894 SECTION VII Pediatric Critical Care Renal airway obstruction (e g , obstructive sleep apnea syndrome and craniofacial disorders), neuromuscular diseases, or central nervous system problems (congen[.]
894 S E C T I O N V I I Pediatric Critical Care: Renal airway obstruction (e.g., obstructive sleep apnea syndrome and craniofacial disorders), neuromuscular diseases, or central nervous system problems (congenital central hypoventilation syndrome).154,155 In these patients with a tenuous respiratory baseline, decompensation can result from infection, use of narcotics, or uncontrolled oxygen therapy.156 These factors superimpose CO2 retention and acidemia on an already elevated baseline CO2 Progressive narcosis and coma (i.e., hypercapnic encephalopathy) may ensue Treating Respiratory Acidosis Treatment of hypoventilation should focus on the underlying cause Depending on the etiology and severity of the clinical situation, hypoventilation may be addressed quickly (e.g., improvement of bronchospasm with a b2 agonist) or may require more slow and careful correction More than the absolute value of Paco2 (or Pao2), it is the condition and trajectory of the patient that is important for planning an intervention In general, noninvasive or invasive mechanical ventilatory support should be considered in an unstable patient or if central nervous system function is deteriorating.157,158 In patients with high Paco2 and low minute ventilation, the level of consciousness may be altered Unless the hypercapnia can be quickly reversed, intubation may be indicated for airway protection and ventilatory assistance.159 Ventilatory strategies should include careful monitoring of endinspiratory and auto–positive end-expiratory pressures to detect any adverse effects of hyperventilation Aggressive reduction in the Paco2 may result in posthypercapnic alkalosis, with potentially serious consequences As mortality is related to hypoxemia and not the level of hypercapnia or acidemia, oxygen administration is critical in the management of respiratory acidosis However, caution must be exercised with treatment of hypoxia in those with hypercarbia, particularly those with chronic lung disease, as oxygen supplementation can suppress respiratory drive and provoke a further increase in Paco2.156 Chronic hypercapnia may downregulate CO2 chemoreceptor sensitivity, meaning that patients with chronic lung pathology are more dependent on hypoxic drive to maintain adequate spontaneous ventilation Hypoxemia is treated with Fio2 supplementation and efforts to improve airspace recruitment (and decrease V/Q mismatching), whereas the usual ventilatory strategy for hypercapnia is to increase minute ventilation In patients with severe ARDS, permissive hypercapnia may be indicated to minimize ventilator-associated lung injury.160 Lungprotective strategies, such as permissive hypercapnia, should be considered if there are no contraindications, such as intracranial hypertension.65,160 Ventilatory strategies should target a pH greater than 7.2, as there is growing evidence that hypercapnia is tolerated in pediatric patients with critical illness.65,160–162 However, this might not be the case for a critically ill child with multiple-system involvement, particularly if there is neurologic involvement.161,163 Respiratory Alkalosis In contrast to respiratory acidosis, if alveolar ventilation rises out of proportion to CO2 production, Paco2 will fall In a patient with critical illness, hyperventilation may occur for a variety of reasons, including early sepsis and hypermetabolic state, hypoxic respiratory disorders (including ARDS), Kussmaul respiration in DKA, hepatic failure, fever, central nervous system abnormalities, salicylate ingestion, and pain or anxiety (see eTable 72.3) Marked alkalemia can occur in certain circumstances: inappropriate mechanical ventilation parameters, central nervous system disorders, and some psychiatric diseases, the last of which are not often seen in children The presence of respiratory alkalosis is an indicator of illness severity, as mortality increases in proportion with the severity of hypocapnia Usually, blood pH does not exceed 7.55 in most cases of respiratory alkalosis, and severe manifestations of alkalemia are unusual Similar to what is seen with acute respiratory acidosis, acute respiratory alkalosis results in a biphasic change in plasma bicarbonate The immediate metabolic compensation is through a moderate decrease in the bicarbonate concentration, which is dictated by the Henderson-Hasselbalch equation (see Eq 72.7 and 72.8) as well as tissue buffering.164,165 With persistent hypocapnia, chloride reabsorption in the kidney changes, leading to a larger decrease of bicarbonate and a rise in urine pH.15,24,29 Within days, this results in a new, lower steady state.15 Of note, arterial hypocapnia does not necessarily imply respiratory alkalosis or the secondary and compensatory response to metabolic acidosis In patients with profound circulatory shock, alveolar ventilation is relatively preserved but profound cardiovascular depression