Snapshot Case- No Day at the Beach

It is a beautiful summer afternoon when you and your partner are called to the beach for a “swimmer in distress”.

Upon your arrival, you find a 48 year old male sitting on a beach towel, appearing to be in some distress.

You are told that he was swimming in the ocean when he began to struggle, and was pulled out by bystanders.

Patient tells you that he developed a constant sharp pain in his chest, along with pain in his right arm, probably from overdoing the swimming he thinks. He says he feels a little better now.

He has no history, takes no meds, and tells you this has never happened before. He denies shortness of breath, lightheadedness, and nausea. Diaphoresis is hard to assess because the patient is still cool and wet from the water.


You get a set of vitals:

  • Pulse: 78 and regular
  • BP: 128/78
  • RR: 18 regular, lungs clear
  • SpO2: 96% on RA
  • Skin: cool and moist (out of the water)


You acquire a 12 lead ECG:




The community hospital is 12 minutes away by ground, and the STEMI center is 30 minutes away requiring Medevac transport.

For context, your system has had an issue with false positive cath lab activations, making activations from the field a little more difficult subject to system review.


Back to this call:

  • What is your ECG interpretation?
  • How will you treat your patient?
  • Will you take your patient to the closest hospital, or activate the cath lab?


59 Year Old Female: Intermittent Head Pain (Conclusion)

This is the conclusion to Wednesday’s post; if you haven’t seen it, I highly suggest checking out the original case description and initial ECG.

Wednesday’s case introduced a 59 year old woman with a chief complaint of intermittent occipital head pain for about 10 days. Recently, it had started radiating into her neck and upper back/shoulders. This was her initial ECG and it is clearly abnormal:

EKG #1

Figure 1. EKG on arrival at the ED.

The computer identifies it as showing left ventricular hypertrophy (LVH) with secondary ST and T-wave abnormalities (which we call a “strain pattern” or just “strain”). LVH with strain is quite common—in fact, it’s the predominant source of false-positive cath lab activations—but is that really what we’re looking at here? That’s a vital question because, if it’s not LVH w/ strain, then we’re probably looking at an inferior STEMI.

Does this tracing show a STEMI mimic? Or a true STEMI mimicking a STEMI mimic?

To start our analysis, I’d first caution anyone against trying to attribute ST/T abnormalities to a “strain pattern” in the absence of obviously large voltages or an old ECG showing a similar pattern. While Fig. 1 does meet a couple of different voltage criteria for LVH (which the computer is excellent at calculating—one of the few things I rely on it for), the voltages really aren’t that impressive. If you’re going to call LVH with strain based on a single ECG, you want it to be something obvious—like the tracing in Fig. 2.

LVH w/ strain

Figure 2. LVH with strain and massive QRS voltages.

On a side note, several commenters noted that they were swayed against the diagnosis of LVH by the absence of high voltage in the precordial leads of Fig. 1. While they were right to be skeptical of LVH, it was for the wrong reasons. Seeing high voltage in only one plane (large complexes in the limb leads but normal complexes in the precordials, or vice-versa) actually doesn’t do much to rule-out the diagnosis of LVH. Fig. 3 shows an ECG where the precordial leads demonstrate huge QRS complexes but the limb leads are perfectly normal.

LVH w/ strain and 2:1 AV-block

Figure 3. LVH with huge precordial QRS complexes but normal limb leads; there is also 2:1 AV-block.

Back to our case…

There are a couple of other findings that also weigh against a strain pattern:

  • Even if we believe there is LVH, the ST-deviations, especially in III and aVL, seem slightly excessive when considered in proportion to the size of QRS complexes. There is no good rule for determining excessive discordance with LVH (that 25% one is okay as a rule-in criteria and better than nothing, but terrible at ruling-out STEMI), but a seasoned eye will note that this seems like just a tiny bit too much elevation with a T-wave in III that is just a bit too tall for the QRS size.
  • There is a convex morphology to the ST-elevation in III that is slightly atypical for LVH.
  • There is a down-up morphology to the ST-depression in I and aVL. While sometimes normal with LVH, this has to be approached as abnormal and ischemic until proven otherwise.
  • There is concordant ST-depression in V2 and V3.
Concordant ST-depression in V2 and V3.

