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Zero to Finals: Medicine A.S. > Cardiology > Flashcards

Cardiology Flashcards

1
Q

list 3 non-modifiable risk factors of CVD

A
  • older age
  • family history
  • being male
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2
Q

list some modifiable risk factors of CVD

A
  • smoking
  • alcohol
  • high sugar / fat, low fruit / veg diet
  • low exercise
  • obesity
  • poor sleep
  • stress
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3
Q

which medical co-morbidities contribute to CVD risk?

A
  • DM
  • HTN
  • CKD
  • inflamm stuff like RA
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4
Q

which conditions can atherosclerosis result in?

A

CARDIAC

  • angina
  • MI

NEURO

  • TIA
  • stroke

PVD

chronic mesenteric ischaemia

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5
Q

how can modifiable risk factors of heart disease be optimised?

A
  • advise on diet, exercise, weight loss
  • stop smoking
  • stop drinking alcohol
  • optimise comorbid condition treatments (like DM)
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6
Q

what is QRISK 3 score? when should a statin be started? what dose?

A
  • the % risk of a patient having a stroke or MI in the next 10 years
  • when risk is >10%
  • atorvastatin 20mg
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7
Q

who should be put on a statin?

A
  • anyone with QRISK 3 score >10%
  • CKD >10 years
  • T1DM >10 years
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8
Q

how can statins affect LFTs? when should LFTs be checked?

A
  • transiently and mildly raised ALT and AST for weeks
  • check LFTs at 3m and 12m
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9
Q

4As of secondary prevention of CVD? (they’re all drugs)

A
  • Aspirin ( + clopidogrel, for DAPT)
  • Atorvastatin
  • Atenolol
  • ACE-i (ramipril)
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10
Q

3 main side effects of statins?

A
  • myopathy (raised CK)
  • T2DM
  • haemorrhagic stroke (rare)
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11
Q

describe the pathophysiology of angina

A
  • narrowed coronary arteries
  • reduced blood flow to myocardium
  • demand > supply
  • causes tight chest pain +/- radiation to jaw / arm
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12
Q

when is angina “stable”?

A

when symptoms are completely relieved by GTN

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13
Q

when is angina “unstable”?

A

when symptoms come on at rest

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14
Q

gold standard investigation for angina?

A

CT coronary angiogram

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15
Q

what are the baseline investigations for angina? why are they each important?

A
  • physical exam (?HF, heart sounds, BMI)
  • ECG
  • FBC (?anaemia)
  • UEs (before starting ACE-i)
  • LFTs (before starting a statin)
  • Lipid profile
  • TFTs
  • HbA1C, fasting glucose (?DM)
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16
Q

RAMP: management of angina?

A
  • Referral to cardiology
  • Advice on Dx, when to seek help etc
  • Meds
  • Procedural (surgical) interventions
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17
Q

which drug classes are used in angina management?

A
  • short acting nitrites (GTN)
  • BB
  • CCB
  • long acting nitrites (isosorbide mononitrate)
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18
Q

what are the 2 surgical interventions for angina treatment?

A
  • PCI (stent)
  • CABG
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19
Q

who gets offered surgical interventions in angina management?

A

those with severe stenosis seen on CT coronary angiography

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20
Q

which 2 surgical scars does CABG leave?

A
  • midline sternotomy scar
  • scar over great saphenous vein on leg
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21
Q

what does the left coronary artery divide into?

A
  • circumflex
  • left anterior descending (LAD)
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22
Q

which areas of the heart does the circumflex artery supply?

A
  • LA
  • posterior of LV
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23
Q

which areas of the heart does the LAD artery supply?

A
  • anterior of LV
  • anterior of septum
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24
Q

which areas of the heart does the right coronary artery (RCA) supply?

A
  • RA
  • RV
  • inferior of LV
  • posterior of septum
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25
Q

what are the 3 types of acute coronary syndrome (ACS)?

A
  • unstable angina
  • STEMI
  • NSTEMI
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26
Q

what are the diagnostic criteria on ECG for a STEMI?

A

either of these:

  • ST elevation
  • new LBBB
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27
Q

if there is no ST elevation on ECG, what is the next investigation for ACS? what would this show?

A
  • troponin blood tests
  • raised trops + other ECG signs = NSTEMI
  • normal trops + normal ECG = UA / other cause of chest pain
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28
Q

1st line investigation in suspected ACS?

A

ECG

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29
Q

ECG changes in NSTEMI?

A
  • ST depression
  • T wave inversion
  • pathological Q waves
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30
Q

symptoms other than chest pain in ACS?

A
  • N+V
  • sweaty, clammy
  • sense of impending doom
  • SOB
  • palpitations
  • jaw / arm pain
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31
Q

other than ECG and troponins, which other investigations could you do in suspected ACS? what would they show?

A
  • CXR (?pulmonary oedema)
  • echocardiogram (shows damage in heart)
  • CT coronary angiogram (?CAD)
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32
Q

what can be offered if someone presents <2h following a STEMI?

A

primary PCI

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33
Q

what can be offered if someone presents 2-12h following a STEMI? which medications are used here?

A
  • thrombolysis
  • streptokinase, alteplase, tenecteplase
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34
Q

BATMAN: medical management of NSTEMI?

