Clinical cardiology + vascular Flashcards

Question

Infective endocarditis - causes

Answer 1

Native valve - Staph. aureus - viridans Strep. - post-dental - Enterococcal (HACEK, Strep. bovis) Prosthetic valve - Staph. epidermidis - Staph. aureus - viridans Strep. (Pseudomonas, HACEK, fungal)

Answer 2

Major - Positive blood cultures - at least 2 taken more than 12hr apart - Imaging evidence on TOE Minor - Predisposing condition - Fevers > 38 - Embolic phenomena e.g. Janeway lesions, septic emboli - Immunological phenomena e.g. Osler's nodes, Roth spots - Microbiological findings Definitive diagnosis requires: 2 major 1 major + 3 minor 5 minor

Answer 3

Native valve: - Min 2-6 weeks of therapy e.g. vancomycin + gentamicin Prosthetic valve: - May require lifelong suppressive therapy e.g. vancomycin + gentamicin + rifampicin Surgery - High mortality and morbidity - May be required if there is acute severe valve dysfunction or aortic root abscess

Answer 4

Neurogenic - T2DM - Parkinson's - SCLC - MGUS Cardiac - Arrhythmias - Aortic stenosis Endocrine - Dehydration - Adrenal insufficiency Medications: - Diuretics - esp. thiazides - Alpha-blockers - Antihypertensives - Insulin - Levodopa

Answer 5

Diagnosis: - SBP drop by 20 mmHg - SBP drop to <90 mmHg - DBP drop by 10 mmHg with symptoms Management: - Fludrocortisone - MRA - Midodrine - alpha-1 agonist

Answer 6

A form of juxta-cardiac AAA which can cause aortic regurgitation and can acutely dissect Aetiology: - Age-related - CTDs e.g. Marfans, vasculitis - HTN

Answer 7

Quiet = low CO - Reduced LV function - Rheumatic MR - Long PR interval (1st degree HB) Loud = high CO - Large stroke volume - Mitral stenosis - Short PR interval

Answer 8

Physiological splitting - AV closes slightly before PV because left contracts before right - Increases with inspiration, decreases with expiration Wide splitting - Delayed RV emptying e.g. RBBB, pulmonary HTN Reverse splitting - Delayed LV emptying e.g. LBBB, LV outflow obstruction Quiet S2 - Aortic stenosis Loud S2 - Systemic or pulmonary HTN

Answer 9

Occurs just after S2 'Lub-dub-ta' Normal if pregnant, febrile, <30 y.o. Otherwise HF, MR. When combined with tachycardia is called a gallop rhythm

Answer 10

The sound of blood being forced into a stiff non-compliant ventricle Just before S1

Answer 11

Rate - R waves x 6 - 300 / no. large squares in R-R interval Rhythm Axis - aVF and I - normal = both positive - left = I +ve, aVF -ve - right = I -ve, aVF +ve Morphology - QRS < 120ms aka 3 small - PR 120-220ms aka 3-5 small - QT < 450ms

Answer 12

aka 1st degree heart block PR > 5 sq or 200ms AVN fibrosis Medication e.g. digoxin, amiodarone, CCBs Hypo or hyperkalaemia

Answer 13

LBBB - Always pathological e.g. posterior STEMI - WiLLiaM - May have TWI in lateral leads RBBB - May be benign - MaRRoW Bifascicular block - RBBB + axis deviation (usually LAD) - LAD = L anterior fascicle - RAD = L posterior fascicle ((((Trifascicular block - RBBB + axis deviation + 1st degree heart block - OLD, TRUE WOULD BE COMPLETE HEART BLOCK))))

Answer 14

Usually occurs alongside inferior ± lateral infarction Obstruction of LCX is most common ST depression V1-V4 Dominant R in V1-V2 ST elevation in V7-V9 New LBBB

Answer 15

Poorest prognosis Obstruction of LAD ST elevation V1-V4 ST depression II, aVF Preceding hyperacute T waves

Answer 16

Obstruction of RCA (80%) or LCX (20%) depending on dominance ST elevation II, III, aVF ST depression aVL Preceding hyperacute T waves Later develop deep Q waves Supplies nodal arteries so risk of new significant heart block

Answer 17

Usually occurs in conjunction with anterior infarction due to involvement of the main LAD Obstruction of small branches of LAD or LCX ST elevation V5-V6, I, aVL ST depression II, aVF

Answer 18

Defined as ECG patterns which do not fully meet the criteria for STEMI but nevertheless suggest coronary occlusion requiring urgent PCI - Elevation in 2 contiguous inferior leads + depression in aVL - New RBBB + LAFB - T waves out of proportion to R waves - ST depression maximal in V1-V4 with progression to V5-V6 - Multilead ST depression + ST elevation in aVR

