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Cardiology Flashcards

1
Q

What are the inferior leads and supplying coronary artery?

A

II, III, aVF: right coronary artery

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2
Q

What are the anteroseptal leads and supplying coronary artery?

A

V1-4: left anterior descending artery

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3
Q

What are the lateral leads and supplying coronary artery?

A

I, aVL, V5-6: circumflex artery

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4
Q

Which territory of the heard is most likely in an MI with bradycardia?

A

inferior - right coronary artery supplies SAN and AVN (also RA, RV, inferior portion LV and posterior septum)

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5
Q

Which 3 medications should be avoided in HOCM?

A
  1. ACE inhibitors
  2. inotropes
  3. nitrates
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6
Q

What are 3 findings on ECHO in HOCM?

A

MR SAM ASH
1. mitral regurgitation
2. systolic anterior motion of the anterior mitral valve leaflet
3. asymmetric hypertrophy

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7
Q

What is the treatment approach to HOCM?

A

A-E
Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis

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8
Q

Which 2 medications do all patients with ACS receive?

A

aspirin 300mg + nitrates

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9
Q

What are the ECG criteria for a STEMI?

A
  • clinical symptoms >20 min
  • persistent (>20 min) ECG features in 2 consective leads of:
  • >2.5mm STE in V2-V3 in men under 40y or >2mm STE in V2-V3 in men >40y
  • >1.5mm STE in V2-V3 in women
  • 1mm STE in other leads
  • new LBBB
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10
Q

What are the 2 branches of the management of STEMI?

A

is PCI available within 120 minutes (2 hours) [of when fibrinolysis can be given]?
* if yes: give prasugrel, give UFH + bailout glycoprotein IIb/IIIa inhibitor, perform PCI preferably with drug-eluting stent
* if no: give antithrombin (e.g. fondaparinux) at the same time as fibrinolysis. afterwards give ticagrelor

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11
Q

How should antiplatelets be managed in STEMI with bleeding risk?

A

if bleeding risk give ticagrelor instead of prasugrel, or clopidogrel instead of ticagrelor
if patients on anticoagulants swap prasugrel for clopidogrel

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12
Q

If patients with STEMI present after 12 hours how should they be managed?

A

consider PCI if ongoing myocardial ischaemia

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13
Q

What should be done if a patient’s ECG shows ongoing ST elevation following fibrinolysis?

A

transfer to centre for PCI

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14
Q

What medical treatments are given before and alongside PCI in STEMI?

A
  • before: DAPT - aspirin + prasugrel (or clopidogrel if on anticoagulation)
  • during: UFH + bailout glycoprotein IIb/IIIa inhibitor. if femoral access - bivalirudin
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15
Q

What medications should be given alongside fibrinolysis for STEMI?

A

antithrombin e.g. fondaparinux

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16
Q

What should be done after fibrinolysis for STEMI?

A

ECG at 60-90 minutes; if ongoing STE -> transfer for PCI

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17
Q

What are 7 signs of severe aortic stenosis?

A
  1. Narrow pulse pressure
  2. Slow rising pulse
  3. Delayed ESM
  4. Soft/ absent S2
  5. S4
  6. Left ventricular hypertrophy or failure
  7. Thrill
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18
Q

What are 5 causes of aortic stenosis?

A
  1. Degenerative calcification (commonest >65y)
  2. Bicuspid valve (commonest <65y)
  3. Williams syndrome (supravalvular)
  4. Rheumatic heart disease
  5. HOCM - subvalvular
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19
Q

What is the main indication for valve replacement in aortic stenosis?

A

Symptomatic

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20
Q

When should surgery be considered for aortic stenosis?

A

If pressure gradient is >40mmHg and presence of left ventricular systolic dysfunction

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21
Q

What are 2 options for surgical management of aortic stenosis?

A
  1. Replacement - surgical AVR or transcatheter AVR (TAVR)
  2. Balloon valvuloplasty
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22
Q

When is surgical AVR the treatment of choice for aortic stenosis?

A

Young, low/medium operative risk patients

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23
Q

When is TAVR the procedure of choice for aortic stenosis?

A

High operative risk patients

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24
Q

What are 2 situations when balloon valvuloplasty is the treatment of choice for aortic stenosis?

A
  • children with no aortic valve calcification
  • adults with critical aortic stenosis who aren’t fit for valve replacement
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25
Q

When does atrioventricular heart block require treatment and how?

A

requires treatment if patient symptomatic (syncope/ pre-syncope/ hypotension/ bradycardia) - trancutaneous pacing

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26
Q

What is the management for isolated systolic hypertension (diastolic BP normal)?