Figure 4. Concordant ST-depression in V2 and V3.

I’ve highlighted that last point because I think it’s the most important and pretty-much seals the diagnosis of STEMI for me. Since we’re already concerned about an inferior MI (based on the findings in III and aVL), and since inferior STEMI’s are often accompanied by posterior involvement, seeing right-precordial ST-depression consistent with posterior STEMI leaves me very confident that the ST/T abnormalities we see in III and aVL are indeed caused by an infero-posterior STEMI.

When we discuss the right-precordial leads in the setting of LVH on this blog [1] [2] [3] [4], it’s usually because the strain pattern often produces ST-elevation in V1 and V2 (and sometimes V3) that mimics STEMI (see Fig. 2). In those cases the ST-elevation is appropriately discordant and direct opposite the negative QRS complexes. It’s less common to see concordant right-precordial ST-depression in those leads when there is LVH.

Figure 5. LVH w/ strain and concordant ST-depression in V3.

Figure 5. LVH w/ strain and concordant ST-depression in V3. This is not a STEMI.

LVH w/ strain and concordant ST-depression in V2 and V3.

Figure 6. LVH w/ strain and concordant ST-depression in V2 and V3. This is not a STEMI.

When we do sometimes see concordant ST-depression with LVH, most of the time is due to chronic diffuse subendocardial ischemia from multi-vessel coronary artery disease or demand ischemia (as in Fig. 5 & 6). The key in those cases is that it’s usually associated with ST-depression in most of the limb leads and ST-elevation in aVR. Looking back on Fig. 1, the limb lead ST-depression in our case is confined to I and aVL and there is no ST-elelvation in aVR.

So that right-precordial ST-depression, combined with the other findings listed above, confirms that we are very likely looking at an infero-posterior STEMI. But we have another issue…

Note that I said it’s “very likely” that we’re dealing with a STEMI, not “certain.” Despite my confidence in the ECG findings, this still isn’t an easy diagnosis because things get much trickier when you take the patient’s symptoms into account. While acute coronary syndrome (ACS) was present on the differential for her initial presentation (hence, why we did the ECG), before we did the test it didn’t seem very likely that her symptoms were due to myocardial ischemia. In other words, her pretest probability (our assumed likelihood that she was experiencing a STEMI prior to performing the ECG) was pretty low.

Now, her pre-test probability of ACS clearly isn’t 0%, but it’s also not very high. As a result, it’s going to take a pretty convincing test to diagnose a STEMI in this patient. That’s unfortunate since we already determined that her ECG, while suggestive of STEMI, wasn’t 100% conclusive.

Large anterior STEMI

Figure 7. If a patient came in with toe pain and this ECG they’d still go for emergent PCI despite an incredibly low pretest probabilty. The ECG is so strongly indicative of acute anterior STEMI that it is capable of swinging us all the way from a pretest probabiltiy of almost 0% to diagnostic certainty. In the case of our 59 year old woman though, even though her pretest probability of ACS was a bit higher than someone with “toe pain,” the ECG is less clear-cut. While we are mildly confident that we are looking at a subtle STEMI, we are not certain because we have a hazy clinical picture combined with a non-pathognomonic ECG.

We’ve moved ACS way-up on the differential, but we haven’t clinched the diagnosis. [On a side note: The ECG is a very subjective test, and while an expert like Dr. Steve Smith would assign a lot of confidence to his interpretation and could very well diagnose STEMI here in-spite of a low pre-test probability, most providers could and should not.] When faced with a non-diagnostic ECG in the face of possible ACS, it’s almost always a smart move to repeat the ECG.

In our case I didn’t see this patient’ EKG until an hour after she arrived, but as soon as I did I expressed my concerns to the treating physician and requested a repeat EKG. To refresh your memory, here’s that initial tracing again, followed by the repeat:

Fig 1.

