24: Bronchospasm and Chronic Obstructive Pulmonary Disease
CHAPTER 24 Bronchospasm and Chronic Obstructive Pulmonary Disease
Karishma Parekh1 and E. Mirna Mohanraj2
1 Mercy Medical Center, Roseburg, OR, USA
2 Icahn School of Medicine at Mount Sinai, New York, NY, USA
Background
Definition of disease
The Global Initiative for Asthma (GINA) defines asthma as a ‘common, chronic, heterogeneous respiratory disease characterized by variable airflow limitation and usually associated with airway hyper‐responsiveness and chronic airway inflammation.’
The Global Initiative for Chronic Obstructive Pulmonary Disease (GOLD) defines COPD as a ‘common preventable and treatable disease, characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases.’
Disease classification
Acute severe asthma (status asthmaticus) is an acute, severe asthma exacerbation that does not respond to initial intensive medical therapy. Patients with acute severe asthma often require ventilatory assistance.
Acute exacerbation of COPD (AECOPD) is a clinical diagnosis characterized by acute worsening of a patient’s respiratory symptoms, including increased cough, sputum production, and/or dyspnea. Severe AECOPD may progress to acute respiratory failure requiring ventilatory assistance.
Incidence/prevalence
More than 25 million people in the USA suffer from asthma. Acute asthma exacerbations account for 1–2 million emergency department visits annually: 25% of these patients require hospitalization; 5–10% of hospitalized patients require ICU admission. In‐hospital asthma mortality is approximately 0.5%.
In the USA, moderate to severe COPD affects more than 65 million people and is the third leading cause of death. COPD is a comorbid condition in nearly 9% of all patients admitted to the ICU and independently contributes to ICU mortality. Severe AECOPD accounts for approximately 2.5% of ICU admissions for acute respiratory failure and carries an estimated in‐hospital mortality rate of 5–20%.
The global prevalence of asthma and COPD is increasing. Important associated factors are socioeconomic status, smoking behaviors, and exposure to outdoor, indoor, and occupational air pollution.
Etiology
The most common causes of acute severe asthma and AECOPD requiring ICU admission are bacterial and viral respiratory tract infections.
Bacterial pathogens are mainly implicated in AECOPD, whereas viral infections are most often associated with acute severe asthma.
In asthmatics, significant exposure to extrinsic allergens, food allergens, or NSAIDs may also trigger sudden exacerbations.
In patients with COPD, undiagnosed venous thromboembolism, decompensated heart failure, and natural progression of disease may contribute to AECOPD.
Additional causes of exacerbation include inadequate baseline control, medication non‐compliance, inhalation of recreational drugs, and exposure to air pollutants.
Pathology/pathogenesis
Airway inflammation and airway wall edema are present in both asthma and COPD.
Inflammation in asthma is triggered by allergic bronchial hyper‐responsiveness to inhaled allergens. The inflammatory response is driven by airway infiltration by eosinophils, neutrophils, stimulated Th2 lymphocytes, and activated mast cells. Cytokine‐mediated airway injury ensues via the release of interleukins (particularly IL‐4, IL‐5), GM‐CSF, allergen‐specific IgE, and leukotrienes.
Inflammatory cells trigger a cytokine cascade that results in bronchoconstriction via smooth muscle contraction, mucous gland secretion, and further airway inflammation.
Airway inflammation in COPD results from inhalation of noxious particles and gases – predominantly cigarette smoke. It is chronic in nature and is characterized by neutrophil‐predominant inflammatory cells with increased mucous production. Continued lung parenchymal destruction leads to emphysema and impaired gas exchange.
Airflow obstruction is the pathophysiologic hallmark of both severe acute asthma and severe AECOPD. Narrowing of the airways leads to airflow limitation and increased airway resistance.
In asthma, airflow obstruction results from a combination of airway inflammation and edema, airway smooth muscle contraction, mucus plugging of the airways, and airway remodeling. Both inspiratory and expiratory flow rates are limited.
