Cardiovascular system Flashcards
what are the clinical features of angina?
Typical symptoms include: chest pressure or squeezing lasting several minutes, provoked by exercise or emotional stress, relieved by GTN.
usually described as a central, crushing, retrosternal chest pain.
what are the risk factors for angina?
smoking hypertension hyperlipdaemia isolated HDL cholesterol diabetes inactivity obesity family history of CHD males illicit drug use
what are the differential diagnosis for chest pain?
acute MI prinzmetal's angina acute pericarditis MSK pain GI reflect Pleuritic chest pain aortic dissection PE oesophagitis, oesophageal spasm anxiety
what is prinzmetals angina?
angina caused by coronary artery spasm and results in angina that occurs without provocation, usually at rest. ECG during pain show ST elevation
what is decubitus angina?
occurs on lying down
what investigations would you perform for stable angina?
CT coronary angiography is the gold standard diagnostic investigation.
resting ECG - often normal but may reveal ST-T changes suggestive of ischemia or Q wave indicative of riot infarction
Haemoglobin levels
fasting lipid profile
fasting blood glucose or HbA1c
Also, consider
TSH
Stress exercise ECG -ST segment elevation elevation and depression identify ischaemia.
angiography
what would an ECG of a person with a stable angina show?
often normal but may reveal ST-T changes suggestive of ischaemia or Q wave indicative of riot infarction
may show ST segment depression and T wave flattening or inversion during an attack.
how is stable angina managed?
1st line - lifestyle education
PLUS - anti platelet therapy (aspirin or clopidogrel)
PLUS - statin e.g. atorvastatin
You can add prophylactic treatment:
Beta blockers (bisoprolol)
calcium channel blockers (amlodipine)
nitrates
revascularisation
GTN spray - sublingual glycerol trinitrate to terminate acute episodes of angina.
why should verapamil and BB not be prescribed together?
risk of complete heart block
how do Beta blockers work?
reduce heart rate and force of ventricular contraction, both of which reduce myocardial oxygen demand.
how do calcium channel blockers work?
block calcium influx into the cell and the utilization of calcium within the cell. They relax the coronary arteries and reduce the force of left ventricular contraction thereby reducing oxygen demand. The side effects (postural dizziness, headache, ankle oedema) are the result of systemic vasodilation
how do nitrates work?
Nitrates reduce venous and intracardiac diastolic pressure, reduce impedance to the emptying of the left ventricle and dilate coronary arteries
what is acute coronary syndrome?
it is usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery.
there are three types
- unstable angina
- ST elevation myocardial infarction
- non-St elevation myocardial infarction
what are the risk factors for ischaemic heart disease?
unmodifiable - increasing age, male gender, family history
modifiable risk factors - smoking, diabetes mellitus, hypertension, hypercholesterolaemia, obesity
what is the pathophysiology of IHD?
- initial endothelial dysfunction is triggered by a number of factors such as smoking, hypertension and hyperglycaemia
- this results in a number of changes to the endothelium including pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability
- fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles
- monocytes migrate from the blood and differentiate into macrophages. These macrophages then phagocytose oxidized LDL, slowly turning into large ‘foam cells’. As these macrophages die the result can further propagate the inflammatory process.
- smooth muscle proliferation and migration from the tunica media into the intima results in formation of a fibrous capsule covering the fatty plaque.
the plaque forms a physical blockage in the lumen of the coronary artery. This may cause reduced blood flow and hence oxygen to the myocardium, particularly at times of increased demand, resulting clinically in angina
the plaque may rupture, potentially causing a complete occlusion of the coronary artery. This may result in a myocardial infarction
in ACS what are the features of the chest pain?
- typically central/left sided
- may radiate to the jaw or left arm
- often described as heavy or constricting
- certain patients e.g. diabetic/elderly may not experience any (silent MI)
other than chest pain, what symptoms do patients experience with ACS?
- nausea and vomiting
- sweating and clamminess
- feeling of impending doom
- shortness of breath
- palpitations
- pain radiating to jaw or arms
symptoms should continue at rest for more than 20 minutes - if they settle with rest consider angia
what ECG changes do you see in STEMI, NSTEMI and unstable angina?
