Endpoints in Tissue Oxygenation - PowerPoint Presentation

1. Endpoints in Tissue OxygenationBarbara McLean, MN, RN, CCNS-BC, NP-BC, CCRN, FCCMClinical Specialist Critical CareGrady Hospital, ATL, GAwww.barbaramclean.combamclean@mindspring.com

2. Grady Hospital, Atlanta GA

3. Shock is defined as inadequate tissueoxygenation

4. Which are the most appropriate cardio-respiratory variables to detect and to monitor the course of tissue hypoxia in the clinical setting ?

5. Conventional cardio-respiratory parameters are of limited value for the assessment of the adequacy of tissue oxygenation !

6. Pflüger 1872The cardio-respiratory system fullfills its physiological task by guaranteeing cellular oxygen supply and to remove the waste products of metabolism

7. Critical Care Medicine PrinciplesFusion of multiple, disparate medical specialties refined by applied bedside physiologyGoal is to improve morbidity, mortality in acute illness and major surgeryOutcome from acute illness is a function of time from diagnosis to initiation of EDGTAll current therapeutic endeavors attempt to contemporaneously improve oxygen delivery and minimize oxygen consumption

8. Three GoalsTissue perfusionLactateScV02, SvO2Base deficitLung oxygenationP/F ratioCompares oxygen assumed to be delivered to alveoli Fi02Oxygen dissolved in arterial blood Pa02Pa02 measured by ABG/Fi02 decimalP/F ratio > 400, ventilated> 0.40 >250Lung clearance of CO2Pv-aCO2ETCO2

9. Delivering and Measuring Tissue perfusionMACROCardiac Output (HR{SV})Stroke volume Systolic blood pressurePulse pressureUrine output in mls/Kg/hrPulsesColor TemperaturerefillMICROBase deficitBicarbonateAnion gapSvO2V-A CO2

10. Composite Value of ABG and VBGMainstays of diagnosis, therapy in acute illnessVBG historically used as: a surrogate measurement of arterial pH, PCO2ScvO2 or SvO2 measurementsOxygenation/perfusion abnormalitiesComposite clinical value rarely discussedSimultaneous initial ABG, VBGPowerful initial diagnostic strategyClinical decision adjunct in EGDT

11. INDICATIONSABGOxygenationVentilationAcid-Base StatusVBGVentilation and Acid-Base StatusCardiac Output (venous arterial PCO2 difference)Endpoint of resuscitation (ScvO2 and PCO2)

12. Blood Gas Report(Arterial)pH (No Units) 7.35-7.45 PaCO2 (mm Hg) 35-45PaO2 (mm Hg) 110 - 0.5(age) HCO3- (mmol/L): calc. 22-26 B.E. (mmol/L) -2 to 2O2 saturation: calc. >90%

13. Blood Gas Report(mixed/central venous)pH = 7.32-7.42PvCO2 = 40 - 50 (mm Hg)PvO2 = 36 - 42 (mm Hg)Oxygen Saturation > 70%Base Excess = -2 to +2

14. The Oxygenation ProfileDirect measure of acidInversely reflects acid (estimates one of the major buffers)pH | pCO2 | pO2 | O2 Sat| (H+)HC03| Base| Total CO2 Components of the ABG and Chemistry Panelthat are indicators in acid-base balance/imbalance.

15. The Oxygenation ProfileAcid-Base DisturbancesAre common in critical patientsMay be complex or mixedAre often confusingRequires accurate analysis to facilitate appropriate treatmentFocus on Metabolic Acidosis

16. The Oxygenation ProfileCells: ProducerProduces acid during metabolism: acid transported as carbonic acidTissue acids increase in insulin deficiency statesTissue acids increase in tissue hypoxia statesCells: Regulate pHAcidosis: acid (H+) uptake in exchange for potassium release provides buffer effect and promotes intracellular hypokalemiaAlkalosis: acid (H+) release in exchange for potassium uptake provides buffer effect and promotes intracellular hyperkalemiaKidney: RegulatorMajor volume and electrolyte regulatorAcid regulatorBase regulatorLung: Acid regulatorRate and depth of breaths depends on the carbonic acid and therefore the pH

17. 17The Oxygenation ProfileDirect Effects from Acid : Presence or AbsencepH: directly reflects acidWhen acid goes up, pH goes downAcids are formed as end products of protein, carbohydrate, and fat metabolism.To maintain the body’s normal pH (7.35-7.45), the H2C03 must be controlled: H+ must be neutralized (buffer and cells) or excreted (requires renal function)C02 must be regulated via ventilation

