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11 Acute Respiratory Distress Syndrome and Lung Protective Ventilation
119
There has also been substantial interest in the role of conservative fl uid management strategies in the treatment of patients with ARDS. The state of increased microvascular permeability present in ARDS potentiates pulmonary edema that may be caused by increased hydrostatic pressure associ­ated with fl uid administration [ 95 , 96 ]. In 2006, the ARDS Network published a comparison of conservative and liberal strategies of fl uid management [
97 ]. There was no signifi -
cant difference in 60-day mortality, but the conservative strategy demonstrated improved oxygenation and decreased duration of MV [ 97 ]. In patients with ARDS who are also hypoproteinemic, albumin administration in conjunction with diuretics in a conservative fl uid management strategy may also improve oxygenation but is not associated with improved survival [ 98 , 99 ]. In surgical and trauma patient populations, however, the role of conservative fl uid manage­ment is usually limited, since it is not recommended for patients who are hypotensive, are oliguric, have recently received vasopressors, or have a central venous pressure (CVP) <4 mmHg [ 91 , 97 , 100 , 101 ].
Corticosteroid utilization to address the fi bro-proliferative and infl ammatory response in ARDS continues to generate debate. Yet another ARDS Network trial examined the use of methylprednisolone in established courses of ARDS (at least 14 days after onset) and, despite improvements in oxygen­ation and reduced duration of MV, showed a signifi cant increase in 60- and 180-day mortality [ 102 ]. Conversely, a later study suggested a trend toward decreased mortality, but patients in this study received corticosteroids early (within 72 h of being diagnosed with ARDS) [ 103 ]. Meta-analysis has confi rmed a trend toward, and in some cases a statisti­cally signifi cant, reduction in mortality with the use of early corticosteroids, without any increase in infectious or CIM complications [ 104 , 105 ]. As a result of the current evidence, a long course (at least 14 days) of methylprednisolone administration, followed by gradual weaning, may be con­sidered in patients with early severe ARDS [ 106 , 107 ].
Inhaled nitric oxide (iNO) improves oxygenation due to selective pulmonary vasodilation, which improves ventila­tion perfusion (V/Q) mismatch and decreases pulmonary arterial pressure [ 91 ]. It has been shown in multiple trials and meta-analyses to improve short-term oxygenation in patients with ARDS but without any impact on duration of MV or mortality [ 108115 ]. The use of iNO should be limited to short-term rescue for life-threatening hypoxemia [ 25 , 91 ]. Inhaled prostacyclins have been investigated as alternatives to iNO, due to their lower cost and similar effects on oxygenation, though evidence to support their use is lacking [ 91 , 110 , 116 ].
Another strategy to improve outcomes in patients with severe refractory hypoxemia in ARDS is prone positioning. The mechanism of improvement is again multifactorial, including increased alveolar recruitment and ventilation in
the dorsal pulmonary segments, decreased shunt physiology, and decreased pulmonary compression by the heart [ 117 , 118 ]. Early studies consistently showed prone posi- tioning to improve oxygenation and gas exchange; however, mortality benefi ts were not shown [ 119122 ]. Subsequent meta- analysis, though, demonstrated improved mortality in patients with severe ARDS [ 123 , 124 ]. This prompted fur- ther investigation in the Proning Severe ARDS Patients (PROSEVA) trial, an RCT that showed signifi cant reduction in mortality in patients with PaO 2 /FiO 2 < 150 who were proned within 48 h of diagnosis of ARDS, for at least 16 consecutive hours/day up to 28 days (16.0 % vs. 32.8 %, p < 0.001), with no increase in complications compared to patients who were supine [ 125 ].
ECLS has been perhaps the most controversial adjunct to MV in patients with severe ARDS. ICUs that offer ECLS are specialized centers with focused providers. The goal is to allow for complete gas exchange by means of an extracorpo­real membrane oxygenation (ECMO) circuit while minimiz­ing VILI by using minimal settings on the ventilator, thus allowing “lung rest”[ 126 ]. Veno-venous ECMO (V-V ECMO) is most commonly used in isolated respiratory fail­ure and employs large central venous catheters (via jugulo­femoral or bifemoral placement) to remove blood from the body, circulate it through an oxygenator that allows for gas exchange, and return oxygenated blood to the patient [ 127 , 128 ]. For years, the only data showing positive results for ECMO in adults were retrospective studies [ 129132 ]. However, most recently, a multicenter prospective RCT (Conventional ventilation or ECMO for Severe Adult Respiratory failure, or CESAR) compared referral to an ECMO center to conventional treatment and showed improved 6-month mortality (63 % vs. 47 %; RR 0.69; 95 % CI 0.05–0.97; p = 0.03) [ 133 ]. Interestingly, only 75 % of the patients referred were actually placed on ECMO, which begs the question whether the survival benefi t was due to ECMO per se or simply transfer to a facility with greater resources and expertise. Despite criticisms of the CESAR trial, it has sparked new debate regarding the advantages of ECMO. Especially relevant to the surgical patient population are reports of its successful use in patients with TBI and mul­tiple injuries, in which heparin-bonded circuits may be used in order to forgo systemic anticoagulation [ 134137 ]. However, restraint is still advised, as the optimal techniques and clinical indications for ECLS continue to be clarifi ed [ 138 , 139 ].
In summary, many adjuncts to MV have been used in the treatment of ARDS and continue to undergo rigorous inves­tigation. While some have demonstrated improvements in mortality, all the adjuncts discussed here have demonstrated improvements in oxygenation. As a result, these therapies may be considered in the setting of life-threatening hypox­emia despite optimized MV.
120
S.E. Greer et al.

Intraoperative MV: A Setup for Disaster?

