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57 year old female CC: Shortness of breath and chest pressure

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Here's an interesting case study from a faithful reader from Ann Arbor, MI who wishes to remain anonymous.

Patient information

Age: 57

Gender: F

Chief complaint: SOB and Chest pressure constant 9/10 which woke her from sleep. Pt also vomited when she woke up and hands tingle. No radiation and nothing makes pain better or worse.

Medical history: Triple bypass x 2 years, Renal Failure, HTN, High cholesterol, Diabetic type 2, family hx of MI, constant vertigo.

Medications: Zoloft, Lisinopril, Rengel, Plaquenil, Levothroid, Plavix, Sodium Bicarb, Coreg, Nephro, Prilosec, ASA, Norco, Leverin, Novalog.

Allergies: Codine, Toradal

Vital signs: 

  • HR 77
  • BP 143/84
  • RR 18
  • BGL 298
  • Skin PWD, Cap-refill >0.2sec

12-lead ECGs are captured about 30 minutes apart.

Physical exam

  • Denies HA or nausea
  • Eyes: PERAL
  • BS: Clear x4, chest = rise/fall, SAT 100 on 6lp NC, speaking full sentences, breathing non-labored
  • ABD: No c/o pain soft non-tender x4, with no rigidity.
  • No edema noted
  • Amputation above knee L-leg
  • Smoker, quit x 8 years

 

Questions:

What do you think about the 12-lead ECGs?

What is the most likely cause of the ST-depression and T-wave inversion?

Sudden Cardiac Arrest podcasts from EMS Today 2011

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PlayPlay

Here's a recap of some of the great podcasts from EMS Today 2011 that specifically addressed sudden cardiac arrest.

In Part I of this podcast, EMS Garage host and "EMS 10" awardee Chris Montera chats with Ben Bobrow, M.D., James Jollis, M.D. and Graham Nichol, M.D. of the Heart Rescue Project. This program looks at the variability of survival rates for sudden cardiac arrest around the country and shares best practices.

In Part II (starting at about the 14:50 mark), the "podmedic" Jamie Davis, Tom Bouthillet, Dana Yost and Tim Noonan discuss process improvement for sudden cardiac arrest. Dana Yost is with Redmond Fire Department (King County Medic One) and shares some insights into their awesome survival rates.

In this segment, Carissa O'Brien conducts a separate interview with Graham Nichol, M.D. of the HeartRescue Project.

In this podcast Tom Bouthillet, Tim Noonan, Dave Hiltz and Lynn White discuss HEARTsafe Communities, the HeartRescue Project and process improvement for cardiac arrest.

Dave Hiltz was named one of the "EMS 10" (Top 10 Innovators in EMS) at EMS Today 2011 and Lynn White literally wrote the book for the HeartRescue Project.

You can find the HEARTsafe Community Facebook page HERE and you can learn more about the HeartRescue Project HERE.

60 year old male CC: Sudden cardiac arrest

34 comments

Here's a great case submitted by a faithful reader who wishes to remain anonymous. Some minor details have been changed to preserve patient confidentiality and some relevant comments and teaching points have been added.

EMS is called to a barbecue festival for 60 year old male, unconscious and unresponsive, possible cardiac arrest.

En route dispatch advises, "the caller states the patient is breathing, CPR in progress." 

While radio transmissions like this often make EMTs and paramedics chuckle, we know that agonal breathing helps predict survival from sudden cardiac arrest.

This is one of the reasons that "look, listen and feel" has been removed from the 2010 AHA ECC guidelines.

"Agonal gasps are common early after sudden cardiac arrest and can be confused with normal breathing. Pulse detection alone is often unreliable, even when performed by trained rescuers, and it may require additional time. Consequently, rescuers should start CPR immediately if the adult victim is unresponsive and not breathing or not breathing normally (ie, only gasping). The directive to "look, listen, and feel for breathing" to aid recognition is no longer recommended."

On arrival, bystander CPR is in progress. Specifically, continuous chest compressions without rescue breathing are in progress. An EMT takes over compressions and the following sequence happens very quickly.

  1. The LP12 is powered on.
  2. The combi-pads are deployed and attached to the patient.
  3. The LEAD button is pushed to get a paddles view.
  4. The monitor is charged to 200 J.