Answer 19

A rare cause of MI most commonly presenting in young healthy women Causes: - Connective tissue disorders - Hormonal changes associated with pregnancy - No association with atherosclerosis or trauma Presentation very similar to NSTEMI/STEMI - Chest pain - Elevated troponin - ST changes Coronary angiogram is key for investigation and treatment

Answer 20

Normal: - Mostly upright - Possible TWI in aVR and V1 - Amplitude <5mm in limb, <10mm in precordial Peaked - Tall, narrow, symmetrical peaked Hyperacute - Broad - Asymmetrically peaked

Answer 21

Can be normal to have TWI in I and aVR. More widespread TWI is normal in childhood due to right-sided predominance Other causes: - BBB - left = I/aVL/V5-6, right = V1-V3 - Hypertrophy - HTN - Heart strain/PE - Ischaemia/infarction - dynamic during, fixed afterwards - HOCM

Answer 22

In which the T wave has two phases, one going up and the other down - MI = up - down - Hypokalaemia = down - up

Answer 23

A pattern of inverted or biphasic T waves in V2-3 which, when accompanied with chest pain, is high suggestive of critical stenosis of the LAD Type 1 (25%) - Biphasic T wave - up then down Type 2 (75%) - Deep, symmetrical TWI

Answer 24

Presence of an accessory conducting pathway (the Bundle of Kent) which allows some electricity to bypass the AVN - Short PR interval - Delta wave Causes two types of SVT - Orthodromic - Narrow QRS - Treat as SVT - Antidromic - Delta wave + broad QRS - Treat with procainamide, cardioversion. Management: - Medical - e.g. flecainide, sotalol, amiodarone - Pathway ablation - If symptomatic, FHx of sudden death, or high- risk professions

Answer 25

An increased awareness of the heartbeat - usually because it is strong, fast, or irregular Causes - Substances - caffeine, alcohol, tobacco, salbutamol - Ectopic beats - Narrow complex tachycardia - Panic attack - Thyrotoxicosis High-risk features: - Previous MI - Previous cardiac surgery - Associated syncope or cardiac chest pain - FHx of sudden death

Answer 26

Ventricular ectopics which are significant because they can lead to VT/VF by setting up circuits - Associated with sudden cardiac death post-MI - More = worse prognosis - In healthy patients can be substance-induced (e.g. caffeine), thyrotoxicosis, iatrogenic (e.g. digoxin) Treatment: - Correct electrolytes - K+ > 4.0, Mg > 1.0 - Improve respiratory state - Avoid triggers

Answer 27

Class I - Block fast sodium channels which cause phase 0 (aka rapid depolarisation) - Slows upstroke, no effect on duration/refractoriness - IA and IC bind both activated and inactivated states so are useful during tachyarrhythmia - IB bind during the inactivated state and are most useful when there is myocardial ischaemia - IA = procainamide, IB = lidocaine, IC = flecainide. Class II - Beta-blockers - esp. action at beta-1-adrenoceptors - Beta-1 = increased SAN firing, increased conduction velocity - e.g. atenolol, bisoprolol etc. Class III - Mechanism variable but lead to prolongation of the cardiac action potential, mainly by inhibition of repolarizing K+ currents and increasing QTc - Esp. potent in suppressing arrhythmias caused by reentrant signs - e.g. amiodarone, sotalol Class IV - Calcium channel blockers - Suppress ectopic pacemaker action, decrease conduction velocity, prolong repolarisation at the AVN - e.g. diltiazem, verapamil Class V - Increase vagal tone at SAN/AVN - e.g. digoxin

Answer 28

Technique: - Implanted in subclavian region on opposite side to dominant hand - Done under local anaesthetic - Up to three leads - right atrial, right ventricular, left ventricular Complications: - Site infection - Pneumothorax - if leads placed via subclavian vein

Answer 29

Right atrial + right ventricular leads - On-demand pacing Lead selection: - Atrial fibrillation = RV only - Paroxysmal AF = RA + RV - Young sick sinus = RA only. Older = RA + RV Pacing cycle: - Intrinsic P wave sensed in RA = A SENSED - If no ventricular contraction in a given time, ventricle is paced = V PACED - After this there is no atrial activity so the atria are paced = A PACED - If ventricular activity is sensed, the RV leads are inhibited = V SENSED

Answer 30

Indications - Primary prevention - high risk of severe ventricular arrhythmia - Inherited e.g. HOCM, Brugada, long QT - Prev. surgical repair of congenital heart disease - Previous MI with LVEF < 35% and symptomatic heart failure - Secondary prevention - known severe ventricular arrhythmia without treatable cause - Spontaneous sustained VT with syncope or instability - Spontaneous sustained VT with LVEF < 35% and NHYA III symptoms or better Technique: - Similar implantation to PPM - Ventricular leads contain additional defibrillation coil

