Cardiology: Myocardial Infarction and Acute Coronary Syndromes (ACS)
Acute Coronary Syndromes (ACS)
This is basically an umbrella term for:
- STEMI – ST elevation MI
- NSTEMI – non-ST elevation MI
- Unstable angina
They are grouped together because – they all have a common mechanism –rupture or erosion of the fibrous cap of a coronary artery plaque.
Imagine it like a spectrum – with unstable angina at one end, and STEMI at the other – NSTEMI is in the middle.
Epidemiology
- It is the most common cause of death in the UK
o 50% of deaths occur within 2 hours of onset of symptoms
- Incidence of 300 000 cases per year
- More than 1.4m people in the UK suffer from angina – this also has incidence of approximately 2%
- CAD accounts for about 3% of admission to UK hospitals each year
Aetiology
- Non-modifiable:
o Age
o Gender (male)
o FH of IHD – only if symptoms present before the age of 55
- Modifiable:
o Smoking
o Hypertension
o Diabetes
o Hyperlipidaemia
o Obesity
o Sedentary lifestyle
- Controversial
o Stress
o Type ‘A’ personality
o LVH – left ventricular hypertrophy
o Cocaine use
o ↑ fibrinogen
Symptoms
- Pain! Can radiate down the inside of the arm, and into the neck and jaw and can last up to a couple of hours. May also radiate to the epigastrium or back
- Distress, also sometimes a ‘feeling of impending doom’
- Breathlessness – indeed in many cases this may be the only symptom – many MI’s actually pass unrecognised – particularly in diabetic patients – ‘silent MI’
- Syncope – fainting – if this occurs, then it will be a result of severe arrhythmia, or severe hypotension.
- Sweating
- Tachycardia
- Vomiting and sinus bradycardia– this may occur as a result of excessive vagal stimulation, which is most common in inferior MI
- Nausea and vomiting may also be aggravated by opiates given for pain relief
- Sudden death – this usually occurs from ventricular fibrillation or asystole. Most of these deaths occur within the first hour.
o If the patient survives the first hour, then the liability of serious arrhythmias remains, but diminishes with each subsequent hour. So, patients have to be educated to get help as soon as possible!
o Cardiac failure is the major cause of death in those that survive the first few hours. Whether or not cardiac failure develops is dependent on the extent of myocardial damage.
- Remember, infarction can occur in the absence of any physical signs
- MI (and stroke) is often more common in the morning. This is thought to be because BP lowers during the night, and then rises again when the person wakes up. This higher BP may then dislodge any thrombus that has formed overnight.
Signs
- Signs of impaired myocardial function
o 3rd / 4th heart sounds
o Pan systolic murmur
o Pericardial rub
o Pulmonary oedema – crepitations in the lungs
o Hypotension
o Quiet first heart sound
o Narrow pulse pressure (difference of <40mmHg)
o Raised JVP
- Signs of sympathetic activation:
o Pallor (basically looking pasty. It can be generalised or localised, but is only really clinically significant if generalised. Most evident in the palms and on the face)
o Sweating
o Tachycardia
Presentation of a ‘silent MI’ (no cardiac pain / chest tightness) – usually in diabetic and/or elderly patients
- Syncope
- Pulmonary oedema
- Epigastric pain
- Vomiting
- Acute confusional state
- Stroke
- Diabetic hyperglycaemia
Pathology
MI is almost always due to occlusive thrombus formation at the site of rupture or erosion of an atheromatous plaque. The pain experienced is usually the same as angina, but lasts longer and may be more severe.
- Patients should call an ambulance if they experience ‘angina type pain’, which, after using GTN spray does not subside within 15 minutes.
- The pain is often excruciating – look at the patients face / expression / pallor to determine the seriousness of the pain
There are two different mechanisms. Either:
- the fibrous cap of the plaque itself gets a superficial injury, and a thrombus forms on it, or,
- in more advanced, unstable plaques, the fibrous cap completely ruptures, and not only can some of the contents escape, but blood can also enter the plaques, forming a thrombus within the remaining cap of the plaque.
