Pul edema

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Pul edema

  1. 1. “When you’re a nurse you know that every day you will touch a life or a life will touch yours”
  2. 2. PULMONARY EDEMA Presented By, Mr. Thomaskutty, RN, MSN, Accident and Emergency, Fujairah
  3. 3. DEFINITION Pulmonary edema is a condition characterized by fluid accumulation in the lungs caused by extravasations of fluid from pulmonary vasculature into the alveoli and interstitial spaces of the lungs
  4. 4. ANATOMY AND PHYSIOLOGY
  5. 5. Lower Respiratory Tract (Cont.)
  6. 6. Respiratory Bronchioles, Alveolar (Cont.) Ducts, and Alveoli • Lungs contain small saccular outpocketings called alveoli. • They have a thin wall specialized to promote diffusion of gases between the alveolus and the blood in the pulmonary capillaries. • Gas exchange can take place in the respiratory bronchioles and alveolar ducts as well as in the alveoli • The spongy nature of the lung is due to the packing of millions of alveoli together.
  7. 7. Surfactant (Cont.)
  8. 8. Capillary Network (Cont.)
  9. 9. (Cont.)
  10. 10. Respiratory Membrane
  11. 11. Cells in Alveolus  Type I cells : simple squamous cells forming lining  Type II cells : or septal cells secrete surfactant  Alveolar macrophages
  12. 12. (Cont.) Normal Physiology Hydrostatic pressure increases or Oncotic pressure decreases Interstitial Edema Continues leak Lymphatics drain excess fluid Alveolar edema
  13. 13. EPIDEMIOLOGY • Pulmonary edema occurs in about 1% to 2% of the general population. • Between the ages of 40 and 75 years, males are affected more than females. • After the age of 75 years, males and females are affected equally. • The incidence of pulmonary edema increases with age and may affect about 10% of the population over the age of 75 years.
  14. 14. CLASSIFICATION • BASED ON INCITING MECHANISM • BASED ON UNDERLINING CAUSE
  15. 15. A. BASED ON INCITING MECHANISM 1. IMBALANCE OF STARLING FORCE A. Increased pulmonary capillary pressure -left ventricular failure -Volume overload B. Decreased plasma oncotic pressure - Hypoalbuminemia due to different cause C. Increased negativity of interstitial pressure -Rapid removal of pneumothorax with large applied negative pressures (unilateral)
  16. 16. Abst ract • Study: Pulmonary edema related to changes in colloid osmotic and pulmonary artery wedge pressure in patients after acute myocardial infarction • Samples: 26 patients with acute myocardial infarction of whom 14 developed pulmonary edema • Findings: Both increases in pulmonary capillary pressure and decreases in colloid osmotic pressure leads to pulmonary edema (P L Luz da; H Shubin; M H Weil; E Jacobson)
  17. 17. BASED ON INCITING AGENT….. 2. ALTERED ALVEOLAR-CAPILLARY MEMBRANE PERMEABILITY o o o o o o o o Infectious pneumonia Inhaled toxins, Aspiration Circulating foreign substances Endogenous vasoactive substances Disseminated intravascular coagulation Immunologic—hypersensitivity pneumonitis, drugs Shock lung in association with non-thoracic trauma Acute hemorrhagic pancreatitis
  18. 18. BASED ON INCITING AGENT….. (Cont.) 3. LYMPHATIC INSUFFICIENCY After lung transplant Lymphangitic carcinomatosis Fibrosing lymphangitis
  19. 19. BASED ON INCITING AGENT….. (Cont.) 4. UNKNOWN OR INCOMPLETELY UNDERSTOOD High-altitude pulmonary edema Neurogenic pulmonary edema Narcotic overdose Pulmonary embolism Eclampsia After anesthesia After cardiopulmonary bypass
  20. 20. B. BASED ON UNDERLINING CAUSE Cardiogenic pulmonary edema Due to increased pressure in the pulmonary capillaries because of cardiac abnormalities Increase in pulmonary venous pressure Non- cardiogenic pulmonary edema Evidence of alveolar fluid accumulation without hemodynamic evidence Hydrostatic pressure is normal Leakage of protein and other molecule into the tissue
  21. 21. PATHOGENESIS OF CPE Congestion & accumulation of blood in the pulmonary area Decrease pumping ability to the systemic circulation Left sided heart failure Fluid leaks out of the intravascular space to the interstitium Accumulation of fluid Pulmonary edema
  22. 22. 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 due to altered alveolar- capillary permeability
  23. 23. (Cont.) Mild: Only engorgement of pulmonary vasculature Moderate: Extravasations of fluid into the interstitial space due to changes in oncotic pressure Severe: Alveolar filling occurs
  24. 24. Causes of Pulmonary Edema o Congestive Cardiac Failure o Over hydration with intravenous Fluids o Hypoalbuminemia: Nephrotic Syndrome Hepatic disease Nutritional Disorders oMalignancies of lymph system
