What is this rhythm?

Unfortunately, I remember who sent this EKG to me, or the clinical information, but it is a very interesting tracing.

What is it?

Below is an annotated version:

There is isorhythmic dissociation (see below), with escape beats in complexes 1-4 and 9-14.  In beat 4, you can see a bit of a P-wave, and then 5 thru 8 have sinus rhythm.

Aside: "Isorhythmic dissociation:" the P-wave just happens to arrive at the same time as the escape beat, so that the P-wave and QRS are dissociated even though they are happening about the same time ("isorhythmic").   ........AV Dissociation does not always mean AV Block!! There can be dissociation without block, as here.  See more posts below.

Whenever the beat is fully sinus, the QRS is normal.

Whenever it is an escape beat, the QRS has a tall R-wave, along with an inferior and right axis, similar to a left posterior fascicular block (LPFB).  

But since there is no LPFB in sinus rhythm, the escape cannot be coming from the AV node; if it were, the QRS would not be different.  [The QRS in sinus rhythm and junctional rhythm are the same, because sinus rhythm goes through the AV node.]

The escape must be originating from a more inferior location that activates the left anterior fascicle preferentially, thus mimicking an LPFB.  

1. This confused me, because any beat that initiates in the left anterior fascicle should also have a RBBB morphology, which is not present here.

2. Also: why does the sinus rhythm come and go?


I asked my very smart friends Ken Grauer and Christopher Watford for their opinions.

Ken gave this great explanation, also referring to insights by Christopher:

"It’s a beautiful example of AV dissociation beginning with beat #4 where the P wave comes right at the onset of the QRS. There is underlying marked sinus arrhythmia with accelerated idioventricular rhythm (AIVR) at a rate of ~80/minute (arising from a septal focus) — such that when the sinus rate is faster (beats #5-thru-8), we have sinus rhythm — and when we have slight slowing of the sinus arrhythmia rate to below ~80/minute — then the accelerated septal focus takes over (beginning with beat #9). Note the sinus P wave peaking back again at the end of the tracing (at the onset of beat #14). So, the mechanism for AV dissociation here is a combination of “default” (when the sinus rate slows to below 80/minute) + “usurpation” (due to the slightly accelerated ventricular septal focus.

"The QRS morphology as Steve and Christopher have described is fairly narrow with left posterior hemiblock (LPHB) morphology, but lacking the RBBB characteristic that is usually seen in V1 with the more typical fascicular ventricular tachycardias...... I imagine, depending on where in the septal the focus is, that you might get a hemiblock pattern with narrow QRS and no RBBB (as we see here)."


Here are more posts on AV dissociation and AV block

AV Dissociation Lecture by K. Wang (28 minutes)

AV Dissociation. Is there AV block?

A Mystery Rhythm, Explained by K. Wang's Ladder Diagram.

Another Guest post from K. Wang: What is the rhythm/conduction problem?

What Kind of AV Block is This? Guest Post by Dr. K. Wang (The Rhythm Master), Using a Ladder Diagram

Atrial Flutter. What else?? (AV dissociation with block)

Wide complex tachycardia at a rate of 270

Unfortunately, this case lacks some of the clinical data, but not so much that we can't learn something from it.

Case

A 50-something male called 911 for central chest pain and palpitations.
PMH: atrial flutter, hypertension, elevated cholesterol
Medications: Digoxin, ramipril, aspirin

The patient was diaphoretic and clammy.  He was hypotensive.

A prehospital rhythm strip was obtained:

A 12-lead is below

A 12-lead was obtained:

Regular Wide Complex Tachycardia
Rate 267, R-R interval 225 ms
What is it? What do you want to do?

There is a wide complex, regular tachycardia at a rate of 267.  The R-R interval is 225 ms.

1. It is regular, so it cannot be atrial fibrillation.
2. It is on the high end of rates for SVT (140-280), so SVT is unlikely.
3. It is too fast for typical ventricular tachycardia, but could be "ventricular flutter," but that is very rare.
4. AV reciprocating tachycardia (AVRT, antidromic) is possible. [WPW with antidromic rhythm: down the accessory pathway (resulting in wide QRS) and up the AV node.]  But this 50 year old has already had cardiac care and does not have a diagnosis of WPW, so that is nearly impossible.

