Quick · a patient's pH is 7.28. Is that acidosis or alkalosis?
1
The Three Numbers That Matter
FOUNDATIONEvery ABG gives you three critical values. Everything else is derived from these:
pH · the verdict. Normal: 7.35 · 7.45. Below 7.35 = acidosis. Above 7.45 = alkalosis. 🔑 7.4 is home base. Think of it like a 4-letter word: SAFE.
pCO2 · the respiratory player. Normal: 35,45 mmHg. CO2 is an acid. More CO2 = more acid. Lungs blow it off in minutes.
HCO3 · the metabolic player. Normal: 22,26 mEq/L. Bicarb is a base. Kidneys adjust it over hours to days.
The golden rule: CO2 and pH move in opposite directions. HCO3 and pH move in the same direction. That's it. That's the whole game.
🔑
CO2 is a contrarian · pH goes down, CO2 goes up. Bicarb is a yes-man · pH goes down, bicarb goes down too.
ABG Collection
2
The 5-Step ABG Algorithm
THE METHODEvery ABG. Same five steps. Same order. Don't skip. Don't freestyle.
1
Look at the pH.
< 7.35 = acidemia. > 7.45 = alkalemia. Normal pH with abnormal CO2/bicarb = compensated or mixed.
< 7.35 = acidemia. > 7.45 = alkalemia. Normal pH with abnormal CO2/bicarb = compensated or mixed.
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2
Is it respiratory or metabolic?
Check which value explains the pH. If pH is low and pCO2 is high → respiratory acidosis. If pH is low and HCO3 is low → metabolic acidosis.
Check which value explains the pH. If pH is low and pCO2 is high → respiratory acidosis. If pH is low and HCO3 is low → metabolic acidosis.
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3
Is there compensation?
The body always tries to compensate. Respiratory problem → kidneys adjust bicarb. Metabolic problem → lungs adjust CO2. Compensation moves toward normal but never overshoots.
The body always tries to compensate. Respiratory problem → kidneys adjust bicarb. Metabolic problem → lungs adjust CO2. Compensation moves toward normal but never overshoots.
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4
If metabolic acidosis: calculate the anion gap.
AG = Na − (Cl + HCO3). Normal = 12 (±2). Elevated = something is adding acid. Normal gap = losing bicarb.
AG = Na − (Cl + HCO3). Normal = 12 (±2). Elevated = something is adding acid. Normal gap = losing bicarb.
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5
If anion gap is elevated: check the delta-deltaThe delta-delta (Δ/Δ) compares: how much the AG rose vs. how much HCO3 fell. If AG rose MORE than bicarb fell, there's a hidden metabolic alkalosis underneath. If AG rose LESS, there's an additional non-gap acidosis hiding..
ΔAG / ΔHCO3. Ratio <1 = additional non-gap acidosis. Ratio >2 = hidden metabolic alkalosis. Ratio 1,2 = pure gap acidosis.
ΔAG / ΔHCO3. Ratio <1 = additional non-gap acidosis. Ratio >2 = hidden metabolic alkalosis. Ratio 1,2 = pure gap acidosis.
Compensation NEVER overshoots. If pH goes past normal in the "compensating" direction, you have a mixed disorder, not overcompensation. Boards love this.
3
Walk Through It
PRACTICEABG comes back: pH 7.30, pCO2 55, HCO3 26. Walk the algorithm.
Step 1 · pH is 7.30. What's the verdict?
4
The Anion Gap
HIGH YIELD→ Cause-by-cause deep dives
When you see metabolic acidosis (low pH + low bicarb), the next question is always: is the gap elevated?
Anion Gap = Na − (Cl + HCO3). Normal ≈ 12.
Elevated gap = something is adding acid to the blood. The unmeasured anions are the new acid.
Normal gap = you're losing bicarb (diarrhea, RTA) or gaining chloride. Cl replaces HCO3 so the gap stays normal.
MUDPILES · causes of anion gap metabolic acidosis:
Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol, Isoniazid/Iron, Lactic acidosis, Ethylene glycol, Salicylates
Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol, Isoniazid/Iron, Lactic acidosis, Ethylene glycol, Salicylates
HARDASS · causes of non-gap (hyperchloremic) metabolic acidosis:
Hyperalimentation, Acetazolamide, RTA, Diarrhea, Adrenal insufficiency, Saline infusion, Spironolactone
Hyperalimentation, Acetazolamide, RTA, Diarrhea, Adrenal insufficiency, Saline infusion, Spironolactone
Albumin affects the gap. Every 1 g/dL drop in albumin below 4 lowers the AG by ~2.5. A "normal" AG of 12 in a patient with albumin of 2 is actually an elevated corrected AG of 17. Always correct for albumin in sick patients.
🧭
pH Compass
INTERACTIVETwo axes. Four disorders. Click a quadrant to see where the body lands and how it compensates.
Compensation Formula
Select a disorder above
☠
The Four Villains
FLIP TO LEARNFour acid-base disorders. Each one wants to kill your patient a different way. Tap a card to flip it.
