Acute coronary syndrome
A new NICE guideline on ACS is expected in 2010. These recommendations are taken from
the SIGN guidelines1
Recognise acute myocardial infarction and use appropriate investigations to confirm the
diagnosis
What is a myocardial infarction?
Not as easy to answer as you might imagine as there are many different definitions. The World
Health Organisation (WHO) say that it may be diagnosed upon two of the following three being
present2:
 A history of cardiac-type ischaemic chest discomfort
 Raised cardiac markers (e.g. tropinin >1.0)
 ECG changes involving the development of Q waves
The Americal College of Cardiology (ACC) and the European Society of Cardiology (ECS) use
the following diagnostic criteria:
 Raised cardiac troponins (>0.01 – note difference to level for WHO) + at least one of
o Ischaemic symptoms (e.g. chest pain, dyspnoea, nausea etc.)
o Development of pathological Q waves on ECG
o ECG changes indicating ischaemia (ST elevation or depression)
o Positive coronary artery intervention e.g. coronary angioplasty
SIGN guideline 93 (2007) encourages yet another way of thinking about myocardial infarct
using the British Cardiac Society guidelines.
The WHO definition states that MI is not diagnosable until a Trop T result of >1.0 – this definition,
however means that many people with a poor 30 and 60 day prognosis may not get treatment
that could benefit them.
The European Society of Cardiology (ESC) and American College of Cardiology (ACC) treat MI
as being diagnosable with a Trop T >0.01.
Troponin is ideally measured at 12 hours after the onset of chest pain and some hospitals keep
rigidly to this guideline, not processing samples taken before this limit. There is a role however for
earlier measurement of troponin to guide early treatment provided that a second test is done at
12 hours if the result is anything but ACS with MI, as management may need to be upgraded.
The British Society of Cardiology gives three classifications:
 ACS with unstable angina
 ACS with myocyte necrosis – probable micro-infarcts but no major tissue damage.
 ACS with clinical myocardial infarction
Both of the last two yield increased mortality at 30 and 60 days over simple unstable angine – this
verifies the ACC/ECS opinion that treatment is suitable at troponin levels >0.01
Elevated troponins can occur without ACS and is associated with poorer outcomes in sepsis, PE,
CKD and CHF. Out of Troponin I and T neither has an obvious advantage.
So how do you decide which diagnostic criteria to use?
Use common sense and err on the side of caution!
Describe immediate management of Acute Coronary Syndrome
The Mnemonic GO CARDIO ABCD can be of help. This mnemonic does not describe the order
of the actions – it simply acts as a reminder not to forget things!
G
O
C
A
R
D
I
O
A
B
C
D
GTN
Oxygen
Clot prevention – Enoxaparin or Clexane
Aspirin + Clopidogrel
Raised position
Diamorphine
Investigations: ECG and Troponin at minimum
Observations: initial and repeat
ACE Inhibitor or ARB
Beta blocker if not in failure
Cholesterol - Statin
Diabetes control
Measures to implement in the acute
setting
Measures to implement after
control of the acute event has been
achieved.
Act appropriately to ensure that those patients likely to benefit receive thrombolysis or
PCI as quickly as possible
There are two types of acute coronary syndrome:
 Non ST Elevation Acute Coronary Syndrome (NSTEACS): Prev. NSTEMI or non-Q-wave MI
 ST Elevation Acute Coronary Syndrome (STEACS): Previously STEMI or Q-wave MI
Q waves are now no longer used as they are relatively late arrivals on an ECG trace and so poor
for guiding need for thrombolysis.

-
For thrombolysis  12 hours should have elapsed since onset of chest pain + one of:
ST elevation >2mm in 2+ chest leads
ST elevation >1mm in 2+ limb leads
Posterior infarction (Dominant R wave + ST depression in V1 – V3.
New onset LBBB
Compared to placebo thrombolysis improves 35 day mortality in STEACS but it is inferior to
primary PCI at all time points. Thrombolysis should be given if it is not possible to start primary
PCI within 90 minutes. There is an increase in mortality of 1.6 / 1000 patients for each hour delay
so thromolysis is extremely time sensitive.
There is certainly no need to learn this table! The important points are that risk of a reinfarct or
recurrent ischaemia is reduced by nearly 60% in PCI compared to thrombolysis and risk of death
is reduced by nearly 40% in PCI compared to thrombolysis.
Control the pain of myocardial infarction
The standard drug is diamorphine – this is given by slow IV injection 5 mg at 1 mg / min + 2.5 – 5
mg extra if required. Half dose in elderly or frail. An antiemetic (e.g. cyclizine 50 mg) should be
given at the same time.
Recognise ventricular fibrillation (and other dangerous rhythms) and carry out immediate
management
There are many rhythms that should indicate the need to do something urgently
– the main ones you need to be aware of are:
Rhythm
Ventricular tachycardia
Ventricular fibrillation
Pulseless electrical activity
Asystole
Action
Shockable - administer shock as soon
as possible and follow the ALS
guideline3
Non-shockable – attempt to convert to
normal or shockable rhythm by
adrenaline and following ALS protocol3
Premature Ventricular Contraction
The QRS complex is early and very wide. These are dangerous when:
 They come "off" the T wave (as here) -- the heart gets confused and is unsure whether to
relax (T wave) or contract (PVC), so it quits.
