Thoracic Epidural Anesthesia in Patients with Unstable Angina Pectoris

  • S. Blomberg
Part of the Anaesthesiologie und Intensivmedizin / Anaesthesiology and Intensive Care Medicine book series (A+I, volume 222)


During acute myocardial ischemia, the sympathetic nervous system is activated rapidly [17, 22]. In addition to chemical factors produced by the ischemic myocardium (e.g. bradykinin, prostaglandins, potassium, and lactic acid) separately [21, 25] or in concert [25], stretching of the ventricular wall during ischemia is also capable of stimulating sensory receptors in the ventricular wall [18]. It is generally agreed that the cardiac symphathetic afferent nerve fibers are the essential pathways for the conduction of anginal pain [26]. The afferent pathways pass through the cervical and the upper thoracic ganglia, project to the five most cranial sympathetic segments [15, 26] of the spinal cord (T 1–T5), and eventually join with the neurons of the spinothalamic tract. The stimulus for activation of the sympathetic efferents, however, is not fully understood. Continuous hemodynamic monitoring in patients with unstable angina [5, 9] has demonstrated that, coincident to the onset of anginal pain (and even in the absence of pain), there is an “overshoot” increase in heart rate and in both systolic and diastolic arterial pressures (a “pressor response”), which most likely reflects a spinal cardiocardiac reflex mediated via sympathetic afferents and efferents activated by myocardial ischemia itself [4, 19]. Input from higher nervous centers such as during mental stress [16] or unloading of baroreceptors consequent to an initial reduction in arterial blood pressure, however, may also contribute. Since it has been speculated that sympathetic nerve activity may cause transient stenotic vasoconstriction [23] and thrombus formation [12, 20], it might be that myocardial ischemia itself will trigger a reflex mechanism, which further aggravates the ischemic process by increasing myocardial oxygen demand, coronary vasoconstriction, and platelet aggregation.


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© Springer-Verlag Berlin Heidelberg 1992

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  • S. Blomberg

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