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_2553_Библиотеки_им_академика_М_И_Перельмана
.pdf
Figure 12.9 A lateral chest X- ray.
https://t.me/med1917
resulting information is processed by a computer
to generate a series of cross- sectional images that
display the various tissues in a slice dependent on
their density. A thoracic CT scan thus is composed
of a series of cross- sectional ‘slices’ through the
thorax either at intervals or much more commonly
as a contiguous set of images.
The CT scan plays a vital part in the imaging of
thoracic pathology. Thin sections aid in the diagnoses
of diffuse/interstitial lung disease and airways disease,
such as bronchiectasis. The investigation, diagnosis
and staging of lung cancer are heavily reliant on CT
imaging. The addition of intravenous contrast that
opacifies the pulmonary arteries allows detection
of emboli as filling defects and has advantages over
isotope lung scanning (see below) in diagnosing
pulmonary embolism in patients with pre- existing
lung disease.
Similarly, opacification of the aorta permits
identification of vascular abnormalities, such as
dissection, and cardiac gating enables the capture
of slices in diastole only allowing accurate pictures
of the coronary arteries to be obtained without the
degrading influence of cardiac motion. In many
cases this technique has replaced conventional
coronary angiography. Using helical CT technology,
scanners capture large volumes of data from which
contiguous thin sections may be reconstructed,
followed by post- processing techniques such as 3D
reconstructions and the more clinically useful multiplanar reconstructions (Fig. 12.10).
SECTION THREE
Respiratory system
Radioisotope imaging
For the lungs, the most widely used radioisotope
technique is combined ventilation and perfusion
scanning, used to aid the diagnosis of pulmonary
embolism.
The perfusion scan is performed by injecting
intravenously a small dose of macroaggregated
human albumin particles labelled with technetium-
99m
99m (
Tc). A gamma- camera image is then built
up of the radioactive particles impacted in the
pulmonary vasculature; the distribution of perfusion
in the lung can then be seen. The ventilation scan
is obtained by inhalation of a radioactive gas, such
as krypton- 81m (
81m
Kr), again using scanning to
identify the distribution of the radioactivity.
Blood is usually diverted away from areas of the
lung that are unventilated, so a matched defect on
both the ventilation and perfusion scans usually
indicates parenchymal lung disease. If areas of
ventilated lung are not perfused (i.e. an unmatched
defect), this is evidence in support of an embolism
to the nonperfused area. Figure 12.11 shows a
ventilation- perfusion isotope scan. The unmatched
defects (areas ventilated by the inspired air but not
perfused by blood) suggest a high probability of
pulmonary embolism.
Magnetic resonance imaging
Magnetic resonance imaging (MRI) is useful in
demonstrating mediastinal abnormalities and can
help evaluate invasion of the mediastinum and
chest wall by tumour. Apart from the fact that it
does not use ionizing radiation, currently it has few
other advantages over CT in imaging the thorax.
MRI is particularly degraded by movement artefact
in imaging the chest because of the relatively long
data acquisition time and therefore is not used for
assessing the lung parenchyma, but faster scanners
are beginning to overcome this drawback.
Ultrasound
Ultrasound reveals much less detail than CT
scanning but has the advantages that it does not
involve radiation and, as it gives ‘real- time’ images,
the operator can visualize what is happening as it
happens. It is used for examining diaphragmatic
movement and, when available, it is recommended
that ward- based pleural procedures, such as chest
drain insertion and pleural aspiration or biopsy, be
undertaken under ultrasound guidance.
A paralysed hemidiaphragm usually results from
damage to the phrenic nerve by a mediastinal
tumour. If the patient is asked to make a sudden
inspiratory effort (e.g. sniffing), the non- paralysed
pressure drops, and the paralysed side moves up.
