Potassium Disorders: Hypokalemia and Hyperkalemia

Quick Answer

Potassium Disorders encompass both hypokalemia (K+ <3.5 mmol/L) and hyperkalemia (K+ >5.5 mmol/L), both of which are life-threatening electrolyte emergencies in the ICU setting due to their profound effects on cardiac conduction and neuromuscular function.

Key Clinical Features:

• Hyperkalemia: ECG changes (peaked T waves → prolonged PR → wide QRS → sine wave → VF/asystole), muscle weakness, paralysis
• Hypokalemia: ECG changes (U waves, flattened T waves, QT prolongation), muscle weakness, ileus, rhabdomyolysis, arrhythmias (Torsades de Pointes)
• Both conditions cause neuromuscular dysfunction and cardiac arrhythmias

Emergency Management:

Hyperkalemia (K+ >6.5 mmol/L with ECG changes):

1. Cardiac membrane stabilisation: Calcium gluconate 10% 10-20 mL IV over 2-5 min (or calcium chloride 10% 5-10 mL via CVC)
2. Shift K+ intracellularly: Insulin 10 units IV + Dextrose 50% 50 mL (or 25 g); Salbutamol 10-20 mg nebulised
3. Remove K+ from body: Dialysis (most effective); Resonium/patiromer/sodium zirconium cyclosilicate
4. Identify and treat cause: Stop K+-sparing drugs, treat AKI, exclude rhabdomyolysis/tumour lysis

Hypokalemia (K+ <2.5 mmol/L or with arrhythmia):

1. IV potassium replacement: 10-20 mmol/h via central line (max 40 mmol/h in emergency)
2. Correct concurrent hypomagnesemia (essential for refractory hypokalemia)
3. Continuous ECG monitoring
4. Identify and treat cause: GI losses, renal losses, redistribution

Mortality:

• Severe hyperkalemia (>6.5 mmol/L): Up to 30% mortality at 24 hours if untreated
• Cardiac arrest from hyperkalemia: 10-15% of ICU cardiac arrests
• Hypokalemia with digoxin: Significantly increased arrhythmia risk

Must-Know Facts:

• 98% of total body potassium is intracellular - small shifts cause large serum changes
• Calcium does NOT lower potassium - it stabilises the cardiac membrane
• Insulin/glucose shifts K+ within 15-30 minutes but wears off in 4-6 hours
• Dialysis is the only treatment that definitively removes potassium from the body
• Always check and replace magnesium in refractory hypokalemia

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CICM Exam Focus

What Examiners Expect

Second Part Written (SAQ):

Common SAQ stems:

• "A 65-year-old male with CKD Stage 4 presents to ICU with K+ 7.2 mmol/L. ECG shows wide QRS complexes. Outline your immediate management and the mechanisms of action of each intervention."
• "A patient post-cardiac surgery develops ventricular ectopy. K+ is 2.8 mmol/L. Discuss the pathophysiology and management of hypokalemia-induced arrhythmias."
• "Compare and contrast the mechanisms and efficacy of interventions used to treat hyperkalemia."
• "A patient with rhabdomyolysis has K+ 6.8 mmol/L. Outline your assessment and management priorities."

Expected depth:

• Systematic approach: ECG → immediate stabilisation → shift → removal → cause identification
• Understanding of K+ distribution: intracellular/extracellular ratio determines membrane potential
• Pharmacology: mechanism, onset, duration of each hyperkalemia treatment
• Evidence for newer K+ binders (patiromer, sodium zirconium cyclosilicate)
• ICU-specific scenarios: post-cardiac arrest, massive transfusion, rhabdomyolysis, tumour lysis syndrome
• Risk stratification for cardiac arrest

Second Part Hot Case:

Typical presentations:

• Post-cardiac surgery patient with hypotension and wide QRS on monitor
• Dialysis patient who missed sessions, now with cardiac arrhythmia
• Trauma patient with crush injury and oliguria
• Oncology patient post-chemotherapy with tumour lysis syndrome
• Patient on ACE inhibitor and spironolactone with deteriorating renal function

Examiners assess:

• Recognition of life-threatening ECG changes
• Immediate structured response (ABC approach)
• Appropriate dosing and route of calcium, insulin/glucose, salbutamol
• Recognition of need for RRT
• Identification of precipitating cause
• Safe communication with team

Second Part Viva:

Expected discussion areas:

• Physiology: Na-K-ATPase, resting membrane potential, aldosterone effects, insulin/catecholamine effects on K+ distribution
• ECG interpretation: Progressive ECG changes in hyperkalemia and hypokalemia
• Pharmacology: Mechanism, onset, duration, adverse effects of each treatment modality
• Dialysis indications: When, how urgently, modality selection (IHD vs CRRT)
• Special populations: Digoxin toxicity, post-cardiac arrest, massive transfusion
• Newer agents: Patiromer, sodium zirconium cyclosilicate - mechanism, evidence, PBS status

Examiner expectations:

• Safe, immediate response to hyperkalemic emergency
• Understanding of physiology underpinning treatment
• Evidence-based practice citing key trials
• Recognition of when dialysis is indicated
• Cultural sensitivity and Indigenous health awareness

Common Mistakes

• Forgetting to give calcium FIRST in hyperkalemia with ECG changes (stabilise membrane before shift)
• Using calcium chloride via peripheral IV (causes tissue necrosis)
• Giving insulin without glucose (causes hypoglycemia)
• Expecting immediate K+ reduction after giving calcium (calcium does not lower K+)
• Not monitoring for rebound hyperkalemia after insulin/salbutamol wear off (4-6 hours)
• Forgetting to treat hypomagnesemia in refractory hypokalemia
• Rapid IV potassium replacement peripherally (max 10 mmol/h peripherally, causes pain and phlebitis)
• Not repeating K+ after treatment to assess response
• Confusing pseudohyperkalemia with true hyperkalemia (haemolysed sample, prolonged tourniquet, thrombocytosis)

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Key Points

Must-Know Facts

1. Potassium Distribution: 98% of total body K+ (3,000-4,000 mmol) is intracellular at ~150 mmol/L; only 2% is extracellular at 3.5-5.0 mmol/L. The ratio determines resting membrane potential.

2. ECG is CRITICAL: In hyperkalemia, ECG changes (peaked T → wide QRS) may precede cardiac arrest. Treat ECG changes immediately regardless of K+ level.

3. Hyperkalemia Treatment Hierarchy: (1) Membrane stabilisation (calcium), (2) Shift (insulin/glucose, salbutamol), (3) Remove (dialysis, resins). Each has different onset and duration.

4. Calcium Mechanism: Does NOT lower potassium - antagonises the effect of hyperkalemia on cardiac membrane by raising threshold potential. Onset 1-3 minutes, duration 30-60 minutes.

5. Insulin/Glucose: Most reliable shift therapy. 10 units insulin + 25g glucose shifts K+ by 0.5-1.2 mmol/L in 15-30 min. Duration 4-6 hours. Monitor BSL q30min for 6 hours.

6. Dialysis is Definitive: Only treatment that removes K+ from the body. IHD can remove 30-40 mmol/h; CRRT removes 10-20 mmol/h. Indicated for severe/refractory hyperkalemia or oliguric AKI.

7. Hypokalemia and Digoxin: Hypokalemia potentiates digoxin toxicity by increasing digoxin binding to Na-K-ATPase. Can precipitate fatal arrhythmias at therapeutic digoxin levels.

8. Magnesium is Essential: Hypomagnesemia causes renal K+ wasting and refractory hypokalemia. Always check and replace Mg2+ (target >0.8 mmol/L) before aggressive K+ replacement.

9. Newer K+ Binders: Patiromer (Veltassa) and sodium zirconium cyclosilicate (Lokelma) are more effective and better tolerated than Resonium. PBS-listed for hyperkalemia with limited criteria.

10. ICU Causes: Post-cardiac arrest (ischaemia-reperfusion), massive transfusion (K+ in stored blood), rhabdomyolysis (muscle breakdown), tumour lysis syndrome (cell lysis), burns, crush injury.

Memory Aids

Mnemonic "MACHINE" for Hyperkalemia Causes:

• M: Medications (ACEi, ARB, K+-sparing diuretics, NSAIDs, trimethoprim, heparin)
• A: Acidosis (metabolic - H+/K+ exchange)
• C: Cellular destruction (rhabdomyolysis, tumour lysis, haemolysis, burns)
• H: Hypoaldosteronism (Addison's, Type 4 RTA, heparin)
• I: Intake (dietary, IV fluids, TPN)
• N: Nephropathy (AKI, CKD, RRT failure)
• E: Excretion failure (oliguria, anuria)

Mnemonic "CALCIUM-BIG-K" for Hyperkalemia Emergency Treatment:

• Calcium (membrane stabilisation)
• Albuterol/salbutamol (shift)
• Lokelma/resins (remove - slower)
• Check glucose, give with insulin
• Insulin + dextrose (shift)
• Use bicarbonate (limited role)
• Monitor ECG continuously
• Bicarbonate (consider if acidotic)
• IHD/RRT (definitive removal)
• Glucose monitoring (prevent hypoglycemia)
• Keep monitoring K+ levels hourly

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Definition & Epidemiology

Definitions

Potassium Disorders are classified based on serum potassium concentration:

Hypokalemia:

Hyperkalemia:

Pseudohyperkalemia: Falsely elevated serum K+ due to:

• Haemolysis during venepuncture (most common - fist clenching, small needle, prolonged tourniquet)
• Marked thrombocytosis (>500 × 10⁹/L) or leukocytosis (>100 × 10⁹/L)
• Delayed sample processing (K+ leaks from cells)
• Diagnosis: Repeat sample with careful technique, plasma K+ (rather than serum)

Epidemiology

International Data (PMID: 28143600, 31533907):

• Hypokalemia: Present in 20% of hospitalised patients
• Hyperkalemia: Present in 10% of hospitalised patients, 40-50% of ICU patients with AKI
• Hyperkalemia-associated cardiac arrest: Incidence 0.5-1% of hospital admissions
• ICU cardiac arrests due to electrolyte abnormalities: 10-20%
• CKD patients: 40-50% lifetime risk of hyperkalemia

