The conclusion to “The path (more) traveled” has been posted.
Did you recognize the rhythm as AF/WPW?
This is one situation where a CCB could be the last medication a patient receives!
Enjoy!
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Here’s a really interesting ECG submitted by my good friend David Hildebrandt.
EMS is called to an assisted living facility for an 88 year old female who is weak and complaining of chest pain.
The patient is found lying on her side in bed.
She appears acutely ill and states she is nauseated.
She is oriented to first and last name and place, but not the day of the week. However, she knows it is 2011 and that Obama is the POTUS.
Past medical history: HTN, CHF, CVA x 4 years ago, osteoporosis, L hip replacement
Medications: Lopressor, Capoten, Lasix
Skin is cool and clammy.
2/4 pitting edema is noted in both ankles which the CNA states is normal for her.
Breath sounds: mostly clear (slight rales)
Vital signs are assessed:
RR: 20
Pulse: 60
NIBP: 150/68
SpO2: 96 on RA
The cardiac monitor is attached and shows sinus rhythm.
A 12-lead ECG is captured.
What is your impression of this ECG?
How would you treat this patient?
See also:
This is the conclusion to 49 year old male CC: Chest pain.
Let's take another look at the 12-lead ECG (the one with lead V4 in the position of right-sided lead V4R).
I was wondering if anyone would notice that I've shown this ECG before. It's from my 3-part tutorial on right ventricular infarction. Specifically it's from Part III.
I had thought the original ECGs were lost but I found them in a folder when I was cleaning out my guest bedroom last week.
So let's take a look at the 12-lead ECG.
At first glance, ST-elevation is clearly present in leads II, III and aVF. ST-elevation is also present in leads V5 and V6.
The R/S ratio is > 1 in lead V2 which could suggest posterior infarction.
What appears to be hyperacute T-waves in the right precordial leads (and lead V2 in particular) could represent so-called posterior reperfusion T-waves secondary to a precarious clot.
So why isn't this ECG a slam dunk?
The thing that makes this ECG both unusual and difficult is the lack of reciprocal changes in the high lateral leads I and aVL.
Consider this comment by Stephen Smith, M.D. (from Dr. Smith's ECG Blog) on the EMCrit podcast.
"…we looked at 160 consecutive inferior STEMIs proven by angiographic occlusion…in 99% of all those occlusions there was either ST-depression or T-wave inversion in lead aVL…"
The absence of ST-depression or T-wave inversion in lead aVL in the setting of acute inferior STEMI is unusual.
Does that mean that no reciprocal changes are present on this ECG?
That depends on whether or not you're willing to accept leads aVR and V1 as reciprocal changes. Some authors contend that these leads should be considered.
Unfortunately, you can also have ST-depression in leads aVR and V1 with pericarditis.
Cases like this are difficult because they don't follow the expected pattern. But sometimes they're still sick patients who require immediate reperfusion!
This patient was in fact experiencing an acute STEMI.
The culprit artery was the circumflex (LCX).
From the archives.
EMS is called to the vacation residence of a 49 year old male complaining of chest pain.
On arrival the patient is found sitting at the kitchen table. He appears anxious and acutely ill.
Past medical history: Healthy
Meds: None
Allergies: NKDA
Skin is cool, pale and diaphoretic.
He confirms that he is experiencing chest pain.
Onset: Sudden while moving furniture 30 minutes prior to contacting 9-1-1
Provoke: Nothing makes the pain better or worse
Quality: “Crushing”
Radiate: The pain does not radiate
Severity: 10/10
Time: No previous episodes
Breath sounds are clear bilaterally.
No JVD or pitting edema.
Vital signs are assessed.
RR: 20
Pulse: 50
NIBP: 138/79
SpO2: 98 on RA
The cardiac monitor is attached.
Sorry about the fading but this is what happens to ECGs over time (which is why they need to be copied or digitally scanned to preserve them for posterity).
A 12-lead ECG is captured.
A second 12-lead ECG is captured with lead V4 in the position of V4R.
Do you think this patient is having a STEMI?
Why or why not?
Describe how you would treat this patient and why.
