Scott talks to Consultant Cardiologists Professor John Somauroo and Dr. Babu Kunadian and Karen Randles, a cardiology specialist nurse at Chester about the assessment of patients presenting with chest pain and the management of Acute Coronary Syndromes (ACS). This includes ST-segment-elevation myocardial infarctions (STEMI) and non-ST-segment elevation myocardial infarctions (NSTEMI).

Check out the podcast below or follow the link to itunes or Podbean (android).

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For example ECGs, visit www.lifeinthefastlane.com

What is ACS?

ACS is an acute medical emergency which encompasses cardiac conditions caused by thrombus formation on an atherosclerotic plaque within the coronary arteries. ACS is usually divided into STEMI, NSTEMI and unstable angina (1).

STEMI occurs if the thrombus formation leads to a complete occlusion of the affected coronary artery.

This is often precipitated by rupture of an atherosclerotic plaque. The blockage causes the cardiac muscle (or myocytes) supplied in the blocked territory to die. As the name describes, this causes ST elevation on the electrocardiogram (ECG) in STEMI (1,2).

NSTEMI occurs when the thrombus formation leads to a partial occlusion of the affected coronary artery. Again, this will be associated with a thrombus forming on an atherosclerotic plaque and reduction in blood flow to the affected territory causes varying degrees of cardiac muscle death. As signified by its name, there is no ST elevation on the ECG. Other ECG changes may be seen including; ST segment depression, T wave inversion or non-specific ST flattening in NSTEMI. ECG changes may only be seen with serial ECGs, and in some cases of NSTEMI, there may be no ECG changes (1,3).

The 12 lead ECG changes seen in STEMI and NSTEMI can be analysed to assess the coronary artery territory that has been affected. Since these two conditions lead to cardiac muscle death, both will cause a rise in serial cardiac enzyme levels as this leaks from the cardiac myocytes which have undergone necrosis. The current cardiac enzyme which is measured as part of their diagnosis is troponin (1,4). Assays for troponin T and Troponin I are available. When looking at the evidence yourself,  it is important to know which is used where you work as they have different cut off levels.

trop_edu_graph1_large_ca6-00042977~9

Other conditions can cause a rise in troponin levels including pulmonary embolism, significant renal disease, heart failure and myocarditis. It is important that troponin is considered together with the history and examinination whether the patient has had an ACS (5).

How do we diagnose a STEMI?

To diagnose STEMI, patients should have symptoms that fit with an acute myocardial infarction together with the ECG changes specific for STEMI. This includes patients who have presented with chest pain that is cardiac and ischaemic in nature and those presenting with a cardiac arrest. The ECG changes specific in the diagnosis of STEMI are:

ST segment elevation of equal to or greater than 1mm in two or more contiguous (leads representing the same infarct territory) leads, except for in the chest leads V2 and V3 where equal to or greater than 2mm in males or more than 1.5mm in females is required.

Image credit: http://www.lifinthefastlane.com

There are also other important ECG changes to remember, which if occurring with symptoms compatible with an acute MI should be treated in the same manner as STEMI.

These changes include new or presumed new Left Bundle Branch Block (LBBB), or acute posterior MI. Should your patient presenting with an old LBBB then the Sgarbossa criteria can be used to assess for a coexisting STEMI (6).

In acute posterior MI, there is greater than or equal to 2mm of ST depression in leads V1 to V3. These changes can be seen in the conventional 12 lead ECG in V1 to V3 in posterior MI because these leads are the reciprocal, or mirror image, of the posterior heart.

PMI10

Image credit: http://www.lifeinthefastlane.com

If posterior MI is suspected, the conventional 12 lead ECG can be modified to cover the additional leads V7 to V9 by removing the leads V1 to V3 and using new stickers to continue V7,8,9 laterally and posteriorly along the same horizontal plane as V4,5,6. This ECG should be labelled appropriately to show it is representing V7 to V9. The actual ST elevation occurring posteriorly can be demonstrated in V7 to V9, where 1mm of ST elevation could be significant in the diagnosis of STEMI. As above, the mirror image of this actual change will be seen as deep ST depression greater than or equal to 2mm in V1 to V3 (1,2).

“What do the changes on the ECG actually mean in patients with STEMI?”.

The ECG changes observed in patients with a STEMI signify a severe acute myocardial injury, which can become transmural (or full myocardial wall thickness) in nature. The changes themselves are caused by an alteration in myocardial repolarisation due to the severe acute myocardial injury caused by the complete occlusion of a coronary artery. Following a STEMI, the permanent myocardial necrosis that has occurred may be seen on a surface 12 lead ECG with pathological Q waves in the affected coronary artery territory (9).

