Background
The clinical impact of prolonged steep Trendelenburg position and CO2 pneumoperitoneum during robot‐assisted radical cystectomy (RC) on intraoperative conditions and immediate ...postoperative recovery remains to be assessed. The current study investigates intraoperative and immediate postoperative outcomes for open RC (ORC) versus robot‐assisted RC with intracorporal urinary diversion (iRARC) in a blinded randomised trial. We hypothesised that ORC would result in a faster haemodynamic and respiratory post‐anaesthesia care unit (PACU) recovery compared to iRARC.
Methods
This study is a predefined sub‐analysis of a single‐centre, double‐blinded, randomised feasibility study. Fifty bladder cancer patients were randomly assigned to ORC (n = 25) or iRARC (n = 25). Patients, PACU staff, and ward personnel were blinded to the surgical technique. Both randomisation arms followed the same anaesthesiologic procedure, fluid treatment plan, and PACU care. The primary outcome was immediate postoperative recovery using a standardised PACU Discharge Criteria (PACU‐DC) score. Secondary outcomes included respiration‐ and arterial O2 saturation scores as well as perioperative interventions and recordings.
Results
All patients underwent the allocated treatment. The total PACU‐DC score was highest 6 h postoperatively with no difference in the total score between randomisation arms (p = 0.80). Both the ORC and iRARC groups maintained a mean respiration‐ and arterial O2 saturation score below 1 (out of 3) throughout PACU stay. The iRARC patients had significantly, but clinically acceptable, higher maximum airway pressure and arterial blood pressure, as well as lower minimum pH levels. The ORC group received significantly more opioids after extubation but marginally less analgesics in the PACU, compared to the iRARC group.
Conclusions
A prolonged Trendelenburg position and CO2 pneumoperitoneum was well‐tolerated during iRARC, and immediate postoperative recovery was similar for ORC and iRARC patients.
Background
Hypotension during major surgery is frequent, resulting in increased need for observation in the post‐anaesthesia care unit and treatment including vasopressors and fluids. However, ...although severe hypotension in the immediate post‐operative recovery phase after major surgery is suggested to be related to increased morbidity and mortality, the underlying risk factors are not well described, hindering advancements in prevention and treatment.
Methods
We performed a retrospective study assessing factors (age, gender, body‐mass index, cardiac co‐morbidity, haemoglobin, absolute and increase in c‐reactive protein on the first post‐operative day, bleeding, fluid balance at the end of surgery and the first post‐operative day) related to severe persistent hypotension (SPH) (SPH: need for noradrenaline to maintain a mean arterial blood pressure (MAP) >65.0 mm Hg on the morning after surgery) and occurrence of other early (24 hours) complications. One hundred patients undergoing pancreaticoduodenectomy (PD) with pre‐operative high‐dose glucocorticoid and goal‐directed fluid therapy were enrolled and perioperative data collected from anaesthetic and medical records.
Results
Forty‐five patients had SPH, who had a significantly higher increase in CRP levels the morning after surgery (median 50 mg L−1 vs 41 mg L−1, SPH vs non‐SPH, respectively, P = .028), and a significantly more positive fluid balance at discharge (median 1457 ml vs 1031 ml, respectively, P = .027) vs patients without SPH.
Conclusions
Severe persistent hypotension after PD was associated with significantly increased inflammatory response and increased need for fluids. Future studies should investigate the effect of further inflammatory control in PD to improve haemodynamics and morbidity.
Summary
Background: Both hypovolemia and a fluid overload are detrimental for outcome in surgical patients but the effort to establish normovolemia is hampered by the lack of an operational clinical ...definition. Manipulating the central blood volume on a tilt table demonstrates that the flat part of the Frank‐Starling curve is reached when subjects are supine and that finding may be applicable for a clinical definition of normovolemia. However, it is unknown whether stroke volume (SV) responds to an increase in preload induced by fluid administration.
Methods: In 20 healthy subjects (23 ± 2 years, mean ± SD), SV was measured by esophageal Doppler before and after fluid administration to evaluate whether SV increases in healthy, non‐fasting, supine subjects. Two hundred millilitres of a synthetic colloid (hydroxyethyl starch, HES 130/0·4) was provided and repeated if a ≥10% increment in SV was obtained.
