Cardiovascular Risk: DISCUSSION

In: Anesthesia

16 Mar 2010

Cardiovascular Risk DISCUSSION

Though local anesthesia induced statistically significant changes to the mean values for HR and SBP for both anesthetic and sedation groups, the physiological magnitude and clinical relevance of such change would best be described as minimal. Maximal values were seen during the phase of surgery and were consistent with the observations of Knoll-Kohler et al and Paramaesvaran and Kingon. Greater hemodynamic changes have been reported for cardiac patients with controlled maximal exercise and isometric muscle testing. However, there were no significant differences between the phases of treatment. Thus to patients with the administration of the local anesthetic appeared to be no more stressful than the phases of stabilization, surgery, or recovery; conversely, to the patient, stabilization, surgery, and recovery were as stressful as anesthesia.

For the ECG, dysrhythmias were common, but their incidence was low. Previous dental studies have been confused on this particular issue, reading significance into prevalence and excluding patients of particular interest—for example, those with known dysrhythmias and ischemic heart disease. However, dynamic electrocardiography has demonstrated the ubiquity of arrhythmias and ischemic change in the general population. Arrhythmias have been recorded in 56% of fit medical students and 90% of individuals with coronary heart disease. Changes in ST segments and T waves have been recorded in 23% of unaffected subjects and 90% of individuals with coronary heart disease. A better judgment on prognosis might therefore be offered by the known hierarchy of risk associated with the more complex or malignant arrhythmia, defining dysrhythmias such as premature supraventricular beats, ventricular ectopics, and pauses as benign and atrial bigeminy, trigeminy, multiple consecutive beats, and sustained supraventricular and ventricular tachycardias as malignant. However, such malignant arrhythmias have also proven to be almost omnipresent in the general population. A number of investigators have looked further for other predictors of sudden cardiac death, without great result apart from the repetition of known associations with heart disease, ischemia, chronic ectopic activity, catecholamine release, circadian rhythm, potassium levels, mental stress, and physical activity. For this investigation, what was surprising was that up to 42% of the total arrhythmic data was accounted for by a single individual and that though dysrhythmias were scattered across all phases of treatment, they were most common during surgery. The latter was also an observation made by Barkin and Middleton. Finally, the use of midazolam sedation improved hemodynamics whether measured in a summarized or extreme manner, but it marginally increased malignant arrhythmic activity, apparently at the expense of benign activity. canadian pharmacy viagra

As to noradrenaline, there is little pharmacological ar­gument for the employment of this particular catecholamine as a vasoconstrictor. Its potency is a quarter that of adrenaline, and because of its tendency to induce hypertensive change, the majority of investigators have always suggested that it should not be employed in such a role. However, in the main study (R. J. Middlehurst, unpublished data, 1999) there was a rank order for the prevalence of arrhythmias with lidocaine anesthesia that was dependent upon adrenaline concentration. Greatest for the combination vasoconstrictor was adrenaline 1:50,000 and vasopressin 0.25 IU/mL; intermediate was lidocaine with adrenaline 1:80,000; and least was the adrenaline-free combination of noradrenaline 1:50,000 and vasopressin 0.25 IU/mL. This may be explained by adrenaline’s major effect as a cardiac stimulant, inducing a tachycardia and, as a consequence, ischemia. Finally, the hemodynamic changes for the extreme responders might represent the capture of intravascular injection sequelae, and a literature review reported the risk for such events at 8%.

The hypothesis argued for the risks of local anesthesia in heart disease is that structural and functional abnormalities have the potential to interact with external triggers, alone or in synergy, to produce the common end point of sudden cardiac stress or death. For dentistry, this remains a simplistic point of view, given the scale of local anesthetic use, with Lilley et al suggesting that in 1978 approximately 70 million injections were given in the United Kingdom. Yagiela has also reported that mortality over a 30-year period ranged from 1 death in 1.4 million to 1 death in 45 million administrations. However, circulatory diseases have been described as the epidemic of our time and are more prevalent with age, and the elderly are a group who will in the future require increasing dental care. It is this context that gives relevance to an information gap regarding the safety of local analgesia.

This study dealt with patients of marked medical compromise. Most were on waiting lists for cardiac surgery and underwent challenging surgical dentistry with substantial quantities of local anesthetic. The resultant hemodynamic and electrocardiographic changes were not clinically significant. Conscious sedation with intravenous midazolam attenuated the sympathoadrenal response, and greater changes were always seen during the phase of surgery. Professional attention should therefore be directed to the management of the whole patient episode, not just perceived problems with the administration of anesthesia.


It is recommended that clinical practice for local anesthesia in patients with cardiovascular disease should fol low established protocols for risk minimization with (a) sensible prescribing for dental treatment, eg, prophylactic and restorative solutions in preference to surgical intervention; (b) behavioral modification; (c) the use of reasonable quantities of a local anesthetic, such as lidocaine 2% with adrenaline at its minimally effective concentration; (d) aspiration on injection; and (e) appropriate monitoring. Finally, the protocol should include the prescription of a sedative agent, such as midazolam, for its attenuation of the sympathoadrenal response.

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