12-Lead ECG Blog - (Cardiology & Electrocardiography Experts)

58 year old male CC: Unconscious - Conclusion

2011-02-03T02:40:00.000Z

Here is the conclusion to 58 year old male CC: Unconscious.

This was an unusual case with an unfortunate outcome.

Let's look at the heart rhythm again.

The rhythm is slow and irregular with strange looking complexes. At first glance it's difficult to distinguish QRS complexes from T-waves. It looks like a pre-morbid rhythm.

However, on closer inspection we can see that the QRS complex is present but near isoelectric. The QRS duration is > 200 ms which is extremely abnormal. Whenever you see a QRS complex > 200 ms you should suspect hyperkalemia!

In addition, when the S and T-waves merge together and the ST-segment becomes non-distinct you've moved into what is sometimes referred to as the "sine wave" ECG. This is an ominous finding.

Unfortunately, at the time this ECG was recorded (several years ago) our paramedics weren't trained to recognize hyperkalemia. It's one of the many ways the paramedic profession has evolved throughout the course of my career.

However, they knew the heart rhythm was "bad" and they wanted to see something a little bit less scary on the monitor so they elected to perform transcutaneous pacing (TCP).

Did they achieve capture? Let's take a look.

They did not achieve capture, although I can understand whey they thought they had intermittent capture.

A shows the morphology of the underlying rhythm. B shows a (presumed to be) transcutaneously paced QRS complex. It is classic for false capture. C shows a "phantom" QRS complex (caused by pacing artifact) that coincidentally falls directly on top of the (unsensed) native QRS complex. This makes it appear as though capture has been achieved. D shows a "phantom" QRS complex falling in the absolute refractory period of the underlying rhythm (proving beyond any shadow of a doubt that these QRS complexes are the result of pacing artifact).

So what ended up happening?

The patient survived to arrival at the emergency department. However, during transfer of care the emergency physician asked that the TCP be turned off so that he could examine the underlying rhythm.

Moments later the patient was shocked x2 by his ICD and the resultant heart rhythm was asystole.

He was not successfully resuscitated.

It was later that they found out the potassium level was > 9 mEq/L (I don't remember the exact value).

I don't know why this patient's ICD shocked him. I was not present when the device was interrogated. But I suspect that it may have been confused by the TCP.

If I am ever faced with a situation in the future where I feel that TCP is indicated and the patient has an ICD I will be contacting Online Medical Control and asking permission to disable tachy therapy with a ring magnet.

Obviously there are a lot of lessons to be learned from this case.

See also:

Transcutaneous pacing (TCP) – The problem of false capture

Transcutaneous pacing (TCP) with a Lifepak 12

Using capnography to confirm capture with transcutaneous pacing (TCP)

Transcutaneous pacing (TCP) for asystole

58 year old male CC: Unconscious

2011-01-24T14:37:00.000Z

EMS is called to the residence of a 58 year old male patient who was found unconscious at the bottom of the stairs by the spouse.

The patient responds to painful stimuli with a grimace.

Respirations are shallow.

Past medical history: MI, pacemaker/ICD, renal insufficiency

Medications: Numerous - unable to locate at the time of evaluation

Radial pulses are absent.

The cardiac monitor is attached and shows strange, slow waves.

By the appearance of the ECG paramedics are surprised that the patient is not in cardiac arrest.

They prepare the patient for immediate transcutaneous pacing (TCP).

Paramedics report capture at 60 PPM and 80 mA.

The patient regains consciousness but is not alert.

He is not conversant but nods his head to simple questions and manages to mouth the word, "Sick."

What do you think is wrong with this patient?

What do you think about the current course of treatment?

See also:

58 year old male CC: Unconscious - Conclusion

41 year old female CC: Chest pain - Conclusion

2011-01-12T13:23:00.000Z

Here is the conclusion to 41 year old female CC: Chest pain

Paramedics give 150 mg amiodarone over 10 minutes via piggyback infusion.

The patient's BP drops to 90/48 and the patient's clinical status is observed to deteriorate.

Synchronized cardioversion is performed.

The rhythm is now narrow complex but extremely fast and unstable.

The ICD delivers a shock and the patient is observed to be in VF.

After waiting a few seconds (to see what the ICD is going to do) paramedics shock the VF.

The rhythm starts to stabilize and the patient's BP comes up to 142/74.

Are you ready to drop this patient off at the emergency department?

41 year old female CC: Chest pain

2011-01-10T12:52:00.000Z

Here's a case submitted by Bob Sullivan from New Castle County EMS.

EMS is called to the residence of a 41 year old female with chest pain.

Onset: Sudden while sweeping the floor
Provoke: Nothing makes the pain better or worse
Quality: Tightness
Radiate: The pain does not radiate
Severity: 8/10
Time: 20 minutes prior to EMS arrival

Past medical history: MI, Pacemaker/ICD
Medications: amiodarone

Vital signs:

RR: 22
Pulse: Very rapid
BP: 150/80
SpO2: Not registering

The cardiac monitor is attached.

A 12-lead ECG is captured.

The patient is placed on O2 via NRB @ 15 LPM and IV access is established.

What do you think the paramedics should do next?

76 year old male CC: "Possible MI"

2011-01-06T13:57:00.000Z

Here is a case submitted by a faithful reader from the UK who wishes to remain anonymous.

Call is received into control via 999 from a General Practitioners Surgery. Call is received as 76 year old male with possible MI.

Presenting Complaint - Chest Pain

History of Present Complaint - 76 year old male, nil cardiac history, known COPD, ex smoker, social drinker.

Awoken at 2 a.m by an acute central chest pain radiating to his left arm.

Male waited till surgery opened and made an emergency appointment.

GP had 12-lead ECG done on patient - noticed ST-elevation and administered 1x400mcg GTN spray SL, 300mg Aspirin PO and O2 therapy. Ambulance contacted via 999.

Here is the first 12-lead ECG taken by the GP.

The second 12-lead ECG taken by the GP was after NTG.

Ambulance..

On Arrival - Patient supine on bed, O2 therapy via NRB administered by GP

On examination:
Alert, orientated and communicable (GCS 15)
Slightly pale
Nil diaphoresis

Nil SOB, clear bi-lateral air entry - nil adventitious breath sounds
R/R 20, SpO2 99% on O2

H/R 89 and regular, BP 149/99

Pyrexial 37.7
B.M 10.6

C/O chest pain..
O - Acute
P - Not affected by breathing. Eases slightly leaning forward. Pain++ on palpation of sternum.
Q - Sharp in chest
R - Central chest radiating left arm
S - Pain score 7/10 eases slightly with GTN
T - 11 hours ago
I - No pain intervention sought.

Nil nausea, nil vomit

Meds - Usual COPD drugs
PMH - COPD
Allergies - NKA

Paramedics switched the patient over to their 12-lead ECG monitor.

What's going on with this patient?

What is your treatment plan?

Where would you transport this patient?

Is there anything unusual about this case?

ECG101:P-Wave

2011-01-05T01:02:00.003Z

It’s all in a P-Wave

You know, the more you learn about medicine, the more you will realize how much there is out there that you will never know. ECGs are no exception. My obsession with cardiology began in paramedic school and it was only natural for me to grow a similar love for ECG interpretation.

Unfortunately, the usual prehospital training for 12-lead ECGs is limited, and generally doesn’t cover much more than STEMI and bundle branch blocks. The traditional resistance to further education usually involves a phrase like “well how is that going to change your treatment?” Nothing irks me more than hearing that stupid question. As if gaining new treatment strategies was the only reason to learn something. In this collection of posts, we will discuss some of the other things that an ECG can be used for, and you may find that it just might change your treatment.

The p-wave
The p-wave is the graphical representation of atrial depolarization. With normal physiology, this is initiated by the sinoatrial, or SA node. The p-wave can tell us many different things. A normal p-wave, married to a normal QRS lets us know that the patient has normal conduction.

There are many abnormals that may clue us in to a few pathologies though. If a p-wave is too tall, or peaked, right atrial enlargement is likely. A p-wave with two humps might indicate left atrial enlargement. The absence of a p-wave lets us know that the pacemaker is somewhere else in the heart. A p-wave that follows the QRS is likely not being used, and indicates that the AV junction is probably controlling the heart rate.

Maybe you have a p-wave that is slowly gaining distance between itself and it’s QRS complex, until finally there is no QRS; which indicates a Wenkebach pattern. The p-wave could be completely divorced from the QRS complex, indicating atrioventricular disassociation, or a complete heart block. It’s funny how much that little deflection can tell us. We often take it for granted, but when it is absent, we want it back desperately.

Above you can see a relatively normal location for a P-wave. 99% of your patients will probably have a similar variation to this.

Below is an example of p-pulmonale, which is an indication of right atrial enlargement.

Why is it called p-pulmonale?

Well, this is enlargement if the right atrium. The right atrium pumps its contents into the right ventricle which eventually empties its contents into the pulmonary trunk, pulmonary arteries, and eventually the lungs. When the pressure is backed up or increased in the lungs from chronic respiratory conditions like COPD, or asthma, or as a result of left ventricular failure, the right ventricle has to work harder. When the right ventricle works harder, so does the right atrium. Consisting of mostly muscle, when the heart works harder it gets bigger, just like your biceps. Consequently, right-sided heart failure is known as cor pulmonale. There are other causes, such as a right ventricular myocardial infarction, but the concept remains the same.

Above, you will see a p-wave with two humps. These p-waves are usually wider than normal, and are an example of p-mitrale, which is indicative of left atrial enlargement.

How does the left atrium enlarge?

The left atrium generally hypertrophies as a result of heart failure. To be more specific, left-sided heart failure. Left ventricular hypertrophy can be expected as well. This doesn't have to be the case though, anything problem that causes the left atrium to increase its workload may result in an increased size.

While biphasic p-waves may be a normal finding in V1 on a 12-lead ECG, if it is deeper than it is tall, it is likely representing left atrial enlargement as well.

You may find that many of your patients have both atria enlarged, and maybe even all four chambers. This cardiomegaly is a very good indicator that your patient may be suffering from heart failure. When you see left atrial enlargement on the 12-lead, don't forget to look for LVH. Remember that LVH can present with a left ventricular strain pattern, and this can mimic STEMI quite well. Check out ems12lead.com for more about that STE-Mimic.

The p-wave and its relationship with the QRS complex can tell you about abnormal conduction from the atria to the ventricles. More specifically, you can diagnose an atrioventricular block by closely examining the p-wave and pr-interval.

How to identify which AV block you are looking at:

Is the PR-Interval a constant length?

Yes > Are there any dropped beats? No > P wave for every QRS?

- Yes = Mobitz 2 - Yes = Mobitz 1/Wencheback

- No = 1st Degree AV Block - No = Complete Heart Block

Using capnography to confirm capture with transcutaneous pacing (TCP)

2010-12-31T13:22:00.002Z

Those of you who have been following me for a while (here and other online forums) know that I have searching for cases where a patient was successfully paced with a Lifepak 12.

I have reviewed dozens of cases where the treating paramedic thought the patient was being paced, but the rhythm strips showed only false capture.

Imagine my surprise when Robbie Murray (Operations Chief for Sussex County EMS) taught a capnography class for Hilton Head Island Fire & Rescue!

It was a wonderful class, and I learned a lot about capnography, but the part that really stood out was a couple of rhythm strips that showed TCP with true electrical capture!

That's just something you don't see every day. Trust me on this point. I've been paying attention!

Robbie was gracious enough to email them to me so I could share them with you.

Apparently for this intubated patient, there was a marked rise in CO2 as soon as electrical (and mechanical) capture was achieved. What a novel and interesting use of waveform capnography!

One thing I'd like to point out is that both of these rhythm strips show TCP @ 140 mA! That's important because the most common mistake I've seen with TCP is failure to increase the milliamperes high enough to achieve electrical capture.

Yours truly captured @ 120 mA with the Lifepak 12.

So, chalk up another "score" for waveform capnography and thanks again to Robbie Murray for sharing these interesting rhythm strips!

See also:

Transcutaneous pacing (TCP) - The problem of false capture

Transcutaneous pacing (TCP) with a Lifepak 12

58 year old male CC: Chest pain

2010-12-25T02:01:00.000Z

Here's an interesting case sent in by a faithful reader who wishes to remain anonymous.

EMS is called to the residence of a 58 year old male complaining of chest discomfort.

On arrival the patient is found sitting on the edge of the bed. He is anxious but alert and oriented to person, place, time, and event.

He was awakened from sleep by chest discomfort.

Onset: 30 minutes ago while sleeping
Provoke: Nothing makes the pain feel better or worse
Quality: Severe pressure or "ache"
Radiate: The pain does not radiate
Severity: 10/10
Time: He has had chest pain before but "not this bad"

Past medical history: HTN, dyslipidemia

Medications: Lipitor, Norvasc, ASA

Vital signs are assessed.

RR: 24
Pulse: 136
NIBP: 160/98
SpO2: 94 on RA

Breath sounds: basilar rales

The patient admits to mild dyspnea. He states that he has "gained a little weight" recently and his doctor was getting ready to put him "on a water pill."

Temp: 99.1
BGL: 138

The cardiac monitor is attached.

A 12-lead ECG is captured.

The patient is given 324 mg of aspirin, 0.4 mg NTG SL spray and placed on CPAP.

Another 12-lead ECG is captured.

The patient is loaded for transport and another rhythm strip is captured.

What do think is going on with this patient's heart rhythm?

What do you think is wrong with this patient?

You are 15 minutes away from the local non-PCI hospital and 60 minutes away from a STEMI receiving center.

Where would you transport this patient and why?

Physio-Control announces LIFENET System 5.0, partnership with AirStrip Technologies

2010-12-20T12:48:00.000Z

Today at the American Heart Association's Scientific Sessions 2010, Physio-Control announced the release of LIFENET 5.0 and a new partnership with AirStrip Technologies.

New features available in LIFENET 5.0 include:

LIFENET Consult – iPhone application allows physicians to perform rapid consults and provides decision support remotely to EMS and hospital care teams. The LIFENET Consult app is available for download from the iPhone App Store.
LIFENET OnePush – Automated protocol activation, notifies necessary caregivers and allows hospital teams more time to prepare for incoming patients.
LIFENET ePCR Delivery – Enables efficient and secure remote delivery of electronic patient care records (ePCR) to hospital printers or electronic medical record systems.
LIFENET Asset –Provides LIFEPAK device overview and management across entire fleet including automated alerts on device status, usage information, management of setup options and software updates.
Enhanced data integration – Enables EMS and hospitals to capture more patient data and combine it for a more-complete view of the patient.

If you're not familiar with AirStrip Technologies some of their mobile wireless solutions were featured in this TED Med talk in October 2009: Eric Topol: The wireless future of medicine.

This post was derived in part from a press release sent by Physio-Control with whom the Cardiology & Electrocardiography Experts blog has no conflict of interest.

60 year old male CC: Syncope

2010-12-20T12:42:00.003Z

Here is yet another awesome case courtesy of Christopher Watford who writes the My Variables Only Have 6 Letters blog.

One of these days Christopher is going to say (in his best Darth Vader voice), "Once you were the teacher but now I am the master!" and it will be completely justified.

EMS is called to evaluate a 60 year old male patient who experienced a syncopal episode.

On arrival the patient is found sitting in the front seat of his car. He is ashen gray and cold to the touch.

He is in moderate respiratory distress.

Past medical history: Brochitis
Medications: None

Breath sounds: clear bilaterally

Vital signs are assessed.

RR: 30
Pulse: 118 (weak and rapid)
BP: 108/64
SpO2: 88 on RA (increases to 94 on oxygen via NC @ 4 LPM)

BGL: 79

The patient states that he "can't afford to go to the hospital."

The cardiac monitor is attached.

A 12-lead ECG is captured.

What do you think is wrong with this guy?

*** Update 12/20/2010 ***

This gentleman was diagnosed with bilateral pulmonary emboli. He was admitted to the hospital on Lovenox (enoxaparin). After almost signing out AHA he was persuaded to stay by a doctor and nurse who informed him in no uncertain terms that he would die if he left.

The most suggestive ECG findings were:

Sinus tachycardia
S1Q3T3 (S-wave in lead I, Q-wave in lead III, inverted T-wave in lead III)
Possible beginnings of an acute right ventricular strain pattern in the right precordial leads

It's important to note that the most common ECG abnormality associated with PE is sinus tachycardia.

78 year old female CC: Headache

2010-12-17T15:12:00.000Z

Here's a case submitted by a faithful reader by the name of Nick Mercer.