STEMI:
ST segment elevation (>20 mins) in leads consistent with an area of ischaemia
New Left Bundle Branch Block also diagnoses a “STEMI”
NSTEMI:
ST segment depression in a region, Deep T Wave Inversion, Pathological Q Waves (suggesting a deep infarct – a late sign)
The ECG may be normal or show non-specific changes
unstable angina - The ECG typically shows ST-segment depression and T-wave inversion, but may be normal
How is ACS usually diagnosed?
it typically requires serial troponins(at baseline and 6 or 12 hours after onset of symptoms
a rise in troponin is consistent with myocardial ischaemia as the proteins are released from the ischaemic muscle however they are non-specific - meaning that a raised troponin does not automatically mean ACS
other than ACS what are some causes of raised troponins?
chronic renal failure sepsis myocarditis aortic dissection PE
what are the different cardiac markers?
Troponins (T or I)
Creatine kinase (CK, specifically CK-MB)
Myoglobin
how do you acutely manage ACS?
MONA - morphine, oxygen, nitrates, aspirin
what investigations other than ECG and troponin would you perform for ACS?
FBC U&E LFT lipid profile TFT HbA1C
plus echo, CXT and CT angiogram to assess for coronary artery disease
how should you manage acute STEMI?
> Primary PCI if available within 2 hours of presetation
> thrombolysis if PCI is not available in 2 hours (streptokinase, alteplase or tenecteplase)
how would you manage acute NSTEMI?
BATMAN
B- beta blockers unless contraindicated
A- aspirin 300mg stat dose
T- ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative)
M - morphine titrated to control pain
A - anticoagulant: low molecular weight heparin at treatment dose
N - nitrates -GTN spray to relieve coronary artery spasm.
what score can be used to give a 6-month risk of death or repeat MI after having an NSTEMI
GRACE score
used to assess the need for PCI in NSTEMI
** if the GRACE score is greater that 3% in NSTEMI so you should do PCI
what are the complications of myocardial infarction?
DREAD
D-death R-rupture of the heart septum or papillary muscles E edema- heart failure A- arrhythmia and aneurysm D - dressler's syndrome
what is dressler’s syndrome?
aka post-MI syndrome.
usually occurs 2-3 weeks after an MI
caused by localised immune response and causes pericarditis
it presents with pleuritic chest pain, low grade fever and a pericardial rub on auscultation
It causes a pericardial effusion and rarely a pericardial tamponade
what investigations for Dressler’s syndrome and what will they show?
ECG - global ST elevation and T wave inversion
Echo - pericardial effusion
Inflammatory markers - CRP and ESR raised
how do you manage Dressler’s syndrome?
NSAIDs and in more severe cases steroids can be used
they may need pericardiocentesis to remove fluid from around the heart
what is the secondary prevention medical management for MI’s
6 As
Aspirin 75mg once daily
Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months
Atorvastatin 80mg once daily
ACE inhibitors (e.g. ramipril titrated as tolerated to 10mg once daily)
Atenolol (or other beta blocker titrated as high as tolerated)
Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)
Dual antiplatelet duration will vary following PCI procedures depending on the type of stent that was inserted. This is due to a higher risk of thrombus formation in different stents.
how do you manage unstable angina?
antiplatelet therapy statin BB ACE i lifestyle
what is heart failure?
when cardiac output is inadequate for the body’s requirements
what are the causes for low output heart failure?
cardiac output is decreased and fails to increase with exertion
Pumps failure -> systolic and or diastolic failure as well as arrhythmias (bradycardia, heart block, tachycardia and anti-arrhythmic (e.g.beta blockers, verapamil)
excessive preload -> aortic or mitral regurgitation, fluid overload
excessive afterload ->aortic stenosis, hypertensions
what are the causes of high output heart failure?
there is right ventricular failure followed by left ventricular failure
causes are:
anaemia, thyrotoxicosis, thiamine deficiency (beri beri), pregnancy, paget’s
what is systolic and diastolic heart failure?
systolic is the inability of the ventricles to contact resulting in decreased cardiac output (heart failure with reduced ejection fraction)
causes: IHD, MI, cardiomyopathy
Diastolic - inability of the ventricles to relax and fill normally - HF with preserved ejection fraction.
Causes: constrictive pericarditis, tamponade, restrictive cardiomyopathy
what are the causes, symptoms and signs of right ventricular failure?
causes - LVF, pulmonary stenosis and lung disease (cor pulmonale)
symptoms and sigs ->peripheral oedema, ascites, nausea, anorexia, facial engorgement, increased JVP, hepatomegaly
what are the causes, symptoms and signs of left ventricular failure?
causes - IHD, idiopathic dilated cardiomyopathy, systemic hypertension, mitral and aortic valve disease, specific cardiomyopathies
symptoms and signs - dyspnoea, poor exercise tolerance, fatigue, orthopnoea, paroxysmal nocturnal dyspnoea, nocturnal cough (plus pink frothy sputum), wheeze, nocturia,cold peripheries, weight loss, muscle wasting
what is acute heart failure ?
new onset or decompensation of chronic
it is characterised by peripheral and/or pulmonary oedema with or without signs of peripheral hypo perfusion
what is chronic heart failure?
