Evidence Of Left Atrial Hypertension Research Articles

A Case Report of Mild TRALI and Literature Review

Abstract Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-associated fatalities. The diagnosis of TRALI is challenging due to lack of pathognomonic laboratory tests and the diagnosis is mainly based on clinical and radiographic findings. The criteria for the diagnosis of TRALI include (1) onset: within 6 hours of transfusion; (2) oxygenation: PAO2/FiO2 ≤300 mm Hg regardless of positive end-expiratory pressure level or oxygen saturation of ≤90% on room air; (3) chest x-ray: bilateral infiltrates on frontal chest radiography; and (4) blood pressure: pulmonary artery occlusion pressure ≤18 mm Hg when measured or no evidence of left atrial hypertension. Although the pathogenesis of TRALI is not fully understood, two different hypothetical pathways have been postulated. One of the pathways is an antibody-mediated, one-hit event (immune TRALI, 89% of cases) and mainly related to the antibodies against the human leukocyte antigen (HLA) or human neutrophil antigen (HNA). The other pathway (nonimmune TRALI) is a two-hit event, and the risk depends on certain predisposing factors, such as underlying pulmonary diseases. However, diagnosis of mild TRALI is challenging due to absence of stridor, wheezing, and rales on physical examination and lack of typical chest x-ray features of TRALI. On the other hand, identification of mild TRALI is important in order to initiate appropriate donor investigation and limit the potential for more severe occurrence in other patients. Recently, we diagnosed a rare case of mild TRALI and report it as follows: A 47-year-old African American male was admitted for relapsed acute myeloid leukemia (AML) who developed therapy-related thrombocytopenia requiring platelet transfusion. Within 15 minutes of starting the transfusion, the patient developed acute dyspnea, hypertension, tachycardia, and hypoxemia with PaO2/FiO2 of 78.9 mm Hg and SaO2 of 92.4%. However, the chest x-ray showed no infiltrates. He was treated with IV steroids, antihistamines, and 15 L of oxygen by face mask with improvement of signs and symptoms within 90 minutes of the reaction. The diagnosis of mild TRALI was confirmed by the detection of anti-HLA class I antibodies in the donor’s plasma. We reviewed the literature, and only four cases of mild TRALI were reported. Mild TRALI can be caused by transfusion of fresh-frozen plasma (2/4), RBCs (1/4), and platelets (1/4). The initial symptoms usually include fever (3/4), chills (4/4), dyspnea (4/4), tachycardia (3/4), and blood pressure changes (2/4 increased in both systolic and diastolic BP, 1/4 increased in systolic BP, 1/4 increased in systolic but decreased in diastolic BP, and 1/4 decreased in diastolic BP). On physical examination, no stridor, wheeze, rales, or urticaria were found (4/4). Laboratory test showed a decrease in the WBC (4/4). Chest x-ray did not show obvious bilateral infiltration and therefore was not required. The symptoms improved rapidly in a few minutes (2/4) to several hours (1/4 in 2 hours and 1/4 in 4 hours). HLA testing showed HLA class I (4/4) or class II (2/4) antibodies in the donor’s plasma. In conclusion, identification of mild TRALI is critical but challenging because diagnosis is based principally on the clinical symptoms and there is no specific laboratory test for mild TRALI. We need to have a high index of suspicion for TRALI in any patient who experiences respiratory symptoms related to transfusion in our daily practice.

