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PHASE 2A > Cardio > Flashcards

Cardio Flashcards

1
Q

Define atherosclerosis

A

Build up of plaque in the intima of an artery

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2
Q

What can an atherosclerotic plaque cause?

A
  1. Heart attack
  2. Stroke
  3. Gangrene
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3
Q

Give 4 risk factors for atherosclerosis

A
  1. Family history
  2. Increasing age
  3. Smoking
  4. High serum cholesterol (LDL)
  5. Obesity
  6. Diabetes
  7. Hypertension
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4
Q

What are the constituents of an atheromatous plaque?

A 
Lipid core 
Necrotic debris 
Connective tissue surrounded by foam cells
Fibrous cap 
Lymphocytes
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5
Q

In which arteries would you most likely find an atheromatous plaque?

A

Peripheral and coronary arteries

Focal distribution along the length

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6
Q

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

A

Media

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7
Q

What is the precursor for atherosclerosis?

A

Fatty streaks

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8
Q

What can cause chemoattractant release?

A

Endothelial cell injury

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9
Q

What is the function of chemoattractants?

A

Signal leukocytes and produce a concentration gradient

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10
Q

What is the function of leukocytes?

A

Leukocytes accumulate and migrate into vessel walls and release cytokines leading to inflammation

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11
Q

What inflammatory cytokines are found in plaques?

A 
IL-1 
IL-6 
IFN-y
MCP-1 
TGF-B
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12
Q

Describe the process of leukocyte recruitment

A
  1. Capture
  2. Rolling
  3. Slow rolling
  4. Adhesion
  5. Transmigration
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13
Q

What types of molecules are present during leukocyte recruitment?

A
  1. Chemoattractants
  2. Selectins (1-3)
  3. Integrins (3-5)
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14
Q

Describe the 5 steps of progression of atherosclerosis

A
  1. Fatty streaks
  2. Intermediate lesions
  3. Fibrous plaque
  4. Plaque rupture
  5. Plaque erosion
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15
Q

At what age do fatty streaks begin to appear?

A

< 10 years old

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16
Q

What are the constituents of fatty streaks?

A

Foam cells and T lymphocytes within the intimal layer of the vessel wall

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17
Q

What are the constituents of intermediate lesions?

A 
Foam cells 
Smooth muscle cells 
T lymphocytes 
Platelet adhesion and aggregation
Extracellular lipid pools
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18
Q

What are the constituents of fibrous plaques?

A 
Fibrous cap overlies lipid core and necrotic debris 
Smooth muscle cells 
Macrophages
Foam cells
T lymphocytes
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19
Q

What are fibrous plaques able to do?

A

Impede blood flow and they are prone to rupture

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20
Q

Why might a plaque rupture?

A

Fibrous plaques are constantly growing and receding
Fibrous cap has to be resorbed and redeposited in order to be maintained
If balance is shifted in favour of inflammatory condition, the cap becomes weak and the plaque ruptures
Thrombus formation and vessel occlusion

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21
Q

What the primary treatment for atherosclerosis?

A

Percutaneous Coronary Intervention (PCI)

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22
Q

What is the major limitation of PCI?

A

Restenosis

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23
Q

How can restenosis be avoided following PCI?

A

Drug eluting stents –> anti-proliferative and drugs that inhibit healing

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24
Q

What drugs can patients be started on following a PCI?

A

Aspirin - antiplatelet
Clopidogrel/Ticagrelor - inhibit P2Y12 ADP receptors on platelets
Statins - cholesterol lowering
Anti-inflammatory drugs - Colchicine, canakinumab

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25
Q

What is the key principle behind pathogenesis of atherosclerosis?

A

It is an inflammatory process

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26
Q

Define atherogenesis

A

The development of an atherosclerotic plaque

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27
Q

What is an electrocardiogram?

A

Representation of electrical events of the cardiac cycle

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28
Q

What can ECGs identify?

A 
Arrhythmias
Myocardial ischaemia and infarction
Pericarditis
Chamber hypertrophy 
Electrolyte disturbances
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29
Q

What is depolarisation?

A

Contraction of any muscle associated with electrical changes

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30
Q

What is the dominant pacemaker of the heart?