Answer 31

Aetiology: - Autosomal dominant channelopathy - 25% have FHx - Usually mutation of SCN5 which encodes cardiac voltage-gated sodium channels Presentation: - Asymptomatic - Syncope - VT/VF - Sudden death ECG when in arrhythmia: - Type 1 - coved ST elevation >2mm in more than one of V1-V3, followed by TWI. - Type 2 - Saddle ST elevation >2mm V1-V3 - Type 3 - Either of the above but ST elevation < 2mm Increased risk of arrhythmia with alcohol, fever, periods of high vagal tone like sleep, rest, or after a meal Definitive management = ICD

Answer 32

LVH with giant QRS in lateral leads and deep dagger Q waves ± arrythymias e.g. AF, SVT, VT, VF

Answer 33

Mnemonic - MR SAM ASH Mitral regurgitation (MR) Systolic anterior motion (SAM) of the anterior mitral valve leaflet Asymmetric hypertrophy (ASH) Evidence of LVOTO - left ventricular outflow tract obstruction - Septal hypertrophy + narrowing of LVOT causes abberrant blood flow which displaces mitral valve leaflets anteriorly. - Mitral valve also anatomically more susceptible to this displacement - Loss of leaflet coaptation -> LVOTO, MR LVOTO may need to be elicited e.g. Valsalva, exercise, strain.

Answer 34

Aetiology: - Unexplained LVH - 1/500 people - Often FHx but not always - 40% due to mutations in beta-myosin heavy chain Signs: - Either ESM (due to LVOTO) or pansystolic (MR) Investigations: - Ambulatory ECG - ECHO - gold-standard - cMRI if echo suboptimal - add late gadolinium enhancement (LGE) to detect secondary myocardial fibrosis - Genetic testing Management: - General: - Mild-to-moderate exercise - Pregnancy safe if condition is stable - Lifestyle changes - Obstructive symptoms: - 1st line - beta-blockers - 2nd line - add diltiazem - 3rd line - surgical e.g. septal ablation, myomectomy - ICD - Known to have had ventricular arrhythmias - FHx of sudden death - Episodes of syncope - Massive LVH - LVEF < 50% - Children with runs of SVT - End-stage: - Consider heart transplant if having ventricular arrhythmias or NYHA III+ symptoms - LVAD if unavailable - CRT if develop LBBB

Answer 35

First detected episode Paroxysmal AF - At least 2 recurrent self-terminating episodes lasting < 7 days Persistent AF - AF which is not self-terminating and has persisted for > 7 days Permanent AF - AF which cannot be cardioverted

Answer 36

Investigations: - Ambulatory ECG - TTE - AF + valve pathology is absolute indication for anticoagulation Rhythm control - If first episode, co-existent HF, reversible cause - Electrical cardioversion - synchronised - Must either have been in AF for < 48h, anticoagulated for 21-28 days, or no evidence of clot on TOE - Will need to stay on anticoagulation for at least 28 days afterwards - Chemical cardioversion - Flecainide - no structural disease, pill in pocket if well with AF and no CKD (dose = 200mg) - Amiodarone - if IP, more unwell, structural disease (- AF ablation) Rate control - Beta-blocker e.g. bisoprolol - Rate-limited CCB e.g. diltiazem, verapamil - Combination therapy - 2/3rds dose of BB + CCB/digoxin - Digoxin used mainly if limited exercise and unable to tolerate other medications

Answer 37

Digoxin effect - normal when taking digoxin - 'Reverse tick' - downsloping ST depression - Flattened, inverted, or biphasic T waves - Short QT Digoxin toxicity - Frequent PVCs e.g. bigeminy, trigeminy - Sinus bradycardia - Slow AF - AV block - VT

Answer 38

Precipitants: - Overdose - Renal failure - Concurrent infection - Hypokalaemia Features: - GI - nausea/vomiting, anorexia, diarrhoea - Visual - blurred vision, yellow/green, haloes - CVS - palpitations, pre-/syncope, SOB - CNS - confusion, fatigue, delirium ECG - can be a number of arrhythmias - Frequent PVCs e.g. bigeminy, trigeminy - Sinus bradycardia - Slow AF - AV block - VT Diagnosis = digoxin levels Management = Digibind, correct electrolytes

