Sign in

Renal Physiology & Acid-Base

Usually weeks 14-15 of a medical physiology course, after cardiovascular and pulmonary

The kidney unit is where the course's earlier ideas all get spent at once: Starling forces decide filtration, transporters from week one decide reabsorption, hormones from the endocrine unit tune the distal nephron, and the lungs' CO2 control becomes half of every acid-base problem. The exam asks it in a few reliable shapes — predict what an arteriolar change does to RPF, GFR, and filtration fraction; calculate a clearance and say what it measures; name the segment and transporter behind a drug or a lab pattern; and walk an arterial blood gas to a diagnosis with the expected compensation. Learn the nephron as a map of segments, each with one job and one drug, and learn acid-base as a fixed sequence of steps you run the same way every time.

On the PANCE this unit feeds:Renal · 5%Cardiovascular · 11%Endocrine · 6%Pulmonary · 9%

This guide is the frame. The exams are written from your lectures— drop this unit's slides on the dashboard to get flashcards and board-style questions from your own course, and quiz them all semester (a course whose exams re-test earlier units rewards nothing more than early, repeated self-testing). The physiology playbook has the weekly loop.

Drop a lecture

Free30 study kits/mo · 1 diagram deck · 1 board-graded quiz · 2 tutor Qs/wk

Pro $20/mono monthly cap (5 kits/day) · 10 diagram decks · See plans →

Lectures you file for this course live under Physiology → My Lectures in your library — pick it from the Module box as you upload, or from any card's Move menu afterwards.

AI-authored study notes, not faculty-reviewed and not medical advice. Verify every mechanism against your course materials and faculty; programs differ in emphasis.

High-Yield Pearl

Treat the kidney as two resistors and a string of transporters — afferent versus efferent tone predicts every RPF, GFR, and filtration-fraction question, and naming each segment's transporter predicts its hormone, its diuretic, and its side effects — then read every blood gas in the same five steps and calculate the compensation before you believe the diagnosis.

