563CHAPTER 50 Asthma intubation should prompt an equipment check and confirmation of tube placement A tension pneumothorax must be considered in patients with hypoxemia and hypotension who fail to imp[.]
intubation should prompt an equipment check and confirmation of tube placement A tension pneumothorax must be considered in patients with hypoxemia and hypotension who fail to improve rapidly after administration of fluids and optimization of ventilation (or brief endotracheal tube disconnection), particularly when unequal breath sounds are present Pressure CHAPTER 50 Asthma Peak inspiratory Peak inspiratory pressure pressure Ventilator Settings The goal of mechanical ventilation in patients with near-fatal asthma is to reverse hypoxemia (if present), relieve respiratory muscle fatigue, and maintain a level of alveolar ventilation compatible with an acceptable pH, while avoiding iatrogenic hyperinflation and levels of intrathoracic pressure that reduce cardiac output Ill-advised attempts to achieve a normal PaCO2 would require fast respiratory rates, high minute volumes, and very high airway pressures, all of which are associated with the development of air leak (pneumothorax and pneumomediastinum) and high mortality rates.202–204 A paradigm shift in the ventilatory management of patients with asthma occurred with the introduction of a strategy of controlled hypoventilation reported by Darioli and Perret.203 Their strategy resulted in no mortality in 34 episodes of mechanical ventilation in 26 patients and significantly lower complication rates in comparison with historical controls.203 This approach used tidal volumes between and 12 mL/kg and targeted peak airway pressures up to 50 cm H2O Tidal volumes were reduced if the peak pressure limit could not be respected and higher Paco2 measurements were tolerated.203 A similar approach using respiratory rates lower than 12 breaths/min, tidal volumes between and 12 mL/kg, peak inspiratory pressures of 40 to 45 cm H2O, and permissive hypercapnia also resulted in very few complications and no mortality or long-term morbidity in 19 mechanically ventilated children with near-fatal asthma.202 The modes of ventilatory support for patients with severe acute asthma can be divided between pressure and volume preset No definitive evidence exists to suggest that one mode of ventilation is superior to the other However, to safely ventilate a patient with asthma, the characteristics of each mode must be fully understood Pressure control modes use a decelerating gas flow and have the advantage of ensuring that a particular inspiratory pressure limit is respected The main disadvantage of pressure control modes is that tidal volumes can vary greatly with changes in airway resistance and respiratory compliance Volume control modes deliver a constant tidal volume provided that there is no significant air leak around the endotracheal tube An added advantage of volume control is that it allows for comparison of peak inspiratory pressure and plateau pressure measurements (peak-to-plateau pressure), which can serve as a longitudinal indicator of airway resistance and response to therapy For these measurements, the plateau pressure is obtained by performing an inspiratory hold and is then compared with the peak inspiratory pressure (Fig 50.3) Increasing peak-to-plateau pressure indicates increasing airway resistance, whereas decreasing peak-to-plateau pressure suggests a response to therapy A disadvantage of volume control ventilation is that very high lung volumes can develop if exhalation is incomplete because tidal volumes remain constant breath to breath The option of using pressure-regulated volume control, a mode available on several ventilators, offers many of the combined advantages of pressure control and of volume control, including optimal decelerating inspiratory gas flow, assured tidal volumes, and minimized airway pressures 563 Inspiratory hold Plateau pressure Time representation of the airway pressure waveform over time during volume control ventilation The peak-to-plateau pressure difference (double-headed arrow) is obtained after an inspiratory hold by comparing the peak pressure and measured plateau pressure • Fig 50.3 Schematic The use of PEEP in intubated patients with asthma has been the focus of controversy Externally applied PEEP may benefit patients with expiratory flow limitation resulting from dynamic compression of small airways by moving the equal pressure point further down the airway and enabling decompression of upstream alveoli.205 The application of low levels of PEEP that are, by definition, lower than the level of auto-PEEP also