S-(-KETAMINE - CARDIOVASCULAR INTERACTI ONS DURING TOTAL INTRAVENOUS ANESTHESIA AND ANALGOSEDATION())

General cardiovascular properties of ketamine: ''In vitro'', ketamine has moderate negative inotropic effects. ''In vivo'', significant cent ral sympathomimetic action with consecutive hemodynamic effects is dom inant. The sympathomimetic potency of ketamine is one of the most sign ificant pharmacological features of the substance with direct clinical implications. Monoanaesthesia with S-(+)-ketamine: After application of racemic ketamine or S(+)-ketamine as well, identic and significant increases in plasma catecholamines, arterial pressure and heart rate a re observed. This outstanding sympathomimetic action is beneficial in induction of patients with shock or asthmatic state. TIVA and analgose dation with S-(+)-ketamine and midazolam: The sympathomimetic effect o f S(+)-ketamine, and racemic ketamine as well, is mitigated by midazol am. Nevertheless, significant increases in heart rate and arteriel pre ssure might be observed. Clinical use of the combination is common in short procedures like reposition maneuvers. Of greater importance is t he use for analgosedation in patients with cardiovascular instability, particularly in patients with exogenous catecholamine demand. TIVA an d analgosedation with S-(+)-ketamine and propofol: When S(+)-ketamine is combined with propofol, the sympatholytic effects of propofol are c ounteracted by S(+)-ketamine, and stable hemodynamic conditions are pr esented. This combination seems useful for TIVA in patients with hypot onic dysregulation or endocrine deficits like hypothyreosis and adrena l insufficiency. Furthermore, analgosedation with S(+)-ketamine and pr opofol is advantageous, when rapid recovery is necessary and negative circulatory effects should be avoided. Conclusion: Sympathoadrenergic and hemodynamic effects of S(+)-ketamine and racemic ketamine are gene rally identical. The distinctest action is observed,when S(+)-ketamine is used as a monoanaesthetic. In combination with midazolam, a signif icant reduction is achieved. In combination with propofol, the sympath olytic effects of this hypnotic agent are compensated by S(+)-ketamine . With respect to sympathoadrenergic and hemodynamic reactions, the cl inical position of S(+)-ketamine is unchanged. Nevertheless, a signifi cant clinical progress can be expected due to improved recovery and re duced substance load, when racemic ketamine is replaced by S(+)-ketami ne.