Tuesday, November 5, 2019

A healthy 30-something presented with nausea, vomiting, benign positional vertigo and atrial fibrillation


A healthy 30-something presented with nausea, vomiting, vertigo and atrial fibrillation.  The vertigo is triggered by head movement and relieved by holding still.  He has severe nausea with it, and epigastric discomfort.

He had an ECG recorded because epigastric discomfort can be due to inferior MI:
This patient is healthy and on no medications.
His electrolytes are normal.
He does not drink alcohol or use drugs.
Thyroid was not checked, as A Fib from thyroid would be very rapid.

What is unusual here, and why?
What is the likely cause of the atrial fibrillation?











There is no real evidence of ischemia.
There is atrial fibrillation.

--First, it is unusual that a young healthy person develops atrial fibrillation.
--Second, a young person should have a rapid ventricular response if there is a healthy AV node and no AV nodal blockers.

Why is the ventricular response below 100 beats per minute?

This patient had no idea that he was in an abnormal rhythm, so it was impossible to say for certain how long he had been in it.

I learned from this case, from our electrophysiologist (Rehan Karim) and from one of our very smart hospitalists, who is particularly smart at cardiology (Meghan Walsh), that extreme vagal tone can BOTH cause atrial fibrillation and then, correspondingly, be associated with a relatively slow ventricular response because of that high vagal tone.

This happens particularly in young healthy athletic men.

So this young man got benign positional vertigo, then severe nausea, which made for high vagal tone, which converted him to atrial fibrillation with a relatively slow response.

His Benign Positional Vertigo was managed successfully with an Epley maneuver.

He ultimately converted back to sinus rhythm spontaneously.


For more, see this article:

Paroxysmal Atrial Fibrillation: A Disorder of Autonomic Tone?


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MY Comment, by KEN GRAUER, MD (11/5/2019):
===================================
This is an important case, in that it brings up a number of underappreciated concepts regarding Atrial Fibrillation (AFib).

The most common sustained cardiac arrhythmia by far is atrial fibrillation. When assessing the patient with new-onset AFib — once you have ensured hemodynamic stability, sequential priorities optimally include: iFinding the cause; ii) “Fixing” the cause (if at all possible); iii) Slowing the rate; iv) Converting the rhythm; andv) Preventing thromboembolism.
  • Most patients with new AFib will not be hemodynamically unstable as a result of the AFib. If they are — then immediate synchronized cardioversion is in order!
  • Once you’ve ensured that the patient is stable — the reason I suggest considering the above 5 clinical priorities in the sequence that I list them — is that IF you can find and fix the cause of new-onset AFib — then you may at the same time slow the rate, convert the rhythm and reduce the chance of stroke (ie, if the cause of new AFib is heart failure — then diuresis may facilitate conversion).

It’s helpful to keep in mind the Common Causes of AFib. There are many ... The 3 most common causes of AFib are:
  • Heart failure/cardiomyopathy.
  • Acute ischemic heart disease (acute MI/acute coronary syndrome).
  • Hypertension (especially when longstanding, because of structural alteration of the heart that longterm hypertension produces).

Among the many other potential causes of AFib are the following:
  • Valvular heart disease
  • Hyperthyroidism (which overall is not a common cause of AFib — but which is still very important, because there is a specific treatment).
  • Drugs (ie, cocaine, sympathomimetics, alcohol use)
  • Pulmonary embolus/hypoxemia
  • Other significant medical illness
  • Sleep apnea
  • Sick sinus syndrome
  • “Lone” AFib (ie, when AFib occurs in a patient under 50-60 years old in the complete absence of underlying heart disease [ie, not even hypertension]).
PEARL #1: Today’s case emphasizes the need to actively consider an additional entity:
  • Vagotonic AFib (discussed more below).

PEARL #2: Description of the rhythm that the patient in this case had as “atrial fibrillation” would be an incomplete description of his cardiac rhythm. WHY ???



ANSWER: The reason that simply saying this 30-year old man presented with “atrial fibrillation” is an incomplete description of the rhythm — is that this description provides NO indication of the average rate of the ventricular response. Knowing the ventricular response of AFib instantly tells you so much about how to proceed with diagnosis and treatment!
  • Figure-1 shows 4 examples AFib. For each of the rhythms shown — there is an irregular irregularity without indication of sinus P waves. The QRS complex is wide in the last example.


QUESTIONS:
  • How would you describe each rhythm in Figure-1?
  • What diagnostic and treatment considerations should be immediately suggested for the examples of AFib that you see in Rhythms A, B, C and D?

Figure-1: Four examples of AFib. How would you describe each of these? (See text).