Australian/NZ Data (ANZICS APD, PMID: 24995628):

• Estimated 15-25% of ICU patients have at least one potassium abnormality
• Hyperkalemia as primary ICU admission diagnosis: 0.5-1% of admissions
• CKD prevalence in Australia: 1.7 million (10% of adults)
• ESKD patients on dialysis: ~26,000 nationally
• Hyperkalemia is leading cause of dialysis emergency presentations

Indigenous Health Considerations (PMID: 30571826, 25564171):

• Aboriginal and Torres Strait Islander peoples: 5-10× higher rates of ESKD
• Earlier onset of CKD (median age ~48 years vs ~65 years)
• Higher rates of diabetes-related CKD
• Remote community challenges: Limited dialysis access, delayed presentations
• Higher rates of medication non-adherence due to access barriers
• Potassium binder availability limited in remote areas
• Māori populations (NZ): 3-4× higher ESKD rates, similar access challenges
• Cultural considerations: Whānau/family involvement in treatment decisions essential

Risk Factors:

Hyperkalemia:

• CKD/ESKD (impaired renal excretion)
• Diabetes mellitus (hyporeninemic hypoaldosteronism)
• Heart failure (RAASi medications, reduced renal perfusion)
• Medications: ACEi, ARBs, K+-sparing diuretics, NSAIDs, trimethoprim, heparin
• Acute tissue injury: Rhabdomyolysis, burns, crush injury, tumour lysis
• Metabolic acidosis (H+/K+ exchange)
• Adrenal insufficiency

Hypokalemia:

• Diuretic use (thiazides, loop diuretics)
• GI losses (vomiting, diarrhoea, NG suction, laxative abuse)
• Renal losses (hyperaldosteronism, Bartter/Gitelman syndrome, RTA)
• Redistribution: Insulin, beta-agonists, alkalosis, hypothermia/rewarming
• Poor dietary intake (alcoholism, anorexia)
• Hypomagnesemia

Outcomes (PMID: 28143600, 26797972):

• Hyperkalemia ≥6.5 mmol/L: 30% 24-hour mortality if untreated
• Hyperkalemia with ECG changes: 3-6× increased cardiac arrest risk
• In-hospital mortality in hyperkalemia: 10-30% depending on severity and comorbidities
• Hypokalemia <3.0 mmol/L: 2× increased in-hospital mortality
• Hypokalemia in acute MI: 2× increased ventricular arrhythmia risk
• Hypokalemia with digoxin: 5× increased mortality

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Applied Basic Sciences

This section bridges First Part basic sciences with Second Part clinical practice

Physiology of Potassium Homeostasis

Total Body Potassium Distribution (PMID: 26452653):

Total body potassium: 50-55 mmol/kg body weight (3,500-4,000 mmol in 70 kg adult)

Clinical Significance: Because only 2% of K+ is extracellular, small shifts between compartments cause large changes in serum K+. A net shift of 1% of intracellular K+ to extracellular compartment increases serum K+ by ~1 mmol/L.

Resting Membrane Potential (PMID: 17079956):

The resting membrane potential (RMP) is determined by the K+ concentration gradient:

• RMP = -70 to -90 mV (intracellular negative)
• Calculated using Nernst equation: E = -61 log ([K+]in/[K+]out)
• Normal ratio ~35:1 (intracellular:extracellular)

Na-K-ATPase (Sodium-Potassium Pump)

Structure and Function (PMID: 23613517):

• Ubiquitous membrane protein present in all cells
• Pumps 3 Na+ OUT and 2 K+ IN per ATP hydrolysed
• Maintains electrochemical gradient
• Consumes 20-30% of cellular ATP at rest

Regulation:

• Insulin: Stimulates Na-K-ATPase activity → K+ shift into cells
• Catecholamines (β2-receptors): Stimulate Na-K-ATPase → K+ shift into cells
• Aldosterone: Long-term upregulation of Na-K-ATPase expression
• Thyroid hormone: Increases Na-K-ATPase expression
• Digoxin: INHIBITS Na-K-ATPase → impairs K+ uptake, explains K+ sensitivity

Renal Potassium Handling

Overview of Renal K+ Excretion (PMID: 26452653):

Daily K+ balance:

• Intake: 40-120 mmol/day (Western diet)
• Renal excretion: 90% (~90 mmol/day)
• GI excretion: 10% (~10 mmol/day)
• Sweat: Negligible

Nephron K+ Handling:

Aldosterone and Potassium (PMID: 23613517):

Aldosterone is the primary hormonal regulator of K+ excretion:

1. Released from adrenal cortex in response to:
   • Hyperkalemia (direct effect on zona glomerulosa)
   • Angiotensin II (RAAS activation)
   • ACTH
2. Actions on principal cells of collecting duct:
   • Increases ENaC expression → Na+ reabsorption → luminal electronegativity
   • Increases ROMK channel expression → K+ secretion
   • Increases Na-K-ATPase activity
3. Time course:
   • Aldosterone release: Minutes after hyperkalemia
   • Genomic effects: 1-2 hours for channel/transporter upregulation
   • Peak kaliuresis: 4-6 hours

Clinical Implications:

• ACE inhibitors/ARBs: Block RAAS → reduced aldosterone → hyperkalemia risk
• K+-sparing diuretics: Block aldosterone effect (spironolactone) or ENaC (amiloride) → hyperkalemia
• Loop/thiazide diuretics: Increase distal Na+ delivery → increased K+ secretion → hypokalemia

Cellular Redistribution of Potassium

Factors Causing K+ Shift INTO Cells (Lower Serum K+) (PMID: 26452653):

Factors Causing K+ Shift OUT OF Cells (Raise Serum K+):

Acid-Base Effects on Potassium (PMID: 25359368):

Important nuance:

• Mineral acidosis (HCl, NH4Cl): Strong K+ shift out of cells (~0.6 mmol/L per 0.1 pH decrease)
• Organic acidosis (lactic, ketoacidosis): Minimal K+ shift (lactate/ketones enter cells with H+)
• Respiratory acidosis: Variable, less pronounced effect than metabolic acidosis
• Alkalosis: K+ shifts into cells (~0.2-0.4 mmol/L per 0.1 pH increase)

Cardiac Electrophysiology and Potassium

Action Potential Phases and K+ Effects (PMID: 25359368):

ECG Changes in Hyperkalemia (Progressive) (PMID: 28143600):

WARNING: ECG changes may occur at any K+ level and do not reliably correlate with serum levels. Some patients develop cardiac arrest at K+ 6.5, others tolerate 8.0. Always treat ECG changes immediately.

ECG Changes in Hypokalemia (PMID: 31340166):

U Wave: Small positive deflection after T wave, most visible in V2-V3. Becomes prominent in hypokalemia.

Pharmacology of Potassium-Modifying Drugs

Hyperkalemia Treatment Agents:

Calcium (Gluconate or Chloride) (PMID: 28143600):

• Mechanism: Raises threshold potential, does NOT lower K+. Widens gap between resting and threshold potentials, restoring normal excitability.
• Onset: 1-3 minutes
• Duration: 30-60 minutes
• Dosing:
  • "Calcium gluconate 10%: 10-20 mL (2.2-4.6 mmol Ca2+) IV over 2-5 min"
  • "Calcium chloride 10%: 5-10 mL (3.4-6.8 mmol Ca2+) IV via CVC over 2-5 min"
• Adverse effects: Bradycardia if given too fast, tissue necrosis (CaCl2 peripheral), digoxin interaction (may precipitate arrhythmia - give slowly over 20-30 min)
• Repeat: Can repeat every 5-10 minutes if ECG changes persist

Insulin + Glucose (PMID: 26272582):

• Mechanism: Insulin stimulates Na-K-ATPase, shifts K+ intracellularly
• Onset: 15-30 minutes
• Peak effect: 30-60 minutes
• Duration: 4-6 hours
• K+ lowering: 0.5-1.2 mmol/L
• Dosing:
  • "Insulin: 10 units regular insulin IV"
  • "Glucose: 25 g (50 mL 50% dextrose, or 250 mL 10% dextrose)"
  • "If BSL >15 mmol/L: May give insulin without glucose"
• Adverse effects: Hypoglycemia (10-75% incidence), monitor BSL every 30 min for 6 hours
• Australian practice: Some centres use higher glucose (50g) to reduce hypoglycemia risk

Salbutamol (Nebulised) (PMID: 28143600):

• Mechanism: β2-adrenergic stimulation → cAMP → Na-K-ATPase activation
• Onset: 15-30 minutes
• Duration: 2-4 hours
• K+ lowering: 0.5-1.0 mmol/L (additive with insulin)
• Dosing: 10-20 mg nebulised (2.5-5 mg MDI with spacer less effective)
• Adverse effects: Tachycardia, tremor, hypokalaemia (paradoxically), lactic acidosis
• Caution: 20-40% of dialysis patients are "non-responders"

Sodium Bicarbonate (PMID: 28143600):

• Mechanism: Alkalinisation shifts K+ into cells (in theory)
• Efficacy: POOR as monotherapy; may be useful if concurrent severe metabolic acidosis
• Onset: Variable, unpredictable
• Dosing: 50-100 mmol (50-100 mL of 8.4%) IV over 5-10 min
• Adverse effects: Fluid overload, hypernatraemia, paradoxical intracellular acidosis
• Current recommendation: NOT first-line; consider only if pH <7.1 and ONLY with other therapies

Potassium Binders:

Dialysis (PMID: 28143600):

• Mechanism: Direct removal of K+ from blood
• Efficacy: Most effective K+ removal
• K+ removal rates:
  • "IHD: 30-40 mmol/hour (1-2 mmol/L reduction per hour)"
  • "CRRT: 10-20 mmol/hour (slower but continuous)"
• Indications: Severe hyperkalemia (>6.5), refractory to medical therapy, oliguric AKI, ongoing K+ release (rhabdomyolysis, tumour lysis)
• Australian context: Most ICUs have CRRT capability; IHD available in tertiary centres

