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Using capnography to confirm capture with transcutaneous pacing (TCP)

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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: Unconscious (Transcutaneous pacing failure in the setting of hyperkalemia)

Transcutaneous pacing (TCP) for asystole

58 year old male CC: Chest pain

20 comments

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?

*** UPDATE ***

This 12-lead ECG was captured en route to the hospital.

And finally this rhythm strip.

Does this shed any light on the mechanism behind the wide complexes?

Rhythm Challenge #5 – Answer

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Here is the solution to Rhythm Challenge #5.

The rhythm is paced and here’s why.

As I explained in Evaluating the Pacemaker Patient – Part I, most modern pacemakers are DDD pacemakers according to the NBG pacemaker code.



Essentially that means that most pacemakers will “track” P-waves and deliver a paced QRS complex (when no native QRS complex appears) after a prescribed PR interval to take advantage of the “atrial kick” and the associated improved hemodynamics.

However, there is a limit. As you might expect, cardiologists don’t want the device to track P-waves and supply paced QRS complexes when the atrial rate goes up to 300 as it does during atrial flutter. That would not be in the patient’s best interest. So there’s an upper rate limit.

Let’s say the cardiologist wants a pacemaker to track a patient’s P-waves but he doesn’t want the paced rhythm to exceed 136 BPM. How can this be achieved? By a parameter called the PVARP or Post-Ventricular Atrial Refractory Period. That means that a pacemaker will “close its eyes” for a prescribed interval after each QRS complex, whether it’s a native QRS complex or a paced QRS complex. In other words, it will ignore P-waves during that period of time.

All of the ECGs in Rhythm Challenge #5 can be explained by a PVARP set for approximately 440 ms or 11 small blocks, which is a heart rate of about 136.

Let’s look at a graphic to see how this played out from the pacemaker’s point of view.

As you can see, when a P-wave falls outside of the PVARP the device waits for a prescribed PR interval and then creates a paced QRS complex if a native QRS complex does not appear first. P-waves that fall inside the PVARP are ignored by the pacemaker.

In other words, this is normal pacemaker behavior! Having said that, the only way to know for sure is to identify the exact type of pacemaker (the manufacturer and model), the indication for the pacemaker, how the pacemaker is programmed, and to read the report after the device is interrogated.

Rhythm Challenge #5

17 comments

@S_Cook_EMTP contacted me on Twitter with regard to a 77 year old male with an interesting heart rhythm.

He subsequently took a picture of the ECG and emailed it to me with this description:

77 yo male with history of COPD, CHF. Initial 4-lead EKG reveals A-Flutter with variable response: 2:1, 3:1, 4:1, and 5:1 is what I saw. Patient would have runs of both bi and trigeminal PVCs then settle back to A-Flutter in the 80s/90s. Then patient developed 20-30 second runs of the attached that ran from ~100BPM to 225BPM.

Best I can think is this is a run of V-Tach. Patient does have an implanted pacer/defib, but relates he hasn’t felt it fire.

Up to about 130 to 140, electrical rate and radial rates were equal.

Otherwise, patient was hemodynamically stable, BPs in the 120s/70s, A&O X 4, with some difficulty breathing.

Patient was recieveing an A&A neb treatment. Initial SaO2 was 75, increasing to 98 during treatment. Heavy smoker. Denies any and all pain and relates he “just feels like $%^*”

Here’s the picture of the ECG in question.

What do you think this heart rhythm is showing?

After I gave my answer, @S_Cook_EMTP shared the following ECGs from the same case, indicating that the treating emergency physician did not agree with my assessment.

However, I still think I’m right!

Of course, I could be wrong (we’ll discuss that a little bit more later).

So, for the sake of Rhythm Challenge #5, to what do you attribute this wide complex tachycardia and why?

See also:

Rhythm Challenge #5 – Answer

Previous “rhythm challenges” can be found here:

What’s the heart rhythm?

