Welcome back to our wonderful journey into History of Pediatric Cardiology.

How many of us can understand the term, “cor biatriatum triloculare”? I think all of us should be indebted to this term. For, it started the scientific journey of Pediatric cardiology in the dawn of 20th century. One such heart was cooling in the shades of dilapidated museum of McGill Medical school at Canada in the turn of 19th to 20th Century. This specimen of heart dated back to AD 1824 and was there only because it was donated to the collection by the first dean of McGill Medical School, Dr Andrew Holmes. The story of how this specimen led to the development of the science of congenital cardiology is quite exciting. Read on..

By the end of 19th century, after much controversy, McGill medical school took its first women candidate for studying Medicine. This lady, despite having had a brilliant academic career till then, was flatly refused admission due to her gender. She fought for her admission and finally made it to become the first lady doctor from McGill. When she applied for a position in the same medical school, she was appointed as the assistant curator of medical museum in AD 1898, largely because nobody else wanted this job. The museum was a disorganized collection of huge number of specimens collected over 75 years. Although some medical data always accompanied the specimen, it was usually stocked with some rubble, quite away from the specimen itself. It would have been maddening and thankless job. No one cared how the museum was.

Kudos to this gutsy lady, she started cataloging the specimens carefully and did a wonderful job. One specimen titled “cor biatriatum triloculare” confused her. She decided to consult Dr William Osler, the ‘Chief’ of McGill. Dr Osler was a phenomenal figure and was knighted by the Queen. On the description of the said specimen by the assistant curator, he immediately identified it and ranted out some history of the specimen. This specimen belonged to a man who died at the age of 22 years in AD 1824, collected to the museum by the first Dean of McGill medical school and reported in Edinburgh Medical Journal. It had two atriae but both AV valves drained into the same ventricle. The other ventricle was reduced to a “nonentity” at the upper right end. The posteriorly located aorta sprung from the main ventricle and the anteriorly located Pulmonary Artery from the diminutive cavity representing the other ventricle.

Either taken away from the charm of Sir Osler, or due to a spring of inspiration from her own innate brilliance, the assistant curator searched for the original article and re-did the article along with her etchings in the McGill Medical Journal in AD 1901. She did an extraordinary cataloging of the specimens of museum, making it a place worth a visit for all the students and faculty. In AD 1904, Sir Osler visited McGill museum and was spellbound by the beauty with which it had metamorphosed in the hands of its assistant curator. He told the Dean of McGill that the museum was “the best that McGill had done to date…there was no collection in North America or Britain that came close to it”. So impressed Sir Osler was, that he asked the young lady doctor to write a chapter for his Magnum Opus, “Systems of Modern Medicine”. She was the only woman contributor in the list of 104 authors. And what a work she did! In a 100-page chapter, she had evaluated 400 cases and correlated the clinical findings with the autopsy reports. Sir Osler wrote a thank you note to her, saying… “It is by far the best thing ever written on the subject in English – possibly any language… For years it will be the standard work on the subject…” She returned the compliments by naming her McGill museum catalogue as ‘The Osler Catalogue’. Although her biographers differ, this was possibly the moment of inspiration for her monumental Atlas.

Her “Atlas of Congenital Cardiac Disease” was published by American Heart Association in AD 1936. The Atlas described 1000 hearts with their pathophysiological and statistical analysis of the clinical and anatomical abnormalities. The frontpiece of the Atlas had Portraits of Senac, Morgagni, Peacock, Rokitansky, and Sir Arthur Keith, demonstrating her gratitude towards the history of the field.

She wrote the following note in the introduction of the Atlas: “This volume presents, in a somewhat unusual form, a pictorial retrospect of the author’s personal experience in what may be considered a specialized field of clinicopathological research. A first-hand knowledge of the exact morphology of a large range of cardiac anomalies obtained in the first place through an intensive study of the rich material accumulated under the author’s care as Curator of the Medical Museum of McGill University, has been continuously applied and amplified through more than three decades of activity, by observations of congenital heart disease in the wards and autopsy rooms of many great hospitals both at home and abroad.”