This is where the "pit crew" concept or "choreographed model" comes into play. There is no reason to hesitate. The monitor should be charged immediately with the expectation that it's a shockable rhythm so that the shock can be delivered as soon as possible.

(Since some are claiming this is "dangerous" please see:

M.S. Lloyd, B. Heeke, P.F. Walter, J.J. Langberg. Hands-on defibrillation: an analysis of electrical current flow through rescuers in direct contact with patients during biphasic external defibrillation. Circulation 117 (2008) (2510 – 2514).

Edelson DP, Robertson-Dick BJ et al. Safety and efficacy of defibrillator charging during ongoing chest compressions: a multi-center study. Resuscitation. 2010 Nov;81(11):1521-6.)

Once these actions are complete, everyone clears the patient with the exception of the chest compression man. When the lead paramedic gives the command (in this case a nod of the head) the chest compression man clears the patient, the lead paramedic confirms that VF is on the monitor, and the shock is delivered with minimal delay between stopping compressions and shocking.

Compressions are resumed immediately. The pulse check does not occur until another complete 2 minute cycle is complete.

Incidentally, some of the highest performing EMS systems in the country handle this in differrent ways. Some perform continuous chest compressions with a non-rebreather mask, some follow the 30:2 recommendation of the AHA (occasionally with a ResQPOD attached to the BVM), others drop a blind insertion airway device like the King LTS-D and deliver asynchronous ventilations at a rate of 8-10/min. (every 6-8 seconds), and some capture the airway with a tracheal tube without interrupting chest compressions.

As the next 2-minute cycle is nearing completion the monitor should be charged again to 300 J (or whatever energy setting your protocols dictate for the second shock). Again, the idea is to avoid ineffficiency.

It shouldn't look like this:

  1. Stop compressions
  2. Read the monitor and decide the patient needs a shock
  3. Start compressions again
  4. Charge the monitor
  5. Stop compressions
  6. Confirm that a shockable rhythm is on the monitor
  7. Go through a lengthy "I'm clear, you're clear, we're all clear" process
  8. Deliver the shock

On the other hand, it is very important that the paramedic who interprets the monitor pay close attention to whether or not it's a shockable rhythm before pushing the SHOCK button.

This can be diffficult when the defibrillator is pre-charged, everyone's watching, and you're trying to balance minimizing the delay between stopping compressions and shocking with making sure the shock will confer a benefit to the patient.

After the second shock it was noted that the patient was "pinkening up."

The defibrillator was pre-charged prior to the end of the next 2 minute cycle. However, this time there was a rhythm on the monitor. It looked something like this.

The patient started to breath spontaneously at a rate of about 30/min which was somewhat surprising. The "airway man" attached the waveform capnography to the BVM and timed small bag squeezes with the patient's spontaneous ventilations. 

This works beautifully if you haven't tried it! Waveform capnography is a very useful tool.

Once the patient was loaded in the back of the ambulance a 12-lead ECG was captured.

Vital signs were assessed.

RR: 20
Pulse: 150 Irregular
NIBP: 155/123 (presumed spurious)
SpO2: 97 and rising

An EMT attempted to confirm the BP by auscultation but was only able to confirm a BP of 150/P.

At this point it was noted that the patient was moving and there was a small amount of vomit in the patient's mouth. 

The patient's airway was suctioned (with difficulty due to a clenched jaw). After a minute or two the patient's jaw relaxed.

The OPA was removed in case the problem was a return of the patient's airway reflexes. By this time the respiratory effort was adequate and the decision was made to switch the patient out to a non-rebreather mask. The patient's head was turned to the side.

This had a positive effect and within a minute or two the patient followed a command to open his eyes.

Another 12-lead ECG was captured.

By arrival at the hospital the patient was confused but talking.

Questions for discussion

Do you follow a "pit crew" concept or choreographed model for sudden cardiac arrest?

What is a normal response in your jurisdiction for sudden cardiac arrest?

Have you read the 2010 AHA ECC Guidelines?

Do you emphasize minimally interrupted chest compressions, controlled ventilations, and shocking in a 2-minute cycle?

Are all other interventions secondary?

Do you think this patient needed antiarrhythmics?

What do you think of the patient's 12-lead ECGs?

What should this patient's post-resuscitation care look like?

See also:

Conclusion to 60 year old male CC: Sudden cardiac arrest

High performance CPR – Seattle Style!

