Acute Coronary Syndromes (1): ST-Segment Elevation

Many emergency departments will have a specific protocol for the management of STE-ACS, consisting of:

Focused clinical assessment (Figure 45.1) and observations, using an ABCDE protocol:
- Time, onset and character of pain
- Past history and risk factors for coronary disease
- Bleeding risk
- Consider alternative diagnoses – could pulmonary embolism or aortic dissection be possible?
12-lead ECG (repeated every 15 min if not initially diagnostic and chest pain persists) and other urgent investigation (Table 45.1). Evaluate carefully for:
- ST-segment elevation >1 mm in 2 or more adjacent leads or
- Complete left bundle branch block not known to be old
Oxygen therapy if indicated:
- Monitor arterial oxygen saturation, aiming for >92%
- Give high-flow oxygen if oxygen saturation is <92% or there is evident respiratory distress or pulmonary oedema
Put in an IV cannula and give opioid analgesia:
- 5 mg morphine IV (2.5 mg if elderly or frail) over 3–5 min, with further doses at 15-min intervals as needed to relieve pain
- Co-administer an antiemetic, for example metoclopramide 10 mg IV

If the clinical presentation and ECG are consistent with STE-ACS:

Give aspirin 300 mg PO unless already administered.
Give a beta blocker (e.g. atenolol 5–10 mg or metoprolol 5–10 mg) IV unless there is pulmonary oedema, or systolic BP is <100 mmHg, or the heart rate is <60/min.
Is primary percutaneous coronary intervention (pPCI) available within 90 min? If so:
- Give an additional antiplatelet agent – clopidogrel, ticagrelor or prasugrel, depending on local protocol
- Transfer the patient to the cardiac catheterization laboratory for immediate angiography and follow-on pPCI
If pPCI not available, assess eligibility for reperfusion therapy:
- Less than 12 h since the onset of symptoms?
- Other causes for ST-segment elevation (pericarditis, early repolarization, acute aortic dissection; see Chapter 7) considered and excluded?
- Contraindications to reperfusion therapy absent? (Table 45.2)
Give thrombolysis if appropriate (Table 45.3):
- Problems encountered with thrombolysis are as shown in Table 45.4.
- Repeat a 12-lead ECG 60 min after start of lytic therapy. If there is persisting ST-segment elevation, transfer for immediate coronary angiography. If ST segment has resolved, and the patient is clinically stable, discuss with a cardiologist inpatient coronary angiography during the same hospital admission.

Problems in the Acute Phase

Delayed presentation of STE-ACS

The benefits of reperfusion therapy fall if the diagnosis of STE-ACS is made more than 12 h after the onset of symptoms, but should still be considered if there is:

Severe heart failure
Haemodynamic disturbance
Recurrent ventricular arrhythmia
Persistent ischaemic pain

If on-site primary PCI is not available, then the decision over reperfusion therapy depends on the time required for transfer and initiation of PCI. Ideally, this should be less than 90 min from diagnosis of STEMI to restoration of flow in the occluded vessel. If it is likely to be longer than 120 min, then fibrinolytic therapy and follow-on angiography maybe more appropriate.

Diagnosis of ST-segment-elevation ACS but normal coronary anatomy

Consider stress cardiomyopathy (Takotsubo syndrome) (Table 45.5). This typically occurs in a female aged >65 following an emotional shock. The diagnosis is suggested by echocardiography showing the wall motion abnormality extending from the apex to the midcavity and crossing more than one arterial territory. Coronary angiography is required to exclude coronary disease, although it is recognized that bystander coronary disease may occur. Other possibilities are myocarditis, resolution of plaque rupture, coronary embolism and coronary spasm (e.g. caused by cocaine).

Hypotension without pulmonary oedema

Hypotension is not always due to cardiac dysfunction. Carefully evaluate for evidence of hypovolaemia which may be due to vomiting or bleeding following percutaneous coronary intervention. If there is no evidence of pulmonary oedema, consider a fluid challenge.

Check the JVP, which will be low in hypovolaemia and high in right ventricular (RV) infarction.
An echocardiogram (Chapter 114) will show:
- RV size and function
- An inferior vena cava, flat in hypovolaemia and engorged in right ventricular infarction
For both hypovolaemia and right ventricular infarction initial treatment is with IV fluid. Give crystalloid 500 mL IV over 15–30 min followed by a further 500 mL over 30–60 min if systolic BP remains <100 mmHg and there is no pulmonary oedema.
If BP remains low start an infusion of dobutamine (Table 2.7 page 13).
If hypotension persists, consider placement of a pulmonary artery catheter to guide further therapy. In right ventricular infarction, the right atrial pressure will be high (12–20 mmHg) and equal or greater than the wedge pressure.
Give more fluid to raise the wedge/pulmonary artery diastolic pressure to 15 mmHg. You can risk pulmonary oedema giving IV fluids without monitoring if there is an associated large inferior infarct.

Hypotension with pulmonary oedema

Review for signs of cardiogenic shock (Chapter 49):

Systolic pressure <90 mmHg
Heart rate either >100 or <40/min
Hypoxaemia (arterial oxygen saturation <90%) or tachypnoea (respiratory rate >30/min)
Poor peripheral perfusion
Sweating and agitation
Oliguria

Cardiogenic shock carries a poor prognosis and is an indication for PCI. Discuss with a cardiologist.