  25. 25. Causes of Pulmonary Edema (Cont.) o Altered Capillary Permeability of Lungs Inhaled Toxins Inflammation Severe Hypoxia o Respiratory Distress Syndrome o Unknown Causes Neurogenic Conditions Narcotic Overdose High altitude
  26. 26. Abst ract • Study: Transfusion-related acute lung injury and pulmonary edema in critically ill patients: a retrospective study • Samples: Consecutive patients at four intensive care units (ICUs) • Findings: 94 required new respiratory support within 6 hours of transfusion Among 49 patients with confirmed acute pulmonary edema, experts identified 7 cases with suspected TRALI • Conclusion: In the ICU, pulmonary edema frequently occurs after blood transfusion (Rana R, Fernández-Pérez ER, Khan SA, Rana S)
  27. 27. Clinical Manifestations • Sudden onset of Dyspnea - Orthopnea, Paroxysmal Nocturnal Dyspnea • Agitated, Pale and possibly Cyanotic • Restlessness and Irritability • Skin- Clammy and Cold
  28. 28. Clinical Manifestations (Cont.) • • • • Wheezing and Coughing Distended Jugular Veins Noisy wet respiration On Auscultation- Bubbling Crackles, Wheezes and Rhonchi • HR is rapid • BP- Elevated or Decreased
  29. 29. Differential diagnosis Pneumothorax Bronchitis Cardiac tamponed COPD Pericarditis Pneumonia (bacterial ,viral , PCP) Pulmonary embolism Shocks (Cardiogenic ,septic ,anaphylactic) Venous air embolism
  30. 30. DIAGNOSTIC STUDY  History and Physical Examination  Blood studies Routine; CBC Liver function tests Renal Function Tests Arterial blood gas analysis Serum cardiac biomarkers
  31. 31. (Cont.)  Chest X-Ray  Hemodynamic Monitoring  Twelve-lead ECG  Echocardiogram  Nuclear imaging studies  Cardiac Catheterization
  32. 32. MEDICAL MANAGEMENT • • • • • • Improving gas exchange and Oxygenation Improved cardiac function Decreased Intravascular Volume Decreased venous return Decreased afterload Reducing Anxiety
  33. 33. DRUG THERAPY • • • • • Morphine Diuretics Digitalis Nitroglycerin Sodium Nitroprusside
  34. 34. (Cont.) • Isotropic Therapy • Digitalis Preparation • Beta- Adrenergic agonists • Phosphodiesterase Inhibitor (Milrinone) • Calcium Sensitizing Agent (Levosimendan) • Human B-type natriuretic peptide • Nesiritide
  35. 35. NURSING DIAGNOSIS 1. Ineffective breathing pattern related to: fatigue and breathing aids installation 2. Impaired gas exchange related to: distention of pulmonary capillaries
  36. 36. NURSING DIAGNOSIS 3. Risk for infection related to: the invasion of microorganisms area secondary to endotracheal tube installation 4. Ineffective tissue perfusion related to: decreased cardiac muscle contractility
  37. 37. NURSING DIAGNOSIS (CONT.) 5. Risk for Injury / trauma related to: anxiety secondary to the installation of breathing aids 6. Anxiety related to: the threat of biological integrity secondary to the actual installation of breathing aids
  38. 38. NURSING DIAGNOSIS (CONT.) 7. Impaired verbal communication related to: installation of endotracheal tube
  39. 39. COMMON INTERVENTIONS • Oxygen • High Fowlers position • Legs in dependent position • Activity restrictions • Emotional rest • Allay the anxiety • Monitor ECG, S. electrolytes
  40. 40. COMMON INTERVENTIONS (CONT.) • Small meals than larger ones • Monitor weight daily • Maintain intake & output chart • Restrict sodium & fluid intake • Self care needs • Increase activity gradually & as tolerated • Medications • Watch for complications of treatment such as electrolyte depletion
  41. 41. COMPLICATION  Leg swelling(edema)  Abdominal swelling (ascites)  Pleural effusion  Congestion & swelling of liver  Acute heart attack (myocardial infarction [MI])  Cardiogenic shock  Arrhythmias  Electrolyte disturbances  Protein enteropathy  Respiratory arrest  Death
  42. 42. • Emphasize reporting early signs of fluid overload • Review all prescribed medications with the patient and Family • Discuss ways to observe physical energy • Teach the patient- How to take slow and deep breath • Na restricted dietary pattern • Need to monitor weight gain
  43. 43. EXPECTED OUTCOMES:  O2 Sat - >95%  RR 12 to 20 breaths/min  Airway Patency - open, clear tracheobronchial passages  ABG • PH 7.35-7.45 • Pa02 80 to 100 mm of Hg • PaCo2 35 to 45 mm of Hg  Knowledge: Medications
  44. 44. BIBLIOGRAPHY Lewis, Heitkemper, Dirksen (2004), MedicalSurgical Nursing, 6th Edition, Mosby,840-853 Manual of Medical & Surgical Nursing Care, Nursing Intervention and Collaborative management , 5th Edition, Mosby, 191-195 Lippincott, Manual of Nursing Practice, 8th Edition, 416-417
  45. 45. (Cont.) Givertz MM, Colucci WS, Braunwald E(2005), Textbook of Cardiovascular Medicine, 7th ed, Elsevier Saunders, Philadelphia,539

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