Acid-base status

Published on 13/02/2015 by admin

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Last modified 22/04/2025

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Acid-base status

Ian MacVeigh, MD

Recognizing, diagnosing, and treating acid-base disorders are absolutely essential skills for all anesthesia providers. Having a clear understanding of the terminology and physiology related to acid-base disorders and employing standard criteria for the assessment and diagnosis of these often-puzzling derangements results in quicker recognition and more effective treatment of acid-base disorders.

Terminology

Normal values of pH, defined as the negative logarithm of the hydrogen ion concentration [H⁺] (expressed in extracellular fluids in nanoequivalents per liter), range from 7.35 to 7.45. Changes in pH are inversely related to changes in [H⁺]: a 20% increase in [H⁺] decreases the pH by 0.1; conversely, a 20% decrease in [H⁺] increases the pH by a 0.1 (Table 47-1).

Table 47-1

pH for Given Hydrogen Ion Concentrations

pH	[H⁺] (nEq/L)
7.0	100
7.1	80
7.2	64
7.3	50
7.4	40
7.5	30
7.6	24
7.7	20

The terms acidemia and alkalemia refer to the pH of blood. Acidosis, on the other hand, refers to the process that either adds acid or removes alkali from body fluids; conversely, alkalosis is the process that either adds alkali or removes acid from body fluids. Compensation refers to the body’s homeostatic mechanisms that generate or eliminate [H⁺] to normalize pH in response to a pathologic acid-base disturbance. Base excess, an assessment of the metabolic component of an acid-base disturbance, quantifies the amount of acid that must be added to a blood sample to return the pH of the sample to 7.40 if the patient’s PaCO₂ were 40 mm Hg. A positive base excess value indicates that the patient has a metabolic alkalosis (acid would have to be added to the blood to reach a normal pH); a negative value indicates that the patient has a metabolic acidosis and alkali would have to be added to normalize the pH. Blood gas results are, by convention, reported as pH, PaCO₂, PaO₂, HCO₃⁻, and base excess; the latter two are calculated. The HCO₃⁻ is derived using the Henderson-Hasselbalch equation, which can be expressed as either of the following:

< ?xml:namespace prefix = "mml" />pH=pKa+PaCO2HCO3–

[H+]=24×PaCO2HCO3–

Tight control of the pH requires a fairly constant PaCO₂/HCO₃⁻ ratio, which allows one to check the validity of an arterial blood gas (ABG) sample (Table 47-2).

Table 47-2

Examples of the Use of Henderson-Hasselbalch Equation to Calculate H⁺ Concentration with a Known HCO₃⁻ and PaCO₂

PaCO₂	HCO₃⁻	[H⁺] (nEq/L) will be	Calculation [H⁺]	pH
40	24	40	24 × 40/24 = 40	7.4
60	24	60	24 × 60/24 = 60	7.2
20	24	20	24 × 20/24 = 20	7.7
40	16	60	24 × 40/16 = 60	7.2
60	16	90	24 × 60/16 = 90	7.05
20	16	30	24 × 20/16 = 30	7.5

Types of acid-base disorders

Acid-base disorders may be simple or mixed. Simple disorders include respiratory acid-base disorders, in which the primary change in pH is secondary to changes in PaCO₂, and metabolic acid-base disorders, in which the primary change involves the [H⁺]. Mixed disorders occur when more than one acid-base disorder coexists in the same patient. Remember that acid-base disorders are simply manifestations of underlying systemic disorders. Determining why the acid-base disorder is present requires the incorporation of information from the patient’s history and the findings on physical examination.

Compensatory responses

Every primary acid-base disorder should have an appropriate compensatory response. A primary respiratory (ventilatory) disorder induces a renal response—reabsorption of HCO₃⁻ in the proximal tubules is altered to compensate for the change in pH induced by the change in PaCO₂. This process is slow, occurring over 24 to 36 h. A primary metabolic disorder, on the other hand, induces a much faster respiratory compensation, in which ventilation changes to increase or decrease PaCO₂ (Table 47-3). The absence of compensation in a timely manner would probably indicate the presence of a secondary disturbance.

