ecg in patients with chest pain
TRANSCRIPT
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The ECG in patients with chest pain: diagnosis andmanagement
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Pre-test
1. An 82 year old woman presents with a two day history of chest tightness,
palpitations, and breathlessness. She has a recent history of increasing
angina symptoms. Her electrocardiogram (ECG) shows atrial fibrillation with
a heart rate of 160 beats per minute. Her high sensitivity troponin T level is
elevated at 475 ng/l and 382 ng/l six hours and 12 hours after presentation.
What is the likely diagnosis?
a.
Acute pulmonary oedema
b.
Supraventricular tachycardia
c.
Atrial fibrillation with fast ventricular response and rate related
ischaemia
d.
Fast atrial fibrillation
e.
Non-ST segment elevation myocardial infarction with atrial fibrillation
A 26 year old woman presents with a three day history of sharp chest pain,
which is exacerbated by deep breaths and lying flat. She has been unwell
with flu-like symptoms. An ECG shows widespread saddle shaped ST
segment elevation. Which one of the following statements about her
prognosis is correct?
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.
Her prognosis is good with complete recovery
a.
She is at high risk of cardiac tamponade
b.
She is at high risk of developing pericardial constriction
c.
There is a high likelihood of recurrence
d.
Corticosteroids are given routinely to reduce the likelihood of
recurrence
A 76 year old woman is admitted with a sudden onset of severe chest pain
that radiated through to her back and caused her to collapse. Her blood
pressure is 180/102 mm Hg in her right arm and 138/60 mm Hg in her left arm.
Her heart rate is 112 beats per minute. Her ECG shows non-specific T wave
inversion in leads II, III, and aVF. Her chest x ray shows clear lung fields.
Which one of the following statements describes the most appropriate
course of action?
.
The history suggests acute coronary syndrome. You should treat with
antiplatelets and wait for troponin level results to confirm the diagnosis
a.
The history suggests acute myocardial infarction. You should treat with
fibrinolysis
b.
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The history suggests thoracic aortic dissection. You should treat
conservatively with antihypertensive drugs
c.
The history suggests thoracic aortic dissection. You should request
urgent computed tomography (CT) or magnetic resonance imaging
(MRI), reduce blood pressure with antihypertensive therapy, and
obtain a cardiothoracic surgical opinion when the diagnosis is
confirmed
d.
The history suggests thoracic aortic dissection. You should treat with
antihypertensive drugs and book an echocardiogram to confirm the
diagnosis
A 28 year old woman presents with her first episode of palpitations. She
had been treated for asthma by her GP. Her blood pressure is 110/70 mm Hg
and her oxygen saturation is 95% on room air. Her presenting ECGs are as
follows:
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What is the immediate management?
.
Immediate electrical cardioversion
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a.
Treat as acute coronary syndrome
b.
Give intravenous digoxin and wait for a senior colleague to review
c.
Give intravenous verapamil in the presence of asthma
d.
Give intravenous flecainide or amiodarone
A 72 year old man with a previous history of angina and hypertension is
admitted with a two hour history of chest pain. He describes the chest pain
as similar to his usual angina but more severe. He has a permanent
pacemaker in situ. His blood pressure is 120/70 mm Hg and heart rate is 70
beats per minute. His ECG shows regular ventricular pacing spikes. What
should you do?
.
Treat as ST segment elevation myocardial infarction and give
fibrinolysis
a.
Give aspirin and pain relief
b.
Treat as high risk acute coronary syndrome
c.
Give aspirin and pain relief and wait for the cardiac troponin level
result
d.
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Admit him under a cardiologist
A 54 year old woman presents with a two day history of pleuritic chest pain
and breathlessness. She is tachypnoeic with a respiratory rate of 30 breaths
per minute. Her oxygen saturations are 88% with 28% oxygen. Her blood
pressure is 102/70 mm Hg and her heart rate is between 140 beats per minute
and 160 beats per minute.
What does her ECG show?
.
Lateral ST depression
a.
Left bundle branch block
b.
Right bundle branch block and S1Q3T3 pattern
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c.
Inferior ST segment elevation myocardial infarction
d.
Paced rhythm
An 86 year old man with a longstanding history of angina is brought to the
emergency department after collapsing at home. Although alert, he appears
weak and reports chest pain. His blood pressure is 80/52 mm Hg and his
heart rate is 40 beats per minute. On listening to his chest there are
widespread bilateral crackles. The chest x ray confirms pulmonary oedema.
He was given atropine in the ambulance.
ECG after giving atropine 3.0 mg in cumulative doses
What should be his immediate management?
.
Fibrinolytic therapy
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a.
Intravenous fluid
b.
Intravenous furosemide
c.
Intravenous nitrate
d.
Temporary pacing
A 56 year old man is admitted with severe central chest and epigastric pain.
He has coffee grounds vomiting. He is a smoker who drinks eight pints of
lager each day. He is normally hypertensive but not compliant with his
medications, which include aspirin. His blood pressure is 90/60 mm Hg. His
ECG shows a sinus tachycardia with a rate of 120 beats per minute. His chest
x ray shows clear lung fields. His haemoglobin level is 79 g/l and his high
sensitivity troponin T level is elevated at 50 ng/l and 83 ng/l (at six hours and
12 hours respectively) after the onset of his symptoms. What should you do
next?
.
Treat as acute coronary syndrome. Give antiplatelet treatment with a
proton pump inhibitor
a.
Give a proton pump inhibitor and a blood transfusion, and stop aspirin
b.
Give an intravenous beta blocker as an anti-ischaemic agent
c.
Give intravenous fluids and analgesia
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A 30 year old man consults his GP because of a cold. He is found to have
an aortic systolic murmur, and an ECG shows voltage criteria for left
ventricular hypertrophy (sum of R wave in V6 and S wave in V1 = 42 mm). He
is otherwise healthy and slim, with a BMI of 25 and a blood pressure of 120/80
mm Hg. Because of these findings he is referred to the outpatient clinic.
Which one of the following investigations is most useful?
.
Carotid Doppler measurements
a.
Dobutamine stress echocardiogram
b.
Transthoracic echocardiogram
c.
Chest radiograph
d.
24 hour ambulatory blood pressure
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Section 3 of 6 - Question 1 (of 11)
The ECG in patients with chest pain: diagnosis andmanagement
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1. A 62 year old man presents to the emergency department with central chest
pain that started one hour ago. He looks pale and clammy. He is a smoker
with a history of hypertension. His blood pressure is 100/60 mm Hg. The
paramedic gave the man oxygen and aspirin in the ambulance.
