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MY PHASE 2A MEDICINE > CARDIO > Flashcards

CARDIO Flashcards

1
Q

Name 4 valvular heart diseases.

A
  1. Aortic stenosis.
  2. Mitral regurgitation.
  3. Mitral stenosis.
  4. Aortic regurgitation.
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2
Q

Briefly describe aortic stenosis.

A

A disease where the aortic orifice is restricted and so the LV can’t eject blood properly in systole = pressure overload.

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3
Q

Describe the aetiology of aortic stenosis.

A
  1. Congenital: bicuspid valve.

2. Acquired: age related degenerative calcification/ rheumatic heart disease.

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4
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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5
Q

Give 3 symptoms of aortic stenosis.

A
  1. Exertional syncope.
  2. Angina.
  3. Exertional dyspnoea.

Onset of symptoms is associated with poor prognosis. ( <25% of normal function)

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6
Q

Give 3 signs of aortic stenosis.

A
  1. pulsus tardus + pulsus parvus
  2. Soft or absent heart sounds.
  3. Ejection systolic murmur: crescendo/decrescendo (right 2nd intercostal space)
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7
Q

What investigation might you do in someone who you suspect to have aortic stenosis?

A

Echocardiography.

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8
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.
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9
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 with moderate/severe aortic stenosis.
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10
Q

What is mitral regurgitation?

A

Back flow of blood from the LV to the LA during systole - LV volume overload

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11
Q

Describe the aetiology of mitral regurgitation.

A
  1. Myxomatous degeneration.
  2. Mitral valve prolapse
  3. Rheumatic heart disease.
  4. IE
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12
Q

What is the pathophysiology of mitral regurgitation?

A

LV volume overload! Compensatory mechanisms: LA enlargement and LVH and increased contractility. Progressive LV volume overload -> dilatation and progressive HF.

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13
Q

Give 2 symptoms of mitral regurgitation.

A
  1. Dyspnoea on exertion.

2. HF.

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14
Q

Give 3 signs of mitral regurgitation.

A
  1. Pansystolic murmur (always there).
  2. Soft 1st heart sound.
  3. 3rd heart sound.

In chronic MR the intensity of the murmur correlates with disease severity.

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15
Q

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

A
  1. ECG.
  2. CXR.
  3. Echocardiogram: estimates LA/LV size and function.
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16
Q

Describe the management of mitral regurgitation.

A
  1. Rate control for AF e.g. beta blockers.
  2. Anticoagulation for AF.
  3. Diuretics for fluid overload.
  4. IE prophylaxis.
  5. If symptomatic = surgery.
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17
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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18
Q

What is the aetiology of aortic regurgitation?

A
  1. Bicuspid aortic valve.
  2. Rheumatic.
  3. IE.
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19
Q

Describe the pathophysiology of aortic regurgitation.

A

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

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20
Q

Give 3 symptoms of aortic regurgitation.

A
  1. Dyspnoea on exertion.
  2. Orthopnea.
  3. Palpitations.
  4. Paroxysmal nocturnal dyspnea.
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21
Q

Give 3 signs of aortic regurgitation.

A
  1. Wide pulse pressure.
  2. Diastolic blowing murmur.
  3. Systolic ejection murmur.
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22
Q

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

A

CXR and echocardiogram.

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23
Q

Describe the management for someone with aortic regurgitation.

A
  1. IE prophylaxis.
  2. Vasodilators e.g. ACEi.
  3. Regular echo’s to monitor progression.
  4. Surgery if symptomatic.
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24
Q

What is mitral stenosis?

A

Obstruction to LV inflow that prevents proper filling during diastole.

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25
Q

Give 3 causes of mitral stenosis.

A
  1. Rheumatic heart disease.
  2. IE.
  3. Calcification.
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26
Q

Describe the pathophysiology of mitral stenosis.

A
  1. LA dilation -> pulmonary congestion.
  2. Increased trans-mitral pressures -> LA enlargement and AF.
  3. Pulmonary venous hypertension causes RHF symptoms.
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27
Q

Give 3 symptoms of mitral stenosis.

A
  1. Dyspnea.
  2. Haemoptysis.
  3. RHF symptoms.
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28
Q

Give 3 signs of mitral stenosis.

A
  1. low volume pulse
  2. Signs of RHF.
  3. MALAR FLUSH (Pink patches on cheeks due to vasoconstriction)
  4. Low pitched diastolic murmur.
  5. Loud opening 1st heart sound snap.
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29
Q

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

A
  1. ECG.
  2. CXR.
  3. Echocardiogram - gold standard.
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30
Q

Describe the management for mitral stenosis.