STEMI Treatment

The treatment for STEMI is an emergency primary percutaneous coronary intervention (PCI). This is available nationally and may require an emergent referral to tertiary centres. Patients suspected of having a STEMI should be referred for this immediately with the aim of achieving primary PCI as soon as possible and within 120 minutes. Paramedics are trained to recognise patients presenting with STEMI on the ECG so they can be taken directly from the community to the appropriate centre offering emergency primary PCI. There are cases where STEMI will occur in a hospital setting or after a patient has presented to the Emergency Department (ED). Therefore, it is still very important to recognise STEMI early and act promptly (1,2,4).

rescue-helicopter-922465_1920

“What should be done in the ED for patients with STEMI prior to urgent transfer for a primary PCI?”.

Hospitals nationally have their own STEMI pathways for assessing suitability and arranging the rapid transfer of affected patients for primary PCI. The pathway used by your hospital should be followed and will have its own inclusion and exclusion criteria. The inclusion criteria will include symptoms compatible with an acute MI, appropriate ECG finding (s) described above, and the patient should usually be alert and able to give their verbal consent to being transferred except for patients who are post cardiac arrest. If a patient is post cardiac arrest and thought to be having a STEMI, they would be unlikely to have the mental capacity to consent and therefore the decision to transfer urgently would be acting in their best interests if the other criteria on the pathway were met.

The transfer of patients with STEMI to a tertiary centre for primary PCI should not be delayed if the patient is stable to transfer. Whilst the emergency transfer is being arranged immediately, treatment for STEMI would be antiplatelets including Aspirin as per the local policy. Patients should be assessed, and given morphine analgesia as this will reduce their pain and anxiety. Traditional teaching has been to provide high flow oxygen, however, the evidence is pointing away from this either showing no benefit (7) or potential increase in infarction size (8). If a patient’s oxygen saturations are low, oxygen should be given through a face mask to achieve normal oxygen saturations of 94-98% for patients with no history of chronic obstructive pulmonary disease (COPD). In patients with a history of COPD, oxygen should be given to achieve oxygen saturations of 88-92%.

gtn

Nitrates should also be considered to relieve pain and improve coronary blood flow through their vasodilatory actions, as long as the patient’s blood pressure permits (if systolic blood pressure is greater than 90mmHg). Nitrates may be given as one or two puffs of Glyceryl Trinitrate (GTN) sublingual spray (400 micrograms per spray) which is rapidly absorbed into the circulation, or as an infusion.  Please remember, your local STEMI pathway should be followed and the transfer of these patients should not be delayed if the patient is stable enough for a transfer (1,2,4).

The above measures can be remembered with the mnemonic MONA: Morphine, Oxygen (remember target the patient’s normal oxygen saturations), Nitrates, and Aspirin.

In the immediate treatment of STEMI, the precise antiplatelets given will be dictated by your local policy. Unless contraindicated would, For example, include aspirin 600mg given as a stat loading dose orally. This would be contraindicated if the patient had a true aspirin allergy. The second antiplatelet might be Ticagrelor given as a 180mg stat loading dose orally. Ticagrelor would be contraindicated here if the patient had a previous history of intra cranial haemorrhage owing to the increased bleeding risk. In this case, an alternative second antiplatelet to give would be Clopidogrel as a 600mg stat loading dose orally (2).

In summary

In patients presenting with a STEMI, the underlying pathology has been caused by a total occlusion of coronary artery where there has been thrombus formation on a ruptured atherosclerotic plaque. Therefore, the important early treatment is to restore coronary artery blood flow with an emergency primary PCI, to help reduce the size of the area of cardiac myocyte necrosis and prevent future events.

NSTEMI 

Case example:

  • 65 year old male
  • Retired builder
  • 20 pack year smoking history (20 cigarettes per day for 20 years)
  • Past medical history of hypertension, and raised cholesterol
  • Not had chest pain before, usually fairly active until recently

Initial Assessment – History

The most important history aspect to gather is assessing the type of pain the patient is presenting with and whether they are presenting with typical ischaemic cardiac chest pain. This includes patients presenting with central and retrosternal chest discomfort which is across the chest and may radiate into the jaw or the arms. It is often described as a tightness or heaviness and, if lasting for 20 minutes or more, strongly suggests the pain may be compatible with that of ACS. Contrary to conventional teaching, pain radiating to the right arm is highly suggestive of a diagnosis of ACS (9).

