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144. Fawzy A, Wu TD, Wang K, etal. Racial and ethnic discrepancy in pulse oximetry and delayed identication of treatment eligibility among patients with COVID-19. JAMA Intern Med. 2022;182(7):730–8. https://doi.org/10.1001/jamainternmed.2022.1906.
145.
146.
147.
148.
149.
150.
151.
152.
153.
154.
155.
156.
157.
158.
159.
160.
eever TM, Hearson G, Housley G, etal. Using venous blood gas analysis in the assess-
McK ment of COPD exacerbations: a prospective cohort study. Thorax. 2016;71(3):210–5. https://
doi.org/10.1136/thoraxjnl- 2015- 207573.
y P, Bennett K, Staunton P, McMahon G.Venous vs arterial blood gases in the
McCann assessment of patients presenting with an exacerbation of chronic obstructive pulmonary disease. Am J Emerg Med. 2012;30(6):896–900. https://doi.org/10.1016/j.ajem.2011.06.011.
varria C, Steer J, Wason J, Bourke S. Oxygen therapy and inpatient mortal-
Eche ity in COPD exacerbation. Emerg Med J. 2021;38(3):170–7. https://doi.org/10.1136/
emermed- 2019- 209257.
O’Driscoll BR, Ho in adults in healthcare and emergency settings. BMJ Open Respir Res. 2017;4(1):e000170.
https://doi.org/10.1136/bmjresp- 2016- 000170.
Austin MA, on mortality in chronic obstructive pulmonary disease patients in prehospital setting: ran­domised controlled trial. BMJ. 2010;341:c5462. https://doi.org/10.1136/bmj.c5462. Osadnik ventilation for the management of acute hypercapnic respiratory failure due to exacerbation of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2017;2017:7. https://
doi.org/10.1002/14651858.CD004104.pub4.
Ameen sure and bilevel positive pressure ventilation in treatment of acute exacerbation of chronic obstructive pulmonary disease. Egypt J Chest Dis Tuberc. 2012;61(3):95–101. https://doi.
org/10.1016/j.ejcdt.2012.10.018.
MacIntyre NR. 2019;64(6):617–28. https://doi.org/10.4187/respcare.06635. Rochwer noninvasive ventilation for acute respiratory failure. Eur Respir J. 2017;50(2):1602426.
https://doi.org/10.1183/13993003.02426- 2016.
Conf tilation in patients with COPD exacerbation. Eur Respir J. 2005;25(2):348–55. https://doi.
org/10.1183/09031936.05.00085304.
Brochard of chronic obstructive pulmonary disease. N Engl J Med. 1995;333(13):817–22. https://doi.
org/10.1056/NEJM199509283331301.
Ornico SR, Lobo SM, Sanches HS, et tion improves weaning outcome after acute respiratory failure: a randomized controlled trial. Crit Care. 2013;17(2):R39. https://doi.org/10.1186/cc12549. Ferrer M, Sellarés J, capnic patients with chronic respiratory disorders: randomised controlled trial. Lancet Lond Engl. 2009;374(9695):1082–8. https://doi.org/10.1016/S0140- 6736(09)61038- 2. Na ure after extubation in high-risk patients. Crit Care Med. 2005;33(11):2465–70. https://doi.
org/10.1097/01.ccm.0000186416.44752.72.
Girault C, Bubenheim M, with chronic Hypercapnic respiratory failure. Am J Respir Crit Care Med. 2011;184(6):672–9.
https://doi.org/10.1164/rccm.201101- 0035OC.
Society BPGL and BT 2002;57(3):192–211. https://doi.org/10.1136/thorax.57.3.192.
CR, Tee VS, Carson-Chahhoud KV, Picot J, Wedzicha JA, Smith BJ.Non-invasive
A, Zedan M, El Shamly M.Comparison between continuous positive airway pres-
g B, Brochard L, Elliott MW, etal. Ofcial ERS/ATS clinical practice guidelines:
alonieri M, Garuti G, Cattaruzza MS, etal. A chart of failure risk for noninvasive ven-
va S, Gregoretti C, Fanfulla F, etal. Noninvasive ventilation to prevent respiratory fail-
ward LS, Earis J, Mak V.British Thoracic Society guideline for oxygen use
Wills KE, Blizzard L, Walters EH, Wood-Baker R.Effect of high ow oxygen
Physiologic effects of noninvasive ventilation. Respir Care.
L, Mancebo J, Wysocki M, etal. Noninvasive ventilation for acute exacerbations
al. Noninvasive ventilation immediately after extuba-
Valencia M, et al. Non-invasive ventilation after extubation in hyper-
Abroug F, etal. Noninvasive ventilation and weaning in patients
. Non-invasive ventilation in acute respiratory failure. Thorax.
L. C. McNamara et al.
cute Exacerbations ofChronic Obstructive Pulmonary Disease
6
A
161. Díaz GG, Alcaraz AC, Talavera JCP, etal. Noninvasive positive-pressure ventilation to treat Hypercapnic coma secondary to respiratory failure. Chest. 2005;127(3):952–60. https://doi.
