s/p Arrest

The study of history teaches us that we do not learn from the study of history.

New EKGs and new insights on a 2010 cold case. To recap:

While vacationing in Saigon a 57 year-old Caucasian female presented to the local emergency center with complaints of nausea and light-headedness. She experienced cardiac arrest, was resuscitated, and was found to have a persistent idioventricular rhythm coupled with significant acidosis and hypotension. She required multiple pressors and ultimately recovered despite a syndrome of multi-system organ failure. She was stabilized and transferred back to the states to a medical rehab facility. Infectious disease work up revealed only Candida Pelliculosa.

After several weeks in rehab, she again presented to the ED with complaints of nausea and light-headedness. Her past medical history included an aortic valve replacement (secondary to aortic stenosis), paroxysmal a-fib, diabetes, and depression. She was taking coumadin, flecainide, lexapro, januvia, and lopressor. Her BP on arrival was 81/44; the following EKG was recorded:

She had no complaints of chest discomfort or shortness of breath. At this time the potassium was 4.1, sodium 133, chloride 104, creatinine 3.1, BUN 31, glucose 114, and lactic acid 1.4. The white blood count was elevated at 15.6k. Amylase, lipase, AST and ALT were all mildly above normal. The pH was 7.01.

Her mental status deteriorated; she was intubated in the ED and transferred to the ICU. That night she suffered a PEA arrest and was resuscitated; multiple pressors were added sequentially for homodynamic support and a dialysis catheter and arterial line were placed. Peri-arrest bradyarrythmias were frequent and a transvenous pacemaker was inserted.

On the second hospital day the following EKG was recorded:

The potassium was 4.9, the sodium 135, chloride 101, creatinine 3.9, BUN 41, glucose 187, and lactic acid 13.

The cardiology consultant believed this to be an idioventricular rhythm of likely metabolic origin, secondary to electrolyte disturbance, possible flecainide or lexapro toxicity, or sepsis. Despite a widened QRS, the echocardiogram revealed a normal EF. Lexapro and flecainide were discontinued at this time.

On the third hospital day this EKG was recorded:

Labs from this date show a potassium of 3.5, sodium 143, chloride 97, creatinine 4.1, BUN 30, glucose 256, and lactic acid 23.

The blood pressure and electrocardiogram gradually stabilized; all cardiac enzyme assays were negative. By the seventh day she was extubated and transferred back to the hospital at which she had been originally treated returning from Vietnam. No bacteria, fungus, or parasites were isolated during this admission, however, she did have a positive hep-c antibody. Prior to discharge this EKG was recorded:

Labs from this date indicate a potassium of 3.4, sodium of 142, chloride 110, creatinine 2.4, BUN 40, glucose 303, and lactic acid 2.4.

She was subsequently lost to follow up.

Discussion

The differential diagnosis for a sinusoidal, wide complex rhythm between 80-120bpm with QRST fusion includes hyperkalemia, sodium channel blocker toxicity, aberrant QRS AIVR, and tachycardia with aberrant conduction and massive ST elevation. In 2010, when I first presented these EKGs,  I believed that this case (in the acute phase) represented AIVR.

The dominant pacemaker may in fact be idioventricular. The presence of AV dissociation would confirm this, but I do not see P waves. The third EKG (hospital day 3) is equivocal. This could also be a-fib with AIVR and dissociation.

Even if the rhythm is AIVR, there is still a more important diagnosis at stake.

For comparison, and to illustrate this, here are some exemplars:

This is typical AIVR:

Image courtesy of Life In The Fast Lane

This is RBBB with LAFB and massive STE:

Image courtesy of Dr. Smith’s ECG Blog

Hear are three cases of sodium channel blockade with TCA cardio-toxicity:

Nortriptyline toxicity. Image courtesy of ECGpedia.

Dothiepin toxicity. Image courtesy of Life In The Fast Lane.

Unknown TCA toxicity. Image courtesy of EB Medicine.

