decreased conditioning-related activity in insula and amygdala in patients with autonomic denervation

The degree to which perceptual awareness of threat stimuli and bodily states of arousal modulates neural activity associated with fear conditioning is unknown. We used functional magnetic neuroimaging (fMRI) to study healthy subjects and patients with peripheral autonomic denervation to examine how the expression of conditioning-related activity is modulated by stimulus awareness and autonomic arousal. In controls, enhanced amygdala activity was evident during conditioning to both "seen" (unmasked) and "unseen" (backward masked) stimuli, whereas insula activity was modulated by perceptual awareness of a threat stimulus. Absent peripheral autonomic arousal, in patients with autonomic denervation, was associated with decreased conditioning-related activity in insula and amygdala. The findings indicate that the expression of conditioning-related neural activity is modulated by both awareness and representations of bodily states of autonomic arousal.

http://www.ncbi.nlm.nih.gov/pubmed/11856537

Effect of sympathectomy on mechanical properties of common carotid and femoral arteries

Compared with the intact animals, sympathectomized rats showed a marked increase in arterial distensibility over the entire systolic-diastolic pressure range. When quantified by the area under the distensibility-pressure curve, the increase was 59% and 62% for the common carotid and femoral arteries, respectively (P<.01 for both). In the femoral but not in the common carotid artery, sympathectomy was accompanied also by an increase in arterial diameter (+18%, P<.05 versus intact). Therefore, in the anesthetized normotensive rat, sympathetic activity exerts a tonic restraint on large-artery distensibility. This restraint is pronounced in elastic vessels and even more pronounced in muscle-type vessels.

http://www.ncbi.nlm.nih.gov/pubmed/9369260

endoscopic sympathicotomy in carotid and vertebral arteries in the surgical treatment of primary hyperhidrosis

Analyze, in patients with primary hyperhidrosis (PH) who was undergone to videothoracoscopic sympathicotomy, the degree of vascular denervation after surgical transection of the thoracic sympathetic chain by measuring ultrasonografic parameters in carotid and vertebral arteries.

METHODS:

Twenty-four patients with PH underwent forty-eight endoscopic thoracic sympathicotomy and were evaluated by duplex eco-Doppler measuring systolic peak velocity (SPV), diastolic peak velocity (DPV), pulsatility index (PI) and resistivity index (RI) in bilateral common, internal and external carotids, besides bilateral vertebral arteries. The exams were performed before operations and a month later. Wilcoxon test was used to analyse the differences between the variables before and after the sympatholisis.

RESULTS:

T3 sympathicotomy segment was the most frequent transection done (95.83%), as only ablation (25%) or in association with T4 (62.50%) or with T2 (8.33%). It was observed increase in RI and PI of the common carotid artery (p < 0.05). The DPV of internal carotid artery decreased in both sides (p < 0.05). The SPV and the DPV of the right and left vertebral arteries also increased (p < 0.05). Asymmetric findings were observed so that, arteries of the right side were the most frequently affected.

CONCLUSIONS:

Hemodynamic changes in vertebral and carotid arteries were observed after sympathicotomy for PH. SPV was the most often altered parameter, mostly in the right side arteries, meaning significant asymmetric changes in carotid and vertebral vessels. Therefore, the research findings deserve further investigations to observe if they have clinical inferences.

http://www.ncbi.nlm.nih.gov/pubmed/16186983

Cardiac Autonomic Function in Patients Suffering from Primary Focal Hyperhidrosis

At the high-frequency band (0.15-0.5 Hz), which represents parasympathetic cardiac innervation, an interaction of type and position influencing spectral power was detected. Our highly interesting findings indicate that primary focal hyperhidrosis is based on a much more complex autonomic dysfunction than generalised sympathetic overactivity and seems to involve the parasympathetic nervous system as well.
Eur Neurol 2000;44:112-116 (DOI: 10.1159/000008207)

the sympathetic block, regularly extends six or more spinal segments above the level of sensory block

Chamberlain et al, using a very sensible technique with thermographic imaging, showed that the sympathetic block, at least partial, regularly extends six or more spinal segments above the level of sensory block [8].

