Snipping the nerve may stop 'flight-or-fight' stress response

What do sweaty palms and abnormal heart rhythms have in common? Both can be initiated by the nervous system during an adrenaline-driven "flight-or-fight" stress reaction, when the body senses danger.

Hyperhidrosis, an abnormal flight-or-fight response of the sympathetic nervous system that causes excessively sweaty palms may also contribute to problems like dangerous irregular rhythms from the lower chambers of the heart, known as ventricular arrhythmias.

UCLA cardiologists have now found that surgery to snip nerves associated with the sympathetic nervous system on both the left and right sides of the chest may be helpful in stopping dangerous, incessant ventricular arrhythmias — known as an "electrical storm" — when other treatment methods have failed. This same type of surgery has been used for years to alleviate hyperhidrosis.

The UCLA team's findings are reported in the Dec. 27–Jan. 3 issue of the Journal of the American College of Cardiology. The study is one of the first to assess the impact of bilateral cardiac sympathetic denervation (BCSD), surgery on both sides of the heart, to control arrhythmias. The research builds on previous work at UCLA in which a similar procedure was performed only on the left side. But for some patients to obtain relief, the researchers said, it must be done bilaterally. 

http://newsroom.ucla.edu/releases/snipping-key-nerves-may-help-life-220281 

Sympathectomy - a neurocardiologic disorder

Bilateral thoracic sympathectomies or sympathotomies are done for refractory palmar hyperhidrosis [85–87]. Iontophoresis, botulinum toxin injection, and glycopyrrolate cream are alternatives. Because sweating is mediated mainly by sympathetic cholinergic fibers, autonomic neurosurgery is usually effective; however, a variety of expected and unexpected consequences can result, including ectopic (e.g., plantar) hyperhidrosis, gustatory sweating, Horner syndrome, and decreased heart rate responses to exercise. The latter seems to be related to partial cardiac denervation [88]. Anecdotally, fatigue, altered mood, blunted emotion, and decreased ability to concentrate can develop after bilateral thoracic sympathectomies. 

β-Adrenoceptor blockers are a mainstay of treatment for CPVT. An automated defibrillator may have to be implanted. Treatment for CPVT also includes left sympathectomy. Such treatment leaves open the theoretical possibilities of denervation supersensitivity of cardiac adrenoceptors and compensatory activation of the adrenomedullary hormonal system; however, plasma levels of catecholamines have not been assessed in CPVT with or without therapeutic cardiac denervation.

Table 1. Neurocardiologic disorders that feature abnormal catecholaminergic function

Disorders where abnormal catecholaminergic function is etiologic Hypofunctional states without central neurodegeneration
Acute, primary
Neurocardiogenic syncope Spinal cord transection Acute pandysautonomia Sympathectomy
Acute, secondary
Drug-related (e.g., alcohol, tricyclic antidepressant, chemotherapy, opiate, barbiturates, benzodiazepines, sympatholytics, general anesthesia)
Seizures
Guillain–Barre syndrome Alcohol

Chronic, primary

Pure autonomic failure
Horner's syndrome
Familial dysautonomia
Carotid sinus syncope

Adie's syndrome Dopamine-β-hydroxylase deficiency
Sympathectomy 

http://onlinelibrary.wiley.com/doi/10.1111/j.1755-5922.2010.00244.x/full

https://archive.is/UMW1w

Patients may develop bradycardia after surgical procedure to treat sweaty hands and blushing

Upper-Thoracic Sympathectomy; Patients may develop bradycardia after surgical procedure

Heart Disease Weekly. Atlanta: Feb 23, 2003. pg. 71

direct injury to the anatomic structure of the autonomic nervous system in the thoracic cavity, and postthoracotomy pain may contribute independently or in association with each other to the development of these arrhythmias

Anesthesiol Res Pract. 2013;2013:413985. doi: 10.1155/2013/413985. Epub 2013 Oct 23.

Supraventricular arrhythmias after thoracotomy: is there a role for autonomic imbalance?

Vretzakis G1, Simeoforidou M, Stamoulis K, Bareka M.

Author information

Abstract

Supraventricular arrhythmias are common rhythm disturbances following pulmonary surgery. The overall incidence varies between 3.2% and 30% in the literature, while atrial fibrillation is the most common form. These arrhythmias usually have an uneventful clinical course and revert to normal sinus rhythm, usually before patent's discharge from hospital. Their importance lies in the immediate hemodynamic consequences, the potential for systemic embolization and the consequent long-term need for prophylactic drug administration, and the increased cost of hospitalization. Their incidence is probably related to the magnitude of the performed operative procedure, occurring more frequently after pneumonectomy than after lobectomy. Investigators believe that surgical factors (irritation of the atria per se or on the ground of chronic inflammation of aged atria), direct injury to the anatomic structure of the autonomic nervous system in the thoracic cavity, and postthoracotomy pain may contribute independently or in association with each other to the development of these arrhythmias. This review discusses currently available information about the potential mechanisms and risk factors for these rhythm disturbances. The discussion is in particular focused on the role of postoperative pain and its relation to the autonomic imbalance, in an attempt to avoid or minimize discomfort with proper analgesia utilisation.

http://www.ncbi.nlm.nih.gov/pubmed/24235971

Infra-stellate upper thoracic sympathectomy results in a relative bradycardia during exercise, irrespective of the operated side

