Evaluation of transthoracic electrical impedance in the diagnosis of pulmonary edema.

Fein, Adam S.; Grossman, Ronald F.; Jones, Jeffrey S.; Goodman, Philip C.; Murray, J. F.

doi:10.1161/01.cir.60.5.1156

Cited by 70 publications

(54 citation statements)

References 13 publications

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“…The thermal dye double-indicator dilution technique remains one of the more accurate methods in intact humans and can determine small changes in EVLW, but it is highly invasive and would be difficult to perform in large numbers of subjects at altitude (42). Transthoracic electrical impedance measurement has been used at altitude (14,43), but the results have been disappointing and changes in lung volume with ventilation and the lack of spatial resolution further complicate the interpretation of results (11).…”

Section: Discussionmentioning

confidence: 99%

Serial changes in nasal potential difference and lung electrical impedance tomography at high altitude

Mason¹,

Petersen

Mélot

et al. 2003

Journal of Applied Physiology

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Mason, Nicholas P., Merete Petersen, Christian Mé lot, Bakyt Imanow, Olga Matveykine, Marie-Therese Gautier, Akpay Sarybaev, Almaz Aldashev, Mirsaid M. Mirrakhimov, Brian H. Brown, Andrew D. Leathard, and Robert Naeije. Serial changes in nasal potential difference and lung electrical impedance tomography at high altitude. J Appl Physiol 94: 2043-2050, 2003. First published December 6, 2002 10.1152 10. /japplphysiol.00777.2002 work suggests that treatment with inhaled ␤2-agonists reduces the incidence of high-altitude pulmonary edema in susceptible subjects by increasing respiratory epithelial sodium transport. We estimated respiratory epithelial ion transport by transepithelial nasal potential difference (NPD) measurements in 20 normal male subjects before, during, and after a stay at 3,800 m. NPD hyperpolarized on ascent to 3,800 m (P Ͻ 0.05), but the change in potential difference with superperfusion of amiloride or isoprenaline was unaffected. Vital capacity (VC) fell on ascent to 3,800 m (P Ͻ 0.05), as did the normalized change in electrical impedance (NCI) measured over the right lung parenchyma (P Ͻ 0.05) suggestive of an increase in extravascular lung water. EchoDoppler-estimated pulmonary artery pressure increases were insufficient to cause clinical pulmonary edema. There was a positive correlation between VC and NCI (R 2 ϭ 0.633) and between NPD and both VC and NCI (R 2 ϭ 0.267 and 0.418). These changes suggest that altered respiratory epithelial ion transport might play a role in the development of subclinical pulmonary edema at high altitude in normal subjects. pulmonary edema; hypobaric hypoxia ALTHOUGH ONLY A MINORITY OF those who go to high altitude develop the potentially fatal condition of highaltitude pulmonary edema (HAPE), there is increasing evidence that the majority of people ascending to altitude may develop subclinical pulmonary edema (9). Forced vital capacity (FVC) falls on ascent to high altitude and is thought to be primarily due to subclinical pulmonary edema (32). The control of pulmonary extravascular lung water (EVLW) has traditionally been attributed to the interplay of Starling forces, with the pulmonary capillary pressure attributed the major regulatory role. It is now realized that sodium transport across the respiratory epithelium plays an important role in the removal of alveolar water (34) and that an intact epithelial barrier is necessary for the resolution of alveolar edema (35). Hypoxia reduces epithelial sodium transport in cultured rat alveolar epithelial monolayers (29) and decreases the expression of alveolar epithelial ion transport proteins (8). In addition, treatment of HAPE-susceptible individuals with inhaled ␤ 2 -agonists, which are known to increase transepithelial sodium transport, decreases pulmonary edema without any effect on pulmonary hemodynamics (44).Measurement of alveolar ion transport in vivo in human subjects is not feasible; however, measurement of the potential difference (PD) generated by ion transport in the nasal mucosa can be used as a marker...

