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Phase 2a > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What are the risk factors for atherosclerosis?

A
  • Age
  • Smoking
  • High serum cholesterol
  • Obesity
  • Diabetes
  • Hypertension
  • Family history
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2
Q

In which arteries would you be most likely to find atheromatous plaques?

A

In the peripheral and coronary arteries - LAD, circumflex, RCA

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3
Q

Describe in 5 steps the progression of atherosclerosis.

A
  1. Fatty streaks
  2. Intermediate lesions
  3. Fibrous plaque
  4. Plaque rupture
  5. Plaque erosion
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4
Q

What is the earliest lesion of atherosclerosis? What do they consist of?

A
  • Fatty streaks (appear at a very early age <10 years)
  • Consist of aggregations of lipid–laden macrophages and T lymphocytes within the tunica intima
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5
Q

What can lesions progress to? What does this contain?

A
  • Intermediate lesion
  • Composed of layers of :
  • Foam cells
  • Vascular smooth muscle cells
  • T lymphocytes
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6
Q

What can intermediate lesions progress to? What do these contain?

A
  • Fibrous plaques or advanced lesions
  • Impedes blood flow
  • Prone to rupture
  • Covered by dense fibrous cap made of ECM proteins including collagen (strength) and elastin (flexibility) laid down by SMC that overlies lipid core and necrotic debris
  • May be calcified
  • Contains: smooth muscle cells, macrophages and foam cells and T lymphocytes
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7
Q

Describe the process of atherosclerosis.

A
  1. High levels of LDL in the blood. Some deposits in the tunica intima and become oxidised - this activates endothelial cells to attract leukocytes (ENDOTHELIAL CELL DYSFUNCTION)
  2. Monocytes etc. are attracted to the site of damage (endothelium) - move to tunica intima (become macrophages)
  3. Macrophages take up oxidised lipid to form foam cells (inflammatory response). These foam cells encourage plaque progression by serving as a source of pro inflammatory cytokines. They also promote the migration of smooth muscle cells from the tunica media to the tunica intima and smooth muscle cell proliferation - this causes heightened synthesis of collagen
  4. Foam cells die - release lipid contents
  5. Fibrous cap maintaining the plaque has to be maintained by resorption and redeposition. However, if the balance is shifted, e.g. in favour of inflammatory conditions we get a plaque rupture. This causes blood coagulation = thrombus = impedes blood flow (occludes vessel)
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8
Q

Describe the process of leukocyte recruitment after the endothelial cells have been activated

A
  1. Capture
  2. Rolling
  3. Slow rolling
  4. Adhesion
  5. Trans-migration
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9
Q

Which histological layer of the artery may be thinned by an atheromatous plaque?

A

The tunica media

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10
Q

What is the treatment for atherosclerosis?

A

Percutaneous coronary intervention (PCI)

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11
Q

What is the major limitation of PCI? How can restenosis be avoided following PCI?

A
  • Restenosis
  • Drug eluting stents: anti-proliferative and drugs that inhibit healing
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12
Q

What is the key principle behind the pathogenesis of atherosclerosis?

A

It is an inflammatory process

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13
Q

What are the functions of the mitral and aortic valves?

A
  • Mitral valve = lets blood flow the left atrium to the left ventricle
  • Aortic valve = opens when the left ventricle squeezes to pump out blood, and closes in between heart beats to keep blood from going backward into the heart
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14
Q

Describe aortic stenosis. How common is it?

A
  • A disease where the aortic orifice (aortic opening) is restricted and so the LV can’t eject blood properly in systole = pressure overload
  • It is the commonest valvular disease
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15
Q

Describe the aetiology of aortic stenosis.

A
  1. Congenital bicuspid aortic valve
  2. Rheumatic heart disease
  3. Senile calcification of the valve
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16
Q

Describe the pathophysiology of aortic stenosis.

A

Aortic orifice is restricted, e.g. by calcific deposits and so there is a pressure gradient between the LV and the aorta. LV function is initially maintained due to compensatory hypertrophy. Overtime this becomes exhausted = LV failure

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17
Q

Give 3 symptoms of aortic stenosis. What is the onset of symptoms associated with?

A
  • SAD:
  1. Exertional syncope
  2. Angina
  3. Exertional dyspnoea
    Onset of symptoms is associated with poor prognosis
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18
Q

Give 3 signs of aortic stenosis including the murmur type.

A
  1. Slow rising carotid pulse and decreased pulse amplitude
  2. Soft or absent heart sounds (S2) if severe
  3. Ejection systolic murmur: <> shape (crescendo-descrendo character)
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19
Q

What investigation might you do in someone who you suspect to have aortic stenosis? Which two measurements are obtained?

A
  • Echocardiography - reduced aortic outflow, LVH
  • Two measurements are obtained: left ventricular size and function + Doppler derived gradient and valve area
  • CXR
  • ECG
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20
Q

Describe the management for someone with aortic stenosis.

A
  1. Ensure good dental hygiene
  2. Consider IE prophylaxis
  3. AORTIC VALVE REPLACEMENT or TAVI (Transcatheter Aortic Valve Implantation)
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21
Q

Who should be offered an aortic valve replacement?

A
  1. Symptomatic patients with aortic stenosis
  2. Any patient with decreasing ejection fraction
  3. Any patient undergoing CABG (coronary artery bypass graft) with moderate/severe aortic stenosis
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22
Q

What is mitral regurgitation? What is it associated with?

A
  • Backflow of blood from the LV to the LA during systole - LV volume overload
  • Associated with ATRIAL FIBRILLATION
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23
Q

Describe the aetiology of mitral regurgitation.

A
  1. Papillary muscle rupture
  2. Mitral valve prolapse
  3. Rheumatic heart disease
  4. IE
  5. Marfan’s syndrome
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24
Q

What is the pathophysiology of mitral regurgitation?

A

LA enlargement and LVH to maintain BP. Progressive LV volume overload -> dilatation and progressive heart failure

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25
Q

Give 3 symptoms of mitral regurgitation.

A

PEF:
1. Palpitations

  1. Exertional dyspnoea
  2. Fatigue
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26
Q

Give 4 signs of mitral regurgitation including its murmur. In chronic mitral regurgitation, what does the intensity of the murmur correlate with?

A
  1. Pansystolic murmur radiating to left axilla (always there)

ADS:

  1. Atrial fibrillation
  2. Displaced, thrusting apex
  3. Soft 1st heart sound + a 3rd heart sound
    In chronic MR, the intensity of the murmur correlates with disease severity
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27
Q

What investigations might you do in someone who you suspect to have mitral regurgitation? What may these show?

A
  1. ECG - may show LA enlargement, atrial fibrillation and LV hypertrophy
  2. CXR - LA enlargment
  3. Echocardiogram: estimates LA/LV size and function
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28
Q

Describe the management of mitral regurgitation.

A
  • Rate control for AF, e.g. beta blockers
  • Vasodilators, e.g. ACEI
  • Anticoagulation for AF
  • Diuretics for fluid overload
  • IE prophylaxis
  • If symptomatic = surgery
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29
Q

What is aortic regurgitation?

A

A regurgitant aortic valve means blood leaks back into the LV during diastole due to ineffective aortic cusps

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30
Q

What is the aetiology of aortic regurgitation?

A
  1. Bicuspid aortic valve (should be tricuspid)
  2. Rheumatic heart disease
  3. IE
  4. Marfan’s syndrome
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31
Q

Describe the pathophysiology of aortic regurgitation.

A

Pressure and volume overload. Compensatory mechanisms - LV dilatation, LVH. Progressive dilation leads to HF

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32
Q

Give 3 symptoms of aortic regurgitation.

A

PAD:

  • Palpitations
  • Angina
  • Dyspnoea
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33
Q

Give 4 signs of aortic regurgitation.

A
  1. Wide pulse pressure
  2. Water hammer pulse
  3. Diastolic blowing murmur
  4. Austin flint murmur
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34
Q

What investigations might you do in someone who you suspect to have aortic regurgitation?

A

CXR and echocardiogram

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35
Q

Describe the management for someone with aortic regurgitation.

A
  • IE prophylaxis
  • Vasodilators e.g. ACEI
  • Regular echocardiograms to monitor progression
  • Surgery if symptomatic
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36
Q

What is mitral stenosis?

A

Obstruction to LV inflow that prevents proper filling during diastole

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37
Q

What is the aetiology of mitral stenosis?

A
  1. Rheumatic heart disease (most common)
  2. Congenital
  3. Calcification
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38
Q

Describe the pathophysiology of mitral stenosis.

A
  1. LA dilation -> pulmonary congestion (as coming in from the pulmonary vein, reduced emptying)
  2. Increased trans-mitral pressures -> LA enlargement and AF
  3. Pulmonary venous hypertension causes RHF symptoms
  4. Hemoptysis: due to rupture of bronchial vessels due to elevated pulmonary pressure
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39
Q

Give 3 symptoms of mitral stenosis.

A
  1. Dyspnoea
  2. Haemoptysis (due to pulmonary oedema)
  3. Palpitations (AF)
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40
Q

Give 5 signs of mitral valve stenosis. What is its murmur?

A
  1. ‘a’ wave in jugular venous pulsations (due to pulmonary hypertension and right ventricular hypertrophy)
  2. Malar flush - pink patches on cheeks due to vasoconstriction
  3. Low pitched diastolic murmur
  4. Loud S1
  5. Tapping apex beat
    - Murmur = rumbling mid-diastolic murmur with opening snap
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41
Q

What investigations might you do in someone who you suspect to have mitral stenosis? What might they show?

A
  1. ECG - atrial fibrillation and LA enlargement
  2. CXR - LA enlargement and pulmonary congestion
  3. Echocardiogram - GOLD STANDARD. Assess mitral valve mobility, gradient and mitral valve area
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42
Q

Describe the management for mitral stenosis.

A
  • If in AF rate control, e.g. beta blockers/CCBs
  • Anticoagulation if AF
  • BALLOON VALVULOPLASTY or valve replacement
  • IE prophylaxis
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43
Q

Why does medication not work for mitral and aortic stenosis?

A

The problem is mechanical and so medical therapy does not prevent progression

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44
Q

Explain the shape of the action potential graph.

A
  • 4 = resting potential (-90mV) = due to Na+/K+ ATPase (3 Na+ move out for 2K+ that move into cell) + Na+/K+ leak channels (100 K+ out for every K+ in, but Na+/K+ ATPase much more prominent)
  • 0 = rapid depolarisation = threshold reached (-70mV), leads to sodium gated fast channels opening. Na+ enters cells + depolarises for +20mV
  • 1 = partial repolarisation = K+ channels open + K+ leaves cell. Inflow of Na+ stops
  • 2 = plateau = voltage-gated Ca2+ channels open. Ca2+ moves in + counters K channels. Lasts approx. 200ms. Entry of Ca2+ into cell results in contraction of myocyte. Contraction of cardiac muscle longer than skeletal due to calcium channels that cause plateau. Less duration in atria than ventricles
  • 3 = repolarisation = K+ outflow and Ca2+ inflow stops until resting potential reached. Closure of Ca2+ channels, opening of more K+ channels
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45
Q

What is an ECG? Give a few examples of conditions that we can identify through ECGs.

A
  • The representation of the electrical events of the cardiac cycle
  • Conditions: arrhythmias, myocardial ischaemia and infarction, pericarditis, electrolyte disturbances
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46
Q

What are the main pacemakers of the heart? Which is the dominant pacemaker?

A
  • SA node = dominant pacemaker (60-100 bpm)
  • AV node = back-up pacemaker (40-60 bpm)
  • Ventricular cells = back-up pacemaker (20-45 bpm)
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47
Q

Starting with the sinoatrial node, where does the electrical impulse travel?

A

SA node - AV node - Bundle of His - Bundle branches - Purkinje fibres

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48
Q

What do the P, QRS and T wave represent?

A
  • P wave = atrial depolarisation (60-80ms)
  • QRS complex = ventricular depolarisation (100-120ms)
  • T wave = ventricular repolarisation (120-160ms)
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49
Q

What does the PR interval represent? Why is it a bit longer?

A
  • Reflects conduction through the AV node
  • Accounts for delay that allows time for atria to contract before ventricles contract
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50
Q

ECG: how long should the PR interval be?

A

120-200ms

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51
Q

ECG: what is the J point?

A

Where the QRS complex becomes the ST segment

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52
Q

ECG: what is the normal axis of the QRS complex?

A

-30° -> +90°

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53
Q

How many seconds do the following represent on ECG paper?
a) small squares

b) large squares

A

a) 0.04s
b) 0.2s

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54
Q

What do the ECG leads measure?

A

The difference in electrical potential between two points

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55
Q

How many electrodes does a 12 lead ECG have?

A

10 electrodes - six on the chest, four on the limbs

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56
Q

What are the typical ECG findings for a right axis deviation? What is a right axis deviation associated with?

A
  • Lead III has the most positive deflection and lead I should be negative
  • Right axis deviation is associated with right ventricular hypertrophy
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57
Q

What are the bipolar and unipolar leads?

A
  • Bipolar leads: measure difference in electrical potential between two different points on the body
  • Unipolar leads: measure difference in electrical potential between one point on the body and a virtual reference point with zero electrical potential, located in the centre of the heart
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58
Q

What are the 12 leads of the ECG?

A
  • 3 standard limb leads
  • 3 augmented limb leads
  • 6 precordial leads
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59
Q

What should the cardiac axis look like in healthy individuals? What should the most positive deflection be in? Why? Where would you see the most negative deflection? Why?

A
  • In healthy individuals, you would expect the cardiac axis to lie between -30°and +90º. The overall direction of electrical activity is therefore towards leads I, II and III. As a result, you see a positive deflection in all these leads, with lead II showing the most positive deflection as it is the most closely aligned to the overall direction of electrical spread
  • You would expect to see the most negative deflection in aVR. This is due to aVR providing a viewpoint of the heart from the opposite direction
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60
Q

What does a positive deflection mean in an ECG? How about a negative deflection? What does the height of a deflection tell us?

A
  • When the electrical activity within the heart travels towards a lead you get a positive deflection
  • When the electrical activity within the heart travels away from a lead you get a negative deflection
  • The height of the deflection represents the amount of electrical activity flowing in that direction (i.e. the higher the deflection, the greater the amount of electrical activity flowing towards the lead
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61
Q

What are the typical ECG findings for a right axis deviation? What is a right axis deviation associated with?

A

Lead III has the most positive deflection and lead I should be negative. Right axis deviation is associated with right ventricular hypertrophy

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62
Q

What does the cardiac axis tell us? What do we need to determine the cardiac axis? What is the pathway of electrical activity in the heart? What do a positive and negative deflection tell us?

A
  • The cardiac axis gives us an idea of the overall direction of electrical activity
  • To determine the cardiac axis, you need to look at leads I, II and III
  • In healthy individuals, the electrical activity of the heart begins at the sinoatrial node then spreads to the atrioventricular (AV) node. It then spreads down the bundle of His and then Purkinje fibres to cause ventricular contraction
  • Whenever the direction of electrical activity moves towards a lead, a positive deflection is produced
  • Whenever the direction of electrical activity moves away from a lead a negative deflection is produced
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63
Q

What are the typical ECG findings for a left axis deviation? What is it associated with?

A
  • Lead I has the most positive deflection
  • Leads II and III are negative
  • Left axis deviation is associated with heart conduction abnormalities
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64
Q

Which leads correspond to which view of the heart? What can we infer from these?

A
  • LEARN:
  • Inferior = II, III, aVF - RCA
  • Lateral = I, aVL, aVR, V5, V6 - LCx
  • Anterior = V3, V4 - LAD
  • Septal = V1, V2 - proximal LAD
  • Understanding which leads represent which anatomical territory of the heart allows you to localise pathology
  • For example, if there is ST elevation in leads V3 and V4 it suggests an anterior myocardial infarction (MI). You can then combine this with some anatomical knowledge of the heart’s blood supply, to allow you to work out which artery is likely to be affected (e.g. left anterior descending artery).
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65
Q

How do we systematically approach interpreting ECGs?

