This is complementary to a recent previous post.
A dialysis patient presented with pedal edema. As a screen for hyperkalemia, an ECG was recorded:
A previous ECG was immediately found at a time when the K was 6.1 mEq/L:
This shows how subtle hyperkalemia can be, and yet still be diagnostic.
See the two side-by-side here:
Previous, with K 6.0 mEq/L This Visit
My previous post showed the failure to recognize such a subtle sign of hyperkalemia and the subsequent v fib arrest.
In RBBB, a QRS duration greater than 175 ms should make you strongly suspect hyperK (see this link!). In this case, in the past, there actually had been such a long QRS in the presence of a normal K, so this case was an exception.
The patient's K was 7.1 mEq/L.
A dialysis patient presented with pedal edema. As a screen for hyperkalemia, an ECG was recorded:
 |
| QRS duration is 183 ms. What do you think? |
A previous ECG was immediately found at a time when the K was 6.1 mEq/L:
 |
| QRS duration is 167 ms, but a previous ECG with a normal K had a QRS of 184 ms. What do you think? |
This shows how subtle hyperkalemia can be, and yet still be diagnostic.
See the two side-by-side here:
Previous, with K 6.0 mEq/L This Visit
 |
| Notice how the ST segment is flatter on the right than on the left (see especially lead V4). Such a flat ST segment is part of what makes the T-wave peaked, as the rise of the T-wave from a flat ST segment is very steep. |
My previous post showed the failure to recognize such a subtle sign of hyperkalemia and the subsequent v fib arrest.
In RBBB, a QRS duration greater than 175 ms should make you strongly suspect hyperK (see this link!). In this case, in the past, there actually had been such a long QRS in the presence of a normal K, so this case was an exception.
The patient's K was 7.1 mEq/L.
Steve...
ReplyDeleteA very interesting case! I seem to recall you having commented on this finding before. Has anyone done the research to determine why and under what circumstances the ST segment may present this way in hyperkalemia? It is certainly not an unusual finding in chronic ischemia and even as a reciprocal change during acute ischemic episodes. One would think that the plateau (Phase 2) of the AP would have to be a bit longer and flatter than usual and repolarization (Phase 3) should have a very acute downslope (perhaps a prolonged inward calcium current with an abrupt end). Most cases of hyperkalemia that I have seen are characterized by a rather short ST segment (if any at all) and I don't recall ever noticing this type of ST segment. After reading your post, I searched the internet for more examples. The vast majority were associated with a short ST or an immediate take off of the T wave from the terminal QRS but I did find several examples with the flat ST segment ending in an acute takeoff of the T wave. I was not able to relate those few to any other particular characteristic other than the fact that all the T waves ended well before the middle of the R-R interval (but so did some of the ECGs with the other more characteristic ST-T changes). And each example of the flat ST segment was associated with more obvious and characteristic changes elsewhere on the 12-lead ECG. Perhaps this would be a good research topic for someone.
Jerry,
DeleteI agree. HyperK usually has a long QT. On the other hand, a high extracellular K would slow the outward potassium flow of phase 2, making for a more prolonged phase 2 and flat ST segment. Then a sudden change in the inward. A decrease in Ca inflow would result in the fast repolarization and short QT.
Steve
Sir please ,How hyperkalemia Usually cause long QT interval , I Think Hypokalemia cause Long QT rather than hyperkalemia ?
ReplyDeleteHere we are talking about the QRS. But, yes, hyperK causes shorter QT and hypoK longer
Delete