Hyperkalaemia and ECG changes

[Phloston]

Hyperkalaemia can cause tall, peaked T waves, followed by a loss of the P waves, followed by QRS widening and a sinusoidal patterning.

Why those specific changes in that sequence.

What's the mechanism at each step. Why.

Cheers,

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[Jabbed]

Hyperkalaemia can cause tall, peaked T waves, followed by a loss of the P waves, followed by QRS widening and a sinusoidal patterning.

Why those specific changes in that sequence.

What's the mechanism at each step. Why.

Cheers,

Effects of Hyperkalemia on Impulse Production and Propagation:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1413606/#__sec3title

Hands down the best explanation that I've seen on this topic. Bear in mind that the changes do not necessarily occur in sequence and are notoriously insensitive markers of [K].

Long and short of it:

• P wave and PR/QRS elongation are due to partial depolarization and inactivation of the sodium channels which decreases maximal conduction velocity.
• T wave peaking is due to rapid and synchronous repolarization of the membrane secondary to increased potassium permeability during phase 2/3 of the action potential. Supposedly, this occurs because the increased extracellular potassium actually triggers the opening of potassium channels and increases the conductance of the membrane to potassium during this phase.

 

[Phloston]

Effects of Hyperkalemia on Impulse Production and Propagation:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1413606/#__sec3title

Hands down the best explanation that I've seen on this topic. Bear in mind that the changes do not necessarily occur in sequence and are notoriously insensitive markers of [K].

Long and short of it:

• P wave and PR/QRS elongation are due to partial depolarization and inactivation of the sodium channels which decreases maximal conduction velocity.
• T wave peaking is due to rapid and synchronous repolarization of the membrane secondary to increased potassium permeability during phase 2/3 of the action potential. Supposedly, this occurs because the increased extracellular potassium actually triggers the opening of potassium channels and increases the conductance of the membrane to potassium during this phase.

Champion. Cheers man

 

[Silverish]

Not sure exact mechanism of the sequence of events, nor do I think anything like that will be asked on STEP1.
However, I did have something like that on my exam - just needed to be able to recognize hyperkalemia on EKG.
I just think thats about as far as you have to go for it.

 

[tasar1898]

I remember reading Qester's explanation simplified somewhere , it sticks if you think Potassium Channels ''love'' having some potassium around to keep them open -->More Potassium--> Inc Conductance --> Rapid Repol --> Peaked T wave

Also increased K increases excitability in the short term ( like seconds to minutes ) due to its effect on the concentration gradient part of K+ efflux --> Less K going out --> Resting Em is closer to 0 . This eventually leads to depolarization of some Na channels which ''locks'' them out of the game , but without producing an AP , so now less Na channels available to fire --> Reduced excitability (minutes until you fix the hyperkalemia)