By the end of this note you will be able to recognise, interpret and initiate appropriate management of the common acid‑base disturbances seen in Kenyan clinical rotations, while remembering to verify drug choices and local protocols against the Kenya MoH guideline and your hospital formulary.
Definition
Acid‑base disorders are abnormalities in the body’s hydrogen ion concentration that disturb the normal pH range (7.35‑7.45). They arise from either an excess of acid, a loss of base, or a failure of compensatory mechanisms, and may be metabolic, respiratory, or mixed.
Anatomy and physiology you need
| System | Key component | Relevance to pH |
|---|---|---|
| Respiratory | Lungs (ventilation) | Expel CO₂ → ↓ H₂CO₃ → ↑ pH |
| Renal | Proximal & distal tubules | Reabsorb HCO₃⁻, secrete H⁺ |
| Buffer | Intracellular proteins, hemoglobin, phosphate, bicarbonate | Immediate neutralisation of H⁺ |
| Cellular metabolism | Aerobic/anaerobic pathways | Produce CO₂ and lactic acid |
| Endocrine | Aldosterone, ADH | Modulate renal H⁺/HCO₃⁻ handling |
Causes and risk factors
| Category | Common causes in Kenya | Specific risk factors |
|---|---|---|
| Metabolic acidosis | Diarrhoea, severe malaria, septic shock, renal failure, keto‑acidosis (diabetes, alcoholic), lactic acidosis (post‑operative, severe anemia) | HIV‑related opportunistic infections, TB meningitis, sickle cell vaso‑occlusive crisis |
| Metabolic alkalosis | Prolonged vomiting, nasogastric suction, diuretic over‑use, mineralocorticoid excess | Chronic rheumatic heart disease with loop diuretic therapy, adrenal tumours |
| Respiratory acidosis | COPD exacerbation, severe pneumonia, airway obstruction, opioid overdose, neuromuscular weakness | TB lung disease, HIV‑related pneumocystis pneumonia |
| Respiratory alkalosis | Hyperventilation from pain, fever, anxiety, high altitude, sepsis | Malaria‑induced fever spikes, pulmonary embolism |
Pathophysiology
Metabolic acidosis → ↑ acid production or ↓ HCO₃⁻ loss → ↓ plasma HCO₃⁻ → ↓ pH → respiratory centre ↑ ventilation → ↓ PaCO₂ (partial compensation).
Metabolic alkalosis → HCO₃⁻ gain or H⁺ loss → ↑ plasma HCO₃⁻ → ↑ pH → respiratory centre ↓ ventilation → ↑ PaCO₂ (partial compensation).
Respiratory acidosis → hypoventilation → ↑ PaCO₂ → ↑ H₂CO₃ → ↓ pH → kidneys ↑ H⁺ secretion, reabsorb HCO₃⁻ (renal compensation).
Respiratory alkalosis → hyperventilation → ↓ PaCO₂ → ↓ H₂CO₃ → ↑ pH → kidneys ↓ H⁺ secretion, excrete HCO₃⁻ (renal compensation).
Mixed disorder → simultaneous primary metabolic and respiratory abnormalities → pH reflects net effect; compensation patterns may be inappropriate or absent.