A

NICE recommends same as standard hypertension

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27
Q

What is the management of SVT (stepwise, 3 aspects)?

A
  1. vagal manouevres (carotid massage, blowing into empty plastic syringe)
  2. IV adenosine
  3. electrical cardioversion (indicated if shock i.e. hypotensive; only if pulse is present)
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28
Q

What doses of adenosine are given in SVT?

A
  • 6mg IV
  • if unsuccessful 12mg
  • if unsuccessful further 18mg
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29
Q

If IV adenosine doesn’t work to arrest SVT what can be tried next?

A

electrical cardioversion

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30
Q

When is adenosine contraindicated for SVT and what can be given instead?

A

asthma - verapamil

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31
Q

What are 2 things that can be used for prevention of paroxysmal SVT episodes?

A
  1. beta blockers
  2. radio-frequency ablation
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32
Q

What are 5 aspects of the management of acute heart failure?

A
  1. high flow O2 and sit upright
  2. morphine if CP / severe distress
  3. IV furosemide
  4. IV GTN (if SBP >90)
  5. CPAP or NIV if acidotic / not responding to above
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33
Q

What are 3 haemodynamic findings in acute cardiac failure?

A
  1. increased right an dleft-sided ventricular filling pressures
  2. reduced cardiac index
  3. reduced cardiac output
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34
Q

What happens to the RAS in heart failure?

A
  • activation of RAS
  • salt and water retention
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35
Q

What are 3 aspects of the management of heart failure once the acute phase has been stabilised?

A
  1. ACEi
  2. beta blockers
  3. aldosterone antagonist e.g. spironolactone
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36
Q

What forms first line therapy for heart failure?

A

ACEi and beta blocker

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37
Q

What is second line therapy in heart failure already on ACEi and beta blocker?

A

Mineralocorticoid antagonists e.g. eplerenone, spironolactone

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38
Q

What drug has increasing evidence to support its use in heart failure (reduce hospitalisation and cardiovascular death) and therefore can be used as add on therapy?

A

SGLT2 inhibitors e.g dapagliflozin

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39
Q

What can be used as an add on to optimised care in heart failure, with evidence of reducing hospitalisation and cardiovascular death?

A

SGLT2 inhibitors

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40
Q

What are 5 options for third line therapy in heart failure?

A
  1. Ivabradine
  2. Digoxin
  3. Sacubitril-Valsartan
  4. Hydralazine + nitrate
  5. Cardiac resynchronisation therapy
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41
Q

What are 2 criteria for starting ivabradine as third line treatment for heart failure?

A
  1. HR > 75bpm
  2. LVEF < 35%
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42
Q

What is the criteria for sacubitril-valsartan for third line heart failure treatment?

A

LVEF <35%

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43
Q

When can sacubitril-valsartan be started in Heart failure treatment?

A

After ACEi/ARB washout period

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44
Q

Does digoxin improve mortality in heart failure?

A

No but can improve symptoms

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45
Q

When is digoxin strongly indicated for heart failure treatment?

A

Coexistence AF

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46
Q

When is hydralazine with a nitrate particularly indicated in heart failure?

A

African Caribbean patients

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47
Q

When is CRT indicated in heart failure?

A

patients with widened QRS E.g. LBBB

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48
Q

What are 5 drugs prescribed first line in stable angina?

A
  1. Aspirin
  2. Statin
  3. GTN
  4. beta blocker OR rate limiting CCB (verapamil / diltiazem)
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49
Q

What is the next step after first line therapy for angina?

A
  • if on beta blocker - add longer acting dihydropyridine CCB E.g. amlodipine
  • if on CCB add beta blocker (avoid verapamil + beta blocker -> heart block)
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50
Q

If a patient with angina is on monotherapy (beta blocker or CCB) what are 4 alternative medications to add if CCB/beta blocker not tolerated?

A
  1. Long-acting nitrate e.g. IMN
  2. Ivabradine
  3. Nicarondil
  4. Ranolazine
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51
Q

Which anti-anginal drug needs asymmetric dosing?

A

STANDARD release ISMN - need 10-14 hour drug free window (due to tolerance - don’t have same issue with MR form)

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52
Q

What is first line line treatment for T2DM if metformin (inc MR) is not tolerated in
a) normal QRISK
b) QRISK >10

A

a) sulphonylurea or DPP4 inhibitor or glitazone
b) SGLT2 inhibitor

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53
Q

What is the definition of prolonged QT interval?

A

Males >450ms
Females >460ms

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54
Q

What is Wolff-Parkinson White syndrome?