See also:
This is the conclusion to 74 year old female CC: Chest pain.
As usual I enjoyed reading the comments! My goal is to get you guys thinking and it’s nice to see you discuss “stable versus unstable”, the need for sedation, and the importance of considering the Hs and Ts!
Let’s take another look at the 12-lead ECG.
This is an unstable wide complex tachycardia which we must presume to be ventricular tachycardia.
We presume it is ventricular tachycardia because that is our default ECG diagnosis for “wide and fast” rhythms.
The fact that she has a history of MI makes VT all the more likely.
We need to avoid the temptation to over-think heart rhythms like this! As much as 12-lead ECGs have advanced the EMS profession, this is one small area where we have taken a step backward, IMHO.
Before 12-lead ECGs a “wide and fast” rhythm like the one you see above was VT. Now you can’t turn around without someone labeling a clear-cut case of VT as “SVT with aberrancy.”
However, in this case (hopefully) the debate is irrelevant because the patient is unstable.
Why?
Because the patient is experiencing chest pain, radial pulses are absent, the patient looks “shocky” and the level of consciousness is diminished.
Immediate synchronized cardioversion is indicated. That’s exactly what this crew decided to do.
About a minute later the rhythm started to stabilize.
What should the crew do next?
If you said, “Obtain a 12-lead ECG!” move to the head of the class!
Now we have some insight as to why this patient was in VT!
Vital signs are re-assessed.
RR: 20
Pulse: 86
BP: 138/92
SpO2: 100 with O2 via NRB @ 15 LPM
If this was your patient what would you do next?
Here’s another great case from Michael M.
EMS is called to the residence of a 74 year old female with a chief complaint of chest pain.
On arrival the patient is found lying on her side in bed. She is conscious but lethargic and it’s clear she has vomited.
Skin is cool, pale and diaphoretic. She looks very ill.
The spouse states that he “thinks it’s her heart.”
Past medical history: MI x 3 years ago with stents, HTN, high cholesterol
Meds: ASA, atenolol, simvastatin, spironolactone
Vital signs are assessed.
RR: 24 shallow
Pulse: radial absent, carotid very rapid
NIBP: unable to auscultate
SpO2 does not register
The cardiac monitor is attached.
Is there anything else you’d like to know about this patient?
What is your interpretation of the ECG?
How would you treat her and why?
See also:
This is the discussion for 50 year old male CC: Chest pain.
You may recall that the patient started experiencing chest pain during sexual intercourse.
Many of you were appropriately concerned about the possible use of drugs for erectile dysfunction that would contraindicate nitroglycerin! Thanks for pointing that out.
In this case the patient was not taking any medication for erectile dysfunction.
Let’s take another look at the 12-lead ECG.
This ECG shows an essentially regular rhythm with no clearly discernible P-waves and wide QRS complexes (but not > 180 ms) at a rate of about 90.
The morphology of the QRS complexes are somewhat unusual, especially in the right precordial leads. If this is a supraventricular rhythm I would call it a non-specific intraventricular conduction defect or atypical left bundle branch block.
Regardless of what kind of conduction delay is present (even if it’s an accelerated idioventricular rhythm) we know that the depolarization is abnormal. T-wave discordance is present throughout the majority of the 12-lead ECG.
So does anything look like an acute injury pattern? Absolutely!
Let’s take a look at high lateral leads I and aVL.
Here we can see significant ST-elevation that is concordant with (in the same direction as) the majority of the QRS complex. It is also concordant with the terminal (last) wave of the QRS complex.
That’s bad! We have already satisfied one of Sgarbossa’s criteria to identify acute STEMI in the presence of left bundle branch block (LBBB).
Another feature worth pointing out is that leads I and aVL show pathological Q-waves.
Now let’s look at inferior leads III and aVF.
Even taking into account the wandering baseline and artifact we can appreciate concordant J-point depression.
Is this concerning? Yes!
Why?
Because of the ST-elevation in the high lateral leads. In the words of Tomas Garcia, M.D., one must always consider the company an ECG abnormality keeps.
Lead’s III and aVF are reciprocal to leads I and aVL. So the fact that ST-depression (or at least J-point depression) is present in two inferior leads while ST-elevation is present in the high lateral leads is troublesome.