A 
Sinoatrial node (SAN) 
60-80 bpm
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31
Q

What are the pacemakers of the heart?

A
  1. Sinoatrial node (dominant)
  2. Atrioventricular node
  3. Ventricular cells
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32
Q

What is the standard calibration of an ECG?

A

25 mm/S
0.1 mV/mm
Electrical impulse that travels towards the electrode produces a positive deflection

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33
Q

What is the route of impulse conduction in the heart?

A

SAN –> AVN –> Bundle of His –> Bundle branches –> Purkinje fibres

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34
Q

What does the P wave represent?

A

Atrial depolarisation

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35
Q

What does the QRS complex represent?

A

Ventricular depolarisation

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36
Q

What does the T wave represent?

A

Ventricular repolarisation

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37
Q

What does the PR interval represent?

A

Atrial depolarisation and delay in AV junction

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38
Q

How long should the PR interval be?

A

120-200 ms

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39
Q

What might a long PR interval indicate?

A

Heart block

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40
Q

How long should the QRS complex be?

A

< 110 ms

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41
Q

What does the ST segment represent?

A

Time between depolarisation and repolarisation of the ventricles (contraction)

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42
Q

What is the J point?

A

Where the QRS complex becomes the ST segment

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43
Q

How many seconds do the following represent on ECG paper?

a) Large squares
b) Small squares

A

a) 0.2s

b) 0.04s

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44
Q

What is the normal axis of the QRS complex?

A

-30° to +90°

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45
Q

What is the QT interval?

A

Time from the beginning of ventricular depolarisation to the end of ventricular repolarisation

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46
Q

How long should the QT interval be?

A

0.35-0.45s

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47
Q

Where would you place lead I?

A

From the right arm to the left arm

At 0°

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48
Q

Where would you place lead II?

A

From the right arm to left leg

At 60°

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49
Q

Where would you place lead III?

A

From the left arm to left leg

At 120°

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50
Q

Where would you place lead aVF?

A

From halfway between the left arm and right arm to the left leg
At 90°

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51
Q

Where would you place lead aVL?

A

From halfway between the right arm and left leg to the left arm
At -30°

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52
Q

Where would you place lead aVR?

A

From halfway between the left arm and left leg to the right arm
At -150°

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53
Q

Where are the chest electrodes placed?

A
  • V1 = 4th intercostal space, right sternal edge
  • V2 = 4th intercostal space, left sternal edge
  • V3 = midway between V2 and V4
  • V4 = 5th intercostal space, midclavicular line
  • V5 = Same horizontal level as V4, left anterior axillary line
  • V6 = same horizontal level as V4 and V5, left mid-axillary line
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54
Q

What leads show the lateral view of the heart on an ECG?

A

Lead I
aVL
V5
V6

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55
Q

What leads show the inferior view of the heart on an ECG?

A

Lead II
Lead III
aVF

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56
Q

What leads show the septal view of the heart on an ECG?

A

V1

V2

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57
Q

What leads show the anterior view of the heart on an ECG?

A

V3

V4

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58
Q

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

A

Leads I and II

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59
Q

In which lead are all waves negative?

A

aVR

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60
Q

In which leads must the R wave grow?

A

From chest leads V1 to V4

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61
Q

In which leads must the S wave grow?

A

From chest leads V1 to V3

Must disappear in V6

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62
Q

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

A

Leads I, II and V2-V6

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63
Q

What might tall pointed P waves on an ECG suggest?

A

Right atrial enlargement

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64
Q

What might notched, ‘m shaped’ P waves on an ECG suggest?

A

Left atrial enlargement

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65
Q

Give 3 signs of abnormal T waves

A
  1. Symmetrical
  2. Tall and peaked
  3. Biphasic or inverted
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66
Q

What happens to the QT interval when HR increases?

A

QT interval decreases

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67
Q

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

A

QT interval

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68
Q

Define angina

A

Type of ischaemic heart disease

It is a symptom of O2 supply/demand mismatch to the heart

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69
Q

What is the most common cause of angina?

