Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2683_Библиотеки_им_академика_М_И_Перельмана.pdf
Cardiovascular system
Modifiable risk factors
Smoking
It is estimated that smoking is responsible for more than
20% of CVD, with mortality from CVD 60% higher in
smokers. Passive smoking increases the risk of developing
CVD by around 25%.
HINTS AND TIPS
The description of symptoms in ischaemic heart
disease is very variable. Patients often use words
such as ‘heaviness’, ‘tightness’ or ‘restriction’
rather than ‘pain’.
Poor nutrition
A diet high in saturated fat, salt and sugar increases the risk
of developing CVD.
Hyperlipidaemia
The risk of CVD increases as serum total cholesterol and
low-density lipoprotein (LDL) cholesterol levels increase.
High-density lipoprotein (HDL) cholesterol is ‘protective’ for CVD, and the risk of CVD decreases as HDL level
increases.
Hypertension
Both systolic and diastolic hypertension are associated with
the risk of developing CVD, as well as hypertensive heart
disease, stroke and renal failure. Treatment of hypertension
with drugs reduces the incidence of cardiac events, particularly in the elderly.
Diabetes mellitus
Diabetes mellitus increases the risk of developing CVD by
three to four times.
Obesity
In addition to being an independent risk factor for CVD,
obesity also increases the likelihood of developing hypertension, hyperlipidaemia and diabetes mellitus.
Pathophysiology
Atherosclerosis is a slowly progressive focal proliferation of
connective tissue within the arterial intima that begins as
early as the second decade of life. It is linked to high lipid
levels. LDL is the main atherogenic lipid, although the principal constituent of atherosclerotic plaques is collagen synthesized by smooth muscle cells.
The initial process involves endothelial dysfunction in
association with high circulating cholesterol levels, inflammation and shear forces. Macrophages enter the arterial
wall between endothelial cells, taking up lipids and forming
foam cells. The accumulation of lipid-laden macrophages
in the subendothelial zone leads to the formation of fatty
streaks. Toxic products released from the macrophages
result in platelet adhesion and smooth muscle cell proliferation and thrombus formation. Subsequently, an atherosclerotic plaque surrounded by a fibrotic cap is formed.
Progressive enlargement of these lesions leads to segmental narrowing of the lumen, which, when sufficient to be
flow limiting on exercise, causes stable exertion-associated
angina.
Atherosclerotic plaques are liable to rupture, resulting
in sudden thrombosis, and ACS. Factors associated with
plaque disruption and consequent thrombosis include a
large lipid core, a high monocyte density and low smooth
muscle cell density.
Clinical features
CVD clinically presents in broadly two categories: stable
angina and ACS. Stable angina is due to a predictable mismatch between oxygen supply and demand of cardiac myocytes (cardiac ischaemia). This is brought on by exertion
and relieved by rest. Symptoms include central chest pain,
heaviness or discomfort commonly radiating to the jaw
or arm, and may be associated with shortness of breath,
sweating, nausea or faintness (see Chapter4). ACS presents
with the same symptoms but, unlike stable angina, occurs
suddenly and is often a result of atherosclerotic plaque
rupture.
Investigations
Although stable angina and ACS present with similar symptoms, they are investigated differently. ACS is a medical
emergency and requires urgent inpatient diagnosis. Stable
angina is commonly managed in primary care with diagnostic investigations arranged as an outpatient.
Electrocardiogram
A normal ECG does not exclude a diagnosis of stable angina or ACS. During attacks, there may be ST-segment depression or symmetrical T-wave inversion (Table27.2). The
ECG may show signs of an old myocardial infarction (MI)
or left ventricular hypertrophy. Comparison with an old
ECG is very useful.
Exercise tolerance test
Also known as ‘exercise ECG’, an exercise tolerance test helps
determine exercise performance, and is an independent indicator of prognosis. It is contraindicated in ACS, severe
aortic stenosis, HOCM, severe pulmonary hypertension and
significant rhythm disturbances. The sensitivity for CVD is
78% and the specificity is 70%. Causes of false- positive tests
include hyperventilation, digoxin, hypokalaemia, hypertension, valvular heart disease, left ventricular hypertrophy
and preexcitation syndromes. The test should be terminated
if there is chest pain, ST elevation, more than 2 mm of ST
depression, a fall in BP or arrhythmia.
