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CHAPTER9 Cardiology and vascular disease
Management ofchronic heartfailure
0 Always look for the underlying cause and treat wherever possible.
Review the basis for historical diagnosis and arrange Echo to conrm if
diagnosis is in doubt.
Driving and heartfailure
• Group1 licence Stop driving and inform the DVLA if severe symptoms
(NHYA IV)
• Group2 licence Inform the DVLA. Can continue driving if mild
symptoms (NYHA Ior II) and LV ejection fraction is >40%
Regular review Every 6mo or more often as needed. Check:
• Clinical state Functional capacity, uid status, cardiac rhythm, cognitive
and nutritional status
• Screen for depression Aects >40%
• Manage co- morbidities
• Medication Ensure drug record is up to date, review compliance and
side eects, change if clinical circumstances/ best practice alter
• Blood U&E, creatinine, and eGFR
Non- drugmeasures
• Educate about the disease, current/ expected symptoms, and need for
treatment. Discuss prognosis. Support with written information
• Discuss ways to make life easier e.g. benets, mobility aids, blue
disability parking badge. Consider referral to social services for
assessment for services such as home care
• Diet Adequate calories, d salt, d weight if obese, restrict alcohol
• Lifestyle measures Smoking cessation (E p. 156); regular exercise
• Restrict uid intake If severe heart failure
• Vaccination Pneumococcal and annual inuenza vaccination
Diuretics Relieve congestive symptoms/ uid retention in all types
of heart failure. Choose a loop diuretic, e.g. furosemide 20– 40mg or
bumetanide 1– 2mg od. Add a thiazide if continued problems with oedema
or hypertension. Titrate dose i or d according to need. Monitor for d K+
and co- treat with amiloride or K+ supplements as needed.
First- line medication for left ventricular systolic dysfunction Start all patients on an ACE inhibitor and a β- blocker. Use clinical
judgement to decide which drug to start rst.
ACE inhibitors Improve symptoms, i exercise capacity, d progression of dis-
ease, d hospital admissions, and i survival in symptomatic and asymptomatic patients. Start at low dose (e.g. ramipril 1.25mg od) and titrate upwards.
Check U&E and Cr before starting, at rst follow- up and after each i in
dose. Use ARB if not tolerated.
0 If neither an ACE inhibitor nor ARB is tolerated rst- line, a combination
of hydralazine with a nitrate is an alternative— seek specialist advice.
- blockers Start a β- blocker licensed for heart failure (e.g. bisoprolol
1.25mg in the morning) in all those with left ventricular dysfunction regardless of whether symptoms persist. Use in a ‘start low, go slow’ manner with
assessment of pulse, BP, and clinical status after each titration.
https://t.me/med1917
MANAGEMENT OFCHRONIC HEARTFAILURE
Heart failure withpreserved ejection fraction (HFPEF) Apart
from diuretics, there is no specic treatment for HFPEF. Treat any comorbidities, e.g. DM, i BP, IHD.
Other drugs toconsider
• Anticoagulation If heart failure + AF, or history of thromboembolism,
left ventricular aneurysm, or intra- thoracic thrombus— E p. 648
• Aspirin 75– 150mg od if heart failure + atherosclerotic arterial disease
(including CHD)
• Statins Only if other indications— E p. 224
• Amlodipine Treatment for angina and i BP. 0 Avoid verapamil,
diltiazem, or short- acting dihydropyridine agents
Referral tocardiology (or other suitable specialist) Consider if
(E= Emergency admission; U=Urgent; S=Soon; R=Routine):
• Heart failure unable to be managed at home— E
• Severe heart failure— U/ S
• Heart failure not controlled by rst- line medication— U/ S/ R
• Angina, AF, or other symptomatic arrhythmia— U/ S/ R
• Heart failure due to valve disease or diastolic dysfunction— R
• Co- morbidity that may impact heart failure, e.g. COPD, renal failure,
anaemia, thyroid disease, PVD, urinary frequency, gout— R
• Woman with heart failure planning pregnancy— R
Treatment underspecialistsupervision
Left ventricular systolic dysfunction Second- line agents include:
• Aldosterone antagonists, e.g. spironolactone
• Combination of hydralazine and nitrate
• ARB— used in combination with ACE inhibitor and β- blocker
Digoxin An antiarrhythmic and a positive inotrope. It is used for worsening
or severe heart failure due to left ventricular systolic dysfunction despite
rst- and second- line treatment. Only check levels (8– 12h after last dose) if
suspected toxicity or non- adherence.
