Cardiology Flashcards
Aspirin MOA
Anti-COX - irreversibly acetylates it. Prevents production of thromboxane A2 - therefore inhibits platelet aggregation.
Aspirin Uses x3
Secondary prevention following MI and TIA/Stroke. Also for patients with angina or peripheral vascular disease.
Clopidogrel and prasugrel MOA - and 1x benefit
ADP (adenosine diphosphate) receptor antagonists - therefore also block platelet aggregation. May cause less gastric irritation
When clopidogrel and prasugrel used? x3
If aspirin intolerant, after coronary stent insertion with aspirin, ACS.
Tirofiban MOA and use
Glycoprotein IIb/IIIa antagonist - anti-platelet - unstable angina and MI - prevention of cardiovascular events
Warfarin MOA
Inhibits vitamin-k dependant synthesis of clotting factors, factor II, VII, IX and X
Warfarin uses x2 and complication
AF and mechanical valves. Needs monitoring of values
Apixaban MOA and Dabigatran MOA. Benefits
Factor Xa inhibitor and Direct thrombin inhibitor. Novel anticoagulant therapy. Don’t require therapeutic monitoring, may have a better risk:benefit ratio
LWH MOA and use
Bind to antithrombin which accelerates its inhibition of activated factor X (factor Xa) - used in ACS
Fondaparinux MOA and use
Factor Xa inhibitor - used in ACS
Bivalirudin MOA and use
Thrombin inhibitor - ACS
Features of angina - pathology, presentation, exacerbation and relieving factors, radiation.
Due to myocardial ischaemia, central tightness or heaviness, brought on by exertion and relieved by rest, radiates to arms, neck, jaw.
Precipitants of angina x3
Cold weather, emotion, heavy meals
Associated symptoms of angina x4
Dyspnoea, sweating, nausea, faintness
Causes of angina x6
Atheroma, anaemia, aortic stenosis, tachyarrhythmias, HCM, arteritis/small vessel disease
Types of angina x4
Stable (worse on exertion, better on rest),
Unstable (gradually increasing, occurs on minimal exertion or rest, greater risk of MI)
Decubitus angina (precipitated by lying flat - usually combination of CAD and heart failure)
Variant (Prinzmetal’s) angina - caused by coronary artery spasm - may coexist with fixed stenoses
Features of variant angina - cause, presentation, ECG, typical patient
Coronary artery spasm and can be in healthy coronary arteries,
Pain usually at rest rather than during activity
ECG during pain = ST elevation, resolves when pain subsides
Patients do not usually have atherosclerosis risk factors
Treatment of variant angina
Calcium channel blockers
Aspirin and B-blockers can exacerbate
Tests in angina x 4
ECG, Angiography, Functional imaging, Stress echo
Conservative management of angina x4
Stop smoking, encourage exercise and weight loss, control HTN and diabetes, decrease cholesterol with statin
Drugs for angina - 1st lines x 3
If b-blocker contraindicated
Extra if not controlled
One final one
Aspirin
B-blockers (eg. atenolol) unless contraindicated)
Nitrates
Long-acting calcium antagonists (eg. amlodipine, diltiazem)
K+ channel activator (eg. nicorandil)
Ivabradine - inhibits funny current in SA node - reduces heart rate
Nitrates use in angina
Symptoms - GTN spray or sublingual spray
Prophylaxis
Isosorbide mononitrate - need 8hour free period to avoid tolerance
Or slow release/adhesive nitrate patches, buccal pills
Surgical treatment of angina
Indications x4
Percutaneous Transluminal Coronary Angioplasty
Balloon dilatation of stenotic vessels - >70% with stent insertion
Poor response/intolerance to medical therapy, refractory not suitable for CABG, previous CABP, post-thrombolysis in patients with severe angina
What does ACS include? x3
Unstable angina, silent ischaemia, evolving MI
Underlying pathology of ACS
Plaque rupture, thrombosis and inflammation - occlusion of coronary artery
Can also get it due to emboli or coronary spasm in normal coronary arteries
Myocardial Infarction definition
Myocardial necrosis in the clinical setting of myocardial ischaemia
Difference between STEMI and NSTEMI
STEMI = full thickness damage of heart muscle due to complete occlusion of major coronary artery
NSTEMI = partial thickness damage due to occlusion of minor coronary artery or partial occlusion of a major coronary artery
Symptoms the same but ECG different
Cardiac markers usually more mild in NSTEMI
UK Incidence of ST elevation
60-70/100,000
Drug which increases risk of MI
Cocaine
3 things which raised levels increase risk of MI
Fibrinogen, Insulin, Homocysteine
2 types of trigger for MI and subtypes
1) Sudden shortage of myocardial oxygen supply
- Acute thrombosis on background of atherosclerosis (vigorous exercise, overeating, hot/cold - Virchow’s)
- Cardiac - unrelated to atherosclerosis (thrombo-embolism, coronary artery dissection, arteritis)
- Reduced oxygen supply (anaemia, hypoxaemia)
2) Sudden excess myocardial oxygen consumption
- Fever
- Thyrotoxicosis
- Hyperadrenergic state
- Increase LV afterload (HTN, AS)
Symptoms of MI x5
Chest pain >20mins, nausea, sweating, dyspnoea, palpitations
Silent infarct presentation of MI- when?