18. The BIG fourWhen you have metabolic acidosisKetonesLactateRenal failureHigh chloride?

19. Standard Bicarbonate:Plasma HCO3 after equilibrationto a PaCO2 of 40 mm Hg: Reflects non-respiratory acid base change: No quantification of the extent of the buffer base abnormality Base Excess: D base to normalise HCO3 (to 24) with PaCO2 at 40 mm Hg(Sigaard-Andersen): Reflects metabolic part of acid base D: No info. over that derived from pH, pCO2 and HCO3: Misinterpreted in chronic or mixed disordersNo click

20. H ION CONC.N.MOLS / L.pH 20 7.70 30 7.52 40 7.40 50 7.30 60 7.22H IONOH ION014pH stand for "power of hydrogen" H+ = 80 - last two digits of pHDon’t click wait …..till Last message …….. “H = 80-last two digits of pH”

21. 74 yo male found unresponsive and pulselessArterial Draw:pH = 7.28, PaCO2 = 34, HCO3 = 16Na = 153 Cl = 106 Total CO2 = 17Alb = 3 g/dL, Saturation = 84%Primary Acid-Base Disturbance?Metabolic Acid-Base Status?

22. Venous DrawpH = 7.08, pCO2 = 75, HCO3 = 21Na = 145, Cl = 103, Total CO2 =22 Alb = 3 g/dL, Saturation = 20%Primary Acid-Base Disorder?Metabolic Acid-Base Status?

23. Oxygen -> lungs -> alveoli -> bloodmuscles + organsOxygencellsOxygenOxygen +GlucoseenergyCO2bloodlungsCO2breathCO2PaCO2ETCO2PvCO2Respiratory Cycle

24. Venous Arterial CO2 DifferenceCirculatory FailureAssociated with Tissue Hypercarbic AcidosisHypovolemia, sepsis, shock …Cardiac Index = Endpoint of Resuscitation

25. PvCO2 and PaCO2 differenceInverse non linear significant relation between oxygen delivery, P(v-a)CO2 and pH(v-a)Brandi. Minerva Anestesio 1995.Increase P(v-a)CO2 mainly related to decrease in cardiac output and increased in ischemic hypoxia not in hypoxic hypoxiaVallet. J Appl Physiol 2000.Circulatory FailureAssociated with Tissue Hypercarbic AcidosisHypovolemia, sepsis, shock …Cardiac Index = Endpoint of ResuscitationDifference should be < 5 mmHg

26. Comparison of PCO2 and SvO2Key Points :SvO2 may reflect the metabolic rate and oxygen consumption PCO2 and/or serial lactate levels and clearance may reflect the adequacy of tissue perfusionAG, Bicarb, BASE reflect adequacy of tissue perfusion

27. Managing Tissue OxygenationOxyHemoglobinDissociationOXYGENDeliveryOXYGENConsumption

28. Why measure SvO2?A decrease in SvO2 is an early indicator of a threat to tissue oxygenationEarlier information results in earlier diagnosis with interventionsNormal range of SvO2 = 60-80%

29.

30. 0.95-1.000.60-0.80Oxygenation

31. Dissociation must be measured in the venous compartmentPv02Sv02Scv02

32. right shift tissues  H+ (Bohr shift)CO2temperature2,3 BPGH+  CO2temperature2,3 BPGleft shiftHold onSummaryAt any PO2 less O2 bound.At any PO2 more O2 bound.Source UndeterminedHemoglobin affinity for oxygen is not static

33. Understanding Tissue OxygenComponents of Oxygen Delivery1. Cardiac Output = Heart rate x stroke volume2. Total hemoglobin (02 carrying capacity)3. Saturation of hemoglobinFirst line compensatory mechanism ( patient)Increase the heart rate and stroke volume to increase delivery when cells are hyper metabolic and/or when oxygen is not functionally dissociating from its’ transporter, hemoglobin.

34. The two main determinants of oxygen supply to the tissues are arterial oxygen content and cardiac output

35. Understanding Tissue OxygenThe amount of oxygen required by the cells changes every secondWhen demand/consumption increases, hemoglobin releases oxygen more rapidlyShift to the right: releaseWhen demand/consumption decreases, hemoglobin decreases release or latches on to oxygenShift to the left: latched onSecond compensatory mechanism: hemoglobin more aggressively releases oxygen to dissolve in the blood (partial pressure) to be used by the cells

36. Understanding Tissue OxygenOxygen dissociation as a compensatory responseShifts in the bound oxygen mean that there is a change in the way oxygen is Taken up by the hemoglobin molecule at the alveolar level (Sa02)Depends on the partial pressure of alveolar gas (PA02)Released related to the partial pressure of capillary oxygen (Pa02, Pcap02)Capillary oxygen depends on the tissue oxygen (Pti02)Tissue oxygen goes down when cells are hypermetabolic and/or the delivery is inadequate

