Cardiology (Structural disease) Flashcards
pericarditis
inflammation of the pericardium
- acute if onset within 4-6 weeks
RF for pericarditis
- Male sex
- Aged 20-50 years
- Post-myocardial infarction
- Cardiac surgery
- Malignancy
- Viral and bacterial infections
- Chronic kidney disease and uraemia
- Dialysis
- Systemic autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis
presentation of pericarditis
Chest pain is the most common presenting complaint:
- Usually acute
- Described as sharp
- Pleuritic – worse with inspiration
- It is usually relieved leaning forward or sitting up
- It is usually worsened lying down
- Tachycardia
- Tachypnoea
- Pericardial friction rub on auscultation
- Fever
- Myalgias
investigations for pericarditis
ECG:
- May show global saddle-shaped ST-elevation with PR depression
- PR depression is most specific for pericarditis
Cardiac troponins:
- May be raised in pericarditis
- Also used to look for acute coronary syndrome
Echocardiography – an essential investigation:
- Detects pericardial effusions, which if large enough, can cause cardiac tamponade, a life-threatening complication
Pericardiocentesis:
- If suspected cardiac tamponade
- Aspirates can be sent for microscopy and cytology to identify underlying causes
Others
- D-dimer to rule out PE
- ESR/ CRP
- FBC, UE, LFTs
- CXR
management of pericarditis
Treat underlying cause
First line NSAIDs + proton pump inhibitors + colchicine
Second line
- Corticosteroids are used under specialist guidance if:
- Infection has been ruled out and NSAIDs and colchicine fail or
- There is a specific indication e.g. autoimmune diseases like systemic lupus erythematosus – in this case, corticosteroids and colchicine are used
complication of pericarditis
- Pericardial effusion and potential cardiac tamponade
- Chronic constrictive pericarditis – relatively rare
- In the healing process, some of the pericardium may be replaced with scar tissue which can interfere with ventricular filling
dressler syndrome
Dressler’s syndrome is thought to be an autoimmune response to the pericardium after myocardial infarction. It is a post-myocardial infarction pericarditis that usually happens 1-6 weeks after the myocardial infarction. In some cases, it may be delayed for as long as 3 months.
cardiac tamponade
accumulation of fluid, blood, pus, clots, or air in the pericardial space leading to restricted heart movement, reduced ventricular filling and haemodynamic compromise.
causes of cardiac tamponade
- Traumatic injury to the chest
- Mlaignnacy e.g. breast or lung cancer
- Acute MI
- Post MI - dressler
- Infective e.g. HIV, TB
- Rheum - SLE, RA
- Radiation
- Chronic kidney disease- uraemia
The classic features of cardiac tamponade are described with
Beck’s triad:
1) Hypotension
- There is a weak pulse and narrowed pulse pressure
2) Muffled heart sounds
3) Raised jugular venous pressure (JVP)
Other features
- Dyspnoea – seen in 90%
- Pulsus paradoxus
- > 10mmHg drop in systolic blood pressure during inspiration
- Tachycardia
- Absent y descent in the JVP
management of cardiac tamponade
Urgent pericardiocentesis
The aspirate should be sent for culture and cytology to identify underlying causes
Myocarditisis
the acute or chronic inflammation of the myocardium. Continued inflammation and destruction of the myocardium can lead to dilated cardiomyopathy. It is a diagnosis that should be considered in younger patients with chest pain.
causes of myocarditis
most common:
Viral
- coxsackievirus, adenovirus, parvovirus, HIV, EBV, hepA, hepC
Bacterial
- Diphtheria
- Syphilis
- TB
Fungal
- Candida
- Aspergillus
Autoimmune
- Sarcoidosis
- SLE
- Hyperthyroid
Drugs
- ethanol
- cocaine
- lithium
myocarditis presentation
- There is often a history of a viral infection 2-3 weeks prior
- Chest pain
- Dyspnoea
- Orthopnoea
- Syncope
- Fatigue
- Palpitations
- May have soft S1
- May have S3 or S4 gallop
*
investigations for myocarditis
12-lead ECG:
* May show non-specific ST and T-wave changes such as ST elevation and ST depression
Chest x-ray:
* Ordered in any patient with shortness of breath
* May show pulmonary infiltrates if myocardial-induced heart failure develops
Cardiac troponins:
* May be elevated
* To screen for myocardial infarction
NT-proBNP:
* May be elevated if myocarditis-induced heart failure develops
Echocardiogram:
* Shows global and regional LV motion abnormalities and dilation
management of myocarditis
Management involves treating the underlying cause and is supportive if patients have no signs of LV dysfunction. Corticosteroids may be used if there is an underlying autoimmune aetiology.
