What is the pathophysiology and management of potassium imbalance, including hypokalemia and hyperkalemia?

Pathophysiology and Management of Potassium Imbalance

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SLIDE 1: Introduction & Learning Objectives

Potassium homeostasis is critical for survival—both hypokalemia and hyperkalemia create a U-shaped mortality curve, with deviations from 4.0-5.0 mEq/L increasing cardiovascular death risk. 1

Learning Objectives:

• Understand the physiological mechanisms maintaining potassium balance
• Recognize clinical manifestations of potassium disorders
• Apply evidence-based treatment algorithms for hypo- and hyperkalemia
• Identify high-risk populations requiring intensive monitoring

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SLIDE 2: Potassium Physiology—The Foundation

Distribution & Homeostasis

• 98% of total body potassium resides intracellularly (140-150 mEq/L), with only 2% extracellular (3.5-5.0 mEq/L)—this means small serum changes reflect massive total body deficits. 2
• The kidneys are the primary regulators, excreting 90% of daily potassium intake through a highly regulated distal nephron secretory process 1, 2
• The GI tract contributes minimally under normal conditions, though becomes significant in diarrheal states 1

Key Regulatory Factors:

• Aldosterone increases distal tubular potassium secretion 2
• Insulin and β2-agonists drive potassium into cells 2
• Acid-base status: acidosis shifts K+ out of cells; alkalosis shifts K+ into cells 2
• Sodium delivery to distal nephron stimulates potassium excretion 2

MCQ #1: A 65-year-old with CKD stage 4 (eGFR 25 mL/min) has serum K+ 5.8 mEq/L. Which compensatory mechanism allows CKD patients to tolerate higher potassium levels? A) Enhanced GI potassium excretion
B) Increased aldosterone-mediated colonic secretion
C) Upregulation of distal tubular flow-dependent secretion
D) Transcellular redistribution via insulin

Answer: B 1—CKD patients develop compensatory increases in aldosterone-mediated colonic potassium secretion, allowing tolerance of K+ 3.3-5.5 mEq/L in stage 4-5 CKD versus 3.5-5.0 mEq/L in normal kidneys.

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SLIDE 3: Hypokalemia—Pathophysiology

Definition & Classification

• Mild: 3.0-3.5 mEq/L
• Moderate: 2.5-2.9 mEq/L
• Severe: <2.5 mEq/L 3, 4

Mechanisms of Hypokalemia:

1. Decreased Intake (rare as sole cause)

• Inadequate dietary potassium (<3,510 mg/day) 4
• Anorexia, alcoholism 4

2. Renal Losses (most common)

• Diuretics (loop and thiazides)—the #1 cause 3
• Hyperaldosteronism (primary or secondary) 4
• Renal tubular acidosis 3
• Hypomagnesemia (causes refractory hypokalemia by impairing Na-K-ATPase) 3

3. GI Losses

• Diarrhea, vomiting, high-output stomas 3
• Laxative abuse 4

4. Transcellular Shifts

• Insulin excess, β2-agonists, thyrotoxicosis 3
• Metabolic alkalosis 4

MCQ #2: A 45-year-old on furosemide 40 mg daily presents with K+ 2.8 mEq/L despite taking KCl 20 mEq daily. Magnesium is 1.2 mg/dL (normal 1.7-2.2). What is the MOST important next step? A) Increase KCl to 60 mEq daily
B) Add spironolactone 25 mg daily
C) Correct magnesium first with IV MgSO4
D) Switch to IV potassium replacement

Answer: C 3—Hypomagnesemia is the #1 reason for refractory hypokalemia and MUST be corrected first (target >0.6 mmol/L or >1.5 mg/dL) before potassium levels will normalize.

