AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Respiratory acidosis occurs when the arterial partial pressure of carbon dioxide (PaCO₂) is elevated above the normal range (>44 mm Hg) leading to a blood pH less than 7.35.¹ Respiratory acidosis is not a specific disease. Instead, it is an abnormality that results from an imbalance between carbon dioxide (CO₂) production by the body and excretion by the lungs, providing adequate minute ventilation. A deficiency of minute ventilation can occur anywhere along the continuum of the respiratory system, from central initiation of ventilation to appropriate gas exchange at the capillary alveolar interface.

Respiratory acidosis may result from an acute or chronic process. Acute respiratory acidosis can be life threatening when a sudden and sharp increase in PaCO₂ is associated with severe hypoxemia and acidemia (see Equation 2). In contrast, chronic respiratory acidosis (>24 h) is characterized by a gradual and sustained increase in PaCO₂.

By definition, the diagnosis of respiratory acidosis requires measurement of the arterial PaCO₂ and pH. When the diagnosis is made, the cause should be thoroughly investigated.

Pathophysiology

PaCO₂ is directly proportional to CO₂ production and inversely proportional to alveolar ventilation. Alveolar ventilation is responsible for CO₂ elimination and is calculated when the respiratory frequency is multiplied by the difference between the tidal volume and the physiologic dead space. Respiratory acidosis results primarily when alveolar ventilation is decreased or if CO₂ production is increased.

Many clinical scenarios contribute to inadequate removal of CO₂ from the blood. A few examples include depressed central respiratory drive, acute paralysis of the respiratory muscles, acute parenchymal lung and airway diseases, and increased dead space or wasted ventilation. If breathing ceases, arterial CO₂ increases further at a rate of 3-6 mm Hg/min. In other cases, hypercarbia gradually develops as it does in a progressive neuromuscular disease, in worsening scoliosis leading to restrictive lung disease, or in chronic pulmonary diseases. In this scenario, persistently elevated PaCO₂ leads to effective compensatory mechanisms.

In rare instances, increased CO₂ production can exceed the patient's ability to compensate, leading to a respiratory acidosis. This situation occurs during hypermetabolic states, such as extensive burn injury, malignant hyperthermia, or fever when the patient is unable to increase minute ventilation. When PaCO₂ accumulates acutely, other organ systems are affected.

General physiologic and metabolic effects

CO₂ is carried in the blood in 3 forms: dissolved gas, bicarbonate, and protein bound. It diffuses freely across cell membranes, and this diffusion allows for its efficient transport from peripheral tissues to the lungs for excretion. When hypercapnia is present, this same property causes excess CO₂ to shift intracellularly and decrease intracellular pH. CO₂ normally combines with water (H₂O) to form carbonic acid (H₂CO₃), which then dissociates to release hydrogen ion [H⁺] and bicarbonate (HCO₃^-) (Equation 1). When a respiratory acidosis is present, excess CO₂ increases H₂CO₃ formation, shifting the equilibrium of the equation toward the accumulation of hydrogen ions.

Equation 1: CO₂ + H₂O ↔ H₂ CO₃ ↔ H⁺ + HCO₃^-

The body has several compensatory systems to minimize the decrease in pH. Intracellular proteins and inorganic phosphates are initially the most effective buffers. The most important blood buffer is hemoglobin. Deoxygenated hemoglobin readily accepts hydrogen ions to prevent substantial changes in pH, and approximately 10% of CO₂ is bound to hemoglobin to form carbaminohemoglobin.

Cellular buffering elevates plasma bicarbonate (HCO₃^-) only slightly and causes plasma HCO₃^- to increase 1 mEq/L for every 10-mm Hg increase in PaCO₂.

Renal compensation for sustained hypercapnia begins in 6-12 hours, but 3-5 days pass before maximal compensation occurs. The kidneys increase excretion of hydrogen ions (predominantly in the form of ammonium [NH₄⁺]) and chloride while retaining HCO₃^- and sodium (Na⁺). This process increases the plasma HCO₃^- concentration by approximately 3.5-4 mEq/L for every 10-mm Hg increase in PaCO₂. As a result, additional NaHCO₃^- is available to buffer free hydrogen ions. Because neonates and infants have a relatively large amount of hemoglobin and interstitial fluid for their body weight, their increase in plasma HCO₃^- concentrations and decrease in plasma hydrogen ion concentrations are greater than those of older children.