Sudden Cardiac Arrest podcasts from EMS Today 2011

Video: Axis Determination

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So you've read our blog, followed us on Facebook, submitted your own case studies, but you're looking for more. You're looking for the next big thing in EMS 12-Lead education. As a test run I've put together a video, shot Kahn Academy style using a pen and tablet, covering rapid axis determination.

When I learned 12-Lead interpretation in paramedic school, axis determination was covered but it never really sank in. A few folks were comfortable with the I-II-III method (up-up-up, up-down-down, etc). Others, like myself, understood what it meant, what it was for, but never really internalized it as a skill.

The technique I've found the easiest is one from Garcia and Holtz's 12-Lead ECG: The Art of Interpretation. It uses only leads I and aVF and could be called the "quadrant method". The best part is the method is easy to apply even when your own heart is racing!

Rapid axis determination using only leads I and aVF

The following video assumes you have a basic understanding of vectors and axes. The objective is to teach you a rapid means of axis determination using only leads I and aVF.

Let us know if this is helpful and let us know if you want more!

May 2011 EMS 12-Lead column at EMS1.com – What in the wide world of sports?

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The May 2011 EMS 12-Lead column has been posted at EMS1.com.

What in the wide world of sports?

If you think you know what's wrong with the patient, leave a comment that includes 1.) your impression and 2.) your treatment plan at EMS1.com.

If (in my completely arbitrary opinion) yours is "the best" you could win an EMS1 t-shirt and key ring bottle opener! Yes, ladies and gentlemen. You heard that correctly. We don't play around.

Good luck! 

Wake County EMS cardiac arrest survival rate among the highest in the country

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via NBC 17 News

In these trying economic times, wouldn't it be nice to enjoy these bragging rights?

It's not so easy for elected officials to cut your budget when you can prove you're a vital public service! 

It feels good to save people, too. As noted by the panelists of the HeartRescue Project at EMS Today 2011, cardiac arrest survivors are powerful allies!

Bring one to a meeting and watch the "anti-champions" crawl under the nearest rock.

Congratulations to Wake County EMS!

See also: On Scene and Hospital Hypothermia – D2B October 2010 Webinar with Brent Myers, M.D.

53 year old male with a suspicious ECG – Conclusion

4 comments

This is the conclusion to 53 year old male with a suspicious ECG.

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

This one was really challenging because we all know that reciprocal changes are strongly supportive of acute STEMI. However, this case is an excellent reminder of something else — the importance of clinical correlation! 

Remember "Step 7" in the Six Step Method for 12-Lead ECG Interpretation? While I acknowlege the possibility of a clinically silent acute myocardial infarction, my department's STEMI Alert protocol requires that the patient be experiencing signs and symptoms consistent with ACS. It need not be chest pain, but it would have to be an anginal equivalent if chest pain were absent.

This ended up being called benign early repolarization at the hospital.

Aside from the lack of clinical correlation, were there any clues that this was not an acute STEMI? 

When I sent this ECG to Stephen Smith, M.D. of Dr. Smith's ECG Blog he pointed out that the QTc was only 360 ms. He gave it a 3% probability of being an acute STEMI (perhaps it would have been less had I told him the patient was completely asymptomatic). That was a very good point! The QTc is almost always prolonged in the setting of ischemia.

I can't give you an exact cut-off but it's something I'll be keeping a close eye on going forward for these tough cases.

Another thing that interests me about this case is that it reminds me of the incredible diversity of ST-changes that fall under the banners of "benign early repolarization", "early repolarization", or "repolarization abnormality".

I think these phrases are often a substitute for "we don't know why ST-elevation is present but we don't think it's a STEMI." However, the phrase "repolarization abnormality" is pretty generic. After all, what is the ST-elevation of acute STEMI if not a repolarization abnormality?

I understand the reluctance of physicians to use the word "benign" especially when some studies suggest that "benign" early repolarization may be a weak marker for sudden cardiac death. But it can all be very confusing for those trying to learn how to differentiate the ST-elevation of acute STEMI from other causes of ST-elevation.

Let's consider some examples.

This is from 23 year old male CC: Chest pain

This one was labeled a "repolarization abnormality". 

Here's another great example from Tweet about ECG leads to mystery – Is this a mimic or the real thing?

This one is similar to our "53 year old male with a suspicious ECG" in that the inverted T-wave in lead aVL looks like a reciprocal change. However, the patient was a 19 year old African American male, ventilator dependent, with an elevated temperature. Not exactly a presentation we associate with acute STEMI.

