Cardiology Flashcards

1
Q

What is essential hypertension?

A

Hypertension with no identifiable cause

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2
Q

What are risk factors for essential hypertension?

A

Increased age, family history, male sex, african-americans

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3
Q

What can essential hypertension lead to (broadly)?

A

Cardiac, renal and cerebral events

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4
Q

In primary care, if a patient has an initial blood pressure reading of >140/90, what should you do?

A

Repeat their blood pressure

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5
Q

In primary care, if a patients second blood pressure reading is again >140/90, what should you do?

A

Offer ambulatory or home blood pressure monitoring

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6
Q

How is ambulatory blood pressure monitoring done?

A

2 blood pressure measurements are taken per hour during usual waking hours (around 14 readings a day). An average blood pressure is then calculated from these

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7
Q

How is home blood pressure monitoring done?

A

2 consecutive blood pressure measurements are taken 1 minute apart, twice daily for 4-7 days. Measurements on day 1 are discarded and then an average of the other readings calculates the blood pressure.

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8
Q

How is end organ damage assessed in essential hypertension?

A

Test urine for proteinuria
Take bloods for glucose, electrolytes, creatinine, eGFR, cholesterol
Examine fundi for hypertensive retinopathy
Arrange a 12-lead ECG

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9
Q

What is stage 1 hypertension defined as (clinic & ABPM readings)?

A

Clinic ≥ 140/90

ABPM ≥135/85

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10
Q

What is stage 2 hypertension defined as (clinic & ABPM readings)?

A

Clinic ≥ 160/100

ABPM ≥ 150/95

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11
Q

What is severe hypertension defined as (clinic readings)?

A

Clinic ≥ 180 systolic or diastolic ≥ 110

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12
Q

What lifestyle interventions can be done for hypertension?

A

Healthy diet, low salt diet
Aerobic exercise
Stop smoking
Decrease alcohol intake

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13
Q

What is the first line treatment for patients under 55 with essential hypertension?

A

ACE inhibitor or ARB (e.g. rampipril or losartan)

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14
Q

What is the first line treatment for patients ≥55 or afro-carribean with essential hypertension?

A

Calcium channel blocker (e.g. amlodipine)

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15
Q

What is the second line treatment for essential hypertension?

A

ACEi/ARB + Calcium channel blocker

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16
Q

What is the third line treatment for essential hypertension?

A

ACEi/ARB + Calcium channel blocker + thiazide diuretic

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17
Q

Which kind of thiazide diuretics should patients be started on for 3rd line essential hypertension treatment?

A

Indapamide or chlortalidone

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18
Q

What drug is added 4th line in essential hypertension if the patients potassium is less than 4.5mmol?

A

Spironolactone

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19
Q

What is the 4th line treatment of essential hypertension if the patients potassium is more than 4.5mmol?

A

Higher dose of thiazide diuretic

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20
Q

How do ACE inhibitors work?

A

Prevent conversion of angiotensin I to angiotensin II leading to vasodilation and decreased BP

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21
Q

What are side effects of ACE inhibitors?

A

Dry cough, hyperkalaemia, fatigues, dizziness, headache

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22
Q

How do ARBs work?

A

Block angiotensin II receptors resulting in vasodilation and decreased BP

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23
Q

What are side effects of ARBs?

A

Dizziness, headache

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24
Q

What type of calcium channel blockers are used in hypertension treatment?

A

Dihydropiridines

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25
Q

What are side effects of dihydropiridines?

A

Flushing, headache, ankle swelling

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26
Q

How do calcium channel blockers work?

A

Block voltage gated calcium channels

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27
Q

How do thiazide diuretics work?

A

Inhibit sodium resorption at the distal convoluted tubule

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28
Q

What are side effects of thiazide diuretics?

A

Postural hypotension, gout, dehydration, electrolyte imbalance

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29
Q

What kind of drug is spironolactone?

A

Aldosterone agonist

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30
Q

What are some side effects of spironolactone?

A

Nausea, vomiting, hyperkalaemia, rashes, gynaecomastia

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31
Q

What does the umbrella term acute coronary syndrome cover?

A

Unstable angina, STEMI, NSTEMI

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32
Q

What are risk factors for acute coronary syndrome?

A

Obesity, smoking, family history, high cholesterol, alcohol

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33
Q

What are the two consequences of atherosclerotic plaque build up in the arteries?

A

Narrowing of the arteries (causing less blood any oxygen)

Sudden plaque rupture causing arterial occlusion

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34
Q

What are symptoms of acute coronary syndrome?

A

Pain - left sided, radiating to jaw and down arm
Breathlessness
Sweating
Nausea & vomiting

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35
Q

What causes STEMI?