Answer 39

Unstable features? e.g. syncope, hypotension, MI, heart failure, shock - DCCV Narrow complex regular - Likely AVNRT or AVRT e.g. SVT - 1st line - vagal manoeuvres - 2nd line - IV adenosine 6mg - 12mg - 18mg or verapamil if asthmatic - 3rd line - cardioversion Narrow complex irregular - Most likely fast AF Broad complex regular - Likely VT unless known BBB - Loading amiodarone (300mg IV over 30 mins) then maintenance infusion (900mg over 24h) - oral loading (10-15g total needed to load, 200mg TDS for 7 days then BD for 7 then OD as long as needed) - NB avoid amiodarone if known long QT Broad complex irregular - Seek expert advice - Most commonly AF + BBB but possibility of torsades de pointes - Do not give amiodarone until confirmed

Answer 40

Monomorphic - Uniform complexes - Originates from a single complex in the ventricles Polymorphic - Complexes of variable amplitude - Sign of more unstable electrical activity

Answer 41

Salvo - 3-5 beats Non-sustained - VT lasting more than 6 beats but less than 30s Sustained - VT lasting >30s or with haemodynamic instability

Answer 42

aka fast AF Triggers - PIRATES Pulmonary embolism Ischaemia Respiratory disease Atrial enlargement or myxoma Thyrotoxicosis Ethanol Sepsis/sleep apnea Unstable - cardioversion Stable - Optimise electrolytes - K+ > 4.0, Mg = 1.0 - Rate control - Beta-blockers - Digoxin loading - Oral - 500mcg, then after 6hr 500mcg, maintenance at 125mcg - IV - 500-1000mcg split over 2 doses and 6hr - Rhythm control - Consider anticoagulation

Answer 43

Alternating bradycardia and paroxysmal tachycardia - Usually supraventricular - After tachy may have delayed sinus recovery causing a sinus pause or exit block - If prolonged can cause syncope Causes - Idiopathic fibrosis (most common, sick sinus syndrome) - Ischaemia - Infiltration - Cardiomyopathy - Congenital - Autonomic dysfunction - Hypothyroidism - Hyperkalaemia - Medications e.g. digoxin, BB, CCBs Management - Treat reversible causes - PPM insertion

Answer 44

Most commonly due to age-related fibrosis but can be secondary to many cardiac conditions e.g. ischaemia, infiltration, SLE, lyme disease Types: - 1st degree - PR > 200ms - 2nd degree - Type I - Progressive PR lengthening until dropped complex - Usually due to reversible conduction block at the level of the AV node - increased fatiguability - Type II - Intermittent dropped beats - Due to failure of the Purkinje fibres, often irreversible damage - 3rd degree/complete - Dissociation between P and QRS Management: - Unstable - Atropine 500mcg IV - up to 3mg total - Transcutaneous pacing - Aim for transvenous pacing + PPM insertion as soon as possible - Stable - 1st degree/2nd degree type 1 - nothing if asymptomatic, else atropine - 2nd degree type 2 + complete - Monitoring, temporary pacing, aim for PPM

Answer 45

C - Congestive heart failure (1) H - Hypertension (or treated hypertension) (1) A2 - Age >= 75 years (2) - Age 65-74 years (1) D - Diabetes (1) S2 - Prior Stroke, TIA or thromboembolism (2) VA -Vascular disease (including ischaemic heart disease and peripheral arterial disease), (1) S - Sex (female) (1)

Answer 46

Replacement for HAS-BLED - Haemoglobin (males < 130, female < 120) or haematocrit (males < 4-0%, female < 36%) = (2) - Age > 74 = (1) - Bleeding hx (GI, intracranial, stroke) = (2) - Renal impairment (eGFR < 60) = (1) - Treatment with antiplatelets = (1) Low risk - 0-2 Medium risk - 3 High risk - 4-7

Answer 47

Cardiovascular - ACS and angina - Myo/pericarditis - Aortic dissection Respiratory - Pneumothorax - Pulmonary embolism - Pneumonia Gastrointestinal - Oesophageal spasm - GORD - Peptic ulcer - Pancreatitis Other - MSK - Radiculopathy - Anxiety - Shingles

Answer 48

Myocarditis is an inflammatory cardiac disorder which can lead to acute heart failure - Fulminant = hours-to-days - Non-fulminant = days-to-weeks Causes: - Viral - coxsackie B, adenoviruses - Eosinophilic - Chagas, parasites hypersensitivity - Granulomatous - TB, sarcoid - Drug-induced - vaccines, chemo, ETOH Features: - Sharp stabbing chest pain - Fever - New heart failure - SOB, orthopnea, dizziness - Palpitations - Recent infectious prodrome - coryza, diarrhoea Investigations: - Bloods incl. viral serology, serial trops - Imaging e.g. cMRI - Myocardial biopsy is gold-standard Management: - Symptomatic relief from acute heart failure - Colchicine for pain, up to 2-3 months after resolution

