Session 5: Group Work Flashcards
- A patient presents to you with the following arterial blood chemistry:
o pH 7.33 (7.35 – 7.45)
o pCO2 6.3 kPa (4.7 -6.0)
o [HCO3-] 25.16 mmol/L (22 – 26).
o pO2 8.8 kPa (9.3 – 13.3)
What is this disturbance of acid base balance called?
Uncompensated respiratory acidosis due to hypoventilation.
You return to the same patient 3 days later, her pCO2 is still 6.3kPa, but
the new plasma pH is 7.4.
What parameter is likely to have changed and why?
What do we call this change in acid base balance?
Compensated respiratory acidosis where HCO3- has increased by reabsorption from kidneys.
pH =7.22
pCO2 = 8.1
HCO3 = 24
pO2 = 8.9
Uncompensated respiratory acidosis
pH =7.22
pCO2 = 4.5
HCO3 = 13
pO2 = 12.4
Partially compensated metabolic acidosis
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Partially compensated respiratory alkalosis
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Uncompensated metabolic acidosis
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Partially compensated respiratory acidosis
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Uncompensated metabolic alkalosis
pH = 7.37
pCO2 = 5.7 HCO3 = 24 pO2 = 12.1
Normal
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Fully compensated respiratory acidosis
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Fully compensated metabolic acidosis
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Uncompensated respiratory alkalosis
- A young man appears in casualty. You note that his respiration is rapid
and quite deep, and suspect that he is anxious and hyperventilating.
His ABG results are as follows:
o pH = 7.2 (7.35 – 7.45),
o pO2 = 12.4 kPa (9.3-13.3),
o pCO2 4.3kPa (4.7 -6.0),
Is your initial suspicion correct? Explain your answer.
No
It is partially compensated metabolic acidosis
If not, what might account for the symptoms? How would your view change if you learned that he had been feeling very tired lately and seemed far thirstier? What other investigation would you perform?
Diabetes mellitus
Glucose test
U&Es
HbA1c
FBC
Urine dip stick
Smell breath
- A patient with longstanding severe Chronic Obstructive Pulmonary
Disease (COPD) is seen in clinic. On looking through his notes the
doctor sees many previous arterial blood gas results which indicate
that he has had chronically low pO2 levels (hypoxia) and elevated pCO2
levels (hypercapnia).
a. In the normal individual breathing is ‘driven’ by carbon dioxide. What
will happen to the response of the central chemoreceptors in
persistent hypercapnia?
Central chemoreceptors respond to changes in pCO2. In this case there is an increase in pCO2. This leads in long term to the choroid plexus cells secreting HCO3- into the CSF to restore the ratio. The ratio is now restored at an elevated pCO2. The central chemoreceptors shut off and no hyperventilation is done anymore by them.
However the pCO2 is still high and the ratio outside of the CSF is still disturbed.
b. What may be in driving respiration in this patient?
Which chemoreceptors are involved?
Peripheral chemoreceptors in response to hypoxia (low pO2)
A few weeks later he is admitted with a chest infection which has worsened his breathlessness. The ABG results on admission (breathing room air) are as follows: pO2= 7.5kPa, pCO2= 7 kPa
He is treated with antibiotics and inhaled oxygen. When repeated 20 minutes later, ABG shows a pO2 of 12 kPa and a pCO2 of 7.5 kPa
Why has the pO2 level increased?
Because the air he is inhaling has a higher pO2 leading to more diffusion.
Why has the pCO2 level increased?
Treating the hypoxia leads to the peripheral chemoreceptors switching off. This means that the patient will stop hyperventilating which was a response also to treat the hypercapnia.
The pCO2 levels will therefore increase.