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Cardiology Flashcards

1
Q

Give 4 methods of secondary prevention of cardiovascular disease

A

4 A’s:
1. Aspirin (+12 months of clopidogrel)
2. Atorvastatin
3. Atenolol (or propranolol)
4. ACE inhibitor (commonly ramipril)

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2
Q

Give the pathophysiology of angina

A

Narrowing of coronary arteries reduces blood flow to myocardium.
In high demand there is insufficient flow.

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3
Q

What is the difference between stable and unstable angina?

A

Stable: relieved by rest/GTN

Unstable: occurs at rest

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4
Q

Give the recommended investigations for angina

A

CT angiography - GOLD STANDARD

ECG, FBC, U&Es, LFTs, Lipid profile, HbA1c

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5
Q

Give the management of angina

A
  1. GTN
  2. Beta-blocker OR CCB
  3. Secondary prevention (4 A’s)
  4. Percutaneous coronary intervention with coronary angioplasty
  5. Coronary artery bypass graft
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6
Q

Give the ECG changes seen in STEMI

A

ST elevation in arterial distribution

New left bundle branch block

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7
Q

What investigations should be undertaken when no ST elevation but strong suspicion of MI?

A
  1. Troponin
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8
Q

Which ECG leads demonstrate the inferior aspect of the heart, and which artery supplies this area?

A

II, III, aVF

Right coronary artery

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9
Q

Which ECG leads demonstrate the septal aspect of the heart and which artery supplies this area?

A

V1, V2

Left anterior descending

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10
Q

Which ECG leads demonstrate the anterior aspect of the heart and which artery supplies this area?

A

V3, V4

Left anterior descending

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11
Q

Which ECG leads demonstrate the lateral aspect of the heart and which artery supplies this area?

A

I, aVL, V5, V6

Circumflex artery

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12
Q

Give the presentation of MI

A
  1. Central crushing chest pain, radiating to L arm and jaw
  2. Nausea and vomiting
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13
Q

What are the differential diagnoses of raised troponin?

A
  1. ACS
  2. Renal failure
  3. Sepsis
  4. Myocarditis
  5. PE
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14
Q

Give the acute management of MI

A

MONA:

  1. Morphine
  2. Oxygen
  3. Nitrates
  4. Aspirin
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15
Q

Give the management of STEMI

A
  1. Primary percutaneous coronary intervention (within 12 hours)
  2. Thrombolysis if PCI not available - alteplase/streptokinase
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16
Q

Give the management of acute NSTEMI

A

BATMAN

  1. Beta blocker (bisoprolol)
  2. Aspirin
  3. Ticagrelor (P2Y12 inhibitor)
  4. Morphine
  5. Anticoagulant (fondaparinux)
  6. Nitrates

PCI if indicated

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17
Q

Give the complications of ACS

A
  1. Cardiogenic shock - presents with low BP
  2. Death
  3. Cardiac failure
  4. Arrhythmia
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18
Q

Which ECG leads demonstrate the posterior aspect of the heart?

A

V1-V3

Posterior MI causes ST depression in these leads

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19
Q

What is Dressler’s syndrome?

A

Autoimmune pericarditis provoked by MI

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20
Q

Give the presentation of Dressler’s syndrome

A
  1. Onset 1-3 weeks post MI
  2. Fever, pericardial effusion, anaemia, cardiomegaly
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21
Q

Give the management of Dressler’s syndrome

A

Self-limiting within a few days

NSAIDs and steroids

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22
Q

Give the triggers of left ventricular failure

A
  1. Iatrogenic
  2. Sepsis
  3. MI
  4. Arrhythmia
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23
Q

Give the presentation of acute left ventricular failure

A
  1. ACUTE BREATHLESSNESS (type 1 resp. failure) - worse when lying flat
  2. Cough
  3. Tachypnoea
  4. Decreased sats.
  5. Bilateral basal crepitations
  6. Hypotension - signifies cardiogenic shock
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24
Q

Give the presentation of right sided heart failure

A
  1. Raised JVP
  2. Peripheral oedema
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25
Q

Give the investigations for left ventricular failure

A
  1. ECG - assess for underlying cause
  2. ABG
  3. CXR
  4. BNP
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26
Q

What does a raised BNP reflect?