Appearance of the QRS in lead V4R (reverse V4): ST elevation
(V7 to V9 are posterior leads and on this ECG have substituted
the usual V4 to V6 positions to show posterior ST elevation, for
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ease of showing all these changes on one ECG. ST elevation in
lead V4R is shown on the next ECG with three beats)
What is the diagnosis?
a.
Anterior ST segment elevation myocardial infarction
b.
Inferior ST segment elevation myocardial infarction
c.
Lateral ST segment elevation myocardial infarction
d.
Inferoposterior ST segment elevation and right ventricular myocardial
infarction
e.
Posterior ST segment elevation myocardial infarction
1. A 62 year old man presents to the emergency department with central chest
pain that started one hour ago. He looks pale and clammy. He is a smoker
with a history of hypertension. His blood pressure is 100/60 mm Hg. The
paramedic gave the man oxygen and aspirin in the ambulance.
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Appearance of the QRS in lead V4R (reverse V4): ST elevation
(V7 to V9 are posterior leads and on this ECG have substituted
the usual V4 to V6 positions to show posterior ST elevation, for
ease of showing all these changes on one ECG. ST elevation in
lead V4R is shown on the next ECG with three beats)
What is the diagnosis?
Youranswer
Coan
a.Anterior ST segment elevation myocardial infarction
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b.Inferior ST segment elevation myocardial infarction
c.Lateral ST segment elevation myocardial infarction
d.Inferoposterior ST segment elevation and right ventricular myocardial infarction
e.Posterior ST segment elevation myocardial infarction
a : Anterior ST segment elevation myocardial infarction
Anterior refers to leads V1 to V6. This patient has inferoposterior ST segment
elevation and right ventricular myocardial infarction.
b : Inferior ST segment elevation myocardial infarction
Inferior refers to leads II, III, and aVF. This patient has inferoposterior ST segment
elevation and right ventricular myocardial infarction.
c : Lateral ST segment elevation myocardial infarction
Lateral refers to leads V5, V6, I, and aVL. This patient has inferoposterior ST
segment elevation and right ventricular myocardial infarction.
d : Inferoposterior ST segment elevation and right ventricular myocardial
infarction
Inferoposterior refers to leads II, III, aVF, and V7 to V9. Right ventricular infarction
can be diagnosed if there is ST segment elevation in the reverse V4 lead (rV4).
ST segment elevation refers to the presence of J point elevation of 2 mm in two or
more adjacent V1 to V3 leads, and/or 1 mm in two or more adjacent V4 to V6, V7
to V9, and/or standard limb leads.
e : Posterior ST segment elevation myocardial infarction
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Posterior ST segment elevation myocardial infarction is diagnosed by the presence
of ST segment elevation in V7 to V9. To diagnose posterior myocardial infarction if
these posterior leads are not available, look for:
ST segment depression in V1 to V3
R/S ratio 1 in V1 or V2
Upright tented T wave in V1 or V2
2. What is the management?
a.
Pain relief
b.
Pain relief and intravenous fluids
c.
Pain relief and beta blockers
d.
Pain relief, clopidogrel, and primary angioplasty or fibrinolysis
e.
Pain relief, clopidogrel, fibrinolysis, and pacing
management
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2. What is the management?
Youranswer
Coan
a.Pain relief
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b.Pain relief and intravenous fluids
c.Pain relief and beta blockers
d.Pain relief, clopidogrel, and primary angioplasty or fibrinolysis
e.Pain relief, clopidogrel, fibrinolysis, and pacing
3. a : Pain relief
4. Pain relief is important but not the only treatment. You should use intravenous
morphine or diamorphine with an antiemetic, such as metoclopramide. Avoid
cyclizine because it can worsen pulmonary oedema by causing peripheral
vasoconstriction.
5. b : Pain relief and intravenous fluids
6. You should avoid intravenous fluids in most episodes of acute myocardial
infarction, except in right ventricular infarction and where there is evidence of
hypovolaemia, such as in patients with low central venous pressure.
7. c : Pain relief and beta blockers
8. Beta blockers reduce death and reinfarction in patients with acute myocardial
infarction.1 2 You should give beta blockers orally in the first 24 hours in patients
without heart failure, cardiogenic shock, asthma, or other contraindications. You
should consider giving beta blockers intravenously at presentation to patients who
are hypertensive and without contraindications.3
9. d : Pain relief, clopidogrel, and primary angioplasty or fibrinolysis
10. Primary percutaneous coronary intervention is the method of choice for
reperfusion.4 It is indicated in patients who present within 12 hours of symptom
onset and are suitable for invasive coronary management. Primary percutaneous
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coronary intervention is associated with a higher rate of infarct related artery
patency, lower stroke and mortality rates, and shorter hospital stays.5 6
11. Fibrinolytic therapy has, until recently, been widely used for coronary reperfusion in
the United Kingdom. If primary percutaneous coronary intervention is not available,
you should aim to give fibrinolytic therapy as soon as possible, preferably within 20
minutes of the patient arriving in hospital, because the benefit is greatest within the
first two hours of symptom onset.7 8
12. You should consider clopidogrel (with aspirin) as additional antiplatelet therapy in
all patients with ST segment elevation myocardial infarction. Clopidogrel reduces
death, myocardial reinfarction, stroke, and recurrent ischaemia needing urgent
revascularisation.9 10 There are other, newer antiplatelet drugs available such as
prasugrel and ticagrelor. You should follow your local guidelines when using them.
13. e : Pain relief, clopidogrel, fibrinolysis, and pacing
14. Transcutaneous or transvenous temporary pacing is indicated for patients with
symptomatic bradycardia, advanced heart block, and asystole accompanied by
haemodynamic instability and/or cardiogenic shock. This patient does not have any
of these indications.
15. KEY POINTS
ST segment elevation myocardial infarction occurs when there is a
complete obstruction of a coronary artery. In clear cases of ST
segment elevation myocardial infarction, patients should receive
reperfusion therapy without delay
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3. A 52 year old heavy goods vehicle driver presents with a three hour history of
retrosternal chest tightness that radiates to his jaw and left arm. He is a
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heavy smoker of 40 cigarettes per day, and has no previous history of heart
disease. When he attended a well man clinic recently, his blood pressure was
high at 150/90 mm Hg.
His BMI is 34 and he has marked central obesity. On arrival at the medical
admissions unit his blood pressure is 152/90 mm Hg, and his oxygen
saturations are 98% on air. His heart sounds are normal and his lungs are
clear.