may relieve dyspnea by facilitating ventilator triggering and synchronization for intubated patients capable of drawing spontaneous breaths.205,206 However, as elegantly demonstrated by Tuxen,207 the use of PEEP in chemically paralyzed patients with severe airflow obstruction is uniformly associated with higher lung volumes, increased airway and intrathoracic pressures, and circulatory compromise (Fig 50.4) Our preference is to use the volume control synchronized mandatory ventilation mode or the pressure regulated volume control mode, with set tidal volumes of to 12 mL/kg, which can be reduced as needed to generate plateau pressures of 30 cm H2O or less Depending on the degree of airway resistance, these tidal volumes may necessitate peak inspiratory pressures in excess of 50 cm H2O in the most severe cases However, those not reflect the plateau pressure to which the alveoli are actually being exposed since peak inspiratory pressure is measured cephalad to the obstruction and is affected by flow and resistance The initial tidal volume target of to 12 mL/kg might seem high, parti cularly in the era of lung-protective ventilation with reduced tidal volumes for patients with acute respiratory distress syndrome However, it is important to note that the typical patient with near-fatal asthma does not have significant parenchymal lung injury or the heterogeneously decreased lung compliance characteristic of patients with acute respiratory distress syndrome Respiratory rate is initially set between and 12 breaths/min, and inspiratory time is set between and 1.5 seconds, allowing for expiratory times between and seconds PEEP is set at zero for the patient under neuromuscular blockade With the intensification of therapy and clinical improvement, neuromuscular blockade is stopped and trigger sensitivity for spontaneous breaths is optimized Once the patient no longer requires neuromuscular blockade, a low level of PEEP (lower than the measured autoPEEP and generally not in excess of cm H2O) is applied to facilitate ventilator-patient synchrony The resultant spontaneous breaths should be assisted by the application of pressure support To be clear: the use of PEEP should be avoided in the patient with near-fatal asthma without significant parenchymal lung disease 564 S E C T I O N V Pediatric Critical Care: Pulmonary Lung volume Tidal ventilation Apnea VT VT A VTrap VEI FRCPEEP FRCPEEP B FRC Time VEI (L) VT VTrap PEEP (cm H2O) RR (breaths/min) FRCPEEP 10 15 10 10 16 15 10 15 22 • Fig 50.4 Top, Schematic representation of the measurement of end-inspiratory lung volume above functional residual capacity both with (A) and without (B) positive end-expiratory pressure (PEEP) by a period of apnea during steady-state ventilation Bottom, Effect of PEEP (0, 5, 10, and 15 cm H2O) on lung volumes at each level of minute ventilation (respiratory rate 10, 16, and 20 breaths/min) Note that the application of PEEP leads to a progressive increase in lung volume due to increased functional residual capacity and volume of trapped gas above functional residual capacity (FRC), particularly at faster respiratory rates FRCPEEP, Functional residual capacity resulting from PEEP; Vei, end-inspiratory lung volume above FRC; RR, respiratory rate; VT, tidal volume; Vtrap, volume of trapped gas above FRC (Modified from Tuxen DV Detrimental effects of positive end-expiratory pressure during controlled mechanical ventilation of patients with severe airflow obstruction Am Rev Respir Dis 1989;140[1]:5–9.) under neuromuscular blockade, as the applied expiratory pressure could translate into a proportional increase in hyperinflation PEEP should be applied to the intubated patient capable of initiating breaths, as it shifts the equal pressure point distally, decreases inspiratory intrathoracic pressure swings, and facilitates ventilator trigger and synchrony The use of a ventilation strategy consisting of pressure support with PEEP has gained increasing acceptance in the management of spontaneously breathing intubated patients with asthma, with the goal of reducing inspiratory work.208 In fact, pressure support with PEEP was the most commonly used strategy (36% of patients) in a study of 261 patients with fatal and near-fatal asthma.8 In this strategy, PEEP is used to facilitate ventilator triggering by narrowing the gap between proximal and distal airway pressures during a hyperinflated obstructed state Pressure support is then applied to facilitate inspiration while reducing associated work of breathing The patient initiates and terminates every breath— dictating the inspiratory time, respiratory rate, and depth of each breath—making