MAP decreased continuously during the study period and 21 patients developed relative hypotension, but only seven had a SAP below 90 mmHg (Table 3). The changes in HR were minimal, and bradycardia (HR < 50 beats min−1) was seen in only one patient. The haemodynamic changes were not significantly related to premedication, bupivacaine dose 15 mg or above, baricity, patient position or use of epidural catheter.
Onset of spinal anaesthesia resulted in reduction in the CO, 0.5 L min−1 on average in elderly patients untreated with fluids or vasopressors. However, CO increased initially reaching a maximum 7 min after the subarachnoid injection. MAP decreased continuously throughout the study period, whereas HR remained virtually unchanged.
In accordance with our findings, an initial increase in CO during onset of spinal anaesthesia was recently found . This study in elderly patients demonstrated that smaller local anaesthetic doses resulted in a significant increase in CO, 2 min after subarachnoid injection. The final CO decrease in our study (8%) is in accordance with another study in elderly men with cardiac disease . These 15 patients with a median sensory block at T4 had a 33% decrease in MAP, 26% decrease in SVR and 10% decrease in CO, as determined by a pulmonary artery catheter. Other studies reported similar changes (10-20% decrease in CO or cardiac index) using thoracic electrical bioimpedance [8-10] or transthoracic echocardiography .
Using thoracic electrical bioimpedance, it was found that a decrease in SV in some elderly patients was compensated by an increase in HR . In our study, CO decreased as a result of reduced SVR and SV that were not compensated by an increase in HR. This, on one hand, may be explained by the impaired baroreceptor activity  and, on the other hand, by the more frequent β-blocker medication in the elderly. However, only four of our patients received β-blockers, and only one of these was unable to increase HR to compensate for a large CO reduction. The lack of HR response in our study is thus most likely to be caused by impaired baroreceptor activity.
The four patients receiving ACE inhibitors had a 0.9 L min−1 CO decrease, but this study was not powered to compare haemodynamic response and concurrent cardiovascular medication.
The initial CO increase in our study may be attributed to a reduction in arterial vascular tone, which preceded the reduction of venous return . Ageing and elevated sympathetic activity increase the SVR . At the time of the largest CO increase, on average 7 min after the intrathecal injection, SVR had decreased 27% in our patients. At the end of data collection, 10 min later, the decrease in SVR was 23%. Thus, we can assume that the initial increase in CO is caused by this large reduction in afterload. This is supported by findings when patients are compared according to hypertension at baseline. In 20 patients with hypertension at the baseline (SAP ≥ 160 mmHg), the initial increase in CO was 1.3 L min−1 vs. 0.8 L min−1 in the 12 patients with normotension at the baseline (P = 0.04). A moderate afterload reduction may thus be associated with increased CO in elderly hypertensive patients.
At end of data collection, we observed a large and significant increase in SVV and PPV. These results should be considered with caution since the patients were not mechanically ventilated, and changes in respiratory cycle during the study period may enhance inter-individual differences in SVV and PPV. However, this suggests that hypotension was caused by decreased venous return.
Further analysis of this study showed that eight patients with sensory block level T3-T5 had a 1.1 L min−1 decrease in CO vs. 0.3 L min−1 in the 24 patients with sensory block level T6-T12 (P = 0.10). This is in accordance with evidence that cardioacceleratory fibres are blocked when spinal anaesthesia involves higher thoracic levels . We must, however, emphasize that this is a post hoc analysis and the overall correlation of final CO change and sensory block level was poor (r = 0.24; P = 0.16). The change in HR was similar in these groups, so the larger decrease in CO may be a consequence of reductions in preload and central venous return rather than a blockade of cardioacceleratory fibres. The interpretation of these findings is furthermore limited by the large inter-individual differences in the assessment of sympathetic block from sensory block level and our sample size provided less than 50% power to detect the observed difference.