A

– Rate

– Rhythm

– Axis

– P, PR, QRS, ST, QT, T

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66
Q

ECG: where would you place lead 1 (bipolar)?

A

From the right arm to the left arm with the positive electrode being at the left arm. At 0°

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67
Q

ECG: where would you place lead 2?

A

From the right arm to the left leg with the positive electrode being at the left leg. At 60°

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68
Q

ECG: where would you place lead 3?

A

From the left arm to the left leg with the positive electrode being at the left leg. At 120°

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69
Q

ECG: where would you place lead avF (unipolar)?

A

From halfway between the left arm and right arm to the left leg with the positive electrode being at the left leg. At 90°

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70
Q

ECG: where would you place lead avL?

A

From halfway between the right arm and left leg to the left arm with the positive electrode being at the left arm. At -30°

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71
Q

ECG: where would you place lead avR?

A

From halfway between the left arm and left leg to the right arm with the positive electrode being at the right arm. At -150°

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72
Q

What are the unipolar chest leads?

A
  • V1 = R. of sternum 4th intercostal space
  • V2 = L. of sternum 4th intercostal space
  • V3 = Inbetween V2 + V4
  • V4 = R. of sternum 5th intercostal space
  • V5 = 5th intercostal space anterior axillary line
  • V6 = 5th intercostal space midaxillary line
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73
Q

What are Chamberlain’s 10 rules of a normal ECG?

A

ECG RULES:

  • Rule 1 = PR interval should be 120 to 200 milliseconds or 3 to 5 little squares
  • Rule 2 = the width of the QRS complex should not exceed 110 ms, less than 3 little squares
  • Rule 3 = the QRS complex should be dominantly upright in leads I and II
  • RULE 4 = QRS and T waves tend to have the same general direction in the limb leads
  • RULE 5 = all waves are negative in lead aVR
  • RULE 6 = the R wave must grow from V1 to at least V4, the S wave must grow from V1 to at least V3 and disappear in V6
  • RULE 7 = the ST segment should start isoelectric except in V1 and V2 where it may be elevated
  • RULE 8 = the P waves should be upright in I, II, and V2 to V6
  • RULE 9 = there should be no Q wave or only a small q less than 0.04 seconds in width in I, II, V2 to V6
  • RULE 10 = the T wave must be upright in I, II, V2 to V6
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74
Q

What is a P wave like in leads I, II and aVR?

A

Always positive in leads I + II, always negative in aVR

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75
Q

What do P waves look like in right and left atrial enlargement? How about in atrial fibrosis, obesity and hyperkalaemia?

A
  • Right atrial enlargement = tall, pointed P wave (P pulmonale)
  • Left atrial enlargement = ‘M’ shaped P wave (P mitrale)
  • Atrial fibrosis, obesity and hyperkalaemia = low amplitude
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76
Q

What can a short PR interval indicate?

A

WPW (Wolff-Parkinson-White syndrome)

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77
Q

What does a long PR interval (>200ms) indicate?

A

First degree heart block

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78
Q

How long should the QRS complex be? When do we get broad QRS complexes, small QRS complexes and tall QRS complexes?

A
  • <110ms
  • Broad QRS = ventricular conduction delay / bundle branch block
  • Small QRS complexes = obese patient, pericardial effusion, infiltrative cardiac disease
  • Tall QRS complexes = left ventricular hypertrophy, thin patient
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79
Q

In which leads would you expect the QRS complex to be upright in?

A

Leads I and II

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80
Q

In which lead are all waves negative?

A

aVR

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81
Q

In which leads should T waves and P waves be upright?

A

Leads 1, 2, V2 -> V6

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82
Q

What part of the ECG does the plateau phase of the cardiac action potential coincide with?

A

QT interval

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83
Q

What happens to the QT interval when HR increases?

A

The QT interval decreases

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84
Q

Give 3 signs of abnormal T waves.

A
  1. Symmetrical
  2. Tall and peaked (hyperkalaemia)
  3. Biphasic (ischaemia or hypokalaemia) or inverted (non-specific but can indicate ischaemia/infarction, hypertrophy, cardiomyopathy)
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85
Q

What is the U wave related to? What is their appearance? When are they more prominent?

A
  • The U wave is related to afterdepolarisations which follow repolarisation
  • U waves are small, round, symmetrical and positive in lead II
  • More prominent in slower heart rates
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86
Q

How do we determine heart rate from an ECG in a regular rhythm? How about in an irregular rhythm?

A
  • Rule of 300: count the number of ‘big boxes’ between each QRS complex and divide this into 300, e.g. 300/6 = 50bpm
  • If a patient’s heart rhythm is irregular the first method of heart rate calculation doesn’t work (as the R-R interval differs significantly throughout the ECG). As a result, you need to apply a different method:
  • Count the number of complexes on the rhythm strip (each rhythm strip is typically 10 seconds long)
  • Multiply the number of complexes by 6 (giving you the average number of complexes in 1 minute)
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87
Q

What does the QRS axis represent? What do QRS axis abnormalities hint at?

A
  • The QRS axis represents the overall direction of the heart’s electrical activity
  • Abnormalities hint at ventricular enlargement and conduction blocks
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88
Q

What aspect of the heart is represented by leads 2, 3 and aVF?

A

The inferior aspect

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89
Q

What might ST elevation in leads 2, 3 and aVF suggest?

A

RCA blockage. These leads show the activity of the inferior aspect of the heart and the RCA supplies the inferior aspect of the heart with blood

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90
Q

What is ischaemic heart disease? What is it broken down into? Which condition has ischaemic heart disease as its main cause?

A
  • Ischaemic heart disease (or coronary artery disease) is a condition where the coronary arteries are narrowed or blocked
  • Broken down into stable angina and acute coronary syndrome
  • Angina’s commonest cause is IHD. This is a symptom of O2 supply/demand mismatch to the heart experienced on exertion
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91
Q

What is IHD primarily caused by? What happens when a coronary artery is 70-80% sclerosed? Why?

A
  • Primarily caused by atherosclerosis = lipid rich plaques in arterial wall. Inflammatory, progressive process
  • When 70-80% sclerosed: exertional symptoms show: angina. Exertional symptoms only as there is increased oxygen demand on exertion: heart muscle cannot access required oxygen volume due to artery occlusion (due to the atherosclerosis), therefore there is a supply-demand mismatch. Pain occurs: angina
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92
Q

What are the modifiable and non-modifiable risk factors for IHD?

A
  • Non modifiable:
  • Family history
  • Age
  • Ethnicity (S. Asian)
  • Modifiable:
  • Smoking
  • Poor nutrition
  • Sedentary lifestyle
  • Alcohol
  • Stress
  • HTN
  • Obesity
  • DM
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93
Q

Give 5 possible causes of angina.

A
  1. Narrowed coronary artery = impairment of blood flow, e.g. atherosclerosis
  2. Increased distal resistance = LV hypertrophy
  3. Reduced O2 carrying capacity, e.g. anaemia
  4. Coronary artery spasm
  5. Thrombosis
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94
Q

Briefly describe the pathophysiology of angina that results from atherosclerosis.

A

On exertion there is increased O2 demand. Coronary blood flow is obstructed by an atherosclerotic plaque -> myocardial ischaemia -> angina

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95
Q

Briefly describe the pathophysiology of angina that results from anaemia.

A

On exertion there is increased O2 demand. In someone with anaemia there is reduced O2 transport -> myocardial ischaemia -> angina

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96
Q

How do blood vessels try and compensate for increased myocardial demand during exercise?

A

When myocardial demand increases, e.g. during exercise, microvascular resistance drops and flow increases

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97
Q

Why are blood vessels unable to compensate for increased myocardial demand in someone with CV disease?

A

In CV disease, epicardial resistance is high meaning microvascular resistance has to fall at rest to supply myocardial demand at rest. When this person exercises, the microvascular resistance can’t drop anymore and flow can’t increase to meet metabolic demand = angina!

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98
Q

What is the typical presentation of someone with IHD? With angina, how do we classify it?

A
  • Central, crushing retrosternal chest pain, radiating into the jaw and typically the left arm
  • Shortness of breath
  • Nausea
  • Sweating
  • Palpitation
  • Angina:
    1. Constricting discomfort in front of chest, neck, shoulders, jaws or arms
    2. Precipitated by physical exertion
    3. Relieved by rest/GTN spray ~5 mins
  • Normal examination
  • All 3 features: typical angina, 2 features: atypical angina, 1/none: non-anginal pain
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99
Q

What are the investigations for IHD?

A
  • ECG: resting and exercise (to induce ischaemia)
  • Blood tests: HbA1c, FBC, cholesterol profile
  • Biological markers: troponin, myoglobin etc.
  • Gold standard angina = CT CORONARY ANGIOGRAPHY
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100
Q

How would you describe the chest pain in angina?

A

Crushing central chest pain. Heavy and tight. The patient will often make a fist shape to describe the pain

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101
Q

Give 5 symptoms of angina.

A
  1. Crushing central chest pain
  2. The pain is relieved with rest or using a GTN spray
  3. The pain is provoked by physical exertion
  4. The pain might radiate to the arms, neck or jaw
  5. Breathlessness
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102
Q

Describe the primary prevention of angina.

A
  1. Risk factor modification
  2. Low dose aspirin
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103
Q

Describe the secondary prevention of angina.

A
  • Aspirin
  • Atorvastatin
  • ACEi
  • PCI/CABG if extensive disease
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104
Q

How do we treat IHD?

A

BANS:

  • Beta-blocker, e.g. propanolol
  • Dual antiplatelet: aspirin and clopidogrel
  • Nitrate: GTN spray (to abort attacks)
  • Statin: simvastatin
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105
Q

What is the symptomatic reflief and long term relief for angina?

A
  • Symptomatic relief = GTN spray
  • Long term symptomatic relief = beta blocker or CCB
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106
Q

Describe the action of beta blockers.

A

Beta blockers are beta-1 specific. They antagonise sympathetic activation and so are negatively chronotropic and inotropic. Myocardial work is reduced and so is myocardial demand = symptom relief

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107
Q

Give 3 side effects of beta blockers.

A
  1. Bradycardia
  2. Tiredness
  3. Erectile dysfunction
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108
Q

When might beta blockers be contraindicated?

A

They might be contraindicated in someone with asthma or in someone who is bradycardic

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109
Q

Describe the action of nitrates.

A

Nitrates, e.g. GTN spray are venodilators. Venodilators -> reduced venous return -> reduced pre-load -> reduced myocardial work and myocardial demand

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110
Q

Describe the action of Ca2+ channel blockers.

A

Ca2+ blockers are arterodilators -> reduced BP -> reduced afterload -> reduced myocardial demand

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111
Q

How does aspirin work?

A

Aspirin irreversibly inhibits COX. You get reduced TXA2 synthesis and so platelet aggregation is reduced.
Caution: Gastric ulcers!

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112
Q

What are statins used for?

A

They reduce the amount of LDL in the blood

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113
Q

Give 2 advantages and 1 disadvantage of PCI.

A
  1. Less invasive than CABG
  2. Convenient and acceptable
  3. High risk of restenosis
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114
Q

Give 1 advantage and 2 disadvantages of CABG.

A
  1. Good prognosis after surgery (preferred in diabetics and those >65)
  2. Very invasive
  3. Long recovery time
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115
Q

Name 3 different types of angina.

A
  1. Stable angina (as we see in IHD) = predictable, happens on exertion
  2. Unstable angina (ACS, later) = unexpected, happens during rest + accelerated during sleep. NOT relieved by rest or GTN spray
  3. Prinzmetal’s angina = sudden, no clear triggers, results from spasms or dysfunctions in coronary artery
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116
Q

What are acute coronary syndromes (ACS)?

A

ACS encompasses a spectrum of acute cardiac conditions including unstable angina, NSTEMI and STEMI

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117
Q

What is the common cause of ACS?

A

Thrombus from an atherosclerotic plaque blocking a coronary artery

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118
Q

What are uncommon causes of ACS?

A
  1. Coronary vasospasm
  2. Drug abuse
  3. Coronary artery dissection
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119
Q

Describe unstable angina, NSTEMI and STEMI.

A
  • Unstable angina (ischaemia)
  • NSTEMI (partial occlusion → subendocardial infarction). Non-ST elevation
  • STEMI (complete occlusion). ST elevation
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120
Q

Describe the differences between stable angina and unstable angina. Include the pathophysiology, ECG and troponin.

A
  • Stable angina: stable atherosclerotic plaque, vessel unable to dilate enough to allow adequate blood flow to meet myocardial demand. Pain upon exertion. Demand ischaemia, no infarct. Normal ECG. Normal troponins
  • Unstable angina: plaque ruptures and thrombus forms, causing partial occlusion of the vessel. Pain at rest or progresses rapidly over a short period of time. Supply ischaemia, no infarct. Normal, inverted T waves, or ST depression. Normal troponins
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121
Q

Describe the differences between NSTEMI and STEMI.

A
  • NSTEMI: the plaque rupture and thrombus formation causes partial occlusion of the vessel that results in injury and infarct to the subendocardial myocardium. Subendocardial infarct. Normal, inverted T waves, or ST depression. Troponin elevated
  • STEMI: complete occlusion of the blood vessel lumen, resulting in transmural injury and infarct to the myocardium, which is related by ECG changes and a rise in troponins. Transmural infarct. Hyperacute T waves or ST elevation. Troponin elevated. Acute changes = ST elevation or hyperacute T waves, hours/days = T wave inversion, pathological Q waves
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122
Q

Why do you see increased serum troponin in NSTEMI and STEMI?

A

The occluding thrombus causes necrosis of cells and so myocardial damage. Troponin is a sensitive marker for cardiac muscle injury and so is significantly raised in reflection to this

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123
Q

What is the presentation of people with ACS?

A
  • Central, constricting chest pain radiating to jaw/arms
  • Sweating
  • SOB
  • >20 minutes
  • Unstable angina: pain not relieved by rest or GTN spray
  • Silent MI: in diabetics
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124
Q

Give 3 signs of unstable angina.

A
  1. Cardiac chest pain at rest
  2. Cardiac chest pain with crescendo patterns; pain becomes more frequent and easier provoked
  3. No significant rise in troponin
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125
Q

Give 6 signs/symptoms of MI.

A
  1. Unremitting and usually severe central cardiac chest pain
  2. Pain occurs at rest
  3. Sweating
  4. Breathlessness
  5. Nausea/vomiting
  6. 1/3 occur in bed at night
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126
Q

What investigations would you do on someone you suspect to have ACS?

A
  1. ECG
  2. Blood tests; look at serum troponin
  3. Coronary angiography
  4. Cardiac monitoring for arrhythmias
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127
Q

A raised troponin is not specific for ACS. In what other conditions might you see a raised troponin?

A
  1. Gram negative sepsis
  2. Pulmonary embolism
  3. Myocarditis
  4. Heart failure
  5. Arrhythmias
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128
Q

Describe the initial management for ACS.

A
  1. Get into hospital ASAP - call 999
  2. If STEMI, paramedics should call PCI centre for transfer
  3. Aspirin 300mg
  4. Pain relief e.g. morphine
  5. Oxygen if hypoxic
  6. Nitrates
  7. Clopidogrel
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129
Q

Describe the management for stable angina.

A
  • Pharmacological: GTN SPRAY (symptomatic relief). Then BETA-BLOCKERS OR CCB, switch, combine
  • Interventional: PERCUTANEOUS CORONARY INTERVENTION (preferred) or CORONARY ARTERY BYPASS GRAFT
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130
Q

Describe the management for NSTEMI/unstable angina.