Answer 49

QTc = An estimate of QT at a standardised heart rate of 60bpm Long if : Men > 440ms Women > 460ms Aetiology: - Hypokalaemia - Hypomagnesaemia - Hypocalacaemia - Hypothermia - Raised ICP - Medications - Ischaemia - Congenital

Answer 50

Beat-to-beat variation in T wave amplitude or polarity Associated with long QT Often secondary to ischaemia, increases risk of re-entrant arrhythmias

Answer 51

Classification: - Type A - 2/3 - ascending aorta - Type B - 1/3 - descending aorta Aetiology: - HTN - Trauma - CTDs - Bicuspid aortic valve, Turner's, Noonan's syndrome Features: - Severe, 'tearing' pain radiating to back - > 20mmHg discrepancy in BP - New AR - Angina, paraplegia, limb ischaemia Imaging: - CT angiograhpy - look for false lumen - TOE - in unstable patients Management: - Type A - surgical repair - Type B - strict BP control (SBP 100-120)

Answer 52

Heart failure: elevated PE: elevated Pericardial effusion: elevated, prominent y descent Pericardial constriction: elevated w kussmauls sign (inc on insp) SVCO: elevated w loss o pulsation Afib: absent a waves Tricuspid stenosis: giant a waves Tricuspid regurg: giant V waves Complete heart block: cannon waves

Answer 53

Most common congenital abnormality in children and second most common in adults Predominantly create pathology through formation of a shunt, with risk of Eisenmenger syndrome Features: - Pansystolic murmur - Heard best at L sternal edge - CHF - Fluid overload, raised JVP etc. - Eisenmenger - Cyanosis - Syncope - Dyspnea - Clubbing Management: - Small = observation - Isolated medium/large = percutaneous closure - Large, complex or haemodynamic compromise = surgical closure

Answer 54

Insertion of Swan-Ganz catheter into the right side of the heart via a large peripheral vein RA < 5 mmHg RV - 15-30 / 3-8 Pulmonary artery - Systolic = RV - 15-25 / 4-12 PCWP - Indirect estimate of LA pressure - Helps to quantify LVF and mitral stenosis - < 12mmHg LV - 100-140 / 3-12 Combination of PA + PCWP, via thermodilution technique, is used to measure pulmonary vascular resistance and therefore diagnose pulmonary HTN

Answer 55

Indications: - AF which has failed first-line medical treatment Must take anticoagulation for 4-6 weeks prior - Do not stop prior to the procedure Stop beta-blockers, CCBs, and antihypertensives pre-procedure Perform wide circumferential ablation around the pulmonary veins

Answer 56

Non-pharmacological: - Stop smoking - Weight loss Pharmacological: - ACEI (NNT = 22) - Statin (NNT = 33) - Aspirin (NNT = 42) - Beta-blocker (NNT = 143)

Answer 57

Inflammation of the pericardium - Can lead to involvement of the epicardium - ECG changes - or effusion - risk of tamponade Causes: - Infection (oft. viral) - Uraemia - Autoimmune - Malignancy (esp. lung) Features: - Sharp stabbing central chest pain - Better leaning forwards - Worse coughing, lying back, moving - May radiate to neck and arm - Pericardial rub - SOB Investigations: - ECG - saddle-shaped ST elevation - Raised troponin - Echo - diagnostic Management: - Treat underlying cause - NSAIDS, colchicine Complications: - Myocarditis - Tamponade

Answer 58

Features: - Beck's triad: - Hypotension - Raised JVP - Muffled heart sounds - Tachycardia - Pulsus paradoxus - SOB with normal lung fields Investigations: - CXR = large globular heart - Echo = diagnostic Management: - Emergency pericardiocentesis

Answer 59

Chronic inflammation leads the pericardium to become dense and fibrous Aetiology: - TB - Trauma - Purulent pericarditis Features: - Peripheral oedema - Dyspnea - Ascites - Hepatomegaly Investigations: - CXR - normal sized heart - Echo - restricted mitral filling, pericardial thickening Management: - Surgical excision

Answer 60

Aetiology: - Coronary atherosclerosis - Tachycardia - Anaemia - Aortic stenosis - LVH - Coronary artery spasm Features: - Cardiac chest pain occurring on exertion - Relieved with GTN - Also fatigue, nausea, belching Classification of severity: - Class I - only with prolonged strenuous activity - Class II - on climbing stairs or walking into wind - Class III - on climbing 1 flight of stairs or going 50-100m on the flat - Class IV - on any physical activity Investigations: - Stress testing - with ECG, echo, etc. - Coronary angiography Management: - Lifestyle advice + secondary prevention meds - Medical: - GTN for breakthrough - CCBs e.g. diltiazem, verapamil or beta- blocker - Consider ivabradine, nicorandil etc. - If not managed with 4 agents, PCI/CABG

