Cardio Flashcards
HTN, HF, IE, AF, valvular disease, PVD, hyperlipidaemia, rheumatic fever, IHD
Infective endocarditis risk factors
recent dental, endoscopic or operative procedures, valve disease (including bicuspid aortic), prosthetic valves, past rheumatic fever, heart disease/operations, IV drug use,
immunosuppression
Signs on exam for Infect Endocarditis
Peripheral
Hands
clubbing
splinter haemorrhages
Osler’s nodes (painful red)
Janeway lesions (non-tender, tiny, red
palms)
Eyes
Roth spots (red haemorrhage w white centre)
Neuro
Signs of peripheral embolic disease forming
abscess (but embolic abscesses can form in
almost any organ)
Heart
Listening for new murmur or changed murmur.
Most often vegetations cause regurgitation
(commonly mitral)
Signs of Cardiac Failure
Source of Infection (+ temperature)
Investigations for IE- expected bugs + abx
Bloods
Cultures – strep viridians (penicillin) and staph aureus (flucloxacillin) predominantly
FBC (raised neutrophils) and ESR (high)
Imaging
CXR (heart failure, cardiomegaly)
ECHO (looking for vegetations,
regurgitation, or abscess) TOE is more sensitive
Other
MSU – for haematuria (from emboli)
Management of IE
IV antibiotics dependent on the organisms
sensitivities –at least 4 weeks but 6-8 if prosthetic valves
Consider cardiac surgery e.g. valve replacement (if severe heart failure, valvular obstruction, abscess) - 50% require surgery
Consider antibiotic prophylaxis (high dose, short term) for future medical/dental procedures – but this is controversial - if patient is already having antibiotics
however it is recommended to cover IE organisms
differential diagnosis for IE
-Rheumatic fever
atrial myxoma (cardiac tumour)
other cardiac neoplasm
SLE
Risk factors for heart failure
Coronary artery disease:
HTN, hyperlipidaemia, DM, smoking,
obesity, physical inactivity, CAD, family
history of heart disease, high alcohol intake
Dilated Cardiomyopathy:
alcohol intake, family history or
cardiomyopathy, haemochromatosis
Exams to do for HF
Cardio , resp, lying and standing BP, PVD brief
exam findings for RHF vs LHF vs both
RHF - pitting oedema, JVP, ascites,
hepatomegaly (congestion)
LHF - cyanosis,cool peripheries, crackles in lung bases, stony dullness (effusion)
BOTH - murmur, conjunctival/palmar crease pallor, AF,
parasternal heave, Cheyne-stokes breathing,
displaced apex beat, S3
Look for cardiac cachexia, pacemaker
NY HA classes of HF - 1 to 4
1 - Cardiac disease, but no symptoms and no limitation in ordinary physical activity,
2 - Mild symptoms (mild shortness of breath and/or angina) and slight limitation during ordinary activitye.g. shortness of breath when walking, climbing stairs etc
3 -Comfortable only at rest. Marked limitation in activity due to symptoms, even during less-thanordinary activity, e.g. walking short distances (20–100 m).
- Severe limitations. Experiences symptoms even while at rest. Mostly bedbound patient
Differentials for HF symptoms
Nephrotic syndrome, liver disease
(decreased albumin), if only LHF think of any lung disease (e.g. Pneumonia, COPD)
Investigations for HF
Bloods
Hb – to exclude anaemia as precipitant
Electrolytes and Creatinine- hyperkalaemia may cause arrhythmias, hyponatraemia may indicate severe long standing cardiac failure
BNP – elevated levels may distinguish
cardiac from non-cardiac dyspnoea. Useful for monitoring response to treatment.
Cr and eGFR - (renal failure as a cause or as a consequence, and also make sure OK to take medications)
TFTs (thyrotoxicosis)
Imaging
CXR – (ABCDE) alv oedema, kurly beeline= fissure, cardiomegaly, distention of sup pul vessels, effusion. Chamber size enlarged.