A

BNP is a protein released by ventricles when excessively stretched.

Indicates fluid overload of heart, tachycardia, sepsis, PE, renal impairment, COPD.

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27
Q

Give the management of acute left ventricular failure

A
  1. Stop IV fluids
  2. Stat dose of furosemide if necessary
  3. Oxygen - if sats falling
  4. Sit up - will relieve symptoms
  5. Inotropes (rarely) - e.g. noradrenaline
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28
Q

What is the method of action of dabigatran

A
  1. Anticoagulant
  2. Direct thrombin inhibitor
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29
Q

What is the reversal method for dabigatran

A

Idarucizumab

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30
Q

Describe the 2 types of chronic heart failure

A
  1. Systolic HF - impaired left ventricular function
  2. Diastolic HF - left ventricular relaxation
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31
Q

Give the presentation of chronic heart failure

A
  1. Breathlessness
  2. Cough
  3. Orthopnoea (SOB when lying flat)
  4. Paroxysmal nocturnal dyspnoea (sudden waking at nights with attacks of SOB and cough)
  5. Peripheral oedema
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32
Q

Describe the diagnosis of chronic heart failure

A
  1. BNP
  2. Echocardiogram
  3. ECG
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33
Q

Give the causes of chronic heart failure

A
  1. IHD
  2. Valvular heart disease (aortic stenosis)
  3. Hypertension
  4. Arrhythmias
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34
Q

Give the management of chronic heart failure

A

First line - ABAL:

  1. ACE inhibitor (ramipril)
  2. Beta blocker (bisoprolol)
  3. Aldosterone antagonist (spironolactone) - if Sx not controlled by 1. and 2.
  4. Loop diuretic (furosemide)

Second line - cardiac resynchronisation therapy

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35
Q

Give the side effects of furosemide

A

Hyponatraemia causing:

  1. Confusion
  2. Somnolence
  3. Peripheral oedema
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36
Q

Give the role of digoxin in chronic heart failure

A

Does not reduce mortality.

Provides symptomatic relief due to it’s inotropic properties.

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37
Q

Give the mechanism of action of digoxin

A

Cardiac glycoside

Positively inotropic, negatively chronotropic.

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38
Q

Give the indications for digoxin use

A
  1. AF - not commonly used
  2. Atrial flutter
  3. Chronic heart failure
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39
Q

Give causes of digoxin toxicity

A
  1. Overdose
  2. Renal failure (digoxin excreted renally)
  3. Hypokalaemia
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40
Q

Give the presentation of digoxin toxicity

A
  1. Xanthopsia – a yellow ring / discolouration of the vision
  2. Bradycardias
  3. Ventricular ectopic beats
  4. Heart block (various types)
  5. VT/VF – rare
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41
Q

Define cor pulmonale

A

Right sided heart failure caused by respiratory disease

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42
Q

Give the causes of cor pulmonale

A
  1. COPD - most common
  2. PE
  3. Cystic fibrosis
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43
Q

Give the presentation of cor pulmonale

A
  1. Often asymptomatic
  2. SOB
  3. Peripheral oedema
  4. Syncope
  5. Hypoxia/cyanosis
  6. Raised JVP
  7. Hepatomegaly

Back-log of blood through venous system leads to 3, 6, 7

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44
Q

Give the management of cor pulmonale

A
  1. Treat underlying cause
  2. Oxygen therapy
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45
Q

What values are considered hypertension?

A

Clinic: 140/90
Ambulatory: 135/85

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46
Q

Give the causes of hypertension

A
  1. Essential HTN
  2. Renal disease
  3. Obesity
  4. Pregnancy
  5. Endocrine (hyperaldosteronism)
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47
Q

Give the complications of hypertension

A
  1. IHD
  2. CVA
    3.Hypertensive retinopathy (diagnose with fundoscopy)
  3. Hypertensive nephropathy (haematuria on dipstick)
  4. Heart failure
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48
Q

