pumonary edema, etiology, investigation, venti management

1. Pulmonary EdemaDR. HARSH PANDYA R1
UNDER GUIDANCE OF
DR.NIPA NAYAK
M.D. ASSO. PROF

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

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
 Pulmonary edema occurs in about 1% to 2% of the general
population.
 Between the ages of 40 and 75 years, males are affected
more than females.
 After the age of 75 years, males and females are affected
equally.
 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
 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
 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
o Cardiogenic pulmonary edema
o Non-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.
o Hydrostatic pressure is increased
and fluid exit capillary at increased
rate

12. Cardiogenic PE
 Basic pathophysiology:
A rise in pulmonary venous and
pulmonary capillary pressures pushes
fluid into the pulmonary alveoli and
interstitium.
CXR: B/L perihilar bat’s wing
appearance,symmetric opacification
of lung fields

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
 Vary by cause
-Leading risk factor is clearly
underlying cardiac disease.

15. Causes of Cardiogenic PE
LV failure is the most common
cause.
Dysrhythmia
LV hypertrophy and
cardiomyopathy
 LV volume over load
Myocardia infarction
 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.
o Characterized by intra pulmonary
shunt with hypoxemia and
decrease lung compliance

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

19. Non- cardiogenic PE
 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. Mild: Only engorgement of
pulmonary vasculature is
seen.
Moderate: There is
extravasation of fluid into the
interstitial space due to
changes in oncotic pressure.
Severe: Alveolar filling occurs.

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

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

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

28. Symptom……
Long term(chronic)
 Paraxosomal nocturnal dyspnea
 orthopnea
 Rapid weight gain
 Loss of appetite
 fatigue
 ankle and leg swelling

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

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

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

32. 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.

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

34. 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
-.

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

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

37.  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

38. 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

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

40. Medications
 Anticoagulants
 Aspirin
 NSAIDs
 Narcotic
 Heroin
 Morphine
 Methadone and
 Dextropropoxyphene

41. INVESTIGATIONS
 CXR-PA view:
unilateral or bilateral involvement,cardiogenic
pattern or non cardiognic pattern(air bronchogram
signs, fluffy opacities, asymmetrical inhomogenous
involvement),lobar involvement in post infectious PE.
 ABG analysis:
hypoxia and hypocapnia initially with respi. alkalois
hypercapnea in later stage with respi and
metabolic acidosis
 Hemodynamic measurement with Swan-Ganz
catheter
 Blood work up and septic screen

42. Management stretagy
 Treat underlying cause : Sepsis,heart failure,high
altitude hypoxia,obstruction,fluid
overload,hypoproteinemia etc.
 Respi support: NIV vs Intubation f/b venti support
Indication for intubation f/b venti support
 Refractive hypoxia
 Excessive work of breathing : rate > 35/min ,
MV>12L/min
 Hemodynamic instability
 Inability to protect airway
 Anticipated rapid clinical deterioration

43. Management stretagy…..
 NIV support:CPAP
Reasonable initial venti settings are EPAP 7 cmH2O
and IPAP of around 15 cm H2O with adjustment
according to patient tolerance and maintaining
SaO2>90%
Decreases work of breathing,FRC is
increased,collapse of alveoli due to edema fluid is
prevented and helps in opening up of already
collapsed alveoli
Good response is generally observed in 30 minutes,if
not so or worsening is seen, consider elective
intubation f/b venti support

44. Management stretagy…
 Principles of mechanical ventilation
Two fundamental principles
1. Prevention of overdistension of alveoli-limiting
tidal volume or inspiratory pressure
2. Choose the level of PEEP sufficiently high to
prevent derecruitment of alveoli at end of
expiration

45. 1. Limiting tidal volume
High TV 12-15 ml per kg are
dangerous in patient with PE
Can lead to VOLUTRAUMA
Tidal volume kept at 6-8 ml per kg
to start with in patient of PE
Then adjusted to keep the plateau
pressure below 30 cm of H2O

46. 2. Use of PEEP
Recruits collapsed alveoli,prevents collapse,improves
V/Q mismatch,decreases shunt and venous
admixture,increases FRC,reduces pathological dead
space
Can allow adequate oxygenation at lower
FiO2,protects from oxygen toxicity
Most patients with ARDS will need PEEP of more than
10 cm H2O at FiO2<0.6
If high level of PEEP causes hemodynamic instability,
use of pressure controlled – inverse ratio ventilation ,
prone posture can be beneficial
Inverse ratio venti:changes inspiration-expiration
ratio,lower peak pressure can be achieved,auto-
PEEP develops,higher mean alveolar pressure with
low peak pressure

47. Treatment in special
conditions
 High altitude pulmonary edema
Slow ascent ,prophylactically tab.nifedipine 20mg
sustained release 8hrly, or tab dexamethasone 8 mg
12hrly,or inhaled salmeterol
Descent and supplemental O2 are definitive Rx
If descent not possible and O2 not available,start
pharmacotherapy to reduce pulmonary artery
pressure
Tab nifedipine 10mg sublingual f/b 20 mg SR tab
6hrly
Also hydralazine,inhaled nitrous oxide
acetazolamide are helpful

48. Post Aspiration PE
 Preop gastric emptying by physical means(ryle’s
tube aspiration) or pharmacological
means(perinorm,atropine,glocopyrolate)
 Anti ematics ondensatron,granisatron injectable
 Induction in lateral position
 Head low position
 Bronchoscopic removal of particulate aspirate
material
 NO BRONCHO-ALVEOLAR LAVAGE-removes
surfactant and promotes collapse
 Supportive sterids
 PEEP and mechanical venti till edema clears

49. THANK YOU