Key Questions For History Of Present Illness In The WCT Patient

Wide Complex Tachycardia: Risk Management Pitfalls

Risk Management Pitfalls:

1. “Look at this rhythm strip. It’s a narrow complex tachycardia. We have an SVT on our hands.” Avoid making a diagnosis of narrow complex tachycardia by one or two lead rhythm strips alone. Only when the QRS is narrow in all 12-leads can a classification of narrow complex tachycardia be used. Many wide QRS tachycardias have a narrow QRS complex in a few leads (because a portion of the QRS is isoelectric in those leads). In the unstable patient with WCT, DC cardioversion is the treatment of choice. The management of stable patients with WCT will be greatly facilitated by a 12-lead ECG that demonstrates the tachycardia.

2. “That looks like VT on the telemetry monitor. Get the paddles.” Avoid making a diagnosis of VT vs. SVT with only a rhythm strip or by monitoring the rhythm on a telemetry screen. If the patient is unstable, then “getting the paddles” is the correct next step (regardless of whether the rhythm is a VT or SVT with AVC). A stable patient will benefit from a paper copy of the 12-lead. Many of the specific signs for VT are quite subtle (e.g., AV dissociation) and need a few minutes of your time with the paper copy of the ECG. Since the specific diagnosis (SVT with AVC or VT) can never be made with 100% certainty in every case, a paper copy of the tachycardia is very useful in the longterm management of the patient.

3. “He looks very good. It’s probably an SVT.” Avoid the assumption that a patient with stable vital signs or minimal symptoms could only have SVT. The literature is also littered with cases of wide complex tachycardias where the incorrect diagnosis of SVT was made partly because of “how well the patient looked.”

4. “This is SVT with aberrancy. See, it meets all the QRS morphological criteria on the 12-lead ECG.” No single electrocardiographic criterion or combination of criteria are adequate to distinguish between SVT and VT. While the Griffith or Brugada algorithms are quite accurate, neither of them is 100% accurate. The patient’s history, physical examination, and laboratory data can be very helpful. Therefore, ask a stable patientmregarding any history of MI, CHF, recent unstable angina, complex congenital heart disease, and allergies.

5. “This is VT. SVT with aberrancy never looks this bizarre.” Do consider electrolyte abnormalities and drug toxicity in the differential. While the timely treatment of VT with cardioversion is quite important, it can sometimes be ineffective in patients with metabolic derangement, especially hyperkalemia or toxic ingestion. If possible, question patients and their families regarding drug ingestion, and check laboratory studies for electrolyte levels.

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Wide Complex Tachycardia: Case Study

Case Study:

It’s actually a slow day in the ED and you make the mistake of saying so. Suddenly, the EMS radio goes off and reports that they are en route with a dyspneic older male, status post recent syncopal event—ETA 10–12 minutes; an ECG rhythm strip is sent for your review. He has a history of myocardial infarction (MI) with congestive heart failure (CHF). His vital signs include a blood pressure (BP) of 100/65 mm Hg, pulse (P) of 170 bpm, respiratory rate (RR) of 28/minute, and oxygen saturation (SAT) of 92% on 4l nasal cannula.

Seconds later, the charge nurse tells you that you should see the elderly lady in room 22 soon. Upon entering the room, you see an awake, alert, elderly female sitting comfortably on the stretcher. She is conversant and in no distress. Her vital signs include a BP of 170/120 mm Hg, pulse 170 bpm, RR of 22/minute, and SAT of 94% on room air; the 12-lead ECG reveals a wide complex tachycardia.

Then, you hear “I need a doctor now” from room 9. You find a young adult male supine on the cot. He is alert and oriented, complaining of extreme dizziness and weakness. He is pale and diaphoretic. The monitor demonstrates a WCT. The examination is significant for a BP of 85 mm Hg by palpation, pulse 190 bpm, RR of 34/minute, and SAT of 96% on room air.

Around the same time, you are called to the telephone regarding a patient a local internist is sending in for evaluation. An elderly male, aged 71 years, presented with palpitations. He has a history of stable angina managed with atenolol. His examination is remarkable for normal vital signs with the exception of a pulse of 190 bpm. The ECG rhythm strip demonstrates a WCT.

Case Study Conclusion:

Patient #1, a 67-year-old male with MI and CHF, demonstrates a WCT. In the prehospital setting, the patient was stable or, more appropriately phrased, not unstable. Unfortunately, he has deteriorated upon arrival. He is lethargic with a BP of 70 mmHg by palpation. The monitor demonstrates the WCT as seen in Figure 1; note the appearance of deflections and irregularities in the QRS complexes—likely representing AV dissociation. A 12-lead ECG of this WCT is shown in Figure 14. The Griffith algorithm reveals a right axis deviation with a left bundle branch morphology WCT and AV dissociation, all of which lead to the diagnosis of VT. You rapidly assess him, noting his significant instability. He is sedated with etomidate and cardioverted at 100 joules to sinus tachycardia and an improved hemodynamic picture. The 12-lead ECG subsequently performed does not demonstrate ACS-related abnormalities; the serum marker analysis is normal. He is admitted to the CCU.

Patient #2, the elderly female with a hemodynamically stable WCT, demonstrates a wide complex rhythm. Her examination is remarkable only for the rapid rate. The 12-lead ECG reveals a WCT with RBBB morphology at a rate of 150 bpm that does not meet the Griffith RBBB criteria. This leads you to a presumptive diagnosis of VT. During your history, the patient notes a history of atrial flutter. You review her prior ECGs, one of which demonstrates sinus rhythm with an identical RBBB morphology as the one today. The other ECG demonstrates atrial flutter with 4:1 conduction (a rate of 75 bpm) with an identical RBBB morphology as the WCT today. She is cautiously diagnosed with atrial flutter with rapid ventricular response (with 2:1 AV conduction) and preexisting bundle branch block. She receives intravenous diltiazem and is admitted to the telemetry unit for further monitoring.

Patient #3, a 19-year-old male with palpitations and weakness, is more problematic. He is somewhat illappearing, yet his BP has improved spontaneously to 105/79 mm Hg. The monitor continues to demonstrate an irregular WCT with the 12-lead ECG revealing a similar finding. Review of the rhythm lead V1 (below the 12-lead ECG in Figure 18) demonstrates no significant (including capture/fusion beats) and doesn’t meet the Griffith criteria for classic LBBB (the “initial r” in V2 is at least 40 ms in width), you diagnose the patient with VT. His history of MI further supports your diagnosis. Due to his stability, he receives intravenous amiodarone over 10 minutes without effect; a repeat infusion of amiodarone results in a conversion to sinus tachycardia (procainamide would also have been a very reasonable choice). His subsequent ED evaluation is unremarkable; he is admitted to a monitored unit for further care.

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