Results: None of the subjects increased SV ≥10% following fluid administration but there was a minor increase in mean arterial pressure (92 ± 15 to 93 ± 12 mmHg, P = 0·01), while heart rate (HR) (66 ± 12 beats min−1; P = 0·32), cardiac output (4·8 ± 1·1 l min−1; P = 0·25) and the length of the systole corrected to a HR of 60 beats/min (corrected flow time; 344 ± 24 ms; P = 0·31) did not change.
Conclusion: Supporting the proposed definition of normovolemia, non‐fasting, supine, healthy subjects are provided with a preload to the heart that does not limit SV suggesting that the upper flat part of the Frank‐Starling relationship is reached.
An estimation of cardiac output can be obtained from arterial pressure waveforms using the Modelflow method. However, whether the assumptions associated with Modelflow calculations are accurate ...during whole body heating is unknown. This project tested the hypothesis that cardiac output obtained via Modelflow accurately tracks thermodilution-derived cardiac outputs during whole body heat stress. Acute changes of cardiac output were accomplished via lower-body negative pressure (LBNP) during normothermic and heat-stressed conditions. In nine healthy normotensive subjects, arterial pressure was measured via brachial artery cannulation and the volume-clamp method of the Finometer. Cardiac output was estimated from both pressure waveforms using the Modeflow method. In normothermic conditions, cardiac outputs estimated via Modelflow (arterial cannulation: 6.1 ± 1.0 l/min; Finometer 6.3 ± 1.3 l/min) were similar with cardiac outputs measured by thermodilution (6.4 ± 0.8 l/min). The subsequent reduction in cardiac output during LBNP was also similar among these methods. Whole body heat stress elevated internal temperature from 36.6 ± 0.3 to 37.8 ± 0.4°C and increased cardiac output from 6.4 ± 0.8 to 10.9 ± 2.0 l/min when evaluated with thermodilution (P < 0.001). However, the increase in cardiac output estimated from the Modelflow method for both arterial cannulation (2.3 ± 1.1 l/min) and Finometer (1.5 ± 1.2 l/min) was attenuated compared with thermodilution (4.5 ± 1.4 l/min, both P < 0.01). Finally, the reduction in cardiac output during LBNP while heat stressed was significantly attenuated for both Modelflow methods (cannulation: -1.8 ± 1.2 l/min, Finometer: -1.5 ± 0.9 l/min) compared with thermodilution (-3.8 ± 1.19 l/min). These results demonstrate that the Modelflow method, regardless of Finometer or direct arterial waveforms, underestimates cardiac output during heat stress and during subsequent reductions in cardiac output via LBNP.
Hyperthermia reduces the capacity to withstand a simulated hemorrhagic challenge, but volume loading preserves this capacity. This study tested the hypotheses that acute volume expansion during ...hyperthermia increases cerebral perfusion and attenuates reductions in cerebral perfusion during a simulated hemorrhagic challenge induced by lower-body negative pressure (LBNP). Eight healthy young male subjects underwent a supine baseline period (pre-LBNP), followed by 15- and 30-mmHg LBNP while normothermic, hyperthermic (increased pulmonary artery blood temperature ~1.1°C), and following acute volume infusion while hyperthermic. Primary dependent variables were mean middle cerebral artery blood velocity (MCAvmean), serving as an index of cerebral perfusion; mean arterial pressure (MAP); and cardiac output (thermodilution). During baseline, hyperthermia reduced MCAvmean (P = 0.001) by 12 ± 9% relative to normothermia. Volume infusion while hyperthermic increased cardiac output by 2.8 ± 1.4 l/min (P < 0.001), but did not alter MCAvmean (P = 0.99) or MAP (P = 0.39) compared with hyperthermia alone. Relative to hyperthermia, at 30-mmHg LBNP acute volume infusion attenuated reductions (P < 0.001) in cardiac output (by 2.5 ± 0.9 l/min; P < 0.001), MAP (by 5 ± 6 mmHg; P = 0.004), and MCAvmean (by 12 ± 13%; P = 0.002). These data indicate that acute volume expansion does not reverse hyperthermia-induced reductions in cerebral perfusion pre-LBNP, but that it does attenuate reductions in cerebral perfusion during simulated hemorrhage in hyperthermic humans.