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SLIDE 4: Hypokalemia—Clinical Manifestations

Cardiac Effects (Most Dangerous)

• ECG changes: ST depression, T-wave flattening, prominent U waves, prolonged QT 3
• Arrhythmias: Ventricular premature beats, ventricular tachycardia, torsades de pointes, ventricular fibrillation 3
• Increased digoxin toxicity even at therapeutic digoxin levels 3

Neuromuscular Effects

• Muscle weakness, cramps, paralysis (especially with K+ <2.5 mEq/L) 4
• Rhabdomyolysis in severe cases 4
• Respiratory muscle weakness 4

Metabolic Effects

• Impaired insulin secretion (worsens hyperglycemia) 4
• Metabolic alkalosis 4
• Nephrogenic diabetes insipidus 4

MCQ #3: A 72-year-old on digoxin 0.125 mg daily for atrial fibrillation has K+ 3.2 mEq/L. ECG shows new ST depression and flattened T waves. What is the target potassium range? A) 3.5-4.0 mEq/L
B) 4.0-4.5 mEq/L
C) 4.5-5.0 mEq/L
D) 5.0-5.5 mEq/L

Answer: C 3—Patients on digoxin require aggressive potassium maintenance at 4.5-5.0 mEq/L because even modest hypokalemia dramatically increases digoxin toxicity risk and arrhythmias.

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SLIDE 5: Hypokalemia—Diagnostic Approach

Initial Assessment

1. Verify true hypokalemia (rule out pseudohypokalemia from leukocytosis) 3
2. Obtain ECG immediately if K+ <3.0 mEq/L or cardiac disease present 3
3. Check concurrent electrolytes:
   • Magnesium (ALWAYS—40% of hypokalemic patients have hypomagnesemia) 3
   • Calcium, sodium, bicarbonate 3
4. Assess renal function (creatinine, eGFR) 3

Determine Etiology

• Medication review: Diuretics, insulin, β2-agonists, corticosteroids 3
• 24-hour urine potassium or spot urine K+:
  • <20 mEq/day = extrarenal losses (GI, inadequate intake, transcellular shift) 4

  • 20 mEq/day = renal losses (diuretics, hyperaldosteronism, RTA) 4

• Acid-base status: Metabolic alkalosis suggests diuretic use or vomiting 4

MCQ #4: A 28-year-old with chronic diarrhea has K+ 2.9 mEq/L. Spot urine K+ is 15 mEq/L. What is the most likely mechanism? A) Renal tubular acidosis
B) Primary hyperaldosteronism
C) GI potassium losses
D) Diuretic abuse

Answer: C 4—Spot urine K+ <20 mEq/L with hypokalemia indicates extrarenal losses; chronic diarrhea causes massive GI potassium wasting.

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SLIDE 6: Hypokalemia—Treatment Algorithm

STEP 1: Assess Severity & Route

Indications for IV Replacement:

• K+ ≤2.5 mEq/L 3, 4
• ECG abnormalities (ST changes, U waves, arrhythmias) 3
• Severe neuromuscular symptoms (paralysis, respiratory weakness) 3
• Active cardiac arrhythmias 3
• Non-functioning GI tract 3

Oral Replacement (Preferred):

• K+ >2.5 mEq/L with functioning GI tract 3
• No ECG changes or severe symptoms 3

STEP 2: Correct Magnesium FIRST

• Target Mg >0.6 mmol/L (>1.5 mg/dL) 3
• Use organic salts (aspartate, citrate, lactate) over oxide for better absorption 3
• IV MgSO4 for severe depletion with cardiac manifestations 3

STEP 3: Potassium Replacement Dosing

Oral Replacement:

• Standard dose: KCl 20-60 mEq/day divided into 2-3 doses 3
• Expected rise: ~0.25-0.5 mEq/L per 20 mEq supplementation 3
• Target range: 4.0-5.0 mEq/L (4.5-5.0 mEq/L if on digoxin or cardiac disease) 3

IV Replacement:

• Peripheral line: Maximum 10 mEq/hour at concentration ≤40 mEq/L 3
• Central line: Up to 20 mEq/hour for severe cases with continuous cardiac monitoring 3
• Severe hypokalemia (K+ <2.0 mEq/L): May require 200-400 mEq total replacement over 24-48 hours 3

MCQ #5: A 55-year-old with K+ 2.2 mEq/L and peaked T waves on ECG requires IV replacement. What is the maximum SAFE peripheral IV rate? A) 5 mEq/hour
B) 10 mEq/hour
C) 20 mEq/hour
D) 40 mEq/hour

Answer: B 3—Peripheral IV potassium should NEVER exceed 10 mEq/hour at concentrations ≤40 mEq/L; rates >20 mEq/hour require central access and continuous cardiac monitoring.

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SLIDE 7: Hypokalemia—Special Populations & Pitfalls

Diuretic-Induced Hypokalemia

• First-line: Add potassium-sparing diuretic (spironolactone 25-100 mg, amiloride 5-10 mg, or triamterene 50-100 mg daily) rather than chronic KCl supplements 3
• Provides more stable levels without peaks/troughs 3
• Monitor K+ and creatinine at 5-7 days, then weekly until stable 3

Patients on RAAS Inhibitors

• Routine KCl supplementation may be unnecessary and dangerous when on ACE-I/ARBs alone or with aldosterone antagonists 3
• These drugs reduce renal K+ losses 3
• If adding spironolactone, STOP KCl supplements to avoid hyperkalemia 3

Heart Failure Patients

• Strict target: 4.0-5.0 mEq/L (both hypo- and hyperkalemia increase mortality) 3
• Consider aldosterone antagonists for mortality benefit while preventing hypokalemia 3

Critical Pitfalls to Avoid:

1. Never supplement K+ without checking Mg first—#1 cause of treatment failure 3
2. Never give digoxin before correcting hypokalemia—life-threatening arrhythmias 3
3. Avoid NSAIDs entirely—worsen renal function and increase hyperkalemia risk 3
4. Separate K+ supplements from other meds by 3 hours (especially with certain formulations) 3

MCQ #6: A 68-year-old on lisinopril 20 mg and furosemide 40 mg has recurrent hypokalemia despite KCl 40 mEq daily. What is the BEST long-term strategy? A) Increase KCl to 80 mEq daily
B) Switch to IV potassium weekly
C) Add spironolactone 50 mg daily and STOP KCl
D) Continue current regimen and recheck in 1 month

Answer: C 3—Potassium-sparing diuretics are superior to chronic oral supplements for diuretic-induced hypokalemia, providing stable levels; MUST stop KCl when adding spironolactone to avoid hyperkalemia.

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SLIDE 8: Hyperkalemia—Pathophysiology

Definition & Classification

• Mild: 5.0-5.9 mEq/L
• Moderate: 6.0-6.4 mEq/L
• Severe: ≥6.5 mEq/L 5

Mechanisms of Hyperkalemia:

1. Impaired Renal Excretion (dominant cause)

• Chronic kidney disease (eGFR <30 mL/min) 1, 5
• Medications: ACE-I, ARBs, MRAs, NSAIDs, trimethoprim, heparin, β-blockers 5
• Hypoaldosteronism (Addison's disease, type IV RTA) 4

2. Transcellular Shifts

• Metabolic acidosis (each 0.1 pH drop raises K+ by ~0.6 mEq/L) 4
• Insulin deficiency, hyperglycemia 4
• Tissue breakdown (rhabdomyolysis, tumor lysis syndrome, hemolysis) 4
• Succinylcholine, digitalis toxicity 4

3. Excessive Intake (only with impaired excretion)

• IV potassium, salt substitutes, high-K+ foods 5
• Blood transfusions (stored blood releases K+) 4

Cardiac Effects (Life-Threatening)

• Hyperkalemia depolarizes cardiac membranes, shortening action potentials and increasing fatal arrhythmia risk 1
• ECG changes (not always present): Peaked T waves → flattened P waves → prolonged PR → widened QRS → sine wave → asystole 5

