An acute exacerbation of asthma or COPD is characterized by worsening respiratory symptoms such as shortness of breath, cough, and wheezing. Initial treatment involves oxygen, inhaled bronchodilators, and systemic glucocorticoids. Severe exacerbations may require hospitalization for monitoring, additional bronchodilators, and noninvasive ventilation. The goal is to relieve symptoms and improve lung function through aggressive medical therapy to prevent respiratory failure or the need for intubation.
2. Definition
An acute state where inflammation, airway edema,
excessive mucus accumulation, and severe
bronchospasm result in a profound airway
narrowing that is poorly responsive to usual
bronchodilator therapy
3. CLINICAL PRESENTATION
Symptoms
◦ Acute distress and severe dyspnea, shortness of breath,
chest tightness, or burning. The patient is only able to say
a few words with each breath.
Signs
◦ wheezing on auscultation, dry hacking cough, tachypnea,
tachycardia, pale or cyanotic skin, hyper-inflated chest, and
hypoxic seizures if very severe.
7. Initial assessment includes history, physical
examination, and objective assessments.
The brief history will assess for: onset and causes
of the exacerbation; severity of symptoms and if
associated with anaphylaxis; medication use,
adherence, and response to current therapy; and
risk factors for asthma-related death.
8. The asthma-related risk factors for death
include:
a history of near-fatal asthma requiring intubation and
mechanical ventilation
hospitalization or emergency care in the past year
current or recent use of oral corticosteroids
no current use of ICSs
over use of short-acting β2-agonist therapy (more than one
canister per month)
history of psychiatric disease or psychosocial problems
poor medication adherence
lack of a written asthma action plan
food allergy.
9. The physical exams:
◦ Vital signs
◦ Any complicating factors such as pneumonia or
anaphylaxis as well as other comorbid conditions that
could be causing acute shortness of breath such as inhaled
foreign body, congestive heart failure, pulmonary infection,
and pulmonary embolism.
10. Objective assessments
◦ should be made before initiation of oxygen or drug
treatment.
◦ Lung function testing by PEF or FEV1
should be measured before treatment if possible and
thereafter at one hour after start of treatment and then
periodically until response is achieved or no further
improvement is evident.
◦ Oxygen saturation: preferably by pulse oximetry
◦ Arterial blood gases
◦ A chest X-ray
◦ Complete blood count
11. Arterial blood gas measurements in
acute asthma are indicated in the
following settings:
Patients with persistent dyspnea whose PEF is
below 25 percent of normal despite initial
bronchodilator therapy
Selected patients with a PEF 25 to 50 percent of
normal whose respiratory status is deteriorating
despite intensive therapy
Patients who are too ill to perform a peak flow
measurement
Patients who demonstrate signs or symptoms of
hypercapnia, such as depressed consciousness,
inappropriately slow respiratory rate, or myoclonus
12. Features suggesting an alternate or
comorbid condition
◦ Concomitant symptoms such as fever,
purulent sputum production, urticaria, or
pleuritic chest pain should raise the
possibility of an alternative diagnosis such
as pneumonia, flare of bronchiectasis,
anaphylaxis, or pneumothorax.
13. A chest radiograph should be obtained
when:
A complicating cardiopulmonary process is
suspected (eg, temperature >38.3ºC,
unexplained chest pain, leukocytosis, or
hypoxemia)
When a patient requires hospitalization,
When the diagnosis is uncertain
17. Oxygen therapy goals:
◦ Arterial oxygen saturation of
93% to 95% in adolescents and adults
94% to 98% in school-aged children and pregnant women or those
with cardiac disease.
19. Systemic glucocorticoids indication:
◦ A severe exacerbation with a peak expiratory flow ≤50
percent of baseline. Immediate administration is warranted.
◦ A moderate exacerbation with a peak expiratory flow >50
but <70 percent of baseline that does not reverse to normal
after initial bronchodilator therapy.
◦ An asthma exacerbation that occurs despite ongoing daily
or alternate-day oral glucocorticoid therapy. Such patients
require supplemental glucocorticoids above their baseline
dose.