ANSWERS:

Rhythm A in Figure-1:
  • This is AFib with a rapid ventricular response — which I define as AFib with a rate averaging over ~120/minute (Note that the R-R interval varies between 2-to-3 large boxes in duration — which is consistent with an average rate of ~120-130/minute). Rapid AFib is by far the most common ventricular response for new-onset AFib. 
  • The reason new-onset rapid AFib in an older population is so commonly associated with heart failure is due to: i) loss of the “atrial kick” (which provides between 5-40% of cardiac output — but typically closer to the higher range in patients with longstanding hypertension who have resultant diastolic dysfunction); and, ii) the rapid rate disproportionately shortens the period of diastole (during which diastolic filling of the left ventricle takes place) — which significantly reduces resultant cardiac output.

Rhythm B in Figure-1:
  • This is AFib with a controlled ventricular response — which I define as AFib with a rate averaging between ~70-110/minute. Attaining rate control is one of the principal goals of treating new-onset rapid AFib with antiarrhythmic medication.
  • Occasionally, an otherwise healthy older adult will present in new AFib with a controlled ventricular response that falls within this rate range. But, as emphasized by Dr. Smith — We should not expect an otherwise healthy young adult (as in this case) to present in AFib with an average heart rate under 100/minute — unless something else (in this case, vagotonic AFib) was going on.

Rhythm C in Figure-1:
  • This is AFib with a slow ventricular response — which I define as AFib with a rate averaging less than ~50-60/minute.
PEARL #3: It is unusual for new-onset AFib to present with a slow ventricular response! When this is seen — it should immediately prompt a different set of diagnostic considerations. These include:
  • Use of rate-slowing drugs (ie, digoxin; ß-blockers; verapamil/diltiazem; amiodarone; sotalol; clonidine; various herbal preparations). Ask about all pills that the patient is taking — including herbal preparations (you may need to look up which of these may be rate-slowing ...)PEARL #4 — Don't forget to ask about eye drops! (ie, ß-blocking eye drops are partially absorbed — and may produce significant bradycardia that resolves when the eye drops are stopped! )
  • Acute ischemic heart disease (ie, from ischemia/infarction; acute coronary syndrome). Recent MI may present with slow AFib without any history of chest pain.
  • Hypothyroidism (abnormal thyroid function may predispose to arrhythmias).
  • Sleep apnea (which is commonly overlooked as a potential cause of bradyarrhythmias).
  • SSS (Sick Sinus Syndrome) — which can only be diagnosed after ruling out causes in the 4 bullets above this! PEARL #5 — Almost by definition, a patient older than 60-70 years old who presents with new-onset slow AFib, but who is not on any rate-slowing drugs — has no acute or recent ischemia — does not have sleep apnea — and has normal thyroid function — will have SSS!

Rhythm D in Figure-1:
  • This is AFib with a very rapid ventricular response. The usual rate range for “rapid” AFib is between ~110-180/minute. This is because the intrinsic refractory period of the normal AV node generally does not allow conduction of more than 200-220 impulses per minute.
  • PEARL #6  IF ever the rate of AFib is significantly above this (ie, >200-220/minute) — the patient probably has an AP (Accessory Pathway) that is bypassing the AV node (ie, WPW = Wolff-Parkinson-White Syndrome).
  • Note in Panel D of Figure-1 — that the QRS complex is wide. AFib in patients with WPW will almost always be antidromic (traveling first down the AP instead of through the AV node, as the path to the ventricles). This is because of the shorter refractory period of the AP. As a result, the QRS complex is typically wide in patients with WPW who develop AFib. As seen in Panel D — the irregularly irregular tachyarrhythmia is characterized by periodic slowing of the rhythm in some places, while attaining exceedingly fast rates that may approach 250-300/minute in other places (CLICK HERE for more on the arrhythmias commonly seen with WPW).


MORE on Vagotonic AFib:
  • Autonomic dysfunction often figures prominently in the onset of AFib. In most instances, there is excessive sympathetic activity — but on occasion, increased vagal tone may trigger AFib episodes (Vagal stimulation shortens the atrial effective refractory period — and therefore enhances the ability of a PACs to induce AFib).
  • Vagotonic AFib  is most commonly seen in younger-to-middle-aged males (ie, 30-50 years old). Active participation in endurance sporting activities (ie, cycling, long-distance running, cross-country skiing, etc.) predisposes to a longterm increase in resting vagal tone.
  • IF episodes of AFib most often occur at rest, after meals, or during sleep — these episodes of AFib are more likely to be vagally stimulated.
  • Episodes of vagotonic AFib are more likely to resolve in the morning or during periods of exercise (ie, when sympathetic tone is increased).
  • AFib recurrence is commonly precipitated by episodes of coughing, intense nausea or vomiting — or after ingestion of especially spicy foods, or very cold food or drinks (all potential stimulators of vagal tone). Sometimes, simply eating a meal may precipitate episodes.
  • If 24-hour Holter monitoring is done — there will often be a period of sinus bradycardia prior to onset of AFib.
  • Episodes of vagotonic AFib typically manifest a relatively slower ventricular response (as occurred in this case).
  • Echo may be normal.