this a comfortable mode for the patient with some degree of awareness Ventilatory Monitoring Regardless of the chosen mode of ventilation, patients with nearfatal asthma undergoing mechanical ventilation require very close monitoring Frequent auscultation provides valuable information regarding symmetry of breath sounds (assessing for pneumothorax or mucus plugging) and optimal length of exhalation Monitoring modules capable of analyzing and displaying permutations of important variables—such as pressure, volume, flow, and time—can provide important information that assists in the optimization of ventilator settings (Fig 50.5) Monitoring the peakto-plateau pressure difference allows for inferences regarding airway resistance and response to treatment The shape of the capnography curve also may provide insights regarding the adequacy of lung emptying (Fig 50.6), while integrated volumetric capnography can track changes in alveolar dead space over time Analgesia, Sedation, and Muscle Relaxation Patients with near-fatal asthma undergoing mechanical ventilation require adequate analgesia and sedation to avoid tachypnea, breath stacking, and ventilator dysynchrony, particularly in the setting of hypercapnia Ketamine is the anesthetic agent of choice because of its bronchodilatory properties Its use with continuous benzodiazepine infusion can provide deep sedation while decreasing the chance of postanesthetic hallucinatory reactions Despite its bronchodilatory effects, the use of ketamine is not favored by some because of concerns about increased secretions on an already hypersecretory and narrowed airway When opiates are used Flow CHAPTER 50 Asthma Flow Time 565 of serious neurologic complications, such as prolonged muscle weakness or paralysis, from the interaction of these agents and corticosteroid drugs.209,210 Reports of prolonged paralysis and myopathy after the concomitant use of corticosteroid drugs and aminosteroid-based neuromuscular blockers, such as vecuronium and pancuronium, led to the preferential use of benzylisoquinolinium compounds, such as cisatracurium, in patients with asthma However, this combination may not be completely safe, because prolonged muscle weakness has also been observed after treatment with cisatracurium and corticosteroids.211 Inhalational Anesthetic Agents Time ETCO2 • Fig 50.5 Schematic representation of the airway flow tracing over time during volume control ventilation Top, Expiratory flow does not return to zero prior to the initiation of the following breath, resulting in auto-PEEP (positive end-expiratory pressure) Bottom, Expiratory flow returns to baseline prior to initiation of the following breath after optimization of ventilator settings (lower respiratory rate and longer expiratory time) ETCO2 Time Time • Fig 50.6 Schematic representation of a capnogram in near-fatal asthma (top) and under normal conditions (bottom) Severe airflow obstruction in persons with near-fatal asthma is manifested by sloping of the expiratory phase tracing and absence of a plateau, suggesting incomplete exhalation prior to the following inspiration ETCO2, End-tidal carbon dioxide instead, fentanyl is the preferred agent because morphine can cause histamine release and, theoretically, aggravate an acute attack Muscle relaxation with neuromuscular blockers should be maintained following initiation of mechanical ventilation until satisfactory gas exchange and clinical stability are achieved Patients who exhibit significant hypercapnia during mechanical ventilation require continuation of neuromuscular blockers to abolish spontaneous respiratory movements that could worsen dynamic hyperinflation However, use of neuromuscular blockers should be discontinued as soon as feasible to reduce the likelihood Inhalational anesthetic agents have been used for their bronchodilatory effects in the treatment of mechanically ventilated patients with near-fatal asthma that is refractory to more conventional treatment modalities.212 The exact mechanism responsible for bronchodilation during inhalational anesthesia is unknown but may involve direct inhibition of vagal tone.213 Various agents have been used successfully in both adult and pediatric patients with refractory near-fatal asthma, including halothane,214 isoflurane,215 enflurane,216 and sevoflurane.216,217 Sevoflurane compares favorably with halothane and appears to be less noxious to human airways than isoflurane or enflurane.218 Inhalational anesthetics can be delivered by means of an anesthesia machine that feeds into the low-pressure gas port of a conventional mechanical ventilator or via a dedicated anesthesia ventilator