Pulmonary edema

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seminar presentation on pulmonary edema by Rodas Temesgen

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Pulmonary edema

  1. 1. Pulmonary Edema
  2. 2. Outline0 Definition0 Epidemiology0 Pathophysiology0 Classifications & causes0 Pathogenesis0 Staging0 Clinical manifestations0 Complications0 Differential diagnosis
  3. 3. DefinitionPulmonary Edema ; is a conditioncharacterized by fluid accumulation inthe lungs caused by extravasation offluid from pulmonary vasculature in tothe interstitium and alveoli of the lungs
  4. 4. The extent to which fluid accumulates in the interstitium of thelung depends on the balance of hydrostatic and oncotic forceswithin the pulmonary capillaries and in the surrounding tissue.Hydrostatic pressure-favors movement of fluid from the capillary into theinterstitium Oncotic pressure-favors movement of fluid into the vesselMaintenance-lymphatic in the tissue carry away the small amounts ofprotein that may leak out-tight junction of endothelium are impermeable to protein
  5. 5. Epidemiology0 Pulmonary edema occurs in about 1% to 2% of the generalpopulation.0 Between the ages of 40 and 75 years, males are affectedmore than females.0 After the age of 75 years, males and females are affectedequally.0 The incidence of pulmonary edema increases with age andmay affect about 10% of the population over the age of 75years.
  6. 6. 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 allow protein toescape capillary bed and enhance movement of fluidin to the tissue of the lung idiopathic or unknown
  7. 7. Classification0 based on inciting mechanism1. Imbalance of Starling forceA. Increased pulmonary capillary pressure-left ventricular failure-Volume overloadB. Decreased plasma oncotic pressure- Hypoalbuminemia due to different causeC. Increased negativity of interstitial pressure-Rapid removal of pneumothorax with largeapplied negative pressures (unilateral)
  8. 8. ClassificationBased on inciting agent…..2. Altered alveolar-capillary membranepermeabilityo Infectious pneumoniao Inhaled toxinso Circulating foreign substanceso Aspirationo Endogenous vasoactive substanceso Disseminated intravascular coagulationo Immunologic—hypersensitivity pneumonitis, drugso Shock lung in association with non-thoracic traumao Acute hemorrhagic pancreatitis
  9. 9. Classification0 Based on inciting agent….3. Lymphatic insufficiency-After lung transplant- Lymphangitic carcinomatosis-Fibrosing lymphangitis4. Unknown or incompletely understood- High-altitude pulmonary edema- Neurogenic pulmonary edema- Narcotic overdose- Pulmonary embolism- Eclampsia-After anesthesia- After cardiopulmonary bypass
  10. 10. ClassificationBase on underlining causeoCardiogenic pulmonary edemaoNon-cardiogenic pulmonary edema
  11. 11. Cardiogenic pulmonary edemaIs Pulmonary edema due to increased pressurein the pulmonary capillaries because of cardiacabnormalities that lead to an increase inpulmonary venous pressure.oHydrostatic pressure is increased and fluidexit capillary at increased rate
  12. 12. Cardiogenic PE0 Basic pathophysiology:A rise in pulmonary venous and pulmonarycapillary pressures pushes fluid into thepulmonary alveoli and interstitium.
  13. 13. Pathogenesis of CPELeft sided heart failureDecrease pumping ability to the systemic circulationCongestion & accumulation of blood in the pulmonary areaFluid leaks out of the intravascular space to the interstitiumAccumulation of fluidPulmonary edema`
  14. 14. Risk Factors0 Vary by cause-Leading risk factor is clearly underlyingcardiac disease.
