports the use of a volume- and pressure-limited approach to mechanical ventilation in patients with acute lung injury. It is not yet clear whether the open-lung approach will further reduce mortality in patients receiving volume- and pressure-limited ventilation support.

Humans↗

Enzymatic basis of renal adaptation to acidosis in the dog.

The effect of pH on the activities of various enzymes along the ammoniagenic pathway was tested on dog kidney cortex homogenates in an attempt to identify the metabolic steps that could be directly influenced by a low pH in this species. The activity of alphaketoglutarate dehydrogenase was markedly stimulated by acidification of the medium that decreased abruptly the km for alphaketoglutarate. By contrast, succinyl CoA synthetase and malate dehydrogenase remained relatively insensitive to pH changes. The apparent km of malic enzyme for malate was markedly decreased by an acid medium. Therefore these findings suggest that an acid pH regulates the ammoniagenic pathway at two critical sites: alphaketoglutarate dehydrogenase and malic enzyme. These stimulated enzymatic activities may account for the changes in renal cortical concentrations of metabolites observed during metabolic or respiratory acidosis.

Acidosis↗

Effects of loaded breathing and hypoxia on diaphragm metabolism as measured by (31)P-NMR spectroscopy.

Diaphragm fatigue may contribute to respiratory failure. (31)P-nuclear magnetic resonance spectroscopy is a useful tool to assess energetic changes within the diaphragm during fatigue, as indicated by P(i) accumulation and phosphocreatine (PCr) depletion. We hypothesized that loaded breathing during hypoxia would lead to diaphragm fatigue and inadequate aerobic metabolism. Seven piglets were anesthetized by using halothane inhalation. Diaphragmatic contractility was assessed by transdiaphragmatic pressure (Pdi) at end expiration with the airway occluded. A nuclear magnetic resonance surface coil placed under the right hemidiaphragm measured P(i) and PCr during four conditions: control, inspiratory resistive breathing (IRB), IRB with hypoxia, and recovery (IRB without hypoxia). IRB alone resulted in hypercarbia (32 +/- 7 to 61 +/- 21 Torr) and respiratory acidosis but no change in diaphragm force output or aerobic metabolism. Combined IRB and hypoxia resulted in decreased force output (Pdi decreased by 40%; from 30 +/- 17 to 19 +/- 11 mmHg) and evidence of metabolic stress (ratio of P(i) to PCr increased by 290%; from 0.19 +/- 0.09 to 0.74 +/- 0.27). We conclude that diaphragm fatigue associated with inadequate aerobic oxidative metabolism occurs in the setting of loaded breathing and hypoxia. Conversely, aerobic metabolism and force output of the diaphragm remain unchanged from control during loaded normoxic or hyperoxic breathing despite the onset of respiratory failure.

Animals↗

Differential effects of acetazolamide, benzolamide and systemic acidosis on hydrogen and bicarbonate gradients across the apical and basolateral membranes of the choroid plexus.

The effect after 1 hr of sulfonamide agents and systemic acidosis on pH (dimethyloxazolidinedione method) and [HCO3-] (calculated from pH and estimated cell pCO2) of choroid plexus epithelium was analyzed in adult Sprague-Dawley rats anesthetized with ether. Acetazolamide (20 mg/kg i.p.) caused a striking increase in choroid cell pH (7.0-7.45) and a substantial elevation in [HCO3-]i, and an alkalinization of cerebrospinal fluid (CSF); effects of benzolamide (3 mg/kg i.v.) were less marked. Acetazolamide-induced augmentation of steady-state pH was found in choroid plexus (0.45 pH unit) but not in submaxillary salivary gland, skeletal muscle, erythrocytes and cerebral cortex. Respiratory acidosis (blood pH 6.94) caused choroid cell pH to decrease less extensively than in the other tissues analyzed; metabolic acidosis (blood pH 7.23) did not significantly alter choroid plexus pH. Both sulfonamide agents and systemic acidoses significantly decreased the pH gradient between arterial blood and cisternal CSF. The sulfonamide-induced increase in choroid cell pH is attributed to suppression of buffering of OH- by CO2, leading to elevated [OH]i; and to a build-up in [HCO3-]i. Acetazolamide caused a reversal of the H+ and HCO3- gradients across the basolateral (plasma-facing) membrane of the choroid plexus. It is postulated that carbonic anhydrase inhibitors decrease CSF formation primarily by reducing Na+-H+ exchange at the basolateral membrane of the choroidal epithelium, and secondarily by slowing down HCO3- and Cl- exit across the CSF-facing membrane.