org/10.1378/chest.127.3.952.
162.
163.
164. Fowler WS. Lung function studies; the respiratory dead space. Am J Physiol.
165.
166.
167.
168. Papachatzakis I, Velentza L, Kontogiannis S, Trakada G.High ow nasal cannula with
169.
170.
171.
172.
173.
174.
175.
176.
177.
owski S, Ergan B, Bos L, etal. ERS clinical practice guidelines: high-ow nasal can-
Oczk nula in acute respiratory failure. Eur Respir J. 2022;59(4):2101574. https://doi.org/10.118
3/13993003.01574- 2021.
T, Turrini C, Eronia N, etal. Physiologic effects of high-ow nasal cannula in acute
Mauri hypoxemic respiratory failure. Am J Respir Crit Care Med. 2017;195(9):1207–15. https://doi.
org/10.1164/rccm.201605- 0916OC.
1948;154(3):405–16. https://doi.org/10.1152/ajplegacy.1948.154.3.405.
W, Celik G, Feng S, etal. Nasal high ow clears anatomical dead space in upper
Möller airway models. J Appl Physiol Bethesda Md 1985. 2015;118(12):1525–32. https://doi.
org/10.1152/japplphysiol.00934.2014.
arke RL, Eccleston ML, McGuinness SP. The effects of ow on airway pressure during
P nasal high-ow oxygen therapy. Respir Care. 2011;56(8):1151–5. https://doi.org/10.4187/
respcare.01106.
, Thille AW, Mercat A, etal. High-ow oxygen through nasal cannula in acute hypox-
Frat JP emic respiratory failure. N Engl J Med. 2015;372(23):2185–96. https://doi.org/10.1056/
NEJMoa1503326.
warm humidied air versus non-invasive mechanical ventilation in respiratory failure type II. Eur Respir J. 2017;50(suppl 61):PA2182. https://doi.org/10.1183/1393003.congress-
A2182.
2017.P
Nishimura M. 2015;3(1):15. https://doi.org/10.1186/s40560- 015- 0084- 5.
AF, Sun X, Johannes RS, Yaitanes A, Tabak YP.Validation of a novel risk score for
Shorr severity of illness in acute exacerbations of COPD.Chest. 2011;140(5):1177–83. https://doi.
org/10.1378/chest.10-
Tabak YP, Sun X, Johannes RS, Gupta V, Shorr AF.Mortality and need for mechanical ven-
tilation in acute exacerbations of chronic obstructive pulmonary disease: development and validation of a simple risk score. Arch Intern Med. 2009;169(17):1595–602. https://doi.
org/10.1001/archinternmed.2009.270.
Squadrone patients with severe acute respiratory failure deemed to require ventilatory assistance. Intensive Care Med. 2004;30(7):1303–10. https://doi.org/10.1007/s00134-
A, Güell R, Gómez J, etal. Predicting the result of noninvasive ventilation in severe
Antón acute exacerbations of patients with chronic airow limitation. Chest. 2000;117(3):828–33.
https://doi.org/10.1378/chest.117.3.828.
Neto SCGB, cal ventilation in people with neuromuscular disease: a systematic review. BMJ Open. 2021;11(9):e047449. https://doi.org/10.1136/bmjopen-
Davidson AC, Banham S, Elliott M, etal. BTS/ICS guideline for the ventilatory management
of acute hypercapnic respiratory failure in adults. Thorax. 2016;71(Suppl 2):ii1–ii35. https://
doi.org/10.1136/thoraxjnl-
TC, Marini JJ.Impact of PEEP on lung mechanics and work of breathing in severe
Smith airow obstruction. J Appl Physiol Bethesda Md 1985. 1988;65(4):1488–99. https://doi.
org/10.1152/jappl.1988.65.4.1488.
MacIntyre NR, McConnell R, Cheng KCG. the inspiratory threshold load of intrinsic PEEP. Chest. 1997;111(1):188–93. https://doi.
org/10.1378/chest.111.1.188.
High-ow nasal cannula oxygen therapy in adults. J Intensive Care.
3035.
E, Frigerio P, Fogliati C, et al. Noninvasive vs invasive ventilation in COPD
004- 2320- 7.
Torres-Castro R, Lima Í, Resqueti VR, Fregonezi GAF.Weaning from mechani-
2020- 047449.
2015- 208209.
Applied PEEP during pressure support reduces
151
152
178. Reddy RM, Guntupalli KK.Review of ventilatory techniques to optimize mechanical venti­lation in acute exacerbation of chronic obstructive pulmonary disease. Int J Chron Obstruct Pulmon Dis. 2007;2(4):441–52.
179.
MacIntyre N, Huang tive pulmonary disease. Proc Am Thorac Soc. 2008;5(4):530–5. https://doi.org/10.1513/
pats.200707- 088ET.
180.
Prediletto I, admission. J Clin Med. 2023;12(10):3369. https://doi.org/10.3390/jcm12103369.
Giancotti G, Nava S.COPD exacerbation: why it is important to avoid ICU
YC.Acute exacerbations and respiratory failure in chronic obstruc-
L. C. McNamara et al.
Chapter 7
Acute Asthma Exacerbation intheIntensive Care Unit
KevinG.Correa andLaurenE.Eggert

