Acid-Base Balance in Surgical Patients — ABG Method, HAGMA/NAGMA, Lactate, Bicarbonate Verdict, Alkalosis, Stewart

The surgical patient rarely offers a single acid-base disorder — so run history, electrolytes, anion gap and pH first, then compensation, then the delta ratio last; correct the gap for albumin before believing it; pair every high gap with an osmolar gap when toxins threaten; sort lactate by production versus removal and clear it rather than chase it; blame saline chloride before blaming dilution; split gut loss from renal loss with the urine anion gap; give bicarbonate only where BICAR earned it (severe acidaemia with kidney injury, or pH at or below 7.10) and never at pH 7.2 or above; read vomit-loss alkalosis as chloride depletion with volume and urine electrolytes first; suspect ketoacidosis behind normal glucose on SGLT2 inhibitors; and use Stewart equations as a second lens with interchangeability humility: because the anion gap is a construct that splits acidosis in two, the delta ratio exposes the hidden second disorder, bicarbonate failed its primary endpoints but cut dialysis, and every number below comes from the paper named beside it.^{[2][3][4][42][44][52][58][68]}

A 64-year-old man is day 2 after emergency laparotomy for small-bowel obstruction on an SGLT2 inhibitor taken the morning of surgery: pH 7.18, bicarbonate 14, chloride 112, albumin 22, lactate 3.1 clearing slowly, ketones positive with glucose 11, potassium 5.6, creatinine rising, urine output falling. Which disorder is primary and which is hiding inside it, whether his gap is worse than it looks, whether bicarbonate helps a shocked acidotic kidney, what the SGLT2 tablet did, and which alkali alternative the ventilator prefers? The examiner will watch you correct the gap for albumin, compute the delta against his own baseline, fence lactate resuscitation to the shock topic while keeping its interpretation, apply the BICAR rule with its exact boundaries, withhold-and-monitor the SGLT2 inhibitor by the 72-hour rule, and read the vomit-loss alkalosis underneath. This page teaches each move with every number taken from the paper named beside it.^{[4][9][36][42][44][73][75]}

The Stepwise ABG Algorithm — history to delta ratio

Diagnose every simple disorder — metabolic acidosis, metabolic alkalosis, respiratory acidosis, respiratory alkalosis — with one fixed sequence: history and examination, then electrolytes with anion gap and pH, then the degree and nature of compensation, and finally the delta anion gap to delta bicarbonate ratio, which also unlocks mixed disorders.^[2] Plot paired PCO2 and bicarbonate ratiometrically rather than reading pH alone: mapping the pair on Cartesian coordinates visually defines the disorder and validates the method when more than a simple disorder is present.^[12] Use a systematic approach for every gas because bedside reads miss mixtures: in 31 critically ill CKD patients the systematic method found mixed disorders in 50% versus 12.9% by bedside read, with findings that correlated to the clinical picture — a small single-centre cohort, but the direction favours discipline.^[15] Published stepwise algorithms package exactly these new concepts for case work, and a pharmacist-led systematic approach improves pharmacotherapy decisions — the method is team-wide, not tribal.^[11][14]

