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Dr A Röschl's picture

Sinus Bradycardia and More

Let's analyze the ECG. It comes from a pacemaker patient whose pacemaker was briefly switched to VVI at 30 bpm due to a stimulation threshold test. The first 3 beats show a sinus rhythm with a frequency of approx. 40 bpm. This is followed by a premature ventricular contraction (PVC). The P wave of the next sinus node beat lands exactly on the T of the PVC. This cannot be conducted to the ventricles, either because the ventricular myocardium is still unexcitable or the PVC has conducted retrogradely into the AV node and this is therefore still refractory.

Dawn's picture

Left Bundle Branch Block

This ECG is taken from an elderly man with heart failure. 

The ECG   The first feature that might capture your attention is the wider-than-normal QRS complex, which is 160 ms (.16 seconds).  The rate is 58 bpm. We do not know the patient’s medications or baseline rate.  There are P waves present, and so the rhythm is SINUS BRADYCARDIA. The P waves are broad , > 110 ms in Lead II (red lines in close up) and bifid, with greater than 40 ms between the two peaks in Lead II (blue lines).  In V1, the P waves are biphasic, with the terminal negative portion greater than 40 ms duration (red lines). This meets the ECG criteria for LEFT ATRIAL ENLARGEMENT, or preferably, LEFT ATRIAL ABNORMALITY. (https://LITFL.com/left-atrial-enlargement-ecg-library/) ECG criteria are not highly accurate for detecting atrial enlargement, and abnormal findings should be confirmed by anatomic measurement. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2244611/).

The QRS complexes, as mentioned, are wide. Because there is sinus rhythm, we know the delay in conduction is due to interventricular conduction delay, and not to ventricular rhythm.  This ECG meets the criteria for LEFT BUNDLE BRANCH BLOCK. 

·        Supraventricular rhythm 

·        Wide QRS (>.12 seconds)

Dawn's picture

High-grade AV Block With Profound Bradycardia

If you are an ECG instructor, you probably carefully choose ECGs to illustrate the topic you are teaching. One of the reasons for the existence of the ECG Guru website is our desire to provide lots of such illustrations for you to choose from.

Sometimes, though, an ECG does not clearly illustrate one specific dysrhythmia well, because the interpretation of the ECG depends on so many other factors.  In order to get it “right”, we would need to know information about the patient’s history, presentation, lab results, or previous ECGs. We might need to see the ECG done immediately before or after the one we are looking at.  Some ECG findings must ultimately be confirmed by an electrophysiology study before we can know for sure what is going on.

For those of us who are “ECG nerds”, it can be fun to debate our opinions and even more fun to hear from wiser, more advanced practitioners about their interpretations.

My belief, as a clinical instructor, is that we must teach strategies for treating the patient who has a “controversial” ECG that take into account the level of the practitioner, the care setting, and the patient’s hemodynamic status.  In some settings, it might be absolutely forbidden for a first-responder to cardiovert atrial fibrillation, for example.  But atrial fib is routinely cardioverted under controlled conditions in hospitals.  The general rule followed by emergency providers that “all wide-complex tachycardias are v tach until proven otherwise” has no doubt prevented deaths in situations where care providers did not agree on the origin of the tachycardia.

The ECG:    We do not have much patient information to go with this ECG, just that it is from a 71-year-old woman who developed severe hypotension and lost consciousness, but was revived with transcutaneous pacing.   Here is what we do know about this ECG:

·        There are regular P waves, at a rate of about 39 bpm (sinus bradycardia).

Dawn's picture

Bifascicular Block and Sinus Bradycardia

Today’s ECG is from a 75 year old man who has been experiencing syncope. 

Examination of the ECG shows a sinus bradycardia at just under 40 bpm.  There is a first-degree AV block, with a PR interval of about .28 seconds (280 ms).  There is a right bundle branch block.  The ECG criteria for right bundle branch block are:  supraventricular rhythm, wide QRS (120 ms in this case), rSR’ pattern in V1, and  a small, wide S wave in Leads I and V6.  There is actually a “terminal delay”, or extra wave at the end of each QRS complex, reflecting late repolarization of the right ventricle. 

This ECG also shows a left anterior fascicular block, also called left anterior hemiblock.  The left bundle branch usually has two main branches, the anterior-superior and the posterior-inferior.  ECG criteria for left anterior fascicular block are: left axis deviation with a small r wave in Lead III and a small q waves with tall R waves in Leads I and aVL.  There is also a prolonged R wave peak time (> 45 ms) in aVL. There is usually a slightly prolonged QRS, but in this case, there is widening of the QRS due to the RBBB.   Because the right bundle branch is blocked, and one fascicle of the left bundle is blocked, the patient is said to have a “bifascicular block”.  Only one fascicle remains available for conduction from the atria to the ventricles.

We have no information about what caused the conduction block in these two fascicles, but should the third fascicle fail, the patient will be in a complete AV block.  An AV block at the level of the bundle branches will result in an idioventricular escape rhythm – wide QRS complexes with very slow rates – which is a low-output rhythm.  

This patient has also had syncope, which was determined to be related to his bradycardia.  He had an AV sequential pacemaker implanted and did well.