Acetazolamide↗

Effect of amiloride on contractility of rat cardiac muscle exposed to chronic hypercapnia and acute acidosis.

Papillary muscle preparations from rats with normal arterial oxygen and carbon dioxide tensions and from rats which had been maintained with normal oxygen tension but with hypercapnia for 28 days (FICO2 = 5%) were subjected to acute hypercapnia with or without amiloride, a competitive inhibitor of the Na+/H+ pump. Acclimatisation to hypercapnia reduced the slope of the line relating log tension against the extracellular pH from 0.96(SEM0.06) to 0.71(0.07) (p less than 0.02). Amiloride increased the slope in unacclimatised muscle to 1.39(0.09), p less than 0.001 and in muscles acclimatised to hypercapnia to 1.03(0.13), p less than 0.05. The slope in acclimatised muscles was significantly less steep than in unacclimatised muscle (p less than 0.05). The sarcolemmal Na+H+ exchanger is important in the protection of rat cardiac muscle against acute respiratory acidosis.

Acidosis↗

[Treatment of Pseudomonas aeruginosa in cystic fibrosis in a child].

The report deals with the case of a 10-year-old girl with chronic cystic fibrosis. She has been repeatedly treated at the hospital. She has been hospitalized due to respiratory deterioration. Cystic fibrosis is a rare disease, inherited autosomaly recessively, but is very complex in terms of diagnostic and treatment. Fibrosis is the formation of scar tissue due to injury or long term inflammation. The diagnosis is confirmed based on a clinical picture of the child, measure of Chloride in the sweat, chest X-ray, CT thorax, laboratory findings--genetic confirmation CFTR genes. The diagnosis is originally set when she was 4 years old. She is now admitted due to a deterioration of the main disease. Five days before the admission, the girl had a higher bodily temperature, cough and difficult breathing. Due to the deteriorated general condition and the respiratory insufficiency and respiratory acidosis in blood gas analysis, the girl was intubated and put on the complete mechanical ventilation (IPPV). Since the girl is a chronic patient with bronchiectasie chronic walls of bronchi changes full of the mucus, who is not responding to conservative treatment (antibiotics), therapeutic and diagnostic flexible bronchoscopy had to be performed, resulting in a gram-negative bacteri Pseudomonas aeruginosa--a typical bacteri for chronically sick C. F. patient. Pseudomonas aeruginosa is typically acquired in early childhood. This bacteria is giving progressive lung disease and often aggravates morbidity and mortality. So the main thing as a respiratory management is prevention of lung infection with this bacteria. A Pseudomonas therapy was prescribed according to the sensitive antibiogram, (Garamycin). Antibiotics are crucial to treating cystic fibrosis lung infections. Therapy with an amynoglicoside in combination with a B-lactam or a quinolone antibiotic is standard. It is a difficult to deliver a high doses at these antibiotics via the iv. route without significant systemic adverse events (otoxicity and nephrotoxicity). A reformulation of the aminoglycoside antibiotic tobramicin or garamycin therapy is solution for inhalation. To be well established infections the suppression of Pseudomonas aeruginosa has been shown to lead to decreasing same bacteria and benefits lung function from antibiotic therapy in a way that can be maintained over extended period. During bronchoscopy was given locally on changes mucous pulmozyme (to destroy a very hard mucous) and garamycin. So, after taking out a lot of mucus, it was later continued spontaneously. Control chest x ray and blood gas analysis are now very improved.

Child↗

[Metabolic acidosis after cardiac surgery with cardiopulmonary bypass revisited with the use of the Stewart acid-base approach].