Chemoreceptors in the brainstem and in the carotid body rapidly detect changes in PaCO₂. CO₂ is a potent respiratory stimulant and elevated levels lead to an increase in minute ventilation to excrete increased quantities of CO₂ and normalize the pH. However, this effect is attenuated if the CO₂ level remains elevated for more than several hours. In general, acute respiratory acidemia causes no change or only a slight increase in extracellular potassium and phosphate levels.

Respiratory effects

When a patient develops a respiratory acidosis while breathing air, the alveolar gas equation predicts that hypoxemia will develop. The alveolar gas equation (Equation 2) states that the alveolar partial pressure of oxygen (P_AO₂) is equal to the partial pressure of inspired oxygen (P_iO₂) minus the quantity of alveolar partial pressure of CO₂ (P_ACO₂) divided by the respiratory quotient (RQ), as follows:

Equation 2: P_AO₂ = P_iO₂ - (P_ACO₂/RQ)

The RQ is the ratio of the volume of CO₂ expired to the volume of O₂ consumed by an organism (see nutrition effects on RQ below). In steady-state conditions, the human body produces CO₂ at a rate of approximately 200 mL/min and consumes O₂ at a rate of 250 mL/min; therefore, RQ = 0.8. If RQ is rounded to 1, the equation reduces to the following (Equation 3):

Equation 3: P_AO₂ = P_iO₂ - P_ACO₂

The P_iO₂ is the difference between the barometric pressure (PB) and the partial pressure of water vapor (PH₂O) multiplied by the fraction of inspired oxygen (F_iO₂), as shown below (Equation 4):

Equation 4: P_iO₂ = F_iO₂ (PB - PH₂O)

If the equation is rearranged, P_ACO₂ is ultimately dependent on the level of inspired O₂ (Equation 5):

Equation 5: P_ACO₂ = F_iO₂ (PB - PH₂O) - P_AO₂

Because PB at sea level is 760 mm Hg and PH₂O in the atmosphere is 47 mm Hg, when a person is breathing air (F_iO₂ = 0.21), the sum of P_ACO₂ and P_AO₂ adds up to approximately 150 mm Hg, as follows (Equations 6 and 7):

Equation 6: P_AO₂ = 0.21 (760 mm Hg - 47 mm Hg) - P_ACO₂

Equation 7: P_AO₂ + P_ACO₂ = 149.7 mm Hg

In the acute setting, PaCO₂ values higher than 80-90 mm Hg while the patient is breathing air are life threatening because of the associated hypoxemia. When the PaCO₂ exceeds 100 mm Hg, an iatrogenic or an acute on chronic condition is present. Hypoventilation can lead to clinically significant hypercarbia without hypoxemia only if a patient is breathing supplemental oxygen.

Consider the case of a child in the pediatric ICU who is breathing supplemental oxygen given by a mask (F_iO₂ = 0.80). The child has partial airway obstruction or central hypoventilation secondary to narcotic administration. Supplemental oxygen allows for an increased PaCO₂ given the principle of the alveolar gas equation without arterial desaturation. The profound acidemia associated with the hypercapnia can lead to bradycardia, the first sign of the problem. Some have used the term supercarbia to describe when the PaCO₂ is greater than 150 mm Hg. In this case, P_AO₂ = [0.80 (760 mm Hg - 47 mm Hg)] - 150 mm Hg = 420 mm Hg.

Hypercapnia is associated with increased pulmonary vascular resistance. However, the absolute CO₂ level does not have the greatest effect on pulmonary vascular tone; rather, decreased serum pH most likely mediates the effect. When hypercapnia is combined with acidemia and hypoxemia, resultant pulmonary vasoconstriction can be severe and life threatening.

Cardiovascular effects

Acute respiratory acidosis increases epinephrine and norepinephrine release. Several studies have shown that acute moderate hypercapnia produces a hyperdynamic state defined by tachycardia, high cardiac output, and reduced systemic vascular resistance. In experimental models, cardiac contractility decreases with acute respiratory acidosis. Some have proposed that the rapid development of intracellular acidosis interferes with the interaction between calcium and myofilaments. This adverse effect of acute moderate hypercapnia on myocardial contractility has not been seen in adult human studies. With severe acidemia at a serum pH of less than 7.20, the catecholamine response is blunted, and this change may contribute to a state of decreased cardiac output.