Ultrasound is also valuable in distinguishing
pleural thickening from pleural fluid. With real- time
imaging, the latter can be seen to move with changes
in posture. When such fluid is present, ultrasound
187
188
https://t.me/med1917
12
Respiratory system
Figure 12.10 Axial images from a CT scan demonstrating
an endobronchial lesion in the right main bronchus (A). The
contiguous nature of the thin axial slices enables the display
of the same structures in multiple planes. The coronal
(B) and sagittal planes (C) have been created, allowing
the surgeon to accurately place the endobronchial lesion
anatomically to aid the planning of the operative resection
(Courtesy of Dr Stephen Ellis.)
A
may be used to aid placement of a catheter to drain
the collection and also to steer a draining catheter
accurately into an intrapulmonary abscess.
Positron emission tomography (PET) scanning
In this technique, a radiolabelled 18- flurodeoxyglucose
(FDG) molecule is administered, which is taken
up by metabolically active tissues, such as cancers,
showing as ‘hot spots’ on the image. It is useful in
detecting regional and mediastinal lymphadenopathy
and is widely used in the staging of lung cancers and
to assess suitability for surgery in patients with lung
cancer.
B
C
Flexible bronchoscopy and endobronchial
ultrasound (EBUS)
Bronchoscopy is an essential tool in the investigation
of many forms of respiratory disease. For discrete
abnormalities, such as a mass seen on chest X- ray
and suspected to be a lung cancer, bronchoscopy
is usually indicated to investigate its nature. Under
local anaesthesia, the flexible bronchoscope is passed
through the nose, pharynx and larynx, down the
trachea, and the bronchial tree is then inspected.
Figure 12.12 shows a lung cancer seen down the
bronchoscope. Flexible biopsy forceps, which are
SECTION THREE
https://t.me/med1917
Respiratory system
Figure 12.11 Ventilation/perfusion
isotope scan of the lungs. Segmental
and subsegmental loss of perfusion (B
and D) can be seen with relatively normal
ventilation (A and C). The clear, punchedout areas in the perfusion (B and D)
scans indicate areas of reduced isotope
concentration during the perfusion scan.
Thus, these are areas of reduced blood flow.
The ventilation scans show normal aeration
of the lungs as depicted by the isotope
distribution in the pulmonary airways.
$
$QWHULRUYHQWLODWLRQ
%
$QWHULRUSHUIXVLRQ
These sequences of scans are suggestive
of pulmonary embolism because they show
impaired perfusion with normal ventilation.
189
& '
Figure 12.12 A lung cancer, seen down the bronchoscope.
3RVWHULRUYHQWLODWLRQ 3RVWHULRUSHUIXVLRQ
passed down a channel inside the bronchoscope,
are used to obtain tissue samples for histological
examination. Similarly, aspirated bronchial secretions
and brushings of any endobronchial abnormality can
be sent to the laboratory for cytological examination.
At bronchoscopy, specimens are also taken for
microbiological examination in order to determine
the nature of any infecting organisms and should
include samples for acid- fast bacilli (AFB). In diffuse
interstitial lung disease, such as sarcoidosis or pulmonary fibrosis, the technique of transbronchial biopsy
can be used to obtain small specimens of lung parenchyma for histological examination to help confirm
the diagnosis.
Endobronchial ultrasound (EBUS) is gradually
becoming more available. It involves a modified
bronchoscope fitted with an ultrasound probe and
a fine- gauge aspiration needle and is used to biopsy
thoracic lymph nodes. The procedure is normally
undertaken as a day case and under sedation. The
scope is thicker than the average bronchoscope and is
passed into the patient’s airways via a plastic mouth
guard rather than the nose. The ultrasound processor
is able to image lymph nodes on the other side of
the bronchial airways; the operator can then use the
aspiration needle to puncture that bronchial wall
and biopsy the lymph nodes. A similar procedure,
endoscopic ultrasound (EUS), can be used via the
oesophagus. Combining these two techniques
allows all of the mediastinal lymph nodes to be
biopsied. In the majority of cases, they have replaced
mediastinoscopy as the biopsy technique of choice
and are particularly useful in the diagnosis and
staging of lung cancer, sarcoidosis and tuberculosis.
