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Questions and Answers
What is the maintenance infusion rate for the neuromuscular blocker?
Why is cisatracurium preferred over other non-depolarizing neuromuscular blockers in asthmatic patients?
What is the main goal of mechanical ventilation?
What does an increasing peak-to-plateau pressure indicate during mechanical ventilation?
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What is a typical tidal volume setting in a paralyzed patient during PRVC mode?
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What is a sign of severe disease indicated by pulsus paradoxus?
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Which treatment is considered a validated mainstay therapy for severe acute asthma?
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In patients with acute severe asthma, which gas level indicates a worsening situation?
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What is a common symptom of an asthma attack?
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Which of the following is NOT typically required for routine monitoring in all asthma patients?
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Which indicates the need for immediate attention in asthmatic patients?
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What is an expected consequence of hypoxemia in status asthmaticus?
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What is the recommended immediate treatment for a patient presenting with a severe asthma attack?
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What is one possible outcome of respiratory muscle fatigue in asthmatic patients?
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Which of the following may be an indicator that a patient is in respiratory distress?
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What is a potential side effect of magnesium sulfate infusion?
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What is the recommended bolus dose for magnesium sulfate in the pediatric population?
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What is the maximum FiO2 requirement for heliox therapy to be effective?
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What characterizes asthma as a chronic inflammatory disease?
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What type of effects does isoproterenol provoke when used as a treatment?
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At what serum level do side effects of aminophylline commonly begin to worsen?
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Which statement accurately describes the prevalence of asthma in children?
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Which factor is NOT associated with near fatal asthma?
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Which of the following should be avoided when using opioids for sedation in an asthmatic patient?
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For patients not responding to conventional therapy, which agent is indicated?
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What is the classic pathophysiologic triad in asthma?
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What role do mast cells play in asthma pathophysiology?
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What is the initial infusion rate of isoproterenol for treating respiratory failure?
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Which medication is primarily responsible for bronchodilation via multiple mechanisms, including phosphodiesterase inhibition?
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Which airway irritant can trigger asthma attacks?
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Which factor limits the use of noninvasive ventilation in young patients?
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What leads to ventilation/perfusion mismatching in asthma?
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Which of the following is NOT a consequence of inflammation in asthma?
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What is the primary effect of beta-2 agonists in treating severe asthma?
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Which beta-agonist is preferred for its selectivity and minimal cardiac effects?
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What is the standard dose of albuterol for severe asthmatics per kilogram of body weight?
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What adverse effect is commonly associated with beta-agonist therapy?
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Which of the following medications is not indicated for acute asthma exacerbations?
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How often can ipratropium bromide be administered alongside albuterol nebulization?
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What distinguishes levalbuterol from albuterol?
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Which beta-agonist is used in anaphylaxis due to its potent Beta-1 effects?
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What role do steroids play in the treatment of status asthmaticus?
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Which adverse effects can result from beta-agonist treatments, other than tachycardia?
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Study Notes
Asthma
- Asthma is a common chronic inflammatory disease affecting the airways, characterized by reversible airflow obstruction, exacerbations, and remissions.
- It is the most common chronic pediatric disease, with a global prevalence of 11-13%.
- In the USA, asthma affects 9.5% of all children.
- Only 8% of hospitalized children with asthma require the ICU.
### Asthma Pathophysiology
- Asthma pathophysiology involves acute and chronic inflammation and airway hyperresponsiveness.
- Bronchial smooth muscle constriction, airway edema, and mucous plugging are the classic pathophysiologic triad in asthma.
- Mast cell activation, denuded airway epithelia, inflammatory cell migration, collagen deposition, and fibrosis below the basement membrane are histological findings.
- Mast cells release mediators like histamine, prostaglandins, and leukotrienes causing bronchoconstriction.
- T-lymphocyte release of cytokines like IL 4, 5, 8, and 13 amplify the inflammatory response.
- B cells produce excessive IgE, stimulating mast cells to release leukotrienes.
- This process leads to excess mucus production, epithelial cell destruction, airway plugging, and airway surface denuding.
### Asthma Triggers
- Airway irritants like cigarette smoke, inhaled particulates, respiratory tract viruses, psychologic stress, and cold air can trigger asthma attacks.
- Increased mucus production with large amounts of cellular debris and increased viscosity contributes to airway obstruction.
- Inflammation-mediated airway edema, mucus hypersecretion, airway plugging, and bronchospasm lead to severe airway obstruction in severe asthma attacks.
### Asthma Exacerbations
- Genetics, environmental exposures, and viruses play key roles in acute exacerbations.
- Acute exacerbations are characterized by a rapid increase in airway resistance, reactive airways, and minimal response to medications.
- Respiratory insufficiency can develop leading to respiratory failure or even death.
- Asthma symptoms include tachypnea, wheezing, persistent coughing, nocturnal coughing, chest pain, chest tightness, dyspnea, and emesis.
