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Exam > Cardiology - my notes > Flashcards

Cardiology - my notes Flashcards

1
Q

Atherosclerosis

A

Atheromas (fatty deposits) and sclerosis (hardening or stiffening of the blood vessel walls).

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2
Q

What causes atherosclerosis?

A

Chronic inflammation and activation of the immune system (in the artery wall)  deposition of lipids in the wall  atheromatous plaques

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3
Q

What do atheromatous plaques result in?

A

Stiffening (HTN)
Stenosis (reduced blood flow)
Plaque rupture (thrombus)

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4
Q

CVD modifiable risk factors

A
  • Raised cholesterol
  • Smoking
  • Alcohol consumption
  • Poor diet
  • Lack of exercise
  • Obesity
  • Poor sleep
  • Stress
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5
Q

CVD non-modifiable risk factors

A
  • Older age
  • Family history
  • Male
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6
Q

Co-morbidities increasing risk of atherosclerosis

A
  • DM
  • HTN
  • CKD
  • RA
  • Atypical antipsychotic medications
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7
Q

End results of atherosclerosis

A
  • Angina
  • MI
  • TIA
  • Stroke
  • Peripheral arterial disease
  • Chronic mesenteric ischaemia
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8
Q

NICE guidelines physical activity recommendations

A
  • Aerobic activity 150min moderate intensity or 75min vigorous intensity
  • Strength training 2x week
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9
Q

QRISK 3

A

% risk of having a stroke or MI in the next 10years

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10
Q

QRISK 3 >10% treatment

A

Atorvastatin 20mg at night

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11
Q

What pts get atorvastatin 20mg as 1* prevention?

A

CKD
T1DM >40yo, or for 10y

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12
Q

Statins mode of action

A

Reduce cholesterol production in the liver by inhibiting HMG CoA reductase

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13
Q

Side effects of Statins

A
  • Myopathy
  • Rhabdomyolysis
  • T2DM
  • Haemorrhagic strokes
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14
Q

Blood tests in pts on statins

A

LFTs at 3 months and 12 months (statins cause ALT and AST rise)

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15
Q

How to check for rhabdomyolysis?

A

Check creatinine kinease levels

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16
Q

2 examples of cholesterol lowering drugs

A

Ezetimibe (reduces cholesterol absorption in intestine)
Monoclonal antibodies

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17
Q

2* prevention CVD

A
  • Antiplatelet medications (aspirin/clopidogrel/ticagrelor)
  • Atorvastatin 80mg
  • Atenolol (or Bisoprolol, Beta blocker)
  • ACE inhibitor (ramipril)
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18
Q

Medications post MI

A

Dual antiplatelet treatment
- Aspirin 75mg daily forever
- Clopidogrel or ticagrelor for 12mth

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19
Q

When is Clopidogrel a preferred antiplatelet?

A

Peripheral arterial disease, and following ischaemic stroke

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20
Q

Familial hypercholesterolaemia

A

AD
- Family history of CVD
- Very high cholesterol 7.5mmol/L
- Tendon xanthomata

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21
Q

Define tendon xanthomata

A

Hard nodules in tendons, containing cholesterol

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22
Q

Mx of familial hypercholesterolaemia

A
  • Genetic testing, specialist referral
  • Statins
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23
Q

What causes angina?

A

Atherosclerosis affecting coronary arteries, and reducing blood flow to the myocardium

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24
Q

Symptoms of angina

A

Constricting chest pain, with or without radiation to jaw and arms

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25
Q

Define stable angina

A

Symptoms only come with exertion, and are relieved by rest or GTN

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26
Q

Define unstable angina

A

Symptoms appear randomly at rest. (Type of Acute coronary syndrome)

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27
Q

Define cardiac stress testing

A

Assessing heart function in exertion – treadmill or dobutamine – assess by ECG, Echo, MRI

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28
Q

Gold standard Ix for coronary artery disease

A

Invasive coronary angiography

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29
Q

Immediate symptomatic relief in angina

A

Sublingual GTN

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30
Q

What is the effect of GTN (and what side effects?)

A

Vasodilation (headache, dizziness)

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31
Q

How to use GTN

A

1st take GTN, after 5 min 2nd dose if symptoms, again after 5 min 3rd dose, after 5min call ambulance

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32
Q

Long term symptomatic relief in angina

A

Beta blocker (bisoprolol) AND/OR Ca Channel blocker (diltiazem/verapamil)

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33
Q

When should diltiazem and verapamil be avoided?

A

In heart failure with reduced ejection fraction

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34
Q

Surgical interventions in Angina

A
  • PCI (coronary angioplasty and stenting)
  • CABG
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35
Q

3 options for graft in CABG

A
  • Saphenous vein
  • Internal thoracic artery
  • Radial artery
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36
Q

Acute Coronary Syndrome

A

Result of a thrombus from atherosclerotic plaque, blocking a coronary artery

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37
Q

3 types of ACS

A
  • Unstable angina
  • STEMI
  • NSTEMI
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38
Q

Right coronary artery supplies (areas)

A

R atrium
R ventricle
Inferior L ventricle
Posterior septum

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39
Q

Left coronary artery branches

A

Circumflex artery, Left anterior descending

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40
Q

Circumflex artery supplies (areas)

A

L atrium
Posterior L ventricle

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41
Q

Left anterior descending supplies (areas)

A

Anterior aspect of L ventricle
Anterior aspect of septum

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42
Q

What pts are at risk of silent MI?

