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Acidosis, Respiratory: Treatment & Medication
Updated: Jan 5, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
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.
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
None reported
Documented hypersensitivity; anuria; uremia
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
More on Acidosis, Respiratory |
| Overview: Acidosis, Respiratory |
| Differential Diagnoses & Workup: Acidosis, Respiratory |
 Treatment & Medication: Acidosis, Respiratory |
| Follow-up: Acidosis, Respiratory |
| References |
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References
Epstein SK, Singh N. Respiratory acidosis. Respir Care. Apr 2001;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. Feb 2002;96(2):283-8. [Medline].
Goldstein B, Shannon DC, Todres ID. Supercarbia in children: clinical course and outcome. Crit Care Med. Feb 1990;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. Jan-Feb 1998;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. Mar 2004;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. May 1998;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. Feb 2004;43(2):196-9. [Medline].
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].
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].
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].
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].
Thome UH, Carlo WA. Permissive hypercapnia. Semin Neonatol. Oct 2002;7(5):409-19. [Medline].
Vavilala MS, Lee LA, Lam AM. Cerebral blood flow and vascular physiology. Anesthesiol Clin North America. Jun 2002;20(2):247-64. [Medline].
Further Reading
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, PaCO2, 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