Hypokalemia Treatment Agents:

Potassium Chloride (IV) (PMID: 31340166):

• Formulation: 1 g KCl = 13.4 mmol K+; commonly 10 mmol/100 mL or 20 mmol/100 mL
• Peripheral IV: Maximum 10 mmol/hour (40 mmol/L concentration) due to pain/phlebitis
• Central IV: Maximum 20-40 mmol/hour (emergency only, with continuous ECG)
• Expected rise: 10 mmol KCl increases serum K+ by ~0.1 mmol/L (highly variable due to transcellular shifts)
• Total body deficit estimation:
  • "K+ 3.0-3.5 mmol/L: ~100-200 mmol deficit"
  • "K+ 2.5-3.0 mmol/L: ~200-400 mmol deficit"
  • "K+ <2.5 mmol/L: ~400-800 mmol deficit"

Magnesium Replacement (PMID: 24445866):

• Essential in refractory hypokalemia: Mg2+ is cofactor for Na-K-ATPase; hypomagnesemia causes renal K+ wasting
• Dosing: MgSO4 10-20 mmol (2.5-5 g) IV over 1-2 hours
• Target: Serum Mg2+ >0.8 mmol/L (preferably >1.0 mmol/L)

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Clinical Presentation

ICU Admission Scenarios

Typical Hyperkalemia Presentations:

Scenario 1: CKD Patient with Medication Non-Compliance

• History: 68-year-old male with CKD Stage 5, missed dialysis sessions, taking lisinopril and spironolactone
• Observations: HR 45, BP 90/60, RR 20, weakness in legs
• ECG: Wide QRS (140 ms), peaked T waves, absent P waves
• K+: 7.8 mmol/L, Creatinine 890 μmol/L

Scenario 2: Post-Cardiac Arrest

• History: 72-year-old male with VF cardiac arrest, 20 minutes CPR, ROSC achieved
• Observations: Intubated, HR 95 (paced), BP 85/50 on noradrenaline
• ECG: Sinus with peaked T waves
• K+: 6.9 mmol/L (ischaemia-reperfusion injury)

Scenario 3: Rhabdomyolysis Following Crush Injury

• History: 45-year-old male, earthquake victim, prolonged entrapment
• Observations: HR 110, BP 130/85, dark urine, leg compartments tense
• K+: 7.2 mmol/L, CK >100,000 U/L, myoglobinuria

Scenario 4: Tumour Lysis Syndrome

• History: 55-year-old female with high-grade lymphoma, Day 2 post-chemotherapy
• Observations: HR 100, BP 140/90, oliguria
• K+: 6.8 mmol/L, phosphate 3.2 mmol/L, urate 0.9 mmol/L, Ca2+ 1.8 mmol/L

Typical Hypokalemia Presentations:

Scenario 1: Post-Cardiac Surgery with Diuretics

• History: 65-year-old male, Day 3 post-CABG, on frusemide infusion
• Observations: HR 100 with frequent VPBs, BP 110/70
• ECG: Prominent U waves, T wave flattening, ventricular ectopy
• K+: 2.7 mmol/L, Mg2+ 0.6 mmol/L

Scenario 2: DKA Treatment

• History: 28-year-old female with Type 1 DM, presenting K+ 5.8 mmol/L, now on insulin infusion
• Observations: HR 110, BP 100/60, polyuric
• K+: 2.5 mmol/L (after 6 hours insulin therapy)

Scenario 3: Digoxin Toxicity with Hypokalemia

• History: 78-year-old female on digoxin for AF, recent gastroenteritis
• Observations: HR 45 (heart block), BP 95/55, nausea, visual disturbance
• ECG: Complete heart block with junctional escape, ST scooping
• K+: 2.8 mmol/L, Digoxin level 3.8 nmol/L (toxic)

Symptoms and Signs

Hyperkalemia (PMID: 28143600):

Neuromuscular:

• Muscle weakness (ascending, proximal > distal)
• Paraesthesias
• Muscle cramps
• Areflexia
• Flaccid paralysis (severe)
• Respiratory muscle weakness (life-threatening)

Cardiovascular:

• Palpitations
• Bradycardia
• Hypotension (cardiogenic)
• Cardiac arrest (VF, asystole)

Gastrointestinal:

• Nausea, vomiting
• Diarrhoea
• Ileus

NOTE: Symptoms often absent until severe hyperkalemia; ECG changes may be first sign.

Hypokalemia (PMID: 31340166):

Neuromuscular:

• Muscle weakness (proximal > distal, lower limbs first)
• Muscle cramps
• Myalgia
• Rhabdomyolysis (severe)
• Respiratory muscle weakness
• Paralysis

Cardiovascular:

• Palpitations
• Arrhythmias (atrial and ventricular)
• Torsades de Pointes
• Digoxin toxicity potentiation

Gastrointestinal:

• Constipation
• Ileus
• Nausea

Renal:

• Polyuria (nephrogenic DI)
• Metabolic alkalosis (renal HCO3 retention)

Severity Scoring and Risk Stratification

Hyperkalemia Cardiac Arrest Risk Stratification (PMID: 28143600):

Hypokalemia Risk Stratification:

Differential Diagnosis

Hyperkalemia - Rule Out:

1. Pseudohyperkalemia: Haemolysis, thrombocytosis, leukocytosis, prolonged tourniquet, fist clenching - Repeat sample
2. Laboratory error: Send fresh sample to verify

True Hyperkalemia - Causes:

1. Reduced Excretion (most common):

   • AKI, CKD, ESKD
   • Hypoaldosteronism (Addison's, Type 4 RTA, heparin)
   • K+-sparing diuretics, ACE inhibitors, ARBs, NSAIDs

2. Increased Intake:

   • Oral/IV K+ supplementation
   • Blood transfusion (especially old blood)
   • High K+ diet in setting of CKD

3. Transcellular Shift:

   • Metabolic acidosis (mineral)
   • Insulin deficiency
   • Beta-blockers
   • Digoxin toxicity
   • Succinylcholine

4. Cell Lysis:

   • Rhabdomyolysis
   • Tumour lysis syndrome
   • Massive haemolysis
   • Burns
   • Crush injury

Hypokalemia - Causes:

1. GI Losses:

   • Vomiting, NG suction (alkalosis causes renal K+ wasting)
   • Diarrhoea (direct K+ loss)
   • Laxative abuse

2. Renal Losses:

   • Diuretics (loop, thiazide)
   • Hyperaldosteronism (primary/secondary)
   • Hypomagnesemia
   • Bartter/Gitelman syndrome
   • RTA Type 1 and 2

3. Transcellular Shift:

   • Insulin
   • Beta-agonists
   • Alkalosis
   • Hypothermia (rewarming causes K+ shift back to ECF)
   • Refeeding syndrome

4. Inadequate Intake:

   • Anorexia
   • Alcoholism
   • TPN without adequate K+

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Investigations

Laboratory Investigations

Bedside Tests:

Arterial Blood Gas:

• pH: Assess acid-base status (acidosis causes K+ shift out of cells)
• K+: Point-of-care K+ useful for rapid assessment
• Lactate: May indicate tissue hypoperfusion or metformin toxicity
• Calculate anion gap if metabolic acidosis present

Blood Glucose:

• Hyperglycemia causes hyperosmolar K+ shift out of cells
• Important for insulin dosing decisions

Blood Tests:

Core Panel:

Urine Studies (for hypokalemia workup):

ECG (Critical Investigation)

Must Perform 12-Lead ECG in All Potassium Disorders:

Hyperkalemia ECG Progression (PMID: 28143600):

Stage 1 - Early (K+ ~5.5-6.0 mmol/L):

• Peaked T waves (tall, narrow, symmetric, "tented")
• Best seen in precordial leads V2-V4
• May be only early sign

Stage 2 - Moderate (K+ ~6.0-6.5 mmol/L):

• Prolonged PR interval (>200 ms)
• Flattened P waves
• Early QRS widening

Stage 3 - Severe (K+ ~6.5-7.5 mmol/L):

• Loss of P waves (atrial standstill)
• Marked QRS widening (>120 ms)
• LBBB or RBBB pattern
• ST segment changes (elevation or depression)

Stage 4 - Pre-Terminal (K+ >7.5 mmol/L):

• Sine wave pattern (QRS merges with T wave)
• Bizarre wide QRS
• May mimic STEMI

Stage 5 - Terminal:

• VF
• Asystole
• PEA

Hypokalemia ECG Changes (PMID: 31340166):

Progressive changes:

1. ST segment depression
2. T wave flattening
3. U wave appearance (positive deflection after T wave)
4. T-U fusion (apparent QT prolongation is actually QU prolongation)
5. Prominent U waves (>1 mm)
6. Torsades de Pointes (polymorphic VT with twisting axis)
7. VF

ECG Red Flags Requiring Immediate Treatment:

• Any QRS widening (>120 ms) in hyperkalemia
• Loss of P waves
• Sine wave pattern
• Torsades de Pointes in hypokalemia
• New arrhythmia with K+ abnormality

Imaging

Renal Ultrasound:

• Rule out obstructive uropathy in hyperkalemia with AKI
• Assess kidney size (small = CKD, normal = AKI)
• Evaluate for hydronephrosis

Chest X-Ray:

• Pulmonary oedema (fluid overload in AKI)
• Cardiomegaly
• Line position post-central access

Physiological Monitoring

Continuous ECG Monitoring:

• Mandatory in all moderate-severe potassium disorders
• Watch for progression of changes
• Arrhythmia detection

Telemetry/ICU Monitoring Indications:

• K+ ≥6.0 mmol/L
• K+ <3.0 mmol/L
• Any ECG changes
• On digoxin with hypokalemia
• Receiving IV potassium replacement
• Post-treatment monitoring

Frequency of K+ Monitoring:

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ICU Management

This is the core clinical section - most detailed

Hyperkalemia Emergency Management

Immediate Actions (First 15 Minutes):

Step 1: Confirm and Assess Severity

• Repeat K+ if time permits (exclude pseudohyperkalemia)
• 12-lead ECG IMMEDIATELY
• Assess haemodynamic stability