A

congenital accessory conducting pathway between atria and ventricles, leading to atrioventricular re-entry tachycardia (AVRT)

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55
Q

What are 4 ECG features in WPW syndrome?

A
  1. short PR interval
  2. slurred upstroke at start of QRS complex - delta wave
  3. wide QRS complexes
  4. left axis deviation if R sided pathway, RAD if L sided pathway
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56
Q

What are types A and B WPW syndrome?

A
  • type A: L sided pathway - dominant R wave in V1
  • type B: R sided pathway - no dominant R waves in V1
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57
Q

What are 5 associations of WPW?

A
  1. HOCM
  2. mitral valve prolapse
  3. Ebstein’s anomaly
  4. thyrotoxicosis
  5. secundum ASD
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58
Q

What is the definitive management of WPW syndrome?

A

radiofrequency ablation of accessory pathway

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59
Q

What are 3 options for medical therapy of WPW?

A
  1. sotalol
  2. amiodarone
  3. flecainide
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60
Q

Which of the options for medical therapy for WPW should be avoided in certain circumstances & when?

A
  • sotalol - avoid in co-existent AF - prolonging refractory period at AV node may increase rate of transmission through accessory pathway, increasing ventricular rate and potentially deteriorating into VF
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61
Q

What 5 drugs for secondary prevention should patients who have had ACS be commenced on?

A
  1. aspirin - indefinitely
  2. clopidogrel - 12 months
  3. ACE inhibitor
  4. beta blocker
  5. statin
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62
Q

How long should beta blockers be continued as secondary prevention after ACS?

A
  • if reduced LVEF - indefinitely
  • if normal - may discontinue >12 months
  • diltiazem or verapamil may be alternative in aptients wihtout pulmonary congestion / reduced LVEF
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63
Q

What are 3 options for the treatment of acute heart failure with hypotension <85 mmHg / cardiogenic shock?

A
  1. inotropic agents e.g. dobutamine (esp. severe LV dysfunction)
  2. vasopressor agents e.g. norepinephrine (if insufficient response to inotropes, end-organ hypoperfusion)
  3. mechanical circulatory assistance e.g. intra-aortic balloon counterpulsation, ventricular assist devices
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64
Q

What is synchronised cardioversion vs. desynchronised?

A
  • synchronised used for unstable AF, atrial flutter, atrial tachycardia, SVTs
  • unsynchronised = defibrillation, indicated for pulseless VT/VF, unstable polymorphic VT
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65
Q

What is the recommended rate control approach for management of AF?

A
  • beta blocker or rate limiting calcium channel blocker (e.g. diltiazem/verapamil) first line
  • if monotherapy not sufficient - add beta blocker, diltiazem, digoxin
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66
Q

How is the CHADSVasc score calculated?

A
  • C = congestive cardiac failure
  • H = hypertension
  • A = age; 1 point for 65-74, 2 points >75
  • D = diabetes mellitus
  • S = prior stroke/ TIA / VTE = 2 points
  • Vasc = ischaemic heart disease or peripheral arterial disease
  • S = sex (female)
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67
Q

What dods the CHADSVascS score translate to in terms of management?

A
  • 0 = no treatment
  • 1 = males - consider anticoag; females = no treatment (just for being female)
  • 2 = offer anticoag
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68
Q

Why is balloon valvuloplasty for aortic stenosis reserved for patients who cannot undergo surgical intervention?

A

efficacy lasts for approximately 6-12 months

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69
Q

What is the first line antiplatelet treatment for medically-managed ACS?

A

aspirin lifelong, ticagrelor 12 months

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70
Q

What is first line antiplatelet treatment for ACS managed with PCI?

A

Aspirin lifelong, prasugrel or ticagrelor 12 months

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71
Q

Why is it very important to recognise long QT syndrome?

A

can lead to ventricular tachycardia/torsade de pointes - can cause collapse/sudden death

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72
Q

What causes the most common variants of LQTS?

A

LQT1 and LQT2: defects in alpha subunit of slow delayed rectifier potassium channel

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73
Q

What are 2 congenital causes of prolonged QT interval?

A
  1. Jervell-Lange-Nielsen syndrome (includes deafness + due to abnormal K+ channel)
  2. Romano-Ward syndrome (no deafness)
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74
Q

What are 10 drugs that can cause long QT syndrome?

A
  1. amiodarone
  2. sotalol
  3. TCAs
  4. SSRIs
  5. methadone
  6. chloroquine
  7. terfenadine
  8. erythromycin
  9. haloperidol
  10. ondansetron
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75
Q

What are 3 electrolyte abnormalities that can cause long QT syndrome?