What the exam asks
Mechanisms, curves, and what happens when each one fails.
  • The nephron as a map of segments. Glomerulus and Bowman capsule filter ~180 L/day of protein-free plasma. The PROXIMAL TUBULE reclaims the bulk isosmotically (~two-thirds of Na+ and water, nearly all glucose and amino acids, most HCO3−) and secretes organic acids and bases. The THIN DESCENDING LIMB is water-permeable and solute-impermeable, so fluid concentrates as it descends. The THICK ASCENDING LIMB pumps NaCl out through the Na+-K+-2Cl− cotransporter (NKCC2) while staying water-impermeable — the diluting segment that builds the medullary gradient (~25% of filtered Na+). The DISTAL CONVOLUTED TUBULE reabsorbs ~5% of Na+ through the Na+-Cl− cotransporter (NCC) and fine-tunes Ca2+ under PTH. The COLLECTING DUCT makes the final adjustments: principal cells handle Na+, K+, and water (aldosterone and ADH), and intercalated cells handle acid and base.
  • Renal blood flow and autoregulation. The kidneys receive ~20–25% of cardiac output (RBF ~1.1–1.2 L/min; renal plasma flow ~600–650 mL/min) through two resistances in series — the afferent arteriole before the glomerulus and the efferent arteriole after it. Over a mean arterial pressure of roughly 80–180 mmHg, RBF and GFR stay nearly constant through two intrinsic mechanisms acting on the AFFERENT arteriole: the MYOGENIC response (stretch of vascular smooth muscle opens cation channels → Ca2+ entry → constriction) and TUBULOGLOMERULAR FEEDBACK (more NaCl reaching the macula densa → ATP/adenosine signaling → afferent constriction, and less renin). Below the range the afferent arteriole is already maximally dilated, so flow and filtration fall with pressure; sympathetic tone and angiotensin II can override autoregulation in shock.
  • GFR — Starling forces and arteriolar tone. GFR = Kf × [(P_GC − P_BS) − (π_GC − π_BS)]. Glomerular capillary hydrostatic pressure (P_GC, roughly 50–60 mmHg) is the main driving force and is unusually high and nearly constant along the capillary because the efferent arteriole sits downstream. Bowman space hydrostatic pressure (P_BS) opposes filtration and rises with urinary obstruction. Glomerular oncotic pressure (π_GC) opposes filtration and RISES along the capillary as protein-free fluid leaves; Bowman space oncotic pressure is essentially zero because protein is not filtered. Kf reflects surface area and permeability — reduced by glomerular disease and mesangial contraction. Filtration fraction (FF) = GFR ÷ RPF, normally ~20%. CONSTRICTING THE AFFERENT arteriole lowers both RPF and P_GC, so RPF and GFR fall together and FF is roughly unchanged (sympathetic tone, NSAIDs removing prostaglandin dilation). CONSTRICTING THE EFFERENT arteriole lowers RPF but RAISES P_GC, so GFR is preserved or rises modestly and FF rises (angiotensin II at moderate levels; very intense efferent constriction eventually lowers GFR as the oncotic pressure climbs). Dilating the efferent (ACE inhibitors, ARBs) lowers P_GC — GFR and FF fall. Raised plasma protein lowers GFR and FF; ureteral obstruction lowers GFR through P_BS. Angiotensin II's preferential efferent effect is how GFR is defended when perfusion falls.
  • Clearance — inulin, creatinine, PAH. Clearance C = (U × V) ÷ P: the volume of plasma completely cleared of a substance per minute. INULIN is freely filtered and neither reabsorbed nor secreted, so its clearance equals GFR (~125 mL/min). CREATININE, made at a steady rate by muscle, is the bedside estimate — it is slightly secreted, so creatinine clearance OVERESTIMATES GFR modestly, and plasma creatinine rises roughly reciprocally as GFR falls (a halved GFR roughly doubles creatinine at steady state). PAH is filtered and so avidly secreted that ~90% is removed in one pass, so PAH clearance estimates effective RENAL PLASMA FLOW; RBF = RPF ÷ (1 − hematocrit). A substance whose clearance is below inulin's is net reabsorbed (glucose, urea, Na+); above it, net secreted (PAH, many drugs).
