Pediatric Respiratory Acidosis

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Respiratory acidosis occurs when the arterial partial pressure of carbon dioxide (P_a CO₂) is elevated above the normal range (>44 mm Hg) leading to a blood pH lower than 7.35. ^[1] By definition, the diagnosis of respiratory acidosis requires measurement of P_a CO₂ and pH. When the diagnosis is made, the underlying cause should be thoroughly investigated.

Respiratory acidosis is not a specific disease. Instead, it is an abnormality that results from an imbalance between production of carbon dioxide by the body and its excretion by the lungs, owing to inadequate minute ventilation. Low 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 and may occur at any age. Acute respiratory acidosis can be life-threatening when a sudden and sharp increase in P_a CO₂ is associated with severe hypoxemia and acidemia. In contrast, chronic respiratory acidosis (>24 h) is characterized by a gradual and sustained increase in P_a CO₂.

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

Many clinical scenarios contribute to inadequate removal of carbon dioxide 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 carbon dioxide 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 P_a CO₂ leads to effective compensatory mechanisms.

In rare instances, increased carbon dioxide production can exceed the patient’s ability to compensate, leading to 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 P_a CO₂ rises acutely, other organ systems are affected.

Carbon dioxide is carried in the blood in 3 forms: dissolved gas, bicarbonate, and protein bound. It diffuses freely across cell membranes, and this diffusion allows it to be efficiently transported from peripheral tissues to the lungs for excretion. When hypercapnia is present, this same property causes excess carbon dioxide to shift intracellularly and decrease intracellular pH.

Carbon dioxide (CO₂) normally combines with water (H₂ O) to form carbonic acid (H₂ CO₃), which then dissociates to release hydrogen ion (H⁺) and bicarbonate (HCO₃^–), as in the following equation:

CO₂ + H₂ O ↔ H₂ CO₃ ↔ H⁺ + HCO₃^–

When respiratory acidosis is present, excess carbon dioxide increases H₂ CO₃ formation, shifting the equilibrium of the equation toward the accumulation of hydrogen ions.

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 carbon dioxide is bound to hemoglobin to form carbaminohemoglobin.

Cellular buffering elevates plasma bicarbonate (HCO₃^–) only slightly and causes plasma HCO₃^– to increase by 1 mEq/L for every 10-mm Hg increase in P_a CO₂.

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 P_a CO₂. 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 P_a CO₂. Carbon dioxide is a potent respiratory stimulant, and elevated levels lead to an increase in minute ventilation to excrete increased quantities of carbon dioxide and normalize the pH. However, this effect is attenuated if the carbon dioxide 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.

When a patient develops 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 carbon dioxide (P_A CO₂) divided by the respiratory quotient (RQ), as follows:

P_A O₂ = P_I O₂ – (P_A CO₂/RQ)

The RQ is the ratio of the volume of carbon dioxide expired to the volume of oxygen consumed by an organism. In steady-state conditions, the human body produces carbon dioxide at a rate of approximately 200 mL/min and consumes oxygen at a rate of 250 mL/min; therefore, the RQ is about 0.8. If the RQ is rounded to 1, the alveolar gas equation is reduced as follows:

P_A O₂ = P_I O₂ – P_A CO₂

The P_I O₂ is equivalent to 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 follows:

P_I O₂ = F_I O₂ (PB – PH₂ O)

In view of this equivalence, the alveolar gas equation may be expressed as follows:

P_A O₂ = F_I O₂ (PB – PH₂ O) – P_A CO₂

If this equation is rearranged, P_A CO₂ is seen to be ultimately dependent on the level of inspired oxygen, as follows:

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:

P_A O₂ = 0.21 (760 mm Hg – 47 mm Hg) – P_A CO₂

P_A O₂ = 149.7 mm Hg – P_A CO₂

P_A O₂ + P_A CO₂ = 149.7 mm Hg

In the acute setting, P_a CO₂ values higher than 80-90 mm Hg while the patient is breathing air are life-threatening because of the associated hypoxemia. When P_a CO₂ 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 an increased P_a CO₂ 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 scenarios in which P_a CO₂ is greater than 150 mm Hg. In the example just given, the alveolar gas equation yields the following results:

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 carbon dioxide 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, the resultant pulmonary vasoconstriction can be severe and life-threatening.