EMS is dispatched to "possible heart attack" in rural Montana.

On arrival they find a 78 year old female lying on the couch where her friends found her in the morning.

The patient is awake and oriented but not alert. Speech is clear and appropriate but sluggish. She states that she has been lying on the couch for less than 1 hour.

The paramedics determine that she is complaining of a headache.

From bystanders they learn the patient as a past medical history of CVA, CHF, and MI.

The patient is cool, pale and diaphoretic.

During a neuro exam paramedics discover right-sided facial palsy and left-sided arm drift.

The patient starts to vomit.

Because they are 50 minutes from the hospital, the paramedics call for aeromedical transport.

The patient's head appears to be atraumatic. She denies recent falls. She denies chest pain or shortness of breath.

Vital signs are assessed.

RR: 24
Pulse: 90
BP: 216/134
SpO2: 98 on oxygen via NRB @ 15 LPM

BGL: 168

A 12-lead ECG is captured.

The patient is more lethargic by the time aeromedical transport arrives although the other neurological symptoms have resolved. She still looks acutely ill.

The patient has vomited a total of six times but stops after being treated with IV Zofran.

Repeat vital signs are assessed.

RR: 20
Pulse: 88
BP: 164/110
SpO2: 99 on oxygen via NRB @ 15 LPM

An additional 12-lead ECG is captured.

What is your impression of this patient?

69 year old male CC: Chest pain

2010-12-13T13:07:00.000Z

Christopher A. Watford from the My Variables Only Have 6 Letters blog has submitting a very interesting case study (actually he submitted two but you'll have to wait for the other one).

EMS is called to the residence of a 69 year old male complaining of chest pain.

On arrival the patient is found sitting in a kitchen chair.

He appears acutely ill.

Skin is ashen, cool, and very diaphoretic.

Levine's sign is present.

It is obvious that the patient is anxious and in severe pain.

Onset: Sudden onset approx 20 minutes before EMS arrival
Provoke: Nothing makes the pain better or worse
Quality: Severe pressure
Radiate: The pain does not radiate
Severity: 10/10
Time: No previous episodes

Breath sounds are clear bilaterally.

Vital signs are assessed.

RR: 20
Pulse: 60 R
BP: 142/68
SpO2: 90 on RA (increases to 96 with oxygen via NRB @ 15 LPM)

BGL: 104

No known drug allergies.
Denies any significant medical history other than "indigestion".

The cardiac monitor is attached.

A 12-lead ECG is captured.

Another 12-lead ECG is captured with modified chest leads V4R, V5R and V6R.

How would you treat this patient?

Is there anything about this case that surprises you?

Conclusion to 43 year old female CC: Chest pain - Angiograms

2010-12-10T13:43:00.000Z

Here is the conclusion to 43 year old female CC: Chest pain.

Let's take another look at her 12-lead ECG.

This patient experienced cardiac arrest on arrival in the emergency department.

She was defibrillated while still on the EMS gurney, stabilized, and then transferred to the cardiac catheterization lab.

Here we see a proximal occlusion of the right coronary artery (RCA). Those of you who suspected right ventricular infarction in addition to acute inferior STEMI were exactly correct.

Here we see the wire crossing the lesion.

Balloon inflation.

More balloon inflation.

Blood flow restored.

The patient was admitted to the ICU and discharged three days later.

Diagnosis: ST-elevation myocardial infarction

43 year old female CC: Chest pain

2010-12-08T15:16:00.000Z

EMS is called to the residence of a 43 year old female with a chief complaint of chest pain.

On arrival, the patient is found supine in bed.

She is alert and oriented to person, place, and time.

She is anxious and diaphoretic.

Past medical history: Hypertension
Surgical history: One kidney removed (unknown reason)
Medications: Azor

She denies shortness of breath and breath sounds are clear bilaterally.

Onset: 1 hour prior to EMS arrival
Provoke: Nothing makes the pain better or worse
Quality: Severe "pressure"
Radiate: The pain radiates down the left arm
Severity: 10/10
Time: No previous episodes of similar pain or pressure

Vital signs:

RR: 18
Pulse: 76
NIBP: 114/71
SpO2: 98 on RA

The cardiac monitor is attached.

A 12-lead ECG is captured.

How would you treat this patient and why?

73 year old female CC: Chest pain - Conclusion (with angiograms)

2010-12-06T20:20:00.000Z

Here is the conclusion to 73 year old female CC: Chest pain.

I'm sorry the conclusion to this case took so long. Due to a clerical error I received a duplicate case.

Let's take another look at the 12-lead ECG.

The patient was emergently cathed and a partially occlusive thrombotic lesion was identified in the mid-RCA.

Here's what it looked like to the invasive cardiologist.

The balloon is inflated (very short clip).

Here is the RCA after the intervention.

No acute lesions were noted on the left side (LCA and its tributaries, the LAD and LCX).

Finally, here is the post-cath 12-lead ECG.

Diagnosis: Acute ST-elevation myocardial infarction

Tom Bouthillet and Jamie Davis discuss the 2010 AHA ECC Guidelines with Monica Kleinman, M.D. and then discuss cardiac arrest and the chain-of-survival

2010-11-30T01:57:00.000Z

Part I - Jamie Davis and Tom Bouthillet discuss the 2010 AHA ECC Guidelines with Monica Kleinman, M.D., incoming Chair of the AHA's ECC Committee.

Part II - Jamie Davis and Tom Bouthillet discuss the 2010 AHA ECC Guidelines with Monica Kleinman, M.D., incoming Chair of the AHA's ECC Committee.

Part III - Jamie Davis and Tom Bouthillet discuss cardiac arrest and the chain-of-survival.

73 year old female CC: Chest pain

2010-11-30T01:52:00.000Z

EMS is called to the residence of a 73 year old female with a chief complaint of chest pain.

On arrival the patient is found sitting on the couch. She appears acutely ill.

Skin is pale and diaphoretic.

Onset: 1 hour ago
Provoke: Nothing makes the pain feel better or worse
Quality: Heaviness or pressure
Radiate: Pain radiates to neck and jaw
Severity: 7/10 and persistent
Time: No previous episodes

Past medical history: HTN, dyslipidemia, breast CA

Medications: Unknown

The patient admits to mild dyspnea but breath sounds are clear.

Vital signs are assessed.

RR: 18
Pulse: 96
BP: 172/72
SpO2: 98 on RA

The cardiac monitor is attached.

A 12-lead ECG is captured.

Displeased with the data quality, paramedics capture another 12-lead ECG.

What do you think is wrong with this patient?

63 year old male CC: Syncope - Conclusion

2010-11-20T15:55:00.000Z

Here is the conlcusion to 63 year old male CC: Syncope.

First, let's take another look at the 12-lead ECG.

This 12-lead ECG shows poor data quality.

This is a problem because the ECG is abnormal and suspicious for acute anterior STEMI.

We need to consider whether or not this could be benign early repolarization or a strain pattern from left ventricular hypertrophy.

This ECG does not meet the voltage criteria for LVH and does not have the general appearance of a "strain pattern" (but it would be nice to be able to take a nuanced look at the ST-segments and T-waves in leads I and aVL).

Could it be benign early repolarization?

Stephen Smith MD from Dr. Smith's ECG Blog has come up with two different decision rules to help distinguish acute anterior STEMI from benign early repolarization.

Here they are in Dr. Smith's own words:

Decision rule #1

If the mean R-wave amplitude from V2-V4 is less than 5 mm, then it is almost certainly MI. If greater than 5 mm, it is probably BER. A cutoff of 5 mm gives a sensitivity for MI of about 70%, but a specificity of greater than 95%.

In this case the first decision rule favors BER.

Decision rule #2

If 2 of the following 3 questions are answered "yes", then it is MI with an accuracy of about 85%: 1) is the QTc > 392 ms? 2) Is the ST elevation at 60 ms after the J-point in lead V4 > 2mm? 3) Is the R-wave in V4 < 13 mm?

In this case the second decision rule favors acute anterior STEMI.

Do you see why this is such a difficult case?

I've said it before and I'll say it again.

Sometimes the "go or no go" decision for the cardiac cath lab comes down to fractions of millimeters!

I really liked the way Tim Phalen explained the importance of serial 12-lead ECGs when we appeared together on the MedicCast at EMS Today 2010. He compared it to taking a single photograph of Old Faithful.

"Maybe it's a geyser. Maybe it's a hole in the ground."

In this case a single 12-lead ECG was captured by the EMS crew. They did, however, obtain another rhythm strip as they were pulling into the hospital.

It appears as though this might show a change from the initial rhythm strip but we're in monitor mode and a diagnostic quality 12-lead ECG should be used to observe changes on serial ECGs.

Let's move on because poor data quality is about to rear its ugly head again. This time inside the hospital.

Here is the 12-lead ECG captured on arrival at the hospital.

Now we have a 12-lead ECG with excellent data quality.

When the medical chart was pulled it was discovered that the patient had a history of "remote inferior wall myocardial infarction".

It was the next ECG that led to the patient becoming a "Code STEMI".

You will note that someone has drawn brackets around the ST-segments in leads II and III.

This problem is, this isn't ST-depression. This is artifact.

The ST-depression is not present in the first cardiac cycle. In addition, the baseline is shifted upwardly prior to the P-wave, marking this as some kind of wandering baseline or loose lead artifact.

Poor data quality continues in the right precordial leads.

From the cath report:

"The initial ECG in the emergency department was of concern because of ST-elevation in the anterior septal leads. This was not clear-cut acute myocardial injury-type ST-elevation. A follow-up ECG revealed the same findings and also non-specific inferior T-wave changes, possibly representing reciprocal changes. These changes were different in comparison with the previous ECG from our office in 2004. Therefore, ER physician's consultation with me, we elected to treat this as a Code STEMI event."

The patient was sent to the cardiac cath lab where angiography revealed no acute lesions.

Serial cardiac biomarkers came back negative.

The patient ruled out for acute myocardial infarction.

Please don't think that I believe I'm perfect. I know that I'm not. All human beings make mistakes and that's why patient safety experts like Peter Pronovost advocate designing systems that help minimize the impact of human error.

The first 12-lead ECG captured in the emergency department might have been reason enough to cath this patient (I am not in possession of the 12-lead ECG from 2004 so it's difficult to speculate).

I also know that emergency physicians are under tremendous pressure not to delay care for acute STEMI patients.

It is impossible to identify acute STEMI with perfect sensitivity and specificity.

Having said that, poor data quality should not enter into the equation.

63 year old male CC: Syncope

2010-11-19T23:13:00.002Z

EMS is called to the home of a 63 year old male who has experienced a syncopal episode.

On arrival the patient is found sitting in a dining room chair that his spouse brought to the foyer. A grocery bag is up-ended with groceries all over the floor.

The patient has vomited but he does not appear to be incontinent of urine.

He appears to be acutely ill.

The patient is awake and oriented to person, place, and time but not event.

Skin is cool, pale, and diaphoretic.

The patient's baseline SpO2 is 96. He is placed on oxygen via NRB mask @ 15 LPM.

He denies chest discomfort, palpitations, or shortness of breath.

Past medical history is significant for hypertension and congestive heart failure.

Medications include aspirin, spironolactone, and carvedilol.

Vital signs are assessed.

RR: 20
HR: 64 R
BP: 102/58

The cardiac monitor is attached.

A 12-lead ECG is captured.

What's next?

60 year old female CC: Dizziness - Discussion

2010-11-15T14:33:00.000Z

Let's talk about this heart rhythm a little bit, and when we do, let's go back to the basics.

Is it regular or irregular?

It's irregular.

Is it regularly irregular or irregularly irregular?

It's irregularly irregular.

Does it have narrow QRS complexes or wide QRS complexes?

It has narrow QRS complexes.

Sight unseen, this heart rhythm has a high probability of being atrial fibrillation. However, wandering atrial pacemaker or multifocal atrial tachycardia is also part of the differential diagnosis.

Is the rate over 100?

Yes.

So is this atrial fibrillation with rapid ventricular response or multifocal atrial tachycardia?

Let's look at the isoelectric line. Does it appear fibrillatory?

No.

We see atrial complexes before the QRS complexes. However, the P-wave morphology is not constant.

When you have 3 or more distinct P-wave morphologies, you are justified in calling a rhythm like this multifocal atrial tachycardia.

Now, I will tell you that on the cardiac unit a rhythm like this is often referred to as either atrial fibrillation or sinus tachycardia with frequent multi-focal PACs, but that is not correct.

Next, let's look at the T-waves, because with a rhythm like this it can sometimes be difficult to differentiate P-waves and T-waves.

To find real T-waves, let's only pay attention to cardiac cycles at the end of clusters of QRS complexes.

This should give you some idea as to the actual amplitude of the T-waves in lead II as well as the QT interval. Once you make a mental note of this, you can go back and decide if the other complexes are T-waves or P-waves superimposed on T-waves.

Now it should be obvious that the cardiac cycle circled in red is showing a P-wave masquerading (isn't that a ridiculous word?) as a T-wave, whereas the cardiac cycle circled in blue shows an actual T-wave unspoiled by a mega P-wave.

Incidentally, these tall, pointy P-waves in lead II suggest significant right atrial enlargement. Remember, enlarged atria are not happy atria. They are predisposed to various arrhythmias like atrial fibrillation, atrial flutter, and multi-focal atrial tachycardia.

Granted, if you look at the 12-lead ECG, a right axis deviation is not present (right atrial enlargement and right ventricular hypertrophy go together) but the patient's history includes "severe heart failure" which means that the patient's entire heart is enlarged, not just the right side.

So what we see is "low voltage" in the limb leads (all QRS complexes < 10 mm), the result of electrical forces on the right and left side canceling each other out.

Especially with the history of COPD, I would call this a pulmonary disease pattern.

So how about the final rhythm strip showing a very fast narrow complex tachycardia?

This is where it's nice to monitor a patient's heart rhythm inside the hospital as opposed to inside the ambulance!

If you see a rapid heart rate inside the hospital you can "go back" in time and examine the onset of the arrhythmia to see whether or not it has a paroxysmal (sudden) onset. That would narrow it down to atrial flutter or some kind of reentrant tachycardia.

On the other hand, if the heart rate histogram shows a gradual increase in heart rate that maxed out at 216 you know it's an automatic focus tachycardia for which adenosine would not be helpful (for example).

This particular arrhythmia turned out to be "self limiting" but even noting the termination of a tachycardia can be helpful in the diagnosis.

Did it stop abruptly (paroxysmal) or did it slow down gradually, revealing flutter waves (again, for example).

Since the patient's chief complaint of dizziness seems to correlate with this rapid heart rate, definitive care for this condition will take place inside the hospital, and possibly the EP lab.

Sometimes the medications used to control rapid heart rates aren't desirable for a patient with severe heart failure. Other times, they're already taking these medications for the heart failure, but they're experiencing rapid heart rates anyway!

I remember one patient with chronic AF who ultimately required RF ablation of the AV node and a pacemaker!

The atria continued to fibrillate but rapid ventricular response was no longer possible due to surgically induced third degree AV block. That was all the way back in 1997! Still pretty cool.

Thanks for the case, Mark!

60 year old female CC: Dizziness

2010-11-14T01:18:00.000Z

Here's an interesting case study from the Right Honorable Mark Glencorse of Tyneside. In addition to being a founding member of EMS 2.0 and the Chronicles of EMS, he also hosts the popular ECG Geek series at 999Medic.com.

Here is the situation (and no, I'm not talking about Mike Sorrentino).

Called to a 60 yr old female patient. She had been suffering with dizzy bouts and collapses for a couple of weeks and had been diagnosed with vertigo.

Has a medical history of MI (with cardiac arrest) in 2009, severe heart failure, COPD with home O2 via NC @ 2 LPM 24hrs per day.

She called 999 as she felt her dizzy bouts were getting worse and the medication that had been given to her for the vertigo was not working.

On arrival she was dyspnoiec (although in her normal state), slightly pallid and feeling dizzy. No chest pain.

Observations :

GCS: 15
Resps : 32, use of accessory muscles
SaO2: 95% on 2 litres/min O2 via nasal cannula (all normal for her)
Pulse: 92, irregular and weak radial pulse
BP: 102/55

Skin was warm to touch and dry.

She complained that her dizzyness was worse today and that sometimes she felt as though she was falling even when she was lying in bed.

Whilst completing my assessment, my partner rechecked her blood pressure and mentioned that her pulse had gone very irregular and she seemed bradycardic.

A rhythm strip was taken.

