Abstract
The fact that temperature influences the electrophysiology of the heart is well
known. However, the effects of their regional variations on the
electrophysiological parameters of myocardium, or its influence on the
activation process during ventricular fibrillation (VF), have not been
sufficiently investigated. In experimental models, the analysis of the
modulation effect caused by local changes of temperature, can contribute to
obtain information on the mechanisms that support the VF, or the procedures
for its effective control. In this doctoral thesis, a new system to perform
changes on myocardial temperature in isolated heart models has been
developed. Specifically, this system allows to cause controlled hypothermia
and hyperthermia in limited regions of the tissue. Applying stimuli and
registering ventricular electrograms at different temperatures, is possible
thanks to an extraflat electrode. This system has been used to quantify the
effects of hypothermia and local hyperthermia on the VF activation frequency
parameters, in isolated and perfused rabbit hearts. The electrophysiological
parameters during basal stimulation have also been obtained. The epicardial
temperature in the free wall of the left ventricle has been modified from 17 ºC
to 42 ºC. The results show that local hypothermia prolongs the ventricular
refractory periods and decreases the conduction velocity during basal
stimulation; hyperthermia has the contrary effect. The wavelength of the
activation process does not suffer significant changes in spite of these
variations. On the other hand, during the VF, local hyperthermia accelerates
the activation in a reversible manner in the zone where it's applied; on the
contrary, hypothermia slows the arrhythmia. In the range of temperatures
studied, there is a lineal relation between the dominant frequency of the VF, or
the average activation interval, and temperature. Finally, the tests carried out
show that, reverse to caused by global hypothermia, the slowing of the VF, in
the zone where the changes of temperature are performed, does not achieve
global modifications of the activation neither the termination of the
arrhythmia.