This document provides an overview of pulmonary edema, including its definition, epidemiology, pathophysiology, classifications, causes, clinical manifestations, diagnosis, and treatment. Pulmonary edema is fluid accumulation in the lungs caused by increased fluid filtration from pulmonary capillaries into lung tissue. It can be cardiogenic, caused by left ventricular failure which increases hydrostatic pressure, or non-cardiogenic, caused by altered capillary permeability independent of cardiac issues. Symptoms include shortness of breath, cough, and hypoxemia. Treatment focuses on supporting oxygenation, reducing preload and afterload on the heart, and addressing any underlying conditions.

1. Pulmonary Edema

2. Outline
0 Definition
0 Epidemiology
0 Pathophysiology
0 Classifications & causes
0 Pathogenesis
0 Staging
0 Clinical manifestations
0 Complications
0 Differential diagnosis

3. Definition
Pulmonary Edema ; is a condition
characterized by fluid accumulation in
the lungs caused by extravasation of
fluid from pulmonary vasculature in to
the interstitium and alveoli of the lungs

4. The extent to which fluid accumulates in the interstitium of the
lung depends on the balance of hydrostatic and oncotic forces
within the pulmonary capillaries and in the surrounding tissue.
Hydrostatic pressure
-favors movement of fluid from the capillary into the
interstitium
 Oncotic pressure
-favors movement of fluid into the vessel
Maintenance
-lymphatic in the tissue carry away the small amounts of
protein that may leak out
-tight junction of endothelium are impermeable to protein

5. Epidemiology
0 Pulmonary edema occurs in about 1% to 2% of the general
population.
0 Between the ages of 40 and 75 years, males are affected
more than females.
0 After the age of 75 years, males and females are affected
equally.
0 The incidence of pulmonary edema increases with age and
may affect about 10% of the population over the age of 75
years.

6. Pathophysiology
 imbalance of starling force
-increase pulmonary capillary pressure
-decrease plasma oncotic pressure
-increase negative interstitial pressure
 damage to alveolar- capillary barrier
 lymphatic obstruction
Disruption of endothelial barrier allow protein to
escape capillary bed and enhance movement of fluid
in to the tissue of the lung
 idiopathic or unknown

7. Classification
0 based on inciting mechanism
1. Imbalance of Starling force
A. Increased pulmonary capillary pressure
-left ventricular failure
-Volume overload
B. Decreased plasma oncotic pressure
- Hypoalbuminemia due to different cause
C. Increased negativity of interstitial pressure
-Rapid removal of pneumothorax with large
applied negative pressures (unilateral)

8. Classification
Based on inciting agent…..
2. Altered alveolar-capillary membrane
permeability
o Infectious pneumonia
o Inhaled toxins
o Circulating foreign substances
o Aspiration
o Endogenous vasoactive substances
o Disseminated intravascular coagulation
o Immunologic—hypersensitivity pneumonitis, drugs
o Shock lung in association with non-thoracic trauma
o Acute hemorrhagic pancreatitis

9. Classification
0 Based on inciting agent….
3. Lymphatic insufficiency
-After lung transplant
- Lymphangitic carcinomatosis
-Fibrosing lymphangitis
4. Unknown or incompletely understood
- High-altitude pulmonary edema
- Neurogenic pulmonary edema
- Narcotic overdose
- Pulmonary embolism
- Eclampsia
-After anesthesia
- After cardiopulmonary bypass

10. Classification
Base on underlining cause
oCardiogenic pulmonary edema
oNon-cardiogenic pulmonary edema

11. Cardiogenic pulmonary edema
Is Pulmonary edema due to increased pressure
in the pulmonary capillaries because of cardiac
abnormalities that lead to an increase in
pulmonary venous pressure.
oHydrostatic pressure is increased and fluid
exit capillary at increased rate

12. Cardiogenic PE
0 Basic pathophysiology:
A rise in pulmonary venous and pulmonary
capillary pressures pushes fluid into the
pulmonary alveoli and interstitium.