Arrows for causal steps:
``` Cause → ↑/↓ acid or base → change in [HCO₃⁻] or PaCO₂ → pH shift → compensatory response → new steady state (or decompensation)
Clinical features
| Aspect | Key questions / findings | Why it occurs |
|---|---|---|
| Onset & tempo | “When did you first notice symptoms? Sudden vs. gradual?” | Acute disturbances (e.g., keto‑acidosis, severe sepsis) produce rapid pH change; chronic disorders (e.g., CKD) evolve slowly. |
| Respiratory symptoms | Dyspnoea, tachypnoea, “air‑hungry” breathing, orthopnoea, cough, sputum colour | Hyperventilation is a compensatory response to metabolic acidosis; hypoventilation may accompany metabolic alkalosis (e.g., vomiting). |
| Neurological status | Confusion, lethargy, headache, seizures, coma, asterixis | Cerebral effects of pH shift: acidosis depresses neuronal activity, alkalosis increases neuronal excitability. |
| Gastro‑intestinal | Nausea, vomiting, diarrhoea, abdominal pain, loss of appetite | Vomiting removes HCl → metabolic alkalosis; diarrhoea loses bicarbonate → metabolic acidosis. |
| Renal history | “Any known kidney disease, recent AKI, use of diuretics, NSAIDs?” | Impaired H⁺ excretion or HCO₃⁻ reabsorption drives metabolic acidosis; diuretics can cause alkalosis. |
| Endocrine / metabolic | Polyuria, polydipsia, weight loss, recent infection, steroid use | Diabetic ketoacidosis, hyperaldosteronism, Cushing’s, thyroid disease affect acid‑base. |
| Infectious / tropical | Recent malaria, TB treatment, HIV status, sickle‑cell crisis, rheumatic fever | Malaria and severe sepsis cause lactic acidosis; TB drugs (e.g., isoniazid) can precipitate metabolic acidosis; HIV‑related opportunistic infections and sickle‑cell vaso‑occlusion generate lactic or ketoacidosis. |
| Medication & toxin exposure | “Any over‑the‑counter meds, antacids, diuretics, laxatives, alcohol, methanol, ethylene glycol?” | Antacids → alkalosis; diuretics → alkalosis; toxins → high‑anion‑gap acidosis. |
| Fluid & electrolyte balance | Recent IV fluids, oral rehydration, salt intake, urine output | Volume status influences renal compensation; chloride‑rich fluids can cause hyperchloraemic acidosis. |
| Physical exam – general | Level of consciousness, skin colour, temperature, capillary refill | Altered mental status reflects severe pH derangement; warm skin may suggest sepsis‑related lactic acidosis. |
| Respiratory | Respiratory rate, depth, use of accessory muscles, arterial CO₂ (if available) | Kussmaul breathing (deep, rapid) = metabolic acidosis; shallow breathing = metabolic alkalosis. |
| Cardiovascular | Blood pressure, pulse, signs of volume overload or depletion | Hypotension → tissue hypoperfusion → lactic acidosis; hypertension may accompany primary alkalosis (e.g., hyperaldosteronism). |
| Abdominal | Tenderness, bowel sounds, signs of obstruction or ileus | Vomiting or diarrhoea clues to loss of H⁺ or HCO₃⁻. |
| Neurological | Tremor, seizures, asterixis, focal deficits | Asterixis is classic for metabolic encephalopathy (uremic, hepatic, severe alkalosis). |
| Skin | Dryness, diaphoresis, flushing | Diaphoresis common in metabolic acidosis; flushing may accompany alkalosis (e.g., hyperventilation). |
| Extremities | Edema, peripheral pulses, capillary refill | Volume status influences renal compensation and guides fluid therapy. |
Differential diagnosis
| Condition | Points toward it | Distinguishing feature |
|---|---|---|
| Diabetic ketoacidosis (DKA) | Polyuria, polydipsia, fruity breath, HIV/TB co‑infection | High anion gap, positive serum/urine ketones, glucose often >250 mg/dL |
| Lactic acidosis (type A) | Sepsis, malaria, severe anaemia, shock, recent surgery | High anion gap, lactate >2 mmol/L, normal/low glucose |
| Hyperchloraemic metabolic acidosis | Large volume normal saline, diarrhoea, renal tubular acidosis | Normal anion gap, ↑Cl⁻, ↓HCO₃⁻ |
| Metabolic alkalosis (vomiting) | Persistent vomiting, nasogastric suction, antacid overuse | Low Cl⁻, high HCO₃⁻, paradoxical aciduria |
| Metabolic alkalosis (diuretic) | Loop/thiazide use, volume depletion, hypertension | Low urine Cl⁻ (<20 mmol/L) if chloride responsive |
| Renal tubular acidosis (RTA) | Chronic kidney disease, nephrocalcinosis, growth failure (pediatrics) | Normal anion gap, urine pH >5.5 (type 1) or >5.5 with low HCO₃⁻ (type 2) |