INTRODUCTION: According to the Stewart approach of acid-base regulation, chloride from either volume replacement or cardiopulmonary bypass (CPB) priming solution may induce metabolic acidosis. The alternative hypothesis stands in volume dilution with solutions free of bicarbonate. OBJECTIVES: Evaluate the acid-base status of patients undergoing cardiac surgery with CPB priming containing chloride and bicarbonate. MATERIAL AND METHODS: Prospective study. METHODS: Twenty-eight patients were prospectively included. Priming of CPB contained 47.4 mmol/l of bicarbonate and 97.7 mmol/l of chloride. Arterial blood samples were taken at 3 timings: prior (T1) and after (T2) CPB, and on arrival in the ICU (T3). Following measurements were performed: Na(+), K(+), Cl(-), Mg(++), Ca(++), phosphates, albumin, lactate and arterial blood gases. RESULTS: After CPB respiratory acidosis was observed. There was a significant increase of chloride with a decrease in apparent strong ion difference (SIDa). At the same time bicarbonate and base excess (BE) remained constant. A significant but weak correlation between BE and SIDa existed (r(2) = 0.06, p=0.024). On the contrary, no correlation was found between variations of BE and SIDa. However, the correlation was stronger between values and variations of bicarbonate and BE (respectively r(2)=0.605, p<0.0001 and r(2)=0.495, p<0.0001). CONCLUSION: No metabolic acidosis occurred after cardiac surgery when CPB was primed with bicarbonate. Therefore, it appears that chloride administration is not the main mechanism being involved in the acid-base regulation. This reinforces the hypothesis that metabolic acidosis during CPB may mainly be due to dilution of bicarbonate.

Acid-Base Equilibrium↗

Cardiopulmonary effects of high-impulse noise exposure.

In high-energy impulse noise environments, the biomechanical coupling process between the external forces and the pathophysiology of cardiopulmonary injury is not well understood. A 12-in-diameter compressed air-driven shock tube with reflector plate was used to induce three levels of pulmonary contusion injury in a large animal model. Twenty-one anesthetized sheep were exposed to the various levels of impulse noise generated by the shock tube, with six additional sheep serving as a control group. Pathologic evaluations, performed 3 hours after exposure, showed pulmonary contusion ranging from minor petechial changes on the surface of the lung parenchyma to diffuse ecchymoses affecting as much as 60% of the lung. The gross pathologic observations of injury produced by exposure to the impulse noise produced by the shock tube were similar to those reported for blunt impact trauma or exposure to chemical or grain-dust explosions. The extent of lung injury (lung injury index) was quantitatively assessed. A semilogarithmic relationship between the lung injury index and the measured peak pressure was demonstrated. A significant linear correlation was demonstrated between lung injury index and lung weight-to-body weight ratio. Significant cardiopulmonary changes were also observed as a result of exposure to high-impulse noise. Although in most cases the degree of change was related to the severity of the injury, significant cardiopulmonary function changes were also observed in the absence of significant grossly observable pulmonary injury. Cardiac injury was indicated by decreased cardiac output and hypotension at all levels of injury and might be the result of myocardial contusion or air emboli. Pulmonary injury was demonstrated by respiratory acidosis, increases in lung resistance, and decreases in lung compliance and lung volume. Arterial PO2 appeared to be the most sensitive parameter of injury and was decreased for all measurement intervals for all exposure groups.

Animals↗

Reversible resistance to the phosphaturic effect of db-cAMP in lithium-treated rats.

Acute lithium administration (5 mmol/kg b.w.) to parathyroidectomized (PTX) rats induces extracellular acidosis, lower plasma phosphate concentration and increased phosphate reabsorption. The present studies evaluate the effect of lithium administration on tissue phosphate distribution, metabolites content in the kidneys and renal phosphate, 2-oxoglutarate and citrate transport in the presence and absence of db-cyclic AMP. Lithium decreased plasma and renal phosphate concentrations and increased phosphate concentration in the skeletal muscle, db-cyclic AMP was not phosphaturic in lithium-treated PTX rats. In PTX rats infused with 20 mM phosphate lithium depressed fractional phosphate excretion induced by db-cyclic AMP from 20 +/- 0.3% to 3.2 +/- 1.0%. However, metabolic or respiratory acidosis restored the responsiveness to db-cyclic AMP. Citraturia and ketoaciduria induced by lithium were depressed in db-cyclic AMP-treated rats. Kidney citrate and 2-oxoglutarate concentrations increased drastically, ATP level fell significantly whereas cAMP content did not change after lithium. We conclude that lithium administration increases phosphate uptake by the muscle which largely accounts for hypophosphatemia. The kidney responds with increased phosphate reabsorption independent of plasma and kidney phosphate concentrations, and with refractoriness to the phosphaturic effects of db-cyclic AMP. Acute lithium administration to rats induces extracellular acidosis and, probably, renal intracellular alkalosis as reflected by citraturia and ketoaciduria as well as the renal metabolite profile. The phosphaturic responsiveness to db-cyclic AMP is dependent, at least in part, on intracellular pH.

