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- •Foreword
- •Foreword
- •Foreword
- •Contents of Volume I
- •Contents of Volume II
- •Contributors
- •1.1 Introduction
- •1.4.3 Acute Stroke
- •1.4.4 CNS Infection
- •1.4.1 Sepsis
- •1.4.2 Acute Encephalopathy
- •1.4.5 Severe Community-Acquired Pneumonia
- •1.4.6 Nosocomial Pneumonia
- •1.4.7 Pulmonary Edema
- •1.4.8 Fever
- •References
- •2.1 Introduction
- •2.4 ECG Nomenclature
- •2.4.1 P Wave
- •2.4.2 PR Interval
- •2.4.3 QRS Complex
- •2.4.4 J Point
- •2.4.5 ST Segment
- •2.4.6 T Wave
- •2.4.7 QT Interval
- •2.4.8 U Wave
- •2.4.9 RR Interval
- •2.5.1 P Wave
- •2.5.1.1 Atrial Arrhythmias
- •Atrial Fibrillation
- •Atrial Flutter
- •Atrial Tachycardia
- •Multifocal Atrial Tachycardia
- •2.5.1.2 Interatrial Blocks
- •Intermittent Interatrial Block (I-IAB)
- •Advanced Interatrial Block (A-IAB)
- •2.5.2 P-QRS Ratio
- •2.5.2.1 Shortened P-QRS Ratio
- •Wolff-Parkinson-White Syndrome (WPW)
- •Junctional Rhythm
- •Atrioventricular Nodal Reentrant Tachycardia (AVNRT)
- •2.5.2.3 Prolonged P-QRS Ratio
- •2.5.3 PR Interval
- •2.5.3.1 Shortened PR Interval
- •2.5.3.2 Prolonged PR Interval
- •2.5.3.3 Second-Degree AV Block
- •Advanced AV Block
- •Third-Degree AV Block (Complete Heart Block)
- •2.5.4 PR Segment
- •2.5.4.1 PR-Segment Elevation
- •2.5.4.2 PR-Segment Depression
- •Acute Pericarditis
- •Acute Myocardial Ischemia
- •2.5.5 Q Waves
- •2.5.6 QRS Complex
- •2.5.6.1 Heart Rate
- •2.5.7 QT Interval
- •2.5.8 ST Segment
- •2.5.8.1 ST-Segment Depression
- •2.5.8.2 ST-Segment Elevation
- •2.5.9 T Waves
- •2.5.9.1 Inverted T Wave
- •2.5.9.2 Flattened T Wave
- •2.5.9.3 Peaked T Wave
- •References
- •Further Reading
- •3.1 Introduction
- •3.2.2 Nasogastric Tube
- •3.2.3 Central Venous Catheters
- •3.2.4 Cardiac Devices
- •3.2.5 Arterial Catheters
- •3.3 Cardiopulmonary Abnormalities
- •3.3.1 Pulmonary Edema
- •3.3.2 Acute Respiratory Distress Syndrome
- •3.3.3 Atelectasis
- •3.3.4 Aspiration
- •3.3.5 Pneumonia
- •References
- •4.1 Introduction
- •4.5 Modes of Mechanical Ventilation
- •4.5.1 Volume Control Ventilation
- •4.5.2 Pressure Control Ventilation
- •4.5.3 Pressure Support Ventilation
- •4.6 Patient-Ventilator Interactions
- •4.6.1 Trigger Dyssynchrony
- •4.6.2 Flow Dyssynchrony
- •4.6.3 Cycle Dyssynchrony
- •4.9.1 Acute Respiratory Distress Syndrome
- •4.9.2 Severe Asthma Exacerbation
- •4.11 Summary
- •5.10 Neuromuscular Blockade
- •References
- •5.1 Introduction
- •5.3 Pathobiology
- •5.4 ARDS Phenotypes
- •5.5 Lung-Protective Ventilation
- •5.6 Positive End-Expiratory Pressure
- •5.7 Conservative Fluid Management
- •5.8 Moderate-to-Severe ARDS
- •5.9 Prone Positioning
- •5.11 Corticosteroids
- •5.12 Inhaled Pulmonary Vasodilators
- •5.13 Veno-Venous Extracorporeal Membrane Oxygenation
- •5.14 Survivorship
- •References
- •6.1 Introduction/Epidemiology
- •6.2 Physiology
- •6.2.2 Physiology During COPD Exacerbation
- •6.4 Pharmacologic Treatment
- •6.4.1 Bronchodilators
- •6.4.1.1 Mechanism
- •6.4.2 Glucocorticoid Therapy
- •6.4.2.1 Mechanism
- •6.4.2.4 Duration
- •6.4.3 Antimicrobials
- •6.4.3.1 Antibiotic Patient Selection
- •6.4.4.1 Nonpharmacologic Interventions
- •6.4.4.2 Opioids
- •6.4.4.3 Benzodiazepines
- •6.4.4.4 Dexmedetomidine
- •6.4.4.5 Ketamine
- •6.4.5 Adjunctive Therapies
- •6.4.5.1 Magnesium
- •6.4.5.3 Vitamin D
- •6.4.5.4 Venous Thromboembolism Prophylaxis
- •6.4.5.5 Smoking Cessation
- •6.4.5.6 Bowel Regimen
- •6.4.5.7 Mucolytics
- •6.4.5.8 Nutrition
- •6.4.5.9 Post-Discharge Adjuncts
- •6.5 ICU-Level Interventions
- •6.5.1 Noninvasive Positive-Pressure Ventilation
- •6.5.2 High-Flow Nasal Canula
- •6.5.3 Invasive Mechanical Ventilation
- •6.6 Conclusion
- •References
- •7.1 Introduction
- •7.1.1 What Is Asthma?
