3. INTRODUCTION
• Pulmonary edema is an acute emergency condition need an active
intervention
• It is due to imbalane of fluid shift in the alveoli that leads to
accumulation of fluid in the alveoli known as pulmonary edema
• Treating the primary cause
4. DEFINATION:
• Pulmonary edema is due to leakage of intravascular fluid into the
interstitium of the lungs and eventually into the alveoli.
• Acute pulmonary edema can be caused by increased capillary pressure
(hydrostatic or cardiogenic pulmonary edema) or by increased capillary
permeability.
• Cardiogenic pulmonary edema is characterized by marked dyspnea,
tachypnea, and signs of sympathetic nervous system activation
(hypertension, tachycardia, diaphoresis) .
• Pulmonary edema caused by increased capillary permeability is
characterized by a high concentration of protein and secretory products
in the edema fluid.
5. • Diffuse alveolar damage is typically present with the increased-
permeability pulmonary edema associated with acute respiratory
distress syndrome (ARDS).
• This “butterfly” fluid pattern is more commonly seen with increased
capillary pressure than with increased capillary permeability.
• The presence of air bronchograms suggests increased-permeability
pulmonary edema
7. PATHOPHYSIOLOGY
• A key component of normal lung function is to maintain a net flux of
fluid through the lung parenchyma.
• The massive surface area of the capillary network provides a low–
hydrostatic pressure (5 to 12 mm Hg) for the blood to come into close
contact with alveolar gases.
• The interstitial space between the alveolus and capillary is very thin
(<0.5 µm) and separated into two compartments: (1) the relatively
stiff alveolar side between the capillaries and the alveolar epithelium
and (2) the more compliant nonalveolar side around the capillary wall
8. • This interstitial fluid leads to a hydrostatic pressure, known as
interstitial pressure, which is similar to but opposes the hydrostatic
pressure in the vascular space.
• The net exchange of fluids between the capillaries and the
interstitium of the lungs is determined by the combined influences of
hydrostatic and osmotic forces within each compartment
• The lung lymphatic drainage system is the primary system for
removing the filtered fluid and protein from the lungs.
• Once the capacity of the interstitium to capture fluid is surpassed and
the rate of fluid accumulation exceeds the rate of lymphatic drainage,
fluid must next begin to accumulate within the alveoli referred to as
pulmonary edema
9.
10. • Forces causing outward movement of fluid from capillaries into
interstitium
• Capillary pressure -7mmHg
• Interstitial fluid colloid osmotic pressure-14mmHg
• Negative interstitial fluid pressure -8mmHg
• Total outward force-29mmHg
• Forcecausing absorption of fluid into capillaries
• Plasmacolloid osmotic pressure-28mmHg
• Total inward force- 28mmHg
14. CARDIOGENIC PULMONARY EDEMA
• Hydrostatic pulmonary edema
• Increased hydrostatic pressures in the pulmonary veins lead to
increased hydrostatic pressures in the alveolar capillaries that
increase fluid leakage out of the capillary.
• In most patients, elevation of pulmonary venous pressures is caused
by increased pressures in left-sided heart pressures
15. • The endothelial and epithelial barriers remain intact and
impermeable to large proteins and molecules.
• The fluid that accumulates within the alveoli Is identical to those of
normal interstitial fluid, which typically contain minimal cells and low
protein levels.
• In CHF, similar fluid can accumulate in other body spaces (e.g., pleural
effusions, peritoneal ascites) for the same reasons and are typically
referred to as transudative fluid collections or transudates.
16. NEUROGENIC PULMONARY EDEMA
• Acute brain injury
• Occurs in minutes to hours
• Massive outpouring of sympathetic impulses from the injured CNS
that results in generalized vasoconstriction and a shift of blood
volume into the pulmonary circulation.
• Difference b/w aspiration and neurogenic Pulmonary edema
• Unlike neurogenic pulmonary edema, chemical pneumonitis resulting
from aspiration frequently persists longer and is often complicated by
bacterial infection.
