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Phase 2a > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Aortic stenosis murmur?

A

Crescendo-decrescendo ejection systolic murmur.

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2
Q

What causes the first heart sounds (S1)?

A

Closing of the AV valves (mitral and tricuspid valves) at the start of systolic contraction.

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3
Q

What causes the second heart sound (S2)?

A

Closing of aortic & pulmonary valves at the end of systole.

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4
Q

What is S3?

A

Third heart sound, heard around 0.1s after S2.

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5
Q

What causes S3?

A

Rapid ventricular filling - chordae tendinae stretch to their full length, creating a ‘twang’.
May indicate stiff and weak ventricles in heart failure.

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6
Q

Is S3 always pathological?

A

No, S3 is normal in young patients.

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7
Q

What is S4?

A

Fourth heart sound, heard directly before S1.

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8
Q

What does S4 indicate?

A

Stiff / hypertrophic ventricle. Turbulent flow from atrial contraction against a non-compliant ventricle.

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9
Q

Is S4 always pathological?

A

Yes, and fairly rare.

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10
Q

Where is the aortic space (auscultation)?

A

2nd intercostal space, right sternal border.

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11
Q

Where is the pulmonary area (auscultation)?

A

2nd intercostal space, left sternal border.

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12
Q

Where is the tricuspid area (auscultation)?

A

5th intercostal space, left sternal border.

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13
Q

Where is the mitral area (auscultation)?

A

5th intercostal space, midclavicular line (apex).

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14
Q

Where is the apex of the heart (bony landmarks)?

A

5th intercostal space, mid-clavicular line.

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15
Q

What is Erb’s point?

A

Best place to auscultate for heart sounds.

3rd intercostal space, left sternal border.

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16
Q

What murmur is heard in mitral stenosis?

Which heart sounds are heard?

A 
Mid diastolic murmur (low pitched and rumbling - slow blood flow).
Loud S1 (stiff valve closure).
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17
Q

What murmur is heard in mitral regurgitation?

Which heart sounds are heard?

A

Pan-systolic murmur (high pitched, whistling - high velocity blood flow).
Soft S1.
S3 may be heard.

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18
Q

What murmur is heard in aortic stenosis?

A

Ejection systolic crescendo-decrescendo murmur (high-pitched).
Radiates to carotids (turbulent blood flow).

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19
Q

When does systole occur (in terms of heart sounds)?

A

Between S1 and S2.

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20
Q

What murmur is heard in aortic regurgitation?

A

Early diastolic soft murmur.

‘Austin flint’ murmur at apex - early diastolic rumbling.

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21
Q

What pulse is associated with aortic regurgitation?

A

Collapsing ‘water hammer’ pulse.

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22
Q

Rate of spontaneous depolarisation of the SAN?

A

60-100 bpm.

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23
Q

Rate of spontaneous depolarisation of the AVN?

A

40-60 bpm.

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24
Q

Rate of spontaneous depolarisation of the ventricles?

A

20-40 bpm.

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25
Q

Where is lead V1 placed?

A

4th intercostal space, right sternal border.

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26
Q

How much time does a small square on an ECG last?

A

0.04s

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27
Q

How much time does a large square on an ECG last?

A

0.2s.

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28
Q

Which ECG leads are inferior?

A

II, III and AVF.

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29
Q

Which limb leads are lateral?

A

I and AVL.

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30
Q

What does lead AVR correspond to?

Is it positive or negative?

A

Right atrium.

Should always be negative.

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31
Q

How long should the QRS complex be?

A

Less than 0.12s.

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32
Q

How long should the PR interval be?

A

0.12 - 0.20s.

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33
Q

How to calculate rate from an ECG (if regular rhythm)?

A

N - number of large boxes in the R-R interval.

Rate is 300/N.

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34
Q

What would indicate an irregular rhythm on an ECG?

A

R-R intervals differ in length.

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35
Q

What does a broad QRS complex indicate?

A

Abnormal rhythm originating from the ventricles.

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36
Q

What is meant by an ectopic beat?

A

When part of the heart depolarises earlier than expected.

Ectopics may originate from the atria, around the AVN, or the ventricles.

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37
Q

What is the normal cardiac axis?

A

-30 degrees to +90 degrees.

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38
Q

What are some causes of left axis deviation?

A
  • left bundle branch block

- left ventricular hypertrophy

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39
Q

What are some causes of right axis deviation?

A
  • chronic pulmonary disease
  • right ventricular hypertrophy
  • lateral MI
  • pulmonary embolism
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40
Q

How do you work out the cardiac axis from an ECG?

A

Evaluate leads I, II, and III - are they predominantly positive or negative?

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41
Q

What does a normal axis look like in leads I, II, and III?

A

I - positive.
II - positive (largest).
III - positive or negative.

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42
Q

What does left axis deviation look like in leads I, II, and III?

A

I - positive.
II - negative.
III - negative.

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43
Q

What does right axis deviation look like in leads I, II, and III?

A

I - negative.
II - positive / negative.
III - positive (largest).

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44
Q

What happens in first degree heart block?

A

PR interval is greater than 0.20s.

There is delayed conduction through the AV node.

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45
Q

What happens in second degree heart block?

A

Intermittent conduction of atrial activity to the ventricles.

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46
Q

What is type I Mobitz conduction?

A

Type of second degree heart block.

Increasing PR interval until a beat is ‘dropped’ (no conduction from atria to ventricles). This process then repeats.

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47
Q

What is type II Mobitz conduction?

A

Type of second degree heart block.
There is a regular pattern of block (e.g. 2:1 ratio between P and R waves) or random ‘dropped’ beats.
PR interval remains constant.

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48
Q

What happens in third degree heart block?

A

Complete failure to conduct atrial activity to the ventricles - AV dissociation.
No correlation between P waves and QRS complexes.
Broad QRS complexes - ventricular depolarisation originates from ventricular pacemaker cells.

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49
Q

What does the left bundle branch divide into?

A

Anterior and posterior fascicles.

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50
Q

What happens to the QRS complex in bundle branch block?

A

Wide QRS complex, because the wave of depolarisation must travel from the opposite ventricle to depolarise the ventricular muscle.

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51
Q

What is the relationship between P waves and QRS complexes in bundle branch block?

A
  • P waves are present.
  • PR interval is constant.
  • 1:1 AV conduction.
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52
Q

What are the ECG features of right BBB?

A

MaRRoW
In lead V1 - M shaped QRS complex.
In lead V6 - W shaped QRS complex.

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53
Q

What are the ECG features of left BBB?

A

WiLLiaM
V1 - W shaped QRS complex.
V6 - M shaped QRS complex.

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54
Q

What ECG features are seen in pericarditis?

A
  • saddle-shaped ST elevation

- PR depression

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55
Q

What is the mechanism of action of adenosine?

A

Causes transient heart block in the AV node.

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56
Q

How should a haemodynamically stable patient with SVT be managed?

A
  1. Valsalva manoeuvre.
  2. Carotid sinus massage.
  3. Chemical cardioversion (adenosine / alternative such as verapamil).
  4. DC cardioversion.
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57
Q

What is atropine used for?

A

Bradycardia (e.g. following MI).

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58
Q

How does atropine work?

A

Increases HR and improves AV conduction by blocking parasympathetic stimulation of the heart.

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59
Q

What are the ECG features of hyperkalaemia?

