Cardiology Flashcards

Question

Which ECG changes occur in acute MI?

Answer 1

ST elevation, tall T waves, LBBB

Answer 2

T wave inversion Pathological Q wave (think longer and over 25% size of the R wave)

Answer 3

A score system to risk stratify patients with diagnosed ACS to estimate in-hospital admission and 6 month to 3 year mortality - it is also used to decide whether to undergo PCI vs conservative Looks at: - age - HR/BP - cardiac and renal function - cardiac arrest on presentation - ECG findings - troponin levels If risk >3% (intermediate), consider PCI within 72h

Answer 4

- Cardiac arrest - Unstable angina - Bradycardias/heart block - Tachyarrhytmias - Heart failure - Pericarditis - DVT/PE - Cardiac tamponade - Mitral regurgitation - Dresslers syndrome

Answer 5

Palpitation, chest pain, syncope, hypotension, pulmonary oedema May be asymptomatic

Answer 6

An inherited condition associated with delayed repolarization of the ventricles which can lead to VT/torsade de pointes. There are 3 types: LQT1 - associated with exertional syncope eg. swimming LQT2 - associated with stress related syncope LQT3 - events occur at night or rest

Answer 7

Congenital: - Jervell-Lange-Nielsen syndrome (includes deafness, due to abnormal K channel) - Romano-Ward syndrome (no deafness) Drugs (the usual mechanism of this is by blocking potassium channels): - Amiodarone, sotalol, class 1a antiarrhythmic drugs - Antidepressants (TCAs, SSRIs esp citalopram) - Methadone - Chloroquine - Erythromycin - Haloperidol - Ondansetron - Terfenadine (non sedating antihistamine) Other: - Electrolytes ( LOW K, Ca, Mg) - Acute MI - Myocarditis - Hypothermia - SAH

Answer 8

WPW syndrome

Answer 9

Hypokalemia Small deflection immediately following the t wave, usually in the same direction

Answer 10

1. Sinoatrial node initiates an electrical impulse causing atrial contraction 2. Atrial depolarisation (P wave) 3. Impulse reaches AV node 4. AV node generates a slow action potential 5. Activation of the bundle of His and generation of a fast action potential (PR interval) 6. Impulse conducted to right and left bundle branches 7. Impulse travels through purkinje fibres causing depolarisation in the ventricles (QRS complex) 8. Ventricles repolarise and myocardium relaxes (T wave) NB - atrial repolarisation hidden in QRS complex on ECG

Answer 11

Cardiac electrical disorder defined as impaired conduction from the atria to the ventricles, shown as PR abnormalities and bradycardia on ECG The severity is described in degrees.

Answer 12

- Levs disease (fibrosis/calcification of conduction system) - Ischaemic heart disease - Cardiomyopathy - Myocarditis - His Purkinje disease - Use of AV nodal blocking agents

Answer 13

Electrical impulse moves more slowly through AV node. Common in athletes (increased vagal tone) and caused by certain drugs. Generally asymptomatic without significant complications. ECG shows increased PR interval >0.2s

Answer 14

aka Wenckebachs PR interval gradually increases until a QRS complex is lost Due to reversible conduction block at the AV node (athletes, drugs, inferior MI, myocarditis) Asymptomatic patients dont require treatment - give atropine if symptomatic and stop AV node blocking drugs (ABCD - adensine, beta blockers, CCBs, digoxin)

Answer 15

Some P waves do not have QRS complexes following them (intermittent non-conducted P waves) without progressive PR prolongation Due to failure of conductive at the His-Purkinje system (below the AV node), due to drugs, ischaemia, structural damage, hyperkalemia, inflammation May be symptomatic. More likely to be associated with haemodynamic instability and asystole so need active management with digoxin/pacemaker

Answer 16

No relation between P waves and QRS complexes Due to complete loss of conduction between atria and ventricles. Perfusing rhythm maintained by a junction or ventricular escape rhythm. Will be symptomatic (fainting, dizziness, fatigue, SOB, chest pain) High risk of sudden cardiac death, need urgent monitoring, digoxin, atropine, temporary/permanent pacing

Answer 17

Syncopal episode due to a cardiac arrhythmia, most commonly bradycardia/complete heart block

Answer 18

Any heart rhythm slower than 60bpm, due to: 1. Reduced automaticity (sinus node dysfunction) due to increased vagal tone 2. Conduction block

Answer 19

Increased vagal tone

Answer 20

>40bpm, asymptomatic - no treatment, treat cause (stop drugs, hypothyroidism, sick sinus syndrome) <40bpm or symptomatic, give atropine up to 6 times > transcutaneous pacing > transvenous pacing or temporary pacing wire if no response

Answer 21

Sinus node dysfunction causing bradycardia and arrest, sinoatrial block or SVT. Often requires a pacemaker!