Anion Gap — Calculate, Correct, Suspect

Start from the construct: the anion gap compares blood sodium against chloride plus bicarbonate, and that single subtraction splits metabolic acidosis into high-gap versus hyperchloraemic families, delimiting the aetiologies — then comparing gap change against bicarbonate change exposes occult coexisting disorders.^[3] Acidosis begins as a primary bicarbonate fall with roughly 1 mmHg of PaCO2 lost per 1 mmol/L of bicarbonate and a falling pH, and the gap formula of sodium minus bicarbonate-plus-chloride sorts normal (hyperchloraemic) from elevated gap — though the categories can overlap as renal failure evolves.^[1] Correct every gap for albumin before trusting it: marked hypoalbuminaemia is the norm in critical illness (nearly half under 20 g/L in Figge's ICU cohort), each g/L of missing albumin hides 0.25 mEq/L of gap anions, and the correction adds 0.25 times the albumin deficit in g/L (2.5 times in g/dL) to return the gap to its familiar scale.^[4] The correction changes management: in shocked children the uncorrected gap found occult tissue anions in 48% of significant samples versus 87% after Figge correction — a paediatric-shock cohort, so borrow the equation generally but fence the percentages there.^[5] Respect the small or negative gap too: it suggests occult disease or measurement artifact rather than reassurance.^[3] Memorise the low-gap traps for the viva — hypoalbuminaemia, cationic paraproteins, halide poisoning, lithium — plus the air-exposure artifact that fakes a high gap with normal pH, and keep the delta ratio plus urine gap ready for complex cases.^[6] Know what generates the gap mechanistically: non-chloride organic acids entering blood create it, which is why chloride stays put while bicarbonate falls.^[7]

Delta Gap and Osmolar Gap — the second disorder and the toxin

Compute the delta ratio after the gap, not before: the change in anion gap over the change in bicarbonate (with the urine gap alongside) dissects complex and mixed disorders that a single gap value cannot.^[2][6] Abandon the 1:1 dogma for early lactic acidosis: in trauma patients sampled before fluids, the mean delta-gap-to-delta-bicarbonate ratio was 1.86 within the first hours — not 1:1 — because endogenous human lactic acidosis carries unmeasured anions that animal acid-infusion models never had.^[8] Correct before you ratio: using an albumin-corrected gap with each patient's own pre-illness baseline gives a mean ratio of 1.20 in septic ICU patients, while mean-normal values inflate it to 1.6–1.8 and can misdiagnose complex disorders — so carry the patient's baseline and albumin into every calculation.^[9] Pair the gap with plasma osmolality and the osmolal gap whenever toxins threaten, since the pair together guides decisions — but never let a normal osmolal gap reassure you: toxic-alcohol ingestion kills within minutes to hours and the osmolal gap is an inadequate substitute for direct testing, so the laboratory's role is urgent confirmation, not screening comfort.^[3][10]

HAGMA Causes in Surgical Patients

Think acute versus chronic by mechanism: acute acidosis overproduces organic acids — ketoacids, lactate — while chronic acidosis wastes bicarbonate or fails renal acidification, with different harms and different alkali logic for each.^[1] Work the Core Curriculum cases from common to rare: the gap points at ketoacidosis, lactate, renal failure and toxins, with albumin and glucose corrections plus osmolal gap completing the hunt.^[3] Suspect starvation ketoacidosis in the re-operative, long-fasted abdomen: the acute-care-surgery case normalised its gap within hours once carbohydrate delivery resumed — a single case, so borrow the suspicion, never a rate, and remember fasting surgical patients need substrate thinking, not just alkali.^[85] Price acute acidosis honestly when counselling: falling cardiac output, vasodilatation with hypotension, altered oxygen delivery, less ATP, arrhythmia tendency and immune impairment — against chronicity's muscle wasting and bone disease.^[1]

Lactate — Classify, Clear, Prognosticate (resuscitation fenced)

Classify L-lactic acidosis by production versus removal rather than alphabet letters: the production/removal frame decides whether you restore perfusion, stop a drug, or support clearance.^[34] Read severity as oxygen debt: lactic acidosis tracks overall oxygen debt and survival, and serial lactate monitors perfusion through resuscitation — yet buffering shock-driven lactic acidosis has never been shown to change outcome.^[33] Clearance predicts: lactate clearance marks lower mortality in the critically ill with optimal clinical utility, so trend it as a prognostic biomarker.^[35] Use Jones narrowly and exactly: 300 ED patients with severe sepsis randomised to lactate-clearance (10% or more) versus ScvO2 (70% or more) goals died 17% versus 23% in hospital with no significant difference — clearance is noninferior as a goal, which licenses goal-choice, not resuscitation detail (pressors, MAP and protocol belong to shock-surgical).^[36] Always exclude drugs: hyperlactataemia is a rare but life-threatening toxicity across drug classes — stop the culprit, use antidotes where they exist, and think toxicology when sepsis, hypotension and hypoxia are absent.^[37] Exempt epinephrine-driven lactate explicitly: beta2-agonist hyperlactataemia reflects accelerated aerobic glycolysis and needs no specific intervention — but still search for remediable hypoperfusion because global delivery numbers can look fine while regions starve.^[38]