  15. 15. Causes of Cardiogenic PE0LV failure is the most common cause.0Dysrhythmia0LV hypertrophy and cardiomyopathy0 LV volume over load0Myocardia infarction0 left ventricular outflow obstruction
  16. 16. Non cardiogenic pulmonaryedemaIt is defined as the evidence of alveolar fluidaccumulation with out hemodynamicevidence that suggest a cardiogenic etiology.Hydrostatic pressure is normalLeakage of protein and other molecule in tothe tissue
  17. 17. Non cardiogenic PEo Associated with dysfunction of surfactantlining the alveoli, increased surface force and apropensity for the alveoli to collapse at lowvolume.oCharacterized by intra pulmonary shunt withhypoxemia and decrease lung compliance
  18. 18. Non cardiogenic pulmonaryedemaMechanism include:0Increased alveolar–capillarymembrane permeability0Decreased plasma oncotic pressure0Increased negativity of pulmonaryinterstitial pressure0Lymphatic insufficiency or obstruction
  19. 19. Non- cardiogenic PE0 causeI. Direct injury to the lungII. Hematogenous injury to the lungIII. possible lung injury plus elevatedhydrostatic pressure
  20. 20. Staging of PEThree stages of PE can be distinguished based on thedegree of fluid accumulation:Stage-1 : all excess fluid can still be cleared bylymphatic drainage.Stage-2 : characterized by the presence of interstitialedema.Stage-3 : characterized by alveolar edema due to alteredalveolor- capillary permeability
  21. 21. 0Mild: Only engorgement of pulmonaryvasculature is seen.0Moderate: There is extravasation offluid into the interstitial space due tochanges in oncotic pressure.0Severe: Alveolar filling occurs.
  22. 22. Unusual type pulmonaryedemaNeurogenic pulmonary edema0 Patients with central nervous system disorders andwithout apparent preexisting LV dysfunctionRe-expansion pulmonary edema0 Develops after removal of air or fluid that has been inpleural space for some time, post- thoracentesis0 Patients may develop hypotension or oliguriaresulting from rapid fluid shifts into lung.
  23. 23. Unusual type pulmonaryedema High altitude pulmonary edema0 occurs in young people who have quickly ascended toaltitudes above2700m and who then engage instrenuous physical exercise at that altitude, beforethey have become acclimatized.0 Reversible (in less than48 hours)
  24. 24. Pathophysiologyon ascending to high altitude, falling level of Po2 trigger hypoxicpulmonary vasoconstrictionThis directs blood flow away from hypoxic areas of lung towardsarea that are well oxygenatedThis results in a rise in mean pulmonary artery pressure & aheterogeneous blood flow to different parts of the lung
  25. 25. Cont…0 In areas that receive high blood flow the capillary trans-mural pressure rises & walls of the capillary &alveolus areexposed to stress failure0 Extensive damage to alveolar capillary membrane0 Edema which is rich in high molecular weight proteins &RBCs to pass freely in to the alveoli & impair oxygenation.0 patient present withHeadache, Insomnia, Fluid retention, Cough,Shortness ofbreath
  26. 26. Clinical manifestationSymptom0 Acute (sudden)0 Chronic (long-term)
  27. 27. SymptomACUTE0 Shortness of breath0 A Feeling of suffocating0 Anxiety ,restlessness0 Cough-frothy sputum that may be tinged with blood0 excessive sweating0 pale skin0 chest pain if PE is cause by cardiac abnormality0 palpitation
  28. 28. symptomLong term(chronic)0 Paraxosomal nocturnal dyspnea0 orthopnea0 Rapid weight gain0 Loss of appetite0 fatigue0 ankle and leg swelling
  29. 29. Sign0 Tachycardia0 Tachypnea0 Confusion0 Agitation0 Anxious0 Diaphoric0 Hypertension0 Cool extremities0 Rales0 Wheezing0 CVS findings ; S3 ,accentuation of pulmonic component of S2,jugular venous distention…..