MCQ #7: A 70-year-old with CKD stage 4 on lisinopril 10 mg and spironolactone 25 mg presents with K+ 6.8 mEq/L. ECG shows peaked T waves and widened QRS. What is the FIRST medication to administer? A) IV insulin 10 units + dextrose 25g
B) IV calcium gluconate 15-30 mL
C) Nebulized albuterol 20 mg
D) Sodium zirconium cyclosilicate 10g PO

Answer: B 5—IV calcium gluconate MUST be given first when ECG changes are present (onset 1-3 minutes) to stabilize cardiac membranes; it does NOT lower K+ but prevents arrhythmias while other therapies take effect.

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SLIDE 9: Hyperkalemia—Diagnostic Approach

STEP 1: Verify True Hyperkalemia

• Rule out pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique 5
• Repeat sample with proper technique or arterial sampling if suspected 5

STEP 2: Obtain ECG Immediately

• ECG changes indicate URGENT treatment regardless of K+ level 5
• Look for: peaked T waves, flattened P waves, prolonged PR, widened QRS 5
• ECG findings are highly variable and less sensitive than labs—absence doesn't exclude danger 5

STEP 3: Assess Clinical Context

• Symptoms: Muscle weakness, paralysis, palpitations (often nonspecific) 5
• Renal function: Creatinine, eGFR, urine output 5
• Medication review: RAAS inhibitors, K+-sparing diuretics, NSAIDs, trimethoprim, heparin 5
• Acid-base status: Venous blood gas (acidosis worsens hyperkalemia) 5

STEP 4: Identify High-Risk Populations

• CKD, diabetes, heart failure 1, 5
• Patients on RAAS inhibitors 1, 5
• Rate of rise matters—rapid increases more dangerous than gradual 1

MCQ #8: A 58-year-old with diabetes and CKD stage 3b has K+ 5.9 mEq/L. ECG shows normal sinus rhythm with no peaked T waves. What is the MOST appropriate initial management? A) IV calcium gluconate immediately
B) Insulin 10 units + dextrose 25g IV
C) Review medications, eliminate NSAIDs, initiate patiromer
D) Emergency hemodialysis

Answer: C 5—Mild-moderate hyperkalemia (5.0-5.9 mEq/L) WITHOUT ECG changes does NOT require acute interventions (calcium, insulin, albuterol); focus on medication review, eliminating contributors, and initiating potassium binders.

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SLIDE 10: Hyperkalemia—Acute Management Algorithm

TIER 1: Cardiac Membrane Stabilization (IMMEDIATE)

IV Calcium Gluconate or Calcium Chloride

• Indications: K+ ≥6.5 mEq/L OR any ECG changes 5
• Dosing:
  • Calcium gluconate 10%: 15-30 mL IV over 2-5 minutes 5
  • Calcium chloride 10%: 5-10 mL IV over 2-5 minutes (central line preferred) 5
• Onset: 1-3 minutes 5
• Duration: 30-60 minutes (temporary only) 5
• Repeat dose if no ECG improvement in 5-10 minutes 5
• CRITICAL: Calcium does NOT lower K+—only stabilizes cardiac membranes 5

TIER 2: Shift K+ Intracellularly (15-60 minutes)

Insulin + Glucose

• Dosing: Regular insulin 10 units IV + dextrose 25g (50 mL D50W) 5
• Onset: 15-30 minutes; Duration: 4-6 hours 5
• Expected K+ drop: 0.5-1.2 mEq/L 5
• Monitor glucose closely—risk of hypoglycemia 5

Nebulized Albuterol

• Dosing: 10-20 mg in 4 mL nebulized over 10 minutes 5
• Onset: 30 minutes; Duration: 2-4 hours 5
• Expected K+ drop: 0.5-1.0 mEq/L 5
• Adjunctive therapy—use with insulin for maximum effect 5