Elderly or diabetics
1) Signs of MI x5
2) If heart failure x3
3) If papillary muscle or ventricular septum dysfunction
1) Distress and anxiety, pallor and sweating, tachycardia, hypotension or hypertension, 4th heart sound
2) If HF - raised JVP, 3rd heart sound, basal creps
3) Pan-systolic murmur
Chest Xray in MI
Look for cardiomegaly, pulmonary oedema or diastinum (aortic rupture)
Creatinine Kinase in MI
x5 1-3 days post acute MI
CK-MB in MI
Isoenzyme of CK
Elevated x4
Increases within 3-12hr of onset of pain
Peak within 24 hour
Aspartate transaminase in MI
Elevated x3
1-3 days after
Lactate dehydrogenase in MI
Elevated x3
2-3days post
Takes 10 days to decrease to baseline
Cardiac troponin in MI
x50 increase
within 2-12 hour
peak at 24-48 hr
back to baseline 5-14 days
DDX of MI x6
Angina Pericarditis Myocarditis Aortic Dissection PE Oesophageal reflux/spasm
Management of STEMI
- 3 aims
1) Restore vessel patency & reperfusion
- Primary angioplasty
- Thrombolysis/fibrinolysis
2) Reverse/prevent thrombosis
- Heparin
- GPIIb/IIa antagonists
- Clopidogrel (2-4hr onset) and prasugrel (30min onset of effect)
3) Reduce myocardial oxygen demand
- Beta-blocker
- Nitrates
- ACE-i eg. lisinopril
Management of NSTEMI
Aspirin, clopidogrel, antithrombosis (fondaparinux), beta-blocker
Use of Coronary angiogram + PCI in MI
Urgent if ongoing pain or ECG changes despite optimal medical therapy, HF or haemodynamic instability
Early
Post MI management
Aspirin, Clopidogrel/ticagrelor/prasugrel for 1 year B-blocker lifelong ACE-i lifelong Statins lifelong (even if not raised cholesterol) Aldosterone lifelong if LVEF
Driving after PCI
Wait 1 week
Work after MI
May return after 2 months - unless danger occupation aka pilot, diver, airtraffic control
Heavy goods vehicles and public service drivers - return if fit criteria
Sex after MI
Best avoided for 1 month
Air travel after MI
Avoid for 2 months
Peak age incidence for Rheumatic Fever
5-15 years
Infective agent in rheumatic fever, presentation and in who
Pharyngeal infection with Lancefield group A β-haemolytic streptococci
2-4 weeks after infection rheumatic fever occurs
In susceptible 2% of population
Pathology of rheumatic fever
Antibody to the carbohydrate cell wall of the streptococcus cross-reacts with valve tissue (antigenic mimicry)
Diagnostic criteria for rheumatic fever
1) Evidence of group A β-haemolytic streptococci infection
2) 2 major criteria
- carditis
- arthritis
- subcutaneous nodules
- sydenham’s chorea
- erythema marginatum
3) 1 major and 2 minor criteria
- Fever
- Raised ESR
- Arthralgia (not if arthritis is the major)
- Prolonged PR interval (not if carditis is the major)
- Previous rheumatic fever
Evidence of group A β-haemolytic streptococci infection X4
1) Positive throat swab (usually -ve by time you get fever)
2) Rapid streptococcal antigen test +ve
3) Elevated or rising streptococcal antibody titre
4) Recent scarlet fever
Evidence of carditis in rheumatic fever x6
Tachycardia, Murmurs (regurgitation or Carey Coombs), Pericardial rub, CCF, Cardiomegaly, Conduction defects (45-70%)
Apical systolic murmur may be the only sign
Arthritis in rheumatic fever
Migratory “flitting” polyarthritis, usually only affecting the larger joints
Subcutaneous nodules in RF
Small, mobile, painless nodules on extensor surfaces of joints and spine (2-20%)
Sydenham’s chorea in RF
Occurs late in 10% - unilateral or bilateral
May be preceded by emotional lability and uncharacteristic behaviour
Erythema marginatum in RF
Geographical type rash with red, raised edges and clear centres - mainly on trunk, thighs and arms
In 2-10%
Management of RF
Including for carditis/arthritis and chorea
Bed rest until CRP normal for 2 weeks (might take 3 months)
Benzylpenicillin or erythromycin or azithromycin if allergic - for 10 days
Analgesia for carditis/arthritis - aspirin (immobilize joints in severe arthritis)
Haloperidol or diazepam for chorea
Prognosis in RF
60% with carditis develop chronic rheumatic heart disease
Recurrence can occur with more infection, pregnancy and use of pill
Cardiac sequelae affects: mitral (70%), aortic (40%), tricuspid (10%) and pulmonary (2%) valves
Prophylaxis in RF
Penicillin or sulfadiazine/erythromycin
If carditis + persistent valvular disease - at least until age 40 - maybe lifelong
If carditis but no valvular disease - continue for 10 years
No carditis - 5 years prophylaxis (until age of 21) is sufficient
When are beta blockers used?
Angina Hypertension Disrhythmias Post MI Heart failure (with caution)
When are loop diuretics used?
Heart failure
When are thiazides diuretics used?
Hypertension
Which two cardiovascular drugs can’t be combined
Verapamil and beta blockers
Risk of severe Bradycardia
When are calcium antagonists used?
Angina and hypertension
Non-hydropyridines eg. Nifedipine and amlodipine - slow conduction at SA and AV node - therefore also used to treat dysrythmia
Digoxin effect and use
Slows pulse - AF
When does digoxin levels need to be altered or alter the level of something else?
If on amiodarone - half dose of digoxin
Cardio version when on digoxin - use less Energy
How do statins work?
Inhibit HMG-COA reductase
Therefore inhibits de novo synthesis of cholesterol in the liver
This increases LDL receptor expression by hepatocytes leading to decreased circulating LDL cholesterol
Best given at night
What is Dressler’s syndrome?
Post MI: 1-3 weeks Recurrent pericarditis Pleural effusions Fever Anaemia Raised ESR
Treated with NSAIDs and steroids of severe
When do you do CABG?
left main stem disease
Mostly - triple vessel disease or abnormal LV function
Or if PCI has failed