Table 47-3

Primary Change and Compensatory Response for the Primary Acid-Base Disorders

Primary Disorder	Primary Change	Compensatory Response*
Respiratory acidosis	↑ PaCO₂	↑ HCO₃⁻
Respiratory alkalosis	↓ PaCO₂	↓ HCO₃⁻
Metabolic acidosis	↓ HCO₃⁻	↓ PaCO₂
Metabolic alkalosis	↑ HCO₃⁻	↑ PaCO₂

^*Homeostatic response in an attempt to maintain constant PaCO₂/HCO₃⁻ ratio.

Metabolic acidosis

Metabolic acidosis provokes stimulation of chemoreceptors, promoting an increase in ventilation. Winter’s formula can be used to calculate the expected PaCO₂ in patients with metabolic acidosis:

Expected PaCO2 = (1.5 × [HCO3−]) + 8 ± 2

If the measured PaCO₂ is equal to the expected PaCO₂, the patient has a compensated metabolic acidosis. If, on the other hand, the measured PaCO₂ is greater than the expected PaCO₂, compensation is inadequate, and the patient has a primary metabolic acidosis with superimposed respiratory acidosis. However, if the measured PaCO₂ is lower than the expected PaCO₂, the patient has a primary metabolic acidosis with superimposed respiratory alkalosis.

Metabolic alkalosis

Metabolic alkalosis can be chloride responsive or resistant. Chloride-responsive states, which are associated with urinary chloride concentrations of less than 15 mEq/L, include vomiting, continuous nasogastric suctioning, and volume-contraction states—the latter being the most common in hospitalized postsurgical patients. Chloride-resistant disorders or conditions, associated with urinary chloride concentrations greater than 25 mEq/L, include hypercortisolism, hyperaldosteronism, sodium bicarbonate therapy, severe renal artery stenosis, hypokalemia, and the use of diuretics, in which case patients may have high urinary chloride concentrations, but the alkalosis nonetheless responds to the administration of chloride. The formula used to calculate the PaCO₂ in patients with metabolic alkalosis is as follows:

Expected PaCO2 = (0.7 × HCO3−) + 21 ± 2

If the measured PaCO₂ is equal to the expected PaCO_2, the patient has a metabolic alkalosis. However, if the measured PaCO₂ is greater than the expected PaCO_2, the patient has a metabolic alkalosis with superimposed respiratory acidosis. Finally, if the measured PaCO₂ is less than the expected PaCO_2, the patient has a primary metabolic alkalosis with superimposed respiratory alkalosis.

Assessment of acid-base disorders secondary to respiratory mechanics

Although equations can be used to calculate the expected change in pH for changes in PaCO₂, the easiest way to assess a patient for the influences of PaCO₂ on pH is to remember that the pH changes inversely 0.08 for every 10-mm Hg change in PaCO₂. For example, if the PaCO₂ equals 50 mm Hg, the pH will be 7.32; if the PaCO₂ is 30 mm Hg, the pH will be 7.48.

Acid-base disorders secondary to respiratory mechanics are the most common acid-base disorders seen in otherwise “healthy” patients anesthetized for surgical procedures.

If respiratory disorders are more longstanding (e.g., respiratory acidosis in a patient with chronic obstructive pulmonary disease or a ventilated patient in the intensive care unit retaining CO₂), then the kidneys will retain HCO₃⁻ to minimize the change in pH.

