Haemodynamic changes and stress responses of piglets to surgery during total intravenous anaesthesia with propofol and fentanyl.

The purpose of the study was to assess the haemodynamic (blood pressure and heart rate) changes and stress responses (serum cortisol and serum amyloid A [SAA] concentrations) to surgery in piglets during total intravenous anaesthesia (TIVA) with propofol and fentanyl. After preanaesthetic medication with intramuscular midazolam (0.5 mg/kg body mass), ketamine (10 mg/kg) and butorphanol (0.5 mg/kg) anaesthesia was induced in five piglets, with intravenous propofol (1 mg/kg) followed by tracheal intubation and mechanical lung ventilation. Soft tissue surgery was performed in the jugular and inguinal regions during TIVA with propofol (8 mg/kg/h) and fentanyl (35 microg/kg/h). Anaesthesia was maintained for 300 min after surgery as the piglets were the control group of a project involving extracorporeal membrane oxygenation. Mean plasma cortisol concentration decreased significantly (P<0.05) from 59+/-39.9 nmol/L (mean+/-1 SD) before surgery to 7.5+/-2.5 nmol/L 300 min after end of surgical procedure. The mean SAA concentrations increased over the same period from 1.6+/-2.3 microg/mL to 4.2+/-5.6 microg/mL without statistical significance. The baseline (presurgery) mean arterial pressure (MAP) was 72+/-9 mmHg compared with 72+/-11 mmHg 300 min after end of surgery. Neither heart rate nor lactate concentrations changed significantly over the same time points: heart rate was 104+/-11 and 103+/-15 beats/min whereas mean lactate concentrations were reduced from 1.14+/-0.45 mmol/L to 0.90+/-0.22 mmol/L. Haemodynamic stability, a decrease in serum cortisol and a non-statistically significant rise in mean SAA concentrations suggest that the anaesthetic described suppresses the stress response of piglets to surgery without adverse cardiovascular effects. Therefore, it may prove useful in cardiovascular research.

The immediate haemodynamic response to the initiation of extracorporeal membrane oxygenation in a piglet model of infant hypoxic respiratory failure.

There is evidence that haemodynamic fluctuations on extracorporeal membrane oxygenation (ECMO) increase the risk of cerebral damage. We hypothesized that initiation of venovenous (VV) or venoarterial (VA) ECMO itself causes haemodynamic fluctuations and, thus, established an infant animal ECMO model in order to discuss this hypothesis. Five piglets were cannulated using the jugular and femoral veins (VV group) and five using the jugular vein and carotid artery (VA group). All animals were subjected to hypoxic ventilation (FiO2 8%) for 10 min, leading to a PaO2 of < 40 mmHg, and subsequently rescued by ECMO. The heart rate (HR) and mean arterial blood pressure (MAP) were recorded at 5-min intervals; the arterial blood lactate was measured prior to and after 5 and 10 min of hypoxia, as well as 30, 60 and 120 min after initiation of ECMO. The response to initiation of ECMO was similar in the VV and VA groups with regard to HR and lactate, but differed significantly in MAP. HR decreased significantly from 135 +/- 7 to 103 +/- 6 beats/min (p < 0.05) and from 132 +/- 8 to 84 +/- 9 beats/min (p < 0.01) at 5 min (p = NS) after installation; lactate increased from 1.4 +/- 0.1 to 1.8 +/- 0.2 mmol/l (p = NS) and from 1.4 +/- 0.2 to 1.6 +/- 0.5 mmol/l (p = NS) after 30 min (p = NS); MAP decreased from 80 +/- 5 to 63 +/- 3 mmHg (p = NS) and increased from 75 +/- 4 to 84 +/- 3 mmHg (p = NS) at 5 min (p = 0.001), respectively. The initiation of ECMO is associated with haemodynamic fluctuations in both modalities, which differ with regard to blood pressure reaction.