Amiodarone May be used to treat arrhythmias associated with heart failure.
It requires specialist initiation and close monitoring with TFTs and LFTs at
least every 6mo once established on a maintenance dose.
Medicaldevices
• Implantable cardioverter debrillator May be tted in patients with left
ventricular dysfunction and previous episodes of ventricular tachycardia
or widened QRS complexes on ECG
• Cardiac resynchronization therapy Considered if severe symptoms on
maximal therapy and in sinus rhythm with prolonged QRS complexes
Prognosis Progressive deterioration to death; 7½ die suddenly—
probably due to arrhythmias. Mortality:Mild/ moderate heart failure— 20–
30% 1y mortality; severe heart failure— >50% 1y mortality
Palliative care E p. 1011
Further information
NICE (2018) Chronic heart failure in adults:management. M www.nice.
org.uk/ guidance/ ng106
Patient information
British Heart Foundation F 0300 330 3311 M www.bhf.org.uk
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CHAPTER9 Cardiology and vascular disease
Pulmonary hypertension and cor
pulmonale
Pulmonary hypertension Normal pulmonary arterial pressure is less
than a fth of that in the systemic circulation. Pulmonary hypertension is
dened as pulmonary artery pressure ≥25mmHg. It is classied according
to cause:
• Group1 Pulmonary arterial hypertension— may be idiopathic or
associated with connective tissue disease (mainly scleroderma)
• Group2 Left heart disease— severe heart failure (systolic or diastolic),
valve disease (e.g. mitral stenosis), congenital heart disease
• Group3 Lung disease— COPD, interstitial lung disease
• Group4 Chronic thromboembolic pulmonary hypertension— PE, sickle
cell disease
• Group5 Unclear and multifactorial mechanisms
Cor pulmonale Right heart failure resulting from chronic pulmonary
hypertension.
Diagnosis Non- specic symptoms often lead to delayed diagnosis.
Presentation Fatigue and breathlessness on exertion ± angina, palpitations,
and pre- syncope. Later, as ventricular failure develops, symptoms include
peripheral oedema, ascites, and syncope.
Examination Check for cyanosis, peripheral oedema, i JVP, 4th heart
sound, diastolic murmur from pulmonary regurgitation, hepatomegaly
± ascites, crepitations at lung bases ± pleural eusion.
Investigations
• CXR Prominent right heart border + enlargement of proximal
pulmonary arteries
• ECG If abnormal— right axis deviation, tall peaked P wave in lead II,
dominant R wave in V1, T- wave inversion in anterior leads or RBBB
Management Refer to a specialist cardiologist or chest physician.
Specialistinvestigation
• Doppler Echo Used to assess ventricular function and give an estimate
of pulmonary arterial pressure
• Right heart catheterization and direct measurement of mean
pulmonary artery pressure Conrms diagnosis, provides information on
prognosis, and determines the treatment plan
• Assessment of functional capacity The 6min walk test is used to give
information about prognosis; <380m at presentation is associated with
poor prognosis
Specialist treatment Depending on the underlying cause, treatment is
usually through a tertiary specialist centre and includes:
• Oxygen therapy for symptomatic relief
• Diuretic treatment for heart failure
• Vasodilation with calcium channel blockers (in the 10– 15% of patients
who are responsive)
• Anticoagulation
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PULMONARY HYPERTENSION AND COR PULMONALE
• Specic drug treatment (group 1 pulmonary hypertension)
• Surgery
Specic drug treatments For group 1 pulmonary hypertension.