If LV dysfunction develops, patients are given heart failure treatment.
primary cardiomyopathies causes
Genetic cardiomyopathies:
* Hypertrophic obstructive cardiomyopathy (HOCM)
* Arrhythmogenic right ventricular cardiomyopathy (ARVC)
* Ion channelopathies including long QT syndrome
Mixed cardiomyopathies:
* Dilated cardiomyopathy
* Restrictive cardiomyopathy
Acquired cardiomyopathies:
* Stress cardiomyopathy (Takotsubo cardiomyopathy)
* Myocarditis
* Peripartum cardiomyopathy
common causes of secondary cardiomyopathies
Infective
- coxsackie B virus
Endocrine
- thyrotoxicosis
Toxic
- alcohol
Autoimmune
- SLE
- Sarcoidosis
Hypertrophic obstructive cardiomyopathy (HOCM)
- Autosomal dominant condition and is the most common cardiomyopathy.
- It is the most frequent cause of sudden cardiac death in young people.
- It is characterised by left ventricular hypertrophy, impaired diastolic filling, and mitral valve abnormalities.
presentation of hypetrophic cardiomyopathy
- Most people are asymptomatic
- Dyspnoea is the most common presenting complaint
- Chest pain
- Palpitations
- Syncope, which may happen on exertion
- Incidentally picked up on ECG/clinical examination
- Dyspnoea/syncope when drinking alcohol
- Features of heart failure
- Ventricular arrhythmias
- Sudden cardiac death, which may happen on exertion
signs on examination of hypertrophic obstructive cardiomyopathy
- Ejection systolic murmur at the lower left edge
- This is made louder with exercise and standing
- This is made quieter when lying supine or squatting
- Fourth heart sound (S4) due to stiff ventricle/impaired diastolic filling
- Features of atrial fibrillation i.e. irregularly irregular pulse
- Double apical impulse
differential for hypertrophic obstructive cardiomyopathy
Athlete’s heart
- Usually patient is an athlete without cardiac symptoms
- No family history of HCM or sudden death
- Hypertrophy regresses when exercise stops
- Echocardiogram shows symmetrical LVH with homogenous myocardial appearance
- LV filling pattern is mostly normal
investigations for hypertrophic obstructive cardiomyopathy
Initial investigations
ECG:
* Prominent Q waves
* Left ventricular hypertrophy
* Atrial fibrillation may be seen
* Giant T wave inversion
Chest x-ray:
* Not very sensitive: may show cardiomegaly, may be normal
Echocardiography – features remembered using MR SAM ASH:
* Mitral regurgitation (MR)
* Systolic anterior motion (SAM) of the anterior mitral valve leaflet
* Asymmetric hypertrophy (ASH)
Holter monitoring and an exercise ECG if tolerated to assess their risk of sudden death.
Factors increasing this risk of sudden death are:
- Family history of sudden death
- Family/personal history of unexplained syncope
- Previous cardiac arrest
- Previous sustained ventricular tachycardia
- Ventricular tachycardia on the Holter monitor
- Abnormal blood pressure responses to exercise
- Massive left ventricular hypertrophy
- Severe outflow obstruction demonstrated on echocardiogram
- Left ventricular ejection fraction <50%
- Presence of left ventricular aneurysm
management of asymptomatic patients with HOCM
High risk of sudden death:
* 1st line: implantable cardioverter-defibrillator (ICD) + avoid high-intensity exercise
Not at high risk of sudden death:
* 1st line: observation
management of symptomatic and preserved systolic function patients with HOCM
1st line: beta-blockers or verapamil
Consider ICD if:
- Higher risk level
- New symptomatic or concerning asymptomatic ventricular arrhythmias develop
Consider amiodarone to prevent recurrences of atrial fibrillation
Consider if medical therapy is inadequate:
- Myectomy or
- Dual-chamber pacing if cannot have surgery/not desired
If patients develop heart failure, they are treated using standard heart failure therapy.