37. Targeting Mixed Venous Saturationnormally 70-75%may be elevated in sepsismaldistribution of blood flowIncreasing LAreduced venous saturation with normal arterial saturation→ increase in O2 extractionimbalance between VO2 and DO2improve supply

38. But …………Sa02 is pre-cell reservoir: 95-100% Sv02 is post cell left over: 60-80%Scv02 is global (upper extremities) post cell left over: 65-85%St02 is specific local post cell left over: 75-80%

39. Arterial Venous Saturation DifferenceSHOCKPaO2 vs PvO2 in Cardiogenic Shock

40. Central Venous Oxygen Saturation ScvO2Allows separation of early and late shockEasily measured with venous blood gasSurrogate measurement of mixed venous oxygen sat.5-18% higherA low ScvO2 always means a low SvO2!Normal ScvO2  68-76%25% extraction coefficient of normal physiology

41. Targeted ScvO2ScvO2 > 70 % reflected adequate oxyhemoglobin BUT not adequate perfusion unless tissue acidosis is absent!Do not keep ScvO2 too highImmediate ScvO2 level will be used for the endpoint if it is on lower siderequire additional parameters to assess perfusion state

42. When delivery is inadequate: look to the tissuesShift to right of oxyhemoglobin dissociation curve: doesn’t matter what Cardiac Output you have measured:Demand is highCardiac Output is poor (relative to demand)Content of oxygen is lowOxyhemoglobin dissociation shifts to right: RISK when RELEASE to RIGHTCell demands more (consumer of oxygen)PaO2 needed to provide to cellsSvO2 to as more oxygen is released to dissolved stae and used

43. When delivery is adequate and cells can utilize oxygenShift to leftDemand may be normalCardiac Output is adequate (relative to demand)Content of oxygen is adequateOxyhemoglobin dissociation shifts to left: LATCHED on to HgB when LEFT: Lactic acid checkCell demands less PaO2 needed to provide to cellsSvO2 as less oxygen is released to dissolved state and used by the cells represents less is needed at cells Validate with arterial blood gas and absence of acidosis when condition warrants it

44. When delivery appears adequate and cells cannot utilize oxygenShift to leftAll appears adequate EXCEPTPatient has acidosisPatient is on vasopressorsPatient requires CRRTOxyhemoglobin dissociation shifts to left: LATCHED on to HgB when LEFT: Lactic acid checkCells cannot utilize what has been deliveredPaO2 available to provide to cells ( poor blood flow or cellular use failure)SvO2 as less oxygen is released to dissolved state and used by the cellsValidate with arterial blood gas, lactic acid and absence of acidosis

45. 74 yo male found unresponsive and pulselessWhy a metabolic acidosis in arterial bed and respiratory acidosis in venous bed?Venous arterial PCO2 difference?PvCO2 (75) - PaCO2 (34) = 41Normal ≤ 6 mm HgVenous vs Arterial saturation difference?PaO2 = 50 mm Hg, saturation = 84%PvO2 =18, Venous Saturation = 20%Increased oxygen extraction from circulatory failure

46. Emergency MedicinePatients Who May BenefitHigh Acuity Elderly TraumaAny ageMechanism of injury puts at risk for bleedingMay have non-alarming vital signsMedical BleedingAll patients at risk for bleeding/suspected of internal bleeding: -Gastrointestinal-Vaginal-NasalOver 65 years old with: -Shortness of breath-Chest pain-Abdominal pain-Falls-Weakness-SyncopeCritical Care Patients described above Patients considered to be resuscitated; have non-alarming clinical signs Patients requiring active treatmentVeening, Crit Care. 2010;14(Suppl 1):P151.Ardolic, Ann Emerg Med. 2010;56:S131.

47. So what about lactate?

48. Measures of Tissue OxygenationLactate/pHNormal lactate – 1-2 mmol > 2 BAD> 4 mmol REALLY bad!pH – normal 7.35-7.4548

49. Oxygen to mitochondriaPatient may have defective oxygen extraction or oxygen may not reach the cells due to micro emboli or shunting of bloodDefective extraction may be due to Mitochondrial injuryShunting of bloodO2lactateCO2vaMicro-EmboliMaldistribution

50. Why Is Oxygen Important?Used in cellular respirationNeeded for energy production by cells and tissuesGLYCOLYSISKREB’S CYCLE+ELECTRON TRANSPORTPyruvateGlucoseOxygen2 ATP34 ATP

51. Why Is Oxygen Important?Used in cellular respirationNeeded for energy production by cells and tissuesGLYCOLYSISKREB’S CYCLE+ELECTRON TRANSPORTPyruvateGlucoseOxygen2 ATP4 ATPLactateDa02 is not adequateConsumption too highCannot use it

