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Cardiology Notes
Aortic Dissection
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1

This is caused by a tear in the tunica intima of the aorta and this creates a false
lumen through which the blood can flow between the inner and outer layers of the
walls of the aorta
Risk factors:
o Hypertension
o Connective tissue disease such as Marfan’s syndrome
o Valvular heart disease
o Cocaine and amphetamine use
Complications- death due to internal haemorrhage, rupture, end organ damage,
cardiac tamponade, stroke, limb ischaemia and mesenteric ischaemia
Stanford Classification of aortic dissections:
o Stanford Type A- this involves the ascending aorta and also the arch of the
aorta and is the most common one found
o Stanford Type B- involves the descending aorta
Clinical features:
o Sudden onset tearing chest pain which radiates to the back
o Presents in males over the age of 50
o Radio radial and radio femoral delay- there is pulse deficit
o Aortic regurgitation- there may be early diastolic murmur which is worse on
expiration or leaning forward
o Blood pressure is differential between the arms
o Syncope and hypotension may happen but they are less common
Investigations:
o ECG- can show ischaemia in specific territories if the dissection extends into
the coronary arteries
...
any patient who comes in with chest pain will need
ECG
o ECHO- will show pericardial effusion and aortic valve involvement and this
needs to be transthoracic
o CXR- widened mediastinum and this is a key feature
o CT angiography tends to be the investigation of choice- false lumen is the key
finding and this is the first line imaging investigation for definitive diagnosis
o Bloods- raised troponin and D dimer may be positive but since D dimer is of
low sensitivity, this doesn’t necessarily mean that there is going to be a PE
Management
o Mortality is high so need to do ABCDE
o Resuscitation, cardiac monitoring

o Metoprolol/ Labetolol infusion for strict blood pressure control
o Type A- will need surgical management (aortic graft)
o Type B- managed with BP control and endovascular repair if there is evidence
of end organ damage
-------------------------------------------------------------------------------------------------------------------------Arrhythmias
Arrhythmia Definition
Tachycardia Heart rate is greater
than 100 beats per
minute

Symptoms
Palpitations
Breathlessness

Investigations
ECG- fast rate
but may still
show sinus
rhythmn
QRS width of
less than 120ms
on the ECG

Bradycardia Heart rate is slower
than 60 beats per
minute and is caused
by- sinus nodal
disease, beta blockers,
CCBs, electrolyte
abnormalities and
hypothyroidism

Dizziness
Syncope
Tiredness
This triad is
classic

ECG- will show
bradycardia

Atrial

Irregularly

ECG- irregularly

2

This is also a type of

Management
If features of HF,
ischaemia, shock
and syncope- give
synchronised DC
shock
In stable
First line- Valsavla
maneouvres such
as blowing into
syringe, carotid
sinus massage etc,
Second line- IV
Adenosine 6mg
Third line- beta
blocker, verapamil
Fourth line- DC
cardioversion
ABCDE
assessment first
If
haemodynamically
unstable- give
500mcg IV
atropine
...
A type of
supraventricular
tachycardia

irregular pulse
Palpitations
Chest Pain
SOB
Dizziness
Difference in
pulses in arms

Atrial
Flutter

Re-entrant
tachycardia in the
macro-circuit within
the right atrium and
can be caused byCOPD, obstructive
sleep apnoea, PE,
pulmonary
hypertension,
ischaemic heart
disease, sepsis,
alcohol, thyrotoxicosis

Lots are
asymptomatic
Palpitations
Dizziness
Chest Pain

Ventricular
Fibrillation

A broad complex
tachycardia

Ventricular

Tachycardia which

Pulseless
rhythmn
Collapse and
loss of
consciousness
Chest pain
Dizziness
Nausea
SOB
Palpitations