Simvastatin to reduce pulmonary dysfunction in patients with acute respiratory distress syndrome: the HARP-2 RCT

Background Acute lung injury is a common devastating clinical syndrome characterised by life-threatening respiratory failure requiring mechanical ventilation and multiple organ failure, and is a major cause of morbidity and mortality. Objective This study tested the hypothesis that treatment with simvastatin would improve clinical outcomes in patients with acute respiratory distress syndrome (ARDS). Design This was a multicentre, allocation-concealed, randomised, double-blind, parallel-group trial. Setting/participants Patients in intensive care units were eligible if they were intubated and mechanically ventilated and had ARDS as defined by a partial pressure of arterial oxygen to fraction of inspired oxygen concentration (PaO2 : FiO2) ratio of ≤ 300 mmHg, bilateral pulmonary infiltrates consistent with pulmonary oedema and no evidence of left atrial hypertension. Intervention Patients were randomised in a 1 : 1 ratio to receive enteral simvastatin 80 mg or identical placebo tablets once daily for up to 28 days. Main outcome measures The primary outcome was the number of ventilator-free days (VFDs) to day 28. Secondary outcomes included the number of non-pulmonary organ failure-free days to day 28, mortality and safety. The biological effect by which simvastatin may modify mechanisms implicated in the development of ARDS was also investigated. A cost-effectiveness analysis was also planned. Results The study was completed when 540 patients were recruited with 259 patients allocated to simvastatin and 281 patients to placebo, with 258 patients in the simvastatin group and 279 patients in the placebo group included in the analysis of the primary outcome. There was no significant difference between study groups in mean [standard deviation (SD)] VFDs [12.6 days (SD 9.9 days) with simvastatin and 11.5 days (SD 10.4 days) with placebo; mean difference 1.1, 95% confidence interval –0.6 to 2.8; p = 0.21], non-pulmonary organ failure-free days [19.4 days (SD 11.1 days) with simvastatin and 17.8 days (SD 11.7 days) with placebo; p = 0.11] or in 28-day mortality (22.0% with simvastatin and 26.8% with placebo; p = 0.23). There was no difference in the incidence of severe adverse events between the groups. Simvastatin did not significantly modulate any of the biological mechanisms investigated. Simvastatin was cost-effective at 1 year compared with placebo for the treatment of ARDS, being associated with both a small quality-adjusted life-year (QALY) gain and cost saving. Limitations One possibility for the lack of efficacy relates to the statin and dosage used. It is possible that adverse effects at the simvastatin dosage used outweighed a beneficial effect, although our data suggest that this is unlikely. The heterogenous cohort of patients with ARDS was an attempt to ensure that our findings would be generalisable; however, it may be more appropriate to target potential therapies based on their proposed biological mechanism for a specific population of patients. The assumptions underpinning the economic benefit are based on the analysis of a subgroup of responders. Conclusions High-dose enteral simvastatin, while safe and with minimal adverse effects, is not effective at improving clinical outcomes in patients with ARDS. There was a small gain in QALYs and a cost saving associated with simvastatin. Future work There is a need to confirm if ARDS endotypes that are more likely to benefit from targeted treatment with simvastatin exist. The potential role of simvastatin in the prevention of ARDS in patients at a high risk of developing ARDS has not yet been evaluated. Trial registration Current Controlled Trials ISRCTN88244364. Funding This project was funded by the Efficacy and Mechanism Evaluation programme, a Medical Research Council and National Institute for Health Research (NIHR) partnership. This study was also funded in the Republic of Ireland by the Health Research Board (HRA_POR-2010-131). In addition, the Health and Social Care Research and Development division of the Public Health Agency in Northern Ireland, the Intensive Care Society of Ireland and REVIVE provided additional funding.

Don't Lose the Lungs for the Brain: Pulmonary Complications After Subarachnoid Hemorrhage

pontaneous subarachnoid hemorrhage (SAH) from a ruptured aneurysm is a catastrophic event. Even if the S patient survives the initial hemorrhage and the aneurysm is safely secured, a whole host of systemic sequelae exist that contribute substantially to morbidity after SAH. Pulmonary complications play a major role in this arena. The principal pulmonary complications are acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). The North American-European Consensus Conference formally defined these 2 entities more than 20 years ago to aid in trial design (1). A diagnosis of ALI required 3 criteria: acute arterial hypoxemia (ratio of partial arterial oxygen pressure to fraction of inspired oxygen <300), bilateral infiltrates on chest x-ray, and no clinical evidence of left atrial hypertension. ARDS is ALI but with more severe arterial hypoxemia (ratio of partial arterial oxygen pressure to fraction of inspired oxygen <200).

