ARF. 8 8 (PaO 2 / FIO 2 ) NPPV NPPV ( P = 0.37) NPPV NPPV. (PaO 2 / FIO 2 > 200 PaO 2 / FIO 2 NPPV > 100) (P = 0.02) NPPV ( NPPV P = 0.

Transcription

1 Monica Rocco, MD; Donatella Dell'Utri, MD; Andrea Morelli, MD; Gustavo Spadetta, MD; Giorgio Conti, MD; Massimo Antonelli, MD; and Paolo Pietropaoli, MD (ARF) (NPPV) 19 ARF ( ) NPPV 19 (PaO 2 / FIO 2 ) NPPV NPPV ( 37% 47%; P = 0.37) 7 (34%) NPPV 14 (74%) NPPV (PaO 2 / FIO 2 > 200 PaO 2 / FIO 2 > 100) (P = 0.02) NPPV (P = 0.02) NPPV ( P = 0.01) NPPV 1 24 h NPPV NPPV (P < 0.001) ARF NPPV ( NPPV ) NPPV (immunocompromised patients); (noninvasive ventilation); (pneumonia) 368

2 (ICU) ICU (acute respiratory failure ARF) [1~3] [4~8] COPD ICU (12 [9] [10,11] ) ARF [12~14] ARF (noninvasive positive pressure ventilation NPPV) NPPV ARF NPPV NPPV 3 y [ ARDS ICU 45 ARF (PaO 2 / FIO 2 ) ] [15] ARF NPPV (simplified acute physiologic score SAPS) [16] ICU ARF SAPS NPPV ARF NPPV (Venturi) < 150 NPPV ARF ( < / µl) (respiratory rate RR) > 30 / min From the Department of Intensive Care (Drs. Rocco, Dell'Utri, Morelli, Spadetta, and Pietropaoli), University of Rome La Sapienza ; and Department of Intensive Care (Drs. Conti and Antonelli), Catholic University of Rome, Rome, Italy. Correspondence to: Monica Rocco, MD, Dipartimento di Anestesia e Rianimazione, Policlinico Umberto Iº, Viale del Policlinico 155, Rome, Italy; monica. rocco@uniroma1. it Glasgow (Glasgow coma scale GCS) 8 ( < 80 mm Hg ) CHEST

3 5 L / s 45º (Castar; Starmed; Mirandola, Italy) NPPV (Vital Sign; Towota, NJ) NPPV Siemens 300 (Siemens; Uppsala, Sweden) 10 cm H 2 O 7 ~ 9 ml / kg < 25 / min [15] PEEP 2 ~ 3 cm H 2 O 3 12 cm H 2 O FIO 2 28 ~ 33cm > 90% 34 ~ 39cm 40 ~ 45cm 5 L / s 45º ( 1) 10 cm H 2 O NPPV 2 ~ 3 cm H 2 O 1995 ICU [10] RR < 25 / min ARF NPPV NPPV 1 24 h NPPV NPPV NPPV 50% ~ 60% (positive end-expiratory pressure FIO 2 = PEEP) 2 ~ 3 cm H 2 O 0.5 < 88% 12 cm H 2 O FIO 2 NPPV 1 24 h > 90% NPPV RR < 25 / min > 160 > 24 h 1 NPPV > 100 (GCS 8) ( < 80 mm Hg ) NPPV 370

4 [17] [10,22] ARF NPPV > 100 NPPV 1 h ( ) 2 ICU / ICU ARDS [18] ; x ± s Student t Mantel-Haenszel χ 2 / ARDS Mann-Whitney Fisher [23] (ventilator-associated pneumonia VAP) [19~21] 1h PaCO 2 ph RR (heart rate HR) 19 ARF (systolic arterial pressure SAP) NPPV 19 NPPV 17 (89%) 4 2 (11%) 3 1h ARF ( 1) ( ) ( ) NPPV 1 > (1) 1 ARF (x ± s, n = 19) P P / HR/ min [ (%)] 13 (68) 12 (63) 0.5 RR / min SAPS SAP / mm Hg GCS ph [ (%)] PaCO 2 / mm Hg (42) 8 (42) (42) 8 (42) 0.63 ARF [ (%)] 3 (16) 3 (16) (37) 8 (42) 0.49 ARDS 12 (63) 11 (58) CHEST

5 2 (x ± s, n = 19) P P 1 h [ (%)] 12 (63) 12 (63) 0.63 / cm H 2 O [ (%)] (1) 7 (37) 14 (74) 0.02 PEEP / cm H 2 O h NPPV / d NPPV / h d h PaCO 2 / mm Hg h PaCO 2 / mm Hg ICU / d h ph [ (%)] 9 (47) 7 (37) 0.37 ph [ (%)] 1 h RR / min (55) 3 (43) 0.5 RR / min NPPV 4 (44) 1 (14) h HR / min GCS < 8 3 (33) 3 (43) 0.54 HR / min ICU [ (%)] 9 (47) 6 (31) h SAP / mmhg [ (%)] 10 (53) 7 (37) 0.26 SAP / mmhg (1) > 200 > 100 (63%) (P = 0.63)NPPV 1 24 h 14 (74%) NPPV (37%) (P = 0.02) (P < 0.001) NPPV PaCO 2 ph RR NPPV ICU 7 (37%) 9 (47%) NPPV (P = 0.37) 3 (43%) 1 5 (55%) (P = (3.7 2) d P = 0.4 (11 3) (13 6) h / d P = 0.15] ( 2) 15 NPPV 0.5) 3 ( 43% 33% P = 3 9 (47%) 0.5) GCS ~ 10 d 2 (14%) 4 (44%) NPPV (P = 0.01) (P = 0.23) 3 (41 28) h NPPV 3 (15%) 2 (10%) VAP (P = 5 (36 32) h 0.5) (P = 0.41) PEEP [(8 2) (7 2) cm H 2 O P = 0.23] [(15 2) (15 2) cm H 2 O P = 0.30] NPPV [(3.3 1) ARF NPPV 372

