Lung Impedance Measurements Research Articles

Informal Caregivers' Experiences with Performing Telemonitoring in Heart Failure Care at Home-A Qualitative Study.

Informal caregivers have an important role in caring for family members at home. Supporting persons with a chronic illness such as heart failure (HF) in managing their self-care is reported to be a challenge and telemonitoring has been suggested to be of support. Aim: to explore informal caregivers’ experiences with performing non-invasive telemonitoring to support persons with HF at home for 30 days following hospital discharge in Norway and Lithuania. Methods: A qualitative explorative study of informal caregivers performing non-invasive telemonitoring using lung-impedance measurements and short message service (SMS). Data was collected using semi-structured interviews with informal caregivers of persons with HF in NYHA class III-IV in Norway and Lithuania. Results: Nine interviews were conducted with informal caregivers of persons with HF who performed non-invasive telemonitoring at home. A sequential process of three categories emerged from the data: access to support, towards routinizing, and mastering non-invasive telemonitoring. Conclusion: Informal caregivers performed non-invasive telemonitoring for the first time in this study. Their experiences were of a sequential process that included access to support from health care professionals, establishing a routine together, and access to nurses or physicians in HF care as part of mastering. This study highlights involving informal caregivers and persons with HF together in the implementation and future research of telemonitoring in HF care.

Self-Care Monitoring of Heart Failure Symptoms and Lung Impedance at Home Following Hospital Discharge: Longitudinal Study.

BackgroundSelf-care is key to the daily management of chronic heart failure (HF). After discharge from hospital, patients may struggle to recognize and respond to worsening HF symptoms. Failure to monitor and respond to HF symptoms may lead to unnecessary hospitalizations.ObjectiveThis study aimed to (1) determine the feasibility of lung impedance measurements and a symptom diary to monitor HF symptoms daily at home for 30 days following hospital discharge and (2) determine daily changes in HF symptoms of pulmonary edema, lung impedance measurements, and if self-care behavior improves over time when patients use these self-care monitoring tools.MethodsThis study used a prospective longitudinal design including patients from cardiology wards in 2 university hospitals—one in Norway and one in Lithuania. Data on HF symptoms and pulmonary edema were collected from 10 participants (mean age 64.5 years; 90% (9/10) male) with severe HF (New York Heart Association classes III and IV) who were discharged home after being hospitalized for an HF condition. HF symptoms were self-reported using the Memorial Symptom Assessment Scale for Heart Failure. Pulmonary edema was measured by participants using a noninvasive lung impedance monitor, the CardioSet Edema Guard Monitor. Informal caregivers aided the participants with the noninvasive measurements.ResultsThe prevalence and burden of shortness of breath varied from participants experiencing them daily to never, whereas lung impedance measurements varied for individual participants and the group participants, as a whole. Self-care behavior score improved significantly (P=.007) from a median of 56 (IQR range 22-75) at discharge to a median of 81 (IQR range 72-98) 30 days later.ConclusionsNoninvasive measurement of lung impedance daily and the use of a symptom diary were feasible at home for 30 days in HF patients. Self-care behavior significantly improved after 30 days of using a symptom diary and measuring lung impedance at home. Further research is needed to determine if daily self-care monitoring of HF signs and symptoms, combined with daily lung impedance measurements, may reduce hospital readmissions.

Aeration changes induced by high flow nasal cannula are more homogeneous than those generated by non-invasive ventilation in healthy subjects

BackgroundNon-invasive mechanical ventilation (NIV) is a standard respiratory support technique used in intensive care units. High-Flow Nasal Cannula (HFNC) has emerged as an alternative, but further evidence is needed. The lung aeration and diaphragm changes achieved with these two strategies in healthy subjects have not been compared to date. MethodsTwenty healthy subjects were recruited. Ten were ventilated with NIV and ten underwent HFNC. Lung impedance and diaphragmatic ultrasound measurements were performed before and after 30 min of respiratory support. The Mar-index was defined as the ratio of the diaphragm excursion-time index to the respiratory rate. ResultsBoth groups showed significant decreases in respiratory rate (NIV: 14.4 (4.1) vs 10.4 (1.6), p = 0.009; HFNC: 13.6 (4.3) vs 7.9 (1.5) bpm, p = 0.002) and significant increases in the end-expiratory lung impedance (EELI) (NIV: 66,348(10,761) vs. 73,697 (6858), p = 0.005; HFNC: 66,252 (9793) vs 69,869 (9135), p = 0.012). NIV subjects showed a significant increase in non-dependent silent spaces (4.13 (2.25) vs 5.81 (1.49)%, p = 0.037) while the increase was more homogeneous with HFNC. The variation in EELI tended to be higher in NIV than in HFNC (8137.08 (6152.04) vs 3616.94 (3623.03), p = 0.077). The Mar-index was higher in HFNC group (13.15 vs 5.27 cm-sec2/bpm, p = 0.02). ConclusionsNIV and HFNC increased EELI in healthy subjects, suggesting an increase in the functional residual capacity. The EELI increase may be higher in NIV, but HFNC produced a more homogeneous change in lung ventilation. HFNC group has a higher MAR-index that could reflect a different ventilatory system adaptation.

