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Breathing pattern in weaning patients: comparison of two inspired oxygen fractions

Abstracts

BACKGROUND AND OBJECTIVES: An inspired oxygen fraction (FiO2) of 40% is often used for weaning patients, but lower FiO2 values are also recommended, if arterial oxygen pressure (PaO2)/ FiO2 >150-200 mmHg. This study aimed to compare respiratory variables and vital data values recorded during use of sufficient FiO2 (ideal) to maintain peripheral oxygen saturation at 92% with values recorded during use of FiO2 established at 40% (baseline) in weaning patients. METHODS: Prospective cross-over study. Respiratory variables (respiratory frequency, tidal volume, occlusion pressure, inspiratory time/total time ratio) and vital data (blood pressure and heart rate) were collected sequentially at 30 and 60 minutes with baseline FiO2, followed by ideal FiO2. These were compared to a generalized linear model for repeated measurements. Comparisons between baseline and ideal FiO2 values, and arterial blood gases were evaluated by the Student's t or Wilcoxon tests. RESULTS: In 30 adult patients the median of ideal FiO2 was 25% (IQ25%-75% 23-28). This was significantly lower than baseline FiO2 (40%) (p< 0.001). No significant difference was found in the PaO2/ FiO2 ratio between baseline FiO2 (269±53) and ideal FiO2 (268±47). Tidal volume was significantly lower during use of ideal FiO2 (p=0.003) and blood pressure was significantly higher during use of baseline FiO2 (p=0.041), but there was no clinical significance. The remaining variables were not affected by reduction in FiO2. The ideal FiO2 did not influence remaining variables. CONCLUSIONS: These results suggest that FiO2 levels sufficient to ensure a SpO2>92% did not alter breathing patterns or trigger clinical changes in weaning patients.

Respiration; Respiratory mechanics; Mechanical ventilation; Oxygen inhalation therapy; Ventilator weaning


INTRODUÇÃO E OBJETIVOS: Frações inspiradas de oxigênio (FiO2) < 40% são recomendadas durante o desmame ventilatório se pressão arterial de oxigênio (PaO2)/FiO2 >150-200 mmHg, O objetivo desse estudo foi comparar as variáveis respiratórias e os dados vitais coletados durante a utilização de uma FiO2 suficiente para manter a saturação periférica de oxigênio em 92% (ideal) com aquelas coletadas durante uma FiO2 rotineiramente ajustada em 40% (basal) em pacientes sob desmame ventilatório. MÉTODOS: Estudo prospectivo cruzado. As variáveis freqüência respiratória, volume corrente, pressão de oclusão, relação tempo inspiratório/tempo total, pressão arterial e freqüência cardíaca foram coletados, seqüencialmente, aos 30 e 60 minutos sob FiO2 basal (40%) e, em seguida sob FiO2 ideal. Essas foram comparadas pelo modelo linear generalizado para medidas repetidas. Para comparar os valores basal e ideal da FiO2 e da PaO2 foram utilizados os testes t Student ou Wilcoxon. RESULTADOS: Em 30 pacientes adultos a mediana da FiO2 ideal foi 25% (IQ25%-75% 23-28), significativamente menor que a basal (40%) (p< 0,001). A relação PaO2/FiO2 não apresentou diferença significativa entre a FiO2 basal (269±53) e a FiO2 ideal (268±47). O volume corrente foi significativamente menor durante a utilização da FiO2 ideal (p=0,003) e a pressão arterial foi significativamente maior durante a utilização da FiO2 ideal (p=0,041), mas sem significância clínica. A FiO2 ideal não influenciou as demais variáveis. CONCLUSÃO: Esses resultados sugerem que níveis de FiO2 suficientes para manter uma SpO2>92% não alteraram o padrão respiratório ou provocaram alterações clínicas em pacientes sob desmame ventilatório.

