Pediatric Respiratory Acidosis Treatment & Management
- Author: Mithilesh K Lal, MBBS, MD, MRCP, FRCPCH; Chief Editor: Timothy E Corden, MD more...
The goals of therapy are to remove the underlying cause and return the arterial partial pressure of carbon dioxide (Pa CO2) to baseline. Patients with acute respiratory acidosis require admission to the intensive care unit (ICU) for close monitoring and possible advanced airway management with mechanical respiratory support.
Failure to aggressively manage acute respiratory acidosis with assisted ventilation can lead to an otherwise avoidable respiratory or cardiovascular arrest. Use of sedative medications in a nonintubated patient can worsen mild respiratory acidosis, leading to unrecognized carbon dioxide narcosis.
If hypoxemia accompanies hypercapnia, oxygen should be administered. Diagnosis and directed therapy must accompany oxygen administration. In chronic hypercapnia, supplemental oxygen therapy can worsen hypercapnia by reducing the respiratory drive and increasing dead-space ventilation through loss of hypoxic pulmonary vasoconstriction.
Some institutions have successfully used extracorporeal membrane oxygenation (ECMO) to reduce high-Pa CO2 states (eg, in treatment of patients with severe asthma).
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 carbon dioxide production. If a metabolic alkalosis develops during diuretic therapy, correct it by replacing chloride and, if needed, careful replacement of potassium.
Noninvasive positive-pressure ventilation
Noninvasive positive-pressure ventilation (NPPV) can be delivered continuously or intermittently to increase alveolar ventilation and decrease work of breathing. It 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 (COPD), early application of NPPV in hypercapnic respiratory failure can decrease the need for invasive mechanical ventilation and decrease length of stay in the hospital.
Advantages of NPPV include a decreased incidence of nosocomial infections (eg, sinusitis or pneumonia), increased comfort in comparison with tracheal intubation, and the ability to maintain verbal communication. Disadvantages include facial skin necrosis, conjunctivitis, and aspiration.
Mechanical ventilation increases minute ventilation and decreases dead space. It 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 (eg, exhaustion, prognosis, and prospect of improvement with concurrent therapy).
In acute hypercapnia, mechanical ventilation usually can quickly and safely correct Pa CO2 to a normal value. In chronic hypercapnia, the goal of mechanical ventilation is near-normal pH with the patient’s baseline Pa CO2. If the Pa CO2 must be normalized, this should be done over 2-3 days to prevent a sudden increase in cerebrospinal fluid (CSF) pH, which can cause seizures.
Intratracheal pulmonary ventilation
Sometimes, mechanical ventilation is ineffective in reducing hypercapnia because of increased dead space. In such cases, intratracheal pulmonary ventilation can help in treating intractable hypercapnia. This procedure involves passing a catheter down the endotracheal tube to produce a reverse flow up the tube. The dead-space gas is flushed out, and rebreathing of carbon dioxide decreases.
In acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), a strategy of low tidal volume (4-6 mL/kg) allows the Pa CO2 to rise to 60-70 mm Hg so as 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.
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 an elevated Pa CO2 may worsen the underlying disease.
Treatment of a concurrent metabolic acidosis or buffering the acidemia with a respiratory acidosis can be considered. Tromethamine (THAM) has been used to prevent and correct systemic or respiratory acidosis. NaHCO3– administration should be used carefully if the patient cannot increase minute ventilation because it increases the amount of carbon dioxide to be excreted. Therefore, NaHCO3– should be administered slowly if it is used.
Disease-specific interventions may be needed, such as the following:
Antibiotics for pneumonia
Naloxone for narcotic-associated hypoventilation
Bronchodilators (eg, albuterol) and steroids for asthma
Complications of Treatment
Respiratory acidosis may precede acute respiratory failure and possible cardiovascular failure. Convulsions may result if Pa CO2 levels are restored too quickly in patients with chronic hypercapnia. Posthypercapnic alkalosis can occur in patients with chronic hypercapnia if Pa CO2 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 without addressing the underlying respiratory acidosis.
Tracheal intubation may lead to upper-airway edema and difficult extubation, especially in chronically ill patients with limited baseline pulmonary reserve. 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 Pa CO2 that could contribute to hemodynamic instability, CNS injury, or cardiopulmonary arrest.
As noted (see Pathophysiology), the respiratory quotient (RQ) is defined as the ratio of carbon dioxide produced to the amount of oxygen consumed while making energy. The RQ varies according to the fuel source substrate: It is 1.0 for carbohydrate, 0.8 for protein, and 0.7 for fat.
Thus, for a given amount of substrate burned, carbohydrate produces the greatest amount of carbon dioxide, and fat produces the least. Patients on a high-carbohydrate diet must be able to accommodate or must be provided with higher minute ventilation in order to balance the increased carbon dioxide load, or else they run the risk of developing a respiratory acidosis.
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 improves 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).
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.
If obesity is contributing to obstructive sleep apnea, a weight-reduction and exercise program should be part of the management plan.
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.
NPPV 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.
Epstein SK, Singh N. Respiratory acidosis. Respir Care. 2001 Apr. 46(4):366-83. [Medline].
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].
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].
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].