Acid-Base Disorders

Henderson-Hasselbalch Equation

pH = pKa + log([HCO₃^-] / 0.03 × PaCO₂)

Where pKa = 6.1, [HCO3-] in mEq/L, PaCO2 in mmHg. This describes the relationship between the metabolic and respiratory components of acid-base balance. The ratio [HCO3-] / (0.03 × PaCO2) determines pH direction.

7.35–7.45

Normal pH

35–45 mmHg

Normal PaCO₂

22–26 mEq/L

Normal HCO₃^-

±2 mEq/L

Base Excess (BE)

8–12 mEq/L

Anion Gap (normal)

95–100 mmHg

Normal PaO₂

Buffer Systems

Bicarbonate Buffer (primary extracellular)

CO2 + H2O ⇌ H2CO3 ⇌ H+ + HCO3-. Most important buffer in ECF. Regulated by lungs (CO2) and kidneys (HCO3-).

Phosphate Buffer

HPO4²- + H+ ⇌ H2PO4-. Important in renal tubules and intracellular fluid. pKa ~6.8.

Protein Buffer (albumin)

Amino acid side chains act as H+ acceptors/donors. Accounts for ~70% of non-bicarbonate buffering in blood.

Haemoglobin Buffer

Deoxyhaemoglobin is a better buffer than oxyhaemoglobin (Haldane effect). Critical in red blood cells during CO2 transport.

Compensation Mechanisms

Respiratory Compensation

Responds within minutes. Changes in RR/TV alter PaCO2. Chemoreceptors detect pH changes and adjust ventilation.

Full respiratory compensation takes 12–24 hours. Immediate response is partial.

Renal Compensation

Responds over 3–5 days. Kidneys regulate HCO3- by reabsorption/excretion and H+ excretion via ammoniagenesis and titratable acids.

Renal compensation is slower but more powerful — can fully correct pH in chronic disorders.

Stewart Approach — Strong Ion Difference (SID)

The Stewart model provides a physicochemical framework for acid-base analysis beyond the traditional HH approach.

SID = (Na⁺ + K⁺ + Ca²⁺ + Mg²⁺) − (Cl^- + lactate^-)

Normal SID ≈ 40–44 mEq/L. When SID falls (e.g. hyperchloraemia), acidosis results. When SID rises, alkalosis results. This explains why normal-AG hyperchloraemic acidosis occurs with saline infusion (dilution of SID) and helps identify complex ICU acid-base disorders not explained by traditional approach.

Stewart model is increasingly used in critical care — explains "unexplained" acidosis from albumin changes, strong ions, and phosphate independently.

Why Acid-Base Balance Matters Clinically

Enzyme Function

Most enzymes have optimal pH 7.35–7.45. Acidosis/alkalosis denatures proteins and impairs metabolic reactions.

O2 Dissociation Curve

Acidosis → right shift (Bohr effect) → reduced O2 binding but increased O2 release to tissues. Alkalosis → left shift → increased affinity but poor release.

Drug Ionisation

pH affects drug ionisation (Henderson-Hasselbalch). Acidosis increases absorption of weak acids; alkalosis increases excretion. Critical for salicylate/tricyclic overdose.

Electrolyte Shifts

Acidosis → hyperkalaemia (K+ moves out of cells). Alkalosis → hypokalaemia. Each 0.1 pH unit change → ~0.6 mEq/L K+ shift inversely.

Cardiac Function

Severe acidosis (pH <7.1) depresses myocardial contractility, causes arrhythmias, and reduces response to catecholamines.

Neurological Effect

Alkalosis → cerebral vasoconstriction → tetany/seizures. Acidosis → cerebral vasodilation; CO2 crosses BBB readily.

Respiratory Acidosis

pH <7.35 | PaCO₂ >45 mmHg | HCO₃^- normal or elevated

Mechanism

Alveolar hypoventilation leads to CO2 retention → carbonic acid accumulation → acidosis.

