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_2720_Библиотеки_им_академика_М_И_Перельмана
.pdf
224
https://t.me/med1917
224
CHAPTER9 Cardiology and vascular disease
Factors toconsider beforestarting astatin
• Discuss risks vs benets. Consider other co- morbidities, polypharmacy,
general frailty, and life expectancy before deciding to prescribe
• Contraindicated in pregnancy, breastfeeding, and for those with active
liver disease (transaminases ≥3× upper limit of normal)
• Drug interactions— statins i eect of warfarin; there is i risk myositis when
statins are taken with other lipid- lowering drugs, macrolide antibiotics (e.g.
erythromycin), antifungals (e.g. ketoconazole), amiodarone, calcium channel
blockers, HIV protease inhibitors (e.g. nelnavir), danazol, or ciclosporin
• Diet restrictions— avoid grapefruit if taking atorvastatin, simvastatin, or
lovastatin, and cranberry juice (uvastatin only)
Baseline assessments beforestarting astatin
• Smoking status
• Alcohol consumption
• BP
Only measure creatine kinase (CK) level if history of unexplained persistent, generalized muscle pain.
• If CK <5× upper limit of normal, start statin at d dose
• If ≥5× upper limit of normal, recheck after 7d— if still ≥5× upper limit
of normal, do not start a statin
• BMI
• Lipid prole
• Liver function
(transaminases)
• HbA1c
• Renal function
• eGFR
• TSH
Starting dose Statins are most eective taken in the evening. Use a high-
intensity statin (d LDL by >40%):
• Primary prevention Start atorvastatin 20mg after optimizing lifestyle
intervention, and treatment of other modiable risk factors
• Secondary prevention Start atorvastatin 80mg immediately
0 Rosuvastatin 10– 40mg is an alternative. Simvastatin 80mg (also a highintensity statin) should not be commenced due to i risk of myopathy.
Target lipid levels Aim to d non- HDL by >40% from baseline.
Follow- up
• Recheck lipid prole in 3mo. If target is not met:promote lifestyle
measures, check concordance, i dose (if tolerated/ not on maximum)
• Check liver function 3mo and 1y after initiating statin/ changing dose; do
not recheck again unless clinically indicated
• Do not routinely check CK levels— only if muscle pain
Benets ofstatins d CVD risk overall by 725%. In general, the higher
the risk of CVD at baseline, the greater the benet of statins. Therefore, for
all patients with established CVD benet of statin treatment (in terms of d
in CVD risk) greatly outweighs risk.
Primary prevention As overall risk is lower in primary prevention, benet of
statin treatment is not so clear cut. Decision aids may help patients to decide whether or not they wish to take a statin. Options:
• NICE— provides a paper- based decision aid in the ‘tools and resources’
section of its lipid modication guidance
• QRisk3 and JBS3 risk calculator tools can both be used to graphically
demonstrate risk reduction likely for individual patients from
modication of lifestyle factors and/ or taking statins— E p. 214
https://t.me/med1917
HYPERLIPIDAEMIA
Adverse eects of statins Overall NNH for high- intensity statin
therapy is 763. If unable to tolerate a statin, consider d dose, or prescribing
an alternative statin or ezetimibe. Specic side eects:
• Myositis Most important adverse eect of statins (11/ 100,000 person
years). Risk is i if elderly or alcohol misuse. Usually arises <6mo after
starting treatment— consider other causes if later. May be genetic
predisposition. Ask patients to report unexplained muscle pain/
weakness— check CK— if >5× upper limit of normal withdraw therapy
• Peripheral neuropathy Stop statins and seek specialist advice if
unexplained peripheral neuropathy develops (12/ 100,000 person years)
• Abnormal liver function Discontinue if serum transaminase i and
remains at >3× upper limit of normal
• Diabetes i risk type 2 DM. Consider screening with HbA1c
Alternative lipid- lowering treatments Do not oer brates, nico-
tinic acid, bile acid sequestrants, or omega- 3 fatty acid for prevention of
CVD. Ezetimibe may be used if statin is contraindicated/ not tolerated, or
combined with low- dose statin to achieve target cholesterol levels.
