Should oxygen be given in myocardial infarction?
BMJ 2010; 340 doi: https://doi.org/10.1136/bmj.c3287 (Published 17 June 2010) Cite this as: BMJ 2010;340:c3287
All rapid responses
The previous contribution on oxygen supplementation in myocardial
infarction (1) has triggered some compelling responses. One is
particularly important, in that it puts forward a recent guideline that
does not recommend normobaric oxygen (2).
The undersigned does principally recommend to follow guidelines, even
though the studies supporting guideline-recommendations may be weak. In
fact, only approx. 10% of all guideline-recommendations in cardiology are
based on evidence class A. Let us therefore examine what the three
authoritative societies in cardiology recommend in their guidelines:
The AHA and ACC (American Heart Association / American College of
Cardiology), guideline on STEMI (2004) gives a class IIa recommendation to
the use of oxygen, by stating that “it is reasonable to administer
supplemental oxygen to all patients with uncomplicated STEMI during the
first 6 hours” (3). As pointed out in the previous correspondence, there
is very little literature covering this topic, hence the level of Evidence
is C.
The ESC guideline on STEMI (2008) states that “oxygen 2-4 L/min by
mask or nasal prongs should be administered to those who are breathless or
who have any features of heart failure or shock.” (4).
It is important to repeat that there is no convincing evidence of
harm regarding the administration of oxygen in myocardial infarction. None
of the five studies selected in the review by Farquhar et al. (5),
irrespective of how profoundly dr. O’Driscoll relies on its conclusions,
dealt with patients suffering from myocardial infarction.
References:
1. Atar D: Should oxygen be given in myocardial infarction? BMJ
2010;340:c3287.
2. O’Driscoll BR, Davison AG, Howard LS: Maintain a normal oxygen
level until more evidence is available. Hyperoxameia reduces coronary
artery blood flow. BMJ 2010;340:c3287 - rapid response.
3. Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, et
al. ACC/AHA guidelines for the management of patients with ST-elevation
myocardial infarction—executive summary: a report of the American College
of Cardiology/American Heart Association. Circulation 2004;110(5):588-636.
4. Van de Werf F, Bax J, Betriu A, Blomstrom-Lundqvist C, Crea F,
Falk V, et al. Management of acute myocardial infarction in patients
presenting with persistent ST-segment elevation: the Task Force on the
Management of STSegment Elevation Acute Myocardial Infarction of the
European Society of Cardiology. European Heart Journal 2008;29(23):2909-
45.
5. Farquhar H, Weatherall M, Wijesinghe M, Perrin K, Ranchord A,
Sommonds M, Beasley R: Systematic review of studies of the effect of
hyperoxia on coronary blood flow. Am Heart J. 2009;158(3):371-7.
Competing interests:
None declared
Competing interests: No competing interests
Cardiologists use the tension time index (TPI) as a measure of
myocardial work each minute, the TPI being derived from the product of the
area under the systolic portion of the left ventricular pressure curve and
the heart rate. They have also used it as a measure of minute myocardial
oxygen demand because the two are correlated. They have used it to define
the threshold minute myocardial oxygen consumption above which angina
occurs in accordance with the Burns thesis by inducing an artifical
tachycardia by pacing the right atrium at progressively increasing rates.
The problem is that no such threshold can be found in some patients and no
universally accepted explanation for this fact has been proposed.
Furthermore there is no satisfactory explanation for the reduction in
exercise tolerance after food. In seeking to explain these anomalies
cardiologists have assumed the latest embodiment of the idea that
ischaemia occurs when the myocardium is stressed beyond the limit of its
metabolic reserve with maximum vasodilatation and oxygen extraction so
that oxygen demand exceeds supply, a thesis that was first proposed by
Burns in 1809, 201 years ago.
We now know that metabolic work depletes ATP pools some 10%, ADP
pools some 0% and increase AMP pools some 600% and that the increase in
AMP is accompanied by a fall in pH for the two are closely related
stochiometrically. This is convenient for the increase in AMP activates
AMPK, and the enzymatic cascade that triggers, the fall in pH has a
negative inotropic effect, seemingly due to inhibiting the inward calcium
slow current, releasing calcium from the sarcoplasmic reticulum and/or
possibly to opening the Katp channel. Collectively these changes act to
preserve and even to restore to normality myocardial tissue energetics
just as presumed to occur following the administration of beta blockers.