Case report: transfusion-related acute lung injury

The diagnostic criteria of transfusion-related acute lung injury (TRALI)consist of hypoxia and bilateral pulmonary edema during or within 6 h of a transfusion,moreover there is no evidence of left atrial hypertension and no preexisting acute lung injury before transfusion.We report a case a female patient,36 years old,who had TRALI during the operation under general anesthesia.Finally,the patient was discharged after treatment. Key words: General anesthesia; Transfusion-related acute lung injury

47 EMF Risk of Acute Lung Injury After Spontaneous Intracerebral Hemorrhage

47 EMF Risk of Acute Lung Injury After Spontaneous Intracerebral Hemorrhage

Prevalence of Acute Lung Injury Among Medical Patients in the Emergency Department

Acute lung injury (ALI) affects an estimated 190,000 persons per year in U.S. intensive care units (ICUs), but little is known about its prevalence in the emergency department (ED). The objective was to describe the prevalence of ALI among mechanically ventilated adult nontrauma patients in the ED. The hypothesis was that the prevalence of ALI in adult ED patients would be low. This was a retrospective cohort study of admitted nontrauma patients presenting to an academic ED. Two trained investigators abstracted data from patient records using a standardized form. The use of mechanical ventilation in the ED was identified in two phases. First, all ED patients were screened for the current procedural terminology (CPT) code for endotracheal intubation (CPT 31500) from January 1, 2003, to December 31, 2006. Second, each patient record was reviewed to verify the use of mechanical ventilation. ALI was defined in accordance with a modified version of the American-European Consensus Conference criteria as: 1) hypoxemia defined as PaO(2) /FiO(2) ratio ≤300 mm Hg on all arterial blood gases (ABGs) in the ED and the first 24 hours of admission, 2) the presence of bilateral infiltrates on chest radiograph, and 3) the absence of left atrial hypertension. Data are presented in absolute numbers and percentages. Interobserver agreement was evaluated using the kappa statistic. Of the 552 patients who received mechanical ventilation in the ED and were subsequently admitted, a total of 134 (24.3%, 95% confidence interval [CI] = 20.8% to 28.0%) met hypoxemia criteria. Of these, 34 had evidence of left atrial hypertension, 52 did not have chest radiograph findings consistent with ALI, and two did not have a chest radiograph performed; the remaining 46 met ALI criteria. An additional two patients who died in the ED had clinical evidence of ALI. Thus, 48 of 552, or 8.7% (95% CI = 6.6% to 11.3%), met criteria for ALI. The kappa value for determination of ALI was 0.84 (95% CI = 0.54 to 1.0). The prevalence of ALI was nearly 9% in adult nontrauma patients receiving mechanical ventilation in the ED. Further study is required to determine which types of patients present to the ED with ALI, the extent to which lung protective ventilation is used, and the need for ED ventilator management algorithms.

First do no harm: surrogate endpoints and the lesson of β-agonists in acute lung injury