  • Filtered load, Tm, and the glucose titration curve. Filtered load = GFR × plasma concentration (for freely filtered solutes); excretion = filtered − reabsorbed + secreted. Carrier-mediated reabsorption saturates at a transport maximum (Tm). For glucose, SGLT2 in the early proximal tubule does most of the work and SGLT1 later mops up the rest; the whole-kidney Tm is ~375 mg/min. Glucose first appears in the urine at the RENAL THRESHOLD (~200 mg/dL plasma), below the plasma level at which Tm is fully reached (~350 mg/dL). The rounded region between them is SPLAY — nephrons differ in filtered load and carrier capacity, and carriers lose some glucose as they approach saturation. Past Tm, excretion rises in parallel with filtered load. SGLT2 inhibitors and pregnancy both lower the threshold.
  • The proximal tubule — the bulk reabsorber. Basolateral Na+/K+-ATPase keeps cell Na+ low; apical Na+ entry is coupled to glucose and amino acids (cotransport) and to H+ secretion through the Na+/H+ exchanger (NHE3). Secreted H+ combines with filtered HCO3− to form CO2 and water (luminal carbonic anhydrase); CO2 enters the cell, is re-formed into HCO3−, and leaves basolaterally — ~80% of filtered HCO3− is reclaimed this way (the acetazolamide target). Water follows solute through a leaky epithelium (aquaporin-1), so the fluid stays ISOSMOTIC while its volume falls by two-thirds; Cl− is reabsorbed later in the segment. The proximal tubule also reclaims phosphate (PTH inhibits it), makes ammonium from glutamine, and secretes organic anions and cations (PAH, penicillin, diuretics reach their luminal targets this way). Glomerulotubular balance keeps the reabsorbed FRACTION constant when GFR changes.
  • Loop of Henle, countercurrent multiplication, and urea. The thick ascending limb transports NaCl out without water, so its fluid leaves HYPOTONIC (~100 mOsm/kg) and the interstitium around it becomes hypertonic; the descending limb, permeable to water, equilibrates with that interstitium and delivers more concentrated fluid back to the pump — the countercurrent MULTIPLIER, which builds a corticomedullary gradient up to ~1200 mOsm/kg. K+ recycling through ROMK creates a lumen-positive potential that drives paracellular Ca2+ and Mg2+ reabsorption. UREA RECYCLING supplies roughly half the inner medullary osmolality: ADH raises urea permeability of the inner medullary collecting duct (UT-A transporters), urea diffuses into the interstitium, and some re-enters the loop. The VASA RECTA are hairpin capillaries acting as countercurrent EXCHANGERS: slow flow lets them carry away reabsorbed water without washing out the gradient.
  • Distal nephron, ADH, aldosterone, and diuretic sites. Principal cells reabsorb Na+ through ENaC and secrete K+ through ROMK; aldosterone (mineralocorticoid receptor) adds ENaC channels and pumps. ADH acts on V2 receptors (Gs → cAMP) to insert aquaporin-2 in the apical membrane, so collecting duct fluid equilibrates with the hypertonic medulla — urine up to ~1200 mOsm/kg; without ADH it can be diluted to ~50. Alpha-intercalated cells secrete H+ (H+-ATPase, H+/K+-ATPase) and return HCO3− via basolateral Cl−/HCO3− exchange; beta-intercalated cells secrete HCO3− through apical pendrin in alkalosis. Diuretic sites follow the map: acetazolamide (proximal carbonic anhydrase), mannitol (osmotic, proximal tubule and loop), loop diuretics (NKCC2 — the most potent), thiazides (NCC), and the K+-sparing agents at the principal cell (spironolactone/eplerenone block the receptor; amiloride/triamterene block ENaC).
  • Potassium handling. About 98% of body K+ is intracellular, so plasma K+ (~3.5–5.0 mEq/L) depends on both INTERNAL balance and renal excretion. Shifts INTO cells: insulin, β2-agonists, and alkalosis (all via the Na+/K+-ATPase or H+ exchange). Shifts OUT: insulin deficiency, β-blockade, digoxin toxicity, hyperosmolarity, cell lysis, strenuous exercise, and inorganic (non-anion-gap) acidosis. In the kidney, most filtered K+ is reabsorbed proximally and in the thick ascending limb regardless of intake; the REGULATED step is principal-cell secretion, increased by aldosterone, a high-K+ diet, high distal flow and Na+ delivery (why loop and thiazide diuretics waste K+), and alkalosis. In K+ depletion, alpha-intercalated cells reabsorb K+ through H+/K+-ATPase.