168
Coronary heart disease
2727
Table27.2 Correlation between myocardial infarction
territory, electrocardiogram leads in which changes are
seen and the artery involved
MI territory Leads Artery
Anterior • ST elevation ± Q
Anteroseptal • ST elevation in
Posterior • Reciprocal
Inferior • ST elevation in
Lateral • ST elevation in
MI, Myocardial infarction.
waves in leads
V1–V6 ± I and aVL
• Reciprocal ST
depression in
leads II, III and
aVF (inferior
leads)
leads V1–V
changes in
leads V1–V4
(anteroseptal
leads)
leads II, III and
aVF
• Reciprocal ST
depression in
lead aVL
leads I, aVL, V5
and V6 (lateral
leads)
• Reciprocal ST
depression in
leads III and aVF
(inferior leads)
4
Left anterior
descending artery
Left anterior
descending and
right coronary
arteries
Right coronary
artery
Left circumflex
coronary artery
Dominant right
coronary artery
(80%)
Any of the other
coronary arteries
Left anterior
descending artery
Right or left
circumflex artery
Nuclear imaging
Radioactive isotopes (e.g. thallium, technetium myocardial
perfusion (MIBI) scan or multigated acquisition (MUGA)
scan) are used to assess myocardial structure and function.
The isotope is taken up by healthy myocardium, whereas
areas of infarction show up as ‘cold spots’.
Coronary angiography
Coronary angiography allows visualization of the coronary
arteries and measurement of intracardiac pressures, blood
oxygen saturation in different cardiac chambers and cardiac
output. It is used as a guide to decide on further management (i.e. medical therapy, coronary angioplasty or coronary artery bypass surgery).
The mortality from the procedure is approximately 1 in
1000. Complications include:
• haemorrhage and haematoma at the site of arterial
puncture;
• emboli into arteries resulting in coronary or peripheral
ischaemia;
• stroke;
• arrhythmias;
• coronary artery dissection.
Treatment
As for all chronic disease, optimal management includes
patient education, lifestyle changes, medication and procedural interventions. Noncoronary causes of angina should
be sought and treated (e.g. valvular heart disease and anaemia). National Institute for Health and Care Excellence
(NICE) guidelines are available for the management of
stable angina, unstable angina, NSTEMI, STEMI and chest
pain of recent onset (see Further reading).
Echocardiography
Echocardiography allows visualization of cardiac structures
and assessment of their function. It is a useful tool to identify valvular heart disease, ventricular dysfunction, structural abnormalities of the heart or pericardial disease.
Echocardiography can be transthoracic (transducer
probe is placed in the intercostal spaces) or transoesophageal (ultrasound probe is passed into the oesophagus). A
transoesophageal echocardiogram is an invasive procedure
but allows better visualization of the posterior structures of
the heart.
CT coronary angiography
CT coronary angiography allows noninvasive assessment of
the coronary arteries. CT scans can be used in CVD risk
stratification through measurement of possible atherosclerosis expressed as ‘calcium score’, or as a noninvasive
method for assessing coronary artery patency.
Lifestyle changes
You should ask about possible risk factors and address
those that are present. Weight loss, smoking cessation, exercise and healthy diet should all be encouraged. Exercise
may improve the collateral circulation in the heart. Factors
precipitating angina (e.g. cold weather or extremes of emotion) should be avoided. All patients should be provided
with a sublingually administered nitrate, either spray or
tablet, for relief of acute attacks or prophylactic use before
exercise.
HINTS AND TIPS
Patients with stable angina should be advised to
seek urgent medical help if their symptoms have
not resolved 5 min after taking the second dose of
a short-acting nitrate such as glyceryl trinitrate.
169
Cardiovascular system
Drug agents
Antiplatelet drugs
Unless contraindicated, aspirin therapy at 75 mg daily
should be started as this lowers the incidence of subsequent
MI and death. If aspirin is contraindicated, then clopidogrel
is an alternative.
Nitrates
Nitrates cause peripheral vasodilation that is most marked
in the veins. This reduces venous return and preload,
thereby decreasing cardiac output and oxygen demand,
resulting in relief of angina. Nitrates are converted to the
active molecule nitric oxide, which results in an increase in
the level of intracellular cyclic guanosine monophosphate in
smooth muscle. This stimulates calcium-binding processes
and reduces the amount of free calcium available to trigger
muscle contraction.
Short-acting nitrates are the mainstay of relief of acute
angina and, when combined with rest, they normally relieve the pain in minutes. If the pain continues, then this
should be a warning sign to patients. Longer-acting nitrates are more stable and can be effective for several hours.
Isosorbide dinitrate is rapidly metabolized by the liver to
mononitrate, which is the main active metabolite. Use of
isosorbide mononitrate may avoid the variable absorption
and unpredictable first-pass metabolism of the dinitrate.
Adverse effects are normally due to arterial dilation, and
include headaches, flushing, hypotension and, rarely, fainting. Patients may become tolerant to nitrates, reducing their
effectiveness. Nitrate ‘holidays’ are the traditional way of
minimizing the problem, although newer once-daily preparations reduce this effect.
β-Blockers
β-Blockers improve oxygen supply and demand balance
by lowering heart rate and BP, decreasing end-systolic
stress and contractility and prolonging diastole, permitting
greater coronary flow.
Typical β-blockers include atenolol, bisoprolol, carvedilol and metoprolol. Contraindications include asthma,
hypotension, marked bradycardia, second- and thirddegree heart block, severe peripheral arterial disease and
uncontrolled heart failure.