Met Acidosis (AG)
Anion gap elevated
tap to flip
Anion Gap Metabolic Acidosis
AG = Na − (Cl + HCO3) > 14
Causes (MUDPILES):
- Methanol / Ethylene glycol
- Uremia
- DKA / Alcoholic ketoacidosis
- Propylene glycol
- Isoniazid / Iron
- Lactic acidosis
- Salicylates
Compensation: Winter's: pCO2 = 1.5(HCO3) + 8 ±2
Then check: delta-delta ratio to find hidden disorder
Met Acidosis (Non-AG)
Normal anion gap
tap to flip
Non-Gap (Hyperchloremic) Metabolic Acidosis
AG normal (8-12). Losing bicarb or gaining Cl−.
Causes (HARDASS):
- Hyperalimentation
- Acetazolamide
- RTA (Types 1, 2, 4)
- Diarrhea (direct HCO3 loss)
- Adrenal insufficiency
- Saline infusion (dilutional)
- Spironolactone
Key: Cl rises to fill the gap as HCO3 falls. Urine AG helps distinguish RTA from diarrhea.
Met Alkalosis
High HCO3, high pH
tap to flip
Metabolic Alkalosis
pH > 7.45, HCO3 > 26. Too much base or lost acid.
Causes:
- Vomiting / NG suction (lose HCl)
- Loop / thiazide diuretics (lose H+ and Cl−)
- Primary hyperaldosteronism (retain HCO3)
- Milk-alkali syndrome
- Pyloric stenosis in infants
Compensation: pCO2 rises ~0.7 per 1 mEq/L HCO3 rise (hypoventilate)
Treat: NS (saline-responsive) or correct aldosterone excess (saline-resistant)
Respiratory Disorders
CO2 is the weapon
tap to flip
Respiratory Acidosis vs Alkalosis
Resp Acidosis: pCO2 > 45 → pH falls
- Hypoventilation: COPD, opioids, obesity hypoventilation, neuromuscular
- Acute: HCO3 rises 1 per 10 pCO2
- Chronic: HCO3 rises 3.5 per 10 pCO2
Resp Alkalosis: pCO2 < 35 → pH rises
- Hyperventilation: anxiety, PE, altitude, sepsis (early), pregnancy
- Acute: HCO3 falls 2 per 10 pCO2
- Chronic: HCO3 falls 5 per 10 pCO2
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Elimination Game
INTERACTIVEA patient presents obtunded. ABG: pH 7.22, pCO2 20, HCO3 8, Na 140, Cl 100. Six possible diagnoses. Each clue eliminates one. Find the answer.
COPD exacerbation
Diabetic ketoacidosis
Severe diarrhea
Renal tubular acidosis
Ethylene glycol ingestion
Lactic acidosis
CLUE 1
pCO2 is 20 (low). The lungs are hyperventilating, compensating for a metabolic problem. This is NOT a respiratory acidosis.
Eliminated: COPD exacerbation · COPD causes high CO2, not low.
CLUE 2
Anion gap = 140 − (100 + 8) = 32. Massively elevated. This is a gap acidosis.
Eliminated: Severe diarrhea & RTA · both cause non-gap acidosis (normal AG).
CLUE 3
Glucose is 95. No ketonuria. This is not a diabetic crisis.
Eliminated: DKA · no hyperglycemia, no ketones.
CLUE 4
Lactate is 1.8 (normal). The tissue oxygenation is fine.
Eliminated: Lactic acidosis · lactate is normal.
FINAL CLUE
Osmolar gap is elevated. Calcium oxalate crystals in the urine. The patient drank something they shouldn't have.
Answer: Ethylene glycol ingestion · gap acidosis + osmolar gap + oxalate crystals = toxic alcohol.
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Compensation Rules
REFERENCEYou don't need to memorize the exact formulas. You need to know the direction and the magnitude.
| Disorder | Primary Change | Compensation | Rule of Thumb |
|---|---|---|---|
| Metabolic acidosis | ↓ HCO3 | ↓ pCO2 (hyperventilate) | Winter's: pCO2 = 1.5(HCO3) + 8 ±2 |
| Metabolic alkalosis | ↑ HCO3 | ↑ pCO2 (hypoventilate) | pCO2 rises ~0.7 per 1 HCO3 rise |
| Acute resp acidosis | ↑ pCO2 | ↑ HCO3 (buffering) | HCO3 rises 1 per 10 pCO2 rise |
| Chronic resp acidosis | ↑ pCO2 | ↑ HCO3 (renal) | HCO3 rises 3.5 per 10 pCO2 rise |
| Acute resp alkalosis | ↓ pCO2 | ↓ HCO3 | HCO3 falls 2 per 10 pCO2 drop |
| Chronic resp alkalosis | ↓ pCO2 | ↓ HCO3 (renal) | HCO3 falls 5 per 10 pCO2 drop |
The body compensates metabolic problems fast (lungs adjust in minutes). It compensates respiratory problems slow (kidneys take hours to days). That's how you tell acute from chronic.
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ABG Interpreter
TOOLPlug in the numbers. Watch the algorithm think out loud. Then try to beat it.