24. Features that help with assessment of severity (may or may not be
present):
◦ Impending respiratory failure:
Cyanosis, inability to maintain respiratory effort, depressed mental status, SpO2 <90%
PaCO2 >40 mmHg
◦ Severe exacerbation:
Speaks in single words
Sits hunched forward
Agitated, diaphoretic
Respiratory rate >30 breaths/minute
Heart rate >120 beats/minute
SpO2 (on air) <90%
PEF ≤50% predicted or personal best
◦ Mild to moderate exacerbation:
Talks in phrases or sentences
Prefers sitting to lying
Not agitated
Respiratory rate 16 to 30 breaths/minute
Heart rate 100 to 120 beats/minute
SpO2 >90%
PEF >50% but <80% predicted or personal best
25. Indications for hospitalization or
discharge
Factors favoring continued observation in patients
with a PEF of 40 to 60 percent of predicted are:
new onset asthma
multiple prior hospitalizations or emergency department
visits for asthma
use of oral glucocorticoids at the time of presentation
with the acute deterioration.
26. Most patients with improving symptoms and a PEF
>60 percent of predicted can be safely discharged,
if they are knowledgeable about their asthma and
have good availability of follow-up care.
27. Magnesium sulfate
◦ MOA: bronchodilation due to inhibition of
calcium influx into airway smooth muscle
cells
◦ Dosage: single Intravenous dose 2 g infused
over 20 min
◦ Suggested for patients who have a life-
threatening exacerbation or whose
exacerbation remains severe (PEF <40% of
baseline) after one hour of intensive
conventional therapy.
◦ Helpful in reducing hospital admissions
28. Nonstandard therapies
Anesthetic agents
◦ IV ketamine, inhaled halothane, isoflurane, and
sevoflurane have bronchodilating effects, and have
favorable responses in patients with refractory status
asthmaticus
◦ Mechanism: inhibition of histamine and acetylcholine-
induced bronchoconstriction and acting as a
sympathomimetic agent.
◦ Ketamine has been recommended for rapid induction
of anesthesia in patients with asthma who require
intubation and mechanical ventilation.
◦ Hypotension is often the limiting factor in the
administration of these agents
29. Enoximone
◦ Phosphodiesterase inhibitors, associated with
ventricular and atrial arrhythmias, hypotension, and
hepatotoxicity.
◦ Further study is needed to evaluate the safety and
efficacy of it
Parenteral beta-agonists — Intravenous and
subcutaneous beta-agonists are generally
avoided when treating asthma exacerbations in
adults, because inhaled short-acting selective
beta agonists have equal or greater efficacy and
lower incidence of adverse effects (eg,
tachycardia, arrhythmias, myocardial injury)
compared with parenteral beta-agonists.
30. Exceptions:
◦ patients suspected of having an
anaphylactic reaction
◦ Those unable to use inhaled
bronchodilators for a severe asthma
exacerbation
◦ Epinephrine or terbutaline subcutaneously
are an alternatives.
31. High-dose inhaled glucocorticoids are
not recommended as an alternative to
oral glucocorticoids for patients with a
discrete asthma exacerbation
32. Leukotriene receptor antagonists
◦ do not administer leukotriene receptor
antagonists as part of routine treatment of
acute exacerbations, except in patients
whose exacerbation was triggered by
ingestion of aspirin or a nonsteroidal anti-
inflammatory drug (NSAID), events
associated with dramatic overproduction
of leukotrienes.
33. Ineffective therapies
Methylxanthines
Empiric antibiotics
hydration (in the absence of evidence
of dehydration)
Expectorants such as guaifenesin
Antihistamines
Chest physiotherapy.