| Salicylate poisoning | Recent aspirin use, tinnitus, hyperventilation | Mixed respiratory alkalosis + metabolic acidosis, anion gap ↑ |
| Methanol / ethylene glycol poisoning | History of ingestion, visual disturbances (methanol) | Very high anion gap, osmolar gap ↑, specific toxic metabolites |
| Chronic respiratory acidosis | COPD, neuromuscular disease, sedative use | Elevated PaCO₂, compensatory ↑HCO₃⁻ (renal). |
| Primary respiratory alkalosis | Hyperventilation from anxiety, high altitude, fever | Low PaCO₂, low HCO₃⁻ (renal compensation). |
Investigations
| Test | What it answers | Typical result interpretation |
|---|---|---|
| Arterial blood gas (ABG) | pH, PaCO₂, HCO₃⁻, base excess | Determines primary disorder, compensation, severity |
| Serum electrolytes (Na⁺, K⁺, Cl⁻, HCO₃⁻) | Anion gap, chloride status | ↑AG = high‑gap acidosis; ↓Cl⁻ = metabolic alkalosis |
| Serum lactate | Presence of lactic acidosis | >2 mmol/L = significant lactic contribution |
| Serum ketones (β‑hydroxybutyrate) | Ketoacidosis | Positive in DKA, alcoholic ketoacidosis |
| Urine ketones | Support DKA | Positive dipstick |
| Serum creatinine & urea | Renal function, uremic acidosis | Elevated → renal contribution |
| Serum glucose | Diabetic vs non‑diabetic acidosis | Hyperglycaemia suggests DKA |
| Serum osmolar gap (if toxic ingestion suspected) | Detects methanol/ethylene glycol | Osmolar gap >10 mOsm/kg suggests toxic alcohol |
| Complete blood count | Infection, malaria, sickle‑cell crisis | Leukocytosis, parasitaemia |
| Chest X‑ray | Pulmonary cause of respiratory disorder | Hyperinflation (COPD), infiltrates (pneumonia) |
| Urine electrolytes (urine Na⁺, Cl⁻) | Distinguish renal vs extrarenal causes of metabolic alkalosis | Urine Cl⁻ <20 mmol/L = chloride‑responsive alkalosis |
| Serum albumin (if low) | Adjusted anion gap | Low albumin reduces calculated AG |
Diagnosis and severity
- Identify the primary disturbance using ABG:
- pH < 7.35 → acidosis; pH > 7.45 → alkalosis.
- Compare PaCO₂ and HCO₃⁻ to expected compensation (e.g., Winter’s formula for metabolic acidosis).
- Classify the metabolic component:
- Anion‑gap = (Na⁺ + K⁺) − (Cl⁻ + HCO₃⁻).
- High‑gap (>12 mmol/L) → ketoacidosis, lactic acidosis, renal failure, toxins.
- Normal‑gap → hyperchloraemic acidosis, RTA, GI bicarbonate loss.
- Assess severity (clinical and laboratory):
- Mild: pH 7.30–7.35, bicarbonate 18–22 mmol/L, no organ dysfunction.
- Moderate: pH 7.20–7.30, bicarbonate 12–18 mmol/L, symptoms (confusion, tachypnoea) but stable vitals.
- Severe / life‑threatening: pH < 7.20, bicarbonate < 12 mmol/L, altered mental status, hypotension, arrhythmia, impending respiratory failure.
- Document mixed disorders when pH does not match expected compensation (e.g., simultaneous metabolic acidosis and respiratory alkalosis).
- Assign a working diagnosis integrating history, exam, and investigations (e.g., “High‑anion‑gap metabolic acidosis secondary to septic‑induced lactic acidosis”).
- Severity guides urgency of therapy: severe cases require ICU‑level monitoring, rapid correction of underlying cause, and careful electrolyte/fluid management.
Management principles (dose‑free):
- Fluid resuscitation with isotonic crystalloids for hypovolaemia; consider balanced solutions to avoid hyperchloraemia.
- Address the underlying cause: insulin‑based protocols for DKA, antibiotics for sepsis/malaria/TB, antiretroviral optimisation for HIV‑related metabolic derangements, exchange transfusion for severe sickle‑cell crisis.
- Correct electrolyte abnormalities: potassium replacement when K⁺ < 3.5 mmol/L (especially before insulin in DKA), calcium for severe hypo‑albuminaemia, magnesium if low.
- Specific acid‑base modifiers:
- Sodium bicarbonate only for severe acidemia (pH < 7.1) or life‑threatening hyperkalaemia, administered cautiously.
- Acetazolamide for certain types of metabolic alkalosis (e.g., high‑altitude, chronic hypoventilation).
- Ventilatory support: adjust tidal volume and respiratory rate to normalize PaCO₂ in pure respiratory disorders; avoid over‑correction in mixed states.
- Monitoring: repeat ABG every 2–4 h until stable, continuous cardiac and pulse‑ox monitoring, strict input‑output charting, serial electrolytes.
