Pulmonary edema is a condition marked by fluid accumulation in the lungs, resulting from various causes, including cardiogenic and non-cardiogenic factors. Symptoms include severe shortness of breath, cough with pink frothy sputum, and cyanosis, with complications such as leg edema and respiratory arrest. Management strategies focus on oxygen supplementation, mechanical ventilation, and medications to reduce preload and afterload.

1. Pulmonary Edema

2. Definition
 Pulmonary edema is a condition characterized by fluid
accumulation in the lungs caused by extravasation of
fluid from pulmonary vasculature into the interstitium
and alveoli of the lungs

3. 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

4. Classification
 Based on underlying cause
 Cardiogenic pulmonary edema
 Non-cardiogenic pulmonary edema
 Neurogenic PE
 High Altitude PE
 Post Aspiration PE
 Re-expansion PE
 Other ( inhaled toxins, lymphatic obstruction, post
lung transplant, etc.)

5. Cardiogenic Pulmonary
edema
 Due to cardiac abnormalities, pulmonary capillary pressure
is increased that increases the pulmonary venous pressure.
CAUSES :
 LV failure is the most common
 Dysrhythmia
 LV hypertrophy and cardiomyopathy
 LV volume overload
 Myocardial infarction
 LV outflow obstruction

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

7. Non-cardiogenic PE
 Neurogenic PE
Patients with CNS disorders and
without apparent preexisting LV
dysfunction
 Re-expansion PE
Develops after removal of air or
fluid, post-thoracocentesis

8.  High Altitude PE
 Occurs in young people who have quickly
ascended to altitudes above 2700m and
who then engage in strenuous physical
exercise at that altitude, before they
have become acclimatized
 Reversible (in less than 48 hours)

9. Staging of PE
 Based on the degree of fluid
accumulation
 Stage- 1:all excess fluid can still be
cleared by lymphatic drainage
 Stage- 2 presence of interstitial edema
 Stage- 3 alveolar edema

10.  Mild: Only engorgement of pulmonary vasculature.
 Moderate: Extravasation of fluid into the interstitial space due to changes
in oncotic pressure
 Severe: Alveolar filling occurs

11. Clinical Presentation
Symptoms:
ACUTE
 Severe shortness of breath
 Cough- with pink frothy sputum
 Profuse sweating
 Cyanosis
 Anxiety, restlessness
 Palpitation
 Chest pain

12.  LONG TERM (CHRONIC)
 Paroxysmal nocturnal dyspnea
 Orthopnea
 Rapid weight gain
 Loss of appetite
 Fatigue
 Ankle and leg swelling

13. Signs
 Tachycardia
 Tachypnea
 Confusion
 Agitation, anxious
 Diaphoriesis
 Hypertension
 Cool extremities
 Crepitant rales, ronchi or wheeze
 CVS findings: S3, accentuation of pulmonic component of S2, jugular
venous distension

14. Complications
 leg edema
 Ascites
 Pleural effusion
 Congestion and swelling of liver
 Myocardial infarction
 Cardiogenic shock
 Arrythmias
 Electrolyte disturbances
 Mesenteric insufficiency
 Protein enteropathy
 Respiratory arrest and death

15. Distinguishing Cardiogenic from
Non cardiogenic PE
Cardiogenic PE Non cardiogenic
PE
CVS findings:
- S3 gallop
- Elevated JVP
- Peripheral edema
- relatively normal in early
stages
cardiomegaly Heart size is normal
Engorgement of vasculature
to the apices
No engorgement
Pleural effusion is common uncommon

16. Cardiogenic PE Non cardiogenic
PE
Perihilar alveolar infiltrate Uniform alveolar infiltrate
Kerley B lines Not present
Hypoxemia due to
ventilation perfusion miss
match
Hypoxemia due to
intrapulmonary shunting
Responds to administration
of oxygen
Persist despite oxygen
supplementation

17. Investigations
 CBC – severe anemia
 Serum electrolytes – Hypokalemia, Hypomagnesemia
 Pulse oximetry – assess
 Hypoxia
 Response to supplemental oxygenation
 ABGs – Initially hypoxia and hypocapnia with respi. Alkalosis
- Later Hypercapnia with respi and metabolic acidosis

18.  ECG- tachydysrhythmia
- bradydysrhythmia
- acute MI
 Ultrasonography – B lines
sensitivity of 94.1%
specificity of 92.4%
 Chest x-ray- 1. enlarged heart
2.inverted blood flow
3. Kerley lines
4. Basilar edema (vs diffuse edema)
5. Absence of air bronchograms
6. bilateral and symmetrical pleural effusions

19.  Echocardiography –
 acute papillary muscle rupture
 acute VSD
 cardiac temponade
 acute severe mitral regurgitation
 aortic regurgitation.
 Pulmonary arterial catheterization :
(Swan-Ganz Catheter)
 PCWP >18mmHg indicates CPE.
 PCWP <18mmHg indicates NCPE

20. General Management
 Initial management - ABCs of
resuscitation
 Supplemental oxygen
 Mechanical ventilation
- noninvasive by face mask
 BiPAP
 CPAP
- invasive as in endotracheal intubation

21. Medical treatment of CPE
 3 main goals
 1. preload reduction:
 (a) Nitroglycerin (sublingual or
intravenous) IV NTG
-10mcg/min, rapidly uptitrated to more
than 100mcg/min
- 3mg IV boluses every 5 minutes
 (b) Diuretics (loop diuretics) Furosemide

22.  (c) Nesiritide (recombinant human BNP)
 2. Afterload reduction:
 (a) ACE inhibitors –
 enalapril 1.25mg IV
 captopril 25mg sublingually
 (b) Angiotensin II receptor blockers –
 Valsartan and candesartan
 (c) Nitroprusside-
 Avoided in acute MI
 Prolonged use causes cyanide toxicity ,
tolerance and reflex tachycardia

23.  (3)Inotropic Support :
(a) Dobutamine
(b) Dopamine
(c) Norepinephrine
 Intra-aortic Balloon pumping –
 reduces afterload
 Increases cardiac output
 Reduces LA pressure and improves CPE

24. Treatment of Neurogenic PE
 Resolves within 48-72 hours in majority
of patients
 Medical care:
 oxygen supplementation
 Diuretics
 Inotropic support
 Surgical Care : directed at the
neurological insult (e.g., intracerebral
hemorrhage, subdural hematoma, etc.)

25. Treatment of High-altitude PE
Descent and supplemental O2
Tab nifedipine 10mg sublingual or
20mg sustained release 6hrly.
Hydralazine
inhaled nitrous oxide
 acetazolamide

26. Thank you!