NAGMA and Hyperchloraemic Acidosis — saline, gut, kidney

Suspect NAGMA early precisely because it is under-recognised: in adults it can be the first clue to autoimmune disease, gammopathy or drug toxicity, so run a pathophysiology framework rather than a single test.^[18] Convict saline first: randomised acute-care comparisons show saline arms more acidotic via rising chloride, and 0.9% NaCl is the leading cause of hyperchloraemic acidosis in the critically ill — with coagulation, renal and mortality signals attached.^[19][20] Expect hyperchloraemia in sepsis whether from disease or intervention, since it drives both acidosis and wider septic pathophysiology.^[21] Then bound the fluid claim with Cochrane honesty: buffered solutions change chemistry (lower chloride, higher bicarbonate and pH) but show no mortality effect versus saline with high certainty, and similar AKI with low certainty — chemistry wins, outcomes tie.^[22] Explain the chloride avidity that maintains the disorder: losing sodium bicarbonate (proximal RTA) or sodium-anion salts (distal RTA) contracts effective volume, which drives dietary chloride reabsorption and locks in the normal-gap acidosis.^[23] Split gut from kidney at the bedside with urine: the urine anion gap estimates ammonium excretion and runs typically negative in diarrhoea-driven normal-gap acidosis — negative points to gut, positive to kidney.^[17] Read postoperative fluids in Stewart terms: the infusate's strong-ion-difference-minus-bicarbonate drives the plasma change during replacement, unmeasured anions contribute, and renal effects are temporally limited over short time frames.^[32]

RTA Subtypes — proximal, distal, hyperkalaemic

Separate the RTAs by what the tubule mishandles: distal and renal-failure RTA cannot regenerate bicarbonate spent buffering endogenous acid, proximal RTA wastes filtered bicarbonate — and as filtration collapses, a normal-gap acidosis eventually gains a gap.^[23] Apply the stone rule that examiners love: citrate in the urine protects (proximal RTA, negligible stones) while its absence condemns (distal RTA, high stones with nephrocalcinosis) — and remember RTA also presents as stones, rickets and growth failure, with alkali treatment still largely empirical.^[24][26] Diagnose by urine function: distal-versus-proximal testing assesses urinary acid and bicarbonate handling, while hyperkalaemic RTA means proving aldosterone deficiency or resistance after excluding other hyperkalaemia — then give alkali to distal/proximal disease and potassium-lowering (diet, newer binders) to hyperkalaemic disease.^[25] Classify distal disease mechanistically with urinary acidification indices while weighing potassium and its excretion — the Batlle discipline that still organises the workup.^[28] File pseudohypoaldosteronism II correctly: laboratory findings confirm PHA2 is compatible with type IV RTA, so hyperkalaemic hyperchloraemic acidosis with hypertension points there.^[29] Place Bartter and Gitelman beside the RTAs as salt-wasting alkalosis mimics: replenish fluid and electrolytes, consider prostaglandin blockade and RAAS disruption, and note genotype-phenotype mapping is still maturing through registries.^[30] Recognise RTA in all its forms early, because naming the right type chooses the therapy and the prognosis — the Chan imperative that has survived four decades.^[27]