A

Diabetic pts

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43
Q

STEMI ECG changes

A

ST elevation
LBBB

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44
Q

NSTEMI ECG changes

A

ST depression
T wave inversion

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45
Q

Pathological Q waves significance

A

Transmural infarction (involving full muscle thickness)
Appear 6h post symptoms onset

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46
Q

Left coronary artery (heart area, ECG leads)

A

Anterolateral, I, aVL, V3-6

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47
Q

Left anterior descending

A

Anterior, V1-4

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48
Q

Circumflex

A

Lateral, I, aVL, V5-6

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49
Q

Right coronary artery

A

Inferior, II, III, aVF

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50
Q

Rise of troponin significance

A

MI

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51
Q

Ix in suspected ACS

A

Troponin (rising or high)
Bloods
Chest x ray
Echocardiogram

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52
Q

STEMI Dx

A

ECG:
- ST elevation
- LBBB

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53
Q

NSTEMI Dx

A

Raised troponin + Normal ECG OR ST depression OR T wave inversion

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54
Q

Unstable angina Dx

A

Symptoms of ACS + normal troponin + normal ECG OR ST depression OR T wave inversion

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55
Q

Acute coronary syndrome initial Mx

A

C- call ambulance
P – perform ECG
A – aspirin 300mg
I – IV morphine with antiemetic (metoclopramide)
N – nitrate (GTN)

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56
Q

Pt pain free, pain in the last 72h Mx

A

Refer for same-day assessment

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57
Q

Pt with STEMI within 12h of onset Mx

A

PCI <2h of presenting OR Thrombolysis <2h of presenting

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58
Q

Define thrombolysis

A

Injecting a fibrinolytic agent (breaks down clots)

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59
Q

Example of thrombolytics

A

Streptokinase, alteplase, tenecteplase

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60
Q

NSTEMI Mx

A

B – Angiography or PCI
A – Aspirin 300mg
T – Ticagrelor 180mg stat
M – morphine
A – antithrombin (fondaparinux)
N – GTN
O2 if saturation drops <95%

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61
Q

Angiography in NSTEMI

A

Immediate angiography in unstable patients

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62
Q

GRACE score

A

6-months probability of death after NSTEMI

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63
Q

=< 3% GRACE score

A

Low risk

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64
Q

> = 3% GRAE score

A

Medium – High risk

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65
Q

Pericarditis

A

Inflammation of the pericardium

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66
Q

2 Most common causes of pericarditis

A

Idiopathic or viral
Other: autoimmune, injury, cancer, uraemia, methotrexate

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67
Q

Pericarditis presentation

A

Chest pain, fever

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68
Q

Tx of pericarditis

A

NSAIDs

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69
Q

Define pericardial effusion

A

Potential space of the pericardial cavity fills with fluids; makes it difficult to expand during diastole

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70
Q

Pericardial/cardiac tamponade

A

Pericardial effusion is large enough to raise intra-pericardial pressure (reduced heart filling in diastole, decreases Cardiac Output in systole)

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71
Q

Describe the character of chest pain in pericarditis

A

Sharp, central, pleuritic – worse with inspiration, worse on lying down, better on sitting forward

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72
Q

Auscultation sign in pericarditis

A

Pericardial rub

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73
Q

Pericardial Ix (blood tests)

A

Raised white cells, CRP, ESR

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74
Q

Pericardial Ix ECG changes

A

Saddle-shaped ST elevation; PR depression

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75
Q

Mx of pericarditis

A

NSTEMI, colchicine (3 months to reduce recurrence risk)

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76
Q

Pericardiocentesis

A

Removal of fluid from around the heart in significant pericardial effusion/tamponade

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77
Q

Acute left ventricular failure

A

Left ventricular unable to move blood through left side of heart info the systemic circulation

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78
Q

Cardiac output

A

Volume of blood ejected by heart per minute

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79
Q

Stroke volume

A

Volume of blood ejected during each beat

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80
Q

Volume of blood ejected during each beat

A

Stroke volume x heart rate

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81
Q

Pulmonary oedema

A

Lung tissue and alveoli are filled with interstitial fluid; interferes with gas exchange and causes SOB and reduced O2 sats

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82
Q

Presentation of acute left ventricular failure

A
  • Acute SOB
  • Exacerbated by lying flat
  • Better by sitting up
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83
Q

What kind of respiratory failure is acute left ventricular failure?

A

Type 1 respiratory failure (low oxygen without increased carbon dioxide)

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84
Q

Symptoms of acute left ventricular failure

A

SOB
Looking unwell
Cough with frothy white or pink sputum

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85
Q

Signs in acute left ventricular failure

A

Raised RR
Reduced SaO2
Tachycardia
3rd heart sound
Bilateral basal crackles (wet sound)
Hypotension

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86
Q

Right sided heart failure symptoms

A

Peripheral oedema (legs ankles sacrum)
Raised JVP (due to backlog of blood in right heart)

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87
Q

B-type Natriuretic Peptide

A

BNP/ hormone released from the heart ventricles when myocardium is too stretched (suggest heart overload)

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88
Q

Action of BNP on cardiac system

A

Relax smooth muscle in blood vessels, reduces systemic vascular resistance

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89
Q

Action of BNP on kidneys

A

Acts as a diuretic to promote water excretion

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90
Q

Ejection fraction

A

Measure of left ventricular function (% of blood pumped out of the ventricle with each contraction) >50%

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91
Q

Cardiomegaly

A

Cardiothoracic ratio >0.5

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92
Q

Lung oedema (fluid leaking) X ray signs

A

Bilateral pleural effusions
Interlobar fissure fluid
Fluid in septal lines (Kerley lines)

