What it is:The body keeps arterial pH between 7.35 and 7.45 by balancing two things: the kidneys' handling of bicarbonate (HCO3-, the metabolic side) and the lungs' handling of CO2 (the respiratory side). An acid-base disorder is what happens when one of those two knobs breaks.
The core problem:There are only four primary disorders, and they pair up by direction. Acidosis(pH low) is either metabolic (HCO3- falls) or respiratory (PaCO2 rises). Alkalosis(pH high) is either metabolic (HCO3- rises) or respiratory (PaCO2 falls). Whichever side didn't cause the problem tries to fix it, that's compensation, and it never fully normalizes pH.
What you do about it:Read the ABG in order (pH, then which value moved with it, then whether the other value moved appropriately), find the primary disorder, decide if compensation is proportional or if there's a second process hiding underneath, then treat the underlying cause. You almost never treat the number itself.
Think of it as one see-saw with two hands on it.The metabolic hand is HCO3-, controlled by the kidney over hours to days. The respiratory hand is PaCO2, controlled by the lungs in minutes. When one hand pushes the see-saw off level, the other hand pushes back partway to compensate, but it can't do the first hand's job completely. That's why compensation is always partial and predictable by formula, never full normalization.
Everything in this chapter is variations on the same equation: CO2 + H2O ↔ H2CO3 ↔ HCO3- + H+.Push it one direction and pH drops (more H+), push it the other and pH rises (less H+, more HCO3-). The lungs control the CO2 side of that equation in real time; the kidneys control the HCO3- side slowly.
| Disorder | Primary change | pH | Compensating organ |
|---|---|---|---|
| Metabolic acidosis | ↓ HCO3- | ↓ | Lungs: hyperventilate to blow off CO2 |
| Metabolic alkalosis | ↑ HCO3- | ↑ | Lungs: hypoventilate to retain CO2 |
| Respiratory acidosis | ↑ PaCO2 | ↓ | Kidneys: reabsorb more HCO3-, secrete more H+ |
| Respiratory alkalosis | ↓ PaCO2 | ↑ | Kidneys: excrete more HCO3- |
The organ that didn't cause the problem is always the one that compensates.A metabolic problem gets a respiratory fix, and a respiratory problem gets a metabolic fix. The lungs respond in minutes because it's just a breathing rate change. The kidneys take hours to days because they have to alter tubular handling of acid and bicarbonate, which is why acute respiratory disorders look uncompensated on an ABG drawn early, and why the same disorder days later shows partial metabolic compensation.
Every ABG question is really the same three questions asked in order. Do them in this sequence and you won't get fooled by a normal-looking number that's actually hiding a second process.
| Disorder | pH | PaCO2 | HCO3- |
|---|---|---|---|
| Respiratory acidosis (uncompensated) | ↓ | ↑ | normal |
| Respiratory alkalosis (uncompensated) | ↑ | ↓ | normal |
| Metabolic acidosis (uncompensated) | ↓ | normal | ↓ |
| Metabolic alkalosis (uncompensated) | ↑ | normal | ↑ |
| Metabolic acidosis, respiratory compensation | ↓ (partially corrected) | ↓ | ↓ |
| Metabolic alkalosis, respiratory compensation | ↑ (partially corrected) | ↑ | ↑ |
| Respiratory acidosis, metabolic compensation | ↓ or near-normal | ↑ | ↑ |
| Respiratory alkalosis, metabolic compensation | ↑ or near-normal | ↓ | ↓ |
In a purely compensated single disorder, pH moves toward normal but never fully gets there and never crosses to the other side.If pH is actually normal (7.35-7.45) but HCO3- and PaCO2 are both abnormal, or if compensation overshoots what the formula predicts, you're looking at two primary disorders happening at once, not one disorder with compensation. Never assume compensation, always check the formula.
Base excess (BE) estimates how much HCO3- is above or below normal without you doing the math. Normal is roughly -2 to +2 mmol/L. BE >+2means excess bicarbonate (metabolic alkalosis or compensation for it). BE <-2means bicarbonate deficit (metabolic acidosis or compensation for it). It's a fast sanity check, not a replacement for working the actual numbers.