The best clue is the history of atrial flutter and that he is at least supposed to be on Digoxin.

Thus, it is almost certainly atrial flutter with 1:1 conduction at a rate of 267 (interval 225 ms).  The R-R interval would then have to be identical to the atrial flutter interval of 225 ms.

Why is there a wide complex?

Probably because the rate is too fast for one of the conducting bundles.  This looks most like a left bundle branch block, but is not clearly LBBB.

More importantly, the patient is unstable, so electrical cardioversion should be the next step, immediately.

This is the next ECG rhythm strip (unfortunately, no 12-lead).  It seems that there was no time for any intervention by the medics.

Now the atrial (flutter) rate is 290 (not 270, as before) and there is 2:1 block
Ventricular rate is 145
R-R interval here is 414 ms, flutter interval is 207 ms (shorter than before)
The QRS is still wide.
What happened?

Paradoxically, the increased atrial rate is associated with a slower ventricular rate, and probably was the cause of the slower ventricular rate. 

A ventricular rate of 290 with 1:1 conduction results in depolarization of the AV node and ventricle every 0.207 seconds (207 milliseconds).   If the AV node takes longer than 207 ms to repolarize (refractory period greater than 207 ms), then at this atrial rate (a beat every 207 ms), only every other (every 2nd) beat can be conducted, and there will be 2:1 conduction.

For an unknown reason, the atrial rate increased and thus the ventricular rate decreased, which is very good for the patient.

Why might this have happened?

Uncertain, but if the patient became more distressed and had increased sympathetic output, then he could have an increased atrial rate.  

        However, increased sympathetic tone also increases AV conduction (makes it more "slick," or "greasy").   This could counteract the faster atrial rate and prevent the slowing of the ventricular rate.   

Why is this concept important for us?

If you see a patient with atrial flutter with 2:1 conduction and you want to convert the atrial flutter chemically with, for instance, procainamide (or any other type 1 antidysrhythmic), you could convert to 1:1 conduction. How?  Procainamide is used to convert flutter to sinus, but before conversion (or if it is ineffective), it will cause the atrial flutter rate to slow to a rate that makes 1:1 AV conduction possible.  

You will have made the situation worse.  

Therefore:

If you ever want to convert atrial flutter by giving procainamide or any other Type 1 antidysrhythmic, you MUST give an AV nodal blocker first, or you will make the patient worse.

I always use electricity to convert atrial flutter.  It is safer.

Similarly:

Any patient who is started on a Type 1 antidysrhythmic (flecainide, for example, to control symptomatic PVCs) should be started on a calcium channel blocker such as Diltiazem (or a beta blocker).  If such a patient were to go coincidentally go into atrial flutter, the flecainide would result in slow atrial flutter that could be slow enough to conduct 1:1.   Diltiazem would prevent 1:1 conduction. 

Digoxin

This patient is probably on Digoxin for the same reason.  It also slows AV conduction.  It is likely that he stopped taking it and this is one of the reasons for his decompensation.

An elderly woman with dyspnea, asystolic arrest, resuscitated

911 was called for a very elderly dialysis patient for acute onset of dyspnea.

On arrival, medics found the patient with agonal respirations.  Chest compressions were started and 2 doses of epinephrine givne, and she was found to be in asystole, which then changed to PEA at some point, then to ventricular tachycardia.  A King airway was placed.

This is her prehospital ECG:

What do you think?
My thoughts are below.

On arrival, she was hypertensive and tachycardic.  Due to concern for hyperkalemia, Calcium was given empirically.  Cardiac ultrasound showed poor LV function and normal RV size.  K returned at 5.8 mEq/L (not high enough to be responsible for all of this).

An ED ECG was obtained:

What do you think?

