Fibrillation and Self-Defibrillation of the Heart in
Deep Body Cooling

Vladimir Kobrin and Marina Tverskaya

Russian State Medical University, Moscow, Russia

Correspondence: VI Kobrin, Russian State Medical University, Ostrovotyanova, 1, 117997, Moscow, Russia.
E-mail: vikobrin@mtu-net.ru, phone +7-095-434-6229, fax +7-095-434-4787

1.  Introduction

It is known the descent of temperature of a body less than 26-28⁰C can lead to the ventricular fibrillation (V.M.Pokrovsky et al., 1984) but the process of ventricular self-defibrillation is not studied by low temperature of a body. The aim of the present study was to investigate the process of spontaneous ventricular fibrillation and self-defibrillation in deep body cooling.

2.  Material and Methods

The guinea-pigs were cooled in the water-ice bath until to +4oC of a body. For control of the TB was used a rectal thermometer. “Swimming” glass microelectrodes were used for recording of transmembrane potentials of ventricular contractile cardiac cells in fibrillation induced by electrical current.

3.  Results and Discussion

The resting potential (RP) was decreased significantly (p<0.05) if the TB was less 20⁰C. The amplitude of action potential (AP) was decreased if the TB was less 25⁰C and according to it the overshoot was decreased too. The increase of action potential duration (APD) was according to the heart rhythm inhibition (Fig. 1, Table 1).

Figure 1. Electrical activity of cardiomyocytes of the left ventricle. Non-stop registration by the deep cooling of a body. 1 –ECG, 2 – AP. 50 mV, 50 ms. Temperature: A – 370, B - 330, C - 250, D – 200, E – 170.

We registered only ventricular asystolia when the TB was less than 12-15⁰C. The electrical threshold of VF was increased from 1.6 V until 300 V by the descent of the TB until 8⁰ C.

Table 1.    The parameters of transmembrane potentials the cells of conractile myocardium in hypothermia.
(* p<0.05)

We could model the ventricular fibrillation if we used the overthreshold irritation. The electrical activity of cardiac cells by the low temperature of the body was the same as in control experiments (Fig.2) but the frequency of APs was lower and the depolarization of cardiomyocytes was not more than 5-7 mV by temperature 25⁰C (instead 30-35 mV in control experiments).

Figure 2. Fibrillation and self-defibrillation by the temperature +25⁰ C. A-B –non-stop registration. On-off –influence of electrical current. 1- ECG, 2- AP.

A comparative research of transmembrane potentials of cardiomyocytes belonging to the left and the right ventricles demonstrated that the difference in the APD appeared, when the TB was less than 18-20⁰C, and the mainly expressed changes were in the cardiomyocytes belonging to the right ventricle (Fig.3).

Figure 3. Electrical activity of cardiomyocytes of the left (2) and right (3) ventricles. 1 – ECG. Temperature +170 C, 100 mV, 100 ms.

Probably, it was according to the fact, that the blood, which flows to the right ventricle, is colder than one flows to the left ventricle (Lloyd and Mitchel, 1974).

So, one of the causes of the absence of spontaneous fibrillation by hypothermia was the decrease of the excitability of myocardium in spite of the fact that there appeared the electrophysiological heterogeneity.

Acknowledgements

Work supported by grant of RFBR № 01-04-48201.

References

Pokrovsky V.M., Sheich-Zade Y.R., Vovereit V.V. A heart by hypothermia. Nauka, Moscow, 1984, 141.

Lloyd E. and Mitchel B. Factors affering of ventricular fibrillation on hypothermia. Lancet.1974., v.2, N7892, p.1294