ECG Case 11: Answers!
A few days ago I posted ECG Case 11: with a couple of questions and am pleased to say a couple of responses!! Brilliant stuff!
If you missed the case the first time have a look here before we go over the answers:
1. What Rhythm is this?
Both of the answers given were spot on: this is a run of self-terminating VT. Nice broad regular complexes which terminate after 14-15 beats lasting for about 10 seconds or so fulfilling the criteria for a run of non-sustained ventricular tachycardia (non-sustained being <30s)
2. What would your initial management be?
Again; both answers given were spot on. First and foremost is to go and assess the patient clinically. The rhythm strip shows restoration of underlying rhythm (sinus) so the chance of him having ongoing symptoms due to his run of VT is unlikely but we need to exclude any ongoing chest pain, dyspnoea and check his current vitals. Get a 12 lead ECG to check for any evolving ischaemic changes which may represent silent ischaemia and as Wanderer said checking his K+, Mg+, PO4+ & Ca++ are essential. I’d aim for a K+>4.5 & Mg+>1.0 in anyone with an arrhythmia both of which can be easily replaced IV/PO. If we were concerned that his VT was ischaemia induced or driving heart failure then checking cardiac markers and CXR would be ordered.
In the absence of any contraindications and provided his BP/HR were acceptable I’d start him on a low dose beta blocker . Beta blockade post MI is well recognised to decrease all cause-mortality (Beta blockade Heart Attack Trial, JAMA) and is one of the must have discharge medications. Beta blockers will increase vagal tone and reduce the frequency of recurrent runs of NSVT
3. What longer term management issues or other investigations are there?
Both responses were along the lines of what I was hoping to hint at and that would be the criteria surrounding the use of implantable cardioverter defibrillators (ICDs). My line of investigations (provided recurrent ischaemia had been excluded) would follow something like this:
- Echo: To assess primarily for LVEF
- 24hr (or longer) Holter: To capture runs of VT
- Depending on the results of the above an EP study (I would leave this one last as it is the most invasive and may not be required depending on the results of the above)
NICE (The National Institute for Clinical Evidence) published comprehensive ICD & ICD-CRT Guidelines in 2006 which can be found here.
The gentleman in our case would just fit in to the primary prevention category (only 3 weeks post-MI) and would fulfill criteria for ICD implantation if the following were met:
LVEF<35% (no worse than Class III NYHA) AND evidence of NSVT on Holter AND inducible VT on EP study
OR
LVEF<30% (no worse than Class III NYHA) AND QRS>120ms
NEJM: July 8 2010
There are a couple of good articles in this weeks NEJM, one in particular which I thought would be of interest to readers.
“Mitral regurgitation due to degenerative valve disease” http://content.nejm.org/cgi/content/full/363/2/156 is part of the NEJM Clinical Practice articles which begins with a short vignette then a review of current evidence and guidelines. In this case the article talks us through the medical and surgical options for patients with degenerative MV disease and highlights the currently accepted best practice.
The article ends with a brief summary of the current recommendations for when patients should be offered surgical intervention:
- Symptomatic or asymptomatic patients with chronic severe MR with evidence of LV dysfunction defined as an LVEF of 30-60% and a LV end systolic dimension of 40mm or greater
- Asymptomatic patients with evidence of raised PA pressure
- Asymptomatic patients with new-onset AF
The article notes that patients with severely reduced LVEF (<30%) are unlikely to benefit Asymptomatic patients with evidence of raised PA pressures
The articles states that endocarditis prophylaxis should be offered to patients with MV disease only after MV replacement (prosthetic or repair with annuloplasty) or where there is a prior history of endocarditis. A few years ago there was a trend for all patients with MV disease (ranging from those with so-called benign MV prolapse to those with chronic severe MR) to be offered prophylaxis but this has now gone out of fashion as re-highlighted here.
ECG Case 11:
A 55 year old man 3 weeks post NSTEMI presents to A&E with a history of palpitations and pre-syncope. Examination is unremarkable apart from a displaced apex (6th intercostal space, mid clavicular line). He is monitored and this rhythm strip is obtained within the first 24hrs of his admission:
Questions:
1. What rhythm is this?
2. What would your immediate management be?
3. What longer-term management issues or other investigations are there?
Answers to follow shortly!!
