Cardiology Flashcards
Midline sternotomy +…
Metallic click
Mechanical valve replacement
Midline sternotomy +…
Murmur
Tissue valve
Valvotomy
Midline sternotomy +…
Vein harvest scars
CABG
Midline sternotomy +…
Old scar, young patient
Repair of congenital defect
Midline sternotomy +…
Immunosuppression
Heart transplant
Midline sternotomy +…
No other findings
Trauma: tamponade,
Internal mammary artery CABG
Tissue valve
Cardiac Causes of Clubbing
Infective endocarditis
Congenital cyanotic heart disease
- Fallot’s tetralogy
- VSD
- Pulmonary stenosis
- Right ventricular hypertrophy
- Overriding aorta
- Transposition of the Great Vessels
Atrial myxoma
Associated with Carney Complex LAMES syndrome
Lentigines: spotty skin pigmentation
Atrial Myxoma
Endocrine tumours: pituitary
Schwannomas
Causes of Collapsing Pulse
Caused by hyperdynamic circulation
ATAP
Aortic regurgitation
Thyrotoxicosis
Anaemia
Pregnancy
Causes of Absent Radial Pulse
Arrest
Trauma
Thrombosis/ embolism
Co-arctation of aorta
Takayasu’s arteritis
Impalpable Apex Beat
COPD
COPD
Obesity
Pericardial effusion
Dextrocardia
Features of Pulmonary Hypertension
Increased JVP
Left parasternal heave
Loud P2 + Pan-systolic murmur of Tricuspid regurgitation
Pulsatile hepatomegaly
Ascites and peripheral oedema
Heart sounds
S1 = mirtal valve closure
S2 = aortic valve closure
S3 = rapid venitrcular filling of dilated left ventricle
S4 = atrial contraction against stiff ventricle
Signs on Examination of Aortic Stenosis
Slow-rising pulse
Narrow pulse pressure <30mmHg
Precordium
Pacemaker
Aortic thrill
Apex: forecful, non-displaced
HS: Quiet A2, S4 (forceful atrial contaction against hypertrophied left ventricle)
Murmur
Early, ejection systolic murmur
Right 2nd ICS
Loudest sitting forward at end-expiration
Radiates to carotids
SEVERE AS
Quiet, absent A2
S4
Narrow pulse pressure
Decompensation: LVF
Significant negatives
Infective endocarditis
LVF
Indicators of severity
Clinical Signs of Severe Aortic Stenosis
Quiet A2
S4
Narrowed pulse pressure
LVF
Differential for Aortic Stenosis
Aortic sclerosis: no radiation to carotids, normal pulse character
Mitral regurgitation (also, systolic murmur)
HOCM: valsalva increases murmur, squatting decreases murmur
Pulmonary stenosis: right sided
Causes of Aortic Stenosis
Age-related senile calcification
Biscuspid aortic valve
Rheumatic heart disease
Clinical symptoms of Severe Aortic Stenosis
Angina: 50% dead in 5 years
Syncope: 50% dead in 3 years
Dyspnoea: 50% dead in 2 years
Clinical signs
Quiet A2
S4
LVF
Narrowed pulse pressure
Echo features of severe Aortic stenosis
Valve area <1cm2
Pressure gradient >40mmHg
Jet velocity >4m/s
Management of Aortic Stenosis
MDT: GP, Cardiologist, Cardiothoracic surgeons, dietician, specialist nurse
Conservative
- Monitor, regular follow-ups with echo
Medical
- Optimise CV risk factors: atorvastatin, Anti-HTN, DM, anti-platelets
Surgical
- if symptomatic then valve replacement
- if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction then consider surgery
- balloon valvuloplasty is limited to patients with critical aortic stenosis who are not fit for valve replacement
- TAVI
Signs of Mitral Regurgitation on Examination
Peripheral inspection: warfarin bracelet
Pulse: Atrial fibrillation
Precordium
Left parasternal heave
Apex: THRUSTING displaced - volume oberload as ventricle has to pump forward systolic volume and regurgitant volume —> eccentric hypertrophy
HS: Soft S1, S2 not heard separately from the murmur (+/- loud P2 if pulmonary hypertension)
Murmur
Blowing: pansystolic murmur
Loudest at apex, left lateral position and on end-expiration
Radiates to axilla
Clinical signs of severe Mitral Regurgitation
Left ventricular failure
Atrial fibrillation
Significant negatives: Infective endocarditis, AF, LVF (indicators of severity)
Differential for Mitral Regurgitation
Aortic stenosis (systolic)
Ventricular septal defect
Tricuspid regurgitation: right-sided
Clinical Signs of Severe Mitral Regurgitation
LVF
AF
Causes of Mitral Regurgitation
Functional: Left ventricular dilatation secondary to hypertension or idiopathic
