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Hyperoxygenation During CPB: When Should We Use It?

Hyperoxygenation During CPB: When Should We Use It?. Gary Grist RN CCP, Chief Perfusionist The Children’s Mercy Hospitals and Clinics Kansas City, Missouri ggrist@cmh.edu No Disclosures.

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Hyperoxygenation During CPB: When Should We Use It?

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  1. Hyperoxygenation During CPB: When Should We Use It? Gary Grist RN CCP, Chief PerfusionistThe Children’s Mercy Hospitals and ClinicsKansas City, Missouriggrist@cmh.eduNo Disclosures

  2. Some consider it a fact that use of hyperoxia on cardiopulmonary bypass (CPB) has negative effects on patient outcome by increasing the danger of oxygen toxicity or reperfusion injury. This belief has become a 'sacred cow' among many perfusionists. However, the manipulation of oxygen on CPB can be used to the patient's benefit. It is incumbent upon the perfusionist to understand the need for the manipulation of oxygen concentration and master the techniques needed to provide the patient with the greatest benefit. A 'one size fits all' approach to oxygenation strategy, be it normoxia, hyperoxia, or something in between can rob the patient of the benefits that the free range of oxygen manipulation, from high to low, can provide. Oxygen Pressure Field Theory conceptualizes the manipulation of oxygen concentration such that the perfusionist can understand the mechanics of microvascular gas exchange. Hyperoxia can be beneficial in one situation and detrimental in another as can normoxia. This presentation discusses oxygen manipulation in six clinical situations. 1. Nitrogen entrainment: Special equipment has shown that gaseous microemboli (GME) may occur in the cerebral circulation of any patient on CPB. The GME are most numerous during interventions by perfusionists and were associated with the worst neuropsychological outcomes. Most bubbles that enter the CPB circuit are initially composed of room air; approximately 70% nitrogen, 19% oxygen, 5% carbon dioxide and 6% water vapor. GMEs of this composition are likely to occlude small arteries and capillaries and cause tissue ischemia. During the periods of high risk for GME generation and by using Boyles Law, the perfusionist can change these bubbles to approximately 0% nitrogen, 89% oxygen, 5% carbon dioxide and 6% water vapor. This GME composition is much less likely to result in capillary occlusion. 2. Hemodilution: The reduced oxygen delivery common during CPB as a result of hemodilution can be counter-acted to a limited degree by the use of hyperoxia. Hyperoxia is commonly used for humans in major, non-cardiac surgery and has shown to 1) be safe during anesthesia with no adverse side effects, 2) reduce the need for blood transfusion, 3) preserve myocardial oxygenation during low hematocrit, 4) reverse anemic hypoxic ECG changes, 5) increase sub-endocardial oxygen delivery, 6) reverse non-cardiac tissue hypoxia caused by anemia and 7) reduce the risk of wound infection. 3. Metabolic acidosis: Increases in base deficient caused by suboptimal perfusion (shock) can be significantly reduced using various degrees of hyperoxia. 4. Deep hypothermic circulatory arrest (DHCA): Hyperoxia can be used prior to DHCA to 'oxygen load' tissues. This can extend the period of safe circulatory arrest before anaerobic metabolism begins by approximately 20 minutes. 5. Oxygen toxicity: Oxygen toxicity is frequently confused with reperfusion injury, but it occurs when circulation is good, there is no acidosis, and the antioxidants are functioning properly. However, the amount of oxygen present in the tissues overwhelms the antioxidants' ability to neutralize reactive oxygen species. The perfusionist who is aware of the circumstances during which oxygen toxicity occurs can take the proper precautions with oxygen manipulation to prevent tissue damage. 6. Reperfusion injury: Reperfusion injury is frequently confused with oxygen toxicity, but it occurs when circulation is poor and acidosis is present which deactivates the antioxidants. Reperfusion injury can occur even during low oxygen concentration and can be caused iatrogenically by the perfusionist. The perfusionist can prevent tissue damage when there is reperfusion injury potential (RIP) and he/she can prevent damage by not allowing RIP to develop; in both instances using oxygen manipulation.