A
  • tall tented T waves
  • flattened P waves
    - PR prolongation
  • wide QRS complex
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60
Q

What are the ECG features of hypokalaemia?

A
  • T wave inversion
  • ST depression
  • prominent U wave
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61
Q

Cause of infective endocarditis (found in oral cavity)?

A

Viridans streptococci.

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62
Q

Gold standard investigation for aortic dissection?

A

CT angiography.

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63
Q

ECG changes in RBBB?

A

R wave in V1 and slurred S wave in V6.

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64
Q

ECG changes in LBBB?

A

Wide QRS with notched top in V6

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65
Q

What murmur is heard in VSD?

A

Pan-systolic, best heard in the left lower sternal border.

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66
Q

What murmur is heard in ASD?

A

Mid-systolic murmur at the upper left sternal border. Wide and fixed splitting of S2.

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67
Q

Which are the lateral ECG leads?

A

I, aVL, V5, V6.

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68
Q

Occlusion of which artery causes a lateral infarct?

A

Left circumflex, or diagonal of LAD.

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69
Q

Which ECG leads are inferior?

A

II, III and aVF.

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70
Q

Occlusion of which artery causes an inferior infarct?

A

Right coronary artery or left circumflex.

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71
Q

Which ECG leads are anterior / septal?

A

V1 - V4

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72
Q

Occlusion of which artery leads to an anterior infarct?

A

Left anterior descending.

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73
Q

What is the definitive treatment for atrial flutter?

A

Catheter ablation.

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74
Q

X ray findings in heart failure?

A
  • alveolar oedema
  • Kerley B lines
  • cardiomegaly
  • dilated upper lobe vessels
  • pleural effusion (blunted costophrenic angle)
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75
Q

What is the full name for BNP?

A

NT-proBNP

N-terminal pro-B-type natriuretic peptide

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76
Q

Pharmaceutical management of heart failure?

A
  • ACE inhibitor (e.g. ramipril)
  • beta blocker (e.g. bisoprolol)
  • aldosterone antagonist (e.g. spironalactone)
  • loop diuretic (e.g. furosemide)
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77
Q

Dose of furosemide in heart failure?

A

40mg once daily

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78
Q

What is the most common cause of secondary hypertension in adults?

A

Primary hyperaldosteronism (Conn’s syndrome).

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79
Q

Scoring system for CVD?

A

QRISK

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80
Q

Medication for QRISK score > 10%?

A

Statin

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81
Q

Common side effect of statins?

A

Myalgia

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82
Q

How should PE be managed?

A 
Give oxygen.
DOAC (e.g. apixaban or rivaroxaban).
Or LMWH (e.g. dalteparin or enoxaparin).
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83
Q

Gold standard investigation for PE?

A

CT pulmonary angiogram.

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84
Q

Prinzmetal’s angina ECG features?

A

ST elevation due to transmural ischaemia.

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85
Q

Pharmacological management for Prinzmetal’s angina?

A

CCB such as verapamil.

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86
Q

Which coronary artery is most commonly occluded in a myocardial infarction?

A

Left anterior descending

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87
Q

What is Dressler’s syndrome?

A

Pericarditis occurring post MI

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88
Q

What do Kerley B lines signify?

A

Interstitial oedema

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89
Q

Cause of a pansystolic murmur?

A
  • mitral regurgitation

- tricuspid regurgitation

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90
Q

Right sided heart failure presentation?

A

Lungs clear but the rest of the body is affected.

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91
Q

What does a positive Buerger’s test indicate?

A

New onset ischaemia

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92
Q

ECG changes in hyperparathyroidism?

A
  • short QT interval

- tall T waves

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93
Q

What is Beck’s triad?

A

Cardiac tamponade:

  • muffled heart sounds
  • hypotension
  • raised JVP
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94
Q

Time window for PCI after MI?

A

2 hours

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95
Q

Management for MI patients after 2 hour time window?

A

Fibrinolysis (IV tenecteplase).

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96
Q

ECG appearance atrial flutter?

A

Sawtooth

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97
Q

ECG appearance AF?

A

Absence of p waves.

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98
Q

What is stable angina?

A

Pain in the chest (also neck, shoulder, jaw or arms) caused by an insufficient blood supply to the myocardium. Occurs predictably with physical exertion or emotional stress, relieved by rest and with sublingual nitrates.

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99
Q

Causes of stable angina?

A
  • coronary artery disease
  • valvular disease
  • hypertrophic obstructive cardiomyopathy
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100
Q

Risk factors for stable angina?

A
  • older age
  • hypertension
  • smoking
  • diabetes
  • family history
  • hypercholesterolaemia
  • physical inactivity
  • excessive alcohol intake
  • obesity
  • chronic kidney disease
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101
Q

Pathophysiology of stable angina?

A
  • imbalance between myocardial oxygen supply and myocardial oxygen demand
  • demand is increased by emotional stress and physical exertion
  • coronary artery stenosis means that the myocardial oxygen supply cannot be upregulated sufficiently to meet increased demand
  • this results in myocardial ischaemia
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102
Q

Pathophysiology of atherosclerosis?

A
  • recurrent endothelial injury results in chronic inflammation, expression of adhesion molecules and increased permeability to LDL
  • LDL and inflammatory cells accumulate in the intimal layer (fatty streak)
  • over time, lipid-laden macrophages (foam cells) die and form a necrotic lipid core
  • attempted tissue repair - platelet-derived growth factor stimulates smooth muscle cell proliferation and migration
  • SMCs deposit collagen, forming a fibrous cap over the lipid core
  • haemorrhage from micro-vessels within the plaque leads to rapid enlargement of the plaque
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103
Q

Atherosclerotic plaque composition?

A
  • central lipid core & foam cells
  • overlying fibrous cap
  • macrophages and T cells
  • calcification in advanced plaques
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104
Q

Clinical manifestations of stable angina?

A
  • constricting discomfort in chest (also neck, shoulders, jaw, arms)
  • relieved by rest or GTN within 5 minutes
  • precipitated by physical exertion
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105
Q

Gold standard investigation for stable angina?

A

coronary angiography

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106
Q

Investigations for stable angina?

A
  • coronary angiography
  • ECG (exercise testing)
  • lipid profile
  • blood pressure
  • HbA1c and fasting glucose
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107
Q

Differentials for stable angina?

A
  • unstable angina
  • MI
  • pericarditis
  • pulmonary embolism
  • GORD
  • peptic ulcer disease
  • costochondritis
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108
Q

Immediate symptomatic relief for stable angina?

A
  • GTN spray
  • if pain unresolved after 5 minutes, repeat dose
  • if pain remains unresolved, call an ambulance
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109
Q

Long term treatment of stable angina?

A 
Symptomatic relief - beta blocker, calcium channel blocker.
Secondary CVD prevention:
- aspirin
- atorvastatin
- ACE inhibitor
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110
Q

Surgery / procedures to treat stable angina?

A
  • PCI (with coronary angioplasty)

- coronary artery bypass graft

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111
Q

What is unstable angina?

A

Sudden new onset of angina, or a significant and abrupt deterioration in stable angina. Pain is experienced at rest.

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112
Q

Investigations for unstable angina?

A
  • coronary angiography
  • ECG
  • serum troponin
  • lipid profile
  • HbA1c and fasting glucose
  • echocardiogram
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113
Q

Acute management of unstable angina?

A
  • aspirin 300mg
  • coronary angiography with PCI
  • coronary artery bypass graft
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114
Q

Long term management of unstable angina?