- •7.2 Diagnosis
- •7.2.1 Physical Examination
- •7.2.2 Laboratory Data
- •7.2.3 Radiographic Findings
- •7.3.1 Standard-of-Care Therapy
- •7.3.3 Potential Adjunctive Therapies
- •7.3.3.1 Inhaled Corticosteroids (ICSs)
- •7.3.3.4 Intravenous (IV) Aminophylline
- •7.3.3.5 Intravenous (IV) Beta2-Agonists
- •7.3.3.6 Leukotriene Antagonists (LTRAs)
- •7.3.3.7 Intramuscular (IM) or IV Epinephrine
- •7.3.3.8 Inhaled Anesthetics
- •7.3.3.9 Inhaled Helium-Oxygen (Heliox)
- •7.3.3.10 Intravenous Ketamine
- •7.3.4.1 Subcutaneous (SC) Biologics
- •7.4.1 Noninvasive Ventilation (NIV)
- •7.4.2 Invasive Mechanical Ventilation (IMV)
- •7.6.1 Outpatient Follow-Up
- •7.7 Summary
- •References
- •8.1 Introduction
- •8.1.3.2 Anatomic Location
- •8.1.3.3 Chronicity
- •8.1.4 Clinical Presentation
- •8.1.4.1 Symptoms
- •8.1.4.2 Physician Examination
- •8.1.4.3 Cardiopulmonary Compromise
- •8.2.1.1 Clinical Pretest/Scores
- •8.2.1.2 D-Dimer-Level Interpretations
- •8.2.2 Computed Tomography Pulmonary Angiography (CTPA)
- •8.2.3 Mortality Risk Assessment
- •8.2.3.1 PE Severity Index Score
- •8.2.3.2 Prognostic Indicators
- •8.3.2 High-Risk PE
- •8.4 Systemic Thrombolytic Therapy
- •8.4.1.1 High-Risk PE
- •8.4.1.2 Intermediate-Risk PE
- •8.4.1.3 Cardiac Arrest
- •8.5.2 Percutaneous Mechanical Interventions
- •8.5.2.2 Catheter-Directed Thrombolysis
- •8.5.3 Surgical Embolectomy
- •8.5.4 Mechanical Circulatory Support
- •8.6.1 PE Response Team (PERT)
- •8.6.3.1 Renal Dysfunction
- •8.6.3.4 Cancer
- •8.6.3.5 Treatment Failure
- •8.7 Conclusion
- •References
- •9.1.2 ECMO Outcomes
- •9.2 ECMO During Cardiopulmonary Resuscitation (eCPR)
- •9.2.1 Extracorporeal Carbon Dioxide Removal
- •9.3 ECMO Management
- •9.3.3 Fluid Management
- •9.4.1 Coagulation Changes
- •9.4.2 Transfusion Thresholds
- •9.4.3.1 Heparin
- •9.4.3.2 Direct Thrombin Inhibitors
- •9.4.4 Monitoring Anticoagulation
- •9.6.2.1 Opioids
- •9.6.2.2 Ketamine
- •9.6.2.3 Propofol
- •9.6.2.4 Benzodiazepines
- •9.6.2.5 Dexmedetomidine
- •9.7.1 Aminoglycosides
- •9.7.2 Beta-Lactams
- •9.7.4 Antifungals
- •9.9 Other Complications
- •9.9.1 Bleeding
- •9.9.2 Thrombosis
- •9.9.3 Neurologic
- •9.10 Conclusion
- •References
- •10.1 Type 1–5 Myocardial Infarctions
- •10.2 Acute Coronary Syndrome (Type 1 MI)
- •10.3 Clinical Presentation/Evaluation
- •10.4 Non-pharmacologic Therapy
- •10.5 Pharmacologic Therapy
- •10.5.1 Fibrinolytics
- •10.5.2 Anticoagulants
- •10.5.2.1 Heparins
- •10.5.2.2 Direct Thrombin Inhibitors
- •10.5.3 Antiplatelets
- •10.5.3.1 Aspirin
- •10.5.3.2 P2Y12 Inhibitors
- •Clopidogrel
- •Prasugrel
- •Ticagrelor
- •10.5.3.3 Glycoprotein IIb/IIIa Receptor Inhibitors
- •10.5.3.4 Cangrelor
- •10.7 Long-Term Management
- •10.7.1 High Bleed Risk (HBR)
- •10.7.2 Statins
- •10.7.3 Beta-Blockers
- •10.7.5 Mineralocorticoid Receptor Antagonists
- •References
- •11.1 Introduction
- •11.2.2 What is Ejection Fraction?
