PULMONARY

EDEMA
PRESENTED BY: MOHAMMED ELIAS
INTRODUCTION
Fluid accumulation in air spaces and parenchyma of the
lungs.
This Leads to impaired gas exchange and may cause
respiratory failure.
 A pathophysiologic condition, not a
disease
Fluid in and around alveoli
Interferes with gas exchange
Increases work of breathing
Two Types
Cardiogenic (high pressure)
Non-Cardiogenic (high permeability)
MECHANISMS OF FLUID ACCUMULATION

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, which is determined by the protein
concentration in the blood, favors movement of fluid into the
vessel.
TYPES

Noncardioge
Cardiogenic
nic
Pulmonary
Pulmonary
Edema
Edema
CARDIOGENIC PULMONARY EDEMA

Cardiac abnormalities

increase in pulmonary venous pressure

Hydrostatic pressure is increased

fluid exits the capillary

Pulmonary edema
PRESENTATION

Symptoms
dyspnea
including orthopnea and paroxysymal nocturnal dyspnea (PND)
Physical exam
bibasilar inspiratory crackles
due to air expanding fluid-filled alveoli
rusty-colored sputum
due to rupture of pulmonary capillaries from elevated hydrostatic
pressure
wheezing
due to peribronchiolar edema
"cardiac asthma"
 Immediate, aggressive therapy is mandatory for survival. The following measures should
be instituted as simultaneously as possible for cardiogenic pulmonary edema:
Administer 100% O2by mask to achieve PaO2>60 mmHg; if inadequate, use positive-
pressure ventilation by face or nasal mask, and if necessary, proceed to endotracheal
intubation.
Reduce preload:
Seat pt upright to reduce venous return, if not hypotensive.
Intravenous loop diuretic (e.g.,furosemide, initially 0.51.0 mg/kg); use lower dose if pt does not take
diuretics chronically.
Nitroglycerin (sublingual 0.4 mg 3 q5min) followed by 520 g/ min IV if needed.
Morphine24 mg IV; assess frequently for hypotension or respiratory depression;naloxoneshould be
available to reverse effects ofmorphineif necessary.
Consider ACE inhibitor if pt is hypertensive, or in setting of acute MI with heart failure.
Consider nesiritide (2-g/kg bolus IV followed by 0.01 g/kg per min) for refractory symptomsdo not use
in acute MI or cardiogenic shock.

Inotropic agents are indicated in cardiogenic pulmonary edema and severe LV

dysfunction:dopamine,dobutamine,milrinone(Chap. 11).
The precipitating cause of cardiogenic pulmonary edema (Table 13-1) should be sought
and treated, particularly acute arrhythmias or infection. For refractory pulmonary edema
associated with persistent cardiac ischemia, early coronary revascularization may be
life-saving. For noncardiac pulmonary edema, identify and treat/remove cause
MANAGEMENT
TAKE HOME POINTS
Take-home points: 1. Elevation of pulmonary wedge
pressures helps to differentiate cardiogenic from non-
cardiogenic causes of pulmonary edema. 2. CXR, ECG,
and ABG are indicated in most patients. History and
physical exam can help differentiate causes. 3. For
treatment think: L-M-N-O-P (Lasix-Morphine-Nitro-
Oxygen-Position/Positive pressure ventilation)