Understanding acid-base balance Find out how to interpret values and steady a disturbed equilibrium in an acutely ill patient. By Susan J. Appel, APRN,BC, CCRN, PhD, and Charles A. Downs, APRN,BC, CCRN, MSN Many critical illnesses can upset a patient’s acid-base bal- generates 50 to 100 mEq/day of acid from metabolism of ance, and a disturbance in acid-base equilibrium may indi- carbohydrates, proteins, and fats. In addition, the body cate other underlying diseases or organ damage. Accurately loses base in the stool. In order to maintain acid-base interpreting acid-base balance requires simultaneous mea- homeostasis, acid production must balance the neutraliza- surements of arterial pH and plasma electrolytes, as well as tion or excretion. The lungs and kidneys are the main reg- knowledge of compensatory physiologic mechanisms. ulators of acid-base homeostasis. The lungs release CO2, an In this article, we’ll review normal acid-base physiol- end product of carbonic acid (H2CO3). The renal tubules, - ogy, acid-base disturbances, and lab techniques and math- with the regulation of bicarbonate (HCO3 ), excrete other ematical calculations used to identify the cause of acid-base acids produced from the metabolism of proteins, carbohy- derangements. Lastly, we’ll discuss potential treatments for drates, and fats.1 acid-base disturbances. M Compensating for changes What’s normal? The body has three compensatory mechanisms to handle A normal range for arterial pH is 7.35 to 7.45. Acidosis is changes in serum pH: a pH less than 7.35; alkalosis is a pH greater than 7.45. • Physiologic buffers, consisting of a weak acid (which Because pH is measured in terms of hydrogen (H+) ion can easily be broken down) and its base salt or of a weak concentration, an increase in H+ ion concentration de- base and its acid salt. These buffers are the bicarbonate- creases pH and vice versa. Changes in H+ ion concentra- carbonic acid buffering system, intracellular protein tion can be stabilized through several buffering systems: buffers, and phosphate buffers in the bone. bicarbonate-carbonic acid, proteins, hemoglobin, and • Pulmonary compensation, in which changes in ventila- phosphates. tion work to change the partial pressure of arterial carbon Acidosis, therefore, can be described as a physiologic dioxide (PaCO2) and drive the pH toward the normal condition caused by the body’s inability to buffer excess H+ range. A drop in pH, for example, results in increased ven- ions. At the other end, alkalosis results from a deficiency in tilation to blow off excess CO2. An increase in pH de- + H ion concentration. Acidemia and alkalemia refer to the creases ventilatory effort, which increases PaCO2 and lowers process of acidosis or alkalosis, respectively, occurring in the pH back toward normal. arterial blood. • Renal compensation, which kicks in when the other Body acids are formed as end products of cellular me- mechanisms have been ineffective, generally after about tabolism. Under normal physiologic conditions, a person 6 hours of sustained acidosis or alkalosis. While respira- Fall 2008 9 ED Insider tory compensation occurs almost immediately, renal Metabolic alkalosis - mechanisms can take hours to days to make a difference. Metabolic alkalosis occurs when HCO3 is increased, usu- In acidosis the kidneys excrete H+ in urine and retain ally as the result of excessive loss of metabolic acids. Causes - HCO3 . In alkalosis, the kidneys excrete bicarbonate and of metabolic alkalosis include diuretics, secretory adenoma retain H+ in the form of organic acids, resulting in near- of the colon, emesis, hyperaldosteronism, Cushing’s syn- normalization of pH.2,3 Lastly, bone may also serve as a drome, and exogenous steroids. buffer because it contains a large reservoir of bicarbonate Some causes of metabolic alkalosis respond to treat- and phosphate and can buffer a significant acute acid ment with 0.9% sodium chloride solution. If the patient’s load. Patients who have low albumin levels and bone urine chloride concentration is less than 15 mmol/L, his density due to malnutrition or chronic disease, and ane- metabolic alkalosis is saline-responsive; urine chloride mic patients, have an ineffective buffering capability.4 levels above 25 mmol/L indicate nonsaline-responsive metabolic alkalosis.2,7 The mechanisms resulting in saline- Common acid-base upsets responsive metabolic alkalosis include GI loss, diuresis, or Generally, if your patient has changes in acid-base home- renal compensation from hypercapnia. Nonsaline respon- ostasis, you’d look for the cause first before intervening to sivemetabolic alkalosis results from mineralocorticoid ex- normalize the pH. But because some acid-base distur- cess or potassium depletion. bances have a limited number of causes, you can systemat- Fluid administration is the foundation for treatment ically eliminate some potential causes. for saline-responsivemetabolic alkalosis.8 In cases of ex- Start by looking at the patient’s arterial blood gas treme alkalosis, the patient may be given dilute hydrochlo- analysis. Many