A
  • BB
  • Aspirin 300mg stat
  • Ticagrelor 180mg (or clopidogrel 300mg - ^ bleeding risk)
  • Morphine
  • Anticoagculant (fondaparinux - LMWH) (unless high bleeding risk)
  • Nitrates (GTN)

+ Ox if sats are dropping (<95%)

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35
Q

what is the GRACE score?

A

6 month risk of death / repeat MI in patients who have had an NSTEMI

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36
Q

what GRACE score would qualify for PCI?

A

>5%

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37
Q

complications of MI?

A

D – Death (cardiac arrest)
R – Rupture of the heart septum or papillary muscles
E – “Edema” (Heart Failure)
A – Arrhythmia and Aneurysm
(VF or VT; AV block ,especially after inferior MI)
( LV aneurysm; )
D – Dressler’s Syndrome

Also

  • VSD
  • acute mitral regurg
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38
Q

what is Dressler’s syndrome? when does it occur?

A
  • post-MI inflammation causing pericarditis
  • 2-3 weeks after an MI
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39
Q

presentation of Dressler’s syndrome?

A
  • pleuritic chest pain
  • fever (low grade)
  • pericardial rub on auscultation
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40
Q

what are the ECG changes in Dressler’s syndrome?

A
  • global ST elevation
  • T wave inversion
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41
Q

investigations for Dressler’s syndrome?

A
  • ECG
  • echocardiogram
  • bloods
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42
Q

echo findings in Dressler’s syndrome?

A

shows pericardial effusion

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43
Q

what is seen on bloods in Dressler’s syndrome?

A

raised CRP and ESR (inflamm markers)

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44
Q

management of Dressler’s syndrome?

A
  • NSAIDs (aspirin, ibuprofen)
  • steroids (prednisolone)
  • pericardiocentesis (removes fluid)
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45
Q

what does secondary prevention of MI involve?

A

6As
- Aspirin 75mg OD
- Another antiplatelet e.g. clopidogrel or ticagrelor (12m)
******DAPT
- atorvastatin (80mg OD)
- ACE-i (ramipril)
- Atenolol (or another BB)
- Aldosterone antagonist (spironolactone, EPLERENONE) if HF also present

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46
Q

how does acute LVF result in oedema?

A
  • LV cannot push all the blood out
  • backlog of blood develops in L atrium, pulmonary veins and lungs
  • fluid leaks out of engorged veins into lungs
  • pulmonary oedema
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47
Q

causes of acute LVF?

A
  • iatrogenic (aggressive IV fluids in someone who is frail)
  • sepsis
  • MI
  • arrhythmias
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48
Q

how does acute LVF present?

A
  • rapid onset SOB
  • worse lying flat + better sitting up
  • cough with frothy white / pink sputum
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49
Q

what signs and symptoms might be present in acute LVF which indicate the underlying cause?

A
  • chest pain (MI)
  • fever (sepsis)
  • palpitations (arrhythmias)
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50
Q

what are the findings on examination in acute LVF?

A
  • increased RR (tachypnoeic)
  • reduced O2 sats
  • tachycardia
  • 3rd heart sound
  • bibasal “wet” crackles on auscultation
  • hypotension if severe (cardiogenic shock)
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51
Q

what are the additional findings if the patient with acute LVF also has right-sided heart failure?

A
  • raised JVP
  • peripheral oedema (ankles, legs, sacrum)
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52
Q

investigations for acute LVF?

A
  • ECG (arrhythmia, MI)
  • ABG (sats)
  • CXR (oedema)
  • FBC, UE (infection, renal function)
  • BNP (CCF)
  • troponin (MI)
  • echocardiogram (shows LV function)
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53
Q

is BNP sensitive or specific? does this mean it is good for ruling in or ruling out HF?

A
  • sensitive but not specific
  • good for ruling OUT HF when negative but can be raised for other causes
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54
Q

other than HF, what else can cause a raised BNP?

A
  • tachycardia
  • sepsis
  • PE
  • renal impairment
  • COPD
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55
Q

what is ejection fraction? what is a normal ejection fraction?

A
  • proportion of blood pumped out of LV with each contraction
  • >50%
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56
Q

ABCDE: CXR findings in acute / chronic HF?

A
  • Alveolar oedema (bat wing)
  • B lines (Kerley)
  • Cardiomegaly (CTR >0.5)
  • Dilated upper lobe vessels
  • Effusion (pleural)
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57
Q

stop IV SODM: management of acute LVF?

A
  • stop IV fluids
  • Sit up
  • Oxygenate
  • Diuretics (IV furosemide 40mg)
  • Monitor fluid input and output
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58
Q

presentation of chronic heart failure? (5)

A
  • SOBOE
  • cough with frothy white / pink sputum
      • orthopnoea (SOB lying flat, ask about pillows)
    • PND
    • peripheral oedema
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59
Q

how is chronic HF diagnosed? (4)

A
  • clinical exam

Investigations:

  • NT-proBNP
  • echocardiogram
  • ECG
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60
Q

what are the causes of chronic HF?

A
  • IHD
  • aortic stenosis
  • HTN
  • AF and other arrhythmias
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61
Q

what level of NT-proBNP needs an urgent specialist referral?