How troublesome?
Troublesome enough for me to call this an acute STEMI.
Now let’s look at the right precordial leads.
Once again we see concordant J-point (and ST-segment) depression in leads V1-V3. Is this concerning? Absolutely! In fact this meets another of Sgarbossa’s criteria.
Finally, we can appreciate ST-elevation in leads V5 and V6 in spite of the wandering baseline there.
I can’t tell you what heart rhythm this patient is in but I feel confident we’re looking at an acute injury pattern.
So what was the outcome?
Unfortunately, this patient experienced cardiac arrest on arrival at the hospital and was not successfully resuscitated (which is more evidence that it was an acute STEMI).
See also:
Here’s a really interesting case submitted by “Anonymous from Ann Arbor, Michigan.” Wolverines! 
Sorry, Buckeyes.
EMS is called to the residence of a 59 year old male with a chief complaint of chest pain.
Past medical history: Dyslipidemia
Meds: Zocor
The patient was given 600 mg ASA by the spouse prior to EMS arrival.
Onset: Fairly rapid during sexual intercourse
Provoke: Nothing makes the pain better or worse, not reproducible on palpation
Quality: Described as pressure
Radiate: Right arm
Severity: 5/10
Time: 30 minutes prior to EMS arrival, no previous episodes
Patient is alert and oriented to person, place, time and event.
Skin is pink, warm and moist.
Breath sounds: clear bilaterally
No JVD or pitting edema.
Vital signs are assessed.
RR: 22
Pulse: 80
BP: 124/84
SpO2: 99 on RA
BGL: 134
The patient was placed on the cardiac monitor and a 12-lead ECG was captured.
What is going on with the patient?
How would you treat the patient and why?
See also:
This is the follow-up and discussion for 85 year old female CC: Respiratory distress. As usual, thank you for all the insightful comments!
The case demonstrates some very important points not the least of which is that the differential diagnosis of shortness of breath can be difficult, even for emergency physicians who have access to chest x-rays and blood tests like the BNP / NT-proBNP.
It also shows why paramedics need to think more more clinicians and less like technicians! Some of us were taught that we “only treat symptoms” but there’s a big difference between treating the shortness of breath associated with asthma or COPD versus CHF versus a tension pneumothorax.
When a patient like this one has co-morbidities it’s not always straight-forward. As some of you mentioned in the comments, it’s entirely possible to have overlapping COPD and CHF. For this case, COPD certainly played a role (how could it not when it’s part of the patient’s history?) but the patient was also in severe acute pulmonary edema.
As some of you also mentioned, acute pulmonary edema can lead to reflex airway spasms that cause wheezing (so-called “cardiac asthma”). In this case, the paramedics placed the patient in high-Fowlers, gave SL NTG, placed the patient on CPAP, and gave an in-line nebulizer treatment. After several minutes the patient was moving enough air for them to appreciate crackles bilaterally in all lung fields.
Let’s take another look at the 12-lead ECG.
I’ve seen this computerized interpretation several times and I always find it a bit confusing because to me, this ECG meets all of the criteria for left bundle branch block (i.e., supraventricular rhythm with a QRS duration > 120 ms, rS complex in lead V1 and a monomorphic (but notched) R-wave in lead I) .
It would be interesting to know why the computer calls it left ventricular hypertrophy with QRS widening.
So what is the rhythm? Based on the appearance of flutter waves in lead V1 I would call this atrial flutter, although it’s entirely possible for a heart rhythm to switch back and forth between atrial flutter and atrial fibrillation. On the cardiac unit we used to call this “fib-flutter” and it’s pretty common.
In this image we can see flutter waves in lead V1 (blue arrows). rS complexes are present in lead V1 and the red dotted lines show where I am measuring the QRS duration.
Here we can see monomorphic R-waves in leads I and V6 (lead I shows an rR’ complex). To me this clinches the ECG diagnosis of left bundle branch block. Your mileage may vary.
So, we all know that new onset pulmonary edema is ACS until proven otherwise.
Could this ECG show acute STEMI in the presence of LBBB?