A
  • dual antiplatelet therapy
  • statin
  • beta blocker
  • ACE inhibitor
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115
Q

What is NSTEMI?

A

Myocardial infarction with an ECG showing non-specific signs of ischaemia, with raised serum troponin.

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116
Q

Causes of NSTEMI?

A
  • atherosclerotic plaque rupture and thrombus formation
  • severe progressive atherosclerosis
  • re-stenosis following PCI
  • coronary artery spasm
  • vasculitis
  • myocardial oxygen supply-demand mismatch (hypovolaemia)
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117
Q

Signs and symptoms of NSTEMI?

A
  • central crushing chest pain (persisting for > 15 minutes)
  • pain may radiate to arm / neck
  • shortness of breath
  • sweating
  • nausea and vomiting
  • palpitations
  • pallor
  • tachycardia
  • hypotension
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118
Q

Patients likely to experience silent MI?

A
  • diabetics

- elderly

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119
Q

Atypical presentation of MI?

A
  • indigestion-like pain
  • back pain
  • arm / jaw pain alone
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120
Q

Investigations for NSTEMI?

A
  • ECG
  • troponin
  • CXR
  • echocardiogram
  • coronary angiography
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121
Q

ECG signs NSTEMI?

A
  • ST depression
  • T wave inversion
  • may be normal
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122
Q

Acute management of NSTEMI?

A 
MONA
- IV morphine + anti-emetic
- oxygen
- nitrates
- aspirin 300mg
Coronary angiography and PCI (for high risk patients) OR anti-thrombotic therapy with fondaparinux.
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123
Q

Long term management of NSTEMI?

A
  • dual anti-platelet therapy
  • beta blocker
  • statin
  • ACE inhibitor
  • cardiac rehabilitation
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124
Q

What is STEMI?

A

Myocardial infarction resulting in myocardial necrosis with ST elevation seen on ECG. Generally due to a complete and persistent blockage of a coronary artery.

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125
Q

Causes of STEMI?

A
  • atherosclerotic plaque rupture and thrombus formation
  • coronary artery dissection
  • coronary artery vasospasm
  • coronary embolism
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126
Q

What is type 1 MI?

A

Primary coronary arterial event caused by atherosclerotic plaque rupture.

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127
Q

What is type 2 MI?

A

Occurs secondary to an acute imbalance in myocardial oxygen supply and demand without atherothrombosis. May result from coronary artery dissection, coronary vasospasm, hypoxia, coronary embolus, etc.

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128
Q

Risk factors for STEMI?

A
  • hypercholesterolaemia
  • diabetes
  • hypertension
  • smoking
  • family history
  • male
  • older age
  • physical inactivity
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129
Q

What is meant by a thin-cap atheroma?

A

Unstable atherosclerotic plaque prone to rupture.

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130
Q

How does a thrombus form due to atherosclerosis?

A
  • plaque rupture exposes thrombogenic lipid core of the plaque
  • this triggers a cascade of platelet adhesion, activation and aggregation, leading to thrombus formation
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131
Q

Signs and symptoms of STEMI?

A
  • central crushing chest pain / discomfort
  • nausea and vomiting
  • pallor
  • shortness of breath
  • sweating and clamminess
  • pain radiating to arm, shoulder, neck, or jaw
  • palpitations
  • feeling of impending doom
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132
Q

Investigations for STEMI?

A
  • ECG
  • coronary angiography
  • serum troponin
  • CXR
  • echocardiogram
  • lipid profile
  • HbA1c and fasting glucose
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133
Q

Acute management of STEMI?

A

MONA

  • PCI within 2 hours
  • fibrinolysis with tissue plasminogen activator (alteplase)
  • revascularisation (stenting / CABG)
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134
Q

Long term management of STEMI?

A
  • dual antiplatelet therapy (aspirin + ticagrelor / clopidogrel)
  • ACE inhibitor
  • statin
  • beta blocker
  • cardiac rehabilitation
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135
Q

Complications of STEMI?

A
  • arrhythmias
  • congestive heart failure
  • Dressler’s syndrome
  • mitral regurgitation
  • heart block
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136
Q

ECG findings in STEMI?

A
  • ST elevation OR

- new left bundle branch block

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137
Q

What is heart failure?

A

Syndrome in which the ability of the heart to maintain adequate blood circulation is impaired, as a result of a structural or function impairment of ventricular filling or ejection.

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138
Q

Ejection fraction in heart failure?

A

Can either be reduced or preserved.

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139
Q

Most common causes of heart failure?

A
  • MI
  • hypertension
  • cardiomyopathies
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140
Q

Causes of heart failure?

A
  • MI
  • hypertension
  • cardiomyopathies
  • valvular heart disease
  • arrhythmias
  • high output state (anaemia, sepsis, thyrotoxicosis)
  • volume overload (end-stage CKD, nephrotic syndrome)
  • pulmonary hypertension
  • amyloidosis
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141
Q

Risk factors for heart failure?

A
  • dyslipidaemia
  • hypertension
  • diabetes
  • obesity
  • smoking
  • older age
  • family history
  • genetics
  • arrhythmias
  • CKD
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142
Q

Pathophysiology of HF-PEF?

A

Structural / cellular alterations lead to an inability of the left ventricle to relax properly.

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143
Q

Pathophysiology of HF-REF?

A

Characterised by acute / chronic loss of cardiomyocytes (or the ability of cardiac myocytes to contract) resulting in systolic dysfunction.

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144
Q

Signs of HF?

A
  • oedema
  • ascites
  • weight gain
  • tachycardia
  • laterally displaced apex beat
  • heart murmurs
  • S3 / S4
  • raised JVP
  • hepatomegaly
  • basal crepitations
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145
Q

Symptoms of HF?

A
  • fatigue
  • breathlessness
  • orthopnoea
  • cough
  • paroxysmal nocturnal dyspnoea
  • syncope
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146
Q

Investigations for heart failure?

A
  • NT-pro-BNP
  • echocardiogram
  • ECG
  • exercise tolerance test
  • lung function tests (spirometry)
  • FBC
  • thyroid function tests
  • HbA1c and fasting glucose
  • lipid profile
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147
Q

Gold standard investigation for heart failure?

A

Echocardiography

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148
Q

Differentials for heart failure?

A
  • COPD
  • nephrotic syndrome
  • severe anaemia
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149
Q

Pharmacological management of heart failure?

A
  • ACE inhibitor
  • beta-blocker
  • aldosterone antagonist
  • loop diuretic
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150
Q

What is cor pulmonale?

A

Right-sided heart failure secondary to respiratory disease.

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151
Q

Causes of cor pulmonale?

A
  • COPD
  • pulmonary embolism
  • interstitial lung disease
  • pulmonary hypertension
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152
Q

Most common cause of cor pulmonale?

A

COPD

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153
Q

Pathophysiology of cor pulmonale?

A
  • chronic hypoxaemia leads to chronic vasoconstriction of pulmonary arteries
  • this increases pulmonary vascular resistance and results in pulmonary artery hypertension
  • pulmonary hypertension increases right-sided filling pressures, causing right heart strain and right ventricular enlargement
  • eventually right ventricle cannot compensate for increased filling pressures and right heart failure develops
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154
Q

Signs and symptoms of cor pulmonale?