Step 2: Cardiac Membrane Stabilisation (If ECG Changes)

Calcium Gluconate 10% (PMID: 28143600):

• Dose: 10-20 mL (2.2-4.6 mmol Ca2+) IV over 2-5 minutes
• Onset: 1-3 minutes
• Duration: 30-60 minutes
• Mechanism: Raises threshold potential, restores excitability
• Can repeat: Every 5-10 minutes if ECG changes persist (max 3 doses)

OR Calcium Chloride 10% (if central line available):

• Dose: 5-10 mL (6.8-13.6 mmol Ca2+) IV over 2-5 minutes via CVC
• Higher Ca2+ content than gluconate (3× more elemental calcium per mL)
• NEVER give peripherally: Causes severe tissue necrosis

Special Consideration - Digoxin Toxicity:

• Calcium should still be given for life-threatening hyperkalemia with ECG changes
• Give SLOWLY over 20-30 minutes to reduce risk of precipitating arrhythmia
• Some sources recommend DigiFab before calcium if digoxin toxicity confirmed

Step 3: Shift Potassium Intracellularly

Insulin + Glucose (PMID: 26272582):

• Dose: Insulin 10 units regular IV bolus + Glucose 25 g (50 mL 50% dextrose OR 250 mL 10% dextrose)
• Onset: 15-30 minutes
• Peak: 30-60 minutes
• Duration: 4-6 hours
• K+ reduction: 0.5-1.2 mmol/L
• If BSL >15 mmol/L: Can give insulin alone initially

CRITICAL - Hypoglycemia Prevention:

• Monitor BSL every 30 minutes for 6 hours
• Hypoglycemia occurs in 10-75% of patients
• Give additional dextrose if BSL <6 mmol/L
• Consider dextrose 10% infusion at 50-100 mL/h post-bolus

Salbutamol Nebulised (PMID: 28143600):

• Dose: 10-20 mg via nebuliser over 10-15 minutes
• Onset: 15-30 minutes
• Duration: 2-4 hours
• K+ reduction: 0.5-1.0 mmol/L (additive with insulin)
• Adverse effects: Tachycardia, tremor, lactic acidosis
• Note: 20-40% of dialysis patients are non-responders (β-receptor downregulation)

Sodium Bicarbonate (Limited Role):

• NOT first-line monotherapy
• Consider only if concurrent severe metabolic acidosis (pH <7.1)
• Dose: 50-100 mmol (50-100 mL of 8.4%) IV over 5-10 minutes
• Effect on K+ is modest and unpredictable

Step 4: Remove Potassium from Body

Dialysis - Most Effective (PMID: 28143600):

• Indications:

  • K+ ≥6.5 mmol/L with inadequate response to medical therapy
  • Oliguric/anuric AKI
  • Ongoing K+ release (rhabdomyolysis, tumour lysis)
  • Volume overload
  • Concurrent severe metabolic acidosis

• Modality Selection:

• Dialysate K+ concentration: 0-2 mmol/L (lower for severe hyperkalemia)
• Caution: Rapid K+ removal may cause arrhythmias; monitor ECG during dialysis

Potassium Binders:

Sodium Zirconium Cyclosilicate (Lokelma) (PMID: 25415805 HARMONIZE):

• Dose: 10 g PO TDS for 48 hours (acute), then 5-10 g daily (maintenance)
• Onset: 1-2 hours
• K+ reduction: 0.7-1.1 mmol/L
• Mechanism: Non-absorbed, exchanges Na+ for K+ throughout GI tract
• PBS listed: Yes (since 2022), restricted benefit criteria
• Advantages: Faster onset than patiromer, well tolerated, can use in ileus
• Adverse effects: Oedema (sodium load), constipation

Patiromer (Veltassa) (PMID: 26272582 OPAL-HK):

• Dose: 8.4-25.2 g PO daily
• Onset: 7 hours (slower)
• K+ reduction: 0.7 mmol/L
• Mechanism: Non-absorbed polymer, exchanges Ca2+ for K+ in colon
• PBS listed: Yes, restricted benefit
• Advantages: Does not contain sodium, suitable for heart failure
• Adverse effects: Constipation, hypomagnesemia
• Drug interactions: Separate from other medications by 3 hours

Resonium A (Sodium Polystyrene Sulfonate) (PMID: 25415805):

• Dose: 15-30 g PO or 30-60 g PR (with sorbitol)
• Onset: 1-2 hours
• K+ reduction: 0.5-1.0 mmol/L
• Mechanism: Exchanges Na+ for K+ in colon
• CAUTION: GI necrosis risk with sorbitol, especially post-operative; avoid in ileus
• Not recommended in acute setting by recent guidelines (AHA 2017)

Step 5: Identify and Treat Underlying Cause

Medication Review:

• STOP: ACE inhibitors, ARBs, K+-sparing diuretics, NSAIDs, trimethoprim
• Review: Potassium supplements, TPN K+ content, blood product K+ load

Treat Underlying Condition:

• AKI: Optimise renal perfusion, remove nephrotoxins, consider RRT
• Rhabdomyolysis: Aggressive fluid resuscitation (aim UO >200 mL/h), early RRT if oliguria
• Tumour lysis syndrome: Rasburicase, allopurinol, hydration, RRT
• Addisonian crisis: Hydrocortisone, fluid resuscitation
• Acidosis: Treat underlying cause (not bicarbonate alone)

Hypokalemia Emergency Management

Immediate Actions:

Step 1: Assess Severity and Urgency

• 12-lead ECG
• Identify arrhythmia risk factors: cardiac disease, digoxin therapy, concurrent hypomagnesemia

Step 2: IV Potassium Replacement (PMID: 31340166)

Peripheral IV:

• Maximum concentration: 40 mmol/L
• Maximum rate: 10 mmol/hour
• Use large vein, dilute solution to reduce pain/phlebitis

Central IV (Emergency):

• Maximum concentration: 100-200 mmol/L
• Maximum rate: 20-40 mmol/hour (with continuous ECG monitoring)
• Requires ICU setting, continuous cardiac monitoring

Replacement Protocol:

Expected Response:

• 40 mmol KCl raises serum K+ by ~0.3-0.4 mmol/L (variable)
• Total body deficit can be 100-400+ mmol; may need prolonged replacement

Step 3: ALWAYS Correct Hypomagnesemia (PMID: 24445866)

• Mg2+ is essential cofactor for Na-K-ATPase
• Hypomagnesemia causes renal K+ wasting via ROMK channel activation
• K+ replacement will be INEFFECTIVE until Mg2+ is corrected

Magnesium Replacement:

• Dose: MgSO4 10-20 mmol (2.5-5 g) IV over 1-2 hours
• Repeat if Mg2+ remains <0.8 mmol/L
• Target: Mg2+ ≥1.0 mmol/L

Step 4: Identify and Treat Cause

GI Losses:

• Vomiting: Anti-emetics, NG suction losses replaced
• Diarrhoea: Treat cause, replace losses

Renal Losses:

• Diuretics: Reduce dose, add K+-sparing diuretic if needed
• Hyperaldosteronism: Spironolactone, investigate cause
• Bartter/Gitelman: Lifelong supplementation, NSAIDs may help

Redistribution:

• Insulin therapy (DKA): Monitor K+ hourly, replace aggressively
• Beta-agonist therapy: Monitor closely
• Alkalosis: Treat underlying cause

Step 5: Special Situations

Digoxin Toxicity with Hypokalemia (PMID: 24445866):

• Hypokalemia potentiates digoxin toxicity (both inhibit Na-K-ATPase)
• Replace K+ carefully (rapid changes can also be arrhythmogenic)
• Target K+ 4.0-5.0 mmol/L
• Consider DigiFab if significant toxicity

Torsades de Pointes (PMID: 31340166):

• IV Magnesium 2 g (8 mmol) over 2-5 minutes (even if Mg2+ normal)
• IV Potassium replacement
• Overdrive pacing or isoprenaline if bradycardic
• Stop any QT-prolonging drugs
• Avoid amiodarone (further prolongs QT)

ICU-Specific Considerations

Post-Cardiac Arrest (PMID: 30571826):

• Hyperkalemia common due to ischaemia-reperfusion injury, tissue hypoperfusion, lactic acidosis
• K+ may rise rapidly in first 1-2 hours post-ROSC
• Treat aggressively; consider early dialysis if refractory
• Monitor K+ hourly for first 6 hours
• Targeted temperature management: Hypothermia causes K+ shift into cells; rewarming causes K+ release

Massive Transfusion (PMID: 25564171):

• Stored RBCs leak K+ (up to 50 mmol/L in unit after 21 days)
• Risk factors: Rapid transfusion, hypothermia, acidosis, renal impairment
• Prevention: Use fresh blood (<7 days), warm blood, monitor K+ frequently
• Treatment: Standard hyperkalemia management; consider washed RBCs for high-risk patients

Rhabdomyolysis (PMID: 24995628):

• K+ release proportional to muscle damage
• CK >10,000 U/L significantly increases hyperkalemia risk
• Aggressive fluid resuscitation (200-300 mL/h) to maintain UO >200 mL/h
• Early dialysis if oliguria or K+ >6.5 mmol/L
• Monitor K+ every 2-4 hours during active muscle breakdown
• May need continuous K+ removal with CRRT

Tumour Lysis Syndrome (PMID: 28143600):

• Rapid cell death releases K+, phosphate, uric acid
• Risk factors: High tumour burden, rapidly proliferative malignancy, chemosensitive tumour
• Prevention: Allopurinol or rasburicase, hydration before chemotherapy
• Treatment: Aggressive hydration, rasburicase (urate), early dialysis for hyperkalemia/hyperphosphatemia
• Monitor K+, phosphate, Ca2+, urate every 6-8 hours during high-risk period

Burns (PMID: 25564171):

• Early (first 48h): Hyperkalemia from tissue destruction
• Late: Hypokalemia from diuresis, wound losses, refeeding
• Succinylcholine contraindicated 24-48 hours post-burn (upregulated receptors → massive K+ release)

