Part XXV- Episode 8- The Art of Reanimation The Advent of Myocardial Protection Standing on Tall Shoulders- The History of Cardiac Surgery Thomas N Muziani PA-C, CP

“Everyone is a prisoner of his own experiences”

Edward R. Murrow- 1953 (1908-1965)

Warm Reanimation:

Of the three completely disparate phases that encompass global myocardial protection- induction, maintenance and reanimation… the reanimation phase is by far the most invalidated and misunderstood. To orchestrate an essentially seamless transition from an unnatural prolonged anaerobic environment-to reanimating the myocardium into normal sinus rhythm- warm, oxygenated blood has proven the vehicle of choice. Substrate enhancement is not sanctum sanctorum for oxygen-rich blood to be considered a “warm shot”. In an effort for brevity, this discussion will not involve incorporating amino acid-enriched solutions. Therefore, when referring to warm reanimation, the delivery agent is warm oxygenated blood without cardioplegia or additives.

The intended predomination of warm induction, cold maintenance and warm reanimation blood cardioplegia delivery, regardless of any specific formulation, will only be efficacious if the plegia is delivered to all myocardial regions in sufficient amounts to promote global myocardial management. Maldistribution of flow is common in patients with coronary artery disease if the primary mode of distribution is strictly antegrade perfusion. Retrograde delivery of cardioplegia compensates for this limitation by providing effective left ventricular protection following coronary sinus or right atrial perfusion.

The original science for delivering warm reanimation was to limit reperfusion injury and wash out completely any remaining potassium, Lidocaine and/or metabolites. The intent was to promote spontaneous conduction into normal sinus rhythm with minimal workload imposed upon the myocardium. Switching to the warm setting on the heater/cooler approximately 5 minutes prior to delivery should ensure a tepid to warm delivery of reanimating blood. Many institutions prefer tepid blood temperature during initial delivery in order to facilitate gradual shifts in myocardial temperature flux.

If whole body hypothermia was employed and the decision is made to rewarm systemic core (whole body) early, caution should be used when raising the myocardial temperature to the point where warmth alone may trigger spontaneous electromechanical activity. This is due to warm non-coronary collateral blood allowing the heart, with retained energy, to commence contraction. Systemic rewarming for an extended period of time without periodic concurrent warm blood perfusion may cause unnecessary ischemic injury due to insufficient non-coronary collateral flow that cannot provide adequate metabolic suffusion.

Ensuring optimal flow while administering antegrade cardioplegia is extremely important. An inadequate flow mindset may be the result of an age old perfusion commandment: “Thou shalt not blow up tubing or coronaries”. No perfusionist enjoys spending 2-3 extra hours mopping up a heart-lung machine due to tubing separation and resultant blood geyser.

When antegrade flow is too low, attendant sub-optimal pressure will prevent closure of the aortic valve. Approached schematically, not closing the aortic valve means your cardioplegia or non-cardioplegic blood is flowing straight down the ventricle and not perfusing the coronaries. Average minimal flow antegrade during reanimation is approximately 150mL/min for 5 to 10 minutes. You should witness a sudden jump in line pressure indicating the aortic valve has closed. Volume delivered may be divided equally between antegrade and retrograde. This would ensure maximum washout of cardioplegia prior to removal of the cross clamp. During this phase you may experience resumption of bradycardic electrical activity prior to cross clamp removal. If Lidocaine was not administered during cardioplegia delivery, consideration should be made to injecting 100mg. during this early restoration of electrical activity. Please titrate Lidocaine slowly (i.e. ⅓ ⅓ ⅓) to avoid instigating ectopic beats or asystole.

Clinical experience has supported that if the heart begins to beat, even in a bradycardic rhythm, increase arterial flow by 400 to 800 ml/min. while constantly observing line pressure. This gentle upsurge in flow has a propensity to gradually increase heart rate and tighten ST segments of the ECG. Attempt to avoid using inotropes or vasopressors during this phase of reanimation. Along with constricting the vascular bed, these drugs also clamp down the coronaries. When overused, they become a crutch providing a false sense of security by displaying fictitious and very transient numbers. Control pressure with flow, not drugs, if at all possible. Working in concert with Anesthesia is ideal during this application.

The heart should recover into spontaneous electrical activity within 3 to 7 minutes after aortic unclamping. Persistent asystole may signify an elevated serum and presumably myocardial potassium or gross air in the coronaries and/or heart. A gentle tapping on the cardiac surface with either a finger or forceps usually stimulates contraction (the original pacemaker).