Fig. 1 (reprising its role).

EKG #2

Figure 8. Repeat ECG 1 hour later.

Well, that’s a bit different. There are several important findings in Fig. 8:

  • The ST-elevation in lead III has disappeared (normalization of the J-point).
  • There are now a terminal T-wave inversions in lead III (reperfusion T-waves).
  • The ST-depression in I and aVL has mostly resolved (normalization of the J-point).
  • The ST-depression in V2 has resolved (normalization of the J-point).
  • The T-waves in V2 and V3 are slightly taller and more symmetric (posterior reperfusion waves).

The most important of those changes is the new terminal T-wave inversions in lead III—these are reperfusion T-waves. Many providers are familar with Wellens syndrome affecting the anterior leads, but they are not aware that you can see similar T-wave inversions in other distubutions.

Wellens syndrome is due to spontaneous reperfusion of an anterior STEMI. When the patient’s LAD is blocked, it results in a typical anterior STEMI pattern…

Subtle Anterior STEMI

Figure 9. Subtle anterior STEMI.

But then if that previously closed LAD spontaneously re-opens, the leads that used to show ST-elevation sometimes develop these classic-looking T-wave inversions described by Dr. Wellens.

Wellens T-wave Inversions

Figure 10. Wellens T-wave inversions indicative of spontaneous reperfusion.

What Dr. Wellens didn’t mention in his original paper—and what is still not well known—is that you can see these sorts of T-wave inversions in any sort of STEMI. If a lateral STEMI suddenly reperfuses, you might see T-wave inversions in the lateral leads. If an inferior STEMI reperfuses, you might see T-wave inversions in the inferior leads (like we do here). And finally, if a posterior STEMI reperfuses, you can see T-wave inversions in the posterior leads. These posterior reperfusion waves are reflected on the standard 12-lead as subtly taller, upright T-waves in V2 and V3 (which we also see here).

Note the other important finding, listed in big text at the top of the Fig. 8: The patient’s pain, while present at a 3 out of 10 during EKG #1, was absent during EKG #2. That confirms that we are looking at reperfusion T-waves in EKG #2, which in-turn means that EKG #1 must have been showing an infero-posterior STEMI!

At this point in the patient’s course I was convinced but no one else was buying that this patient with a “headache” was actually experiencing an intermittent and spontaneously reperfusing STEMI.

Thankfully her troponin-I (ref <= 0.04 ng/mL) came back mildly elevated at 0.80 ng/mL right around that time, buying her some stronger consideration for ACS. She received aspirin, nitro paste, metoprolol, clopidogrel, and enoxaparin in the ED and preparations were made to admit her for an unstable angina/NSTEMI workup.

About 90 minutes after EKG #2 the patient began to complain of slight pain again and another EKG was recorded, including posterior leads:

Subtle infero-posterior STEMI

Figure 11. Repeat ECG showing subtle infero-posterior STEMI (again).

Inferior STEMI, Posterior ECG

Figure 12. Posterior ECG (V7–V9) showing no ST-elevation in the posterior leads.

The T-waves in lead III are now purely upright again—this is a phenomenon known as pseudo-normalization. Rather than being normal and reassuring, it is actually an indication of re-occlusion of the culprit artery. When dealing with reperfusion T-waves, an inverted T-wave becomes a good thing because it means the previously blocked artery is now open. A sudden reversion of an inverted reperfusion T-wave to a normal, upright configuration is usually associated with re-occlusion of that temporarily unclogged coronary artery.

As I was the electrocardiograph wires after EKG #4, the patient mentioned that her pain had completely resolved again, so of course I reattached her and ran another tracing:

Infero-posterior reperfusion

Figure 13. Infero-posterior reperfusion pattern… again.

This EKG suggest that she is in the process of reperfusion yet again, though there is still some mild residual ST-depression. The most important thing that that the T-wave in lead III has returned to its flipped “reperfusion” morphology—a good thing!

For a better visualization of changes across these last three EKG’s over the course of six minutes, check out the gif below.