with its own vaporizer It is important to ensure proper disposal of exhaled gases into a scavenger system to prevent release of the anesthetic agent into the environment A monitor capable of continuously analyzing inspiratory and expiratory drug concentrations is helpful in ascertaining the actual amount delivered and signaling inadvertent interruptions in therapy, such as those caused by an empty vaporizer reservoir or failure to resume therapy after a refill Usual doses of isoflurane range from 0.5% to 2% and should be titrated for effect Clinical response usually can be observed within 30 minutes Therapy with an inhaled anesthetic agent for persons with refractory near-fatal asthma should be performed in a well-monitored ICU under the direction of personnel experienced in the administration of these agents and knowledgeable of their adverse effects Patients treated with halothane can experience significant hypotension as a result of myocardial depression and require rapid fluid expansion and inotropic support.219,220 Halothane is associated with cardiac arrhythmias, particularly during concurrent administration of epinephrine,221 which explains why many physicians prefer a nonarrhythmogenic alternative such as isoflurane Isoflurane does not have negative inotropic effects but may still cause hypotension because of vasodilation.191 Considering that halothane and isoflurane result in equivalent bronchodilation, isoflurane is preferred for use in children because of its less significant adverse effects The use of subanesthetic doses of inhalational anesthetic agents in attempts to avoid mechanical ventilation in spontaneously breathing patients with severe asthma during maximal medical treatment is an intriguing strategy that warrants further study.222 Antibiotics In children, acute asthma exacerbations frequently are triggered by a viral infection Thus, antibiotic agents are not indicated as part of standard treatment A subset of school-aged children may 566 S E C T I O N V Pediatric Critical Care: Pulmonary present to the hospital with shortness of breath, accessory muscle use, hypoxemia, and expiratory wheezing caused by Mycoplasma pneumoniae that simulates an acute asthma exacerbation These patients usually have bilateral interstitial disease on a chest radiograph and should be treated with appropriate antibiotics, such as a macrolide Patients with near-fatal asthma who require intubation and prolonged mechanical ventilation should be monitored for the development of nosocomial infections The presence of fever and abundant thick white or purulent tracheal secretions warrants obtaining a protected tracheal specimen for Gram stain and culture to guide appropriate antibiotic coverage Bronchoscopy Increased bronchial secretions and mucus plugging play a major role in the continued deterioration observed in some patients.49–51 Mucous plugging and casts can cause atelectasis of large segments and worsen the heterogeneity of ventilation and dynamic hyperinflation Thus, a small percentage of mechanically ventilated patients with severe near-fatal asthma may require selective suction of mucus plugs, casts, or thick secretions by bronchoscopy.223 The combination of bronchial lavage with mucolytic agents such as N-acetylcysteine224 or recombinant human deoxyribonuclease225 and aggressive selective suction through a bronchoscope may be beneficial in patients with clinically significant mucous plugging who fail to respond to maximal therapy and traditional tracheal suction Extracorporeal Life Support The use of extracorporeal life support (ECLS) has been reported in the management of the very few patients with near-fatal asthma who continue to exhibit a profound degree of clinical instability despite maximal therapy.226,227 Such cases are the exception and comprise less than 4% of patients in the Extracorporeal Life Support Organization registry who received ECLS for a pulmonary indication (1140 of 28,369 [3.9%] pediatric and adult ECLS runs).228 The survival rate for persons with near-fatal asthma necessitating ECLS is approximately 81%,228 which is remarkable considering that the vast majority of these patients were extraordinarily sick and had failed to respond to very aggressive treatment Prognosis The prognosis of patients with critical or near-fatal asthma who receive proper medical therapy is excellent Better understanding of the pathophysiology of airway obstruction and dynamic hyperinflation, coupled with improved mechanical ventilation strategies and aggressive pharmacologic treatment, has reduced the ICU mortality rate to nearly zero in these patients.8,229–231 Asthma fatalities still