DKA/HHS (PMID: 26452653):

• Presenting K+ often normal or high (despite total body K+ deficit)
• Insulin therapy causes rapid K+ shift into cells
• K+ falls 0.4-0.6 mmol/L per hour with treatment
• DO NOT start insulin if K+ <3.5 mmol/L - replace K+ first
• Replace K+ if <5.5 mmol/L before insulin; add 20-40 mmol/L to IV fluids

Australian-Specific Protocols

PBS Availability of Potassium Binders:

Therapeutic Guidelines Australia Recommendations:

• Calcium gluconate first-line for membrane stabilisation
• Insulin/glucose as primary shift therapy
• Consider salbutamol as adjunct
• Resonium not recommended for acute hyperkalemia (slow onset, GI risks)
• Newer binders (patiromer, SZC) preferred if available

State-Based Protocols:

• NSW Clinical Excellence Commission: Hyperkalemia pathway available
• Victorian Safer Care Victoria: K+ disorder guidelines
• QLD Health: Statewide protocol for electrolyte emergencies

Monitoring and Ongoing Management

Hyperkalemia Monitoring:

Hypokalemia Monitoring:

Rebound Hyperkalemia:

• Insulin/glucose effect wears off at 4-6 hours
• Salbutamol effect wears off at 2-4 hours
• Re-check K+ at 2, 4, and 6 hours post-treatment
• May need repeat dosing or dialysis

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Monitoring & Complications

ICU-Specific Monitoring

Daily Parameters:

• Serum K+: At least every 12 hours (more frequently if abnormal)
• Mg2+, Ca2+, phosphate: Daily
• Renal function (creatinine, urea): Daily
• Fluid balance: Daily (affects K+ concentration)
• Medications: Review K+-affecting drugs daily

Trend Monitoring:

• K+ trends over time
• Correlation with renal function
• Correlation with acid-base status
• Response to interventions

Complications

Complications of Hyperkalemia:

Cardiac Arrest (PMID: 28143600):

• Incidence: 10-15% of ICU cardiac arrests have hyperkalemia as contributing factor
• Rhythm: Usually VF or asystole (less commonly PEA)
• Risk factors: Rapid rise in K+, concurrent acidosis, digoxin, cardiac disease
• Management: Standard ACLS with additional calcium, consider dialysis during resuscitation

Arrhythmias:

• Bradycardia (SA node suppression)
• AV blocks (all degrees)
• Wide-complex ventricular rhythms
• VF, asystole

Neuromuscular:

• Ascending weakness
• Respiratory failure (diaphragm weakness)
• Paralysis

Complications of Hypokalemia:

Arrhythmias (PMID: 31340166):

• Atrial fibrillation/flutter
• Premature ventricular contractions
• Ventricular tachycardia
• Torsades de Pointes (polymorphic VT)
• VF

Rhabdomyolysis:

• Severe hypokalemia causes muscle cell dysfunction and breakdown
• Releases myoglobin → AKI
• Paradoxically releases K+ (may mask ongoing hypokalemia)

Ileus:

• Smooth muscle dysfunction
• May impair oral K+ absorption

Respiratory Failure:

• Respiratory muscle weakness
• May require mechanical ventilation

Digoxin Toxicity Potentiation:

• Hypokalemia increases digoxin binding to Na-K-ATPase
• Arrhythmias occur at "therapeutic" digoxin levels

Complications of Treatment:

Hyperkalemia Treatment:

• Hypoglycemia (insulin): Monitor BSL q30min for 6 hours
• Tissue necrosis (calcium chloride peripherally): Use gluconate or CVC for chloride
• Volume overload (sodium bicarbonate, Lokelma): Monitor fluid status
• GI necrosis (Resonium with sorbitol): Avoid in post-operative patients
• Arrhythmia during dialysis (rapid K+ shift): Slow dialysis rate, monitor ECG

Hypokalemia Treatment:

• Phlebitis (peripheral IV K+): Use dilute solutions, central line for concentrated
• Overcorrection (hyperkalaemia): Monitor K+ frequently
• Arrhythmia during replacement: Continuous ECG, slow rate

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Prognosis & Outcome Measures

Mortality

Hyperkalemia (PMID: 28143600, 26797972):

• Mild (5.5-5.9): No significant increase in mortality
• Moderate (6.0-6.4): 1.5× increased in-hospital mortality
• Severe (≥6.5): 3× increased in-hospital mortality
• K+ ≥7.0 with ECG changes: Up to 30% 24-hour mortality if untreated
• Post-cardiac arrest due to hyperkalemia: 60-70% in-hospital mortality

Hypokalemia (PMID: 31340166):

• K+ <3.0: 2× increased in-hospital mortality
• K+ <2.5: 4× increased mortality
• Hypokalemia in acute MI: 2× increased VF/VT risk
• Hypokalemia with digoxin: 5× increased arrhythmia mortality

Cardiac Arrest Risk Stratification

Hyperkalemia Cardiac Arrest Predictors (PMID: 28143600):

• K+ level (especially ≥7.0 mmol/L)
• Rate of K+ rise (>1 mmol/L/hour = high risk)
• ECG changes (QRS >120 ms = imminent risk)
• Concurrent hypocalcemia
• Concurrent acidosis
• Digoxin therapy
• Pre-existing cardiac disease
• Ongoing K+ release (rhabdomyolysis, tumour lysis)

Hypokalemia Cardiac Arrest Predictors:

• K+ <2.5 mmol/L
• Concurrent hypomagnesemia
• Digoxin therapy
• QT-prolonging drugs
• Pre-existing QT prolongation
• Structural heart disease
• Recent MI

Prognostic Factors

Favourable Prognosis:

• Rapidly reversible cause (medication-related, dietary)
• Normal renal function
• No structural heart disease
• Early recognition and treatment
• Normal ECG despite K+ abnormality

Poor Prognosis:

• CKD/ESKD (ongoing issue)
• Cardiac arrest presentation
• Delayed treatment
• Concurrent multi-organ failure
• Underlying malignancy (tumour lysis)
• Unable to remove precipitating medications (RAASi in heart failure)

Long-Term Outcomes

CKD Patients with Hyperkalemia (PMID: 31533907):

• 50-70% have recurrent hyperkalemia within 1 year
• Often limits RAASi therapy (cardioprotective)
• Newer K+ binders allow continued RAASi use

Quality of Life:

• Recurrent episodes require dietary restriction, frequent monitoring
• Dialysis initiation may be required for recurrent severe hyperkalemia
• Medication regimens become complex

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Progressive Difficulty Assessments

Basic Level (Foundation Knowledge)

Question 1: Definition

Q: Define hyperkalemia and hypokalemia. What are the normal reference ranges for serum potassium?

A:

• Normal serum K+: 3.5-5.0 mmol/L
• Hyperkalemia: K+ >5.5 mmol/L (mild 5.5-5.9, moderate 6.0-6.4, severe ≥6.5)
• Hypokalemia: K+ <3.5 mmol/L (mild 3.0-3.4, moderate 2.5-2.9, severe <2.5)

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Question 2: Potassium Distribution

Q: What percentage of total body potassium is intracellular vs extracellular? Why is this clinically important?

A:

• Intracellular: 98% (concentration ~150 mmol/L)
• Extracellular: 2% (concentration 3.5-5.0 mmol/L)
• Clinical importance: Small shifts between compartments cause large changes in serum K+ and can significantly affect cardiac membrane potential

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Question 3: ECG Changes

Q: List the progressive ECG changes seen in hyperkalemia in order of severity.

A:

1. Peaked T waves (tall, narrow, tented) - earliest sign
2. Prolonged PR interval
3. Flattened P waves
4. Widened QRS complex (>120 ms)
5. Loss of P waves (atrial standstill)
6. Sine wave pattern (QRS merges with T wave)
7. VF or asystole

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Question 4: Calcium Mechanism

Q: How does calcium work in hyperkalemia? Does it lower the potassium level?

A:

• Calcium does NOT lower potassium level
• Mechanism: Raises the threshold potential, widening the gap between resting membrane potential and threshold
• Effect: Restores normal cardiac excitability despite elevated K+
• Onset: 1-3 minutes; Duration: 30-60 minutes
• This is "membrane stabilisation"
• buys time for other treatments to lower K+

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Intermediate Level (Applied Knowledge)

Question 1: Case-Based Scenario

Stem: A 72-year-old male with CKD Stage 4 presents to ED with generalised weakness. He takes lisinopril and spironolactone for heart failure. K+ = 7.1 mmol/L, Creatinine 450 μmol/L. ECG shows wide QRS (145 ms) with peaked T waves.

Q1: What is your immediate management? (5 marks)

A1:

1. Call for help, prepare for potential cardiac arrest (1 mark)
2. Calcium gluconate 10% 10-20 mL IV over 2-5 min (membrane stabilisation) (1 mark)
3. Insulin 10 units IV + Glucose 25 g (50 mL 50% dextrose) (1 mark)
4. Salbutamol 10-20 mg nebulised (1 mark)
5. Stop lisinopril and spironolactone, call nephrology for urgent dialysis (1 mark)

Q2: Explain why calcium is given before insulin in this patient. (3 marks)

A2:

• The wide QRS indicates severe cardiac toxicity and imminent arrest risk (1 mark)
• Calcium works within 1-3 minutes to stabilise cardiac membrane (1 mark)
• Insulin takes 15-30 minutes to shift K+ - too slow if cardiac arrest imminent (1 mark)

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Question 2: Medication Interaction

Q: A patient on digoxin develops K+ 2.6 mmol/L. Why is this particularly dangerous, and how should you manage this?

A: Danger:

• Both digoxin and hypokalemia affect Na-K-ATPase
• Hypokalemia increases digoxin binding to Na-K-ATPase
• Results in enhanced digoxin toxicity at "therapeutic" levels
• Significantly increased arrhythmia risk

Management:

• Check digoxin level (may be therapeutic but toxic)
• IV potassium replacement with continuous ECG monitoring
• Replace magnesium (also affects digoxin toxicity)
• Target K+ 4.0-5.0 mmol/L
• Consider DigiFab if significant digoxin toxicity
• Slow, careful replacement (rapid changes also arrhythmogenic)

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Question 3: Refractory Hypokalemia

Q: A patient's K+ remains 2.9 mmol/L despite receiving 80 mmol KCl over 8 hours. What is the most likely reason, and what should you do?