In bringing order to what had previously been a disorganized array of fascinating, but poorly understood, congenital malformations of the heart, she divided these patients into three groups: Those with no abnormal communications, those with a left-to-right shunt (acyanotic), including patients with shunt reversal later in life (cyanose tardive), and those with permanent right-to-left shunt (Morbus coeruleus). For each she developed a diagram of the circulation.

Recognizing the importance of preventing these malformations, she developed the following 6 “ever-pertinent” questions to learn their etiology.
1. Did the abnormality result from a fault in the germ plasm?
2. Was the abnormality inherited?
3. Did the abnormality occur because of a change in the environment of the embryo in utero?
4. Was the abnormality a result of maternal disease?
5. Was the abnormality due to fetal trauma or a uterine disorder?
6. Did a disease affecting the early embryo cause the abnormality?

It is probably the time to remember the person who provided an impetus for our modern understanding of the etiologies of congenital heart disease. Called by various names as “The beneficent Tornado”, “The Saint”, “The big chief of Heart” etc, but I personally prefer to call her the “God-Mother” of Congenital heart diseases. We are referring to Dr Maude Elizabeth Abbott. The “cor biatriatum triloculare” that we spoke of at the start of this session is today known as the “Holmes’ Heart”. It is probably very important for every student of Congenital Cardiology to know the background, which this heart has provided for this science and the person who made it possible for all of us.

The coming 2nd of September commemorates the 69th death anniversary of Dr Maude Abbott. In view of many authorities on the subject, if we have to name one keystone person for the development of Congenital Cardiology, it would be Dr Abbott. Please vote your views after reading today’s piece again!

March 18th happens to be the birthday of Dr Maude Abbott. I personally wish to see every hospital delivering Congenital Heart care to celebrate this day meaningfully.

(Ref: Abbott ME. Atlas of Congenital Heart Disease. New York, NY: American Heart Association; 1936

MacDermot HE. Maude Abbott. A Memoir. Toronto, Canada: Macmillan; 1941

Wiglesworth FW. Maude E. Abbott.Perspect Pediatr Pathol. 1984;8:291-294)

Next time, lets see the history of Pediatric Cardiology in the first half of 20th century.

On a personal note, we at Narayana Hrudayalaya are witnessing a change in the state of affairs. New branches are coming up. The Health city is progressing. New cases of Novel H1N1 are getting diagnosed! In next few weeks we shall come with new developments and their repercussions.

Hearty congrats to our chairman, Dr Devi Prasad Shetty, for having named as a member of National Human Resource Commission, led by the Prime Minister himself. It is another feather in the cap of Dr Shetty, who can do wonders given the right position at any level – National or International. Many states of India now are trying to replicate our Yeshaswini scheme and getting advice from him.

We never cease to learn; all that is required is to keep the senses open. Our weekly Cath meetings are always filled with new outlooks, new discussions and learnings. It is wonderful to be a part of such illuminating brains that can think laterally so well.

How to proceed in a case of {S,L,L} dextrocardia, Ebsteins anomaly, juxtaposed atrial appendages, Severe PAH in a 9 month old child? Though the ventricles are of good size, juxtaposed appendages are an impediment for double switch. Can we consider PA banding? Would it be final palliation? Is Senning/Mustard cannot be done in any case of juxtaposed atrial appendages? Let me know your views on it.

What to do if a clot gets totally organized to an atrial wall? On echo, it does not show any sign of movement. How to make sure that patient would have no problem with this at home? How does such things generally behave?

When we are balloon opening a tight aortic valve, should we start with 80% balloon size to begin with? Or should we start with a smaller balloon and progressively dilate the valve? Any comparative trails or personal experiences?

