To our knowledge, this is the second case report documenting ECG changes during hanging [9]. While changes in the ECG of hanging survivors, such as elongated QTc intervals and initial ventricular fibrillation, are widely described [10], evidence of cardiophysiological stigmata in cases of complete hanging remains scarce.

In the present case, there was an abrupt onset of bradycardia, followed by the progression of AV blocks. Although the other published case [9] did not discuss the ECG findings in detail, a photograph of the trace was taken. A cardiologist conducted a comparative interpretation of these two ECGs and found a similar electrophysiological picture. In our case, an asystole of about four minutes preceded the onset of bradycardia and the consecutive progression of AV blocks. In the other published case, a second-degree AV block with a conduction pattern of 2:1, then 3:1, and then 4:1 was observed. Subsequently, no QRS complexes were noted, and finally, the P-waves ceased as well.

Based on these observations, we propose that the abrupt onset of bradycardia marks the moment of hanging when the carotid sinus is compressed. This indicates that the pressure on the baroreceptors caused by the ligature may also play a role during hanging.

The reason for the initial asystole of about 20 s in the present case can only be hypothesized. The ECG showed no signs of disturbance, as would be expected in artifacts caused by seizures. One possible explanation is an initial attempt at hanging, where either the ligature broke or the attempt was abandoned. However, no morphological signs of a first attempt of hanging was found on the body, especially no second ligature mark.

Another possible explanation is that the initial asystole marks the point of hanging. The later noted bradycardia could be interpreted as a heart rhythm resulting from the dying of the heart itself, which is not directly linked to the cause of death. In the literature, the rhythm of the dying heart is described as different types of arrhythmias, with terminal irregular idioventricular rhythms and gradual slowing and disappearance of P waves [11]. These kinds of changes were not observed in our ECG. Instead, the final rhythm recorded showed only P waves. The other published case showed a similar pattern, with only p waves as the final rhythm before asystole.

Different modes and mechanisms of death in hanging are discussed in the literature [4]. In 1870, Ecker reported a hanging which resulted in an obstruction of the airways [12], later Langreuter identified four different mechanisms of death in 1886. These authors proposed that death by strangulation could result from compression of the airways, compression of the blood vessels supplying oxygen to the brain, compression of the vagal nerve, or injuries to the spine [13]. It is also possible that negative chronotrope and negative dromotrope effects on the heart due to compression of the nerves along the carotid arteries contribute to the cause of death [8].

Especially in atypical hangings, compression of venous vessels without complete compression of arterial vessels is observed, resulting in congestion and the occurrence of petechial hemorrhages above the strangulation level [14]. Death is typically attributed to brain hypoxia [2, 14]. One mechanism worth discussing is whether pressure on the carotid sinus induces a vagal reflex, thereby leading to bradycardia [7].

Based on experiments conducted by Brinkmann et. al. on dogs, [15] it has been determined that in atypical hangings, there is a drop in heart rate and blood pressure. Consciousness is typically lost after about 8 s, and breathing activity ceases. Asphyxia could be induced by clamping the endotracheal tube used for ventilation, resulting in corresponding changes in the ECG such as ventricular fibrillation, followed by progression to AV block and ultimately pulseless electrical activity [16]. While direct comparisons with humans can be challenging, similar results have been observed in cases of survived hanging, where ventricular fibrillation may occur initially [10].

In self-hanging experiments conducted by Minovici in 1904, loss of consciousness occurred after 8–9 s when the knot was located laterally on the neck [17].

In the present case, no ventricular fibrillation could be observed. This suggests that the observed changes are not consistent solely with those resulting from oxygen deprivation, thereby making the involvement of vagal reflex mechanisms even more likely. According to the literature, cessation of blood circulation in the brain, which is the predominant factor in hanging, leads to loss of consciousness within 6–10 s [2]. In contrast, experiments involving the cessation of blood flow to the brain in volunteers using mechanical cuffs over a period of 100 s did not report significant health effects [18].

While slowing of the heart can be observed in asphyxia [19], the abrupt onset of bradycardia in the current case needs to be discussed. Bradycardia occurred abruptly within seconds in the present case, suggesting that it was not solely due to cessation of brain circulation. Based on current evidence, it could be stipulated that there was a failure of the central regulatory mechanisms that control the heart and breathing. Lack of oxygen and brain congestion can lead to a Cushing reflex and subsequent increase in sympathetic output [20]. These effects contrast with the ECG recordings in the present case, which showed progressive AV block due to activation of the parasympathetic nervous system. Such activation of the parasympathetic nervous system can be induced by pressure on the carotid baroreceptors.

The effects of alcohol consumption on the ECG should also be discussed. While the recorded changes in the ECG are likely directly linked to the hanging and subsequent death, the presence of 1.44 ‰ of alcohol may have also contributed to these changes. Most ECG changes recorded during acute alcohol intoxication include atrial fibrillation or premature ventricular contractions, but in some cases, atrioventricular conduction disturbances could be observed. However, based on the balance of probabilities, the recorded ECG changes were more likely a result of increased vagal tone rather than the effects of alcohol itself [21].

Due to the small number of cases, with only two publications including the one we presented, it remains questionable whether our findings can be generalised to other similar cases. One opportunity for a larger dataset could arise from the increasing number of smartwatches with ECG recording capabilities, which may provide new insights into the cardiac pathophysiology of hanging.