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93
Q

Mx of pleural effusion

A

Sit up
O2
Diuretics (IV furosemide)
IV fluids STOPPED

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94
Q

Positive inotropes

A

Increase the contractility of the heart  increase CO and MAP

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95
Q

Vasopressors

A

Cause vasoconstriction, increase systemic vascular resistance and MAP

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96
Q

Heart failure with reduced ejection fraction

A

Ejection fraction <50%

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97
Q

Heart failure with preserved ejection fraction

A

> 50%; diastolic dysfunction

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98
Q

Causes of chronic heart failure

A
  • Ischaemic heart disease
  • Valvular heart disease (aortic stenosis)
  • Hypertension
  • Arrhythmias (AF)
  • Cardiomyopathy
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99
Q

Symptoms of chronic heart failure

A
  • Breathlessness, worsened by exertion
  • Cough (frothy white/pink sputum)
  • Orthopnoea
  • Paroxysmal nocturnal dyspnoea
  • Peripheral oedema
  • Fatigue
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100
Q

Signs of examination in chronic heart failure

A
  • Tachycardia
  • Tachypnoea
  • HTN
  • 3rd heart sound
  • Bilateral basal crackles (sounding “wet”) on auscultation of the lungs, indicating pulmonary oedema
  • Raised jugular venous pressure (JVP
  • Peripheral oedema
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101
Q

Orthopnoea

A

Breathlessness when lying flat, relieved by sitting or standing (ask how many pillows they use)

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102
Q

Paroxysmal Nocturnal Dyspnoea

A

suddenly waking at night with a severe attack of shortness of breath, cough and wheeze

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103
Q

Dx of heart failure

A

ECG
Echocardiogram
NT-proBNP

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104
Q

New York Heart Association (NYHA)

A

Grades severity of symptoms related to heart failure

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105
Q

Classes of NYHA

A
  • Class I: No limitation on activity
  • Class II: Comfortable at rest but symptomatic with ordinary activities
  • Class III: Comfortable at rest but symptomatic with any activity
  • Class IV: Symptomatic at rest
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106
Q

Mx if NT-proBNP 400-2000 ng/litre

A

Seen and Echo within 6 weeks

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107
Q

Mx if NT-proBNP >2000 ng/litre

A

Seen and Echo within 2 weeks

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108
Q

Tx of chronic heart failure

A

Ace inhibitor (ramipril)
Beta blocker (bisoprolol)
Aldosterone antagonist (when symptoms not controlled with A and B – spironolactone or eplerenone
Loop diuretics (furosemide or bumetanide)

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109
Q

Which drugs must be avoided in valvular heart disease?

A

ACE inhibitors

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110
Q

When are aldosterone antagonists used in reduced EF?

A

When symptoms are not controlled on ACEi + B Blocker

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111
Q

Who needs a implantable cardioverter defibrillators?

A

Pts with shockable arrythmia such as ventricular tachycardia OR ventricular fibrillation

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112
Q

Cardiac resynchronisation therapy

A

Used in EF <35%
Biventricular (Triple chamber)pacemaker – RA, RV, LV

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113
Q

Hypertension (levels)

A

> 140/90 clinical setting;
135/85 home/ambulatory

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114
Q

Essential hypertension

A

~primary hypertension / no secondary cause

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5
Perfectly
115
Q

2* hypertension causes

A

Renal disease
Obesity
Pregnancy/Pre-eclampsia
Endocrine
Drugs (alcohol, nsaids, oestrogen, liquorice)

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116
Q

Most common cause of 2* HTN

A

Renal disease (renal artery stenosis)

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117
Q

How is renal artery stenosis diagnosed?

A

Duplex ultrasound or MR/CT angio

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118
Q

If HTN <40 yo

A

Specialist investigations

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119
Q

Endocrine cause of HTN

A

Hyperaldosteronism (Conn’s syndrome)

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120
Q

BP >140/90 steps

A

24h ambulatory BP or home readings

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121
Q

White coat effect

A

> 20/10 difference in BP between clinic and home

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122
Q

HTN stage 1

A

Clinic >140/90; Home 135/85

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123
Q

HTN Stage 2

A

Clinic >160/100; Home 150/95

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124
Q

HTN Stage 3

A

> 180/120

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125
Q

What to test in pts with new HTN diagnosis?

A
  • HbA1c, renal function, lipids
  • Urine Albumin:Creatinine
  • Proteinura and dipstick for haematuria
  • ECG for left ventricular hypertrophy
  • Eye exam
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126
Q

QRISK

A

Risk of stroke or MI in next 10 years

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127
Q

QRISK >10%

A

Take atorvastatin 20mg at night

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128
Q

What are the steps of HTN medications in Black African / Black Caribbean people?

A

ARB – instead of ACEi (candesartan)
B blocker (bisoprolol)
Ca channel blocker (amlodipine)
Diuretic (thiazide like) (indapamide)

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129
Q

Which HTN drugs are not used together?

A

ARB and ACEi

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130
Q

What drug is given if pt doesn’t tolerate Calcium channel blockers?