A
  • shortness of breath
  • peripheral oedema
  • syncope
  • hypoxia and cyanosis
  • raised JVP
  • third heart sound
  • pan-systolic murmur (tricuspid regurgitation)
  • hepatomegaly
155
Q

Gold standard investigation for cor pulmonale?

A

Right-heart catheterisation to measure pulmonary artery pressure.

156
Q

Investigations for cor pulmonale?

A
  • CXR
  • ECG
  • echocardiography
157
Q

Management of cor pulmonale?

A
  • treat symptoms (e.g. diuretic)
  • treat underlying cause
  • long term oxygen therapy
158
Q

What is primary / essential hypertension?

A

Hypertension with no identifiable cause.

159
Q

Threshold for hypertension?

A

Clinic BP > 140/90 mmHg

Ambulatory / home BP > 135/85 mmHg

160
Q

Stages of hypertension?

A
  1. > 140/90
  2. > 160/100
  3. > 180/120
161
Q

What is secondary hypertension?

A

Hypertension with a known underlying cause (CKD, Cushing’s disease, Conn’s syndrome etc).

162
Q

Risk factors for essential hypertension?

A
  • older age
  • Black ethnicity
  • family history
  • low socioeconomic group
  • smoking
  • excess alcohol
  • excess salt
  • obesity
  • physical inactivity
  • stress and anxiety
  • diabetes
163
Q

Complications of hypertension?

A
  • retinopathy
  • visual changes
  • CVD
  • CKD
  • stroke
  • peripheral arterial disease
  • heart failure
164
Q

Anti-hypertensive drug treatment?

A
  1. ACEi / CCB
  2. CCB / ACEi or thiazide-like diuretic
  3. ACEi + CCB + thiazide-like diuretic
  4. spironalactone or beta blocker if potassium > 4.5
165
Q

What is atrial fibrillation?

A

Supraventricular tachycardia resulting from disorganised electrical activity and ineffective contraction of the atria.

166
Q

Most common causes of AF?

A
  • sepsis
  • mitral valve pathology
  • ischaemic heart disease
  • thyrotoxicosis
  • hypertension
167
Q

Risk factors for AF?

A
  • older age
  • hypertension
  • heart failure
  • obstructive sleep apnoea
  • obesity
  • coronary artery disease
  • valve disease
  • cardiomyopathy
  • hyperthyroidism
168
Q

Pathophysiology of AF?

A
  • atrial stress results in dilatation with fibrosis / inflammation
  • this leads to tissue heterogeneity, where there is a difference in refractory periods within atrial tissue
  • there is chaotic depolarisation and electrical conduction in the atria
  • this leads to irregularly irregular ventricular contraction and tachycardia
169
Q

Signs and symptoms of AF?

A
  • palpitations
  • dyspnoea
  • syncope
  • reduced exercise tolerance
  • fatigue
  • tachcardia
  • irregular pulse
170
Q

Gold standard investigation for AF?

A

12 lead ECG

171
Q

Investigations for AF?

A
  • 12 lead ECG
  • clotting profile
  • thyroid function tests
  • CXR
  • echocardiography (for assessment of function, also may identify left atrial clot)
172
Q

ECG findings in AF?

A
  • no P waves
  • chaotic baseline
  • irregularly irregular ventricular rate
  • tachycardia
173
Q

Management of AF?

A

Anticoagulation & avoid stroke:
- CHA2DS-VASc score for stroke risk
- ORBIT score for bleeding risk
- anticoagulation (DOAC)
- left atrial appendage occlusion if anticoagulation contraindicated
Better symptom management:
- rate control with beta blocker or rate-limiting CCB
- pharmacological cardioversion with amiodarone
- DC electrical cardioversion
- left atrial ablation
Cardiovascular and co-morbidity optimisation:
- manage underlying cause
- modify lifestyle factors

174
Q

Complications of AF?

A
  • stroke
  • heart failure
  • sudden cardiac death
175
Q

What is atrial flutter?

A

Re-entrant rhythm in atrium stimulates atrial contraction at 300bpm.

176
Q

Rate of ventricular contraction in atrial flutter?

A

150 bpm due to AV node refractory period.

177
Q

ECG appearance of atrial flutter?

A

Sawtooth - most prominent in II, III, aVF, V1.

178
Q

Gold standard management of atrial flutter?

A

Radiofrequency ablation of re-entrant rhythm.

179
Q

Management of stable heart block?

A

Observation

180
Q

Management of unstable heart block?

A
  • atropine 500 mcg IV
  • transcutaneous cardiac pacing with a defibrillator
  • pacemaker
181
Q

How does atropine work?

A

Anti-muscarinic that inhibits parasympathetic stimulation of the heart.

182
Q

What is supraventricular tachycardia?

A

Self-perpetuating loop of an electrical signal re-entering the atria from the ventricles, then travelling back through the AV node and causing another ventricular contraction.

183
Q

ECG findings in SVT?

A
  • narrow complex tachycardia (QRS < 0.12s)

- QRS complex followed immediately by T wave, then another QRS complex, etc.

184
Q

Management of acute SVT?

A
  • valsalva manoeuvre
  • carotid sinus massage
  • adenosine
  • DC cardioversion
185
Q

Definitive management of SVT?

A

Radiofrequency ablation.

186
Q

How does adenosine work?

A

Slows cardiac conduction through the AV node to reset SVT to sinus rhythm. Causes a brief period of asystole before sinus rhythm returns.

187
Q

What is ventricular tachycardia?

A

Shockable rhythm with a ventricular rate > 100 bpm. Wide complex tachycardia originating from one of the ventricles.

188
Q

ECG findings in VT?

A

Wide complex tachycardia - QRS > 0.12s.

189
Q

Management of VT?

A

Stable - amiodarone.

Unstable - up to 3 shocks, amiodarone.

190
Q

What is an ectopic beat?

A

Heart skips or adds a beat, not usually a cause for concern.

191
Q

What is prolonged QT?

A

Prolonged repolarisation of cardiac muscle cells after contraction.

192
Q

What is torsades de pointes?

A

Polymorphic ventricular tachycardia occurring in patients with a prolonged QT interval.

193
Q

Causes of prolonged QT?

A
  • inherited long QT syndrome
  • medications (amiodarone)
  • electrolyte disturbance (hypokalaemia)
194
Q

Pathophysiology of torsade de pointes?

A
  • prolonged repolarisation of cardiac muscle cells can result in random spontaneous depolarisations in some cells (‘afterdepolarisations’)
  • these depolarisations spread throughout the ventricle, leading to ventricular contraction before repolarisation has fully occurred
  • if torsade de pointes progresses to VT, it can lead to cardiac arrest
195
Q

ECG signs of torsade de pointes?

A
  • VT with QRS complex twisting around the baseline

- height of QRS complexes gets progressively smaller

196
Q

Management of prolonged QT?

A
  • avoid QT-prolonging medications
  • correct electrolyte disturbances
  • beta blocker (not sotalol)
  • pacemaker / implantable defibrillator
197
Q

What is Wolff-Parkinson-White syndrome?

A

Arrhythmia caused by an extra electrical pathway connecting the atria and the ventricles (bundle of Kent).

198
Q

ECG findings in WPW sydrome?

A
  • short PR interval (< 0.12s)
  • wide QRS complex (> 0.12s)
  • delta wave - slurred upstroke on QRS complex
199
Q

Management of WPW syndrome?

A

Radiofrequency ablation of accessory pathway.

200
Q

What should be avoided in patients with AF and WPW?