ECGs:

Prehospital:
--There is sinus tachycardia.
--The large R-wave in V1, with wide S-wave in V5 and V6 shows late forces toward V1 and away from V5 and V6, and is therefore diagnostic of right bundle branch block (RBBB).
--The large inferior S-waves, with a small q- and large R-wave in aVL are diagnostic of left anterior fascicular block.
--(Bifascicular block, RBBB and LAFB).
--Importantly, the PR interval is normal.  If prolonged, there would be so-called trifascicular block.

These findings alone are very suggestive of LAD or left main occlusion.  Every such case I have ever encountered was in a patient with either left main occlusion or LAD occlusion and the patient was near death or post-arrest.

This is a very bad sign, and the ST Elevation in these cases is frequently very subtle.

Finally, there are very large (hyperacute) T-waves in II, III, aVF and in V4-V6.  These are diagnostic of either hyperkalemia or of acute STEMI.

Here are some cases of STEMI with RBBB and LAFB

Wide Complex Tachycardia; It's really sinus, RBBB + LAFB, and massive ST elevation

don't miss this one!

What, besides large anterior STEMI, is so ominous about this ECG?

Chest Pain and Right Bundle Branch Block

68 minutes with chest compressions, full recovery. Plus recommendations from a 5-member panel on cardiac arrest.

____________________________

ED ECG:
--Sinus tachycardia with RBBB and LAFB
--There is subtle ST elevation in V2-V5

Here the precordial leads are magnified:

Notice that there is almost 2 mm ST Elevation in V2
2 mm ST elevation in V3
1 mm ST Elevation in V4

RBBB should not have ANY ST elevation, so this is STEMI until proven otherwise.

In fact, in leads with a prominent R'-wave (here, as is usual: V1-V3), there should be ST depression that is discordant to the prominent R'-wave)

Here is an example of RBBB without any ischemia:

Note normal (non-ischemic) ST depression in V1-V3, discordant to positive R'-wave

The ST elevation was not seen.

She had fever and elevated lactate.

Sepsis and pulmonary embolism were suspected.

CT pulmonary angiogram was negative.

After this, she had another brady-asytolic arrest and was resuscitated again.

Another ECG was obtained:

Now the anterior STEMI is obvious
 (in addition to right bundle branch block and left anterior fascicular block) 

Further comment on this ECG:
--The ST elevation is greatest in V1
--There is also ST Elevation in lead III, and reciprocal ST depression in aVL
--There is ST depression in V5 and V6

Notice the RBBB with LAFB is gone!  I cannot explain this except to say that any new bundle branch block in any situation can be transient.

One might suspect these findings to indicate an inferior and right ventricular infarct, but a (left ventricular) septal infarct with a wraparound LAD to the inferior wall will give the same pattern and is more likely, especially due to the bifascicular block.


Now the etiology of her entire clinical presentation (except fever) is obvious.

She arrested again before she could get to the cath lab.  So no angiogram was done.

An 82 year old with syncope

An 82 yo male stopped for lunch after cycling. Witnesses reported a syncopal episode lasting approximately 30 seconds. He has a history of prior MI with 3 stents placed. There was no other significant hx. 

The patient denied any chest discomfort, dyspnea, or n/v or any complaints and did not wish to go to the hospital.  However, he did not protest transport.  

BP was 134/66, and heart rate remained around 60, which he said was normal for him. 

A 12-lead ECG was recorded:

Sinus rhythm, rate 64.
There are features here that one can recognize in retrospect, but in a patient with no current symptoms, it is all nonspecific.
For instance, there is a long ST segment and negative T-wave in lead III.  But the QRS axis is also negative, so not truly T-wave inversion.
Lead aVF has a very subtle up-down T-wave
There is a sagging ST segment in lead V3

The medic is very good at recording serial ECGs, and did so this time at 9 minutes even though there were no new symptoms (patient asymptomatic).

Sinus rhythm.
Note there is new ST elevation in lead II, aVF, V5, and V6.
There is also increased sagging of the ST segment in V1-V3.
The computer surprisingly reads "Meets STEMI critiera" !!