Rhythm challenge #1

Rhythm challenge #2

Rhythm challenge #3

Rhythm challenge #4

Rhythm challenge #4 – Discussion

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

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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

60 year old male CC: Syncope

18 comments

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 12/10/2010 ***

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

29 comments

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

29 comments

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?

*** Update 12/13/2010 ***

What Christopher and I both found unusual about this case is that the GE-Marquette 12SL interpretive algorithm was not giving the ***ACUTE MI SUSPECTED*** message, even though it was giving messages like “ST-elevation consider anterolateral or acute infarct” and “inferior injury pattern” which I had always thought automatically trigged an accompanying ***ACUTE MI SUSPECTED*** message.

This is especially important because some EMS systems require the ***ACUTE MI SUSPECTED*** message in order for paramedics to bypass the local non-PCI hospital for the STEMI Receiving Center!

So, I contacted a friend at Physio-Control who put me in touch with the person responsible for the computerized interpretive algorithm. He was also surprised that the ***ACUTE MI SUSPECTED*** message was not present on these 12-lead ECGs. So he turned to a “veteran 12SL designer”.

Together they figured out the problem.

Mystery solved! The 12SL expert said that the 12SL algorithm would definitely give the Acute MI statement for the first cse that you sent me. So I turned to the setup choices (LP12 Operating Instructions, chapter 9). One of the setup menu items is “ACUTE MI”. The description is “Print Acute MI message”. Further explanation says, “ON: Prints on the 12-lead reports when criteria are met.”

I think that the LP12 is set up with the ACUTE MI option turned off. I suggest that you get back to the customer and have them turn ACUTE MI on in the setup menu for this LP12 and any others that they have.

So, if you have a Lifepak 12 and you’re not receiving the ***ACUTE MI SUSPECTED*** message for obvious acute STEMIs, you might want to check this parameter.

LIFEPACK 12 Defibrillator/Monitor – Operating Instructions

Conclusion to EMS1.com case study “Changing Channels”

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Part II of my introductory column at EMS1.com has been posted. Enjoy!

Changing Channels: Patient follow-up.

43 year old female CC: Chest pain

40 comments

Don’t worry, I haven’t forgotten about the 73 year old female CC: Chest pain.

The conclusion will be posted as soon as it’s available. In the meantime, here’s another case for you to ponder.

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?

See also:

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

73 year old female CC: Chest pain

29 comments

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?

See also:

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

63 year old male CC: Syncope – Conclusion

5 comments

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

30 comments

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?

See also:

63 year old male CC: Syncope – Conclusion

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

15 comments

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:

  1. Insignificant epicardial coronary artery narrowing in a right dominant system.
  2. Congenitally absent left main (normal variant).
  3. Severely reduced left ventricular systolic function, left ventricular ejection fraction 35% with a large anterolateral and apical area of akinesis. The apex is aneurysmal.
  4. 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

9 comments

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?

See also:

76 year old female CC: Chest pain

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

76 year old female CC: Chest pain

13 comments

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.

What should the paramedics tell her and why?

*** Update 09/06/2010 ***

By request, here are the serial prehospital 12-lead ECGs for the case.

See also:

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

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

37 year old male CC: “Light-headedness” – DISCUSSION

2 comments

This is the discussion for the case study: 37 year old male CC: “Light-headedness” (posted earlier this week).

Here’s the question asked by the paramedic who submitted the case.

“The first 12 lead ECG shows Q-waves in the inferior leads. Perhaps this isn’t a surprise considering the patient’s history of MI. But what about the flipped T-waves? Do prior MIs flip the T-waves at all?”

Answer: Yes.

Consider the following graphic.

Granted, the patient states his MI was 2 years ago, but in my experience the T-wave does not always recover.

Now I’d like to address those of you who are questioning why Brian H. et al. suspect the possibility that a stent in the RCA is re-occluded. I have to admit, I didn’t see these very subtle findings until they were brought to my attention. That’s probably because I focused on the question that was asked.

