UTAH PROTOCOL by Thomas N. Muziani PA-C, CP June 30, 2005- revised December 23, 2018

This protocol’s premise is based upon a microplegia philosophy and application.  Its clinical efficacy reflects 50 years clinical cardiac experience of-what will work and what does not. The basic postulation of the UTAH PROTOCOL (UP) on first review is counterintuitive to conventional myocardial protection dogma…with UP there are no volume or time constraints. You have the option to provide unlimited cardioplegia as often as your surgeon and/or surgical demands require. Near-continuous or continuous flow is not a detriment- and always an option.

The ultimate goal of this protocol is to create Aerobic Arrest not Ischemic Arrest.

When utilized with the Quest MPS:

  1. One 50ml syringe with 40mg. Adenosine, 40mg Lidocaine, 4Gm Magnesium (ALM) and 16.7ml NaCl. This will give you 40mls in a 50ml syringe
  2. Initial Additive setting:  20mls/L/min*-  *↑Amount = Faster arrest
  3. Upon achieving quiescence reduce setting to 10mls/L/min

When used with Syringe Pump:

  1. Place ALM in syringe pump with setting on “Induction”

 INDUCTION PHASE:

With the MPS:

  1. Temperature Setting: Warm (37°)
  2. Additive Setting: 20
  3. Arrest Setting: 20-25

With Syringe Pump:

  1. CPB temperature is Warm (37°)
  2. Syringe Pump Setting: “Induction”

Upon Application of Cross-Clamp:

  1. Ramp up Antegrade flow quickly to 500ml/min with constant observation of cardioplegia pressure. This is to insure closure of aortic valve.
  2. Once you insure closure of Aortic Valve (CPG pressure will jump from ~150Torr  to ~250Torr)- IMMEDIATELY reduce antegrade flow to ~300-350mls/min and continue to flow
  3. Reduce Additive Setting to 15mls/L/min
  4. Give ~300cc’s of Warm Antegrade- Once assured of prolonged quiescence, switch to Cold
  5. If giving Retrograde CPG- Give 400cc’s Cold
  6. Lower Additive Setting: 4– Most “Preconditioning” of the heart has now occurred. You are now into the Maintenance Phase of arrest

 MAINTENANCE PHASE:

  1. If you are performing a CABG- and distals are sewn first- After first graft, hook up graft to multi-vessel cannulae (Medusa, “Chicken Feet”, and Christmas Tree etc.) Ramp up flow very slowly, keeping in mind there is some “lag” time- to achieve a coronary pressure of ~150Torr.
  2. Inform the surgeon what the flow is. This will accomplish several goals:
  1. You have a controlled mechanical device with the capacity to determine the patency of the graft utilizing the Gold Standard of pressure to flow ratio
  2. The surgeon has the means to check for hemostasis of the anastomotic site, especially on the back side of the heart
  3. You have the capability to deliver antegrade (through the vessel cannulae) to the target site beyond disease And retrograde simultaneously if desired- This is the most ideal of all protection
  4. If the procedure requires multiple grafts, and you continue to flow cardioplegia down the grafts…The graft that was perfused first should be the graft disconnected first. The rest of the grafts follow sequentially the same order.

REPERFUSION/REANIMATION PHASE:

When approaching the last 10 minutes of cross-clamp, preparations are made for the Reperfusion/Reanimation Phase. This includes:

  1. Water Setting to:                 Warm
  2. Potassium Setting to:          Zero
  3. Additive Setting on MPS:   Zero    On Syringe Pump: “Reperfusion”
  4.  ALM alone will keep the heart quiet. Therefore, keep the setting on zero. Continue giving just warm, oxygen rich blood.
  5. DO NOT GIVE ANY ADDITIONAL LIDOCAINE OR MAGNESIUM, EITHER PRIOR TO X-CLAMP REMOVAL OR AFTER IT’S REMOVED. IT IS NOT NECESSARY AND MAY INHIBIT SPONTANEOUS CONDUCTION

From a myocardial protection strategy, this technique should provide one of the most complete forms of myocellular energy/oxygen preservation. This is accomplished by neutralizing and/or reversing the oxygen supply/oxygen demand ratio. You are providing more oxygen to the patient’s heart than it is demanding. If performed properly, you should avoid iatrogenic injury that results from CPB and aortic cross clamping. Other goals are to terminate clinical ischemia and, hopefully, mitigate the possibility of reperfusion injury.

________________________________________________________________

FAQ SHEET ON MICROPLEGIA

What is the real benefit of microplegia?

First of all, other than hypothermia, microplegia is the oldest form of myocardial protection. Dr. Denis Melrose, in 1955, utilized a concentration of potassium citrate in a 30ml syringe and injected directly into the aorta to achieve rapid arrest. Oxygen rich blood with micro-titrations of drugs to create a quiet, bloodless field and prevent the onset of ischemia and or reperfusion injury.

 Ischemic injury, to a large extent, is dependent upon the duration of the ischemic event, whether regional or global in nature. With ischemia being defined as the mismatch between oxygen supply (coronary blood flow and oxygen extraction) and oxygen demand (determined by the work load, wall stress and inotropic state of the heart), the severity of ischemia is an extremely important factor in determining subsequent injury.

The severity of ischemia can be offset and even neutralized by increased collateral blood flow. This is the whole premise and design behind microplegia.