Enter ABG Values
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Don't Kill Them
QUIZFour patients just rolled in with ABGs. Figure out what's wrong before something bad happens. No pressure.
Q1 of 8
A 68-year-old with COPD presents with confusion and shallow breathing. ABG: pH 7.29, pCO2 68, HCO3 31. Which statement best characterizes this disorder?
A. Acute metabolic alkalosis with respiratory compensation
B. Acute respiratory acidosis, uncompensated
C. Chronic respiratory acidosis with appropriate renal compensation
D. Mixed metabolic and respiratory acidosis
Q2 of 8
A 19-year-old presents with anxiety and tingling around her mouth after a panic attack. ABG: pH 7.54, pCO2 24, HCO3 19. What is the primary mechanism causing her paresthesias?
A. Hyperkalemia from alkalosis-driven potassium shift
B. Alkalosis increases albumin binding of calcium, reducing ionized calcium
C. Cerebral vasoconstriction from elevated CO2
D. Hypomagnesemia secondary to hyperventilation
Q3 of 8
ABG: pH 7.24, pCO2 22, HCO3 9, Na 138, Cl 108. The anion gap is:
A. 21 (elevated gap acidosis)
B. 21 (wait, let me recalculate: 138 minus 108 minus 9 = 21 · elevated gap acidosis)
C. 11 (non-gap hyperchloremic acidosis)
D. 29 (massively elevated, likely toxic alcohol)
Q4 of 8
A 52-year-old with vomiting for 3 days. ABG: pH 7.51, pCO2 48, HCO3 38. What is the primary disorder and how should you treat it?
A. Respiratory alkalosis · decrease respiratory rate
B. Metabolic alkalosis · IV normal saline to replace chloride
C. Mixed metabolic and respiratory alkalosis · no treatment needed
D. Acute respiratory acidosis · intubation required
Q5 of 8
A diabetic patient has ABG: pH 7.18, pCO2 26, HCO3 9, Na 141, Cl 102. AG = 30. Winter's formula predicts pCO2 should be ____. The actual pCO2 is ____. What does this mean?
A. Expected 21, actual 26 · appropriate compensation, pure gap acidosis
B. Expected 21, actual 26 · the patient has additional respiratory alkalosis
C. Expected 21.5 (plus/minus 2), actual 26 · pCO2 higher than expected, additional respiratory acidosis present
D. Expected 34, actual 26 · appropriate for this level of acidosis
Q6 of 8
ABG: pH 7.40, pCO2 55, HCO3 33. Na 142, Cl 98, albumin 2.0 g/dL. What is the corrected anion gap?
A. 11 (normal, no gap acidosis)
B. 16 (borderline elevated)
C. 16, corrected to 21 (each 1 g/dL drop in albumin below 4 adds 2.5 to expected AG)
D. Cannot calculate without potassium
Q7 of 8
A critically ill patient has ABG: pH 7.32, pCO2 38, HCO3 19, Na 140, Cl 100, AG = 21. The delta-delta ratio is approximately 0.6. What does this reveal?
A. Pure anion gap metabolic acidosis (ratio 1-2 = pure gap)
B. Hidden metabolic alkalosis underlying the gap acidosis (ratio greater than 2)
C. Additional non-gap (hyperchloremic) acidosis on top of the gap acidosis (ratio less than 1)
D. The delta-delta only applies when the AG is above 30
Q8 of 8
A 44-year-old alcoholic found down. ABG: pH 7.21, pCO2 18, HCO3 7, Na 139, Cl 101. AG = 31. Lactate = 1.5 (normal). Urine shows calcium oxalate crystals. What is the diagnosis and antidote?
A. Methanol poisoning · fomepizole, then dialysis
B. Ethylene glycol poisoning · fomepizole to block alcohol dehydrogenase, then dialysis
C. Lactic acidosis from sepsis · broad-spectrum antibiotics
D. Alcoholic ketoacidosis · dextrose and thiamine
Q9 of 25
A 78-year-old with heart failure and diuretic use. ABG: pH 7.46, pCO2 50, HCO3 35, Na 138, Cl 90, K 2.8. What best describes the acid-base status?
A. Pure metabolic alkalosis with respiratory compensation
B. Contraction alkalosis with hypokalemia from loop diuretics
C. Concurrent respiratory acidosis masking a severe metabolic alkalosis
D. Acute respiratory alkalosis with compensatory metabolic acidosis
The high pH (7.46) and high HCO3 (35) indicate metabolic alkalosis. The elevated pCO2 (50) is appropriate respiratory compensation. But the critical clue is the low chloride (90) and dangerously low potassium (2.8).
Loop diuretics like furosemide cause contraction alkalosis. Fluid loss contracts the extracellular volume, the kidney interprets this as needing to retain sodium. To reabsorb sodium, the kidney must reabsorb bicarbonate. The patient also loses potassium and chloride, which worsens the alkalosis. This is chloride-responsive alkalosis.