Speaking of which, has anyone read The Invisible Gorilla?

Before I go further, I am not saying this ECG shows a STEMI. I’m saying this ECG is very suspicious.

Take a look at the following graphics.



Once again I will invoke Tomas Garcia MD’s rule to “consider the company” any ECG abnormality keeps.

If we accept the possibility that the Q-waves and inverted T-waves in the inferior leads are this patient’s “normal” baseline then we need to amend our approach slightly.

You can see that the ST-segments and T-waves in lead aVL are “pulled down” (flat ST-segments and smaller T-waves) at 21:31:30.

Whenever I see flat T-waves in the high lateral leads I get suspicious! This is often the earliest indication of acute inferior STEMI. The reciprocal changes usually come first according to computer modeling and my own anecdotal experience.

By 21:49:05 this finding disappears. One has to wonder if this is due to oxygen and nitroglycerin!

I realize that no one is disputing this patient is most likely experiencing ACS. The question on the table is whether or not this could be an early STEMI.

Let’s move on to lead III.

These ST-segments are also flattening at 21:31:30, but they appear to be “flattening” in the wrong direction! I say this because the depth of the T-wave is less. In other words, this could be early pseudo-normalization of a baseline inverted T-wave.

What does that mean? It means that if your baseline T-wave is inverted, acute STEMI can “recover” the T-wave prior to ST-segment elevation. That’s why this finding is suspicious.

The finding disappears by 21:49:05.

It’s the reciprocal nature of the changes viewed in leads III and aVL that is troubling!

Finally, let’s look at the right precordial leads V2 and V3.

You can see that the ST-segments are depressed at 21:31:30 and back to normal by 21:49:05. Again, this is troubling because ST-depression in the high lateral leads and the right precordial leads frequently accompanies acute inferior STEMI.

Would an “old” ECG help for comparison? Without question!

The paramedic who submitted the case is attempting to follow up on the case. I’m sure you’d all be interested in the final diagnosis.

37 year old male CC: “Light-headedness”

19 comments

I received an excellent question this week from a reader who chooses to remain anonymous.

Before we get to his question (and my answer) let’s take a look at the case that prompted the question.

EMS is called to the residence of a 37 year old male c/o “light-headedness”.

Upon EMS arrival the patient is found lying supine on a bench. He is still “light-headed”, appears diaphoretic and also complains of “chills”.

Editor’s side-note: I hope this would be enough for anyone reading this to perform a 12-lead ECG, regardless of the medical history.

The patient denies shortness of breath or chest pain/discomfort.

The patient admits to some nausea but has not vomited.

No feelings of arm heaviness or tingling.

Past medical history is significant for MI x2 years ago which required a stent being placed.

Disturbingly, the patient reports that today’s symptoms remind him of the symptoms he experienced 2 years prior.

Vital signs are assessed.

RR: 20
HR: 92 R
BP: 162/88
SpO2: 100 RA

Breath sounds are clear bilaterally.

A 12-lead ECG is captured.

A second 12-lead ECG is captured en route to the hospital.

What is your impression?

See also:

37 year old male CC: “Light-headedness” – DISCUSSION

71 year old male CC: Seizures

59 comments

EMS is called to the residence of a 71 year old male for seizures.

On arrival the patient’s spouse meets the ambulance outside and hurries the paramedics along saying “Come quickly! Please help him!”

The paramedics arrive at the patient’s side just in time to see him receive an ICD shock.

They ask how long this had been going on.

“That was my 15th shock!”

The patient states that he “felt himself going faint” just prior to the first shock.

The cardiac monitor was attached and the following rhythm strips were recorded.


How would you proceed?

*** Update 08/22/2010 ***

The patient appears anxious.

Skin is pink, warm, and moist.

The patient has numerous skin tears in his arms which the spouse states are related to convulsions induced by the ICD shocks.