Develops/progresses slowly
venous congestion common
arterial pressure maintained until late
what criteria is used to diagnose congestive cardiac failure
the Framingham criteria - at least two major criteria or 1 major and 2 minor criteria
Major criteria
- paroxysmal nocturnal dyspnoea
- crepitaitions
- s3 gallop
- cardiomegaly
- increased central venous pressure
- weight loss greater than 4.5kg in response to treatment
- neck vein distension
- acute pulmonary oedema
- hepatojugular refiux
Minor criteria
- bilateral ankle oedema
- nocturnal cough
- dyspnoea on ordinary exertion
- hepatomegaly
- tachycardia
- pleural effusion
- decreased vital capacity
what is it called when right and left sided heart failure occur together?
congestive cardiac failure
what investigations would you perform for heart failure ?
1st line - N-terminal pro-B-type natriuretic peptide (NT-pro BNP)- if levels are high then arrange a specialist assessment in 2 weeks, if levels are raised arrange a specialist assessment with in 6 weeks
transthoracic echo
ECG
CXR
bloods- FBC,U&E,LFTs, LFTs, lipid profile
what factors may increase and decrease BNP?
increase: left ventricular hypertrophy, ischaemia, tachycardia, right ventricular overload, hypoxaemia, GFR<60mls/min, sepsis, COPD, Diabetes, age >70, liver cirrhosis
Decrease: obesity diuretics, ACEi, beta blockers, angiotensin 2 receptor blockers, aldosterone antagonists
what would a chest x-ray show in heart failure?
ABCDE A - alveolar oedema B- kerley B lines C- cardiomegaly D- dilated upper lobe vessels E - pleural effusion
what is the New York classification of heart failure?
1 - not limitation of activity
2 - comfortable at rest, dyspnoea on ordinary activity
3 - marked limitation of ordinary activity
4 - dyspnoea @ rest, all activity leads to discomfort
what is it called when someone has acute heart failure without a past history of heart failure?
de-novo acute heart failure
what can cause de-novo acute HF?
De-novo heart failure is caused by and increased cardiac filling pressures and myocardial dysfunction usually as a result of ischaemia. This causes reduced cardiac output and therefore hypoperfusion. This, in turn can cause pulmonary oedema. Other less common causes of de-novo AHF are:
Viral myopathy
Toxins
Valve dysfunction
what are themes common precipitating causes of decompensated acute heart failure?
acute coronary syndrome
hypertensive crisis
acute arrhythmia
valvular disease
how is acute heart failure managed?
Management options in acute heart failure include: oxygen loop diuretics opiates vasodilators inotropic agents CPAP ultrafiltration mechanical circulatory assistance: e.g. intra-aortic balloon counterpulsation or ventricular assist devices
Consideration should be given to discontinuing beta-blockers in the short-term
how is heart failure managed?
Lifestyle changes
1st line - ACE inhibitor
plus a beta blocker (primary options carvedilol, other options include metoprolol, bisoprolol)
treatments that can be added
- diuretics (furosemide)
- aldosterone antagonist (spironolactone)
- vasodilators - hydralazine and isosorbide dinitrate
- digoxin
- ivabradine
- vasopressin antagonist
give annual influenza vaccine and offer one-off pneumococcal vaccine
if intolerant to ACE i - first line would be beta blocker plus angiotensin 2 receptor antagonist
invasive therapies
cardiac resynchronisation +/- ICD
LVAD
heart transplantation
what are risk factors for heart failure?
65 and older African descent men (due to lack of protective effect provided by oestrogen resulting in the early onset IHD in men) obesity previous MI
what is mitral regurgitation?
Mitral regurgitation is when an incompetent mitral valve allows blood to lead back through during systolic contraction of the left ventricle. It results in congestive cardiac failure because the leaking valve causes a reduced ejection fraction and a backlog of blood that is waiting to be pumped through the left side of the heart.