Sodium Bicarbonate (ONLY if metabolic acidosis present)

• Dosing: 50 mEq IV over 5 minutes 5
• Indications: pH <7.35, bicarbonate <22 mEq/L 5
• Onset: 30-60 minutes 5
• DO NOT use without acidosis—ineffective and wastes time 5

TIER 3: Remove K+ from Body (Definitive)

Loop Diuretics

• Dosing: Furosemide 40-80 mg IV 5
• Requires adequate renal function (eGFR >30 mL/min) 5
• Titrate to maintain euvolemia, not primarily for K+ management 5

Hemodialysis

• Most effective and reliable method for severe hyperkalemia 5
• Indications: Severe hyperkalemia unresponsive to medical management, oliguria, ESRD 5
• Removes 25-50 mEq K+ per hour 5

Potassium Binders (Chronic or Subacute)

• Sodium zirconium cyclosilicate (SZC/Lokelma): 10g PO TID x 48 hours, then 5-15g daily (onset ~1 hour) 5
• Patiromer (Veltassa): 8.4g PO daily with food, titrate to 25.2g (onset ~7 hours) 5
• Avoid sodium polystyrene sulfonate (Kayexalate)—delayed onset, risk of bowel necrosis 5

MCQ #9: A 62-year-old with ESRD on hemodialysis presents with K+ 7.2 mEq/L and sine wave pattern on ECG. After IV calcium gluconate, what are the NEXT TWO therapies to administer simultaneously? A) Insulin + glucose AND nebulized albuterol
B) Sodium bicarbonate AND furosemide
C) Patiromer AND sodium bicarbonate
D) Hemodialysis only

Answer: A 5—After calcium stabilizes the membrane, give ALL shifting agents together (insulin + glucose AND albuterol) for maximum effect; sodium bicarbonate ONLY if acidosis present; hemodialysis is definitive but takes time to arrange.

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SLIDE 11: Hyperkalemia—Chronic Management

STEP 1: Medication Optimization (DO NOT Discontinue RAAS Inhibitors)

For K+ 5.0-6.5 mEq/L on RAAS Inhibitors:

• Initiate potassium binder (patiromer or SZC) while MAINTAINING RAAS inhibitor therapy 5
• RAAS inhibitors provide mortality benefit in cardiovascular disease, heart failure, and proteinuric CKD 5
• Temporarily reduce or hold RAAS inhibitors ONLY if K+ >6.5 mEq/L, then restart at lower dose once K+ <5.0 mEq/L with concurrent binder 5

Eliminate Contributing Medications:

• NSAIDs, trimethoprim, heparin, β-blockers 5
• Potassium supplements, salt substitutes 5
• Avoid triple combination (ACE-I + ARB + MRA)—excessive hyperkalemia risk 5

STEP 2: Potassium Binder Therapy

Patiromer (Veltassa):

• Starting dose: 8.4g once daily with food 5
• Titration: Increase weekly by 8.4g increments to max 25.2g daily based on K+ 5
• Mechanism: Exchanges calcium for K+ in colon 5
• Separate from other meds by 3 hours 5
• Monitor magnesium—can cause hypomagnesemia 5

Sodium Zirconium Cyclosilicate (SZC/Lokelma):

• Acute phase: 10g PO TID x 48 hours 5
• Maintenance: 5-15g once daily 5
• Mechanism: Exchanges hydrogen and sodium for K+ 5
• Onset ~1 hour—suitable for urgent outpatient scenarios 5
• Monitor for edema (sodium content) 5

STEP 3: Dietary Counseling (Less Restrictive with Binders)

• Evidence linking dietary K+ to serum levels is limited 5
• Potassium-rich diets provide cardiovascular benefits (BP reduction) 5
• Newer binders may allow less restrictive dietary restrictions 5
• Eliminate high-K+ salt substitutes, herbal supplements (alfalfa, dandelion, horsetail, nettle) 5