European Journal of Cardio-Thoracic Surgery > 2001 > 20 > 6 > 1095-1100

chronic interference with β-adrenergic receptors (via either sympathectomy or β-blockade) on cardiac mast cell morphology/activation and on interstitial collagen deposition

In the present study we investigated the effects of chronic interference with β-adrenergic receptors (via either sympathectomy or β-blockade) on cardiac mast cell morphology/activation and on interstitial collagen deposition. In rats subjected to chemical sympathectomizy with the neuro- toxin 6-hydroxydopamine (6-OHDA) we observed a significant increase of mast cell density, and in particular of degranulat- ing mast cells, suggesting a close relationship between the cardiac catecholaminergicsystem and mast cell activation. In parallel, chronic 6-OHDA treatment was associated with increased collagen deposition. The influence of the β-adren- ergic receptor component was investigated in rats subjected to chronic propranolol administration, that caused a further significant increase in mast cell activation associated with a lower extent of collagen deposition when compared to chem- ical sympathectomy. These data are the first demonstration of a close relationship between rat cardiac mast cell activation and the catecholaminergic system, with a complex interplay with cardiac collagen deposition. Specifically, abrogation of the cardiac sympathetic efferent drive by chemical sympathectomy causes mast cell activation and interstitial fibrosis, possibly due to the local effects of the neurotoxin 6-hydroxy- dopamine. In contrast, β-adrenergic blockade is associated with enhanced mast cell degranulation and a lower extent of collagen deposition in the normal myocardium. In conclusion, cardiac mast cell activation is influenced by β-adrenergic influences. 

http://www.ejh.it/index.php/ejh/article/viewFile/985/1108

Correspondence: Rosanna Nano,

Department of Animal Biology, University of Pavia,

European Journal of Histochemistry

2006; vol. 50 issue 2 (Apr-Jun):133-140

Chronic bradycardia can cause fatigue, shortness of breath on exertion and dizziness

Bradycardia is defined as a heart rate below 60 beats per minute. However, slow heart rates are often found in normal people, especially at rest or if very fit. Sinus bradycardia, junctional escape rhythm and Wenckebach block can also be seen in normal people and are usually asymptomatic.

Patients with asymptomatic bradycardia usually need no treatment.

Intermittent severe bradycardia can cause syncope. Chronic bradycardia can cause fatigue, shortness of breath on exertion and dizziness. Severe bradycardia can cause haemodynamic consequences of hypotension, altered conscious state, poor perfusion, ischaemic chest pain and cardiac failure. However, in the presence of bradycardia and haemodynamic compromise it is important to look for other factors such as myocardial infarction or poor ventricular function.

Patients with syncope, other symptoms or haemodynamic compromise due to bradycardia should be referred urgently for consideration of pacemaker implantation.

Transcutaneous pacing may be required in the emergency setting for acute severe bradycardia causing severe haemodynamic compromise. Temporary transvenous pacing may be required in patients with acute, symptomatic bradycardia. Patients with chronic symptomatic bradycardia and some patients with asymptomatic but significant bradyarrhythmias require permanent pacemaker implantation.

Revised February 2012. ©Therapeutic Guidelines Ltd (etg43demo November 2014) 

http://www.tg.org.au/etg_demo/desktop/tgc/cvg6/2878.htm 

regional myocardial denervation creates autonomic and electrophysiological heterogeneity and the substrate for heterogeneous drug actions

These data show that regional myocardial denervation creates autonomic and electrophysiological heterogeneity and the substrate for heterogeneous drug actions. This drug-induced electrophysiological heterogeneity may be another mechanism for proarrhythmia. 

Circulation. 1991 Oct;;84(4):1709-14.
Modulation of drug effects by regional sympathetic denervation and supersensitivity.
Stanton MS, Zipes DP.
Krannert Institute of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis 46202. 

chronic interference with β-adrenergic receptors (via either sympathectomy or β-blockade) on cardiac mast cell morphology/activation and on interstitial collagen deposition

In the present study we investigated the effects of chronic interference with β-adrenergic receptors (via either sympathectomy or β-blockade) on cardiac mast cell morphology/activation and on interstitial collagen deposition. In rats subjected to chemical sympathectomizy with the neuro- toxin 6-hydroxydopamine (6-OHDA) we observed a significant increase of mast cell density, and in particular of degranulat- ing mast cells, suggesting a close relationship between the cardiac catecholaminergic system and mast cell activation. In parallel, chronic 6-OHDA treatment was associated with increased collagen deposition. The influence of the β-adren- ergic receptor component was investigated in rats subjected to chronic propranolol administration, that caused a further significant increase in mast cell activation associated with a lower extent of collagen deposition when compared to chem- ical sympathectomy. These data are the first demonstration of a close relationship between rat cardiac mast cell activation and the catecholaminergic system, with a complex interplay with cardiac collagen deposition. Specifically, abrogation of the cardiac sympathetic efferent drive by chemical sympathectomy causes mast cell activation and interstitial fibrosis, possibly due to the local effects of the neurotoxin 6-hydroxy- dopamine. In contrast, β-adrenergic blockade is associated with enhanced mast cell degranulation and a lower extent of collagen deposition in the normal myocardium. In conclusion, cardiac mast cell activation is influenced by β-adrenergic influences. 

http://www.ejh.it/index.php/ejh/article/viewFile/985/1108

Correspondence: Rosanna Nano,
Department of Animal Biology, University of Pavia,

European Journal of Histochemistry

2006; vol. 50 issue 2 (Apr-Jun):133-140