The platelets then release serotonin and thromboxane A2 and this causes vasoconstriction in the area resulting in reduced bloodflow to the myocardium, and ischaemic injury.
Differentiating types of MI
Transmural MI – this is an infract that causes necrosis of tissue through the full thickness of the myocardium
Nontransmural – this is an MI that does not cause necrosis through the full thickness of the myocardium
Diagnosis
Essentially 2 out of the following 3:
- Suggestive history
o Sign/symptoms
o Risk factors
- ECG changes
- Positive cardiac enzymes tests
o Troponin T
o Troponin I
Differentials
- Cardiac
o Angina
o Pericarditis
o Myocarditis
o Aortic dissection
- Pulmonary
o PE
o Pneumothorax
o Anything that causes pleuritic chest pain
- Oesophageal
o Oesophageal reflux / spasm
o Tumour
o Oesophagitis
Acute Management
Pre-hospital
- Call ambulance
- Aspirin 300mg orally – unless an obvious contraindication
- Pain relief, e.g. 5-10mg morphine + metoclopramide (anti-emetic)10mg IV - avoid IM injections as there is a risk of bleeding - and you just gave loads of aspirin!
- Sublingual GTN (unless hypotensive)
o You can give up to 3 sprays of GTN – but don’t give any if the HR <50, or the systolic BP <90.
Hospital
- Attach ECG – make a recording – it is also reasonably likely that this will have been done in the ambulance. You have to differentiate raised ST segment Mi from non-raised ST segment MI.
- High-flow O2 by venturi mask[non rebreathing] (careful if COPD) – try and maintain sats of above 90 – the ischaemia is hypoxic, so try and counteract this
o If you’re worried about COPD don’t be! Give the O2, but keep an eye on the sats; and adjust if CO2 retention
- Get IV access – take bloods for
o FBC, U+E, glucose, lipids, cardiac enzymes
- Take history / make brief assessment
o History of CHD?
o Risk factors?
o Contra-indications to thrombolysis
- Do a cardiac examination:
o Pulse
o BP
o JVP
o Murmurs
o Signs of heart failure
o Peripheral pulses
o Signs of previous surgery
o ECG – do this before you give thrombolysis to differentiate raised ST segment or not MI
- Give 300mg aspirin if not already administered
- Give 5-10mg morphine and metoclopramide 10mg IV if not already administered
o Be careful! – giving pain relief can mask whether there is still ongoing pain, and thus you aren’t able to tell if you’re GTN is working!
- Give GTN sublingually, 2 sprays or one tablet if not already given –BUT don’t give with systolic BP <90, or with a HR <50
- In STEMI - GIVE THOMBOLYSIS – the sooner you give it the better – the greatest benefit is seen within the first 12 hours of chest pain, but may still be beneficial up to 12 hours. The British Heart Foundation advises that it should be given no greater than 90 minutes after initial onset of chest pain, and ideally no greater than 60 minutes if possible
o The pain experienced during an MI is related to myocardial ischaemia – if the pain goes away its probably too late to save the heart muscle.
o Streptokinase is the usual drug used.
o BUT – DONT GIVE THROMBOLYSIS TO THOSE WITHOUT ST ELEVATION!
- Give a β-blocker – usually atenolol 5mg IV. Do not give if asthma or right ventricular failure!
- Give CXR – you should always give the anticoagulant first, unless you suspect aneurysm!