34. MECHANICAL VENTILATION
Indication:
Slowing of the respiratory rate
depressed mental status
inability to maintain respiratory effort,
worsening hypercapnia and associated
respiratory acidosis
inability to maintain an oxygen saturation >92
percent despite high-flow supplemental oxygen
35. Virtually every patient who has
suffered an asthma attack severe
enough to require urgent care should
receive an inhaled glucocorticoid as
part of his or her discharge medication
plan
39. Definition
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
40. Acute change in one or more of the
following cardinal symptoms:
Cough increases in frequency and severity
Sputum production increases in volume and/or
changes character
Dyspnea increases
41. Clinical features
Features of COPD exacerbation: Diffuse
wheezing, distant breath sounds, barrel-shaped
chest, tachypnea, tachycardia, smoking >20 pack
years
Features of severe respiratory insufficiency: Use
of accessory muscles; brief, fragmented speech;
inability to lie supine; profound diaphoresis;
agitation; asynchrony between chest and
abdominal motion with respiration; failure to
improve with initial emergency treatment
Features of impending respiratory arrest:
Inability to maintain respiratory effort, cyanosis,
hemodynamic instability, and depressed mental
status
42. Associated features that would
suggest an alternate diagnosis or
comorbidity include:
Constitutional symptoms (eg, fever, chills, night
sweats)
Chest pain, chest pressure, or peripheral
edema
Risk factors for thromboembolic disease or
coronary disease
Upper respiratory symptoms that might suggest
a viral respiratory infection
43. RISK FACTORS FOR COPD
EXACERBATION :
Advanced age
Duration of COPD
COPD-related hospitalization within the
previous year
Theophylline therapy
Having one or more comorbidities (eg,
ischemic heart disease, chronic heart failure, or
diabetes mellitus)
44. Exacerbation risk
Low risk: Typically GOLD 1 or 2 (mild
to moderate airflow limitation) and/or 0
to 1 exacerbation per year, no
hospitalization due to an exacerbation
High risk: Typically GOLD 3 or 4
(severe or very severe airflow
limitation) and/or ≥2 exacerbations per
year or ≥1 hospitalization due to an
exacerbation
45. Staging Acute Exacerbations of
COPD
Mild (type 1)
One cardinal symptoma plus at least
one of the following: URTIb within 5
days, fever without other
explanation, increased wheezing,
increased cough, increase in
respiratory or heart rate >20% above
baseline
Moderate (type 2) Two cardinal symptomsa
Severe (type 3) Three cardinal symptomsa
46. Factors Favoring Hospitalization for Treatment of COPD
Exacerbation
Presence of high risk comorbidity (eg, 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
47. Diagnostic testing
Look at S/S
Obtain ABG in all patients with severe COPD exacerbation
Assess oxygen saturation with continuous pulse oximetry
Do not assess peak expiratory flow or spirometry in acute severe COPD
exacerbations as results are not accurate
Obtain portable chest radiograph: Look for signs of pneumonia, acute
heart failure, pneumothorax
Obtain complete blood count, electrolytes (Na+, K+, Cl–, HCO3–), BUN,
and creatinine; also obtain cardiac troponin, BNP, or NT-proBNP, if
diagnosis is uncertain
Test for influenza infection during influenza season
Obtain ECG: Look for arrhythmia, ischemia, cor pulmonale
48. Criteria for ICU admission include:
•Patients with high-risk comorbidities (pneumonia, cardiac arrhythmia,
heart failure, diabetes mellitus, renal failure, liver failure)
•Continued need for NPPV or invasive ventilation
•Hemodynamic instability
•Need for frequent nebulizer treatments or monitoring
49. Monitoring
Perform continual monitoring of oxygen saturation, blood pressure,
heart rate, respiratory rate
Close monitoring of respiratory status
Continuous ECG monitoring
Monitor blood glucose
51. Provide combination of aggressive
bronchodilator therapy and ventilatory
support (NPPV or invasive ventilation)
52. Noninvasive positive pressure
ventilation (NPPV):
◦ Appropriate for the majority of patients with
severe exacerbations of COPD unless immediate
intubation is needed or NPPV is otherwise
contraindicated
◦ Contraindications to NPPV include: Severely
impaired consciousness, inability to clear
secretions or protect airway, high aspiration risk
53. Tracheal intubation and mechanical
ventilation:
◦ Indicated for patients with acute respiratory
failure, hemodynamic instability (eg, heart rate
<50/minute, uncontrolled arrhythmia) and those
in whom NPPV is contraindicated or who fail to
improve with NPPV and aggressive
pharmacotherapy
54. Therapy Comments
Antibiotics
Recommended if two or more of the following
are present:
•Increased dyspnea
•Increased sputum production
•Increased sputum purulence
Corticosteroids
Oral or IV therapy may be used.
If IV is used, it should be changed to oral after
improvement in pulmonary status.
If continued longer than 14 days, then the dose
should be tapered to avoid HPA Axis
suppression.
Bronchodilators
MDIs and DPIs equal in efficacy to
nebulization.
β-Agonists also may increase mucociliary
clearance.
Long-acting β-agonists or long-acting
antimuscarinics should not be used for quick
relief of symptoms or on an as-needed basis.