A

Most anti-arrhythmic medications are contra-indicated. They reduce conduction through the AV node, promoting conduction through the accessory pathway. This increases the risk of polymorphic wide complex tachycardia.

201
Q

What is an abdominal aortic aneurysm?

A

Dilation of the abdominal aorta (diameter > 3cm).

202
Q

Risk factors for AAA?

A
  • males
  • increasing age
  • smoking
  • hypertension
  • family Hx
  • existing CVD
203
Q

Screening for AAA?

A
  • all men over 65 offered ultrasound scan

- screening also considered in women over 70 with risk factors

204
Q

Clinical presentation of ruptured AAA?

A
  • severe abdominal pain
  • haemodynamic instability (hypotension & tachycardia)
  • pulsatile and expansile abdominal mass
  • collapse
  • loss of consciousness
205
Q

Investigations for AAA?

A
  • ultrasound

- CT angiogram

206
Q

Intervention for stable AAA?

A

Elective surgical repair - open repair via laparotomy, or endovascular aneurysm repair (EVAR) with stent inserted via femoral artery.

207
Q

What is aortic dissection?

A

Tear forms in the tunica intima of the aorta, allowing blood to flow between the intima and the media. This creates a false lumen full of blood within the wall of the aorta.

208
Q

Most common site for aortic dissection?

A

Right lateral area of the ascending aorta (under most stress from blood exiting the heart).

209
Q

Risk factors for aortic dissection?

A
  • male
  • older age
  • smoking
  • hypertension
  • physical inactivity
  • hypercholesterolaemia
  • biscuspid aortic valve
  • aortic valve replacement
  • coarctation of the aorta
  • CABG
  • Marfan’s, EDS type IV
210
Q

Possible triggers for aortic dissection?

A

Events temporarily causing a massive increase in BP:

  • weightlifting
  • cocaine use
211
Q

Signs and symptoms of aortic dissection?

A
  • acute severe ripping / tearing chest pain
  • pain may change location with extending dissection
  • blood pressure differential > 20 mmHg between arms
  • reduced / absent pulses
  • diastolic murmur (aortic valve incompetence)
  • syncope
  • hypotension
212
Q

Investigations for aortic dissection?

A
  • CT angiogram
  • CXR
  • ECG
213
Q

Management of aortic dissection?

A
  • morphine IV
  • beta blocker
  • open surgery to replace affected section of aorta with a synthetic graft
  • TEVAR (thoracic endovascular aortic repair) with catheter inserted via femoral artery to insert a stent graft
214
Q

Complications of aortic dissection?

A
  • MI
  • stroke
  • cardiac tamponade
  • aortic regurgitation
  • death
215
Q

What is claudication?

A

Crampy pain that predictably occurs after walking a certain distance, as a result of peripheral arterial disease. Pain relieved by rest. Most commonly affects calves, also affects thighs / buttocks.

216
Q

What is critical limb ischaemia?

A

Reduced / absent blood supply to limb due to peripheral arterial disease.

217
Q

Signs and symptoms of critical limb ischaemia?

A
  • pale
  • perishing cold
  • pulseless
  • paralysis
  • paraesthesia
  • pain
  • atrophic skin / ulceration / gangrene
  • positive Buerger test
218
Q

Investigations for critical limb ischaemia?

A
  • ankle brachial pressure index
  • doppler ultrasound
  • CT angiography
  • cardiovascular risk assessment
219
Q

Normal vs critical limb ischaemia ABPI?

A

Normal is > 0.9, less than 0.5 indicates critical limb ischaemia.

220
Q

Management of critical limb ischaemia?

A
  • angioplasty & stenting
  • bypass grafting
  • amputation
  • long-term statin and antiplatelet therapy (clopidogrel 75mg daily)
221
Q

Complications of critical limb ischaemia?

A
  • sepsis

- gangrene

222
Q

What is pericarditis?

A

Inflammation of the lining of the heart.

223
Q

Acute vs chronic pericarditis?

A

Acute - usually self-limiting without significant complications.
Chronic - inflammation > 3 months, usually follows an acute episode. Complications include pericardial effusion and constrictive pericarditis.

224
Q

Causes of pericarditis?

A
  • idiopathic
  • viral (coxsackievirus B, influenza, adenovirus, enterovirus)
  • bacterial (haematogenous spread, spread from pulmonary infection, complication of endocarditis)
  • tuberculosis
  • Dressler’s syndrome
225
Q

Signs and symptoms of pericarditis?

A
  • sharp, pleuritic chest pain
  • pain improves sitting up / leaning forwards
  • fever
  • breathlessness (effusion)
  • cough
  • pericardial friction rub
  • Beck’s triad (cardiac tamponade)
226
Q

Investigations for pericarditis?

A
  • ECG
  • CXR
  • blood cultures
  • echocardiogram
  • serum troponin
  • pericardiocentesis
227
Q

Diagnostic criteria for pericarditis?

A

2 of:

  • pericardial friction rub
  • widespread ST elevation / PR depression
  • new or increasing pericardial effusion
228
Q

ECG findings in pericarditis?

A
  • widespread saddle-shaped ST elevation

- PR depression

229
Q

Differentials for pericarditis?

A
  • pulmonary embolism
  • pneumonia
  • MI
  • pneumothorax
230
Q

Gold standard investigation for pericarditis?

A

Pericardiocentesis guided by echocardiography.

231
Q

Management of pericarditis?

A
  1. NSAID
  2. Colchicine (continue for 3 months).
    Broad-spectrum antibiotics if purulent (rare).
232
Q

Complications of pericarditis?

A
  • cardiac tamponade

- constrictive pericarditis

233
Q

What is endocarditis?

A

Infection and inflammation of the endocardial surface of the heart, typically involving heart valves or intracardiac devices.

234
Q

Most common cause of infective endocarditis?

A

staph aureus

235
Q

Staph aureus IE is associated with?

A
  • IVDU
  • prosthetic heart valves
  • aggressive course native valve IE
236
Q

Causes of IE?

A
  • staph aureus
  • viridans strep
  • staph epidermidis
  • enterococci
  • candida
  • aspergillus
237
Q

What is Libman-Sacks endocarditis?

A

Non-infective endocarditis, due to:

  • advanced malignancy
  • SLE
238
Q

Risk factors for IE?

A
  • older age
  • IVDU
  • poor dental hygiene
  • recent dental procedure
  • congenital heart disease
  • valvular heart disease
  • prosthetic valve
  • previous IE
  • intravascular devices
  • immunosuppression
239
Q

Valve most frequently affected in IE?

240
Q

Pathophysiology of IE?

A
  • bacteria in the bloodstream deposit onto the endocardial surface of the heart
  • bacteria adhere and aggregate to form vegetations
  • this leads to invasion and destruction of valve leaflets
  • vegetation fragments may break off (septic emboli) and deposit in organs (e.g. cerebral abscess)
241
Q

Signs and symptoms of IE?

A
  • fever
  • malaise / fatigue / anorexia
  • shortness of breath
  • chest pain
  • palpitations
  • pansystolic murmur
  • splinter haemorrhages
  • petechiae
  • janeway lesions
  • osler nodes
  • roth spots
242
Q

What are Roth spots?

A

Retinal lesions seen in IE

243
Q

Investigations for infective endocarditis?

A
  • blood cultures (3 sets taken before initiation of antibiotics)
  • transthoracic echocardiography
  • transoesophageal echocardiography (gold standard)
  • CRP / ESR
  • FBC (raised WCC)
244
Q

Criteria for IE?

