Medical Director Message February 2025
Dr. Kathrina Consing
Dr. Consing is an EMS Medical Director
February 3, 2025
The Global Initiative for Chronic Obstructive Lung Disease (GOLD) and the World Health Organization (WHO) defines chronic obstructive pulmonary disease (COPD) as “a heterogeneous lung condition characterized by chronic respiratory symptoms (dyspnea, cough, expectoration, exacerbations) due to abnormalities of the airway (bronchitis, bronchiolitis) and/or alveoli (emphysema) that cause persistent, often progressive, airflow obstruction."
Chronic bronchitis – Defined as a chronic productive cough, with periods of at least 3 months in 2 years, in whom other causes of chronic cough have been ruled out. The diagnosis may precede or follow the development of airflow limitation.
Emphysema – The enlargement of the airspaces distal to the terminal bronchioles accompanied by the destruction of airspace walls. Patients clinically present with decreased breath sounds and hyperinflation of the lungs. It is frequently associated with dyspnea.
Airflow limitation – Physiologically defined as abnormally reduced ability to exhale efficiently. The expiratory phase of respiration is normally passive (without the need for active muscle use). Individuals with airflow limitation may have to actively participate in exhalation to improve the amount of air they breathe out.
Asthma – Chronic inflammatory disorder of the airways that leads to recurrent episodes of wheezing, breathlessness, chest tightness, and coughing. Associated with episodes of airflow obstruction. Adults with longstanding asthma can develop persistent airflow limitation.
There are interrelationships among these conditions.
COPD exacerbations generally include an acute change of one or more of the following:
Increase in cough frequency and severity
Increase in the volume of sputum production and/or changes in the characteristics of the sputum
Increase in shortness of breath
Physical exam findings of an acute exacerbation may include:
Wheezing (may not appreciate wheezing in a patient with poor air movement)
Tachypnea
Difficulty speaking due to increased respiratory effort
Use of accessory respiratory muscles
Tachycardia
Altered mental status from hypercapnia or hypoxemia
The major components of acute management of COPD exacerbations in the pre-hospital setting include reversing airflow limitation with inhaled short-acting bronchodilators and systemic steroids and ensuring appropriate oxygenation.
Maintain SpO2 at 88% - 92% — This minimizes the risk of worsening hypercapnia with excess supplemental oxygen. A small, randomized trial showed that titrating oxygen to SpO2 of 88%- 92% resulted in lower mortality compared with high flow (non-titrated) oxygen in a pre-hospital setting. In a separate retrospective analysis study, COPD patients with SpO2 maintained between 88% and 92% had a lower adjusted risk of death compared to patients who received supplemental oxygen results in higher percentages of SpO2.
Albuterol and ipratropium (DuoNeb) — Albuterol is a short-acting beta-adrenergic agonist with rapid onset action and efficacy in producing bronchodilation. Ipratropium is a short-acting muscarinic antagonist that also aids in bronchodilation. The combination of albuterol and ipratropium, compared to either medication used alone, has shown extensive evidence of superior bronchodilation in longer-term studies.
Systemic glucocorticoids — Glucocorticoid steroids such as methylprednisolone (Solu-Medrol) provide an anti-inflammatory response to the patient’s treatment. Pre-hospital providers will not see an immediate change in the patient’s presentation as the onset of action of the medication is about one hour. However, glucocorticoid administration has shown multiple beneficial effects in studies including a reduction in the rate of exacerbation relapse, treatment failure, decreased shortness of breath, greater improvement in airflow limitation, and decreased length of hospital stay.
Magnesium — Inhibits the influx of calcium into the smooth muscle cells of the airways which results in bronchodilation. Magnesium should be used in patients who do not respond to albuterol and ipratropium. A systematic review of magnesium administration in COPD exacerbations found a decrease in hospitalizations compared to placebo.
COPD has a high prevalence and chronicity that results in high resource utilization with frequent outpatient office visits, multiple hospitalizations from acute exacerbations, and the need for chronic therapy. The early recognition of an acute COPD exacerbation and its treatment in the prehospital setting can help reduce hospital admissions and hospital length of stay.
Stay warm! Stay Safe!
Kathrina Consing, MD
February 10, 2025
Not all respiratory distress arises from issues with the pulmonary system. Other common causes of respiratory distress include, but are not limited to, cardiovascular, metabolic, and toxic exposures. As there are many causes for respiratory distress, determining an accurate diagnosis is difficult in the prehospital setting. Examining the patient and closely monitoring vital signs, cardiac rhythm with an EKG, pulse oximetry, and waveform capnography will not only assist with determining the severity of the disease but also aid in the diagnosis and appropriate treatment of the patient.
Acute coronary syndrome (ACS) is important to consider with patients presenting with shortness of breath. Shortness of breath associated with ACS may not be accompanied by chest pain or discomfort. This atypical presentation is more common in women, patients with diabetes, and older individuals. ACS can present as cardiogenic shock with acute pulmonary edema and subsequent difficulty breathing. Patients in cardiogenic shock may also have cool or clammy skin, mottled extremities, and weak pulses. Another cardiac etiology of respiratory distress includes dysrhythmias. Obtaining a 12-lead EKG in all patients with respiratory distress may reveal a cardiac etiology of their symptoms whether it be an acute myocardial infarction or a dysrhythmia.