Calcium channel blockers
Calcium antagonists inhibit the influx of calcium into the
myocyte during the action potential and relax peripheral
vascular smooth muscle. They relieve angina by a combination of reduced afterload (and hence myocardial oxygen
demand) plus reduced heart rate and increased coronary
vasodilation. They are especially useful if there is a degree of
coronary artery spasm. Dihydropyridines such as nifedipine
can cause reflex tachycardia secondary to peripheral vasodilatation, and therefore may be combined with a β-blocker.
Verapamil is the drug of choice for supraventricular tachycardias (SVTs) if β-blockers are contraindicated (verapamil
and β-blockers must never be coprescribed). All calcium
channel blocking drugs are negatively inotropic to some
degree and, although safety of amlodipine has been demonstrated in heart failure, care should be taken when you are
prescribing any of them in left ventricular impairment.
Side effects include headache, flushing, dizziness, consti-
pation and gravitational oedema.
CLINICAL NOTE
TREATMENT OF STABLE ANGINA
Patients with stable angina should be treated with
either a β-blocker or a calcium channel blocker.
Second-line therapies include long-acting nitrates,
ivabradine, nicorandil and ranolazine.
Potassium channel activators
Nicorandil has arterial and venous vasodilating properties,
and is useful in patients refractory to treatment with other
antianginal agents.
Angiotensin-converting enzyme inhibitors
Unless contraindicated, angiotensin-converting enzyme
(ACE) inhibitor therapy should be started in patients with
stable angina and left ventricular dysfunction and/or diabetes.
Lipid-lowering drugs
Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase
inhibitors) are the mainstay of lipid-lowering therapy. They
may also help to stabilize atherosclerotic plaques and reduce
the frequency of acute cardiac events. Most patients with
CVD should be taking a statin even if their cholesterol level
is within the normal range.
CLINICAL NOTE
MEASURING CHOLESTEROL
The National Institute for Health and Care
Excellence currently recommends the use of nonhigh-density lipoprotein (HDL) cholesterol (total
cholesterol minus HDL cholesterol) as a guide to
starting therapy with statins.
Revascularization
Revascularization should be considered in patients with stable angina in whom symptoms are not controlled by medical management. This can be achieved by percutaneous
coronary intervention (PCI) or coronary artery bypass graft
(CABG). The choice of which procedure is performed depends on clinical assessment and patient preference. Groups
of patients who benefit from CABG rather than PCI are described in clinical notes: patient factors associated with reduction in mortality with coronary artery bypass graft.
170
Acute coronary syndrome
2727
CLINICAL NOTES
PATIENT FACTORS ASSOCIATED WITH
REDUCTION IN MORTALITY WITH CORONARY
ARTERY BYPASS GRAFT
• Left main stem stenosis.
• Triple-vessel coronary artery disease.
• Two-vessel disease with proximal left anterior
descending coronary artery disease.
• Left ventricular impairment (benefit is greater).
PCI involves use of a balloon catheter to widen the coronary artery. Bare metal or drug-eluting stents are usually
used after dilation to reduce rates of restenosis.
CABG is a surgical technique where vessels are harvested from another part of the body and used to replace
the stenosed coronary artery. A bypass procedure using one
or both of the internal mammary arteries is preferred to the
traditional vein graft as it results in better patency and flow.
In all patients who have undergone revascularization,
lifelong aspirin therapy is started. Patients with stents should
be receiving dual antiplatelet therapy (usually aspirin and
clopidogrel). This is continued for at least 1month in case
of bare metal stents and 12months for drug-eluting stents.
ACUTE CORONARY SYNDROME
Table27.3 Changes induced by acute myocardial
infarction
Time after onset
of symptoms
Up to 18 hours None None
24–48 hours Pale oedematous
3–4days Yellow rubbery
3–6weeks Silvery scar
Macroscopic
changes
muscle
centre with
haemorrhagic
border
becoming rough
and white
Microscopic
changes
Oedema, acute
inflammatory
cell infiltration,
necrosis of
myocytes
Obvious necrosis
and inflammation,
early granulation
tissue
Dense fibrosis
thrombus overlying an ulcerated or fissured stenotic plaque.
Underlying most cases there is a dynamic interaction between severe coronary atherosclerosis, an acute atheromatous plaque change, superimposed thrombosis, platelet
activation and vasospasm. The microscopic changes of acute
MI follow a predictable sequence (Table27.3). Almost 50% of
myocardial tissue that lies in the area of ischaemia dies within
1 hour of occlusion, and more than 60% dies within 3 hours;
thus restoration of coronary blood flow is a key treatment
goal. NICE recommends use of the universal definition of MI
when one is making the diagnosis (clinical notes: universal
definition of myocardial infarction).
