Management of severe hyperkalemia in the ED

Syed Shahrul Naz Bin Syed ShamsuddinM.D (UKM)

Emergency Medicine Resident

Outline

• Potassium• Hyperkalemia• Clinical Manifestations of Hyperkalemia

• EKG findings• Management of Hyperkalemia

• History and Physical Examination• Diagnostics• Management

– Rapid-Transient – Potassium Excretion

• A 60 y/o male presented with 2 weeks of intermittent chest pain. He has a history of MI and renal insufficiency. Now he feels weak. His pulse is 42 with a BP of 140/35.

Here is his initial ECG:

• His charts showed he had presented to a clinic 2 months prior with chest pain and had an identical ECG which was read as "no change from old". The ECG prior to that one, however, did not have bradycardia (so there really was a change from old). The patient had been sent home from clinic.

Rhythm analysis: • there is a regular rhythm with a QRS that is borderline prolonged

at 110 ms (QRS on the previous truly normal ECG was 105 ms). Are there p-waves? Yes, but they are after the QRS, and they are inverted. And the R-P interval is very prolonged at about 440 ms. So there is either sinus arrest or severe sinus bradycardia (such that the junction or bundle of HIS escapes before the sinus node can fire). There is atrial activity (the p-wave); it is inverted because it is being activated from below.

• Diagnosis: Sinus arrest or extreme bradycardia with junctional escape and retrograde p-waves with prolonged VA conduction.

What are the common causes:

1. hyperkalemia2. Ischemia (no evidence of ischemia on this ECG)3. Drugs (he was not on any that woul do this): digitalis, beta blockers, calcium channel blockers, Na channel modulators4. Sick sinus5. Increased vagal tone, but this would also slow the escape. 6. Variety of other less common etiologies, such as Lyme, infiltrative diseases

• Atropine 1 mg was given without change. Potassium returned at 6.2 mEq/L. 3g of Calcium gluconate were given and the rate immediately went to 60.

Here is the subsequent ECG:

• The patient ruled out for MI by serial troponins.

• When a patient has bradycardia, always think of hyperkalemia among other etiologies.

Case 2 A 52-year-old man with hypertension and diabetes complains of weakness,

nausea, and a general sense of illness, that has progressed slowly over 3 days. His medications include a sulphonylurea, a diuretic, and an ACE inhibitor. On examination, he appears lethargic and ill. His BP is 154/105 mm Hg, HR 70bpm, temperature 98.6° F, and respiratory rate 22 breaths/min. The physical examination reveals moderate jugular venous distension, some minor bibasilar rales, and lower extremity edema. He is oriented to person and place but is able to give further history. The ECG shows a wide complex rhythm.

Laboratory studies performed are significant for potassium 7.8 mEq/L, BUN is 114 mg/dL and creatinine is 10.5.

Potassium homeostasis: depends on maintenance of external and internal potassium balance.

Potassium homeostasis: depends on maintenance of external and internal potassium balance.

Determinants of Serum Potassium Concentration

HyperkalemiaK > 5.0 meq/L

R/O PseudohyperkalemiaHemolysis, Leucocytosis, Thrombocytosis

Excess K Intake

K SupplementsK Penicillin

Stored Blood Salt Substitutes

Translocation from ICF to ECF Acidosis Severe Catabolism Rhabdomyolysis

Tissue NecrosisInsulin DeficiencyMineralocorticoid deficiencyPeriodic ParalysisAldosterone ToxicityDigitalis ToxicitySuccinylcholineB blockersHyperosmolarityCatecholamine Deficiency

Decreased Excretory Capacity

Renal FailureOliguriaRenal Tubular DiseaseK sparing DiureticsHypoaldosteronismCyclosporineACE inhibitorsNSAIDsUreterojejunostomy

Clinical Manifestations of Hyperkalemia

Serious manifestationsMuscle weakness or paralysisCardiac Conduction abnormalitiesCardiac Arrhythmias

ECG Changes of Hyperkalemia

• Easily Distinguished ECG signs:– peaked T wave. – prolongation of the PR interval– ST changes (which may mimic myocardial infarction)– very wide QRS, which may progress to a sine wave pattern

and asystole.

• Patients may have severe hyperkalemia with minimal ECG changes, and prominent ECG changes with mild hyperkalemia.