- •11.4 Understanding Blood Pressure
- •11.5 Preload vs. Afterload
- •11.6 Acute Decompensated Heart Failure
- •11.6.2 Etiology
- •11.8 Treating Volume Overload
- •11.8.1 Loop Diuretics
- •11.9 Intravenous Vasodilators
- •11.10 Cardiogenic Shock
- •11.10.1 Inotrope Clinical Pearl
- •11.12 Digoxin
- •11.12.3 Loading Dose
- •11.12.4 Maintenance Dosing
- •11.12.5 Monitoring
- •11.12.7 Distribution
- •11.12.8 Drug-Drug Interactions
- •11.12.9 Digoxin Toxicity
- •11.13 ADHF Clinical Pearls
- •11.13.3 Avoid Phenylephrine
- •11.13.4 Use Mean Arterial Pressure (MAP)
- •11.14 Guideline-Directed Medical Therapy
- •11.15 Venous Thromboembolism (VTE) Prophylaxis
- •11.16 Conclusion
- •References
- •12.1 Introduction
- •12.3 Diagnostic Findings
- •12.4.1 Oxygen Therapy
- •12.4.2 Pharmacological Management
- •12.4.3 Mechanical Circulatory Support (MCS)
- •12.5 Pulmonary Hypertension
- •12.6 The Pharmacist’s Role
- •12.7 Conclusion
- •References
- •13.1 Introduction
- •13.2 Atrial Arrhythmias
- •13.2.2 Atrioventricular Blocks
- •13.2.3 Atrial Fibrillation
- •13.2.3.2 Anticoagulation
- •13.2.3.3 Rate vs. Rhythm Control
- •13.2.4 Atrial Flutter
- •13.2.5 Supraventricular Tachycardia (SVT)
- •13.3 Ventricular Arrhythmias
- •13.3.1 Premature Ventricular Complexes
- •13.3.2 Ventricular Tachycardia
- •13.3.2.1 Torsades de Pointes
- •13.3.3 Ventricular Fibrillation
- •13.3.4 Ventricular Arrhythmia Treatment Strategies
- •13.3.4.1 ICD Implantation
- •13.3.4.2 Pharmacologic Treatments
- •13.3.4.3 Catheter Ablation
- •13.4 Conclusion
- •References
- •14.1 Introduction
- •14.3.2 Laboratory Assessment
- •14.3.3 Imaging
- •14.3.4 Invasive Hemodynamic Monitoring
- •14.4.1 Distributive
- •14.4.2 Cardiogenic
- •14.4.3 Hypovolemic
- •14.4.4 Obstructive
- •14.5 Management
- •14.6 Conclusion
- •References
- •15.1 Background
- •15.2 Diagnosis
- •15.3 Management
- •References
- •16.1 Introduction
- •16.3 Hemodynamics
- •16.5 Pharmacological Management
- •16.5.1 Hyperosmolar Therapy
- •16.5.3 Barbiturate Coma
- •16.6 Nonpharmacological Treatments
- •16.6.2 Temperature Management
- •16.6.3 Prophylactic Hypothermia
- •16.7 Adjunct Therapies
- •16.7.2 Venous Thromboembolism (VTE) Prophylaxis
- •16.7.3 Antibiotic Prophylaxis
- •16.7.4 Stress Ulcer Prophylaxis (SUP)
- •16.7.5 Tranexamic Acid
- •16.7.6 Glucose Targets
- •16.7.7 Steroids
- •16.8 Complications
- •16.8.1 Paroxysmal Sympathetic Hyperactivity
- •16.8.3 Central Fever
- •16.8.4.1 Diabetes Insipidus
- •16.8.4.3 Cerebral Salt Wasting Syndrome
- •16.9 Conclusion
- •References
- •17.1 Introductory Case
- •17.2 Introduction
- •17.4 Pathophysiology
- •17.5 Acute Therapies
- •17.5.1 Thrombolytic Therapy
- •17.5.2 Thrombectomy
- •17.5.3 Blood Pressure Management
- •17.5.4 Acute Anticoagulation
- •17.5.5 Antiplatelet Therapy
- •17.6 Early Complications
- •17.6.1 Hemorrhagic Conversion
- •17.6.2 Angioedema
- •17.6.3 Malignant Cerebral Edema
- •17.7 Secondary Prevention
- •References
- •18.1 Introduction
- •18.4 Therapeutic Drug Monitoring
- •18.5 Adverse Drug Effects
- •18.7 Anti-seizure Medications
- •18.7.1 Available Parenteral Preparations
- •18.7.1.1 Benzodiazepines: GABAA Receptor Activation
- •18.7.1.2 Other GABAergic Therapies
- •Barbiturates: GABAergic
- •Phenobarbital
- •Pentobarbital Infusion
- •Propofol Infusion: GABAergic
- •18.7.1.3 Second-Line Non-anesthetic ASMs
- •Levetiracetam: Synaptic Vesicle Protein 2A Binding

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Chapter 7
Acute Asthma Exacerbation
intheIntensive Care Unit
KevinG.Correa andLaurenE.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
inammation [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 airow 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 1second (FEV-1), and
forced vital capacity (FEV-1/FVC) ratio, and sometimes there is also evidence of air
trapping or hyperination [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 inammation to reduce obstructive symptoms