Annular calcification —> contraction
Rheumatic heart disease
Mitral valve prolapse
ECG changes in Mitral Regurgitation
P-mitrale (atrial hypertrophy)
Arrhythmias
- Atrial premature beats
- Paroxysmal supraventricular tachycardia
- Ventricular premature beats
- Complex ventricular ectopy
Left ventricular hypertrophy
Echo features of severe Mitral Regurgitation
Jet width of >0.6cm
Systolic pulmonary flow reversal
Regurgitant volume >60ml
Management of Mitral Regurgitation
MDT: GP, cardiologist, cardiothoracic surgeon, dietician, specialist nurse
Optimise cardiovascular risk factors: Atorvastatin, anti-platelet, anti-HTN, DM
Specific
AF: rate control and anti-coagulate
Reduce afterload: ACE-inhibitor or b-blocker (esp Carvedilol)
Surgical:
Valve replacement or repair
If unfit: ?Percutaneous mitral valve leaflet repair for mitral regurgitation
Aim to replace the valve before significant LV dilatation and dysfunction
Indications for surgery: symptomatic
Eponymous signs of Aortic Regurgitation
Quincke’s sign: capillary pulsation in nail beds
Corrigan’s: visible vigorous carotid pulsation
De Musset’s: head bopping
Traube’s: pistol-shot femorals (pistol-sound heard over femorals)
Durozieze’s: systolic murmur over femoral artery with proximal compression, diastolic murmur with distal compression
Mueller’s: systolic pulsations of uvula
Rosenbach’s: systolic pulsations of the liver
Causes of Aortic Regurgitation
Marfan’s
Tall, thin, long arms, high-arched palate
Ankylosing spondylitis: cervical kyphosis
Signs of Aortic Regurgitation on Examination
Pulse: Collapsing
Wide pulse pressure e.g. 180/45
Precordium
Aortic thrill
Apex: displaced (volume overload)
HS: soft S2, +/- S3
Murmur
High-pitched early diastolic murmur
Loudest on lower left sternal edge (parasternal 3rd IC), sitting forward in end-expiration
Additional murmurs:
Ejection systolic flow murmur
Austin-flint murmur = rumbling mid-diastolic murmur secondary to regurgitant jet fluttering the anterior of mitral valve
Clinical Signs of Severe Aortic Regurgitation
Collapsing pulse
Wide pulse pressure
Left ventricular failure
Significant negatives: infective endocarditis, indicators of severity (LVF, wide pulse pressure, collapsing pulse)
Clinical Signs of Severe Aortic Regurgitation
Collapsing Pulse
Wide pulse pressure
Left ventricular failure
Causes of Aortic Regurgitation
Chronic
Bicuspid aortic valve
Rheumatic heart disease
Autoimmune: ankylosing spondylitis
Connective tissue disease: Marfan’s, Ehlers-Danlos
Acute
Infective endocarditis
Type A aortic dissection
Differential for Aortic Regurgitation
Mitral stenosis
Pulmonary regurgitation, tricuspid stenosis: right-sided
Echo findings in Aortic Regurgitation
Severe
Jet width >65% of outflow tract
Regurgitant jet volume
Premature closure of mitral valve
Management of Aortic Regurgitation
MDT: GP, cardiologist, cardiothoracic surgeon, dietician, specialist nurse
Optimise cardiovascular risk factors: Atorvastatin, anti-platelet, anti-HTN, DM
Specific
Reduce afterload: ACE-inhibitor, or b-blockers (carvedilol) OR diuretics
Surgical: valve replacement (before LV dilatation)
Indications: NYHA >2, LV dysfunction
Pulse pressure >100mmHg
ECG changes: T invesion in lateral leads
LV enlargement on CXR or EF <50%
Signs of Mitral Stenosis on Examination
Peripheral inspection: middle-aged female, wafarin bracelet, malar flush
Pulse: Atrial fibrillation
Precordium
Left parasternal heave: Right ventricular hypertrophy secondary to pulmonary hypertension
Apex: Tapping (palpable S1), non-displaced
HS: Loud S1, +/- Loud S2 if Pulmonary hypertension
Murmur
Rumbling mid-diastolic murmur
Loudest at the apex, left lateral position, with the bell, radiating to axilla
+/- Graham Steell (early diastolic) murmur due to pulmonary regurgitation secondary to pulmonary hypertension
Clinical Signs of Severe Mitral Stenosis
Malar flush
Long murmur
LVF
Significant Negatives: infective endocarditis, indicators of seveirty, evidence of pulmonary hypertension (raised JVP with large v waves, left parasternal heave, loud P2)