Give the investigations for hypertension

A

24 hour ambulatory BP monitoring - indicated if clinic BP is high

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49
Q

Describe the first line management of hypertension

A
  1. Age <55 and non-black: ACE inhibitor (ramipril)
  2. Age >55 or black: CCB (amlodipine)
  3. Diabetic: ACEi/ARB regardless of age
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50
Q

Describe the second line management of hypertension

A
  1. Non-black: ACEi + CCB (ramipril + amlodipine)
  2. Black: CCB + ARB (amlodipine + candesartan)
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51
Q

Describe the third line management of hypertension

A

ACEi + CCB + Thiazide Diuretic (indapamide)

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52
Q

Give the fourth line management of hypertension

A

ACEi + CCB + Thiazide Diuretic + Beta-Blocker/A-Blocker (bisoprolol/doxazosin)

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53
Q

Give 3 side effects of thiazide diuretics and their presentation

A

Erectile dysfunction

Hypokalaemia
ECG:
1. T wave depression
2. ST sagging
3. U wave prominence
4. Prolonged P-R interval

Hypercalcaemia

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54
Q

When are aldosterone antagonists indicated in hypertension?

A

When thiazides cause hypokalaemia - spironolactone is potassium sparing.

*ACEi and spironolactone both cause hyperkalaemia - monitor U&Es

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55
Q

Give the role of verapamil in hypertension

A

Verapamil is a CCB

Contra-indicated as is rate-limiting.
B-blocker + verapamil may cause asystole.

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56
Q

What action causes the S1 heart sound?

A

AV valves closing

‘lub dub’

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57
Q

What action causes the S2 heart sound?

A

Semi-lunar valves closing

‘lub dub’

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58
Q

What action causes the S3 heart sound?

A

Chordae-tendinae ‘twang’ - normal in young people. Indicates heart failure in older people due to stiffening of ventricles and chordae tendinae.

‘lub de dub’

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59
Q

What action causes the S4 heart sound?

A

Stiff or hypertrophic ventricle - demonstrates turbulent flow from atria to non-compliant ventricle

‘le lub dub’

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60
Q

Where can the pulmonary valve be auscultated?

A

2nd ICS - L sternal edge

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61
Q

Where can the aortic valve be auscultated?

A

2nd ICS - R sternal edge

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62
Q

Where can the tricuspid valve be auscultated?

A

5th ICS - L sternal edge

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63
Q

Where can the mitral valve be auscultated?

A

5th ICS - mid-clavicular line (apex space)

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64
Q

When is mitral stenosis most audible?

A

When lying on left hand side

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65
Q

When is aortic regurgitation most audible?

A

When sat up, leaning forward and holding exhalation

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66
Q

Which murmur radiates to the carotid arteries?

A

Aortic stenosis

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67
Q

How are murmurs described?

A

SCRIPT:

  1. Site
  2. Character
  3. Radiation
  4. Intensity
  5. Pitch
  6. Timing (systolic/diastolic)
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68
Q

How are murmurs graded?

A
  1. Difficult to hear
  2. Quiet
  3. Easy to hear
  4. Easy to hear with palpable thrill
  5. Can be heard with stethoscope barely on chest
  6. Can be heard with stethoscope off chest
69
Q

Give the cause of mitral stenosis

A
  1. Rheumatic heart disease
  2. Infective endocarditis
70
Q

Give the pathophysiology of mitral stenosis

A

Causes left atrial hypertrophy

71
Q

Describe the murmur heard in mitral stenosis

A

Mid-diastolic, low-pitched rumbling

72
Q

Give the cause of mitral regurgitation

A
  1. Idiopathic
  2. IHD
  3. Infective endocarditis
  4. Rheumatic heart disease
  5. Ehler’s Danlos/Marfan Syndrome
73
Q

Give the pathophysiology of mitral regurgitation

A

Left atrial dilation

Results in congestive cardiac failure

74
Q

Describe the murmur heard in mitral regurgitation

A

Pan-systolic high-pitched whistling

75
Q

Give cause of aortic stenosis

A
  1. Idiopathic calcification
  2. Rheumatic heart disease
76
Q

Describe the pathophysiology of aortic stenosis

A

Causes left ventricular hypertrophy

77
Q

Describe the murmur heard in aortic stenosis

A

Ejection-systolic crescendo-decrescendo high-pitched murmur radiating to the carotids