Vital signs are assessed.

Resp: 20
NIBP: 108/72
Pulse: 60 and irregular
SpO2: 98 on RA

Past medical history:

The EMS crew learns that this patient survived two sudden cardiac arrests prior to receiving his first ICD in 1992. The device was replaced in 2008. The patient does not have his device ID card but knows that it was made by St. Jude Medical.

Medications:

The patient states he takes several medications but he can only remember one of them: Coumadin.

The patient is placed on 100% oxygen.

The EMS crew contacts Online Medical Control and receives permission to apply a ring magnet to the device. The magnet is applied and taped in place. The tape doesn’t hold and a FF is assigned to hold the magnet over the device pocket.

A 12-lead ECG is captured.

And another.

The rhythm appears more stable on the monitor.

The patient is loaded for transport.

IV access is achieved.

En route the the hospital serial 12-lead ECGs are captured.

Vital signs are re-assessed.

Resp: 18
Pulse: 75 and slightly irregular
NIBP: 102/70
SpO2: 100 w/ oxygen via NRB @ 15 LPM

The patient feels much calmer and says, “Please don’t let that thing shock me again.”

This 12-lead ECG was captured on arrival at the hospital.

What do you think of the way this EMS crew handled the call?

What do you think the patient would say was the most important thing the EMS crew did for him?

See also:

Inappropriate or ineffective ICD shocks – Part I

Inappropriate or ineffective ICD shocks – Part II

Inappropriate or ineffective ICD shocks – Part III

81 year old female CC: ICD shocks x6

79 year old female CC: Unresponsive

27 comments

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?

*** UPDATE ***

Here are some additional 12-lead ECGs.

58 year old male CC: Chest discomfort

8 comments

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?

54 year old male CC: Chest pain – Discussion

4 comments

This is the discussion for 54 year old male CC: Chest pain.

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

19 comments

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?

See also:

54 year old male CC: Chest pain – Discussion

69 year old male CC: “Indigestion”

16 comments

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.

What is your impression?

*** UPDATE ***

The patient lost consciousness and the monitor showed ventricular fibrillation. A shock was delivered at 200J.

The patient experienced return of spontaneous circulation.

A few minutes later the heart rhythm returned to baseline.

Emergent cath revealed 100% occlusion of the LAD.

79 year old male CC: Shortness of breath

19 comments

Here’s another interesting case submitted by Geoff Dayne.

79 y/o male c/o non-provoked SOB without CP.

Patient was found sitting upright, tripodding, 1 word dyspnea.

Lung sounds: extremely decreased tidal volume. EMS crew was unable to tell if there was rales or wheezing.

Past medical history: HTN, dyslipidemia, CHF, pacemaker (recently implanted within a week or so), diabetes, emphysema.

Drug allergies: Sulfa

Current meds: Glipizide, Omerprazole, Hydralizine, Lovastatin, Lasix, Albuterol

Vital signs:

B/P: 154/84
Pulse: 134 Strong/Irregular
Resp: 30
SpO2: 84 on RA

They treated w/ O2 and put him on the patient’s home BiPAP and transported.

A 12-lead ECG was captured.



And a rhythm strip.



I think this case is an excellent example of the real-life difficulties paramedics face in the field when it comes to the triage of possible ACS patients.

What would you do next as the treating paramedic?

See also:

Identifying AMI in the presence of LBBB – Sgarbossa’s Criteria Part I

Identifying AMI in the presence of LBBB – Sgarbossa’s Criteria Part II

Discordant ST-segment elevation in LBBB or paced rhythm

Found on the Lifenet Receiving Station (LBBB with concordant ST-depression in leads V3 and V4)

62 year old male CC: Chest pain (LBBB with ST-elevation > 0.2 the QRS complex)

58 year old female CC: Chest pain

58 year old female CC: Chest pain – Conclusion (meets all 3 of Sgarbossa’s criteria)