A
  1. If in AF rate control e.g. beta blockers/CCB.
  2. Anticoagulation if AF.
  3. Balloon valvuloplasty or valve replacement.
  4. IE prophylaxis.
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31
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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32
Q

What is the main pacemaker in the heart?

A

Sino atrial node

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33
Q

What controls the sinus node discharge rate?

A

The autonomic nervous system.

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34
Q

Define sinus rhythm.

A

Sinus rhythm - a P wave precedes each QRS complex.

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35
Q

Give 3 symptoms of arrhythmia.

A
  1. Sudden death.
  2. Syncope.
  3. Dizziness.
  4. Palpitations.
  5. Can also be asymptomatic.
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36
Q

Define bradycardia.

A

<60 bpm

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37
Q

Define tachycardia

A

> 100 bpm

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38
Q

Give the two broad categories of tachycardia.

A
  1. Supra-ventricular tachycardia’s.

2. Ventricular tachycardia’s.

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39
Q

Where do supra-ventricular tachycardia’s arise from?

A

They arise from the atria or atrio-ventricular junction.

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40
Q

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

A

NARROW

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41
Q

Where do ventricular tachycardia’s arise from?

A

Ventricles (duh)

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42
Q

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

A

BROAD

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43
Q

Name 4 supra-ventricular tachycardia’s.

A
  1. Atrial fibrillation.
  2. Atrial flutter.
  3. AV node re-entry tachycardia (AVNRT).
  4. Atrioventricular reciprocating tachycardia (AVRT)
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44
Q

Give 4 causes of sinus tachycardia.

A
  1. Physiological response to exercise.
  2. Fever,
  3. Anaemia.
  4. Heart failure.
  5. Hypovolemia.
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45
Q

Give an example of an Atrioventricular reciprocating tachycardia (AVRT)

A

Wolff-Parkinson-White syndrome (WPW)

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46
Q

Describe 3 characteristics of an ECG taken from someone with atrial fibrillation.

A
  1. ’Irregularly irregular’
  2. No clear P waves
  3. QRS is rapid and irregular
  4. F waves
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47
Q

Give 4 causes of atrial fibrillation

A
  1. Heart failure
  2. hypertension
  3. rheumatic heart disease
  4. thyrotoxicosis
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48
Q

Give 4 symptoms of atrial fibrillation

A
  1. Palpitations.
  2. Shortness of breath.
  3. Fatigue.
  4. Chest pain.
  5. Increased risk of thromboembolism and therefore stroke.
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49
Q

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

A

CHADS2 VASc.

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50
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:

  1. Congestive heart failure
  2. Hypertension
  3. Age >75 (2)
  4. DM
  5. Stroke/TIA in past. (2)
  6. Vascular disease
  7. Sex = female.

A score >2 indicates the need for anticoagulation.

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51
Q

Describe the treatment for atrial fibrillation.

A
  1. Rate control - beta blockers, CCB and digoxin.
  2. Rhythm control - electrical cardioversion or pharmacological cardioversion using flecainide.
  3. Flecainide can be taken on a PRN basis in people with infrequent symptomatic paroxysms of AF.
  4. Long term - catheter ablation and a pacemaker.
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52
Q

Atrial fibrillation treatment: what might you give someone to help with rate control?

A

Beta blockers, CCB and digoxin.

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53
Q

Atrial fibrillation treatment: what might you give someone to help restore sinus rhythm (rhythm control)?

A

Electrical cardioversion or pharmacological cardioversion using flecainide.

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54
Q

What is the long term treatment of atrial fibrillation?

A

Catheter ablation - it targets the triggers of AF.

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55
Q

Describe the ECG pattern taken from someone with atrial flutter.

A
  1. Narrow QRS.

2. ‘sawtooth’ flutter waves.

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56
Q

Give 3 extrinsic causes of bradycardia

A
  1. BB/ digoxin
  2. hypOthyroidism/hypOthermia
  3. raised ICP
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57
Q

Give 3 intrinsic causes of bradycardia

A
  1. Acute ischaemia
  2. Infarction of SAN
  3. Sick sinus syndrome
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58
Q

How would you treat bradycardia?

A
  1. Underlying cause if extrinsic
  2. ATROPINE if intrinsic
  3. Surgery = pacemaker
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59
Q

ECG: what might a long PR interval indicate?

A

Heart block

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60
Q

Give 3 causes of heart block.

A
  1. CAD.
  2. Cardiomyopathy.
  3. Fibrosis.
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61
Q

What kind of heart block is associated with wide QRS complexes with an abnormal pattern?

A

RBBB or LBBB

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62
Q

What is 1st degree heart block characterised by?

A
  1. Asymptomatic!
  2. Caused by myocarditis/hypokalaemia
  3. Delayed AV conduction —> PR interval prolonged >0.2s
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63
Q

What are the two types of second degree heart block?