Causes of Mitral Stenosis
Rheumatic heart disease
Other rarer causes: prosthetic valve, congenital
Echo features of Severe Mitral Stenosis
Valve orifice <1cm2
Pressure gradient >10mmHg
Pulmonary artery systolic pressure >50mmHg (pulmonary hypertension)
Management of Mitral Stenosis
MDT: GP, cardiologist, cardiothoracic surgeon, dietician, specialist nurse
Optimise cardiovascular risk factors: Atorvastatin, anti-platelet, anti-HTN, DM
Specific
AF: Rate control with b-blockers, anti-coagulate
Diuretics for symptomatic relief
Surgical
Indicated in mod-severe mitral stenosis
Percutaneous balloon valvuloplasty
CI: atrial mural thrombus
Valve replacement
Pathophysiology of Rheumatic Fever
Antibiody cross-reactivity following Strep pyogenes infection
Leading to a Type II hypersensitivity reaction (molecular mimicry)
Antibodies cross-react with myosin, muscle glycogen and smooth muscle cells
Histology: Aschoff bodies and Anitschkow myocytes
Revised Jones Criteria
Evidence of Group A strep infection
AND
either
2 major criteria
OR
1 major + 2 minor criteria
Major Criteria (Jones) Rheumatic Fever **PASES**
PASES
Pancarditis
Arthritis
Subcutaneous nodules
Erythema marginatum
Sydenham’s chorea
Minor Criteria (Jones) Rheumatic Fever
FEPAP
Fever
ESR / CRP raised
Prolonged PR interval (not if carditis is major)
Arthralgia (not if arthritis is major)
Previous rheumatic fever
Management of Rheumatic Fever
Bed rest for 2 weeks
Benpen for strep throat
Naproxen for arthritis
Diazepam if chorea not settling
Causes of recurrence of rheumatic fever
Strep throat infection again
Pregnancy
OCP
Valve disease in rheumatic heart disease
Mitral: 70%
Aortic: 40%
Tricuspid: 10%
Pulmonary: 2%
Regurgitation —> stenosis
Rheumatic fever prognosis
resolves within ~3 months
60% of those with carditis will have rheumatic heart disease
Secondary prophylaxis against rheumatic fever
Pen V 250mg / 12h
For at least five years or until age 21 years, whichever is longer.
This should be for ten years for RF with carditis but no valvular disease (or well into adulthood, whichever is longer).
However, with substantial valvular disease this should be continued longer. In severe valvular damage, or with valve surgery, prophylaxis should be continued for life
Signs of Valve Replacement on Examination
General: audible click, bruising from anti-coagulation, warfarin bracelet, anaemia
Scars
- Midline sternotomy: CABG, aortic valve replacement, mitral valve replacement
- Left lateral inferior thoracotomy: mitral valve replacement, mitral valvotomy
- Neck scars: central line insertion
- Groin / femoral / wrist scars from angiography
- Vein harvesting
Pulse:
AF suggestive of mitral replacement due to mitral stenosis
Time click with pulse, occurs in time = mitral valve (systole –> mitral closure)
Precordium
3 artifical sounds = Starr-Edwards
1 artifical sound = tilting disc or bileaflet
No sounds - biological valve
Aortic replacement: lub-click
+/- systolic flow murmur
Mitral replacement: click-dub
+/- diastolic flow murmur
Murmurs
well-seated valves –> flow murmurs
Aortic: systolic
Mitral: diastolic
Poorly seated valves –> regurgitation
Aortic: diastolic
Mitral: systolic
Starr-Edwards Valve
3 artifical sounds
Quiter click as valve opens
Loud thud as valve closes
Rumbling sound as ball rolls in cage
Tilting disc valve
Bileaflet valve
1 artificial sound
high-pitched click as valve closes
Complications of valve replacement
Thromboembolism: 1-2% per annum despite warfarin
Anaemia: haemolysis
Bleeding
Infective endocarditis
Failure
Acute: breakage, thrombus, dehiscence
Chronic: stenosis or incompetence
Risk Factors for Infective Endocarditis
IVDU
Skin wounds
Immunosuppression: Chronic Renal Failure, Diabetes Melitus
Organisms causing Infectiv Endocarditis
Strep viridans (most common)
Staph aureus (IVDU)
S.epidermidis
S. bovis (needs colonoscopy for colonic neoplasm)
HACEK = culture negative IE
Clinical Features of Infective Endocarditis
Hands
Clubbing
Splinter haemorrhages
Janeway lesions
Osler nodes
Cardiac
New/changing murmur
Mitral regurgitation: 85%
