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PubMed1990

Low oxygenation index and pulmonary artery hypertension in predicting early death from adult respiratory distress syndrome (ARDS).

Hemodynamic and respiratory parameters were continuously monitored in 45 septic shock patients, 15 of whom developed adult respiratory distress syndrome (ARDS). Low oxygenation index (OI = PaO2/FIO2), pulmonary artery hypertension (high mean pulmonary artery pressure, MPAP) and elevated pulmonary vascular resistance (PVR) were observed in all ARDS, as well as in non-ARDS septic patients, as a baseline. These same pulmonary factors were compared between those who survived and those who died during the first few days (early fatalities) in both the ARDS group (5 patients) and the non-ARDS group (8 patients). The results showed that the early fatalities in the ARDS group had a significantly lower (p less than 0.001) OI than the survivors, as well as a lower MPAP (p less than 0.01). In the non-ARDS group, the MPAP of the early fatalities was significantly lower (p less than 0.01) than that of survivors, but their OI was not significantly lower. PVR, when compared between groups (ARDS versus non-ARDS) or between subgroups within each group, was elevated concurrently with the elevation of MPAP. It is concluded that patients with septic shock and ARDS who show a severely depressed OI and a modestly elevated MPAP and PVR during the first few days can be predicted to have a poor outcome.

Adult↗
PubMed1985

An investigation of the relationship between cesarean section birth and respiratory distress syndrome of the newborn.

To clarify the nature of the association between respiratory distress syndrome and Cesarean section birth, a study was conducted which compared 273 premature (36 weeks or less) Cesarean-delivered infants with 341 premature vaginally delivered infants who were born at the University of Washington Hospital from January 1, 1977 through March 31, 1980. The gestational age-adjusted probability of respiratory distress syndrome was higher among the Cesarean cohort compared with the vaginal cohort (38.2% vs. 27.6%, odds ratio = 1.63, 95% confidence interval = 1.11-2.39). Three alternative explanations for the association of Cesarean section with respiratory distress syndrome other than causation were tested, and each was rejected. The association was not explained by 1) improper timing of elective Cesarean deliveries; 2) misclassification of cases of mild, transient respiratory distress (which may be more common after Cesarean birth) as respiratory distress syndrome; or 3) the differences in the occurrence of pregnancy complications preceding Cesarean births compared with vaginal births. Lack of labor appears to account for part of the increased risk of respiratory distress syndrome among infants delivered by Cesarean section. The gestational age-adjusted probabilities of respiratory distress syndrome were 47.0% for Cesarean birth without labor, 35.4% for Cesarean birth preceded by labor, and 27.6% for vaginal birth.

Birth Weight↗
PubMed2005

Corticosteroids in acute respiratory distress syndrome.

Improving the course and outcome of patients with acute respiratory distress syndrome presents a challenge. By understanding the immune status of a patient, physicians can consider manipulating proinflammatory systems more rationally. In this context, corticosteroids could be a therapeutic tool in the armamentarium against acute respiratory distress syndrome. Corticosteroid therapy has been studied in three situations: prevention in high-risk patients, early treatment with high-dose, short-course therapy, and prolonged therapy in unresolving cases. There are differences between the corticosteroid trials of the past and recent trials: today, treatment starts 2-10 days after disease onset in patients that failed to improve; in the past, the corticosteroid doses employed were 5-140 times higher than those used now. Additionally, in the past treatment consisted of administering one to four doses every 6 h (methylprednisolone, 30 mg/kg) versus prolonging treatment as long as necessary in the new trials (2 mg kg(-1) day(-1) every 6 h). The variable response to corticosteroid treatment could be attributed to the heterogeneous biochemical and molecular mechanisms activated in response to different initial insults. Numerous factors need to be taken into account when corticosteroids are used to treat acute respiratory distress syndrome: the specificity of inhibition, the duration and degree of inhibition, and the timing of inhibition. The major continuing problem is when to administer corticosteroids and how to monitor their use. The inflammatory mechanisms are continuous and cyclic, sometimes causing deterioration or improvement of lung function. This article reviews the mechanisms of action of corticosteroids and the results of experimental and clinical studies regarding the use of corticosteroids in acute respiratory distress syndrome.