All patients with HCM should:
- Avoid high-intensity athletics
- Undergo regular testing with echocardiography, Holter monitors, ECGs etc. to assess their risk of sudden cardiac death and consideration of an ICD to prevent it
- Be considered for anticoagulation if they develop atrial fibrillation
- Be followed-up lifelong
- Seek medical help if they have exertional chest pain, dyspnoea, palpitations, presyncope/syncope
Takosubo cardiomyopathy also known as
stress cardiomyopathy or ‘broken heart syndrome’
Takosubo cardiomyopathy
- a type of non-ischaemic cardiomyopathy characterised by a sudden transient weakening and ballooning of the myocardium.
Pathophysiology
- Its pathophysiology is not fully understood, but it is thought that significant elevations in catecholamines may cause microvascular spasms and injury to the myocardium.
- Stress cardiomyopathy is more common in post-menopausal women
- Oestrogen promotes vasodilation in the cardiovascular system, therefore, in times of vasoconstriction, it is exaggerated in post-menopausal women
presentation of takotsubo (stress cardiomyopathy)
Patients present with chest pain with or without features of heart failure following physical or psychological stress (e.g. finding out bad news, such as a relative passing away). Features include:
- Chest pain
- Dyspnoea
- Syncope
- Features of heart failure
investigations for takotsubo
ECG:
* May show ST-elevation
Troponins:
* May be mildly elevated
Transthoracic echocardiogram:
* Shows apical ballooning of the left ventricle
management of takotsubo
observation and monitoring, along with supportive treatment.
Most patients improve with supportive treatment.
infective endocarditis
infection of the endocardium of the heart
- non specific symptom
- causes vegetation of the valves of the heart
- mitral valve most commonly affected
- IVDU- tricuspid valve more commonly affected
infective endocarditis causes
- Staphylococcus aureus is the most common cause in developed countries and IVDUs
- Streptococcus viridans (Streptococcus mitis and Streptococcus sanguinis) are the most common in developing countries and in patients with poor dental hygiene following a dental procedure
- Staphylococcus epidermidis and other coagulase-negative Staphylococci are a common cause in indwelling lines or prosthetic valves in the first 2 months
- After 2 months, Staphylococcus aureus predominates
- HACEK species – Haemophilus, Aggregatibacter, Cardiobacterium hominis, Eikenella corrodens, and Kingella species
Risk Factors IE
- Previous infective endocarditis
- Valvular heart disease
- Valve replacements
- Structural congenital heart disease, even if it has been corrected
- Hypertrophic cardiomyopathy
- Intravenous drug use
- Invasive vascular procedures e.g. haemodialysis
IE should be suspected in any patients with
- Fever and signs and symptoms of embolism
- Fever and heart failure with risk factors for IE
- Fever and a new/worsening murmur – this is rare
Other symptoms
* Fever/chills
* Heart murmurs
* Night sweats
* Malaise
* Fatigue
* Anorexia
* Weight loss
* Myalgias
* Joint pain
* Headaches
* Shortness of breath
* Weakness e.g. asymmetric weakness consistent with a stroke
Signs of IE on Examination
- Fever
- Heart murmurs
- Petechiae in the conjunctiva, on the chest or abdominal wall, dorsum of the hands and feet, or in the oral mucosa and soft palate
- Splinter haemorrhages
- Osler’s nodes
- Clubbing – usually if long-standing
- Roth’s spots – retinal haemorrhages with pale centres
- Janeway’s lesions – usually with Staphylococcus aureus IE
- Meningism
=
investigations for IE
Blood cultures:
* If the patient is septic, do not delay giving empirical antibiotics
* If possible, take 3 blood cultures at different venepuncture sites at 30-minute intervals before giving empirical antibiotics
Transoesphageal Echocardiography:
* May show valvular, mobile vegetations
Full blood count (FBC):
* May show normocytic anaemia
* May show leukocytosis
C-reactive protein (CRP):
* A non-specific marker of inflammation, may be elevated
* Useful for monitoring treatment
Urea and electrolytes (U&Es):
* As a baseline
