Page 43 - Medicine and Surgery

P1: JYS
BLUK007-02 BLUK007-Kendall May 25, 2005 17:25 Char Count= 0

Chapter 2: Ischaemic heart disease 39

Table 2.7 Distribution of ECG abnormalities in Creatine kinase peaks within 24 hours; it is also pro-
myocardial infarction ducedbyskeletalmuscleandbrain.CKMBisanisoen-
Infarct site Leads Artery zyme that is specific for myocardial damage.
Myoglobin levels rise within 2–3 hours of muscle in-
Anteroseptal V1–V3 Septal
Anterior V2–V5 LAD jury, reach their highest levels by about 8–12 hours
Anterolateral V1–V6, I, aVL Left main stem and fall back to normal by about 1 day.
Lateral I, II, aVL Diagonal (branch
of LAD) Management
Inferior II, III, aVF Right or
Oral aspirin (300 mg) should be given as quickly as
circumflex
Posterior V1, V2 (reciprocal Circumflex possible, followed by lifelong low-dose daily aspirin.
i.e. ST depression) The pain of a myocardial infarction should be con-
trolled using diamorphine (with metoclopramide or
cyclizine as an antiemetic).
High flow oxygen should be given unless contraindi-
with a high ESR; anti-inflammatory and steroid ther-
cated.
apy may be necessary. It occurs 1–4 weeks after an
infarction and presents with fever, chest pain and a Thrombolytic therapy is routinely given as soon as
pericardial rub on auscultation. possible after confirmation of the diagnosis and usu-
ally up to 12 hours after the onset of symptoms. Strep-
tokinase is used in most patients. Recombinant tissue
Investigations plasminogen activator (tPA) is used in young patients
ECG: The earliest change seen is ST segment elevation, (<50 years), patients with anterior myocardial infarc-
the T wave then becomes inverted. The development of tion, hypotension or in patients previously exposed
persistent Q waves usually denotes a more substantial in- to streptokinase. Contraindications to thrombolysis
farct. The site of ischaemia and which artery is affected must be excluded, e.g. pregnancy, recent surgery, ac-
may be deduced from the site of ECG changes (see Ta- tive bleeding or uncontrolled hypertension. Intra-
ble 2.7). venous heparin is given in conjunction with all forms
Biochemical markers of myocardial damage (see of tPA.
Fig. 2.5): β-blockers reduce myocardial demand and may limit
Cardiac troponin is highly sensitive and specific; it theextentofinfarctionifgivenearly;however,theycan

is released early and persists for 7–10 days. It is also increase the risk of cardiac failure and hypotension.
raised in NSTEMI (see page 36). It is now available as These should be given to all patients without evidence
abedside test. of heart failure unless contraindicated.
ACE inhibitors should be given to patients following

infarction, even without evidence of cardiac failure.
They reduce mortality, reduce the number who de-
velop cardiac failure and slow progression of the in-
Myoglobin
farct, by improving the remodelling of myocardium
postinfarct. Therapy is usually commenced the fol-
Serum levels Cardiac troponin lowing day.
Post-MI all patients should be commenced on a statin
CK-MB lipid lowering drug.
Diabetic patients should be treated with an intra-

venous insulin sliding scale to ensure good glycaemic
0 1 2 3 4 5 6 7 8 control, avoiding hypo- and hyperglycaemia. All di-
Days after onset of acute Ml
abetic patients should be treated with subcutaneous
insulin for 3 months after discharge rather than oral
Figure 2.5 Biochemical markers of myocardial damage. agents.