A

Complete occlusion of a coronary artery due to plaque rupture, leading to myocardial ischaemia

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36
Q

What ECG changes do you see in STEMI?

A

ST elevation, T wave inversion, Q waves

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37
Q

What are the 3 criteria on an ECG that would be suggestive of STEMI?

A

≥1mm elevation in 2 adjacent limb leads OR
≥2mm elevation in 2 contiguous chest leads OR
New LBBB

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38
Q

Is troponin elevated in STEMI?

A

Yes

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39
Q

What leads will you see ST elevation in an inferior MI?

A

II, III, aVF

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40
Q

What artery is occluded in an inferior MI?

A

Right coronary artery

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41
Q

Why is an inferior MI likely to cause arrythmias?

A

As the RCA supplies the AV node and sometimes the SA node

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42
Q

What leads will you see ST elevation in an anterior MI?

A

V1-V6

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43
Q

What leads will you see ST elevation in an anteroseptal MI?

A

V1-V4

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44
Q

What leads will you see ST elevation in an anterolateral MI?

A

I, aVL, V5. V6

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45
Q

What artery is occluded in an anterior MI?

A

Left anterior descending (LAD)

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46
Q

What artery is occluded in a lateral MI?

A

Left circumflex

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47
Q

What leads will you see ECG changes in a posterior STEMI?

A

V1-V3 - ST DEPRESSION

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48
Q

What is an NSTEMI?

A

ACS where there is plaque rupture but transient/non-complete arterial occlusion

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49
Q

What are the ECG changes in NSTEMI?

A

Normal or ST depression and T wave inversion

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50
Q

Is troponin elevated in NSTEMI?

A

YES

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51
Q

What is unstable angina?

A

An ACS with no evidence of cardiac damage

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52
Q

What are the ECG changes in unstable angina?

A

Normal or ST depression and T wave inversion

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53
Q

Is troponin elevated in unstable angina?

A

NO

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54
Q

What drugs should all patients presenting with ACS be given ASAP?

A

Aspirin 300mg
Ticagrelor 180mg
Metoprolol 50-100mg/5-15mg IV

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55
Q

If a patient has ST elevation, how long is the window for doing PCI from diagnosis?

A

<120 minutes

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56
Q

If a patient with ST elevation is not able to get PCI within 120 minutes from diagnosis, how should you manage them?

A

Thrombolysis IV (Alteplase) and fondaparinux

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57
Q

After thrombolysis, when should you perform an ECG?

A

90 minutes later to check for resolution of ST elevation

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58
Q

How should patients with no ST elevation be managed first (following aspirin, ticagrelor & metoprolol)?

A

Fondaparinux or LMWH SC

Nitrates IV

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59
Q

After initial management of no ST elevation ACS, what should be calculated?

A

GRACE Score - estimates risk of death/MI

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60
Q

If the GRACE score is medium to high what should be done?

A

Coronary angiography

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61
Q

Following ACS, what antiplatelet therapy should all patients be on and for how long?

A

6 months dual antiplatelet therapy - aspirin 75mg and ticagrelor 90mg BD
Then aspirin 75mg lifelong

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62
Q

What other maintenance medications should all patients with ACS be put on?

A

ACE inhibitor - lifelong
Statin - lifelong
Beta-blocker - at least 12 months/lifelong

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63
Q

What is heart failure?

A

When cardiac output is inadequate for the bodies requirements

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64
Q

What is the pathophysiology of the systolic nature of heart failure?

A

Inability of the ventricle to contract normally, leading to a decreased ejection fraction and therefore decrease CO

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65
Q

What is the pathophysiology of the diastolic nature of heart failure?

A

Inability of the ventricle to relax and fill normally causing increased filling pressures (note that systolic and

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66
Q

What are the main causes of left heart failure?

A

MI, hypertension, CHD

67
Q

What are the symptoms of left heart failure?

A

Dyspnoea, fatigue, orthopnoea, PND, nocutrnal cough with pink frothy sputum

68
Q

What are the signs of left heart failure?

A

Displaced apex, gallop rhythm, murmurs (aortic stenosis/mitral regurgitation)

69
Q

What are the causes of right sided heart failure?

A

Left heart failure, pulmonary stenosis, cor pulmonale

70
Q

What are the symptoms of right sided heart failure?

A

Peripheral oedema, ascites, nausea, anorexia, facial engorgement

71
Q

What are the signs of right sided heart failure?

A

Pulsation in face and neck

Tricuspid regurgitation

72
Q

What is congestive cardiac failure?

A

Both right and left sided heart failure

73
Q

How is congestive cardiac failure classified?

A

Framingham criteria

74
Q

If you are suspicious of a diagnosis of heart failure, what is the first line investigation for a patient who has had an MI?