* Urea may be elevated
Urinalysis:
* To look for the distal spread of IE
* May show haematuria, RBC casts, white cell casts, proteinuria, pyuria
ECG:
* Progression of IE may lead to conduction abnormalities
* May cause PR prolongation or AV node blocks
Echocardiography – a key investigation:
May show vegetations
criteria for IE
Modified Duke criteria
IE is diagnosed if any of the following are met:
- A pathological criterion is positive
- 2 major criteria
- 1 major and 3 minor criteria
- 5 minor criteria
Pathological criteria:
- Microorganisms demonstrated by culture or on histological examination of valve tissue, vegetation, a vegetation that has embolised, or an intracardiac abscess sample
Major criteria for Dukes
- Positive blood cultures for IE
- Evidence of endocardial involvement
Minor criteria:
- Predisposing heart condition of IVDU
- Fever over 38°C
- Vascular phenomena: Major arterial emboli, septic pulmonary emboli, intracranial haemorrhage, conjunctival haemorrhage, Janeway lesions
Immune phenomena: Glomerulonephritis, Osler nodes, Roth spots, and Rheumatoid factor present
Microbiology:
* Positive blood cultures that do not meet major criteria
* Identification of previous recent embolic events or infectious aneurysms by imaging
Initial “blind” therapy for IE
- Native valve endocarditis: amoxicillin (or ampicillin) + consider low-dose gentamicin
- If penicillin allergic/suspected MRSA/severe sepsis: vancomycin + low-dose gentamycin
- Prosthetic valve endocarditis: vancomycin + rifampicin + low-dose gentamicin
Native valve endocarditis due to Staphylococcus
- Flucloxacillin
- If penicillin allergic/MRSA: vancomycin + rifampicin
Prosthetic valve endocarditis due to Staphylococcus
- Flucloxacillin + rifampicin + low-dose gentamicin
- If penicillin allergic/MRSA: vancomycin + rifampicin + low-dose gentamicin
Endocarditis caused by fully-sensitive Streptococcus
- Benzylpenicillin
- If penicillin allergic: vancomycin (or teicoplanin) + low-dose gentamicin
Endocarditis caused by less-sensitive Streptococci
- Benzylpenicillin + low-dose gentamicin
- If penicillin-allergic or highly penicillin-resistant: vancomycin (or teicoplanin) + low-dose gentamicin
Endocarditis caused by enterococci
- Amoxicillin (or ampicillin) + low-dose gentamicin or
- Benzylpenicillin + low-dose gentamicin
- If penicillin-allergic or penicillin-resistant: vancomycin (or teicoplanin) + low-dose gentamicin
- If gentamicin resistant: amoxicillin (or ampicillin) + streptomycin
Endocarditis caused by HACEK organisms
- Amoxicillin (or ampicillin) + low-dose gentamicin
- If amoxicillin-resistant: ceftriaxone (or cefotaxime) + low-dose gentamicin
surgery and IE
Surgery is indicated if:
- Heart failure develops
- There is severe valvular dysfunction
- There is an uncontrolled infection which may be characterised by:
- Abscess formation
- Enlarging vegetation
- Prosthetic valve endocarditis due to Staphylococcus or non-HACEK gram-negative bacteria
- Fungal or multidrug-resistant organism endocarditis
- Recurrent embolic events e.g. stroke
aortic stenosis
Narrowing of the aortic valve
- obstructs blood flow
- can be caused by valve fibrosis and calcification
causes of aortic stensosis
- Degenerative calcification and fibrosis – most common
- Congenital bicuspid valves (Turner’s syndrome)
- Rheumatic heart disease
presentation of aortic stenosis
- Exertional dyspnoea is the most common symptom
- Exertional syncope
- Fatigue
- Chest pain
aortic stenosis murmur
- Ejection systolic murmu
- Louded over right upper sternal border
- radiates to carotids
- louder on inspiration
investigations for AS
- Transthoracic echocardiogram
- ECG
- CXR
management of AS
Asymptomatic
- watch and wait
Asymptomatic but LVEF <50%
- Aortic valve replacement
Symptomatic
- Aortic valve replacement
Unfit for surgery
- Balloon vlvuloplasty
Complications of AS
Acute heart failure
Cardiac arrest
Infective endocarditis
Prosthetic valve infection
Mechanical valve thrombosis
aortic regurgitation
inadequate closure of the aortic valve leading to the backflow of blood during diastole. It can be due to problems with the aortic valve or the aortic root.