Controlled oxygen therapy
Titrate oxygen to desired oxygen saturation
(>90%).
Monitor arterial blood gas for development of
hypercapnia.
Noninvasive mechanical ventilation
Consider for patients with acute respiratory
failure.
Not appropriate for patients with altered mental
status, severe acidosis, respiratory arrest, or
cardiovascular instability.
55. Pharmacotherapy
Inhaled beta agonist: Albuterol 2.5 mg diluted to 3 mL via nebulizer or 4 to 8
inhalations from MDI every hour
Inhaled anticholinergic agent: Ipratropium 500 micrograms via nebulizer or 4 to 8
inhalations from MDI every four hours
Intravenous glucocorticoid (eg, methylprednisolone 60 mg to 125 mg IV, repeat
every 6 to 12 hours)
Antibiotic therapy: Appropriate for majority of severe COPD exacerbations; select
antibiotic based on likelihood of particular pathogens (eg, Pseudomonas risk factors,
prior sputum cultures, local patterns of resistance)
Antiviral therapy (influenza suspected)*: Oseltamivir 75 mg orally every 12 hours
OR peramivir 600 mg IV once (for patients unable to take oral medication)
56. Patient Characteristics Likely Pathogens Recommended Therapy
Uncomplicated
exacerbations
<4 exacerbations per year
No comorbid illness
FEV1 >50% of predicted
S. pneumoniae
H. influenzae
M. catarrhalis
H. parainfluenzae
Resistance uncommon
Macrolide (azithromycin,
clarithromycin)
Second- or third-generation
cephalosporin
Doxycycline
Therapies not recommendeda:
TMP/SMX, amoxicillin, first-
generation cephalosporins,
and erythromycin
Complicated exacerbations:
Age ≥65 and >4
exacerbations per year
FEV1 <50% but >35% of
predicted
As above plus drug-resistant
pneumococci, β-lactamase–
producing H. influenzae and
M. catarrhalis
Amoxicillin/clavulanate
Fluoroquinolone with
enhanced pneumococcal
activity (levofloxacin,
gemifloxacin, and
moxifloxacin)
Complicated exacerbations
with risk of P. aeruginosa
Chronic bronchial sepsisb
Need for chronic
corticosteroid therapy
Resident of nursing home
with <4 exacerbations per
year
Some enteric gram-negatives
As above plus P. aeruginosa
Fluoroquinolone with
enhanced pneumococcal and
P. aeruginosa activity
(levofloxacin)
IV therapy if required: β-
lactamase resistant penicillin
with antipseudomonal activity
3rd- or 4th-generation
cephalosporin with
antipseudomonal activity
57. Supportive care
Cigarette smoking cessation
Thromboprophylaxis
Nutritional support
58. Roflumilast
Is a phosphodiesterase 4 inhibitor indicated
to reduce risk of exacerbations in patients
with severe COPD
Roflumilast may be beneficial in patients with
severe or very severe COPD who are at high
risk of exacerbation (Group C and D) and are
not controlled by inhaled bronchodilators. It
may also be considered for patients who are
intolerant or unable to use inhaled
bronchodilators or corticosteroids. Roflumilast
is not recommended for us with theophylline
because the drugs share similar
mechanisms.
General
An episode can progress over several days or hours (usual scenario) or progresses rapidly over 1 to 2 hours.
The goals of initial home management are to relieve symptoms and prevent deterioration to a severe and potentially life-threatening attack.
Patients with a history of recurrent, severe asthma exacerbations may have been prescribed oral glucocorticoids to have available at home and may be advised by their clinician to take an initial dose (eg, prednisone 40 mg) and notify their clinician.
UPTODATE page 4+5
It is important that therapy not be delayed, so the history and physical examination should be obtained while initial therapy is being provided
Oxygen saturation: preferably by pulse oximetry and is a key parameter in young children who may not be able to perform lung function Patients with signs of impending respiratory failure should not be asked to perform peak flow. Current guidelines recommend the use of transcutaneous pulse oximetry monitoring particularly among patients who are in severe distress, have a forced expiratory volume in one second (FEV1) or peak expiratory flow less than 50 percent of baseline, or are unable to perform lung function measurements [2]. There is no contraindication to the use of continuous transcutaneous oximetry during all asthmatic attacks.