A

Narrowing of the coronary arteries due to atherosclerosis

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70
Q

Give 5 possible causes of angina

A
  1. Impairment of blood flow = narrowed coronary artery (e.g. atherosclerosis)
  2. Increased distal resistance (e.g. LV hypertrophy)
  3. Reduced O2 carrying capacity of blood (e.g. anaemia)
  4. Coronary artery spasm
  5. Thrombosis
  6. Aortic stenosis
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71
Q

How reduced does the diameter of an artery need to be before symptoms occur?

A

Diameter has to fall below 70%

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72
Q

Name 4 types of angina

A
  1. Stable angina
  2. Unstable angina
  3. Cescendo angina
  4. Prinzmetal’s angina
  5. Microvascular angina (syndrome X)
  6. Decubitus angina
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73
Q

Name 3 non-modifiable risk factors for angina

A
  1. Increasing age
  2. Family history
  3. Gender - Male
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74
Q

Give 5 modifiable risk factors for angina

A
  1. Smoking
  2. Diabetes
  3. Hypertension
  4. Hypercholesterolaemia
  5. Sedentary lifestyle/obesity
  6. Stress
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75
Q

Name 3 exacerbating factors for angina that effect the supply of O2

A
  1. Anaemia
  2. Hypoxaemia
  3. Polycythaemia
  4. Hypothermia
  5. Hyper/hypovolaemia
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76
Q

Name 3 exacerbating factors for angina that effect the demand of O2

A
  1. Hypertension
  2. Tachyarrhythmia
  3. Valvular heart disease
  4. Hyperthyroidism
  5. Cold weather
  6. Heavy meals
  7. Emotional stress
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77
Q

Briefly describe the pathophysiology of angina that results from atherosclerosis

A

On exertion there is increase O2 demand

Coronary blood flow is obstructed by an atherosclerotic plaque –> myocardial ischaemia –> angina

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78
Q

Briefly describe the pathophysiology of angina the results from anaemia

A

On exertion there is increased O2 demand

In someone with anaemia there is reduced O2 transport –> myocardial ischaemia –> angina

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79
Q

Briefly describe the pathophysiology of Prinzmetal’s angina

A

Occurs due to coronary artery spasm

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80
Q

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

A

When myocardial demand increases, microvascular resistance drops and flow increases

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81
Q

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

A

In CVD, epicardial resistance is high meaning microvascular resistance has to fall at rest to supply myocardial demand at rest
When this person exercise, microvascular resistance can’t drop anymore and flow can’t increase to meet metabolic demand = angina

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82
Q

Name 3 differential diagnoses for angina

A
  1. Pericarditis/myocarditis
  2. PE
  3. Chest infection
  4. Dissection of aorta
  5. GORD
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83
Q

How would you describe the chest pain in angina?

A

Crushing central chest pain that is heavy and tight

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84
Q

What 3 things are used to assess whether it is typical angina, atypical pain or non-anginal pain?

A
  1. Have central, tight, radiation to arms, jaw and neck
  2. Precipitated by exertion
  3. Relieved by rest or GTN spray
    3/3 = Typical angina
    2/3 = Atypical pain
    1/3 = Non-anginal pain
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85
Q

Give 5 symptoms of angina

A
  1. Crushing central chest pain
  2. Pain is relieved with rest or GTM spray
  3. Pain is provoked by physical exertion
  4. Pain may radiate to arms, neck or jaw
  5. Dyspnoea
  6. Nausea
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86
Q

What tool can you use to determine the best investigations and treatment in someone you suspect to have angina?

A

Pre-test probability of CAD

It takes into account gender, age and typicality of pain

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87
Q

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

A
  1. ECG - usually normal, sometimes ST depression, flat or inverted T waves
  2. Echocardiogaphy
  3. CT angiography - high NPV and good at excluding disease
  4. Exercise tolerance test - induces ischaemia
  5. Invasive angiogram - tells you FFR (pressure gradient across stenosis)
  6. SPECT - radio labelled tracer taken up by metabolising tissues
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88
Q

A young, healthy, female patient presents to you with what appears to be the signs and symptoms of angina. Would it be good to do CT angiography on this patient?

A

Yes

CT angiography has a high NPV, so is ideal for excluding CAD in younger, low risk patients

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89
Q

How can angina be reversed?

