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Pulmonary embolism 2

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Otherwise called Pulmonary Vascular Diseases / Venous Thromboembolism (VTE)

Venous thromboembolism encompasses deep venous thrombosis (DVT) and Pulmonary embolism (PE)

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Venous thrombi dislodge from site of formation embolize to pulmonary arterial circulation and sometimes to arterial circulation through a patent foramen ovale or atrial septal defect

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Most common gas exchange abnormalities are hypoxaemia (decreased arterial PO2) and an increased alveolar arterial O2 tension gradient

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Other pathological abnormalities1. Increased pulmonary vascular resistance

2. Impaired gas exchange due to increased alveolar dead space from vascular obstruction

3. Alveolar hypoventilation due to reflex stimulation of irritant receptors

4. Increased airway resistance due to constriction of airways distal to bronchi

5. Decreased pulmonary compliance due to lung edema, lung hemorrhage or loss of surfactant

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Clinical features –

VTE is difficult to diagnose It is fore most to find out the risk factors for VTE

Risk factors for VTE-

1. Surgery- Major abdominal surgery Post operative intensive care Hip/knee surgery

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2. Obstretics- Pregnancy Puerperium

3. Lower limb problems- Fracture Varicose veins Stroke /spinal cord injury

4. Cardio-respiratory diseases- . COPD

. Congestive cardiac failure

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5. Malignant diseases- Abdominal/pelvic Concurrent chemotherapy

6. Miscellaneous- Increasing age Previous proven VTE Immobility Trauma

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Features of pulmonary thromboembolism : A. Acute massive PE :

I .Pathophysiology: Cardiac output acute right heart failure

II. Symptoms: faintness or collapse crushing central chest pain

Apprehension Severe dyspnoea

III. Signs: Tachycardia Hypotension JVP Rt. Ventricular gallop rhythm loud P2

Severe cyanosis Urinary output

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IV. Chest X-ray:Usually normalmay be subtle oligaemic

V. ECG:S1 Q3 T3 anterior T-wave inversion

Rt. Bundle branch block (RBBB)VI. ABG:

PaO2 and PaCo2Metabolic acidosis

VII. D/D: Myocardial infarction

Pericardial tamponade Aortic dissection

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B. Chronic PE:I. Pathophysiology:

Chronic occlusion of pulmonary microvasculature, Rt. Heart failure

II. Symptoms:

Exertional dyspnoea

III. Signs:

May be minimal early in disease

Later RV heave, loud P2

Termnal: signs of right heart failure

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IV. Chest X-ray:

Enlarged pulmonary artery trunk

Enlarged heart

Prominent RV


RV hypertrophy and strain


Exertional PaO2 or desaturation on formal exercise testing

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INVESTIGATIONS:1. Chest x-ray :

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2. ECG:

3. Arterial blood gases: Reduced PaO2

Normal or low PaCo2 and an increased alveolar-arterial oxygen gradient

4. D-dimer studies: D-dimer is a specific degradation product released into

the circulation when cross linked fibrin undergoes endogenous fibrinolysis

An elevated D-dimer is of limited value

D-dimer :

Myocardial infraction


Sepsis along with pulmonary embolism

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5. Imaging : CT pulmonary angiography (CTPA) is most commonly

used to diagnose PE

Ventilation Perfusion Scanning is less commonly used as its utility is limited in patients with pre-existing chronic cardiopulmonary pathology and the scan is most frequently regarded as indeterminate. Color Doppler ultrasound of the leg veins remains the investigation of choice in patients with suspected DVT

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6. Echocardiography:

Extremely useful in differential diagnosis and assessment of acute circulatory collapse

RA, RV dilatation in massive PE and thrombus (embolism in transit) may be vissible.

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General measures:

Prompt recognition and treatment is life saving especially in cases of massive PE

Oxygen –all hypoxaemic patients to maintain Sao2 >90 %

Circulatory shock treated with IVF, plasma expanders.

Ionotropic agents are of limited value as the hypoxic dilated Rt. Ventricle is maximally stimulated by endogenous catecholamines

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Diuretics and vasodilators should be avoided as they cause cardiac output

Opiates may be necessary to relieve pain and distress, but should be used with caution in hypotensive patients

Resuscitation by external cardiac massage may be successful in the moribund patients by dislodging and breaking up a large central embolus.

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B. Anticoagulation: Commenced immediately if established


-reduces further propagation of clot - the risk of further emboli, - lowers the mortality

Low molecular weight heparin (LMWH) –

The duration of LMWH treatment should be at least 5 days, during which time oral warfarin is commenced. LMWH should not be discontinued until the INR is greater than 2

Patients with persistent prothrombotic risk factors require 3 months of therapy

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C. Thrombolytic Therapy: Indicated in any patient presented with massive PE

accompanied by cardiogenic shock

Helpful in patients with Rt. Ventricular dilatation, hypokinesia or sever hypoxaemia

Selected patients –surgical pulmonary embolectomy

D. Caval filters : Inferior vena caval filters


i. massive haemorrhage on anticoagulation therapy

ii. Recurrent VTE despite anticoagulation

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