Untitled Flashcards Set
Acute coronary syndromes (ACS)
Defi nitions ACS includes unstable angina and myocardial infarctions (MIs). These
share a common underlying pathology—plaque rupture, thrombosis, and infl ammation.
However, ACS may rarely be due to emboli, coronary spasm, or vasculitis (p556)
in normal coronary arteries. Myocardial infarction means there is myocardial cell
death, releasing troponin. Ischaemia means a lack of blood supply, °”cell death. MIS
have troponin rises, unstable angina does not. An MI may be a STEMI—ACS with STsegment
elevation (may only be present in V7–V9 if posterior STEMI) or new-onset
LBBB; or an NSTEMI—trop-positive ACS without ST-segment elevation—the ECG may
show ST depression, T-wave inversion, non-specifi c changes, or be normal. The degree
of irreversible myocyte death varies, and signifi cant necrosis can occur without
ST elevation.
Risk factors Non-modifi able: age, gender, family history of IHD (MI in 1st-degree
relative <55yrs). Modifi able: smoking, hypertension, DM, hyperlipid aemia, obesity,
sedentary lifestyle, cocaine use. Controversial risk factors include: stress, type A
personality, LVH, fi brinogen, hyperinsulinaemia, homocysteine levels, ACE genotype.
Incidence 5/1000 per annum (UK) for ST-segment elevation (declining in UK & USA).
Diagnosis An increase in cardiac biomarkers (eg troponin) and either: symptoms of
ischaemia, ECG changes of new ischaemia, development of pathological Q waves, new
loss of myocardium, or regional wall motion abnormalities on imaging.
Symptoms Acute central chest pain, lasting >20min, often associated with nausea,
sweatiness, dyspnoea, palpitations. ACS without chest pain is called ‘silent’; mostly
seen in elderly and diabetic patients. Silent MIs may present with: syncope, pulmonary
oedema, epigastric pain and vomiting, post-operative hypotension or oliguria,
acute confusional state, stroke, and diabetic hyperglycaemic states.
Signs Distress, anxiety, pallor, sweatiness, pulse or , BP or , 4th heart sound.
There may be signs of heart failure (JVP, 3rd heart sound, basal crepitations) or a
pansystolic murmur (papillary muscle dysfunction/rupture, VSD). Low-grade fever
may be present. Later, a pericardial friction rub or peripheral oedema may develop.
Tests ECG: (See fi g 3.21.) STEMI: classically, hyperacute (tall) T waves, ST elevation,
or new LBBB occur within hours. T-wave inversion and pathological Q waves follow
over hours to days (p98). NSTEMI/unstable angina: ST depression, T wave inversion,
non-specifi c changes, or normal. In 20% of MI, the ECG may be normal initially.
Paced ECGs and ECGs with chronic bundle branch block are unhelpful for diagnosing
NSTEMIs14 and may hinder STEMI15 diagnosis; in these cases, clinical assessment
and troponin levels are especially important. CXR: Look for cardiomegaly, pulmonary
oedema, or a widened mediastinum. Don’t routinely delay treatment whilst waiting
for a CXR. Blood: FBC, U&E, glucose, lipids, cardiac enzymes. Cardiac enzymes: (See
BOX ’Troponin‘.) Cardiac troponin levels (T and I) are the most sensitive and specifi
c markers of myocardial necrosis. Diff erent hospitals use diff erent assays: check
the required timing of troponin blood samples where you work (eg two samples 3h
apart). Other cardiac enzymes (see fi g 3.22) are sensitive but less specifi c; their role
in ACS diagnosis is decreasing as troponin testing improves. Echo: Regional wall
abnormalities.
Diff erential diagnosis (p94.) Stable angina, pericarditis, myocarditis, Takotsubo
cardiomyopathy (p145), aortic dissection (p655), PE, oesophageal refl ux/spasm, pneumothorax,
musculoskeletal pain, pancreatitis.
Management See p120, pp798–801.
Mortality 50% of deaths occur within 2h of onset of symptoms. Up to 7% die before
discharge. Worse prognosis if: elderly, LV failure, and ST changes. 16
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Fig 3.22 Enzyme changes following acute MI. Increasingly, high-sensitivity troponins are used
alone for routine investigation of ACS.