NEJM April 15 2010
Apologies for the pause between posts; I’ve haven’t forgotten about cardiologycases!
As a brief stop gap before the next set of cases I recommend taking a look at this weeks NEJM. 3 Cardiology specific articles caught my eye
1. “The Beat Goes On“: An excellent interactive case which explores a young man with dilated cardiomyopathy and syncope
2. “Lenient vs. Strict Rate Control in AF“: An interesting study looking at outcome of varying degrees of rate control in patients with AF.
3. “Duration of Dual Antiplatelet Therapy after implantation of Drug-eluting Stents“: An important first (of many!) step in furthering our knowledge in the optimum duration of antiplatelet agents; such an important topic in our aging and increasingly frail patient population with multiple medical comorbidities.
The rest of the NEJM issue is also excellent from a GIM (internal) medicine perspective with an excellent overview of the management of severe COPD; an interesting case of PML and interesting image challenges. I would highly recommend an online subscription for the budding physician (no COI!)
NEJM March 11 2010
Another week and another two fantastic articles concerning Cardiology from the New England Journal of Medicine
1. Low Diagnostic Yield of Elective Coronary Angiography. “In this national registry of data on cardiac catheterization, only 38% of elective, diagnostic coronary angiograms showed obstructive lesions, and 39% of angiograms were interpreted as showing no disease, while the procedure exposes patients to substantial radiation.” An interesting sub-study of a much large cohort analysing patients without known coronary artery disease undergoing angio.
2. Commotio Cordis. A review article which covers what we know about commotio cordis and a look at current strategies to reduce the incidence. Slide from NEJM
ECG Case 10: Anterior STEMI
A 53 year old caucasian woman presents with a 4 day history of severe central chest pain on exertion, alleviated with rest. Over the last 24 hours the pain has increased in severity and frequency and is now present at rest as well as exertion. Her medical history includes type 2 diabetes, hypertension and hypercholestrolaemia.
On examination she appears unwell; in pain; sweaty and grey. Her ECG is shown below
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This ECG is about as classic as you’re ever likely to see for an acute anterior ST-elevation MI with the large “tombstone” like ST segment elevation evident in V1-V4. This is a medical emergency in the true sense and needs urgent intervention ASAP. Fortunately the patient was transferred to the local primary PCI centre and had her angiogram within 60 minutes of initially presenting to hospital.
Her coronary angiogram showed 100% LAD stenosis (almost “expected” given the ischaemic change in LAD territory) and 80% stenosis in her left circumflex (LCx). She underwent primary PCI to her LAD with two stents (with planned repeat PCI to LCx after 6-8 weeks) and her ECG post intervention is below
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We can see that her ST segments have begun to resolve and although still elevated have lost that ominous tombstone look that they had on presentation. Note also the development of Q waves in V1-V3.
She undergoes a relatively unremarkable recovery and is discharged home 4 days post PCI with the ECG below
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For further reading about the management of patients with ST-elevation MI I suggest reading through the 2004 ACC/AHA Guidelines for Management of Patients with ST-elevation MI & the 2009 Focused Update which provide a more than comprehensive overview of all aspects of management.
Two take home messages which struck me from this case:
- The “leave-alone” strategy during her primary PCI which is in-keeping with guidelines to “restore flow in the infarct artery as quickly as possible to improve myocardial perfusion in the infarct zone”
- If possible give the patient a copy of his/her ECG. The importance of comparing old ECGs with new if this patient was to represent cannot be stressed enough and may save her an unnecessary trip to the cath lab!!
ECG Case 9: Careful Observation
As well as highlighting interesting and hopefully useful cases I want to also show some more basic ECGs and talk through common, simple mistakes and how we try to avoid repeating them! See what you think of this case; any and all comments welcome!
A 45 year old lady presented with acute onset dyspnoea and chest pain; her ECG is shown below:
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Her ECG was intepreted as “new” (i.e. acute, ischaemic) LBBB and compared with an old, normal sinus rhythm ECG from 3 years previous and she was transferred for primary PCI.
