Transpulmonary pressure and lung elastance can be estimated by a PEEP-step manoeuvre.

BACKGROUND: Transpulmonary pressure is a key factor for protective ventilation. This requires measurements of oesophageal pressure that is rarely used clinically. A simple method may be found, if it could be shown that tidal and positive end-expiratory pressure (PEEP) inflation of the lungs with the same volume increases transpulmonary pressure equally. The aim of the present study was to compare tidal and PEEP inflation of the respiratory system. METHODS: A total of 12 patients with acute respiratory failure were subjected to PEEP trials of 0-4-8-12-16 cmH2O. Changes in end-expiratory lung volume (ΔEELV) following a PEEP step were determined from cumulative differences in inspiratory-expiratory tidal volumes. Oesophageal pressure was measured with a balloon catheter. RESULTS: Following a PEEP increase from 0 to 16 cmH2O end-expiratory oesophageal pressure did not increase (0.5 ± 4.0 cmH2O). Average increase in EELV following a PEEP step of 4 cmH2O was 230 ± 132 ml. The increase in EELV was related to the change in PEEP divided by lung elastance (El) derived from oesophageal pressure as ΔPEEP/El. There was a good correlation between transpulmonary pressure by oesophageal pressure and transpulmonary pressure based on El determined as ΔPEEP/ΔEELV, r(2) = 0.80, y = 0.96x, mean bias -0.4 ± 3.0 cmH2 O with limits of agreement from 5.4 to -6.2 cmH2O (2 standard deviations). CONCLUSION: 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.

High-Sensitive Troponin T and N-Terminal Pro B-Type Natriuretic Peptide for Early Detection of Stress-Induced Cardiomyopathy in Patients with Subarachnoid Hemorrhage.

BACKGROUND: Patients developing stress-induced cardiomyopathy (SIC) after subarachnoid hemorrhage (SAH) have increased risk of vasospasm, delayed cerebral ischemia and death. We evaluated whether high-sensitive troponin T (hsTnT) and N-terminal pro B-type natriuretic peptide (NTproBNP) are useful biomarkers for early detection of SIC after SAH. METHODS: Medical records of all patients admitted to our NICU with suspected or verified SAH from January 2010 to August 2014 were reviewed. Patients in whom echocardiography was performed and blood samples for measurements of hsTnT and/or NTproBNP were obtained, within 72 and 48 h, respectively, after onset of symptoms, were included. SIC was defined as reversible left ventricular segmental hypokinesia diagnosed by echocardiography. RESULTS: A total of 502 SAH patients were admitted during the study period, 112 patients fulfilled inclusion criteria and 25 patients fulfilled SIC criteria. Peak levels of hsTnT and NTproBNP were higher in patients with SIC (p < 0.001). hsTnT had its peak on admission, while NTproBNP peaked at days 2-4 after onset of symptoms. A hsTnT > 89 ng/l or a NTproBNP > 2,615 ng/l obtained within 48 h after onset of symptoms had a sensitivity of 100% and a specificity of 79% in detecting SIC. CONCLUSIONS: 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.

Lung elastance and transpulmonary pressure can be determined without using oesophageal pressure measurements.

INTRODUCTION: The aim of the present study was to demonstrate that lung elastance and transpulmonary pressure can be determined without using oesophageal pressure measurements. METHODS: Studies were performed on 13 anesthetized and sacrificed ex vivo pigs. Tracheal and oesophageal pressures were measured and changes in end-expiratory lung volume (ΔEELV) determined by spirometry as the cumulative inspiratory-expiratory tidal volume difference. Studies were performed with different end-expiratory pressure steps [change in end-expiratory airway pressure (ΔPEEP)], body positions and with abdominal load. RESULTS: A PEEP increase results in a multi-breath build-up of end-expiratory lung volume. End-expiratory oesophageal pressure did not increase further after the first expiration, constituting half of the change in ΔEELV following a PEEP increase, even though end-expiratory volume continued to increase. This resulted in a successive left shift of the chest wall pressure-volume curve. Even at a PEEP of 12 cmH(2) O did the end-expiratory oesophageal (pleural) pressure remain negative. CONCLUSIONS: 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.

Positive end-expiratory pressure-induced changes in end-expiratory lung volume measured by spirometry and electric impedance tomography.