Fig 3.21 Sequential ECG changes following acute MI.
Troponins are proteins involved in cardiac and skeletal muscle contraction
(fi g 3.23). When myocardial cells are damaged, troponins are released and enter
the bloodstream. The levels of troponin in the blood can therefore help with
diagnosing myocardial damage. Troponins I and T are most specifi c to the heart.
Troponin levels are most commonly measured when ACS is suspected. In this
circumstance, one would expect troponin levels to rise in the hours following the
insult (fi g 3.22). Troponin levels can be high with other causes of myocardial damage,
for example myocarditis, pericarditis, and ventricular strain. With these conditions,
the troponin levels are likely to change little hour by hour as the insults are
ongoing. Discrete episodes of tachyarrhythmias may cause troponin rises similar
to in ACS. Troponin levels can also be raised iatrogenically, eg following CPR, DC
cardioversion, ablation therapy.
A troponin rise may have a non-cardiac aetiology. This can be indirectly related
to the heart, eg a massive PE causing right ventricular strain, or have no clear cardiac
connection, eg subarachnoid haemorrhage, burns, or sepsis. A common cause
of consistently elevated troponin is renal failure. Hence, when measuring troponin,
change in level is often more important than the level itself.
Fig 3.23 Diagram of myocardial contraction unit. The troponin complex controls when the myosin
heads can bind to the actin chain, shortening the muscle fi bre.
Reproduced from Barnard et al., Cardiac Anaesthesia, 2010, with permission from Oxford University Press.
Troponin
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Management of ACS
ACS management depends on whether the ACS is ‘ST elevated’ or not:
1 ST elevated myocardial infarction (STEMI): this category includes ACS with ST elevation
on ECG (fi g 3.9) but also ACS with new LBBB (fi g 3.7); and posterior MIs
(fi g 3.24) where ST elevation may only be seen with extra leads (V7–V9). Urgent
revascularization is essential. p796.
2 ACS without ST elevation: serial troponins are needed to diff erentiate non-ST elevated
MIs (NSTEMIs) (trop rise) from unstable angina (no trop rise). p798.
After the immediate actions described on pp796–9, treatment of ACS17 focuses on
managing symptoms, secondary prevention of further cardiovascular disease, revascularization
(if not already undertaken), and addressing complications.
Symptom control
Manage chest pain with PRN GTN and opiates. If this proves insuffi cient, consider a
GTN infusion (monitor BP, omit if recent sildenafi l use). If pain is deteriorating, seek
senior help. Manage symptomatic heart failure, p136.
Modify risk factors
• Patients should be strongly advised and helped to stop smoking (p93).
• Identify and treat diabetes mellitus, hypertension, and hyperlipidaemia.
• Advise a diet high in oily fi sh, fruit, vegetables, & fi bre, and low in saturated fats.
• Encourage daily exercise. Refer to a cardiac rehab programme.
• Mental health: fl ag to the patient’s GP if depression or anxiety are present—these
are independently associated with poor cardiovascular outcomes.
Optimize cardioprotective medications
• Antiplatelets: aspirin (75mg OD) and a second antiplatelet agent (eg clopidogrel)
for at least 12 months to vascular events (eg MI, stroke). Consider adding a PPI (eg
lansoprazole) for gastric protection.
• Anticoagulate, eg with fondaparinux, until discharge.
• -blockade reduces myocardial oxygen demand. Start low and increase slowly,
monitoring pulse and BP. If contraindicated, consider verapamil or diltiazem.
• ACE-i in patients with LV dysfunction, hypertension, or diabetes unless not tolerated
(consider ARB). Titrate up slowly, monitoring renal function.
• High-dose statin, eg atorvastatin 80mg.
• Do an echo to assess LV function. Eplerenone improves outcomes in MI patients
with heart failure (ejection fraction <40%).
