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The Role of Oxygen in Acute Coronary Syndromes

The Role of Oxygen in Acute Coronary Syndromes. Stephen L. Rennyson MD October 28, 2010. Cardiovascular Disease. Over 2 million ACS patients yearly, tremendous improvement in mortality

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The Role of Oxygen in Acute Coronary Syndromes

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  1. The Role of Oxygen in Acute Coronary Syndromes • Stephen L. Rennyson MD • October 28, 2010

  2. Cardiovascular Disease • Over 2 million ACS patients yearly, tremendous improvement in mortality • One of the most widely studied clinical scenarios with robust data for almost all clinical interventions employed http://www.nhlbi.nih.gov/about/factbook-07/chapter4.htm

  3. What is the role of oxygen therapy in the ACS patient?

  4. Oxygen Thearpy • Historical Perspective • Initial ACC/AHA ACS treatment algorithm • The Evidence of Oxygen Therapy in ACS • Initial studies of oxygen therapy in ACS • Randomized Trials • Oxygen Therapy -- Potentially Harmful Mechanisms -- studies outside ACS • Effect on coronary blood flow • Effect on stroke volume and cardiac output • Effects on peripheral vascular resistance • Oxygenation and clinical evaluation • Critical Care Medicine • Arterial Hyperoxia after Cardiac Arrest • ARDSNet • Rivers and Early Goal Directed Therapy in Sepsis • Conclusions

  5. Historical Perspective • 1900 described the use of oxygen in patients with myocardial infarction • Improving angina • 1940 Bolan described oxygen use to relieve anginal pain in ACS

  6. Historical Perspective • Initial theory for oxygen therapy: • Treating local and systemic hypoxia

  7. Historical Perspective • Local (myocardial) supply and demand problem: • Coronary artery plaque rupture -- vessel occlusion • Myocardial hypoxia distal to the occlusion • Oxygenation or systemic hypyeroxia can improve oxygen delivery to the myocardium

  8. Historical Perspective • Systemic hypoxia from an ACS • Acute LV failure, increased PCWP, pulmonary edema • Neuro-endocrine function of pain and anxiety • Oxygen therapy will improve myocardial hypoxia -- thus alleviate the cascade of events

  9. Historical Perspective • Supplemental Oxygen if able to improve local tissue hypoxia should: • Relieve anginal symptoms • Decrease arrhythmias • Decrease infarct size

  10. Oxygen Thearpy • Historical Perspective • Initial ACC/AHA ACS treatment algorithm • The Evidence of Oxygen Therapy in ACS • Initial studies of oxygen therapy in ACS • Randomized Trials • Oxygen Therapy -- Potentially Harmful Mechanisms -- studies outside ACS • Effect on coronary blood flow • Effect on stroke volume and cardiac output • Effects on peripheral vascular resistance • Oxygenation and clinical evaluation • Critical Care Medicine • Arterial Hyperoxia after Cardiac Arrest • ARDSNet • Rivers and Early Goal Directed Therapy in Sepsis • Conclusions

  11. Acute Coronary SyndromesACC/AHA Guidelines

  12. ACC/AHA Guidelines • Management Section -- Routine Measures • Oxygen • Analgesia • Morphine • Nitrates • Aspirin • Beta-blockade where appropriate Circulation. 2004;110:588-636.

  13. ACC/AHA Guidelines • Establish Coronary Blood Flow: • Door to reperfusion time of less than 90 minutes (PCI) • Fibrinolytics < 30 minutes • Facilitated PCI Circulation. 2004;110:588-636.

  14. Specific recommendations • Class I • Supplemental oxygen should be administered to patients witharterial oxygen desaturation (SaO2 less than 90%). (Level ofEvidence: B) • Class IIa • It is reasonable to administer supplemental oxygen to all patientswith uncomplicated STEMI during the first 6 hours. (Level ofEvidence: C) Circulation. 2004;110:588-636.

  15. Goals of Oxygen Thearpy • Oxygen therapy imbedded in guidelines with little evidence that -- beyond treating hypoxia -- there is benefit in ACS

  16. Oxygen Thearpy • Historical Perspective • Initial ACC/AHA ACS treatment algorithm • The Evidence of Oxygen Therapy in ACS • Initial studies of oxygen therapy in ACS • Randomized Trials • Oxygen Therapy -- Potentially Harmful Mechanisms -- studies outside ACS • Effect on coronary blood flow • Effect on stroke volume and cardiac output • Effects on peripheral vascular resistance • Oxygenation and clinical evaluation • Critical Care Medicine • Arterial Hyperoxia after Cardiac Arrest • ARDSNet • Rivers and Early Goal Directed Therapy in Sepsis • Conclusions

  17. Kenmure 1968 • Measure the effects of oxygen in 50 ACS patients • Not randomized, no controls • Observational study pre and post administration of high flow oxygen • PaO2 increased from a mean of 65 to 433 Br Med J. 1968 Nov 9;4(5627):360-4

