The cause of hypercapnia is often independent of hypoxemia. Both can cause altered mental status.

” The clinical manifestations of hypoventilation syndromes usually are nonspecific, and in most cases, they are secondary to the underlying clinical diagnosis. Manifestations vary depending on the severity of hypoventilation, the rate of development of hypercapnia, and the degree of compensation for respiratory acidosis that may be present.” Hypoventilation Syndromes Clinical Presentation

Type 2 ( Ventilatory /Hypercapnic Respiratory Failure):

Physiologic causes of Hypercapnia:

  1. Increased COproduction (fever, sepsis, burns, overfeeding)
  2. Decreased alveolar ventilation
  • decreased RR
  • decreased tidal volume (Vt)
  • increased dead space (Vd)

The cause of hypercapnia is often independent of hypoxemia. Hypercapnia results from either increased CO2production secondary to increased metabolism (sepsis, fever, burns, overfeeding), or decreased CO2 excretion. CO2excretion is inversely proportional to alveolar ventilation (VA). VA is decreased if total minute ventilation is decreased – secondary to either a decreased respiratory rate (f) or a decrease in tidal volume (Vt); or if the deadspace fraction of the tidal volume is increased (Vd/ Vt).

PACO2 = k x  VCO2 / VA, therefore….

PACO2 = k x  VCO2 / VE(1 –  Vd/ Vt) = k x  VCO2 / (Vt x f) (1-  Vd/ Vt)

since VA = (Vt –  Vd)f

where VCO2 is carbon dioxide production, VA is alveolar ventilation, VE is total minute ventilation, and Vd/Vt is the fraction of dead space over tidal volume.

Causes of decreased alveolar ventilation:

  1. Decreased CNS drive ( CNS lesion, overdose, anesthesia). The patient is unable to sense the increased PaCO2. The patient “won’t breathe”.
  2. Neuromuscular disease ( Myasthenia Gravis, ALS, Guillian-Barre , Botulism, spinal cord disease, myopathies, etc.). The patient is unable to neurologically signal the muscles of respiration or has significant intrinsic respiratory muscle weakness. The patient “can’t breathe”.
  3. Increased Work Of Breathing leading to respiratory muscle fatigue and inadequate ventilation. 
    • Asthma/ COPD
    • Pulmonary fibrosis
    • Kyphoscoliosis
  4. Increased Physiologic Dead Space (Vd). When blood flow to some alveoli is significantly diminished, CO2 is not transferred from the pulmonary circulation to the alveoli and CO2 rich blood is returned to the left atrium. Causes of increased dead space ventilation include pulmonary embolus, hypovolemia, poor cardiac output, and alveolar over distension. Dead space can be quantified using the Bohr equation and a Douglas bag, or with the use of a “metabolic cart”.

Evaluation of Hypercapnia:

The physiologic reasons for hypercapnia can be determined at the bedside.

  • Minute Ventilation, measurements of [RR] Respiratory Rate , Vt,
  • Assessment of patient’s work of breathing – accessory respiratory muscle use, indrawing, retractions, abdominal paradox. etc…

Clinical Signs and Symptoms of Acute Respiratory Failure

Clinical manifestations of respiratory distress reflect signs and symptoms of hypoxemia, hypercapnia, or the increased work of breathing necessary. These include

  • Altered mental status (agitation, somnolence)
  • Peripheral or central cyanosis or decreased oxygen saturation on pulse oximetry
  • Manifestations of a “stress response” including tachycardia, hypertension, and diaphoresis
  • Evidence of increased respiratory work of breathing including accessory muscle use, nasal flaring, intercostal indrawing, suprasternal or supraclavicular retractions, tachypnea
  • Evidence of diaphragmatic fatigue (abdominal paradox)
  • Abnormal arterial blood gas results

Management of Acute Respiratory Failure

The management of acute respiratory failure can be divided into an urgent resuscitation phase followed by a phase of ongoing care. The goal of the urgent resuscitation phase is to stabilize the patient as much as possible and to prevent any further life-threatening deterioration. Once these goals are accomplished the focus should then shift towards diagnosis of the underlying process, and then the institution of therapy targeted at reversing the primary etiology of the ARF.


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