Effect of unilateral diaphragmatic paralysis on postpneumonectomy lung growth.

Respiratory muscle-associated stretch has been implicated in normal lung development (fetal breathing movements) and postpneumonectomy lung growth. To test the hypothesis that mechanical stretch from diaphragmatic contraction contributes to lung growth, we performed left phrenic nerve transections (PNT) in mice with and without ipsilateral pneumonectomy. PNT was demonstrated by asymmetric costal margin excursion and confirmed at autopsy. In mice with two lungs, PNT was associated with a decrease in ipsilateral lung volume (P<0.05) and lung weight (P<0.05). After pneumonectomy, PNT was not associated with a change in activity level, measureable hypoxemia, or altered minute ventilation; however, microCT scanning demonstrated altered displacement and underinflation of the cardiac lobe within the first week after pneumonectomy. Coincident with the altered structural realignment, lung impedance measurements, fitted to the constant-phase model, demonstrated elevated airway resistance (P<0.05), but normal peripheral tissue resistance (P>0.05). Most important, PNT appeared to abrogate compensatory lung growth after pneumonectomy; the weight of the lobes of the right lung was significantly less than pneumonectomy alone (P<0.001) and indistinguishable from nonsurgical controls (P>0.05). We conclude that the cyclic stretch associated with diaphragmatic muscle contraction is a controlling factor in postpneumonectomy compensatory lung growth.

A model of end-expiratory lung impedance dependency on total extracellular body water

Electrical impedance tomography (EIT) is an attractive method for clinical monitoring of patients during mechanical ventilation. This study evaluates lung impedance measurements using Dräger PulmoVista 500 EIT system on an animal model. Mechanically ventilated model was created. Vital signs were monitored as well as mechanical ventilation parameters. Extracellular fluid balance and blood volume were handled as follows: 30–40% of total blood volume were removed and returned back, 0.5 to 1 litre of Ringer's solution was injected afterwards. The quantity of injected fluids was recorded for each animal. During this process thoracic electrical impedance measurement was performed. Recorded data from PulmoVista 500 EIT system were analysed using the official Dräger EIT Data Analysis Tool. The dependency of end-expiratory lung impedance on the change of fluid balance was observed. The relation between end-expiratory (minimum impedance value) frames and changes of fluid balance is shown. Preliminary results strongly support the expectation that electrical impedance of thorax can be affected by total extracellular fluid change.

Mechanostructural adaptations preceding postpneumonectomy lung growth

ABSTRACTIn many species, pneumonectomy results in compensatory growth in the remaining lung. Although the late mechanical consequences of murine pneumonectomy are known, little is known about the anatomic adaptations and respiratory mechanics during compensatory lung growth. To investigate the structural and mechanical changes during compensatory growth, mice were studied for 21 days after left pneumonectomy using microCT and respiratory system impedance (FlexiVent). Anatomic changes after left pneumonectomy included minimal mediastinal shift or chestwall remodeling, but significant displacement of the heart and cardiac lobe. Mean displacement of the cardiac lobe centroid was 5.2 ± 0.8 mm. Lung impedance measurements were used to investigate the associated changes in respiratory mechanics. Quasi-static pressure–volume loops demonstrated progressive increase in volumes with decreased distensibility. Measures of quasi-static compliance and elastance were increased at all time points postpneumonectomy (P < .01). Oscillatory mechanics demonstrated a significant change in tissue impedance on the third day after pneumonectomy. The input impedance on day 3 after pneumonectomy demonstrated a significant increase in tissue damping (5.8 versus 4.3 cmH2O/mL) and elastance (36.7 versus 26.6 cmH2O/mL) when compared to controls. At all points, hysteresivity was unchanged (0.17). We conclude that the timing and duration of the mechanical changes was consistent with a mechanical signal for compensatory growth.

