ASSESSMENT

The patient should be assessed in a safe environment with oxygen, monitoring and a cannula in situ. Look for ACS with ECG changes, known as ST-segment elevation myocardial injury (STEMI), indicating recent coronary artery occlusion, or ACS without new ECG changes, now known as ‘non-ST-segment elevation acute coronary syndrome’ (NSTEACS). NSTEACS patients can then be stratified as high risk, medium risk or low risk.

In some cases no ACS can be demonstrated and an alternative diagnosis is established, such as aortic dissection, pericarditis or pulmonary embolism

Table 7.1 Initial patient assessment and stratification

STEACS	NSTEACS
ST-elevation acute coronary syndrome usually referred to as STEMI (ST–segment elevation myocardial injury)	Non-ST-elevation acute coronary syndrome Stratify: → HIGH RISK → INTERMEDIATE RISK → LOW RISK

or a non-cardiovascular cause such as pneumonia, musculoskeletal pain or gastro-oesophageal disease may be identified. In a significant subgroup of presentations, immediately serious illness can be excluded and, although no diagnosis is reached, the patient can be discharged for follow-up outpatient assessment.

DIAGNOSING AND STRATIFYING ACUTE CORONARY SYNDROMES

History, examination, investigation and management proceed rapidly and concurrently and senior staff should be contacted as soon as possible (see Figure 7.1).

Figure 7.1 Chest pain pathway

Typical presentations of ACS involve chest discomfort at rest or for prolonged periods (prolonged is defined as > 10 minutes, not relieved by sublingual nitrates) or recurrent chest discomfort or discomfort associated with syncope or acute heart failure.

Some important points of immediate history include the time of onset of pain, exertionally-related pain, risk factors and comorbidities, allergies and contraindications to treatments.

Physical examination may show tachycardia or bradycardia, hyper- or hypotension, sweating, nausea or evidence of heart failure (dyspnoea, basal crepitations, third heart sound, poor peripheral perfusion). Importantly there may be no specific physical findings in some patients with ACS.

Note that although cardiac myonecrosis is demonstrated by increased levels of cardiac biomarkers (troponins, creatine kinase-myocardial band (CK-MB)) and can occur in ACS with or without ECG changes, the indication for initial urgent reperfusion therapy is acute ECG change.

Tests to include are listed in Table 7.2.

Table 7.2 Tests to aid in the diagnosis and stratification of patients with ACS ^∗

Test	Comment
Full blood count	Anaemia or polycythaemia may need treatment, baseline platelet count (particularly if heparin is to be used)
Coagulation PT and APTT	Guides anticoagulant therapy
Serum chemistry	Hypokalaemia increases the risk of arrhythmia. Hypomagnesaemia may be present if patient taking some diuretics or has liver/renal disease
Renal function	Creatinine (and, if elevated, eGFR calculation). Kidney disease is a risk factor for high- and intermediate-risk NSTEACS
Troponin I or T^∗∗	May take up to 6 hours to rise, two or more measurements over time may be required; remains elevated 5–14 days
Serum lipids	Initiating treatment of hyperlipidaemia within the first few days may be required
Blood glucose	Diabetes may be undiagnosed (especially mild NIDDM); close control of blood glucose levels improves outcomes
Chest X-ray	May show heart failure, cardiomegaly. Do not delay urgent treatment to obtain a CXR. Do not send potentially unstable patient out of resuscitation monitoring area for CXR

APTT, activated partial thrombin time; CXR, chest X-ray; eGFR, estimated glomerular filtration rate; NIDDM, non-insulin dependent diabetes mellitus; PT, prothrombin time

∗ Additional tests such as high-sensitivity C-reactive protein (CRP) and B-type natriuretic protein (BNP) or Pro-BNP are still being evaluated. In some settings bedside cardiac echocardiography can be valuable as it may be able to provide information on wall motion (myocardial ischaemia or infarction), ejection fraction (heart failure, systolic or diastolic dysfunction), valvular disease (aortic stenosis, acute mitral valve chordae disruption), free wall rupture, aortic or pericardial disease. Drug screening (cocaine, amphetamines) may be relevant. An alternative diagnosis of pulmonary embolism can sometimes be made when significant right heart abnormality is seen on echo.

∗∗

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