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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

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

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.

CAUSES OF HYPERCAPNIA

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

Increased Work of Breathing

Fatigue and Anxiety

Decreased cough
Decreased tidal volumes
Atelectasis, pneumonia
Added catechol release

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)

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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