a) K>5 with any hyperkalemia ECG changes or

b) K>6.5 regardless of ECG findings

↓
Eliminate K through the kidneys and GI tract while achieving euvolemia
and establish good urine flow

Episode 86 – Hyperkalemia Normal Saline IV boluses if hypovolemia

Furosemide IV only if hypervolemic
PEG 3350 17g orally for alert patients remaining in your ED for
prolonged period of time
With Dr. Ed Etchells & Dr. Melanie Baimel Dialysis for arrest, peri-arrest, dialysis patient or severe renal
Prepared by Dr. Michael Kilian & Anton Helman, Sept 2016 failure
↓
Monitor rythym strip, glucose at 30 mins, K and ECG at 60 mins
and repeat as needed until the K is below 6, ECG has normalized and/or
dialysis has been started
General Approach to Emergency Management of
Hyperkalemia
The ECG in Emergency Management of
Place the patient on a cardiac monitor, establish IV access and obtain an
Hyperkalemia
ECG
↓ The ECG changes associated with hyperkalemia do not always happen in a
If the patient is stable, consider the cause and rule out pseudohyperkalemia step-wise fashion with predictable serum potassium levels. Although it is
(from poor phlebotomy technique, thrombocytosis or leucocytosis) and generally true that higher levels of potassium correlate with progressive
repeat the potassium to confirm hyperkalemia. ECG changes, the more acute the hyperkalemia the more likely the ECG
↓ changes occur. It is possible for a hyperkalemic patient to progress rapidly
Stabilize the cardiac membrane with Calcium Gluconate 1-3 amps from a normal ECG to ventricular fibrillation.
(or Calcium Chloride 1 amp if peri-arrest/arrest) if:
a) K>6.5 or The classic ECG progression in hyperkalemia
b) wide QRS or
c) absent p waves or 1. Peaked T wave (K approx 5.5-6.5)
d) peri-arrest/arrest
↓
Peaked T waves reflect faster repolarization of the myosite. A sensitive sign
Drive K into cells with 2 amps D50W + Regular Insulin 10 units IV push
is if the amplitude of the T exceeds the amplitude of the R. This
followed by B-agonists 20mg by neb or 8 puffs via spacer if:
distinguishes peaked T waves of hyperkalemia from hyperacute T waves 2. Prolonged PR interval and flattening
of early MI which tend to have a broader base T wave.
or disappearance of the P wave (K approx 6.5-7.5)

The resting potential of myosite becomes more positive which slows

depolarization.

Peaked T waves of Hyperkalemia. Note the amplitude of the T exceeds the
amplitude of the R. Care of Life in The Fast Lane blog.

Example of bradycardia with absent or flattened p waves in hyperkalemia.
Care of Dr. Smith’s ECG blog.

3. Widening of the QRS

The increasingly positive membrane potential leads to progressively slowed

depolarization and widening of the QRS.
Hyperacute T waves of early MI. Note the broad-based T waves in the
anterior leads to help distinguish from peaked T waves of hyperkalemia.
Care of Dr. Smith’s ECG blog.
 Hyperkalemia is the Great ECG Imitator

These ECG findings are not specific to hyperkalemia alone. Given the broad
differential for these ECG changes, hyperkalemia has been dubbed the
“Great ECG Imitator”. It is important to consider the patient’s presentation,
clinical complaints and trends on the ECG.
PEARL: Hyperkalemia has been known to cause almost any
dysrhythmia. Pay special attention to patients in “slow VT” and wide-
complex bradycardia and consider treating them empirically as
hyperkalemia.