But, as the biochemistry textbooks point out, the rise in AMP may be
induced not only by an increase in workload but also by a decrease in the
availablity of nutrient for ATP resynthesis. Indeed were it not for the
availability of nutrient, fatty acids, glucose and lactate in the case of
the heart, no ATP could be produced. The same cannot be said for oxygen.
On the contrary the most active metabolic states, such as the growth of an
embryo, wound healing and neoplastic growth, rely upon anaerobic
metabolism to generate their ATP needs. This is not surprising for the
products of glycolysis and the Krebs cycle include protons, NADH and FADH2
and carbon dioxide and it is only the electron transport chain that
requires oxygen to be the last electron acceptor before the formation of
water. Furthermore in our dog experiments, cited in my earlier rapid
response, "the intramural pH and O2 consumption did not decrease in the
hypoxic group". Thus it would seem that is the availability of nutrient
and not of oxygen that is ever likely to be the rate limiting factor even
in stable angina.
Herein may lie a satisfactory explanation for the reduction in
exercise tolerance after food and the failure to find a threshold in some
patients.
Competing interests:
None declared
Competing interests: No competing interests
As a medical registrar in the late 1970's, sometimes admitting
patients to coronary care for myocardial infarction, I used to wonder why
everyone ended up with intranasal oxygen when it is was only in the
minority of cases who were in severe cardiac failure or cardiogenic shock
who had low oxygen saturations. However, the practice has persisted
regardless, and I believe the reason is something far more subliminal than
those elegant physiologic arguments outlined above.
When a patient is admitted to a cardiac ward, he or she is suddenly
"contained" in a psychiatric sense by warm hands, chatty nurses, bleebing
monitors, clean sheets and pumping blood pressure cuffs. One is now "safe"
and a pinch of oxygen intranasally adds to this delusion as even a layman
knows that oxygen is good and carbon dioxide and monoxide are bad. Chicken
soup is also good and a wee dram of whisky is also good.
Life is full of 'Yings' and 'Yangs' and get them out of kilter means
bad things can happen. The average patient does not care a fig about the
oxygen dissociation curve and that most oxygen is glued to haemoglobin and
that only a tiny fraction is dissolved in plasma, a bit like gas in ginger
ale. I suspect this also escapes most our cardiologists who are steeped in
American cardiology and a culture of "Big Mac" paradigms.
Thus oxygen is to patients what chicken soup is to a Jewish mother or
even to Hippocrates. Finally, as a thoracic physician, I have often
thought that intranasal oxygen in these patients is also reassuring to the
cardiologist. We are treating the doctor as well as the patient. Now that
the lungs are under control, that only leaves the heart.
As for the lungs, it was thought until Dr. John Mayow's "Tractatus
Quinque" (1674) that their job was to cool the blood and as cardiologists
don't "get" the lungs, oxygen always seemed "cool".
In my medical career, I have witnessed the demise of so many dogmas,
and the older I become, the more I see that the foundation of the Temple
of Hygeia is based more on shifting sediments than a batholith.
Competing interests:
None declared
Competing interests: No competing interests
In his rapid response to Dan Atar's editorial (1) B Ronan O'Driscoll,
Consultant Respiratory Physician, wrote, "In considering areas of
medicine where evidence is weak, the physician is faced with a choice. The
first principle he or she will apply is that of "primum non nocere" or
first do no harm. He or she will ask if there is any evidence that giving
oxygen is beneficial, the answer to which is “no”. He or she will then ask
if there is evidence of harm to which the answer is “maybe” based on the
recent Cochrane review that Professor Atar criticises. In response to this
alone the answer should be to limit oxygen to those who are
hypoxaemic......A systematic review by Farquhar and colleagues reported a
mean reduction in coronary artery blood flow of 8-29% in five studies
where oxygen was given to patients with heart disease and there was a 21-
41% increase in coronary vascular resistance and a mean reduction of 15-
27% in myocardial oxygen consumption. Giving oxygen to a patient with
normal haemoglobin oxygen saturation (96-98%) can increase the blood
oxygen content by only 2-4% because very little oxygen is carried in the
blood independently of haemoglobin. This small rise in blood oxygen
content cannot compensate for the reduced coronary blood flow found in all
published studies. Oxygen has similar effects on cerebral blood flow and
oxygen was given routinely to normoxaemic patients with strokes until it
was shown to increase mortality significantly in patients with mild and
moderate strokes with no mortality effect in severe strokes..It is
regrettable that the BMJ failed to have this editorial peer reviewed
because the views expressed are so far out of line with current UK
guidance and the author appears to be unaware of the overwhelming
physiological evidence that hyperoxia causes a reduction, not an increase
in oxygen delivery to ischaemic myocardium".
