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2)
HYPER METABOLISM-INDUCED
RESPIRATORY
FATIGUE
(POWER FAILURE)
Pathophysiology:
The
increase in oxygen consumption and
carbon dioxide production during this
period will require increased gas
exchange relative to that seen in the
previous periods. A 50 to 100%
increase in carbon dioxide production
will be seen with burns in excess of
50% total body surface. In addition,
the severe catabolism, initiated by
the inflammatory response, can lead to
not only extremity weakness, but also
weakness of the chest wall muscle.
Chronic pain and anxiety will lead to
sleep deprivation and fatigue. Common
causes of impaired oxygenation during
this period are heart failure leading
to lung edema and
hypoventilation-induced atelectasis as
fatigue develops. The major problem
during this period is, however,
usually not hypoxemia but rather
hypercapnia because carbon dioxide
removal is directly dependent on
alveolar minute ventilation.
A
doubling of carbon dioxide production
means a doubling of alveolar
ventilation to maintain a normal PaCO2.
Increased ventilation means increased
work of breathing, especially if a
decrease in compliance or an increase
in dead space is also present. Large
tidal volumes are necessary to
maintain adequate alveolar ventilation
because small tidal volumes ventilate
little more than airway dead space.
Increased tidal volumes require an
increased inspiratory force and the
added work must be sustained 24 hours
a day. If fatigue develops, impaired
clearance of secretions will also
occur, which can lead to nosomial
pneumonia as well as hypercapnia.
Diagnosis:
- Shortness
of breath
- Increasing
respiratory rate
- Decreasing
tidal volume
- Use
of accessory muscles
- Signs
of patient patient
fatigue - weak cough
- Hypercarbia
- Diffuse
atelectasis on X-ray
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Alveolar
ventilation - total ventilation - dead
space ventilation
Is
the Cause an Increased Carbon Dioxide
Production or Increased Dead Space?
If
mechanical factors are not present,
the differential diagnosis includes:
an increase in carbon dioxide
production, and an increase in dead
space ventilation, VD/VT.
Increased
dead space can be due to a decrease in
regional lung perfusion relative to
ventilation, often due to lung over
expansion. Vascular occlusion from
pulmonary emboli must also be
considered. The distinction can be
made by directly measuring carbon
dioxide production and then
calculating VD/VT.
Thus, diagnosis includes:
- Assessing
tidal volume, vital
capacity, inspiratory
force
- Measuring
carbon dioxide
production: VDVT,
respiratory quotient
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Serial
measurements of tidal volume, vital
capacity, and inspiratory force will
allow one to detect early
deterioration. In addition, the
measurements of carbon dioxide
production will allow one to determine
whether the production is in excess of
that predicted for the burn size
alone. Oxygen consumption can also be
measured directly using available
spirometric techniques or the Fick
method and the respiratory quotient
directly calculated.
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CAUSES
OF HYPERCAPNIA
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Extrapulmonary
- Impaired
Ventilatory Response to
CO2
- Central nervous
system-depressant drugs,
head trauma, starvation,
hypothyroidism,
hypophosphatemia, metabolic
alkalosis
-
Increased CO2 Production
-
Increased temperature (6% -
10% per C)
-
Increased muscle activity:
shivering, seizures
-
Increased respiratory
quotient from excess
carbohydrate calories
- Sepsis
Pulmonary
- Airway
obstruction
- Impaired
Chest Wall Motion
- Chest wall trauma,
instability
- Chest
wall pain, splinting
-
Neuromuscular disorders
-
Increased Dead space
Ventilation
- Shallow
breathing
-
Vascular obstruction,
pulmonary emboli
- Low
cardiac output, hypovolemia,
impaired perfusion
-
Positive-pressure
ventilation
-
Increased airway pressure,
impaired perfusion
|
| |
| Hypercarbia
in patients receiving
mechanical ventilation |
Correct
Mechanical Problems
Endotracheal tube leak,
plugging
Air leak
from lung, chest tubes
Leak in
ventilator
Airways
plugging
Correct
Increased Dead space
Treat
hypovolemia
Decrease
mean airway pressure
Control
pulmonary emboli
Correct
Increased CO2 production
Control
fever
Decrease
activity
Control
sepsis
Avoid
excess CHO leading to
increasing RQ
|
| CHO,
carbohydrate, RQ,
Respiratory Quotient |
| Mechanism
of Power Failure |
Increased
oxygen demands
Increased energy demands
Increased CO2 production
Catabolism induced
weakness
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Increased
Work of Breathing
|
Fatigue
and Anxiety
|
Decreased
cough
Decreased tidal volumes
Atelectasis, pneumonia
Added catechol release
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Respiratory
Distress
-
hypoxemia
- lung
sepsis
|
| |
Treatment
- Optimize
nutrition (avoid excess
CO2 production)
- Maintain
adequate rest periods
- Consider
partial ventilatory
assist to avoid fatigue
(tracheostomy useful)
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Protection
of the lung against processes that
will impair function is the best form
of support. Controlling edema and
infection while maintaining nutrition
and adequate rest as well as chest
wall exercise are key components.
Excess carbon dioxide production
should be controlled by avoiding
excess carbohydrate calories and
controlling excessive hyperthermia.
The nutrient mix should be well
controlled in order to avoid too few
or too many calories. Fatigue and
early evidence of respiratory
compromise should be treated with
assisted ventilatory support. An
increase in VDVT
due to low blood volume or excessive
positive end-expiratory pressure
(PEEP) can be in part corrected by
volume loading.
Partial
ventilatory support via a tracheostomy
may be useful, especially if the
anticipated problem will last several
weeks, as is the case with a large
body burn. Adequate rest must be
assured as well as control of pain and
anxiety, which can lead to a further
increase in catechols and resulting
hypermetabolism. The patient receiving
an anesthetic must be accurately
evaluated preoperatively to determine
intraoperative ventilatory needs. In
addition, added ventilatory support
should be provided in the early
postoperative period until the patient
can resume sufficient spontaneous
ventilation.
  
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