Synchronized Cardioversion: What Happened?

EMS was dispatched for a 62 year old male with an altered mental status. Upon their arrival they found the patient to be non-communicative, responsive to verbal stimuli, in moderate respiratory distress, with pale, diaphoretic skin, and weakly palpable radial pulses. The patient was placed on the monitor during their initial assessment:

Wide complex tachycardia of unknown etiology.

A blood pressure was unobtainable, however a pulse of 150 was palpable at the carotid. Labored respirations were present, with clear breath sounds bilaterally. The patient had an extensive cardiac history, renal failure, and insulin dependent diabetes mellitus. The patient's blood sugar was 300 mg/dL.

A 12-Lead was obtained and interpreted as presumed ventricular tachycardia:

Wide complex tachycardia, interpreted as presumed ventricular tachycardia.

Differentials of a wide complex tachycardia at 150 bpm include: ventricular tachycardia, SVT with aberrancy, sinus tachycardia with aberrancy, and 2:1 atrial flutter with aberrancy. No previous 12-Lead was available for comparison.

Given the presence of a WCT with hemodynamic instability the patient was prepped for synchronized cardioversion. Combo-pads were placed anterio-laterally, the Sync button was pressed, and sync markers were noted with each QRS complex.

The patient was then synchronized cardioverted at 100J biphasic:

100J synchronized cardioversion.

A rhythm change was noted on the monitor:

Ventricular fibrillation post cardioversion.

With ventricular fibrillation present, the paramedic disabled synchronization and delivered a 200J biphasic shock:

200J defibrillation of ventricular fibrillation.

After defibrillation, the patient regained consciousness and palpable radial pulses were present. Emergency transport was initiated. During transport, a sustained run of ventricular tachycardia occurred and the patient was given 100 mg lidocaine IV with a subsequent conversion of a sinus rhythm (not captured). The patient experienced multiple episodes of non-sustained ventricular ectopy during transport.

In this case the paramedic did not appreciate that oversensing was present from the cardiac monitor's display. It was not until after the summary printed that the ineffective synchronization was discovered.

Oversensing during synchronized cardioversion--highlighted in red--resulting in therapy delivery during the vulnerable period.

As the ventricular myocardium repolarizes, it may not do so homogeonously. This window of non-uniformity, with both absolutely and relatively refractory myocardium present is known as the Vulnerable Period. Electrical stimulation during the vulnerable period of ventricular repolarization may result in ventricular tachyarrhythmias.

Illustration of the vulnerable period of ventricular repolarization. Adapted from Reilly et al. 1998 pp 188 Fig 5.19.

This is best appreciated during episodes of a prolonged QT interval. An early-cycle premature ventricular contraction may result in the so called "R-on-T" phenomenon initiating Torsades de Pointes.

A prolonged QT interval and an "R-on-T" PVC resulting in Torsades de Pointes. Used with permission from Dr. Ken Grauer's ECG Web Brain.

In this case, the electrical stimulation was provided by inappropriately synchronized biphasic shock. By default the synchronization used Lead II, which featured proportionately smaller negative complexes when compared to their T-waves. Sometimes atrial tachyarrhythmias, such as atrial flutter or atrial fibrillation, may produce deflections sufficient to trigger R-wave deflection as well.

Oversensing of atrial fibrillation. Adapted from Resuscitation 82 (2011):135-136,Fig.1.

Appropriate lead section is important when performing synchronized cardioversion in order to avoid delivering the therapy while the myocardium is vulnerable. If synchronization is not accurate the operator of the cardiac monitor should switch leads, increase the gain, or change pad placement.

• Reilly J. Patrick. Applied Bioelectricity: From Electrical Stimulation to Electropathology. Springer-Verlag: New York (1998); pp 188.
• Dr. Ken Grauer's ECG Web Brain. Accessed online 26 July 2012. [https://www.kg-ekgpress.com/]
• Sodeck GH, Huber J, Stollberger C. Letter to the Editor: Electrical cardioversion - Misinterpretation of the R-wave. Resuscitation 82 (2011): 135-136. [PubMed]

Incidence of cardiac rhythms as determined by Paramedics on an ALS ambulance

The following are the incidence of various cardiac rhythms as determined by the treating Paramedic for an ALS ambulance from October 2007 to June 2012. Outlier data were examined for correctness, including all interpretations of rhythms with less than 2% incidence. Incomplete data for each record was added if available, otherwise the record was ignored. AV Nodal Blocks and Bundle Branch Blocks were not recorded in this data set.

• Patients: 3528 (47% male)

• Age: 8 hours - 110 years (avg 56 yr, median 60 yr)

• First Contact Heart Rate (>0): 22-260 bpm (avg 91 bpm, median 90 bpm, stdev 29.5)

• First Contact Rhythm:

Count		Rhythm
1841	52.18%	Normal Sinus Rhythm
995	28.20%	Sinus Tachycardia
145	4.11%	Paced Rhythm
139	3.94%	Sinus Bradycardia
114	3.23%	Atrial Fibrillation
88	2.49%	Asystole
68	1.93%	Sinus Arrhythmia
67	1.90%	Atrial Fibrillation w/ RVR
19	0.54%	Pulseless Electrical Activity
18	0.51%	Supraventricular Tachycardia
11	0.31%	Ventricular Fibrillation
10	0.28%	Atrial Flutter
5	0.14%	Ventricular Tachycardia
4	0.11%	Junctional Rhythm
2	0.06%	Idioventricular Rhythm
1	0.03%	Ectopic Atrial Tachycardia
1	0.03%	Junctional Tachycardia

EKG Myth - "Can't be Ventricular Tachycardia with that Axis"

This is part of a series of posts detailing common electrocardiogram myths.