  30. 30. Special considerationsUnilateral pulmonary edema after rapid evacuation oflarge pneumothorax0 Findings may be apparent only by radiography.0 Occasionally, dyspnea with physical findings localized toedematous lung
  31. 31. Special considerationLymphatic blockade secondary to fibrotic andinflammatory diseases or lymphangiticcarcinomatosis0 Both clinical and radiographic manifestations aredominated by the underlying disease process.Neurogenic pulmonary edema0 Symptoms usually occur within minutes to hours of theinjury
  32. 32. Complications leg swelling(edema), abdominal swelling(ascites), Pleural effusion, Congestion & swelling of liver, acute heart attack (myocardial infarction [MI]), cardiogenic shock, arrhythmias, electrolyte disturbances, mesenteric insufficiency, protein enteropathy, respiratory arrest, and death.
  33. 33. Differential diagnosis0Pneumothorax0Bronchitis0Cardiac tamponed0COPD0Pericarditis0Pneumonia (bacterial ,viral , PCP)0Pulmonary embolism0Shocks (cardiogenic ,septic ,anaphylactic)0Venous air embolism
  34. 34. Distinguishing Cardiogenic from Non-cardiogenic Pulmonary EdemaFinding suggesting cardiogenic edema-S3 gallop-elevated JVP-Peripheral edemaFindings suggesting non-cardiogenic edema-Pulmonary findings may be relatively normal inthe early stages-.
  35. 35. Distinguishing …..Chest radiographyA cardiogenic cause is favored with0 Cardiomegaly0 Kerley B lines and loss of distinct vascular margins0 Cephalization: engorgement of vasculature to the apices0 Perihilar alveolar infiltrate0 Pleural effusionNon cardiogenic cause-Heart size is normal-Uniform alveolar infiltrate-pleural effusion is uncommon-lack of cephalization
  36. 36. Distinguishing….. Hypoxemia0 Cardiogenic- due to ventilation perfusion miss match-respond to administration of oxygen0 Non cardiogenic-due to intrapulmonary shunting-persist despite oxygen supplimentation
  37. 37. Exertional DyspneaOrthopneaAspiration of food or foreign bodyDirect Chest injuriesWalking High altitudeChest Pain(right or left)Leg pain or swelling(Pulmonary Embolism)A cough that produces frothy sputum that may be tingedwith blood(cardiogenic)History TakingApproach a Patient withPulm.Edema
  38. 38. Cont…PalpitationsExcessive sweatingSkin color change-Pale skinChest pain(if it is Cardiogenic)Rapid weight gain(cardiogenic)FatigueLoss of appetiteSmoking History
  39. 39. Past Medical HistoryCOPD, heart failure, HIV risk factors(pulmonary Kaposi’s sarcoma). Prior chest X-rays,CT scans,tuberculin testing (PPD).
  40. 40. Medications0 Anticoagulants0 Aspirin0 NSAIDs0 Narcotic0 Heroin0 Morphine0 Methadone and0 Dextropropoxyphene
  41. 41. Physical ExaminationGeneral AppearanceVital signsHEENTLymphoglandular systemRespiratory systemCardiovascular systemAbdomenMusculoskeletal……
  42. 42. Laboratory InvestigationsRoutine; CBCLiver function testsRenal Function TestsArterial blood gas analysisSerum cardiac biomarkers
  43. 43. INVESTIGATIONImaging chest radiographyEchocardiographyUltrasound
  44. 44. INVESTIGATION…..Pulmonary artery catheterizationindicated when;-Cause remains uncertain-Pulmonary edema which is refractory to therapy-PE accompanied by hypotensionPulmonary capillary wedge pressure < 18 mmHg isconsistent with a non-cardiogenic cause.Pulmonary capillary wedge pressure >20 mmHgfavors a cardiogenic cause.
  45. 45. Treatment approachEmergence management-Support of oxygenation and ventilation-oxygen therapy-positive pressure ventilation0 Reduction of pre load-loop diuretics-nitrate- morphine
  46. 46. Treatment approachreduction of after load and inotropic supportcondition that complicate PE must be corrected-infection-academia-renal failure-anemia

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