Metabolic Alkalosis Flashcards
pH = 7.45 HCO3 = 34 pCO2 = 51 Anion gap = 14
male in ER because of weakness. tachy, flat JVP, low BP. Eating disorder (anorexia and bulemia). What acid-base problem is happening?
pattern between pH and bicarb– both elevated. metabolic alkalosis. look at compensation; in bicarb is incresaed by 10, proper compensation is for CO2 to increase by 7 for every 10 bicarb increase. in this case, CO2 should be 47. here, it’s higher than it should be (51). that means there is a respiratory acidosis.
look at anion gap. 14. 12+/-2 –> normal.
therefore there are two disorders here:
- metabolic alkalosis
- rspiratory acidosis.
metabolic alklaosis is usually due to:
Metabolic alkalosis is usually due to increased HCO3- reabsorption and/or production in the kidne
two ways that the body is tricked into maintainine metabolic alkalosis
- reduced EABV via angiotensin II.
- hypokalemia
outline how metabolic alkalosis is maintained when there is a low EABV
tubular lumen contains bicarb that we wanna reaborb. we absorb that by moving H+ out of the tubular lumen, moving Na+ in from the lumen. RAS system increases the activity of this sodium- hydrogen xchanger on the tubular lumen– so that we can reabosrb more na+ to correct the EABV. however, more H+ goes out to the lumen. more H+ in lumen = more bicarb being reabsorbed, creating a serum high pH. the bicarb threshold increases to 28 or 32 instaed of 24, and will stay at that level until you correct the EABV and shut off the RAS.
recall; metabolic alkalosis can be maintained by a low EABV when the RAS system is turned on, causing the PCT to increase bicarbonate reabsorption in response to Na+-H+ exhcnager activation.
How can you tell the SITE of volume loss that resulted in this low EABV?
Urine chloride to decide if its GI loss (kidney should behaving appropriately by adequately retaining salt), or if its renal loss (ex/ if taking diuretics or pt with gitelmans, then thye will be wasting salt, and urine chloride will be HIGH)
in our patients case ( see case in previous cards), the Cl- is low, so the source of volume loss is from the GI tract rather than the kidney.
normally in the GI tract, there is secretion of HCl into the stoamch by parietal cell. the Cl- gets into stomach by exchanging from the parietal cells. this doesn’t persist though becuase when we enter the duodenum, the bicarbonate secretion neutralizes everything. there is not net gain or loss of bicarb.
in VOMITING, we lose HCl from the body in the vomiuts, so there is a net gain of sodium and bicarb, causing an increase in bicarb in the blood. this is not the reason wy we maintain a bicarbonate alkalois since it is readily excreted by kidney. it’s because we also lose sodium and potassium positively charged ions as they are being dragged out by the bicarb.
therefore in vomiting, you see an ___ urine, a very low __, and a __ concentration that is too hgih for the low chloride because it’s being dragged out and excreted. by the bicarb.
normally in the GI tract, there is secretion of HCl into the stoamch by parietal cell. the Cl- gets into stomach by exchanging from the parietal cells. this doesn’t persist though becuase when we enter the duodenum, the bicarbonate secretion neutralizes everything. there is not net gain or loss of bicarb.
in VOMITING, we lose HCl from the body in the vomiuts, so there is a net gain of sodium and bicarb, causing an increase in bicarb in the blood. this is not the reason wy we maintain a bicarbonate alkalois since it is readily excreted by kidney. it’s because we also lose sodium and potassium positively charged ions as they are being dragged out by the bicarb.
therefore in vomiting, you see an alkaline urine, a very low chloride, and a sodium concentration that is too hgih for the low chloride because it’s being dragged out and excreted. by the bicarb.
Hypokalemia via intracellular acidosis also maintains metabolic alkalosis How?
hypokalemia can be caused in multiple ways Ex/ aldosterone in CCT. usually there is a tendency for K+ to move into lumen in ECF. when the ICF loses potassium, it tries to restore balance by hanging onto other cations. Na+ is one choice, but the sodium ATPase prevents that from happening. the onyl otehr option is H+. H+ normally is produced inside the cell throguh metabolism.
therefore in hypokalemia, we hold onto H+, causing an acidosis. When an acidosis happens, the PCT tries to fix this situation by activating glutaminase, which forms ammonium and bicarbonate via AKG. when hypokalemia causes an intracellular acidosis, it leads to increase bicarbonate production at the PCT. the PCT will continue to produce more bicarb, until you correct the potassium levels which are causing the original acidosis.
Outline what you should consider if the patient doesnt hav ea low EABV– how do you explain met alkalosis?
almost always due to hypokalemia== something is driving the principle cell and causing increased renal loss of K+, causing a high acid in ICF, and the cell is causing more bicarb secretion. but what is causing this? too much aldosterone? bicarb infusion? mineralcorticoid receptor stimulation?
treating metabolic alkalosis
- for reduced eABV and hypokalemia
- give NaCl to fix EABV to restore normal threshold for bicarb reabsorption proximally
- fix potassium to stop the kidney from producing bicarb in response to high ICF H+
- stop vomiting, give PPI or something
treating a patient with metabolic alkalosis but with an expanded EABV
usually this is due to principle cell dysfunction. block the aldosterone/mineral corticoid function.
- can also stop at the PCT by blocking carbonic anhydrase inhibitor. This is also a diuretic.
5 KEY POINTS
- Metabolic alkalosis is usually due to increased HCO3- reabsorption and/or production in the kidney
- Reduced EABV via Angiotensin II maintains metabolic alkalosis
- Urine Cl- identifies the site of volume loss
- Hypokalemia via intracellular acidosis maintains metabolic alkalosis
- Treatment of metabolic alkalosis typically involves correction of maintenance mechanism(s)
