Cardiovascular Flashcards
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
- For all ACS (STEMI/NSTEMI/UA) - give aspirin life-long
- STEMI within 12hrs Sx-onset & can do PCI within 120 mins - corronary angio + PCI, if not:
- If within 12hrs - fibrinolysis
- If not within 12hrs but myocardial ischaemia/cardio shock - angio
- Otherwise add Ticagrelor (Clopidogrel if high bleed risk)
- After angio add prasugrel (if no previous anticoag, otherwise clopi), if done via radial route give unfr heparin, femoral give bivalirudin (either with bailout GPI) - NSTEMI/UA - give fondaparinux (if low bleed risk, CR >265 consider unfr heparin) –> do GRACE/HEART score:
- If low risk add Ticagrelor
- If high risk/young for angio - Secondary prevention - ACEi, DAPT (12m), B-blocker (12m or forever if rLVEF, if CI for diltiazem/verapamil), Statin
- IF heart failure with rLVEF start aldosterone antag e.g. spironolactone (3-14d post-MI, after ACEi)
Give an overview of pericarditis
- Inflam of pericardium
- Acute form - new onset inflam lasting under 6-weeks
- Triad - chest pain, pericardial friction rub on auscultation, ECG widespread ST elevation (other Ix - bloods inflam, echo - pericardial effusion)
- Tx - NSAIDs + Colchicine
- Complications - recurrence, tamponade, constrictive pericarditis
Give an overview of aortic dissection
- Seperation in aortic wall intima –> blood flow into false channel (inner & outer layers of media)
- > 50yrs, sudden tearing substernal/intrascapular pain (+/- syncope, heart/renal failure, mesenteric/limb ischaemia)
- Ix with CT/MRI/ECHO
- If ascending aorta/arch - URGENT repair, otherwise b-blocker (or surgery if complicated), needs lifelong surveillance
After how long do trop levels peak after MI? Other causes of raised trop?
- rise 2-4hrs, peak 18-24hrs, last several days
- PE, other heart issue, renal failure, sepsis, rhabdomyolysis
Driving rules for MI
- Cease for 1wk if - successful angioplasty (incl in STEMI)/PPM-insertion
- Cease 4wk if - CABG/MI
- Cease completely if unstable angina uncontrolled
- Notify DVLA if AAA ≥6cm (disqualified if ≥6.5cm) or arrythmia (incapacitated)
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?
- Arrythmias - VF/VT (20%), AF (15%)
- Ischaemia (high CK) - re-occlusion, postinfarct angina –> angio + corronary revasc
- Mechanical:
- LVSD/HF - Killip’s classification (severity of HF post-MI)
- 24h-7d: 1) Ventricular septal - angina/pul oedema, new pansystolic murmur LLSB -> surgery. 2) free wall rupture - bleeding into pericardium (-> tamponade) -> needs pericardiocentesis/surgery
NOTE: pseudoaneurysm = contained left ventricular free walk rupture - Acute MR (normally inf/posterior infarct from isch/necrosis/papillary muscle rupture) = pansystolic murmur
- L. vent aneurysm, R vent failure, L vent outflow obstruction
- Inflammatory - Dressler’s syndrome (pericarditis) - 2-4wks post-MI - self-limiting fever + pericardial/pleural pain –> Tx with NSAIDS/steroids/drainage
- Systemic - PE/DVT, mural thrombosis & systemic embolism
- Depression - suicide
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?
- Bat wing opacities 2. Kerley B lines 3. Cardiomegaly 4. Dilated upper lobe vessels 5. Pleural effusion
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?
- Beck’s triad - JVP, low BP, reduced HS
- Pulsus paradoxus - >12mmHg/9% normal insp decrease in SBP (also caused by const pericarditis, restrictive CMO, severe obs pul disease, PE)
- Kussmaul sign - increased venous pressure/distension on inspiration
- Ewart/Pins sign - if large pericardial effusion, dullness/bronchial breath sounds/bronchophony below angle L scapula
ECG - sinus tachy, low voltage QRS, electrical alternans, PR segment depression
Pericardiocentesis
Mx of stable angina?
- B-Blocker and/or CCB (amlodipine/nifedipine)
- Add/switch to long-acting nitrate/nicorandil (risk of ulceration)
- Ivabradine/Ranolazine
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%):
- Raised JVP
- Muffled heart sounds
- Hypotension
Mx:
- IV fluids (RV filling depends on venous pressure & effusion is constricting)
- Echo –> refer to cardiology for pericardiocentesis
- Coagulation profile (to prep for pericardiocentesis)
Acute limb ischaemia - Def? Presentation? Ix? Mx?