A

Thiazide-like diuretic

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131
Q

SE of calcium channel blockers (amlodipine)

A

Ankle oedema

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132
Q

HTN drugs steps in <55 or any age diabetes

A

1: ACEi or ARB
2: A + C or A + D
3: A + C + D
4. K+ <4.5 then low dose spironolactone
K+ >4.5 then alpha or beta blocker

133
Q

HTN drugs steps in >=55 (no diabetes) or black

A

1: C
2: C + A or C + D
3: A + C + D
4. K+ <4.5 then low dose spironolactone
K+ >4.5 then alpha (Doxazosin) or beta blocker (atenolol)

134
Q

Mode of action of aldosterone

A

Blocks action of aldosterone in the kidneys (sodium excretion, potassium reabsorption)

135
Q

SE of thiazide diuretics

A

Cause hypokalaemia

136
Q

SE of spironolactone or ACE i

A

hyperkalaemia

137
Q

<80 yo BP target

A

<140 / <90

138
Q

> 80 yo BP target

A

<150 / <90

139
Q

Malignant hypertension

A

BP > 180/120, retinal haemorrhages or papilloedema

140
Q

Hypertensive emergency drugs

A
  • Sodium nitroprusside
  • Labetalol
  • Glyceryl trinitrate
  • Nicardipine
141
Q

first heart sound (S1)

A

closing of the atrioventricular valves (the tricuspid and mitral valves) at the start of the systolic contraction of the ventricles.

142
Q

second heart sound (S2)

A

closing of the semilunar valves (the pulmonary and aortic valves) once the systolic contraction is complete.

143
Q

third heart sound (S3)

A

0.1 sec after S2 – gallop rhythm – due to pulling the chordae tendineae

144
Q

What does gallop rhythm / S3 indicate in elderly?

A

Heart failure
- S3 normal in 15-40yo

145
Q

fourth heart sound (S4)

A

Heard directly before S1 – ALWAYS abnormal

146
Q

What does S4 indicate?

A

Stiff or hypertrophic ventricle

147
Q

Where is Erb’s point?

A

3rd intercostal space, left sternal border – best to hear S1 and S2

148
Q

How to hear mitral stenosis better?

A

Pt lying on left side

149
Q

How to hear aortic regurgitation better?

A

Pt sat up, leaning forward, holding exhalation

150
Q

Which murmur is heard over carotids?

A

Aortic stenosis

151
Q

Which murmur is heart in the left axilla?

A

Mitral regurgitation

152
Q

Which valvular disease causes hypertrophy?

A

Stenosis (mitral or aortic)

153
Q

What does mitral stenosis cause?

A

Left atrial hypertrophy

154
Q

What does aortic stenosis cause?

A

Left ventricular hypertrophy

155
Q

What valvular disease causes dilatation?

A

Regurgitation (mitral or aortic)

156
Q

What does mitral regurgitation cause?

A

Left atrial dilatation

157
Q

What does aortic regurgitation cause?

A

Left ventricular dilatation

158
Q

Most common valvular heart disease?

A

Aortic stenosis

159
Q

Most common indication for valve replacement?

A

Aortic stenosis

160
Q

Aortic stenosis

A

Narrowing of the aortic valve – restricting blood flow from left ventricle to aorta

161
Q

Aortic stenosis murmur characteristics

A

Ejection – systolic
High-pitched
Crescendo-decrescendo
Radiates to carotids
Narrow pulse pressure
Slow rising pulse
Exertional syncope

162
Q

Causes of aortic stenosis

A

Idiopathic age-related calcification
Bicuspid aortic valve
Rheumatic heart disease

163
Q

Aortic regurgitation

A

Incompetent aortic valve – blood flows back from the aorta to the left ventricle

164
Q

Aortic regurgitation murmur characteristics

A

Early diastolic
Soft murmur
Collapsing pulse
Wide pulse pressure
Heart failure and pulmonary oedema
Also: Austin-Flint murmur – heard at apex

165
Q

Collapsing pulse

A

In aortic regurgitation
Also called water hammer pulse – appearing and rapidly disappearing pulse – felt in the radial artery (when arm held straight upward)

166
Q

Causes of aortic regurgitation

A
  • Idiopathic age-related weakness
  • Bicuspid aortic valve
  • Connective tissue disorders, such as Ehlers-Danlos syndrome and Marfan syndrome
167
Q

Narrowed mitral valve, restricting blood flow from the left atrium to the left ventricle

A

Narrowed mitral valve, restricting blood flow from the left atrium to the left ventricle

168
Q

Mitral stenosis murmur

A

Mid diastolic
Low pitched (rumbling)
Loud S1 (tapping apex beat)
AF – irregularly irregular pulse
Malar flush

169
Q

Malar flush

A

Present in mitral stenosis; red discolouration of the skin of cheeks and nose; due to back pressure of pulmonary system causing a rise in CO2 and vasodilation

170
Q

Causes of mitral stenosis

A
  • Rheumatic heart disease
  • Infective endocarditis
171
Q

Mitral regurgitation

A

Incompetent mitral valve – blood flows back from left ventricle to the left atrium during systolic contraction (causes reduced ejection fraction and congestive cardiac failure)

172
Q

2nd most common cause of valve replacement

A

Mitral regurgitation (1st is aortic stenosis)

173
Q

Mitral regurgitation murmur

A

Pan-systolic
High-pitched (whistling)
Radiates to left axilla
3rd heart sound
Thrill
AF – irregularly irregular pulse
Heart failure and pulmonary oedema

174
Q

Causes of mitral regurgitation

A
  • Idiopathic
  • Ischaemic heart disease
  • Infective endocarditis
  • Rheumatic heart disease
  • Connective tissue disorders, such as Ehlers-Danlos syndrome or Marfan syndrome
175
Q

Tricuspid regurgitation

A

Incompetent tricuspid valve – blood flows back from right ventricle to the right atrium during systolic contraction

176
Q

Tricuspid regurgitation murmur

A

Pan-systolic
Split 2nd heart sound (pulmonary valve closes faster than aortic valve/ left ventricle empties faster than right)
Raised JVP
Giant C-V waves (Lancisi’s sign)
Pulsatile liver
Peripheral oedema
ascites

