Pulmonary

Edema
• Presentor : Dr. Yojana Goyal
• Moderator : Dr. Asmita Karnalkar
Pulmonary Edema
 Accumulation of intravascular fluid into the
interstitium of the lungs and into the alveoli.

 The extent to which fluid accumulates in the interstitium of the

lung depends on the balance between hydrostatic and oncotic
forces within the pulmonary capillaries and in the surrounding
tissue
Basic dynamics of fluids in the
body
• Hydrostatic pressure
• Oncotic pressure
•4 Starling forces
•Hydrostatic pressure:

• The pressure exerted by a fluid at equilibrium at a given

point within the fluid, due to the force of gravity

•Oncotic pressure:
•Itis exerted by proteins, notably albumin, in the plasma
(blood/liquid) that tends to pull water into the circulatory
system.
•PRINCIPLE of starling forces:

• The fluid movement due to the filtration across the capillary wall
is dependent on the balance between the HYDROSTATIC
PRESSURE GRADIENT and ONCOTIC PRESURE
GRADIENT across the capillary wall

• Starling Equation:

Fluid Movement =k[(Pc – Pi) – (πc - πi) ]

where:
 K = Capillary Filtration Coefficient

 K depends upon permeability and the area

available
Pulmonary edema results
When there is:
• Imbalance of starling force
•increased pulmonary capillary pressure
•decreased plasma oncotic pressure
•increased negative interstitial pressure

• Damage to alveolar- capillary barrier

• Lymphatic obstruction or decreased lymphatic clearance
• 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
Pathophysiology
Increase in fluid filtration into
interstitial spaces of lungs

Movement of fluid from interstitium

to alveolar walls

Damage to alveolar epithelium

Accumulation of fluid in alveoli

Types of PE
• Based on cause

Pulmonary
edema

Non
Cardiogenic
Cardiogenic
Cardiogenic PE
•Itis due to increased pressure in the pulmonary capillaries
because of cardiac abnormalities that lead to an increase in
pulmonary venous pressure.

•Hydrostatic pressure is increased and fluid exit capillary at

increased rate
Causes of Cardiogenic PE
 LV failure is the most common cause

 LV hypertrophy and cardiomyopathy

 LV volume over load

 Myocardial infarction

 Left ventricular outflow obstruction

Pathophysiology of CPE
Left sided heart failure

Decreased pumping ability to systemic circulation

Congestion and accumulation of blood in the pulmonary area

Fluid leaks out of intervascular space to the interstitium

Pulmonary Edema
Non Cardiogenic PE
• It is defined as the presence of alveolar fluid accumulation with
absence of hemodynamic changes that suggest a cardiogenic
etiology

• It may be due to

 Increased alveolar–capillary membrane permeability

 Decreased plasma oncotic pressure
 Increased negativity of pulmonary interstitial pressure
 Lymphatic insufficiency or obstruction
Causes of Non Cardiogenic PE

Lung injury plus

Hematogenous
Direct Injury to Lung elevated Hydrostatic
Injury to Lung
Pressure
• Chest trauma • Sepsis • High altitude PE
• Pulmonary • Pancreatitis • Neurogenic PE
contusion • Multiple • Re-expansion PE
• Aspiration transfusions
• Smoke inhalation • Intravenous drug
• Pneumonia use (eg : Heroine)
• Pulmonary
embolism
High Altitude PE
•Occurs due to:
 Rapid ascent
 Doing heavy physical work during first 3to 4 days after rapid
ascent to high altitude.

 Mechanism
•Increased sympathetic activity

•Produces vasoconstriction which leads to increase in pulmonary

capillary hydrostatic pressure
•Drives the fluid out of pulmonary capillaries producing pulmonary
edema
Neurogenic PE
• Develops in small proportions patients experiencing acute brain
injury.
• This
form of pulmonary edema occurs minutes to hours after
CNS injury and manifests during the perioperative period.
 Sympathetic over activity from injured CNS

Generalised Vasoconstriction

Shift of blood volume into pulmonary circulation

Increased pulmonary capillary pressure

Transudation of fluid into interstitium and alveoli

Re- expansion PE
•General Considerations:

• Rare complication of rapid expansion of the lung passively collapsed by

a large pleural effusion or pneumothorax

• Greatest risks are in young patients with large pneumothoraces, pulmonary

collapse of more than 7 days, or removal of up to 3 liters of pleural fluid at
one time
◦ But it has been reported to occur with as little as 1 liter of fluid
removed.

• Pathophysiology not known

Negative Pressure Pulmonary
Edema (NPPE)
• Negative pressure pulmonary edema
(NPPE) represents a pure form of
hydrostatic edema.
• NPPE has also been referred to as ‘post-
obstructive pulmonary edema (POPE) ’ or ‘
laryngospasm- induced pulmonary edema’.
• It
usually occurs after laryngospasm, due to
forced inspiratory effort against closed glottis,
creating increased hydrostatic pressure in
pulmonary capillaries, leading to edema.
How does laryngospasm occur?
• Laryngospasm involves the reflex
arc consisting of Trigeminal,
Glossopharngeal, Superior and
Inferior laryngeal branches of Vagus
Nerves which innervates the mucosal
lining of nasopharynx till vocal cords.