3

irregular pulse
Absent A wave
on JVP

haemodynamically
unstable, use DC
cardioversion
Rate control- first
line strategy with
beta blockers,
CCBs and digoxin
Rhythmn controlelectric or
pharmacological
cardioversion
...
QRS
1mg adrenaline
complexes are
and 300mg
polymorphic and amiodarone
irregular
administered after
the shock has
been given
Tachycardia
Unsynchronised

tachycardia

starts in the ventricles

Dizziness
Lightheadedness
Chest Pain
SOB
Cardiac arrest

Torsades
des Pointes

A form of polymorphic
ventricular
tachycardia which is
caused by QT
prolongation
...
Use
cardioversion if all else fails but use beta blockers and verapamil first
 If bradycardia- use atropine 500mcg and transcutaneous pacing as second line
 Atrial flutter- beta blockers and CCBs first and then electric cardioversion if all else fails
 Fast heart so use adenosine as the drug (after manouvres fail)
 Slow heart so use atropine (then use transcutaneous pacing)
 Symptoms are similar for all arrhythmias
o Dizzinesss and syncope
o SOB and lightheadedness
o Chest Pain
o Palpitations
 AF- rate control is more important so use beta blockers and CCBs and digoxin unless it is
their first AF or features of heart failure in which case cardioversion is more important
via
o Electric DC cardioversion
o Pharmacological- flecainide for the younger patients and amiodarone for the
older
o Need long term anticoagulation via DOACs as well

4

Acute Coronary Syndrome- MI
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5

It is an umbrella term which covers a number of acute presentations of ischaemic
heart disease which include:
o ST elevation myocardial infarction- STEMI
 Caused by COMPLETE occlusion of a coronary artery
o Non ST elevation myocardial infarction
 Incomplete stenosis/ occlusion of a coronary artery
o Unstable angina- in angina, there is no death of myocardial tissue whereas in
an MI, there is
Condition typically develops in people who have ischaemic heart disease which
happens due to the development of plaques and the process is:
o Monocyte infiltrate the damaged endothelium in areas with vulnerable shear
stress
 Endothelium has pro-inflammatory, pro-oxidant and reduced nitric
oxide bioavailability
o The monocytes then mature into macrophages and take up oxidised LDLs to
form foam cells which become the core of the lesions
o The oxidised LDLs stimulate the macrophages to release more cytokines to
allow for monocyte recruitment further- this is basically a vicious cycle
o Cytokines then stimulate smooth muscle cell proliferation and connective
tissue synthesis to form a fibrous plaque
o Plaque will rupture and this is what leads to the issues
o So an acute coronary syndrome therefore happens when:
 Sudden plaque rupture- the fatty plaque which have built up in the
endothelium will occlude the artery and this can lead to no blood
reaching the myocardium
 Gradual narrowing- less blood and so oxygen reaches the myocardium
at times of increased demand at a lower capacity and this is what
leads to angina
Risk factors:
o Hypertension- major reason for atherosclerosis formation
o Smoking- can also worsen issues such as Diabetes and insulin resistance
o Diabetes and insulin resistance can contribute to the hypertension
o Obesity and hypercholesterolaemia
o Age and male gender
o Family history
o South Asian ethnicity
Clinical features:
o Central/ left sided chest pain which may radiate to the jaw/ arms
...

 Coronary angiography will be done for high risk patients
 Targeted oxygen therapy
 Loading PO 300mg aspirin dose with fonduparinux
 Calculate GRACE score and then provide either prasugrel or
ticagrelor if they have anything but a low risk scoreclopidogrel instead if high risk of bleeding
 Sublingual GTN spray for symptom relief
 IV morphine
 Start antithrombin therapy with low dose molecular weight heparin
o Secondary prevention:
 Lifelong therapy which includes DUAPT, Beta blockers, ACE inhibitors
and a statin
 Aspirin 75mg + 75mg clopidogrel or 90mg ticagrelor
 Beta blocker- bisoprolol
 ACE inhibitor- ramipril
 High dose statin- atorvastatin 80mg ON
 All need an ECHO to assess systolic function
 Cardiac rehab
Complications of condition

o Ventricular arrhythmia, recurrent ischaemia, congestive heart failure, heart
block, left ventricular thrombus, acute mitral regurgitation, ventricular septal
defect, dressler’s syndrome
...
There may also
be SOB
o This triad is more towards the end stage of disease and patients may remain
asymptomatic for a long period of time
o Exertional dyspnoea and also decreased exercise tolerance is a key feature
o Signs
 Slow rising carotid pulse and narrow pulse pressure- features of
severe aortic stenosis
 Non displaced apex beat which is heaving
 Ejection systolic murmur which is heart best on the second intercostal
space on the right and it will radiate to the carotids- this is a key
feature
 Valsalva manoeuvre will decrease the intensity of the murmur
 Soft S2 with an ejection click may be heard in some cases
...
There is a criteria for this
 Symptomatic- all will need intervention
 Reduced ventricular ejection fraction
o If asymptomatic- they will need observation