Here's an ECG that I had forgotten about until I found it on my hard drive last week. I don't remember who sent it to me but I remember being told that the potassium came back in the normal range (and that it was not a STEMI).

This is an impressive looking ECG! I would definitely be worried about acute anterior STEMI. However, two findings point toward benign early repolarization. First, the QTc is only 389 ms! Second, R-wave progression is intact (average R-wave height in leads V2-V4 is greater than 5 mm).

Finally, let's look at a "classic" case of benign early repolarization (BER). This is from the "Early Bird Gets the Worm" case at EMS1.com.

Now we see all of the classical features of benign early repolarization. Notched J-points. Upwardly concave ST-elevation. Short QTc. Absence of reciprocal changes.

Unfortunately, as you can see, it's not always this easy! 

So what should you do?

Remember the 41 year old male CC: Chest pain?

In this case the QTc was relatively short at 394 ms and R-wave progression is intact. However, something about it doesn't look right. The ST-segments in lead aVL are upwardly convex (non-concave) and the ST-segments are flat and almost downsloping in lead III (a possible reciprocal change).

This turned out to be acute STEMI but it was serial ECGs that clinched the diagnosis! That and the fact that the "story was good."

So remember, always correlate the ECG to the history and clinical presentation and perform serial ECGs.

High Performance CPR – Seattle Style!

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Editor's note: Since it's all over the news that Seattle's "save rate" for cardiac arrest (witnessed collapse, presumed cardiac etiology, shockable rhythm) is over 50%, I asked Dave Hitlz of the HEARTsafe Community page on Facebook if I could re-post an article he and Mathias Duschl wrote about their experience at the Resuscitation Academy. He graciously agreed.

High Performance CPR: Seattle Style!

Written by:

Mathias Duschl, from Gattikon, Switzerland
David B. Hiltz, from Westerly, Rhode Island

Recently, the two of us had the tremendous opportunity to attend the Resuscitation Academy, whose mission is to improve survival from out of hospital cardiac arrest.

The Academy, conducted by Seattle Medic One and King County EMS, convenes EMS managers, EMS directors and EMS medical directors in a “mini-fellowship” program that consists of Pre-Fellowship assigned readings, a 4-day intensive and immersive experience discussing Quality Improvement (QI), education, science and leadership in system approaches to optimizing outcomes from out of hospital cardiac arrest (OOHCA), and post-fellowship QI projects.

The experience was remarkable, and provided both of us with improved knowledge, understanding and perception of complex subjects relating to the public health issue of cardiac arrest. Despite having people from different continents, we all had the same mind set and came together to work on strategies that can help save more lives in our communities.

The evolution of discussions at the Academy led to the identification of deliberate approaches to optimizing outcomes from OOHCA. We truly believe that the experience gained through the mini-fellowship program to be highly beneficial and we encourage agencies, EMS systems, local governments and administrations (like county boards of health in the U.S.) to send representatives to the Academy with a goal of developing localized strategies to save lives. 

Among the essential components of a system of care for cardiac arrest victims is “high performance CPR” (HP-CPR) and we have decided to share this, our perspective, on the subject. Neither of us intends to portray ourselves as experts and all-knowing, but simply applying one viewpoint on one subject in a cardiac arrest QI montage.

High quality resuscitation and improved outcomes are highly dependent on a foundation of high quality CPR by prehospital care providers. Advanced cardiac life support must be positioned in a way that does not get in the way of, but instead enables this high quality CPR. The approach requires a teamwork approach by EMS systems, agencies and providers alike.

The American Heart Association has released the revised BLS for HCP course. In Europe, the European Resuscitation Council ERC provides PowerPoint presentations, posters etc. about the new BLS strategies as downloads in several languages via their website. These materials, in the hands of qualified instructors, will continue to be a cornerstone in resuscitation education for countless providers. But AHA-ERC certification is just the beginning…not an end point in our efforts to save more lives.

Resuscitation training and education should not be thought of as a course or single “event”, but rather a long-term progression in development of CPR quality and an ongoing quest for better insight on the science, practice and performance of resuscitation. Continuity in education and repetitive training in CPR can lead to better results in real-life situations. A goal of highly choreographed HP-CPR is extremely desirable, but like most things, it won’t happen through desire alone. Action is required if we are to expect improvement.

