Management of Acute Asthma and COPD Exacerbations
systemic corticosteroids reduce
mucus production, reduce bronchial hyper responsiveness, reduce airway edema and exudation
Acute Severe COPD- increased
muscle fatigue
systemic corticosteroids increases
receptor density 4 hours after administration
Corticosteroids shorten
recovery time
Acute Asthma Presentation may progress over
several days to hours Some patients progress rapidly over 1-2 hours
Ipratropium is indicated in
severe asthma exacerbation not completely responsive to beta 2 agonists
Uncontrolled asthma progresses to
severe bronchospasm that results in profound airway narrowing Inflammation Airway edema Excessive mucus accumulation
Corticosteroids longer courses are not more efficacious than
short courses Patients with frequent exacerbations may require higher doses and longer courses of therapy with tapering
Acute Severe COPD- Increased inflammatory mediators in the
sputum i. Neutrophils, eosinophils
Ipratropium reverses cholinergic-mediated bronchoconstriction induced by
triggers: histamine prostaglandins exercise allergens
Antibiotics usual duration
5-10 days
Goal O2 saturation
88-92% may need home o2 at rest or with acitivity
Goal SPO2
>90% (EPR-3) or 93-95% (GINA)
Ipratropium produces a further improvement in
lung function of 10-15% over Beta 2 agonists alone
Acute Severe COPD- COPD is characterized by recurrent exacerbations
Change in patient's baseline symptoms Cough, dyspnea, sputum production
Acute respiratory failure is an acute drop in
PaO2 of 10-15mmHg
Factors Favoring Hospitalization
Presence of high risk comorbidity i. pneumonia, arrhythmia, CHF, diabetes, renal or hepatic failure Suboptimal response to outpatient management Marked worsening of dyspnea Inability to eat or sleep due to symptoms Worsening hypoxemia or hypercapnia Mental status changes Lack of home support for care Uncertain diagnosis
Acute Severe Asthma is poorly responsive to
bronchodilators
Systemic corticosteroids indication
can prevent/reverse down-regulation and desensitization of β2 receptors in the lung
Acute respiratory failure Acute increase in PaCO2 with
decreased pH to ≤7.3
Acute Severe Asthma Treatment is characterized by
early initiation and intensification of treatment
Albuterol Administration
every 20 minutes or continuously shows higher efficacy Continuous administration via nebulizer shows decreased hospitalization and greater FEV1/PEF improvements compared to hourly at the same total dose
Discharge Criteria
-Able to use long acting bronchodilators with or without inhaled corticosteroids -Short acting β2-agonist no more than q 4 hours -Patient able to walk across room if ambulatory -Patient able to eat/sleep without frequent dyspnea -Clinically stable for 12-24 hours -Stable ABGs for 12-24 hours -Understands home medication i. Assess need for home O2- necessary if O2 sat 88% or less at rest or during ambulation -Follow up arranged within 4-6 weeks
Acute Severe Asthma Treatment - Goals of Therapy
-Correction of significant hypoxemia -Rapid reversal of airflow obstruction -Reduction of the likelihood of relapse of the exacerbation -Reduction of the likelihood of future recurrence of severe airflow obstruction -Development of a written asthma action plan in case of a further exacerbation
Indications for Mechanical Ventilation- Invasive
-NIV failure -Respiratory arrest -Inability to remove secretions -Bradycardia with AMS -Hemodynamic instability -Ventricular arrhythmias -Life-threatening hypoxemia
Goals of COPD Exacerbation Treatment
-Prevent hospitalization or reduce duration of stay -Prevent acute respiratory failure and death -Resolution of exacerbation symptoms -Return to baseline clinical status and quality of life
Acute asthma mild to moderate presentation
-Talks in phrases -Prefers sitting to lying -Not agitated -Respiratory rate increased -Accessory muscles not used -Pulse 100-120 bpm -O2 sat 90-95% -PEF > 50% predicted or best
systemic corticosteroids - treatment duration
5-7 day course in adults, 3-5 days in children
Short Acting Bronchodilators
Bronchodilation as well as decreased mucous production Nebulizer may be more convenient for patient, but overall efficacy is equal to MDI Usually use albuterol plus ipratropium combination therapy See asthma section for dosing guidelines
Albuterol- Nebulizer vs. MDI in severe acute asthma
Controversy regarding most efficacious route
Oxygen description
Hypoxemia from ventilation-perfusion mismatch should be immediately correctible via low flow O2
Acute asthma -Life threatening
Drowsy, confused Silent chest- not enough air movement to produce wheezing
Indications for Mechanical Ventilation- Noninvasive
Respiratory acidosis- arterial pH ≤7.35 / PaCO2 ≥ 45mmHg Severe dyspnea with increased work of breathing i. Use of accessory muscles ii. Paradoxical motion of the abdomen iii. Retraction of intracostal spaces
Acute Severe Asthma Attacks may correspond with triggering event:
Respiratory infection Allergens or environmental factors Exercise Medications
Acute Respiratory Failure manifestations
Restlessness Confusion Tachycardia Diaphoresis Cyanosis Hypotension Irregular breathing
Uncomplicated exacerbations- recommended therapy
macrolide (azithromycin, clarithromycin) second or third generation cephalosporin doxycline therapies not recommended: TMP/SMX, amoxicillin, first generation cephalosporins, and erythromycin
Ipratropium has poor absorption across mucosae and blood brain barrier
Low incidence of side effects Slower onset than β2 agonists (30-60min)
COPD Exacerbations
An acute event characterized by a worsening of the patient's respiratory symptoms that is beyond normal day-to-day variations and leads to a change in medication.