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 by 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 carbon dioxide gas can be administered to preoperative neonates with hypoplastic left heart syndrome and low systemic cardiac output associated with high arterial saturations (> 85%). P_a CO₂ is maintained above 40 mm Hg, and the patient is mechanically ventilated, sedated, and paralyzed to prevent a compensatory tachypnea.

Inspired 3% carbon dioxide 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.

The clinical manifestations of acute hypercapnia are primarily neurologic. Acute elevations of P_a CO₂ above 60 mm Hg cause confusion and headache. A P_a CO₂ higher than 70 mm Hg produces a hypercapnic encephalopathy or carbon dioxide 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 P_a CO₂ was 269 mm Hg) did not have long-term adverse neurologic or developmental effects. ^[3]

Acute elevations in P_a CO₂ increase intracranial pressure by increasing cerebral blood flow (CBF) and cerebral blood volume secondary to vasodilatation. With a P_a CO₂ of 40-80 mm Hg, CBF increases by 1-2 mL per 100 g of brain per minute for each 1-mm Hg increase in P_a CO₂. A P_a CO₂ 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, carbon dioxide 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 carbon dioxide by the lungs). If the CSF acidosis persists for several hours, HCO₃^– levels in the CSF gradually increase to normalize the pH. In general, the response of the cerebral circulation to P_a CO₂ increases during development from the neonatal period to adulthood.

Causes of respiratory acidosis related to central nervous system (CNS) respiratory drive suppression include the following:

Trauma

Infection (eg, encephalitis, meningitis, or respiratory syncytial virus infection)

Neoplasm

Stroke

Hypoxia

Toxins, overdose (eg, of narcotics or alcohol)

Seizures – Postictal state

Spinal causes (eg, trauma to C3-C5 or impairment of phrenic nerve function)

Nerve-related causes include the following:

Spinal muscular atrophy

Guillain-Barré syndrome

Poliomyelitis

Phrenic nerve trauma

Neuromuscular junction–related causes include the following:

Myasthenia gravis

Botulism

Neuromuscular blockade

Muscle causes (eg, muscular dystrophy)

Airway-related causes include the following:

Loss of CNS control (eg, from brain injury, toxin or overdose, trauma, angioedema, tonsillar adenoid hypertrophy, thermal or chemical burn, foreign body, pharyngeal abscess, epiglottitis, or paralyzed vocal cords)

Congenital lesions (eg, subglottic stenosis, laryngomalacia, craniofacial abnormalities, tracheal rings, or vascular slings)

Laryngotracheobronchitis (croup)

Neoplasm, mediastinal mass

Bronchiolitis

Asthma

Acute lung injury–related causes include the following:

Pneumonia

Pulmonary edema

Lung contusion

Bronchiolitis

Chronic lung disease–related causes include the following:

Bronchopulmonary dysplasia

Cystic fibrosis

Chronic bronchitis

Chronic obstructive pulmonary disease

Causes related to chest wall restriction and reduced respiratory compliance include the following:

Flail chest

Pneumothorax

Pleural effusions

Kyphoscoliosis

Abdominal distention

Causes related to increased carbon dioxide production causes the following:

Malignant hyperthermia

Extensive burns

Overfeeding

The effects of respiratory acidosis vary according to the severity, the duration, the underlying disease, and the associated arterial saturation. Hypercapnic neurologic changes are reversible with no residual effect. The most important consideration may be the degree to which hypercarbia or the underlying disease adversely affects arterial oxygenation.

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). It may also be the sign of an irreversible progressive disease that leads to death (eg, idiopathic pulmonary hypertension).

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Ramamoorthy C, Tabbutt S, Kurth CD, et al. Effects of inspired hypoxic and hypercapnic gas mixtures on cerebral oxygen saturation in neonates with univentricular heart defects. Anesthesiology. 2002 Feb. 96(2):283-8. [Medline].