Bicarbonate — the BICAR verdict and bedside rule

Start from controversy, not habit: bicarbonate for severe metabolic acidaemia was possible but unproven on clinical outcomes — which is exactly what BICAR-ICU was built to test.^[42] Quote BICAR-ICU precisely (389 patients, pH 7.20 or below): the composite of 28-day death plus day-7 organ failure hit 71% control versus 66% bicarbonate (absolute difference −5.5%, p=0.24, null), with 28-day survival 46% versus 55% (p=0.09, null) — but the prespecified AKIN 2–3 stratum survived 54% versus 37% (p=0.0283), a stratum signal inside a null trial.^[42] Update with BICARICU-2 (627 analysed, severe acidaemia plus moderate-to-severe AKI, pH target 7.30 or higher): day-90 death 62.1% versus 61.7% (difference 0.4, p=0.91, null) with no day-28 or day-180 effect — yet kidney replacement fell from 50% to 35% (difference −15.5) — mortality null, dialysis cut.^[43] Close with the individual-patient synthesis of both trials (1,016 patients): 90-day mortality risk ratio 0.96 (null), dialysis initiation risk ratio 0.69 (NNT 6.3) with more dialysis-free days — and a depth interaction (p=0.006) where pH 7.10 or below cut mortality (risk ratio 0.80) while above 7.10 did nothing (risk ratio 1.05).^[44] State the bedside rule in one sentence: no mortality benefit overall, fewer dialysed, possible mortality gain only at pH 7.10 or below — bicarbonate to avoid dialysis and for profound acidaemia, not as routine correction.^[44] Set the floor from the reviews: limited benefit below pH 7.1 with bicarbonate under 6 except with AKI where survival improves; no mortality difference in high-gap (mostly lactic) acidosis; Bayesian hints of mortality benefit remain inconclusive pending larger trials.^[46][47][48] Set the ceiling at pH 7.2: no known benefit correcting at or above 7.2 with only sparse evidence below it — and if given, slow infusion with adequate ventilation and calcium replacement.^[52] Treat the cause first in shock lactate: reversing hypoperfusion is the therapy, with slow alkali only as adjunct plus a CO2-clearance plan and ionised-calcium correction (a 10% fall impairs heart, vessels and catecholamine response) — preferring bicarbonate-based over citrate replacement fluids on continuous dialysis since citrate may widen the strong ion gap.^[51] Price the harms before prescribing: hypercapnia, hypokalaemia, ionised hypocalcaemia and QTc prolongation, plus the BICAR-observed alkalosis, hypernatraemia and hypocalcaemia (no life-threatening events reported).^[50][42] Tailor rather than protocolise: correction tracks haemodynamics poorly, so weigh alkali and dialysis risks per patient while awaiting definitive trials — the scoping review concurs that data are too thin to support routine use and a proper investigation programme is justified — and note survivors carry reduced long-term physical quality of life either way.^[53][49][45] Name the open DKA question honestly: bicarbonate efficacy below pH 6.9 in DKA still needs prospective randomised proof.^[79] The BICARICU-2 protocol paper itself contributes design only — severe acidosis with moderate/severe AKI tested against day-90 mortality — with no outcome numbers borrowed from it.^[54]

THAM and Dialysis Buffers — the alternative alkali

Offer THAM where bicarbonate's baggage hurts: equivalent pH correction with less hypercarbia and hypernatraemia — priced as hyperkalaemia, hypoglycaemia, ventilator depression and extravasation necrosis, with high-quality evidence still lacking.^[55] Choose THAM over bicarbonate specifically for hypercapnic acidosis (and only buffer hypercapnia for a concrete indication such as haemodynamic instability): it corrects pH better without generating CO2.^[56] Predict dialysis swings from the bag: the intensity of plasma-water exchange plus the buffer content — lactate, acetate, citrate or bicarbonate — governs the acid-base effect with or without renal failure, so the prescription must name its buffer deliberately.^[57]