Respiração; Mecânica respiratória; Ventilação mecânica; Oxigenoterapia; Desmame do respirador


ORIGINAL ARTICLE

Breathing pattern in weaning patients: comparison of two inspired oxygen fractions

Gisele do Carmo Leite Machado DinizI; Walter Araújo ZinII; Fernando Antônio BotoniIII; Aldemar Vilela de CastroIV; Maria da Glória Rodrigues-MachadoV

IMaster, Professor of the Physiotherapy Department, Pontifícia Universidade Católica de Minas Gerais - PUC-Minas - Betim (MG), Minas Gerais, Brazil

IIPhD, Professor of the Biophysics Institute Carlos Chagas Filho, Universidade Federal do Rio de Janeiro - UFRJ - Rio de Janeiro (RJ), Brazil

IIIPhD, Professor of the Department of Internal Medicine, Faculdade de Medicina - Universidade Federal de Minas Gerais - UFMG - Belo Horizonte (MG), Minas Gerais, Brazil

IVPhD of the Ophtalmology Clinic at Hospital Governador Israel Pinheiro - HGIP - Belo Horizonte (MG), Minas Gerais, Brazil

VMaster, Professor from Faculdade de Ciências Médicas de Minas Gerais - Belo Horizonte (MG), Minas Gerais, Brazil

Author for Correspondence

ABSTRACT

BACKGROUND AND OBJECTIVES: An inspired oxygen fraction (FiO2) of 40% is often used for weaning patients, but lower FiO2 values are also recommended, if arterial oxygen pressure (PaO2)/ FiO2 >150–200 mmHg. This study aimed to compare respiratory variables and vital data values recorded during use of sufficient FiO2 (ideal) to maintain peripheral oxygen saturation at 92% with values recorded during use of FiO2 established at 40% (baseline) in weaning patients.

METHODS: Prospective cross-over study. Respiratory variables (respiratory frequency, tidal volume, occlusion pressure, inspiratory time/total time ratio) and vital data (blood pressure and heart rate) were collected sequentially at 30 and 60 minutes with baseline FiO2, followed by ideal FiO2. These were compared to a generalized linear model for repeated measurements. Comparisons between baseline and ideal FiO2 values, and arterial blood gases were evaluated by the Student's t or Wilcoxon tests.

RESULTS: In 30 adult patients the median of ideal FiO2 was 25% (IQ25%-75% 23-28). This was significantly lower than baseline FiO2 (40%) (p< 0.001). No significant difference was found in the PaO2/ FiO2 ratio between baseline FiO2 (269±53) and ideal FiO2 (268±47). Tidal volume was significantly lower during use of ideal FiO2 (p=0.003) and blood pressure was significantly higher during use of baseline FiO2 (p=0.041), but there was no clinical significance. The remaining variables were not affected by reduction in FiO2. The ideal FiO2 did not influence remaining variables.

CONCLUSIONS: These results suggest that FiO2 levels sufficient to ensure a SpO2>92% did not alter breathing patterns or trigger clinical changes in weaning patients.

Keywords: Respiration; Respiratory mechanics; Mechanical ventilation; Oxygen inhalation therapy; Ventilator weaning

INTRODUCTION

Supplemental inspired oxygen fraction (FiO2) is a mechanical ventilation parameter often used to optimize tissue oxygenation. However, an inadequate adjustment of FiO2 may lead to hypoxia or hyperoxia and, consequently, to noxious effects.(1-3) Several cellular alterations and an increased anaerobic metabolism are some of the consequences of tissue hypoxia.(4) When an individual is in a situation of acute hypoxemia, there may be an increased stimulus of peripheral chemoreceptors and therefore increase of respiratory drive, which is defined as the lowest central stimulus able to generate a motor response in the inspiratory muscles.(5) In patients under mechanical ventilation, respiratory drive is directly related to the patient and mechanical ventilator interaction.(6) The respiratory pattern is directly influenced by the drive and is regarded as a set of factors related to respiratory frequency and depth, such as flow, minute volume, inspiration and expiration times as well as associated variables such as the inspiratory time/total time ratio (Ti/Ttot).(7)

