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p. 555

Acid–base analysis should proceed in a stepwise approach to avoid

missing complicated disorders that may not be readily apparent.

Case 26-1 (Question 1),

Case 26-2 (Question 1),

Case 26-3 (Question 1),

Case 26-4 (Question 2),

Case 26-5 (Question 3),

Case 26-6 (Question 1)

A normal anion gap metabolic acidosis is most commonly found in

patients who have either diarrhea or are receiving large amounts of

isotonic crystalloid infusions. A less common cause of a normal anion

gap metabolic acidosis occurs with patients who present with one of

several types of renal tubular acidosis.

Case 26-1 (Questions 2–6)

A metabolic acidosis with an elevated anion gap is created by a disease

process that produces an acid, which is buffered by the major

extracellular buffer, bicarbonate. It is important to include a calculation

of the anion gap in the workup of all patients considered for acid–base

analysis.

Case 26-2 (Questions 1–4)

Metabolic alkaloses can be classified according to a patient’s volume

status and responsiveness to the administration of chloride-containing

solutions. A contraction alkalosis, also called chloride-responsive

alkalosis, is generally caused by diuretic administration whereas a

chloride-nonresponsive alkalosis may be caused by glucocorticoid

administration.

Case 26-3 (Questions 1–4)

A respiratory acidosis can be acute, chronic, or acute-on-chronic. The

best way to differentiate these disorders is with a careful patient history

and review of previous blood gas values looking for elevated carbon

dioxide levels when a patient is at his or her baseline.

Case 26-4 (Questions 1–4)

Unlike respiratory acidosis, most patients presenting with a respiratory

alkalosis do so acutely. There are a relatively small number of

conditions that cause an acute respiratory alkalosis, which can aid in the

diagnosis when it is not apparent.

Case 26-5 (Questions 1–4)

Mixed metabolic and respiratory acid–base disorders occur commonly in

acutely ill patients. Acid–base analysis can assist in the diagnosis of

Case 26-6 (Questions 1–3)

clinically difficult cases. Following a stepwise approach in the analysis

of acid–base disorders should identify all clinically important

abnormalities.

Understanding the etiology of a clinically important acid–base disturbance is

important because therapy generally should be directed at the underlying cause of the

disturbance rather than merely the change in pH. Severe acid–base disorders can

affect multiple organ systems, including cardiovascular (impaired contractility,

arrhythmias), pulmonary (impaired oxygen delivery, respiratory muscle fatigue,

dyspnea), renal (hypokalemia, nephrolithiasis), or neurologic (decreased cerebral

blood flow, seizures, coma).

ACID–BASE PHYSIOLOGY

To protect body proteins, acid–base balance must be tightly controlled in an attempt

to maintain a normal extracellular pH of 7.35 to 7.45 and an intracellular pH of

approximately 7.0 to 7.3.

1 This narrow range is maintained by complex buffer

systems, ventilation to expel carbon dioxide (CO2

), and renal elimination

p. 556

p. 557

of acids and reabsorption of bicarbonate (HCO3

).

2 At rest, about 200 mL of CO2

,

and even more during exercise, is transported from the tissues and excreted in the

lungs.

3 Although HCO3

is responsible only for about 36% of intracellular buffering,

it provides about 86% of the buffering activity in extracellular fluid (ECF).

1

Extracellular fluid contains approximately 350 mEq of HCO3

, which buffers

generated H+

.

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