Abstract
Pulmonary embolism (PE) is a common emergency presenting among high risk patients. It is important to have a structured approach to clinical assessment, diagnosis and management of this potentially life-threatening emergency. Clinical and management pathways have improved over the last 10 years as clear guidelines have emerged. Newer diagnostic modalities have become available and will hopefully improve the pick-up rate of PE and reduce the morbidity and mortality. High level evidence presented by the American Society of Haematology and the European Society of Cardiology forms the basis for this review.
Highlights
Pulmonary embolism (PE) and deep vein thrombosis (DVT) are clinical manifestations of venous thrombo-embolic disease (VTE) and both have similar risk factors
Treated patients with no right ventricular dysfunction have a mortality rate of 2% which increases to 30% in patients who present with shock
CI =confidence interval; VQ = Ventilation perfusion scan; VQ 1, high probability scan interpreted as positive, low/nondiagnostic/normal scan interpreted as negative; VQ 2, high/low/nondiagnostic probability scan interpreted as positive, normal scan interpreted as negative; VQ 3, high probability scan interpreted as positive, normal scan interpreted as negative
Summary
Pulmonary embolism (PE) and deep vein thrombosis (DVT) are clinical manifestations of venous thrombo-embolic disease (VTE) and both have similar risk factors. Patients who present with cardiac arrest have a mortality rate of 65%.3 It is important for a primary care physician to identify high risk patients, consider the diagnosis of PE in acutely ill patients and follow a structured approach to diagnosis and management. The manifestations of PE are predominately haemodynamic and become apparent when greater than 30–50% of the pulmonary arterial bed is obstructed by emboli. This acutely increases pulmonary artery pressures and causes an overloading effect of the right ventricle (RV) which is not able to cater for the afterload needed for the systemic circulation resulting in electromechanical dissociation and sudden death. Patients who survive have sympathetic nervous system activation resulting in an inotropic and chronotropic response which aims at stabilising the systemic circulation.[1]
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