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

2 Serum buffer bases are given by:

A - [HCO 3 - ] + [proteinate]
B - [Cl - ] + [HCO 3 - ] + [HPO 4 2− ] + [lactate]
C - [HCO 3 - ] + [CO 3 2− ]

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

A - finding increased values ​​of "anion gap"
B - reduction of pO 2 in arterial or central venous blood
C - low hemoglobin in the blood
D - increased lactate in the blood

4 Significant hypoproteinemia with a decrease in residual anions leads to: '

A - MAL
B - MAC
C - RAL + MAC
D - MAC + RAC


Case reports[edit | edit source]

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

A 17-year-old patient was admitted to hospital with a congestive heart defect and scoliosis. Upon admission, the laboratory was examined and again 24 hours later.

Power:

  • protein 1 g
  • pH = 6
  • 3-6 hyaline cylinders
  • other findings normal
+ Laboratory results
- 'reception' 'in 24 hours' - pH 7.2 7.46 - pCO 2 14.0 kPa 5.3 kPa - HCO 3 - 40 mmol / l 29 mmol / l - BE 5.0 mmol / l 5.0 mmol / l - pO 2 17.6 kPa 17.6 kPa - saturation O 2 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 - glycaemia 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 μcat / l 2.4 μcat / l - LD 4.1 μcat / l 3.8 μcat / l - Hb 189 g / l 165 g / l - Hematocrit 58.80% 50.70%

'Questions:'

  1. 'What was the ABR failure on reception?'
  2. 'What was the ABR disorder after 24 hours?'
  3. 'What caused the decrease in serum K + in 24 hours?'
  4. 'Does the clinical condition match the laboratory findings?'
Answers -
  1. RAC partially compensated (HCO rise 3 - and BE)
  2. MAL, apparently chloride-responsive after hypercapnia.
  3. Because pH directly affects K + movement, a change in pH leads to a change in K + in ECT unless K + is therapeutically delivered. An increase in pH by 0.1 leads to a decrease in K + by about 0.6 mmol / l, ie an increase in pH by 0.26 → a decrease in K + , by 2.6 × 0.6 = 1.56, in our case a decrease in K + by 1.70 mmol /l# A similar situation occurs with multiple syndromes. Scoliosis makes deep breathing difficult, and the reduction in minute volume seems to have worked together. The subsequent decrease in HCO 3 - can be explained by a congestive heart defect (hypoxic lactic acidosis). However, the retention of CO 2 was probably of a different origin (difficulty breathing).

Patient in acute respiratory distress[edit | edit source]

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

+ Laboratory results on admission
-

pH || 7.41

- pCO 2 5.4 kPa - HCO 3 - 26.0 mmol / l - pO 2 17.6 kPa -

saturation O 2 || 76%

- carbonylHb 11,50% - venous saturation 54% - P 50 4.33 kPa -

2,3-bisphosphoglycerate || 5.3 (standard 3.3-5.3)

- Hb 201 g / l

'Questions:'

  1. 'How do you rate ABR at the time of admission?'
  2. 'Is the oxyhemoglobin dissociation curve shifted?'
  3. 'What is the significance of the other results?'
Answers -
  1. ABR is normal.
  2. Yes, the curve is shifted to the right. Normally, P 50 is 3.4-3.6 kPa; Thus, P 50 is higher with virtually no increase in 2,3-bisphosphoglycerate. Thus, the affinity of Hb for oxygen is significantly reduced.
  3. Hemoglobin is elevated, this secondary polycythemia is not common in chronic respiratory diseases. Although there is no high saturation of arterial blood (probably due to lung damage), which does not allow quality replacement, the tissues receive quite a lot of oxygen due to the arteriovenous difference.

Patient in diabetic coma[edit | edit source]

A 15-year-old girl is brought in a coma to ARO. She is a diabetic for 7 years, she took insulin. She already had several seizures hypoglycemia and ketoacidosis. She's been learning a lot at school lately and may have neglected some insulin injections.

+ Laboratory results on admission
- 'blood' 'urine' - pH 7.11 ketonuria 3 - pCO 2 2,7 kPa glycosuria 3 - HCO 3 - 8 mmol / l - pO 2 12.7 kPa - saturation O 2 97.90% - glycemia 58.3 mmol / l - Na + 148 mmol / l - K + 5.8 mmol / l - Cl - 87 mmol / l -

lactate ||||||

- urea 5 mmol / l - creatinine 122 μmol / l - Osmolality 385 mmol / kg -

calculated osmolarity || 346 mmol / l ||||

- anion gap 58.3 mmol / l

'Questions:'

  1. What is the diagnosis?
  2. Calculate the anion gap (AG), what is the cause of high AG?
  3. What is the significance of increased osmolality?
  4. Why are chlorides and HCO 3 - reduced, what is the meaning of "normal" Na + and increased K +  ?
Answers -
  1. Diabetic ketoacidosis (hyperglycemia, acidosis, ketonuria, glycosuria).
  2. AG = Na + + K + - HCO 3 - - Cl - = 58.8 mmol / l; the cause is ketoacidosis (other causes are lactic acidosis, uremia, intoxication ...).
  3. Increased serum osmolality is due to water loss by osmotic diuresis and hyperglycemia. This is common in ketoacidosis.
  4. Diabetic ketoacidosis is a form of MAC that leads to a decrease in HCO 3 - . Patients breathe rapidly to compensate for acidosis and this leads to a reduction in pCO 2 (pO 2 is usually normal). Hypochloridemia occurs due to osmotic diuresis. High Na + is a relative effect of water loss. The patient is thirsty, but usually drinks fluids without enough Na + and other electrolytes. Plasma K + levels should be evaluated carefully. Of the total body K + , only about 2-3% are in the ECT. Hyperkalaemia is caused by severe acidosis and partly also osmotic diuresis. (K + stores in a diabetic coma are always greatly reduced and K + is required to correct the condition.

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

Patient 55 years old, with chronic pulmonary obstructive disease who has been treated with thiazide drugs for a long time (such as diuretic).

Laboratory results on admission

pH || 7.42
- pCO 2 11,6 kPa - HCO 3 - 55 mmol / l - pO 2 8,4 kPa - K + 2.6 mmol / l

'Questions:'

  1. 'What ABR fault is this?'
Answers -
  1. Chronic lung disease leads to reduced gas exchange: CO retention 2 → respiratory acidosis, O 2 deficiency → hypoxia → hypoxic lactic acidosis. Long-term use of thiazide preparations leads to loss of K + in the urine → hypokalaemic metabolic alkalosis.

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Template:Pathobiochemistry of metabolic pathways (Masopust)

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