A patient has malar flush and rumbling mid-diastolic murmur (loudest on exp on left side). What is the Dx?
Mitral stenosis
Pan systolic murmur following MI with features of heart failure - what is the murmur?
Mitral regurgitation - due to ischaemic to papillary muscles
Most common heart defect in Down’s?
AVSD (others - VSD, ASD, PDA, ToF)
How does a thrombolytic/fibrinolytic agent work? What different types exist?
Plasminogen activators - dissolve IV clots to Tx acute MI, DVT/PE, acute ischaemic stroke, occlusion of indwelling catheter etc.
During thrombosis platelets activate prothrombin to form thrombin. This converts fibrinogen to fibrin forming a matrix.
This is counterbalanced by plasmin derived from plasminogen. tPA is a natural fibrinolytic in epithelial cells. All thrombolytic agents are proteases cleaving plasminogen to plasmin.
Agent types:
1. Fibrin-specifc agents - need fibrin present for conversion and work best for STEMI/PE/acute ischaemic stroke. E.g. alteplase
2. Non-fibrin-specific agents - act systemically as don’t require fibrin present e.g. streptokinase (less efficacy but reduced risk of IC haemorrhage, increased risk of allergy, no repeat use for 6 months), urokinase (used for indwelling catheters/PV thrombosis)
TXA can be used to reverse action of these agents.
ECG findings based on electrolyte abn?
K:
* Hyperkalaemia - ECG tall tented T-waves, wide QRS, prolonged PR - causes cardiac toxicity/muscle weakness - caused by drugs (k-sparing diuretics, ACEi/ARB, digoxin), Addison’s.
* Hypokalaemia - ECG U-waves (V2/3), T-waves wide/flat, ST depression - causes muscle weakness/resp failure - caused by diarrhoea/vom, malnutrition, aldosteronism, drugs (insulin, corticosteroids)
Ca:
* Hypercalcaemia - ECG short ST, wide T-wave - causes thrones, stones, bones, grones, and psychic moans - caused by primary hyperparathryoidism, malignancy
* Hypocalcaemia - long ST, long QT - causes neuro Sx - caused by pancreatitis, rhabdomyolysis etc
Na - no effect on ECG:
* Hypernatremia - causes thirst/neuro Sx - caused by dehydration, diabetes insipidus, hyperaldosteronism
* Hyponatremia - causes neuro Sx - caused by diuretics, SIADH, heart/liver/renal disease, diarrhoea
Summarise ACS guidelines
Give an overview of pericarditis
Give an overview of aortic dissection
After how long do trop levels peak after MI? Other causes of raised trop?
Driving rules for MI
Other to note - no sex for 1/12, return to work after 2/12 (stop if pilot/air traffic control)
ECG changes depending on STEMI location? How long for ECG changes to resolve?
Lateral leads - left circumflex/LAD
Inferior leads (or posterior) - RCA/LCx
Anterior/septal - LAD
ST-T changes resolve in days-weeks (longer if ischaemia causes infarction)
QRS including pathological Q-wave - PERMANENT
What are the complications of MI by time period after the event?
Give an overview of chronic heart failure
Classification:
- LVEF (<40 low, 41-49 mild, 50 preserved)
- NYHC (1 - no limit on physical activity, 2 - slight, 3 - marked, 4 - Sx at rest)
NT-proBNP > 2000 - 2wk referral/echo, 400-2000 - 6wk referral/echo
Acute heart failure findings on CXR? Ix? Mx?
Sit upright and 15L NRM, consider IV dia/morphine, Furosemide IV (x2 oral dose), GTN IV 0.5mg/hr (only if BP >90), consider CPAP/NIV if acidotic
If BNP > 100 or NT-proBNP > 300 transthoracic echo
Acute severe MR - surgical replacement
Critical AS - surgical replacement/TAVI
LVSD - ACEi, Aldosterone antag, B-blocker (d/c after stable for 48hrs)
Hypertension Management
BP in clinic >140/90 —> repeat (both arms should be measured if >15 repeat then use measurement in higher arm)
BP 140/90-180/120 - AMBM (ambulatory - 2 measurements/hr requiring 14 measurements)/HBPM (Home - x2 measurements daily for 4-7d, discard 1st day) to confirm Dx
>180/120 with retinal haemorrhage/papilloedema/Sx - same day specialist R/V
Classification:
1 >140/90 with AMBM 135/85
2 >160/100 with AMBM 150/95
3 >180/120
Accelerated/malignant = signs of retinal haemorrhage/papilloedema
?secondary cause of HTN if: <40yrs, Low Na/High K, eGFR <60, Pro/Blood in urine
Most common secondary cause: Renal
Signs of cardiac tamponade? Possible ECG findings? Tx?
ECG - sinus tachy, low voltage QRS, electrical alternans, PR segment depression
Pericardiocentesis
Mx of stable angina?
Secondary prevention: consider Aspirin, Statins, ACEi
Cardiac tamponade - key finding on exam? Triad? Mx?
Pulsus paradoxus - BP variation between inspiration & expiration (≥10)
Beck’s triad (50%):
Mx:
Acute limb ischaemia - Def? Presentation? Ix? Mx?

Peripheral vascular (arterial) disease - Def? RFs? Spectrum? Ix? Special test?
Def: limb ischemia (chronic) from atherosclerosis in lower limb vasculature
RFs: male, older, smoker, HTN, DM
Spectrum:
Ix:
Mx: dealt with by vascular surgeons –> optimise meds + surgery (bypass)
Chronic venous insufficiency & varicose veins - presentation? Ix? Mx? Complications of varicose veins?
Presentation:
Ix: duplex USS (allow DVT to be ruled out)
Venous insufficiency Mx:
Varicose Veins complications:
AAA key Sx & ruptured Sx? Ix? Mx?
Sx:
Ruptured AAA Sx:
Ix:
Mx:

How to calculate ABPI? ABPI value range?
Range:
Aortic dissection - def? Sx? Ix? Mx?
Def: tear in tunica intima (inner layer of BV) –> blood collection between tunica intima and tunica media –> false lumen (can occlude blood flows through aorta) –> AR, myocardial ischaemia, stroke
Sx: sudden onset, central tearing chest pain –> radiating to between shoulder blades
Ix:
Mx:
