Part XXIV- Episode 7- The Art of Perfusion- The Advent of Myocardial Protection Standing on Tall Shoulders- The History of Cardiac Surgery Thomas N Muziani PA-C, CP

“Happiness is nothing more than good health and a bad memory” – Albert Schweitzer MD (1875-1965)

Prologue:

This past month (Dec. 2018) a large group of surgeons invited me to discuss the more subtle nuances of myocardial protection. They were specifically interested in the consequences of high potassium on patients with metabolic or renal disorders. The negative ramifications of high potassium on humans warrants a more comprehensive article at another date.

During the discussion phase of the presentation the subject of transformational surgical advances in cardiac repair and replacement over the last thirty years were broached. At one point this author mentioned that the video camera should be considered a major advancement for the art of perfusion…which immediately prompted collective quizzical stares from the surgeons. Not from the perfusionists. My definition for the “art” of perfusion is rather simple. Coalescing all your acquired knowledge from scholastic to experiential trial and error… then refine it to insure consistently optimal outcomes no matter the procedure, no matter the surgeon.

The “art” of perfusion is intrinsic to the DNA of pediatric perfusionists. Two hundred extra milliliters of crystalloid solution means nothing to an adult, but it will kill a neonate. Baby anatomy is pure celestial by nature but does not suffer fools gladly. Neonatal cardiac malformations may sometimes be like solving a Rubik’s cube, but God does not make mistakes.

With no video camera, perfusion is solely reliant upon the surgeon, anesthesia or assistants to determine what is “going on up at the field”. Without the camera it is somewhat analogous to flying a plane strictly by instruments in extreme fog or severe cloud cover on a moonless night. The camera provides real-time visual cues of what the heart is actually doing; if it is truly beating, sequestering blood or an air bubble floating in the coronary grafts. Air bubbles in the heart make it difficult to insure spontaneous conduction upon cross clamp removal. The TEE will validate the fireflies (air bubbles). For those of us that have relied upon spontaneous conduction as an indices for complete myocardial protection, the onus falls upon us to at least suggest to your surgeon to check for air if the heart should have restarted and will not.

The first visual indication of a heart beginning to beat may be just a very slight quiver from the right atrial appendage, the most delicate and diaphanous of tissues.  This quivering may fail to even trigger an electrical impulse on the ECG waveform in the early stages. But the camera is a perfusionist’s friend and will not lie. ECG machines are notorious for being very quirky. A loose or wet ECG patch may prompt extraneous artifact or no waveform at all, and attempting to correct it requires going under the drapes which is no easy task. Without the camera you have to ask yourself- is it truly electrical activity or electrical artifact? Chasing false numbers or erroneous artifact routinely is not universally considered perfusion maxima.

If you experience an early return of electromechanical activity, either a beating or fibrillating heart, within a relatively short timeframe (2 to 6 minutes) post cardioplegia administration…this is indicative cardioplegia had been washed away by non-cardioplegic blood. Non-coronary collateral flow does not cause such prompt resumption of contractile function. A mechanical or technical malfunction emanating from the surgical field should be investigated as step one.

Back to my metaphor on flying; approximately thirty years ago, several prominent but disparate Asian airlines experienced an unusually high number of fatal accidents. After intense and thorough investigation, it was finally surmised that the problem was deeply embedded in an ancient Asian culture. The crashes and subsequent fatalities were the end result. The root cause was archaic Asian nurturing of differential respect where you never ever correct an elder. The first officer or flight engineer were pawns to this antiquated caste system where the senior person (Captain) was omnipotent. You do not correct or instruct the Captain that he is wrong and we’re all flying into a mountain. Everyone took that humble respect to their grave. The first officer or flight engineer were too frightened or embarrassed to speak up.

When this author first became involved in medicine in the late 1960’s, there were too many cardiac surgeons that were all too reticent to make any correction based solely upon input from perfusion. The operating room of the 60’s definitely maintained a caste system which clamped a firm muzzle on conversation. One extremely tall surgeon insisted on draping the venous return line over the ether screen to prevent it from oscillating (which it always did) naturally in front of his waist. Then, he would proceed to place his left elbow and forearm on the venous line and partially occlude it. When perfusion spoke up about lack of return volume, his instinctive guttural response was: “deal with it!” This would invariably be followed within a nanosecond his screaming frustration: “the heart is beating! More potassium!” This scenario routinely played out like old stale and tired Kabuki Theater.

If the heart starts to beat within a short post cardioplegia delivery period of 2 to 6 minutes, the first place investigated for resolution should be on the field. Not from the pump. Not adding more potassium.

The aortic cross clamp will, on rare occasions, fail to occlude the aorta if it is heavily calcified. Palpating the aorta prior to applying the clamp should provide confirmation if the aorta is filled with plaque. An incompetent cross clamp should divulge itself in several ways;

1) Inadequate venous drainage which can be verified by a full pulmonary artery signifying blood has evaded capture into the venous cannulae.

