Overview on Pulmonary Embolism | Open Access Journals

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Overview on Pulmonary Embolism

Usha Sangana*

Aditya Institute of Pharmaceutical sciences and research, Affliated to Andhra University, Surampalem, Andhra Pradesh, India.

*Corresponding Author:
Usha Sangana
Aditya Institute of Pharmaceutical sciences and research
Surampalem, Andhra Pradesh, India.
E-mail: ushar.pharmazone@gmail.com

Received date: April 25, 2016; Accepted date: April 30, 2016; Published date: May 08, 2016

Visit for more related articles at Research & Reviews: Journal of Pharmacology and Toxicological Studies


Pulmonary Embolism, blood clots, shortness of breath, immobility


Pulmonary embolism (PE) is defined as a blockage in one of the pulmonary arteries or one of its branches in lungs. In most cases, embolism is caused by blood clots that travel from different parts of body to lungs (deep vein thrombosis). Because embolism nearly always happens in conjunction with deep vein occlusion, most doctors refer the conditions together as venous thromboembolism [1]. The obstruction of the blood flow through the lungs and also the resultant pressure on the proper ventricle of the center result in the symptoms and signs of alphabetic character. The chance of alphabetic character is increased in varied things, like cancer or prolonged bed rest [2].

Pulmonary embolism is mostly developed by some factors like immobility, travelling for long time. Pulmonary embolism might be life-threatening, but immediate diagnosis and treatment can decrease the risk of death [3].

Pulmonary embolism isn't a disease rather; it's a complication of underlying phlebothrombosis. Symptoms of Pulmonary Embolism [4-6].

Many symptoms are associated like shortness of breath, syncope, chest pain, cough, leg pain, haemoptysis and hypoxia. Most of the patients don’t have significant signs and symptoms but they vary.

Acute embolism is related to a broad spectrum of clinical severity. However, despite the varied displays, medical care is primarily restricted to medical care. The sole wide accepted exception to the employment of medical care alone in those patients with massive acute embolism. Massive embolism is outlined as acute embolism with sustained cardiovascular disease (systolic vital sign <90 torr for a minimum of quarter-hour or demand of inotropic support), pulselessness, or cardiac arrhythmia with signs of shock [7]. In patients with huge embolism and a suitable risk of hurt, general disintegration is usually thought of the fore most acceptable possibility [8-10]. In patients with massive embolism and contra indications to general disintegration, persistent shock despite general disintegration, or shock possible to cause death before general disintegration will get, surgical cutting out has historically been offered [11]. However, the simplest surgical outcomes are achieved in precisely those centers those centers in embolectomy [12-14].

Pulmonary embolism is diagnosed by so many physical examinations like blood tests. These tests include CT scan, ECG, Doppler ultrasound and X-ray [15].

Causes and Risk Factors

There are so factors which may responsible for blood clots, certain clots will increase the risk of pulmonary embolism. Some factors like family history, heart disease, cancer, immobility, long journeys, smoking and overweight [16,17].

Some drugs are responsible for pulmonary embolism. Prolong intake of some drugs causes pulmonary embolism.

Pulmonary embolism is presently thought to be the results of associate degree interaction between patient-related and setting-related risk factors. Patient related predisposing factors sometimes permanent, whereas setting-related risk factors of typically temporary. Commonly, over one risk issue is present, illustrating that pulmonary embolism may be a multi-causal disorders. However, pulmonary embolism will occur in patients with none diagnosable predisposing factors [18-22].


Pulmonary embolism may be life-threatening and one third of individuals with unknown and untreated embolism do not survive. Once the condition is diagnosed and treated promptly, however, that variety drops dramatically [23].

In very rare cases, blood clots occur frequently and develop for a long time, leading to chronic pulmonary hypertension, also called chronic thromboembolic pulmonary hypertension [24].


Several methods exist for the treatment of venous thromboembolism. The first line of treatment is chemical anticoagulation, usually with heparin. Anticoagulant treatment resolves venous thromboembolism and its associated symptoms [25-27]. In some cases, however, anticoagulation is contraindicated. Contraindicated patients include patients who are non-ambulatory or comatose. Treatment with anticoagulants in these cases can lead to haemorrhage and associated morbidity and mortality [28].

When anticoagulants are contraindicated, VTE can be treated endovascularly, most often with filters. VTE filters are placed most frequently in the inferior vena cava (IVC) to prevent a circulating clot from becoming a pulmonary embolism. IVC filters have been shown to be extremely effective in preventing the development of pulmonary embolism and in decreasing the morbidity and mortality of patients known to be harboring VTE of any kind [29-31]. An inferior venous blood vessel (IVC) filter is usually placed to stop continual pulmonary embolism.

Some of the drugs used to treat pulmonary embolism are anticoagulants like Warfarin, Heparin. Rivaroxaban, Fondaparinux [32].

The risk stratification has spot on such patients which has emerged as a crucial element of care. The therapeutic goals for pulmonary embolism are interference of coagulum growth, restoration of respiratory organ blood flow, and interference of recurrences. The treatment of pulmonary embolism begins with the combination of 2 blood thinners they are heparin, which can be administered intravenously or by injection, and second one is warfarin, blood thinner which can be administer orally. Heparin comes two principal forms. The traditional unfractionated form ordinarily requires intravenous administration. There is no fixed dose for this type of heparin. Instead, the dose is titrated to a blood test called the partial thromboplastin time [33-36].

This biopsy is performed many times daily for the primary few days and so once daily henceforth. Additional, low-molecular-weight anticoagulants have begun exchange unfractionated heparin. Low-molecular-weight heparins are normally prescribed in proportion to the patient’s weight, need no blood testing, and necessitate injection once or twice daily [37,38].


I would like to acknowledge the support of my colleagues in assisting with proper guidance. This content is reviewed and approved by Murali M.