  3. OBJECTIVES To briefly describe the oxygen pressure field theory and discuss scenarios where oxygen manipulation on cardiopulmonary bypass may be helpful to improve patient outcomes. Six situations for oxygen manipulation: • Nitrogen entrainment • Hemodilution • Metabolic acidosis • Hypothermic arrest • Oxygen toxicity • Reperfusion injury

  4. 1. NITROGEN ENTRAINMENT • CNS complications from CPB • stroke = 1.5% (CABG) to 10% (valves) • asymptomatic brain infarct by MRI = 18% • Floyd et al. 2006 • Gerriets et al. 2010 • Sources of emboli • atheroemboli from aortic manipulation • thromboemboli • bubbles of air • Raymond et al. 2001

  5. 1. NITROGEN ENTRAINMENTBrain Emboli: Cardiopulmonary Bypass Principles & Practice, Gravlee et al, Ed., 1993, pg 549

  6. 1. NITROGEN ENTRAINMENTAir bubbles in the venous return line Wang S, Undar A . Vacuum-assisted venous drainage and gaseous microemboli in cardiopulmonary bypass.J Extra Corpor Technol. 2008 Dec;40(4):249-56.

  7. 1. NITROGEN ENTRAINMENTBlood emulsification with air by the vent and suckers:Making bloody meringue! Ashby MF. The properties of foams and lattices. Philos Transact A Math Phys Eng Sci. 2006 Jan 15;364(1838):15-30. Cheng KT. Air-filled, cross-linked, human serum albumin microcapsules. Molecular Imaging and Contrast Agent Database (MICAD) [Internet]. Bethesda (MD): National Center for Biotechnology Information (US); 2004-2010. 2006 Jul 06 [updated 2008 May 08].

  8. 1. NITROGEN ENTRAINMENTBorger MA, Feindel CM. Cerebral emboli during cardiopulmonary bypass: effect of perfusionist interventions and aortic cannulas. J Extra Corpor Technol 2002; 34(1):29-33.

  9. 1. NITROGEN ENTRAINMENTDealing with bubbles • Use an arterial filter/bubble trap w/ purge • CO2 flush the surgical field • Add volume to the venous reservoir • Slow down the suckers and vent • Limit perfusionist interventions • Use a circuit or MCA Doppler • Ask the surgeon to stop what he is doing and fix the bubble source • Increase sweep FiO2

  10. 1. NITROGEN ENTRAINMENTConverting N2 bubbles in blood to O2 bubblesVann RD, Butler FK, Mitchell SJ, Moon RE.Decompression illness. Lancet. 2011 Jan 8;377(9760):153-64.

  11. Understanding The Oxygen Pressure Field: Krogh Cylinder Model Capillary radius: r = 5µ Capillary X-section : A =  r 2 = 78.5 µ2 Cylinder radius: R = 10 Cylinder X-section: A =  R2 = 314 µ2 Ratio: Capillary X-section Cylinder X-section = 1/4 Highest ptO2: 79 mmHg OPF Range: 79 ~ 1 mmHg Lowest ptO2: 1 mmHg R r Blood Flow paO2 = 80 mmHg pvO2 = 40 mmHg Avg. ptO2 = 20 mmHg Avg. ptO2 = 10 mmHg O2 radial vectors

  12. PERFUSED CAPILLARY DENSITY (PCD) R R Low PCD: Single capillary unit High PCD: Multiple capillary units Closed capillary unit Increasing PCD • WORKING MUSCLE RESTING MUSCLE NORMAL ORGAN FUNCTION ORGAN SHOCK Decreasing PCD

  13. Capillary radius: r = 5µ Capillary X-section : A =  r 2 = 78. 5 µ2 Cylinder radius: R = 20 Cylinder X-section: A =  R2 = 1256 µ2 Ratio: Capillary X-section Cylinder X-section = 1/16 Anoxic tissue 1 mmHg pO2 line ANOXIC LETHAL CORNER R Highest tissue pO2: 79mmHg r Blood Flow paO2 = 80mmHg pvO2 = 40 mmHg ANOXIC LETHAL CORNER 1 mmHg pO2 line O2 radial vectors

  14. 2. HEMODILUTIONShould Perfusionists Use A Transfusion TriggerOn Cardiopulmonary Bypass? • Patients with ≥ 25% Hct = 2% mortality. • Patients with ≤ 19% Hct = 4% mortality. • DeFoe et al. 2001. • Should 19% be a trigger point? • Reduce the mortality from 4% to 2% • NNT: Transfuse 90/100 low hematocrit patients • 2 additional patients survive • 88 patients unnecessarily transfused • Grist G. AmSECT Today 2009.