### Physical Examination and Assessment
- Physical examination findings include wheezing, diminished breath sounds, prolonged expiratory phase, pulsus paradoxus, accessory muscle use, nasal flaring, and abdominal breathing.
- Pulsus paradoxus of >20 mm Hg indicates severe disease.
- Mental status changes like irritability, restlessness, lethargy, and confusion may be signs of respiratory failure and necessitate immediate attention.
- A clinical asthma score can help identify near-fatal asthma.
- Scores of >5 on the Wood asthma score indicate respiratory failure.
### Imaging and Diagnostic Studies
- Chest X-ray should be performed in severely ill asthmatics. Patients with a focal pulmonary asculatory finding or suspected airleak (i.e. pneumothorax, pneumomediastinum) should also undergo imaging.
- Arterial blood gas monitoring is not routinely necessary in all patients.
- Patients early in their asthma exacerbation often present with hypoxia and hypocarbia.
- A PaCO2 >40 torr in a severe exacerbation implies developing respiratory muscle fatigue.
### Laboratory Tests
- Electrolytes and blood counts in acute severe asthma may reflect dehydration and acidosis.
- Patients may be hypokalemic secondary to beta-agonist treatments.
- Myoglobin may be elevated in near-fatal asthma.
- Troponin may be elevated in critical asthma due to sustained diastolic hypotension and decreased coronary perfusion.
### Management of Severe Asthma
- Treatment of severe, acute status asthmaticus can be divided into validated and non-validated therapies.
- Validated mainstay therapies include oxygen, hydration, beta-agonists, steroids, anticholinergics, and mechanical ventilation for respiratory failure.
- Non-validated therapies include magnesium sulfate, bicarbonate, mucolytic drugs, chest physiotherapy, heliox, antibiotics, high-frequency oscillatory ventilation, and inhaled anesthetics.
### Oxygen Therapy
- Hypoxemia in status asthmaticus results from ventilation-perfusion mismatch due to bronchial obstruction.
- Bronchodilators can exacerbate hypoxemia by abolishing regional pulmonary hypoxic vasoconstriction.
- Early, humidified oxygen in acute severe asthma management is supported by clinical experience.
- Various oxygen delivery methods should be used to maintain oxygen saturation greater than 92%.
### Emergency Department Management of Acute Asthma
- For mild asthma attacks, one or more treatments with inhaled B2-agonists and a 3-5 day course of oral steroids may suffice.
- For moderate or severe asthma attacks, patients require more aggressive treatment with supplemental oxygen delivery immediately, with SPO2 maintenance above 92%.
### Nebulized B-2 Agonists
- Nebulized B-2 agonists are commonly used as first-line treatment after oxygen.
- Albuterol is administered at a dose of 0.15 mg/kg up to 5 mg, repeated every 10-20 minutes.
- Systemic corticosteroids (oral prednisone, IV methylprednisolone, or IM dexamethasone) should be administered.
### Anticholinergic Agents
- Nebulized anticholinergic agents (ipratropium bromide) can be added to intermittent albuterol administration.
- Magnesium sulfate can be given IV and has been shown to reduce ICU admissions.
### PICU Admission
- Patients remaining in respiratory distress after receiving aggressive therapy for more than an hour or who are deteriorating during emergency department treatment may require PICU admission.
### Hydration
- Most asthmatics are dehydrated on presentation.
- Fluid replacement and maintenance are crucial to correct dehydration and minimize thickening of secretions.
### Beta-Agonist Therapy
- Beta-agonists are a first-line treatment in status asthmatics, causing bronchial smooth muscle relaxation, increased diaphragmatic contractility, enhanced mucociliary clearance, and inhibition of bronchospastic mediators.
- Albuterol and terbutaline are generally preferred due to their beta-2 receptor selectivity, minimizing cardiac effects.
- Severe asthmatics are generally given intermittent high-flow nebulized albuterol at a dose of 0.05-0.15 mg/Kg to a maximum of 5 mg every 6-2 hours, depending on clinical status and response.
- Continuous nebulized albuterol may be superior for severe asthmatics.
- IV beta-agonist therapy (terbutaline) should be considered if the patient is unresponsive to continuous albuterol.
### Levalbuterol
- Levalbuterol is the pure (R)-albuterol isomer.
- It is as effective as albuterol but significantly more expensive.
### Epinephrine
- Epinephrine is an adrenergic drug with alpha, beta-1, and beta-2 effects.
- It is generally reserved for bronchospasm associated with anaphylaxis.
### Isoproterenol
- Isoproterenol is a potent beta-1 and beta-2 agonist.
- Isoproterenol use has been supplanted by terbutaline.
- Salmeterol is a long-acting beta-agonist, not indicated in the acute setting and associated with patient death.
### Steroid Therapy
- Steroids are mandatory first-line treatment in status asthmaticus.
- Steroids inhibit pro-inflammatory gene expression, with anti-inflammatory effects occurring between 6-12 hours after administration.