Other
Daily weights
ECG – arrhythmia, signs of ischaemia or old infarct, LVH, LBBB
ECHO – if the diagnosis is not already
obvious. May show regional (infarct) or global (dilated cardiomyopathy) wall motion abnormalities, estimate EF, identify valvopathy
Coronary angiography (plus troponins and ETT) to exclude coronary artery disease
RV biopsy to determine aetiology – rare
how can you correct the underlying cause of HF as part of management
Correct Underlying Cause
rate control arrhythmias (pacemaker or meds)
thrombolysis for acute infarct
CABG or angioplasty for ischaemia
Medication review
Control thyroid disease
Valve replacement
Transfusion for anaemia
Management of acute HF
Manage Failure (Acute)
Sit upright
Morphine
Oxygen
GTN
Frusemide +/- thiazide
DO NOT GIVE BETA BLOCKERS
Management of HF - non pharm pharm
Non Pharmacological
Bed rest if unwell
Low salt diet
Fluid restriction (1 – 1.5L/day)
Control CV risk factors (smoking cessation, weight loss, alcohol reduction, exercise)
Annual influenza vaccination (increased risk)
Educate around sx and have action plan in place for exacerbations
ACP/ resus
Pharmacological - HFRef
1st- Furosemide initially for fluid overload
2nd- ACEI or ARB
3rd- BB once no more overload - bisoprolol titrate max dose
4th- still symptomatc spironolactone
5th-entresto –>stop the arb/ace i
5th SGLT2 inhibitor - empag -
- digoxin/anticoag for AF
-Iv irons for anaemia
Only use ARBs if side effect (usually cough) to ACEi
Avoid calcium channel blockers (negative inotropes) and NSAIDs (worsen renal function)
Symptom improvement = diuretics, beta blockers, ACEi, hydralazine + nitrate, digoxin, spironolactone
Increased survival = beta blockers, ACEi,
hydralazine + nitrate, spironolactone
For HFpEF its optimisation f other comorbidities
Possible causes of HF
Causes =
IHD (most common), arrythmias, valvulopathy, hypertension, cardiomyopathy, myocarditis,
-chronic lung disease (cor pulmonale), pulmonary embolism,
-medications with negative inotropic properties (beta blockers and verapamil)
-high output status (anaemia,thyrotoxicosis, pregnancy etc).
Note that RVF is usually due to lung disease, LVF, or pulmonary stenosis.
HTN important complications, 2ndary causes of htn, other aspects of hx to ask for someone with htn
o Stroke
o Heart failure or PVD
o Renal failure
Symptoms of malignant hypertension (severe headache)
Potential secondary cause
o Phaeochromocytoma if paroxysmal sweating, palpitations and headache
o OSA if daytime sleepiness
o Renal artery stenosis or CKD
o Coarctation of aorta
o Adrenal tumour, conns or Cushing’s
o Meds- COC, NSAIDS
o Pregnancy
o However 95% are idiopathic/primary
Other risk factors for vascular
disease
o Type 2 diabetes
o Hyperlipidaemia
o Family history of coronary or CVD
Lifestyle factors
o Obesity, lack of physical activity, excessive alcohol intake, high salt
diet
o Ask about attempts and success with any of these
Exam for HTN
Cardiovascular disease (look for postural BP drop, and do BP in both arms)
- Look for signs of Cushing’s (moonfaced, weight gain, purple striae, buffalo hump, proximal muscle weakness)
-Remember radio femoral delay (coarctation)
Fundoscopy (looking for hypertensive retinopathy –flame haemorrhages and cotton wool spots, AV nipping, exudates, papilledema)
Ix for HTN - primary and secondary
Bloods
U+E, creat – to look for renal disease
ECG – to look for LVH and evidence of IHD
CXR – to exclude cardiomegaly, LVH,CHF
Urine analysis – looking for proteinuria
(renal failure caused by HTN. If positive can do 24 hour urine collection and work out ACR
HBA1C and lipids – to assess for other cardiovascular risks
Aldosterone/renin ration – to detect primary hyperaldosteronism i.e. Conns (especially if hypokalaemic and not on diuretics; high Plasma Aldosterone :Plasma Renin Activity ratio (plasma ) Also renin secreting cancers
24 hour catecholamines if symptoms consistent with phaeochromocytoma
Serum cortisol if investigating for Cushing’s/ dexamethasone suppression test/ ACTH stimulation test
Renal artery Doppler study for patients with intractable hypertension renal artery stenosis
Sleep study if considering sleep apnoea
Ambulatory BP- at home BP record
Dx and classes of HTN
Dx = BP of over 140/90 on three separate occasions a week apart (unless severe HTN with end organ MI, LVH, HF, stroke, renal damage, retinopathy)
Preferably ambulatory BP monitoring will be used at home to make diagnosis (to prevent white coat HTN)
Classes
Mild (Grade 1) 140-159/90-99
Moderate (Grade 2) 160-179/100-109
Severe (Grade 3) >180 syst +/- >110 dias
Management of HTN based on CVD risk - basic principles (risk by gender, age, ethnicity, BP, TC/HDL ratio, smoke, DM, fam hx). Target BP?