Infero STEMI and reperfusion gif

Figure 14. The continuum between inferior STEMI and spontaneous reperfusion.

Follow each lead individually:

  • Lead III transitions from mild ST-elevation with an upright T-wave (STEMI) to an upright T-wave with no elevation to finally an inverted reperfusion T-wave.
  • aVL goes from showing ST-depression with a steep downslope (reciprocal changes) to an isoelectric J-point with very little downslope to the T-wave.
  • V3 initially shows concordant ST-depression with a small T-wave (posterior STEMI), but eventually evolves to showing a isoelectric J-point with a T-wave that is slightly taller than before (mirror image of a posterior reperfusion wave).

Just because we can, here’s a similar animation of all five ECG’s over the patient’s ED course.

Infero-posterior STEMI to reperfusion gif

Figure 15. The process of intermittent injury and spontaneous reperfusion over the patient’s ED course.

The patient was admitted to telemetry where her troponin-I values (ref <= 0.04 ng/mL) every 6 hours trended as:

  • 0.80 ng/mL
  • 0.75 ng/mL
  • 0.79 ng/mL

Echo the next morning showed normal left ventricular size and function with no regional wall motion abnormalities and a preserved EF of 55%. There was no echocardiographic evidence of LVH. That day she was transferred to the CCU at a nearby hospital where she experienced an uneventful course and underwent coronary angiography a couple of days later,  as planned.

Unremarkable left coronary system

Figure 16. Unremarkable left coronary system.

RCA culprit lesion

Figure 17. The right coronary system shows a culprit lesion in the RCA.

Cath showed a culprit lesion in the right coronary artery (RCA), perfectly consistent with the pattern of infero-posterior injury and reperfusion we were seeing on the patient’s ECG’s! She received a single drug-eluting stent and had a good outcome with no significant loss of LV function or other sequelae.

Open RCA

Right coronary artery status-post PCI and a single stent.

It might seem crazy that this patient was experiencing anginal pain in the back of her head, but that’s actually a well documented (though not really well known) presentation of myocardial ischemia known as “cardiac cephalgia.” We’ll discuss this a bit more in a couple of days but I think we’ve covered more than enough ground for today.

Let me know if you have any questions in the comments or in response to our links to this case on Facebook and Twitter!

59 Year Old Female: Intermittent Head Pain (Part 1)

One of my co-workers told me that she wants to see more case studies.

A 59-year-old female presents to the emergency department with a chief complaint of “head pain that comes and goes.”

She describes the pain as a dull ache in her occiput that’s been striking without warning a couple of times per day for the past ten days. Over the last three days she’s noted that it has also been radiating into her neck and upper back/shoulders.

Onset – 10 days prior
Provocation/Palliation – None that she can identify
Quality – Dull ache that gradually worsens over the first few minutes
Radiation – Sometimes to her neck and upper back/shoulders
Severity – Around 9 out of 10 at its worst
Timing – Intermittent, each episode lasting ~10–15 minutes

Signs/Symptoms – A well-appearing 59yo F in no acute distress; symptoms as described above. She denies any associated nausea/vomiting/shortness-of-breath/lightheadedness/palpitations/syncope, but has occasionally experienced blurred-vision.
Allergies – No known drug allergies
Medications – Metformin, sitagliptin, insulin glargine, lisinopril
Past Medical History – Type II diabetes mellitus, hypertension, occasional migraines, appendectomy (40 years prior)
Last Oral Intake – Dinner three hours prior to arrival
Events Preceding Presentation – She experienced another spell at dinner and it self-resolved, but then a few hours later it came back and disappeared again. Realizing the episodes were becoming more frequent, she decided to get checked-out and drove to the ED. While she is signing in at triage she mentions that the pain is starting to come back.

Temperature – 36.9 C (98.4 F)
Heart Rate – 80 bpm
Blood Pressure – 142/88 mmHg (NIBP)
Respiratory Rate – 15 /min
SpO2 – 97% (room air)

Because of her vague symptoms and pain that involves her back/shoulders, a 12-lead ECG is performed soon after arrival.

