Mechanisms behind and treatment of sudden, unexpected circulatory collapse during central neuraxis blockade.
Judging from the number of cases reported in the literature, severe bradycardia and/or asystole in association with central neuraxis blockade fortunately seems a rare complication. However, short periods of extreme bradycardia may go unnoticed and manifest cases, especially when outcome is favourable, may go unreported, and thus the real incidence may be much higher. Although the decrease in systemic blood pressure as a result of central neuraxis blockade is caused by various mechanisms, the most important factor causing severe hypotension, bradycardia and circulatory collapse is decreased venous return, and both prevention and treatment are aimed at preserving or restoring adequate venous return to the heart. Correction of preoperative hypovolaemia, limiting the extent of sensory blockade and positioning the patient so that gravity promotes venous return are the most significant preventive measures. Although a widespread custom, controversy exists regarding the efficacy of a preload; for certain categories of patients intravenous volume loading may be deleterious, and rather than a routine measure, the decision to administer a preload should be based on the clinical situation and the condition of the individual patient. For the treatment of mild bradycardia, anticholinergic drugs are the first choice. Hypotension may be treated by promoting venous return using gravity, by intravenous fluid infusion, by intravenous administration of sympathomimetic drugs, or by a combination of all three measures. In the event of sudden circulatory collapse, the first therapeutic measure that is usually immediately effective is elevation of the legs, thus promoting venous return.
Stienstra
R
R
Department of Anesthesiology, Leiden University Medical Center, The Netherlands. r.stienstra@lumc.nl
D006339:Heart Rate / Q000502:physiology; D006801:Humans; D009407:Nerve Block / Q000009:adverse effects*; D012769:Shock / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*