Adrenal Cortex Hormones↗
PubMed1993

Alveolar surfactant and adult respiratory distress syndrome. Pathogenetic role and therapeutic prospects.

The adult respiratory distress syndrome (ARDS) is characterized by extended inflammatory processes in the lung microvascular, interstitial, and alveolar compartments, resulting in vasomotor disturbances, plasma leakage, cell injury, and complex gas exchange disturbances. Abnormalities in the alveolar surfactant system have long been implicated in the pathogenetic sequelae of this life-threatening syndrome. This hypothesis is supported by similarities in pulmonary failure between patients with ARDS and preterm babies with infant respiratory distress syndrome, known to be triggered primarily by lack of surfactant material. Mechanisms of surfactant alterations in ARDS include: (a) lack of surface-active compounds (phospholipids, apoproteins) due to reduced generation/release by diseased pneumocytes or to increased loss of material (this feature includes changes in the relative composition of the surfactant phospholipid and/or apoprotein profiles); (b) inhibition of surfactant function by plasma protein leakage (inhibitory potencies of different plasma proteins have been defined); (c) "incorporation" of surfactant phospholipids and apoproteins into polymerizing fibrin upon hyaline membrane formation; and (d) damage/inhibition of surfactant compounds by inflammatory mediators (proteases, oxidants, nonsurfactant lipids). Alterations in alveolar surfactant function may well contribute to a variety of pathophysiological key events encountered in ARDS. These include decrease in compliance, ventilation-perfusion mismatch including shunt flow due to altered gas flow distribution (atelectasis, partial alveolar collapse, small airway collapse), and lung edema formation. Moreover, more speculative at the present time, surfactant abnormalities may add to a reduction in alveolar host defense competence and an upregulation of inflammatory events under conditions of ARDS. Persistent atelectasis of surfactant-deficient and in particular fibrin-loaded alveoli may represent a key event to trigger fibroblast proliferation and fibrosis in late ARDS ("collapse induration"). Overall, the presently available data on surfactant abnormalities in ARDS lend credit to therapeutic trials with transbronchial surfactant administration. In addition to the classical goals of replacement therapy defined for preterm infants (rapid improvement in lung compliance and gas exchange), this approach will have to consider its impact on host defense competence and inflammatory and proliferative processes when applied in adults with respiratory failure.

Apoproteins↗
PubMed1996

Respiratory function and treatment in dogs with acute respiratory distress syndrome: 19 cases (1985-1993).

OBJECTIVE: To characterize respiratory function and treatment in dogs with findings compatible with those of human adult respiratory distress syndrome (ARDS) and to evaluate the application in dogs of clinical for diagnosis of ARDS. DESIGN: Retrospective review of medical records. ANIMALS: 19 dogs with acute respiratory distress syndrome. RESULTS: Arterial blood pH was 7.30 +/- 0.59 (mean +/- SD). Nine dogs had metabolic acidosis. In nonmechanically ventilated dogs, PaCO2 was 15.0 to 54.9 mm of Hg. Respiratory acidosis developed in 2 mechanically ventilated dogs. Hypoxemia was observed in 4 of 5 dogs breathing room air. In 4 mechanically ventilated dogs, oxygenation was inadequate, despite use of > 60% inspired O2 and positive end-expiratory pressure in 3 dogs. Alveolar-to-arterial oxygen tension gradients were widened in 4 dogs breathing room air and in 6 dogs ventilated with 100% O2. Ten dogs were mechanically ventilated; ventilatory rate was 18 to 60 breaths/min. Tidal volume was 12 +/- 3.8 ml/kg of body weight in 4 dogs, minute ventilation > 400 ml/kg/min in 2 dogs, and peak airway pressures > 25 cm of H2O in 6 dogs. Positive end-expiratory pressure was used in 8 dogs. Pneumothorax was detected in 5 ventilated dogs. Human clinical criteria for diagnosis of ARDS were fulfilled in 7 dogs. Fluid treatment consisted of IV crystalloids and synthetic colloids. Drugs most often administered were antibiotics and loop diuretics. CLINICAL IMPLICATIONS: Human clinical criteria for identification of ARDS may be helpful in diagnosis of acute respiratory distress syndrome in dogs.

