but still had an svt attack of 250 bpm and chest pain. We have now been told he has to be admitted to hospital to be given Flecainide, is this save on a child this age or is there any other drugs that can be used. He has an extra electrical pathway in his heart which we discovered 8 months ok.
18 Feb 2010
You need to trust in the doctors you have chosen to treat your child ask them all the questions you need to ask even get a second opinion Last but not least Trust in God I know nothing about the proceedure but I am sure you are terrified and have the right to be. BELIEVE in you Doctor your choices and God Hope this helps and good luck with this let me know how it works out God bless Barb
18 Feb 2010
I do understand the tenormin. That soounded really great. But with a heart rate that high, I am so sorry that did not work. But I had not heard of this drug. I did find this interesting article:
This is mainly about adults.
"Under one year of age, current available data are limited but suggest that the half-life at birth may be as long as 29 hours, decreasing to 11-12 hours by three months of age and 6 hours by one year of age. The pharmacokinetics in hydropic infants have not been studied, but case reports suggest prolonged elimination. In children aged 1 year to 12 years the half-life is approximately 8 hours. In adolescents (age 12 to 15) the plasma elimination half-life is approximately 11-12 hours. Since milk may inhibit absorption in infants, a reduction in Flecainide dosage should be considered when milk is removed from the diet (e.g., gastroenteritis, weaning). Plasma trough Flecainide levels should be monitored during major changes in dietary milk intake."
The last is the best... I went to google, typed in the word google scholar.
Clicked that and typed in flecainide for atrial fibrillation in children
I found that this medication was a first line of treatment. So it sounds like you are on the right track.
"Most patients in the younger group (17 of 22) received digoxin and/or a beta-blocker as the first line of medical therapy. Additional first line medications in the younger patients included flecainide (3 patients), amiodarone (1 patient), and a combination of digoxin and sotalol (1 patient). Responders to first line therapy included eight of the 17 who were treated with digoxin and/or a beta-blocker, as well as two of the three who were on flecainide. The patients started on sotalol or amiodarone as first line therapy did not achieve control until additional medications were added.
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Table 1 Medical Management in Children <3 Years of Age (n = 22)
Drug toxicity occurred in two patients in the younger group. One child who was receiving flecainide developed a new right bundle branch block with an accelerated ventricular rhythm, and a second child had a toxic flecainide level (flecainide level 1,700 ng/dl on 120 mg/m2/day) without evidence of clinical toxicity.
Excluding four patients in the younger group who were still on drug therapy, 14 of the possible 18 (78%) patients had complete resolution. The mean duration of therapy in those patients whose AET did spontaneously resolve was 12 ± 7 months.
Only two of the 22 patients in the younger group who were diagnosed at less than three years of age underwent RFA; both were successful in the short term. Their ages at the time of RFA were six months and nine years. The six-month-old underwent RFA due to a progressive cardiomyopathy despite medical therapy with amiodarone. The ablation was successful with an early recurrence of AET. The AET focus was modified by the RFA as it was more easily controlled with medication after ablation, followed by resolution once antiarrhythmics were discontinued. The older of these two patients had been on multiple antiarrhythmic combinations and ultimately underwent a successful RFA secondary to family preference.
None of the patients in the younger group required surgical intervention.
All three of the patients who presented with myocardial dysfunction in the younger group had improved function after intervention. The two patients who presented with mild-to-moderate myocardial dysfunction both had improved function while on antiarrhythmic therapy. The single patient in the younger group with a severe cardiomyopathy was discussed above. He was tried on multiple medical regimens without success and ultimately underwent RFA at six months of age. Due to recurrence of AET after RFA, he was placed on, and responded to, amiodarone with normalization of function.
Group 2. Patient profile
There were 46 patients diagnosed with AET at 3 years of age (median, 10 years; range, 3 to 18 years). The mean follow-up time was 20 months (range, 1 week to 120 months). There were three patients in the older group who were lost to follow-up.
Common reasons for referral included irregular heart rate (16 patients), tachycardia (13 patients), palpitations (11 patients), and for other reasons (6 patients). At presentation, echocardiograms were performed in 40 of 46 (87%) in the older group. There was echocardiographic evidence of decreased function in eight patients with a severe cardiomyopathy resulting in referral for transplant evaluation in two patients (ejection fractions by Simpson's biplane method of 16% and 20%). The single anatomic abnormality in the older group consisted of a quadricuspid aortic valve that was neither stenotic nor regurgitant.
Antiarrhythmic medications were used as the initial therapy in 35 of 46 (76%) of the older patients, with a median of two drugs (range, 1 to 5) per patient. Similar to the younger group, drug doses were typically increased to achieve clinical control or until measured serum levels were therapeutic. Control of AET while on antiarrhythmic therapy was achieved in only 13 of 35 (37%) of the older children. Drugs used in the older group and their effects are detailed in Table 2. As with the younger group, most patients (30 of 35) in the older group were initially started on digoxin and/or beta-blocker therapy. Additional first line medications included procainamide (1 patient), ethmozine (1 patient), flecainide (1 patient), and a combination of digoxin and quinidine (2 patients). There were 13 patients in the older group who achieved control, nine of whom received digoxin and/or beta-blocker therapy. Additional medications used to achieve control in the older group included ethmozine (1 patient), flecainide with a beta blocker (1 patient), and digoxin with flecainide (2 patients). There were no toxic side effects in the older group. "
I will keep your family in my prayers and know that there is a rainbow after the storm. Just look for it.
- Flecainide Information for Consumers
- Flecainide Information for Healthcare Professionals (includes dosage details)
- Side Effects of Flecainide (detailed)
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Whether esmolol can be used to control SVT & severe HT?
1 answer • 9 Sep 2009
I am not on any other drugs and I have not had any heart work ups yet other than a echo cardia I have had 3 trips to er via ambulance for what the er ...
1 answer • 20 Jun 2010
... which runs between 80 to 270 does depending on activity does anyone else have this issue?
1 answer • 20 Jan 2013
Does it stop rapid heartbeat happening or does it just control? the onset of SVT?
2 answers • 17 days ago