177
Q

Causes of tricuspid regurgitation

A
  • Infective endocarditis
  • Rheumatic heart disease
  • Carcinoid syndrome
  • Ebstein’s anomaly
  • Connective tissue disorders, such as Marfan syndrome
178
Q

Pulmonary stenosis

A

Narrowed pulmonary valve – restricts blood flow from right ventricle to pulmonary arteries

179
Q

Pulmonary stenosis murmur

A

Ejection systolic (louder with inspiration)
Split 2nd heart sound (left ventricle empties faster than the right)
Raised JVP
Giant A waves (right atrium contracts against right hypertrophic ventricle)
Peripheral oedema
ascites

180
Q

Pulmonary stenosis causes

A

Congenital:
- Noonan syndrome
- Tetralogy of fallot

181
Q

Tetralogy of fallot

A
  • Ventricular septal defect (VSD)
  • Overriding aorta
  • Pulmonary valve stenosis
  • Right ventricular hypertrophy
182
Q

Bioprosthetic valve

A

Limited life span (10 years)
Porcine valves – come from pigs

183
Q

Mechanical valves

A

20 y life span
Lifelong anticoagulation with warfarin
INR target 2.5-3.5

184
Q

AF INR target

A

2-3

185
Q

Metallic mitral valves click

A

Replaces S1

186
Q

Types of valves

A

Starr Edwards (with ball in a cage) – not used due to thrombus formation
Tilting disc valve – single tilting disc
St Jude valves – bileaflet valves – smallest risk of thrombus

187
Q

Metallic aortic valves click

A

Replaces S2

188
Q

Mechanical heart valves complications

A
  • Thrombus formation (blood stagnates and clots)
  • Infective endocarditis (infection in the prosthesis)
  • Haemolysis causing anaemia (blood gets churned up in the valve)
189
Q

TAVI

A

Transcatheter aortic valve implantation – treatment for severe aortic stenosis – catheter inserted into femoral artery, implanting a bioprosthetic valve

190
Q

Infective endocarditis mortality rate

A

15%

191
Q

Infective endocarditis causative organisms

A

Gram-positive cocci
* Staphylococcus
* Streptococcus
* Enterococcus

192
Q

Infective endocarditis

A

Infection of the endothelium (inner heart surface) – affects heart valves and can be acute/subacute/chronic

193
Q

Risk factors for infective endocarditis

A
  • Intravenous drug use
  • Structural heart pathology
  • Chronic kidney disease
  • Immunocompromised (e.g., cancer, HIV or immunosuppressive medications)
  • History of infective endocarditis
194
Q

Structural pathologies increasing risk of endocarditis

A
  • Valvular heart disease
  • Congenital heart disease
  • Hypertrophic cardiomyopathy
  • Prosthetic heart valves
  • Implantable cardiac devices (e.g.,pacemakers)
195
Q

Causes of infective endocarditis

A
  • Staphylococcus aureus.
  • Streptococcus (viridans)
  • Enterococcus (e.g., Enterococcus faecalis)
196
Q

Symptoms of infective endocarditis

A

Fever
Night sweats
Muscle ache
Loss of appetite

197
Q

Examination findings in infective endocarditis

A
  • New or “changing” heart murmur
  • Splinter haemorrhages
  • Petechiae
  • Janeway lesions
  • Osler’s nodes
  • Roth spots (haemorrhages on the retina)
  • Splenomegaly
  • Finger clubbing
198
Q

Petechiae

A

(small non-blanching red/brown spots) on the trunk, limbs, oral mucosa or conjunctiva

199
Q

Osler’s nodes

A

(tender red/purple nodules on the pads of the fingers and toes)

200
Q

Janeway lesions

A

(painless red flat macules on the palms of the hands and soles of the feet)

201
Q

Blood tests for infective endocarditis

A

Blood cultures – 3 cultures separated by 6h from 3 different sites

202
Q

Imaging in infective endocarditis

A

Echocardiography, transoesophageal echocardiography,
For prosthetic valves: PET/CT or SPECT/CT

203
Q

Modified Duke criteria

A

Diagnosis of infective endocarditis (1 major + 3 minor OR 5 minor)

204
Q

Duke criteria (major and minor)

A

Major: +ve blood cultures, imaging findings
Minor: predisposition, fever, vascular phenomena, immunological phenomena, microbiological phenomena

205
Q

Mx of infective endocarditis

A

IV broad spectrum abx (amoxicillin and optional gentamycin)
- 4 weeks for native valves
- 6 weeks for prosthetic valves

206
Q

When is surgery required in infective endocarditis?

A
  • Heart failure relating to valve pathology
  • Large vegetations
  • Infections not responding to abx
207
Q

Hypertrophic obstructive cardiomyopathy (HOCM)

A

Left ventricle becomes hypertrophic
Autosomal Dominant (defect in gene of sarcomere proteins)

208
Q

left ventricular outflow tract obstruction

A

Hypertrophic obstructive cardiomyopathy asymmetrically affects the septum, blocking the outflow of blood from the left ventricle

209
Q

HOCM examination findings

A

Ejection systolic murmur (lower left sternal vorder)
4th heart sound
Trhill (lower left sternal border)

210
Q

What medications are avoided in HCOM?

A

ACE inhibitors and nitrates are avoided as they can worsen the LVOT obstruction.