The ECG does not, strictly speaking, meet STEMI criteria: note on the side there are measurements of ST elevation at the J-point: it is correctly reading more than 1 mm ST elevation in 2 leads (II and V5), but these are not consecutive leads. STEMI criteria require the findings to be present in at least 2 consecutive leads. 


The medic was now very worried in spite of absence of symptoms, and recorded another ECG 6 minutes later:

Now the T-wave in lead III is much less negative.
There appears to be LESS ST elevation in II, V5, and V6

The medic noticed these dynamic findings and activated the cath lab!  

They were headed to a non-PCI center, so activating meant activating a transfer.  But they were too close to bypass the smaller hospital, so they stopped and the patient had an immediate ECG in the ED, still with no symptoms!!:

Atrial flutter with slow and variable conduction
Obvious inferior - posterior - lateral STEMI
Note that inferior T-waves have "pseudonormalized" (become upright)
See here for more on pseudonormalization

The patient was immediately transported to the PCI hospital, where an ostial RCA 95% thrombotic occlusion was found and opened and stented.

Comment

Should we get serial ECGs on asymptomatic syncope patients?  Maybe.  The literature on serial ECGs, which is pretty old, would say that among patients who are unlikely to have ACS, or at least dynamic ACS, it takes more resources than it is worth.  One should clearly get serial ECGs on a patient with ongoing chest pain, but for a single episode of syncope without ongoing symptoms?  

But in the ambulance, the ECG leads may remain attached, so why not record multiple tracings?

In contrast, in the ED, there is much demand for the ECG machine and tech, and it is more use of resources to keep the machine attached and record multiple tracings, so I would not advocate for that.


Learning Points

1. If it does not strain resources, record serial ECGs whenever there is any suspicion for ACS.

In this case, suspicion was very low but the medic is an incredibly skilled ECG reader (I know him) and he noticed these slight abnormalities which made him record more and then activate the cath lab.

2. In this case, the computer was very sensitive for STEMI.

Acute Respiratory Distress and Pulmonary Edema

A 60-something called 911 for respiratory distress of acute onset.  Medics found him hypoxic with wet sounding lungs.  He was put on CPAP with improvement.  BP was 250/140 by manual measurement.

He was brought to the ED.  There was vomitus in his CPAP mask, and he began vomiting again.

He was intubated before he could even be placed on a cardiac monitor.

A bedside echo was performed.


There is an irregularly irregular rhythm with rapid response.
The myocardium is very thick (concentric ventricular hypertrophy)
There is very little ventricular filling, and thus very little cardiac output.
There is good LV function

There were many B lines and a very filled inferior vena cava.


Obviously, even without an ECG or monitor, this is atrial fibrillation with rapid ventricular response.

What do we do?

1.  Immediately cardiovert?  This will restore the important atrial contribution to ventricular filling, and we can see that ventricular filling is a big issue.  This will only work reliably in paroxysmal atrial fib.  Chronic atrial fib is unlikely to convert.  Furthermore, if it is chronic, then there is a stroke risk.
2. Slow the rate with an AV nodal blocker?  Diltiazem?  Esmolol?   This will not restore the atrial contribution, but will slow the ventricular rate and allow for more filling.
3. Give diuretics? This will worsen ventricular filling.

Figuring out whether this is chronic or paroxysmal is important.

The big question is: What initiated the critical situation?

1.  The patient has concentric LVH and suddenly developed atrial fibrillation.
Pulmonary Edema developed due to high left sided pressures due to poor forward flow due to:
          a) No atrial contribution to ventricular filling, and
          b) A rate too rapid for ventricular filling, this patient who has a stiff and noncompliant ventricle suddenly has a precipitous drop in cardiac output and develops pulmonary edema.

Catecholamine surge leads to peripheral vasoconstriction and very elevated BP (in spite of poor cardiac output), further diminishing cardiac output.

2.  Alternatively, there is chronic atrial fibrillation and something else caused the rapid response:
a. Patient became septic, dehydrated, had GI Bleed, etc.  However, this would lead to shock but not pulmonary edema.  And the inferior vena cava would show evidence of volume depletion.