A
  1. Mobitz type 1 (Wenckebach) - progressive prolongation of PR interval
  2. Mobitz type 2 - fixed PR interval

(an occasional QRS is dropped)

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64
Q

What is 3rd degree heart block?

A

COMPLETE heart block

All atrial activity fails to conduct to the ventricles – there is no association between atrial and ventricular activity

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65
Q

What would the ECG look like of a patient with 3rd degree heart block?

A
  1. P waves and QRS complex are independent

2. Ventricular contractions are sustained by spontaneous escape rhythm

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66
Q

What is the treatment for complete heart block

A
  1. IV atropine (acute)

2. pacemaker insertion

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67
Q

LBBB: what would you see in lead V1 and V6?

A

A ‘W’ shape would be seen in the QRS complex of lead V1 and a ‘M’ shape in V6

WiLLiaM

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68
Q

RBBB: what would you see in lead V1 and V6?

A

A ‘M’ shape would be seen in the QRS complex of lead V1 and a ‘W’ shape in V6.

MaRRoW.

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69
Q

A patient enters the clinic with BP of 140/90 mmHg. What would you management plan be?

A
  1. Offer 24hr ambulatory BP monitoring
  2. Assess end organ damage/ DM/QRISK2
  3. Lifestyle advice!
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70
Q

What are 7 risk factors for developing hypertension?

A
  1. Family history
  2. Old age
  3. Male
  4. Afro-Carribeans
  5. Lack of physical activity
  6. Unhealthy diet
  7. Obesity
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71
Q

What would be the BP of a patient with
- moderate
- severe
HTN?

A

Moderate = 160/100 mmHg

Severe = 180/110 mmHg

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72
Q

What are the two main types of treatment for hypertension?

A
  1. Lifestyle modification: reduce salt intake, lose weight, reduce alcohol.
  2. Drug therapy: ABCD.
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73
Q

What drugs might you give to someone with hypertension?

A

A - ACEi e.g. rampiril or ARB e.g. candesartan.
B - beta blockers e.g. bisoprolol.
C - Calcium CB e.g. amlodipine, diltiazem or verapamil.
D - diuretics e.g. bendroflumethiazide or furosemide.

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74
Q

A patient with hypertension has come to see you about their medication. You see in their notes that ACE inhibitors are contraindicated. What might you prescribe them instead?

A

An Angiotensin 2 Receptor Blocker (ARB) e.g. candesartan

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75
Q

A patient comes to see you who has recently started taking calcium channel blockers for their hypertension. They complain of constipation. What calcium channel blocker might they be taking?

A

Verapamil

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76
Q

You see a 45 y/o patient who has recently been diagnosed with hypertension. What is the first line treatment?

A

ACE inhibitors e.g. ramapril or ARB e.g. candesartan.

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77
Q

You see a 65 y/o patient who has recently been diagnosed with hypertension. What is the first line treatment?

A

Calcium channel blockers (as this patient is over 55) e.g. amlodipine.

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78
Q

You see a 45 y/o patient who has recently started taking ACE inhibitors for their hypertension. Unfortunately their hypertension still isn’t controlled. What would you do next for this patient?

A

You would combine ACE inhibitors or ARB with calcium channel blockers.

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79
Q

You see a 45 y/o patient who has been taking ACE inhibitors and calcium channel blockers for their hypertension. Following several tests you notice that their blood pressure is still high. What would you do next for this patient?

A

You would combine the ACEi/ARB and calcium channel blockers with a thiazide diuretic e.g. bendroflumethiazide.

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80
Q

Give 5 causes of hypertension.

A
  1. Kidney disease (CKD)
  2. Genetics and family history.
  3. Lifestyle factors e.g. high salt diet, excess alcohol, obesity, stress, caffeine.
  4. Recreational drug use e.g. cocaine.
  5. Drugs such as OCP and NSAIDS.
  6. Hyperaldosteronism.
  7. Pregnancy!
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81
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.
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82
Q

Give 3 side effects of amlodipine.

A

Side effects of dihydropyridines (CCB):

  1. Flushing.
  2. Headache.
  3. Oedema.
  4. Palpitations.
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83
Q

Diuretics: where do in the kidney do thiazides work?

A

The distal tubule.

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84
Q

Name a thiazide.

A

Bendroflumethiazide.

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85
Q

Name 2 loop diuretics.

A
  1. Furosemide.

2. Bumetanide.

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86
Q

Name a potassium sparing diuretic.

A

Spironolactone.

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87
Q

Why are potassium sparing diuretics especially effective?

A

They have anti-aldosterone effects too.

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88
Q

In what diseases are diuretics clinically indicated?

A
  1. HF

2. HTN

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89
Q

Give 5 potential side effects of diuretics.

