eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Critical Care

Acidosis, Respiratory

Margaret A Priestley, MD, Assistant Professor of Clinical Anesthesiology and Critical Care, University of Pennsylvania School of Medicine; Clinical Director, Pediatric Intensive Care Unit, The Children's Hospital of Philadelphia
Ronald Litman, DO, Associate Professor of Anesthesiology and Pediatrics, University of Pennsylvania School of Medicine

Updated: Jan 5, 2009

Introduction

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 Pathophysiology). 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 (H₂ O) to form carbonic acid (H₂ CO₃), which then dissociates to release hydrogen ion [H⁺] and bicarbonate (HCO₃ ^-) (Equation 1). When a respiratory acidosis is present, excess CO₂ increases H₂ CO₃ formation, shifting the equilibrium of the equation toward the accumulation of hydrogen ions.

Equation 1: CO₂ + H₂ O ↔ 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_A O₂) is equal to the partial pressure of inspired oxygen (P_i O₂) minus the quantity of alveolar partial pressure of CO₂ (P_A CO₂) divided by the respiratory quotient (RQ), as follows:

Equation 2: P_A O₂ = P_i O₂ - (P_A CO₂/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_A O₂ = P_i O₂ - P_A CO₂

The P_i O₂ is the difference between the barometric pressure (PB) and the partial pressure of water vapor (PH₂ O) multiplied by the fraction of inspired oxygen (F_i O₂), as shown below (Equation 4):

Equation 4: P_i O₂ = F_i O₂ (PB - PH₂ O)

If the equation is rearranged, P_A CO₂ is ultimately dependent on the level of inspired O₂ (Equation 5):

Equation 5: P_A CO₂ = F_i O₂ (PB - PH₂ O) - P_A O₂

Because PB at sea level is 760 mm Hg and PH₂ O in the atmosphere is 47 mm Hg, when a person is breathing air (F_i O₂ = 0.21), the sum of P_A CO₂ and P_A O₂ adds up to approximately 150 mm Hg, as follows (Equations 6 and 7):

Equation 6: P_A O₂ = 0.21 (760 mm Hg - 47 mm Hg) - P_A CO₂

Equation 7: P_A O₂ + P_A CO₂ = 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_i O₂ = 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_A O₂ = [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. Inspired 3% CO ₂ improved cerebral oxygenation measured by near-infrared spectroscopy and mean arterial pressure in preoperative neonates with single ventricles.² 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.³

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 cerebrospinal fluid (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

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 CO ₂ production causes include the following:
  • Malignant hyperthermia
  • Extensive burns
  • Overfeeding

Differential Diagnoses

Workup

Laboratory 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

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.⁴
  • 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.⁵
  • 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.⁶
  • 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 pCO ₂ states such as when treating patients with severe asthma.

Diet

• As described above, the respiratory quotient (RQ) describes the ratio of CO₂ produced to the amount of O₂ 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.
  • The function of selected micronutrients, including those that serve antioxidant roles, is important in the course of ARDS and should be considered in the care of patients. Relevant antioxidants include vitamins E and C and the carotenoids.
  • One commercially available formula is Oxepa (Abbott Laboratories; Abbott Park, IL).

Medication

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.

Tromethamine (THAM)

Also known as tris [hydroxymethyl]-aminomethane. Combines with hydrogen ions to form HCO₃ ^- buffer. Used to prevent and correct systemic or respiratory acidosis. Biologically inert weak base that can buffer excess CO₂. Used to correct acute respiratory acidosis, as follows: R-NH₂ + CO₂ + H₂ O = R-NH₃ + HCO₃
At 37°C, pKa is 7.8; therefore, more effective buffer than NaHCO₃ ^- in physiologic blood pH range. Not protein bound and distributed primarily in extracellular space. When protonated, excreted by kidneys and acts as osmotic diuretic. Most appropriately administered as short-term infusion during therapeutic window to correct acute respiratory acidosis.

Dosing

Adult

Estimate IV loading dose by the following equation: Volume (mL) of 0.3-M solution = lean body weight (kg) X base deficit (mEq/L) X 1.1
Typical adult dose is about 500 mL (150 mEq) of 0.3-M solution; may use up to 1000 mL in severe situations; titrate to serum pH (some authors practice using half the calculated replacement dose and consider further replacement based on results); 1 mMol = 3.3 mL of 0.3-M solution

Pediatric

Estimate IV loading dose by the following equation: Volume (mL) of 0.3-M solution = lean body weight (kg) X base deficit (mEq/L) X 1.1
Do not exceed 40 mL/kg/d IV; infusion rate not to exceed 3-16 mL/kg/h; titrate to serum pH

Interactions

None reported

Contraindications

Documented hypersensitivity; anuria; uremia

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May induce respiratory depression and hypoglycemia (require ventilatory assistance and glucose administration); reduce dose in renal impairment; monitor serum and urine pH

Follow-up

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

Medicolegal 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

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Keywords

respiratory acidosis, carbon dioxide acidosis, CO₂ acidosis, acute respiratory acidosis, chronic respiratory acidosis, hypercapnia, hypercarbia, supercarbia, acidemia, blood pH, acid-base balance, pCO₂, minute ventilation, bicarbonate, hypercapnic acidosis, arterial partial pressure of carbon dioxide, hypoxemia, PaCO_2, depressed central respiratory drive, acute paralysis of the respiratory muscles, acute parenchymal lung and airway diseases, increased dead space, wasted ventilation, scoliosis, pulmonary vasoconstriction, supraventricular arrhythmias, hypoplastic left heart syndrome, hypercapnic encephalopathy, myasthenia gravis, bronchopulmonary dysplasia, asthma, emphysema, encephalitis, meningitis

Contributor Information and Disclosures

Author

Margaret A Priestley, MD, Assistant Professor of Clinical Anesthesiology and Critical Care, University of Pennsylvania School of Medicine; Clinical Director, Pediatric Intensive Care Unit, The Children's Hospital of Philadelphia
Margaret A Priestley, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Ronald Litman, DO, Associate Professor of Anesthesiology and Pediatrics, University of Pennsylvania School of Medicine
Ronald Litman, DO is a member of the following medical societies: American Academy of Pediatrics, American Society of Anesthesiologists, and Society for Pediatric Anesthesia
Disclosure: Nothing to disclose.

Medical Editor

G Patricia Cantwell, MD, Associate Clinical Professor, Department of Pediatrics, University of Miami; Director of Pediatric Critical Care Medicine, Miller School of Medicine, Jackson Children's Hospital
G Patricia Cantwell, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Emergency Physicians, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Barry J Evans, MD, Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center
Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

CME Editor

Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Professor of Clinical Pediatrics, State University of New York at Stony Brook; Director of Children's Sleep Services, Winthrop University Hospital
Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians
Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

Chief Editor

Timothy E Corden, MD, Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin
Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, and Wisconsin Medical Society
Disclosure: Nothing to disclose.

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