Chest electrodes were applied and a 12 Lead ECG was captured.

Patient was moved to the ambulance via carry chair and once on the stretcher called out to say that she had gone dizzy again. Leads were immediately attached to the monitor again which showed the following rhythm strip.

What do you think of these ECGs?

47 year old female CC: Chest pain - Discussion

2010-11-08T17:07:00.000Z

Obviously, this is a scary looking ECG because there is significant ST-elevation in the precordial leads.

However, this ECG also meets the voltage criteria for LVH.

Could it be a strain pattern (typical secondary repolarization abnormality)?

No.

It's difficult to tell with the wandering baseline throughout this ECG, but if you line up the point at which the PR-segment hits the QRS complex in leads V1, V2, and V3 you can see that each of these leads shows approximately 4 mm of ST-elevation.

You will recall that with a "strain pattern" the degree of ST-elevation is proportional to the depth of the S-wave in the opposite direction! So the lead with the deepest S-wave should have the most significant ST-T wave abnormality in the opposite direction.

It's not easy to tell the exact depth of the S-wave because the complexes are running together, but these measurements are probably fairly close.

There's no way that a typical strain pattern would show the same amount of ST-elevation in one lead with S-waves that are 22.5 mm deep and another with S-waves that are only 6 mm deep.

Here's the most disturbing finding, in my opinion.

There appears to be reciprocal behavior between the inferior leads and the high lateral leads.

So, if this is a STEMI mimic (for example, benign early repolarization superimposed on top of left ventricular hypertrophy) it's a darned good one!

So what should the hospital do when they are in receipt of a patient like this?

I asked Stephen Smith MD from Dr. Smith's ECG Blog and here's what he said.

"If I were the ED physician, I would aggressively treat the blood pressure with NTG (up to 250 mcg/min or even higher) until the BP came way down. I would do a bedside cardiac ultrasound and look for anterior wall motion. If pain did not go away, and echo did not definitely show good wall motion, I would activate the cath lab."

It's always nice to get Dr. Smith's perspective! I've learned a lot from his blog over the past 2 years. If you're not familiar with his website you should take the time to check it out! His case studies are top notch!

47 year old female CC: Chest pain

2010-11-04T16:37:00.000Z

Here's a case study from a faithful reader who wishes to remain anonymous.

EMS is dispatched to a 47 year old female complaining of chest pain.

On arrival paramedics find the patient seated on the floor. She appears acutely ill. Her skin is cool, pale, and diaphoretic.

The patient confirms that she is experiencing severe, sub-sternal chest discomfort.

Onset: 15 minutes prior to EMS arrival
Provoke: Nothing makes the pain better or worse
Quality: "Very bad" (language barrier)
Radiate: The pain does not radiate
Severity: 8/10
Time: No previous episodes

She is also complaining of palpitations.

First responders initially suspect symptoms of anxiety based on her young age.

The patient's son relates that the patient is a diabetic and hands paramedics a bottle of lisinopril and glipizide.

Paramedics ask the patient if she has a history of heart problems. She says "yes" but can not give specifics other than "blood pressure."

Due to the patient's poor appearance the EMS crew immediately loads her for transport.

In the back of the ambulance vital signs are assessed.

RR: 18
HR: 80
NIBP: 240/120 (confirmed with manual BP)
SpO2: 97 with NRB @ 15 LPM

Breath sounds are clear bilaterally.

The cardiac monitor is attached and a 12-lead ECG is captured.

What is your impression and what should the EMS crew do next?

37 year old male CC: Unconscious - Discussion

2010-10-27T02:37:00.000+01:00

Here is the follow-up to: 37 year old male CC: Unconscious.

This is the 12-lead ECG that was presented.

There are a few difficulties involved with this case.

First, we have the syncopal episode with possible seizure-like activity and slurred speech.

Second, we have an abormal ECG.

Third, there is a recent history of chelation therapy which may or may not be playing a role in what's happening.

For any patient who experiences a syncopal episode the ECG should be reviewed for high-risk features like cardiac arrhythmias, a prolonged QT-interval, Brugada's syndrome, a Wolf-Parkinson-White pattern, or hypertrophic cardiomyopathy.

Unfortunately, this is an endurance athlete, and it's notoriously difficult (if not impossible) to distinguish between an "athlete's heart" and hypertrophic cardiomyopathy without the aid of an echocardiogram to examine the exact dimensions and shape of the left ventricle.

To me, this ECG clearly shows left ventricular hypertrophy complete with a "strain pattern" (or secondary ST-T wave abnormality).

Remember, left ventricular hypertrophy is considered a "STEMI mimic" and an acute anterior STEMI mimic in particular.

If you're screening the ECG for STEMI and you don't have ST-elevation in the anterior leads, there's no need to measure for the voltage criteria.

Of course, if you've been reading my blog for a while, there's very little reason to measure the voltage criteria if you can identify a "strain pattern".

Consider the following graphics.

ST-elevation is present and the degree of ST-elevation appears to be proportional to the depth of the S-wave. Note that the S-wave is "cropped" in lead V3 by the bottom of the ECG graph paper.

It's worth mentioning that Stephen Smith, MD from Dr. Smith's ECG Blog has stated:

"[I]t is very difficult to find a case of anterior MI with extreme voltage like this; this is probably because profound ischemia of LAD occlusion (STEMI) alters the QRS voltage and attenuates the severity of the electrocardiographic LVH voltage."

It is so rare in fact that he has asked that anyone who has seen an acute anterior STEMI with deep S-waves suggestive of LVH to please contact him! Keep in mind, he wrote the book The ECG in Acute MI.

So, when ST-elevation in the anterior leads is associated with deep S-waves suggestive of LVH, slow down. Take a closer look. You're probably dealing with a STEM mimic!

Now let's look at the lateral leads.

Here again we see "T-wave discordance". In other words, the T-waves are deflected opposite the main deflection of the QRS complex (which is what we're looking for to identify a "strain pattern" with LVH). In addition, the degree of the ST-T wave abnormality is proportional to the size of the QRS complex, but in the opposite direction.

This can sometimes be difficult to appreciate on the prehospital 12-lead ECG because the QRS complexes run together. So take your time and try to identify the true amplitude in each lead.

Finally, take a look at the transition of the T-wave in the precordial leads. By the "transition" I mean the manner in which the T-wave transitions from positively deflected in lead V1 to negatively deflected in lead V6.

As the QRS complex transitions from negative to positive, the T-wave transitions from positive to negative! This is what is meant by "widened QRS/T angle".

If you look at the QRS and T axis at the top of the ECG the QRS axis is 43 and the T axis is 144 which makes the QRS/T angle 101. That's abnormal and suggests T-wave discordance.

So it's clear we're dealing with left ventricular hypertrophy and a strain pattern. Is it "normal" for an endurance athlete? Quite possibly, but it's not our place to make that determination in the field, particularly with the immediate history of syncope.

The best thing the EMS crew did for this patient was take him to the hospital.

If the syncope wasn't reason enough (and in my opinion it most certainly was) the patient had a recent history of chelation therapy. I don't know if the chelation therapy was oral or IV but it doesn't matter. It can contribute to loss of electrolytes and nutrients.

Finally, the slurred speech and loss of clear eye contact. That's what upset the patient's spouse the most, and sometimes we need to stop and listen to the people who know the patient the best. Occasionally this means listening to a mother about about her baby. In this case it means listening to a wife about her husband.

So what was the outcome?

The patient ended up receiving a CT scan of the head at the receiving hospital. A slow venous bleed was discovered. He was transferred to a tertiary care center for more advanced care.

To the best of my knowledge this was the patient's normal ECG.

See also:

Left ventricular hypertrophy - Part I

Left ventricular hypertrophy - Part II

41 year old male CC: Chest pain

41 year old male CC: Chest pain - Answer

37 year old male CC: Unconscious

2010-10-24T16:25:00.000+01:00

EMS is called to evaluate an unconscious 37 year old male.

En route to the scene dispatch advises paramedics that the patient is now conscious and may have experienced a syncopal episode and seizure-like activity. The spouse believes that the patient may be having a stroke.

On arrival the patient is found lying in bed. He is alert and oriented to person, place and time, but not event.

He appears to be in excellent shape.

The spouse informs the EMS crew that the patient is an endurance athlete who has recently undergone chelation therapy to "clean out his system." It's clear this has been controversial topic their relationship. The spouse is not pleased about it.

She is clearly shaken by what has happened and is particularly concerned that the patient slurred his speech immediately after re-gaining consciousness.

The patient states that he was "worked up for chest pain" about 3 months ago and all tests came back negative. Otherwise he states that he has been healthy. He takes no meds.

Vital signs are assessed.

RR: 18
HR: 80 R
BP: 140/90
SpO2: 98 on RA

Breath sounds are clear bilaterally.

BGL: 108

The cardiac monitor is attached.

A 12-lead ECG is captured.

The paramedics sit the patient up to check orthostatics. The patient's eye contact becomes less focused and his speech becomes slurred. He seems weak.

What are your concerns?

60 y/o male, c/o dizziness, nausea & vomiting

2010-10-10T22:57:00.000+01:00

PMH: Of similar episodes under investigation by cardiologist, no other relevant medical information.

No observations provided on this p/t, this is just an exercise in 12-lead ECG interpretation…

Here’s a little help from me, please provide your ECG analysis.

Rate:

Atrial: Unable to determine.

Ventricular: 90-160 bpm.

Waves: P waves present: Difficult to identify, best seen in V2-3, appearance is fibrillation pattern, P waves NOT consistent, no relation to QRS, no Q waves present that are pathological, T waves are present with no significant abnormalities.

Intervals: P-R consistent, QRS: 0.16 secs, appearance: rSR’ in V1-2, consistent; QT interval 0.40 secs.

Axis: Quadrant:??? Please give your analysis…J Degrees -80 (aVF and Lead II mostly isoelectic slightly positive.

Hypertrophy: No atrial or ventricular detected.

Other info: Q waves none significant for AMI, no significant elevation, ST depression in V2, no possible drug effects noted.

69 y/o male, 12-Lead ECG, done under routine medical examination

2010-10-10T21:33:00.001+01:00

PMH: Angina, Gastric ulcer, no other relevant info, no information on p/t’s medications… This is just an exercise in 12-lead ECG interpretation…

Here’s a little help from me, please provide your ECG analysis & interpretation.

Rate:
Atrial: Unable to determine, irregular

Ventricular: 75-150, irregular.

Waves: Difficult to identify P waves, but can be identified in aVF, other appearance is fibrillation pattern, not consistent… Relation to QRS – None… Q waves NOT present… T waves present “Morpholology – Fused with QRS.

Intervals: P-R consistent, QRS: 0.16 secs, appearance: consistent, wide, positive RS in V6, negative QS in V1… QT interval: 0.40.

Axis: Quadrant: LAD… Degrees -40 (aVF and Lead II mostly isoelectic slightly negative.

Hypertrophy: No atrial or ventricular detected.

Other info: Q waves none significant for AMI… I see some ST displacement: ST elevation II, III, aVF, V1-5… ST depression 1, aVL, V6, no possible drug effects noted.

78 year old male CC: Chest pain - Discussion

2010-10-06T20:30:00.000+01:00

I posted this case for a few reasons, but not because it was difficult. So if you were looking for a zebra, I'm sorry to disappoint you!

I have noticed on many occasions that a paramedic's inability to recognize a paced rhythm can lead to incorrect interpretations of the 12-lead ECG. That's why it's important to look (and feel) for a pacemaker can when you do your physical exam!

You do perform a physical exam, right? (Say yes.)

When you completely undress your patient from the waist up, it helps with proper lead placement, reveals surgical scars and implantable medical devices, and allows you to assess breath sounds more accurately. It's just a good habit to get in to.

For this case there are a couple of big tip-offs that we're dealing with a paced rhythm.

It's a supraventricular rhythm with a wide QRS complex, left axis deviation, and LBBB morphology in lead V1. This is the most common morphology for paced rhythm and suggests that the pacing lead is in the apex of the right ventricle.

You will also note negative concordance of the QRS complexes across the precordial leads which is suggestive of a ventricular rhythm. Negative concordance of the QRS complex is not always present but it's a common feature of ventricular paced rhythms.

In addition, pacer spikes (or blips or "nubbins" since Christopher is making up his own words) are visible in a few leads, most notable of which is lead V4. This makes sense when you think about it because lead V4 is in close proximity to the apex of the right ventricle.

This case is also a nice example of appropriate T-wave discordance. Since all of the precordial leads show negative QRS complexes, let's arrange them smallest to largest and see if we notice anything.

See how the T-wave gets larger and larger as the S-wave gets deeper and deeper? The more times you look at this in a "normal" paced rhythm or left bundle branch block ECG, the easier it will be for you to identify when something looks "wrong".

I have no idea what was causing this man's chest pain but I feel confident it wasn't an acute STEMI.

Speaking of acute STEMI, I was recently made aware of another case where a computer algorithm incorrectly identified a WPW Type B pattern.

This was sent to me by Dr. Jody Griswold.

This is an interesting case in its own right and Dr. Griswold wrote a very informative paper about it which you can download here (with Dr. Griswold's permission):

WPW_Type_B_versus_STEMI (This is a Word .doc).

Just to show that the GE-Marquette 12SL interpretive algorithm gets it right sometimes, check out:

Wolf-Parkinson-White (WPW) - STEMI Mimic.

78 year old male CC: Chest pain

2010-10-04T00:29:00.000+01:00

EMS is called to the residence of a 78 year old male.

It's the middle of the night. The patient's spouse meets you at the front door and brings you back to the bedroom.

The patient is sitting on the edge of his bed. He is highly anxious and complaining of chest discomfort and palpitations.

Onset: During sleep
Provoke: Running made the sensation feel better earlier the previous day
Quality: An "electric" sort of "full" feeling in his chest
Radiate: The sensation does not radiate
Severity: 5/10
Time: Started earlier the previous day but went away after running

The patient takes several deep breaths during EMS evaluation and seems upset that it doesn't correct the problem.

Skin is pink, warm, and moist.

Breath sounds are clear bilaterally.

Vital signs are assessed.

RR: 20 and shallow
HR: 100
BP: 160/98
SpO2: 98 on RA

The cardiac monitor is attached.

A 12-lead ECG is captured.

And another.

What's going on here?

Could this be WPW?

Why or why not?

76 year old female CC: Chest pain - Conclusion (Tako-Tsubo Cardiomyopathy)

2010-09-17T22:01:00.000+01:00

Here is the conclusion to the most recent case: 76 year old female CC: Chest pain.

To see Part I click HERE. To see Part II click HERE.

The patient was transported to the emergency department where she was treated for a possible acute coronary syndrome.

Serial 12-lead ECGs and cardiac biomarkers were performed.

This 12-lead ECG was captured at 1407.

This is fairly similar to the prehospital 12-lead ECGs.

The next 12-lead ECG is from 1722.

This ECG is significantly different from the prehospital 12-lead ECGs.

You will note that the hyperacute T-waves are gone, as are the ST-elevation and reciprocal changes.

Let's look at the cardiac biomarkers.

1407

CPK.............................38
CKMB........................2.56
Troponin..................< 0.01

1730

CPK............................72
CKMB.....................12.30(H)
Troponin..................0.562(H)

The patient was admitted to the hospital.

Echocardiogram showed a large anteroseptal wall motion abnormality.

0610 (the following morning)

CPK............................48
CKMB.......................7.46(H)
Troponin..................0.211(H)

It should be noted that with changes on serially obtained ECGs and a rise and fall of cardiac biomarkers, the WHO criteria for the diagnosis of acute myocardial infarction has been met.

The patient was sent to the cardiac cath lab for PTCA and stents if needed.

Results:

Insignificant epicardial coronary artery narrowing in a right dominant system.
Congenitally absent left main (normal variant).
Severely reduced left ventricular systolic function, left ventricular ejection fraction 35% with a large anterolateral and apical area of akinesis. The apex is aneurysmal.
Likely apical ballooning syndrome versus spasm in the left anterior descending coronary as a cause of the apical wall motion abnormality.

So, what is "Apical Ballooning Syndrome"?

It is also called "Tako-Tsubo Cardiomyopathy," "Stress Cardiomyopathy," or "Broken Heart Syndrome."

"Tako" is the Japanese word for octopus and "Tsubo" is the Japanese word used for pot or trap. The Japanese physician who first described this condition noted that the end-systolic ventriculogram took on the shape of an "octopus pot" and hence the name "Tako-Tsubo" or "Takotsubo".

