Background The purpose of the present study is to determine whether airway pressure release ventilation (APRV) can safely enhance hemodynamics in patients with acute lung injury (ALI) and/or adult respiratory distress syndrome (ARDS), relative to pressure control ventilation (PCV). Method Patients with severe acute lung injury or ARDS who were managed with inverse-ratio pressure control ventilation, neuromuscular blockade and a pulmonary artery catheter were switched to APRV. Hemodynamic performance, as well as pressor and sedative needs, was assessed after discontinuing neuromuscular blockade Results Mean age was 58 ± 9 years (n = 12) and mean Lung Injury Score was 7.6 ± 2.1. Temperature and arterial oxygen tension/fractional inspired oxygen (FiO2) were similar among the patients. Peak airway pressures fell from 38 ± 3 for PCV to 25 ± 3 cmH2O for APRV, and mean pressures fell from 18 ± 3 for PCV to 12 ± 2 cmH2O for APRV. Paralytic use and sedative use were significantly lower with APRV than with PCV. Pressor use decreased substantially with ARPV. Lactate levels remained normal, but decreased on APRV. Cardiac index rose from 3.2 ± 0.4 for PCV to 4.6 ± 0.3 l/min per m2 body surface area (BSA) for APRV, whereas oxygen delivery increased from 997 ± 108 for PCV to 1409 ± 146 ml/min for APRV, and central venous pressure declined from 18 ± 4 for PCV to 12 ± 4 cmH2O for APRV. Urine output increased from 0.83 ± 0.1 for PCV to 0.96 ± 0.12 ml/kg per hour for APRV. Conclusion APRV may be used safely in patients with ALI/ARDS, and decreases the need for paralysis and sedation as compared with PCV-inverse ratio ventilation (IRV). APRV increases cardiac performance, with decreased pressor use and decreased airway pressure, in patients with ALI/ARDS.

Background: Various estimates of the incidence and mortality rate of the acute (adult) respiratory distress syndrome (ARDS) have been published. The studies that led to those estimates were based on relatively small patient populations and employed variable diagnostic identifiers of ARDS. The purpose of this study was to estimate the incidence of ARDS and its mortality rate from a large database to which refined diagnostic criteria were applied. We conducted a retrospective review of all hospital discharges over a 4-year period, using screening criteria designed to select patients with ARDS. Discharges from all acute care hospitals in the state of Maryland were reviewed using a computer database from the Health Services Cost Review Commission (HSCRC). Patients ≥ 12 years of age were included. Screening criteria consisted of ICD-9 codes 518.5 and 518.82 cross-referenced with procedural codes for ventilatory support (96.70, 96.71 and 96.72). Data were normalized to the number of cases per 100,000 people. Results: During the 4-year study period there were 2,501,147 hospitalizations. Applying the ICD-9 ARDS criteria yielded lower and upper limits of 159-205, 439-568, 531-694 and 529-720 cases of ARDS for 1992, 1993, 1994 and 1995, respectively. Normalizing for a population of 5 million yields yearly lower and upper limit rates of 3.2-4.2, 8.8-11.4, 10.6-13.8 and 10.5-14.2 cases of ARDS per 100,000 people. Mortality upper and lower limit rates based upon the same duration, admissions and population were 38-49%, 39-52%, 36-47%, and 36-49%, respectively. Conclusions: The incidence of ARDS in Maryland is in the range of 10-14 cases per 100,000 people. The ARDS mortality rate is 36% to 52%, similar to that calculated in previous studies.

상급 종합병원의 중환자실의 경우 환자 중 40% 이상 인공호흡기를 적용하지만 사망률은 15~23%로 높고, 지역별 및 전담 전문의 배치에 따른 사망률 편차가 크기 때문에 호흡부전 환자에서 근거 중심의 표준화 지침에 따른 양질의 인공호흡기 치료가 필수적임.

Hypoxic pulmonary vasoconstriction continues to attract interest more than half a century after its original report because of persistent mystery about its biochemical mechanism and its exact physiological function. Recent work suggests an important role for pulmonary arteriolar smooth muscle cell oxygen-sensitive voltage-dependent potassium channels. Inhibition of these channels by decreased PO2 inhibits outward potassium current, causing membrane depolarization, and calcium entry through voltage-dependent calcium channels. Endothelium-derived vasoconstricting and vasodilating mediators modulate this intrinsic smooth muscle cell reactivity to hypoxia. However, refined modeling of hypoxic pulmonary vasoconstriction operating as a feedback mechanism in inhomogeneous lungs, using more realistic stimulus-response curves and confronted with direct measurements of regional blood flow distribution, shows a more effective than previously assessed ability of this remarkable intrapulmonary reflex to improve gas exchange and arterial oxygenation. Further studies could show clinical benefit of pharmacological manipulation of hypoxic pulmonary vasoconstriction, in circumstances of life-threatening hypoxemia.

Although mechanical ventilation is instituted as a life-saving technique, it may lead to complications that can negatively impact on patients' morbidity and/or mortality. Ventilator associated pneumonia (VAP) is one such complication that is a common challenge to intensivists. Although most experts would agree that early 'appropriate' antibiotic use is essential in patients who develop VAP, the best diagnostic test to guide decision-making is far from clear. One diagnostic test that is capable of providing microbiological samples from the lower respiratory tree is invasive bronchoscopy with a protected specimen brush. Such a procedure has long been available to intensivists and is frequently employed in many intensive care units. However, this procedure has associated costs and potential complications, and its utility in VAP has been challenged. In this issue of Critical Care Forum, the two sides of this debate are brought forward with compelling arguments. The authors' arguments should fuel future trials.

Our current state of knowledge on noninvasive positive pressure ventilation (NPPV) and technical aspects are discussed in the present review. In patients with chronic obstructive pulmonary disease, NPPV can be considered a valid therapeutic option to prevent endotracheal intubation. Evidence suggests that, before eventual endotracheal intubation, NPPV should be considered as first-line intervention in the early phases of acute exacerbation of chronic obstructive pulmonary disease. Small randomized and non-randomized studies on the application of NPPV in patients with acute hypoxaemic respiratory failure showed promising results, with reduction in complications such as sinusitis and ventilator-associated pneumonia, and in the duration of intensive care unit stay. The conventional use of NPPV in hypoxaemic acute respiratory failure still remains controversial, however. Large randomized studies are still needed before extensive clinical application in this condition.

According to the Frank-Starling relationship, a patient is a 'responder' to volume expansion only if both ventricles are preload dependent. Mechanical ventilation induces cyclic changes in left ventricular (LV) stroke volume, which are mainly related to the expiratory decrease in LV preload due to the inspiratory decrease in right ventricular (RV) filling and ejection. In the present review, we detail the mechanisms by which mechanical ventilation should result in greater cyclic changes in LV stroke volume when both ventricles are 'preload dependent'. We also address recent clinical data demonstrating that respiratory changes in arterial pulse (or systolic) pressure and in Doppler aortic velocity (as surrogates of respiratory changes in LV stroke volume) can be used to detect biventricular preload dependence, and hence fluid responsiveness in critically ill patients.