Now look again carefully at her first ECG and this second trace and see if you spot the problem…
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What wasn’t initially evident on the first trace has shown itself on her second ECG: Pacing Spikes!! Look carefully again:
The clues that we could/should have led us to think that this wasn’t truely acute ischaemic LBBB are:
- Presence of PPM clinically (examination is suprisingly often forgotten about in the “drama” of a STEMI/acute LBBB)
- ECG Sign 1: Pacing spikes; difficult to see unless you look very closely
- ECG Sign 2: LBBB morphology and LAD deviation; remember that it is the RV which is being paced hence there is a relative delay in conduction of the left ventricle compared with the right resulting in LBBB & LAD
Don’t let it happen to you!!
BHF: Images from Inside the Heart
From the BBC:
“The British Heart Foundation (BHF) has announced the winners of its “Reflections of Research” competition.
Scientists across the UK submitted videos which represented their field of research. The images show the variety of pioneering work that is helping unearth new ways to tackle heart and circulatory disease.”
Click through for 3 fantastic videos
ECG Case 8: Dizziness ?cause
This is a difficult one and shows how tricky clinical medicine can be.
An 84 year old lady presented with a 6 week history of feeling episodically dizzy and 2 episodes of near collapse (pre-syncope). She also admitted to mild dyspnoea on exertion which she had noticed over the same 6 week period. She had no previous cardiac history and was only on medications for constipation.
Let’s cut to the chase as this is a cardiology website and hence I’ll tell you that the cause of her dizziness, pre-syncope & dyspnoea is (we think!) cardiac. What do you think of her ECG?
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Confused? If in doubt repeat the trace; what about this one?
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The rhythm is irregularly irregular and at first we wondered whether her symptoms could be due to paroxysmal AF (this led us to wonder whether she was having posterior circulation TIAs and dizziness secondary to this) but then we looked at the rhythm strip with more care and we see this:
These are p waves which (by definition) represent organised atrial activity although we noticed that there were at least 3 distinct morphologies and the PR interval was variable. This satisfies the criteria for the ECG diagnosis of “wandering atrial pacemaker” which occurs when the atria depolarise from different sites other than the SA node.
However, this diagnosis alone doesn’t usually cause symptoms (and indeed doesn’t usually need treatment) so we put a 24 hour tape on to see whether there was evidence of sinus or AV node disease. We gave strict instructions for her to be mobile when the tape was on so we could assess her response to exertion.
We found 2 things on her 24 hr tape:
- A HR range of 60-70bpm over 24 hours (a so-called “flat” trace) which was despite exercise and in the absence of rate-limiting medications; this is chronotropic incompetence which is part of the spectrum of sinus node dysfunction
- A dropped p wave (see below:) which raises the possibility of her suffering from occasional AV block (2:1)
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Chronotropic incompetence is tricky to spot but should always be considered in an elderly patient who is breathless on exertion (assuming the other “common” causes aren’t apparent). The rest of her workup was unremarkable and we decided that given our findings we could justify a dual-chamber pacemaker to protect against higher degrees of block and optimise her rate response to exercise.
Interestingly symptomatic chronotropic incompetence is a Class I indication for PPM insertion according to the ACC/AHA guidelines; available here
This was a challenging case and I hope I’ve presented it in a useful way; please feel free to comment or suggest improvements!
ECG Case 7: ??
A short case which can sometimes catch people out.
53yr old hypertensive male in hospital with headache. ECG below
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In summary: Sinus Rhythm, large p waves with borderline PR interval, normal axis, large R waves V3-V6, ST depression & deep T wave inversion V4-V6, T wave inversion I, aVL & V3.
Any thoughts?
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This is classical LVH with strain pattern. Don’t confuse it for ischaemia!! (although these patients are higher risk for coronary artery disease)
There are multiple LVH “criteria” indexes including Cornell, Estes, Sokolow-Lyon but the most important thing I think is seeing the pattern and recognising it in future!
Also remember that LVH itself isn’t a “disease” but can be thought of as a marker or result of other disease processes and the finding of LVH on ECG should trigger a slew of further investigations and a hunt for hypertension, aortic stenosis or regurgitation, HOCM, drug misuse (cocaine). All these patients need a full history, examination, echo and treatment of underlying cause.
Cardiology Cases 