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REBEL Core Cast 125.0 – Hyperkalemia

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Manage episode 425734789 series 3381424
Content provided by Salim R. Rezaie, MD, Salim R. Rezaie, and MD. All podcast content including episodes, graphics, and podcast descriptions are uploaded and provided directly by Salim R. Rezaie, MD, Salim R. Rezaie, and MD or their podcast platform partner. If you believe someone is using your copyrighted work without your permission, you can follow the process outlined here https://player.fm/legal.

Take Home Points

  • Always obtain an EKG in patients with ESRD upon presentation
  • Always obtain an EKG in patients with hyperkalemia as pseudohyperkalemia is the number one cause
  • If the patient with hyperkalemia is unstable or has significant EKG changes (wide QRS, sine wave) rapidly administer calcium salts
  • In patients who are anuric, early mobilization of dialysis resources is critical

REBEL Core Cast 125.0 – Hyperkalemia

Definition: A serum potassium level > 5.5 mmol/L

Epidemiology

  • Common electrolyte disorder
  • 10% of hospitalized patients (Elliott 2010)

Causes

  • Pseudohyperkalemia: extravascular hemolysis
  • Renal failure (potassium is primarily eliminated by the kidneys)
  • Acidosis
  • Massive cell death (tumor lysis syndrome, rhabdomyolysis, burns, crush injuries, hemolysis)
  • Drugs: ACEI, ARBs, Spironalactone, NSAIDs, Succinycholine

Clinical Manifestations

  • Mild hyperkalemia often asymptomatic
  • Cardiac Effects
    • Increased potassium raises the resting membrane potential of cardiac myocytes
    • Slows ventricular conduction
    • Decreases length of action potential
    • Increases cardiac myocyte excitability
    • Cardiac effects can manifest in lethal dysrhythmias
  • Neuromuscular Effects
    • Paresthesias
    • Weakness
    • Flaccid paralysis
    • Depressed or absent deep tendon reflexes

Diagnosis

  • Suspect hyperkalemia in ALL patients with renal impairment, especially end-stage renal disease (ESRD)
  • Serum potassium
    • Can be artificially elevated by extravascular hemolysis
    • Blood gas results may differ from standard metabolic panels by up to 0.5mmol/L
  • 12-Lead EKG
    • Screening test that can rapidly detect severe cardiac manifestations of hyperkalemia
    • A normal EKG with a significant serum potassium elevation should raise concerns for spurious results (extravascular hemolysis)
    • Sensitivity of EKG to detect hyperkalemia is poor (Wrenn 1991, Aslam 2002, Montague 2008)
    • Classic EKG findings
      • PR prolongation
      • Peaked T waves
      • Loss of P waves
      • Widening of QRS complex
      • Sine wave
      • Ventricular Fibrillation
      • Asystole
    • Note: Hyperkalemia can present with a number of “non-classic” EKG findings including AV blocks and sinus bradycardia (Mattu 2000)
    • Note: Hyperkalemic EKG changes do not necessarily occur in order (i.e. patients can jump from peaked T waves to sine wave)

Management

Basics: ABCs, IV, O2, Cardiac Monitor and, 12-lead EKG

  • Identify + treat underlying cause of hyperkalemia (i.e. rhabdomyolysis -> hydration)
  • Remove inciting factors (i.e. stop ACEI, NSAIDs etc)

Asymptomatic Patients without EKG Changes

  • Eliminate potassium from the body
    • Binding agents (SPS, Sodium zirconium cyclosilicate etc)
    • Enhance renal elimination
      • Intravenous hydration if volume depleted
      • Consider potassium wasting loop diuretics (i.e. furosemide)
    • Dialysis for anuric patients (i.e. ESRD)

Symptomatic Patients or Significant EKG Changes

  • Stabilize cardiac myocytes with calcium salts
    • Mechanism: Recreates the electrical gradient leading to rapid reversal of cardiac effects and rapid stabilization
    • Two Options: CaGluconate, CaCl2
    • Onset of action: seconds to minutes
    • Duration: 20-30 minutes
  • Shift potassium into intracellular space (temporary)
    • Insulin (Moussavi 2021)
      • Mechanism: Activation of the Na-K-ATPase
      • Dose: 5-10 units IV
      • Onset of Action: < 15 min
      • Effect: Lowers potassium by about 0.6 mmol
      • Duration of action: 30-60 min
      • Give with dextrose (0.5 – 1 g/kg) unless hyperglycemia present
      • Caution: Duration of action of insulin may outlast administered dextrose. Be vigilant for hypoglycemia
    • Beta-adrenoreceptor agonists (i.e. albuterol)
      • Mechanism: Activation of beta receptors
      • Dose: 10-20 mg inhaled (4-8 standard ampules)
      • Onset of Action: < 15 min
      • Effect: Lowers potassium by about 0.6 mmol
      • Duration of action: 30-60 min
      • Additive effect with insulin (Allon 1990)
      • Note: Unlikely to have effect in patients taking beta-adrenoreceptor blocker medications
    • Sodium Bicarbonate (NaHCO3)
      • Evidence for the efficacy of NaHCO3 to lower serum potassium is scant and contradictory (Elliott 2010, Weisberg 2008)
  • Eliminate potassium from the body (see above)