7.1 Introduction

7.1.1 What Is Asthma?

Asthma is a heterogeneous, chronic respiratory disease that is characterized by vari­able airway obstruction through hyperresponsive bronchoconstriction and bronchial inammation [1]. The diagnosis of asthma is made based on a combination of clini­cal symptoms such as cough, wheezing, shortness of breath, and chest tightness and a demonstration of variable airow obstruction [1, 2]. Asthma on spirometry typi­cally presents as a reversible, obstructive ventilatory defect notable for a reduced peak expiratory ow (PEF), forced exhalatory volume in 1second (FEV-1), and forced vital capacity (FEV-1/FVC) ratio, and sometimes there is also evidence of air trapping or hyperination [1, 2]. The severity of asthma symptoms may correlate to the severity of a decrease in PEF and FEV-1 at home or in clinic and can be used to trend response to therapeutic agents [1, 2]. The cornerstone management of asthma revolves around controlling airway inammation to reduce obstructive symptoms by targeting the several molecular pathways that lead to inammation and broncho­constriction [1]. As a result of chronic inammation, the airway, or bronchioles, may undergo remodeling, leading to increased bronchoconstriction, thickened bronchioles, and mucus production [3] (Fig.7.1).
Asthma is one of the most common inammatory diseases and is known to affect more than 300million individuals worldwide [1]. The prevalence of asthma varies from country to country, with estimates ranging from 1% to 29% of the population. It is one of the few diseases that can develop in people of all ages, from young
K. G. Correa (*) · L. E. Eggert Division of Pulmonary, Allergy, and Critical Care Medicine, Stanford University, Palo Alto, CA, USA e-mail: correak@stanford.edu; leggert1@stanford.edu
Switzerland AG 2025 Y. Alzaidi, M. A. Gebily (eds.), The Pharmacist’s Expanded Role in Critical Care Medicine, https://doi.org/10.1007/978-3-031-77335-8_7
153© The Author(s), under exclusive license to Springer Nature
154
Relaxed
ned
during attack
Air trapped
K. G. Correa and L. E. Eggert
smooth
muscles
Wall inflamed and thickened
Asthmatic airwayNormal airway
in alveoli
Asthmatic airway
Tighte smooth muscles
Fig. 7.1 Diagram depicting the bronchioles, or airways, in normal, asthma, and exacerbation state. Note the decreased lumen size and increased bronchoconstriction in the asthmatic and exac­erbation airways
children to late adulthood, with onset and severity closely linked to genetics and environmental factors [1]. Social factors have also been shown to play a signicant role in the severity and control of asthma with worse outcomes in populations iden­tied as minorities and from lower socioeconomic backgrounds [1]. Asthma is het­erogeneous, and several distinct phenotypes have been described, including but not limited to the following: allergic, exercise-induced, obesity- associated, and nonal­lergic [1]. To address asthma’s large global health impact, the Global Initiative for Asthma (GINA) was created which provides guidance to clinicians regarding asthma management in an evidence-based manner [2].
7.1.2 What Is anAsthma Exacerbation?
The key goal of asthma management is to target minimal to no day-to-day symp­toms and minimize the risk for exacerbations. The range of medications required to keep an individual’s asthma under control varies widely, which owes to the disease’s heterogeneity. Several disease-specic questionnaires have been developed to assess one’s asthma symptoms and can be used as an objective measurement of a medication’s impact on their asthma control. Given asthma’s close interplay with environmental factors, control can vary throughout the year and medication changes may be necessary in one’s disease course.
