Accidental intravascular injection of local anaesthetics occurs occasionally in the course of regional anaesthesia and can cause hemodynamic changes (Chapter 36). The magnitude of these changes depends upon the potency of the local anaesthetic injected and also upon a number of factors, such as:
1. site and speed of injection,
2. mass of local anaesthetic,
3. cardiac output,
4. Arterial PCO2,
5. acid-base status, and
6. patient-related factors (2).
Convulsant doses of lidocaine occur usually when plasma levels exceed 10 mcg/ml, (Table E.2). Serious hemodynamic changes do not occur until plasma levels far exceed these values (3). (Table 57.3) Supraconvulsant doses of lidocaine alter cardiac conductivity, automaticity and contractility leading to cardiovascular collapse, profound bradycardia and sinus arrest (2).
Bupivacaine, when injected intravascularly, causes serious cardiac arrhythmias (Table 36.6). Parturients may be more susceptible to these cardiotoxic effects (4).
Ropivacaine is a new, long acting, amide local anaesthetic currently undergoing clinical investigation (Chapter 4). Studies to date indicate that it is pharmacodynamically similar to bupivacaine but is less cardiotoxic (5, 6).
Hemodynamic effects of epidurally administered local anaesthetics:
Hemodynamic changes induced by epidural injection of local anaesthetics depend upon a number of factors including:
1. the extent of sympathetic blockade,
2. the site of blockade,
3. absorption of local anaesthetics,
4. the addition or absence of epinephrine, and
5. patient-related factors (7).
Obstetric patients are somewhat unique in their hemodynamic response to epidural anaesthesia. The large uterine mass interferes with venous drainage from the lower extremities causing engorgement of vertebral vessels in the epidural space. Therefore, a given injection of local anaesthetics into the epidural space will spread further and uptake of local anaesthetics into the circulation is more rapid. However, when one compares hemodynamic changes induced by epidural anaesthesia in pregnancy with those in the non-pregnant state the effects are far greater in pregnancy (8).
In late pregnancy, the uterus is extremely vascular and is a huge repository for venous blood. Furthermore, epidural anaesthesia impairs the homeostatic responses which would normally occur during aortocaval compression by the enlarged uterus (Figure 28.1) (Chapter 28). Finally, pooling of blood in the lower extremities, enhanced by uterine contractions, may add to this impairment of venous return. The key to the prevention of most of these problems is patient positioning (Figure 28.2) and intravenous fluid loading. Vasopressors may also be necessary. Patients should be nursed on the left side with slight elevation of the lower extremities.
Rapid uptake of epinephrine containing local anaesthetics adds further to hemodynamic changes (Table 57.4).
References:
1. Covino BG Epidural Anesthesia and Analgesia. Grune & Stratton Inc. 1985
2. Covino BG. Local Anesthetics. Grune & Stratton. 1976
3. Liu PL. Anesth Analg 62:375,1983
4. Albright GA Cardiac arrest following regional anesthesia with etidocaine or bupivacaine Anesthesiology 1979 51:4:285-287
5. Feldman HS. Anesth Analg 1989; 69:794
6. Scott DB Anesth Analg 1989;69:563
7. Bromage PR Epidural Anaesthesia. WB Saunders & Co Philadelphia. 1978
8. Assali NS J Clin Invest 1950;29:1354