We have examined, "changes in O2 consumption, O2 extraction, and
intramural pH, resulting from a decreasing O2 delivery, ..in the intact
dog intestine. The O2 delivery was decreased by ischemia, hypoxia, and
combined hypoxia-ischemia. A noninvasive approach for determining
intramural pH based on the principle of tonometry was used. There was a
strong correlation between the changes in intramural pH and intestinal O2
consumption as O2 delivery was decreased. Intramural pH and O2 consumption
were initially maintained in the face of decreasing O2 delivery, but after
a critical point they decreased. This critical point was 60.3 +/- 1.6% of
base-line O2 delivery in the ischemic group and 51.3 +/- 2.7% of base line
in the hypoxic-ischemic group. Despite a decrease to 36.0 +/- 5.6% of base
-line O2 delivery, the intramural pH and O2 consumption did not decrease
in the hypoxic group. O2 extraction increased with decreasing O2 delivery
but did not plateau, indicating no diffusion limitation. The data suggest
that blood flow is the major factor limiting intestinal O2 consumption"
(2). Thus the addition of hypoxaemia to vascular occlusion rendered the
gut mucosa more susceptable to the fall in O2 delivery. The inference is
that had the hypoxaemia been reversed the risk of developing an
intramucosal acidosis, which we now know to be a very good predictor of
impending mucosal injury and its associated organ failures (3),should have
been reduced.
Why was hypoxaemia alone not able to cause an intramucosal acidosis?
Because the dogs died from a cardiac arrest suggesting that the heart was
more vulnerable than the gut mucosa in these circumstance, probably
because of the increasing myocardial workload induced by the compensatory
increase in cardiac output (4). The inference is that the intramucosal pH
might have fallen even though the intramucoal pH had not.
The fall in intramucosal pH may increase the efficiency of oxidative
phosphorylation independently of substrate change from glucose to fatty
acids, induced by the inhibition of glycolysis by the accompanying
inhibition of phosphofructokinase, by increasing the proton gradient
driving ATP resynthesis. Furthermore in increasing the net yield of ATP
from each mole of substrate utilized the shift to fatty acid consumption
can be expected to decrease the rate of blood flow needed to maintain the
same rate of ATP resynthesis. This may explain the bradycardia that
occurs with the onset of haemorrhage and that seen by free divers and
those swimming in very cold water. What then of the effects of hyperoxia?
Stoneham and Martin's reported two patients, who became
neurologically obtunded during awake carotid surgery, whose neurological
deficits were reversed by the administration of oxygen 100% through a
tight-fitting anaesthetic face mask and circle-breathing system. In
discussing these cases I asked how these neurological deficits might have
been reversed? "By inducing an acute lipid shift? If so, what was the
trigger? Free radicals?" (5). Free radicals increase mitochondrial
membrane permeability and in so doing increase the proton leak which is
said to be associated with an increase in heat production relative to ATP
resynthesis. Giving thyroxine, which is an uncoupler, to a patient with
myxoedema increases the rate of ATP yield and of heat production and is,
therefore, beneficial. Giving thyroxine to a patient who is thyrotoxic
will, however, compound the metabolic disturbances present and is likely
to be harmful, the net ATP yield being a function of ambient temperature.
In the same way increasing mitochondrial membrane permeability may have
both positive and negative effects on energy metabolism. These effects
might account for the reversal of the neurological deficits in these two
patients but, as I observed in my letter, that did not preclude the
possiblity of the hyproxia contributing to the development of secondary
brain injury.
Dan Atar stated with some finality that, "oxygen therapy in stable
angina is a cornerstone of treatment because this disease is caused by a
lack of oxygen supply to the ischaemic myocardium. Its role in this
contest is indisputable". Lionel Opie makes the point that by increasing
oxygen consumption giving fatty acids increases infarct size (6) by,
presumably, increasing myocardial workload in the penumbra in which
oxidative phosphorylation is marginal. The observation sugggests that ATP
resynthesis may be driven by mass action. If oxygen therapy does the same
it might be expected to do the same even in stable angina.