Navigational bronchoscopy is a developing
specialist technique. It takes place with the
anaesthetized patient lying on an electromagnetic
table. This is linked to the patient’s most up- todate CT scan of the thorax via a computer using
appropriate software to produce a 3D map of the
thorax. It allows the operator, via a bronchoscope, to
190
https://t.me/med1917
12
Respiratory system
guide a probe into a diseased area of lung, either for
biopsy to make a diagnosis or to deliver treatment,
such as microwave ablation directly to a tumour.
Pleural aspiration and biopsy
A pleural effusion (Fig. 12.15) can give rise to
diagnostic problems and, sometimes, management
problems when the amount of fluid causes respiratory
embarrassment. When a pleural effusion is seen as a
presenting feature in a middle- aged or older patient,
the most likely cause is a malignancy. Less commonly,
particularly in younger patients, it may be owing
to tuberculosis. In either case, the diagnosis is best
obtained by both aspiration of the fluid and pleural
biopsy. Aspiration alone has a lower diagnostic yield.
After anaesthetizing the skin, subcutaneous tissues
and pleura, pleural fluid may be aspirated by syringe
and needle for microbiological and cytological
examination. Large pleural effusions may need to be
drained by an indwelling catheter, left in situ until
the fluid has been fully removed. As noted above,
ultrasound guidance can be helpful, particularly if
the fluid is loculated in various pockets, and should
be used whenever equipment and trained personnel
are available.
Cytological examination of pleural fluid may
demonstrate the presence of malignant cells.
Many polymorphs may be seen if the effusion is
secondary to an underlying pneumonic infection.
With tuberculosis, the fluid usually contains many
lymphocytes, although tubercle bacilli are rarely
seen. Therefore, all pleural fluid samples should
be cultured for possible tuberculosis, because this
infection can coexist with other pathologies and it
is so important not to miss it. In empyema, pus is
present in the pleural cavity. It has a characteristic
appearance and is full of white cells and organisms.
An indwelling catheter should be left in situ to drain
an empyema when possible.
The pleural fluid should also be examined for
protein content. A transudate (resulting from
cardiac or renal failure) can be distinguished from an
exudate (from pleural inflammation or malignancy)
by its lower protein content (<30 g/l). Light’s criteria
may also be applied (Box 12.20). When infection is
suspected, pleural fluid pH should be measured in
non- purulent effusions and, if not available, pleural
fluid glucose should be assessed. A pH < 7.2 strongly
suggests the need for pleural drainage (pleural
fluid glucose <3.4 mmol/l). Pleural fluid lactate
dehydrogenase (LDH) is also raised in the presence
of infection.
It is recommended that pleural biopsies are
undertaken under CT or ultrasound guidance, where
available, and whilst Abram’s pleural biopsy needles
continue to be used in some centres, they are no
longer the first choice of technique. Samples should
be sent for histological examination, microscopy,
culture and sensitivity (MC&S) and, whenever TB is
a possibility, for AFB staining and TB culture.
Box 12.20
An effusion is exudative if it meets one of the following
criteria:
Pleural fluid protein/serum protein > 0.5
Pleural fluid lactate dehydrogenase (LDH)/serum LDH
ratio > 0.6
Pleural fluid LDH > two- thirds the upper limit of normal
serum LDH
Light’s criteria for diagnosing a pleural effusion
Ridge thoracoscopy and video- assisted
thoracoscopic surgery (VATS)
These techniques enable the pleural cavity to be
examined directly and biopsies taken; VATS is now
becoming the procedure of choice. The ridge method
is normally performed under a general anaesthetic
by a surgeon who uses direct vision down a rigid thoracoscope after the lung has been deflated. Increasingly, however, more minimally invasive procedures
using flexible thoracoscopes attached to cameras are
being used—VATS, and are not only able to biopsy
the pleura but also biopsy the lung, mediastinal
nodes and tumours, decortication of empysemas,
lobectomy and pneumonectomy, pleurodesis and
endoscopic stapled bullectomy (lung volume reduction surgery).
Lung biopsy
As noted above, the technique of transbronchial
biopsy can be used to obtain samples of lung
parenchyma, but often samples are too small for
diagnosis. In this circumstance, biopsies of the lung
taken at thoracoscopy may be of value. Occasionally,
a formal open lung biopsy obtained at thoracotomy
may be necessary.