-------------------------------------------------------------------------------------------------------------------------Atrial Fibrillation
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10

When there is uncoordinated atrial contraction- there tends to be a delay at the AV
node and this means that only some of the atrial impulses are conducted to the
ventricles and this leads to an irregular ventricular response
Pathophysiology- dilation of the atria through inflammation and fibrosis leads to
discrepancies in the refractory periods within the atrial tissue and this means there is
re-entry within the atria and recurrent uncoordinated atrial contraction
Complications- heart failure, stroke, GI bleeding, intracranial bleeds,
Causes:
o Ischaemic heart disease, hypertension, rheumatic heart disease, peri and
myocarditis
o Dehydration
o Endocrine causes- hyperthyroidism
o Pulmonary causes- pneumonia and PE
AF classification:
o Acute- will last less than 48 hours
o Paroxysmal- lasts less than 7 days and is intermittent
o Persistent- lasts more than 7 days but is fine after cardioversion
o Permanent- lasts more than 7 days and is not amenable to cardioversion
Symptoms
o Palpitations
o Irregularly irregular pulse- key feature
o SOB and dizziness
o Single waveform on the JVP
o Fatigue and anxiety
o Chest pain, tightness and discomfort
Investigations:

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o ECG- will show an irregularly irregular pulse and this will need to be done
immediately
o Essentially check the entire body for cause and most things will be normal:
 Troponin may be elevated but this DOES NOT have to mean a heart
attack
Management
o Focussed on rate or rhythmn control
o ABCDE approach first ALL THE TIME
 Assess for haemodynamic instability- shock may suggest end organ
hypoperfusion, syncope may be due to brain hypoperfusion, chest
pain may be due to myocardial ischaemia and pulmonary oedema
may be due to heart failure
 If unstable- IMMEDIATE DC Cardioversion
o Rate Control in AF: this is the first thing to use in haemodynamically stable
patients with AF
 Beta blocker bisoprolol is the most commonly one used in AF
 Do not use in COPD, Asthma, hypotension
 Calcium channel blocker- diltiazem or verapamil
 Do not use in heart failure since there is negative inotropy
 These two are the most commonly used in AF
 Digoxin- only use if there is hypotension, co-existent heart failure but
do avoid in younger people
o Rhythmn Control in AF
 Electric cardioversion- DC cardioversion should be used if there is
acute AF
 If the AF has been going on for more than 48 hours, then there
needs to be anticoagulation for 3 weeks before DC
cardioversion can be done
 Anticoagulation:
o Use the CHADVASC2 score- if the score is more than 1
for males and 2 for females, there needs to be
anticoagulation
o Also calculate HASBLED score since anticoagulation can
lead to increased bleeding- may be an ORBIT score now
o Choice of anticoagulants:
 DOAC- first choice and includes edoxaban,
apixaban, rivroxaban and dabigatran
 Warfarin- needs LMWH first and needs regular
INR monitoring and is not as ideal as DOACs
o Continue anticoagulant even after cardioversion
 Pharmacological cardioversion

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Flecainide- preferred in younger patients who have
structurally normal hearts
Amiodarone- only for older and sedentary patients since there
are a lot of side effects
Sotalol- only use if not possible to use the other two

-------------------------------------------------------------------------------------------------------------------------Angina
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12

