Cardiovascular responses to different stages of restorative dental treatment unaffected by local anaesthetic type


Address for correspondence:
Professor Carina Gisele Costa Bispo
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Background:  The aim of this study was to evaluate the cardiovascular effects of maxillary infiltration using 2% lidocaine with 1:100 000 adrenaline, 4% articaine with 1:200 000 adrenaline, and 4% articaine with 1:100 000 adrenaline in different stages during restorative dental procedures.

Methods:  Twenty healthy patients randomly received 1.8 mL of the three local anaesthetics. Systolic blood pressure, average blood pressure, diastolic blood pressure, and heart rate were evaluated by the oscillometric and photoplethysmograph methods in seven stages during the appointment.

Results:  Statistical analysis by ANOVA and Tukey tests of cardiovascular parameters did not show significant differences between the anaesthetic associations. There were significant differences for the parameters among different clinical stages.

Conclusions:  The variation of cardiovascular parameters was similar for lidocaine and articaine with both adrenaline concentrations and showed no advantage of one drug over the other. Cardiovascular parameters were influenced by the stages of the dental procedures, which showed the effect of anxiety during restorative dental treatment.

Abbreviations and acronyms:

diastolic blood pressure


heart rate


mean blood pressure


systolic blood pressure


Since its introduction, lidocaine has been the most common dental local anaesthetic due to its clinical efficiency and safety.1,2 Articaine, another amide type local anaesthetic, is also a widely used local anaesthetic and was compared to lidocaine in previous studies.3,4

The vasodilator properties of amide justify the addition of a vasoconstrictor in order to increase the duration of action and decrease systemic toxicity. Lidocaine and articaine present almost identical vasodilator features.5

Adrenaline, the most common vasoconstrictor associated with local anaesthetics, is a neurotransmitter that stimulates alpha adrenergic receptors, especially in the peripheric blood vessels, and beta receptors, in the heart. Its principal effect in the vessels is the increase of its resistance, a consequence of an arteriolar dose-dependent vasoconstriction due to its effect on alpha receptors. The heart effects of adrenaline are an increase in the force and frequency of heart contractions due to its effect on beta 1 receptors, and the vasodilatation of skeletal musculature due to its effect on beta 2 receptors. The clinical manifestation of these actions can be an increase in systolic blood pressure and heart rate, and a decrease in diastolic pressure.2,6

Anderson and Reagan7 affirmed that a vasoconstrictor should have its maximum activity in alpha receptors, since it would result in the contraction of the unstriated musculature of arterioles, along with minimum activity in beta receptors in order to avoid undesirable cardiac effects. However, adrenaline is a low selective vasoconstrictor, with significant action in alpha and beta receptors. It is available in concentrations of 1:200 000 to 1:50 000.6,8

A systematic review of the cardiovascular effects of local anaesthesia with adrenaline in non-controlled hypertensive patients found a minimal risk, with small, non-significant increases in systolic and diastolic pressure.9

In normotensive patients, the principal causes of local anaesthetic systemic effects are incidental intravascular injection or excessive vascular administration, with high levels of the drug in blood and tissue levels. Systemic alterations induced by intravascular injection occur, especially with cardiovascular and central nervous system manifestations. However, appropriate local anaesthesia does not result in any systemic effect.6,10

Psychological stress can produce effects in a variety of psychological systems that are similar to those produced by physical challenges due to the activation of two stress response systems: the sympathetic or autonomic system and the hypothalamus-pituitary-adrenal axis. Situations involving pain, anxiety and acute tissue injury, such as dental stimuli, increase the activity of the hypothalamus-pituitary-adrenal axis which in turn enhance secretion of cortisol. Even in simple and painless dental procedures, such as low complexity restorative treatment, anticipating pain can increase anxiety and create a stressful situation with possible cardiovascular alterations.11

The effects of local anaesthetics and dental anxiety on the cardiovascular and central nervous systems are always important topics for the clinician. The objective of this study was to evaluate and compare the possible cardiovascular alterations of articaine and lidocaine with adrenaline and the effect of anxiety in different stages of low complexity dental procedures.