STEP 4: Monitoring Protocol

• Check K+ within 1 week of starting/escalating RAAS inhibitors 5
• Reassess at 7-10 days after initiating binder therapy 5
• Individualize frequency based on: eGFR, heart failure, diabetes, history of hyperkalemia 5
• High-risk patients: Weekly during titration, then 1-2 weeks, 3 months, then every 6 months 5

MCQ #10: A 65-year-old with HFrEF on lisinopril 40 mg and spironolactone 25 mg has K+ 5.7 mEq/L. What is the BEST management strategy? A) Stop lisinopril and spironolactone permanently
B) Reduce lisinopril to 20 mg and stop spironolactone
C) Initiate patiromer 8.4g daily and MAINTAIN current RAAS therapy
D) Initiate furosemide 40 mg daily and dietary K+ restriction

Answer: C 5—NEVER permanently discontinue RAAS inhibitors in heart failure—they provide mortality benefit; instead, initiate potassium binders (patiromer or SZC) to enable continuation of life-saving medications.

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SLIDE 12: Special Populations & Clinical Pearls

CKD Patients

• Optimal K+ range is BROADER in advanced CKD: 3.3-5.5 mEq/L for stage 4-5 CKD vs. 3.5-5.0 mEq/L for stage 1-2 1, 5
• CKD patients tolerate higher K+ due to compensatory mechanisms (increased aldosterone-mediated colonic secretion) 1
• Maintain RAAS inhibitors aggressively using binders—these drugs slow CKD progression 5

Heart Failure Patients

• Strict target: 4.0-5.0 mEq/L (both hypo- and hyperkalemia increase mortality) 3, 5
• Aldosterone antagonists provide mortality benefit—use binders to enable therapy 5

Diabetic Ketoacidosis (DKA)

• Total body K+ deficit is 3-5 mEq/kg despite initially normal/elevated serum K+ 3
• Add 20-30 mEq/L K+ to IV fluids once K+ <5.5 mEq/L with adequate urine output 3
• Delay insulin if K+ <3.3 mEq/L—restore K+ first to prevent life-threatening arrhythmias 3

Hemodialysis Patients

• Target predialysis K+ 4.0-5.5 mEq/L to minimize mortality 5
• K+ can rebound 4-6 hours post-dialysis as intracellular K+ redistributes 5
• Use SZC 5g daily on non-dialysis days or patiromer 8.4g daily 5

Critical Pitfalls Across All Populations:

1. Never delay calcium if ECG changes present—waiting for repeat labs can be fatal 5
2. Never use sodium bicarbonate without metabolic acidosis—ineffective 5
3. Never give insulin without glucose—hypoglycemia is life-threatening 5
4. Remember: Calcium, insulin, and β-agonists are temporizing only—they do NOT remove K+ from the body 5

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SLIDE 13: Monitoring & Follow-Up Protocols

Hypokalemia Monitoring:

• Initial: Recheck K+ and renal function within 3-7 days after starting supplementation 3
• Titration phase: Every 1-2 weeks until values stabilize 3
• Maintenance: At 3 months, then every 6 months 3
• More frequent if: Renal impairment, heart failure, diabetes, or on medications affecting K+ 3

Hyperkalemia Monitoring:

• Acute phase: Every 2-4 hours during active treatment until stabilized 5
• Post-intervention: Within 1-2 hours after IV K+ correction or insulin/glucose 5
• RAAS inhibitor initiation: Check K+ within 7-10 days 5
• Binder therapy: Reassess at 1 week, then weekly during titration 5
• High-risk patients: Individualize based on CKD stage, heart failure, diabetes 5

Red Flags Requiring Immediate Reassessment:

• New ECG changes (either hypo- or hyperkalemia) 3, 5
• Neuromuscular symptoms (weakness, paralysis) 3, 5
• Arrhythmias 3, 5
• Acute kidney injury or worsening renal function 5
• Addition of new medications affecting K+ homeostasis 3, 5

