Pathology: Embolusin the pulmonary vasculature that has classically travelled from a deep vein ofthe leg (DVT) via the right heart or a right atrial thrombus in AF.
Venous stasise.g. immobility, CCF, dehydration and venous obstruction
Endothelial Injury e.g. trauma, inflammation and previous thrombosis
Hypercoagulable state e.g. malignancy, oestrogen therapy, surgery and
abnormalities of the clottingcascade
Symptoms: Acute Minor: Pleuritic pain, dyspnoea
Acute Major: Central chest pain, dyspnoea
Signs: Acute Minor: hyperventilation,haemoptysis, hypoxia, fever, effusion
Acute Major: As above + hypotension, cyanosis, engorgedneck veins and collapse
Sub-Acute/Chronic: hyperventilation, raised JVP
Investigations: Chest X-Ray: Often normal, elevation ofa hemi-diaphragm and linear atelectasis,
small effusions or wedged shaped infarcts may be present
ECG: Sinus tachycardia, right heart strain or S1Q3T3
ABG: Low PaO2 and PaCO2
D-dimer: If clinical probability is intermediate or lowthen a negative d-dimer is a
reliable rule-out of thromboembolicdisease
CTPA: Initial investigation for non-massive PE’s
V/Q Scan: Used in those who can not tolerate CT contrast
Treatment: Thrombolysis: Clinically massive PE andmarked haemodynamic compromise
Anticoagulation: Low molecular weight heparin thenWarfarin with a target INR of 2.0-3.0.
LMWHcontinued until 2 consecutive days of target INR achieved due to initialprothrombotic effect of Warfarin.
IVC filter: Aim to prevent further clot reaching pulmonaryvasculature.
Complications: Pulmonaryhaemorrhage, pulmonary hypertension, CCF, recurrent episodes
Prognosis: MassivePE 30-60% mortality, most occur in the first 1-2 hours of care
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