An embolism is a foreign mass that travels through the intravascular space carried by the systemic circulation. The mass may be solid, liquid or gaseous. The circulation carries the embolus through vessels to parts of the body where it can cause obstruction or occlusion. The Pulmonary Embolism (PE) occurs when the embolism causes an obstruction or occlusion of the pulmonary artery or one of its branches, which in turn reverts pressure on the right ventricle. A solid embolus can be a thrombus, also known as a blood clot, which traveled through the circulation to cause obstruction or occlusion in a location istant from its origin.
A thrombus is always a solid, non- traveling stationary body that causes obstruction or occlusion at the site of its origin. Once a thrombus breaks loose and travels through the circulation it becomes a thromboembolism. A solid embolus can also be fat tissue from fractured tubular bones that leaks into ruptured vessels, fat emulsions that are intravenously injected, pus from sepsis, tissue dislodged from cancerous metastasis, bullet fragments in the circulation, broken intravenous catheter tips, or talc added to drugs of intravenous drug abusers.
A gas embolus can be air or other gases found in or introduced into the circulation. An air embolus can be introduced through the rupture of alveoli, through being inhaled and leaked into the blood vessels, through the intravenous injection of air or from the accidental rupture of the subclavian vein allowing air to be sucked into the veins by the negative pressure of chest expansion during inspiration. An embolus from other gasses can be observed with deep-sea diving. Gases in the blood are dissolved during the descent into deep water.
When the diver ascends to normal atmospheric ressure too fast the gases can become insoluble, forming bubbles in the blood causing Decompression Sickness, also called The Bends. A liquid embolus can be from amniotic fluid introduced into the blood stream as a rare complication of childbirth or from intravenously injected fluid thick enough to cause obstruction or occlusion. Each year more than six- hundred thousand (600,000) people in the United States are diagnosed with PE. (Rahimtoola and Bergin) These cases result in between 50,000 (Rahimtoola and Bergin) and 200,000 deaths per year in the United States. Kumar and Robbins) Those ospitalized are around 1% at risk of developing PE (Wood).
The rate of fatal PE has declined from 6% to 2% over the last 25 years in the United States. (Kumar and Robbins) Diagnosing Pulmonary Embolism There is a significant overlap of signs and symptoms between acute coronary syndromes and PE. There should be a high index of suspicion for PE when a patient presents with signs and symptoms of acute coronary syndrome and a history that is suggestive for PE. The patient experiencing PE will generally present with difficulty breathing, chest pain on inspiration, and palpitations.
Patient assessment will typically show signs of decreased oxygen saturation (SpO2), cyanosis, rapid breathing, and a rapid heart rate. Severe cases of PE may include syncope, low blood pressure, and sudden death (Goldhaber, Pulmonary Thromboembolism). In the instance of a significant occlusion of the pulmonary artery the immediate result is sudden dilatation of the right ventricle and right auricle, also known as acute cor pulmonale. (Mcginn and White) When presentation is suggestive for PE, evaluation risk factors and additional clinical signs can increase the index of suspicion.
Risk factors for PE include: urgery within the past three (3) months, recent period of immobilization, previous venous thromboembolism (VTE), family history of VTE, current cancer treatment, smoking and the use of oral contraception. Additional clinical signs of PE include: dyspnea, pleuritic chest pain, non-retrosternal chest pain, hemoptysis, pleural rub, heart rate > 90 beats/min, leg symptoms such as DVT, low-grade fever, chest radiograph compatible with PE, syncope, and electrocardiographic (ECG) signs of PE.
Based on the clinical presentation and the index of suspicion for PE, laboratory tests and imaging studies can onfirm the diagnosis. The D-dimer is a laboratory test that measures the amount of protein fragments found in the blood after clot degradation through fibrinolysis. Fibrin degradation products (FDPS) are released into the body during the coagulation process so they are not normally found in the blood. When the body is unable to dissolve a clot, abnormal levels of FDPS will be found in the blood. D-dimer is the most detectable FDP.