A

>2000 ng/L

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62
Q

ABAL: drug management of chronic HF? hint: 2 diuretics

A
  • ACE-i (ramipril, avoid if valve disease)
  • BB (bisoprolol)
  • Aldosterone antagonist (spironolactone)
  • Loop diuretic (furosemide)
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63
Q

other than drugs, what else is there in the management of chronic HF?

A
  • advise and explain the condition
  • specialist referral
  • surgery if caused by AS or MR
  • involve the HF specialist nurse
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64
Q

what is cor pulmonale?

A

RSHF caused by respiratory disease (e.g. COPD)

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65
Q

causes of cor pulmonale?

A
  • COPD (commonest)
  • PE
  • interstitial lung disease
  • CF
  • primary pulmonary HTN
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66
Q

how does cor pulmonale present?

A
  • often asymptomatic!
  • SOB(OE)
  • peripheral oedema
  • syncope
  • chest pain
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67
Q

what are the findings on examination in cor pulmonale?

A
  • hypoxia
  • cyanosis
  • raised JVP
  • peripheral oedema
  • 3rd heart sound
  • murmur (if underlying valve disease)
  • hepatomegaly (hepatic vein congestion)
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68
Q

management of cor pulmonale?

A
  • treat underlying cause
  • long term O2 therapy
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69
Q

what is normal BP defined as?

A

< 120/80

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70
Q

ROPE: secondary causes of hypertension?

A
  • Renal disease
  • Obesity
  • Pregnancy-induced HTN / Pre-eclampsia
  • Endocrine (Conns syndrome)
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71
Q

complications of HTN?

A
  • IHD
  • cerebrovascular accident (stroke / haemorrhage)
  • retinopathy
  • nephropathy
  • HF
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72
Q

how is HTN diagnosed?

A

either:
- several raised clinic readings
- raised 24h ambulatory readings

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73
Q

what is classed as stage 1 HTN? clinic and ambulatory readings

A
  • clinic: >140/90
  • ambulatory: >135/85
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74
Q

what is classed as stage 2 HTN? clinic and ambulatory readings

A
  • clinic: >160/100
  • ambulatory: >150/95
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75
Q

ABCD: drugs used in HTN management?

A
  • ACE-i (ramipril) / ARB (candesartan)
  • BB (bisoprolol)
  • CCB (amlodipine)
  • diuretic (thiazide-like, indapamide)
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76
Q

what are 1st and 2nd medical treatments for someone <55 years old and not Black with HTN?

A
  • 1st: ACE-i (ARB if not tolerated)
  • 2nd: ACE-i + CCB
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77
Q

what are 1st and 2nd medical treatments for someone >55 years old or Black with HTN?

A
  • 1st: ARB if Black
  • 2nd: ACE-i/ARB + CCB
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78
Q

what are 3rd and 4th line treatments of HTN? (hint: same for everyone)

A
  • 3rd: ACE-i/ARB + CCB + diuretics
  • 4th: ACE-i/ARB + CCB + 2 diuretics
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79
Q

what kind of diuretic is spironolactone? how does it work?

A
  • K+ sparing
  • blocks aldosterone action
  • causes Na+ excretion and K+ reabsorption
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80
Q

why is it important to closely monitor UEs on ACE-i and diuretics?

A

they can all cause hyperkalaemia

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81
Q

what is the target BP in diabetics with HTN?

A

< 130/80

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82
Q

what is the target BP in <80 year olds with HTN?

A

< 140/90

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83
Q

what is the target BP in >80 year olds with HTN?

A

< 150/90

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84
Q

what is the first line drug treatment for HTN in diabetics?

A
  • CCB for women of child-bearing age
  • ACEi + CCB for Black people
  • ACE-i for everyone else
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85
Q

what is the initial management of HTN (before meds)?

A
  • investigate for causes
  • investigate for end organ damage
  • advise on lifestyle, salt intake and exercise
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86
Q

what causes the first heart sound (S1)?

A

atrioventricular (tricuspid and mitral) valves closing as the ventricles contract

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87
Q

what causes the second heart sound (S2)?

A

pulmonary and aortic valves closing at the end of ventricular contraction

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88
Q

what causes an S3 sound? who is this normal in?

A
  • chordae tendinae being twanged like a guitar string lol
  • young people
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89
Q

what might an S3 sound indicate in older patients?

A

heart failure

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90
Q

when is S4 heard? what causes it?

A
  • before S1
  • always pathological!
  • hypertrophic ventricle
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91
Q

where is Erb’s point? what can be heard here?

A
  • 3rd IC space, L sternal border
  • S1 and S2
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92
Q

how can you emphasise the mitral stenosis murmur?

A

roll the patient over onto their L side

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93
Q

how can you emphasise the aortic regurgitation murmur?

A

have the patient sit up, lean forward, exhale and then hold it like that

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94
Q

what does mitral stenosis result in?

A

L atrial hypertrophy (thickening)

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95
Q

what does aortic stenosis result in?

A

L ventricular hypertrophy (thickening)

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96
Q

what does mitral regurg result in?

A

L atrial dilatation (thinning out)

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97
Q

what does aortic regurg result in?

A

L ventricular dilatation (thinning out)

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98
Q

describe the pathophysiology of mitral stenosis

A
  • narrowed mitral valve
  • makes it difficult for L atrium to push blood into L ventricle
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99
Q

main 2 causes of mitral stenosis?