Acid-Base Equilibrium↗
PubMed1999

Continuous flow peritoneal dialysis as a method to treat severe anasarca in children with acute respiratory distress syndrome.

OBJECTIVE: To describe a method of rapid fluid removal in children with anasarca and the acute respiratory distress syndrome (ARDS) secondary to sepsis or the systemic inflammatory response syndrome. DESIGN: Consecutive case series. SETTING: Pediatric Intensive Care Unit of a children's hospital. PATIENTS: Six patients with ARDS secondary to sepsis or systemic inflammatory response syndrome, who had persistent anasarca complicating their respiratory course despite intravenous diuretic therapy. INTERVENTIONS: Continuous flow peritoneal dialysis (CFPD) was instituted after percutaneously inserting two Tenckhoff dialysis catheters into the peritoneal cavity of each patient and tunneling them through the subcutaneous tissue to exit from opposite lower abdominal quadrants. A dialysis solution with 2.5% dextrose was administered continuously via one of the catheters at a rate ranging from 10-30 mL/kg/hr, and concomitantly drained via the other catheter. The concentration of the dialysis solution and rate of inflow were adjusted as needed to achieve the desired peritoneal outflow rate. CFPD was discontinued when adequate weight loss had occurred and the patient's daily urine output exceeded their daily fluid intake. The patient's overall fluid balance and change in weight were recorded daily. The PaO2/FiO2 ratio, alveolar-arterial oxygen gradient, and oxygenation index were also calculated daily. MEASUREMENTS AND MAIN RESULTS: Six patients with ARDS, mean age 18.7+/-37.0 months were mechanically ventilated for 8.0+/-4.0 days before CFPD, during which time average body weight increased to 63%+/-22% above admission body weight, despite the use of intravenous diuretic therapy. They underwent CFPD for 126.7+/-60.0 hrs, during which time their body weight decreased to 30%+/-12% above admission weight (p<.05). During dialysis, the dialysis outflow rate exceeded the inflow rate by 4.2+/-0.9 mL/kg/hr. When compared with values calculated immediately before starting CFPD, post-CFPD PaO2/FiO2 increased from 97.0+/-32.0 to 215.0+/-40.4 mm Hg (12.9+/-4.3 to 28.7+/-5.4 kPa) (p<.05), post-CFPD alveolar-arterial oxygen gradient decreased from 390.7+/-85.8 to 206.7+/-72.8 mm Hg (52.1+/-11.4 to 27.6+/-9.7 kPa) (p<.05), and post-CFPD the oxygenation index decreased from 29.6+/-9.8 to 11.8+/-5.6 (p<.05). There were no complications associated with dialysis catheter insertion or CFPD therapy. Four patients survived. Two patients had an irreversible course of infections and septic shock and died. CONCLUSION: Severe anasarca in the course of ARDS can be effectively treated in pediatric patients with continuous flow peritoneal dialysis, resulting in a significant improvement in respiratory status.

Blood Gas Analysis↗
PubMed2005

Blood L-arginine levels in early respiratory distress syndrome.

