Pulmonary oedema

a presentation on pulmonary oedema

1. PULMONARY OEDEMA Prajjwal Malla MDGP Resident 3 rd year

2. D efinition A condition characterized by fluid accumulation in the lungs caused by extravasation of fluid from pulmonary vasculature into the interstitium and alveoli of the lungs.

3. Etiopathogenesis Imbalance of the following forces Increased pulmonary capillary pressure Decreased plasma oncotic pressure Increased negative interstitial pressure Damage to the alveolar-capillary barrier Lymphatic obstruction Idiopathic mechanism

4. CLASSIFICATION CARDIOGENIC NON CARDIOGENIC

5. PATHOPHYSIOLOGY

6. CAUSES OF CARDIOGENIC PULMONARY EDEMA Hypertension Left Ventricular Failure Valvular H eart Disease Cardiomyopathy

7. Common causes of Non Cardiogenic Pulmonary Oedema Direct injury to Lung Hematogenous injury to Lung Possible lung injury plus elevated hydrostatic pressure Chest trauma Sepsis High altitude pulmonary oedema Pulmonary contusion Pancreatitis Neurogenic pulmonary oedema Aspiration Multiple transfusions Reexpansion pulmonary oedema Smoke inhalation Intravenous drug use Pneumonia Cardiopulmonary bypass Oxygen toxicity Pulmonary embolism, reperfusion

8. CARDIOGENIC vs NONCARDIOGENIC CARDIOGENIC NON-CARDIOGENIC S3 gallop Relatively normal in early stages Elevated JVP Peripheral edema Rales and wheezes on auscultation CXR - Enlarged cardiac silhouette - Heart size normal - Vascular redistribution - Uniform alveolar infiltrates - Interstitial thickening - Pleural effusions uncommon - Perihilar alveolar infiltrates - Pleural effusions - Kerley lines

9. Approach to a Patient with Pulmonary Oedema Exertional dyspnoea √ Palpitation Orthopnoea √ Excessive sweating Aspiration of food or √ S kin colour change – pale skin foreign body Direct chest injuries √ Chest pain (if cardiogenic) Walking high altitude √ R apid weight gain (cardiogenic) Chest pain (right or left) √ Fatigue Leg pain or swelling (Pulmonary embolism) √ L oss of appetite Cough with blood tinged sputum √ S moking history

10. LABORATORY INVESTIGATIONS Routine CBC Renal Function Test Liver Function Test Arterial blood gas analysis Serum cardiac biomarkers Ultrasound Echocardiograpy

11. Investigation….. Pulmonary artery catheterization is indicated when Cause remain uncertain Pulmonary edema refractory to therapy Pulmonary edema accompanied by hypotension

12. Complications Pulmonary edema, especially acute, can lead to fatal respiratory distress or cardiac arrest due to hypoxia. Assisted ventilation is provided if signs of respiratory fatigue - lethargy , fatigue, diaphoresis, worsening anxiety Sudden cardiac death secondary to cardiac arrhythmia- continuous monitoring of the heart rhythm Non-cardiogenic PE – resolves much less quickly, and most require mechanical ventilation

13. TREATMENT APPROACH EMERGENCY MANAGEMENT Upright sitting posture Support of oxygenation and ventilation Oxygen therapy Positive pressure ventilation REDUCTION OF PRELOAD AND INOTROPIC DRUGS Loop diuretics Nitrates Morphine Dopamine Your text here

14. LMNOP LASIX MORPHINE NITRATES OXYGEN POSITION

15. TREATMENT APPROACH….. Condition that complicate PE must be corrected Infection Renal failure Anemia

16. OXYGEN THERAPY Is essential to ensure adequate O2 delivery to peripheral tissues, including heart . When hypoxemia (PO2<60 mmHg) without hypercapnia – O2 given either by nasal prongs or Venturi mask with reservoir . If PO2 cannot be maintained at or near 60 mmHg despite inhalation of 100% O2 at 20L/min, or if progressive hypercapnia , mechanical ventillation is needed

17. NON INVASIVE VENTILLATION Continuous Positive Airway Pressure (CPAP) Non-invasive Intermittent Positive-pressure Ventillation (NIPPV ) CPAP maintains the same positive-pressure support throughout the respiratory cycle NIPPV increases airway pressure more during inspiration than during expiration compared to CPAP, NIPPV produces greater improvements in oxygenation and carbon dioxide clearance and a greater reduction in the work of breathing in patients with pulmonary oedema . Intubation and mechanical ventilation

18. REDUCTION OF PRELOAD Diuretics : 0.5-1.0 mg/kg The loop diuretics - furosemide, bumetanide , and torsemide are effective in most forms of pulmonary edema, even in the presence of hypoalbuminemia , hyponatremia , or hypochloremia .

19. Nitrates : Nitroglycerin and isosorbide dinitrate - venodilators but have coronary vasodilating properties as well. Sublingual nitroglycerin (0.4 mg × 3 every 5 min) first-line therapy for acute cardiogenic pulmonary edema . Morphine : Given in 2- to 4-mg IV boluses, morphine is a transient venodilator that reduces preload while relieving dyspnea and anxiety.

20. ACE inhibitors : reduce both afterload and preload and are recommended for hypertensive patients . Physical Methods: In nonhypotensive patients, venous return can be reduced by use of the sitting position with the legs dangling along the side of the bed

21. Inotropics : agents are indicated in patients with cardiogenic pulmonary edema and severe LV dysfunction Digitalis Glycosides: useful for control of ventricular rate in patients with rapid atrial fibrillation or flutter and LV dysfunction

22. Sinus tachycardia or atrial fibrillation can result from elevated left atrial pressure and sympathetic stimulation . may require cardioversion

23. Reexpansion pulmonary edema can develop after removal of longstanding pleural space air or fluid . These patients may develop hypotension or oliguria resulting from rapid fluid shifts into the lung. Diuretics and preload reduction are contraindicated I ntravascular volume repletion often is needed while supporting oxygenation and gas exchange.

24. High-altitude pulmonary edema can be prevented by use of dexamethasone, calcium channel–blocking drugs, or long-acting inhaled β2-adrenergic agonists. Treatment descent from altitude bed rest oxygen inhaled nitric oxide. Nifedipine may also be effective.

25. Prognosis In-hospital death rates - cardiogenic PE- as high as 15-20 % Myocardial infarction, associated hypotension, and a history of frequent hospitalizations for CPE generally increase the mortality risk

26. Take Home Message Clinical suspicion should be made when a patient with acute onset shortnes s of breath presents in ER. Try to find the cause for the condition. Promp t positioning and proper treatment would help relief the patient and could be life saving. Prognosis depends upon the severity of the condition.

27. References Harrison’s Principles of Internal Medicine 18 th edition Uptodate Medscape Online journals