pulmonaryedema basic classifications.pptx

basics of pulmonary edema

1. Pulmonary Edema

2. Definition Pulmonary edema is 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. Pathophysiology Imbalance of starling force -Increase pulmonary capillary pressure -decrease plasma oncotic pressure -increase negative interstitial pressure Damage to alveolar – capillary barrier Lymphatic obstruction Disruption of endothelial barrier

4. Classification Based on underlying cause Cardiogenic pulmonary edema Non- cardiogenic pulmonary edema Neurogenic PE High Altitude PE Post Aspiration PE Re-expansion PE Other ( inhaled toxins, lymphatic obstruction, post lung transplant, etc.)

5. Cardiogenic Pulmonary edema Due to cardiac abnormalities, pulmonary capillary pressure is increased that increases the pulmonary venous pressure. CAUSES : LV failure is the most common Dysrhythmia LV hypertrophy and cardiomyopathy LV volume overload Myocardial infarction LV outflow obstruction

6. Pathogenesis of CPE Left sided heart failure Decreased pumping ability to the systemic circulation Congestion and accumulation of blood in pulmonary area Fluid leaks out of intravascular space to the interstitium Accumulation of fluid Pulmonary edema

7. Non- cardiogenic PE Neurogenic PE Patients with CNS disorders and without apparent preexisting LV dysfunction Re-expansion PE Develops after removal of air or fluid, post- thoracocentesis

8. High Altitude PE Occurs in young people who have quickly ascended to altitudes above 2700m and who then engage in strenuous physical exercise at that altitude, before they have become acclimatized Reversible (in less than 48 hours)

9. Staging of PE Based on the degree of fluid accumulation Stage- 1: all excess fluid can still be cleared by lymphatic drainage Stage- 2 presence of interstitial edema Stage- 3 alveolar edema

10. Mild: Only engorgement of pulmonary vasculature. Moderate: E xtravasation of fluid into the interstitial space due to changes in oncotic pressure Severe: Alveolar filling occurs

11. Clinical Presentation Symptoms: ACUTE Severe shortness of breath Cough- with pink frothy sputum Profuse sweating Cyanosis Anxiety, restlessness Palpitation Chest pain

12. LONG TERM (CHRONIC) Paroxysmal nocturnal dyspnea Orthopnea Rapid weight gain Loss of appetite Fatigue Ankle and leg swelling

13. Signs Tachycardia Tachypnea Confusion Agitation, anxious Diaphoriesis Hypertension Cool extremities Crepitant rales, ronchi or wheeze CVS findings : S3, accentuation of pulmonic component of S2, jugular venous distension

14. Complications leg edema Ascites Pleural effusion Congestion and swelling of liver Myocardial infarction Cardiogenic shock Arrythmias Electrolyte disturbances Mesenteric insufficiency Protein enteropathy Respiratory arrest and death

15. Distinguishing Cardiogenic from Non cardiogenic PE Cardiogenic PE Non cardiogenic PE CVS findings : - S3 gallop - Elevated JVP - Peripheral edema - relatively normal in early stages cardiomegaly Heart size is normal Engorgement of vasculature to the apices No engorgement Pleural effusion is common uncommon

16. Cardiogenic PE Non cardiogenic PE Perihilar alveolar infiltrate Uniform alveolar infiltrate Kerley B lines Not present Hypoxemia due to ventilation perfusion miss match Hypoxemia due to intrapulmonary shunting Responds to administration of oxygen Persist despite oxygen supplementation

17. Investigations CBC – severe anemia Serum electrolytes – Hypokalemia, Hypomagnesemia Pulse oximetry – assess Hypoxia Response to supplemental oxygenation ABGs – Initially hypoxia and hypocapnia with respi . Alkalosis - Later Hypercapnia with respi and metabolic acidosis

18. ECG - tachydysrhythmia - bradydysrhythmia - acute MI Ultrasonography – B lines sensitivity of 94.1% specificity of 92.4% Chest x-ray - 1. enlarged heart 2.inverted blood flow 3. Kerley lines 4. Basilar edema (vs diffuse edema) 5. Absence of air bronchograms 6. bilateral and symmetrical pleural effusions

19. Echocardiography – acute papillary muscle rupture acute VSD cardiac temponade acute severe mitral regurgitation aortic regurgitation. Pulmonary arterial catheterization : (Swan- Ganz Catheter) PCWP >18mmHg indicates CPE. PCWP <18mmHg indicates NCPE

20. General Management Initial management - ABCs of resuscitation Supplemental oxygen Mechanical ventilation - noninvasive by face mask BiPAP CPAP - invasive as in endotracheal intubation

21. Medical treatment of CPE 3 main goals 1. preload reduction : (a) Nitroglycerin (sublingual or intravenous) IV NTG -10mcg/min, rapidly uptitrated to more than 100mcg/min - 3mg IV boluses every 5 minutes (b) Diuretics (loop diuretics) Furosemide

22. (c) Nesiritide (recombinant human BNP) 2. Afterload reduction: (a) ACE inhibitors – enalapril 1.25mg IV captopril 25mg sublingually (b) Angiotensin II receptor blockers – Valsartan and candesartan (c) Nitroprusside - Avoided in acute MI Prolonged use causes cyanide toxicity , tolerance and reflex tachycardia

23. (3) Inotropic Support : (a) Dobutamine (b) Dopamine (c) Norepinephrine Intra-aortic Balloon pumping – reduces afterload Increases cardiac output Reduces LA pressure and improves CPE

24. Treatment of Neurogenic PE Resolves within 48-72 hours in majority of patients Medical care : oxygen supplementation Diuretics Inotropic support Surgical Care : directed at the neurological insult (e.g., intracerebral hemorrhage, subdural hematoma, etc.)

25. Treatment of High-altitude PE Descent and supplemental O2 Tab nifedipine 10mg sublingual or 20mg sustained release 6hrly. Hydralazine inhaled nitrous oxide acetazolamide

26. Thank you!