One potential method to improve CPR is to develop a “team strategy” with clear roles and is translated into “team practice” of HP-CPR. View the videos from the Resuscitation Academy, where a team approach is portrayed. Whether you call it Choreographed CPR, HP-CPR, Crisis Resource Management in CPR or use of an Incident Command strategy at the scene of a cardiac arrest, the essential goal is improved teamwork, and teamwork requires PRACTICE.

Initiating team practice does not have to be elaborate or complicated. Informal and formal practice sessions are both reasonable and recommended strategies to improve future performance. Use of observers with equipped with stopwatches, checklists, video recorders, and/or instrumented manikins along with practiced and non-punitive debriefing skills will improve results.

Use a “let’s just do it” approach. Don’t wait for an overly-detailed plan to begin the process of quality improvement. Read the Guidelines for CPR and ECC and understand the science Make resuscitation quality a priority (culture of excellence) Use courses like the AHA BLS HCP course to establish baselines Begin practicing HP CPR Collect CPR performance data through observation or instrumentation.

Ongoing and routine debriefing regarding CPR performance

All personnel involved in practice should have an opportunity to contribute to the QI process. Exercise facilitators should use a structured and consistent approach to debriefing of rescuers. The practice of clinical event debriefing can also be very valuable in the QI process and development of HP CPR.

Improving OOHCA outcomes is challenging to say the least. Individual clinical excellence is just one factor in a life-saving formula…but at the same time an integral and core component in a process that involves the implementation of strategies to optimize recognition, response, care and outcomes for cardiac arrest patients. The incremental value of ongoing system quality improvement (public health surveillance), early recognition and emergency number activation, pre-arrival instructions, bystander initiated CPR, really fast “shock strategies”, HP- CPR, and regional systems of care (incorporating therapeutic hypothermia and other evidence based recommendations) is essential.

Performing high quality CPR, with minimal delays and interruptions is a core strategy to improving outcomes. Quality improvement strategies should aim to encourage, enable, and direct the ongoing practice and pursuit of high performance CPR. High Performance CPR is not, and should not be complicated. In fact, we believe it is relatively easy to implement. It does however require action in order to get the process going, commence practice, and begin the process of developing a culture of excellence.

“Measure, improve, measure, improve, measure, improve”- Dr. Mickey Eisenberg.

See also:

Resuscitation Academy

HEARTsafe Community page on Facebook

53 year old male with a suspicious ECG

28 comments

Here's another interesting case brought to my attention by the one and only David Hildebrandt.

EMS is called to a local medical clinic to transfer a 53 year old male to the emergency department.

It turns out the patient was in for a regular check-up.

He appears to be in excellent physical condition and states that he is a personal trainer at the local gym.

Past medical history: Hypertension
Medication: Atenolol

Vital signs are assessed.

RR: 12
Pulse: 44
NIBP: 132/78
SpO2: 99 on RA

A 12-lead ECG is captured which matches the ECG taken at the clinic.

Why is the physician at the clinic concerned?

See also:

53 year old male with a suspicious ECG – Conclusion

58 year old female CC: Chest pain – Conclusion

11 comments

This is the conclusion to 58 year old female CC: Chest pain.

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

Remember, ST-elevation needs to be explained, and if the etiology involves myocardial infarction, urgent time-sensitive decisions need to be made.

In this case, we have ST-elevation in leads V1-V5, which suggests the possibility of acute LAD occlusion.

This finding is all-the-more concerning when we consider that R-wave progression is poor (absent) and the QTc is prolonged at 481 ms. Both of these findings point away from benign early repolarzation.

It's all too easy to dismiss a patient like this as having a mere anxiety attack. We need to keep an open mind and careful not to stimatize our patient.

How else might we explain the ST-elevation in the precordial leads?

We can consider the possibility that the ST-elevation is "old" or from a previous MI (the ECG finding we sometimes refer to as left ventricular aneurysm).

However, when we measure the T/QRS ratio we see that the T-waves are far more acute-looking than we would expect with left ventricular aneurysm.

The T/QRS ratio is 0.45 in lead V2 which is way above our threshold of 0.36.

Another possibility that some of you very astutely pointed out in the comments is Tako-Tsubo (or Takotsubo) Cardiomyopathy. I found that suggestion particularly interesting because it does seem to tie together all of the elements of this case.

