[11] Severe cases can lead to passing out, abnormally low blood pressure, obstructive shock, and sudden death.

[6] The risk of blood clots is increased by advanced age, cancer, prolonged bed rest and immobilization, smoking, stroke, long-haul travel over 4 hours, certain genetic conditions, estrogen-based medication, pregnancy, obesity, trauma or bone fracture, and after some types of surgery.

[19] More severe cases can include signs such as cyanosis (blue discoloration, usually of the lips and fingers), collapse, and circulatory instability because of decreased blood flow through the lungs and into the left side of the heart.

The strain on the right ventricle may be detected as a left parasternal heave, a loud pulmonary component of the second heart sound, or raised jugular venous pressure.

[22] As smaller pulmonary emboli tend to lodge in more peripheral areas without collateral circulation, they are more likely to cause lung infarction and small effusions (both of which are painful), but not hypoxia, dyspnea, or hemodynamic instability such as tachycardia.

Larger PEs, which tend to lodge centrally, typically cause dyspnea, hypoxia, low blood pressure, fast heart rate and fainting, but are often painless because there is no lung infarction due to collateral circulation.

This is a cause of obstructive shock, which presents as sustained low blood pressure, slowed heart rate, or pulselessness.

[25] The rare venous thoracic outlet syndrome can also be a cause of DVTs, especially in young men without significant risk factors.

[citation needed] VTE is much more common in immunocompromised individuals as well as individuals with comorbidities including: The development of thrombosis is classically due to a group of causes named Virchow's triad (alterations in blood flow, factors in the vessel wall, and factors affecting the properties of the blood).

[41] In the 2000 publication, Wells proposed two different scoring systems using cutoffs of 2 or 4 with the same prediction rule, and also included D-dimer testing in the rule-out of PE in low probability patients.

The rationale behind this decision is that further testing (specifically CT angiogram of the chest) may cause more harm (from radiation exposure and contrast dye) than the risk of PE.

This includes a full blood count, clotting status (PT, aPTT, TT), and some screening tests (erythrocyte sedimentation rate, kidney function, liver enzymes, electrolytes).

[62] According to a cohort study, single-slice spiral CT may help diagnose detection among people with suspected pulmonary embolism.

It is particularly useful in people who have an allergy to iodinated contrast, impaired kidney function, or are pregnant (due to its lower radiation exposure as compared to CT).

Historically, the gold standard for diagnosis was pulmonary angiography by fluoroscopy, but this has fallen into disuse with the increased availability of non-invasive techniques that offer similar diagnostic accuracy.

[76] ECG findings associated with pulmonary emboli may suggest a worse prognosis since the six findings identified with RV strain on ECG (heart rate > 100 beats per minute, S1Q3T3, inverted T waves in leads V1-V4, ST elevation in aVR, complete right bundle branch block, and atrial fibrillation) are associated with increased risk of circulatory shock and death.

[78] In massive and submassive PE, dysfunction of the right side of the heart may be seen on echocardiography, an indication that the pulmonary artery is severely obstructed and the right ventricle, a low-pressure pump, is unable to match the pressure.

People are often admitted to hospital in the early stages of treatment and tend to remain under inpatient care until the INR has reached therapeutic levels (if warfarin is used).

As vitamin K antagonists do not act immediately, initial treatment is with rapidly acting injectable anticoagulants: unfractionated heparin (UFH), low molecular weight heparin (LMWH), or fondaparinux, while oral vitamin K antagonists are initiated and titrated (usually as part of inpatient hospital care) to the international normalized ratio, a test that determines the dose.

[5] In terms of injectable treatments, LMWH may reduce bleeding among people with pulmonary embolism as compared to UFH.

Known as the directly acting oral anticoagulants, these treatments are now preferred over vitamin K antagonists by American professional guidelines.

[5] A Cochrane review found that there is no evidence of a difference between oral DTIs (dabigatran, rivaroxaban, edoxaban, apixaban) and standard anticoagulation in the prevention of recurrent pulmonary embolism.

[87] In people with cancer who develop pulmonary embolism, therapy with a course of LMWH is favored over warfarin or other oral anticoagulants.

[5][88] Similarly, pregnant women are treated with low molecular weight heparin until after delivery to avoid the known teratogenic effects of warfarin, especially in the early stages of pregnancy, but it can be used while breastfeeding.

Medication that breaks up blood clots is released through the catheter so that its highest concentration is directly next to the pulmonary embolus.

These include hypotension, cardiogenic shock, syncope, evidence of right heart dysfunction, and elevated cardiac enzymes.

[citation needed] That said, the reported mortality rate of 26% in the placebo group is probably an overstatement, given that the technology of the day may have detected only severe PEs.

The PESI and sPESI (= simplified Pulmonary Embolism Severity Index) scoring tools can estimate the mortality of patients.

[27] This is likely due to there being a generally lower level of activity among the elderly, resulting in higher rates of immobility and obesity.

[109] In Europe, an average of approximately 40,000 deaths per year with pulmonary embolism as the primary cause was reported between 2013 and 2015, a conservative estimate because of potential underdiagnosis.