  • Volume vs osmolarity — two separate control systems. ECF VOLUME is set by total body Na+ content and is defended by sensors of effective circulating volume (carotid and aortic baroreceptors, afferent arteriolar pressure, atrial stretch) acting through the renin-angiotensin-aldosterone system, sympathetic nerves, and ANP (which raises GFR and causes natriuresis). Plasma OSMOLARITY — and therefore the plasma Na+ concentration — is set by WATER balance and is defended by hypothalamic osmoreceptors driving ADH and thirst, responding to a 1–2% change. A severe volume loss can also release ADH, overriding osmolar control, which is why hypovolemic patients become hyponatremic. Keep the rule: sodium CONTENT decides volume; water decides sodium CONCENTRATION.
  • Acid-base: buffers, Henderson-Hasselbalch, and renal acid excretion. Normal arterial pH 7.35–7.45, PaCO2 35–45 mmHg, HCO3− 22–26 mEq/L. Henderson-Hasselbalch: pH = 6.1 + log[HCO3− ÷ (0.03 × PaCO2)] — at 24 and 40 the ratio is 20:1 and pH is 7.40. The bicarbonate system dominates the ECF because it is OPEN: the lungs set PaCO2 and the kidneys set HCO3−. Intracellular proteins, hemoglobin, phosphate, and bone buffer too. Metabolism produces ~1 mEq/kg/day of nonvolatile acid, which the kidney excretes while regenerating the HCO3− it consumed. Net acid excretion = titratable acid (H+ carried mainly on filtered phosphate) + NH4+ − excreted HCO3−. Each H+ excreted as titratable acid or as ammonium (from proximal glutamine metabolism, trapped in the collecting duct lumen) generates a NEW HCO3− for the blood; ammonium is the adaptable route that rises severalfold in chronic acidosis. Reclaiming filtered HCO3− adds no new base.
  • The four primary disorders, compensation, and the stepwise ABG. Step 1: acidemia or alkalemia (pH). Step 2: is the primary change in PaCO2 (respiratory) or HCO3− (metabolic) — the one that moved in the direction that explains the pH. Step 3: check compensation. Metabolic acidosis: expected PaCO2 = 1.5 × HCO3− + 8 ± 2 (Winter's formula). Metabolic alkalosis: PaCO2 rises ~0.7 mmHg per 1 mEq/L rise in HCO3−. Respiratory acidosis: HCO3− rises ~1 per 10 mmHg PaCO2 acutely and ~3.5–4 per 10 chronically. Respiratory alkalosis: HCO3− falls ~2 per 10 acutely and ~4–5 per 10 chronically. A value outside the expected range means a second primary disorder; compensation never returns pH fully to normal. Step 4 (metabolic acidosis): anion gap = Na+ − (Cl− + HCO3−), normal ~8–12 mEq/L (lower it with low albumin). High-gap causes are the unmeasured-acid list — ketoacidosis, lactic acidosis, renal failure, toxic alcohols, salicylates; normal-gap (hyperchloremic) causes are HCO3− loss (diarrhea, renal tubular acidosis) or chloride loading. Step 5: the delta-delta compares the rise in gap with the fall in HCO3− — a ratio well below 1 hides a normal-gap acidosis, well above 2 hides a metabolic alkalosis.
Worth drilling · 45 concepts
Each with the one fact that identifies it. Your course's slides are the authority; use this to check your list against.
  1. 1Proximal convoluted tubule — reclaims about two-thirds of filtered Na+ and water isosmotically, plus nearly all glucose and amino acids
  2. 2Thin descending limb — water-permeable, solute-impermeable; tubular fluid concentrates as it descends
  3. 3Thick ascending limb — NKCC2 segment impermeable to water; the diluting segment and loop diuretic site
  4. 4Distal convoluted tubule — Na+-Cl− cotransporter segment; thiazide site and PTH-regulated Ca2+ reabsorption
  5. 5Principal cell — ENaC Na+ reabsorption and ROMK K+ secretion, boosted by aldosterone
  6. 6Alpha-intercalated cell — H+-ATPase acid secretion with basolateral HCO3− return
  7. 7Beta-intercalated cell — pendrin secretes HCO3− in exchange for Cl− during alkalosis
