pulmonary embolism 2

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  1. 1. PULMONARY EMBOLISM DR. ASWINI KUMAR MOHAPATRA PROFESSOR AND HEAD PULMONARY MEDICINE
  2. 2. PULMONARY EMBOLISM- Otherwise called Pulmonary Vascular Diseases / Venous Thromboembolism (VTE) Venous thromboembolism encompasses deep venous thrombosis (DVT) and Pulmonary embolism (PE)
  3. 3. Pathophysiology 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
  4. 4. Physiology- Most common gas exchange abnormalities are hypoxaemia (decreased arterial PO2) and an increased alveolar arterial O2 tension gradient
  5. 5. Other pathological abnormalities 1. 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
  6. 6. 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
  7. 7. 2. Obstretics- Pregnancy Puerperium 3. Lower limb problems- Fracture Varicose veins Stroke /spinal cord injury 4. Cardio-respiratory diseases- . COPD . Congestive cardiac failure
  8. 8. 5. Malignant diseases- Abdominal/pelvic Concurrent chemotherapy 6. Miscellaneous- Increasing age Previous proven VTE Immobility Trauma
  9. 9. 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
  10. 10. IV. Chest X-ray: Usually normal may be subtle oligaemic V. ECG: S1 Q3 T3 anterior T-wave inversion Rt. Bundle branch block (RBBB) VI. ABG: PaO2 and PaCo2 Metabolic acidosis VII. D/D: Myocardial infarction Pericardial tamponade Aortic dissection
  11. 11. 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
  12. 12. IV. Chest X-ray: Enlarged pulmonary artery trunk Enlarged heart Prominent RV V. ECG: RV hypertrophy and strain VI. ABG: Exertional PaO2 or desaturation on formal exercise testing
  13. 13. INVESTIGATIONS: 1. Chest x-ray :
  14. 14. 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 Pneumonia Sepsis along with pulmonary embolism
  15. 15. 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
  16. 16. 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.
  17. 17. MANAGEMENT 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
  18. 18. 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.
  19. 19. B. Anticoagulation: Commenced immediately if established Heparin- -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
  20. 20. 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 Indications: i. massive haemorrhage on anticoagulation therapy ii. Recurrent VTE despite anticoagulation
  21. 21. THANK YOU