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Section: Discussionmentioning

confidence: 99%

Serial changes in nasal potential difference and lung electrical impedance tomography at high altitude

Mason¹,

Petersen

Mélot

et al. 2003

Journal of Applied Physiology

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“…Various studies describe the assessment of lung edema by transthoracic bioimpedance measurements in pulmonary critical care, but the method has been found to be critical in lung tissue [17,18] . Measurements depend on the variations of air volume within the tissue, on a number of factors including body weight and position, lung volume and pleural effusions.…”

Section: Discussionmentioning

confidence: 99%

Monitoring of Lung Edema by Microwave Reflectometry during Lung Ischemia-Reperfusion Injury in vivo

et al. 2006

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It is still unclear whether lung edema can be monitored by microwave reflectometry and whether the measured changes in lung dry matter content (DMC) are accompanied by changes in PaO₂ and in pro- to anti-inflammatory cytokine expression (IFN-γ and IL-10). Right rat lung hili were cross-clamped at 37°C for 0, 60, 90 or 120 min ischemia followed by 120 min reperfusion. After 90 min (DMC: 15.9 ± 1.4%; PaO₂: 76.7 ± 18 mm Hg) and 120 min ischemia (DMC: 12.8 ± 0.6%; PaO₂: 43 ± 7 mm Hg), a significant decrease in DMC and PaO₂ throughout reperfusion compared to 0 min ischemia (DMC: 19.5 ± 1.11%; PaO₂: 247 ± 33 mm Hg; p < 0.05) was observed. DMC and PaO₂ decreased after 60 min ischemia but recovered during reperfusion (DMC: 18.5 ± 2.4%; PaO₂: 173 ± 30 mm Hg). DMC values reflected changes on the physiological and molecular level. In conclusion, lung edema monitoring by microwave reflectometry might become a tool for the thoracic surgeon.

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“…Later, clinical studies have employed the more conventional four-electrode configuration, 2 where the transthoracic impedance along the long axis of the thorax is measured. [3][4][5][6][7] This methodology was found to be better resistant to changes in tidal volume and chest movement errors. Still, these studies have shown inconsistent results, while not specifically measuring the lungs' impedance but rather that of the whole thoracic volume.…”

Section: Monitoring Lung Resistivity Changes In Congestive Heartmentioning

confidence: 98%

Monitoring Lung Resistivity Changes in Congestive Heart Failure Patients Using the Bioimpedance Technique

Zlochiver

Radai

Barak-Shinar

et al. 2005

Congestive Heart Failure

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The feasibility of a novel, dedicated system for monitoring lung resistivity in congestive heart failure patients, implementing a hybrid approach of the bioimpedance technique, was assessed in this preliminary study. Thirty‐three healthy volunteers and 34 congestive heart failure patients were measured with the PulmoTrace system (Cardiolnspect, Tel Aviv University, Tel Aviv, Israel) during tidal respiration, and the ability to monitor the respective lung resistivity values was assessed. Mean left and right lung resistivity values of 1205±163 and 1200±165 Ω·cm for the control group and 888±193 and 943±187 Ω·cm for the congestive heart failure group were found, indicating a significant (p<2·10−7) difference between the two groups. The results of long‐term monitoring of two patients during medical treatment are also shown. This hybrid approach system is believed to improve diagnostic capabilities and help physicians to better adjust medication dosage on a frequent basis.

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Evaluation of transthoracic electrical impedance in the diagnosis of pulmonary edema.

Cited by 70 publications

References 13 publications

Serial changes in nasal potential difference and lung electrical impedance tomography at high altitude

Serial changes in nasal potential difference and lung electrical impedance tomography at high altitude

Monitoring of Lung Edema by Microwave Reflectometry during Lung Ischemia-Reperfusion Injury in vivo

Monitoring Lung Resistivity Changes in Congestive Heart Failure Patients Using the Bioimpedance Technique

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