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Cardiovascular Alterations and Management 221

Thrombolytic therapy
TABLE 10.2 Thrombolysis in Myocardial Infarction Thrombolytic therapy has been demonstrated to show a
(TIMI) flow grades in coronary arteries 15 significant reduction in mortality in the high-risk group
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described above. The greatest reduction in mortality
TIMI 0 No perfusion and no antegrade flow beyond the occurs if the reperfusion occurs within the first ‘golden’
occlusion.
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hour of presentation. Thrombolysis can be delivered
TIMI 1 Penetration with minimal perfusion, and contrast does effectively in many settings where other methods of
not opacify the entire bed distal to the stenosis during reperfusion are not available.
the picture run.
Clots formed in response to injury normally dissolve
TIMI 2 Partial perfusion and contrast opacifies the entire
coronary bed distal to the stenosis, although entry to using the body’s fibrinolytic processes as tissue repair
this area is slower than with unaffected coronary beds. takes place. This requires the presence of the proenzyme
plasminogen, which is converted into the enzyme plasmin
TIMI 3 Complete perfusion and filling and clearance of contrast
is rapid and comparable to other coronary beds. when activated by macrophages and degrades the clot.
Thrombolytic agents, including streptokinase and tissue-
type plasminogen activator (tPA), have been developed
that trigger conversion of plasminogen to plasmin and
therefore break down clots. It is essential to screen patients
clearly ACS or AMI, this step can wait until after thromboly- for contraindications to thrombolysis quickly but thor-
sis or PCI. oughly so that therapy can be commenced as soon as
possible. Contraindications are given in the National
Collaborative Management of Angina and Health Foundation of Australia (NHFA) Guidelines.
Acute Coronary Syndrome
The management of stable angina patients is aimed at: Streptokinase and tenecteplase are the most commonly
prescribed thrombolytic agents. Streptokinase is pre-
(a) secondary prevention of cardiac events; (b) symptom pared from beta-haemolytic streptococci and is a potent
control with medication; (c) revascularisation; and (d) plasminogen activator. Streptokinase is not thrombus-
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rehabilitation (see Figure 10.6). (Revascularisation by specific, so plasmin is released into the general circula-
coronary artery bypass graft is reviewed in Chapter 12; tion that may break down any recent clot formed as a
revascularisation by percutaneous coronary angioplasty is result of surgery, injection or healing, leading to a poten-
reviewed in the next section.) tial increase in haemorrhagic episodes. Streptokinase is
Treatment of acute coronary syndrome aims at rapid bacterial in origin, so it is antigenic. Most individuals
diagnosis and prompt re-establishment of flow through have been exposed to beta-haemolytic streptococci so
the occluded artery to ensure myocardial perfusion antibodies are often present, which means a higher dose
and reduce size of infarction. In addition, treatment may be required owing to the destruction of some of the
aims to: 18 enzyme when administered. Occasionally an escalated
allergic response will occur and will need urgent treat-
● minimise the area of myocardial ischaemia by increas- ment. This is more likely if streptokinase has been
ing coronary perfusion and decreasing myocardial administered in the previous 6 months. Streptokinase is
workload given intravenously over 60–90 minutes, because it has a
● maximise oxygen delivery to tissues short half-life.
● control pain and sympathetic stimulation
● counter detrimental effects of reperfusion The drug tissue-type plasminogen activator (tPA) is avail-
● preserve ventricular function able as alteplase, tenecteplase and reteplase. These agents
● reduce morbidity and mortality. are of human origin, made by recombinant DNA tech-
niques. The drug activates only plasminogen present in
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The ideal place to manage ACS or MI patients is in the blood clots, so the risk of haemorrhage is decreased.
coronary care unit, where continuous, specialised nursing Unlike streptokinase, tPA can be given repeatedly without
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care is available and there is rapid access to treatments. risk of anaphylactic reaction. However, tPA costs about 10
Secondary prevention of cardiac events includes the pro- times as much as streptokinase, so it is occasionally still
vision of medications, such as antiplatelet therapy and reserved for patients who have recently received streptoki-
lipid-lowering therapy. nase or are at risk of allergic reaction. Often patients with
anterior ischaemic changes are treated with tPA (alteplase)
Reperfusion therapy based on the GUSTO-1 trial that showed improved out-
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Reperfusion therapy includes coronary angioplasty, comes in terms of reduction of ischaemia. Alteplase is
ideally with stent and thrombolytic therapy (also termed usually given by infusion, whereas reteplase, which has a
fibrinolysis). Patients fast-tracked for reperfusion therapy longer half-life, can be given in two bolus injections.
have one or more of the following indications: (a) isch- Nursing management of patients post-thrombolysis
aemic or infarction symptoms for longer than 20 minutes; focuses on monitoring and detection of bleeding compli-
(b) onset of symptoms within 12 hours; (c) ECG changes cations and/or return of ischaemia. Care is as follows:
(ST elevation of 1 mm in contiguous limb leads, ST eleva-
tion of 2 mm in contiguous chest leads; left bundle ● Observations. Assess neurological state including ori-
branch block). entation, any IV sites and urinalysis for the presence