Supraventricular arrhythmias are increased in the presence of a severe respiratory acidosis, but these problems are most likely caused by concomitant hypoxemia, electrolyte shifts, and increased catecholamines rather than a direct hypercapnia-induced cardiac irritability. Cardiovascular symptoms of respiratory acidosis are often difficult to discern because of the concomitant effects of hypoxemia and metabolic acidosis.

Inhaled CO₂ gas can be administered to preoperative neonates with hypoplastic left heart syndrome and low systemic cardiac output associated with high arterial saturations (>85%). PaCO₂ is maintained above 40 mm Hg, and the patient is mechanically ventilated, sedated, and paralyzed to prevent a compensatory tachypnea. The inhaled CO₂ increases pulmonary vascular resistance, thereby shunting blood flow to the systemic circulation away from the pulmonary system, resulting in improved systemic oxygen delivery and cerebral oxygenation. Experimental evidence also suggests that hypercarbia may have some beneficial effects at assisting the mechanical recovery of hypoxic injured myocytes; however, further human clinical correlation is still needed.

CNS effects

The clinical manifestations of acute hypercapnia are primarily neurologic. Acute elevations of PaCO₂ greater than 60 mm Hg cause confusion and headache. PaCO₂ more than 70 mm Hg produces a hypercapnic encephalopathy or CO₂ narcosis manifesting as drowsiness, depressed consciousness, or coma. However, the neurologic changes associated with hypercarbia are reversible. In one report, children without hypoxemia but with severe respiratory acidosis (lowest pH was 6.76, and highest PaCO₂ was 269 mm Hg) did not have long-term adverse neurologic or developmental effects.²

Acute elevations in PaCO₂ increase intracranial pressure by increasing cerebral blood flow (CBF) and cerebral blood volume secondary to vasodilatation. With a PaCO₂ of 40-80 mm Hg, CBF increases 1-2 mL per 100 g of brain per minute for each 1-mm Hg increase in PaCO₂. A PaCO₂ of 80 mm Hg or more produced a maximal increase in CBF in anesthetized animals. During sustained hypercapnia, CBF returns to baseline after about 36 hours as brain extracellular pH is corrected.

In acute hypercapnia, CO₂ rapidly diffuses across the blood-brain barrier, which leads to accumulation of hydrogen ions in the CSF. This change in pH is rapidly detected by the brainstem, causing rapid compensation (ie, increased elimination of CO₂ by the lungs). If the CSF acidosis persists for several hours, CSF HCO₃^- levels gradually increase to normalize the pH. In general, the response of the cerebral circulation to PaCO₂ increases during development from the neonatal period to adulthood.

Frequency

See Background.

Mortality/Morbidity

The effects of respiratory acidosis vary according to the severity, the duration, the underlying disease, and the associated arterial saturation. The most important consideration may be the degree to which hypercarbia or the underlying disease adversely affects arterial oxygenation.

Race

No racial distribution is known.

Age

Respiratory acidosis can occur at any age.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

The following questions should be assessed:

• Does the patient have a history of headaches? With chronic hypercapnia, headaches typically occur at nighttime or when the patient awakens in the morning.
• Does the patient have disturbed sleep patterns? Chronic hypercapnia can disturb sleep patterns, leading to a reversed sleep-wake cycle.
• Is the patient irritable or anxious or is he or she having trouble concentrating?
• Does the patient have a possible or known exposure to sedatives (eg, narcotics, benzodiazepines, tricyclic antidepressants)? Is the patient recovering from a procedure in which general anesthesia was used?
• Does the patient have symptoms of neuromuscular weakness or paralysis?
• • Bulbar dysfunction suggesting myasthenia gravis
  • Proximal or distal weakness suggesting a myopathy or Guillain-Barré syndrome
  • Apnea associated with a traumatic injury suggesting an injury to the cervical spinal cord
• Does the patient have a long-standing pulmonary disease, such as bronchopulmonary dysplasia, CF, asthma, or emphysema?
• Does the patient have an acute change in mental status (eg, signs of stroke, postictal state)?
• • Is the change in mental status associated with a fever, which may suggest encephalitis or meningitis?
  • Does the patient have signs of increased intracranial pressure (eg, headaches, visual changes, emesis)?
• Does the patient have a potential for an anaphylactic reaction?
• Does the patient have a potential traumatic mechanism leading to brain injury?

