ACUTE PULMONARY EDEMA

Definition: an increase in pulmonary extravascular water, which occurs when transudation or exudation exceeds the capacity of lymphatic drainage.

ANATOMICAL ASPECTS
Pulmonary capillary endothelial cells

meets in a fairly loose fashion-gap junction are~5nm wide and permit moderately large protein molecules. Alveolar epithelial cells meet at tight junctions~1nm wide and virtually impermeable to protein.

Cont
Lungs have well developed lymphatic system. It lies in the potential space around air passages and vessels, separating them from the lung parenchyma. Pulmonary lymphatics often cross the midline and pass independently into the juntions of IJ and SC veins. Normal lymphatic drainage from human lungs is~10 ml/ hr.

STAGES OF PULMONARY OEDEMA

1. 2. 3. 4.

it has 4 stages Interstitial pulmonary oedema Cresentic alveolar filling Alveolar flooding Airway flooding With gradual onset these may be identifiable clinically, however with fulminant disease progression may be obscured There is usually prodromal stage in which lymphatic drainage is increase, though there is no detectable increase in lung water

Interstitial pulmonary oedema

Microscopically - detected as cuffing of distended lymphatics around branches of the bronchi and larger pulmonary vessels Interstitial lung water is increase but there is no passage of fluid into the alveoli. This produces the butterfly shadow or bat wings on CXR Physical signs are generally absent and the PA-aO2 gradient is small. PCO2 may be normal or subnormal

CRESENTIC ALVEOLAR FILLING

Interstitial oedema increases and there is

passage of fluid into the alveoli However, some centre of the alveoli and the most of the alveoli walls remain clear Pt might become tachypnoeic and bilateral fine crepts are heard Gas exchange remains little affected and the PA-aO2 gradient remains small.

ALVEOLAR FLOODING
Quantal alveolar flooding Some alveolar are totally flooded,while

others only cresentic filling Fluid enters the alveoli in a crescentic fashion until the surface tension rises sharply and further fluid is drawn into the alveolus as the pressure gradient rises exponentially

CONT
The alveolar edema ensues with outpouring of liquid which contains both RBC and macromolecules This cause severe distruption of the alveolarcapillary membrane and edematous liquid floods the alveoli and airways.
phenomenon is believed responsible for the all or none filling of individual alveoli

CONT
Clearly no gas exchange can occur in flooded alveoli. At this point, full blown clinical pulmonary edema with bilateral wet crepitation and rhonci are heard. typically pt. is anxious and perspire freely, and the sputum is frothy and blood-tinged The CXR shows a butterfly pattern with interstitial markings (Kerley B lines) and overall hazzines with greater density in the more proximal region.

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. The arterial PCO2 will be increased

This subsequently leads to the 4th stage

AIRWAY FLOODING, which effectively blocks air passages preventing any meaningful gas exchange and is rapidly fatal unless treated.

AETIOLOGY
Falls into 5:
Increased capillary pressure Increased alveolar/capillary permeability Decreased plasma oncotic pressure Lymphatic obstruction

Miscellaneous

Increased capillary pressure

a. Absolute hypervolaemia
-

overtransfusion/overperfusion pulonary edema Decreased H2O clearance-fluid overload in renal failure pt

CONT
b. Relative pulmonary hypervolaemia - Postural - Vassopressor c. Increased pulmonary venous pressure - LV failure - Dysarthythmias - MV disease eg : mitral stenosis - Increased pulmonary arterial pressure( socall overperfusion pulmonary edema

CONT
d. Increased pulmonary blood flow - left/right shunt - Anaemia e. Subatmospheric airway pressure - it assoc with severe physical exertion and far more common in person under age of 25 years dt high- pressure pulmonary edema .

INCREASED ALVEOLAR ( ARDS)

a.Direct injury -infection: bacteria or virus -aspiration of gastric content -lung contusion -near drowning

CONT
b. Indirect -sepsis syndrome -extensive burn -drug overdose

DECREASED PLASMA ONCOTIC PRESSURE

Esp in hypoalbuminemic state eg., severe

liver disease,nephrotic syndrome or protien losing-enteropathy This is seldom the primary cause of PE However, is common in seriously ill pt and may contribute significantly to their degree of oedema

LYMPHATIC OBSTRUCTION
a. Infection- bacterial or viral
b. Tumour c. Transplantation/surgical

MISCELLANEOUS a. neurogenic-head injury b. Narcotic overdose

MANAGEMENT
Oxygen give at high concentration to maintain an adequate PCO2 b. Posture - if feasibly,sitting the patient reduces central blood volume ( prop-up) c. Diuretics-frusemide (iv 80-120mg) usually produces an effect in 10 mins dt the dugs venodilator- reduces in preload-in absent of hypotension
a. -

CONT
d. e. -

Morphine reduces anxiety and causes vasodilation 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

CONT
Vasodilators- nitrates,ACE inhibitors, frusemide. f. Dobutamine indicated 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
-

CONT
because this agent may cause constriction of pulmonary vein-will increased in pulm capillary hydrostatic pressure and lung accumulation.

CPAP
- if the arterial PO2 remain low after treatment with o2 and appropriate diuretics and cardiac drugs, mask Continuous Positive Airway Pressure ( 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

CONT
- Generally,CPAP is most useful in awake,

oriented and cooperative pt. - Invasive mechanical ventilation with PEEP should be applied if the arterial Po2 remains below 60mmhg and increased Pco2 above 70-80mmhg when the pt is breathing approximately 50% o2 thru mask CPAP.

Invasive ventilation
In left ventricular dysfunction, preload is

elevated PEEP elevates intrathoracic pressure,reduces venous return and decreases preload, so may improve left ventricular function PEEP also improve left ventricular afterload

Ventilator setting
CMV selected, either preesure or volume ventilation is acceptable Tidal volumes-8 to 10 mL/kg RR > 10 to achieve eucapnia Peak alveolar pressure should be <30cm H2O Inspiratory time should be short ( 1 to 1.5s) Fio2 should initially set at 1,titrated per Po2 PEEP of 5 to 10 H20 should be applied to support for failing heart.

MONITORING
Cvp
Systemic hemodynamics Pulse oximetry and serial ABG Strict I/O chart , fluid restriction is a must

and monitor urine output Electrolyte balance

WEANING
Weaning is relatively easy, provided no u/lying chronic pulmonary disease or 20 pulmonary problems develop and the left heart failure is appropriately managed.
In COPD pt, it generate large intrathoracic pressure swings during spontaneous breathing, thus elimination of mechanical ventilator- increase in left ventricular preload and pulmonary edemea.

CONT
Weaning may progress rapidly to low level of PS, FiO2 and CPAP, but pulmonary edema may develop when positive pressure ventilation is discontinued Some pt may develop ischemic changes during weaning Ventilatory support must be continued until therapy is directed at improving cardiac functionsuch as proper fluid balance afterload reduction and inotropic support

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