Improve symptoms, delay disease progression, and prolong survival. Always
initiated in specialist centres:
• Prostanoids e.g. epoprostenol, iloprost, selexipag
• Endothelin receptor antagonists e.g. bosentan, ambrisentan,
macitentan— require monthly monitoring with LFTs
• Phosphodiesterase inhibitors e.g. sildenal, tadalal
• Other agents e.g. riociguat (causes arterial dilatation by action on an
enzyme that mediates the vasomotor eect of nitric oxide in the lungs)
Pulmonary endarterectomy Treatment of choice for patients with
cardio- thromboembolic pulmonary hypertension. The majority can be
cured with normalization of pulmonary pressure following surgery (>90%
5y survival).
Bilateral heart/ lung transplantation For those who have severe
symptoms despite optimal treatment. 5y survival following transplantation
is 50– 60%.
Driving and heart failure E p. 234
Patient information
Pulmonary Hypertension Association (PHA) UK F 01709 761450
Mwww.phauk.org
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CHAPTER9 Cardiology and vascular disease
Tachycardia
Tachycardia is a heart rate >100bpm. It is often felt as palpitations. Common
and may be an incidental nding. History and examination can exclude signicant problems in most patients.
Driving and arrhythmia E p. 241
History Ask about:
• Palpitations Duration, frequency and pattern, rhythm (ask the patient to
tap it out if not present when seen)
• Precipitating/ relieving factors
• Associated symptoms Chest pain, collapse or funny turns, sweating,
breathlessness or hyperventilation
• Past history e.g. previous episodes, heart disease, thyroid disease
• Family history e.g. any cardiac/ rhythm disorders, sudden death
• Lifestyle Drug history; caeine/ alcohol intake; smoking
• Occupation Arrhythmias may aect driving and/ or work
• Red agsymptoms
• Pre- existing cardiovascular disease
• FH of syncope, arrhythmia, or sudden death
• Arrhythmia associated with falls and/ or syncope
Examination
• General examination For anaemia, thyrotoxicosis, anxiety, other
systemic disease
• Cardiovascular examination Heart size, pulse rate and rhythm, JVP, BP,
heart sounds and murmurs, evidence of left ventricular failure
Investigations Resting ECG is all that is needed for many patients.
Consider further investigations if ECG is abnormal or other concerning features (e.g. syncope, breathlessness, prolonged episodes):
• Blood:TFTs, FBC, ESR/ CRP, U&E, FBG/ HbA1c, Ca2+, albumin
• Ambulatory ECG or cardiac memo
• Echo if <50y or murmur/ heart failure detected
• Exercise tolerance test if exercise related
• Ventricular tachycardia (VT) Broad (>3 small squares) QRS
complexes at a rate of >100bpm on ECG. Admit as a ‘blue- light’ emergency. Meanwhile give O2 if available ± 100mg IV lidocaine. If no pulse treat
as VF cardiac arrest (E p. 1066). If recurrent VT, may require surgery,
insertion of a pacemaker or implantable cardioverter debrillator (ICD).
Ventricular ectopic beats Additional broad QRS complexes, without
Pwaves, superimposed on regular sinus rhythm. Common. Usually of no
clinical signicance. Rarely, a presenting feature of viral myocarditis.
• Frequent ectopics (>100/ h) on ECG Urgent cardiology referral
• R on T phenomenon on ECG Rarely ectopics can lead to VF,
particularly if they coincide with the T wave of a preceding beat (‘R on
T phenomenon’). Admit if this occurs >10×/ min on ECG
• After MI Associated with i mortality— refer to cardiology
• No sinister features on ECG Explain benign nature. Advise avoidance
of caeine, alcohol, smoking, and fatigue. β- blockers can be helpful if
unable to tolerate ectopics despite reassurance
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TACHYCARDIA
Long QT syndrome (LQTS) ECG shows prolonged QT interval.
Heart is structurally normal. Associated with ventricular arrhythmias which
may lead to syncope/ sudden death, often triggered by excitement/ exercise. If inherited, may be autosomal dominant or recessive. Refer any patient with FH of sudden cardiac death for specialist assessment. Antenatal
screening is possible.
Brugada syndrome Particularly aects people of SE Asian origin;
♂>> ♀. Autosomal dominant inheritance but FH in only 750%. Results in
syncope/ sudden death (usually <45y) due to ventricular arrhythmias, often
at night. ECG shows ‘Brugada’ sign— coved ST i of ≥2mm in V1/ V2, followed by a −ve T wave— but may be transient/ absent. Treatment is with
an ICD. Arrange same- day cardiology review if suspected.
