Erectile dysfunction and sexual health counselling after myocardial infarction treated with percutaneous coronary intervention.

Brain injury accounts for approximately two-thirds of mortality in resuscitated out-of-hospital cardiac arrest (OHCA) patients. Central to neuroprotection is optimizing cerebral blood flow, which is determined by mean arterial pressure (MAP) and local cerebrovascular resistance. The optimal blood pressure in resuscitated OHCA patients is unknown; current standard-of-care uses a MAP target of ≥65 mmHg, a practice adopted from septic shock guidelines. This target has been associated with decreased cerebral oxygenation during the critical first 6–12 h post-ROSC., Additionally, randomized controlled trials comparing fixed MAP targets after OHCA have been uniformly neutral., , The difficulty in defining optimal MAP targets stems from marked pathophysiological heterogeneity. Cerebral autoregulation may be totally absent in some patients and significantly impaired in others, with the preserved range varying substantially across individuals., Furthermore, cerebral blood flow demonstrates a characteristic temporal pattern of early hyperemia, prolonged hypoperfusion, and later partial normalization, superimposed on regional microcirculatory heterogeneity. Consequently, the cerebrovascular response to any given MAP differs between patients and across post-resuscitation phases, rendering any fixed target liable to produce hypoperfusion at some timepoints and hyperperfusion at others. An individualized blood pressure strategy tailored to real-time cerebral blood flow is a biologically plausible alternative, but must be instituted early post-ROSC, while secondary injury is still modifiable, and dynamically adjusted as autoregulatory status evolves. Transcranial Doppler ultrasound (TCD) and near-infrared spectroscopy (NIRS) provide complementary, non-invasive, bedside measurements of cerebral blood flow velocity and regional cerebral oxygen saturation (rSO), enabling autoregulation assessment by correlating slow signal changes with MAP fluctuations, to derive the autoregulatory limits and the individualized optimal MAP (MAPopt).,