Causes

Category	Examples
Obstructive lung	COPD exacerbation, severe asthma
Obesity/Restrictive	Obesity hypoventilation syndrome (OHS)
Neuromuscular	GBS, MG crisis, ALS, phrenic nerve palsy
CNS depression	Opioids, benzodiazepines, anaesthetic agents
Thoracic	Flail chest, massive pleural effusion, kyphoscoliosis
Airway obstruction	Foreign body, severe OSA

Renal Compensation

Acute: HCO₃^- rises 1 mEq/L per 10 mmHg ↑ PaCO₂

Chronic: HCO₃^- rises 3.5 mEq/L per 10 mmHg ↑ PaCO₂

Respiratory Alkalosis

pH >7.45 | PaCO₂ <35 mmHg | HCO₃^- normal or decreased

Mechanism

Alveolar hyperventilation → CO2 washout → reduced carbonic acid → alkalosis.

Causes

Category	Examples
Psychogenic	Anxiety, panic attacks, pain
Hypoxaemia	High altitude, pulmonary oedema, PE, pneumonia
Iatrogenic	Mechanical over-ventilation (high RR/TV)
CNS stimulation	Cerebral oedema, meningitis, stroke
Metabolic	Liver failure (NH3), sepsis, thyrotoxicosis
GCC-specific	Pregnancy (progesterone), heat exhaustion

Renal Compensation

Acute: HCO₃^- falls 2 mEq/L per 10 mmHg ↓ PaCO₂

Chronic: HCO₃^- falls 5 mEq/L per 10 mmHg ↓ PaCO₂

Ventilator Management & Acid-Base Implications

Respiratory Rate (RR)

↑ RR → ↓ PaCO2 → respiratory alkalosis risk. Target RR 12–20/min. In COPD allow permissive hypercapnia (pH >7.25).

Tidal Volume (TV)

Lung-protective: 6 mL/kg IBW. High TV causes hypocapnia + barotrauma. Low TV causes CO2 retention.

PEEP

PEEP recruits alveoli → improves V/Q matching → reduces hypoxic respiratory drive. Does not directly alter PaCO2.

Driving Pressure

Driving pressure = Plateau P – PEEP. Target <15 cmH2O. High driving pressure = lung injury risk, worsens acidosis.

Permissive Hypercapnia

In ARDS: accept PaCO2 up to 60–80 mmHg (pH >7.2) to limit lung injury. Contraindicated in raised ICP.

Weaning Targets

pH 7.35–7.45, PaCO2 near baseline, RR <25, RSBI <105, minimal pressure support (<8 cmH2O).

Anion Gap Calculation

AG = Na⁺ − (Cl^- + HCO₃^-) Normal: 8–12 mEq/L

Albumin-corrected AG = AG + 2.5 × (Normal Albumin − Measured Albumin[g/dL])

Or if albumin in g/L: AG + 0.25 × (40 − measured albumin). Every 10 g/L drop in albumin reduces AG by ~2.5 mEq/L — hypoalbuminaemia masks high AG acidosis in ICU patients.

Metabolic Acidosis — High AG

HCO₃^- <22 | pH <7.35 | AG >12

Mnemonic: MUDPILES

Letter	Cause	Key Feature
M	Methanol	Visual disturbance, osmolar gap
U	Uraemia	Renal failure, ↑ creatinine
D	Diabetic Ketoacidosis	Ketonuria, hyperglycaemia, ↑ ketones
P	Propylene glycol	IV medications (lorazepam), osmolar gap
I	Isoniazid / Ibuprofen	Drug history, seizures (INH)
L	Lactic acidosis	↑ Lactate >2 mmol/L
E	Ethylene glycol	Antifreeze ingestion, oxalate crystals in urine
S	Salicylates	Aspirin OD, mixed resp. alkalosis + met. acidosis

Metabolic Acidosis — Normal AG

HCO₃^- <22 | pH <7.35 | AG normal (8–12) | Hyperchloraemia

Mnemonic: USED CARP

Letter	Cause
U	Ureteral diversion (ileal conduit)
S	Saline excess (hyperchloraemic acidosis)
E	Extra-renal HCO3- loss (pancreatic fistula)
D	Diarrhoea (HCO3- lost in stool)
C	CARbonic anhydrase inhibitors (acetazolamide)
A	Adrenal insufficiency
R	Renal tubular acidosis (Types 1, 2, 4)
P	Post-hypocapnia (correction of chronic resp. alkalosis)

