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MBBS Y5 > MEDICINE - CARDIOLOGY test > Flashcards

MEDICINE - CARDIOLOGY test 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
  • angina - MI- 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

BATMEN: medical management of NSTEMI?

A
  • BB- Aspirin 300mg stat- Ticagrelor 180mg (or clopidogrel 300mg)- Morphine - Enoxaparin (or other LMWH) - Nitrates (GTN)
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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
  • cardiac arrest- cardiogenic shock- chronic heart failure- VF or VT- AV block, esp after inferior MI- pericarditis (Dressler’s syndrome)- LV aneurysm- LV free wall rupture- 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
  • DAPT (Aspirin and clopidogrel)- atorvastatin - ACE-i (ramipril)- BB (atenolol)- aldosterone antagonist (spironolactone) 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?

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?

A
  • clinical exam- 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?

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 - HTNothers:- 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

02-Mar

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

MBBS Y5 (27 decks)

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