Here's an image that shows a side-by-side of the patient's ventriculogram (end-diastole on the left and end-systole on the right).

This is a fairly obscure but well documented STEMI mimic (although one article I found from Mayo Clinic Proceedings suggests that spontaneous aborted MI is a more likely scenario).

If you would like to learn more about Tako-Tsubo Cardiomyopathy you can see the Wikipedia article HERE. The eMedicine article is HERE. The Medscape article is HERE.

From the Medscape article:

"Patients often present with chest pain, have ST-segment elevation on electrocardiogram, and elevated cardiac enzyme levels consistent with a myocardial infarction.1 However, when the patient undergoes cardiac angiography, left ventricular apical ballooning is present and there is no significant coronary artery stenosis."

"One of the more unique features of TCM is the association with a preceding emotionally or physically stressful trigger event, occurring in approximately two thirds of patients."

"Recently, TCM has been reported after near drowning episodes."

How about that, Dr. House?

See also:

76 year old female CC: Chest pain

76 year old female CC: Chest pain - The case for this being an acute anterior STEMI

76 year old female CC: Chest pain - The case for this being an acute anterior STEMI

2010-09-15T22:11:00.000+01:00

I find this case to be extremely interesting for a variety of reasons. (Click HERE to see the original post).

As many of you pointed out, the history and clinical presentation isn't exactly screaming "Acute Coronary Syndrome!"

But then, as others have pointed out, the elderly often have atypical or vague symptoms.

Let's look at the 12-lead ECG itself (I will post the serial ECGs to the original case study so you can see those, too).

First question, does it meet the ACC/AHA STEMI criteria (imperfect though it may be). I have to admit, when I first reviewed this case I didn't see it, but the answer is, "Yes."

Hyperacute T-wave are visible in several leads, the most noticeable of which are leads V4 and V5.

Here's an important teaching point, courtesy of Dr. Smith from Dr. Smith's ECG Blog in reference to this case.

"The T-wave is the best indicator of viable myocardium at risk."

Is ST-elevation also present?

Some of you have been taught that 2 mm of ST-elevation is required in two contiguous precordial leads. That is only the case for leads V2 and V3. This is probably due to the fact that leads V2 and V3 often have deep S-waves.

In this case, lead V4 has about 2 mm of ST-elevation and lead V5 has 1 mm of ST-elevation.

Couldn't this be benign early repolarization? In theory, yes, although BER is not particularly common in elderly female patients.

There's also another way to tell. Look at the R-wave progression in leads V1-V4. It's non-existent, which points away from benign early repolarization.

Do any other leads show ST-elevation?

As some of you mentioned in the comments, ST-elevation is present in the high lateral leads I and aVL. However, it's less than 1 mm. So it's not significant. Right?

Wrong.

It's significant due to the low amplitude of the QRS complex! You have to consider proportionality.

To illustrate this point consider the following graphics that "stretch" leads I and aVL vertically while preserving the ST/QRS ratio.

This is the same image side-by-side but the image on the right has been "stretched" vertically. It's a single cardiac cycle in lead I. It looks much worse when it's stretched, doesn't it? But the ST/QRS ratio is exactly the same!

Here's another example of lead I.

Here's lead aVL, normal on the top and "stretched" vertically on the bottom.

If only there were reciprocal changes to firm up the diagnosis!

You will notice a flattening of the ST-segment in leads III and aVF that by itself would not seem particularly significant in a 76 year old female with a history of emphysema. However, it's all about context! Over and over again I have preached Tomas Garcia, MD's admonition to "consider the company" that any ECG abnormality keeps.

A flattening of the ST-segments in the inferior leads when the anterior and high lateral leads are suspicious for acute STEMI should be considered reciprocal changes.

Now what do you think? Are you sold or do you still have doubts?

76 year old female CC: Chest pain

2010-09-14T17:39:00.000+01:00

EMS is called to the beach for a 76 year old female complaining of shortness of breath. Past medical history of emphysema.

On arrival, the patient is found sitting in a beach chair alert and oriented to person, place, time, and event. She does not appear to be in any acute distress.

The patient states that she was out wake-boarding when she fell and "got a mouth full of water." She coughed profusely and then experienced some chest discomfort.

She denies having experienced any shortness of breath.

She denies any other significant medical history other than a little bit of emphysema and states that she takes an inhaler but rarely uses it.

The patient is embarrassed but consents to further evaluation in the back of the ambulance. It takes some convincing for the patient to allow EMS personnel to carry her off of the beach (she wants to walk the 100 yards to the ambulance).

In the back of the ambulance, vital signs are assessed.

RR: 18
HR: 80
BP: 132/74
SpO2: 94 on RA

The cardiac monitor is attached.

A 12-lead ECG is captured.

The patient states she feels better and wants to know if it's really necessary for her to go to the hospital.

Should they transport her to the hospital?

79 year old female CC: Unresponsive

2010-08-20T03:25:00.000+01:00

Here's a very interesting and unusual case submitted by a long-time reader of the Prehospital 12-Lead ECG blog named Christopher Linke (aka SoCalMedic).

I'll warn you up front that the patient insisted on being transported to a hospital without specialty services so we have no information about diagnostic testing that might confirm the diagnosis.

EMS is called to the scene of an "unresponsive" patient.

Upon arrival, paramedics find a 79 year old female with no complaints. The patient's family states that the patient's eyes rolled back into her head and she became unresponsive.

More disturbingly, the family states that she was not breathing and did not have a pulse prior to EMS arrival. CPR was performed.

At the time of EMS evaluation the patient is oriented to person and place but not time or event.

Vital signs:

Resp: 26
Pulse: 112
BP: 125/77
SpO2: 84 RA

Patient is resting in her right side.

Skin is pink, moist, and hot to the touch with no cyanosis.

No accessory muscle usage. No JVD, tracheal deviation or pitting edema.

The family states that the patient was diagnosed with ventricular tachycardia within the past week for which she takes amiodarone.

No known drug allergies.

Patient was placed on the cardiac monitor (this rhythm strip was captured later in the call).

A 12-lead ECG was captured.

Serial ECGs were performed en route to the hospital.

Do you see anything unusual that is cause for concern?

40 y/o Female C/C Chest Pain

2010-08-12T03:50:00.000+01:00

Submission thanks to Tim Waters, CCEMTP of Lee County Medstar

40 yo female, thin build with no history/meds/allergies. + smoker. Works as painter outside and was painting when developed pain in her upper chest/left arm which is the same she uses to paint. Also adds that she has been moving and lifting numerous heavy objects over the past week and since then has been having these episodes of shoulder discomfort. Pain is non-radiating with moderate reproducibility with movement and inspiration. I forget what severity scale she gave it but was definitely uncomfortable. Onset was about 3 ½ hours prior to presentation while painting with her trying to work through the pain until it became to unbearable.. Denies nausea, is diaphoretic but has been working outside.

58 year old male CC: Chest discomfort

2010-08-10T13:57:00.002+01:00

Here's another case from a faithful reader who wishes to remain anonymous.

No, these are not all from the same anonymous reader! :)

EMS responds to a 58 year old male complaining of chest discomfort.

Onset: 30 min ago while mopping hot tar on roof
Provoke: Nothing makes the pain better or worse
Quality: Dull pressure
Radiate: The discomfort does not radiate
Severity: 4/10
Time: Persistent with no previous episodes

The patient is found supine on the ground appearing acutely ill and diaphoretic.

The patient was moved to air conditioned room, skin dried.

Pt denies SOB, allergies, meds, history.

GCS: 15

Vital signs:

Pulse: 66
BP: 116/78
RR: 16
SpO2: 99 on RA

BGL: 92

Breath sounds: clear bilaterally

12-lead ECG was captured.

Crew initiates CP protocol to include O2, ASA, NTG.

The patient declines intravenous access.

Vital signs remained unchanged.

The patient stated that he felt better and did not want to be transported to the emergency department.

The EMS crew was concerned about the patient's decision and spent the next 40 minutes persuading the patient to be seen at the hospital.

Finally the patient agreed.

The patient was loaded for transport, the monitor was re-attached, and en route other 12 lead ECG was captured.

Are you noticing a trend here?

Got a case you'd like to see featured on the Prehospital 12-Lead ECG blog?

Email me at ems12lead@gmail.com.

54 year old male CC: Chest pain - Discussion

2010-08-06T21:44:00.000+01:00

Once again we see the importance of serial ECGs in the treatment of a suspected ACS patient. The difference between the first and second 12-lead ECG is the key to solving this case.

As you can see, the T-waves become more pronounced in leads V2-V5 (blue) and the ST-depression becomes more obvious in leads III and aVF (red).

When you consider any ECG abnormality you should "consider the company it keeps".

Without the benefit of the first ECG that provides the baseline, you might be forgiven for thinking the T-waves in the second ECG represent benign early repolarization.

However, with changes on serially obtained ECGs that correspond to new symptoms, the T-wave changes strongly suggest acute developing anterior STEMI.

The reciprocal changes in the inferior leads remove all doubt.

See also:

To see previous cases involving serial ECGs CLICK HERE.

54 year old male CC: Chest pain - Discussion

2010-08-06T21:40:00.000+01:00

Once again we see the importance of serial ECGs in the treatment of a suspected ACS patient. The difference between the first and second 12-lead ECG is the key to solving this case.

As you can see, the T-waves become more pronounced in leads V2-V5 (blue) and the ST-depression becomes more obvious in leads III and aVF (red).

When you consider any ECG abnormality you should "consider the company it keeps".

Without the benefit of the first ECG that provides the baseline, you might be forgiven for thinking the T-waves in the second ECG represent benign early repolarization.

However, with changes on serially obtained ECGs that correspond to new symptoms, the T-wave changes strongly suggest acute developing anterior STEMI.

The reciprocal changes in the inferior leads remove all doubt.

54 year old male CC: Chest pain

2010-08-04T18:14:00.002+01:00

Here's an interesting case submitted by Terry Weatherford, NREMT-P.

EMS responds to a report of a 54 year old male complaining of chest discomfort.

O—Sudden onset
P—Nothing made the pain better or worse
Q—Stabbing
R—Radiated to left shoulder
S—9/10
T—Less than 30 minutes

Vital signs:

B/P 110/78
HR—70
Resp—20/min.
Pulse ox 100% with O2.

S—Nausea no vomiting
A—Morphine
M—NTG, Lisinopril, Insulin
P—MI with stents placed, diabetes and HTN
L—Breakfast 1 hr ago
E—Taking a shower

The patient informs paramedics that his pain resolved prior to EMS arrival. He states that he does not want to go to the hospital because he knows they will keep him for 4 to 5 hours and it will turn out to be nothing.

A 12-lead ECG is captured.

The paramedics tell the patient that with his past medical history he should go to the hospital by ambulance for an evaluation. He adamantly refused treatment even with 3 paramedics explaining the possible consequences of refusing care.

Suddenly, the patient's chest pain returns. He appears diaphoretic.

A second 12-lead ECG is captured.

What is your impression?

58 year old female CC: Chest pain - Conclusion

2010-07-29T15:29:00.002+01:00

ere's the conclusion to the 58 year old female with chest pain and left bundle branch block.

To refresh your memory here is the 12-lead ECG.

And for those of you who requested lead V4R.

This ECG meets all 3 of Sgarbossa's criteria to identify acute STEMI in the presence of left bundle branch block.

Keep in mind, it only has to meet one criterion in one lead!

(Please note: One criterion has been modified from its original form. Instead of discordant ST-elevation > 5 mm we are looking for discordant ST-elevation > 0.2 the depth of the S-wave. Credit to Dr. Smith of Dr. Smith's ECG Blog.)

Angiography revealed 100% occlusion of the LCX and 99% occlusion of the RCA.

Thanks to everyone who commented on the case!

See also:

AMI in the presence of LBBB - Sgarbossa's Criteria Part I

AMI in the presence of LBBB - Sgarbossa's Criteria Part II

Sgarbossa's criteria - new graphic

"New" LBBB - What's the big deal?

Discordant ST-Segment Elevation in LBBB or Paced Rhythm

58 year old female CC: Chest pain

2010-07-26T02:21:00.002+01:00

Here's another case study from an international reader who wishes to remain anonymous.

Presenting Complaint - Chest Pain

History of Present Complaint - 58 year old female, nil cardiac history, mild smoker, social drinker and overweight.

Complaining of acute central chest pain @ rest. Awoken by pain.

On Arrival - Sat upright on settee (Editor's note: One of you Brits will have to interpret that for me!)

On examination:

Alert, orientated and communicable (GCS 15)
Pale, cool dry skin.

Nil SOB, clear bi-lateral air entry - nil adventitious breath sounds
R/R 19, SpO2 99%

H/R 68 and irregular, BP 125/74

Temp 36.8
B.M 7.2 (Editor's note: B.M. is BGL measured in millimoles. 1 mmol/L of glucose is equivalent to 18 mg/dL. Hence, this patient's sugar is about 130).

C/O chest pain.

O - Acute. Awoken from sleep.
P - Nothing makes pain better. Not affected by breathing
Q - Non specific compressing type pain
R - Central chest pain radiating left arm
S - Pain score 6/10
T - 30 mins
I - No pain intervention sought.

Slight nausea, nil vomit

The cardiac monitor is attached.

A 12-lead ECG is captured.

Once again, I am impressed at the power of Web 2.0.!

Getting case studies like this from thousands of miles away is a real privilege and it makes me very happy to be able to share them with my colleagues from around the world!

This ECG meets all 3 of a certain criteria.

What criteria are we talking about and how would you treat this patient?

While you're at it, please CLICK HERE if you missed my previous post and cast your vote!

69 year old male CC: "Indigestion"

2010-07-23T16:35:00.000+01:00

Here's a case from a faithful reader who wishes to remain anonymous.

In his own words:

Presenting Complaint - Chest Pain

History of Present Complaint - 69 year old male, nil cardiac history, none smoker, social drinker.
Complaining of indigestion last 2-3 weeks with noticably increase in belching.
This a.m acute onset of burning heavy central chest pain radiating to neck.

On Arrival - Semi-recumbent in bed

On examination:
Alert, orientated and communicable (GCS 15)
Pallor
Diaphoretic

Nil SOB, clear bi-lateral air entry - nil adventitious breath sounds
R/R 16, SpO2 98%

H/R 90 and irregular, Hypertensive 168/110

Temp 36.5 C (97.7 F)
B.M 9.0

C/O chest pain..
O - Acute
P - Nothing makes pain better. Not affected by breathing
Q - Heavy in chest, burning in throat
R - Retrosternal and radiating to neck
S - Pain score 10/10
T - 15 mins
I - No pain intervention sought.

Nil nausea, nil vomit

The cardiac monitor is attached.

A 12-lead ECG is captured.

The patient loses consciousness and the monitor shows ventricular fibrillation. A shock is delivered at 200J.

The patient experiences return of spontaneous circulation.

A few minutes later the heart rhythm returns to baseline.

What is this patient's problem?

Chronicles of EMS - Here Are the Finalists! VOTE NOW!

2010-07-23T15:02:00.002+01:00

As you may have heard, the finalists are in for the Chronicles of EMS "Change the Name" competition! The field has now been narrowed from over 500 entries to just 5!

It just so happens that my girlfriend Kelly is one of the finalists.

Now, I don't want to influence your decision in any way....

So please CLICK HERE to cast your vote NOW!

Select one of the following:

Beyond the Lights and Sirens

Mobile Medicine

Frontline Medicine

Medicine in the Streets

Real Life, Real Emergencies

Again, just choose from your heart.

Don't be influenced by the fact that this could lead to a trip to Europe for Kelly and me! :)

See also:

Chronicles of EMS - "Change the Name" Competition!

A 58 year old women presents with episodes of "greying out" with exertion

2010-06-14T14:33:00.006+01:00

Here's great case submitted by Dr John M

A 58 year old women presents with episodes of "greying out" with exertion. She has had a slightly higher than usual heart rate for a few days, but of late, any exertion brings on near syncopal episodes.

Past history includes long-standing atrial fibrillation. In the past two years, she has had two left atrial ablations. The first ablation included pulmonary vein isolation alone, but the second one, done 3 months prior included repeat pulmonary vein isolation, plus left a left atrial roof line, mitral isthmus line and multiple ablations of complex-fractionated electrograms.

Exam: She is an obese female, with a BMI of 38, BP 98/58, HR- 170, RR-24.
She appears anxious and slightly diaphoretic.
Neck veins not distended
Lungs are clear
Heart exam reveals tachycardia
No peripheral edema

The first ECG is here...