Answer 61

Presence of an accessory pathway connecting the atria to the bundle of His, leading to bypass of the AVN - vs WPW where it connects to the ventricular myocardium ECG - short PR, no delta waves Management: - Beta-blockers - Pathway ablation

Answer 62

Myoglobin: - Released within 1hr of myocardial cell damage, elevated for 1-2 days afterwards Troponins: - Released within 4-6 hours of myocardial cell damage and remain elevated for up to 2 weeks - TnI and Tnt are most sensitive Creatinine kinase: - Released c. 24h after myocardial cell damage and remain elevated for 3-4 days

Answer 63

Relative: - Prolonged traumatic CPR - Recent surgery - Bleeding disorders - Pregnancy - On anticoagulation and/or INR > 1.8 Absolute: - BP > 180/110 - Head trauma within 2/52 - Known intracranial malignancy - Active bleeding - Stroke < 2/12 ago - Suspected aortic dissection

Answer 64

ACEi - Decrease circulating ATII -> decreased aldosterone -> decreased Na+ reabsorption - Also increase bradykinin levels - Dry cough - Angioedema ARBs: - Blockade of AR2 - Useful in those who don't tolerate ACEi Thiazides: - Inhibit the Na/Cl symporter in the DCT -> decreased Na+ reabsorption - Takes 12 weeks to come into effect - Early reduction in blood volume - Slower vasodilation CCBs: - Predominantly blockade of L-type voltage-gated calcium channels - Affects vascular tone + heart contractility - Only amlodipine can be used in CHF patients

Answer 65

Ivabradine - Inhibition of If within the SAN - hyperpolarization-activated cyclic-nucleotide gated K+ channel Hydralazine - Direct-acting smooth muscle relaxant working primarily in resistance arterioles - Inhibits inositol triphosphate-induced Ca2+ release from the sarcoplasmic reticulum Nicorandil - Nitrate + activates ATP-sensitive K+ channels -> induces hyperpolarization Clopidogrel: - Inhibitor of a P2YR, inhbiting ADP-mediated platelet aggregation - Prodrug requiring activation by CYP2C19 which is active in only 2/3rds the population

Answer 66

Presents on a spectrum from stable angina to ACS with potential to cause ischaemia Most likely to occur at night due to increased activity of the PNS although SNS is also implicated in it's pathophysiology Investigations: - Coronary angiography with provocative testing - Need ECG changes, >50% luminal narrowing, and symptoms

Answer 67

Pacemaker: - Cannot drive car for 1 week - Cannot drive group 2 vehicles for 6 weeks ICD - Car - Primary prevention = 1 month - Secondary prevention = 6 months - Cannot drive for 6 months after any shock - Cannot drive group 2

Answer 68

Group 1 - Cannot drive for 1 week if had successful angioplasty - Cannot drive for 4 weeks if either angioplasty was unsuccessful or didn't happen. Group 2 - Cannot drive for 6 weeks

Answer 69

Type 1 - coronary artery-based Type 2 - increased demand/reduced supply states with normal coronaries Type 3 - sudden cardiac death from MI Type 4 - due to PCI or stent thrombosis Type 5 - due to cardiac surgery

Answer 70

Myocardial infarction secondary to ischaemia due to either increased oxygen demand or decreased supply - e.g. vasospasm, hypovolaemia, sepsis, PE Diagnosis: - Elevated by changing troponin - Clinical features inconsistent with type 1 MI - Clinical conditions known to increase oxygen demand and/or decrease supply Management: - Treat underlying insult - Screen for coronary artery lesions

Answer 71

Specific: - Atrial fibrillation - Pulmonary HTN - Pericardial effusion - Pleural effusion (40%) - Stroke - Renal injury - Haemodynamic instability General: - Sternal wound infections - Graft failure - Pneumonia - VTE phenomena

Answer 72

L-> R shunt - Enlarged heart - Prominant pulmonary vasculature - Fluid in lung fields Aortic stenosis - Prominent LV - Aortic dilatation Pulmonary stenosis - Post-stenotic pulmonary artery dilatation Coarctation of the aorta - Prominent LV - Rib notching Tetralogy of Fallot - Boot-shaped heart - apex above L hemidraphram + concave L heart border - Small pulmonary arteries - Oligaemic lung fields Transposition of the Great Arteries - Egg-on-side appearance Total anomalous pulmonary venous drainage - Small heart - Pulmonary congestion - can be white-out Ebstein's anomaly - Massively enlarged heart - Pulmonary oligaemia