A: Most likely reason: Concurrent hypomagnesemia

Explanation:

• Mg2+ is a cofactor for Na-K-ATPase function
• Hypomagnesemia activates ROMK channels causing renal K+ wasting
• K+ replacement is ineffective until Mg2+ is corrected

Action:

• Check serum Mg2+
• Replace with MgSO4 10-20 mmol IV over 1-2 hours
• Target Mg2+ ≥1.0 mmol/L
• Continue K+ replacement concurrently

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Exam Level (CICM Second Part Standard)

See SAQ Practice section below.

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SAQ Practice (Full Exam-Level)

SAQ 1: Hyperkalemia Emergency

Time Allocation: 10 minutes
Total Marks: 20

Stem: A 58-year-old male with Type 2 diabetes and CKD Stage 4 (eGFR 22 mL/min) presents to ICU following a witnessed collapse at home. Paramedics documented VF arrest with ROSC after 12 minutes of CPR and 3 shocks.

Medications: Metformin, lisinopril, spironolactone, atorvastatin

Observations on arrival to ICU:

• Intubated and sedated
• HR: 55 bpm (sinus bradycardia)
• BP: 95/60 mmHg on noradrenaline 0.15 mcg/kg/min
• Temperature: 35.5°C (targeted temperature management initiated)

Investigations:

ABG (FiO2 0.6):

• pH: 7.18
• PaCO2: 38 mmHg
• PaO2: 145 mmHg
• HCO3: 14 mmol/L
• Lactate: 6.8 mmol/L
• K+: 7.4 mmol/L

Bloods:

• Creatinine: 580 μmol/L (baseline 220)
• CK: 12,500 U/L
• Troponin: 850 ng/L

ECG: Sinus bradycardia 55/min, QRS 148 ms, peaked T waves V1-V4, no P waves visible

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Question 1.1 (8 marks)

Outline your immediate management of the hyperkalemia in this patient, including specific drug doses and monitoring.

Question 1.2 (6 marks)

Discuss the pathophysiological mechanisms contributing to hyperkalemia in this patient.

Question 1.3 (6 marks)

What are the indications for renal replacement therapy in this patient, and what modality would you choose? Justify your answer.

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Model Answer SAQ 1

Question 1.1 (8 marks total)

Immediate Management of Hyperkalemia:

1. Cardiac Membrane Stabilisation (2 marks)

• Calcium gluconate 10% 20 mL IV over 2-5 minutes (0.5 marks)
• Can repeat after 5 minutes if ECG changes persist (0.5 marks)
• Monitor ECG continuously for response (narrowing of QRS) (0.5 marks)
• Duration of effect 30-60 minutes - need follow-up treatments (0.5 marks)

2. Shift Potassium Intracellularly (2 marks)

• Insulin 10 units regular IV bolus (0.5 marks)
• PLUS Glucose 25 g (50 mL 50% dextrose) IV (0.5 marks)
• Monitor BSL every 30 minutes for 6 hours (hypoglycemia risk) (0.5 marks)
• Salbutamol 20 mg nebulised as adjunct (0.5 marks)

3. Prepare for Potassium Removal (2 marks)

• Urgent nephrology consultation for dialysis (0.5 marks)
• CRRT preferred due to haemodynamic instability (0.5 marks)
• Insert dialysis access (vascath) (0.5 marks)
• Sodium zirconium cyclosilicate 10 g PO/NG as adjunct if available (0.5 marks)

4. Address Precipitants (2 marks)

• Stop lisinopril and spironolactone (0.5 marks)
• Stop metformin (lactic acidosis, renal failure) (0.5 marks)
• Repeat K+ in 1 hour to assess response (0.5 marks)
• Optimise volume status and renal perfusion (0.5 marks)

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Question 1.2 (6 marks total)

Pathophysiological Mechanisms of Hyperkalemia:

1. Pre-existing Renal Impairment (1 mark)

• CKD Stage 4 (eGFR 22) → reduced renal K+ excretion capacity
• Baseline vulnerability to hyperkalemia

2. Medication-Related (1 mark)

• Lisinopril (ACE inhibitor) → reduced aldosterone → impaired renal K+ secretion
• Spironolactone (K+-sparing diuretic) → blocks aldosterone receptor → further impairs K+ secretion
• Combined RAASi blockade in CKD = high risk

3. Acute Kidney Injury (1 mark)

• Creatinine risen from 220 to 580 (AKI on CKD)
• Likely combination of prerenal (arrest/hypoperfusion) and ischaemic ATN
• Oliguria/anuria → inability to excrete K+

4. Ischaemia-Reperfusion Injury (1 mark)

• Cardiac arrest with 12 minutes CPR → global tissue ischaemia
• Reperfusion after ROSC releases intracellular K+ from damaged cells
• Elevated CK (12,500) indicates muscle breakdown (possible rhabdomyolysis component)

5. Metabolic Acidosis (1 mark)

• pH 7.18 with metabolic acidosis (low HCO3)
• Lactic acidosis from tissue hypoperfusion
• H+ enters cells, K+ exits to maintain electroneutrality
• ~0.6 mmol/L K+ rise per 0.1 pH decrease (mineral acidosis)

6. Hypothermia (1 mark)

• Targeted temperature management at 35.5°C
• Hypothermia initially causes K+ shift into cells
• BUT reduced renal function and drug metabolism may contribute
• Rewarming will cause K+ shift back to ECF (monitor closely)

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Question 1.3 (6 marks total)

Indications for RRT:

Absolute Indications Present (3 marks)

• Severe hyperkalemia (K+ 7.4) with ECG changes refractory/likely refractory to medical therapy (1 mark)
• Severe metabolic acidosis (pH 7.18) contributing to haemodynamic instability (1 mark)
• Oliguria/AKI with ongoing K+ release (ischaemia-reperfusion, possible rhabdomyolysis) - medical therapy alone will not address ongoing K+ load (1 mark)

Modality Selection: CRRT (CVVHDF) (3 marks)

Rationale:

• Haemodynamic instability (on vasopressors) - CRRT better tolerated than IHD (1 mark)
• Continuous K+ removal matches ongoing K+ release from tissue injury (1 mark)
• Allows concurrent targeted temperature management without thermal instability (0.5 marks)
• Provides continuous acid-base correction (0.5 marks)

CRRT Prescription:

• Modality: CVVHDF at 25-30 mL/kg/h
• Dialysate K+: 2 mmol/L initially (not 0, to avoid rapid shifts)
• Anticoagulation: Citrate preferred (reduced bleeding risk post-arrest)
• Monitor K+ hourly during initiation

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Common Mistakes:

• Not giving calcium first (goes straight to insulin)
• Using calcium chloride peripherally
• Not recognising multiple contributing mechanisms
• Choosing IHD in unstable patient
• Forgetting to stop offending medications

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SAQ 2: Hypokalemia with Arrhythmia

Time Allocation: 10 minutes
Total Marks: 20

Stem: A 68-year-old female is Day 4 post-CABG × 3 (LIMA-LAD, SVG-OM, SVG-RCA). She has been receiving frusemide 80 mg IV BD for fluid management. The nurse calls you urgently as the patient has developed palpitations and lightheadedness.

Past Medical History: Hypertension, Type 2 DM, chronic AF (on digoxin 125 mcg daily)

Observations:

• HR: 140 bpm (irregularly irregular with frequent VPBs)
• BP: 95/55 mmHg
• RR: 22
• SpO2: 94% on 2L NC
• Alert but anxious

Investigations:

ECG: AF with RVR ~140/min, frequent multifocal VPBs, non-sustained VT (3-beat run), prominent U waves V2-V4, QTc 520 ms

Bloods:

• K+: 2.4 mmol/L
• Mg2+: 0.58 mmol/L
• Digoxin: 2.6 nmol/L (therapeutic range 0.6-1.3)
• Creatinine: 145 μmol/L (baseline 110)

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Question 2.1 (8 marks)

Outline your immediate management of this patient, including specific interventions and monitoring.

Question 2.2 (6 marks)

Explain the interaction between hypokalemia, hypomagnesemia, and digoxin toxicity in causing arrhythmias.

Question 2.3 (6 marks)

How would you manage this patient's electrolyte replacement over the next 24 hours? Include specific targets and monitoring.

