ABB/Questions and Case Studies

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Questions[edit | edit source]

1 The concentration of hydrogen ions (H+) in body fluids is in the order of:

A – μmol/l
B – nmol/l
C – mmol/l
D – pmol/l

2 The urinary excretion of H+ in 24 h in an adult is on average around the value:

A – 200 mmol
B – 40 μmol
C – 70 mmol
D – 7 mmol/l

3 The serum buffer bases are given by the values:

A – [HCO3 ] + [Proteinate]
B – [Cl] + [HCO3 ] + [HPO42− ] + [lactate]
C – [HCO3 ] + [CO32−]

4 Recognition of metabolic acidosis (MAC) in mixed ABR disorder allows:

A – finding of elevated "anion gap" values
B – decrease in pO2 in arterial or central venous blood
C – low haemoglobin in the blood
D – increased blood lactate

5 Significant hypoproteinemia with a decrease in residual anions leads to:


Case Studies[edit | edit source]

Patient with scoliosis and cardiac defect[edit | edit source]

A 17-year-old patient admitted to the hospital with congestive heart defect and scoliosis. Laboratory investigated on admission and again 24 h later.


  • Proteins 1 g
  • pH = 6
  • 3-6 hyaline cylinders
  • other findings normal
Laboratory results
on admission after 24 h
pH 7,2 7,46
pCO2 14,0 kPa 5,3 kPa
HCO3 40 mmol/l 29 mmol/l
BE 5,0 mmol/l 5,0 mmol/l
pO2 17,6 kPa 17,6 kPa
saturace O2 97,90 % 99 %
Na+ 146 mmol/l 139 mmol/l
K+ 5,0 mmol/l 3,3 mmol/l
Cl 94 mmol/l 96 mmol/l
glycemia 6,9 mmol/l 4,8 mmol/l
urea 6,0 mmol/l 1,7 mmol/l
creatinine 45 μmol/l 75 μmol/l
CK 3,6 μkat/l 2,4 μkat/l
LD 4,1 μkat/l 3,8 μkat/l
Hb 189 g/l 165 g/l
hematocrit 58,80 % 50,70 %


  1. What was the ABB disorder on admission?
  2. What was the ABB impairment after 24 h?
  3. What was the cause of the decrease in serum K+ over 24 h?
  4. Does the clinical status correspond to the laboratory findings?
  1. RAC partially compensated (rise of HCO3- and BE)
  2. MAL, probably chloride-responsive after hypercapnia.
  3. Because pH directly affects K+ movement, a change in pH leads to a change in K+ in the ECT unless K+ is therapeutically added. A 0.1 increase in pH leads to a decrease in K+ of about 0.6 mmol/l, thus a 0.26 increase in pH → a decrease in K+, 2.6 × 0.6 = 1.56, in our case a decrease in K+ of 1.70 mmol/l
  4. A similar situation occurs in several syndromes. Scoliosis makes deep breathing more difficult, the decrease in minute volume seems to be a contributory factor. The subsequent decrease in HCO3- may be explained by congestive heart defect (hypoxic lactic acidosis). However, CO2 retention was probably of a different origin (difficulty in breathing).

Patient in acute respiratory distress[edit | edit source]

A 51-year-old man admitted to hospital with acute respiratory distress syndrome (ARDS). The patient smokes 3 packs of cigarettes a day.

Laboratory results on admission
pH 7,41
pCO2 5,4 kPa
HCO3 26,0 mmol/l
pO2 17,6 kPa
saturation O2 76 %
carbonylHb 11,50 %
venous saturation 54 %
P50 4,33 kPa
2,3-bisphosphoglycerate 5,3 j. (norma 3,3-5,3)
Hb 201 g/l


  1. How do you rate ABB at the time of patient admission?
  2. Is the oxyhemoglobin dissociation curve shifted?
  3. What is the significance of the other results?
  1. ABB is normal.
  2. Yes, the curve is shifted to the right. Normally, P50 is 3.4-3.6 kPa; thus, P50 is higher with virtually no increase in 2,3-bisphosphoglycerate. Thus, the affinity of Hb for oxygen is greatly reduced.
  3. Hemoglobin is elevated; this secondary polycythemia is not common in chronic respiratory disease. Although there is not a high saturation of arterial blood (probably due to lung damage), which does not allow a good quality exchange, the tissues receive quite a lot of oxygen due to the arterio-venous difference.

Patient in diabetic coma[edit | edit source]

A 15-year-old girl is brought to the E.R. in a coma. She's been diabetic for 7 years, taking insulin. She's had several bouts of hypoglycemia and ketoacidosis. She has had a lot of studying at school recently and may have neglected some insulin injections.

Laboratory results on admission
blood urine
pH 7,11 ketonuria 3
pCO2 2,7 kPa glycosuria 3
HCO3 8 mmol/l
pO2 12,7 kPa
saturation O2 97,90 %
glycemia 58,3 mmol/l
Na+ 148 mmol/l
K+ 5,8 mmol/l
Cl 87 mmol/l
urea 5 mmol/l
creatinin 122 μmol/l
osmolality 385 mmol/kg
calculated osmolarity 346 mmol/l
anion gap 58,3 mmol/l


  1. What is the diagnosis?
  2. Calculate the anion gap (AG), what is the cause of the high AG?
  3. What is the significance of the increased osmolality?
  4. Why are chloride and HCO3- decreased, what is the significance of "normal" Na+ and increased K+?
  1. Diabetic ketoacidosis (hyperglycemia, acidosis, ketonuria, glycosuria).
  2. AG = Na+ + K+ - HCO3- - Cl- = 58.8 mmol/l; the cause is ketoacidosis (other causes are lactic acidosis, uremia, intoxication...).
  3. Increased serum osmolality is from water loss by osmotic diuresis and from hyperglycemia. It is common in ketoacidosis.
  4. Diabetic ketoacidosis is a form of MAC that leads to a decrease in HCO3-. Patients breathe rapidly to compensate for acidosis and this leads to a decrease in pCO2 (pO2 tends to be normal). Hypochloridemia occurs due to osmotic diuresis. High Na+ is relative to the effect of water loss. The patient is thirsty but usually drinks fluids without enough Na+ and other electrolytes. Plasma K+ levels should be assessed with caution. Only about 2-3% of total body K+ is in ECT. Hyperkalemia here is due to severe acidosis and partly also to osmotic diuresis. (Body K+ stores in diabetic coma are always very reduced and K+ administration is necessary to correct the condition.

Patient with pulmonary insufficiency and hypokalemia[edit | edit source]

Patient 55 years old, with chronic obstructive pulmonary disease, who was treated for a long time with thiazide preparations (as a diuretic).

Laboratory results on admission

pH 7,42
pCO2 11,6 kPa
HCO3 55 mmol/l
pO2 8,4 kPa
K+ 2,6 mmol/l


  1. What is the fault in ABB?
  1. Chronic lung disease leads to reduced gas exchange: CO2 retention → respiratory acidosis, O2 deficiency → hypoxia → hypoxic lactic acidosis. Long-term use of thiazide preparations leads to urinary K+ loss → hypokalemic metabolic alkalosis.

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