The incidence of hypotension in this study was 66% and 22%, when defined as a decrease in MAP > 25% and SAP below 90 mmHg, respectively. This compares well with previous findings in elderly patients [4,6,7], as well as with the study by Carpenter and colleagues . In their study, 33% of 952 patients had hypotension, defined as a SAP < 90 mmHg or a 10% decrease from baseline. Other investigations reported incidences of hypotension as low as 15%, when defined as a decrease in arterial pressure greater than 30% or a SAP below 85 mmHg  and 8% when defined as a decrease in MAP > 30% . In elderly patients, it was recently reported that 22 of 25 patients required treatment with ephedrine as a consequence of a decrease in SAP > 25% or SAP below 100 mmHg after spinal anaesthesia for hip repair .
The strength of our study is the high time-resolution of data, which may follow the haemodynamic changes during onset of spinal anaesthesia more closely than other methods. Although we observed a statistically significant reduction in CO from baseline, this reduction was smaller than the estimated reduction in our sample size calculation. Thus, we cannot conclude that spinal anaesthesia per se is associated with a clinically important reduction in CO. In the patients with high sensory blockade, we observed a trend towards a larger CO decrease. Although most of the observed changes in CO were often of minor clinical relevance, describing the CO changes every 10 s provides better knowledge of the underlying physiology of spinal anaesthesia.
One limitation of our study is that we did not control the final sensory block level. It is likely that the block would have been higher in some patients after 30 min . However, we did not wish to delay treatment of hypotension to 30 min after subarachnoid injection. We collected haemodynamic data representing onset of spinal anaesthesia, and not spinal anaesthesia together with fluid preloading, ephedrine, elevation of legs, etc. Spinal anaesthesia was performed as decided by the attending anaesthesiologist, who chose the dose and bupivacaine baricity, to achieve the optimal anaesthesia for the given patient and type of surgery. The placement of epidural catheter after subarachnoid injection was unlikely to influence haemodynamic or the sensory block level. No medication was given through the catheter, apart from a 2 mL bupivacaine test dose 5 min before termination of data collection.
Although cardiovascular medications and atrial fibrillation can influence haemodynamic responses, these do not necessarily impair the ability of using the LiDCO™plus, and we eliminated artefacts due to large beat-to-beat variation in pulse amplitude. Benzodiazepine premedication may be another limitation of our study. This may attenuate the arterial baroreflex [19-21]. However, premedication did not show a significant association with hypotension in another study of spinal anaesthesia . A total of 47% of patients had premedication.
We did not try to compare our CO measurements to a gold standard, but the purpose of this study was neither to evaluate the LiDCO™plus haemodynamic monitor nor to compare it with a pulmonary artery catheter. The LiDCO™plus monitor has been validated previously (limits of agreement from −26% to +21% when compared to thermodilution) and appears reliable without recalibration, for at least 8 h after cardiac surgery, a situation with frequent changes in arterial resistance [22,23].
This study shows that it is feasible to use the LiDCO™plus monitor to follow changes in haemodynamics at short intervals during onset of spinal anaesthesia. Future studies should include longer observation time. This will allow evaluation of different regimes to maintain haemodynamic stability.
In conclusion, biphasic changes in CO were observed during spinal anaesthesia in elderly patients using a method with high time-resolution. Initially, CO increased. Subsequently, it decreased significantly from baseline, although this decrease was of minor clinical importance.
The authors wish to thank The Danish Medical Research Council (Grant number: 22-04-0019) and Oberstinde Kirsten Jensa la Cour's foundation for supporting this research.
1. Greene NM. Physiology of Spinal Anaesthesia
. Baltimore: Williams & Wilkins, 1981.