1. Dan Atar. Should oxygen be given in myocardial infarction?
BMJ 2010; 340: c3287
2. C. M. Grum, R. G. Fiddian-Green, G. L. Pittenger, B. J. Grant, E.
D. Rothman and D. R. Dantzker. Adequacy of tissue oxygenation in intact
dog intestine. J Appl Physiol 56: 1065-1069, 1984.
3. Fiddian-Green RG. Associations between intramucosal acidosis in
the gut and organ failure. Critical Care Medicine February 1993 - Volume
21 - Issue 2
4. Gross BD, Sacristán E, Peura RA, Shahnarian A, Devereaux D, Wang
HL, Fiddian-Green R. Supplemental systemic oxygen support using an
intestinal intraluminal membrane oxygenator. Artif Organs. 2000
Nov;24(11):864-9.
5. C. H. E. Imray, A. J. Thacker and M. K. Mead, Fiddian-Green RG.
Oxygen administration can reverse neurological deficit following
carotid cross-clamping.
Br J Anaesth. 2005 Aug;95(2):274-5
6. Opie LH. Metabolism of free fatty acids, glucose and
catecholamines in acute myocardial infarction. Relation to myocardial
ischemia and infarct size. Am J Cardiol. 1975 Dec;36(7):938-53.
Competing interests:
None declared
Competing interests: No competing interests
So "sliding scale insulin coverage", which came from the era of
treating the results of urine glucose testing,and was long
extrapolated,without study,to current finger-stick blood glucose testing
has finallybeen put to rest [1].The long interval between Holler's[2] case
report documenting life threatening hypokalemia during treatment of
diabetic ketoacidosis( DKA)with insulin without potassium supplements and
potassiums ultimate inclusion in current treatment protocols is an
historic fact.Metformin was tarred with the same brush that eliminated
Phenformin from the American market, again without study, resulting in
more than 3 decades of unavailability in the U.S.
We still use "normal" or 0.9% saline for everything intravenous
despite its dubious history and excellent reasons to replace it with more
physiologic electrolyte solutions[3].And industrial dose insulin therapy
of DKA based solely on "expert opinion" persisted long after studies
demonstrated the adequacy of low-dose insulin regimens[4].
The current suggestion that supplemental oxygen in myocardial
infarction may be harmful[5] and,at a minimum, has never been shown to be
beneficial has engendered the "expert opinion" argument and defense of
the status quo[6].As Tatsioni,et.al.[7] note ,it can be "difficult to
discern whether perpetuated beliefs are based on careful consideration of
all evidence and differential interpretation,inappropriate entrenchment of
old information,lack of dissemination of newer data, or purposeful
silencing of their existence".
References:
1. Shagan BP.Does anyone here know how to make insulin work backward;
Why sliding scale insulin coverage doesn't work.Practical Diabetes
1990;9(#3);1-4.
2.Holler JW.Potassium deficiency occuring during the treatment of
diabetic acidosis.JAMA 1946;132:1186-1189.
3.Awad S,Allison SP,Lobo DN.The history of 0.9% saline. Clinical
Nutrition.2008; 27:179-188.
4.Carroll P,Matz R.Uncontrolled diabetes mellitus in adults:
experience with low-dose insulin and a uniform treatment regimen(1976-
1982). Diabetes Care 1983; 6: 579-585.
5.Cabello JB, Burls A, Emparanza JI, Bayliss S,Quinn T.Oxygen therapy
for acute myocardial infarction.Cochrane Database Syst Rev 2010;
6:CD007160.
6.Atar D. Editorial: Should oxygen be given in acute myocardial
infarction? BMJ 2010;340:C3287.