Toxic effects of oxygen are not well established in humans, but when administered in high doses or for a prolonged period, oxygen can cause pulmonary and systemic injuries.(8,9) In case of hyperoxia, the principal mechanism involved in these injuries is oxidative stress.(10,11) This can lead to degenerative processes of organic biomolecules, with subsequent cell failure and death.(12) Concerning pulmonary inflammation, activation and recruitment, of neutrophils and alveolar macrophages may occur , resulting in hyaline membrane formation, edema, hyperplasia and proliferation of type II alveolar epithelial cells, type I epithelial cells destruction, interstitial fibrosis and vascular pulmonary remodelling.(13)

To avoid harmful effects of hypoxia or hyperoxia on the organism, a FiO2 higher than that of the surrounding air is recommended as adjuvant therapy when arterial oxygen pressure (PaO2) is below 60 mmHg or SaO2< 90%.(14) For weaning adult patients, criteria for assessment of mechanical ventilation discontinuation are adequate oxygenation (eg, PaO2/ FiO2 ratio > 150 to 200; requiring positive end-expiratory pressure [PEEP] < 5 to 8 cmH2O; FiO2 < 40 to 50%).(15) Many patients undergoi prolonged mechanical ventilation(16,17) and consequently prolonged use of oxygen. These patients should receive a FiO2 sufficient to meet their needs without changes in their breathing patterns and vital data. As such, , the aim of this study was to compare respiratory variables and vital data values recorded during use of FiO2 at sufficient levels to maintain peripheral oxygen saturation (SpO2) > 92% with variables recorded during use of a baseline FiO2 at 40% in stable patients being weaned from mechanical ventilation. The secondary objective was to determine the effect of exposure time on these variables of each FiO2 level. The hypothesis was that such patients would exhibit no significant alterations in their respiratory variables and vital data values, because a SpO2 level considered safe enough to avoid hypoxia in stable patients would be ensured.

METHODS

Study Patients

This was a prospective cross-over study that took place between April and December 2006, in one intensive care unit (ICU). The sample comprised 30 weaning patients, over 18 years of age, who had been on mechanical ventilation for more than 48 hours, due to different causes of respiratory failure. At the time of the study, all patients were on weaning from mechanical ventilation and on a 40% baseline FiO2. Criteria used for considering patients as undergoing weaning from mechanical ventilation were those described in literature.(15)

Exclusion criteria were hemodynamic instability, severe cardiomyopathy or recent acute coronary syndrome. Patients with hemoglobin levels below 8 g/dL; those without adequate monitoring of SpO2; with significant hydroelectrolytic, acid-base and metabolic disorders, neuromuscular diseases or need for sedation were also excluded. This study was approved by the Ethics Committee of the Governador Israel Pinheiro Hospital. Terms of informed consent were signed either by the patients or legal guardians.

Study Protocol

Respiratory pattern and drive variables were assessed from the mechanical ventilator monitor. The mechanical ventilator used was the Servoi® (Maquet Critical Care AB, Solna, Sweden). This model has an automatic calibration of FiO2 and continuously monitors pressure in the first 100 milliseconds of an occluded inspiration (P0.1) (used to estimate respiratory drive)(18) and the Ti/Ttot ratio (reflecting contraction duration of the inspiratory muscles).(7) Respiratory frequency (f), tidal volume (VT) and Ti/Ttot ratio were recorded from a single measurement. P0.1 was obtained from the average of three consecutive measurements. Patients on pressure support ventilation (PSV) were studied. Professionals who had no knowledge about this study defined all ventilatory parameters in accordance with each patient's clinical conditions.

Heart rate (HR), mean arterial pressure (MAP) and SpO2 were monitored using Dixtal heart and oximetric monitors (DX 2010®, Dixtal Biomédica, São Paulo) and values were recorded throughout all phases of the study. The sampled arterial blood was analyzed periodically using a calibrated ABL 520 gasometer (Radiometer®, Copenhagen, Denmark). Complementary data was obtained from each patient at the time of collection.