‘Acute coronary syndrome’ (ACS) is a term that encompasses
a range of diagnoses, including STEMI, NSTEMI and unstable angina. It is a medical emergency. ACS usually results from
atherosclerotic plaque rupture, leading to sudden reduction of
blood flow to the myocardium and sometimes the formation
of emboli. Presenting symptoms include severe pain in the
chest, jaw, arms and/or back that may be associated with sweating, breathlessness and nausea and vomiting (see Chapter4).
Despite uniform clinical features, the underlying disorders
differ: STEMI is usually a result of a large territory myocardial
damage, NSTEMI is a consequence of a relatively smaller injury, and angina is caused by narrowing, but not complete obstruction, of the coronary arteries. Angina is termed ‘unstable’
if it is not relieved by rest or medical treatment.
ACS is common (incidence 15 in 1000). Around 60% of
patients present with an STEMI and around 40% present
with an NSTEMI and/or unstable angina.
ST elevation myocardial infarction
General overview
The incidence of STEMI has been decreasing in the past
20years and is estimated to range between 750 and 1250 per
million in the United Kingdom. In-hospital mortality is about
5%. Most STEMIs are caused by an occlusive intracoronary
CLINICAL NOTES
UNIVERSAL DEFINITION OF MYOCARDIAL
INFARCTION
The universal definition of myocardial infarction, as
published in the Journal of the American College of
Cardiology in 2012 by Thygesen etal. (see Further
reading) and described by the National Institute for
Health and Care Excellence, is as follows:
Detection of rise and/or fall of cardiac biomarkers
(preferably troponin) with at least one value above
the 99th percentile of the upper reference limit,
together with evidence of myocardial ischaemia
with at least one of the following:
• Symptoms of ischaemia.
• ECG changes indicative of new ischaemia (new
ST-T changes or new LBBB).
• Development of pathological q wave changes
• Imaging evidence of new loss of viable
myocardium or new regional wall motion
abnormality.
171
Cardiovascular system
Normal Hours Days Weeks Months
Days
45
Serum enzyme levels
Clinical features
Patients commonly present with acute-onset chest, jaw,
back or arm pain (see Chapter 4), although occasionally
ACS may be ‘silent’. Associated features include nausea,
vomiting, sweating, palpitations, dyspnoea, syncope and/
or pulmonary oedema. The patient will often be distressed.
Investigations
The earliest ECG changes or ‘hyperacute’ changes consist
of tall, pointed T waves and subsequent ST elevation. This
is followed by T-wave inversion, decreasing R-wave voltage
and the development of q waves. After weeks or months,
the T wave may become upright again, but the q waves will
remain (Fig. 27.1). The site of the infarction may be deduced from the affected leads on the ECG (see Table27.2).
Reciprocal ECG changes with ST depression in leads opposite the site of infarction may also be present.
Cardiac biomarkers are intracellular molecules which
leak out of infarcted myocardium into the bloodstream
(Fig.27.2):
• Elevated troponin I or troponin T concentrations are
highly reliable markers of myocardial damage. Serum
levels increase within 3–12 hours of the onset of pain
and peak at 24–48 hours. They remain elevated for
1–2weeks.
• Myocardial muscle creatine kinase (CK-MB) levels
increase within 3–12 hours and peak at 24 hours. They
remain elevated for 48–72 hours.
• Aspartate aminotransferase and lactate dehydrogenase
were formerly used to assess MI as their levels remain
elevated for several days. Their use is now largely
obsolete.
Management
Acute management
Follow the ABCDE approach. The aim of treatment is to
prevent ischaemia and alleviate pain and anxiety. Pain
can be managed with sublingually or buccally administered glyceryl trinitrate (GTN) and intravenous opioids.
In addition to providing analgesia, morphine compounds
also reduce cardiac workload by vasodilation and alleviating sympathetic activation. Antiemetics should be
administered with opiates. Aspirin (300 mg) should be
given as soon as possible, and this is often done by the
paramedic crew.
NICE recommends coronary angiography with
follow-on PCI if the intervention can be delivered within
120 minutes of the time when fibrinolysis could have been
given for patients with STEMI. If a delay is expected, fibrinolysis should be considered (see Table27.4 for contrain-
dications to thrombolytic therapy). Glycoprotein IIb/IIIa
inhibitors should not routinely be given to patients undergoing PCI; instead any of the three antiplatelet agents
should be given: clopidogrel, prasugrel or ticagrelor.
Non-ST elevation myocardial infarction and unstable angina
General overview
NSTEMI is diagnosed in patients who fit the criteria for MI
but do not have persistent ST elevation on ECG, whereas
unstable angina is diagnosed in patients without elevated
biomarker values.
Clinical features
The history and clinical features are the same as those for
STEMI. Patients with stable angina may note that their pain
is no longer relieved fully by GTN, that it is increasing in
intensity or that it is occurring at rest.
Fig.27.1 Progressive electrocardiogram changes in
myocardial infarction.
Key
= CK
= LDH
= AST
= Troponin
0
01 23
Fig.27.2 The pattern of serum markers after acute
myocardial infarction. AST, Aspartate aminotransferase;
CK, creatine kinase; LDH, lactate dehydrogenase.
