Acute pulmonary edema

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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 - PowerPoint PPT Presentation

Transcript of Acute pulmonary edema

Page 1: Acute pulmonary edema
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ACUTE PULMONARY EDEMAWilliam 2001

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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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Study: HF Preeclampsia Fluid overload Tocolytics Infection RF – HF

Tocolytics = 5% of obstetric causes

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Commonly associated with: Preeclampsia 28% PTL 24% Fetal surgery 17% Infection 14%

If iatrogenic causes are excluded ,most cases are:

Old

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Obese Chronic HTN + superimposed

preeclampsiaPrecipitation factors:

Operative delivery acute blood loss Anemia Infection

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Some causes of RF: -Pneumonia - Drug abuse

-Sepsis - Arsenic poisoning -Hemorrhage - Pancreatitis -Preeclampsia - CT disease

-Embolism - Pheochromocytoma

-Irritant inhalation - Burns

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ACUTE RESPIRATORY DISTRESS SYNDROME

=Worst form of RFMortality:

Nonpregnant = 40 – 50% ( ↑to 90% if + infection)

Pregnant women = 25%Pathophysiological diagnosis include:

Alveolar epithelial injuries Endothelial injuries

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Chemokines neutrophils recruitment ↑ cytokines tissue injury ↑ pulmonary capillary permeability ↓ lung volume ↑ arterial hypoxemia Criteria of diagnosis differ from:

Mild pulmonary insufficiency toTotal mechanical ventilation

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Diagnosis: X - ray diffuse infiltrates PaO2 : FiO2 < 200 – 250 No evidence of HF

Most common cause: Nonpregnant = sepsis Pregnant = sepsis 40%

= preeclampsia = hemorrhage

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7% of cases are combination of: -Sepsis - Trauma

-Shock - Fluid overloadClinical coarse depend on:

Magnitude of insult Ability to compensate Stage of disease

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Very early: Hyperventilation Accentuation of pregnancy metabolic

alkalosis + arterial O2 normalLater on:

X - ray and auscultatory evidence of lung disease

↓ lung compliance

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↑ Intrapulmonary blood shunting Progressive alveolar and

interstitial edema

Extravagation of WBCs and RBCsIf not diagnosed RF:

Marked dyspnea Marked tachypnea Marked hypoxemia

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With further ↓ of lung volume: ↓↓ lung capacity ↑↑ intrapulmonary blood

shuntingX–ray and chest auscultation

Bilateral diffuse infiltrationsLethal if not treated with

+ ve airway pressure

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

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Histology of end stage: Intra-alveolar fibrosis Fibroblastic infiltration Massive tissue plates

Management: O2 Fluids/blood Empirical antibiotics

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Points: O2 α 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

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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

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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 affinityPaO2 in maternal alveoli > tissue PaO2

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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 )

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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

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Mechanical ventilation: In early stages O2 mask In immanent RF intubation

and artificial ventilationAdjustment of volume/cycle:

PaO2 ≥ 60 mmHg PaCO2 35 – 45 mmHg Hemoglobin saturation 90%

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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

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Close PEEP during measuring PCWP higher results

Other causes of high PCWP: Overdistended alveoli ↓ Compliance Barotrauma

Fluid therapy:Fluid overload worsen lung condition

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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

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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

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