Body out of balance: Understanding metabolic acidosis and alkalosis 
Rhonda Lawes RN, CNE, MSN 

November 2009 
Volume 39 Number 11
Pages 50 - 54

MAINTAINING HOMEOSTASIS is a delicate, yet critically important balancing act. By understanding the main factors that affect homeostasis and blood pH, you can quickly recognize signs and symptoms of metabolic acidosis and alkalosis and intervene appropriately. This article examines these two common, potentially life-threatening metabolic imbalances and discusses the usefulness of an arterial blood gas (ABG) analysis in the patient's plan of care.

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pH and homeostasis

The state in which the body's hormones, neurotransmitters, enzymes, and metabolic processes function most effectively is called homeostasis. One measurement of homeostasis is a serum pH between 7.35 and 7.45, the designated normal range for hydrogen ion concentration in the extracellular fluid. Arterial pH is obtained by ABG analysis; the ABG sample is generally obtained by a percutaneous arterial puncture, but can also be obtained from an indwelling arterial cannula or catheter, especially if multiple samples are needed.

The three values important to basic ABG interpretation are pH, PaCO2 (normal range, 35 to 45 mm Hg), and HCO3- (bicarbonate, normal range, 22 to 26 mEq/L).

Keeping pH in balance

The pH value is a reflection of the ratio between the serum concentrations of HCO3- and PaCO2. When the ratio of HCO3- to PaCO2 is 20:1, the pH is within the normal range. A change in HCO3- has little or no effect on pH as long as there's an accompanying change in PaCO2, and vice versa.1 Maintaining this ratio, which maintains homeostasis, is the driving force behind the body's compensatory response to changes in the pH.

The body's first line of defense in maintaining a normal pH are the buffer systems. Acting like chemical shock absorbers, buffers absorb or release hydrogen ions in response to pH changes. The three major buffer systems are body proteins, the bicarbonate buffer system, and the transcellular hydrogen-potassium exchange system. Although the buffer systems can respond immediately to pH changes, they have only a limited effect on pH, and can't correct large or long-term pH changes. When the buffer systems are overwhelmed and can't normalize the pH, the respiratory system (the second line of defense) and renal system (the third line of defense) respond. The respiratory response, a change in respirations, occurs within minutes, compared with the renal response, which can take 24 to 48 hours to make a difference.

To further understand how the body compensates for disturbances in pH, think of serum HCO3- as a base or alkalinizer, and PaCO2 as an acid. (Although CO2 isn't an acid, in the bloodstream, a small percentage of the gas combines with water to form carbonic acid [H2CO2]. Carbonic acid is almost impossible to measure, so dissolved PaCO2 measurements are substituted when calculating pH.)1 In short, increased hydrogen ion concentration reduces pH, and increased base (or alkaline content) raises pH.

For example, if your patient's pH is less than 7.35 because of excess CO2 (acid), the body will respond by increasing HCO3- (base) in an effort to increase the pH back toward the normal range. If your patient's pH is less than 7.35 because of a decrease in HCO3-, the body will respond by decreasing CO2 to help to increase the pH toward normal.

Understanding metabolic acidosis

Respiratory and metabolic acidosis are both characterized by a pH less than 7.35, but in metabolic acidosis, the patient's HCO3- is less than 22 mEq/L either because of an excess of acids or a loss of bicarbonate.1

Causes of metabolic acidosis include:

* increased acids from ketoacidosis (as in uncontrolled diabetes, starvation or fasting, or alcohol abuse), lactic acidosis, ingestion of toxins such as ethylene glycol (antifreeze) or cyanide, or ingestion of certain medications and other substances, such as excessive amounts of aspirin, iron, or paraldehyde

* loss of HCO3- from diarrhea, gastric tubes or ileostomies, or Type 2 (proximal) renal tubular acidosis

* decreased acid excretion from renal failure or Type 1 (distal) renal tubular acidosis

* decreased production of HCO3- from renal, hepatic, or pancreatic failure.1

To treat metabolic acidosis, the healthcare team must quickly identify and treat the underlying cause. This is where the anion gap comes in. To maintain electrical balance and normal body functions, the number of cations (positive ions such as sodium and potassium) should equal the number of anions (negative ions such as chloride and bicarbonate). Not all serum cations and anions are routinely measured, but unmeasured cations and anions need to be accounted for when interpreting ABGs. Normally, unmeasured anions outnumber unmeasured cations—this is called the anion gap.