by targeting the several molecular pathways that lead to inammation and bronchoconstriction [1]. As a result of chronic inammation, 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 inammatory diseases and is known to affect
more than 300million 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 signicant
role in the severity and control of asthma with worse outcomes in populations identied 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 anAsthma 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-specic 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 dened as asthma with rapidly worsening symptoms and
clinical deterioration [1]. The hyperresponsive and inamed bronchioles of the airway lead to overt bronchoconstriction and airow obstruction, which can be demonstrated by worsening obstruction on spirometry and/or a decreased PEF [4]. In

7
cute Asthma Exacerbation intheIntensive Care Unit
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155
addition, the remodeled bronchioles are subjected to mucus hypersecretion, which
additionally leads to further airway occlusion and subsequent hyperination [4].
Prompt recognition of exacerbation symptoms is crucial as early assessment and
intervention are necessary to prevent signicant 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 andRisk Factors forMore
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. Table7.1 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
Wildres or pollution
Strong odors
Gastric reux
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 difcult-to-control asthma, steroid-dependent
asthma, elderly patients with signicant 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 identication 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, signicant 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 specic ndings on the exam which can signal patients at higher risk for
needing ICU level of care. Table7.2 highlights the main physical exam ndings that
are indicative of a severe or life-threatening exacerbation.

7 Acute Asthma Exacerbation intheIntensive 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
hyperination)
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, inammatory 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 inuenza 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
hyperination
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 hyperination
and attened diaphragms due to air trapping from airway obstruction. A CT of the
chest may demonstrate ndings that are consistent with chronic airway inammation 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 ofExacerbations
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 intheIntensive Care Unit
159
inammation and bronchoconstriction. The backbone of exacerbation management
is thus through corticosteroids to temper airway inammation 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 inammation and bronchoconstriction. This poses a clinical challenge as
continued patient deterioration may occur despite initiating the correct therapies. In
these difcult cases, several other therapies have been proposed with varying
degrees of potential clinical benet 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 inammation [1, 5]. These are given in addition to
bronchodilators which act to relieve bronchial wall smooth muscle constriction.
Together, these therapies act to alleviate airow obstruction, reduce air trapping
and hyperination, 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 benet with higher doses of systemic corticosteroids compared to lower doses
[7]. Low-dose corticosteroids were dened as ≤80mg 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 inammation is key
for optimal outcomes. In adult subjects in this study, the dosage of corticosteroid
ranged from 500mg of IV hydrocortisone (equivalent to 100mg of methylprednisolone) to 125mg 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
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