  18. Kenmure 1968 • Hemodynamics • Cardiac output decreased secondary to a decreased SV (HR stable) • Increased SVRI • Blood Gas • No change in the pH, pCO2, marked increase in PaO2 • Decreased serum lactate with oxygen treatment Br Med J. 1968 Nov 9;4(5627):360-4

  19. Davidson 1973 • Evaluate effects of Oxygen on a large group of patients with an ACS. • Compared room air to 100% oxygen via NRB for 10 minutes in the catheterization lab • Blood gas response • Hemodynamic response Circulation. 1973 Apr;47(4):704-11

  20. Davidson 1973 • 60 patients with ACS - within 1hour of presentation • confirmed MI by ECG and cardiac enzymes • Assigned to one of 4 clinical classes -- based on presentation • No overt heart failure (28) • 13 pts classified as Ib group (level II or greater) • Mild to moderate CHF (19) • Overt CHF - pulmonary edema (9) • Cardiogenic shock (4) • Compared to 9 Controls -- Admitted wih suspected ACS and ruled out Circulation. 1973 Apr;47(4):704-11

  21. Davidson 1973 • Blood Gas Response • Degree of blood gas response paralleled the degree of LV dysfunction • Predict preclinical CHF by their blood gas response (class Ib patients) Circulation. 1973 Apr;47(4):704-11

  22. Davidson 1973 • Hemodynamic Response • Uncomplicated pts (group I) equaled controls • decrease HR SV • increase in PVR Circulation. 1973 Apr;47(4):704-11

  23. Davidson 1973 • Most profound change in Hemodynamic Response in those who achieved a PaO2 of > 200 mmHg (all statistically significant changes): • Decreased HR, CI, SI • Increased PVR • Compared with those who never achieved a PaO2 > 200 mmHg after supplemental O2 • No statistical change in HR, CI, SI, PVR Circulation. 1973 Apr;47(4):704-11

  24. Madias 1976 • Measure the effects of high flow oxygen on patients with Anterior STEMI • 17 patients • 49 lead ECG pre, during, and post oxygen therapy -- summation of ST elevation • PaO2 increased from a mean of 70 to 278 Circulation 1976;53;411-417

  25. Madias 1976 • Noted decrease in ST segments with oxygen administration • No correlation with level of PaO2 and change in ST segments • After returning to ambient air: • ST segment elevations returned to prior elevation • No change in hemodynamics • No change in pain control Circulation 1976;53;411-417

  26. Wilson 1997 • Initially looked at CCU’s across United Kingdom • Only 50% utilized oxygen therapy routinely • Determine the incidence of hypoxemia in ACS • Evaluate the utility of oxygen therapy with ACS J R Coll Physicians Lond. 1997 Nov-Dec;31(6):657-61

  27. Wilson 1997 • 50 patients with ACS and treated with thrombolysis • Randomized to 4L/min of oxygen vs Compressed air for 24 hours J R Coll Physicians Lond. 1997 Nov-Dec;31(6):657-61

  28. Wilson • No Oxygen Thearpy • Hypoxemia noted in 70% (<90% SpO2) • Oxygen Thearpy • Hypoxemia noted in 27% (<90% SpO2) J R Coll Physicians Lond. 1997 Nov-Dec;31(6):657-61

  29. Wilson • Results • Hypoxemia is common • No difference in arrhythmias • No difference ST segment changes • Conclusions • Measuring oxygen saturations is justified • Oxygen use routinely is not necessary J R Coll Physicians Lond. 1997 Nov-Dec;31(6):657-61

  30. Rawles • 1976 study of ACS patients • Double blind, randomized trial of 200 patients • Suspected ACS -- 43 pts without ACS excluded • 6 L/min oxygen vs compressed air for 24 hours • Exclusions: • CHF, COPD, Cardiogenic shock, SCD, clinically short of breath Br Med J. 1976 May 8;1(6018):1121-3.

  31. Rawles • Compare oxygen thearpy with compressed air • Infarct size (AST) • Mortality • Ventricular Tachycardia • Pain control (opiate use) Br Med J. 1976 May 8;1(6018):1121-3.

  32. Rawles • 6 L/Min Oxygen (80 patients) • Infarct Size: • Aspartate Amiontransferase 99.9 IU/ml • Mortality: • 9 of 80 (11.3%) • Compressed Air (77 patients) • Infarct Size: • Aspartate Amiontransferase 80.7 IU/ml • Mortality: • 3 of 77 (3.9%) Br Med J. 1976 May 8;1(6018):1121-3.

  33. Rawles • 6 L/Min Oxygen • Ventricular Tachycardia: • 11/80 (13.8%) • Opiate Use: • 57/80 (71.3%) • Compressed Air • Ventricular Tachycardia: • 5/77 (6.5%) • Opiate Use: • 52/77 (67.5%) Br Med J. 1976 May 8;1(6018):1121-3.

  34. Rawles • Oxygen therapy during ACS does not appear to offer an advantage • Suggests a “deleterious effect of oxygen” • Little place for routine oxygen administration for all ACS patients Br Med J. 1976 May 8;1(6018):1121-3.

