Noninvasive monitoring of maximumexpiratory and inspiratory flows(MIF and MEF,respectively)via electrical impedance tmography(EIT)may allow forthe early detection of changes inthe mechanical properties of the respiratory systemin responsetonew conditions or inresponse totreatment.We sought to confirmEIT-basedmeasuresofMIFandMEF against spirometryof intubatedhypoxemic patients during controlled ventilationand breathing spontaneously.Furthermore, the spatial distribution ofmaximal airflows may be influenced bylungpathology and increasethelikelihood of additional ventilationinjury.Thus, we also aimedtoinvestigate the effectsofdifferent settings for mechanical ventilation onregions ofMIFandMEF.
Methods
The present study was a reanalysisofthe dataof two randomised, prospectivecross-sectionalstudies.We examined intubated patientsadmitted to theintensive care unit (ICU) withacute hypoxemic respiratory failure(AHRF)and acute respiratory stress syndrome(ARDS)that were undergoing pressure-supportventilatory(PSV, n10) andvolume-controlled ventilation(VCV, n20).We measured MIF and MEFthrough spirometry and EIT in6 different ventilation configurations that werehigherthan. lower supportinPSV, and higherthan. lowerpositive end-expiratory pressure(PEEP)inbothVCV and PSV.Regional airflows were determined byEITin both dependent and non-dependentlung regionsas well.
Results
MIF and impedanztomographie determinedthroughEIT weretightly correlated withthose measured using spirometry underthe entire range of conditions(rangeinR2 0.629-0.776 and R2 0.606-0.772respectively, p<0.05acrossall) which was within clinically acceptablelimits of agreement.Higher PEEP significantly improveduniformity in thepatternof MIF and MEFwhen ventilated with volume control,by increasing airflows to theareas of the lung that are dependent and decreasingthem in non-dependent areas.
Conclusions
EITgives accurate, non-invasive measurementofMIFandMEF.The current study also supportsthenotionthat EITcould guidePSV and PEEPset-upsto increase the homogeneity and consistency ofspreading and deflating regional airflows.
Introduction
Electric impedance tomography(EIT)can be described asanoninvasive bedside, radiation-freetechnology for lung imaging that is dynamic. EITprovides intrathoracic maps oflung impedance fluctuations that are referenced toa baseline(i.e.,the volume of the lungs at the end of expiration frompreviousbreath) every20-50 ms ([1].Intrathoracic impedance changes measuredbyEIT are linearlyrelated tothe global and regional volume of tidal and this correlation issustained at higher positive end-expiratorypressure (PEEP) levels [22.This means thatEITgives a noninvasive bedside continuousmeasurement oflung volumechanges betweeninspiratory and expiration.
Inspiratory and expiratory flows correspondto thespeed at whichthe lung’s volume as it changesintime.For patients intubated,they aretraditionally measured throughan spirometer attachedto the ventilator circuit prior tothetube for endotracheal intubation or withinthe ventilator.Global maximum inspiratory as well asexpiratoryflows(MIF and MEF respectively)measured bystandard spirometry depend uponphysical properties in the respiratory system(namely, lung compliance andresistance of the airway) [33.Thus, monitoringMIF andMEF couldbe helpful in guidingairway settings(e.g. by selectingthepressure level positive associatedwithbettermechanics)or to determinetheefficacy of pharmacologic treatments(e.g. the increase inMIFand/or MEF followingbronchodilator medication) [4].However, spirometry provides onlygeneral measures of MIF andMEF, whereas heterogeneous distributionofabnormal lung mechanics can be ahallmark of acute hypoxemic respiratorydysfunction(AHRF)as well as acute respiratory distress syndrome(ARDS) [55.In the event of an alveolar injury, it can lead to thean elongation of lung tissuesadjacent to normal-, partiallyand excessively inflated units creatingan imbalancein regionalMIFas well asMEF values.These imbalances could increasetherisk of a ventilator-induced lung injury(VILI)by a variety of mechanisms[6], and settingsto achieve more homogeneous regional flowscould decrease the risk. Externalclassic spirometry sometimes leadstoaltered respiratory patterns andincorrect measurements,too[77.Therefore, a non-invasivebedsidemethod for measuringregional and global MIF andMEFvalues canmake a great contribution tostudyingAHRF and ARDSsufferers’ pathophysiology, andto help guide treatment options.