The nurse calls to tell me she has converted to Sinus Rhythm. After looking at this second ECG, do you concur?

After a brief procedure later in the day, this ECG is recorded.

12-Lead Differential Diagnosis: Syncope

2010-06-12T01:43:00.001+01:00

12-Lead Differential Diagnosis: Syncope

By Adam Thompson, EMT-P

There are many causes of syncope. Syncope is the medical term for fainting. Most of us are pretty familiar with the common vasovagal cause. Fortunately syncope is often self-correcting; the patient hypo-perfuses, they blackout and fall, their body perfuses better, they wake up. This post will be dedicated to 12-lead presentations that may indicate causes of syncope.

I have decided to use some exerts from my favorite emergency physician/presenter, Dr. Amal Mattu. Dr. Mattu has spoke and written on these topics multiple times.

Bradycardia

This first one is easy, and you wouldn't even need a 12-lead to determine it's malignancy.

What do you notice about the 12-lead above? How about the rate? This is an example of bradycardia. Bradycardia may cause hypo-perfusion, leading to syncope. This would classify them as symptomatic, and they may require treatment.

*It is important to remember that there are many tachycardic arrhythmias that could cause syncope as well.

Acute Myocardial Infarction

An acute myocardial infarction (AMI) is the most common reason we use a 12-lead for diagnostic purposes. An AMI may cause syncope amongst many other signs and symptoms. Syncope would be an atypical (not usual) presentation for an AMI. I am not going to elaborate much on this presentation because it requires much teaching for those who are unfamiliar with STEMIs (ST-Elevated Myocardial Infarction). Please head over to the prehospital 12-lead blog for some great education on STEMIs.

Long QT Syndrome

Long QT Syndrome, or LQTS may lead to arrhythmias that lead to syncope. This happens due to something called an R on T phenomenon. The most common arrhythmia due to LQTS is Torsades de Pointes, however monomorphic ventricular tachycardia is possible. Syncope and/or seizures are common symptoms of the rhythms associated with LQTS.

Torsades de Pointes

From Dr. Amal Mattu:

Prolonged QT-Interval

• Prolonged QT-interval predisposes to torsades de pointes
• One of the key “can’t miss” diagnoses associated with syncope
• Perhaps a more common cause of syncope and sudden death than previously recognized?

Causes of QT-prolongation
• Electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia)
• Sodium channel blocking medications (many!)
• Includes Type IA medications, anticholinergics, cocaine, many antipsychotics, some antibiotics
• Acute myocardial ischemia (usually associated with inverted T-waves)
• CNS lesions, e.g. intracerebral hemorrhage (often associated with giant inverted T-waves)
• Hypothermia
• Congenital

How long is too long?
• QT-interval will vary based on patient’s heart rate
• Measure QT from beginning of the QRS complex to the end of the T-wave, and average over 3-5 beats
• “Corrected” QT-interval (Bazett formula): QTc = QT/√(RR)
• QTc is considered prolonged when > 450 msec in men and > 460 msec in women and children
• Major risk occurs in patients with QTc > 500 msec

Treatment
• Search for and correct underlying cause (e.g. correct electrolyte abnormalities, discontinue responsible medications, etc.)
• Congenital or idiopathic causes: beta-blocking medications attenuate adrenergic-mediated trigger mechanisms
• Treatment of torsades de pointes: cardioversion/defibrillation, magnesium if relatively stable (e.g. intermittent torsades): 2 grams IV over 2-3 minutes followed by infusion
• Overdrive pacing? Isoproterenol? Atropine? These are listed as possible treatments in acquired (not for congenital) cases, but rarely needed
• Post-conversion treatment with magnesium, not lidocaine/amiodarone/ procainamide! (unlike other forms of ventricular tachycardia); for congenital cases, add beta-blocking medications

Click here or here to learn about Long QT Syndrome

Brugada Syndrome

ECG example of Brugada Syndrome

Brugada syndrome is becoming more and more well known recently. It is associated with specific ECG changes and an increased risk for sudden cardiac arrest. Only known cause of Sudden Unexpected Death Syndrome (SUDS)--according to Wikipedia. The ECG changes associated with Brugada Syndrome are most visible in V1, and V2. Non-STEMI-like ST-elevation that cannot be explained by another pathological cause (ie. LVH, LBBB, BER) may be Brugada Syndrome. These individuals may be otherwise very healthy and/or young.

Some features of the different types of Brugada Syndrome include:

a RBBB pattern in V1 without terminal S-waves in lead I and V6.
A saddleback ST-elevation pattern (type 2 below)
Coved J-point elevation in V1, V2, V3 that gradually slopes down (type 1 below)

From Dr. Amal Mattu:

Brugada Syndrome

More common cause of sudden death than previously recognized
• May be responsible for up to 20% of sudden deaths in individuals without structural heart disease
• Responsible for 4-5% of all sudden deaths
• Incidence varies in different populations (some genetic factors involved)
• Most common in young males (< 50 yo.)
• First onset of symptoms approximately 40 yo.
• Mortality approximately 10% per year if not treated with an internal cardioverter-defibrillator (ICD), regardless of whether or not antiarrhythmics are used

Syndrome characterized by
• ECG abnormalities in leads V1 – V3
• Polymorphic or monomorphic (less common) ventricular tachycardia
• Causes syncope if self-terminating
• Causes sudden death if persists and not terminated by treatment
• Structurally normal heart
• Familial occurrence in approximately half of patients

ECG findings in leads V1 – V3
• Right bundle branch block (RBBB) or incomplete RBBB pattern
• ST-segment elevation — 2 types
• “coved-type” (most common)
• “saddle-type”
• ECG findings can vary with time depending on the autonomic balance, administration of antiarrhythmic and other drugs affecting channel function, body temperature, and other unknown factors

Definitive diagnosis can be made with electrophysiologic testing
• Challenge with an intravenous class I medication (e.g. ajmaline, procainamide, flecainide)
• Will induce increased ST-segment elevation and “coving”
• Programmed electrical stimulation of the heart
• Can induce ventricular tachycardia

Treatment
• Placement of an ICD is the only effective treatment
• Antiarrhythmic drugs (including beta blockers, amiodarone, etc.) ineffective

Click here or here for more on Brugada Syndrome

Hypertrophic Cardiomyopathy

From Dr. Amal Mattu:

Hypertrophic Cardiomyopathy (AKA IHSS, ASH, HOCM, etc.)

• Prevalence — 0.02% – 0.2% of the general population
• Genetic factors involved
• Hypertrophied but nondilated left ventricle
• Thickening is usually asymetric, involving the septum to a greater extent than the free ventricular wall
• Cardiomegaly usually not present on chest x-ray
• Mortality 3.5% per year
• Diagnosis often made only when the patient experiences sudden death
• Usually occurs during exertion \
• Average age at diagnosis is 30 – 40 yo.
• Patients may also experience syncope, angina, palpitations, dyspnea (often associated with exertion)

ECG findings
• Normal in 7% – 15%
• Typical abnormalities
• Deep narrow Q-waves in the inferior and/or lateral leads – I, aVL, V5-6 (simulates MI, but Q-waves are “too narrow” for MI)
• Very specific for this condition
• Q-waves in lateral leads are more common than inferior leads, very commonly misdiagnosed as lateral MI
• Left atrial enlargement
• High left ventricular voltage/left ventricular hypertrophy
• Other less common abnormalities
• Tall R-wave in lead V1 (simulates posterior MI)
• Deep narrow Q-waves in the inferior leads (simulates inferior MI)
• Don’t rely on your cardiologists to make the Dx on ECG! Clinical diagnosis
• Systolic murmur at apex or LLSB
• Murmur increases with valsalva, standing
• Murmur decreases with trendelenburg position, isometric exercise, squatting
• Definitive diagnosis — doppler echocardiography

Treatment
• Beta blockers, calcium channel blockers to improve LV filling and diastolic \function ]
• Amiodarone if ventricular dysrhythmias present

Unrecognized Killers in Emergency Electrocardiography

Amal Mattu, MD 7

81 year old male CC: "Cold and shaky" - Conclusion

2010-06-08T04:52:00.002+01:00

Here is the update to 81 year old male CC: "Cold and shaky"

The patient was sent to the cardiac cath lab where angiography revealed 100% occlusion of the right coronary artery (RCA). A stent was successfully placed and the patient is doing well.

Before - 100% occlusion of right coronary artery (RCA)

Balloon inflation

After successful stent placement

Diagnosis: Acute Inferior ST-Elevation Myocardial Infarction

81 year old male CC: "Cold and shaky"

2010-06-06T23:09:00.002+01:00

An 81 year male reports to the fire station to have his blood pressure checked.

He tells the paramedics he had just finished a round of golf and was sitting in the clubhouse when he felt, "cold and shaky."

He relocated to his car with the windows rolled up and the A/C turned off. The ambient temperature was very warm but he still felt cold.

That's when he decided to drive to the fire station.

At the time of evaluation his BP was 120/70 and his pulse was 76 and regular, which was consistent with the other vital signs recorded on his BP card over the past 2 weeks.

When he left the fire station he did not appear acutely ill.

Two hours later an ambulance was dispatched for a male patient with shortness of breath.

The paramedics recognized the man standing on the side of the road wearing a jogging suit as the same man who was at the fire station earlier for a BP check.

He states that he called his doctor who was out of town, and the on-call physician advised him to call 9-1-1.

The man was helped into the back of the ambulance and undressed from the waist-up. A surgical scar is noted down the center of his chest.

Past medical history: MI and CABG x3 in 1985

Meds: Unknown

His vital signs were assessed.

Resp: 18
Pulse: 80
BP: 114/76
SpO2: 96 on RA

He states that "nothing has really changed" since he was at the fire station.

When asked about shortness of breath, he denies it.

The cardiac monitor is attached.

When specifically asked about chest discomfort he states, "Well, I do a little bit of chest pressure, but it's nothing like when I had my heart attack."

A 12-lead ECG is captured.

What is your impression?

66 year old male CC: Chest pain

2010-05-29T18:09:00.001+01:00

Here's another great case submitted by Nick Ciaravella of Grady EMS in Atlanta, GA.

66 year old male presents to EMS with chest pain.

S - Chest Pain
A - None
M - Atenolol, HCTZ
P - HTN
L - meal, 7 hours prior to event
E - Mowing his lawn

O - Started while mowing his lawn
P - Provoked while exerting himself, Palliated initially when he sat down to rest
Q - Sharp
R - Substernal, initially radiating to his jaw, when he rested the pain was only in his chest
S - Initially 10/10, upon ems arrival 4/10, en route 8/10, 9/10, and 10/10 upon arrival at ED
T - No previous episodes

The patient initially presented to EMS with 4/10 pain and vitals as follows, 148/84, pulse 72, 18 respirations, SPO2 96%, Lung sounds clear and equal, BGL 103.

The patient was placed on 3 LPM O2 via NC, given 324 mg Aspirin PO, given 0.4 mg Nitro Tablet Sublingual and then 1 inch of Nitro Paste Transdermal. The Patients pain increased en route to the ED and began to radiate down his left arm en route.

12-lead ECG #1

12-lead ECG #2 (about 15 minutes later)

What do you think?

See also:

Anterior ischemia or posterior STEMI?

26 year old male CC: Chest pain

74 year old male CC: Chest pain

50 year old male CC: Respiratory distress, chest pain

48 year old male CC: Chest discomfort, shortness of breath

Pure (Isolated) Posterior STEMI -- not so rare, but often ignored! - Dr. Smith's ECG Blog

41 year old male CC: Chest pain - Answer

2010-05-27T12:42:00.000+01:00

This was not a STEMI.

It was most likely left ventricular hypertrophy with a strain pattern and mild hyperkalemia.

First, let's look at the 12-lead ECG and make the case for LVH. You'll recall from my previous posts on the topic that I've said it's more important to recognize the so-called "strain pattern" than the voltage criteria.

The reason is simple. If the "strain pattern" isn't causing a problem (mimicking an acute anterior STEMI) then you're waisting your time calculating the QRS voltage.

This ECG has the general appearance of "T-wave discordance". In other words, the T-waves are deflected opposite the main deflection of the QRS complex, which is highly suggestive of a secondary ST-T wave abnormality. In this case, the most likey cause is left ventricular hypertrophy.

I say "generally appearance of T-wave discordance" because it's not true in every lead. That's why I mentioned in a previous post that there are "some caveats".

When I'm looking for appropriate T-wave discordance, I mentally remove isoelectric or equiphasic leads, particularly in the transition zone (the point at which a QRS goes from mostly negative to mostly positive in the precordial leads).

Let's circle the leads I would mentally remove from this 12-lead ECG to decide whether or not "T-wave discordance" is present.

With those leads removed, are the T-wave deflected opposite the QRS complexes?

Absolutely!

Could that be a coincidence?

Highly unlikely!

The high lateral leads in particular are showing a very typical looking strain pattern.

This can be a problem because it could easily be mistaken for "lateral ischemia" or reciprocal changes secondary to acute STEMI!

Does this ECG meet the voltage criteria for LVH?

Not exactly, but I believe we can make the case using the Romhilt-Estes point scoring system. This ECG would get at least a 4 (probable LVH), and it's right on the borderline for left atrial enlargement and delayed intrinsicoid deflection in leads V5 and V6 which would give it a score of 5 or 6.

But I don't think that's important.

The next question we want to ask is, is the degree of the secondary ST-T wave abnormality proportional to the amplitude of the QRS complex in the opposite direction?

The answer is yes.

Remember, we're looking at the ST-segments and the T-waves together.

At first glance it looks like there might be more ST-elevation in lead V1 than lead V2. However, I believe this is an optical illusion created by the biphasic P-waves in lead V1, as well as the more defined (less diffuse) J-points in lead V1.

Let's blow this up a little bit.

When we use the TP-segments as a baseline, we can see that it's debatable as to whether or not lead V1 shows more ST-elevation, but it's obvious that lead V2 shows a more pronounced ST-T wave abnormality.

The T-waves seem a little bit narrower than we might have expected with LVH, perhaps with a slightly later take-off. Also, the QTc is well within "normal" at 419 ms.

I don't have the exact lab value, but the feedback I received on this case was that the patient had a potassium level that was "on the high end of mild" (so I'm guessing between a 6 and 7).

Consider the following graphic that compares the T-waves of hyperkalemia to the T-waves of acute anterior STEMI.

There isn't much documentation out there as to what hyperkalemia is supposed to look like in the presence of a secondary ST-T wave abnormality, but you'll notice that with hyperkalemia, the T-waves are narrow and have a late take-off, while with acute anterior STEMI, the T-waves are more "broad-based".

This was a very difficult case. So what can we learn from it?

In my mind, it's very simple (and it needs to be simple for field use -- complicated equations involving calipers are not simple).

T-wave discordance strongly suggests the possibility of a secondary ST-T wave abnormality. That being the case, I would wait for changes on serially obtained ECGs before calling a STEMI Alert.

Remember, in some studies LVH is the most common cause of ST-elevation in chest pain patients, so we need a solid strategy to deal with this STE-mimic!

41 year old male CC: Chest pain

2010-05-26T19:18:00.002+01:00

A 41 year old male is pulled over during morning rush-hour by sheriff's deputies.

He states that he is on his way to the hospital because he is having chest pain. EMS is called to the scene.

The patient is awake, alert, and oriented to person, place, time, and event.

His skin is pink, warm, and moist.

He appears acutely ill and anxious.

He states that he has a history of high blood pressure and renal insufficiency. He takes several medications, but he can only recall that one of them is a beta blocker.

Onset: 1 hour ago while sleeping.
Provoke: Nothing makes the pain better or worse.
Quality: Patient describes the pain as a poorly localized "fullness" or "pressure".
Radiate: The patient cannot tell whether or not the pain radiates.
Severity: The patient reluctantly gives the pain a 7/10.
Time: The patient states he has had the pain on several occasions over the past few months but did not seek medical treatment.

Vital signs are assessed.

Resp: 20
Pulse: 76
BP: 138/78
SpO2: 99 on RA

The cardiac monitor is attached.

A 12-lead ECG is captured.

What is your analysis of this ECG?

Does anything about it concern you?

Is this a STEMI?

Why or why not?

Note: This 12-lead ECG was captured in the back of an ambulance with the motor and generator running, but it shows excellent data quality.

62 year old male CC: Chest pain

2010-05-19T21:47:00.001+01:00

62 year old male presents to the emergency department complaining of chest discomfort.