2nd most common valve disease after aortic stenosis
what kind of murmur does mitral regurgitation cause?
pan systolic high pitched “whistling murmur’ due to high velocity blood flow through the leaky valve.
The murmur radiates to the left axilla
there may be a third heart sound heard
what are the causes of mitral regurgitation?
idiopathic weakening of the valve with age
Ischaemic heart disease
mitral valve prolapse
Infective Endocarditis
Rheumatic Heart Disease
Connective tissue disorders such as Ehlers Danlos syndrome or Marfan syndrome
what are some RF for mitral regurgitation?
Female sex Lower body mass Age Renal dysfunction Prior myocardial infarction Prior mitral stenosis or valve prolapse Collagen disorders e.g. Marfan's Syndrome and Ehlers-Danlos syndrome
what are the symptoms of mitral regurgitation?
often asymptomatic
symptoms may be due to failure of the left ventricle, arrhythmias or pulmonary hypertension - which would present as SOB and oedema, decreased exercise tolerance
what investigations would you perform for mitral regurgitation?
transthoracic echo - crucial to diagnosis and assessment of severity
ECG (may show a broad P wave which is indicative of atrial enlargement)
CXR - cardiomegaly may be seen
how is mitral regurgitation managed?
if asymptomatic give ACEi (captopril or enalapril) and BB (metoprolol or atenolol)
If symptomatic - medical option - ACEi (captopril or enalapril) and BB (metoprolol or atenolol) plus diuretic (furosemide or indapamide) with an intra-aortic balloon counterpulsation
if acute and severe - surgery is indicated
surgical options
repair over replacement is better in degenerative regurgitation
valve replacement with either artificial valve or pig valve can be considered
what is the most common cause of mitral stenosis?
Rheumatic fever
rarer causes that may be seen include mucopolysaccharidoses, carcinoid and endocardial fibroelastosis
how does mitral stenosis affect the heart?
there is narrowing of the mitral valve orifice which causes decreased filling of the left ventricle, while simultaneously increasing left atrial pressure - as disease progresses pulmonary hypertension and right heart failure occur.
what murmur is heard in mitral stenosis ?
It causes a mid-diastolic, low pitched “rumbling” murmur due to a low velocity of blood flow.
There will be a loud S1 due to thick valves requiring a large systolic force to shut, then shutting suddenly.
You can palpate a tapping apex beat due to loud S1.
what features is mitral stenosis associated with?
malar flush - this is due to back-pressure of blood into the pulmonary system causing a rise in CO2 and vasodilation
Atrial fibrillation. This is caused by the left atrium struggling to push blood through the stenotic valve causing strain, electrical disruption and resulting fibrillation.
there may be orthopnoea as a consequence of increased left atrial pressure
Dyspnoea - there is increased left atrial pressure which results in pulmonary congestion
Neck vein distension - sign of pulmonary hypertension and/or right ventricular failure
what investigations would you perform for mitral stenosis?
Transthoracic echo - hockey stick shaped mitral deformity
CXR - left atrial enlargement may be seen (indicated by double right heart border), prominent pulmonary artery and kerley B lines (a radiological change of pulmonary venous hypertension)
ECG - may show AF, left atrial enlargement, right ventricular hypertrophy
how is mitral stenosis managed?
if asymptomatic - no treatment needed
balloon valvotomy
diuretics can be added - furosemide or bumetanide
what kind of murmur does aortic stenosis cause?
It causes an ejection-systolic, high pitched murmur (high velocity of systole).
This has a crescendo-decrescendo character due to the speed of blood flow across the value during the different periods of systole. Flow during systole is slowest at the very start and end and fastest in the middle.
what are the causes of aortic stenosis?
degenerative calcification (most common cause in older patients > 65 years)
bicuspid aortic valve (most common cause in younger patients < 65 years)
William’s syndrome (supravalvular aortic stenosis)
post-rheumatic disease
subvalvular: HOCM
what are the clinical features of aortic stenosis?
chest pain
dyspnoea
syncope
what signs other than murmur might you find in aortic stenosis?
The murmur radiates to the carotids as the turbulence continues up into the neck
Slow rising pulse
narrow pulse pressure
second heart sound soft or absent
what investigations for aortic stenosis?
transthoracic doppler echo - will show an elevated aortic pressure gradient.
ECG - may demonstrate left ventricular hypertrophy and absent Q waves, AV block, hemiblock or bundle branch block
how do you manage aortic stenosis?
if asymptomatic - observe (serial echos every 3-5 years)
if symptomatic then valve replacement
**cardiovascular disease may coexist. For this reason an angiogram is often done prior to surgery so that the procedures can be combined
balloon valvuloplasty is limited to patients with critical aortic stenosis who are not fit for valve replacement
what kind of murmur does aortic regurgitation cause?