A
  • GTN SPRAY (symptomatic relief) and BETA BLOCKERS, e.g. bisoprolol or CCB if beta-blockers are CONTRAINDICATED
  • Use GRACE score to predict 6 month mortality + risk of further cardio events
  • Fondaparinux
  • Low risk: ticagrelor (P2Y12 receptor antagonist) and aspirin
  • Med/high risk: angiography + PCI, prasugrel (P2Y12 receptor antagonist) and aspirin
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131
Q

Describe the management for STEMI.

A
  • PCI within 120 mins
  • Fibrinolysis (if PCI not possible in <120 mins), e.g. alteplase
  • Clopidogrel or prasugrel and aspirin
  • Ticagrelor and aspirin
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132
Q

Describe the immediate management for a myocardial infarction.

A
  • Prehospital: ASPIRIN 300mg and GTN SPRAY
  • HOSPITAL - IMMEDIATE MANAGEMENT:

M - Morphine

O - Oxygen

N - Nitrates (GTN)

A - Aspirin (300mg)

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133
Q

Describe the secondary prevention for ACS.

A
  • ACEi
  • Clopidogrel
  • Aspirin + atorvastatin
  • Beta blocker
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134
Q

What are some complications that can happen post MI?

A
  • Death
  • Rupture of heart septum/papillary muscles
  • Oedema (heart failure)
  • Arrhythmias and aneurysm
  • Dressler’s syndrome
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135
Q

What is the function of P2Y12?

A

It amplifies platelet activation

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136
Q

Give 3 potential side effects of P2Y12 inhibitors.

A
  1. Bleeding
  2. Rash
  3. GI disturbances
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137
Q

What are the 5 classes of risk factors for IHD?

A
  • Clinical risk factors (hypertension, lipids, diabetes)
  • Lifestyle risk factors (smoking, diet, physical inactivity)
  • Environmental risk factors (air pollution, chemicals)
  • Demographic risk factors (age, sex, ethnicity, genetic)
  • Psychosocial risk factors (behaviour pattern, depression/anxiety, work, social support)
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138
Q

What are the layers of the heart wall?

A
  • Endocardium = innermost layer, lines the cavities and valves of the heart
  • Myocardium = composed of cardiac muscle, responsible for the contractions of the heart
  • Epicardium = outermost layer of the heart, formed by the visceral layer of the PERICARDIUM. It is composed of connective tissue and fat. The connective tissue secretes a small amount of lubricating fluid into the pericardial cavity
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139
Q

What are the two layers of pericardium? How much serous fluid is there between these layers? What is the function of this fluid?

A
  • Visceral and parietal pericardium
  • 50ml
  • It acts as a lubricant and so allows smooth movement of the heart inside the pericardium
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140
Q

What lies within the pericardium?

A

Great vessels

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141
Q

The pericardial sac has a small reserve volume. What happens if this volume is exceeded? What is Tamponade physiology?

A
  • If this volume is exceeded, the pressure is translated to the cardiac chambers
  • Tamponade physiology: small amount of volume added to space has dramatic effects on filling but so does removal of a small amount
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142
Q

What is pericarditis?

A

Inflammation of the pericardium with/without effusion

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143
Q

What are the causes of pericarditis?

A
  • Infectious:
  • Viral: coxsackievirus
  • Bacterial: mycobacterium tuberculosis
  • Histoplasma spp. (most likely type found in immunocompromised)
  • Non-infectious:
  • Trauma (common) and iatrogenic
  • Autoimmune: rheumatoid arthritis, Sjogren’s syndrome, SLE
  • Secondary metastatic tumours
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144
Q

What is the pathophysiology of pericarditis?

A
  • Inflammation of the pericardium (pericardial vascularisation, polymorphonuclear leukocyte infiltration)
  • This leads to the narrowing of the pericardial space and scarring of the fibrous pericardium
  • IF UNTREATED, we get a fibrinous reaction = a build up of exudate and adhesions in the pericardial space = PERICARDIAL EFFUSION
  • Pericardial effusion puts pressure on the cardiac myocytes = cardiac dysfunction. The fluid may be serous or haemorrhagic
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145
Q

What are the symptoms of pericarditis?

A

• Severe chest pain

  • Sharp, pleuritic, rapid onset
  • Worse when laying flat + inspiration
  • Relieved by sitting forward
  • Radiates to trapezius ridge
  • Dyspnoea
  • Cough
  • Hiccups
  • Fever
  • Myalgia
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146
Q

What are the signs of pericarditis?

A
  • Pericardial rub friction rub on auscultation - high pitched scratchy sound heard loudest on the midline during inspiration
  • Tachycardia
  • Peripheral oedema
  • Increased JVP
  • PERICARDIAL EFFUSION:
  • Bronchial breathing at left base
  • Muffled heart sounds
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147
Q

What are the investigations for pericarditis? What would these show?

A
  • ECG: DIAGNOSTIC
  • Saddle-shaped ST elevation
  • PR depression
  • CXR:

• Effusion may cause cardiomegaly

  • Serum troponin, CRP
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148
Q

How do we treat pericarditis?

A
  • NSAIDS with gastric protection: ibuprofen for two weeks, aspirin for two weeks. Colchicine for three months to reduce recurrence risk
  • Reduce physical activity until symptoms resolve
  • Treat the cause
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149
Q

How do we treat pericardial effusion?

A
  • Treat the cause
  • Pericardiocentesis
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150
Q

What is a cardiac tamponade? What is the pathophysiology? What are the symptoms? What are the investigations? What is the treatement?

A
  • Cardiac tamponade = life threatening condition whereby there is an accumulation of fluid in the pericardial space → compression of the heart chambers → decrease in venous return → decrease in filling in the heart → reducing cardiac output. Major COMPLICATION of pericarditis
  • Beck’s triad: falling BP, rising JVP, and muffled heart sound. Also pulsus paradoxus (large decrease in stroke volume → systolic blood pressure drops by > 10mmHg on inspiration)
  • Investigations: echocardiogram = gold standard
  • Treatment = pericardiocentesis
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151
Q

What is the difference between pericardial effusion and pericardial tamponade?

A
  • Pericardial effusion = happens when pericardial fluid builds up slowly over time, which allows the pericardium to stretch out to accommodate bigger and bigger volumes of fluid without compressing the heart. Over time, it can cause chest pain, shortness of breath, and compression of near structures. Ultimately, if the pressure inside the pericardial cavity increases enough to compress the heart muscle, it may lead to pericardial tamponade.
  • Pericardial tamponade = when there’s a sudden fluid accumulation, the pericardium has no time to adjust, so even small amounts can cause a dramatic increase of pressure inside the pericardial sac, resulting in acute pericardial tamponade
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152
Q

What are the causes of pericardial tamponade?

A
  • Chest trauma, e.g. stab wound or blunt trauma, rupture of the aorta, rupture of the ventricle after a heart attack, or as a complication of cardiac surgery
  • It can also appear more gradually in individuals with pericardial infection, pericarditis or cancer, due to a progressive build-up of pericardial fluid over time
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153
Q

What are the signs of pericardial tamponade?

A
  • Beck’s triad:
  • Low blood pressure
  • Distension of the jugular veins
  • Muffled heart sounds
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154
Q

What investigations should be done for a pericardial tamponade?

A
  • CXR - enlargement of the heart
  • Echocardiogram - right-sided chamber collapse during diastole
  • ECG - low voltage QRS complex
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155
Q

How do we manage pericardial tamponade?

A

Pericardiocentesis

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156
Q

You are a junior doctor and see a 26 year old woman who came to A&E complaining of chest pain. She has a past medical history of type 1 diabetes, and has a family history of rheumatoid arthritis. You decide to perform an ECG, and whilst you’re placing the leads you notice a widespread rash on the patient’s cheeks, neck and chest, which she says gets worse after she’s been in the sun.

The ECG shows widespread saddle-shaped ST elevation.

What is the likely cause of her chest pain?

a. STEMI
b. Infective Endocarditis
c. Prinzmetal Angina
d. Pericarditis

A

D. Pericarditis

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157
Q

You are a junior doctor and see a 26 year old woman who came to A&E complaining of chest pain. She has a past medical history of type 1 diabetes, and has a family history of rheumatoid arthritis. You decide to perform an ECG, and whilst you’re placing the leads you notice a widespread rash on the patient’s cheeks, neck and chest, which she says gets worse after she’s been in the sun.

The ECG shows widespread saddle-shaped ST elevation.

What is the most likely underlying cause?

a. Her Type 1 Diabetes Mellitus
b. Rheumatoid arthritis
c. Systemic Lupus Erythematosus
d. Mycobacterium Tuberculosis

A

C. Systemic Lupus Erythematosus (SLE)

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158
Q

What is the definition of heart failure? What happens in order for cardiac output to be maintained? What happens eventually?

A
  • Inability of the heart to deliver blood and thus oxygen at a rate that is commensurate with the requirements of the body. Can result from STRUCTURAL/FUNCTIONAL cardiac disorder that impairs the heart’s ability to function
  • Compensatory physiological changes occur in order to maintain cardiac output. They are eventually overwhelmed and become pathophysiological:
  • [sympathetic system activation] BP falls → detected by baroreceptors → sympathetic activation → positively inotropic/chronotropic → CO increases
  • RAAS system
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159
Q

What are the different types of heart failure?

A
  • Acute heart failure = new onset acute or decompensation of chronic
  • Chronic heart failure = develops/progresses slowly and arterial pressure is well maintained until late
  • Systolic failure = inability of the ventricle to contract normally
  • Diastolic failure = inability of the ventricle to relax and fill normally
  • Left ventricular failure = either systolic or diastolic failure of the left ventricle
  • Right ventricular failure = either systolic or diastolic failure of the right ventricle
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160
Q

What is the aetiology of left sided heart failure?

A
  • Coronary artery disease
  • Myocardial infarction
  • Cardiomyopathy
  • Valvular heart disease
  • Arrhythmias
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161
Q

What is the aetiology of right sided heart failure?

A
  • Right ventricular infarct
  • Pulmonary hypertension
  • Pulmonary embolism
  • COPD
  • Progression of left sided heart failure
  • COR PULMONALE (disease of lung/pulmonary vessels → pulmonary hypertension → RV hypertrophy → RHF with venous overload, peripheral oedema, hepatic congestion)
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162
Q

What is the aetiology of systolic heart failure?

A
  • ISCHAEMIC HEART DISEASE
  • Myocardial infection
  • Cardiomyopathy
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163
Q

What is the aetiology of diastolic heart failure?

A
  • Aortic stenosis
  • Chronic hypertension
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164
Q

What is the pathophysiology of heart failure?

A
  • Myocardium fails, so there is a decreased volume of blood ejected. This causes an increase in preload
  • An increase in ventricular load causes hypertrophy of the myocardium. An increase in the size and number of cells causes an increase in myocardial demand for oxygen. This causes the myocardium to become ischaemic = patchy fibrosis = stiffness and reduced contractibility
  • Reduced contractibility = increased workload and amount of blood remaining. More force needed to maintain cardiac output = cells become tired = pathological
  • Increased afterload and preload = increased cardiac work = damage to myocytes = decreased cardiac output = reduced blood flow to kidneys etc. = activates RAAS system and adrenergic pathway. This causes Na2+ and water retention, increased HR and contraction force, and cardiotoxicity
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165
Q

What are the symptoms of left sided heart failure? Why?

A
  • 3 cardinal symptoms: SHORTNESS OF BREATH, FATIGUE, ANKLE SWELLING
  • EXERTIONAL DYSPNOEA - this is because blood backs up to the lungs via pulmonary vein as not pumped around the body
  • FATIGUE
  • PAROXYSMAL NOCTURNAL DYSPNOEA
  • Orthopnoea
  • Poor exercise tolerance
  • Nocturnal cough
  • Wheeze
  • Nocturia
  • Cold peripheries
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166
Q

What are the symptoms of right sided heart failure? Why? What is the classifcation for heart failure

A
  • Peripheral OEDEMA (ankle swelling) - this is because blood backs up to the body via the vena cava
  • ASCITES
  • RAISED JVP
  • HEPATOMEGALY
  • Nausea
  • Facial engorgement
  • Epistaxis
  • Cyanosis
  • NEW YORK CLASSIFICATION
  • Hypotension
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167
Q

What are the symptoms and signs of heart failure?

A
  • 3 cardinal symptoms: SHORTNESS OF BREATH, FATIGUE, ANKLE SWELLING

SOFA PC:

  • Shortness of breath
  • Orthopnoea
  • Fatigue
  • Ankle swelling
  • Pulmonary oedema (due to backflow from decreased CO; produced cough with pink frothy sputum)
  • Cold peripheries
  • Raised JVP
  • End respiratory crackles
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168
Q

What are the investigations for heart failure? What is the mnemonic for assessing heart failure through a chest X-ray?

A
  • NT-pro BNP (BRAIN NATRIURETIC PEPTIDE) = a marker of heart failure, released when the myocardial walls are under stress
  • ECG
  • Transthoracic ECG: wall motion abnormalities, valvular disease, cardiomyopathies
  • GOLD STANDARD = ECHOCARDIOGRAPHY
  • Chest X-ray (ABCDE):

– Alveolar oedema (bat wing shadowing)

– Kerley B Lines

– Cardiomegaly

– Dilated upper lobe vessels of lungs

– Effusions (pleural)

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169
Q

What is the treatment for acute heart failure? What is the treatment for chronic heart failure? Why?

A
  • Acute HF = OMFG: oxygen, morphine, furosemide, GTN spray
  • Chronic HF:
  • Lifestyle changes: stop smoking, low salt, weight and nutrition
  • Medication:
  • 1st line = ACEIs, e.g. ramipril and BETA BLOCKERS, e.g. bisoprolol
  • 2nd line = ALDOSTERONE RECEPTOR ANTAGONISTS, e.g. spironolactone
  • 3rd line = Digoxin
  • Symptomatic relief: DIURETICS - excretion of water = reduces preload and BP. Loop diuretics (furosemide), thiazide diuretics (bendroflumethiazide), aldosterone antagonists (spironolactone)
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170
Q

What is Cor Pulmonale?

A

Right sided heart failure caused by chronic pulmonary arterial hypertension

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171
Q

What are the causes of Cor Pulmonale?

A
  • Chronic lung disease, e.g. COPD
  • Pulmonary vascular disorders
  • Neuromuscular and skeletal diseases
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172
Q

What are the symptoms of Cor Pulmonale?

A
  • Dyspnoea
  • Fatigue
  • Syncope
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173
Q

What are the signs of Cor Pulmonale?

A
  • Cyanosis
  • Tachycardia
  • Raised JVP
  • RV heave
  • Pan-systolic murmur due to tricuspid regurgitation
  • Hepatomegaly
  • Oedema
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174
Q

What are the investigations for Cor Pulmonale?

A
  • ABG – hypoxia +/- hypercapnia
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175
Q

What is the management for Cor Pulmonale?

A
  • TREAT UNDERLYING CAUSE
  • Give oxygen to treat respiratory failure
  • Treat cardiac failure the same, e.g. diuretics
  • Consider venesection if haematocrit >55
  • Consider heart-lung transplantation in young patients
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176
Q

A patient with recently diagnosed heart failure comes to your GP practice for a check-up and medication review. He tells you that he has felt a little weaker and more tired than usual recently. His current medications include: Furosemide, Ramipril, Bisoprolol

His blood results show: Sodium: 142 (135-145) Potassium: 2.4 (3.5-5.5)

  1. Which of the following drugs is the most likely cause of the electrolyte abnormality?
    a. Furosemide
    b. Ramipril
    c. Bisoprolol
    d. None of the above
A

A. Furosemide

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177
Q

A patient with recently diagnosed heart failure comes to your GP practice for a check-up and medication review. He tells you that he has felt a little weaker and more tired than usual recently. His current medications include: Furosemide, Ramipril, Bisoprolol

His blood results show: Sodium: 142 (135-145) Potassium: 2.4 (3.5-5.5)

  1. Which of the following diuretics is the most appropriate for this patient?
    a. Furosemide
    b. Bendroflumethiazide
    c. Spironolactone
    d. Verapamil
A

C. Spironolactone

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178
Q

What is the Tetralogy of Fallot? What is it characterised by?