In this case, the treating paramedic wasn't sure what to make of the ST-elevation in the precordial leads so he transmitted it over the LIFENET to the receiving hospital.

The two ED physicians weren't sure what to make of it either, but to be on the safe side they called a "Code STEMI".

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

The differences between this ECG and the previous ECG are not dramatic, but if you scrutinize the two you will see that there are differences in QRS, ST and T wave morphology.

By the time the patient arrived in the emergency department her chest pain was completely gone.

After a discussion with the cardiologist she consented to cardiac catheterization.

There was an acute 99% occlusion of the LAD which was successfully stented.

Diagnosis: Acute ST-elevation myocardial infarction.

See also:

81 year old male CC: Palpitations

76 year old female CC: Chest pain

58 year old female CC: Chest pain

25 comments

EMS is called to the residence of a 58 year old female complaining of chest pain.

On arrival the patient is found walking around the kitchen. She is anxious and hyperventilating.

Past medical history: Hypertension (controlled with diet and exercise)
HTN Medications: Xanax

The patient is asked to sit down in a kitchen chair and to control her breathing.

Onset: Sudden after coming home from the gym
Provoke: Nothing makes the pain better or worse
Quality: Unable to describe
Radiate: The pain does not radiate
Severity: 8/10
Time: No previous episodes

The patient appears to be in excellent physical condition and states that she works out several times a week.

Skin is warm, pink and moist.

Breath sounds are clear bilaterally.

Vital signs are assessed.

RR: 36
Pulse: 104
NIBP: 155/93
SpO2: 99 on RA

The cardiac monitor is attached.

Paramedics press the PRINT button to obtain a cleaner tracing.

A 12-lead ECG is captured.

What is your impression of this 12-lead ECG?

How would you treat this patient and why?

See also:

58 year old female CC: Chest pain – Conclusion

Found on the LIFENET 05/2011

22 comments

Found on the LIFENET.

What is your impression of this ECG?

 

*** UPDATE ***

Consider this recent case from Dr. Smith's ECG Blog.

ST-elevation in aVR, with widespread ST-depression

"ST elevation in aVR is often thought to represent left main occlusion. However, it really just signifies widespread and diffuse subendocardial ischemia which could be due to left main or 3-vessel disease, or severe proximal LAD disease. Left Main occlusion generally causes rapid death; most who survive left main ACS have some flow and thus often have widespread ST depression."

See also:

63 year old male CC: Chest pain

An unusual case of left bundle branch block

82 year old male CC: Shortness of breath – Conclusion

7 comments

This is the conclusion to 82 year old male CC: Shortness of breath.

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

This ECG shows a severe bradycardia.

We need to ask a couple of very important questions.

Is the patient stable or unstable?

The patient is unstable. In fact, the patient is periarrest.

We cannot be lulled into a false sense of security because the NIBP reads 142/122.

In the first place, that's an extremely difficult BP to believe.

I've seen this happen on more than one occasion. The last was a patient with a ruptured abdominal aortic aneurysm. Radial pulses were absent but the NIBP was reading very similar to this case (very high diastolic pressure with a narrow pulse pressure).

I tried to confirm it manually but I was unable to auscultate a BP in the back of the ambulance. Of course, the air conditioner and generator were running and the sirens were blaring. Let's face it. Sometimes it's not easy to auscultate a BP or breath sounds in the back of the ambulance!

I trusted my instincts and gave a fluid bolus. It turned out that the NIBP had given a spurious reading.

As I have mentioned before, I absolutely despise the mantra, "Treat the patient not the monitor!" I think it's one of the most misunderstood (and overused and abused) sayings in all of EMS.

A much better alternative is, "Correlate the monitor to the patient's history and clinical presentation." 

It's easy to second-guess or criticize the actions of someone else. I wasn't on this call, but tossing around a case like this gives all of us an opportunity to learn.

Very often I'm the one preaching to leave a patient alone and "do no harm". Too often EMS does more harm than good because we feel like we have to "do something" even though the patient is hemodynamically stable.

This is not one of those occasions.

So how do we determine our course of action?

2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science – Part 8: Adult Advanced Cardiovascular Life Support – Part 8.3: Management of Symptomatic Bradycardia and Tachycardia

There are some important statements here that deserve to be read very carefully.