Aspiration of pulmonary secretions was performed 30 minutes prior to data collection. Each patient was then placed in supine position with the headrest at 45 degrees. The variables of interest were then collected in two phases, each lasting one hour. The first phase was denominated baseline FiO2 and was carried out with the patient on 40% FiO2. The second was denominated ideal FiO2 because it used an acceptable SpO2 for stable patients,(14) in which SpO2 was adjusted to a level sufficient to maintain it at 92% for Caucasians and 95% for Black individuals.(19) Ideal FiO2 was determined after completion of the first phase; the FiO2 was adjusted to 25% for all patients and observed for ten minutes. According to Cakar et al.,(20) this is sufficient time for a balance of the PaO2 and SpO2 following FiO2 alterations in stable patients. After 10 minutes, FiO2 was readjusted only if the desired SpO2 had not yet been achieved and the same stabilization period was maintained until the ideal FiO2 was obtained. Once this FiO2 was determined, the second phase of the study began.

Data collection of respiratory variables and vital data were made every 30 and 60 minutes after onset of each phase to determine a possible influence of time. Arterial blood sample for blood gas analysis and lactate measurement was collected only 30 minutes after onset of each phase, to minimize the discomfort of radial artery punction. Pressure support and positive end-expiratory pressure (PEEP) remained unchanged throughout the study period. In accordance with the routine protocol of the service, FiO2 of each patient was readjusted to 40% after completion of the second stage.

Statistical analysis

Data were analyzed using the SPSS 11.5 (SPSS Inc. Chicago, Illinois) and Prism 3 (GraphPad Software, San Diego) software programs. The information collected was presented either in absolute values, median (IQ25%-75%) or as the mean ± SD.

Respiratory variables and vital data were analyzed using the generalized linear model for repeated measurements with the Wilk's Lambda test, which investigated two effects: FiO2 (baseline and ideal) and time (30 and 60 minutes). According to the test for normality, the paired Student's t test or the Wilcoxon test were used to compare PaO2, arterial carbon dioxide pressure (PaCO2), pH, arterial oxygen saturation (SaO2), lactate, SpO2, ideal FiO2 in relation to baseline FiO2, and the PaO2/ FiO2 ratio between the two study phases (use of different FiO2 values). A two-sided p-value < 0.05 was considered significant.

RESULTS

All the 30 patients initially recruited completed the protocol. Of these 21 were male, mean age was 61±14 years and main reasons for mechanical ventilation were: pneumonia, complications after abdominal surgery, sepsis and stroke. Their demographic and clinical characteristics are shown in table 1. The median of ideal FiO2 was 25% (IQ25%-75% 23-28). This result was significantly lower than baseline FiO2 (40%) (p<0.001). PaO2, SaO2 and SpO2 were significantly lower at 30 minutes during use of ideal FiO2 (p<0.001, p<0.001, p<0.001, respectively), whereas no significant difference was observed regarding PaCO2 (p=0.21) (Table 2). Lactate (1.42±0.56 and 1.41±0.52 mmol/L) and PaO2/ FiO2 (268±47 and 269±53) values obtained from ideal FiO2 and baseline ideal, respectively, were not significantly different between the two phases. Among all patients studied, four (13%) had a PaO2 < 60 mmHg during use of ideal FiO2. Table 3 shows the PaO2, SaO2, SpO2, f and HR values during the two study phases.

Respiratory variables and vital data assessed throughout the study time using different FiO2 values are shown in table 4. Tidal volume (VT) was significantly lower at 30 minutes during use of ideal FiO2 in comparison to that at 30 and 60 minutes after onset of baseline FiO2, and no significant difference was observed in intragroup analyses. When considering interaction between the two FiO2 levels used and the two patient exposure times for each FiO2, a significant difference was observed only in the MAP variable. It was significantly higher during the first 30 minutes of the baseline FiO2 phase then at other times of exposure. The remaining variables demonstrated no significant alterations with regard to different FiO2 levels or exposure times.

