The following arterial blood gas and biochemistry results are from a patient with cardiac and respiratory disease and recent profuse vomiting.
|
Parameter |
Patient |
Reference |
|
FiO2 |
0.4 |
|
|
pH |
7.5* |
7.35 – 7.45 |
|
PaO2 |
58.0 mmHg (7.6 kPa) |
|
|
PaCO2 |
47 mmHg* (6.2 kPa*) |
35 – 45 (4.6 – 6.0) |
|
HCO3 |
34.8 mmol/L* |
22 – 27 |
|
Base Excess |
10.2 mmol/L* |
-2.0 – +2.0 |
|
Sodium |
137 mmol/L |
135 – 145 |
|
Potassium |
2.5 mmol/L* |
3.5 – 5.0 |
|
Chloride |
92 mmol/L* |
95 – 105 |
a) Explain the acid-base status (1 marks)
b) List the potential causes of the acid-base abnormalities in this patient (3 marks)
Syllabus topic/section: 2.1.5 Respiratory Intensive Care: Interpretation of arterial blood gases and 2.1.7 Renal Intensive Care: Blood gas analysis
Discussion:
This section was relatively well answered with a metabolic alkalosis and incomplete respiratory compensation mostly recognised. Common causes of this clinical picture from volume contraction, diuretic therapy and vomiting were expected to be included for an at standard answer. Higher marks were achieved if candidates also recognised the specific causes associated with chronic cardiac and respiratory disease.
a) "cardiac and respiratory disease and recent profuse vomiting" already shouts "diuretics, steroids, hypovolemia and chloride loss in the gastric fluid" but let's be systematic before jumping to the obvious conclusions:
b) With this exercise now behind us, we may safely conclude that the explanation is diuretics, steroids, hypovolemia and chloride loss in the gastric fluid. If one takes the stance that CO2of 44 is lower than expected, and this alkalosis is in fact incompletely compensated, then this can also be explained by the hypoxia, as it would be perfectly reasonable to have a higher respiratory rate in that context.
Khanna, Apurv, and Neil A. Kurtzman. "Metabolic alkalosis." studies 28 (2006): 29.