Remember, patients who are elderly or have a history of Diabetes Mellitus may experience pain differently and can present with atypical symptoms, other equivalent symptoms including shortness of breath, or no symptoms, which can be referred to as a silent MI. All patients presenting with acute chest pain should be assessed for ACS and other life threatening causes of acute chest pain including pneumonia, aortic dissection, pneumothorax, pulmonary embolism and oesophageal rupture. Following this, other causes of chest pain should be considered (1,11).

A pneumonic you may remember from medical school is SOCRATES (Site, Onset, Character, Radiation, Associated symptoms, Timing, Exacerbating factors and Severity). Ask about previous episodes of chest pain. A pain that is worse than the patient’s usual angina pain or different needs taking seriously.

Ask the patient about their past medical history including whether they have had any previous heart problems or previous MIs. This could mean they are more likely to be presenting with an MI now. A previous history of other vascular disorders including a previous history of stroke or peripheral vascular disease could increase the patient’s risk of MI by up to 40%.

Ask the patient/assess as appropriate about risk factors for arterial disease including whether they have hypertension, a smoking history, raised cholesterol (hyperlipidaemia), are male and over the age of 40. Include whether there is a history of Diabetes Mellitus and a family history of MI in a 1st degree relative below 55 years of age- i.e. in one or both of the patient’s parents, their brother and/or sister. The presence of any of these would all increase the chances that the patient is presenting with ACS.

Assess what medications the patient is currently taking because:

1) This may provide a clue as to their past medical history if they are already taking an antihypertensive or statin.

2) In case they are already taking an antiplatelet drug or anticoagulant, so we know what drugs may or may not be appropriate to add into their current prescription.

3) Allergies should be asked about in case of a true allergy or history of anaphylaxis which would contraindicate the use of a medication.

Initial Assessment – Examination

First of all, the most important thing to assess is whether the patient is cardiovascularly stable. Are their other vital signs including oxygen saturations and respiratory rate stable? If the patient is unstable, they would need to be kept in the resuscitation room in the ED or high dependency unit (HDU)/critical care environment until they have been stabilised, and can monitored appropriately with continuous ECG monitoring.

We would then examine for any of the acute complications of ACS. This includes looking for evidence of pulmonary oedema or fluid overload, which includes a raised Jugular Venous Pressure (JVP), bilateral chest crackles on auscultation and/or the coughing of pink frothy sputum. The presence of these features could indicate a patient who is becoming unstable requiring even more urgent treatment. In the case of pulmonary oedema consider intravenous diuretic or nitrate therapy and the provision of early continuous positive airways pressure (CPAP) for associated type 1 respiratory failure.

Other acute complications to examine for would be any cardiac murmurs. A murmur may have been present previously.  In the setting of a patient presenting with ACS, a loud parasternal murmur would make us concerned that the patient may have developed a ventricular septal defect as a result of an acute MI. A loud pansystolic murmur at the apex of the heart could signify the development of acute mitral regurgitation of ischaemic damage to the papillary muscles which attach to the cusp of the mitral valve. Again, the presence of these features indicates a patient who has become unstable requiring increasingly urgent treatment and discussion with cardiothoracic surgery for acute intervention to correct the new defect.

Other examination signs to look for would include evidence of previous cardiac surgery including scars from previous coronary artery bypass grafting (CABG), in the central chest from the thoracotomy itself, and harvest vein site. Finally, examine for signs of the risk factors for arterial disease including the presence of nicotine staining in the fingers of patients who smoke, and the presence of any xanthelasma around the eyes which could signify the presence of hypercholesterolaemia (3).

Initial Assessment – Investigations

An immediate ECG should be completed within 5 to 10 minutes of the patient arriving.

nstemi1

The ECG should be examined for features compatible with NSTEMI. The initial ECG may be normal, or may show high risk features for a NSTEMI including ST segment depression or T wave inversion. A repeat ECG should be taken in all cases another 10 to 20 minutes after arrival to look for any serial changes in appearance which may occur in evolving NSTEMI cases.  Further serial ECGs should be taken in the event of evolving changes or ongoing chest pain.