A

A congenital heart defect characterised by 4 defects:

  1. Ventricular septal defect (a hole allowing blood to flow between the two ventricles)
  2. Over-riding aorta (aorta expands to allow blood from both ventricles to enter)
  3. RV hypertrophy
  4. Pulmonary stenosis (narrowing of the exit of the right ventricle)
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179
Q

What is the physiology of Tetralogy of Fallot?

A
  • The stenosis of the RV outflow leads to the RV being at a higher pressure than the left
  • Therefore deoxygenated blood passes from the RV to the LV
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180
Q

Would a baby born with Tetralogy of Fallot be cyanotic?

A

YES! There is a greater pressure in the RV than the LV and so blood is shunted into the LV -> CYANOSIS!

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181
Q

What are the signs, investigations and treatment of Tetralogy of Fallot?

A
  • Signs: cyanosis, harsh systolic ejection murmur, tachypnoea
  • Investigations = pulse oximetry, echocardiogram, ECG, CXR
  • Treatment = surgical repair
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182
Q

What is ventricular septal defect? Would a baby born with ventricular septal defect be cyanotic?

A
  • An abnormal connection between the two ventricles
  • No. There is a higher pressure in the LV than the RV and so blood is shunted from the left to right meaning there is an increased amount of blood going to the lungs; not cyanotic
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183
Q

What are the signs of a large VSD? How about a small VSD?

A
  • Moderate-large show exercise intolerance
  • SOB
  • Poor weight gain
  • Harsh systolic murmur
  • Very high pulmonary blood flow
  • Usually asymptomatic if small
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184
Q

What might VSD lead onto?

A

Eisenmenger’s syndrome

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185
Q

What are the investigations and treatment for VSD?

A
  • Investigations: echocardiogram, ECG, CXR
  • Tx: small asymptomatic = no intervention. Larger + symptoms = consider surgical repair
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186
Q

Describe Eisenmenger’s syndrome. What is its physiology?

A
  • When shunting through septal defect is from right to left, resulting in deoxygenated blood in the systemic circulation
  • High pressure pulmonary blood flow damages pulmonary vasculature -> there is increased resistance to blood flow (pulmonary hypertension) -> RV pressure increases -> shunt direction reverses (RV to LV) -> CYANOSIS!
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187
Q

Describe 3 risks associated with Eisenmenger’s syndrome.

A
  1. Risk of death
  2. Endocarditis
  3. Stroke
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188
Q

What is atrial septal defect?

A

An abnormal connection between the two atria; it is fairly common

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189
Q

Would a baby born with ASD be cyanotic?

A

No. There is a higher pressure in the LA than the RA and so blood is shunted from the left to right, therefore not cyanotic

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190
Q

What are the signs of ASD?

A
  1. Significant increase in blood flow through the right heart and lungs - pulmonary flow murmur
  2. Enlarged pulmonary arteries
  3. Right heart dilatation
  4. SOBOE
  5. Increased chest infection
  6. Ejection systolic murmur on auscultation
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191
Q

What are the investigations and treatment of ASDs?

A
  • Investigations: echocardiogram, ECG, CXR
  • Treatments: most close spontaneously, some require corrective closure
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192
Q

What is AVSD?

A

Atrio-ventricular septal defects. Basically a hole in the very centre of the heart. Involves the ventricular septum, the atrial septum, the mitral and tricuspid valves

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193
Q

Give 2 clinical signs of AVSD.

A
  1. Breathless
  2. Poor feeding and poor weight gain
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194
Q

What is a patent ductus arteriosus?

A
  • A patent ductus arteriosus (PDA) occurs when it fails to close - the ductus arteriosus is a vascular foetal structure that connects the pulmonary artery and the aorta and usually closes in the first 48 hours after birth
  • Persistence of the ductus arteriosus can result in heart failure, increased pulmonary pressures, and endarteritis
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195
Q

What are the signs of a patent ductus arteriosus?

A
  • CONTINOUS ‘MACHINERY’ MURMUR
  1. Torrential flow from the aorta to the pulmonary arteries can lead to pulmonary hypertension and RHF
  2. Breathless
  3. Poor feeding, failure to thrive
  4. May be asymptomatic
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196
Q

What are the investigations of patent ductus arteriosus?

A
  • Investigations: echocardiogram, ECG, CXR
  • Treatment: varies. Surgical closure
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197
Q

What is the coarctation of the aorta? Describe its pathophysiology.

A
  • Narrowing of the aorta at the site of insertion of the ductus arteriosus
  • Excessive sclerosing that normally closes the ductus arteriosus extends into the aortic wall leading to narrowing
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198
Q

What are the signs of coarctation of aorta?

A
  • RIGHT ARM Hypertension
  • Differential upper and lower extremity blood pressures - RADIO ‘FEMORAL’ PULSE
  • Systolic ejection murmur
199
Q

What are the investigations and treatment for a coarctation of aorta?

A
  • Investigations: ECG, CXR, echocardiogram
  • Treatment: surgery
200
Q

What do the numbers mean in a blood pressure reading? From which artery is blood pressure usually measured?

A
  • Top number = systolic blood pressure = arterial blood pressure when the heart is contracting
  • Bottom number = diastolic blood pressure = arterial blood pressure when the heart is relaxing
  • Usually measured from brachial artery (as if high there then it’s probably high elsewhere)
201
Q

What do the terms isolated systolic hypertension and isolated diastolic hypertension mean?

A
  • Isolated systolic hypertension = only systolic pressure raised
  • Isolated diastolic hypertension = only diastolic pressure raised
202
Q

What are the hospital and non-hospital readings for hypertension (stage 1)?

A
  • BP >140/90 in clinic = White coat syndrome
  • BP >135/85 with ABPM/home readings
203
Q

What are the causes of hypertension?

A
  • 95% idiopathic = Essential hypertension (usually diagnosed by screening of an asymptomatic individual)
  • 5% underlying cause = Secondary hypertension. ROPE:
  • Renal disease
  • Obesity
  • Pregnancy (pre-eclampsia)
  • Endocrine (Conn’s syndrome)
204
Q

What are the modifiable and non-modifiable risk factors for hypertension?

A
  • Modifiable:
  • Alcohol intake
  • Sedentary lifestyle
  • DM
  • Sleep apnoea
  • Smoking
  • Non-modifiable:
  • Age (>65)
  • FHx
  • Ethnicity (Afro-Caribbean)
205
Q

On average, by how much does having high blood pressure shorten life?

A

7 years. Although this depends on onset and severity

206
Q

Name 5 conditions that hypertension is a major risk factor of.

A
  1. MI (IHD)
  2. Stroke
  3. Heart failure
  4. Chronic renal disease
  5. Dementia
207
Q

If you gave someone 1 blood pressure tablet by how much would you expect their blood pressure to decrease?

A

1 tablet = 10mmHg reduction in BP

208
Q

What are the symptoms of different types of hypertension? What are some complications?

A
  • Primary HTN = usually none
  • Secondary HTN = symptoms relate to underlying cause
  • Hypertensive crisis = confusion, drowsiness, chest pain, breathlessness
209
Q

What investigations might you do in someone with hypertension?

A
  1. If clinical BP is >140/90:
    - Recheck BP on 2-3 occasions over the next few weeks/months
    - If persistently high, offer 24h ambulatory blood pressure >135/85 will confirm the diagnosis
    - If stage 1 diagnosed → do QRISK to decide treatment
    - If stage 2 diagnosed → start antihypertensive treatment
  2. We then need to identify possible causes of secondary hypertension
    - ECG (cardiovascular complications, e.g old infarction)
    - Urine ACR (albumin:creatinine ratio): ?proteinuria, dipstick: ?microscopic haematuria, bloods: renal function (GFR), Hb
    - Hypertensive retinopathy = fundus examination
    - Others:
    - HbA1c (DM)
    - Lipids
210
Q

What are the classifications of the different stages of blood pressure for both clinic BP and ABPM BP? What is the classification for a hypertensive crisis and what is the treatment?

A
  • Clinic BP:
  • Stage 1 = >140/90
  • Stage 2 = >160/100
  • ABPM BP:
  • Stage 1 = >135/85
  • Stage 2 = >150/95
  • Stage 3 (hypertensive crisis) = >180/120. With organ damage, this is known as maligant HTN = medical emergency - SAME DAY ADMISSION AND START ANTIHYPERTENSIVE DRUG IMMEDIATELY
211
Q

What is the treatment for hypertension?

A
  • Lifestyle changes
  • Hypertension with type 2 diabetes or without T2DM but <55 and not Afro-Caribbean = ACEi or ARB
  • Hypertension without T2DM but >55 or Black-African or Afro-Caribbean (any age) = CCB
  • May have to include these with thiazide-like diuretics if worse
  • For diabetics, ACE-i is ALWAYS first line
  • For black patients, start with CCB as they are not responsive to ACE-i
  • Give CCB before diuretics, unless evidence of oedema/intolerance
  • ACE-i are CI in pregnancy/if patient is on general anaesthesia
212
Q

What drugs might you give to someone with hypertension?

A
  • ABCD:

A - ACEi, e.g. ramipril or ARB (if they develop a cough with ramirpil), e.g. candesartan
B - beta blockers, e.g. bisoprolol
C - CCB, e.g. amlodipine
D - diuretics, e.g. bendroflumethiazide

213
Q

Give 5 potential side effects of rampiril.

A

Side effects of ACE inhibitors:

  1. Hypotension
  2. Acute renal failure
  3. Hyperkalaemia
  4. Teratogenic
  5. Cough, rash, anaphylactoid due to increased kinin production
214
Q

On what receptor does valsartan act?

A

AT-1, prevents Ang 2 binding

215
Q

Give 4 side effects of valsartan. How about a contraindication?

A
  • Side effects of valsartan:
    1. Hypotension
    2. Renal dysfunction
    3. Hyperkalaemia
    4. Rash
  • Contraindiated in pregnancy!
216
Q

Give 5 side effects of bisoprolol.

A

Side effects of beta blockers:

  1. Hypotension
  2. Fatigue
  3. Headache
  4. Erectile dysfunction
  5. Bradycardia
217
Q

Give 3 side effects of amlodipine.

A

Side effects of dihydropyridines (CCB):

  1. Flushing
  2. Headache
  3. Oedema
218
Q

Give 3 side effects of verapamil.

A

Side effects due to being negatively chronotropic:
1. Bradycardia
2. AV block
Side effects due to being negatively inotropic:
1. Worsening of cardiac failure

219
Q

Give 5 side effects of bendroflumethiazide.

A

Side effects of diuretics:

  1. Hypovolemia
  2. Hypotension
  3. Reduced K, Na, Mg, Ca
  4. Hyperuricaemia -> gout
  5. Erectile dysfunction
220
Q

Why are men more commonly affected by heart failure than women?

A

Women have ‘protective hormones’ meaning they are less at risk of developing heart failure

221
Q

What are the compensatory mechanisms in heart failure?

A
  1. Sympathetic system
  2. RAAS
  3. Natriuretic peptides
  4. Ventricular dilation
  5. Ventricular hypertrophy
222
Q

Explain how the sympathetic system is compensatory in heart failure and give one disadvantage of sympathetic activation.

A

The sympathetic system improves ventricular function by increasing HR and contractility = CO maintained.
BUT it also causes arteriolar constriction which increases after load and so myocardial work

223
Q

Explain how RAAS is compensatory in heart failure and give one disadvantage of RAAS activation.

A

Reduced CO leads to reduced renal perfusion; this activates RAAS. There is increased fluid retention and so increased preload.
BUT it also causes arteriolar constriction which increases after load and so myocardial work

224
Q

Give 3 properties of natriuretic peptides that make them compensatory in heart failure.

A
  1. Diuretic
  2. Hypotensive
  3. Vasodilators
225
Q

Give an example of an ACE inhibitor that is commonly used in HF.

A

Perindopril

226
Q

Name 4 beta blockers that are used in the treatment of heart failure.

A
  1. Metoprolol
  2. Bisoprolol
  3. Carvedilol
  4. Nebivolol
227
Q

What is an arrhythmia? Give a list of common arrhythmias.

A
  • Arrhythmia = an abnormality in cardiac rhythm:
  • Atrial fibrillation
  • Atrial flutter
  • Heart block
  • Tachycardia
  • Bradycardia
  • Prolonged QT
  • WPW syndrome
  • BBB
228
Q

What is the definition of tachycardia?

A

Heart rate > 100bpm

229
Q

What is atrial tachycardia? How does it appear on an ECG?

A
  • Atrial tachycardia occurs when the electrical signal that controls the heartbeat starts from an unusual location in the upper chambers (atria) and rapidly repeats, causing the atria to beat too quickly
  • In an ECG we have:
  • Abnormal P waves
  • Normal QRS
  • >150bpm
230
Q

What is AV nodal re-entrant tachycardia? What is the main symptom? What does it look like on an ECG? How do we treat it?

A
  • Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common form of paroxysmal supraventricular tachycardia (PSVT) encountered in clinical practice
  • Main symptom = sudden development of regular rapid palpitations
  • ECG:
  • Absent P wave
  • Normal QRS
  • Treatment = involves anything blocking the AV node, e.g. carotid sinus massage, Valsalva manoeuvre
231
Q

What is a ventricular tachycardia? How is this different to a supraventricular tachycardia? What does it look like on an ECG?

A
  • It occurs when the ventricles of the heart beat too fast. It is a BROAD-COMPLEX (QRS COMPLEX >120ms)
  • A supraventricular tachycardia occurs when the atria beat too fast
  • ECG:
  • No P waves
  • Regular, wide QRS
  • No T waves
232
Q

Do supraventricular tachycardia’s have narrow or broad QRS complexes? Do ventricular tachycardia’s have narrow or broad QRS complexes?

A
  • Supraventricular tachycardias are often associated with narrow complexes
  • Ventricular tachycardias are often associated with broad complexes
233
Q

Give 4 causes of sinus tachycardia.

A
  1. Physiological response to exercise
  2. Fever
  3. Anaemia
  4. Heart failure
234
Q

Name 5 supraventricular tachycardias. What is the first line management in SVT’s?

A
  1. Atrial fibrillation
  2. Atrial flutter
  3. AVRT
  4. AV node re-entry tachycardia (AVNRT)
  5. Focal atrial tachycardia

1st line management in SVT is ADENOSINE.

235
Q

What is atrial fibrillation? What is its pathophysiology? How does it appear on an ECG?

A
  • Atrial fibrillation = chaotic irregular rhythm with an irregular ventricular rate - IRREGULARLY IRREGULAR
  • Pathophysiology = continuous rapid activation of the atria with no organised mechanical action
  • ECG:
  • No P waves - irregular line
  • Irregularly irregular QRS
236
Q

What are the causes of atrial fibrillation?

A
  • Idiopathic
  • Hypertension
  • Heart failure
  • Coronary artery disease
  • Valvular heart disease
  • Cardiac surgery
  • Cardiomyopathy
  • Rheumatic heart disease
237
Q

What are the risk factors for atrial fibrillation?

A
  • Aged 60+
  • Diabetes
  • High BP
  • Coronary artery disease
  • Past MI
  • Structural heart disease
238
Q

What is the clinical presentation of atrial fibrillation?

A
  • Asymptomatic
  • Palpitations
  • Dyspnoea
  • Chest pains
  • Fatigue
  • NO P WAVES ON ECG
  • Rapid/irregular QRS
  • Apical pulse>radial
239
Q

How do we treat atrial fibrillation?