CVD < 5%
o Lifestyle advise
o Discuss harms and benefits of BP lowering and statin meds
o Further assessment 5 – 10 years
CVD 5-15%
o Individualized lifestyle advise
o Commence BP lowering +/ statin
o Further assessment 1 – 2 years
CVD > 15% and established CVD or anyone with BP 160/100
o Intensive lifestyle advise
o BP lower + statin + antiplatelet therapy
o Annual review
Target BP
o <140/90 if >80 or significant
concern of frailty/hypotension
o <130/80 in most cases/ high risk patients
Management of HTN - pharm + non pharm
What are some examples of the drugs (give names), and contraindication
Non-Pharmacological
Diet - reduced salt, fats and sugars
Physical activity – 30 mins a day, green prescription
Weight – BMI < 25
Smoking cessation – ask, brief advice and offer of help, cessation support, document
Alcohol reduction
Pharmacological
Recommendation to commence on a low dose of a single therapy, followed by addition of a low dose of a second medication rather than increasing the dose of the first to avoid S/E
When choosing medication, consider previous intolerance, known contraindications, interaction with other meds, existing medical problems that favour use of a certain class.
o 1st ACEi monotherapy if young/close to target or DM,
- CCB if >55 or black
o 2nd add other ( or start w two low dose if elderly
o 3rd thiazide
o 4th add spironolactone or other medicine (bb)
Swap ACEi for ARB- (Cilazapril for candesartan) if side effects (usually cough)
ACEi - Not female reproductive age
Calcium Channel Blockers
Felodipine (targets vessels) Diltiazem (targets vessels and cardiac),
Verapamil (targets cardiac tissue) Beneficial for angina
Beta blockers. Less effective on own and not common or recommended for HTN Metoprolol, Bisoprolol, (HF)
Benefit: Angina, HF, MI
Contraindicated: asthma, DM, heart block, PVD
Specific indications
o BPH –alpha blocker
DIFFERENTIAL DIAGNOSIS OF IRREGULARLY
IRREGULAR BEAT
D Atrial fibrillation
Ventricular ectopic beats
Complete heart block with variable ventricular escape
Atrial flutter
Precipitants (for AF)
A- age
T- thyrotoxicosis
M – mitral valve disease
I – ischaemic heart disease
S – surgery, sleep apnoea,
smoking
H – hypertension
A – alcohol binge or caffeine
P – PE
CKD, DM, male, obesity
exam for AF
Cardiovascular exam
Heart rate and rhythm
Radial pulse!
Thoracotomy scars, pacemakers, implanted
defibrillators
Signs of cardiac failure, valvular heart disease
Evidence of recent abdominal surgery
Thyrotoxicosis
Ix for AF - specific signs on most important
ECG
o Resting ECG
o 24 ECG Holter monitor if symptomatic
o AF specific signs
No p waves
Irregular QRS
EPS (electrophysiological studies)
Assess inducibility of
arrhythmias before and after
treatment
ETT
If associated symptoms or
known IHD
ECHO
Valve disease, cardiomyopathy,
hypertrophy, atrial size,
segmental wall abnormalities
Bloods
U+E, TFT’s, serial trops
Management of symptomatic bradycardia, Ventricular tachy
Symptomatic brady
- atropine 1mg every 3-5 min then transcutaneous pacing or epinephrine ot dopamine infusion
- Consider permanent pacemaker if completeheart block, second degree AV block, sinus node dysfunction
VT
- Consider implanted cardioverterdefibrillators if
- VF/VT with haemodynamic
instability, contraindications to drug treatment or non-response, symptomatic long QT, persistently inducible VF/VT,VF/VT
Works by overdrive pacing before administering DC shock
Acute management of AF
Acute Management
< 48 hours – cardioversion
o DC cardioversion if haemodynamically unstable/unconscious
o Medical cardioversion with amiodarone 5mg/kg over one hour followed by infusion 900mg over 23 hours (rule out thyrotoxicosis first)
> 48 hours – do not cardiovert (unless TOE has proven no intracardiac thrombus). Thus rate control.