Answer 22

Any heart rate above 100bpm, due to: 1. Increased automaticity (exercise, ectopic firing) 2. Triggered activity (abnormal APs triggered by preceding AP) 3. Reentry

Answer 23

Narrow complex means that the signal must pass through the AV node - Sinus tachycardia - Supraventricular tachycardia (p wave absent or inverted) - AF (wandering baseline) - Atrial flutter (sawtooth) - Atrial tachycardia - Junctional tachycardia

Answer 24

1. If patient compromised use DC cardioversion 2. If not, identify underlying rhythm and treat accordingly 3. Transient AV block through vagal manoeuvres or IV adenosine

Answer 25

1. Vagal manoeuvres 2. IV adenosine (6m > 12mg > 18mg UNLESS ASTHMATIC) 3. IV verapamil (if asthmatic) 4. DC cardioversion (if treatment refractory or if haemodyamically unstable) Prevention of future episodes with beta blockers or radiofrequency ablation

Answer 26

1. Stop digoxin if this is the cause | 2. Maintain potassium levels

Answer 27

Junctional rhythms occur when the AV node takes over as the main pacemaker of the heart. BUT, AV node can only conduct 40-60 beats Regular rate, absent p waves, normal QRS Types of junctional tachycardia: 1. AV nodal re-entry tachycardia 2. AV re-entry tachycardia 3. His bundle tachycardia OFTEN REQUIRE PACING

Answer 28

1. Vagal manoeuvres 2. IV adenosine 3. If recurrence, beta blocker or amiodarone 4. Radiofrequency ablation

Answer 29

Congenital accessory conduction pathway between the atria and ventricles. ECG shows short PR interval, wide QRS complex (due to slurred upstroke/delta wave) Patients present with SVT, AF or atrial flutter. Refer to cardiologist for electrophysiology and ablation of accessory pathway

Answer 30

Acute arhythmmias due to binge drinking, usually causing SVT and AF

Answer 31

Supraventricular tacchyarrhythmia, characterised by uncoordinated atrial activity. Causes cardiac output to drop as the ventricles aren't primed reliably by the atria. ECG shows absent p waves, and irregularly irregular pulse, wandering baseline.

Answer 32

Paroxysmal - episode of AF that terminates spontaneously or with intervention in less than 7 days Persistent - each episode lasts for longer than 7 days Permanent - AF that cannot be controlled by medication

Answer 33

Palpitations, dyspnoea, angina, dizziness, syncope May present as stroke, HF

Answer 34

Haemodynamically unstable: - DC cardioversion Haemodynamically stable: Offer either rate or rhythm control RHYTHM Heparin and either: - DC cardioversion (this option if haemodynamically unstable) - Pharmacological cardioversion; IV amiodarone (if structural heart disease) or flecanide RATE - Beta blocker/CCB/digoxin OFFER DOAC IF SINUS RHYTHM NOT ACHIEVED AFTER 48H, HIGH RISK OF RECURRENCE OR HIGH RISK OF STROKE

Answer 35

- AF with a reversible causes - HF thought to be caused by AF - New onset AF - Atrial flutter

Answer 36

Offer either rate or rhythm control: RATE - Rate control with beta blocker/CCB (verapamil or diltiazem). - 2nd line - add digoxin - Consider rhythm if symptoms not controlled on rate control RHYTHM: - Amiodarone/dronedarone for 4 weeks then DC cardioversion, then continue amiodarone/dronedarone for 12 weeks after - Consider anticoagulation using CHA2DS2VASc score (offer if >=1 in men or >= 2 in women) - Lifelong treatment even if reverts to NSR NB - if cha2ds2vasc 0, needs to have had an echo to exclude valvular heart disease which would be an indication for anticoagulation

Answer 37

- Pill in the pocket - sotalol or flecainide if no structural heart disease - Anticoagulation - Consider digoxin mono therapy if very sedentary

Answer 38

Offer left atrial catheter ablation- This is a keyhole technique (surgery performed through a tiny incision), which directs a small, flexible tube (or catheter) to a specific area inside the heart. Once there, it uses heat energy to damage (or ablate) the abnormally active heart muscle.

