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Phase 2a Medicine > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is the principal cause of heart attack, stroke and gangrene of extremities?

A

Atherosclerosis

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2
Q

What is the best known risk factor for coronary artery disease?

A

Age

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3
Q

Besides age, what are five other risk factors for atherosclerosis?

A
  1. Smoking
  2. Obesity
  3. Family history
  4. High serum cholesterol (LDL)
  5. Diabetes
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4
Q

What 4 things make up an atherosclerotic plaque?

A
  1. Lipid
  2. Necrotic core
  3. Connective tissue
  4. Fibrous ‘cap’
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5
Q

What two things can happen to an atherosclerotic plaque?

A
  1. It can occlude the vessel lumen, restricting blood flow

2. It can rupture, leading to thrombus formation

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6
Q

Why do high LDL levels increase the risk of coronary artery disease?

A

LDL can pass in and out of the arterial wall and can be oxidised and glycated when it accumulates in the arterial wall. This can lead to endothelial dysfunction, causing the endothelium to not relax properly.

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7
Q

How is GTN used to prevent arterial disease?

A

GTN converts to nitrous oxide in the body and relaxes the vessel walls

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8
Q

What two things might be elevated in the bloods of a patient who has had a recent MI?

A

C-reactive protein (non-specific inflammatory marker)

Troponin (indicator of whether heart has been damaged)

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9
Q

How can canakinumab and tocilizumab be used to treat atherosclerosis?

A

Antibodies to IL-1 and IL-6 respectively, decreases inflammation in the vessel by decreasing the chemoattractants.

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10
Q

What is stage 1 of atherosclerosis?

A

Fatty streaks consisting of aggregations of lipid-laden macrophages and T lymphocytes within the intimal layer of the vessel wall.

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11
Q

What are stage 2 (intermediate lesions) of atherosclerosis comprised of?

A 
Lipid laden macrophages (foam cells)
Vascular smooth muscle cells (abnormal)
T lymphocytes
Platelets (complete with aggregation and adhesion to vessel wall)
Isolated pools of extracellular lipid
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12
Q

Stage 3 atherosclerotic plaques can impede blood flow and are prone to rupture. What prevents contact with the flowing blood?

A

They are covered with a dense fibrous cap made of ECM proteins including collagen and elastin.

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13
Q

Why would an atherosclerotic plaque rupture? (stage 4)

A

Because the fibrous cap has to be constantly resorbed and deposited to be maintained. If the balance is shifted in favour of inflammatory conditions (i.e. increased enzyme activity), the plaque becomes weak and can rupture.

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14
Q

What is stage 5 of atherosclerosis?

A

Plaque erosion

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15
Q

What is PCI?

A

Percutaneous coronary intervention, i.e. stents

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16
Q

How does aspirin help prevent coronary artery disease?

A

Irreversible inhibitor of COX, inhibits platelet aggregation

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17
Q

How do clopidogrel and ticagrelor help prevent coronary artery disease?

A

Inhibit platelet aggregation by inhibiting the P2Y12 ADP receptor on platelets

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18
Q

How do statins help prevent coronary artery disease?

A

Inhibit HMG CoA reductase, thereby reducing cholesterol synthesis

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19
Q

What drug used for gout and pericarditis may be repurposed for patients with recent MI?

A

Colchicine - has been found to lower risk of ischaemic events in patients with recent MI

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20
Q

What are the 3 types of pacemakers found in the heart?

A
  1. SA node (dominant pacemaker, intrinsic rate of 60-100bpm)
  2. AV node (backup pacemaker, intrinsic rate of 40-60bpm)
  3. Ventricular cells (backup pacemaker, intrinsic rate of 20-40bpm)
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21
Q

On an ECG, what does the P wave represent?

A

Atrial depolarisation

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22
Q

On an ECG, what is the PR interval and what does it represent?

A

Starts at origin of P wave to start of QRS complex - includes SA depolarisation, atrial depolarisation and conduction through the AV node and bundle of His.

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23
Q

How much time do the large and small boxes on the ECG represent? (Horizontally)

A

Small box = 0.04s

Large box = 0.2s

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24
Q

What voltage does a large box on an ECG represent vertically?

A

0.5mV

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25
Q

Which ECG leads show activity on the lateral right side?

A

I and aVL

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26
Q

Which ECG leads show activity on the lateral left side?

A

V5 and V6

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27
Q

Which ECG leads show activity on the inferior surface of the heart?

A

II, III and aVF

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28
Q

Which ECG leads show septal activity in the heart?

A

V1 and V2

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29
Q

Which ECG leads show anterior activity in the heart?

A

V3 and V4

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30
Q

What is Rule 1 for a normal ECG?

A

PR interval should be 120-200ms (3-5 little squares)

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31
Q

What is Rule 2 for a normal ECG?

A

The width of the QRS complex should not exceed 110ms (3 little squares)

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32
Q

What is Rule 3 for a normal ECG?

A

QRS complex should be dominantly upright in leads I and II

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33
Q

What is Rule 4 for a normal ECG?

A

QRS and T waves tend to have the same general direction in the limb leads

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34
Q

What is Rule 5 for a normal ECG?

A

All waves are negative in aVR

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35
Q

What is Rule 6 for a normal ECG?

A

R wave progression - R wave must get larger from V1 to at least V4 and the S wave must get larger from V1 to at least V3 and disappear in V6

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36
Q

What is Rule 7 for a normal ECG?

A

The ST segment should start isoelectric except in V1 and V2, where it may be elevated

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37
Q

What is Rule 8 for a normal ECG?

A

The P waves should be upright in I, II and V2 to V6

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38
Q

What is Rule 9 for a normal ECG?

A

There should be no Q wave or only a small q <0.04s in width in I, II and V2 to V6

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39
Q

What is Rule 10 for a normal ECG

A

The T wave must be upright in I, II, V2 to V6

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40
Q

The P wave is best seen in which lead?

A

Lead II

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41
Q

What can tall P waves (>2.5 little squares) indicate?

A

Right atrial enlargement

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42
Q

What can bifid (M shaped) P wave in limb leads represent?

A

Left atrial enlargement

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43
Q

What might cause a short PR interval?

A

An accessory pathway, which bypasses the AV node and allows early activation of the ventricle (as seen in Wolff-Parkinson-White syndrome)

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44
Q

What does a long PR interval signify?

A

A first degree heart block

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45
Q

What does the T wave on an ECG represent?

A

Ventricular repolarisation

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46
Q

What does a normal T wave look like?

A

Asymmetrical with a more gradual slope in the first half, at least 1/8 but <2/3 of the amplitude of the R wave, following the direction of the QRS deflection.

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47
Q

In which lead is the QT interval measured?

A

aVL

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48
Q

What is the QT interval and what does it measure?

A

Beginning of QRS complex to the end of the T wave, measures total duration of depolarisation and repolarisation.

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49
Q

What happens to the QR interval when heart rate increases?

