Obstruction

Definition/Etiology:

• Chronic obstructive pulmonary disease: persistent airflow obstruction due to abnormalities in alveoli and airways, usually caused by exposure to noxious particles and gasses.
• Chronic bronchitis: chronic productive cough for 3 months in each of 2 years, in patients without other causes like bronchiectasis.
• Emphysema: abnormal and permanent enlargement of the airspaces distal to the terminal bronchioles that is accompanied by destruction of the airspace walls, without obvious fibrosis.
• Asthma: chronic inflammation with airway hyperresponsiveness and widespread airflow obstruction within the lung, often reversible either spontaneously or with treatment. Can be exercise-induced, particularly in cold air.

Pathophysiology:

• Chronic inflammation is a hallmark of these diseases. Increased mucus production occurs as well as hyperactivity of cells that fight infection. Allergic mediators play an active role, especially in asthma. In emphysema, destruction of alveoli occurs, and surface area for gas exchange diminishes.
• Stridor is an acute, transient sign of upper airway obstruction from edema, foreign object, infection, allergy, smoke inhalation, etc. It is high-pitched and heard best over the neck.
• Alveolar destruction in emphysema causes loss of spongy recoil in the lungs. This loss of elasticity causes airways to close early during exhalation. This traps air distally in the lungs.
• High CO2 levels in the blood are called hypercapnia. Our drive to breathe is normally based on CO2 levels in the blood. When high, we are triggered to breathe. In chronic pulmonary patients, this can change, and giving them too much oxygen can lessen their drive to breathe. Patients can develop acute hypercapnia, or acute-on-chronic hypercapnia.

Clinical Presentation:

• Exertional dyspnea is the earliest symptom
• Dyspnea at rest develops later
• Chronic sputum production
• Chronic cough
• If wheezing/stridor, look for other s/s systemic allergy
• Doorway assessment: are they toxic? (infection)
• If stridor, assess for aspiration of foreign object
• Chest tightness (less common)
• Tripoding?
• Assess sputum. Color? Frothy?
• Assess work of breathing
• Quiet/focused/nervous vs agitated/frantic
• If sluggish, sleepy, or agitated, consider high CO2
• If home O2, increased AP diameter, clubbing of fingernails, etc, consider chronic CO2 retainer
• If they get quiet, pay attention. Are they moving enough air to wheeze?

Collaborative Management:

Testing:

• Labs: CBC, BNP, CMP, ABG, possibly Alpha 1 antitrypsin
• Pulmonary function testing
• Pre/post bronchodilator spirometry to detect partial/full reversibility of airflow limitation
• Pulse oximetry

CXR:

• Increased AP diameter is common
• Rule out other causes like CHF, pneumonia
• Darker lung fields can indicate emphysema (alveolar destruction), and flattening of the diaphragm from air trapping

Respiratory therapy:

• Meds: steroids, bronchodilators
• Racemic epinephrine nebulizer if stridor
• Bipap, vent for acute exacerbation

Evaluation | Patient Monitoring | Education:

• Outpatient allergy testing
• Outpatient pulmonary rehab
• Home monitoring of peak flow
• Home nebulizer
• Smoking cessation
• Pulmonary rehab

Linchpins: (Key Points)

• Recognize and treat both high CO2 and low O2.
• Both quiet/nervous and agitated/frantic can be bad signs.
• Patient may be a chronic CO2 retainer.
• Treat the factors that we can in order to manage the acute-on-chronic exacerbation.