In COPD with emphysema, airflow limitation is most pronounced during expiration. Parenchymal destruction leads to a loss of airway tethering with intrapulmonary airway collapse during expiration.
Dynamic hyperinflation:
Tachypnea in the setting of airflow limitation results in incomplete exhalation and hyperinflation. This leads to the increases in end‐expiratory lung volumes and alveolar pressures referred to as intrinsic PEEP or auto‐PEEP.
In an effort to completely exhale each breath, expiratory muscles are recruited with an increase in pleural pressures. This is often insufficient to overcome severe airways obstruction and hyperinflation worsens with each breath.
Hyperinflation also results in diaphragm flattening and inefficient expiratory muscle contraction, further worsening expiratory flow and dynamic hyperinflation.
In patients with severe AECOPD, increased pleural pressures will cause airway collapse and progressive hyperinflation.
Consequences of persistent and progressive airways obstruction:
Increased dead space ventilation results in severe ventilation–perfusion (V/Q) mismatch and hypoxemia.
Alveolar overdistension introduces high risk for barotrauma with ventilatory and hemodynamic compromise.
Air trapping increases intrathoracic pressure, which impedes systemic venous return. Decreases in right ventricular preload and stroke volume cause hypotension and may lead to shock.
The high work of breathing cannot be sustained. A combination of increased metabolic demands of the respiratory muscles, hypoxemia, and hypoperfusion worsens hypercapnia and results in respiratory failure.
Persistent hypoxemia may have additional harmful effects including neurologic damage, cardiac arrhythmia, and cardiac ischemia.
Predictive/risk factors
Patients requiring mechanical ventilation for either acute severe asthma or severe AECOPD are at high risk for death.
Secondary complications from severe airways obstruction and/or mechanical ventilation include hemodynamic instability from dynamic hyperinflation, barotrauma, and severe acidemia.
Cough, sputum retention, recurrent infections, airway collapse and air trapping on dynamic CT chest
Pulmonary embolism
Pleuritic chest pain, symptoms of deep vein thrombosis, filling defect on chest CT angiography
Congestive heart failure exacerbation
Orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema, rales, evidence of volume overload, pulmonary edema on chest radiograph, elevated BNP
Myocardial infarction
Angina pectoris, ECG consistent with myocardial ischemia, elevated cardiac biomarkers
Paradoxical vocal fold motion
Recurrent wheezing, stridor, abnormal vocal cord adduction on direct laryngoscopy
Hyperventilation syndrome
Intermittent hyperventilation with spontaneous resolution, sense of fear or anxiety, parasthesias
Typical presentation
Patients with acute severe asthma present with severe dyspnea even at rest, wheezing, difficulty speaking and chest tightness. Patients may have had recent exposure to known or unknown triggers. Patients typically report worsening symptoms despite increased use of short‐acting β2‐agonist therapy.
Patients with severe AECOPD present with progression of their baseline symptoms including worsening dyspnea, cough, wheezing, and exercise intolerance. They may report discoloration and increased volume of sputum. Overt hemoptysis is rare, but streaks or flecks of blood in the sputum are not uncommon.
Clinical diagnosis
History
Presence of constitutional symptoms.
Presence of respiratory symptoms including dyspnea, cough, wheezing, hemoptysis, sputum production (volume, color, change from baseline), pleuritic or exertional chest pain, orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema.
Onset, duration, frequency, and timing of symptoms.
Symptoms include sleep disturbance, exercise intolerance, or limitation in activities of daily living.
Alleviating and exacerbating factors.
Exposure to sick contacts, significant allergens at home or work.
Prior history of exacerbations, use of oral corticosteroids, emergency care or hospitalizations.
Prior intubation or ICU admission.
Adherence to medication regimen, frequency of rescue medication use, recent changes in medication regimen.
Physical examination
Document vital signs including temperature, blood pressure, heart rate, respiratory rate, and continuous pulse oximetry. Pulsus paradoxus indicates severe airflow obstruction.
Examine the patient’s general appearance. Agitation, anxiety, upright or forward‐leaning position indicates severe disease.