Animals↗

[A case of myotonic dystrophy with morning headache following sleep apnea syndrome].

We reported a 39-year-old man with myotonic dystrophy. He suffered from morning headache. Respiratory function tests showed restrictive pattern and arterial gas analysis showed hypoxia and hypercapnia with respiratory acidosis (PaCO2 50.8 mmHg, PaO2 63.8mmHg, pH 7.317, SaO2 89.8%). Polysomnograph showed central apneas exclusively in light sleep (stage 1 and 2). O2 saturation fell at most to as low as 50% during the apneas. We conclude that sleep apnea should be consider in patients with myotonic dystrophy associated with morning headache.

Adult↗

Late-onset encephalopathy associated with a C11777A mutation of mitochondrial DNA.

A 67-year-old man presented with cognitive deficits, status epilepticus, left hemiparesis, and severe lactic acidosis. Respiratory chain enzyme analysis of skeletal muscle revealed a defect in complex I activity, associated with a heteroplasmic C11777A mutation in the mitochondrial ND4 gene. This case is remarkable not only because of the late onset of symptoms, but because this mutation affects the identical ND4 codon as the G11778A mutation that causes Leber hereditary optic neuropathy.

Acidosis, Lactic↗

[Correlation between the area of arterial blood gases graph and the acid-base disturbance in 92 cases with chronic obstructive pulmonary disease].

OBJECTIVE: To study the correlation between the area of arterial blood gases graph (ABGG) and the acid-base disturbance (ABD). METHODS: Using the software developed by ourselves, the results of arterial blood gases and concomitant electrolyte (K(+), Na(+), Cl(-), HCO(3)(-)) determination in 313 episodes were analyzed in 92 cases with chronic obstructive pulmonary diseases (COPD) during hospitalization, and the correlation was studied. RESULTS: (1)On admission, among 92 cases, in 9 cases the results of blood gas analysis were in the area of compensated ventilation and deranged gas exchange (area IV), in 82 cases the results were in the area of insufficient ventilation and deranged gas exchange (area V), and 1 case in the area of excessive ventilation and deranged gas exchange (area VI). There were 8 types of the ABDs, and respiratory acidosis (RAC)+metabolic alkalosis (MAL), RAC, RAC+metabolic acidosis (MAC) with increase in anion gap (AG) ranked in above order. (2)At the time of discharge, in 2 cases the distribution of ABGG was in the normal area (area I), 5 cases in the area IV, 20 cases in the area V, and 1 case in the area VI. There were 5 types of the ABDs. RAC+MAL and RAC ranked in the first two positions. (3)During hospitalization, the correlations between the area of ABGG and ABD in 313 episodes were as follows: ABD normal and MAC of AG increased in the area I; ABD normal and MAL, MAC with AG increased, RAC+MAC, respiratory alkalosis (RAL)+MAL, MAL+MAC of AG increased, RAC+MAL+MAC of AG increased and RAL+MAL+MAC of AG increased in the area IV; RAC, MAL, RAC+MAL, RAC+MAC of AG increased, MAL+MAC of AG increased, and RAC+MAL+MAC of AG increased in the area V; MAC of AG increased, RAC+MAC, RAL+MAL, MAL+MAC of AG increased, and RAL+MAL+MAC of AG increased in the area VI. No ABD occurred in the areas II and III. CONCLUSION: The correlation between ABGG and ABD can be analyzed easily and quickly and the accuracy of results is ensured by using the software.

