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This dialysis patient called 911 for weakness. Medics found the patient to be hypotensive and bradycardic.
The patient was taking carvedilol and amlodipine, but denied overdose.
The medics recorded this ECG:
The patient was stable enough that no therapy was needed, but the correct therapy would be IV Calcium. This ECG represents hyperkalemia until proven otherwise and, if it is due to hyperK, it will often respond immediately to calcium therapy.
He arrived and had this ED ECG recorded:
Hyperkalemia can abolish atrial activity and eliminate P-waves, even though the sinus node may still be generating a rhythm. So, in this case, there may be an underlying sinus rhythm that is generating the impulse we see. Or it could be a slow junctional rhythm. The distinction is academic.
Note the T-waves are only minimally peaked (II, and V4-V6 especially) and would not even be noticed by many observers.
We administered Calcium Chloride 1 gram x 3 as well as atropine, and the pulse increased to 60 beats per minute.
We gave calcium chloride because there is a shortage right now of calcium gluconate. Had we given gluconate, it would have required 9 grams to obtain the same molar amount. Calcium chloride is safe to give through a peripheral vein if it is a high quality IV and it is given slowly. I gave it for years as a young physician with no adverse events. It does cause skin necrosis if it infiltrates.
The K returned at 8.1 mEq/L.
We also gave albuterol, insulin, and dextrose, as well as bicarb (the patient was not fluid overloaded).
The heart rate increased and he went immediately to dialysis.
It is wise to place external pacing pads!
Learning Points:
1. Bradycardia is hyperkalemia until proven otherwise because it is very common, very easily ruled in or out with a K level, and very easily and safely treated with calcium.
2. The only ECG sign of severe and life threatening hyperK may simply be bradycardia. There may be no QRS widening or peaking of T-waves.
The patient was taking carvedilol and amlodipine, but denied overdose.
The medics recorded this ECG:
 |
| The medics were considering external pacing. What is a better initial therapy? |
The patient was stable enough that no therapy was needed, but the correct therapy would be IV Calcium. This ECG represents hyperkalemia until proven otherwise and, if it is due to hyperK, it will often respond immediately to calcium therapy.
He arrived and had this ED ECG recorded:
 |
| There are no visible P-waves. Rate is 35. There is a narrow complex bradycardic rhythm. It appears to be junctional. |
Hyperkalemia can abolish atrial activity and eliminate P-waves, even though the sinus node may still be generating a rhythm. So, in this case, there may be an underlying sinus rhythm that is generating the impulse we see. Or it could be a slow junctional rhythm. The distinction is academic.
Note the T-waves are only minimally peaked (II, and V4-V6 especially) and would not even be noticed by many observers.
We administered Calcium Chloride 1 gram x 3 as well as atropine, and the pulse increased to 60 beats per minute.
We gave calcium chloride because there is a shortage right now of calcium gluconate. Had we given gluconate, it would have required 9 grams to obtain the same molar amount. Calcium chloride is safe to give through a peripheral vein if it is a high quality IV and it is given slowly. I gave it for years as a young physician with no adverse events. It does cause skin necrosis if it infiltrates.
The K returned at 8.1 mEq/L.
We also gave albuterol, insulin, and dextrose, as well as bicarb (the patient was not fluid overloaded).
The heart rate increased and he went immediately to dialysis.
It is wise to place external pacing pads!
Learning Points:
1. Bradycardia is hyperkalemia until proven otherwise because it is very common, very easily ruled in or out with a K level, and very easily and safely treated with calcium.
2. The only ECG sign of severe and life threatening hyperK may simply be bradycardia. There may be no QRS widening or peaking of T-waves.
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