Comparison of the Predictive Values of NT-proBNP and Lung Impedance Measurements in the Course of BNP-Guided Treatment of CHF Patients

Percutaneous Ventricular Restoration Therapy Using the Parachute Device in Patients With Ischemic Heart Failure and Dilated Left Ventricles: The U.S. Pivotal Trial Design William T. Abraham, Michael Pencia, Serjan Nikolic, Thomas Engels, Marco A. Costa; Division of Cardiovascular Medicine, The Ohio State University, Columbus, OH; Harvard Clinical Research Institute, Harvard University, Boston, MA; Cardikinetix Inc., Menlo Park, CA; Division of Cardiology, Case Western Reserve University, Cleveland, OH

Corrigendum

CORRIGENDUMCorrigendumPublished Online:01 Jan 2008https://doi.org/10.1152/japplphysiol.zdg-7692-corr.2008Original articleMoreSectionsPDF (16 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Volume 103, November 2007 Cohen JC, Hudak J, et al. Comments on Point:Counterpoint: Lung impedance measurements are/are not more useful than simple measurements of lung function in animal models of pulmonary disease. J Appl Physiol 103: 1905–1908, 2007; doi:10.1152/japplphysiol.00759.2007. The final letter in this compilation of comments was written solely by Lennart K. A. Lundblad. Brett A. Simon was incorrectly listed as a coauthor. Simon coauthored a previous comment with David W. Kaczka.This article has no references to display. Download PDF Previous Back to Top Next FiguresReferencesRelatedInformationRelated ArticlesLung impedance measurements are/are not more useful than simpler measurements of lung function in animal models of pulmonary disease 01 Nov 2007Journal of Applied Physiology More from this issue > Volume 104Issue 1January 2008Pages 317-317 Copyright & PermissionsCopyright © 2008 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.zdg-7692-corr.2008History Published online 1 January 2008 Published in print 1 January 2008 Metrics

Lung impedance measurements are/are not more useful than simpler measurements of lung function in animal models of pulmonary disease

The following letters are in response to Point:Counterpoint: “Lung impedance measurements are/are not more useful than simpler measurements of lung function in animal models of pulmonary disease” that appears in this issue. To the Editor : Mitzner argues that constant phase modeling is not more

Last Word on Point:Counterpoint: Lung impedance measurements are/are not more useful than simpler measurements of lung function in animal models of pulmonary disease