A
  • hypokalaemia
  • hypocalcaemia
  • hypomagnesaemia
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76
Q

Other than electrolyte abnormalities and drugs, what are 4 acquired causes of long QT syndrome?

A
  1. acute MI
  2. myocarditis
  3. hypothermia
  4. subarachnoid haemorrhage
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77
Q

What clinical features differentiate long QT1/QT2/QT3?

A
  • QT1: exertional syncope, swimming
  • QT2: syncope from emotional stress, exercise or auditory stimuli
  • QT3: events occur at night/rest
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78
Q

What are 3 aspects of the management of long QT syndrome?

A
  1. avoid drugs which prolong QT + other precipitants e.g. strenuous exercise
  2. beta blockers (NOT sotalol)
  3. implantable cardioverter defibrillators in high risk cases
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79
Q

What are 5 ECG findings in hypokalaemia?

A
  1. u waves
  2. small or absent T waves (occasionally inverted)
  3. prolonged PR interval
  4. ST depression
  5. long QT
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80
Q

Which artery supplies the inferior heart (leads II, III, aVF)?

A

Right coronary artery

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81
Q

Which artery supplies the anterolateral heart (leads I, V1-V6, aVL)?

A

Proximal left anterior descending artery

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82
Q

Which artery supplies the lateral heart (I, aVL, +- V5-6)?

A

Left circumflex

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83
Q

What ECG changed will be seen in a posterior STEMI?

A
  • changes in V1-3
  • horizontal ST depression
  • tall, broad R waves
  • upright T waves
  • dominant R wave in V2
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84
Q

Which arteries supply the posterior heart?

A

L circumflex and R coronary

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85
Q

What ECG changes are seen in posterior STEMI?

A
  • changes in V1-3
  • horizontal ST depression
  • tall, broad R waves
  • upright T waves
  • dominant R wave in V2
86
Q

What is the algorithm for ALS with shockable rhythms (VF, pulseless VT)?

A
  • chest compressions: ventilation 30:2
  • single shock followed by 2 minutes CPR
  • adrenaline 1mg once chest compressions restarted after 3rd shock
  • amiodarone 300mg after 3 shocks
  • further dose amiodarone 150mg after 5 shocks
87
Q

What is the algorithm for ALS with non-shockable rhythms (PEA, asystole)?

A
  • chets compression: ventilation ratio 30:2
  • adrenaline 1mg ASAP
  • repeat adrenaline 1mg every 3-5 minutes while ALS continues
  • NO amiodarone
88
Q

How can shocks be delivered for a shockable rhythm in an arrest that is witnessed in a monitored patient (e.g. in CCU)?

A

up to 3 quick successive (stacked) shocks

89
Q

What should be attempted if IV access is not possible during an arrest?

A

intraosseous route

90
Q

What can be used as an alternative to amiodarone if it is not available?

A

lidocaine

91
Q

What are the target oxygen saturations after ROSC following an arrest?

A

aim 94-98% to avoid potential harm caused by hyperoxaemia

92
Q

In a R sided accessory pathway in Wolff-Parkinson-White syndrome which way will the axis be?

A

L axis deviation (if L sided pathway - RAD)

93
Q

What is a major disadvantage of biological (bioprosthetic) valves?

A

structural deterioration and calcification over time

most older patients receive bioprosthetic valves

94
Q

What anticoagulation is required for bioprosthetic valves?

A
  • long-term anticoagulation not usually needed; warfarin may be given for first 3 months depending on patient factors
  • low dose aspirin given long-term
95
Q

What is the most common type of mechanical valve and what other types were previously popular?

A

bileaflet valve; ball and cage valves now rarely used

96
Q

What is the major disadvantage of mechanical valves?

A

increased risk of thrombosis - require long-term anticoagulation with warfarin

97
Q

What is the target INR for patients taking warfarin for mechanical heart valves?

A
  • aortic: 3.0
  • mitral: 3.5
98
Q

Which valve is classically affected in infective endocarditis in IVDU?

A

tricuspid valve

99
Q

In patients without risk factors / previously normal valves, which valve is most commonly affected in infective endocarditis?

A

mitral valve

100
Q

What is the most common organism to cause infective endocarditis?

A

Staphylococcus aureus

101
Q

Which patients with I.E. caused by IV drug use what is the commonset organism?

A

staph aureus

102
Q

Which organisms that cause I.E. are linked to dental hygiene?