210
Q

Ix in HOCM

A

Echocardiogram or cardiac MRI
Genetic testing
Chest x ray (normal/pulmonary oedema)
ECG (left ventricular hypertrophy)

210
Q

Mx of HOCM

A
  • Beta blockers
  • Surgical myectomy
  • Alcohol septal
  • Implantable cardioverter defibrillator
  • Heart transplant
210
Q

Dilated cardiomyopathy

A

heart muscle becomes thin and dilated

211
Q

Alcohol-induced cardiomyopathy

A

dilated cardiomyopathy caused by long-term alcohol use.

211
Q
A
212
Q

Restrictive cardiomyopathy

A

heart becomes rigid and stiff, causing impaired ventricular filling during diastole.

213
Q

Arrhythmogenic cardiomyopathy

A

Genetic condition
Heart muscle is replaced with fibrofatty tissue
->Cause of sudden cardiac death in athletes

213
Q

Takotsubo cardiomyopathy

A

Left ventricular dysfunction and weakness
Follows emotional stress – Broken heart syndrome

213
Q

Symptoms of AF

A

SOB
Dizziness
Syncope
Stroke
Palpitations
Irregularly irregular choice

213
Q

AF

A

Electrical activity in the atria becomes disorganised; fibrillation – random muscle twitching
- Irregularly irregular ventricular contractions
- Tachycardia
- Heart failure
- Increased stroke risk

213
Q

2 differential diagnoses for irregularly irregular pulse:

A

AF
Ventricular ectopics (Disappear at high heart rate)

213
Q

Causes of AF

A

Sepsis
Mitral valve pathology (stenosis or regurgitation)
Ischaemic heart disease
Thyrotoxicosis
Hypertension
Alcohol and caffeine

214
Q

ECG in AF

A

Absent P waves
Narrow QRS tachycardia
Irregularly irregular ventricular rhythm

214
Q

Paroxysmal atrial fibrillation

A

episodes of atrial fibrillation that reoccur and spontaneously resolve back to sinus rhythm. they last between 30sec - 48 hours.

215
Q

Ix for Paroxysmal atrial fibrillation

A
  • 24-hour ambulatory ECG (Holter monitor)
  • Cardiac event recorder lasting 1-2 weeks
216
Q

Valvular Atrial Fibrillation

A

AF with significant mitral stenosis or a mechanical heart valve. (AF without valve pathology is non-valvular AF)

217
Q

AF treatment

A
  • Rate or rhythm control
  • Anticoagulation to prevent strokes
218
Q

Rate control

A

1st step for pts with AF (except reversible cause of AF, onset within 48h, heart failure)
Aim for Heart rate <100

218
Q

Rate control drugs

A

B blocker (1st line) – atenolol, bisoprolol
Ca channel blocker (diltiazem or veramapil) – DO NOT give in heart failure
Digoxin – only in sedentary people, toxic, needs close monitoring

218
Q

Rhythm control

A

Aims to restore normal sinus rhythm
Offered to pts with:
- Reversible cause AF
- New onset AF within 48h
- Heart failure caused by atrial fibrillation

219
Q

Rhythm control process

A

Either
- Cardioversion (immediate or delayed)
- Long-term rhythm control

220
Q

Immediate cardioversion

A
  • AF for less than 48 hours
  • Causing life-threatening haemodynamic instability
  • Either electrical or pharmacological
220
Q

Immediate pharmacological cardioversion

A
  • Flecainide
  • Amiodarone
220
Q

Drug of choice in AF cardioversion in structural heart disease?

A

amiodarone

220
Q

Electrical cardioversion

A

Shock the heart back into sinus rhythm (cardiac defibilator, sedation or general anaesthesia)cardioversion

221
Q

Delayed cardioversion

A

Used in AF >48h
- Electrical
- Transoesophageal echocardiography-guided cardioversion
- Amiodarone added before and after electrical cardioversion to prevent recurrence

221
Q

Anticoagulation in delayed cardioversion

A

For at least 3 weeks before cardioversion
Pts are rate controlled in the meantime

221
Q

Long term rhythm control drugs

A
  • Beta blockers 1st
  • Dronedarone 2nd
  • Amiodarone is useful in patients with heart failure or left ventricular dysfunction
221
Q

Mx of paroxysmal AF

A

Pill-in-the-pocket
For pts with infrequent episodes and no structural heart disease
Take a pill when symptoms starting

221
Q

Paroxysmal AF drugs

A

Flecainide – pill in the pocket – might convert AF into atrial flutter with 1:1 AV conduction

222
Q

When is ablation needed?

A

When rate or rhythm control drug treatment is inadequate

223
Q

Atrioventricular node ablation

A

Destroys the av node; permanent pacemaker is required to control ventricular contraction

223
Q

Anticoagulation in AF

A

DOAC 1st line
Warfarin

223
Q

Left atrial ablation

A

Performed in cath lab under sedation/GA – catheter inserted into femoral vein to the left atrium- radiofrequency ablation (heat) burns the abnormal electrical activity areas

223
Q

Risk of stroke in AF

A

Without anticoagulation: 5%
With 1-2% per year

223
Q

DOAC

A

Do not require INR monitoring
6-14h half life

223
Q

Direct thrombin inhibitor

A

Dabigatran

223
Q

Direct Xa factor inhibitors

A

Apixaban, edoxaban and rivaroxaban

224
Q

Which DOACs are taken 1x daily

A

edoxaban and rivaroxaban

224
Q
A
224
Q

Which DOACs are taken 2x daily

A

Apixaban and dabigatran

225
Q

How to reverse apixaban and rivaroxaban action?

A

Andexanet alfa

226
Q

How to reverse dabigatran action?