Asymptomatic Patients with Minor EKG Changes

  • Minimal recommendations on managing this clinical entity
  • Eliminate potassium from the body (see above)
  • Consider calcium salt administration: patients can rapidly progress through EKG changes and calcium administration may prevent this from occurring. However, the effects of calcium are temporary and offer no long-term protection
  • Consider medications to shift potassium intracellularly while waiting for elimination

Take Home Points

  • Always obtain an EKG in patients with ESRD upon presentation
  • Always obtain an EKG in patients with hyperkalemia as pseudohyperkalemia is the number one cause
  • If the patient with hyperkalemia is unstable or has significant EKG changes (wide QRS, sine wave) rapidly administer calcium salts
  • In patients who are anuric, early mobilization of dialysis resources is critical

References

Elliott MJ et al. Management of patients with acute hyperkalemia. CMAJ 2010; 182(15): 1631-5. PMID: 20855477

Wrenn K et al. The ability of physicians to predict hyperkalemia from the ECG. Ann Emerg Med 1991; 20(11): 1229-32. PMID: 1952310

Aslam S et al. Electrocardiography is unreliable in detecting potentially lethal hyperkalaemia in hemodialysis patients. Nephrol Dial Transplant 2002; 17: 1639-42. PMID: 12198216

Montague BT et al. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol 2008; 3:324–330. PMID: 18235147

Mattu A et al. Electrocardiographic manifestations of hyperkalemia. Am J Emerg Med 2000; 18: 721-9. PMID: 11043630

Allon M, Copkney C. Albuterol and insulin for treatment of hyperkalemia in hemodialysis patients. Kidney Int 1990; 38:869–872. PMID: 2266671

Weisberg LS. Management of hyperkalemia. Crit Care Med 2008; 36: 3246-51. PMID: 18936701

Moussavi K et al. Reduced alternative insulin dosing in hyperkalemia: a meta-analysis of effects on hypoglycemia and potassium reduction. Pharmacotherapy 2021; 41(7): 598-607. PMID: 33993515

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)

The post REBEL Core Cast 125.0 – Hyperkalemia appeared first on REBEL EM - Emergency Medicine Blog.

  continue reading

25 episodes

Artwork
iconShare
 
Manage episode 425734789 series 3381424
Content provided by Salim R. Rezaie, MD, Salim R. Rezaie, and MD. All podcast content including episodes, graphics, and podcast descriptions are uploaded and provided directly by Salim R. Rezaie, MD, Salim R. Rezaie, and MD or their podcast platform partner. If you believe someone is using your copyrighted work without your permission, you can follow the process outlined here https://player.fm/legal.

Take Home Points

  • Always obtain an EKG in patients with ESRD upon presentation
  • Always obtain an EKG in patients with hyperkalemia as pseudohyperkalemia is the number one cause
  • If the patient with hyperkalemia is unstable or has significant EKG changes (wide QRS, sine wave) rapidly administer calcium salts
  • In patients who are anuric, early mobilization of dialysis resources is critical

REBEL Core Cast 125.0 – Hyperkalemia

Definition: A serum potassium level > 5.5 mmol/L

Epidemiology

  • Common electrolyte disorder
  • 10% of hospitalized patients (Elliott 2010)

Causes

  • Pseudohyperkalemia: extravascular hemolysis
  • Renal failure (potassium is primarily eliminated by the kidneys)
  • Acidosis
  • Massive cell death (tumor lysis syndrome, rhabdomyolysis, burns, crush injuries, hemolysis)
  • Drugs: ACEI, ARBs, Spironalactone, NSAIDs, Succinycholine

Clinical Manifestations

  • Mild hyperkalemia often asymptomatic
  • Cardiac Effects
    • Increased potassium raises the resting membrane potential of cardiac myocytes
    • Slows ventricular conduction
    • Decreases length of action potential
    • Increases cardiac myocyte excitability
    • Cardiac effects can manifest in lethal dysrhythmias
  • Neuromuscular Effects
    • Paresthesias
    • Weakness
    • Flaccid paralysis
    • Depressed or absent deep tendon reflexes