Determine the Cause of Hyperkalemia
Widened QRS in severe hyperkalemia (Care of Dr. Melanie Baimel)
First rule out pseudohyperkalemia which accounts for 20% of
hyperkalemia lab values.
Pseudohyperkalemia is caused by hemolyzed sample, poor phlebotomy
4. Sine Wave: pre-terminal rhythm technique leukocytosis or thrombocytosis.
Then treat the underlying cause:
As the depolarization slows, the widening QRS begins to merge with the T
wave. This is a pre-terminal rhythm which can deteriorate rapidly into • Medications: ACEi, Potassium sparing diuretics, B-
Ventricular Fibrillation. Blockers, NSAIDs, Trimethoprim (Septra) and Non-
prescription salt substitutes
• Renal Failure
• Cell death: Secondary to rhabdomyolisis, massive
transfusion, crush or burn injuries.
• Acidosis: Consider Addisons crisis, primary adrenal
insufficiency and DKA.
Sine wave in severe hyperkalemia, a pre-arrest rhythm.
PEARL: If hyperkalemia cannot be explained by any other cause and the
patient has unexplained hypotension, draw a random cortisol and ACTH
level and give 100 mg IV solucortef for presumed adrenal insufficiency.
Medications in the Emergency Management of There is no good literature to help guide whether calcium gluconate or
calcium chloride is better for stabilizing the cardiac membrane in
Hyperkalemia hyperkalemia. The most important difference to remember is that calcium
chloride has 3 times more elemental calcium than calcium gluconate (6.8
Three main principles mEq/10 mL vs 2.2 mEq/10 mL) and has greater bioavailability. However,
calcium gluconate has less risk of local tissue necrosis at the IV site.
1. Stabilize cardiac membrane Therefore, if you decide to give calcium gluconate, ensure you are giving
sufficient doses of calcium since one amp may not be enough. Three amps
2. Shift potassium intracellularly of calcium gluconate are often required to start to see the ECG changes
3. Eliminate potassium of hyperkalemia resolve. Remember that calcium does not lower the
potassium level.
There are specific treatments geared at targeting each of these three main
principles, which we will discuss below. Unfortunately, there is no clear Our experts recommend using calcium chloride through a large well-
evidence to guide exactly when to initiate specific treatments for flowing peripheral IV or central line in the arrest or peri-arrest patient.
hyperkalemia. Our experts recommend using two factors to guide your Calcium gluconate is recommended for all other patients given it’s lower
management: risk for local tissue necrosis.

1. Serum potassium level and Routine use: 1 gram of 10% calcium gluconate (i.e. 10 ml mixed with
100cc of D5W or NS in a mini-bag) over 5-10 minutes. Repeat as needed to
2. ECG achieve QRS <100ms and p waves re-appear.

with the following indications for immediate treatment of hyperkalemia in Arrest or Pre-arrest: Push 1 amp (1 gram) of 10% calcium chloride
the ED: through a large bore well-running peripheral IV or central line
(preferable). Repeat as needed to achieve QRS <100ms and p waves re-
appear.

In patients taking digoxin the traditional teaching is that calcium is

contraindicated. The so-called “stone heart” from the administration of
calcium in patient with digoxin toxicity has been largely debunked. A small
case-controlled study found no mortality differences between 23 patients
with hyperkalemia and digitalis toxicity who were treated with calcium and
Principle 1: Stabilize the cardiac membrane 136 patients who were not.

If digoxin toxicity is suspected in the setting of severe hyperkalemia, our

experts recommend giving calcium cautiously, at a slower rate than usual:
1 gram of 10% calcium gluconate in 100 cc of D5W or NS over 15-
30 minutes (rather than 5 minutes).
 Bicarbonate is also known to shift bicarbonate into cells. Our experts do
Principle 2: Shifting potassium into cells: not recommend the routine use of bicarbonate in the treatment of
hyperkalemia. It may have a role to play in a small subset of patients who
The choices for shifting potassium into cells include intravenous insulin and also have a non-anion gap metabolic acidosis such as those patients with
glucose, beta-agonists and bicarbonate. The indications for starting insulin renal tubular acidosis.
and glucose include a K>5 mmol with ECG changes or a K> 6.5 mmol
regardless of ECG changes. Observational studies have shown that many Principle 3: Eliminate Potassium
patients treated with insulin and glucose for hyperkalemia become
hypoglycemic when given 1 amp of D50W followed by 10 units of humulin The kidneys are the main route for eliminating of potassium. Ensuring
R. Therefore, based on a recent systematic review our experts recommend euvolemia and appropriate urine output is the mainstay of treatment.
the following approach to initiating insulin and glucose therapy: Inserting a foley catheter will allow you to monitor urine output. Many
patients will be hypovolemic and will need fluid resuscitation with
2 amps of D50W followed by 10 units IV humulin R (rapid injection) crytalloid. If you need to volume resuscitate your patient, the initial fluid of
choice is Normal Saline even though with huge doses hypercholoremic
Monitor glucose q30 minutes metabolic acidosis can occure. Ringer’s Lactate contains 4mmol/L of
potassium, which poses obvious risks of increasing serum potassium if
Repeat K at 60 minutes appropriate renal elimination has not started.

