A 60'ish male presented with 2 weeks of intermittent chest pain. He has a history of MI and renal insufficiency. Now he feels weak. His pulse is 42 with a BP of 140/35. Here is his initial ECG:
His charts showed he had presented to a clinic 2 months prior with chest pain and had an identical ECG which was read as "no change from old". The ECG prior to that one, however, did not have bradycardia (so there really was a change from old). The patient had been sent home from clinic.
Rhythm analysis: there is a regular rhythm with a QRS that is borderline prolonged at 110 ms (QRS on the previous truly normal ECG was 105 ms). Are there p-waves? Yes, but they are after the QRS, and they are inverted. And the R-P interval is very prolonged at about 440 ms. So there is either sinus arrest or severe sinus bradycardia (such that the junction or bundle of HIS escapes before the sinus node can fire). There is atrial activity (the p-wave); it is inverted because it is being activated from below.
Diagnosis: Sinus arrest or extreme bradycardia with junctional escape and retrograde p-waves with prolonged VA conduction.
One might also say there is a severe 1st degree AV block because of the long R-P (not P-R) interval, but our electrophysiologist, Rehan Karim, states that:
"One cannot infer that VA conduction tells you what AV conduction would be. It is well known that patients who have complete AV block may have intact VA conduction. That is, a ventricular beat gives rise to retrograde p waves, but the P-waves or atrial pacing does not conduct to the ventricles. Same is true with adenosine: there can be few times when adenosine will affect AV conduction but may or may not affect VA conduction."
What are the common causes:
1. hyperkalemia
2. Ischemia (no evidence of ischemia on this ECG)
3. Drugs (he was not on any that woul do this): digitalis, beta blockers, calcium channel blockers, Na channel modulators
4. Sick sinus
5. Increased vagal tone, but this would also slow the escape.
5. Variety of other less common etiologies, such as Lyme, infiltrative diseases
Atropine 1 mg was given without change. Potassium returned at 6.2 mEq/L. 3g of Calcium gluconate were given and the rate immediately went to 60. Here is the subsequent ECG:
The patient ruled out for MI by serial troponins.
When a patient has bradycardia, always think of hyperkalemia among other etiologies.
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| What is the rhythm, and what the etiology? |
His charts showed he had presented to a clinic 2 months prior with chest pain and had an identical ECG which was read as "no change from old". The ECG prior to that one, however, did not have bradycardia (so there really was a change from old). The patient had been sent home from clinic.
Rhythm analysis: there is a regular rhythm with a QRS that is borderline prolonged at 110 ms (QRS on the previous truly normal ECG was 105 ms). Are there p-waves? Yes, but they are after the QRS, and they are inverted. And the R-P interval is very prolonged at about 440 ms. So there is either sinus arrest or severe sinus bradycardia (such that the junction or bundle of HIS escapes before the sinus node can fire). There is atrial activity (the p-wave); it is inverted because it is being activated from below.
Diagnosis: Sinus arrest or extreme bradycardia with junctional escape and retrograde p-waves with prolonged VA conduction.
One might also say there is a severe 1st degree AV block because of the long R-P (not P-R) interval, but our electrophysiologist, Rehan Karim, states that:
"One cannot infer that VA conduction tells you what AV conduction would be. It is well known that patients who have complete AV block may have intact VA conduction. That is, a ventricular beat gives rise to retrograde p waves, but the P-waves or atrial pacing does not conduct to the ventricles. Same is true with adenosine: there can be few times when adenosine will affect AV conduction but may or may not affect VA conduction."
What are the common causes:
1. hyperkalemia
2. Ischemia (no evidence of ischemia on this ECG)
3. Drugs (he was not on any that woul do this): digitalis, beta blockers, calcium channel blockers, Na channel modulators
4. Sick sinus
5. Increased vagal tone, but this would also slow the escape.
5. Variety of other less common etiologies, such as Lyme, infiltrative diseases
Atropine 1 mg was given without change. Potassium returned at 6.2 mEq/L. 3g of Calcium gluconate were given and the rate immediately went to 60. Here is the subsequent ECG:
 |
| Sinus rhythm with a PR interval of approximately 200 ms. The QRS is acttually slightly longer, at 113 ms. |
The patient ruled out for MI by serial troponins.
When a patient has bradycardia, always think of hyperkalemia among other etiologies.
HyperK is the Syphilis of the EKG:The Great Imitator
ReplyDeleteHi Dr Smith
ReplyDeleteYet another fascinating and informative case. From a junior doc, thanks for all the work you do to educate us. It truly is amazing and what is even more spectacular is that it is free!
Can I ask, how did you determine the p-waves in the initial ECG? When I first looked at it, I was thinking biphasic T-waves or U-waves.
Thanks
Ryan
Ryan, thanks for the kind words. As for recognizing the p-waves, always look in leads II and V1. In II, the negative deflection is just to abrupt to be a biphasic T- or U-wave. In V1, in which normal p-waves are always biphasic (up then down), the wave here is biphasic (down then up!). So it must be a p-wave.
Deletethank you Dr smith, i'm also a hunior doctor from Algeria, i would ask about the tall and large T waves in V2 V3 ? what's their signification ?
ReplyDeletethank you merci beaucoup
They are partly due to hyperkalemia, and became smaller after treatment for hyperK.
DeleteJe vous en prie!
Steve Smith
Hi, I just discovered this wonderful blog, hence the late reply.
ReplyDeleteMay I enquire as to why you did not include third degree SA block as a differential diagnostic.
Also, what can account for the huge gap between systolic and diastolic BP ?
Thanks for your time.
Stanley, you are absolutely correct that third degree SA block should be on the differential. Thanks.
DeleteSteve Smith
Also, bradycardia leads to a high pulse pressure because it gives the elastic recoil of the aorta much time to release its pressure: so much time that little elastic recoil is left and you get a low diastolic pressure.
Delete