A
  • rheumatic heart disease
  • infective endocarditis
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100
Q

describe the mitral stenosis murmur

A
  • mid-diastolic
  • low-pitched
  • rumbling (low velocity in diastole)
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101
Q

what might be palpated in mitral stenosis? what causes this?

A
  • a tapping apex beat
  • loud S1
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102
Q

which 2 conditions are associated with mitral stenosis?

A
  • malar flush
  • atrial fibrillation
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103
Q

how does mitral stenosis cause malar flush?

A
  • blood gets blacklogged in the pulmonary system
  • CO2 rises
  • results in vasodilation
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104
Q

what is mitral regurgitation?

A

incompetent mitral valve allowing blood to leak back into the L atrium

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105
Q

describe the mitral regurg murmur. where does it radiate it?

A
  • pansystolic
  • high-pitched
  • whistling (high velocity in systole)
  • radiates to L axilla
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106
Q

what does mitral regurg result in?

A

congestive cardiac failure (is there a 3rd heart sound?)

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107
Q

causes of mitral regurg? 6

A
  • ageing (valve weakens)
  • IHD
  • infective endocarditis
  • rheumatic heart disease
  • papillary muscle infarction
  • conn tissue disorders (Ehlers-Danlos, Marfan syndrome)
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108
Q

what is the most common valve disease?

A

aortic stenosis

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109
Q

describe the murmur in aortic stenosis. where does it radiate to?

A
  • ejection-systolic
  • high-pitched (high velocity in systole)
  • crescendo-decrescendo (diff stages of systole)
  • radiates to carotids
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110
Q

other than a murmur, what are the other signs of aortic stenosis?

A
  • slow rising pulse
  • narrow pulse pressure
  • exertional syncope
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111
Q

causes of aortic stenosis?

A
  • age-related calcification
  • rheumatic heart disease
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112
Q

describe the murmur in aortic regurg

A
  • early diastolic
  • soft
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113
Q

what kind of pulse is aortic regurg associated with?

A

collapsing pulse at carotids

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114
Q

what is an Austin-Flint murmur? which valve disease can cause this?

A
  • early diastolic
  • rumbling
  • heard at the apex
  • aortic regurg can cause this
115
Q

describe the scar seen on patients who have had a mitral / aortic valve replacement

A

midline sternotomy scar (same as the CABG scar)

116
Q

what is the surgical management for severe aortic stenosis? do they need to be on warfarin afterwards?

A
  • transcatheter aortic valve implantation (TAVI)
  • no, this valve is bioprosthetic
117
Q

what is the most common complication following valve replacement?

A

infective endocarditis

118
Q

which 3 gram +ve cocci can cause infective endocarditis?

A
  • staphylococcus
  • streptococcus
  • enterococcus
119
Q

explain the pathophysiology of AF

A
  • disorganised electrical activity overriding signals from the SAN
  • causes irregular atrial and ventricular contractions
120
Q

signs on examination of AF?

A
  • irregularly irregular pulse
  • tachycardia
  • HF (due to poor filling in diastole)
121
Q

what is the major complication caused by AF? how could this happen?

A
  • embolic (ischaemic) stroke
  • blood pools in the atria and clots
  • the clots can then break off and travel to the cerebral arteries
122
Q

how might AF present?

A
  • asymptomatic, incidental finding
  • palpitations
  • SOB
  • dizziness / syncope
  • symptoms of underlying pathology, e.g. thyrotoxicosis / sepsis signs
123
Q

what are the 2 differentials for an irregularly irregular pulse?

A
  • AF
  • ventricular ectopic beats
124
Q

ECG findings in AF?

A
  • absent P waves
  • narrow QRS complex tachycardia
  • irregularly irregular ventricular rhythm
125
Q

when is AF classed as “valvular”?

A

when the pt also has either:

  • severe mitral stenosis
  • a mechanical heart valve
126
Q

when is AF classed as “non-valvular”?

A

when the pt also has either:

  • no underlying valve disease
  • a valve disease which is NOT mitral stenosis
127
Q

SMITH: commonest causes of AF?

A
  • Sepsis
  • Mitral stenosis / regurgitation
  • IHD
  • Thyrotoxicosis
  • HTN

others:
- DM
- obesity
- HF
- cardiomyopathies

128
Q

what are the 3 main categories of treatment in AF?

A
  • rate control
  • rhythm control
  • anticoagulation (to prevent stroke)
129
Q

what is the aim of rate control in AF management?

A

to get the HR below 100bpm so the ventricles can fill properly

130
Q

what are the drug options for rate control?

A
  • BB (atenolol)
  • CCB (diltiazem), avoid in HF
  • digoxin, only in sedentary patients
131
Q

in which groups of AF patients can rhythm control be offered?

A
  • reversible cause
  • new onset AF <48h
  • AF is causing HF
  • symptomatic despite rate control
132
Q

what is the aim of rhythm control in AF? what does it involve?

A
  • to produce normal sinus rhythm
  • cardioversion
133
Q

what are the 2 forms of rhythm control in AF?

A
  • pharmacological cardioversion
  • electrical cardioversion
134
Q

when is immediate cardioversion used vs delayed in AF?

A
  • immediate is when AF <48h onset or they are haemodynamically unstable
  • otherwise it is delayed
135
Q

drugs used acutely for pharmacological cardioversion?