A

Echocardiogram within 2 weeks

75
Q

If you are suspicious of a diagnosis of heart failure, what is the first line investigation for a patient who has NOT had an MI?

A

Measure serum brain natruretic peptide (BNP)

76
Q

What is BNP?

A

A hormone produced by the left ventricle in response to stress/strain

77
Q

What do high levels of BNP correlate with in heart failure?

A

A poor prognosis

78
Q

If the BNP levels are high, what should you do?

A

Echocardiogram within 2 weeks

79
Q

If BNP levels are raised but not very high, what should you do?

A

Echocardiogram within 6 weeks

80
Q

What other investigations are important in heart failure?

A

FBC, U&Es, CXR, ECG

81
Q

What does CXR show in left ventricular failure?

A
Alveolar shadowing
Kerly B lines
Cardiomegaly
Dilated vessels
Effusion (pleural)
82
Q

How should you treat acute heart failure?

A

Oxygen
Diuretics, vasodilators, ionotropes
CPAP
Mechanical circulatory interventions

83
Q

What is the first line drug treatment for heart failure?

A

ACE inhibitor + betablocker

84
Q

What are the second line add on treatments for heart failure?

A

Addition of either
Aldosterone agonist (spironolactone)
ARB
Hydralazine and nitrate

85
Q

If heart failure persists after first and second line treatment, what should be considered?

A

Cardiac resynchronization OR
Digoxin OR
Ivabradine

86
Q

When should diuretics be used in heart failure?

A

Only if evidence of fluid overload

87
Q

What is stable angina?

A

Syndrome caused by plaques in the coronary arteries restricting blood flow and causing symptoms

88
Q

What are symptoms of stable angina?

A

Chest pain lasting minutes provoked by exercise or emotion, relived by rest/GTN

89
Q

What medication should all patients with stable angina be put on for cardioprotection?

A

Long term aspirin and statin

90
Q

What is the first line therapy for stable angina?

A

Betablocker

91
Q

What is the first line therapy for stable angina if the patient cannot tolerate a beta-blocker?

A

Rate limiting CCB - Verapamil or Diltiazem

92
Q

What is the second line treatment option for stable angina?

A

Betablocker + dihydropiridine CCB (Amlodipine, nifedipine)

93
Q

What treatment should be given to patients with stable angina for symptomatic relief?

A

GTN spray for prevention and relief

94
Q

What other therapies are available for stable angina?

A

Isosorbide mononitrate
Ivabradine
Nicorandil

95
Q

What causes murmurs?

A

Audible turbulent blood flow as a consequence of valve disease

96
Q

What is the diagnostic investigation for murmurs?

A

Echocardiogram

97
Q

‘Ejection systolic murmur best heard at the aortic region that radiates to the carotids’

A

Aortic stenosis

98
Q

‘Slow rising pulse’

A

Aortic stenosis

99
Q

What are causes of aortic stenosis?

A

Congenital bicuspid valve, rheumatic heart disease, age related calcification

100
Q

What sort of murmur does pulmonary stenosis cause?

A

Ejection systolic

101
Q

‘Pansystolic murmur best heart at the apex, radiating to the axilla’

A

Mitral regurgitation

102
Q

‘Displaced apex beat’

A

Mitral regurgitation

103
Q

‘Harsh pansystolic murmur’

A

Ventricular septal defect

104
Q

What are causes of a late systolic murmur?

A

Mitral valve prolapse

Coarctation of aorta

105
Q

‘Early diastolic murmur best heard when patient is sitting forward on expiration’

A

Aortic regurgitation

106
Q

‘Wide pulse pressure, collapsing pulse’

A

Aortic regurgitation

107
Q

‘High pitched blowing murmur’

A

Aortic regurgitation

108
Q

What are some causes of aortic regurgitation?

A

Endocarditis, aortic dissection, marfans, vasculitis

109
Q

‘Rumbling mid-diastolic murmur, best heard on expiration with patient lying on their side’

A

Mitral stenosis

110
Q

‘Opening snap, malar flush, tapping apex’

A

Mitral stenosis

111
Q

What are the causes of mitral stenosis?

A

Rheumatic fever, congenital

112
Q

‘Continuous machine like murmur’

A

Patent ductus arteriosis

113
Q

What are the features of innocent murmurs?

A

Soft, early systolic and vary with position

114
Q

Where do supraventricular arrhythmias originate from?

A

Above the ventricle (e.g. SA node, AV node, bundle of His)

115
Q

What are some examples of supraventricular tachycardias?

A

Atrial fibrillation
Atrial flutter
Ectopic atrial tachycardia

116
Q

What are examples of supraventricular bradycardias?