-
Def: a sudden decrease in limb perfusion that threatens the viability of limb
- AF = major RF for acute limb ischemia
-
Presentation - 6Ps:
- Pale
- Pulseless
- Painful
- Perishingly cold
- NOTE: need immediate vascularisation (<6hrs) if:
- Paralysis
- Paraesthesia (esp worrying)
-
Ix (after initial Mx):
- Bedside: ABPI (PAD), ECG (AF)
- Bloods: FBC, U&E, clotting, HbA1c, lipid profile
- Imaging: duplex USS, CT/MR angiography
-
Mx:
- Initial:
- A-E, IV access, analgesia
- IV heparin infusion - reduces the chance of the clot getting worse
- Limb viability:
- Immediate - tender muscles, loss of power, loss of sensation
- Urgent - pale, pulseless, painful, cold
- Irreversible - fixed, mottled skin, woody, hard muscles
- Refer to vascular surgery:
- Thrombotic - local intra-arterial thrombolysis, angioplasty, bypass
- Embolic - embolectomy/local intra-arterial thrombolysis/bypass
- Initial:

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:
-
Intermittent claudication (mild) - cramping leg pain after walking (& have to stop) + relieved by rest
- NOTE: the equivalent of stable angina (worse on exertion)
- Worse going uphill/upstairs
-
Critical limb ischemia (severe) - ulcers, gangrene, night pain & rest pain
- NOTE: the equivalent of unstable angina (present at rest)
Ix:
- Bedside:
- Exam special test = Buerger’s angle - elevation pallor –> sudden drop feet down = sunset sign
- exercise-treadmill ABPI (ankle-brachial pressure index) - <0.8 (<0.3 = CLI)
- Bloods - FBC, U&E, LFTs, CRP, clotting
- Imaging:
- Arterial duplex USS
- CT/MR angiography
Mx: dealt with by vascular surgeons –> optimise meds + surgery (bypass)
- Conservative: smoking cessation
- Medical: ACEi, clopidogrel, statin, DM control
- Surgery: angioplasty/stent/bypass graft/amputation
Chronic venous insufficiency & varicose veins - presentation? Ix? Mx? Complications of varicose veins?
Presentation:
- Oedema, haemosiderin deposition, lipodermatosclerosis (inverted-champagne bottle), eczema, venous ulcers
- Varicose veins - dilated tortuous, superficial veins
- Pain, swelling, itching, restless legs, cramps
- Feel for thrombosis (hard = thrombophlebitis)
- Cough impulse at SFJ (for Saphena Varix - dilation of saphenous vein @junction w/ femoral vein)
-
Trendelenburg test
- Lying flat, lift up leg & empty veins
- Compression over SFJ –> stand up (maintain pressure) - if do not fill = competent valves below SFJ
- If do fill = incompetent valves below SFJ (blood flow from deep to superficial vein via perforating veins)
- Repeat with pressure lower down until filling stops
- Perthe’s test - apply tourniquet to mid-thigh + walk for 5-mins –> compresses superficial vein
- Less distended - normal deep veins as calf compression pushes blood into deep venous system
- Remain distended - impaired deep veins
- Doppler US for reflux
- Warfarin - previous DVT
- Abdo mass with compression
Ix: duplex USS (allow DVT to be ruled out)
Venous insufficiency Mx:
- ABPI > 0.8 –> Compression bandaging
- Varicose veins:
- Conservative - weight loss, avoid standing for prolonged periods
- Minimally invasive procedures - injection sclerotherapy, endovenous radiofrequency ablation
- Surgical - vein ligation
Varicose Veins complications:
- thrombophlebitis - Tx for superficial: NSAIDs
- Eczema
- Bleeding
- Haemosiderin deposition
- Lipodermatosclerosis (champagne bottle)
- Ulceration
AAA key Sx & ruptured Sx? Ix? Mx?
Sx:
- Central abdo pain
- Radiates to back
- Bloating
- Pulsatile mass on palpation (expansile - moves to sides)
- NOTE: always consider if abdo pain + RFs (male, >65yrs, HTN, smoking etc.)
Ruptured AAA Sx:
- Severe pain radiating to back
- Visible pulsating abdo mass
- Shock (circulatory compromise)
Ix:
- Abdo duplex USS if part of national screening - male age 65yrs
- CT angiography if stable but suspicious of rupture
Mx:
-
<5.5cm –> Conservative: monitor w/ USS + RF modification
- <4.5cm –> yearly USS
- 4.5≤x<5.5com –> 3 monthly USS
- Medical: optimise BP control, statin, aspirin
- Sx/>5.5cm/expanding >1cm/yr –> Surgical: endovascular (catheter into aorta to insert stent)/open repair

How to calculate ABPI? ABPI value range?
