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4 things EMS providers need to know about pulmonary embolism

Careful diagnosis of respiratory and circulatory compromise will help you choose the most appropriate treatment and destination for patients with suspected pulmonary embolism

By Bob Sullivan

Pulmonary embolism can strike people at any age and any baseline health status. It is the second leading cause of sudden death in the United States and is responsible for over 250,000 hospitalizations in the United States each year [1, 2].

Pulmonary embolism often presents with vague symptoms and is a difficult condition to diagnose. Here are four things you need to know about how to identify and treat pulmonary embolism:

1. Pulmonary embolism compromises both circulation and respiration.

Pulmonary embolism occurs when a foreign body becomes lodged in a pulmonary artery and obstructs blood flow to a section of the lungs. Most pulmonary emboli begin as a blood clot that formed in a vein of a lower leg, known as a deep vein thrombosis, or DVT. Pulmonary emboli can also originate as blood clots in the pelvis, kidneys, arms or right chambers of the heart [1].

When part or all of the clot breaks loose it forms a thromboembolism, which travels through the venous bloodstream, through the right chambers of the heart and into the pulmonary artery, where it becomes lodged in the pulmonary vasculature.

Severity of a pulmonary embolism depends on its size and the location of the obstructed pulmonary blood vessel. A massive pulmonary embolism obstructs a proximal pulmonary artery and causes rapid hypotension and shock. Patients with emboli lodged in more distal pulmonary vasculature may be hemodynamically stable initially, but they can quickly decompensate and are at risk of a larger pulmonary embolism if not treated [1].

Death from pulmonary embolism is usually caused by obstructive shock [1, 3]. The blockage in the pulmonary artery increases the pressure the right ventricle must pump against, causing the right ventricle to dilate and strain, which displaces the septum into the left ventricle. This reduces preload to the left side of the heart and impairs contractility of the left ventricle, resulting in hypotension and shock from reduced cardiac output.

Pulmonary embolism can also cause respiratory distress and failure by reducing the surface area available for gas exchange in the lungs. An obstructed pulmonary artery causes a ventilation-perfusion mismatch, where oxygen-rich air reaches alveoli on inhalation but no blood is available for gas exchange. Less of the inhaled oxygen is then diffused across the alveoli into the bloodstream, causing hypoxia, and less CO2 is released from the bloodstream into the alveoli for exhalation, leading to hypocapnea [1, 4].

2. Look for signs and symptoms of a DVT when assessing patients with respiratory distress and shock.

Pulmonary embolism can present with a wide spectrum of symptoms, none of which are specific to pulmonary embolism, and all of which can also be caused by other conditions. One study found that 40 percent of patients who died from a pulmonary embolism were seen by a physician in the weeks before their deaths [1].

The key to identifying pulmonary embolism is to look for signs and risk factors of peripheral blood clots, along with any respiratory and cardiovascular complaints.

Patient history: Patients with pulmonary embolism often complain of difficulty breathing, which may come on suddenly from a large pulmonary embolism, or come on gradually, intermittently or with exertion from small emboli. They may also have a nonproductive cough, hemoptysis or low-grade fever.

Pleuritic chest pain – chest pain described as sharp or stabbing, and which increases with cough, movement or inspiration – is another common symptom of pulmonary embolism. Syncope and altered mental status, which suggest a compromised cardiac output, are additional signs of a pulmonary embolism [1].

Inquire about symptoms and risk factors for a DVT, which include extremity immobilization, recent surgery, recent travel over four hours, pregnancy, oral contraceptive use and smoking. Patients may complain of localized leg pain with a DVT or abdominal or flank pain from a thromboembolism that formed in the pelvis, abdomen or kidneys [1].

Physical exam: Observe patients for signs of respiratory distress, right-side heart failure and peripheral blood clots on a head-to-toe exam. Patients with pulmonary embolism are usually tachypneic and tachycardic, and their skin may be pale, diaphoretic and cyanotic. Lung sounds may be clear or have basilar crackles or wheezes.