Lead V3 shows greater than 5 mm of discordant ST-elevation which is cause for concern. However, we don’t know if the ST-segments are excessively discordant when taking into account the depth of the S-wave because the S-waves are cut off by the bottom of the ECG paper.
Fortunately, the ECG was transferred over the LIFENET and that ECG does show the depth of the S-wave.
With calipers, the S-waves in lead V3 measure about 60 mm deep. Using a ST/QRS ratio of 0.2 as a cut-off, we would require at least 12 mm of ST-elevation in lead V3 to be significant for this patient!
She ruled-out for acute myocardial infarction.
EMS is called to a local nursing home for a 85 year old female with a chief complaint of respiratory distress.
On arrival the patient is found lying in bed in obvious distress.
Respirations are 40 and shallow with a prolonged expiratory phase and accessory muscle usage.
Auscultation of the chest reveals a poor tidal volume with tight expiratory wheezes.
There are signs of cyanosis around the mouth and nail beds.
The patient appears weak and listless.
Past medical history: CHF, COPD, NIDDM, Breast CA, Depression
Medications: Numerous
Vital signs are assessed.
RR: 40
Pulse: 130 and irregular
NIBP: 170/91
SpO2: 74
The patient’s external jugular veins appear prominent but the patient is lying flat.
A 12-lead ECG is captured.
What is your interpretation of this ECG?
What do you think is wrong with the patient?
What is your treatment plan?
See also:
Part I of the April 2011 EMS 12-Lead column is now posted at EMS1.com.
The Path (More) Traveled – Part I
Enjoy!
Many apologies for the delay, your author worked a 48 over the weekend and was unable to get time to type up this article!
This is the conclusion to 78 year old male CC: Dizziness.
There were so many great comments on this case, including some great discussion on classifying wide complex tachycardias!
The first rhythm strip clearly shows a wide complex tachycardia. An important point to note is the rate is well above the predictive maximal sinus rate for our patient’s age. This rules out sinus tachycardia with a bundle branch block. At this point, providers may ask themselves if this is Ventricular Tachycardia or SVT with aberrancy.
If we take a look at the 12-Lead ECG, we can look for signs which rule-in Ventricular Tachycardia.
We have a QRS duration of ≥140 ms, amplitude of R > R’ in V1, a non-specific IVCD, and an R wave in aVR; all of these point to Ventricular Tachycardia. Additionally, the patient has a significant cardiac history. Some readers noted the normal axis and what potentially are P- or F-waves. I would offer that these points are moot: from this ECG alone we cannot rule-out Ventricular Tachycardia.
Wide and fast is Ventricular Tachycardia until proven otherwise.
Besides, our patient is unstable and needs immediate synchronized cardioversion.
Which is just what the crew did! Given the potential for atrial flutter, the initial cardioversion setting was 50 J. With no conversion they increased the energy to 100 J.
No change was noted. A supervisor on scene mixed up 150 mg of amiodarone and began a 10 minute infusion. After no change with two cardioversions, the decision was made to move the patient to the unit.
In the back of the truck a sudden change of responsiveness was noted. The energy setting was increased to 150 J.
At 150 J the cardioversion was successful!
The post-cardioversion 12-Lead showed diffuse ischemia and the patient ended up receiving an Automatic Implantable Cardioverter-Defibrillator. Great job by the responding crew!
UPDATED 12 APRIL 2011
Jeremy asked how the QRSd was measured in this case. Usually I try and find the earliest onset and match that with the latest end in a grouping of leads, then use the largest value to map each grouping. The following image may help illustrate this point.
I first saw this visualization on Dr. Smith’s ECG Blog, where he uses it for more than just determining the QRS duration in “Cardiac Arrest, Wide Complex, Is it STEMI?” and “Wide Complex Tachycardia; It’s really sinus, RBBB + LAFB, and massive ST elevation”.