Acute respiratory acidosis prior to onset of renal compensation:

Expected pH = 7.40 − (0.008 × PaCO2) ΔpH = 0.008 × ΔPaCO2

Acute respiratory alkalosis prior to onset of renal compensation:

Expected pH = 7.40 + [0.008 × (40 − PaCO2)] ΔpH = 0.008 × ΔPaCO2

Chronic respiratory acidosis, renal compensation fully developed:

Expected pH = 7.40 − [0.003 × (PaCO2 − 40)] ΔpH = 0.003 × ΔPaCO2

Chronic respiratory alkalosis, renal compensation fully developed:

Expected pH = 7.40 + [0.003 × (40 − PaCO2)] ΔpH = 0.003 × ΔPaCO2

Respiratory acidosis

Causes of respiratory acidosis include airway obstruction, central nervous system depression, the use of opioids, restrictive lung disease (kyphoscoliosis, fibrothorax), and neuromuscular diseases.

Respiratory alkalosis

Causes of respiratory alkalosis include psychogenic hyperventilation, encephalitis, early pneumonia, early stages of bronchial asthma, pulmonary embolism, hepatic failure, early sepsis, and pregnancy. The lowest PaCO₂ achieved by hyperventilation is approximately 16 mm Hg, and the pH is approximately 7.6 before renal compensatory changes occur.

Assessment of acid-base disorders secondary to metabolic disorders

Metabolic acidosis

If, on an ABG analysis, the pH is less than 7.35 and the base excess is negative (a base deficit), then the patient has a metabolic acidosis, assuming that the PaCO₂ is equal to 40 mm Hg. The first step is to calculate the anion gap (AG), which can be done by subtracting the sum of Cl⁻ and HCO₃⁻ from the Na⁺ concentration. Normal values are 12 ± 4 mEq/L. This gap represents the unmeasured negatively charged ions (anions) that are balancing the electrical charge of the positively charged ions (cations) in human bodies.

Causes of an increased anion gap

Causes of an increase in the AG (mnemonic, DARLINGS ARE IMP) include diabetic ketoacidosis (anions = acetoacetate, β-hydroxybutyrate), alcohol use, renal failure (anions = phosphate, sulfate), lactic acidosis, iron poisoning, no food (starvation), generalized seizures, sepsis, aspirin poisoning, rhabdomyolysis, ethylene glycol ingestion, the use of isoniazid (INH), and methanol or paraldehyde exposure.

Causes of a decreased anion gap

Processes that decrease the unmeasured anions or increase the unmeasured cations will decrease the AG. Albumin is an anion and is responsible for approximately half of the normal AG of 12 mEq/L. If the albumin concentration is low, the AG will be lower than normal (i.e., <12 mEq/L), decreasing by approximately 2 to 3 units for every 1-g decrease in serum albumin concentration.

Conversely, immunoglobulins are cations, and if they increase (i.e., in paraproteinemias, such as multiple myeloma), the kidneys retain additional chloride to maintain electrical neutrality, and the AG decreases.

Causes of non–anion gap metabolic acidosis

In metabolic acidosis without an AG, the loss of bicarbonate is compensated for by a rise in chloride. Primary causes of a metabolic acidosis without an AG include gastrointestinal losses (diarrhea, small bowel fistula, ileostomy, ureterosigmoidostomy, or an ileal conduit for an ureter), urinary losses (proximal and distal renal tubular acidosis, acetazolamide therapy, urinary obstruction, pancreatic fistula, or the correction phase of diabetic ketoacidosis), and infusion of isotonic saline.

δanion gap strategy

The ΔAG strategy is used in patients with metabolic acidosis to detect the possibility of a superimposed metabolic disorder, either a metabolic alkalosis or a non-AG metabolic acidosis. The following three steps are required:

1. ΔAG = patient-calculated AG – normal AG (12 mEq/L)

2. Calculate the corrected HCO₃⁻ = measured HCO₃⁻ + ΔAG

3. Compare corrected HCO₃⁻ to a normal HCO₃⁻ = 24 mEq/L

If the corrected HCO₃⁻ is higher than the normal HCO₃⁻, then the patient has a superimposed metabolic alkalosis; if the corrected HCO₃⁻ is lower than the normal HCO₃⁻, then the patient has non-AG metabolic acidosis.

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