Hyperkalemia is a severe and deadly event which means there is an excessive amount of potassium in the blood. The normal concentration of potassium in the blood is around 3.5-5.0 mmol/L. Hyperkalemia is caused by many different things and it effects vital body functions. The causes of hyperkalemia can be broken down into three categories.
- Potassium excretion
- Potassium shifts
- Increased potassium intake
Potassium is the most abundant intracellular cation in the body and is excreted from the body with the help of the kidneys.
Potassium is filtered in the Glomerulus along with the proximal convoluted tubule and the distal tubule and is excreted out of the body in urine. The distal tubule’s ability to filter potassium is affected by the hormone aldosterone which is created in the adrenal cortex. Aldosterone binds to the mineralocorticoid receptor which activates sodium/potassium ATPases. These pumps help shift potassium and sodium using the help of ATP. ATP binds to the pump which promotes the ions to enter/leave the pump depending on if they have a low or high affinity to the binding sites. ATP releases an inorganic phosphate which causes a conformational change in the pump.
So, for the potassium excretion aspect of hyperkalemia, we need to think of injury (acute or chronic) to the kidneys and various pathways that cause a decrease in aldosterone. Injury to kidneys causes a decrease in glomerular filtration rate which decreases the amount of potassium being filtered this causes a build up of potassium in the blood.
The normal Renin Angiotensin Aldosterone system (RAAS) goes as the following:
- Angiotensinogen is secreted by the liver due to Sodium changes or decreased BP
- Renin is secreted by the kidneys
- Renin cleaves the angiotensinogen to create Angiotensin I
- Angiotensin I is converted into Angiotensin II by the enzyme Angiotensin-converting enzyme (ACE) which is found in the pulmonary circulation.
- Angiotensin II goes to the adrenal cortex and promotes the secretion of aldosterone
So, we know that low levels of aldosterone can cause hyperkalemia, but several drugs can impact the RAAS. ACE inhibitors cause a decrease in angiotensin II being created which in turn decreases the amount of aldosterone. NSAIDs decrease Renin production in the kidneys which in turn decreases the amount of aldosterone. And potassium sparing diuretics (Spironolactone, Amiloride, Eplerenone) block aldosterone from binding to the receptors in the distal convoluted tubule which causes the kidneys to pass more fluid through while retaining potassium.
A normal cell usually has more potassium in it in comparison to the extracellular space. If a cell is excitatory in nature, there needs to be a shift of ions, and this is accomplished by the sodium-potassium ATPases we talked about earlier. One hormone that affects these pumps is insulin. Insulin increases the cell surface expression of the Na/K ATPases which increases the activity of the pumps. If a patient has diabetes, insulin is unable to activate and stimulate the pumps effectively which prevents potassium from being pushed into the cell. To help combat the decrease in pH, the cells pull in a H+ ion into cells but because H+ is positively charged, a K+ ion is pumped out which causes an increase of potassium in the blood. The body enjoys things being in equilibrium and ions shift from higher to lower concentrations which can cause hyperkalemia.
The next part talks about the various medications we administer which can inhibit Na/K pumps. Beta blockers that bind to Beta-2 receptors and inhibit NA/K ATPase pumps and so does Digoxin.
And the final cause of hyperkalemia due to potassium shifts can be contributed to rhabdomyolysis. Remember that our cells are packed full of potassium so when they burst, potassium floods into the blood stream. Myoglobin is also released from skeletal cells which is difficult for the kidney to filter which can cause acute kidney injuries. This can exacerbate the build up of potassium in the blood.
Increased Potassium Intake
The final cause of hyperkalemia is due to an increased intake. This can occur orally by consuming foods or potassium supplementation by hospital providers.
Hyperkalemia works by increasing the threshold potential of the myocytes which is shown below. As many of us know, hyperkalemia basically widens the ECG out until you reach the very stable rhythm of asystole. To my surprise, I have learned that a lot of providers just think that the “peaked T waves” is the only sign. So here is the normal progression of hyperkalemia.
I want to make it clear that it isn’t super reliable to look at the morphology of the QRS and be able to accurately determine what the K+ is. This is because your average joe might follow this progression well, patients who are more resistant to hyperkalemia due to dialysis might have different QRS morphologies such as just a peaked T wave with a potassium of 9. The typical progression of hyperkalemia goes:
- Peaked T waves due to repolarization abnormalities
- Prolonged PRI due to atrial paralysis (showing a first degree AV block)
- P wave is flattened until it no longer exists
- QRS widening until it reaches a Sine wave pattern due to conduction abnormalities
To get more into the various morphologies, hyperkalemia causes the peaked T waves due to shortening of the action potential duration which causes synchronous repolarization throughout the ventricular wall. The P wave eventually vanishes due to slowing conduction velocity because the heart is in a bath of potassium ions.
