全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

Interest of Monitoring Diaphragmatic Electrical Activity in the Pediatric Intensive Care Unit

DOI: 10.1155/2013/384210

Full-Text   Cite this paper   Add to My Lib

Abstract:

The monitoring of electrical activity of the diaphragm (EAdi) is a new minimally invasive bedside technology that was developed for the neurally adjusted ventilatory assist (NAVA) mode of ventilation. In addition to its role in NAVA ventilation, this technology provides the clinician with previously unavailable and essential information on diaphragm activity. In this paper, we review the clinical interests of EAdi in the pediatric intensive care setting. Firstly, the monitoring of EAdi allows the clinician to tailor the ventilatory settings on an individual basis, avoiding frequent overassistance leading potentially to diaphragmatic atrophy. Increased inspiratory EAdi levels can also suggest insufficient support, while a strong tonic activity may reflect the patient efforts to increase its lung volume. EAdi monitoring also allows detection of patient-ventilator asynchrony. It can play a role in evaluation of extubation readiness. Finally, EAdi monitoring provides the clinician with better understanding of the ventilatory capacity of patients with acute neuromuscular disease. Further studies are warranted to evaluate the clinical impact of these potential benefits. 1. Introduction In the pediatric intensive care unit (PICU), up to half of patients require mechanical ventilation (MV) [1]. The objectives of this therapy are to support the failing respiratory muscles and allow better gas exchange while awaiting recovery. As simple a concept as MV may seem, it can be also detrimental and delay healing if not judiciously adjusted to the individual patient. Ventilation not synchronized with patients’ efforts, as well as both insufficient or excessive support, can delay recovery, prolong the MV duration, and contribute to muscle wasting [2, 3]. It has long been considered crucial to monitor the respiratory activity of critically ill patients in order to limit these complications, but available monitoring methods were complex and rarely used in clinical practice [4, 5]. Over the last decade, a new minimally invasive technology has been developed to continuously record the electrical activity of diaphragm (EAdi) at bedside. The main purpose of this technology is to synchronize and adapt the ventilatory support following the EAdi signal during the neurally adjusted ventilatory assist (NAVA) mode [6]. In addition to NAVA ventilation, EAdi monitoring also provides the clinician with a comprehensible continuous evaluation of the diaphragm’s function. The aim of this paper is to emphasize the importance of this new information in clinical practice. 2. Materials and

