Dear Cricket -

I'm not so sure about a link between SVT and CRPS. For one thing, I just searched the two acronyms on PubMed and came up with nothing - as in zero hits - which is weird where PubMed is nicely programed to read medical acronyms as the phrases for which they stand, and vice versa. Searches of "SVT RSD," "cardiac plexus CRPS" and "cardiac plexus RSD" were similarly unproductive.

Secondly, the two cardiac related conditions that appear to be related to CRPS in the literature, are (1) orthostatic and/or cardiac sympatho-vagal dysregulation - which is in turn distinguished from postural orthostatic tachycardia syndrome (POTS) - and (2) atypical chest pain caused by the sensitization of the intercostobrachial nerve (ICBN), in CRPS patients with brachial plexus involvement. See, e.g.:

Complex regional pain syndromes in children and adolescents: regional and systemic signs and symptoms and hemodynamic response to tilt table testing, Meier PM, Alexander ME, Sethna NF, De Jong-De Vos Van Steenwijk CC, Zurakowski D, Berde CB, Clin J Pain 2006 May;22(4):399-406, FULL ONLINE TEXT @ http://www.rsds.org/pdfsall/Meier_ClinJPain_2006.pdf

Abstract
OBJECTIVE: Complex regional pain syndromes (CRPS) involve neuropathic limb pain and localized circulatory abnormalities. The authors hypothesized that (1) pediatric CRPS patients exhibit systemic autonomic symptoms and orthostatic and/or cardiac sympatho-vagal dysregulation and (2) their orthostatic regulation differs from healthy controls and pediatric patients with postural orthostatic tachycardia syndrome (POTS).

METHODS: CRPS children and adolescents (n=20) underwent a 6-week trial of physical therapy and cognitive-behavioral treatment. Measures included pain and function scores, regional and systemic autonomic symptom profiles, heart rate and blood pressure with tilt, heart rate variability indices, and baroreflex gain. Systemic autonomic symptoms were recorded in 55 healthy pediatric controls. Tilt responses in CRPS patients were compared with those of 21 POTS patients and 39 healthy controls.

RESULTS: CRPS patients' regional autonomic symptoms, pain, and limb function improved over 6 weeks (P<0.01). At baseline CRPS patients reported more systemic autonomic symptoms than controls (P<0.05). Tilt table test showed orthostatic stability, but the mean heart rate increase with tilt was greater in CRPS patients than controls (P<0.001). POTS patients showed significant increases with tilt in mean heart rate and diastolic and systolic blood pressures compared with controls (P<0.001). There were significant increases in the mean systolic and diastolic blood pressures in POTS compared with CRPS patients but no difference in the mean heart rate between groups.

DISCUSSION: CRPS patients reported multiple regional and systemic autonomic symptoms that improved during the study course, and they experienced minimal and transient tilt table-induced hemodynamic changes compared with POTS patients but relatively similar to controls.

PMID: 16691095 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/19787018

AND

Atypical chest pain: evidence of intercostobrachial nerve sensitization in Complex Regional Pain Syndrome, Rasmussen JW, Grothusen JR, Rosso AL, Schwartzman RJ, Pain Physician 2009 Sep-Oct;12(5):E329-34, FULL ONLINE TEXT @ http://www.painphysicianjournal.com/...;E329-E334.pdf

Abstract
BACKGROUND: Atypical chest pain is a common complaint among Complex Regional Pain Syndrome (CRPS) patients with brachial plexus involvement. Anatomically, the intercostobrachial nerve (ICBN) is connected to the brachial plexus and innervates the axilla, medial arm and anterior chest wall. By connecting to the brachial plexus, the ICBN could become sensitized by CRPS spread and become a source of atypical chest pain.

OBJECTIVE: To evaluate the sensitivity of chest areas in CRPS patients and normal controls.

DESIGN: Prospective investigation of pressure algometry in chest areas to determine chest wall sensitivity.

METHODS: CRPS patients and normal controls volunteered to participate in our study. Each individual was examined to meet inclusion criteria. Patients' report of chest pain history was collected from every participant. Pressure algometry was used to measure pressure sensitivity in the axilla, anterior axillary line second intercostal space, mid-clavicular third rib, mid-clavicular tenth rib, and midsternal. Each of these measurements were compared to an intra-participant abdominal measure to control for an individuals generalized sensitivity. The ratios of chest wall sensitivities were compared between CRPS patients and normal controls.

RESULTS: A history of chest pain was reported by a majority (94%) of CRPS patients and a minority (19%) of normal controls. CRPS patients reported lifting their arm as a major initiating factor for chest pain. To pressure algometry, the ratios of CRPS patients were significantly greater than control subjects (p< 0.02 throughout), indicating increased chest wall sensitivity.

LIMITATIONS: This study is limited by the relatively small number of patients (n=35) and controls (n=21) used.

CONCLUSION: The results of this study support the idea that chest pain is greater in CRPS patients than normal controls. The ICBN could be the source of this sensitization by CRPS spread from the brachial plexus.

PMID: 19787018 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/19787018

And neither of them sound anything like what you've got.

That said, a couple of years ago, my wife (who does not have RSD/CRPS) became ill with what was believed to be SVT, getting worse over a number of months, whereupon she was referred not to a Cardiologist, but to an Electrophysiologist: doctors who specialize only in the electrical activity of the heart. A practice so specialized that it takes 7 to 8 years after medical school, 3 years of Internal Medicine residency, 3 years of Clinical Cardiology fellowship, and 1 to 2 (in most instances) years of a Clinical Cardiac Electrophysiology fellowship on top of that!.

I have forgotten the medication she was put on initially, but the point is that she was given a very specialized type of halter monitor to wear for a fairly long period of time. The idea being that as soon as you felt something going, you hit the button which started the recording, and were then given a number to call 24/7 where she then downloaded the information via an audible tone, which was read by a tech who stayed with her until he got her doctor on the phone. In any event, while monitored, one night she hit 300 b.p.m. - she never would have guessed it was that high - went into shock and the paramedics were called. It took two rounds of IV adenosine before they determined that she was "stable enough to transport," but by then the adenosine had done the trick and she walked out of the ER 2 hours later. Long story short, with the fire department's EKG tape, they got it down to a subset of SVT: AV nodal reentrant tachycardia (AVNRT). http://en.wikipedia.org/wiki/AV_noda...nt_tachycardia At which point her Electrophysiologist was able to schedule a 3-hour cardiac cath. procedure using "cold ablation" or "cryoablation" http://en.wikipedia.org/wiki/Cryoablation and the errant pair of nerves were put out of their misery. And she hasn't had a problem in the 2 years since.

My suggestion: get a referral to a board certified electrophysiologist. But for all I know, you are already be seeing one!

Good luck. I have no doubt that you will figure this one out.

Mike