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View Full Version : And here's a 2nd question that came up today...


neecheepure
04-15-2012, 22:39
How much stomach acid does an adult have to vomit (volume) in order to make themselves alkolotic? This came up specifically in regards to N/V in a heat casualty, so the follow up is this: In a heat casualty, whose blood levels of potassium and sodium are likely already decreased, how much vomiting is it going to take to make them alkolotic? What acute problems could this akolotic state potentially cause that would compound a heat casualty's other issues?

I understand that these are broad questions that may not have an exact-amount type of answer; I'm looking for wisdom and experience beyond my own here, not an exact mL amount.

As always, thanks to all!

scooter
04-15-2012, 22:53
Vomiting results in the loss of hydrochloric acid (hydrogen and chloride ions) with the stomach contents. Severe vomitting also causes loss of potassium (hypokalaemia) and sodium (hyponatraemia). The kidneys compensate for these losses by retaining sodium in the collecting ducts at the expense of hydrogen ions (sparing sodium/potassium pumps to prevent further loss of potassium), leading to metabolic alkalosis.

Compensation for metabolic alkalosis occurs mainly in the lungs, which retain carbon dioxide (CO2) through slower breathing, or hypoventilation (respiratory compensation). CO2 is then consumed toward the formation of the carbonic acid intermediate, thus decreasing pH. Respiratory compensation, though, is incomplete. The decrease in [H+] suppresses the peripheral chemoreceptors, which are sensitive to pH. But, because respiration slows, there's an increase in PCO2 which would cause an offset of the depression because of the action of the central chemoreceptors which are sensitive to the partial pressure of CO2 in the blood. So, because of the central chemoreceptors, respiration rate would be decreased.

Renal compensation for metabolic alkalosis, less effective than respiratory compensation, consists of increased excretion of HCO3- (bicarbonate), as the filtered load of HCO3- exceeds the ability of the renal tubule to reabsorb it.