Metabolic Alkalosis

HCO₃^- >26 | pH >7.45 | PaCO₂ normal or elevated

Saline-Responsive (Urine Cl^- <20 mEq/L)

Cause	Mechanism
Vomiting / NG suction	Loss of HCl → net HCO3- gain
Diuretics (loop/thiazide)	Cl- and K+ loss → contraction alkalosis
Post-hypercapnia	Renal HCO3- retention persists after CO2 correction

Saline-Resistant (Urine Cl^- >20 mEq/L)

Cause	Note
Primary hyperaldosteronism	Conn's syndrome — HTN + hypokalaemia
Cushing's syndrome	Cortisol excess → mineralocorticoid effect
Bartter/Gitelman syndrome	Tubular channel defects
Exogenous steroids	High-dose corticosteroids

Treatment: normal saline (if Cl-responsive), KCl replacement, address underlying cause.

Respiratory Compensation for Metabolic Disorders

For Metabolic Acidosis (Winter's Formula)

Expected PaCO₂ = (1.5 × HCO₃^-) + 8 ± 2

If actual PaCO2 > expected → additional respiratory acidosis. If actual PaCO2 < expected → additional respiratory alkalosis (mixed disorder).

For Metabolic Alkalosis

Expected PaCO₂ = (0.7 × HCO₃^-) + 21 ± 2

Compensation is usually incomplete — body doesn't hypoventilate to the point of significant hypoxia.

Compensation never overcorrects pH. If pH is normalised by compensation alone, consider a mixed disorder.

Complete Compensation Formulae Reference

Disorder	Expected Compensation	Timeframe
Metabolic Acidosis	PaCO2 = (1.5 × HCO3-) + 8 ± 2 (Winter's)	12–24 hours
Metabolic Alkalosis	PaCO2 = (0.7 × HCO3-) + 21 ± 2	24–36 hours
Acute Resp. Acidosis	HCO3- = 24 + (PaCO2 − 40) / 10	Minutes
Chronic Resp. Acidosis	HCO3- = 24 + (PaCO2 − 40) × 3.5 / 10	3–5 days
Acute Resp. Alkalosis	HCO3- = 24 − (40 − PaCO2) × 2 / 10	Minutes
Chronic Resp. Alkalosis	HCO3- = 24 − (40 − PaCO2) × 5 / 10	3–5 days

Delta-Delta Ratio — Mixed Disorder Detection

Delta-Delta = (AG − 12) / (24 − HCO₃^-)

Used when AG metabolic acidosis is present. Compares expected vs actual HCO3- fall to detect a second metabolic disorder.

Ratio	Interpretation	Clinical Meaning
<0.4	Non-AG acidosis coexists	Concurrent hyperchloraemic acidosis (e.g. diarrhoea + DKA)
0.4–1.0	Mixed: High AG + Non-AG acidosis	Both types contributing
1.0–2.0	Pure high AG metabolic acidosis	Expected — no mixed disorder
>2.0	Metabolic alkalosis coexists	Concurrent vomiting + lactic acidosis

Remember: Delta-delta is only valid when AG is elevated above 12. Do not apply to normal-AG acidosis.

Recognising Mixed Disorders

Common Mixed Disorder Patterns

Pattern	Example	ABG Clue
Met. Acidosis + Resp. Alkalosis	Sepsis, salicylate OD	pH may appear normal; both HCO3- ↓ and PaCO2 ↓
Met. Acidosis + Resp. Acidosis	Cardiac arrest	Very low pH; inadequate compensation
Met. Alkalosis + Resp. Acidosis	COPD + vomiting	Normal or near-normal pH; high HCO3- + high PaCO2
Met. Alkalosis + Resp. Alkalosis	Liver failure + NG suction	Very high pH; both HCO3- ↑ and PaCO2 ↓
Triple disorder	Alcoholic ketoacidosis + vomiting + resp. alkalosis	Complex — requires delta-delta + full history

Key Rules for Mixed Disorders

1. If compensation is not within expected range → second disorder present.

2. If pH is normal but PaCO2 and HCO3- are both abnormal → mixed disorder.

3. Two disorders that both cause acidosis or both cause alkalosis cannot compensate each other.

4. Apply Winter's formula — if actual PaCO2 deviates from expected, a respiratory component is added.

Diabetic Ketoacidosis (DKA)

Acid-Base Pattern

High anion gap metabolic acidosis due to accumulation of beta-hydroxybutyrate and acetoacetate. AG typically 20–30+.

