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Not so fast...

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January 05, 2011


EMS 12-Lead
by Tom Bouthillet

Not so fast...

Can you interpret these ECGs?

By Tom Bouthillet

Editor's note: We're pleased to introduce a new competition this month connected to "EMS 12-Lead." Think you know what's going on in this latest scenario? Read the details and the 12 Lead ECG below and submit your diagnosis and how you would treat this patient – get it right and you could win an EMS1 T-shirt and bottle opener. Enter your thoughts in the comments section. And good luck!

--> UPDATED: 01/20/2011 - Patient Follow-Up Posted.  CLICK HERE FOR THE ANSWER

Here's an interesting case submitted by Stephen Moorhead of Greenville County EMS.

EMS is called in the early morning to the residence of a 85-year-old male with a chief complaint of chest pain.

On arrival the patient is found sitting on the edge of his bed. He appears anxious and acutely ill.

His skin is pink, warm, and moist.

He states that he was awoken from sleep with severe chest pain.

Onset: 20 minutes prior to EMS arrival
Provoke: Nothing makes the pain better or worse
Quality: "Heaviness" and "constricting"
Radiate: The patient does not radiate
Severity: 10/10
Time: No previous episodes

Past medical history: HTN, dyslipidemia, MI, CABG, pacemaker

Medications: Lisinopril, metropolol, niacin, calcium

Vital signs:

RR: 20
Pulse: 136
BP: 150/96
SpO2: 96 on RA

The cardiac monitor is attached.

 


A 12-lead ECG is captured.



How would you treat this patient and why? Tell us in the comments below— get it right and you could win an EMS1 T-shirt and bottle opener.

 

About the author


Tom Bouthillet is a Fire Captain/Paramedic with Hilton Head Island Fire & Rescue, Editor of the EMS 12-Lead blog, host of the Code STEMI web series at First Responders Network, a member of the Editoral Advisory Board of EMS World Magazine, and developer of the 12-Lead ECG Challenge smartphone app. He has taught nationally in the Critical Care Transport (CCEMT-P) program out of UMBC and his writings have been referenced in the American Heart Journal, the Journal of the American College of Cardiology: Cardiovascular Interventions and the EP Lab Digest. Contact Tom at tom.bouthillet@ems1.com.

Comments
The comments below are member-generated and do not necessarily reflect the opinions of EMS1.com or its staff.
Frank Amanze Frank Amanze Monday, April 09, 2012 5:14:10 AM going to say VT as it fits the criteria of ERAD with a positive V1.
??? ??? Monday, April 09, 2012 6:05:40 AM This is VT according to morphologic criteria. It's verapamil sensitive VT. Verapamil 10mg IV is treatment of choice.
Kevin Mazza Kevin Mazza Monday, April 09, 2012 6:40:33 AM Amiodarone 150mg over 10 minutes.
Nick Adams Nick Adams Monday, April 09, 2012 7:00:12 AM ERAD with a positive V1 = 99% VT, plus a negative complex in V6. V6 being at the apex of the heart and V1 being proximal to that shows that a negative complex in V6 and a positive complex in V1 is the electrical impulse originating in the ventricals and traveling upwards, away from lead V6, and towards the V1 lead. This is most certainly VT even though I can seen what appears to be retrograde PW's in leads III, aVF, and V4, but I think that it's apart of the QRS complex itself. The pt's CP is most likely secondary to the cardiac disfunction and HR, which causes ischemia and pain. Slow the rate first. O2 is NOT necessary because a RR of 20 is most likely secondary to anxiety, and the pt's SpO2 is 96% on RA. IV, ECG (3), pre-ECG (12), Protocols state Adenosine @ 6mg IVP as a first-line drug, even though I don't think it will work. Amiodarone @ 150mg IV gtt over 10 minutes. Once the VT breaks, a post 12-lead EKG is indicated. If the pt is still experiencing CP after the rate has been reduced, especially if there is evidence of post conversion ischemia or infarction, ASA @ 324mg, NTG x3 @ 0.4mg SL Q 5minutes followed by a gtt @ 10 mcg/min and titrating up 10 mcg as long as the SBP remains >100 mmHg, 5mg of Morphine IVP (slow) for pain control and preload reduction through histamine release and vasodilation, or 1mcg/kg of fentanyl IVP (slow) for pain, which both reduces myocardial work load secondary to pain reduction......transport to cardiac center.
Kathie Magin Kathie Magin Mon Apr 9 08:21:29 PDT 2012 NERD!!!!! giggle. :)
Chee Yong Chuan Chee Yong Chuan Monday, April 09, 2012 7:08:52 AM ECG shows a wide complex tachycardia.The usual dilemma occurs when the patient is hemo-dynamically stable and in this patient a normal blood pressure(hypertensive actually) in the absence of pulmonary edema/altered mental status/severe ischemic chest pain. Things are less complicated when it comes to unstable VT-->DC cardioversion. Now there are 3 possibility to this ECG: 1) Ventricular Tachycardia 2) SVT with aberrancy 3) SVT with an underlying accessory pathway. I would go with the diagnosis of VT for several reasons. 1) A patient with an underlying history of CAD/previous MI and CABG makes VT more likely. 2) AV dissociation is present. If you could have a closer look at the first image(rhythm strip of lead I, you could make out small P waves in between the broad QRS complexes. 3) QRS complexes are very broad >400ms. 4) Positive concordance over pre-cordial leads. 5) Couldn't appreciate a typical LBBB/RBBB morphology. 6) Josephson's sign, in the long lead II, there is a notch near the nadir of S wave. 7) I think Brugada sign is present too. Just have a look at lead II, the onset of QRS to the nadir of S wave is about 3 small boxes, which is more than 100ms. The only ones absent are capture and fusion beats I guess. With regards to treatment, when in doubt/when patients become unstable treat as VT. Treat the patient and not the ECG! Based on ACLS 2010, we could possible try a dose of adenosine 6mg fast push IV since this is a stable regular wide complex tachycardia. With regards to choice of drug, procainamid(class IIa) over amiodarone(class IIb), depending on what you have. Still, prepare for cardioversion.
El Taco El Taco Monday, April 09, 2012 6:55:47 PM Could this be a mediate pacemaker tachycardia. I would suggest a carotid sinus massage or AV nodal blocking drugs such as adenosine, verapamil, or beta-blockers that could block VA conduction.
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