Assess for signs of impending respiratory failure including cyanosis, nasal flaring, suprasternal retractions, accessory muscle use, paradoxical breathing (abnormal or dysynchronous movement of the chest wall and/or abdomen during respiration), and the inability to complete full sentences. Ominous signs include confusion or somnolence, ‘silent chest,’ hypotension, and bradycardia.
Inspect the oral airway to prepare for potential intubation.
Auscultate the lungs to identify inspiratory and/or expiratory wheezing, diminished breath sounds, or other sounds that may support an alternate diagnosis.
Listen for stridor.
Auscultate the heart for brady‐ or tachyarrhythmias. Note the presence of jugular venous distension, hepatojugular reflex, and lower extremity edema.
Identify clubbing of the extremities.
Evaluate for signs of barotrauma including absent breath sounds, jugular venous distension, subcutaneous emphysema, and deviated sternal notch.
In the ventilated patient, serial examinations should assess for barotrauma and the development of auto‐PEEP:
Auscultate for bilateral, symmetric breath sounds.
Palpate the neck and chest wall for subcutaneous emphysema.
Listen carefully to the expiratory phase; if the next ventilator breath interrupts complete exhalation, the patient is likely developing auto‐PEEP.
Laboratory diagnosis
List of diagnostic tests
Arterial blood gas should be routinely ordered for patients with acute severe asthma or severe AECOPD.
AECOPD may present with acute or acute‐on‐chronic CO2 retention. An elevated bicarbonate level may be a clue to chronic hypercapnia in an individual with known severe COPD. Hypoxemia may also be present, but use of chronic supplemental oxygen should be considered in the interpretation.
Acute severe asthma often presents with hypoxemia and hypocapnia. Normocapnia or mild hypercapnia may indicate impending respiratory failure.
CBC should be ordered in all patients with AECOPD and status asthmaticus.
Serum electrolytes (potassium, magnesium, phosphate) should be monitored in patients using frequent β2‐agonist therapy.
ECG should be routinely ordered to evaluate for myocardial ischemia, arrhythmia, and right ventricular strain pattern.
Consider obtaining cardiac biomarkers (troponin‐T, BNP) in patients with AECOPD or with presentation concerning for myocardial ischemia, left‐sided heart failure, or cor pulmonale.
Obtain theophylline level for asthmatics taking this medication.
Influenza/viral culture and/or bacterial sputum culture should be obtained in patients with relevant symptoms of infection.
List of imaging techniques
Chest radiograph: evaluate for consolidation, barotrauma (pneumothorax, pneumomediastinum, pneumoperitoneum, subcutaneous emphysema (Figure 24.1)), and pulmonary edema.
CT angiography: consider when presentation is suspicious for acute pulmonary embolism. Increased index of suspicion is recommended in AECOPD patients without a clear precipitating factor.
Serial peak expiratory flow (PEF) monitoring is recommended for patients with asthma who are able to participate in testing. A decrease in PEF to less than 40% predicted or personal best indicates a severe exacerbation. Improvements in PEF indicate a response to therapy.
In centers with appropriate ultrasound expertise, point‐of‐care chest ultrasonography may be used to detect pneumothorax in mechanically ventilated patients with acute severe asthma or AECOPD.
Potential pitfalls/common errors made regarding diagnosis of disease
Incomplete history of prior exacerbations or respiratory failure that may inform risk stratification.
Failure to maintain a broad differential diagnosis.
Delayed recognition of impending respiratory failure, particularly in acute severe asthma.
Treatment
Treatment rationale
Immediate assessment and treatment of compromised respiratory and hemodynamic status is critical to preventing and managing respiratory failure and cardiovascular collapse.
Invasive and non‐invasive positive pressure ventilation are life‐saving therapies for patients with acute respiratory failure from obstructive airways processes. Careful patient selection (for invasive versus non‐invasive ventilation strategies) and appropriate monitoring is critical.
First line pharmacologic therapy for both acute severe asthma and AECOPD is the administration of bronchodilators and corticosteroids.