A
  • flecanide (1st line)
  • amiodarone if structural heart disease
136
Q

drugs used for long term rhythm control?

A
  • BBs
  • dronedarone
  • amiodarone
137
Q

what is paroxysmal AF?

A
  • AF which comes and goes in episodes
  • not lasting longer than 48h
138
Q

management of paroxysmal AF? when is this drug avoided? why?

A
  • anticoagulated if CHADVASc score is >1
  • “pill in the pocket” approach with flecanide
  • avoided in atrial flutter due to risk of tachycardia
139
Q

where is blood most likely to clot in AF?

A

the atrial appendage

140
Q

without anticoagulation, what is the risk of stroke in AF?

A

5%

141
Q

with anticoagulation, what is the risk of stroke in AF?

A

1-2%

142
Q

what is the HASBLED score?

A

risk of having a bleed whilst on an anticoagulant

143
Q

what is the target INR range in AF?

A

2-3

144
Q

which foods / drinks affect INR?

A
  • leafy green veg (contain vit K)
  • cranberry juice
  • alcohol
145
Q

what is the half-life of warfarin? how is an OD reversed?

A
  • 1-3 days
  • vitamin K
146
Q

give 3 examples of DOACs

A
  • apixaban
  • dabigatran
  • rivaroxaban
147
Q

advantages of DOACs over warfarin?

A
  • no monitoring
  • no major interactions
  • better at preventing strokes
  • lower risk of bleeding
148
Q

what does CHA2DS2-VASc stand for?

A
  • Congestive HF
  • HTN
  • Age >75 (2)
  • Diabetes
  • Stroke / TIA Hx (2)
  • Vascular disease
  • Age 65-74
  • Sex is female
149
Q

at which CHA2DS2-VASc score do you consider anticoag? when do you offer it?

A
  • 1 to consider
  • >1 to offer
150
Q

what does HASBLED stand for?

A
  • HTN
  • Abnormal renal / liver function
  • Stroke
  • Bleeding
  • Labile INRs on warfarin
  • Elderly
  • Drugs or alcohol
151
Q

what are the four possible rhythms in cardiac arrest?

A
  • ventricular tachycardia (VT)
  • ventricular fibrillation (VF)
  • pulseless electrical activity (PEA)
  • asystole
152
Q

which 2 cardiac arrest rhythms are “shockable”?

A
  • VT
  • VF
153
Q

which 2 cardiac arrest rhythms are “non-shockable”? what does this mean?

A
  • PEA
  • asystole
  • defibrillation will not work
154
Q

management of tachycardia in an unstable patient?

A
  • up to 3 synchronised DC shocks
  • amiodarone infusion
155
Q

pathophysiology of atrial flutter?

A
  • re-entrant rhythm
  • electrical signals stuck in self-perpetuating loop
156
Q

what is the ECG finding in atrial flutter? what causes it?

A
  • sawtooth appearance
  • P wave after P wave with no ventricular activity in between
157
Q

which conditions are associated with atrial flutter?

A
  • HTN
  • IHD
  • cardiomyopathy
  • thyrotoxicosis
158
Q

management of atrial flutter?

A
  • similar to AF
  • rate / rhythm control
  • treat any reversible underlying condition (e.g. HTN, thyrotoxicosis)
  • radiofrequency ablation of re-entrant rhythm
  • anticoagulate if CHA2DS2-VASc score >1
159
Q

what causes supraventricular tachycardia (SVT)?

A

electrical signal re-entering atria from the ventricles

160
Q

is SVT narrow or broad complex?

A
  • narrow QRS complex
  • QRS <0.12
161
Q

what are the 3 types of SVT? how are they classified?

A
  • AV nodal re-entrant tachycardia
  • AV re-entrant tachycardia
  • atrial tachycardia
  • based on the re-entry point for the electrical signal
162
Q

what is Wolff-Parkinson-White syndrome?

A

atrioventricular re-entrant tachycardia (a type of SVT)

163
Q

management of stable patients with an SVT?

A
  • continuous ECG monitoring
  • valsalva manoeuvre
  • carotid sinus massage
  • adenosine (alt: verapamil)
  • DC cardioversion
164
Q

how does adenosine work?

A
  • interrupts accessory pathway in SVT
  • slows conduction and HR
165
Q

what might immediately happen after adenosine administration?

A
  • bradycardia or asystole
  • should fix itself very quickly
166
Q

what should patients be warned about before giving adenosine?

A

feeling of impending doom on injection

167
Q

where is adenosine contraindicated?

A
  • asthma or COPD
  • HF
  • heart block
  • severe hypotension
168
Q

definitive treatment of WPW syndrome?

A

radiofrequency ablation of accessory pathway

169
Q

ECG changes seen in WPW syndrome?

A
  • short PR interval (<0.12)
  • wide QRS complex (>0.12)
  • delta wave (upstroke on QRS complex)
170
Q

how is catheter ablation carried out?

A
  • catheter inserted into femoral vein under X-ray guidance
  • fed through to the heart
  • once abnormal area is found, radiofrequency ablation (heat) applied
171
Q

which conditions can be cured with radiofrequency ablation?

A
  • AF
  • atrial flutter
  • SVTs
  • WPW syndrome
172
Q

what is torsades de pointes?