Paroxysmal supraventricular tachycardia (SVT) Narrow QRS
complex tachycardia with a regular rate >100bpm on ECG.
If seen duringan attack Get an ECG if possible. Try carotid sinus massage
(unless elderly, IHD, digoxin toxicity, carotid bruit, history of TIAs), the
Valsalva manoeuvre, and/ or ice on the face (especially eective for children). Admit as an emergency if attack continues.
If attack terminates or not seen during attack SVT may be diagnosed on
12- lead resting ECG or 24h ECG/ cardiac memo. Refer to cardiology for
assessment and initiation of treatment— urgently if chest pain, dizziness, or
breathlessness during attacks. Include ECG if available.
Ongoing care Avoid caeine, alcohol, and smoking. Treatment:catheter ab-
lation or drug therapy (sotalol, diltiazem, verapamil, or ecainide).
Wol– Parkinson– White (WPW) syndrome A congenital acces-
sory conduction pathway is present between atrium and ventricle (bundle
of Kent). Predisposes to SVT and AF. ECG shows a short P– R interval
followed by slurred upstroke (‘delta wave’) into the QRS complex. Refer
to cardiology. Treatment is with antiarrhythmics (SVT— verapamil; AF—
amiodarone or DC shock) ± ablation of the accessory pathway.
Sinus tachycardia Consider infection, pain, MI, shock, exercise, emo-
tion (including anxiety), heart failure, thyrotoxicosis, drugs.
Inappropriate sinus tachycardia Diagnosis of exclusion. Persistent tachycardia of >95bpm averaged over 24h, with night- time rate dipping. Can
result in palpitations, breathlessness, fatigue/ exercise intolerance, and syncope/ pre- syncope. Cause is unknown. Treatment (if needed) is with β-
blockers or rate- limiting calcium channel blockers.
Postural tachycardia syndrome (POTS) Change from lying to standing causes
an exaggerated i in pulse rate of >30bpm. ♀ >> ♂. May be a FH. Average
age of presentation is 20y. Suspect if palpitations, weakness, and/ or syncope/ pre- syncope (but no d in BP) on standing. Diagnosis is conrmed
by tilt- table testing. Treatments include behavioural modication and drugs,
e.g. β- blockers. Cause is unknown. May spontaneously remit.
Atrial brillation/ utter E p. 240
No tachycardia and no ECG abnormalities Reassure. Explore the
possibility of anxiety disorder (E p. 970).
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CHAPTER9 Cardiology and vascular disease
Atrialfibrillation (AF)
Common disturbance of cardiac rhythm characterized by rapid irregularly
irregular narrow QRS complex tachycardia with absence of P waves. May
be episodic (paroxysmal) or chronic. Aects 1.5– 2% of the UK population.
Prevalence i with age:<0.5% aged 40– 50y; 5% >65y; 10% >75y.
Causes Usually idiopathic— may occasionally be due to atrial dilata-
tion (e.g. in association with valve disease, inammation, or brosis of the
atrium), or i in muscle mass (e.g. LVH 2° to i BP or cardiomyopathy).
Acute AF May be precipitated by acute infection, high alcohol intake, surgery, electrocution, MI, pericarditis, PE, or hyperthyroidism.
Presentation Often asymptomatic— detected if chance nding of ir-
regular pulse or following stroke/ TIA. If symptomatic:palpitations, breathlessness, dizziness, postural hypotension, and/ or chest discomfort.
Examination Aims to conrm AF and exclude underlying causes. Check
pulse rate/ rhythm (apex rate > radial pulse rate if in AF), BP, heart size,
heart sounds/ murmurs, JVP, signs of LVF. Check for signs of systemic disease, e.g. anaemia, thyrotoxicosis.