A

It decreases

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50
Q

How long should the QT interval be?

A

0.35-0.45s, not more than half the R-R interval

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51
Q

What is a U wave?

A

A small, round, symmetrical wave, which has a positive deflection in lead II (same as T wave) and is more prominent in slower heart rates. It signifies after-depolarisations which follow repolarisation.

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52
Q

What are the 4 most common diseases of the heart valves and which one is by far the most common?

A
  1. Aortic stenosis (most common)
  2. Mitral regurgitation
  3. Aortic regurgitation
  4. Mitral stenosis
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53
Q

What is the normal aortic valve area?

A

3-4cm2

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54
Q

At what point do symptoms of aortic valve stenosis normally occur?

A

When the valve area is reduced to about 1/4 of normal

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55
Q

Give a congenital cause of aortic valve stenosis

A

Congenital bicuspid valve

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56
Q

Bicuspid aortic valve affects about 0.5-2% of the population. At what age do symptoms generally appear?

A

30s-50s

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57
Q

What are two more common causes of acquired aortic stenosis?

A
  1. Degenerative calcification - usually doesn’t cause symptoms until 70s-80s
  2. Rheumatic heart disease leading to adhesions and fusion of commissures and cusps
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58
Q

How does the heart initially compensate for aortic stenosis?

A

Increased afterload due to pressure gradient between the left ventricle and aorta leads to compensatory left ventricular hypertrophy.

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59
Q

Name 4 ways in which symptomatic aortic stenosis can present

A
  1. Syncope (heart works harder, but BP drop due to aortic stenosis)
  2. Angina (due to increased myocardial oxygen demand)
  3. Dyspnoea (on exertion)
  4. Sudden death (<2%)
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60
Q

Describe what might be heard on auscultation of a patient with aortic stenosis

A
  1. Soft/absent second heart sound (second heart sound = closure of aortic valve)
  2. S4 gallop due to left ventricular hypertrophy
  3. Ejection systolic murmur (crescendo-decrescendo due to turbulence across the aortic valve)
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61
Q

What measurements would be obtained on an echocardiogram for a patient with suspected aortic valve stenosis?

A
  1. Left ventricular size (check for hypertrophy), dilation and ejection fraction to check function)
  2. Gradient and AVA (aortic valve area)
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62
Q

Aortic stenosis can be graded as mild, moderate or severe. What measurements are used to grade?

A

Aortic valve area

Velocity of blood flow

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63
Q

Why do patients with aortic stenosis need to be really careful about their dental hygiene?

A

Because of the increased risk of infective endocarditis

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64
Q

Why does medical management play a limited role in aortic stenosis?

A

AS is a mechanical problem

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65
Q

What kind of drugs are contraindicated in severe aortic stenosis?

A

Vasodilators

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66
Q

What procedure is normally used to replace a stenotic aortic valve?

A

TAVI = transcatheter aortic valve implantation

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67
Q

Which patients are candidates for aortic valve replacement?

A
  1. Any symptomatic patient with severe aortic stenosis (including symptoms with exercise)
  2. Any patient with decreasing ejection fraction
  3. Any patient undergoing CABG with moderate/severe AS
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68
Q

What are the signs of mitral regurgitation on auscultation?

A
  1. Pansystolic murmur at the apex radiating to the axilla
  2. S3 sound (due to congestive heart failure or LA overload)
  3. Displaced hyperdynamic apex beat
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69
Q

Patients with asymptomatic severe mitral regurgitation have a 5%/year mortality rate. At what point does mortality rise sharply?

A

Once the patient’s ejection fraction drops below 60% or the patient becomes symptomatic (e.g. decreased exercise tolerance)

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70
Q

What investigations should be requested if mitral regurgitation is suspected?

A

ECG, chest x-ray, echo (particularly transoesophageal echo)

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71
Q

What might an ECG show if a patient has mitral regurgitation?

A

Signs of left atrial enlargement, atrial fibrillation and left ventricular hypertrophy

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72
Q

What 4 types of medication might be given for mitral regurgitation?

A
  1. Vasodilators (e.g. ACE inhibitors, hydralazine)
  2. Beta blockers/calcium channel blockers/digoxin for rate control
  3. Anticoagulation for AF and flutter
  4. Diuretics for fluid overload
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73
Q

What is used to monitor mitral regurgitation?

A

Serial echocardiography - frequency depends on severity

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74
Q

What are the indications for surgery in cases of severe mitral valve regurgitation?

A

Any symptoms at rest or exercise

In asymptomatic patients: if ejection fraction drops below 60% or if LVESD >45mm

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75
Q

What is the definition of aortic regurgitation?

A

Leakage of blood into the left ventricle during diastole due to ineffective coaptation of the aortic cusps

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76
Q

What are three possible causes of chronic aortic regurgitation?

A
  1. Bicuspid aortic valve
  2. Rheumatic causes
  3. Infective endocarditis
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77
Q

Aortic regurgitation results in pressure and volume overload. What compensatory mechanisms might be seen?

A

Left ventricle dilatation and hypertrophy

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78
Q

What would BP measurements in a patient with aortic regurgitation likely show?

A

Wide pulse pressure

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79
Q

What would auscultation examination of a patient with aortic regurgitation likely show?

A
  1. Diastolic blowing murmur at the left sternal border
  2. Austin flint murmur (apex) caused by vibration of the anterior mitral valve leaflet
  3. Systolic ejection murmur due to increased blood flow across the aortic valve
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80
Q

Around what age does aortic regurgitation normally become symptomatic?

A

40s-50s

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81
Q

What are the progressive symptoms of aortic regurgitation?

A

Dyspnoea (exertional, orthopnoea and paroxysmal nocturnal dyspnoea)
Palpitations due to increased force of contraction and ectopics

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82
Q

How would aortic regurgitation be evaluated radiologically?

A
  1. Chest x-ray would show enlarged cardiac silhouette and aortic root enlargement
  2. Echo can be used to assess LV dimensions and function
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83
Q

How is aortic regurgitation managed?

A
  1. Consider IE prophylaxis
  2. Vasodilators (ACEis can be used to improve stroke volume and reduce regurgitation if patient is symptomatic or hypertensive)
  3. Serial echocardiograms to monitor progression
  4. Surgical treatment (definitive)
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84
Q

What are the indications for surgical treatment of aortic regurgitation?

A
  1. Any symptoms at rest or exercise

2. If asymptomatic: if EF drops below 50% or if LV becomes dilated

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85
Q

What is the definition of mitral stenosis?

A

Obstruction of the LV inflow that prevents proper filling during diastole

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86
Q

What is the predominant cause of mitral stenosis?

A

Rheumatic carditis

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87
Q

What are two less common causes of mitral stenosis?

A

Infective endocarditis and mitral annular calcification

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88
Q

Progressive dyspnoea can occur in patients with mitral stenosis as a result of left atrial dilation, which causes pulmonary congestion due to reduced emptying. What might trigger this symptom?

