Genel anestezi esnasında peep uygulamasının arteriyel oksijenizasyona etkileri

Genel anestezi sırasında bozulabilen arteriyel oksijenizasyonım asıl nedeni atelektazilerin oluşmasıdır. Çalışmamızda anestezi sırasında PEEP uygulamasının arteriyel oksijenizasyon üzerindeki etkilerini araştırdık. Alt abdominal cerrahi girişim geçirecek, akciğer problemi olmayan, ASA I-II, premedikasyon verilmeyen, 24 yetişkin olgu çalışmaya alındı. 3 dakikalık preoksijenasyondan sonra anestezi indüksiyonunda tiyopental (3 mg kg'1), veküronyum (0.08 mg kg'1) vefentanil (3 yg kg'1); idame de %50-50 O2/N2O içinde %l-2 oranında sevofluran verildi. Rasgele 3 gruba ayrılan olgularda Grup F de PEEP uygulanmadı. İndüksiyondan 30 dk sonra, Grup II'de 5 cmH20 PEEP operasyon bitimine kadar uygulanırken, Grup III'de PEEP 5'er dk süreyle ve 5 cmH20'lik artışlarla 15 cmH20'ya kadar titre edildi. Daha sonra 5 cmH20'ya indirildi. İndüksiyon öncesi ve sonrasında 15 dakikalık aralarla hemodinamik değişiklikler, peak ve plato basınçları, kompliyans ve arter kan gazları değerlendirildi. Önemli hemodinamik değişiklikler olmadan, Grup I'e göre Grup IH'de, peak ve plato basınçlarının yanısıra arteri-yel oksijen basıncı ve oksijen satürasyonunda anlamlı artış saptandı (p

Effects of peep administration arterial oxygenation under general anesthesia

The main cause of deteriorated arterial oxygenation during general anesthesia is the formation of athelectasias. in this study, we examined the effects of PEEP administration on arterial oxygenation under general anesthesia. Twenty-four ASA I-II group adult patients, with no lung problems and no premedication undergoing abdominal surgery were included in the study. After 3 minutes of preoxygenation, thiopental (3 mg kg'1), vecuronium (0.08 mg' kg'1) andfentanyl (3 ftg kg-') were used for induction of anesthesia. Anesthesia was maintained with 50-50 % N2O/O2 and 1-2% sevoflurane. Patients were randomly allocated into 3 groups. Group I received no PEEP. 5 cmH2O PEEP was administered to Group II starting from 30* minute after induction, until the end of the surgery. 5 cmH2O PEEP was commenced to Group III30 minutes after induction and PEEP was increased with 5 cmH2O increments at 5 mi-nutes intervals until 15 cmH2O. PEEP was then reduced to 5 cmH2O with 5 cmH2O decrements at 5 minutes intervals. Hemodynamic parameters, peak and plateau airway pressures, compliance and arterial blood gas analysis were re-corded before induction and at 15 minutes intervals after induction. Peak and plateau airw/ay pressures, arterial oxygen pressure and oxygen saturations were significantly higher in Group III with respect to Group I without any important hemodynamic changes (p<0.05). Increases in peak and pla-teau pressures, arterial oxygen pressure and saturation were not statistically significant in Group H. We concluded that a significant increase in PaO2 and SaO2 may be provided by application of higher PEEP levels during general anesthesia.

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  • 1. Benumof J. Respiratory physiology and respiratory function during anesthesia. In: Miller RD (ed) Anesthesia, New York, Churchill Livingstone 1994; 577-620.
  • 2. Moller JT, Johannessen NW, Berg H, Espersen K, Larsen LE. Hypoxaemia during anaesthesia- An observer study. Br J Anaesth 1991; 66:437-44.
  • 3. Hedenstiema G, Tokics L, Strandberg A, Lundquist H, Brismar B. Correlation of gas exchange impairment to development of atelec-tasis during anaesthesia and muscle paralysis. Acta Anaesth Scand 1986; 30: 183-91.
  • 4. Rothen HU, Sporre B, Engberg G, Wegenius G, Reber A, Hedenstiema G. Prevention of atelectasis during general anaesthesia. Lancet 1995; 345:1387-91.
  • 5. Lindberg P, Gunnarsson L, Tokics L, et al. Atelectasis and lung function in the postoperative period. Acta Anaesth Scand 1992; 36: 546-53.
  • 6. Rothen HU, Sporre B, Engberg G, Wegenius G, Hedenstiema G. Reexpansion of atelectasis during general anaesthesia may have a prolonged effect. Acta Anaesth Scand 1995; 39: 118-25.
  • 7. Klingstedt C, Hedenstiema G, Baehrendtz S, et al. Ventilation-perfusion relationships and atelectasis formation in the supine and lateral positions during conventional mechanical and differential ventilation. Acta Anaesth Scand 1990; 34: 421-9.
  • 8. Tokics L, Hedenstiema G, Strandberg A, Brismar B, Lundquist H. Lung collapse and gas exchange during general anesthesia: Effects of spontaneous breathing, muscle paralysis and positive end-expiratory pressure. Anesthesiology 1987; 66:157-67.
  • 9. Strandberg A, Tokics L, Brismar B, Lundquist H, Hedenslierna G. Constitutional factors promoting development of ateleclasis during anaesthesia. Acta Anaesth Scand 1987; 31: 21-4.
  • 10. Gunnarsson L, Tokics L, Gustavsson H, Hedenstiema G. Influence of age on ateiectasis formation and gas exchange impairment during general anaesthesia. Br J Anaesth 1991; 66: 423-32,
  • 11. Rothen HU, Sporre B, Engberg G, Wegenius G, Hogman M, Hedenstiema G. Influence of gas composition on recurrence of atelectasis after a reexpansion maneuver during general anesthesia. Anesthesioiogy 1995; 82: 832-42.
  • 12. Neumann P, Rothen HU, Berglund JE, Valtysson J, Magnusson H, Hedenstiema G. Positive end-expiratory pressure prevents atelectasis during general anaesthesia even in the presence of a high inspired oxygen concentration. Acta Anaesth Scand 1999; 43: 295-301.
  • 13. Serafini G, Cornara G, Cavalloro F, et al. Pulmonary atelectasis during paediatric anaesthesia: CT scan evaluation and effect of positive end expiratory pressure (PEEP). Paediatr Anaesth 1999; 9: 225-8.
  • 14. Tusman G, Böhm SH, Vazquez GF, Campo JL, Lachmann B. "Alveolar recruitment strategy" improves arterial oxygenation during general anaesthesia. Br J Anaesth 1999; 82: 8-13.
  • 15. Clarke JP, Schuitemaker MN, Sleigh JW. The effect of intraoperative ventilation strategies on perioperative atelectasis.Anaesth Intensive Care 1998;26:262-6.