Familial dyslipidaemia Screen 1st- degree blood relatives aged >18y
every 5y with fasting lipids if FH of familial hyperlipidaemia and/ or FH of
premature CVD (♂ <55y, ♀ <65y). Exclude secondary causes of hyperlipidaemia (Box 9.1, E p. 223). Refer ifN:
• Total cholesterol >7.5mmol/ L and FH of premature CVD
• Total cholesterol >9mmol/ L, non- HDL cholesterol >7.5mmol/ L; or
TGs >10mmol/ L on repeat fasting sample (urgently if >20mmol/ L)
Common types offamilial dyslipidaemia
• Polygenic hypercholesterolaemia Most common. Presents with FH of
premature CHD + i total cholesterol >6.5mmol/ L
• Familial combined hyperlipidaemia Polygenic. Aects 0.5– 1% of the
population and 715% having MI <60y. Associated with obesity, insulin
resistance/ DM, i BP, xanthelasma, corneal arcus and premature IHD. i
total cholesterol (6.5– 10mmol/ L); i TGs (2.3– 12mmol/ L)
• Familial hypercholesterolaemia Autosomal dominant. Heterozygous
form aects 1 in 500 individuals. Associated with tendon xanthomata
and FH premature IHD. i LDL (>4.9mmol/ L); i total cholesterol
(>7.5mmol/ L); normal TGs
• Familial hypertriglyceridaemia Autosomal dominant. Aects 71% of
the population and 75% having MI <60y. Associated with DM, obesity,
gout, eruptive xanthomas, and pancreatitis. Normal (or slightly i) total
cholesterol; i TGs (2.3– >10mmol/ L)
Further information
NICE (2014, updated 2016)Cardiovascular risk assessment and the modication of blood lipids for the primary and secondary prevention of cardiovascular disease. M www.nice.org.uk/ guidance/ cg181
NICE (2008, updated 2017)Familial hypercholesterolaemia. M www.nice.
org.uk/ guidance/ cg71
SIGN (2017) Risk estimation and the prevention of cardiovascular disease.
M https:// www.sign.ac.uk/ sign- 149- risk- estimation- and- the- preventionof- cardiovascular- disease.html
Patient information
British Heart Foundation F 0300 330 3311 M www.bhf.org.uk
ALGRAWANY
225
226
https://t.me/med1917
226
CHAPTER9 Cardiology and vascular disease
Angina
Aects 8% ♂ and 3% ♀ in the UK. Incidence i with age. Coronary artery
disease is the most common cause. Rarer causes include HOCM, valve
disease, hypoperfusion during arrhythmia, arteritis, anaemia or thyrotoxicosis. Mortality (usually sudden death, acute coronary syndrome, or LVF) is
70.5– 4%/ y— doubled if coexistent left ventricular dysfunction.
Chest pain ofrecent onset E p. 1064
Presentation ofstable angina Diagnosis is usually made on history:
• Pain Episodic central- crushing or band- like chest pain that may radiate
l jaw/ neck and/ or 1 or both arms. Pain in the arms/ neck may be the
only symptom. Ask about frequency, severity, duration, and timing
• Precipitating/ relieving factors Precipitated by exertion, cold, emotion,
and/ or heavy meals. Pain stops with rest or GTN spray
• Associated symptoms Pain may be associated with palpitations,
sweating, nausea, and/ or breathlessness during attacks
• Presence of risk factors Smoking history; family history; history of other
vascular disease, e.g. CVA/ TIA, peripheral vascular disease
Examination There are usually no physical signs although anaemia may
exacerbate symptoms. Check BMI and BP. Look for murmurs (especially
ejection systolic murmur of aortic stenosis) and evidence of peripheral
vascular disease and carotid bruits (especially in patients with DM).
First- lineinvestigations
• Blood FBC, fasting lipid prole, fasting blood glucose. Consider checking
ESR (to exclude arteritis) and TFTs if suspicion of thyrotoxicosis
• 12- lead resting ECG Provides information on rhythm, presence of heart
block, previous MI, myocardial hypertrophy and/ or ischaemia
0 Anormal ECG does not exclude coronary artery disease, but an abnormal ECG identies those at higher risk of cardiac events in the next
year— consider referral for further investigation.
Dierential diagnosis Chest pain— E p. 1065
Referral ofpatients with suspected stable angina For patients
with new- onset intermittent chest pains, refer to a rapid access chest pain
clinic for prompt specialist assessment to:
• Conrm/ refute angina
• Perform appropriate investigations, e.g. cardiac MRI (E p. 210)
• Provide information on treatment options available including the merits
of revascularization for the individual
0 Patients with pre- existing cardiac disease (e.g. previous MI, valve disease, cardiomyopathy) are often excluded from rapid access chest pain
clinic referral. Refer to cardiology direct.