Hypokalemia from diuretics blocks renal H+ secretion and forces continued bicarb reabsorption. The patient CANNOT fix the alkalosis until potassium and chloride are replaced. Treating this with volume alone (without KCl) won't work. The board loves testing whether you know the pathophysiology: contraction + diuretics = chloride and potassium loss = alkalosis locked in place until electrolytes are restored.
Q10 of 25
A 52-year-old with severe diarrhea for 2 weeks. ABG: pH 7.28, pCO2 32, HCO3 14, Na 135, Cl 98, K 2.9. What is the primary disorder?
A. Metabolic acidosis with respiratory compensation
B. Hyperchloremic metabolic acidosis from bicarbonate loss in stool
C. Mixed metabolic and respiratory acidosis
D. Respiratory alkalosis driving secondary metabolic acidosis
The low pH (7.28) and low HCO3 (14) indicate metabolic acidosis. The low pCO2 (32) is appropriate hyperventilation to compensate. But notice the normal-to-low chloride (98) with low sodium (135). This pattern is hyperchloremic (non-gap) acidosis.
Diarrhea loses bicarbonate directly in stool. Chloride is reabsorbed preferentially in the colon, so the kidney responds to volume depletion by reabsorbing sodium with chloride, not bicarbonate. The result is normal anion gap (Na minus Cl minus HCO3 = 135 minus 98 minus 14 = 23, but this is still around 10-12 normal). The anion gap is normal because bicarbonate is lost, not accumulated acid.
This is a non-gap acidosis from bicarbonate loss. The board will try to confuse you with the low potassium (2.9) and ask if this is a potassium-depletion metabolic alkalosis instead. Nope. The pH is LOW. The HCO3 is LOW. This is ACIDOSIS. Treat with IV normal saline and potassium replacement.
Q11 of 25
A 34-year-old Type 1 diabetic found with ABG: pH 7.22, pCO2 18, HCO3 7, Na 139, Cl 105, K 6.2. AG = 27. What is missing from this picture?
A. Pulmonary embolism blocking respiratory compensation
B. Concurrent normal anion gap acidosis in addition to DKA
C. Lactic acidosis explaining the anion gap
D. Hyperchloremic acidosis masking the true gap
The massive anion gap (27) with low HCO3 (7) screams DKA. The low pCO2 (18) is appropriate Kussmaul respiration. But the chloride is HIGH (105, normal 98-107), which doesn't fit pure DKA. In pure DKA, chloride should be LOW because sodium is reabsorbed without chloride to balance the negative ketones.
This patient has TWO problems: DKA from hyperglycemia, AND concurrent non-gap acidosis from volume depletion and renal dysfunction. The high chloride relative to sodium suggests chloride is being reabsorbed preferentially, creating a "double acidosis" → high gap from ketones, PLUS normal gap from chloride retention.
Calculating the delta-delta here reveals it. Expected HCO3 fall due to AG increase: 27 minus 12 (normal AG) = 15. Expected new HCO3: 24 minus 15 = 9. But we got 7. That means HCO3 is 2 mEq/L LOWER than expected, indicating additional non-gap loss. This patient needs insulin, fluids, and careful monitoring of electrolytes. Pure DKA treatment alone will fail.
Q12 of 25
A 67-year-old with ESRD on hemodialysis (last session 4 days ago). ABG: pH 7.29, pCO2 30, HCO3 13, Na 140, Cl 102, K 6.8. AG = 25. What is the primary disorder?
A. Uremic acidosis (gap acidosis from renal failure) with respiratory compensation
B. Mixed high-gap and normal-gap acidosis from renal failure and hyperkalemia
C. Pure respiratory alkalosis from uremia driving hyperventilation
D. Metabolic acidosis with concurrent alkalosis from contraction
The low pH (7.29), low HCO3 (13), and elevated AG (25) indicate a high-gap metabolic acidosis. The low pCO2 (30) is appropriate respiratory compensation. The patient is in renal failure, accumulating unmeasured anions (phosphate, sulfate, urate).
In ESRD, the kidneys cannot excrete metabolic waste. Hydrogen ions and organic acids accumulate, creating an anion gap acidosis. This is called uremic acidosis. The patient's last dialysis was 4 days ago, so the gap has widened. The hyperkalemia (6.8) is also from renal retention. The HCO3 is LOW because buffering capacity is exceeded.
The board loves testing whether you know uremic acidosis is a REAL gap acidosis, not just "the kidneys can't compensate." The kidneys aren't compensating here → they're FAILING to clear acid. This patient NEEDS dialysis urgently. Treating the HCO3 alone (bicarb administration) won't fix this; you must remove the accumulated anions via hemodialysis.
Q13 of 25
A 45-year-old with pneumonia, on mechanical ventilation. Settings: RR 18, minute ventilation 8 L/min. ABG: pH 7.55, pCO2 28, HCO3 24. What adjustment is needed?
A. Increase respiratory rate to blow off more CO2
B. Decrease respiratory rate or tidal volume to allow pCO2 to rise
C. Give sodium bicarbonate to correct the alkalemia
D. Increase oxygenation to improve compensation
The high pH (7.55) and low pCO2 (28) indicate respiratory alkalosis. The HCO3 (24) is normal, so this is a PRIMARY respiratory alkalosis from mechanical ventilation settings, not a compensatory response.
