cardiac surgery


The dawn of heart surgery.

Clarence Walton Lillehei was known as the “father of open heart surgery”. Indeed, hardly any other cardiac surgeon has introduced a greater number of innovative techniques and concepts.

During his career, Dr Lillehei focused his efforts on cardiac surgery, particularly the development of open heart operations. The difficulty of operating on a beating heart and the hypoperfusion of the vital organs were serious and frequent complications of heart surgery. In 1953, Dr John Gibbon of Philadelphia successfully closed an atrial septal defect using a complex screen oxygenator and roller pumps. However, the mortality of open heart surgery remained high, mainly because of oxygenator-related problems, and many surgeons despaired of ever being able to correct complex intracardiac defects. 

This situation was changed in March 1954 when Dr Lillehei and his associates—Morley Cohen, Herb Warden, and Richard Varco— used controlled cross-circulation to correct a ventricular septal defect in an 11-year-old boy. The boy’s anesthetized father served as the oxygenator. Blood flow was routed from the patient’s caval system to the father’s femoral vein and lungs, where it was oxygenated and then returned to the patient’s carotid artery. The cardiac defect was repaired with a total pump time of 19 minutes. Over the ensuing 15 months, Lillehei operated on 45 patients with otherwise irreparable complex interventricular defects; most of these patients were less than 2 years old. Although cross-circulation was a major advance, it was not adopted for widespread use because it posed a serious risk to the “donor”. Nevertheless, this method paved the way for the open heart surgery era.

That same year, Dr Richard A. DeWall and Dr Lillehei introduced the first clinically successful bubble oxygenator, which remained the standard for extracorporeal circulation until the late 1970s. Dr Lillehei also helped pioneer hemodilution and moderate hypothermia techniques for open heart surgery. 


Human heart in ventricular fibrillation.

Ventricular fibrillation is a condition in which there is uncoordinated contraction of the cardiac muscle of the ventricles in the heart, making them quiver rather than contract properly. It is the most commonly identified arrhythmia in cardiac arrest patients.

While there is some activity, the lay person is usually unable to detect it by palpating (feeling) the major pulse points of the carotid and femoral arteries. Such an arrhythmia is only confirmed by electrocardiography.

Ventricular fibrillation is a medical emergency that requires prompt Advanced Life Support interventions. If this arrhythmia continues for more than a few seconds, it will likely degenerate further into asystole (“flatline”). This condition results in cardiogenic shock and cessation of effective blood circulation. As a consequence, sudden cardiac death (SCD) will result in a matter of minutes. If the patient is not revived after a sufficient period (within roughly 5 minutes at room temperature), the patient could sustain irreversible brain damage and possibly become brain-dead, due to the effects of cerebral hypoxia. On the other hand, death often occurs if sinus rhythm is not restored within 90 seconds of the onset of VF, especially if it has degenerated further into asystole.

Causes of ventricular fibrillation are:

  • Abnormal automaticity: In the healthy myocardium, the rhythm of contraction is regulated by sinoatrial node,that acts like a pacemaker and generates the normal sinus rhythm. Automaticity is a measure of the propensity of a fiber to initiate an impulse spontaneously, separated from the sinoatrial node. The product of a hypoxic myocardium can be hyperirritable myocardial cells and these may then act as pacemakers. The ventricles are then being stimulated by more than one pacemaker. Scar and dying tissue is inexcitable, but around these areas usually lies a penumbra of hypoxic tissue that is excitable. Ventricular excitability may generate re-entry ventricular arrhythmia. It is interesting to note that most cardiac myocardial cells with an associated increased propensity to arrhythmia development have an associated loss of membrane potential.
  • Re-entry: The role of re-entry or circus motion was demonstrated separately by Mines and Garrey. Mines created a ring of excitable tissue by cutting the atria out of the ray fish. Garrey cut out a similar ring from the turtle ventricle. They were both able to show that, if a ring of excitable tissue was stimulated at a single point, the subsequent waves of depolarisation would pass around the ring. The waves eventually meet and cancel each other out, but, if an area of transient block occurred with a refractory period that blocked one wavefront and subsequently allowed the other to proceed retrogradely over the other path, then a self-sustaining circus movement phenomenon would result. For this to happen, however, it is necessary that there be some form of non-uniformity. In practice, this may be an area of ischaemic or infarcted myocardium, or underlying scar tissue.

