Mechanical stimuli may trigger or terminate cardiac arrhythmias. This ‘duality’ is similar to that of electrical stimulation, which currently is the intervention of choice for cardiac resuscitation. It is interesting to note that only 4% of the current, applied externally for ventricular defibrillation, actually traverses the cardiac muscle (Lerman et al. 1990). This requires very high energies for resuscitation (150-300 J). Mechanical interventions, such as the pre-cordial thump (PT), offer a low-energy alternative, where stimuli of less than 1 J may trigger ectopic ventricular excitation, and impacts of 4-8 J may terminate ventricular tachycardia (VT) and fibrillation. PT is understood to be a relatively safe intervention, with the exception of pre-existing severe anoxia of the myocardium. The effect of PT on cardiac electrophysiology is based on mechano-electric feedback, whereby mechanical stimuli are translated into increased open probability of cardiac stretch-activated channels (SAC, for review see Kohl et al. 1999). There are two main SAC populations: cation non-selective (SACNS, reversal potential near -10 mV) and K+ selective (SACK, reversal potential near -95 mV) (Craelius et al. 1988; van Wagoner, 1993). One representative of SACK is the ATP-inactivated K+ channel, which is mechanically-activated and ligand-inactivated. Interestingly, reduction in ATP content sensitizes this channel to mechanical stimulation (van Wagoner, 1993), and we propose that this may explain the reduced utility of PT in the ischaemic heart. We simulated VT either as a single spiral wave or as figure-of-eight reentry, using a 2D ventricular model (Garny & Kohl, 2004). In short, a 2.5×2.5 cm mesh containing 63,001 ventricular cells was implemented. Re-entrant excitation was generated via localised S1-S2 stimulation protocols, and PT was simulated by brief (5 ms) activation of SACNS and SACK in variable ratios. Our results show that activation of SACNS terminates re-entry via depolarisation of cells in the excitable gap. Shifting the modelled stretch-effect from SACNS only towards increasing co-activation of SACK (to represent ischaemic conditions with loss of ATP-dependent channel inactivation) decreased the efficacy of defibrillation. This is caused by the progressive shift towards a more negative reversal potential of the ‘net stretch-induced current’. As a consequence, resting cells in the excitable gap are depolarised to a lesser extent, while action potential duration of excited cells is reduced. The former has no lasting effect on the excitable gap, while the latter temporarily reduces electrical cycle length, thereby facilitating re-entry. The increasing contribution of SACK may explain why PT is less efficient in hypoxic conditions, which is now subject of experimental validation.