L-arginine is the precursor of nitric oxide which plays an important role on pulmonary circulation and pulmonary vascular tone. Our aim was to compare the levels of L-arginine between infants with respiratory distress syndrome and infants without respiratory distress syndrome and to determine the relationship between plasma L-arginine concentrations and severity of disease. Thirty premature infants who were admitted to our neonatal intensive care unit were included the study. Seventeen of these infants with respiratory distress syndrome were study group and the other 13 infants without respiratory distress syndrome served as controls. Blood collection was made before any treatment or intervention given to infants and tandem mass spectrometry was used for laboratory testing. In the respiratory distress syndrome group mean L-arginine level was 33.0 (+/- 11.5) mM/l, and in controls it was 79.0 (+/- 23) mM/l. This difference was statistically significant (P < 0.05). There was a reverse relationship between L-arginine levels and oxygenation index (r = 0.732, P = 0.001). If level of L-arginine is low or insufficient in respiratory distress syndrome patients' nitric oxide level would decrease in pulmonary circulation and results increased pulmonary resistance and severity of respiratory distress syndrome. We concluded that L-arginine levels are low in patients with rspiratory distress syndrome and for further investigations, supplementation of respiratory distress syndrome patients with L-arginine may decrease disease severity.

Arginine↗
PubMed1996

Exogenous surfactants in a piglet model of acute respiratory distress syndrome.

Evidence for surfactant dysfunction in acute respiratory distress syndrome (ARDS) suggests a role for exogenous surfactant which contains apoprotein for resistance to protein inhibition. We compared the effects of KL-4-Surfactant, an artificial preparation containing a synthetic 21 amino acid peptide with SP-B-like activity, with Exosurf, an artificial protein-free surfactant, and Survanta, a bovine protein-containing surfactant, in a saline lung lavage model of ARDS in neonatal piglets. Two sequential series of lung lavages were performed to lower PaO2 < 100 mm Hg, each followed by administration of surfactant or air and a 90-min observation period. Progressive lung injury was demonstrated by deterioration in pulmonary function, increasing bronchoalveolar lavage protein, and changes in histopathology. All surfactants improved oxygenation, although oxygenation was generally better with Survanta and KL-4-Surfactant. Further, Survanta and KL-4-Surfactant groups showed improvement in ventilation, with decreases in PaCO2 and increases in FRC. Only KL-4-Surfactant demonstrated greater pressure-volume characteristics and lower bronchoalveolar protein than those of Controls. We conclude that the physiologic effects of KL-4-Surfactant are more like Survanta in this model. We speculate that KL-4-Surfactant may improve pulmonary function, reduce alveolar protein leak, and thus be efficacious in the treatment of ARDS.

Animals↗
PubMed2002

Adult respiratory distress syndrome: do selective anticoagulants help?

The adult respiratory distress syndrome (ARDS) is a form of acute lung injury that is characterized by florid extravascular fibrin deposition. Thrombosis in the pulmonary vasculature and disseminated intravascular coagulation have also been observed in association with ARDS. Fibrin deposition does not occur in the normal lung but is virtually universal in acute lung injury induced by disparate insults. A large body of basic and preclinical evidence further implicates abnormalities of pathways of fibrin turnover in the pathogenesis of acute inflammation and fibrotic repair. Coagulation is locally upregulated in the injured lung, while fibrinolytic activity is depressed. These abnormalities occur concurrently and favor alveolar fibrin deposition. The systemic derangements of fibrin turnover in sepsis are similar to those that occur in the injured lung. Recent clinical trials demonstrate that interventions using selective anticoagulation can provide a mortality advantage and that selective anticoagulants differ in their ability to provide clinical benefit. Preclinical trials in primates with sepsis-induced ARDS now indicate that anticoagulant interventions that block the extrinsic coagulation pathway can protect against the development of pulmonary fibrin deposition as well as lung dysfunction and acute inflammation. These observations provide proof of principle that key steps in the coagulation cascade are appropriate therapeutic targets to prevent the development of acute lung injury in ARDS. Ongoing studies and prior publications also support the hypothesis that reversal of the fibrinolytic defect in ARDS could protect against the development of acute lung injury. In all, these studies suggest that fibrin deposition in the injured lung as well as abnormalities of coagulation and fibrinolysis are integral to the pathogenesis of ARDS. The ability of selective anticoagulants to effectively and safely alter clinical outcome in ARDS remains to be determined.