These are the exact formulas that separate "appropriately compensated" from "there's a second disorder here too." They come straight from the guideline table your professor tests from, and yes, you have to know acute vs. chronic for the respiratory ones.
| Primary disorder | Expected compensation |
|---|---|
| Metabolic acidosis | PaCO2 falls 1.25 ×the fall in HCO3- (mm Hg per mEq/L) |
| Metabolic alkalosis | PaCO2 rises 0.6 ×the rise in HCO3- |
| Acute respiratory acidosis | HCO3- rises 0.1 ×the rise in PaCO2 |
| Chronic respiratory acidosis | HCO3- rises 0.4 ×the rise in PaCO2 |
| Acute respiratory alkalosis | HCO3- falls 0.2 ×the fall in PaCO2 (rarely below 18 mEq/L) |
| Chronic respiratory alkalosis | HCO3- falls 0.4 ×the fall in PaCO2 (rarely below 14 mEq/L) |
The metabolic compensation for a respiratory problem takes the kidney 12-24 hours to even begin and days to complete, because it requires upregulating proximal tubular bicarbonate reabsorption, ammoniagenesis, and distal H+ secretion. An ABG drawn 2 hours into an asthma exacerbation should show a near-normal HCO3- (acute, uncompensated). The same PaCO2 in a COPD patient who's been retaining CO2 for years shows a much higher HCO3-, because chronic compensation had time to fully develop. Same PaCO2, very different HCO3-, because of time, not severity.
64-year-old with COPD, worsening dyspnea and cough x4 days. pH 7.26, PaCO2 8.2 kPa (61 mm Hg, high), HCO3- 28 (high), BE +4. Low pH driven by high PaCO2 = respiratory acidosis. HCO3- is elevated, meaning the kidney is compensating, and the several-day timeline plus COPD history makes this look chronic-on-acute (an acute flare on top of chronic CO2 retention), not a fresh, fully uncompensated process.
Primary problem:HCO3- falls, either because the kidney can't hold onto bicarbonate, because acid is being generated or ingested faster than it can be buffered and excreted, or because bicarbonate itself is being lost (diarrhea, some renal tubular disorders). Compensation:hyperventilation blows off CO2 to partially correct the pH; that's the deep, rapid Kussmaul-type breathing you see in severe cases.
When IV sodium bicarbonate is used, the target is to raise pH to roughly 7.2and plasma HCO3- to 8-10 mEq/L, not to normalize either value. Sodium bicarbonate replaces fluid and electrolytes and raises arterial pH, but it does not improve cardiac function, organ perfusion, or intracellular pH.Overcorrecting is a real risk: it causes volume overload, hypernatremia, and can worsen intracellular acidosis paradoxically. This is a classic exam distractor, students assume "more bicarb is better."
LD (mEq) = Vd × BW × (desired [HCO3-] − current [HCO3-])
Vd for bicarbonate = 0.5 L/kg; BW = body weight in kg. Plug in the current HCO3- from the ABG and your target (usually 8-10 mEq/L in acute severe acidosis), and that gives you the total mEq needed.
Generated by:reduced renal HCO3- excretion, loss of H+ from the kidney or stomach (vomiting, NG suction), or a gain of bicarbonate-rich fluids/excess alkali intake. Maintained by:an abnormal kidney that can't excrete the excess bicarbonate, usually because it's busy conserving sodium and chloride at the expense of bicarbonate (volume depletion) or because of ongoing mineralocorticoid excess. Compensation:hypoventilation raises PaCO2, but this is limited because the body won't tolerate severe hypoxemia just to buffer pH.