Complications to watch for: cardiac arrhythmias (from K⁺/Ca²⁺ shifts), cerebral oedema (rapid correction of severe hyponatraemia or DKA), hypoglycaemia (insulin therapy), renal failure progression, pulmonary oedema from aggressive fluid therapy, rebound alkalosis after bicarbonate use.
Management
| Step | What to do | Rationale |
|---|---|---|
| Airway‑breathing‑circulation | Give supplemental O₂ if SpO₂ < 94 % or respiratory distress; consider non‑invasive ventilation for severe metabolic acidosis with Kussmaul breathing. | Improves tissue oxygenation and reduces work of breathing. |
| Correct life‑threatening derangements | • Rapid IV sodium bicarbonate only for pH < 7.1 with haemodynamic compromise or severe hyper‑K⁺. <br>• IV calcium gluconate (or chloride) for imminent hyper‑K⁺‑induced arrhythmia. | Bicarbonate buffers H⁺; calcium stabilises myocardial membranes. |
| Identify and treat the primary disorder | • Respiratory acidosis – improve ventilation (e.g., treat COPD exacerbation, reverse opioid overdose, consider BiPAP). <br>• Respiratory alkalosis – treat underlying hyperventilation (pain, anxiety, sepsis, high‑altitude). <br>• Metabolic acidosis – give the missing anion (e.g., insulin + dextrose for DKA, thiamine for alcoholic ketoacidosis, folate for methanol/ethylene glycol). <br>• Metabolic alkalosis – replace volume and chloride (IV saline), give potassium if low, stop excess alkali. | Targeting the root cause stops ongoing acid/base shift. |
| Electrolyte optimisation | Replace K⁺ cautiously (avoid rapid shifts), correct Mg²⁺, monitor Na⁺ and Cl⁻. | Electrolyte disturbances perpetuate acid‑base imbalance and arrhythmias. |
| Fluid management | Give isotonic saline for volume depletion; avoid excessive chloride‑rich fluids in chloride‑responsive metabolic alkalosis. | Restores perfusion and influences strong ion difference. |
| Monitoring | • Serial ABG (or VBG) every 2–4 h until stable. <br>• Continuous ECG for arrhythmia risk. <br>• Urine output, serum lactate, glucose, renal function. | Detects over‑correction, emerging complications, and guides therapy titration. |
| Definitive therapy | Treat underlying disease: antiretroviral optimisation for HIV‑related renal tubular acidosis, anti‑TB drugs with renal dose adjustment, malaria antimalarials, disease‑modifying therapy for sickle cell crisis, etc. | Prevents recurrence and addresses the systemic cause. |
| Safety / Contra‑indications | • Avoid bicarbonate in pure respiratory alkalosis, in chronic compensated metabolic alkalosis, or when pH > 7.45. <br>• Do not give potassium without ECG monitoring in severe hyper‑K⁺. <br>• Caution with rapid fluid shifts in severe heart failure or pulmonary oedema. | Prevents iatrogenic harm. |
Complications and prognosis
- Cardiac arrhythmias (especially with severe acidosis, hyper‑K⁺, or rapid correction).
- Cerebral oedema in profound metabolic acidosis (e.g., DKA) if over‑corrected too quickly.
- Hypotension / shock from massive bicarbonate administration (due to CO₂ generation and vasodilation).
- Renal impairment progression when underlying cause (e.g., HIV‑associated nephropathy) is untreated.
- Respiratory failure if ventilatory drive is blunted by over‑correction of respiratory alkalosis.
Prognosis hinges on rapid identification of the primary disorder and timely definitive therapy. In resource‑limited Kenyan settings, early recognition of tropical infections (malaria, TB) and prompt antimicrobial therapy markedly improve outcomes.
High‑yield exam points
- Look‑alike: Metabolic acidosis with respiratory compensation vs. primary respiratory alkalosis – check the anion gap and expected PaCO₂ (Winter’s formula).
- Common mistake: Giving bicarbonate for all metabolic acidoses; examiners expect you to reserve it for severe pH < 7.1 or hemodynamic instability.
- Bedside question: “Why does a patient with severe vomiting develop a metabolic alkalosis?” – loss of gastric HCl → rise in serum HCO₃⁻ and chloride depletion.
- Tricky: Distinguish renal tubular acidosis (normal anion gap, inappropriate urine pH) from diarrhoeal acidosis (low urine pH).
- Examiner cue: “What is the next step after you have identified a high‑anion‑gap metabolic acidosis in a diabetic?” – check glucose, ketones, give insulin, and monitor potassium.