The normal range for the anion gap is 8 to 12 mEq/L.1 Because the anion gap can't be directly measured, it's determined by the formula Na+ - (Cl- + HCO3-). The formula assumes that the patient has a normal albumin level—low serum albumin significantly reduces the accuracy of the anion gap formula.

The anion gap is categorized as high (increased), normal, or low, with low occurring infrequently. Each of the three classifications have specific causes (for example, an increased anion gap is associated with increased acid) and help the healthcare provider determine the most effective treatment plan for treating the acidosis. For more details, see The anion gap and metabolic acidosis.

The two causes of metabolic acidosis you're most likely to see in a hospitalized patient are lactic acidosis and ketoacidosis.

Lactic acidosis, the most common cause of metabolic acidosis in hospitalized patients, is the result of excess lactic acid production or reduced lactic acid removal from the blood.2 Lactic acid, a byproduct of anaerobic glucose metabolism, is removed by the liver and kidneys.1

Patients at risk for developing lactic acidosis include those with cardiopulmonary failure, shock, acute pulmonary edema, carbon monoxide poisoning, cyanide intoxication, smoke inhalation, severe hypoxemia (PaO2 less than 40 mm Hg), sepsis, trauma, grand mal seizure, thiamine deficiency, adverse reactions to drugs or toxins, alcohol abuse, liver disease, cancer, AIDS, various acquired and congenital diseases, and pheochromocytoma. In rare cases, patients taking metformin develop lactic acidosis.3

Ketoacidosis, the other major cause of metabolic acidosis, is a common complication of diabetes. Increased fatty acid metabolism and ketoacid accumulation can occur in patients with type 1 diabetes with acute, temporary increased insulin requirements.4

Starving patients and patients who abuse alcohol and have a poor diet also can develop ketoacidosis, because of decreased gluconeogenesis.5 For signs and symptoms of metabolic imbalances, see Recognizing metabolic acidosis and alkalosis.

Because metabolic acidosis has many underlying causes, a wide range of treatments are used to help patients return to homeostasis. Let's look at three cases:

* Ashleigh Dautermann, 23, has had severe diarrhea for the past 3 days and has just been admitted to your monitored medical-surgical unit. Her initial ABGs showed a pH of 7.33, PaCO2 of 35 mm Hg, and HCO3- of 18 mEq/L, indicating metabolic acidosis caused by a depletion of base due to severe diarrhea. As you complete your assessment, she complains of a headache and feeling extremely tired.

Because Ms. Dautermann's pH is close to normal, her body should be able to correct the pH if the diarrhea is resolved and her fluid volume is replaced I.V.

* Chad Ray, 39, has a history of alcohol abuse, and was found unresponsive. He was admitted to the ED with a pH of 7.24, PaCO2 of 36 mm Hg, and HCO3- of 14 mEq/L. His metabolic acidosis calls for administration of an I.V. alkalizing solution to raise his pH. Monitor Mr. Ray closely for signs of overcorrection, such as metabolic alkalosis, hypokalemia, hypernatremia, and hypersomolality, which can lead to fluid retention, fluid volume overload, and hypertension. Administer additional 0.9% sodium chloride solution and I.V. glucose as prescribed.5

* Alonna Triplett, 26, who has type 1 diabetes, was admitted with a diagnosis of diabetic ketoacidosis. Her blood glucose level is 510 mg/dL (normal range, 60 to 110 mg/dL). Her pH is 7.28, PaCO2 is 35 mm Hg, and HCO3- is 14 mEq/L. She has positive serum ketones, and ketones and glucose in her urine. Her potassium level is 3.2 mEq/L (normal range, 3.5 to 5.1 mEq/L). She says she's exhausted and has worn herself out going to the bathroom frequently to vomit or urinate.