| Saline (chloride) responsive | Saline (chloride) resistant | |
|---|---|---|
| Mechanism | Volume depletion + chloride loss | Mineralocorticoid excess or profound hypokalemia keeping the kidney "stuck" excreting acid |
| Typical causes | Vomiting, NG suction, diuretic therapy | Bartter/Gitelman syndrome, Liddle syndrome, exogenous corticosteroids, primary hyperaldosteronism |
| Fix | Normal saline to replete volume and chloride | Treat the underlying cause; saline won't fix it and may make sodium-intolerant patients worse |
Assess intravascular volume and chloride stores first. Volume down →give normal saline to replete chloride, that alone often resolves it. Volume up or sodium-intolerant →think endogenous or exogenous mineralocorticoid excess. If it's exogenous corticosteroid, corticosteroid dose exceeded need, or drugs like spironolactone/amiloride/triamterene are already on board incorrectly, adjust the regimen. If it's endogenous (Bartter, Gitelman) and K+ <3 mEq/L, replete potassium and start amiloride or triamterene. If K+ isn't the driver and pH is still <7.55, acetazolamide 250-375 mg PO once or twice daily (plus potassium if K+ <3.5) helps the kidney dump bicarbonate. Persistent alkalosis or an initial pH >7.55 escalates to hydrochloric acid infusion (preferred in renal failure, liver failure, or decompensated CHF where you can't just give more saline) or ammonium chloride/arginine monohydrochloride as alternatives, with surgery considered if nothing works.
pH >7.55 risks cardiac arrhythmias, hyperventilation-driven hypoxemia, and neuromuscular irritability. This is the threshold where you escalate past saline/potassium fixes to acid infusion.
Mechanism:PaCO2 falls because ventilation is clearing CO2 faster than the body produces it, i.e., hyperventilation. Causes split into central/peripheral neurochemical drive (anxiety, pain, fever, sepsis, salicylate toxicity, CNS lesions) and mechanical over-ventilation (voluntary or from a ventilator).
Clinical picture:often asymptomatic, but can cause light-headedness, confusion, syncope, or seizures from reduced cerebral blood flow, plus nausea/vomiting from cerebral hypoxia, and arrhythmias if severe. Electrolytes shift too: chloride typically rises while potassium, phosphorus, and ionized calcium fall.
The immediate response is chemical buffering (H+ released from intracellular proteins, phosphate, hemoglobin). If it persists beyond 6 hours, the kidney starts inhibiting proximal tubular bicarbonate reabsorption and serum HCO3- starts to fall, that's the metabolic compensation kicking in.
Treatment:usually unnecessary since most cases are mild (pH rarely exceeds 7.50) and self-limited. Fix the underlying trigger: treat pain, hypovolemia, fever, infection, or salicylate overdose. A rebreathing device (paper bag) helps anxiety-driven hyperventilation. On a ventilator, correct it by decreasing the set respiratory rate, fine-tuning with capnography/spirometry, or adding dead space to the circuit.
Mechanism:PaCO2 rises and pH falls because ventilation isn't clearing CO2 adequately. Causes: central respiratory center suppression (opioids, sedatives, CNS injury), neuromuscular disease impairing the bellows (myasthenia, Guillain-Barre, high spinal injury), pulmonary perfusion problems, or intrinsic airway/parenchymal lung disease (COPD, severe asthma, pneumonia). Acute respiratory acidosis with hypoxemia and hypercarbia together is life-threatening.
Neurologic findings dominate: altered mental status, abnormal behavior, seizures, stupor, coma. Hypercapnia can even mimic a stroke or CNS tumor with headache, papilledema, focal paresis, and abnormal reflexes, all from increased cerebral blood flow.
Chemical buffering happens immediately. Metabolic (renal) compensation doesn't start until the disorder has been present 12-24 hours: enhanced proximal bicarbonate reabsorption, ammoniagenesis, and distal H+ secretion raise serum HCO3- and push pH back toward normal. This is exactly why "acute" and "chronic" get different compensation multipliers in the formula table above.
Give oxygen carefully and only if PaO2 <50 mm Hg.In chronic CO2 retainers, the drive to breathe has shifted to depend on hypoxemia rather than hypercarbia. Over-correcting oxygenation can blunt respiratory drive and worsen CO2 retention. This distinction between acute and chronic O2 targets is a favorite trap question.
