Double counting heart rate - Littmann sign in electrocardiogram

Abstract

This report highlights necessity of correctly and quickly identifying Littmann sign. Littmann sign is not common in clinical practice, which is easily overlooked by most physicians, leading to delays in the treatment of hyperkalemia. A 68 year old patient with hyperkalemia was found to have inconsistent heart rate displayed on electrocardiogram monitoring with cardiac auscultation and synchronous electrocardiogram in the early stages of onset. Hyperkalemia was highly suspected by the Littmann sign. After completing arterial blood gas analysis, hyperkalemia was identified and active potassium lowering treatment was immediately initiated. The Littmann syndrome disappeared, and the patient eventually recovered.

1. Introduction

The phenomenon of double counting the true heart rate in the electrocardiogram (ECG) is called Littmann sign in clinical practice. The main cause of Littmann sign is severe hyperkalemia. This sign is often a critical indication that can help identify those patients with hyperkalemia who require prompt intervention[ [1]].

1.1. Case presentation

A 68-year-old dialysis-dependent woman with a history of diabetic nephropathy and cerebral hemorrhage sequelae was admitted to the hospital due to fever and cough for the past 3 days. ECG (Fig. 1A) and cardiac ultrasound (Fig. 1B) were normal at admission. Linezolid, levofloxacin, and fluconazole were given in combination with anti-infective therapy during hospitalization, along with a nasal feeding homogenization diet, glycaemic regulation, and regular dialysis. On the 5th day of treatment, the patient suddenly developed malaise, accompanied by sweating all over the body. Blood pressure was 90/40 mmHg, and fingertip oxygen saturation was unremarkable. Capillary blood glucose level was elevated, at 17 mmol/L. Cardiac auscultation revealed rhythmic bradycardia. ECG monitoring was immediately performed, and a heart rate of 80 beats/min was observed (Fig. 2A). A 12-lead ECG was simultaneously obtained, but the heart rate indicated 41 beats/min (Fig. 2B).

Questions

Why is the heart rate of ECG monitoring inconsistent with cardiac auscultation and ECG? What clinical diagnosis does this sign suggest? How should this patient be treated?

Fig. 1.

The patient's initial ECG (A) and echocardiographic images (B).

Fig. 2.

ECG monitoring (A) and a synchronized 12-lead ECG (B) obtained at patient's condition changes. The monitoring showed a ventricular bigeminy with a heart rate of 80 beats/min (red rectangular box)，and showed the pulse with a rate of 38 beats/min (white rectangular box). The 12-lead ECG showed a bradycardia with a pulse rate of 41 beats/min, and R–R interval (horizontal blue line) was measured at 1480 ms. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

1.2. Interpretation

The ECG monitor (Fig. 1A) showed a ventricular bigeminy with a heart rate of 80 beats/min. The height of the T waves were similar to that of the R waves. However, the pulse on the monitor showed 38 beats/min. The synchronized ECG (Fig. 1B) showed a bradycardia at approximately 40 beats/min. The rhythm seems to be quite regular, and the R–R interval was measured at 1480 ms. No P waves were noted. The QRS complexes have normal morphologies, measuring approximately 90 ms. The ST segments were aligned with the baseline of the ECG, without elevation or depression. The T-waves were tall and peaked, symmetrical and tent-shaped, especially on the chest leads V3 and V4, measuring a height of about 1.5mv. The QTc interval was in the upper limit of normal and calculated at 463 ms according to Bazett's formula. All in all, the true heart rate was repeatedly counted (Littmann sign) on the bedside ECG monitor, tall and peaked T waves, and absence of sinus rhythm renders the ECG unusual looking.