A

Idarucizumab

227
Q

Indications for DOACs

A
  • Stroke prevention in patients with AF
  • Treatment of (DVT) and (PE)
  • Prophylaxis of venous thromboembolism (DVTs and PEs) after a hip or knee replacement
228
Q

Advantages of DOACs over warfarin

A

No monitoring required
No major interactions
Less bleeding risk than warfarin
Better control of strokes in AF than warfarin

229
Q

Warfarin

A

Vit K antagonist – prolongs prothrombin time (time taken for blood to clot)

230
Q

INR

A

Assesses how coagulated pt is
INR 1 – normal prothrombin time
INR 2 – prothrombin time twice as normal

231
Q

Target INR for AF

A

2-3

232
Q

TTR time in therapeutic range

A

Refers to percentage of time that INR is in the target range (when INR is too low, risk of stroke, when too high, risk of bleeding)

232
Q
A
232
Q

CHA2DS2-VASc

A

Assess whether patient with AF should start anticoagulation. The higher the score, the higher risk of stroke or TIA

232
Q

How to reverse vit K effects?

A

Vit K

232
Q

CHA2DS2-VASc of 2

A

Offer anticoagulation

232
Q

CHA2DS2-VASc score

A
  • C – Congestive heart failure
  • H – Hypertension
  • A2 – Age above 75 (scores 2)
  • D – Diabetes
  • S2 – Stroke or TIA previously (scores 2)
  • V – Vascular disease
  • A – Age 65 – 74
  • S – Sex (female)
232
Q

ORBIT score

A

Assesses risk of major bleeding in pts with AF taking anticoagulation

232
Q

CHA2DS2-VASc of 1

A

Consider anticoagulation in men (women automatically score of 1)

232
Q

CHA2DS2-VASc of 0

A

No anticoagulation

232
Q

ORBIT score factors

A
  • O – Older age (age 75 or above)
  • R – Renal impairment (GFR <60)
  • B – Bleeding previously (history of gastrointestinal or intracranial bleeding)
  • I – Iron (low haemoglobin or haematocrit)
  • T – Taking antiplatelet medication
232
Q
A
233
Q

Left atrial appendage occlusion

A

Used in pts with contraindications for anticoagulation and high stroke risk
Plug is placed in left atrial appendage preventing blood pooling/accessing the area

233
Q

Supraventricular tachycardia

A

Caused by electrical signal re-entering the atria from the ventricles; the signal travels through atrioventricular node again -> narrow complex tachycardia (QRS has a duration of <0.12 seconds)

234
Q

AF on ECG

A
  • Absent P waves
  • Narrow QRS complex tachycardia
  • Irregularly irregular ventricular rhythm
235
Q

Atrial flutter on ECG

A

Atrial rate is 300 beats
Saw-tooth pattern
2 atrial contractions per 1 ventricular contraction

235
Q

Sinus tachycardia on ECG

A

Normal P wave, QRS, T wave

235
Q

3 types of SVT

A
  • Atrioventricular nodal re-entrant tachycardia
  • Atrioventricular re-entrant tachycardia
  • Atrial tachycardia
235
Q

Supraventricular tachycardia on ECG

A

QRS followed immediately by T wave
P waves are present by buried in the T waves
Different from AF – regular rhythm
Different from atrial flutter – no saw-tooth pattern
Narrow complex tachycardia
Occurs at rest with no cause (sinus tachy has gradual onset and explanation – pain/fever)

235
Q

Atrioventricular re-entrant tachycardia

A

Re-entry point is an accessory pathway (somewhere between atria and ventricles)
- This is called Wolff-Parkinson-White syndrome

235
Q

What is a Delta wave on ECG

A

Slurred upstroke on QRS complex

235
Q

Atrioventricular nodal re-entrant tachycardia

A

The re-entry point is via atrioventricular node (most common type of SVT)

235
Q

Atrial tachycardia

A

Electrical signal originates in the atria but outside the sinoatrial node (abnormally generated electrical activity)

235
Q

Treatment for WPW syndrome

A

Radiofrequency ablation of the accessory pathway

235
Q

Wolff-Parkinson-White syndrome

A

Extra electrical pathway connecting the atria and ventricles (also called pre-excitation syndrome)
Extra pathway is called Bundle of Kent

235
Q

Wolff-Parkinson-White on ECG

A
  • Short PR interval, less than 0.12 seconds
  • Wide QRS complex, greater than 0.12 seconds
  • Delta wave
235
Q

Valsalva manoeuvres

A

Increase thoracic pressure (pt blows against resistance for 10-15sec)

236
Q

vagal manouvres

A

Stimulate the vagus nerve, increase the activity of parasympathetic nervous system (slow conduction of electrical activity in the heart)

236
Q

What drugs are contraindicated in WPW?

A

Anti-arrhythmic (beta blockers, calcium channel blockers, digoxin, adenosine) – as they promote conduction through the accessory pathway and lead to wide complex tachycardia

236
Q

WPW treatment

A

Step 1: Vagal manoeuvres
Step 2: Adenosine
Step 3: Verapamil or a beta blocker
Step 4: Synchronised DC cardioversion (IV amiodarone added if DC unsuccessful)

237
Q

How to give adenosine?

A

Rapid IV bolus, grey cannula
* Initially 6mg
* Then 12mg (after 2 mins)
* Then 18mg

238
Q

Carotid sinus massage

A

Stimulating baroreceptors

239
Q

adenosine

A

Slows cardiac conduction through AV node (might inially cause asystole or bradycardia)

239
Q

When is Synchronised DC applied?

A

During R wave (ventricular contraction)
Avoid T wave – will cause ventricular fibrillation

239
Q

What arrhythmias can be resolved by radiofrequency ablation?