Is there a role of DC Cardioversion in cases of chronic tachycardia induced cardiomyopathy? We saw a 10-year-old girl, who was diagnosed as Dilated Cardiomyopathy and referred. We saw 6-month old ECG traces showing a ventricular rate of around 300/min with SVT pattern. This girl hardly has any LV contraction. She is currently on life support measures. Is it terminal? Can the situation be improved? This girl emphasized the need for a good training of physicians in the peripheries in identifying simple problems and timely advice. Lest, this is what we would witness time and again.

Dr Amol Morey, who was with us for a 6-month training has gone back to Australia. He shared an interesting case scenario with us. I would like him to be a part of our team from that distance to contribute his overseas experience. Thanks Dr Amol, for that update.

I am off to a medical camp at Ranibennur, a small town about 7 hours from Bangalore. I shall narrate my experiences next time.

Let me know your comments. I am yet to receive any response from our PITU team on their postings. I hope to get it soon and let you know about it.

Regards

Kiran

Before we start this session of our Voyage into History of Pediatric cardiology, I have a small disclaimer to make!

I had some criticism from some readers that the details on Dr Thomas Peacock were too exhaustive. Few argued that brevity is the soul of interesting writing. So, I felt I should make this clarification.

I was interested in giving some details on works of Dr Peacock, more than as a passing reference. When I searched Wikipedia for some details, there was no write up on this person who contributed so much to the science of Congenital Cardiology. It was painful.

I would like to quote Dr Miguel A. Chiong of Queen's University Kingston, Ont. “We don't remember our medical heroes, but, as everyone knows, most of us mortals need to be reminded of most things most of the time. Since medical history is at the bottom of the medical curriculum, there is no curiosity or incentive to find our medical roots, and the young grow woefully unaware of those on whose shoulders they now stand…. Perhaps it should be the task of departments of medical history across the country to remind the medical profession of its forgotten or almost forgotten heroes so we can pay our respects on time!” I felt Dr Peacock is one such forgotten hero.

(Ref: CAN MED ASSOC J 1990;143 (10) 995)

The history of a period happens by references of the era and the persons who made the era memorable. However, old times have to be gauged by works, as reliable biographies of the people who made them are not available. But, in case of living memory, a biographical sketch of a person adds up to the work of the period. As Booker Washington once quoted, it is not only the achievement of a person that carries importance, but the circumstances through which the person had to pass to achieve the glory. So was my decision to write some extra stuff on Dr Peacock. I intend to follow this style for future references too. If the readership feels that the details are asynchronous with the spirit of flow, then I shall cut short.

With this, lets continue our journey!

The publications of Dr Thomas Peacock arouse a great deal of interest in the professional circles and prompted more physicians to look for congenital heart diseases. The blue babies aroused interest but no one kept a sustained interest, as no available treatment was effective. Even then few sustained their interest. One among them was a big name then and a bigger name now! He is Etienne-Louis Arthur Fallot, the same person on whom the tetralogy is eulogized.

Fallot taught pathological anatomy to students. In AD 1888, he coined the term “tetralogy” and clarifies the concept of a cardiovascular malformation with four distinctive characteristics that today is universally known as the tetralogy of Fallot. He had no wish for this lesion-complex to be named after him; nor he made any statement about him ‘discovering’ this entity. He studies 3 cases personally and exclaimed that it was a ‘happy hazard’ for him to have witnessed this rare and curious lesion thrice over few years duration. After a description of his findings in Part 1 of his article, Fallot reviewed the available literature on this lesion in Parts 2 to 6 of his work. Apart from 3 cases seen by himself, Fallot nicely reviewed and summarized 68 other cases of blue disease, whether or not they had tetralogy. Fallot referred to and summarized the first known case of Stenson (Steno) in AD 1671, the second known case of Sandifort in AD 1777, the cases of Hunter in AD 1784 and many more.

