Question 1:
PH = 7.58, that is Alkalaemia (Moderate)
HCO3 = 45.3, so we have metabolic alkalosis. Next we check the compensation.
For metabolic alkalosis, the expected PCO2 = 0.7 x [HCO3] + 20 (+/- 5). Accordingly, the expected PCO2 in this case is: 0.7 x 45.3 + 20 = 46 – 56. PCO2 in this case is 48, it fits within this range. According to that there are no additional metabolic processes.
Other abnormal findings:
K = 1.8 that is severe hypokalaemia( not clear if it is acute or chronic).
CK = 17000, creatine kinase usually released from muscles tissue. Any condition that causes muscle damage or interferes with muscle energy production can lead to increase CK level.
Lactate level is slightly elevated = 2.4 (Mild lactataemia).
Question 2:
C – contraction alkalosis: possible contributing factor. Need to check hydration status
L – liquorice, laxative abuse. Possible contributing factor. Can be ruled out by taking good history
E – endocrine (Conn’s, Cushing’s), unlikely
V – vomiting, GI loss (villous adenoma), nothing in the history to suggest that
E – excess alkali (antacids), nothing in the history to suggest that
R – renal (Bartter’s), severe K depletion… Rare, and it is an acute condition.
P – post hypercapnia, no..
D – diuretics…. (These cause metabolic alkalosis and hypokalaemia), body builders tend to use multiple substances (Anabolic steroids (even sometimes fast acting insulins for their anabolic effects), Thyroid hormones, human growth hormones, they also use diuretics to make their muscles more prominent (usually around competition times or when they are trying to attract attention).
This patient was using diuretics.
Question 3:
Diuretics such as frusemide and thiazides interfere with reabsorption of chloride and sodium in the renal tubules leading to increase urinary loss of chloride that exceed the urinary loss of bicarbonate. Diuretics increase sodium delivery to the distal segment of the distal tubule; this increases potassium loss because the increase in distal tubular sodium concentration stimulates the aldosterone-sensitive sodium pump. That increases sodium reabsorption in exchange for potassium and hydrogen ion, which are lost to the urine. The increased hydrogen ion loss can lead to metabolic alkalosis.
Rhabdo is caused by impairment of blood flow in the muscles secondary to hypokalaemia, (dehydration may be a contributing factor).
Knochel and Schlein showed that muscles blood flow is severely impaired in hypokalaemic dogs.
Potassium plays a major role in regulating skeletal muscle blood flow, increase potassium in muscles during activity leads to vasodilatation, in hypokaelemia this mechanism is lost which lead to relative ischemia in the active muscles, this usually leads to muscles cramps and in severe cases will lead to muscle necrosis and rhabdo.
Hypokalaemia also might affect the metabolic mechanisms in muscles which might contribute to muscles dysfunction.