Setting: ED
CC: “I think I have palpitations.”
VS: R: 34 breaths/minute; BP: 138/88 mm Hg; P: 160 beats/minute; T: 99.8°F
HPI: A 19-year-old woman presents to the ED complaining of palpitations. She is anxious and her chest is uncomfortable from the rapid heart rate. She is not confused, and there is no “chest pain.” She is a generally healthy person, and this is the first time she has been to an ED. She drank four Red Bull energy drinks today.
PMHX: none
Medications: none
Initial Orders:
CHEM-7
CBC
Echocardiogram
ECG
Calcium and magnesium levels
What does the ECG show (Figure 1-7)?
Figure 1-7. Supraventricular tachycardia. (Reproduced with permission from Conrad Fischer.)
a. AFib
b. Atrial flutter
c. Supraventricular tachycardia (SVT)
d. VT
Answer c. Supraventricular tachycardia (SVT)
The first part of the ECG reading, on the left, shows sinus rhythm because of the presence of P waves and a normal QRS duration <100 msec. On the right, there is a narrow complex (<100 msec) tachycardia with no P waves, no fibrillatory waves, and no flutter waves. That is the definition of SVT. If there are clear P waves, then it is not SVT.
SVT and atrial flutter are regular in rhythm. Fibrillation is irregular.
What is the mechanism of the patient’s SVT today?
a. Caffeine
b. Ischemia
c. Abnormal conduction pathway at the AV node
d. Ectopic focus in the ventricle
e. Thrombus in the atrium
Answer c. Abnormal conduction pathway at the AV node
The vast majority of SVT is based on abnormal “wiring” at the AV node or an AV nodal reentry. Caffeine does not create SVT. Ischemia is a prominent cause of ventricular arrhythmias but, virtually never, atrial arrhythmias. Ectopic ventricular foci create VT, not SVT. AFib leads to stasis in the atrium that creates thrombi, but thrombi do not create SVT.
The patient is lying on her stretcher continuing to feel palpitations. Her BP is now 112/82 mm Hg. Carotid sinus massage is attempted, but it is not effective. Adenosine is given with two sequential boluses, but the SVT persists. Move the clock forward 5 to 10 minutes on CCS after vagal maneuvers and adenosine administration.
Carotid massage increases vagal tone to convert SVT.
Adenosine most often works to convert SVT.
If you are uncertain about patient status, click on “Interval History” to getan update.
Because the patient is hemodynamically stable, there is no indication for cardioversion. Palpitations do not count as hemodynamic instability. BP remains at 118/80 mm Hg. Diltiazem or verapamil is given as an IV bolus, and you move the clock forward 5 to 10 minutes. All IV agents that may potentially affect the cardiac conduction system should be given under telemetry or continuous cardiac monitoring. The telemetry monitor now shows VT (Figure 1-8).
Figure 1-8. Ventricular tachycardia. (Reproduced with permission from Stern SDC, et al. Symptom to Diagnosis: An Evidence-Based Guide. New York: McGraw-Hill; 2010.)
What should you do first?
a. Consult cardiology.
b. Transfer the patient to the ICU.
c. Check vital signs.
d. Perform synchronized cardioversion.
e. Perform unsynchronized cardioversion.
Answer c. Check vital signs.
Any change in a patient’s cardiac rhythm requires the BP to be checked immediately. If VT results in hypotension, you need immediate synchronized cardioversion. If VT persists, but BP stays normal, use amiodarone first, possibly followed by lidocaine or procainamide if there is no response to amiodarone.
Do not ever order consultations for a person who is unstable and needs immediate help. The CCS Step 3 examination expects you to help the patient, not to defer responsibility. On CCS, consultants never tell you what to do. They just say “I saw your patient; I have no specific recommendations. Do what you think is right.”
Do not ever transfer an unstable or potentially unstable patient to another part of the hospital without first starting treatment and ordering tests. Both a transfer and a consultation are inappropriate first responses on the Step 3 examination because they make you look like an idiot who cannot care for a sick patient.
Shock Unstable Ventricular Tachycardia Unstable =
• Chest pain
• Systolic <90 mm Hg
• CHF
• Confusion from hypoperfusion
As you order vital signs, the clock will automatically move forward 2 minutes. If you have not already done so, order calcium, magnesium, oxygen, and potassium levels. Low levels of all of these are associated with developing arrhythmias, particularly ventricular arrhythmias. Do not wait for the results to give magnesium. Giving magnesium can help correct ventricular arrhythmia. Do not give calcium or potassium without being sure the level is low.