- BP cuff above ankle with leads upwards – find dorsalis pedis pulse with doppler
- Inflate cuff until signal disappears – let down cuff until signal reappears = ankle pressure
- Repeat procedure in arm using brachial artery signal to record the brachial pressure
- ABPI = ankle pressure/brachial pressure
Range:
- 0.8-1 = normal
- 0.6-0.8 = claudication (may only drop to this with exercise)
- Below 0.6 = critical limb ischaemia
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
- Hx of intermittent claudication
- Haemodynamic instability (high HR, low BP)
- Before left subclavian artery - left arm smaller than right arm
- After left subclavian artery - lower body less developed than upper body
Ix:
- BP in both arms - radio-radial delay
- ECG, CXR (widened mediastinum)
- Gold-standard: CT-aortogram w/ contrast
Mx:
- Stanford A (ascending aorta) - more WORRYING (compromise blood to brain, cause aortic regurg):
- BP control - B-blockers & CCB (aim 100-120mmHg)
- Immediate referral for vascular surgery
- Stanford B (descending aorta)
- BP control - B-blockers & CCB (aim 100-120mmHg)
- Urgent referral to vascular surgery (repair likely if complicated)

Comparing different types of vascular ulcers:
- Hx
- Location
- Characteristics - ulcer & surrounding skin
- Tx
Venous:
- Hx: varicose veins, previous DVT, obesity, preg, recurrent phlebitis
- Location: lower calf-medial malleolus
- Characteristics: mild pain
- Ulcer - shallow/flat margins, exudate, sloughing @base, granulation tissue
- Surrounding skin - haemosiderin staining, eczematous, oedematous, thickening skin, (normal CRT)
- Tx: compression bandaging, leg elevation, surgical Mx
Arterial:
- Hx: HTN, DM, smoking, prev vascular disease
- Location: pressure points, toes/feet, lateral malleolus, tibia
- Characteristics: painful
- Ulcer - punched-out/deep, irreg shape, necrosis, no exudate (unless inf)
- Surrounding skin: thin, shiny, reduced hair, 6Ps (pallor, pain, perishingly cold, pulselessness, paraesthesia, paralysis)
- Tx: revascularization (e.g. bypass), anti-platelet, manage RFs
Neuropathic:
- Hx: DM (peripheral neuropathy), trauma, prolonged pressure
- Location: plantar foot, tip of toe, lateral-fifth metatarsal
- Characteristics: no pain
- Ulcer - deep, surrounded by callus, insensate (no feeling)
- Surrounding skin - dry, cracked, callus, insensate
- Tx: off-loading pressure, topical GF
Pressure:
- Hx: limited mobility
- Location: bony prominence, heel
- Characteristics:
- Ulcer - deep, macerated (moist, wrinkly)
- Surrounding skin - atrophic skin, lost muscle mass
- Tx: off-loading pressure, reduced moisture, increased nutrition

Hypertension BP targets? Ix? Mx?
BP targets:
- <140/90
- <150/95 for over 80yrs
- Causes of hypertensive crisis ≥180/120: pregnancy, scleroderma, vasculitis, renovascular, endo, cocaine –> reduce BP slowly
Ix:
- Bedside - ECG, urine dip
- Bloods - FBC, U&E, lipids, BM, TFTs
Drug treatment:
- Conservative management - diet (low salt), exercise, reduce alcohol
- a) <55yrs/DM –> ACEi (ramipril)/ANG-II receptor antagonist (Losartan)
- b) ≥55yrs/black –> CCB (amlodipine)/thiazide diuretic (bendroflumethiazide)
- ACEi + CCB OR ACEi + thiazide diuretic
- ACEi + CCB + thiazide diuretic
- Add:
* Spironolactone (or other diuretic)
* Alpha-blocker
* Beta-blocker
* Specialist advice
- Add:
DVT - def? RFs? Presentation? Scoring & Ix? Mx?
Def: occlusion of deep vein in lower limb
RFs: SICC - Surgery, Immobility, Cancer, COCP
Presentation: pain, swelling (if extends proximally to iliacs –> bilateral swelling), pitting oedema, warmth, erythema
Scoring & Ix: Well’s score
- 0-1= D-Dimer –sign raised–> as below
- ≥2 = proximal leg vein USS + D-Dimer
- Obtain baseline before starting anti-coag: FBC, U&E, LFTs, clotting screen
Mx:
- Ongoing anticoagulation - DOAC/Warfarin
- Provoked - 3 months (SICC)
- Unprovoked - >6 months + thrombophilia testing
IHD - RFs? Types? Definition? Dx? Mx? Complications?