Although lung protective ventilation is the standard of care in ICU patients with ARDS, it is still not widely practiced in the operating room (OR) – in fact, the use of high V T and zero PEEP is still commonplace, with fewer than 20 % of patients receiving protective ventilation in routine anesthetic practice [ 140 , 141 ].
Early studies that investigated intra operative factors asso- ciated with post operative pulmonary complications (PPC) focused primarily on patient variables (age, smoking, arterial- alveolar differences, and pulmonary function tests (PFTs)), surgical events (estimated blood loss and transfu­sion volumes), and types of procedures (vascular, cardiac, abdominal), rather than the impact of MV itself on outcomes [ 142144 ]. Even in a trial designed specifi cally to defi ne risk factors for postoperative morbidity, parameters for MV during surgery were not examined [ 142 ]. Though there are currently no standardized guidelines for intraoperative MV, it is becoming increasingly clear that lung protective ventila­tion is one of the many important modalities associated with postoperative outcomes [ 145147 ].
General anesthesia can result in both atelectasis and decreased pulmonary blood fl ow [ 148 ]. Intra-abdominal sur- gery can induce atelectasis due to the direct pressure of the operative fi eld onto the (basilar) lungs. Atelectasis may also be present with lateral positioning, Trendelenburg, lithot­omy, or intra-abdominal insuffl ation – even in patients who are previously healthy. Within 5 min of induction of anesthe­sia, increased densities have been shown in the dependent regions of both lungs [ 149 ]. Furthermore, pulmonary blood fl ow may be reduced for several reasons: systemic vasodila­tion, high V T ventilation, patient position (blood fl ow may be decreased to nondependent areas), or HPV. HPV occurs when the partial pressure of oxygen in a given lung region falls, and vascular smooth muscle in the pulmonary circula­tion contracts in an effort to maintain V/Q matching. Vasodilators (including inhaled anesthetics) inhibit HPV [ 150 ] and may thus contribute to an increase in the shunt fraction; conversely, intravenous anesthetics do not have this effect [ 151 ].
Evidence supporting intraoperative lung protective venti­lation strategies to improve oxygenation and respiratory mechanics, and to decrease PPC, has now been shown in sev­eral studies [ 152156 ]. One prospective RCT in patients undergoing open abdominal surgery compared protective MV ( V T 7 mL/kg, PEEP 10 cm H 2 O with RMs) to “standard” ventilation ( V T 9 mL/kg, zero PEEP): patients in the protec­tive MV group had improved oxygenation, better PFTs, and fewer alterations in chest X-ray (CXR) postoperatively [ 145 ]. Recent meta-analysis also demonstrated an associa- tion between lower V T and decreased rates of PPC (2.0 % vs.
4.7 %; RR 0.40; 95 % CI 0.22–0.70) [
146 ].
To further confi rm this fi nding in a large RCT, the Intraoperative Protective Ventilation (IMPROVE) investiga­tors studied patients undergoing major abdominal surgery, with risk factors for PPC [ 147 ]. During anesthesia, patients were randomized to protective ventilation ( V PEEP 6–8 cm H ( V
10–12 mL/kg, zero PEEP, and no RMs). Over the 7-day
T
O with RMs) vs. non-protective ventilation
2
6–8 mL/kg,
T
postoperative study period, 5.0 % of patients in the protective group compared to 17.0 % of patients in the non-protective group required noninvasive ventilation (NIV) or intubation (RR 0.29; 95 % CI 0.14–0.61; p = 0.001). The protective ven- tilation group also demonstrated a signifi cantly shorter hos­pital stay (mean difference −2.45 days; 95 % CI −4.17 to
−0.72; p = 0.006) [ 147 ].
Once again, however, parsing the relative contributions of V T and PEEP has not been straightforward. Several meta- analyses have shown a benefi cial effect of higher PEEP: it has been associated with decreased rates of PPC (1.4 % vs. 4.9 %; RR 0.29; 95 % CI 0.14–0.60) [ 146 ] and reduced postoperative atelectasis [ 157 ]. However, this was not confi rmed in the large PROtective Ventilation ( PROVE) Network trial comparing high vs. low PEEP in the OR [ 158 ]. In 30 centers across Europe, North, and South America, patients at high risk of PPC undergoing abdominal procedures were randomized to high (12 cm H 2 O) or low (2 cm H 2 O) PEEP, using a consistent V T of 8 mL/kg. PPC were seen in 40 % of patients in the high PEEP group and in 39 % in the low PEEP group; furthermore, patients in the high PEEP group had more hypotension and required more vasoactive medications [ 158 ].
The largest and most recent meta-analysis sought to clar­ify the role of intraoperative PEEP and the frequency of PPC [ 159 ]. As previously demonstrated, rates of PPC were lower in patients assigned to low V T – but there was no statistical difference between low V T /high PEEP and low V T /low PEEP (8.9 % vs. 12 %; adjusted RR 0.93; 95 % CI 0.64–1.37; p = 0.72) over the 2,127 patients analyzed. Furthermore, there was no dose-response relationship found between rates of PPC and level of PEEP ( R
2
= 0.08) [ 159 ]. The optimal level of PEEP in intraoperative ventilation, therefore, remains unclear.
It is worth noting that many of the studies referenced above refer to specifi c types of surgery (neurosurgery, tho­racic surgery, oncologic surgery, general surgery) and to patient populations with an increased risk of PPC due to pre­existing comorbidities. The healthy patient undergoing elec­tive surgery is not well studied with regard to optimal ventilator settings, and it is unknown if V T or PEEP impacts their postoperative outcomes. Finally, there is also a paucity of data on the intraoperative management of trauma and acute care surgery patients – who may have been healthy prior to their precipitating event but then develop an infl am­matory response and/or hemodynamic instability before they
11 Acute Respiratory Distress Syndrome and Lung Protective Ventilation
121
reach the operating room. Given the increased mortality and substantial economic burden of PPC, further research on their prevention could have a great impact [
160 ].

Summary

ARDS and PPC in surgical patients contribute substantially to mortality and to the economic burden on the health-care system – although progress has been made, and ARDS has shown recent declines. The Berlin Defi nition for ARDS will help clarify populations of interest in future studies. At pres­ent, the standard of care in MV for patients with ARDS remains an open lung protective ventilation strategy, with low V T and relatively higher PEEP. A more nuanced under­standing of the effect of pressure settings is beginning to emerge and may further delineate the most benefi cial aspects of MV. Additionally, as further evidence accumulates, the prevention rather than the treatment of both ARDS and VILI may ultimately prove to be most effi cacious, with strategies such as early APRV holding great promise. Finally, in the comprehensive management of critically ill surgical patients, the lines between ICU and OR often blur – making recent investigations of intraoperative lung protective strategies all the more important. Despite the already vast literature, there is more work to be done.

