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William 2001 Causes:  HF  Permeability edema  Both Most obstetric APE are due to noncardiogenic causes = 5% of ICU admissions = 0.5% of deliveries.

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Presentation on theme: "William 2001 Causes:  HF  Permeability edema  Both Most obstetric APE are due to noncardiogenic causes = 5% of ICU admissions = 0.5% of deliveries."— Presentation transcript:

1

2 William 2001

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

4 Study:  HF  Preeclampsia  Fluid overload  Tocolytics  Infection  RF – HF Tocolytics = 5% of obstetric causes

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

6  Obese  Chronic HTN + superimposed preeclampsia Precipitation factors:  Operative delivery  acute blood loss  Anemia  Infection

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

8 = Worst form of RF Mortality:  Nonpregnant = 40 – 50% ( ↑ to 90% if + infection )  Pregnant women = 25% Pathophysiological diagnosis include:  Alveolar epithelial injuries  Endothelial injuries

9 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

10 Diagnosis:  X - ray  diffuse infiltrates  PaO 2 : FiO 2 < 200 – 250  No evidence of HF Most common cause:  Nonpregnant = sepsis  Pregnant = sepsis 40% = preeclampsia = hemorrhage

11 7% of cases are combination of: - Sepsis - Trauma - Shock - Fluid overload Clinical coarse depend on:  Magnitude of insult  Ability to compensate  Stage of disease

12 Very early:  Hyperventilation  Accentuation of pregnancy metabolic alkalosis + arterial O 2 normal Later on:  X - ray and auscultatory evidence of lung disease  ↓ lung compliance

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

14 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

15 Final phase:  ↑↑ intrapulmonary shunts ≥ 30%  Severe hypoxemia  ↑↑ dead space  60% of tidal volume  Hypercapnia ( = ↑ CO 2 )  Metabolic and respiratory acidosis  Myocardial irritability  HF

16 Histology of end stage:  Intra-alveolar fibrosis  Fibroblastic infiltration  Massive tissue plates Management:  O 2  Fluids/blood  Empirical antibiotics

17 Points:  O 2 α CO  Increasing PaO 2 to 100 – 200 mmHg  minimal ↑ of O 2 delivery  Correction of anemia  ↑↑ O 2 delivery ( Each 1 gm of Hb carries 1.25 mL O 2 when 90% saturated )  Delivery does not improve hypoxia

18 Goals:  PaO 2 = 60 mmHg  Or 90% oxyhemoglobin saturation  At an inspired O 2 content of < 50%  With PEEP of < 15 mmHg Oxygen dissociation curve: Describes the propensity of Hb molecule to release O 2

19 ODC is divided into:  Upper ODC represents alveolar - capillary environment  Low O 2 affinity  high tissue capillary O 2 exchange  Lower ODC represents tissue - capillary environment  High O 2 affinity PaO 2 in maternal alveoli > tissue PaO 2

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

21 Fetal Hb is characterized by:  ↑ O 2 affinity  Left shift  Constantly in tissue portion of ODC - At any given PaO 2  F Hb carries more O 2 # M Hb - At high altitude  maternal PaO 2 = 60 mmHg while fetal PaO 2 is at sea level

22 Mechanical ventilation:  In early stages  O 2 mask  In immanent RF  intubation and artificial ventilation Adjustment of volume/cycle:  PaO 2 ≥ 60 mmHg  PaCO 2 35 – 45 mmHg  Hemoglobin saturation 90%

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

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

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

26 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

27 Other therapy:  Surfactant  Nitric oxide  Corticosteroids  Immune therapy  Lipid mediator antagonists  Antioxidants


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