A 60-something with h/o cirrhosis and diabetes called 911 because he felt sick and was unable to move his lower extremities.
Comment: There is also a very wide QRS. The regular rate suggests: Junctional with aberrancy, or ventricular escape, or sinus bradycardia with an invisible P-wave (this happens in hyperK). The regular rate rules out atrial fib, unless there is atrial fib with complete AV block and an escape.
Whenever there is bradycardia or a wide QRS, especially BOTH, it is hyperkalemia until proven otherwise. Hyperkalemia often results in PseudoSTEMI patterns, especially in V1 and V2, but also in inferior leads.
See these other cases of PseudoSTEMI due to hyperkalemia. Some were unrecognized, resulted in inappropriate cath lab activation, and then resulted in death.
Based on the initial ECG, the providers activated the Cath Lab.
However very shortly after activation, they received the initial labs.
Unmeasurable lactate over 12
Metabolic acidosis with a pH of 7.08
Bicarb of 11, with no significant respiratory compensation with a PCO2 of 40
Acute renal failure with a potassium of 8.8 and a creatinine of 2.38.
With this information, they deactivated the Cath Lab and focused our treatment on acute hyperkalemia.
They administered 6 grams of calcium gluconate (equivalent to 2 g of CaCl), 10 units of IV regular insulin, D50, and 10 mg of nebulized albuterol.
A repeat ECG was recorded:
On arrival he was bradycardic and hypotensive.
He stated that starting approximately 7 hours prior the he felt that he was unable to feel his extremities. At some point after that he contacted his neighbor who came to check on him and called 911. On arrival to the stabilization room he says he can feel his extremities and and states that he just generally feels unwell. He denies any chest pain or shortness of breath.
EMS reports that when they arrived to the scene he had a heart rate in the 40s with very weak and thready peripheral pulses and altered mental status. He had a syncopal episode while getting into the EMS cart. He maintained pulses but was ashen and diaphoretic. He was largely unresponsive to voice during his transport to the hospital.
BP systolic 60.
Ultrasound revealed global dilation of all 4 chambers of the heart with poor contractility, a IVC that measured 2.4 cm, no significant B-lines in lung fields nor large pleural effusions.
An ECG was recorded:
 |
| No definite P-waves, Bradycardic, Regular, lots of artifact. There is ST Elevation in V1 and V2 What do you think? |
Comment: There is also a very wide QRS. The regular rate suggests: Junctional with aberrancy, or ventricular escape, or sinus bradycardia with an invisible P-wave (this happens in hyperK). The regular rate rules out atrial fib, unless there is atrial fib with complete AV block and an escape.
Whenever there is bradycardia or a wide QRS, especially BOTH, it is hyperkalemia until proven otherwise. Hyperkalemia often results in PseudoSTEMI patterns, especially in V1 and V2, but also in inferior leads.
See these other cases of PseudoSTEMI due to hyperkalemia. Some were unrecognized, resulted in inappropriate cath lab activation, and then resulted in death.
Based on the initial ECG, the providers activated the Cath Lab.
However very shortly after activation, they received the initial labs.
Unmeasurable lactate over 12
Metabolic acidosis with a pH of 7.08
Bicarb of 11, with no significant respiratory compensation with a PCO2 of 40
Acute renal failure with a potassium of 8.8 and a creatinine of 2.38.
With this information, they deactivated the Cath Lab and focused our treatment on acute hyperkalemia.
They administered 6 grams of calcium gluconate (equivalent to 2 g of CaCl), 10 units of IV regular insulin, D50, and 10 mg of nebulized albuterol.
A repeat ECG was recorded:
 |
| Dramatic improvement Peaked T-waves remain in all leads, and QRS is still wide, but much better. |
A good example of what I would call an "acquired" Brugada ECG pattern from hyperkalemia. What is Brugada syndrome? A congenitally defective sodium channel causing ST elevation in V1-2. Hyperkalemia, hyperthermia or several other conditions are also known to disable the sodium channel in some patients, causing a Brugada ECG pattern.
ReplyDeleteK. Wang.
Thanks (!) for your comment K. Hyperkalemia clearly IS one of the more common causes of Brugada phenocopy (a number of these cases have been published on Dr. Smith’s ECG blog). There is however a lot of artifact on the initial ECG in this case — and I thought this made it harder to identify a Brugada-1 pattern.
Deleteoooooooooh very nice
ReplyDeleteWhenever there is bradycardia or a wide QRS, especially BOTH, it is hyperkalemia until proven otherwise. Hyperkalemia often results in PseudoSTEMI patterns, especially in V1 and V2, but also in inferior leads.
@ Unknown — Yes, Yes & Yes to your comments — :)
DeleteHi Prof Smith,
ReplyDeleteThanks for this interesting case. Reading the presenting complaints my first thought was that bilateral muscle weakness seems unlikely to be result of focal neurology . When the cluster of symptoms seem non-specific when taken together. In the context of a diabetic person I would have initially done his capillary glucose and ketone level, and checked his electrolytes.
The bloods seem to suggest that he might be a type 1 diabetic who has diabetic ketoacidosis, with acute kidney injury secondary to dehydration. Was he non-compliant with insulin?
I am unsure of why the cath lab was activated in the first instance before waiting for the electrolytes, especially considering there is no chest pain history at all!
Another thing I don't understand is the significance of the echo showing dilation in all four chambers. Would that be an expected finding in hyperkalaemia?
@ Sahib — THANKS for your comment. Unfortunately, more history is not known on this case. The major learning point in this case is (as you say) — that the cath lab should not have been immediately activated. Instead, the bradycardia and wide QRS should immediately suggest hyperkalemia — correction of which becomes the highest priority. Chamber dilation is not an expected finding in hyperkalemia.
Deletefirst:
ReplyDeletehappy holidays, team. and that includes our global team of women and men who have chosen to do what we do.
second: cool post, Steve. and i do not mean cool as in you must be pretty darn cool up there in minneapolis. yes, you have taught us before: listen to the patient. ill, weak, no chest pain. look. brady and ugly complexes, no or hard to see P waves.
cool case.
happy holidays, Steve.
Thanks, tom!
DeleteHi Dr. Smith, I have two questions:
ReplyDelete-What was the cause of ARF with lactic acidosis and low blood pressure(if you learned anything about it)? Was he septic, taking Metoformin for diabetes or beta-blockers for cirrhosis-related portla hypertension? This latter eventuality, in particular, would explain almost everything about the clinical scenario and the ECG findings (not only bradycardia but, by some means, even hyperkalemia cause by hyporeninemic hypoaldosteronism)
-Surely hyperkaliemia fits, especially in the setting of bradycardia without any clear P vawe and large and "misshapen" QRS (Broad, Brayd and Bizarre9. Nontheless, QRS morphology in lead V1 and V2 potentially looked like Brugada (or Brugada-like!) to me. What do you think about it?
Thanks!
@ Anonymous — Unfortunately, additional history was not available on this case. Hyperkalemia is among the more common causes of Brugada Phenocopy (ie, some other condition that may produce a Brugada-1 ECG pattern — but which resolves after correction of in this case the electrolyte disorder). That said, there is so much artifact on the initial ECG that I was not at all certain if there was a Brugada-1 ECG pattern here ... (but other cases in which there was definite Brugada Phenocopy have been published previously on this blog). THANKS for your comment — :)
Delete