Written by Sean Trostel MD, peer reviewed by Meyers, Smith, Grauer, etc.
A man in his 60s with a history of severe alcohol use disorder and epidural abscess on long-term ciprofloxacin presented to the emergency department after an episode of syncope while standing in line at a grocery store.
He did not have chest pain.
Here is his triage ECG:
 |
| What do you think? |
My interpretation:
Sinus rhythm, normal QRS, widespread wavy ST depression leading into late T/U-waves with very prolonged QT. No evidence of OMI. QTc/QUc is in the range of 630 msec.
What is the most likely cause of the patient’s ECG findings, and what would be your first step in management?
ECG is consistent with severe hypokalemia and/or hypomagnesemia causing prolonged QT (QU) at high risk of Torsades (which is polymorphic ventricular tachycardia in the setting of a long QT interval).
A prior ECG was available for comparison:
 |
| Normal |
One might be tempted to interpret the ST depression as ischemia, but as Smith says, "when the QT is impossibly long, think of hypokalemia and a U-wave rather than T-wave."
Check out this case:
Are These Wellens' Waves??
The Queen of Hearts PM Cardio AI app was fooled into saying "OMI with low confidence," but she has never been trained in hypokalemia. We just finished training version 2 with some cases of hypokalemia, so that is in the future. Moreover, the Queen is only supposed to be used with a high pretest probability of ACS/OMI.
The patient’s VBG resulted as I was speaking with him and confirmed my suspicions, showing a potassium of 1.6 mEq/L. Magnesium later resulted at 0.8 mg/dL, and ionized calcium was 0.73 mmol/L.
The patient had pads placed in case of PMVT/VF, was immediately given 2g magnesium sulfate and 40mEq oral potassium, and had additional IV access obtained to start IV KCl.
This patient has many reasons to have long QT in this case:
Hypokalemia
Hypomagnesemia
Chronic ciprofloxacin use
Hypocalcemia (contributes to long QT but lower risk of TdP as discussed in this post)
With a chief complaint of syncope, it should be suspected that the patient went into torsades de pointes prior to arrival. The patient was admitted to the ICU for close monitoring and electrolyte repletion and had an uneventful hospital course.
The patient had pads placed in case of PMVT/VF, was immediately given 2g magnesium sulfate and 40mEq oral potassium, and had additional IV access obtained to start IV KCl.
This patient has many reasons to have long QT in this case:
Hypokalemia
Hypomagnesemia
Chronic ciprofloxacin use
Hypocalcemia (contributes to long QT but lower risk of TdP as discussed in this post)
With a chief complaint of syncope, it should be suspected that the patient went into torsades de pointes prior to arrival. The patient was admitted to the ICU for close monitoring and electrolyte repletion and had an uneventful hospital course.
See these other relevant cases:
What are these bizarre bigeminal PVCs??
More cases of long QT not measured correctly by computer (these are all fascinating ECGs/cases):
Bupropion Overdose Followed by Cardiac Arrest and, Later, ST Elevation. Is it STEMI?
Another diagnostic ECG of a potentially deadly condition
===================================
MY Comment, by KEN GRAUER, MD (10/19/2023):
===================================
Today's excellent case discussion by Drs. Trostel and Meyers brings home a number of important points regarding assessment of the QT interval. I focus my comment on some additional observations
- For clarity in Figure-1 — I've labeled the initial tracing in today's case.
-USE.png) |
| Figure-1: The initial ECG in this case — and a rapid method for estimating the QTc (See text). |
MY Thoughts on Today's CASE:
Essential for assessment of the initial ECG — is the history. The patient is a man in his 60s with established severe alcohol use disorder — and epidural abscess being treated with longterm Ciprofloxacin — who presented to the ED following a syncopal episode.
- NOTE: Each of the bolded words in the above paragraph are essential to our assessment.
As per Drs. Trostel and Meyers — the ECG in Figure-1 shows sinus rhythm with normal PR interval and normal QRS duration — but with a markedly prolonged QTc interval. The frontal plane axis is normal — and there is no chamber enlargement. There is diffuse ST segment depression, seemingly with terminal T wave positivity in multiple leads.
QUESTION #1:
- Did YOU notice that beat #4 is a PVC with fusion?
=================================
WHY is this PVC Potentially Relevant to Today's Case?
RED arrows in the long lead II rhythm strip in Figure-1 highlight sinus P waves. Note that the PINK arrow P wave is right on time! — but that the PR interval preceding beat #4 is slightly shorter than the PR interval of other beats in this long lead rhythm strip.
- That beat #4 is a fusion beat — is best seen by looking at simultaneously-recorded beat #4 in lead aVL, in which the small, negative QRS complex clearly looks different than the small, upright QRS for beats #5 and #6 in lead aVL.
- The reason for this difference in QRS morphology — is that this is a late-cycle (ie, end-diastolic) PVC — in which the on-time PINK arrow P wave begins to conduct to the ventricles — but before it can complete its path there, it encounters a ventricular impulse, thereby resulting in an intermediate (fusion) form sharing morphologic features of normal and ventricular conduction.
- PEARL #1: Late-cycle PVCs are a common form of reperfusion arrhythmia — such that whenever I see them, I take an extra close look at the tracing to make sure there are no indications of recent infarction (More on this in a moment with regard to today's case!).
==============================
QUESTION #2:
- If it were not for the markedly prolonged QTc — Wouldn't ECG #1 look like diffuse subendocardial ischemia?
ANSWER:
As we've discussed on numerous occasions in Dr. Smith's ECG Blog — the diagnosis of diffuse subendocardial ischemia (DSI ) is made by the finding of ST depression in multiple (usually at least 6-7) leads in association with ST elevation in lead aVR (and sometimes also in lead V1).