Hypoplastic Left Heart Syndrome (HLHS)

HLHS is exactly what it sounds like: the left sided structures of the heart are hypoplastic or underdeveloped. While the exact features can vary between patients (HLHS variants), typically HLHS describes 6 defects. 

  1. Mitral valve atresia
  2. Severe aortic valve stenosis
  3. Hypoplastic left ventricle 
  4. Atrial septal defect (ASD)
  5. Hypoplastic ascending aorta
  6. Patent ductus arteriosus (PDA)

Mitral valve atresia. The mitral valve allows blood between the left atrium and the left ventricle. In atresia, the mitral valve does not open. Blood cannot enter the left ventricle, causing the left ventricle to become severely underdeveloped. 

Severe aortic valve stenosis. The aortic valve allows blood into the aorta from the left ventricle. Stenosis means the valve does not open completely. This (combined with mitral valve atresia and left ventricular hypoplasia), means blood cannot enter the aorta where it normally does. Instead, it bypasses the ascending aorta and enters near the aortic arch through the PDA. This decreased blood flow causes the ascending aorta to become severely underdeveloped. 

Hypoplastic left ventricle. Normally, the left ventricle is the strongest in the heart. It pumps blood out through the aorta into the body (systemic circulation). When the ventricle become hypoplastic, it cannot adequately supply the body with oxygenated blood. This is why HLHS is referred to as a single ventricle defect: the right ventricle is the only effective pumping chamber in the heart.

Atrial septal defect. An atrial septal defect is a hole between the atria of the heart. This allows blood to be shunted between them, bypassing the left ventricle and entering the right ventricle. The right ventricle is now responsible for pumping blood to both the body and the lungs. As you might expect, this causes oxygenated and deoxygenated blood to become mixed together. 

Hypoplastic ascending aorta. Because the ascending aorta is underdeveloped, the surgery for HLHS involves constructing a new aorta from the base of the pulmonary artery (one step of the Norwood procedure, the initial surgery for HLHS). 

Patent ductus arteriosus. This isn’t technically a defect, as all babies normally have a PDA that closes shortly after birth. I feel it’s worth noting, though, as the PDA will need to be kept open in babies with HLHS. The PDA is a connection between the pulmonary artery and aorta. When blood is pumped from the right ventricle into the pulmonary artery, the PDA allows some of it to flow into the aorta as well. This is the only way blood is able to enter systemic circulation. Life is dependent upon the PDA in this defect, and prostaglandin must be infused to keep it open until surgery can be performed.

Surgery for HLHS is initiated within the first few weeks after birth, as this defect is incompatible with life without it. Surgeries typically occur in stages as the heart matures. The first being the Norwood procedure, followed by the Glenn procedure and the Fontan. It should be noted that none of these surgeries can create a “normal” heart, but can redirect blood flow so that the body is perfused much more effectively. 

This picture says it all for me.

All my life people tell how can I not believe in god, it’s thanks to him I’m here and I should be thankful and praise him.
That, however, is a false statement if there is a god then he is a sick fuck who wanted me dead at birth. People say “thank god you lived”, NO don’t,  instead try thanking the doctors and surgeons at Johns Hopkins Hospital who gave their time and effort to learning and practicing the skills and knowledge that were used to allow me to live this long. I will soon see myself complete 22 years of living and that is not thanks to any god but to a man who wanted me to have a chance to experience this glorious world. So thank you from the bottom of my heart to all surgeons and doctors who allow people like myself to live full lives, even when people constantly bash you, never give thanks, and threaten your livelihood on a regular basis just to make a quick buck or make them feel better.


This photo is of Polish surgeon, Dr. Zbigniew Religa. 

He performed the first successful heart transplant in Poland. 

This picture was taken in 1987. The man on the operating table, Tadeusz Żytkiewicz is still alive. He’s now 88 years old. He outlived Dr. Religa who sadly died in 2009 due to lung cancer. 

I’m posting this because I just got done watching an amazing movie about the topic. The film is called Bogowie (and yes to answer dxmedstudent’s question it does translate to Gods. It’s about a surgeon would you expect any less?).  