17.
18. DRUG INDUCED PULMONARY EDEMA
• Opioids and cocaine
• Cocaine can also cause pulmonary vasoconstriction, acute myocardial
ischemia, and myocardial infarction.
• Treatment of patients who develop drug-induced pulmonary edema
is supportive and may include tracheal intubation for airway
protection and mechanical ventilation.
19. HIGH ALTITUDE PULMONARY EDEMA
• 2500-5000mts
• Rate of ascent
• Fulminant pulmonary edema may be preceded by the less severe
symptoms of acute mountain sickness.
• The cause of this highpermeability pulmonary edema is presumed to
be hypoxic pulmonary vasoconstriction, which increases pulmonary
vascular pressure.
• Treatment includes administration of oxygen and prompt descent
from the high altitude. Inhalation of nitric oxide may improve
oxygenat
20.
21. RE-EXPANSION PULMONARY EDEMA
• Rapid expansion of a collapsed lung may lead to pulmonary edema in
that lung.
• The risk of reexpansion pulmonary edema after relief of a
pneumothorax or pleural effusion is related to the amount of air or
liquid that was present in the pleural space (>1 liter increases the
risk), the duration of collapse (>24 hours increases the risk), and the
rapidity of reexpansion.
• The high protein concentration in this edema fluid suggests that
enhanced capillary membrane permeability is important in the
development of this form of pulmonary edema.
• Treatment of reexpansion pulmonary edema is supportive.
22.
23. NEGATIVE PRESSURE PULMONARY EDEMA
• Releif after acute airway obstruction
• Also called as post obstruction pulmonary edema
• Occurs in few min to 2-3hrs after obstruction
• Pathogenesis -Development of high negative intrapleural pressure by
vigorous inspiratory efforts against an obstructed upper airway.
• This high negative intrapleural pressure decreases the interstitial
hydrostatic pressure, increases venous return, and increases left
ventricular afterload.
24. • In addition, such negative pressure leads to intense sympathetic
nervous system activation, hypertension, and central displacement of
blood volume.
• Together these factors produce acute pulmonary edema by
increasing the transcapillary pressure gradient.
• Maintenance of a patent upper airway and administration of
supplemental oxygen are usually sufficient treatment
• Mechanical ventilation may occasionally be needed for a brief period.
• Radiographic evidence of this form of pulmonary edema resolves
within 12–24 hours.
25.
26. CLINICAL FEATURES
• Dyspnea
• Tachypnea
• Orthopnea
• Hypertension
• Cough with forthy pink sputum
• Extensive use of accessory muscles
• Jugular venous pressure increases
• Wet crackles
27.
28. Kerley B lines are short parallel lines located at the
lung periphery.
•Represent distended interlobular septa
•Usually less than 1 cm in length and parallel to one
another at right angles to the pleura
•May be seen in any zone but are most frequently
located at the lung bases
29. wing or butterfly pulmonary
opacities a radiologic sign.
•Bilateral perihilar shadowing
•Classically described on a frontal chest
radiograph
Shown below is a chest x ray with the
yellow arrow which demonstrate bat's
wing.
30. Peribronchial cuffing is a radiologic sign, also referred to
as peribronchial thickening or bronchial wall thickening.
•Occurs when excess fluid buildup in the small airway
•Causes the area around the bronchus to appear more
prominent on an X-ray
•Thin bronchial walls are thickened and take on a
doughnut-like appearance
Shown below is a chest x ray with the red arrows which
demonstrate thickened bronchial walls that have a
doughnut-like appearance.
31. Cardio-thoracic ratio is useful for assessing an
underlying cardiogenic cause of pulmunary
edema.
•The cardiothoracic ratio is calculated by
measuring the transverse diameter of
the heart on a posterior/anterior chest X Ray,
and dividing it by the diameter of the thoracic
cage
•A value > 0.5 or one half is consistent with
enlargement of the heart