occur in patients with sudden onset of severe airway obstruction who not come to medical attention prior to the development of respiratory failure or cardiorespiratory arrest.232,233 The homegoing treatment plan for patients admitted to the hospital with critical or near-fatal asthma should be carefully reviewed prior to discharge to ensure adequate outpatient therapy, education, and follow-up in an attempt to reduce the likelihood of a preventable recurrence Such patients should be followed by an asthma expert in addition to a pediatrician Key References Kenyon N, Zeki AA, Albertson TE, Louie S Definition of critical asthma syndromes Clin Rev Allergy Immunol 2015;48(1):1-6 Newth CJ, Meert KL, Clark AE, et al Fatal and near-fatal asthma in children: the critical care perspective J Pediatr 2012;161(2): 214-221 e213 Grunwell JR, Travers C, Fitzpatrick AM Inflammatory and comorbid features of children admitted to a PICU for status asthmaticus Pediatr Crit Care Med 2018;19(11):e585-e594 Sullivan PW, Ghushchyan V, Navaratnam P, et al National prevalence of poor asthma control and associated outcomes among school-aged children in the United States J Allergy Clin Immunol Pract 2018; 6(2):536-544 e531 Biagini Myers JM, Simmons JM, Kercsmar CM, et al Heterogeneity in asthma care in a statewide collaborative: the Ohio Pediatric Asthma Repository Pediatrics 2015;135(2):271-279 Bratton SL, Newth CJ, Zuppa AF, et al Critical care for pediatric asthma: wide care variability and challenges for study Pediatr Crit Care Med 2012;13(4):407-414 Tse SM, Samson C Time to asthma-related readmission in children admitted to the ICU for asthma Pediatr Crit Care Med 2017;18(12): 1099-1105 Kikuchi Y, Okabe S, Tamura G, et al Chemosensitivity and perception of dyspnea in patients with a history of near-fatal asthma N Engl J Med 1994;330(19):1329-1334 Sur S, Crotty TB, Kephart GM, et al Sudden-onset fatal asthma A distinct entity with few eosinophils and relatively more neutrophils in the airway submucosa? Am Rev Respir Dis 1993;148(3):713-719 Wenzel SE Asthma phenotypes: the evolution from clinical to molecular approaches Nature medicine 2012;18(5):716-725 Kuyper LM, Pare PD, Hogg JC, et al Characterization of airway plugging in fatal asthma Am J Med 2003;115(1):6-11 Hays SR, Fahy JV The role of mucus in fatal asthma Am J Med 2003;115(1):68-69 Rodriguez-Roisin R, Ballester E, Roca J, Torres A, Wagner PD Mechanisms of hypoxemia in patients with status asthmaticus requiring mechanical ventilation Am Rev Respir Dis 1989;139(3):732-739 Stalcup SA, Mellins RB Mechanical forces producing pulmonary edema in acute asthma N Engl J Med 1977;297(11):592-596 Jardin F, Farcot JC, Boisante L, Prost JF, Gueret P, Bourdarias JP Mechanism of paradoxic pulse in bronchial asthma Circulation 1982;66(4):887-894 Simmons DH, Linde LM, Miller JH, O’Reilly RJ Relation between lung volume and pulmonary vascular resistance Circ Res 1961;9:465-471 Gorelick MH, Stevens MW, Schultz TR, Scribano PV Performance of a novel clinical score, the Pediatric Asthma Severity Score (PASS), in the evaluation of acute asthma Academic emergency medicine 2004;11(1):10-18 Bekhof J, Reimink R, Brand PL Systematic review: insufficient validation of clinical scores for the assessment of acute dyspnoea in wheezing children Paediatric respiratory reviews 2014;15(1):98-112 Kussmaul A Ueber schwielige mediastino-pericarditis und den paradoxen puls Berl Klin Wschr 1873;38(10):433-435 Bilchick KC, Wise RA Paradoxical physical findings described by Kussmaul: pulsus paradoxus and Kussmaul’s sign Lancet 2002; 359(9321):1940-1942 Knowles GK, Clark TJ Pulsus paradoxus as a valuable sign indicating severity of asthma Lancet 1973;2(7842):1356-1359 Mountain RD, Heffner JE, Brackett NC, Jr., Sahn SA Acid-base disturbances in acute asthma Chest 1990;98(3):651-655 Meert KL, McCaulley L, Sarnaik AP Mechanism of lactic acidosis in children with acute severe asthma Pediatr Crit Care Med 2012;13(1): 28-31 Sarnaik SM, Saladino RA, Manole M, et al Diastolic hypotension is an unrecognized risk factor for beta-agonist-associated myocardial injury in children with asthma Pediatr Crit Care Med 2013;14(6): e273-279 CHAPTER 50 Asthma Matson JR, Loughlin GM, Strunk RC Myocardial ischemia complicating the use of isoproterenol in asthmatic children J Pediatr 1978; 92(5):776-778 Rowe BH, Spooner C, Ducharme FM, Bretzlaff JA, Bota GW Early emergency department treatment of acute asthma with systemic corticosteroids Cochrane Database Syst Rev 2000(2):CD002178 Davies AO, Lefkowitz RJ Regulation of beta-adrenergic receptors by steroid hormones Annu Rev Physiol 1984;46:119-130 Shein SL, Speicher