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Model Answer SAQ 2

Question 2.1 (8 marks total)

Immediate Management:

1. Stabilise and Monitor (2 marks)

• Transfer to ICU/CCU for continuous monitoring (0.5 marks)
• Continuous ECG monitoring - watch for VT/VF, Torsades (0.5 marks)
• IV access, supplemental oxygen (0.5 marks)
• Have defibrillator and pacing equipment available (0.5 marks)

2. Treat Hypomagnesemia FIRST (2 marks)

• MgSO4 10 mmol (2.5 g) IV over 10-20 minutes (can give rapidly if VT) (1 mark)
• Mg2+ is cardioprotective, reduces digoxin toxicity, and essential for K+ repletion (1 mark)

3. Treat Hypokalemia (2 marks)

• Central IV access for rapid K+ replacement (0.5 marks)
• KCl 20-40 mmol/h via central line with continuous ECG (0.5 marks)
• Target K+ 4.0-4.5 mmol/L (higher target due to digoxin) (0.5 marks)
• Check K+ every 2 hours during replacement (0.5 marks)

4. Address Digoxin Toxicity (2 marks)

• Hold digoxin (0.5 marks)
• Consider DigiFab if life-threatening arrhythmia develops (VT, high-grade AV block) (0.5 marks)
• DigiFab dosing: Number of vials = (digoxin level in ng/mL × weight in kg) / 100 (0.5 marks)
• Avoid cardioversion if possible (may precipitate refractory VF) until digoxin level falls (0.5 marks)

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Question 2.2 (6 marks total)

Interaction Between Hypokalemia, Hypomagnesemia, and Digoxin:

1. Digoxin Mechanism and K+ Interaction (2 marks)

• Digoxin inhibits Na-K-ATPase on cardiac myocytes (0.5 marks)
• Hypokalemia increases digoxin binding affinity to Na-K-ATPase (0.5 marks)
• Results in enhanced digoxin effect (toxicity) at "therapeutic" levels (0.5 marks)
• Leads to increased intracellular Ca2+ → triggered arrhythmias (DADs) (0.5 marks)

2. Hypomagnesemia Effects (2 marks)

• Mg2+ is cofactor for Na-K-ATPase function (0.5 marks)
• Hypomagnesemia → reduced Na-K-ATPase activity → enhanced digoxin effect (0.5 marks)
• Mg2+ also stabilises cardiac membrane and suppresses afterdepolarizations (0.5 marks)
• Mg2+ deficiency causes renal K+ wasting (ROMK channel activation) → worsens hypokalemia (0.5 marks)

3. Combined Arrhythmogenic Effect (2 marks)

• Hypokalemia causes prolonged repolarization (QT prolongation, U waves) (0.5 marks)
• Digoxin toxicity causes DADs (delayed afterdepolarizations) and triggered activity (0.5 marks)
• Combination creates substrate for both triggered arrhythmias (VPBs, VT) and re-entry (0.5 marks)
• Both must be corrected for arrhythmia control - K+ replacement ineffective without Mg2+ (0.5 marks)

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Question 2.3 (6 marks total)

Electrolyte Replacement Strategy (24 hours):

1. Potassium Replacement (2 marks)

• Acute phase: KCl 20-40 mmol/h via central line until K+ >3.5 mmol/L (0.5 marks)
• Maintenance: 10-20 mmol/h until K+ 4.0-4.5 mmol/L (0.5 marks)
• Estimate total deficit: K+ 2.4 = ~400 mmol deficit (0.5 marks)
• Do NOT replace too rapidly - risk of rebound hyperkalemia and arrhythmias (0.5 marks)

2. Magnesium Replacement (2 marks)

• Acute: MgSO4 20 mmol (5 g) IV over 2-4 hours (0.5 marks)
• Check Mg2+ at 4 hours - repeat if <0.8 mmol/L (0.5 marks)
• Target Mg2+ ≥1.0 mmol/L (0.5 marks)
• Continue maintenance 10-20 mmol/day until levels stable (0.5 marks)

3. Monitoring Plan (2 marks)

• K+ every 2 hours during active replacement, then 4-hourly (0.5 marks)
• Mg2+ every 6-8 hours (0.5 marks)
• Continuous ECG for arrhythmia detection and QT monitoring (0.5 marks)
• Digoxin level in 24-48 hours (after distribution phase) (0.5 marks)

Targets:

• K+ 4.0-4.5 mmol/L (higher target due to digoxin)
• Mg2+ ≥1.0 mmol/L
• QTc normalisation
• Resolution of VPBs/non-sustained VT

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Common Mistakes:

• Replacing K+ without replacing Mg2+ first
• Using cardioversion for AF (dangerous with digoxin toxicity)
• Replacing K+ too aggressively (causing overcorrection)
• Not recognising the synergistic toxicity of all three factors
• Forgetting to stop digoxin

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Hot Case Scenarios

Hot Case 1: Post-Cardiac Surgery Hyperkalemia

Setting: ICU Bed 6
Duration: 20 minutes (10 min assessment + 10 min discussion)

Actor/Simulator Briefing:

Patient Details:

• Age: 67 years
• Gender: Male
• Admission diagnosis: CABG × 4, Day 1 post-operative
• Aboriginal Australian from remote Northern Territory community

History (if asked):

• Presented with unstable angina 3 days ago
• Transferred from Alice Springs Hospital
• Past history: T2DM, CKD Stage 3b (eGFR 38), HTN
• Medications pre-op: Metformin, lisinopril, aspirin, atorvastatin
• Family present at bedside, concerned about complications
• Cultural liaison officer available

Examination Findings:

• General: Intubated, sedated, RASS -2
• Airway: ETT in situ, secured at 23 cm
• Breathing: Mechanical ventilation, clear chest, bilateral air entry
• Circulation: Epicardial pacing wires in situ (not pacing), HR 48 (sinus bradycardia), BP 92/55 on noradrenaline 0.1 mcg/kg/min, cool peripheries
• Disability: Pupils 3 mm bilateral reactive, sedated
• Exposure: Median sternotomy dressing dry, chest drains 200 mL total, UO 15 mL last hour

Charts/Data Available:

• Admission K+ (theatre): 4.2 mmol/L
• Current K+ (ICU, 6 hours post-op): 6.9 mmol/L
• Creatinine: 285 μmol/L (baseline 180)
• Hb: 82 g/L
• Lactate: 4.2 mmol/L
• pH: 7.26, pCO2 36, HCO3 16
• Received 6 units PRBC intraoperatively

ECG: Sinus bradycardia 48/min, peaked T waves, QRS 128 ms

Current Management:

• Ventilator: SIMV, FiO2 0.4, PEEP 5
• Noradrenaline 0.1 mcg/kg/min
• Propofol 50 mg/h
• Fentanyl 50 mcg/h
• Heparin 500 units/h

---

Expected Performance:

Assessment Phase (10 minutes):

Systematic A-E Examination:

• A: ETT secure, appropriate position
• B: Clear lungs, appropriate ventilation
• C: Bradycardia 48 (RED FLAG - may be hyperkalemia-related), hypotension, low UO (oliguric AKI), cool peripheries, epicardial wires available
• D: Appropriately sedated
• E: Recent cardiac surgery, chest drains patent

Key Findings to Identify:

• Hyperkalemia 6.9 mmol/L with ECG changes (peaked T, widened QRS)
• Oliguric AKI (15 mL/h, creatinine risen)
• Metabolic acidosis (pH 7.26, low HCO3)
• Elevated lactate (low cardiac output, tissue hypoperfusion)
• Bradycardia (hyperkalemia effect)
• Massive transfusion (6 units PRBC - K+ load from stored blood)
• CKD baseline (impaired K+ excretion)

One-Minute Summary: "This is a 67-year-old Aboriginal man, Day 1 post-CABG × 4, with severe hyperkalemia (K+ 6.9) and ECG changes including bradycardia and wide QRS. He has oliguric AKI with metabolic acidosis and is on vasopressor support. This is a life-threatening emergency requiring immediate cardiac membrane stabilisation with calcium, followed by potassium-shifting therapies and likely renal replacement therapy. Key contributing factors include massive transfusion, baseline CKD, pre-operative RAASi use, and post-operative low cardiac output state."

---

Discussion Phase:

Q1: "What is your immediate management?"

Expected Answer:

1. Calcium gluconate 10% 20 mL IV over 2-5 minutes (membrane stabilisation)
2. Insulin 10 units + glucose 25 g IV (K+ shift)
3. Consider temporary epicardial pacing if bradycardia worsens
4. Salbutamol 20 mg nebulised (additive shift)
5. Urgent nephrology referral for RRT
6. Stop heparin infusion, hold ACE inhibitor
7. Repeat K+ in 1 hour

Q2: "What are the causes of hyperkalemia in this patient?"

Expected Answer:

• Massive transfusion (stored blood K+ 20-50 mmol/L per unit)
• Pre-existing CKD (impaired excretion)
• Pre-operative lisinopril (impaired aldosterone)
• Post-operative AKI (low cardiac output, CPB-related injury)
• Metabolic acidosis (H+/K+ shift)
• Possible ongoing myocardial ischaemia/injury

Q3: "The family is very anxious. How would you communicate with them?"

Expected Answer:

• Acknowledge their concerns and the seriousness of the situation
• Involve Aboriginal Health Worker/cultural liaison officer
• Use simple language, avoid medical jargon
• Explain the problem (potassium too high, affecting heart rhythm)
• Explain immediate treatment plan
• Ensure family has opportunity to ask questions
• Offer to have family present (if appropriate for culture)
• Regular updates

Q4: "When would you consider dialysis?"

Expected Answer:

• If K+ does not respond to medical therapy (remains >6.5 after 1-2 hours)
• If ongoing K+ load expected (ongoing low cardiac output, continuing transfusion)
• If oliguric/anuric AKI persists
• If severe acidosis not responding to treatment
• Would use CRRT (CVVHDF) due to haemodynamic instability
• Discuss with cardiac surgery regarding anticoagulation (citrate preferred, avoid heparin if bleeding risk)

---

Hot Case 2: Digoxin Toxicity with Hypokalemia

Setting: ICU Bed 12
Duration: 20 minutes

Patient Details:

• Age: 82 years
• Gender: Female
• Māori patient from Auckland, whānau present
• Admission: Collapse at home, bradyarrhythmia

Examination Findings:

• General: Alert, nauseated, "yellow vision" reported
• A: Patent
• B: Clear, RR 18
• C: HR 38 (complete heart block with junctional escape), BP 85/50, transcutaneous pacing pads on
• D: GCS 14 (confused), visual disturbance
• E: No oedema

Data:

• K+: 2.6 mmol/L
• Mg2+: 0.52 mmol/L
• Digoxin: 4.8 nmol/L (toxic)
• Creatinine: 180 μmol/L

ECG: Complete heart block, junctional escape 38/min, ST scooping ("reverse tick"), bidirectional VT beats

---

Expected Performance:

Key Issues to Identify:

• Digoxin toxicity (level 4.8, clinical features)
• Severe hypokalemia (K+ 2.6)
• Severe hypomagnesemia (Mg2+ 0.52)
• Complete heart block (requiring pacing)
• Synergistic toxicity of all three

Management:

1. Prepare for transcutaneous pacing (bradycardia)
2. IV Magnesium 10 mmol over 10 minutes
3. IV Potassium 20-40 mmol/h via central line
4. Hold digoxin
5. DigiFab consideration (complete heart block, bidirectional VT = life-threatening)
6. Involve whānau in discussions, cultural support

DigiFab Indication:

• Life-threatening arrhythmia (complete heart block, bidirectional VT)
• Calculate dose based on digoxin level
• Expect K+ to RISE after DigiFab (releases K+ from cells as digoxin effect reversed)

---

Viva Questions

Viva 1: ECG Interpretation and Hyperkalemia Management

Stem: "A 55-year-old male with ESKD on haemodialysis missed his last two sessions. He presents to ED with weakness. This is his ECG."