3. The patient has chronic atrial fib and now has fluid overload.  But in such a case, the ventricular cavity would be dilated and filling well.

4. The patient has a sudden change in ventricular function (e.g., ischemia, ACS).  This is not supported by this echo which shows good LV function.

5. Valvular dysfunction: the only valvular dysfunction that is associated with a small ventricle is mitral stenosis.  This is a possibility and would be associated with atrial fibrillation and pulmonary edema.  However, it is relatively rare in the U.S. and it is also more likely to be a chronic problem.

Aortic insufficiency, Aortic stenosis, and Mitral insufficiency are all associated with a well-filling ventricle.


The typical patient who has chronic atrial fibrillation and has a rapid ventricular response is ill with second pathology that overlays the atrial fib, and cardioversion will not work and will not correct the situation.  Most of these patients have sepsis, hypoxia, resp failure, GI bleed, dehydration.  They are older and have become ill more slowly.  Their ventricles are usually dilated, not small and with concentric LVH.  This represents about 80-90% of ED patients with atrial fib and RVR who are ill.

But a younger patient with sudden symptoms, a tiny ventricle, and severe pulmonary edema is likely to have paroxysmal atrial fib and to benefit from cardioversion.

The risk of stroke is much lower as well.

Case progression

The patient was cardioverted after etomidate sedation with 200 J of biphasic synchronized cardioversion.

Here is the post cardioversion ultrasound:



Cardiac output is far better.  Filling is far better.

His clinical condition rapidly improved.

Here is the post conversion ECG:

Sinus rhythm.  LVH with typical ST-T (repolarization) abnormalities.

His blood pressure came down to 134/92, 158/97 without any ED medications.

This turned out to be his first episode of atrial fibrillation.  So, as expected, it was paroxysmal and was the initiating factor to his pulmonary edema.

Cardioversion was the exact right thing to do.

The patient did well.

Learning Points.

1. Even without the past history, one can make a very good assessment as to the chronicity of atrial fibrillation in critically ill patients.

2. Cardioversion can restore the atrial contribution to ventricular filling.

3. A slower rate can improve cardiac output.

4. Patients with LVH have very stiff ventricles that require particularly high filling pressures.

A 60-something dialysis patient with complete heart block: ultrasound before and after treatment

A 60-something dialysis patient complained of weakness.  He was hypoxic and in some respiratory distress.


He had these prehospital ECGs:

Rhythm Strip only, with very slow rate.  There appear to be some P-waves that are dissociated from the QRS.  This appears to be complete heart block with ventricular escape.

More of the same, but with some narrow complex beats, perhaps junctional, or perhaps with some conduction.
The exact ECG diagnosis is not as important as the management.

A 12-lead was recorded:

P-waves are difficult to consistently identify, but there is a wide complex ventricular escape, with a RBBB and LAFB morphology, consistent with a posterior fascicle escape.
Notice also the deep T-wave inversions.
These are common in third degree heart block but do not usually represent ischemia due to ACS.

Syncope with 3rd degree heart block often has huge inverted T-waves.


He arrived in the ED without any IV access. Obtaining access was very difficult and the patient was refusing many attempts.

Since hyperkalemia was presumed, 0.50 mg intramuscular terbutaline while attempting IV access.

A bedside ultrasound was done:


Here you can see the mitral valve opening at an irregular rate that is faster than the left ventricle, and with the two dissociated.  This confirms third degree (complete) AV heart block.


Finally, an ultrasound guided IV was obtained and he given 3 g of calcium gluconate.

His heart rate increased, with this subsequent ultrasound:


Rate is irregular and much faster now.  Cardiac output is much higher.

Symptoms resolved.

He was also shifted with insulin, and glucose.


A repeat ECG was recorded:

Sinus rhymth with PACs and Left Bundle Branch Block
Normal ST-T for LBBB
Previous ECGs showed both sinus rhythm and atrial fib
They showed LVH without LBBB

The K returned at 6.6 mEq/L.  The repeat value 34 minutes later was 6.0 mEq/L.  The value prior to obtaining blood may have been a bit higher than 6.6.