Aortic regurgitation typically causes an early diastolic, soft murmur - intensity is increased with the handgrip manouver
other than murmur what signs does aortic regurgitation cause?
- It is also associated with a Corrigan’s pulse. A Corrigan’s pulse is also called a collapsing pulse and is a rapidly appearing and disappearing pulse at carotid as the blood is pumped out by the ventricles and then immediately flows back through the aortic valve back into the ventricles
- wide pulse pressure
- Quincke’s sign (nailbed pulsation)
- De Musset’s sign (head bobbing)
- mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams
what are the causes of aortic regurgitation?
Causes (due to valve disease)
- rheumatic fever
- infective endocarditis
- connective tissue diseases e.g. RA/SLE
- bicuspid aortic valve
Causes (due to aortic root disease)
- aortic dissection
- spondylarthropathies (e.g. ankylosing spondylitis)
- hypertension
- syphilis
- Marfan’s, Ehler-Danlos syndrome
what investigations should be performed for aortic regurgitation?
ECG - may show non specific SR-T wave changes, left axis deviation or conduction abnormalities
CXR - may show cardiomegaly
Ehco - visualisation of the origin of regurgitant jet and its width, detection of aortic valve pathology.
colour flow doppler, pulsed wave doppler, continuous wave doppler
what signs would you get in tricuspid regurgitation?
pan-systolic murmur
prominent/giant V waves in JVP
pulsatile hepatomegaly
left parasternal heave
what are some causes of tricuspid regurgitation?
right ventricular infarction pulmonary hypertension e.g. COPD rheumatic heart disease infective endocarditis (especially intravenous drug users) Ebstein's anomaly carcinoid syndrome
what investigations would you perform for tricuspid regurgitation?
transthoracic or transoesophageal echocardiogram
ECG may show af
LFTs may be abnormal due to chronic TR from chronic congestion
how is tricuspid regurgitation managed?
treat underlying cause
manage heart failure
if symptomatic - consider valve repair or replacement
how is aortic stenosis managed?
if symptomatic - aortic valve replacement
long term infective endocarditis antibiotic prophylaxis
what causes pulmonary stenosis?
majority of cases of congenital
what murmur is it in pulmonary stenosis?
pathological systolic ejection murmur with or without systolic click
where should you listen for valve murmurs?
Pulmonary: 2nd I.C.S left sternal boarder
Aortic: 2nd I.C.S right sternal boarder
Tricuspid: 5th I.C.S left sternal boarder
Mitral: 5th I.C.S mid clavicular line (apex area)
Patient on their left hand side (mitral stenosis)
Patient sat up, learning forward and holding exhalation (aortic regurgitation)
what are the types of valve replacement?
Valves can be either replaced by a bioprosthetic or a metallic mechanical valve. “Porcine” bioprosthetic valves come from a pig.
Bioprosthetic valves have a limited lifespan of around 10 years.
Mechanical valves have a good lifespan (well over 20 years) but require lifelong anticoagulation with warfarin. The INR target range with mechanical valves is 2.5 – 3.5.
*Mechanical valves cause a click
A click replaces S1 for metallic mitral valve
A click replaces S2 for metallic aortic valve
what are the different types of mechanical heart valve?
Starr-Edwards valve
- Ball in cage valve
- Very successful but no longer being implanted
- Highest risk of thrombus formation
Tilting disc valve
- A single tilting disc
St Jude Valve
- Two tilting metal discs
- The two discs mean they are called bileaflet valve
- Least risk of thrombus formation
what are the major complication of mechanical valve replacement?