References

1. Ashbaugh D, Bigelow DB, Petty T, Levine B. Acute respiratory distress in adults. Lancet. 1967;290(7511):319–23.
2. Bernard GR, Artigas A, Brigham KL, Carlet J, Falke K, Hudson L, et al. The American-European Consensus Conference on ARDS. Defi nitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med. 1994;149(3):818–24.
3. ARDS Defi nition Task Force, Ranieri VM, Rubenfeld GD, Thompson BT, Ferguson ND, Caldwell E, et al. Acute respiratory distress syndrome: the Berlin defi nition. JAMA. 2012;307(23): 2526–33.
4. Ferguson ND, Fan E, Camporota L, Antonelli M, Anzueto A, Beale R, et al. The Berlin defi nition of ARDS: an expanded ratio­nale, justifi cation, and supplementary material. Intensive Care Med. 2012;38(10):1573–82.
5. Ware LB, Matthay MA. The acute respiratory distress syndrome. N Engl J Med. 2000;342(18):1334–49.
6. Hedenstierna G, Strandberg A, Brismar B, Lundquist H, Svensson L, Tokics L. Functional residual capacity, thoracoabdominal dimensions, and central blood volume during general anesthesia with muscle paralysis and mechanical ventilation. Anesthesiology. 1985;62(3):247–54.
7. Carney D, DiRocco J, Nieman G. Dynamic alveolar mechanics and ventilator-induced lung injury. Crit Care Med. 2005; 33(Supplement):S122–8.
8. Gajic O, Dabbagh O, Park PK, Adesanya A, Chang SY, Hou P, et al. Early identifi cation of patients at risk of acute lung injury: evaluation of lung injury prediction score in a multicenter cohort study. Am J Respir Crit Care Med. 2011;183(4):462–70.
9. Rubenfeld GD, Caldwell E, Peabody E, Weaver J, Martin DP, Neff M, et al. Incidence and outcomes of acute lung injury. New Engl J Med. 2005;353(16):1685–93.
10. Martin M, Salim A, Murray J, Demetriades D, Belzberg H, Rhee P. The decreasing incidence and mortality of acute respira­tory distress syndrome after injury: a 5-year observational study. J Trauma. 2005;59(5):1107–13.
11. Li G, Malinchoc M, Cartin-Ceba R, Venkata CV, Kor DJ, Peters SG, et al. Eight-year trend of acute respiratory distress syndrome: a population-based study in Olmsted County, Minnesota. Am J Respir Crit Care Med. 2011;183(1):59–66.
12. Ferguson ND, Slutsky AS. Point: counterpoint: high-frequency ventilation is/is not the optimal physiological approach to venti­late ARDS patients. J Appl Physiol. 2008;104:1230–1.
13. Dos Santos CC, Slutsky AS. The contribution of biophysical lung injury to the development of biotrauma. Annu Rev Physiol. 2006;68:585–618.
14. Tremblay LN, Slutsky AS. Ventilation-induced lung injury: from barotrauma to biotrauma. Proc Assoc Am Physicians. 1998;110: 482–8.
15. Tremblay LN, Slutsky AS. Ventilator-induced lung injury: from the bench to the bedside. Intensive Care Med. 2006;32:24–33.
16. Fan E, Villar J, Slutsky AS. Novel approaches to minimize ventilator- induced lung injury. BMC Med. 2013;11(1):85.
17. Slutsky AS, Tremblay LN. Multiple system organ failure: is mechanical ventilation a contributing factor? Am J Respir Crit Care Med. 1998;157(6):1721–5.
18. Ranieri VM, Suter PM, Tortorella C, De Tullio R, Dayer JM, Brienza A, et al. Effect of mechanical ventilation on infl ammatory mediators in patients with acute respiratory distress syndrome: a randomized controlled trial. JAMA. 1999;282(1):54–61.
19. Lachmann B. Open up the lung and keep the lung open. Intensive Care Med. 1992;18(6):319–21.
20. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory dis­tress syndrome. N Engl J Med. 2000;342(18):1301–8.
21. Amato MBP, Barbas CSV, Medeiros DM, Magaldi RB, Schettino GP, Lorenzi-Filho G, et al. Effect of a protective-ventilation strat­egy on mortality in the acute respiratory distress syndrome. New Engl J Med. 1998;338(6):347–54.
22. Villar J, Kacmarek RM, Perez-Mendez L, Aguirre-Jaime A. A high positive end-expiratory pressure, low tidal volume ventila­tory strategy improves outcome in persistent acute respiratory dis­tress syndrome: a randomized, controlled trial. Crit Care Med. 2006;34(5):1311–8.
23. Burns K, Adhikari N, Slutsky AS, Guyatt GH, Villar J, Zhang H, et al. Pressure and volume limited ventilation for the ventilatory management of patients with acute lung injury: a systematic review and meta-analysis. PLoS One. 2011;6(1):e14623.
24. Briel M, Meade M, Mercat A, Brower RG, Talmor D, Walter SD, et al. Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome: systematic review and meta-analysis. JAMA. 2010;303(9): 865–73.
25. Hemmila MR, Napolitano LM. Severe respiratory failure: advanced treatment options. Crit Care Med. 2006;34(9 Suppl): S278–90.
26. Esan A, Hess DR, Raoof S, George L, Sessler CN. Severe hypox­emic respiratory failure: part 1—ventilatory strategies. Chest J. 2010;137(5):1203–16.
27. Amato MB, Meade MO, Slutsky AS, Brochard L, Costa EL, Schoenfeld DA, et al. Driving pressure and survival in the acute respiratory distress syndrome. N Engl J Med. 2015;372(8): 747–55.
28. Gattinoni L, Pesenti A. The concept of “baby lung”. Intensive Care Med. 2005;31(6):776–84.
122
S.E. Greer et al.
29. Fan E, Needham DM, Stewart TE. Ventilatory management of acute lung injury and acute respiratory distress syndrome. JAMA. 2005;294(22):2889–96.
30. Serpa Neto A, Cardoso SO, Manetta JA, Pereira VGM, Espósito DC, Pasqualucci Mde O, et al. Association between use of lung­protective ventilation with lower tidal volumes and clinical out­comes among patients without acute respiratory distress syndrome: a meta-analysis. JAMA. 2012;308(16):1651–9.
31. Webb HH, Tierney DF. Experimental pulmonary edema due to intermittent positive pressure ventilation with high infl ation pres­sures. Protection by positive end-expiratory pressure 1–4. Am Rev Res Dis. 1974;110(5):556–65.
32. Dreyfuss D, Basset G, Soler P, Saumon G. Intermittent positive­pressure hyperventilation with high infl ation pressures produces pulmonary microvascular injury in rats 1–3. Am Rev Res Dis. 1985;132(4):880–4.
33. Tsuno K, Miura K, Takeya M, Kolobow T, Morioka T. Histopathologic pulmonary changes from mechanical ventilation at high peak airway pressures. Am Rev Respir Dis. 1991;143(5 Pt 1):1115–20.
34. Eisner MD, Thompson BT, Schoenfeld D, Anzueto A, Matthay MA. Airway pressures and early barotrauma in patients with acute lung injury and acute respiratory distress syndrome. Am J Respir Crit Care Med. 2002;165(7):978–82.
35. Weg JG, Anzueto A, Balk RA, Wiedemann HP, Pattishall EN, Schork MA, et al. The relation of pneumothorax and other air leaks to mortality in the acute respiratory distress syndrome. N Engl J Med. 1998;338(6):341–6.
36. Anzueto A, Frutos–Vivar F, Esteban A, Alía I, Brochard L, Stewart T, et al. Incidence, risk factors and outcome of barotrauma in mechani­cally ventilated patients. Intensive Care Med. 2004;30(4):612–9.
37. Dreyfuss D, Soler P, Basset G, Saumon G. High infl ation pressure pulmonary edema: respective effects of high airway pressure, high tidal volume, and positive end-expiratory pressure. Am Rev Res Dis. 1988;137(5):1159–64.
38. Brower RG, Lanken PN, MacIntyre N, Matthay MA, Morris A, Ancukiewicz M, et al. Higher versus lower positive end- expiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med. 2004;351(4):327–36.
39. Meade MO, Cook DJ, Guyatt GH, Slutsky AS, Arabi YM, Cooper DJ, et al. Ventilation strategy using low tidal volumes, recruitment maneuvers, and high positive end-expiratory pressure for acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2008;299(6):637–45.
40. Mercat A, Richard J, Vielle B, Jaber S, Osman D, Diehl J, et al. Expiratory pressure (express) study group. Positive end- expiratory pressure setting in adults with acute lung injury and acute respira­tory distress syndrome: a randomized controlled trial. JAMA. 2008;299(6):646–55.
41. Lapinsky SE, Mehta S. Bench-to-bedside review: recruitment and recruiting maneuvers. Crit Care. 2005;9(1):60–5.
42. Fan E, Wilcox ME, Brower RG, Stewart TE, Mehta S, Lapinsky SE, et al. Recruitment maneuvers for acute lung injury: a system­atic review. Am J Respir Crit Care Med. 2008;178(11):1156–63.
43. Hess DR, Bigatello LM. Lung recruitment: the role of recruitment maneuvers. Respir Care. 2002;47(3):308–17; discussion 17–8.
