acute pulmonary edema 1

7/28/2019 Acute Pulmonary Edema 1

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ACUTE PULMONARY

EDEMA

Definition:

an increase in pulmonary extravascularwater, which occurs when transudation or

exudation exceeds the capacity of

lymphatic drainage.


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ANATOM ICAL ASPECTS

Pulmonary capillary endothelial cells

meets in a fairly loose fashion-gap junction

are~5nm wide and permit moderately largeprotein molecules.

Alveolar epithelial cells meet at tight

junctions~1nm wide and virtuallyimpermeable to protein.


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Cont

Lungs have well developed lymphatic system.

It lies in the potential space around air

passages and vessels, separating them fromthe lung parenchyma.

Pulmonary lymphatics often cross the midlineand pass independently into the juntions of IJ

and SC veins.Normal lymphatic drainage from human

lungs is~10 ml/ hr.


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STAGES OF PULMONARY

OEDEMA

it has 4 stages

1. Interstitial pulmonary oedema

2. Cresentic alveolar filling3. Alveolar flooding

4. Airway flooding

With gradual onset these may be identifiableclinically, however with fulminant diseaseprogression may be obscured

There is usually prodromal stage in whichlymphatic drainage is increase, though thereis no detectable increase in lung water


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Interstitial pulmonary oedema

Microscopically - detected as cuffing ofdistended lymphatics around branches of thebronchi and larger pulmonary vessels

Interstitial lung water is increase but there isno passage of fluid into the alveoli.

This produces the butterfly shadow or bat

wings on CXRPhysical signs are generally absent and the

PA-aO2 gradient is small. PCO2 may benormal or subnormal


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ALVEOLAR FLOODING

Quantal alveolar flooding

Some alveolar are totally flooded,while

others only cresentic fillingFluid enters the alveoli in a crescentic

fashion until the surface tension rises

sharply and further fluid is drawn into thealveolus as the pressure gradient risesexponentially


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CONT

The alveolar edema ensues with outpouring of

liquid which contains both RBC and

macromoleculesThis cause severe distruption of the alveolar-

capillary membrane and edematous liquid

floods the alveoli and airways.

phenomenon is believed responsible for the

all or none filling of individual alveoli


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CONT

Clearly no gas exchange can occur in floodedalveoli.

At this point, full blown clinical pulmonaryedema with bilateral wet crepitation andrhonci are heard. typically pt. is anxious andperspire freely, and the sputum is frothy andblood-tinged

The CXR shows a butterfly pattern withinterstitial markings (Kerley B lines) andoverall hazzines with greater density in themore proximal region.


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CONT

There is severe hypoxemia with a low

PCO2 in the early stages, but as the work

of breathing is increased with the

reduction in lung compliance and

increased in airway resistance. Thearterial PCO2 will be increased


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This subsequently leads to the 4th stage

AIRWAY FLOODING, which effectively

blocks air passages preventing anymeaningful gas exchange and is rapidly

fatal unless treated.


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AETIOLOGY

Falls into 5:

Increased capillary pressure

Increased alveolar/capillary permeability

Decreased plasma oncotic pressure

Lymphatic obstructionMiscellaneous


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Increased capillary pressure

a. Absolute hypervolaemia

- overtransfusion/overperfusion pulonary

edema

- Decreased H2O clearance-fluid overload

in renal failure pt


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CONT

b. Relative pulmonary hypervolaemia

- Postural

- Vassopressorc. Increased pulmonary venous pressure

- LV failure

- Dysarthythmias

- MV disease eg : mitral stenosis

- Increased pulmonary arterial pressure( so-call overperfusion pulmonary edema


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CONT

d. Increased pulmonary blood flow

- left/right shunt

- Anaemiae. Subatmospheric airway pressure

- it assoc with severe physical exertion and

far more common in person under age of25 years dt high- pressure pulmonaryedema .


