In Veterinary medicine, in healthy dogs, for our premedication prior to general anaesthesia we tend to use an alpha-2 adrenoceptor agonist such as medetomidine or its active enantiomer, dexmedetomidine. The resulting bradycardia, although being a normal response, can be disconcerting for some practitioners who then tend to reverse the alpha-2 and lose, with the sedation, its analgesic effect. Others, although discouraged by different papers in the literature, give an anticholinergic which then results in hypertension. Following the advice of a more experience anaesthetist, I tend nowadays to give 2 mg/kg IV of lido to increase the HR in those patients. The effect is usually a mild increase and of short duration. The experimented anaesthetist referred to a technique or info from the 70"s. I have asked around me since, and can not get the explanation for the mechanism. Naturally, I would have expected an injection of lido to result in a decrease of the HR as we observed when we treat ventricular rhythm disturbances such as V-Tach. Even when I look at data sheets, slower HR (bradycardia) is a side-effect, not faster heart rate. Does anyone have any idea?
Cheers
Good morning
There may be a central effect from the administration of 2 mg/kg of lidocaine in a bradycardic patient. My first question is why is the patient bradycardic? If there is some conduction defect, I suggest the lidocaine would have no effect. If it is simply a sinus bradycardia, the central mechanism of heart rate may be involved.
There is, in the brain, a neuronal pool called the nucleus tractus solitarius (NTS) which regulates heart rate (See Guyton's textbook of medical physiology, 12th Ed, pp 206 and 7). Stimulation of the NTS results in excitation of the parasympathetic stimulatory center, resulting in decreased heart rate. A bolus dose of a local anesthetic such as you describe may have transient CNS depressant effects. If you depress this center, you depress the ability to slow heart rate (decrease centrally mediated vagal tone), so heart rate can increase.
This is common in the early stages of an inadvertent overdose of local anesthetic (excitatory stage), but is followed, in the case of a large overdose, by bradycardia and cardiovascular collapse. A more complex explanation can be found at Journal of the Autonomic Nervous System Volume 23, Issue 2, August 1988, Pages 161–174 Evidence for a sympathoexcitatory pathway from the nucleus tractus solitarii to the ventrolateral medullary pressor area Raymond W. Urbanski2,
Hreday N. Sapru, 1, 2
Please note this is my "best guess", and am happy to entertain other ideas
Cheers
Rich
Good afternoon.
The case I am descibing is one we see everyday when using an alpha2 adrenoceptor agonist in the premedication. The resulting bradycardia, a response to increase peripheral vascular resistance (vaso constriction) can sometimes be important. The administration of lidocaine during the anaesthesia to increase the heart rate may possibly have a positive effect on the MAC value of the inhalant. There is at least one human paper (Hamp et al, 2013) showing a significant MAC reduction on Sevoflurane after an injection of 1.5 mg/kg of Lido. The level of Sevo decreased by a mean of about 0.23%. . In 2009, Matsubara et al showed a decreased of the MAC value of Sevo in dog with lidocaine infusion (50 and 200 micg/kg /min); Valverde in 2004 with similar infusion rate showed a MAC reduction of Iso in dog too while Doherty in 1998 in Poneys showed a MAC reduction in Haltothane with similar infusion rate.
So I agree with Anhubav that the patient may be deeper...but that would still not explain the increase in HR. In the human I mentioned earleir (Ham et al) they see no changes in HR, possibly a slight decrease if anything!!!
Hi Geoffrey,
Your guess is a good one.. But I think I have seen that effect even after phase 1, but I could not swear it , but me feeling is...long enough to be passed the phase 1...as I always make sure that the effect (bradycardia) could be alpha2 related. and that an anticholinergic might not be appropriate.(hypertension).
Hi Geoffrey
Dose is usually less than 5 mic/kg if IM and nomore than 3 if IV...with an opioid.
Time in the 30 min window...
Hello everyone,
I might have found an answer to my question. I found the following paper, or at least its abstract: : The effects of lidocaine on electrical and mechanical activity of the heart", 1968, lieberman et al., Amer J. of Cardiol. 22(3), pp.3 75-380. In the abstratc it is said:"Lidocaine has a negative chronotropic effect on automatic pacemakers of the ventricles and, to a lesser extent, of the atria. However, under conditions of increased vagal activity, a vagolytic effect capable of increasing the rate of the S-A node was demonstrated...". So what we see might be the vagolytic effect?
I cant get the full paper and would love to read it...would be great if someon had the chanse to access it and sendint me a copy...cheers
Thierry
Hi Geoffrey,
usually the heart rate increases by about 10-20% at best. Blood pressure follows, but usually no hypertension per se. No arrhythmias observed so far, but N is low...about 20-30 dogs. Haven't tried in cats yet...
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