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
left subclavian artery. The condition is a cause of secondary
hypertension. It encourages the formation of a collateral arterial circulation involving the intercostal arteries. In 30% of
patients, there is an associated bicuspid aortic valve.
In adults the condition is often asymptomatic until long-standing hypertension becomes apparent. When
present, symptoms include headache, left ventricular failure, stroke and endocarditis. On examination the femoral
pulses are weak or absent and there is radiofemoral delay.
The upper limbs may be hypertensive or have unequal BP,
and the lower limbs have a low BP. There may be features of
left ventricular hypertrophy. There is a mid-systolic or latesystolic murmur over the upper praecordium or back due to
turbulent flow through the coarctation. Collateral murmurs
may be heard over the scapulae, and there may be an aortic
systolic murmur of an associated bicuspid valve.
There may be left ventricular hypertrophy on ECG,
and CXR shows tortuous and dilated collaterals that may
erode the under surface of the ribs to produce ‘rib notching’. There may be a double aortic knuckle due to stenosis
and poststenotic dilatation. Cardiomegaly may indicate left
ventricular enlargement. MRI and aortography confirm
the diagnosis.
Treatment is by surgical resection or balloon angioplasty.
Aortic and pulmonary stenosis
Clinical features and management of aortic stenosis have
been covered previously in this chapter. The commonest
congenital abnormality is a bicuspid valve (1%–2%) which
results in chronic turbulent flow leading to calcification of
the leaflets. Supravalvular aortic stenosis is associated with
Williams syndrome.
Pulmonary stenosis is rare and often asymptomatic until severe. Patients can present with exertional dyspnoea,
light-headedness and symptoms of right-sided heart failure. It is associated with Noonan syndrome and Alagille
syndrome. In general, invasive intervention is recommended (valvotomy is very effective).
Cyanotic conditions
Tetralogy of Fallot
This represents 6%–10% of cases of congenital heart disease. The four features composing the tetrad are:
• VSD;
• right ventricular outflow obstruction (pulmonary
stenosis—infundibular or valvar);
• the aorta being positioned over the ventricular septum
(‘overriding aorta’);
• right ventricular hypertrophy.
Because there is right ventricular outflow obstruction, the
shunt through the VSD is from right to left. This results in
central cyanosis.
Children may present with deep cyanosis and syncope. Squatting helps to decrease the right-to-left shunt
by increasing systemic resistance. Signs include cyanosis
and finger clubbing. There is a parasternal heave and systolic murmur in the pulmonary area (second left intercostal space), P2 is soft or absent, and there may be growth
retardation.
ECG features include right atrial and ventricular hypertrophy. The heart is boot-shaped (coeur en sabot) and
the pulmonary artery is small with oligaemic lung fields.
Echocardiography can be diagnostic, but it may be necessary to proceed to cardiac catheterization studies to confirm
the disorder.
Management is by total surgical correction. Palliative
procedures as holding measures can be used (e.g. the modified Blalock–Taussig shunt, which produces an anastomosis
between a subclavian artery and a pulmonary artery to increase pulmonary blood flow).
Chapter Summary
• Cardiovascular disease (CVD) is one of the biggest killers in the United Kingdom.
Modifiable risk factors include hypertension, diabetes mellitus, obesity and smoking. It
can present as stable angina or acute coronary syndrome. Both of those syndromes
result from inadequate oxygenation of the cardiac muscle.
• Drug treatments for CVD include antiplatelet agents, nitrates, β-blockers, calcium
channel blockers, potassium channel activators, angiotensin-converting enzyme (ACE)
inhibitors and lipid-lowering drugs.
• Acute coronary syndrome is a medical emergency that includes ST elevation myocardial
infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI) and unstable angina.
It usually results from atherosclerotic plaque rupture. If STEMI is present, urgent
percutaneous coronary intervention should be undertaken if it can be delivered within 120
minutes of the time when fibrinolysis could be given. Revascularization can be delayed in
NSTEMI unless patients have an immediate or higher risk of death or future
cardiovascular events (calculated by an established scoring system such as the Global
Registry of Acute Cardiac Events score).
198
Further reading
• Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia. Causes can
include CVD, valvular disease, infection or electrolyte disturbances. Two approaches to
treatment exist: rate control and rhythm control. Generally, rate control is recommended
as the first-line option unless the patient has a reversible cause of the arrhythmia, the
patient has heart failure, the AF is of new onset or rhythm control is deemed more
suitable. Anticoagulation should be considered in all patients with AF.