172
Table27.4 Contraindications to thrombolytic therapy
Contraindications Relative contraindications
Stroke Transient ischaemic attack
Major surgery, trauma or
head injury within 3weeks
Gastrointestinal bleed Pregnancy
Known bleeding disorder Noncompressible punctures
Suspected dissecting
aneurysm
Cerebral neoplasm Refractory hypertension
Recent retinal laser
SBP, Systolic blood pressure.
in the preceding 6months
Warfarin therapy
Traumatic resuscitation
(SBP >200 mmHg)
treatment
Acute coronary syndrome
2727
Investigations
Investigations are the same as those for STEMI. The ECG
may show ST-segment depression, T-wave flattening, biphasic changes or inversion. The initial ECG may be normal, and serial ECGs are needed, preferably when pain
occurs, to demonstrate the dynamic ischaemia.
Patients with troponin-positive NSTEMI are at high risk
of experiencing further events (30% chance of STEMI at
1month).
HINTS AND TIPS
Old ECGs are invaluable in assessing patients with
chest pain, allowing comparison.
Risk scoring
All patients who present with ACS should undergo risk
stratification. This allows clinicians to identify those who
are most likely to benefit from early therapeutic intervention such as PCI or CABG. Identification of individuals at
increased risk of adverse future events is performed with an
established scoring system such as the Global Registry of
Acute Cardiac Events (GRACE) score (clinical notes: components of the grace score). The GRACE score is validated
as a prognostic tool to predict mortality and MI risk in hospital and at 6months.
CLINICAL NOTES
COMPONENTS OF THE GRACE SCORE
• Age
• Heart rate
• Systolic blood pressure
• Creatinine level
• Congestive heart failure
• Cardiac arrest on admission
• ST-segment deviation on admission
• Elevated levels of cardiac enzymes
A score of more than 3% to 6% indicates an
intermediate risk of future adverse cardiovascular
events. A score of more than 6% indicates high
risk.
Management
Acute management
The initial emergency management of NSTEMI and
unstable angina is identical to that of STEMI: aspirin
(300 mg), morphine and nitrates. Antithrombin therapy
with fondaparinux should be offered unless angiography
is planned within 24 hours of presentation to hospital, in
which case unfractionated heparin is given. Patients with
a predicted 6-month mortality greater than 1.5% and those
in whom PCI is planned within 24 hours should be offered
clopidogrel (300 mg). The glycoprotein IIb/IIIa inhibitors
eptifibatide and tirofiban should be considered for patients
with a predicted 6-month mortality greater than 3.0% in
whom angiography is planned within 96 hours.
Role of revascularization—The big difference between
NSTEMI and STEMI is the role of PCI – it has no demonstrated benefit for patients who do not have ST elevation or
new left bundle branch block (LBBB), unless specific factors
are present.
Coronary angiography with follow-on PCI or CABG, if
indicated, is recommended for patients with NSTEMI or
unstable angina who have an intermediate or higher risk of
mortality or future cardiovascular events (calculated by use
of an established scoring system such as the GRACE score).
This should be performed within 72 hours. If patients are
clinically unstable, they should undergo coronary angiography as soon as possible but no later than 24 hours. Clinical
instability is defined as pain despite treatment, haemodynamic instability, left ventricular failure and/or dynamic
ECG changes.
Subsequent inpatient management of patients with acute coronary syndrome
Long-term drug treatment—All patients should have
their cardiovascular risks assessed and modified. Daily use
of aspirin is continued indefinitely after MI. It reduces the
risk of reinfarction and death by 25%. There is no clear benefit of oral anticoagulation over antiplatelet therapy, although
it may be considered for patients with left ventricular aneurysm, atrial fibrillation (AF) or echocardiographically
proven left ventricular thrombus. If aspirin is contraindicated, clopidogrel monotherapy should be considered.
Dual antiplatelet therapy with aspirin and another agent
is recommended following an MI. Clopidogrel is a treatment option in any patient who has had an NSTEMI and
in those who have had an STEMI and received a bare-metal
or drug-eluting stent or who underwent CABG. For these
patients, clopidogrel therapy should be continued for up
to 12months. In medically managed patients with STEMI,
clopidogrel can be given but the period for which this is
continued ranges between 1month and 12months.
Prasugrel is a treatment option in combination with aspirin in patients undergoing PCI. Treatment is continued
for up to 12months.
Ticagrelor is a treatment option in combination with aspirin in patients with ACS. Treatment is continued for up
to 12months.
Rivaroxaban is a treatment option in combination with
aspirin and clopidogrel or aspirin alone for people who have
had an STEMI or NSTEMI. Treatment is continued for up
to 12months.