A

Streptococcus viridans:
* Steptococcus mitis
* Streptococcus sanguinis

103
Q

Which organisms cause infective endocarditis following prosthetic valve surgery due to perioperative contamination?

A

Streptococcus epidermidis

104
Q

What pre-existingi disease is linked with infective endocarditis caused by Streptococcus bovis?

A

colorectal cancer (subtype Streptococcus gallolyticus most linked)

105
Q

What is Libman-Sacks endocarditis?

A

endocarditis associated with systemic lupus erythematosus

106
Q

What is an example of an inotrope?

A

dobutamine

107
Q

What is an example of a vasopressor?

A

noradrenaline

108
Q

What is an indication for inotropes e.g. dobutamine in acute heart failure?

A

LVSD

109
Q

When are vasopressors (e.g. noradrenaline) used in the treatment of acute heart failure?

A

when there is poor response to inotropes and evidence of end-organ hypoperfusion

110
Q

Should ACEi and beta-blockers be stopped in an acute exacerbation of heart failure?

A

no - only stop beta blockers if HR <50, second or third degree AV block, or shock

111
Q

What are 2 categories of causes of aortic regurgitation?

A
  1. valve disease
  2. aortic root disease / ascending aorta disease
112
Q

What are 5 valve disease causes of aortic regurgitation?

A
  1. rheumatic fever (commonest in West)
  2. calcific valve disease
  3. connective tissue diseases e.g. RA, SLE
  4. bicuspid aortic valve
  5. infective endocarditis (acute presentation)
113
Q

What are 6 causes of aortic regurgitation due to aortic root disease?

A
  1. bicuspid aortic valve
  2. spondyloarthropathies e.g. ankylosing spondylitis
  3. HTN
  4. syphilis
  5. Marfan’s, Ehler’s Danlos syndrome
  6. aortic dissection
114
Q

What are 6 clinical features of aortic regurgitation?

A
  1. early diastolic murmur (increased by handgrip manoeuvre)
  2. collapsing pulse
  3. wide pulse pressure
  4. Quincke’s sign (nailbed pulsation)
  5. De Musset’s sign (head bobbing)
  6. mid-diastolic Austin-Flint murmur if severe
115
Q

What is the management of aortic regurgitation?

A
  • medical management of any HF
  • surgery if symptomatic + severe, asymptomatic but severe with LVSD
116
Q

What echocardiography finding in the newborn is indicative of transposition of the great arteries?

A

parallel aorta and pulmonary trunk

117
Q

What causes transposition of the great arteries?

A

failure of aorticopulmonary septum to spiral during septation - aorta leaves right ventricle, pulmonary trunk leaves left

118
Q

What is a risk factor for transposition of the great arteries?

A

diabetes in the mother

119
Q

What x-ray appearance is seen in transposition of the great arteries?

A

egg-on-side appearance

120
Q

What is the management of transposition of the great arteries?

A

prostaglandin E1 to maintain ductus arteriosus patency; surgical correction is definitive

121
Q

What is the presentation of left ventricular aneurysm following a recent MI?

A

persistent ST elevation after recent MI, no chest pain, left ventricular failure

increases risk of ventricular thrombus formation

122
Q

What are 10 complications of acute myocardial infarction?

A
  1. cardiac arrest
  2. cardiogenic shock
  3. chronic heart failure
  4. tachyarrhythmias
  5. bradyarrhythmias
  6. pericarditis
  7. left ventricular aneurysm
  8. left ventricular free wall rupture
  9. ventricular septal deefct
  10. acute mitral regurgitation
123
Q
A
124
Q

What is the most common cause of death following an MI?

A

ventricular fibrillation and arrest

125
Q

Within what time period can pericarditis commonly occur following transmural MI?

A

first 48 hours

126
Q

When does Dressler’s syndrome tend to develop following MI?

A

2-6 weeks following MI

127
Q

What is thought to be the underlying pathophysiology of Dressler’s syndrome?

A

autoimmune reaction against antigenic proteins formed as myocardium recovered

128
Q

What are the clinical features of Dressler’s syndrome?

A

fever, pleuritic pain, pericardial effusion, raised ESR

129
Q

what is the treatment of Dressler’s syndrome?

A

NSAIDs

130
Q

How soon after myocardial infarction does left ventricular free wall rupture tend to occur?

A

1-2 weeks afterwards

131
Q

How do patients present with left ventricular free wall rupture?

A

raised JVP, pulsus paradoxus, diminished heart sounds

132
Q

What is the management of left ventricular free wall rupture?

A

urgent pericardiocentesis and thoracotomy

133
Q

When does ventricular septal defect occur following MI?