Answer 39

A score used to determine whether a patient with AF should have long term anticoagulation. Points scored: Congestive HF (1) Hypertension (1) Age >65 (1) Diabetes (1) Stroke/TIA/VTE (2) Vascular disease (1) Age >65 (1) Female (1) Score 1 or more - consider antiplatelet/anticoagulant Score 2 or more - start anticoagulant Note - if pt reverts back to sinus rhythm after 2 episodes, they should stillcontinue anticoagulation

Answer 40

DOAC- offer if CHADvasc >2, consider if >1

Answer 41

A score calculating bleeding risk whilst on an anticoagulant Score 1 for: Age >74 Treatment with antiplatelets GFR <60 Score 2 for: Bleeding history Hb <12 in females, >13 in males 0-2 LOW 3 MODERATE 4-7 HIGH

Answer 42

Tachyarrhythmia in which the atria and ventricles beat at different speeds, usually due to a reentry circuit in the right atrium. Associated with AF! ECG shows sawtooth appearance, may have 2:1 AV block nb - AF is when the atria beat irregularly. Flutter is when the atria beat regulalry but at a differet speed to the ventricles

Answer 43

Haemodynamically unstable: - DC cardioversion Stable: 1. B-blocker/CCB/amiodarone (+ anticaog if appropriate) 2. If unsuccessful, DC cardioversion or ablation (more successful in Afl)

Answer 44

Rate >100 + QRS >120s (3 small sq). This is a tachycardia in which there is dysfunction of the ventricular conduction system (BBB) or a problem with the ventricles themselves.

Answer 45

- VT (most common) - includes torsades de pointes | - VF

Answer 46

VF (looks like bag of worms?) | Pulseless VT

Answer 47

Regular: Unstable VT/VF: SHOCK Stable VT: oxygen, IV amiodarone if monomorphic (load then 24h infusion), IV Mg if polymorphic torsades, consider DC cardioversion May need ICD long term Irregular (AF with BBB, AF with ventricular pre-excitation, torsades de pointes): Seek expert help!

Answer 48

VT with varying axis (looks like VF) - due to increased QT interval, electrolyte imbalances

Answer 49

- Symptomatic bradycardia, unresponsive to atropine - After acute MI - Suppression of drug-resistant tachyarrhytmias

Answer 50

- Complete AV block - Mobitz type II - Symptomatic bradycardiac - Heart failure

Answer 51

Cardiac arrhythmia in which one or both bundles of His are delayed or blocked, causing ventricles to beat abnormally

Answer 52

RBBB - wide S wave, triphasic QRS (M in V1 and W in V6 MaRRoW) -this can be normal in young healthy patients LBBB - large R wave, large Q wave (W in V1 and M in v6 WiLLiaM) - this could be a new MI, htn, AS, cardiomyopathy

Answer 53

Systolic - inability of ventricle to contract normally causing decreased CO, EF<40% Caused by IHD, MI, cardiomyopathy Diastolic - inability of ventricle to relax normally causing increased filling pressures, EF>50% Caused by constrictive pericarditis, tamponade, restrictive cardiomyopathy, hypertension These two types usually co-exist?

