ECG Blog #61 — What is Vagotonic Block?

The series of rhythm strips shown in Figures 1,2,3, and 4 were obtained from a young adult recovering from recent surgery.

• How would you interpret these tracings?
• Is the conduction disturbance due to 2nd degree AV block Mobitz Type I (AV Wenckebach)? – or to Mobitz II? – or to complete (3rd degree) AV block?
• Is this patient likely to need a pacemaker?

Figure 1 – First in a series of Holter tracings obtained from a young adult with recent surgery (See text).

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Figure 2 – Second in a series of 4 tracings (See text).

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Figure 3 – Third in a series of 4 tracings (See text).

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Figure 4 – Fourth in a series of 4 tracings (See text).

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INTERPRETATION: Clinical assessment of what we are seeing over this series of 4 tracings is best accomplished by first noting all findings, and then putting them together into a single cohesive explanation.

• Figure 1 – The QRS complex is narrow. The R-R interval is the same between beats #2-3 and #3-4 – but it varies for other beats on this tracing. This suggests that beats #3 and #4 (which each end a longer R-R interval cycle) may be junctional escape beats. Supporting this supposition is at least transient AV dissociation (there seems to be no relation between P waves and the QRS in the middle of the tracing) – and – slightly different QRS morphology for beats #3 and #4 compared to the other beats on the tracing (the S wave seems deeper for both beats #3 and 4). The P-P interval varies greatly throughout the tracing (See arrows in Figure 5) – much more so than one would normally expect for simple sinus arrhythmia. Finally – Beats #1 and #5 may be conducting, albeit with a long PR interval (the PR interval appears to be the same for beats #1 and #5). If this were true (that beats #1 and #5 are conducting) – then there would be a Wenckebach cycle with progressive lengthening of the PR interval preceding beat #2 compared to #1 – with non-conduction of the P wave that notches the T wave of beat #2. That said - interpretation of Figure 1 is complex and clearly atypical from the usual appearance of 2nd degree AV block, Mobitz Type I .

Figure 5 – Red arrows highlight the marked P-P irregularity seen in Figure 1. Variation in the P-P interval is clearly more marked than is normally seen with simple sinus arrhythmia.

• Figure 2 – Interpretation of this second tracing is even more complex than was the rhythm strip in Figure 1. The QRS complex is narrow, with slight variation in QRS morphology that is difficult to characterize (the QRS is seen to vary more in lead V1 than in lead II). The P-P interval is even more irregular than it was in Figure 1. It is difficult to determine IF the reason P wave morphology in lead V1 is changing is due to shift in the site of the atrial pacemaker (?) – vs acceptable variation in P wave morphology as a result of baseline artifact. It is equally difficult to determine if beats #2, 3 and 4 make up a Wenckebach cycle (with progressive PR interval lengthening until a beat is dropped) vs some other random occurrence accounting for the change in P wave and QRS morphology with marked variation in P-P interval. More questions are raised by Figure 2 than are answered .

• Figure 3 – We know beat #2 is not conducting (the PR interval preceding beat #2 is clearly too short for conduction). We wonder if beats #3 and #5 are sinus conducted with 1st degree AV block (both have similar albeit prolonged PR intervals). Although at first glance one might think beat #1 is conducted in the same manner – measurement (with calipers) of the PR interval preceding beat #1 reveals slight-but-real lengthening compared to the PR interval preceding beats #3 and 5. The cause for this is uncertain from assessment of Figure 3 alone.

• Figure 4 – More of the same variation is seen in this fourth and final tracing. We suspect beats #2 and 4 are conducting (they have similar PR intervals to each other, and to other beats we thought were conducting on previous tracings). That said – we are once again at a loss to explain the variation in QRS morphology and marked change in both P-P and R-R intervals.

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IMPRESSION: The usual rules for rhythm interpretation and assessment of AV blocks and AV dissociation are not closely followed here. Instead – We see dramatic variation in P-P interval and elements resembling Mobitz Type I AV block, higher-grade 2nd degree AV block, and AV dissociation. That said – there IS one phenomenon that readily explains ALL findings seen in this series of 4 tracings – which is Vagotonic AV Block.

• The literature is scant regarding vagotonic AV block. This unusual conduction disturbance occurs far less often than other forms of AV block – which may in part account for the difficulty in recognizing it.