Increase the inspired oxygen concentration, aiming for oxygen saturation >92% (PaO₂ >8 kPa).
Consider a continuous positive airway pressure (CPAP) system if this target is not achieved (Chapter 113).
Start inotrope/vasopressor therapy (Table 45.6) if hypotension persists.
Use intravenous nitrates if systolic BP >100 mmHg.
Place a bladder catheter and aim for a urine output >30 mL/h.
Arrange urgent echocardiography to assess ventricular function and assess for structural complications.
For pulmonary oedema without significant hypotension:
- Give furosemide 40–80 mg IV
- Start a nitrate infusion

Arrhythmias

Bradycardia (Chapter 44)Bradycardia (Chapter 44)

Give IV atropine 0.6–1.2 mg IV if symptomatic bradycardia <40/min.
Temporary pacing is occasionally indicated (Table 45.7): discuss with a cardiologist. The procedure risks perforation of infarcted myocardium and triggering of ventricular arrhythmia.

Tachyarrhythmia (Chapters 39, 40, 41, 42, 43)Tachyarrhythmia (Chapters 39–43)

Broad complex tachycardia should be treated as ventricular tachycardia. If there is haemodynamic compromise, DC cardioversion should be done promptly (Chapter 121).
Ensure serum potassium is maintained between 4 and 5 mmol/L.

Outline

General Supportive Care
Drug Therapy
Glycaemic Control
Managing Recurrent Pain
New Murmur
Rehabilitation and Secondary Prevention
Assessment of Lv Systolic Function
Testing for Inducible Myocardial Ischaemia
Discharge Checklist

General Supportive Care

Bed/chair rest for 24 h, then mobilization.
Oxygen is not required if normal oxygen saturation and clear chest X-ray.
Fever and leucocytosis are common in response to infarction, but ensure no evidence of thrombophlebitis, pericarditis or lower respiratory tract infection complicating resolving pulmonary oedema (Table 45.8).
Continuous ECG monitoring (by bedside monitor or telemetry) for 48 h.
Thromboprophylaxis with low-molecular-weight heparin.
Cardiopulmonary examination at least daily. Causes of a murmur are given in Table 45.9.
Review all usual medication and stop any drugs that are contraindicated post-infarction:
- Non-steroidal anti-inflammatory drugs should be avoided as increased bleeding risk
- Pro-arrhythmic agents including some antidepressant and anti-epileptic drugs
- Drugs that may depress myocardial function, for example calcium channel blockers

Drug Therapy

Aspirin 75 mg daily for life.
Second antiplatelet agent (P2Y₁₂ inhibitor, e.g. clopidogrel) in addition to aspirin for one year.
Oral beta blocker the next day:
- Delay if heart failure
- Caution if low cardiac output
- Delay or avoid if high risk for heart block
- Contraindicated in true reactive asthma (but not COPD)
An ACE inhibitor should be started on the morning of the day after admission unless there is a contraindication:
- Highest value in patients with anterior infarction
- Prognostic value if LV ejection fraction <40%
- Can be replaced by angiotensin receptor blocker if required, but not in addition
High-dose statin therapy should be commenced in all patients irrespective of initial lipid profiles – dose and agent can be modified in the recovery phase if required.

Glycaemic Control

In patients with known diabetes or an elevated blood glucose on arrival (>10 umol/L) start a variable rate insulin infusion (Chapter 82).
Post-infarction treatment with subcutaneous insulin is preferred unless prior glycaemic control (and an HbA1c measurement) was excellent on oral hypoglycaemia agents. Input and education from a specialist diabetes team should be requested.

Managing Recurrent Pain

Chest soreness is common after infarction and can be severe following cardiopulmonary resuscitation, which may result in rib fracture.
Pericarditis occurs in 20% of patients and can cause pain similar to infarction but less severe, and usually postural and affected by respiration. Treat with higher dose aspirin or non-steroidal anti-inflammatory agents with gastro-protection.
Re-infarction presenting with recurrence of infarct symptoms and new ST elevation should be managed as acute STE-ACS with urgent revascularization unless contraindicated.

New Murmur

A pericardial friction rub may be mistaken for a murmur.
Request an echocardiogram for all murmurs, either electively or as an emergency, if there is hypotension or pulmonary oedema:
- Soft systolic murmurs are usually benign, but may occasionally result from an early ventricular septal rupture, while still limited or from significant mitral regurgitation with an eccentric jet.
- A loud systolic murmur suggests aortic stenosis and the murmur may become obvious as LV function improves.
- Pan systolic murmurs may be due to ventricular septal rupture or mitral regurgitation, which may be chronic, but can be acute following papillary muscle disruption or rupture.

Rehabilitation and Secondary Prevention

Give advice on diet, exercise and driving/work implications.
Smoking cessation advice and nicotine replacement therapy if needed.
Seek advice on management of diabetes from the specialist diabetes team.
Treat hypertension aiming for BP <140/85 or <130/80 mmHg if diabetic.
Continue high-dose statin; if the initial lipid profile showed severe hypercholesterolaemia or hypertriglyceridaemia, refer to a lipid specialist.
Involve hospital rehabilitation team and enrol in post-discharge support programme.
Psychological support may be needed.

Assessment of Lv Systolic Function

Echocardiography to assess LV systolic function should be done before discharge. If LV ejection fraction is <40%, seek advice on management from a cardiologist prior to discharge.

Testing for Inducible Myocardial Ischaemia

As the majority of patients will undergo reperfusion with primary PCI and the culprit lesion treated with a stent there is no requirement for pre-discharge stress testing unless multivessel disease was identified with significant bystander disease.
Exercise electrocardiography is safe if there are no recurrent symptoms and no arrhythmia for 72 h prior to the test. Pharmacological stress testing with assessment of ischaemia by non-invasive imaging (e.g. stress echocardiography or myocardial perfusion scintigraphy) is also safe and can be performed pre-discharge or in the recovery period to help guide the need for further revascularization.

Discharge Checklist

See Table 45.10.

section name header

Information ⬇

Priorities ⬆ ⬇

Further Management ⬆ ⬇

Further Reading ⬆