What is the most likely initial diagnosis?
a.
Acute coronary syndrome
b.
Non-ST segment elevation myocardial infarction
c.
Pulmonary embolism
d.
Pericarditis
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e.
Hypertensive heart disease
You have changed your answer. Your first answer will count.
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3. A 52 year old heavy goods vehicle driver presents with a three hour history of
retrosternal chest tightness that radiates to his jaw and left arm. He is a
heavy smoker of 40 cigarettes per day, and has no previous history of heart
disease. When he attended a well man clinic recently, his blood pressure was
high at 150/90 mm Hg.
His BMI is 34 and he has marked central obesity. On arrival at the medical
admissions unit his blood pressure is 152/90 mm Hg, and his oxygen
saturations are 98% on air. His heart sounds are normal and his lungs are
clear.
What is the most likely initial diagnosis?
Youranswer
Coan
a.Acute coronary syndrome
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b.Non-ST segment elevation myocardial infarction
c.Pulmonary embolism
d.Pericarditis
e.Hypertensive heart disease
a : Acute coronary syndrome
Acute coronary syndrome is a term used to describe a constellation of clinical
symptoms that are related to acute myocardial ischaemia. It broadly comprises ST
segment elevation myocardial infarction and non-ST segment elevation acute
coronary syndromes. The latter are further subdivided into non-ST segment
elevation myocardial infarction and unstable angina, depending on the presence or
absence of evidence of myocardial necrosis.11 12
Patients with acute coronary syndrome and ST segment depression are at high risk
of developing heart failure or death, and you should actively treat them with
antiplatelet agents (aspirin and clopidogrel) and anticoagulant therapy
(fondaparinux (factor Xa inhibitor) or low molecular weight heparin), unless
contraindicated.
b : Non-ST segment elevation myocardial infarction
Non-ST segment elevation myocardial infarction describes acute myocardial
infarction with an ECG pattern other than ST segment elevation (ST segment
depression, T wave inversion, normal ECG, bundle branch block, or paced rhythm).
Acute myocardial infarction is diagnosed by the presence of a typical rise and fall in
cardiac biomarkers, with characteristic ischaemic symptoms or ECG changes of
acute ischaemia, or both.11
c : Pulmonary embolism
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Pulmonary embolism is a differential diagnosis. Here the chest pain is characteristic
of cardiac ischaemia, and normal oxygen saturation makes pulmonary embolism
less likely.
d : Pericarditis
Symptoms of pericarditis are usually more insidious. Chest pain is characteristically
sharp and stabbing, and is exacerbated by inspiration, movement, and supine or
erect posture. There may be a recent history of viral illness with symptoms such as
running nose, cough, pyrexia, myalgia, or arthralgia.
e : Hypertensive heart disease
Hypertensive heart disease can present with chest pain, and usually occurs inpatients with uncontrolled hypertension. Left ventricular hypertrophy may be
present on the ECG. This diagnosis can coexist with other cardiac diseases, such
as acute coronary syndrome, and should be made only after excluding other
causes of chest pain.
KEY POINTS
Non-ST segment elevation acute coronary syndrome is much more
common than ST segment elevation myocardial infarction
Non-ST segment elevation acute coronary syndrome presents with a
variety of ECG changes. High risk features include ST segment
depression, transient ST elevation, bundle branch block or paced
rhythm on the ECG, and elevated cardiac troponin
CLINICAL TIPS
Start treatment for acute coronary syndrome promptly to stabilise
patients
Consider early invasive coronary revascularisation in suitable
patients
4. A 78 year old man presents with a three day history of breathlessness and a
cough productive of green purulent sputum. His blood pressure is 120/78 mm
Hg and his oxygen saturations are 97% on 28% oxygen. His chest x ray
shows patchy consolidation in the right lower zone. His high sensitivity
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troponin T level is 35 ng/l and 36 ng/l (on admission and six hours later
respectively. The normal level is
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e.
Start treatment for pneumonia and acute coronary syndrome
5. A 70 year old man presents with a four day history of feeling breathless and a
cough productive of green purulent sputum. On examination his pulse is 145
beats per minute and irregularly irregular. His blood pressure is 120/78 mm
Hg and his oxygen saturations are 97% on 28% oxygen. His chest x ray
shows patchy consolidation in the right lower zone. His high sensitivity
troponin T level is 35 ng/l and 36 ng/l (on admission and six hours later
respectively. The normal level is
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troponin T level is 35 ng/l and 36 ng/l (on admission and six hours later
respectively. The normal level is
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Sepsis
Bleeding (remember that a patient with upper gastrointestinal
bleeding may present with severe chest pain as well as epigastric
pain)
Renal failure
Pulmonary embolism
Stroke
Multiorgan failure.
The most likely diagnosis in this patient is pneumonia precipitating atrial fibrillation.
b : The troponin level is spuriously elevated so you should ignore it
The newer generation of troponin bioassays are highly sensitive and specific, so
the level is unlikely to be spuriously elevated.
c : The troponin level is elevated because of the tachyarrhythmia and
pneumonia, and is a marker for an adverse prognosis
Given the history and ECG changes it is highly likely that the troponin level is
elevated because of the tachyarrhythmia and pneumonia. A raised troponin level is
a marker for adverse prognosis, in both acute coronary syndrome and other
conditions.16 17
d : A single raised level of cardiac troponins is sufficient to make a diagnosis
of acute myocardial infarction
The new universal definition of acute myocardial infarction requires two or more
measurements of cardiac troponins, showing a rise and/or fall pattern, and also in
the presence of an appropriate clinical setting.18
Learning bite: Universal definition of acute myocardial
infarction18
It is possible to confirm a diagnosis of acute myocardial infarction in an appropriate
clinical setting (for example, where the patient has chest pain lasting 15 minutes or
longer) by the presence of a rise and/or fall pattern of cardiac troponins where at
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least one value is above the normal reference value and there is at least one of the
following clinical features:
Symptoms of cardiac ischaemia (for example, chest pain that is
ischaemic in nature, or pain in the shoulder or arm that has no other
causes such as musculoskeletal pain)
New changes on the electrocardiogram indicating ischaemia (ST-T
changes, left bundle branch block, or development of a Q wave)
New regional wall abnormality on echocardiography, or another
imaging modality showing new loss of viable myocardium.
e : You should always interpret a troponin result in conjunction with other
cardiac enzymes, such as creatine kinase
In the context of acute coronary syndrome, a raised troponin level may or may not
be accompanied by a rise in other cardiac enzymes. A raised troponin level in the
absence of a rise in other cardiac enzymes, for example, creatine kinase, is usually
the result of a small infarct.
