For background regarding EKG double counting and Littmann’s sign of hyperkalemia, see March, 2012.
The following was recorded from an 82 year-old female with lethargy and malaise; electrolyte status is unknown, as is any further clinical data.
This is a 10 second strip with 9 QRS complexes; the true heart rate is thus 54bpm. The GE-Marquette 12SL interpretation algorithm has counted 163bpm, (3 x 54 = 162). Assuming that this is a result of systematic error and not coincidence, both the mechanism and significance of triple counting remain unclear.
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.
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:
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.
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.
In April of 2011 I presented a case of subtle hyperkalemia. A reader, Dr. George Nikolic, author of Practical Cardiology 2nd Ed., responded with the following commentary,
“The QT is unusually long for hyperkalemia; the lady may have additional pathology (e.g., myxoedema) or be on some QT prolonging medication. The commonest cause of low voltage is large or multiple infarcts in the past. What were her other medical problems?”
I was unable to follow up on this case until recently. Here is what I uncovered:
The patient was an 81 year-old caucasian female nursing home resident of unknown social background with a past history of hypertension, dyslipidemia, diabetes, colon cancer (s/p diverting ileostomy), depression and dementia. Despite numerous cardiac risk factors, she had no explicit history of myocardial infarction, coronary disease, or CHF. There was no history of thyroid disease or obesity.
Her medications consisted of Lexapro 10mg, Aricept 5mg q.h.s, Lopressor 12.5mg b.i.d., folic acid, and Imdur 30mg daily.
She had visited the Emergency Department 12 days prior to this episode with complains of weakness and bradycardia. At that time her BUN was 22, Creatinine 0.8, Sodium 136, Potassium 3.7, and Calcium 9.1. The following EKG was recorded:
Cardiology was consulted and a differential of sick-sinus syndrome vs. beta-blocker toxicity was considered. The Lopressor was reduced, and, following a 48-hour admission, she was discharged back to the nursing home with a slightly increased heart rate.
Two weeks later, on the date in question, she again presented to the ED with complaints of syncope and generalized weakness. This EKG was recorded on arrival:
The hospitalist’s admission note described a provisional diagnosis of acute renal failure secondary to dehydration and possible UTI. Obstructive failure was also considered in light of the cancer history. Most revealing, a thorough chart review revealed two prior admissions for acute renal failure secondary to dehydration from high-output ileostomy syndrome.
Echocardiography on the second hospital day reported no chamber enlargement, no increased wall thickness, no wall motion abnormalities, no valvular disease, no pericardial or pleural effusion, and a normal systolic function with an EF > 55%.
On the third hospital day she was discharged back to her nursing facility with the following EKG:
The differential diagnosis for low voltage is broad; neoplastic, metabolic, autoimmune, infectious, genetic, and acquired disease states are all represented.
When bradycardia is added, the field narrows: thyroid disease, acute or chronic ischemia, and hypothermia are among the most common etiologies.
In hyperkalemia, it is traditionally understood that when the QRS is normal, the QTc should be either shortened or unremarkable. (Smith, Jan 12, 2010; Lipman-Massie, p.579) In this case, the QTc at 6.4mEq K+ (394) is practically identical to the QTc at 4.0 mEq K+ (394). I do not know if the GE-Marquette algorithm uses the Bazett formula for QTc, but this formula is known to under-correct at abnormally low heart rates. (Wikipedia, 2012) Therefore, although the QTc here may be longer than the computer estimates, in an adult female, a QTc of 395 remains if anything on the short side of normal. Regarding medications, however, Lexapro is known to cause QT prolongation.
There was no effusion, as I had originally hypothesized in 2011. We do not have a solid culprit for the low voltage. The QT looks relatively normal. I am grateful for Dr. Nikolic’s attention and comments regarding this case. Fortunately for the patient, the clinical correlations do not seem to support either of our theories.
Dunn, B. and Lipman, B. (1989) Lipman-Massie Clinical Electrocardiography, 8th Ed. Yearbook Medical Publisher Inc.
Smith, S. (2010) Hyperkalemia with cardiac arrest. Peaked T waves: hyperacute (STEMI) vs. early repolarization vs. hyperkalemia. http://hqmeded-ecg.blogspot.com/2010/01/peaked-t-waves-hyperacute-stemi-vs.html
Wikipedia. (2012) QT interval. http://en.wikipedia.org/wiki/QT_interval
In 2007, Littmann and colleagues presented a novel EKG indicator of hyperkalemia based on the computerized “double counting” of heart rate. Over a 13-year period they identified 33 cases in which the GE-Marquette computerized 12SL EKG interpretation algorithm “double counted” or “near double counted” the actual heart rate seen on electrocardiogram. All 33 patients had hyperkalemia (between 5.3-8.8 mEq/L K+) as confirmed by serology taken within two hours of the double-counted EKG recording.