AG = Na − (Cl + HCO3) >12 + ketonaemia

Bicarbonate Therapy

Only consider NaHCO3 if pH <6.9 (severe). Routine bicarbonate is harmful — worsens hypokalaemia, paradoxical CNS acidosis, delays ketone clearance.

Management Priorities

Priority	Action	Acid-Base Effect
1	IV fluids (0.9% NaCl then 0.45%)	Restores renal perfusion → ↑ ketone excretion
2	Insulin infusion (0.1 U/kg/hr)	Suppresses lipolysis → closes AG
3	K+ replacement	Prevents hypokalaemia from insulin/correction
4	Monitor ABGs q2–4h	Track AG closure — target AG <12

Resolution: AG closes before pH normalises. Hyperchloraemic acidosis often persists post-DKA from saline loading.

Lactic Acidosis

Type A — Tissue Hypoperfusion

Anaerobic metabolism due to inadequate O2 delivery. Lactate >2 mmol/L (significant >4 mmol/L).

Cause	Management
Septic shock	Fluids, antibiotics, vasopressors
Cardiogenic shock	Inotropes, revascularisation
Haemorrhage	Blood products, surgery
Mesenteric ischaemia	Urgent surgical review

Treat the underlying cause. Bicarbonate does not improve outcomes in Type A — address O2 delivery.

Type B — No Hypoperfusion

Cause	Note
Metformin toxicity	Inhibits mitochondrial complex 1; CRRT if severe
Liver failure	Reduced lactate clearance; transplant consideration
Malignancy	Warburg effect (aerobic glycolysis)
HIV medications	Nucleoside analogues — mitochondrial toxicity
Thiamine deficiency	Pyruvate dehydrogenase inhibition — IV thiamine

Metformin-associated lactic acidosis (MALA): consider continuous renal replacement therapy (CRRT) to remove metformin and correct acidosis.

Renal Tubular Acidosis (RTA) — Types & Features

Type	Name	Defect	K+	Urine pH	Key Associations
Type 1	Distal RTA	Failure to excrete H+ in distal tubule	↓ Hypokalaemia	>5.5	Nephrolithiasis, nephrocalcinosis, Sjögren's, amphotericin B
Type 2	Proximal RTA	Failure to reabsorb HCO3- in proximal tubule	↓ Hypokalaemia	Variable	Fanconi syndrome, myeloma, carbonic anhydrase inhibitors, Wilson's disease
Type 4	Hyperkalaemic RTA	Hypoaldosteronism → reduced NH3 excretion	↑ Hyperkalaemia	<5.5	Diabetes, ACE inhibitors, spironolactone, Addison's, obstructive uropathy

Type 3 RTA (combined 1+2) is rare and seen mainly in carbonic anhydrase II deficiency. Types 1 and 2 are the clinically important exam types.

Hyperchloraemic Acidosis — Fluid Choice Matters

Fluid	Cl^- content	Acid-Base Effect
0.9% NaCl (Normal Saline)	154 mEq/L	Causes hyperchloraemic acidosis
Hartmann's (Ringer's Lactate)	111 mEq/L	Balanced — metabolised to HCO3-
PlasmaLyte	98 mEq/L	Best balance — gluconate/acetate
5% Dextrose	0	No Cl- load but no volume support

Large volume normal saline administration in surgery/ICU → dilutes SID → hyperchloraemic acidosis. Balanced crystalloids (Hartmann's, PlasmaLyte) preferred for volume resuscitation.

In DKA: 0.9% NaCl initially then switch to balanced fluids once glucose <14 mmol/L reduces post-DKA hyperchloraemic acidosis.

Complete Acid-Base Interpreter

PaCO₂ (mmHg)

HCO₃^- (mEq/L)

Na⁺ (mEq/L)

Cl^- (mEq/L)

Albumin (g/L) optional

Lactate (mmol/L) optional

5-Step ABG Interpretation Method (with Worked Example) ▶

Assess pH — Is it acidaemia or alkalaemia?

pH <7.35 = acidaemia | pH >7.45 = alkalaemia | pH 7.35–7.45 = normal (but may still have a disorder)

Identify the primary disorder — Respiratory or Metabolic?