When the clock is moved forward 2 minutes, the patient’s BP is 140/90 mm Hg. Palpitations are the only symptom. VT persists.
What should you do?
a. Perform synchronized cardioversion.
b. Perform unsynchronized cardioversion.
c. Give amiodarone.
d. Give quinidine.
Answer c. Give amiodarone.
Use amiodarone first for hemodynamically stable VT. Amiodarone is a clear first choice as an antiarrhythmic for both VT and ventricular fibrillation. Although lidocaine is a second-line drug, Step 3 does not put you in “hairsplitting” decisions where lidocaine could be a choice. The wrong answers are clearly wrong. Quinidine is a rarely used class Ia agent for atrial arrhythmias, and there is no point in cardioverting VT until medications have been tried and failed.
After amiodarone, the rhythm converts to normal sinus at a rate of 70 beats/minute. Symptoms of palpitations resolve.
What most likely led to this situation in which SVT deteriorates to VT after the use of verapamil?
a. Dilated cardiomyopathy
b. Hypertrophic cardiomyopathy
c. WPW syndrome
d. Brugada syndrome
Answer c. WPW syndrome
WPW is notorious for worsening after the use of CCBs (Figure 1-9). WPW is one of the only syndromes to alternate SVT with VT. Dilated cardiomyopathy may have worsening systolic function with the use of a prominent negative inotrope such as verapamil, but neither dilated nor hypertrophic cardiomyopathy alone will result in an arrhythmia just from use of a CCB.
Figure 1-9. Left: Wolff-Parkinson-White (WPW)-type preexcitation and short PR-type preexcitation. Right: (top) Delta waves of different magnitude: (A) minor preexcitation and (B, C) significant preexcitation; middle: three consecutive QRS complexes with evident preexcitation; (below) short PR-type preexcitation. (Reproduced with permission from Fuster V, et al., ed. Hurst’s The Heart, 13th ed. New York: McGraw-Hill; 2011.)
Brugada syndrome is a genetic disorder leading to syncope and sudden death in association with a right bundle branch block pattern on an ECG. It is more common in persons of Asian ethnicity.
What is the mechanism of arrhythmia formation in WPW?
a. Elimination of normal AV node
b. Bundle branch block in ventricles
c. Accessory bundle of Kent
d. Loss of normal calcium channel in the AV node
Answer c. Accessory bundle of Kent
WPW is an anatomic defect in the conduction system of the AV node. An abnormal accessory pathway is present. Calcium channel blocking medications produce blockade in the normal AV nodal tissue forcing cardiac conduction down the abnormal accessory pathway in the bundle of Kent. This can lead to either SVT or VT, although SVT is more common.
Besides the CCBs that were used in this patient, what is the medication most dangerous in WPW?
a. Digoxin
b. Beta-blockers
c. Procainamide
d. Sotalol
Answer a. Digoxin
Digoxin has a strong blocking effect on normal AV nodal conduction tissue. This effect forces conduction down the abnormal pathway. This occurrence is much less common with beta-blockers. Procainamide is the best therapy for WPW during arrhythmia. In this case, it was not known that WPW was the cause of the VT and that is why the standard of care for VT, which is amiodarone, was used. In the future, if WPW leads to SVT or VT, procainamide is the best drug therapy.
Which part of the ECG is most affected by WPW (Figure 1-10)?
Figure 1-10. The PR interval is shortened (double arrow) and a delta wave (upsloping initial QRS segment) is seen (arrow, shaded area). (Reproduced with permission from Knoop KJ, et al. The Atlas of Emergency Medicine, 3rd ed. New York: McGraw-Hill; 2010.)
a. PR segment depression
b. PR interval <120 msec
c. PR interval >200 msec
d. Wide QRS complex
e. Long QT interval
Answer b. PR interval <120 msec
The accessory bundle of Kent conducts faster than the normal AV node. This make the PR interval shorter than the lower limit of normal, which is 120 msec.
The slowest conduction in the normal heart is the AV node.
The patient is admitted to the ICU, which is appropriate for patients with WPW presenting with VT. Patients with asymptomatic WPW or just SVT can be sent to the regular hospital ward. Order an echocardiogram if not already done. Now that the patient is stable, consult cardiology and electrophysiology. The patient needs evaluation for a permanent repair with radiofrequency catheter ablation.
WPW syndrome is readily cured with catheter ablation.