A
  1. Hypovolemia.
  2. Hypotension.
  3. Reduced serum Na+/K+/Mg+/Ca2+.
  4. Increased uric acid -> gout.
  5. Erectile dysfunction.
  6. Impaired glucose tolerance.
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90
Q

What is heart failure?

A

A complex clinical syndrome of signs and symptoms that suggest the efficiency of the heart as a pump is impaired.

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91
Q

What is the most common cause of heart failure?

A

IHD

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92
Q

How do you calculate CO?

A

CO = HR x SV

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93
Q

What hormones does the heart produce?

A

Atrial natriuretic peptide (ANP)

Brain natriuretic peptide (BNP)

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94
Q

What is the counter regulatory system to RAAS?

A

ANP/BNP hormones.

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95
Q

What are the two broad categories of heart failure?

A
  1. Systolic failure: the ability of the heart to pump blood around the body is impaired.
  2. Diastolic failure: the heart is pumping blood effectively but is relaxing and filling abnormally.
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96
Q

How does the ejection fraction differ in systolic and diastolic HF?

A

Systolic: EF <40%
Diastolic: EF>50%

97
Q

Give 3 diseases that cause

  • systolic HF
  • diastolic HF
A

Systolic - IHD, MI, cardiomyopathy

Diastolic - Constrictive pericarditis, cardiac tamponade, hypertension

98
Q

Briefly describe the pathophysiology of heart failure.

A
  1. When the heart fails, COMPENSATORY mechanisms attempt to maintain CO.
  2. As HF progresses, these mechanisms are exhausted and become PATHOLOGICAL.
99
Q

What is preload?

A
  1. Left ventricular end-diastolic pressure (LVEDP),

2. the amount of ventricular stretch at the end of diastole

100
Q

What is after load?

A
  1. Systemic vascular resistance (SVR)
  2. the amount of resistance the heart must overcome to open the aortic valve and push the blood volume out into the systemic circulation
101
Q

Describe low-output HF

A

Decreased CO, fails to increase with exertion

102
Q

What are 3 causes of low output HF

A
  1. Pump failure
  2. Excessive pre-load
  3. Chronic increased afterload
103
Q

What is high output HF? What can cause it?

A
  1. Demands of body are too high

2. Pregnancy/ anaemia / hyperthyroidism

104
Q

What are the compensatory mechanisms in heart failure?

A
  1. Sympathetic system.
  2. RAAS.
  3. Inflammation

ALSO

Natriuretic peptides/ Ventricular dilation/Ventricular hypertrophy.

105
Q

Explain how the sympathetic system is compensatory in heart failure and how that can be damaging

A
  1. improves ventricular function by increasing HR and contractility = CO maintained.
  2. Increases afterload by causing peripheral vasoconstriction
106
Q

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

A
  1. Reduced CO leads to reduced renal perfusion; this activates RAAS.
  2. Increased fluid retention + vasoconstriction = increased preload AND afterload
107
Q

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

A
  1. Diuretic.
  2. Hypotensive.
  3. Vasodilators.
108
Q

How do cardiac myocytes change to compensate for HF

A
  1. Ventricular dilation

2. Myocyte hypertrophy

109
Q

What are the 3 cardinal symptoms of HF?

A
  1. Shortness of breath.
  2. Fatigue.
  3. Peripheral oedema.
110
Q

Give 4 signs of left heart failure.

A
  1. Cardiomegaly (displaced apex beat)
  2. 3rd and 4th heart sounds
  3. Crepitations in lung bases
  4. Tachycardia
111
Q

Give 3 symptoms of LHF

A
  1. Exertional dyspnoea
  2. Fatigue
  3. Paroxysmal Nocturnal Dyspnoea
    - pink, frothy sputum
112
Q

Give 4 signs of RHF

A
  1. Raised JVP
  2. Hepatomegaly
  3. Pitting oedema
  4. Ascites
113
Q

What investigations might you initially do in someone who has the signs/symptoms suggestive of HF?

A
  1. ECG.
  2. CXR
  3. Natriuretic peptide levels - raised BNP (not specific!)
114
Q

What would you observe on a CXR of a patient with heart failure

A 
Alveolar oedema (Bat wings)
B Kerley B lines
Cardiomegaly 
Dilated prominent upper lobe vessels
E Pleural Effusion
115
Q

What is the management for a patient with heart failure?

A
  1. Lifestyle!!
  2. (first line) Loop diuretics (furosemide)
  3. ACE inhibitor (ramipril) + Beta blocker (bisoprolol)
116
Q

When would the prescription of a beta blocker be contraindicated?

A
  1. ASTHMA

2. 2nd and 3rd degree heart block

117
Q

How do you calculate Stroke volume?