BACKGROUND: A bedside tool for monitoring changes in end-expiratory lung volume (ΔEELV) would be helpful to set optimal positive end-expiratory pressure (PEEP) in acute lung injury/acute respiratory distress syndrome patients. The hypothesis of this study was that the cumulative difference of the inspiratory and expiratory tidal volumes of the first 10 breaths after a PEEP change accurately reflects the change in lung volume following a PEEP alteration. METHODS: Changing PEEP induces lung volume changes, which are reflected in differences between inspiratory and expiratory tidal volumes measured by spirometry. By adding these differences with correction for offset, for the first 10 breaths after PEEP change, cumulative tidal volume difference was calculated to estimate ΔEELV(VT) ((i-e)) . This method was evaluated in a lung model and in patients with acute respiratory failure during a PEEP trial. In patients, ΔEELV(VT) ((i-e)) were compared with simultaneously measured changes in lung impedance, by electric impedance tomography (EIT), using calibration vs. tidal volume to estimate changes in ΔEELV(EIT) . RESULTS: In the lung model, there was close correlation (R(2) = 0.99) between ΔEELV(VT) ((i-e)) and known lung model volume difference, with a bias of -4 ml and limits of agreement of 42 and -50 ml. In 12 patients, ΔEELV(EIT) was closely correlated to ΔEELV(VT) ((i-e)) (R(2) = 0.92), with mean bias of 50 ml and limits of agreement of 131 and -31 ml. Changes in EELV estimated by EIT (ΔEELV(EIT) ) exceeded measurements by spirometry (ΔEELV(VT) ((i-e)) ), with 15 (±15)%. CONCLUSIONS: 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.

A Scandinavian survey of drug administration through inhalation, suctioning and recruitment maneuvers in mechanically ventilated patients.

BACKGROUND: The aim was to describe current practices for drug administration through inhalation, endotracheal suctioning and lung recruitment maneuvers in mechanically ventilated patients in Scandinavian intensive care units (ICUs). METHODS: We invited 161 ICUs to participate in a web-based survey regarding (1) their routine standards and (2) current treatment of ventilated patients during the past 24 h. In order to characterize the patients, the lowest PaO(2) with the corresponding highest FiO(2), and the highest PaO(2) with the corresponding lowest FiO(2) during the 24-h study period were recorded. RESULTS: Eighty-seven ICUs answered and reported 186 patients. Positive end-expiratory pressure (PEEP) levels (cmH(2)O) were 5-9 in 65% and >10 in 31% of the patients. Forty percent of the patients had heated humidification and 50% received inhalation of drugs. Endotracheal suctioning was performed >7 times during the study period in 40% of the patients, of which 23% had closed suction systems. Twenty percent of the patients underwent recruitment maneuvers. The most common recruitment maneuver was to increase PEEP and gradually increase the inspiratory pressure. Twenty-six percent of the calculated PaO(2)/FiO(2) ratios varied >13 kPa for the same patient. CONCLUSION: 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.

Bronchoscopic suctioning may cause lung collapse: a lung model and clinical evaluation.

OBJECTIVE: To assess lung volume changes during and after bronchoscopic suctioning during volume or pressure-controlled ventilation (VCV or PCV). DESIGN: Bench test and patient study. PARTICIPANTS: Ventilator-treated acute lung injury (ALI) patients. SETTING: University research laboratory and general adult intensive care unit of a university hospital. INTERVENTIONS: Bronchoscopic suctioning with a 12 or 16 Fr bronchoscope during VCV or PCV. MEASUREMENTS AND RESULTS: Suction flow at vacuum levels of -20 to -80 kPa was measured with a Timeter(trade mark) instrument. In a water-filled lung model, airway pressure, functional residual capacity (FRC) and tidal volume were measured during bronchoscopic suctioning. In 13 ICU patients, a 16 Fr bronchoscope was inserted into the left or the right main bronchus during VCV or PCV and suctioning was performed. Ventilation was monitored with electric impedance tomography (EIT) and FRC with a modified N(2) washout/in technique. Airway pressure was measured via a pressure line in the endotracheal tube. Suction flow through the 16 Fr bronchoscope was 5 l/min at a vacuum level of -20 kPa and 17 l/min at -80 kPa. Derecruitment was pronounced during suctioning and FRC decreased with -479+/-472 ml, P<0.001. CONCLUSIONS: 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.