44. Hickling K, Henderson S, Jackson R. Low mortality associated with low volume pressure limited ventilation with permissive hypercapnia in severe adult respiratory distress syndrome. Intensive Care Med. 1990;16(6):372–7.
45. Hickling KG, Walsh J, Henderson S, Jackson R. Low mortality rate in adult respiratory distress syndrome using low-volume, pressure-limited ventilation with permissive hypercapnia: a pro­spective study. Crit Care Med. 1994;22(10):1530–9.
46. Bidani A, Tzouanakis AE, Cardenas VJ, Zwischenberger JB. Permissive hypercapnia in acute respiratory failure. JAMA. 1994;272(12):957–62.
47. Bulger EM, Jurkovich GJ, Gentilello LM, Maier RV. Current clini­cal options for the treatment and management of acute respiratory distress syndrome. J Trauma Acute Care Surg. 2000;48(3):562–72.
48. Kregenow DA, Rubenfeld GD, Hudson LD, Swenson ER. Hypercapnic acidosis and mortality in acute lung injury. Crit Care Med. 2006;34(1):1–7.
49. Broccard AF, Hotchkiss JR, Vannay C, Markert M, Sauty A, Feihl F, et al. Protective effects of hypercapnic acidosis on ventilator- induced lung injury. Am J Respir Crit Care Med. 2001;164(5):802–6.
50. Metnitz PG, Metnitz B, Moreno RP, Bauer P, Del Sorbo L, Hoermann C, et al. Epidemiology of mechanical ventilation: analysis of the SAPS 3 database. Intensive Care Med. 2009;35(5):816–25.
51. Fessler HE, Derdak S, Ferguson ND, Hager DN, Kacmarek RM, Thompson BT, et al. A protocol for high-frequency oscillatory ventilation in adults: results from a roundtable discussion. Crit Care Med. 2007;35(7):1649–54.
52. Stawicki SP, Goyal M, Sarani B. High-frequency oscillatory ven­tilation (HFOV) and airway pressure release ventilation (APRV): a practical guide. J Intensive Care Med. 2009;24(4):215–29.
53. Greer SE, McCunn M. High-frequency oscillatory ventilation. Curr Probl Surg. 2013;50(10):471–8.
54. Derdak S, Mehta S, Stewart TE, Smith T, Rogers M, Buchman TG, et al. High-frequency oscillatory ventilation for acute respira­tory distress syndrome in adults: a randomized, controlled trial. Am J Respir Crit Care Med. 2002;166(6):801–8.
55. Bollen CW, van Well GT, Sherry T, Beale RJ, Shah S, Findlay G, et al. High frequency oscillatory ventilation compared with con­ventional mechanical ventilation in adult respiratory distress syn­drome: a randomized controlled trial [ISRCTN24242669]. Crit Care. 2005;9(4):R430–9.
56. Ferguson ND, Cook DJ, Guyatt GH, Mehta S, Hand L, Austin P, et al. High-frequency oscillation in early acute respiratory distress syndrome. New Engl J Med. 2013;368(9):795–805.
57. Young D, Lamb SE, Shah S, MacKenzie I, Tunnicliffe W, Lall R, et al. High-frequency oscillation for acute respiratory distress syn­drome. N Engl J Med. 2013;368(9):806–13.
58. Gu X, Wu G, Yao Y, Shi D, Song Y. In adult acute respiratory distress syndrome patients, is high-frequency oscillatory ventila­tion more effective and safer than conventional protective ventila­tion? A meta-analysis of randomized controlled trials. Crit Care. 2014;18:R111.
59. Malhotra A, Drazen JM. High-frequency oscillatory ventilation on shaky ground. N Engl J Med. 2013;368(9):863–5.
60. Downs J, Stock M. Airway pressure release ventilation: a new concept in ventilatory support. Crit Care Med. 1987;15(5):459.
61. Andrews P, Habashi N. Airway pressure release ventilation. Curr Probl Surg. 2013;50(10):462–70.
62. Maung AA, Kaplan LJ. Airway pressure release ventilation in acute respiratory distress syndrome. Crit Care Clin. 2011;27(3):501–9.
63. Protti A, Andreis DT, Monti M, Santini A, Sparacino CC, Langer T, et al. Lung stress and strain during mechanical ventilation: any difference between statics and dynamics? Crit Care Med. 2013;41(4):1046–55.
64. Putensen C, Zech S, WRIGGE H, Zinserling J, Stuber F, VON SPIEGEL T, et al. Long-term effects of spontaneous breathing during ventilatory support in patients with acute lung injury. Am J Respir Crit Care Med. 2001;164(1):43–9.
65. Wrigge H, Zinserling J, Neumann P, Muders T, Magnusson A, Putensen C, et al. Spontaneous breathing with airway pressure release ventilation favors ventilation in dependent lung regions and counters cyclic alveolar collapse in oleic-acid-induced lung injury: a randomized controlled computed tomography trial. Crit Care. 2005;9(6):R780.
66. Walkey AJ, Nair S, Papadopoulos S, Agarwal S, Reardon CC. Use of airway pressure release ventilation is associated with a reduced incidence of ventilator-associated pneumonia in patients with
11 Acute Respiratory Distress Syndrome and Lung Protective Ventilation
123
pulmonary contusion. J Trauma Acute Care Surg. 2011;70(3): E42–7.
67. Hering R, Bolten JC, Kreyer S, Berg A, Wrigge H, Zinserling J, et al. Spontaneous breathing during airway pressure release venti­lation in experimental lung injury: effects on hepatic blood fl ow. Intensive Care Med. 2008;34(3):523–7.
68. Hering R, Viehofer A, Zinserling J, Wrigge H, Kreyer S, Berg A, et al. Effects of spontaneous breathing during airway pressure release ventilation on intestinal blood fl ow in experimental lung injury. Anesthesiology. 2003;99(5):1137–44.
69. Kreyer S, Putensen C, Berg A, Soehle M, Muders T, Wrigge H, et al. Effects of spontaneous breathing during airway pressure release ven­tilation on cerebral and spinal cord perfusion in experimental acute lung injury. J Neurosurg Anesthesiol. 2010;22(4):323–9.
70. Neumann P, Wrigge H, Zinserling J, Hinz J, Maripuu E, Andersson LG, et al. Spontaneous breathing affects the spatial ventilation and perfusion distribution during mechanical ventilatory support*. Crit Care Med. 2005;33(5):1090–5.
71. Kaplan LJ, Bailey H, Formosa V. Airway pressure release ventila­tion increases cardiac performance in patients with acute lung injury/adult respiratory distress syndrome. Crit Care. 2001; 5(4):221.
72. Maung AA, Luckianow G, Kaplan LJ. Lessons learned from air­way pressure release ventilation. J Trauma Acute Care Surg. 2012;72(3):624–8.
73. Rasanen J, Cane RD, Downs JB, Hurst JM, Jousela IT, Kirby RR, et al. Airway pressure release ventilation during acute lung injury: a prospective multicenter trial. Crit Care Med. 1991;19(10): 1234–41.
74. Maxwell RA, Green JM, Waldrop J, Dart BW, Smith PW, Brooks D, et al. A randomized prospective trial of airway pressure release ventilation and low tidal volume ventilation in adult trauma patients with acute respiratory failure. J Trauma. 2010;69(3):501– 10; discussion 11.
75. Andrews PL, Shiber JR, Jaruga-Killeen E, Roy S, Sadowitz B, O’Toole RV, et al. Early application of airway pressure release ventilation may reduce mortality in high-risk trauma patients: a systematic review of observational trauma ARDS literature. J Trauma Acute Care Surg. 2013;75(4):635–41.
76. Varpula T, Valta P, Niemi R, Takkunen O, Hynynen M, Pettilä V. Airway pressure release ventilation as a primary ventilatory mode in acute respiratory distress syndrome. Acta Anaesthesiol Scand. 2004;48(6):722–31.
77. Dart IV BW, Maxwell RA, Richart CM, Brooks DK, Ciraulo DL, Barker DE, et al. Preliminary experience with airway pressure release ventilation in a trauma/surgical intensive care unit. J Trauma Acute Care Surg. 2005;59(1):71–6.
78. Navarrete-Navarro P, Rodriguez A, Reynolds N, West R, Habashi N, Rivera R, et al. Acute respiratory distress syndrome among trauma patients: trends in ICU mortality, risk factors, complications and resource utilization. Intensive Care Med. 2001;27(7):1133–40.
79. Roy S, Sadowitz B, Andrews P, Gatto LA, Marx W, Ge L, et al. Early stabilizing alveolar ventilation prevents acute respiratory distress syndrome: a novel timing-based ventilatory intervention to avert lung injury. The J Trauma Acute Care Surg. 2012;73(2): 391–400.
80. Roy S, Habashi N, Sadowitz B, Andrews P, Ge L, Wang G, et al. Early airway pressure release ventilation prevents ARDS-a novel preventive approach to lung injury. Shock. 2013;39(1):28–38.
81. Emr B, Gatto LA, Roy S, Satalin J, Ghosh A, Snyder K, et al. Airway pressure release ventilation prevents ventilator-induced lung injury in normal lungs. JAMA Surg. 2013;148(11):1005–12.
82. Smith BJ, Lundblad LK, Kollisch-Singule M, Satalin J, Nieman G, Habashi N, et al. Predicting the response of the injured lung to the mechanical breath profi le. J Appl Physiol. 2015;118(7): 932–40.
