MORCORE

KEYWORDS

PULMONARY EDEMA, ACUTE MANAGEMENT

Keywords: Pulmonary edema
Author: Kristina Eng MD
Date 1/15/12

Introduction/pathophysiology
*This brief review will focus on the treatment and management of cardiogenic pulmonary edema*
Pulmonary edema results from transudation of fluid from pulmonary capillaries  interstitial space 
alveoli

Pathophysiology
Fluid in interstitial space and alveoli = extravascular lung water
Movement of water across pulmonary capillaries is similar to what occurs in other capillary beds
and can be expressed by Starling equation:
o
 Q – net flow across the capillary
 K – filtration coefficient
 Pc’ and Pi – capillary and interstitial hydrostatic pressure
 πc’ and πi – capillary and interstitial oncotic pressure
o Normally, forces favoring transudation of fluid are balanced by forces favoring
reabsorption
o Net amount of fluid that moves out of pulmonary capillaries is small (10-20 ml/h in adults)
and is rapidly removed by pulmonary lymphatics
o Net movement of water becomes positive when the normally negative Pi becomes
positive relative to atmospheric pressure
 Because of lung’s capacity to increase lymph flow, pulmonary interstitium usually
accommodates large increases in capillary transudation before Pi becomes
positive
 When reserve capacity is exceeded, pulmonary edema develops
Stages of pulmonary edema
Stage Physiology Signs/symptoms CXR findings
I Only interstitial edema Decreased pulmonary Increased interstitial
present compliance  markings
tachypnea
Peribronchial cuffing
II Fluid fills interstitium
and beings to fill alveoli
III Alveolar flooding – Large increase in A-a “Butterfly pattern” –
many alveoli no longer gradient bilateral perihilar
contain air distribution of infiltrates
Dyspnea
Most prominent in

Pulmonary edema
 dependent areas Hyperventilation
Hypoxemia
Hypocapneia
IV Airway frothing Severe hypoxemia Diffuse bilateral
interstitial infiltrates
Progressive
hypercapneia Air-bronchograms

Two main causes of pulmonary edema

o Increase in net hydrostatic pressure across capillaries  cardiogenic due to left
ventricular (LV) failure
 Ejection fraction of the LV falls when the stroke volume decreases
 Ventricle dilates with an increase in end-diastolic volume (LVEDV)
 This causes an increase in myocardial oxygen demand and increased potential
for ischemia
 Progressive LV dysfunction can be manifested by increasing heart rate as failing
LV tries to compensate for decreased stroke volume
 Pulmonary congestion  pulmonary edema as LVEDV and LV end-diastolic
pressure (LVEDP) increases
 Also, hypotension develops as cardiac output falls
 Hypotension + pulmonary edema = cardiogenic shock
o Increases in alveolar-capillary membrane permeability  non-cardiogenic
Several ways to determine etiology
o PAOP – if >18 mm Hg, indicates that hydrostatic pressure is involved
o Protein content of edema fluid – fluid due to hemodynamic edema has low protein
content; fluid due to permeability edema has high protein content
Less common causes
o Prolonged severe airway obstruction – pulmonary edema results from increase in
transmural pressure across pulmonary capillaries associated with markedly negative
hydrostatic pressure
o Re-expansion of collapsed lung – related to amount of air or liquid present in pleural
space (>1L associated with increased risk), duration of collapse (>24 hours associated
with increased risk), and rate of re-expansion
o High altitude – 2000-5000 meters; influenced by rate of asecent, onset is gradual but
within 48-72 hours
o Pulmonary lymphatic obstruction
o Severe head injury – neurogenic pulmonary edema related to increase in sympathetic
tone, causing severe pulmonary hypertension  disruption of alveolar/capillary
membrane
o Drug-induced pulmonary edema - Can occur after administration of many drugs,
especially opiates (heroin) and cocaine

Anesthetic management

Pulmonary edema 2
Ultimately, management involves decreasing the pressure in the pulmonary capillaries
If identified preoperatively, elective surgery should be delayed and efforts should be made to
optimize cardiorespiratory function prior to returning
ABC
o 100% oxygen
o Auscultate to determine airway patency
o Consider intubation for patients with significantly increased work of breathing
 If ventilated, maintain tidal volumes in 6 ml/kg range to minimize lung
parenchymal trauma
o Blood pressure
o ST changes? – nondiagnostic ECG findings are more common in elderly, diabetics, and
those with previous myocardial infarctions
o Consider administration of small amounts of opiates in awake patient
Determine cardiogenic vs. noncardiogenic cause for pulmonary edema
o History of CHF? Valvular conditions? Other cardiac conditions?
o History of COPD? Pneumonia? ALI/ARDS? Other intrinsic lung disease?
Consider invasive monitoring, if not already present
Measures to improve left ventricular function
o Afterload reduction  may improve cardiac output
 IV nitroglycerin
Use intial low dose and gradually increase dose until mean SBP fall by
10-15%
Avoid SBP < 90 mm Hg – can cause frank signs of poor peripheral
perfusion
o Vasopressor/Inotropic support
 If patient initially hypotensive (SBP < 80 mm Hg), administer norepinephrine until
SBP ~ 90 mm Hg
Can also use dopamine
 Once BP reaches 90 mm Hg, add dobutamine to reduce requirement for
vasopressor
 Milrinone may be considered as inotrope but may require concomitant
vasopressor
o Consider cardiology consult for intra-aortic balloon counterpulsation
Correct fluid overload with diuretics
o Loop diuretics commonly used
 Monitor for electrolyte disturbances
Reduce pulmonary blood flow
o IV nitroglycerin will also reduce preload  decrease pulmonary congestion

Pulmonary edema 3
ACC/AHA algorithm for management of acute pulmonary edema, hypoperfusion,
and CHF

References:
American Heart Association: Guidelines 2000 for cardiopulmonary resuscitation and emergency
cardiovascular care: International consensus on science. Circulation 102:I-I204, 2000
Barash PG, Cullen BF, Stoelting RK. Clinical Anesthesia. Philadelphia, PA. Lippincott Williams and
Wilkins; 5th ed, 2006
Hines RL, Marschall K. Stoelting’s Anesthesia and Co-existing Disease. Philadelphia, PA: Churchill
Livingstone; 5th ed. 2008
Jessup M, Abraham W, Casey D, Feldman A, Francis G, Ganiats T, Konstam M, Mancini D, Rahko P,
Silver M, Stevenson L, Yancy C. 2009 Focused Update: ACCF/AHA Guidelines for the Diagnosis and
Management of Heart Failure in Adults. J Am Coll Cardiol. 2009;53:1343-1382
Morgan GE, Mikhail, MS, Murray M. Clinical Anesthesiology. New York, NY: McGraw-Hill; 4th ed, 2006

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