If your surgeon has a preference for performing the proximal anastomoses after the aorta is unclamped and while the heart is rewarming, a standard, proven technique is proffered:

  1. Non-cardioplegic warm blood is perfused through the grafts while the other proximal anastomoses are constructed. It has been validated that a simple coronary, very easy to access, such as the distal right will perfuse 70% of the myocardium during this coronary perfusion.
  2. Normally the graft to the largest vascular bed is connected last to the aorta to ensure viable perfusion beyond the proximal coronary stenosis.
  3. Normal sequential discontinuance of coronary perfusion is: first graft perfused, first graft discontinued. Continue the same sequence with the rest of the grafts.
  4. This machine-driven coronary perfusion provides an additional benefit: validating through the Gold Standard of pressure-to-flow ratio in determining actual flow through the grafts and into the coronaries. It will also expose lack of patency, by high pressure and low flow, while still amenable to reconstruction.
  5. All flows and sizers should be charted, including pump record and provided to your surgeon for dictation. These flows provide the one true validation the grafts were patent and flowing well post insertion. Example: OM- 1.5- mild- 150ml/min
  6. Also, an excellent opportunity to check for hemostasis at the graft site, especially the back wall.

Another frequent “habit” that perfusion should be apprised of is the instinctive penchant of surgeons to lift the heart and check for bleeding on the backside the moment cross clamp is removed. More often than not, this lifting tactic will obliterate the outflow tract of the aorta triggering PVC’s or ectopic beats.  Obliterating the outflow tract (as graphically displayed on the physiologic monitor with an arterial flat line and precipitant pressure) during this period of immediate cross clamp removal is the antithesis to reinvigorating a starved heart. Providing an extended recovery period allowing the heart to recuperate after clamp removal plus gentle care while lifting the heart produces amazing outcomes. Ventricles of a heart do not require being pointed to the lights to gain optimal visualization. Confer with your surgeon.

A long established procedure utilized during warm retrograde non-cardioplegic blood infusion:

  • Warm retrograde is commenced prior to the last suture being cinched down on the internal mammary artery (IMA) anastomosis in order to de-air the vascular bed. The bulldog clamp on the IMA is removed transiently to facilitate de-airing the graft and the suture line is cinched down.
  • If utilizing a stopcock for antegrade/retrograde selection- switch the stopcock to antegrade mode after suture line is cinched down on the IMA graft, and
  • Vent is closed after starting antegrade flow. This should purge any residual air from the antegrade line.

This technique will facilitate administration of warm antegrade blood while tacking sutures into the IMA pedicle and securing. This will also allow for site selection and placement of the last proximal graft. The aortic valve will normally remain competent despite any possible distortion due to pads intentionally remaining beneath the heart for visualization of the LAD to IMA grafting. Non-cardioplegic flow is slightly increased by approximately 300 to 350ml/min after proximals are completed.

One of the true hallmarks of warm reanimation provided in copious amounts during the final phase of aortic cross clamping is this; if delivered at appropriate flows while warm, this technique transmigrates from ischemic arrest to aerobic arrest. You are actually providing more oxygen to the myocardium than it is demanding. It has been well documented that patients presenting to the operating room with severe left ventricular dysfunction or cardiogenic shock have a pronounced reduction in tolerating aortic cross clamping. This is most likely due to pre-ischemic depletion of their myocardial energy stores. When maintaining strict adherence to all three forms of myocardial protection modalities- an expected result should be recovery of the depleted myocardial energy stores. Resuscitating the energy stores provides improved overall hemodynamics and ventricular function allowing for an accelerated, uneventful recovery.

Over the last forty years blood cardioplegia, primarily due to widespread empirical validation, emerged as the preferred cardio-protective strategy, especially with very sick patients. The numerous benefits included; versatility, since a blood vehicle for delivery will blend onconicity, buffering, rheology and antioxidant benefits. It was also discovered to be capable of augmenting oxygen delivery along with the ability to “resuscitate the heart”, “prevent ischemic injury”, “limit reperfusion damage”, and “reverse” ischemic-reperfusion injury.

I welcome any questions. Please contact me: muziani@hotmail.com

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Perfusion Theory is an educational platform for the Oxygen Pressure Field Theory (OPFT). August Krogh’s theoretical concept of the oxygen pressure field is explained and then applied to clinical applications in perfusion practice.