In his own words, “Blue disease had hardly been described clinically when the cardiac alterations which caused it were simultaneously established. Knowledge of the symptoms and lesions have, one might say, marched together. It is sufficient to go over the observations of Hunter, Sandifort, Duncan, and Pallois, etc to find indicated here in a fashion most clear and detailed, our pathologic anatomic tetralogy: stenosis of the pulmonary artery, interventricular communication, hypertrophy of the right ventricle, and deviation of the aorta to the right. One asks oneself why a group of facts so numerous and of such demonstrable value has not already become established in science. Above all, one has trouble in comprehending how, despite the opinion of Gintrac, Senior, and of Cruveilhier, it has been possible for this belief, so profoundly erroneous, to be born, to grow, and to develop to the point of becoming almost universal: the belief that blue disease is linked to failure of the hole of Botallo to close (the foramen ovale)”

Fallot never applied his name to tetralogy. He never wished to, as he knew he was not the first to describe it. He wanted to call this condition la maladie bleue, i.e., the blue disease, or morbus caeruleus (in Latin). Till his death in AD 1911, the lesion-complex did not bear his name. It is to the credit of Maude E. Abbott, who coined the diagnosis “tetralogy of Fallot” in AD 1924, probably for the sake of convenience!

(Ref: Fallot A (1888) Contribution a l’anatomie pathologique de la maladie bleue. Marseille-Medical 25:77-93, 138- 158, 207-223, 270-286, 341-354, 403-420 (in 6 parts)
Abbott ME, Dawson WT (1924) The clinical classification of congenital cardiac disease, with remarks upon its pathological anatomy, diagnosis and treatment. Int Clin 4: 156-188
Allwork SP (1988) Tetralogy of Fallot: the centenary of the name, a new translation of the first of Fallot’s papers Em J Cardio-thorac Surg 2:386-392)

Next time we shall see further developments of end of 19th century and beginning of 20th century.

On a personal note, it was a pleasant experience for me to have delivered a talk at Hassan, a town located about 200 km from Bangalore. It was a satellite CME, in collaboration with ISRO at their Master Control Facility auditorium. The CME was uplinked using the Edusat (Indian satellite dedicated for educational purposes) facility. It could be downlinked by any person or institute who has a small dish antenna to capture Edusat signals, totally free of cost. The CME also had star speakers like Dr Krishnakumar and Dr Zulfikar Ahmed. An added incentive was our visit to the world-famous temples at Belur and Halebid. After visiting the temples and witnessing the splendor of architecture, we wondered if these are any less than Taj Mahal. Yet, it pains to see the neglect of them by our system. Tourism has so much potential in India. Why is that the private sector still not attending to such things? Few “good for nothing” rock formations at west are given such a hype that we travel across continents to see them. But, we forget the million times more magnificence at our backyard, just because we care a damn for our own culture! I feel few entrepreneurs should put their hands together to glamorize our own symbols of splendor to draw our own folks to it! I bet it would be reaping them the moolah in no time.

I should mention a word about the Pediatric fraternity at Hassan. For a small branch of around 20 members, Hassan branch of IAP has been awarded “Best IAP branch of country” for 3 years in succession! Their way of conducting the satellite CME was amazing. They are showing how to integrate the technology to spread good among the masses through out the country. They do not see the audience directly during CME, as it is beamed through satellite. Yet, their impetus does not wither. There are no applause or “pats on back”. But they don’t care for the acknowledgement. They conduct the CMEs for the greater benefit of Doctors across country, with no expectations. I think, they exemplify the social commitment of our fraternity, with no returns. In fact, they spend money on transport, accommodation and hospitality of all speakers, all at their own cost. Kudos to Dr Dinesh, Dr Sudhir Bangalore, Dr Lakshmikanth and others for their service to Medical community of India. I wish many more years of “Best IAP branch of the country” award for them in future.

