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1 Hyperoxygenation During CPB: When Should We Use It? Gary Grist RN CCP, Chief Perfusionist The Childrens Mercy Hospitals and Clinics Kansas City, Missouri.

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Presentation on theme: "1 Hyperoxygenation During CPB: When Should We Use It? Gary Grist RN CCP, Chief Perfusionist The Childrens Mercy Hospitals and Clinics Kansas City, Missouri."— Presentation transcript:

1 1 Hyperoxygenation During CPB: When Should We Use It? Gary Grist RN CCP, Chief Perfusionist The Childrens Mercy Hospitals and Clinics Kansas City, Missouri No Disclosures

2 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 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: 1.Nitrogen entrainment 2.Hemodilution 3.Metabolic acidosis 4.Hypothermic arrest 5.Oxygen toxicity 6.Reperfusion injury

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

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

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

7 7 1. NITROGEN ENTRAINMENT Blood 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 Jan 15;364(1838): 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); Jul 06 [updated 2008 May 08].

8 8 1. NITROGEN ENTRAINMENT Borger 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 9 1. NITROGEN ENTRAINMENT Dealing with bubbles Use an arterial filter/bubble trap w/ purge Use an arterial filter/bubble trap w/ purge CO 2 flush the surgical field CO 2 flush the surgical field Add volume to the venous reservoir Add volume to the venous reservoir Slow down the suckers and vent Slow down the suckers and vent Limit perfusionist interventions Limit perfusionist interventions Use a circuit or MCA Doppler Use a circuit or MCA Doppler Ask the surgeon to stop what he is doing and fix the bubble source Ask the surgeon to stop what he is doing and fix the bubble source Increase sweep FiO 2 Increase sweep FiO 2

10 10 1. NITROGEN ENTRAINMENT Converting N2 bubbles in blood to O2 bubbles Vann RD, Butler FK, Mitchell SJ, Moon RE.Decompression illness. Lancet Jan 8;377(9760): Pre- oxygenator bubble Post- oxygenator bubble Gas in the bubble FiO2 = 21% FiO2 = 40% FiO2 = 100% N270%54%0% O219%35%89% CO25%5%5% H2O6%6%6%

11 11 O2 radial vectors r R Capillary radius: r = 5µ Capillary X-section : A = r 2 = µ 2 Cylinder radius: R = 10 Cylinder X-section: A = R 2 = 314 µ 2 Capillary X-section Cylinder X-section Ratio: = 1/4 paO2 = 80 mmHgpvO2 = 40 mmHg Avg. ptO2 = 20 mmHg Avg. ptO2 = 10 mmHg Blood Flow Understanding The Oxygen Pressure Field: Krogh Cylinder Model Highest ptO2: 79 mmHg Lowest ptO2: 1 mmHg OPF Range: 79 ~ 1 mmHg

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

13 13 O2 radial vectors 1 mmHg pO2 line ANOXIC LETHAL CORNER paO2 = 80mmHgpvO2 = 40 mmHg Highest tissue pO2: 79mmHg Anoxic tissue Capillary radius: r = 5µ Capillary X-section : A = r 2 = µ2 Cylinder radius: R = 20 Cylinder X-section: A = R2 = 1256 µ2 Ratio: Capillary X-section Cylinder X-section = 1/16 r R Blood Flow

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

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

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

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

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

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

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

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

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

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

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

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

26 26 4. HYPOTHERMIC ARREST Profound Hypothermic Bypass And Circulatory Arrest: The Need for Dissolved Oxygen Hemodilution reduces DO2 Hemodilution reduces DO2 Hypothermia & alpha stat impairs O2 off loading Hypothermia & alpha stat impairs O2 off loading Hyperoxia provides dissolved O2 Hyperoxia provides dissolved O2 Dissolved oxygen satisfies most of the brain's oxygen requirements during profound hypothermic cardiopulmonary bypass. Dissolved oxygen satisfies most of the brain's oxygen requirements during profound hypothermic cardiopulmonary bypass. Dexter et al. 1997Dexter et al 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. 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. 1999Nollert et al. 1999