A

Duke criteria

245
Q

Major criteria for IE?

A
  • two positive blood cultures with typical endocarditis organisms
  • evidence of echocardiographic involvementr (vegetation, new valve regurgitation, new dehiscence of prosthetic valve)
246
Q

What are considered typical endocarditis organsims?

A
  • s. aureus
  • s. epidermidis
  • s. viridans
247
Q

Minor criteria for IE?

A
  • IVDU
  • fever > 38 degrees
  • Osler nodes / Roth spots
  • glomerulonephritis
  • embolic phenomena (Janeway lesions)
  • positive blood culture not meeting major criteria
248
Q

Treatment of IE caused by strep?

A

4 weeks of amoxicillin OR 2 weeks amoxicillin and gentamicin.
Vancomycin if allergic to penicillin.

249
Q

Treatment of IE caused by staph aureus?

A

4-6 weeks IV flucloxacillin.

4-6 weeks IV vancomycin.

250
Q

Management of IE?

A
  • empirical antibiotics (broad-spectrum)
  • antibiotics based on culture results
  • surgical removal of infected tissue
251
Q

What antibiotics may be used as prophylaxis for dental procedures to prevent IE?

A
  • amoxicillin

- clindamycin

252
Q

Complications of infective endocarditis?

A
  • heart failure
  • pericarditis
  • stroke
  • cerebral abscess
  • glomerulonephritis
253
Q

What is aortic stenosis?

A

Obstructive of blood flow across the aortic valve, typically due to calcification.

254
Q

What valve area is classed as aortic stenosis?

A

< 1.5 - 2.0 cm2

Normal is 3.0 - 4.0 cm2

255
Q

Which valve disease is most common?

A

Aortic stenosis

256
Q

Causes of aortic stenosis?

A
  • calcification
  • congenital bicuspid aortic valve
  • rheumatic heart disease
257
Q

Risk factor for aortic stenosis?

A
  • increasing age
  • hypercholesterolaemia
  • hypertension
  • smoking
  • diabetes
  • bicuspid aortic valve
  • previous episode of rheumatic fever
258
Q

Pathophysiology of aortic stenosis?

A
  • aortic stenosis impedes LV outflow
  • LVH occurs as a compensatory mechanism to maintain the ejection fraction
  • LVH may lead to diastolic dysfunction due to impaired relaxation and reduced compliance of the ventricle
  • eventually systolic dysfunction occurs as the ventricle’s ability to compensate is exhausted, leading to left sided HF
259
Q

Link between aortic stenosis and von Willebrand factor deficiency?

A

Patients may acquire vWF deficiency due to turbulent flow and high shear forces across the aortic valve, inducing structural changes to the protein.

260
Q

Signs and symptoms of aortic stenosis?

A
  • exertional syncope
  • fatigue
  • breathlessness
  • angina
  • ejection systolic crescendo-decrescendo murmur
  • slow-rising pulse
  • narrow pulse pressure
  • epistaxis and bruising
  • S4 heart sound
261
Q

Gold standard investigation for valvular heart disease?

A

Echocardiography (transthoracic)

262
Q

Management of aortic stenosis?

A
  • percutaneous balloon valvotomy
  • open valve replacement
  • transcatheter aortic valve replacement
263
Q

Complications of aortic stenosis?

A
  • congestive heart failure
  • sudden cardiac death
  • prosthetic valve infection
  • prosthetic valve thrombosis
  • valve dehiscence
264
Q

What is mitral stenosis?

A

Narrowing of the mitral valve orifice, with fusion of the valve commissures and thickening of the valve leaflets.

265
Q

What valve area is considered mitral stenosis?

A

< 1.5 cm2

Normal is 4-6 cm2

266
Q

Causes of mitral stenosis?

A
  • rheumatic heart disease
  • calcification
  • congenital mitral stenosis
267
Q

Risk factors for mitral stenosis?

A
  • streptococcal infection (rheumatic fever)
  • female
  • SLE
  • amyloidosis
268
Q

Pathophysiology of mitral stenosis?

A
  • increased left atrial pressure
  • left atrial enlargement
  • raised atrial pressure translates to pulmonary venous pressures, resulting in pulmonary hypertension
  • eventually right-sided heart failure develops
269
Q

Signs and symptoms of mitral stenosis?

A
  • exertional dyspnoea
  • angina (increased oxygen demand)
  • mid-diastolic murmur
  • loud S1
  • AF
  • mitral facies
  • raised JVP
  • peripheral oedema
270
Q

What is Ortner syndrome?

A

Left atrial enlargement causes a left recurrent laryngeal nerve palsy, resulting in hoarse voice. May be seen in mitral stenosis.

271
Q

Signs of mitral stenosis on CXR?

A
  • double right heart border
  • prominent atrial appendage
  • dilated pulmonary vessels
272
Q

ECG signs in mitral stenosis?

A
  • AF
  • p-mitrale
  • right-sided hypertrophy
273
Q

Gold standard treatment for mitral stenosis?

A

Percutaneous mitral commissurotomy - inflation of balloon delivered via catheter, to relieve stenosis.

274
Q

Medical management of mitral stenosis?

A
  • treat AF

- anticoagulation (if left atrium enlarged)

275
Q

Complications of mitral stenosis?

A
  • AF
  • stroke
  • infective endocarditis
276
Q

Causes of aortic regurgitation?

A
  • rheumatic heart disease
  • bicuspid aortic valve
  • calcification
  • infective endocarditis
  • aortic dissection
  • Marfan’s syndrome
  • EDS
  • aortitis
277
Q

Pathophysiology of acute aortic regurgitation?

A

Acute rise in left atrial pressure results in pulmonary oedema and cardiogenic shock. Reduced coronary flow results in angina or MI in severe cases.

278
Q

Pathophysiology of chronic aortic regurgitation?

A
  • increase in LV end-diastolic volume
  • LV dilatation occurs to compensate for regurgitation and maintain stroke volume
  • eventually worsening regurgitation cannot be compensated for and heart failure develops
279
Q

Signs and symptoms of aortic regurgitation?

A
  • dyspnoea
  • raised JVP
  • palpitations
  • angina
  • water hammer / collapsing pulse
  • wide pulse pressure
  • early diastolic murmur
  • soft S2
  • fatigue
  • oedema
280
Q

Presentation of acute aortic regurgitation?

A
  • chest pain
  • bi-basal crepitations due to pulmonary oedema
  • shortness of breath
281
Q

Eponymous signs of aortic regurgitation?

A
  • de Musset’s sign (head nodding with each beat)
  • Muller’s sign (vibrating uvula)
  • Traube’s sign (pistol shot femoral pulses)
  • Quincke’s sign (pulsating nail beds)
282
Q

How does LVH appear on ECG?

A
  • deep S waves in V1 and V2
  • tall R waves in V5 and V6
    WiLLiaM
283
Q

Management of aortic regurgitation?

A

TAVI (transcatheter aortic valve implantation) or open surgery.

284
Q

Complications of aortic regurgitation?

A
  • MI
  • infective endocarditis
  • heart failure
285
Q

Primary causes of mitral regurgitation?

A
  • calcification and degeneration
  • infective endocarditis
  • rheumatic heart disease
  • congenital abnormalities
286
Q

Secondary causes of mitral regurgitation?