Adult↗
PubMed1985

Distribution of ventilation and perfusion during positive end-expiratory pressure in the adult respiratory distress syndrome.

The response of respiratory gas exchange to incremental increases in positive end-expiratory pressure (PEEP) was studied in patients with the adult respiratory distress syndrome (ARDS). Fifty total changes in PEEP were studied in 19 PEEP trials performed in 16 patients. The initial patterns of ventilation-perfusion distribution as measured by the multiple inert gas elimination technique showed a large shunt flow (32 +/- 14% of total cardiac output), which was accompanied in half of the patients by perfusion to a region of low ventilation-perfusion ratio (VA/Q ratio less than 0.1). In 17 PEEP trials, there was an improvement in PaO2 (increase in PaO2 greater than 10 mmHg over control value) with at least one level of PEEP tested. In the 38 PEEP increments in these trials where PaO2 did improve, there was either a reduction in shunt alone, a reduction in ventilation-perfusion regions alone, or a redistribution in blood flow from shunt to regions of low or normal ventilation-perfusion ratio. In the increments where no increase was observed in PaO2, this reduction in blood flow to shunt or low VA/Q regions did not occur. In some instances, there was an increase in ventilation to unperfused alveoli and evidence of high ventilation-perfusion ratio (VA/Q greater than 10) as the level of PEEP increased. Because patients had an adequate pulmonary artery wedge pressure at the start of the PEEP trial (mean wedge pressure, 12.8 +/- 1.5 mmHg) improvements in oxygenation could usually be attained with only mild decreases in cardiac output.

Adult↗
PubMed2006

Why do patients who have acute lung injury/acute respiratory distress syndrome die from multiple organ dysfunction syndrome? Implications for management.

Acute respiratory distress syndrome (ARDS) affects some 10% to 15% of ICU patients and is associated with mortality rates of 40% to 50%. Although ARDS is the most severe form of acute respiratory failure, refractory hypoxia is an uncommon cause of death in these patients. The majority of patients who have ARDS die from multiple-organ dysfunction syndrome (MODS), and ARDS should, therefore, be seen as a systemic disease. Improved understanding of the systemic factors involved in the development and evolution of ARDS and MODS should facilitate the development of new therapeutic agents that will improve outcomes in these patients.

Anti-Infective Agents↗
PubMed2002

Reactive oxygen species as mediators of organ dysfunction caused by sepsis, acute respiratory distress syndrome, or hemorrhagic shock: potential benefits of resuscitation with Ringer's ethyl pyruvate solution.

Reactive oxygen species are reactive, partly reduced derivatives of molecular oxygen. Important reactive oxygen species in biological systems include superoxide radical anion, hydrogen peroxide, and hydroxyl radical. Peroxynitrite, is another important species in biological systems. A variety of enzymatic and non-enzymatic processes can generate reactive oxygen species in mammalian cells. An extensive body of experimental evidence from studies using animal models supports the view that reactive oxygen species are important in the pathogenesis of ischemia-reperfusion syndromes, sepsis, acute respiratory distress syndrome, and multiple organ dysfunction syndrome. This view is further supported by data from clinical studies that correlate biochemical evidence of reactive oxygen species-mediated stress with the development of acute respiratory distress syndrome or sepsis in patients. Ethyl pyruvate, a simple derivative of pyruvic acid, has been shown to be efficacious in several animal models of critical illness, and warrants further evaluation in this regard.

Adult↗
PubMed2004

Acute lung injury and acute respiratory distress syndrome in pregnancy.

Acute respiratory failure can be the result of a variety of clinical conditions, such as congestive heart failure, pneumonia, pulmonary embolism, exacerbation of obstructive lung diseases, and acute respiratory distress syndrome (ARDS). This article focuses on developments related to acute lung injury and ARDS and reviews epidemiology, pathogenesis and therapeutic advances with an emphasis on the obstetric population. A brief discussion of tocolytic-induced pulmonary edema, preeclampsia, venous air embolism, and aspiration-related ARDS is included. Management of pregnant women with ARDS is outlined.