See Also:
Differential diagnosis of wide complex tachycardias – Part I
Differential diagnosis of wide complex tachycardias – Part II
Differential diagnosis of wide complex tachycardias – Part III
Differential diagnosis of wide complex tachycardias – Part IV
Differential diagnosis of wide complex tachycardias – Part V
Differential diagnosis of wide complex tachycardias – Part VI
Podcast: Play in new window | Download
In this special episode of the EMS Research podcast Tom Bouthillet and Tim Noonan (RogueMedic) interview Dave Hiltz (Heart Safe Community) and Lynn White (Heart Rescue Project) about best practices to optimize survival from sudden cardiac arrest.
Download the full episode at the ProMed Network here.
Hot on the heels of the last case is another great case study, this one is from a reader named Baby Medic. I hope you enjoy it!
It is a busy Halloween night, when you and your EMT partner are dispatched to an outlying address in your service area for a 78 year old male complaining of dizziness.
After navigating a mess of rural farm roads, you arrive at a small house off a long dirt driveway. Out front you are met by the patient’s wife, who frantically directs you inside and down to the basement. There you find your patient, a noticeably larger man, sitting in a recliner with one hand on his chest. As your partner kneels down to obtain vitals, you ask him what is going on.
Onset: Chest pain started about 15 minutes ago, while watching TV
Provocation/Palliation: Nothing makes it better or worse
Quality: “Something is pushing on my chest”
Radiation: The pain is only localized retrosternal
Severity: 10 of 10
Timing: The pain is constant
Your partner briefly interrupts to say he cannot find a radial pulse. You continue with your history.
Allergies: NKDA
Medications: He can’t remember (you send his wife to find them)
Past Medical History: Extensive cardiac history, including CABG, HTN, and he was recently discharged from the hospital after carotid artery surgery
Last Ins/Outs: Normal dinner
Events: “Sitting in my chair, watching TV, got real dizzy and then the pain started.”
Your partner anxiously relays the patient’s vitals while he attaches the cardiac monitor.
Pulse: Could not palpate a radial pulse
BP: 82/54
RR: 24, labored; lungs clear and equal bilaterally
SaO2: Beeps and displays E34
A physical exam reveals no JVD, a soft, non-tender obese abdomen, and good pulse/sensory/motor in all extremities. The only remarkable feature is dusky, cool, diaphoretic skin.
An alarm sounds on the cardiac monitor as the initial rhythm strip is printed.
Your partner acquires a 12-Lead ECG while you interpret the rhythm strip.
What rhythm is present? Does the 12-Lead ECG help with your interpretation?
You’re 20 minutes from the nearest hospital and 45 minutes from a PCI capable facility. How would you treat this patient?
This is the conclusion to 54 year old female CC: BLS intercept.
I did not expect to get so many comments! Great discussion on many points. It even afforded an opportunity to review atrioventricular blocks.
Going back to the case let’s look at the initial 12-Lead ECG.
As many readers noted, there is a lot of baseline wander. This is not the most helpful of 12-Leads. On scene the crew attempted multiple 12-Leads, however, the patient would not sit still and that was the best one.
I think a close look at the Initial 12-Lead has enough information to make a field diagnosis.
Leads III and aVF have subtle ST-elevation and Q-waves, which without any cardiac history are likely new. More importantly, the ST-elevation in III and aVF is proportionately large compared to the QRS amplitude. Leads aVL, V2, and V3 all have at least 1mm of ST-depression without question. I’ve borrowed Tom’s technique of using PowerPoint to stretch the leads vertically while preserving the ST/QRS ratio to help illustrate these findings.
Is ST-elevation present in two or more contiguous leads?
Yes.
Additionally, we should take into account all of our findings which strongly suggest an MI.
- Chest pain which awoke the patient from sleep
- Left sided paresthesia
- ST-elevation in two contiguous leads, with reciprocal changes
- 3° AV Block, with a junctional escape
- Hypotension
This constellation of findings would be expected with an occlusion of the RCA, potentially with right ventricular and/or posterior involvement. We can solidify our hunch with knowledge that the AV node is fed by the RCA in right-dominant individuals. ST-elevation in Lead III > Lead II is suggestive of RCA occlusion.
The crew in this case activated the cath lab from the field. They gave 324 mg ASA, started bilateral lines, gave multiple fluid boluses, placed pads for pacing, and administered 0.5 mg atropine while preparing the patient for transcutaneous pacing.