Thrombus formation (blood stagnates and clots) Infective endocarditis (infection in prosthesis) Haemolysis causing anaemia (blood gets churned up in the valve)
what causes infective endocarditis?
historically - streptococcus viridans - now only the most common cause in developing countries
Staphylococcus aureus now most common cause
Those who have had valve replacement - coagulase negative staphylococci - often staphylococcus epidermidis (after 2 months the most common cause is staph aureus)
what are the risk factors for infective endocarditis?
prior history of infective endocarditis
presence of artificial prosthetic heart valves
certain types of congenital heart disease
post-heart transplant
IV drug users
recent piercings
what valve is most commonly affected in infective endocarditis?
mitral valve
what criteria is used for infective endocarditis?
modified duke criteria Infective endocarditis diagnosed if pathological criteria positive, or 2 major criteria, or 1 major and 3 minor criteria, or 5 minor criteria
Pathological criteria
Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)
Major criteria
Positive blood cultures
two positive blood cultures showing typical organisms consistent with infective endocarditis, such as Streptococcus viridans and the HACEK group, or
persistent bacteraemia from two blood cultures taken > 12 hours apart or three or more positive blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis, or
positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci, or
positive molecular assays for specific gene targets
Evidence of endocardial involvement positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves), or new valvular regurgitation
Minor criteria
predisposing heart condition or intravenous drug use
microbiological evidence does not meet major criteria
fever > 38ºC
vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots
what are the features of infective endocarditis?
fever/chills night sweats, malaise, fatigue, weight loss - non specific symptoms weakness arthralgia headaches SOB janeway lesions osler nodes roth spots splinter haemorrhages cutaneous infarcts
what investigations would you perform for infective endocarditis?
FBC - most patients will have an anaemia
blood cultures
ECG - prolonged PR interval, non-specific ST/T wave abnormalities, AV block
Echo - will show mobile vegetation’s
urinalysis - septic emboli are common complication and may cause RBC casts WBC casts, protinuria, pyuria
what are poor prognostic factors in infective endocarditis?
Poor prognostic factors
Staphylococcus aureus infection (see below)
prosthetic valve (especially ‘early’, acquired during surgery)
culture negative endocarditis
low complement levels
Mortality according to organism
staphylococci - 30%
bowel organisms - 15%
streptococci - 5%
how do you manage infective endocarditis?
suspected with native valve - amoxicillin (consider adding low dose gentamicin) if allergic to penicillin - vancomycin
suspected with prosthetic valve - vancomycin, rifampicin and low dose gentamicin
if native valve and caused by staphylococci - flucloxacillin or vancomycin and rifampicin if allergic to penicillin.
If prosthetic valve and caused by staph - flucloxacillin (vancomycin if allergic to penicillin) , rifampicin and low dose gentamicin
if caused by viridans - benzylpenicllin or vancomycin plus low dose gentamicin.
what are the indications for surgery in infective endocarditis?
severe valvular incompetence
aortic abscess (often indicated by a lengthening PR interval)
infections resistant to antibiotics/fungal infections
cardiac failure refractory to standard medical treatment
recurrent emboli after antibiotic therapy
what prophylaxis is given for infective endocarditis?
amoxicillin
what is rheumatic fever?
an autoimmune disease that may occur following group A streptococcal throat infection
what is the pathogenesis of rheumatic fever?
Streptococcus pyogenes infection → activation of the innate immune system leading to antigen presentation to T cells
B and T cells produce IgG and IgM antibodies and CD4+ T cells are activated
there is then a cross-reactive immune response (a form of type II hypersensitivity) thought to be mediated by molecular mimicry
the cell wall of Streptococcus pyogenes includes M protein, a virulence factor that is highly antigenic. It is thought that the antibodies against M protein cross-react with myosin and the smooth muscle of arteries
this response leads to the clinical features of rheumatic fever
Aschoff bodies describes the granulomatous nodules found in rheumatic heart fever
what gives evidence of streptococcal infection?
raised or rising streptococci antibodies,
positive throat swab
positive rapid group A streptococcal antigen test
How is rheumatic fever diagnosed?
JONES criteria
evidence of recent strep infection plus 2 major criteria or 1 major criteria with 2 minor criteria
JONES CAFE PAL
Major criteria = JONES J - joint involvement O - heart looks like an O - myocarditis N - nodules - subcutaneous E - erythema marginatum S - Sydenham chorea
Minor criteria = CAFE PAL C - CRP elevated A - arthralgia F - fever E - elevated ESR
P - prolonged PR interval
A - anamnesis of rheumatism
L - Leukocytosis
what investigations would you consider doing for rheumatic fever?
ESR CRP WBC count blood cultures ECG CXR echo throat swab and culture rapid antigen test for group A streptococci anti-streptococcal serology
how is rheumatic fever managed?
benzathine benzylpenicillin, secondary options are erythromycin base or phenoxymethypenicllin
if there is arthritis - salicylate therapy or NSAID
if there is heart failure - diuretic +/- ACEi
all patients following acute treatment need secondary prophylaxis - benzylpenicillin every 3-4 weeks