Management ofpatients withstable angina Provide information
about angina and its treatment.
• Driving Group1 licence:no need to inform DVLA— must not drive
when symptoms occur at rest, with emotion or at the wheel. Group2
licence:notify the DVLA— must not drive when symptoms occur; licence
is revoked if symptoms continue; restored if no angina for ≥6wk +
DVLA functional test requirements are met
https://t.me/med1917
ANGINA
• Occupation May be unable to undertake heavy work— give advice/
support. Special rules apply to some occupations, e.g. merchant seamen,
airline pilots. Advise to consult occupational health
Non- drug treatment Aimed at secondary prevention of CHD:
• Smoking cessation E p. 156
• Hypertension Check BP and treat if >140/ 90mmHg— E p. 218
• Diet Advise healthy diet (oily sh, low cholesterol, i fruit and
vegetables, d salt) and, if obese, aim to d weight until BMI <25kg/ m
• d alcohol To ≤14U/ wk; <3– 4U/ d (♂) or <2– 3U/ d (♀) maximum
• Exercise i aerobic exercise within the limits set by the disease state;
consider referral for cardiac rehabilitation
• Diabetes Treat any underlying DM— E p. 320
• Cardiac rehabilitation May be helpful for patients with angina and/ or
after surgery
Drug treatment E p. 228
Referral tocardiology E= Admit; U=Urgent; S=Soon; R=Routine.
• Unstable angina/ rapidly progressive symptoms— E
• Aortic stenosis with angina— U
• Angina following MI— U/ S
• Abnormal ECG at diagnosis— U/ S
• Angina not controlled by medication with 2 drugs— U/ S/ R
• If diagnosis is in doubt— S/ R
• Strong family history— R
• Other factors, e.g. occupation aected— R
H Unstable angina Pain on minimal or no exertion, pain at rest (may
occur at night) or angina which is rapidly worsening in intensity, frequency,
or duration. Incidence:6/ 10,000/ y; 15% suer MI in <1mo.
Management Urgent referral to cardiology. Admit if attacks are severe,
occur at rest or last >10min even with GTN spray.
227
2
Surgical intervention Consider referral for coronary revascularization
with bypass surgery (CABG) or percutaneous intervention (PCI) if symptoms
are not controlled with antianginal drug intervention (2 drugs). Both procedures d symptoms, but CABG confers a survival advantage if DM, age >65y,
left anterior descending (LAD) artery disease, or complex 3- vessel disease.
Prinzmetal (variant) angina Angina at rest resulting from coronary
artery spasm. ECG shows ST elevation. Refer to cardiology to exclude MI
and atherosclerotic angina. GTN alleviates immediate episodes. Calcium
channel blockers are used to prevent angina.
Cardiac syndrome X Ongoing angina symptoms despite normal cor-
onary angiography. Treat with β- blockers and/ or calcium channel blockers
(if eective) but not secondary prevention agents.
Further information
Cardiac rehabilitation M www.cardiacrehabilitation.org.uk
NICE (2011, updated 2016)Stable angina:management. M www.nice.org.
uk/ guidance/ cg126
Patient information
British Heart Foundation F 0300 330 3311 M www.bhf.org.uk
ALGRAWANY
228
https://t.me/med1917
228
CHAPTER9 Cardiology and vascular disease
Drug treatment ofangina
Symptomcontrol
‘As required’ medication Glyceryl trinitrate (GTN) spray is used for ‘as required’ symptom relief for angina. Advise 1– 2 pus as needed in response
to pain and before engaging in activities that bring on pain. Warn about side
eects— ushing, headaches, and light- headedness (sit down or nd something to hold onto if this occurs).
• If used for chest pain:advise patients to repeat the dose of GTN after
5min if the pain has not gone. If the pain has not gone 5min after the
second dose, advise to call for an emergency ambulance.
Regular treatment Drugs for regular symptomatic treatment— Table 9.6.
