Secondary Logo

Journal Logo


Spontaneous restoration of decreased systemic vascular resistance after spinal anaesthesia

Kamenik, M.

Author Information
European Journal of Anaesthesiology (EJA): November 2002 - Volume 19 - Issue 11 - p 848-850
  • Free


The mechanisms involved in blood pressure control during spinal anaesthesia are still not completely understood. Analysing the time course of the haemodynamic changes during spinal anaesthesia gives important information about the mechanisms involved in maintaining blood pressure during a sympathetic block. However, such an analysis is often impossible because the hypotensive events during spinal anaesthesia, which occur daily in our practice, are not sufficiently documented to permit a time course analysis of changes of blood pressure, cardiac output (CO) and systemic vascular resistance (SVR). In this correspondence, we analysed the time course of the haemodynamic changes in a patient developing severe hypotension during spinal anaesthesia. The patient was taking part in a study of the haemodynamic changes during spinal anaesthesia so that blood pressure and CO were continuously measured, allowing a detailed analysis.

Lidocaine (2% 3 mL) was injected intrathecally at the L2-3 interspace in a 41-yr-old female (weight 80 kg, height 160 cm) scheduled for arthroscopic knee surgery after the circulation had been preloaded with 8 mL kg−1 body weight Ringer's solution. CO, heart rate (HR) and stroke volume (SV) were measured continuously by impedance cardiography (NCCOM®; BoMed Medical Manufacturing, Irvine, CA, USA). Systolic and diastolic pressures were measured with an automated device (Corometrics Model 555®; Corometrics Medical Instruments, Inc, Wallingford, CT, USA), and mean arterial pressure (MAP) and SVR were calculated. The measurements started 7 min before and continued for 25 min after beginning spinal anaesthesia. No surgery was performed during this period.

The patient's baseline haemodynamic measurements were: systolic blood pressure 115 mmHg, MAP 90 mmHg, CO 6.7 L min−1 and SVR 1104 dyne s cm−5. The time courses of these variables during spinal anaesthesia are shown in Figure 1. Systolic pressure decreased to 73 mmHg and MAP to 55 mmHg 6 min after beginning spinal anaesthesia (Fig. 1). This was accompanied by a decrease of SVR to 610 dyne s cm−5 and a transient increase of CO to 7.1 L min−1. HR increased by up to 21 beats min−1 during the first minutes after inducing spinal anaesthesia but it started to decrease after 7 min (Fig. 1). The infusion of Ringer's solution was started immediately and the blood pressure started to increase. Twelve minutes after the lidocaine injection, systolic pressure was at an acceptable level (94 mmHg) (Fig. 1). This was accompanied by an increase of SVR to 1036 dyne s cm−5 and a decrease of CO to 5.6 L min−1. By that time, the patient had received about 250 mL Ringer's solution. Because of the decreasing HR (Fig. 1), atropine 0.5 mg was administered 15 min after beginning spinal anaesthesia at which time the HR was 71 beats min−1. Blood pressure was stable during the operation and no vasopressors were needed. The patient developed a sensory block up to the T3 dermatome.

Figure 1
Figure 1:
Time course of mean arterial pressure (MAP), cardiac output (CO), systemic vascular resistance (SVR), heart rate (HR) and stroke volume (SV) in a patient developing severe hypotension during spinal anaesthesia.

Hypotension during spinal anaesthesia is common in elderly patients, in patients developing a high sensory block [1] and in obstetric patients where an incidence as high as 50-80% has been reported [2]. However, hypotension necessitating the use of vasopressors is rare in middle-aged patients without concurrent disease undergoing arthroscopic surgery. In our patient, the primary cause of severe hypotension after spinal anaesthesia was a large decrease of SVR caused by sympathetic block. The SVR decrease occurred very soon after the lidocaine injection and activated the baroreceptor reflex, as indicated by the immediate increase of HR and CO. This increase of HR excludes vasovagal syncope as a likely cause of hypotension. After about 6 min, HR started to decrease, probably caused by the rostral spread of the local anaesthetic blocking the sympathetic innervation of the heart. We immediately started infusing Ringer's solution and decided to delay the administration of a vasopressor since the blood pressure had started to increase and the patient felt no discomfort. Twelve minutes after beginning spinal anaesthesia (6 min after the severe hypotension), the systolic blood pressure was at an acceptable level (94 mmHg). The blood pressure increase during this period was caused by a gradual increase of SVR since CO was actually decreasing. To our knowledge, a spontaneous restoration of SVR and blood pressure in a patient developing severe hypotension after spinal anaesthesia has never been recorded before. The restoration of SVR after an initial decrease without vasopressors indicates that endogenous mechanisms involved in blood pressure regulation by arteriolar vasoconstriction despite the presence of the sympathetic block were active. There are many reports in the literature indicating that the sympathetic block during spinal anaesthesia is incomplete even in patients developing high sensory block [3,4]. These reports are in agreement with the reports in the literature showing an attenuated but preserved cardiovascular response to the Valsalva manoeuvre during spinal anaesthesia [5]. A possible cause of vasoconstriction is the release of vasopressin in response to the blood pressure decrease caused by the sympathetic block. Vasopressin release after central neuraxial block has been reported in animals as well as in human beings [6,7]. Ecoffey and colleagues [7] measured a threefold increase in plasma vasopressin concentrations within 5 min after a decrease in blood pressure induced by a 30° head-up-body tilt in patients receiving epidural anaesthesia. Since vasopressin is a potent vasoconstrictor, it could have been partially responsible for the spontaneous increase of SVR in our patient.

Our case shows that the mechanisms involved in restoring the decreased SVR after the sympathetic block are not completely abolished even in patients developing a high sensory block during spinal anaesthesia. Further controlled stud-ies are needed to understand better the relationship between the degree of sympathetic block and the degree of haemodynamic changes after spinal anaesthesia.

M. Kamenik

Maribor Teaching Hospital; Department of Anaesthesiology; Intensive Care and Pain Management; Maribor, Slovenia


1. Carpenter RL, Caplan RA, Brown DL, Stephenson C, Wu R. Incidence and risk factors for side effects of spinal anaesthesia. Anesthesiology 1992; 76: 906-916.
2. Karinen J, Rasanen J, Alahuhta S, Jouppila R, Jouppila P. Effect of crystalloid and colloid preloading on uteroplacental and maternal haemodynamic state during spinal anaesthesia for Caesarean section. Br J Anaesth 1995; 75: 531-535.
3. Stevens RA, Frey K, Liu SS, et al. Sympathetic block during spinal anesthesia in volunteers using lidocaine, tetracaine and bupivacaine. Reg Anesth 1997; 22: 325-331.
4. Gratadour P, Viale JP, Parlow J, et al. Sympathovagal effects of spinal anesthesia assessed by the spontaneous cardiac baroreflex. Anesthesiology 1997; 87: 1359-1367.
5. Macfie AG, Brimacombe J. Response to the Valsalva manoeuvre after spinal anaesthesia. Anaesthesia 1992; 47: 13-16.
6. Peters J, Kutkuhn B, Medert HA, et al. Sympathetic blockade by epidural anesthesia attenuates the cardiovascular response to severe hypoxemia. Anesthesiology 1990; 72: 134-144.
7. Ecoffey C, Edouard A, Pruszczynski W, Taly E, Samii K. Effects of epidural anesthesia on catecholamines, rennin activity and vasopressin changes induced by tilt in elderly men. Anesthesiology 1985; 62: 294-297.
© 2002 European Academy of Anaesthesiology