Two mechanisms produce a mixed picture: failure of compensationgives you mixed acidosis (respiratory + metabolic) or mixed alkalosis (respiratory + metabolic) stacking in the same direction. Excess compensation, or really two opposing primary processes,gives you metabolic acidosis with respiratory alkalosis, or metabolic alkalosis with respiratory acidosis.
| Mixed pattern | Typical setting | Treatment focus |
|---|---|---|
| Respiratory + metabolic acidosis | Cardiorespiratory arrest; chronic lung disease in shock; metabolic acidosis progressing to respiratory failure | Oxygen and ventilation support for the respiratory component; appropriate alkali for the metabolic component |
| Respiratory + metabolic alkalosis(most common mixed pattern) | Critically ill surgical patients: mechanical ventilation, hypoxia, sepsis, hypotension, pain driving respiratory alkalosis, plus vomiting/NG suction or massive transfusion driving metabolic alkalosis | NaCl/KCl solutions for the metabolic side; adjust ventilator or treat the hyperventilation trigger for the respiratory side |
| Metabolic acidosis + respiratory alkalosis | Advanced liver disease, salicylate intoxication, pulmonary-renal syndromes | Treat the underlying cause directly |
| Metabolic alkalosis + respiratory acidosis | COPD with chronic respiratory acidosis, treated with salt restriction, diuretics, +/- glucocorticoids | pH often near-normal since the two push in opposite directions, but still manage PaO2/PaCO2; sodium/potassium chloride lowers plasma bicarbonate and lets the kidney excrete the retained bicarb from diuretic-driven alkalosis |
Salicylate toxicity is the textbook example of mixed metabolic acidosis and respiratory alkalosis in one patient: salicylates directly stimulate the medullary respiratory center (respiratory alkalosis) while also uncoupling oxidative phosphorylation and generating organic acids (metabolic acidosis). If you see that combination on a board question, salicylate overdose should be on your differential.
For the gradual correction of mild to moderate metabolic acidosis. Choice depends mostly on whether the patient needs sodium or potassium as the accompanying cation, and on renal function (avoid potassium-containing salts if the kidney can't excrete potassium).
| Product | Alkali delivered | Cation |
|---|---|---|
| Sodium citrate/citric acid solution | 1 mEq bicarbonate per mL | Sodium |
| Sodium bicarbonate tablets | 3.9 mEq (325 mg tab) or 7.8 mEq (650 mg tab); baking soda powder ~60 mEq/teaspoon | Sodium |
| Potassium citrate ER tablets | ~5, 10, or 15 mEq bicarbonate per tablet | Potassium |
| Potassium bicarbonate/potassium citrate effervescent tablets | ~10, 20, or 25 mEq bicarbonate per tablet | Potassium |
| Potassium citrate/citric acid packets or solution | ~30 mEq bicarbonate per packet; ~2 mEq per mL as solution | Potassium |
| Sodium citrate/potassium citrate/citric acid solution | ~2 mEq bicarbonate per mL (1 mEq Na+ and 1 mEq K+ per mL) | Both sodium and potassium |
If the patient is already hyperkalemic or has poor renal clearance of potassium, reach for a sodium-basedproduct. If they're hypokalemic (common in some renal tubular acidoses and GI losses), a potassium-basedcitrate product corrects two problems at once. Citrate salts are metabolized to bicarbonate in the liver, so hepatic impairment can blunt their effect, sodium/potassium bicarbonate itself doesn't need that conversion step.
| Parameter | When | Watching for |
|---|---|---|
| ABG (pH, PaCO2, HCO3-, BE) | Baseline and serially through treatment; this is the primary tool for evaluating outcome | Direction and magnitude of pH correction; whether compensation is proportional to the compensation formulas |
| Serum electrolytes (Na, K, Cl, HCO3-) | Baseline, then regularly during IV alkali therapy or aggressive diuresis | Overcorrection, hypokalemia (common as acidosis corrects and K+ shifts intracellularly), hypernatremia from sodium-based alkali |
| Volume status / daily weight, BP | Throughout treatment of metabolic alkalosis | Adequacy of saline repletion in chloride-responsive alkalosis; fluid overload from sodium bicarbonate load |
| Mental status | Every assessment in acidosis or alkalosis of any origin | Both severe acidemia and alkalemia cause neurologic symptoms; a change signals the disorder is worsening or overcorrecting |
| Cardiac rhythm / telemetry | Severe acidemia (pH <7.2) or severe alkalemia (pH >7.55) | Arrhythmia risk rises sharply at these extremes |
| Renal function (BUN, SCr) | Alongside any acid-base workup | Underlying or contributing renal dysfunction; SCr lags true kidney function by days, so trend it, don't rely on one value |