Chronic Obstructive Pulmonary Disease (COPD) and Emphysema in Emergency Medicine Workup

Arterial blood gas

Arterial blood gas (ABG) analysis provides the best clues as to acuteness and severity. In general, renal compensation occurs even in chronic CO₂ retainers (ie, bronchitics); thus, pH usually is near normal. Generally, consider any pH below 7.3 a sign of acute respiratory compromise.

Serum chemistry

These patients tend to retain sodium. Diuretics, beta-adrenergic agonists, and theophylline act to lower potassium levels; thus, serum potassium should be monitored carefully. Beta-adrenergic agonists also increase renal excretion of serum calcium and magnesium, which may be important in the presence of hypokalemia.

CBC count

CBC count may reveal polycythemia.

Brain natriuretic peptide (BNP)

Human BNP binds to particulate guanylate cyclase receptors of vascular smooth muscle and endothelial cells. Binding to the receptors causes an increase in cyclic guanosine monophosphate (GMP), which serves as a secondary messenger to dilate veins and arteries. By measuring the BNP level, it was thought that the ability to differentiate between CHF and COPD exacerbations in blue bloaters would have become much easier. However, clinical observation and research has demonstrated that, in the cases of mild CHF exacerbations, the ability to differentiate between CHF and COPD is still not straightforward. A mild elevation of a BNP level still must be taken in context with the overall clinical picture.

Lactate level

With the use of beta-adrenergic agents during acute exacerbations (eg, albuterol), there can be a notable increase in serum lactate levels, which can confuse the clinical picture.

Albuterol functions by activating beta2-adrenergic receptors on airway smooth muscles, stimulating adenyl cyclase and increasing production of cyclic adenosine monophosphate (cAMP), causing relaxation of the smooth muscle and bronchodilation. Beta-2 receptor activation produces excess glycogenolysis and lipolysis. Increased glycogenolysis eventually leads to increased concentrations of pyruvate. Pyruvate is converted to acetyl coenzyme A (CoA), which enters the citric acid cycle. If pyruvate does not enter this aerobic pathway, it is converted to lactate instead, thereby potentially causing lactic acidosis. In addition, an increased lipolysis also increases acetyl CoA concentration through a different pathway. An increased acetyl CoA concentration potentially further inhibits pyruvate oxidation to acetyl CoA and leads to excess pyruvate. Finally, beta-2 receptor stimulation also inhibits the pyruvate dehydrogenase complex, and this might even further limit the rate that pyruvate is oxidized to acetyl CoA. ^[4] It is also thought that albuterol creates a hyperadrenergic state. High levels of these catecholamines can aggravate hyperlactatemia by reducing tissue perfusion and overstimulating the beta-2 adrenoceptor. ^[5] This, in turn, enhances glycogenolysis and gluconeogenesis and subsequently increases glycolysis and pyruvate production.

This is important to remember during treatment for COPD exacerbations. Patients with wheezing are usually initially treated with albuterol, among other strategies (see Treatment). When a patient has had too much albuterol and a subsequent increase in lactic acid, it creates a paradoxical picture. The bronchospasm may improve, but the patient may appear more dyspneic or tachypneic. Initially with the increased respiratory rate, patients are physiologically compensating for the metabolic acidosis that is occurring. This may lead providers to interpret these signs and symptoms as worsening asthma and therefore give more albuterol, which may not be indicated.

Astute clinical observation of the patient, repeated reexamination of the breath sounds, and discussion with the patient of how he or she is feeling should be part of the basics of treatment with these patients. This will most often yield a much better clinical picture of response to treatment than relying on a simple lactate level.

Chest radiography

Chronic bronchitis is associated with increased bronchovascular markings and cardiomegaly.

Emphysema is associated with a small heart, hyperinflation, flat hemidiaphragms, and possible bullous changes. Typical findings are shown in the radiographs below.

Chronic obstructive pulmonary disease (COPD). A lung with emphysema shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragms on lateral chest radiograph.

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Chronic obstructive pulmonary disease (COPD). A lung with emphysema shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragms on posteroanterior chest radiograph.

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Posteroanterior (PA) and lateral chest radiograph in a patient with severe chronic obstructive pulmonary disease (COPD). Hyperinflation, depressed diaphragms, increased retrosternal space, and hypovascularity of lung parenchyma is demonstrated.

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Subcutaneous emphysema and pneumothorax.

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Pulse oximetry

Pulse oximetry does not offer as much information as ABG analysis. When combined with clinical observation, this test can be a powerful tool for instant feedback on the patient's status.

Electrocardiography

The presence of underlying cardiac disease is highly likely. Establish that hypoxia is not resulting in ischemia. Establish that the underlying cause of respiratory difficulty is not cardiac in nature. It is also important to look for changes associated with potassium abnormalities.

Pulmonary function tests

Forced expiratory volume in 1 second (FEV₁) is decreased, with concomitant reduction in FEV₁/forced vital capacity (FVC) ratio. Patients have poor/absent reversibility with bronchodilators. FVC is normal or reduced. Total lung capacity (TLC) is normal or increased. Residual volume (RV) is increased. Diffusing capacity is normal or reduced.