Within any drug class, use the cheapest preparation that the patient can
tolerate, will comply with, and which controls symptoms. Assess response
every 2– 4wk after initiating/ changing drug therapy:
• First- line agent β- blocker or calcium channel blocker— choice depends
on co- morbidities, contraindications, and patient preference
• If treatment is ineective/ not tolerated Switch to whichever rst-
line agent has not been tried and/ or combine a β- blocker and
dihydropyridine calcium channel blocker
Alternative regular treatments Include long- acting nitrates, ivabradine,
nicorandil, and ranolazine. Consider:
• Monotherapy if both rst- line agents (β- blockers and calcium channel
blockers) are contraindicated or not tolerated
• In combination with a rst- line agent if symptoms are not controlled
with one rst- line agent alone and the other rst- line agent is
contraindicated or not tolerated
• As a third antianginal agent if symptoms are not controlled with 2
antianginal drugs and the person is either not suitable for CABG/ PCI or
is awaiting CABG/ PCI
Secondaryprevention
Aspirin d mortality by 34%. Unless contraindicated, give 75mg od to all pa-
tients with angina. Consider clopidogrel 75mg od if aspirin intolerant.
Statin A reduction in total cholesterol and LDL by 25– 35% results in a reduction of CHD mortality by 25– 35%. Trial data suggest all patients with
proven CHD benet from statin treatment irrespective of initial cholesterol
concentration— E p. 223.
ACE inhibitors Signicantly d cardiovascular deaths (RR 0.83) and all- cause
mortality (RR 0.87)— even in the absence of left ventricular dysfunction.
https://t.me/med1917
DRUG TREATMENT OFANGINA
Table9.6 Drug treatment ofangina
Drug Treatment notes
-blockers
0 May
accumulate in
patients with
renal failure—d
dose
Dihydropyridine
calcium channel
blockers
Rate-limiting
calcium channel
blockers
Long-acting
nitrates
Potassium
channel activator
Ivabradine Lowers the heart rate by its action on the sinus node
Ranolazine Aects sodium-dependent calcium channels
Eective for symptom control and to prevent vascular events.
Check fully β-blocked by monitoring heart rate—resting
heart rate ≤65bpm; post-exercise (e.g. walking up 2 ights of
stairs) heart rate ≤90bpm. Further i in dose once adequately
Warn patients not to stop suddenly or run out. If the patient
needs to stop the drug, tail o over 4wk
In patients with asthma/COPD in whom β-blockade is
essential, use cardio-selective β-blockers (e.g. atenolol,
bisoprolol, metoprolol, nebivolol) with care
In patients with left ventricular failure, start at very low dose
and titrate dose over weeks/months
e.g. amlodipine, felodipine
All equally eective in symptom control. No evidence of
cardioprotective eect
Contraindications:vary. Do not use if aortic stenosis, <1mo
post-MI or uncontrolled heart failure except with specialist advice
e.g. diltiazem, verapamil
Contraindications:avoid if heart block or heart failure
• Do not combine with β-blockers
e.g. isosorbide mononitrate (ISMO)
Oral and patch preparations (dosages ≤ 10mg/24h) are available.
Start with a low dose and i as tolerated. Side eects are common
Side eects:headache, postural hypotension and dizziness—
wear o with use. Reex tachycardia may d coronary blood
ow and worsen angina
Tolerance:many patients rapidly develop tolerance with d
therapeutic eect. To avoid this allow a nitrate-free period of
4–8h/d overnight by removing patches at night or giving the
2nd dose of ISMO at 4p.m.
Contraindications:HOCM, aortic stenosis, constrictive pericarditis,
mitral stenosis, severe anaemia, closed-angle glaucoma
e.g. nicorandil
Headache is common—usually transitory
Contraindications:left ventricular failure; hypotension
Contraindications:avoid if heart rate <60bpm, heart block, or
heart failure
Contraindications:renal/liver failure; use with caution if CCF or
weight <60kg
229
Further information
NICE (2011, updated 2016)Stable angina:management. M www.nice.org.
uk/ guidance/ cg126
Patient information
British Heart Foundation F 0300 330 3311 M www.bhf.org.uk
ALGRAWANY
230
https://t.me/med1917
230
CHAPTER9 Cardiology and vascular disease
After myocardialinfarction
Acute coronary syndrome E p. 1066
Modication ofrisk factors afterMI Secondary prevention:
• Cholesterol All with proven CHD benet from d in total cholesterol
and LDL irrespective of initial cholesterol level. Areduction of 25– 35%
using statin therapy results in 25– 35% d in CHD mortality. Serum
cholesterol levels d after MI and remain d for several weeks
• β- blockers Unless contraindicated, start on an oral β- blocker (e.g.
atenolol) soon after MI and titrate to target or maximum tolerated
dose. Continue for 12mo, or indenitely if LVF. Prevents 712 deaths
/ 1000 treated/ y. If contraindicated, consider a rate- limiting calcium
channel blocker (e.g. diltiazem or verapamil) instead
ACE inhibitors d myocardial work and deaths <1mo post MI by 5/
1000 treated. Titrate to target or maximum tolerated dose in 4– 6wk.