RFs: HTN, DM, Smoking, FHx IHD, Hypercholesterolaemia
Stable angina - chest pain on exertion relieved by rest
- Path - mismatch in O2 supply and demand to the myocardium
- Ix: CT-angiogram
- Mx:
- B-blocker/CCB (e.g. verapamil) - reduces HR req for activity –> reduced likelihood of mismatch in O2 supply & demand
- GTN spray - reduce myocardial preload + reduces strain
- RF modification –> reduced risk of progression
Acute coronary syndrome - Sx caused by sudden reduced BF to the myocardium
- Dx:
- ST-elevation = STEMI
- Troponin raised = NSTEMI (+ dynamic T-wave inversion, ST depression)
- Unstable angina pectoris (pain at rest) = ischemia NOT infarct
- Generic ACS Mx - MONA BASH
- ALL immediate:
- 5-10mg Morphine IV + Nitrates (GTN spray)
- Dual antiplatelet therapy (DAPT) - 300mg Aspirin STAT + 300mg Clopidogrel STAT (or 180mg PO Ticagrelor)
- ALL long-term:
- Continue DAPT
- 1 year: 75mg OD Aspirin + 75mg OD Clopidogrel (or 90mg BD Ticagrelor)
- >1yr - 75mg OD Aspirin
- B-blocker (1.25-10mg Bisoprolol OD)
- ACEi (1.25-10mg Ramipril OD)
- Statin (80mg Atorvastatin OD)
- Continue DAPT
- ALL immediate:
- STEMI Mx: establish coronary reperfusion ASAP
- Sx under 12hrs for PCI, BUT if no PCI within 2hrs Dx > thrombolysis (e.g. tPA - tissue plasminogen activator)
- Sx >12hrs: invasive coronary angiography ± PCI if needed
- PCI:
- If having PCI give Prasugrel (instead of Clopi/Ticagrelor)
- PCI accessed via radial (or femoral) artery, guidewire passed via X-ray guidance into the affected coronary artery AND IV unfractionated heparin during the procedure –> stent inserted impregnated with an anti-proliferative agent (e.g. Tacrolimus - to prevent adverse tissue reaction) –> takes longer for endothelialization of stent so DAPT needed for 1yr
- If PCI with stents inserted –> DAPT 12 months
- NSTEMI Mx:
- 2.5mg SC Fondaparinux (direct factor 10a inhibitor)
- Risk stratify - GRACE criteria (& others)
- High risk = invasive coronary angiography (within 48-72hrs)
Complications: FAP (failure, arrhythmias, pericarditis)
- Heart failure, arrhythmias (incl. VF)
- Pericarditis
- Early - positional chest pain day after MI –> give NSAIDs
- Late - Dressler’s syndrome - immune response @6wks (fever, pleuritic chest pain, pericarditis/pericardial effusion)

Heart failure def? Causes? Pathophysiology? Categories & Causes? Classification? Ix? Mx?
Def: pumping of blood by heart insufficient to meet the demands of the body
Causes:
- RVF:
- Acute: MI, inf endocarditis, PE
- Chr: Cor pulmonale, LVF
- LVF:
- Acute: ischaemic/hypertensive CMO, valvular HD
- Chr: MI, inf endocarditis
Pathophysiology:
- RHF - right side of the heart pumps deoxygenated blood from the body to the lungs to be reperfused - if the RH is not pumping effectively you get the fluid collection in the peripheries = PERIPHERAL OEDEMA
- LHF - left side of the heart pumps oxygenated blood from the lungs to the body - if the LH is not pumping effectively you pooling of blood in the lungs = PULMONARY OEDEMA
- Reduced CO –> shock, tachycardia, AKI
- CO = SV*HR
- Ejection fraction = SV/End-diastolic Volume
Categories:
- HF w/ preserved ejection fraction (left ventricular >50%) = inadequate filling of ventricles during diastole (from ventricular stiffness)
- Causes of ventricular stiffness:
- Volume overload (valve regurg)
- Pressure overload (HTN)
- Decreased distensibility (constrictive pericarditis)
- Causes of ventricular stiffness:
- HF w/ reduced ejection fraction (left ventricular <40%) = inadequate emptying of ventricles during systoles (from outflow obstruction/impaired contractility)
- Causes of outflow obstruction/impaired contractility:
- MI, Cardiomyopathy, Arrythmia
- Causes of outflow obstruction/impaired contractility:
NYHA classification:
- 1 - no limitation on activity