A

Exercise, fever, tachycardia and pregnancy

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89
Q

Besides dyspnoea, what are the other clinical features of mitral stenosis?

A

LA enlargement
Atrial fibrillation
Haemoptysis (due to rupture of bronchial blood vessels due to pulmonary hypertension)
Right ventricular hypertrophy
Mitral facies (vasoconstriction as a result of diminished cardiac output –> pink-purple patches on cheeks)

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90
Q

What causes people to die from mitral stenosis?

A

Progressive pulmonary congestion
Infection
Thromboembolism

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91
Q

What distinctive heart sounds are heard in patients with mitral stenosis?

A
  1. Diastolic murmur - low pitched diastolic rumble most prominent at the apex
  2. Loud opening S1 ‘snap’ due to abrupt halt in leaflet motion in early diastole
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92
Q

What investigations are used to evaluate mitral stenosis?

A

ECG, chest x-ray, echo

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93
Q

What might an ECG show in cases of mitral stenosis?

A

Atrial fibrillation and evidence of left atrial enlargement

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94
Q

What might be seen on a chest x-ray of a patient with mitral stenosis?

A

Left atrial enlargement and pulmonary congestion, possible calcification of mitral valve

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95
Q

What three things are used to categorise mitral stenosis as mild, moderate or severe?

A
  1. Mean pressure gradient
  2. Pulmonary artery systolic pressure
  3. Valve area
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96
Q

Mitral stenosis is a mechanical problem and medication cannot halt progression. However, beta blockers, calcium channel blockers and digoxin might still be prescribed. Why?

A

These drugs have a chronotropic effect on the heart- slowing the heart rate prolongs diastole and allows improved diastolic filling.

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97
Q

Which patients should be considered for mitral valve replacement?

A
  • Any symptomatic patient

- Asymptomatic moderate/severe MS with a pliable valve suitable for percutaneous mitral balloon valvotomy

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98
Q

When might physiological hypertrophy of the heart occur?

A

In athletes and during pregnancy

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99
Q

Congenital heart disease affects up to 1% of all live births. What are the four most common congenital heart conditions?

A

Ventriculoseptal defect
Atrioventricular defect
Patent ductus arteriosus
Tetralogy of Fallot

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100
Q

Give four potential causes of congenital heart disease

A
  1. Genetic causes e.g. trisomy 21, Turner syndrome, homeobox gene mutations
  2. Infections e.g. rubella
  3. Drug and alcohol use
  4. Diabetes
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101
Q

Acute rheumatic fever is associated with which pathogenic organism?

A

Group A beta-haemolytic strep

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102
Q

Acute rheumatic fever is most common in which age group?

A

Peak age 9-11 years but can occur in adults

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103
Q

What are the clinical features of acute rheumatic fever?

A

Carditis, polyarthritis, chorea, erythema marginatum and subcutaneous nodules

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104
Q

How does acute rheumatic fever affect the heart?

A

The antibodies that are produced in response to the group A beta-haemolytic strep infection cross-react with cardiac myocytes and valvular glycoproteins, resulting in inflammation and scarring. This messes up the valves and results in progressive cardiac dysfunction. Also provides a favourable site for bacterial infection, increasing risk of infective endocarditis.

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105
Q

Name three inflammatory disorders other than acute rheumatic fever that can affect cardiac valves

A
  1. Systemic lupus erythematosus
  2. Rheumatoid arthritis
  3. Ankylosing spondylitis
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106
Q

What is the most common aetiology of myocarditis?

A

Viral (Coxsackie, adenovirus, ECHO, influenza)

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107
Q

What is the most common type of vasculitis?

A

Giant cell arteritis

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108
Q

Giant cell arteritis is more likely to affect which groups of people?

A

Female, 70+

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109
Q

Where are berry aneurysms found?

A

In the cerebral circulation, particularly between branching points of the circle of Willis

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110
Q

What is the major risk of a berry aneurysm?

A

Subarachnoid haemorrhage, leading to sudden death

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111
Q

What is a dissecting aneurysm?

A

When a haematoma forms within the arterial wall with blood entering under pressure from the luminal surface, which then results in dissection along the length of the media.

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112
Q

Name 2 things that increase the risk of dissecting aneurysm

A
  1. Hypertension

2. Degenerative arterial disease (e.g. Marfan syndrome)

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113
Q

What is Virchow’s triad?

A

Three things that lead to thrombus formation:

  1. Endothelial injury
  2. Stasis/turbulence of blood flow
  3. Increase in blood coagulation
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114
Q

What is an embolus?

A

A detached intravascular solid, liquid or gas bolus that moves from one part of the circulation to another - most are thrombus in origin but can be e.g. cholesterol, foreign body, tumour etc.

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115
Q

What is a haemangioma?

A

Benign proliferation of blood vessel tissue

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116
Q

What is a haemangioendothelioma?

A

A vascular tumour of endothelial cells of low grade malignancy

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117
Q

What is an angiosarcoma?

A

A highly aggressive neoplasm of endothelial cells, can be caused by environmental carcinogens such as arsenic and vinyl chloride

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118
Q

What is Ehlers-Danlos syndrome?

A

A group of disorders with abnormal collagen synthesis

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119
Q

Which type of Ehlers-Danlos syndrome is associated with spontaneous arterial rupture and aneurysm formation in early adulthood?

A

Type IV

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120
Q

What causes angina?

A

A mismatch of oxygen supply and demand caused by a narrowed artery. If a patient exerts themselves, the blood can’t reach the distal myocardium in required amount, leading to pain

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121
Q

What are the 6 most important predisposing factors to ischaemic heart disease?

A
  1. Age
  2. Smoking
  3. Family history
  4. Diabetes mellitus
  5. Hypercholesterolaemia
  6. Hypertension
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122
Q

Name 5 conditions that can exacerbate ischaemic heart disease

A
  1. Anaemia (decreases supply)
  2. Hypoxia (decreases supply)
  3. Hypertension (increases demand)
  4. Tachyarrhythmia (increases demand)
  5. Hyperthyroidism (increases demand)
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123
Q

Name 4 environmental factors that can exacerbate ischaemic heart disease

A
  1. Exercise
  2. Cold weather
  3. Heavy meal
  4. Emotional stress
    (anything that increases cardiac output/oxygen demand)
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124
Q

When does myocardial ischaemia occur?

A

When there is an imbalance between the heart’s oxygen demand and supply, usually because of an increase in demand (e.g. from exertion) accompanied by a limitation of supply (e.g. from impairment of blood flow or increased resistance)

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125
Q

What cardiac symptoms tend to accompany ischaemic heart disease?

A

Central chest pain/tightness/discomfort

Breathlessness without fluid retention

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126
Q

What cardiac symptoms do not tend to accompany ischaemic heart disease?