This is purported cocaine cardiotoxicity with features of sodium channel blockade:

Image courtesy of ECGpedia.

Two cases of flecainide toxicity:

Image courtesy of Bond et. al., Heart 2010. 

Image courtesy of EB Medicine.

Sodium channel blocker and specifically flecainide toxicity has been covered extensively in the literature; the following excerpts are particularly relevant in light of this case.

“Flecainide is an increasingly used class 1C antiarrhythmic drug used for the management of both supra-ventricular and ventricular arrhythmias. It causes rate-dependent slowing of the rapid sodium channel slowing phase 0 of depolarization and in high doses inhibits the slow calcium channel.” (Timperley, 2005)

“Cardiac voltage-gated sodium channels reside in the cell membrane and open in response to depolarization of the cell. The sodium channel blockers bind to the transmembrane sodium channels and decrease the number available for depolarization. This creates a delay of sodium entry into the cardiac myocyte during phase 0 of depolarization. As a result, the upslope of depolarization is slowed and the QRS complex widens.” (Hollowell, p.880– graphic and text.)

“Bradydysrhythmias are rare in sodium channel blocking agents because many of these also possess anticholinergic or sympathomimetic properties. These agents can, however, affect the pacemaker cells that are dependent on sodium entry, thus causing bradycardia. In severe poisoning, the combination of a wide QRS complex and bradycardia is a sign of overwhelming sodium channel blockade of all channels, including the pacemaker cells.” (Delk, p.683)

“Due to its significant effect on sodium channels, flecainide prolongs depolarization and can slow conduction in the AV node, the His-Purkinje system, and below. These changes can lead to prolongation of the PR interval, increased QRS duration, and first- and second-degree heart block. ….In contrast, flecainide does not affect repolarization and therefore has little effect on the QT interval.” (Giardina, G. 2010)

“Impending cardiovascular toxicity in adult patients [with TCA poisoning] is usually preceded by specific ECG abnormalities: the majority of pateints at significant risk will have a QRS duration >100ms or a rightward shift (130-270) of the terminal 40ms of the frontal plane QRS vector. The later finding is characterized by a negative deflection of the terminal portion of the QRS complex in lead I and a positive deflection of the same portion in lead avR.” (Van Mieghem, p.1569)

“In severe cases [of sodium channel blocker toxicity], the QRS prolongation becomes so profound that it is difficult to distinguish between ventricular and supraventricular rhythms. Continued prolongation of the QRS complex may result in a sine wave pattern and eventual asystole.” (Holstege, p166.)

There are multiple mechanisms for flecainide toxicity in this case.

  • Reduced metabolism and elimination due to impairment of liver and renal function.
  • Significant acidosis resulting in a decrease in protein bound flecainide and an increase in the free (active) agent in the blood stream.
  • Borderline hyponatremia as a potential predisposing condition for over-therapeutic sodium channel blockade.
The root cause of all of this remains unclear.

References

Bond, R., et al. (2010). Iatrogenic flecainide toxicity. Heart (2010), 96:2048-2049 doi:10.1136/hrt.2010.202101

Delk, C., et al. (2007). Electrocardiographic abnormalities associated with poisoning. American Journal of Emergency Medicine, (2007), 25, 672-687.

Giardina, G. (2010). Major side effects of flecainide. UpToDate.

Harrigan, R., et al. (1999). ECG abnormalities in tricyclic antidepressant ingestion. American Journal of Emergency Medicine, (1999), July 17(4), 387 – 393.

Hollowell, H. et al. (2005) Wide-complex tachycardia: beyond the traditional differential diagnosis of ventricular tachycardia vs supraventricular tachycardia with aberrant conduction. American Journal of Emergency Medicine, (2005), 23, 876 – 889.

Holstege, C., et al. (2006). ECG manifestations: The poisoned patient. Emerg Med Clin N Am, 24 (2006) 159–177. Free full text.