A

Resting - reducing myocardial demand

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90
Q

Describe the primary prevention for angina

A
  1. Modify risk factors
  2. Treat underlying causes
  3. Low dose aspirin
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91
Q

Describe the secondary prevention of angina

A
  1. Modify risk facotrs
  2. Pharmacological therapies for symptom relief and to reduce the risk of CV events
  3. Interventional therapies (e.g. PCI)
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92
Q

Name 3 symptom reliving pharmacological therapies the might be used in someone with angina

A
  1. Beta blockers (e.g. atenolol, propranolol, bisoprolol)
  2. Nitrates (e.g. GTN spray)
  3. Calcium channel blockers
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93
Q

Describe the action of beta blockers

A

Beta 1 specific
Antagonise sympathetic activation and so are negatively chronotropic and inotropic
Myocardial work is reduced and so is myocardial demand = symptom relief

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94
Q

Give 3 side effects of beta blockers

A
  1. Bradycardia
  2. Tiredness
  3. Erectile dysfunction
  4. Cold peripheries
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95
Q

When might beta blockers be contraindicated?

A

Someone with asthma or someone who is bradycardic

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96
Q

Describe the action of nitrates

A

Venodilators

Reduce venous return –> reduced preload –> reduced myocardial work and myocardial demand

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97
Q

Describe the action of Calcium channel blockers

A

Arterodilators

Reduce BP –> Reduce afterload –> reduced myocardial demand

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98
Q

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

A
  1. Aspirin
  2. Clopidogrel
  3. Statins
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99
Q

How does aspirin work?

A

Antiplatelet

Irreversibly inhibits COX –> reduced thromboxane 2 synthesis –> platelet aggregation reduced

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100
Q

What is a caution when prescribing aspirin?

A

Gastric ulceration

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101
Q

How does clopidogrel work?

A

Antiplatelet

P2Y12 inhibitor –> prevents platelet activation

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102
Q

What are statins used for?

A

To reduce the amount of LDL in the blood

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103
Q

What is revascularisation?

A

Used to restore coronary artery and increase blood flow

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104
Q

Name 2 types of revascularisation

A
  1. Percutaneous coronary intervention (PCI)

2. Coronary artery bypass graft (CABG)

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105
Q

Give 2 advantages and 1 disadvantage of PCI

A 
ADVANTAGES 
1. Less invasive 
2. Convenient and acceptable
DISADVANTAGES 
1. High risk of restenosis
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106
Q

Give 1 advantage and 2 disadvantages of CABG

A 
ADVANTAGES 
1. Good prognosis after surgery 
DISADVANTAGES 
1. Very invasive 
2. Long recovery time
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107
Q

Name 2 complications of angina

A
  1. Acute coronary syndromes
  2. Congestive cardiac failure
  3. Conduction disease
  4. Arrhythmia
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108
Q

What are acute coronary syndromes?

A

Encompasses a spectrum of acute cardiac conditions from unstable angina, NSTEMI and STEMI

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109
Q

What is the common cause of ACS?

A

Rupture of an atherosclerotic plaque and subsequent arterial thrombosis

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110
Q

What are uncommon causes of ACS?

A
  1. Coronary vasospasm
  2. Drug abuse
  3. Coronary artery dissection
  4. Thoracic aortic dissection
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111
Q

Briefly describe the pathophysiology of ACS

A

Atherosclerosis –> plaque rupture –> platelet aggregation –> thrombus formation –> ischaemia and infarction –> encores of cells –> permanent heart muscle damage and ACS

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112
Q

Describe type 1 MI

A

Spontaneous MI with ischaemia due to plaque rupture

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113
Q

Describe type 2 MI

A

MI secondary to ischaemia due to increased O2 demand

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114
Q

What is troponin a marker for?