DISCUSSION

The main finding of the present study was that reduction of 40% FiO2 to a level sufficient to assure SpO2 > 92% did not alter the breathing pattern and/or trigger clinical changes in stable patients undergoing weaning from mechanical ventilation. However, there was a significant difference between baseline FiO2 and tideal FiO2 values for each patient. The clinical implication of these findings is that it is possible to reduce FiO2 without affecting the PaO2 / FiO2, ensuring gas exchange.

No significant alterations in variables related to the respiratory pattern and drive were observed in this study, except for a reduction in VT 30 minutes after onset of the ideal FiO2 phase. However, this finding does not seem to have clinical significance, as the VT value considered ideal during weaning from mechanical ventilation ranges from 4 to 6 mL/kg of ideal weight. One reason for reduction in VT is the inhibition of chemoreceptors through reduction of PaCO2. In our study, no significant variation was observed in PaCO2 levels during the different FiO2 regimens used. This may be due to the fact that patient respiratory patterns did not change. Values of average lactate and Ti/Ttot ratio remained within ranges considered normal with both FiO2 levels and no significant differences between them was found.

Unlike our results, Volta et al.(21) found that respiratory pattern and drive were modulated by variations in FiO2. The authors observed that reduction of FiO2 was associated to a significant increase of VT, f, P0.1 and dyspnea. However, differences of the ventilatory parameters used may explain the divergence from our results. Volta et al. compared predetermined FiO2 levels (21 and 30%) to the 40% FiO2 and found a significant difference only when FiO2 was decreased from 40 to 30%. The pressure support level used for similar VT in the two studies was also greater in the population of the Volta et al. study. This suggests that our patients were most likely at a greater mechanical advantage, which may have reflected positively on our results. In patients under adequate pressure support level, there is less overload on respiratory muscles, which translates to lower P0.1 values.(22) Differences in methods of measuring time applied to the variables may also have favored divergences between results. Pesenti et al.(23) found an increased hypoxic respiratory drive after 20 minutes, even when SpO2 was maintained at values considered adequate (90 to 95%). However, differences between the populations studied are also evident, especially because our patients were not under the effect of sedatives. The diagnostic heterogeneity of our population provides a greater clinical applicability of results. Furthermore, our patients were studied for a longer time than those of the studies cited, which may also have influenced findings.

Sensitivity to increase or decrease of oxygen level occurs through specialized chemoreceptor cells that regulate respiratory and cardiovascular response. This takes place acutely through activation of pre-existing proteins and chronically by regulation of genetic transcription.(24) However, hypoxic stimulation in the carotid body, only occurs where there is an important reduction in arterial oxygen content or when PaO2 is lower than 60 mmHg. This stimulates neurosecretion by the glomic cells and causes the sensation of dyspnea.(25) Although dyspnea was not objectively assessed in this study, there was no report of respiratory discomfort by patients and, upon inspection, no accessory muscle action was observed.

No significant HR alterations were observed in this study. Thomson et al.(26) found an increased HR when assessing the effect of hypoxemia on the cardiovascular function of healthy volunteers. However, these individuals were exposed to 80 percent SpO2, which is different from that in our population. Regarding MAP, a significantly higher value was observed in the first 30 minutes of the study. This may have occurred because patients were alert and possibly anxious in relation to the initial procedures of the study.