Physical

• Neurologic findings
• • Early signs include anxiety, disorientation, confusion, and lethargy.
  • Somnolence or coma occurs when PaCO₂ is greater than 70 mm Hg.
  • Tremor, myoclonus, or asterixis are occasionally seen.
  • Brisk deep tendon reflexes are seen in mild-to-moderate respiratory acidosis.
  • Depressed deep tendon reflexes are seen in severe respiratory acidosis.
  • Papilledema or blurring of the optic disc may be present.
• Cardiovascular findings
• • Tachycardia
  • Bounding arterial pulses
  • Hypotension (severe respiratory acidosis or acidemia and hypoxemia)
• Skin findings
• • Warm, flushed, or mottled
  • Diaphoretic
• Respiratory findings
• • Acute hypercapnia is seen in association with increase work of breathing
  • Tachypnea, dyspnea, or deep labored breaths may be observed.
  • Accessory muscle use and nasal flaring are usually present.
  • With CNS or peripheral nervous system disease, respiratory distress may not be present.
  • Decreased aeration, crackles, wheezes, or other signs of airway disease may be observed.
  • Clubbing is a sign of chronic respiratory disease.

Causes

• CNS respiratory drive suppression causes include the following:
• • Trauma
  • Infection (eg, encephalitis, meningitis, respiratory syncytial virus)
  • Neoplasm
  • Stroke
  • Hypoxia
  • Toxins, overdose (eg, narcotics, alcohol)
  • Seizures - Postictal state
• Spinal causes include trauma (C-spine C3-C5, phrenic nerve function).
• Nerve causes include the following:
• • Spinal muscular atrophy
  • Guillain-Barré syndrome
  • Poliomyelitis
  • Phrenic nerve trauma
• Neuromuscular junction causes include the following:
• • Myasthenia gravis
  • Botulism
  • Neuromuscular blockade
• Muscle causes include muscular dystrophies.
• Airway causes include the following:
• • Loss of CNS control
  • • Brain injury
    • Toxin, overdose
  • Trauma
  • Angioedema
  • Tonsillar adenoid hypertrophy
  • Thermal or chemical burn
  • Foreign Body
  • Pharyngeal abscess
  • Epiglottitis
  • Paralyzed vocal cords
  • Congenital lesions
  • • Subglottic stenosis
    • Laryngomalacia
    • Craniofacial abnormalities
    • Tracheal rings
    • Vascular slings
  • Laryngotracheobronchitis (croup)
  • Neoplasm, mediastinal mass
  • Bronchiolitis
  • Asthma
• Acute lung injury causes include the following:
• • Pneumonia
  • Pulmonary edema
  • Lung contusion
  • Bronchiolitis
• Chronic lung disease causes include the following:
• • Bronchopulmonary dysplasia
  • CF
  • Chronic bronchitis
  • Chronic obstructive pulmonary disease
• Chest wall restriction and reduced respiratory compliance causes include the following:
• • Flail chest
  • Pneumothorax
  • Pleural effusions
  • Kyphoscoliosis
  • Abdominal distension
• Increased CO₂ production causes include the following:
• • Malignant hyperthermia
  • Extensive burns
  • Overfeeding