The ventilator is set to RR 18 with an 8 L/min minute ventilation, which is TOO AGGRESSIVE. The patient is hyperventilated, blowing off CO2 faster than normal. In pneumonia, tachypnea is common, but the ventilator amplifies it. Over-ventilation causes respiratory alkalosis. The kidneys would normally compensate by excreting bicarbonate, but this takes hours. The immediate problem is the ventilator itself.
Decreasing the respiratory rate or tidal volume will allow pCO2 to rise back toward 40. This is a ventilator management question, not a metabolic problem. The board tests this because clinicians often panic about "low pCO2" and increase ventilation → exactly the WRONG move. You need to decrease minute ventilation.
Q14 of 25
An 8-year-old with severe gastroenteritis and 8% dehydration. ABG: pH 7.20, pCO2 28, HCO3 11, Na 148, Cl 110, K 3.2. AG = 19. What is the acid-base disturbance?
A. Pure metabolic acidosis with appropriate respiratory compensation
B. Mixed metabolic acidosis (gap) and hyperchloremic acidosis from dehydration
C. Respiratory alkalosis masking an underlying metabolic acidosis
D. Metabolic alkalosis with respiratory compensation
The low pH (7.20) and low HCO3 (11) indicate metabolic acidosis. The elevated AG (19) suggests a gap component. But the chloride is high (110), and the patient is severely dehydrated with hypernatremia (148), suggesting concurrent volume depletion.
In severe gastroenteritis, the child loses both bicarbonate (small bowel diarrhea) and free water. The sodium concentration rises (hypernatremia, 148) because water is lost disproportionately. The chloride is high because it's reabsorbed preferentially during volume depletion. The AG is slightly elevated because small amounts of unmeasured anions accumulate during the early shock state. This is a MIXED picture: gap acidosis from early renal dysfunction, plus hyperchloremic acidosis from bicarbonate loss and chloride retention.
Treating this with saline alone will worsen the hyperchloremic component. The child needs HYPOTONIC fluids (0.45% saline with dextrose) to free water replete while correcting electrolytes. This is a pediatric board favorite because it combines dehydration, hypernatremia, mixed acidosis, and hypokalemia → all common in severe gastroenteritis.
Q15 of 25
A 72-year-old with COPD, acute exacerbation on day 3 of prednisone. Baseline ABG: pH 7.35, pCO2 55, HCO3 30 (chronic compensation). Current ABG: pH 7.28, pCO2 65, HCO3 31. What happened?
A. The patient developed acute on chronic respiratory acidosis
B. The patient's kidneys improved compensation
C. The prednisone is worsening respiratory drive
D. Concurrent metabolic alkalosis is masking the severity
Comparing to baseline, the pH dropped (7.35 to 7.28) and pCO2 ROSE (55 to 65). The HCO3 stayed about the same (30 to 31). This is acute decompensation of chronic respiratory acidosis.
The baseline shows chronic respiratory acidosis with renal compensation. The kidneys have adjusted to the chronic high pCO2 by retaining bicarbonate. But during the acute exacerbation, the pCO2 spiked to 65. The kidneys can't respond that fast → renal compensation takes hours. So there's an acute increment on top of the chronic baseline. The HCO3 didn't rise from 30, meaning the kidneys haven't had time to compensate for the acute CO2 rise.
The danger here is underestimating severity. A baseline pH of 7.35 looked "compensated," but during acute exacerbation, the pCO2 spike outpaces renal compensation. The patient is acidemic and at risk for respiratory failure. Aggressive bronchodilators and possibly BiPAP/intubation are needed. This is a classic USMLE scenario: chronic vs acute respiratory acidosis differentiation.
Q16 of 25
A 28-year-old with a 4-day alcohol binge. ABG: pH 7.29, pCO2 22, HCO3 10, Na 137, Cl 102, K 3.4, Lactate 3.2 (elevated), Beta-hydroxybutyrate 4.2 mmol/L (elevated). AG = 33. What is the diagnosis?
A. Alcoholic ketoacidosis (AKA)
B. Lactic acidosis from cirrhosis
C. Methanol poisoning
D. Combined lactic and ketoacidosis
The elevated AG (33) with low HCO3 (10) and appropriate respiratory compensation (low pCO2) indicates a gap metabolic acidosis. The presence of both elevated lactate (3.2) and elevated beta-hydroxybutyrate (4.2) suggests mixed lactic and ketoacidosis.
Alcoholic ketoacidosis happens during or shortly after alcohol binge with poor nutrition. Ethanol metabolism produces acetyl-CoA, driving ketone body production. Simultaneously, hypoglycemia and poor perfusion drive lactic acid accumulation. The AG rises from BOTH ketones and lactate. Unlike DKA, glucose is usually LOW or normal (not > 300), and HCO3 is very low (10 vs 7-15 in DKA).