LETTERS TO THE EDITORLast Word on Point:Counterpoint: Lung impedance measurements are/are not more useful than simpler measurements of lung function in animal models of pulmonary diseaseWayne MitznerWayne MitznerPublished Online:01 Nov 2007https://doi.org/10.1152/japplphysiol.00748.2007MoreSectionsPDF (27 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat THE ABILITY TO MAKE A MEASUREMENT IS NOT A SUFFICIENT CONDITIONto the editor: After reading all the comments (2) on our debate (1, 3), it may seem that Jason has won this round, with five letters clearly in support of his position, one relatively neutral, one with lukewarm support of both of us (thank you, Ken), and one that dumped on both of us. However, of these writers, since five have had part of their careers invested in such impedance modeling, perhaps this first round vote tally is not entirely unbiased. Nevertheless, despite these otherwise thoughtful comments, still no one has told me what any measurement of G has done to improve our understanding of lung structure or pathology. This is after 15 years of making such measurements. And although Dr. Hantos tried to link G to older measures of tissue resistance, no one can even explain what the structural origins of “tissue” resistance are. Furthermore, despite Fredberg's mathematical rearrangement to focus on eta, reports of eta with experimental manipulations, mice are often as variable as they are constant. So perhaps the constant phase model as applied to the intact lung is not so constant after all.The critically important issue is that the great majority of researchers using animal models of lung disease are now making measurements of impedance for no other reason than it is now very easy (and acceptable) to do. Dr. Zeldin and colleagues suggest that we measure and report both impedance variables along with traditional R and E, but then why not also include the slope of phase III or N2 washout, or closing volume, or frequency dependence of compliance, or DLCO, or etc., etc., etc.? All of these many pulmonary function indexes might also provide improved ability to separate pathology from normal, but they are not included because they are just not so easy to measure in mice. In the recent past, many investigators with little knowledge of pulmonary function, but with a critical need to measure it, were unfortunately hoodwinked into buying snake oil (i.e., Penh). When that elusive and mysterious variable was unmasked, another system took its place that can provide indexes more acceptable to pulmonary physiologists and bioengineers. So now we have mouse asthma models reporting G and eta, without any discussion of what they mean. The primary goal of an animal model of any disease is to help learn something relevant about the disease. As I emphasized previously (1), experimental data without some meaningful link to structure and function provide little insight into what we really want to know. If investigators can't intelligently discuss what each of their measured variables means, it still seems entirely inappropriate to include them in publications or grant applications.REFERENCES1 Bates JH. Point: Lung impedance measurements are more useful than simpler measurements of lung function in animal models of pulmonary disease. J Appl Physiol; doi:10.1152/japplphysiol.00369.2007.Google Scholar2 Cohen JC, Hudak J, Fredberg JJ, Hantos Z, Zeldin DC, Card JW, Carey MA, Voltz JW, Suki B, Lutchen KR, Kaczka DW, Simon BA, Lundblad LKA. Comments on Point:Counterpoint “Lung impedance measurements are/are not more useful than simpler measurements of lung function in animal models of pulmonary disease.” J Appl Physiol; doi:10.1152/japplphysiol.00759.2007.Google Scholar3 Mitzner W. Counterpoint: Lung impedance measurements are not more useful than simpler measurements of lung function in animal models of pulmonary disease. J Appl Physiol; doi:10.1152/japplphysiol.00369.2007a.Google ScholarAUTHOR NOTESAddress for reprint requests and other correspondence: W. Mitzner, 615 N. Wolfe St, Baltimore, MD 21205 (e-mail: [email protected]) Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation More from this issue > Volume 103Issue 5November 2007Pages 1910-1910 Copyright & PermissionsCopyright © 2007 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00748.2007History Published online 1 November 2007 Published in print 1 November 2007 Metrics

Counterpoint: Lung Impedance Measurements are not More Useful than Simpler Measurements of Lung Function in Animal Models of Pulmonary Disease

Counterpoint: Lung Impedance Measurements are not More Useful than Simpler Measurements of Lung Function in Animal Models of Pulmonary Disease

