Every procedure elicits a physiological stress-response. This response is initiated by tissue injury and mediated primarily by the sympathoadrenal system. Sympathoadrenal activity can induce tachycardia and hypertension and increase myocardial oxygen demand. The magnitude of procedure-related stress is predicated on the extent of procedure-related tissue trauma, duration of the procedure, volume of blood loss, fluid shifts, and changes in core body temperature.1
The rates of catecholamine release are the primary determinants of the biologic expression of sympathoadrenal activity. The basal range steady-state plasma concentration for epinephrine is 10-70 pg/ml.2 Specific effects, e.g., changes in heart rate and blood pressure, are produced at particular threshold plasma concentrations. In two studies in dental settings, the resting supine steady-state plasma concentration of epinephrine was reported to be 27±4 and 28±8 pg/ml, respectively.3,4
The first study evaluated the sympathoadrenal and hemodynamic effect of local dental anesthesia (administered as a mandibular nerve block).3 The administration of 1.8 cc of lidocaine 2% without epinephrine did not significantly alter the resting supine steady-state plasma epinephrine concentrations of 27±4 pg/ml over the 60 minute study period. Similarly, heart rate (HR) and mean arterial pressure (MAP = systolic blood pressure + 2(diastolic blood pressure)/3) were also unaltered following injection.
The administration of 1.8 cc of lidocaine 2% with epinephrine 1:100,000 (administered as a mandibular nerve block) resulted in a transient elevation of epinephrine from the resting supine steady-state plasma of 27±4 pg/ml to a maximum of 94 pg/ml at 8 minutes after injection.3 MAP was unaffected. Threshold concentrations required to affect diastolic blood pressure (BP) range from 150-200 pg/ml.2 HR increased by only a few beats per minute for the initial 2 minutes after injection. Threshold concentrations required to affect heat rate range from 50-100 pg/ml.2
The second study evaluated the sympathoadrenal and hemodynamic effect of routine restorative dental care (two or three surface amalgams) under local dental anesthesia.4 Following the administration of 1.8 cc of lidocaine 2% with epinephrine 1:100,000 (administered as a mandibular nerve block) plasma epinephrine levels increased from the resting supine steady-state plasma epinephrine concentrations of 28±8 pg/ml to 105±28 pg/ml and 73±14 pg/ml at 5 and 10 minutes after injection, respectively.
After rubber dam application (13 to 18 minutes after injection) the plasma epinephrine level had further decreased to 51±7 pg/ml and within minutes returned to resting supine steady-state levels. One procedure was done on each patient and the total chair-time per procedure was 60±4 minutes. Corresponding to increased plasma epinephrine concentrations at 5 and 10 minutes after injection, HR increased by only a few beats per minute (threshold concentrations required to affect heat rate range from 50-100 pg/ml. No significant alterations were noted in MAP.
Surgical stress can also cause alterations in the balance between prothrombotic and fibrinolytic factors, resulting in hypercoagulability and possible coronary thrombosis (elevation of fibrinogen and other coagulation factors, increased platelet activation and aggregation, and reduced fibrinolysis).1 The extent of such changes is proportional to the degree and duration of surgical stress. These factors can contribute to myocardial ischemia and heart failure.
Perioperative cardiac risk, defined as myocardial infarction and cardiac death within 30 days of noncardiac procedures, has been assessed.5 It was concluded that non-cardiac procedures can be divided into high-, intermediate-, and low-stress groups with estimated rates of cardiac events of >5%, 1-5%, and < 1%, respectively (Box 1). With low-stress non-cardiac procedures the risk of a cardiac event is negligible unless strong patient-specific risk factors are present.5
|High-stress procedures||Intermediate-stress procedures||Low-stress procedures|
There are no adequately controlled or randomized clinical trials that help define perioperative cardiac risk for various dental procedures. However, according to a retrospective analysis of EMS data in Seattle and King Counties, WA, with a combined population 1.5 million, over a seven-year period six major cardiac events were documented in community based dental practices for an annual incidence of < 0.002 per dental practice.6
Two independent prospective surveys over a 10-year period, involving 4,309 dentists, documented a total of 30,602 medical emergencies.7 Based on these data, the number of medical emergencies per dental practice per year was 0.5. Cardiovascular emergencies included postural hypotension (17.8%), angina pectoris (4.6%), myocardial infarction (1.4%), and cardiac arrest (1.1%) at an annual rate of 0.08, 0.02, 0.007, and 0.005 per dental practice per year, respectively.
It can be concluded that the risk of perioperative cardiac events in association with dental procedures is low-to-very low. In a low-risk situation the likelihood of a major cardiac event (MACE) of death or myocardial infarction (MI) is < 1%.8 Elevated-risk defines a situation in which the risk of MACE is ≥1%.8 Consequently, dental procedure-specific variable are less important than patient-specific variables in predicting a MACE in oral healthcare settings.