Situs ambiguous never cease to surprise a Pediatric Cardiologist! How many variants are possible? I think there is no such number. We saw common AV valve with TAPVC with pulmonary atresia with Situs ambiguous. We had recently seen cTGA with d-malposed great vessels with ambiguous situs. Another combination was criss-cross ventricles with VSD with situs ambiguous. It is fascinating to deduct them sequentially and make the defect unravel and managable. I wonder how anyone would have managed these before the “Sequential Analysis” pattern of van Praagh!

In any criss-cross ventricle, should the patch closing a VSD pass though the axis of AV valves? In that case, does every VSD of criss-cross ventricle not closable? What does the literature say? Any inputs? Please let me know.

In a sequential lesion, how to assess the relative importance of individual lesions? We had an infant with multiple VSDs with Supramitral membrane and closely placed papillary muscles. The MS gets overestimated and VSDs get underestimated. Our surgeons felt that the mitral valve may be unmanageable and closing VSDs alone may not be fruitful. It was the sheer logical approach of Dr Sejal Shah, which prompted them to open up the supramitral membrane and correction of VSDs, without touching the mitral valve per-se. The infant is recovering well, with minimal gradient across the mitral valve. Great go indeed!

Has anyone had any experience with spontaneous closure of a mild LV to RA jet in a postoperative VSD closure? How do these lesions behave? If anyone has any data or reference, please let me know.

Our PITU team is interested in posting their experiences in this blog. We have perhaps the largest Cardiac PITU in the world, with atleast 80 beds and equally massive and varied challenges! The inputs might be very informative for all interested in Pediatric Cardiac care. I welcome the move with all earnestness. This would definitely enhance the gravity of content in the blog. May be, from next few posts, one can read a substantial amount of our PITU experiences too. I would certainly invite our surgical team also to share this platform for posting their views. But as of now, they are not finding enough time to do so. May be, sometime in future.

Please send in your inputs. If anyone has anything interesting to share, either post a reply or send the info to my mail drkiranvs@gmail.com I shall post the content on your behalf.

Regards

Kiran

Welcome back to our fascinating journey via the historical course of Pediatric cardiology.

It would be unjust not to write more about the towering figure of Thomas Bevill Peacock. No other name appears with such consistency as this in the monumental textbook called “Clinical Recognition of Congenital Heart Diseases” by Joseph K Perloff. Dr Perloff’s eye for historical details is a phenomenon by itself. That naturally endears the reverence for Thomas Peacock.

Thomas Peacock was writing in an era when Cardiology was gaining grounds. The first authentic English text in Cardiology was published in AD 1809 by Allan Burns of Glasgow. It was titled, “Observations on some of the most Frequent and Important Diseases of the Heart”. He gave neat and clear descriptions of cardiac murmurs. His classification of the heart disease was in three categories: (1) Sympathetic, deriving from other organs of the body, (2) 'Malformations' or Congenital defects, and (3) Organic diseases of the heart. Peacock’s contemporaries also included people like Stokes, Graves, Corrigan and Cheyne who extended the knowledge of physical signs and revived interest in treatment of heart ailments.

Peacock’s inspiration for heart ailments and motivation to write about them probably came from two contemporaries of his: James Hope, who in AD 1831 published “A Treatise on the Diseases of the Heart and Great Vessels” and Peter Latham, who was a known authority on Rheumatic Heart Disease. Latham’s “Lectures on Subjects Connected with Clinical Medicine Comprising Diseases of the Heart” published in AD 1845 remains both epigrammatic and entertaining. Between AD 1846 and AD 1862, Peacock worked on Cardiology related issues. His works spread across: Dissecting aneurysm of aorta, Valvular heart disease, Congenital heart disease, and Measurements of the normal and diseased heart.

