III_B.  HYPERMETABOLISM UNDUCED RESPIRATORY DYSFUNCTION (Power Failure)

Pathophysiology:

There are a group of patients who develop further respiratory dysfunction as a result of the added metabolic stress of the hypermetabolic-catabolic state after burns.^97-99  This process of respiratory fatigue or power failure is most evident in the elderly and the patient with inhalation injury or other pre-existing lung problems like COPD.  The added work of breathing and need for increased gas exchange can exceed their lung capacity.

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 both large burns and the inflamed lung of smoke inhalation.^99,100 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. Lean mass loss is significant.^101-103 Chronic pain and anxiety can also 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.  The intense systemic inflammatory response, also present, adds to the increased pulmonary demands.

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 nosocomial pneumonia as well as hypercapnia.  The increased CO₂ production is difficult to manage if lungs are compromised.^104-107

A common period for fatigue to occur is in the perioperative period.  Underestimation of the increased ventilatory needs of the burn patient can lead to hypercapnia during the anesthesia period.  The immediate postoperative period is the most vulnerable time because oxygen consumption and carbon dioxide production return to or exceed preoperative values nearly immediately after the anesthetic has been turned off.¹⁰⁸  However, the return of chest wall muscle and diaphragm muscle function can lag for several hours after the anesthesia period.^109-111    The patient is often assumed to be ventilating adequately if a minute ventilation of 5 to 6 L is being generated.  This volume, however, is often inadequate for the carbon dioxide production.  The resulting hypercapnia is difficult to correct in view of the need to increase alveolar ventilation even further.  An increase in arterial carbon dioxide tension and resulting acidosis produces an intense catechol release, anxiety, and a further increase in oxygen demands and carbon dioxide production.¹⁰⁰  An additional increase in carbon dioxide will also be produced if an excess amount of carbohydrate is infused.  The respiratory quotient for carbohydrate burned for energy is 1.0 and for excess carbohydrate conversion to fat the value approaches 8.0.

Diagnosis

Dyspnea occurs if the ability to adequately remove carbon dioxide is impaired and hypercarbia develops. Fatigue develops if lung mechanics are not adequate to clear carbon dioxide with a reasonable work effort, i.e., if the dead space ventilation to tidal volume ratio (v_D/V_T) is increased or more work per breath is required.

Alveolar ventilation = total ventilation – dead space ventilation

If dead space remains constant but tidal volume decreases due to fatigue, a further increase in rate will be required, which leads to more fatigue.  Fatigue with its effects on impaired cough and a decrease in tidal volume, is often subtle, with the first clear evidence being a deterioration in blood gases or a new infiltrate on radiographs.^113-117

The remaining differential diagnosis for hyperiopnia during this period includes: an increase in carbon dioxide production, or an increase in dead space ventilation, v_D/V_T.^113-117.

Treatment

Protection of the lung against processes that will impair function is the best form of support.  Controlling edema and infection while maintaining optimum 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 v_D/V_T due to low blood volume or excessive positive end-expiratory pressure (PEEP) can be in part corrected by volume loading.^113-117

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