Rhythm Challenge #2

Hmmm, quite a humdinger! I'm still at uni and have no other comments to go from so I'm sure my guess will be horribly off the mark, however I'm bound to learn from it!I think I've figured out where the baseline is, and the QRS looks wide, leading me to think that the rhythm is ventricular in origin. It looks as though there is ST depression, and perhaps a retrograde p wave suggesting a junctional rhythm, but it doesn't really fit with my ventricular origin theory. Will be interested to see what comes up!

Thanks for that Tom. Thought junctional rhythms could only be of an atrial nature, so thanks for the tip

Rules:- P-waves present, upright, peaked (p-pulmonale criteria met)- Regular save for 3rd complex- Rate 70-75- P-waves are associated- PRi is around normal 0.12- QRSd is wide (quite wide)Sinus rhythm with a bundle branch or abberant conduction.I'm concerned that it appears there is ST-depression or concordant T waves when there shouldn't be. I'm considering potassium changes as well (w/ such a significant QRSd). Obviously any rhythm like this gets a 12-L.

I'd also want a 12-lead to assess for BBB. This strip reminds me of a three lead where all the medics were scratching their heads looking at the monitor (thinking we mixed up the leads) until we did a 12-lead and it was like an "Ah hah!" moment (LBBB).

Anonymous – Right atrial enlargement is a fairly obscure finding for a lowly amateur! I can see where you would think that based on this ECG.Tom

Scott -Awesome job calculating the rate! May I please know what method you used?Tom

Anonymous – You're absolutely correct with regard to the P-waves in the setting of hyperkalemia.I wonder if those are really P-waves…Tom

Sooo…maybe ask him what color his urine is? Assess the arm for shunts? Trying throwing a little albutrol, sodium bicarb and calcium chloride at him and see if that does anything?! If it really is hyperkalemia…I would be guessing it's reaching the unhappy place of around 10 mEq

Okay I posted about the p waves as anonymousRe: second strip–we're really working on getting to the sine wave stage!Re: third strip–those "p" waves very well may be part the widened QRS. They just look like p-waves. V1 is typically also a good lead to look for p-waves, and there's none there. Based on the change between the two rhythm strips, the lack of p waves and the non-specific and grossly prolonged non-specific intraventricular conduction delay, I would say this is almost certainly hyperkalemia. The rhythm is most likely sinus, the hyperkalemia has basically erased the visible p-waves (but really they are still there most likely). Next stop, sine wave and cardiac arrest. This patient doesn't need labs BEFORE treatment especially if there is a likely hx. Even without a dialysis or other likely hx, there is new-onset acute renal failure to consider.

I don't see p waves, so I'd call it an idioventricular rhythm unless the pt had a hx of a ventricular pacemaker.

Okay, it looks like AIVR, but if you treat it with Ca, Sodium Bicarb, Albuterol, Kayexalate, Insulin-glucose, dialysis—the p waves should gradually reappear in their usual location as the QRS gradually narrows. AIVR implies the rhythm is originating in the ventricles. I believe the actual source of the impulses is the SA node (or at least not the ventricles). The p waves are just so impacted by the hyperkalemia that they get smaller and smaller, until the disappear from the surface EKG.

Tom, 300, 150, 100, 75 ….the original strip was just a touch to the left of the 75 block marker …so ~ 80.

"I remember because I kept palpating his chest looking for a pacemaker!"At least I got one part right…

Here a couple of better explanations for why the P-wave gradually goes away, and then gradually reappears with treatment. I am interested in hearing about other theories."Hyperkalemia preferentially affects atrial tissue and suppresses the appearance of P-waves, even when sinus node activity is still present and activating the ventricle….When treatment is initiated, the P-waves seem to reappear. In reality, sinus activity was always present but simply not visible as P-waves." Amal Mattu, ECG's for the Emergency Physician 2"As the potassium level increases…the amplitude of the P waves decreases. Eventually you will not be able to see them. Why? As the potassium level increases, the atrial myocardial cells will stop depolarizing. The SA node and the special conduction system of the atria will continue to function but the myocardial cells will not. Because the atrial myocardium creates the atrial vectors as the P-waves, we do not see any atrial activity [P-waves] on the ECG." Garcia & Holtz, 12-lead ECG: The Art of Interpretation.

Mike -Emergency treatment of suspected hyperkalemia from ACLS for Experienced Providers (2003) p.162.For moderate elevation (6 to 7 mEq/L):Initiate a temporary intracellular shift of potassium using the following agents:* Sodium bicarbonate: 50 mEq IV or up to 1 mEq/kg over 5 minutes* Glucose/insulin: Mix 10 U regular insulin and 25 g (50 mL of D50) glucose, and give IV over 10 to 15 minutes* Nebulized Albuterol: 5 to 20 mg over 15 min.For the periarrest patient, they recommend 10 mL of 10% calcium chloride IV over 2 to 5 minutes as the most important immediate therapy, and then the other therapies, along with diuretics and dialysis as required.In my service, we carry calcium gluconate.Tom

I was thinking Hyper K+ almost immediately. The widening of the QRS along with slow merging of the T's into the QRS making it a borderline sinoventricular rhyhm…not quite the sine wave (ran a pt that labs came back 8.8 K+, & was in the pre-arrest sine wave of about 40-60 BPM) but pretty close. I wish more agencies pushed for fiekd Tx's of Hyper K+, we don't do it but have all the drugs except CA-gluconate (you're lucky if you do!) or insulin. My research has lead me to this being one of the few things you can Dx in the field from a 12-Lead only before labs are drawn. I'm fascinated with what the heart can & will do.