Answer 54

THINK where does the heart back up to Left heart failure - causes respiratory symptoms, dyspnoea, poor exercise tolerance, orthopnea, PND, nocturnal cough with pink froth sputum, cardiac asthma Right heart failure - peripheral oedema, ascites, nausea, pulsation in neck and face Usually these occur together causing congestive cardiac failure

Answer 55

Acute - new onset or acute decompensation with pulmonary/peripheral oedema, may have signs of hypo perfusion Chronic - develops slowly with venous congestion Management is different for both

Answer 56

Framingham - CCF requires at least 2 major or 1 major + 2 minor criteria

Answer 57

ECG (may indicate cause) , BNP (>400)- if either abnormal, do ECHO to confirm diagnosis Caution - BNP may be falsely high in MI, AF, PE, COPD, liver failure, sepsis, diabetes, renal impairment. - BNP may be falsely low if the patient is on aldosterone antagonists, ACE inhibitors, ARB, beta blockers or diuretics

Answer 58

- Cardiomegaly (>50% of the thorax) - Kerley B lines - Batwing pulmonary oedema - Pleural effusions - Prominent upper lobe veins

Answer 59

Cachexia, increased RR and HR, JVP, murmur (if valvular disease), 3rd heart sound, bibasal crops, pitting oedema

Answer 60

LMNOP Loop diretics - IV furosemide Morphine Nitrates Oxygen Positioning

Answer 61

1st line: - ACE-inhibitors - symptomatic and prognostic - Beta blockers - prognostic - Loop diuretics - this is symptomatic, not related to mortality 2nd line: - Spironolactone/eplerenone - add if ongoing symptoms in pts with reduced EF - SGLT-2 inhibitors, particularly if diabetic 3rd line: - Ivabradine - if HR >75, EF<35% - Sacubitril-valsartan - if symptomatic on ACEi/ARB - Digoxin - if co-existent AF - Vasodilators (isosorbide, hydralazine) - if intolerant of ACEis/ARB, particularly in Afro-Caribbean patients - Cardiac resynchronisation therapy (for patients with heart faiure and wide QRS)

Answer 62

Inflammation of the pericardium causing sharp severe chest pain, worse on inspiration and supine position. Classically in younger males, after cardiac surgery, viral/bacterial infection or neoplasm, also associated with autoimmune disorders

Answer 63

1. Retrosternal chest pain 2. Pericardial friction rub (high pitched, squeaky rub at left sternal edge with patient leaning forwards at end-expiration) 3. Serial ECG changes (PR DEPRESSION IS SPECIFIC, widespread saddle ST elevation) Usualy troponin will be NORMAL, as oppose to myocarditis where it will be high

Answer 64

ALL PATIENTS SHOULD HAVE TTE If no risk factors - manage as outpatient with NSAIDs/colcihcine and 1 week follow up - continue treating until symptom resolution/normal inflam markers and taper dose If febrile, high trop or high risk - admit for observation If purulent - pericardiocentesis and antibiotics If tamponade - pericardiocentesis

Answer 65

Chronic recurrent pericarditis Constrictive pericarditis Cardiac tamponade

Answer 66

Thickened, fibrotic pericardium limiting cardiac function - due to long term inflammation of the pericardium. Treat as heart failure

Answer 67

Accumulation of pericardial fluid, blood, pus or air within the pericardial space. This increases pressure, restricting cardiac filling and decreasing cardiac output - MEDICAL EMERGENCY

Answer 68

Symptoms - chest pain, syncope Signs - tachycardia, hypotension (shock), muffled heart sounds, elevated JVP, pulses paradoxus (a fall in BP during inspiration by >10mmHg), positive rub

Answer 69

ECG - electrical alternans (varying height of QRS complex) ECHO - large effusion, chamber collapse

Answer 70

Haemodynamically stable (sBP>110) - anti-inflammatories and observe Haemodynamically unstable - pericardiocentesis and surgical drainage

Answer 71

Perciarditis after MI - will have fever, chest pain, pericarditis

Answer 72

Pharyngeal infection with group A beta-haemolytic streptococci. Antibody cross reacts with valve tissue and may cause permanent heard damage

Answer 73

Inhibit action of HMG-CoA reductase which is an enzyme involved in cholesterol synthesis LFTs at baseline, 3 months and 12 months - discontinue treatment if serum transaminases concentrations rise to and persist at 3x the upper limit of the reference range CI: macrolides, pregnancy

Answer 74

1st - previous episode of endocarditis Other - rheumatic valve disease. prosthetic valves, congenital heart defects, IVDU, recent piercings

Answer 75

1. Staph aureus (particularly if acute presentation or IVDU) 2. Streptococcus viridans (number 1 in developing countries or post dental procedure) 3. Staph epidermis 4. Strep bovis (linked with colorectal cancer)