• Stimulation with foreign materials

like blood, secretions, gastric contents
stimulates the arc

• Causes bradycardia followed by

tachycardia
Types of NPPE
• Type I NPPE
• Seen in acute obstruction
• Mainly after surgical manipulation or laryngospasm
• Also called Laryngospasm induced PE or Post extubation edema.

• Type II NPPE
• Seen in chronic obstruction
• Enlarged tonsils, hypertrophied adenoids, redundant uvula.
Pathophysiology of NPPE

Muller’s Maneuver
Causes of NPPE
Type I NPPE Type II NPPE
• Postextubation • Post tonsillectomy
laryngospasm • Post adenoidectomy
• Epiglottitis
• Choanal stenosis
• Choking/ foreign body • Hypertrophic redundant
• Strangulation/ hanging uvula
• ETT obstruction, biting
• Laryngeal tumor, goiter
• Post op Vocal cord paralysis
• Near drowning
Clinical features of PE
• Acute • Chronic

 Shortness of breath  Paroxysomal nocturnal dyspnea

 A Feeling of suffocating  Orthopnea

 Anxiety ,restlessness  Rapid weight gain

 Pinky -frothy sputum

 Loss of appetite

 Excessive sweating  Fatigue

 Chest pain  Ankle and leg swelling

Signs of PE
• Tachycardia
• Cool extremities
• Tachypnea
• Rales
• Confusion
• Wheezing
• Agitation
• CVS findings : S3 gallop ,
• Anxious
accentuation of pulmonic
• Diaphoric component of S2, jugular

• Hypertension venous distention.

Investigations
Blood tests
 CBC – severe anemia

 Cardiac myocytes of left ventricle secrete BNP in response to

stretching caused by increased ventricular blood volume or increased
intracardiac pressures.
 BNP
 < 100 pg/ml – Non cardiac PE
 > 500 pg/ml – Cardiac PE
 100- 500 pg/ml – Seen in critically ill patients

 Serum electrolytes – rules out fluid overload

 Pulse oximetry – assess Hypoxia
Response to supplemental oxygenation

 ABGs – Initially hypoxia and hypocapnia with respiratory

Alkalosis
•Later Hypercapnia with respiratory and metabolic
acidosis
•This is due to increased dead space ventilation.
•Increased arterial alveolar gradient also seen.

 ECG-
• Tachydysrhythmia , Bradydysrhythmia signs of ischemia or
acute MI
Imaging findings
• Radiographic findings can lag behind physiologic changes

•The key findings of cardiogenic pulmonary edema:

◦ Kerley B lines (septal lines)

◦ Pleural effusions
◦ Fluid in the fissures
◦ Kerley B lines (septal lines)
• Seenat the lung bases, usually no more than 1 mm thick and
1 cm long, perpendicular to the pleural surface
◦ Pleural effusions
• Usually bilateral, frequently the right side being larger than
the left
• If unilateral, more often on the right

◦ Fluid in the fissures

• Thickening of the major or minor fissure
Non cardiogenic PE
• Bilateral peripheral air space
disease with air bronchograms or
central batwing appearance
• Kerley B lines and pleural
effusions are uncommon
• Typicallly occurs 48 hours or more
after the initial insult
• Stabilises at around 5 days and
make take weeks to completely
clear.
CT findings
• Gravity-dependent
consolidation or ground
glass opacification and
typical batwing pattern from
center to periphery

• Air bronchograms are

common
Echocardiography findings
• Pulmonary Capillary Wedge pressure helps differentiate between
cardiogenic and non cardiogenic PE
• IF PCWP < 18 mm Hg- Non cardiogenic PE
• Ventricularcontractility, Vena cava dimensions and compressibility
gives idea about fluid overload.

POCUS (Point of Care Ultrasound Lung)

• Bedside, non invasive and rapid and uses a phased array probe.
• Helps in perioperative diagnosis and management of hypoxia.
Pulmonary artery catheterisation
It is 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.
Treatment approach

Emergence management:

 Support of oxygenation and ventilation

 Oxygen therapy ( NRM at 15 L/ min)
 Positive pressure ventilation ( invasive or non invasive)
 Larson’s manoeuvre – breaks laryngospasm by pressing between mastoid
process and ramus of mandible
 Succinylcholine in low doses of 0.5- 1 mg/kg helps break laryngospasm
with low doses of propofol.
 Steroids (Dexamethasone/ Hydrocortisone )
Reduction of Preload
• Loop diuretics (Furosemide )
• Betaagonists- acts on cellular level and removes fluid by cation
transport mechanism
• Morphine

Reduction of Afterload
• ACE inhibitors
• Angiotensin II receptor blockers
• Nitroprusside

Ionotropic support
• Dobutamine
• Dopamine
• Norepinephrine
Conditions that complicate PE must also be corrected
• Infection
• Acidosis
• Renal failure
• Anemia
Differential diagnosis of NPPE
• Cardiogenic PE
• Anaphylaxis
• Acute lung injury
• Aspiration
• Neurogenic PE
• Covid lung
• Sympathetic crashing Acute PE ( Takotsubo syndrome – TTS)
• Fluid overload