Antibiotics should be administered in patients with signs and symptoms of infection.
Adjunctive therapies to mechanical ventilation including deep sedation, neuromuscular blockade, anesthetic agents (intravenous ketamine, inhaled anesthetics), ECMO, and ECCO2R (extracorporeal CO2 removal) should be considered for refractory cases.
When to hospitalize
Indicators of need for hospitalization in AECOPD:
Older age.
Severe underlying COPD.
Use of long‐term oxygen therapy.
Difficulty managing disease at home.
Significant cardiac comorbidities.
Failure to respond to initial medical treatment.
Signs of overt or impending respiratory failure.
Indicators of need for hospitalization in acute asthma exacerbation:
Severe underlying asthma.
Failure to respond to initial medical treatment.
Post‐treatment improvement in PEF remains less than 40% predicted or personal best.
ICU admission for overt or impending respiratory failure, respiratory arrest, impaired consciousness, or refractory hypoxemia or hypercarbia.
Managing the hospitalized patient
Overview of management for acute severe asthma or AECOPD
Oxygen supplementation
Target saturation 88–92% Excessive oxygen may have deleterious effects in AECOPD
Non‐invasive positive pressure ventilation
First line therapy in carefully selected patients with respiratory failure from AECOPD
Mechanical ventilation
Target low respiratory rate to allow prolonged expiratory time Maintain plateau pressures <30 cmH2O Monitor for auto‐PEEP
Inhaled bronchodilators
Administer every 20 minutes to every hour Continuous delivery may be required
Systemic corticosteroids
Administer equivalent of methylprednisolone 60–125 mg IV every 6 hours Taper with clinical improvement
Antibiotics
Initiate antibiotic treatments in patients with evidence of infection
Sedation
Target ventilator synchrony
Neuromuscular blockade
Administer for ventilator asynchrony, severe auto‐PEEP, and poorly controlled airway pressures
ECMO and ECCO2R
Consider expert consultation in patients on maximal therapy with refractory hypoxemia, hypercapnia, or hemodynamic compromise
Anesthetic agents
Consider expert consultation in patients on maximal therapy with refractory acidosis, life‐threatening auto‐PEEP, and poorly controlled airway pressures
Supplemental oxygen
Target saturation in acute severe asthma and severe AECOPD is 88–92%.
Excessive oxygen supplementation may have deleterious effects in AECOPD patients including progressive hypercapnia from V/Q mismatch, decreased binding of carbon dioxide to hemoglobin due to the Haldane effect, and blunted ventilatory drive.
Non‐invasive positive pressure ventilation (NPPV)
NPPV is increasingly being used as first line ventilatory support in patients with severe AECOPD.
Positive expiratory pressure leads to airway dilation, improves ventilation, and improves gas exchange. Positive inspiratory pressure alleviates the work of inspiratory muscles and relieves dyspnea.
In AECOPD, the use of NPPV can prevent intubation, shorten length of stay, and significantly reduce mortality (NNT = 4). This mortality reduction is largely attributed to the avoidance of invasive mechanical ventilation‐associated complications.
Patients on NPPV must be monitored closely. Improvement in respiratory acidosis, work of breathing, and confusion should be observed within 1–2 hours of initiation. If no improvement or decline, rapidly move to invasive mechanical ventilation.
The use of NPPV for acute asthma exacerbation remains controversial. NPPV may be used in selected asthmatics with caution and vigilance in monitoring.
Indications for NPPV in AECOPD
Respiratory acidosis.
Evidence of respiratory muscle fatigue.
Use of accessory muscles, paradoxical respiratory pattern.
Contraindications to NPPV
Cardiopulmonary arrest.
Hemodynamic instability.
Altered mental status (excluding hypercapnic encephalopathy).
Inability to protect the airway.
Active emesis, hematemesis, copious oral secretions.
Increase IPAP in increments of 2–4 cmH2O (up to 10–20 cmH2O) as tolerated, with goals:
Alleviation of dyspnea.