Aortic regurgitation: 55%
Other
Fever
Roth spots
Splenomegaly
Haematuria
Duke Criteria for Infective Endocarditis
2 major
OR
1 major AND 3 minor
OR
All 5 minor
Major Duke Criteria
1) Positive blood culture
Typical organism in 2 separate cultures OR persistently +ve cultures e.g. 3 >12 h apart
2) Endocardial involvement
+ve echo vegetation, abscess, dehiscence
OR
New valvular regurgitation
Minor Duke Criteria (5)
- Predisposition: IVDU, cardiac lesion
- Fever >38
- Emboli: septic infarcts, splinters, janeway lesions
- Immunological phenomena: Glomerulonephritis, Osler nodes, Roth spots, RF
- +ve blood culture not meeting major criteria
Treatment of Infective Endocarditis
Acute severe:
Flucloxacillin OR Vancomycin IV
+ Gentamicin IV
Subacute:
Benpen + Gentamicin IV
Apex Beat Displacement
Thrusting displaced apex beat is caused by volume overload: an active large stroke volume ventricle eg aortic or mitral regurgitation or left to right shunts.
Sustained apex beat is caused by pressure overload eg aortic stenosis, gross hypertension.
Tapping apex beat - mitral stenosis.
Diffuse pulsation asynchronous with apex beat - left ventricular aneurysm.
Double or triple impulse may occur in hypertrophic obstructive myopathy.
Impalpable apex beat - obesity, overinflated chest, pericardial effusion. Also consider dextrocardia.
Signs of Atrial Fibrillation on Exmaination
On inspection:
Hyperthyroidism: tremor, thin, palmar erythema, sweating, eye signs
Mitral stenosis: malar flush
Pneumonia: bronchial breath sounds + added sounds
Pulse: irregularly irregular
Precordium
Mitral stenosis: mid-diastolic murmur
Mitral regurgitation: pan-systolic murmur
Significant negatives: murmur, evidence of hyperthyroidism, LVF, bruising from warfarin
Causes of Atrial Fibrillation
Common
IHD
Rheumatic herat disease
Thyrotoxicosis
HTN
Other
Pneumonia
PE
Post-op
Potassium: hypokalaemia
Poison: alcohol
Painful joints: rheumatoid arthritis
Differential diagnosis of irregularly irregular pulse
AF
Remains when exercising the patient
Multiple ventricular ectopics
As patient exercises, pulse appears regular as there is reduced window for ectopics
Pulse deficit
Difference ub HR at the wrist and at the apex
CHA2DS2-VASc Score
Determine the necessity of anticoagulation in AF
Congestive heart failure/left ventricular dysfunction (heart failure with reduced ejection fraction, or people with recent decompensated heart failure requiring hospitalization, irrespective of ejection fraction) = 1
Hypertension (defined as a resting blood pressure greater than 140 mmHg systolic and/or greater than 90 mmHg diastolic on at least 2 occasions or current antihypertensive pharmacologic treatment) = 1
A2ge older than or equal to 75 years = 2
Diabetes mellitus (defined as fasting plasma glucose level of 7.0 mmol/L [126 mg/dL] or more or treatment with oral hypoglycaemic drugs and/or insulin) = 1
S2troke/TIA/thromboembolism = 2
Vascular disease (prior myocardial infarction, peripheral arterial disease, or aortic plaque) = 1
Age 65–74 years = 1
Sex category (female) = 1
Anticoagulation treatment = CHA2DS2VASc score of 2 or above,
Consider offering it to men with a CHA2DS2VASc score of 1
Weigh up with HASBLED
HAS-BLED Score
Identify people at high risk of bleeding who could benefit from increased vigilance and a specific focus on correction of modifiable risk factors
- Uncontrolled hypertension
- Poor control of INR
- Concurrent medication (for example concurrent use of aspirin or a nonsteroidal anti-inflammatory drug)
- Harmful alcohol consumption
Hypertension (uncontrolled, greater than 160 mmHg systolic)
Abnormal liver function / Abnormal renal function
Stroke (previous history, particularly lacunar)
Bleeding (bleeding history or predisposition)
Labile international normalized ratios (INRs, therapeutic time in range less than 60%)
Elderly (aged over 65 years)
Drugs (antiplatelet agents or nonsteroidal anti-inflammatory drugs)
Harmful alcohol consumption
Management of new-onset AF
Admit if they present with severe symptoms or a serious complication of AF.