KEY POINTS
Atrial fibrillation with a fast ventricular rate is a common acute
medical problem
You should:
Identify and treat precipitating conditions
Maintain haemodynamic stability
Consider anticoagulation.
CLINICAL TIPS
Beta blockers (if not contraindicated) are a useful and reliable way ofcontrolling heart rate
Atrial fibrillation with a fast ventricular rate, of less than 48 hours
onset and without a precipitating cause may be suitable for
antiarrhythmic or synchronised electrical cardioversion
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6. A 72 year old man presents with a two hour history of central chest pain
radiating to his jaw and left arm. He is known to suffer with angina. His pain
came on at rest, feels worse than his usual angina, and is not relieved by his
glyceryl trinitrate spray. He is pale, clammy, and breathless. He has a
previous history of hypertension, myocardial infarction, and coronary artery
bypass grafting, and he has a permanent pacemaker.
What is the most likely diagnosis?
Youranswer
Coan
a.Acute coronary syndrome with left bundle branch block
b.Acute coronary syndrome with right bundle branch block
c.
Acute coronary syndrome with idioventricular rhythm
d.Acute coronary syndrome with paced rhythm
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e.Acute coronary syndrome with biventricular paced rhythm
a : Acute coronary syndrome with left bundle branch block
This patient has a dual chamber permanent pacemaker and acute coronary
syndrome. Left bundle branch block morphology consists of:
Positive R wave in the left ventricular leads (V5, V6, I, and AVL)
Secondary R wave in the left ventricular leads, with an M shaped
QRS complex in these leads
QRS duration 120 ms.
ECG showing left bundle branch block
b : Acute coronary syndrome with right bundle branch block
This patient has a dual chamber permanent pacemaker and acute coronary
syndrome. Right bundle branch block morphology consists of:
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Secondary R wave in the right ventricular leads (V1, V2) with an M
shaped complex in these leads
Broad S wave in the left ventricular leads, especially lead I
QRS duration 120 ms.
ECG showing right bundle branch block
The QRS morphology in lead V1 in right bundle branch block,
showing a typical M appearance
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c : Acute coronary syndrome with idioventricular rhythm
This patient has a dual chamber permanent pacemaker and acute coronary
syndrome. Idioventricular rhythm consists of a monomorphic broad complex
ventricular rhythm at a rate of less than 100 beats per minute. This is also known
as accelerated idioventricular rhythm, with a faster rate of up to 120 beats per
minute.19
ECG showing an idioventricular rhythm (broad ventricular
complexes at a rate of less than 100 beats per minute)
d : Acute coronary syndrome with paced rhythm
This patient has a dual chamber permanent pacemaker. The ECG shows the
pacemaker is sensing native atrial depolarisation and pacing the ventricle.
Ventricular pacing is commonly right ventricular apical pacing. As ventricular
depolarisation starts in the right ventricle by the pacemaker and spreads to the left
ventricle, this results in left bundle branch block type morphology. Unlike the usual
left bundle branch block, a pacing spike is usually visible at the start of each QRS
complex.
You should regard patients with symptoms of acute coronary syndrome who
present with a paced rhythm as being at high risk. This is because important
ischaemic ECG changes are often masked by the paced QRS complex. Moreover,
patients with pacemakers are usually older and have other comorbidities.
Fibrinolytic therapy is not indicated because ST repolarisation changes are often
present in ventricular paced beats, and are not a reliable guide for fibrinolytic
therapy.
e : Acute coronary syndrome with biventricular paced rhythm
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Biventricular pacing represents cardiac resynchronisation therapy. There are two
ventricular leads: the first is in the right ventricle, while the second is placed through
the coronary sinus into one of the cardiac veins, and onto the epicardial surface of
the left ventricle. The aim is to achieve synchronised depolarisation and contraction
within the left ventricle and between the right and left ventricles. The QRS complex
in biventricular pacing usually shows a fusion of both left and right bundle branch
block type morphology.
ECG showing biventricular pacing with atrial flutter and a right
bundle branch block pattern in V1
KEY POINT
Treat patients presenting with acute coronary syndrome and paced
rhythm with care because ischaemic changes on the ECG are often
masked by pacing
CLINICAL TIP
In patients with acute coronary syndrome and paced rhythm,
ischaemic changes on the ECG are often masked by pacing. You
should use other risk markers, such as cardiac troponin levels and
pulmonary oedema, to further risk stratify a patient for acute
coronary syndrome
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7. A 38 year old woman presents with a three week history of exertional chest
pain and palpitations. She is a non-smoker and has no other medical
problems. You note that her younger sister had a pacemaker fitted recently,
and an older brother died suddenly at age 42.
What is the diagnosis from the ECG?
Youranswer
Coan
a.Ischaemic lateral ST segment depression
b.Within normal limits
c.QT prolongation
d.Left ventricular hypertrophy with a repolarisation abnormality (also referred to as strain)
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e.Right ventricular hypertrophy
a : Ischaemic lateral ST segment depression
Left ventricular hypertrophy with a repolarisation abnormality (also referred to as
strain) refers to the presence of ST segment depression and T wave inversion in
the left ventricular leads (I, aVL, V5, and V6).20
In the presence of left ventricular hypertrophy, ST depression may indicate strain,
ischaemia, or both. You should consider ST depression as possibly ischaemic in
origin in patients presenting with chest pain. Serial ECGs and comparison with an
old ECG may help you to differentiate ischaemia from strain. ST segment
depression is an adverse prognostic feature in acute coronary syndrome.
Because this patient is a young woman with no cardiovascular risk factors, she is
unlikely to have ischaemia. Conversely, she has a highly significant ECG showing
left ventricular hypertrophy with massive voltage.
b : Within normal limits
This is an abnormal ECG.
c : QT prolongation
Long QT syndrome is a group of hereditary genetic mutations involving cardiac cell
membrane ion channel subunits. It is suspected when the QTc interval is 450 ms
if accompanied by symptoms, or 470 ms in asymptomatic people. The QT is
normal in this ECG. QTc is best interpreted with a non-acute ECG. Computer
analysis tends not to be accurate in the presence of tachycardia, beat to beat RR
interval difference, indistinct T wave ending, and motion artefact. For clarity, it
would be better to blank out the QTc measurement on the ECG. Genetic historyand testing confirm the diagnosis. Patients with long QT syndrome are at risk of
ventricular arrhythmias, particularly torsades de pointes and sudden cardiac death.
