You are on page 1of 80

ASTHMA

What is Asthma
A Chronic disease of the airways
that may cause:
Wheezing
Breathlessness
Chest tightness
Nighttime or early morning coughing

The bronchospasm characteristic


of the acute asthmatic attack is
typically reversible. It improves
spontaneously or within minutes to
hours of treatment

Asthma can exist by itself or


coexist with chronic bronchitis,
emphysema, or bronchiectasis

Symptoms/Chief
Complaint
Progressive dyspnea
Cough
Chest tightness
Wheezing/coughing

The rapidly reversible airflow


obstruction of asthma is mainly
due to bronchial smooth muscle
contraction

Focus of Therapy
Pharmacologic manipulation of airway smooth
muscle
Do not overlook physiologic impairment caused by
mucous production and mucosal edema
Bronchospasm can be reversed in minutes
Airflow obstruction due to mucous plugging and
inflammatory changes in bronchial walls may not
resolve for days/weeks may lead to atelectasis, infectious bronchitis,
pneumonitis

Asthma Triggers

Immunologic reaction
Viral respiratory/sinus infections
change in temperature/humidity
Drugs/Chemicals aspirin, NSAIDS

Exercise
GE reflux
Laughing/coughing
Environmental factors strong odors, pollutants, dust, fumes

Patient Exam
Wheezing
may be audible w/o stethoscope

Use of accessory muscles of inspiration


diaphragmatic fatigue
Paradoxical respirations
- reflect impending ventilatory failure

Altered mental status lethargy, exhaustion, agitation, confusion

Patient Exam
Hyperrsonance to percussion
decreased intensity of breath
sounds
prolongation of expiratory phase w
or w/o wheezing

Patient Exam
The intensity of the wheeze may
not correlate with the severity of
airflow obstruction
quiet chest - very severe airflow
obstruction

Risk factors for death from


asthma
Past history of sudden severe
exacerbations
Prior intubation for asthma
Prior admission for asthma to an intensive
care unit
Two or more hospitalizations for asthma in
the past year
Three or more emergency care visits for
asthma in the past year
Hospitalization or emergency care visit for
asthma within the past month

Risk factors cont..


Use of more than two canisters per month of inhaled
short-acting 2-agonist
Current use of systemic corticosteroids or recent
withdrawal from systemic corticosteroids
Difficulty perceiving airflow obstruction or its severity
Comorbidity, as from cardiovascular diseases or
chronic obstructive pulmonary disease
Serious psychiatric illness or psychosocial problems
Low socioeconomic status in urban residents
Illicit drug use

Asthma Treatment
Nebulized B-adrenergic drugs
Corticosteroids
Nebulized anticholinergics
Magnesium sulfate
Oxygen
Long acting beta-agonists
Inhaled steroids

Managing Asthma:
Indications of a severe attack:
Breathless at rest
hunched forward
talking in words rather than
sentences
Agitated
Peak flow rate less than 60% of
normal

Treatment Goals of Severe


Asthma
Improve airway function rapidly
Avoid hypoxemia
Prevent respiratory failure and
death

Classifying Severity of
Asthma Exacerbations
Symptoms

Mild

Moderate

Breathlessness
walking
Position
Talks in

Alertness

walking

Can lie down

talking

at rest
rest

Prefers sitting

Sentences

May be agitated

Severe

Phrases

upright

Words

Usually agitated

Classifying Severity of
Asthma Exacerbations
Signs

Mild

Moderate

Severe

Classifying Severity of
Asthma Exacerbations
Functional assessment

Mild

Moderate

Severe

Classifying Severity of
Asthma Exacerbations
Functional assessment
Peak expiratory flow

% predicted or

Mild

Moderate

80%

5080%

Normal

>60 mm Hg

% personal best

PaO2 (on air)

Severe

<50% or
response lasts<2h
<60 mm Hg:

possible cyanosis

PaCO2
<42 mm Hg
<42 mm Hg
possible respiratory failure

> 42 mm Hg:

SaO2%

(on air) at sea level

>95

%9195%

<91%

Respiratory Arrest
Imminent
Drowsy or confused
Paradoxical thoracoabdominal
movement
AbsentWheeze
Bradycardia
Absence Pulsus paradoxus suggests
respiratory muscle fatigue

Asthma Mimickers

Congestive heart failure ("cardiac asthma")


Upper airway obstruction
Aspiration of foreign body or gastric acid
Bronchogenic carcinoma with endobronchial
obstruction
Metastatic carcinoma with lymphangitic
metastasis
Sarcoidosis with endobronchial obstruction
Vocal cord dysfunction
Multiple pulmonary emboli (rare)

treatment of acute asthma


Goal in the ED
reverse airflow obstruction rapidly
by repetitive or continuous
administration of inhaled 2-agonists
ensure adequate oxygenation
relieve inflammation

Initial Assessment
History
physical examination
(auscultation use of accessory muscles,
heart rate, respiratory rate)

PEFR or FEV
oxygen saturation
other tests as indicated

Diagnosis
Bedside spirometry
rapid, objective assessment ,guide to
the effectiveness of therapy.
The forced expiratory volume in 1 s
(FEV1)
peak expiratory flow rate (PEFR)

Sequential measurements
management decisions

Pulse oximetry
assessing oxygenation and
monitoring oxygen saturation
during treatment.
ABG is not indicated in most
patients with mild to moderate
asthma exacerbation

ABG
assess for hypoventilation with carbon dioxide
retention and respiratory acidosis
clinical evidence of severe attacks
PEFR or FEV1 of less than 25 percent predicted
With acute attacks, ventilation is stimulated,
resulting in a decrease in partial pressure of
carbon dioxide (PaCO2)
normal or slightly elevated PaCO2 (e.g., 42 mm Hg)
indicates extreme airway obstruction and fatigue and
may herald the onset of acute ventilatory failure

radiography
clinical indication of a complication
pneumothorax, pneumomediastinum,
pneumonia, or other medical concern

one-third of asthma exacerbations


requiring admission, will
demonstrate an abnormality on
chest radiograph

CBC
not indicated
modest leukocytosis secondary to
administration of B -agonist therapy
or corticosteroid treatment
In patients taking theophylline before
ED presentation, a serum
theophylline level

ECG
Routine electrocardiogram is unnecessary
right ventricular strain, abnormal P waves,
or nonspecific ST- and T-wave
abnormalities, which resolve with
treatment
Older patients, especially those with
coexisting heart disease, should have
cardiac monitoring during treatment

Impending or Actual
Respiratory
Arrest
Intubation and mechanical ventilation
with 100% 02
Nebulized B2 agonist and anticholinergic
Intravenous steroid
Admit to ICU

FEV1 or PEFR <50%


(Severe Exacerbation)

Repeat Assessment
Symptoms.
physical examination.
PEFR.
02 saturation.
other test as needed

Severe Exacerbation

Moderate Exacerbation

Good Response

Discharge Home

Poor Response

Poor Response

Incomplete Response

Poor Response

medications are used in the


treatment of acute asthma

adrenergic agonists
anticholinergics
glucocorticoids
Magnesium, heliox (mixture of helium and
oxygen), and ketamine may be considered
when the aforementioned medications fail
to relieve bronchospasm.
Mast cell-stabilizing agents,
methylxanthines, and leukotriene
modifiers are currently reserved for
maintenance therapy only

Adrenergic Agents
Adrenergic receptors
Stimulation of B 1-receptors increases rate
and force of cardiac contraction and
decreases small intestine motility and tone
B2-adrenergic stimulation promotes
bronchodilation, vasodilation, uterine
relaxation, and skeletal muscle tremor