78
Q

Give the cause of aortic regurgitation

A
  1. Idiopathic age-related weakness
  2. Ehler’s Danlos/Marfan
79
Q

Give the pathophysiology of aortic regurgitation

A

Causes left ventricular dilation

80
Q

Describe the murmur heard in aortic regurgitation

A

Soft early diastolic murmur associated with collapsing pulse and head nodding (De Mussett’s sign)

81
Q

Give the lifespan of biosynthetic prosthetic valves

A

10 years

82
Q

Give the lifespan of mechanical valves

A

20+ years

Require life-long warfarin with target INR of 2.5-3.5

83
Q

Give the clotting screen results seen on warfarin

A

Prolonged prothrombin time, with a normal activated partial prothrombin time (APTT).

84
Q

Give the major complications of prosthetic heart valves

A
  1. Infection endocarditis (staphylococcus, streptococcus, enterococcus)
  2. Thrombus formation
  3. Haemolysis
85
Q

Which valvular disease is associated with polycystic kidney disease?

A

Mitral valve prolapse

86
Q

Define atrial fibrillation

A

Uncoordinated, rapid, irregular contraction of the atria due to disorganised electrical activity.

87
Q

Give the presentation of AF

A
  1. Irregularly irregular pulse
  2. Tachycardia
  3. Heart failure
  4. Palpitations
  5. SOB
  6. Syncope
88
Q

Describe the ECG presentation of AF

A
  1. Absent p waves
  2. Narrow QRS
  3. Irregularly irregular ventricular rhythm
89
Q

Give the causes of AFM

A

“AF affects Mrs Smith”

  1. Sepsis
  2. Mitral valve pathology
  3. IHD
  4. Thyrotoxicosis
  5. Hypertension
90
Q

Define paroxysmal AF

A

Comes and goes, with attacks not lasting longer than 48 hours.

91
Q

Give the management of paroxysmal AF

A

Flecanide

“Pill-in-pocket” approach - carry medication, take when have attacks.

Anti-coagulate based on CHADS-VASc

92
Q

Give the first-line management of atrial fibrillation

A

Rate control:

  1. Allows for adequate ventricular filling
  2. B-blocker (atenolol)/CCB (diltiazem)/digoxin
93
Q

Give the second-line management of atrial fibrillation

A

Rate control - if rhythm control not indicated, e.g.
1. Cause is reversible
2. New onset
3. AF causing heart failure

Rate control:
1. Cardioversion - immediate if AF onset <48 hours or patient unstable
2. Cardioversion can be pharmacological (flecanide/amiodarone) or electrical (defibrillation under GA/sedation)

94
Q

Describe anticoagulation therapy in AF

A

First-line:
1. NOAC - e.g. apixaban/rivaroxaban (Xa inhibitor)
2. Reverse using andexanet alfa

Second-line:
1. Warfarin (vitamin K antagonist)
2. Target INR 2-3

95
Q

Describe the CHADS-VASc score

A

Assesses risk of developing stroke or TIA in the presence of AF

Score >1 indicates anticoagulant recommendation

C - congestive heart failure
H - hypertension
A2 - age >75
D - diabetes
S2 - stroke or TIA previously
V - vascular disease
A - age 65-74
S - sex (female)

96
Q

What are the 4 cardiac arrest rhythms?

A

Shockable:
1. Ventricular fibrillation
2. Ventricular tachycardia

Non-Shockable:
1. Pulseless electrical activity (PEA)
2. Asystole

97
Q

Describe the presentation of atrial flutter on ECG

A
  1. HR >150bpm
  2. ‘Saw tooth’ appearance
98
Q

Give the management of atrial flutter

A
  1. Rate control: beta blocker
  2. Rhythm control: cardioversion
  3. Treat underlying cause (IHD, HTN, cardiomyopathy)
99
Q

Give the pathophysiology of supra-ventricular tachycardia

A

Electrical signals re-enter the atria from the ventricles - then travel back through the AV node to cause an additional contraction.