Decreased respiratory rate.
Adjust to deliver VT 6–8 mL/kg predicted body weight.
Patient–ventilator synchrony.
Invasive mechanical ventilation (IMV)
The aim of IMV is to assume the work of breathing and maintain gas exchange while avoiding the complications of dynamic hyperinflation.
Early intubation is advised for patients who do not respond to aggressive treatment, deteriorate despite aggressive treatment, or show signs of impending respiratory failure.
Indications for IMV
Respiratory or cardiac arrest.
Inability to tolerate NPPV or NPPV failure.
Hemodynamic instability.
Inability to clear secretions.
Persistent diminished consciousness or agitation.
Refractory hypercapnia or hypoxemia.
Intubation
Physicians experienced with difficult airway management should perform intubation in a controlled setting.
Anticipate and prepare for post‐intubation hemodynamic instability. Venous return is impaired by the presence of dynamic hyperinflation and worsened with positive pressure ventilation. Intravenous fluid resuscitation and vasopressors may be required.
Ventilator settings
Controlled modes of ventilation – either pressure controlled or volume controlled – are recommended.
Initial settings for volume‐controlled ventilation should target a low tidal volume 6–8 mL/kg predicted body weight, respiratory rate of 10–12 breaths/min, and FiO2 of 100%. Respiratory rate is set low in order to prolong expiratory time and allow expiratory flow to reach zero before the next inhalation (Figure 24.2).
Initial PEEP setting of 0–5 cmH2O is recommended in patients with acute severe asthma or severe AECOPD.
Intrinsic PEEP should be measured using an expiratory hold maneuver (Figure 24.3). However, caution must be exercised to not underestimate auto‐PEEP in patients with severe airways obstruction. With severe bronchospasm, airways that are not in communication with main airways may be obstructed due to edema and mucous and, although overdistended, not measured as auto‐PEEP. If a patient has hemodynamic signs consistent with auto‐PEEP and clinical examination showing continued expiration when the next ventilator breath is given, assume there is significant auto‐PEEP.
Significant auto‐PEEP must be treated. This may be achieved with improved patient–ventilator synchrony, reduced inspiratory to expiratory time ratio, and continued medical treatment of bronchoconstriction.
Extrinsic PEEP can be added for patients with severe air trapping who are allowed spontaneous breaths. This may reduce work of breathing to trigger inspiration, but may also result in worsened air trapping and dangerously high inspiratory pressure if not performed under expert supervision and monitoring.
Plateau pressures should be monitored closely and maintained below 30 cmH2O. Peak pressures should be maintained as low as possible.
For pressure‐controlled ventilation, ensure that adequate tidal volumes are achieved.
Permissive hypercapnia refers to permitting a PaCO2 of 60–80 mmHg and pH as low as 7.2. Elevated PaCO2 is the result of reducing minute ventilation, allowing prolonged time for exhalation in order to reduce auto‐PEEP. Permissive hypercapnia is typically necessary in acute severe asthma to allow auto‐PEEP reduction strategies. Permissive hypercapnia is problematic for patients with increased intracranial pressure, severe coronary disease, or severe metabolic acidosis.
Deep sedation is typically required to ensure patient–ventilator synchrony and to reduce risk of barotrauma.
Neuromuscular blockade may be required in severe cases.
Sedation for IMV
Continuous sedative infusion is a mainstay of therapy, particularly for mechanically ventilated patients with status asthmaticus.
A validated sedation scale, such as the Richmond Agitation‐Sedation Scale (RASS), should be utilized. Until airflow limitation state has improved, patients with acute severe asthma or severe AECOPD typically require moderate to deep sedation (often RASS –3 to –4) to achieve comfort and ventilator synchrony.
Propofol by continuous infusion is commonly used and may have additional bronchodilator effects.
Additional opiate and/or benzodiazepine infusions may be required to achieve desired level of sedation and ventilator synchrony. Morphine is associated with histamine release but this seems to have minimal clinical importance. Fentanyl is not associated with histamine release.