Serum potassium > 5.5 mEq/L is associated with repolarization abnormalities:

• Peaked T waves (usually the earliest sign of hyperkalaemia)

Tall tented T waves

Serum potassium > 6.5 mEq/L is associated with progressive paralysis of the atria:

• P wave widens and flattens• PR segment lengthens• P waves eventually disappear

Prolonged PR segment

Loss of P waves

Serum potassium > 7.0 mEq/L is associated with conduction abnormalities and bradycardia:

• Prolonged QRS interval with bizarre QRS morphology• High-grade AV block with slow junctional and

ventricular escape rhythms• Any kind of conduction block (bundle branch blocks,

fascicular blocks)• Sinus bradycardia or slow AF• Development of a sine wave appearance (a pre-

terminal rhythm)

Junctional bradycardia

Sine wave

Serum potassium level of > 9.0 mEq/L causes cardiac arrest due to:

• Asystole• Ventricular fibrillation• PEA with bizarre, wide complex rhythm

12-lead ECG from an 82-year-old man with acute renal failure and hyperkalemia (serum potassium 8.6 mEq/dL).

12-lead ECG from same patient following treatment of hyperkalemia with intravenous calcium gluconate, insulin, glucose, normal saline, and oral kayexalate (serum potassium 6.2 mEq/dL).

EKG and Hyperkalemia

• PR interval prolongation (>7.0meq/L)

Peaked T-Waves (6meq/L)

Absent P wave with widen QRS complex

• SWAT Nurses lurking around your patient

Analysis• Diagnosis: Hyperkalemia- Severe

– Classification of Hyperkalemia• NORMAL: 3.5 to 5.0 mEq/L. • MILD: 5.5 to 6.0 mEq/L• MODERATE :> 6.0 mEq/L• SEVERE: Levels of 7.0 mEq/L or greater

• It is important to suspect this condition from the history and ECG, because laboratory test results may be delayed and the patient could die before those test results become available.

Approach to Hyperkalemia

• Basis

– Antagonizing the membrane effects of potassium with calcium

– Driving extracellular potassium into the cells– Removing excess potassium from the body

• History and Physical Exam• Rule out Pseudohyperkalemia?• Cardiac status• Treatments

– Rapid and Transient acting– Potassium Excretion

Principles of Treatment

1. Antagonize the effect of K on excitablecell membranes.2. Redistribute extracellular K into cells.3. Enhance elimination of K from thebody.

Weisberg LS. Management of severe hyperkalemia. Crit Care Med. 2008 Dec;36(12):3246-51.

Rapidly acting transient therapies

• Indications• (+) Electrocardiographic changes• Potassium > 6.5 to 7 meq/L (6.5 to 7.0 mmol/L)• Rapidity of increase in potassium-Etiology of

Hyperkalemia• Agents– Calcium Gluconate– Insulin with glucose, – Beta 2 adrenergic agonists – Sodium bicarbonate (Metabolic Acidosis?)

Calcium

MOA: Directly antagonizes the membrane actions of hyperkalemia. Kinetics:

– Begins within minutes– short lived (30-60mins)– Indications: EKG findings of widening of QRS complex or loss of P waves

(insulin and glucose acts 30-60 minutes patient might be in assystole by that time) .

Forms– Calcium gluconate 1000 mg over 2-3 mins repeated Q5 minutes

• Can be given peripheraly– Calcium Chloride 500-1000mg over 2-3 mins repeated Q5 mins.

• Irritating to veins- given in central or deep vein

Side effect: – Rapid IV: cardiotoxic, hypotension and phlebities– Caution in digitalized patients and renal disease:– Antidote: IV Magnesium Sulphate

Insulin

• MOA: Enhancement of the activity of Na-K-ATPase pump in skeletal muscle.

• Kinetics: – Onset: 10-20 mins– Peaks 30-60 mins and lasts for 4-6 hours.

• Administration: – if the serum glucose is > 250mg/dl , insulin alone will suffice– Regimen:

• 10 Units of Regular insulin then 50mg of 50% glucose.• Higher insulin concentrations have a higher potassium lowering effect.• 75% of patients treated becomes hypoglycemia.

• Potassium concentration drops by 0.5-1.2meq/L• Renal failure resistant to glucose lowering effect of insulin-not resistant to

the hypokalemic effect of enhanced Na-KATPASE effect.• Common Side effect: Hypoglycemia

Beta-2 Adrenergic Agonists

• MOA: Increases activity of the Na-K-ATPAse pump/activation of inwardly directed Na-K-2Cl co transporter

• Kinetics: peak effect seen within 30 mins with IV and 90 mins with nebulization

• Dosing: • Albuterol: 10-20mg in 4 ml saline by nebulization over 10 minutes (4-8x dose used for

bronchodilation) which is 4 to 8 times the dose used for bronchodilation• Lowers the serum potassium by 0.5 to 1.5meq/L• Addititive effect of albuterol, insulin with glucose decreases

serum potassium by approximately 1.2-1.5 meq/L• Side effects – Tachycardia– Induction of angina/CAD patients/ ESRD patients –subclinical or overt CAD

Sodium Bicarbonate

• Raises systemic pH—movement of Hydrogen ion release from cells—to maintain neutrality potassium moves into the cells.

• Administration is not recommended• Isotonic solution 150meq/L D5W over two to

4 hours.