100
Q

Give the management of supra-ventricular tachycardia

A
  1. Valsalva manoeuvre - blowing hard against resistance (e.g. sealed syringe)
  2. Carotid sinus massage
  3. Adenosine bolus
  4. Direct current cardioversion - if systolic BP <90
101
Q

Describe the mechanism of action of adenosine

A
  1. Slows conduction through the AV node, to ‘reset’ back to sinus rhythm
  2. Causes brief asystole/bradycardia - causes sense of impending doom/chest pain
102
Q

Describe the pathophysiology of Wolff-Parkinson-White syndrome

A
  1. Extra electrical pathway connecting the atria and ventricles
  2. Causes SVT

ECG: short PR, wide QRS

103
Q

Describe the management of Wolff-Parkinson-White

A

Radiofrequency ablation of additional pathway

Heat applied to burn areas of heart and convert to non-conducting scar tissue.

Curative in AF, atrial flutter, WPW, SVT.

Will need to continue lifelong clopidogrel for anticoagulation after ablation even if curative.

104
Q

Describe the pathophysiology of Torsades de Pointes

A

Ventricular tachycardia in which the height of the QRS complex progressively gets smaller, then larger again, then smaller again etc.

105
Q

Give the causes of Torsades de Pointes

A
  1. Hypokalaemia/hypocalcaemia/hypomagnasaemia
  2. Antipsychotics
  3. Citalopram (also causes QT prolongation)
  4. Amiodarone
  5. Macrolides (e.g. clarithromycin)
106
Q

Give the management of Torsades de Pointes

A
  1. Correct underlying cause
  2. Magnesium infusion
  3. Defibrillation if necessary
  4. Beta blocker
  5. Pacemaker
107
Q

Give the pathophysiology of ventricular ectopics

A

Premature ventricular beats, presenting with brief palpitations

108
Q

Give the ECG presentation of ventricular ectopics

A

Random, abnormal brief broad QRS complexes on an otherwise normal ECG

109
Q

Give the management of ventricular ectopics

A

Correct underlying electrolyte disturbance

Reassurance - no treatment required in healthy individuals

110
Q

Define 1st degree heart block

A

PR interval <0.2s with no beats dropped

111
Q

Describe 2nd degree heart block

A

Mobitz I: progressive prolongation of PR interval until a beat is dropped

Mobitz II: constant PR interval with occasional dropped beats

112
Q

Describe third degree heart block

A

P waves and QRS complexes with no association

Significant risk of asystole

113
Q

Describe the ratio of chest compressions:ventilation:defibrillation in adult advanced life support

A

30 chest compressions:2 breaths

Single shock delivered with 2 minutes of CPR between shocks

114
Q

Describe the drug management in adult advanced life support

A

Adrenaline: 1mg ASAP if non-shockable rhythm. 1mg after 3rd shock in VT/VF, repeat every 3-5 minutes

Amiodarone: 300mg after 3rd shock in VT/VF (used to treat arrhythmias - if patient has non-shockable rhythm then is not indicated)

Thrombolysis: if PE suspected, then continue CPR for 60-90 minutes

115
Q

Give the management of AV node block (heart block)

A
  1. Atropine (IV bolus) - if no improvement then repeat up to 6x with increasing doses
  2. Inotroped (e.g. noradrenaline)
  3. Transcutaneous cardiac pacing
  4. Pacemaker
116
Q

Give the mechanism of action of atropine

A

Anti-muscarinic (anti-cholinergic) - acts to inhibit the parasympathetic nervous system and increase heart rate

117
Q

Define cardiac tamponade

A

Condition where the heart becomes compressed by fluid in the pericardial space, limiting its expansion and reducing diastolic filling.

May cause cardiac arrest.

