Acid–Base Disorders

(1)

Professor of Medicine, Department of Medicine, Chief, Division of Nephrology and Hypertension, Rutgers New Jersey Medical School, Newark, NJ, USA

Keywords

Metabolic acidosisMetabolic alkalosisRespiratory alkalosisRespiratory acidosisTriple acidBase disorders

A mixed acid–base disorder is defined as the coexistence of two or three primary disorders in the same patient. These disorders can occur simultaneously or at different times. Two groups of patients are at risk for mixed acid–base disturbances: the critically ill patients in the intensive care units and the elderly. Also, diabetic or alcoholic subjects may present to the Emergency Department with a double or triple acid–base disturbance.

In general, the critically ill patients have multiple medical conditions that can elicit a mixed acid–base disturbance. For example, a septic or liver failure patient can present initially with a respiratory alkalosis and subsequently develops a high anion gap (AG) metabolic acidosis due to hypotension. The other group of patients, the elderly, may have a chronic disease such as chronic obstructive pulmonary disease (COPD) with respiratory acidosis and subsequent development of metabolic alkalosis due to a thiazide or loop diuretic for treatment of cor pulmonale.

Recognition of a mixed acid–base disorder by the clinician is extremely important for appropriate care of the patient. For example, failure to recognize the metabolic alkalosis superimposed on chronic respiratory acidosis may aggravate hypoxemia because both disorders are associated with an increase in pCO₂. Also, vigorous saline administration may improve the underlying metabolic alkalosis while lowering the pH to a dangerous level. To avoid these changes, it is extremely important to recognize both disorders and treat them simultaneously so that the patient’s condition would ultimately improve.

Furthermore, identification of a mixed acid–base disorder may provide a clue to the onset of a new condition, particularly in a critically ill patient. For example, a patient with severe pneumonia and respiratory alkalosis may start developing an increase in AG within a few hours of admission. This suggests that the patient may be generating lactic acid due to septic shock.

Analysis of Mixed Acid–Base Disorders

Mixed acid–base disorders should be suspected whenever (see also Chap. 4):

1.

There is no compensatory response or overcompensation for a primary simple acid–base disorder
2.

The pH and [HCO₃ ⁻] are normal, but the AG is high (mixed metabolic acidosis and metabolic alkalosis)
3.

The pH is near normal, but [HCO₃ ⁻] is low (mixed metabolic acidosis and respiratory alkalosis)
4.

The pH is low (<7.4), but [HCO₃ ⁻] is normal or slightly low (mixed metabolic acidosis and respiratory acidosis)
5.

The pH is near normal, but [HCO₃ ⁻] is high (mixed metabolic alkalosis and respiratory acidosis)
6.

The pH is high (>7.4), but [HCO₃ ⁻] is normal (mixed metabolic alkalosis and respiratory alkalosis)

Several factors should be taken into consideration in analyzing a mixed acid–base disorder. Such factors include:

1.

Medical and clinical settings: stable or unstable, intubation, sepsis, hypotension, nasogastric suction, or ketoacidosis, etc
2.

Drug administration: sedation
3.

Evaluation of pH: lower than before (additive), or normal (counterbalancing), or high (additive)
4.

AG: normal or high
5.

Time course of pH changes: acute or chronic disturbance

The following discussion will focus on the clinical settings in which a common mixed acid–base disorder occurs with characteristic electrolyte and arterial blood gas (ABG) values. Note that these laboratory values vary depending on the presence of dominant disturbance and the duration of the coexisting disorder. Table 14.1 summarizes the most frequently observed mixed acid–base disorders in hospitalized patients.

Table 14.1

Common mixed acid–base disorders, pH and electrolyte profiles

Acid–base disorder	Clinical setting	pH	pCO₂ ^a	Na⁺	K⁺	Cl⁻	HCO₃ ^−a	AG
Double acid–base disorders
Metabolic acidosis and metabolic alkalosis	Renal failure (CKD 4 and 5), diabetic ketoacidosis, lactic acidosis with vomiting, or diuretics	N	N	N/↓	N↓	N↓	~N	↑
Metabolic acidosis and respiratory alkalosis	Renal failure (CKD 4 and 5) with sepsis, or salicylate intoxication, or pulmonary embolus	~N	↓↓	N	N	N/↑	↓↓	↑ or N^b
Metabolic acidosis and respiratory acidosis	Cardiac arrest or renal failure with emphysema, or sedatives, or narcotics	↓↓	N/↑	N	N	N	N/↓	↑ or N^b
Metabolic alkalosis and respiratory alkalosis	Vomiting, diuretics with pneumonia, or hepatic failure, or pregnancy	↑↑	N/↓	~ N	↓	N	N/↑	Slight↑
Metabolic alkalosis and respiratory acidosis	Vomiting or diuretics with emphysema, or sedatives	N/↑	↑↑	N/↓	N/↓	N	↑↑	N
Triple acid–base disorders
Metabolic acidosis, metabolic alkalosis, and respiratory alkalosis	Ketoacidosis with vomiting and abdominal pain, or pneumonia	↑	↓	N	N/↓	N/↓	Slight↓	↑
Metabolic acidosis, metabolic alkalosis and respiratory acidosis	Ketoacidosis with vomiting, or sedative, or COPD	↓↓	↓	N	N	N	↓↓	↑

