1 / 59

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

shad-adams
Download Presentation

The Role of Oxygen in Acute Coronary Syndromes

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  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

More Related