Rate control
o BB - Metoprolol ( not if in acute HF)
o CCB - Diltiazem – short acting (15mg or 30mg) initially then long acting.
o Digoxin
Thromboprophylaxis
o Dabigatran normally first line now
(no monitoring required)
o LMWH then commence warfarin if high risk, stop LMWH once therapeutic INR – not as common now, if dabigatran not appropriate discuss with cardio
o No anti-coagulation needed if stable sinus rhythm restored, no risk factors, and recurrence unlikely – discuss with cardio
Chronic management of AF - rate and rhythm control methods + drugs
Rate control just as good as rhythm control
Rhythm control - Consider if symptomatic, CCF, younger, 1st presentation, or persistence despite corrected
precipitant.
o Electric cardioversion if unstable (after at least three weeks of therapeutic anticoagulation before)
o Flecainide if no structural heart disease
o Amiodarone if structural heart disease
o Note can do ‘pill in pocket’ approach with sotalol or flecainide if infrequent PAF
Rate control
o Metoprolol or diltiazem, if that fails add digoxin (not for renal failure), if that fails try amiodarone with expert advice.
Anticoagulation
Noacs or warfarin
o If CHA2DS2VSc score > 1
CHA2DS2Vsc score (stroke risk) means what vs HASBLED (bleeding risk)
chadsvasc - stroke risk for patients w AF
C – CHF (1)
H – HTN (1)
A – Age (1 if 65 – 74, 2 if 75 or more)
D – DM (1)
S – Stroke (2), TIA (1)
V – Vasc disease (1)
S – Sex female (1)
Hasbled- major bleeding risk on anticoagulation
HTN
Abnormal renal/liver fx
Stroke hx
prev Bleed
Labile INR
Elderly >65
medication usage predisposing to bleeding, etOH >8 units a week
Mitral stenosis causes, complications, differential dx
Causes
Rheumatic heart disease 99%
Congenital, prosthetic valve
Complications
– Pulmonary hypertension,
emboli, pressure symptoms from large LA including hoarse voice and dysphagia
Differential Diagnosis
Atrial/ Ventricular septal defect, patent DA
Carey coombs (A rheumatic fever)
Ix and management of Mitral stenosis
Investigations
ECG
o May be in AF
o signs of L) atrial enlargement - P mitrale if in sinus
o RVH
CXR
o L atrial enlargement
o Pulmonary oedema
o Mitral valve calcification
ECHO
o For diagnosis
Managements
Medical
o If in AF, rate control + anticoagulate
o Diuretics to reduce preload and pulmonary congestion
o Long term antibiotic prophylaxis against recurrent rheumatic fever
o Short term antibiotic prophylaxis against IE for dental, GI and GU procedures may be indicated
Surgical (if medical not controlling sx)
o Balloon valvuloplasty
o Open mitral valvotomy or valve replacement
Signs of mitral stenosis on exam vs mitral regurgitation
Mitral stenosis
o Malar flush
o Low volume pulse
o AF (common)
o Loud S1 + tapping apex
o Mid diastolic murmur, heard loudest over apex in expiration on left lateral side
Mitral regurg
o +/- AF
o Displaced, hyperdynamic apex
o Pansystolic murmur, loudest over apex, radiating to the axilla, heard loudest in expiration on left lateral
side
o Soft first heart sound, possible third heart sound
Mitral regurg causes, differential dx
Causes
Functional (LV dilatation) – secondary mitral insufficiency
Congenital
Annular calcification
Rheumatic fever/IE
Papillary muscle dysfunction/rupture
Connective tissue disorders e.g Marfan’s - Mitral valve prolapse/ruptured C.T
Differential Diagnosis
Ventricular Septal Defect (esp if post MI), TR (V wave + pulse liver)
Ix and management mitral stenosis
Investigations
ECG
o May be in AF
o P mitrale if in sinus
o RVH
CXR
o Enlarged LA
o Mitral valve calcification
o Pulmonary oedema
ECHO (with Doppler)
o Diagnose and ascertain aetiology
o Size and site of regurgitant jet
o Assess LV function
Cardiac catheterization
Management
Rate control if in AF
Anticoagulate if in AF, hx of embolism or additional mitral stenosis
Diuretics or ACEi for patients with hypertension to decrease afterload
Surgery to replace/replace the valve before LV irreversibly impaired (balloon valvuloplasty, open mitral valvotomy/ replacement
Antibiotic prophylaxis before procedures to be considered
What is the cause, symptoms, sign, ix and management of mitral valve prolapse
Causes
Atrial Septal Defect/Patent Ductus Arteriosus, Wolf PW
Turners/Marfan’s syndrome
Symptoms
None or atypical chest pain, palpitations
Autonomic dysfunction (anxiety, syncope)
Signs
- Mid systolic click + late systolic murmur
Ix
ECHO is diagnostic
ECG may show T wave inversion
Treatment
Surgery if severe
Aortic stenosis causes, signs, ecg and differentials
Causes
Senile calcification (most common – this is essentially a disease of older people)
Bicuspid valve
Rheumatic heart disease
Signs
o Slow rising pulse with narrow pulse
pressure
o P – Non displaced apex, LV heave, aortic thrill
o A – ejection systolic murmur heart
loudest at the base/left sternal edge/aortic area radiating to carotids, ejection click.