Other important investigations to be taken when obtaining initial intravenous access include:

  • Troponin – for myocardial damage
  • Full Blood Count – looking for anaemia which could contribute to cardiac ischaemia or infection with a high or low white cell count which may have been a precipitator for the ACS
  • Renal Profile – for prescribing purposes, to assess of any potential systemic effects of the ACS, and looking for chronic kidney disease, which is associated with an increased risk for vascular events including ACS
  • Liver Function Tests – for prescribing purposes prior to considering a statin and to assess for any potential systemic effects of the ACS
  • Cholesterol – risk factor

The first troponin is taken on arrival to hospital at the ED/MAU. The result is normally available within 30 minutes to 1 hour. Troponin is a cardiac muscle enzyme released when there is cardiac myocyte death. Therefore, with severe myocardial ischaemic or infarction the troponin level will rise in the blood usually within 1 to 2 hours of the onset of symptoms (1,3,4).

doctor-2346235_1920

When is the second troponin taken?

At present, local policies will vary so you should follow your local hospital policy. Often, a second troponin is taken at 6 hours after admission at present. There are newer high sensitivity troponin assays now included in guidance from the national institute for clinical excellence (NICE) which some trusts will be using and can be taken 3 hours after the initial (1,2,3,4).

What other investigation would be important in patients with a suspected ACS?

chest X-ray (CXR) should also be performed in suspected cases of ACS/NSTEMI. The CXR is looking for any evidence of acute heart failure, occurring as an immediate complication of the ACS, or pneumonia which may have precipitated the ACS. Alternatively, it could show an alternative cause of severe chest pain including a pneumothorax. If heart failure is suspected or shown by its CXR appearances including cardiomegaly, pulmonary venous congestion and/or pleural effusion(s), treatment with a loop diuretic should be commenced promptly. Likewise, appearances of consolidation suggesting a pneumonia would prompt the urgent administration of antibiotics and following the sepsis protocol if sepsis is suspected (1,12).

What might make you think that a patient with ACS was too unstable to move departments within the hospital?

Use an A,B,C approach according to advanced life support (ALS) guidance to assess a patient’s stability. Any significant problem identified with this approach should identify unstable patients. Look for specific features for a patient with ACS that suggest they may be unstable for transfer. These features could include (1,13):

  • The presence of ongoing chest pain
  • Evidence of arrhythmia or haemodynamic instability (with compromised blood pressure, or significant disturbances in heart rate with a tachy or bradycardia)
  • The presence of dynamic ECG changes (ECG changes which are rapidly progressively worsening, including a worsening severity of ST elevation or depression)

When would it be appropriate to do a bedside echocardiogram in the ED/MAU/Resuscitation area for a patient presenting with ACS?

A bedside echocardiogram would be appropriate in patients suspected of having acute heart failure and those with a new acute murmur suspected of having a VSD or acute mitral regurgitation. It is important to recognise and diagnose these complications early to enable their prompt treatment. This will hopefully prevent worsening haemodynamic compromise and worsening of the ACS (14).

NSTEMI Treatment

As discussed and remembered overall with the MONA pneumonic earlier, if a patient’s oxygen saturations are low (less than 94% in individuals with no history of COPD, or less than 92% in individuals with COPD) oxygen should be administered to target the 94-98% target range in those with no history of COPD, and 88-92% target range in those with a history of COPD (15).

It was previously standard practice to use a non-rebreather oxygen mask at 15L/minute for patients with ACS. However, this has been replaced by the above guidance in line with evidence, including from systematic reviews, that hyperoxaemia, or over oxygenation, can reduce coronary blood flow and could cause harm in the initial treatment of MI (16).

The next important thing to do would be to give Aspirin. This may have already been given by the paramedic crew, but if it hasn’t yet, given aspirin 300mg loading stat dose orally (unless contraindicated, for example, by a history of previous anaphylaxis to aspirin. In such cases, an alternative such as clopidogrel could be considered).

In addition, it is important to relieve the significant pain that can be associated with NSTEMI through the use of morphine. Morphine may be given intravenously, and should usually be given with an intravenous antiemetic such as metoclopramide to prevent nausea which can occur because of the NSTEMI/ACS itself and/or the use of an opiate.

A nitrate can be used also include Glyceryl Trinitrate (GTN) to relieve pain and improve coronary blood flow through its vasodilatory effects as discussed earlier, as long as the systolic blood pressure is above 90mmHg (3). It can cause a drop in blood pressure which may sometimes precipitate the patient collapsing. In this situation, you should satisfy yourself first that the ACS has not caused the collapse before deciding the nitrates were the cause.