At the receiving facility, after they switched to the ED’s monitor, the patient’s rhythm changed to a 2° AV Block Type II with a ventricular rate of 70, easily palpable radials, and improved skin color.
In the cath lab, the following was found:
Diagnosis: Acute ST-elevation myocardial infarction.
Take another look at the rhythm strip from the current case study, “54 year old female CC: BLS Intercept”:
As many readers have pointed out, there exists some level of atrioventricular block. The question then is, which one is it: is it a second degree AV block or a third degree AV block?
In order to answer this question, we should start with the basics.
The conduction system of a normal heart begins in the right atrium at the sinoatrial, or SA, node. From here, the impulse travels through the internodal pathways (and to the left atrium through Bachmann’s Bundle) before reaching the atrioventricular, or AV, junction located inside Koch’s Triangle.
It is at this point that our case picks up.
Inside the AV junction is the AV node, a compact, specialized area of myocardium responsible for delaying impulses traveling from the atria to the ventricles. This ensures the atria and ventricles operate in a coordinated fashion. On a surface ECG this delay is realized, in part, through the length of the PR interval illustrated below:
After an impulse leaves the AV node, it travels through the Bundle of His and on through to the Right and Left Bundle Branches, finally terminating in the ventricles with the Purkinje Fibers.
When the AV node becomes ischemic, injured, diseased, or otherwise compromised, the conduction system becomes impaired. Collectively, these impairments of the AV node are referred to as Atrioventricular Blocks. There are three degrees of atrioventricular blocks, each representing an increasing amount of AV node impairment.
Before we return to the case study, we will cover the rules for differentiation of atrioventricular blocks on the ECG:
A 1° Atrioventricular Block is not a block, per se, but rather an increased delay in the AV node. On the surface ECG this is realized through a prolonged PR interval. Otherwise this block has no other effect on the ECG.
1° Atrioventricular Block
Rate: Unaffected
Regularity: Unaffected
P-Waves: Unaffected
PR Interval: Prolonged, >0.2 s
QRS Duration: Unaffected
2° Atrioventricular Blocks are broken into two types, each representing an increasing level of impairment in the AV node. In a Mobitz Type I, or Wenkebach, block the delay at the AV node gradually increases until conduction to the ventricles is blocked, resulting in a missing QRS complex. Recognition of Wenkebach conduction requires at least 3 P-waves and 2 QRS complexes in order to identify the progressive lengthening of AV nodal delay.
2° Atrioventricular Block: Mobitz Type I (Wenkebach)
Rate: Depends on the underlying atrial rate
Regularity: Regularly irregular
P-Waves: More P-waves than QRS complexes, associated with each conducted QRS complex
PR Interval: Progressively lengthens until a QRS complex is dropped
QRS Duration: Unaffected
In a Mobitz Type II block, the AV node fails to conduct impulses through to the ventricles, resulting in missing QRS complexes. However, the AV nodal delay is not impacted, resulting in a stable PR interval for all associated P-waves.
2° Atrioventricular Block: Mobitz Type II
Rate: Depends on the underlying atrial rate and the ratio of conducted complexes
Regularity: Regular, regularly irregular, or irregular (based on the ratio of conducted complexes)
P-Waves: More P-waves than QRS complexes, associated with each conducted QRS complex
PR Interval: Unaffected
QRS Duration: Unaffected
Finally, a 3° Atrioventricular Block is a complete heart block. The AV node no longer allows atrial impulses to conduct through to the ventricles. Atrial activity proceeds independent of ventricular activity, known as AV disassociation. The rate of ventricular activity depends on the escape rhythm present. If the block is high enough in the AV node, a junctional rhythm may exist with narrow QRS complexes. If the block is lower in the AV node, a ventricular rhythm may exist, with wide QRS complexes.
3° Atrioventricular Block: Complete Heart Block
Rate: Atrial rate will be independent of ventricular rate. V-rate depends on escape. Junctional rhythms 40-60, ventricular rhythms 20-40.
Regularity: Atrial rate will be regular, ventricular rate will be regular.
