I don’t normally blog about animal studies, but on reading a review of recent(-ish) shock research I was interested in the following piece that describes the effect of diffrent induction agents on rat heart muscle:
Sedation is frequently necessary in patients with septic shock, and therefore Zausig and colleagues investigated the effects of dose-dependent effects of various induction agents (propofol, midazolam, s(+)-ketamine, methohexitone, etomidate) in a Langendorff heart preparation from rats rendered septic by CLP. Propofol exerted the most pronounced depressant effects on both the maximal systolic contraction and the minimal diastolic relaxation, and cardiac work. Furthermore, propofol only adversely deleteriously affected the myocardial oxygen supply- demand ratio. In contrast, s(+)-ketamine was associated with the best maintenance of cardiac function. Within the limits of the study – that is, the use of an ex vivo isolated organ model – the authors concluded that s(+)-ketamine may be an alternative to the comparably inert etomidate, the use of which is, however, limited due to its endocrine side effects.
Of course we should be cautious about extrapolating animal lab work to clinical practice, but this supports my position of vehement opposition to the injudicious use of propofol for RSI in critically ill patients!
Year in review 2009: Critical Care – shock
Critical Care 2010, 14:239 Full text