O2_MI_ppt Nov 18

Re-thinking the O2 in MONA:: 

Re-thinking the O 2 in MONA: Considerations for the RT treating MI patients

"It AIN'T so much the things we don't know that get us into trouble. It's the things we know that just ain't so.“ - Josh Billings : 

"It AIN'T so much the things we don't know that get us into trouble. It's the things we know that just ain't so.“ - Josh Billings

Current Practice: 

Current Practice “… 98.3% said they always or usually use oxygen... while only 1.3% reported that they thought 'it may even increase the risk of death.” Burls A, Emparanza JI, Quinn T, Cabello JB. Oxygen use in acute myocardial infarction: an online survey of health professionals' practice and beliefs. Emergency Medicine Journal : EMJ 2010, 27(4):283-286

Slide 6: 

Why do we give O 2 for the MI patient?

Basis for O2 therapy in MI patients: 

Basis for O2 therapy in MI patients Animal studies showed reduction of infarct size with supplemental O2

Basis for O2 therapy in MI patients: 

Basis for O2 therapy in MI patients ECG and pain management studies Reduction in ST elevation Less analgesia requirements Criticized for not being well controlled

Slide 10: 

What sort of physiological things would not be favourable with an MI patient?

Slide 11: 

↓ HR ↓ SV ↓ Cardiac Index ↑ PVR ↑ SVR ↑ BP

Slide 12: 

Cardiovascular effects of Hyperoxemia ↓ HR ↓ SV ↓ Cardiac Index ↓ Myocardial Oxygen Consumption ↑ PVR ↑ SVR ↑ BP

Slide 13: 

Cardiovascular effects of Hyperoxia Thomas, et al. Hemodynamic effects of Oxygen in patients with myocardial infarction. Brit. Heart J., 1965, 27, 401.

Slide 14: 

. McNulty P H et al. Am J Physiol Heart Circ Physiol 2005;288:H1057-H1062 ©2005 by American Physiological Society Right Coronary Angiogram

Slide 15: 

McNulty, 2004

Slide 16: 

Cardiovascular effects of Hyperoxia A few considerations regarding heart failure If your cardiac index was greater than 2.5 L/min/m 2 tended to exhibit all the effects listed above. If your initial cardiac index was less than 2.5 L/min/m 2 your vascular response was muted or you had a small improvement in cardiac output. Davidson et al. Blood-gas and Hemodynamic responses to Oxygen in Acute Myocardial Infarction. Circulation 1973. Vol 47. p. 707

Cardiovascular effects of Hyperoxia: 

Cardiovascular effects of Hyperoxia “From these observations, we have concluded that the major determinant of the hemodynamic response to inhalation of oxygen in patients with acute myocardial infarction is the rise in arterial PO 2 ” The 200 mmHg Threshold Davidson et al. Blood-gas and Hemodynamic responses to Oxygen in Acute Myocardial Infarction. Circulation 1973. Vol 47. p. 707

Slide 18: 

Cardiovascular effects of Hyperoxia “ The decrease in myocardial blood flow prevents any additional oxygen delivery to the heart despite a considerable increase in arterial oxygen content; indeed the decrease in blood flow may be so great as to reduce the total amount of oxygen available to the heart .” Rawles, J M., Kenmure, A C F., Controlled trial of oxygen in uncomplicated mycardial infarction. BMJ 1976; Volume 1, p. 1123

Slide 19: 

Cardiovascular effects of Hyperoxia “Angina pectoris is accompanied by a rise of LVEDP to about 30 mmHg and might reflect cessation of blood flow to certain subendocardial areas of the myocardium. The increased amount of oxygen in the arterial blood during oxygen breathing might therefore not be transported to these ishaemic parts of the heart.” Lecerof, Harry. Central haemodynamics during oxygen breathing in angina pectoris. Thorax. 1974. Vol 29, p675-676

Our Best Evidence…: 

Our Best Evidence…

Slide 21: 

Randomized Controlled Trials Summaries Rawles and Kenmure in 1976 published in the British Medical Journal 200 patients but 157 only in statistical analysis 6 lpm of either oxygen or air via mask – gas identity hidden Variables looked at Size of infarct – inferred from AAT levels Arrhythmias Mortality Need for analgesia HR Duration of stay Followed till discharge

Slide 22: 

Randomized Controlled Trials Summaries Rawles and Kenmure in 1976 published in the British Medical Journal Results Statistically significant increase in sinus tachycardia Double the rate of V-Tach although not statistically significant Statistically significant increase in infarct size as inferred by AST 9 deaths in O2 group vs 3 in AIR group (not statistically significant)

Slide 23: 