&.Tatsioni A, Bonitsis NG, Ioannidis JPA.Persistance of contradicted
claims in the literature.JAMA 2007;298:2517-2526
Competing interests:
None declared
Competing interests: No competing interests
We read with some surprise the editorial by Professor Atar, although
had it been peer-reviewed it would have been more alarming. The question
of whether to administer oxygen in non-hypoxaemic acute coronary syndrome
was give considerable thought in preparing the British Thoracic Society
Emergency Oxygen Guidelines published in 2008 of which we were co-
authors.1
In considering areas of medicine where evidence is weak, the
physician is faced with a choice. The first principle he or she will
apply is that of "primum non nocere" or first do no harm. He or she will
ask if there is any evidence that giving oxygen is beneficial, the answer
to which is “no”. He or she will then ask if there is evidence of harm to
which the answer is “maybe” based on the recent Cochrane review that
Professor Atar criticises. In response to this alone the answer should be
to limit oxygen to those who are hypoxaemic.
The next area a physician can turn to is expert opinion. Experts too
will consider the principle of doing no harm, but may look to extrapolate
from other knowledge, in this case oxygen physiology. Professor Atar
recommends oxygen on these grounds, citing that the principal problem in
myocardial ischaemia is a lack of oxygen where in fact it is a lack of
blood flow. A systematic review by Farquhar and colleagues reported a
mean reduction in coronary artery blood flow of 8-29% in five studies
where oxygen was given to patients with heart disease and there was a 21-
41% increase in coronary vascular resistance and a mean reduction of 15-
27% in myocardial oxygen consumption.2 Giving oxygen to a patient with
normal haemoglobin oxygen saturation (96-98%) can increase the blood
oxygen content by only 2-4% because very little oxygen is carried in the
blood independently of haemoglobin. This small rise in blood oxygen
content cannot compensate for the reduced coronary blood flow found in all
published studies. Oxygen has similar effects on cerebral blood flow and
oxygen was given routinely to normoxaemic patients with strokes until it
was shown to increase mortality significantly in patients with mild and
moderate strokes with no mortality effect in severe strokes.3 For these
reasons and because published studies have shown a non-significant
increase in death and a significant increase in aspartate aminotransferase
when oxygen was given to non-hypoxaemic patients with myocardial
infarction, the British Thoracic Society Guideline for emergency oxygen
use recommends that oxygen should be given to heart attack patients (and
angina patients) only if they are hypoxaemic (oxygen saturation below
94%).3 This guideline was endorsed by the British Cardiovascular Society
and by 21 other Societies and also by the recent NICE guideline for the
management of acute chest pain of suspected cardiac origin.4
Professor Atar appears to be unaware of any of these publications. He
states that the use of oxygen for patients with angina is “a cornerstone
of treatment” and “undisputed” whereas he is directly contradicting the
BTS and NICE Guidelines for oxygen use in ischaemic heart disease. He has
offered no evidence other than “custom and practice” to support the
continuation of a form of therapy where there is strong physiological
evidence and weak clinical evidence of harm but no proven benefit.
Professor Atar uses the argument that hyperbaric oxygen may reduce
complications in myocardial infarction. It is conceivable that such high
partial pressures may be beneficial in overcoming the reduction in flow,
but this cannot be extrapolated back to using normobaric oxygen for the
reasons given above. It is clear that further trials of normobaric
hyperoxaemia and hyperbaric hyperoxaemia for patients with acute
myocardial ischaemia will be required but clinicians should aim to
maintain normoxaemia until such trials have been concluded.
It is regrettable that the BMJ failed to have this editorial peer
reviewed because the views expressed are so far out of line with current
UK guidance and the author appears to be unaware of the overwhelming
physiological evidence that hyperoxia causes a reduction, not an increase
in oxygen delivery to ischaemic myocardium. We would suggest publishing a
prominent editorial comment or a statement of retraction.
References:
1. O'Driscoll BR, Howard LS, Davison AG; British Thoracic Society. BTS
guideline for emergency oxygen use in adult patients. Thorax. 2008 Oct;63
Suppl 6:vi1-68
2. Farquhar H, Weatherall M, Wijesinghe M, Perrin K, Ranchord A,
Simmonds M,
Beasley R. Systematic review of studies of the effect of hyperoxia on
coronary
blood flow. Am Heart J. 2009 Sep;158(3):371-7
3. Rønning OM, Guldvog B. Should stroke victims routinely receive
supplemental
oxygen? A quasi-randomized controlled trial. Stroke. 1999 Oct;30(10):2033-
7
4 National Clinical Guideline Centre for Acute and Chronic
Conditions. Chest pain of recent onset: Assessment and diagnosis of
recent onset chest pain or discomfort of suspected cardiac origin
http://guidance.nice.org.uk/CG95
Competing interests:
We are the lead authors of the British Thoracic Society Guideline for emergency oxygen use in adult patients (2008)
Competing interests: No competing interests
Oxygen is a drug, whose sole indication is hypoxemia. All drugs are
used for specific indications, at specific doses for specific times, while
monitoring therapeutic response. No physician would suggest a hypoglycemic
agent prophylactically. Why do we, then, automatically prescribe oxygen in
acute MI, when pulse oximetry immediately provides information regarding
oxygenation status, when there is at least a potential theoretical and
actual risk of deleterious effects?