Adrenergic Agents
stimulation of the enzyme adenyl cyclase, which
converts intracellular adenosine triphosphate
into cyclic adenosine monophosphate
enhances the binding of intracellular calcium to
cell membranes, reducing the myoplasmic
calcium concentration, and results in relaxation
of bronchial smooth muscle
inhibit mediator release and promote
mucociliary clearance.

side effect of B-adrenergic


drugs

skeletal muscle tremor (most common)


nervousness, anxiety,
insomnia, headache,
hyperglycemia,
palpitations, tachycardia, and hypertension
potential cardiotoxicity(combination with
theophylline not significant problems)
Arrhythmias and evidence of myocardial
ischemia( rare)

Inhaled short-acting B-2


agonists
Albuterol
Nebulizer solution (5 mg/mL)
2.55.0 mg every 20 min for 3 doses
then 2.510 mg every 14 h as needed or 1015
mg per h continuously

Only selective B-2 agonists are


recommended
for optimal delivery, dilute aerosols to minimum
of 4 mL at gas flow of 68 L per min

Albuterol
MDI (90 g/puff)
48 puffs every 20 min up to 4 h
then every 14 h as needed
As effective as nebulized therapy if patient
is able to coordinate inhalation maneuver;
use spacer/holding chamber

Inhaled short-acting B-2


agonists
Bitolterol
Nebulizer solution (2 mg/mL)
MDI (370 macg/puff)

Pirbuterol
MDI (200 g/puff)

Inhaled short-acting B-2


agonists
Systemic (injected), B-2 agonists
Epinephrine (1:1000 or 1 mg/mL)
0.30.5 mg SC every 20 min for 3 doses

Terbutaline (1 mg/mL)
0.25 mg SC every 20 min for 3 doses

No proven advantage of systemic


therapy over aerosol

Anticholinergics
potent bronchodilators in patients with asthma and
other forms of obstructive lung disease
anticholinergics affect large, central airways,
whereas B-adrenergic drugs dilate smaller airways
competitively antagonize acetylcholine at the
postganglionic junction between the parasympathetic nerve
terminal and effector cell
blocks the bronchoconstriction induced by vagal cholinergicmediated innervation to the larger central airways
concentrations of cyclic guanosine monophosphate in
airway smooth muscle are reduced,further promotin
bronchodilation

Anticholinergics
Ipratropium bromide
Nebulizer solution (0.2 mg/mL)
0.5 mg every 30 min for 3 doses
then every 24 h as needed
Should not be used as first-line therapy;
should be added to 2 agonist therapy;
may mix in same nebulizer with albuterol

MDI (18 g/puff)


48 puffs every 68 h

side effects
dry mouth
Thirst
difficulty swallowing
Less commonly
tachycardia, restlessness, irritability,
confusion, difficulty in micturition,
ileus, blurring of vision, or an increase
in intraocular pressure

Corticosteroids
highly effective drugs in asthma
exacerbation
one of the cornerstones of treatment
mechanism of action is unknown
Restoring B-adrenergic responsiveness
reducing inflammation

The onset of anti-inflammatory effect is


delayed at least 4 to 8 h after
intravenous or oral administration.

Corticosteroids
administered within 1 h of arrival in the ED
reduces the need for hospitalization
prednisone 40 to 60 mg, oral
methylprednisolone 60 to 125 mg IV

High-dose corticosteroid therapy offers no advantage


Additional doses should be given every 4 to 6 h until
significant subjective and objective improvements
are achieved
discharging all patients with mild persistent or more
severe asthma on maintenance inhaled
corticosteroids in addition to a burst of oral
corticosteroid

Corticosteroids

Prednisone
Methylprednisolone
Prednisolone
120180 mg per d in 3 or 4 divided doses for
48 h,
then 6080 mg per d until FEV1, or PEFR
reaches 70% of predicted or personal best
For outpatient "burst," use 4060 mg per d, for
310 d in adults

Theophylline
no longer considered a first-line
treatment
in combination with inhaled B 2adrenergic drugs,
increase the toxicity, but not the efficacy, of
treatment

more sustained bronchodilator effect,


improving respiratory muscle endurance
improving resistance to fatigue
anti-inflammatory

Theophylline
side effects
nervousness, nausea, vomiting,
anorexia, and headache
At plasma levels greater than 30
g/mL, there is a risk of seizures
and cardiac arrhythmias.

magnesium sulfate
acute, very severe asthma
(i.e., FEV1 <25 percent predicted)

The dose is 1 to 2 g IV over 30


min.