In the present studyfollowing preliminary findings from ananimal models[8], our goal wastoverify inan intubatedAHRFandARDS patientsreceivingcontrolledventilation andspontaneous breathing EIT-based measures ofMIF and MIF global againststandardspirometry.In addition, we examinedtheeffect of higher vs. lowerpressure supports on theregionalflows.our hypothesis isthat higherlevels of PEEPand lower pressure support couldprovide a more homogeneous distribution ofthe regionalMIFas well asMEF.
Materials and methods
Studypopulations
We performed a new analysis of data collected during two prospective randomized crossover studies: in the first (pressure support ventilation (PSV) study) [9], ten intubated patients recovering from ARDS [10], lightly sedated (RASS – 2/0), undergoing PSV and admitted to the intensive care unit (ICU) of the university-affiliated San Gerardo Hospital, Monza, Italy, were enrolled; and in the second (volume-controlled ventilation (VCV) study) [11], twenty intubated, deeply sedated and paralyzed patients with AHRF (i.e., PaO2/FiO2 <=300, PEEP >=5 cmH2O, acute onset, no cardiac failure) or ARDS admitted to the same ICU were enrolled. Theethical committee ofSan Gerardo Hospital, Monza, Italy, approved thestudies,in accordance with the informed consent givenas perlocalregulations.Further details regardingtheinclusion and exclusion criteriaforbothstudies are availableinan online supplement to the data(Additionalfile1.).
Demographic data collection
Werecorded sex and age, Simplified Acute Physiology Score IIvalues, etiology, diagnosis andseverityof ARDS, days onmechanical ventilationprior to study enrollmentforeachpatient.The mortality rate in hospital was also recordedtoo.
EIT andmonitoring of ventilation
Ineach patient, an EIT-dedicatedbelt,with 16 equallyspaced electrodes was placedaround the thorax atthefifth or sixthintercostalspace and connected toan commercialEIT monitor (PulmoVista 500, Drager Medical GmbH, Lubeck, Germany).Throughout all study phases,EITinformation was generated throughthe application of tinyelectrical currents which rotated around thean individual’s thorax. They were continuously recordedat 20 Hz. These data were storedfor offline analysis as previouslydescribed in [1212.When synchronized toEITtracer data as well as airway pressure andthe flow of air fromMechanical ventilators werecontinuously recorded.
Interventions
Further details aboutthe two protocolscan be foundin theonline data supplement(Additionalto file1.).
In short, inthisPSV study,patients underwentthe followingsteps of crossover with each one lasting 20 minutes:
- 1.
The support level at PEEP for clinical patients is low(PSV low)as compared to.more support atPEEP in the clinical setting(PSV high);
- 2.
Clinical supportatlow PEEP(PSV-PEEP low)vs.help from clinical specialists at higher pressure(PSV-PEEP high).
Within theVCV study,the following phaseswere performedin crossover randomized order,each lasting20 minutes:
- 1.
Protection VCV in low-PEEP(VCV-PEEP low)contrasts with.the protective VCV atPEEPand 5cmH 2O (VCV-PEEP high).
EIT andventilation data
Analyzing offline theEITtracer data collected duringthefinal minutesin each of the phases(analysis oftenbreaths) We determinedboth the global and regional(same-sizedependent and non-dependent lung regions) noninvasive airflows’ waveform,similar to the one described previously[88.Simply, instantaneous global as well asregionalexpiratory and inspiratoryairflowswere recorded asvariationsin global and regionalimpedance measured every 50 ms, multiplied by the tidalvolume/tidal-impedance ratio fromthestudy phase in question anddivided by 50milliseconds. EIT airflow data wereconverted from mL/msec intoL/min (Fig. 1), and the maximumMIF global and regional derived by EITand MEF (MIFglob, MIFnon-depand MIFdep;MEFglob with MEFnon-dep, MEFglob andMEFdep and MEFdep, respectively) wereidentified and thevalues averaged across5-10breathingcycles.