An exacerbation is dened as asthma with rapidly worsening symptoms and clinical deterioration [1]. The hyperresponsive and inamed bronchioles of the air­way lead to overt bronchoconstriction and airow obstruction, which can be dem­onstrated by worsening obstruction on spirometry and/or a decreased PEF [4]. In
7
cute Asthma Exacerbation intheIntensive Care Unit
A
155
addition, the remodeled bronchioles are subjected to mucus hypersecretion, which additionally leads to further airway occlusion and subsequent hyperination [4]. Prompt recognition of exacerbation symptoms is crucial as early assessment and intervention are necessary to prevent signicant morbidity and mortality. The range of severity of an asthma exacerbation can be from mild which can be managed as an outpatient to severe and life-threatening, requiring admission to the intensive care unit (ICU). Asthma exacerbations are a frequent cause of emergency room visits and hospital admissions [5]. The presence and rate of exacerbations have become a standard benchmark for assessing a patient’s asthma control. Preventing exacerba­tions is a key therapeutic target for medical treatment of asthma.
7.1.3 Exacerbation Triggers andRisk Factors forMore
Severe Exacerbations
In many exacerbations, there is a clear culprit responsible for causing the acute asthma symptoms. These triggers can be infectious or noninfectious, such as smoke, pollution, cold weather, or allergen exposure [1]. As individuals understand their asthma symptoms in relation to their environment, they will become more familiar with their triggers and can work to purposefully avoid such exposures. Asthmatics will have their own threshold on how much exposure of a trigger they need to pro­voke an exacerbation. Additionally, repeated exposures may provoke further immune system sensitization leading to more pronounced symptoms with decreased trigger exposure [1]. Unfortunately, many asthma triggers are variable and unpre­dictable, hence the importance of obtaining baseline asthma control. Table7.1 high­lights some of the most common triggers for asthma exacerbations.
Table 7.1 Review of common triggers of asthma exacerbations
Category Trigger
Infectious Bacterial infections (bronchitis, tracheitis, pneumonia)
Allergens Pollen
Irritants Cleaning agents and solutions
Miscellaneous Aspirin (aspirin exacerbated respiratory disease ie. AERD)
Viral infections (rhinovirus, SARS-CoV-2, RSV, etc.) Fungal spores, aspergillus colonization
Grasses Trees Dust mites, cockroaches Pet dander
Preservatives Cold air or weather changes Wildres or pollution Strong odors
Gastric reux Exercise
156
The major challenge that presents to clinicians is gauging the severity and trajec­tory of an asthmatic presenting to seek care with an exacerbation. Not all exacerba­tions that present for medical evaluation require hospitalization, and many can be safely treated as an outpatient with oral corticosteroids, inhaled bronchodilators, and close outpatient follow-up. If present, there are several risk factors that raise concern for increased risk of a severe exacerbation requiring hospital admission including escalation to the ICU. Risk factors include prior asthma exacerbation requiring ICU level of care, need for invasive or noninvasive ventilation, history of recent exacerbation with known difcult-to-control asthma, steroid-dependent asthma, elderly patients with signicant comorbidities, and pregnant individuals presenting with exacerbation [4, 5]. Upon arrival to the emergency department, patients experiencing an asthma exacerbation should be assessed in a timely manner as early identication and management of ICU-bound patients are vital.
K. G. Correa and L. E. Eggert