Assess severity European Heart Rhythm Association (EHRA) Score:
I No symptoms II Mild symptoms, normal activity not aected
III Severe symptoms, normal activity aected
IV Disabling symptoms, normal activity discontinued
Investigations
• ECG— if paroxysmal AF is suspected but not captured on ECG,
consider 24h- ECG monitoring, or cardiac memo
• Blood tests— FBC; U&E/ eGFR; TFTs (anaemia, hyperthyroidism or
electrolyte imbalance trigger AF; renal function aects drug choice)
• CXR— to evaluate the size of the heart and identify lung disease
• Echocardiography— to check left atrial size and left ventricular function
Management If acutely, severely compromised, admit to hospital.
Rate limitation If the heart is beating too fast, it cannot rell before the next
beat and becomes an inecient pump. Controlling ventricular rate in AF allows the heart to work more eectively. Choice of drugs— Figure 9.3. Oer
as the rst- line strategy to people with AF, except if:
• AF has a reversible cause (e.g. alcohol binge, chest infection)
• Heart failure caused by AF • New- onset AF
• Atrial utter suitable for ablation
• Rhythm control would be more suitable
Restoration ofsinus rhythm Successful cardioversion is most likely in young
patients with a structurally normal heart where duration of AF is <12mo.
Consider referral for DC cardioversion if:
• Heart failure associated with AF
• Recent- onset AF with low risk of recurrence, i.e. obvious precipitant
(e.g. pyrexia, alcohol, or post- op) and no structural heart disease
• Intolerable symptoms despite adequate rate control
• High risk from anticoagulant therapy
Otherwise oer rate control as the rst- line strategy.
0 Patients are usually started on amiodarone prior to DC cardioversion
and for 1y following the procedure to maintain sinus rhythm.
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ATRIALFIBRILLATION (AF)
Figure9.3 Choice of drugs for rate limitation in AF
Prevention ofthromboembolic complications E p. 536. AF is associated with an
i risk of peripheral thromboembolism including stroke (5× i risk). All patients
with valvular AF and moderate/ high- risk patients with non- valvular AF should
be considered for anticoagulation with warfarin or a direct oral anticoagulant
(DOAC, e.g. rivaroxaban, apixaban) to d stroke risk. Do not oer aspirin for AF.
Weigh risk of thromboembolism against risk of bleeding (E p. 537).
The Keele University decision support tool may be useful— M www.
anticoagulation- dst.co.uk
‘Pill- in- the- pocket’ approach toparoxysmal AF Consider self- medication with
a β- blocker prn (e.g. atenolol 50– 100mg od) if infrequent symptomatic
paroxysms and no history of LV dysfunction or valvular/ ischaemic heart
disease; systolic BP >100mmHg and resting heart rate >70bpm; able to
understand when and how to take the medication.
Referral tocardiology
E=Emergency admission; U=Urgent; S=Soon; R=Routine
• Acutely unwell with AF— E
• For consideration of cardioversion— E/ U
• Abnormality on echocardiogram requiring referral— S/ R
despite rate control or frequent attacks of paroxysmal AF— S/ R
• <30y of age— S/ R • Heart failure— S/ R
Atrial utter ECG shows regular saw- tooth baseline at rate of 300bpm
with a narrow QRS complex tachycardia superimposed at a rate of 100 or
150bpm. Manage as for AF (specialist drug treatment may dier).
Driving and arrhythmia Stop driving if arrhythmia has or is likely to
cause incapacity.
• Group1 licence Restart driving when underlying cause identied and
arrhythmia controlled for ≥4wk. Inform the DVLA only if underlying
cause not found and arrhythmia not controlled for ≥4wk
• Group2 licence Inform the DVLA. Licence restored if underlying cause
found, arrhythmia controlled ≥3mo + LV ejection fraction >40%
Further information
NICE (2014) Atrial brillation:management. M www.nice.org.uk/ guidance/ cg180
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CHAPTER9 Cardiology and vascular disease
Bradycardia
Heart rate <60 bpm.
Presentation Often an incidental nding but may present with faints or
blackouts, drop attacks, dizziness, breathlessness, or lack of energy.
Examination Slow pulse rate; normal/ low BP ± evidence of secondary
heart failure. There may also be symptoms/ signs of associated disease.