A

EDV-ESV

118
Q

What is ASD?

A

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

119
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.

120
Q

Give 4 clinical signs of a large ASD.

A
  1. Pulmonary flow murmur
  2. Fixed split second heart sound (delayed closure of PV because more blood has to get out)
  3. CXR - enlarged pulmonary arteries
  4. Cardiomegaly
121
Q

Give 2 symptoms of ASD

A
  1. SOBOE

2. Inc no. of chest infections

122
Q

What is AVSD?

A

Atrio-ventricular septal defects. Basically a hole in the very centre of the heart.

123
Q

Give 2 clinical signs of AVSD.

A
  1. Breathless.

2. Poor feeding and poor weight gain.

124
Q

What is VSD?

A

An abnormal connection between the two ventricles.

125
Q

Would a baby born with VSD be cyanotic?

A

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.

126
Q

Give 4 clinical signs of a large VSD.

A
  1. High pulmonary blood flow.
  2. Breathless, poor feeding, failure to thrive.
  3. Increased respiratory rate,
  4. Tachycardia.
127
Q

What syndrome might VSD lead on to?

A

Eisenmenger’s syndrome

128
Q

Briefly describe the physiology of Eisenmengers syndrome.

A
  1. High pressure pulmonary blood flow damages pulmonary vasculature
  2. increased resistance to blood flow (pulmonary hypertension)
  3. RV pressure increases
  4. shunt direction reverses (RV to LV) -> CYANOSIS!
129
Q

What are the risks associated with Eisenmengers syndrome?

A
  1. Death
  2. Stroke
  3. Endocarditis
130
Q

What is PDA?

A

Patent Ductus Ateriosus

- torrential flow from aorta to pulmonary arteries

131
Q

Give 3 clinical signs of PDA.

A
  1. Pulmonary hypertension and RHF.
  2. Breathless.
  3. Poor feeding, failure to thrive.
132
Q

What can be a complication of having a bicuspid aortic valve?

A
  1. Aortic stenosis

2. Aortic regurgitation

133
Q

Describe the pathophysiology behind coarctation of the aorta.

A

Excessive sclerosing that normally closes the ductus arteriosus extends into the aortic wall leading to narrowing.

134
Q

How would severe correction of the aorta present?

A

Collapse with heart failure

135
Q

How would mild coarction of the aorta present?

A
  1. Raised BP
  2. Systolic murmur (best heard over left scapula, ‘scapula bruit’)
  3. Radio-femoral delay, BP in right arm > than left arm
136
Q

How would you manage correction of the aorta?

A

Surgical repair/Stent

137
Q

What are the four main features of tetralogy of fallot?

A
  1. Ventricular septal defect.
  2. Over-riding aorta.
  3. RV hypertrophy.
  4. Pulmonary stenosis.
138
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!

139
Q

What may be seen on CXR of a child with TOF?

A

Boot shaped heart

140
Q

Why do children with TOF squat?

A
  1. Increases TPR

2. Alleviates R -> L shunt

141
Q

What is pulmonary stenosis?

A

Narrowing of the RV outflow tract.

142
Q

Name 3 congenital heart defects that are not cyanotic.

A
  1. VSD.
  2. ASD.
  3. PDA.

Left to right shunt! This is okay but a bit insufficient and there is a risk of Eisenmengers syndrome.

143
Q

Give 3 causes of IHD

A
  1. Reduced blood flow to the heart muscle (clot or atheroma)
  2. Increased distal resistance (LV hypertrophy)
  3. Reduced O2 carrying capacity (anaemia) or availability (hypoxia)
144
Q

Give 4 modifiable risk factors of IHD

A
  1. Smoking
  2. Obesity/ sedentary lifestyle
  3. Hypertension
  4. diet (High cholesterol = LDL)
145
Q

Give 3 non-modifiable risk factors for IHD

A
  1. age
  2. genetics
  3. gender (male)
146
Q

Give examples of 2 psychosocial risk factors for IHD

A
  1. High demand, low control jobs (high stress)

2. low social interaction and support

147
Q

What is the QRISK2?

A

Predicts risk of CVD in next 10 years

148
Q

What is the most common manifestation of stable IHD?

A

Angina pectoris

149
Q

What is the most common cause of angina?

A

Narrowing of the coronary arteries due to atherosclerosis.

150
Q

Briefly describe the pathophysiology of angina that results from atherosclerosis.

A
  1. On exertion there is increased O2 demand.
  2. Coronary blood flow is obstructed by an atherosclerotic plaque
  3. Myocardial ischaemia -> angina.
151
Q

Give 5 symptoms of angina.

A
  1. Crushing central chest pain.
  2. The pain RAPIDLY RESOLVES 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.
152
Q

What investigations might you do in someone you suspect to have angina?