Clinical case
Patient: 28‑year‑old male, known HIV (on ART), presents with 2‑day history of vomiting, diffuse abdominal pain, and lethargy.
Key findings:
- BP 110/70 mmHg, HR 118 bpm, RR 28 /min, SpO₂ 96 % on room air.
- Dry mucous membranes, Kussmaul breathing.
- ABG: pH 7.09, PaCO₂ 22 mmHg, HCO₃⁻ 8 mmol/L, anion gap 22 mmol/L.
- Serum K⁺ 3.2 mmol/L, glucose 210 mg/dL, urine positive for ketones.
Questions
- What is the primary acid‑base disorder?
Answer: High‑anion‑gap metabolic acidosis with appropriate respiratory compensation (Kussmaul breathing).
- What is the most urgent immediate intervention?
Answer: Start IV insulin infusion with dextrose to halt keto‑acid production, and begin cautious potassium replacement because insulin drives K⁺ intracellularly.
- Which underlying cause is most likely in this patient?
Answer: Diabetic ketoacidosis precipitated by infection (possible opportunistic infection in HIV) and vomiting‑induced volume depletion.
Practice questions
Question 1
A 45‑year‑old woman with severe malaria is obtunded, breathing rapidly (RR 30/min). ABG: pH 7.48, PaCO₂ 28 mmHg, HCO₃⁻ 22 mmol/L. What is the next best step?
A. Give IV sodium bicarbonate
B. Start mechanical ventilation
C. Treat underlying malaria and give analgesia
D. Administer IV saline bolus
Answer: C. treat underlying malaria and give analgesia
Explanation: The picture is primary respiratory alkalosis from hyperventilation; correcting the underlying infection and pain will resolve it. Bicarbonate or ventilation would worsen alkalosis.
Question 2
A 60‑year‑old man with chronic obstructive pulmonary disease presents with dyspnoea. ABG: pH 7.30, PaCO₂ 58 mmHg, HCO₃⁻ 28 mmol/L. Which intervention is contraindicated?
A. Initiate non‑invasive positive pressure ventilation
B. Give IV sodium bicarbonate
C. Administer bronchodilators
D. Provide supplemental oxygen to keep SpO₂ > 90 %
Answer: B. give IV sodium bicarbonate
Explanation: This is chronic respiratory acidosis with renal compensation; bicarbonate would further raise CO₂ retention and worsen acidosis.
Question 3
A child with sickle cell disease presents with severe pain crisis, vomiting and a serum Na⁺ 130 mmol/L, Cl⁻ 95 mmol/L, HCO₃⁻ 12 mmol/L. What explains the low chloride?
A. Renal loss of bicarbonate
B. Gastrointestinal loss of HCl
C. Dilutional hyponatraemia from IV fluids
D. Hyperventilation
Answer: B. gastrointestinal loss of HCl
Explanation: Vomiting leads to loss of gastric HCl, causing metabolic alkalosis; the low chloride here reflects a mixed picture with concurrent renal tubular acidosis common in sickle cell.
Question 4
A patient on antiretroviral therapy develops a normal‑anion‑gap metabolic acidosis (pH 7.20, HCO₃⁻ 10 mmol/L, PaCO₂ 25 mmHg). Urine pH is 7.5. What is the most likely diagnosis?
A. Lactic acidosis from ART
B. Diarrhoeal acidosis
C. Type 1 renal tubular acidosis
D. Hyperchloraemic metabolic alkalosis
Answer: C. type 1 renal tubular acidosis
Explanation: Normal anion gap, inappropriate alkaline urine despite systemic acidosis points to distal RTA, a recognised ART adverse effect.
Question 5
A 70‑year‑old man with severe heart failure receives large volumes of normal saline for hypotension. After 12 h his ABG shows pH 7.45, PaCO₂ 40 mmHg, HCO₃⁻ 30 mmol/L. What complication has occurred?
A. Metabolic alkalosis due to chloride‑responsive volume expansion
B. Respiratory acidosis from pulmonary oedema
C. Lactic acidosis from tissue hypoperfusion
D. Hyperchloraemic metabolic acidosis
Answer: A. metabolic alkalosis due to chloride‑responsive volume expansion
Explanation: Excessive saline raises extracellular volume and stimulates renal bicarbonate reabsorption, producing a non‑anion‑gap metabolic alkalosis.
Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.