  15. 2. HEMODILUTIONCounter-acting Hemodilution With Hyperoxia • Hyperoxia use in non-cardiac surgery • Safe • No adverse side effects (human experience) • Habler et al. 2002 • Reduces the need for transfusion • Less allogenic blood given (human experience) • Kemming et al. 2003 • Preserves myocardial oxygenation during low hematocrit • Reverses anemic hypoxic ECG changes (human experience) • Increases sub-endocardial O2-delivery 24% (animal study) • Kemming et al. 2004 • Reverses tissue hypoxia at low hematocrit • Tissue pO2 increases from 10 to 18 mmHg (animal study) • Meier et al. 2004 • Reduces risk of wound infection • Supplemental O2 (80% vs 30%) reduces infections by 39% (human experience) • Brasel et al. 2005

  16. 2. HEMODILUTION Formation Of An Anoxic Lethal Corner Due To Low Hematocrit O2 Axial Vectors 1 mmHg tissue pO2 line Low Hct paO2 = 150 mmHg Anoxic Tissues Lethal Corner Forms O2 Radial Vectors

  17. 2. HEMODILUTION Augmented Axial Vectors (Hyperoxia) Redistributes O2 To Prevent An Anoxic Lethal Corner Augmented O2 Axial Vectors Potential Lethal Corner Line Low Hct paO2 = 400 mmHg Tissues Oxygenated Lethal Corner Obliterated Augmented O2 Radial Vectors

  18. 3. METABOLIC ACIDOSISPoor perfusion = decreased perfused capillary density (PCD)causing tissue anoxia R R Low PCD: Single capillary unit High PCD: Multiple capillary units Increasing PCD Closed capillary unit • WORKING MUSCLE RESTING MUSCLE NORMAL ORGAN FUNCTION SHOCK Decreasing PCD

  19. 3. METABOLIC ACIDOSISNormal Capillary Configuration Lowest tissue pO2: 1mmHg Highest tissue pO2: 99mmHg paO2 = 100mmHg SAO2 = 99% pvO2 = 40 mmHg SVO2 = 75% Blood Flow pvCO2 = 45 mmHg Lowest tissue pCO2: 42mmHg paCO2 = 40 mmHg Highest tissue pCO2: 47mmHg O2 radial vectors CO2 radial vectors

  20. 3. METABOLIC ACIDOSISCapillary Configuration In The Shock Patient paO2 = 100mmHg SAO2 = 99% pvO2 = 40 mmHg SVO2 = 75% Blood Flow pvCO2 = 60 mmHg paCO2 = 40 mmHg Anoxic &/or Hypercapnic Lethal Corner O2 radial vectors CO2 radial vectors

  21. 3. METABOLIC ACIDOSIS Poor Perfusion = Decreased Perfused Capillary Density Causing Tissue Anoxia ANOXIC LETHAL CORNER Blood Flow paO2 = 150 mmHg O2 RADIAL VECTORS O2 AXIAL VECTORS

  22. 3. METABOLIC ACIDOSIS Axial Kick = Oxygen Redistributed To The Lethal Corner NO ANOXIC LETHAL CORNER R r Blood Flow paO2 = 500 mmHg AUGMENTED O2 RADIAL VECTORS AUGMENTED O2 AXIAL VECTORS

  23. 3. METABOLIC ACIDOSIS FiO2 = 50% FiO2 = 50% FiO2 = 52% FiO2 = 46% FiO2 = 45% FiO2 = 42%

  24. 3. METABOLIC ACIDOSISAxial Kick Keeps Potential Lethal Corner Oxygenated Augmented O2 Axial Vectors Potential 1 mmHg tissue pO2 line paO2 = 150 mmHg Augmented O2 Radial Vectors

  25. 3. METABOLIC ACIDOSIS Reduced Axial Kick Causes Formation Of A Lethal Corner With Development Of A Base Deficit Reduced O2 Axial Vectors 1 mmHg tissue pO2 line paO2 = 100 mmHg Lethal Corner Forms: Anoxic tissue O2 Radial Vectors

  26. Hemodilution reduces DO2 Hypothermia & alpha stat impairs O2 off loading Hyperoxia provides dissolved O2 “Dissolved oxygen satisfies most of the brain's oxygen requirements during profound hypothermic cardiopulmonary bypass.” Dexter et al. 1997 “Used prior to DHCA normoxic CPB increases brain damage compared to hyperoxic CPB. The mechanism is hypoxic injury, which overwhelms any injury caused by oxygen free radicals.” Nollert et al. 1999 4. HYPOTHERMIC ARRESTProfound Hypothermic Bypass And Circulatory Arrest:The Need for Dissolved Oxygen

  27. 4. HYPOTHERMIC ARRESTBypass Hypothermia To Oxygen Load Tissues

  28. 4. HYPOTHERMIC ARRESTCirculatory Arrest: Extending The Safe Arrest Time Adult Brain MET @ 18°C = 0.7 cc/kg/min

  29. 4. HYPOTHERMIC ARREST Perfused Capillary Density (PCD): alpha stat vs. pH stat R R Low PCD: Single capillary unit High PCD: Multiple capillary units Open capillaries Increasing PCD Closed capillaries pH stat: 1. systemic vasodilation 2. increased PCD 3. high CO2 (relative acidosis) 4. oxyhemoglobin unloading promoted • Alpha stat: • systemic vasoconstriction • reduced PCD • low CO2 (relative alkalosis) • oxyhemoglobin unloading inhibited High PCD and high CO2 enhances tissue oxygen loading prior to deep hypothermic circulatory arrest

  30. 4. HYPOTHERMIC ARRESTAcid Produced During 60 Minutes Arrest @ 18C Normoxia = pvO2 <150 mmHg Hyperoxia = pvO2 > 300 mmHg Pearl, Grist et al. 2000.