Female↗
PubMed1993

Randomized study of high-frequency oscillatory ventilation in infants with severe respiratory distress syndrome. HiFO Study Group.

We conducted a multicenter, prospective, noncrossover, randomized study to determine whether high-frequency oscillatory ventilation (HFOV) would decrease the development or progression of air leak syndrome in infants with severe respiratory distress syndrome. Air leak syndrome was defined as pulmonary interstitial emphysema or gross air leak such as pneumothorax. Infants were eligible for study entry if they were less than 48 hours of age and had severe respiratory distress syndrome, defined by peak inspiratory pressure or the presence of air leak syndrome. Infants who weighed > or = 0.5 kg at birth were randomly assigned to receive either conventional ventilation (CV) or HFOV. HFOV was provided by a ventilator that operated at 15 Hz, with a 1:2 inspiratory/expiratory ratio and no background tidal breaths. Severity of pulmonary interstitial emphysema was scored independently by two neonatologists unaware of the infants' ventilatory group. Gross air leak severity was scored according to the number of chest tubes required and duration of air leak. Eighty-six infants received HFOV; 90 received CV. During the first 24 hours of the study, patients in the HFOV group received significantly higher mean airway pressure and lower inspired oxygen concentration, had significantly lower arterial carbon dioxide tension, and had a higher ratio of arterial to alveolar oxygen tension. When the HFOV and CV groups were compared with control for birth weight strata, study site, and inborn versus outborn status, HFOV significantly reduced the development of air leak syndrome in those patients who entered the study without the syndrome. We conclude that HFOV, when the strategy employed in this study is used, provides effective ventilation, improves oxygenation, and significantly reduces the development of air leak syndrome in infants with severe respiratory distress syndrome.

Female↗
PubMed1994

Oxidative damage to plasma proteins in adult respiratory distress syndrome.

There is evidence that patients with adult respiratory distress syndrome are under severe oxidative stress that leads to molecular damage. Oxidative stress appears to be inherent in the disease process as well as an unfortunate complication of essential treatment with oxygen. Eight critically ill patients with an established diagnosis of adult respiratory distress syndrome requiring high inspired oxygen concentrations administered by ultra high frequency jet ventilation, were studied. Three patients survived (38%). For the group as a whole, there was evidence of increased protein damage, measured on serial plasma samples as an increase in protein carbonyls (mean +/- SEM, 1.41 +/- 0.09 nmol/mg protein), compared with Intensive Care Unit (ICU) controls (1.24 +/- 0.09 nmol/mg protein), and normal healthy controls (0.940 +/- 0.04 nmol/mg protein). Protein thiol groups were decreased in the ARDS group (4.56 +/- 0.50 nmol/mg protein) compared with ICU controls (5.5 +/- 0.27 nmol/mg protein), and the normal healthy controls (6.55 +/- 0.52 nmol/mg protein). However, when ARDS patients were grouped as survivors and non-survivors, total plasma protein levels were lower in survivors (53.9 +/- 2.15 mg/ml) compared with non-survivors (78.2 +/- 4.68 mg/ml); but the protein thiol content was significantly higher (p = < 0.001) in survivors (6.24 +/- 0.09 nmol/mg protein) compared with non-survivors (3.56 +/- 0.16 nmol/mg protein). Serial plasma measurements of protein damage indicated two different patterns. Survivors had higher total plasma thiol values (protein corrected), which increased as the lung injury resolved, and failing protein carbonyl values. By contrast, non-survivors had low and failing protein thiols often accompanying rising carbonyls.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Proteins↗
PubMed2002

[Prophylaxis and treatment of respiratory distress syndrome with different surfactants].

