Acid-base balance disorders – case histories
Case 1
Ms M.M., 72 years old, treated for a long time for chronic obstructive lung disease, now admitted for
dyspnoea. Reported to have been febrile and coughing for the last three days.
Admission Astrup
pH
pCO2
pO2
HCO3BE




7.325
7.42 kPa
6.42 kPa
30.1 mM
- 7.2 mM
What type of ABB disorder can be seen in this patient?
Recall the mechanisms of control of breathing.
What pH of urine would you expect in this patient?
Explain the mechanism of bicarbonate re-absorption in the kindneys.
Patient M.M. was administered oxygen (by mask, 4L/min) to alleviate nocturnal dyspnoea. After an
hour dyspnoea disappeared, patient became, however, confused and sleepy. The result of arterial
Astrup was as follows:
pH
pCO2
pO2
HCO3BE


7.210
9.86 kPa
11.2 kPa
31.0 mM
- 7.9 mM
How would you explain the extreme rise in pCO2?
Would you administer sodium bicarbonate in this case?
Upon standard antibiotic and bronchodilation treatment the patient’s state improved in 10 days. The
final Astrup result was:
pH
pCO2
pO2
HCO3BE
7.45
3.9 kPa
9.2 kPa
27.0 mM
+3.0 mM
Case 2
34 year old woman was operated for acute thrombotic occlusion of mesenteric vein and most of the
intestine was resected. Only 70 cm of proximal jejunum was left – jejunostomy was performed. The
patient afterwards lost weight - from 55 kg to 43 kg within one month – produced less than 0.5 liters of
urine per day, her wound became dehiscent. She was losing more than 4 liters of fluid through the
jejunostomy. Basic examination suggested deep dehydration and malnutrition.
Lab results: Na=124 mM, K = 3.9 mM, Cl=69 mM… Astrup:
pH
pCO2
pO2
HCO3BE


7.550
7.2 kPa
7.7 kPa
42mM
+18 mM
What kind of ABB disorder is this? What is the probable cause?
What would be the appropriate treatment?
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Case 3.
68 year old K.M., homeless, was admitted unconscious. As reported by the police he was found in a
park. Physical examination shows no gross pathology, except deepened breathing, 20 breaths per
minute.
Lab results: Na 141 mM, K = 5.8 mM, Cl = 103 mM, Glycaemia 7.4 mM, Urea 6.98 mM, Creatinin 114
M, ALT 19.5 kat/l, AST 25.3 kat/l
Urine: pH 4.5, otherwise normal (negative for protein, glucose, ketone bodies)
Astrup:
pH
pCO2
pO2
HCO3BE




7.010
2.1 kPa
12.2 kPa
11.0 kPa
- 16 mM
Look at the lab results, decide which of these are normal and which abnormal. What state
are they pointing to?
What type of ABB disorder is this? Explain the hyperpnoea.
Calculate anion gap. Which substances can be responsible for the increased AG?
What then could be the cause for the patient’s state?
Toxicology was positive for ethyleneglycol.
Case 4.
26 year old man (65kg) was admitted with severe head injury after a car accident. Artificial ventilation
was started with 40% oxygen, tidal volume 600 mL, breathing frequency of 18 per minute.
Astrup result after 30 minutes of this ventilation regime was as follows:
pH
pCO2
pO2
HCO3BE