13. Pathogenesis of CPE
Left sided heart failure
Decrease pumping ability to the systemic circulation
Congestion & accumulation of blood in the pulmonary area
Fluid leaks out of the intravascular space to the interstitium
Accumulation of fluid
Pulmonary edema
`

14. Risk Factors
0 Vary by cause
-Leading risk factor is clearly underlying
cardiac disease.

15. Causes of Cardiogenic PE
0LV failure is the most common cause.
0Dysrhythmia
0LV hypertrophy and cardiomyopathy
0 LV volume over load
0Myocardia infarction
0 left ventricular outflow obstruction

16. Non cardiogenic pulmonary
edema
It is defined as the evidence of alveolar fluid
accumulation with out hemodynamic
evidence that suggest a cardiogenic etiology.
Hydrostatic pressure is normal
Leakage of protein and other molecule in to
the tissue

17. Non cardiogenic PE
o Associated with dysfunction of surfactant
lining the alveoli, increased surface force and a
propensity for the alveoli to collapse at low
volume.
oCharacterized by intra pulmonary shunt with
hypoxemia and decrease lung compliance

18. Non cardiogenic pulmonary
edema
Mechanism include:
0Increased alveolar–capillary
membrane permeability
0Decreased plasma oncotic pressure
0Increased negativity of pulmonary
interstitial pressure
0Lymphatic insufficiency or obstruction

19. Non- cardiogenic PE
0 cause
I. Direct injury to the lung
II. Hematogenous injury to the lung
III. possible lung injury plus elevated
hydrostatic pressure

21. Staging of PE
Three stages of PE can be distinguished based on the
degree of fluid accumulation:
Stage-1 : all excess fluid can still be cleared by
lymphatic drainage.
Stage-2 : characterized by the presence of interstitial
edema.
Stage-3 : characterized by alveolar edema due to altered
alveolor- capillary permeability

22. 0Mild: Only engorgement of pulmonary
vasculature is seen.
0Moderate: There is extravasation of
fluid into the interstitial space due to
changes in oncotic pressure.
0Severe: Alveolar filling occurs.

23. Unusual type pulmonary
edema
Neurogenic pulmonary edema
0 Patients with central nervous system disorders and
without apparent preexisting LV dysfunction
Re-expansion pulmonary edema
0 Develops after removal of air or fluid that has been in
pleural space for some time, post- thoracentesis
0 Patients may develop hypotension or oliguria
resulting from rapid fluid shifts into lung.

24. Unusual type pulmonary
edema
 High altitude pulmonary edema
0 occurs in young people who have quickly ascended to
altitudes above2700m and who then engage in
strenuous physical exercise at that altitude, before
they have become acclimatized.
0 Reversible (in less than
48 hours)

25. Pathophysiology
on ascending to high altitude, falling level of Po2 trigger hypoxic
pulmonary vasoconstriction
This directs blood flow away from hypoxic areas of lung towards
area that are well oxygenated
This results in a rise in mean pulmonary artery pressure & a
heterogeneous blood flow to different parts of the lung

26. Cont…
0 In areas that receive high blood flow the capillary trans-
mural pressure rises & walls of the capillary &alveolus are
exposed to stress failure
0 Extensive damage to alveolar capillary membrane
0 Edema which is rich in high molecular weight proteins &
RBCs to pass freely in to the alveoli & impair oxygenation.
0 patient present with
Headache, Insomnia, Fluid retention, Cough,Shortness of
breath

27. Clinical manifestation
Symptom
0 Acute (sudden)
0 Chronic (long-term)

28. Symptom
ACUTE
0 Shortness of breath
0 A Feeling of suffocating
0 Anxiety ,restlessness
0 Cough-frothy sputum that may be tinged with blood
0 excessive sweating
0 pale skin
0 chest pain if PE is cause by cardiac abnormality
0 palpitation

29. symptom
Long term(chronic)
0 Paraxosomal nocturnal dyspnea
0 orthopnea
0 Rapid weight gain
0 Loss of appetite
0 fatigue
0 ankle and leg swelling

30. Sign
0 Tachycardia
0 Tachypnea
0 Confusion
0 Agitation
0 Anxious
0 Diaphoric
0 Hypertension
0 Cool extremities
0 Rales
0 Wheezing
0 CVS findings ; S3 ,accentuation of pulmonic component of S2,
jugular venous distention…..