Materials and methods

After approval was granted from the Ethics in Research Committee, this study was performed in the dental office of the Department of Stomatology, University of São Paulo.

Twenty healthy patients (5 males and 15 females, aged 18–31 years) with three maxillary posterior teeth in need of restorative treatment were selected and informed written consent was obtained. Only small occlusal cavities (Class I) were selected and the extent of the restorative procedure took a similar time for each patient, a maximum 20 minutes. The same operator conducted the three appointments for each patient, with an interval of at least one week between appointments. One tooth was treated per session (a total of 60 appointments).

Patients were not smokers, pregnant, or hypersensitive to the drugs used in the study. Female patients always attended in the first week after menstruation. At each appointment, the tooth that would be treated received 1.8 mL of one of the three local anaesthetics: (1) 2% lidocaine with 1:100 000 adrenaline (L) – (Lidocaína 100, DFL®); (2) 4% articaine with 1:100 000 adrenaline (A1) (Septanest 1:100 000®, Septodont); and (3) 4% articaine with 1:200 000 adrenaline (A2) (Septanest 1:200 000®, Septodont).

Every patient had every anaesthetic solution (one for each tooth) and the order of application was chosen randomly. The injection technique was the maxillary infiltration described by Malamed.2 A self-aspiration syringe was used.

Systolic blood pressure (SBP), mean blood pressure (MBP), diastolic blood pressure (DBP) and heart rate (HR) were obtained by oscillometric and photoplethysmograph methods with an automatic non-invasive monitor model NIBP Schollar II (Criticare S.TM Inc., EUA) in different stages of the treatment. The cuff was positioned on the left arm and the photoplethysmograph device on the right hand middle finger.

An electric pulp-tester (Vitality Scanner Model 2005®; Analytic Endodontics, CA, USA), which is an electric device of low frequency designed to determine the response of a pulp to an electrical stimulus, was also used to evaluate onset and duration of local anaesthetics; the results can be found in a previous publication.12

Cardiovascular parameters were recorded in seven different stages during the dental appointment: Stage 1 (T1) – during the 10 minutes to record threshold values of cardiovascular parameters before electric stimulation; Stage 2 (T2) – during the five minutes the tooth was pulp tested; Stage 3 (T3) – during the 10 minutes to record threshold values of cardiovascular parameters before anaesthetic injection; Stage 4 (T4) – during the two minutes of anaesthetic injection; Stage 5 (T5) – during the evaluation anaesthetic’s onset period (using pulp tester); Stage 6 (T6) – during tooth restoration (using burs); and Stage 7 (T7) – during the 10 minutes after the conclusion of restoration.

In each stage (one minute), the one with the highest value for each parameter was evaluated to be considered in the statistical analysis.

The cardiovascular effects of the local anaesthetics were compared during the different clinical stages with the ANOVA parametric test and the Tukey auxiliary test, with a significance level of 1% (p < 0.01).


There were no intravenous injections and no markedly anxious states. The comparison of local anaesthetic solutions showed no significant difference (p > 0.01) among the cardiovascular parameters (SBP, MBP, DBP, HR). There was no significant difference (p > 0.01) in the interaction of local anaesthetics and clinical stages. However, the comparison among clinical stages showed significant differences for all of the cardiovascular variables.

There was a significant difference in HR (p < 0.01) before electric stimulation and during the anaesthetic injection (T1 > T4), during the anaesthetic injection and during pulp tester use (T4 < T5), and during pulp tester use and filling procedure (T4 < T6).

A significant difference was also found in SBP (p < 0.01) before and during electric stimulation (T1 > T2), before electric stimulation and during the anaesthetic injection (T1 > T4), and during injection and after the conclusion of the restoration (T4 < T7).

There was a significant difference in MBP (p < 0.01) before and during electric stimulation (T1 > T2), before electric stimulation and during the anaesthetic injection (T1 > T4), and before and during the anaesthetic injection (T3 > T4).