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INCREASED ALVEOLAR

( ARDS)

a.Direct injury

-infection: bacteria or virus

-aspiration of gastric content

-lung contusion

-near drowning


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CONT

b. Indirect

-sepsis syndrome

-extensive burn

-drug overdose


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DECREASED PLASMA

ONCOTIC PRESSURE

Esp in hypoalbuminemic state eg., severe

liver disease,nephrotic syndrome or protien

losing-enteropathyThis is seldom the primary cause of PE

However, is common in seriously ill pt and

may contribute significantly to their degreeof oedema


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LYMPHATIC OBSTRUCTION

a. Infection- bacterial or viral

b. Tumour

c. Transplantation/surgical

MISCELLANEOUS

a. neurogenic-head injury

b. Narcotic overdose


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MANAGEMENT

a. Oxygen

- give at high concentration to maintain an

adequate PCO2b. Posture

- if feasibly,sitting the patient reduces centralblood volume ( prop-up)

c. Diuretics-frusemide (iv 80-120mg) usuallyproduces an effect in 10 mins dt the dugsvenodilator- reduces in preload-in absent ofhypotension


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CONT

d. Morphine

- reduces anxiety and causes vasodilation

e. Treat the u/lying problems- severe HPT-nitroprusside is indicated if PE

is dt severe HPT or mechanical cx acute MI

- Manage cardiac arrhythmias-digoxin to

reduce the ventricular response in AF- Treat the infection using appropriate

antibiotics


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CONT

- Vasodilators- nitrates,ACE inhibitors,

frusemide.

f. Dobutamineindicated if the above measures fail to control

pulmonary edema in the presence of mild

hypotension and severe LV systolic dysfx. If

resp failure complicates pulm edema,

dopamine should be avoided


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CONT

because this agent may cause constriction

of pulmonary vein-will increased in pulm

capillary hydrostatic pressure and lungaccumulation.


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CPAP

- if the arterial PO2 remain low after treatment

with o2 and appropriate diuretics and cardiac

drugs, mask Continuous Positive AirwayPressure ( CPAP) should be initiated

- It reduces the work-of-breathing and the work

of the myocardium.

- Also increases Pao2, decreases Pao2, reduces

the need for intubation


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CONT

- Generally,CPAP is most useful in awake,

oriented and cooperative pt.

- Invasive mechanical ventilation withPEEP should be applied if the arterial

Po2 remains below 60mmhg and

increased Pco2 above 70-80mmhg whenthe pt is breathing approximately 50%

o2 thru mask CPAP.


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Invasive ventilation

In left ventricular dysfunction, preload iselevated

PEEP elevates intrathoracicpressure,reduces venous return anddecreases preload, so may improve leftventricular function

PEEP also improve left ventricularafterload


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Ventilator setting

CMV selected, either preesure or volumeventilation is acceptable

Tidal volumes-8 to 10 mL/kg

RR > 10 to achieve eucapnia

Peak alveolar pressure should be


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MONITORING

Cvp

Systemic hemodynamics

Pulse oximetry and serial ABG

Strict I/O chart , fluid restriction is a must

and monitor urine output

Electrolyte balance


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WEANING

Weaning is relatively easy, provided no u/lying

chronic pulmonary disease or 20 pulmonary

problems develop and the left heart failure isappropriately managed.

In COPD pt, it generate large intrathoracic

pressure swings during spontaneous

breathing, thus elimination of mechanicalventilator- increase in left ventricular preload

and pulmonary edemea.


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CONT

Weaning may progress rapidly to low level ofPS, FiO2 and CPAP, but pulmonary edemamay develop when positive pressure

ventilation is discontinued

Some pt may develop ischemic changes duringweaning

Ventilatory support must be continued untiltherapy is directed at improving cardiacfunctionsuch as proper fluid balance afterloadreduction and inotropic support


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THANK YOU

Hope you will be awake by now

acute pulmonary edema 1

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