Metabolic Alkalosis — generation versus maintenance

Separate generation from maintenance or mistreat every case: acid loss (gut or kidney) or alkali gain generates it, but persistence means the kidney's bicarbonate-excretion defences have failed.^[58][59] Memorise the six maintenance saboteurs — volume contraction, low filtration, potassium deficiency, hypochloraemia, aldosterone excess, high CO2 — and expect them stacked in the vomiting postoperative patient.^[58] Respect the mortality line: pH 7.55 or above in critical illness carries significantly increased mortality, so severe alkalosis gets aggressive management, not reassurance.^[58][60] Start every workup with volume examination plus urine electrolytes inside Seldin's ECF-volume framework — still the most straightforward diagnostic and therapeutic model — because urine chloride separates saline-responsive (vomiting, diuretics) from resistant (mineralocorticoid, Bartter/Gitelman) disease.^[60][61] List the generators for the viva: vomiting, aldosterone/cortisol excess, liquorice, chloruretic diuretics, calcium-alkali excess, Bartter/Gitelman and cystic fibrosis.^[58] Treat by reversing drivers first; severe cases earn acetazolamide, acid infusion or low-bicarbonate dialysis — without dosing detail here.^[60]

Respiratory Disorders Perioperative

Derive respiratory acidosis from CO2 retention through three doors — failed gas exchange, failed chest wall and muscles, or a silenced medullary centre — and walk the oversedated, splinted postoperative patient through each.^[62] Define respiratory alkalosis numerically: hyperventilation driving arterial PCO2 below 35 mmHg with alkalinisation — pain, anxiety, hypoxia, sepsis and iatrogenic hyperventilation all qualify.^[62] Remember why ventilation matters quantitatively: the open CO2 buffer clears volatile acid from fat and carbohydrate oxidation at far greater scale than nonvolatile handling, so removing ventilatory compensation crashes the compensated metabolic-acidosis patient.^[62] Fence the respiratory-cohort numbers: in acute respiratory disease, bicarbonate-gap above 11.6 and corrected gap above 19.88 each predicted unmeasured-ion acidosis near-perfectly — borrow the corrected-gap/Stewart-Figge-over-base-excess method point generally, never the cutoffs outside that cohort.^[72][67]

Stewart versus Henderson-Hasselbalch — equations with humility

State the Stewart ontology plainly: abnormalities come from PCO2, strong ion difference and weak acids (chiefly albumin), with base excess as their net — computable rigorously only by machine, estimable mentally with discipline.^[64] Compute Story's two bedside lines: sodium-chloride effect equals sodium minus chloride minus 38, and albumin effect equals 0.25 times (42 minus albumin in g/L) — mental arithmetic that agreed with the full equations in 300 ICU blood samples.^[63] Estimate Boyle's way: SID effect as measured SID (sodium plus potassium minus chloride plus lactate) against the normal 42, albumin effect as 0.25 times the albumin deficit, predicted base excess as their sum — with clinically acceptable bias for finding components, but poor agreement for quantifying gap ions, so never dose decisions off the BE-gap.^[64] Deliver the humility verdict the examiner respects: the largest comparison found Stewart and conventional methods interchangeable with no meaningful gain in understanding, diagnosis or treatment — and all three schools find unmeasured-anion acidosis equally while further delineation lacks proven benefit.^[68][69] Keep Stewart for its three keep-cases: simplified equations unmask otherwise-invisible mixed disorders; apparently normal gases can hide hyperchloraemic low-SID plus high-gap acidosis offset by hypoalbuminaemic alkalosis; and corrected gap or Stewart-Figge beats standard base excess for unmeasured anions and hyperlactataemia prediction.^[65][66][67] Close the loop with urine and volume: expanding extracellular volume acidifies by diluting SID while contraction alkalinises — so urinary SID belongs in every assessment — and integrate base excess with Stewart rather than preaching either church.^[71][70]