7.2 Diagnosis

Evaluation of the asthmatic presenting in an exacerbation requires a comprehensive review of the patient’s clinical presentation and available objective data. Triage and initial management in the rst hour within emergency department arrival are crucial as clinical deterioration can occur rapidly. Early interventions performed in the emergency department can shape the hospital course for a patient. The main indica­tions for an asthmatic to require ICU level of care include worsening clinical status refractory to initial therapies, increased work of breathing with concern for impend­ing respiratory failure, carbon dioxide retention with respiratory acidosis or respira­tory failure requiring invasive or noninvasive ventilation, signicant comorbidities that may complicate hospital course, and a history of a prior exacerbation requiring ICU-level care [4, 5].

7.2.1 Physical Examination

The initial physical examination is fundamental to correctly identifying the level of care a patient needs upon presentation to the emergency department. In addition to the initial exam, serial examinations are necessary to assess a patient’s response to initial interventions, especially because clinical status can quickly change during the course of severe exacerbations [5]. When in doubt about the level of care, it is always better to monitor an exacerbation in the ICU, as delays or transfers of care can lead to increased morbidity. Therefore, clinicians should pay particular atten­tion to specic ndings on the exam which can signal patients at higher risk for needing ICU level of care. Table7.2 highlights the main physical exam ndings that are indicative of a severe or life-threatening exacerbation.
7 Acute Asthma Exacerbation intheIntensive Care Unit
Table 7.2 Common physical exam ndings in asthma exacerbations
Organ system Exam nding
Neurologic Altered mental status (CO Head, eyes, ears, nose, and
throat (HEENT) Cardiovascular Tachycardia, hypotension (can be if in the setting of anaphylaxis) Pulmonary Tachypnea, use of accessory breathing muscles (tripod breathing),
Abdominal Paradoxical abdominal breathing, emesis, and diarrhea (can be in
Extremities/ musculoskeletal
Nasal aring, stridor (can be if in the setting of anaphylaxis), sternocleidomastoid (SCM) retractions, pursed-lip breathing
wheezing, decreased breath sounds (“silent chest” due to hyperination)
the setting of anaphylaxis) Cyanosis, skin rash, or ushing (can be in the setting of
anaphylaxis)
narcosis), fatigue, lethargy
2
157

7.2.2 Laboratory Data

As highlighted previously, the underlying etiology of an asthma exacerbation can be infectious or noninfectious. Therefore, initial workup sent in an exacerbation should include labs to rule out common triggers. Initial labs should include a complete blood cell count with differential to assess for leukocytosis and eosinophilia and basic met­abolic panel to evaluate for any electrolyte abnormalities and renal function for med­ication dosing. In noninfectious triggers of exacerbations, laboratory studies may be completely normal [5]. Initial infectious workup may include laboratory tests such as a nasal swab testing for common respiratory viruses and serum procalcitonin to help assess the likelihood of bacterial infection. If supported by further clinical symptoms or data, additional studies could be considered such as respiratory gram stain and culture, blood cultures, inammatory markers, and a troponin and NT-proBNP to rule out comorbid cardiac disease [5]. Certain infectious triggers of exacerbations may have treatment options to either shorten the duration of exacerbation or prevent progression to severe disease such as inuenza and SARS-CoV-2 infections.
Patients in exacerbation are tachypneic and have a degree of hyperventilation that can be expected. Since asthma is a disease of the airways and not the lung parenchyma, oxygen saturation can be expected to be normal in a mild-moderate exacerbation. If an arterial blood gas is obtained in exacerbation, then the expected ndings range from normal to a mild respiratory alkalosis occurring from hyperven­tilation. If serial blood gases demonstrate retention of CO2 (hypercapnia), a patient may become hypoxic due to hypercapnia, which is a key concern for impending respiratory failure because of respiratory fatigue or “tiring out,” and the patient may require urgent ventilatory support [4].
Given that corticosteroids are the cornerstone of asthma exacerbation manage­ment, close attention should be paid to blood glucose in patients with a known his­tory of diabetes or insulin resistance as uncontrolled hyperglycemia can lead to further adverse events. In the ICU, patients can have their hyperglycemia readily addressed with either subcutaneous insulin or a continuous insulin infusion.
158
Fig. 7.2 Chest X-rays in the majority of asthma exacerbations are low yield. One of the more common ndings as demonstrated below is hyperination
K. G. Correa and L. E. Eggert

