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Acute pulmonary edema

William 2001. Acute pulmonary edema. Causes: HF Permeability edema Both Most obstetric APE are due to noncardiogenic causes = 5% of ICU admissions = 0.5% of deliveries. Study: HF Preeclampsia Fluid overload Tocolytics Infection RF – HF

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Acute pulmonary edema

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  1. William 2001 Acute pulmonary edema

  2. Causes: • HF • Permeability edema • Both Most obstetric APE are due to noncardiogenic causes = 5% of ICU admissions = 0.5% of deliveries

  3. Study: • HF • Preeclampsia • Fluid overload • Tocolytics • Infection • RF – HF Tocolytics = 5% of obstetric causes

  4. Commonly associated with: • Preeclampsia 28% • PTL 24% • Fetal surgery 17% • Infection 14% If iatrogenic causes are excluded, most cases are: • Old

  5. Obese • Chronic HTN + superimposed preeclampsia Precipitation factors: • Operative delivery • acute blood loss • Anemia • Infection

  6. Some causes of RF: - Pneumonia - Drug abuse - Sepsis - Arsenic poisoning - Hemorrhage - Pancreatitis - Preeclampsia - CT disease - Embolism - Pheochromocytoma - Irritant inhalation - Burns

  7. = Worst form of RF Mortality: • Nonpregnant = 40 – 50% ( ↑ to 90% if + infection ) • Pregnant women = 25% Pathophysiological diagnosis include: • Alveolar epithelial injuries • Endothelial injuries Acute respiratory distress syndrome

  8. Chemokines neutrophils recruitment  ↑ cytokines  tissue injury  ↑ pulmonary capillary permeability  ↓ lung volume  ↑ arterial hypoxemia Criteria of diagnosis differ from: Mild pulmonary insufficiency to Total mechanical ventilation

  9. Diagnosis: • X - ray  diffuse infiltrates • PaO2 : FiO2 < 200 – 250 • No evidence of HF Most common cause: • Nonpregnant = sepsis • Pregnant = sepsis 40% = preeclampsia = hemorrhage

  10. 7% of cases are combination of: - Sepsis - Trauma - Shock - Fluid overload Clinical coarse depend on: • Magnitude of insult • Ability to compensate • Stage of disease

  11. Very early:  Hyperventilation  Accentuation of pregnancy metabolic alkalosis + arterial O2 normal Later on: • X - ray and auscultatory evidence of lung disease • ↓ lung compliance

  12. ↑ Intrapulmonary blood shunting • Progressive alveolar and interstitial edema • Extravagation of WBCs and RBCs If not diagnosed  RF: • Marked dyspnea • Marked tachypnea • Marked hypoxemia

  13. With further ↓ of lung volume: • ↓↓ lung capacity • ↑↑ intrapulmonary blood shunting X–ray and chest auscultation  Bilateral diffuse infiltrations Lethal if not treated with  +ve airway pressure

  14. Final phase: • ↑↑ intrapulmonary shunts ≥ 30% • Severe hypoxemia • ↑↑ dead space  60% of tidal volume • Hypercapnia ( = ↑ CO2 ) • Metabolic and respiratory acidosis • Myocardial irritability • HF

  15. Histology of end stage: • Intra-alveolar fibrosis • Fibroblastic infiltration • Massive tissue plates Management: • O2 • Fluids/blood • Empirical antibiotics

  16. Points: • O2α CO • Increasing PaO2 to 100 – 200 mmHg  minimal ↑ of O2 delivery • Correction of anemia  ↑↑ O2 delivery ( Each 1 gm of Hb carries 1.25 mL O2 when 90% saturated ) • Delivery does not improve hypoxia

  17. Goals: • PaO2 = 60 mmHg • Or 90% oxyhemoglobin saturation • At an inspired O2 content of < 50% • With PEEP of < 15 mmHg Oxygen dissociation curve: Describes the propensity of Hb molecule to release O2

  18. ODC is divided into: • Upper ODC represents alveolar - capillary environment  Low O2 affinity  high tissue capillary O2 exchange • Lower ODC represents tissue - capillary environment  High O2 affinity PaO2 in maternal alveoli > tissue PaO2

  19. With higher PaO2 in alveoli  maternal Hb is maximally saturated Causes of right ODC shift: • Hypercapnia • Acidosis • ↓ temp • ↑ 2,3, diphosphglycerate level ( ↑ 30% during pregnancy  ↑ O2 delivery to the mother and fetus )

  20. Fetal Hb is characterized by: • ↑ O2 affinity • Left shift • Constantly in tissue portion of ODC - At any given PaO2 F Hb carries more O2 # M Hb - At high altitude  maternal PaO2 = 60 mmHg while fetal PaO2 is at sea level

  21. Mechanical ventilation: • In early stages  O2 mask • In immanent RF  intubation andartificial ventilation Adjustment of volume/cycle: • PaO2 ≥ 60 mmHg • PaCO2 35 – 45 mmHg • Hemoglobin saturation 90%

  22. Positive-end-diastolic pressure: For severe pulmonary injury + highintrapulmonary shunting  Filling of collapsed alveoli 5 – 15 mmHg  no need for cardiovascular monitoring 15 mmHg  ↓ VR ↓ CO  ↓ uteroplacental circulation

  23. Close PEEP during measuring PCWP  higher results Other causes of high PCWP: • Overdistended alveoli • ↓ Compliance • Barotrauma Fluid therapy: Fluid overload worsen lung condition

  24. Daily record: • Fluid intake/output • Body weight Mechanical ventilation add 1 L/day ↑ Permeability ↑ interstitial fluid Aim: Lowest PCWP possible + no ↓ CO Pregnancy changes:  ↑ risk of lung injury from fluid therapy

  25. Colloid oncotic pressure ( COP ): • Early during pregnancy = 28 mmHg • At term = 23 mmHg • During puerperium= 17 mmHg • Preeclampsia at term = 16 mmHg • During puerperium= 14 mmHg • COP/PCWP gradient = >8 mmHg • COP/PCWP gradient = ≤4 mmHg  ↑ risk of pulmonary edema

  26. Other therapy: • Surfactant • Nitric oxide • Corticosteroids • Immune therapy • Lipid mediator antagonists • Antioxidants

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