Abstract
In oleci acid-induced pulmonary oedema (OAPO) sequential intrapulmonary fluid accumulation occurs leading to different expiratory flow pattern in dependent lung regions. The potential effects on efficacy of high-frequency jet ventilation (HFJV, f=3 Hz, I: E=0.43, FiO2=0.4) were studied and compared with continous positive pressure ventilation (CPPV, f=12–18/min, I:E=0.5, TV=12 ml/kg, PEEP=0.5 kPa, FiO2=0.4) in a dog model of OAPO. In the control state (lung-healthy dogs), 15 min afteroleic acid lung injury (interstitial oedema, period I) and 60 min after onset of OAPO (alveolar oedema, period II), gas exchange, lung volumes, compliance, resistance and haemodynamics were measured. The course of lung oedema was determined indirectly by means of washout curvesof helium (foreign gas bolus-test, FGB) and nitrogen (single breath-test for oxygen, SBO2). During control, there were no significant differences between the HFJV-group (n=7) and the CPPV-group(n=6) by virtue of gas exchange, lung volumes and haemodynamics. During period I, PaO2 decreased signiicantly both with HFJV (p<0.01) and CPPV (p<0.05), being lower in the HFJV-group (p<0.05). PaCO2, pulmonary and haemodynamic parameters were unchanged. Onset of phase IV of the alveolar plateau (closing volume CV) occurred significantly earlier (p<0.05) in all animals. Impaired ventilation of dependent lung regions, increased maldistribution of intrapulmonary gas and VA/Q-mismatching may be the underlying mechanisms for lower efficacy of HFJV during interstitial lung oedema. In period II, pulmonary and cardiocirculatory parameters had changed significantly in both groups. CV had decreased, indicating a biphasic behavior of washout curves, which is due to changes of regional FRC, resistance and compliance after onset of alveolar flooding. Oxygenation was significantly more impaired in the HFJV-group (p<0.05). CPPV is superior to HFJV in maintaining sufficient gas exchange both during interstitial and alveolar oedema in dogs with oleic acid-induced lung injury.
Article PDF
Similar content being viewed by others
Avoid common mistakes on your manuscript.
References
Simon BA, Winmann GA, Mitzner W (1984) Mean airway pressure and alveolar pressure during high-frequency ventilation. J Appl Physiol 57:1069–1078
Saari AF, Rossing TH, Solway J, Drazen JM (1984) Lung inflation during high-frequency ventilation. Am Rev Resp Dis 129:332–336
Eliasen K, Mogensen T, Andersen JB (1986) Peripheral airway pressure during high-frequency ventilation. Acta Anaesth Scand 30:97–100
Rouby JJ, Simmoneau G, Benhamou D, Sartene R, Sardnal F, Deriaz H, Duroux P, Viars P (1985) Factors influencing pulmonary volumes and CO2-elimination during high-frequency ventilation. Anesthesiol 63:473–493
Lemen R, Graf G, Jones RD, Cowan G (1975) “Closing volume” changes in alloxan-induced pulmonary edema in dogs. J Appl Physiol 39:235–241
Staub NC, Nagano H, Pearce ML (1967) Pulmonary edema in dogs: especially the sequence of fluid accumulation in lungs. J Appl Physiol 22:227–240
Montaner JSG, Tsang J, Evans KG, Mullen JBM, Burns AR, Walker DC, Wiggs B, Hogg JC (1986) Alveolar epithelial damage. A critical difference between high pressure and oleic acid-induced low pressure pulmonary edema. J Clin Invest 77:1786–1796
Derks CM, Jacobovitz Derks D (1977) Embolic pneumopathy induced by oleic acid. Am J Pathol 87:143–158
Schoene RB, Robertson TM, Thorning DR, Springmeyer SC, Hlastala MP, Cheney FW (1984) Pathophysiological patterns of resolution from oleic acid lung injury in the dog. J Appl Physiol 56:472–481
Henning RJ, Heyman U, Alcover I, Romeo S (1986) Cardiopulmonary effects of oleic acid-induced pulmonary edema and mechanical ventilation. Anesth Analg 65:925–932
Iliff LD, Greene RE, Hughes JMB (1972) Effect of interstitial edema on distribution of ventilation and perfusion in isolated lung. J Appl Physiol 33:462–467
Hogg JC, Agarawal JB, Gardiner AJS, Palmer WH, Macklem PT (1972) Distribution of airway resistance with developing pulmonary edema in dogs. J Appl Physiol 32:20–24
Hedenstierna G, Santesson J (1979) Airway closure during anesthesia: a comparison between resident-gas and argon-bolus techniques. J Appl Physiol 47:874–881
Rehder K, Marsh HM, Rodarte JR, Hyatt RE (1977) Airway closure. Anesthesiol 47:40–52
Thompson WK, Marchak BE, Froese AB, Bryan AC (1982) High-frequency oscillation compared with standard ventilation in pulmonary injury model. J Appl Physiol 52:534–548
Wright K, Lyrene RK, Truog WE, Standaert TA, Murphy J, Woodrum DE (1982) Ventilation by high-frequency oscillation in rabbits with oleic acid lung injury. J Appl Physiol 50:1056–1060
Breen PH, Ali J, Wood LDH (1984) High-frequency ventilation in lung edema: effects on gas exchange and perfusion. J Appl Physiol 56:187–195
Muir AL, Hogg JC, Naimark A, Hall DL, Cherneck W (1975) Effect of alveolar liquid on distribution of blood flow in dog lungs. J Appl Physiol 39:885–890
Hachenberg T, Wendt M, Meyer J, Wrenger K, Lawin P (1988) “Closing volume” during high-frequency ventilation in anesthetized dogs. Acta Anaesth Scand:140–146
Wagner PD, Lavaruso LB, Goldzimmer E, Naumann PF, West JB (1975) Distribution of ventilation-perfusion ratios in dogs with normal and abnormal lungs. J Appl Physiol 38:1099–1109
Frostell C (1986) Lung fluid balance during mechanical ventilation. Thesis, Karolinska Institute Stockholm
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Hachenberg, T., Wendt, M., Hermeyer, G. et al. High-frequency jet ventilation during oleic-acid induced pulmonary oedema. Intensive Care Med 15, 105–110 (1989). https://doi.org/10.1007/BF00295986
Received:
Accepted:
Issue Date:
DOI: https://doi.org/10.1007/BF00295986