A healthy 50-something who exercises regularly had new onset of dyspnea on even the slightest exertion for the previous 2 days. He reports he is physically fit and has never had this problem before. Also reports new onset substernal non-radiating chest pain with exertion that started today. Patient reports that he had to run today to catch a ride and he could only get a few steps before being completely drenched in sweat and so out of breath he had sit down.
He denies any history of this in the past, denies cardiac history or lung problems.
He is on no medications.
He presented to the ED and had an ECG, which had a very strong clue as to etiology:
There is a PR interval of 330 ms. First degree AV block is generally considered benign. Any PR interval of longer duration than 200 ms is defined as first degree AV block, but the vast majority are still under 300 ms. 330 ms is very long. The QRS duration is a bit long as well. The QRS in most healthy adults is less than 100 ms, though it can be up to 110 ms. A QRS of 109 ms suggests that the site of AV conduction delay may be below the bundle of His and not in the AV node. This would suggest a serious conduction delay.
The clinical presentation is very worrisome for severe exertional ischemia due to a tight coronary stenosis, but this ECG finding of a very long PR interval may provide an alternative explanation for the symptoms.
Potassium was normal. Serial troponins were all below the level of detection.
Because of exertional symptoms, he was tested with a treadmill ECG test, and after walking on the treadmill for one minute, he developed AV block progressing with increasing heart rate to second degree block Mobitz II (2:1 block). His heart rate dropped from 88 to 50, with reproduction of the symptoms. This was suggestive of infranodal disease (in the bundle of His).
The patient had a dual chamber pacemaker placed.
No etiology was found, but MRI was to be done later as an outpatient.
First Degree AV Block
1. Etiology
a. Increased Vagal Tone, particularly in athletes
b. Hyperkalemia
c. Drugs
---that affect the AV node: (digoxin, beta blockers, non-dihydropyridine calcium channel blockers such as diltiazem or verapamil)
---that affect the Bundle of His: Type 1a antidysrhythmics such as procainamide, quinidine, disopyramide and also type 1c such as flecainide.
d. Myocardial infarction, acute or old.
----When anterior MI, then it is below the AV node (bundle branch or fascicle) and more dangerous.
----When inferior MI, it is the AV node that is ischemic. It is less likely to progress to complete AV block and more likely to be sensitive to atropine.
e. Underlying AV nodal structural abnormalities
f. Infiltrative diseases such as sarcoidosis, amyloidosis, and hemochromatosis
g. Lyme Carditis
h. Other
2. Sites of delay
AV node is most common. This is measured by the atrial-His (AH) time measured by His bundle ECG. Normal AH time is 60-125 ms. A narrow QRS strongly implies that the site of delay is the AV node.
Bundle of His or lower. Usually associated with a wide QRS.
3. Presentation
There are rarely symptoms of first degree AV block and it is almost always benign. When associated with a wide QRS, it is likely that the block is below the AV node. This is important because it is more likely to progress to complete heart block. Especially when there is RBBB + fascicular block + first degree AV block, there is risk of progression to complete heart block. This situation has the misnomer of "Trifascicular block." This would literally imply complete heart block if all 3 fascicles were blocked (right bundle, left anterior fascicle, and left posterior fascicle). But it may indeed progress to complete heart block. Certainly any symptoms associated with both prolonged PR interval and bundle branch and/or fascicular blocks are very worrisome, especially in the context of ischemia.
See this post on "Trifascicular block"
Pacemaker syndrome (rare)
If the delay is very long, then the atrium contracts too shortly after the previous ventricular contraction, which leads to incomplete atrial filling and to a decrease in stroke volume and chest discomfort.
Summary:
It was not difficult to determine the significance of the AV conduction delay. Since the symptoms were induced by exertion, the test of choice was clearly an exercise stress test, and this produced the diagnosis. Such symptoms would more commonly be due to severe coronary stenosis, but in this case the stress test clearly showed the problem to be AV node conduction.
Article:
There are other longitudinal studies which did NOT show increased long term risk.
He denies any history of this in the past, denies cardiac history or lung problems.
He is on no medications.