A

Palpitations and syncope

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127
Q

Name 7 possible causes of chest pain

A
  1. Ischaemic heart disease
  2. Pericarditis/myocarditis
  3. Pulmonary embolism/pleurisy
  4. Chest infection/pleurisy
  5. GORD
  6. Musculoskeletal chest pain (particularly in arthritis)
  7. Psychological
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128
Q

How is chronic stable angina treated?

A
  1. Lifestyle changes (smoking cessation, weight loss, exercise, dietary changes)
  2. Advice for emergency (999 if pain is prolonged and feel ill)
  3. Medication - GTN spray for when it comes on, aspirin, beta blocker, statin, ACEI
  4. Consider revascularisation if patient is unresponsive to medication
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129
Q

What is the first line of investigation for patients with suspected coronary disease?

A

CT coronary angiography

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130
Q

If a patient with suspected coronary disease has an exercise test, what should you look out for?

A

ST depression on ECG caused by differences in spread of electricity through the ischaemic myocardium.

131
Q

How do beta blockers help to treat ischaemic heart disease?

A

By reducing the heart’s oxygen demand by reducing heart rate and contractility

132
Q

What are the side effects of beta blockers?

A

Bradycardia, cold peripheries due to vasoconstriction, erectile dysfunction, tiredness

133
Q

When are beta blockers contraindicated?

A

In patients with severe asthma (due to risk of bronchoconstriction), patients already bradycardic (e.g. athletes) and patients with heart blocks.

134
Q

What two invasive treatments can be used to treat coronary disease if not controlled by medical treatment?

A
  1. PCI - percutaneous coronary intervention (stenting)

2. CABG - coronary artery bypass surgery

135
Q

A clinical diagnosis of acute pericarditis is made from at least 2 out of which 4 clinical features?

A
  1. Chest pain
  2. Friction rub
  3. ECG changes
  4. Pericardial effusion
136
Q

What pathogens can cause infectious pericarditis?

A

Usually viruses - enteroviruses, herpes viruses, adenoviruses, parvovirus B19. Also Mycobacterium tuberculosis, rarely other bacteria

137
Q

Give 5 non-infectious aetiologies of pericarditis

A 
Autoimmune
Metabolic
Traumatic
Neoplastic
Iatrogenic
138
Q

Describe the chest pain normally characteristic of pericarditis

A

Severe, sharp pain of rapid onset in the left anterior chest/epigastrium, which radiates to the arm. Usually relieved by sitting forward and exacerbated by lying down.

139
Q

What symptoms can sometimes accompany pericarditis?

A

Dyspnoea, cough, hiccups and systemic disturbances (e.g. fever, rash, joint pain, eye symptoms)

140
Q

What tests would be ordered to investigate a case of suspected pericarditis?

A

ECG, bloods, chest x-ray, echocardiogram

141
Q

What ECG changes may be caused by pericarditis?

A

ST segment elevation

PR depression

142
Q

What might blood tests for pericarditis show?

A 
Increased WCC
Elevated troponin (may suggest myopericarditis)
143
Q

What might a chest x-ray for pericarditis show?

A

In idiopathic pericarditis (most cases), a chest x-ray will be normal. May show pneumonia in cases of bacterial pericarditis.

144
Q

How is pericarditis managed?

A
  • In athletes: limit exertion until symptoms resolve and ECG/CRP are normal
  • NSAID or aspirin
  • Colchicine appears to reduce recurrence
145
Q

What is unstable angina?

A

Angina that includes chest pain at rest, episodes of which become more frequent and prolonged.

146
Q

Would troponin levels be expected to be elevated in a patient with unstable angina?

A

Not significantly

147
Q

How is non-ST elevation MI diagnosed?

A

In retrospect, once troponin (and other) results are available, which show damage to the myocardium.

148
Q

In STEMI, ST elevation reciprocal changes are seen in which lead?

149
Q

How does a non Q-wave MI present on ECG?

A
  • Poor R wave progression (less than expected in V3)
  • Slight ST elevation
  • Biphasic T wave often seen in recovering MI
150
Q

How does a Q wave MI present on ECG?

A

Complete loss of R wave on V3 with no upward deflection and a pathological Q wave with no significant R wave, straight into a segment of ST elevation.

151
Q

How does cardiac chest pain associated with MI differ from that associated with angina?

A

It is usually unremitting, severe, occurs at rest (often in bed at night)

152
Q

What symptoms often occur alongside chest pain in MI and why?

A

Sweating, breathlessness and nausea/vomiting due to activation of the vagus nerve

153
Q

How should MI be managed initially?

A
  • Call 999, paramedics should perform ECG and contact PCI centre for transfer if ST elevation is present
  • Take 300mg aspirin immediately
  • Pain relief
154
Q

Arterial thrombosis is the most common cause of MI. What is the predominant cause of arterial thrombosis?

A

Rupture of an atherosclerotic plaque

155
Q

Most MIs due to acute coronary thrombosis can be prevented with which drugs?

A

Anti-platelet drugs

156
Q

What is the treatment of choice for STEMI?

A

Primary PCI (percutaneous coronary intervention) - stent

157
Q

How does clopidogrel work?

A

Prodrug, metabolised in the liver and then binds irreversibly to P2Y12 receptor.

158
Q

What is the main problem with clopidogrel?

A

It is not very efficient and not much better than a placebo in up to 30% of patients. Many factors influence response to clopidogrel e.g. age, weight, diabetes, other drugs, genetic abnormalities

159
Q

Why might prasugrel be preferred over clopidogrel?

A

It is more effectively converted to its active form than clopidogrel

160
Q

What are the advantages of ticagrelor over clopidogrel?

A

It is a reversibly binding non-prodrug so is both activated and inactivated more quickly

161
Q

What is the disadvantage of ticagrelor compared with clopidogrel?

A

More likely to cause bleeding in non-surgical intervention

162
Q

What is heart failure?

A

The inability of the heart to deliver blood (and oxygen) at a rate commensurate with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures.

163
Q

What causes heart failure?

A

Anything that can cause myocardiac dysfunction - most commonly ischaemia caused by coronary disease but also hypertension, alcohol excess, valve problems, endocarditis, cardiomyopathy.

164
Q

At what age does the incidence of heart failure start to rise exponentially?

165
Q

What are the symptoms of heart failure?

A 
Breathlessness
Tiredness
Cold peripheries
Leg swelling
Weight gain
166
Q

What are the clinical signs of heart failure?

A 
Tachycardia
Displaced apex beat
Raised jugular venous pressure
Added heart sounds and murmurs
Hepatomegaly
Peripheral and sacral oedema
Ascites
167
Q

What parameters make breathlessness more likely to be due to heart failure?

A

Past medical history of heart failure
Paroxysmal nocturnal dyspnoea (breathlessness that wakes patient up)
S3 gallop
Chest x-ray showing pulmonary venous congestion
Atrial fibrillation on ECG

168
Q

Heart failure is classified into four classes: I to IV. How is it assessed?