From Uptodate…• “Given the limited efficacy, we do not recommend the

administration of sodium bicarbonate as the only therapy for the acute management of hyperkalemia, even in patients with mild to moderate metabolic acidosis

• However, prolonged bicarbonate therapy appears to be beneficial in patients with metabolic acidosis.

• In one series, for example, the administration of isotonic sodium bicarbonate in a constant infusion to patients with a baseline serum bicarbonate of 18 meq/L had little effect at one and two hours but significantly lowered the serum potassium from 6 meq/L at baseline to 5.4 and 5.3 meq/L at four and six hours; the serum bicarbonate increased to 28 meq/L at one hour and 30 meq/L at six hours.”

Potassium Excretion

Diuretics:

– Loop and thiazide diuretics increases potassium loss in the urine in patients with normal or mild to moderately impaired renal function.

– Chronic diuretic therapy is more effective– Add saline hydration to maintain distal

sodium delivery and flow.

Sodium Polystyrene Sulfonate

• MOA: removes potassium by exchanging sodium ions for potassium ions in the intestine (large intestine).

• Kinetics– Onset of action:2-24 hours, Fall of 0.4meq/L in first 24 hours– Absorption: none– Excretion: Completely feces (primarily as potassium polystyrene

sulfonate)• Adverse reactions

– Electrolytes derangement– GIT: Anorexia, Colonic necrosis, constipation/diarrhea

• Contraindications: – Hypersensitivity reactions, Obstructive bowel disease

• Dosing – SPS without or with sorbitol – oral dosing is

effective if intestinal motility is not impaired– 15 to 30 gm every 4-6 hours as necessary– Can also be give as enema in Tap water– May add lactulose or Miralax

• Intestinal Necrosis?

Dialysis

• Indicated – if the rest of the treatments were insufficient. – Hyperkalemia is severe or is expected to increase rapidly– If the patient is hemodialysis dependent.

• Hemodialysis can remove 25-50 meq of potassium per hour• Post dialysis potassium rebound

– Seen in Tumor Lysis Syndrome, Rhabdomyolysis– Effect of rapidly acting transient therapies in HD dependent

Patients– Serum potassium should usually not be measure soon after the

completion of hemodialysis

History and PE

Find and treat Underlying cause Remove offending drugs

If Potassium >6 or with EKG Findings

Check EKG

Ca Gluconate 10ml of 10%

solution infused over 2-3mins

D50 1 amp+10 U insulin IV Kayexalate 30-60 gm PO 1-4x

B-agonist inhaled10-20mg neb 30-60 mins

DialysisVascular AccessHD Dependent

Antagonize membrane effects

Drive Extracellular potassium into the cells

Excrete excess Potassium from the Body

Cardiac Monitor

Lactulose/Miralax

Check EKG/Cardiac Monitor after 10 minutes

Check Potassium after 2 hours

If Potassium <6 without EKG Findings

Check Potassium after 2 hours

QUESTION 1:

A 55-year-old man presents in cardiac arrest. A dialysis fistula is present in the right arm. In addition to standard ACLS therapies, which of the following is most appropriate for this patient?

A. 25 g of 50% dextrose, IV push. B. Sodium bicarbonate, 50-mL IV push. C. Begin immediate hemodialysis. D. Calcium gluconate, slow intravenous push.

QUESTION 2:

A 45-year-old man is brought into the emergency center due to significant dehydration and weakness. His potassium level is noted to be 7 mEq/L. Which of the following statements is most accurate regarding his potassium level?

A. Hyperkalemia can usually be diagnosed by symptoms alone. B. An ECG showing peaked T waves means the patient is stable and treatment can safely wait until

laboratory results are obtained. C. Hyperkalemia can mimic a myocardial infarction on the ECG. D. Hyperkalemia is synonymous with kidney disease.

QUESTION 3:

Which of the following statements regarding treatment of hyperkalemia in patients with some renal function is incorrect?

A. Administration of normal saline may hasten the excretion of potassium. B. Administration of furosemide can hasten the excretion of potassium. C. The combination of saline with a diuretic is often indicated because hyperkalemic patients are

frequently dehydrated. D. Patients with some renal function do not need dialysis even for severe hyperkalemia.

QUESTION 4:

A patient with severe renal disease is found to have hyperkalemia, with tall, peaked T waves on ECG. Vascular access cannot be readily obtained, but vital signs are stable. Which of the following would be appropriate temporizing measures?

A. Inhaled albuterol 2.5 mg in 3 mL saline B. Oral sodium bicarbonate with rectal sodium polystyrene sulfonate C. Inhaled albuterol 20 mg, with oral or rectal sodium polystyrene sulfonate, 30 g D. Oral dextrose 25 g

Thank You Do you know your resuscitation room?