These have greater efficacy than streptokinase, but are relatively short-acting agents and, therefore, there is a risk of re-occlusion. Anticoagulation is recommended for 48 h following administration. Commonly, an infusion of unfractionated heparin is used; however, there is increasing evidence for the use of LMWH (for administration and doses see ‘Heparin’, p. 109). While the efficacy of tenecteplase (TNK) and recombinant tissue plasminogen activator (r-tPA) are similar, TNK can be given as a single bolus. Therefore, it is often chosen because of its ease of administration, e.g. for use in out-of-hospital thrombolysis. Since the risk of stroke is increased in patients over 75 years old given fibrin-specific lytics, some centres advocate the use of streptokinase in this population (check your local protocol).

Streptokinase has a more prolonged anticoagulant effect than the fibrin-specific lytics. Therefore, unfractionated heparin is often not given to patients treated with this form of thrombolysis. However, recent evidence suggests benefit from low molecular weight heparin as an adjunct to streptokinase. This has been added to many CCU protocols, but you should check your local guidelines.

Common side-effects of streptokinase include nausea, vomiting, hypotension and anaphylaxis. Streptokinase is a bacterial enzyme which can induce an antibody response; therefore, repeated administration beyond 4 days of the original dose is not advised due to an increased risk of anaphylaxis and reduced efficacy. Hypotension can be dangerous in unstable patients, but can be ameliorated by stopping the infusion temporarily and re-starting it at half the previous flow rate.

Many patients will have already received 300 mg in the ambulance. However, you should not assume that this is the case and always actively ensure that it has been given. If it has not, it should be given immediately after the ECG.

There is evidence that patients receiving thrombolysis, especially those within 12 h of the onset of their myocardial infarction, should also receive clopidogrel. 300 mg should be given at the time of thrombolysis (reduced to 75 mg in patients over 75 to reduce the risk of bleeding complications) and then continued at a daily dose of 75 mg, irrespective of age.

Troponin-negative patients (i.e. ACS without myocyte necrosis) may be at a greater short-term risk than those with positive results if other risk factors are present, e.g. age, ST changes, known coronary disease. This concept is the basis of risk stratification scores such as GRACE and TIMI. GRACE scores are more accurate at predicting short-term outcome, but more complicated than TIMI scores (Table 5.2 and Table 5.3) which can be calculated easily during an on-call shift. This risk stratification can identify those at greatest risk, in whom early investigation, e.g. arteriography, should be performed.

A chest X-ray should be considered in all patients with chest pain and performed urgently in those with symptoms or signs of pneumothorax. Patients with pulmonary thromboembolism may have a normal CXR. In those with an aortic dissection, the CXR may show mediastinal widening, with or without a pleural effusion.

This is unnecessary in the acute setting, but should be considered in patients with myocardial infarction or suspected LV dysfunction. It may be diagnostic in acute thoracic aortic dissection and massive PTE (see p. 154).

Urgent spiral CT should be performed if aortic dissection is suspected. Cardiac MRI can accurately quantify infarct size, using gadolinium contrast, in addition to LV function and myocardial viability. MRI can also differentiate acute myocarditis from myocardial infarction in patients with atypical chest pain and an elevated troponin. This difference can have significant long-term implications.

These drugs are short-acting but potent inhibitors of platelet aggregation. They are usually reserved for high-risk patients with ongoing chest pain or dynamic ECG changes, or those in whom early PCI is contemplated (see indications for further investigation below). Check your unit’s protocol; if used, remember to adjust the dose in renal impairment.

Patients who have been in AF for >48 h may have developed atrial clot and are at risk of systemic embolization on reversion to sinus rhythm. In this situation, patients should be anticoagulated unless there is a contraindication, pending a decision between DC cardioversion and rate control. Note that LMWH is not licensed for use in AF; unfractionated IV heparin should be used. Initiate warfarin and discontinue heparin once the INR is over 2 (see also ‘Warfarin’, p. 110).

In patients with persistent AF, long-term anticoagulation should be considered. The benefit of this should be balanced against potential risks, e.g. GI bleeding, intracranial haemorrhage, especially in those prone to falls or in whom compliance may be a problem.

As with any tachyarrhythmia, AF causing significant haemodynamic compromise should be managed by emergency DC cardioversion (see also ‘Defibrillation and cardioversion’, p. 58). This should not be performed in patients with long-standing AF, and is unlikely to produce maintainable sinus rhythm if precipitants are not addressed.

Elective cardioversion, e.g. for persistent AF, requires at least 3 weeks of anticoagulation with warfarin and an interval transoesophageal echocardiogram to ensure that there is no intracardiac thrombus.

Immediate chemical cardioversion should only be attempted if, from the patient’s history, the onset of AF clearly occurred <48 h ago and there is a haemodynamic advantage to be gained. Otherwise, elective DC cardioversion can be considered at a later date, once anticoagulation has been established and information on cardiac function is available.

If chemical cardioversion is desired, all patients should be anticoagulated as above. Success is most likely in those with AF of a short duration. If the patient is asymptomatic, with a normal blood pressure, consider rate control (see below), anticoagulation and management of any likely precipitant (see Table 5.4). Pharmacological options for chemical cardioversion include:

Rate control is the treatment of choice where cardioversion is not appropriate, e.g. in patients who have been in AF for more than 48 h. In patients with adequate left ventricular systolic function, a β-blocker should be considered first, e.g. atenolol (25–50 mg twice daily). If this fails, consider adding a rate-limiting calcium channel antagonist, e.g. diltiazem (60 mg 8-hourly) or amiodarone; see below. If this fails, or in patients unable to tolerate β-blockers or calcium channel antagonists, due to LV dysfunction or hypotension, use digoxin. The loading dose of digoxin is dependent on the volume of distribution; for a standard 70 kg male, 500 μg is given PO/IV and then again 6–8 h later; lower doses should be considered for smaller patients and the elderly. The maintenance dose needed, e.g. 125 μg PO daily, is dependent on renal function.

If the ECG shows δ waves, Wolff–Parkinson–White syndrome should be considered (see also ‘ECGs’, p. 85). In this condition, digoxin and verapamil are contraindicated; they may accelerate conduction down the accessory pathway leading to VT or VF. If rate control proves difficult, consider elective DC cardioversion (see above).

In patients who describe paroxysmal symptoms, and in whom periods of AF with a rapid ventricular response arise suddenly and without warning, useful treatments are sotalol (40–80 mg twice daily) and amiodarone (100 mg PO 8-hourly for 1 week, then 100 mg twice daily for 1 week, followed by a maintenance dose of 100 mg orally once daily). However, amiodarone has a large number of side-effects and the risk of developing them is dose dependent and cumulative.