Therefore, it seems that a partial sympathetic blockage exists on substantial area over and under of the level of somatic block. In fact, preganglionic sympathetic fibers, once they quit the dura, enter the paravertebral sympathetic chain. From there, these fibers can ascend or descend, synapsing with up to 18 postganglionic fibers, which may project to dermatomes well above and below the spinal segment from which they originated [9].

Bradycardia associated with spinal block is usually light, and contributes modestly to the drop of blood pressure. Rarely, bradycardia is associated with cardiac collapse. Traditional explanation of this bradycardia originating from a spinal anesthesia is the blockage of cardiac accelerator sympathetic nerves (T1-4). Many studies showed than the incidence and the severity of bradycardia is not related to the height of the sensory block.

Onset time of the bradycardia has poor relation with the timing of the spinal block [10]. Carpenter, in a prospective study on 1000 patients under spinal block., showed that bradycardia occured in 13% (heart rate < 50/min) with an onset time of 47 min (range from1 to 204).

There is a pulse rate paradoxical response to movement of the operation table. Under a spinal or epidural anesthesia, when one lift patient head, blood pressure decreases caused by pooling of the venous blood. But in place of a reflex tachycardia mediated by baroreceptors, there is a paradoxical bradycardia. Interestingly, in situation associated with severe reduction of venous return, paradoxical bradycardia can be seen even in the absence of sympathetic block.

There is similarities between hypotension related to bradycardia of the spinal anesthesia and vasovagal reaction. Vasovagal shock is characterized by hypotension and bradycardia, and can progress to syncope. It has a central or a peripheral etiology.

Because of their rare occurrence, almost all studies on cardiac arrest during spinal anesthesia are retrospective, therefore limited in their ability to identify variables and incidents of such events.

Caplan [14] in 1988 has identified 14 cases of sudden cardiac arrest on patients in good health and undergoing minor surgical procedures. None of these patients had unusually high block, nor received badly inadequate resuscitative care. Despite all this, only 8 of 14 patients survived, and only one survivors had acceptable neurological functions Retrospectively, respiratory insufficiency was suspected, secondary to a strong sedation, as the main etiology of the cardiac arrest. Even a complete sympathectomy leaves a good arterial vascular tone, but in presence of hypoxia and acidosis can lead to a fall in arterial tone, to an exaggerated decrease in blood pressure and cardiac collapse. Early sympathetic responses to hypoxia, which are tachycardia and vasoconstriction, are almost severely blunt by spinal anesthesia [15].

Mackey reported 3 cases of severe bradycardia during spinal anesthesia in the absence of hypoxia and strong sedation [16]. He concludes that severe bradycardya was caused by a drop in venous return triggering Bezold-Jarisch reflex which in presence of sympathetic block led to exaggerated bradycardia, hypotension and arrest.

http://www.esra-learning.com/site/generalites/pathology/b_haemodynamic.htm

Depressed heart rate variability has independent prognostic value in patients with chronic heart failure; spectral analysis identifies an increased risk for sudden death in these patients

http://www.ncbi.nlm.nih.gov/pubmed/10681488

In a person who had a sympathectomy, the sympathetic component of the baroreceptor mechanism is absent

The baroreceptor reflex is only a short-term regulator of blood pressure because the receptors adapt by raising the threshold and lowering discharge rate.
8. Describe the reflex compensations when someone suddenly stands up from a supine position. What would happen in a patient who just had a sympathectomy?

Sudden standing causes pooling of blood in the leg veins. This results in decreased venous return to the heart, which leads to decreased cardiac output (Frank-Starling mechanism), which leads to decreased MAP. This decrease in MAP is detected by the carotid sinus baroreceptors, which relay a message to the medullary cardiovascular control center, which increases sympathetic outflow and decreases parasympathetic outflow, this causes:

* An increase in HR and myocardial contractility, tending to restore cardiac output.
* Vasoconstriction in skeletal musculature, skin, kidneys and gut, reducing blood flow to these organs and increasing TPR.
* Venoconstriction decreasing capacitance and increasing venous return

A patient with a sympathectomy would experience what's referred to as orthostatic hypotension (which might lead to syncope). Orthostatic hypotension is a decrease in arterial pressure when going from supine to a standing position. A person with a normal baroreceptor mechanism will try to restore MAP. In a person who had a sympathectomy, the sympathetic component of the baroreceptor mechanism is absent.

