Picking up hyperkalemia on an EKG can be lifesaving.
We all know about "peaked T-waves," but the underlying pathophysiological basis for the various EKG changes is confusing and unintuitive.
A thread on EKG findings in hyperkalemia!
- Thead -
Disclaimers
Though these are the "classic" EKG changes, patients do not necessarily progress in this order.
EKGs do not always correlate with the actual K level - it depends on the chronicity of the elevation.
Lastly, EKG changes are NOT sensitive for hyperkalemia.
Why does HyperK lead to EKG changes?
The "less-negative" membrane potential initially leads to excitability
It then leads to incomplete or delayed depolarization
Lastly, zones of differential excitability form, leading to reentrant circuits or uncoordinated contraction
Some key pearls to appreciate:
1. Atria are more susceptible to changes in K. This is why we see effects on the PR interval and p-waves earlier than in the QRS.
2. HyperK is one of the "H's and T's" etiologies of cardiac arrest. It can lead to VFib, PEA, or asystole.
Here are the "classic" EKG changes, courtesy of @LITFLblog and @Core_EM (their excellent blog posts linked at the end of the thread!)
1. Peaked T-waves
2. Prolonged PR and flat p-waves
3. Sinusoidal Wave or life-threatening arrythmia
Let's discuss each.
1. Mild: K 5.5-6.5 mEq/L
Peaked T-waves
The earliest change associated with hyperK is accelerated REpolarization of ventricular cells.
This is due to more outward K current in repolarization and more cells repolarize at the same time, creating the sharp, steep T-waves.
This first phase seemed unintuitive to me.
If there is more K outside the cell already and the concentration gradient is now "less negative," why would more K leave the cell?
It's because we are talking about REpolarization and not DEpolarization.
Despite a reduced gradient, the cells are closer to the threshold potential, so they are able to return to their resting state more quickly.
K channels may also become more active or open longer due to the altered membrane potentials, facilitating efflux.
2. Moderate: K 6.5-8.0 mEq/L
Prolonged PR Interval
Flattened P-waves
At these levels, the DEpolarization of the atria begins to be affected, leading to prolonged PR (delayed conduction from the atria to the ventricles).
Eventually, the p-waves flatten and disappear.
QRS Widening
The QRS represents ventricular depolarization. As the speed of ventricular depolarization decreases, conduction across the ventricle is decreased, widening the QRS.
At higher levels, the QRS becomes so long that it merges with the T-wave.
Again, unintuitive.
If the cells are more excitable with "less negative" potentials, why would PR increase and p-waves go away?
As hyperK progresses, the resting membrane potential becomes so depolarized that it leads to the inactivation of voltage-gated sodium channels.
These sodium channels are crucial for initiating an action potential.
Thus, when they are inactivated, it becomes difficult to initiate a new action potential.
The AV node is particularly sensitive, resulting in a prolonged PR interval.
3. Severe: K > 8.0 mEq/L
Sine Wave Pattern
Severe disturbances of depolarization and repolarization lead to the complete joining of the QRS complex and T-wave.
Commit these images to memory. You may save someone's life.
VFib and Arrythmias
In zones of differential excitability, some areas may respond quickly to an electrical impulse, while others respond more slowly or not at all.
This can lead to uncoordinated contraction of the venticular muscle (resulting in VFib or PEA).
Here are some of my favorite posts about EKG changes and HyperK from the MedTwitter community!
First, @EM_RESUS - my go-to educational source for all things related to EM and EKGs!
"Slow VTach" may be hyperK!
twitter.com/EM_RESUS/status/950058330118074369