Answer 76

Mitral valve Tricuspid valve if IVDU

Answer 77

Stage 1: Clinic BP >140/90 and average ABPM/HBPM > 135/85 Stage 2: Clinic BP >160/100 and average ABPM/HBPM >150/95 Severe: Clinic BP >180 or diastolic >120

Answer 78

Treat if <80yo and any of the following apply: - Target organ damage - Established cardiovascular disease - Renal disease - Diabetes - 10y cardiovascular Qrisk >10% Note if pts <40yo, consider specialist referral to exclude secondary causes

Answer 79

Step 1: If <55 or bg T2DM - ACEi/ARB If >55, afrocaribbean - CCB or thiazide-LIKE diuretic eg. indapamide (oedema, HF) If diabetic, regardless of age or ehtnicity - ACEi/ARB Step 2: If <55 - add CCB/diuretic If >55 - add ACEi/ARB/diuretic (note if afrocaribbean, choose ARB over ACEi) Step 3: A + C + D Step 4 (resistant HTN): Seek specialist advice before adding a fourth drug, consider spironolactone (if K <4.5) /alpha/blocker/beta blocker (if K >4.5) Remember lifestyle factors! - Aim <3g/day of salt daily - Reduce caffeine intake NB if pt has a history of gout, give CCB instead of thiazide-like diuretic as it may exacerbate his gout

Answer 80

Worrying features or acute BP>200 systolic or 120 diastolic No end-organ damage - oral therapy with CCB/ACe i Organ damage - admit, closely monitor BP, neuro state, fluid balance, ECG, and give IV labetolol or furosemide (+ hydralazine?)

Answer 81

1. Cardiac arrest 2. Cardiogenic shock - if a large part of the myocardium is damaged the EF may decrease causing cardiogenic shock, often need inotropes 3. Chronic heart failure 4. Tachyarrhythmias - most common is VF 5. Bradyarrhythmias - AV block more common after inferior MIs 6. Pericarditis - common in first 48h following transmural MI - may hear a pericardal rub and see an effusion - Dresslers is an autoimmune type of pericarditis in which a reaction forms against antigenic proteins formed as the myocardium recovered. Typical to see widespread ST elevation with PR depression, treat with NSAIDs 7. Left ventricular aneurysm - ischaemic damaged from MI weakens the myocardium causing an anuerysm formation - this would cause persistent ST elevation and LVF - pts should be anticoagulated due to stroke risk 8. Left ventricular free wall rupture - presents as acute HF with features of cardiac tamponade 1-2 weeks post MI - urgent pericardiocentesis and thoracotomy are required 9. Ventricular septal defect - presents as acute HF with pansystolic murmur 1 week post MI - urgent surgery required 10. Acute MR - common with infero-posterior infarction, due to ischaemia of rupture of papillary muscle - presents as acute hypotension and pulmonary oedema with early-to-mid systolic murmur - treat with vasodilators, may require surgical repair

Answer 82

- Usually bovine or porcine - Structurally deteriorate and calcify over time therefore only given to patients over 65/70 yo - Advantage is long term anticoagulation not needed (except for warfarin in first 3 months) - Pts will be on life long aspirin

Answer 83

- Usually bileaflet - Low failure rate - Major disadvantage is increased thrombosis risk > lifelong warfarin (aim 2.5-3.5 aortic aim 3-4 mitral) - Give aspirin if additional indication

Answer 84

eg. varices, ICH - Stop warfarin - Give IV vit K 5mg PCC (FFP if not available)

Answer 85

Major bleeding: - Stop warfarin - Give IV vit K1-3mg - Repeat vit K if INR still high after 24h - Restart warfarin when INR >5 Minor bleeding: - Stop warfarin - Give vit K 1-5mg PO (use IV orally) - Repeat vit K if INR still high after 24h - Restart warfarin when INR >5

Answer 86

Minor: - Stop warfarin - Give IV vit K 1-3mg - Restart when INR >5 No bleeding: - Withhold 1-2 doses of warfarin - Reduce subsequent maintenance dose

Answer 87

- Often asymptomatic - Mild/moderate AS causes chest pain, dyspnoea, syncope - EJECTION SYSTOLIC MURMUR RADIATING TO CAROTIDS (decreased after valsalva) Severe features: - Narrow pulse presure - Slow rising pulse - Delayed ESM - Soft or absent S2 or new S4 - Thrills - LVH or failure