  35. Oxygen Thearpy • Historical Perspective • Initial ACC/AHA ACS treatment algorithm • The Evidence of Oxygen Therapy in ACS • Initial studies of oxygen therapy in ACS • Randomized Trials • Oxygen Therapy -- Potentially Harmful Mechanisms -- studies outside ACS • Effect on coronary blood flow • Effect on stroke volume and cardiac output • Effects on peripheral vascular resistance • Oxygenation and clinical evaluation • Critical Care Medicine • Arterial Hyperoxia after Cardiac Arrest • ARDSNet • Rivers and Early Goal Directed Therapy in Sepsis • Conclusions

  36. Ganz circulation 1972 • Evaluate effects of hyperemia in pts with CAD (9) vs Controls (6) • Average PaO2 >400 • HR and CI decreased • Increased MAP in the CAD group • Decreased coronary sinus flow in CAD group secondary to increased resistance Circulation. 1972 Apr;45(4):763-8

  37. McNulty 2007 • Evaluate the effect of oxygen on coronary blood flow (and see effects of Vitamin C) • 12 patients total: • Patients with angina or abnormal stress • Coronary angiogram with moderate grade LAD stenosis J Appl Physiol. 2007 May;102(5):2040-5. Epub 2007 Feb 15.

  38. McNulty • Patients given 100% FiO2 • Measured HR, Blood Pressure, PCO2, PaO2, • As well measured LAD diameter, coronary blood flow, coronary vascular resistance J Appl Physiol. 2007 May;102(5):2040-5. Epub 2007 Feb 15.

  39. McNulty • Blood Gas • PaO2 average 321 • No change in pH or PCO2 • Hemodynamics • No change in HR, MAP • 20% decrease in coronary blood flow • associated with a 23% increase in coronary resistance • Angiography • LAD diameter -- no change J Appl Physiol. 2007 May;102(5):2040-5. Epub 2007 Feb 15.

  40. McNulty • Hyperoxia is associated with an decrease in coronary blood flow • No change in LAD diameter • Thus, the hemodynamic changes seen are likely the result of microcirculation changes J Appl Physiol. 2007 May;102(5):2040-5. Epub 2007 Feb 15.

  41. Hyperoxia in Heart Failure • End stage CHF patients -- supplemental O2 • Increased PVR • Lowered CO • Increased PCWP • Ventricular Assist Devices • Those with a fixed CO -- Increased PVR with hyperoxia J Appl Physiol. 1997 May;82(5):1601-6.

  42. Crawford • Supplemental oxygen increases peripheral vascular resistance -- even in those with an LVAD • Supplemental oxygen does not change sympathetic outflow • What is the mechanism? J Appl Physiol. 1997 May;82(5):1601-6.

  43. Crawford • Measuring PVR in those after 10 minutes of forearm circulatory arrest -- Hyperemic blood flow response alone and with hyperoxia (100% FiO2 for 15 minutes) • Oxygen demonstrated an increase in vascular resistance and a decrease in blood flow J Appl Physiol. 1997 May;82(5):1601-6.

  44. Crawford • Overcome the vasodilator response of ischemia • Proposed mechanism -- degradation of NO -- known to be destroyed by free radical and simply oxygen J Appl Physiol. 1997 May;82(5):1601-6.

  45. Oxygen Thearpy • Historical Perspective • Initial ACC/AHA ACS treatment algorithm • The Evidence of Oxygen Therapy in ACS • Initial studies of oxygen therapy in ACS • Randomized Trials • Oxygen Therapy -- Potentially Harmful Mechanisms -- studies outside ACS • Effect on coronary blood flow • Effect on stroke volume and cardiac output • Effects on peripheral vascular resistance • Oxygenation and clinical evaluation • Critical Care Medicine • Arterial Hyperoxia after Cardiac Arrest • ARDSNet • Rivers and Early Goal Directed Therapy in Sepsis • Conclusions

  46. Oxygenation • Supplemental • Nasal Canula • Approximately each liter/min will increase the FiO2 by about 3 % • Face Mask -- Can attain FiO2 100% • Invasive and noninvasive mechanical ventilation • CPAP/BiPAP • Mechanical Ventilator • Increase oxygenation with FiO2 and PEEP

  47. Oxygenation • How is it measured? PaO2, SpO2, CaO2 • Blood gasses • Pulsoximeter • Requires Knowledge of the Oxygen Content (CaO2) equation • CaO2 = (SaO2 x Hb x 1.34) + .003(PaO2)

  48. Blood Gasses • Typical Blood gas provides: • pH, CO2, PaO2, Calculated HCO3 • PaO2 • Measure of the dissolved oxygen in blood • Reflects the atmospheric oxygen -- assuming normal lungs • CaO2 = (SaO2 x Hb x 1.34) + .003(PaO2)

  49. Oxygen • Oxygen dissociation curve: • PaO2 of 60 mmHG generally equates to a 90% saturation • Once hemoblobin saturated it is shifted into oxygen tension in blood (PaO2)

  50. Pulsoximetry • CaO2 = (SaO2 x Hb x 1.34) + .003(PaO2) • Pulsoximeter provides the SaO2 • Hemoglobin measurement

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