Aerobic arrest versus Ischemic arrest:

By definition, maintenance of cardiac aerobic metabolic patterns during arrest requires oxygen supply to match oxygen demand. Consequently, if one assumes that oxygen demand has been, once and for all, drastically reduced by adequate Induction and Maintenance of asystole, it results that the prerequisites for sustained aerobiosis primarily have to deal with the modalities of oxygen supply.

These modalities can be summarized as follows:

  1. Oxygen must be present in sufficient quantities. There is now convincing evidence that the hematocrit be at least equal to 24%.
  2. Oxygen and blood must be delivered at a sufficient flow rate. Too low of flow will not inure closure of aortic valve
  3. Oxygen should be delivered in as near a continuous fashion as possible, without restricting the surgeon’s view, because it is consumed over time. No matter what the “safe” ischemic interval is in experimental models, it is virtually impossible to predict in a given patient, the time point beyond which myocardial metabolism is going to shift to anaerobic patterns as well as the extent and reversibility of tissue damage that may occur beyond this cut-off time mark.

There are numerous victims of ischemic-reperfusion injury. The myocyte is an extremely important casualty in the injury process, because it is the metabolic and functional center of the heart; it requires the greatest oxidative metabolism and ATP turnover rate to support its relentless energy demand.

Although the myocyte has been most commonly recognized as the primary casualty of surgical ischemic-reperfusion injury, another victim has been identified, most notably the coronary vascular endothelium. The coronary endothelium is not merely an inert cellophane layer or boundary at the vascular interface. It is the immediate interface between the blood and underlying myocardium and myocytes, a location that implies a gatekeeper function.

The endothelium plays a dual role; not only is it a source of deleterious activators (including platelet activating factor, endothelium-1, superoxide anion, histamine) that may injure coronary vascular endothelium, but the endothelium is also a source of nitric oxide, adenosine and prostacyclin, which protect against endothelial cell injury.

The goal of UP has always been to provide a safe, easy and reproducible method to insure global distribution of cardioplegia down to the myocyte and endothelium. This requires several simple tenets remain constant.

They are:

  1. Warm Induction- Cold creates constriction and when coupled with diffuse disease, inhibits the ability to achieve global distribution of cardioplegia down to the myocyte. Warm Induction will naturally dilate the heart and coronaries, facilitating global distribution of cardioplegia, even through diseased areas of the heart. The heart will become bradycardic…and then go to sleep…pink and flaccid. Not squeezed tight like a prune.
  2. Active Maintenance Phase- The capacity to provide as much cardioplegia as often as required. This demands a fluid understanding of micro titration of drugs administered during cardioplegia to mitigate hyperkalemia and hyperglycemia.
  3. Warm Reperfusion/Reanimation- This demands an adequate “warm shot” (min. 2L) prior to removing x-clamp. This will wash out potassium, Lidocaine and metabolites and provide a seamless transition to aerobiosis and cross clamp removal.

Any questions, comments, or if you require further details, please contact me anytime;

Remember- Successful reanimation of the heart without pacers or inotropes is one of the most rewarding benefits of perfusion. It is no small thing to bring a heart back vibrant. tnm

Thomas N Muziani PA-C, CP

tmuziani@aol.com

Hemo-Stat Blood Management Consulting

 

Addendum to Utah Protocol- Separate Dedicated ALM Delivery Line

Thomas N Muziani PA-C, CP

Upon reviewing the latest publication of the Utah Protocol (UP) I realized that I omitted the single most important advantage with this administering technique; ALM’s own dedicated delivery line. (Adenosine, Lidocane, Magnesium)  TNM 8 March 2019

The Rationale:

Adenosine has a half-life of twenty seconds once it makes contact with blood. It is rapidly cleared from the circulation via cellular uptake. This is a primary reason why it is the drug of choice utilized for individuals undergoing a cardiac stress test that will not tolerate walking on a treadmill. When adenosine is utilized to cardiovert an abnormal rhythm, it is normal for the heart to enter ventricular asystole for a few seconds prior to conversion.

By effectively separating ALM from potassium and blood delivery, perfusion is now provided with unlimited options;

  • Blood delivery only
  • ALM and blood with no K+
  • ALM alone
  • ALM with ↓K+ and blood

Recommended Schematic:

  1. One (1) three-way stopcock placed on port of 50ml ALM syringe
  2. One (1) 6ft. monitoring line attached to end of stopcock. Ideally this will be a male-to-male 6ft. line in order to attach to stopcock and delivery port.
  3. If possible- one way valve connected to 6ft. line to prevent back pressure
  4. One (1) multi-attachment delivery port. Must have leur fittings (i.e. drug delivery port)
  5. The delivery port is extremely important. This is placed next to open chest at the antegrade/retrograde port site and attached to the cardioplegia line. The cardioplegia line and ALM line are both attached to this delivery port.

Advantage:

You have now isolated all aspects of cardioplegia. Having double lines for ALM and blood/K+ delivery allows for a myriad of combinations and options for delivery. All blood, no K+ or ALM, increase ALM and no K+ for control of arrest with no ↑ K+. Continuous cardioplegia with control of K+ and ALM.

Any questions or require further information; muziani@hotmail.com

Leave a Reply

Your email address will not be published. Required fields are marked *

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.