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A Review of Venous Thromboembolism for Paramedics

Abbreviations and acronyms used in this document.

DVT: Deep Vein Thrombosis

VTE: Venous Thromboembolism

PE: Pulmonary Embolism

SVR: Systemic Vascular Resistance

PVR: Pulmonary Vascular Resistance

CO: Cardiac Output

LVOT: Left Ventricular Outflow Tract

SpO2: Oxyhemoglobin Saturation

FiO2: Fraction of Inspired Oxygen

CVA: Cerebrovascular Accident

MI: Myocardial Infarction

JVD: Jugular Venous Distension

EMS: Emergency Medical Services

AHA: American Heart Association

MAP: Mean Arterial Pressure

RSI: Rapid Sequence Induction

HR: Heart Rate

RR: Respiratory Rate

mmol/L: Millimole Per Litre 

Venus Thromboembolism (VTE) is a common and potentially fatal condition comprising Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE). DVT occurs when venous thrombosis forms in an intact vein, usually in the lower extremities. DVT can break off, that is embolize, and follow venous return to the right heart. Pass through the pulmonary valve and lodge in a pulmonary artery.

VTE has an incidence of 150 events per year per 100,000 population. Every year 900,000 people in the United States are affected by VTE.  Ten percent will die within one month of diagnosis and sudden hemodynamic instability and death is the first symptom in 25% of cases. Up to 8% of the population has upwards of 7 risk factors for the disease (1).

Deep vein thrombosis and its commonly associated severe complication of pulmonary embolism presents a diagnostic challenge for front line paramedics and ER staff. Due to non-specific signs and symptoms, limitations in physical exam and diagnostic tools unfortunately proper treatment is often delivered too late.


We will begin our overview with the pathophysiology of deep vein thrombosis. Clots may develop in various large veins, most commonly in the legs as venous return is often the slowest. The most probable sites for deep vein thrombus formation are the superficial femoral (a deep vein despite name), popliteal and the three paired calf veins (anterior and posterior tibial and peroneal veins). Risk factors have been identified as venous stasis, endothelial injury and coagulopathy; this is known as the Virchow Triad (6). Venus stasis is most commonly encountered in immobilized or paralyzed patients as muscular contraction and movement in the inferior limbs is needed to maintain adequate venous return and avoid blood pooling. Endothelial injury may result from recent surgery or trauma or intra-venous lines. Coagulopathy or hyper-coagulability may be present for a myriad of reasons and characterized as inherited and acquired thrombophilia. Acquired thrombophilia include cancer, hormone treatments or conditions involving elevated levels of estrogen such as birth control medications and pregnancy.  Antiphospholipid antibody syndrome (antibodies that activate the hemostatic system) (7). Inherited thrombophilia include factor 5 Leiden, prothrombin gene variant, anti-thrombin deficiency, and protein C deficiency and S deficiency.

It would not be out of the ordinary for a patient to be positive for all risk categories in the triad, such as a bed ridden osteosarcoma patient who recently underwent excision of a mass in the lower limbs.

Once a clot is formed in a major vessel it may dislodge spontaneously and travel following blood-flow towards the heart. Once in the right atrium in the absence of VSD or ASD the only place for the clot to go is the pulmonary vasculature (9). When a thrombus is lodged in the pulmonary arteries, we refer to it as a pulmonary embolism, depending on the size or number of clots (expressed as clot burden) two major consequences arise. The first and most common cause of death for these patients is the hemodynamic collapse that occurs as blood flow from the right side of the heart to the left is severely diminished, this leads to significant lack of preload for the left ventricle and subsequent decrease in cardiac output. When a large clot is lodged into the pulmonary artery, the afterload for the right ventricle is severely elevated, this leads to over stretching of the ventricle and decreased contractility based on starlings’ law. The right ventricle is usually capable of overcoming increased PVR in a controlled setting. Such as anesthesiology collapsing a lung for improved access to the thoracic viscera during surgery. Why does the RV tolerate this extreme change in pulmonary circulation under these circumstances but fails when an equal amount of pulmonary vasculature is occluded by a thrombus? The answer may lie in the composition of the clot itself. A component of hemostasis in the early stages is a rapid vascular spasm of the affected blood vessels. This vasoconstriction brought on by exposure to endothelin-1 may be responsible for this massive increase in pulmonary vascular resistance and subsequent RV failure. When the volume overloaded right ventricle is dilated to such an extent there may be septal shifting to the left side resulting in left ventricular outflow tract obstruction and decreased cardiac output from the left ventricle due to increased afterload. This acute cardiac compromise can provoke significant hypotension and systemic hypoperfusion leading to a low flow shock state.