A

in the first week

134
Q

What are the features of a ventricular septal defect following MI?

A

acute heart failure associated with pansystolic murmur

135
Q

What is diagnostic of ventricular septal defect following MI and why else is it useful?

A

echocardiogram - excludes acute mitral regurgitation (presents similarly)

136
Q

What is the management of ventricular septal defect following MI?

A

acute surgical correction

137
Q

What is the presentation of acute mitral regurgitation following MI?

A

acute hypotension and pulmonary oedema, early to mid systolic murmur

138
Q

Which type of MI is more commonly associated with acute mitral regurgitation as a complication?

A

infero-posterior infarction - due to ischaemia or rupture of the papillary muscle

139
Q

What is the treatment of acute mitral regurgitation due to MI?

A

vasodilator therapy, often require emergency surgical repair

140
Q

What are 4 medications that can exacerbate heart failure?

A
  1. thiazolidinediones (pioglitazone)
  2. verapamil
  3. NSAIDs / glucocorticoids
  4. class I antiarrhythmics - flecainide
141
Q

What is the first-line treatment for Torsades-de-Pointes?

A

IV magnesium sulfate

NB: amiodarone CI as can prolong QT interval

142
Q

What is are the management options for atrial flutter?

A
  • similar to AF
  • more sensitive to cardioversion - lower energy levels can be used
  • radiofrequency ablation of tricuspid valve isthmus - curative in most
143
Q

What drug should be started in patients with a background of type 2 diabetes who are newly diagnosed with hypertension?

A

ACE inhibitor or angiotensin receptor blocker, regardless of age

144
Q

What is the pathophysiology of HOCM?

A
  • usually mutation in the gene encoding β-myosin heavy chain protein or myosin-binding protein C
  • predominantly diastolic dysfunction: left ventricle hypertrophy → decreased compliance → decreased cardiac output
  • characterized by myofibrillar hypertrophy with chaotic and disorganized fashion myocytes (‘disarray’) and fibrosis on biopsy
145
Q

What are 5 symptoms of HOCM?

A
  1. often asymptomatic
  2. exertional dyspnoea
  3. angina
  4. syncope - often following exercise
  5. sudden death (ventricular arrhythmias)
146
Q

What are 6 examination signs of HOCM?

A
  1. arrhythmias
  2. heart failure
  3. jerky pulse
  4. large a waves
  5. double apex beat
  6. systolic murmurs - ejection systolic / pansystolic
147
Q

What causes syncope in HOCM?

A

subaortic hypertrophy of ventricular septum - functional aortic stenosis

148
Q

What is the most common cause of sudden death in HOCM?

A

ventricular arrhythmias

149
Q

What causes systolic murmurs in HOCM?

A
  • ejection systolic murmur: L ventricular outflow tract obstruction
  • pansystolic murmur - systolic anterior motion of mitral valve - causes mitral regurgitation
150
Q

What are 2 conditions associated with HOCM?

A
  1. Friedrich’s ataxia
  2. Wolff-Parkinson White
151
Q

What are 4 ECG findings in HOCM?

A
  1. L ventricular hypertrophy
  2. non-specific ST segment and T waves abnormalities (progressive T wave inversion)
  3. deep Q waves
  4. AF (occasionally)
152
Q

What are the classes of NYHA for heart failure?

A
  • I: no symptoms, no limitations to ordinary physical exercise
  • II: mild symptoms, slight limitation of ordinary physical activity but comfortable at rest
  • III: moderate symptoms, marked limitation of less than ordinary physical activity but comfortable at rest
  • IV: severe symptoms, unable to carry out any physical activity without discomfort, symptoms at rest
153
Q

What is used to risk-stratify patients with NSTEMI to guide management, and what 6 things does this take into account?

A

GRACE score
1. age
2. heart rate + BP
3. cardiac (Kilip class) and renal function (creatinine)
4. cardiac arrest on presentation
5. ECG findings
6. troponin levels

154
Q

What are 3 options for management of patients with NSTEMI after MONA depending on risk stratification?

A
  1. immediate PCI (+UFH) - clinically unstable e.g. hypotensive
  2. PCI within 72h (+ fondaparinux immediately) - GRACE > 3% (intermediate, high or highest risk) or ischaemia after admission
  3. conservative management - DAPT
155
Q

What guides DAPT in NSTEMI managed conservatively?

A
  • all have aspirin
  • high bleeding risk: clopidogrel
  • not high bleeding risk: ticagrelor
156
Q

What are 2 types of non-drug management for heart failure?