- 2 - comfortable at rest but dyspnoea on ordinary activity
- 3 - marked limitation on ordinary activity
- 4 - dyspnoea at rest
Ix:
- Bedside: ECG - detects if anything precipitating HF (arrhythmia/ischaemic event)
- Bloods: ABG (if resp compromise from pul oedema), troponin (ACS), BNP (HF screening)
- Imaging: CXR (visualise pul oedema, cardiomegaly), ECHO (valvular abn/regional wall mov abn)
Mx: MON BA (out of MONA BASH)
- Immediate:
- Sit the patient up (reduce venous return to heart –> less strain)
- O2 15L/min NRM
- Medical:
- IV furosemide (loop diuretic) - remove excess fluid + venous dilation (reduce preload)
- Nitrates (GTN/Isosobide Mononitrate) AND Morphine - reduce preload on the heart
- Long-term:
- Reduced ejection fraction - prognostic benefit:
- B-blocker (bisoprolol) - reduce strain on heart, do not give acutely if severe HF as will kill them
-
ACEi - reduce strain on heart
- After the above if LVEF <35% & Sx –> mineralocorticoid antagonist e.g. spironolactone
- 3rd line - by specialist: Sacubitril/Valsartan (entresto), Ivabradine & CRT
- SGLT2 inhibitors (dapagliflozin)
- RF modification - poor glycaemic control/high cholesterol
- Sx (diuretics)
- Reduced ejection fraction - prognostic benefit:
Complications:
- Reduced CO (SV*HR) –> shock, tachycardia, AKI
- Congestion –> pulmonary oedema + peripheral oedema

Atrial fibrillation (AF)
- Def? Causes? Ix? Mx?
Def: rapid, chaotic, and ineffective atrial electrical conduction
- ECG def: irregularly irregular narrow complex tachycardia with no p waves
Causes: idiopathic, cardio (IHD, valvular disease, cardiomyopathy), resp (PE, pneumonia), hyperthyroidism, alcohol
Ix: ECG (absence of p-waves, irregularly irreg rhythm)
Mx:
- Haemodynamically unstable (≤90 BP, chest pain, acute HF) –> DC Cardioversion
OR
- Rate control –> B-blocker (bisoprolol) OR rate-limiting CCB (verapamil - asthma)
OR
- Rhythm control - ONLY if clear reversible cause
- Sx onset <48hrs –> DC/chemical cardioversion (amiodarone/flecanide)
- NOTE: IV heparin started prior to cardioversion
- Sx onset >48hrs –> anticoagulate for 3wks –> elective cardioversion (also anticoag for 4wks after)
- Sx onset <48hrs –> DC/chemical cardioversion (amiodarone/flecanide)
AND
- Stroke risk - CHADS-Vasc Vs Orbit/HAS-BLED score –> DOAC (Apixaban)
- If metallic heart valve –> warfarin INR 3-3.5
- Otherwise DOAC
- NOTE: if incidental non-symptomatic AF - normal rate, no other RFs, CHA2DS2-VASc 0 –> anticoagulation not recommended
-
CHF, HTN, Age ≥75rs (2), DM, Stroke (2), Vascular disease, Age 65-74, Sex - female
- Score 1 - consider; ≥2 - DOAC/Warfarin needed
- Lifetime risk = annual risk x estimated years of life left (up to 80 yrs e.g. if 60 then x annual risk by 20)
SVT - Def? Types? Presentation - case example? Mx?

Def: regular narrow-complex tachycardia with no p-waves + supraventricular origin
Junctional types:
- AVNRT - local re-entry circuit within AV node
- AVRT - re-entry circuit between atria and ventricles –> after SVT termination = delta wave = WPW syndrome:
- Assoc w/ HOCM
- Avoid digoxin, verapamil, amiodarone (reduce conduction down SAN –> worsen retrograde conduction –> risk of VT)
- Can use B-blocker/flecainide instead
Case example: 23yrs, 1-hr palpitations + SoB, 2 similar episodes prev following alcohol, this time severe chest pain
Mx:
- Unstable tachycardia (<90 BP/chest pain/acute heart failure) –> synchronised DC Cardioversion
-
Vagal manoeuvres (increase parasympathetic stim via vagus nerve to slow conduction via AV node)
- Valsalva manoeuvre (blow out through nose while pinching + shut mouth) - breath through 50ml syringe
-
Adenosine 6mg –> 12 mg –> 12mg
- NOTE: if adenosine CI (e.g. asthma) –> VERAPAMIL (rate-limiting CCB)
- Other:
- IV B-blocker/amiodarone/digoxin
- Synchronised DC Cardioversion

Key heart murmurs?
