28: 58-year-old man with shortness of breath Flashcards
Causes of dyspnea
- cardiac
- heme
- pulm
- psychogenic
- other: neuromu, metabolic, deconditioning
Orthopnea Definition
Dyspnea which occurs when lying flat, forcing the person to have to sleep propped up in bed or sitting in a chair. It is commonly measured according to the number of pillows needed to prop the patient up to enable breathing (Example: “three pillow orthopnea”).
Dyspnea Definition
Dyspnea is defined as an uncomfortable awareness of breathing.
Paroxysmal nocturnal dyspnea (PND) - Definition, Etiology, Symptoms
Definition
Sudden, severe shortness of breath at night that awakens a person from sleep, often with coughing and wheezing.
Etiology
It is most closely associated with congestive heart failure.
Symptoms
PND commonly occurs several hours after a person with heart failure has fallen asleep. PND is often relieved by sitting upright, but not as quickly as simple orthopnea. Also unlike orthopnea, it does not develop immediately upon lying down.
acute vs chronic bronchitis
Acute Bronchitis
Productive cough lasting 1-3 weeks
Chronic Bronchitis
Productive cough for at least three months for the past two years
Classic Findings on Physical Exam for COPD
> > Increased anteroposterior (AP) diameter of the chest
Decreased diaphragmatic excursion
Wheezing (often end-expiratory)
Prolonged expiratory phase
Four items predicted the presence of COPD:
> > Smoking more than 40 pack-years
Self-reported history of chronic obstructive airway disease
Maximum laryngeal height of 4 cm or less,
Age at least 45 years
Chronic Obstructive Pulmonary Disease (COPD) - Definition, Epidemiology, Diagnosis
Definition
COPD encompasses both chronic bronchitis and emphysema and is characterized by airflow limitation that is progressive and not fully reversible with bronchodilators.
Epidemiology
While it is currently estimated by the World Health Organization to be the twelfth commonest cause of morbidity and the fourth commonest cause of death worldwide, COPD is set to become the fifth most common cause of morbidity and third most common cause of death by 2020. Twelve million Americans are diagnosed with COPD; yet an additional 12 million Americans may have COPD and remain undiagnosed.
Diagnosis
A clinical diagnosis of COPD should be considered in any middle-aged or older adult who has:
»dyspnea
»chronic cough or sputum production, or
»a history of tobacco use
The diagnosis should be confirmed by spirometry.
Differences between the mechanisms underlying COPD and asthma include:
Cigarette smoke is more of a causal agent in COPD,
Mast cells, T helper cells, and eosinophils play more of a role in what appears to be an allergic bronchoconstrictive response in asthma
Macrophages, T killer cells, and neutrophils play a role in an inflammatory and destructive process in COPD.
As noted on the previous card, a post-bronchodilator FEV1/FVC ratio < 70% confirms the presence of airflow limitation that is not fully reversible (hence a diagnosis of COPD).
Significant reversibility is defined as an increase in FEV1 ≥ 12% after bronchodilator.
Distinguishing COPD from Asthma
Air-flow obstruction in asthma is reversible, but in COPD it is not .
The major distinction between asthma and COPD is the reversible nature of asthma’s obstruction to air flow.
By definition, FEV1/FVC is decreased in COPD, but can be decreased or normal in asthma if the FEV1 and FVC are both decreased proportionally.
FVC is normal to decreased in COPD, but always decreased in asthma.
Macrophages and T killer cells play a role in COPD.
The major benefit occurred in the first year after smoking cessation.
“Your lungs will work better within that first year of quitting smoking.”
“When you quit smoking, your lungs will not ‘age’ as quickly as if you continued smoking.” “Even if you quit and then start smoking again, there may be benefit to you.”
Therapy for Moderate & Severe COPD
Therapy for Moderate COPD
For patients whose FEV1 is between 50 and 80% of predicted, maintenance therapy of inhaled anticholinergics (ipratroprium or tiotroprium) alone or in combination with short-acting beta agonists may be utilized.
Therapy for Severe COPD
In symptomatic COPDera whose FEV1 is < 50% of predicted and who have repeated exacerbations, it is recommended that inhaled glucocorticosteroids be added to bronchodilator tx. The combo of an inhaled glucocorticosteroid combined with a long-acting ß2-agonist is more effective than each individual component, although the addition of a gc may increase the risk of pna.
GOLD Spirometric Criteria for COPD Severity
Mild
FEV1/FVC < 0.7 FEV1 ≥ 80% predicted
At this stage, the patient is probably unaware that lung function is starting to decline.
Moderate
FEV1/FVC < 0.7
50% ≤ FEV1 < 80% predicted
Symptoms during this stage progress, with shortness of breath developing upon exertion.
Severe
FEV1/FVC < 0.7
30% ≤ FEV1 < 50% predicted
Shortness of breath becomes worse at this stage, and COPD exacerbations are common.
Very Severe
FEV1/FVC < 0.7
FEV1 < 30% predicted, or
FEV1 < 50% predicted with chronic respiratory failure
Quality of life at this stage is gravely impaired. COPD exacerbations can be life threatening.
Bronchodilators include:
inhaled short-acting and long-acting beta-2-agonists inhaled long-acting anticholinergics, and oral methylxanthines
Bronchodilators are essential for symptom management in COPD. According to the Global Initiative for Chronic Obstructive Lung disease:
All symptomatic patients with COPD should be prescribed a short-acting bronchodilator (e.g., albuterol) on an as-needed basis.
If symptoms are still inadequately controlled, a daily dose of long-acting bronchodilator should be added.
The choice between beta-2-agonist, anticholinergic, theophylline, or combination therapy depends on availability and individual response in terms of symptom relief and side effects.
Combining bronchodilators of different pharmacological classes may improve efficacy and decrease the risk of side effects compared to increasing the dose of a single bronchodilator.