causes of aortic regurgitation
- Rheumatic fever
- Degenerative calcification
- Connective tissue disorders e.g. Marfans, Ehlers danlos
- IE
- Bicuspid aortic valve
aortic regurgitation murmr
Early diastolic murmur
- louder on sitting forward
- louder on expiration
- Collapsing pulse
Other signs
- Quinckes sign- nailbed pulsation
- De Mussets sign- head bobbing
investigation AR
ECG
- Left axis deviation
CXR
- cardiomegaly
Echocardiogram
management of aortic regurgitation
- Medical management of any associated heart failure
- Surgery: aortic valve indications include
* symptomatic patients with severe AR
* asymptomatic patients with severe AR who have LV systolic dysfunction
pulmonary stenosis
describes the narrowing of the tricuspid valve leading to obstructed blood flow through the pulmonary valve, which separates the right ventricle and pulmonary artery.
This obstruction can lead to increased workload on the right ventricle and right ventricular hypertrophy.
Causes pulmonary stenosis
Tetralogy of Fallot
Noonan syndrome
Maternal rubella syndrome
Infective endocarditis
Carcinoid syndrome
Marfan syndromeCauses
pulmonary stenosis presentation
- Shortness of breath
- Chest pain
- Exertional syncope
- Sudden cardiac death
- Critical PS – causes cyanosis in neonates
pulmonary stenosis murmur
ejection systolic murmur
- louder on inspiration
investigations for pulmonary stenosis
- ECG
-CXR - Echo
pulmonary stenosis management
treating the underlying cause, managing heart failure, and surgery.
Pulmonary regurgitation (PR)
describes the inadequate closure of the pulmonary valve leading to the backflow of blood during diastole. The pulmonary valve normally separates the right ventricle and pulmonary artery. It occurs rarely as a congenital abnormality.
pulmonary regurgitation causes
- Congenital
- Rheumatic fever
- Infective endocarditis
- Pulmonary hypertension and its causes
- Marfan syndrome
presentation of pulmonary regurg
PR is generally asymptomatic.
Right sided heart failure - results in systmeic congestion:
* Peripheral oedema, classically ankle or sacral oedema
* Raised jugular venous pressure
* Hepatomegaly which may be pulsatile
* Weight gain due to fluid retention
* Anorexia
pulmonary regurg murmur
early diastolic murmur in the left upper sternal edge that is louder on inspiration
Mitral stenosis
describes the narrowing of the mitral valve leading to obstructed blood flow through the mitral valve, which separates the left atrium and left ventricle of the heart. This obstructed flow results in increased pressures in the left atrium, pulmonary vasculature, and the right side of the heart.
Over time, continued increased left atrial pressure can lead to left atrial hypertrophy and atrial fibrillation.
causes of mitraql stenosis
- Rheumatic fever is the most common cause
- Degenerative calcification
- Carcinoid syndrome
- Autoimmune diseases (e.g. rheumatoid arthritis, systemic lupus erythematosus)
presentation of mitral stenosis
- Progressive shortness of breath on exertion
- Haemoptysis: due to increased left atrial pressure leading to the rupture of bronchial veins
- Atrial fibrillation: due to left atrial enlargement
mitral stenosis murmur
Mid-late diastolic murmur that is louder in the left lateral position in expiration
mitral stenosis: key signs on examination
- malar flush
- elecated JVP
investigations for mitral stenosis
ECG:
* May show atrial fibrillation
* May show bifid P waves
Chest x-ray:
* May show left atrial enlargement
* May show features of pulmonary oedema (e.g. Kerley B lines)
Transthoracic echocardiogram:
* Confirms mitral stenosis
management of mitral stenosis
If atrial fibrillation is present: lifelong warfarin
If asymptomatic:
* Monitor with regular echocardiography
If symptomatic– treat, options include:
* Percutaneous mitral balloon valvotomy
* Mitral valve surgery (e.g. valve replacement or commissurotomy)
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mitral regurg
A
second most common valve disease after aortic stenosis
is the result of the mitral valve failing to close properly, leading to leakage of blood from the left ventricle through the mitral valve and back into the left atrium when the left ventricle contracts.