27 27 4. HYPOTHERMIC ARREST Bypass Hypothermia To Oxygen Load Tissues

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

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

30 30 4. HYPOTHERMIC ARREST Acid Produced During 60 Minutes 18 C Normoxia = pvO2 <150 mmHg Hyperoxia = pvO2 > 300 mmHg Pearl, Grist et al

31 31 Oxygen Toxicity vs Reperfusion Injury Oxygen toxicity Oxygen toxicity normal capillary blood flow normal capillary blood flow intracellular pH normal intracellular pH normal active antioxidants active antioxidants too much O 2 too much O 2 Reperfusion injury Reperfusion injury poor capillary blood flow poor capillary blood flow intracellular pH change intracellular pH change deactivated antioxidants deactivated antioxidants reperfusion of capillaries & tissues reperfusion of capillaries & tissues injury increases w/ O 2 increase injury increases w/ O 2 increase AOX = antioxidants ROS = reactive oxygen species

32 32 5. OXYGEN TOXICITY Off Gassing To Remove Nitrogen From Microemboli In The Body And 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. Because of the effective defense systems (functioning antioxidants), the tolerance of viable human cells to (reactive oxygen species) is relatively high. Bauer & Bauer Bauer & Bauer USN uses 100% O2 to off gas N2 causing decompression sickness 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 Oxygen toxicity prevented by five minute air breaks taken intermittently restore antioxidant reserve capacity Air breaks reduce CNS and pulmonary complications. Air breaks reduce CNS and pulmonary complications. U.S Navy Diving Manual U.S Navy Diving Manual Take away lesson for perfusionists: R 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 33 5. OXYGEN TOXICITY Neurologic Complication Comparison: CPB vs. Hyperbaric Hyperoxia CNS complications from CPB CNS complications from CPB stroke = 1.5% (CABG) to 10% (valves) stroke = 1.5% (CABG) to 10% (valves) asymptomatic brain infarct (MRI) = 18% asymptomatic brain infarct (MRI) = 18% Floyd et al. 2006Floyd et al Hyperbaric hyperoxia 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 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% CNS event < 0.01% Neumeister. 2008Neumeister The risk of stroke is times greater during CPB than during hyperbaric hyperoxia The risk of stroke is times greater during CPB than during hyperbaric hyperoxia

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

35 35 6. REPERFUSION INJURY Reperfusion 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. 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 Shock: inadequate blood flow = poor tissue oxygenation & CO2 removal Cardiogenic Cardiogenic Septic Septic Traumatic Traumatic Hypovolemic septic Hypovolemic septic Neurogenic Neurogenic Shock: a state of insufficient perfusion that holds the potential for reperfusion injury if normothermic oxygenation is suddenly restored. Shock: a state of insufficient perfusion that holds the potential for reperfusion injury if normothermic oxygenation is suddenly restored. Low CPB flow at normothermia Low CPB flow at normothermia Transplanted organs Transplanted organs A cause of acute organ failure in transplants.

36 36 6. REPERFUSION INJURY ECPR Hemodilution/Hypothermia To Prevent Reperfusion Injury Patients develop RIP during resuscitation Patients develop RIP during resuscitation Hypothermia reduces O2 need Hypothermia reduces O2 need Hemodilution reduces oxygen delivery to tissues Hemodilution reduces oxygen delivery to tissues Allows high blood flow without excessive O2 delivery to facilitate CO2 removal. Allows high blood flow without excessive O2 delivery to facilitate CO2 removal. Capillaries damaged during reperfusion Capillaries damaged during reperfusion Reduced viscosity counters no reflow phenomenon (aka DIC) Reduced viscosity counters no reflow phenomenon (aka DIC) care/critical-care-research/animal-models-of-acute-lung-injury.html Normal mouse lung Mouse lung after gastric ischemic/hypoxia reperfusion

37 37 6. Reperfusion Injury Perfusionists 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. 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 Ihnken et al. 1995


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