Heart Physiology II

M.A.S.T.E.R. Learning Program, UC Davis School of Medicine
Date Revised: Jan 16, 2002
Revised by: Gordon Li and Carolyn Nguyen

blunted hypoxic pulmonary vasoconstriction due to partial interruption of the sympathetic nerve supply to the lung by bilateral thoracic sympathectomy

Anaesth Intensive Care. 2003 Oct;31(5):581-3.

Orthodeoxia--an uncommon presentation following bilateral thoracic sympathectomy.

van Heerden PV, Cameron PD, Karanovic A, Goodman MA.

Source

Departments of Intensive Care and Vascular Surgery, Sir Charles Gairdner Hospital, Pharmacology Unit, School of Medicine and Pharmacology, University of Western Australia, Perth, Western Australia.

Abstract

We present a case of orthodeoxia (postural hypoxaemia) which resulted from a combination of lung collapse/consolidation and blunted hypoxic pulmonary vasoconstriction due to partial interruption of the sympathetic nerve supply to the lung by bilateral thoracic sympathectomy.

http://www.ncbi.nlm.nih.gov/pubmed/14601286

Bezold-Jarisch Reflex and Sympathectomy

Much attention has been focused on the Bezold-Jarisch Reflex as the cause of sudden acute bradycardia during spinal or epidural anesthesia. The basis of this reflex is a decrease in stretch tension on mechanoreceptors located in the left ventricle. A sudden empty left ventricle triggers this paradoxical reflex which resulst in increased parasympathetic activity. Sympathetic output is also inhabited. Anything that decreases left ventricular end-diastolic volume suddenly, such as spinal anesthesia may rigger his reflex.

   By contrast, bradycardia that is slow on onset, developing after administration of spinal anesthesia, has been recognized and attributed to decreased activity of the cardioaccelerator nerves to the heart. This is a different phenomenon than the sudden bradycardia or asystole in the patient presented above. Complete sympathectomy of the heart itself reduces heart rate by about 20%.

Complications of regional anesthesia

Brendan T. Finucane

Springer, 2007 - 506 pages

An unopposed vagal tone secondary to sympathectomy

1.) An unopposed vagal tone secondary to sympathectomy. This sympathectomy occurs 2-6 dermatomes higher than sensory block, so that a sensory block of T6 can conceivably inhibit all of the sympathetic innervation to the heart.

2.) The Bezold-Jarisch reflex – which may be widely under appreciated phenomenon. You’ll be surprised how many clinicians are not well versed in this essential physiology.

Sympathectomy → reductions in venous tone → profound decreased venous return. This activates mechanoreceptors embedded within the walls of the myocardium → stimulating vagal afferents → vasomotor center of medulla → increased vagal tone to the heart, thus slowing or stopping the heart entirely to allow enough filling time to generate an effective stroke volume. 
http://allnurses.com/certified-registered-nurse/sympathectomies-and-atropine-124910.html

A depression in the heart rate and decrease in response to stress is expected to some degree in all patients after sympathectomy

A depression in the heart rate with resultant drop in the heart rate product and decrease in response to stress is expected to some degree in all patients. Some series have described this finding in most patients, whereas others report at least a 10% drop in heart rate in all patients. This is a possible major cause for postoperative dysfunction and should be cautiously sought after. Patients with resting heart rate that is below 50 to 60 beats/min should undergo electrocardiography. It is recommended that if the heart rate is low on a subsequent electrocardiogram as well, that a tilt test should be performed to exclude patients in whom there is an inordinately high risk of postoperative bradycardia.

In conclusion, thoracoscopic sympathectomy can be done as an outpatient procedure safely and efficiently. Debate continues about the correct transection levels, but at this time there is a consensus that division or clipping is equal to resection. Although the procedure has several severe side effects, they are rare. The predominant complication remains compensatory sweating, which may occur regardless of the level transected or the indication. Future clinical trials should compare some of the different techniques to achieve a global consensus of the surgical approach.

http://ats.ctsnetjournals.org/cgi/content/full/85/2/S764