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Pulmonary edema
- 1. Dr. Amna Akram CMH,Multan
- 2. Pulmonary edemais 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. Imbalance ofstarling 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. Based onunderlying 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. Due tocardiac 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. Left sided heartfailure 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. Neurogenic PE Patientswith CNS disorders and without apparent preexisting LV dysfunction Re-expansion PE Develops after removal of air or fluid, post-thoracocentesis
- 8. High AltitudePE 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. Based onthe 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: Onlyengorgement of pulmonary vasculature. Moderate: Extravasation of fluid into the interstitial space due to changes in oncotic pressure Severe: Alveolar filling occurs
- 11. Symptoms: ACUTE Severe shortnessof 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. 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. 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. Cardiogenic PE Non cardiogenicPE 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 cardiogenicPE 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. 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. Bat wing edema ina 71-year-old woman with fluid overload and cardiac failure.
- 20. Neurogenic PE in a patientwith subdural hematoma. Bilateral alveolar filling process and a normal- sized heart.
- 21. Patient admitted with progressive respiratory distress 24 hoursafter arriving at town at 2700 meters above sea level. Right greater than left indistinct airspace opacity
- 22. 12 hours later (same patient) Marked improvement in airspace opacity.
- 23. Echocardiography – acutepapillary 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
- 24. Initial management- ABCs of resuscitation Supplemental oxygen Mechanical ventilation - noninvasive by face mask BiPAP CPAP - invasive as in endotracheal intubation
- 25. 3 maingoals 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
- 26. (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
- 27. (3)Inotropic Support: (a) Dobutamine (b) Dopamine (c) Norepinephrine Intra-aortic Balloon pumping – reduces afterload Increases cardiac output Reduces LA pressure and improves CPE
- 28. Resolves within48-72 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.)
- 29. Descent andsupplemental O2 Tab nifedipine 10mg sublingual or 20mg sustained release 6hrly. Hydralazine inhaled nitrous oxide acetazolamide