A
  • “twisting of tips”
  • polymorphic ventricular tachycardia
  • QRS complex is twisting around the baseline
173
Q

causes of prolonged QT interval?

A
  • long QT syndrome (inherited)
  • drugs
  • electrolyte imbalances
174
Q

drug causes of prolonged QT interval?

A
  • antipsychotics
  • citalopram
  • flecainide
  • sotalol
  • amiodarone
  • macrolide antibiotics (e.g. clarithromycin)
175
Q

electrolyte disturbance causes of prolonged QT interval?

A
  • hypokalaemia
  • hypomagnesaemia
  • hypocalcaemia
176
Q

acute management of torsades de pointes?

A
  • correct underlying drug / electrolyte cause
  • magnesium infusion
  • defibrillation if VT occurs
177
Q

long term management of long QT syndrome?

A
  • avoid drugs which worsen it
  • BBs (except sotalol)
  • pacemaker / implantable defibrillator
178
Q

what are ventricular ectopic beats? what causes these?

A
  • premature ventricular beats
  • due to random electrical discharge from outside the atria
179
Q

how might ventricular ectopics present?

A

random, brief palpitations

180
Q

ECG changes seen in ventricular ectopics?

A
  • absent P waves
  • individual random broad QRS complexes
  • otherwise normal
181
Q

what is bigeminy?

A

when ventricular ectopic beats occur regularly after every sinus beat

182
Q

management of ventricular ectopics?

A
  • check bloods for anaemia / thyroid / electrolyte disturbances
  • reassure healthy people
  • seek expert advice if underlying heart conditions
183
Q

what is first degree heart block? how does it look on an ECG?

A
  • delayed conduction through the AVN
  • long PR interval >0.20 secs (1 big square)
184
Q

what is second degree heart block? what are the 3 types?

A
  • some of the atrial impulses don’t make it to the ventricles
  • Mobitz type 1
  • Mobitz type 2
  • 2:1 block
185
Q

what is the other name for Mobitz type 1 block? how does it look on an ECG?

A
  • Wenckebach’s phenomenon
  • increasing PR interval until a QRS complex is dropped, then PR interval returns to normal, then repeats
186
Q

how does Mobitz type 2 block look on ECG?

A
  • a set ratio of P waves to QRS complexes
  • e.g. 3 P waves then a QRS complex is 3:1
187
Q

what is the main risk associated with Mobitz type 2?

A

asystole

188
Q

how does 2:1 block look on ECG?

A

2 P waves then 1 QRS complex

189
Q

management of heart block in an unstable patient / risk of asystole?

A
  • atropine 500mcg IV
  • 2nd line is to repeat this up to 6 times
  • then noradrenalin
  • transcutaneous cardiac pacing with a defibrillator
190
Q

management of heart block where there is HIGH risk of asystole?

A
  • temporary transvenous cardiac pacing
  • permanent implantable pacemaker
191
Q

what class of drug is atropine? common side effects?

A
  • antimuscarinic
  • dilated pupils
  • urinary retention
  • dry eyes
  • constipation
192
Q

risk factors for asystole?

A
  • Mobitz type 2
  • third degree (complete) heart block
  • previous asystole
193
Q

what is third degree heart block?

A
  • complete block
  • no association between P waves and QRS complexes
194
Q

how long do the batteries in a pacemaker last?

A

5 years

195
Q

indications for a pacemaker?

A
  • symptomatic bradycardia
  • Mobitz type 2 block
  • third degree block
  • severe HF
  • HOCM
196
Q

what is cardiac tamponade?

A

heart gets compressed by excess fluid in pericardium

197
Q

main complication of cardiac tamponade?

A

cardiac arrest

198
Q

causes of cardiac tamponade?

A
  • traumatic injury to chest
  • pericarditis
  • cancer
  • iatrogenic (post-surgery)
199
Q

what is becks triad? where is it seen?

A
  • hypotension
  • muffled heart sounds
  • distended jugular veins
  • seen in cardiac tamponade
200
Q

presentation of cardiac tamponade?

A
  • becks triad
  • tachycardia
  • SOB
  • chest pain
  • pulsus paradoxus
201
Q

investigation for cardiac tamponade?

A

bedside USS (called FAST)

202
Q

management of cardiac tamponade?

A
  • pericardiocentesis
  • surgery to make a pericardial window
  • pericardiectomy
203
Q

what is cardiomyopathy?

A

any heart muscle disorder without another obvious heart deformity

204
Q

3 main types of cardiomyopathy?

A
  • dilated
  • hypertrophic
  • restrictive
205
Q

most common cause of unexpected death in children?

A

hypertrophic cardiomyopathy

206
Q

causes of cardiomyopathy?

A
  • idiopathic (primary)
  • connective tissue disorders
  • endocrine
  • drugs
  • infection
  • nutrition
  • genetic (e.g. DMD)
207
Q

which connective tissue disorders can cause cardiomyopathy?

A
  • sarcoidosis
  • SLE
208
Q

which endocrine disorders can cause cardiomyopathy?

A
  • DM
  • thyroid disease
  • acromegaly
209
Q

drug causes of cardiomyopathy?

A
  • chemo
  • cocaine
  • alcohol
210
Q

nutritional causes of cardiomyopathy?

A
  • obesity
  • B1 def
  • Ca def
  • Mg def
211
Q

commonest type of cardiomyopathy?