A

Cardiac muscle injury

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115
Q

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

A

The occluding thrombus causes necrosis of cells and so myocardial damage causing troponin to be raised

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116
Q

Give 3 signs of unstable angina

A
  1. Cardiac chest pain at rest
  2. Cardiac chest pain with crescendo pattern
  3. No significant rise in troponin
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117
Q

Give 4 symptoms of MI

A
  1. Unremitting and usually severe central cardiac chest pain
  2. Pain occurs at rest
  3. Sweating
  4. Breathlessness
  5. Nausea and vomiting
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118
Q

Give 3 signs of MI

A
  1. Hypo/hypertension
  2. 3rd/4th heart sound
  3. Signs of congestive heart failure
  4. Ejection systolic murmur
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119
Q

Name 3 possible differential diagnoses of MI

A
  1. Pericarditis
  2. Stable angina
  3. Aortic dissection
  4. GORD
  5. Pneumothorax
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120
Q

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

A
  1. ECG
  2. Blood tests - troponin levels and rule out anaemia
  3. Coronary angiography
  4. Cardiac monitoring for arrhythmias
  5. Chest x-ray
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121
Q

What might the ECG of someone with unstable angina show?

A

May be normal, or might show T wave inversion and ST depression

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122
Q

What might the ECG of someone with NSTEMI show?

A

May be normal or might show T wave inversions and ST depression
Might also be R wave regression, ST elevation and biphasic T wave in lead V3

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123
Q

What might the ECG of someone with STEMI show?

A

ST elevation in the anterolateral leads

After a few hours, T waves inlet and deep, broad, pathological Q waves develop

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124
Q

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

A

Normal

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125
Q

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

A

Significantly raised

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126
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. PE
  3. Myocarditis
  4. Heart failure
  5. Arrhythmias
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127
Q

Describe the initial management of ACS

A
  1. Get into hospital ASAP - 999
  2. If STEMI, paramedic call PCI centre for transfer
  3. Aspirin 300 mg
  4. Pain relief - opioid
  5. Oxygen if hypoxic
  6. Nitrates
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128
Q

What is the treatment of choice for STEMI?

A

PCI

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129
Q

What is the function of P2Y12?

A

It amplifies platelet activation

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130
Q

Give 2 potential side effect of P2Y12 inhibitors

A
  1. Bleeding
  2. Rash
  3. GI disturbances - ulceration
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131
Q

Describe the secondary prevention therapy for people after having a STEMI

A
  1. Aspirin - antiplatelet
  2. Clopidogrel - P2Y12 inhibitor
  3. Statins
  4. Metoprolol - beta blocker
  5. ACE inhibitor - ramipril, lisinopril
  6. Modification of risk factors
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132
Q

What is involved in antithrombotic therapy?

A 
Dual antiplatelet therapy = aspirin and clopidogrel 
Anticoagulant = heparin
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133
Q

Give 5 potential complications of MI

A
  1. Heart failure
  2. Rupture of infarcted ventricle
  3. Rupture of intraventricular septum
  4. Mitral regurgitation
  5. Arrhythmias
  6. Heart block
  7. Pericarditis
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134
Q

Give 2 possible sequelae to MI

A
  1. Shock
  2. Heart failure
  3. Pericarditis
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135
Q

What is a DVT?

A

Blood clot within a blood vessel of the lower limb

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136
Q

What are the symptoms of DVT?

A

Non-specific symptoms

Pain and swelling

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137
Q

What are the signs for DVT?

A

Tenderness, warmth and discolouration

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138
Q

What investigations might be done in order to diagnose a DVT?

A
  1. D-dimer (blood test) - look for fibrin breakdown products –> normal excludes DVT diagnosis (abnormal does NOT confirm)
  2. Ultrasound compression test of proximal veins - if you can’t squash the vein = clot
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139
Q

What is the treatment for DVT?

A
  1. LMW heparin
  2. Oral warfarin or direct acting oral anticoagulant (DAOC)
  3. Compression stockings
  4. Treat the underlying cause (e.g. malignancy or thrombophilia)
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140
Q

Name the types of DVT

A
  1. Spontaneous

2. Provoked - incidence of recurrence is low if you remove the stimulus

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141
Q

Give 5 risk factors for DVT

A
  1. Surgery, immobility, leg fracture
  2. Combined oral contraceptive pill, HRT
  3. Long haul flights
  4. Genetic predisposition
  5. Pregnancy
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142
Q

How can DVTs and PEs be prevented?

A
  1. Hydration
  2. Early mobilisation
  3. Compression sticking/pumps
  4. Low dose LMW heparin
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143
Q

What is low risk thromboprophylaxis treatment?