Acid-Base Equilibrium↗

Combined high-frequency ventilation for management of terminal respiratory failure: a new technique.

Seven patients with severe adult respiratory distress syndrome (ARDS) developed terminal respiratory failure and severe hypoxemia (PaO2 below 50 mm Hg) with death imminent despite maximal ventilatory support with intermittent positive-pressure ventilation (IPPV) and positive end-expiratory pressure (PEEP). High-frequency positive-pressure ventilation (HFPPV) was used in these patients for one day at a rate of 250 breaths/min, with slight improvement of PaO2 to a mean of 80 mm Hg. High-frequency oscillatory (HFO) ventilation was used during the second day at a rate of 2000 breaths/min; this provided adequate oxygenation with a mean PaO2 of 244 mm Hg. Nonetheless, during HFO there was progressive CO2 retention and respiratory acidosis (mean PCO2 67 mm Hg). On the third study day, all seven patients were ventilated with combined high-frequency ventilation (CHFV) for a period from 5-21 days. CHFV is based on the administration of HFPPV simultaneously with HFO and provided adequate oxygenation by accelerated gas diffusion and CO2 elimination by convection. PaO2 was maintained during CHFV at a mean of 280 mm Hg. CO2 elimination was adequate with a mean PaCO2 of 32 mm Hg. Cardiac output also was adequately maintained during CHFV. Moreover, CHFV was well tolerated in our patients, allowing them to communicate with their families and nurses. CHFV successfully treated the hypoxemia of respiratory failure in all the patients. However, five patients (71%) died of cardiac arrest as a result of multisystem failure despite adequate oxygenation (PaO2 above 80 mm Hg).

Adolescent↗

Noninvasive continuous positive airway pressure ventilation using a new helmet interface: a case-control prospective pilot study.

OBJECTIVE: To evaluate the clinical efficacy of noninvasive continuous positive airway pressure ventilation (CPAP) using a new interface, constituted by a cephalic plastic helmet, in comparison with a standard facial mask. DESIGN AND SETTING: A prospective pilot study with matched-control group, in the emergency department of a teaching hospital. PATIENTS AND METHODS: Eleven consecutive adult patients with acute hypoxemic respiratory failure related to cardiogenic pulmonary edema (whether hypercapnic or not) were enrolled in the study, after failure of the initial medical treatment. Each patient treated with CPAP, using the helmet in addition to a standardized medical treatment, was matched with historical control-patient treated with CPAP using a standard facial mask, and selected by gender, age, and PaCO2 levels on admission. Primary end points were improvements of gas exchanges and clinical parameters of respiratory distress. tolerance was evaluated after each CPAP trial. RESULTS: The 22 patients and controls had similar characteristics at baseline. PaCO2 levels, and clinical parameters improved similarly in both groups. No interface intolerance was reported whether using standard facial mask or the helmet. No complications were observed in either group. The helmet allowed CPAP administration for a longer period of time (p=0.045). In-hospital mortality was not different between the two groups. CONCLUSION: Despite a high dead-space volume (9-15 l), this new helmet interface is an efficient alternative to standard face mask during CPAP, even in cases of severe respiratory acidosis and hypercapnia. It allowed to provide long-duration CPAP, without any adverse events or clinical intolerance.

Acute Disease↗

Adenosine and the acid-base state of vascular smooth muscle.

Hog carotid artery media was incubated under conditions of normocapnia (95% O2-5% CO2) and hypercapnia (nominally 75% O2-25%CO2). The intracellular pH (pHi) was determined from the distribution of 14C-labeled 5,5-dimethyloxazoladine-2,4-dione, alpha- and beta-receptor antagonists were used to block the effects of endogenous catecholamines. With 5% CO2, adenosine had no effect on the pHi. High K+ (25mM) and dipyridamole (DPM) induced a cellular metabolic acidosis that was reversed by adenosine and not affected by 0.5 mM ca2+ or ouabain. Hypercapnia decreased the resting pHi from 7.30 to 6.79. Adenosine significantly attenuated this decrease. With high K+ or DPM, a similar degree of hypercapnia only depressed the pHi to 6.91 and 6.90, respectively. The alkalinizing effect of high K+ and DPM was not altered by 0.5 mM Ca2+, was partically reversed by ouabain, and was completely reversed by adenosine. These results suggest that, under normocapnic conditions, although adenosine relaxes the contraction associated with K+-depolarization, it does not do so by elevating cellular proton levels. However, adenosine may decrease a tissue's ability to attenuate a local respiratory acidosis characteristic of increased O2 demand, resulting in relaxation under hypercapnic conditions. In any case, this demonstrates an interaction, with respect to the acid-base state of the vascular smooth muscle cells, among adenosine, K+, and H+, all suggested components of the metabolic theory of blood flow autoregulation.