A
  1. cardiac resynchronisation therapy
  2. exercise training
157
Q

Does CRT improve patient outcomes in heart failure?

A

yes - improves symptoms and reduces hospitalisation in NYHA class III patients

158
Q

Which patients with heart failure should have CRT?

A

wide QRS

159
Q

What are the outcomes for patients with exercise training who have heart failure?

A

improves symptoms but not hospitalisation / mortality

160
Q

What are 4 normal variants on ECG when seen in athletes?

A
  1. sinus bradycardia
  2. junctional rhythm
  3. first degree heart block
  4. Mobitz type 1 (Wenckebach phenomenon)
161
Q

What is the name of the triad of features in cardiac tamponade?

A

Beck’s triad
1. hypotension
2. raised JVP
3. muffled heart sounds

162
Q

What is the classic JVP sign in cardiac tamponade?

A

absent Y descent (due to limited R ventricular filling)

163
Q

What is pulsus paradoxus (seen in cardiac tamponade)?

A

abnormally large drop in BP during inspiration

164
Q

What can be seen on an ECG in cardiac tamponade?

A

electrical alternans

165
Q

What are 4 differences between cardiac tamponade and constrictive pericarditis?

A
  1. in cardiac tamponade there is absent Y descent, X+Y present in constrictive pericarditis
  2. cardiac tamponade has pulsus paradoxus but this is absent in constrictive pericarditis
  3. Kussmaul’s rare in CT but present in constrictive pericarditis
  4. Pericardial calcification on CXR in constrictive pericarditis
166
Q

What is the management of cardiac tamponade?

A

urgent percardiocentesis

167
Q

What are the 2 types of aortic dissection per the Stanford classification?

A
  • type A: ascending aorta, 2/3 of cases
  • type B: descending aorta, distal L subclavian origin, 1/3 of cases
168
Q

What proportion of aortic dissections are Stanford type A vs B?

A
  • A: 2/3
  • B: 1/3
169
Q

What is the DeBakey classification of aortic dissection?

A
  • type I: originates in ascending aorta, extends to aortic arch +- distally
  • type II: originates in + confined to ascending aorta
  • type III: originates in descending arta (can extend distally, rarely proximally)
170
Q

What is the investigation of choice for aortic dissection and what is the key finding?

A

CT angiography chest, abdo pelvis - false lumen

171
Q

When is TOE used in diagnosis of aortic dissection?

A

patients too unstable to take to CT

172
Q

What is the management of Stanford type A dissection?

A
  • surgical
  • BP must be controlled to target SBP 100-120 whilst awaiting surgery
173
Q

What is the management of Stanford type B dissection?

A
  • conservative
  • bed rest
  • IV labetalol to reduce BP
174
Q

What are the possible complications of aortic dissection?

A
  • backward tear: aortic incompetence / reugurgitation, inferior MI
  • forward tear: unequal arm pulses, stroke, renal failures
175
Q

When can PDE5 inhibitors (e.g. sildenafil) be given in patients after MI?

A

6 months afterwards - but avoid in patients prescribed either nitrates or nicorandil

176
Q

When should aldosterone antagonist e.g. eplerenone be used post MI

A

symptoms and/or signs of heart failure and LVSD - initiate within 3-14 days of MI (after ACEi)

177
Q

What is the mechanism of action of aspirin?

A
  • non-reversible COX 1 and 2 inhibitor
  • inhibits conversion of arachidonic acid to prostaglandin, prostacyclin and thromboxane
  • thromboxane A2 promotes platelet aggregation and vasoconstriction
178
Q

What are 3 drugs that aspirin potentiates?

A
  1. oral hypoglycaemics
  2. warfarin
  3. steroids
179
Q

Why should aspirin be used in children <16 y?

A

risk of Reye’s syndrome (with exception fo Kawasaki disease)

180
Q

When is statin offered in CKD?

A

if eGFR < 60

181
Q

In primary prevention, when should the dose of atorvastatin be increased from 20mg ON?

A

if non-HDL cholesterol doesn’t fall by 40% and eGFR > 30, at 3 months

182
Q

What is DVLA guidance on driving after ACS that has been successfully treated by coronary angioplasty?

A

stop driving for at least 1 week, no need to inform DVLA as long as:
* no other urgent revascularisation (< 4weeks) is planned
* L ventricular ejection fraction at least 40% prior to d/c
* no other disqualifying condition

183
Q

What is DVLA guidance on driving after ACS that has not been treated by coronary angioplasty?

A
  • driving can recommence after 4 weeks provided no other disqualifying condition
184
Q

What is the guidance for bus / taxi / lorry drivers after ACS?

