We conclude that spirometric measurements of inspiratory-expiratory tidal volumes agree well with impedance changes monitored by EIT and can be used bedside to estimate PEEP-induced changes in EELV.

PEEP inflation of the respiratory system is extremely slow, and allows the chest wall complex, especially the abdomen, to yield and adapt to intrusion of the diaphragm. As a consequence a change in transpulmonary pressure is equal to the change in PEEP and transpulmonary pressure can be determined without oesophageal pressure measurements.

A PEEP increase resulted in a less than expected increase in end-expiratory oesophageal pressure, indicating that the chest wall and abdomen gradually can accommodate changes in lung volume. The rib cage end-expiratory spring-out force stretches the diaphragm and prevents the lung from being compressed by abdominal pressure. The increase in transpulmonary pressure following a PEEP increase was closely related to the increase in PEEP, indicating that lung compliance can be calculated from the ratio of the change in end-expiratory lung volume and the change in PEEP, ΔEELV/ΔPEEP.

BackgroundPatients with subarachnoid haemorrhage (SAH) frequently develop cardiac complications in the acute phase after the bleeding. Although a number of studies have shown that increased levels of cardiac biomarkers after SAH are associated with a worse short-term prognosis, no prospective, consecutive study has assessed the association between biomarker release and long-term outcome. We aimed to evaluate whether the cardiac biomarkers, high-sensitive troponin T (hsTnT) and N-terminal pro B-type natriuretic peptide (NTproBNP), were associated with poor 1-year neurological outcome and cerebral infarction due to delayed cerebral ischaemia (CI-DCI).MethodsIn this single-centre prospective observational study, all consecutive patients admitted to our neurointensive care unit from January 2012 to December 2013 with suspected/verified SAH with an onset of symptoms <72 hours were enrolled. Blood samples for hsTnT and NTproBNP were collected during three consecutive days following admission. Patients were followed-up after 1 year using the Glasgow Outcome Scale Extended (GOSE). Poor neurological outcome was defined as GOSE ≤4.ResultsOne hundred and seventy seven patients with suspected SAH were admitted during the study period; 143 fulfilled inclusion criteria and 126 fulfilled follow-up. Forty-one patients had poor 1-year outcome and 18 had CI-DCI. Levels of hsTnT and NTproBNP were higher in patients with poor outcome and CI-DCI. In multivariable logistic regression modelling age, poor neurological admission status, cerebral infarction of any cause and peak hsTnT were independently associated with poor late outcome. Both peak hsTnT and peak NTproBNP were independently associated with CI-DCI.ConclusionIncreased serum levels of the myocardial damage biomarker hsTnT, when measured early after onset of SAH, are independently associated with poor 1-year outcome. Furthermore, release of both hsTnT and NTproBNP are independently associated with CI-DCI. These findings render further support to the notion that troponin release after SAH is an ominous finding. Future studies should evaluate whether there is a causal relationship between early release of biomarkers of myocardial injury after SAH and neurological sequelae.

Suction flow through the bronchoscope at the vacuum levels commonly used is well above minute ventilation in most ALI patients. The ventilator was unable to deliver enough volume in either VCV or PCV to maintain FRC and tracheal pressure decreased below atmospheric pressure.

The cardiac biomarkers, hsTnT and NTproBNP, are increased early after SAH and levels are considerably higher in patients with SIC. These biomarkers are useful for screening of SIC, which could make earlier diagnosis and treatment of SIC in SAH patients possible.

Frequent use of drug administration through inhalation and endotracheal suctioning predispose to derecruitment of the lungs, possibly resulting in the large variations in PaO(2)/FiO(2) ratios observed during the 24-h study period. Recruitment maneuvers were performed only in one-fifth of the patients during the day of the survey.

Objective: Protective ventilation should be based on lung mechanics and transpulmonary driving pressure (ΔPTP), as this “hits” the lung directly. Approach: The change in end-expiratory lung volume (ΔEELV) is determined by the size of the PEEP step and the elastic properties of the lung (EL), ΔEELV/ΔPEEP. Consequently, EL can be determined as ΔPEEP/ΔEELV. By calibration of tidal inspiratory impedance change with ventilator inspiratory tidal volume, end-expiratory lung impedance changes were converted to volume changes and lung P/V curves were obtained during a PEEP trial in ten patients with acute respiratory failure. The PEEP level where ΔPTP was lowest (optimal PEEP) was determined as the steepest point of the lung P/V curve. Main results: Over-all EL ranged between 7.0-23.2 cmH2O/L. Optimal PEEP was 12.9 cmH2O (10-16) with ΔPTP of 4.1 cmH2O (2.8-7.6). Patients with highest EL were PEEP non-responders, where EL increased in non-dependent and dependent lung at high PEEP, indicating over-distension in all lung. Patients with lower EL were PEEP responders with decreasing EL in dependent lung when increasing PEEP. Significance: PEEP non-responders could be identified by regional lung P/V curves derived from ventilator calibrated EIT. Optimal PEEP could be determined from the equation for the lung P/V curve.