A
  • Treat underlying cause, e.g. alcohol, hypertension
  • Rate control, e.g. BETA BLOCKERS, CCBs
  • Give a LWMH, e.g. dalteparin to prevent thromboembolism
  • Restore sinus rhythm = electrical or pharmacological cardioversion
  • Maintain sinus rhythm, e.g. by using flecainide
240
Q

What is the long term treatment of atrial fibrillation?

A

Catheter ablation - it targets the triggers of AF

241
Q

The ECG taken from someone with atrial fibrillation shows a fine oscillation of the baseline and absent P waves. Why?

A

The atria fire a lot, it is chaotic. The AV node and ventricles can’t keep up -> irregularly irregular pulse

242
Q

What score can be used to calculate the risk of stroke in someone with atrial fibrillation?

A

CHADS2 VASc

243
Q

What does the CHADS2 VASc score take into account?

A

The CHADS2 VASc score is used to calculate the risk of stroke in patients with atrial fibrillation. It considers:
- Congestive heart failure/LV dysfunction

  • Hypertension
  • Age >75 (2)
  • Diabetes mellitus
  • Stroke/TIA/thrombo-embolism (2)
  • Vascular disease
  • Age 65-74
  • Sex category

Out of 9 in total. A score >2 indicates the need for anticoagulation

244
Q

Why does the stroke risk increase in atrial fibrillation?

A

Stroke risk increase due to static blood in the atria – it pools and it remains still, causing it to clot and embolise

245
Q

What is an atrial flutter? How is it different to atrial fibrillation? What is its pathophysiology? What does it look like on an ECG?

A
  • Atrial flutter = organised atrial rhythm
  • In atrial fibrillation, the atria beat irregularly. In atrial flutter, the atria beat regularly, but faster than usual and more often than the ventricles - regularly irregular
  • Pathophysiology: the re-entry mechanism - there is blockage of the normal circuit. Another pathway forms, takes a different course and re-enters the circuit -> tachycardia
  • ECG = saw-tooth pattern (F-waves) - DEFINITIVE DIAGNOSIS
246
Q

What are the causes of atrial flutter?

A
  • Idiopathic
  • Coronary heart disease
  • Obesity
  • Hypertension
  • Heart failure
  • COPD
  • Pericarditis
247
Q

What are the risk factors for atrial flutter?

A

Atrial fibrillation

248
Q

What is the clinical presentation of atrial flutter?

A
  • Palpitations
  • Breathlessness
  • Chest pain
  • Dizziness
  • Syncope
  • Fatigue
  • Sign: narrow QRS and ‘sawtooth’ flutter waves
249
Q

Describe the ECG pattern taken from someone with atrial flutter.

A
  1. Narrow QRS
  2. ‘sawtooth’ flutter waves
250
Q

What is the treatment for atrial flutter?

A
  • DEFINITIVE = CATHETER ABLATION
  • Cardioversion - give a LMWH (pharmacological), shock with defibrillator (electrical)
  • IV Amiodarone - restore sinus rhythm
251
Q

What is the acute management of haemodynamically stable patients with superventricular tachycardia?

A
  1. VALSALVA MANOUEVRE
  2. CAROTID SINUS MASSAGE
  3. Chemical cardioversion:
    i. ADENOSINE
    ii. Alternative to adenosine, e.g. verapamil
  4. Direct current (DC) cardioversion
252
Q

What is the definition of bradycardia?

A

Slow heart rate <60 bpm

253
Q

What does bradycardia look like on an ECG?

A
  • PR interval between 0.12 and 0.20 seconds
  • QRS complex <0.12 seconds
254
Q

What is a bundle branch block? What are the two types?

A
  • Bundle branch block = a block in the conduction of one of the bundle branches, so the ventricles don’t receive impulses at the same time
  • Right bundle branch block and left bundle branch block
255
Q

What is the pathophysiology of a right bundle branch block? What are the causes?

A
  • Pathophysiology = right bundle doesn’t conduct, so impulse spreads from left ventricle to right, resulting in a late activation of RV
  • Causes:
  • Pulmonary embolism
  • IHD
  • Atrial Ventricular Septal Defect
256
Q

What is the clinical presentation of right bundle branch block?

A
  • Asymptomatic
  • Syncope/Presyncope
257
Q

How do we diagnose a right bundle branch block through an ECG?

A
  • MaRRoW (the M and W stand for shapes in V1 and V6, the RR means it’s right)
  • Wide QRS
258
Q

How do we treat a right bundle branch block?

A
  • Pacemaker
  • CRT - cardiac resynchronisation therapy
  • Reduce blood pressure
259
Q

What is the pathophysiology of a left bundle branch block? What are the causes of a left bundle branch block?

A
  • Pathophysiology: left bundle doesn’t conduct, so the impulse spreads from right ventricle to left, resulting in a late activation of LV
  • Causes:
  • IHD
  • Aortic valve disease
260
Q

What is the clinical presentation of left bundle branch block?

A
  • Asymptomatic
  • Syncope/Presyncope
261
Q

How do we diagnose a left bundle branch block from an ECG?

A
  • WiLLiaM (W in V1, LL for left and M in V6)
  • Wide QRS and notched top
  • T wave inversion in lateral leads
262
Q

How do we treat left bundle branch block?

A
  • Pacemaker
  • CRT – cardiac resynchronisation therapy
  • Reduce blood pressure
263
Q

What is a heart block? What are the different types of heart block?

A
  • Heart block = a block at any level of the conduction system in which conduction seizes
  • 1st degree heart block, 2nd degree heart block (Mobitz I), 2nd degree heart block (Mobitz II), 2nd degree heart block (2:1), 3rd degree heart block
264
Q

What do the degrees of heart block represent?

A

How severe the block is, e.g. first degree = delayed but still makes it, PR interval > 200ms

265
Q

What are the causes of heart block?

A
  • Athletes
  • Sick sinus syndrome
  • IHD - esp MI
  • Acute myocarditis
  • Drugs
  • Congenital
  • Aortic valve calcification
  • Cardiac surgery/trauma
266
Q

What is first degree heart block? How do people with first degree heart block present? What does first degree heart block look like on an ECG?

A
  • First degree heart block = occurs where there is delayed atrioventricular conduction through the AV node. Despite this, every atrial impulse leads to a ventricular contraction, meaning every p waves results in a QRS complex. On an ECG this presents as a prolonged PR interval
  • Presentation = asymptomatic
  • ECG: PR interval > 200ms
267
Q

What is a second degree heart block?

A

Second degree heart block is where some of the atrial impulses do not make it through the AV node to the ventricles. This means that there are instances where p waves do not lead to QRS complexes. There are several patterns of second degree heart block

268
Q

What is a second degree heart block (Mobitz I)? How does this show on an ECG?

A
  • Where the atrial imputes becomes gradually weaker until it does not pass through the AV node. After failing to stimulate a ventricular contraction the atrial impulse returns to being strong. This cycle then repeats.
  • PR interval gradually increases until AV node fails and no QRS complex is seen. The PR interval then returns to normal but progressively becomes longer again until another QRS complex is missed. This cycle repeats itself
269
Q

What is a second degree heart block (Mobitz II)? What does the ECG look like? What is there a risk of?

A
  • This is where there is intermitted failure or interruption of AV conduction
  • This results in missing QRS complexes. There is usually a set ratio of P waves to QRS complexes, for example 3 P waves to each QRS complex would be referred to as a 3:1 block. The PR interval remains normal
  • There is a risk of ASYSTOLE with Mobitz Type 2
270
Q

How would someone with a second degree heart block (Mobitz I) present? What would their ECG look like?

A
  • Presentation:
  • Light headedness
  • Dizziness
  • Syncope
  • ECG:
  • Progressive lengthening of PR interval
  • One non-conducted P wave
  • Next PR interval is shorter
271
Q

What would the ECG of someone with a second degree heart block (Mobitz II) look like?

A
  • Constant PR
  • Occasional non-conducted P-waves
  • Wide QRS
272
Q

What is a second degree heart block (2:1)? What is it caused by? What is the clinical presentation of someone with a second degree heart block (Mobitz II (2:1)) and what would their ECG look like?

A
  • Where there are 2 P waves for each QRS complex. Every second p wave is not a strong enough atrial impulse to stimulate a QRS complex. It can be caused by Mobitz Type 1 or Mobitz Type 2 and it is difficult to tell which
  • Clinical presentation:
  • SOB
  • Postural hypotension
  • Chest pain
  • ECG:
  • Two waves per QRS
  • Normal consistent PR intervals
273
Q

Describe a third degree heart block. What is there a significant risk of?

A
  • Third degree heart block (complete heart block) = atrial activity fails to conduct to the ventricles. P waves and QRS complexes therefore occur independently (no observable relationship)
  • Significant risk of asystole
274
Q

What happens in a third degree heart block? What is the clinical presentation of third degree heart block?

A
  • In a third degree heart block, the signal is completely blocked
  • Clinical presentation = dizziness and blackouts
275
Q

What is the shape of an ECG in a third degree heart block?

A
  • P waves and QRS at different rates (dissociation)
  • Abnormally shaped QRS
276
Q

What is the treatment for a third degree heart block?

A
  • Permanent pacemaker
  • IV atropine
277
Q

What are the investigations and treatment for heart block?

A
  • Investigations = ECG
  • Treatment = cardioversion (give a LWMH, shock with defribrillator), catheter ablation (creates a conduction block), IV amiodarone (restore sinus rhythm)
278
Q

Wolff-Parkinson White syndrome (an accessory pathway syndrome) is a type of arrhythmia. What happens in this syndrome? What is the extra pathway called?

A
  • WPW syndrome is caused by an extra electrical pathway connecting the atria and ventricles. Normally there is only one pathway connecting the atria and ventricles called the atrio-ventricular node
  • The extra pathway that is present in Wolff-Parkinson White Syndrome is often called the Bundle of Ken
279
Q

What does the ECG of some with Wolff-Parkinson-White syndrome look like?

A
  • Pre-excitation:
  • SHORT PR interval
  • Wide QRS complex that begins slurred - DELTA WAVE
280
Q

What are the causes of Wolff-Parkinson-White syndrome (an accessory pathway syndrome)?

A
  • Congenital
  • Hypokalaemia
  • Hypocalcaemia
  • Drugs: amiodarone, tricyclic antidepressants
  • Bradycardia
  • Acute MI
  • Diabetes
281
Q

What is the clinical presentation of Wolff-Parkinson-White syndrome?

A
  • Palpitations
  • Severe dizziness
  • Dyspnoea
  • Syncope
282
Q

What is the treatment for Wolff-Parkinson-White syndrome?

A
  • Definitive treatment = RADIOFREQUENCY ABLATION of the accessory pathway
  • Vagal manoeuvre: breath holding, carotid massage, valsalva manoeuvre
  • IV adenosine
283
Q

Describe the pathophysiology of focal atrial tachycardia.

A

Another area of the atrium becomes more autonomic than the sinus node and so sinus node function is taken over -> focal atrial tachycardia

284
Q

What might you see on an ECG taken from someone with focal atrial tachycardia?

A

Abnormal P waves appear before a normal QRS

285
Q

What are ectopic beats and what are they caused by? What might the patient complain of?

A

Very common, generally benign arrhythmias caused by premature discharge. The patient may complain of symptoms of ‘skipped beats’

286
Q

What is prolonged QT syndrome? What does the ECG look like?

A
  • Prolonged repolarisation of the muscle cells in the heart after a contraction
  • The QT interval is greatly increased
287
Q

What are the causes of prolonged QT syndrome?

A
  • Congenital
  • Hypokalaemia
  • Hypocalcaemia
  • Drugs: amiodarone, tricyclic antidepressants
  • Bradycardia
  • Acute MI
  • Diabetes
288
Q

What is the clinical presentation of prolonged QT syndrome? What might it progress to?

A
  • Palpitations
  • Syncope
  • May progress to VF (shockable cardiac arrest rhythm)
289
Q

What is the treatment for prolonged QT syndrome?

A
  • Treat underlying cause, e.g. electrolyte management
  • Defribrillation if VF occurs
  • If acquired (not congential) = IV isoprenaline
290
Q

What is Torsades de pointes? Who does it occur in? What does its ECG look like?

A
  • Torsades de pointes is a type of polymorphic (multiple shape) ventricular tachycardia
  • It occurs in people with PROLONGED QT SYNDROME
  • It looks like normal ventricular tachycardia on an ECG, however there is an appearance that the QRS complex is twisting around the baseline. The height of the QRS complexes progressively get smaller, then larger then smaller and so on
291
Q

A patient presents to A and E following an episode where they lost consciousness. They were alone so are unsure how long they were out for. On questioning, you find out that the episode was preceded by palpitations, dizziness and shortness of breath, and that they have a family history of ‘heartbeat problems’.

You perform an ECG, which shows a sawtooth pattern.

  1. What is the most likely diagnosis?
    a. Atrial fibrillation
    b. Atrial flutter
    c. Mobitz II heart block
    d. Tachycardia
A

B. Atrial flutter

292
Q

What is infective endocarditis? Which 2 symptoms/signs signal towards infective endocarditis?

A
  • An infection of the endocardium or vascular endothelium of the heart
  • Fever + new murmur = infective endocarditis until proven otherwise
293
Q

Which bacteria cause infective endocarditis?

A
  • STAPHYLOCOCCUS AUREUS (most common - IV drug users)
  • STREPTOCOCCUS VIRIDANS (poor dental health - most common in non-IVDU)
  • Pseudomonas aeruginosa
  • Staphylococcus epidermis (prosthetic valves)
294
Q

Based on the bacterial causes of infective endocarditis, in which individuals do we usually find infective endocarditis?

A
  • IV drug users
  • Immunocompromised patients
  • People with prosthetic valves
  • Aortic/mitral valve disease
  • Poor dental hygiene
  • Pacemakers
  • IV Cannula
295
Q

Describe the pathophysiology of infective endocarditis.

A
  • Abnormal cardiac endothelium (damaged by turbulent blood flow, this is why valves are often affected. We get platelet and fibrin deposition and then a thrombus) and organisms in the bloodstream = adherance and growth of organisms to thrombus in affected area
  • Virulent organisms destroy the valve = valve regurgitation and worsening of heart failure
296
Q

Which area of the heart is usually affected by infective endocarditis? What is the exception?

A
  • Left side of the heart (MITRAL (most common) and aortic valves)
  • Exception = IV drug users = affects the right side of the heart
297
Q

What are the symptoms and signs of infective endocarditis?

A
  • Symptoms:
  • Fever
  • Rigors
  • Night sweats
  • Malaise
  • Weight loss
  • Signs:
  • Anaemia
  • Splenomegaly
  • Clubbing
  • New murmur
  • Sepsis of unknown origin
  • Embolic events of unknown
298
Q

What are some signs to look out for when investigating infective endocarditis (common exam question)?

A
  • Hands = splinter haemorrhages, Janeway lesions, Osler’s nodes
  • Eyes = Roth spots
  • Skin = embolic skin lesions, petechiae
299
Q

What are the investigations for infective endocarditis?

A
  • Use Duke Criteria: Major = POSITIVE BLOOD CULTURE, endocardium involved. Minor = FEVER > 38, predisposition, vascular phenomena (Janeway’s lesions etc.), immunological lesions (Osler’s nodes etc.), positive blood culture that doesn’t meet major criteria. 2 major or 1 major and 2 minor or 5 minor
  • IN EXAM: TRANSOESOPHAGEAL ECHOCARDIOGRAM = more sensitive, uncomfortable, better at diagnosing
  • ECG: long PR interval, regular
300
Q

How do we treat infective endocarditis?

