Altered Mental Status, Bradycardia

911 was called for an elderly woman who fell and was confused.  Medics found her unresponsive, with “convulsive” movements.  They could not find a pulse.  They performed CPR, gave epinephrine, and intubated the patient and regained a pulse, at which time she became responsive and had this prehospital ECG:

On arrival, heart rate was 87 and she was hypotensive at 52/21, with a palpable pulse and cardiac function present on echo.  She was intubated (by medics), but awake and alert and nodding to questions, shaking her head “no” to chest pain, headache, or SOB.  Repeat pulse was slow and irregular.  She was non-focal and followed commands.

Her heart rate dropped back down and an ECG was recorded:


First, there are very sublte regular P-waves at a rate just over 100, seen best in lead II across the bottom.  The ventricular response is irregular and dissociated, and narrow, so there is complete AV block with variable junctional escape.

And one other finding.   At conference, one of our smart faculty, Dr. Richard Gray, immediately made the diagnosis without any other clinical information, though it is very subtle.  What is it?

This magnification of lead III may help, though it is still very subtle:

What is that bump at the end of the QRS?

The diagnosis was not suspected based on either clinical or ECG grounds.  The patient was given atropine 0.5 mg x 3 with no response.

Labs were:
VBG: 7.21/59/39/23
Lactate: 4.8
Hgb: 13.7
Na: 138
Cl: 109
K: hemolyzed at 8.1
CO2: 23
Cr: 2.62

After ketamine sedation, transcutaneous pacing was begun at a rate of 70, with capture at 48 milliamps.

It was found that the patient was on metoprolol and diltiazem, so Calcium gluconate 3 grams was given for both possible hyperkalemia and calcium channel blocker (CCB) toxicity.  Glucagon 1 mg was given for possible BB toxicity.

High dose insulin (HDI) was started at 1unit/kg for probably CCB and BB toxicity.

At 60 minutes, transcutaneous pacing was stopped and another ECG was recorded:

The finding is still very subtle.

It is very small Osborn waves.  In the second ECG, it is most apparent in lead V6, though still extremely subtle.

This is a diagnosis that should be made clinically.  One would think that you don’t need an ECG to diagnose hypothermia, but sometimes the temperature is not easy to get. 

In this case, they had trouble obtaining a rectal temperature.  This alone is a clue that it may be very low.  When they finally did get a temperature by urinary catheter probe, it was 29 degrees C, or 84 degrees F.

In this case, the ECG had atrial fibrillation with a very slow ventricular response.  One should not only suspect hypothermia, but also hyperkalemia and drug toxicity.  All three contributed here.  Transcutaneous pacing and treatment for all 3 disorders was undertaken with success.

Ultimately, the patient was found to be uroseptic.

Tiny Osborn waves.

If you don’t believe the finding in lead III, look at this series of ECGs that start at 23 degrees and end at 29 degrees.  Look at lead III on the 4th (last, at 29 degrees) ECG.

Massive Osborn Waves of Severe Hypothermia (23.6 C), with Cardiac Echo

Learning Point:

1. Always obtain an accurate temperature in critically ill patients.  Rectal temp may not record accurately.  If the temp does not record, consider that it is too low.  Or get an EKG (just kidding).

2.  Use transcutaneous pacing when bradycardia results in cardiac output that is insufficient (shock, in this case manifested by ).

Everything you need to know about transcutaneous pacing:

Emergency Transvenous Cardiac Pacing

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