2. 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. 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. 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. 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. 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. 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. 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. 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
14. 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. 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. 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. Bat wing
edema in a
71-year-old
woman with
fluid overload
and cardiac
failure.
20. Neurogenic
PE in a
patient with
subdural
hematoma.
Bilateral
alveolar
filling
process and
a normal-
sized heart.
24. Initial management - ABCs of
resuscitation
Supplemental oxygen
Mechanical ventilation
- noninvasive by face mask
BiPAP
CPAP
- invasive as in endotracheal
intubation
25. 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
26. (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
27. (3)Inotropic Support :
(a) Dobutamine
(b) Dopamine
(c) Norepinephrine
Intra-aortic Balloon pumping –
reduces afterload
Increases cardiac output
Reduces LA pressure and improves
CPE
28. 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.)