I suggest that the norm should be: measurement of arterial oxygen
saturation while the patient is breathing room air, and prescription of
the lowest oxygen concentration producing an acceptable saturation (e.g.
>95%).
Competing interests:
None declared
Competing interests: No competing interests
Dear Editor,
Professor Dan Atar's editorial reminds me of the time when I was once
accused of not following the protocol of giving routine IV lignocaine to
every one admitted to the CCU at The Middlesex Hospital. I had
specifically asked the SHO not to administer liognocaine as both of us
thought, at that time, that the said patient did not have any acute MI. He
was discharged the following day when all tests proved negative.
Since the boss was away I had to take the responsibility as the SR.
That was the time I found out, to defend myself, way back in 1972, that
while there were only two studies out of the total of seventeen,
supporting the use of routine lignocaine to suppress arrhythmias,
remaining 15 studies did not support that belief. Despite that lignocaine
became the standard protocol! Both my consultants, Late Walter Somerville
and Richard Emanuel, stood by me. I survived.
When one goes deep into any practice on the bed side one could find
situations like giving oxygen routinely to every acute MI without solid
data to back it. Another was administering morphia in acute LVF. We could
expect to see in the near future the dangers of suppressing the autonomic
nervous system in acute MI like situations with beta-blockers and ACE
inhibitors. The autonomic nervous system initiates and completes the
natural remodelling of the left ventricle after an AMI. That could be
interfered with by suppressing the inbuilt repair mechanism mediated
through the autonomic nervous system. [1]
Professor Beasley was one of the persons who has gone deep into
oxygen therapy in AMI. His study of the limited number of controlled
trials did show that routine oxygen, in fact, harmed patients. [2]
Beasley’s historical perspective is exhaustive for anyone interested in
this area. [3] It was Steele who started this practice through his article
in the BMJ in 1900. [4] But even as far back as 1949, 1950, 1965 and 1976
there were enough studies showing that routine oxygen is harmful in AMI
[4, 5, 6, 7, 8] One study even showed that good risk AMI patients below
the age of 70 are much better off left at home than being rushed to CCUs
in those ambulances hurtling through dense traffic with their shrill
sirens. [9]
However, the common man gets upset if the patient does not get oxygen
as the media and, even the motion picture industry, depict routine oxygen
mask after a heart attack as a must! Cochrane group has asked for more
detailed RCTs on the subject, preferably placebo controlled. That might
take time and lots of money. I doubt if that would take knowledge any
further as the weight of existing evidence is against giving routine
oxygen in acute ischaemia. Excess oxygen is shown to reduce blood flow to
the heart, brain or kidney when they have an ischaemic episode unless
there is severe hypoxia.
Yours ever,
Bmhegde
References:
1) Poise and CADD studies.
2) Beasley et. al. Oxygen in acute AMI. Heart 2009; 95: 198-202.
3) Beasley et. al. Oxygen in AMI-history. J. R. Soc. Med 2007; 100: 06-
0065.
4) Steele C. Severe anginal pain relieved by oxygen. BMJ 1900; 2: 1568.
5) Boland EW. Oxygen and pain relief in acute coronary thrombosis. JAMA
1940; 114:1512.
6) Russek HI, Regan FD, Neagele CF. 100% oxygen in AMI and severe angina.
JAMA 1950; 144: 373.
7) Thomas M, Malmcrona R, Shillingford J. Haemodynamics of oxygen in acute
MI. Br. Heart J 1965; 27: 401.
8) Rawles JM, Kenmure ACF. Controlled trials of AMI. BMJ 1976;53: 411-417.