Hyperkalemia is the great imitator and can mimic anything from heart blocks, VT, Brugada syndrome, to STEMIs. This should be familiar to those who appreciate Dr. Amal Mattu’s lectures. So now we get into the various ECGs to show you hyperkalemia.
Here is an example of the “typical” hyperkalemia that we should be used to. You have the narrow, symmetrical, peaked T waves easily seen in the precordial leads.
Here is a typical “sine wave” pattern which is very wide and is named after the math “Sine Wave” as we should remember from our traumatic time in college.
Here is hyperkalemia mimicking a STEMI. You can see elevation in the inferior leads (II, III, and aVF) with reciprocal depression in I and aVL. But if you look at the T waves in the inferior leads, you will notice they are that wide based coved top that you expect with a STEMI. There is a peaked T wave in there. And there are massive, peaked T waves in your precordial leads.
This shows hyperkalemia mimicking ventricular tachycardia. If you do the big box method, you can see the rate is around 150 BPM. But if you measure the QRS (as seen in V3) it is about 1 big box wide. If a QRS is 1 big box wide or nearing 1 big box you instantly need to think of a tox/metabolic issue because VT can’t produce QRS complexes that wide.
Here is another example of hyperkalemia mimicking VT. Some of the QRS complexes are 1 big box wide.
So how do you narrow down your diagnosis to hyperkalemia due to the various morphologies? It comes down to PATTERN RECOGNITION. All ECG interpretation is understanding and interpreting patterns. Hyperkalemia has a very distinct pattern. If you think the term “wide and bizarre” think hyperkalemia every day and twice on Sunday. If the QRS is over 1 big box wide, think the patient has a tox/metabolic issue.
The normal treatment for hyperkalemia is:
- Priority CALCIUM to stabilize the myocardium
- Insulin in conjunction with glucose
- Beta 2 agonist (albuterol)
- Sodium Bicarbonate
- Emergency Hemodialysis
Calcium lowers the threshold potential to a safer level which prevents the patients from deteriorating. Glucose and insulin administration helps drive the potassium into cells by increasing the Na/K ATPase activity which we discussed in the patho part. A beta 2 agonist works similarly to glucose and insulin by increasing Na/K ATPase activity. And finally, Sodium bicarbonate can push potassium into cells by alkalinizing the serum which can cause a switching of protons (H+) and K+ ions in an out of cells which we discussed in the patho region. The sodium bicarbonate treatment might not be the most efficient treatment as there is a solvent drag effect. This happens with hypertonic bicarb because the hypertonic solution pulls the fluid and thus potassium back out of the cells so isotonic bicarb is the preferred treatment.
But what happens if we mistake hyperkalemia for ventricular tachycardia and we administer a sodium channel blocker or amiodarone? It is simple, you will get a “clean kill” as Dr. Amal Mattu states. Amiodarone is typically a class III antiarrhythmic drug that primarily focuses on the potassium channels of the heart that are responsible for the repolarization process in the phase 3 of cardiac action potential. Amiodarone is normally not marketed this way, but it also acts on beta-adrenergic receptors, calcium channels, and sodium channels. Hyperkalemia is thought to be a sodium channelopathy so when given a sodium channel blocker to already poisoned sodium channels, the patient will code.
We should be able to diagnose hyperkalemia on an ECG without the use of labs just like we should be able to diagnose ventricular tachycardia without an EP study. Always remember that if the words “wide and bizarre” enter your mind, think hyperkalemia.
This site is meant to be used for educational use only. We strive to push evidence-based medicine with no bias to help you obtain all of the important information. You should always follow your protocols that have been set in place.
-Scopeducation Team (Matt)
Farkas, J. (2022, June 11). Hyperkalemia. EMCrit Project. Retrieved July 5, 2022, from https://emcrit.org/ibcc/hyperkalemia/
Lehnhardt, A., & Kemper, M. J. (2011, March). Pathogenesis, diagnosis and management of Hyperkalemia. Pediatric nephrology (Berlin, Germany). Retrieved July 5, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3061004/
Weiss, J. N., Qu, Z., & Shivkumar, K. (2017, March). Electrophysiology of hypokalemia and Hyperkalemia. Circulation. Arrhythmia and electrophysiology. Retrieved July 5, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5399982/