When there is a discrete, localized lesion, it may
be possible to obtain a biopsy percutaneously with
the aid of CT scanning to direct the insertion of the
biopsy needle (Fig. 12.13). All samples should be
sent for histology, microbiology and TB culture.
Immunological tests
Asthma attacks may be caused by type I immediate
hypersensitivity reactions on exposure to common
environmental proteins known as allergens.
In such individuals, an inherited tendency to
produce exaggerated levels of immunoglobulin
E (IgE) against these allergens is responsible.
Part of the assessment of such allergic patients
might include skin- prick tests (see Chapter 20).
Alternatively, serum levels of specific (individual)
IgEs against allergens may be measured by blood
tests (formerly known as radioallergosorbent
(RAST) tests) to demonstrate sensitization. The
total IgE level is often raised in patients with
asthma, rhinitis or eczema. Delayed (type IV,
cell- mediated) hypersensitivity is shown by the
Mantoux and Heaf skin tests, used to detect the
presence of sensitivity to tuberculin protein.
SECTION THREE
https://t.me/med1917
Respiratory system
191
Figure 12.13 A CT- guided percutaneous biopsy in progress.
The radiodense (white) structure penetrating the chest wall is the
biopsy needle.
Figure 12.14 Chest X- ray showing right apical scarring and
tracheal deviation (detectable clinically) from previous tuberculosis
and hyperinflation of the lungs caused by chronic obstructive
pulmonary disease in a 66- year- old long- term smoker with 5 years
of increasing breathlessness.
Precipitating immunoglobulin G (IgG) antibodies
in the circulating blood are present in patients with
some fungal diseases, such as bronchopulmonary
aspergillosis or aspergilloma. In patients suspected
of having an allergic alveolitis, IgG antibodies may
be demonstrated to the relevant antigens.
Tests for tuberculosis (TB)
Tuberculosis continues to be a worldwide problem,
occurring most frequently as a pulmonary infection,
but also commonly in the lymph nodes, as well as
Figure 12.15 Chest X- ray showing a large left pleural effusion in
a young man with a 4- month history of malaise, fever, night sweats
and weight loss. The diagnosis of tuberculosis was confirmed on
histology of a pleural biopsy and culture of the pleural fluid.
Figure 12.16 Chest X- ray showing a right basal pneumonia
in a previously fit 40- year- old man with fever, breathlessness,
central cyanosis and pleuritic pain. Chest signs included bronchial
breathing and a pleural rub in the right lower zone. The cyanosis
was caused by the shunting of deoxygenated blood through the
consolidated lung, the increased respiratory rate leading to a low
PaCO2 because of increased clearance of carbon dioxide by the
unaffected alveoli. Streptococcus pneumoniae was grown on blood
cultures.
being able to affect any organ of the body. As outlined
above, sending relevant samples for smear and culture
is essential and often forgotten in hospitals where
TB is less common. Sputum can easily be tested by
light microscopy using a Zeihl- Neelsen or auramine
stain to look for the AFB. Where available, culture
192
https://t.me/med1917
12
Respiratory system
should be undertaken as drug monoresistance and
multidrug- resistant TB (MDR TB) continue to be
a major problem in the fight against the infection.
Newer techniques help to diagnose active infection
and drug resistance using molecular methods to
detect Mycobacterium tuberculosis (MTB) complex
DNA (e.g. the polymerase chain reaction (PCR))
assay Xpert® MTB/RIF (Cepheid, California, United
States) and the line probe assay MTBDRplus®
(Hain Lifescience, Nehren, Germany). More
recently whole genome sequencing (WGS) is
replacing routine culture and sensitivity testing to
include different strains of mycobacterium and drug
resistance.
Tests for latent TB and the Heaf and Mantoux
skin tests are still widely used to look for evidence
of previous TB exposure. In many centres, they
are being superseded by blood tests that use the
interferon gamma- releasing assay (IGRA), which
measures interferon gamma released from Tcells activated by the presence of Mycobacterium
tuberculosis. At the present time, the IGRA blood
test does not differentiate between active and
latent TB and should be used only to diagnosis
latent disease. False-negative results can occur in
disseminated and non- pulmonary active disease and
can therefore be misleading when diagnosing active
infection.
SECTION THREE
https://t.me/med1917
BASIC SYSTEMS
Cardiovascular system
Andrew Archbold, Adam Timmis, and Ceri Davies
13
Introduction
Recent decades have seen major changes in
patterns of cardiovascular disease. In the developed
world, syphilitic and tuberculous involvement of
the cardiovascular system has become rare, and
the incidence of rheumatic disease has declined
considerably. Myocardial and conducting tissue
diseases are diagnosed with increasing frequency
and the importance of arterial hypertension has
become recognized. Coronary artery disease has
emerged as the major cardiovascular disorder of the
era, becoming the most common cause of premature
death throughout Europe, North America and
Australasia. In the last 30 years, there has been a
steady fall in age- specific death rates from coronary
artery disease in Western societies, but elsewhere
its prevalence is increasing; in the underdeveloped
world it now threatens to overtake malnutrition and
infectious disease as the major cause of death.
As patterns of cardiovascular disease have changed,
so have the cardiologist’s diagnostic tools, although
a good history and thorough clinical examination
remain cornerstones of the assessment of patients
with cardiovascular disease. A century that started
with the stethoscope, the sphygmomanometer, the
chest X- ray and a very rudimentary electrocardiogram
saw the development of a variety of new imaging
modalities, using ultrasound, radioisotopes, X- rays
and magnetic resonance. This non- invasive capability
was complemented by the introduction of the
catheterization laboratory, permitting angiographic
imaging, electrophysiological recording and tissue
biopsy of the heart. Add to this the resources of
the chemical pathology, bacteriology and molecular
biology laboratories, and the array of diagnostic
technology available to the modern cardiologist
becomes almost overwhelming.
The cardiac history
The history should record details of presenting
symptoms, of which the most common are chest
pain, fatigue and dyspnoea, palpitations, and
presyncope or syncope (see below and Box 13.1).
Previous illness should also be recorded, as it may
provide important clues about the cardiac diagnosis;
thyroid, connective tissue and neoplastic disorders,
for example, can all affect the heart. Rheumatic
fever in childhood is important because of its
association with valvular heart disease, and diabetes
and dyslipidaemias because of their association
with coronary artery disease. Smoking is a major
risk factor for coronary artery disease. Alcohol
abuse predisposes to cardiac arrhythmias and
cardiomyopathy. The cardiac history should quantify
both habits in terms of pack- years smoked and units
of alcohol consumed. The use of other recreational
drugs (in particular cocaine) can be associated with
acute presentations of chest pain and intravenous
drug use is an increasingly important cause of
infective endocarditis.
The family history should always be documented
because coronary artery disease and hypertension
often run in families, as do some of the less common
cardiovascular disorders, such as hypertrophic
cardiomyopathy. Indeed, in patients with
hypertrophic cardiomyopathy, a family history of
sudden death is probably the single most important
indicator of risk. Finally, the drug history should be
recorded, because many commonly prescribed drugs
are potentially cardiotoxic. β- Blockers and some
calcium channel blockers (diltiazem, verapamil),
for example, can cause symptomatic bradycardias,
and tricyclic antidepressants and β agonists can
cause tachyarrhythmias. Vasodilators cause variable
reductions in blood pressure, which can lead to
syncopal attacks, particularly in patients with aortic
stenosis. The myocardial toxicity of certain cytotoxic
drugs (notably doxorubicin and related compounds)
is an important cause of cardiomyopathy.
Chest pain
Myocardial ischaemia, pericarditis, aortic dissection
and pulmonary embolism are the most common
causes of acute, severe chest pain. Chronic, recurrent
chest pain is usually caused by angina, oesophageal
reflux or musculoskeletal pain.