Rebuttal from Dr. Bates

POINT-COUNTERPOINTRebuttal from Dr. BatesPublished Online:01 Nov 2007https://doi.org/10.1152/japplphysiol.00369.2007bMoreSectionsPDF (37 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Dr. Mitzner and I clearly differ in our opinions about the usefulness of lung impedance (4, 6). However, we do agree on certain key things, such as the lack of utility of Penh, which, as my worthy opponent rightly points out, has seduced many investigators solely on account its ease of use (1). But then he makes the error of suggesting that this unfortunate state of affairs also applies to impedance because equipment is now available to measure it with relative ease (6). While there is no question that a certain amount of confusion currently reigns over the physiological interpretation of lung impedance, this is not a reflection of any fundamental shortcoming in the quantity itself. Rather, the shortcoming resides in the community of scientists who use it. Indeed, Dr. Mitzner says as much, for example, when he accuses investigators of lack of consistency in the use of the constant-phase model parameter G (6). As I stated previously (4), in a homogeneous lung G reflects the dissipative properties of the lung tissues. However, both analytical investigation (2) and simulation studies with anatomically accurate models of the lung (5, 7) have shown that changes in G relative to H (tissue elastance) can be used to infer the development of lung derecruitment versus regional ventilation heterogeneities. These are nontrivial physiological insights that, along with those provided by RN (airway resistance) and H, have been used to advantage in several recent studies (e.g., Refs. 3, 5, 8). Dr. Mitzner also charges that “investigators often just extract airway resistance from the impedance” (6). This is true, but again it simply reflects ignorance, not fundamental futility. If investigators choose to discard some of the information present in an experimental measurement, the fault (if there is any) lies with them. To be fair, lung impedance can only be properly interpreted in physiological terms in the context of a mathematical model of the lung (5, 7). This introduces a level of technical complexity that goes beyond what many biomedical researchers are used to, which probably explains how far we have not come in 30 years (6). The utility of impedance thus comes down to an issue of intellectual accessibility, which is consequently its greatest impediment to widespread acceptance. Nevertheless, I firmly believe that an appreciation of the utility of lung impedance is potentially within the grasp of any trained scientist and well worth the effort.REFERENCES1 Bates J, Irvin C, Brusasco V, Drazen J, Fredberg J, Loring S, Eidelman D, Ludwig M, Macklem P, Martin J, Milic-Emili J, Hantos Z, Hyatt R, Lai-Fook S, Leff A, Solway J, Lutchen K, Suki B, Mitzner W, Pare P, Pride N, Sly P. The use and misuse of Penh in animal models of lung disease. Am J Respir Cell Mol Biol 31: 373–374, 2004.Crossref | PubMed | ISI | Google Scholar2 Bates JH, Allen GB. The estimation of lung mechanics parameters in the presence of pathology: a theoretical analysis. Ann Biomed Eng 34: 384–392, 2006.Crossref | PubMed | ISI | Google Scholar3 Bates JH, Wagers SS, Norton RJ, Rinaldi LM, Irvin CG. Exaggerated airway narrowing in mice treated with intratracheal cationic protein. J Appl Physiol 100: 500–506, 2006.Link | ISI | Google Scholar4 Bates JHT. Point: Lung impedance measurements are more useful than simpler measurements of lung function in animals models of pulmonary disease. J Appl Physiol; doi:10.1152/japplphysiol.00369.2007.Google Scholar5 Lutchen KR, Greenstein JL, Suki B. How inhomogeneities and airway walls affect frequency dependence and separation of airway and tissue properties. J Appl Physiol 80: 1696–1707, 1996.Link | ISI | Google Scholar6 Mitzner W. Counterpoint: Lung impedance measurements are not more useful than simpler measurements of lung function in animals models of pulmonary disease. J Appl Physiol; doi:10.1152/japplphysiol.00369.2007a.Google Scholar7 Thorpe CW, Bates JH. Effect of stochastic heterogeneity on lung impedance during acute bronchoconstriction: a model analysis. J Appl Physiol 82: 1616–1625, 1997.Link | ISI | Google Scholar8 Wagers S, Lundblad LK, Ekman M, Irvin CG, Bates JH. The allergic mouse model of asthma: normal smooth muscle in an abnormal lung? J Appl Physiol 96: 2019–2027, 2004.Link | ISI | Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation More from this issue > Volume 103Issue 5November 2007Pages 1903-1904 Copyright & PermissionsCopyright © 2007 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00369.2007bHistory Published online 1 November 2007 Published in print 1 November 2007 Metrics

Last Word on Point:Counterpoint: Lung impedance measurements are/are not more useful than simpler measurements of lung function in animal models of pulmonary disease

Last Word on Point:Counterpoint: Lung impedance measurements are/are not more useful than simpler measurements of lung function in animal models of pulmonary disease

Point:Counterpoint: Lung impedance measurements are/are not more useful than simpler measurements of lung function in animal models of pulmonary disease

Research on pulmonary disease relies increasingly on the use of animal models, commensurate with the progression of our ability to manipulate the genome and recreate noxious environmental conditions in the laboratory. Accordingly, any self-respecting biomedical research institution these days will

Hysteresivity of the lung and tissue strip in the normal rat: effects of heterogeneities

We measured lung impedance in rats in closed chest (CC), open chest (OC), and isolated lungs (IL) at four transpulmonary pressures with a optimal ventilator waveform. Data were analyzed with an homogeneous linear or an inhomogeneous linear model. Both models include tissue damping and elastance and airway inertance. The homogeneous linear model includes airway resistance (Raw), whereas the inhomogeneous linear model has a continuous distribution of Raw characterized by the mean Raw and the standard deviation of Raw (SDR). Lung mechanics were compared with tissue strip mechanics at frequencies and operating stresses comparable to those during lung impedance measurements. The hysteresivity (eta) was calculated as tissue damping/elastance. We found that 1) airway and tissue parameters were different in the IL than in the CC and OC conditions; 2) SDR was lowest in the IL; and 3) eta in IL at low transpulmonary pressure was similar to eta in the tissue strip. We conclude that eta is primarily determined by lung connective tissue, and its elevated estimates from impedance data in the CC and OC conditions are a consequence of compartment-like heterogeneity being greater in CC and OC conditions than in the IL.

Mechanical factors in distribution of pulmonary ventilation.

Mechanical factors in distribution of pulmonary ventilation.