A negative D-dimer rules out thromboembolism leaving no need for further diagnostic testing for PE. Wiener, Ouellette and Diamond) D-dimer greater than ive-hundred nanograms per milliliter (> 500 ng/mL) or 10 times the patient’s age in years over 50 (Age X 10) is suggestive for thromboembolism and justifies further testing. False positive D- dimer results can be seen in patients with liver disease, high rheumatoid factor, inflammation, malignancy, trauma, pregnancy, recent surgery or advanced age. False negative results can be seen in patients when the sample is taken too soon after thrombus formation, when testing is not done for several days after initial presentation or when patients are on anti-coagulation therapy (Es, Mos and Douma).
Tools like the Wells Score are used to justify additional testing when the D- dimer is positive. This approach prevents unnecessary radiation exposure or costly procedures for the patient. (Wiener, Ouellette and Diamond). The Wells score was developed as a prediction tool for PE based on clinical criteria. (Philip S. Wells, David R. Anderson and Marc Rodger)
Clinical Criteria Clinically suspected DVT Alternative diagnosis is less likely than PE – 3. 0 points • Tachycardia (heart rate > 100) – 1. 5 points • Immobilization (2 3d)/surgery in previous four weeks – 1. points •History of DVT or PE – 1. 5 points 3. 0 points Hemoptysis – 1. 0 points Malignancy (with treatment within 6 months) or palliative – 1. 0 points Traditional interpretation Score >6. 0 – High (probability 59% based on pooled data) • Score 2. 0 to 6. 0 – Moderate (probability 29% based on pooled data) • Score 4 – PE likely. Consider diagnostic imaging. Score 4 or less – PE unlikely. Consider D-dimer to rule out PE. Ultrasound, ventilation-perfusion lung scan (V/Q scan) and/or Computed Topography (CT) scans are additional diagnostic studies for confirming the diagnosis.
The ability to perform each test is limited by the availability of the equipment to perform he test. The V/Q scan shows the circulation of air and blood in the lungs measuring the ability for air to move through every part of the lungs and the efficiency of blood circulating in the lungs. The preferred method of definitively diagnosing PE is the CT pulmonary angiogram (CTPA), a minimally invasive scan performed through an intravenous line. (Fedullo and Tampson) CTPA is considered the gold standard for PE testing but is contraindicated in pregnant patients, those allergic to radioactive contrast (iodine) and patients with renal failure.
When contraindicated, a positive ultrasound for deep vein hrombosis (DVT) when symptoms are suggestive for PE is considered diagnostic. A thoracic ultrasound (TUS) with a high sensitivity and diagnostic accuracy was found to diagnose PE in 30 patients with a diagnostic accuracy of 78% when the patient presented with clinical findings suspicious for PE. A negative TUS cannot rule out PE but a positive finding can increase the index of suspicion enough to justify proceeding with treatment for PE. (Ericsoussi) PE causes an increase in the dead space in the lungs thereby decreasing the alveoli available to offload carbon dioxide.
A rapid decrease of the end-tidal carbon dioxide (ETCO2) level in the absence of changes in blood pressure, central venous pressure and heart rate have been shown to definitively indicate an air embolism or thromboembolism. As the size of air embolism increases, a reduction in cardiac output occurs that further decreases the EtCO2 level. A reduced cardiac output by itself can decrease ETCO2. In the event of a rapid decrease in EtCO2 associated with a reduction in cardiac output, a rise in the pulmonary arterial pressure confirms the occurrence of pulmonary embolism.
This decrease indicates that he right pulmonary artery (RPA) is potentially occluded thereby reducing the amount of CO2 exhaled per breath. Progressive decrease in ETCO2 reflects increasing dead space as experienced during: cardiac arrest, large pulmonary emboli (air, gas, blood or fat) and severe bronchospasm. In trauma patients the decline in CO2 could be indicative of fat embolism. End tidal CO2 in the lungs is directly proportional to pulmonary blood flow and ultimately cardiac output (Shibutani, Muraoka and Shirasaki). On the ECG tachycardia should always be considered suspicious for impending cardiogenic shock or PE.