Myth: Ventricular Tachycardia always has an extreme axis

When evaluating a wide complex tachycardia, many providers will look at the QRS axis to rule out ventricular tachycardia if an extreme axis is not present. An extreme right axis deviation, also known as No Man's Land, is easiest to appreciate when leads I, II, and III are almost wholly negative.

The absence of an extreme right axis deviation does not rule out ventricular tachycardia.

In fact, the sensitivity of an extreme right axis deviation may only reach 20%^[1]. More commonly, VT features a left axis deviation^[2].

In 70% (n=172) of VT cases studied by Brugada et al had a Left axis deviation^[2].

As with any cardiac rhythm, the axis is dependent on the origin and subsequent activation of the myocardium.

VT origin and QRS axis. An apical origin results in a superiorly directed axis in the frontal plane. In contrast, a basal origin leads to an inferior QRS axis (lower panel)^[3].

In VT arising from the left ventricle, a RBBB-like morphology is most common^[4]. If the origin is in the apex of the left ventricle near the inferiolateral wall, the classic extreme right axis deviation (right superior axis) will be present. Whereas, if the origin is in the left free wall a right inferior axis deviation will be present^[5].

Two cases of Ventricular Tachycardia with an (A) inferior axis and a (B) right axis deviation^[6].

In VT arising from the right ventricle, a LBBB-like morphology is most common^[7]. If the origin is closer to the septum, a right axis deviation will be present. If the origin is the Right Ventricular Outflow Tract (RVOT), an inferior axis will be present with characteristic broad, monomorphic R-waves in leads II, III, and aVF. RVOT-VT is a common ventricular tachycardia in patients without known cardiac disease^[8]. In some cases, VT arising from the right ventricle will have a normal axis.

VT with a normal axis, misclassified as SVT^[9].

Any approach to the diagnosis of a wide complex tachycardia should include ruling in Ventricular Tachycardia if an extreme right axis deviation is present. However, clinicians should be mindful that the absence of an extreme right axis deviation cannot rule out Ventricular Tachycardia.

1. Vereckei A, et al. New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia. Heart Rhythm 2008;5:89–98. [PubMed]
2. Brugada P, et al. A New Approach to the Differential Diagnosis of a Regular Tachycardia with a Wide QRS Complex. Circulation 1991;83:1649-1659. [Full Text PDF]
3. Wellens HJJ. Ventricular tachycardia: diagnosis of broad QRS complex tachycardia. Heart 2001;86:579-585. [Full Text]
4. Surawicz B, Knilans TK. Chou's Electrocardiography in Clinical Practice: Adult and Pediatric, 6th ed. Philadelphia, PA. Saunders, 2008.
5. Pellegrini CN, Scheinman MM. Clinical Management of Ventricular Tachycardia. Curr Probl Cardiol. 2010;35:453-504. [PubMed]
6. Ibid 2.
7. Ibid 4.
8. Ibid 5.
9. Ibid 2.

J-waves after ROSC and Intra-arrest Therapeutic Hypothermia

The following is the post-resuscitation 12-Lead electrocardiogram of an 82 year old female who received intra-arrest therapeutic hypothermia, via chilled saline and ice packs, as part of a new protocol for cardiac arrest management. The patient also received three defibrillations and was administered epinephrine, naloxone, and amiodarone during the resuscitation.

12-Lead ECG obtained approximately 5 minutes after ROSC

The post arrest 12-Lead ECG shows a sinus rhythm with frequent premature atrial and ventricular ectopic complexes. The LifePak 12, which uses the GE Marquette 12SL algorithm, displayed the ominous *** ACUTE MI SUSPECTED *** message and suggested a lateral injury pattern.

Closer inspection of the lateral precordial leads reveals the ST-elevations present are actually giant J-waves, or Osborn waves.

J-waves--or Osborn waves--appreciated in the lateral precordial leads

Recognizing this finding is present, a closer look at the entire 12-Lead ECG shows that subtle J-waves are present in almost every lead group.

Subsequent 12-Lead ECG obtained 17 minutes after ROSC

A repeat 12-Lead ECG acquired 12 minutes later shows a sinus tachycardia with a single PAC, without the giant J-waves from the initial ECG, diffuse ST/T-wave changes consistent with ischemia are also present. However, small J-point elevation persists in the lateral precordials. The computerized interpretation no longer believes a STEMI-pattern is present and incorrectly identifies the rhythm as atrial fibrillation.

Comparison of the precordial leads between the first and subsequent 12-Lead ECG.

A side by side look at the precordial leads provides an interesting look at the near resolution of the giant J-waves post-ROSC.

One explanation for the normalization of the traditional electrocardiographic findings of hypothermia may be related to the management of the patient's ventilation both intra-arrest and post-arrest. As the patient's pH normalized with mechanical ventilation and a perfusing rhythm, so did the repolarization abnormalities (visualized as J-waves).

References

1. Antzelevitch C, Yan GX. J Wave Syndromes. Heart Rhythm. 2010; 7(4):549-558. [FullText]
2. Fenstad ER, et al. Therapeutic hypothermia in out of hospital sudden cardiac arrest: Significance of J-waves. J Am Coll Cardio. 2011; 57(14):Suppl 5, E1002. [PDF FullText]
3. Edelman ER, Joynt K. J Waves of Osborn Revisited. J Am Coll Cardio. 2010; 55(20):2287. [PubMed]
4. Dr. Smith's ECG Blog: Osborn Waves and Hypothermia.