Look for signs of right-side heart failure, such as jugular venous distention and peripheral edema. Inspect and palpate the legs for localized pain, swelling, warmth or redness from a DVT [1].

Respiratory and cardiac monitoring: Pulse-oximetry and waveform capnography provides feedback on both respiration and perfusion status in pulmonary embolism, both at baseline and after treatment. Hypoxia from decreased blood oxygen concentration causes low a pulse-oximetry reading, or low SPO2 [1]. Decreased perfusion to the lungs and reflex hyperventilation to compensate decreases end-tidal CO2, or ETCO2 [5].

Because pulmonary embolism obstructs pulmonary blood vessels, not the airways, capnography waveform would have a normal, crisp shape. Thus, low SPO2, low ETCO2 with a normal capnography waveform and clear lung sounds strongly suggest pulmonary embolism.

Dysrhythmias and EKG changes may also be found with right ventricular strain and hypoxia from pulmonary embolism, which is associated with worse outcomes. Patients may have a resting sinus tachycardia or new onset of atrial fibrillation. A 12-lead EKG may show a new onset of a right bundle branch block, T-wave inversion in the anterior leads, or SQ3T3 pattern – a deep S wave in lead 1, along with a Q wave and inverted T wave in lead III [1,2].

3. Aim to improve oxygenation and cardiac output without adding stress to the right ventricle.

Treatment goals for pulmonary embolism are to improve oxygenation and cardiac output. Administer supplemental oxygen via nasal cannula or non-rebreather mask to maintain SPO2 above 94 percent.

Be aware that reduced blood flow to the lungs may prevent improvement of hypoxia from oxygen administration. For patients with an adequate blood pressure who remain hypoxic, CPAP may help by increasing oxygenation delivery to the lower airways that are perfused. Note that CPAP is contraindicated in patients who are hypotensive, as it may increase intrathoracic pressure and further compromise cardiac output.

While necessary for patients in respiratory failure, positive pressure ventilation with a bag valve mask also compromises cardiac output. Deliver only enough tidal volume needed to make the chest rise, and use waveform capnography to guide ventilation rate.

Start a large bore IV on patients with suspected pulmonary embolism, but limit IV fluid administration, as this adds stress to the failing right ventricle. Use a vasopressor to treat sustained hypotension, preferably norepinephrine, which works by increasing afterload of the left ventricle without adding stress to the right side of the heart [5].

4. Consider transporting unstable pulmonary embolism patients to a specialty center.

Like trauma, STEMI and stroke, definitive care for a massive pulmonary embolism is only available at tertiary care centers.

Once a pulmonary embolism is detected, eligible patients may receive heparin and thrombolytic medications to reduce clotting and dissolve the embolus. More invasive treatment includes catheter-based intervention (similar to a cardiac catheterization) or surgery to remove the clot, and placement on Extracorporeal Membrane Oxygenation, or heart-lung bypass device [5].

Consult with medical control and local protocols to determine the best destination for unstable pulmonary embolism patients.

1. Ouellette D. Pulmonary Embolism. Medscape. 2016 June 22. Retrieved from: http://emedicine.medscape.com/article/300901-overview

2. Jaff MR, McMurtry MS, Archer SL et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation. 2011 April 26; 123(16):1788-830.

3. ED ECMO. Ornato lives! How ECMO saved a pillar of resuscitation. 2015, July 14. Retrieved from: http://edecmo.org/edecmo-23-ornato-lives-how-ecmo-saved-a-pillar-of-resuscitation/

4. Walls R, Murphy M. Manual of emergency airway management. (2012). Philadelphia: Lippincott Williams & Wilkins.

5. Ventetuolo C, Klinger J. Management of acute right ventricular failure in the intensive care unit. (2013). Annals of the American Thoracic Society. 2014; 11 (5) 811-822. 

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