Familial screening and genetic counselling are indicated. QT prolongation can also
be an acquired condition.
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d : Left ventricular hypertrophy with a repolarisation abnormality (also
referred to as strain)
There are many different ECG criteria for left ventricular hypertrophy. In general
terms, the likelihood of left ventricular hypertrophy is increased when more of the
following criteria are met20:
Sum of R wave in V5 or V6 and S wave in V1 35 mm
Sum of tallest R wave in V4, V5 or V6 and deepest S wave in V1, V2
or V3 40 mm
R wave in lead I or aVL 13 mm
R wave in V4, V5 or V6 27 mm
R wave in aVF 20 mm when the frontal plane QRS axis is vertical
S wave in V1 or V2 25 mm
ST depression and T wave inversion in the left ventricular leads (I,
AVL, V5, and V6)
Slow ventricular activation time 50 ms
Left axis deviation.
Causes of left ventricular hypertrophy on the ECG include:
Systemic hypertension
Aortic stenosis or regurgitation
Hypertrophic cardiomyopathy
Coarctation of the aorta
Athletes heart.
It may also be a normal variant, especially in thin people.
e : Right ventricular hypertrophy
Right ventricular hypertrophy is shown on an ECG by:
A dominant R wave in V1 with an R/S ratio 1
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Right axis deviation
ST or T wave changes in the right ventricular leads (V1 and V2).
ECG showing right ventricular hypertrophy
Causes of right ventricular hypertrophy include:
Pulmonary hypertension (primary or secondary)
Cor pulmonale
Fallots tetralogy
Pulmonary stenosis.
KEY POINT
Left ventricular hypertrophy is commonly seen in clinical practice.
Ensure that the ECG is correctly calibrated, that is 10 mm/millivolt
and 25 mm per second
CLINICAL TIPS
Transthoracic echocardiography is a useful tool for investigating the
cause of left ventricular hypertrophy
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The ECGs of slim people sometimes show apparent voltage criteria
for left ventricular hypertrophy. You should exclude left ventricular
hypertrophy by measuring the thickness of the ventricle wall using
an echocardiogram. If left ventricular hypertrophy is confirmed, you
can consider further investigating its cause
8. A 32 year old woman presents with a three day history of left sided chest pain
that worsens with inspiration, coughing, and lying flat. She has been feeling
unwell and notices she has a mild temperature. She has no significant past
medical history.
What is the most likely diagnosis?
Youranswer
Coan
a.Pleurisy
b.Acute coronary syndrome
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c.Acute pericarditis
d.Brugada syndrome
e.Pulmonary embolism
a : Pleurisy
Pleurisy is a differential diagnosis, but pleurisy alone is not associated with these
ECG changes unless accompanied by coexisting pericarditis.
b : Acute coronary syndrome
Acute coronary syndrome can present with atypical symptoms, and ECG changes
can resemble those of acute pericarditis. Varying degrees of ST elevation in more
than one coronary artery territory support the diagnosis of acute pericarditis.
Repeating the ECG at regular intervals can help you to distinguish between
pericarditis and acute coronary syndromes. Progressive loss of R wave,
development of Q wave or T wave inversion in the leads with initial ST segment
elevation, or the presence of reciprocal ST segment depression support the
diagnosis of acute coronary syndrome.
c : Acute pericarditis
These symptoms and ECG changes are characteristic of acute pericarditis. A
pericardial rub would help to confirm the diagnosis, but is usually transient. Beside
saddle shaped ST segment elevation, PR segment deviation occurs early in acute
pericarditis.21 Later, T wave inversion appears and can occasionally persist after
recovery. The presence of pr-depression on the ECG is pathognomonic of acute
pericarditis.
If a patient has uncomplicated pericarditis, you can discharge them from hospital
quickly. A raised cardiac troponin level in a patient with pericarditis should alert you
to the possibility of coexisting myocarditis, and you should arrange a transthoracic
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echocardiography. Cardiomegaly on a posterior-anterior chest radiograph suggests
the presence of pericardial effusion or myocarditis.
d : Brugada syndrome
Brugada syndrome is characterised by the presence of right bundle branch block,
persistent ST segment elevation in leads V1-3, and sudden cardiac death in the
absence of structural heart disease.22 In familial cases, Brugada syndrome is
inherited in an autosomal dominant manner. There are three classic ECG features:
Type I - "coved" - which is diagnostic of the condition
Types II and III - "saddle back" - which are suspicious but not
diagnostic.
Type III can also be found in healthy people.
ECG showing Brugada syndrome (ST elevation changes in lead
V1)
Published with permission from Brugada R, Brugada P, Brugada J.
Electrocardiogram interpretation and class I blocker challenge in Brugada
syndrome. J Electrocardiol2006;39(4 Suppl):S115-18.
e : Pulmonary embolism
From the history pulmonary embolism is a differential diagnosis, and you should
use your clinical judgment to exclude it. However, pericarditis is much more likely.
KEY POINTS
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More benign conditions (such as acute pericarditis) commonly
present in younger people with chest pain
More serious chest pain problems (such as ischaemic heart disease
and pulmonary embolism) are more common in older people
CLINICAL TIP
If you suspect that a patient has pericarditis, ask about a recent
history of viral illness
A 72 year old woman collapses with chest pain while gardening. On waking, she recalls having
severe central chest pain that radiated to her back between her shoulder blades. She has type 2 diabetes
mellitus and a history of hypertension. On examination she is alert, but pale and clammy. Her blood pressure
is 92/60 mm Hg.
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What is the most likely diagnosis?
Youranswer
Coan
a.Acute coronary syndrome
b.Bilateral hilar lymphadenopathy
c.Acute thoracic aortic dissection
d.Tension pneumothorax
e.Pulmonary embolism
a : Acute coronary syndrome
Aortic dissection causes an instantaneous shearing chest pain. Acute coronary
syndrome is a differential diagnosis. The onset of cardiac chest pain that is
ischaemic in origin is normally slower, persistent, or crescendo in nature.
b : Bilateral hilar lymphadenopathy
Her chest x ray shows a widened mediastinum and not bilateral hilar
lymphadenopathy. The sudden onset of severe chest pain and the widened
mediastinum should make you suspect aortic dissection in this patient.
c : Acute thoracic aortic dissection
Clinical signs of acute thoracic aortic dissection can be subtle and few. Beside
characteristic symptoms, look for blood pressure or pulse difference in both arms.Examine all pulses. The presence of aortic regurgitation suggests aortic root
dissection. The coronary arteries can be affected.
d : Tension pneumothorax
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Pneumothorax has a specific appearance on the chest x ray: the lung collapses
towards the mediastinum and there is a lack of pulmonary vascular markings
peripherally. Tension pneumothorax is associated with a contralateral shift of the
mediastinum due to high intrapleural pressure on the affected side. You should
treat it urgently.
e : Pulmonary embolism
Pulmonary embolism is a differential diagnosis and can be difficult to differentiate
from aortic dissection clinically. You should arrange urgent investigations to confirm
the diagnosis.