- Identify and manage any underlying causes or triggers of AF.
- Treat the arrhythmia :
- rate-control treatment (beta-blocker or a rate-limiting calcium-channel blocker) is recommended for most people with AF
- Referral for rhythm-control treatment (cardioversion) may be appropriate for people:
- With new-onset AF.
- Whose AF has a reversible cause (for example a chest infection).
- Who have heart failure thought to be primarily caused, or worsened, by AF.
- With atrial flutter and is considered suitable for an ablation strategy to restore sinus rhythm.
- Rate-control or rhythm-control treatment should be considered for people with AF presenting acutely with non-life threatening haemodynamic instability, depending on the time of onset of arrhythmia.
- Assess stroke risk using the CHA2DS2VASc assessment tool.
- Assess risks and benefits of anticoagulation , and start treatment if appropriate.
- The HAS-BLED assessment tool should be used to assess the risk of a major bleed and to identify and manage modifiable risk factors for bleeding, such as uncontrolled hypertension, harmful alcohol consumption, and concurrent use of aspirin or a nonsteroidal anti-inflammatory drug.
Arrange follow up :
- After starting rate-control treatments — to assess their effectiveness and tolerability.
- After starting anticoagulation treatment — to assess compliance and adverse effects.
Provide advice and information on AF, its treatments, and where to find support groups.
Management of AF
1st Line
- Offer a rate-control treatment to most people with atrial fibrillation
- Offer a beta-blocker (see Choice of beta-blocker) or a rate-limiting calcium-channel blocker (diltiazem [off-label use] or verapamil)
- Consider digoxin monotherapy for people with non-paroxysmal AF only if they have a sedentary lifestyle (that is, they do little or no exercise)Follow up within 1 week of starting rate-control treatment to assess tolerance to treatment and to review symptom control, heart rate, and blood pressure.
Refer to a cardiologist for consideration of rhythm-control treatment (cardioversion), people:
- With new-onset AF.
- Whose AF has a reversible cause (for example a chest infection).
- Who have heart failure thought to be primarily caused, or worsened, by AF.
- With atrial flutter who are considered suitable for an ablation strategy to restore sinus rhythm.
- For whom a rhythm-control strategy would be more suitable based on clinical judgement.
For people with AF presenting acutely with non-life threatening haemodynamic instability, rate-control or rhythm-control treatment should be considered, depending on the time of onset of arrhythmia.
- If the onset of arrhythmia is within 48 hours, offer rate-control treatment or refer the person to an acute medical unit for consideration of immediate cardioversion (without the need for anticoagulation treatment).
- If the onset of arrhythmia is more than 48 hours or uncertain, start rate-control treatment. If referral for consideration for rhythm-control treatment (cardioversion) is thought to be necessary using clinical judgement, cardioversion should be delayed until the person has been maintained on therapeutic anticoagulation for a minimum of 3 weeks.
Rhythm-control treatments used by specialists include:
- Electrical cardioversion.
- Pharmacological cardioversion with antiarrhythmic drugs (such as amiodarone or sotalol).