31. Special considerations
Unilateral pulmonary edema after rapid evacuation of
large pneumothorax
0 Findings may be apparent only by radiography.
0 Occasionally, dyspnea with physical findings localized to
edematous lung

32. Special consideration
Lymphatic blockade secondary to fibrotic and
inflammatory diseases or lymphangitic
carcinomatosis
0 Both clinical and radiographic manifestations are
dominated by the underlying disease process.
Neurogenic pulmonary edema
0 Symptoms usually occur within minutes to hours of the
injury

33. Complications
 leg swelling(edema),
 abdominal swelling(ascites),
 Pleural effusion,
 Congestion & swelling of liver,
 acute heart attack (myocardial infarction [MI]),
 cardiogenic shock,
 arrhythmias,
 electrolyte disturbances,
 mesenteric insufficiency,
 protein enteropathy,
 respiratory arrest, and death.

34. Differential diagnosis
0Pneumothorax
0Bronchitis
0Cardiac tamponed
0COPD
0Pericarditis
0Pneumonia (bacterial ,viral , PCP)
0Pulmonary embolism
0Shocks (cardiogenic ,septic ,anaphylactic)
0Venous air embolism

35. Distinguishing Cardiogenic from Non-
cardiogenic Pulmonary Edema
Finding suggesting cardiogenic edema
-S3 gallop
-elevated JVP
-Peripheral edema
Findings suggesting non-cardiogenic edema
-Pulmonary findings may be relatively normal in
the early stages
-.

36. Distinguishing …..
Chest radiography
A cardiogenic cause is favored with
0 Cardiomegaly
0 Kerley B lines and loss of distinct vascular margins
0 Cephalization: engorgement of vasculature to the apices
0 Perihilar alveolar infiltrate
0 Pleural effusion
Non cardiogenic cause
-Heart size is normal
-Uniform alveolar infiltrate
-pleural effusion is uncommon
-lack of cephalization

37. Distinguishing…..
 Hypoxemia
0 Cardiogenic
- due to ventilation perfusion miss match
-respond to administration of oxygen
0 Non cardiogenic
-due to intrapulmonary shunting
-persist despite oxygen supplimentation

38. Exertional Dyspnea
Orthopnea
Aspiration of food or foreign body
Direct Chest injuries
Walking High altitude
Chest Pain(right or left)
Leg pain or swelling(Pulmonary Embolism)
A cough that produces frothy sputum that may be tinged
with blood(cardiogenic)
History Taking
Approach a Patient with
Pulm.Edema

39. Cont…
Palpitations
Excessive sweating
Skin color change-Pale skin
Chest pain(if it is Cardiogenic)
Rapid weight gain(cardiogenic)
Fatigue
Loss of appetite
Smoking History

40. Past Medical History
COPD,
 heart failure,
 HIV risk factors
(pulmonary Kaposi’s sarcoma).
 Prior chest X-rays,
CT scans,
tuberculin testing (PPD).

41. Medications
0 Anticoagulants
0 Aspirin
0 NSAIDs
0 Narcotic
0 Heroin
0 Morphine
0 Methadone and
0 Dextropropoxyphene

42. Physical Examination
General Appearance
Vital signs
HEENT
Lymphoglandular system
Respiratory system
Cardiovascular system
Abdomen
Musculoskeletal……

43. Laboratory Investigations
Routine; CBC
Liver function tests
Renal Function Tests
Arterial blood gas analysis
Serum cardiac biomarkers

44. INVESTIGATION
Imaging
 chest radiography
Echocardiography
Ultrasound

45. INVESTIGATION…..
Pulmonary artery catheterization
indicated when;
-Cause remains uncertain
-Pulmonary edema which is refractory to therapy
-PE accompanied by hypotension
Pulmonary capillary wedge pressure < 18 mmHg is
consistent with a non-cardiogenic cause.
Pulmonary capillary wedge pressure >20 mmHg
favors a cardiogenic cause.

46. Treatment approach
Emergence management
-Support of oxygenation and ventilation
-oxygen therapy
-positive pressure ventilation
0 Reduction of pre load
-loop diuretics
-nitrate
- morphine

47. Treatment approach
reduction of after load and inotropic support
condition that complicate PE must be corrected
-infection
-academia
-renal failure
-anemia