Acid-Base Equilibrium↗

Acute quadriplegic myopathy in a 16-month-old child.

We present a case of a 16-month old previously healthy child who was hospitalized because of an acute respiratory insufficiency most likely caused by a viral infection and who then developed a severe acute quadriplegic myopathy (AQM). Initial clinical symptoms were respiratory acidosis, dypnea, intense wheezing, and deterioration of the level of consciousness, which required orotracheal intubation and mechanical ventilation. We administered neuromuscular blocking agents, corticosteroids, and antibiotics. After 9 days the clinical picture improved. An attempt to wean from the ventilator failed. We diagnosed AQM. This paper discusses AQM and its clinical importance.

Humans↗

Blood acid-base status of an awake heterothermic rodent, Spermophilus tereticaudus.

The desert ground squirrel Spermophilus tereticaudus is shown to show both reptilian style alphastat regulation and the pH-stat regulation typical of mammalian hibernation, depending upon the range of body temperature and the state of vigilance. Temperature corrected arterial pH and PCO2 of torpid squirrels (Tb 11-28 degrees C) were independent of Tb and about equal to euthermic values at 37 degrees C. Torpid squirrels show a progressive respiratory acidosis as Tb is lowered. In awake heterothermic squirrels (Tb 30-42.5 degrees C), blood acid-base status is like that of many ectothermic vertebrates: from 30 to 40 degrees C delta pHa/delta Tb was -0.0121, delta PaCO2/delta Tb was 1.057 and [HCO3-] remained about constant. Arterial blood from awake heterothermic squirrels measured at standard temperature (37 degrees C) showed no significant change with Tb, similar to blood undergoing anaerobic temperature changes in vitro. In vitro, the delta pH/delta T of blood of constant CCO2 was -0.014. Constant blood pH with change in Tb is thus not a general feature of mammalian acid-base regulation but appears in this species to be a feature of the respiratory and metabolic poise of torpor.

Acid-Base Equilibrium↗

Prospective, randomized, controlled pilot study of partial liquid ventilation in adult acute respiratory distress syndrome.

We evaluated the safety and efficacy of partial liquid ventilation (PLV) with perflubron in adult patients with acute lung injury and the acute respiratory distress syndrome (ARDS) in a multicenter, prospective, controlled, randomized exploratory clinical trial. Ninety adult patients with PaO2/FIO2 ratios > 60 and < 300 with ARDS for no more than 24 hours were randomized to receive PLV (n = 65) with administration of perflubron through an endotracheal tube sideport or conventional mechanical ventilation (CMV, n = 25) for a maximum of five days. Although a significant reduction in progression to ARDS was noted among patients with PLV, no significant differences in the number of days free from the ventilator at 28 days (CMV = 6.7 +/- 1.8, PLV = 6.3 +/- 1.0 days, p = 0.85), the incidence of mortality (CMV = 36%, PLV = 42%, p = 0.63), or any pulmonary-related parameter were observed. During a post hoc subgroup analysis, significantly more rapid discontinuation of mechanical ventilation (p = 0.045) and a trend toward an increase in the number of days free from the ventilator at 28 days (CMV = 3.2 +/- 1.9, PLV = 8.0 +/- 2.2 days, p = 0.06) were observed during PLV among those patients under 55 years of age with acute lung injury or ARDS. Episodes of hypoxia, respiratory acidosis, and bradycardia occurred more frequently in the PLV group, but these were transient and self-limited. Further evaluation of PLV is warranted to further define beneficial effects in well-defined groups of patients and also to gain additional information regarding safety.

Adult↗