Unless contraindicated, following an MI, treatment with
a β-blocker (reduces mortality and reinfarction rates), ACE
173
Cardiovascular system
inhibitor (reduce the risk of death and heart failure) and a statin (statins have antiinflammatory plaque-stabilizing effects)
should be started. Calcium channel blockers such as diltiazem
or verapamil can be used in patients in whom β-blockers are
contraindicated. In patients with signs of heart failure or left
ventricular systolic dysfunction, aldosterone antagonist therapy should be started. Use of β-blockers is continued for at
least 12months in patients without left ventricular systolic
dysfunction, and indefinitely in those with left ventricular
systolic dysfunction. ACE inhibitors are given lifelong.
Other management—All patients who have had an MI
should undergo left ventricular function assessment, most
commonly done by the use of echocardiography. Cardiac
rehabilitation programmes of exercise and information sessions should be offered to all patients following an acute MI.
People should be advised regarding lifestyle modifications:
eating a Mediterranean-style diet, physical activity for 20–
30 minutes per day, smoking cessation. Overweight patients
should be offered weight management advice.
Complications of myocardial infarction
A summary of the complications that may occur as a result
of MI is given in Table27.5.
Cardiac failure and cardiogenic shock
Overt left ventricular failure after MI is associated with a
poor prognosis. Cardiogenic pulmonary oedema is a common finding (Table27.6). The management of heart failure
is described later in this chapter.
Table27.6 Killip classification for assessment of heart
failure
Class Features
1 No crepitations or third heart sound
2 Crepitations over less than 50% of lung fields
or third heart sound
3 Crepitations over 50% of the lung fields
4 Shock
Cardiogenic shock is described as secondary to pump
failure, inadequate end-organ perfusion and subsequent
tissue hypoxia. MI-related cardiogenic shock occurs as a result of damage to the myocardium leading to a mechanical
insufficiency. Other causes of shock include hypovolaemia,
vasovagal reactions, drugs or arrhythmias. Ventricular and
valvular function should be evaluated by echocardiography.
Inotropic agents are of value: dobutamine or milrinone are
positive inotropes that enhance cardiac contractility.
Cardiac rupture
Free wall rupture, if acute, is usually fatal within minutes. If subacute, there is haemodynamic deterioration with hypotension
and signs of cardiac tamponade. Immediate surgery is needed.
Postinfarction ventricular septal defects (VSDs) are rare
but associated with high mortality without prompt surgical repair. They should be suspected if there is clinical deterioration
and a loud pansystolic murmur at the left sternal edge.
Table27.5 Complications of myocardial infarction.
Complication Interval Mechanism
Sudden death Usually within hours Often ventricular fibrillation
Arrhythmias First few days —
Persistent pain 12 hours to a few days Progressive myocardial necrosis (extension
Angina Immediate or delayed (weeks) Ischaemia of noninfarcted muscle
Cardiac failure Variable Ventricular dysfunction following muscle
Mitral incompetence First few days Papillary muscle dysfunction, necrosis or
Pericarditis 2–4days Transmural infarct with inflammation of the
Cardiac rupture and ventricular septal
defects
Mural thrombus 1week or more Abnormal endothelial surface following
Ventricular aneurysm 4weeks or more Stretching of newly formed collagenous
Dressler syndrome Weeks to months Autoimmune
Pulmonary emboli 1week or more Deep vein thrombosis in lower limbs
Late ventricular arrhythmias — —
3–5days Weakening of wall following muscle
of myocardial infarction)
necrosis; arrhythmias
rupture
pericardium
necrosis and acute inflammation
infarction
scar tissue
174
Arrhythmias
2727
Mitral regurgitation
Development of mitral regurgitation is a poor prognostic factor. It usually occurs within the first week after MI.
Mortality without surgical intervention is high.
Arrhythmias and conduction disturbances
These are extremely common in the early period following
MI. Often, the arrhythmias are not hazardous in themselves
but are a manifestation of a serious underlying disorder
such as continuing ischaemia, vagal overactivity or electrolyte disturbance, particularly potassium and magnesium.
Arrhythmias can also occur following reperfusion. The
management of arrhythmias is covered in detail later in this
chapter.
Ventricular arrhythmias—Ventricular arrhythmias
may present as ventricular ectopics, ventricular tachycardia
(VT) or ventricular fibrillation (VF).
Ventricular ectopics are almost universal on the first day
and require no treatment if the patient is asymptomatic.
Short episodes of VT may be well tolerated and require no
treatment. More prolonged episodes may cause hypotension and heart failure. VF is associated with approximately
5% of MI. It is rapidly fatal if not treated. If VF occurs, immediate defibrillation should be performed as part of the
advanced life support protocol.
When arrhythmias occur late in the course of MI, they
are likely to recur, and are associated with a high risk of
death. If it is probable that the arrhythmia is induced by
ischaemia, revascularization should be considered. If this
is unlikely, antiarrhythmic agents (e.g. β-blockers and
amiodarone) and electrophysiologically guided treatment
may be given. In some cases, an implantable defibrillator
is indicated.
Supraventricular arrhythmias—AF complicates 15%–
20% of MIs, and is often associated with severe left ventricular damage and heart failure; it is usually self-limiting.