A

Sinus bradycardia

Sinus pauses

117
Q

Where do ventricular arrhythmias originate from?

A

The ventricle

118
Q

What are examples of ventricular arrythmias?

A

Ventricular ectopics
Premature ventricular complexes
Ventricular tachycardia
Ventricular fibrillation

119
Q

What are causes of arrhythmias?

A

Abnormal anatomy (e.g. LVH, accessory pathways)
Autonomic nervous system (e.g. increased vagal tone)
Metabolic (hypoxia, electrolyte imbalance)
Inflammation (myocarditis)
Drugs
Genetic

120
Q

What are ectopic beats?

A

Beats originating from somewhere other than the SA node

121
Q

What is re-entry tachycardia?

A

More than 1 conduction pathway in the heart results in different depolarisation speeds and a paroxysmal tachycardia as the depolarisation travels back up the accessory pathway reactivating the atria

122
Q

What is a congenital cause of re-entry tachycardia?

A

Wolff-Parkinson White syndrome

123
Q

What two classes of antiarrhythmic drugs are rhythm control?

A

Class I and II

124
Q

What two classes of antiarrhythmic drugs are rate control?

A

Class II and class IV

125
Q

What are some class I anti-arrhythmics?

A

Lignocaine, flecainide, quinidine

126
Q

What are some class II anti-arrythmic drugs?

A

Beta-blockers (bisoprolol)

127
Q

What are some class III anti-arrhytmic drugs?

A

Amiodarone, sotalol, dronedarone

128
Q

What is a class IV anti-arrhythmic drug?

A

Verapamil

129
Q

What is radiofrequency ablation?

A

Selective cautery of tissue to prevent tachycardia

130
Q

What is implantable cardioversion defibrillation?

A

Terminates arrhythmia by dose of electrical current

131
Q

What are the 3 types of atrial fibrillation?

A

Permanent Paroxysal Persistent

132
Q

What are the two main treatment areas for permanent atrial fibrillation?

A

Rate control

Anti-coagulation

133
Q

What are options for rate control in AF?

A

Beta-blocker (bisoprolol)
Rate limiting CCB (diltiazem, verapamil)
Digoxin

134
Q

What score is used to assess whether anti-coagulation is necessary?

A

CHA2DS2VASc

135
Q

What are the two ways of cardioverting patients?

A

Chemical

DC

136
Q

What time period do you have after the onset of symptoms of persistent AF to cardiovert the patient?

A

48 hours

137
Q

What is it important to carry out before cardioversion?

A

Anticoagulation

138
Q

What are drug options for chemical cardioversion?

A

Amiodarone

Flecainide

139
Q

How is tachycardia with adverse features treated?

A

DC Cardioversion

140
Q

How is regular broad complex tachycardia treated?

A

Amiodarone 300mg IV over 20-60min then 900mg over 24hrs

141
Q

How is regular narrow complex tachycardia treated?

A

Vagal manouevres

Adenosine (6mg->12mg->12mg)

142
Q

What is an irregular narrow complex tachycardia likely to be and how is it treated?

A

Probably AF

Betablocker or diltiazem

143
Q

How is bradycardia with adverse features managed?

A

Atropine 500mcg (repeat up to 3mg)

144
Q

What is the normal PR interval on an ECG?

A

0.12-0.2s

145
Q

What is the normal QRS complex length?

A

<0.12 s

146
Q

‘Tall tented T waves’

A

Hyperkalaemia

147
Q

Flattened T waves

A

Hypokalaemia

148
Q

S wave slurring

A

Digoxin toxicity

149
Q

Delta waves

A

Wolff-Parkinson White

150
Q

Shortened QT interval

A

Hypercalcaemia

151
Q

Lengthened QT interval

A

Hypocalcaemia

152
Q

Saddle shaped ST elevation

A

Pericarditis

153
Q

Absent P waves

A

Atrial fibrillation

154
Q

Irregularly irregular pulse

A

Atrial fibrillation

155
Q

J Waves on ECG

A

Hypothermia

156
Q

U waves on ECG

A

Hypocalcaemia

157
Q

S1 Q3 T3 Pattern

A

Pulmonary embolus

158
Q

Saw tooth baseline

A

Atrial flutter

159
Q

Prominent P waves in leads II and III

A

COPD

160
Q

Rightwards shift of QRS axis and poor progression of R wave

A

COPD

161
Q

Fibrinoid necrosis and BP of 200/140

A

Malignant hypertension

162
Q

What is Dresslers syndrome?

A

Post MI pericarditis

163
Q

What CHA2DS2VASC score do you anticoagulate?

A

2 and above

164
Q

How do you investigate pericarditis?

A

Echocardiogram