7.2.3 Radiographic Findings

The role of radiologic studies in asthma exacerbations is limited. Unless the exacer­bation was triggered by pneumonia which can be seen on a chest X-ray or high­resolution computed tomography (CT) scan of the chest, most asthma exacerbations have an unremarkable chest X-ray [5]. Chest X-ray may demonstrate hyperination and attened diaphragms due to air trapping from airway obstruction. A CT of the chest may demonstrate ndings that are consistent with chronic airway inamma­tion such as bronchial wall thickening, and mucus plugging. Normal imaging nd­ings do not exclude the diagnosis of an asthma exacerbation. Even in the ICU setting, there is limited utility to obtaining serial imaging unless there were prior ndings requiring follow-up. In many instances, imaging is used to rule out an alter­native diagnosis such as pulmonary embolism, pneumothorax, or pneumonia (Fig.7.2).
7.3 Medical Management ofExacerbations
The management of an acute asthma exacerbation centers around reversing the underlying pathophysiology. As described previously, an exacerbation is repre­sented by uncontrolled hyperresponsiveness of the airway as a result of
7 Acute Asthma Exacerbation intheIntensive Care Unit
159
inammation and bronchoconstriction. The backbone of exacerbation management is thus through corticosteroids to temper airway inammation and inhaled broncho­dilators to relieve bronchoconstriction [5]. In severe exacerbations requiring the medical ICU, there may be limited initial response to treatment due to the degree of airway inammation and bronchoconstriction. This poses a clinical challenge as continued patient deterioration may occur despite initiating the correct therapies. In these difcult cases, several other therapies have been proposed with varying degrees of potential clinical benet and data to support their use.

7.3.1 Standard-of-Care Therapy

Corticosteroids are the mainstay of therapy for acute asthma exacerbations by acting to decrease airway inammation [1, 5]. These are given in addition to bronchodilators which act to relieve bronchial wall smooth muscle constriction. Together, these therapies act to alleviate airow obstruction, reduce air trapping and hyperination, and, thus, relieve patient symptoms and improve clini­cal status.
Ideal dosing of systemic corticosteroids in asthma exacerbations remains unclear. A previously published meta-analysis and systematic review comparing low-dose versus high-dose systemic corticosteroids for asthma exacerbations found no addi­tional benet with higher doses of systemic corticosteroids compared to lower doses [7]. Low-dose corticosteroids were dened as 80mg of methylprednisolone or 400 mg of hydrocortisone per day. However, patients who were in the ICU or receiving mechanical ventilation were excluded from these trials. There are no ran­domized controlled trials to dictate the dosing of systemic corticosteroids for patients requiring systemic corticosteroids in the intensive care unit, and thus, it is often left to clinician discretion. In general, higher dosages of systemic steroids and IV formulations tend to be used more frequently for patients admitted to the ICU, especially if requiring invasive ventilation.
While dosing remains nebulous, what is known is that earlier time to corticoste­roid administration is associated with improved outcomes. Studies have demon­strated that patients who receive corticosteroids within 1 hour of emergency department arrival have fewer admissions for asthma [8]. While these studies did not evaluate ICU patients, it does suggest that early control of inammation is key for optimal outcomes. In adult subjects in this study, the dosage of corticosteroid ranged from 500mg of IV hydrocortisone (equivalent to 100mg of methylpredniso­lone) to 125mg of IV methylprednisolone, which is the most frequently used dos­age in emergency departments in the United States [5].
There are two major types of inhaled bronchodilators that are used in acute asthma management: short-acting beta short-acting anticholinergics (SAAC). The most encountered type of SABA is salbu­tamol, better known as albuterol, and for SAAC, it is ipratropium. Albuterol and ipratropium can be given as either a nebulizer or a metered-dose inhaler (MDI).
adrenergic receptor agonists (SABAs), and
2