A
  • Antibiotics:
  • FIRST LINE (before organism identified) = FAG: flucloxacillin, ampicillin + gentamicin
  • If staphylococcus: flucloxacillin, rifampicin + gentamicin
  • MRSA = VGR: VANCOMYCIN, GENTAMICIN + RIFAMPICIN
  • Not staphylococcus: benzylpenicillin and gentamycin
  • Treat any complications, e.g. heart failure, embolism etc.
  • Surgery: Replace the valve if infection can’t be treated with antibiotics. Remove and replace infected devices. Remove large vegetations at risk of embolising
301
Q

How can we try to prevent infective endocarditis?

A

Good oral health, no IV drug use, educate surgery patients on symptoms

302
Q

You are the on-call doctor for the cardiology ward, and the dental hospital sends you an urgent referral for a patient who they are treating for gum disease, who has signs of sepsis. The patient is a known intravenous drug user.

  1. What diagnosis springs to mind without even seeing the patient?
    a. Pericarditis
    b. Infective endocarditis
    c. NSTEMI
    d. Rheumatic fever
A

B. Infective endocarditis

303
Q

You are the on-call doctor for the cardiology ward, and the dental hospital sends you an urgent referral for a patient who they are treating for gum disease, who has signs of sepsis. The patient is a known intravenous drug user.

  1. Which of the following signs would help towards your diagnosis
    a. Splinter haemorrhages
    b. Roth spots
    c. Neither
    d. Both
A

D. Both

304
Q

You take blood cultures, which show MRSA growth.

  1. What antibiotics do you use?
    a. Rifampicin
    b. Vancomycin + Rifampicin
    c. Erythromycin + Vancomycin
    d. Amoxicillin
A

B. Vancomycin + Rifampicin

305
Q

What is rheumatic fever? What is it caused by? What is its pathophysiology?

A
  • Autoimmune condition common in developing countries from a Lancefield group A B-haemolytic streptococci (typically STREPTOCOCCUS PYOGENES)
  • It is caused by ANTIBODIES created against the streptococcus bacteria that also target tissues in the body - Type II hypersensitivity
  • An antibody from the cell wall cross-reacts with valve tissue which can cause permanent damage to the heart valves
306
Q

What are the symptoms and signs of rheumatic fever?

A
  • Symptoms:
  • Fever
  • Arthritis - painful, tender joints
  • Chest pain
  • SOB
  • Fatigue
  • Chorea - jerky movements
  • Signs:
  • Tachycardia
  • Murmur - dependent on the valve
  • Pericardial rub
  • Erythema marginatum - red rash with raised edges and clear centre on trunk, thighs or arms
  • Prolonged PR interval
307
Q

What are the investigations for rheumatic fever?

A
  • Erythrocyte sedimentation rate (ESR) and CRP
  • WBC count
  • Blood cultures
  • JONES criteria: recent strep. infection and 2 major or 1 major and 2 minor criteria:
  • Major:
  • Carditis: tachycardia, murmurs, pericardial rub, cardiomegaly
  • Arthritis: polyarthritis – usually larger joints
  • Erythema marginatum – red rash with raised edges and clear center
  • Sydenham’s chorea – unilateral/bilateral involuntary semi-purposeful movements
  • Minor:
  • Fever
  • Raised ESR/CRP
  • Arthralgia (as long as no arthritis)
  • Prolonged PR interval
  • Previous rheumatic fever
308
Q

How do we treat rheumatic fever?

A
  • Best rest until CRP is normal for 2 weeks consistently
  • FIRST LINE: Benzylpenicillin IV, then phenoxymethylpenicillin for ten days
  • Analgesia - aspirin
  • Haloperidol/Diazepam for chorea
309
Q

Mrs S is a 56-year-old woman who comes to GP complaining of increased fatigue and palpitations. On examination, you hear a pansystolic murmur at the apex that radiates into the axilla.

  1. Which pathology causes this murmur?
    a. Mitral stenosis
    b. Aortic stenosis
    c. Mitral regurgitation
    d. Aortic regurgitation
A

C. Mitral regurgitation

310
Q

When you ask about previous episodes of palpitations, Mrs S tells you that when she was around 12 and still lived in India, she did experience palpitations, fever and a rash on her torso which she thinks happened around 3 weeks after she had a sore throat.

What was the likely cause of her childhood illness?

a. Infective endocarditis
b. Rheumatic fever
c. Scarlet fever
d. Hypertension

A

B. Rheumatic fever

311
Q

What are cardiomyopathies? What are the four types?

A
  • A group of diseases of the myocardium that affect mechanical or electrical function
  • 4 types:
  • Hypertrophic
  • Dilated
  • Restrictive
  • Right ventricular arrhythmogenic
312
Q

What is dilated cardiomyopathy? What are the causes?

A
  • Dilated cardiomyopathy = the left ventricle is dilated, with thin muscles, so contracts poorly
  • Causes:
  • Ischaemia
  • Alcohol
  • Thyroid disorder
  • Genetic
313
Q

What is the pathophysiology of dilated cardiomyopathy?

A
  • Poorly generated contractile force = progressive dilation of the heart
  • Diffuse interstitial fibrosis
  • Systolic dysfunction of the left or both ventricles
314
Q

What are the symptoms and signs of dilated cardiomyopathy?

A
  • Symptoms:
  • Shortness of breath
  • Fatigue
  • Dyspnoea
  • Signs:
  • Heart failure
  • Arrhythmia
  • Thromboembolism
  • Increased JVP
  • Sudden death
315
Q

What are the investigations for dilated cardiomyopathy?

A
  • CXR = cardiac enlargement
  • ECG = tachycardia, arrhythmia, T-wave changes
  • Echocardiogram = dilated ventricles
316
Q

What is hypertrophic cardiomyopathy? What are its causes?

A
  • Hypertrophic cardiomyopathy = ventricular hypertrophy, causing the obstruction of the outflow tract
  • Causes:
  • Genetic - autosomal dominant
  • 50% sporadic

It is the commonest cause of sudden death in young people

317
Q

What is the pathophysiology of hypertrophic cardiomyopathy?

A
  • Gene mutation for the sarcomere protein
  • Impaired diastolic filling
  • Reduced stroke volume
  • Reduced cardiac output
318
Q

What are the signs and symptoms of hypertrophic cardiomyopathy?

A
  • Symptoms:
  • Sudden death may be the first symptom
  • Chest pain/angina
  • Dyspnoea
  • Dizziness
  • Palpitations
  • Syncope
  • Signs:
  • Ejection-systolic murmur
  • Jerky carotid pulse
  • Left ventricular outflow obstruction
319
Q

What are the investigations for hypertrophic cardiomyopathy?

A
  • ECG: T wave inversion, deep Q waves
  • Genetic analysis
320
Q

How do we treat hypertrophic cardiomyopathy?

A
  • Amiodarone - anti-arrhythmic
  • CCB - verapamil
  • Beta-blocker - atenolol
321
Q

What is restrictive cardiomyopathy? What are the causes?

A
  • Restrictive cardiomyopathy = scar tissue replaces the normal heart muscle and the ventricles become rigid so don’t contract properly
  • Causes:
  • Amyloidosis
  • Idiopathic
  • Sarcoidosis
  • End-myocardial fibrosis
322
Q

What is the pathophysiology of restrictive cardiomyopathy?

A
  • Normal/decreased volume in both ventricles
  • Bi-atrial enlargement
  • Impaired ventricle filling
  • Rigid myocardium restricts ventricular filling
323
Q

What are the symptoms and signs of restrictive cardiomyopathy?

A
  • Symptoms:
  • Dyspnoea
  • Fatigue
  • Embolic symptoms
  • Signs:
  • Increased JVP, diastolic collapse, elevated on inspiration
  • Hepatic enlargement
  • Ascites
  • Oedema
  • Third and fourth heart sounds
324
Q

What are the investigations and treatment for restrictive cardiomyopathy?

A
  • Investigations = cardiac catheterisation diagnostic
  • Treatment = no treatment - poor prognosis
325
Q

What is right ventricular arrhythmogenic cardiomyopathy?

A
  • Arrhythmogenic right ventricular cardiomyopathy is a rare familial disorder that may cause ventricular tachycardia and sudden cardiac death in young, apparently healthy individuals
  • Progressive loss of myocardium and its replacement by fatty tissue
326
Q

What are the 2 most common presenting complaints for right ventricular arrhythmogenic cardiomyopathy?

A
  • Palpitation
  • Effort induced syncope
327
Q

How do we manage right ventricular arrhythmogenic cardiomyopathy?

A
  • Implantable cardioverter defribrillator
  • Beta blockers
  • Cardiac ablation
328
Q

22 year old presents to the GP saying sometimes he experiences ‘his heart racing’ and he gets really dizzy. He sometimes gets chest pain during these episodes. His dad and grandad both died in their twenties/thirties, but he doesn’t remember what from, and he is scared that he has the same condition.

Which of the following differential diagnoses is the most common cause of sudden cardiac death in young people (and the most likely differential)?

a. Restrictive cardiomyopathy
b. Dilated cardiomyopathy
c. Hypertrophic cardiomyopathy
d. Pericarditis

A

C. Hypertrophic cardiomyopathy

329
Q

What is an aneurysm? What is the most common vessel aneurysm? What is the major complication of an anuerysm?

A
  • Aneurysm = weakening of vessel wall followed by dilation due to increased wall stress. True and false
  • Abdominal Aortic Aneurysm = most common vessel aneurysm
  • The RUPTURE of the aneurysm is the major complication
330
Q

Describe the pathogenesis of an abdominal aortic aneurysm.

A
  • Inflammation and degeneration of SMC in high-risk patients → loss of structural integrity of the aortic wall → widening of the vessel → mechanical stress (e.g., high blood pressure) acts on weakened wall tissue → dilation and rupture may occur
  • The aneurysmatic dilatation of the vessel wall may cause disruption of the laminar blood flow and turbulence → possible formation of thrombi in the aneurysm → peripheral thromboembolism
331
Q

What are the risk factors for an abdominal aortic aneurysm?

A
  • Smoking - MAJOR
  • Family history
  • Connective tissue disorders - Marfan’s, Ehlers-Danlos
  • Age
  • Atherosclerosis
  • Male
332
Q

What is the clinical presentation of an abdominal aortic aneurysm?

A
  • Patients with unruptured AAAs are usually asymptomatic
  • Cause symptoms if expanding rapidly: lower back/abdominal pain, hypotension
  • Usually discovered on routine examinations and imaging. Pulsatile mass on palpation if it is big; bruit on auscultation. Commonly found below the renal arteries (infrarenal)
333
Q

What are the investigations for an abdominal aortic aneurysm?

A
  • 1st line: ULTRASONOGRAPHY
  • May consider ESR/CRP, FBC
334
Q

How do we manage abdominal aortic aneurysms?

A
  • Patients presenting with a ruptured aneurysm require urgent repair
  • For patients with symptomatic aortic aneurysms, repair is indicated regardless of diameter
  • For asymptomatic AAA detected as an incidental finding, surveillance is preferred to repair until the risk of rupture is high. Repair is usually indicated when diameter exceeds 5.5 cm in men or 5.0 cm in women
  • All MALES at AGE 65
335
Q

What are the complications of an abdominal aortic aneurysm?

A
  • Rupture of AAA = urgent surgery
  • Thromboembolisms
  • Fistula formation
336
Q

What is the clinical presentation of a ruptured abdominal aortic aneurysm? What is the treatment?

A
  • Ruptured AAA is the most feared complication of AAA
  • Presentation:
  • Acute onset of severe, tearing abdominal pain with radiation to back, flank, groin
  • Painful pulsatile mass
  • Hypovolemic shock
  • Syncope
  • Nausea, vomiting
  • Treatment: do NOT waste time with imaging if the presentation seems clear. Treatment is URGENT SURGERY and maintaining haemodynamic stability - EVAR = Endovascular Aneurysmal Repair
337
Q

What is aortic dissection? Who does most commonly occur in? In which blood vessel do most cases occur?

A
  • Aortic dissection is a tear in the intimal layer of the aorta which leads to a collection of blood between the intima and medial layers
  • Most often occurs in men; 40-60
  • 65% of cases in the ascending aorta
338
Q

What is the pathophysiology of aortic dissection?

A
  • Tear in the intimal layer → blood then passes through the media propagating distally or proximally → false lumen
  • As the dissection propagates, flow through the false lumen can occlude flow through branches of the aorta, including the coronary, brachiocephalic, intercostal, visceral and renal, or iliac vessels 🡪 ischaemia of supplied regions
339
Q

What are the risk factors for aortic dissection?

A
  • Hypertension - most common risk factor
  • Trauma
  • Vasculitis
  • Cocaine use
  • Connective tissue disorders - cause aortic dissection in younger adults
340
Q

What are the clinical features of aortic dissection?

A
  • Sudden and SEVERE TEARING PAIN in chest radiating to back
  • Hypotension
  • ASYMMETRICAL BLOOD PRESSURE
  • Syncope
341
Q

What are the investigations for aortic dissection?

A
  • ECG
  • CXR
  • CT scanning - definitive imaging
342
Q

How do we treat aortic dissection?

A
  • Maintain haemodynamic stability - fluid resuscitation, inotropes, noradrenaline
  • Opioid analgesia for pain control
  • Surgical intervention: Endovascular stent-graft repair
  • Put patient on antihypertensives following surgery and recovery
  • Type A and Type B (add to this)
343
Q

What is peripheral vascular disease? What is its pathophysiology?

A
  • Peripheral vascular disease = when blood vessels (except those supplying the heart and brain) become narrowed and reduce blood flow, e.g. to arms, legs. POPLITEAL ARTERY IS MOST AFFECTED
  • FONTAINE CLASSIFICATION:
    1. Asymptomatic
    2. Intermittent claudication
    3. Ischaemic rest pain
    4. Ulceration/gangrene (Critical ischaemia)
  • Pathophysiology:
  • Commonly ATHEROSCLEROSIS leading to claudication of vessels
  • Other (rarer) causes of claudication: aortic coarctation, temporal arteritis, Buerger’s disease
344
Q

What are the risk factors for peripheral vascular disease?

A
  • Smoking
  • Diabetes
  • HTN
  • Sedentary lifestyle
  • Hyperlipidaemia
  • History of CAD
  • Age (< 40)
345
Q

What is end stage PVD called? How does this present?

A
  • End stage PVD = acute limb ischaemia
  • Pain
  • Parasthesia
  • Pulselessness
  • Pallor
  • Paralysis
  • Poikilothermia (perishingly cold)
346
Q

What is the clinical presentation of peripheral vascular disease?

A
  • Pain in lower limbs on exercise, relieved on rest - INTERMITTENT CLAUDICATION
  • Severe: unremitting pain in foot (esp. at night - HANGS FOOT OUT OF BED)
  • Leg may be pale, cold, loss of hair, skin changes
347
Q

What are the investigations for PVD? Explain this procedure.

A
  • Ankle Brachial Pressure Index (ABPI): PAD = 0.5-0.9, critical limb ischaemia = <0.5
  • ABPI is doppler ultrasonography = measures ratio of systolic BP at ankle and in arm to provide measure of blood flow at level of ankle, should be 1
  • 1st line = COLOUR DUPLEX ULTRASOUND
348
Q

How do we treat PVD?

A
  • Control risk factors:
  • Smoking cessation
  • Regular exercise
  • Weight reduction
  • BP control, DM control
  • Statin
  • Antiplatelet therapy = aspirin/clopidgrel
349
Q

How do we treat critical limb ischaemia?

A
  • How we treat PVD, e.g. controlling risk factors and antiplatelet therapy, PLUS:
  • Revascularisation, e.g. stenting, angioplasty, bypassing
  • Amputation if unsuitable
350
Q

What is shock? What are the different types?

A
  • Shock is a life-threatening situation where the body doesn’t have enough blood flow, which means cells and tissue don’t receive oxygen which can lead to multiple organ failure
  • Different types:
  • Cardiogenic
  • Hypovolaemic - either non-haemorrhagic or haemorrhagic
  • Septic
  • Anaphylactic
  • Neurogenic
351
Q

What is hypovolaemic shock? Describe the two types.