A 
< 40 years 
Surgery < 30 mins 
Early mobilisation and hydration
No chemical 
TED if surgical
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144
Q

What is high risk thromboprophylaxis?

A

Hip, knee, pelvis, malignancy, risk factors, prolonged immobility
All immobile medical, many surgical - Dalteparin s/c od

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145
Q

What might be the consequence of a dislodged DVT?

A

Pulmonary embolism

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146
Q

Give 2 symptoms of a PE

A
  1. Breathlessness

2. Pleuritic chest pain

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147
Q

Give 2 signs of a PE

A
  1. Tachycardia

2. Tachypnoea

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148
Q

What investigations might be done to diagnose a patient with PE?

A

ECG sinus tachycardia - to exclude cardiac cause
Blood gases - to exclude respiratory causes
D-dimer - normal excludes diagnosis
CTPA spiral with contrast - gaps in dye if PE has occurred
Ventilation/perfusion scan (used in pregnancy)

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149
Q

What is the treatment for a PE?

A

LMW heparin, oral warfarin for 6 months
DOAC - for outpatient with a relatively minor PE
Treat cause if possible

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150
Q

If a patient can not be placed on anticoagulation following a PE, what alternative treatment should be considered?

A

IVC filter - prevents more clot travelling from the leg to the lungs

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151
Q

Define thrombosis

A

Blood coagulation inside a vessel

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152
Q

How would you describe an arterial thrombus?

A

Platelet rich (a ‘white thrombosis’)

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153
Q

How would you describe a venous thrombosis?

A

Fibrin rich (a ‘red thrombosis’)

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154
Q

What are the potential consequences of an arterial thrombosis?

A
  1. Coronary circulation = MI
  2. Cerebral circulation = Stroke
  3. Peripheral circulation = Peripheral vascular disease (e.g. gangrene)
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155
Q

What investigations would you do to diagnose an arterial thrombosis?

A 
MI = history, ECG, cardiac enzymes
Stoke = History and examination, CT/MRI scan
PVD = History and examination, ultrasound, angiogram
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156
Q

What is the treatment for arterial thrombosis?

A
  1. Aspirin
  2. LMW heparin
  3. Thrombolytic therapy: streptokinase tissue plasminogen factor
  4. Treat risk factors
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157
Q

What are the potential consequences of a venous thrombosis?

A

Deep vein thrombosis

Pulmonary embolism

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158
Q

Name 4 causes of a venous thrombosis

A 
Circumstantial 
 - surgery 
 - immobilisation
 - malignancy
Genetic 
 - factor V Leiden 
 - antithrombin deficiency 
 - protein C or S deficiency 
Acquired 
 - Anti-phospholipid syndrome
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159
Q

How does heparin work?

A

Inhibits thrombin and factor Xa

Indirect thrombin inhibitor - binds to antithrombin and increased its activity

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160
Q

How do you monitor heparin?

A

Activated partial thromboplastin time

Aim ratio: 1.8-2.8

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161
Q

Why is LMW heparin often used instead of normal heparin?

A

Smaller molecule, less variation in dose and renally excreted

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162
Q

How does warfarin work?

A

Inhibits production of vitamin K dependent clotting factors (2, 7, 9, 10)
Prolongs the prothrombin time

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163
Q

What is warfarin an antagonist of?

A

Vitamin K

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164
Q

Why is warfarin difficult to use?

A

Lots of interactions
Needs almost constant monitoring
Teratogenic

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165
Q

How is warfarin measured?

A

Using International Noramlised Ratio (derived from prothrombin time)
Usual target = 2-3
Higher range = 3-4.5

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166
Q

How does Direct Acting Oral Anticoagulant (DAOC) work?

A

Directly acts on factor 2 (thrombin) or 10

No blood test or monitoring needed just given od or bd

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167
Q

How much serous fluid is there between the visceral and parietal pericardium?

A

50 ml

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168
Q

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

A

Lubricant and so allows smooth movement of the heart inside the pericardium

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169
Q

What is the function of the pericardium?

