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.
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.
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:
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.
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.
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.