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Acute coronary syndrome

Discuss the Published Evidence in regard to Oxygen Therapy of the Compromised Myocardium. Would you Change or Maintain the Oxygen Administration Therapy Reported in both Mr Hertz and Mika's Management? Explain.

Acute coronary syndrome compromises myocardium, a common cause of death in US and Europe. Myocardial infarction (heart attack) and unstable angina are its constituents resulting from sudden reduction in blood (oxygen) supply to the cardiac muscles. This reduction is as a result of formation of blood clots when an atheroma ruptures within a coronary artery. The time length blood flow is blocked, the location of the blockage and the damage that occurs on the tissue determines the type of acute coronary syndrome.

Compromised myocardium in acute coronary syndrome ACS: In many cases it is as a result of narrowing of the blood vessels due to atheroma within the artery lining. Atheroma is plaques or fatty patches. They form over years; each atheroma has an outer film of soft inner fatty core. When they rupture they cause a thrombus formation, platelets activation and adherence and activation of the coagulation cascade. Other uncommon causes of ANS includes: inflammation of the coronary artery, a heart stab wound, a blood clot that travels and was formed from other parts of the body to the coronary artery, cocaine use usually causes coronary artery spasm, complications of heart surgery.

Predisposition factors to acute coronary syndrome are: Hypertensive persons, overweight persons, and people with a high cholesterol, inactive persons, and unhealthy diets, diabetic. Symptoms of compromised myocardium: severe chest pain is the most common. Feels like a heavy pressure on the chest. The pain at times travels up to the jaws and down to the left arm or at times to both is similar to stable angina but lasts longer and more severe. It can last for 15 minutes to hours. Sweating, fainting, feeling sick and shortness of breath are common too. In some people especially the old and elderly and diabetic they may not have pain.

The following tests are usually done: electrocardiogram, blood test and echocardiogram. An electrocardiograph (ECG) has typical changes, in some it’s normal. Blood tests measure of chemical troponin; it is a test of heart muscle damage. Its level rises in heart attack but not in unstable angina. Echocardiogram is an ultrasound of the heart to show the blockage or the infarction.

Oxygen therapy is one of the treatment modes to these patients. As mentioned earlier, all the symptoms are as a result of reduced/no oxygen supply to cardiac muscles. On inhalation oxygen is drawn into the lungs where it dissolves in plasma and binds to hemoglobin. This oxygen is delivered to all cells for respiration (energy production) oxygen combines with glucose to give us ATP and carbon dioxide. In hypoxia there is anaerobic respiration where by glucose breaks down to lactic acid and ATP is generated. Lactic acid causes pain to the muscles s it irritates the nerves. Lactic accumulation leads to acidosis which is fatal to cells. To avoid this, these patients are supplemented with oxygen.

Compromised myocardium in acute coronary syndrome ACS

Oxygen stress refers to the production of reactive oxygen species. These species interact with the cell contents and bring about physiological alteration. Some may react with the cell membrane contents thereby compromising its function. Some may react with the genetic material and hence destroying the nucleus. These cases have been associated with oxygen intoxication. This condition has been associated with diseases that bring about degeneration in some organs due to destruction of cells.

According to the case scenario, the following can be deduced as the Patient presentation: Responsive to the environment, respiratory rate 26 breathes per minutes. This is quite high and can be considered abnormal.82 beats/minute, warm to touch, capillary refill of 2 seconds, nauseated, alert, blood pressure 105/89 ,saturation pressure of oxygen 99%,temperatures 36.8 ‘C, crushing central chest pain ,ECG 2 results ST segment elevation,T wave inversion, flat T wave, on blood test troponin is elevated ,creatinine kinase is elevated,

In this case, the risk factors are: ischemic heart disease, an ex-smoker, Hypercholesterolemia

Crushing central chest pain exceeding 40 minutes, it is relieved and after 24 hours the pain recurs and he complains of the pain being as severe as the previous.

Routine blood tests

Aspirin 300mg

Clopidogrel 600mg

Heparin 4000 units IV bolus





Reopro (abcimab): in situ 42mls per hour for 12 hours.

2 bare metal stents on the left anterior descending artery.

Oxygen therapy via face mask at 6litres per minute

Owing to the oxygen therapy being used as an intervention, the question of whether this is necessary arises. Considering the benefits and the demerits, a choice has to be made.

Mony.  S., Dan. A., Philippe.G, (2016) European Heart Journal, All patients who presents with acute coronary syndrome they are treated with oxygen supplementation regardless of the saturation levels. Hypoxemic patients highly appreciate this as it increases the delivery of oxygen to cells and reverse hypoxia effects. On the other hand it can be hazardous. Most of the acute coronary syndrome is not hypoxemic and the value of oxygen therapy is unknown. The 2014 American (AHA/ACC) ST-elevation myocardial infarction guideline recommends admission of oxygen to patients who are hypoxemic with a saturation pressure less than 90% and also to all patients admitted for the first 6 hours. The current European NSTEMI-ACS guidelines advocates for oxygen supplementation when the saturation is less than 90% ,the European STEMI-ACS guidelines recommends oxygen supplementation at less than 95% oxygen saturation.

Predisposition factors to acute coronary syndrome

Oxygen therapy increases dissolved plasma oxygen which cannot be monitored and most significantly the effects of these high levels. This therapy increases the delivery of oxygen to tissues. This can also be lead to formation of the reactive oxygen species (ROS) which in turns causes oxidative stress.