Metabolic acidosis normally generates a respiratory response and can present as shortness of breath. The most likely scenarios that prehospital providers may encounter with metabolic acidosis include diabetic ketoacidosis (DKA) and sepsis. Patients with type 1 diabetes (pancreas does not produce insulin) are more likely to develop DKA than those with type 2 diabetes (pancreas does not produce enough insulin or the body is resistant to insulin). However, patients with type 2 diabetes can develop DKA if their pancreas stops producing insulin or their body becomes increasingly resistant to insulin (insulin-dependent type 2 diabetes). Insulin is needed for sugar to enter cells in the body. Without insulin, the body’s cells do not have the required sugar to create energy. In this case, the body breaks down fat for energy. The breakdown of fat creates acidic ketones, which build up in the bloodstream and ultimately result in metabolic acidosis. The body compensates for this metabolic acidosis by increasing the respiratory rate to exhale excessive acids to create a metabolic alkalosis. If the metabolic acidosis persists, patients in DKA may develop Kussmaul’s respirations, characterized by deep and fast breaths. Patients with sepsis may also develop shortness of breath, even in non-pulmonary sources of infection. In this scenario, septic patients can develop poor peripheral perfusion resulting in cells not receiving enough oxygen to compensate for the increased metabolic demand in fighting off an infection. This leads to cells utilizing anaerobic metabolism to meet the increased demand resulting in the production of lactate. Lactate is an acidic product that builds up in the bloodstream resulting in metabolic acidosis. Similar to patients in DKA, septic patients will normally compensate by increasing their respiratory rate to exhale out excess acid.
Thinking broadly when caring for patients with respiratory distress or shortness of breath is important. Your suspicion for a non-pulmonary etiology of the patient’s presentation should be especially high in patients with clear lung sounds. For this reason, it is important to obtain a 12-lead EKG in all patients presenting with shortness of breath. If you are concerned about DKA, obtaining blood sugar will aid in that diagnosis. Determining the etiology of respiratory distress in the prehospital setting is difficult. However, obtaining a complete assessment and keeping a broad differential for your diagnosis will aid in performing the appropriate care for your patients.
Stay warm! Stay Safe!
Kathrina Consing, MD
February 17, 2025
You are dispatched to a call for respiratory distress.
When you arrive on scene, you find that the patient has a tracheostomy tube in place. A tracheostomy is an opening between the tracheal rings with a tracheostomy tube placed in a stoma to assist with ventilation. Trachs are placed for various reasons, such as the inability to breathe independently, an abnormality of the larynx or trachea, cancer of the neck or airway, or to prevent aspiration when paralysis of the larynx muscles affects swallowing. Patients with a trach may be supported with a ventilator or have no difficulty breathing on room air. The main components of trachs include a removable inner cannula and an outer cannula (also called a tracheostomy tube). The outer cannula may or may not have an inflatable cuff. Most pediatric trachs do not have an inner cannula because of the small inner diameter of the outer cannula.
Patients with trachs can develop respiratory distress from trach-related issues in addition to more traditional etiologies. When going through the ABCs of a primary survey, the “A” of the airway is the trach. Problems that can arise with a trach include obstruction, dislodgment, bleeding, and infection.
Complications with a trach generally arise from airway obstruction. Secretions can cause mucus plugs or can dry inside the cannula. These secretions can act as a ball-valve mechanism; patients can inhale air but have difficulty exhaling air. Before suctioning a trach tube, it is important to pre-oxygenate at the trach site. If the patient breathes spontaneously, place a non-rebreather mask on the trach. If the patient is ventilator-dependent or not breathing spontaneously, a Bag-Valve-Mask (BVM) can be used. The patient should be oxygenated for 30 seconds with 100% oxygen. Once the patient is adequately pre-oxygenated, a soft flexible suction catheter can be inserted into the trach through the inner cannula to the site of the sternal notch or a cough reflex is stimulated. Apply suction only as the catheter is being pulled out. Each suction attempt should occur for a maximum of 10 seconds. If additional attempts at suctioning are needed, do not forget to pre-oxygenate the patient. If thick secretions are encountered, 3-5 mL of sterile saline or water can be instilled into the trach to soften and break up the secretions before suctioning. If there is no relief despite effectively suctioning the inner cannula, the outer cannula (trach tube) can be removed. Inspect the inner cannula and clean off any secretions or debris. Suctioning through the trach tube can be attempted. If the obstruction is relieved after suctioning through the trach tube, the inner cannula can be re-inserted after it is cleaned with hydrogen peroxide or warm water.
If the patient continues to have respiratory distress despite suctioning through the trach tube, the trach tube can be removed and the patient can be suctioned through the stoma. Before removing the tube, determine if a replacement trach is available. If the patient does not have an extra trach, a 6 mm endotracheal tube (ETT) can be used instead. After ensuring a replacement airway, pre-oxygenate the patient, deflate the cuff if the trach tube has one, and insert a bougie through the trach tube. The bougie will ensure the appropriate placement of the new tube and prevent placement in a false trach. Remove the trach tube by pulling outward and downward towards the chest. Leave the bougie in the stoma, then attempt suctioning the stoma with a soft flexible catheter. After suctioning, lubricate the new trach tube or ETT tube with lubricating jelly or saline/water. Insert the new trach tube over the bougie through the stoma in an inward and downward motion toward the lungs. Insert a new trach tube until the hub meets the skin. If using an ETT, advance the tube until just after losing site of the cuff. Do not advance the trach tube or ETT if you meet resistance. Once you confirm appropriate tube placement with end tidal CO2 and good chest rise, secure the tube.
Tracheostomies can be intimidating, especially if you do not frequently encounter them. Not all patients with trachs are ventilator dependent—some do not even need supplemental oxygen! It is important to familiarize yourself with the different components of a trach so you are more comfortable when you encounter them. Trach obstructions are a major cause of respiratory distress in this patient population. However, it is still possible for them to develop a different disease process contributing to their difficulty breathing including COPD exacerbations and pulmonary edema. It is still important to keep your differential diagnosis broad when caring for a patient with a trach.
Stay warm! Stay Safe!
Kathrina Consing, MD