Look at PaCO2 and HCO3-. If pH ↓ and PaCO2 ↑ → Respiratory Acidosis. If pH ↓ and HCO3- ↓ → Metabolic Acidosis. Apply same logic for alkalosis.

Is compensation appropriate?

Apply compensation formulae. If actual value matches expected → appropriate (simple disorder). If not → mixed disorder.

Calculate Anion Gap (if metabolic acidosis)

AG = Na − (Cl + HCO3-). If >12 → high AG. Correct for albumin. Classify as MUDPILES or USED CARP.

Delta-Delta ratio (if high AG metabolic acidosis)

DD = (AG−12)/(24−HCO3-). <0.4 = additional non-AG acidosis. >2 = additional metabolic alkalosis. 1–2 = pure high AG acidosis.

Worked Example: pH 7.28 | PaCO2 20 | HCO3- 9 | Na 140 | Cl 104
Step 1: pH 7.28 → Acidaemia. Step 2: HCO3- low → Metabolic Acidosis. PaCO2 also low = compensation.
Step 3: Winter's: (1.5×9)+8=21.5 ±2. Expected PaCO2=19.5–23.5. Actual=20 → appropriate compensation, simple metabolic acidosis.
Step 4: AG = 140−(104+9) = 27 → High AG. Step 5: DD = (27−12)/(24−9) = 15/15 = 1.0 → Pure high AG acidosis.
Diagnosis: Pure high AG metabolic acidosis — consider MUDPILES (DKA, lactic acidosis, uraemia)

MUDPILES — High AG Metabolic Acidosis Causes (Quick Reference) ▶

M — Methanol

Osmolar gap elevated. Visual disturbance "snowstorm blindness". Treat: fomepizole, dialysis.

U — Uraemia

CKD/AKF. Accumulation of organic acids (sulfate, phosphate). Treat: dialysis, conservative management.

D — DKA

Beta-hydroxybutyrate + acetoacetate. Urine ketones +. Glucose usually >11 mmol/L. Insulin + fluids.

P — Propylene Glycol

Solvent in IV lorazepam/diazepam. Osmolar gap. Seen in ICU with prolonged infusions. Stop medication.

I — INH / Ibuprofen

Isoniazid: seizures + lactic acidosis. Ibuprofen overdose rare cause. Drug history essential.

L — Lactic Acidosis

Type A (hypoperfusion) or Type B (metformin, malignancy). Lactate >4 mmol/L = severe. Treat cause.

E — Ethylene Glycol

Antifreeze. Oxalate crystals in urine. Osmolar gap. Treat: fomepizole, ethanol infusion, dialysis.

S — Salicylates

Aspirin OD. Mixed high AG metabolic acidosis + respiratory alkalosis (direct stimulation of resp. centre). Urine alkalinisation + dialysis if severe.

Winter's Formula — Quick Reference Calculator ▶

Expected PaCO₂ = (1.5 × HCO₃^-) + 8 ± 2

HCO₃^- (mEq/L)

Actual PaCO₂

GCC-Specific Clinical Contexts

Heat Exhaustion Acid-Base Changes (Gulf Climate)

Extreme heat → hyperventilation → respiratory alkalosis (PaCO2 ↓, pH ↑). If severe/prolonged: dehydration → ↓ perfusion → lactic acidosis (mixed disorder). Heatstroke: combined high AG metabolic acidosis + multi-organ failure.

In Hajj/Heatwave cases: mixed respiratory alkalosis + lactic acidosis. Initial ABG may show normal pH despite significant disorder.

Ramadan Fasting — Metabolic Effects

Prolonged fasting (16–18h): mild ketonaemia → slight AG elevation. Dehydration → ↓ renal HCO3- excretion → relative alkalosis. Diabetic patients: high risk of DKA. Hypoglycaemia in insulin-dependent patients → lactic acidosis risk.

Monitor T1DM patients on Ramadan waiver programs. Pre-Ramadan ABG baseline useful in complex patients.