There was a good outcome.

Learning points

Bradycardia and block may be due exclusively to hyperkalemia, and reversed by Calcium.  There is no dose of calcium too high for such critically ill patients.

See this case in which I gave 15 grams of Calcium gluconate:

Weakness, prolonged PR interval, wide complex, ventricular tachycardia

A 50-something woman with chest pain and dyspeoa (an Aussie)

This case comes from Max Nelson, a paramedic in Australia.

See also this post:

40-something with severe CP. True + vs. False + high lateral MI. ST depression does not localize.

Case

I was dispatched to a middle age woman (~50YO) with chest pain and nausea.

Exam: pt is huddled around toilet bowel, naked and shivering. Pt appears “well” but with pallor.

Hx: pt was woken from sleep after midnight with chest aching, dyspnoea and significant nausea. Pt moved to the toilet and had one bilious vomit. The ambulance was called and arrived approx 20 minutes later.

Signs and symptoms: nausea, dyspneoa, cold, pallor.

Now states chest pain/tightness has resolved (gone).

Hx of pain:

D- aching

O- tonight roughly 30 minutes before assessment. First experienced 2 days ago while “rushing at work” with several intermittent pains since then.

L- central chest

O- nausea, dyspnoea. Unchanged on inspiration, palpation, movement.

R- nil radiation, relieved tonight with vomit, relieved past two days with rest, rated 7/10 (not current).

Risks: postmenopausal woman, paternal CABG. Non smoker.

Allergy: penicillin

Medication: anti-depressant

Past medical history: depression

VSS: GCS 15, PERRLA, 140/80, 96BPM, 22RPM, 98% ORA, 35.5*C, 6mmol/L.

Here is the ECG, after patient's pain has resolved:

Click here to enlarge
Automated interpretation: NSR, Normal

What do you think?

Smith comment: I see significant ST depression in inferior leads.    Remember that when there is inferior ST depression, it is NOT "inferior ischemia," as subendocardial ischemia does not localize.  When you see this, it is nearly always reciprocal to ST elevation in aVL that may be very difficult to appreciate, often because of very low voltage in aVL.  Indeed, if you look at aVL, the QRS voltage is not even 0.2 mV (2 mm) and so the ST elevation (less than 0.5 mm) then is proportionally significant.

Also, the T-waves are down-up, which is particularly indicative of ischemia (or of hypokalemia, if QT interval is very long -- really a QU-interval).

See these posts about down-up T-waves.

Case continued

Patient is moved to ambulance with wheelchair, develops pain and second ECG is recorded roughly 7 minutes later (with pain):

Click here to enlarge 
Automated interpretation: NSR, ST depressionWhat do you think?

Smith comment:

The "inferior ST depression" is more pronounced.  There is now higher T-wave voltage in V2-V4.  It is beginning to look like an LAD occlusion, proximal to the first diagonal.

Mobile Intensive Care Ambulance (MICA) requested for worsening depression.

Two further ECGs are recorded roughly 8 minutes apart en route to RV:

Click here to enlarge
Automated interpretation: "NSR, ST depression, consider subendocardial ischaemia"

Smith interpretation: ST depression is deeper.  STE in aVL is higher.  There is new ST elevation in V1 and V2, and a bit in aVR.  T-waves are now hyperacute in V1-V5.  There is ST depression now in V5 and V6.
This is a proximal LAD occlusion and may in fact be proximal to the septal perforator.  This results in ST elevation in V1 and aVR, and can also result in reciprocal ST depression in V5 and V6, which are opposite the septum.


4th ECG:

Click here to enlarge
Not much different than the 3rd

Further ECGs (not shown) displayed developing elevation in anterior leads leads with runs of ventricular bigeminy.

Outcome

This woman had thrombotic occlusion of the LAD

Smith: It was reportedly of the mid-LAD, though I am skeptical, and suspect that the report was miscommunicated because the ECG clearly shows high lateral involvement.