Accentuation manoeuvres?
Causes?
Left vs right heart valve abn epidemiology?
Mx?
Complications of prosthetic heart valves?
Key murmurs:
-
AS = ejection systolic + radiates to carotids, slow rising pulse, narrow pulse pressure, heaving apex beat
- Sound: Wooooshhh
- Severe AS - absent/soft 2nd heart sound, reversed splitting of 2nd HS, heaving apex beat
- A longer murmur is worse (small space for blood to pass through = takes longer)
-
MS = mid-diastolic + LLP, malar flush, AF, loud/palpable S1 “tapping” apex, pul HTN (loud P2 - pul thrill)
- Sound: Wooosh de (loud S1) de (early diastolic snap)
-
AR = early diastolic + sitting forward (LLSE), collapsing pulse, wide pulse pressure, displaced apex
- Sound: de woooshhhh
- Severe AR –> Austin-flint murmur = ‘Rumbling mid-diastolic murmur’
- Best heard at apex, caused by blood flowing back through aortic valve and over mitral valve
- Shorter murmur is worse (quicker to flow back through large hole)
-
MR = pan-_systolic_ + radiates to left axilla, AF, displaced thrusting apex, LVF/pul HTN
- Sound: Woooooshhh (holosystolic)
- NOTE: same pattern for pulmonary & tricuspid (pul stenosis & tricuspid regurgitation = systolic)
- TR - pulsatile liver
- PS - radiates to back, assoc w/ Noonan’s (AD, webbed neck, wide-spaced eyes etc.)
Accentuation manoeuvres:
- R-sided murmurs (tricuspid + pulmonary) –> louder on INspiration = blood goes IN to right-side of heart
- L-sided murmurs (aortic + mitral) –> louder on EXpiration = blood EXits left-side of heart
- AS radiates to the carotids + louder on leaning forward + listen on right sternal edge
- MS louder on turning to the left, MR radiates to axilla
Causes:
- AS (stenosis/sclerosis): senile calcification (aortic valve)
-
MR:
- Acute: - IHD (papillary-muscle dysfunction post-MI), Infective endocarditis, cardiomyopathy, RHD
- Chronic - myxomatous degeration
-
AR:
- Acute (infective endocarditis, aortic dissection)
- Chronic (CTD, RHD, HTN, congenital)
- MS: rheumatic heart disease (RHD)
Left vs Right valve abn:
- Left = more common as higher pressure system, more likely in damaged valves, commonly Strep Viridans
- Right = more common in IV drug users –> tricuspid valve is first valve reached, commonly S. aureus
Management:
- AS:
- C: 6-monthly ECHO, exercise-stress test if asymptomatic
- M: RF optimisation (statins, HTN, DM), HF Sx (diuretics, ACEi)
- S: Based on severity/comorbid - STS-PROM (surgical risk calc)
- If severe AS:
- Medically fit (req midline sternotomy & cardiopul bypass) = Surgical aortic valve replacement (SAVR)
- Not fit = Transcatheter aortic valve replacement (TAVR)
- Acutely Sx/cardiogenic shock = Balloon valvuloplasty
- If severe AS:
- MR:
- M:
- ACEi ± B-blockers (as HTN worsens MR)
- Tx AF & anti-coagulate
- Diuretic (if refractory to surgery)
- S: for acute MR (post-MI, chordae tendinae rupture), asymptomatic LVEF <60%, symptomatic LVEF >30%
- Valve _R_epair > _R_eplacement
- M:
- AR:
- M: asym + Reassurance (good prog)
- Unfit for surgery/waiting - ACEi & vasodilators (e.g. hydralazine)
- S: acute/Sx/severe = surgery
- Valve _R_eplacement > _R_epair
- M: asym + Reassurance (good prog)
-
MS:
- C: asymptomatic - Monitor
- M:
- AF Tx, anti-coagulate & diuretics (if Sx/severe)
- S: Sx/severe - can do balloon valvuloplasty/replacement
- Valvuloplasty = lateral thoracotomy scar
- Do not do percutaneously if persistent left atrial thrombus/rigid calcified valve –> need open heart surgery (CABG, concurrent severe MS)
Complications of prosthetic heart valves: FIBAT
- Failure
- Infection
- Bleeding - MAHA
- Anaemia
- Thromboembolic phenomena

Infective endocarditis - RFs? Ix? Dx criteria? Mx?
Acute vs subacute bacterial endocarditis - what hearts affected? who are commonly affected? What bacteria most likely?