Investigations
• ECG 12- lead resting ECG; ambulatory ECG may help with diagnosis of
intermittent bradycardia (e.g. sick sinus syndrome)
• Blood TFTs, FBC, ESR, U&E, LFTs, digoxin levels (if taking digoxin)
Sinus bradycardia Constant bradycardia. P waves present and P– R
interval <0.2sec (1 large square). Causes:
• Physiological, e.g. athletes
• Vasovagal attack
• Drugs, e.g. β- blockers, digoxin
• Inferior MI
• Sick sinus syndrome
Management Admit acutely if symptomatic. Refer for cardiology opinion
if asymptomatic but HR <40bpm despite treatment of reversible causes.
AV node block (heart block) Causes :
• IHD
• Drugs (digoxin, verapamil)
• Myocarditis
Types ofheartblock
• 1st- degree block Fixed P– R interval >200msec (1 large square)
• 2nd- degree block:
• Mobitz type I(Wenckebach)— progressively lengthening P– R interval
followed by a dropped beat
• Mobitz type II— constant P– R interval with regular dropped beats
(e.g. 2:1— every second beat is dropped— consider drug toxicity)
• 3rd- degree block (complete heart block)— P– P intervals are constant
and R– R intervals are constant but not related to each other
Management Untreated 2nd- and 3rd- degree heart block have a mortality of 735%. Refer all patients to cardiology even if asymptomatic. If
symptomatic (d BP <90mmHg systolic, left ventricular failure, heart rate
<40bpm) admit as an emergency— give IV atropine and O2 (if available)
while awaiting admission.
Stokes Adams attacks Cardiac arrest due to AV block. Results in
sudden loss of consciousness ± some limb twitching due to cerebral anoxia.
The patient becomes pale and pulseless but respiration continues. Attacks
usually last 730 sec although occasionally are fatal. On recovery the patient
becomes ushed. Refer to cardiology if suspected.
• Hypothyroidism
• Hypothermia
• i ICP
• Jaundice
• Cardiomyopathy
• Fibrosis
• Lyme disease (rare)
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BRADYCARDIA
Sick sinus syndrome Due to sinus node dysfunction causing:
• Bradycardia ± asystole
• Sinoatrial block (complete heart block)
• AF or SVT alternating with bradycardia (tachy/ brady syndrome)
Common among elderly patients. If symptomatic, heart rate <40bpm or
pauses >3sec on ECG, refer to cardiology for pacemaker insertion.
Pacemakers Electrically stimulate the heart to beat. Indications:
• Symptomatic bradycardia
• 2nd- or 3rd- degree heart block
• Suppression of resistant tachycardia
Insertion Pacemaker box is attached under the skin of the chest— usually
medial to the left axilla— under LA. Wires are fed into the great veins of the
chest and thus to the heart under X- ray and/ or US guidance.
Types Classied according to:
• Chamber paced— atrium, ventricle, or both (‘dual’)
• Chamber sensed— atrium, ventricle, or both (‘dual’)
• Mode of response to sensing— inhibited output, triggered, inhibited, and
triggered (‘dual’)
Thus a VVI pacemaker both paces and senses the ventricle in inhibited
mode— i.e. if the ventricle beats spontaneously, the pacemaker will not re.
ECG changes witha pacemaker If the pacemaker is in operation, a pacing
‘spike’ (vertical line) is seen on ECG.
0 In devices pacing on demand, a spike will not be seen if the natural rate
is in excess of the rate set on the pacemaker.
Lifespan Pacemakers last 7– 15y. Regular checks are made by pacemaker
clinics to ensure the pacemaker remains operational. Reprogramming
through the skin is possible. Batteries can be changed via a small surgical
procedure under local anaesthetic.
Driving and arrhythmia E p. 241
Driving with a pacemaker Inform DVLA and insurance company. Stop
driving for 1mo after insertion.
243
• Pacemakers must be removed after death before cremation can occur.
Afee is payable.
Further information
NICE (2010, updated 2014)Transient loss of consciousness (blackouts) in
over 16s. M www.nice.org.uk/ guidance/ cg109
NICE (2014) Bradycardia:dual chamber pacing. M www.nice.org.uk/
guidance/ ta324
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