Download Dyspnea

ASTHMA
What is Asthma
• A Chronic disease of the airways that
may cause:
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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
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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
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Immunologic reaction
Viral respiratory/sinus infections
change in temperature/humidity
Drugs/Chemicals • aspirin, NSAIDS
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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
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Nebulized B-adrenergic drugs
Corticosteroids
Nebulized anticholinergics
Magnesium sulfate
Oxygen
Long acting beta-agonists
Inhaled steroids
Managing Asthma:
• Indications of a severe attack:
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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
• Breathlessness walking
Moderate
talking
Severe
at rest
• Position
Can lie down
Prefers sitting
upright
• Talks in
Sentences
Phrases
Words
• Alertness
May be agitated
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
% personal best
Mild
80%
Moderate
50–80%
Severe
<50% or
response lasts<2h
PaO2 (on air)
Normal
>60 mm Hg
<60 mm Hg:
possible cyanosis
PaCO2
<42 mm Hg
<42 mm Hg
> 42 mm Hg:
possible respiratory failure
SaO2%
(on air) at sea level
>95
%91–95%
<91%
Respiratory Arrest Imminent
• Drowsy or confused
• Paradoxical thoracoabdominal
movement
• Absent Wheeze
• Bradycardia
• Absence Pulsus paradoxus suggests
respiratory muscle fatigue
Asthma Mimickers
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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
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ensure adequate oxygenation
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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
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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
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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
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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)
• 2.5–5.0 mg every 20 min for 3 doses
• then 2.5–10 mg every 1–4 h as needed or 10–15
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 6–8 L per min
Albuterol
• MDI (90 g/puff)
• 4–8 puffs every 20 min up to 4 h
• then every 1–4 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)
• 0.3–0.5 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 2–4 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)
• 4–8 puffs every 6–8 h
side effects
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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
• 120–180 mg per d in 3 or 4 divided doses for 48 h,
• then 60–80 mg per d until FEV1, or PEFR reaches
70% of predicted or personal best
• For outpatient "burst," use 40–60 mg per d, for 3–10
d in adults
Theophylline
• no longer considered a first-line treatment
• in combination with inhaled B 2-adrenergic
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
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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
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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
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secondary polycythemia
cyanosis
tremor
somnolence and confusion due to
hypercarbia
• Secondary pulmonary HTN w or w/o cor
pulmonale
COPD Treatment Strategy
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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 patient’s 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
patient’s overdose was complicated by
aspiration pneumonitis and that the patient
required treatment with antibiotics in addition
to mechanical ventilation.
Questions ?