6 3 67% ICU (n = 19) 2 mo P [ (%)] 10 (53) 6 (31) / ICU [ (%)] 5 / 5 (26) 3 / 2 (15) / 2 (10) 3 / 2 (15) / 7 (37) 4 / 3 (21) 0.23 NPPV [ (%)] 9 (47) 2 (10) (0.5) 0 (0) 0.5 [10,11] ARF NPPV Antonelli [10] 40 ARF NPPV NPPV ICU Hilbert [11] ARF NPPV NPPV NPPV NPPV ICU ARF < 150 ARF [10,11] ICU ( < 200) NPPV NPPV NPPV 1 24 h NPPV ICU Antonelli [10] Hillbert [1~3] [11] ARF NPPV [5~8] [24,25] VAP 45 min 3 h [26~28] [7,12~14] NPPV Tognet [12] ARF NPPV ARF [11] 33% ICU ICU Conti [13] 16 ICU ARF NPPV ICU ARF Rocco [14] [15] 21 ARF NPPV ( ARDS [14] 18 AIDS ) ARF [7] NPPV NPPV CHEST

7 NPPV NPPV ARF COPD [30] COPD NPPV NPPV ARF CO 2 ARF ARF NPPV 18 ~ 48 h NPPV NPPV 1 24 h NPPV ( NPPV ARF PEEP FIO 2 1 Pingleton S. Am Rev Respir Dis 1988;137: ventilation. NY: McGraw-Hill 1994; ARDS ARF ( ) NPPV 4 Estopa R, et al. Crit Care Med 1984;12: Blot F, et al. Eur J Cancer 1997;33: NPPV 6 Ewing S, et al. Eur Respir J 1998;12: NPPV 163: Antonelli M, et al. JAMA 2000;283: Hilbert G, et al. N Engl J Med 2001;344: Tognet E, et al. Clin Intensive Care 1994; Stauffer JL. In: Tobin MJ Principles and practice of mechanical 3 Chantila WM, et al. Respir Care Clin N Am 2002;8: Confalonieri M, et al. Intensive Care Med 2002;28: Rubenfeld GD, et al. Ann Intern Med 1996;125: American Thoracic Society, et al. Am J Respir Crit Care Med 2002; 13 Conti G, et al. Intensive Care Med 1998;24: Rocco M, et al. Intensive Care Med 2001;27: ( ) 15 Antonelli M, et al. Crit Care Med 2002;30: Le Gall JR, et al. JAMA 1993;270: Antonelli M, et al. Intensive Care Med 2001;27: [29] 19 Meduri GU, et al. Chest 1992;102 (Suppl):557S 564S 20 Bone RC, et al. Chest 1992;101: y 22 Antonelli M, et al. N Engl J Med 1998;339: NPPV State University Press, Richards MJ, et al. Crit Care Med 1999;27: Vincent JL, et al. JAMA 1995;274: Cook DJ, et al. JAMA 1998;279: Bregeon F, et al. Anesthesiology 2001;94: Ventilation with lower tidal volumes for acute lung injury and the acute respiratory distress syndrome: the Acute Respiratory Distress Syndrome Network. N Engl J Med 2000;342: Bernard GR, et al. Am J Respir Crit Care Med 1994; 149: Snedecor GW, et al. Statistical methods. Sixth ed. Ames, IA: Iowa 374

8 28 Heyland DK, et al. Am J Respir Crit Care Med 1999;159: Sacks H, et al. Am J Med 1982;72: Antonelli M, et al. Anesthesiology 2004;100:16 24 CHEST 2004;126: CHEST No CHEST D. Arterial PCO 2 is reduced. Pregnancy produces a variety of anatomic and functional changes to the respiratory system. Hormonal changes affect the upper airway, causing hyperemia, edema, and increased friability. The anatomy of the thoracic cage is altered by the expanding uterus and by hormonally induced ligamentous laxity. Although the diaphragm is displaced upwards, this is usually offset by an increase in the anteroposterior and transverse diameters and widening of the subcostal angle. In healthy pregnant individuals,there is usually a 20 to 30% fall in arterial PCO 2 to 28 to 32 mm Hg (therefore, choice D is correct). An increase in respiratory drive due to elevated serum progesterone levels is partly responsible and causes a state of relative hyperventilation that exceeds that required by the increase in metabolic CO 2 production that also occurs with pregnancy. Similarly, tidal volume increases beginning in the first trimester and reaches 30 to 35% above baseline at term (choice C). In health, measurements of airflow are not significantly affected by pregnancy, because the increased diameter of the thoracic cage results in an increase in inspiratory capacity and preservation of FEV 1 and vital capacity (choice A). Other anatomical changes in pregnancy produce alterations in lung volume that are measurable at 16 to 24 weeks gestation. Elevation of the diaphram and the gravid uterus cause a reduction of expiratory reserve volume by 8 to 40% and a decrease in residual volume by 7 to 22%. This is turn leads to a progressive decease in functional residual capacity (FRC) that reaches 10 to 25% by term (choice B). Despite these anatomical changes, alveolar-to-arterial oxygen tension gradient is similar to non-pregnant values, and mean arterial PO 2 is usually greater than 100 mm Hg in healthy individuals (choice E). Mild hypoxemia may develop in the supine position as FRC decreases near term, but more importantly, oxygen consumption also increases, reaching 20 to 30% above baseline at term. This combination can make the pregnant patient susceptible to the rapid development of hypoxia in the event of hypoventilation or apnea. CHEST