Def: infection of heart valves (typically mitral/aortic or tricuspid in IVDU)
RFs: bacteraemia (long-term lines, IVDU, dental work), abn valves (prosthetic, RHD), prev endocarditis, VSD, piercings
Presentation: low-grade fevers, night sweats
- Exam:
- Splenomegaly
- Splinter haemorrhages, osler’s nodes, Janeway lesions, petechiae, Roth spots (eyes)
- Chronic = clubbing (rare, mostly acute now)
Ix:
- Urine dip - haematuria
- Serial BCs (x3 but start empirical abx), ESR
- Transoesophageal Echo (TOE - vegetations)
Dx: DUKE’S CRITERIA (2 major OR 1 major + 3 minor OR 5 minor):
- Major: +ve BC (typical organism), new regurg murmur/veg on echo
- Minor: RF, fever (>38), embolic (vascular) phenomena, immune phenomena, +ve BC (another organism)
- Mx: IV abx for 6wks – fluclox/vanc/gent
Acute in structurally normal heart – In IV drug user the first valve met is tricuspid valve, commonly S. aureus (also most common cause in prosthetic valve endocarditis)
Subacute in structurally abn heart – mitral & aortic valves more commonly affected as high pressure system, more likely damaged valves, commonly Strep Viridans (overall most common cause of endocarditis)
3rd & 4th heart sounds - sounds & cause?
3rd = rapid ventricular filling = volume overload e.g. HF (reduced EF/systolic)
- KEN…TU.CKY (deee. de.de)
4th = atrial contraction against stiff ventricles = pressure overload e.g. longstanding AS & other causes of left ventricular hypertrophy (HTN heart disease, HOCM, HF with preserved EF/diastolic)
- TE.NE..SSEE (de.de.deee)
2 days of chest pain following 4 days of generalised muscle aches
- Worse on inspiration & lying flat
- Low-grade fever
- Exam: pericardial rub
Causes? Dx? Ix? Mx?
Pericarditis
Causes:
- Viral (most common)
- MI (can be Dressler’s syndrome)
- TB (constrictive)
- Uraemia (CKD where urea high –> pericarditis) = indication for haemodialysis (HUMP)
- Hydralazine (AI pericarditis)
- NOTE: also causes drug-induced lupus
- SLE, RF, radiation
Presentation:
- Pleuritic chest pain, worse lying flat
- Exam: pericardial rub - “creaking/scratching”
- Tip - put on all-fours, put stethoscope on sternal edge, hold inspiration
Ix:
- ECG: ST elevation widespread
- Only slightly raised/normal troponin
Mx: colchicine (3 months) + NSAIDs (ibuprofen, max 2wks)
Causes of raised JVP (>4cm)?
JVP + hepatojugular pressure (RUQ), rockstar hand
PQRST:
- Pul HTN/PE/Pericarditis/Pericardial effusion/PS
- Quantity of fluid (fluid overloaded)
- RHF
- SVC obstruction
- Tamponade/TR
SVC obstruction - presentation? Tx?
Presentation: swollen face and neck and distended veins on her chest in background of cancer
Mx: dexamethasone to reduce tumour swelling
- Insert EV stent if stridor (after intubation and steroids)
Bradycardia arrhythmia with a palpable pulse (peri-arrest) - Mx?
Innitial: A-E
- If unstable - 500mcg IV atropine (/5mins up to 3mg)
- Also considered unstable if:
- Recent asystole >3s/Mobitz T2 AV block/3rd degree heart block
- Caution in acute MI, C/I if heart transplant
- Also considered unstable if:
- If persistent –> transcutaneous pacing + analgesia/sedation (very painful)
- If can’t be achieved properly –> IV isoprenaline/adrenaline (specialist help)
- Arrange transvenous pacing (temporary if recent asystole >3s/Mobitz T2 AV block/3rd degree heart block)
Heart block causes? types? Ix? Mx? Complications?