Individual trust protocols may vary, but often a subcutaneous injection of Fondaparinux 2.5mg stat s/c would be given unless contraindicated. The intended benefit of fondaparinux is to try to reduce the size of the thrombus or prevent extension of it. Balanced against this, there is a bleeding risk associated with its use which would need to be explained to the patient. Its use and the use of a related low molecular weight heparin would be contraindicated in patients with a high bleeding risk, identified using the CRUSADE score (http://www.crusadebleedingscore.org), and in those already on warfarin anticoagulation with an INR above 2 (17).

In patients with an eGFR (identified from their renal profile and subsequent calculation) less than 20mls/minute, Enoxaparin 1mg/Kg once daily s/c is often used instead of Fondaparinux but will be advised by your local policy.

Further medications to be initiated could include the beta blocker bisoprolol, usually given as a stat dose 2.5mg and then continued once daily, aiming for a heart rate of 60-70bpm. Beta blockers reduce myocardial oxygen demands and can relieve ischaemia. Additionally, it is important to commence a statin early to help prevent future ACS events. The importance of this has been demonstrated in the MIRACL study where the dose of atorvastatin 80mg once daily orally prevented subsequent episodes of MI in hospital, and this dose is now often used in protocols nationally (3,18).

What second antiplatelet agent should be used in patients with a NSTEMI?

This will vary according to local policies and risk of the individual patient. In addition to the initial aspirin, most hospitals now use ticagrelor and is becoming the trend nationally in the UK. Some hospitals are using other antiplatelet agents including clopidogrel or prasugrel (3,4).

How are patients with NSTEMI risk assessed to guide their subsequent management?

Patients are risk assessed using the GRACE score, which is a recognised validated tool at www.gracescore.org

The GRACE score allows the user to input certain parameters including the patient’s age, heart rate, systolic blood pressure, serum creatinine, presence of heart failure, ST-segment ECG changes, troponin result, and the presence of cardiac arrest at admission. It then uses these to calculate a risk score for the patient, including the patient’s individual risk of death at 6 months (19). If a patient’s risk of death at 6 months after the NSTEMI is less than 3%, they are considered at low risk of further cardiovascular events and death. These patients may be able to go to a cardiology or acute medical ward and require consideration for cardiac monitoring.

If a patient’s risk is 3-6% they are considered at intermediate risk. Above 6%, patients are considered at high risk and above 9% is very high risk. Any patients with a risk of 3% or higher, as well as any patients with ongoing chest pain, haemodynamic instability or dynamic ECG changes which includes ST depression, transient ST elevation or T wave inversion should be considered for admission to the coronary care unit (CCU) and require cardiac monitoring. CCU would be essential for any patients with a risk of 6% or higher, and those in the highest risk group of 9% or above not only require CCU, but a discussion with the regional tertiary cardiac centre for considering transfer of their care there if they are stable to undergo a transfer (1,3,19).

When a patient is admitted to CCU, what are the most important things to observe for?

electrocardiogram-16948_1280

Patients admitted to the CCU during and following a NSTEMI/ACS are at high risk for arrhythmias including ventricular arrhythmias and cardiac arrest. They are therefore continually monitored with telemetry and any arrhythmias should be observed for and treated as appropriate, according to ALS algorithms (13).

To help prevent arrhythmias by stabilising the electrochemistry of cells, the concentration of the patient’s blood potassium is often maintained within a target range of 4 to 5mmol/L, and their magnesium concentration maintained at a target of 1mmol/L. The patient may require oral or intravenous supplementation to their diet to achieve.

The features of complications of NSTEMI/ACS including new acute murmurs or pulmonary oedema should be examined for daily and treated appropriately as described earlier, and patients should have a daily 12 lead ECG done on CCU. Any features of instability in these patients at any time should prompt discussion with a senior doctor and the regional tertiary cardiac centre as it may be appropriate for their care to be transferred there (13).

What medications should patients with NSTEMI be continued on following admission?

In hospital, patients should be continued on regular aspirin 75mg once daily orally (unless contraindicated by a history of true allergy/anaphylaxis), and usually according to local policies, unless contraindicated, either ticagrelor 90mg twice daily orally, or clopidogrel 75mg once daily.

These are prescribed together with atorvastatin 80mg once daily orally and provided that a beta blocker is tolerated without a significant drop in blood pressure or heart rate, bisoprolol should be continued aiming for at least 2.5mg once daily orally if this is possible.