1169 - 01a

What do you see?

What are your next steps in workup/management?

No, doubling the paper speed will not reveal hidden P-waves

Apparently I went to the Rick Bukata School of Titling Articles.

A 22-year-old male presents with agitation and delirium after smoking an unknown substance that an equally unknown person on the street offered him. You note a rapid radial pulse at around 150 bpm and attach him to the cardiac monitor:

Figure 1. Initial rhythm at normal paper speed.

Figure 1. Initial rhythm at normal paper speed (25 mm/s).

Well now we’re in a tough spot. It’s difficult to tell whether Fig. 1 shows sinus tachycardia or some non-sinus narrow-complex tachycardia (we’ll use the colloquial shorthand of “SVT” to include all those other options on the differential, including AVNRT, AVRT, ectopic atrial tachycardia, junctional tachycardia, etc…). If it is indeed sinus tach, then the requisite P-waves must be those upright deflections in II and III and superimposed on the T-waves.

Is there something we could do to see if those really are P-waves buried in the T-waves?

If you’re like me, you were probably taught that it would be a clever move to double the paper speed in a situation like this to separate the P’s from the T’s, revealing the diagnosis of sinus tachycardia. Let’s see what happens when we do that.

Here’s the same rhythm strip run at double-speed:

Figure 2. Double-speed

Figure 2. The same rhythm strip as Fig. 1 but performed at double the paper speed (50 mm/s). [Note: this is only the first 5 seconds of the full 10-second strip. Since the paper’s going twice as fast, a 10-second strip at 50 mm/s ends up twice as long, which is a bit unwieldy for posting.]

We still can’t distinguish P-waves from the T-waves..

Then this must be SVT, not sinus tachycardia!

[Spoiler] But this is sinus tachycardia!

It turns out that changing the paper speed does nothing to reveal waves buried in the ECG. I’ll admit, I used to think it would help too since several instructors suggested it would and I never bothered to try it out. Five years ago I even included it in my first list of pointers for spotting 2:1 atrial flutter—a tip I’ve since redacted. The rationale for why this maneuver’s not helpful has to do with the simple reason why ECG waves end up superimposed in the first place:

There are two events happening at the same time!

A P-wave ends up on top of a T-wave when atrial de-polarization and ventricular re-polarization occur simultaneously. No adjustment to the paper speed is going to change that fluke of timing. It doesn’t matter if the paper if going 10 mm/s or 100 mm/s—if the P-wave is happening at the same time as the T-wave, they’re always going to be superimposed on the ECG.

Don’t believe me?

Let’s look at the normal-speed tracing from Fig. 1 again, but this time I’m going to crop it so that we only see the first half of the strip:

Figure 3. This is identical to Fig. 1 except cropped to show only the first 5 seconds.

Figure 3. This is identical to Fig. 1 except cropped to show only the first 5 seconds.

Now, rather than changing the paper speed, I’m going to stretch the image above by doubling its width.

Figure 4. This is the same image as Fig. 3 except stretch horizontally to double the width.

Figure 4. This is the same image as Fig. 3 but stretch horizontally to double the width.

We can now compare our true double-speed printout (Fig. 2) with this simulated version (Fig. 4). It turns out they are absolutely identical.

Figure 5. The top strip is Fig. 2 (50 mm/s) and the bottom strip Fig. 4 (25 mm/s stretched).

Figure 5. The top strip is Fig. 2 (50 mm/s) and the bottom strip is Fig. 4 (25 mm/s, stretched horizontally).

Another way of understanding this is that all of the information contained on the 50 mm/s strip is already available on the standard 25 mm/s strip. Running the paper at double-speed does nothing to uncover “hidden” complexes since every aspect of the ECG is stretched equally.