AG anion gap, COPD chronic obstructive pulmonary disease, CKD chronic kidney disease

^aConcentrations of these vary depending on the severity of the dominant acid–base disorder

^bAG depends on the etiology of metabolic acidosis

Metabolic Acidosis and Metabolic Alkalosis

This disorder can be seen in two clinical settings:

1.

Metabolic acidosis due to chronic kidney disease (CKD) stages 4 and 5 (renal failure), or ketoacidosis, or lactic acidosis with a superimposed metabolic alkalosis due to vomiting, or nasogastric suction. The most compatible electrolyte and ABG values are as follows:

Serum	ABG
Na⁺ = 138 mEq/L	pH = 7.39
K⁺ = 3.6 mEq/L	pCO₂ = 39 mmHg
Cl⁻ = 96 mEq/L	pO₂ = 92 mmHg
HCO₃ ⁻ = 23 mEq/L	HCO₃ ⁻ = 22 mEq/L
Creatinine = 4.6 mg/dL
BUN = 48 mg/dL
AG = 19

ABG arterial blood gas, AG anion gap, BUN blood urea nitrogen

2.

Metabolic alkalosis due to loop or thiazide diuretic use with a superimposed metabolic acidosis due to ketoacidosis or renal failure. Compatible laboratory results are:

Serum	ABG
Na⁺ = 130 mEq/L	pH = 7.41
K⁺ = 3.2 mEq/L	pCO₂ = 41 mmHg
Cl⁻ = 86 mEq/L	pO₂ = 92 mmHg
HCO₃ ⁻ = 25 mEq/L	HCO₃ ⁻ = 24 mEq/L
Creatinine = 1.4 mg/dL
BUN = 28 mg/dL
AG = 19

ABG arterial blood gas, AG anion gap, BUN blood urea nitrogen

Note that electrolyte and ABG values vary depending on the dominant acid–base disorder. The effect on pH by these acid–base disorders is to bring it to near normal (counterbalancing). One consistent abnormality is serum AG, which is elevated. If diarrhea is the cause for metabolic acidosis, the AG may not be that high.

Metabolic Acidosis and Respiratory Alkalosis

The clinical setting is usually renal failure, ketoacidosis, or lactic acidosis with sepsis. Salicylate overdose or pulmonary embolism can produce both metabolic acidosis and respiratory alkalosis. The representative electrolyte and ABG are shown in the following table. The AG is elevated. The effect on pH is counterbalancing, so that the pH is brought to near normal, but the fall in pCO₂ is greater with both disorders. In salicylate overdose, the initial acid–base disorder is respiratory alkalosis due to direct central nervous system (CNS) stimulation followed by the development of metabolic acidosis. The presence of dominant disorder can be identified by calculation of appropriate secondary response. For example, if metabolic acidosis is the dominant acid–base disorder, the superimposed respiratory alkalosis can be diagnosed by a greater fall in pCO₂ than expected for a simple metabolic acidosis. If respiratory alkalosis is the dominant disturbance, a coexisting metabolic acidosis can be identified by a greater fall in serum [HCO₃ ⁻] than expected for a simple respiratory alkalosis.

The laboratory values shown in the following table indicate that metabolic acidosis is the dominant acid–base disturbance. The expected pCO₂ should be 26 ± 2 mmHg (1.5 × serum HCO₃ ⁻ + 8 ± 2 = 18 + 8 = 26 ± 2). Instead, the reported pCO₂ is 22 mmHg, indicating that the patient is more hypocapnic than expected. Thus, respiratory alkalosis is superimposed on metabolic acidosis.

Serum	ABG
Na⁺ = 129 mEq/L	pH = 7.36
K⁺ = 3.4 mEq/L	pCO₂ = 22 mmHg
Cl⁻ = 92 mEq/L	pO₂ = 90 mmHg
HCO₃ ⁻ = 12 mEq/L	HCO₃ ⁻ = 11 mEq/L
Creatinine = 8.6 mg/dL
BUN = 68 mg/dL
AG = 25