[Show ECG with peaked T waves, absent P waves, wide QRS 160 ms]

Opening Question: "Describe the ECG and your immediate concerns."

Expected Answer (2-3 minutes):

• "This ECG shows severe hyperkalemia changes:
  • No visible P waves (atrial standstill)
  • Wide QRS complex (160 ms, normal <120 ms)
  • Peaked, tall T waves
  • Suggests K+ likely >7.0 mmol/L
• Immediate concerns:
  • Risk of cardiac arrest (VF or asystole) is imminent
  • The wide QRS indicates severe conduction delay
  • This is a time-critical emergency
• I would treat immediately without waiting for laboratory confirmation"

---

Follow-up Question 1: "Walk me through your management."

Expected Answer:

1. Immediate (within 60 seconds):

   • Call for help, ensure defibrillator available
   • Calcium gluconate 10% 20 mL IV over 2-5 minutes
   • Can repeat in 5 minutes if no ECG improvement

2. Next 15 minutes:

   • Insulin 10 units IV + glucose 25 g
   • Salbutamol 20 mg nebulised
   • Establish IV access, continuous ECG monitoring

3. Next 1-2 hours:

   • Urgent dialysis (patient is dialysis-dependent)
   • Contact nephrology for emergency IHD
   • Check K+ at 1 hour
   • Monitor BSL q30min for hypoglycemia

4. Address cause:

   • Determine why dialysis was missed
   • Dietary counselling
   • Social support if needed

---

Follow-up Question 2: "The patient's K+ returns at 8.1 mmol/L. You give calcium and the QRS narrows to 100 ms. What do you expect the K+ to be now?"

Expected Answer:

• "The K+ will still be 8.1 mmol/L - calcium does not lower potassium
• Calcium works by raising the threshold potential
• It restores normal cardiac excitability despite the elevated K+
• This is 'membrane stabilisation' - it buys time but doesn't treat the underlying problem
• The effect lasts only 30-60 minutes
• I need to proceed immediately with insulin/glucose and dialysis to actually lower the K+"

---

Follow-up Question 3: "The patient is stable after dialysis. His K+ is now 5.2 mmol/L. Discuss how you would prevent future episodes."

Expected Answer:

• "Prevention requires multifaceted approach:

  1. Dialysis adherence:

     • Explore barriers to attendance (transport, timing, cultural factors)
     • Social work involvement
     • Consider home dialysis if appropriate

  2. Dietary modification:

     • Dietitian referral for low-K+ diet education
     • Identify high-K+ foods patient regularly consumes
     • Culturally appropriate dietary advice

  3. Medications:

     • Consider chronic K+ binder (patiromer or SZC) if recurrent
     • Review other K+-raising medications

  4. Emergency action plan:

     • Patient education on symptoms of hyperkalemia
     • When to seek medical attention
     • Emergency contact numbers

  5. Follow-up:

     • Close nephrology follow-up
     • Frequent K+ monitoring initially"

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Viva 2: Hypokalemia Pathophysiology and Management

Stem: "A 45-year-old female presents to ICU with profound weakness. She admits to using large amounts of laxatives daily. K+ is 1.8 mmol/L."

Opening Question: "What are your immediate concerns and how would you manage this?"

Expected Answer: "This is life-threatening severe hypokalemia requiring immediate ICU management.

Immediate concerns:

• Cardiac arrhythmias (Torsades de Pointes, VF)
• Respiratory muscle weakness (may need intubation)
• Rhabdomyolysis (muscle breakdown at this K+ level)

Immediate management:

1. Continuous ECG monitoring, defibrillator available
2. Check Mg2+ (likely also low)
3. Central IV access for concentrated K+ replacement
4. MgSO4 10-20 mmol IV over 20-30 minutes
5. KCl 20-40 mmol/hour via central line
6. Frequent K+ monitoring (every 1-2 hours)
7. Monitor for respiratory compromise
8. Check CK for rhabdomyolysis"

---

Follow-up Question 1: "Why did you give magnesium before aggressive potassium replacement?"

Expected Answer: "Magnesium is critical for two reasons:

1. Na-K-ATPase function:

   • Mg2+ is an essential cofactor for Na-K-ATPase
   • Without adequate Mg2+, the pump cannot effectively transport K+ into cells
   • K+ replacement will be ineffective

2. Renal K+ wasting:

   • Hypomagnesemia activates ROMK channels in the collecting duct
   • This causes ongoing renal K+ excretion
   • Patient loses K+ as fast as we give it

3. Cardiac protection:

   • Mg2+ has independent anti-arrhythmic properties
   • Suppresses early afterdepolarisations
   • Reduces risk of Torsades de Pointes

The K+ will be refractory to replacement until Mg2+ is corrected."

---

Follow-up Question 2: "You've given 160 mmol KCl over 4 hours. The K+ has only risen from 1.8 to 2.4 mmol/L. Why?"

Expected Answer: "Several factors explain the slow response:

1. Massive total body deficit:

   • At K+ 1.8, total body deficit may be 500-1000 mmol
   • Only about 2% of administered K+ stays in serum
   • Most redistributes to intracellular compartment

2. Transcellular shift:

   • As K+ is replaced, it moves into cells
   • This is appropriate - restoring intracellular K+
   • Serum K+ rises slowly

3. Ongoing losses:

   • Need to stop laxative abuse
   • May have ongoing renal/GI losses
   • Check urine K+

4. Inadequate magnesium:

   • Recheck Mg2+ level
   • May need more Mg2+ replacement

Management:

• Continue aggressive replacement
• Address underlying cause (laxative abuse - requires psychiatric/psychological input)
• May need >500 mmol replacement over 24-48 hours"

---

Follow-up Question 3: "This patient discloses that she has anorexia nervosa and has been restricting food and using laxatives for weight control. How does this change your approach?"

Expected Answer: "This significantly changes the clinical picture:

1. Refeeding syndrome risk:

   • Very high risk given chronic starvation
   • As we replace K+ and start nutrition, phosphate will drop
   • Need to monitor phosphate, Mg2+, thiamine closely
   • Start nutrition cautiously (10-15 kcal/kg/day)

2. Other deficiencies likely:

   • Phosphate (refeeding will cause drop)
   • Thiamine (must give before glucose)
   • Multiple vitamin deficiencies

3. Multidisciplinary care:

   • Psychiatry consultation essential
   • Eating disorders specialist
   • Dietitian involvement
   • May need Medical Emergency Team for eating disorders (METED) if available

4. Medical complications to monitor:

   • Cardiac: Prolonged QT, cardiomyopathy
   • Metabolic: Hypoglycemia
   • GI: Delayed gastric emptying, constipation

5. Cultural/psychosocial:

   • Sensitive, non-judgmental approach
   • Involve family with patient consent
   • Long-term psychiatric follow-up essential"

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Interactive Elements

[INTERACTIVE: ECG Library - Potassium Disorders]

Hyperkalemia ECG Progression:

ECG 1: Mild Hyperkalemia (K+ 5.8 mmol/L)

• Findings: Peaked T waves (tall, narrow, symmetric) in V2-V4
• Normal PR, QRS, QT
• Action: Medical management, monitor closely

ECG 2: Moderate Hyperkalemia (K+ 6.5 mmol/L)

• Findings: Peaked T waves, PR interval 240 ms, P waves flattening
• QRS normal
• Action: Calcium + insulin/glucose + salbutamol

ECG 3: Severe Hyperkalemia (K+ 7.2 mmol/L)

• Findings: No visible P waves, QRS 145 ms, peaked T waves
• Action: IMMEDIATE calcium, prepare for dialysis

ECG 4: Critical Hyperkalemia (K+ 8.0 mmol/L)

• Findings: Sine wave pattern (QRS merges with T wave)
• Action: Immediate calcium, CPR standby, emergency dialysis

Hypokalemia ECG Progression:

ECG 5: Mild Hypokalemia (K+ 3.2 mmol/L)

• Findings: ST depression, T wave flattening
• Small U waves visible V2-V3

ECG 6: Moderate Hypokalemia (K+ 2.5 mmol/L)

• Findings: Prominent U waves, T wave inversion, ST depression
• QTc prolonged (actually QU interval)

ECG 7: Severe Hypokalemia (K+ 1.9 mmol/L)

• Findings: Giant U waves, T-U fusion, apparent QT >600 ms
• Frequent PVCs

ECG 8: Torsades de Pointes

• Findings: Polymorphic VT with twisting axis
• Preceded by long QT
• Action: IV Magnesium, overdrive pacing if bradycardic

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[INTERACTIVE: Potassium Calculator]

Hyperkalemia Treatment Calculator:

Input:

• Current K+ level: [___] mmol/L
• ECG changes: [None / Peaked T only / Wide QRS / Sine wave]
• Renal function: [Normal / AKI / Oliguric AKI / ESKD]

Output:

• Risk level: [Low / Moderate / High / Critical]
• Recommended treatment:
  • "Calcium gluconate: [Yes/No] - Dose: [___]"
  • "Insulin/glucose: [Yes/No] - Dose: [___]"
  • "Salbutamol: [Yes/No] - Dose: [___]"
  • "Dialysis: [Not needed / Consider / Urgent / Emergency]"

Hypokalemia Replacement Calculator:

Input:

• Current K+ level: [___] mmol/L
• Access: [Peripheral IV / Central line]
• Cardiac history: [Yes / No]
• Digoxin therapy: [Yes / No]

Output:

• Severity: [Mild / Moderate / Severe]
• Replacement rate: [___] mmol/hour
• Estimated deficit: [___] mmol
• Mg2+ check: [Recommended / Not essential]