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VAGOTONIC AV BLOCK:

Clinical characteristics of vagotonic AV block include the following:

• Presence of a condition consistent with increased vagal tone (the patient in this case is in the early post-operative period). Other situations in which enhanced vagal tone may be seen include persistent vomiting; performance of a medical procedure; athletic training. Vagotonic AV block may also be seen in healthy adults during normal sleep (and especially in individuals with sleep apnea).
• Sinus arrhythmia which may be marked – and which especially slows just prior to and during periods of AV block.
• Mixed forms of AV block including Mobitz I 2nd degree AV block – 2nd degree AV block with 2:1 AV conduction — Mobitz II — and periods of high-grade or even complete AV block.
• Frequent switching back-and-forth between two or more of the above forms of AV block, often punctuated by periods of P-P irregularity, sinus rate slowing, and sometimes unexpected change in the PR interval.

KEY Point: Fortunately — the clinical course of vagotonic AV block in otherwise healthy adults without underlying heart disease is most often benign. It does not generally progress to significant AV conduction system disease — and pacing is rarely needed. That said — more severe, symptomatic cases not responding to simple measures should be referred.

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SUMMARY: It is well to be aware of the phenomenon of Vagotonic AV block. This conduction disturbance may be transiently seen during Holter monitoring of otherwise healthy individuals during sleep or in a situation of increased vagal tone (ie, persistent vomiting).  It should be thought of in such situations when serial tracings reveal marked and unpredictable P-P interval variation with mixed and atypical AV block conduction disturbances (such as those illustrated in Figures 1-thru-4). The course is usually benign, such that pacing is rarely needed – but persistent symptomatic cases may merit referral.

• A related arrhythmia to be aware of is Vagotonic AFib! You may occasionally see a younger-to-middle-aged adult (occurs most often in males) — who through participation in endurance sports or activities, develops AFib at a relatively slower rate. Vagotonic AFib most often occurs at night; at rest; after eating; or following an episode of coughing or vomiting (all potentiating causes of vagal tone).  
• CLICK HERE — for My Comment in the November 5, 2019 post on Dr. Smith's ECG blog, in which we discuss a case of Vagotonic AFib in detail.

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• ACKNOWLEDGMENT: My appreciation goes to Dr. Faisal Qadir (from Karachi, Pakistan) – for allowing me to use this ECG and this clinical case.

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- For more information - GO TO:

1) See Section 20.0 (from ACLS-2013-ePub) on the Basics of AV Block. The part on Vagotonic Block begins in Section 20.30. 

2) Zysko D, Gajek J, Kozluk E, Mazurek W: ECG Characteristics of AV Block Induced by Tilt Testing. Europace 11:225-230, 2009.

3) Brignole M: Different ECG Manifestations of the Cardioinhibitory Vasovagal Reflex. Europace 11:144-146, 2009.
4) Korantzopoulos et al: Markedly Prolonged AV Block with Ventricular Asystole During Sleep. S Med J 102:872-873, 2009. You have to READ this 2 page Letter (beginning on page 872) to believe it — a 25 second period of vasovagally-induced ventricular asystole during sleep!

5) Jaiswal S, Aldave APN, Wool KJ: Ventricular Standstill (VS): An Uncommon Electrophysiological Abnormality Caused by Profound Vagal Tone. N Am J Med Sci 6(4):178-180, 2014. (Prolonged asymptomatic periods of VS!).

ECG Blog #60 — LVH/Acute MI vs Normal Variant?

The ECG in Figure 1 was on my desk for interpretation.

• How would you interpret this ECG?
• Does this ECG Reflect ACS (Acute Coronary Syndrome) and/or Acute STEMI (ST Elevation Myocardial Infarction)?
• What clinical information is lacking?
• Is there LVH (Left Ventricular Hypertrophy) – at least by voltage?

Figure 1 – Does this ECG suggest acute ischemia and/or infarction?

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INTERPRETATION: Our Descriptive Analysis of this tracing begins as follows: Sinus arrhythmia (as determined by slight but definite variation in the R-R interval); normal intervals; marked left axis (approximately -40 degrees – which is consistent with LAHB = Left Anterior HemiBlock).

• At this point - further interpretation requires some information about the patient (namely age of the patient and whether or not the patient is healthy and asymptomatic vs an older adult with new-onset chest pain).
• HALF STANDARDIZATION: It is easy to overlook that this 12-lead ECG was obtained at HALF standardization. Note that the standardization rectangle (seen at the very beginning of the tracing) is only 5mm (=1 large box) tall. Actual amplitude is therefore double that seen in Figure 1 (ie, the S wave in lead V2 is really 24mm in depth – not the 12mm that we count on this tracing).
• Regarding Q-R-S-T Changes: No Q waves are seen. Transition occurs early (ie, between V1-to-V2). That said - the most remarkable finding on this tracing relates to the ST-T waves, which show ST segment coving with symmetric T wave inversion in many leads. There is at least slight ST elevation in leads V2,V3,V4.