He presented to the ED and had an ECG, which had a very strong clue as to etiology:
 |
| What do you think? The computerized QRS duration is 109 ms |
There is a PR interval of 330 ms. First degree AV block is generally considered benign. Any PR interval of longer duration than 200 ms is defined as first degree AV block, but the vast majority are still under 300 ms. 330 ms is very long. The QRS duration is a bit long as well. The QRS in most healthy adults is less than 100 ms, though it can be up to 110 ms. A QRS of 109 ms suggests that the site of AV conduction delay may be below the bundle of His and not in the AV node. This would suggest a serious conduction delay.
The clinical presentation is very worrisome for severe exertional ischemia due to a tight coronary stenosis, but this ECG finding of a very long PR interval may provide an alternative explanation for the symptoms.
Potassium was normal. Serial troponins were all below the level of detection.
Because of exertional symptoms, he was tested with a treadmill ECG test, and after walking on the treadmill for one minute, he developed AV block progressing with increasing heart rate to second degree block Mobitz II (2:1 block). His heart rate dropped from 88 to 50, with reproduction of the symptoms. This was suggestive of infranodal disease (in the bundle of His).
The patient had a dual chamber pacemaker placed.
No etiology was found, but MRI was to be done later as an outpatient.
First Degree AV Block
1. Etiology
a. Increased Vagal Tone, particularly in athletes
b. Hyperkalemia
c. Drugs
---that affect the AV node: (digoxin, beta blockers, non-dihydropyridine calcium channel blockers such as diltiazem or verapamil)
---that affect the Bundle of His: Type 1a antidysrhythmics such as procainamide, quinidine, disopyramide and also type 1c such as flecainide.
d. Myocardial infarction, acute or old.
----When anterior MI, then it is below the AV node (bundle branch or fascicle) and more dangerous.
----When inferior MI, it is the AV node that is ischemic. It is less likely to progress to complete AV block and more likely to be sensitive to atropine.
e. Underlying AV nodal structural abnormalities
f. Infiltrative diseases such as sarcoidosis, amyloidosis, and hemochromatosis
g. Lyme Carditis
h. Other
2. Sites of delay
AV node is most common. This is measured by the atrial-His (AH) time measured by His bundle ECG. Normal AH time is 60-125 ms. A narrow QRS strongly implies that the site of delay is the AV node.
Bundle of His or lower. Usually associated with a wide QRS.
3. Presentation
There are rarely symptoms of first degree AV block and it is almost always benign. When associated with a wide QRS, it is likely that the block is below the AV node. This is important because it is more likely to progress to complete heart block. Especially when there is RBBB + fascicular block + first degree AV block, there is risk of progression to complete heart block. This situation has the misnomer of "Trifascicular block." This would literally imply complete heart block if all 3 fascicles were blocked (right bundle, left anterior fascicle, and left posterior fascicle). But it may indeed progress to complete heart block. Certainly any symptoms associated with both prolonged PR interval and bundle branch and/or fascicular blocks are very worrisome, especially in the context of ischemia.
See this post on "Trifascicular block"
Symptomatic Bradycardia. So-called Trifascicular Block. Occum's Razor and Hickum's dictum.
Pacemaker syndrome (rare)
If the delay is very long, then the atrium contracts too shortly after the previous ventricular contraction, which leads to incomplete atrial filling and to a decrease in stroke volume and chest discomfort.
Summary:
It was not difficult to determine the significance of the AV conduction delay. Since the symptoms were induced by exertion, the test of choice was clearly an exercise stress test, and this produced the diagnosis. Such symptoms would more commonly be due to severe coronary stenosis, but in this case the stress test clearly showed the problem to be AV node conduction.
Article:
Long-term Outcomes in Individuals With Prolonged PR Interval or First-Degree Atrioventricular Block
This was a longitudinal study of 7575 asymptomatic patients in the Framingham study, of whom 124 had first degree AV block at baseline, and were followed up for 35 years. Compared to those with normal PR intervals, in multivariable analyses, each 20-millisecond increment in PR above 200 ms was associated with an adjusted hazard ratio (HR) of 1.11 for Atrial Fib, 1.22 for pacemaker implantation, and 1.08 for all-cause mortality. So the hazard ratio for a PR interval of 330 ms would be quite significant. This study was on asymptomatic patients.There are other longitudinal studies which did NOT show increased long term risk.
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