A

By ability to cope with exertion - from class I (asymptomatic, no limitation) to class IV (inability to carry out any physical activity without discomfort)

169
Q

What is HF-REF?

A

Heart failure with reduced ejection fraction - LVEF <40%

170
Q

What is HF-PEF?

A

Heart failure with preserved ejection fraction - LVEF >50%

171
Q

How can NTproBNP be used to help diagnose heart failure?

A

NTproBNP is a peptide released by the heart when it is stretched. It causes excretion of sodium from the kidneys and subsequent diuresis and vasodilation. 92% of patients with NTproBNP levels above 2000 have heart failure.

172
Q

Which hormones are always elevated in patients with heart failure?

A

Arg vasopressin, renin and noradrenaline

173
Q

How is HF-PEF managed?

A
  1. Manage co-morbidities (e.g. hypertension, atrial fibrillation, IHD, diabetes)
  2. Commence exercise-based cardiac rehabilitation
174
Q

How is HF-REF managed?

A
  1. ACEI and beta blockers
  2. If symptoms continue, add aldosterone (mineralocorticoid) receptor antagonist e.g. spironolactone
  3. If symptoms persist, seek specialist advice
175
Q

What are the four elements that make up tetralogy of Fallot?

A
  1. Right ventricular hypertrophy
  2. Pulmonary stenosis
  3. Overriding aorta
  4. Ventricular septal defect
176
Q

How do babies with tetralogy of Fallot present?

A

Increased pressure in the outflow tracts when the babies feed/cry leads to hypoxia and therefore cyanosis

177
Q

What issues can tetralogy of Fallot cause following repair?

A

Pulmonary valve regurgitation in adulthood (requires redo surgery)
Arrhythmias
Endocarditis risk
Small risk of sudden death

178
Q

What is ventricular septal defect?

A

An abnormal connection between the two ventricles

179
Q

A small VSD can often be asymptomatic and require no intervention (although there is an increased risk of endocarditis). What tends to happen in babies born with a larger VSD?

A

High pulmonary blood flow leads to breathlessness, poor feeding and failure to thrive. Can lead to severe fixed irreversible pulmonary hypertension if not treated (Eisenmenger’s syndrome).

180
Q

What is Eisenmenger’s syndrome?

A

High pressure pulmonary blood flow in the infant damages the pulmonary vasculature, increasing the resistance to blood flow through the lungs.
This increases right ventricular pressure, reverses the shunt direction and causes cyanosis.

181
Q

What is an atrial septal defect?

A

An abnormal connection between the atria

182
Q

Why are patients with ASD not cyanosed?

A

The pressure in the left atrium is higher than that in the right, so the shunt is from left to right, resulting in increased blood flow to the right heart and lungs.

183
Q

What are the clinical signs of ASD?

A

Pulmonary flow murmur
Fixed split second heart sound (closure of the pulmonary valve is delayed because more blood has to get out)
Big pulmonary arteries and heart on chest x-ray

184
Q

What is an AVSD?

A

Atrioventricular septal defect - a hole in the very centre of the heart involving the ventricular septum, atrial septum, mitral and tricuspid valves.

185
Q

How would a neonate with a complete AVSD present?

A

Breathless, poor feeding and weight gain, with torrential pulmonary blood flow. Eisenmenger syndrome develops quickly.

186
Q

What is a PDA?

A

Patent ductus arteriosus. The ductus arteriosus supplies the fetal lungs until first breath is taken. If it does not close, there is a shunt between the pulmonary artery and aorta, resulting in high pressure flow into the pulmonary circulation and subsequent cyanosis and possible Eisenmenger’s syndrome if left untreated.

187
Q

What is coarctation of the aorta?

A

Narrowing of the aorta around the site of insertion of the ductus arteriosus. Collateral vessels form around the narrowing to try and compensate. The reduced flow activates the sympathetic system.

188
Q

Severe coarctation of the aorta results in complete or almost complete obstruction to aortic flow resulting in collapse with heart failure. How does mild coarctation of the aorta present?

A

Hypertension in right arm, weak femoral arteries and an incidental murmur with bruits over scapulae and back from collateral vessels.

189
Q

What two types of repair can be used to fix coarctation of the aorta surgically?

A

End to end repair or subclavian flap repair

190
Q

What long term problems are sometimes associated with coarctation of the aorta?

A

Hypertension (and therefore coronary artery disease, strokes, subarachnoid haemorrhage)
Re-coarctation requiring repeat intervention
Aneurysm formation at site of repair.

191
Q

What is a BAV?

A

Bicuspid aortic valve, less efficient at allowing flow through that normal tricuspid valve. Will normally develop regurgitation/stenosis in 20s/30s.

192
Q

What is pulmonary stenosis?

A

Obstruction of the right heart due to narrowing of the outflow of the right ventricle.

193
Q

What procedure is performed on patients with a univentricular heart?

A

Fontan procedure - formation of a single ventricle circuit for hearts with only one usable ventricle. Involves passive connection of great veins to pulmonary artery.

194
Q

What causes deviation of the heart axis?

A

Fascicular blocks, bundle blocks, ventricular hypertrophy

195
Q

What is the definition of bradycardia?

196
Q

What is the definition of tachycardia?

197
Q

What do supraventricular rhythms all have in common?

A

Narrow QRS complexes

198
Q

Why do ventricular rhythms have broad QRS complexes?

A

The rhythm arises from the ventricles and therefore doesn’t use the His-Purkinje system. Electrical activity is therefore propagated from cell to cell and takes longer.

199
Q

Give 4 causes of bradycardia

A
  1. Conduction tissue fibrosis
  2. Ischaemia
  3. Drugs (prescribed)
  4. Inflammation
200
Q

What is the difference between Mobitz type I and type II second degree heart blocks?

A

Type I - PR interval gradually lengthens until AV node fails and no subsequent QRS complex, then the pattern starts again.
Type II - Sudden unpredictable loss of AV conduction and loss of QRS - PR interval is constant, but QRS missing every now and then.

201
Q

How can a left bundle branch block be recognised on an ECG?

A

WiLLiaM

i.e. “W” shape in the V1 and “M” shape in V6

202
Q

How can a right bundle branch block be recognised on an ECG?

A

MaRRoW

i.e. “M” shape in V1 and “W” shape in V6

203
Q

Which coronary artery supplies the inferior surface of the heart?

A

In most people, the right coronary artery, but in one-third of people, the left anterior descending branch of the left coronary artery

204
Q

What happens to the ECG in cases of hyperkalaemia?

A

Tall T waves, flattened P waves, broad QRS complexes

205
Q

What effect does hypokalaemia have on an ECG?

A

Flattened T waves, QT prolongation

206
Q

What effect does hypercalcaemia have on the ECG?

A

QT shortening

207
Q

What effect does hypocalcaemia have on the ECG?