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Importance of Clinical History:

This is an interesting ECG, in that its interpretation will be very different, depending on the clinical setting. In actual fact – this ECG was obtained as part of a “pre-participation physical” performed on an otherwise healthy 20-year-old football player. Past medical history was negative – and physical exam was normal (no heart murmur).

• ST segment coving with slight elevation and T wave inversion (as present in Figure 1) – may occasionally be seen in healthy young adults as a less common type of normal repolarization variant. Given this patient’s age and absence of symptoms – that almost certainly is the explanation here.
• Nevertheless – this is an unusual tracing for a healthy young adult. The surprisingly tall R wave already by lead V2 suggests prominent septal forces. We would therefore advise obtaining an Echocardiogram prior to clearing this individual for active sports participation to rule out anatomic abnormality (such as hypertrophic cardiomyopathy).

An entirely different interpretation would be in order IF the ECG in Figure 1 was instead obtained from an older adult with chest pain. In this case:

• The ST segment coving with slight elevation and symmetric T wave inversion in multiple leads might clearly reflect acute ischemia/infarction. This would need to be ruled out.
• Voltage for LVH would be present (deepest S in V1,V2 + tallest R in V5,V6 definitely exceeds 35mm given half standardization).

FINAL THOUGHT: It may be helpful to make a wallet-sized copy of this ECG for this individual to carry as record of their baseline ECG. Having this copy could prove invaluable for comparison purposes if this individual ever developed chest discomfort.

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- For more information - GO TO:

• See Section 09.0 (from ECG-2014-ePub) for more on Repolarization Variants. The part on Early Repolarization begins in Section 09.14. - 

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ECG Blog #59 — Giant T - Ischemia -Yamaguchi

No history is available for the ECG shown in Figure 1. That said:

• How would you interpret this ECG?
• What clinical conditions should be considered?

Figure 1:  No history is available. What clinical conditions should be considered?

INTERPRETATION: 

The rhythm is sinus bradycardia and arrhythmia, with an overall heart rate just under 60/minute. All intervals (PR/QRS/QT) are normal. The axis is normal at +50 degrees. Voltage for LVH is present (deepest S in V1,V2 + tallest R in V5,V6 ≥35mm). The most remarkable changes are seen with respect to Q-R-S-T Changes:

• There are no Q waves.
• Transition occurs slightly early (between leads V2-to-V3) – with relatively tall R waves in leads V1,V2.
• There is diffuse, deep symmetric T wave inversion. T wave inversion is almost 15mm deep in leads V2,V3.
• Other subtle-but-real ST-T wave findings include 1-2mm of J-point ST depression in multiple leads – suggestion of ST segment coving in leads I, aVL, V2,V3,V4 – and a hint of ST elevation in leads III, aVR and V1.

Giant T Wave Syndrome

The overall impression is consistent with Giant T Wave Syndrome. Although some T wave inversion is common in many conditions — the term “giant T waves” is reserved for a select number of clinical entities that produce truly deep (>5-10 mm amplitude) T wave inversion. When this clinical picture is seen (as it is in Figure 1) — one should think of the following diagnostic entities.

• Apical (Yamaguchi) Cardiomyopathy.
• Takotsubo Cardiomyopathy.
• Severe CNS disorders (increased intracranial pressure).
• Stokes-Adams attacks (especially when due to severe bradycardia, complete AV block).
• Acute ischemia/coronary artery disease.
• Post-Tachycardia Syndrome (ie, Cardiac "Memory" effect).
• Massive Pulmonary Embolism (acute right heart strain).

Without any history — it is impossible to know which of the above entities is most likely:

• We doubt massive PE (Pulmonary Embolism) — because none of the other stigmata of acute right heart strain are present (no right or indeterminate axis, no right atrial enlargement, no T inversion in lead III, no tall R wave in lead V1). T wave inversion with acute PE is most often limited to right-sided leads (V1,V2,V3 and II,III,aVF) — and is usually not nearly as deep as seen here.

Any of the other entities on the above list are possible.