Littmann’s sign can be seen in the following EKG, initially presented here as a study in hyperkalemia in September of 2010.
A 65 year-old Caucasian man with sepsis and HHNKC; the potassium was 7.7mEq/L. The heart rate is 72 bpm; the computer counts 137 bpm.
Although the GE algorithm is proprietary and unavailable for analysis, they argue that, “The QRS width and axis measurement by the interpretation software suggested that, on many occasions, the computer recognized the T waves as being the QRS complexes….” (p.586)
Littmann et al. conclude stating, “Although interpretation software double counting of heart rate appears to be quite specific for hyperkalemia, its sensitivity is almost certainly very low.” (p.586)
While this research represents an intriguing new insight, it leaves many open questions. How were these 33 EKG cases identified? Were certain populations screened for this anomaly? How many total EKGs were reviewed in the course of this investigation?
Littmann claims that double counting “appears to be quite specific” presumably because all 33 EKGs were associated with underlying hyperkalemia. Yet without insight into the methods used to assemble this case series, I remain skeptical that these investigators did not succumb to confirmation bias in the process of collecting their EKGs. The existence of non-hyperkalemic double counting is not discussed in this publication and no differential diagnosis is presented regarding alternative etiologies.
In fact, concerning alternative etiologies and the specificity of double QRS counting, it turns out that this phenomenon has been extensively described in the pacemaker literature for over a decade. A Pubmed search using the combined terms “double counting QRS” produces numerous references. (Al-Ahmad A, Barold SS, Boriani G)
I reviewed 22 pacemaker EKGs collected over a 10 month period, recorded pre-hospitaly using the same GE-Marquette algorithm. This is what I found:
Looking further through ~50 EKGs collected over the same 10 months I found this as well:
In the first pair of EKGs, the computer appears to be confusing the pacemaker spike for a QRS complex; this is clearly “double counting of the QRS.”
The second pair is more complicated. This is not technically “double counting” of the QRS; there is not a 1:1 relationship between each QRS and a particular artifactual deflection. This is over-counting with a coincidental but not precise 2:1 relationship between the total count made by the computer and the total number of true QRS complexes. The interpretation of “Atrial Fibrillation” supports this in that it suggests that numerous complexes are counted during the first 5 seconds and then much fewer in the last 5. Although Littmann’s sign is not technically present here, the 12-lead EKG must be scrutinized to reach this conclusion. This seems problematic given Littmann’s stated goal of elucidating an “objective”, and “easily identifiable” indicator. (p.586)
No clinical data is available on these EKGs and it cannot be proven that these patients did not in fact have elevated potassium.
While producing these two hypothetical “false positives” hardly constitutes significant evidence, it is interesting that such counterpoints to Littmann’s specificity claims were so easily identified. Of further concern is the distinction between perfect double counting as seen in the pacemaker case and “near double counting” as seen in both the hyperkalemia case from Sept. 2010 and artifact case. What bearing this has on Littmann’s argument remains unclear.
Although a novel indicator, I am not sure that there is as yet persuasive evidence for what exactly Littmann’s sign indicates or how often this indication is specific for any one underlying clinical etiology.
Littmann L, Brearley WD, Taylor L, Monroe MH. Double counting of heart rate by interpretation software: a new electrocardiographic sign of severe hyperkalemia. Am J Emerg Med 2007;25:584-90.
Tomcsányi J, Wágner V, Bózsik B. Littmann sign in hyperkalemia: double counting of heart rate. Am J Emerg Med. 2007 Nov;25(9):1077-8.
Al-Ahmad A, Wang PJ, Homoud MK, Estes NA 3rd, Link MS. Frequent ICD shocks due to double sensing in patients with bi-ventricular implantable cardioverter defibrillators. J Interv Card Electrophysiol. 2003 Dec;9(3):377-81.
Barold SS, Herweg B, Gallardo I. Double counting of the ventricular electrogram in biventricular pacemakers and ICDs. Pacing Clin Electrophysiol. 2003 Aug;26(8):1645-8.
Boriani G, Biffi M, Frabetti L, Parlapiano M, Galli R, Branzi A, Magnani B. Cardioverter-defibrillator oversensing due to double counting of ventricular tachycardia electrograms. Int J Cardiol. 1998 Sep 1;66(1):91-5.
An 81 yr old white female with multiple medical problems presents to the ED complaining only of syncope and weakness; the routine 12-lead EKG is pictured below.