Peacock’s Magnum Opus was published in AD 1858 and was titled, “On Malformations of the Human Heart”. The book started as a compilation of series of lectures that he gave to the students of St. Thomas's Hospital in AD 1854. The era had evoked a great interest on Congenital Heart Disease. Hence, he published them in the Medical Times and Gazette which had a great response from medical fraternity. After careful revision and greater elaboration, he produced the book. The period had an incomplete anatomical and physiological knowledge on the subject. One can imagine problem of classifying the many unexplained defects that were being set up in to an orderly arrangement. For example, the cause of cyanosis was completely unknown at that time and as previously described (see the previous post), Peacock held a strong opposition to the admixture of blood as the cause of cyanosis. He had firmly believed that the cyanosis was due to venous stasis and obstruction to the flow. Peacock came up with a novel idea to solve the problem of classification: He combined an anatomical with embryological classification. This is very evident from the book’s “Table of Contents”.

His account of “Fallot’s Tetralogy”, 42 years prior to Fallot’s description is indeed interesting. It goes something like this:
MALFORMATION OF THE HEART, CONSISTING IN CONTRACTION OF THE ORIFICE OF THE PULMONARY ARTERY WITH DEFICIENCY AT THE BASE OF THE INTERVENTRICULAR SEPTUM.
In this case there existed extreme contraction of the orifice of the pulmonary artery, with a deficiency in the interventricular septum, and the aorta arose in chief part from the right ventricle. The right auricle and ventricle were of large size, and the walls of the latter thick and very firm. The left ventricle was, on the contrary, small, and its walls thin and flaccid. The left auricle was also small. The foramen ovale and ductus arteriosus were both closed. The heart was taken from a child two years and five months old, who had exhibited well-marked symptoms of cyanosis, which commenced three months after birth. It was remarked that though the recorded cases are numerous in which, with more or less contraction of the orifice of the pulmonary artery, the septum of the ventricles is found deficient, it is far from frequent to meet with these malformations, with, as in the present instance, a closed state of the foramen ovale; and especially so, when the degree of contraction of the pulmonary artery is extreme. The intensity of the cyanosis, and the duration of life in these cases, bears a general relation to the amount of contraction of the pulmonary orifice and the freedom of communication between the right and left cavities of the heart, through the medium of the open foramen ovale and the aperture in the interventricular septum. Dr. Peacock, 7th of December, 1846.

Peacock makes many interesting observations: the difference between valvular and infundibular type of pulmonary stenosis, pulmonary valves often becoming the seat of subsequent disease, “and display recent deposits or vegetation . .. in some cases, indeed, the obstruction is mainly due to warty growths from the valves”.
Peacock also noticed the susceptibility of congenitally abnormal aortic and pulmonary valves to chronic inflammatory changes.

In 186o, Peacock reported a case to the Pathological Society, which had the features of Infective Endocarditis. The comments at the end of the report reads as following:
The great interest of the case Dr. Peacock considered to be:
1. The existence of disease both in the aortic and mitral valves, which had been manifested by distinct physical signs, so that a correct diagnosis had been effected during life.
2. The musical character of the murmur heard at the base with the diastole of the heart, and which was clearly traceable to the loose retroverted edge of the posterior semilunar valve.
The great concern with which the physical signs can lead to a correct anatomical diagnosis without any mention of the etiological possibilities is the point of concern here, considering the time when etiological diagnosis was not easy.

Peacock’s contribution to Valvular heart disease was equally noteworthy. However, it should be noted that Peacock was not an exclusive cardiac physician. He was more of a general physician with special interest in pathological anatomy. His name remains remembered even today in Cardiology for his exhaustive observations, deep interest in understanding the new concepts, the orderly fashion in which he arranges the details and his beautiful and masterly illustrations. In Maude Abbott’s words, “The first comprehensive study, covering the whole field and reviewing the earlier literature may be said to be Peacock's, which remains a classic and is still the leading authority in English upon the subject”. Considering Abbott’s contribution to this field, these words stand as the testimony of Peacock’s contribution to the subject of Pediatric Cardiology.