exists, resulting in a pseudo-respiratory alkalosis, sometimes referred to as venoarterial CO2 gradient.71 Occurring despite a reduced pulmonary blood flow and decreased CO2 delivered to the lungs, the CO2 balance of the body is positive due to tissue acidosis reflected in mixed venous blood acidemia, usually involving both metabolic and respiratory components.101 The metabolic component derives from tissue hypoperfusion and hyperlactatemia In patients with cardiogenic and septic shock, the venoarterial Pco2 gradient decreases as hemodynamic variables improve.88 Mixed Acid-Base Derangements Coexisting metabolic acidosis and respiratory acidosis are seen commonly in the setting of critical illness Complex alterations in acid-base balance can be seen in cardiopulmonary arrest, underlying chronic lung disease complicated by pneumonia and resulting septic shock, coexisting kidney and pulmonary insufficiency, and as a consequence of certain toxic agents that may provoke both central nervous system changes (resulting in hypoventilation) and cardiocirculatory collapse (causing metabolic acidosis).1,54,151 In order to appropriately address the underlying disorder, more complex evaluation of acid-base derangements may need to be employed In complex cases such as this, using the physicochemical and modified SBE approaches can assist with evaluating coexisting mixed acid-base disorders Such an approach can reveal both components of the acid-base derangement in order to target treatment to the underlying disorder Knowledge of the extent of kidney and respiratory compensations allows more complex disturbances to be diagnosed (see eTable 72.1) Mixed alkalosis may occur in patients with chronic kidney disease in whom primary hypocapnia develops In this setting, inappropriately high plasma bicarbonate levels occur due to inadequate kidney response to acid-base derangements These abnormalities may continue to persist despite dialytic therapy, as hemodialysis and hemofiltration are most commonly an alkalinizing therapy and are much less effective in compensating alkalemia than acidemia.57 CHAPTER 72 Acid-Base Disorders 895 Summary Key References In a critically ill child with an acid-base derangement, the first step is to define the disorder using various tools to determine whether the patient has acidosis or alkalosis, acidemia or alkalemia, acute or chronic, simple or mixed An easily accessible tool to evaluate acid-base status is through the bicarbonate (or CO2TOT) concentration While an abnormal value may provide a clue to the etiology of the imbalance, a normal concentration does not rule out the possibility of an acid-base derangement If the bicarbonate is abnormal or if a complex or mixed acid-base disorder is suspected, an arterial blood gas can provide invaluable information on pH, Paco2, and SBE Further evaluation with AG evaluation and lactate concentration should be considered if metabolic acidosis exists (with or without acidemia) If the patient’s history documents resuscitation with large volumes of normal saline, special attention must be given to chloride concentrations There is compelling evidence that abnormal pH by itself may not be as dangerous as once thought However, an individualized approach must be taken to decide whether a given patient may benefit or not from modifying the patient’s pH and acid-base status Finally, none of the approaches for interpreting acid-base homeostasis is without limitations or drawbacks Careful and close attention should be given to the interactions between acidbase balance and clinical status as well as the trajectory of the patient’s clinical course and acid-base status Gomez H, Kellum JA Understanding acid base disorders Crit Care Clin 2015;31(4):849-860 Kishen R, Honoré PM, Jacobs R, et al Facing acid-base disorders in the third millennium - the Stewart approach revisited Int J Nephrol Renovasc Dis 2014;7:209-217 Mehta AN, Emmett JB, Emmett M GOLD MARK: an anion gap mnemonic for the 21st century Lancet 2008;372(9642):892 Story DA Bench-to-bedside review: a brief history of clinical acid-base Crit Care 2004;8(4):253-258 Kraut JA, Madias NE Approach to patients with acid-base disorders Respir Care 2001;46(4):392-403 Kellum JA Clinical review: reunification of acid-base physiology Crit Care 2005;9(5):500-507 Kraut JA, Madias NE Lactic acidosis N Engl J Med 2015;372(11): 1078-1079 MW, Self WH, Wanderer JP, et al Balanced crystalloids versus saline in critically ill adults N Engl J Med 2018;378(9):829-839 Rodríguez Soriano J Renal tubular acidosis: the clinical entity J Am Soc Nephrol 2002;13(8):2160-2170 Sabatini S, Kurtzman NA Bicarbonate therapy in severe metabolic acidosis J Am Soc Nephrol 2009;20(4):692-695 Adrogué HJ, Gennari FJ, Galla JH, Madias NE Assessing acid-base disorders Kidney Int 2009;76(12):1239-1247 The full reference list for this chapter is available at ExpertConsult.com e1 References Gunnerson KJ Clinical review: the meaning of acid-base abnormalities in the intensive care unit part I - epidemiology Crit Care 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