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Management of severe

hyperkalemia in the ED
Syed Shahrul Naz Bin Syed Shamsuddin
M.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. hyperkalemia
2. 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
modulators
4. Sick sinus
5. 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
Hyperkalemia
K > 5.0 meq/L
R/O Pseudohyperkalemia
Hemolysis, Leucocytosis, Thrombocytosis
Excess K Intake

K Supplements
K Penicillin
Stored Blood
Salt Substitutes
Translocation from ICF to ECF

Acidosis
Severe Catabolism
Rhabdomyolysis
Tissue Necrosis
Insulin Deficiency
Mineralocorticoid deficiency
Periodic Paralysis
Aldosterone Toxicity
Digitalis Toxicity
Succinylcholine
B blockers
Hyperosmolarity
Catecholamine Deficiency

Decreased
Excretory Capacity

Renal Failure
Oliguria
Renal Tubular Disease
K sparing Diuretics
Hypoaldosteronism
Cyclosporine
ACE inhibitors
NSAIDs
Ureterojejunostomy
Clinical Manifestations of Hyperkalemia
Serious manifestations
Muscle weakness or paralysis
Cardiac Conduction abnormalities
Cardiac 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 excitable
cell membranes.
2. Redistribute extracellular K into cells.
3. Enhance elimination of K from the
body.
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 pHmovement of Hydrogen
ion release from cellsto 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 inhaled
10-20mg neb 30-60 mins
Dialysis
Vascular Access
HD 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
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