References

[1]  M. Santschi, P. Jouvet, F. Leclerc et al., “Acute lung injury in children: therapeutic practice and feasibility of international clinical trials,” Pediatric Critical Care Medicine, vol. 11, no. 6, pp. 681–773, 2010.
[2]  F. Lemaire, “Difficult weaning,” Intensive Care Medicine, vol. 19, Supplement 2, pp. S69–S73, 1993.
[3]  A. W. Thille, P. Rodriguez, B. Cabello, F. Lellouche, and L. Brochard, “Patient-ventilator asynchrony during assisted mechanical ventilation,” Intensive Care Medicine, vol. 32, no. 10, pp. 1515–1522, 2006.
[4]  M. J. Tobin, “Respiratory monitoring during mechanical ventilation,” Critical Care Clinics, vol. 6, no. 3, pp. 679–709, 1990.
[5]  J. W. Fitting, “Respiratory muscle function in the critically ill patient,” Acute Care, vol. 14-15, pp. 313–349, 1989.
[6]  C. Sinderby, P. Navalesi, J. Beck et al., “Neural control of mechanical ventilation in respiratory failure,” Nature Medicine, vol. 5, no. 12, pp. 1433–1436, 1999.
[7]  J. Beck, C. Sinderby, L. Lindstr?m, and A. Grassino, “Influence of bipolar esophageal electrode positioning on measurements of human crural diaphragm electromyogram,” Journal of Applied Physiology, vol. 81, no. 3, pp. 1434–1449, 1996.
[8]  J. Beck, C. Sinderby, J. Weinberg, and A. Grassino, “Effects of muscle-to-electrode distance on the human diaphragm electromyogram,” Journal of Applied Physiology, vol. 79, no. 3, pp. 975–985, 1995.
[9]  C. A. Sinderby, J. C. Beck, L. H. Lindstr?m, and A. E. Grassino, “Enhancement of signal quality in esophageal recordings of diaphragm EMG,” Journal of Applied Physiology, vol. 82, no. 4, pp. 1370–1377, 1997.
[10]  C. Sinderby, J. Beck, J. Spahija, J. Weinberg, and A. Grassino, “Voluntary activation of the human diaphragm in health and disease,” Journal of Applied Physiology, vol. 85, no. 6, pp. 2146–2158, 1998.
[11]  R. V. Louren?o, N. S. Cherniack, J. R. Malm, and A. P. Fishman, “Nervous output from the respiratory center during obstructed breathing,” Journal of Applied Physiology, vol. 21, no. 2, pp. 527–533, 1966.
[12]  S. Levine, T. Nguyen, N. Taylor et al., “Rapid disuse atrophy of diaphragm fibers in mechanically ventilated humans,” The New England Journal of Medicine, vol. 358, no. 13, pp. 1327–1335, 2008.
[13]  S. Jaber, B. J. Petrof, B. Jung et al., “Rapidly progressive diaphragmatic weakness and injury during mechanical ventilation in humans,” American Journal of Respiratory and Critical Care Medicine, vol. 183, no. 3, pp. 364–371, 2011.
[14]  A. S. Knisely, S. M. Leal, and D. B. Singer, “Abnormalities of diaphragmatic muscle in neonates with ventilated lungs,” Journal of Pediatrics, vol. 113, no. 6, pp. 1074–1077, 1988.
[15]  S. K. Powers, A. N. Kavazis, and K. C. DeRuisseau, “Mechanisms of disuse muscle atrophy: role of oxidative stress,” American Journal of Physiology, vol. 288, no. 2, pp. R337–R344, 2005.
[16]  R. A. Shanely, M. A. Zergeroglu, S. L. Lennon et al., “Mechanical ventilation-induced diaphragmatic atrophy is associated with oxidative injury and increased proteolytic activity,” American Journal of Respiratory and Critical Care Medicine, vol. 166, no. 10, pp. 1369–1374, 2002.
[17]  R. A. Shanely, D. Van Gammeren, K. C. DeRuisseau et al., “Mechanical ventilation depresses protein synthesis in the rat diaphragm,” American Journal of Respiratory and Critical Care Medicine, vol. 170, no. 9, pp. 994–999, 2004.
[18]  T. Vassilakopoulos and B. J. Petrof, “Ventilator-induced diaphragmatic dysfunction,” American Journal of Respiratory and Critical Care Medicine, vol. 169, no. 3, pp. 336–341, 2004.
[19]  L. Brochard, A. Harf, H. Lorino, and F. Lemaire, “Inspiratory pressure support prevents diaphragmatic fatigue during weaning from mechanical ventilation,” American Review of Respiratory Disease, vol. 139, no. 2, pp. 513–521, 1989.
[20]  E. Futier, J. M. Constantin, L. Combaret et al., “Pressure support ventilation attenuates ventilator-induced protein modifications in the diaphragm,” Critical Care, vol. 12, no. 5, article R116, 2008.
[21]  M. B. Hudson, A. J. Smuder, W. B. Nelson, C. S. Bruells, S. Levine, and S. K. Powers, “Both high level pressure support ventilation and controlled mechanical ventilation induce diaphragm dysfunction and atrophy,” Critical Care Medicine, vol. 40, no. 4, pp. 1254–1260, 2012.
[22]  D. Colombo, G. Cammarota, V. Bergamaschi, M. De Lucia, F. D. Corte, and P. Navalesi, “Physiologic response to varying levels of pressure support and neurally adjusted ventilatory assist in patients with acute respiratory failure,” Intensive Care Medicine, vol. 34, no. 11, pp. 2010–2018, 2008.
[23]  M. Alander, O. Peltoniemi, T. Pokka, and T. Kontiokari, “Comparison of pressure-, flow-, and NAVA-triggering in pediatric and neonatal ventilatory care,” Pediatric Pulmonology, vol. 47, no. 1, pp. 76–83, 2012.
[24]  A. A. Colin, M. E. B. Wohl, J. Mead, F. A. Ratjen, G. Glass, and A. R. Stark, “Transition from dynamically maintained to relaxed end-expiratory volume in human infants,” Journal of Applied Physiology, vol. 67, no. 5, pp. 2107–2111, 1989.