Diagnosis

  • Suspect hyperkalemia in ALL patients with renal impairment, especially end-stage renal disease (ESRD)
  • Serum potassium
    • Can be artificially elevated by extravascular hemolysis
    • Blood gas results may differ from standard metabolic panels by up to 0.5mmol/L
  • 12-Lead EKG
    • Screening test that can rapidly detect severe cardiac manifestations of hyperkalemia
    • A normal EKG with a significant serum potassium elevation should raise concerns for spurious results (extravascular hemolysis)
    • Sensitivity of EKG to detect hyperkalemia is poor (Wrenn 1991, Aslam 2002, Montague 2008)
    • Classic EKG findings
      • PR prolongation
      • Peaked T waves
      • Loss of P waves
      • Widening of QRS complex
      • Sine wave
      • Ventricular Fibrillation
      • Asystole
    • Note: Hyperkalemia can present with a number of “non-classic” EKG findings including AV blocks and sinus bradycardia (Mattu 2000)
    • Note: Hyperkalemic EKG changes do not necessarily occur in order (i.e. patients can jump from peaked T waves to sine wave)

Management

Basics: ABCs, IV, O2, Cardiac Monitor and, 12-lead EKG

  • Identify + treat underlying cause of hyperkalemia (i.e. rhabdomyolysis -> hydration)
  • Remove inciting factors (i.e. stop ACEI, NSAIDs etc)

Asymptomatic Patients without EKG Changes

  • Eliminate potassium from the body
    • Binding agents (SPS, Sodium zirconium cyclosilicate etc)
    • Enhance renal elimination
      • Intravenous hydration if volume depleted
      • Consider potassium wasting loop diuretics (i.e. furosemide)
    • Dialysis for anuric patients (i.e. ESRD)

Symptomatic Patients or Significant EKG Changes

  • Stabilize cardiac myocytes with calcium salts
    • Mechanism: Recreates the electrical gradient leading to rapid reversal of cardiac effects and rapid stabilization
    • Two Options: CaGluconate, CaCl2
    • Onset of action: seconds to minutes
    • Duration: 20-30 minutes
  • Shift potassium into intracellular space (temporary)
    • Insulin (Moussavi 2021)
      • Mechanism: Activation of the Na-K-ATPase
      • Dose: 5-10 units IV
      • Onset of Action: < 15 min
      • Effect: Lowers potassium by about 0.6 mmol
      • Duration of action: 30-60 min
      • Give with dextrose (0.5 – 1 g/kg) unless hyperglycemia present
      • Caution: Duration of action of insulin may outlast administered dextrose. Be vigilant for hypoglycemia
    • Beta-adrenoreceptor agonists (i.e. albuterol)
      • Mechanism: Activation of beta receptors
      • Dose: 10-20 mg inhaled (4-8 standard ampules)
      • Onset of Action: < 15 min
      • Effect: Lowers potassium by about 0.6 mmol
      • Duration of action: 30-60 min
      • Additive effect with insulin (Allon 1990)
      • Note: Unlikely to have effect in patients taking beta-adrenoreceptor blocker medications
    • Sodium Bicarbonate (NaHCO3)
      • Evidence for the efficacy of NaHCO3 to lower serum potassium is scant and contradictory (Elliott 2010, Weisberg 2008)
  • Eliminate potassium from the body (see above)

Asymptomatic Patients with Minor EKG Changes

  • Minimal recommendations on managing this clinical entity
  • Eliminate potassium from the body (see above)
  • Consider calcium salt administration: patients can rapidly progress through EKG changes and calcium administration may prevent this from occurring. However, the effects of calcium are temporary and offer no long-term protection
  • Consider medications to shift potassium intracellularly while waiting for elimination

Take Home Points

  • Always obtain an EKG in patients with ESRD upon presentation
  • Always obtain an EKG in patients with hyperkalemia as pseudohyperkalemia is the number one cause
  • If the patient with hyperkalemia is unstable or has significant EKG changes (wide QRS, sine wave) rapidly administer calcium salts
  • In patients who are anuric, early mobilization of dialysis resources is critical

References

Elliott MJ et al. Management of patients with acute hyperkalemia. CMAJ 2010; 182(15): 1631-5. PMID: 20855477

Wrenn K et al. The ability of physicians to predict hyperkalemia from the ECG. Ann Emerg Med 1991; 20(11): 1229-32. PMID: 1952310

Aslam S et al. Electrocardiography is unreliable in detecting potentially lethal hyperkalaemia in hemodialysis patients. Nephrol Dial Transplant 2002; 17: 1639-42. PMID: 12198216

Montague BT et al. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol 2008; 3:324–330. PMID: 18235147

Mattu A et al. Electrocardiographic manifestations of hyperkalemia. Am J Emerg Med 2000; 18: 721-9. PMID: 11043630

Allon M, Copkney C. Albuterol and insulin for treatment of hyperkalemia in hemodialysis patients. Kidney Int 1990; 38:869–872. PMID: 2266671

Weisberg LS. Management of hyperkalemia. Crit Care Med 2008; 36: 3246-51. PMID: 18936701

Moussavi K et al. Reduced alternative insulin dosing in hyperkalemia: a meta-analysis of effects on hypoglycemia and potassium reduction. Pharmacotherapy 2021; 41(7): 598-607. PMID: 33993515

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)

The post REBEL Core Cast 125.0 – Hyperkalemia appeared first on REBEL EM - Emergency Medicine Blog.

  continue reading

25 episodes

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