Question: I have persistent sinus tach(112-128bpm resting/sleep without decrease), with no orthostatic changes, CP, angina, can do rapid rising and exertions with expected HR increase(no BP drops) and have no lipid/cardiac hx(54yo MD) or early Fam Hx; was athletic in heavy exertion/endurance sports and labor(Expedition Medicine) with P-60's, BP 100-10/60s, Tot. Chol <170 all life) until neck injury C5/6 and C6/7 disc extrusions with C5/6 anter. cord indentation(10-15 % at MRI/CT MYelogram at rest/neutral posture) and radicular encroachment. All thyroid.adrenal levles WNL;EKG,Echo,Holter WNl with just "IST", all chems WNL and tachy parallels post neck activity and irritation which also parallels atenolol requirement to control rate. Severe neck s/s induces BP surges to 130-140s/90s(high for my norm 100-110/60s) but IST occurs when BP nomrmal, too. I believe the C5/6 and C6/7 disc environment peri-cord vaso congestion/neural root edema/inflamation spread is source irritant to cardiac accelerator pathways from middle and inferior cervical ganglion input connections, but local cardiologists and neurologists seem disinterested or unknowledgeable. Only ANS symptoms are apparent gastric and increased peristalsis without emptying pc.(as if pyloric tone increased). No lower tract spinal symptoms, but significan C6 classic paresthesaias bilateral with use/posture and muscle pattern twitches, fasciculations and occasional postural spasms. I need advocacy and references for this presumption for stubborn Work Comp system. I was previously healthy and expedition conditioned for >ten yrs, no illnesses until the neck injury plus torn labrum/cuffs both shoulders and right knee form labor accident. The cervical stimulation of the IST and BP surges seems the first remaining choice, and life on beta blockers not desired, nor is ablation. Disc surgery review presently pending by insurer.

IST is Inappropriate Sinus Tachycardia. If hormones/endocrineWNL, no toxins, heart shows no damage, then the source of continuous cardiac acceleration comes from degrading Sinus atrial node or its neurologic input from the middle and inferior cardiac nerves(right >Left input) originating from the Inferior(stellate) and middle cervical Sympathetic ganglis, lying near C6 and C8/T1. Not only can the cardiac accelerator nerves be effected by peri cervical damage through reacive nerve edema to cervical branches, tissue engorgement from herniation pressured peri spinal cord fat pad and venous plexus(C6 indentation 10-15% with C6 and C7 R>L foramenal encroachment), but the mere feed back through these leveles from both the cervical injuries and bilateral shoulder labral tears/rotator cuff and articular cartilage tears and left para labral cyst can induce sympathetic reactions with feed crossover to the cardiac accelerators. Especiall since the left labral tear was inferior with para labral cyst encroaching on axillary nerve, causing quadralateral space syndrome in the shoulder, and temporary thoracic outlet mass effect paralysis of the left hand intrinsics/sensory(Ulnar trunk pattern) until CT needle aspiration resolved the TOS component. The reactivity is exactly same mechanism as other organ-SANS feed back reflexive tissue changes, as in gastroparesis with angina/ vomiting, etc, only this is neck or shoulder feedback, or direct tissue environment spread effecting the cardiac accelerator pathways enough to irritate them, not block them, causing upper body/ neck activity dependent tachycardia and BP surges. Such pathway function/feedback has long been known with stellate ganglion and segmental cervical blocks to isolate the pathway and control the tachycardia while finding origin. Perhaps I must relay on an anesthesiologist to do this, or simply have the neck surgery and left shoulder surgery completed with paralabraql cyst dissection from the nerve encraoched/tethered environ, and just see if the tachycardia/ BP surges with activity resolves. Simply condemning to beta blocker use or cardiac ablation is not conducive to addressing the cause, and will destroy 20yrs+ anticipated lifestyle for no good medical reason. This didn't happen due to some predisposition, family history. Ockham's Razor-- the simplest and most obvious, by history and change in history, is the injury. Sources to show the insurer would help though.

Sorry, but all chiropractic and osteopathic literature seems to specifically address vertebral nerve and vertebral artery irritation and encroachment by disc protrusion, tissue inflamation and edema, especially at C5/6 right side>Left, which is the major disc extrusion with broad spinal cord indentation and foramenal encroachment. This, and Ockham's Razor, where coincidental primary development is far outweighed by lack of family Hx, genetic traits and prior pure clean health and superior stamina/physical conditioning, suddenly changing, after injury, to drastic relative HR(60s-110-120s) and BP changes (110/60s-->130s/90s surges) paralleling neck symptoms after use most definitely leaves the neural and vascular regional influence and feed back loops as candidates over primary organ origins, especially since all endocrine and cardiac screening WNL. If simple physical upper body use reproduces the syrges and pattern of increased beta-blocker dosage and frequency, what els need be proven? I will not believe functional testing, and a possible blockage, inhibition to the stimulation would not clarify this. Isolated lower leg exertion(upper body relaxed) does not produce BP surge results afterwards, or Beta blocker dosage changes if done with no resultant neck/shoulder irritation. The source is continually illuistrated functionally. Sources should be treated before condemning someone to unecessary and limiting medication. Changiong symptomatic address is not what Medicine is about. Determining a treatable source existence is. Why MD literature is deficient is uncertain, unless indexing is poor. Much exists in print about complications of accelerator nerve and SANS damage post surgery or through stellate/injections. The events prove that inflamatory influence or feedback loops can also contribute. Infrequency in reporting is not a reason to discount a source. Living with dependent medication tachycardia is not acceptable, whatever the meds. It doesn't correlate with physiology of aging in this case.

I'm sorry, but I am a 25 yr medical professional and well capable to not trust mere MR and CT findings, which are highly unreliable in standard T2 weighting patterns when age of injury, size of defect and neural/tissue edema is subtle, especially when performed in neutral, unloaded supine resting position, a completely unnatural presentation. If cervical motion, Light activity(non cardiac stressing)upper body tensioning and posture induces cardiac breakthrough IST despite beta blockade, and HTN surges correlate with more severe incitement of cervical symptoms, Ockham's Razor and functional medicine at the orthopedic, neurologic and cardiac level prove such functional effect. Since no other neck/chest head tissue was involved, the answer is the disc/foramenr/C6 level effects contiguous to vertebral artery and anterior spinal cord venus plexus flow which can effect tissue edema and innervation coating the vessels for feedback to regulatory centers by sub pathways. Your denials of association seem straightforward from classic textbook symptoms and associations. Such are the minority in true clinical picture, and gray zone admixed symptoms and accomodation for functional demponstrated effects are of paramount importance. You cannot explain the functional effects given, so your answer is unacceptable. Remove my inquiries, please, as the answers presented are unqualified. All answers given were of no help, did not even reflect the reading of the full information, and generate doubt.