A
  • myocardial infarction
  • dilated / hypertrophic cardiomyopathy
  • chordae tendineae rupture
287
Q

Pathophysiology of chronic mitral regurgitation?

A
  • backflow of blood from LV into LA during systole
  • results in a reduced ejection fraction and increased atrial pressure
  • compensated phase - dilatation of LV and LA maintains ejection fraction and prevents rise in atrial / pulmonary pressure
  • decompensation results in heart failure with reduced ejection fraction, and increased pulmonary pressures
288
Q

Pathophysiology of acute mitral regurgitation?

A
  • increased pressure in left atrium is translated to the pulmonary veins, causing pulmonary hypertension
  • pulmonary oedema develops
  • fall in ejection fraction leads to tachycardia
  • cardiogenic shock often occurs as the tachycardic response is insufficient to maintain cardiac output
289
Q

Clinical manifestations of acute mitral regurgitation?

A
  • rapid development of heart failure with inadequate cardiac output
  • flash pulmonary oedema
  • dyspnoea and tachycardia
  • cardiogenic shock
290
Q

Clinical manifestations of chronic mitral regurgitation?

A
  • fatigue and malaise
  • dyspnoea and orthopnoea
  • peripheral oedema
291
Q

Signs of mitral regurgitation?

A
  • lateral displacement of apex beat
  • pansystolic murmur
  • soft S1
  • S3
  • bi-basal lung crepitations
  • peripheral oedema
292
Q

CXR signs of mitral regurgitation?

A
  • double right heart border

- pulmonary oedema

293
Q

ECG sign of left atrial enlargement?

294
Q

ECG signs of mitral regurgitation?

A
  • p-mitrale

- signs of LVH

295
Q

Medical management of mitral regurgitation?

A
  • ACE inhibitor
  • beta blocker
  • spironalactone
  • loop diuretic
296
Q

Surgical management of mitral regurgitation?

A

Valve repair or replacement.

297
Q

Complications of mitral stenosis?

A
  • AF
  • pulmonary hypertension
  • congestive heart failure
298
Q

What is shock?

A

Life-threatening generalised acute circulatory failure. Inadequate oxygen delivery to tissues results in multiple organ dysfunction and damage, and may lead to death.

299
Q

Categories of shock?

A
  • distributive
  • cardiogenic
  • hypovolaemic
  • obstructive
300
Q

Causes of distributive shock?

A
  • sepsis
  • anaphylaxis
  • neurogenic (brainstem / spinal cord injury)
301
Q

Causes of cardiogenic shock?

A
  • MI

- acute valvular incompetence

302
Q

Causes of hypovolaemic shock?

A
  • GI bleeding
  • trauma
  • burns
  • DKA
303
Q

Causes of obstructive shock?

A
  • cardiac tamponade

- tension pneumothorax

304
Q

How does sepsis cause shock?

A

Sepsis causes pathological vasodilation, resulting in a loss of perfusion pressure due to decreased systemic vascular resistance.

305
Q

Signs and symptoms of shock?

A
  • hypotension
  • tachycardia
  • cool, clammy peripheries
  • mottled ashen appearance
  • sweating
  • cyanosis
  • oliguria
  • agitation, confusion, distress
  • dyspnoea and tachypnoea
  • hypoxaemia
  • fever (septic shock)
306
Q

Management of shock?

A
  • ABCDE approach
  • arterial blood gas (metabolic acidosis)
  • oxygen
  • IV fluids / blood transfusion
  • check blood glucose
  • identify and treat underlying cause
307
Q

What conditions can ventricular septal defects be associated with?

A
  • Down’s syndrome

- Turner’s syndrome

308
Q

Pathophysiology of VSD?

A
  • left to right shunt eventual leads to right-sided overload, right heart failure, and pulmonary hypertension
  • initially the infant remains acyanotic because blood is still being oxygenated
  • may progress to Eisenmenger syndrome
309
Q

What is Eisenmenger syndrome?

A

Pressure on the right side of the heart becomes greater than the left, causing shunt reversal (right-to-left). This results in cyanosis as blood bypasses the lungs.

310
Q

Clinical manifestations of VSD?

A
  • poor feeding
  • dyspnoea
  • tachypnoea
  • failure to thrive
  • pansystolic murmur
  • systolic thrill
311
Q

Gold standard investigation for VSD?

A

Echocardiogram

312
Q

Management of VSD?

A

Watchful waiting for spontaneous closure / surgical correction.

313
Q

Cause of atrial septal defects?

A

Defects in fusion of the septum primum / septum secondum with the endocardial cushion, resulting in a hole between the two atria.

314
Q

What is a patent foramen ovale?

A

Small hole in the septum secondum, normally closes at birth. Not a true ASD.

315
Q

Pathophysiology of ASD?

A
  • left-to-right shunt

- may progress to Eisenmenger’s syndrome

316
Q

Signs and symptoms of ASD?

A
  • mid-systolic crescendo-descrendo murmur
  • fixed splitting of S2
  • dyspnoea
  • difficulty feeding
  • poor weight gain
317
Q

Gold standard investigation for ASD?

A

Echocardiogram

318
Q

Management of ASD?

A

Watchful waiting or surgical correction.

319
Q

Complications of ASD?

A
  • stroke
  • atrial fibrillation
  • pulmonary hypertension
  • right-sided heart failure
  • Eisenmenger syndrome
320
Q

What is the ductus arteriosus?

A

Connection between the aorta and pulmonary artery, enabling blood in the foetal circulation to bypass the lungs.

321
Q

When does the ductus arteriosus close?

A

Stops functioning within 1-3 days of birth, fully closes within 2-3 weeks.

322
Q

Risk factor for patent ductus arteriosus?

A

Prematurity

323
Q

Pathophysiology of PDA?

A
  • left-to-right shunt occurs, with blood flowing from the aorta to the pulmonary artery
  • leads to pulmonary hypertension and eventually right heart strain and hypertrophy
  • increased blood return from pulmonary vessels on the left side of the heart results in LVH
324
Q

Signs and symptoms of PDA?

A
  • shortness of breath
  • difficulty feeding
  • poor weight gain
  • continuous crescendo-decrescendo machinery murmur
325
Q

Gold standard investigation for PDA?

A

Echocardiogram

326
Q

Management of PDA?

A
  • echocardiogram monitoring until 1 year of age

- surgical closure

327
Q

Complication of PDA?

A

Heart failure

328
Q

What is coarctation of the aorta?

A

Congenital condition where there is narrowing of the aortic arch, usually around the ductus arteriosus.

329
Q

What condition is coarctation of the aorta associated with?

A

Turner’s syndrome

330
Q

Pathophysiology of CoA?

A
  • reduced BP in arteries distal to narrowing
  • increased BP in arteries proximal to narrowing (heart, first three branches of the aorta)
  • right & left ventricular hypertrophy
331
Q

Signs and symptoms of CoA?

A
  • weak femoral pulses
  • high blood pressure in limbs supplied before the narrowing, low blood pressure in limbs supplied after the narrowing
  • systolic murmur heard in the left infraclavicular area
  • tachypnoea
  • poor feeding
  • grey / floppy appearance
  • underdeveloped left arm / legs
  • left ventricular heave
332
Q

Investigations for CoA?

A
  • ECG (signs of RVH / LVH)
  • CXR (cardiomegaly)
  • echocardiogram
  • CT angiography (gold standard)
333
Q

Management of CoA?