- Patients with diabetes, consider:
o Glucose
o Insulin
o Potassium
- Consider DVT prophylaxis
- Continue all medications further (unless contraindicated), except calcium channel-agonists, until reviewed for long-term treatment
Note that morphine is also a vasodilator
Investigations
ECG Showings – most commonly, a STEMI
- Early – within hours
o Peaked T wave (very tall T wave)
o Raised ST segment
- Within 24h
o Inverted T waves – this may or may not persist
o ST segment returns to normal. Raised ST segments may persist if a left ventricular aneurysm develops
- Within days
o Pathological Q waves form – these may resolve in 10% of cases
§ We say the Q wave is pathological if it is >25% of the height of the R wave, and/or it is greater than 0.04s width (1 small squares) and/or greater than 2mm height (2 small squares)
§ Q waves are also a sign of a previous MI – the changes in Q waves are generally permanent. The changes in T waves may or may not revert. The ST segment can return to normal within hours.
§ Non-q-wave infarcts are infarcts that occur without the changes seen in the Q waves, but still with the ST and T changes.
Typical picture of changes:
ST elevation – then later, T inversion - , then later, Q wave appears
Other patterns of ECG change:
- ST- depression
- Reciprocal change - sometimes seen in STEMI. This refers to a phenomenon whereby there is ST DEPRESSSION in some leads, in the presence of ST elevation in others. this occurrs as the ECG leads are viewing the heart from different angles. the ST depression will typically occur in leads viewing the heart at the opposite angle to those showing ST elevation. The presence of reciprocal change is thought to indicate an earlier presentation of MI but is not particularly associated with different outcomes.
**20% of patients will initially have no ECG changes**
- Patients without ST elevation are said to have had a NSTEMI
REMEMBER!:
- ST depression – Ischaemia – the damage is reversible (with the right treatment)
- ST elevation – Infarction – damage is irreversible
CXR
- Don’t delay treatment whilst waiting for the CXR! Changes may include:
o Cardiomegaly
o Pulmonary oedema
o Widened mediastinum
Blood Tests
- Cardiac enzymes – troponin T and I
o Troponin T – most commonly used test.
§ Level should be 2x greater than normal to be diagnositc
§ Peak level of elevation is 12-24 hours – perform the test 12h after onset. Levels usually raised for about a week
§ Specific for heart muscle – but not for MI – be wary of other causes of heart muscle damage (e.g. severe tachycardia, heart failure, myocarditis, myopericarditis)
§ Helps to differentiaite between unstable angina and MI
· If troponin T and ECG are both normal after 6 hours, risk of MI is only 0.3%
o Creatine kinase (CK)
§ Found in skeletal and myocardial muscle
§ Raised after any sort of muscle trauma
- Glucose – not only does this help you treat any diabetes present, but evidence suggests that patients with a high glucose on admission have a worse prognosis- thus you should treat these patients more aggressively.
- Lipids – checking for raised cholesterol – although this isn’t actually necessary as all MI patients are given a potent statin (e.g. atorvastatin) regardless of the cholesterol level.
- FBC – get a provisional platelet level before anticoagulation. Check for anaemia
Give thrombolysis – IF APPROPRIATE!
Indications for giving thrombolysis
The patient presents within 12 hours of chest pain, and:
- There is ST elevation of 2mm or more in 2 or more chest leads
- There is ST elevation of 1mm or more in 2 or more limb leads
- There is new onset LBBB
- There is evidence of a posterior infarct:
o Dominant R waves and ST depression in V1-V3
OR
The patient presents within 12-24 hours of onset of chest pain
- and there is continuing chest pain
- OR there is ST elevation
Contraindications for thrombolysis
- Internal bleeding
- Prolonged or traumatic CPR
- Heavy vaginal bleeding
- Acute pancreatitis
- Active lung disease with cavitation
- Recent surgery or trauma (<2 wks)
- Cerebral neoplasm
- Severe hypertension (>200/120)
- Suspected aortic dissection
- Previous allergic reaction
- Pregnancy
- <18 weeks postnatal
- Severe liver disease
- Oesophageal varices
- Recent head trauma
- Recent haemorrhagic stroke
if ANY of these are present, then you should consider giving urgent angioplasty instead
1 in 200 patients who receive thrombolysis will have a stroke! Do not give thombolysis to those without ST elevation.