Perioperative Ketoacidosis — SGLT2i EDKA front and centre

Suspect euglycaemic DKA by its disguise: atypical, near-normal glucose, under-recognised — so perioperative ketone vigilance (plasma or capillary) is the diagnostic move, not glucose-watching.^[73] Name the entity precisely: SGLT2i-associated perioperative ketoacidosis (SAPKA), estimated at 0.17% for elective but 1.1% for emergent procedures — an infographic estimate, so quote it as estimated while letting the tenfold emergency gradient sharpen vigilance.^[74] Apply the 72-hour rule: withhold SGLT2 inhibitors for 72 hours (five half-lives) before elective surgery with multidisciplinary input for diet-altering procedures and cardiac/renal/diabetic complexity; around emergency surgery or recent dosing, check ketones 6-hourly for 24 hours postoperatively until full diet resumes, restarting only when eating and ketone-free.^[75] Admit the guideline mess behind the rule: perioperative SGLT2i guidance is inconsistent across bodies and poorly understood, which is exactly why a written local protocol (STOP-GAP/STOP DKA-2 style algorithms exist as expert-opinion tools) beats memory.^[76][84] Set DKA fluids honestly: balanced crystalloids show better biochemistry than saline in DKA but time-to-resolution effects remain uncertain — definitive practice awaits better evidence.^[77] Run the DKA backstop without dosing detail here: aggressive rehydration, insulin, electrolyte replacement and precipitant treatment — with most type-2 postoperative DKA preventable or treatable when recognised early, especially the euglycaemic form that glucose-monitoring overlooks.^{[78][83][81][82]} Remember the trajectory: DKA mortality has fallen remarkably with better understanding while hyperosmolar-state mortality stays alarmingly high in older comorbid patients — prevention spending pays.^[80]

Mixed Disorders and Vignette Traps

Expect mixtures as the default in the critically ill: opposing disturbances normalise pH while additive ones crash it, so interrogate compensation appropriateness, serum and urine electrolytes and urinary acid excretion on every gas.^[16] Spring the low-gap and atypical traps: hypoalbuminaemia, paraproteins, halides and lithium shrink the gap, air exposure fakes a high one — and ethylene-glycol poisoning can even present without gap elevation, so the exception proves testing beats pattern-matching.^[6] Use veins wisely: venous gases are diagnostically equivalent in appropriate contexts — faster, less invasive — while arteries stay mandatory when precision (oxygenation, ventilator titration) matters.^[13] Price high-output gut loss: high-output enterocutaneous fistulae lose fluid and electrolytes at 10–20% mortality in series — quote the stakes here, fence closure technique to the fistula topic — and adjudicate gut-versus-kidney with the urine gap.^[31][17]

Prognosis Markers — what predicts, what does not

Rank markers with their caveats: lactate clearance predicts lower mortality; lactic acidosis, base excess and strong ion gap flag death risk — but unmeasured-anion variables (gap, corrected gap, base-excess-from-unmeasured-anions, strong ion gap) predict hyperlactataemia well yet hospital mortality poorly, whichever school computes them.^[35][41][40] Prefer lactate over SIG explicitly: strong ion gap's prognostic value is modest and inferior to arterial lactate — read lactate whatever interpretive school you belong to.^[39] State the Winter's omission out loud: Winter's formula and Fulop's rule carry large prediction errors at least in dialysis cohorts, where expected PCO2 as bicarbonate-plus-15 proved interchangeable with the practical rule — the coefficients were unverified in this topic's sources and are therefore absent; compensation here runs on Kraut's ~1 mmHg per 1 mmol/L.^[86][1]

