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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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