Causes:
- MI/IHD (MOST COMMON)
- Inf (RHD, IE)
- Drugs (digoxin)
- Metabolic (hyperkalaemia)
- Infiltration of conducting system (e.g. sarcoidosis)
- Degeneration of conducting system
Types:
- First Degree AV block - fixed prolonged PR interval (> 0.2 s) - ASYMPTOMATIC
- Second degree AV block:
- Mobitz TI (Wenckebach) - progressively prolonged PR interval –> P-wave NOT followed by a QRS complex = ‘going, going, gone’
- Normally asymptomatic
- Mobitz Type II - intermittently P wave NOT followed by a QRS
- May be regular pattern of P waves not followed by QRS (e.g. 2:1 or 3:1)
- Can cause:
- Stokes-Adams Attacks (syncope caused by ventricular asystole)
- Dizziness, palps, chest pain, HF
- Mobitz TI (Wenckebach) - progressively prolonged PR interval –> P-wave NOT followed by a QRS complex = ‘going, going, gone’
- Complete AV heart block - no relationship between P waves and QRS complexes
- Presentation as in Mobitz T2
Ix: ECG
- Bloods: TFTs, Digoxin, cardiac enzymes (troponin, CK, BNP)
- CXR (cardiac enlargement, pulmonary oedema)
- Echo (wall motion abn, aortic valve disease, vegitations)
Mx:
- Acute block - if clinical deterioration:
- IV atropine
- Consider temporary transcutaneous pacing
- Chronic block:
- 1st degree monitored
- Permanent pacemaker in:
- Symptomatic Mobitz T1
- Advanced Mobitz T2
- Complete heart block
Complications: asystole, cardiac arrest, HF, surgical complications of pacemaker insertion
Types of pacemaker? When to use each type? Complications?
Types:
- Implantable Cardioverter Defibrillator (ICD, has a thicker end)
- Single-chamber pacemaker (right ventricle)
- Used in permanent AF (no organised atrial contraction so atrial lead not required to sense contraction)
- Rarely can have atrial lead only - if SA disease in young with good AV conduction
- Dual-chamber pacemaker (right atrium & ventricle)
- Can have ICD dual-chamber pacemaker
- Used in paroxysmal AF/all other scenarios (there is sometimes organised atrial contraction - this is sensed by the atrial lead)
- Cardiac Resynchronisation Therapy/Biventricular pacemaker (right ventricle, left ventricle ± right atrial lead)
- Can have ICD biventricular pacemaker
When to use each type:
- Atrial lead only → Sino-atrial disease in young people with good AV node conduction
- RV lead only → Pacing whilst in permanent atrial fibrillation
- Dual-lead → All other scenarios (paroxysmal AF, bradycardia)
- CRT → LV dysfunction + broad QRS –> end-stage HF
- Indications for ICD:
- Primary prevention = @risk of serious ventricular arrhythmia
- Familial cardiac conditions (hypertrophic cardiomyopathy, long QT)
- Previous surgical repair of congenital HD
- Previous MI + LVEF <35% + HF Sx
- Secondary prevention = had previous serious ventricular arrhythmia wo/ treatable cause
- Cardiac arrest from VT/VT
- Spontaneous sustained VT AND:
- Syncope/haemodynamic compromise OR
- LVEF <35% + sign HF Sx (NYHA 3+)
- NOTE: VT/VF from STEMI has treatable cause (open occluded vessel)
- Primary prevention = @risk of serious ventricular arrhythmia
Complications:
- Surgical complications - infection, bleeding, damage to underlying structures
- Displacement (of lead)
- Pacemaker syndrome (if ventricular lead with no atrial) –> AV node conducts in retrograde direction = mitral/tricuspid regurge + HF Sx
Different pulse forms? Causes?
Pulsus paradoxus - greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or absent pulse in inspiration
- severe asthma, cardiac tamponade
Slow-rising/plateau
- AS
Collapsing
- AR, PDA
- hyperkinetic states (anaemia, thyrotoxic, fever, exercise/pregnancy)
Pulsus alternans - regular alternation of the force of the arterial pulse
- severe LVF
Bisferiens pulse - ‘double pulse’ - two systolic peaks
- Mixed aortic valve disease
- HOCM (also causes ‘Jerky’ pulse)
Ventricular tachycardia - Dx? Presentation? Ix - appearance on ECG? Mx?
VT or SVT w/ aberrancy
- SVT >200bpm, also often irregular
- VT more likely if LAD
- Acutely treat any broad complex tachy as VT until proven otherwise
Presentation: palpitations, light-headed, chest pain, syncope, seizure
- Tachycardia, LVF
- ACS most common cause
- NEVER IGNORE palpitations & light-headedness
Ix: ECG - regular broad complex tachycardia
- U&E (Mg, Ca, K), TFTs, Troponins
Mx:
- Unstable tachycardia (BP <90, chest pain, acute cardiac failure) = DC cardioversion
- Stable:
- IV amiodarone, b-blocker –> prepare for DC cardioversion

Cardiac tamponade - key finding on exam? Triad? Mx?
Pulsus paradoxus - BP variation between inspiration & expiration (≥10)
Beck’s triad (50%):
- Raised JVP
- Muffled heart sounds
- Hypotension
Mx:
- IV fluids (RV filling depends on venous pressure & effusion is constricting)
- Echo –> refer to cardiology for pericardiocentesis
- Coagulation profile (to prep for pericardiocentesis)