• Heart failure is a clinical syndrome where the heart cannot meet the demands placed on it
by the body. It can present as an acute problem or it can be of chronic nature. Acute heart
failure is a medical emergency. ACE inhibitors and diuretics are the mainstay of treatment.
β-Blockers are used in chronic heart failure. Nondrug treatments include implantable
cardiac devices.
• Hypertension can be essential (no underlying cause identified) or secondary (to, e.g.
kidney or heart disease). Treatment includes a stepwise approach of introduction of drugs
depending on the patient’s age and ethnicity. Patients older than 55years and all black
people of African or Caribbean family origin should initially be given calcium channel
blockers. All other patients should be given an ACE inhibitor first.
• Rheumatic fever is the most common cause of mitral stenosis. Aortic stenosis is usually
the result of a calcified bicuspid valve.
• Pericarditis can lead to the development of cardiac tamponade. Cardiac tamponade is a
medical emergency. Treatment is with pericardiocentesis.
• Hypertrophic obstructive cardiomyopathy is an autosomal dominant genetic disorder
that leads to left ventricular hypertrophy and cardiac dysfunction. Patients are at risk of
sudden cardiac death.
• Staphylococcus aureus is the commonest pathogen responsible for infective
endocarditis. Modified Duke criteria are used for diagnosis.
• Rheumatic fever is a multisystem immune disease that follows an infection with a group A
β-haemolytic streptococcus.
2727
FURTHER READING
British Heart Foundation: https://www.bhf.org.uk.
The American College of Cardiology publishes guidelines and re-
views on all aspects of cardiology. They are available on its web-
site: www.acc.org.
NICE, 2016. Chest pain of recent onset: assessment and diagnosis.
NICE, 2013a. Myocardial infarction with ST-segment elevation:
acute management.
NICE, 2013b. Unstable angina and NSTEMI: early management.
NICE, 2016a. Stable angina: management.
NICE, 2016b. Cardiovascular disease: risk assessment and reduc-
tion, including lipid modification.
NICE, 2016c. Chest pain of recent onset: assessment and diagnosis.
NICE, 2014. Acute coronary syndromes in adults.
Thygesen, K., Alpert, J.S., Jaffe, A.S., Simoons, M.L., etal., 2012.
Third universal definition of myocardial infarction. J Am Coll
Cardiol 60 (16), 1581–1598.
NICE, 2014a. Atrial fibrillation: management.
NICE, 2014b. Acute heart failure: diagnosis and management.
NICE, 2010. Chronic heart failure in adults: management.
NICE, 2016. Hypertension in adults: diagnosis and management.
199
This page intentionally left blank
VQ/
( )
Respiratory system
28
RESPIRATORY FAILURE
General overview
Respiratory failure is defined as dysfunction of gas exchange resulting in abnormalities of oxygenation or ventilation, leading to hypoxia (low blood oxygen levels) and/or
hypercapnia (high blood carbon dioxide levels).
Respiratory failure is said to be present in a patient
breathing air at sea level when the oxygen partial pressure in arterial blood (Pa2) is less than 8.0 kPa. If hypoxia
is combined with a normal or low CO2 partial pressure
(Pa2), this is type I (hypoxaemic) respiratory failure. The
primary cause of type I respiratory failure is ventilation–
perfusion
with a raised Pa2 (>6.0 kPa), type II (hypercapnic) respiratory failure is present. The underlying cause of type II
respiratory failure is alveolar hypoventilation, with or without
gradient). Measurement of arterial blood gas (ABG) is essential to the diagnosis of respiratory failure.
ventilation by central stimulation of the respiratory centres
in the medulla, resulting in an increase in minute ventilation to lower Pa2. In type II respiratory failure, this mechanism fails, and there is effective alveolar hypoventilation.
This can be due to several causes (see later).
of as those due to hypoxaemia (present in both type I and
type II) and those due to hypercapnia (type II). Hypoxia
causes dyspnoea, restlessness, central cyanosis and eventually impaired consciousness. Hypercapnia causes headache,
tachycardia with bounding pulse, tremor and clouding of
consciousness.
• Full blood count (FBC): look for anaemia,
• Chest X-ray (CXR); CT pulmonary angiogram (CTPA)
• Sputum microscopy, culture and sensitivities.
• Spirometry.
The course of the disease and its prognosis depend to a
great extent on the underlying disorder and the premorbid
condition of the patient.
mismatch (see also clinical notes: alveolar-arterial
In a healthy person a rise in Pa2 causes an increase in
The clinical features of respiratory failure can be thought
Investigations useful in respiratory failure include:
polycythaemia, leucocytosis; ABG; urea and
electrolytes (U&Es); C-reactive protein (CRP); blood
cultures if the patient is pyrexial.
if pulmonary embolism (PE) is suspected.
mismatch. When hypoxia is combined
CLINICAL NOTES
ALVEOLAR–ARTERIAL GRADIENT
Alveolar–arterial (A–a gradient) is a measure
used to determine the origin of hypoxemia
(intrapulmonary or extrapulmonary). It is the
difference between the alveolar (A) and arterial
(a) oxygen concentration. It is calculated from
the following formula: A–a Gradient = [(Fio2) ×
(Atmospheric Pressure − H2O Pressure)
− (Paco2/0.8)] − Pao2.
Elevated A–a gradient indicates
shunt or alveolar hypoventilation as the cause of
hypoxaemia, whereas a depressed A–a gradient
points towards hypoventilation or low inspired
oxygen levels.
mismatch,
Type I respiratory failure
Causes
Type I respiratory failure can occur as a result of:
• low inspired oxygen concentration (Fi2), for example
at high altitude.
•
• shunt, for example right-to-left shunt where mixing
• alveolar hypoventilation (e.g. neuromuscular disorders
• altered gas diffusion (e.g. pneumonia, acute respiratory
Management
The main therapeutic objective in acute hypoxaemic respiratory failure is to ensure oxygen delivery to vital organs.
Hypoxia is life-threatening, and oxygen therapy is indicated
to maintain saturations of more than 90% (Pa2 > 8 kPa).
Although high concentrations of inspired oxygen (Fi2 >
50%) are safe in patients with type I respiratory failure, pulmonary oxygen toxicity is a risk if the Fi2 remains above
60% for more than 48 hours continuously. The British
Thoracic Society (BTS) recommends an upper limit of 98%
for oxygen saturations for most patients.
mismatch (e.g. PE, atelectasis).
of oxygenated and nonoxygenated blood occurs (e.g.
patent foramen ovale, atrial septal defects).
causing respiratory muscle weakness, chest wall
deformity, interstitial lung disease (ILD)).
distress syndrome (ARDS), pulmonary fibrosis).
201
Respiratory system
Assisted ventilation may be necessary (clinical notes:
assisted ventilation). Noninvasive ventilation reduces morbidity and mortality in selected patients. Continuous positive airway pressure (CPAP) is particularly useful in type I
respiratory failure.
Assisted ventilation is associated with airway and alveolar damage through mechanisms such as oxygen toxicity,
volutrauma (overstretching), barotrauma (over pressure),
biotrauma (shear forces) and cardiac overstimulation.
Therapeutic objectives include:
• specific therapy of the underlying cause (e.g.
antimicrobial therapy for pneumonia, bronchodilators
and steroids for asthma or chest drain insertion for
pneumothorax).
• general supportive care: adequate hydration, nutrition and
electrolyte balance and endotracheal intubation if needed.
CLINICAL NOTES
ASSISTED VENTILATION
‘Assisted ventilation’ describes the delivery
of ventilatory support to assist or replace
spontaneous respiration.
Modes of assisted ventilation include:
• Noninvasive ventilation: without the use of an
invasive artificial airway.
• High-flow nasal oxygen: heated, humidified,
high-flow oxygen is delivered through nasal
cannula, facilitating gas exchange. Fio2 achieved
can be as high as 100% in a flow of up to 60 L/
min. Generated positive end-expiratory pressure
impedes atelectasis and reduces the work
of breathing. It is well tolerated by patients.
Impaired respiratory drive is a contraindication
to its use.
○
Continuous positive airway pressure (CPAP):
continuous positive pressure is delivered
through all phases of ventilation, facilitating
oxygenation. It promotes alveolar opening,
increases the functional residual capacity
and reduces left ventricular transmural
pressure, increasing cardiac output. CPAP
is particularly useful in obstructive sleep
apnoea and congestive cardiac failure. Care
should be taken in patients with low blood
pressure as CPAP reduces venous return.
○
Bilevel positive airway pressure: this pressure-
limited ventilation delivers inspiratory positive
airway pressure and expiratory positive airway
pressure. ‘Expiratory positive airway pressure’
is synonymous with ‘positive end-expiratory
pressure’. This cyclical mode of ventilation
facilitates CO2 clearance and airway
opening and reduces the work of breathing.
It is particularly useful in CO2 retention or
chronic obstructive pulmonary disease. High
expiratory positive airway pressure reduces
preload and therefore decreases stroke
volume.
• Invasive ventilation: support is administered with
the use of an invasive artificial airway. This can
be penetrating through the nose (nasotracheal),
mouth (endotracheal) or skin (tracheostomy).
Type II respiratory failure
Causes
Type II respiratory failure can occur as a result of:
• reduced breathing effort, including reduced central
drive (e.g. sedation and brainstem disorders, obesity,
drugs).
• neuromuscular disease (e.g. Guillain–Barré
syndrome, motor neurone disease, spinal cord lesions,
poliomyelitis, myasthenia gravis and diaphragmatic
palsy).
• thoracic wall abnormalities (e.g. kyphoscoliosis).
• increased airway resistance (e.g. asthma, chronic
obstructive pulmonary disease (COPD), pneumonia
and lung fibrosis).
Management
As in type I failure, ensuring adequate oxygenation is key.
However, care must be taken when high oxygen concentrations are being delivered to patients with chronic type II
respiratory failure who rely on their hypoxic drive for ventilation because of chronic CO2 retention.
Oxygen therapy must be carefully controlled. Venturi
masks, which deliver a fixed oxygen concentration, are used
to maintain oxygen saturations of 88%–92% (target saturation for patients at risk of CO2 retention). Oxygen concentration is titrated to achieve normoxaemia without acidosis.
(See BTS Guideline for oxygen use in adults in healthcare
and emergency settings. May 2017.)
Other therapeutic objectives include:
• specific therapy of the underlying cause (e.g.
antimicrobial and bronchodilator therapy for an
infective exacerbation of COPD).
• general supportive care as for type I failure.
HINTS AND TIPS
Always note the inspired oxygen concentration
when you are taking an arterial blood gas sample.
202
Asthma
2828
ASTHMA
General overview
Asthma is a disease of the airways characterized by an increased responsiveness of the tracheobronchial tree to many
different stimuli, resulting in paroxysmal reversible airway
obstruction. It manifests itself as episodes of shortness of
breath, cough, chest tightness and wheeze. These symptoms
may resolve spontaneously or may be relieved by treatment.
Asthma is episodic, with acute exacerbations interspersed by symptom-free periods. Most attacks are short
(minutes to hours), with complete clinical recovery.
In severer asthma, patients can experience some degree
of airway obstruction daily, with accompanying symptoms.
Asthma is common, with a prevalence of approximately
12% of the population in the United Kingdom. The incidence is higher in children. There are no major sex differences. In the United Kingdom, more than 1000 people die
of acute asthma attacks every year.
Aetiology
Asthma is likely to be a combination of multiple environmental and genetic factors.
Many people with asthma are atopic, with the production
of IgE in response to an antigenic challenge. Atopic asthma
can be associated with a personal or family history of allergy
such as hay fever, urticaria and eczema. There may also be
increased levels of IgE in the serum and a positive response to
provocation tests (e.g. histamine or methacholine challenge).
‘Intrinsic asthma’ is a term used to describe patients with
no personal or family history of allergy, negative skin test
results and normal serum levels of IgE. Many develop typical symptoms following an upper respiratory tract infection.
Many patients do not fit into either category but fall into
a group with a mixture of allergic and nonallergic features.
Pathophysiology
Many theories and mediators are proposed regarding the
mechanisms for asthma. The role of IgE, various cytokines and
chemokines, mast cells, histamine, eosinophils, leucotrienes,
cell adhesion molecules and activated T lymphocytes—in
particular the balance between Th1 and Th2 cells—provides
much academic debate and has provided new therapeutic targets such as monoclonal antibodies against IgE.
The clinical features of asthma probably derive from
chronic airway inflammation causing denuded airway epithelium, inflammatory cell infiltrate, mast cell activation
and smooth muscle and mucous gland hypertrophy.
The two main pathophysiological events responsible
for acute asthma exacerbations are bronchospasm (smooth
muscle spasm leading to airway narrowing) and airway
plugging secondary to excessive secretions. Vascular congestion and oedema formation are also involved.
A number of factors interact with normal airway respon-
siveness and provoke acute episodes, including:
• allergens (e.g. house dust mites and animal dander);
• drugs (e.g. β-blockers and nonsteroidal
antiinflammatory drugs);
• environmental factors (e.g. climatic conditions and air
pollution);
• occupations (e.g. exposure to industrial chemicals,
drugs, metals, dusts);
• infections (e.g. viral and bacterial);
• exercise;
• emotion;
• cigarette smoke.
Clinical features
The classic symptoms of asthma consist of shortness of breath,
wheeze, chest tightness and cough. In its most typical form,
asthma is an episodic disease and the symptoms coexist.
At the onset of an attack, patients experience tightness in
the chest, often with a nonproductive cough. Breathing becomes audibly harsh, speech is difficult, wheezing becomes
prominent and expiration is prolonged as airflow is reduced.
Patients are frequently tachypnoeic and tachycardic. If the
attack is severe or prolonged, there may be a loss of breath
sounds, and the wheeze becomes either very high-pitched or
inaudible as airflow is severely compromised. Accessory muscles of respiration are used, and pulsus paradoxus can develop.
Less typically, a patient with asthma may present with intermittent episodes of nonproductive cough or shortness of
breath on exertion. Such patients often have normal physical examination findings but may wheeze after repeated
forced exhalations or may show evidence of airway obstruction with spirometry.
Nocturnal symptoms (e.g. waking up short of breath,
coughing or wheezing) are very common features.
Investigations
The diagnosis of asthma is established by demonstration of
reversible expiratory airflow obstruction. NICE recommends
different investigations that can be used. These include:
bronchodilator reversibility (BDR) test – in adults positive
if improvement in the forced expiratory volume in 1 second
(FEV1) of 12% or more and increase in volume of 200ml or
more is observed following administration of a β2-agonist;
fractional exhaled nitric oxide [FeNO] test, used to measure
the level of airway inflammation – in adults positive if a result of 40 parts per bilion (ppb) or more is obtained; peak
expiratory flow rate (PEFR) diurnal variation – positive if
variability is greated than 20% on more than 3 days in a week
for 2 weeks; obstructive spirometry showing FEV1/FVC ratio of less than 70%; and direct bronchial challenge test with
histamine or methacholine - positive if provocative concentration of methacholine causing a 20% fall in FEV1 (PC20) is
8 mg/ml or less. Notably, in asymptomatic patients, normal
203
Respiratory system
spirometry findings do not exclude asthma. Once the diagnosis has been confirmed, measurement of PEFR at home,
or FEV1 in the clinic, can be used to monitor the course of
the illness and the effectiveness of therapy. Eosinophilia and
high serum IgE levels may be supportive but are not specific
for asthma and are not recommended. Very high serum IgE
levels or eosinophilia is not typical for asthma and may indicate asthma plus another diagnosis (e.g. allergic bronchopulmonary aspergillosis (ABPA)).
CLINICAL NOTES
DIFFERENTIAL DIAGNOSIS OF ASTHMA
In a small minority of patients, the diagnosis can
cause some difficulty and differential diagnoses
should be considered:
• chronic obstructive pulmonary disease;
• upper airway obstruction: tumour, vocal cord
dysfunction and laryngeal oedema;
• endobronchial disease: foreign body aspiration,
neoplasm, bronchial stenosis;
• left ventricular failure;
• carcinoid tumours;
• recurrent pulmonary emboli;
• eosinophilic pneumonia;
• systemic vasculitis with pulmonary involvement.
Management
Chronic asthma requires long-term management (see BTS/
Scottish Intercollegiate Guidelines Network asthma guideline,
September 2016; NICE, 2017. Asthma: diagnosis, monitoring
and chronic asthma management). A patient-centred model
of care, which should characterize supporting all patients with
a chronic illness, should be applied (i.e. patient education and
empowerment, pharmacological therapy and a multidisciplinary approach in hospital and in the community).
The therapeutic targets of medications used for asthma
include:
• drugs that inhibit smooth muscle contraction (e.g. β2agonists, anticholinergics and methylxanthines such as
theophylline)
• drugs that prevent or reverse airway inflammation (e.g.
corticosteroids and mast cell stabilizing agents)
• drugs that modify the action of leucotrienes (e.g.
leucotriene antagonists or 5-lipoxygenase inhibitors)
Emergency management
Emergency treatment of acute asthma is one of the most
common emergencies seen in medical practice. Senior help
should be involved early.
Features indicating severe asthma include the inability to
speak in sentences, tachypnoea, tachycardia, PEFR less than
50%, low oxygen saturations, the use of accessory muscles
of respiration (sternocleidomastoid, scalene muscles), quiet
chest, cyanosis and a tiring patient. Measurements of ABGs
and PEFR or FEV1 help in assessing the severity and will
guide management. The approach to assessment and treatment of these patients is summarized in Table28.1.
Table28.1 Checklist for the emergency assessment and
treatment of acute severe asthma
Tasks to consider Comment
Assessment Clinical features indicating severe
Immediate
treatment
Criteria for
hospital
admission
attack:
• inability to speak sentences in
one breath
• respiratory rate >25/min
• heart rate >110 bpm
• peak flow rate 33%–50% best or
predicted
Features indicating life-threatening
attack:
• peak expiratory flow rate <33%
best or predicted
• oxygen saturation <92%
• Pao2 <8 kPa
• Paco2 normal or high
• cyanosis
• poor respiratory effort and silent
chest
• confusion, coma or exhaustion
High concentration of oxygen—aim
for saturations of 94%–98%
Back to back nebulized salbutamol
(5 mg) with ipratropium bromide
(500 μg) if severe attack. Use
oxygen-driven nebulizers if
possible
Systemically acting corticosteroids
(hydrocortisone 100 mg IV or
prednisolone 40–50 mg orally)
Magnesium sulphate intravenously
as a bronchodilator (1.2–2 g
intravenously over 20 min)
Intravenous bronchodilators
(aminophylline or salbutamol)
Any life-threatening attack
All severe attacks that do not
respond to initial treatment
If peak expiratory flow rate >75%
best 1 hour after treatment,
consider discharge from the
accident and emergency
department
Consider short-stay observation
wards for other patients
Do not discharge patients in the
late evening if the presentation was
recent, and they are apparently
better as they may have an early
morning dip unless they are
completely better!
204
Asthma
2828
Table28.1 Checklist for the emergency assessment and
treatment of acute severe asthma—Cont’d
Tasks to consider Comment
Referral to
intensive care
Further
investigations
Duration of
hospital stay
Drugs on
discharge
Treatment
changes on
discharge
ABG, Arterial blood gas; CXR, chest X-ray; ECG,
electrocardiogram; FBC, full blood count; PaCo2, partial pressure
of carbon dioxide; Po2, partial pressure of oxygen; U&Es, urea
and electrolytes.
Persisting or worsening hypoxia
Worsening peak flow despite treatment
Exhaustion, poor respiratory effort
Hypercapnia or acidosis on ABG
measurements
Coma or respiratory arrest
CXR (not routine):
• if severe or life-threatening attack
• if other disease is considered
(pneumothorax, consolidation)
Regular ABG measurements
(irrespective of pulse oximetry
saturations)
FBC, U&Es, ECG (older patients)
Until symptoms and lung function
are stable
Peak expiratory flow rate >75% at
best or predicted
Peak expiratory flow rate diurnal
variation <25%
No nocturnal symptoms
Oral steroids for 1–3weeks
Inhaled steroid therapy
Inhaled short-acting β2-agonist
Other medications as per stepwise plan
Taking inhaled medications (no
nebulizers) for 24–48 hours before
discharge
GP review within 48 hours of discharge
Inhaler technique reviewed
Appropriate lifestyle advice given
Clinic follow up arranged
Patient action plan to promote
self-management
Drug level monitoring if needed
Long-term management
The aim of management is control of the disease. Patient education, enabling self-management, is essential and involves
identifying triggers and avoiding precipitants (e.g. smoking), monitoring the severity of the illness (PEFR diaries),
adherence to medication and regular multidisciplinary
reviews.
HINTS AND TIPS
If asthma control is poor, do not forget to assess
inhaler technique.
Drug therapy should be kept as simple as
possible. Many patients find the division of
drugs into ‘preventers’ and ‘relievers’ useful to
understand their disease and its treatment. A
stepwise approach to management of asthma
is recommended. The British Thoracic Society
guidelines are summarized in Table28.2. Treatment
is stepped up when symptoms (e.g. nocturnal
wakening, morning dips) are not controlled. Shortacting β2-agonists are the first step, then inhaled
corticosteroids, which can then be combined
with long-acting β2-agonists, anticholinergics, oral
steroids, leucotriene modifiers and theophyllines
added in various combinations. When control is
obtained, treatment should be reduced to the
lowest feasible level.
In patients aged 6years or older with poorly
controlled (requiring at least four courses of
oral corticosteroids in the previous year) severe
persistent confirmed allergic IgE-mediated disease,
the anti-IgE monoclonal antibody omalizumab may
be used, as recommended by the National Institute
for Health and Care Excellence.
COMMON PITFALLS
• Raised respiratory rate in a patient who appears
otherwise well may be the only sign of a severe
attack.
• Silent chest with no evidence of wheeze in a
patient with asthma attack signifies poor air
entry and is a very poor prognostic sign.
• Patients with increased work of breathing
will tire after a period. Reduced respiratory
rate (exhaustion) and/or altered state of
consciousness (CO2 retention) is a sign of
deterioration.
COMMUNICATION
Asthma control can be greatly improved with a
clear self-management plan enabling the patient
to lead in the symptom control. Asthma nurse
specialists and physiotherapists can be crucial in
promoting independence—involve them!
All patients with asthma should have a
personalized asthma action plan.
205
Respiratory system
COMMUNICATION
The Royal College of Physicians devised three
simple questions that aid in determining asthma
control:
• Have you had difficulty sleeping because of your
asthma symptoms (including cough)?
• Have you had your usual asthma symptoms
during the day (e.g. cough, wheeze, chest
tightness, or breathlessness)?
• Has your asthma interfered with your usual
activities (e.g. housework, work, school)?
Table28.2 Stepped care plan for the management of
chronic asthma
Step Measures
1. Mild intermittent asthma Inhaled short-acting
2. Regular preventer
therapy
3. Initial add-on
therapy
4. Persistent poor control Trial of high dose of regular
5. Oral steroid Add lowest dose of oral
Treatment is started at the step most appropriate for the initial
severity, and a ‘rescue’ course of prednisolone can be given at
any time and with any step to cover an exacerbation. Move up
the ladder if relief bronchodilators are needed frequently or nighttime symptoms occur. Check adherence and inhaler technique,
and consider the use of spacer devices. (After British Thoracic
Society.)
β2-agonist as required
Start inhaled steroid
therapy regularly at
200–800 μg/d (e.g.
beclomethasone,
budesonide or fluticasone)
Add long-acting β2-agonist
regularly
Increase dose of regular
inhaled steroid
Add third medication,
theophylline or leucotriene
receptor antagonist
inhaled steroid up to 2000
μg/d
Addition of medications
not used in step 3
steroid to achieve control
of symptoms
Continue with maximum
dose of inhaled steroid
Must be under the care of
a respiratory physician
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
General overview
The term ‘chronic obstructive pulmonary disease’
(COPD) includes both chronic bronchitis and emphysema
caused by chronic inflammation. It is defined by expiratory airflow limitation with an FEV1 to forced vital capacity ratio of less than 0.7 and limited reversibility with
bronchodilators.
Chronic bronchitis is defined by excessive mucus production sufficient to cause cough with sputum for at least
3months of the year for more than two consecutive years
in the absence of another condition known to cause sputum
production. Emphysema is permanent, abnormal distension of the air spaces distal to the terminal bronchioles with
destruction of alveolar walls.
Aetiology
Cigarette smoking
Cigarette smoking is the most commonly identified factor in
COPD, thought to be causative in 90% of cases. Prolonged
cigarette smoking impairs ciliary movement, inhibits function of alveolar macrophages (dust cells) and leads to hypertrophy and hyperplasia of mucus-secreting glands. An
accurate smoking history should be taken and expressed as
a pack year history (20 cigarettes per day for 1year equates
to 1 pack year).
HINTS AND TIPS
Number of Pack Years = (Number of Cigarettes
Smoked per Day/20) × Number of Years Smoked.