2) Incompetent cross clamp. It may be defective or was not closed completely or did not occlude the aorta entirely. If the clamp does not occlude the aorta, the aorta remains tumescent after antegrade is halted. The aorta should collapse during retrograde when suction is applied to the antegrade line. The heart will resist arresting during antegrade with an incompetent clamp and will wake up early.

3) All extension lines for cardioplegia delivery may not be attached securely.

4) One or more components of the cardioplegia delivery line or “Christmas tree” for flowing down vein grafts may have been inadvertently opened or unsecured with resultant cardioplegia flowing into the drapes and/or onto the floor.

The Dark Age of Stone Heart:

For anyone who is now in the category of seasoned senior perfusionist, the recollection of Stone Heart, whether first hand or anecdotal knowledge, may still send shivers down ones spine. The first reports of stone heart were published between 1967 and 1969 (Taber et al. 1967; Najafi et al. 1969). It was documented as transmural or subendocardial myocardial necrosis with low cardiac output post valve replacement (Cooley et al. 1972). Cooley, in 1972, was a very convincing advocate of normothermic ischemic arrest. From all investigation it appears Cooley coined the term “Stone Heart” which referenced irreversible contracture that may manifest during and/or following non-protected aortic occlusions…especially prevalent in hypertrophied hearts. The key words are non-protected.

During the early 1970’s, this outcome to an otherwise pristine perception of cardiac surgery was a clarion call to all biochemists throughout the world to actively seek resolution. It quickly became evident that some sort of ATP depletion was triggering the etiological factor behind stone heart formation. Hearse, in 1977, experimented with isolated rat hearts utilizing left ventricular pressure recordings along with tissue ATP measurements at brief intervals. The recordings and measurements verified the onset of contracture (the rise in resting tension) during ischemia when ATP was diminished by 50%, which lead to ATP-hydrolysis and accelerated contracture almost immediately afterwards. The exact time-to-onset could be diminished by direct interventions which would reduce myocardial energy demands.

These interventions included; potassium chloride arrest, magnesium elevation, calcium antagonists and hypothermia. From exhaustive further experimentation, it was concluded that ischemic contracture manifested from ATP depletion formed rigor complexes between actin and myosin. The onset of contracture was solely ATP related and the final degree of contracture was heavily influenced by calcium-sensitive mechanisms.

The final outcome from this unfortunate experience was a severe wake-up call to all cardiac surgeons and perfusionists throughout the world to effectively re-think and thoroughly comprehend all minutiae that encompassed a robust approach to myocardial protection. Protecting the heart through all phases; induction, maintenance and reanimation, down to the myocyte, cannot be treated with nonchalant indifference. From this tragic and rather frightening experience, myocardial protection was catapulted to a new level of understanding and provided the foundation for how we approach complete protection for the electromechanically arrested heart today.

My humble thanks to Dr. Jeffrey Milliken, Cardio-thoracic surgeon extraordinaire, for his invaluable input, generous insight and most of all, his compassionate friendship.

Addendum by Gary Grist RN CCP Emeritus: Thomas asked me to comment about pediatric perfusionists, so here it is:

I agree with Thomas’ statement about peds perfusionist: “The “art” of perfusion is intrinsic to the DNA of pediatric perfusionists.”  Of course, I am biased in that area. For many years we were hampered because when disposables became available they were keyed towards adult patients and adult perfusionists.  And peds perfusionists needed to make a lot of modifications to make a pediatric circuit work.

A peds perfusionst can pump the average adult CABG or valve repair/replacement.  But I do not think that an adult perfusionist could pump the average congenital child safely, particularly infants, IMHO.  They could not even prime the pump properly without supervision or practice blood conservation efficiently.  And don’t even get me started on univentricular cases dealing with A-P collateral vessels, hypertrophic hearts or redos on congenital patients.

And then there is being ready for post-pump ECMO support.  There was a time, many years ago, when a child who wouldn’t wean from CPB (sometimes with Stone heart like Thomas describes) was just allowed to die on the table.  I saw many of these and even baptized a few on their foreheads before stopping the pump. One of our cardiac anesthesiologists always carried a bottle of “Holy water” in his bag for just such an occasion.  But now, nobody dies in the OR. They go on ECMO and at least make it to the ICU so their parents can see them.  ECMO saves about 50% of them, who without ECMO would be dead. We started offering ECMO for failure-to-wean kids in about 1988. No cardiac surgery deaths in the OR after that.

I remember one legendary and “seasoned senior” perfusionist often saying at society meetings that ANY perfusionist should be able to pump ANY case that comes through the door. That is a reflection of the early days of the profession that I call the “age of arrogant self-reliance”, when perfusionists felt that they could safely handle any situation or emergency on CPB.   That was never true then and nobody in perfusion should be thinking like that today. But many old timers thought that way including me, I guess….. afraid to admit that I might fail. With age comes wisdom and I learned that self-confidence is one thing, but arrogance is self-deceptive hubris.