Revascularization
• STEMI patients and very high-risk NSTEMI patients (eg haemodynamically unstable)
should receive immediate angiography °” PCI. NSTEMI patients who are high risk (eg
GRACE score >140) should have angiography within 24h; intermediate risk (eg GRACE
109–140) within 3d; low-risk patients may be considered for non-invasive testing.
• Patients with multivessel disease may be considered for CABG instead of PCI (p123).
Manage complications See p122.
Discharge Address any questions the patient has. Discuss ‘red fl ag’ symptoms and
where to seek medical advice should they arise. Ensure the management plan is
communicated to the patient’s GP. Book clinic and cardiac rehab appointments.
General advice
• Driving:18 drivers with group 1 licences (car and motorcycle) can resume driving
1wk after successful angioplasty, or 4wk after ACS without successful angioplasty,
if their ejection fraction is >40%. Group 2 licence holders must inform the DVLA of
their ACS and stop driving; depending on the results of functional tests, they may
be able to restart after 6wk.
• Work: how soon a patient can return to work will depend on their clinical progress
and the nature of their work. They should be encouraged to discuss speed of return
°” changes in duties (eg to lighter work if manual labour) with their employer. Some
occupations cannot be restarted post-MI: eg airline pilots & air traffi c controllers.
Drivers of public service or heavy goods vehicles will have to undergo functional
testing (eg exercise test), as mentioned previously.
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Fig 3.24 Acute postero-lateral MI. The posterior infarct is evidenced by the reciprocal changes seen in V1–3: dominant R waves (‘upside-down’ pathological Q waves)
and ST depression (‘upside-down’ ST elevation). If extra chest leads were added (V7–9), we would see the classic ST elevation pattern, see p 98. The ST elevation in V6 suggests
lateral infarction. A blockage in the circumfl ex coronary artery could explain both the posterior and lateral changes.
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Complications of MI
Cardiac arrest (See p894, fi g A3.) Cardiogenic shock (p802.) Left ventricular
failure (p136, p800, p802.)
Bradyarrhythmias Sinus bradycardia: See p808. Patients with inferior MIs may
suff er atropine-unresponsive bradycardia due to infarction of nodal tissue. 1st-degree
AV block: Most commonly seen in inferior MI. Observe closely as approximately
40% develop higher degrees of AV block (in which case calcium channel blockers and
-blockers should be stopped). Wenckebach phenomenon: (Mobitz type I) Does not
require pacing unless poorly tolerated. Mobitz type II block: Carries a high risk of
developing sudden complete AV block; should be paced. Complete AV block: Usually
resolves within a few days. Insert pacemaker (may not be necessary after inferior
MI if narrow QRS, reasonably stable and pulse 40–50). Bundle branch block: MI
complicated by trifascicular block or non-adjacent bifascicular disease (p132) should
be paced.
Tachyarrhythmias NB: K+, hypoxia, and acidosis all predispose to arrhythmias and
should be corrected. Sinus tachycardia: Can myocardial O2 demand, treat causes
(pain, hypoxia, sepsis, etc.) and add -blocker if not contraindicated. SVT: p126. AF
or fl utter: If compromised, DC cardioversion. Otherwise, medical therapy as per
p130. Frequent PVCs (premature ventricular complexes) and non-sustained VT (≥3
consecutive PVCS >100bpm and lasting <30s) are common after acute MI and are associated
with increased risk of sudden death. Correct hypokalaemia and hypomagnesaemia
and ensure the patient is on -blockers, if not contraindicated.19 Sustained
VT: (Consecutive PVCS >100bpm and lasting >30s.) Treat with synchronized DC shock
(if no pulse, treat as per advanced life support algorithm, see p894, fi g A3). Use
anti-arrhythmics only if VT recurrent and not controlled with shocks. Consider ablation
+/or ICD. Ventricular fi brillation: 80% occurs within 12h. VF occuring after 48h
usually indicates pump failure or cardiogenic shock. : DC shock (see p894, fi g A3),
consider ICD.
Right ventricular failure (RVF)/infarction Presents with low cardiac output and
JVP. Fluid is key; avoid vasodilators (eg nitrates) and diuretics.20 Inotropes are required
in some cases.
