2) Hypercarbic respiratory failure is characterized by alveolar hypoventilation and respiratory acidosis. Hypercarbic respiratory failure results from decreased minute ventilation and/or increased physiologic dead space. Conditions associated with hypercarbic respiratory failure include neuromuscular diseases (e.g., myasthenia gravis), disease processes causing diminished respiratory drive (e.g., drug overdose, brainstem injury), and respiratory diseases associated with respiratory muscle fatigue (e.g., exacerbations of asthma and chronic obstructive pulmonary disease [COPD]). In acute hypercarbic respiratory failure, PaCO2 is typically >50 mmHg. With acute-on-chronic respiratory failure, as is often seen with COPD exacerbations, considerably higher PaCO2 values may be observed. The degree of respiratory acidosis, the pt’s mental status, and the pt’s degree of respiratory distress are better indicators of the need for mechanical ventilation than a specific PaCO2level in acute-on-chronic respiratory failure.

Hypercarbic respiratory failure is characterized by alveolar hypoventilation and respiratory acidosis.

Hypercarbic respiratory failure results from decreased minute ventilation and/or increased physiologic dead space. Conditions associated with hypercarbic respiratory failure include neuromuscular diseases (e.g., myasthenia gravis), disease processes causing diminished respiratory drive (e.g., drug overdose, brainstem injury), and respiratory diseases associated with respiratory muscle fatigue (e.g., exacerbations of asthma and chronic obstructive pulmonary disease [COPD]). In acute hypercarbic respiratory failure, PaCO2 is typically >50 mmHg. With acute-on-chronic respiratory failure, as is often seen with COPD exacerbations, considerably higher PaCO2 values may be observed. The degree of respiratory acidosis, the pt’s mental status, and the pt’s degree of respiratory distress are better indicators of the need for mechanical ventilation than a specific PaCO2 level in acute-on-chronic respiratory failure.

 

 

This type of respiratory failure is a consequence of alveolar hypoventilation and results from the inability to eliminate carbon dioxide effectively.

Mechanisms are categorized by

  • impaired central nervous system (CNS) drive to breathe
    • drug overdose
    • brainstem injury
    • sleep-disordered breathing
    • severe hypothyroidism.
  • impaired strength with failure of neuromuscular function in the respiratory system,
  • and increased load(s) on the respiratory system. Reduced strength can be due to impaired neuromuscular transmission (e.g., myasthenia gravis, Guillain-Barré syndrome, amyotrophic lateral sclerosis) or respiratory muscle weakness (e.g., myopathy, electrolyte derangements, fatigue).

The overall load on the respiratory system can be subclassified into resistive loads (e.g., bronchospasm), loads due to reduced lung compliance (e.g., alveolar edema, atelectasis, intrinsic positive end-expiratory pressure [auto-PEEP]—see below), loads due to reduced chest wall compliance (e.g., pneumothorax, pleural effusion, abdominal distention), and loads due to increased minute ventilation requirements (e.g., pulmonary embolus with increased dead-space fraction, sepsis).

The mainstays of therapy for type II respiratory failure are directed at reversing the underlying cause(s) of ventilatory failure. Noninvasive positive-pressure ventilation with a tight-fitting facial or nasal mask, with avoidance of endotracheal intubation, often stabilizes these patients. This approach has been shown to be beneficial in treating patients with exacerbations of chronic obstructive pulmonary disease; it has been tested less extensively in other kinds of respiratory failure but may be attempted nonetheless in the absence of contraindications (hemodynamic instability, inability to protect the airway, respiratory arrest).

 

 

 

 

2. Treatment

Treatment for both Type 1 and Type 2 ARF is aimed at stabilizing and reversing the derangements in the patient's ability to properly exchange gases in the lung. Diagnosing and treating the underlying issue is important, but acute strategies to augment oxygenation and support the ventilatory release of CO2 must also be utilized to relieve the patient's symptoms and prevent organ failure.

