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 ( 8 8 3 ) 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
(ICU) ICU (acute respiratory failure ARF) [1~3] [4~8] COPD 2001 1 2002 12 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 ) 125 43] [15] ARF NPPV (simplified acute physiologic score SAPS) [16] 4 10 15 ICU ARF SAPS NPPV ARF NPPV (Venturi) < 150 NPPV ARF ( < 1 000 / 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, 00161 Rome, Italy; e-mail: monica. rocco@uniroma1. it Glasgow (Glasgow coma scale GCS) 8 ( < 80 mm Hg ) www.chestjournal.org.cn CHEST 2005 6 2 6 369
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
[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 > 200 12 (1) 1 ARF (x ± s, n = 19) P P / 49 14 51 14 0.27 HR/ min -1 114 20 114 20 0.98 [ (%)] 13 (68) 12 (63) 0.5 RR / min -1 37 5 37 11 1 SAPS 42 8 43 14 0.37 SAP / mm Hg 136 21 136 19 0.99 GCS 14 1 14 1 1 ph 7.43 0.08 7.42 0.07 0.70 [ (%)] PaCO 2 / mm Hg 41 10 41 15 0.97 8 (42) 8 (42) 0.63 101 34 109 34 0.44 8 (42) 8 (42) 0.63 ARF [ (%)] 3 (16) 3 (16) 0.67 7 (37) 8 (42) 0.49 ARDS 12 (63) 11 (58) 0.49 www.chestjournal.org.cn CHEST 2005 6 2 6 371
2 (x ± s, n = 19) P P 1 h [ (%)] 12 (63) 12 (63) 0.63 / cm H 2 O 15 2 15 2 0.30 [ (%)] (1) 7 (37) 14 (74) 0.02 PEEP / cm H 2 O 7 2 8 2 0.23 1 h 202 61 224 111 0.45 NPPV / d 3.7 2 3.3 1 0.4 178 61 247 131 0.04 NPPV / h d -1 13 6 11 3 0.15 1 h PaCO 2 / mm Hg 39 8 39 9 0.91 24 h 2.94 1.02 1.21 1.18 0.001 PaCO 2 / mm Hg 40 6 40 8 0.95 ICU / d 9 4 9 9 0.96 1 h ph 7.42 0.06 7.43 0.07 0.08 [ (%)] 9 (47) 7 (37) 0.37 ph 7.42 0.04 7.41 0.08 0.64 [ (%)] 1 h RR / min -1 27 4 27 9 0.96 5 (55) 3 (43) 0.5 RR / min -1 29 7 26 11 0.35 NPPV 4 (44) 1 (14) 0.23 1h HR / min -1 100 17 101 17 0.41 GCS < 8 3 (33) 3 (43) 0.54 HR / min -1 106 21 98 20 0.20 ICU [ (%)] 9 (47) 6 (31) 0.25 1h SAP / mmhg 135 15 135 20 0.98 [ (%)] 10 (53) 7 (37) 0.26 SAP / mmhg 128 16 137 13 0.06 (1) > 200 > 100 (63%) (P = 0.63)NPPV 1 24 h 14 (74%) NPPV 1.2 1 7 (37%) (P = 0.02) 2.9 1 (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 8 1 7 ~ 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
3 67% ICU (n = 19) 2 mo P [ (%)] 10 (53) 6 (31) 0.16 2.4 2 1 / ICU [ (%)] 5 / 5 (26) 3 / 2 (15) 0.34 2 / 2 (10) 3 / 2 (15) 0.5 7 / 7 (37) 4 / 3 (21) 0.23 NPPV [ (%)] 9 (47) 2 (10) 0.01 1 (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 www.chestjournal.org.cn CHEST 2005 6 2 6 373
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;137:1463 1493 ventilation. NY: McGraw-Hill 1994;711 747 ARDS ARF ( ) NPPV 4 Estopa R, et al. Crit Care Med 1984;12:26 28 5 Blot F, et al. Eur J Cancer 1997;33:1031 1037 NPPV 6 Ewing S, et al. Eur Respir J 1998;12:16 122 NPPV 163:281 291 10 Antonelli M, et al. JAMA 2000;283:235 241 11 Hilbert G, et al. N Engl J Med 2001;344:481 487 12 Tognet E, et al. Clin Intensive Care 1994;282 288 2 Stauffer JL. In: Tobin MJ Principles and practice of mechanical 3 Chantila WM, et al. Respir Care Clin N Am 2002;8:631 647 7 Confalonieri M, et al. Intensive Care Med 2002;28:1233 1238 8 Rubenfeld GD, et al. Ann Intern Med 1996;125:625 633 9 American Thoracic Society, et al. Am J Respir Crit Care Med 2002; 13 Conti G, et al. Intensive Care Med 1998;24:1283 1288 14 Rocco M, et al. Intensive Care Med 2001;27:1622 1626 ( ) 15 Antonelli M, et al. Crit Care Med 2002;30:602 608 16 Le Gall JR, et al. JAMA 1993;270:2957 2963 17 Antonelli M, et al. Intensive Care Med 2001;27:1718 1728 [29] 19 Meduri GU, et al. Chest 1992;102 (Suppl):557S 564S 20 Bone RC, et al. Chest 1992;101:1644 1655 12 y 22 Antonelli M, et al. N Engl J Med 1998;339:429 435 NPPV 200 700 State University Press, 1967 24 Richards MJ, et al. Crit Care Med 1999;27:887 892 25 Vincent JL, et al. JAMA 1995;274:639 644 26 Cook DJ, et al. JAMA 1998;279:1605 1606 27 Bregeon F, et al. Anesthesiology 2001;94:554 560 18 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;342:1301 1308 21 Bernard GR, et al. Am J Respir Crit Care Med 1994; 149:818-824 23 Snedecor GW, et al. Statistical methods. Sixth ed. Ames, IA: Iowa 374
28 Heyland DK, et al. Am J Respir Crit Care Med 1999;159:1249 1256 29 Sacks H, et al. Am J Med 1982;72:233 240 30 Antonelli M, et al. Anesthesiology 2004;100:16 24 CHEST 2004;126:1508-1515 CHEST No.21 359 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. www.chestjournal.org.cn CHEST 2005 6 2 6 375