Despite deep sedation, patients with persistent ventilator asynchrony or progressive dynamic hyperinflation may require neuromuscular blockade. Cisatracurium loading dose followed by continuous infusion is frequently used.
Adjunctive therapies
Bronchoscopy may be rarely required for airway clearance in intubated patients with severe mucous plugging. Procedure duration should be minimized. Monitor the patient closely for worsening airway resistance, barotrauma, and hemodynamic instability during the procedure.
Routine bronchoscopy in patients with severe AECOPD is not beneficial.
Inhaled β2‐agonist treatments act within 5 minutes to decrease airway inflammation, relax airway smooth muscle, and decrease mucous production. For a patient in respiratory distress, repeated doses may be given at intervals of every 20 minutes to every hour. Continuous nebulization may be required. Administration via a nebulizer or MDI has equivalent effects; however, nebulized treatment is recommended for patients in respiratory distress to ensure adequate medication delivery.
Inhaled ipratroprium bromide may be added to β2‐agonist therapy to augment the bronchodilator effect. Due to its slow onset of action, it should not be used as a stand‐alone bronchodilator.
Parenteral methylxanthine administration is generally not recommended in the acute setting.
Subcutaneous, endotracheal, or parenteral epinephrine may be considered in patients refractory to inhaled bronchodilator therapy.
Table 24.2Frequently used medications in acute severe asthma and severe AECOPD.
Drug name
Recommended dosage
Frequency
Nebulized albuterol
2.5 mg to 5 mg
Every 20 minutes initially then every 4–6 hours in the stabilized patient Severe disease may require continuous administration
Nebulized ipratropium
0.5 mg (2.5 mL)
Every 6–8 hours
Nebulized albuterol/ipratropium
2.5 mg/0.5 mg per 3 mL
Every 4–6 hours
Methylprednisolone
60–125 mg IV
Every 6 hours until stabilized
Magnesium sulfate
2 g IV
One time dose given over 20 minutes
Epinephrine
0.1–0.3 mg subcutaneous
Every 20 minutes (to a maximum of 0.01 mg/kg)
Lorazepam
0.01–0.1 mg/kg/h continuous infusion
Titrate to targeted level of sedation and patient–ventilator synchrony
Midazolam
0.02–0.1 mg/kg/h continuous infusion
Titrate to targeted level of sedation and patient–ventilator synchrony
Morphine
2–30 mg/h continuous infusion
Titrate to targeted level of sedation and patient–ventilator synchrony
Fentanyl
0.7–10 μg/kg/h continuous infusion
Titrate to targeted level of sedation and patient–ventilator synchrony
Propofol
0.3–3 mg/kg/h continuous infusion
Titrate to targeted level of sedation and patient–ventilator synchrony
Early corticosteroid administration improves lung function and decreases duration of exacerbation by reducing inflammation and mucous production.
Administer methylprednisolone 60–125 mg IV every 6 hours. Transition to lower dosing or oral therapy once symptoms have improved. However, evidence is lacking for benefit of higher dose (>80 mg) or intravenous compared to oral route.
Antibiotics:
Antibiotics should be started in asthmatics with signs and symptoms of bacterial infection.
Antibiotics should be administered to COPD patients with moderate to severe exacerbation who meet the Winnipeg criteria (increased dyspnea, increased sputum volume, increased sputum purulence) or who require invasive mechanical ventilation.
Antibiotic selection should be based on local bacterial resistance pattern and/or sputum culture results for high risk patients (recent antibiotic use, recent intubation).
Parenteral magnesium sulfate may have beneficial bronchodilator effects in adult asthmatics with severe airflow limitation. This treatment does not benefit patients with AECOPD.
Leukotriene‐receptor antagonist therapy has not been well studied in patients with acute severe asthma or severe AECOPD. It is not a recommended therapy at this time.
Mucolytics and chest physical therapy are suitable for asthma and COPD patients with copious or retained secretions. Airway clearance devices may also be beneficial for secretion clearance, but critically ill patients are unlikely to use these effectively.