The treatment is dextrose and thiamine. Dextrose stops ketone production (by suppressing lipolysis) and restores glucose. Thiamine prevents Wernicke encephalopathy, a board-favorite complication. This is NOT DKA. The blood glucose distinguishes them: DKA > hyperglycemic, AKA > normoglycemic or hypoglycemic. The boards test this distinction relentlessly.
Q17 of 25
A 56-year-old with cirrhosis on lactulose presents with confusion. ABG: pH 7.48, pCO2 30, HCO3 22, Na 135, Cl 99, K 3.0. AG = 14 (normal). What is the acid-base status?
A. Primary metabolic alkalosis from lactulose-induced potassium loss
B. Primary respiratory alkalosis from hepatic encephalopathy
C. Combined metabolic and respiratory alkalosis
D. Respiratory compensation for underlying metabolic acidosis
The high pH (7.48) indicates alkalemia. The HCO3 (22) is normal-to-high, and the pCO2 (30) is low. Both are DRIVING alkalemia, not compensating. This is a COMBINED acid-base problem.
Lactulose causes osmotic diarrhea, losing both potassium and bicarbonate. With hypokalemia (3.0), the kidney reabsorbs bicarbonate preferentially (paradoxically making HCO3 "normal" or high despite losses). Meanwhile, hepatic encephalopathy ITSELF drives hyperventilation, lowering pCO2. The patient has both metabolic (from lactulose/K loss) AND respiratory (from encephalopathy) alkalosis.
This is a HIGH-risk scenario for cardiac arrhythmias (hypokalemia + alkalosis = QT prolongation). The patient is confused partly from encephalopathy, partly from the alkalosis itself (which worsens mental status). Treatment: KCl supplementation, continue lactulose for encephalopathy, and treat the underlying liver disease. Don't just chase the acid-base numbers → fix the potassium.
Q18 of 25
A 3-year-old with prolonged vomiting (pyloric stenosis suspected). ABG: pH 7.56, pCO2 48, HCO3 42, Na 140, Cl 85, K 2.5, Urine Cl less than 10 mEq/L. What is the acid-base status?
A. Severe metabolic alkalosis with respiratory compensation
B. Chloride-responsive metabolic alkalosis
C. Chloride-resistant metabolic alkalosis from hyperaldosteronism
D. Mixed metabolic and respiratory alkalosis
The very high pH (7.56), high HCO3 (42), and elevated pCO2 (48) indicate metabolic alkalosis with respiratory compensation. The chloride is LOW (85), potassium is LOW (2.5), and urine chloride is very LOW (less than 10).
Vomiting from pyloric stenosis loses acid (HCl) directly. The stomach secretes HCl; loss of this acid leaves an excess of bicarbonate. Volume depletion from vomiting triggers aldosterone, causing sodium reabsorption WITH bicarbonate (not chloride, because chloride is already depleted). The kidneys CANNOT excrete bicarbonate without chloride to accompany sodium. So the alkalosis is LOCKED IN by chloride depletion.
This is a chloride-responsive alkalosis. Treatment is IV 0.9% saline (normal saline, which contains chloride). DO NOT give potassium-sparing diuretics or acetazolamide → these make it worse by depleting chloride further. The urine chloride less than 10 is the KEY sign that this is chloride-responsive (vs chloride-resistant, which would have urine Cl greater than 20). The board loves this scenario because it tests whether you know the mechanism: the kidneys want to excrete bicarbonate, but CANNOT do so without chloride.
Q19 of 25
A 64-year-old with acute coronary syndrome, on high-flow oxygen therapy (FiO2 100% for 6 hours). ABG: pH 7.32, pCO2 45, HCO3 21, Na 140, Cl 102, K 4.0. Why is the pH low despite normal pCO2 and HCO3?
A. This is a measurement error; the pH should be normal
B. Hyperoxia drives mild metabolic acidosis (oxygen toxicity)
C. The HCO3 is ACTUALLY low when corrected for hypokalemia (paradoxical alkaluria)
D. This is normal; 7.32 is only mildly low and within compensation range
The pH is 7.32 (acidemia) with normal pCO2 (45) and near-normal HCO3 (21). If both pCO2 and HCO3 were normal, pH should be normal. The low pH indicates a metabolic acidosis that isn't obvious from HCO3 alone.
Hyperoxia causes production of reactive oxygen species, which drive metabolic acidosis. Additionally, high oxygen increases chloride reabsorption in the kidney, creating a mild hyperchloremic metabolic acidosis. The HCO3 hasn't dropped dramatically (still 21) because the process is mild and acute. But the low pH reveals it's present.
This is a rarely-tested board phenomenon, but it's real. The treatment is to WEAN oxygen once the ACS crisis stabilizes. Prolonged high-flow oxygen creates an iatrogenic metabolic acidosis. Target oxygen saturation of 90-95% is safer than 100%. This teaches a practical lesson: normal HCO3 does NOT guarantee normal acid-base status → always look at the pH first.
Q20 of 25
An 18-year-old girl with anorexia nervosa, presenting with chest pain. ABG: pH 7.54, pCO2 32, HCO3 26, Na 138, Cl 94, K 2.0 (CRITICAL), Mg 1.3 (low). What is the immediate life threat?