Her clinical course was aspirin, GTN, opioid analgesia, anti-emetic, heparin bolus pre-hospital with uncomplicated angiogram and stent at cath lab. Discharged home two days later with full recovery.

Some thoughts on the ECG from Max:

• ECG 1: bad tracing on limb leads but inferior ST depression is the most obvious abnormality here. Both the poor tracing and ischaemic pattern should prompt serial ECGs. aVL is concerning: there is very slight ST elevation that, when interpreted in the context of the QRS amplitude, is not so slight.
• ECG 2: there is obviously a better trace and there is progression of the inferior depression (most notable in aVF). There is also progression of the elevation in aVL, which, at this point, is diagnostic of MI. Also note the changes in anterior T-wave morphology and the gradual straightening of the ST segment in the anterior leads.
• ECG 3, 4: obvious progression in above findings. Now with some elevation in precordial leads and notably in aVR. Low lateral depression (V5, V6)

There is very little to say about this except to highlight the importance of serial ECGs. This woman is obviously very unwell but it is feasible that, with early morning night shift brain, her symptoms may have been interpreted incorrectly and the history of the pain brushed over.

In addition to that, the computer did not interpret these as “****STEMI****, acute infarct, etc.” Don’t trust the computer! It’s generally pretty good but it cannot see your patient. You do not need to be able to pick which vessel or to able to intimately explain the changes of the ECG. Simply recognising something that is abnormal/changing is better than relying on a computer. Do not take these people to a non-PCI capable hospital!

I want to commend Max on a great job.

Learning Points:
1. Recognize that "inferior ST depression" is reciprocal to high lateral MI (aVL)
2. Do serial ECGs
3. Don’t trust the computer interpretation.

An interesting finding, and absence of another, in an intoxicated patient found down

This was a male in his 20s who was found down, intoxicated presumably with an opiate, perhaps methadone.  He awoke very slowly with naloxone, probably because his brain had been hypoxic for a while.   

He had an ECG recorded. 

Sinus tachycardia.  
Computer reads QRS as 114 ms.
What else?

Notice that at the end of the QRS in leads II and V4-V6 there is a distortion: these "J-waves" are very large.  They are, in fact, Osborn waves.  They result in the QRS measurement being wide (114 ms).

The K at this point was 4.6 mEq/L.

His rectal temp was taken and it was 33.2 C.

He was externally warmed.  He became hypotensive and was resuscitated, and another ECG was recorded at a temp of 34.5 degrees C:

The Osborn waves persist, but with less voltage.  However, the QRS also has less voltage, so the Osborn waves remain proportionally unchanged.  Computer again reads QRS duration as 114 ms.

Do you see anything else?

Only one thing: There is a negative P-wave axis now.  So there is now either a low atrial rhythm or a high junctional rhythm (both will have negative P-waves that are see before the QRS -- a low junctional rhythm with result in P-wave in, or after, the QRS.

All I see is the change in P-wave axis, and that is what is interesting: in the time between ECGs, the K had risen to 7.6 mEq/L.  The patient had rhabodmyolysis and was rapidly releasing potassium into the circulation.

Other than the change in P-wave axis, I could not find any evidence of hyperkalemia on this ECG, compared to the previous.  And I cannot prove that the change in P-wave axis is due to hyperkalemia.

We treated with calcium and shifting: intramuscular terbutaline, insulin, glucose, furosemide, and precious bicarbonate because there was rhabdomyolysis.   We placed a dialysis catheter in anticipation of continued release of potassium and possible severe kidney injury.

Rhabdomyolysis patients can have a huge continued ongoing release of potassium that sometimes even dialysis cannot keep up with.

The patient did well in spite of a CK rise to above 100,000.

Learning Points:

1. Recognize Osborn waves.
2. Significant hyperkalemia can (rarely) be nearly invisible on the ECG, even with a previous ECG for comparison.  In this case,  the only possible clue was a change in P-wave axis, and I cannot even
3. Beta-2 Agonists are useful in lowering K, but only in high nebulized doses or parenteral administration.