P-Waves: Present and disassociated from the ventricular activity
PR Interval: Non-existent
QRS Duration: Narrow (≤0.11s) with junctional escape rhythms, wide (>0.11s) with ventricular escape rhythms
With these rules in mind we can analyze the rhythm strip from the case study, marching out the P-waves and the QRS complexes:
Rate: Bradycardic ventricular rate of ~45 bpm
Regularity: Regular P-P, Regular R-R
P-Waves: Rounded, upright, symmetrical; rate of ~100 bpm; no apparent association with QRS complexes
PR Interval: Non-existent (appears to lengthen and shorten erratically)
QRS Duration: Narrow, 0.1s
Given these findings and the rules we covered before, this rhythm is a sinus tachycardia with a 3° atrioventricular block and a junctional escape rhythm.
When working to differentiate between the atrioventricular blocks, it is important to follow your rules and march out the atrial and ventricular impulses in order to make an accurate determination of the rhythm.
See also: Rhythm Challenge #3
Tom, our Editor-in-Chief, and David, an Associate Editor, are gone on vacation. As a send-off, I am presenting the following case. I hope you enjoy it!
It is just after 3am when you are called to intercept a BLS unit on scene with a 54 year old female with a low heart rate.
Upon your arrival, you find two EMT-Basics attending to a small woman lying in bed, who appears acutely ill.
The patient is alert, oriented, and answers all of your questions appropriately. She states that she woke up not feeling well and called 911 when she could not get out of bed.
Past Medical History: hysterectomy, cholecystectomy, breast cancer
Medications: Ambien and Zoloft (she denies depression)
Allergies: Aspirin gives her heartburn
You ask her if anything else is going on and she states that her chest, “feels funny”.
Onset: woke her up from her sleep
Provocation/Palliation: nothing makes it better or worse
Quality: she points to the middle of her chest as the source of the funny feeling
Radiation: when asked, she mentions her left leg is tingling
Severity: repeated questioning only elicits, “it isn’t that bad”
Time: 20 minutes
Her vital signs are reassessed in the Trendelenburg position.
Pulse: 44, regular, no radial pulses present, however weak brachials are palpable
Respirations: 12, unlabored, bilaterally clear breath sounds
BP: 54/0, unable to accurately auscultate the diastolic
SpO2: 96% on O2 via NRB at 15 L/min
Besides her cold, ashen gray skin, her physical examination is unremarkable.
The cardiac monitor is attached.
A 12-Lead ECG is acquired.
A final 12-Lead ECG is acquired as you arrive at the receiving facility.
What is your interpretation of the initial 3-Lead and 12-Lead? How would you treat this patient?
Given the final 12-Lead, does this change your interpretation?
See Also:
This is the conclusion to 77 year old female CC: Chest pain.
Thanks for all the great comments! You guys never disappoint.
Let's take another look at the initial 12-lead ECG.
Here is one of the serial 12-lead ECGs taken about 15 minutes later.
It's subtle but there are clear changes in QRS, ST and T wave morphology between these 12-lead ECGs (nice catch NJ Newbie). This suggests that a dynamic process is at work. Namely, the dynamic oxygen supply vs. demand characteristics of true ACS.
But is it a STEMI?
There are several things that make this case confusing.
In the first place, PR-depression is present in several leads, and we're already thinking about the possibility of pericarditis because of the unusual constellation of ST-elevation (and the atypical nature of the chest pain). But, women often present with atypical symptoms!
Second, pathological Q-waves are present in the inferior leads (nice catch Dave O and Neil H) but he is correct in that this finding could be old or new. Normally lead aVL is our "go to" lead to help confirm acute inferior STEMI and while there is the tiniest little "dip" after the J-point in this lead, I'm not prepared to call it a reciprocal change.
Third, low voltage is present throughout the 12-lead ECGs which makes analysis of the ST-segments and T-waves more difficult. To help, we can use the "rule of proportionality". That means that our threshold for ST/T wave abnormalities is lower when the QRS complex is smaller. In other words, we don't necessary need 1 (or 2) mm of ST-elevation to be significant, especially when the QRS complex is < 5 mm in amplitude. We also need to be suspicious when the T-waves appear disproportionately large for the size of the QRS complex (again, nice catch Dave O).