Goldstein B, Shannon DC, Todres ID. Supercarbia in children: clinical course and outcome. Crit Care Med. 1990 Feb. 18(2):166-8. [Medline].

Makhoul IR, Bar-Joseph G, Blazer S, et al. Intratracheal pulmonary ventilation in premature infants and children with intractable hypercapnia. ASAIO J. 1998 Jan-Feb. 44(1):82-8. [Medline].

Laffey JG, O’Croinin D, McLoughlin P, Kavanagh BP. Permissive hypercapnia–role in protective lung ventilatory strategies. Intensive Care Med. 2004 Mar. 30(3):347-56. [Medline].

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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].

Brian JE. Carbon dioxide and the cerebral circulation. Anesthesiology. 1998 May. 88(5):1365-86. [Medline].

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. 2004 Feb. 43(2):196-9. [Medline].

Kiely DG, Cargill RI, Lipworth BJ. Effects of hypercapnia on hemodynamic, inotropic, lusitropic, and electrophysiologic indices in humans. Chest. 1996 May. 109(5):1215-21. [Medline].

Low JM, Gin T, Lee TW, Fung K. Effect of respiratory acidosis and alkalosis on plasma catecholamine concentrations in anaesthetized man. Clin Sci (Lond). 1993 Jan. 84(1):69-72. [Medline].

Mas A, Saura P, Joseph D, et al. Effect of acute moderate changes in PaCO2 on global hemodynamics and gastric perfusion. Crit Care Med. 2000 Feb. 28(2):360-5. [Medline].

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. 2004 Jul. 14(7):596-603. [Medline].

Thome UH, Carlo WA. Permissive hypercapnia. Semin Neonatol. 2002 Oct. 7(5):409-19. [Medline].

Vavilala MS, Lee LA, Lam AM. Cerebral blood flow and vascular physiology. Anesthesiol Clin North America. 2002 Jun. 20(2):247-64. [Medline].

Mithilesh K Lal, MD, MBBS, MRCP, FRCPCH, MRCPCH(UK) Consultant Neonatologist, Clinical Director for Neonatal Services, Associate Medical Director (Revalidation), The James Cook University Hospital, South Tees Foundation NHS Trust, UK

Mithilesh K Lal, MD, MBBS, MRCP, FRCPCH, MRCPCH(UK) is a member of the following medical societies: American Pediatric Society, Society for Pediatric Research, British Association of Perinatal Medicine, British Medical Association, Neonatal Society, Nepal Medical Association, Royal College of Paediatrics and Child Health, Royal College of Physicians

Disclosure: Nothing to disclose.

Margaret A Priestley, MD Associate Professor of Clinical Anesthesiology and Critical Care, Perelman School of Medicine at the University of Pennsylvania; 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, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Ronald Litman, DO Professor of Anesthesiology and Pediatrics, Perelman School of Medicine at the University of Pennsylvania; Attending Anesthesiologist, Hospital of the University of Pennsylvania and Children’s Hospital of Philadelphia

Ronald Litman, DO is a member of the following medical societies: American Medical Association, Institute For Safe Medication Practices, Malignant Hyperthermia Association of the United States, Society for Pediatric Anesthesia

Disclosure: Nothing to disclose.

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, Wisconsin Medical Society

Disclosure: Nothing to disclose.

G Patricia Cantwell, MD, FCCM Professor of Clinical Pediatrics, University of Miami, Leonard M Miller School of Medicine; Chief, Division of Pediatric Critical Care Medicine, Medical Manager, Urban Search & Rescue, South Florida TF-2, Medical Director, Holtz Children’s Hospital Palliative Care Team, Medical Director, Tilli Kids – Pediatric Initiative of Hospice Care of SE Florida, Director, Pediatric Critical Care Transport, Holtz Children’s Hospital/Jackson Memorial Hospital

G Patricia Cantwell, MD, FCCM is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

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.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Pediatric Respiratory Acidosis

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