9) H G Mather, D C Morgan, N G Pearson, K L Read, D B Shaw, G R Steed, M G
Thorne, C J Lawrence, I S Riley. To compare the results of home and
hospital treatment in men aged less than 70 years. Br Med J 1976;1:925-929
(17 April), doi:10.1136/bmj.1.6015.925.
Competing interests:
None declared
Competing interests: No competing interests
Routine oxygen therapy in myocardial infarction--primum non nocere
It has been a concern reading from afar the recent editorial comment
[1,2] proposing that there is no convincing evidence of harm with the
routine administration of oxygen in myocardial infarction. We suggest
that this statement is not consistent with available evidence. We also
suggest that the relevant issue to consider is the balance of available
evidence for both the efficacy and safety of oxygen therapy in the routine
treatment of myocardial infarction.
Arterial oxygen tension is a major determinant of coronary artery
tone, with any increment in arterial oxygen content reducing coronary flow
regardless of initial saturation. In human studies of subjects with
cardiac disease, hyperoxia from high concentration oxygen therapy causes a
marked reduction in coronary blood flow [3]. In patients with myocardial
infarction, high concentration oxygen therapy also causes a reduction in
cardiac output and stroke volume, and increases systemic vascular
resistance and blood pressure.
There is little evidence by which to determine the efficacy and
safety of high concentration oxygen therapy in myocardial infarction [4-
6]. The evidence that does exist indicates that the use of high
concentration oxygen therapy in uncomplicated myocardial infarction
results in a significant increase in infarct size (as determined by
cardiac enzyme levels) [5] and possibly mortality with an odds ratio of
death of 3.03 (95% CI 0.93 to 9.83) [6].
In terms of resuscitation following cardiac arrest, oxygen therapy
resulting in hyperoxia is independently associated with increased
mortality, compared with either hypoxia or normoxia [7].
As a result, there is no convincing evidence of benefit with the
routine use of oxygen therapy in myocardial infarction, and indeed, the
balance of the limited evidence that does exist suggests potential harm
with this approach. We propose from afar that the current recommendation
of the New Zealand Branch of the Cardiac Society of Australia and New
Zealand, that “oxygen should be administered to keep the saturations
around 96%” [8] is evidence-based and sound advice. We also refer
clinicians to the excellent British Guidelines on Oxygen Therapy which
recommend that oxygen should be prescribed for defined indications in
which the benefits outweigh the risks, and that the dose, method and
duration of delivery is specified and the patient’s response to oxygen
therapy is monitored [9].
REFERENCES
1. Atar D. Should oxygen be given in myocardial infarction? BMJ
2010; 340: c3287.
2. Atar D. Oxygen for myocardial infarction. BMJ 2010; 340: (Letter).
3. Farquhar H, Weatherall M, Wijesinghe M, Perrin K, Ranchord A, Simmonds
M, Beasley R. Systematic review of studies of the effect of hyperoxia on
coronary blood flow. Am Heart J 2009; 158:371-7.
4. Wijesinghe M, Perrin K, Ranchord A, Simmonds M, Weatherall M, Beasley
R. Routine use of oxygen in the treatment of myocardial infarction:
systematic review. Heart 2009; 95:198-202.
5. Rawles JM, Kenmure AC. Controlled trial of oxygen in uncomplicated
myocardial infarction. BMJ 1976; 1: 1121-3.
6. Cabello JB, Burls A, Emparanza JI, Bayliss S, Quinn T. Oxygen therapy
for acute myocardial infarction (Review). The Cochrane Library 2010,
Issue 6. 2010: The Cochrane Collaboration, John Wiley & Sons Ltd.
7. Kilgannon JH, Jones AE, Shapiro NI, Angelos MG, Milcarek B, Hunter K,
et al. Association between arterial hyperoxia following resuscitation from
cardiac arrest and in-hospital mortality. JAMA; 303:2165-71.
8. ST-Elevation Myocardial Infarction Guidelines Group and the New Zealand
Branch of the Cardiac Society of Australia and New Zealand. ST-elevation
myocardial infarction: New Zealand management guidelines. NZMJ 2005;118:1
-21.
9. O'Driscoll BR, Howard LS, Davison AG, British Thoracic S. BTS guideline
for emergency oxygen use in adult patients. Thorax 2008; 63 Suppl 6:vi1-
68.
Competing interests:
None declared
Competing interests: No competing interests