A

dilated cardiomyopathy (DCM)

212
Q

describe the ventricles in DCM

A
  • larger in size
  • normal wall thickness
213
Q

which demographics are more affected by cardiomyopathy?

A

Black men aged 20-60

214
Q

presentation of DCM? hint: think HF

A
  • SOBOE
  • fatigue
  • peripheral oedema
  • raised JVP (if RV affected)
  • loud S3 and S4
  • arrhythmia (e.g. AF, AVNB)
215
Q

infective causes of DCM?

A
  • bacterial
  • HIV
  • coxsackie viruses
  • viral myocarditis
216
Q

investigations in DCM?

A
  • ECG
  • CXR
  • echo
  • cardiac muscle biopsy (rare)
217
Q

changes seen on ECG in DCM?

A
  • sinus tachycardia
  • T-wave inversion and Q-waves (even without Hx of MI)
  • ST depression
  • LBBB
218
Q

changes seen on CXR in DCM?

A

signs of HF (ABCDE)

219
Q

changes seen on echo in DCM?

A

dilated, hypokinetic chambers

220
Q

management of DCM?

A
  • treat underlying cause
  • start anticoag (warfarin or NOAC)
  • treat any arrhythmia
  • consider pacemaker if AVNB
  • treat HF
  • consider ICD
  • consider transplant
221
Q

in the context of cardiomyopathy treatment, what’s an ICD? when is it used?

A
  • implantable cardioverter defibrillator
  • if high risk of arrhythmia
222
Q

prognosis in DCM?

A
  • extremely poor
  • 30% survive 5 years past diagnosis
223
Q

markers of worse prognosis in DCM?

A
  • being peripartum
  • thin ventricular wall
  • ventricles markedly dilated
224
Q

inheritance pattern for hypertrophic cardiomyopathy (HCM)?

A

autosomal dominant

225
Q

what is the effect of HCM on heart function?

A

diastolic dysfunction +/- outflow obstruction

226
Q

which chamber is affected in HCM?

A

LV

227
Q

presentation of HCM?

A
  • mostly asymptomatic
  • SOB
  • chest pain
  • syncope, especially after exercise
  • palpitations
  • sudden death
228
Q

what causes sudden death in HCM? hint: 2 ways

A
  • arrhythmia
  • outflow tract obstruction
229
Q

top differential for unexplained syncope in athlete?

A

hypertrophic cardiomyopathy (HCM)

230
Q

signs O/E in HCM?

A
  • forceful apex beat
  • late ejection systolic murmur, does not radiate
  • abnormal rise in BP in response to exercise
  • signs of AF (20%)
231
Q

nature of murmur in HCM?

A
  • late ejection systolic
  • no radiation
  • best heard at L sternal edge, 3-4th IC space
  • reduced on squatting
232
Q

diagnostic investigation for HCM? findings?

A
  • echocardiogram
  • asymmetrical septal hypertrophy >15mm
  • non-dilated LV space
  • thickened LV wall
233
Q

investigations for HCM?

A
  • ECG
  • echo
  • CXR
  • cardiac MRI
234
Q

management of HCM?

A
  • control arrhythmia, consider ablation
  • anticoag if AF
  • BBs
  • verapamil
  • avoid ACEi, ARBs, nitrites and diuretics (opp to DCM)
  • ICD if high risk sudden death
  • consider transplant
235
Q

why do a lot of HF drugs need to be avoided in HCM?

A

they decrease chamber size by decreasing preload, making symptoms worse

236
Q

main complication in HCM?

A

sudden death

237
Q

risk factors for sudden death in HCM?

A
  • unexplained syncope episodes
  • VF / VT episodes
  • abnormal rise in BP in exercise
  • FHx sudden death
  • age <30
238
Q

how can sudden death be prevented?

A

implantable cardioverter defibrillator (ICD)

239
Q

describe restrictive cardiomyopathy (RCM)

A

reduced compliance of ventricular walls in diastolic filling

240
Q

how can RCM be categorised?

A
  • some are caused by invasion of myocardium
  • others aren’t
241
Q

what could invade the myocardium and cause RCM?

A
  • amyloid plaques
  • sarcoidosis
  • iron, in haemachromatosis
242
Q

which chamber is most commonly affected in RCM?

A

LV

243
Q

main risk factors for RCM?

A
  • old age
  • PMH: amyloidosis, sarcoidosis, haemochromatosis
244
Q

presentation of RCM?

A
  • signs of heart failure (incl on CXR)
  • signs of RV failure maybe
  • AF in 75% cases
  • other arrhythmias
245
Q

investigations for RCM?

A
  • ECG
  • CXR
  • echo
246
Q

management of RCM?

A
  • treat underlying cause
  • avoid certain drugs
  • heart transplant
247
Q

which drugs should be avoided in RCM management? why?

A
  • diuretics, reduce preload
  • digoxin, amyloidosis patients are very sensitive to this
  • nitrites, can cause HTN
248
Q

differentials for cardiomyopathy?

A
  • IHD
  • mitral / aortic valve disease
  • pericarditis
  • pulmonary stenosis
  • VSD
249
Q

pathophysiology of aortic dissection?

A

tear in tunica intima layer of aortic wall, causing blood to leak out

250
Q

main risk factor for aortic dissection?

A

HTN

251
Q

which conditions are associated with aortic dissection?

A
  • HTN
  • trauma
  • bicuspid aortic valve
  • syndromes (marfan’s, ehlers-danlos, turner’s, noonan’s)
  • pregnancy
  • syphilis
252
Q

presentation of aortic dissection?

A
  • tearing, severe chest pain
  • radiates to back
  • weak / absent peripheral pulses
  • difference in BP between arms
  • limb ischamia if distal aorta affected
  • paraplegia if spinal arteries affected
253
Q

management of acute bradycardia?

A
  • 500 micrograms of atropine IV
  • repeat every 3-5 mins
  • max dose 3mg
254
Q

what is levine’s sign? what does it indicate?

A
  • curling a fist over chest
  • ischaemic chest pain
255
Q

differentials for pleuritic chest pain?

A
  • pulmonary embolism
  • aortic dissection
256
Q

ECG changes seen in pericarditis?

A
  • global ST elevation (saddle-shaped slope)
  • PR depression
257
Q

what are the big 5 risk factors to ask about in a cardiac history?

A
  • Smoking
  • HTN
  • DM
  • hypercholesterolaemia
  • FH
258
Q

signs O/E of acute heart failure?

A
  • raised JVP
  • peripheral oedema
  • crackles bibasally
259
Q

causes of aortic regurgitation?

A
  • age-related weakening of the valve
  • aortic dissection
260
Q

features of aortic regurgitation?

A
  • difference in BP between arms
  • absence of peripheral pulses
  • delayed peripheral pulses
  • severe pain, not relieved by opiates
261
Q

what might be picked up on FBC in chest pain?

A
  • anaemia
  • infection (?pneumonia)
262
Q

which bloods get done for chest pain patients?

A
  • FBC
  • UEs
  • clotting screen
  • troponin
  • D dimer
  • cholesterol
  • glucose, HbA1c
263
Q

criteria for a primary PCI?

A

either 1 of the following:

  • ST elevation >2mm in 2 contiguous chest leads
  • >1mm in 2 contiguous limb leads
  • new LBBB
264
Q

adverse effect of giving morphine following MI? what should be co-prescribed?

A
  • delays absorption of antiplatelets (e.g. clopidogrel)
  • metoclopramide
265
Q

trend in troponin after an MI?

A
  • rises rapidly
  • falls over following days
266
Q

if initial troponins raised (positive), when should they be repeated?

A

in 3 hours

267
Q

in which scenario does a negative troponin NOT rule out MI?

A

chest pain with onset <6 hours ago

268
Q

non-ACS causes of MI?

A
  • major haemorrhage
  • pneumonia
  • PE
269
Q

what is the HEART score?

A

a score to determine management of chest pain

270
Q

what are the components of the HEART score?

A
  • History
  • ECG
  • Age
  • Risk factors
  • Troponin
271
Q

how is the HEART score interpreted?

A
  • 0-3 = discharge
  • 4-6 = observe
  • 7-10 = treatment
272
Q

RFs for infective endocarditis?

A
  • strongest one is past episode of IE
  • rheumatic valve disease
  • prosthetic valves
  • congenital heart disease
  • IVDU
  • recent piercings
273
Q

which valve does the vegetation grow on in an IVDU with IE?

A
  • tricuspid
  • this is the first valve it hits on the way back to the heart (venous system)
274
Q

scoring criteria used to diagnose infective endocarditis?

A

modified duke’s criteria

275
Q

what modified duke’s criteria scores indicate infective endocarditis?

A

any of the following:

  • pathological criteria positive
  • 2 major criteria
  • 1 major + 3 minor criteria
  • 5 minor criteria
276
Q

describe the pathological criteria (modified duke’s) of infective endocarditis

A

the pathological organisms found on histology / microbiology of the biopsied valve tissue

277
Q

give some examples of major criteria (modified duke’s) in infective endocarditis

A
  • 2 +ve blood cultures
  • persistent bacteraemia on bloods
  • echo showing endocardial enlargement
  • new valvular regurg
278
Q

give some examples of minor criteria (modified duke’s) in infective endocarditis

A
  • predisposing heart condition
  • IVDU
  • fever >38C
  • vascular phenomena
  • immunological phenomena
279
Q

what vascular phenomena are seen in infective endocarditis?

A
  • major emboli
  • splenomegaly
  • clubbing
  • splinter haemorrhages
  • janeway lesions
  • petechiae / purpura
280
Q

what immunological phenomena are seen in infective endocarditis?

A
  • glomerulonephritis
  • osler’s nodes
  • roth spots
281
Q

poor prognostic factors in infective endocarditis?

A
  • staph aureus infection (30% mortality!)
  • prosthetic valve
  • culture -ve endocarditis
  • low complement levels
282
Q

initial ABx of choice for infective endocarditis?

A
  • if native valve: amoxicillin + low-dose gentamicin (vancomycin if pen allergic)
  • if prosthetic valve: vancomycin + rifampicin + low-dose gentamicin
283
Q

indications for surgery in infective endocarditis?

A
  • severe valvular incompetence
  • aortic abscess (lengthening PR interval on ECG)
  • ABx resistant infections
  • HF resistant to treatment
  • recurrent emboli after ABx

Zero to Finals: Medicine A.S. (11 decks)

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