Myocardial ischaemia
Ischaemia of the heart results from an imbalance
between myocardial oxygen supply and demand,
194
https://t.me/med1917
13
Cardiovascular system
Box 13.1
Presenting complaint (PC)
The symptom that prompts the patient to seek medical
History of presenting complaint (HPC)
This should define the nature of the symptoms, initially
− Chest pain: site, radiation, character, duration,
− Breathlessness: orthopnoea, paroxysmal nocturnal
− Palpitation: sudden onset and offset, ‘thumps’ or
− Dizziness/syncope: provoking factors, warning,
Risk factors for cardiovascular disease
Smoking, hypertension, hypercholesterolaemia, diabetes,
Past medical history (PMH)
Stroke or transient ischaemic attack (TIA), renal
Operations, hospital clinic attendances
Family history
Cardiac disease, sudden death
Drug history
Include quantification of alcohol intake
If a patient with known cardiovascular disease is not
producing pain called angina (Boxes 13.2 and 13.3).
Angina is usually a symptom of atherosclerotic
coronary artery disease, which impedes myocardial
oxygen supply. Other causes of coronary artery
disease (Box 13.4) are rare. However, it is important
to be vigilant for causes of angina owing to increased
myocardial oxygen demand, such as aortic stenosis.
The history is diagnostic for angina if the location
of the pain, its character, its relation to exertion
and its duration are typical. The patient describes
retrosternal pain, which may radiate into the arms,
the throat or the jaw. It has a constricting character,
is provoked by exertion and relieved within minutes
by rest. The patient’s threshold for angina is typically
reduced after eating or in cold weather owing to
the diversion of blood to the gut and the increased
myocardial work consequent upon peripheral
vasoconstriction, respectively. Occasionally angina is
Structure for the cardiac history
attention—commonly chest pain, breathlessness
(dyspnoea), palpitation, dizziness or blackouts (syncope)
through open questioning. Closed questions are used to
elicit the presence or absence of features which help to
differentiate between diagnoses:
provoking and relieving factors, associated
symptoms?
dyspnoea, ankle swelling, cough, wheeze,
haemoptysis?
‘pauses’, presyncope or syncope?
duration, recovery?
family history of premature vascular disease
impairment, rheumatic fever, peripheral vascular
disease, other
taking the recognized standard treatment, the reason
for this should be established. For example, why no
statin treatment in a patient with previous myocardial
infarction?—‘Because it caused muscle pains’.
Box 13.2
Typical patient
Middle- aged or elderly man or woman often with a family
history of coronary heart disease and one or more of the
major reversible risk factors (smoking, hypertension,
hypercholesterolaemia, diabetes)
Major symptoms
Exertional chest pain and shortness of breath. Pain often
described as ‘heaviness’ or ‘tightness’, and may radiate into
arms, neck or jaw. Pain comes predictably after exertion
Major signs
None, although hypertension and signs of
hyperlipidaemia (xanthelasmata, xanthomas) may be
present
Peripheral vascular disease, evidenced by absent pulses
or arterial bruits, is commonly associated with coronary
heart disease
Diagnosis
Typical history is most important diagnostic tool
Electrocardiogram (ECG): often normal; may show Q
waves in patients with previous myocardial infarction
Exercise ECG test: exertional ST depression
Isotope or magnetic resonance perfusion scan: stress-
induced perfusion defects
Coronary angiogram: confirms coronary artery disease
Additional investigations
Blood sugar and lipids to rule out diabetes and
dyslipidaemia
Comments
A careful history is the single most important means of
diagnosing angina
Box 13.3
Impaired myocardial oxygen supply
Coronary artery disease:
− atherosclerosis
− arteritis in connective tissue disorders
− diabetes mellitus
Coronary artery spasm
Congenital coronary artery disease:
− arteriovenous fistula
− anomalous origin from pulmonary artery
Severe anaemia or hypoxia
Increased myocardial oxygen demand
Left ventricular hypertrophy:
− hypertension
− aortic valve disease
− hypertrophic cardiomyopathy
Tachyarrhythmias
Angina
Causes of angina
SECTION THREE
https://t.me/med1917
Cardiovascular system
195
Box 13.4
Atherosclerosis
Arteritis:
− systemic lupus erythematosus
− polyarteritis nodosa
− rheumatoid arthritis
− ankylosing spondylitis
− syphilis
− Takayasu’s disease
Coronary dissection:
− spontaneous
− catheter or angioplasty induced
Embolism:
− infective endocarditis
− left atrial/ventricular thrombus
− left atrial/ventricular tumour
− prosthetic valve thrombus
− paradoxical embolism
− complication of cardiac catheterization
Coronary mural thickening:
− amyloidosis
− radiation therapy
− Hurler’s disease
− pseudoxanthoma elasticum
Other causes of coronary luminal narrowing:
− aortic dissection
− coronary spasm
Congenital coronary artery disease:
− anomalous origin from pulmonary artery
− arteriovenous fistula
provoked only by the first significant activity of the
day, a phenomenon known as the ‘warm- up effect’,
which is caused by myocardial preconditioning. Less
commonly, myocardial ischaemia may manifest as
breathlessness, fatigue or symptoms that the patient
finds difficult to describe—‘I just have to stop’—in
which case the clues to the diagnosis are the relation
of the symptoms to exertion, the presence of risk
factors for coronary artery disease and the absence
of an alternative explanation for the symptoms, such
as heart failure.
Causes of coronary artery disease
Acute coronary syndromes
In acute coronary syndromes, which are lifethreatening cardiac emergencies, the pain is similar
in location and character to angina, but is usually
more severe, more prolonged and unrelieved by rest
(Box 13.5).
Pericarditis
Pericarditis causes central chest pain, which is sharp
in character and aggravated by deep inspiration,
cough or postural changes. Characteristically, the
pain is exacerbated by lying recumbent and reduced
by sitting forward. Pericarditis is usually idiopathic
or caused by Coxsackie B infection. It may also
Box 13.5
Typical patient
Middle- aged (male) or elderly (either sex) patient, often
with a family history of coronary artery disease and one
or more of the major reversible risk factors (smoking,
hypertension, hypercholesterolaemia, diabetes). Care
must be taken in female patients: coronary artery disease
occurs frequently and is often under-diagnosed.
In many patients, there is no preceding history of angina.
Major symptoms
Chest pain and shortness of breath. Pain usually
prolonged and often described as ‘heaviness’ or
‘tightness’, with radiation into arms, neck or jaw.
Alternative descriptions include ‘congestion’ or ‘burning’,
which may be confused with indigestion.
Major signs
Frequently none
Autonomic disturbance, sweating, vomiting – implies
myocardial infarction
Tachycardia (anterior myocardial infarction), bradycardia
(inferior myocardial infarction)
Fourth heart sound, dyskinetic precordial impulse,
pulmonary oedema with large infarcts
Diagnosis
(STEMI = ST elevation myocardial infarction)
Acute coronary syndromes
Unstable
STEMI Non- STEMI
ECG ST
elevation
Cardiac
biomarkers
(e.g. troponin
I or T)
Additional investigations
Biochemistry: blood sugar and lipids to rule out diabetes
and dyslipidaemia
Risk stratification: echocardiogram (left ventricular
function), coronary angiogram in high- risk patients,
perfusion imaging in low- risk patients
Comments
History and troponin testing most useful diagnostic tools
in non- ST elevation acute coronary syndromes
occur as a complication of myocardial infarction,
but other causes are seen less commonly (Box
13.6). Myocardial involvement—myocarditis—
is increasingly recognized. It is associated with
the release of cardiac enzymes and abnormalities
on the electrocardiogram (ECG) that can be
indistinguishable from myocardial infarction.