Past medical history is significant for dyslipidemia and ulcerative colitis. Also prior history of significant tobacco use. Maternal history of CAD. Maternal and paternal history of CVA.

The patient's only medication is Lipitor but he took an aspinin en route to the hospital.

Onset: Patient states the pain started that morning and became progressively worse since lunch time.

Provoke: Nothing makes the pain better or worse.

Quality: Sharp and nonpleuritic

Radiate: The pain radiates down the right arm to the bicep.

Severity: 7/10

Time: Patient states he experienced a similar pain in his right upper chest several days prior while playing tennis. He stopped exercising and the pain resolved.

The pain makes the patient feel "a little clammy." He denies shortness of breath. He states that he feels "a little dizzy" but denies palpitations. He had a negative stress test 3-4 years ago.

He has a known history of left bundle branch block.

The patient's skin is warm and dry.

Breath sounds clear bilaterally. No JVD.

Neuro exam normal.

Vital signs:

Resp: 18

Pulse: 60

BP: 140/72

SpO2: 98 on RA

A 12-lead ECG is captured and presented to the ED physician within 5 minutes of arrival.

An "old" ECG is pulled from the computer system for comparison.

What is your impression?

** Update 05/19/2010 **

After oxygen and nitroglycerin the patient reports a significant decrease in pain.

An additional 12-lead ECG is captured.

There is now slightly less ST-elevation in leads V3 and V4.

Remember that a secondary ST-segment abnormality (as opposed to a primary ST-segment abnormality) should not "improve" with oxygen and nitroglycerin!

In other words, if this ST-elevation was caused just by the LBBB, it shouldn't be "getting better". Changing ST-segments suggest the dynamic supply vs. demand characteristics of ACS!

Now, let's go back to the initial 12-lead ECG. Is the ST-elevation in the anterior leads cause for concern?

Go back and read Identifying AMI in the presence of left bundle branch block (or paced rhythm). Remember, discordant ST-elevation = or > 5 mm is the least specific of Sgarbossa's criteria! That's why we use the modified rule that I learned from Dr. Stephen Smith of Dr. Smith's ECG Blog.

That criterion states that discordant ST-elevation should not be more than 0.2 (or 20%) the depth of the S-wave in the setting of left bundle branch block (ST/S ratio).

Using that criterion, how does this ECG measure up? Let's take a look.

Ladies and gentlemen, we have a winner!

The patient was ultimately cathed and angiography revealed 100% occlusion of the LAD.

Final thought:

Does it get any more difficult that that? If Dr. Smith's decision rule works this great, shouldn't we be shouting it from the rooftops?

See also:

Discordant ST-elevation in LBBB or paced rhythm

Identifying AMI in the presence of LBBB

Sgarbossa's criteria - new graph

"New" LBBB - What's the big deal?

New left bundle branch block is a poor indicator of coronary occlusion - Dr. Smith's ECG Blog

STEMI best seen in PVC (Dr. Smith's ECG Blog)

67 y/o male CC: Syncope

2010-05-17T17:57:00.006+01:00

A 67 y/o male has fallen to the ground at his residence. His "partner" called 911 after seeing that he was unconscious. Upon your arrival the patient is alert and requesting that you pick him up because he really needs to make a bowel movement. The patient denies syncope but states that he does not remember falling.

Here is the initial ECG and the subsequent 12-lead ECG. Sorry for the poor quality.

What do you see?

What do you want to know?

What do you want to do?

****Update 5/20/2010****

His Vital Signs

HR correlates with monitor, pulse not palpable at radial.

Initial BP 78/60

AAOx3, normal mental status, just wants to make a bowel movement.

Skin - Pale, more pronounced and white from the waste down. Skin was relatively dry.

****Update 5/23/2010****

A new 12-lead ECG is captured during transport.

The patient's vital signs do not improve dramatically with IV fluids.

96 y/o Female Near Syncope

2010-05-14T21:04:00.003+01:00

Thank you to Jason for the invite to post on this site. If you don;t know me, I am the creator of Paramedicine 101. I am a paramedic with Lee County FL and an EMS educator with the local college. I will drop by here to provide interesting ECGs from time to time. This is one from the Paramedicine 101 archive.

As you arrive, the patient is sitting on the ground. She states that she felt weak, so she sat down. She did not lose consciousness and appears atraumatic.

S - Feels weak

A - PCN

M - Atenolol, Lasix, ASA

P - She thinks she may have had a "mild heart attack" in the past, HTN.

L - Coffee

E - She has not done any strenuous activity. She is at home, and was heading to the kitchen.

No chest pain, mild dyspnea with exertion.

12-Lead:

Please provide your impressions.

26 year old male CC: Chest pain

2010-05-14T11:57:00.001+01:00

Here's a great case submitted by a faithful reader who wishes to remain anonymous.

EMS is called to a 26 year old male complaining of chest pain.

On arrival patient is found sitting on his living room couch. He appears anxious and acutely ill.

He states that he was riding his bike when he became anxious, had a "coughing spell" and started to experience chest discomfort. The location of the chest discomfort is in the center of his chest and slightly to the left.

Onset: Sudden while riding a bike

Provoke: Nothing makes the pain better or worse

Quality: Difficult to describe but with prompting the patient calls it "pressure"

Radiate: Left jaw and left arm

Severity: 7/10

Time: No previous episodes

The patients skin is warm and moist. The color is normal.

The patient denies shortness of breath. Breath sounds are clear bilaterally.

He is nauseated but he has not vomited.

Past medical history: Healthy

Medications: None

Vital signs are assessed.

Resp: 22

Pulse: 98

BP: 140/84

SpO2: 100 with oxygen via NRB @ 15 LPM

The cardiac monitor is attached.

A 12-lead ECG is captured.

What is your impression?

*** Update 05/14/2010 ***

The importance of serial ECGs cannot be over-emphasized.

In this case, a second 12-lead ECG was captured just prior to arrival at the hospital.

Does this new information shed any light on the probably diagnosis?

What else could you have done?

Final update for 74 year old male CC: Chest pain

2010-04-30T15:56:00.003+01:00

Here's the final update on the most recent case.

First of all, this was a male, not a female. I don't know how that misunderstanding happened.

At any rate, here are the notes from the ED physician.

Medical screening exam undertaken.

HPI text: This a 74 year-old white male reports onset of pressure in the anterior chest radiating into the left arm at approximately 2:15 p.m. today. He had just finished eating a large lunch with his wife and a friend. They were walking when the pain started. The pain has been persistent for three hours or more by the time he is brought to the emergency department by ambulance. The pain has worsened throughout the afternoon. His wife and friend both report that the patient was diaphoretic, weak, and at times blue in the lips. He seemed to be breathing heavily as well. The patient initially refused to come to the hospital stating that he was having indigestion. No previous history of coronary artery disease although treated for hypertension and dyslipidemia. Positive family history of coronary artery disease. The patient does not smoke cigarettes. No diabetes mellitus. The patient reports no back pain or abdominal pain. He has a history of chronic edema of the ankles. No previous DVT or PE.

Review of symptoms

Constitutional

General: No recent fever

Head: No recurrent headaches

ENT: No recurrent infections

Eyes: No recent infections

Pulmonary: No asthma. No recent cough.

Cardiovascular: Current chest pain. Hypertension. Dyslipidemia.

GI: No recurrent vomiting. No dyspepsia.

Neurologic: Awake and conversant. Generally weak without focal component.

Remaining review of symptoms reviewed and negative.

Exam

General: 74 year-old white male who appears diaphoretic and pale. He is awake and conversant. Blood pressure was 84 systolic when he arrived. He is clutching his chest and appears uncomfortable.

Head: No swelling or discoloration to the scalp.

Face: No facial swelling or discoloration.

Eyes: No scleral icterus.

Oral cavity: No lesions including tongue and lips.

Neck: No discoloration or swelling.

Chest wall: No deformities or tenderness.

Lungs: Breath sounds are symmetrical. There are a few dry crackles at the bases bilaterally.

Cardiac: Regular rate (62) and rhythm without murmurs, clicks, or rubs.

Abdomen: Soft and nondistended. Bowel sounds are active. Nontender. No pulsatile mass.

Extremities: The hands and feet are cool. Mild cyanosis of the fingertips and toe tests.

Cath report

The patient was taken to the cardiac cath lab. The patient was hypotensive, developed acute respiratory distress, vomited x2 and at times became bradycardic into the mid-high 30s. Oxygen via NRB @ 15 LPM was required to maintain SpO2 > 90%.

Two stents were placed in the RCA (mid and distal).

The main lesion was in the mid-RCA; 99% stenosis with partial flow and partial perfusion.

Before

After

Left coronary artery

After the procedure an IABP was placed and the patient was sent to recovery.

No further information is available.

Update to 74 yof CC: Chest pain

2010-04-27T02:16:00.001+01:00

Here are the serial prehospital 12-lead ECGs from the case.

Angiograms and cath report to follow.

Pay close attention to the right precordial leads (V1-V3).

Consider the following graphic.

The most important changes occur between 16:41:26 and 16:50:30.

Just for fun, here it is "flipped".

74 year old female CC: Chest pain

2010-04-23T01:03:00.002+01:00

74 year old female presents to EMS with a chief complaint of chest pain.

Onset approximately 1 hour prior to the 9-1-1 call.

No further details of the OPQRST are currently available. I will update the case with this information as soon as it is available, along with the physical exam.

Vital signs:

Resp: 20
Pulse: 56
NIBP: 97/57
SpO2: 100 on RA

Past medical history: HTN

Meds: Unkown

The cardiac monitor is attached.

A 12-lead ECG is captured.

What is your impression?

Would you call a STEMI Alert?

Why or why not?

What additional action(s) might you take?

46 year old male CC: Chest Pain

2010-04-02T02:08:00.002+01:00

Here's an interesting case submitted by Christopher Watford. Chris is paramedic and computer programmer and a long-time follower of the Prehospital 12-Lead ECG blog.

He is a recent addition to the Paramedicine 101 bloggers and has his own blog called My Variables Only Have 6 Letters.

46 year old male presents to EMS complaining of chest pain.

After sitting down on the gurney the gurney states, "My heart is jumping out of my chest!"

Onset: Sudden while doing yard work.
Provoke: Nothing makes the pain better or worse.
Quality: Heaviness and "jumping" sensation.
Radiate: The pain does not radiate although his hands are numb and tingling.
Severity: Not reported.

The patient is alert and oriented to person, place, time and event.

Skin: mottled, cool, diaphoretic.

Vital signs were assessed.

Resp: 18
Pulse: Too rapid to count
BP: 120/60
SpO2: Not reported.

Breath sounds: Clear bilaterally.

Capillary refill: 5+ seconds

BGL: 140 mg/dL

The cardiac monitor is attached.

A 12-lead ECG is captured.

What is your differential diagnosis?

What is your treatment plan?

*** Update 04/02/2010 ***

The treating paramedics gave 1.5 mg/kg lidocaine.

After administration of the drug the following rhythms were noted on the monitor.

Pay close attention to this rhythm change....

There is a critical clue here, and it has to do with the R-R interval.

Now take a look at a 12-lead ECG of the irregular rhythm.

Was lidocaine the best possible choice?

Is there a safe antiarrhythmic for a patient like this?

Is this patient at-risk for sudden cardiac arrest?

Why or why not?

23 year old male CC: Chest Pain

2010-03-25T19:59:00.002Z

Here's a fascinating case submitted by Geoff Dayne.

EMS is called to a VA clinic for a 23 year old male who came in to get checked into the system. Somewhere in the exchange, he mentioned that he had been experiencing chest pain off & on for just over a month.

Onset: Today's pain came on gradually.
Provoke: Nothing makes the pain better or worse.
Quality: Pain described as "pressure".
Radiate: Occasionally radiates to the jaw.
Severity: "Mild" (no pain scale)
Time: Several previous episodes over the past month.

The patient denies shortness of breath. There is no nausea and the patient has not vomited.

A 12-Lead ECG is captured at the clinic.

And another.

9-1-1 was contacted.

The patient was given O2, ASA, and NTG at the clinic.

EMS arrives and performs their own assessment.

(Vital signs not available -- let us assume they are within normal limits, stable, and not otherwise helpful to the assessment).

The cardiac monitor is attached.

The paramedics capture their own 12-lead ECG.

Are you concerned about this ECG?

Why or why not?

Should a STEMI Alert be called from the field?

Why or why not?

Would you bypass the local non-PCI hospital for a STEMI receiving hospital?

Why or why not?

*** Update 03/25/2010 ***

Here are some serial ECGs captured in the field.

Does this help?

12 year old male: Chief complaint: Palpitations

2010-03-20T13:52:00.002Z

Here's a case submitted by Bob Sullivan, NREMT-P from New Castle County EMS in Wilmington, DE.

The case occurred six years ago so certain details are missing. However, there is more than enough here to discuss the most relevant points about the case.

The patient was a 12 year old male whose only complaint was palpitations.

The patient's pulse was extremely rapid. However, he appeared to be perfusing adequately and the blood pressure was stable.

A 12-lead ECG was captured.

And another.

Online Medical Control was contacted and the treating paramedic was advised to watch the patient's blood pressure and cardiovert if the patient became unstable.

The patient converted after the ambulance went over a bump. Unfortunately, a post-conversion 12-lead ECG was not recorded.

At the time, Mr. Sullivan was a new paramedic. He states that his co-workers felt that he should have given adenosine, since a 12 year old "could not be in VT." He also mentions that he's gotten different interpretations from each doctor he's shown it to.

The case has been bothering him ever since.

What do you think is the best field treatment for a patient like this?

What do you think of Online Medical Control's advice?

What do you think is wrong with this patient?

56 year old male c/o Chest Pain

2010-03-13T09:48:00.007Z

56 year old male presents with acute onset of sudden central chest pain radiating down both arms with pins & needles sensation, patient found sitting in chair.

This p/t has had 4 previous MI's with stents fitted, p/t stated that pain feels different from previous MI's. Patient stated he had the feeling of impending doom.

Skin: dry, look well perfused (pink)... but had been on oxygen for some time given by the responder, before the arrival of the crew...

Pain score 08/10

No nausea or vomiting

Past medical history:

Hypertension

Previous MI's

Angina

Vital signs:

BP: of 123/49 (Low for this p/t)
HR: 72
RR: 22
SpO2: 99%, 100 on O2 via NRB mask @ 15 LPM

BM: (blood sugar) 5.4 mmol/l

Temp: 36.7

Lead III strip above and Pre-hospital 12-lead ECG

Ventricular rate: 80

PR interval: 120 ms

QRS Duration: 166 ms

QT/QTc: 418/482 ms

P-R-T axes 13 72 -3

Emergency Department 12-Lead ECG

Please comment on the features of this ECG:

What findings do you see ?

For experienced members in cardiology, please use this ECG as a teaching tool, passing on your knowledge and experience to others.

63 year old male with sudden onset shortness of breath

2010-03-01T14:37:00.002Z

This is an interesting case submitted by Tom Bernesser who is a paramedic from North Carolina.

I got to know Tom through the EKG Challenge forum at the EMS Village where he always posted fascinating case studies.

Here's the story.

63 year old male presents with acute onset of dyspnea.

He reported 4 previous MI's with similar presenation, only dyspnea - no pain or discomort as was the case on this morning.

Past medical history:

NIDDM, HTN, MI, CHF, CVA and is bed-confined for the most part. He's also fairly obese.

Vital signs:

BP of 146/90
HR 104
RR 24
SpO2: 87 on RA, 100 on O2 via NRB mask @ 15 LPM

BGL: 141 mg/dL.

He did have diminished lung sounds bilaterally, maybe some rales in the bases but was able to speak in full sentences.

He also had some pedal edema, but wasn't taking any diuretics.

He's at a Skilled Nursing Facility (SNF) but of course there is no old EKG on site for comparison.

Another note, he did have occasional bouts of multifocal PVC's probably about 10-15/min.

Here is the 12-lead ECG.

Here is the computerized interpretive statement.

As you can see, it's giving the >>>> ACUTE MI <<<< message.

Would you activate the cardiac cath lab?

Why or why not?

57 yom CC: Cardiac arrest

2010-02-25T12:24:00.000Z

Here's another interesting case submitted by a reader who wishes to remain anonymous.

While we're on the subject, I'd like to thank my readers for the interesting case studies that have been coming in!

This is what the Web 2.0 experience is all about! We're learning a lot from each other and that's the difference between editing a blog and writing a book.

EMS is called to a seizure patient. According to the patient's girlfriend, he had been feeling weak and vomiting about an hour earlier. She states that he had a "short seizure" after which he was unresponsive. She didn't call 9-1-1 right away because the patient has a history of seizures.