A. Metabolic alkalosis causing seizures
B. Hypokalemia and hypomagnesemia causing cardiac arrhythmia (sudden death risk)
C. Respiratory alkalosis causing cerebral vasoconstriction
D. Concurrent metabolic and respiratory alkalosis
The pH is high (7.54), indicating alkalemia from both metabolic (HCO3 26) and respiratory (low pCO2 32) contributions. But the CRITICAL values are potassium (2.0) and magnesium (1.3).
Severe malnutrition in anorexia nervosa causes total body potassium and magnesium depletion. Refeeding worsens this paradoxically (refeeding syndrome). Hypokalemia plus hypomagnesemia creates a PERFECT STORM for sudden cardiac death: QT prolongation, U waves, torsades de pointes, and ventricular fibrillation.
The acid-base disturbance is almost secondary to the electrolyte emergency. Stabilization requires SLOW refeeding with aggressive potassium and magnesium replacement BEFORE nutrition. Inpatient ICU monitoring with telemetry is mandatory. This is a board-loved high-acuity scenario because it teaches: severe electrolyte abnormalities can coexist with seemingly "mild" acid-base changes, but the electrolytes are what kill the patient.
Q21 of 25
A 42-year-old with metformin-associated lactic acidosis (MALA) on dialysis. ABG: pH 6.89 (CRITICAL), pCO2 12, HCO3 2 (CRITICAL), Na 135, Cl 102, Lactate 18 (CRITICAL), AG = 31. eGFR less than 15 mL/min/1.73m2. What is the primary therapy?
A. Sodium bicarbonate bolus (1-2 amps) to correct the severe acidemia
B. Emergent hemodialysis or hemofiltration to remove lactate and provide ECMO if needed
C. Aggressive hyperventilation to blow off CO2 and raise pH
D. Thiamine and dextrose to reduce lactate production
The pH is CRITICAL at 6.89, and HCO3 is nearly zero (2). The lactate is massively elevated at 18 (normal less than 2). This is the WORST acid-base emergency possible → near-fatal lactic acidosis.
MALA happens when metformin accumulates in renal failure. The kidneys cannot clear the drug, and lactic acid production overwhelms buffering. A pH of 6.89 is incompatible with life for long. The pCO2 is already at the floor (12) → the lungs are compensating maximally. Sodium bicarbonate at this pH has LIMITED utility because the patient is ANION-RICH (all the anions are lactate, which bicarbonate cannot directly fix).
The ONLY definitive therapy is emergent DIALYSIS to remove lactate. High-volume hemofiltration or veno-venous extracorporeal membrane oxygenation (VV-ECMO) with dialysis is often used in ICU. Temporary pH support with sodium bicarbonate may help, but it's a bridge to dialysis, not a solution. This is a teaching case: identify renal failure + metformin = STOP METFORMIN immediately. The patient should have never been on metformin with eGFR less than 30. A missed diagnosis cost them their life.
Q22 of 25
A 38-year-old on topiramate for migraine prophylaxis for 8 weeks. ABG: pH 7.31, pCO2 38, HCO3 18, Na 140, Cl 108, K 3.2. What is the acid-base disturbance?
A. Respiratory acidosis from topiramate-induced hypoventilation
B. Hyperchloremic metabolic acidosis from topiramate's renal tubular effects
C. Anion gap metabolic acidosis from drug toxicity
D. Primary metabolic alkalosis with respiratory compensation
The low pH (7.31) and low HCO3 (18) indicate metabolic acidosis. The pCO2 (38) is normal, so the lungs are NOT compensating → this is a PRIMARY metabolic process. The chloride is high (108) relative to normal, and anion gap is low (12 or less).
Topiramate is a carbonic anhydrase inhibitor (like acetazolamide). It blocks H+ secretion in the kidney's proximal tubule, preventing bicarbonate reabsorption. The result is urinary bicarbonate wasting and HYPERCHLOREMIC metabolic acidosis. The kidney reabsorbs chloride preferentially to maintain electroneutrality, so chloride rises while bicarbonate falls.
This is a known side effect of topiramate → hyperchloremic metabolic acidosis with hypokalemia. Long-term topiramate use, especially in patients with renal impairment, can cause this. The boards love testing whether you recognize drug-induced hyperchloremic acidosis. Treatment: replace bicarbonate with acetazolamide (paradoxically), or switch to a different migraine prophylaxis agent. Potassium supplementation is also needed.
Q23 of 25
A 31-year-old with acute salicylate overdose (aspirin, multiple doses in confusion). ABG: pH 7.21, pCO2 18, HCO3 7, Na 140, Cl 100, K 3.8, Lactate 2.1, Salicylate level 78 mg/dL (TOXIC greater than 30). AG = 33. What is the acid-base status?
A. Pure metabolic acidosis with appropriate respiratory compensation
B. Mixed high-gap metabolic acidosis and respiratory alkalosis (CLASSIC salicylate pattern)
C. Respiratory acidosis with compensatory metabolic alkalosis
D. Lactic acidosis from shock
The low pH (7.21) and low HCO3 (7) indicate metabolic acidosis with appropriate respiratory compensation (low pCO2 of 18). But the AG (33) is VERY high, indicating substantial unmeasured anions. The toxic salicylate level confirms the diagnosis.