Characterised by chest pain and is caused by ischaemic disease since there is an
inability to provide adequate blood supply to the myocardium and so, there is pain
when this happens
o Caused by atherosclerosis of the coronary arteries
o Stable angina- this is constriction like pain which is temporary and is brought
on by exertion
o Unstable angina- when the pain lasts longer than a few minutes and stays
constant and this is basically an ACS event
Clinical features
o Constriction like pain in the chest, neck, arm and jaw
o Brought on by physical activity
o Alleviated by rest of GTN within minutes
o If there are only 2/3 features then it can be described as atypical angina
Investigations
o CT coronary angiography is indicated for the angina if there is high clinical
suspicion and high risk factors- also if ECG shows ischaemic changes in chest
pain with less than 2 features of angina and this is the first line investigation
o Myocardial perfusion scan, stress echo and MRI should be done as second
line investigations- they will show signs of ischaemia
o Coronary angiogram if there are inconclusive results from non-invasive
testing
o Lipid profile since hypercholesterolaemia is a risk for the condition
Management
o Conservative management- smoking cessation, glycaemic control,
hypertension, hyperlipidaemia, weight loss, alcohol intake
o First line management
 Aspirin and Statin- all should receive this in the absence of any
contraindications
 Sublingual GTN- may lead to headaches, flushing or dizziness
...
Verapamil is negatively inotropic
so has a risk of further complicating the heart
 Side effects of:
o CCB- headaches, flushing and ankle oedema with
verapamil causing constipation
o Beta blocker- bronchospasm in asthmatics, fatigue,
cold peripheries and sleep disturbances
o Nitrates- headaches, postural hypotension, tachycardia
o Nicorandil- headache, flushing and anal ulceration
o Ivabradine- visual effects, headaches, bradycardia or
heart block
 If symptomatic after monotherapy, add the other one so
either a beta blocker or a CCB
o Add these if they cannot tolerate the beta blocker or
CCB
 Long acting nitrate- people taking nitrate may
develop tolerance and so, the dosing should be
asymmetric to maintain the dose and reduce
the risk of nitrate tolerance
 Ivabradine- this is a funny current inhibitor and
therefore reduces the cardiac pacemaker
activity
 Nicorandil- vasodilatory drug which is a
potassium channel activator and vasodilation is
through activation of guanylyl cyclase which
leads to increased cGMP
...
Heart failure can
either be:
o Systolic- impaired myocardial contraction during systole and it can be caused
by:
 Ischaemic heart disease, dilated cardiomyopathy, myocarditis and
infiltration via haemachromatosis or sarcoidosis
o Diastolic- impaired ventricular filling during diastole and it can be caused by:
 Hypertrophic obstructive cardiomyopathy, restrictive
cardiomyopathy, cardiac tamponade and constrictive pericarditis
There is a failure of the heart to generate sufficient cardiac output to meet the
metabolic demands of the body
...

 Clinical features: similar to lots of pulmonary conditions but be careful
as it may not be
 SOB on exertion and orthopnoea- this is a key feature of HF so
if the person needs pillows to stay asleep or keeps waking up
due to SOB, assume it is HF
 PND- another key feature of the condition
 Nocturnal cough with pink frothy sputum
 Tachypnoea
 Bibasal fine crackles on auscultations of the lungs
 Cyanosis, hypotension and prolonged cap refill
 Central oedema is a sign of left sided heart failure
o Right heart failure- this causes venous congestion since pressure builds up
behind the right heart and there is pulmonary hypoperfusion due to reduced
right heart output #
 Clinical features
 Ankle swelling and peripheral oedema- a key differentiator
between the right and left heart failure
o The oedema may be pitting
o Ascites is also common
 Abdominal distension
 Anorexia and nausea
 Raised JVP
 Tender smooth hepatomegaly

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15

Transudative PE- this is a key cause of transudates in Pleural
effusion (alongside cirrhosis and also nephrotic syndrome)

Investigations
o ECG
o NT- proBNP- BNP is released by the ventricles in response to myocardial
stretch and this is a good negative predictor of the condition- if the BNP is not
raised, then the diagnosis of congestive cardiac failure is not likely
 >2000ng/L so the patient will need an urgent 2 week referral and
ECHO
 400-2000ng/L- 6 week referral and ECHO
o Transthoracic echocardiogram- will show whether or not there is ventricular
dysfunction and this is measured by the ejection fraction
 40% means that there is heart failure with a reduced ejection fraction
 >40% but raised BNP- means the heart failure is present but there is
preserved ejection fraction
o CXR- remember the ABCDEF mnemonic for this
 A- alveolar oedema and will show a batwing peri-hilar shadowing
 B- Kerley B lines which are caused by interstitial oedema
 C- cardiomegaly
 D- upper lobe blood diversion
 E- pleural effusion which is bilateral since it is mostly transudate
 F- fluid in horizontal fissure
Management
o Lifestyle modifications- smoking cessation, supervised cardiac rehab and also
salt and fluid restriction
o Influenza and pneumococcal vaccine
o Pharmacological
 ACE inhibitor- this is the first line and since it can affect renal function,
may not be that good if there is renal mortality- consider ARBs in this
case
 Hyperkalaemia, renal impairment, dry cough, lightheadedness,
fatigue, GI disturbances and angioedema
 Beta blockers- bisoprolol along with ACE is the first line therapy
 Side effects- bradycardia, hypotension, fatigue and dizziness
 Loop diuretics- furosemide improves the symptoms but NOT the
mortality
 Side effects- hypotension, hyponatraemia and hypokalaemia
 If symptoms persist:
 Aldosterone antagonists such as spironolactone- they improve
mortality