83. Warr J, Thiboutot Z, Rose L, Mehta S, Burry LD. Current thera­peutic uses, pharmacology, and clinical considerations of neuro­muscular blocking agents for critically ill adults. Ann Pharmacother. 2011;45(9):1116–26.
84. Hansen-Flaschen JH, Brazinsky S, Basile C, Lanken PN. Use of sedating drugs and neuromuscular blocking agents in patients requiring mechanical ventilation for respiratory failure: a national survey. JAMA. 1991;266(20):2870–5.
85. Mehta S, Burry L, Fischer S, Martinez-Motta JC, Hallett D, Bowman D, et al. Canadian survey of the use of sedatives, analge­sics, and neuromuscular blocking agents in critically ill patients*. Crit Care Med. 2006;34(2):374–80.
86. Gainnier M, Roch A, Forel JM, Thirion X, Arnal JM, Donati S, et al. Effect of neuromuscular blocking agents on gas exchange in patients presenting with acute respiratory distress syndrome. Crit Care Med. 2004;32(1):113–9.
87. Forel JM, Roch A, Marin V, Michelet P, Demory D, Blache JL, et al. Neuromuscular blocking agents decrease infl ammatory response in patients presenting with acute respiratory distress syn­drome. Crit Care Med. 2006;34(11):2749–57.
88. Papazian L, Forel J-M, Gacouin A, Penot-Ragon C, Perrin G, Loundou A, et al. Neuromuscular blockers in early acute respira­tory distress syndrome. N Engl J Med. 2010;363(12):1107–16.
89. Neto AS, Pereira VG, Esposito DC, Damasceno MC, Schultz MJ. Neuromuscular blocking agents in patients with acute respiratory distress syndrome: a summary of the current evidence from three randomized controlled trials. Ann Intensive Care. 2012;2(1):33.
90. Alhazzani W, Alshahrani M, Jaeschke R, Forel JM, Papazian L, Sevransky J, et al. Neuromuscular blocking agents in acute respi­ratory distress syndrome: a systematic review and meta-analysis of randomized controlled trials. Crit Care. 2013;17(2):R43.
91. Raoof S, Goulet K, Esan A, Hess DR, Sessler CN. Severe hypox­emic respiratory failure: part 2 – nonventilatory strategies. Chest. 2010;137(6):1437–48.
92. Hraiech S, Dizier S, Papazian L. The use of paralytics in patients with acute respiratory distress syndrome. Clin Chest Med. 2014;35(4):753–63.
93. Slutsky AS. Neuromuscular blocking agents in ARDS. New Engl J Med. 2010;363(12):1176–80.
94. Papazian L, Hraiech S. Spontaneous breathing in acute respiratory distress syndrome: friend and foe?*. Crit Care Med. 2013; 41(2):685.
95. Groeneveld AB. Vascular pharmacology of acute lung injury and acute respiratory distress syndrome. Vascul Pharmacol. 2002;39(4–5):247–56.
96. Arif SK, Verheij J, Groeneveld JA, Raijmakers PG. Hypoproteinemia as a marker of acute respiratory distress syndrome in critically ill patients with pulmonary edema. Intensive Care Med. 2002; 28(3):310–7.
97. Wiedemann H, Wheeler A, Bernard G, Thompson B, Hayden D, DeBoisblanc B, et al. National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network. Comparison of two fl uid-management strategies in acute lung injury. N Engl J Med. 2006;354(24):2564–75.
98. Martin GS, Moss M, Wheeler AP, Mealer M, Morris JA, Bernard GR. A randomized, controlled trial of furosemide with or without albumin in hypoproteinemic patients with acute lung injury. Crit Care Med. 2005;33(8):1681–7.
99. Finfer S, Bellomo R, Boyce N, French J, Myburgh J, Norton R, et al. A comparison of albumin and saline for fl uid resuscitation in the intensive care unit. N Engl J Med. 2004;350(22):2247–56.
100. Calfee CS, Matthay MA. Nonventilatory treatments for acute lung injury and ARDS*. Chest J. 2007;131(3):913–20.
101. Schuster KM, Alouidor R, Barquist ES. Nonventilatory interven­tions in the acute respiratory distress syndrome. J Intensive Care Med. 2008;23(1):19–32.
124
S.E. Greer et al.
102. Steinberg KP, Hudson LD, Goodman RB, Hough CL, Lanken PN, Hyzy R, et al. Effi cacy and safety of corticosteroids for persistent acute respiratory distress syndrome. New Engl J Med. 2006; 354(16):1671–84.
103. Meduri GU, Golden E, Freire AX, Taylor E, Zaman M, Carson SJ, et al. Methylprednisolone infusion in early severe ARDS results of a randomized controlled trial. Chest J. 2007;131(4):954–63.
104. Tang BM, Craig JC, Eslick GD, Seppelt I, McLean AS. Use of corticosteroids in acute lung injury and acute respiratory distress syndrome: a systematic review and meta-analysis. Crit Care Med. 2009;37(5):1594–603.
105. Peter JV, John P, Graham PL, Moran JL, George IA, Bersten A. Corticosteroids in the prevention and treatment of acute respi­ratory distress syndrome (ARDS) in adults: meta-analysis. BMJ. 2008;336(7651):1006–9.
106. Marik PE, Pastores SM, Annane D, Meduri GU, Sprung CL, Arlt W, et al. Recommendations for the diagnosis and management of corticosteroid insuffi ciency in critically ill adult patients: consen­sus statements from an international task force by the American College of Critical Care Medicine. Crit Care Med. 2008;36(6): 1937–49.
107. Marik PE, Meduri GU, Rocco PR, Annane D. Glucocorticoid treatment in acute lung injury and acute respiratory distress syn­drome. Crit Care Clin. 2011;27(3):589–607.
108. Dellinger RP, Zimmerman JL, Taylor RW, Straube RC, Hauser DL, Criner GJ, et al. Effects of inhaled nitric oxide in patients with acute respiratory distress syndrome: results of a randomized phase II trial. Crit Care Med. 1998;26(1):15–23.
109. Taylor RW, Zimmerman JL, Dellinger RP, Straube RC, Criner GJ, Davis Jr K, et al. Low-dose inhaled nitric oxide in patients with acute lung injury: a randomized controlled trial. JAMA. 2004; 291(13):1603–9.
110. Walmrath D, Schneider T, Schermuly R, Olschewski H, Grimminger F, Seeger W. Direct comparison of inhaled nitric oxide and aerosolized prostacyclin in acute respiratory distress syndrome. Am J Respir Crit Care Med. 1996;153(3):991–6.
111. Lundin S, Mang H, Smithies M, Stenqvist O, Frostell C. Inhalation of nitric oxide in acute lung injury: results of a European multi­centre study. Intensive Care Med. 1999;25(9):911–9.
112. Troncy E, Collet J-P, Shapiro S, Guimond J-G, Blair L, Ducruet T, et al. Inhaled nitric oxide in acute respiratory distress syndrome: a pilot randomized controlled study. Am J Respir Crit Care Med. 1998;157(5):1483–8.
113. Griffi ths MJD, Evans TW. Inhaled nitric oxide therapy in adults. New Engl J Med. 2005;353(25):2683–95.
114. Adhikari NK, Burns KE, Friedrich JO, Granton JT, Cook DJ, Meade MO. Effect of nitric oxide on oxygenation and mortality in acute lung injury: systematic review and meta-analysis. BMJ. 2007;334:779.
115. Adhikari NK, Dellinger RP, Lundin S, Payen D, Vallet B, Gerlach H, et al. Inhaled nitric oxide does not reduce mortality in patients with acute respiratory distress syndrome regardless of severity: system­atic review and meta-analysis*. Crit Care Med. 2014;42(2):404–12.
116. Lowson SM. Inhaled alternatives to nitric oxide. Crit Care Med. 2005;33(Supplement):S188–95.
117. Guerin C, Badet M, Rosselli S, Heyer L, Sab J-M, Langevin B, et al. Effects of prone position on alveolar recruitment and oxy­genation in acute lung injury. Intensive Care Med. 1999;25(11): 1222–30.
118. Albert RK, Hubmayr RD. The prone position eliminates compres­sion of the lungs by the heart. Am J Respir Crit Care Med. 2000;161(5):1660–5.
119. Gattinoni L, Tognoni G, Pesenti A, Taccone P, Mascheroni D, Labarta V, et al. Effect of prone positioning on the survival of patients with acute respiratory failure. New Engl J Med. 2001;345(8):568–73.
120. Guerin C, Gaillard S, Lemasson S, Ayzac L, Girard R, Beuret P, et al. Effects of systematic prone positioning in hypoxemic acute respiratory failure: a randomized controlled trial. JAMA. 2004;292(19):2379–87.
121. Taccone P, Pesenti A, Latini R, Polli F, Vagginelli F, Mietto C, et al. Prone positioning in patients with moderate and severe acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2009;302(18):1977–84.
122. Fridrich P, Krafft P, Hochleuthner H, Mauritz W. The effects of long-term prone positioning in patients with trauma-induced adult respiratory distress syndrome. Anesth Analg. 1996;83(6):1206–11.
123. Gattinoni L, Carlesso E, Taccone P, Polli F, Guerin C, Mancebo J. Prone positioning improves survival in severe ARDS: a patho­physiologic review and individual patient meta-analysis. Minerva Anestesiol. 2010;76(6):448–54.