- For people having cardioversion for atrial fibrillation (AF) that has persisted for longer than 48 hours, electrical (rather than pharmacological) cardioversion is used
Contrainidcations to Warfarin
Coagulopathues
Compliance issues
Risk of falls
PUD
Pregnancy
Patient choice
Signs of Pacemaker on Examination
Inspection: groin scars from insertion, Medic alert bracelet
Pulse: AF
Precordium
Left infraclavicular incisional scar
Palpable pacemaker: if large ? defibrillator
Murmur ?aortic stenosis
Significant negatives: AF, LVF, valvuar pathology, complications of pacemaker (infection or erosions)
Signs of pacemaker on ECG
Pacing spikes
Physiological ECG trace does not include vertical signals
Evidence of ischaemia
Permanent pacemaker indications
Complete AV block
Mobitz type II
Symptomatic bradycardia e.g. sick sinus syndrome
Drug-resistant tacharrhythmias
Biventricular pacing in chronic heart failure
Letters of pacemaker
1st: chamber paced (A, V, or D)
2nd: chamber sensed (A, V, or D)
3rd: Response (Inhibited, Triggered, Dual)
Number of Pacemaker Leads
Single lead: one lead senses and responds
e.g. VVI
Dual lead: sense and respond in either chamber
Biventricular: leads to both ventricles +/- right atrium
Used for cardiac resynchronisation therapy in HF
Dual lead pacemaker
One lead in rigth atrium
One in right ventricle
Single lead pacemaker
Biventricular pacemaker
Right atrium and right venbtricle lead inserted intravenously
Left ventricle lead was placed epicardially via mini-sternotomy and tunneled up to the prepectoral pocket
Implantable defibrillator
Can be incorporated into any pacemaker
Complications of a Pacemaker
Insertion
Bleeding
Arrhythmia
Post-insertion
Erosion
Lead migration
Pocket infection
Malfunction
Definition of Chronic Heart Failure
Cardiac output is inadequate for the body’s requirments despite adequate filling pressures
Caues of Left-sided heart failure
Ischaemic heart disease
Idiopathic dilatated cardiomyopathy
Systemic hypertension
Mitral and aortic valve disease
Signs and Symptoms of Left-Sided Heart Failure
Signs
Cold peipheries +/- cyanosis
AF
Cardiomegaly with displaced apex beat
S3 + tachycardia = gallop rhythm
Wheeze (cardiac asthma)
Bibasal crepitations
Symptoms
Fatigue
Exertional dyspnoea
Orthopnoea and paroxysmal nocturnal dyspnoea
Nocturnal cough (+forthy pink sputum)
Weight loss and muscle wasting
Causes of Right-Sided Heart Failure
Left ventricular failure
Cor pulmonale
Tricuspid and pulmonary valve disease
Signs and Symptoms of Right-Sided Heart Failure
Signs
Increased JVP + jugular venous distension
Tender smooth hepatomegaly (may be pulsatile)
Pitting oedema
Ascites
Symptoms
Anorexia
Nausea
New York Classification of Heart Failure
I: nil shortness of breath
II: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: Shortness of breath at rest
NT-proBNP
Secreted from ventricles in response to stretch and increased HR
Increased levels are sensitive marker of HF
If low, revise diagnosis
CXR changes in heart failure
Alveolar shadowing
Kerley B lines
Cardiomegaly
Upper lobe Diversion
Effusions
Fluid in the fissures
ECG findings in chronic heart failure
Ischaemia
Hypertrophy
AF / arrhythmias
Echo findinds in CHF
Focal / global hypokinesia
Hypertrophy
Valve lesions
Ejection fraction reduced (normally 60%)
Can be normal HF PEF
Management of CHF
MDT: Gp, cardiologist, physio, dietician, specialist nurse
Optimise CVS risk factors: statins, Anti-HTN, DM, anti-platelet
Specific
1st-line treatment for all patients is both an ACE-inhibitor and a beta-blocker
2nd- line treatment is now either an aldosterone antagonist, angiotensin II receptor blocker or a hydralazine in combination with a nitrate
3rd -line: If symptoms persist cardiac resynchronisation therapy or digoxin* should be considered. A
n alternative supported by NICE in 2012 is ivabradine. The criteria for ivabradine include that the patient is already on suitable therapy (ACE-inhibitor, beta-blocker + aldosterone antagonist), has a heart rate > 75/min and a left ventricular fraction < 35%
Adjuncts
diuretics should be given for fluid overload
offer annual influenza vaccine
offer one-off** pneumococcal vaccine
Trials for Heart Failure Drugs
ACE inhibitors (SAVE, SOLVD, CONSENSUS)
spironolactone (RALES)
beta-blockers (CIBIS)
hydralazine with nitrates (VHEFT-1)