o Side effects- hyperkalaemia, renal impairment,
gynaecomastia, breast tenderness and hair growth in
women as well as changes in libido
o This is the second line therapy
 Hydralazine for Afro-Caribbean patients
o Side effects- headaches, palpitations and flushing
 Digoxin- if there is AF but this can only improve morbidity
 Side effects- dizziness, blurred vision and GI disturbances
 This along with ivabradine is third line
o Surgical
 Cardiac resynchronisation therapy if there is prolongation of QR or
risk of sudden cardiac death
o Acute heart failure:
 Sit the patient up and give them oxygen
 IV furosemide 40mg or more and close fluid balance to maintain a
negative balance and maintain furosemide for 24 hours
 SC morphine
 CPAP
-------------------------------------------------------------------------------------------------------------------------Heart block
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16

First Degree Heart Block- this is caused by prolongation of electrical activity through
the AV node and is characterised by a prolonged PR interval of more than 200ms
o Causes- high vasal tone, acute inferior MI, hyperkalaemia, CCBs, digoxin, beta
blockers and cholinesterase inhibitors
o Management- often asymptomatic and does not need treatment and tends
to be benign but do need to treat the underlying factors
Second Degree Heart Block
o Mobitz Type 1/ Wenckebach
 Block due to reversible conduction block at the AV node and is
characterised by progressive lengthening of the PR interval and this
leads to a P wave that cannot conduct a QRS since it is too far apart
 ECG features- PR interval progressively getting longer with
dropped QRS complexes
 Causes- inferior MI, beta blockers, CCBs, digoxin, professional
athletes, myocarditis and cardiac surgery
 Management- generally also asymptomatic and there may be
bradycardia so it may need atropine
o Mobitz Type 2-

There will be intermittent non conducted P waves with the PR interval
being constant but there being occasional dropped QRS complexes
 ECG features- constant PR interval with the occasional
dropped QRS complex
 This heart block has a higher risk of progressing to a higher
and more dangerous type of heart block and also sudden
cardiac death
 Causes- infarction and particularly anterior, mitral valve or septal
ablation, rheumatic heart disease, SLE, myocarditis, sarcoidosis,
haemochromatosis, beta blockers, calcium channel blockers, digoxin
and amiodarone
 Management- since patients are at risk of complete heart block, and
haemodynamic unstable, there needs to be insertion of a permanent
pacemaker
Third Degree Heart Block/ Complete Heart Block
o The atrial impulse fails to be conducted to the ventricles and there are clinical
features present in this condition
 Syncope or cardiac arrest tend to be some of the first symptoms
 ECG will show severe bradycardia with no association between the P
waves and the QRS complex
o Causes- inferior MI, beta blockers, CCBs, idiopathic fibrosis
o Management is with a permanent pace marker insertion due to the risk of
sudden death with this condition
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Hypertension
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17

Occurs as a result of reduced elasticity of the large arteriesatherosclerosis, degradation of arterial elastin
...
Ramipril, Lisinopril etc
...
Nefedipine, Amlodipine and
NOT for diabetes
o ARB IF THEY CANNOT TOLERATE ACE INHIBITORSCandesartan
 Stage 2- If step 1 fails
o Combine CCB with ACE/ ARB
 Stage 3- if step 2 fails
o Thiazide like diuretic- indapamide, chlortalidone
 Stage 4- if step 3 fails
o Spironolactone if the potassium is low- ONLY in
hypokalaemia
o Increase indapamide dose if high level of potassium
o Alpha and Beta blockers- DO NOT USE IN STAGE 1,
THOSE ARE BETA BLOCKERS AND NOT CCBs