A

DVLA needs to be informed, driving needs to cease for at least 6 weeks

185
Q

What is the rule for driving after CABG?

A

4 weeks off driving

186
Q

What is the guidance for driving with angina?

A

driving must cease if symptoms occur at rest / the wheel

187
Q

What is the guidance for driving after pacemaker insertion?

A

1 week off driving

188
Q

What is the guidance for driving with an ICD?

A
  • if implanted for sustained ventricular arrhythmia: cease driving for 6 months
  • if implanted prophylactically then cease driving for 1 month
  • Having an ICD results in a permanent bar for Group 2 drivers
189
Q

What are the rules for driving after successful catheter ablation for an arrhythmia?

A

2 days off driving

190
Q

What are the rules for driving wiht an aortic aneurysm?

A

if 6cm or more - notify DVLA, licensing will be permitted subject to annual review
aortic diameter of 6.5cm or more disqualified patients from driving

191
Q

What are the rules for driving after heart transplant?

A

do not drive for 6 weeks, no need to notify DVLA

192
Q

What are 9 causes of pericarditis?

A
  1. viral infections - coxsackie
  2. TB
  3. uraemia
  4. post MI (early 1-3 days - fibrinous, late weeks/months - autoimmune, Dressler’s)
  5. radiotherapy
  6. conntective tissue disease - SLE, RA
  7. hypothyroidism
  8. malignancy - lung, breast
  9. trauma
193
Q

What are the 2 points at which pericarditis can occur post -MI?

A
  • Early, 1-3 days: fibrinous pericarditis
  • Late, weeks-months: autoimmune pericarditis (Dressler’s syndrome)
194
Q

What is the most specific ECG marker for pericarditis?

A

PR depression

195
Q

What investigation should be performed in all patients with suspected acute pericarditis?

A

transthoracic echocardiography

196
Q

When should patients with pericarditis be managed a an inpatient?

A
  • majority can be OP
  • high risk features: fever > 38, raised troponin - IP
197
Q

What should be advised about physical activity in pericarditis?

A

strenuous physical activity should be avoided until symptom resolution and normalisation of inflammatory markers

198
Q

What is considered first line management for idiopathic or viral pericarditis?

A

NSAIDs and colchicine (until sx resolution / normal IFM) then tapering of dose

199
Q

What are 5 drug causes of secondary hypertension?

A
  1. steroids
  2. monoamine oxidase inhibitors
  3. COCP
  4. NSAIDs
  5. leflunomide
200
Q

What should be the management of Hb < 80 in acute ACS?

A

transfusion of packed red cells (anaemia can worsen ischaemia)

201
Q

Wat is the Hb concentration target after transfusion in ACS?

A

80-100

202
Q

What is the threshold for transfusion in patients a) without ACS b) with ACS?

A
  • without: 70
  • with: 80
203
Q

How is a diagnosis of Brugada syndrome made?

A

Coved ST segment in V1-V3 followed by inverted T-wave on ECG - seen in southeast asian males in 20s-30s

204
Q

What is the management of Brugada syndrome?

A

same day assessment by cardiology, implantable cardioverter defibrillator (only proven treatment)

205
Q

What is the management of symptomatic bradycardia if atropine fails?

A

external (transcutaneous) pacing

next: isoprenaline/adrenaline infusion

206
Q

What are 4 steps in the management of symptomatic bradycardia?

A
  • atropine 500mcg IV (repeated up to maximum of 3mg)
  • transcutaneous pacing
  • isoprenaline/adrenaline infusion titrated to response
  • transvenous pacing
207
Q

What are 6 factors that can falsely decrease BNP?

A
  1. obesity
  2. diuretics
  3. ACE inhibitors
  4. beta blockers
  5. angiotensin 2 receptor blockers
  6. aldosterone antagonists

DOWN with DRUGS and being FAT

208
Q

What are 10 factors that can falsely increase BNP levels?

A
  1. LVH
  2. ischaemia
  3. tachycardia
  4. R ventricular overload
  5. hypoxaemia (inc PE)
  6. GFR < 60
  7. sepsis
  8. COPD
  9. diabetes
  10. age > 70
  11. liver cirrhosis

INCREASE with being ILL

209
Q

What are 5 drug options to use for accelerated hypertension to lower BP?

A
  1. GTN
  2. sodium nitroprusside
  3. labetalol
  4. nicardipine
  5. phentolamine
210
Q

What is the target for reducing HTN in the first 24-48h?

A

reduction of 25%

too quick will lead to end organ hypoperfusion

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