118
Q

Give the causes of cardiac tamponade

A
  1. Trauma (particularly penetrating injury of the chest allowing blood to accumulate)
  2. Pericarditis
  3. Cancer
119
Q

Give the presentation of cardiac tamponade

A

Beck’s Triad:
1. Hypotension
2. Distended neck veins
3. Muffled heart sounds

  1. Tachycardia
  2. SOB
  3. Chest pain
  4. Pleural effusion
120
Q

Give the management of cardiac tamponade

A
  1. Pericardiocentesis - insertion of wide-bore cannula to drain fluid
  2. Surgery
  3. Conservative management
121
Q

Give the pathophysiology of aortic dissection

A

Tear in the tunica intima of the aortic wall

122
Q

Give the causes of aortic dissection

A
  1. Hypertension
  2. Trauma
  3. Ehler’s Danlos syndrome
  4. Marfan syndrome
  5. Turner syndrome
  6. Noonan syndrome
123
Q

Give the presentation of aortic dissection

A
  1. Chest/back pain - tearing in nature.
  2. Pulse deficit
  3. Hypertension
124
Q

Which classification of aortic dissection most commonly presents with chest pain?

A

Type A

125
Q

Which classification of aortic dissection most commonly presents with back pain?

A

Type B

126
Q

Describe the classification system used for aortic dissection

A

Stanford classification

Type A: ascending aorta (2/3 of cases)
Type B: descending aorta distal to L subclavian origin

Type A = Ascending Aorta

127
Q

Describe the pathophysiology of obstructive hypertrophic cardiomyopathy

A

An autosomal dominant disorder of muscle tissue caused by defects in the genes encoding contractile proteins.

128
Q

Describe the management of obstructive hypertrophic cardiomyopathy

A

ABCDE:

  1. Amiodarone
  2. Beta blocker
  3. Cardioverter defibrillator
  4. Dual chamber pacemaker
  5. Endocarditis prophylaxis
129
Q

Give the presentation of obstructive hypertrophic cardiomyopathy

A
  1. Often asymptomatic
  2. Exertional dyspnoea
  3. Angina
  4. Syncope
  5. Mitral regurgitation
  6. Sudden cardiac death
130
Q

Give the pathophysiology of infective endocarditis

A

Infection of the endocardium by bacteria, most commonly affecting the valves.

Commonly caused by staphylococcus, streptococcus, enterococcus.

131
Q

Which valve is commonly affected by infective endocarditis in IVDU?

A

Tricuspid valve - most commonly by Staph. aureus

132
Q

Give the causes of infective endocarditis

A
  1. IVDU
  2. Poor dental hygiene
  3. Cannulae
  4. Surgery
133
Q

Describe the presentation of infective endocarditis

A

New murmur PLUS fever is infective endocarditis until proven otherwise!

  1. Petechiae
  2. Cardiac/renal failure
  3. Night sweats
  4. Rigors/malaise/fatigue
  5. Splinter haemorrhages
  6. Roth spots
  7. Janeway lesions
  8. Osler nodes

ECG: non-specific saddle shaped ST elevation

134
Q

Define Roth spots

A

Retinal haemorrhages with a pale centre

135
Q

Define Janeway lesion

A

Non-tender small lumps on palms or soles

136
Q

Define Osler nodes

A

Painful red lesions on palms or soles

137
Q

How is infective endocarditis diagnosed?

A
  1. Blood culture (x3 in 24 hours)
  2. Echocardiogram
  3. ECG - non-specific ST elevation
138
Q

Give the management of infective endocarditis

A

Gentamycin + fluclox OR benzylpenicillin

If artificial valve: Gentamycin + vancomycin + rifampicin

If penicillin allergy: Gentamycin + vancomycin

If resistant to Abx: Surgery to replace or repair valve

139
Q

Describe the pathophysiology of left ventricular aneurysm

A

The ischaemic damage sustained during MI may weaken the myocardium resulting in aneurysm formation.

140
Q

Describe the presentation of left ventricular aneurysm

A
  1. Left ventricular failure
  2. Ankle oedema
  3. Dull chest pain

ECG: persistent ST elevation

141
Q

Give the management of left ventricular aneurysm

A

Anticoagulation - thrombus may form within the aneurysm

142
Q

Give the management of ventricular tachycardia

A

No adverse signs:
1. Amiodarone
2. Electrical cardioversion (if amiodarone fails)

Adverse signs (e.g. low BP):
1. Immediate electrical cardioversion

143
Q

Describe the presentation of left ventricular free wall rupture

A

Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds).

This is seen in around 3% of MIs and occurs around 1-2 weeks afterwards

144
Q

Describe the management of left ventricular free wall rupture

A

Urgent pericardiocentesis and thoracotomy are required.