Survival advantage is sustained >1y even if treatment is not continued.
Eects are greater for patients with heart failure at presentation. Long- term
ACE inhibitors:trials show d mortality for all patients. If ACE inhibitors are
not tolerated, use an ARB.
Antiplateletmedication
Aspirin Starting aspirin 75mg od <24h after MI prevents 80 vascular events
over the next 2y/ 1000 patients treated. Unless contraindicated, continue
lifelong.
Clopidogrel 75mg od— prescribe in addition to aspirin for:
• 12mo if non- ST elevation MI (NSTEMI)/ unstable angina
• 1mo following ST elevation MI (STEMI) with no coronary stenting
• 3mo following STEMI with bare- metal stenting
• 12mo following STEMI with drug- eluting stenting
Alternatives toclopidogrel In certain circumstances, newer antiplatelet agents
(e.g. prasugrel or ticagrelor) may be used in combination with aspirin after
ACS and PCI.
Anticoagulation Occasionally required if AF, left ventricular aneurysm,
or if clopidogrel/ aspirin are not tolerated.
Drug treatment ofangina E p. 228
Heart failure/ left ventricular dysfunction Consider treatment
with an aldosterone antagonist (e.g. spironolactone 25mg od, i in <1mo
to 50mg od), starting 3– 14d after MI if symptoms/ signs of heart failure and
left ventricular systolic dysfunction (ejection fraction <0.4).
Cardiac rehabilitation d risk of death by 20– 25%. Provided by spe-
cialist multidisciplinary teams. Components include: psychological support,
information about CHD, structured exercise programme, and modication
of other risk factors.
Advice toprovide afterdischarge
Physical activity Advise gradual i in activity. Ensure goals given match those
given by local cardiac rehabilitation. Guide:
• Up to 2wk— stroll in the garden or street
https://t.me/med1917
AFTER MYOCARDIALINFARCTION
• 2– 6wk— walk ½ mile/ d aiming to i to 2 miles/ d by 6wk
• From 6wk— i speed of walking— aim 2 miles in <30min
Sexual activity Resume as comfortable— usually after ≥4wk. A leaet is
available from the British Heart Foundation.
Return towork Guide:
• Sedentary workers:4– 6wk after uncomplicated MI
• Light manual workers:6– 8wk after uncomplicated MI
• Heavy manual workers:3mo after uncomplicated MI
Psychological eects 750% are depressed 1wk after MI; 25% after 1y. Educate
about CHD. Check for depression (E p. 173), counsel, and treat as needed.
Driving Group1 licence No need to notify the DVLA. Stop driving. Restart
after 1wk if successful PCI and no other revascularization planned in <4wk.
Otherwise driving can restart 4wk after the event.
Driving Group 2 licence Inform the DVLA. Licence is revoked; reinstated
after ≥6wk if LV ejection fraction is ≥40% + DVLA functional test requirements are met.
Flying Most airlines will not carry passengers for 2wk after MI and then only
if able to climb 1 ight of stairs without diculty.
Ongoing GP follow- up
Monitoring health Continue regular reviews at least annually lifelong. Check
for symptoms and signs of cardiac dysfunction (breathlessness, palpitations,
angina); depression; carer stress.
Monitoring drug therapy Ongoing prescription of drugs, monitoring of compliance and side eects, changing medication if clinical circumstances or best
practice alter.
Secondaryprevention
• Smoking cessation E p. 156. d risk of death by 50% over 15y
• Hypertension Check BP and treat if >140/ 90mmHg— E p. 218
• Diet Mediterranean- style diet (low cholesterol, i fruit/ vegetables,
dsalt) and, if obese, aim to d weight until BMI <25kg/ m2. Do not
advise oily sh to d risk of further MI (but no evidence of harm)
• d alcohol to ≤14U/ wk; <3– 4U/ d (♂) or <2– 3U/ d (♀) maximum
• Exercise i aerobic exercise within the limits set by the disease state
• Diabetes Treat any underlying DM— E p. 320
• Reinforce information given during cardiac rehabilitation
Dressler syndrome (post- MI syndrome) Develops 2– 10wk after
MI or heart surgery as a result of autoantibodies to heart muscle. Presents
with recurrent fever and chest pain ± pleural and/ or pericardial eusion.