Anyway, because it’s not in English I’m sure it hasn’t gotten the press it deserves. But, if you get the chance check it out (subtitles aren’t that bad). It really is a great film and I promise you won’t be disappointed!

It never ceases to amaze me how far medicine has come and how much we still have to learn. This was only 28 years ago. What will we achieve in another 28 years? 

Would you like to be awake while having open-heart surgery?

This is the astonishing picture of Swaroup Anand, a 23-year-old patient that went under the knife in Bangalore at Wockhardt Hospital while he was still very much awake. Doctors chose to numb his body with an epidural to the neck rather than send him to sleep with general anaesthesia. 

Lead surgeon Dr Vivek Jawali, said they had performed more than 600 operations this way since 1999. Speaking from his hospital in India, he said: “There has been a huge effort in recent times to make heart surgery less invasive. This can be done in two ways. Firstly smaller cuts can be made and this is helped with modern technology and robotics. Secondly we are trying to interfere as little as possible with the body’s natural functions.”

“The patients are given a mild sedative rather than being knocked out - this drops their heart rate but means they can respond to commands. The patients are drowsy so they can be aroused but are also able to drift into sleep,” Dr Jawali said. “If we need them to cough or breathe more deeply to clear air from their heart they can respond. This makes the procedure a lot easier to perform.”

(Read more).

List of Cardiac Defects and Their Associated Repairs

Please note: This is by no means a comprehensive list. There are other surgical procedures so please don’t treat this post like the Bible of cardiac defect repairs. Every child is different, every anatomy is different, and many patients will require nontraditional repairs. I did not mention certain procedures (such as the hemi-Fontan or Sano modification, etc) because that’s just too much information. One day I may make a surgical repair post for each defect (and at that time would detail modified, Hybrid, non-traditional approaches, etc), but until then: keep in mind that these are not the ONLY options.

Atrial Septal Defect/Ventral Septal Defect - Self-resolving, simple suture or patch repair.

Coarctation of the Aorta - End-to-end anastomosis, subclavian flap angioplasty

Double Inlet Left Ventricle - Damus-Kaye-Stansel procedure, single ventricle palliation

Double Outlet Right Ventricle - Rastelli procedure, RV to PA conduit

Ebstein’s Anomaly of the Tricuspid Valve - Blalock-Taussing shunt, Carpentier’s procedure, Tricuspid valve repair, Starnes procedure

Hypoplastic Left Heart Syndrome - Norwood procedure, Bidirectional Glenn procedure, Fontan procedure

Pulmonary Atresia with Intact Ventricular Septum - Balloon atrial septostomy, pulmonary valvotomy, PDA stent

Pulmonary Atresia with Ventricular Septal Defect - RV to PA conduit and VSD repair

Transposition of the Great Arteries - Arterial switch operation

Brace yourselves.

For I have applied and been accepted for an extra internship in intervention radiology department. 

Because it´s fun! And anatomy! And blood(vessels)! And catheters! And scary close to vascular and cardiac surgery!

Intervention radiology is an invasive (of course) field of radiology concerned mostly with treatment of blood vessel disorders/trauma.. which doesn´t need to be or can´t be treated by surgeon. It also solves problems concerning any other tubular organs, but the main focus is put on blood vessels. The line in between vascular and cardiac surgery and intervention radiology is very thin and most of the time only defined by cooperation in between these departments. Most of the techniques concern wires which are navigated through the blood vessels to treat aneurysms, bleeding, dissolve an embolism or create one for purpose of safer course of surgery. Apart from that it is also required for picturing the course of blood flow in blood vessels in order to expose the defect, stenosis or anything that is wrong.. which can be useful in deciding whether the patient (most often diabetic) will undergo a simple or more complicated surgery or an amputation. 

It´s like playing the labyrinth games just under Xray control with a tiny wire. 

I think it´s about time I finally learnt the branches of external carotid. 

Originally posted by poporonn


Pulmonary atresia is a congenital heart defect affecting pulmonary circulation. The pulmonary valve does not form correctly, preventing the flow of blood into the lungs. Because of this lack of blood flow, the right ventricle and tricuspid valve do not grow appropriately and are hypoplastic.