  8. 8Macula densa — thick ascending limb plaque sensing NaCl delivery for tubuloglomerular feedback
  9. 9Juxtaglomerular cells — modified afferent arteriolar smooth muscle that secretes renin
  10. 10Myogenic response — afferent arteriole constricts when rising pressure stretches it
  11. 11Tubuloglomerular feedback — more NaCl at the macula densa constricts the afferent arteriole via adenosine
  12. 12Autoregulatory range — mean arterial pressure of about 80–180 mmHg over which RBF and GFR hold steady
  13. 13Filtration fraction — GFR divided by renal plasma flow; normally about 20%
  14. 14Glomerular capillary hydrostatic pressure — the main force favoring filtration; raised by efferent constriction
  15. 15Glomerular oncotic pressure — climbs along the capillary as protein-free fluid is filtered, opposing filtration
  16. 16NSAID effect on the kidney — removes prostaglandin dilation of the afferent arteriole; RPF and GFR fall
  17. 17ACE inhibitor effect on the kidney — loses angiotensin II efferent tone; GFR and filtration fraction fall
  18. 18Clearance — plasma volume completely cleared of a substance per minute, UV ÷ P
  19. 19Inulin — freely filtered, never reabsorbed or secreted; its clearance equals GFR
  20. 20Creatinine clearance — bedside GFR estimate that runs slightly high because of tubular secretion
  21. 21PAH clearance — filtered plus nearly complete secretion; measures effective renal plasma flow
  22. 22Filtered load — GFR multiplied by the plasma concentration of a freely filtered solute
  23. 23Transport maximum — carrier-saturated reabsorption rate; about 375 mg/min for glucose
  24. 24Renal threshold for glucose — plasma level near 200 mg/dL where glucose first appears in urine
  25. 25Splay — rounded gap between threshold and Tm from nephron heterogeneity
  26. 26SGLT2 — high-capacity early proximal tubule Na+-glucose cotransporter; the -gliflozin target
  27. 27Countercurrent multiplier — thick ascending limb salt pumping that builds the medullary gradient
  28. 28Vasa recta — slow-flowing hairpin capillaries that exchange countercurrently and preserve the gradient
  29. 29Urea recycling — ADH-stimulated inner medullary urea transport supplying about half the interstitial osmolality
  30. 30Aquaporin-2 — water channel ADH inserts into the collecting duct's apical membrane via V2 receptors
  31. 31Carbonic anhydrase inhibitor — acetazolamide; proximal HCO3− wasting and a mild hyperchloremic acidosis
  32. 32Loop diuretics — block NKCC2; most potent, waste K+, Ca2+, and Mg2+
  33. 33Thiazide diuretics — block NCC; increase Ca2+ reabsorption and risk hyponatremia
  34. 34Potassium-sparing diuretics — act at the principal cell: spironolactone and eplerenone block the aldosterone receptor, amiloride and triamterene block ENaC
  35. 35Transcellular potassium shift — insulin, beta-2 agonists, and alkalosis drive K+ into cells
  36. 36Henderson-Hasselbalch equation — pH = 6.1 + log of HCO3− over 0.03 × PaCO2
  37. 37Titratable acid — H+ excreted on filtered buffers, mainly phosphate
  38. 38Ammoniagenesis — proximal glutamine metabolism yielding NH4+ and new HCO3−; the adaptable acid route
  39. 39Bicarbonate reclamation — proximal H+ secretion and carbonic anhydrase recover filtered HCO3− with no net acid excreted
  40. 40Anion gap — Na+ minus Cl− and HCO3−; normal about 8–12 mEq/L
  41. 41Winter's formula — expected PaCO2 = 1.5 × HCO3− + 8 ± 2 in metabolic acidosis
  42. 42Delta-delta — compares the gap's rise with the HCO3− fall to unmask a second metabolic disorder
  43. 43Distal renal tubular acidosis — collecting duct cannot secrete H+; urine pH stays above 5.5, stones and hypokalemia
  44. 44Proximal renal tubular acidosis — lowered HCO3− reclamation threshold; urine can still acidify once plasma HCO3− falls
  45. 45Hyperkalemic renal tubular acidosis — hypoaldosteronism or resistance; high K+ suppresses ammoniagenesis
Practice it
Active recall over the drill list — flip and claim, match the pairs, produce the answers cold, fill in the diagram, or read the curves like the exam does.