The next problem that results from a large clot in the pulmonary vasculature is significant ventilation and perfusion mismatching where gas is being delivered to the alveoli but the absence of perfusion of the alveolar unit produces no gas exchange. This can be expressed a V/Q value of infinity in the affected area (see figure 1) (10).

Figure 1.

This ventilation and perfusion mismatch make it difficult to correct for profound hypoxia as even high levels of FiO2 may not yield higher SpO2 values.

Less common complications of DVT involve systemic distribution of the emboli due to atrial septal defect or ventricular septal defect leading to CVA, MI, renal artery infarct and other complications due to infarcted circulation on the systemic side.


A large part of the recognition and diagnosis of pulmonary embolism is the patient history and complaint. Patients will often complain of pain that is abnormal and difficult to describe, it will often, but not always, be pleuritic in nature and is often associated, but not always, with increased shortness of breath and exercise intolerance. PE may also present with isolated shortness of breath without chest pain. PE may also be entirely asymptomatic. History of ongoing illness and treatments are vital to the clinical diagnosis to elicit the risk factors discussed above. Decision tools such as the PERC rule and Geneva Score may be helpful in stratifying these patients and determining the statistical likelihood of pulmonary embolus. Physical exam for DVT consists of key findings such as unilateral swelling, erythema, cyanosis and calf of thigh pain (2,5). Findings for PE, other than tachycardia, hypotension and hypoxia more subtle and physical exam is of limited value, however assessing for S3, JVD and normal breath sounds might be a clue that it is PE. Vital signs and EMS capable test results may present as tachycardia, refractory hypoxia, tachypnea. ECG findings include tachycardia, inverted T waves and incomplete RBBB (11).

In a hospital setting, ancillary diagnostic tests including CXR, D-Dimer, cardiac enzyme measurements and echocardiography. CT pulmonary angiogram and V/Q scanning are the current gold standard diagnostic tests to solidify or refute a diagnosis of PE (9.)

On CXR, usually very little is seen with the most common finding being atelectasis (often due to splinting from chest pain). A patient that is suspected to have a pulmonary embolus with an RV/LV ratio of over 1.5 suggests that RV strain is present. The classic finding of an enlarged right ventricle that loses its crescent shape as it pushes towards the left ventricle and begins to resemble the shape of a D. This provides a representation of the effect that RV dilation can have on the LVOT and CO (13).

In the hospital a D-dimer test may be ordered and useful when it is negative. In combination with a low pre-test probability a negative D-Dimer can exclude PE without the need for additional testing. EMS D-dimer testing, in a point of care package, could be useful for the prehospital clinician when rapidly assessing a patient and determining management pathways. The key role EMS providers can play in decreasing the mortality of VTE is early recognition and proper transfer of care. In the future, early point of care D-dimer, for at risk patient presentations, may be a way forward that deserves further investigation (14).     


Paramedic treatment and management of pulmonary embolism should focus on early recognition and early departure to the appropriate facility for definitive management by a specialized care team. However, when faced with an acutely crashing patient that is suspected of having a pulmonary embolism aggressive management must be performed by the paramedic team. Standard interventions such as adequate airway management and maximized oxygen delivery should be performed early. The sedation and intubation of these patients should be done only when absolutely necessary and with extreme caution as the patient’s spontaneous ventilation through negative pressure may play a large role in maintaining what little cardiac output remains. Taking away the RV saving negative pressure of spontaneous ventilation with paralytics and sedation followed by replacing it with positive pressure ventilation may further decrease cardiac output and lead to PEA arrest18. The use of fluid boluses should also be performed with caution as the right ventricle is often overloaded and increased preload will not yield a higher cardiac output. However, a small bolus of 500ml or less may help gain traction on the starling curve and increase cardiac output in a volume depleted patient. If available, ultrasound should be used to determine the need for fluid resuscitation. A view of the heart for RV dilation and an IVC measurement may be helpful. As for the chemical hemodynamic support of these patients, norepinephrine has been coined the drug of choice (2), however its effects on afterload may be detrimental if cardiac dyskinesia is present. An inotrope such as dobutamine that also has the added benefit of decreasing pulmonary vascular resistance is an excellent option as add on therapy (15). When using these hemodynamic support medications, it would be advisable to begin with norepinephrine as it provides some alpha stimulation optimizing SVR prior to administering dobutamine that has the benefits of decreasing PVR, but also SVR is recommended. This strategy is optimal as it compounds both agents in a way that potentiates their supportive qualities yet spares the cardiovascular system of their unwanted effects.