But if the blood doesn’t flow to the lungs, how is the baby alive? How are they oxygenating? Pulmonary atresia is a ductal-dependent defect, meaning that blood flow is dependent on the PDA (patent ductus arteriosis). The PDA is a connection between the aorta and pulmonary artery that is normally present in all babies, but closes shortly after birth. A medication called prostaglandin can be administered to keep this duct open. Blood then flows from the left ventricle into the aorta, through the PDA, to the pulmonary artery and then to the lungs. Because oxygenated and deoxygenated blood are now mixed together, the patient will have decreased sats. Surgery will be needed to ultimately correct this defect. 

Why Michael’s death is really a game changer

Let me preface this by stating that I have not seen Monday night’s episode. I have no plans to watch it, or really any future episode of Jane the Virgin. I normally livestream JTV but this week I didn’t. I found out about Michael’s death by watching a promo for next week’s episode. 

I’m upset. I’m irritated. Mostly I’m just sad. I began watching JTV after the S1 finale. I had read EW recaps periodically out of curiosity because the premise seemed so bizarre, but after watching the S1 finale and subsequent S2 premiere is when I became hooked. My main hook was Jane and Michael’s relationship. I fell in love with them as solo entities, but their relationship hit me right in the feels. It was so genuine, so supportive, it felt as real as a fictional relationship could, like I could walk past them at a bookstore laughing about the next Angelique Harper. 

I loved Jane the Virgin. The writing was so clever, so funny and heartfelt, the characters were so interesting and their relationships were so well developed. But Michael’s death changes all of that for me. I thought Jenni Snyder Urman was a genius for creating this show, for taking the concept of this telenovela but grounding it, making fun of some of the tropes, never really going into the campiness that Shondaland shows (closest things to a soap these days) sometimes head into. But the unnecessary death of Michael Cordero Jr. takes that opinion away. THIS is campy. This is killing off people for shock value/lazy storytelling in the age of HTGAWM and Game of Thrones. If this was truly the plan all along then I’m sorry but you had a shitty plan. 

There was no valid reason for Michael to die other than it was the only way for them to put Jane and Rafael back together. You’re not doing it to flip Jane’s world/path around à la the pilot if theres a time jump. You’re killing Michael because you painted yourself into a corner with how lovely Villadero’s relationship was because it would be completely OOC for Jane to leave Michael AGAIN when she’s repeatedly chosen him over Raf. And the bullshit company line of “when we slipped that line in in S1, we were setting you up for Michael’s death”. Nope. That line could’ve meant that Michael would love Jane until his dying breath at 110. If we’re looking at lines, what about the one about his “illustrious detective career” in the pilot? 3(?) years as a detective where you were fired twice and never caught Sin Rostro is not what I would consider an illustrious career. Especially since Michael died after taking his LSAT. You being “stuck with a plan” even though you were able to prolong his death because you “loved Brett so much” is the HIMYM excuse of 2017. Not to mention the way you killed him was extremely weak. Michael is presumably no more than 6 months out from being shot, where he had major cardiac trauma and surgery. NO ONE is going to say to him “Oh you’re having chest pains? Let’s not brush that off until after your LSATs, we’re going to the ER right now. You were shot in the chest!!!” (Seriously the Jane we love would’ve done that)

Finally, I want to talk about how this really messes up the show. You’ve just severed your tie to Sin Rostro, which in the absence of this first half of the season, made the show a bit weaker. I really don’t care about Raf’s parent problems, or Xo’s career, I wanted Michael back on the force looking for Sin Rostro, protecting his family and getting that victory. Supposedly Michael’s detective friend will be the new tie to this investigation but again, he’s Michael’s friend, Michael is now dead and he has no real ties to anyone else the way Michael did. You’ve just lost a source of some good parenting storylines involving Jane and Raf’s co-parenting with Michael as Mateo’s stepdad. If Jane and Raf get back together there will be no parenting dramas for B-storylines as Raf will go back to his “what can I do to make Jane happy?” days. And do I even need to mention the loss of the bromance?

TLDR: I’m done. I’m sad that I am because I will miss this show, but you know what? Michael’s death just proved that this show wasn’t great to begin with. 

anonymous asked:

Kaz, you're literally a cardiac surgeon! Cutting hearts with precision and put them back together with GREAT SKILLS! < 3 <3

Haha, I wish! If I could do actual cardiac surgery I wouldn’t have to cry over how bad I am at cardio anatomy!