145
Q

Give the adverse effects of loop diuretics

A
  1. hypotension
  2. hyponatraemia
  3. hypokalaemia, hypomagnesaemia
  4. hypochloraemic alkalosis
  5. ototoxicity
  6. hypocalcaemia
  7. renal impairment (from dehydration + direct toxic effect)
  8. hyperglycaemia (less common than with thiazides)
  9. gout
146
Q

Give the features of acute heart failure on chest xray

A

Bilateral fluffy opacification with Kerley-B lines

147
Q

Give the mechanism of action of loop diuretcs

A

Furosemide and bumetanide are loop diuretics that act by inhibiting the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of the loop of Henle, reducing the absorption of NaCl.

148
Q

What is the most appropriate management of complete heart block following an inferior MI?

A

Atropine

External pacing not indicated

149
Q

What is the most appropriate management of wide complex tachyarrhythmias with hypotension?

A

DC cardioversion

150
Q

Give the presentation of right axis deviation on ECG

A

Negative QRS complex in lead I and positive QRS complex in lead II and aVF

151
Q

Give the presentation of Takotsubo cardiomyopathy

A

History of acute or subacute chest pain in a post-menopausal woman after an emotionally stressful experience or situation is typical of Takotsubo cardiomyopathy

Shortness of breath, dizziness and syncope

152
Q

What are xanthomata suggestive of?

A

Hypercholesterolaemia/hyperlipidaemia

Xanthomata: yellowish papules and plaques commonly seen on eyelids

153
Q

Give the first line management for stable angina

A
  1. GTN
  2. A beta-blocker or a calcium channel blocker is used first-line to prevent angina attacks
154
Q

Give the ECG presentation of hypokalaemia

A

Hypokalaemia - U waves on ECG

155
Q

Give the management of symptomatic aortic stenosis

A

Symptomatic aortic stenosis:
1. surgical AVR for low/medium operative risk patients
2. transcatheter AVR for high operative risk patients

156
Q

Give the indications for PCI in acute STEMI

A

should be offered if the presentation is within 12 hours of the onset of symptoms AND PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given (i.e. consider fibrinolysis if there is a significant delay in being able to provide PCI)

157
Q

Give the management of provoked PE

A

‘Provoked’ pulmonary embolisms are typically treated for 3 months with apixaban

158
Q

Give 1 drug interaction for simvastatin

A
  1. Clarithromycin
159
Q

What tool should be used to assess bleeding risk in AF when considering anticoagulation?

A

ORBIT score

160
Q

Give 1 medication which causes Torsades de Pointes

A

Macrolides can cause torsades de pointes
(e.g. erythromycin)

161
Q

Give 1 medication which causes hypocalcaemia

A

Hypocalcemia is a side effect of loop diuretics (e.g. furosemide)

162
Q

Give the management of aortic dissection

A

Type A: IV labetalol + surgery

Type B: IV labetalol

163
Q

Give the ECG changes seen in hypokalaemia

A

presence of U waves (small upward deflections seen after the T waves), flattened T waves, and a borderline elongated PR interval.

164
Q

When is cardiac resynchronisation therapy indicated in chronic heart failure?

A

heart failure not responding to ACE-inhibitor, beta-blocker and aldosterone antagonist therapy, a widened QRS complex favours cardiac resynchronisation therapy

165
Q

Describe the New York Heart Association grading of chronic heart failure

A

NYHA Class I
1. no symptoms
2. no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations

NYHA Class II
1. mild symptoms
2. slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea

NYHA Class III
1. moderate symptoms
2. marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms

NYHA Class IV
1. severe symptoms
2. unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity

166
Q

What does PCI involve?

A

administration of prasugrel, unfractionated heparin and a bailout glycoprotein IIb/IIIa inhibitor.

167
Q

Give 1 example of a long-acting nitrate

A

Ivabradine

168
Q

Give the management of acute pericarditis

A

First line management of acute pericarditis involves combination of NSAID and colchicine

169
Q

Give the mechanism of action of dabigatran

A

Direct thrombin inhibitor

Finals (11 decks)

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