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• ABG analysis
• • The ABG is diagnostic of a respiratory acidosis.
  • The serum HCO₃^- level and pH can be helpful in distinguishing acute hypercapnia from chronic hypercapnia. If the pH is greater than 7.45, elevated PaCO₂ may compensate for metabolic alkalosis and not a primary process.
• Tests for acute respiratory acidosis
• • pH decreases 0.08 for every 10-mm Hg increase in PaCO₂.
  • HCO₃^- increases by 1 mEq/L for every 10-mm Hg increase in PaCO₂.
  • If PaCO₂ increases acutely to 80 mm Hg, the pH is 7.12 and the HCO₃^- value is 28 mEq/L.
• Tests for chronic respiratory acidosis
• • pH decreases 0.03 for every 10-mm Hg increase in PaCO₂.
  • HCO₃^- concentration equals 24 mmol/L ± 4 for every 10-mm Hg increase in PaCO₂ greater than 40 mm Hg.
  • For example, if the PaCO₂ is 80 mm Hg, the pH is 7.28, and the HCO₃^- value is 40 mEq/L ± 4.
• Evaluation of HCO₃^- resorption
• • The HCO₃^--resorption process is efficient.
  • If a patient with chronic hypercapnia has a pH of more than 7.20, a superimposed acute on chronic respiratory acidosis or concomitant metabolic acidosis is most likely occurring as well.
• Toxicology screen for narcotics, benzodiazepines, alcohol, or tricyclic antidepressants if indicated
• Electrolyte assessment for abnormalities associated with muscle weakness (eg, hypophosphatemia, hypokalemia, hypomagnesemia, hypocalcemia)

Imaging Studies

• Chest radiography findings may help in the diagnosis.
• CT scanning of the chest is indicated if the history and physical findings suggest primary pulmonary disease.
• CT angiography may be indicated to rule out pulmonary embolus.
• CT scanning or MRI of the brain is indicated if the history and physical findings suggest signs of an intracranial process.
• MRI of the spine may be indicated by the history and physical findings.

Other Tests

• Pulmonary function tests, including spirometry if the child can cooperate
• Electromyelography (EMG), if indicated to evaluate neuromuscular disease
• Polysomnography, or sleep study, to evaluate for obstructive or central sleep apnea, if indicated

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

• The goals of therapy are to remove the underlying cause and return the PaCO₂ level to baseline.
• If hypoxemia accompanies hypercapnia, oxygen should be administered.
• • Diagnosis and directed therapy need to accompany oxygen administration.
  • In chronic hypercapnia, supplemental oxygen therapy can worsen hypercapnia by reducing the respiratory drive and increasing dead-space ventilation due to a loss of hypoxic pulmonary vasoconstriction.
• Disease-specific interventions may be needed.
• • Antibiotics for pneumonia
  • Naloxone for narcotic associated hypoventilation
  • Bronchodilators (eg, albuterol) and steroids for asthma
• Noninvasive positive-pressure ventilation (NPPV) may be needed.
• • NPPV can be delivered continuously or intermittently to increase alveolar ventilation and decrease work of breathing.
  • NPPV is effective in the treatment of chronic respiratory failure in patients with restrictive lung disease (eg, neuromuscular disease or kyphoscoliosis).
  • In patients with chronic obstructive pulmonary disease, early application of NPPV in hypercapnic respiratory failure can decrease the need for invasive mechanical ventilation and decrease their length of stay in the hospital.
  • Advantages include a decreased incidence of nosocomial infections such as sinusitis or pneumonia, increased comfort compared with tracheal intubation, and the ability to maintain verbal communication.
  • Disadvantages include facial skin necrosis, conjunctivitis, or aspiration.
• Mechanical ventilation may be needed.
• • Mechanical ventilation increases minute ventilation and decreases dead space. This approach is the mainstay of treatment for acute hypercapnia.
  • The decision to start mechanical ventilation when an underlying disease is associated with chronic respiratory acidosis should be well thought out and well informed. Because of limited baseline pulmonary reserve, weaning from ventilatory support and extubation is usually difficult.
  • Various clinical factors determine the proper timing and method of mechanical ventilation, including the etiology of the ventilatory failure and patient factors, such as exhaustion, prognosis, and prospect of improvement with concurrent therapy.
  • Acute hypercapnia can be quickly and safely corrected to a normal PaCO₂.
  • In chronic hypercapnia, the goal of mechanical ventilation is near-normal pH with the patient's baseline PaCO₂. If the PaCO₂ must be normalized, this should be done over 2-3 days to prevent a sudden increase in CSF pH, which can cause seizures.
• Intratracheal pulmonary ventilation may be needed.³
• • Sometimes, mechanical ventilation is ineffective in reducing hypercapnia because of increased dead space.
  • Intratracheal pulmonary ventilation can help in treating intractable hypercapnia.
  • In this procedure, a catheter is placed down the endotracheal tube to produce a reverse flow up the tube. The dead space gas is flushed out, and rebreathing of CO₂ decreases.
• Permissive hypercapnia might be considered.⁴
• • In acute lung injury and acute respiratory distress syndrome (ARDS), a strategy of low tidal volume (4-6 mL/kg) allows the PaCO₂ to rise to 60-70 mm Hg in order to avoid stretch induced lung injury.
  • In a multicenter randomized trial, mechanical ventilation with a low tidal volume decreased mortality and increased the number of days without ventilator use.⁵
  • A respiratory acidosis (pH >7.25) is acceptable as long as adequate oxygenation and cardiovascular stability are maintained.
  • Permissive hypercapnia is contraindicated in patients with traumatic brain injury, pulmonary hypertension, or renal disease because elevated PaCO₂ levels may worsen their underlying disease.
• Treatment of a concurrent metabolic acidosis or to buffer the acidemia with a respiratory acidosis can be considered.
• • Tromethamine (THAM) (see Medication)
  • NaHCO₃^- administration should be used carefully if the patient cannot increase minute ventilation because it increases the amount of CO₂ to be excreted. Therefore, NaHCO₃^- should be administered slowly if it is used.