ROS molecules formed during oxygen metabolism, causes damage to cells. Post ischemic injury which triggers inflammation as a result of leucocytes chemotaxis, they damage electron transport in the mitochondrion all this leads to cell vascular smooth muscle cells, cardiac myocytes, myocytes ROS molecules causes enhanced tone as they lead to increased production of angiotensin 1 all this are associated to these reactive molecules in ischemia .they have also been associated lethal types of arrhythmia: ventricular tachycardia and ventricular fibrillation. These effects are lethal and despite these there has not been proven antioxidant.

Hyperbaric oxygen insufflation: there were two clinical trials which treated there patients with intermittent inhalation of 100% oxygen at atmospheric pressures more than one, this was aimed at elevating plasma concentration of dissolved oxygen. In the first study 74 MI patients were enrolled and the results was end systolic volume index reduced by 20.0% cardiac output increased by 10.0%.the second study was HOT study.121 patients with MI were chosen and it demonstrated a shorter pain relief there was no change in cardiac markers, diastolic and stiffness in the left ventricular were unaffected by oxygen therapy.

Hyperemic reperfusion therapy: a multicenter AMIHOT trial: 20 patients in oxygen and 22 patients as control. The results were the left ventricular volume remained the same and in oxygen group EF increased significantly, no changes in the control group. Other parameters were unchanged.

Hemodynamic effects in oxygen therapy: studies have been done and proven oxygen therapy being non beneficial. It was done on volunteers and it showed a decline of left ventricular perfusion by 23%, cardiac output CO by 10% due to decreased heart rate, stroke volume remains unchanged. Coronary artery disease patients increased production of lactate was noted probably due to reduced coronary flow.

Coronary vasculature and oxygen therapy: studies have shown that coronary sinus blood flow in both normal patients and coronary artery diseases patients decreased on oxygen therapy.  This is attributed to increased left ventricular coronary resistance which leads to vascular tone. These vasoconstrictor effects are hazardous especially to patients who undergo coronary stenting as there is underestimation of the coronary stents which causes sudden cardiac death and thrombosis.

Pain assessment

Random controlled clinical trials: first study by Rawles and Kenmure  ,second study by Wilson and channer and last study by UKholkin they all enrolled patients with myocardial infarction and the results showered the negative effects of oxygen therapy outweighs its benefit.

Management of Mr. Herz condition.

From all the above its so clear oxygen therapy will do more harm than good to our patient so it has to be minimized and avoided where necessary. However, admission of oxygen for the first six hours was necessary just as stipulated by European NSTEM-ACS guidelines.


Twenty breaths per minute:  accompanied by signs of shortness of breath.

Circulation: blood pressure 122/52mmHg, well perfused, capillary return is 2 sec,

Temperature 37.2’C, responsive to environment

There is normal chest movement, no murmurs, no jugular distension.

Tests done

A normal chest x ray.

Anteroseptal left ventricular wall from the ape, depressed left systolic function with hypokinesis of the anterior shown by a transthoracic echocardiography.


No oxygen, pain relief was given

Cardiac catheterization done immediately .it relived 80% obstruction.

Cardiac surgical resection of tumor performed 6 days later.

Acute coronary syndrome as shown from above usually occurs in elderly patients according to the predisposing factors.Mika’s obstruction was as a result of a tumor, it was all fixed surgically .The patient was breathing fine (20 breaths per minute, no physical signs of respiratory distress), was not in danger, the air was clear, so there were no reasons for oxygen therapy.

In conclusion it is evidently that oxygen therapy has more risks than benefits in patients suffering from acute coronary syndrome; arrhythmias, cell death, sudden cardiac arrest. The breathing/blood circulation is improved by a very small percentage or at times no significant changes in these patients. Most of the guidelines have discouraged its use although they recommend its admission for the first 6 hours.


Wijesinghe, M., Perrin, K., Ranchord, M., (2010) Routine use of oxygen in treatment of myocardial infarction, available

Thomas, K. John, K. (2014) On Treatment of Myocardial Infarction in Care Unit .The American Journal of Cardiology. Volume (20), pp, 457-464.Available at

Jeffery, L. et al. (2016) Guideline on Management of Unstable Angina/Non –ST-elevation myocardial infarction. American College of Cardiology Journal. Volume 50(7). Available at

Cabello, JB. et al. (2010) Oxygen therapy for acute myocardial infarction.Sao Paulo Medical .Journal .at

Roffi, M,. Patrono, JP (2015) guideline for management of acute coronary syndrome (online)

Manoukian, SV,. Feit. F,. (2016) Outcomes in Patients with Acute Coronary Syndrome, Journal of The American College of Cardiology pp,738

Bassand, JP., Hamm, CW (2016) Guidelines for the Diagnosis and Treatment of non-ST-elevated myocardial infarction, European Soc 2136

Davies, MJ,. Woolf, N,. (1997) Pathology Of Acute Myocardial Infarction, British Heart Journal (online) pp, 317

Thygesen, K,.  Alpert, JS,. (2017) Universal Definition of Myocardial Infarction, Journal of The American College cardiology (online)

Capes, SE,. Hunt, D,. (2010) Stress hyperglycemia and increased risk of death after myocardial infarction, The Lancet.

Maddox, TM,. Wang, L., (2011) Long Term Outcomes after Stent Implantation (online)

Rioufol, G., Finet, G., (2012) Multiple atherosclerotic plaque rupture in Acute Coronary Syndrome, Circulation .at

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