The end of Thomas Peacock was probably as he wished for it: on 30 May 1882, at the age of 70 years. It happened in the St. Thomas's Hospital, which he had served for 28 years and had retired as the Dean. After having attended a lecture by James Paget, he was accompanying some friends, to whom he was proudly showing the hospital. “He fell down in one of the corridors and was carried into the ward to which he had formerly been physician, and died that same evening in the very place which probably in health he would have chosen to die.” It was probably the way our ancient Indian seers wished to end the present journey of life. Peacock was a seer in all the respects, including the end.

(Ref:
Peacock TB. On Malformations of the Human Heart. London, J. Churchill, 1858.

ABBOTT, M. E. Congenital cardiac disease. In Osler, Sir William, Modern Medicine, vol. IV, Philadelphia and New York, Lea and Febiger, 1908.

Malformation of the heart, consisting in contraction of the orifice of the pulmonary artery with deficiency at the base of the interventricular septum.
Trans. path. Soc. Lond., 1846:8;52

Malformation of the heart. Stenosis at the commencement of the conus arteriosus of the right ventricle and at the origin of the pulmonary artery; aperture in septum ventriculorum and aorta arising partly from right side; foramen ovale and ductus arteriosus closed. Cyanosis. Trans. path. Soc. Lond., 1875-6, 27, 131-6

Retroversion of one of the aortic valves, and destruction of some of the chordae tendinaea of the mitral valve. Ibid., 59-61

BRISTOW, J. S. Obituary of Dr. T. B. Peacock. St. Thos. Hosp. Rep., 1882, 12, 1, 79

Flaxman, N. Peacock and congenital heart disease. Bull. Hist. Med., 1939:7;1061-1103)

Next time, we shall see further progress of the field in 19th century.

On a personal note, it was a pleasant surprise for me when the issue of this blog was discussed in one of our academic sessions. The ever-dependable Dr Vishal Changela (who also happens to be one of the very first followers of this blog), vehemently and passionately advertised my blog to the team in words, which I could probably not have bettered. His rhetoric was so convincing and pressing that the blog had many new visitors and few new followers. I also got the suggestion to post-script all my email communications with the blog id. It is indeed a good thing. Hope the list of people who read this blog grows!

How to approach an infant with ASD, Ebstenoid TV and PDA, in which the PDA shunts bi-directional? Even when infant desaturates a bit, closing PDA should not be a problem, as ASD can still tackle the PAH. Is there a role of cath study for operability? Our team had a split opinion on this. What is your take? Please send them.

Does {S,D,L} DORV with subaortic VSD always needs a homograft? On Echo, it looks as if routing the VSD to Aorta would solve the problem. But the surgeons, (who would obviously think in 3D) feel that doing such a thing would isolate PA from RV. This is because the aorta is anterior and the patch closing VSD would come in the way of RV to PA path. Anyone has any experience in this regard? Please let me know.

In refractory VF, how many DC shocks are permitted? I don’t know if there is a fixed upper limit. The objective would be to save the patient rather than count the numbers! However, we had an interesting discussion on this today, brought up by our fellow, Dr Karunakar.
As per the PALS guidelines, 3 shocks are mentioned. What if patient does not revert with this? There are always instances of multiple shocks, nearly charring the skin of patient, but successfully defibrillating and saving the patient at the end. Is the issue ethical if the effort finally makes the patient survive? Let me know your take on it.

Thanks to our new followers: Dr Raghunath is our senior pediatric Intensivist, trained at Australia. He has been instrumental in formulating the PITU protocols along with the other colleagues of his team.
Dr Amit Misri is a senior member of our team; very skillful and dependable. To be short about him, he is an asset to any establishment he belongs to!

Advanced wishes to Dr Anamika, who would be presenting “Usual device; Unusual heart” tomorrow in the CSI meet. Also, thanks for her wise comments on the blog.

Please send in you inputs. For all the new followers, if you find any problem in posting your comments, please email them to me. I shall post it on your behalf.

Regards

Kiran