Individual cardiovascular response to different levels of sympathetic blockade varies widely, depending on the degree of sympathetic tone before the block

The cardiovascular responses to epidural anaesthesia are almost entirely due to the fact that the local anaesthetic injected into the epidural space not only blocks somatic, sensory and motor fibres, but also produces preganglionic sympathetic denervation.

Postganglionic sympathetic nerves play an important role in controlling cardiac function and vascular tone. The most important of the cardiovascular effects are related to blockade of vasoconstrictor fibres (below T4) with resulting dilatation of resistance and capacitance vessels and/or cardiac sympathetic fibres with loss of chronotropic and inotropic drive to the myocardium (T1-5) (Figure 1).

The cardiac sympathetic outflow emerges from C5 to T5 levels, with the main supply to the ventricles from T1 to T43. A significant part of the chronotropic and inotropic control of the heart is mediated through the upper four thoracic spinal segments.
Denervation of preganglionic cardiac accelerator fibres leaving the cord at T1-T5 results in minimal vasodilatory consequences. Changes however in heart rate, left ventricular function and myocardial oxygen demand may occur due to high thoracic epidural blockade and are discussed below.

The major determinant of heart rate is the balance between sympathetic and parasympathetic systems with the latter predominating. A high thoracic epidural anaesthesia (TEA) covering the cardiac segments (T1-T4) produces small but significant reductions in heart rate4-8. During cardiac sympathetic denervation, parasympathetic cardiovascular responses, including those involved in baroreflexes, may dominate.


It was suggested that the sympathetic control of heart rate modified the dominating parasympathetic tone, rather than functioning as an active cardiac accelerator. In this study there was no compensation for changes in preload;
therefore cardiopulmonary baroreceptors affected by changes in central volume secondary to peripheral vasodilatation or vasoconstriction might have altered arterial baroreceptor heart rate reflex as well.



High TEA added to general anaesthesia significantly decreased the cardiac acceleration in response to decreasing blood pressure, suggesting that baroreflex-mediated heart rate response to a decrease in arterial blood pressure depends on the integrity of the sympathetic nervous system. However general anaesthesia, in addition to high levels of epidural anaesthesia, may have modified the balance between sympathetic and parasympathetic tone as well.
By applying power spectral analysis, i.e., frequency analysis of electrocardiographic R-R interval, the individual components of the autonomic nervous system can be discerned and can be used as a sensitive indicator of sympathovagal interaction.


Individual cardiovascular response to different levels of sympathetic blockade varies widely, depending on the degree of sympathetic tone before the block.
Anaesth Intensive Care 2000; 28: 620-635
B. T. VEERING*, M. J. COUSINS†
Department of Anesthesiology, Leiden University Medical Center, Leiden, The Netherlands and Department of Anaesthesia and
Pain Management, University of Sydney, Royal North Shore Hospital, Sydney, New South Wales

diabetic autonomic neuropathy has already sympathectomized the patient

Although not specific, the symptoms suffered by diabetics from sweating disturbances are fairly typical [5]. Initially there is heat intolerance accompanied by hyperhidrosis of the upper half of the body, particularly affecting the face, neck, axillae and hands. It is of interest that these patients rarely perspire excessively below the umbilicus. This diabetic syndrome has been attributed to a lesion of the sympathetic nerve fibres which control sweat secretion [11] and follow the course of the peripheral nerves [12]. This affects the efferent branch of the reflex arch and is identical to that occurring distal to a surgical sympathectomy [13].

There was no difference found between the histological changes in the nerves of the spontaneous anhidrotic patients
(Fig. 1) and those of the two previously sympathectomized patients.

A number of papers have been published which stressed [22-24] the high failure rate of sympathectomy operations in diabetics. We believe that the failure of the operation is due to the fact that diabetic autonomic neuropathy has already sympathectomized the patient. The results of the present study are compatible with this idea.
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