Sinus achycardia accompanied by the S1Q3T3 phenomenon is consistent with a right sided heart strain (acute cor pulmonale) which is often seen with patients with PE. S1Q3T3 presents as an S wave in lead one (the first down slope after the first upslope in the QRS complex) a Q wave in Lead 3 (first down slope in lead 3) and T-wave inversion in lead 3(T3). Other ECG findings in PE include transient right bundle branch block which suggests acute cor pulmonale as electric conduction traverses down the right bundle and T-wave inversions across the anterior leads. (Goddard and Scofield). S1Q3T3 can be seen in other athologies.
It is not singularly diagnostic for PE. It is used with other diagnostic tools to increase the index of suspicion. (Watford) Treating Pulmonary Embolism Treatment is typically pharmacologic using anticoagulant medications, including heparin or warfarin. Severe cases may require thrombolysis using tissue plasminogen activator (tPA), or may require surgical intervention via pulmonary thrombectomy (Silverstein, Heit and Mohr). Depending on the clinical presentation, anticoagulant therapy may be started as soon as the D-dimer result does not rule out PE while other tests are scheduled.
The therapeutic goals for acute PE are to relieve symptoms, prevent the development of pulmonary hypertension and right ventricular failure, and ultimately, diminish the risk of death. Thrombolytic therapy is the first-line treatment in patients with high-risk PE presenting with cardiogenic shock and/or persistent arterial hypotension because it rapidly exerts beneficial effects on hemodynamic parameters. The Pre-hospital Environment In the pre-hospital environment the goal is to evaluate the clinical presentation and rule out everything else, settling on PE when it is the most probable diagnosis.
PE can be ruled in but it cannot be ruled out without testing. Confirming PE through the testing process is required to begin anticoagulant or thrombolytic treatment. This section explores advances in testing and research that could feasibly be performed in the pre-hospital environment to confirm PE with an increased level of certainty that may justify starting therapy before reaching the hospital. As discussed, the D-Dimer can definitively rule out but not rule in PE. In 2007, Roche Diagnostics launched the Cobas H 232 Meter, a handheld laboratory instrument that can measure cardiac markers, to include D-Dimer.
It has a 10 hour rechargeable battery; some test strips require refrigeration and test times range from 8-12 minutes. The device was marketed to Emergency departments and pre-hospital agencies but is not available in the United States (U. S. ). (n. p. and n. d. ). In the U. S. , the Alere Triage® MeterPro is a compact device used to measure 20 immunoassays, including D-dimer. The test strip uses a sample of blood from a finger-stick and returns results within 20 minutes. (N. p. : n. p. )
Combining the D-Dimer result with a pre-test probability score and diagnostic algorithm, e. g. Wells, probability of PE could be improved. When PE is ruled in further testing could be performed using ultrasound in the prehospital setting. In 2003 the Odessa Fire Department in Odessa, Texas began using portable ultrasound monitors on ambulances. In 2005 they were recognized by the First World Congress on Ultrasound for being the first paramedic ultrasound program in the world (Smith). While the Odessa was done primarily for trauma, other studies have shown that early echocardiography screening in patients with dyspnea or with high clinical probability of PE was sufficient to justify thrombolytic therapy in the field.
Several studies have shown that paramedics can be training in obtaining and reading US images in the prehospital environment. Training ranged from two to six hours with continuing education. Physician overseers were used to validate readings and found that paramedics were able to arrive at the same conclusion as the physician 100% of the time. Training on the use of ultrasound by paramedics can be done in 1 hour with a comparative rating of 100% to the diagnostic assessment of a paramedic vs. a cardiologist. (Chin, Chan and Mortazavi) (Heegaard, Hildebrandt and Spear).