Answer 88

- Degenerative calcification (most common in patients >65) - Bicuspid aortic valve (most common in patients <65) - William's syndrome (supravalvular aortic stenosis = narrowing of aorta just above the valve) - Post-rheumatic disease - Subvalvular HCOM

Answer 89

Asymptomatic > observe Asymptomativ with valve gradient >40 with severe features > consider surgery with valve replacement Symptomatic > valve replacement Options for AVR: - Surgical AVR if low risk - TAVI if high risk - Balloon valvuloplasty in children without calcification or adults with critical AS

Answer 90

Can be causes by diseae of aortic valve or by distortion or dilation of the aortic root and ascending aorta Acute valvular disease: - Infective endocarditis Acute aortic root disease: - Aortic dissection Chronic valvular disease: - Rheumatic fever (no 1) - Calcific valve disease - Connective tissue disease (RA/SLE) - Bicuspid aortic valve Chronic aortic root disease: - Bicuspid aortic valve - Spondyloarthropathies - Hypertension - Syphilis - Marfans/ehlers danlos

Answer 91

- Early diastolic murmur (intensity increased by handgrip manoeuvr and leaning forward/breathe out and hold) - Collapsing pulse - Wide pulse pressure - Quincke's sign (nailbed pulse) - De Musset's sign (head bobbing) - mid-diastolic Austin-Flint murmur in severe AR

Answer 92

- Medical management of associated HF - Surgery if severe symptomatic or LVEF asymptomatic

Answer 93

- Obstruction of blood flow across mitral valve leading to increased pressure within the left atrium, pulmonary vasculature and right side of heart - Dyspnoea due to PVH - Haemoptysis due to pulmonary pressure - Mid-late diastolic murmur, best heard when rolling patient to left hand side - Loud S1 - Opening snap (indicates mitral valve leaflets are still mobile) - Low volume pulrse - Malar flush - AF secondary to high atrial pressure and enlargement

Answer 94

- Rheumatic fever (main cause)

Answer 95

Asymptomatic > regular echos to monitor Symptomatic > percutaneous mitral balloon valvotomy or mitral valve surgery Associated AF > anticoagulate with warfarin

Answer 96

- Second most common valvular disease after AS - Asymptomatic common in healthy patients and doesnt necessarily need treatment - Symptoms include fatigue, SOB, oedema due to LVH/arrhythmias/pulmonary hypertension - Pansystolic murmur best at apex and radiating to axilla - Quiet S1 and split S2 - Broad p wave on ECG

Answer 97

- Post-MI/coronary artery disease - Mitral valve prolapse (trivial) - Infective endocarditis (vegetations prevent valve from closing properly) - Rheumatic fever - Congenital

Answer 98

- Acutely given nitrates, diuretics, inotropes, balloon pump - ACEis/B-blockers for heart failure - Surgery if acute and severe > aim to repair rather than replace

Answer 99

Louder on expiration > AS, HOCM Louder on inspiration > PS, atrial septal defect

Answer 100

- Mitral/tricuspid regurgitation - Ventricular septal defect

Answer 101

- Mitral valve prolapse - Coarctation of the aorta

Answer 102

- Aortic regurgitation (high pitched and blowing) - Pulmonary regurgitation

Answer 103

- Mitral stenosis (rumbling) - Severe aortic regurgitation (asutin flint)

Answer 104

S3: Caues by the twanging of the chordae tendinae - in young pts this can be normal but in older pts this is likely due to HF as the chordae are weaker S4: Always abnormal Caused by a stiff/hypertrophic ventricle 'Le lub dub'

Answer 105

AKA thromboangitis obliterans - Small and medium vessel vasculitis that is strongly associated with smoking - Symptoms include extremity ischaemia, claudication, ischaemic ulcers, superfical thrombophlebitis and Raynauds

Answer 106

- Haemmorhage - Teratogenic (can be used in breastfeeding mothers) - Skin necrosis due to reduced protein C (avoid by concurrent heparin) - Purple toes