• Apical cardiomyopathy — is an uncommon variant of the more commonly encountered hypertrophic cardiomyopathy (HCM). The increased voltage seen in Figure-1 is consistent with apical cardiomyopathy (which may produce identical ST-T wave changes as seen in today's tracing). 
• Takotsubo Cardiomyopathy may produce a somewhat localized or generalized Giant T wave pattern, often with a prolonged QTc (dependent on what areas of the heart are affected).
• Anterior ischemia/infarction from high-grade LAD (Left Anterior Descending) coronary artery narrowing/occlusion should be high on the differential list, because of the J-point ST depression, ST segment coving, and subtle ST elevation in leads III, aVR and V1.
• Acute CNS disorders (stroke, subarachnoid or intracranial hemorrhage, seizure, coma, brain tumors, trauma) may produce some of the most bizarre ST-T wave abnormalities. That said — the QT interval will usually be prolonged with CNS disorders and there will often be manifest T wave broadening (neither of which is seen here).
• Finally — a less commonly appreciated cause of diffuse T wave inversion is post-tachycardia syndrome. Diffuse T wave inversion not due to ischemia/infarction may sometimes transiently be seen following conversion of sustained SVT/VT rhythms.

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NOTE: Although many authorities suggest a minimum of ≥10mm for T wave depth sufficient to qualify as "Giant T waves" — for practical purposes (ie, in our experience) — the entities suggested by the above bullets should be considered in cases in which very deep (ie, ≥5mm) but not necessarily "giant" T waves are seen in a number of leads.
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— For more information — GO TO:

• See Section 10.51 on Giant T Wave Syndrome - 
• See ECG Blog #120 ( = Video-16) -

ECG Blog #58 — AV Dissociation vs Block?

The ECGs in Figure 1 and Figure 2 were both interpreted as showing 3rd degree (complete) AV block.

• Do you agree?

Figure 1: Lead II rhythm strip. Is this complete AV block? 

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Figure 2: Lead MCL-1 rhythm strip. Is this complete AV block? 

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INTERPRETATION: We assess both rhythm strips by the Ps,Qs & 3R Approach, looking for: i) Presence (or absence) of P waves (atrial activity?); ii) QRS width (>0.10 sec is wide?); iii) Regularity of the rhythm; iv) Rate; and v) If P waves are present - Are P waves Related to the QRS (Are P waves conducting?).

FIGURE 1: — The QRS complex is narrow. The first 3 beats show sinus bradycadia at ~55/minute. The PR interval then noticeably shortens (ie, the PR preceding beats #4,5, and 6 is clearly too short to conduct!). Thus, there is transient AV Dissociation (since P waves are at least temporarily unrelated to the QRS).

• Beats #7 and 8 represent a junctional rhythm at ~58/minute.
• It is because the sinus rate slows (to 55/minute) that a slightly faster junctional rhythm can take over (beginning with beat #4).
• We see NO evidence of any AV block on Tracing A — because P waves never fail to conduct when given a chance to do so (P waves before #4,5,6 don't have a chance to conduct ...).

FIGURE 2: — shows complete (3rd degree) AV Block. Note that the QRS does not necessarily have to be overly wide for there to be 3rd degree AV block.

• The atrial rate is regular (marched out in Figure 3 with RED arrows).
• There is also a regular ventricular rhythm — but P waves at all points in the cardiac cycle fail to conduct despite having adequate opportunity to do so (P waves "march through" the QRS).

Figure 3: Arrows indicate regular atrial activity that "marches through the QRS" in this patient with 3rd degree AV block (See text).

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AV Dissociation vs Complete AV Block

AV Dissociation is not the same as 3rd degree AV block. The term, "AV dissociation" merely means that one or more P waves is not related to a neighboring QRS. AV dissociation may be transient or permanent. It may be due to pathologic conditions such as 2nd or 3rd degree AV block — or it may be a benign manifestation of the simple fact that the sinus node temporarily slows down and is replaced in its pacemaker function by an appropriate AV nodal escape rate between 40-60/minute.

• Always try to determine the cause of AV dissociation - of which there are three: 1) AV block itself (could be 2nd or 3rd degree AV block); 2) Usurpation — in which P waves transiently do not conduct because an accelerated junctional rhythm takes over ("usurps" — as commonly occurs with Dig toxicity); and, 3) Default - in which a junctional escape rhythm takes over by default" (because of SA node slowing).
• Figure 1 is an example of AV dissociation by "default" (slowing of the rate from sinus bradycardia that allows emergence of an appropriate junctional escape rhythm).
• PEARL: In order to confidently diagnose complete AV block — the ventricular rate needs to be slow enough (usually <45-50/minute) in order to guarantee that P waves will occur in all phases of the cardiac cycle, yet still fail to conduct despite having adequate "opportunity" to conduct. This clearly occurs in Figure 3.

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For more information - GO TO:

• ECG Basics of AV Block (in ECG-2014-ePub) - 

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