Differential Diagnosis
Aortic Sclerosis
o Senile degeneration of valve
o Normal pulse, no radiation of murmur to carotids (elderly)
Hypertrophic cardiomyopathy
(HCM)
o LV outflow tract obstruction due to asymmetric septal hypertrophy
o Risk of sudden death – leading cause
in the young
o May show LVH, progressive T wave
inversion and deep Q waves on inferior and lateral leads on ECG
Ix + management for aortic stenosis
ECG
o P mitrale
o LVH with strain pattern
o LBBB or complete AV block
CXR
o LVH
o Calcified aortic valve
ECHO
o Diagnose and classify severity
Cardiac catheterization
o Assess valve gradient, LV function, risks emboli
Management
Prompt valve replacement
Percutaneous valvuloplasty (TAVI) if unfit
for surgery
Causes - acute + chronic, signs and differential for Aortic regurgitations
Causes
Acute
o IE
o Ascending aortic aneurysm
Chronic
o Rheumatic heart disease
o Connective Tissue disease (SLE, RA, Marfan’s)
o Seronegative spondyloarthritides (ank spond, psoriatic arthropathy)
o Hypertension
Signs
o Water hammer/collapsing pulse
o Wide pulse pressure
o Nailbed pulsations (Quincke’s sign)
o Carotid pulsations (Corrigan’s Sign)
o Head nodding (de Musset’s sign)
o Pulsating Uvula (Mueller’s sign)
Cardiac
o P – thrusting displaced apex
o A – high pitched early diastolic murmur heard best in expiration with patient sitting forward
Differential MS (mid diastolic murmur
Ix and management of Aortic regurgitations
Investigations
ECG - LVH
CXR o Cardiomegaly,
pulmonary oedema
ECHO
o Diagnostic (TOE)
Cardiac catheterization
o Severity of lesion, anatomy of aortic root, LV function, coronary artery disease
Managements
Medical
o Reduce systolic hypertension (ACEi, diuretics)
Surgical
o Indications – worsening symptoms, not responding to medical therapy,ECG changes, enlarging heart
- Replace valve before significant LV dysfunction occurs
what are the systolic murmurs vs non systolic murmurs
Systolic - Aortic stenosis, mitral regurg
Diastolic - mitral stenosis, aortic regurg
PVD - Arterial vs chronic venous insufficiency hx questions, differential dx
Arterial Questions
How far can you walk? What causes relief?
How long do you need to rest for? How long
has it been this bad? When could you last…?
Do you ever get pain at rest?