A

QT lengthening

208
Q

What are the possible consequences of high burden ventricular ectopy and high burden atrial ectopy?

A

High burden VE can cause heart failure

High burden AE can progress to AF

209
Q

What are the possible treatments for atrial fibrillation?

A
  1. Treat underlying cause (e.g. alcohol, thyroid disease, hypertension, heart failure, obesity)
  2. Rate control via beta blockers/calcium channel blockers/digoxin
  3. Restore sinus rhythm via electrical or pharmacological cardioversion
  4. Maintain sinus rhythm (flecainide, dronedarone, sotalol, amiodarone)
210
Q

What scoring system is used to assess stroke risk in patients with atrial fibrillation?

A

CHA2DS2-VASc

CHF/LVEF<40%, hypertension, age > 75 - 2 points, diabetes, stroke, vascular disease, age 65-75, sex

211
Q

Which patients who require anti-coagulation therapy would be given warfarin instead of DOACs?

A

Those with mechanical prosthetic heart valves or those with poor kidney function (DOACs renally excreted)

212
Q

What 3 DOACs inhibit Xa?

A

Rivaroxiban, apixaban, edoxaban

213
Q

Give an example of a DOAC that is a direct thrombin inhibitor.

A

Dabigatran

214
Q

What surgical treatment can be used to prevent further atrial fibrillation?

A

Pulmonary vein isolation (ablation treatment that causes electrical isolation of pulmonary veins)

215
Q

What non-invasive measures can be used to interrupt or prevent attacks of supraventricular tachycardia?

A

Valsalva manoeuvres increase vagal tone and can interrupt the short circuit that causes SVT
Beta blockers/calcium channel blockers can be used to prevent further attacks of SVT

216
Q

How does supraventricular tachycardia normally present?

A

Recurrent episodes of heart racing with sudden onset and breathlessness

217
Q

How does atrioventricular nodal re-entry tachycardia (the most common type of supraventricular tachycardia) present on an ECG?

A

Narrow QRS complexes with P waves buried within the QRS complexes - caused by re-entry circuit around the AV node, which means atrial and ventricular contraction occurs near simultaneously.

218
Q

How can AVNRT be treated invasively?

A

Ablation - catheter inserted into femoral vein, radiofrequency applied to ablate the short circuit

219
Q

What is an ‘electrical storm’?

A

3 or more sustained episodes of VT/VF or appropriate intracardiac device shocks during a 24 hour period

220
Q

What treatment might be an option if ventricular tachycardia can’t be controlled pharmacologically?

A

Catheter ablation can be used to ablate muscle strands causing the problem

221
Q

How does ventricular tachycardia appear on an ECG?

A

Broad QRS complexes, rapid rhythm, VA dissociation (P waves present, but fewer P waves than QRS complexes).

222
Q

What causes ventricular tachycardia?

A

If the heart has been damaged, there can be some surviving fibres within a diseased area that allow slow conduction in that area, resulting in further activation of the ventricle following ‘normal’ activation.

223
Q

What is infective endocarditis?

A

Infection of heart valves or other endocardial structures e.g. septal defects, pacemaker leads, surgical patches

224
Q

Name 5 risk factors for infective endocarditis

A
  1. Age
  2. Abnormal/prosthetic valve
  3. Previous infective endocarditis
  4. IV drug use
  5. Congenital heart disease
225
Q

How does infective endocarditis present?

A

Often with non-specific symptoms of systemic infection - fever, sweats etc.

226
Q

What are the 2 major criteria for IE diagnosis

A
  1. Pathogen grown from blood cultures that would be expected in a case of IE
  2. Evidence of endocarditis on echo (e.g. vegetations/new valve leak)
227
Q

What are the 5 minor criteria for IE diagnosis?

A
  1. Predisposing factors (e.g. IV drug use, prosthetic valve)
  2. Fever
  3. Vascular phenomena
  4. Immune phenomena
  5. Equivocal blood cultures
228
Q

How many criteria need to be satisfied to make a diagnosis of infective endocarditis?

A

2 major
OR 1 major + 3 minor
OR 5 minor

229
Q

What investigations should you carry out if you suspect infective endocarditis?

A

Blood cultures

Echocardiogram (may need transoesophageal echo if more detailed images required)

230
Q

What 3 types of lesions might be seen in the hands of a patient with infective endocarditis in later stages?

A
  1. Splinter haemorrhages (especially on multiple fingers)
  2. Osler nodes (tender nodules in patient’s digits)
  3. Janeway lesions (haemorrhages and nodules in the fingers)
231
Q

What is the standard treatment for infective endocarditis?

A

Intravenous antimicrobials for around 6 weeks depending on culture sensitivities

Treat complications such as arrhythmia, heart failure, embolism etc.

232
Q

Which patients with infective endocarditis might require surgery?

A
  1. Those whose infection cannot be cured with antibiotics
  2. Those with infected devices
  3. Those with complications requiring surgical management e.g. aortic root abscess
  4. Those with large vegetations that require removal before they embolise and cause further complications.
233
Q

What is sometimes the first sign of infective endocarditis in patients on warfarin?

A

INR shoots up

234
Q

What is thrombosis?

A

Blood coagulation inside a vessel

235
Q

Arterial thrombosis affects which territories?

A

Coronary circulation
Cerebral circulation
Peripheral circulation

236
Q

What is the most common aetiology of arterial thrombosis?

A

Atherosclerosis

237
Q

What drives thrombosis in arteries?

238
Q

How does arterial thrombosis present?

A

Depends on the system/arterial tree effected
Coronary arteries –> angina/MI
Cerebral/carotid arteries –> CVA
Peripheral vascular disease/ischaemia

239
Q

How is arterial thrombosis in the coronary circulation treated?

A
  • Aspirin/other anti-platelet
  • LMWH/fondraparinux
  • Thrombolytic therapy (streptokinase tissue plasminogen activator) to dissolve the clot
  • Reperfusion e.g. stents, catheter treatment to break up clot
240
Q

How is arterial thrombosis in the cerebral circulation treated?

A
  • Aspirin/other anti-platelet therapy
  • Thrombolytic therapy (streptokinase)
  • Reperfusion (stents, catheter treatment)

NOT HEPARIN due to risk of haemorrhagic transformation

241
Q

Venous thrombosis affects which territories?

A

Mainly peripheral territories e.g. ileofemoral and femoro-popliteal veins but can also appear in other sites e.g. cerebral veins, visceral veins.

242
Q

What are the 5 most common inherited pro-thrombotic conditions?

A
  1. Factor V Leiden
  2. PT20210A
  3. Antithrombin deficiency
  4. Protein C deficiency
  5. Protein S deficiency
243
Q

What are the 3 most common acquired pro-thrombotic conditions?

A
  1. Anti-phospholipid syndrome
  2. Lupus anticoagulant
  3. Hyperhomocysteinaemia
244
Q

What are the possible treatment options for venous thrombosis?