  31. Oxygen Toxicity vs Reperfusion Injury • Oxygen toxicity • normal capillary blood flow • intracellular pH normal • active antioxidants • too much O2 • Reperfusion injury • poor capillary blood flow • intracellular pH change • deactivated antioxidants • reperfusion of capillaries & tissues • injury increases w/ O2 increase • AOX = antioxidants • ROS = reactive oxygen species

  32. 5. OXYGEN TOXICITYOff Gassing To Remove Nitrogen From Microemboli In The BodyAnd Resetting The “Oxygen Clock” • “Because of the effective defense systems (functioning antioxidants), the tolerance of viable human cells to (reactive oxygen species) is relatively high.” • Bauer & Bauer. 1999 • USN uses 100% O2 to off gas N2 causing decompression sickness • Oxygen toxicity prevented by five minute ‘air breaks’ taken intermittently restore antioxidant reserve capacity • Air breaks reduce CNS and pulmonary complications. • U.S Navy Diving Manual. 1991 Take away lesson for perfusionists: Reset the oxygen clock and reduce the potential for cardiac oxygen toxicity or reperfusion injury by reducing FiO2 prior to cross clamp removal.

  33. 5. OXYGEN TOXICITYNeurologic Complication Comparison:CPB vs. Hyperbaric Hyperoxia • CNS complications from CPB • stroke = 1.5% (CABG) to 10% (valves) • asymptomatic brain infarct (MRI) = 18% • Floyd et al. 2006 • Hyperbaric hyperoxia • pO2 = 1520 mmHg (2 atm) to 2280 mmHg (3 atm) for 1 to 10 hours: decompression sickness, wound healing, infection, CO poisoning, radiation injury/necrosis, tissue grafts, burns • CNS event < 0.01% • Neumeister. 2008 • The risk of stroke is 150 - 1800 times greater during CPB than during hyperbaric hyperoxia

  34. 6. REPERFUSION INJURYMyocyte Cell Death By Ischemic Anoxia And Subsequent Reperfusion (Reoxygenation) 21% O2 on for 3 hr: 60% mortality Experimental Group O2 off for 1 hr: 0% mortality Control Group O2 off for 4 hours: 14% mortality Becker. 2004

  35. 6. REPERFUSION INJURYReperfusion Injury Potential (RIP)Acronym for “Rest In Peace” RIP: the hidden risk of a lethal reperfusion injury upon the sudden reperfusion of ischemic tissues, i.e., the presence of a lethal corner. Shock: inadequate blood flow = poor tissue oxygenation & CO2 removal Cardiogenic Septic Traumatic Hypovolemic septic Neurogenic Shock: a state of insufficient perfusion that holds the potential for reperfusion injury if normothermic oxygenation is suddenly restored. Low CPB flow at normothermia Transplanted organs A cause of acute organ failure in transplants.

  36. 6. REPERFUSION INJURYECPR Hemodilution/Hypothermia To Prevent Reperfusion Injury Patients develop RIP during resuscitation Hypothermia reduces O2 need Hemodilution reduces oxygen delivery to tissues Allows high blood flow without excessive O2 delivery to facilitate CO2 removal. Capillaries damaged during reperfusion Reduced viscosity counters ‘no reflow’ phenomenon (aka DIC) www.benbest.com/cryonics/ischemia.html Mouse lung after gastric ischemic/hypoxia reperfusion Normal mouse lung • http://www.thoracic.org/sections/clinical-information/critical-care/critical-care-research/animal-models-of-acute-lung-injury.html

  37. 6. Reperfusion InjuryPerfusionists need to identify patients at risk for reperfusion injury on CPB • “Hyperoxemic (paO2 ~ 400 mmHg) cardiopulmonary bypass… did not produce oxidant damage or reduce functional recovery after cardiopulmonary bypass in non-hypoxemic controls….“In contrast, abrupt and gradual reoxygenation(of pre-CPB hypoxemic subjects)...produced significant lipid peroxidation, lowered antioxidant reserve capacity and decreased functional recovery.” • Ihnken et al. 1995

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