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References
1. Dyspnea. Mechanisms, assessment, and management: A consensus
statement. American Thoracic Society. Am J Respir Crit Care Med
1999; 159: 321.
2. Simon PM, Schwartzstein RM, Weiss JW, et al. (1989)
Distinguishable sensations of breathlessness induced in normal
volunteers. Am Rev Respir Dis 140(4): 1021.
3. Banzett RB, Lansing RW, Reid MB, et al. (1989) Air hunger’ arising
from increased PCO2 in mechanically ventilated quadriplegics.
Respir Physiol 76(1): 53–67.
294
E. Barna
Fig. 1. Diagnostic approach to dyspnea.
GENERAL HISTORY
EXPANDED QUALITATIVE HISTORY
PHYSICAL EXAM
CXR
No clear diagnostic direction Clear diagnostic direction
Directed Testing
CARDIAC PULMONARY METABOLIC NEURO/MUSCULAR
ECG Arterial Blood Gas
Cardiac Biomarkers Pulmonary Function Salicyclate level Salicyclate level
BNP
Echocardiogram HRCT
TFT
CT-Angiography
V/Q Scan
Methanol
Ethylene Glycol
Blood Glucose
Acetone
CT Head
4. Banzett RB, Lansing RW, Brown R, et al. (1990) Air hunger’ from
increased PCO2 persists after complete neuromuscular block in
humans. Respir Physiol 81(1): 1–17.
5. Scano G. Stendardi L, Grazzini M, et al. (2005) Understanding
dyspnea by its language. Eur Respir J 25(2): 380–5.
295
Approach to the Patient with Dyspnea
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Asthma
Gwen S. Skloot *
Key Pearls
• Prior severe exacerbations, multiple annual hospitalizations or
Emergency Department visits, overuse of beta-agonist, poor perception of respiratory symptoms, other underlying cardiopulmonary or
psychiatric illness, lack of a written action plan, mold sensitivity, low
socioeconomic status and illicit drug use are all factors that increase
mortality risk of an asthma exacerbation.
• Oxygen saturation and lung function (in all but the most severely ill
patients) are key objective tests, while most other studies are not routinely required.
• The mainstay of inpatient asthma management includes systemic
steroids, short-acting beta agonists, and supplemental oxygen.
• Consultation with an asthma specialist should be considered early
in high-risk patients or those who do not respond to therapy as expected.
• Readiness for discharge hinges on return toward normal subjective
and objective function (i.e. Peak Expiratory Flow Rate returns to 70%
of predicted or personal best).
Introduction
Asthma is a chronic inflammatory disorder of the airways characterized by
airway obstruction that is generally reversible, and by hyperresponsiveness
297
27
Chapter
*Mount Sinai School of Medicine, New York, NY, USA.
to a variety of stimuli.1More than 22 million Americans are believed to
have the disease.
2
Although it is encouraging that for the first time in
decades, asthma death rates are decreasing,
3
morbidity remains quite high.
Healthcare costs due to treatment of asthma in the acute care setting total a
staggering $18 billion dollars per year.
3
Definition, Precipitating Factors and Mortality Risk
Asthma exacerbations are defined by progressive worsening of respiratory symptoms such as shortness of breath, wheezing, cough and chest
tightness, accompanied by decreases in lung function.
1
All patients with
asthma are at risk for developing an acute exacerbation regardless of the
underlying severity of their disease.
4
Respiratory viruses are recognized
as the most important precipitating factor for acute exacerbations.
It is important to be familiar with patient characteristics predictive
of increased mortality risk related to exacerbations.
1
Prior severe exacerbations with Intensive Care Unit (ICU) admission, multiple
Emergency Department (ED) visits or hospitalizations within the year,
using more than two canisters of short acting beta-agonist per month,
poor perception of respiratory symptoms, lack of a written action plan,
and mold sensitivity are historical factors associated with increased risk
of death. Social factors such as low socioeconomic status or inner city
residence, illicit drug use and major psychosocial problems are also
important. Finally, other chronic cardiopulmonary disease or psychiatric
illness can identify patients at high risk.
Evaluation of Patients Hospitalized with an Asthma Exacerbation
History
The clinician should take a focused history to determine the rate of progression of the exacerbation, the factors that may have precipitated the
attack, the therapy that has been used and the time of the last dose.
1
298
G. Skloot
Attention should be paid to risk factors predictive of poor outcome.
