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.

High Performance CPR – Performance Not Protocol!

Pit Crew CPR Positions jpg

This is a supplement to Adult Pit Crew CPR and Pediatric Pit Crew CPR.

Specifically, this is how we have modified our training process since attending the Resuscitation Academy in Seattle / King County.

Each rescuer should experience each position at least twice. In other words, you run the drill, stop and switch, run the drill, stop and switch. This drill is very well received by EMTs and paramedics! It’s fun to watch the performance improve over time.

That’s what it’s all about — perfecting resuscitation!

In a perfect world you would use an instrumented manikin to measure rate, depth, recoil; and volume of air when you squeeze the bag.

The Resuscitation Academy uses Laerdal‘s Resusci Anne QCPR AED Torso with Shock Link and SimPad in each “pod” of 6 rescuers. Each setup retails for about $6,000.00. I like how this particular setup “feels”. We have several different manikins and the more “advanced” ones don’t feel quite right when performing chest compressions.

We break our training down into four positions.

  • Position 1: Monitor / Code Commander
  • Position 2: Chest Compressions
  • Position 3: Airway
  • Position 4: Assistant / Next on Chest Compressions

Once High Performance CPR is up and running we allow two additional rescuers to arrive on scene so we can establish IV/IO access and give epinephrine. We teach our teams to defer advanced airway management for the first 5 cycles unless it’s absolutely necessary (e.g., asphyxial arrest, unable to ventilate, need to protect airway).

Position 1

  • Places monitor at 45 degree angle to left shoulder (monitor can be set back a few feet from working area)
  • Checks pulse and announces “no pulse, begin CPR”
  • Attaches capnography circuit to monitor
  • Extends pads and coordinates placement with rescuer on chest compressions
  • Changes monitor to pediatric mode if applicable
  • Deploys metronome at a rate of 110
  • When appropriate pre-charges the monitor at correct energy dose and coordinates peri-shock pause
  • Acts as Code Commander, gives clear directions, solves problems

Position 2

  • “Hovers” during pulse check
  • Performs CPR at correct rate, depth, and recoil
  • Accepts feedback from crew members about CPR quality
  • Coordinates pad placement with rescuer on monitor
  • Counts out loud “13, 14, 15” or “28, 29, 30” to prompt rescuer on airway to give breaths
  • Waits two full seconds for airway man to give breaths and continues compressions
  • Helps keep track of 2 minute cycle
  • When Code Commander announces “stop CPR” at the beginning of the peri-shock pause this rescuer clears out of the way

Position 3

  • Announces “I’ve got airway”
  • Selects the correct sized BVM and attaches capnography between mask and bag
  • Announces “ready for 15:2” or “ready for 30:2”
  • Reminds rescuer on compressions to count last three
  • Ventilations are given correctly (just enough to produce chest rise with full release between ventilations)
  • Manages the patient’s airway as necessary

Position 4

  • Immediately deploys and tests suction unit
  • Turns on oxygen and hooks up BVM to oxygen at 15 LPM
  • If necessary takes out Handtevy book and determines child’s age
  • Announces child’s age and weight in kilograms
  • Selects correct sized OPA for the rescuer on the airway
  • Hands Hantevy book to rescuer on monitor
  • This rescuer is next on chest compresssions

So far our crews have really enjoyed this method of training. When is the last time you’ve heard cheering and applause during a CPR class?

Check out the South Carolina Resuscitation Academy on Facebook!

See also

Adult Pit Crew CPR – The Explicit Details

Pediatric Pit Crew CPR

High Performance / Pit Crew CPR on the EMS Nation Podcast

Continuous Chest Compressions vs. 30:2. Does it matter? Depends on the quality! 

Pit Crew / High Performance CPR on the EMS Nation Podcast

Editor-in-Chief Tom Bouthillet (@tbouthillet) was on the EMS Nation podcast (@EMS_Nation) for EMS Week. The topic was Pit Crew / High Performance CPR and Systems of Care.

ems nation podcast cpr

Click HERE to open in iTunes.

Click HERE to open in Libsyn (with built-in media player).