Salicylate toxicity causes TWO simultaneous acid-base disturbances: (1) Direct salicylate accumulation raises the AG (salicylate itself is an anion). (2) Salicylate uncouples oxidative phosphorylation, increasing cellular metabolism, heat production, and lactic acid. Both elevate the gap. The respiratory response (low pCO2 of 18) IS appropriate for the metabolic acidosis, but salicylate also DIRECTLY stimulates the respiratory center, driving hyperventilation independent of acid-base needs. This creates a paradoxical picture: severe metabolic acidosis with OVER-compensation (pCO2 very low). Some textbooks call this "mixed metabolic acidosis and concurrent respiratory alkalosis," though both are happening simultaneously, not sequentially.
Treatment is urgent removal via hemodialysis (salicylate is dialyzable). Sodium bicarbonate raises urine pH and alkalemia, both of which trap salicylate in urine and prevent reabsorption. Do NOT give acetazolamide or aggressive hyperventilation (patient is already hyperventilating). The goal is dialysis + supportive care until the drug is cleared. This is a medical emergency because the acidosis worsens neurologic symptoms and cardiotoxicity.
Q24 of 25
A 67-year-old with new-onset atrial fibrillation on day 1 of diuretic therapy for hypertension. ABG: pH 7.49, pCO2 40, HCO3 29, Na 132, Cl 92, K 2.8 (CRITICAL). EKG shows prolonged QT and U waves. What is the mechanism of the arrhythmia?
A. Hyperkalemia from diuretic-induced renal loss
B. Hypokalemia from diuretics, causing QT prolongation and Afib trigger
C. Metabolic alkalosis from diuretic-induced bicarbonate retention
D. Hyponatremia causing cerebral edema and arrhythmia
The pH is high (7.49), HCO3 is high (29), and the pCO2 is normal → this is metabolic alkalosis. The CRITICAL value is potassium at 2.8 (normal 3.5-5.0). The EKG shows signs of hypokalemia (prolonged QT, U waves). The patient is in new-onset Afib.
Loop diuretics cause alkalosis by several mechanisms: (1) volume depletion triggers secondary hyperaldosteronism, increasing sodium and bicarbonate reabsorption. (2) Direct loss of chloride forces bicarbonate reabsorption. (3) Potassium loss activates the pump that exchanges intracellular H+ for extracellular K+, driving net bicarb retention. The hypokalemia is the ARRHYTHMOGENIC factor here. Low potassium prolongs repolarization, lengthening the QT interval. This creates a substrate for re-entrant arrhythmias, Afib, and sudden death.
Diuretic-induced electrolyte losses are a common cause of new-onset Afib in elderly patients started on diuretics for hypertension. The treatment is potassium supplementation, preferably with a potassium-sparing diuretic. NSAIDs can help preserve potassium by blocking aldosterone. This is a board-tested scenario because it requires understanding the interplay of acid-base, electrolytes, and arrhythmias.
Q25 of 25
A 76-year-old with COPD EXACERBATION, presenting with respiratory distress, ABG on 6L O2: pH 7.28, pCO2 68, HCO3 31, Na 141, Cl 101, K 4.8. Baseline (2 months prior): pH 7.36, pCO2 52, HCO3 30. SpO2 88%, RR 28, using accessory muscles. What is the IMMEDIATE intervention?
A. Intubation and mechanical ventilation
B. Bilevel positive airway pressure (BiPAP) mask with warm-up time
C. Aggressive diuretics to reduce pulmonary edema
D. Supplemental oxygen alone until pCO2 improves
This patient has ACUTE worsening of chronic respiratory acidosis. The pCO2 rose from 52 to 68, and the pH dropped from 7.36 to 7.28. The HCO3 rose slightly (30 to 31), but not enough to compensate for the pCO2 rise, indicating ACUTE decompensation. The patient is hypoxic (88%) and tachypneic (28), using accessory muscles → signs of respiratory distress.
The patient has chronic CO2 retention from COPD (baseline pCO2 52), so the kidneys have adapted (HCO3 30). An acute exacerbation (infection, bronchospasm) causes pCO2 to SPIKE. The kidneys cannot respond acutely (takes hours to days), so pH drops. The patient needs ventilatory support to reduce the work of breathing and allow CO2 elimination. BiPAP is the first-line noninvasive option.
Intubation is NOT first-line for acute COPD exacerbation → BiPAP is preferred because it avoids the risks of intubation (ventilator-associated pneumonia, tracheal stenosis, dependency). However, if BiPAP fails, intubation is needed. The key is recognizing ACUTE-ON-CHRONIC: the baseline shows the kidneys have already compensated for chronic hypercapnia. Any ACUTE rise in pCO2 will drop the pH sharply. This is a high-stakes board scenario because the difference between BiPAP (success) and intubation (complications) hinges on rapid recognition and early intervention.