What it does succeed at, however, is making ECG interpretation more difficult for providers who don’t usually reading tracings at 50 mm/s (probably 99% of our readers and certainly all of our editors). Outside of the electrophysiology lab and a few countries where 12-lead printouts often include a 50 mm/s rhythm strip, these sorts of tracings are a rarity. And since most of ECG interpretation comes down to pattern-recognition, changing the speed of even simple tracings interrupts all the mental shortcuts we’ve spent years building—forcing experienced providers to approach double-speed tracings with the deliberate, uncertain, and unpracticed eyes of novices.

While it’s possible to read ECG’s that way, it’s not fun.

The Outcome

The trick we do suggest in this situation isn’t that tricky: run a 12-lead.

Figure 5. 12-lead ECG run simultaneously with the prior rhythm strips.

Figure 6. 12-lead ECG run simultaneously with the prior rhythm strips.

V1 in the ECG above confirms that, without a doubt, those are P-waves we are looking at in the T-waves. Their timing raises another issue however: The Bix Rule suggests that whenever you see P-waves positioned halfway between R-waves, you need to worry that there could be hidden P-waves buried within the R-waves as well.

So rather than sinus tachycardia at 140 bpm, could we be dealing with atrial tachycardia at 280 /min with 2:1 conduction?

Figure 7. Blue arrows denote P-waves, while red arrows show where buried P-waves could be hidden as predicted by the Bix Rule.

Figure 7. Blue arrows denote P-waves, while red arrows show where buried P-waves could be hidden as predicted by the Bix Rule.

Thankfully, given a short period of time, in a case like this it’s pretty easy to rule-in sinus tachycardia since it will usually respond to management of the underlying condition. The patient was treated with a small dose of lorazepam and supportive care and a repeat tracing run about 15 minutes later.

Figure 8.

Figure 8. 15 minutes later, it is now clear that we are dealing with sinus tachycardia.

For the curious, I’ve also printed the rhythm from Fig. 8 at double-speed.

Figure 9.

Figure 9. The same strip as Fig. 8, this shows sinus tachycardia at double-speed.

And, finally, the 12-lead.

Figure 10.

Figure 10. This 12-lead, again confirming sinus tachycardia, was performed simultaneously with the rhythm strips in Fig. 8 and 9.

So, the next time someone tries to be clever and identify sinus tachycardia by printing a 50 mm/s rhythm strip, be extra clever and don’t waste your time. There’s no workaround for superimposed complexes and unless you’re in the EP lab, a tracing at standard speed has all the information you could possibly need.


After sharing this on various social media platforms I was glad to see a bunch of comments from readers suggesting that running a Lewis lead rhythm strip might have a role here. The Lewis lead is a relative of V1 (though definitely not identical), and since V1 is our best lead for picking out P-waves on that first 12-lead (Fig. 6), it makes sense that the Lewis lead should offer a similarly useful view of the atria. I didn’t mention that option in my original article for two reasons:

  1. I’m prone to digressions so I’m trying to kept my posts “tighter” these days.
  2. I didn’t think of it.

For more information on how to obtain the Lewis lead and some examples of situations in which it might be helpful I suggest starting with the posts below:


RCP de Alto Desempaño – ¡Rendimiento sobre Protocolo!

Pit Crew CPR Espanol

Esta entrada es un complemento a Pit-Crew CPR en Adultos y Pit-Crew CPR Pediátrica.

En concreto, esta es la forma en la que hemos modificado nuestro proceso de formación tras asistir a la Resuscitation Academy en Seattle / King County.

Durante el re-entrenamiento, cada rescatador debe experimentar cada posición al menos dos veces. Dicho de otro modo: se ejecuta el ejercicio, parar y cambiar, ejecutar el ejercicio, parar y cambiar. ¡Esta práctica es muy bien recibida por los técnicos de emergencias médicas y paramédicos! Resulta divertido ver como el rendimiento mejora con el tiempo.

Eso es lo que se trata todo esto ¡perfeccionar la reanimación!

En un mundo perfecto usted usaría un maniquí instrumentado para medir la velocidad, la profundidad, el retroceso del pecho, la fracción de compresión y el volumen de aire cuando se aprieta la bolsa.