Answer 73

Friedrich ataxia - HOCM Marfans - aortic dissection/aneurysm/regurg Glycogen storage disease - type 2 cardiomyopathy Noonan's - pulmonary stenosis William's - supravalvular aortic stenosis, pulm sten Romano-ward syndrome - long QT Tuberous sclerosis - rhabdomyoma Turners - bicuspid aortic valve

Answer 74

Alcohol - ASD, TOF Rubella - PDA, coarctation, TOF Phenytoin - pulm stenosis Lithium - ebstein anomaly

Answer 75

Fever Prolonging PR interval + reducing QRS voltages Increasing heart size on CXR

Answer 76

Aetiology: - Embolic (50%) - Arrhythmia - Valve pathology - Post-MI mural thrombus - Aortic aneurysm - Thrombotic (25%) - Atherosclerosis - Shock (20%) - Mesenteric venous thrombosis (<10%) - Dissection - Vasculitis Investigations: - Blood gas - Routine bloods - CT angiography Management: - Urgent surgery - Angioplasty/embolectomy - Bowel resection if necrotic - Usually requires relook laparotomy in 24-48hr

Answer 77

Plaque mostly found at the bifurcation of the CCA or within the proximal ICA Can present with TIA/amaurosis fugax but then rapidly progresses to full stroke Investigation: - Duplex USS Management: - Lifestyle modification - Medications e.g. statin, clopidogrel - Surgery: - If >50% stenosis on one side with sx or >70% and asymptomatic - Balance risk of future stroke with risk of stroke due to intervention

Answer 78

aka aortoilliac occlusive disease Due to severe atherosclerosis of the distal aorta or proximal common iliac Classic triad: - Thigh/buttock claudication - Absent femoral pulses - Male impotence

Answer 79

Used in the investigation of potential peripheral vascular disease > 1.3 = arterial calcification 0.9 - 1.3 = normal 0.6 - 0.9 = mild PVD 0.3 - 0.6 = moderate-severe PVD < 0. 3 = severe to critical PVD

Answer 80

Most commonly due to atherosclerosis of the peripheral arteries, with acute presentations due to thrombus formation Intermittent claudication: - Leg pain on exertion which is relieved by rest - Investigations = ABPI - Management: - Lifestyle modification - Supervised exercise training - Statins, clopidogrel - Revascularisation procedures Critical (chronic) limb ischaemia - Presence of claudication pain at rest, due to critical compromise of blood flow Acute limb ischaemia - A sudden decrease in limb blood flow which threatens viability, usually due to acute thrombus formation - Features = 6 Ps - Investigation = angiography - Management: - Medical - analgesia + unfractionated heparin - IR - stenting, balloon - Surgical - embolectomy, endarterectomy - Limb amputation - A key complication is compartment syndrome following limb reperfusion injury

Answer 81

Aetiology: - Trauma e.g. IV line insertion - Lupus - Cancer - migratory, due to hypercoagulable state - Berger's syndrome Features: - Low-grade fever - Local redness or swelling along course of vein - Symptoms worse when limb lowered Management: - Elevation + compression - NSAIDs - Abx if concurrent infection present

Answer 82

Common in older life. Can also occur in pregnancy, usually resolving upon delivery Investigations: - ABPI - to rule-out arterial pathology prior to compression stockins - Duplex USS - prior to surgical referral Management: - Weight loss - Leg elevation - Compression stockings (incl. in pregnancy) - Refer to vascular if symptomatic - Pain, itchiness, heaviness, swelling, chronic venous insufficiency - Endothermal ablation, foam sclerotherapy, ligation + stripping

Answer 83

Uncommon condition resulting from acute, massive venous thromboembolism - Mostly veins of the leg (iliofemoral), rarely arm - Linked to hypercoagulable state - esp. malignancy Features: - Phlegmasia alba dolens - Initial phase - Progresses over hours to days - Severe pain + limb pallor + edema - Phlegmasia cerulea dolens - Second phase - Severe pain + cyanosis -> bullae and necrosis Management: - Limb elevation - Analgesia + fluids - Thrombolysis - Thrombectomy

Answer 84

Aetiology: - Post-surgical esp. for cancer - Radiotherapy - Infection - filariasis - Psoriasis - DVT/varicose veins Investigation: - Rarely required - MRI or lymphoscintogram Management: - Exercise - Limb elevation - Limb massage - Skin/nail care - Liposuction or lipovascular anastomosis done in a minority of cases at speciality centres

Answer 85

For men 65+ or women 70+ with risk-factors < 3.0 - discharge 3.0 - 4.4 - repeat in 12 months 4.5 - 5.4 - repeat in 3 months > 5.5 or growing > 1.0 in 1 year - vascular referral Symptomatic - urgent vascular referral