There was also significant difference in DBP (p < 0.01) before electric stimulation and during the anaesthetic injection (T1 > T4), before and during anaesthetic injection (T3 > T4), and during injection and after the conclusion of the restoration (T4 < T7).

Figures 1–4 show the behaviour of three local anaesthetics (L, A1 and A2) in the seven clinical stages (T1, T2, T3, T4, T5, T6 and T7), respectively for the parameters HR, SBP, DBP and MBP.

Figure 1.

 Heart rate variation during clinical stages (p < 0.01: between a and b).

Figure 2.

 Systolic blood pressure variation during clinical stages (p < 0.01 between a and b, and between c and d).

Figure 3.

 Diastolic blood pressure during clinical stages (p < 0.01 between a and b).

Figure 4.

 Mean blood pressure variation during clinical stages (p < 0.01 between a and b, and between c and d).


The present study on the variation of cardiovascular parameters with maxillary infiltration of lidocaine and articaine with adrenaline in dental restorative procedures showed that the three solutions had similar reactions and there was no advantage of one anaesthetic over the other in terms of cardiovascular effects. Other studies also compared articaine and lidocaine through the evaluation of the efficacy of clinical variables of onset and duration,3,12 anaesthetic effectiveness,13–16 clinical safety,4,17,18 and postoperative pain,19 and found similarities as well.

The results are in accordance with Khoury et al.20 who compared 2% lidocaine with 1:100 000 adrenaline and 4% articaine with 1:100 000 and 1:200 000 adrenaline, and did not find significant differences in BP and HR. Essentially, lidocaine and articaine with different percentages of the vasoconstrictor are effectively all the same.

The values of SBP and MBP in the first stage of the treatment (T1) – Record of threshold values – that were higher than in the following stage (T2) – application of pulp tester – and also values of HR, SBP, MBP and DBP in the first stage of the treatment were higher than in the stage of anaesthetic injection (T4). This can be interpreted as evidence that the anxiety of anticipating dental treatment may be due to pain expectation,11 and is likely to be the principal cause of cardiovascular alterations21 (Figs 3 and 4).

This affirmation is reinforced by the data that show that MBP and DBP were higher in Stage T3, before anaesthetic injection, than in stage T4, during anaesthetic injection (Fig 4). This is in agreement with Brand and Abraham-Inpijn,22 who reported higher cardiovascular parameters immediately before local anaesthetic injection.

Significant lower values of HR were found during the injection of local anaesthetics (T4) than in stages T5 (evaluation of onset period with the pulp tester) and T6 (during the restoration with burs) and significant lower values of SBP and DBP in stage T4 than in stage T7 (after the conclusion of the restoration). These results seem to eliminate the hypothesis of vasoconstrictors causing cardiovascular alterations in normotensive patients with previous aspiration, and is in agreement with many other studies about this topic.6,10,23,24

The results of the present study indicate some cardiovascular variation among clinical stages. It is probably associated with stress and does not create any risk for a normotensive patient. Cardiac or non-controlled hypertensive patients must receive more attention, although it was found in a systematic review that even in non-controlled hypertension, the effects of local anaesthesia using adrenaline is minimal.9

It must be emphasized that although some significant differences among the stages were found by statistical analysis, during the experiments no alterations or symptoms were observed or reported by the patient that could be associated with the administration of local anaesthetics or with the clinical stages, confirmed in other studies.25,26

It is also important to emphasize that the present study tested maxillary infiltration effects of local anaesthetics. A similar study for mandibular block injections may produce different results because of the different injection technique used.

The key finding of this paper was that cardiovascular events are not a response to the local anaesthetic, but a response to the stage of dental treatment and associated with dental anxiety, even in cases of low complexity restorative dental treatment.


In the present study, three anaesthetic solutions containing adrenaline showed similar reaction for cardiovascular parameters and were found to be safe for routine use in dentistry. There is influence in clinical stages on the cardiovascular dynamic which shows the effect of anxiety during dental restorative procedures.