Beta agonists are also useful to rapidly shift potassium into cells. They act There is no role for diuretics in the routine management of hyperkalemia
synergistically with insulin and can lower serum potassium by 1.2 mmol in unless the patient is hypervolemic.
an hour. Paradoxically, one third of patients will not have the predicted drop
in serum potassium, and observational data has shown a very transient Regarding potassium binding agents such as Kayexalate, a 2005 Cochrane
initial rise in potassium up to 0.4 mmol after administration of beta review did not show any evidence that they improve potassium levels.
agonists. Therefore, B-agonists should NOT be used as mono- There have also been case reports of Kayexelate causing GI necrosis and
therapy and insulin/glucose be given first. The doses of beta agonists for perforation. Our experts conclude that there is no role for kayexcelate in the
hyperkalemia are generally higher than what you would use in asthma: ED.

Salbutamol 8 puffs by aerochamber or 20mg nebulized Consider PEG 3350 orally to help eliminate potassium through the GI tract
if the patient is likely to stay in your ED for a prolonged period of time.
Insulin and beta agonists will start to take effect within 15min with their Given that most patients with hyperkalemia will have some element of renal
peak effect being at 60min. insufficiency it is important to remember that milk of magnesia and fleet
enemas are both contraindicated as they will cause magnesium and
Pitfall: If B-agonists are given before insulin/glucose they may cause a phosphate toxicity, respectively.
transient rise in the serum potassium level. Always give B-agonists after
insulin/glucose.
Hyperkalemia in Cardiac Arrest Intra-arrest Dialysis
In cardiac arrest, case reports have demonstrated successful ROSC and
Based on the principles of treatment and indications discussed above, our good neurologic outcomes despite prolonged arrest when dialysis is
experts recommend the following approach to suspected hyperkalemia initiated during CPR to correct hyperkalemia.
(based on patient history and rhythm strip) or confirmed hyperkalemia
(based on a point of care blood gas) in cardiac arrest in addition to usual
ACLS measures: Future Directions in Emergency Management of
Push 1 amp calcium chloride in well running peripheral IV or central
Hyperkalemia
line and repeat until the QRS is <100ms
↓ A new potassium binding drug, ZS-9 shows promise in the acute treatment
Epinephrine 5-20 mcg q2-5 minutes (shifts K intracellularly) of hyperkalemia and may make it possible to avoid or postpone the most
↓ effective therapy, emergency hemodialysis.
Sodium Bicarbonate 1 amp IV (if suspect severe acidosis)
↓ Other FOAM Resources for Hyperkalemia:
Bolus IV NS Rebel EM on kayexalate and ECG changes in hyperkalemia
↓ EMBasic on hyperkalemia
Shift potassium with Insulin and Glucose followed by B-agonist Life in the Fast Lane on hyperkalemia management
↓ Academic Life in EM on preventing hypoglycemia from insulin in
Dialysis hyperkalemia
First10EM on initial management of hyperkalemia
Rebound Hyperkalemia Dr. Smith’s ECG blog on ECG changes with hyperkalemia
In cases of cardiac arrest due to hyperkalemia, perform CPR until the
hyperkalemia is corrected. This may be a much longer time than usual. Dr. Etchelles, Dr. Bailel, Dr. Helman & Dr. Kilian have no conflicts of
When ROSC is achieved, it will be primarily due to the effects of calcium interest to declare.
rather than decreased potassium levels. The effect of calcium can last 20-
30min. Since the stabilizing effects of calcium will wear off, you must References:
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