Nasal application of adrenaline-containing local anaesthetic is widely used in endoscopic sinus surgery (ESS). However, some recent clinical observations have shown that, in healthy adults, nasal infiltration with 2% lidocaine or physiological saline with adrenaline (1: 200 000) caused a significant mean arterial pressure (MAP) decrease, which indicates that a low dose of adrenaline is related to marked hypotension [1–4].
The present study is a prospective, randomized and double-blinded clinical study. The study was approved by the Institute Ethics Committee of Beijing Institute of Otolaryngology and conducted according to the Helsinki Declaration. The observation was from January to August 2006. Written informed consent was obtained from all the patients. All patients were ASA physical status I or II without a history of coronary artery disease, hypertension, arrhythmia, diabetes or previous ESS. Group I received 1% tetracaine with 1: 10 000 adrenaline for nasal anaesthesia; group II received 1% tetracaine only. An appointed nurse prepared the different solutions; neither the surgeons nor the anaesthetists, including the observer, knew which solution was used. Without premedication, anaesthesia was induced with midazolam 0.03 mg kg−1, remifentanil 1.5 μg kg−1 and propofol 2 mg kg−1. Atracurium 0.5 mg kg−1 was used to facilitate orotracheal intubation with a cuffed tube. Anaesthesia was maintained with 1% isoflurane, nitrous oxide 60% in oxygen. The patients were mechanically ventilated to maintain the end tidal carbon dioxide tension at around 35–40 mmHg. Plasma expanders (hetastarch 3–6 ml kg−1) and crystalloid (Ringer's lactate 3–6 ml kg−1) were infused to prevent MAP and heart rate (HR) fluctuation before nasal packing. Ten minutes after the induction of general anaesthesia and endotracheal intubation, two tetracaine (with or without adrenaline)-soaked cotton plugs were inserted into each nasal cavity (common meatus and middle meatus) and removed 5 min later. The amount of tetracaine solution absorbed by one plug was about 2 ml. A radial artery cannula was inserted before the induction of anaesthesia and blood pressure could be monitored directly and continuously. Systolic blood pressure (SBP), MAP, diastolic blood pressure (DBP) and HR were recorded continuously at the following 11 time points: before tamponade (baseline) and every minute after tamponade until the 10th minute.
Thirty adult patients, including 19 men and 11 women, were recruited, with 15 patients in each group. The mean age was 38 years with a range of 18–50 years. There was no significant difference between the two groups of patients with regard to age, sex, body weight, and volume of intravenous fluid infusion, baseline of BP and baseline of HR. In group I and group II, at all the observation time points after tamponade, SBP, DBP and MAP showed no significant changes compared with baseline. Whereas HR in group II showed no significant changes compared with baseline (P > 0.05), HR in group I showed a transient increase, starting from 1 min (80.3 ± 6.8 beats min−1, P < 0.05). It reached a peak (84.2 ± 10.1 beats min−1, P < 0.05) during the next minute and then decreased by the 3 min point (79.3 ± 10.2 beats min−1, P < 0.05). Moreover, at these three time points, HR was also higher than that in group II (P < 0.05). From the 4th minute to the end of the observation, HR slowed down towards the baseline level and showed no differences from that in group I at the same time point (Fig. 1).
Topical application of local anaesthetics with adrenaline is widely used to relieve pain, decrease surgical bleeding and allow better visualization of the surgical field in ESS. It has been generally accepted that no severe cardiovascular event is related to this procedure [5,6]. However, some studies [1–4] revealed different haemodynamic changes after local infiltration of adrenaline. The controversy was based on different local anaesthesia techniques and adrenaline concentrations (for example 1: 1000 for topical , 1: 80 000 , 1: 100 000 , 1: 200 000 [1,2] and 1: 400 000  for infiltration).
According to our findings, in healthy adults undergoing ESS under general anaesthesia, no significant blood pressure changes were detected after nasal packing with 1% tetracaine-soaked (with or without 1: 10 000 adrenaline) plugs.
The HR changes in different studies are also controversial. We found nasal packing with 1: 10 000 adrenaline-soaked plugs caused a transient and significant increase in HR, and restored quickly within 4 min, which is consistent with the findings of John et al., although they used infiltration with 1: 80 000 adrenaline. The increase in HR might be mainly the result of baroreceptor reflex and some stimulation of β1-receptors [1,2].
Effects of adrenaline on arterial pressure and HR are dose dependent. As a direct acting α-receptor and β- receptor agonist produced by the adrenal medulla, adrenaline may activate different types of sympathetic receptors at different doses. A dose of less than 2 μg should predominantly activate β2-receptors, resulting in vascular relaxation; a dose of 2–10 μg should predominantly activate β1-receptors to increase HR, contractility and conduction and decrease the refractory period. Doses in excess of 10 μg cause marked α-stimulation with resultant generalized vasoconstriction. Thus, the plasma concentration of adrenaline should have a close relationship with activation of sympathetic receptors.
Systemic absorption of adrenaline may occur when local infiltration or topical tamponade or both are applied. Systemic effects of adrenaline are variable in different patients and are related to the blood concentrations. Various studies have shown that the haemodynamic changes after local infiltration of adrenaline also depend on the physical status of the patient, vascularity of the site of administration and the rate of absorption from the area infiltrated . Also, the plasma concentration of adrenaline might be affected by other factors such as the anaesthesia method and the depth of general anaesthesia.
In addition, the plasma concentration of adrenaline is made up of endogenous adrenaline and exogenous adrenaline. Pain or surgery may produce much more endogenous adrenaline than the exogenous amount of adrenaline absorbed from the local applications. This could explain why, in spite of several studies having been carried out, no defined correlations between the amount of local application and plasma concentration of adrenaline has been established. Therefore, the haemodynamic changes are not merely the result of a low dose of adrenaline as a local vasoconstrictor.
Local anaesthetic technique might be another explanation why we detected only increased HR, but not marked hypotension. Local infiltration or topical application might influence the amount of adrenaline absorbed; the procedure per se causes different pain impulses and accordingly the plasma concentration of adrenaline could be different. Therefore, hypotension, hypertension or HR increase might be the result. Our study showed that topical use of tetracaine and adrenaline did not cause blood pressure changes under general anaesthesia, which at least suggests that nasal tamponade might be better than local infiltration in ESS as there are adverse effects.
Deep anaesthesia may be a prerequisite for the adrenaline-induced hypotension . Li et al. reported recently that relatively light anaesthesia can reduce the severity of adrenaline-induced hypotension during ESS. And accordingly, the increase in HR was significantly lower. In our study, the inhaled concentration of isoflurane was only 1%, which also represented a relatively light general anaesthesia and no severe hypotension was seen either.
As most clinical observations, including ours, did not measure the plasma concentration, we can only compare changes in BP and HR. The reason might be that the different plasma concentrations of adrenaline resulted in the activation of different sympathetic receptors; ultimately, a faster HR with or without hypotension could be observed.
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