# Lab case 355 interpretation

Question1:

PH = 6.71, that is severe, life threatening acidaemia

pCO2 = 125 mmHg,  Very high. So we have respiratory acidosis. This can be acute, chronic or acute on chronic.

The compensation for respiratory acidosis is by retaining HCO3, so in both acute and chronic respiratory acidosis we expect the HCO3 to be more than 24.

In this case, HCO3 is low (15 mmol), So we have additional metabolic acidosis.

Because we established that there is metabolic acidosis, next we need to know which type of metabolic acidosis we have here. That can be achieved by calculating the anion gap.

Since K is higher than 6, we will include the K in the calculation and we will consider the normal anion gap value to be 16. Accordingly AG for this patient will be:

(Na + K) -(Cl + HCO3) = (141 + 7) – (109 + 15) = 24. So, we have HAGMA.

Next we will calculate the delta ratio to exclude the presence of other metabolic process. For this patient is calculated as the following:

Delta ratio =  (AG – 16) / (24 – HCO3) = 0.88. So, we have a pure HAGMA. (Ratio between 0.8 and 2).

So we have combined respiratory acidosis and HAGMA.

Other abnormal findings:

K = 7.1 mmol/L. That is severe hyperkaelemia, However, in the presence of acidosis, serum K level is elevated due to shifting outside the cells. Usually, serum K level increases by 0.6 mmol/L for every 0.1 PH below 7.4. PH here is 6.7, that is 0.7 less than 7.4.. Accordingly, the corrected K level will be 7.1 – (0.6 x 0.7 / 0.1) = 2.9.

Cl = 109 mmol/L, that is mild hyperchlraemia.

Creatinine is 536, very high. For a 70 year old man, that will give him eGFR of 9, that is stage 5, end stage CKD.

Lactate = 9.6, extremely high, a reflection of poor tissue oxygenation and excessive anaerobic metabolism.

Final conclusion, Severe combined respiratory and high anion gap metabolic acidosis associated with end stage renal failure and severe hyperkaelaemia.

Question 2:

Heart rate in this patient didn’t respond to adrenaline because Beta receptors become less responsive to adrenaline effect in severe acidosis.

Other circulatory effects of acidosis:

• Acidosis has direct effect on arteries leading to arteriodilatation.
• Acidosis leads to catecholamine release this will  lead to arterioconstriction and venoconstriction, This will lead increase venus return, pulmonary congestion and increase pulmonary arterial pressure.

Cardiac effects: in mild to moderate acidosis

• Direct myocardial depression, impaired contractility and reduce responsiveness to circulating catecholamine.
• Reduce threshold for arrhythmias (Catecholamine release).

Severe metabolic acidosis leads to myocardial depression. Many organelles within the cardiac cells are affected by hydrogen ion.

The tension generated by isolated myofibers at a fixed calcium concentration is reduced by low PH. The dominant mechanism for reduced contractility is competitive inhibition of slow calcium current by hydrogen ion. (Similar to the effect of hypocalcemia).

In an animal study, fast responding extracellular electrodes showed that in ischemic tissue, acidosis develops only seconds after contractile failure.

Effect of acidosis on muscular tissues (Diaphragm).

Acidosis causes muscle weakness, altered O2 delivery will lead to reduce ATP production.  Physiologically, the effect of acidosis on muscular fibers are:

• Small effect on force production.
• Significantly decrease shortening velocity
• Significantly reduce power generating capacity

The research has shown fall of function of diaphragm with respiratory acidosis but not with lactic acidosis. Intracellular PH plays a role in respiratory muscles fatigue.

Other effects of acidosis

• Resistance to insulin action
• Stimulation of apoptosis

***** Treatment of metabolic acidosis with bicarbonate may induce cerebral acidosis and worsen cerebral oedema (During ketoacidosis).