A

Surgical repair

334
Q

What is tetralogy of Fallot?

A
  • ventricular septal defect
  • overriding aorta
  • pulmonary valve stenosis
  • RVH
335
Q

Risk factors for tetralogy of Fallot?

A
  • maternal rubella infection
  • increased maternal age
  • alcohol consumption during pregnancy
  • maternal diabetes
336
Q

Pathophysiology of tetralogy of Fallot?

A
  • VSD and overriding aorta means that a greater proportion of deoxygenated blood enters the aorta from the right side of the heart
  • pulmonary valve stenosis provides greater resistance and encourages blood flow across the VSD
  • right-to-left shunt causes cyanosis
  • RVH results from increased right heart strain
337
Q

Signs and symptoms of ToF?

A
  • ejection systolic murmur (pulmonary stenosis)
  • cyanosis
  • clubbing
  • poor feeding and weight gain
  • cyanotic ‘tet’ spells when right-to-left shunt becomes temporarily worsened
338
Q

Gold standard investigation for ToF?

A

Echocardiogram

339
Q

What is hypertrophic cardiomyopathy?

A

Increased ventricular wall thickness or mass, not caused by pathological loading conditions.

340
Q

Causes of HCM?

A

Genetic mutations in components of the cardiac sarcomere.

341
Q

Pathophysiology of HCM?

A
  • hypertrophy is usually asymmetrical, involving the interventricular septum the left ventricle
  • causes left ventricular outflow obstruction
  • abnormal filling in diastole due to fibrosis and hypertrophy
  • decreased contractility and reduction in LVEF
  • arrhythmias may occur due to remodelling
342
Q

Signs and symptoms of HCM?

A
  • fatigue
  • shortness of breath
  • orthopnoea
  • peripheral oedema
  • chest pain (microvascular angina)
  • exertional syncope
  • ejection systolic crescendo-decrescendo murmur (outflow obstruction)
  • palpitations
  • pansystolic murmur (mitral regurgitation)
  • raised JVP
  • bi-basal lung crepitations
343
Q

Gold standard investigation for HCM?

A

Echocardiography

344
Q

Management of HCM?

A
  • beta blocker
  • calcium channel blockers (verapamil, diltiazem)
  • implantable defibrillator
  • anticoagulation (DOAC)
  • surgical interventions
  • diuretics for heart failure
345
Q

Complications of HCM?

A
  • sudden death
  • infective endocarditis
  • AF
  • ischaemic stroke
346
Q

What is dilated cardiomyopathy?

A

Ventricular enlargement and impaired contraction.

347
Q

Causes of dilated cardiomyopathy?

A
  • idiopathic
  • infection
  • pregnancy
  • drugs
  • inherited abnormal sarcomere genes
348
Q

Pathophysiology of DCM?

A
  • progressive dilatation of the left ventricle (and other chambers)
  • this leads to progressive systolic dysfunction and heart failure
  • conduction abnormalities may develop, causing arrhythmias
349
Q

Clinical manifestations of DCM?

A

Heart failure

350
Q

Gold standard investigation for DCM?

A

Echocardiography

351
Q

Management of DCM?

A
  • medical management of heart failure

- heart transplant

352
Q

What is restrictive cardiomyopathy?

A

Abnormal filling of non-dilated, non-hypertrophied ventricles.

353
Q

Causes of restrictive cardiomyopathy?

A
  • infiltrative diseases (amyloidosis, haemochromatosis, sarcoidosis)
  • inherited abnormal sarcomere genes
  • glycogen storage disease
354
Q

Pathophysiology of restrictive cardiomyopathy?

A
  • infiltration of the heart results in reduced compliance, so there is inadequate ventricular filling in diastole
  • this results in increased atrial pressures, dilated atria, and the development of diastolic heart failure
355
Q

Clinical manifestations of restrictive cardiomyopathy?

A

Heart failure

356
Q

Gold standard investigation for restrictive cardiomyopathy?

A

Echocardiography

357
Q

Management of restrictive cardiomyopathy?

A
  • treat underlying cause

- medical management of heart failure

358
Q

What is Takotsubo’s cardiomyopathy?

A

‘Broken-heart syndrome’ - stressful event leads to characteristic apical ballooning with transient systolic dysfunction.
Exact cause is unknown but thought to be related to catecholamine-induced spasm of small vessels in the cardiac microvasculature.

359
Q

What group of patients is most commonly affected by Takotsubo’s cardiomyopathy?

A

Postmenopausal women.

360
Q

Which arteries does atherosclerosis most commonly affect?

A
  • left anterior descending
  • left circumflex
  • right coronary artery
361
Q

What is Prinzmetal’s angina?

A

Angina caused by coronary artery vasospasm, occurs at rest and at night.

362
Q

Blood markers for myocardial infarction?

A
  • troponin
  • myoglobin
  • creatinine kinase
363
Q

Ejection fraction criteria for HF-REF and HF-PEF?

A

HF-REF ejection fraction is < 40%

HF-PEF ejection fraction is > 40%

364
Q

Management of acute heart failure?

A

OMFG

  • oxygen
  • morphine
  • furosemide
  • GTN spray
365
Q

Eye manifestations of hypertension?

A
  • papilloedema

- cotton wool spots

366
Q

Renal manifestations of hypertension?

A
  • haematuria

- proteinuria

367
Q

Can you give ACE inhibitors in pregnancy?

A

No they are contraindicated.

368
Q

Pathophysiology of cardiac tamponade?

A
  • accumulation of fluid in the pericardial space
  • compression of heart chambers and decrease in venous return
  • this results in decreased filling of the heart and reduced cardiac output
369
Q

What is pulsus paradoxus?

A

There is a large decrease in stroke volume on inspiration, resulting in systolic blood pressure drop > 10mmHg.

370
Q

Signs and symptoms of cardiac tamponade?

A
  • Beck’s triad (muffled heart sounds, elevated JVP, hypotension)
  • pulsus paradoxus
371
Q

Gold standard investigation for cardiac tamponade?

A

Echocardiogram

372
Q

Management of cardiac tamponade?

A

Pericardiocentesis

373
Q

S. epidermidis infective endocarditis particularly affects what group of patients?

A

Patients with prosthetic valves.

374
Q

Empirical treatment of IE?

A

flucloxacillin + ampicillin + gentamicin

375
Q

Which transporters do thiazide diuretics act on?

A

Block the Na+/Cl- symporter at the beginning of the DCT.

376
Q

Complications 0-24hrs post MI?

A
  • ventricular arrhythmia
  • heart failure
  • cardiogenic shock
377
Q

Histology 0-24hrs post MI?

A
  • early coagulative necrosis
  • neutrophils
  • wavy fibres
  • hypercontraction of myofibrils
378
Q

Complications 1-3 days post MI?

A

Fibrinous pericarditis

379
Q

Histology 1-3 days post MI?

A
  • extensive coagulative necrosis

- neutrophils

380
Q

Complications 3-14 days post MI?

A
  • free wall rupture & mitral regurgitation
  • papillary muscle rupture
  • LV pseudoaneurysm
381
Q

Histology 3-14 days post MI?

A

Macrophages and granulation tissue at margins.

382
Q

Complications 2 weeks - several months post MI?

A
  • Dressler syndrome
  • heart failure
  • arrhythmias
  • mural thrombus
383
Q

Histology 2 weeks - several months post MI?

A

Contracted scar complete

Phase 2a (10 decks)

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