A
  • Hypovolaemic shock = shock induced by a low fluid volume of blood
  • Non-haemorrhagic = the loss of fluid volume IS NOT from bleeding, e.g sweating + dehydration. So low fluid volume = low blood volume = shock
  • Haemorrhagic = loss of blood volume from ruptured blood vessels. EDV decreases, so stroke volume decreases, so CO decreases, so blood pressure decreases
352
Q

What are the causes of hypovolaemic shock? What is its pathophysiology?

A
  • Causes:
  • Low fluid volume
  • Haemorrhage
  • Dehydration
  • Pathophysiology = decreased CO and decreased MAP
353
Q

What is the presentation of hypovolaemic shock?

A
  • Tachypnoea
  • Weak rapid pulse
  • Cyanosis
  • Increased capillary refill time
354
Q

How do we treat hypovolaemic shock?

A
  • ABCDE
  • Resuscitation (includes CPR, fluids, oxygen)
  • Fluids
  • Vasodilators (GTN spray)
355
Q

What is cardiogenic shock? What are its causes? What is its pathophysiology?

A
  • Where there is trauma or obstruction to the heart, therefore it cannot pump enough blood to the body’s tissues, e.g. due to myocardial infarction or pericarditis
  • Causes: pump failure, MI, cardiac arrest
  • Pathophysiology = decreased CO, decreased MAP
356
Q

What is the presentation of cardiogenic shock?

A
  • Tachycardia + tachypnoea
  • Decreased urinary output and BP
  • Cold peripheries
  • Chest pain
357
Q

How do we treat cardiogenic shock?

A
  • ABCDE
  • Resuscitation
358
Q

What is septic shock? What are its causes? What is its pathophysiology? How do we treat it?

A
  • Septic shock = when blood pressure drops to a low level after infection
  • Causes: bacterial toxins
  • Pathophysiology: blood vessels dilate + increased permeability due to toxins = decreased SVR = decreased BP
  • BUFALO: blood culture, urine output, fluids, antibiotics, lactate, oxygen
359
Q

What is the presentation of septic shock? How do we treat it?

A
  • Presentation:
  • Tachycardia
  • D+V
  • Decreased UO, O2 and BP
  • Treatment:
  • Broad spectrum IV antibiotics
  • Fluid, O2
360
Q

What is anaphylactic shock? What are its causes? What is its pathophysiology?

A
  • Anaphylactic shock = severe allergic reaction
  • Causes = bee stings, food allergies, drug allergies, IV contrast
  • Pathophysiology = histamine release causes vasodilation + increases permeability, therefore fluid can leak out + BP decreases (also there is less oxygent to tissues/organs = ischaemic = necrotic = failure), hypoxia due to bronchoconstriction
361
Q

What is the presentation of anaphylactic shock?

A

Skin rash, N+V, and a rapid, weak pulse

362
Q

How do we treat an anaphylactic shock?

A
  • Resuscitation
  • Adrenaline to constrict the blood vessels to retain BP
  • Anti-histamines to block histamine receptors
363
Q

What are the main causes of neurogenic shock?

A
  • Acute spinal cord injury
  • Regional anaesthesia
364
Q

What is the clinical presentation of neurogenic shock?

A
  • Unopposed vagal tone causes:
  • Bradycardia
  • Vasodilation = decreased SVR = decreased BP = ischaemia, necrosis etc.
365
Q

What is the treatment for neurogenic shock?

A
  • Vasopressors, e.g. dobutamine, epinephrine
  • IV fluids to stabilise blood volume
366
Q

What is a deep vein thrombosis? What are its risk factors? What are its causes? What is its pathophysiology?

A
  • Deep vein thrombosis = blood clot (thrombus) in the deep veins, usually in the lower leg
  • Risk factors = smoking, obesity, sitting for long periods of time, prolonged bed rest, injury or surgery
  • Causes = Virchow’s triad: reduced blood flow, blood vessel injury, increased coagulability
  • Pathophysiology = endothelium damaged = vasoconstriction + platelets adhere = activated by tissue factor + collagen = recruit more + form platelet plug. Coagulation cascade starts when a clotting factor gets proteolytically cleaved, which then causes this clotting factor to proteolytically cleave the next clotting factor. Fibrinogen then gets activated to fibrin, which deposits and polymerises to form a mesh around the platelet plug
367
Q

What are the signs and symptoms of DVT?

A
  • Often asymptomatic
  • Swelling in the affected leg
  • Pain in the leg
  • Red or discoloured skin on the leg
  • Warmth in the leg
  • Prominent superficial veins
  • Unilateral
  • Positive Wells score, e.g. HR > 100, haemoptysis
368
Q

What are the investigations for DVT?

A
  • Wells score - > 2 points = proximal leg USS, < 2 points = D-dimer
  • Quantitative D-dimer level - positive D-dimer is not diagnostic (can be positive in cancer, pregnancy, and post-operatively), but a negative D-dimer exclude DVT
  • Venous ultrasound - Doppler ultrasound
  • FBC
  • Urea and creatine
  • CT/MRI venography
369
Q

How do we treat DVT?

A
  • Anticoagulant (LMWH) if suspected
  • If diagnosed, anticoagulants (warfarin, rivaroxaban) for 3 months min. - target INR of 2.5
  • DOAC - apixaban (note: not with warfarin)
  • Compression stockings
  • Inferior Vena Cava Filter Placement - prevents PE
370
Q

What is the major complication of DVT? Explain how this occurs.

A

Pulmonary embolism - thrombus travels back to heart through vena cava, right atrium, right ventricle, and gets stuck in the pulmonary artery

371
Q

What does a pulmonary embolism usually arise from? What are its rarer causes? What are the risk factors?

A
  • Commonly arises from DVT
  • Rare causes include sepsis, parasites, fat embolism, neoplastic cells
  • Risks include: recent surgery, hip/knee replacement, immobility, malignancy, pregnancy, combined contraceptive pill, HRT
372
Q

What are the signs and symptoms of a pulmonary embolism?

A
  • ACUTE ONSET SHORTNESS OF BREATH
  • Unilateral pleuritic chest pain
  • Leaning forward to breathe
  • Tachycardia
  • Tachypnoea
  • Haemodynamic instability - pallor, hypotension, shock, collapse
  • Haemoptysis
  • Signs of concurrent DVT
373
Q

What are the investigations for a pulmonary embolism?

A
  • COMPUTED TOMOGRAPHIC PULMONARY ANGIOGRAPHY (CPTA)! If Wells score >4 then immediate CPTA, <4 = D-dimer
  • Echocardiography
  • D-dimer
  • FBC
  • ABG
  • CXR and ECG - look for alternate causes
374
Q

What is the treatment for a pulmonary embolism?

A
  • If PE suspected but unable to investigate, start anticoagulation: APIXABAN (DOAC) or RIVAROXABAN or LMWH
  • If delay on CTPA give LMWH, e.g. Delteparin
  • Patient presenting with hypotension and raised JVP = acutely unwell. Offer O2 if <90%, continuous UNFRACTIONATED HEPARIN and THROMBOLYSIS - senior decision - ALTEPLASE, consider IV fluids
  • Surgical pulmonary embolectomy
  • Major complications can occur in pregnant women
375
Q

How does warfarin work? What is warfarin the antagonist of? Why is warfarin difficult to use?

A
  • It produces NON-functional clotting factors 2, 7, 9 and 10
  • Vitamin K
  • Lots of interactions, teratogenic, needs almost constant monitoring
376
Q

What are the main clinical indications of ACE inhibitors? Give some examples of ACE inhibitors.

A
  • Hypertension
  • Heart failure
  • Diabetic nephropathy
  • Examples: ramipril, enalapril, perindopril, trandalopril
377
Q

What are the main side effects of ACE inhibitors?

A
  1. Related to reduced angiotensin II formation
    a. Hypotension
    b. Acute renal failure
    c. Hyperkalaemia
    d. Teratogenic effects in pregnancy
  2. Related to increased kinin production
    a. Cough
    b. Rash
    c. Anaphylactoid reactions
378
Q

What are the main clinical indications of Angiotensin II Receptor Blockers (ARBs)? Give some examples.

A
  • Hypertension
  • Diabetic nephropathy
  • Heart failure (when ACE-I contraindicated)
  • Examples: candesartan, valsartan, losartan, irbesartan, telmisartan
379
Q

What are the main adverse effects of ARBs?

A
  • Symptomatic hypotension (especially volume deplete patients)
  • Hyperkalaemia
  • Potential for renal dysfunction
  • Rash
  • Angio-oedema
380
Q

What are the main clinical indications of CCBs? Give some examples.

A
  • Hypertension
  • Ischaemic heart disease (IHD) – angina
  • Arrhythmia (tachycardia)
  • Examples: amlodipine, felodipine, lacidipine
381
Q

What are the adverse effects of CCBs?

A
  1. Due to peripheral vasodilatation (mainly dihydropyridines):
    - Flushing
    - Headache
    - Oedema
    - Palpitations
  2. Due to negatively chronotropic effects (mainly verapamil/diltiazem)
    - Bradycardia
    - Atrioventricular block
  3. Due to negatively inotropic effects (mainly verapamil)
    - Worsening of cardiac failure
  4. Verapamil causes constipation
382
Q

What are the main clinical indications of beta-adrenoreceptor blockers?

A
  • Ischaemic heart disease (IHD) – angina
  • Heart failure
  • Arrhythmia
  • Hypertension
  • Examples: bisoprolol, atenolol, propanolol
383
Q

What are the main adverse effects of beta blockers?

A
  • Fatigue
  • Headache
  • Sleep disturbance/nightmares
  • Bradycardia
  • Hypotension
  • Cold peripheries
  • Erectile dysfunction
384
Q

What are the main clinical indications of diuretics? What are the four main classes?

A
  • Hypertension
  • Heart failure
  • Examples: thiazides and related drugs (distal tubule), loop diuretics (loop of Henle, potassium-sparing diuretics, aldosterone antagonists
385
Q

Give examples of these different classes of diuretics:

a) Thiazide and related diuretics
b) Loop diuretics
c) Potassium-sparing diuretics

A

a) bendroflumethiazide, hydrochlorothiazide
b) furosemide, bumetanide
c) spironolactone, amiloride

386
Q

What are the main adverse effects of diuretics?

A
  • Hypovolaemia (mainly loop diuretics)
  • Hypotension ( “ )
  • Hypokalaemia
  • Hyponatraemia
  • Hypomagnesaemia
  • Hypocalcaemia
  • Hyperuricaemia - gout
  • Erectile dysfunction (mainly thiazides)
  • Impaired glucose tolerance ( “ )
387
Q

What is the most commonly involved coronary artery in MI?

A. RCA

B. LAD

C. LCA

D. PDA

A

C

388
Q

What is the key complication in the first 24h of an MI?

A. Fibrinous pericarditis

B. Coronary artery spasm

C. Arrhythmia

D. Mitral Insufficiency

A

C

389
Q

48 y.o. woman diagnosed with hypertension. She presents to you with a dry cough that is not getting better despite taking antibiotics. Which medication could be causing her symptoms?

A. Amlodipine

B. Lisinopril

C. Bendroflumethiazide

D. Mitral Insufficiency

A

B

390
Q

45 year old female patient came into the clinic with acute chest pain that is relieved by leaning forward. What is the gold standard investigation?

A. ECG

B. Chest X-ray

C. Echocardiogram

D. Blood culture

A

C

391
Q

A woman presented with dyspnoea, malar flush and new atrial fibrillation. What murmur should you expect from this lady?

A. Rumbling mid diastolic murmur with opening snap

B. Pansystolic murmur radiating to axilla

C. Ejection systolic murmur

D. Early diastolic murmur

A

A

392
Q

Lidocaine is effective in the treatment of ventricular tachycardias because it:

  1. Slows conduction in healthy heart tissue
  2. Opens sodium channels
  3. Blocks sodium channels at rest
  4. Blocks the activation gate of the sodium channel
  5. Blocks the inactivation gate of the sodium channel
A
  1. Blocks the inactivation gate of the sodium channel
393
Q

Digoxin can be a useful drug in the treatment of supraventricular tachycardias because it:

  1. Stimulates the release of acetylcholine from sympathetic nerves
  2. Is inotropic
  3. Makes the membrane potential more positive releasing acetylcholine from parasympathetic nerves
  4. Inhibits calcium channels
  5. Stimulates sodium/calcium exchange
A
  1. Makes the membrane potential more positive releasing acetylcholine from parasympathetic nerves
394
Q

Amlodipine and verapamil are both calcium channel blockers, what property makes verapamil the more effective anti-arrhythmic agent?

  1. Additional sodium channel blockade
  2. Once daily treatment
  3. Lack of effect on the calcium channel at rest
  4. Blockade of all calcium channel types (L, N & T)
  5. Additional potassium channel blockade
A
  1. Lack of effect on the calcium channel at rest
395
Q

Which additional property makes propranolol the most useful beta blocker to help control the arrhythmias which occur immediately following a heart attack?

  1. Calcium channel block
  2. Potassium channel block
  3. Heart block
  4. Sodium channel block
  5. Parasympathetic activation
A
  1. Sodium channel block
396
Q

In the treatment of heart failure, which transport protein or ion channel is inhibited by the loop diuretic, furosemide?

  1. Na/K ATP-ase
  2. Epithelial Na channel
  3. K channel
  4. Na/K/2Cl transporter
  5. Na/Cl transporter
A
  1. Na/K/2Cl transporter
397
Q

ACE inhibitors reduce the circulating levels of which adrenal hormone?

  1. Aldosterone
  2. Adrenaline
  3. Cortisone
  4. Angiotensin II
  5. Atrial Natriuretic Peptide
A
  1. Aldosterone
398
Q

Which drug exerts a direct inotropic effect (+ force of contraction) on heart muscle?

  1. Ramipril
  2. Furosemide
  3. Losartan
  4. Digoxin
  5. Spironolactone
  6. Glyceryl Trinitrate
A
  1. Digoxin
399
Q

In chronic heart failure beta blockers are:

  1. Contra-indicated
  2. Beneficial by slowing the heart rate
  3. Beneficial by depressing the myocardium
  4. Beneficial by increasing oxygen demand
  5. Effective by blocking reflex sympathetic responses which stress the failing heart
A
  1. Effective by blocking reflex sympathetic responses which stress the failing heart
400
Q

For which CVS drug is BRONCHOSPASM a potential side effect?

  1. Morphine
  2. Beta blocker
  3. Calcium Antagonist
  4. Aspirin
  5. Nitrate
  6. ACE inhibitor
A
  1. Beta blocker
401
Q

For which CVS drug is COUGH a potential side effect?

  1. Morphine
  2. Beta Blockers
  3. Calcium antagonists
  4. Aspirin
  5. Nitrates
  6. ACE inhibitors
A
  1. ACE inhibitors
402
Q

For which CVS drug is TOLERANCE a potential side effect?

  1. Bendroflumethazide
  2. Beta blockers
  3. Calcium antagonist
  4. Aspirin
  5. Nitrate
  6. ACE inhibitor
A
  1. Nitrate
403
Q

Which CVS drug is most likely to induce POSTURAL HYPOTENSION as a potential side effect?

  1. Morphine
  2. Beta blocker
  3. Calcium antagonist
  4. Aspirin
  5. Nitrate
  6. ACE inhibitor
A
  1. Calcium antagonist
404
Q

Doxazosin is an antagonist at which type of peripheral receptor?

  1. Alpha-1 adrenoceptor
  2. Purine receptor
  3. Angiotensin II receptor
  4. Vasopressin receptor
  5. Beta-1 adrenoceptor
  6. Dopamine receptor
A
  1. Alpha-1 adrenoreceptor
405
Q

Atenolol is an antagonist at which type of peripheral receptor?