Randomized Controlled Trials Summaries Rawles and Kenmure in 1976 published in the British Medical Journal “Thus oxygen treatment far from achieving the desired effect of limiting the ischemic area might actually result in an extension of the area of infarction… …the administration of oxygen does not appear to be of any benefit to patients with uncomplicated myocardial infarction. “ Rawles, J M., Kenmure, A C F., Controlled trial of oxygen in uncomplicated myocardial infarction. BMJ 1976; Volume 1, p. 1123

Slide 24: 

Randomized Controlled Trials Summaries Ukholkina in 2005 published in The International Journal of Interventional Cardoangiology 137 patients Confirmed uncomplicated MI 58 in O2 group – 79 in Air group Followed for 10 days Death Recurrent AMI Post-infarction angina Heart failure Area of tissue damage measured by ECG Cardiac Enzymes

Slide 25: 

Randomized Controlled Trials Summaries Ukholkina in 2005 published in The International Journal of Interventional Cardoangiology Results 1 death in O2 group None in Air group Complication of MI were higher in the Air group (8/58 for O2, 24/79 for Air)

Slide 26: 

Randomized Controlled Trials Summaries Ukholkina in 2005 published in The International Journal of Interventional Cardoangiology The authors concluded: Oxygen “reduced the area of necrosis and peri-infarction area, improved central hemodynamic, and decreased the rate of postoperative rhythm disorders as compared to patients breathing ambient air” as reported in Burls et al. Emerg Med J 2011;28:917-923

Slide 27: 

Randomized Controlled Trials Summaries Ukholkina in 2005 published in The International Journal of Interventional Cardoangiology This trial has been criticized for “irregularities” Air group on average was revascularized earlier Oxygen patient were generally “sicker” = poor randomization Gas source was not blinded Cardiac enzyme measurement was not standardized (variable time from infarct to sample) Complications rate did not seem to be analyzed appropriately

Slide 28: 

Two trials with conflicting results = we need more studies!

Slide 29: 

“... these findings provide no support for the view that oxygen therapy was either beneficial or safe in terms of either the size of the mycardial infarction or mortality rate, which would have been necessary to justify the use of a therapeutic intervention (i.e. first do no harm)...” Beasly et al. Oxygen therapy in myocardial infarction: an historical perspective. Journal of the Royal Society of Medicine. Vol 100. March 2007. p130-133

Slide 30: 

While death wasn’t significant even with meta-analysis there was definitely no demonstration of benefit for O 2 therapy Burls et al. Emerg Med J 2011;28:917-923

Slide 31: 

So now what do I do?

Slide 32: 

Don’t fight the body’s Adaptation The body’s response to hypoxia is increased blood flow! Results of Russek as reported in Beasly, Richard., Aldington, Sarah., Weatherall, Mark., Robinson, Geoffrey., McHaffie, David. Oxygen therapy in myocardial infarction: an historical perspective. Journal of the Royal Society of Medicine. Vol 100. March 2007. p130-133 Russek et al. One hundered percent oxygen in the treatment of acute mycardial infarction and severe angina pectoris. JAMA 1950. Vol 144 p. 373-375.

Slide 33: 

The Body’s Adaptation Neill’s experiments suggest that there may myocardial metabolism may not be compromised until SpO2 reaches 50% in normal subjects. This number obviously has to be adjusted for those with advanced coronary artery disease. Neill, William A. Effects of arterial hypoxemia and hyperoxia on oxygen availability for myocardial metabolism. American Journal of Cardiology Volume 24, Issue 2 , Pages 166-171, August 1969 (abstract only)

Slide 34: 

Nobody needs to be Hypoxic or Hyperoxic Keep SpO2 low normal ~94%  this may mean you don’t need any oxygen for many patients Caution - with known exterme athereosclerosis, triple vessel disease.

Slide 35: 

Nobody needs to be Hypoxic or Hyperoxic Common practice has been for basic EMT's to administer oxygen during the initial assessment of patients with suspected ACS. However, there is insufficient evidence to ‘support or refute oxygen use in uncomplicated ACS. If the patient is dyspneic, hypoxemic, has obvious signs of heart failure, or an oxyhemoglobin saturation <94%, providers should administer oxygen and titrate therapy to provide the lowest administered oxygen concentration that will maintain the oxyhemoglobin saturation ≥94% (Class I, LOE C). (Robert, S694-695) 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science

Slide 36: 

The take home… Oxygen is in fact a vasoactive substance! Patients with advanced coronary artery disease are theoretically in the most danger from a relfex coronary vasocontriction Data for oxygen’s use is limited – No harm but no benefit either Titrate aggressively for ~ 94%