The use of PCI (percutaneous coronary intervention – i.e. angioplasty)
Angioplasty is the first line recommended treatment for STEMI (and also high risk NSTEMI) patients. Evidence suggests it is more effective than thrombolysis However, it is not available at all NHS hospitals in the UK. It is mainly available at ‘tertiary centres’. This term basically means a hospital specialised to perform this treatment. i.e. primary care – GP, secondary care – hospital, tertiary care – specialist hospital.
SO – you should only use thrombolysis if:
- The patient has no contra-indications
- they have a STEMI (not NSTEMI)
- angioplasty (PCI) is not available
Differences between STEMI, NSTEMI and unstable angina
- STEMI – the most serious type of ACS. Caused myocardial infarction and ischaemia.
o Management
§ PCI / Thrombolysis. PCI if available. If not, thrombolyse if no CI's
§ Beta-blocker – unless contraindicated (e.g. asthma) – e.g. lisinopril 5mg IV
§ ACE-i – start ASAP – usually within 24hours, particularly if there are signs of LV dysfunction - e.g. lisinopril
- NSTEMI – less serious then STEMI, but still causes damage to the myocardium.
- Unstable angina – does not cause myocardial damage in itself, but may progress to MI
o Management of NSTEMI/Unstable angina
§ Beta-blocker – unless contraindicated (e.g. asthma) - e.g. atenolol 5mg IV
§ LMWH – e.g. enoxaparin – for 2-8 days
§ Nitrates – usually given IV
§ Clopidogrel – may be considered in addition to aspirin, for up to 12 months – especially in patients with raised troponin. These patients are considered high risk
· In patients with normal troponin, you may consider discharge after 48h, as these are low risk
NHS policy – you have to treat MI within 36 minutes – ‘door to needle’ time - a maximum of 36 minutes between a raised ST segment MI patient coming in to the emergency department and receiving PCI / thrombolysis.
MONA LISA Mnemonic for acute management of MI
M- morphine
O- oxygen
N- nitrates
A- Aspirin
L – loop diuretic
I – IV access – for bloods, for IV GTN etc
S – streptokinase (thrombolysis) / PCI - if STEMI
A – Antiplatelets (e.g. clopidogrel)
Subacute Management
- Bed rest for 48h, with constant ECG monitoring
- Examine daily – including heart lungs and legs – for complications
- Cardiac enzymes – every day for 3 days – should see troponin levels begin to fall
- Prophylaxis against thromboembolism, at least until fully mobile, e.g. heparin
o Warfarin recommended for at least 3 months in those with large anterior MI, due to high risk of embolus as a result of LV dysfunction.
- Beta-blocker – should be continued for 1 year+. Does should be high enough o reduce pulse to <60bpm
o Long term beta-blocker use reduces the risk of mortality by 25%
- ACE-i – should be continued. Reduces mortality by 25-30% at 2 years
- DISCHARGE – if no complications, discharge after 5-7 days.
o Work – patients should return to work after 2 months. Certain careers may no longer be allowed:
§ Airline pilot
§ Air-traffic controller
§ Driver
· Some driving jobs allow patients to return to work if they meet certain criteria
§ Some physically demanding jobs (e.g. involving heavy lifting) may not be suitable.
Long term management (secondary prevention measures)
Cardiac rehabilitation programs
All patients should be offered places on these programs, and programs should always involve an exercise component. You should not exclude a patient from any part of the program if they chose not to attend any individual parts
These programs generally offer support to achieve the goals listed below:
- Smoking cessation
- Increase in exercise – encourage regular daily exercise, and at least 30 minutes, 3x/week strenuous exercise
o Sex – Should avoid for 1 month after MI
o Travel – avoid air travel for 2 months
- Reduction in weight
- Reduction in alcohol intake
- Dietary modification (reduced fat intake) – diet should be:
o High in – oily fish, fibre, fresh fruit and veg
o Low in – saturated fat
Drug treatment
All patients should be placed on the following medications:
- Aspirin
o This is an anti-platelet drug. If the patient is hypersensitive, then consider clopidogrel. Some patients may be put on aspirin and clopidogrel in the acute phase after an MI; but they should not be on this combination for more than 12 months.
o In patients with dyspepsia, you should also consider giving a PPI with aspirin to reduce the risk of ulceration.