- In Figure-1 — there is ST depression in no less than 9 leads — with ST elevation in both leads aVR and V1 — such that IF the QTc would not be as prolonged as it is — our differential diagnosis would focus on conditions associated with DSI (diffuse subendocardial ischemia).
- PEARL #2: It is important to remember that the ECG shows us the "net effect" of all that is going on. The relevance of this concept to today's case is that IF a patient has more than a single underlying condition (ie, severe hyper- or hypokalemia and ischemia) — then the ECG manifestations of one of these conditions may "mask" the other. BOTTOM Line: Given all of the ST depression seen in ECG #1 — it will be impossible to rule out DSI until the ECG is repeated after correction of this patient's severe hypokalemia, hypomagnesemia and hypocalcemia.
- PEARL #3: As we've often emphasized — DSI is not an indicator of OMI. Instead — it commonly reflects ischemia from severe underlying coronary disease. And although today's patient did not complain of chest pain — given his history of severe alcohol use, his longterm neurologic condition (ie, epidural abscess) — and his reason for hospital admission (ie, a syncopal episode) — the finding of the late-cycle PVC noted above provides one more reason for extra caution in this patient (who may not reliably recall all that he has experienced) — to rule out a recent event by repeat ECG after correction of his severe electrolyte disturbance.
==============================
How to Quickly Estimate the QTc:
As per Drs. Trostel and Meyers — the QTc in markedly prolonged in today's case.
- The quick and easy way to tell at a glance if the QTc is likely to be prolonged is the "eyeball" method. Assuming the heart rate is not too rapid (this method works less well with heart rates >90-100/minute) — one may suspect that the QTc will be long if the longest QT interval that you can clearly see on the tracing is more than half the R-R interval.
- Measurement of intervals is one of the tasks that the computerized ECG interpretation is usually very accurate with (assuming that the computer correctly identifies the end point of the T wave).
- PEARL #4: To quickly estimate a numerical value for the QTc — I developed a Correction Factor that has been surprisingly accurate for me in assessing too-numerous-to-count QTc values that I’ve estimated over the past 3+ decades. As per the text under the ECG in Figure-1 — you only need to remember 3 values (ie, 1.1 for a rate ~75/min; 1.2 for ~85/min; and 1.3 for ~100/minute). With a little practice using this method — you can estimate the QTc within seconds.
- Applying my method to the case at hand — the rhythm in ECG #1 is regular, with an R-R interval sightly under 4 large boxes. I therefore estimated the heart rate at ~80/minute (ie, a bit faster than 300÷4).
- I selected lead V3 as one of the leads where we can clearly define the onset and offset of the QT interval. I measure the QT in this lead to be ~530 msec. Using a correction factor of 1.15 (since the heart rate ~80/minute) — I estimate the QTc = 530 + [530 X .15 = 80) = 530 + 80 ~610 msec. For speed and ease of calculation — I usually round off values (it’s all an estimate anyway! ) — but I’ve enjoyed being able to get very close to computer-calculated QTc values by this simple correction factor method.
- PEARL #5: Over the years, I have found recall of a short LIST of Causes of QT Prolongation to be of invaluable assistance. As per My Comment in the March 19, 2019 post of Dr. Smith’s ECG Blog — Assuming there is no bundle branch block, ischemia or infarction (as these entities can prolong the QT) — THINK OF: i) DRUGS (many drugs prolong the QT interval — and combinations of drugs may result in marked prolongation); ii) LYTES (ie, Think of low K+ and/or low Mg++ and/or low Ca++); and/or, iii) a CNS Catastrophe (ie, stroke, bleed, coma, seizure, trauma, brain tumor).
==============================
Which of the 3 Causes in the above LIST are Likely?
Actually — each of the above causes in my LIST may be contributing to the markedly prolonged QTc in today's case.
- DRUGS — Today's patient has been on longterm Ciprofloxacin for treatment of epidural abscess. Cipro is one of a number of drugs implicated in potentially significant prolongation of the QTc (including predisposition to Torsades de Pointes) — especially if administered with other agents that may affect the QTc or when there are other predisposing factors that might affect "repolarization reserve" (such as severe electrolyte depletion) — Prabhakar and Krahn (Heart Rhythm 1(5):624-6, 2004) — and — Blondeau JM (Clin Ther 21(1):3-40, 1999).
- LYTES — All 3 of the electrolyte disturbances cited by Drs. Trostel and Meyers have been associated with QTc prolongation (ie, hypokalemia, hypomagnesemia and hypocalcemia). Hypokalemia and hypomagnesemia have been associated with identical ECG manifestations — that typically include diffuse ST segment flattening and/or depression and U waves (especially when U wave amplitude surpasses T wave amplitude!). Although difficult to prove in ECG #1 — I suspect that the reason for the very prominent terminal T wave positivity in multiple leads is that giant U waves are fusing with the end of the T wave (in which case rather than a very long "QTc" — we are probably looking at a long QU interval).
- CNS — As a patient with longterm severe alcohol use disorder and a chronic epidural abscess — with the reason for hospital admission being a new syncopal episode — today's patient presented a series of potential neurological conditions that may be contributing to his marked QTc prolongation (ie, Rather than an episode of Torsades as the reason for this patient's prehospital syncope — perhaps he had an alcohol-related seizure?).
Our THANKS to Drs. Trostel and Meyers for today's interesting case!
- I'd love to see the follow-up ECG after correction of this patient's multiple electrolyte disorders.
No comments:
Post a Comment
DEAR READER: I have loved receiving your comments, but I am no longer able to moderate them. Since the vast majority are SPAM, I need to moderate them all. Therefore, comments will rarely be published any more. So Sorry.