Parenteral Beta Agonists for Hyperkalemia (Terbutaline, Albuterol)

Previous post with more references: 
Terbutaline and Albuterol for Lowering of Plasma Postassium

--0.5 mg of IV albuterol reduces K by about 1.2 mEq/L. 

--A 20 mg neb (most for bronchospasm are only 2.5 mg) lowers it by about 1.0 mEq/L.  

--A 10 mg neb lowers it by about 0.6 mEq/L.

I give 0.25 mg of IM terbutaline to an adult, but only if it is critical, and add nebulized albuterol also.  

I've never given it IV, as I'm a bit reluctant to risk the cardiac irritability.

Here are a couple abstracts on beta agonists in hyperkalemia:

TI

Subcutaneous terbutaline use in CKD to reduce potassium concentrations.

AU

Sowinski KM, Cronin D, Mueller BA, Kraus MA 

SO

Am J Kidney Dis. 2005;45(6):1040. 

BACKGROUND: Acute hyperkalemia is a frequent and potentially life-threatening medical problem in patients on maintenance hemodialysis therapy. beta-Adrenergic receptor (betaAR) stimulation causes potassium cellular influx and a decline in plasma potassium concentrations. Therefore, betaAR agonists are used in the treatment of patients with hyperkalemia. The goal of this study is to evaluate the utility of weight-based subcutaneous terbutaline dosing to reduce plasma potassium concentrations in a group of subjects with chronic kidney disease (CKD) requiring hemodialysis.

METHODS: Fourteen subjects with CKD receiving long-term hemodialysis were administered terbutaline, 7 microg/kg, subcutaneously. Heart rate measurements and blood samples for potassium concentration determinations were made serially for 420 minutes. Effects of terbutaline on heart rate and potassium responses were determined in each subject.

Results: Terbutaline significantly reduced plasma potassium concentrations and significantly increased heart rates during the time course of the study.  Mean reduction was -1.31 +- 0.5 mEq/L and increase in peak heart rate was 25.8 +/- 1, both highly significant.  No adverse events were reported.

CONCLUSION: Administration of subcutaneous terbutaline obviates the need for intravenous access and should be considered as an alternative to nebulized or inhaled beta-agonists to treat acute hyperkalemia in patients with CKD. As with the use of any beta-adrenergic agonist, close cardiovascular monitoring is necessary to avoid or minimize toxicity during therapy.

Hypokalemic effects of intravenous infusion or nebulization of salbutamol in patients with chronic renal failure: comparative study.

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Liou HH, Chiang SS, Wu SC, Huang TP, Campese VM, Smogorzewski M, Yang WC 

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Am J Kidney Dis. 1994;23(2):266. 

To examine and compare the efficacy and safety of different routes of administration of salbutamol in treating hyperkalemia, 15 patients with chronic renal failure (blood urea nitrogen>80 mg/dL, serum creatinine>8.0 mg/dL) were enrolled to sequentially receive either intravenous infusion (0.5 mg) or nebulization (10 mg) of salbutamol. Five of these patients (33.3%) did not respond to the intravenous salbutamol and were excluded from the study. Both treatments significantly decreased plasma potassium in 10 patients and the decrease was sustained for at least 3 hours. After infusion, the maximal reduction in plasma potassium levels was 0.92 +/- 0.10 mEq/L and occurred after 30 minutes. On the other hand, the maximal reduction in plasma potassium after nebulization (0.85 +/- 0.13 mEq/L) was similar to that after infusion, but it occurred after 90 minutes. Insulin and blood glucose increased, whereas blood pH, PCO2, sodium, osmolality, and blood pressure did not change after either treatment. Heart rate increased significantly after both treatments, but less after nebulization than after infusion. It is concluded that both infusion and nebulization are simple, effective, and safe therapeutic modalities for the treatment of hyperkalemia in patients with chronic renal failure. Infusion should be used in patients requiring a rapid decrease in plasma potassium; nebulization, on the other hand, should be used in patients with coronary artery diseases.