RH, Filho JO, Gaston B, Rotta AT Contemporary treatment of children with critical and near-fatal asthma Rev Bras Ter Intensiva 2016;28(2):167-178 Qureshi F, Zaritsky A, Lakkis H Efficacy of nebulized ipratropium in severely asthmatic children Ann Emerg Med 1997;29(2):205-211 Qureshi F, Pestian J, Davis P, Zaritsky A Effect of nebulized ipratropium on the hospitalization rates of children with asthma N Engl J Med 1998;339(15):1030-1035 Ciarallo L, Sauer AH, Shannon MW Intravenous magnesium therapy for moderate to severe pediatric asthma: results of a randomized, placebo-controlled trial J Pediatr 1996;129(6):809-814 Scarfone RJ, Loiselle JM, Joffe MD, et al A randomized trial of magnesium in the emergency department treatment of children with asthma Ann Emerg Med 2000;36(6):572-578 Tal A, Pasterkamp H, Leahy F Arterial oxygen desaturation following salbutamol inhalation in acute asthma Chest 1984;86(6): 868-869 Gleeson JG, Green S, Price JF Air or oxygen as driving gas for nebulised salbutamol Arch Dis Child 1988;63(8):900-904 Kantor DB, Hirshberg EL, McDonald MC, et al Fluid balance is associated with clinical outcomes and extravascular lung water in children with acute asthma exacerbation Am J Respir Crit Care Med 2018;197(9):1128-1135 Katz RW, Kelly HW, Crowley MR, Grad R, McWilliams BC, Murphy SJ Safety of continuous nebulized albuterol for bronchospasm in infants and children Pediatrics 1993;92(5):666-669 Papo MC, Frank J, Thompson AE A prospective, randomized study of continuous versus intermittent nebulized albuterol for severe status asthmaticus in children Crit Care Med 1993;21(10): 1479-1486 Asmus MJ, Hendeles L, Weinberger M, et al Levalbuterol has not been established to have therapeutic advantage over racemic albuterol J Allergy Clin Immunol 2002;110(2):325; author reply 325-328 567 Craven D, Kercsmar CM, Myers TR, O’Riordan M A, Golonka G, Moore S Ipratropium bromide plus nebulized albuterol for the treatment of hospitalized children with acute asthma J Pediatr 2001;138(1):51-58 Dib JG, Engstrom FM, Sisca TS, Tiu RM Intravenous magnesium sulfate treatment in a child with status asthmaticus Am J Health Syst Pharm 1999;56(10):997-1000 Ciarallo L, Brousseau D, Reinert S Higher-dose intravenous magnesium therapy for children with moderate to severe acute asthma Arch Pediatr Adolesc Med 2000;154(10):979-983 Devi PR, Kumar L, Singhi SC, Prasad R, Singh M Intravenous magnesium sulfate in acute severe asthma not responding to conventional therapy Indian Pediatr 1997;34(5):389-397 Shein SL, Farhan O, Morris N, et al Adjunctive pharmacotherapies in children with asthma exacerbations requiring continuous albuterol therapy: findings from the Ohio Pediatric Asthma Repository Hosp Pediatr 2018 Strauss RE, Wertheim DL, Bonagura VR, Valacer DJ Aminophylline therapy does not improve outcome and increases adverse effects in children hospitalized with acute asthmatic exacerbations Pediatrics 1994;93(2):205-210 Rodrigo C, Rodrigo G Treatment of acute asthma Lack of therapeutic benefit and increase of the toxicity from aminophylline given in addition to high doses of salbutamol delivered by metered-dose inhaler with a spacer Chest 1994;106(4):1071-1076 Gupta VK, Cheifetz IM Heliox administration in the pediatric intensive care unit: an evidence-based review Pediatr Crit Care Med 2005;6(2):204-211 Darioli R, Perret C Mechanical controlled hypoventilation in status asthmaticus Am Rev Respir Dis 1984;129(3):385-387 Tuxen DV Detrimental effects of positive end-expiratory pressure during controlled mechanical ventilation of patients with severe airflow obstruction Am Rev Respir Dis 1989;140(1):5-9 Wetzel RC Pressure-support ventilation in children with severe asthma Crit Care Med 1996;24(9):1603-1605 Rampa S, Allareddy V, Asad R, Nalliah RP, Allareddy V, Rotta AT Outcomes of invasive mechanical ventilation in children and adolescents hospitalized due to status asthmaticus in United States: a population based study J Asthma 2014:1-8 The full reference list for this chapter is available at ExpertConsult.com ... reducing associated work of breathing The patient initiates and terminates every breath— dictating the inspiratory time, respiratory rate, and depth of each breath—making this a comfortable mode for... used strategy (36% of patients) in a study of 261 patients with fatal and near-fatal asthma.8 In this strategy, PEEP is used to facilitate ventilator triggering by narrowing the gap between proximal... pressure support with PEEP has gained increasing acceptance in the management of spontaneously breathing intubated patients with asthma, with the goal of reducing inspiratory work.208 In fact, pressure