Surgical Care

Some institutions have successfully used extracorporeal membrane oxygenation (ECMO) to reduce high pCO₂ states such as when treating patients with severe asthma.

Diet

• As described above, the RQ describes the ratio of CO₂ produced to the amount of oxygen consumed while making energy; the RQ varies depending on the fuel source substrate. The RQ for carbohydrate is 1.0, the RQ for protein is 0.8, and the RQ for fat is 0.7. For the same amount of substrate burned, carbohydrate produces the greatest amount of CO₂, and fat produces the least. Patients on a high carbohydrate diet must be able to accommodate or must be provided higher minute ventilation in order to balance the increased CO₂ load or run the risk of developing a respiratory acidosis.
• If obesity is contributing to obstructive sleep apnea, a weight-reduction and exercise program should be part of the management plan
• Data have suggested that a specialized enteral formula can be a useful adjunctive therapy in the management of ARDS because it reduces lung inflammation and improving oxygenation.
• • The prototype is a low-carbohydrate, calorically dense formula containing eicosapentaenoic acid (EPA) from fish oil, gamma-linolenic acid (GLA) from borage oil, and elevated levels of antioxidants.
  • One commercially available formula is Oxepa (Abbott Laboratories; Abbott Park, IL).

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Drug Category: Alkalinizing agents

Mechanical ventilation is the mainstay of therapy for respiratory failure associated with hypercapnia until the precipitating disease state can be reversed. In certain cases, THAM may be helpful.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Patients with acute respiratory acidosis require admission to the ICU for close monitoring and possible advanced airway management with mechanical respiratory support.
• Avoid use of narcotics, sedatives, or other respiratory depressants when the patient is breathing spontaneously.
• Correct electrolyte abnormalities associated with muscle weakness, such as hypophosphatemia, hypokalemia, hypomagnesemia, and hypocalcemia.
• Maximize nutrition, but avoid overfeeding and high carbohydrate content because these can increase CO₂ production.
• If a metabolic alkalosis develops during diuretic therapy, correct it by replacing chloride and, if needed, careful replacement of potassium.

Further Outpatient Care

• For chronic respiratory acidosis, frequent follow-up with pulmonary function testing is necessary to provide a reference baseline and to monitor for changes during acute illness.
• Noninvasive positive-pressure ventilation is an effective home therapy for chronic respiratory failure caused by obstructive sleep apnea, obesity hypoventilation syndrome, or neuromuscular disease. Therapy can be continuous, intermittent with certain activities, or nocturnal.
• Home nursing can provide additional care.

Complications

• Respiratory acidosis may precede acute respiratory failure and possible cardiovascular failure.
• Convulsions may result if PaCO₂ levels are restored too quickly in patients with chronic hypercapnia.
• Posthypercapnic alkalosis can occur in patients with chronic hypercapnia if PaCO₂ is rapidly reduced with mechanical ventilation.
• • The kidneys have a relatively slow mechanism to correct the HCO₃^- excess.
  • The metabolic alkalosis can be treated by replacing chloride, potassium, or by increasing renal HCO₃^- excretion with acetazolamide. Care must be taken not to correct a compensating metabolic alkalosis with out addressing the underlying respiratory acidosis.
• If tracheal intubation is required in a spontaneously breathing person with high minute ventilation, care must be taken to maintain that level of minute ventilation to avoid a sudden increase in PaCO₂ that could contribute to hemodynamic instability, CNS injury, or cardiopulmonary arrest.
• Tracheal intubation may lead to upper-airway edema and difficult extubation, especially in chronically ill patients with limited baseline pulmonary reserve.