Refractory respiratory failure in mechanically ventilated patients
Severe airways disease is dynamic and requires time for treatments to work. Patients may demonstrate respiratory acidosis for 1–2 days.
If there is lack of response or worsening clinical condition despite above measures, we consider this to be refractory respiratory failure:
Hypoxemia despite high FiO2.
Severe persistent hypercapnia (PaCO2 >80 mmHg, pH <7.2).
Inability to achieve tidal volumes due to elevated airway pressures.
Additional treatments for patients with refractory respiratory failure
Neuromuscular blockade may be necessary for patients with ventilator asynchrony, severe auto‐PEEP, and poorly controlled airway pressures. Patients must be adequately sedated. The neuromuscular‐blocking agent should be discontinued as soon as safely possible.
ECMO and ECCO2R may be considered in patients with acute severe asthma with refractory hypoxemia or hypercapnia and/or hemodynamic compromise.
Ketamine is a parenteral anesthetic used in refractory acute severe asthma as an anticholinergic bronchodilator. Evidence does not demonstrate additional benefit over conventional therapy. There is no indication for its use in AECOPD.
Inhaled halogenated anesthetics (isoflurane, sevoflurane) may be administered for patients with refractory acidosis, life‐threatening auto‐PEEP, and poorly controlled airway pressures despite maximal therapy inclusive of neuromuscular blockade. Anesthetic agents must be administered by an anesthesiologist. These agents have both direct and indirect bronchodilator effects that should be evident shortly after administration. Current data do not associate use of inhaled anesthetics with improved outcomes. There is no indication for use of inhaled anesthetics in AECOPD.
Heliox (helium) is a low density gas that can be mixed with supplemental oxygen to reduce turbulent flow and increase airflow through constricted airways. The mixture includes only up to 30% O2, thus is not practical for patients with a greater degree of hypoxemia. Limited data support the routine use of heliox for severe obstructive airways disease. It may be utilized as an adjunctive therapy for difficult to ventilate asthmatics.
Prevention/management of complications
In patients requiring mechanical ventilation, complications of dynamic hyperinflation – including pulmonary barotrauma and hemodynamic compromise – may occur suddenly and can be life threatening.
Pulmonary barotrauma may present with sudden worsening in hypoxemia, hypotension, or clinical exam findings such as: absent or diminished breath sounds, tracheal deviation, subcutaneous emphysema, and jugular venous distension.
An acute increase in peak and plateau pressures should also raise suspicion for pulmonary barotrauma.
If clinical exam suggests tension pneumothorax with instability, immediate needle compression should be performed as a temporizing measure. Tube thoracostomy must then be placed.
In the hemodynamically stable patient, there should be prompt evaluation for pneumothorax with CXR and/or bedside ultrasonography in experienced hands.
Bedside tube thoracostomy should be performed for definitive management of pneumothorax.
Surgical consultation is recommended for management of pneumomediastinum, pneumoperitoneum, and persistent air leaks.
If hypotension is attributed solely to dynamic hyperinflation, a brief apnea trial (30–60 seconds of prolonged exhalation) may be attempted. This should be done under the supervision of a senior clinician.
Patients should be closely monitored for signs of sepsis or venous thromboembolism.
Prolonged immobilization while on mechanical ventilation, in conjunction with the use of glucocorticoids, sedatives, and neuromuscular blockade agents, may lead to ICU‐acquired weakness. With physical rehabilitation, patients typically recover to their pre‐hospitalization functional status.
Special populations
Pregnancy
Status asthmaticus in pregnancy is rare but poses life‐threatening challenges to both mother and fetus.
Pregnant patients have decreased functional residual capacity, increased airway edema, increased mucous secretion, and reduced respiratory reserve placing them at high risk for respiratory failure.
Maternal hypoxia must be avoided to prevent intrauterine growth retardation and fetal death. A target PaO2 of greater than 65 mmHg is considered safe.