"Electrocardiographic (ECG) and rhythm information should be interpreted within the context of total patient assessment. Errors in diagnosis and treatment are likely to occur if advanced cardiovascular life support (ACLS) providers base treatment decisions solely on rhythm interpretation and neglect clinical evaluation. Providers must evaluate the patient's symptoms and clinical signs, including ventilation, oxygenation, heart rate, blood pressure, level of consciousness, and signs of inadequate organ perfusion."

and

"Unstable and symptomatic are terms typically used to describe the condition of patients with arrhythmias. Generally, unstable refers to a condition in which vital organ function is acutely impaired or cardiac arrest is ongoing or imminent. When an arrhythmia causes a patient to be unstable, immediate intervention is indicated. Symptomatic implies that an arrhythmia is causing symptoms, such as palpitations, lightheadedness, or dyspnea, but the patient is stable and not in imminent danger. In such cases more time is available to decide on the most appropriate intervention. In both unstable and symptomatic cases the provider must make an assessment as to whether it is the arrhythmia that is causing the patient to be unstable or symptomatic."

and

"[A] patient in septic shock with sinus tachycardia of 140 beats per minute is unstable; however, the arrhythmia is a physiologic compensation rather than the cause of instability. Therefore, electric cardioversion will not improve this patient's condition. Additionally, if a patient with respiratory failure and severe hypoxemia becomes hypotensive and develops a bradycardia, the bradycardia is not the primary cause of instability. Treating the bradycardia without treating the hypoxemia is unlikely to improve the patient's condition. It is critically important to determine the cause of the patient's instability in order to properly direct treatment. In general, sinus tachycardia is a response to other factors and, thus, it rarely (if ever) is the cause of instability in and of itself."

A strange omission in the "streamlined" 2010 Adult Bradycardia With Pulse algorithm (that was present in the 2005 Bradycardia Algorithm) is the box that shows the Hs and Ts.

As Einstein is reported to have said, we must "make things as simple as possible but not simpler." 

Obviously we must correct hypoxemia.

However, if the rate does not bounce back we must consider other causes of the bradycardia.

In this case, the patient's potassium was very high (it turned out to be over 8.0).

I will grant you that this ECG does not show the classic "sine wave" or "Z-fold" pattern that is typical of life-threatening hyperkalemia (the QRS duration is well below 180 ms and there is no "merging together" of the S-wave and T-wave). On the other hand, there is very little risk to giving calcium and a huge upside potential for the periarrest patient.

Whether hyperkalemia was suspected or not, it would have been appropriate (according to the 2010 guidelines) to attempt to correct the heart rate using atropine, epinephrine, dopamine or transcutaneous pacing.

Would it have worked? I don't know.

Unfortunately, transcutaneous pacing is a skill that is poorly performed by all levels of health care providers. It is very unusual to see cases where patients were successfully paced using this technique. Far more often we see "false capture" with transcutaneous pacing.

This patient went into cardiac arrest in the cardiac cath lab while they were trying to insert a transvenous pacing lead.

Due to some kind of error, there was a significant delay in the lab. By the time they found out about the potassium level (a "critical value") it was too late.

You might recall the 58 year old male who was found unconscious at the bottom of the stairs. He was also suffering from life-threatening hyperkalemia and had a poor outcome.

Remember the ECGs from Rhythm Challenge #2?

In that case (which was far more obvious) hyperkalemia was also missed and the patient had a poor outcome.

The take-home message is that hyperkalemia can be profoundly life-threatening but it can't be treated if it's not suspected.

Consider this conversation between Stephen Smith, M.D. (from Dr. Smith's ECG Blog) and Scott Weingart, M.D. on the EMCrit podcast:

SW: "I know I've learned from being burned many times, that when I have a profound bradycardia or heart block, as my residents are getting excited to place in a pacer, even if the patient has no preexisting history, I do a trial of calcium chloride or calcium gluconate because I've just had so many cases where it turned out to be hyperkalemia. Is that your experience as well?"

SS: "That is my experience as well and I think it's very wise you're giving calcium before you start pacing. By far, more common than intrinsic causes of bradycardia and heart block is hyperkalemia — so common — and so frequently overlooked. It's a great imitator, I think. There are so many ways the ECG can manifest with severe hyperkalemia — life-threatening hyperkalemia. Again, the treatment is benign, and cheap! So how many life-threatening diseases can you treat benignly and cheaply?"

