Fernando Suarez Sipmann

Chest electrical impedance tomography examination, data analysis, terminology, clinical use and recommendations: consensus statement of the TRanslational EIT developmeNt stuDy group

Electrical impedance tomography (EIT) has undergone 30 years of development. Functional chest examinations with this technology are considered clinically relevant, especially for monitoring regional lung ventilation in mechanically ventilated patients and for regional pulmonary function testing in patients with chronic lung diseases. As EIT becomes an established medical technology, it requires consensus examination, nomenclature, data analysis and interpretation schemes. Such consensus is needed to compare, understand and reproduce study findings from and among different research groups, to enable large clinical trials and, ultimately, routine clinical use. Recommendations of how EIT findings can be applied to generate diagnoses and impact clinical decision-making and therapy planning are required. This consensus paper was prepared by an international working group, collaborating on the clinical promotion of EIT called TRanslational EIT developmeNt stuDy group. It addresses the stated needs by providing (1) a new classification of core processes involved in chest EIT examinations and data analysis, (2) focus on clinical applications with structured reviews and outlooks (separately for adult and neonatal/paediatric patients), (3) a structured framework to categorise and understand the relationships among analysis approaches and their clinical roles, (4) consensus, unified terminology with clinical user-friendly definitions and explanations, (5) a review of all major work in thoracic EIT and (6) recommendations for future development (193 pages of online supplements systematically linked with the chief sections of the main document). We expect this information to be useful for clinicians and researchers working with EIT, as well as for industry producers of this technology.

Rationale of Dead Space Measurement by Volumetric Capnography

Dead space is the portion of a tidal volume that does not participate in gas exchange because it does not get in contact with blood flowing through the pulmonary capillaries. It is commonly calculated using volumetric capnography, the plot of expired carbon dioxide (CO2) versus tidal volume, which is an easy bedside assessment of the inefficiency of a particular ventilatory setting. Today, Bohrs original dead space can be calculated in an entirely noninvasive and breath-by-breath manner as the mean alveolar partial pressure of CO2 (PACO2) which can now be determined directly from the capnogram. The value derived from Enghoffs modification of Bohrs formula (using PaCO2 instead of PACO2) is a global index of the inefficiency of gas exchange rather than a true “dead space” because it is influenced by all causes of ventilation/perfusion mismatching, from real dead space to shunt. Therefore, the results obtained by Bohrs and Enghoffs formulas have different physiological meanings and clinicians must be conscious of such differences when interpreting patient data. In this article, we describe the rationale of dead space measurements by volumetric capnography and discuss its main clinical implications and the misconceptions surrounding it.

Noninvasive monitoring of lung recruitment maneuvers in morbidly obese patients: the role of pulse oximetry and volumetric capnography

BACKGROUND:We conducted this study to determine whether pulse oximetry and volumetric capnography (VCap) can determine the opening and closing pressures of lungs of anesthetized morbidly obese patients. METHODS:Twenty morbidly obese patients undergoing laparoscopic bariatric surgery with capnoperitoneum were studied. A lung recruitment maneuver was performed in pressure control ventilation as follows: (1) During an ascending limb, the lungs’ opening pressure was detected. After increasing positive end-expiratory pressure (PEEP) from 8 to 16 cm H2O, fraction of inspired oxygen (FIO2) was decreased until pulse oximetric arterial saturation (SpO2) was <92%. Thereafter, end-inspiratory pressure was increased in steps of 2 cm H2O, from 36 to a maximum of 50 cm H2O. The opening pressure was attained when SpO2 exceeded 97%. (2) During a subsequent decreasing limb, the lungs’ closing pressure was identified. PEEP was decreased from 22 to 10 cm H2O in steps of 2 cm H2O. The closing pressure was determined as the PEEP value at which respiratory compliance decreased from its maximum value. We continuously recorded lung mechanics, SpO2, and VCap. RESULTS:The lungs’ opening pressures were detected at 44 (4) cm H2O (median and interquartile range) and the closing pressure at 14 (2) cm H2O. Therefore, the level of PEEP that kept the lungs without collapse was found to be 16 (3) cm H2O. Using respiratory compliance as a reference, receiver operating characteristic analysis showed that SpO2 (area under the curve [AUC] 0.80 [SE 0.07], sensitivity 0.65, and specificity 0.94), the elimination of CO2 per breath (AUC 0.91 [SE 0.05], sensitivity 0.85, and specificity 0.98), and Bohr’s dead space (AUC 0.83 [SE 0.06], sensitivity 0.70, and specificity 0.95] were relatively accurate for detecting lung collapse during the decreasing limb of a recruitment maneuver. CONCLUSIONS:Lung recruitment in morbidly obese patients could be effectively monitored by combining noninvasive pulse oximetry and VCap. SpO2, the elimination of CO2, and Bohr’s dead space detected the individual’s opening and closing pressures.

Heart-lung interactions in acute respiratory distress syndrome: pathophysiology, detection and management strategies

Acute respiratory distress syndrome (ARDS) is the most severe form of acute respiratory failure characterized by diffuse alveolar and endothelial damage. The severe pathophysiological changes in lung parenchyma and pulmonary circulation together with the effects of positive pressure ventilation profoundly affect heart lung interactions in ARDS. The term pulmonary vascular dysfunction (PVD) refers to the specific involvement of the vascular compartment in ARDS and is expressed clinically by an increase in pulmonary arterial (PA) pressure and pulmonary vascular resistance both affecting right ventricular (RV) afterload. When severe, PVD can lead to RV failure which is associated to an increased mortality. The effect of PVD on RV function is not only a consequence of increased pulmonary vascular resistance as afterload is a much more complex phenomenon that includes all factors that oppose efficient ventricular ejection. Impaired pulmonary vascular mechanics including increased arterial elastance and augmented wave-reflection phenomena are commonly seen in ARDS and can additionally affect RV afterload. The use of selective pulmonary vasodilators and lung protective mechanical ventilation strategies are therapeutic interventions that can ameliorate PVD. Prone positioning and the open lung approach (OLA) are especially attractive strategies to improve PVD due to their effects on increasing functional lung volume. In this review we will describe some pathophysiological aspects of heart-lung interactions during the ventilatory support of ARDS, its clinical assessment and discuss therapeutic interventions to prevent the occurrence and progression of PVD and RV failure.