Exam Synthesis & Fence Map — what acid-base-balance owns

This topic owns seven things and fences everything else: the stepwise ABG algorithm with albumin-corrected gap; delta, osmolar and urine gaps; HAGMA/NAGMA sorting with RTA subtypes; lactate interpretation and clearance; the bicarbonate verdict with its AKI and pH boundaries plus THAM/buffer alternatives; alkalosis generation-versus-maintenance; and perioperative ketoacidosis recognition — with Stewart as the second lens.^{[2][4][9][25][35][44][58][63][73]} Crystalloid-trial ladders, RELIEF/GDT strategy, sodium/potassium/magnesium/phosphate/calcium management and overload belong to fluids-electrolytes; pressors, MAP and resuscitation protocols to shock-surgical; KDIGO staging and RRT timing to acute-kidney-injury-surgical; SOFA trajectories to multiorgan-dysfunction; bundles and source control to postoperative-sepsis; ventilation mechanics to ards-surgical; feeding regimens to icu-nutrition-surgical; blood products and TXA to massive-transfusion and damage-control-resuscitation; fistula closure to the fistula topic.^{[22][36][57][31]} The one-paragraph acid-base story for the viva: correct the gap for albumin, ratio the delta against the patient's own baseline, clear lactate rather than buffer it, give bicarbonate for severe acidaemia with kidney injury or pH 7.10-or-below and never at 7.2-or-above, read saline as chloride load and vomit-loss as chloride depletion, withhold SGLT2 inhibitors 72 hours and check ketones, and let Stewart unmask what Henderson-Hasselbalch hides — while admitting the schools tie.^{[4][9][33][44][52][58][68][75]}

Exam Pearls — the one-liners that score

• History, electrolytes-gap-pH, compensation, delta ratio last — the Williamson order that finds mixtures.^[2]
• Albumin-corrected gap = gap + 0.25 × deficit (g/L), 2.5 × in g/dL — half of ICU patients sit under 20 g/L albumin.^[4]
• Early-lactate delta ratio runs ~1.86, not 1:1; individual-baseline corrected ratio ~1.20 — mean-normal values misdiagnose.^[8][9]
• Lactate clearance predicts survival; Jones 17% versus 23% makes clearance noninferior to ScvO2 as a goal — interpretation here, resuscitation fenced.^[35][36]
• Saline acidifies via chloride (randomised arms prove it); buffered fluids fix chemistry without moving mortality or AKI.^[19][22]
• Urine gap negative means gut (diarrhoea); citrate-free urine means stones (distal RTA); PHA2 is type IV RTA.^[17][24][29]
• BICAR-ICU null overall (71% versus 66%, p=0.24) with AKIN stratum signal; BICARICU-2 mortality null (62.1% versus 61.7%) with dialysis 35% versus 50%; pooled pH-7.10-or-below mortality risk ratio 0.80, dialysis NNT 6.3.^[42][43][44]
• Never alkali at pH 7.2 or above; slow infusion with ventilation and calcium if below; DKA pH-under-6.9 efficacy unproven.^[52][79]
• THAM equals bicarbonate on pH with less CO2 and sodium — priced as potassium rise, glucose fall, ventilator depression, extravasation injury.^[55]
• Severe alkalosis at pH 7.55-plus kills; assess volume plus urine electrolytes first inside Seldin's frame.^[58][60][61]
• Respiratory acidosis is CO2 retention via lung, pump or centre; alkalosis is PCO2 under 35 — buffer hypercapnia only for cause, THAM over bicarbonate.^[62][56]
• Stewart: Na−Cl−38 and 0.25×(42−albumin) at the bedside; interchangeable with conventional overall — keep it for hidden mixtures.^[63][68]
• SGLT2i: withhold 72 hours electively, ketones 6-hourly post-op, SAPKA ~0.17% elective/~1.1% emergent estimated; euglycaemia never rules out ketoacidosis.^[75][74][81]
• SIG loses to lactate prognostically; unmeasured-anion maths predicts lactate, not death.^[39][40]

Revision summary

Acid-base in surgical patients reduces to seven examined moves: run history-gap-compensation-delta in order with albumin correction and the patient's own baseline; sort high-gap causes against hyperchloraemic saline/gut/kidney disease with the urine gap and stone rules; classify and clear lactate while fencing resuscitation detail; give bicarbonate only for severe acidaemia with kidney injury or pH 7.10-or-below and never at 7.2-or-above (THAM for hypercapnia); split alkalosis into generation versus maintenance with volume-plus-urine-chloride first aid; withhold SGLT2 inhibitors 72 hours with ketone surveillance for perioperative ketoacidosis; and wield Stewart's two bedside equations with interchangeability humility — every number from the live PubMed abstract beside it.^{[2][4][17][24][36][44][52][58][63][68][75]}

References86ShowHide

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