Generally, treatment strategies are the same as in non‐pregnant patients but several areas warrant special attention:
Short‐acting β2‐agonists and corticosteroids are generally considered safe for the treatment of acute severe asthma in pregnancy.
The safety of continuous sedative infusion in pregnancy is unknown.
Propofol (pregnancy category B) is commonly used and may have additional bronchodilator effects. Caution must be exercised to avoid hypotension. Excessive dosing may lead to decreased uterine smooth muscle tone.
Opiates (pregnancy category C) are used for short‐term continuous sedation and analgesia in pregnancy. These medications cross the placenta. Longer‐term use – or third trimester use – might affect fetal neurologic development or result in neonatal withdrawal syndrome.
Benzodiazepines (pregnancy category D) should be avoided. These medications cross the placenta and pose fetal risk.
If neuromuscular blockade is required, short‐term use of cisatracurium (pregnancy category B) is recommended. Longer term use may result in fetal arthrogryposis.
NPPV should be used only in highly selected patients. Pregnant patients are at higher than normal risk for gastric distension and aspiration.
Mechanical ventilation in pregnant asthmatics poses particular challenges and should be managed by expert practitioners. The intensivist must work with the obstetrician and maternal–fetal specialist as a team to manage these patients.
Permissive hypercapnia strategies may be life‐saving, but have not been studied specifically in pregnancy.
Due to increased minute ventilation in pregnancy, baseline PaCO2 levels are lower in pregnancy.
Higher PaCO2 levels may have deleterious effects, including decreased uterine blood flow and fetal respiratory acidosis.
While controversial, permissive hypercapnia has been used successfully with excellent pregnancy outcomes. In pregnant patients with refractory respiratory failure despite aggressive treatment, permissive hypercapnia may be exercised with caution.
Prognosis
Prognosis for treated patients
AECOPD:
Admission for AECOPD is associated with a 1 year mortality of 1–9% with significantly increased rates for patients requiring mechanical ventilation.
Several risk factors portend a worse prognosis – severity of underlying COPD, need for long‐term oxygen therapy, comorbid conditions, older age – with 1 year mortality rates surpassing 25–40%.
Patients who can be managed with NPPV have lower mortality and shorter length of stay.
Postextubation, many patients will not return to their baseline respiratory status.
Acute severe asthma:
Patients requiring mechanical ventilation for acute severe asthma have low immediate mortality but maintain a high risk for recurrence of status asthmaticus.
Mortality at 1 year has been cited as high as 10% for patients with recurrent acute severe asthma needing intubation.
Excluding patients with out of hospital respiratory and cardiac arrest, the majority of patients admitted with acute severe asthma return to baseline functional status.
Follow‐up tests and monitoring
Post‐discharge, patients should have prompt follow‐up with a pulmonologist.
Pulmonary function testing should be performed following the exacerbation.
Patients with AECOPD should be evaluated for pulmonary rehabilitation once they have recovered from the acute phase of disease.
Several factors require iterative education including: reliable and rapid access to medical care, adherence to medication regimen, appropriate inhaler therapy technique, understanding signs and symptoms of exacerbation, monitoring increased use of rescue medications, and trigger avoidance.
Reading list
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Guidelines
National society guidelines
Title
Source
Date and weblink
National Asthma Education and Prevention Program: Expert panel report III – Guidelines for the Diagnosis and Management of Asthma
GINA Report: Global Strategy for Asthma Prevention and Management
Global Initiative for Asthma
2020 www.ginasthma.org
Global Strategy for the Diagnosis, Management and Prevention of COPD
Global Initiative for Chronic Obstructive Lung Disease
2020 www.goldcopd.org
Images
Figure 24.1 Barotrauma in a patient with status asthmaticus. Patient has extensive subcutaneous emphysema and required chest tubes for bilateral pneumothorax.
Figure 24.2 Flow versus time tracing showing optimization of prolonged expiratory phase so that expiratory flow reaches zero before the next inhalation (dashed line).
Figure 24.3 Pressure versus time profile demonstrating auto‐PEEP using an expiratory hold maneuver.
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