Detection of 'best' positive end-expiratory pressure derived from electrical impedance tomography parameters during a decremental positive end-expiratory pressure trial

Introduction: This study compares different parameters derived from electrical impedance tomography (EIT) data to define 'best' positive end-expiratory pressure (PEEP) during a decremental PEEP trial in mechanically-ventilated patients. 'Best' PEEP is regarded as minimal lung collapse and overdistention in order to prevent ventilator-induced lung injury.Methods: A decremental PEEP trial (from 15 to 0 cm H2O PEEP in 4 steps) was performed in 12 post-cardiac surgery patients on the ICU. At each PEEP step, EIT measurements were performed and from this data the following were calculated: tidal impedance variation (TIV), regional compliance, ventilation surface area (VSA), center of ventilation (COV), regional ventilation delay (RVD index), global inhomogeneity (GI index), and intratidal gas distribution. From the latter parameter we developed the ITV index as a new homogeneity parameter. The EIT parameters were compared with dynamic compliance and the PaO2/FiO2 ratio.Results: Dynamic compliance and the PaO2/FiO2 ratio had the highest value at 10 and 15 cm H2O PEEP, respectively. TIV, regional compliance and VSA had a maximum value at 5 cm H2O PEEP for the non-dependent lung region and a maximal value at 15 cm H2O PEEP for the dependent lung regio

Impact of medical treatment on the outcome of patients after aneurysmal subarachnoid hemorrhage

BACKGROUND AND PURPOSE: The rationale behind early aneurysm surgery in patients with subarachnoid hemorrhage (SAH) is the prevention of rebleeding as early as possible after SAH. In addition, by clipping the aneurysm as early as possible, one can apply treatment for cerebral ischemia more vigorously (induced hypertension) without the risk of rebleeding. Hypervolemic hemodilution is now a well-accepted treatment for delayed cerebral ischemia. We compared the prospectively collected clinical data and outcome of patients admitted to the intensive care unit in the period 1977 to 1982 with those of patients admitted in the period 1989 to 1992 to measure the effect of the change in medical management procedures on patients admitted in our hospital with SAH. METHODS: We studied 348 patients admitted within 72 hours after aneurysmal SAH. Patients with negative angiography results and those in whom death appeared imminent on admission were excluded. The first group (group A) consisted of 176 consecutive patients admitted from 1977 through 1982. Maximum daily fluid intake was 1.5 to 2 L. Hyponatremia was treated with fluid restriction (<1 L/24 h). Antihypertensive treatment with diuretic agents was given if diastolic blood pressure was >110 mm Hg. Patients in the second group (172 consecutive patients; group B) were admitted from 1989 through 1992. Daily fluid intake was at least 3 L, unless cardiac failure occurred. Diuretic agents and antihypertensive medications were avoided. Cerebral ischemia was treated with vigorous plasma volume expansion under intermittent monitoring of pulmonary wedge pressure, cardiac output, and arterial blood pressure, aiming for a hematocrit of 0.29 to 0.33. Aneurysm surgery was planned for day 12. RESULTS: Patients admitted in group B had less favorable characteristics for the development of cerebral ischemia and for good outcome when compared with patients in group A. Despite this, we found a significant decrease in the frequency of delayed cerebral ischemia in patients of group B treated with tranexamic acid (P=0.00005 by log rank test) and significantly improved outcomes among patients with delayed cerebral ischemia (P=0.006 by chi2 test) and among patients with deterioration from hydrocephalus (P=0.001 by chi2 test). This resulted in a significant improvement of the overall outcome of patients in group B when compared with those in group A (P=0.006 by chi2 test). The major cause of death in group B was rebleeding (P=0.011 by chi2 test). CONCLUSIONS: We conclude that the outcome in our patients with aneurysmal SAH was improved but that rebleeding remains a major cause o

Cardioprotection in pigs by exogenous norepinephrine but not by cerebral ischemia-induced release of endogenous norepinephrine

BACKGROUND AND PURPOSE: Endogenous norepinephrine release induced by cerebral ischemia may lead to small areas of necrosis in normal hearts. Conversely, norepinephrine may be one of the mediators that limit myocardial infarct size by ischemic preconditioning. Because brief ischemia in kidneys or skeletal muscle limits infarct size produced by coronary artery occlusion, we investigated whether cardiac norepinephrine release during transient cerebral ischemia also elicits remote myocardial preconditioning. METHODS: Forty-one crossbred pigs of either sex were assigned to 1 of 7 experimental groups, of which in 6 groups myocardial infarct size was determined after a 60-minute coronary occlusion and 12

Purinergic signalling links mechanical breath profile and alveolar mechanics with the pro-inflammatory innate immune response causing ventilation-induced lung injury

Severe pulmonary infection or vigorous cyclic deformation of the alveolar epithelial type I (AT I) cells by mechanical ventilation leads to massive extracellular ATP release. High levels of extracellular ATP saturate the ATP hydrolysis enzymes CD39 and CD73 resulting in persistent high ATP levels despite the conversion to adenosine. Above a certain level, extracellular ATP molecules act as danger-associated molecular patterns (DAMPs) and activate the pro-inflammatory response of the innate immunity through purinergic receptors on the surface of the immune cells. This results in lung tissue inflammation, capillary leakage, interstitial and alveolar oedema and lung injury reducing the production of surfactant by the damaged AT II cells and deactivating the surfactant function by the concomitant extravasated serum proteins through capillary leakage followed by a substantial increase in alveolar surface tension and alveolar collapse. The resulting inhomogeneous ventilation of the lungs is an important mechanism in the development of ventilation-induced lung injury. The high levels of extracellular ATP and the upregulation of ecto-enzymes and soluble enzymes that hydrolyse ATP to adenosine (CD39 and CD73) increase the extracellular adenosine levels that inhibit the innate and adaptive immune responses rendering the host susceptible to infection by invading microorganisms. Moreover, high levels of extracellular adenosine increase the expression, the production and the activation of pro-fibrotic proteins (such as TGF-β, α-SMA, etc.) followed by the establishment of lung fibrosis