People with mild-moderate MR may be asymptomatic for a long time, but as the disease progresses, the myocardium hypertrophies leading to left ventricular dysfunction and heart failure.
causes of mitral regurg
- Degenerative changes
- Infective endocarditis
- Myocardial ischaemia – papillary muscle dysfunction or rupture can happen after a myocardial infarction
- Acute rheumatic fever
- Connective tissue disease e.g. systemic lupus erythematosus, Ehlers-Danlos syndrome, Marfan’s syndrome
- Congenital heart disease
mitral regurg symptoms
Chronic mitral regurgitation may have:
- No symptoms
- Shortness of breath on exertion
- Decreased exercise tolerance
- Peripheral oedema – typically the lower limb
- Palpitations
- Features of left ventricular dysfunction e.g. orthopnoea/paroxysmal nocturnal dyspnoea
Acute mitral regurgitation leads to rapid pulmonary oedema and is a medical emergency, as it can be life-threatening. This requires emergency valve repair surgery.
pulmonary regurg murmur
pansystolic (holosystolic), blowing murmur at the apex that radiates to the axilla
management of acute mitral regurg
emergency surgery:
* They may need preoperative diuretics: furosemide is used
* Surgical options are: annuloplasty, bioprosthesis/mechanical valve replacement
management of asymptomatic chronic mitral regurg
Depends on left ventricular ejection fraction (LVEF):
* If LVEF >60%: 1st line: ACE inhibitors and beta-blockers
* If LVEF ≤60%: surgery
management of symptomatic chronic mitral regurgitation
LVEF ≥30%:
* Surgery and ACE inhibitors + beta-blockers + diuretics (furosemide or indapamide)
* Surgical options are: annuloplasty, bioprosthesis/mechanical valve replacement
LVEF <30%:
* ACE inhibitors + beta-blockers + diuretics (furosemide or indapamide)
* Surgery is not indicated due to significant operative risk
rheumatoid fever
is an autoimmune disease that may happen following a throat infection with group A Streptococcus i.e. Streptococcus pyogenes.
Pathophysiology
- It is thought to be the result of molecular mimicry.
- This is where the antigens presented on the bacterium are mistaken to be the same as antigens on the human host tissue.
The disease can affect joints, skin, the heart, and the nervous system. It can lead to mitral stenosis and congestive heart failure.
risk factors rheumatic fever
Risk Factors
- Younger age
- Poverty
- Overcrowding in living conditions
- Family history
diagnosis of rheumatic fever
Jones Criteria
Diagnosis is based on the Jones criteria (mentioned in presentation). Diagnosis can be made if there is:
- Evidence of recent streptococcal infection and two major criteria or
- Evidence of recent streptococcal infection and one major and two minor criteria
investigations for rheumatic fever
Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP):
* Usually raised
Full blood count (FBC):
* May have elevated white cells
Blood cultures:
* To rule out sepsis or infective endocarditis
ECG:
* May show PR prolongation which is an acute criterion
Chest x-ray:
* May show cardiomegaly and congestive cardiac failure
Echocardiogram:
* May show valvular dysfunction e.g. mitral regurgitation
Throat swab and culture:
* May show group A Streptococci e.g. Streptococcus pyogenes
* Provides evidence of a streptococcal infection
Throat swab and rapid antigen test for group A Streptococci
* Provides evidence of a streptococcal infection
Anti-streptococcal serology – anti-streptolysin:
- May be positive
- Provides evidence of a streptococcal infection
Throat swab and polymerase chain reaction (PCR):
- May be positive
- Provides evidence of a streptococcal infection
management of rheumatic fever
1st line:
* IM benzathine benzylpenicillin or oral phenoxymethylpenicillin (penicillin V)
* If allergic then give erythromycin
If arthritis present:
* NSAIDs: ibuprofen or naproxen
If heart failure develops:
* Treat with standard heart failure treatment