A

GOLD = Coronary Angiography – shows luminal narrowing

ECG – usually normal, may show ST depression and T wave inversion.

Bloods – anaemia?

CXR – check heart size and pulmonary vessels

153
Q

Describe the primary prevention of angina.

A
  1. Risk factor modification.

2. Low dose aspirin.

154
Q

Describe the secondary prevention of angina.

A
  1. Risk factor modification.
  2. Pharmacological therapies for symptom relief and to reduce the risk of CV events.
  3. Interventional therapies e.g. PCI.
155
Q

Name 3 symptom relieving pharmacological therapies that might be used in someone with angina.

A
  1. Beta blockers.
  2. Nitrates e.g. GTN spray.
  3. Calcium channel blockers.
156
Q

Describe the action of beta blockers.

A
  1. Antagonise sympathetic activation and so are negatively chronotropic and inotropic.
  2. Myocardial work is reduced and so is myocardial demand = symptom relief.
157
Q

Give 3 side effects of beta blockers.

A
  1. Bradycardia.
  2. Tiredness.
  3. Erectile dysfunction.
  4. Cold peripheries.
158
Q

When might beta blockers be contraindicated?

A
  1. Asthma
  2. Bradycardia
  3. Heart block
159
Q

Describe the action of nitrates.

A

Nitrates e.g. GTN spray are VENODILATORS

  1. Venodilators -> reduced venous return -> reduced pre-load -> reduced myocardial work and myocardial demand.
160
Q

Describe the action of Ca2+ channel blockers.

A

Ca2+ blockers are ARTERODILATORS

Reduced BP -> reduced afterload -> reduced myocardial demand.

161
Q

Name 2 drugs that might be used in someone with angina or in someone at risk of angina to improve prognosis.

A
  1. Aspirin

2. Statins

162
Q

How does aspirin work?

A

Aspirin irreversibly inhibits COX. You get reduced TXA2 synthesis and so platelet aggregation is reduced.

Caution: Gastric ulcers!

163
Q

What are statins used for?

A

Reduce the amount of LDL in the blood

164
Q

What is revascularisation?

A

Revascularisation might be used in someone with angina. It restores the patent coronary artery and increases blood flow.

165
Q

Name 2 types of revascularisation.

A
  1. PCI

2. CABG

166
Q

Give 2 advantages and 1 disadvantage of PCI.

A
  1. Less invasive.
  2. Convenient and acceptable.
  3. High risk of restenosis.
167
Q

Give 1 advantage and 2 disadvantages of CABG.

A
  1. Good prognosis after surgery.
  2. Very invasive.
  3. Long recovery time.
168
Q

What is the common cause of ACS?

A

Rupture of an atherosclerotic plaque and subsequent arterial thrombosis.

169
Q

Briefly describe the pathophysiology of ACS?

A
  1. Atherosclerosis
  2. plaque rupture
  3. platelet aggregation
  4. thrombosis formation
  5. ischaemia and infarction
  6. necrosis of cells
  7. permanent heart muscle damage and ACS.
170
Q

What are uncommon causes of ACS?

A
  1. emboli
  2. coronary vasospasm
  3. vasculitis
171
Q

What might the ECG of someone with unstable angina/NSTEMI show?

A
  1. Normal

2. May show T wave inversion and ST depression.

172
Q

What might the ECG of someone with STEMI show?

A
  1. ST elevation in the anterolateral leads
  2. After a few hours, T waves invert
  3. deep, broad, pathological Q waves develop.
173
Q

What would the serum troponin level be like in someone with unstable angina?

A

Normal

174
Q

What would the serum troponin level be like in someone with NSTEMI/STEMI?

A

Significantly raised

175
Q

What other cardiac enzymes are indicators for myocyte damage?

A
  1. CK: CK-MB (creatine kinase - muscle/brain) rise within 3-12h of onset of pain
  2. Myoglobin: rises within 1-4h of onset of pain, highly sensitive but not specific
176
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.
177
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.
178
Q

What is unstable angina?

A

An ACS that is defined by the absence of biochemical evidence of myocardial damage

179
Q

What is a myocardial infarction?

A

Plaque rupture leads to a clot forming which then occludes one of the coronary arteries causing myocardial cell death and inflammation.

180
Q

What are the symptoms of an MI?

A
  1. acute central chest pain
  2. radiating to jaw or shoulder
  3. lasting >20 mins
  4. nausea
  5. SOB
  6. palpitations.
181
Q

Give 4 signs of an MI

A
  1. clammy and pale
  2. 4th heart sound
  3. pansystolic murmur,
  4. may later develop peripheral oedema
182
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/ anti - emetic
  5. Oxygen if hypoxic.
  6. Nitrates.
183
Q

What is the long term management for an MI?

