Pulmonary

Pulmonary Edema
Edema
RIANA SARI
BALAI BESAR KESEHATAN PARU
MASYARAKAT (BBKPM)
SURAKARTA

Pulmonary Edema:
Pathophysiology
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)

Mechanism: normal lung

Fluid and protein leakage (small gaps

between capillary endothelial

cells)alveolar interstitial space ( do not
enter the alveoli because the alveolar
epithelium is composed of very tight
junctions) proximally into the
peribronchovascular spacelymphatics
remove most of this filtered
Movement of larger plasma proteins is
restricted
hydrostatic force for fluid filtration across
the lung microcirculation is approximately
equal to the hydrostatic pressure in the

Mechanism: cardiogenic
rapid increase hydrostatic pressure

increased transvascular fluid filtration

elevated pulmonary venous pressure from
increased left ventricular end-diastolic
pressure and left atrial pressure.
Mild elevations of left atrial pressure (18 to
25 mm Hg) cause edema in the
perimicrovascular and
peribronchovascular interstitial spaces.
Left atrial pressure rises further (>25 mm
Hg), edema fluid breaks through the lung
epithelium, flooding the alveoli with
protein-poor fluid

Cardiogenic
Pulmonary Edema

increased pulmonary venous pressure without

left ventricular failure (eg. Mitral Stenosis)

increased pulmonary venous pressure
secondary to left ventricular failure
increased pulmonary capillary pressure
secondary to increased pulmonary arterial
pressure

Cardiogenic Pulmonary
Edema: Etiology
Left ventricular failure
Valvular heart disease
Stenosis
Insufficiency

Hypertensive crisis (high afterload)

Volume overload

Increased Pressure in Pulmonary Vascular Bed

Mechanism:
noncardiogenic
increase in the vascular permeability of

the lung,
increased flux of fluid and protein
Noncardiogenic pulmonary edema : high
protein content
The net quantity of accumulated
pulmonary edema : balance between the
rate is filtered into the lung and the rate
removed from the air spaces and lung
interstitium.

Non-cardiogenic Pulmonary Edema

Decreased plasma oncotic pressure

Increased negativity of interstitial pressure
Altered alveolar-capillary membrance

permeability(ARDS)
lymphatic insufficiency
others: high-altitude, neurogenic, narcotic
overdose

Non-Cardiogenic Pulmonary
Edema: Etiology

Toxic inhalation
Near drowning
Liver disease
Nutritional deficiencies
Lymphomas
High altitude pulmonary edema
Adult respiratory distress syndrome
Increased Permeability of Alveolar-Capillary Walls

Pulmonary Edema: Signs

&Symptoms

Dyspnea on exertion
Paroxysmal nocturnal dyspnea
Orthopnea
Noisy, labored breathing
Restlessness, anxiety
Productive cough (frothy sputum)
Rales, wheezing
Tachypnea
Tachycardia

Chest Radiography

Management of Non-Cardiogenic
Pulmonary Edema

Position
Oxygen
PPV / Intubation
CPAP
PEEP

IV Access; Minimal fluid administration

Treat the underlying cause
Diuretics usually not helpful; May be harmful

Transport

Definition of ARDS
acute onset
bilateral infiltrates on chest radiography
pulmonary-artery wedge pressure <= 18mmHg
or absence of clinical evidence of left atrial
hypertension
acute lung injury: PaO2:FiO2 <= 300
ARDS: PaO2:FiO2 <= 200
(definition recommended by American-European Consensus Conference Committee)

Clinical Features of ARDS

rapid onset
severe dyspnea
severe tachypnea
arterial hypoxemia refractory to O2 therapy
decreased pulmonary compliance

Radiographic Features

in hydrostatic pulmonary edema

interstitial edema (15-25 mmHg)
mild enlargement of peribronchovascular
spaces
appearance of Kerley lines

alveolar flooding (>25 mmHg)

sudden extension of edema into alveolar
spaces, creating tiny nodular or acinar areas
of increased opacity

in ARDS
Exudative stage
interstitial edema, followed rapidly by perihilar areas of
increased opacity

Proliferative stage
organization of the fibrinous exudate
inhomogeneous pattern of ground-glass areas of
increased opacity

Fibrotic stage
subpleural and intrapulmonary cystic lesion be
observed

Swan-Ganz catheters
Pulmonary-artery wedge pressure:
cardiogenic: high, > 18 mmHg
non-cardiogenic: normal or low, <=18
mmHg

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