- Steroids reverse the downregulation of the beta-2 receptor after prolonged beta-agonist use.
- Oral and parental steroids are acceptable.
### Anticholinergic Agents
- The most commonly used anticholinergic agent is ipratropium bromide.
- It may be administered with albuterol nebulization and given as often as every 2 hours during continuous albuterol administration.
- Anticholinergic agents have synergistic effects with beta-agonists.
### Magnesium Therapy
- Magnesium inhibits calcium uptake, relaxes bronchial smooth muscle, and inhibits acetylcholine release.
- Magnesium sulfate infusion can cause side effects, including hypotension, facial flushing, muscle weakness, and absent reflexes.
- At the recommended dose of 25-50 mg/Kg, magnesium sulfate is relatively safe in the pediatric population.
### Heliox
- Heliox is a mixture of 30% oxygen and 70% helium.
- The lower density of helium reduces the Reynolds number, facilitating aerosol delivery to distal lung units and reducing work of breathing.
- The patient's oxygen requirement is a limiting factor as at least 60% helium is necessary for optimal effect.
- Heliox is a safe therapy with no known published adverse effects.
- It is considered an unproven therapy and should be used only in patients not responding to conventional therapy.
### Intravenous Isoproterenol
- Intravenous isoproterenol was previously the last resort prior to intubation in a patient with impending or established respiratory failure.
- It is a potent beta-1 and beta-2 agonist with a short duration of action, requiring continuous drip administration.
- Side effects include myocardial ischemia, cardiac dysrhythmias, and hyperglycemia.
- Isoproterenol has been largely supplanted by terbutaline and albuterol.
### Aminophylline
- Aminophylline was a mainstay of therapy for years, producing bronchodilation through various mechanisms.
- Side effects are common and worsen with levels greater than 20 mcg/dL.
- Aminophylline use should be restricted to children who respond poorly or fail to improve on maximal beta-agonist therapy.
### Ketamine
- Ketamine is a dissociative anesthetic with bronchodilator effects.
- It is often used during intubation in near-fatal asthmatic patients.
- Ketamine increases sialorrhea and bronchial secretions.
- Typically, the increased heart rate limits the use of ketamine over time.
- Ketamine infusion has not shown benefit to standard therapy in non-intubated patients in the emergency department.
### Noninvasive Ventilation
- Noninvasive ventilation may benefit patients with respiratory muscle fatigue.
- BiPAP can relieve anxiety and allow standard therapy to relieve symptoms.
### Intubation and Mechanical Ventilation
- Mechanical ventilation in an asthmatic is rare and used only when other treatments have failed.
- It carries a high risk of air trapping and the development of airleak syndrome.
### Sedation and Paralysis
- Patients should be sedated heavily and many are paralyzed prior to intubation.
- Benzodiazepines (midazolam) should be used due to their anxiolytic properties.
- Most opioids should be avoided as they produce additional histamine release.
Fentanyl
- Fentanyl is an analgesic agent that can be used in doses of 1-5 mcg/Kg.
- Fentanyl has less histamine release compared to other analgesics in the same class.
Induction
- Succinylcholine (2mg/Kg) can be used for induction.
- An NG tube is recommended during succinylcholine induction due to the high likelihood of vomiting.
Neuromuscular Blockade
- Cisatricurium is used to maintain neuromuscular blockade.
- The maintenance infusion rate for cisatricurium is 0.2-0.3 mg/Kg/hr.
- Cisatricurium is less likely to cause prolonged paresis in asthmatic patients compared to other non-depolarizing neuromuscular blocking agents, because it does not have a steroid based chemical structure.
Sedation
- IV Ketamine (1-2mg/Kg) can be used as a sedative and induction agent.
- Ketamine is preferred as it also has bronchodilator effects.
Mechanical Ventilation
- The goal of mechanical ventilation is to reverse hypoxemia, maintain acceptable pH, and avoid iatrogenic hyperinflation.
- Iatrogenic hyperinflation can lead to reduced cardiac output and air-leak syndrome.
- Achieving normal PaCO2 is not a primary objective.
- Pressure-regulated volume control (PRVC) mode is recommended.
- PRVC mode allows decelerating inspiratory gas flow, assured tidal volumes, and minimized peak airway pressures.
- Longitudinal comparison of peak inspiratory pressure (PIP) to plateau pressure (Pplat) can indicate airway resistance and response to therapy.
- Increasing PIP-to-Pplat ratio indicates increasing airway resistance.
- Decreasing PIP-to-Pplat ratio indicates response to therapy.
- Typical settings in a paralyzed patient during mechanical ventilation: PRVC mode, tidal volume 4-8 mL/Kg, and peak pressure to be monitored.
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Description
Explore the complexities of asthma, a prevalent chronic inflammatory disease affecting airways. This quiz covers its pathophysiology, including the classic triad of bronchial smooth muscle constriction, airway edema, and mucous plugging. Understand the role of mast cells and cytokines in exacerbating asthma's symptoms.
