MVS Pathophysiology: Asthma

community acquired pneumonia | pulmonary embolism | pneumothorax | asthma

Definition and Prevalence Pathophysiology Clinical Features Diagnosis Management

A. Definition and Prevalence

Asthma is an episodic reactive airway disease characterized by inflammation of the airways resulting in hyperresponsiveness, bronchoconstriction, and infiltration of airways with inflammatory cells and edema fluid. Common triggers to an attack include upper respiratory tract infections, common allergens, irritants, exercise and various drugs, including NSAIDs. There is often no identifiable trigger.

This condition is very common, especially in children, with estimates of its prevalence ranging as high as 15% of the child population. Most children with asthma improve significantly as they mature.

The exact etiology of asthma is unknown. However, there is often a family history of atopy in affected individuals suggesting a genetic component to this condition.

There are 2 types of asthma.
1) Extrinsic asthma is a type I hypersensitivity response that involves IgE binding to mast cells. It is a childhood condition that most commonly occurs in patients with a history of allergy
2) Intrinsic asthma is an adult conditon that is not associated with a history of allergy. It may be accompanied by chronic bronchitis.

Asthma triad: asthma, ASA/NSAID sensitivity, nasal polyps

B. Pathophysiology

The pathogenesis of asthma consits of a series of immediate and late immunologic responses that are too detailed to describe completelely here.

Briefly, the immediate response consists of antigen binding to IgE receptors on mast cells. The mast cells release either preformed or newly generated mediators whose effects are bronchoconstriction, increased vascular congestion and permeability with edema, and increased mucus secretion.

The late response involves the eosinophil recruitment (blocked by corticosteroids), neutrophils, macrophages, and lymphocytes and cytokines.

Pathological Microscopic Findings in Bronchial Asthma	Bronchial smooth muscle hypertrophy resulting in airway wall thickening
	Bronchial submucosal and goblet cells hyperplasia contribute to increased airway resitance and atelectasis
	Mucus plugs (containing Curschmann's spirals, eosinophils, and Charcot-Leyden crystals) in the airways

C. Clinical Features

During an asthma attack, patients will experience dyspnea, coughing, wheezing and anxiety. Patients are usually tachypneic and tachycardic. Pulsus paradoxus is also a common finding. When an attack is not present, patients may exhibit similar symptoms to an attack but to a lesser extent. However, in certain cases, a cough, hoarseness or an inability to sleep may be the only symptoms.

In severe cases, the patient may present with status asthmaticus which is defined as an attack of increased severity that is not responsive to routine therapy. It is a dangerous presentation which may suddenly become fatal. The patient usually has a hitory of increased bronchiodilator use. Clinical signs of status asthmaticus are severe exacerbation, pulsus paradoxus, accessory muscle aided breathing, diaphoresis, orthopnea, decreased mental status, and fatigue. Hypoxemia is frequently present and may be accompanied by respiratory and metabolic acidosis. These patients often must be intubated and mechanically ventilated.

D. Diagnosis

Diagnosis relies very much history and physical exam. However, the following tests may confirm your diagnosis.

Asthma Investigations
pulmonary function tests (PFT)	decreased FVC, decreased FEV1, hyperinflation that improves with bronchodilator, increased RV, TLC, and lung compliance
specialized PFT	eg cold air challenge, portable peak flow measurement
CXR	large mucus plugs, hyperinflation, pneumothorax caused by rupture of alveolar tissue by high intraalveolar pressure
pulse oxymetry	hypoxemia
ABG	done if venous PCO2 < 50 mmHG, decreased mental status, deterioration despite treatment, peak flow < 30% predicted, O2 sat < 90% on 100% oxygen

E. Management

Control of asthma is defined as:
1) minimization of symptoms, ideally none
2) ability to conduct normal activities of daily living
3) use of inhaled beta-agonist to no more than twice per day, ideally none
4) normal or near normal airflow rates at rest
5) normal airflow rates after use of inhaled beta-agonist
6) daily variations in PEFR (peak expiratory flow rate) < 20%, ideally < 10%
7) minimal side effects from treatment

The principle classes of agents used to treat asthma are:

The current mainly therapy of asthma consist of inhaled beta-agonist and inhaled corticosteroids.

In the acute emergency department setting, therapy is aimed at relieving hypoxemia, airflow limitation, and airway inflammation. In addition, acute management also tries to avoid toxicity from overdose with bronchodilator.

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