α1-Antitrypsin deficiency
Patients homozygous (1 in 625 to 1 in 2000) for a deficiency
of the protease inhibitor α1-antitrypsin have a greatly increased incidence of early-onset emphysema. The protein
is a protease inhibitor, encoded by a gene on chromosome
14, that protects cells against protease such as neutrophil
elastases. The defect is in release from the liver, where the
protein is synthesized. Patients with the ZZ genotype have
blood levels 10% of those with the normal MM genotype.
As well as being at increased risk of developing emphysema,
patients with the ZZ genotype are also at risk of chronic
liver disease.
206
Chronic obstructive pulmonary disease
2828
Occupation
Occupational exposure to a variety of dusts and fumes
(e.g. gold and coal mining) may contribute to the development of COPD, particularly in nonsmokers, and
results in a higher prevalence of chronic bronchitis
among employees.
COMMUNICATION
Stopping smoking is one of the most important
steps in the management of chronic obstructive
pulmonary disease. Smoking cessation
programmes should be encouraged at every
opportunity. Involving family/carers can be of
benefit. Although smoking cessation should
be reinforced in all consultations, do not
antagonize the patient. It can be useful to express
understanding as to how hard it is to stop smoking
and how addictive smoking is and to not let the
patient become despondent after one attempt fails.
Pathophysiology
The hallmark of chronic bronchitis is hypertrophy of the
mucus-producing glands found in the submucosa of large
cartilaginous airways. Postmortem lungs show goblet cell
hyperplasia, mucosal and submucosal inflammatory cells,
oedema, peribronchial fibrosis, intraluminal mucous plugs
and increased smooth muscle in small airways.
Inflammation in chronic bronchitis occurs at the alveolar epithelium, and differs from the predominantly eosinophilic inflammation of asthma by the predominance of T
lymphocytes and neutrophils.
Emphysema is classified according to the pattern of involvement of the gas-exchanging units (acini) of the lung
distal to the terminal bronchiole. In centriacinar emphysema
the distension and destruction are mainly limited to the respiratory bronchioles, with relatively less change peripherally
in the acinus; these are the changes found in smokers. They
are more prominent in the upper lobes. Panacinar emphysema involves both the central and the peripheral portions
of the acinus; these changes are those seen in α1-antitrypsin
deficiency and occur more commonly in the lower lobes.
The chronic airflow limitation is a consequence of small
airway disease. There is narrowing and blockage of small
airways by an inflammatory bronchiolitis, and airways collapse in expiration because of the loss of elastic recoil and
radial traction to balance the positive transmural pressure.
This limits airflow and results in the air trapping and hyperinflation seen on CXR and lung function tests.
Clinical features
The most common feature of COPD is breathlessness—initially during activity but progressively at rest. Other symptoms include cough, sputum production (particularly in
chronic bronchitis), wheeze, prolonged expiratory phase
and tiredness. Patients with severe COPD may develop respiratory failure. Most patients have features of both chronic
bronchitis and emphysema.
An acute exacerbation of COPD is a common cause for
hospital admission, and is defined as a sudden worsening of
symptoms (increased cough, sputum production and dyspnoea) often, but not always, caused by bacterial or viral
infections.
Patients may present in respiratory distress: increased
respiratory rate, use of accessory muscles of respiration,
pursed lip breathing, drowsiness.
PATIENT SAFETY
Ask about exercise tolerance (e.g. climbing
stairs, walking distance to the shop), home
nebulizers, long-term home oxygen therapy and
the number of previous hospital admissions for
acute exacerbations to aid in establishing disease
severity.
Investigations
Diagnosis is established on the basis of history, examination
and demonstrating airflow obstruction with no or limited
reversibility. Spirometry is the gold standard. The CXR may
show hyperexpansion, and is used to rule out alternative diagnoses. An FBC should be routinely performed to identify
anaemia or polycythaemia. The body mass index needs to
be calculated for all patients. It may be difficult to differentiate COPD and asthma. The two may also overlap each
other. Table28.3 lists the characteristic features of COPD
and asthma.
Patients who present with an acute exacerbation of
symptoms require a CXR, serial ABG measurements, FBC,
U&E, CRP and an ECG. Where an infective exacerbation is
suspected, blood cultures should be sent to the laboratory if
patients are pyrexic. Sputum cultures, legionella and pneumococcal urinary antigen testing and a respiratory virus
screen should be considered.
Management
Management of patients with COPD is based on an accurate diagnosis, assessment of the severity of symptoms and
degree of airflow obstruction, smoking status, the extent
207