2. Salinas FV, Sueda LA, Liu SS. Physiology of spinal anaesthesia
and practical suggestions for successful spinal anaesthesia
. Best Pract Res Clin Anaesthesiol
3. Priebe HJ. The aged cardiovascular risk patient. Br J Anaesth
4. Critchley LA, Stuart JC, Short TG, Gin T. Haemodynamic effects of subarachnoid block in elderly patients. Br J Anaesth
5. Rooke GA, Freund PR, Jacobson AF. Hemodynamic response and change in organ blood volume during spinal anesthesia in elderly men with cardiac disease. Anesth Analg
6. Coe AJ, Revanäs B. Is crystalloid preloading useful in spinal anaesthesia
in the elderly? Anaesthesia
7. Favarel-Garrigues JF, Sztark F, Petitjean ME, Thicoipe M, Lassie P, Dabadie P. Hemodynamic effects of spinal anesthesia in the elderly: single dose versus titration through a catheter. Anesth Analg
8. Chan VW, Chung F, Gomez M, Seyone C, Baylon G. Anesthetic and hemodynamic effects of single bolus versus incremental titration of hyperbaric spinal lidocaine through microcatheter. Anesth Analg
9. Fanelli G, Casati A, Aldegheri G et al.
Cardiovascular effects of two different regional anaesthetic techniques for unilateral leg surgery. Acta Anaesthesiol Scand
10. Kamenik M, Paver-Erzen V. The effects of lactated Ringer's solution infusion on cardiac output
changes after spinal anesthesia. Anesth Analg
11. Donati A, Mercuri G, Iuorio S et al.
Haemodynamic modifications after unilateral subarachnoid anaesthesia evaluated with transthoracic echocardiography. Minerva Anestesiol
12. Jonas MM, Tanser SJ. Lithium dilution measurement of cardiac output
and arterial pulse waveform analysis: an indicator dilution calibrated beat-by-beat system for continuous estimation of cardiac output
. Curr Opin Crit Care
13. Carpenter RL, Caplan RA, Brown DL, Stephenson C, Wu R. Incidence and risk factors for side effects of spinal anesthesia. Anesthesiology
14. Mark JB, Slaughter TF. Cardiovascular monitoring. In: Miller R. ed. Miller's Anesthesia
. Philadelphia, USA: Elsevier Churchill Livingstone, 2005: 1265-1362.
15. Asehnoune K, Larousse E, Tadie JM, Minville V, Droupy S, Benhamou D. Small-dose bupivacaine-sufentanil prevents cardiac output
modifications after spinal anesthesia. Anesth Analg
16. Tarkkila PJ, Kaukinen S. Complications during spinal anesthesia: a prospective study. Reg Anesth
17. Hartmann B, Junger A, Klasen J et al.
The incidence and risk factors for hypotension
after spinal anesthesia induction: an analysis with automated data collection. Anesth Analg
18. Olofsson C, Nygards EB, Bjersten AB, Hessling A. Low-dose bupivacaine with sufentanil prevents hypotension
after spinal anesthesia for hip repair in elderly patients. Acta Anaesthesiol Scand
19. Farmer MR, Vaile JC, Osman F, Ross HF, Townend JN, Coote JH. A central gamma-aminobutyric acid mechanism in cardiac vagal control in man revealed by studies with intravenous midazolam. Clin Sci (London)
20. Ikeda T, Doi M, Morita K, Ikeda K. Effects of midazolam and diazepam as premedication on heart rate variability in surgical patients. Br J Anaesth
21. Taneyama C, Goto H, Kohno N, Benson KT, Sasao J, Arakawa K. Effects of fentanyl, diazepam, and the combination of both on arterial baroreflex and sympathetic nerve activity in intact and baro-denervated dogs. Anesth Analg
22. Hamilton TT, Huber LM, Jessen ME. PulseCO: a less-invasive method to monitor cardiac output
from arterial pressure after cardiac surgery. Ann Thorac Surg
23. Linton NW, Linton RA. Estimation of changes in cardiac output
from the arterial blood pressure waveform in the upper limb. Br J Anaesth
Keywords:© 2007 European Society of Anaesthesiology
CARDIAC OUTPUT; HYPOTENSION; INDICATOR DILUTION TECHNIQUES; LITHIUM CHLORIDE; SPINAL ANAESTHESIA