Professional Documents
Culture Documents
What is Asthma
A Chronic disease of the airways
that may cause:
Wheezing
Breathlessness
Chest tightness
Nighttime or early morning coughing
Symptoms/Chief
Complaint
Progressive dyspnea
Cough
Chest tightness
Wheezing/coughing
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
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
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
Classifying Severity of
Asthma Exacerbations
Symptoms
Mild
Moderate
Breathlessness
walking
Position
Talks in
Alertness
walking
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
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%
>95
%9195%
<91%
Respiratory Arrest
Imminent
Drowsy or confused
Paradoxical thoracoabdominal
movement
AbsentWheeze
Bradycardia
Absence Pulsus paradoxus suggests
respiratory muscle fatigue
Asthma Mimickers
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
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
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
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.
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
Pirbuterol
MDI (200 g/puff)
Terbutaline (1 mg/mL)
0.25 mg SC every 20 min for 3 doses
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
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
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
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
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)
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 - Advanced Dx
secondary polycythemia
cyanosis
tremor
somnolence and confusion due to
hypercarbia
Secondary pulmonary HTN w or
w/o cor pulmonale
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 ?