Yet the most remarkable feature of this case is the disarmingly low voltage. Although the electrocardiographic attributes of hyperkalemia remain well exemplified (peaked, sharply pointed T-waves, bradycardia, and a somewhat elongated PR interval), the attention-grabbing mountainous T-waves are conspicuously absent. This is because the EKG must be seen in the context of its own voltage. When viewed against the background of the low-voltage QRS amplitude, the T-waves are proportionally massive, just as in the classic case. Given the considerable incidence of pericardial effusion in pts with renal disease, it is not unreasonable to imagine both of these pathologies contributing to the appearance of this electrocardiogram.
In this case, laboratory assays returned showing a potassium level of 6.4 mEq/L; the pt was temporized in the ED and ultimately admitted for further evaluation. The presence or absence of pericardial effusion could not be confirmed.
Over the past year a variety of superior resources have been released dealing with the problem of critical hyperkalemia, its electrocardiographic manifestations, and its treatment. As it would be a great challenge to improve on what has been done here, I am simply going to replicate the links below.
Link No. 1: Dr. Stephan Smith of Dr. Smith’s ECG Blog has posted a video covering 4 critical hyperkalemia cases with notable EKG presentations. Be sure to take a look at his first case, second EKG, for a valuable signature morphology which can easily be misinterpreted as STE anterior MI.
Link No. 4: Scott Weingart of the EMCrit Podcast has released an incisive 15-minute Pod-Cast covering cutting edge hyperkalemia treatment paradigms. There may be some practice-changing insights here, so check it out.
Link No. 5: Jeffrey Guy of the Surgery ICU Rounds Podcast has a 30-minute overview and discussion of hyperkalemia, normal potassium physiology, and treatment approaches. This is a hospital/ICU-oriented discussion addressing burn medicine, trauma, rhabdomyolysis, etc. More in-depth, more information.
Please feel free to suggest additional resources; also note that the September 2010 case study published here, “Unconscious with Wide Complex Rhythm,” involves a more comprehensive discussion of hyperkalemic EKG changes.
This patient is a 64 year-old cachectic white male, admitted to ICU with a five day history of nausea, vomiting, and upper abdominal discomfort. The following EKGs were collected in the ED before and after treatment. His history includes HTN, alcoholism, and IDDM.
Classic electrocardiographic indications of hyperkalemia include sharply peaked, symmetrical T-waves, suppression of atrial activity, bradycardia, a markedly widened QRS and a short QT interval. Note how the rhythm in this case approaches the appearance of a sign wave as the QT narrows and the ventricular complexes widen; this is representative of the course in worsening hyperkalemia and is sometimes responsible for the idoventricular or agonal appearance of some hyperkalemic EKGs. This should not be considered a mere “agonal appearance,” however, as typically broad and flattened P-waves with an elongated PR interval will progress toward complete atrial paralysis, frank idoventricular activity below 40bpm, and subsequent hemodynamic collapse.
Distinguishing between the T-wave morphologies of hyperkaemia, early-repolarization, and hyperacuity in early MI can become problematic for pt. outcomes in the acute setting, particularly in the latter case, and a good discussion of this issue can be found at Dr. Smith’s EKG blog. It has been said that hyperkalemic T-waves are “tented” and should be pointed enough to prick your finger. Also note Lipman and Massie’s observation that, “The uniformly wide complex in hyperkalemia differs from the wide QRS in bundle branch block (terminal QRS sluring) or pre-excitation (initial sluring) in that the uniform widening of the QRS in hyperpotassemia affects both the initial and terminal QRS portions.” Lab values are as follows:
Despite resuscitation in the ED this patient arrived in the ICU with a BP of 70/40, HR 60bpm, RR of 30, and a room air SpO2 of 88%. The patient was ultimately stabilized over a matter of days but required extensive pressor support for evolving bacteremia and HHNKC. An ultrasound of the upper abdomen revealed fatty infiltration of the liver but no cholecystitis or cholangitis. It should be noted that although a history of recent complaints could be obtained from the patient’s family members, he initially presented in a comatose state.
Of additional relevance in this case may be Lipman-Massie’s further contention that, “Low sodium levels tend to exaggerate and high sodium levels tend to neutralize the ECG effects of hyperpotassemia.”
Dramatic recordings of progressing or resolving hyperkalemia are not difficult to find about the internet. Dr. M. Rosengarten has a fine series here.
Quotations from Lipman-Massie Clinical Electrocardiography, 8th Ed. Marvin I. Dunn MD, Bernard S. Lipman MD. Yearbook Medical Publisher Inc. ©1989. See pp. 240-243.