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SLIDE 14: Team-Based Approach & Patient Education

Multidisciplinary Team:

• Cardiologists, nephrologists, primary care physicians for medication optimization 5
• Pharmacists for medication reconciliation and interaction screening 5
• Dietitians for individualized dietary counseling 5
• Nurses for patient education and monitoring adherence 5
• Social workers for access to medications and follow-up 5

Patient Education Essentials:

• Hypokalemia patients:

  • Avoid high-K+ foods when on K+-sparing diuretics 3
  • Separate K+ supplements from other meds by 3 hours 3
  • Report muscle weakness, palpitations, or cramps immediately 3

• Hyperkalemia patients:

  • Avoid salt substitutes (high K+ content) 5
  • Limit processed foods rich in bioavailable K+ 5
  • Avoid herbal supplements (alfalfa, dandelion, horsetail, nettle) 5
  • DO NOT stop RAAS inhibitors without consulting physician 5

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SLIDE 15: Take-Home Messages

Key Principles:

1. Target serum K+ 4.0-5.0 mEq/L in ALL patients—both hypo- and hyperkalemia create a U-shaped mortality curve. 1, 3

2. Hypokalemia: ALWAYS check and correct magnesium FIRST (target >0.6 mmol/L)—this is the #1 reason for treatment failure. 3

3. Hyperkalemia with ECG changes: IV calcium gluconate FIRST (onset 1-3 minutes) to stabilize cardiac membranes, then shift K+ intracellularly with insulin + glucose AND albuterol simultaneously. 5

4. NEVER permanently discontinue RAAS inhibitors for hyperkalemia in heart failure, CKD, or cardiovascular disease—use potassium binders (patiromer or SZC) to enable life-saving therapy. 5

5. Diuretic-induced hypokalemia: Potassium-sparing diuretics (spironolactone, amiloride, triamterene) are SUPERIOR to chronic oral K+ supplements—provide stable levels without peaks/troughs. 3

6. CKD patients tolerate higher K+ levels (3.3-5.5 mEq/L in stage 4-5) due to compensatory mechanisms, but maintaining 4.0-5.0 mEq/L minimizes mortality risk. 1, 5

7. Calcium, insulin, and β-agonists are temporizing measures ONLY—they do NOT remove K+ from the body; definitive treatment requires diuretics, binders, or dialysis. 5

8. Sodium polystyrene sulfonate (Kayexalate) should be AVOIDED—serious GI adverse effects including bowel necrosis; use patiromer or SZC instead. 5

9. Monitor K+ within 1 week of starting/escalating RAAS inhibitors, especially in high-risk patients (CKD, diabetes, heart failure). 5

10. Individualize monitoring frequency based on clinical context—high-risk patients need weekly checks during titration, then 1-2 weeks, 3 months, and every 6 months. 3, 5

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Final MCQ #11 (Integrative): A 58-year-old with HFrEF (EF 25%), CKD stage 3b (eGFR 38 mL/min), and diabetes on lisinopril 40 mg, spironolactone 50 mg, and furosemide 80 mg presents with K+ 6.3 mEq/L. ECG shows peaked T waves. What is the COMPLETE management strategy?

A) Stop lisinopril and spironolactone, give IV calcium, insulin + glucose, then furosemide 80 mg IV
B) IV calcium gluconate, insulin + glucose, nebulized albuterol, reduce spironolactone to 25 mg, initiate patiromer 8.4g daily, maintain lisinopril
C) Emergency hemodialysis only
D) Sodium bicarbonate 50 mEq IV, stop all RAAS inhibitors, dietary K+ restriction

Answer: B 5—Correct sequence: (1) IV calcium for ECG changes, (2) shift K+ with insulin + glucose AND albuterol, (3) reduce (not stop) spironolactone temporarily, (4) initiate binder to enable RAAS continuation, (5) maintain lisinopril for mortality benefit in HFrEF.