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18

Infective Endocarditis
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19

This is caused by infection of the endovascular structures of the heart and
It can be caused by:
 Risk factors- increasing age, male sex, IV drug use or devices/
haemodialysis
 IV Drug use greatly increases the risk since there is a predisposition to
staph
...
This will
typically cause infection in people who have poor dental hygiene and
potentially following a dental procedure
 Co-morbid conditions- rheumatic heart disease, mitral valve prolapse,
aortic valve disease, congenital heart disease, pulmonary stenosis,
ventricular septal defect, Previous history of condition
 HIV infection
Clinical features
o The symptoms present acutely and can then progress rapidly with symptoms
of heart failure
o Fever- this is the most common symptom
o Fever + new murmur- always suspect infective endocarditis
 Murmur can be anything
o Anorexia and weight loss- this is also common
o Myalgia and arthralgia
o Night sweats
o Abdominal pain
o Cough with pleuritic pain- there may be PND or SOB if there are features of
heart failure
o Clinical signs:
 Janeway lesions- non tender macules on the palms and soles
 Osler nodes- tender subcutaneous nodules on the finger pads and
toes
 Splinter haemorrhages- essentially, anyone with fever and either of
these three signs should always be suspected of having this condition
 PR Prolongation with complete AV node block- suggests there is an
abscess in the aortic root


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Roth spots- retinal lesions which are surrounded by haemorrhages
which are detected on fundoscopy

Investigations
o Blood cultures- will show the causative organism- at least three blood
cultures need to be taken at different times from various sites
o Echocardiography- will show mobile vegetations in the valves
...

Management
o Mainstay of treatment is long term IV antibiotics- typically, beta lactam,
vancomycin and gentamycin- for 6 weeks but not longer so no prophylaxis
once this is finished
...

 The echo is transthoracic
o ECG- will show left axis deviation, left ventricular hypertrophy and a broad
notched P wave due to left atrial enlargement
o CXR- may shoe pulmonary oedema and also left atrial enlargementcardiomegaly
o Essentially, this and aortic have the same symptoms and investigations and
the key difference is the aortic has an early diastolic murmur and this has a
pansystolic murmur
Management
o Treat the complications
 AF- this will need anticoagulation and rate control
 Thromboembolism- this will need anticoagulation
 Heart failure- diuretics, ACE inhibitors and beta blockers
o Diuretics- furosemide and indapamide can be used
o Chronic MR: medical management can help but surgery will always be the
first option
 ACE Inhibitors- captopril, enalapril, lisinopril
 Plus beta blockers- metoprolol, atenolol and nadolol
o Surgery is the definitive management
 Mitral valve repair is preferred over mechanical/ bioprosthetic mitral
valve replacement
o
o
o
o
o

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21

-------------------------------------------------------------------------------------------------------------------------Pericarditis
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22

There are two kinds of pericarditis:
o Acute pericarditis- this is inflammation of the pericardium and can be caused
by:
 Infection- due to staph
...

 Rheumatological causes- SLE, RA, Sarcoidosis, Vasculitis
 Renal failure and uraemia is common
 Hypothyroidism and IBD
o Constrictive pericarditis- when the pericardium becomes thickened and
scarred and in turn can lead to less blood being pumped since the heart
cannot fully function
...
It does not peak like it does in MI and will stay consistently
elevated
o ECHO- will show the vegetation growth etc
...

tuberculosis

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23

o CRP- elevated
Management
o Exercise restriction and NSAIDs are the first line management with colchicine
alongside
 Be careful and do not give if hepatic or renal impairment
 Give omeprazole a PPI alongside since there needs to be
gastroprotection
 Aspirin or ibuprofen are the major NSAIDs to be used
o Corticosteroids are second line for people who cannot tolerate NSAIDs or
have non viral pericarditis and this should be a low dose of corticosteroids
 Prednisolone is the first line one to use
o IV antibiotics for bacterial causes or if the centesis shows an exudateespecially if the pericarditis is purulent
o Important to treat the underlying cause as well



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