Anesthesia Consideration in pulmonary embolism .pptx

This information regarding pulmonary embolism will immensely help the healthcare workers to understand and manage accordingly. It will also enable them to promptly act on this situation to save the life of such PE individual.

1. Anesthesia Consideration in Pulmonary Embolism

2. Definition Pulmonary Embolism is defined as a blood clot ( thrombus) that becomes lodged in the lungs, blocking one or more arteries and disrupting blood flow. Thrombus is mostly from a deep venous thrombosis. Other forms of Emboli to note include; 1. Air embolus 2. fat embolus 3. Amniotic fluid embolus – labor & delivery/postpartum 4. Septic/bacterial embolus – IV drug users with infective endocarditis

3. Risk Factors T - Trauma/travel H - Hypercoaguable state/hormone replacement R - Recreational drugs (IV) O - Older age group M - Malignancy B - Birth control pills O - Obstetric/Obesity S - Surgery I - Immobilization S - Sickness/Sepsis

4. Pathophysiology of PE A clot from the deep vein gets dislodged > enters the main circulation traveling into the lungs via right side of the heart. Clot blocks one or more arteries & affects the perfusion of affected alveoli. Results in HYPOXEMIA ( low pulse ox reading) as a result of reduced O2 blocked perfusion This tends to affect V/Q ratio resulting in an increase in V/Q ratio (increase alveolar arterial gradient). Hypoxemia activates the chemoreceptors (carotid bodies) that in turn stimulates cranial nerves IX (glossopharyngeal) & X ( vagus ) resulting in tachypnea (rate & depth).

5. Cont … Tachypnea results in excess exhalation of CO2 resulting in hypocapnia leading to respiratory alkalosis. Tachycardia occurs as the body tries to push more blood to the lungs to increase oxygenation. Clot has platelet deposits that releases enzymes into the system that act on the bronchial smooth muscles leading to bronchospasm. Also lead to pulmonary vasoconstriction in an attempt to bypass the obstruction- leading to reduced blood supply to the lungs resulting in an infarction & hemoptysis Increased systemic vascular resistance leads to increased after load & BP within pulmonary system- results into right ventricular dilatation 7 dysfunction.

6. Sign & Symptoms 1. Sudden onset of pleuritic chest pain 2. Shortness of breath 3. Hypoxia 4. Tachypnoea 5. Tachycardia 6. Haemoptysis 7. Jugular venous distension ( right heart failure)

7. PE Death Spiral

8. Diagnosis/Rule out criteria Wells score Years criteria- clinical signs of DVT, hemoptysis, PE as the most likely diagnosis PERC (Pulmonary Embolism Rule out Criteria)

9. Massive Vs Sub-massive PE PE can range from asymptomatic to life threatening Massive PE is defined as acute PE with obstructive shock or SBP< 90mmHg for 15 to 30 mins . Sub massive PE is acute PE without systemic hypotension but with either RV dysfunction or myocardial necrosis

10. Pulmonary Embolism Algorithm

11. Intervention Monitoring Check ABC Provide CPR Defibrillation Thrombolyse RBS

12. Investigations/Lab Testing WBC U/E/C LFTs Coagulation profile D-Dimmer ABG Troponin levels

13. Patients with PE may present with atypical symptoms, such as the following: Seizures Syncope Abdominal pain Fever Productive cough Wheezing Decreasing level of consciousness New onset of atrial fibrillation Hemoptysis Flank pain Delirium (in elderly patients) 

14. Management Admission to monitored setting  O2 supplementation as required Consultation with ICU/ respirology   Start anticoagulation immediately (IV heparin, low molecular weight heparin)  If anticoagulation contraindicated → consider IVC filter (controversial) Hemodynamic instability: similar to treatments of pulmonary hypertension:  Vasopressors to maintain RV perfusion Intravascular fluid therapy as per CVP, PAC, TEE Cautious especially with RV dysfunction: only 500-1000 cc at a time  Inotropes if RV dysfunction: dobutamine , epinephrine  Inodilators : milrinone   Pulmonary artery dilators: nitric oxide, epoprostenol ( flolan )

15. Intubation & ventilation: Avoid if possible  If necessary: Very high risk for cardiac collapse  Ensure pre-induction arterial line/central line if possible  Have vasopressors in-line  Titrated induction with avoidance of hypoxemia/ hypercarbia (bag mask once not breathing)  Avoid high intrathoracic pressures,  hypercarbia & hypoxemia 

16. Thrombolytic therapy:  Indications:  Shock: sBP <90 or ↓ sBP of 40 from baseline  Cardiac arrest  Severe hypoxemia  RV dysfunction  Patent foramen ovale   Dose: tPA 100mg IV over 2 hours  Embolectomy :  Catheter embolectomy   Surgical embolectomy   ECMO if all else fails