Arterial blood gases are typically reserved for patients who are poorly responsive to initial treatment or deteriorating.
A chest X-ray is rarely indicated unless there are physical signs of other or additional complicating features such as foreign body aspiration.
A complete blood count may be appropriate for patients with fever or purulent sputum, but modest leukocytosis is common in asthma exacerbations due to viral infection or secondary to corticosteroid administration. Leukocytosis associated with corticosteroid administration does not cause a shift to the left as is seen in bacterial infections.
Serum electrolytes should be monitored in patients who take diuretics regularly and in patients with coexistent cardiovascular disease as short-acting inhaled β2-agonists can produce transient decreases in potassium, magnesium, and phosphate.2 The combination of high-dose β2-agonists and systemic corticosteroids occasionally may result in excessive elevations of glucose and lactic acid
Patients with persistent dyspnea whose PEF is below 25 percent of normal despite initial bronchodilator therapy (meaning that if the PEF is this low initially, give bronchodilator and see if there is improvement rather than doing an immediate ABG)
— Supplemental oxygen should be administered to most patients with a moderate or severe asthma exacerbation, particularly those who are hypoxemic (SpO2 <90 percent) or for whom continuous oxygen saturation monitoring is not available. Usually, oxygenation is easily maintained with nasal cannula, but occasionally face mask delivery is needed.
----- three treatments are administered within the first hour. The delivery method varies with the setting and severity of the attack (table 3) [2]: High-dose inhaled SABA therapy can be associated with hypokalemia and lactic acidosis.
●Standard nebulization – Albuterol 2.5 to 5 mg by jet (also called "hand-held" or "updraft") nebulization every 20 minutes for three doses, then 2.5 mg to 5 mg every one to four hours as needed. Of note, the higher doses are associated with more frequent and severe sympathomimetic side effects and are generally reserved for very severe, refractory attacks
*(MDI) – Albuterol by MDI with a spacer or valved-holding chamber device (eg, Aerochamber, Optichamber, Vortex, and others), four to eight puffs every 20 minutes, for the first hour. Most patients can then transition to dosing every one to four hours, and rarely require dosing at more frequent intervals.
●Continuous nebulization –
* Four to six carefully administered inhalations from an MDI with chamber/spacer have generally been found to equal one nebulizer treatment, Many emergency departments (including our own) continue to rely on nebulized administration of beta agonists for acutely ill asthmatic patients, taking advantage of the simplicity of delivery during the patient's tidal breathing. As patients recover in the hospital from acute, severe attacks, the transition can be made from nebulized beta agonists to beta agonists by MDI with a valved holding chamber (“spacer”) without loss of efficacy and with the opportunity for patient education in proper inhaler technique
---- We typically stop inhaled short-acting anticholinergic therapy once the patient is admitted to the hospital, except in patients with refractory asthma who require treatment in the intensive care unit, are on monoamine oxidase inhibitor therapy (who may have increased toxicity from sympathomimetic therapy due to impaired drug metabolism), have chronic obstructive pulmonary disease with an asthmatic component, and those whose asthma has been triggered by beta-blocker therapy.
The primary therapy of acute exacerbations is pharmacologic, which includes short-acting inhaled β2-agonists and, depending on the severity, systemic corticosteroids, inhaled ipratropium, and O2. Treatments are typically administered concurrently to facilitate rapid improvement
New evidence supports the use of heliox versus oxygen for nebulized β2-agonist administration in patients with moderate to severe exacerbations who do not respond to standard therapy.3,30 Heliox is a combination of helium and oxygen (often 70:30) that has a lower density than air which reduces resistance to flow and increases ventilation by converting turbulent flow to more efficient laminar flow.31 Limited data suggest that the benefits with heliox therapy are apparent in those with severe exacerbations by improving PEF and reducing the risk of hospitalizations in both children and adults
onset of action of systemic glucocorticoids is not clinically apparent until as long as six hours after administration. Thus, the beneficial effect is not likely to be observed during the few hours that the patient spends in the medical office or emergency department [42]. Early administration helps to minimize the delay in improvement anticipated with systemic glucocorticoids
in the absence of vomiting or respiratory failure, oral administration can be used instead of intravenous administration. Oral prednisone and methylprednisolone are rapidly absorbed (peak serum levels achieved at one hour after ingestion) with virtually complete bioavailability, and their efficacy is comparable to intravenous methylprednisolone. Thus, 40 to 60 mg of prednisone administered in a medical office may provide the maximal benefit to be derived from systemic glucocorticoids in acute asthma.