I would like to thank our anonymous contributor for sharing this important case.

82 year old male CC: Shortness of breath

25 comments

Here's an interesting and somewhat unusual case submitted by a faithful reader who wishes to remain anonymous.

EMS is called to the residence of a 82 year old male complaining of shortness of breath and weakness.

On arrival the patient is found slumped sideways in a chair.

He is weak and in significant distress, repeating, "Oh Lord…. Oh Lord…"

Past medical history: HTN, NIDDM
Medications: Unknown

The patient is African American.

Skin is diaphoretic. Nail beds are bluish. Capillary refill is delayed.

Breath sounds: Basilar rales

Vital signs are assessed.

RR: ~30 (estimated)
Pulse: 36 Irregular
NIBP: 142/122
SpO2: 88 on RA

The cardiac monitor is attached.

A 12-lead ECG is captured.

And another.

An IV is established and labs drawn.

BGL: 450

How would you describe this patient's condition?

What is your treatment plan?

See also:

82 year old male CC: Shortness of breath – Conclusion

88 year old female CC: Chest pain – Conclusion

4 comments

This is the conclusion to 88 year old male CC: Chest pain.

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

This ECG shows acute STEMI in the presence of left bundle branch block.

It's also an excellent example of the value of using "excessive discordance" to identify acute STEMI in the presence of left bundle branch block.

For a more extensive discussion of this topic see:

Excessive discordance as a marker of acute STEMI in LBBB

First, let's see if we can make the case for acute STEMI using Sgarbossa's original criteria.

As a refresher, here are Sgarbossa's criteria to identify AMI in the presence of LBBB

1.) ≥ 1 mm of concordant ST-elevation (in the same direction as the majority of the QRS complex) in at least one lead
2.) ≥ 1 mm of ST-depression in lead V1, V2 or V3
3.) ≥ 5 mm of discordant ST-elevation (opposite the majority of the QRS complex) in at least one lead

According to the original scoring algorithm, the more of these criteria that are met, the higher the probability of AMI.

 

So, let's apply these criteria to this case.

Do we see ST-elevation that is concordant with the majority of the QRS complex in at least one lead?

This criterion appears to be met in lead II.

Do we see ST-depression in leads V1, V2 or V3?

Possibly. I bring up data quality so often on this blog that I probably sound like a broken record, but it's rare that I run a case study where we don't have to compensate for poor data quality in one way or another. In this case it appears that ST-depression may be present in lead V1.

How about discordant ST-elevation = or > 5 mm?

This finding is absent on this 12-lead ECG. However, it doesn't really matter because this finding is (by far) the least specific of Sgarbossa's criteria. It's the least specific because it doesn't take into account the depth of the S-wave (rule of proportionality).

In other words, the deeper the S-wave, the greater the ST-elevation, and this is normal.

That's why we use the modified criterion proposed by Stephen Smith, M.D. (Dr. Smith's ECG Blog).

Rather than look for ST-elevation that is = or > 5 mm, we look for ST-elevation that is > than 0.2 (or 1/5) the depth of the S-wave!

To put this in a quick "rule of thumb" for you, for every 5 mm of S-wave depth, we allow 1 mm of ST-elevation.

Or, you can break out the calipers and calculate the ST/QRS ratio.

Let's apply the modified criterion to this case.

Do we see any leads with a ST/QRS ratio > 0.2?

We certainly do (and it's not even close).

So, lead II meets one of Sgarbossa's original criteria (concordant ST-elevation = or > 1 mm) while leads III and aVF meet Smith's modified criterion (ST/QRS ratio > 0.2).

This is more than enough evidence to call this an acute inferior STEMI in the presence of LBBB.

But we aren't finished yet!

Smith et al. discovered that "excessive discordance" works for positive and negative QRS complexes!

With this in mind, do we see "excessive discordance" anywhere else in this ECG?

Yes we do! Lead aVL shows ST-depression that is "excessively discordant" with the QRS complex.

Is lead aVL reciprocal to leads II, III and aVF?

Yes it is.

Point, game and match.

BTW, I also made the calculations for lead V4 because it looked close to me.

It was close, but no cigar. So take a good look at lead V4! This shows close to the maximum ST-elevation that is permitted for a QRS complex of this size.

Once you train your eye it's much easier to spot excessive discordance!

See also:

80 year old male CC: Chest pain

58 year old female CC: Chest pain