Expanded abstractCitationMatthay MA, Brower RG, Carson S, Douglas IS, Eisner M, Hite D, Holets S, Kallet RH, Liu KD, MacIntyre N, Moss M, Schoenfeld D, Steingrub J, Thompson BT: Randomized, placebo-controlled clinical trial of an aerosolized β-agonist for treatment of acute lung injury. National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network. Am J Respir Crit Care Med 2011, 184:561-568.Backgroundβ2-Adrenergic receptor agonists accelerate resolution of pulmonary edema in experimental and clinical studies of acute lung injury (ALI).MethodsObjective: To determine whether an aerosolized β2-agonist would improve clinical outcomes in patients with ALI.Design: Multi-center, phase III randomized, placebo-controlled clinical trial.Setting: 33 hospitals participating National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network.Subjects: Patients who were intubated and receiving mechanical ventilation, had bilateral infiltrates consistent with edema on frontal chest radiograph, had a ratio of PaO2 to FIO2 (fraction of inspired oxygen) of 300 or less, and not had clinical evidence of left atrial hypertension. A maximum enrolment of 1,000 patients was planned.Intervention: Patients were randomized to receive aerosolized albuterol (5 mg) or saline placebo every 4 hours for up to 10 days.Outcomes: The primary outcome variable was ventilator-free days (VFD). Secondary outcome measures included mortality before hospital discharge on day 60 and day 90, the number of intensive care unit (ICU)-free days and the number of organ failure-free days.ResultsThere were 282 patients enrolled before the trial was stopped for futility after the second interim analysis. The VFDs difference with albuterol treatment was unfavourable by -2.2 days, well past the futility boundary of -0.4 VFDs. VFDs were not significantly different between the albuterol and placebo groups (means of 14.4 and 16.6 days, respectively; 95% confidence interval for the difference, -4.7 to 0.3 days; P = 0.087). Rates of death before hospital discharge and the number of organ failure-free days were also not significantly different between the two groups. The number of ICU-free days was lower in the albuterol group in comparison with the placebo group (means of 13.5 and 16.2 days respectively; 95% confidence intervals for the mean difference, -4.9 to -0.4 days; P = 0.023). Overall, heart rates were significantly higher in the albuterol group by approximately 5 beats/minute in the first 2 days after randomization (P < 0.05), but rates of new onset atrial fibrillation (10% in both groups) and other cardiac dysrhythmias were not significantly different.ConclusionsThese results suggest that aerosolized albuterol does not improve clinical outcomes in ALI patients. Routine use of β2 agonist therapy in mechanically ventilated ALI patients cannot be recommended.

Management of Acute Lung Injury/ARDS

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are disorders of pulmonary inflammation characterized by hypoxemia and respiratory failure. Children have varying incidence of ALI/ARDS from 2.2 to 16 per 100,000 pediatric population associated with high morbidity, mortality, and financial burden. The diagnostic criteria include: acute onset, severe arterial hypoxemia resistant to oxygen therapy alone (PaO₂/FIO₂ ratio ≤ 200 for ARDS and ≤ 300 for ALI), diffuse pulmonary inflammation (bilateral infiltrates on chest radiograph) and No evidence of left atrial hypertension. Management includes ventilatory therapy including lower tidal volume, relatively high PEEP and supportive care. Guidelines for diagnosis, ventilator management, rescue therapies and supportive care are being discussed in the protocol.