6 Worked Clinical Scenarios

Scenario 1 — 28yo Male, Vomiting 3 Days

pH 7.52PaCO2 48HCO3- 36Na 138Cl 88

Metabolic Alkalosis (saline-responsive)
Step 1: pH 7.52 → Alkalaemia. Step 2: HCO3- 36 ↑ → Metabolic Alkalosis. Step 3: Expected PaCO2 = (0.7×36)+21 = 46.2 ±2 → Actual 48 = appropriate compensation. AG = 138−(88+36) = 14 → mildly elevated (may reflect hypoalbuminaemia or contraction). Urine Cl- <20 expected. Diagnosis: Metabolic alkalosis from vomiting/HCl loss. Treat with IV NaCl + KCl.

Scenario 2 — 65yo COPD, Drowsy at Home

pH 7.30PaCO2 72HCO3- 34Na 140Cl 100

Chronic Respiratory Acidosis with appropriate renal compensation
Step 1: pH 7.30 → Acidaemia. Step 2: PaCO2 72 ↑ → Respiratory Acidosis (primary). Step 3: HCO3- expected (chronic) = 24 + (72−40)×3.5/10 = 24+11.2 = 35.2 → Actual 34 ≈ appropriate. AG = 140−(100+34) = 6 → Normal. Diagnosis: Chronic respiratory acidosis (COPD exacerbation). Treat: controlled O2 therapy (28–35%), consider NIV (BiPAP), avoid over-oxygenation.

Scenario 3 — 22yo T1DM, Polyuria and Vomiting

pH 7.18PaCO2 22HCO3- 8Na 132Cl 96Glucose 28

DKA — High AG Metabolic Acidosis with appropriate respiratory compensation
AG = 132−(96+8) = 28 ↑ (high AG). Winter's: (1.5×8)+8 = 20 ±2. Actual PaCO2 = 22 → appropriate. Delta-delta = (28−12)/(24−8) = 16/16 = 1.0 → pure high AG acidosis. Diagnosis: DKA. pH >6.9, no bicarbonate needed. Start insulin infusion 0.1 U/kg/hr, IVF (0.9% NaCl), replace K+ (ensure >3.3 before insulin), hourly glucose monitoring.

Scenario 4 — 55yo Septic Shock Post-Surgery

pH 7.22PaCO2 28HCO3- 11Na 141Cl 113Lactate 6.2

Mixed: High AG metabolic acidosis (lactic) + Normal AG (hyperchloraemic) acidosis
AG = 141−(113+11) = 17 → elevated but less than expected for degree of acidosis. Corrected AG (if albumin low) may be higher. Delta-delta = (17−12)/(24−11) = 5/13 = 0.38 → <0.4 → concurrent non-AG acidosis. Diagnosis: Lactic acidosis (Type A, sepsis) + hyperchloraemic acidosis (excess NaCl resuscitation). Management: treat sepsis source, switch to balanced fluids (PlasmaLyte/Hartmann's), vasopressors, consider CRRT.

Scenario 5 — 40yo on Mechanical Ventilation (Post-Cardiac Surgery)

pH 7.55PaCO2 28HCO3- 23Na 139Cl 103

Iatrogenic Respiratory Alkalosis (over-ventilation)
pH 7.55 → Alkalaemia. PaCO2 28 ↓ → primary respiratory alkalosis. HCO3- 23 normal → acute. Renal compensation minimal (acute). AG = 139−(103+23) = 13 (borderline normal). Diagnosis: Mechanical over-ventilation causing respiratory alkalosis. Risk: cerebral vasoconstriction, seizures, hypokalaemia. Action: reduce RR (e.g. from 18 to 12), or decrease TV slightly. Target PaCO2 35–45 mmHg.

Scenario 6 — 70yo with Confusion, CKD Stage 4, on Metformin

pH 7.08PaCO2 18HCO3- 5Na 136Cl 100Lactate 12.4

Severe Metformin-Associated Lactic Acidosis (MALA)
AG = 136−(100+5) = 31 → Very high AG. Winter's: (1.5×5)+8 = 15.5 ±2. Actual PaCO2 = 18 → appropriate maximal compensation (Kussmaul breathing). Delta-delta = (31−12)/(24−5) = 19/19 = 1.0 → pure high AG. Lactate 12.4 → severe lactic acidosis. Diagnosis: MALA — metformin accumulation in CKD (metformin should be stopped at eGFR <30). Management: STOP metformin, ICU, CRRT to clear metformin + correct acidosis. Consider bicarbonate if pH <6.9 as bridge to CRRT.