Answer 107

- Autosomal dominent disorder of muscle tissue - Mutation in gene encoding B-myosin heavy chaing or myosin-binding protein C - Causes LVH > decreased compliance >decreased cardiac output - Biopsy shows myofibrillar hypertrophy with chaotic and disorganised fashion myocytes - Echo shows MR, SAM ASH - MR, systolic anterior motion, asymmetric hypertrophy - Prevalence 1/500 - Associated with Friedreich's ataxia and WPW - Commonly associated with supraventricular arrhythmias

Answer 108

Ventricular tachycardia secondary to ischaemia in the context of extreme exertion

Answer 109

- High dose beta blockers or CCBs (verapamil, diltiazem) - Surgical septal myectomy if drug refractory and resting gradient >50 mmHg - Dual chamber pacing - Alcohol septal ablation (inject alcohol into LAD to cause septal MI which reduces septal hypertrophy) If sustained or symptomatic VT/VF or high risk for sudden death > offer ICD and/or amiodarone

Answer 110

- 90% of cases - Causes; idiopathic, IHD, peripartum, HTN, iatrogenic, alcohol/cocaine, inherited, DMD - Dilated heart leads to predominantly systolic dysfunction - All 4 chambers dilated but left ventricle more so - Causes classical findings of HF - Balloon appearance on CXR

Answer 111

- Diastolic dysfunction of a non-dilated ventricle - Least common of cardiomyopathies - Caused by amyloid/sarcoid/genetics

Answer 112

AKA broken heart syndrome - Sudden dysfunction of the left ventricle of heart, symptoms alike MI but in the absence of significant CAD - Usually due to severe emotional or physical stress - Treat similar to STEMI with antiplatelets, statins, beta blockers, ACE/ARB

Answer 113

- Second most common cause of sudden death after HOCM - Autosomal dominant - Right ventricular myocardium replaced by fatty and fibrofatty tissue - Mutation in gene which encodes desmosome - Presents as palpitations/syncope/SCD - ECG shows epsilon wave and TWI v1-v3 - Echo not particularly helpful, MRI shows fibrofatty tissue

Answer 114

- Sotalol - Catheter ablation to prevent VT - ICD

Answer 115

- Autosomal recessive variant of ARVC - Causes triad of ARVC, palmoplantar keratosis and wooly hair

Answer 116

- Autosomal dominant disease with mutation in SCN5A gene which encodes the myocardial sodium ion channel protein - May present as sudden cardiac death - More common in Asians - ECG shows convex ST elevation and partial RBBB - ECG changes EXACERBATED by fleicanide or ajmaline; this is diagnositc - Manage with ICD

Answer 117

- Congenital accessory conducting pathway between atria and ventricles leading to atrioventricular re-entry tachycardia - Can degenerate radpidly to VF - ECG shows short PR, wide QRS with slurred upstroke (delta wave) - Associated with HOCM, mitral valve proplapse, thyrotoxicosis

Answer 118

Type A - left sided pathway, causes RAD and dominant R wave in V1 Type B - right sided pathway, causes LAD and NO dominant R wave

Answer 119

Definitive - radiofrequency ablation of accessory pathway Medical - sotalol (provided no AF), amiodarone, flecanide

Answer 120

Use - vasodilatory drug used in angina SE - headache, flushing, skin/mucosal/eye/GI ulcers

Answer 121

MI has affected inferior leads (right coronary arteries also provide blood supply to the AV node) - II, III, avF will have ST elevation

Answer 122

Hypertension: - Can drive unless Group 2 in which you can only drive if <180/100 consistently Angioplasty: - 1 week off CaBG: - 4 weeks off ACS (medical treatment): - 4 weeks off Pacemaker: - 1 week off Angina: - Cannot drive if symptoms at rest of at the wheel ICD: - 1 month if prophylactic insertion - 6 monhts if implanted for sustained ventricular arrhythmia Aortic aneurysm: - If >6cm, notify VLA, they will decide - If >6.5cm, can't drive Heart transplant: - 6 weeks off, no need to notify DVLA

Answer 123

- Check U&Es before treatment initiation and after increasing dose - A change in the creatinine of up to 30% from baseline and potassium up to 5.5 is deemed acceptable

Brainscape's Knowledge GenomeTM

Cardiology Flashcards

Brainscape's Knowledge Genome^TM