BACKGROUND: Etiological treatment of respiratory distress syndrome due to lung immaturity with exogenous surfactant is of proven efficacy. However, it is not clear whether all the exogenous surfactants available, both natural and synthetic, are of equal efficacy. OBJECTIVE: To evaluate whether there is any evidence to support the efficacy of one exogenous surfactant over that of the others in the prophylaxis and treatment of respiratory distress syndrome. METHODS: To identify all the comparative studies of tensoactive compounds, an intensive bibliographic search was performed in several databases. RESULTS: Data was found to corroborate that natural surfactants improve oxygenation more rapidly than synthetic surfactants. Natural surfactants also have lower complication and mortality rates. Of the two natural surfactants available in Spain, the porcine-derived surfactant (poractant-alfa) seems to present some advantages over the bovine-derived surfactant (beractant), such as faster action, expressed as a more favourable PaO2/PAO2 ratio during the first 24 hours of treatment. There is also a trend indicating that newborns treated with porcine surfactant have a lower overall mortality rate (3 %) compared with those treated with bovine surfactant (12.5 %). CONCLUSION: No scientific evidence supports the current use of commercialised synthetic surfactants. The porcine-derived surfactant can be considered as the preparation of choice, although additional studies confirming this finding would be useful.

Humans↗
PubMed1977

Continuous positive airway pressure versus positive end-expiratory pressure in respiratory distress syndrome.

The hemodynamic and respiratory effects of spontaneous ventilation with continuous positive airway pressure (CPAP) and mechanical ventilation with positive end-expiratory pressure (PEEP) were compared in nine patients who had adult respiratory distress syndrome. These patients were capable of maintaining spontaneous ventilation (tidal volume above 300 ml. and PaCO2 below 45 torr). Arterial and mixed venous blood gases, cardiac output, oxygen delivery and consumption, pulmonary artery pressure, and pulmonary wedge pressure were measured in 11 instances, with each patient on 5 or 10 cm. H2O CPAP or PEEP, and in nine instances, with each patient on the ventilator but without PEEP (O PEEP). During CPAP, when compared to PEEP at the same level of end-expiratory pressure, mean PaO2 increased significantly (p less than 0.05) and mean physiological shunt decreased (p less than 0.05). In nine of 11 instances, cardiac output was higher on CPAP than on a corresponding level of PEEP. Thus CPAP was more effective than the same amount of PEEP in improving arterial oxygenation by the lung without adversely affecting cardiac output.

Adolescent↗
PubMed1997

Surfactant proteins and stable microbubbles in tracheal aspirates of infants with respiratory distress syndrome: relation to the degree of respiratory failure and response to exogenous surfactant.

UNLABELLED: Surfactant proteins (SP-A and SP-BC), albumin (ALB), and stable microbubble (SM) count were measured in tracheal aspirates from infants with respiratory distress syndrome (RDS) receiving single-dose Surfactant-TA (surfactant group, n = 32) or no surfactant (control group, n = 12), and those without RDS (non-RDS group, n = 8) to determine biochemical and biophysical status of surfactant in the course of RDS after surfactant replacement. Surfactant therapy resulted in immediate and sustained elevations of SP-BC/ALB and SM count with a rapid fall in ventilatory index to levels measured in the non-RDS group, whereas these indices improved slowly in the control group. The SP-A/ ALB was initially low in both RDS groups and increased to levels measured in the non-RDS group by age 48 h. Multiple regression analysis showed that SP-BC/ALB, postnatal age, SM count, SM count/SP-A plus SP-BC, and surfactant therapy were independently associated with the severity of RDS as assessed by ventilatory index (r = 0.75, P < 0.0001; number of samples = 256). Infants with a relapse response to surfactant (n = 9) had levels of SP-A/ALB and SP-BC/ALB similar to those measured in the sustained group (n = 23), but had significantly lower SM count and SM count/SP-A plus SP-BC between 24 and 96 h of age. CONCLUSION: Surfactant therapy normalizes the surfactant and respiratory status of infants with RDS. Surfactant dysfunction rather than depletion may explain the relapse response seen in some surfactant recipients.

Albumins↗