If the heart rate is fast, bisoprolol or digoxin is effective in
slowing the rate, but amiodarone is more efficacious in terminating the arrhythmia.
Other supraventricular arrhythmias are rare but are also
usually self-limiting. They may respond to carotid sinus
massage. β-Blockers may be effective and direct current
(DC) cardioversion should be used if the arrhythmia is associated with haemodynamic instability.
Sinus bradycardia and heart block—Sinus bradycardia
is common early on, especially in inferior MI, and responds
to atropine.
Atrioventricular (AV) block is common in inferior MI
as the right coronary artery supplies the AV node. The bradycardia may respond to atropine, although patients may
go on to need a permanent pacemaker. Heart block with
anterior MI is ominous because it indicates a large infarct.
The development of LBBB or bifascicular block may presage complete heart block and is an indication for temporary
pacemaker insertion. If complete heart block does occur
and persists, a permanent pacemaker will be needed.
Pericarditis—This usually develops within 24–96 hours
after an MI, causing pain that is sharp in nature and varies with posture and respiration. Treatment is with nonsteroidal antiinflammatory drugs (NSAIDs). Dressler
syndrome is a form of secondary pericarditis that occurs
up to 3 months after MI. Clinical features include fever,
leucocytosis, pericarditis and serositis. Treatment is as for
pericarditis.
ARRHYTHMIAS
General overview
An arrhythmia is a disturbance of normal sinus cardiac
rhythm. Arrhythmias are very common, are often intermittent, but may cause cardiac compromise. They are
commonly secondary to CVD. Other causes include drugs
(prescribed or illicit), cardiomyopathy, myocarditis, thyroid
dysfunction and electrolyte disturbances.
Arrhythmias may present with palpitations (see Chapter
7), dizziness, angina, shortness of breath (see Chapter5),
syncope, cardiac arrest or sudden death; they may also be
asymptomatic. The history taking should focus on symptoms and possible underlying causes.
Investigations
An ECG will allow diagnosis of the arrhythmia if it is
present at the time of the test. Make sure to look for signs
of ischaemia. For infrequent symptoms, a 24-hour ECG
(Holter monitoring) may record the rhythm disturbance.
Other routine investigations should include full blood
count (FBC), urea and electrolytes (U&Es), calcium,
magnesium, thyroid function tests (TFTs) and chest X-ray
(CXR). An echocardiogram should be considered to look
for structural cardiac disease. More prolonged ambulatory monitoring over weeks or months should be considered if the diagnosis is difficult to make. Specialized
electrophysiological studies may reveal an arrhythmogenic focus; radiofrequency ablation can then be used to
destroy this focus.
Supraventricular arrhythmias
Sinus tachycardia
This is defined as a heart rate of more than 100 bpm originating from the sinoatrial (SA) node (sinus rhythm). It can
be entirely physiological (e.g. during exercise) but may be
pathological. Causes include anaemia, pulmonary embolism, pain, fever, sepsis, thyroid toxicosis, hypovolaemia,
anxiety and heart failure. Treating the underlying cause
should resolve the tachycardia. Rarely patients have idiopathic inappropriate sinus tachycardia, which is thought to
be due to abnormal autonomic tone.
175
Cardiovascular system
A
B
Atrial fibrillation
Aetiology and pathophysiology
AF is the most common sustained cardiac arrhythmia. It is
an irregular, chaotic atrial rhythm at a rate of 300–600 bpm.
It is transmitted to the ventricles via the AV node at different intervals, leading to an irregular heart rate, dependent
on the speed of AV node conduction and how refractory
the AV node is. The incidence rises with age, and is more
than 10% in those older than 75years. It may be idiopathic,
secondary to chronic heart disease or a response to acute
illness. Causes include:
• CVD;
• hypertension;
• mitral valve disease;
• electrolyte disturbances;
• hyperthyroidism;
• infection, including endocarditis;
• drugs (e.g. thyroxine, bronchodilators);
• pericarditis;
• cardiomyopathy;
• excess alcohol consumption;
• atrial myxoma;
• infiltrative diseases of the heart (e.g. sarcoidosis).
Clinically, there is an irregularly irregular pulse, and the apical rate can be greater than the rate at the radial artery since
the pulse volume varies. The first heart sound is of variable
intensity.
The ECG shows absent P waves and irregular narrow
QRS complexes (unless there is associated bundle branch
block) (Fig.27.3).
Complications
The most common complication associated with AF is
thromboembolic disease. Poor synchronization of atrial
contraction and the resultant stagnation of blood in the atria
leads to thrombus formation. The thrombus can embolize
to anywhere in the systemic circulation, but stroke and ischaemic gut are the most common presentations. NICE recommends risk stratification with the CHA2DS2-VASc score
(see Chapter32). Patients with a score of 2 should be offered
anticoagulation. Anticoagulation should be considered in
men with a score of 1. Anticoagulation can be achieved with
novel oral anticoagulants or warfarin (see Chapters28 and
32). If anticoagulation is contraindicated, dual therapy with
aspirin and clopidogrel may be considered.