  1. Alpha-1 adrenoceptor
  2. Purine receptor
  3. Angiotensin II receptor
  4. Vasopressin receptor
  5. Beta-1 adrenoceptor
  6. Dopamine receptor
A
  1. Beta-1 adrenoreceptor
406
Q

The antihypertensive action of lisinopril is due to inhibition of which peripheral enzyme?

  1. Kininase II
  2. Renin
  3. Na/K ATP-ase
  4. Angiotensin Converting Enzyme (ACE)
  5. DOPA decarboxylase
A
  1. Angiotensin Converting Enzyme (ACE)
407
Q

Which of the following drug side effects is less likely to be seen when treating hypertension with an angiotensin receptor blocker (ARB) rather than an ACE inhibitor?

  1. Hyperkalaemia
  2. Cough
  3. Angioedema
  4. Renal failure in the presence bilateral renal stenosis
  5. Cold hands/cold feet
A
  1. Cough
408
Q

How do beta-blockers work to relieve the pain from angina pectoris?

  1. Reduce O2 demand by slowing the heart rate
  2. Reduce O2 demand by reducing myocardial contractility
  3. Improve O2 distribution by slowing the heart rate
  4. Increase O2 supply by dilating coronary arteries
  5. Increase O2 supply by stimulating respiration
A
  1. Reduce O2 demand by slowing the heart rate
  2. Reduce O2 demand by reducing myocardial contractility
  3. Improve O2 distribution by slowing the heart rate
409
Q

What is the major mechanism by which glyceryl trinitrate can relieve the pain of angina pectoris?

  1. Dilatation of veins to reduce the preload on the heart
  2. Dilatation of arterioles to reduce the after load on the heart
  3. Dilatation of coronary arteries to increase cardiac perfusion
  4. Opening of collateral blood vessels to improve cardiac perfusion
  5. A positive inotropic effect
A
  1. Dilatation of veins to reduce the preload on the heart
410
Q

Which of the following drugs is likely to be more suitable for the treatment of variant angina due to coronary artery vasospasm?

  1. Bumetanide
  2. Losartan
  3. Isosorbide
  4. Amlodipine
  5. Glyceryl trintrate
A
  1. Amlodipine
411
Q

Which of the following drugs might be used to reduce atheromatous disease, the underlying cause of angina pectoris?

  1. Atenolol
  2. Amlodipine
  3. Simvastatin
  4. Glyceryl trinitrate
  5. Enalapril
A
  1. Simvastatin
412
Q
A

D. Increase heart rate

413
Q
A

C. Crista terminalis

414
Q
A

C. Digoxin

415
Q
A

E. T wave

416
Q
A

C. Isovolumetric relaxation

417
Q
A

D. Pericarditis

418
Q
A

C. Increase cGMP

419
Q
A

A. Connection between two atria to bypass the pulmonary circulation and foetal lungs

420
Q
A

D. Left anterior descending (LAD)

421
Q
A

B. Papillary muscles and/or chordae tendinae

422
Q
A

B. Vasomotor centre inhibition

423
Q
A

C. Right coronary

424
Q
A

B. Morphine, Oxygen, Aspirin 300mg, GTN spray

425
Q
A

C. 2nd degree AV block (Mobitz Type I)

426
Q
A

D. Amlodipine

427
Q
A

E. All of the above

428
Q
A

E. Atrial fibrillation

429
Q
A

B. Can be safely administered with macrolide antibiotics

430
Q
A

C. Infective endocarditis

431
Q
A

E. Aortic dissection

432
Q

Complete this table.

A
433
Q

A 75 year-old male presents with swelling in both of his ankles, a NT-proBNP test comes back raised.

What treatment is not indicated in his treatment?

A. Ramipril

B. Furosemide

C. Verapamil

D. Carvedilol

E. Spironolactone

A

C. Verapamil

434
Q

What drug should be given for hypertension?

a) A 54-year-old Black African male:
b) A 75-year-old White female with T2DM:
c) A 62-year-old African Caribbean female already being treated with amlodipine and ramipril:

A

a) A 54-year-old Black African male: amlodipine
b) A 75-year-old White female with T2DM: ramipril
c) A 62-year-old African Caribbean female already being treated with amlodipine and ramipril: hydrochlorothiazide

435
Q

Which of these is not an effect of ramipril?

A. Dilation of vasculature

B. Reduction in sympathetic activity

C. Renal excretion of Na+ and H2O

D. Bradykinin metabolism inhibition

E. Exacerbation of hypertension

A

E. Exacerbation of hypertension

436
Q
A

C

437
Q
A

D

438
Q
A

E

439
Q
A

C. Hilar haziness is alluding to pleural effusions

440
Q
A

B

441
Q
A

B

442
Q
A

E

443
Q

William is a 54 y.o gentleman presenting to the GP with recurrent chest pain. The pain is intermittent and seems to come more often at night. He describes the pain to be a tightness over his chest. He also has shortness of breath.

William has GORD, hypertension and high cholesterol levels. He has a pack history of 20 years.

ECG shows ST segment elevation. There is no increase in Troponin.

Based on the history, which is the most likely diagnosis?

A. Stable angina

B. Unstable angina

C. Myocardial infarction

D. Variant angina

E. GORD

A

D. Variant angina (Prinzmetal’s angina)

444
Q

A 23 y.o university student had a sudden loss of consciousness while playing football with his mates. Fortunately, CPR was administered in time and he was saved. A medical student was around and quickly did an examination and found the presence of an ejection systolic murmur. The murmur increases with intensity when standing from a supine position and disappears on squatting.

No past medical history. Family history is significant for a brother who died suddenly in his 20s.

Based on the above history, what is the underlying cause?

A. Aortic stenosis

B. Hypertrophic cardiomyopathy

C. Acute heart failure

D. Vasovagal syncope

E. Cardiogenic shock

A

B. Hypertrophic cardiomyopathy

445
Q

Matthew is a 45 y.o. man coming into the GP for a routine check-up. He denies any past medical history but his blood pressure is raised. He has a 20-pack year history. His has a family history of heart disease for which his dad had an MI at the age of 56. Physical examination is notable for obesity and blood pressure of 150/100mmHg. As the GP, you started him on some medications for hypertension.

However 2 weeks later, he starts complaining of swelling in his lower limbs. Which drug is the most likely cause for his problem?

A. Amlodipine

B. Digoxin

C. Enalapril

D. Losartan

E. Spironolactone

A

A. Amlodipine

446
Q

A 56 y.o. man presents to the A&E with chest tightness and breathlessness. His symptoms came on 1 hour ago and has not stopped at all. He has an irregularly irregular pulse between 90-110 bpm. He has a past medical history of hypertension and high cholesterol levels.

His obs are Temp: 37.00c, RR: 31, PR: 90-110, BP: 80/65mmHg and 02: 96%

ECG shows absent p-waves and an irregularly irregular rhythm. Based on the history above, what would your next step in management be?

A. Give Flecainide

B. Anticoagulate and DC cardioversion

C. Anticoagulate and give bisoprolol

D. Give amiodarone

E. Digoxin and DC cardioversion

A

B. Anticoagulate and DC cardioversion

447
Q

Alex is brought into the A&E with chest pain. He describes the pain to be crushing in nature and it radiates to his left arm. An ECG revealed ST-segment elevation and raised Troponins. He was treated for myocardial infarction.

He was later given several medications for secondary prevention. What is the mechanism of action of aspirin?

A. Non-selective inhibitors of COX1 enzymes

B. Irreversibly binds to P2Y12 receptors

C. Reversibly binds to Factor Xa

D. Inhibit HMG CoA reductase

E. Irreversibly binds to GP IIb/IIIa receptor sites

A

A. Non-selective inhibitors of COX-1 enzymes

448
Q

A 30 y.o gentleman comes into the A&E with severe chest pain. He describes himself gardening an hour ago when the pain suddenly came on. Nothing like that has ever happened and he is worried about a heart attack.

He has a past medical history of hypertension. Family history is significant for MI of his father at 59 and more cardiovascular events.

O/E: Tall and long fingers, sunken chest, high-arched palate, radial-radial delay

Based on the above, what is the most likely diagnosis?

A. Abdominal aortic aneurysm

B. Aortic dissection

C. ST-elevation myocardial infarction

D. Pulmonary embolism

E. Pericarditis

A

B. Aortic dissection

449
Q

Malcolm is a 76 y.o. gentleman presenting to the A&E with difficulty breathing and chest pain. It came on gradually an hour ago and it is a lot more severe now. The pain is constant and not associated with movement. He has a 50-pack year history.

He has lung cancer for which he is on chemo and immunotherapy.

His obs are Temp: 37.1oc, RR: 19, PR: 98, BP: 88/65 mmHg and O2: 98%.

O/E: Elevated JVP, muffled heart sounds, pulsus paradoxus

Based on the most likely diagnosis, what would be the definitive management for this presentation?

A. Percutaneous coronary intervention

B. Surgical drainage

C. Pericardiocentesis

D. Colchicine

E. Pericardiectomy

A

B. Surgical drainage

450
Q

Martha is a 73 y.o. woman presenting at the A&E with light headedness, dizziness and sweaty and clammy skin. She looks very pale. She has a history of HF and previous MI. Her BP is 103/66 and RR of 27. She is afebrile (no fever). She has had no recent trauma. Bloods show no signs of anemia. What is the most probable diagnosis?

A: Septic Shock

B: Hypovolemic Shock

C: Cardiogenic Shock

D: Neurogenic Shock

E: Anaphylactic Shock

A

C. Cardiogenic shock

451
Q

Joe is a 57 y.o man with BP of 162/88. He has been diagnosed with essential hypertension. He does not like taking Ramipril because of the cough that it gives. What is the best first line drug that he should take for his hypertension?

A: Losartan

B: Furosemide

C: Lisinopril

D: Spironolactone

E: Amlodipine

A

E. Amlodipine

452
Q

Mary is a 28 y.o woman of Caucasian heritage. She is 26 weeks pregnant and has been diagnosed with hypertension. Which of these drugs should she NOT take no matter what?

1: Losartan
2: Ramipril
3: Spironolactone
4: Amlodipine
5: Bendroflumethiazide

A. 1 and 4

B. 1 and 2

C. 2

D. 2, 3, 4 and 5

E. 1, 2, and 3

A

B. 1 and 2

453
Q

Michael is a 23 y.o man presenting with pain in the loin when urinating, foul-smelling urine and a fever of 38 degrees Celsius. He also pees with increased frequency and nocturia. While admitted, his fever has gotten much worse to 39 degrees Celsius. His HR is 115, BP of 101/63 and RR of 29. He looks very weak, pale, and clammy. He is barely conscious. What is the appropriate management?

  1. Give oxygen
  2. Measure urine
  3. Give fluids
  4. Give IV antibiotics
  5. Take blood cultures
  6. Measure lactate levels

A. 1,3,5,4,2,6

B. 1,5,4,3,2,6

C. 3, 1, 5, 4, 2, 6

D. 1, 3, 4, 5, 2, 6

E. 1, 2, 3, 5, 4, 6

A

B. 1, 5, 4, 3, 2, 6

454
Q

A 67 y.o. African American man comes to the hospital presenting with dizziness, fatigue and SOB. He feels especially dizzy when suddenly standing up. He has recently acquired a clear productive cough. He has no peripheral swelling. A systolic murmur is heard. What is the most likely diagnosis?

A. Mitral stenosis

B. Tricuspid Regurgitation

C. Pulmonary Stenosis

D. Aortic Regurgitation

E. Aortic stenosis

A

E. Aortic stenosis

455
Q

A 67 y.o. African American man comes to the hospital presenting with dizziness, fatigue and SOB. He feels especially dizzy when suddenly standing up. He has recently acquired a clear productive cough. He has no peripheral swelling. A systolic murmur is heard. What is the most likely cause of his diagnosis?

A. Calcified aortic valve

B. Congenital bicuspid aortic valve

C. Myxomatous degeneration

D. Endocarditis

E. Rheumatic fever

A

A. Calcified aortic valve

456
Q

Man presents to A+E with sudden shortness of breath, chest pain and hemoptysis. He has felt very weak and has muscle aches for the last couple of days. He has a on examination a systolic murmur at T5 mid-clavicular is found. He has a T of 38, RR of 23, HR of 94 and BP of 112/81. He is determined to have a cardiological cause for his symptoms.

A. What is the likely diagnosis?

B. What are the gold standard diagnostic investigations need to be done to definitely diagnose this illness?

A

A. Endocarditis

B.

2 separate blood cultures with positive IE microorganisms or 3 positive blood cultures 12 hours apart

Echocardiogram positive for IE

457
Q

Patient arrives at A+E with severe dyspnoea and raised jugular vein at each inspiration. He has crushing chest pain that radiates to the the trapezius. He was better when he was sitting and standing but got worse when he was laid onto the bed, he got worse. He has had chills the last few days and is presenting with a fever. On examination his heart sounds are present but muffled. His T is 38.3, HR is 112, RR 26 and BP 106/71. What is the gold standard diagnostic investigation for this illness?

A. Blood cultures

B. CXR

C. ECG

D. Echocardiogram

E. FBC

A

C. ECG

458
Q

A 27 y.o. homeless man arrives at A+E with a fever and light headedness. He has been extremely fatigued the last few days and have been lying on the ground the whole time. He has no cough and no headache. On examination, the patient was in extreme pain when his fingers were palpated. There were lesions on his palm and black spots throughout his arm. His teeth were mostly rotten and smelled very bad. He has no history of drug use. What bacteria is the most likely cause of his illness?

A. Pseudomonas Aeruginosa

B. Strep. Pneuminae

C. Strep. Viridans

D. Haemophilus Influenza

E. Staph Aureus

A

C. Strep. viridans

459
Q

Josh, a 27 y.o man comes into the clinic. He seems perfectly fine but explains that sometimes he gets headaches, nose bleeds and vision gets a bit blurry. He complains that both his legs usually feel very cold and look pale. His HR is 74, RR 16, and BP was 162/96. What is a likely differential?

A. Aortic Regurgitation

B. TIA

C. Acute limb ischaemia

D. Coarction of Aorta

E. LVH failure

A

D. Coarctation of aorta

460
Q
A

d) Saddle-shaped ST segment

461
Q
A

d) PR > 200ms

462
Q
A

a) Ramipril (ACEi) - this question tricks you because they are Afro-Caribbean (so think amlodipine), but they have T2DM!

463
Q
A

e) Verapamil (CCB)

464
Q
A

b) 2nd degree heart block - Mobitz I

465
Q
A

c) ABPI and duplex ultrasound scan

466
Q
A

e) Troponin

467
Q
A

b) Cardioversion with adenosine

468
Q
A

a) Hyperkalaemia

469
Q
A

a) Tall tented T-waves

470
Q
A

d) Blood culture. Infective endocarditis

471
Q
A

a) Viridans streptococci

472
Q
A

a) CT angiography. Aortic dissection

473
Q
A

b) Torsades de pointes

474
Q
A

e) Right bundle branch block (RBBB). R wave resembles an ‘M’, slurred S wave represents a ‘W’

475
Q
A

d) Pulmonary embolism

476
Q
A

c) Ventricular septal defect

477
Q
A

b) Streptococcus pyogenes

478
Q
A

c. Metoprolol

479
Q
A

B. Aortic stenosis

480
Q
A

D) Atenolol

481
Q
A

d. Right coronary

482
Q
A

d. Left ventricular hypertrophy

483
Q
A

B. Furosemide

484
Q
A

d) Send directly to A+E

485
Q
A

b) Factor Xa

486
Q
A

E. Catheter ablation

487
Q
A

a) Postural hypotension secondary to medications

488
Q
A

d) Drug/alcohol use

489
Q
A

c) Diastolic ventricular dysfunction

490
Q
A
491
Q
A
492
Q
A
493
Q
A
494
Q
A

Phase 2a (13 decks)

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