Timperley, J., et al. (2005). Flecainide overdose– support using an intra-aortic balloon pump. BMC Emergency Medicine, (2005), 5: 10. doi:  10.1186/1471-227X-5-10

Van Mieghem, C., et al. (2004). The clinical value of the ECG in noncardiac conditions. Chest (2004), 125, 1561-1576.

Williamson, K., et al. (2006). Electrocardiographic applications of lead aVR. American Journal of Emergency Medicine (2006), 24, 864-874.


Case No. 5: Coded in a Vietnamese ICU, now Lethargic in a US Rehab

While vacationing in Vietnam two months ago, this 57 yr old white female presented to an urgent care center with complaints of nausea and weakness. Within twenty-four hours she had coded and was on life support in a Vietnamese ICU.

Now she is home, in a rehab center, recuperating as mysteriously as she had fallen ill. Her medical team believes that perhaps she had been given a paralytic agent in the Vietnamese ED; theoretically, this may have resulted in elevated potassium and a state of recurrent iatrogenic cardiac arrest. She has been feeling progressively better, she states, until this morning, when she began experiencing an unusual nausea and sense of weakness.

She is ill appearing and hypotensive, near syncopal on ambulation. The following ECG is recorded by EMS at the scene:

And in the ED:

The Accelerated Idioventricular Rhythm was first characterized as a distinct pathophyiological entity in 1950 by A.S. Harris following the ligation and reperfusion of coronary vessels in animal models. A reperfusion based etiology has continued to predominate as the leading documented setting for AIVR, particularly in light of the growing population of post-PCI patients receiving telemetry services. Incidence has also been well established, however, in structural heart disease– both congenital as well as acquired forms– and in the setting of presumed pharmacological effects. Digitalis, cocaine, halothane, and desfurane, among others, have all been cited in the literature as culprit agents, believed to accelerate the phase 4 action potential depolarization of His-Purkinje pacemaker sites, leading to the possibility of rate competition between atrial and ventricular foci. Less pathological contexts have also been reported, however, and include highly conditioned athletes, pregnant women, and some pediatric populations. A.R. Perez Riera et al. hypothesize that a hypervagotonic / hyposympathetic mechanism is at work here, facilitating the automaticity of ventricular activity by suppressing sino av-nodal pacemakers; work in animal models seems to support this, and there is case documentation in the literature of AIVR resolving through treatment with vagolytic agents such as atropine.

Electrocardiographically, AIVR may be identified when a monomorphic wide complex ventricular rhythm supervenes over the atrial rate, persisting between 60-100bpm. Fusion beats, capture complexes, and retrograde atrial depolarization may be observed, and it is not unusual to note frank evidence of AV dissociation. These findings, including clinical evidence of cannon A waves, may expedite or cement the diagnosis as it does in VT as well as 3rd degree block. AIRV is often spontaneously initiating and resolving, and it is frequently seen as a transient phenomenon– again, most typically post reperfusion or resuscitation. While some patients predisposed to cardiac insufficiency may experience critical loss of ejection fraction as a result of AV dissociation, AIVR is not typically associated with a declining clinical picture. Treatment of the condition should, as always, reflect respect for the pt’s clinical presentation rather than certainty in the pathology of the rhythm; over-treatment may be a greater clinical risk than under-treatment.

An excellent case of AIVR can be seen here at Dr. Wiki, showing fusion and capture complexes, or here, at Medscape ECG of the week. The Emergency Medicine site, Life In The Fast Lane, has also presented a case of AIVR in the highly conditioned athlete which demonstrates subtle isorhythmic AV dissociation.

In the case presented above, our patient suffered a precipitous cardiovascular collapse shortly after admission to the intensive care service; she was resuscitated from PEA arrest twice on the first hospital day and required ventilatory support and renal replacement therapy for most of her 12-day course. Ultimately, a transfer to a large academic medical center with more extensive capabilities was arranged and the patient was subsequently lost to follow up.