In patients with Type 1 ARF, providing supplemental oxygen is key. This can be done most easily through a nasal cannula, the use of which allows patients to continue to eat, drink, and speak easily. Unfortunately, since much of the oxygen supplied is lost to the air around the patient, oxygen by nasal cannula is only useful for patients who require low flow rates (2–5 L) to support their oxygen levels. Patients who require higher flow rates of oxygen require venturi masks, which can deliver FiO2s of up to 50% or non-rebreather masks, which have a 1-way valve that prevents exhaled gases from diluting the delivered oxygen, resulting in 80% to 90% O2 concentrations. All of these methods of increased oxygen delivery should be used cautiously in patients with chronic lung disease, in whom an increased pO2 can result in the loss of their hypoxic drive and subsequent retention of pCO2. Although these patients may initially present as Type 1 ARF, they may need treatment strategies more in line with Type 2 ARF patients, as described below. Patients exhibiting severe levels of hypoxia, unstable vital signs, mental status changes that make them unable to protect their airway, or stridor should proceed immediately to intubation and mechanical ventilation.

Patients with Type 2 ARF require ventilatory support so that they can “blow off” their excess CO2. They may also need supplemental oxygen. As above, patients who are hemodynamically unstable or unable to protect their airway should be intubated and ventilated. In more stable patients, a course of noninvasive ventilation can be very helpful. Two types of noninvasive ventilation are commonly used—continuous positive airway pressure (CPAP) masks and bilevel positive airway pressure (BiPAP) masks.

CPAP masks are tight-fitting apparati that support the patient's ventilatory effort by adding a few centimeters of pressure to the air they breathe. This decreases the workload of breathing and gives patients some rest so that they can improve their ventilatory effort. Supplemental levels of oxygen can be given through the mask if needed. BiPAP masks provide heavier pressure with inhalation and a lower level of pressure with exhalation. This decreases the workload of breathing and improves gas exchange by preventing alveolar collapse on exhalation.

It is important to remember that noninvasive methods of supporting ventilation are only for temporary use while the underlying cause of ARF is diagnosed and treated. Patients who are on CPAP or BiPAP therapy for ARF should be reassessed with an ABG 1 hour after beginning treatment. If significant improvement in their pCO2 and pO2 levels is not seen after this period of time, patients should be intubated and mechanically ventilated.

 

ARF is defined as a sudden (minutes to hours) inability of the lungs to maintain normal respiratory function, resulting in abnormal arterial oxygen or carbon dioxide levels.

Whether classified as Type 1 (hypoxemic) or Type 2 (hypercarbic), ARF represents a major immediate threat to homeostasis and is a medical emergency.

Patients with Type 1 ARF have hypoxemia as their predominant blood gas abnormality. Typically, these patients are anxious and intensely focused on relieving their dyspnea. When you attempt to obtain their history, they may not be able to cooperate, repeating phrases like “I can't breathe” or “Help me.” You may note use of accessory muscles of respiration and, in severe cases, cyanosis. The patient may exhibit unstable vital signs as well. Your differential should include parenchymal and interstitial disease (pneumonia, aspiration, COPD or CHF exacerbation, ARDS) as well as diseases that can cause an acute right-to-left shunt (pulmonary embolism).

Patients with Type 2 ARF have high pCO2 levels as their predominant blood gas problem. They may be hypoxemic as well. These patients can exhibit a “narcosis,” appearing confused, intoxicated, or unresponsive. On physical examination, you may find a tremor or asterixis, peripheral vasodilation with pink nail beds, and significant bradycardia or sinus pauses. Your differential should include disease states that can induce a shallow or inadequate respiratory effort such as asthma or COPD exacerbation in a patient who has “tired out,” neuromuscular issues such as Guillain-Barré syndrome, oversedation with narcotic medications, strokes or brain stem lesions, and structural issues such as severe kyphoscoliosis. In the hospital setting, a few of these issues can combine to turn a chronic condition into an acute problem. For instance, a patient with morbid obesity and resultant sleep apnea who is then hospitalized for a knee replacement and given narcotics for pain control could develop significant hypercarbia due to an acute worsening of the sleep apnea from the sedating effects of the analgesics.

Mechanical Ventialtion

  • ABGs are essential for the correct diagnosis and treatment of ARF, and doctors should not hesitate to order them when appropriate.
  • Do not hesitate to intubate and mechanically ventilate a patient with ARF who is not appropriate for or not responding to noninvasive ventilation. A calm, organized intubation is much safer and results in better clinical outcomes than an emergent intubation done after a patient has become unstable or suffered a cardiopulmonary arrest.
  • Many patients have undiagnosed chronic hypoxia with few clinical signs or symptoms. When hospitalized, the addition of supplemental oxygen, sedating medications, or the stress of an acute illness can cause hypercarbic ARF, which often manifests clinically as altered mental status or delirium.

 

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