Physical changes – cool, pale, ulcers
CVD risk factors
Venous Questions
Risk factors – pregnancy, past history of
trauma/fractures/surgery, hormones,
obesity, smoking
Personal or family history of thrombophilia,
DVT, PE
Varicose veins
Physical changes – swelling, eczema,
pigmentation, ulcers
DIFFERENTIAL DIAGNOSIS
Arterial
Neurogenic claudication (spinal stenosis)
Osteoarthritis of hip/knee
Peripheral neuropathy
Venous
HF, liver cirrhosis, nephrotic syndrome, GI
Exam findings arterial vs venous PVD
Arterial
o Pallor, mottling, gangrene
o Amputation, wasting
o Scars, hair loss
o Ulcers – ‘punched out’, peripheries,
deep, regular, painful, pale base, minimal exudate
o Onychogryphosis, onychomycosis
Venous
o Varicose veins
o Hemosiderosis (red/brown from deposition of haemosiderin from RBCs)
o Oedema
o Lipodermatosclerosis (shiny + red above ankles)
o Eczema
Ulcers – gaiter area, shallow,
irregular, painless, lots of exudate (wet)
Ix and management of arterial and venous pvd
INVESTIGATIONS
Basic bloodwork – FBC, lipids, UEC, BGLs –
for treatment/ secondary prevention
Arterial
- ABP1 - 1-1.2 normal, <0.9 arterial disease, <0.4 critical limb, >1.2 calcified
- Duplex USS
- CT - angiography/MR angiography –
if considering intervention
Venous
Duplex ultrasound
CT and MR venography reserved for patients with complex abnormalities.
ABPI to rule out concurrent arterial
insufficiency before prescribing compression stockings
MANAGEMENT
Arterial
Risk factor management – smoking cessation, regular exercise
Antiplatelet therapy (clopidogrel 1st line)
Statins
- Surgical
o Revascularization
Endovascular
Bypass grafting
Amputation
Venous
Weight loss, exercise
Compression stockings
Education about prolonged standing and
elevating when possible
Endovascular surgery
Hyperlipidaemia exam findings, investigation and management
EXAMINATION
- Cardio exam
- Corneal arcus, xanthelasma (yellow, lipid
plaques around eyes), or xanthomata
(elsewhere eg tendons)
INVESTIGATIONS
-Lipids –normal =LDL <2, HDL >1, Triglycerides <1.7, total cholesterol <4, TC / HDL ratio <4
-Creatinine Kinase – after starting statins
-LFTs – to look for fatty liver and to look for
damage after starting statins
MANAGEMENT
- lifestyle advice (reduce BMI, reduce saturated
fats in diet, increase fresh fruit and vegetables,
increase exercise)
- treat cause if secondary
Medications:
-Who? – those with known CVD, those with
DM, those with CVD risk >20%
-1st line = Statins (eg simvastatin 40mg po
nocte). Reduce cholesterol synthesis in liver.
Side effects = myalgia (check CK), and increased LFTs
-2nd line = Fibrates (eg bezafibrate - useful in
mixed hyperlipidaemias) or Cholesterol absorption inhibitors (eg ezetimibe).
Fibrates best for hypertriglyceridemia.
Ix for rheumatic fever
Bloods
FBC, ESR, CRP
Blood cultures if febrile
Antistrep serology
o Anti streptolysin
o Anti-DNase B
Imaging
CXR
ECHO
Other
ECG
Throat swab
Dx criteria for rheumatic fever
DIAGNOSIS (JONES CRITERIA)
1. Evidence of recent strep infection AND
2. 2 major criteria OR
3. 1 major and 2 minor criteria
Evidence of recent strep infection
- Positive throat culture (usually negative by
the time symptoms appear)
Rapid streptococcal antigen test
Elevated or rising streptococcal antibody
titre
Recent scarlet fever
Major Criteria
- Joints
o Arthritis (Pain + ROM + hot), usually of large joints, Migratory polyarthritis (can be
monoarthritis in high risk
populations)
Carditis
o Can be endocarditis, myocarditis, or
valvulitis
o Look for tachycardia, murmur,
cardiomegaly, CCF, conduction defects
o Sometimes subclinical – ECHO evidence
Subcutaneous nodules
o Rare but highly specific
o Small, hard, mobile, painless subcutaneous nodules on extensor surfaces of joints and spine
Erythema Marginatum
o Rare
o Blanching, circular macules with red
raised edges and clear centres.
o Trunk and proximal extremities
o Not itchy or painful
Sydenham’s Chorea
o Jerky, uncoordinated movements
o Hands, feet, tongue, face
o Bilateral or unilateral
o Useful signs
Milkmaids grip
Pronator sign (arms and
palms turn outward when arms
held above head)
Inability to maintain
protrusion of tongue
Minor Criteria
fever
raised ESR or CRP
Arthralgia (not if arthritis is a major criteria)
Prolonged PR interval (not if carditis is a major criteria)
Previous rheumatic fever
Acute management of Rheumatic fever
Acute Management
- Antibiotics
o Penicillin for 10 days (or
benzylpenicillin IM single dose)
o Erythromycin if penicillin allergy
Anti-inflammatories
o Aspirin/NSAIDS (be wary of toxicity)
Bed rest
o Until CRP normalized
o Gradual return to activities
Treat any heart failure
Surgery
o Emergency valve replacement/
repair if valve leaflet or chordae
tendineae rupture. Otherwise
deferred until active inflammation
has subsided.