Vasopressin may also be initiated; it is suggested to administer this medication as it will increase vascular resistance and MAP without increasing pulmonary vascular resistance. Vasopressin appears to work best as a non-titratable agent that will synergize with other medications to increase potency while decreasing toxicity. It is an excellent agent in PE as there are no vasopressin (V1) receptors in the pulmonary vasculature therefor PVR and RV afterload will not be increased.

These patients will benefit from many of the same treatment models available for pulmonary hypertension patients. Some experts suggest inhaled pulmonary vasodilators as adjunctive therapy in order to decrease the stress put on the RV.

The only treatment that addresses the true cause of the disease is fibrinolysis, however controversial and possibly dangerous this line of treatment may be, it is one of the only options for partially restoring hemodynamics. Without access to an interventional radiology suite or surgical theater this is the only treatment that addresses the root cause of the patient’s disease state. The same guidelines for the use of systemic thrombolysis in the setting of myocardial infarct should be used when considering its use for pulmonary embolism. The AHA has clearly defined relative and absolute contraindications that should be followed in this setting (4).

Performing fibrinolysis may be indicated and is available to some Paramedics. MD consultation is usually required to determine the dose and infusion rate of this medication. Some studies suggest that we may be able to achieve the desired hemodynamic stabilization with lower doses of fibrinolytic. Fibrinolysis may also be considered in patients with PEA arrest where there is a very high likelihood of PE.

Patients with a history of DVT/VTE

Patients with a history of deep vein thrombosis and or pulmonary embolism may be prescribed medications and or have permanent changes to their pulmonary status that add a layer of complexity to their care. These patients may activate EMS and require paramedic services for any other medical or traumatic event and the paramedic must take past illness into account. Patients with DVT/VTE may be prescribed anticoagulant therapy as secondary prevention to prevent recurrent VTE such as Rivaroxaban (Xarelto) and Apixaban (Eliquis) (the two most commonly prescribed NOACs) or older therapies such as vitamin K antagonists (warfarin aka Coumadin), heparin or low molecular weight heparin (SC injections). These medications are effective in preventing unwanted coagulation and thrombotic events, but unfortunately, they put these patients at risk of bleeding complications including GI bleeds and disabling/fatal intracranial hemorrhage. Anticoagulants significantly increase the risk of exsanguination in a traumatic event. Anticoagulant effects of these medications can be reversed but require specific reversal agents and blood products to do so. 

Patients who have suffered DVT may present with post-thrombotic syndrome. This chronic complication leads to persistent pain or discomfort in the affected leg along with signs of poor venous circulation such as swelling and pain with prolonged standing and even ulcers may develop (typically medial malleolar) (16).

Pulmonary embolism patients may suffer from decreased pulmonary function and experience symptoms ranging from limited exercise tolerance to shortness of breath at rest. The Paramedic must keep these complications in mind while excluding and or treating life threatening and reversible causes of dyspnea and or respiratory compromise.

In conclusion, the astute paramedic should keep DVT and PE in mind when assessing and intervene appropriately when the suspicion for DVT or PE is raised. 


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Keep Reading from this Edition

Jakob Rodger

Jakob Rodger

Jakob Rodger completed his Primary Care Paramedic program at LaCite in 2018 and is currently completing his Advanced Care Paramedic Graduate Certificate at Durham College.  He is also completing his Bachelors in Paramedicine with Charles-Sturt University. 

Jakob's professional practice interests are pulmonary embolism, specifically pertaining to pre-hospital diagnosis and management. He is also interested in developing procedural check lists to support high quality patient care and decision making in the field.

Jakob is currently working as a Primary Care Paramedic for The County of Lennox and Addington Paramedic Service, providing emergency medical care to the rural areas of Eastern Ontario.

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