Heliox, Ketamine, and Halothane


Mast Cell Modifiers
Leukotriene Modifiers

Mechanical Ventilation
progressive hypercarbia and acidosis
Exhausted
confused,
does not relieve the airflow obstruction
eliminates the work of breathing and
enables the patient to rest while the
airflow obstruction is resolved
Direct oral intubation

COPD

COPD
Hallmark symptom - Dyspnea
Chronic productive cough
Minor hemoptysis
pink puffer
blue bloater

COPD- pulmonary hyperinflation- the diaphragms are at


the level of the eleventh posterior ribs and appear flat.

COPD - Physical Findings


Tachypnea
Accessory respiratory muscle use
Pursed lip exhalation
Weight loss due to poor dietary
intake and excessive caloric
expenditure for work of breathing

Dominant Clinical Forms of


COPD
Pulmonary emphysema
Chronic bronchitis

Most patients exhibit a mixture of


symptoms and signs

COPD - Advanced Dx
secondary polycythemia
cyanosis
tremor
somnolence and confusion due to
hypercarbia
Secondary pulmonary HTN w or
w/o cor pulmonale

COPD Treatment Strategy


Elimination of extrinsic irritants
bronchodilator & glucocorticoid
therapy
Antibiotics
Mobilization of secretions
respiratory vaccines
Oxygen therapy - if oxygen saturation
<90% at rest on room air

Spirometry

A-a gradient
A-a gradient = predicted pO2 observed PO2
PAO2 = (FIO2 X 713) (PaCO2/0.8) at sealevel
PAO2 = 150-(PaCO2/0.8) at sealevel on room air
Normal range 10-15mm > 30 years of age
Normal range 8mm < 30 years of age
Increased A-aDO2=diffusion defect
Right to left shunt
V/Q mismatch

Examples
A doubel overdose brings two 30 yr old
patients to the ED. Both have ingested
substantial amounts of barbiturates and
diazepam. Blood gases drawn on room
air revealed these values:
patient 1- pH =7.18, PCO2 = 70mmHg,
PO2=50mmHg, HCO3=24mEq/L;
patient2- pH =7.31, PCO2=50mmHg,
PO2=50mmHg, HCO3=25mEq/L

Comment
The A-a gradient calculation for patient
1 is as follows:
A-a DO2 = PAO2 PaO2
PAO2 = 150 (1.25x PCO2)
PAO2 = 150 (1.25x 70)

PAO2 = 62
A-a =62 50
A-a = 12

Comment
The calculation reveals a normal
gradient, indicating that the
etiology for hypoxemia and
hypoventilation is extrinsic to the
lung itself.

Comment
The A-a gradient calculation for
patient 2 is as follows:
PAO2 = 150 (1.25 x PCO2)
PAO2 = 150 (1.25 x 50)
PAO2 = 150 63
PAO2 = 87
Therefore, A-a = 87 50 =37 (an
abnormally increased gradient)

Comment
We can be reasonably confident
that patient 1 suffered
hypoventilation due to the effect of
the ingested drugs on the brain
stem.
Temporary mechanical ventilation
restored this patients gas
exchange.

Comment
Patient 2, on the other hand, had an
increased A-a gradient, indicating a lung
problem in addition to any central cause
for hypoventilation.
The chest x-ray film revealed that this
patients overdose was complicated by
aspiration pneumonitis and that the
patient required treatment with antibiotics
in addition to mechanical ventilation.

Questions ?