11. A 45 year old bus driver is brought into hospital after developing sudden
onset left sided chest pain and breathlessness while at work. His chest painis worse on inspiration. He is sweaty and clammy. His blood pressure is
70/40 mm Hg and his oxygen saturation is 93% on 10 l of oxygen through a
rebreather bag. His high sensitivity troponin T level is elevated at 285 ng/l at
four hours after onset of chest pain.
What is the most likely diagnosis?
Youranswer
Coan
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a.Acute massive pulmonary embolism
b.Acute coronary syndrome
c.Acute pulmonary oedema
d.Acute pericarditis
e.Acute myocarditis
a : Acute massive pulmonary embolism
ECG changes for acute pulmonary embolism are often non-specific and can be
confused with those of acute coronary syndrome. The ECG shows a
supraventricular tachycardia with complete right bundle branch block, most likely
sinus in origin, at 125 beats per minute, with inferior T wave inversion and lateral
ST depression and T wave inversion. The most common ECG change is sinus
tachycardia.
You should also look for:
Right ventricular strain - dominant R wave V1 to V3 with ST
depression, T wave inversion, or both
New partial or complete right bundle branch block
Right axis deviation
P pulmonale - a taller, peaked p wave that reflects right atrial strain
Classic S1Q3T3 changes - this pattern is present in only 20% of
patients with acute pulmonary embolism and comprises an S wave
in lead I, and Q wave and T wave inversion in lead III. It has a
sensitivity of 54% and a specificity of 62%.23
b : Acute coronary syndrome
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Acute coronary syndrome is a differential diagnosis, but the history and ECG in this
man make it less likely than a pulmonary embolism.
c : Acute pulmonary oedema
Acute pulmonary oedema is a differential diagnosis. A chest x ray is an important
part of management in both conditions because it can help you to narrow the
diagnosis. In pulmonary embolism look for pulmonary oligaemia - a reduction or
absence in pulmonary vascular markings, a "pear shaped" hilum due to blockage of
pulmonary arterial branches, and a pulmonary infarct - one or more radio-opaque
densities within the lung parenchyma, and a pleural effusion.
d : Acute pericarditis
Acute pericarditis is usually more gradual in onset, and does not usually cause
hypotension or systemic desaturation.
e : Acute myocarditis
Acute myocarditis causing systemic oxygen desaturation and hypotension suggests
widespread and severe myocardial impairment. Myocarditis is most commonly
preceded by constitutional symptoms such as pyrexia and flu-like symptoms, which
may be followed by symptoms and signs of heart failure.
Learning bite: managing patients with massive or submassive
pulmonary embolism
Emergency pulmonary embolectomy in a highly specialised surgical unit has been
shown to be successful in some patients with massive or submassive pulmonary
embolism.24 However, you should consult with a senior colleague about the
appropriateness of the referral.
Because of anticipated complications and the high mortality associated with shock
and poor oxygenation, admission to the intensive care unit would be advantageous.
Low molecular weight heparin is the mainstay of treatment in pulmonary embolism.
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Although definite evidence of benefit is lacking in pulmonary embolism, you should
consider fibrinolytic therapy in massive pulmonary embolism associated with
haemodynamic instability.25
KEY POINTS
Acute pulmonary embolism can be diagnosed by a lung perfusion
ventilation (V/Q) scan, or by CT of the pulmonary artery
ECG changes and chest x ray findings in acute pulmonary embolism
can be non-specific and easily missed
Right ventricular dysfunction or failure, haemodynamic instability,
and a raised cardiac troponin level are markers for increased
mortality and complications26
CLINICAL TIPS
A normal D dimer level can have a negative predictive value of
>99% for patients with a low or intermediate likelihood of having
pulmonary embolism, depending on the assay used27
A normal jugular venous pressure and oxygen saturation 94% on
air make the diagnosis of acute pulmonary embolism less likely
Learning bite
As soon as the diagnosis of unstable angina or NSTEMI is made, and aspirin and antithrombin therapy have been
offered, formally assess individual risk of future adverse cardiovascular events using an established risk scoring
system that predicts six month mortality (for example, Global Registry of Acute Cardiac Events (GRACE)).
Include in the formal risk assessment:
A full clinical history (including age, previous myocardial infarction (MI), and
previous percutaneous coronary intervention (PCI) or coronary artery bypass
grafting (CABG))
A physical examination (including measurement of blood pressure and heart rate)
Resting 12-lead electrocardiography (ECG) (looking particularly for dynamic or
unstable patterns that indicate myocardial ischaemia)
Blood tests (such as troponin I or T, creatinine, glucose, and haemoglobin).
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Record the results of the risk assessment in the patient's care record.
Use risk assessment to guide clinical management, and balance the benefit of a treatment against any risk of related
adverse events in the light of this assessment.
Use predicted six month mortality to categorise the risk of future adverse cardiovascular events as follows:
Predicted six month mortality Risk of future adverse cardiovascular events
1.5% or below Lowest
>1.5 to 3.0% Low
>3.0 to 6.0% Intermediate
>6.0 to 9.0% High
over 9.0% Highest
The NICE Guideline Development Group selected six month mortality as the outcome measure for risk stratification
because:
Mortality is a hard endpoint, which is available for most clinical trials
Mortality cannot be misinterpreted (as can an endpoint such as myocardial
infarction, the definition of which has evolved over time, and varies between trials)
A six month time frame captured the majority of clinical events that occur after
presentation with unstable angina or NSTEMI, and which may be influenced by an
in hospital intervention (pharmacological or interventional). Shorter follow up
intervals may miss events related to the index acute coronary syndrome event,
and longer follow up may become increasingly influenced by other factors such as
the effects of post-discharge secondary prevention interventions. Moreover, trials
often do not report findings beyond the six month follow up period.