A
  1. Lifestyle- modifiable risk factors!!
  2. B-blocker: metoprolol - if CI then verapamil.
  3. ACE-I
  4. Statin: reduced cholesterol post MI beneficial
  5. Aspirin: 75mg OD

Advice: return to work after 2 months (not all jobs). Encourage exercise and no air travel for 2 months.

184
Q

What are 3 complications that could occur within 24 hours of an MI?

A
  1. Ventricular arrhythmia
  2. Bradyarrhythmia (due to AV block)
  3. Cardiogenic shock
185
Q

What are 3 complications that can occur within 3 days and 2 weeks of an MI?

A
  1. Mitral regurgitation (due to papillary muscle infarction)
  2. Ventricular septal rupture
  3. Rupture of left ventricle free wall
186
Q

What are 2 complications that could occur 2 weeks + after an MI?

A
  1. Chronic pericarditis (Dressler syndrome)

2. Life threatening arrhythmia (ventricular tachycardia)

187
Q

What are 2 complications that could occur anytime after an MI?

A
  1. AF

2. HF

188
Q

What is the DdX for chest pain?

A
  1. Cardiac: ACS, aortic dissection, pericarditis, myocarditis
  2. Respiratory: PE, pneumonia, PT, pleurisy, ca. lung
  3. Musculoskeletal: rib fracture, chest trauma
    Costochondritis
  4. GORD/Oesophageal spasm
  5. Anxiety/panic attack
189
Q

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

A

In peripheral and coronary arteries

190
Q

Why is lidocaine an effective treatment for ventricular tachycardias?

A

It blocks the INactivation gate of the sodium channel

191
Q

Why is digoxin a useful drug in the treatment of supra ventricular tachycardias?

A

It makes the membrane potential more positive releasing acetylcholine from parasympathetic nerves

192
Q

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

A

Is also a sodium channel blocker

193
Q

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

A

Na/K/2Cl transporter

194
Q

What is the purpose of beta blockers in chronic heart failure?

A

Block reflex sympathetic responses which stress the failing heart

195
Q

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

A

CCB

196
Q

What is the cardinal symptom of Peripheral Vascular Disease?

A

Intermittent Claudication

  • cramping pain in calves, thighs and buttocks
  • brought on by exercise
  • relieved by rest!!
197
Q

What can intermittent claudication lead on to if left untreated?

A

Critical Ischaemia

198
Q

Give 6 symptoms of acute limb ischaemia.

A
  1. Pain.
  2. Pale.
  3. Paralysis.
  4. Paraesthesia.
  5. Perishing cold.
  6. Pulseless.
199
Q

Give 5 risk factors for peripheral vascular disease.

A
  1. Hypertension.
  2. Hyperlipidaemia.
  3. Diabetes.
  4. Smoking.
  5. Obesity.
200
Q

Give 3 signs of Peripheral Vascular Disease

A
  1. absent pulses
  2. punched out ulcers
  3. postural colour change (Buerger’s Test)
201
Q

What would the Ankle Brachial Pressure Index (ABPI) be in a patient with PVD?

A 
Normal =  1 - 1.2
PAD = 0.5 - 0.9
202
Q

What investigations would you carry out on a patient with suspected PVD?

A
  1. ECG - check for evidence of CAD
  2. Rule out DM, arteritis, anaemia, renal disease
  3. ABPI
  4. Colour Duplex ultrasound!
  5. CT angiography
  6. Blood test - CK-MM raised (muscle damage)
203
Q

How would you manage patients with peripheral vascular disease?

A
  1. Risk factor modification
  2. Anti-platelet, clopidogrel (1st line).
  3. Exercise programmes
    - reduce claudication by improving blood flow.
  4. PTA or surgery if severely stenosed.
204
Q

Give 4 signs of critical ischaemia (as well as 6 Ps)

A
  1. PAIN AT REST
  2. Classically nocturnal.
  3. Ulceration.
  4. Gangrene.
205
Q

How would you differentiate acute ischaemia from gout/cellultitis?

A

Acute ischaemia

  1. Deep duskiness of limb
  2. Sudden deterioration
206
Q

What is shock?

A

Circulatory failure resulting in inadequate organ perfusion

207
Q

Give 7 signs/symptoms of shock.

A
  1. Pale.
  2. Sweaty.
  3. Cold.
  4. Pulse is weak and rapid.
  5. Reduced urine output.
  6. Confusion.
  7. Weakness/collapse.
208
Q

What would the BP be of someone in shock?

A

systolic <90 mmHg

209
Q

What can cause hypovolemic shock?

A
  1. Loss of blood e.g. acute GI bleeding, trauma, post-op, splenic rupture.
  2. Loss of fluid e.g. dehydration, burns, vomiting, pancreatitis.
210
Q

What is the function of the serous fluid between the visceral and parietal pericardium?