Despite consultation with Cardiology, Infectious Disease, and Critical Care services, no definitive diagnostic position was ever reached in this case. Cardiac enzymes, echo, electrolytes, and cultures were all unrevealing. I developed a close relationship with this patient and even now remain discouraged that we had nothing to say to her and her family when so much was at stake.

References

I am indebted to A.R. Perez Riera et al. for their excellent review and discussion of the literature; many of the following references are via their guidance.

Harris AS. Delayed development of ventricular ectopic rhythms following experimental coronary occlusion. Circulation 1950; 1:1318-1328.

Marret E, Pruszkowski O, Deleuze A, et al. Accelerated idioventricular rhythm associated with desflurane administration. Anesth Analg 2002; 95: 319-321.

Jonsson S, O’Meara M, Young JB. Acute cocaine poisoning. Importance of treating seizures and acidosis. Am J Med. 1983; 75: 1061-1064.

Bonnemeier H, Ortak J, Wiegand UK, et al. Accelerated idioventricular rhythm in the post-thrombolytic era: incidence, prognostic implications, and modulating mechanisms after direct percutaneous coronary intervention. Ann Noninvasive Electrocardiol 2005; 10: 179-187.

Scheinman MM, Thorburn D, Abbott JA. Use of atropine in patients with acute myocardial infarction and sinus bradycardia. Circulation 1975; 52: 627-633.

Basu D, Scheinman M. Sustained accelerated idioventricular rhythm. Am Heart J 1975; 89: 227-231.


Case No. 3: Status Post Cardiac Arrest

An 84yr old white female, s/p VT/PEA arrest.

This ECG demonstrates AV dual sequenced pacing with loss of atrial capture. Note the high left axis in the x-y plane, consistent with typical pacer findings, but an atypical rightward shift of electrical forces across the precordial z-axis (inverse R-wave progression). Traditionally ventricular pacing electrodes are deployed in the right heart and result in a LBBB ECG morphology as the myocardial tissue depolarizes from right to left. Yet in this case we see a dramatic RBBB pattern, raising concerns about displacement or septal perforation, particularly given that the pt. has received CPR. The etiology of RBBB pacer morphology is not exclusively pathological, however, and receives a good discussion on Dr. S. Venkatesan’s Cardiology Blog. Note that the QRS in this case is elongated above 160ms, and necessarily reflects slow and poorly coordinated ventricular contraction, perhaps betraying a newly aberrant interventricular conduction pathway, even for this 100% paced patient.

Another interesting example of a similar RBBB effect can be seen at Dr. M. Rosengarten’s electrocardiography site, and there is a thorough case report and research analysis of the phenomenon in The Journal of Electrocardiography Vol.6 No. 1, 2003.

Shortly after this 12-lead was captured, the pt. again deteriorated into PEA and was lost to resuscitative efforts.


Case No. 2: Status Post Cardiac Arrest

A 19yr old white male, s/p cardiac arrest, now with transtentorial herniation.

As with this case, ECG patterns in the context of acute CNS disease have been primarily associated with ventricular repolarization, i.e. the morphology of the QT segment and T-wave, and the presence of prominent U-waves (not present here). Although little sensitivity or specificity has been accorded to this connection, the phenomenon raises interesting questions of nerocardiac interrelation. Most explicitly, bradycardia as a result of hypervagotonia is often noted in the setting increased intracranial pressure. Yet more difficult to explain are the deep, symmetrical T-wave inversions and prolonged Q-T frequently described as more specific indicators of intracranial pathology. It has been hypothesized that these effects are due to an autonomicaly mediated catocholamine surge causing transient coronary vasospasm and subsequent myocardial ischemia.

The ST segments in this case are of a somewhat novel morphology, perhaps even reminiscent of the scooped out troughs seen as a common Digitalis effect.

This pt. was taken to the OR for withdrawal of ventilatory support and organ donation later in the night.