Every concept on the drill list, one card at a time — the name up front, the fact that identifies it on the flip. Claim each card honestly and the deck learns what to lead with next time. Progress lives in this browser only.

What everyone misses
The distinctions that lose points on this material, year after year.
  • Efferent constriction RAISES GFR while RPF falls. Students reason 'constriction = less flow = less filtration' for both arterioles. The efferent arteriole is downstream, so constricting it backs pressure up into the glomerulus: RPF falls, P_GC rises, GFR is preserved or increases, and filtration fraction climbs. Only the AFFERENT arteriole moves RPF and GFR in the same direction. Draw the two resistors in series before answering any arteriole question.
  • Renal threshold is not Tm. Glucose appears in the urine (threshold, ~200 mg/dL) BEFORE the carriers are fully saturated (Tm reached at ~350 mg/dL), because some nephrons saturate early — the splay. A question asking 'at what point does glucosuria begin' wants threshold; 'at what point is reabsorption maximal' wants Tm. Past Tm, excretion rises parallel to filtered load, not faster.
  • The thick ascending limb dilutes — ADH does not act there. Fluid leaving the thick ascending limb is hypotonic whether ADH is present or not, because the segment removes salt without water. ADH acts downstream on the collecting duct (and on medullary urea permeability). Students who place ADH in the loop miss why loop diuretics impair BOTH concentrating and diluting ability — they abolish the gradient and the diluting step at once.
  • Plasma sodium reports water, not volume. A low sodium concentration is read as 'low sodium, give salt' or 'volume depleted.' Hyponatremia means too much water relative to sodium, and it occurs with low, normal, or high ECF volume (vomiting, SIADH, heart failure). Assess volume from the exam and history; use the sodium concentration to reason about water and ADH.
  • Compensation never overshoots — and rarely normalizes pH. If the pH is normal or on the 'wrong' side despite a clearly abnormal PaCO2 and HCO3−, that is not 'complete compensation' — it is a mixed disorder. Always calculate the expected compensation (Winter's formula, the 0.7 rule, the 1/3.5 and 2/4–5 rules) and treat any mismatch as a second primary process.
  • Creatinine clearance is not a perfect GFR. Creatinine is freely filtered AND slightly secreted, so its clearance reads a little above true GFR — increasingly so as GFR falls. Plasma creatinine also depends on muscle mass: a frail older adult can have a 'normal' creatinine with a markedly reduced GFR. Inulin is the reference standard; PAH measures plasma FLOW, not filtration.
  • Reclaiming bicarbonate is not making new bicarbonate. Proximal H+ secretion that recovers filtered HCO3− only prevents loss; it adds no base and excretes no acid. New HCO3− is generated only when secreted H+ leaves the body as titratable acid or ammonium. Questions asking how the kidney COMPENSATES for chronic acidosis want increased ammonium excretion, not proximal reclamation.
Clinical correlations
Where this unit shows up again — in clinic, on rotations, and on the boards.
  • The NSAID + ACE inhibitor + diuretic combination. An older patient with heart failure on an ACE inhibitor and a diuretic starts ibuprofen for knee pain, then presents with a rising creatinine and hyperkalemia. Volume contraction lowers renal perfusion, NSAIDs remove the prostaglandin dilation of the afferent arteriole, and the ACE inhibitor removes angiotensin II's efferent support — both defenses of GFR are gone at once. It is the arteriole table as a hospital admission.
  • Bilateral renal artery stenosis and ACE inhibitors. When perfusion pressure is low, GFR depends on angiotensin II constricting the efferent arteriole. Start an ACE inhibitor or ARB and that support vanishes: creatinine climbs sharply within days. A marked creatinine rise after starting these drugs should prompt evaluation for renovascular disease — and a modest rise (up to about 30%) is expected and tolerated in other patients.
  • Diabetic ketoacidosis as an acid-base exercise. Glucose 520 mg/dL, HCO3− 10, anion gap 24, PaCO2 23: an anion-gap metabolic acidosis from ketoacids with appropriate respiratory compensation (Winter's: 1.5 × 10 + 8 = 23 ± 2) — the deep Kussmaul breathing. Plasma K+ is often high despite a total-body deficit (insulin lack and hyperosmolarity shift it out), which is why potassium is monitored and replaced as insulin drives it back into cells.
  • Vomiting and contraction alkalosis. Gastric HCl loss generates metabolic alkalosis; the accompanying volume loss activates angiotensin II and aldosterone, which keep the kidney reclaiming HCO3− and secreting H+ and K+ — hypokalemia and sometimes paradoxically acidic urine. Urine chloride is low (<20 mEq/L), marking a saline-responsive alkalosis: restoring volume and chloride lets the kidney excrete the excess HCO3−. Hyperaldosteronism or ongoing diuretic use gives a high urine chloride instead.
  • Diuretic side-effect patterns. Loop and thiazide diuretics both cause hypokalemia and metabolic alkalosis (more distal Na+ and flow, plus volume contraction). They split on calcium: loop diuretics abolish the lumen-positive potential and cause calciuria (useful in hypercalcemia), while thiazides increase distal Ca2+ reabsorption (useful for calcium stones, a cause of mild hypercalcemia). Thiazides are the classic cause of hyponatremia. Spironolactone, eplerenone, amiloride, and triamterene cause hyperkalemia, especially with ACE inhibitors or kidney disease.
  • SGLT2 inhibitors — glucosuria by design. Blocking the proximal Na+-glucose cotransporter lowers the renal threshold, so glucose is excreted at ordinary plasma levels. Benefits include lower glucose, modest natriuresis, and kidney and heart failure protection (partly by restoring tubuloglomerular feedback). The side effects follow the mechanism: genital mycotic infections, volume depletion, and euglycemic ketoacidosis. Normal pregnancy produces a milder version — higher GFR and a lower threshold can cause glucosuria with normal blood glucose.
  • Chronic respiratory acidosis in COPD. PaCO2 60, HCO3− 31, pH 7.34: over days the kidney raised HCO3− about 3.5–4 per 10 mmHg of CO2 by excreting more ammonium, softening the acidemia. If such a patient is intubated and ventilated to a normal PaCO2 too quickly, the retained HCO3− is suddenly unopposed — post-hypercapnic metabolic alkalosis, which can cause arrhythmias and seizures.
  • Salicylate toxicity — a mixed disorder by design. Aspirin directly stimulates the respiratory center (respiratory alkalosis, early) and uncouples oxidative metabolism, raising lactate and other organic acids (anion-gap metabolic acidosis, later). The ABG shows a PaCO2 lower than Winter's formula predicts — the fingerprint of two primary processes. Tinnitus plus an unexplained anion gap should prompt a salicylate level.

Frequently asked

← Pulmonary PhysiologyGastrointestinal Physiology →