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
=