124. Sud S, Friedrich JO, Taccone P, Polli F, Adhikari NK, Latini R, et al. Prone ventilation reduces mortality in patients with acute respiratory failure and severe hypoxemia: systematic review and meta-analysis. Intensive Care Med. 2010;36(4):585–99.
125. Guérin C, Reignier J, Richard J-C, Beuret P, Gacouin A, Boulain T, et al. Prone positioning in severe acute respiratory distress syn­drome. New Engl J Med. 2013;368(23):2159–68.
126. Gattinoni L, Pesenti A, Bombino M, Pelosi P, Brazzi L. Role of extracorporeal circulation in adult respiratory distress syndrome management. New Horiz. 1993;1(4):603–12.
127. Allen S, Holena D, McCunn M, Kohl B, Sarani B. A review of the fundamental principles and evidence base in the use of extracor­poreal membrane oxygenation (ECMO) in critically ill adult patients. J Intensive Care Med. 2011;26(1):13–26.
128. Gattinoni L, Carlesso E, Langer T. Clinical review: extracorporeal membrane oxygenation. Crit Care. 2011;15(6):243.
129. Hemmila MR, Rowe SA, Boules TN, Miskulin J, McGillicuddy JW, Schuerer DJ, et al. Extracorporeal life support for severe acute respiratory distress syndrome in adults. Ann Surg. 2004;240(4):595.
130. Kolla S, Awad SS, Rich PB, Schreiner RJ, Hirschl RB, Bartlett RH. Extracorporeal life support for 100 adult patients with severe respiratory failure. Ann Surg. 1997;226(4):544–64; discussion 65–6.
131. Peek GJ, Moore HM, Moore N, Sosnowski AW, Firmin RK. Extracorporeal membrane oxygenation for adult respiratory fail­ure. Chest J. 1997;112(3):759–64.
132. Nehra D, Goldstein AM, Doody DP, Ryan DP, Chang Y, Masiakos PT. Extracorporeal membrane oxygenation for nonneonatal acute respiratory failure: the Massachusetts General Hospital experi­ence from 1990 to 2008. Arch Surg. 2009;144(5):427–32.
133. Peek GJ, Mugford M, Tiruvoipati R, Wilson A, Allen E, Thalanany MM, et al. Effi cacy and economic assessment of conventional ven­tilatory support versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): a multicentre randomised controlled trial. Lancet (Lond, Engl). 2009;374(9698):1351–63.
134. Szerlip NJ, Bholat O, McCunn MM, Aarabi B, Scalea TM. Extracorporeal life support as a treatment for neurogenic pul­monary edema and cardiac failure secondary to intractable intra­cranial hypertension: a case report and review of the literature. J Trauma Acute Care Surg. 2009;67(3):E69–71.
135. Michaels AJ, Schriener RJ, Kolla S, Awad SS, Rich PB, Reickert C, et al. Extracorporeal life support in pulmonary failure after trauma. J Trauma Acute Care Surg. 1999;46(4):638–45.
136. Messing JA, Agnihothri RV, Van Dusen R, Najam F, Dunne JR, Honig JR, et al. Prolonged use of extracorporeal membrane oxy­genation as a rescue modality following traumatic brain injury. ASAIO J. 2014;60(5):597–9.
137. Neff LP, Cannon JW, Stewart IJ, Batchinsky AI, Zonies DH, Pamplin JC, et al. Extracorporeal organ support following trauma: the dawn of a new era in combat casualty critical care. J Trauma Acute Care Surg. 2013;75(2 Suppl 2):S120–8; discussion S8–9.
11 Acute Respiratory Distress Syndrome and Lung Protective Ventilation
125
138. MacLaren G, Combes A, Bartlett RH. Contemporary extracorpo­real membrane oxygenation for adult respiratory failure: life sup­port in the new era. Intensive Care Med. 2012;38(2):210–20.
139. Combes A, Brodie D, Bartlett R, Brochard L, Brower R, Conrad S, et al. Position paper for the organization of extracorporeal membrane oxygenation programs for acute respiratory failure in adult patients. Am J Respir Crit Care Med. 2014;190(5):488–96.
140. Jaber S, Coisel Y, Chanques G, Futier E, Constantin JM, Michelet P, et al. A multicentre observational study of intraoperative venti­latory management during general anaesthesia: tidal volumes and relation to body weight. Anaesthesia. 2012;67(9):999–1008.
141. Hess DR, Kondili D, Burns E, Bittner EA, Schmidt UH. A 5-year observational study of lung-protective ventilation in the operating room: a single-center experience. J Crit Care. 2013;28(4):533. e9–e15.
142. Hall J, Tarala R, Hall J, Mander J. A multivariate analysis of the risk of pulmonary complications after laparotomy. Chest J. 1991;99(4):923–7.
143. Jayr C, Matthay M, Goldstone J, Gold W, Wiener-Kronish J. Preoperative and intraoperative factors associated with pro­longed mechanical ventilation. A study in patients following major abdominal vascular surgery. Chest J. 1993;103(4):1231–6.
144. Mitchell C, Garrahy P, Peake P. Postoperative respiratory morbid­ity: identifi cation and risk factors. Aust N Z J Surg. 1982; 52(2):203–9.
145. Severgnini P, Selmo G, Lanza C, Chiesa A, Frigerio A, Bacuzzi A, et al. Protective mechanical ventilation during general anesthesia for open abdominal surgery improves postoperative pulmonary function. Anesthesiology. 2013;118(6):1307–21.
146. Hemmes SN, Serpa Neto A, Schultz MJ. Intraoperative ventila­tory strategies to prevent postoperative pulmonary complications: a meta-analysis. Curr Opin Anaesthesiol. 2013;26(2):126–33.
147. Futier E, Constantin J-M, Paugam-Burtz C, Pascal J, Eurin M, Neuschwander A, et al. A trial of intraoperative low-tidal-volume ventilation in abdominal surgery. New Engl J Med. 2013;369(5): 428–37.
148. Duggan M, Kavanagh BP. Pulmonary atelectasis: a pathogenic perioperative entity. Anesthesiology. 2005;102(4):838–54.
149. Brismar B, Hedenstierna G, Lundquist H, Strandberg Å, Svensson L, Tokics L. Pulmonary densities during anesthesia with muscular relaxation – a proposal of atelectasis. Anesthesiology. 1985;62(4):422–8.
150. Pagel PS, Fu JL, Damask MC, Davis RF, Samuelson PN, Howie MB, et al. Desfl urane and isofl urane produce similar alterations in
systemic and pulmonary hemodynamics and arterial oxygenation in patients undergoing one-lung ventilation during thoracotomy. Anesth Analg. 1998;87(4):800–7.
151. Van Keer L, Van Aken H, Vandermeersch E, Vermaut G, Lerut T. Propofol does not inhibit hypoxic pulmonary vasoconstriction in humans. J Clin Anesth. 1989;1(4):284–8.
152. Michelet P, D’Journo X-B, Roch A, Doddoli C, Marin V, Papazian L, et al. Protective ventilation infl uences systemic infl ammation after esophagectomy: a randomized controlled study. Anesthesiology. 2006;105(5):911–9.
153. Lin W-Q, Lu X-Y, Cao L-H, Wen L-L, Bai X-H, Zhong Z-J. Effects of the lung protective ventilatory strategy on proinfl ammatory cytokine release during one-lung ventilation. Ai Zheng. 2008; 27(8):870–3.
154. Licker M, Diaper J, Villiger Y, Spiliopoulos A, Licker V, Robert J, et al. Impact of intraoperative lung-protective interventions in patients undergoing lung cancer surgery. Crit Care. 2009; 13(2):R41.
155. Weingarten T, Whalen F, Warner D, Gajic O, Schears G, Snyder M, et al. Comparison of two ventilatory strategies in elderly patients undergoing major abdominal surgery. Br J Anaesth. 2009;104:16–22. aep319.
156. Yang M, Ahn HJ, Kim K, Kim JA, Chin AY, Kim MJ, et al. Does a protective ventilation strategy reduce the risk of pulmonary com­plications after lung cancer surgery?: a randomized controlled trial. Chest J. 2011;139(3):530–7.
157. Imberger G, McIlroy D, Pace NL, Wetterslev J, Brok J, Moller AM. Positive end-expiratory pressure (PEEP) during anaesthesia for the prevention of mortality and postoperative pulmonary com­plications. Cochrane Database Syst Rev. 2010;(9):CD007922.
158. Hemmes SN, de Abreu MG, Pelosi P, Schultz MJ, Severgnini P, Hollmann MW, et al. High versus low positive end-expiratory pressure during general anaesthesia for open abdominal surgery (PROVHILO trial): a multicentre randomised controlled trial. Lancet. 2014;384(9942):495–503.
159. Serpa NA, Hemmes S, Barbas C, Beiderlinden M, Biehl M, Binnekade J, et al. Protective versus conventional ventilation for surgery: a systematic review and individual patient data meta­analysis. Anesthesiology. 2015;123(1):66–78.
160. Shander A, Fleisher LA, Barie PS, Bigatello LM, Sladen RN, Watson CB. Clinical and economic burden of postoperative pul­monary complications: patient safety summit on defi nition, risk­reducing interventions, and preventive strategies. Crit Care Med. 2011;39(9):2163–72.