Answer 86

A syndrome of channelopathies leading to prolonged QT with risk of arrhythmia and sudden death Often present in unstable monomorphic VT Aetiology: - LQT1 - Most common - KCNQ1 on Chr 11 - Slow delayed rectifier K+ channel - LQT2 - KCNH2 on Chr 7 - Rapid delayed rectifier K+ channel - LQT3 - SCN5A on Chr 3 - Slow Na+ channel Management: - Medical - Beta-blockade - ICD - Mainly for LQT2/3 as higher risk of sudden death

Answer 87

Produced by closure of the mitral and tricuspid valves - Mitral closes just before tricuspid - Wide splitting is always pathological Associated with the ECG R-wave Quiet S1 - rigid valve or delayed LV systole - Mitral regurgitation - Long PR interval - Obesity - 1st degree heart block - LBBB Loud S1 - long diastole, high volume - Mitral stenosis - Hyperdynamic states - Tachycardia - Low BMI - Atrial myxoma Widely split S1 - RBBB - Ebstein's anomaly - Ventricular tachycardia Variable intensity S1 - due to variable PR interval - Complete heart block

Answer 88

Produced by closure of the aortic and pulmonary valves - Some splitting is typical - aortic closes before pulmonary due to high systemic pressures - Splitting increases in inspiration Loud - HTN Quiet/absent - Severe aortic stenosis Widely split - Pathology which delays the end of right ventricular systole or slows exit of blood from the RV e.g. RBBB, Pulmonary stenosis, VSD, Mitral regurgitation Fixed splitting - aka no change with inspiration - because ASD allows equalisation of pressures between both side e.g. ASD Reversed splitting - Closure of PV prior to AV - Delayed LV systole - LBBB - Slowed LV outflow - AS - Additional supply of blood delaying closure - PDA

Answer 89

An uncommon complication of angiography Features: - Recent arterial instrumentation - Marked eosinophilia - AKI - Livedo retricularis - Acrocyanosis - Limb ischaemia and other embolic phenomena Management: - Supportive - No good evidence for thrombolysis, anticoagulation, or re-intervention

Answer 90

aka right ventricular dysplasia 2nd most common cause of sudden death in the young Features: - Palpitations - Syncope - Cardiac arrest - Progressive RV failure ECG: - TWI in V1-3 without RBBB - Epsilon potential - small deflection at end of QRS complex due to RV conduction delay Echo: - Dilated, hypokinetic RV with prominent apical trabeculae and dilated outflow tract Histology: - Fatty infiltration of RV myocytes with subsequent fibrosis

Answer 91

A complication of congenital heart disease in which large anatomical shunts are present e.g. VSD, ToF, large ASDs Pathophysiology: - Initial L -> R shunting - Elevated RV and pulmonary pressures - Eventual pulmonary arterial hypertension and elevated venous resistance - Then R -> L shunting Features: - Cyanosis - Hypoxaemia despite maximal oxygen therapy (due to mixing) - Other cardiac stress - oedema, chest pain, syncoep, SOBOE Management: - Only curative treatment is a heart transplant - Vasodilators e.g. endothelin antagonists

Answer 92

Triad of aortic stenosis, GI bleeding, and acquired von Willebrand syndrome Pathophysiology: - Shear stresses + increased velocity across stenotic aortic valve cause unfolding and activation of vWF - Uses up vWF and so less is available for normal clot formation, in particular predisposing to GI bleeding Management: - Aortic valve replacement

Answer 93

A rare (5%) cause of cardiomyopathy, presenting in a similar way to constrictive pericarditis Aetiology: - Idiopathic - Infiltrative disease - esp amyloidosis - Radiation therapy - Hypereosinophilia Features: - Right heart failure - raised JVP, peripheral oedema, hepatomegaly, cachexia - SOB, PND, orthopnea Investigations: - ECG - non-specific repolarisation disturbances, small complexes - Bloods - Echo - small ventricles, LVH, speckling - Cardiac biopsy - +ve Congo Red staining for amyloid Management: - Supportive - diuretics - AF control

Answer 94

A cardiac tumour formed from the atrial muscle - Most common cardiac tumour - Mostly on L side - Benign - F > M Features arise from embolisation, intra-atrial obstruction of cardiac output, and constitutional symptoms of malignancy Features: - Symptoms - Fever - Weight loss - SOB - Syncope - Signs - Transient mitral stenosis - Early diastolic 'plop' - Distal embolisation - Finger clubbing Investigations: - Bloods - Raised WCC, low PLT, variable Hb - Imaging: - CXR - enlarged heart - Echocardiogram Management: - Urgent surgical resection as high risk of growth and embolisation