GCC Exam MCQs — DHA/MOH/SCFHS/QCHP Style

Q1. A 45-year-old patient presents with pH 7.25, PaCO2 60 mmHg, HCO3- 25 mEq/L. What is the most likely acid-base disorder?

A. Metabolic acidosis with appropriate compensation B. Acute respiratory acidosis without compensation C. Chronic respiratory acidosis with inadequate compensation D. Mixed respiratory and metabolic acidosis

Correct Answer: B — Acute respiratory acidosis without compensation
Explanation: pH low (acidaemia), PaCO2 high (respiratory acidosis). Expected HCO3- for acute = 24 + (60−40)/10 = 26. Actual HCO3- = 25 ≈ expected for acute. This is acute respiratory acidosis (minimal renal compensation as it's acute). No chronic compensation (which would give HCO3- ~31).

Q2. A diabetic patient has pH 7.32, HCO3- 12, PaCO2 24 mmHg, Na 140, Cl 98. What does the delta-delta ratio indicate?

A. Pure high AG metabolic acidosis B. Concurrent metabolic alkalosis C. Concurrent non-AG metabolic acidosis D. Appropriate compensation only

Correct Answer: A — Pure high AG metabolic acidosis
Explanation: AG = 140−(98+12) = 30. Delta-delta = (30−12)/(24−12) = 18/12 = 1.5. Range 1.0–2.0 = pure high AG metabolic acidosis. Winter's: (1.5×12)+8 = 26 ±2. Actual PaCO2 = 24 → appropriate compensation. Diagnosis: Pure high AG metabolic acidosis (likely DKA given context).

Q3. Which electrolyte change is expected with Type 4 Renal Tubular Acidosis?

A. Hypokalaemia and nephrocalcinosis B. Hypokalaemia and bicarbonate wasting C. Hyperkalaemia and hypoaldosteronism D. Hypernatraemia and hypophosphataemia

Correct Answer: C — Hyperkalaemia and hypoaldosteronism
Explanation: Type 4 RTA is caused by aldosterone deficiency or resistance (hypoaldosteronism). Aldosterone normally promotes K+ excretion and H+ excretion. Without it: hyperkalaemia + normal AG hyperchloraemic acidosis. Common in diabetics, CKD, on ACE inhibitors/spironolactone. Type 1 → hypokalaemia + stones. Type 2 → hypokalaemia + HCO3- wasting.

Q4. A 30-year-old woman in her 3rd trimester of pregnancy has pH 7.44, PaCO2 30 mmHg, HCO3- 20 mEq/L. What is the most accurate interpretation?

A. Respiratory alkalosis with inadequate compensation B. Normal physiological adaptation of pregnancy C. Metabolic acidosis D. Mixed metabolic and respiratory alkalosis

Correct Answer: B — Normal physiological adaptation of pregnancy
Explanation: Progesterone stimulates respiratory drive → chronic respiratory alkalosis (PaCO2 ~28–32 mmHg). Kidneys compensate by excreting HCO3- → HCO3- falls to ~18–22 mEq/L. pH remains slightly alkaline or normal. This is expected in pregnancy — not a pathological disorder. Chronic resp. alkalosis compensation: HCO3- = 24 − (40−30)×5/10 = 24−5 = 19. Actual 20 → appropriate.

Q5. A patient with septic shock receives 6L of 0.9% NaCl. ABG shows: pH 7.28, PaCO2 36, HCO3- 16, Na 142, Cl 118. What is the primary acid-base disorder?

A. High AG metabolic acidosis (lactic acidosis) B. Hyperchloraemic normal AG metabolic acidosis C. Respiratory acidosis D. Mixed metabolic acidosis and respiratory alkalosis

Correct Answer: B — Hyperchloraemic normal AG metabolic acidosis
Explanation: AG = 142−(118+16) = 8 → Normal AG. Cl- is markedly elevated (118) → hyperchloraemia from massive 0.9% NaCl infusion (154 mEq/L Cl). This dilutes SID and causes hyperchloraemic acidosis. Winter's: (1.5×16)+8 = 32 ±2. Actual PaCO2 = 36 → inadequate respiratory compensation → mild additional component. Management: switch to balanced crystalloid (PlasmaLyte/Hartmann's), treat sepsis.

