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3)
ADULT
RESPIRATORY DISTRESS SYNDROME (LOW
PRESSURE PULMONARY EDEMA)
ARDS
is the name given to the clinical
manifestation of a number of indirect
lung injury states characterized by
dyspnea, severe hypoxemia, and
decreased lung compliance with
radiographic evidence of diffuse
bilateral pulmonary infiltrates.
Alveolar consolidation with fluid,
protein, and inflammatory cells in the
presence of a normal capillary or
wedge pressure is also a
characteristic finding, i.e., low
pressure pulmonary edema. The altered
permeability results in a rapid
movement of fluid from plasma to
interstitial space with even a normal
capillary (wedge) pressure. The causes
and differential diagnosis of ARDS are
presented.
Adult Respiratory Distress Syndrome
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Causes
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Differential
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- Tissue
inflammation
- Infection-sepsis
- Non-lung
trauma
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- High
pressure edema
- Inhalation
injury
- Pneumonia
- Focal
atelectasis
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Pathophysiology
and Diagnosis
The
lung damage is the result of a
systemic process initiated by burn
tissue, infection or inflammation
rather than a direct lung injury.
However, the term "ARDS" is
commonly but inappropriately used to
describe direct lung injury processes,
such as an inhalation injury. There
are probably several distinct ARDS
state, each with a different cause.
Although the pathophysiology may be
extremely complex and the etiologic
agents varied, the presenting signs
and symptoms for the ARDS states are
nearly identical. The hypoxemia
produced is characteristically
refractory to an increase in
fractional inspired oxygen, indicating
increased shunting. In addition, the
degree of shunt is not directly
correlated with the degree of
increased water content, as is the
case with cardiogenic edema.
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Diagnosis
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- Progressive
hypoxemia, shunt
- Decreased
lung compliance
- Bilateral
diffuse lung infiltrate
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Typical
histologic findings with ARDS which
includes alveolar inflammation,
thickened septal from protein leak
(pink), congestion and decreased
alveolar volume
There
is definitely a significant
ventilatory impairment or airways
component to the disease process not
related to water. There is a decrease
in dynamic compliance and functional
residual capacity resulting in
increased ventilation to perfusion
mismatch, probably due to
mediator-induced broncho constriction.
ARDS
Treatment Summary
Administer
oxygen: maintain oxygen saturation
more than 90%
Determine and delete source of
lung response
Maintain perfusion but avoid
volume overload
- Phase
2 (2-7 days post-onset)
Administer
oxygen; maintain oxygen saturation
more than 90%
May need positive airway pressure
(PEEP, CPAP)
Avoid volume overload (consider
pulmonary artery catheter)
Requires
positive pressure ventilation; add
PEEP
Needs pulmonary artery catheter
Adjust PEEP, tidal volume to
improve static compliance and
arterial oxygen tension but not
impair oxygen delivery
Maintain wedge pressure below
15mmHg, preferably 10 to 12 mmHg.
Maintain blood volume and
hemoglobin

Typical
patterns of ARDS with diffuse internal
infiltrates
| Positive
end-expiratory pressure |
| Advantages
- Increases functional
residual capacity
-
Recruits additional lung
units improving compliance
- Reduces
pulmonary shunt fraction
- Allows
for a decrease in FIO2
- Can
decrease preload in
congestive heart failure
Disadvantages
- Increase mean airway
pressure leading to reduced
venous return
- Can
increase VD/VT
by impairing perfusion to
hyper expanded
lung
- Can
increase pulmonary vascular
resistance and right-heart
dsyfunction
- Altered
renal blood flo with
increase in ADH release
-
Barotrauma caused by
increased pressure
Primary
Indications
- Treat hypoxemia when
patient already receiving an
FIO2 of less
than or
equal to 0.5 and with
bilateral diffuse pulmonary
infiltrates
- Treat a
shunt of less than or equal
to 20% in patient with
diffuse
disease
- To
maintain FRC after airway
injury such as smoke
inhalation
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| VD/VT,
physiologic deadspace ratio;
ADH, antidiuretic hormone;
FRC, functional residual
capacity. |
Common
Pitfalls
Underestimation
of Risks for Pneumonia:
Once
resuscitation is completed and the
patient has become stabilized and is
beginning to be more active, there is
a tendency to be lulled into
complacency regarding pulmonary
support. The patient remains at high
risk for pneumonia for several weeks.
Underestimation
of Increased Ventilatory Requirements
in
Perioperative
Period:
Maintenance
of a "normal" minute
ventilation in the perioperative
period is not adequate in a patient
generating up to twice the normal
amount of carbon dioxide. Hypercapnia
in the intraoperative or early
postoperative period with its
resultant massive catecholamine
release can almost always be avoided
by maintaining preoperative
ventilatory needs in the intra- and
postoperative period.
Underestimation
of the Workload of Breathing During
the
Hypermetabolic
State:
A
two- to threefold increase in minute
ventilation is a substantial work
load. Ventilatory assist may be needed
and should be initiated before
respiratory deterioration.
Underutilization
of the Tracheostomy:
Although
a tracheostomy is usually not
indicated in the first several days
and is contraindicated through burn
tissue, its use for chronic
respiratory support is very
advantageous. A tracheostomy through a
non-burn or excised and grafted skin
can improve pulmonary toilet, improve
rehabilitation efforts by physical
therapy, and will improve comfort.
THIS
CONCLUDES THE END
OF PULMONARY PROBLEMS
 
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