Noninvasive Ventilation in the Perioperative Period

Kimberly M. Ramonell , Richard P. Ramonell , and Kevin W. McConnell
1 2

Introduction and Physiology

Noninvasive ventilation (NIV) is defi ned as ventilatory sup­port that is delivered in a spontaneously breathing patient without establishing an endotracheal airway [ noninvasive ventilation is delivered through a tight-fi tting mask applied to the face.
Like mechanical ventilation via endotracheal intubation, the goals of positive pressure noninvasive ventilation are the same: correct the underlying respiratory abnormality by improving oxygenation, ventilation, or both. To accomplish this task, patients who have an indication for NIV are con­nected to a ventilator circuit via a nasal mask or face mask. Depending on the clinical scenario, the ventilator is then either set to a volume-controlled setting or a pressure- controlled set­ting. Earlier noninvasive ventilators used volume ventilation settings that allowed for the delivery of a specifi c volume dur­ing the inspiratory cycle and were shown to be associated with improvement in acute respiratory failure [ 2 , 3 ]. However, this mode is more diffi cult to tolerate for patients, and as the venti­lator automatically adjusts airway pressures to achieve a speci­fi ed volume, it can result in high inspiratory pressures and air leaks around the face or nose mask [ 4 ].
Since the early 1990s, pressure-controlled settings have been more commonly utilized, and their success has been demonstrated across levels of care and a variety of indications. Specifi cally, continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BPAP) are the two most com­monly used modes of noninvasive ventilation both of which can be delivered either by standard ICU ventilators or portable
K. M. Ramonell , MD • K. W. McConnell , MD (*) Department of General Surgery , Emory University Hospital , Atlanta , GA 30322 , USA
kmhemph@emory.edu; kevin.w.mcconnell@emory.edu
e-mail: R. P. Ramonell , MD
Department of Internal Medicine , Emory University Hospital , Atlanta , GA 30322 , USA
richard.paul.ramonell@emory.edu
e-mail:
1 ]. Instead,
ventilators. Almost every mode of ventilation that can be delivered invasively can also be delivered noninvasively. However, certain modes are used more frequently. Here we will discuss BPAP and CPAP modes, but it is important for the provider to be aware that alternative modes of ventilation can be utilized (pressure support ventilation, assist control, pro­portional assist ventilation). The use of noninvasive ventilation in the medical population with acute COPD exacerbations and acute cardiogenic pulmonary edema is well established and beyond the scope of this chapter. Here we will focus our review on the physiology, rationale for use, equipment, indica­tions, contraindications, and complications of NIV in the pre­operative, intraoperative, and postoperative populations.

Continuous Positive Airway Pressure (CPAP)

CPAP applies a fi xed amount of positive pressure to be deliv­ered continuously throughout the respiratory cycle and as such is a constant pressure but variable fl ow mode. This mode increases the functional residual capacity without increasing the tidal volume resulting in decreased atelectasis and reduced work of breathing [ 59 ]. Since CPAP does not provide additional pressure during inspiration, it technically does not directly support ventilation, but it does exert some effects that can indirectly improve ventilation. For example, by mitigating against atelectasis through increased alveolar recruitment, CPAP decreases the ventilation-perfusion mis­match caused by non-ventilated alveoli and improves hypox­emia. However, because CPAP cannot increase tidal volume, it is not indicated in the treatment of hypercapneic respira­tory failure.

Bilevel Positive Airway Pressure (BPAP)