BACK to THIS CASE  It is of interest that this patient was totally unaware that he was in AFib! That said — he apparently converted to sinus rhythm after his vertigo was successfully treated with an Epley maneuver.
  • Given this history — I suspect this patient was probably having frequent episodes of vagally-induced AFib — that spontaneously resolved when vagal tone decreased. The fact that he is unaware of AFib episodes when they occur complicates management. Nevertheless — Holter monitoring with a DIARY may prove insightful for indicating which activities of daily living are most likely to precipitate episodes. There may be certain precipitants of his vagal-induced AFib episodes that can be avoided, or at least minimized.
  • Rate-slowing drugs, such as ß-blockers should be avoided in treatment — because these may result in further imbalance of parasympathetic tone (since ß-blockers reduce sympathetic tone).
  • Antiarrythmic medications that reduce vagal tone (such as flecainide, disopyramide) may be effective.
  • Ultimately, if episodes of vagotonic AFib are frequent and persistent — referral to EP cardiology may be indicated. Some patients require ablation for control of vagotonic AFib ...
  • BOTTOM LINE Think of Vagotonic AFib as a possibility the next time you see new AFib in an otherwise healthy younger adult — especially if the rate of the AFib is relatively slow, and the patient is male and involved in endurance activities.
  • PEARL #7: A related phenomenon to be aware of is Vagotonic AV Block — in which an otherwise healthy individual during sleep or some other situation associated with increased vagal tone (ie, persistent vomiting) presents with a very atypical AV block conduction disturbance, in which unpredictable variation in PR and R-R intervals defy classification according to the "usual rules" for the 3 degrees of AV block. (CLICK HERE for a fascinating case discussion of this phenomenon).

Our THANKS to Dr. Smith for this interesting case!



2 comments:

  1. Thanks Dr Smith and Dr Grauer for the case and explanation

    The ECG fulfills a criteria for LVH S wave in V2 + R wave in V5 almost 8 large boxes

    Is not it an indication for echo?

    Best regards

    ReplyDelete
    Replies
    1. @ Mustafa — THANK YOU for your comment. I have always used an AGE qualification for the ECG diagnosis of LVH — such that SUM of deepest S in V1,V2 + tallest R in V5,V6 ≥35mm is ONLY valid IF the patient is at least 35 years of age. To emphasize — there is no “clear cut limit” (ie, on the day of one’s 35th birthday, it is not as if all of a sudden you “have LVH”) — but as it is generally known that younger adults often have increased QRS amplitude WITHOUT true chamber enlargement — I favor “reversing” these numbers (ie, using “53” instead of “35”) for this voltage criteria in a younger adult (NOTE: I do not have studies verifying use of this “53” criterion — instead, I base it on my 3+ decades of personal experience … with hope that this easy-to-remember criterion will reinforce the key concept that younger adults often have increased QRS amplitude without true chamber enlargement ). To emphasize — that IF there is “reason” for LVH in a younger adult (ie, known severe hypertension, cardiomyopathy, etc.) — and IF ST-T wave changes of LV “strain” ARE present — then 35mm is “more than enough” to qualify for the ECG diagnosis of LVH. Alas, we are told the “30-something” man in this case (ie, Who knows if he is older or younger than “35”?) was previously healthy — and there is no ST-T wave indication of LV “strain” on his ECG — therefore I felt the diagnosis of LVH by ECG was not justified. That said — ANY patient with new AFib should have an ECHO (You’ll note in My Comment above, that patients with Vagotonic AFib often have a normal Echo — but an Echo NEEDS to be done). P.S. I’ve provided info on “My Take” for the ECG diagnosis of LVH on a number of posts in Dr. Smith’s ECG Blog — Please CHECK OUT — June 15, 2019 — http://hqmeded-ecg.blogspot.com/2019/06/patient-with-dyspnea-you-are-handed.html — and also April 27, 2019 — http://hqmeded-ecg.blogspot.com/2019/04/is-this-terminal-qrs-distortion-is.html — Thanks again for your Comment! — :)

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