Index of Suspicion

Index of Suspicion

Trauma and Acute Respiratory Distress Syndrome

Trauma and Acute Respiratory Distress Syndrome

Fluid Therapy for Acute Lung Injury

Source: The National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network. Comparison of two fluid-management strategies in acute lung injury. N Engl J Med. 2006;354:2564–2575; doi:10.1056/NEJMoa062200To evaluate the use of “conservative” versus “liberal” fluid management, investigators for the Acute Respiratory Distress Syndrome (ARDS) network screened 11,512 adult patients in 20 North American centers. Criteria for ARDS were a ratio of the partial pressure of arterial oxygen (PaO2) to the fraction of inspired oxygen (FiO2) of less than 300 and bilateral pulmonary infiltrates on chest radiograph without evidence of left atrial hypertension. Fluid management was guided by assessments using either a pulmonary artery catheter or a central venous catheter. Patients were assessed every 4 hours for blood pressure, urinary output, and either cardiac output or clinical assessment of circulation. The primary outcome was 60-day mortality, and secondary outcomes included ventilator- and ICU-free days as well as number of organ failure days assessed at day 28.One thousand patients were recruited with 503 randomized to “conservative” and 497 to “liberal” fluid management. Patients had similar demographic and hemodynamic characteristics at the time of enrollment. All patients received mechanical ventilation according to the ARDS Network protocol for lower tidal volumes.1Patients in the “liberal” arm had a positive fluid balance each day for the first 7 days of study ranging from 2.5 liters to 483 ml daily, compared to the “conservative” group which had a positive fluid balance only on day 1 of study, and afterwards had slightly negative fluid balance ranging from −144 ml to −408 ml daily. The in-hospital death rate at 60 days was 25% in the “conservative” arm and 28% in the “liberal” arm; however, the “conservative” arm had greater ventilator-free days (15 vs 12) compared to the “liberal” group (P<.01) and more ICU-free days (13 days vs 11 days; P<.001). The number of organ failure-free days was similar between groups with the exception of central nervous system failure, which was more common in the “conservative” group. Of note, although not statistically significant, use of dialysis was more common in the “liberal” fluid management arm (14% vs 10%). The authors concluded that “conservative” fluid management was associated with a decrease in duration of mechanical ventilation and ICU days.Dr. Bratton has disclosed no financial relationship relevant to this commentary. This commentary does not contain a discussion of a commercial product/device. This commentary does not contain a discussion of an unapproved/investigative use of a commercial product/device.Need for higher airway pressures with mechanical ventilation as well as capillary leak due to inflammatory processes both diminish intravascular volume and cardiac filling pressures and require administration of supplemental fluid to treat hemodynamic compromise. Studies have shown that failure to treat shock in children2 and adults3 increases risk of mortality. However, the present study nicely demonstrates that this initial insult is generally time-limited. Children with severe lung injury, like adult patients, gain fluid but those who gain less water have been shown to have improved survival.4 This report supports use of “conservative” fluid management to minimize positive fluid balance and decrease extravascular lung water leading to improved lung function. The authors showed that in the first day or so of acute respiratory failure all patients required supplemental fluid to support adequate hemodynamics and organ perfusion; however, over time patients tolerated diuretic therapy and lower intravascular filling pressures without development of additional organ failure. Use of less fluid was associated with shorter time of mechanical ventilation and ICU stay.Although pediatric mortality from acute lung injury is lower than for adult patients, recent mortality rates of 22%5 confirm that acute lung injury/ARDS remains an important pediatric critical illness. Application of the present study to pediatric practice requires use of age-appropriate blood pressure and careful assessment of hemodynamic status with a central venous catheter, a common pediatric ICU practice.

“Imitators” of the ARDS: Implications for Diagnosis and Treatment

Acute lung injury (ALI) and ARDS (ALI/ARDS) are defined as follows: (1) an illness having an acute onset, (2) an arterial oxygen tension/inspired oxygen fraction ≤ 200 mm Hg (or ≤ 300 mm Hg for ALI), (3) the presence of bilateral infiltrates on frontal chest radiographs, and (4) a pulmonary artery occlusion pressure ≤ 18 mm Hg if measured, or no clinical evidence of left atrial hypertension when not measured.12

Prone Positioning of Trauma Patients With Acute Respiratory Distress Syndrome and Open Abdominal Incisions

Diagnostic criteria for ARDS are respiratory failure as indicated by evidence of acute bilateral infiltrates on chest radiographs, severe hypoxemia (ratio of PaO2 to fraction of inspired oxygen <200), and no evidence of left atrial hypertension (as indicated by clinical examination or pulmonary artery occlusion pressure <18 mm Hg). The mortality rate for patients with ARDS is as high as 40% to 60%. The actual survivability depends on multiple factors, including predisposing conditions, severity of illness, age, comorbid conditions, and, in patients with trauma, severity of the underlying lung injury. Sepsis is the most frequently identified risk factor for ARDS; other factors are aspiration of gastric material, severe pneumonia, severe trauma, use of cardiopulmonary bypass, multiple transfusions, fat embolism, and pancreatitis. For patients with multiple trauma, factors thought to contribute to the development of ARDS include pulmonary Tracy A. Murray is a nurse practitioner in Miamisburg, Ohio. At the time this article was written, she was a trauma nurse practitioner at Miami Valley Hospital in Dayton, Ohio.