After the patient was unresponsivee for longer than usual she contacted 9-1-1. When asked by EMS personnel, she estimates that the patient had not been breathing for 3-5 minutes prior to EMS arrival. She did not attempt CPR.

The patient is a 57 year old male.

Past medical history: CVA, NIDDM, and seizures

Medications: Tylenol, Trileptol

Pulselessness was confirmed and chest compressions were initiated.

The combo-pads were attached.

Here is the initial rhythm (with CPR artifact).

It was confirmed as asystole a short time later.

CPR was continued. The airway was managed with an OPA and BVM. An 18 ga IV was established in the LAC and run w/o. Epinephrine and atropine were administered.

A rhythm change was noted on the monitor.

A weak carotid pulse was palpated although radial pulses were absent and a BP could not be auscultated.

The patient was relocated to the ambulance. The patient was intubated with an ETCO2 in the mid 50s.

A 12-lead ECG was captured.

The paramedics left the scene en route to a PCI-hospital.

At this point the patient had radial pulses but for some reason the paramedics were still unable to auscultate a blood pressure.

The rhythm continued to be irregular and polymorphic.

Another 12-lead ECG was captured.

Some significant asystolic pauses were noted on the monitor.

As the last 12-lead ECG was captured the patient lost pulses.

By now the ambulance was arriving at the PCI hospital. CPR was resumed. Another round of epinephrine was given and the patient re-gained pulses.

The ED staff identified the prehospital 12-lead ECGs as showing "STEMI".

Do you agree? Why or why not?

Should it matter at this point? In other words, should the patient be cathed anyway (assuming the patient is stable enough for a cath)?

68 yom CC: Chest Pain

2010-02-21T19:34:00.001Z

Here's another great case submitted by Robert Bees.

EMS is called in the very early morning to a 68 year old male complaining of chest pain and shortness of breath.

On arrival, the patient is anxious and appears acutely ill. He is oriented to person, place, and time.

Skin is cool, pale, and diaphoretic.

The patient feels light-headed and admits to nausea but has not vomited.

Onset: While sleeping
Provoke: Nothing makes the pain better or worse
Quality: Poorly localized heavy pressure
Radiate: The pain does not radiate to the arms, back, neck or jaw
Severity: 8/10
Time: Patient states he occasionally "feels bad" but "not like this"

Past medical history: MI with stents x 2 years ago.

Medications: ASA, Lipitor, Tenormin, NTG

Patient states he took NTG x 1 prior to EMS arrival which made him "feel worse"

Vital signs:

Resp: 22 shallow
Pulse: 140
BP: 88/54
SpO2: 92 on RA

Breath sounds: rales - patient becomes very light-headed sitting up

The cardiac monitor is attached.

A 12-lead ECG is captured.

What now?

Should you ever give a calcium channel blocker to a wide complex tachycardia?

2010-02-17T21:31:00.000Z

Some of you are probably wondering whether or not I'd ever condone giving a calcium channel blocker to a wide complex tachycardia in the field.

A recent case submitted by Robert Bees demonstrates a situation where I might consider it (or at least not criticize someone for considering it).

EMS is called to a 90 year old female with a chief complaint of difficulty breathing and weakness.

On arrival, the patient is alert and oriented to person, place, and time.

Vital signs:

Resp: 20 and non-labored
Pulse: 80 and regular
BP: 180/82
SpO2: 96 on RA

BGL: 121

Breath sounds are clear bilaterally.

Past medical history: HTN, asthma

Medications: prednisone, albuterol

The patient states that she used her inhaler prior to EMS arrival with no relief.

The patient denies chest discomfort. She states that she is not nauseated and she has not vomited.

The cardiac monitor was attached and a 12-lead ECG was captured.

The patient is placed on oxygen via NC @ 2 LPM and loaded for transport.

An IV is established in the left arm and 0.9% NS is run KVO.

Shortly after leaving the scene, a rhythm change is noted on the monitor.

Another 12-lead ECG is captured.

The patient became markedly more tired and went from alert to responsive to verbal stimuli.

What do these ECGs show?

The second 12-lead ECG shows a rhythm that is wide (QRS > 120 ms) and fast (HR > 100).

Is it ventricular tachycardia?

How do you know?

How would you treat this patient?

72 yom CC: Unknown Problem (Man Down) - Conclusion

2010-02-14T23:47:00.002Z

You may recall the recent case of the 72 year old male who became dizzy, fell, and hit his head.

Here was the initial 12-lead ECG.

Based on this ECG the lead paramedic called a "STEMI Alert" and transmitted the ECG to the receiving hospital.

The on-duty ED physician received the ECG and the paramedic's radio report.

The ED physician called up the patient's records on the computer system. It turned out that the patient had been to the hospital before.

There was a copy of a prehospital 12-lead ECG from March 2009 on file in the patient's chart.

Based on the similarities between this ECG and the ECG recorded on this call (and the fact that the presentation did not exactly scream ACS) the ED physician did not call the "Code STEMI" while EMS was still in the field.

It would prove to be the correct decision.

This is the 12-lead ECG that was captured on arrival.

You will note that this ECG is very similar to the prehospital 12-lead ECG captured back in March 2009. However, it's slightly different from the prehospital 12-lead ECG taken earlier that evening.

Go back up and look at the prehospital 12-lead ECG.

The frontal plane axis is off by about 15 degrees, the T-wave inversion in lead aVL is more subtle, and the R/S ratio in lead V2 is > 1.

Since these findings are not present in the 12-lead ECG taken on arrival at the hospital, it can probably be explained by lead placement.

Paramedics often project that attitude that skin prep and electrode placement are a low priority, but this case demonstrates why it's essential to quality patient care.

With careful lead placement and excellent data quality, the GE-Marquette 12SL interpretive algorithm does not give the ***ACUTE MI SUSPECTED*** message.

In addition, the ST-depression / inverted T-wave was a critical finding on the prehospital 12-lead ECG, because it suggested the possibility of a reciprocal change to the spurious ST-elevation in lead III.

The presence of the inverted T-wave on the "old" ECG made the ED physician take this finding with a grain of salt.

There's nothing wrong with having multiples sets of "critical eyes" looking at an ECG prior to calling in the cavalry, especially for a marginal ECG where it's questionable as to whether or not the "1 mm of ST-segment elevation in 2 or more anatomically contiguous leads" criterion is met.

That's how we minimize false positives, control health care costs, and do the right thing for the patient.

So we're 0 for 1 with our STEMI Alert protocol. However, on this particular day, the system demonstrated a hidden strength! The STEMI Alert allowed for a quick comparison to an "old" ECG.

64 yom CC: Chest Pain

2010-02-12T18:00:00.003Z

Here's another great case submitted by a faithful reader who wishes to remain anonymous.

The patient is a 64 year old male with a chief complaint of substernal chest pain.

Onset: Sudden onset at rest.
Provoke: Nothing makes the pain better or worse.
Quality: Patient describes the pain as "sharp".
Radiate: Pain radiates to right arm.
Severity: Patient gives the pain a 15/10.
Time: 10 minutes prior to EMS activation.

Skin is cool, pale, and diaphoretic.

He denies shortness of breath. He admits to nausea but has not vomited.

Past medical history: CVA with right side deficit. IDDM with below knee amputation. Electric wheelchair bound.

Allergies: No known drug allergies

Medications: Vicodin

Vital signs:

Resp: 18
Pulse: very rapid, weak
BP: 103/81
SpO2: 99 on RA

BGL: 283

Breath sounds are clear bilaterally.

The cardiac monitor is attached.

A 12-lead ECG is captured.

And another.

What's next?

*** Update 02/13/2010 ***

A rhythm change is noted on the monitor.

An additional 12-lead ECG is captured.

And another.

Does this shed some light on the situation?

50 yom (Asian) CC: left-sided chest and arm pain/weakness.

2010-02-12T12:01:00.013Z

Is this patient having an Acute Myocardial Infarction at this present time or did he have the infarct 2 weeks ago when the patient first had central chest pain?

This is an interesting case... The story here is:... an good friend and colleague of my recently got a call for a immediate transfer from one hospital to another to take a patient for PCI... My colleague was stuck in the middle of 3 consultant cardiologist's aurguing whether the patient was having an AMI at the present time or is the ECG changes from 2 weeks ago when the patient actually had the first chest pain.

Outcome was 2 cardiologists decided that the patient was having an AMI now, and the 3rd cardiologist thoughts were these events are from when the patient first infarcted 2 weeks ago. In the end the outcome was they decided NOT to PCI this patient.

Sorry I have not much clinical information on this patient whether he has any cardiac history, I understand the patient's english was very poor... Observation's were recorded as follows:

HR: 89

BP: 110/69

SPO2: 99% O2

RR: 22

SKIN: No details: just my colleague stated that this patient did not present like he was having a AMI.

No other info on this patient regarding blood results...etc.

My Questions are:

1) What your opinion on this case study?

2) After looking at these ECG's, do you think present events or is the infarct 2 weeks old?

3) Would you PCI ?

4) Give evidence and your reasons from the features on the 12 lead ECG, whether this is 2 weeks old or AMI?

Lead II taken from the rhythm strip

Hospital captured 12 Lead ECG

This is a interesting case to hear from cardiologists with their opinions on this case study, or any other health care professional's sharing their views... Look forward to all your comments...:-)

72 yom CC: Unknown Problem (Man Down)

2010-02-08T17:43:00.002Z

EMS is dispatched to a 72 year old male patient. Third party call. History of Parkinson's Disease. Patient is conscious. No further information.

On arrival, EMS finds a 72 year old Spanish-speaking male. Through an interpreter the lead paramedic determines that the patient became dizzy, fell down, and hit his head. A small hematoma is visible above the patient's right eye.

The patient is awake but somnolent. He is oriented to person, place, time, and event. The remainder of the neurological exam was normal.

Since the patient is not alert the crew applies manual C-spine stabilization and continues the exam.

The patient denies chest pain or shortness of breath.

Breath sounds are clear bilaterally.

The patient denies any significant medical history and states that he takes no medications.

Vital signs are assessed.

Resp: 18
Pulse: 80
BP: 104/70
SpO2: 98 on RA

The cardiac monitor is attached.

A 12-lead ECG is captured.

The lead paramedic notes that the arm leads are reversed. The problem is corrected and another 12-lead ECG is captured.

The black electrode is replaced and a third 12-lead ECG is captured.

What is your impression and what would you do next?

*** Update 02/09/2010 ***

In the first graphic you can see that it's debatable as to whether or not 1 mm of ST-segment elevation is actually present in the 12-lead ECG when you use the TP segment as the baseline.

The first complex in lead III helps foster the perception, probably due to wandering baseline.

Compounding the illusion is the ST-depression in lead aVL! This is one of the first things I look for when considering the ECG diagnosis of acute inferior STEMI.

It's helped me pick up on dozens of subtle presentations!

In the second graphic I've blown up lead II so you can clearly see the PR-segment depression.

This is important for two reasons. First, it fools your eye into the thinking that ST-segment elevation is present. Secondly, it fools the GE-Marquette 12SL interpretive algorithm!

Having said that, I have respect for the GE-Marquette 12SL interpretive algorithm, and I'm certain it also picked up on the ST-depression in lead aVL.

Keep in mind that the ACC/AHA STEMI criteria is far from perfect. I've called STEMIs before with less than 1 mm of ST-segment elevation, specifically when ST-depression was present in lead aVL.

Do you remember this 12-lead ECG from a previous post?

The patient ended up having a 100% occlusion of the RCA!

I've had some really great comments on this case so far. Is your perception of this ECG changing?

Does this case demonstrate that sometimes, the emergency department is exactly where a suspected acute STEMI patient (with a marginal ECG) belongs until the diagnosis can be confirmed through other means?

I'll be posting the conclusion to the case in the next couple of days.

73 yom CC: Chest Pain

2010-02-01T15:21:00.003Z

Here's a case that was submitted by a reader from the UK.

He's a new EMT in his first 6 months who has chosen to remain anonymous.

In his own words:

Presenting Complaint: Chest Pain

History of Presenting Complaint: 73 year old male with cardiac history complained of retrosternal chest pain whilst getting out bed in the a.m.

The pain radiated left shoulder, left arm.

The male took his gtn sublingual spray and the pain eventually eleviated after x3 spray's.

4 hours later male is persuaded to call ambulance to inform of this episode of pain.

On arrival: Patient self mobile to door - nil obvious difficulties.

On examination:

Alert, orientated with good colour - GCS 15.
R/R 19, with good clear bilateral air entry.
Sats 97% on air. Patient communicable.
Good strong radial H/R 85.
Nil chest pain/discomfort.
Nil diaphoresis.
BP - Systolic elevated - 200/83
All other obs within normal parameters

3 lead - see attachment.

12 lead done in situ - see attachment

Past Medical History: Cardiac hx = Angina, Bypass (12 years), valve replacement (u/k which - 1 years)

Allergies - Clopidogrel

Treatment: 300mg aspirin and transport to A&E

A&E department ecg - see attached.

What do you think?

Discordant ST-Segment Elevation in LBBB or Paced Rhythm

2010-01-27T16:20:00.002Z

If you've been following the Prehospital 12-Lead ECG blog for a while, you know that I'm advocate of using Sgarbossa's criteria to help identify acute STEMI in the presence of left bundle branch block (LBBB) or paced rhythm.

According the Sgarbossa's original criteria, 5 mm of discordant ST-segment elevation is required to identify AMI in the presence of LBBB.

Why 5 mm when normally we require only 1 or 2 mm of ST-elevation?

Because in the setting of left bundle branch block or paced rhythm, it's normal for the ST-segment and T-wave to be defected opposite the main deflection of the QRS complex!

That's why it's necessary to consider the depth of the QRS complex when examining the amount of discordant ST-segment elevation. The deeper the S-wave, the greater the secondary ST-T wave abnormality in the opposite direction!

In the original article I wrote on the topic, I showed this example 12-lead ECG to show why the 5 mm criterion is problematic.

As you can see, this 12-lead ECG shows sinus rhythm with left bundle branch block and > 5 mm of discordant (opposite the QRS complex) ST-elevation in leads V1, V2, and V3 (the right precordial leads). The T-wave are huge!

The problem is, this patient was not experiencing acute myocardial infarction. The ST-segments are elevated > 5 mm because the S-waves are extremely deep (off the bottom of the ECG paper for leads V2 and V3).

Had we used the modified criterion of discordant ST-elevation that is = or > to 0.25 the QRS complex (credit to Dr. Smith), we would have seen that in lead V1 the S-wave is 50 mm deep. Thus, we would require at least 12.5 mm of ST-segment elevation to consider this finding positive for acute STEMI.

There's another way the modified criterion can help you!

Consider this 12-lead ECG that shows a ventricular paced rhythm. It's been in my collection for many years, and I regret that I no longer recall where it came from.

This ECG does not meet Sgarbossa's criteria for diagnosing AMI in the presence of LBBB. With the exception of lead V6, the paced QRS complexes show appropriate T-wave discordance, and none of the ST-segments are elevated to 5 mm or more.

But wait! The ST-segments are elevated far greater than 0.25 the depth of the QRS complex in leads II, III, and aVF! This patient is experiencing acute inferior STEMI!

The intrinsic QRS complex in the right precordial leads also shows an > R/S ratio in lead V1 and V2 and ST-segment depression suggesting posterior extension, which clinches the diagnosis.

So remember, when using Sgarbossa's criteria, huge QRS complexes can cause false positive and tiny QRS complexes can cause false negatives, unless you use the modified rule that considers ST-segment elevation as a percentage of the QRS complex!

See also:

Identifying AMI in the presence of LBBB

Sgarbossa's criteria - new graph

"New" LBBB - What's the big deal?

STEMI best seen in PVC (Dr. Smith's ECG Blog)

Wolff-Parkinson-White (WPW) - STEMI Mimics

2010-01-15T17:14:00.002Z

A really interesting 12-Lead ECG was posted to the Cardiology & Electrocardiography (ECG, EKG) Experts group on Facebook the other day.

If you're not familiar, this is one of the groups / fan pages on Facebook I help moderate with Jason Winter who also started the Cardiology & Electrocardiography Experts blog.

What's so interesting about this ECG is that it shows a relatively infrequent STEMI mimic. In addition, it helps demonstrate a point I've been pondering about several of the STEMI mimics in general.

Let's take a look.