A 
Heparin/LMWH
Warfarin
DOAC
Endovascular treatments
Surgery
245
Q

What drives venous thrombosis?

246
Q

How can venous thrombosis in recovering patients be prevented?

A

Early mobilisation
Good hydration
Chemical prophylaxis with anticoagulants
Mechanical prophylaxis with compression stockings

247
Q

How does heparin work and how is it administered?

A

Given via continuous infusion, binds to antithrombin and increases its activity, leading to increased breakdown of thrombin

248
Q

What are the advantages of low molecular weight heparin over unfractionated heparin?

A

It is a smaller molecule, which is renally excreted. It can therefore be given once daily via subcutaneous administration.

249
Q

How does warfarin work?

A

Vitamin K antagonist (therefore giving vitamin K can reverse the effect of warfarin)

250
Q

How do DOACs work?

A

Act directly on factor II or factor X

251
Q

What are the signs and symptoms of deep vein thrombosis?

A

Symptoms: leg pain, swelling
Signs: tenderness, swelling, warmth, discolouration

252
Q

What scoring system is used to categorise a patient’s DVT risk?

A

Well’s score

253
Q

What test can be used to exclude a diagnosis of DVT?

254
Q

What is the main investigation for suspected DVT?

A

Ultrasound compression

255
Q

How is DVT treated?

A
  • LMWH s/c od for at least 5 days
  • Oral warfarin (aim for INR 2-3) for 3-6 months
  • DOAC
  • Compression stockings
  • Treat underlying cause
256
Q

Which surgical patients are considered low risk and don’t require chemical thromboprophylaxis?

A

Those under 40 with surgery <30 minutes

257
Q

How is pulmonary embolism investigated?

A
  • Chest x-ray –> should be normal
  • ECG will show sinus tachycardia
  • Blood gases will show type 1 respiratory failure (decreased O2 and CO2)
  • D-dimer –> excludes PE if normal
  • Spiral CT with contrast to visualise major segmental thrombi
258
Q

How is PE treated?

A
  • Supportive treatment (analgesia and O2, fluids)
  • LMWH s/c od for five days
  • Oral warfarin INR 2-3 for 6 months
  • DOAC
  • Treat underlying cause
259
Q

What are the clinical features of a massive pulmonary embolism?

A 
Haemodynamic instability
Hypotension
Cyanosis
Severe dyspnoea
Right heart strain/failure
260
Q

What invasive treatments can be used to treat (large) pulmonary embolisms?

A
  • Catheter mechano-chemical thrombectomy

- Surgical thrombo-embolectomy

261
Q

Which patients should be screened for underlying causes of hypertension?

A
  1. Those with early onset (<30 years with no risk factors)
  2. Those with resistant hypertension (3 drugs not sorting the problem)
  3. Those with malignant hypertension (so bad it’s damaging the blood vessels)
  4. Those with specific features that suggest an underlying cause e.g. phaeochromocytoma
262
Q

What might spontaneous hypokalaemia in response to thiazides represent?

A

Hyperaldosteronism

263
Q

What are the clinical features of malignant hypertension?

A

Evidence of damage to vessels, e.g. papilloedema, bleeding on the retina, acute kidney injury, acute stroke, acute coronary syndrome, aortic dissection

264
Q

What is the threshold for drug treatment for hypertension?

A

Low CVD risk: 160/100mmHg
High CVD risk: 140/90mmHG

(Clinic thresholds)

265
Q

What symptoms does hypertension usually cause?

A

Usually none, although some patients might suffer with headaches

266
Q

What is the target clinic BP for a patient who has had a previous stroke/heavy proteinuria/CKD and diabetes?

A

<130/80 mmHg

267
Q

What is the (clinic) target BP for patients over 80?

A

<150/90 mmHg

268
Q

What illnesses are often caused by hypertension?

A
  • Stroke
  • Dementia
  • MI
  • Heart failure
  • Renal failure
  • Peripheral vascular disease
269
Q

What lifestyle changes might decrease blood pressure?

A

Weight loss
Salt restriction
Exercise
Alcohol reduction

270
Q

What are the 4 types of drugs that can lower blood pressure?

A
  1. ACE inhibitors
  2. Calcium channel blockers
  3. Diuretics
  4. Beta blockers
271
Q

What types of drugs can increase blood pressure?

A

NSAIDs
SNRIs
Corticosteroids
Oestrogen-containing contraceptives
Stimulants e.g. methylpenidate used in ADHD
Anxiolytics e.g. gabapentin
Anti-TNFs used in e.g. inflammatory arthritis, cancer treatment

272
Q

When should blood pressure medications be stopped?

A

If a patient is undergoing a procedure under general anaesthesia as antihypertensives might block interventions needed to raise blood pressure.

273
Q

What are the (clinic) thresholds for stage 1 and stage 2 hypertension?

A

Stage 1: 140/90mmHg

Stage 2: 160/100mmHg

274
Q

Antihypertensive drug treatment should be offered to patients under the age of 80 with stage 1 hypertension who have at least one of which 5 conditions?

A
  1. Target organ damage
  2. Established cardiovascular disease
  3. Renal disease
  4. Diabetes
  5. A 10 year cardiovascular risk of 20% or greater
275
Q

What are the possible targets for hypertension treatment?

A

Cardiac output and peripheral resistance

276
Q

What two systems are targeted by antihypertension therapy?

A
  1. Renin-angiotensin-aldosterone system

2. Sympathetic nervous system (noradrenaline)

277
Q

What three types of antihypertensive drugs affect the renin-angiotensin-aldosterone system?

A
  1. Renin inhibitors
  2. ACE inhibitors
  3. Angiotensin receptor blockers
278
Q

What 2 types of antihypertensive drugs affect the sympathetic nervous system?

A
  1. Alpha blockers (peripheral resistance)

2. Beta blockers (cardiac output)

279
Q

What class of antihypertensive drug decreases peripheral resistance but does not affect the RAAS or SNS?

A

Calcium channel blockers

280
Q

Name 4 adverse effects of ACE inhibitors related to decrease in angiotensin II formation

A
  1. Hypotension
  2. Acute renal failure
  3. Hyperkalaemia
  4. Teratogenic effects during pregnancy
281
Q

Name 3 adverse effects of ACE inhibitors related to increased bradykinin (peptide the promotes inflammation) production

A
  1. Cough
  2. Rash
  3. Anaphylactoid reactions
282
Q

Give some examples of ACE inhibitors

A

Ramipril, enalapril, perindopril, trandolapril

283
Q

Give some examples of angiotensin II receptor blockers

A

Candesartan, losartan, valsartan, irbesartan, telmisartan

284
Q

What are the main adverse effects of ARBs?

A
  1. Hypotension
  2. Hyperkalaemia
  3. Renal dysfunction
  4. Rash
  5. Angio-oedema
285
Q

Give some examples of calcium channel blockers

A

Amlodipine, nifedipine, felodipine, lacidipine, diltiazem, verapamil

286
Q

Why are dihydropyridines preferred over phenylalkylamines and benzothiazepines for treatment of hypertension?

