Interesting reading about vasovagal mechanism and came across BJR with its share of cardiovascular suppressing entities. This is basically a reflex which would leads to a marked increase in parasympathetic tone as a result of the activation of chemo- &/or mechano- receptors of the left ventricles; which leads to the activation of unmyelinated vagal afferent C fibres. The triad of resulting changes are hypotension, bradycardia and coronary artery dilatation (1). Natriuetic peptide receptors may modulate such response as BJR may be less pronounced in patients with hypertrophy or AF (1). It explains the sinus bradycardia in the initial phase of acute MI. It also happens in patients with nitrates therapy, serotonin agonists, and may explain circulatory collapse in spinal anaesthesia (2).
1. Miller's anaestheisa 7th edition.
2. Wikipedia.
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