- β – blocker
o this has antihypertensive effects, by encouraging peripheral vasodilation, and it also reduces cardiac output, by reducing the rate and contractility of the heart. It also reduces renin secretion.
- ACE inhibitor (or alternative anti-aldosterone drug)
o Not only does this drug help to reduce blood pressure and reduce the risk of chronic renal failure, but it also helps to reduce/delay the onset of heart failure, by preventing remodelling of the left ventricle.
- Statin
o This is useful even in patients with a normal cholesterol level! Some trusts treat all MI patients with a statin, others only treat those with total cholesterol >4mmol/L
Review
- At 5 weeks – for complications, and angina. Treat angina in normal method. Consider angioplasty if severe
- At 3 months – check for raised cholesterol and consider statin if not already prescribed.
COBRA-A mnemonic for Secondary Prevention in ACS
- C – Clopidogrel – antiplatelets
- O – Omacar – Omega 3
- B – Bisoprolol – β-blocker
- R – Ramipril – ACE-i
- A – Aspirin
- A – Atorvastatin – very potent statin!
Complications of MI
- Cardiac arrest
- Unstable angina
- Bradycardia, heart block
- Tachyarrhythmias
- Left ventricular failure
- Right ventricular failure
- Pericarditis
- DVT & PE
- Systemic embolus
- Cardiac tamponade
- Mitral Regurg
- Ventricular septal defect
- Late malignant ventricular arrhythmias
- Dressler’s syndrome
- Left ventricular aneurysm
- Mural thrombus – this is a thrombus attached to the wall of the endocardium in a damaged area, or sometimes it is attached to the aortic wall over an intimal lesion.
o MI leads to akinetic areas of ventricular wall. This stasis allows the formation of a thrombus on the wall. The larger the infarct, the greater the risk of thrombus. Parts of the thrombus can easily break off an embolise. Common sites of ischaemia are; brain, spleen, gut, kidney, lower limbs.
- Ventricular wall rupture – this occurs about 5-10 days after the initial infarct. At this time the myocardium is particularly soft. Blood can then come out of the rupture, and enter the pericardial sack, causing haemopericardium. This usually leads to cardiac tamponade as it is an acute effect.
o This classically presents with electromechanical dissociation – a perfectly normal ECG, but no cardiac output and no pulse. As you know – PEA (pulseless electrical activity) is a non-shockable rhythm – and thus almost always results in death
- Ventricular aneurysm – this is a late complication of a transmural MI. the infracted muscle will be replaced by a thin layer of collagenous scar tissue, that will gradually stretch as intraventricular pressure rises during systole. The aneurysm itself has complications of left ventricular failure, arrhythmias, mural thrombus. Rupture of the aneurysm is rare.
- Mitral valve incompetence – commonly caused by ischaemic damage to the papillary muscles, especially in posterior infarcts. Post ischaemic fibrosing and shortening of the papillary muscles can also cause incompetence
o In some patients, the papillary muscles can be completely destroyed by the infarct, resulting in instant and complete torrential mitral valve incompetence.
Dressler’s syndrome
An autoimmune pericarditis, provoked by MI. Occurrs in 5-10% of cases of MI. Onset 1-3 weeks post MI. Localised pericarditis. Causes fever, pericardial effusions, anaemia, raised ESR, enlarged heart on CXR, pericardial rub (on auscultation). may be similar to PE - another post-MI complicatio
It is often self-limiting, and symptoms last a few days.
Treated with NSAID’s, and in more serious cases, steroids.
Notes by Tom Leach
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