A

It acts as a lubricant and so allows smooth movement of the heart inside the pericardium.

211
Q

What is the function of pericardium?

A

It restrains the filling volume of the heart.

212
Q

Describe the aetiology of pericarditis.

A
  1. Idiopathic (80-90%)
  2. Infection (more commonly virus)
  3. Autoimmune
  4. Dressler syndrome (inflammation of pericardium after MI damaging it)
213
Q

How would a patient with acute pericarditis describe their pain?

A
  1. Central pain
  2. NOT WORSE on exertion
  3. But WORSE on inspiration / lying flat
  4. Relieved by sitting forward
214
Q

What would you hear upon auscultation with a stethoscope of a patient with acute pericarditis?

A

Pericardial friction rub

215
Q

What would you see on the ECG of a patient with acute pericarditis?

A
  1. Concave (saddle-shaped) ST segment elevation in all leads

2. PR Depression

216
Q

What is the major differential diagnosis of acute pericarditis?

A

MI - rule this out ASAP!

217
Q

What is the treatment for pericarditis?

A
  1. Patients are advised to avoid strenuous activity until symptom resolution.
  2. NSAID or aspirin - high doses.
  3. PPI for gastric protection
  4. Colchicine (anti-inflammatory).
218
Q

How does colchicine have an anti-inflammatory effect?

A

Inhibits migration of neutrophils to site of inflammation

219
Q

Give 2 complications of acute pericarditis

A
  1. Fluid accumulation = PERICARDIAL EFFUSION

2. Fibrosis = CHRONIC CONSTRICTIVE pericarditis

220
Q

What can pericardial effusion progress to?

A

Cardiac tamponade!

221
Q

What 3 signs are cardiac tamponade characterised by?

A

BECK’S TRIAD

  1. Falling BP
  2. Rising JVP
  3. Muffled heart sounds
222
Q

A lady presents with a tearing pain and is found to have hypertension. A CT scan is done and a ‘tennis ball sign’ is observed. What is the likely pathology behind the patient’s pain?

A

Aortic dissection!

223
Q

What is the difference between a true and a false aneurysm?

A
  1. True aneurysm:
    - Affect all 3 layers (intimal, media, adventitia)
  2. False aneurysm:
    - A collection of blood under adventitia only
224
Q

Give 3 causes of aneurysms

A
  1. Atheroma (persistent inflammation weakens the arterial wall)
  2. Trauma
  3. Connective tissue disorders; (eg: Marfan’s, Ehlers-Danlos)
225
Q

How is the screening carried out for AAA?

A

Aortic Ultra Sound

226
Q

What signs and symptoms would you observe of a patient with AAA

A
  1. Symptoms
    - asymptomatic
    - sometimes with abdominal / back pain
  2. Signs
    - Pulsatile (normal; but if >5.5cm suggests unruptured)
    - EXPANSILE = abdominal mass (suggests rupture)
227
Q

What is aortic dissection?

A
  1. Blood flows into media
  2. Tearing of INTIMA
  3. Occlusion of branches of aorta
228
Q

What pain would a patient describe who was experiencing an aortic dissection?

A

‘Sudden tearing chest pain, radiating to the back’

229
Q

What are the different types of aortic dissection and how would you treat them?

A

Type A = Involves ascending aorta (surgery)

Type B = Doesn’t involve ascending aorta (surgery/antihypertensives)

230
Q

Name 3 cardiomyopathies.

A
  1. Hypertrophic (HCM).
  2. Dilated (DCM).
  3. Arrhythmogenic right/left ventricular (ARVC/ALVC).
231
Q

What can cause HCM?

A

Sarcomeric gene mutations

232
Q

What is the usual inheritance pattern for cardiomyopathies?

A

Autosomal dominant

233
Q

Describe the pathophysiology of HCM.

A
  1. Systole is normal but diastole is affected

2. heart is unable to relax properly due to thickening of the ventricular walls.

234
Q

Describe the pathophysiology of DCM.

A

Ventricular dilation and dysfunction = poor contractility.

235
Q

Give 3 symptoms of HCM.

A

SAD ( young)

  1. Syncope
  2. Angina
  3. Dyspnoea
236
Q

What might an ECG look like from a person with HCM.

A
  1. Large QRS complexes

2. Large inverted T waves

237
Q

What is restrictive cardiomyopathy?

A

Poor dilation of the heart restricts diastole.

238
Q

What is the commonest cause of restrictive cardiomyopathy?

A

Amyloidosis (extra-cellular deposition of an insoluble fibrillar protein - amyloid).

MY PHASE 2A MEDICINE (14 decks)

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