[25]  G. Emeriaud, J. Beck, M. Tucci, J. Lacroix, and C. Sinderby, “Diaphragm electrical activity during expiration in mechanically ventilated infants,” Pediatric Research, vol. 59, no. 5, pp. 705–710, 2006.
[26]  N. E. L. Meessen, C. P. M. Van Der Grinten, H. T. M. Folgering, and S. C. M. Luijendijk, “Tonic activity in inspiratory muscles during continuous negative airway pressure,” Respiration Physiology, vol. 92, no. 2, pp. 151–166, 1993.
[27]  E. D'Angelo, M. Pecchiari, F. Acocella, A. Monaco, and F. Bellemare, “Effects of abdominal distension on breathing pattern and respiratory mechanics in rabbits,” Respiratory Physiology and Neurobiology, vol. 130, no. 3, pp. 293–304, 2002.
[28]  A. Ma, M. Bravo, and C. T. Kappagoda, “Responses of bronchial C-fiber afferents of the rabbit to changes in lung compliance,” Respiratory Physiology and Neurobiology, vol. 138, no. 2-3, pp. 155–163, 2003.
[29]  S. Gunawardena, K. Ravi, J. C. Longhurst et al., “Responses of C fiber afferents of the rabbit airways and lungs to changes in extra-vascular fluid volume,” Respiratory Physiology and Neurobiology, vol. 132, no. 3, pp. 239–251, 2002.
[30]  S. N. Hussain, “Regulation of ventilatory muscle blood flow,” Journal of Applied Physiology, vol. 81, no. 4, pp. 1455–1468, 1996.
[31]  F. Bellemare and A. Grassino, “Effect of pressure and timing of contraction on human diaphragm fatigue,” Journal of Applied Physiology, vol. 53, no. 5, pp. 1190–1195, 1982.
[32]  F. Laghi, S. E. Cattapan, A. Jubran et al., “Is weaning failure caused by low-frequency fatigue of the diaphragm?” American Journal of Respiratory and Critical Care Medicine, vol. 167, no. 2, pp. 120–127, 2003.
[33]  G. K. Wolf, B. K. Walsh, M. L. Green, and J. H. Arnold, “Electrical activity of the diaphragm during extubation readiness testing in critically ill children,” Pediatric Critical Care Medicine, vol. 12, no. 6, pp. e220–e224, 2011.
[34]  L. Liu, H. Liu, Y. Yang et al., “Neuroventilatory efficiency and extubation readiness in critically ill patients,” Critical Care, vol. 16, no. 4m article R143, 2012.
[35]  R. Kuhlen, S. Hausmann, D. Pappert, K. Slama, R. Rossaint, and K. Falke, “A new method for P0.1 measurement using standard respiratory equipment,” Intensive Care Medicine, vol. 21, no. 7, pp. 554–560, 1995.
[36]  S. N. Nemer, C. S. V. Barbas, J. B. Caldeira et al., “Evaluation of maximal inspiratory pressure, tracheal airway occlusion pressure, and its ratio in the weaning outcome,” Journal of Critical Care, vol. 24, no. 3, pp. 441–446, 2009.
[37]  A. Bordessoule, G. Emeriaud, N. Delnard, J. Beck, and P. Jouvet, “Recording diaphragm activity by an oesophageal probe: a new tool to evaluate the recovery of diaphragmatic paralysis,” Intensive Care Medicine, vol. 36, no. 11, pp. 1978–1979, 2010.
[38]  D. C. Chao, D. J. Scheinhorn, and M. Stearn-Hassenpflug, “Patient-ventilator trigger asynchrony in prolonged mechanical ventilation,” Chest, vol. 112, no. 6, pp. 1592–1599, 1997.
[39]  M. de Wit, S. Pedram, A. M. Best, and S. K. Epstein, “Observational study of patient-ventilator asynchrony and relationship to sedation level,” Journal of Critical Care, vol. 24, no. 1, pp. 74–80, 2009.
[40]  D. Colombo, G. Cammarota, M. Alemani et al., “Efficacy of ventilator waveforms observation in detecting patient-ventilator asynchrony,” Critical Care Medicine, vol. 39, no. 11, pp. 2452–2457, 2011.
[41]  J. Beck, M. Tucci, G. Emeriaud, J. Lacroix, and C. Sinderby, “Prolonged neural expiratory time induced by mechanical ventilation in infants,” Pediatric Research, vol. 55, no. 5, pp. 747–754, 2004.
[42]  A. Bordessoule, G. Emeriaud, S. Morneau, P. Jouvet, and J. Beck, “Neurally Adjusted Ventilatory Assist (NAVA) improves patient-ventilator interaction in infants compared to conventional ventilation,” Pediatric Research, vol. 72, no. 2, pp. 194–202, 2012.
[43]  J. Spahija, M. De Marchie, M. Albert et al., “Patient-ventilator interaction during pressure support ventilation and neurally adjusted ventilatory assist,” Critical Care Medicine, vol. 38, no. 2, pp. 518–526, 2010.
[44]  J. Beck, M. Reilly, G. Grasselli et al., “Patient-ventilator interaction during neurally adjusted ventilatory assist in low birth weight infants,” Pediatric Research, vol. 65, no. 6, pp. 663–668, 2009.
[45]  C. Breatnach, N. P. Conlon, M. Stack, M. Healy, and B. P. O'Hare, “A prospective crossover comparison of neurally adjusted ventilatory assist and pressure-support ventilation in a pediatric and neonatal intensive care unit population*,” Pediatric Critical Care Medicine, vol. 11, no. 1, pp. 7–11, 2010.
[46]  K. C. Clement, T. L. Thurman, S. J. Holt, and M. J. Heulitt, “Neurally triggered breaths reduce trigger delay and improve ventilator response times in ventilated infants with bronchiolitis,” Intensive Care Medicine, vol. 37, no. 11, pp. 1826–1832, 2011.
[47]  G. F. Rafferty, N. Mustfa, W. D. Man et al., “Twitch airway pressure elicited by magnetic phrenic nerve stimulation in anesthetized healthy children,” Pediatric Pulmonology, vol. 40, no. 2, pp. 141–147, 2005.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133