AF can also lead to development of heart failure. This
occurs as a result of reduction in cardiac output.
Management
Underlying causes should be treated. Management of AF
involves rate and rhythm control. NICE recommends rate
control as first-line treatment except in patients:
• with AF with a reversible cause;
• with heart failure primarily caused by AF;
• with new-onset AF;
• with atrial flutter, suitable for ablation;
• who are more suitable for rhythm control (on the basis
of clinical judgement).
The ventricular rate can usually be controlled with a standard
β-blocker (a β-blocker other than sotalol) or a rate- limiting
calcium channel blocker. Digoxin can be considered in sedentary patients. Other classes of drug may sometimes be
required. If the AF is of recent onset, electrical DC cardioversion or pharmacological cardioversion with amiodarone
or flecainide may be attempted. After more than 48 hours
of AF, the patient should be fully anticoagulated for at least
3weeks before electrical cardioversion.
Atrial flutter
This is due to a regular circus movement of continuous
atrial depolarization. As the AV node cannot conduct that
fast, it is usually transmitted with a degree of block (e.g. 2:1,
3:1).
The causes and treatment are similar to those for AF.
The ECG shows a ‘sawtooth’ appearance to the baseline at rates of up to 350 bpm due to flutter or F waves
(Fig.27.4). The ventricular rate is usually divisible into this
(e.g. 150 bpm in 2:1 block or 100 bpm in 3:1 block).
Fig.27.3 Electrocardiograms of atrial fibrillation with a slow ventricular rate (A) and fast ventricular rate (B).
176
Arrhythmias
A
B
Fig.27.4 Electrocardiograms of atrial flutter. (A) Atrial flutter with 4:1 block. (B) Atrial flutter with 2:1 block.
2727
Paroxysmal supraventricular tachycardia
SVT is generally divided into AV reentry tachycardia
(AVRT), AV nodal reentry tachycardia (AVNRT) and atrial
tachycardia. It is caused by either abnormalities of impulse
initiation or disorders of impulse conduction (the presence
of an accessory pathway between the atria and ventricles,
reentrant tachycardias). SVT is usually paroxysmal. In reentrant tachycardias, one pathway is fast- and the other
slow-conducting. This leads to ante or retrograde conduction and formation of a reentrant circuit. The result is premature atrial contraction and ventricular depolarization
giving rise to a fast ventricular rate. The refractory period
for an accessory pathway may be shorter than the AV node,
leading to ventricular rates exceeding 200 bpm.
Atrioventricular reentry tachycardia
This condition is due to a re-entry accessory circuit not involving the AV node. Patients tend to present at a younger
age, as these pathways are often congenital. AVRTs frequently settle with flecainide but may require accessory
pathway ablation to cure the condition. Wolff–Parkinson–
White syndrome is an example of a congenital AVRT.
Atrioventricular nodal reentry tachycardia
This is the commonest cause of a narrow complex tachycardia. By definition, the reentry is through the AV node.
The predominant symptom is palpitations. The condition
is commonly benign, and may require no treatment beyond
termination of the tachycardia (see later).
Management
In haemodynamically stable patients, vagal stimulation can
be tried initially. This can be achieved in the following ways:
• Valsalva manoeuvre: blowing against resistance (the
closed glottis) for approximately 15 seconds. The
tachycardia usually terminates in the relaxation
(parasympathetic) phase.
• Carotid sinus massage: massage of the carotid artery at
the level of the thyroid cartilage.
If vagal manoeuvres are not successful, intravenously administered adenosine is used (as per the tachycardia algorithm of the Resuscitation Council).
If the arrhythmia is poorly tolerated, synchronized DC
cardioversion should be used.
HINTS AND TIPS
Adenosine can be administered intravenously to
reveal the underlying rhythm in supraventricular
tachycardias by temporary blocking of the AV
node.
Ventricular tachycardia
VT is a broad complex (wide QRS complexes >120 ms)
tachycardia defined as three or more consecutive ventricular extrasystoles with a rate greater than 120 bpm (Fig.27.5).
Use the ABCDE approach. If there is no pulse, follow
the adult advanced life support algorithm for VF/VT of the
Resuscitation Council. If the patient is unstable, treat the
patient with synchronized DC cardioversion. Signs of instability include reduced consciousness, chest pain, systolic
BP of less than 90 mmHg and heart failure. If the patient is
conscious, sedation or general anaesthesia will be required.
Stable patients with VT are treated with amiodarone.
Electrolyte abnormalities should be corrected.
Torsades de pointes
This is a special form of polymorphic VT, associated with
a prolonged QT interval. QRS complexes are of variable
amplitude, appearing as if they were twisting around the
Fig.27.5 Electrocardiogram of ventricular tachycardia.
177