1.3. Clinical course

In the setting of a shock patient presenting with the above-mentioned ECG abnormalities, acute myocardial infarction (AMI) should be suspected first. AMI can occur secondary arrhythmias, such as premature ventricular contractions. When the infarction involves the atrial muscle, P-wave changes can occur, but they are mostly manifested in leads related to the infarction, and rarely disappear. Moreover，the hyperacute phase T wave changes in AMI can also be manifested as towering, but manifested as asymmetric double branches of the T wave, widened bottom, and dynamic evolution, accompanied by subsequent changes in ST segments, which is inconsistent with the T wave morphology in this case. In conclusion, in view of the patient's diabetes nephropathy and recent persistent infection status, her specific ECG changes supported the findings by Littmann et al [ [2][]] that double counting of heart rate by ECG interpretation software may be a sign of severe hyperkalemia. Arterial blood gas analysis was performed and showed hyperkalemia, at 7.0 mmol/L, which was confirmed on venous blood analysis. The patient received 10% intravenous calcium gluconate in 3 ampoules (30 mL) (1 ampoule every 15 minutes)，followed by an intravenous bolus of 12 units of short-acting insulin. An oral administration of 15 g of sodium polystyrene sulfonate was provided, and ECG and blood glucose changes are closely monitored. The double counting heart rate sign disappeared on the ECG monitor 4 hours after treatment onset（Fig. 3A）. The patient's mental state improved, sweating symptoms disappeared, blood pressure was 149/43 mmHg, fingertip oxygen saturation was 100%, and respiratory rate was 20 breaths/min. Repeated 12 lead ECG examination indicated restoration of sinus rhythm (75 beats/minute), with both P-wave and T-wave in normal morphology (Fig. 3B).. Repeated blood potassium and the capillary blood glucose measurements showed 5.8 mmol/L and 8.4 mmol/L. Considering the patient's anuria and infection status, continuous renal replacement therapy was given. Blood potassium was reduced to 4 mmoL/l 10 hours after treatment, and no further abnormal changes in the ECG and monitor. The specific time evolution of the entire clinical history and events is shown in Table 1.

Fig. 3.

ECG monitoring (A) and a 12-lead ECG (B) obtained 4 hours after treatment initiation and a potassium level of 5.8 mmol/L. The Littmann sign disappeared and sinus rhythm restored.

Table 1.

Evolution of disease.

Time of disease progression	0 hour	4 hour	10 hour
Clinical manifestation	Mental lethargy and sweating profusely	Improvement in mental state and disappearance of sweating	Mental state returns to normal
Blood pressure	90/40 mmHg	149/43 mmHg	138/45 mmHg
Littmann sign	Yes	No	No
ECG	Peaked T waves and no P waves	Normal	Normal
Potassium/Glucose（mmol/L）	7/17	5.8/8.4	4.0/7.9
Potassium lowering therapy	Calcium gluconate、Insulin、Sodium polystyrene sulfonate	Continuous renal replacement therapy	No

2. Discussion

The phenomenon of double counting heart rate is called the Littmann sign, which is not frequently observed in clinical practice. Littmann et al. reported that double counting automatically analyzed by ECG software suggested recognizable signs of hyperkalemia in 2007[ [2]]. The exact reason for double counting is still unclear, but it is most likely due to software mistaking the T-waves for the QRS waves[ [3]]. When blood potassium levels rise to a certain level, the widening of the QRS waves often accompanies the narrowing of the T wave, and even the QRS-T complexes may fuse into sine waves[ [2,4]]. In both cases, ECG counting software may have difficulty distinguishing between QRS complexes and T waves. In this case, Littmann sign disappeared when the potassium level decreased establishing a cause effect relation. In patients with hyperkalemia, double heart rate counting is often a warning of critical illness. If clinical physicians neglect observation or lack awareness of this sign, they may mistakenly assume that the ECG monitor has wrongly alarmed and unable to provide timely response, thereby delaying the treatment of hyperkalemia, and even cardiac arrest in severe cases[ [5]]. However, Atsushi Mizuno et al. reported that Littmann sign may be the sole sign of hyperkalemia, not necessarily accompanied by significant signs such as tall peaked T waves, shortened QT intervals, or a progression of PR and QRS intervals[ [3]]. This requires that we should interpret the ECG on our own, not completely rely on the automatic interpretation of software, and closely combine clinical signs, and cannot ignore the importance of physical examination[ [6]]. Since this report is a discussion of the original observations, some limitations of this study might be of concern.

2.1. Take-home points

• •ECG changes in hyperkalemia are proportional to the degree and speed of kalemia increase, and the overall unusual-looking ECG associated with clinical picture should be suggestive.

• •Littmann sign is caused by software mistakenly mistaking high and narrow T-waves for QRS waves. In general, we should interpret ECGs on our own and cannot rely completely on the automatic interpretation of software.

In patients with hyperkalemia, Littmann sign is an early warning of critical illness, and may be the sole sign of hyperkalemia, and early recognition is extremely important.

Ethics declarations

The patients’ legal guardian provided informed consent for the publication of her anonymised case details and images.

Data availability statement

The authors confirm that the data supporting the findings of this study are available within the article.

CRediT authorship contribution statement

Wei Wang: Writing – review & editing, Writing – original draft, Data curation. Mei-yu Deng: Data curation. Wen-Hui Zhai: Writing – review & editing. Jian-hui Ma: Writing – review & editing. Ying Zhang: Writing – review & editing. Jian-xin Ma: Writing – review & editing. Jin-ping Zhang: Writing – review & editing, Supervision, Project administration, Data curation.

Declaration of competing interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.