Absence of clinical and breathing pattern changes in our results may be explained by two main reasons. The first is that, at the time of the study, our patients no longer exhibited signs or symptoms of acute respiratory failure as demonstrated by a close to normal PaO2/ FiO2 . Despite this clinical condition, all patients were using a 40% baseline FiO2. Moreover, average PaO2 was higher than 65 mmHg in the population studied. Four patients had a PaO2 of less than 60 mmHg, which probably occurred due to the 2 to 4% variability presented by most pulse oximeters. Adjustment of FiO2 to an "ideal" value in this study was based on SpO2, however, blood gas analyses were used only for control of blood gas data. For that, purpose FiO2 was set at a value that would ensure a SpO2 of 92%. Oximeter variability may have caused an improper adjustment of FiO2 in these patients and therefore a PaO2 of less than 60 mmHg. Respiratory frequency and heart rate increased in these four patients, probably in response to hypoxemia. The ideal FiO2 should be higher than the adjusted, therefore risk of hypoxemia in these patients could be avoided if the SpO2 cut-off point were raised to 94%.(27,28)

There are some limitations in our study: (1) lack of a control group, (2) non-randomization of the patients studied and (3) non-assessment of the clinical outcome of these patients. According to Benchetrit,(7) choice of control individuals is difficult in studies that involve ventilatory alterations due to the considerable variability regarding the diverse components of the respiratory pattern. In order to minimize this bias, each individual served as his own control. Assessment of the clinical outcome of weaning patients submitted to different FiO2 levels could provide relevant information on oxygen use in this population. The total time of each patient on mechanical ventilation after data collection was not assessed, since this was not an objective of the present study.

CONCLUSION

This study suggests that FiO2 levels sufficient to ensure a SpO2 > 92% did not alter breathing patterns or trigger clinical changes in stable adult patients undergoing weaning from mechanical ventilation.