Management:Refer urgently for cardiology advice. Treatment is with steroids and NSAIDs.
Further information
Cardiac rehabilitation M www.cardiacrehabilitation.org.uk
NICE (2013) Myocardial infarction:cardiac rehabilitation and prevention
of further cardiovascular disease. M www.nice.org.uk/ guidance/ cg172
Patient information
British Heart Foundation F 0300 330 3311 M www.bhf.org.uk
231
ALGRAWANY
232
https://t.me/med1917
232
CHAPTER9 Cardiology and vascular disease
Chronic heartfailure
Chronic heart failure occurs when output of the heart is inadequate to meet
the body’s needs. It is the end stage of all diseases of the heart. 900,000
people in the UK have heart failure; prevalence i with age.
Acute heart failure E p. 1068
Causes ofchronic heartfailure
High- output The heart is working at normal or i rate but the needs of the
body are i beyond that which the heart can supply, e.g. hyperthyroidism,
anaemia, Paget’s disease, AV malformation.
Low- output d heart function. Causes:
• i pre- load e.g. mitral regurgitation, uid overload
• Pump failure:
• Cardiac muscle disease— IHD (46%), cardiomyopathy
• d expansion of the heart and restricted lling— restrictive
cardiomyopathy, constrictive pericarditis, tamponade
• Inadequate heart rate— β- blockers, heart block, post MI
• Arrhythmia— AF is the most common
• d power— negatively ionotropic drugs, e.g. verapamil, diltiazem
• Chronic excessive afterload i BP, aortic stenosis
Presentation Clinical diagnosis is dicult. Take a detailed history and do
a clinical examination to exclude other disorders.
Algorithm fordiagnosing heart failure Figure 9.2
Dierentialdiagnosis
• Obesity
• Respiratory disease
• Venous insuciency in lower limbs
• Drug- induced ankle swelling (e.g.
calcium channel blockers) or uid
retention (e.g. NSAIDs)
• Intrinsic renal or hepatic disease
Causes offalsely i natriureticpeptide
• Structural or functional cardiac disease of any cause, including MI
• Baseline is i in ♀ and in those >70y
• Lung disease, including COPD and PE
• Renal impairment
Causes offalsely d natriureticpeptide
• Obesity
• Diuretics
• ACE inhibitors/ ARBs
• β- blockers
Classication
• Left ventricular systolic dysfunction d left ventricular ejection fraction
(LVEF) on echocardiography
• Heart failure with preserved ejection fraction (HFPEF) Also termed
diastolic dysfunction— signs/ symptoms of heart failure with normal
LVEF on echocardiogram
• Pulmonary embolic disease
• Hypoalbuminaemia
• Depression and/ or anxiety
• Bilateral renal artery stenosis
• Severe anaemia
• Thyroid disease
• DM
• Liver failure
• Sepsis
• Aldosterone antagonists
https://t.me/med1917
CHRONIC HEARTFAILURE
Other tests toconsider To exclude aggravating factors/ other causes
of symptoms— urinalysis, blood (FBC, U&E, creatinine, eGFR, TFTs, FBG/
HbA1c), ECG, CXR, and PEFR/ spirometry.
Grading ofseverity The NewYork Heart Association (NYHA) classi-
cation is widely used:
• I No limitation:ordinary physical exercise does not cause undue fatigue,
dyspnoea, or palpitations
• II Slight limitation of physical activity:comfortable at rest but ordinary
activity results in fatigue, palpitations, or dyspnoea
• III Marked limitation of physical activity:comfortable at rest but less
than ordinary activity results in symptoms
• IV Unable to carry out any physical activity without discomfort:
symptoms of heart failure are present even at rest with i discomfort
with any physical activity
233
Figure9.2 Algorithm for diagnosing heart failure
Further information
NICE (2018) Chronic heart failure in adults:diagnosis and management.
M www.nice.org.uk/ guidance/ ng106
Patient information
British Heart Foundation F 0300 330 3311 M www.bhf.org.uk
ALGRAWANY
Соседние файлы в папке Библиотека им академика М.И. Перельмана