Referenced in this podcast

Adult Pit Crew CPR – The Explicit Details

Continuous chest compressions vs. 30:2. Does it matter? Depends on the quality! 

Resuscitation Academy

The Science of CPR with Peter Kudenchuk, M.D.


Cardiac arrest and deep T wave inversions

The paramedic swung the stretcher into the resus bay, and started giving report. As the team of RNs, techs, and residents swung into action, I noted that the young adult patient didn’t look very sick at all. Confused, yes, and perhaps a bit anxious, but this seemed like an over-triage.

“Paramedic Battistelli,” I called out, “why is this 38 year-old female patient here, instead of in fast track?”

“Hey Dr. Walsh! We were called for a seizure, but she looked fine when we got to the house. She denied any problems, but family said she was just lying on the bed, no warning, when she started convulsing. Vitals and sugar were fine.  Listen, I didn’t think I should call in the cath lab team, but I didn’t like the looks of this.”  And he handed me his 12-lead:


“Well.,” I responded, “look at these deep T wave inversions in V1-V4. This looks like Wellens syndrome. We better get the cath lab rolling! When did she stop having chest pain?”

“Doc, she denied chest pain, pressure, burning – everything.”

“Okay. Then this is probably the anterior T wave inversions you see with a massive pulmonary embolism! We might need to give her tPA. Was she very hypoxic?”

“No, in fact she never so much as coughed. No trouble breathing, sats were great.”

“Well, it’s kind of rare, but you can see these sorts of inversions with Takotsubo cardiomyopathy too. Let me guess,” I asked loudly, “she must have had a terrible scare right before the seizure. Or maybe a nasty argument, or some other emotionally charged moment?”

“Nope. She had been napping on the bed with her mother.”

I asked to repeat the ECG, figuring that the leads had been misplaced, or there was some artifact, or the EMS monitor had some bad filter setting..


Crud, this looked worse.

“Medic Battistelli, this shows clear signs of Wellens at this point. As you know, women often don’t feel any pain with their MIs. I’m activating the cath lab.”

“Ok, sounds fine,” he interjected, “but I saw something else on the ECG. It sounds crazy, but…”

“Dr Walsh!” The RN grabbed my arm. “She’s seizing again – and look at the monitor!”



Palpation of her carotid confirmed pulselessness. CPR was started, and the a single defibrillation restored sinus rhythm, as well as consciousness. “Looks like that was VT triggered by ischemia,” I told the team, “let’s focus on getting her to the cath lab as quickly as possible.”

“Doctor Walsh, I was wondering,” asked Mike, “should we try one thing before sending her to the lab?”

What was Mike suggesting for therapy?


Magnesium, as therapy for Torsades de Pointes (TdP).


The arrest rhythm was a wide-complex tachycardia, and thus overwhelmingly likely to be a form of ventricular tachycardia. This VT does not have the usual monomorphic morphology, however, and is instead called polymorphic VT (PVT). One might be tempted to leap to calling this TdP based on this rhythm, given the dramatic appearance of the “twisting points,” but it’s crucial to remember that you can only diagnose TdP when the QTc is long. If the QTc was not prolonged here, this would be just PVT, which is usually caused by cardiac ischemia.


A look back at the EMS ECG shows that the QTc is quite prolonged, > 600 ms, and so we can diagnose TdP.

Why does this matter for therapy?

Well, as mentioned, PVT is usually caused by cardiac ischemia, so evaluation and treatment should first focus on ACS. TdP, by contrast, often has a metabolic (± genetic) cause, and these should be sought and corrected.


Most importantly, distinguishing between PVT and TdP is crucial when selecting an antiarrhythmic medication.

  • For PVT associated with cardiac ischemia, beta-blockers and amiodarone are considered a class I intervention.
  • For TdP, however, magnesium plays a central role (after defibrillation!), while amiodarone has no established or theorized benefit.

Interestingly, many clinicians have been taught that amiodarone is dangerous in TdP, since it is well-recognized as causing a prolonged QTc. There seems to be little evidence for this, and it appears that amio only rarely is implicated as a cause of TdP.