Acid-Base Quick Reference Card

pH 7.35–7.45

Normal Blood pH

PaCO2 35–45

mmHg (respiratory)

HCO3- 22–26

mEq/L (metabolic)

AG 8–12

mEq/L (normal)

Disorder	pH	PaCO2	HCO3-	Mnemonic
Resp. Acidosis	↓	↑	↑ (comp)	COPD, OHS, opioids
Resp. Alkalosis	↑	↓	↓ (comp)	Anxiety, pregnancy, liver failure
Met. Acidosis	↓	↓ (comp)	↓	MUDPILES / USED CARP
Met. Alkalosis	↑	↑ (comp)	↑	Vomiting, diuretics, Conn's

Memory Aid: "ROME" — Respiratory Opposite (pH and PaCO2 move opposite), Metabolic Equal (pH and HCO3- move in same direction).

Henderson-Hasselbalch Equation

Buffer Systems

Bicarbonate Buffer (primary extracellular)

Phosphate Buffer

Protein Buffer (albumin)

Haemoglobin Buffer

Compensation Mechanisms

Respiratory Compensation

Renal Compensation

Stewart Approach — Strong Ion Difference (SID)

Why Acid-Base Balance Matters Clinically

Enzyme Function

O2 Dissociation Curve

Drug Ionisation

Electrolyte Shifts

Cardiac Function

Neurological Effect

Respiratory Acidosis

Mechanism

Causes

Renal Compensation

Respiratory Alkalosis

Mechanism

Causes

Renal Compensation

Ventilator Management & Acid-Base Implications

Respiratory Rate (RR)

Tidal Volume (TV)

PEEP

Driving Pressure

Permissive Hypercapnia

Weaning Targets

Anion Gap Calculation

Metabolic Acidosis — High AG

Mnemonic: MUDPILES

Metabolic Acidosis — Normal AG

Mnemonic: USED CARP

Metabolic Alkalosis

Saline-Responsive (Urine Cl- <20 mEq/L)

Saline-Resistant (Urine Cl- >20 mEq/L)

Respiratory Compensation for Metabolic Disorders

For Metabolic Acidosis (Winter's Formula)

For Metabolic Alkalosis

Complete Compensation Formulae Reference

Delta-Delta Ratio — Mixed Disorder Detection

Recognising Mixed Disorders

Common Mixed Disorder Patterns

Key Rules for Mixed Disorders

Diabetic Ketoacidosis (DKA)

Acid-Base Pattern

Bicarbonate Therapy

Management Priorities

Lactic Acidosis

Type A — Tissue Hypoperfusion

Type B — No Hypoperfusion

Renal Tubular Acidosis (RTA) — Types & Features

Hyperchloraemic Acidosis — Fluid Choice Matters

Complete Acid-Base Interpreter

Assess pH — Is it acidaemia or alkalaemia?

Identify the primary disorder — Respiratory or Metabolic?

Is compensation appropriate?

Calculate Anion Gap (if metabolic acidosis)

Delta-Delta ratio (if high AG metabolic acidosis)

M — Methanol

U — Uraemia

D — DKA

P — Propylene Glycol

I — INH / Ibuprofen

L — Lactic Acidosis

E — Ethylene Glycol

S — Salicylates

GCC-Specific Clinical Contexts

Heat Exhaustion Acid-Base Changes (Gulf Climate)

Ramadan Fasting — Metabolic Effects

6 Worked Clinical Scenarios

Scenario 1 — 28yo Male, Vomiting 3 Days

Scenario 2 — 65yo COPD, Drowsy at Home

Scenario 3 — 22yo T1DM, Polyuria and Vomiting

Scenario 4 — 55yo Septic Shock Post-Surgery

Saline-Responsive (Urine Cl^- <20 mEq/L)

Saline-Resistant (Urine Cl^- >20 mEq/L)