A

Dihydropyridines mainly affect vascular smooth muscle to reduce peripheral resistance, whereas phenylalkylamines and benzothiazepines act more on the heart.

287
Q

Give some examples of beta-adrenoreceptor blockers

A

Bisoprolol, atenolol, propranolol, carvedilol, nadolol, metoprolol

288
Q

Which beta blockers tend to select beta-1 receptors?

A

Bisoprolol and metoprolol

289
Q

What are the main adverse effects of beta blockers? (7)

A
  1. Fatigue
  2. Headache
  3. Sleep disturbance/nightmares
  4. Bradycardia
  5. Hypotension
  6. Cold peripheries
  7. Erectile dysfunction
290
Q

What are the 4 classes of diuretics?

A
  1. Thiazides and related drugs
  2. Loop diuretics
  3. Potassium sparing diuretics
  4. Aldosterone antagonists
291
Q

Give some examples of thiazide and related diuretics

A

Bendromflumethiazide, hydrochlorothiazide, chlorthalidone

292
Q

Give two examples of loop diuretics

A

Furosemide, bumetanide

293
Q

Give some examples of potassium-sparing diuretics

A

Spironolactone, eplerenone, amiloride, triamterine

294
Q

What are the main adverse effects of diuretics?

A 
Hypovolaemia
Hypotension
Hypokalaemia
Hyponatraemia
Hypomagnesaemia
Hypocalcaemia
Raised uric acid
Erectile dysfunction
Impaired glucose tolerance (link to diabetes)
295
Q

What is doxazosin?

A

An alpha-1 adrenoreceptor blocker

296
Q

Which centrally-acting hypertensive drug is really only used for treating pregnancy-induced hypertension?

A

Methyldopa

297
Q

What is the first line antihypertensive treatment for a patient under 55 years of age and not of Afro-Caribbean descent?

A

ACE inhibitor or Angiotensin receptor blocker

Hypertension in these groups more likely to be driven by RAAS

298
Q

What is the first line antihypertensive treatment for a patient over 55 years or a patient of Afro-Caribbean descent of any age?

A

Calcium channel blocker

299
Q

What is the second line of antihypertensive treatment?

A

Patient is on ACE inhibitor or calcium channel blocker already - add in the other one

300
Q

What is the third line of antihypertensive treatment?

A

If patient is on ACEI/ARB and CCB already, add in a thiazide-like diuretic

301
Q

What other drugs can be considered if hypertension is not responding to 3 drugs?

A

Spironolactone/high dose thiazide-like diuretic, alpha blocker, beta blocker (depending on patient)

302
Q

What is the most common cause of heart failure in the UK?

A

Coronary artery disease

303
Q

What 5 types of drugs can be used in heart failure?

A
  1. ACE inhibitors
  2. Angiotensin receptor blockers
  3. Beta blockers
  4. Diuretics
  5. Aldosterone antagonist
304
Q

Why are diuretics and aldosterone antagonists used in heart failure?

A

To reduce sodium and water retention, which is a big problem for patients with heart failure.

305
Q

What is the first line treatment for patients with heart failure?

A

ACE inhibitors and beta blockers (introduce gradually due to risk of hypotension), then aldosterone antagonist (usually spironolactone)

306
Q

What other drugs can be considered for heart failure patients who are intolerant to ACEI and ARB?

A

Hydralazine/nitrate combination
ARNI (aldosterone receptor antagonist with neprilysin inhibitor - Entresto)
SGLT2 inhibitors

307
Q

How do nitrates help in the treatment of ischaemic heart disease and heart failure?

A

By causing dilation of both arteries and veins, reducing both the preload and the afterload of the heart.

308
Q

What kind of drugs can be used to correct arrhythmias?

A

Those that manipulate ion channels –> affects action potential

309
Q

Name some drugs that can influence the early stage of the cardiac action potential.

A

Sodium channel blockers
Disopyramide, quinidine, procainamide
Lidocaine, mexilitene
Flecainide

310
Q

Name 2 drugs that can be used to prolong the QT interval

A

Amiodarone, sotalol

311
Q

Digoxin inhibits the Na/K pump. What effects does it have on the heart?

A

Bradycardia, slowing of AV conduction, increased ectopic activity, increased force of contraction

312
Q

What is the main problem with digoxin?

A

The Na/K pump is found all over the body, therefore it has a very narrow therapeutic range and the toxic effects such as nausea, vomiting, diarrhoea and confusion can be easily mistaken for something else.

313
Q

How does digoxin treat atrial fibrillation?

A

Reduces the ventricular rate response by blocking the AV node

314
Q

What is the most common cardiomyopathy?

A

Hypertrophic cardiomyopathy

315
Q

What are the three main types of cardiomyopathy?

A
  1. Hypertrophic
  2. Dilated
  3. Arrhythmogenic
316
Q

Why might hypertrophic cardiomyopathy cause circuit arrhythmias?

A

Because fibrosis infiltrates the myocardium - the fibrosis is an electrical insulator, so the electrical impulses are forced to go around it.

317
Q

What features are generally seen on an ECG of a person with hypertrophic cardiomyopathy?

A

Large voltages due to thick myocardium with inverted T waves, bursts of ventricular tachycardia often seen with Holter monitor.

318
Q

How does dilated cardiomyopathy present?

A

Thin-walled heart with dilation of left ventricle and possibly dilation of all four chambers. Symptoms same as that of heart failure.

319
Q

What happens to the right ventricle in cases of arrhythmogenic cardiomyopathy?

A

It becomes replaced with fibrous tissue and fat

320
Q

What causes arrhythmogenic cardiomyopathy?

A

Mutation disrupts the proteins that form the desmosomes between myocardial cells, disrupting electrical conduction.

321
Q

Name 6 electrical disorders of the heart that don’t affect structure

A
  1. Long QT syndrome
  2. Brugada syndrome
  3. CPVT (catecholaminergic polymorphic VT)
  4. WPW (Wolff-Parkinson-White - delta waves)
  5. Progressive conduction disease
  6. Idiopathic ventricular fibrillation
322
Q

Why do patients with long QT syndrome have to be very careful with drugs?

A

A lot of drugs, e.g. antidepressants can prolong the QT interval, which could lead to cardiac arrest in these patients.

323
Q

What might show up on an ECG of a patient with Brugada syndrome?

A

Characteristic pattern in V2 - looks like a dip followed by a mountain

324
Q

What are the clinical features of familial hypercholesterolaemia?

A

LDL can’t be removed from the blood as effectively due to mutation in the receptor, so it builds up in the blood.

  • Fatty deposits around knuckles and eyes
  • Evidence of coronary artery stenosis
  • Evidence of peripheral vascular disease

Phase 2a Medicine (13 decks)

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