Nitrates may be required for ongoing pain including either sublingual spays or intravenous nitrates, titrated to pain and to maintain systolic blood pressure above 90mmHg. In the event of pulmonary oedema developing or heart failure, a loop diuretic such as Furosemide may be required, orally or intravenously, and this may be given as a continuous infusion in unstable patients with decompensated heart failure.

Fondaparinux, or enoxaparin, unless contraindicated are continued once daily with review from the cardiology team for their duration but this does not usually exceed one week in cases where they are being prescribed for NSTEMI/ACS.

Patients should be reviewed by the local cardiology team prior to discharge to assess their individual discharge prescription according to their past medical history, previous medications and current events (2,3,4,20,21).

In summary

The evaluation of a patient with chest may not be straightforward every time. You need to take not just the ECG but the patients symptoms and biochemical test in context with what presents to you. If in doubt, give your senior a call and ask their advice.

We encourage you to read the evidence we present in this discussion and post for yourself in order to fully understand your evaluation and treatment of patients.

I’d like to thank Professor John Somauroo and Dr. Babu Kunadian, consultant cardiologists, and Karen Randles, a cardiology specialist nurse at Chester for their time and efforts in producing this podcast, and the medical education department at Chester for their continued support.

 

Speak soon,

Scott

 

Email any feedback or comments

Email: foamdation@gmail.com

Twitter: @FOAMdation @scottymwilliams

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References:

  1. NICE Clinical Guideline 95. Chest pain of recent onset: assessment and diagnosis, March 2010. Website: www.nice.org.uk/guidance/cg95 Accessed 02/05/17
  2. NICE Clinical Guideline 167. Myocardial infarction with ST-segment elevation: acute management, July 2013. Website: www.nice.org.uk/guidance/cg167 Accessed 03/05/17
  3. NICE Clinical Guideline 94. Unstable angina and NSTEMI: early management, March 2010. Website: www.nice.org.uk/guidance/cg94 Accessed 05/05/17
  4. NICE Quality standard 68. Acute coronary syndromes in adults, September 2014. Website: www.nice.org.uk/guidance/qs68 Accessed 02/05/17
  5. Korff S et al. Differential diagnosis of elevated troponins, Heart 2006; 92(7): 987-993
  6. Sgarbossa et al. Electrocardiographic Diagnosis of Evolving Acute Myocardial Infarction in the Presence of Left Bundle-Branch Block, NEJM 1996; 334: 481-487
  7. Cabello et al. Oxygen therapy for acute myocardial infarction, Cochrane Database of Systematic Reviews, Dec 2016.
  8. Stub D et al, Air Versus Oxygen in ST-Segment-Elevation Myocardial Infarction, Circulation. 2015 Jun 16;131(24):2143-50
  9. Body R et al, The Manchester Acute Coronary Syndromes (MACS) decision rule for suspected cardiac chest pain: derivation and external validation. Heart. 2014 Sep 15;100(18):1462-8
  10. Nagase, K et al. Significance of Q-wave regression after anterior wall acute myocardial infarction, European Heart Journal 1998; 19: 742–746
  11. Parsonage et al. The approach to patients with possible cardiac chest pain, The Medical Journal of Australia 2013; 199(1): 30-34
  12. Website: http://bestpractice.bmj.com/bestpractice/monograph/245/treatment/step-by-step.html Accessed 10/5/17
  13. Website: https://www.resus.org.uk/resuscitation-guidelines/ Accessed 11/5/17
  14. Website: https://www.escardio.org/static_file/Escardio/Subspecialty/EACVI/position-papers/echocardiography-acute-cardiovascular-care.pdf Accessed 11/5/17
  15. Website: https://www.brit-thoracic.org.uk/standards-of-care/guidelines/bts-guideline-for-emergency-oxygen-use-in-adult-patients/ Accessed 9/5/17
  16. O’Driscoll, BR et al. Should oxygen be given in myocardial infarction? British Medical Journal 2010; 340: c3287
  17. Website: http://www.crusadebleedingscore.org Accessed 10/5/17
  18. Schwartz GG et al. Effects of atorvastatin on early recurrent ischemic events in acute coronary syndromes: the MIRACL study: a randomized controlled trial. The Journal of the American Medical Association 2001; 285(13): 1711-8.
  19. Website. www.gracescore.org Accessed 9/5/17
  20. Kristian Thygesen et al. Expert consensus document. Universal definition of myocardial infarction. European Heart Journal 2007; 28: 2525–2538
  21. Kristian Thygesen et al. The Writing Group on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction: Third universal definition of myocardial infarction. Eur Heart J 2012; 33: 2551-2256.

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