Comorbidities that can contribute to asthma such as allergic rhinitis,
sinusitis, Gastroesophageal Reflux Disease (GERD), obesity, sleep
disordered breathing and depression should be noted. The differential
diagnosis of severe asthma
1,5
includes chronic obstructive pulmonary
disease (chronic bronchitis or emphysema), cystic fibrosis, congestive
heart failure (CHF), pulmonary embolism, vocal cord dysfunction,
bronchiectasis, sarcoidosis, hypersensitivity pneumonitis and bronchiolitis
obliterans.
Physical Examination
Examination should be targeted to confirm that the process is indeed an
asthma exacerbation and to identify the severity of the attack. Physical
findings typical of a severe asthma exacerbation are shown in Table 1.
1,4,6
Focus should be on the patient’s level of alertness, hemodynamics, fluid
status, and the presence of cyanosis, respiratory distress and wheezing.
Some typical warning signs (tachypnea and tachycardia) may actually
wane as a patient begins to fatigue. Patients may appear anxious and
scared. Accessory muscle use is an indication of increased work of breathing. Although wheezing is generally thought of as a typical marker of an
asthma attack, a quiet chest is more ominous.
7
and louder wheezing may
actually be a sign of improvement.
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Asthma
Table 1. Physical Findings During a Severe Asthma Exacerbation
Difficulty talking in full sentences
Patient seated upright and unable to lie flat
Cyanosis and diaphoresis
Decreased level of consciousness
Confusion
Use of accessory muscles (sternocleidomastoid retraction)
Respiratory rate > 30 breaths/min
Heart rate > 120 beats/min or < 60 beats/min with hypotension
Pulsus paradoxus (>15 mm Hg decrease with inspiration)
Quiet chest
Objective Testing
Very few tests are routinely recommended in the assessment of patients
hospitalized for an asthma exacerbation. Table 2 summarizes the indications for lung function, chest radiography, and laboratory testing. Some
measurement of lung function is helpful to stratify the severity of an attack
and to assess response to therapy.
1
Spirometry (i.e., FEV1) is preferable to
peak expiratory flow (PEF) since the latter test cannot distinguish as well
between obstructive disease and impairment due to other conditions (i.e.,
pneumonia or neuromuscular disease) or simply to reduced effort. FEV
1
or
PEF should be measured upon admission and at least daily thereafter until
discharge. In particular, measurement 15–20 minutes following bronchodilator is recommended with comparison to baseline. Large swings in
lung function during a 24-hour period (i.e., morning and evening) are
300
G. Skloot
Table 2. Indications for Specific Objective Testing in Inpatient
Asthma Evaluation
Test Patient Candidate
Lung Function:
FEV
1
or PEF All patients if possible
Pulse Oximetry All patients
Chest Radiography Suspect alternative diagnosis or
complication (e.g. pneumonia,
atelectasis, pneumothorax, etc.)
Laboratory Studies:
ABG Severe distress, suspected
hypoventilation, SpO
2
< 90%,
FEV
1
or PEF ≤ 25% predicted
CBC Suspect infection
Serum electrolytes Concurrent cardiovascular
disease, on diuretic
Therapeutic Drug Monitoring On methyxanthine formulation
FEV1= forced expiratory volume in 1 second; PEF = peak expiratory flow;
ABG = arterial blood gas; SpO
2
= oxygen saturation by pulse oximetry;
CBC = complete blood count.
thought to portend a poorer prognosis. Patients with such fluctuations or
those with baseline values < 25% predicted and < 10% increase after bronchodilator should be triaged for possible ICU transfer. Oxygen saturation
should be monitored by pulse oximetry (SpO
2
) in all patients. The goal
should be to maintain SpO
2
> 90% in all patients and > 95% in pregnant
women and in patients with cardiovascular disease.
In situations in which other respiratory conditions or complications
are suspected (i.e., pneumonia, atelectasis, pneumothorax or pneumomediastinum), chest radiography can play a helpful role but otherwise should
not be routinely ordered. Patients with severe respiratory distress, with
hypoxia or persistently low lung function after treatment or, with suspected hypoventilation are candidates for arterial blood gas (ABG) monitoring. The most common finding is respiratory alkalosis.
4
A normal or
elevated arterial carbon dioxide tension is an alarming finding that may
signal respiratory muscle fatigue with impending respiratory failure.
When the exacerbation is of longer duration, a compensatory nonaniongap metabolic acidosis may be present.