Prognosis

• Hypercapnic neurologic changes are reversible with no residual effect.
• The prognosis depends on the underlying etiology
• • Respiratory acidosis can be an acute and transient event with no long-term sequelae if it is not associated with hypoxemia (eg, seizure and treatment-associated hypoventilation).
  • Respiratory acidosis may be associated with a chronic disease that has associated morbidity (eg, asthma or Duchenne muscular dystrophy).
  • Respiratory acidosis may be the sign of an irreversible progressive disease that leads to death (eg, idiopathic pulmonary hypertension).

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to aggressively manage acute respiratory acidosis with assisted ventilation can lead to an otherwise avoidable respiratory and/or cardiovascular arrest.
• Use of sedative medications in a nonintubated patient can worsen mild respiratory acidosis, leading to unrecognized CO₂ narcosis.
• Primary respiratory acidosis must be distinguished from secondary hypercapnia due to metabolic alkalosis.
• Failure to consider a mixed acidosis can lead to missed therapies and diagnosis. Always critically analyze acid-base values by assessing the pH, PaCO₂, and HCO₃^- measurement.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

1. Epstein SK, Singh N. Respiratory acidosis. Respir Care. Apr 2001;46(4):366-83. [Medline].
2. Goldstein B, Shannon DC, Todres ID. Supercarbia in children: clinical course and outcome. Crit Care Med. Feb 1990;18(2):166-8. [Medline].
3. Makhoul IR, Bar-Joseph G, Blazer S, et al. Intratracheal pulmonary ventilation in premature infants and children with intractable hypercapnia. ASAIO J. Jan-Feb 1998;44(1):82-8. [Medline].
4. Laffey JG, O'Croinin D, McLoughlin P, Kavanagh BP. Permissive hypercapnia--role in protective lung ventilatory strategies. Intensive Care Med. Mar 2004;30(3):347-56. [Medline].
5. ARDS Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med. 2000;342:1301-8. [Medline].
6. Annane D, Orlikowski D, Chevret S, Chevrolet JC, Raphael JC. Nocturnal mechanical ventilation for chronic hypoventilation in patients with neuromuscular and chest wall disorders. Cochrane Database Syst Rev. 2007;(4):CD001941. [Medline].
7. Brian JE. Carbon dioxide and the cerebral circulation. Anesthesiology. May 1998;88(5):1365-86. [Medline].
8. Halpern P, Raskin Y, Sorkine P, Oganezov A. Exposure to extremely high concentrations of carbon dioxide: a clinical description of a mass casualty incident. Ann Emerg Med. Feb 2004;43(2):196-9. [Medline].
9. Kiely DG, Cargill RI, Lipworth BJ. Effects of hypercapnia on hemodynamic, inotropic, lusitropic, and electrophysiologic indices in humans. Chest. May 1996;109(5):1215-21. [Medline].
10. Low JM, Gin T, Lee TW, Fung K. Effect of respiratory acidosis and alkalosis on plasma catecholamine concentrations in anaesthetized man. Clin Sci (Lond). Jan 1993;84(1):69-72. [Medline].
11. Mas A, Saura P, Joseph D, et al. Effect of acute moderate changes in PaCO2 on global hemodynamics and gastric perfusion. Crit Care Med. Feb 2000;28(2):360-5. [Medline].
12. Mazzeo AT, Spada A, Pratico C, et al. Hypercapnia: what is the limit in paediatric patients? A case of near-fatal asthma successfully treated by multipharmacological approach. Paediatr Anaesth. Jul 2004;14(7):596-603. [Medline].
13. Thome UH, Carlo WA. Permissive hypercapnia. Semin Neonatol. Oct 2002;7(5):409-19. [Medline].
14. Vavilala MS, Lee LA, Lam AM. Cerebral blood flow and vascular physiology. Anesthesiol Clin North America. Jun 2002;20(2):247-64. [Medline].

Article Last Updated: Jan 9, 2008