En la Resuscitation Academy se utiliza un torso Resusci Anne QCPR AED® de Laerdal con ShockLynk® y SimPad® por cada grupo de 6 reanimadores. Cada set tiene un costo aproximado de $6,000.00 USD. Me gusta como se siente el equipo con esta configuración en particular. Contamos con varios maniquíes diferentes y los más “avanzados” no se sienten del todo bien al realizar las compresiones torácicas.

Dividimos nuestro entrenamiento en cuatro posiciones:

  • Posición 1: monitor / Líder de código.
  • Posición 2: compresiones torácicas.
  • Posición 3: vía aérea.
  • Posición 4: asistente / Siguiente en compresiones torácicas.

Una vez que la RCP de Alto Desempeño ha sido puesta en marcha, se permite el acceso a dos reanimadores adicionales para establecer acceso IV/IO y administrar epinefrina. Les enseñamos a nuestros equipos a postergar el manejo avanzado de la vía aérea durante los primeros 5 ciclos a menos que sea absolutamente necesario (por ejemplo, paro por asfixia, incapacidad de ventilar, necesidad urgente de proteger las vías respiratorias).

Posición 1

  • Coloca el monitor en ángulo de 45 grados hacia el hombro izquierdo (el monitor puede ajustarse unos pasos de la zona de trabajo),
  • Busca el pulso y anuncia “no tiene pulso, comiencen RCP”.
  • Conecta el circuito de capnografía.
  • Despliega los electrodos y coordina su colocación con el reanimador en las compresiones torácicas.
  • Cambia el monitor a modo pediátrico si es necesario.
  • Inicia el metrónomo a una velocidad de 110 bpm.
  • Cuando es necesario, pre-carga el monitor a la dosis de energía correcta y coordina la pausa peri-choque.
  • Actúa como líder de código: coordina, da instrucciones claras y resuelve problemas.

Posición 2

  • “Flota” (sus manos en posición de RCP, sin tocar a la víctima) durante la comprobación del pulso.
  • Lleva a cabo la RCP con velocidad, profundidad y el retroceso del pecho correctos.
  • Acepta comentarios de la tripulación sobre la calidad de la RCP.
  • Coordina la colocación de los electrodos con el reanimado al monitor.
  • Cuenta en voz alta “13, 14, 15” o “28, 29, 30” para alertar al socorrista en la vía aérea para dar respiraciones.
  • Espera solo dos segundos para que el reanimador en la vía respiratoria dé respiraciones y continúa comprimiendo.
  • Ayuda a mantener un registro de ciclo de 2 minutos.
  • Cuando el Líder de código anuncia “detener la RCP” al comienzo de la pausa peri-choque, este rescatador se pone fuera del camino.

Posición 3

  • Anuncia “Voy a la vía aérea”.
  • Selecciona la BVM del tamaño correcto y acopla la línea de capnografía entre la mascarilla y la bolsa.
  • Anuncia “listo para el 15×2” o “listo para el 30×2”.
  • Recuerda al reanimador en las compresiones de contar las tres últimas compresiones.
  • Ventila correctamente (solo lo suficiente para elevar el pecho, con liberación completa entre ventilaciones).
  • Maneja la vía aérea del paciente según necesidades del código.

Posición 4

  • Inmediatamente despliega y prueba la unidad de aspiración.
  • Conecta la BVM al tanque de oxígeno y abre el regulador a 15 LPM.
  • Se ser necesario saca el libro del Método Handtevy y determina la edad del niño.
  • Anuncia la edad y el peso (en kilogramos) del niño.
  • Selecciona la COF del tamaño correcto y la entrega al renimador en la vía aérea
  • Entrega el libros Hantevy al reanimador en el monitor.
  • Este reanimador es el siguiente en dar compresiones torácicas.

Hasta ahora, nuestros equipos han disfrutado mucho este método de entrenamiento. ¿Cuándo fue la última vez que usted ha oído vítores y aplausos durante una clase de RCP?

Traducido por Dr. Gerardo Gastélum P
Director Académico en RCP para Vivir.