 There are more than 2 in a row.
 There are more than 6 per minute (some sources say 8 or 10)
 This may progress to ventricular tachycardia
Ventricular Tachycardia (VT or V Tach)
 Usually, there are no P waves visible
 When P waves are detectable they are not related to QRS complexes (atrioventricular
dissociation is present)
 The QRS complexes are wide (> 0.12 s) - they appear in a regular rhythm in monophasic VT
(where the cause is an anatomical re-entry pathway) or in irregular rhythm in polyphasic VT
(where the cause is a constantly changing re-entrant pathway e.g. due to ischaemia).
 The rate of QRS complexes is between 100 and 260 beats per minute (usually between 180
and 250
 This may progress to VF
Ventricular Fibrillation
This is ineffective, disorganized ventricular beating. It is INCOMPATIBLE with life.
Asystole
Usually follows V fib unless it is interrupted by CPR that actually works or by a defibrillator. It
indicates cardiac arrest -- or that your patient has become unattached from the electrodes!
Correctly place paddles / electrodes to safely deliver defibrillating shock




One electrode should be placed at the upper right sternal
border directly below the right clavicle.
The other should be placed lateral to the left nipple with the
top margin of the pad about 7 cm below the axilla.
The correct position is usually indicated on the electrode
packet or shown in a diagram on the machine itself. It may be
necessary to dry the chest if the patient has been sweating
noticeably or shave hair from the chest in the area where the
pads are applied. A sharp razor should be carried with the
machine for this purpose.
Each minute of delay in restoring normal heart rhythm
increases mortality by 7-10%.
Recognise the need for further active management in the medium to long term
Recommendations in the SIGN guidance 2007 include the following to be started BEFORE
discharge:
Unstable
NSTEACS
STEACS
angina
Aspirin 75 mg – 150 mg
Not routine
Long term
Long term
Clopidogrel 75 mg
Not routine
3 months
1 month normally
6 months if stent fitted
Statin e.g. simvastatin 40 mg od
Not routine
Long term (irrespective of lipid levels)
Beta blocker*
Long term
Long term
Long term
Nitrates
For Pain
Not routine
Not routine
Calcium channel blockers
Not routine
Not routine
Not routine
ACE inhibitors
Long Term
Long term and within 36 hours
Angiotensin receptor blockers
Long term as an alternative if non-tolerant of ACE I
Aldosterone receptor antagonist
Not routine
Long term in certain cercumstances**
*Use with care at least 3 days after onset in Left ventricular failure – expert opinion advised.
** Strong benefit in diabetic patients, those with clinical heart failure or LVF ejection fraction <40%
Describe the features of the underlying pathophysiological changes which can be used to
develop treatment and prevention strategies
Ischaemia is basically a mismatch between oxygen demand and oxygen supply
There are three determinants of oxygen demand in the heart
Ventricular wall stress: this is the force acting tangentially on myocardial
fibres that tries to push them apart. Energy must be spent to oppose this
=
force. Wall stress (s) is related to systolic ventricular pressure (P), ventricular
radius (r) and (ventricular wall thickness (h) as in the equation (right).
 Factors increasing P include hypertension and aortic stenosis
 Factors increasing r (increased LV filling) include aortic stenosis and regurgitation.
 Wall thickness increases in compensation to pressure overload
Heart rate
Contractility
Pr
2h
Oxygen supply to the heart is via the coronary vessels (see below). There are two main
factors that interfere with this supply
Fixed vessel narrowing: All other factors being equal, flow is proportional to r4. This means that
even a small change in radius results in a large change in flow. In practice if a lesion occupies
70% of the diameter of the lumen then symptoms will be seen on exercise. At ~90% these
symptoms will be present at rest. Collateral channels may develop in compensation but these are
usually not sufficient.
Endothelial cell dysfunction: endothelial cells accomplish a number of functions
 They secrete vasodilator factors (e.g. NO) that outweigh the action of vasoconstrictors such
as catecholamines.
 They secrete factors that inhibit platelet aggregation
Without these functions it can be seen that the balance between vasodilators and
vasoconstrictors is tipped toward the latter and in addition, platelet aggregation is more likely
producing both a physical barrier and secreting their own procoagulants and vasoconstrictors.
Other causes of poor supply include: anaemia and hypoxaemia:
1) http://www.sign.ac.uk/guidelines/fulltext/93-97/index.html
2) Heart 2002 October; 88(4): 343-347 Myocardial infarction
redefined: The new ACC/ESC definition, based on cardiac troponin,
increases the apparent incidence of infarction, Ferguson et al
3) http://www.resus.org.uk/pages/als.pdf
http://www.resus.org.uk/pages/als.pdf