Management of Patients Hospitalized with an Asthma Exacerbation
Medications
The mainstay of pharmacologic inpatient asthma management includes
short-acting beta-agonists (SABA) and systemic corticosteroids. The
frequency of administration of SABA depends upon improvement in
airflow obstruction and associated symptoms. The onset of action is
generally within five minutes and the duration, while uncertain in severe
exacerbations, likely ranges between 3–6 hours.
4
Adverse effects include
tremors and tachycardia or tachyarrthymias; therefore, more selective
agents (i.e. levalbuterol) are preferred when high doses are required.
SABA may be administered via metered dose inhaler (MDI) with a
valved holding chamber (VHC) when the patient is cooperative and
the exacerbation not severe. An MDI with a VHC is as effective as a
301
Asthma
nebulizer for treatment of acute asthma.6Four to eight puffs of an MDI
are approximately equivalent to one nebulizer treatment. For severe
asthma exacerbations or when the patient cannot cooperative effectively,
nebulizer therapy is appropriate.
All hospitalized patients should receive systemic corticosteroids since
these medications reverse airway inflammation and thus hasten recovery.
High dose steroids are no longer considered advantageous and oral therapy is preferred, provided that gastrointestinal transit time or absorption is
not compromised.
1
The total course of therapy may range from 3–10 days
depending upon the severity of the exacerbation and the patient’s
response. There is no need to taper systemic steroids in patients who are
treated for less than one week. The recommended dose of prednisone or
the equivalent is 40–80 mg/day given in 1–2 divided doses until a PEF of
70% of predicted or personal best is achieved. Patients should continue on
their inhaled corticosteroids while in the hospital.
Additional pharmacologic therapies have been studied as a possible
way to avoid intubation though intubation should not be delayed once it
is judged necessary. Such therapies include intravenous magnesium sulfate, heliox-driven albuterol nebulization, intravenous beta-2-agonists,
intravenous leukotriene receptor antagonists and noninvasive ventilation.
Only intravenous magnesium sulfate and heliox merit consideration at
this time based on available data. These therapies should be reserved for
patients with severe exacerbations who are not responding to traditional
treatment.
Medications not recommended include methylxanthines and antibiotics (unless there are symptoms or signs of infection including purulent
sputum, fever, or evidence of pneumonia). Although inhaled ipratropium
bromide is recommended in the ED setting, it is not thought to be of additive benefit once a patient is hospitalized with an exacerbation.
Adjunct Therapy
Oxygen therapy is generally given until there is a demonstrable response
to beta-agonist with improvement in symptoms, physical findings and
302
G. Skloot
lung function. Low-flow oxygen is usually sufficient and in fact, highdose oxygen may precipitate hypercapnia in some patients.
8
Other adjunct
therapies commonly employed in the past are no longer recommended.
These include aggressive hydration, chest physiotherapy, mucolytics such
as acetylcysteine since they may actually worsen cough or airflow
obstruction, and sedation due to the risk of respiratory depression.
Monitoring Parameters
Patients hospitalized with an asthma exacerbation should be assessed frequently since acute deteriorations can occur. Evaluation should include
monitoring of symptoms, vital signs, lung exam, pulmonary function and
SpO
2
or ABG measurements as necessary.1Patients who are awake and
alert, able to talk in full sentences without respiratory distress or accessory
muscle use and who are able to lie down comfortably are manifesting
improvement. Dyspnea may still be present but should occur only on exertion. Heart rate and respiratory rate should decrease to normal. Blood pressure should be normal without signs of pulsus paradoxus. While wheezing
may persist in some patients, it is more important to note good air entry on
examination. The goal for peak flow parameters is a return to ≥70% of predicted or personal best. Spirometry may still show obstruction but should
be less severe. SpO
2
should exceed 95% on room air. In such a case, ABGs
are not necessary. Indicators of improvement should be sustained for 60
minutes after the last SABA treatment.
Treatment of Comorbid Conditions
Certain comorbid conditions may complicate care of the hospitalized
asthmatic. COPD or cardiovascular disease can lead to more severe illness
or in the case of CHF, potential difficulty in identifying the patient’s primary problem. Obese patients may be more at risk for worse outcomes
related either to disease severity
9
or concurrent conditions such as GERD,
obesity hypoventilation syndrome or obstructive sleep apnea syndrome
(OSAS).
1
Such patients may have a blunted response to corticosteroids
10
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Asthma