The patient was a 29 year old male with no complaints. The ECG was captured during a routine workup according to the contributor Chris de Beer (thanks again for the interesting ECG, Chris).

The ECG shows a WPW pattern as evidenced by a short PR interval and delta waves. The delta waves create a pseudo-infarct pattern (Q-waves) in the septal leads.

You might recall from my previous post about left ventricular hypertrophy (LVH) that I think recognizing the so-called "strain pattern" is actually more important than knowing the "voltage criteria" for LVH.

I'm sure some of you are waiting for "Part II" of the left ventricular hypertrophy series, but I'm still waiting for inspiration! :)

What does this ECG have in common with a strain pattern from left ventricular hypertrophy (LVH)? What does it have in common with left bundle branch block (LBBB)? What does it have in common with ventricular rhythms? Including paced rhythms?

The answer is, it has a widened QRS-T angle! To put it another way, the T-waves and ST-segments are deflected opposite the main deflection of the QRS complex, and (this point is the most critical) the degree of the ST-T abnormality is proportional to the size of the QRS complex.

Think of this as a supplement to Sgarbossa's criteria and the "rule of appropriate T-wave (and ST-segment) discordance".

Here's a graphic to help illustrate the point.

When you see a pattern like this, regardless of cause, it should set off alarm bells that you are dealing with a STE-mimic and not acute STEMI!

Note that the S-wave in lead V3 is cut off by the bottom of the ECG paper. This is a common problem with prehospital 12-lead ECGs! We must presume that the S-wave would be the deepest in lead V3 if we were able to view the entire QRS complex.

That doesn't mean the patient isn't experiencing acute myocardial infarction (although this patient is asymptomatic so let's pretend he was over the age of 30 and complaining of chest discomfort).

It just means you should wait before pulling the trigger on the cardiac cath lab.

Look for changes on serially obtained ECGs instead!

See also:

Left ventricular hypertrophy

Identifying AMI in the presence of LBBB

Sgarbossa's criteria - new graphic

ECG mimics of acute STEMI

Can you see ST-Elevation???

2010-01-14T12:34:00.001Z

This ECG was captured from a patient, I have found out since this patient was c/o chest pain, p/t had a AMI, about 2 years ago... This was given to me by a good friend and colleague... Who stated the doctor in the Emergency Dept.. Give my colleague a telling off for not recognizing ST ELEVATION

DO YOU SEE ANY ST SEGMENT ELEVATION ???

Please discuss the ECG and the features... Sorry about the not having no history on this patient!!!

"New" LBBB - What's the big deal?

2010-01-11T16:19:00.000Z

Cross-posted to the Prehospital 12-Lead ECG blog and Paramedicine101.

In the January 2010 EMCast at EMedHome.com, Amal Mattu MD reviews Chang AM, Shofer FS, Tabas JA, et al. Lack of association between left bundle-branch block and acute myocardial infarction in symptomatic ED patients. Am J Emerg Med 2009;27:916-921.

His comments confirm what I have suspected for a long time with regard to LBBB in the setting of suspected ACS.

"This is a really interesting and provocative article that may bust the traditional myth that we should be thrombolysing or cathing everybody with chest pain who presents with a new left bundle branch block."

"They found that there was no significant difference in the rate of acute myocardial infarction between patients that were presenting with a new, or presumed new left bundle branch block pattern versus patients with a known old left bundle branch block pattern […] In other words, when patients presented with a new left bundle branch pattern, those patients did not rule-in at any greater increased frequency compared to the other patients, and based on this data the argument is certainly made that when patients have chest pain and they present with the left bundle branch block pattern, there’s not necessary a need purely based on the presence of a new left bundle to assume that that patient is having an acute MI, and therefore that patient needs to get thrombolytics or go immediately to the cath lab."

"As I mentioned before, there is reasonable data to indicate that if the patient has a left bundle branch block – whether it’s new or old – and they demonstrate Sgarbossa criteria, then those patients do end up ruling-in for acute myocardial infarction […] Simple presence of a new left bundle branch block pattern does not appear to warrant immediate activation of the cath lab or immediate thrombolytics according to this study."

Amal Mattu MD does add the caveat that the guidelines still state that patients with new LBBB are supposed to get reperfusion therapy.

See also:

Identifying AMI in the presence of LBBB

False positive cardiac cath lab activations

Review of Factors Associated With False-Positive Emergency Medical Services Triage for Percutaneous Coronary Intervention

Sgarbossa's criteria - new graph

52 year old female "off legs".

2010-01-03T11:47:00.004Z

EMS are called to a 52 yof who has been "off legs" for over 2 months.

This p/t is a diabetic, controlled with Metformin, currently on treatment by her GP for a UTI.

Over the past few months this lady has had reduced mobility and an increasing Shortness of Breath on excertion...

PMH:

Renal problems

Heart problems

Diabetic: (Tablet & diet controlled)

UTI's

Poor mobility

Vital signs:

HR: 154

BP: 134/56

SPo2: 94% on air. 100% via 28% therapy mask

BM: Blood sugar 33 mmol/L

Skin: Dry

Temp: 36.9

What features on the 12 lead ECG captured do you see ?

12 lead ECG captured

94 yof CC: Chest Pain

2009-12-30T15:54:00.000Z

Cross posted to the Prehospital 12-Lead ECG blog.

Here is an interesting case submitted by Billy Eskridge.

EMS is called to an assisted living facility to evaluate a 94 year old female complaining of chest pain.

History of present illness:

Approximately 1 hour prior to EMS arrival, the patient had complained of a headache. A nurse gave the patient a Lortab. About 15 minutes later the patient started complaining of chest discomfort.

The nurse gave the patient two 0.4 mg NTG tablets over 20 minutes with no relief of the chest pain. The patient requested to be seen by a physician.

Paramedic evaluation:

Patient is slightly confused and lethargic but states that she feels "sick all over." The nurse states this is unusual for the patient.

Past medical history:

Complex medical history including hypertension, aortic stenosis, and mitral regurgitation

Vital signs:

Resp: 24
Pulse: 68
BP: 184/72
SpO2: 85 on RA

The cardiac monitor is attached.

A 12-lead ECG is captured.

Here are the computer measurements and interpretive statements.

Billy Eskridge asks the following questions:

Since this patient has an internal pacemaker and wide QRS complexes, is it possible to identify the ST/T changes of ischemia or acute injury?

I have also observed that not every beat is paced, and that there are come supraventricular beats which are also wide complex, showing a LBBB.

I know that there are certain tricks for diagnosing acute MI in LBBB, but I'm not familiar with them.

I am also aware that normal ST changes in wide complex rhythms can be used for diagnosis of MI if an old 12 lead is available to compare the current one to, but is this valid for both paced and supraventricular rhythms with a BBB?

If this rhythm was paces every beat without any apparent conduction abnormality can you scan it for AMI?

Discussion:

In the first place, even though the pacing spikes seem to "disappear" occasionally in the rhythm strip, it shows 100% pacing. I suspect that the pacing spikes are simply lining up perfectly with the lines on the graph paper, but regardless, we can rest assured that it's 100% paced because there is no change whatsoever in the R-R interval or QRS morphology.

In this case, the 12-lead ECG shows a fairly typical looking paced rhythm consistent with a pacing lead in the apex of the right ventricle. Namely, it shows LBBB morphology in lead V1 with a left axis deviation. It also shows negative concordance in the precordial leads, which is a common finding with paced rhythms.

You will note that the ST-segments and T-wave are deflected opposite the main deflection of the QRS complex (which is also the terminal deflection of the QRS complex). This is consistent with a "normal" paced rhythm and the "rule of appropriate T-wave (and ST-segment) discordance" with LBBB or paced rhythm.

Another important finding is that the larger the QRS complex, the more pronounced the secondary ST-T wave abnormality in the opposite direction. This is also true with strain patterns with left ventricular hypertrophy (LVH).

However, there are limits as to the expected amount of discordant ST-segment elevation in the presence of LBBB or paced rhythm.

According to Sgarbossa's Criteria, discordant ST-elevation (that's ST-elevation that is opposite the main deflection of the QRS complex -- in other words, ST-elevation in a lead with a negative QRS complex) > 5 mm is suggestive of AMI.

The problem is that QRS complexes with extremely deep QRS complexes will show more ST-elevation, and that's normal for LBBB and paced rhythm. For example, if you have a QRS complex in the right precordial leads with an S-wave that is 50 mm deep, you can have 5 mm of discordant ST-elevation and the ST-elevation is only 10% the depth of the QRS complex, which is fine.

Dr. Smith and colleagues from Hennepin County Medical Center propose a modified rule for discordant ST-elevation where you look for discordant ST-elevation that is 0.25 (or 1/4) the depth of the QRS complex.

Regardless, this 12-lead ECG shows a normal looking paced rhythm with appropriate T-wave discordance and ST-segments that are normal looking within the context of paced rhythms.

To learn more about Sgarbossa's Criteria and the "rule of appropriate T-wave discordance" see these previous posts:

Identifying AMI in the presence of LBBB - Sgarbossa's Critera - Part I

Identifying AMI in the presence of LBBB - Sgarbossa's Criteria - Part II

57 yom CC: Chest pain

2009-12-27T13:54:00.000Z

Cross-posted to the Prehospital 12-Lead ECG blog

Here's a very interesting case submitted by FF/medic Tim Porter (c/o a faithful reader).

The patient is a 56 year old male with a chief complaint of chest pain.

Onset: Approximately 30 minutes prior to EMS arrival
Provoke: Nothing makes the pain better or worse
Quality: Described as intense pressure
Radiate: The pain does not radiate to the arms, back, neck, or jaw
Severity: 6/10
Time: Unknown whether the patient has experienced previous similar episodes

The patient denies shortness of breath.

The patient's skin is pink, warm, and dry.

Past medical history is significant for cardiac stent 2 years prior.

Medications: unknown.

Vital signs are assessed:

Resp: 18
Pulse: 1oo
BP: 160/90
SpO2: 97 on RA

A 12-lead ECG is captured.

The patient is loaded for transport.

An additional 12-lead ECG is captured en route to the local non-PCI hospital.

Of particular interest to me, in the absence of an obvious STEMI, this paramedic's EMS system allows bypass to a STEMI center when 2 of 5 secondary criteria are present.

They include:

Obesity
Smoker
Hypertension
Diabetes
Prior history

In this case, the patient only had prior history.

So, what is your impression?

More to follow...

60 year old male c/o loss of balance

2009-12-21T10:16:00.004Z

Lead II strip

Pre-hospital 12 lead

12 lead ECG capture in the ED

This 60 year old male patient rang for an 999 emergency ambulance... c/o loss of balance... No other symptoms... On the arrival of the ambulance crew... This 60 year old male greeted them at the door, the patient seemed to be very unsteady on is feet and leaning postural wise to the left.

On examination this patient had a positive FAST test, slight problems getting is words out, slight facial drooping on the left side, and unequal grip strength... Patient denies any aches or pains and states he just wants to go to work for is last day before he retires...

Baseline observations taken from this patient are as follows:

HR: 81 bpm

BP: 135/75

Sp02: 98% on air

Blood sugar: 7.1 mmol/l

Resps: 20

GCS - 15 / p/t fully alert and well perfused (pink)

Temp: 36.7

This patient is normally fit & well... Nil reg meds ever taken... Patient never been diagnosed with any previous conditions.

Patient denies any previous episodes of any chest pain, no N&V, skin was dry, non-sweaty, no visual problems or headache...etc... just unsteadiness on his feet, losing is balance.

What do you think about this patient's ECG's???

Questions:

What does the ECG's show?
What are the likely mechanism of this?
What are the likely causes of this?
What are the key issues in managing this patient?

What's features does this ECG show ?

2009-12-20T16:25:00.000Z

What's features does this ECG show ?

Approach To Arrythmias

2009-12-15T00:18:00.001Z

Check out this SlideShare Presentation:

Approach To Arrythmias

View more presentations from Mari Caban.

The 80 lead ECG

2009-12-11T18:23:00.000Z

ST elevation myocardial infarction (STEMI) is the most serious form of heart attack. The ST segments elevate because the full thickness of heart muscle is injured (transmural injury). This full thickness injury and ST elevation is the result of a total occlusion of a coronary artery. Some STEMIs, particularly those involving the posterior or back surface of the heart, may be missed by the present traditional system of placing a limited number of leads on the front of the chest.

In contrast to the 12 leads of data and the limited anterior or front view of the heart from a traditional ECG, an 80 lead ECG (such as the PRIME ECG®) utilizes 80 leads placed on both the front and back of the patient to analyze a 360-degree spatial view of the heart. This new technology may allow the more rapid and accurate detection of STEMI and thereby potentially speed the delivery of care.

Analysis is performed on a computer selected representative beat. ST-segment elevation and depression are translated into colors (red = elevation, blue = depression) and displayed against a 3 dimensional torso image for physician review. These images allow for rapid pattern recognition that identifies problem areas that correlate with regions of ischemia or infarction. This use of graphic imaging allows the physician to quickly focus on specific ECG morphology that contains the most valuable diagnostic information without having to expend time exploring data from all 80 leads. System software facilitates examination of the actual ECG trace for each of the 80 recordings. The user places a cursor over the suspect area and a pop-up window reveals the underlying electrode tracing and provides the value of elevation or depression at that lead. Ten years of clinical data and in-hospital experience have demonstrated an increase in sensitivity over the 12 lead ECG in the range of 18% with no loss in specificity. As a result, there is the potential to detect up to 40% more ST Elevation MIs (serious heart attacks) than the traditional 12-lead ECG.

Registry data from the National Registry of Myocardial Infarction (NRMI), CRUSADE and GRACE have demonstrated that there are significant opportunities for improvement in door-to-balloon time and door-to-needle time in the management of serious heart attacks (STEMI). The 80 lead ECG may provide a technological advance that would speed the correct diagnosis of ST elevation MI. A substantial number of patients have a non-diagnostic 12-lead and these patient may wait for extended periods in the emergency room pending the results of enzymes released into the bloodstream (biomarkers) to diagnose a heart attack.

Heart attacks involving the back side of the heart may cause ST depression rather than ST elevation (STEMI) becuase the pattern of electrical injury is reversed on the traditional 12 lead ECG. One of These patients may currently be receiving less aggressive care because of a diagnosis of non-ST-elevation MI (NSTEMI) based on ST-depression, which may in fact be ST-elevation in a portion of the heart not visible with the 12 lead. Assuming approximately 20-30% of diagnosed MI patients are now diagnosed as STEMI patients and 70-80% are diagnosed as NSTEMI, the PRIME data would indicate that approximately 1 in every 3 patients may be in fact a higher risk category and be suitable for more aggressive care.

A nurse places an 80 lead EGG on a patient

Shown to the right is the 12 lead ECG in a patient that presented with substernal chest pain. Note that there are non diagnostic changes. There is no evidence of ST segment elevation.

An 80 lead ECG vest was then placed. Shown to the right are the 80 EKG lead tracings displayed individually. The anterior leads are displayed on the left had side. The posterior or back of the heart leads are displayed on the right hand side of the figure. For instance lead 68 shows ST elevation. Posterior and right-sided leads reveal ST-elevation, where the 12-lead was silent.

In order to display the data in a more clinically relevant and intuitive fashion, the area of injury is shown in red on the patient's back, corresponding to the inferior-posterior location of the MI.

Cardiovascular disorders in children

2009-12-08T17:02:00.001Z

04 2 25 Cardiac新2009

View more presentations from deepak15.

48 year old male... Post PEA cardiac arrest.

2009-12-08T13:55:00.001Z

EMS called to an 48 year old male, found collapsed on the floor with a GCS of 3, clinical presentation & observations are showed as follows:

Resps 6 per min
Pale and diaphoretic
HR: - 74
BP: - 70/49
GCS - 3
Sp02: 89%, 100% achieved after ventilation using B.V.M
Blood sugar: - 4.1 mmol/I
Not on any regular meds, and no relevant medical Hx
Patient been fit & well up to this time

Patient was ventilated using a B.V.M on 100% O2, IV access obtained, carotid pulse was felt: which was absent, CPR was then commenced on the patient and BLS & ALS skills performed... 1st ECG capture as shows below:

ECG - 1: Patient in PEA.

ECG - 2 capture follows the one above, after return of circulation, post arrest, note the patient's blood pressure now on the top of the ECG strip.

12 - lead ECG capture on route to hospital after return of spontaneous circulation (ROSC).

This patient is now fully recovered and left hospital a week later, the medical staff at the hospital, gave the following explanations on what could have happen to this patient, do you agree with their thoughts: