Initial 40 msec of the QRS is normal in right bundle branch block (RBBB). The QRS width is more than or equal to 120 msec. Lead V1 shows and rSR pattern. The secondary R wave is taller than the initial r wave. The initial r wave may be absent when there is anterior wall myocardial infarction, resulting in QR pattern in V1. There will be associated ST segment depression and T wave inversion, in anterior leads known as secondary ST – T changes. The secondary ST – T changes are repolarisation abnormalities secondary to an abnormal depolarisation sequence due to the conduction abnormality. Lead I and V6 shows a slurred S wave in RBBB. The QRS axis is normal in isolated right bundle branch block. Left axis deviation indicates associated left anterior hemiblock and right axis deviation indicates associated left posterior hemiblock. Brugada syndrome comes in the differential diagnosis of an RBBB pattern. But the ST segment is elevated in V1 in Brugada syndrome while it is depressed in RBBB. Left ventricular ectopic beats and paced rhythm from the left ventricle also have right bundle branch block pattern.

Similar posts: cardiology

The girls had a visit with the cardiologist this morning. 2 1/2 hours at the doctor with two squirmy girls meant I got myself Chick-Fil-A afterward! :) I left Bubs with a sitter! It's always nice visiting our cardiologist because we've been with this group for over 5 years now. I went for the very first time when I was pregnant with Darah because her heart defect was found prenatally. They were all very excited to meet the new baby. They truly are family!

Reese's update: Baby girl is hovering at 19 lbs, 4 oz and is 29" tall. Not only is she our best eater in the family, she also has the healthiest heart! Show-off! ;) Her heart is absolutely perfect! This isn't a surprise to us because her heart was checked in Ukraine by a Ukrainian doctor, but we needed to confirm those results with our cardiologist. We walked Reese out of there WITHOUT a follow-up appointment because she doesn't need to go back. Yay!!

Darah's update: D weighed in at 29 lbs and is 36 1/2" tall. Her cardiology visits always give me anxiety. She has pulmonary hypertension which we have to watch closely and it's a very scary medical condition. She is and always has been medically stable and doing fine, but her pulmonary artery pressures have been twice what they should be. Today they were a little more than twice what they should be. Not too much higher, but higher scares me. Her cardiologist said that I shouldn't panic or worry, but we do need to do another sleep study to see what is going on with her sleep apnea since that can really exacerbate her pulmonary artery pressures. The numbers have been higher than what they are before and six months later have settled back into her "norm," so I will not be surprised if in six months, they are right back at double what they should be. Her little VSD she's had from some stitches coming lose from her open heart surgery is not visible. It's still there because we could see some leaking on the echo, but our doctor couldn't see the hole. So, that's good news! The other good news is we didn't have to increase her current heart medicines or add any new ones. That's always nice.

Con goes back to the cardiologist in August to have his VSD looked at which I'm nervous about, but we'll not worry about that until we need to! And someday, I am going to get my very own designated parking space at that office! I think I've probably earned that much!

Here's a pic of the two oldest enjoying some of our heat.

Similar posts: cardiology

Her pediatrician seemed baffled at her progress. He didn't expect her to be so happy...or to be growing new teeth or to be progressing developmentally. No one that he's talked to expected her to be doing this well. He tried to be very careful to not get our hopes up....but he's very interested to see if she has increased heart function. (I guess the cardiologist doesn't send the results fast enough...Pediatrician asked me to call him Friday to tell him how things go.

Similar posts: cardiology

In my first 3 days, Ive:
x heard an ejection systolic murmur over the aorta, radiating to the carotids (83 yo woman with aortic stenosis that has progressively worsened over several years)
x heard a diastolic murmur over the apex (mitral stenosis)
x auscultated a pt who had 2 prosthetic valves (mitral and aortic) put in. metallic-clicking sound.
x seen a stress test being done
x sat in on echocardiography
x tried to cannulate, been cannulated and finally did one successfully (albeit a little messily!)
x watched a patient get an ABG and cannula this morning. This afternoon, we watched this same patient get a pleural tap and ascitic tap - pleural tap took 3 goes and 2 people to get it, and ascitic tapprobably more than 5 tries by various people with a progressively larger needle (final one was a spinal tap needle), and they still couldnt get it! Patient had lots of oedema and surgical scarring though, so it was hard. Felt kind of bad for him nonetheless.
x taken some histories, examinations
x wrote in patient notes with the SOAP system
Nonetheless, theres still some quiet time (usually when the RMO or registrar is busy) and Ive learnt how to blend into the wall. Victor seems really pro at everything.  xD
Main impressions so far:
x Lots of old patients!! Most of the patients Ive seen are over 80 with so many comorbidities on top of their cardiac disease.
x Did not realise ward rounds went on for so long.
x Nurses are actually pretty nice, they helped me read medcharts and gave us people to cannulate, but then I havent been yelled atyet.
x How crazy is Grand Rounds food?! And where on earth is Surgical Grand Rounds? Haha.
x Cardio Blue team seems M.I.A. LOL.
This patient we met today smoked 40/day. Ive never SEEN such a massive pack of cigarettes. He calls it going out for fresh air.  ._.
TIREDDDD!
Perhaps Ill leave with a quote:
The young man knows the rules, but the old man knows the exceptions.

Similar posts: cardiology

Well we made it through. The past two days have been filled with lots of doctors and lots of talking!

PULMONARY:

We were very happy with this appointment. I really like our doctor. He listened to everything, explained the difference between obstructive sleep apnea vs. central hypoventilation and how they see it in a sleep study, he had talked to Oncology before meeting with us so he already knew about Haven and pulled up her records while we were in there. It was great. We spent over an hour with him.

A few areas discussed:

Haven's breathing and where she is right now: he noted that her sleep studies were pretty good right now and that we would continue to monitor her closely for any changes. He said her last sleep study showed her highest CO2 level at 49 and when she starts to pass 50 is where the concern would be. We have a sleep study scheduled for August 15th and a follow up appointment with him on July 23rd.

He did say he didn't expect Haven would suddenly stop breathing in the next month or even the next 6 months but then reminded us that he can never say that for certainty because we don't know how ROHHAD acts in every child. At most, he said she would probably only need to go on a bi-pap machine in the next 6 months but didn't think we should worry about that yet.

He mentioned bringing Neurology in now to monitor possible seizure activity during her next sleep study. Doesn't mean she is going to have a seizure but Haven has a history and since this hasn't been monitored in over a year he would like another record of her brain in that department.

He is a bit concerned with her sleep walking and talking. More for her safety than anything plus we were sure to explain to him that although her sleep walking drives us crazy and doesn't let us sleep - it also comforts us because if she's screaming and talking we know she's breathing.

He ordered a pulse oximeter for Haven to use at night while sleeping. They said it would be set to alarm if she reaches 94....I am sure we will hear many alarms as Haven is usually around 95-96 and a little drop will cause an alarm. Kris received a call tonight about the delivery! I did briefly discuss her sleep walking and machines but he was not worried. We will have to spot check her stats - we'll have different times at night that we will have to record them.

We discussed her ABG results that were done while under anesthesia. He is almost discounting them because the readings would be altered by the intubation and oxygen given to her. So we will have to have an ABG test while awake. We did not do this today - as he wanted Haven to meet him first without pokes and it hurts a lot.

He is highly recommending us to go to Chicago to meet with Dr. Weese-Mayer. He said he has talked to her and discussed Haven. Oncology has also talked with her about Haven. He is concerned that there could be something they are missing and wants to have a full evaluation done by Dr. Weese-Mayer and then get the results back here. He also would like to have Haven's full studies in the research paperwork to help other children with ROHHAD. I have emailed the team at RUSH (thank you Julie for all the paperwork). We'll discuss this with Oncology next week.

We discussed Haven's allergy to Ketamine. He absolutely doesn't believe it's specifically Ketamine related. He told us that a ROHHAD episode (Respiratory Failure) can easily be triggered by ANY anesthesia. Haven must be required to be intubated without question at any procedure done. He told us to make sure when she does have anesthesia that we require them to monitor her CO2 levels while giving her oxygen. He said CO2 levels can rise dangerously if not monitored at the same time in a ROHHAD child. We have agreed to have her intubated on every anesthesia procedure due to her seizure activities and respiratory failure a few times while under anesthesia.

The funniest thing we heard: he said he bets that Haven can stay under water for a couple of minutes and have no problem at all. She lacks the function of panic that would tell her she needs to get to the surface to breathe. She can withstand a high level of CO2 - which a normal person can not and they would rush to the surface. We didn't take him up on the bet!


ONCOLOGY:

We went to Oncology following Pulmonary. Haven needed to have her levels and blood work done. When we met with Cardiology yesterday he wanted to have her tested for Anemia. So this was done today as well. We will not have results back until next week. Everything went as planned here.

Child Life talked to us about Sunrise Camp for Kids with Cancer. So we are going to sign Haven up in the 5 year old camp. It's a daily camp (she doesn't stay over). It's only for kids with Cancer. There are Pediatric Oncologists and Oncology nurses on site. Our own Nurse Katie volunteers at the camp and Kim at Child Life is there. We think it will be really good for Haven. It's free for her to go and she will have a blast doing crafts. This will be in August.

CARDIOLOGY

Next we went over to Pediatric Cardiology to get Haven hooked up on her holter. We are monitoring her heart rate. She runs high so the doctor said he would like to see her have fluctuations and get down in to the 80's during sleep. We will get the results from him next week. He doesn't want to put her on medication because she is already on so much. He wants to have an Echocardiogram done every 4 - 6 months to monitor her.

Similar posts: cardiology

I had just spend an hour with the patient and her husband who lived here in Chicago discussing her condition and treatment options. So it was a strange moment when the husband of my patient walked out to me and handed me the phone.

"Can you talk to him?" he asked.

"Who's that?" I asked.

"Dr. Frigamafratz. He's our (concierge) doctor in Baltimore."

"Baltimore? Uh, sure."

I held the phone to my ear.

"Dr. Fisher?", a woman's voice asked.

"Yes?"

"Please hold one second while I get Dr. Frigamafratz on the phone," a lady with a very business-like demeanor said.

I heard static, popping, a voice come and go... then...

"Hello, Dr. Fisher?" (static, hissss, clicks, hisss) "I'm Dr. Frigamafratz. Can you tell me what's going on?"

I told him about the situation, about the fact that those skipped heart beats she had been experiencing and intermittent periods of lightheadedness were likely caused by brief bursts of right ventricular outflow tract tachycardia. About her workup. About her structurally normal heart. About her treatment options and the various options for treatment that I had recommended.

"Uh, yes..." (static...click....hisss) "Well, I see," he said.

Then silence.

"Hello? Hello?" I called.

The pleasant young lady came back on the line. "Yes, Dr. Fisher, I'm here. I'm sorry we must have lost Dr. Frigamafratz. I'd be happy to tell him the situation."

Frustrated and pushed for time, I capitulated and summarized the situation again to the lady on the phone, then handed the phone back to the husband. He thanked me for talking with their concierge doctor and I went on to complete my consult note and forwarded it back to the local referring physician. A while later, I returned to the room to see if my patient and her husband had decided on their course of therapy.

They chose medicines over ablation, much to my surprise given our conversation, but I understood her reluctance and respected her decision.

Later that evening, the patient's internist here in Chicago called me. I learned that our mutual patient had spoken with her concierge doctor, Dr. Frigamafratz, while I was writing my note. The internist was livid. Dr. Frigamafratz had not communicated with the internist about his input to the patient's care. (Doctors reading this know this is basic profesional ethics). I learned that Dr. Frigamafratz was a retired Emergency Room doctor and started this concierge's business to cater to high-end, well-traveled clients. I learned that the pleasant people on the phone were not nurses, but secretaries. Finally, I learned that Dr. Frigamafratz had recommended a therapy to my patient, yet knew nothing about her most recent situation and conducted his entire assessment over the phone without setting eyes on her or examining her.

No wonder the internist was livid.

As we plotted the next steps for our patient's treatment, I reflected on the growing movement for online, mobile, and internet-based physician care and suspect that we can expect more of these "who's on first" experiences in the years to come.

Similar posts: cardiology

Status:

Lungs: still have a little fluid
Heart: a bit large (mostly due to the right ventricle being big)
Truncal valve: mildly leaky, no backwards flow
RA-PV conduit: mildly leaky (the doctor says they all are and Oliver's looks like it should)
Breathing: He still breathes fast and hard.
Heart rate: Is still "above average" and he still has occasional extra heart beats (PACs)
Head shape: Is odd
Drugs: He's on three

Treatment:

Lungs: will clear with time
Heart: muscle of right ventricle will thin with time Oliver will grow into it
Truncal valve: will need to be replaced at some point (years).
RA-PV conduit: If he doesn't outgrow it within his first year, it will most likely last for years. He was fortunate that he had 2 weeks to grow before his surgery: the surgeons were able to put in a larger conduit which will (hopefully) "fit" for longer.
Breathing: He'll most likely outgrow it
Heart rate: PACs are not a concern. Rate should slow as his heart continues to heal (the cardiologist said it takes a year for the heart muscle to heal entirely)
Head shape: cardiologist said its common and should normalize
Drugs: His doses are the same. He will be allowed to outgrow two (the diuretic and the reflux med). He will stay on captopril until his truncal valve is replaced. It helps prevent blood from flowing backwards.

Reaction:
Whew!!!!

Yesterday was a bad day. Everything seemed gloomy. Today's news (and a good night's sleep for me) made everything seem better.

Similar posts: cardiology

No parent wants to hear that their child will have to undergo another heart operation in the future, but it was confirmed that she will need her pulmonary valve replaced sometime during her adolescence or early adult years. Its not uncommon for patients with Tetralogy of Fallot to undergo this surgery later in life. Her pulmonary valve is leaky and the blood flowing into her lungs returns back into her right ventricle which is called pulmonary regurgitation. Over the years, the right valve will become weaker and will need to be replaced. Who knows what kind of medical interventions and surgery techniques will be available by the time she needs to have this operation. We continue to have faith in modern medicine and arent going to let this news bring us down.

For now, she is not restricted in her physical activity and she does not need any maintenance medication. Her cardiologist said that he doesnt expect us to see any symptoms of fatigue with exercise until she reaches 8- 12 years old (if at all).

Similar posts: cardiology

In May 2008, we launched Cardiovascular eNewsletter to better address the questions on your minds. Encouraged by your extensive feedback, we launched Issue #2, dedicated to Stroke TIA (Transient Ischemic Attack) management.
Stroke is a common but serious disorder. Hospitalizations attributable to stroke appear to be increasing, suggesting that the care of Stroke TIA patients continues to be a significant health-care issue for the foreseeable future. Accordingly, in this new issue, we highlighted the role of Clinical Education and Service by explaining the novel approaches behind them, and that of CT MRI via a clinical case in the successful delivery of Stroke TIA care. We have also included the announcement of the UK Stroke Forum Conference where these topics were discussed.
If you did not receive the newsletter click here to read about our Stroke TIA solutions.
To register for receiving our newsletter click here.

Similar posts: cardiology

I flip out my cell phone and text a message to a friend living in Los Angeles. I write an e-mail to another friend: hes living in Arkansas, but he drives a big rig. I have no idea where he is, but hell read my e-mail on his laptop. I post on this blog and I receive comments from Canada, Great Britain, and even Australia.  Instant, worldwide communication is a wonderful thing.
I was born on a Tuesday, the doctors didnt detect my heart defect until Friday. There was no resource except the local library, and they had practically nothing.
No other survivors in the area. No support groups. No internet.
Every answer the doctors gave began with the words The books say We didnt have those books, and probably couldnt understand them if we did.
No Echos No MRI.
As my father has said, We were grasping at straws.
How in the world did parents raise a sick kid in the bad old days? Especially when there was next to nothing known about the illness? When it feels like you are just struggling in the dark, trying to find the light switch in a room that you have never been in before?
One of the few answers available is The best you can, but that is a throwaway answer. A platitude. Like the TV shows when the cop tells someone m sorry for your loss. - you know he probably doesnt mean it, or isnt truly sorry, but that is what is required of him. So he spits it out and everyone knows it is a false sentiment.
Our personal philosophy is that we live to fight another day. In fact, that has actually been said before: Albert Pacifico looked my father in the eye and told him I was bleeding profusely in the operating room. It was possible to continue the operation, but the outcome was liable to be bad. What would you have me to do? And my father told him to stop operating and get out the best he could. Wed live to fight another day.
The actual quote is He who fights and runs away will live to fight another day. That implies weakness the inability or the unwillingness to stand and fight. But really, it means that we pick the battlefield and the weapon. At that time - 1988 - daddy told the surgeon to get out, wed fight this battle on our own terms. Pacifico probably thought there was no battle left to be fought: You cant open his chest without massive bleeding, therefore no more surgeries. Now you can do some operative procedures without opening the chest and more are coming.
We choose the battlefield and we choose the weapons. I always choose a major medical center and a team of exceptional, never say quit cardiologists. Because when I fight, I refuse to fight fair.

Similar posts: cardiology

Heart diseases detected on second day of life
Valvular stenotic lesions or regurgitations
Coarctation of aorta
Cyanotic congenital heart disease
Breath holding spell
Breath holding spell has a precipiating factor which causes the child to cry incessantly and this is followed by breath holding. Breath holding does not occur abruptly. Child may become cyanosed after prolonged breath holding which may also lead on to seizures.
Williams syndrome
Williams syndrome is characterised by supravalvar aortic stenosis, elfin facies and hypercalcemia. Learning disability is often associated. Peripheral pulmonary stenosis is also an association. In supravalvar aortic stenosis, the right upper limb blood pressure can be more than that in left upper limb (anisopsphygmia) because the jet is directed towards the brachiocephalic artery. This is known as Coanda effect.
Differentiation of supravalvar aortic stenosis from valvar and subvalvular variety
Murmur of subvalvular aortic stenosis is unlikely to radiate to the carotids. Supravalvar aortic stenosis may radiate more to the right carotid. Ejection click is in favour valvular aortic stenosis. Supravalvar aortic stenosis is unlikely to be associated with aortic regurgitation, while it can occur in valvar and subvalvular variety.
Biventricular outflow obstruction in a child
Noonan syndrome can cause biventricular outflow obstruction due to hypertrophic cardiomyopathy and pulmonary stenosis.
Structural heart diseases associated with WPW syndrome
Ebsteins anomaly, hypertrophic cardiomyopathy, mitral valve prolapse
Causes of dynamic left ventricular outflow tract (LVOT) obstruction
Hypertrophic cardiomyopathy is the most important cause of dynamic LVOT obstruction. In transposition of great arteries (TGA) with intact interventricular septum LVOT obstruction due to systolic anterior motion of mitral valve (SAM) is possible. SAM can also occur transiently following surgery for aortic stenosis and mitral valve repair and cause LVOT obstruction. Dynamic LVOT obstruction is also described as a rare association with myocardial infarction possibly due to SAM. Dobutamine can worsen the LVOT obstruction in this situation.

Similar posts: cardiology

Heart diseases detected on second day of life
Valvular stenotic lesions or regurgitations
Coarctation of aorta
Cyanotic congenital heart disease
Breath holding spell
Breath holding spell has a precipiating factor which causes the child to cry incessantly and this is followed by breath holding. Breath holding does not occur abruptly. Child may become cyanosed after prolonged breath holding which may also lead on to seizures.
Williams syndrome
Williams syndrome is characterised by supravalvar aortic stenosis, elfin facies and hypercalcemia. Learning disability is often associated. Peripheral pulmonary stenosis is also an association. In supravalvar aortic stenosis, the right upper limb blood pressure can be more than that in left upper limb (anisopsphygmia) because the jet is directed towards the brachiocephalic artery. This is known as Coanda effect.
Differentiation of supravalvar aortic stenosis from valvar and subvalvular variety
Murmur of subvalvular aortic stenosis is unlikely to radiate to the carotids. Supravalvar aortic stenosis may radiate more to the right carotid. Ejection click is in favour valvular aortic stenosis. Supravalvar aortic stenosis is unlikely to be associated with aortic regurgitation, while it can occur in valvar and subvalvular variety.
Biventricular outflow obstruction in a child
Noonan syndrome can cause biventricular outflow obstruction due to hypertrophic cardiomyopathy and pulmonary stenosis.
Structural heart diseases associated with WPW syndrome
Ebsteins anomaly, hypertrophic cardiomyopathy, mitral valve prolapse
Causes of dynamic left ventricular outflow tract (LVOT) obstruction
Hypertrophic cardiomyopathy is the most important cause of dynamic LVOT obstruction. In transposition of great arteries (TGA) with intact interventricular septum LVOT obstruction due to systolic anterior motion of mitral valve (SAM) is possible. SAM can also occur transiently following surgery for aortic stenosis and mitral valve repair and cause LVOT obstruction. Dynamic LVOT obstruction is also described as a rare association with myocardial infarction possibly due to SAM. Dobutamine can worsen the LVOT obstruction in this situation.

Similar posts: cardiology

Imagine if every physician's internal billing department or cardiology billing company pursued every claim until it was paid in full. The payers would see their cost to adjudicate the claims rise and they would see their payments to providers rise because the lost/under paid claim games would no longer prevent providers from ultimately being paid. This combination would lead to each physician ultimately being paid quickly and without fuss because the insurance companies would lose significant money by playing games ($25 per extra phone call generated by the games) and they would gain nothing since payments would only be delayed, not avoided.

Similar posts: cardiology

Torcetrapib was the first cholesteryl ester transfer protein (CETP) inhibitor to be used in clinical trials. Even though it raised the HDL cholesterol levels and reduced LDL cholesterol levels, it failed to produce regression of atherosclerosis and increased all cause mortality. Two potential reasons have been suggested for the lack of benefit of torcetrapib. One hypothesis is that the HDL particles produced by CETP inhibition do not participate in reverse cholesterol transport. Another possibility is that torcetrapib has some toxicity that counterbalances the beneficial effects of increasing HDL cholesterol by CETP inhibition.
A recent substudy of the ILLUSTRATE (Investigation of Lipid Level Management Using Coronary Ultrasound to Assess Reduction of Atherosclerosis by CETP Inhibition and HDL Elevation) by Nicholls SJ et al sought to find out the reason by a subgroup analysis. They found that majority of the torcetrapib treated patients showed no regression of atherosclerosis as assessed by intravascular ultrasound. Regression was seen only with the highest levels of HDL cholesterol. Serum sodium levels were elevated and serum potassium lowered on torcetrapib treatment, indicating and aldosterone like effect. This may explain the substantially increased blood pressure in the torcetrapib treatment group. In fact the ILLUMINATE trial was stopped prematurely because of an increased risk of death and cardiovascular events in patients receiving torcetrapib. That study had shown a 72.1% rise in HDL cholesterol and 24.9% reduction in LDL cholesterol as well as 5.4 mm Hg increase in systolic blood pressure at 12 months. There was a decrease in serum potassium, and increases in serum sodium, bicarbonate, and aldosterone levels in the study. Further development of the drug (torcetrapib) was stopped following the study results. It is thought that other CETP inhibitors without this off target toxicity may produce regression of atherosclerosis. Even though the blood pressure was elevated in ILLUMINATE trial, stroke rate which is generally considered a sensitive indicator of the adverse clinical effect of rise in blood pressure, was not documented. So it is possible that torcetrapib has some unkown toxicity which deters its beneficial effect on regression of atherosclerosis by raising HDL levels.

Similar posts: cardiology

Heart.org today:
Physicians need to understand that using generics can have a real
impact on patient's survival and quality of life. "Lower-cost generic drugs, which are available for nearly every therapeutic drug class, can be a part of a medication regimen that leads to better patient adherence to important cardiovascular drugs. If patients aren't taking their drugs because they are expensive, and the economy is in difficult times, and they don't have full drug insurance, and they're doing that because they think they need a brand-name drug, that is a suboptimal outcome," Kesselheim stressed to heartwire. "To improve the clinical care of patients, we think that generic drugs should be a part of a physician's prescribing patterns. This study should give some reassurance to physicians that in the cardiovascular arena. There's no evidence that brand-name drugs are superior.

Similar posts: cardiology

Ventricular tachycardia in structurally normal heart constitutes about 10% of patients with ventricular tachycardia. Echocardiogram and coronary angiorams are normal in these cases, but MRI may show subtle abnormalities. Localized sympathetic denervation may be seen in some of them. Baseline ECG normal in many situations.
Following are the main types of ventricular tachycardia (VT) with structurally normal heart:
Right ventricular outflow tract (RVOT) VT
Left ventricular outflow tract (LVOT) VT
Idiopathic left ventricular tachycardia (ILVT)
Catecholaminergic polymorphic VT (CPVT)
Ventricular tachycardia in Brugada syndrome
Ventricular tachycardia in Long QT syndrome
The first three are monomorphic VT while the latter three are polymorphic in nature.
Right ventricular outflow tract (RVOT) VT
Right ventricular outflow tract (RVOT) VT is a wide QRS tachycardia with LBBB pattern and inferior axis. It occurs in third to fifth decade and consitutes about 90% of outflow VTs. There are two types - Nonsustained, repetitive variety and Paroxysmal, exercise-induced, sustained variety. Both are terminated by adenosine, in contrast from VT in arrhythmogenic right ventricular dysplasia (ARVD).
Exercise stress testing to is used to initiate and evaluate RVOT VT. Initiation depends on a critical heart rate which differs in each patient. MRI may show abnormalities of right ventricle in up to 70%, which include focal thinning, diminished systolic wall thickening, and abnormal wall motion.
Differential Diagnosis of RVOT VT
Differential diagnosis of RVOT VT include ARVD, Mahaim fiber tachycardia, AVRT using a right-sided accessory pathway and VT in patients after repair of tetralogy of Fallot.
Mechanism of RVOT VT
Intracellular calcium overload is thought to be the mechanism which enhances function of Na+/Ca++ exchanger, thereby increasing inward Na+ current and delayed after depolarisation which initiate tachycardia.
Role of adenosine, beta blockers and verapamil in RVOT VT
cAMP regulates intracellular calcium. Increased levels of cAMP will increase intracellular calcium levels.
Adenosine acts by lowering cAMP concentration. Beta-blockers act by inhibiting adenylate cyclase which mediates the synthesis of cAMP. Verapamil has its action by inhibiting L-type Ca++ channels.
Treatement of RVOT VT
Beta-blockers, Verapamil or diltiazem can control RVOT VT with about 25% to 50% efficacy. Class IA, IC, III including amiodarone have been tried in the treatment of RVOT VT. Radiofrequency catheter ablation has cure rates of 90% and is the preferable option, given the young age of patients with RVOT VT.
Left ventricular outflow tract (LVOT) VT
Left ventricular outflow tract (LVOT) VT is characterised by S waves in lead I, and R-wave transition in V1/ V2 and constitutes about 10% of outflow VT. There are two varieties of LVOT VT -supravalvular and infravalvular. Absence of S wave in V5/V6 is suggestive of supravalvular origin, while the presence of S wave in V5/V6 indicates infravalvular origin.
Ablation of LVOT VT
There is a risk of left main coronary artery (LMCA) occlusion while ablating LVOT VT. Hence coronary angiography before, during and after ablation is recommended. The ablation catheter tip has to be kept 1 cm away from the ostia of the coronary arteries.
Idiopathic left ventricular tachycardia
Idiopathic left ventricular tachycardias (ILVT) are verapamil-sensitive intrafascicular tachycardias. Three types are described: RBBB, left-axis pattern - originating from left posterior fascicle (90 - 95%); RBBB, right-axis pattern - originating from left anterior fascicle and left septal fascicular tachycardia with normal axis. It is seen in 2nd - 4th decade and more in men (60%-80%).
Treatment of ILVT
ILVT can be terminated with intravenous verapamil. Long-term therapy with verapamil is also feasible.
Radiofrequency catheter ablation is highly effective (85%-90%) in those with severe symptoms.
Identifying the focus of ablation can be achieved by the recognition of Purkinje potential, late diastolic potential, or earliest ventricular activation.
Purkinje potential
Purkinje potentials are high frequency, short duration, potentials preceding the QRS complex. They are also called P potential and diastolic potential. Purkinje potentials can be recorded both in sinus rhythm and during VT. Pacing at sites of earliest P potential produces QRS identical to that of the clinical tachycardia. They occur 30 to 40 ms before the VT QRS complex.
Primary ablation of ILVT
Primary ablation of ILVT has been suggested by some authors because fascicular VT is sometimes difficult to induce despite pharmacological provocation. Primary ablation has a higher success rates, lesser procedure time, lower fluoroscopy time and requires lesser number of RF energy deliveries.
Catecholaminergic Polymorphic VT
Catecholaminergic Polymorphic VT (CPVT) is a bidirectional polymorphic VT, which is induced by exercise or catecholamine infusion. Family history of premature SCD / stress-related syncope is obtained in one third of the patients. Exercise or acute emotion triggers the syncope in CPVT. Symptoms typically manifest in childhood. CPVT has a genetic basis with three types of mutations being described. Ryanodine receptor 2 (RyR2) mutation is transmitted as an autosomal dominant trait, while calsequestrin (CASQ2) mutation is transmitted as autosomal recessive variety. Ankyrin B mutation has been proposed as a second form of autosomal dominant variety.
Treatement of catecholaminergic polymorphic VT
Beta-blockers are the preferred therapy in CPVT. ICD may be required in 30% of patients, but a word of caution is needed since there is a risk of electrical storm with ICD discharge which can cause an emotional strees and a vicious cycle of CPVT and shocks.
Ventricular tachycardia in Brugada syndrome
Brugada syndrome is characterised by an apparent RBBB pattern with ST elevation in V1 to V3, associated with life-threatening cardiac arrhythmias, typically polymorphic VT. There is a tendency for familial occurrence and it is associated with SCN5A mutation, with a loss of function. Loss of the action potential dome in the epicardium but not endocardium causes the right precordial ST elevation in Brugada syndrome.
Ventricular tachycardia in Long QT syndrome
There are at least seven genotypes of long QT syndrome. Phenotypically LQT1 has broad-based T waves with indistinct onset while LQT2 has bifid T waves and LQT3 a long isoelectric ST segment.
Treatment of LQTS
First and foremost in the treatment of long QT syndrome is the excludison of acquired LQTS, which is much more common. Avoidance of QT prolonging drugs is essential. Beta-blockers are the most useful therapy in LQTS. Surgical sympathectomy is rarely done these days. Oral potassium may be useful in some cases. ICD placement, along with beta-blocker therapy is the best option for secondary prevention in a case of long QT syndrome with history of arrhythmic syncope.

Similar posts: cardiology

Commotio cordis is the term given to sudden arrhythmic death due to blunt chest wall trauma. Death is almost instantaneous and the victims are in ventricular fibrillation. Usually there is no structural damage to the heart or thoracic structures. Impacts which occur in the vulnerable phase of ventricular repolarisation just before the peak of the electrocardiographic T wave result in ventricular fibrillation. Rapid rise in ventricular pressure due to the impact possibly causes activation of ion channels by mechano-electric coupling. This causes a ventricular ectopic beat which triggers ventricular fibrillation. Commotio cordis has to be differentiated from contusio cordis in which there is direct myocardial tissue damage and damage to overlying structues of the chest due to a high velocity projectile impact. United States Commotio Cordis Registry instituted in 1996 has collected over 180 cases. Generally commotio cordis is caused by impact by a ball with a dense solid core like base ball. Balls with non-solid core tend to collapse on contact and absorb most of the impact energy so that commotio cordis is quite rare with impact by an air filled soccer ball.
Commotio cordis is more likely to occur in younger individuals, possibly because of greater transmission of the impact energy by a compliant chest wall. Only 28% of cases in the United States Commotio Cordis Registry were over 18 years and the oldest victim was 44 years old. Resuscitation is often difficult in commotio cordis with overall survival of only 15%. An excellent review on the pathophysiology of commotio cordis by Christopher Madias and associates is available, free full text online [Indian Pacing Electrophysiol. J. 2007;7(4):235-245].

Similar posts: cardiology

Coarctation of aorta is a narrowing in the proximal descending aorta. It can be a discrete narrowing or a tubular one. Usual site is opposite the erstwhile ductus arterious and it is thought to be due to an extension of the process of natural closure of the ductus to the aorta. The usual location is post subclavian though it can be before the origin of the left subclavian. When a patent ductus arterious is associated with coarctation of aorta in a child, the coarctation can be easily missed as the lower limb pulses may not be feeble as in isolated coarctation. This is because the ductal ampulla opposite the ductus reduces the narrowing of the aorta. In a neonate with severe coarctation, symptoms may start with the spontaneous closure of the ductus.
The important physical findings of coarctation are the delayed demoral pulses (brachio-femoral or radio-femoral delay) and the collateral pulsations in the region of the scapula. Systolic or continous murmur may be heard at over the site of the coarctation at the back. Findings of associated bicuspid valve with aortic stenosis or regurgitation may also be noted.
Electrocardiogram may show left ventricular hypertrophy due to the hypertension or associated aortic stenosis. X-ray chest shows the characteristic rib notching of the lower borders of 3rd to 8th ribs due to the erosion by the tortuous posterior intercostal arteries. The notchng is not seen in small children. It becomes more prominent as age increases and the sclerosis at the edge of the notch makes it quite visible. Rib notching is not seen in the upper intercostal spaces as both the posterior and anterior intercostal arteries arise from the high pressure zone proximal to the coarctation, while in the lower spaces, the posterior intercostal arteries arise from the low pressure zone below the coarctation. Unilateral rib notching occurs in presubclavian coarction, on the right side only as both anterior and posterior intercostal arteries will be in the low pressure zone in this case. Collateral pulsations may be felt posteriorly in the region of the scapula.
The natural history of unrepaired coarctation of aorta is poor and is charcterised by aneurysm formation / dissection of the aorta, hypertension, heart failure and premature coronary artery disease. Even individuals whose coarctation has been repaired are more prone for hypertension and coronary artery disease.
The important methods of repair are by patch aortoplasty, either resection and anastomosis or subclavian flap angioplasty. Alternatively, a bypass graft can be used to bypass the obstruction.
Interventional treatment in the form of balloon dilatation and stenting are becoming increasingly common, though it is ideal for re-coarctation after an initial surgical repair.

Similar posts: cardiology

MarketingHire.com features marketing jobs including many Fortune 500 marketing jobs from Disney, Unilever, Google, eBay, GE, Dell, Accenture, Progressive, Newell Rubbermaid, Hewlett Packard (HP), Dow Jones, Abbott, Shell Oil, Intuit, Yahoo, Comcast, US Cellular, Dyson, Eddie Bauer, FedEx, General Motors (GM), Gap Inc, Priceline, Sony, Watson Wyatt, KPMG, Kellogg, Prentice Hall, Philips, Del Monte Foods, CDW, J Walter Thompson (JWT), Honda, L'oreal, Dominos, LexisNexis, Time Warner, Blue Cross/Blue Shield, Capital One, Western Union, Young and Rubicam, Bosch, McGraw-Hill, March of Dimes, AHA, NBA, Coors, Hilton, HSN, Victoria's Secret, DHL, Sith Barney, Maidenform, Godiva, Transunion, TV Guide, Boise Cascade, Williams Sonoma, JP Morgan, Charles Schwab, Equity Office, Motorola, Dyson, HR Block, Vanguard, Yamaha, Thomson, The American Red Cross, Sage Software, Bacardi, Georgia-Pacific, Siemens, Malt-O-Meal, Virgin, Marriott, Princess Cruises, Booz Allen Hamilton, John Hancick, Amp'd Mobile, Merril Lynch, McCann Erickson, Visa, Jockey International, United Airlines, Harte Hanks, Wells Fargo, Home Shopping Network (HSN) ...Search current marketing jobs to find out who's hiring now.

Similar posts: cardiology

Caden goes today to the cardiologist. Since I have to miss half a day of work tomorrow, Paul is trying to convince me that he can do it by himself. Well, I believe that both of them will survive, but if any of you have ever been through an ECHO with a near 2 year old, it's not fun! I'm hoping that this time, he handles it better than the last few times. He just hates that goop all over him, and she has to push that wand thing into that dip his collar bone, pointing down, to see the top of his heart. That's usually the last thing they do, but let me tell you, it's the grand finale.

The appointment starts at 3:30, but first they have to weigh him, and she comes in to ask a bunch of questions... ie: "does he pass out, does he sweat a lot, does he seem to be sleeping more than usual..." Yada yada yada. I know that some parents may not pay too close attention to that stuff, but you bet your butt if he started showing signs of heart failure, I'd be in there before his normal appointment was scheduled!!!

Anyway, then she has to listen to him, feel for his liver, push on his chest a bit (not hard), blah blah blah. Then we go to a different room, where they pull out the ancient TV and VCR. The nurse gives him an EKG, the doctor comes in a few minutes later, looks at it, then turns off the lights to do the actual ECHO. Well, Caden might not take it so bad if he didn't have to watch the same Barney video over and over again. But, last time we remembered his blankie, and he did better having that to rub on his face. He just hates to lay there so still for that long. Usually by the time they're done with the EKG and the ECHO, it's been about an hour or so of him laying there. That's not easy for any of us, especially Caden!

I haven't decided if I'm going to leave a little bit early today or not. Maybe if I take a really short lunch, then it'll make up for it. The ECHO won't start till 4:00-ish, so if I leave at 4, then I'll only miss one hour today. Then I'll miss three hours tomorrow. Maybe nothing else will come up the rest of this week. Cross your fingers for us!!.

Similar posts: cardiology