It is recommended that treatment with clopidogrel in combination with low dose aspirin should be continued
for 12 months after the most recent acute episode of non-ST segment elevation ACS. Thereafter, standard
care, including long term treatment with low dose aspirin alone, is recommended.
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Current NICE guidance for drug eluting stents does not recommend any specific duration of clopidogrel
therapy in addition to aspirin. However, NICE refers to the recommendations from the American College
of Cardiologists/American Heart Association PCI guidelines and the British Cardiovascular Intervention
Society advising a duration of at least 12 months, after which time continuation of clopidogrel should be
reviewed taking into account the risk of further ischaemic events (particularly the risk of subsequent
stent thrombosis) and potential bleeding complications on an individual patient basis.
A 2010 interim analysis of data from two studies (Park S-J, et al. Duration of dual antiplatelet therapy
after implantation of drug-eluting stents. N Engl J Med2010. Published online 15 March (doi:
10.1056/NEJMoa1001266) suggests no benefit for continuing to use clopidogrel in addition to aspirin for
more than 12 months after implantation of drug eluting stents. However, because of limitations, further
studies are required to confirm or refute these findings. The findings of this analysis are insufficient to
recommend a change in practice.
Learning bite
Consider discontinuing clopidogrel treatment five days before CABG in patients who have a low risk of
adverse cardiovascular events. For patients at intermediate or higher risk of adverse cardiovascular
events, discuss the continuation of clopidogrel before CABG with the cardiac surgeon and base the
decision on the balance of ischaemic and bleeding risk.
Offer fondaparinux to patients who do not have a high bleeding risk, unless coronary angiography is planned within
24 hours of admission. Based on the OASIS-5 trial, the NICE guideline advocates fondaparinux as the routine
antithrombin
1. : Eptifibatide or tirofiban
Consider intravenous eptifibatide or tirofiban as part of the early management for patients who have an
intermediate or higher risk of adverse cardiovascular events (predicted six month mortality above 3.0%),
and who are scheduled to undergo angiography within 96 hours of hospital admission. Consider
abciximab, usually in the catheter laboratory, as an adjunct to PCI for patients at intermediate or higher
risk of adverse cardiovascular events who are not already receiving a glycoprotein IIb/IIIa inhibitor.
Balance the potential reduction in a patient's ischaemic risk with any increased risk of bleeding, when
determining whether a GPI should be offered.
Full details, including contraindications, adverse effects, dosage regimens, and modifications are in the
makers Summary of Product Characteristics which can be found athttp://www.medicines.org.uk
http://dx.doi.org/10.1056/NEJMoa1001266http://dx.doi.org/10.1056/NEJMoa1001266http://www.medicines.org.uk/http://www.medicines.org.uk/http://www.medicines.org.uk/http://www.medicines.org.uk/http://dx.doi.org/10.1056/NEJMoa1001266 -
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Offer unfractionated heparin as an alternative to fondaparinux to patients who are likely to undergo coronary
angiography within 24 hours of admission, and use monitoring of blood clotting (such as the activated clotting time
(ACT)) to determine the appropriate dose.
4. You should give unfractionated heparin.
Learning bite
Carefully consider the choice and dose of antithrombin in patients who have a high
risk of bleeding associated with any of the following:
Advancing age
Known bleeding complications
Renal impairment
Low body weight.
Offer systemic unfractionated heparin (50-100 U/kg) in the cardiac catheter
laboratory to patients receiving fondaparinux who are undergoing PCI.
As an alternative to the combination of a heparin plus a GPI, consider bivalirudin for
patients who:
Are at intermediate or higher risk of adverse cardiovascular events
(predicted six month mortality above 3.0%), and
Are not already receiving a GPI or fondaparinux, and
Are scheduled to undergo angiography (with follow on PCI if
indicated) within 24 hours of admission.
As an alternative to the combination of a heparin plus a GPI, consider bivalirudin for
patients undergoing PCI who:
Are at intermediate or higher risk of adverse cardiovascular events,
and
Are not already receiving a GPI or fondaparinux.
CLINICAL TIP
All anticoagulants are necessarily associated with a risk of bleeding complications
and weighing this risk against the potential benefits of such agents requires an
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understanding of the factors associated with bleeding risk, measures by which the
magnitude of this risk can be estimated, and the potential for benefit from these
agents in reducing the rate of ischaemic events. Close attention to appropriate
dosing of these agents is particularly important
Offer coronary angiography (with follow on PCI if indicated) within 96 hours of first admission to hospital to patients
who have an intermediate or higher risk of adverse cardiovascular events (predicted six month mortality above 3.0%)
if they have no contraindications to angiography (such as active bleeding or comorbidity). Perform angiography as
soon as possible for patients who are clinically unstable or at high ischaemic risk. An early invasive strategy does
have benefit, mainly in reducing recurrent ischaemia/infarction in the short term, but also in reducing longer term
mortality or reinfarction. However, this benefit appears to be greatest in those people at higher absolute risk of such
events (with the most benefit seen in those at the highest risk).
1. Assessment of LV function is recommended in all patients who have had an MI.
Consider assessing LV function in all patients with unstable angina.
Record measures of LV function in the patient's care record and in correspondence
with the primary healthcare team and the patient.
It is logical to assess LV function in all people with unstable angina and NSTEMI so
that specific treatment for LV dysfunction can be offered to improve symptoms and
outcome. Left ventricular function may improve after an acute ischaemic event with
the resolution of myocardial stunning and the onset of healing. It may also
deteriorate because of myocardial remodelling or progression of coronary disease.
It may therefore also be important to monitor LV function during follow up, because
of this potential for change with time.
b : Assessing his LV function is not needed as he is at low risk
Assessment of LV function is recommended in all patients who have had an MI.
Learning bite
To detect and quantify inducible ischaemia, consider ischaemia testing before
discharge for patients whose condition has been managed conservatively and who
have not had coronary angiography.
If untreated, the prognosis of patients with non-ST elevation myocardial infarction is
poor and mortality high, particularly in people who have had myocardial damage
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1. In May 2009 the product information for all clopidogrel containing medicines was amended to discourage the
concomitant use of PPIs and clopidogrel unless absolutely necessary.
Since then, the Committee for Medicinal Products for Human Use (CHMP) has
become aware of the results of a number of new studies, some of which put in
question the clinical relevance of interactions between PPIs as a class and
clopidogrel. However, two studies, completed at the end of August 2009, looked
into the effect of omeprazole on the blood levels of the active form of clopidogrel.
