Lecture Notes

Chapter 3: Asthma

Objectives

Define asthma and status asthmaticus

List the potential causes of asthma attacks

Describe the effect of asthma attacks on lung

function

List the clinical features of patients having an

asthma attack

List the treatments and indications for

mechanical ventilation in asthma

Introduction

Obstructive pulmonary disease

Diffuse airway inflammation and narrowing

Entirely or partially reversible

Excessive airway secretions

Status asthmaticus

Asthma attack refractory to conventional treatment

Occupational asthma (work place)

Stable asthma (4 weeks no symptoms)

Unstable asthma (increasing symptoms)

Between attacks, the asthmatic often has normal lung

function.

Etiology

Genetic

Atopy (allergic to

specific allergens)

Triggers

Infection

Exercise

Dust

Pollens

Cold air

Air pollution

Pathophysiology

Bronchospasm - Mucus plugging - Mucosal edema

↑ airway resistance

V/Q mismatching

hypoxemia

↑ pulmonary vascular resistance

Airway obstruction primarily affects exhalation. This results in air

trapping and progressive hyperinflation of the lungs.

Clinical Features: History

Chief complaints

Chest tightness

Difficulty breathing

Wheezing

Coughing

Rapid onset may disappear rapidly with

appropriate treatment

Clinical Features: Physical Exam

Inadequate assessment = insufficient treatment

and monitoring.

Tachypnea

Use of accessory muscles

Prolonged exhalation

Increased A-P chest diameter

Expiratory polyphonic wheezing

Diaphoresis

Intercostal retractions https://www.youtube.com/watch?v=Hv68EQ3tCBI

Clinical Features: Physical Exam

in Severe Asthma

Pronounced use of accessory muscles https://www.youtube.com/watch?v=kPWovH4fpFg

Paradoxical pulse decrease in systolic blood pressure.

Inability to speak

Inspiratory and expiratory wheezing

Decreased peak flows (maximum speed of expiration)

Diaphoresis

Abdominal paradox

Abnormal sensorium (late finding)

Clinical Features: Chest

Radiograph

Often normal or hyperinflation

In presence of complications

Pneumonia

Atelectasis

Pneumothorax

Clinical Features: Pulmonary

Function Studies (Severe Asthma)

Peak flows < 100 L/min

FEV1 < 1.0 L

Methacholine provocation (will cause

bronchospasm)

To determine degree of airway reactivity if normal

PFTs

FEV1 decreased by 20%

Clinical Features: Arterial Blood

Gases

Degree of hypoxemia and hypercapnia =

reliable indicators of severity of airway

obstruction

PaCO2 initially decreased

Normal or increased PaCO2 suggests

Severe degree of obstruction

Respiratory muscle fatigue

Treatment: Pharmacological

Agents

Beta-adrenergics

Rapid onset of action

Lower dose requirements

Lower incidence of systemic effects

Albuterol

Q3 to Q6 hours

Q 20 minutes x 3 in acute attack

Continuous therapy when refractory (10 mg/h)

Small-volume nebulizer (SVN)

Metered-dose inhaler (MDI)

Treatment

Pharmacological Agents

Anticholinergics

Combination with β-agonists

Safe and may be more effective than either drug

alone

Small-volume nebulizer (SVN)

Metered-dose inhaler (MDI)

Treatment: Pharmacological

Agents

IV Corticosteroids

With failure of inhaled β-agonists

Anti-inflammatory effects may take hours

Methylprednisolone 100–500 mg IV

Prednisone 60–80 mg PO

Treatment

IV Aminophylline

Not used for therapy of acute attack high

incidence of adverse effects.

Heliox

Low density gas

Severe acute asthma

Treatment: Pharmacological

Agents

Magnesium sulfate

Smooth muscle relaxant

Severe asthma

Medications to avoid in acute attack

Sedatives can induce ventilatory failure

Acetylcysteine

Cromolyn sodium

Dense aerosols

These agents tend to be irritating to the

airways

Treatment: Pharmacological

Agents

Anti Ig-E antibodies

Ig-E plays major role in pathogenesis of allergic

diseases

Omalizumab (Xolair)

Reduces number of exacerbations

Reduces use of corticosteroids

Improves overall quality of life

Treatment: Indications for

Endotracheal Intubation

Fatigue

Rising PaCO2

Deteriorating sensorium

Abdominal paradox

Decreased peak flow

Respiratory failure

Refractory hypoxemia

Severe acidemia (pH < 7.25)

Central cyanosis

Cardiac arrest

Treatment: Mechanical Ventilation

Sedative agents

Reduce oxygen consumption

Improve patient comfort

Ventilatory strategy

Tidal volume < 8 mL/kg

Rate 8–12 breaths/min

Flow 80–100 L/min

Keep Pplateau < 35 cm H2O

Adequate expiratory time

Permissive hypercapnia acceptance higher values of arterial

CO2 tension (Paco2)

Prevention

Assess asthma severity

Careful history

PFTs

Investigate provoking agents

Patient education

Avoid provoking agents

Use of medications and side effects

Use of peak flow meter

Cromolyn sodium stabilizing the mast cells to prevent the

release of mediators, such as histamine, that can cause bronchospasm.

Prognosis

predicting the outcome

Excellent if patient has a good response to

conventional treatment

Prior history of respiratory failure and intubation

increases mortality

Adult patients with asthma at greater risk for

bronchitis and emphysema