Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department. Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions.
The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation). This first involves checking the patient for a patent airway. A simple method to assess the airway is to ask the patient to speak and listen for the voice. A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present. Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath. Endotracheal intubation may need to be performed before moving forward. Breathing is assessed by evaluating the function of the lungs. Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds. A low oxygen level should be immediately addressed with supplemental oxygen before moving forward. The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment. Lastly, circulation should be assessed. Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage. The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause. After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted.
Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below.
Select Causes of Shortness of Breath (Dyspnea)
Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD
Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)
Diabetic ketoacidosis (Kussmaul breathing)
Salicylate overdose, or any ingestion that causes a severe metabolic acidosis
Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)
Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)
Rib fracture, flail chest
Anxiety, Panic attack
Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma
This patient arrives to the Emergency Department with shortness of breath and generalized weakness or 3 days. On physical exam, there is tachycardia, tachypnea, normal oxygen saturation, and a markedly elevated glucose. The Chest X-ray provided is normal; there are no lung infiltrates or pleural effusions.
This patient has diabetic ketoacidosis (DKA). DKA is a serious condition of insulin deficiency characterized by hyperglycemia, metabolic acidosis, and ketosis. Presenting symptoms include weakness, increased thirst (polydipsia), increased hunger (polyphagia), increased urination (polyuria), abdominal pain, or vomiting. Shortness of breath can also be seen in DKA as the metabolic ketoacidosis triggers an increased respiratory rate to drive more exhaled carbon dioxide out of the body. This deep rapid breathing seen in severe DKA is known as Kussmaul breathing. The treatment of DKA involves IV fluids for hydration, insulin infusion, and close monitoring for electrolyte derangements (potassium abnormalities are common). DKA patients are severely dehydrated due to osmotic diuresis from their hyperglycemic state. For this reason, IV fluid resuscitation is the first step to DKA management. Either normal saline or lactated ringers (Choice B) can be used, although large volumes of normal saline can worsen the acidotic state by causing a hyperchloremic metabolic acidosis. Intravenous fluids should be started with a 20-30cc/kg bolus. IV insulin infusion (Choice A) should never be started without a potassium level, and no potassium level is provided in the question stem. Insulin lowers potassium, and administration of insulin without a potassium level can result in hypokalemia, arrythmia, and death. Endotracheal intubation (Choice D) should be avoided in DKA whenever possible as the patient’s respiratory status serves as a compensation for the metabolic acidosis. This patient is tachypneic and mildly confused, but he is not somnolent and does not require immediate intubation. Intubated DKA patients need carefully monitored ventilator settings in combination with blood gas measurements to avoid worsening acidosis and cardiac arrest. Nebulized beta-2 agonist (i.e., albuterol, salbutamol) is helpful in asthma, however this patient has DKA and not an asthma exacerbation. IV lactated ringers solution (Choice B) is the best next step.
- Alexander, D. (2016). Approach to tachypnea in the ED setting. EM Docs. http://www.emdocs.net/approach-tachypnea-ed-setting/
- Swaminathan, A. (2016). Diabetic Ketoacidosis (DKA). CORE-EM. https://coreem.net/core/dka/