A
  • Atrial fibrillation
  • Atrial flutter
  • Supraventricular tachycardias
  • Wolff-Parkinson-White syndrome
239
Q

Mx of paroxysmal SVT

A
  • Long term (b blockers, ca channel blockers, amiodarone)
  • Radiofrequency ablation
239
Q

Diving reflex

A

Submerging pt’s face in cold water

239
Q

Which pts shouldn’t take adenosine?

A
  • Asthma
  • COPD
  • Heart failure
  • Heart block
  • Severe hypotension
  • Potential atrial arrhythmia with underlying pre-excitation
240
Q

Shockable pulseless rhythms

A
  • Ventricular tachycardia
  • Ventricular fibrillation
241
Q

non shockable pulseless rhythm

A
  • Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)
  • Asystole (no significant electrical activity)
242
Q

Narrow complex tachycardia (4 differentials)

A

QRS complex <0.12 sec (3 small squares)
- Sinus tachycardia
- Supraventricular tachycardia (vagal manouvres and adenosine)
- Atrial fibrillation (rate control or rhythm control)
- Atrial flutter (rate control or rhythm control)

243
Q

Broad complex tachycardia (4 differentials)

A

QRS >0.12 sec (3 small squares)
- Ventricular tachycardia (treated with IV amiodarone)
- Polymorphic ventricular tachycardia, such as torsades de pointes (treated with IV magnesium)
- Atrial fibrillation with bundle branch block (treated as AF)
- Supraventricular tachycardia with bundle branch block (treated as SVT)

244
Q

Life threatening arrythmia features – treatment

A

Synchronised DC cardioversion under sedation/GA
IV amiodarone added if DC shock unsuccessful

245
Q

Prolonged QT interval

A
  • > 440 milliseconds in men
  • > 460 milliseconds in women
246
Q

Torsades de pointes

A

Polymorphic ventricular tachycardia

247
Q

Prolonged QT causes

A
  • Long QT syndrome (inherited)
  • Medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide)
  • Electrolyte disturbance
248
Q

Treatment for prolonged QT interval

A

B Blocker (not sotalol)
Pacemaker or implacntable cardioverter

249
Q

Acute Mx of torsades de pointes

A
  • Magnesium infusion
  • Defibrillation if ventricular tachycardia present
250
Q

Ventricular ectopics

A

Premature ventricular beats

251
Q

bigeminy

A

Every other beat is a ventricular ectopic (normal beat on ECG followed by ectopic beat) – b blockers might be used to manage symptoms

252
Q

First-degree heart block

A

PR >0.2 seconds (5 small or 1 big square)

253
Q

Second-degree heart block

A

When at instances P waves don’t follow QRS (some impulses don’t reach atrioventricular node and ventricles)

254
Q

Mobitz type 1 / Wenckebach phenomenon

A

Longer longer longer drop – increasing PR interval until P wave is not followed by QRS (2nd degree heart block)

255
Q

Mobitz type 2

A

Intermittent failure of conduction though av node – not all P waves are followed by QRS – ex ratio 3:1 or 2:1. PR interval remains normal

256
Q

Third-degree heart block

A

Complete heart block; no relation between P waves and QRS complex (risk of asystole)

257
Q

Bradycardia 3 main causes

A

Medications
Heart block
Sick sinus syndrome

258
Q

Sick sinus syndrome

A

dysfunction of the sinoatrial node (idiopathic degenerative fibrosis)

259
Q

Risk factors for asystole

A
  • Mobitz type 2
  • Third-degree heart block (complete heart block)
  • Previous asystole
  • Ventricular pauses longer than 3 seconds
260
Q

atropine

A

Antimuscarinic, inhibits parasympathetic nervous system – leads to pupil dilation, dry mouth, urinary retention, constipation

260
Q

Temporary cardiac pacing

A
  • Transcutaneous pacing
  • Transvenous pacing
261
Q

pacemaker

A

Consists of pulse generator and the pacing leads that carry electrical impulses to the parts of the heart. The wires are fed into the left subclavian vein and the chambers of the heart.

261
Q

Mx of unstable pts and at risk of asystole

A
  • Intravenous atropine (first line)
  • Inotropes (e.g., isoprenaline or adrenaline)
  • Temporary cardiac pacing
  • Permanent implantable pacemaker, when available
261
Q

Which medical equipment is not compatible with the pacemakers

A

MRI scans, TENS machines, diathermy

261
Q

Indications for a pacemaker

A
  • Symptomatic bradycardias (e.g., due to sick sinus syndrome)
  • Mobitz type 2 heart block
  • Third-degree heart block
  • Atrioventricular node ablation for atrial fibrillation
  • Severe heart failure (biventricular pacemakers)
262
Q

Biventricular / triple-chamber pacemaker

A

Have leads in right atrium, right ventricle, left ventricle
Usually in patients with severe heart failure (cardiac resynchronisation therapy)

262
Q

Dual chamber pacemaker

A

Have leads in the right atrium and right ventricle

262
Q

Single chamber pacemaker

A

Has leads in a single chamber: right atrium or right ventricle

263
Q

Implantable cardioverter defibrillators

A

Continually monitor the heart and apply a defibrillator shock if they identify ventricular tachycardia or ventricular fibrillation

264
Q

Conditions requiring implantable cardioverter

A
  • Previous cardiac arrest
  • Hypertrophic obstructive cardiomyopathy
  • Long QT syndrome
264
Q

Single chamber pacemaker on ECG

A

A line before either the P wave or QRS complex but not the other

264
Q

Dual chamber pacemaker on ECG

A

A line before both the P wave and QRS complex

Exam (17 decks)

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