disorders are mild and don’t require treat- ric acid. Saline-resistant alkalosis is treated by addressing ment, and in some cases, too-hasty treatment can do more the underlying etiology. harm than the imbalance itself. Also, critically ill patients may have more than one acid-base imbalance simultane- Respiratory acidosis ously. In respiratory acidosis, the patient’s pH is less than 7.35 The most common acid-base derangements can be di- and his PaCO2 is above 45 mm Hg (the upper limit of nor- vided into four categories: metabolic acidosis, metabolic mal). Alveolar hypoventilation is the only mechanism that alkalosis, respiratory acidosis, and respiratory alkalosis. causes hypercarbia, or a PaCO2 above the upper limit of Let’s look at each and how you’d respond. normal. The amount of alveolar ventilation necessary to maintain normal PaCO2 varies depending upon CO2 pro- Metabolic acidosis duced. - Metabolic acidosis is an increase in the amount of absolute The relationship between PaCO2 and plasma HCO3 body acid, either from excess production of acids or exces- determines arterial pH. Generally, acute increases in PaCO2 sive loss of bicarbonate, sodium, and potassium. Causes of are accompanied by only minimal changes in serum - metabolic acidosis include lactic acidosis, diabetic ketoaci- HCO3 . However, over a period of 1 to 3 days, renal con- - 9 dosis, and loss of bicarbonate through severe diarrhea or servation of HCO3 results in an increase in pH. bicarbonate wasting through the kidneys or gastrointesti- Chronic respiratory acidosis occurs secondary to a nal (GI) tract. chronic reduction in alveolar ventilation—for example, in In general, the kidneys attempt to preserve sodium by chronic lung diseases such as chronic obstructive pul- exchanging it for excreted H+ or potassium. In the presence monary disease (COPD). Acute respiratory acidosis is of an H+ load, H+ ions move from the extracellular fluid caused by an acute change in alveolar ventilation; respira- into the intracellular fluid.2 For this process to occur, tory depression from acute opioid ingestion is one cause. potassium moves outside the cell into the extracellular Treatment for respiratory acidosis is largely supportive, but fluid to maintain electroneutrality. In severe acidosis, sig- if opioid ingestion is suspected, I.V. naloxone may be given nificant overall depletion of total body potassium stores as an antidote. can occur despite serum hyperkalemia. This is why I.V. potassium is given to patients with diabetic ketoacidosis Respiratory alkalosis early in treatment, despite the often-elevated serum potas- Common in critical care, respiratory alkalosis occurs 5,6 sium level. External and internal potassium balances are when PaCO2 is reduced, causing an increase in pH. regulated to maintain an extracellular fluid concentration The most common cause of respiratory alkalosis is of 3.5 to 5.5 mEq/L and a total body content of about 50 increased alveolar ventilation, which can happen in mEq/kg (40 mEq/kg in females).6 hyperventilation, mechanical overventilation, hepatic ED Insider 10 Fall 2008 disease, pregnancy, and septicemia. Determining appropriate compensatory Comparing acid-base imbalances - changes in HCO3 is key to determining if the - patient also has a concomitant metabolic dis- Condition pH PaCO2 HCO3 order. In chronic respiratory alkalosis, the Pure respiratory alkalosis High Low Normal compensatory mechanisms result in mild re- - Pure respiratory acidosis Low High Normal duction in plasma HCO3 levels to maintain a near normal or normal pH. This causes a Pure metabolic alkalosis High Normal High mixed acid-base disorder, which will be dis- cussed later. Pure metabolic acidosis Low Normal Low Treatment of respiratory alkalosis is di- Metabolic alkalosis with partial High High High rected at discovering and correcting the un- respiratory compensation derlying etiology. For example, if a patient is Metabolic acidosis with partial Low Low Low hyperventilating from anxiety, have him respiratory compensation breathe into a paper bag. In mechanically ven- tilated patients with mechanical overventila- tion, reducing the minute ventilation or tidal volume will anion gap, then a non-anion gap metabolic acidosis is con- increase PaCO2 and reduce pH. Monitor the patient sidered to be present and is worsening the anion gap aci- closely, because a rapid reduction of PaCO2 in a patient dosis. For more examples, see Comparing acid-base with chronic respiratory alkalosis may cause acute meta- imbalances. bolic acidosis.10 Caring for the critically ill Mixed acid-base imbalances Acid-base imbalances are common in critically ill patients. When a patient has two or three acid-base imbalances si- By understanding the basic physiology of acid-base balance multaneously, he’s said to have a mixed acid-base imbal- and what can go wrong, you can help your patient get back ance.7 Examples include: in balance. I • respiratory alkalosis or acidosis that shrouds a metabolic acidosis or alkalosis REFERENCES • metabolic alkalosis or acidosis that shrouds another 1.