BiPAP, on the other hand, delivers variable positive pressure assistance to the patient at different phases of the respiratory cycle, in contrast to a set pressure applied continuously
© Springer International Publishing Switzerland 2016 N.D. Martin, L.J. Kaplan (eds.), Principles of Adult Surgical Critical Care, DOI 10.1007/978-3-319-33341-0_12
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throughout the respiratory cycle as in CPAP mode. The terms “BiPAP” and “BIPAP” are often used incorrectly to refer to NIV in the BPAP mode. “BiPAP” refers to the BPAP mode of ventilation delivered by a specifi c portable ventilator man­ufactured by Respironics Corporation. Similarly, “BIPAP” stands for biphasic positive airway pressure and refers to a time-cycled, pressure-controlled mode that is also a constant pressure variable fl ow mode with a period of fl ow cessation for CO2 clearance available on ventilators produced by Draeger Medical, Inc. These are just two of the many venti­lators that can deliver BPAP. Once this mode of NIV has been selected, the provider must then select the inspiratory positive airway pressure (IPAP) value and the expiratory positive airway pressure (EPAP) value. Unlike CPAP, BPAP will vary the pressure support delivered during inspiration and expiration and therefore must use a sensor which trig­gers alternation between the two pressures. This trigger is usually a fl ow or volume trigger that detects fl ow, volume, or pressure at the proximal airways.
Once the ventilator detects that a patient is exhaling, it will maintain positive pressure assistance equal to the EPAP value. When inspiration is detected, the ventilator delivers positive pressure assistance equal to the IPAP value in addi­tion to the EPAP, which is continuously delivered. For instance, if a ventilator were set to an EPAP of 5 cm H
O and
2
an IPAP of 10 cm H 2 O, the machine would maintain 5 cm H 2 O of positive pressure during expiration and deliver gas fl ow to establish 15 cm H 2 O during inspiration. Commonly, inspiratory positive pressure assistance lasts until the ventila­tor detects a 25 % decrease in peak inspiratory fl ow or 3 s elapses, whichever comes fi rst [ 5 ].
Like CPAP, BPAP increases the functional residual capac­ity and can recruit atelectatic lung segments, thereby decreas­ing shunting. Unlike CPAP, however, the addition of extra inspiratory pressure increases tidal volume. Augmentations in tidal volume subsequently cause increases in minute ven­tilation and thus give BPAP the ability to treat hypercapneic respiratory failure in addition to hypoxemic respiratory fail­ure. Finally, the addition of IPAP also decreases the work of breathing and total lung resistance, which is particularly ben­efi cial in patients who require BPAP for an acute or severe indication [ 5 ].
There is abundant high-quality evidence to recommend the use of NIV in specifi c medical conditions, including acute cardiogenic pulmonary edema, obstructive sleep apnea, and acute COPD exacerbations [ 1012 ]. These indi- cations allowed NIV to gain signifi cant popularity and expand its applicability to medical patients over the last two decades. Increasingly, NIV is being applied to specifi c popu­lations of surgical patients with similar improvements in out­comes as outlined later in this chapter.
Respiratory dysfunction in the postoperative patient rep­resents a complex clinical challenge that differs from the medical patient. Intensive care providers must take into con­sideration several factors before using NIV for a postopera­tive patient including clinical status, surgical procedures performed including anatomic and physiologic alterations, and the potential for further surgical intervention.
Although supplemental oxygen administration and incen­tive spirometry are effective in treating mild postoperative hypoxemia, endotracheal intubation and mechanical ventila­tion may be required in 8–10 % of patients who develop acute postoperative respiratory failure [
13 ]. The use of endotracheal
intubation and invasive mechanical ventilation has been shown to increase the risk of nosocomial infections, utilization of critical care resources, prolong length of hospital stay, and increase overall morality [ 14 ]. There is compelling evidence that demonstrates the benefi ts of NIV for both the patient and health-care utilization through avoidance of invasive ventila­tion [ 12 ]. Additionally, increased recognition of postoperative patients’ exceptional vulnerability to hypercapnia due to inci­sional pain, opioid agents, and unrecognized sleep apnea has led to increased use of NIV in the perioperative period.

Equipment

NIV can be delivered by standard ICU ventilators or por­table ventilators. Modern ICU ventilators can provide higher inspiratory fl ow rates, have separate inspiratory and expiratory tubing which minimizes carbon dioxide rebreathing, are capable of delivering a higher fraction of inspired oxygen (F i O 2 ), and have more appropriate moni­tors and alarms [ 15 ].

Rationale and Epidemiology

The most important advantage that NIV offers is avoidance of invasive endotracheal intubation and the associated dele­terious effects including airway injury, sedation, and ventilator- associated infections and conditions. Unlike intu­bated patients, noninvasively ventilated patients have the ability to be liberated from the ventilator intermittently, which promotes progressive mobility, pulmonary toilet/ coughing, eating, and speaking.

Interface

The ideal interface is one that minimizes air leakage and is most comfortable, thus promoting effi cacy and compliance. The most commonly used interface in the critical care setting is the oronasal mask [ nasal prongs (pillows), a full-face mask (covers the mouth, nose, and eyes), a nasal mask, and a helmet. Regardless of the interface chosen, they should be properly fi tted, comfort­able, effective, and minimize leakage to maximize effi cacy.
16 ]. Other available interfaces include
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Equipment Complications

Patient discomfort and thus compliance with NIV is a limit­ing factor in its clinical applicability and contributes signifi ­cantly to NIV failure rate. The most common complications of NIV equipment include air leakage, pressure ulceration, and patient-ventilator dyssynchrony.

Pressure Ulceration

Facial skin lesions, including ulceration and necrosis, are pressure-related lesions that result from prolonged contact with tight-fi tting masks and predominantly develop on the bridge of the nose. Their development is directly related to the duration of NIV therapy. Factors that have been associ­ated with formation of nasal skin lesions, and must be con­sidered at initiation of NIV therapy, include progressive tightening of the harness, increasing the air volume in the mask cushions, and increasing inspiratory pressures [ 17 ].

Patient-Ventilator Dyssynchrony

Dyssynchrony occurs when the phases of ventilator- delivered breaths do not match with the patient’s. This results in poor tolerance of NIV and can be alleviated by using an alternative ventilator mode (pressure support ventilation allows the patient to trigger each breath and may be more comfortable for some patients) or minimizing mask leaks [ 18 ]. Air leakage increases the time required for the ventilator to reach its pressure target, thus prolonging inspiration and causing discomfort.

Early Recognition of NIV Failure

Improvement in respiratory status is usually apparent within the fi rst 1–2 h after initiation of NIV. The absence of improve­ment in a patient’s respiratory status is a strong indication to promptly proceed with intubation. Delays in recognition of NIV failure and postponing invasive ventilation result in increased morbidity and mortality and should be avoided. Predictive factors associated with an increased risk of NIV failure include advanced age, high-acuity illness score at admission, presence of ARDS, sepsis, or multisystem organ failure (MSOF). In ARDS patients, an arterial oxygen ten­sion/inspired oxygen fraction (P a O 2 /F I O 2 ) ratio <175 mmHg drawn 1 h following initiation of a NIV trial accurately pre­dicts failure [ 19 ].
NIV should be initiated and continuously monitored in a critical care setting with a multidisciplinary team familiar with this therapy and advanced airway techniques; NIV as rescue therapy is generally not appropriate for ward care. There is no established consensus on NIV failure criteria; however, general recommendations including failure to clin­ically improve, unrelieved dyspnea, worsening P a O 2 /F I O 2 ratio, and increasing oxygen or pressure requirements should prompt transition to invasive ventilation. Should the provider anticipate failure, it is essential to promptly proceed to intu­bation while the patient is still able to adequately pre­oxygenate, allowing a safe window of time to perform endotracheal intubation. Patients requiring 100 % F I O 2 on BPAP are prone to respiratory arrest due to a lack of pulmo­nary reserve and rapid desaturation during intubation. High­fl ow NC O2 may be used as an aid in maintaining oxygenation in the period between removing the BPAP mask and estab­lishing a defi nitive airway.

Patient Selection

Prior to discussing the indications for NIV, it is important to understand the constituents of appropriate patient selection and the contraindications to NIV. Patient selection and continuous monitoring are critical to recognizing and reducing NIV failure. In general, the most important factors to consider when selecting patients for NIV are patient cooperation, ability to protect the airway, and their unique risk of aspiration. NIV should not be used in patients with altered mental status, severely agitated or obtunded patients, hemodynamically unstable patients, and those suffering from claustrophobia either due to an inability to cooperate or an impaired ability to protect their airway. Patients with obvious respiratory distress, proximal gastrointestinal hem­orrhage, active emesis, facial trauma or burns, and those with neuromuscular dysfunction are at an increased risk of aspiration and should avoid NIV. These patients warrant prompt endotra­cheal intubation and mechanical ventilation. Similarly, patients with impending respiratory failure due to copious secretions that they are unable to clear are poor candidates for NIV.

Protocol for Initiating NIV

Parameters to be set upon initiation of NIV will be guided by the mode of ventilation chosen. Currently, there is not a uni­versally accepted established protocol for initial NIV set­tings; however, general recommendations can be made. It is imperative to tailor the ventilator mode and settings to each clinical scenario and adjust parameters as needed to alleviate respiratory distress. Table recommended settings for initiation of BPAP [ 16 ].
12.1 presents some commonly
Specifi c Indications and Patient Considerations
NIV is now generally regarded as safe in most surgical patients and provides the most benefi t to patients with rap­idly reversible physiology (atelectasis, acute pulmonary edema, etc.) and patients with an oropharynx prone to