7.490
1.86 kPa
16.2 kPa
24 mM
+6.8 mM
Explain the type of ABB disorder.
What would be the treatment?
SOLUTION
CASE 1
Part A
 What type of ABB disorder can be seen in this patient?
Respiratory acidosis with partial metabolic compensation
 Recall the mechanisms of control of breathing.
Central chemoreceptors in brainstem register pCO2 (or a fall in pH as CO2 difuses through blood
brain barrier). Peripheral receptors in big vessels register pO2. As far as pO2 is within normal
range, breathing is regulated by central receptors according to subtile pCO2 changes.
Nevertheless, as pO2 fall bellow 7-8 kPa, peripheral receptors stimulate breathing regardless the
pCO2 level
 What pH of urine would you expect in this patient?
Acidic – metabolic compensation
 Explain the mechanism of bicarbonate re-absorption in the kindneys
See figure from the lecture: proton secretion, carboanhydrase....
Part B
 How would you explain the extreme rise in pCO2?
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In this patient, breathing has been stimulated by low pO2 (peripheral receptors), because central
receptors already had adapted for high CO2 in chronic lung disease. After oxygen administration,
increasing pO2 in alveoli and subsequently in blood, impulses from peripheral receptors disappeared,
and breathing became shallow. This led to further increase in pCO2 (approaching narcotic
concentration) and worsening of both acidosis and clinical sings (consciousness).

Would you administer sodium bicarbonate in this case?
Certainly not. Bicarbonate administration would only increase endogenous CO2 production. The only
way how to improve the matter is to eliminate CO2 from the body, even by using artificial ventilation.
CASE 2
 What kind of ABB disorder is this? What is the probable cause?
Metabolic alkalosis with partial respiratory compensation (an increase in pCO2 is higher than is
commonly seen, because a substantial increase in pCO2 is usually not possible due to limitation by
pO2). The state could be caused by (1) chlorine loss from fistula leading to hypochloridemia and
bicarbonate increase by Hamburger effect. Potassium depletion (2) could also participate. Loss of K+
is replaced from intracellular space by H+/K+ exchange. Protons are therefore disposed and buffered
within cells during hypokalemia – this condition is sometimes called hypokalemic alkalosis.
 What would be the appropriate treatment?
Supplementation of lost ions (Na+, Cl- a K+) is of crucial importance. “Normal saline” contains 150mM
of chloride (whilst ECS only 100mM) and has acidifying properties (replaces bicarbonate with
chloride).
CASE 3
 Look at the lab results, decide which of these are normal and which abnormal. What state are
they pointing to?
Slightly increased potassium (probably due to acidosis, see above), incrased transaminases (pointing
to liver damage), borderline hyperglycaemia (probably without causative relations to acidosis).
 What type of ABB disorder is this? Explain the hyperpnoea.
Severe metabolic acidosis with partial respiratory compensation. Hyperpnoea (deep and rapid
ventilation), is a sign of respiratory compensation, sometimes called Kussmaul breathing.
 Calculate anion gap. Which substances can be responsible for the increased AG? What then
could be the cause for the patient’s state?
AG = (Na + K) - (Cl + HCO3-), is increased in this case. Possible causes: ketones (not in this case, no
severe hyperglycaemia, no koteons found in the urine), lactate (is measurable, was sent and found
normal in this case), inorganic acids (phosphate, sulphate; usually in case of renal failure, not in this
case – creatinine is normal, kidneys are probably normal). Other: e.g. poisons...
We must consider poisoning in this case, because we still did not explain increased anion gap...
Toxicology samples revealed ethylenglycole poisoning
Commentary: Ethylenglycole is a component of antifreeze mixtures, quite common cause of poisoning
in low social class (e.g. homeless, prisoners). It is oxidized up to oxalate, which causes severe and
life-threating acidosis. Treatment: dialysis, bicarbonate. Prognosis: poor (The patient died after 4 days
under the picture of multiple-organ failure).
CASE 4
 Explain the type of ABB disorder.
Respiratory alkalosis – acute, without metabolic compensation (as it requires hours and days to
develop). It is caused by inappropriate ventilator setting – minute volume is too high.
 What would be the treatment?
Correction of ventilator settings: a decrease of tidal volume or frequency or both.
Commentary: Artificial hyperventilation causing alkalosis leads to contraction of brain arteries and a
decrease in cerebral blood (See also cerebral blood flow autoregulation in physiology).
František Duška
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