Ms. Triplett will need short-acting I.V. insulin to address her elevated glucose. She'll receive a bolus dose initially, followed by an infusion; the dosage will be titrated as her glucose changes. Frequently monitor her serum glucose and potassium levels and ABGs. Insulin causes an intracellular shift of potassium, which can worsen the patient's hypokalemia. Administer potassium replacement as prescribed.

Because patients with diabetic ketoacidosis typically are volume-depleted, in the first 12 hours of treatment, administer 8 to 10 L of fluid, which can be given orally along with I.V. 0.9% or 0.45% sodium chloride solution, depending on the course of her recovery.3

Metabolic alkalosis: Causes and cures

Metabolic alkalosis is the most common acid-base abnormality in hospitalized adults.6 Metabolic alkalosis is the result of excess HCO3- (from overzealous treatment of acidosis with alkalizing solutions such as sodium bicarbonate) or decreased acid, which has the effect of relatively increasing the patient's HCO3- level and making pH rise.

Decreased acid can occur three ways:

* gastrointestinal losses, as from gastric suctioning or drainage or from vomiting

* renal losses, including increased renal excretion of hydrogen ion in hypokalemia, diuretic therapy that leads to sodium and chlorine losses

* Other causes include primary aldosteronism and activation of the renin-angiotensin-aldosterone system.1,7

The most common risk factors for metabolic alkalosis are gastric suctioning, diuretic therapy, mineralcorticoid excess, and hypokalemia.

As with metabolic acidosis, treatment for metabolic alkalosis focuses on identifying and treating the underlying cause and normalizing pH. Administer an antiemetic for relief of vomiting if prescribed. As ordered, discontinue long-term nasogastric suctioning or drainage and diuretic therapy until the imbalance is resolved. The healthcare provider may prescribe acetazolamide, a carbonic anhydrase inhibitor, to increase renal excretion of HCO3-. Monitor the patient's ABGs until pH and HCO3- return to normal ranges, and closely monitor serum potassium and chloride levels.

Table. Recognizing m... - Click to enlarge in new window Table. Recognizing metabolic acidosis and alkalosis

Being prepared

By understanding the complex processes involved in maintaining the delicate balance of homeostasis, and the role of ABG analysis, you'll be prepared to provide effective care for patients at risk for developing these potentially life-threatening imbalances.

The anion gap and metabolic acidosis

The patient's anion gap can point to the possible cause of metabolic acidosis.


1. Porth CM. Essentials of Pathophysiology: Concepts of Altered Health States, 2nd ed. Philadelphia, Pa., Lippincott Williams & Wilkins, 2006. [Context Link]

2. Rose BD. Causes of lactic acidosis. UpToDate. [Context Link]

3. Lehne RA. Pharmacology for Nursing Care, 7th ed. St. Louis, Mo., Elsevier Saunders Inc., 2009. [Context Link]

4. Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, Loscalzo J, eds. Harrison's Principles of Internal Medicine, 17th ed. New York, NY. McGraw-Hill Medical, 2008. [Context Link]

5. Post T. Approach to the adult with metabolic acidosis. UpToDate. [Context Link]

6. Lennox H, Huang M. Metabolic alkalosis. [Context Link]

7. Rose BD. Causes of metabolic alkalosis. UpToDate. [Context Link]

Lactic acidosis.

Kaplan LJ, Kellum JA. Comparison of acid base models for prediction of hospital mortality after trauma. Shock. 2008;29(6):662–666.

Moviat M, Terpstra AM, Ruitenbeek W, Kluijtmans LAJ, Pickkers P, van der Hoeven JG. Contribution of various metabolites to the "unmeasured" anions in critically ill patients with metabolic acidosis. Crit Care Med. 2008; 36(3):752–758.

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