Management of Exacerbations
Assess severity of symptoms, blood gases, chest radiograph Administer supplemental oxygen Bronchodilators i. Increase dose and frequency of short-acting agents ii. Combine short-acting β-2 agonists and anticholinergics iii. Use spacers or nebulizers Add oral or intravenous corticosteroids Consider antibiotics if signs of bacterial infection Consider noninvasive mechanical ventilation
Treatment of Acute Asthma Options
Inhaled short acting β2 agonists Systemic corticosteroids Inhaled ipratropium Oxygen
Albuterol
Beta 2 agonist Most effective bronchodilators for asthma Fast onset (5-10 min)
Acute Asthma Signs
Expiratory and inspiratory wheezing Dry hacking cough Tachypnea Tachycardia Pale skin PEF & FEV1 <40% of normal predicted value, Decreased PaO2 and O2 saturation (<90% is severe)
Acute Severe Asthma Treatment- close monitoring of objective measures of oxygenation and lung function
FEV1 30 minutes following B2 agonist O2 saturation
ipratropium reduce hospitalization rate in patients with
FEV1 <30%
Corticosteroid improve
FEV1 and PAO2
Complicated exacerbations with risk of P aeruginosa
Fluoroquinolone with enhanced pneumococcal and p aeruginosa (levofloxacin)
Antibiotics- Pseudomonas in
GOLD 3 and GOLD 4 patients
Antibiotics
Hemophilus influenzae, Streptococcus pneumoniae, and Morexella catarrhalis are most common bacterial pathogens
Mag Sulfate indication
Indicated for ED administration after bronchodilators used for 1 hour without appropriate response
Acute Severe COPD Severity
Mild One cardinal symptom plus one of the following URTI within 5 days, fever, increased wheezing, increased cough, tachycardia or tachypnea >20% above baseline Moderate- two cardinal symptoms Severe- three cardinal symptoms
Management of COPD Exacerbations
Monitor fluid balance and nutrition Consider venous thromboembolism prophylaxis Identify and treat associated conditions i. Heart failure ii. Arrhythmias Closely monitor condition of patient
Helium- Inert gas given in combination with oxygen to:
Reduce resistance to gas flow Increase ventilation i. Low density decreases the pressure gradient needed to achieve a given level of airflow ii. Converts turbulent flow to laminar flow
systemic corticosteroids - multiple daily administration warranted in severe patients initially
Severe airway inflammation decreases binding affinity of corticosteroid receptors in the lung May transition to once daily dosing after patient stabilizes
Indications for ICU Admission
Severe dyspnea that responds inadequately to initial emergency therapy Mental status changes Persistent or worsening hypoxemia despite supplemental oxygen and noninvasive ventilation i. PaO2 <40mmHg ii. Worsening respiratory acidosis pH <7.25 Need for mechanical ventilation Hemodynamic instability i. Need for vasopressors
Acute asthma severe presentation
Talks in words Sits hunched forward Agitated Respiratory rate > 30/min Accessory muscles being used Pulse rate >120bpm O2 sat < 90% (on room air) PEF 50% or lower than predicted/best
May use PO or IV initially
The GOLD guidelines recommend 40mg PO prednisone for 5 days There is insufficient evidence to provide firm conclusions on the optimal duration of corticosteroids
COPD exacerbation
Un-hospital mortality as high as 6-8% for hospitalized patients Many patients do not return to baseline clinical status for several weeks As many as half readmitted within 6 months Mortality after hospitalization i. 1 year: 22-43% ii. 2 years: 36-49%
Antibiotics indication
Worsening dyspnea Increase in sputum volume Increase in sputum purulence May use if 2/3 as long as sputum purulence is one of them OR Mechanical ventilation
Acute Severe COPD Cardinal symptoms
Worsening dyspnea Increase in sputum volume Increase in sputum purulence
Acute Severe COPD- worsening lung hyperinflation
Worsening dyspnea and poor gas exchange Chronic airflow limitation may not change remarkably
Oxygen- Some severely resistant patients may proceed to
acute respiratory distress syndrome and require invasive ventilation (covered in IS-XI)
Complicated exacerbations- recommended therapy
amoxicillin/clavulanate, fluoroquinolone with enhanced pneumococcal activity (levofloxacin, gemifloxacin, moxifloxacin)
Some antibiotics such as azithromycin also have
anti-inflammatory effect
Acute Severe Asthma usually results from
failure of a therapeutic regimen for persistent asthma
Mag Sulfate AEs
hypotension, facial flushing, sweating, nausea, loss of deep tendon reflexes, and respiratory depression
Acute Severe COPD has profound
hypoxemia, hypercapnia Respiratory acidosis Respiratory failure
Magnesium sulfate description
moderately potent bronchodilator