Anti-chorea meds
(Only if severe/distressing/risky)
o Carbamazepine
Secondary prophylaxis of Rheumatic fever
Choice of antibiotic
1st Line - IM benzathine penicillin every 4
weeks
2nd Line – Oral penicillin twice daily
3rd Line – Oral erythromycin twice daily if
allergy
Time period
ARF + no or mild carditis
o Minimum 10 years or until 21 years old (whichever is longer)
ARF + moderate carditis
o Minimum 10 years after most recent episode or until 30 years (whichever
is longer)
ARF + severe carditis
o Minimum 10 years after most recent episode or until 30 years (whichever
is longer) then review by specialist to consider lifelong
Differentials for IHD, complications of MI, Ix
DIFFERENTIAL DIAGNOSIS
GORD
Oesophageal Spasm
MSK
PE
Acute pericarditis
Pneumonia
MI Complications
Arrhythmias
Bradycardias
Heart failure
Further ischaemia
INVESTIGATIONS
- ECG – current or old changes
- Troponins – note they don’t rise until about 6hours after MI and so repeat troponin is usually done after this 6 hour period to ensure MI not missed. Can remain elevated for 2 weeks (not always specific - lots of things raise troponins)
- FBC, UEC, TFTs, Lipids, HbA1C
- CXR
- ETT – to stimulate ischaemia if needed
- ECHO – to look for valvular pathology and heart function
- Angiogram
Immediate management of stable angina, unstable angina, STEMI and NSTEMI
Immediate
Stable Angina – primarily treated with GTN spray
(be careful with Sildenafil). Can add beta blockers.
Unstable angina – aspirin, GTN, consider beta
blockers. Basically all of the secondary prevention
stuff below. Consider angiogram +/- angioplasty
STEMI:
Morphine, oxygen, short acting nitrate,
DAPT, and antiemetics - metoclopromide
Admit to CCU for continuous ECG monitoring
PCI/angioplasty (door to balloon in 90 mins)
o If not offered in hospital, transfer is preferable over thrombolysis if transport time is 2 – 3 hours.
o Reduced mortality compared with thrombolysis
o Can’t do if previous bypass
Thrombolysis
o < 85 years – IV Tenecteplase (tPA,
tissue plasminogen activator). Converts plasminogen to plasmin,
initiating fibrinolysis.
o >/= 85 years – Streptokinase, unless
there is prior use, risk of reaction.
ACEi and beta blockers - long term management
Non-STEMI
Morphine, oxygen, short acting nitrates,
DAPT, anti-emetics - metoclopromide
Admit to CCU for continuous ECG
monitoring
early revascularization, not as urgent (up to 24 hours after MI)
ACEi and beta blockers for long term management
Secondary prevention for ischaemic heart disease
Non pharmacological
o Diet, physical activity, smoking cessation
o Cardiac rehabilitation programme
Pharmacological
o BP lowering - ACE-i are the drug of choice
o Statins
- Antiplatelet - (aspirin-forever and ticagralor-12month)
o Anti-anginal
Beta blocker
Diltiazem
Nitrates
Surgical
Patients with three vessel
disease, LV damage, L main
coronary stenosis or proximal LAD stenosis may
benefit from CABG.
CABG not usually done in acute ACS unless angioplasty and thrombolysis have failed
Thromboprophylaxis - drugs moa + pros and cons
- Dabigatran - direct thrombin inhibitor - (pros -no regular testing, antidote= idarucizumab, cons - renal excretion, GI SE).
- Rivaroxaban factor 10a inhibitor - (not easily reversed, not for severe renal disease)
- Warfarin - Vit K antagonist, target INR 2-3. Pro - effective, antidote. cons - regular INR testing, GI, IC haemarrhoage, skin necrosis, teratogenic. CI in those conditions + liver disease).