Raised Raised Normal
Normal, ST
depression,
T- wave
inversion
angina
Normal, ST
depression,
T- wave
inversion
Aortic dissection
Aortic dissection produces severe tearing pain in
either the front or the back of the chest. The onset
196
https://t.me/med1917
13
Cardiovascular system
Box 13.6
Idiopathic
Infective:
− viral (Coxsackie B, influenza, herpes simplex)
− bacterial (Staphylococcus aureus, Mycobacterium
Connective tissue disease:
− systemic lupus erythematosus
− rheumatoid arthritis
− polyarteritis nodosa
Uraemia
Malignancy (e.g. breast, lung, lymphoma, leukaemia)
Radiation therapy
Acute myocardial infarction
Post- myocardial infarction/cardiotomy (Dressler’s
syndrome)
Box 13.7
Typical patient
Middle- aged or elderly patient with a history of
Occasionally younger patient with aortic root disease
Major symptoms
Chest pain, typically interscapular
Major signs
Often none
Sometimes regional arterial insufficiency (e.g. occlusions
Diagnosis
Chest X- ray: widened mediastinum, occasionally with left
Transoesophageal echocardiogram, computed
Comments
Type A dissections involve the ascending aorta and are
is abrupt, unlike the crescendo quality of ischaemic
cardiac pain (Box 13.7).
Causes of acute pericarditis
tuberculosis)
Aortic dissection
hypertension or arteriosclerotic disease
(e.g. Marfan’s syndrome)
of coronary artery causing myocardial infarction, carotid
or vertebral artery causing stroke, spinal artery causing
hemi- or quadriplegia, renal artery causing renal failure);
subclavian artery occlusion may cause differential blood
pressure in either arm; aortic regurgitation; cardiac
tamponade; sudden death.
pleural effusion
tomography (CT) scan or magnetic resonance imaging
(MRI) scan: confirms dissection
usually treated surgically. Type B dissections involve the
arch and/or descending aorta and are usually managed
medically or with an endovascular stent.
Pulmonary embolism
Peripheral pulmonary embolism causes suddenonset sharp, pleuritic chest pain, breathlessness and
haemoptysis. Major, central pulmonary embolism
Box 13.8
Typical patient
Recent surgery, lower limb fracture or long- distance air
travel; obese; sedentary; heart failure; malignancy
Major symptoms
Chest pain, dyspnoea, haemoptysis, syncope
Major signs
Peripheral emboli: pleural rub
Large, central emboli: tachycardia, hypotension,
cyanosis, raised jugular venous pressure (JVP)
Diagnosis
D- Dimer: a negative D- dimer in a low- risk patient makes
pulmonary embolism very unlikely.
ECG: sinus tachycardia; right bundle branch block
(RBBB); classic ‘S1, Q3, T3’ pattern uncommon
Chest X- ray: normal; wedge- shaped peripheral
opacification; absent pulmonary vascular markings
Echocardiogram: dilated right heart in some cases of
large central pulmonary embolism
CT pulmonary angiogram: has superseded V/Q scanning
as the diagnostic test of choice.
Comments
Suspect pulmonary embolism in patients with
unexplained hypoxia. Thrombolytic therapy should
be considered for patients with pulmonary embolism
associated with shock and/or a dilated right heart
on echo. Patients with no risk factors for pulmonary
embolism should be investigated for prothrombotic
states.
presents with breathlessness, chest pain that can
be indistinguishable from ischaemic chest pains
and syncope. Risk factors for pulmonary embolism
should be sought in the history (Box 13.8).
Rare cardiovascular causes of chest pain include
mitral valve disease associated with massive left
atrial dilatation. This causes discomfort in the back,
sometimes associated with dysphagia owing to
oesophageal compression. Aortic aneurysms can also
cause pain in the chest owing to local compression.
Pulmonary embolism
Dyspnoea
Dyspnoea is an abnormal awareness of breathing
occurring either at rest or at an unexpectedly low
level of exertion. It is a major symptom of many
cardiac disorders, particularly left heart failure
(Table 13.1), but its mechanisms are complex. In
acute pulmonary oedema and orthopnoea, dyspnoea
is caused mainly by elevated left atrial pressure
that characterizes left heart failure (Box 13.9). This
produces a corresponding elevation of the pulmonary
capillary pressure and increases transudation into
the lungs, which become oedematous and stiff.
Oxygenation of blood in the pulmonary arterioles
is reduced, causing hypoxaemia, and this, together
Соседние файлы в папке Библиотека им академика М.И. Перельмана