Clinicians inevitably encounter patients who meet the diagnostic criteria for the metabolic syndrome (MetS); these criteria include central obesity, hypertension, atherogenic dyslipidaemia, and hyperglycaemia. Regardless of the variations in its definition, MetS may be associated with adverse outcomes in patients undergoing both cardiac and non-cardiac surgery. There is a paucity of data concerning the anaesthetic management of patients with MetS, and only a few observational (mainly retrospective) studies have investigated the association of MetS with perioperative outcomes. In this narrative review, we consider the impact of MetS on the occurrence of perioperative adverse events after cardiac and non-cardiac surgery. Metabolic syndrome has been associated with higher rates of cardiovascular, pulmonary, and renal perioperative events and wound infections compared with patients with a non-MetS profile. Metabolic syndrome has also been related to increased health service costs, prolonged hospital stay, and a greater need for posthospitalization care. Therefore, physicians should be able to recognize the MetS in the perioperative period in order to formulate management strategies that may modify any perianaesthetic and surgical risk. However, further research is needed in this field.

The present work investigated the dynamic changes in stressed volume (Vs) and other determinants of venous return using a porcine model of hyperdynamic septic shock. Septicemia was induced in 10 anesthetized swine, and fluid challenges were started after the diagnosis of sepsis-induced arterial hypotension and/or tissue hypoperfusion. Norepinephrine infusion targeting a mean arterial pressure (MAP) of 65 mmHg was started after three consecutive fluid challenges. After septic shock was confirmed, norepinephrine infusion was discontinued, and the animals were left untreated until cardiac arrest occurred. Baseline Vs decreased by 7% for each mmHg decrease in MAP during progression of septic shock. Mean circulatory filling pressure (Pmcf) analogue (Pmca), right atrial pressure, resistance to venous return, and efficiency of the heart decreased with time (p < 0.001 for all). Fluid challenges did not improve hemodynamics, but noradrenaline increased Vs from 107 mL to 257 mL (140%) and MAP from 45 mmHg to 66 mmHg (47%). Baseline Pmca and post-cardiac arrest Pmcf did not differ significantly (14.3 ± 1.23 mmHg vs. 14.75 ± 1.5 mmHg, p = 0.24), but the difference between pre-arrest Pmca and post-cardiac arrest Pmcf was statistically significant (9.5 ± 0.57 mmHg vs. 14.75 ± 1.5 mmHg, p < 0.001). In conclusion, the baseline Vs decreased by 7% for each mmHg decrease in MAP during progression of hyperdynamic septic shock. Significant changes were also observed in other determinants of venous return. A new physiological intravascular volume existing at zero transmural distending pressure was identified, termed as the rest volume (Vr).

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Background:Mean systemic filling pressure (Pmsf) is a quantitative measurement of a patient's volume status and represents the tone of the venous reservoir. The aim of this study was to estimate Pmsf after severe hemorrhagic shock and cardiac arrest in swine anesthetized with propofol-based total intravenous anesthesia, as well as to evaluate Pmsf's association with vasopressor-free resuscitation. Methods: Ten healthy Landrace/Large-White piglets aged 10-12 weeks with average weight 20 ± 1 kg were used in this study. The protocol was divided into four distinct phases: stabilization, hemorrhagic, cardiac arrest, and resuscitation phases. We measured Pmsf at 5-7.5 seconds after the onset of cardiac arrest and then every 10 seconds until 1 minute postcardiac arrest. During resuscitation, lactated Ringers was infused at a rate that aimed for a mean right atrial pressure of ≤ 4 mm Hg. No vasopressors were used. Results: The mean volume of blood removed was 860 ± 20 ml (blood loss, ~61%) and the bleeding time was 43.2 ± 2 minutes while all animals developed pulseless electrical activity. Mean Pmsf was 4.09 ± 1.22 mm Hg, and no significant differences in Pmsf were found until 1 minute postcardiac arrest (4.20±0.22 mm Hg at 5-7.5 seconds and 3.72±0.23 mm Hg at 55-57.5 seconds; P=0.102). All animals achieved return of spontaneous circulation (ROSC), with mean time to ROSC being 6.1 ±1.7 minutes and mean administered volume being 394 ±20 ml. Conclusions: For the first time, Pmsf was estimated after severe hemorrhagic shock. In this study, Pmsf remained stable during the first minute post-arrest. All animals achieved ROSC with goal-directed fluid resuscitation and no vasopressors.