Let's take a closer look at some of the most suspicious leads. Here I have used PowerPoint to "stretch" the leads vertically while preserving the ST/QRS ratio.
These T-waves are way too large considering the relatively small size of the QRS complex.
But what about ST-elevation?
Let's take a close look at leads V4 and V5 (I'd include lead V3 but there's some wandering baseline that makes finding the TP segment too difficult).
First lead V4 (again stretched vertically while preserving the ST/QRS ratio).
When we compare the TP segment to the J-points we can see that ST-elevation is clearly present.
Next we'll look at lead V5 (stretched vertically while preserving the ST/QRS ratio).
Again, when we compare the TP segment to the J-points we see that ST-elevation is present.
Just "eye-balling" it we can also appreciate ST-elevation in lead V3. So, do we have ST-elevation in 2 or more contiguous leads?
Yes.
In this case, the cardiac cath lab was activated while paramedics were still out in the field and the cath team was waiting when the patient came through the door.
So, what did they find?
Diagnosis: Acute ST-elevation myocardial infarction
EMS is called to a residence on a horse farm for a 77 year old female with chest pain.
On arrival, the patient is found sitting on a wooden bench. She appears anxious and acutely ill.
Skin is warm, flushed and diaphoretic. She is rubbing her chest.
Onset: 20 minutes prior to 9-1-1 call
Provoke: Slightly worse with deep inspiration
Quality: Unable to describe but when pressed “more sharp than dull”
Radiate: The pain does not radiate
Severity: 5/10
Time: She’s had chest pains before but not recently and “nothing this bad”
Past medical history: Hypothyroidism, dyslipidemia
Medications: Synthroid, Lipitor
Vital signs are assessed.
RR: 24
Pulse: 104
NIBP: 201/118
SpO2: 97 on RA
She admits to feeling short of breath.
Breath sounds are clear bilaterally.
The cardiac monitor is attached.
A 12-lead ECG is captured.
What would you do next?
*** UPDATE ***
By request here is another 12-lead ECG taken approximately 15 minutes later.
See also:
Report: Aspirin Taken Daily With Fifth Of Bourbon Greatly Reduces Awareness Of Heart Attacks
4 commentsPHILADELPHIA- In a medical breakthrough that should come as welcome news for millions of at risk Americans, University of Pennsylvania cardiologists announced Tuesday that taking one aspirin tablet and a fifth of bourbon daily can “significantly reduce” an individual’s awareness of heart attacks.
“This study represents a major victory in the fight against heart disease, America’s number-one killer,” said Dr. Arthur Katzeff, head of the University of Pennsylvania team. “Each year, more than two million Americans clutch their chests in terror and exclaim, ‘Jesus Christ! I’m having a fucking heart attack!’ With this revolutionary new aspirin-bourbon treatment, however, such fully conscious incidents of cardiac arrest may soon be a thing of the past.”
According to Katzeff, test subjects who were administered a single aspirin in the morning, followed by a fifth of bonded Kentucky bourbon over the next several hours, were 85 percent less likely to realize that they were having a heart attack than those who did not take the aspirin with bourbon.
Americans are excited about the findings. “My four heart attacks have all been hellish, “ said Ronald Diering, and Evansville, IN, auto mechanic. “I was aware of everything that was happening, and I was gripped by the fear that I was going to die. But with this new aspirin-bourbon treatment, future heart attacks should be much less traumatic.”
“Who wants to spend what could be their last moments on Earth in terror?” asked Alex Broadhurst of San Jose, CA. “Better to enjoy another swig of bourbon and lie on the floor waiting for the ambulance to show up!”
University of Pennsylvania researchers said individuals who take aspirin and bourbon in the prevention of heart attack awareness may experience certain side effects, including slurred speech, euphoria, diminished inhibition, impaired vision, and vomiting.
Upon waking from a heart attack, researchers said, there is also a chance of experiencing “a wicked hangover.” In such cases, individuals are strongly advised to avoid bright lights and loud noises, and not move around too much.
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