The studies confirmed that omeprazole can reduce the levels of the active form of
clopidogrel in the blood and reduce its antiplatelet effects, therefore supporting the
conclusion that there is an interaction between clopidogrel and omeprazole and
esomeprazole.
Taking all of the currently available data into account, the CHMP and its
Pharmacovigilance Working Party concluded that there are no solid grounds to
extend the warning to other PPIs. The class warning for all PPIs has been replaced
with a warning stating that only the concomitant use of clopidogrel and omeprazole
or esomeprazole should be discouraged
KEY PRINCIPLES
You should adapt your consultation style to the needs of individual patients so
that all patients have the opportunity to be involved in decisions about their
medicines at the level they wish
Establish the most effective way of communicating with each patient and, if
necessary, consider ways of making information accessible and understandable
(for example, using pictures, symbols, large print, different languages, an
interpreter, or a patient advocate)
Offer all patients the opportunity to be involved in making decisions about
prescribed medicines. Establish what level of involvement in decision making the
patient would like
Be aware that increasing patient involvement may mean that the patient decides
not to take or to stop taking a medicine. If in the healthcare professional's view
this could have an adverse effect, then the information provided to the patient on
risks and benefits and the patient's decision should be recorded
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Accept that the patient has the right to decide not to take a medicine, even if you
do not agree with the decision, as long as the patient has the capacity to make an
informed decision and has been provided with the information needed to make
such a decision
Be aware that patients' concerns about medicines, and whether they believe they
need them, affect how and whether they take their prescribed medicines
Offer patients information that is relevant to their condition, possible treatments,
and personal circumstances, and that is easy to understand and free from jargon
Recognise that non-adherence is common and that most patients are non-
adherent sometimes. Routinely assess adherence in a non-judgmental way
whenever you prescribe, dispense, and review medicines
Be aware that although adherence can be improved, no specific intervention can
be recommended for all patients. Tailor any intervention to increase adherence to
the specific difficulties with adherence the patient is experiencing
Review patient knowledge, understanding, and concerns about medicines, and a
patient's view of their need for medicine at intervals agreed with the patient,
because these may change over time. Offer repeat information and review to
patients, especially when treating long term conditions with multiple medicines
KEY POINTS
As soon as the diagnosis of unstable angina or NSTEMI is made, and aspirin and
antithrombin therapy have been offered, formally assess individual risk of future
adverse cardiovascular events using an established risk scoring system that
predicts six month mortality (for example, Global Registry of Acute Cardiac
Events (GRACE))
Consider intravenous eptifibatide or tirofiban as part of the early management for
patients who have an intermediate or higher risk of adverse cardiovascular events
(predicted six month mortality above 3.0%), and who are scheduled to undergo
angiography within 96 hours of hospital admission
Offer coronary angiography (with follow on PCI if indicated) within 96 hours of first
admission to hospital to patients who have an intermediate or higher risk of
adverse cardiovascular events (predicted six month mortality above 3.0%) if they
have no contraindications to angiography (such as active bleeding or
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comorbidity). Perform angiography as soon as possible for patients who are
clinically unstable or at high ischaemic risk
When advising patients about the choice of revascularisation strategy (PCI or
CABG), take account of coronary angiographic findings, comorbidities, and the
benefits and risks of each intervention. When the role of revascularisation or the
revascularisation strategy is unclear, resolve this by discussion involving an
interventional cardiologist, cardiac surgeon, and other healthcare professionals
relevant to the needs of the patient. Discuss the choice of revascularisation
strategy with the patient
To detect and quantify inducible ischaemia, consider ischaemia testing before
discharge for patients whose condition has been managed conservatively and
who have not had coronary angiography
Before discharge offer patients advice and information about:
Their diagnosis and arrangements for follow up
Cardiac rehabilitation
Management of cardiovascular risk factors and drug therapy for
secondary prevention
Lifestyle changes
CLINICAL TIPS
NICE Technology Appraisal 182 states "Prasugrel in combination with aspirin is recommended as an option for
preventing atherothrombotic events in people with acute coronary syndromes having percutaneous coronary
intervention, only when:
Immediate primary percutaneous coronary intervention for ST-segment-elevation
myocardial infarction is necessary
Stent thrombosis has occurred during clopidogrel treatment
The patient has diabetes mellitus."
The common side effects of clopidrogel include bruising, haematoma (normally seen associated with a procedure,
surgery, or trauma), epistaxis, gastrointestinal haemorrhage, diarrhoea, abdominal pain, dyspepsia, bleeding at
puncture site.
THE ALGORITHM
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To download this algorithm please go to:
4. NICE Technology Appraisal 182 states Prasugrel in combination with aspirin is recommended as an
option for preventing atherothrombotic events in people with acute coronary syndromes having
percutaneous coronary intervention, only when:
Immediate primary percutaneous coronary intervention for ST-segment-elevation
myocardial infarction is necessary
Stent thrombosis has occurred during clopidogrel treatment
The patient has diabetes mellitus."
Prasugrel is currently a black triangle medicine. A black triangle is assigned to a product if the drug is an
active substance which has been newly licensed for use in the UK. The black triangle symbol is not
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removed until the safety of the drug is well established. The MHRA wishes to receive all reports of
suspected adverse reactions associated with black triangle products, in order to:
Confirm risk/benefit profiles established during the premarketing phase
Increase our understanding of the safety profiles of new medicines
Ensure that previously unrecognised side effects are identified as quickly as possible.
Specific contraindications to prasugrel are:
Hypersensitivity to the active substance or to any of the excipients
Active pathological bleeding
History of stroke or transient ischaemic attack (TIA)
Severe hepatic impairment (Child-Pugh class C).
Full details of caution in use and side effects are included in the makers SPC available at
http://www.medicines.org.uk/emc/
Safety in patients with acute coronary syndrome undergoing PCI was evaluated in one clopidogrel
controlled study (TRITON) in which 6741 patients were treated with prasugrel (60 mg loading dose and
10 mg once daily maintenance dose) for a median of 14.5 months (5802 patients were treated for over
six months, 4136 patients were treated for more than one year). The rate of study drug discontinuation
due to adverse events was 7.2% for prasugrel and 6.3% for clopidogrel. Of these, bleeding was the
most common adverse reaction for both drugs leading to study drug discontinuation (2.5% for prasugrel
and 1.4% for clopidogrel).
http://www.medicines.org.uk/emc/http://www.medicines.org.uk/emc/http://www.medicines.org.uk/emc/