Definition, Pathophysiologie und Epidemiologie des akuten Lungenversagens

The American-European Consensus Conference recently recommended the following criteria for diagnosis of ARDS: (1) acute onset; (2) PaO2/FiO2≤200 mmHg regardless of PEEP level; (3) bilateral infiltrates seen on frontal chest radiograph; (4) PCWP ≤ 18 mmHg when measured or no clinical evidence of left atrial hypertension. Pathophysiologically, ARDS is characterized by pulmonary edema owing to injury of the capillary-alveolar membranes and increased pulmonary artery pressure. It is further distinguished by severe hypoxemia unresponsive to the usual methods of support for respiratory failure. Hypoxemia is caused by intrapulmonary right-to-left shunting due to to persistent perfusion of non-ventilated alveoli. Another characteristic feature in ARDS is the low thoracopulmonary compliance. Latest studies suggest that the incidence of the syndrome is in the range of 3–10 cases / 100,000 inhabitants / year. Mortality rates are a major concern: old and new reports continue to report mortality rates of 50–60%.

Acute lung injury and the acute respiratory distress syndrome.

To review acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS) in light of recent information about the definitions, epidemiology, pathophysiology, management, and outcome of these conditions. The author's personal files as well as the computerized MEDLINE database. STUDY SOLUTION: Studies were selected for their relevance to the conditions of ALI and ARDS. The author extracted all applicable data. The diagnostic criteria for ALI and ARDS include a) acute onset; b) bilateral chest radiographic infiltrates; c) a pulmonary artery occlusion pressure of < or =18 mm Hg or no evidence of left atrial hypertension; and d) impaired oxygenation manifested by a PaO2/FIO2 ratio of < or =300 torr (< or =40 kPa) for ALI and < or =200 torr (< or =27 kPa) for ARDS. The incidence of ALI and ARDS are approximately 70 and 7 patients out of 100,000 of the total U.S. population per year, respectively. The conditions result from direct or indirect injury to the pulmonary epithelium and endothelium that causes edema, atelectasis, inflammation, and fibrosis. This "diffuse alveolar damage" is actually patchy in many patients. Therapy of ALI and ARDS is largely supportive, although new approaches in mechanical ventilation, patient positioning, and pharmacologic therapy have been introduced. The mortality rate of ARDS has improved to <50%, but the reasons for this improvement are unclear. ALI and ARDS are better defined and understood than ever before, and their outcome has improved for unclear reasons.

Electrocardiographic evidence of left atrial hypertension in acute myocardial infarction.

The relationship between mean left atrial pressure (LA m ) and P-wave abnormalities in lead V 1 of standard 12-lead electrocardiograms was evaluated in 30 patients with acute myocardial infarction. In each patient pulmonary artery diastolic pressure or pulmonary wedge pressure was measured, and these values were used as an estimate of LA m . Electrocardiograms recorded at the time of the pressure measurements were used for P-wave analysis. Patients with a history of hypertension were excluded from analysis. There was a significant correlation between the magnitude of the P terminal force in lead V 1 (PTF-V 1 ) and the estimated LA m (r = –0.78, P &lt; 0.001). Sixteen patients had a normal PTF-V 1 on admission; 11 of them had a normal LA m . All 14 patients with an abnormal PTF-V 1 (more negative than –0.03 mm-sec) on admission had an elevated LA m (&gt;12 mm Hg). Thus, in 25 of the 30 patients, the PTF-V 1 correctly identified whether the LA m was normal or abnormal on admission. On subsequent days, simultaneous measurements of PTF-V 1 and estimated LA m were made in 27 of the patients. Significant changes occurred in both PTF-V 1 and LA m ; discordant changes were observed on only seven of 56 occasions. Measurement of PTF-V 1 appears to be a useful and reliable estimate of left ventricular filling pressure in patients with acute myocardial infarction.