EMS Field Identification Of Chronic Obstructive Pulmonary Disease (COPD)

Issues of Concern

In a poor resource setting, be it an ambulance, the wilderness, or any other pre-hospital setting, the EMS provider must utilize the tools available at their disposal. This places more emphasis on the history and physical exminaton, forcing the EMS professional to operate effectively and efficiently. If the patient has a known history of COPD, then they need only to determine if there is a baseline worsening of their disease or if there is a new etiology to sush patient's health status. If the patient denies a known history or is unable to provide a clear history, then the provider must assess as best as possible for known risk factors and red flags.[2][4]

History

Understand that some patients are not familiar with the term "COPD" and may know their disease by another name. The EMS professional should ask about lung disease, chronic bronchitis, or emphysema. If the patient is a poor historian, are there bystanders who know the patient and can help provide insight? Is there a significant smoking exposure (usually 40 pack years or greater), or dust/chemical exposure from work, what about family history? Alpha-antitrypsin deficiency is a rare cause, but a young patient in their 30s with a known family history and non-smoker may still have COPD. Otherwise, most patients with COPD are going to be older than 50 years old. Do they cough more days than not? Is there regular sputum production? Do they experience shortness of breath with activities of daily living or more difficulty completing tasks than age-matched peers? Can you look at the list of medications or do you see them laying around? Do they take medications like inhalers, nebulizer, albuterol, ipratropium, both combined, inhaled steroids, novel long-acting medications (tiotropium, fluticasone/salmeterol, fluticasone furoate/vilanterol, budesonide/formoterol)? Most importantly do they require supplemental oxygen at home, if so how much and how often. Many times patients are supposed to wear their oxygen more than they do, or you may also notice that they have extremely long supply hoses attached to a flow of 2 liters per minute. This length of cord diminishes the benefit greatly. Inquire if the patient is still smoking.[5][6][3][7]

The above establishes a baseline, follow up a history taking with recent changes to their normal routine. If they are short of breath, how long has it been? How far from their baseline, and what have they done thus far? The 3 big questions here are: increased oxygen demand/worsening shortness of breath? Increased cough? Increased Sputum? Note the answers and report them to the receiving facility.

Physical

An exam is focused on the cardiovascular and respiratory systems. The first thing you note as you approach the patient is always scene safety and general appearance. Is the patient in obvious distress? Are there signs of impending failed airway? One may see tripod position, altered mental status, gasping for air, or frank breath sounds. Is the patient able to speak in full sentences? Any deviation from the above indicates the rapid need for supplemental oxygen while obtaining additional needed information. Check capillary refill time while waiting for pulse-oximetry, auscultate lung sounds while your partner readies a 12 lead ECG. Note the abnormalities. If there is chest pain, is it positional, pleuritic, or tender? If the answer is yes to any of the above, the likelihood a cardiac origin is diminished, and concerns for respiratory etiology increase.[8][4]

A history and physical are never linear processes. The history, physical, and treatment are dynamic processes. An appropriate flow of patient care is developed over time; emphasis is placed on maintaining the patient’s ABCs (airway, breathing, circulation) as always.

Clinical Significance

While oxygen should never be withheld to someone with dyspnea, before initiation of further treatment, the need for differentiation of other etiologies is prudent. Previously in literature, there was a large concern for COPD patients losing their respiratory drive with prolonged supplemental oxygen at high levels. Recent studies have shown this to be of little concern in the initial 24 hours of treatment. You are unlikely to alter the hypercarbic respiratory drive of an acutely decompensating patient during the duration of standard care. However, treatment guidelines indicate a titration to the effect of supplemental oxygen, which means goal SpO2 92% or better, do not attempt to reach 100% and stay there, titrate down. Before positive pressure ventilation (PPV) or nebulized medication therapy, you must ensure your diagnosis of COPD without other underlying pathology.[4][7]

Before PPV ensure there is no pneumothorax, auscultate lung sounds bilaterally for diminished unilateral sounds, look for equal rise and fall of the chest, and ensure a midline trachea. Abnormalities here, especially after trauma are concerning for pneumothorax and PPV will acutely worsen the prognosis. Instead, treat appropriately with needle decompression if pneumothorax is suspected.[2][3][7]

Before nebulized albuterol, ipratropium, or lev-albuterol assess for cardiac etiology. Obtain an ECG to rule out ST elevation or dysrhythmias. Assess fluid status and auscultate lungs, wet lungs, pitting edema, white sputum, and worsening orthopnea, especially in a patient with known CHF is highly suspect. You can also assess for jugular venous distention or hepatojugular reflex to indicate fluid overload and a pump (cardiac) problem. If your unit has the equipment to monitor waveform capnography, this is the perfect opportunity. This can be performed in-line with PPV if necessary and depending on your model either as a nasal cannula underneath or on the mask itself. ‘Shark Fin’ with hypercarbia is the classic pattern produced by bronchiolar constriction and CO2 retention in COPD exacerbation and indicate the patient would benefit from bronchodilator (albuterol) therapy. However, if a normal pattern is visualized and the patient is a normocarbia concern for congestive heart failure (CHF) is greater, as this indicates a perfusion pathology with normal functioning ventilation. Albuterol and stimulants should be avoided in acute coronary syndromes, acute myocardial infarctions, and congestive heart failure exacerbations as the increased stress demand on the heart coupled with decreased filling time from tachycardia can worsen the strain and subsequent damage. Conversely, the treatment for cardiac and perfusion pathology is commonly sublingual nitroglycerin which may decrease perfusion while failing to improve ventilation in the COPD patient.[5][6][8]