REFERENCES

  • 1. Crapo JD. Morphologic changes in pulmonary oxygen toxicity. Annu Rev Physiol. 1986;48:721-31.
  • 2. Barazzone C, Horowitz S, Donati YR, Rodriguez I, Piguet PF. Oxygen toxicity in mouse lung: pathways to cell death. Am J Respir Cell Mol Biol. 1998;19(4):573-81.
  • 3. Barazzone C, White CW. Mechanisms of cell injury and death in hyperoxia: role of cytokines and Bcl-2 family proteins. Am J Respir Cell Mol Biol. 2000;22(5):517-9.
  • 4. Scheufler KM. Tissue oxigenation and capacity to deliver O2 do the two go together? Transfus Apher Sci. 2004;31(1):45-54.
  • 5. Treacher DF, Leach RM. Oxygen transport-1. Basic principles. BMJ. 1998;317(7168):1302-6.
  • 6. Dick CR, Sassoon C. Patient-ventilator interactions. Clin Chest Med. 1996;17(3):423-38.
  • 7. Benchetrit G. Breathing pattern in humans: diversity and individuality. Respir Physiol. 2000;122(2-3):123-9.
  • 8. Bryan CL, Jenkinson SG. Oxygen toxicity. Clin Chest Med. 1988;9(1):141-52. Review.
  • 9. Durbin CG Jr, Wallace KK. Oxygen toxicity in the critically ill patient. Respir Care. 1993;38:739-53.
  • 10. Quinn DA, Moufarrej RK, Volokhov A, Hales CA. Interactions of lung stretch, hyperoxia, and MIP-2 production in ventilator-induced lung injury. J Appl Physiol. 2002;93(2):517-25.
  • 11. Sinclair SE, Altemeier WA, Matute-Bello G, Chi EY. Augmented lung injury due to interaction between hyperoxia and mechanical ventilation. Crit Care Med. 2004;32(12):2496-501.
  • 12. Weinberger B, Laskin DL, Heck DE, Laskin JD. Oxygen toxicity in premature infants. Toxicol Appl Pharmacol. 2002;181(1):60-7.
  • 13. Jackson RM. Molecular, pharmacologic, and clinical aspects of oxygen-induced lung injury. Clin Chest Med. 1990;11(1):73-86.
  • 14. Kallstrom TJ; American Association for Respiratory Care (AARC). AARC Clinical Practice Guideline: oxygen therapy for adults in the acute care facility--2002 revision & update. Respir Care. 2002;47(6):717-20.
  • 15. MacIntyre NR, Cook DJ, Ely EW Jr, Epstein SK, Fink JB, Heffner JE, Hess D, Hubmayer RD, Scheinhorn DJ; American College of Chest Physicians; American Association for Respiratory Care; American College of Critical Care Medicine. Evidence-based guidelines for weaning and discontinuing ventilatory support: a collective task force facilitated by the American College of Chest Physicians; the American Association for Respiratory Care; and the American College of Critical Care Medicine. Chest. 2001;120(6 Suppl):375S95S.
  • 16. MacIntyre NR, Epstein SK, Carson S, Scheinhorn D, Christopher K, Muldoon S; National Association for Medical Direction of Respiratory Care. Management of patients requiring prolonged mechanical ventilation: report of a NAMDRC consensus conference. Chest. 2005;128(6):3937-54.
  • 17. Steban A, Alía I, Ibañez J, Benito S, Tobin MJ. Modes of mechanical ventilation and weaning. A national survey of Spanish hospitals. The Spanish Lung Failure Collaborative Group. Chest. 1994;106(4):1188-93.
  • 18. Whitelaw WA, Derenne JP. Airway occlusion pressure. J Appl Physiol. 1993;74(4):1475-83. Review.
  • 19. Jubran A, Tobin MJ. Reliability of pulse oximetry in titrating supplemental oxygen therapy in ventilator-dependent patients. Chest. 1990;97(6):1420-5.
  • 20. Cakar N, Tuörul M, Demirarslan A, Nahun A, Adams A, Akýncý O, et al. Time required for partial pressure of arterial oxygen equilibration during mechanical ventilation after a step change in fractional inspired oxygen concentration. Intensive Care Med. 2001;27(4):655-9.
  • 21. Volta CA, Alvisi V, Bertacchini S, Marangoni E, Ragazzi R, Verri M, Alvisi R. Acute effects of hyperoxemia on dyspnoea and respiratory variables during pressure support ventilation. Intensive Care Med. 2006;32(2):223-9.
  • 22. Perrigault PF, Pouzeratte YH, Jaber S, Capdevila XJ, Hayot M, Boccara G, et al. Changes in occlusion pressure (P0.1) and breathing pattern during pressure support ventilation. Thorax. 1999;54(2):119-23.
  • 23. Pesenti A, Rossi N, Calori A, Foti G, Rossi GP. Effects of short-term oxygenation changes on acute lung injury patients undergoing pressure support ventilation. Chest. 1993;103(4):1185-9.
  • 24. Michiels C. Physiological and pathological responses to hypoxia. Am J Pathol. 2004;164(6):1875-82.
  • 25. Weir EK, López-Barneo J, Buckler KJ, Archer SL. Acute oxygen-sensing mechanisms. N Engl J Med. 2005;353(19):2042-55. Review.
  • 26. Thomson AJ, Drummond GB, Waring WS, Webb DJ, Maxwell SR. Effects of short-term isocapnic hyperoxia and hypoxia on cardiovascular function. J Appl Physiol. 2006;101(3):809-16.
  • 27. Perkins GD, McAuley DF, Giles S, Routledge H, Gao F. Do changes in pulse oximeter oxygen saturation predict equivalent changes in arterial oxygen saturation? Crit Care. 2003;7(4):R67.
  • 28. Van de Louw A, Cracco C, Cerf C, Harf A, Duvaldestin P, Lemaire F, Brochard L. Accuracy of pulse oximetry in the intensive care unit. Intensive Care Med. 2001;27(10):1606-13.
  • Autor para correspondência:

    Gisele do Carmo Leite Machado Diniz
    Centro Clínico de Fisioterapia da PUC Minas - Betim
    Rua do Rosário, 1.081. Bairro Angola
    32630-000 - Betim (MG), Brasil
    Fax: +55 (31) 3539-6820
    E-mail:
  • Publication Dates

    • Publication in this collection
      30 Oct 2009
    • Date of issue
      Aug 2009

    History

    • Accepted
      04 Sept 2009
    • Received
      04 Dec 2008
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