52. Lactic Acid Table

53. Lactate LevelsUtility of a single high initial lactate have been debatedpoor sensitivity and specificityLactate clearance is a better predictor of mortalityLac-time: time it takes to clear 10% of lactateTime to clear < 24 hours , improves survival in Severe sepsisLac-time also directly correlated with number of organ failuresOne lactate (lactic acid ) level is not as predictive or evaluative as a series over 24 hours ( i.e., Q6H) Bakker, J., Coffernils, M., Leon, M., Vincent, J.L. (1991). Blood lactate levels are superior to oxygen-derived variables in predicting outcomes in human patient shock. Chest, 99, 956-962.Bakker, J., Gris, P., Coffernils, M., Kahn R.J., Vincent, J.L. (1996). Serial blood lactate levels can predict the development of multiple organ failure following septic shock. Am J Surg, 171(2), 221-226.Nguyen, H.B., Rivers, E.P., Knoblich, B.P., et al. (2004). Early lactate clearance is associated with improved outcome in severe sepsis and septic shock. Crit Care Med, 32(8), 1637-1642.

54. Anion GapIf Metabolic acidosis is present, is anion gap wide (> 20)?Calculate the anion gap (AG). If the anion gap is ≥ 20, there is a primary metabolic acidosis regardless of pH or serum bicarbonate concentration. The acidosis is due to increased H+Gap is generally wide only with ↑ metabolic ACID production ( Lactic Acid/ Ketoacid)Principle: The body does not generate a wide anion gap as a compensatory mechanism for a primary disorder. With a wide AG, metabolic acidosis is ALWAYS the primary disorder!

55. Anion GapUsed to confirm type of metabolic acidosis with ABGUsed to diagnose metabolic acidosis without ABGAffected by:albumin (for each 1 gm decrease in albumin , add three points to gap)hyperchloremia (usually from fluid resuscitation)High Cl- causes decrease in available HC03-High Cl- binds to H+ → HClCannot compensate because is not a compound that can be blown offMetabolic acidosis with normal gap: non-gap acidosis most commonly occurs in hyperchloremia

56. What do these patients have in common?Patient 1Patient 2Patient 3HR 127133113RR 342818Pa02 70PaC02 23Fi02 1.0PEEP 12Rate 20 ACMV91PaC02 350.70PEEP 15Rate 15 SIMV100PaC02 390.5PEEP 20Rate 10 SIMVBPS 80 BPD 55BPS 80 BPD 40BPS 100 BPD 60SV 25SV 40SV 60Sv02 45%Sv02 70%Sv02 65AG 34AG 41AG 13LA 6.1LA 7.2LA 2.8

57. Match the ABG VBG with the Associated Condition(a) pH = 7.25, PCO2 = 30, PaO2 = 75, saturation = 97%, BE = -15, LA = -15(v) pH = 7.20, PCO2 = 36, PvO2 = 25, venous saturation = 45%(a) pH = 7.30, PCO2 = 25, PaO2 50, saturation = 85% BE = -10, LA = -10(v) pH = 7.20, PCO2 = 50, PvO2 = 25, venous saturation = 45%Hemorrhagic ShockCardiogenic Shock

58. Category One: Oxygenation and VentilationHR _______Stroke volume________RR ________The ventilator rate is ______PEEP __________MawP __________breathing ________ above the ventilator.Most recent ABG (if done )Pa02____________pH_____________PaC02 __________Base/Bicarb______HgB ________Anion Gap ______ScV02 or SvO2 _________ (if done)Cont or intP/F __________HgB____________OI_____________ETC02 ____________Sp02 ____________Category Two: Vascular tone (vessels)His systolic BP is _________His diastolic BP is ________His mean BP is ___________Currently on vasopressors (see side one)__________Base Deficit__________K+_________________Category Three: Volume (perfuion)His SV is _________________His SVV is ________________His CVP is ________________His U/O in mg/kg/hr is ______His IAP is _________________Any abnormal volume labs: Na+, BUN, Cr, Osmo, Base , Bicarb, HcTCategory Four: Ventricles (perfusion)His systolic BP is _________His diastolic BP is ________His mean BP is ___________His SVI ___________________His CI is __________________Any abnormal cardiac measures: echo, EKG, BNP, Troponin, arrythmia

59. SummarySimultaneous ABG and VBGInitial O2 delivery and consumption stateSerial measurements adequacy of interventionsABGOxygenation via Alveolar Gas EquationVentilation by PaCO2Acid Base Status by pH, PCO2, HCO3, SBEVBG (mixed or central)Oxygen extraction ratioScvO2 or SvO2Veno-arterial CO2 difference for cardiac output

60. Essentials of Hemodynamics:Focus on tissue oxygenationBarbara McLean, MN, RN, CCNS-BC, NP-BC, CCRN, FCCMClinical Specialist Critical CareGrady Hospital, ATL, GAwww.barbaramclean.combamclean@mindspring.com