Dawn's picture

ECG Basics: Sinus Bradycardia

Sinus bradycardia.  This strip meets the criteria of:  regular rhythm, rate less than 60 bpm (40 bpm in this case), regular P waves before every QRS.  Sinus bradycardia can have many causes from a completely normal variation to a malfunction of the sinus node.  In some cases, enhanced parasympathetic tone causes sinus bradycardia.  Well-conditioned athletes typically have sinus bradycardia. Treatment depends upon the cause and the patient's response to the rate.  If the rate does not cause hemodynamic impairment, treatment may not be necessary.

Dawn's picture

Electrolyte Effects

This ECG is from a 46-year-old woman with diabetes mellitus.  She presented to the Emergency Dept. with a complaint of weakness.  Her BP was elevated at 186/102.  Her blood glucose was 936 mg/dL (normal 70-105). 

So, what does her ECG show?

1) Sinus bradycardia at 55 bpm.  The rhythm is regular, with no extrasystoles.

2) A slightly prolonged PR interval at 218 ms (.218 seconds). Normal is 120-200 ms. 

3) A “wide side of normal” QRS duration at 109 ms. Normal is 70-100, but can be a little longer in normal individuals.

4) A prolonged QTc interval at 520 ms.  Normal QTc is 460 ms or less in women. A helpful rule of thumb is that the QT should be less than half the preceding RR. 

5) Normal P waves.

6) Normal axes of P, QRS, and T waves.

7) A large Q wave in Lead III which is not repeated in aVL.  This can be inconsequential when confined to Lead III, or can be a pathological Q wave, especially if also seen in aVF. 

8) Flat ST segments.  Normal ST segments are convex upward, like a smile.

9) Tall, peaked T waves in precordial leads V2 through V6, and in Lead II. 

What does it mean?

Unfortunately, we do not have complete labs for this patient, or any information about her outcome.

We know that patients who have uncontrolled diabetes are at risk for renal failure, so we should consider electrolyte imbalances when we see abnormalities in the ECG. 

Dawn's picture

Inferior Wall M.I.

This ECG shows a common manifestation with inferior wall M.I., BRADYCARDIA.  We see the signs of acute inferior wall M.I. in the inferior leads:  II, III, and aVF all have ST segment elevation.  There almost appear to be pathological Q waves in Leads III and aVF.  There are still VERY tiny r waves, and the downward deflections are not wide, but should full-blown Q waves develop in these leads, they would signify necrosis in the area.  A repeat ECG would certainly be warranted. 

Another sign that there is an inferior wall STEMI is the ST segment depression in Leads I and aVL, which are reciprocal to Lead III.  ST depression can have many meanings, but when it is localized in the leads which are opposite ST elevation, it is reciprocal.  There is also ST depression in Leads V1 and V2.  These leads are reciprocal to the POSTERIOR wall, otherwise known as the upper part of the inferior wall.  If an inferior wall M.I. is large enough, it can produce ST elevation in the posterior leads (not performed in this case), and ST depression in the anterior leads, especially V1, V2, and V3. 

The rhythm is a marked sinus bradycardia, at just under 40 beats per minute.  Sinus bradycardia is very common in inferior wall M.I., because the inferior wall and the sinus node are usually both supplied by the right coronary artery.  AV blocks can also occur because the AV node is also supplied by the RCA in most people. 

It is important to remember that bradycardia does not always need to be treated.  In patients with acute M.I., a well-tolerated bradycardia may actually be beneficial to the injured heart, reducing supply/demand ischemia.  A well-tolerated bradycardia is a rate that does not produce low blood pressure and poor peripheral perfusion.  Some people tolerate rates in the 40’s quite well.  If the patient shows signs of poor perfusion: low BP, decreased mentation, pallor, shortness of breath, the rate should be cautiously increased with medication or electronic pacing.  

 

Dawn's picture

ECG Basics: Sinus Bradycardia With A Premature Atrial Contraction

This strip shows an underlying sinus bradycardia with a rate less than 40/min.  There is one "premature" beat, which can be considered to be ectopic, because it interrupts an otherwise regular rhythm.  The interesting thing is that the premature beat is not terribly early - it is about 740 ms from the previous beat.  If all the beats were spaced like this, the heart rate would be about 84/min.  There is probably an element of "escape" here, in that the ectopic beat is able to express itself due to the slow rate.  A faster sinus rate would override this ectopic focus.  So, we could view this early beat as a help, rather than a problem.  The most important consideration here is to address the cause of the bradycardia, and treat appropriately. 

Dawn's picture

ECG Basics: Sinus Bradycardia With First-degree AV Block

This is a nice teaching strip of a slowing sinus bradycardia that began around 40 bpm, and is slowing.  It is a good example of how the sinus node slows down - there is no abrupt change of rates, rather a change with each R-to-R interval.  There is also a first-degree AV block, reflecting slowing of conduction in the AV node.  The PR interval is slightly variable at .28 sec. to about .32 sec.  This is a good strip to begin talking about treatment of bradycardias with beginner students, as there is no second- or third-degee AVB, but the patient is very likely to be symptomatic now, or very soon.  Atropine would probably improve this rate in a symptomatic patient, but if there is time, a 12-Lead would be a good idea to rule out acute M.I.  Inadvertently raising the rate too much in the injured heart can lead to pump failure, while leaving the patient poorly-perfused in a bradycardia will starve the heart.  A transthoracic or temporary IV pacemaker might be a better choice for some patients because of our ability to choose the rate.

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