Pericarditis Central chest pain, relieved by sitting forwards. ECG: saddle-shaped ST
elevation, see fi g 3.51, p155. Treatment: NSAIDS. Echo to check for eff usion.
Systemic embolism May arise from LV mural thrombus. After large anterior MI,
consider anticoagulation with warfarin for 3 months.
Cardiac tamponade (p802) Presents with low cardiac output, pulsus paradoxus,
Kussmaul’s sign,3 muffl ed heart sounds. Diagnosis: echo. Treatment: pericardial aspiration
(provides temporary relief, see p773 for technique), surgery.
Mitral regurgitation May be mild (minor papillary muscle dysfunction) or severe
(chordal or papillary muscle rupture secondary to ischaemia). Presentation: pulmonary
oedema. Treat LVF (p800) and consider valve replacement.
Ventricular septal defect Presents with pansystolic murmur, JVP, cardiac failure.
Diagnosis: echo. Treatment: surgery. 50% mortality in fi rst week.
Late malignant ventricular arrhythmias Occur 1–3wks post-MI and are the cardiologist’s
nightmare. Avoid hypokalaemia, the most easily avoidable cause. Consider
24h ECG monitoring prior to discharge if large MI.
Dressler’s syndrome (p698) Recurrent pericarditis, pleural eff usions, fever, anaemia,
and ESR 1–3wks post-MI. Treatment: consider NSAIDS; steroids if severe.
Left ventricular aneurysm This occurs late (4–6wks post-MI), and presents with
LVF, angina, recurrent VT, or systemic embolism. ECG: persistent ST-segment elevation.
Treatment: anticoagulate, consider excision.
3 JVP rises during inspiration. Adolf Kussmaul was a prominent 19th-century physician and the fi rst to
attempt gastroscopy. Inspired by a sword swallower he passed a rigid tube into the stomach, however light
technology was limited and it was not until years later that gastroscopists could visualize the stomach.
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CABG is performed in left main stem disease; multi-vessel disease; multiple severe
stenoses; patients unsuitable for angioplasty; failed angioplasty; refractory
angina.
Indications for CABG—to improve survival:
• Left main stem disease.
• Triple-vessel disease involving proximal part of the left anterior descending.
Indications for CABG—to relieve symptoms:
• Angina unresponsive to drugs.
• Unstable angina (sometimes).
• If angioplasty is unsuccessful.
NB: when CABG and percutaneous coronary intervention (PCI, eg angioplasty) are
both clinically valid options, NICE recommends that the availability of new stent
technology should push the decision towards PCI. In practice, patients with singlevessel
coronary artery disease and normal LV function usually undergo PCI, and
those with triple-vessel disease and abnormal LV function more often undergo
CABG.
Compared with PCI, CABG results in longer recovery time and length of inpatient
stay. Recent RCTs indicate that early procedural mortality rates and 5-year survival
rates are similar after PCI and CABG. Compared with PCI, CABG probably provides
more complete long-term relief of angina in patients, and less repeated revascularization.
Procedure: The heart is usually stopped and blood pumped artifi cially by a machine
outside the body (cardiac bypass). Minimally invasive thoracotomies not
requiring this are well described, 21 but randomized trials are few. The patient’s
own saphenous vein or internal mammary artery is used as the graft. Several
grafts may be placed. >50% of vein grafts close in 10yrs (low-dose aspirin helps
prevent this). Internal mammary artery grafts last longer (but may cause chestwall
numbness).
On-pump or off-pump:
Seems to make little diff erence. 22
After CABG: If angina persists or recurs (from poor graft run-off , distal disease,
new atheroma, or graft occlusion) restart antianginal drugs, and consider angioplasty.
Ensure optimal management of hypertension, diabetes, and hyperlipidaemia,
and that smoking is addressed. Continue aspirin 75mg OD indefi nitely;
consider clopidogrel if aspirin contraindicated. Mood, sex, and intellectual problems
23 are common early. Rehabilitation helps:
• Exercise: walkcycleswimjog.
• Drive at 1 month: no need to tell DVLA if non-HGV licences, p158.
• Return to work, eg at 3 months.