Dysautonomia And Concussion

[Guest ANCY]

Thanks Corina! I spent the night around 34 bpm and am sitting around 37 bpm today. I honestly don't know how you deal with it! I'm glad it is not all the time for you.

[Amalia01]

How are you doing Ancy?

[Guest ANCY]

Amalie, thanks for asking. Its a comfort to know people care.

Bradycardia is still proving to be difficult to manage... My overnight avg has been between 30-32 the last two nights with several dips down in the 20s.Thankfully my dog (possibly having her trained as a service dog since she alerts me to syncope) has been waking me up when it goes to low. Daytime/awake avg has been between 34-37 so overall it seems to be droping lower. I have an appointment Tuesday with MY cardiologist but my nurse case manager really wants me seen today so she is calling them. She is very concerned because im pasing out 20+ times a day and have presyncope symptoms almost constantly as well as constant chest pain. Trying fluid loading but not making a difference really... My physical therapist came out yesterday and during his entire visit my heart rate never went over 48. We were unsuccessful at raising my heart rate more than a couple seconds with any of the exercises so  Because he is concerned about overworking my heart, he has put PT on hold and told me only very light activity until I see Cardio. 

Thank you so much for caring!

[SarahA33]

Ancy, you poor thing. I am so sorry.   This is a perfect reason why the forum exists - to support and encourage each other! Especially when we are down and out (no pun!). I've read in the past that your fam sounds pretty awesome, but at times, try as they may,  just can't grasp the emotional and physical toll this can take.  You just hang in there, it seems like your doing a good job of that!

When you pass out, how long are you out for, and are they always when you are standing? (as opposed to sitting, reclined, etc) , and do your eyes ever remain open when you pass out? I ask because there are many types of seizures, and non epileptic seizures can occur with "floor drops" and happen multiple times a day. I was curious about the eyes thing because usually when you've blacked out, your eyes are closed. And in a seizure, I believe they are open. During these events, Bradycardia or Tachycardia can occur. Have they ever had you wear a holter monitor to record one of these events? 

Ancy here is an article by Dr. Grubb that discusses POTS and overlapping NCS. - I pasted it from dynakids, so it may look kind of funny.

Neurocardiogenic Syncope Coexisting with Postural Orthostatic Tachycardia Syndrome in Patients Suffering from Orthostatic Intolerance: A Combined form of Autonomic Dysfunction KHALIL KANJWAL, M.D.,* MUJEEB SHEIKH, M.D.,† BEVERLY KARABIN, PH.D.,* YOUSUF KANJWAL, M.D.,* and BLAIR P. GRUBB, M.D.* From the *Section of Electrophysiology, Division of Cardiology, Department of Medicine, The University of Toledo Medical Center, Toledo, Ohio; and †Division of Internal Medicine, Department of Medicine, The University of Toledo Medical Center, Toledo, Ohio
Introduction: There is anecdotal evidence that one or more forms of orthostatic intolerance (OI) subgroups may coexist in the same patients. However, there is a paucity of published data on the clinical featuresandmanagementofpatientswhosufferfromcoexistingfeaturesofposturaltachycardiasyndrome (POTS) and neurocardiogenic syncope (NCS). We herein present our experience of 18 patients who we found displayed evidence of coexisting NCS and POTS. Methods: We reviewed charts of 300 POTS patients seen at the University of Toledo Syncope and Autonomic Disorders Center from 2003 to 2010 and found 18 patients eligible for inclusion in this study. Patients were included in this study if they reported clinical symptoms consistent with bothPOTS and NCS and then demonstrated atypical lPOTS pattern(arise in heart rate without change in blood pressure[BP]) on head up tilt table(HUTT)within the first 10minutes off upright posture followed by a neurocardiogenic pattern (a sudden fall in heart rate and/or fall in blood pressure) reproducing symptoms that were similar to the patients spontaneous episodes. Results: We found 18 patients, mean age (30 ± 12), with 15 (84%) women and three (16%) men, who met the inclusion criterion for this study. Each of these 18 patients demonstrated a typical POTS pattern within the rst 10 minutes on initial physical exam and on a HUTT. Continued tilting beyond 10 minutes resulted in a sudden decline in heart rate (which in some patients manifested as an asystole that lasted anywhere between 10 and 32 seconds [mean of 18 seconds]) and/or a fall in BP in each of these patients demonstrating a pattern consistent with neurocardiogenic subtype of OI.The meantime to the NCS pattern of a fall in BP and heart was 15 minutes with a range of 13–20 minutes. This group of patients was highly symptomatic and reported frequent clinical symptoms that were suggestive of OI. Recurrent presyncope, syncope,orthostatic palpitations,exercise intolerance, and fatigue were the principal symptoms reported. Conclusion: NCS may coexist with POTS in a subgroup of patients suffering from OI. (PACE 2010; 1–6) orthostatic intolerance, postural tachycardia syndrome, neurocardiogenic syncope
Introduction Orthostatic intolerance (OI) syndromes refer to a heterogeneous group of disorders of hemodynamic regulation that are characterized by excessive pooling of blood in the dependent areas of the body during upright posture, thereby resulting in insufcient cerebral perfusion during upright posture causing a variety of symptoms
Address for reprints: Blair P. Grubb M.D., F.A.C.C., Division of Cardiology, Department of Medicine, The University of Toledo Medical Center, Mail Stop 1118, 3000 Arlington avenue, Toledo, OH 43614. Fax: 419-383-3041; e-mail: blair.grubb@utoledo.edu Received September 12, 2010; revised October 13, 2010; accepted October 31, 2010. doi: 10.1111/j.1540-8159.2010.02994.x
that are relieved by recumbency. Symptoms may include syncope, near syncope, fatigue, palpitations, exercise intolerance, lightheadedness, diminished concentration, and headache.1–4 Based on clinical presentation and head up tilt table response (HUTT), OI can be broadly divided into subgroups that include neurocardiogenic syncope (NCS), postural tachycardia syndrome (POTS), and dysautonomic (autonomic failure) syndromes. There is anecdotal evidence that one or more forms of these subgroups may coexist in the same patients. However, there is paucity of published data on the clinical features and management of patients who suffer from coexisting features of POTS and NCS. We herein present our experience of 18 patients who we found displayed evidence of coexisting NCS and POTS.
C 2010, The Authors. Journal compilation C 2010 Wiley Periodicals, Inc. PACE 2010 1
KANJWAL, ET AL.
Methods This was a retrospective study approved by our Institutional Review Board (IRB) at the University of Toledo. We reviewed charts of 300 POTS patients seen at our autonomic center at the UniversityofToledofrom2003to2010andfound 18 patients eligible for inclusion in this study.
Criterion for Diagnosis of OI As mentioned earlier, OI consists of a heterogeneous group of disorders of hemodynamic regulation characterized by excessive pooling of blood in the dependent areas of the body during upright posture resulting in insufcient cerebral perfusion causing symptoms during upright posture relieved by recumbency.
POTS POTS was dened as ongoing symptoms o fOI (of greater than 6 months duration) accompanied by a heart rate increase of at least 30 beats/min (or a rate that exceeds 120 beats/min) observed during the rst 10 minutes of upright posture or HUTT occurring in the absence of other chronic debilitating disorders.1,2 Symptoms may include fatigue, orthostatic palpitations, exercise intolerance, lightheadedness, diminished concentration, headache, near syncope, and syncope. In a retrospective chart review, we collected data, including demographic information, presenting symptoms,laboratory data,tilt-tableresponse,and treatment outcomes.
Neurocardiogenic syncope NCS was dened as episodic syncope (transient loss of consciousness) with spontaneous recovery. Criterion for diagnosis of NCS included a HUTT response consistent with NCS (a sudden decrease in heart rate and/or decrease in blood pressure) that reproduced a patient’s spontaneous symptoms of recurrent transient loss of consciousness with spontaneous recovery.
Protocol for HUTT The protocol used for tilt table testing has been described elsewhere,1–8 but basically consisted of a 70-degree baseline upright tilt for a periodof30minutes,duringwhichtimeheartrate and blood pressure were monitored continually.If no symptoms occurred,the patient was lowered to the supine position and an intravenous infusion of isoproterenol started with a dose sufcient to raise the heart rate to 20%–25% above the resting value. Upright tilt was then repeated for a period of 15 minutes.
Criterion for Diagnosis of Combined OI Patients where included in this study if they reported clinical symptoms consistent with both POTS and NCS and then demonstrated a typical POTS pattern (a rise in heart rate without change in blood pressure) on assuming upright posture or HUTT within the rst 10 minutes followed by a neurocardiogenic pattern on continued HUTT (a sudden fall in heart rate and/or fall in blood pressure)reproducingsymptomsthatweresimilar to the patients spontaneous episodes. Treatment Protocol The treatment protocol semiployed were based on our previous experiences with orthostatic disorders and are described in detail elsewhere.1–8 Briey, a sequence of therapies was employed that included physical counter maneuvers and aerobic and resistance training as well as increased dietary uids and sodium. If these were ineffective, pharmacotherapy was initiated in a sequence generally consisting of β-blockers, central sympatholytics, udrocortisone, midodrine, and selective serotonin reuptake inhibitors, either alone or in combination. If patients failed to respond to these medications, second- and third-line medications such as octreotide, erythropoietin, and pyridostigmine were employed. As this was a retrospective chart review, a formal questionnaire to assess the response to treatment or assessment of response to treatment by HUTT testing was not employed. The information about the subjective symptoms and sense ofwellbeingfromeachpatientwascollectedfrom thepatientcharts,physiciancommunications,and directpatientinquiry.Atreatmentwasconsidered successful if the patient reported that it provided symptomatic relief. Statistics This is an observational study. The statistical analysis was done by using SPSS 17 version (SPSS Inc., Chicago, IL, USA). Continuous data are presented as mean ± standard deviation and categorical data as percentages. A t-test was used for comparisons of means, and a statistical signicance was reached at a P value of <0.05.
Results A total of 300 charts of patients followed at the University of Toledo Syncope and Autonomic Disorders center were screened. These patients had been seen over a period of 7 years. We found 18 patients, mean age (30 ± 12), with 15 (84%) women and three (16%) men, who met the inclusion criterion for this study. Table I summarizes
2 2010 PACE
COEXISTING POTS AND NCS
Table I. Baseline Clinical Characteristics of the Study Patients (N=18) Age (years) 30±12 Sex (females) 15 (84%) Symptoms of orthostatic intolerance Orthostatic palpitations 17 (95%) Dizziness 16 (89%) Inability to concentrate 16 (89%) Syncope 18 (100%) Presyncope 18 (100%) Fatigue 17 (95%) Chest pain 11 (61%) Medications β-blockers 9 (50%) Selective serotonin reuptake 8 (45) inhibitors (SSRI) Norepinephrine reuptake inhibitors/SSRI 11 (61%) Midodrine 9 (50%) Modanil 3 (16%) Fludrocortisone 4 (22%) Pyridostigmine 17 (94%) Octreotide 1 (6%) Erythropoietin 4 (22%) Comorbid conditions Hypermobility 4 (22%) Hypertension 4 (22) Diabetes Mellitus 1 (6%) Migraine 9 (50%) Precipitating factor None 10 (83.3%) Infectious mononucleosis 2 (16.6%)
the clinical features, comorbid conditions, and medications used in these patients. This group of patients was highly symptomatic with frequent clinical symptoms that were suggestive of OI. Recurrent presyncope, syncope, orthostatic palpitations, exercise intolerance, and fatigue were the dominant symptoms reported. Each of these patients carried a diagnosis of POTS initially, but due to the nature of their symptoms each patient was further evaluated by a HUTT. HUTT Response All the patients reported here had clinical features and a physical exam consistent with the diagnosis of POTS. In view of their refractory symptoms and frequent syncope, they were referred to our center for further evaluation. A detailed physical examination was performed in each of these patients .All of these patients demon
Table II. Hemodynamic Parameters as Assessed in an Outpatient Ofce. Most of These Patients Demonstrated This Pattern of Increase in Heart Rate Without Signicant Change in Blood Pressure (POTS Pattern) within 5 Minutes of Standing
trated a typical POTS pattern with minimal change in blood pressure and an increase in heart rate in an ofce-based physical examination, conrming their diagnosis of postural orthostatic tachycardia (Table II). Each of these patients was further evaluated by a standard HUTT. The HUTT conrmed the diagnosis of POTS, but in addition, continuing the tilt beyond 10 minutes demonstrated a response consistent with NCS. Thus, a dual response was noted on a HUTT with initial POTS followed by neurocardiogenic decompensation pattern (see Table III and Fig. 1). Continued tilting beyond 10 minutes resulted in a sudden decline in heart rate (which in some patients manifested as an asystole that lasted anywhere between 10 and 32 seconds, mean of 18 seconds). The mean time to the NCS pattern of a fall in bloodandheartwas15minuteswitharangeof13– 20 minutes. Thirteen patients demonstrated NCS without a provocative isoproterenol infusion and three patients demonstrated NCS response after isoproterenol infusion.
Table III. Heart Rate and Blood Pressure Response in Patients with Combined Orthostatic Intolerance on a HUTT. Note a Dual Response with Initial Pattern Consistent with POTS (Increase in Heart and Minimal Change in Blood Pressure); Prolonged Tilting at 20 Minutes Demonstrated a Typical Neurocardiogenic Pattern with Fall in Heart Rate Associated with Fall in Blood Pressure
0 minutes 10 minutes 20 minutes
Heart rate (beats 73±10 123±15 43±15 per minute) Blood pressure 126±15 118±14 75±12 (mmHg)
PACE 2010 3
KANJWAL, ET AL.
Figure 1. Line diagram demonstrating a dual response with initial pattern consistent with POTS (increase in heart and minimal change in blood pressure);prolonged tilting at 20 minutes demonstrated a typical neurocardiogenic pattern with fall in heart rate associated with fall in blood pressure.
Response to Medications All of these patients failed rst-line medications. Second-line medications including pyridostigmine was tried in 17 of 18 patients. Of these 17 patients, improvement in symptoms of OI was observed in ve patients only. None of these patients had complete elimination of their syncope. However, a subjective improvement in the severity and frequency of symptoms of OI intolerance was reported by ve (30%) of the patients treated with pyridostigmine. One patient is being treated with octreotide and another four with erythropoietin, as pyridostigmine failed to improve heart rate and blood pressure in these patients. Pacemaker Implantation Nine patients were further evaluated by implantable loop recorder (ILR). Five patients demonstrated prolonged periods of complete heart block and asystole on the tracings that were downloaded following episodes of abrupt onset of convulsive syncope. Each of these ve patients received dual chamber closed loop cardiac pacemaker with near complete elimination of their episodic loss of consciousness. Discussion The exact pathophysiology of postural tachycardia syndrome remains elusive. Our understanding of the disorder now called POTS has substantially increased in the last two decades. The early descriptions of the disorder focused on a group of patients who had been previously healthy until a sudden febrile illness (presumably viral) brought on an abrupt onset of symptoms.9 Later investigations revealed that POTS is better un
derstood as a physiological state most commonly due to inability of the peripheral vasculature to maintain adequate resistance in the face of orthostatic stress,allowing for excessivepoolingof bloodinthemoredependentareasofthebody.10,11 The resultant functional decline in circulatory volume elicited a compensatory increase in heart rate and myocardial contractility. While compensatory in mild cases, this mechanism is unable to fully compensate in more severe cases, resulting in a reduction in effective circulation and varying degrees of cerebral hypoperfusion. Later investigations revealed that POTS is not a singlecondition,butratheraheterogeneousgroup of disorders resulting in similar physiological state.9–13 Recentresearchhasshownthatthissyndrome may have multiple etiologies and we now know that POTS can have multiple variants such as partial dysautonomia,9 centrally mediated hyperadrenergic stimulation,12,13 norepinephrine transporterdysfunction,14 andanautoimmuneantibody against acetylycholinesterase receptors,15 POTS associated with deconditioning,15 and hypovolumia.16 In a recently published study, it was reported that POTS may be a manifestation of autonomic cardiac neuropathy.17 More recently, interest has grown in the assessment of parasympathetic function in patients sufferingfromPOTS.RajreportedagroupofPOTS patients in whom vagal function was preserved as assessed by normal sinus arrhythmia ratio on deep breathing.18 Alshekhlee et al. describe a series of four POTS patients who had a surge of parasympathetic activity resulting in marked cardioinhibition and vasodepression.19 They postulated that either a compensatory parasympathetic surge or a central aberration altering both sympathetic as well as parasympathetic output in a balanced fashion may account for increased parasympathetic activity in this group of patients. We postulate that an initial compensatory increase in sympathetic outow that increases the inotropy as well as chronotropy of the heart may fatigue or norepinephrine stores may become exhausted,resultinginastateofrelativesympathetic withdrawal causing a state of bradycardia and hypotension in this group of patients. Assessing bothsympatheticaswellparasympatheticnervous system function at various stages of the HUTT may answer many of the questions, which our report could not address. Ojha et al. have reported that as many as 38% of patients suffering from POTSexperiencesyncopeduringHUTT,andthey suggest that the low-pressure baroreceptors that have been implicated as contributing to some forms of POTS may confer upon these patients an increased riskofsyncope.20 Inarecentstudyfrom
4 2010 PACE
COEXISTING POTS AND NCS
Fuetal.,21 itwasobservedthatpatientswithPOTS haveasmallerheartincomparisontothecontrols. Also they observed that the autonomic function was intact in their group of patients. In this report, exercise training improved or even cured symptoms of POTS. With continued research in the area of OI, we hope to learn more about the pathophysiology of the POTS and its related syndromes. There were some interesting observations from our study. Syncope (which, as mentioned previously, occurs in 10%–38% of historical controls of POTS patients in general) occurred in all patients in this group. This observation could be explained by a late-phase surge in parasympathetic tone or sympathetic withdrawal leading to both cardio inhibition as well as vasodepression. Almost all patients in this study had difculty treating OI with each patient failing rst- and second-line medications. Response to third-line medication, including Pyridostigmine, was also modest. Recently, Ivarbidine, a selective inhibitorofacardiacpacemakercurrentinhibitor, has been reported to be effective in patients with inappropriate sinus tachycardia,22 tachycardia with POTS,23 and tachycardia associated with autonomic dysfunction.24 In one report,23 Ivarbidine was reported to improve symptoms of POTS in a patient who had failed multiple other medications. The patient described in the report had history of intermittent bradycardia and heart block for which he had received a pacemaker. Since these results were recently published, none of our patients had received Ivarbidine so far. But
Ivarbidine therapy may be benecial in patients sufferingfromPOTS.Inthefuture,weexpectmore studies will be published on the use of Ivarbidine in postural tachycardia that will dene the role of this therapy in POTS patients a better way. In our study, the patients who were found to have prolonged episodes of asystole or complete heart block on ILR subsequently beneted from dual-chamber pacemaker placement. Thus, POTS patients who present with unusually frequent and severe episodes of syncope should be considered for evaluation by an ILR to assess whether baradycardia and/or asystole occurs during clinical events. Limitations There were several important limitations in the current study. The study was retrospective and included small number of patients. None of the patients underwent additional autonomic function assessment besides HUTT. Response to therapy was subjective and not objectively assessed by a formal questionnaire or a response to a repeat HUTT. Conclusion NCS may coexist with POTS in a subgroup of patients suffering from OI. This group of patients with mixed-form OI may be difcult to treat and may have syncope as a dominant symptom. Also, POTS patients presenting with unusually frequent and severe episodes of syncope may benet from further evaluation by ILR, as some of these patients, having NCS as well, may be candidates for cardiac pacing.

 

Anyway, all my best!

Sarah
 

 

[corina]

I'm so sorry Ancy. I think you're passing out due to brady. My doc told me that when I get to this point we will talk seriously about getting a pacemaker. I hope you can be seen by your doctor asap and that s/he will be able to figure things out and come up with a treatment plan. Warm wishes, Corina

[Guest ANCY]

Sarah, thank you so much for taking the time to post that article for me! I'm going to try and print it out and bring it to my appointment. I have been diagnosed with both already so maybe my dr will find it useful. I was very interested in the part about pacemakers! Although I don't know how helpful that will be since they said they are not seeing any heart block, they said that's why they don't want to place a pacemaker... I'm at the point I just want then to do SOMETHING to help me feel better. Yes it's reassuring I'm not going to die, but I don't want to feel like it either lol! 

I do have an amazing family who is very supportive and right now as frustrated as me with all that's going on. 

 

My baseline before 2 weeks ago was passing out 2-3 times a day for 30 seconds to 4 minutes because of bp dropping. I did NOT pass out laying down. Post concussion and start of the bradycardia, I have been passing out 20+ times a day for varying lengths of time, most around a minute and a half. My eyes are shut when I pass out and drs are certain that I am not having seizure activity. I have worn a Holter monitor in the past that showed sinus tachycardia when I was passing out. When I was in the hospital they had me on heart monitor and saw sinus bradycardia the entire time. There were no stops or pauses which is why they said no pacemaker.

 

Corina, I would think that my syncope is happening largely in part to the bradycardia. If not, secondary to inability to compensate for blood pressure drops like I was with the tachycardia. I hope you don't reach the point of passing out from it! But I do hope you and your Dr can make a wise decision about a pacemaker.

 

Thank you both for caring!

[Amalia01]

I'm really sorry to hear that this has persisted.  Has anyone consulted with your ANS specialist?

[Guest ANCY]

Wouldn't really say I have an ANS specialists... My Neurologist is great but not an ANS Dr, and no, to my knowledge, has not been consulted. I have not called them because im 90% sure they'd just tell me to see cardio any way, and they're rather difficult to get a hold of. My cardiologist is probably the most familiar with Dysautonomia of any of my medical team so hopefully he will have some answers Tuesday. My nurse called this evening and said she had no luck on getting them to move up my appointment.   Although my heart rate is still dropping i am determined to make it through the weekend without going to the hospital, would be the third weekend in a row lol! Must make it to this appointment! 

[SarahA33]

Ancy, have you checked our physicians list for anyone in your area? One of our medical advisors, Dr. Blitsheyn does Skype or phone consults, she specializes in autonomic disorders.  Brady must be terrible. I suppose I'll take tachy if I have to pick. Ugh!

http://circ.ahajournals.org/content/111/7/839.full   This article is by Dr. Goldstein from the NIH. Neurocirculatory Abnormalities in Chronic Orthostatic Intolorance

http://www.dinet.org/index.php/information-resources/ncs/ncs-links  Here's our site's NCS info, not sure if you've seen it.

I'll keep looking for you. Feel Better

Sarah

 

 

[Guest ANCY]

Yes there is one in Denver but she does not take my insurance. Thank you for the med article I will read it later when I'm feeling a little better. Will look into dr Blitsheyn. I would have to say I would choose tachy over brady every time!? I have read over the info about NCS but will look through it again. Thanks so much Sarah!

[Katybug]

Thinking of you, Ancy. Hope this gets better soon.

[Guest ANCY]

Thank you Katy! I hope to see some improvment soon it has been a looooooong  lesson in patience with all this lol! So tired of all this just want my life back!

[Amalia01]

Hang in there Ancy (I know it's easy for me to say). I cannot imagine what you are going through but I'm glad you are seeing your doctor tomorrow. It's nice that there is a little more information for you.  Wishing you the best.

[yogini]

Ancy, sorry if I missed this in your replies, but what is your blood pressure when your HR is so low? Is your BP very low?  If so maybe you want to talk to your doctor about a stimulant, such as caffeine.

Or maybe your  BP very high when your HR is so low? I see you are on Florinef and midodrine

Anyway I hope you are able to connect with your doctor soon as he or she can best help you. Hope you feel better soon!

[Guest ANCY]

Thank you Amalia! Can't wait for tomorrow.

Yogini- 

My blood pressure avg during this bradycardia is between 80/30-90/60.  Prior to the concussion and bradycardia my avg was around 110/80. I do still get  spike in blood pressure after passing out but it doesn't stay around for long. I had to push diet Coke (caffeine) through my J tube to unclog it last week and the caffeine seemed to raise my heart rate temporarily but was concerned about the other effects it has on me. 

I have an appointment with cardiologist PA tomorrow at 3:30 so hopefully he will have some ideas. I'm so ready to be done with this bradycardia!

[Amalia01]

Any changes or news?

[Guest ANCY]

Made it to my cardiologist appointment today, most helpful dr through this latest mess... He had a very different tune than all the other cardiologists I saw, probably because he knows my baseline. He has sent me to bed for the next week until I see him again. So I will have to say see you later to all you great folks while I hibernate, he literally wants me to sleep the entire time, no books, no electronics, no exercise, no PT, no movies ect... he is hoping that removing ALL stimulus will allow my brain to heal from the concussion.

EKG showed heart rate of 32 with prolonged QT. He is taking me off of zofran, Compazine, aND domperidone because they all can worsen the QT. Going to try scapolamine patches instead to control the nausea. Hoping they will be effective. 

He does believe that something stimulated the vagus nerve which brought on the bradycardia. Wether it was the concussion or all the vomiting there's still not much they can do except symptom control. He did order a repeat CT scan of my head just to be sure there's not anything going on there.

He was able to explain a little more about pacemakers and the reason they don't want to place one in somebody my age. Mostly because it is very dangerous to remove so once you have one it's the rest of your life. I know it would be a last resort and he is not convinced this is not a temporary problem because of concussion. So wants to wait it out another week and see what can be done with rest.

He is also recheck in electrolytes just to be sure there's no problems there.

Thanks so much for all the prayers and well wishes! I'm going to miss you all!

[corina]

Seems like a great doctor! I hope things will work out just as he thinks and once the concussion heals the brady will heal too! Sending good thoughts Ancy!

[Guest ANCY]

Thank you Corina! My overnight lows have been dropping into the 20s this last week and average was between 29-35. 

PA is still convinced it's part of post concussion syndrome so he has ordered me to bed again for another week. CT was unremarkable and blood work was normal, for me lol! EKG showed sinus Bradycardia at 34 bpm. Good news is my QT is back within range. Yeah! PA thinks probably the bradycardia combined with the drugs is what messed it up since I've taken them for years. He  is going to consult with MD and get back to me if MD wants something else doNE or doesn't want to wait any longer to place a pacemaker. 

Thank you everyone for being so supportive! 

 

[Katybug]

Hoping this is resolved soon, Ancy. It must be scary aside from feeling like ick.

[Guest ANCY]

Thank you Katy. I don't think that the gravity of the situation has really sunk in yet... right now it's kind of dealing with it day to day just to make it through.

[Guest ANCY]

Just got a call from cardio office MD wants me to come in today to talk about pacemaker. Please pray for wisdom! (For those of you who pray ?) 

Thanks so much!

[dancer65]

Thinking of you sending you all the best vibes I can ! 

Hope they can sort this out soon for you can't imagine what your going through 

hugs ?

[Guest ANCY]

Thank you dancer!

Cardiologist said that he thinks the bradycardia is a new manifestation of my dysautonomia not directly from concussion... he does not want to wait it out any longer because the longer we wait the more deconditioned i get so scheduled to have a dual chamber pacemaker put in Tuesday morning. Looking forward to feeling better! I'm sure I'll feel at least somewhat better with my heart rate more normal. 

[Katybug]

Hoping for a great outcome for you!