Stress-induced hypothalamic activation increases epinephrine secretion from the adrenal medulla immediately after tissue injury.1-3 Maximum levels are reached in 24 to 48 hours. Direct cardio-pulmonary stimulation increases pulse rate, blood pressure, myocardial contractility, cardiac output, oxygen consumption and the rate of respiration. The hemodynamic and metabolic effects of epinephrine are detected at specific threshold concentrations (Table 2).5-7
|Epinephrine in pg/ml||Effect|
|10 to 70||Basal or resting state|
|50 to 100||Increased heart rate|
|75 to 125||Increased systolic blood pressure|
|150 to 200||Decreased diastolic blood pressure
Increased glycogenolysis and gluconeogenesis
|>400||Decreased insulin secretion|
Epinephrine also promotes renin synthesis. This enzyme is responsible for the conversion of angiotensin I to angiotensin II, which catalyzes aldosterone synthesis in the adrenal cortex. Increased aldosterone concentration leads to sodium and water retention and contributes to volume expansion. Peripheral and splanchnic vasoconstriction and coronary and cerebral vasodilation lead to altered blood volume distribution.
Cardiac risk is predicated primarily on the severity of autonomic response to surgical stress. Surgical procedures can be divided into high-, intermediate-, and low-stress groups and dental procedures have been identified as being low-stress procedures.8 Retrospective and prospective surveys have confirmed that the incidence of dental procedure-induced major adverse cardiac events is low.9,10 A discussion of cardiac risk with dental procedures is presented elsewhere.11-13
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