Intravenous glucocorticoids should be given to patients who present with impending or actual respiratory arrest, or are intolerant of oral glucocorticoids [2]. The exact dose of glucocorticoids to use for patients with life-threatening asthma is largely based on expert opinion
Transition from parenteral to oral administration of glucocorticoids can occur when the patient can tolerate and absorb oral medication.
Duration: As a rough guide, most severe attacks that require hospitalization will resolve (with return of lung function to baseline) in 10 to 14 days. The duration of glucocorticoid therapy can be tailored to individual responses. Patients can stop their oral glucocorticoids upon resolution of their symptoms together with recovery of their self-monitored peak flow values (eg, when peak expiratory flow is greater than 70 percent of baseline) as long as they begin or maintain use of inhaled glucocorticoids following discontinuation of oral glucocorticoids.
Tapering oral glucocorticoids is not necessary if the duration of glucocorticoid treatment is less than three weeks (a duration too brief to cause adrenal atrophy) and if inhaled glucocorticoids are concomitantly prescribed for ongoing therapy (to prevent relapse
patients should receive close monitoring, including serial measurements of vital signs, pulse oximetry, and lung function (eg, peak expiratory flow), to assess the response to treatment.
Discharge planning after an ED visit or hospitalization includes arrangement for follow-up care within one week
myocardial depression and increased ventricular irritability have been observed with halothane, particularly when used in the presence of acidosis, beta-agonists, and theophylline.
full-time anesthesiologist at the bedside
Sedatives should not be given because anxiety may be a sign of hypoxemia, which could be worsened by central nervous system depressants.
Leukotriene receptor antagonists are an established therapy for chronic asthma, but the role of these medications in the management of acute exacerbations is unclear [80-84].
-MethylxanthinesThese agents are not as potent as the beta agonists when used alone for the treatment of asthma and provide no further bronchodilation beyond that achieved with inhaled beta agonists alone when used in combination (figure 3) [86,87]. In addition, methylxanthines appear to increase the incidence of adverse effects when combined with beta-agonist bronchodilators. For patients who are taking oral theophylline at presentation, we typically continue maintenance oral therapy (and check a theophylline blood level) during hospitalization; but if continued oral intake is not possible, we would very rarely use intravenous therapy with aminophylline or theophylline.
2. because most respiratory infections that trigger an exacerbation of asthma are viral rather than bacterial [3]. In general, we reserve antibiotics for treatment of suspected bacterial sinusitis or pneumonia complicating an asthmatic attack. It is possible that measurement of serum procalcitonin levels will allow identification of a bacterial etiology among patients whose asthma exacerbations are triggered or complicated by a respiratory tract infection
3. increased fluid therapy is not indicated in acute asthma management because the capillary leak from cytokines and increased negative intrathoracic pressures may promote edema in the airways
In the absence of anticipated intubation difficulty, rapid sequence intubation is preferred. Nasal intubation is not recommended.
TRIGGERS — Respiratory infections are estimated to trigger approximately 70 percent of chronic obstructive pulmonary disease (COPD) exacerbations. Viral and bacterial infections cause most exacerbations, whereas atypical bacteria are a relatively uncommon cause. The remaining 30 percent are due to environmental pollution, pulmonary embolism, or have an unknown etiology
complication of severe exacerbation is acute respiratory failure.
ABG usually is obtained to assess the severity of an exacerbation.
The diagnosis of acute respiratory failure in COPD is made based on an acute drop in PaO2 of 10 to 15 mm Hg or any acute increase in PaCO2 that decreases the serum pH to 7.3 or less.
Additional acute clinical manifestations of respiratory failure include restlessness, confusion, tachycardia, diaphoresis, cyanosis, hypotension, irregular breathing, miosis, and unconsciousness.
the severity of symptoms (based on instruments such as the COPD Assessment Test [CAT] and the modified Medical Research Council Dyspnea Scale), the degree of airflow limitation (based on the FEV1)
10 to 14 days can be effective for most patients
Therapy with antibiotics generally should be continued for at least 7 to 10 days.