A

Restrains the filling volume of the heart

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170
Q

Describe the aetiology of pericarditis

A
  1. Viral (common) - e.g. enteroviruses
  2. Bacterial - e.g. mycobacterium tuberculosis
  3. Autoimmune - e.g. Sjören syndrome
  4. Neoplastic
  5. Metabolic - e.g. uraemia
  6. Traumatic and iatrogenic
  7. Idiopathic (90%)
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171
Q

Define acute pericarditis

A

Acute inflammation of the pericardium with or without effusion

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172
Q

Give 5 symptoms of pericarditis

A
  1. CHEST PAIN
  2. Dyspnoea
  3. Cough
  4. Hiccups
  5. Skin rash
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173
Q

Describe the chest pain in acute pericarditis

A

Severe, sharp, pleuritic, rapid onset, can radiate to arm

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174
Q

Why might someone with pericarditis have hiccups?

A

Due to irritation to the phrenic nerve

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175
Q

What is the major differential diagnosis of acute pericarditis?

A

Myocardial infarction

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176
Q

Name 3 differential diagnoses for acute pericarditis

A
  1. MI
  2. Angina
  3. Pneumonia
  4. Pleurisy
  5. PE
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177
Q

What investigations might you do on someone who you suspect to have pericarditis?

A
  1. ECG
  2. CXR
  3. Bloods - FBC, ESR and CRP, Troponin
  4. Echocardiogram - usually normal, rule out silent pericardial effusion
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178
Q

What might the ECG look like in someone with acute pericarditis?

A
  1. Saddle shaped ST elevation

2. PR depression

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179
Q

What does a raised troponin in acute pericarditis suggest?

A

Myopericarditis

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180
Q

How can acute pericarditis be clinically diagnosed?

A

Patient has to have at least 2 of the following:

  1. Chest pain
  2. Friction rub
  3. ECG changes
  4. Pericardial effusion
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181
Q

What is the treatment for pericarditis?

A
  1. Restrict physical activity until symptoms resolve
  2. NSAID or aspirin
  3. Colchicine - reduces recurrence
  4. Treat the cause
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182
Q

What is pericardial effusion?

A

Abnormal accumulation of fluid in the pericardial cavity

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183
Q

What is a complication of pericardial effusion?

A

Cardiac tamponade

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184
Q

Why does chronic pericardial effusion rarely cause tamponade?

A

Parietal pericardium is able to adapt when effusion accumulate slowly and so tamponade is prevented

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185
Q

Briefly explain the pathophysiology of cardiac tamponade

A

Accumulation of pericardial fluid –> increase in intra-pericardial pressure –> poor ventricular filling –> decrease in CO

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186
Q

What are the signs of Cardiac tamponade?

A

Beck’s triad:
1. Decreased BP
2. Increased jugular venous pressure
3. Quiet heart sounds
Pulsus paradoxus = pulses fade on inspiration
Kussmaul’s sign = rise in jugular venous pressure with inspiration

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187
Q

What is the treatment of cardiac tamponade?

A

Pericardiocentesis (drainage)

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188
Q

What is chronic constrictive pericarditis?

A

Calcification thickens the pericardium and affects cardiac effusion

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189
Q

What is the treatment for chronic constrictive pericarditis?

A

Surgical excision of thickened pericardium

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190
Q

Name 3 major predictive markers for complications for pericarditis

A
  1. Fever >38 degree
  2. Subacute onset
  3. Large pericardial effusion
  4. Cardiac tamponade
  5. Lack of response to aspirin or NSAIDs after at least 1 week of therapy
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191
Q

What is haemopericaridum?

A

Direct bleeding from vasculature through the ventricular wall following MI

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192
Q

What can cause myocarditis?

A

Viral infection

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193
Q

Give 5 risk factors for peripheral vascular disease

A
  1. Hypertension
  2. Hyperlipidaemia
  3. Diabetes
  4. Smoking
  5. Obesity
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194
Q

Give 4 treatments for peripheral vascular disease

A
  1. Risk factor modification
  2. Vein bypass for critical leg ischaemia
  3. Balloon angioplasty
  4. Stenting of occlusion
  5. Amputation
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195
Q

What is critical ischaemia?

A

Blood supply is barely adequate for life
No reserve for an increase in demand
Very severe, cells are dying
O2 is always low, even at rest

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196
Q

Give 4 signs of critical ischaemia

A
  1. Rest pain
  2. Classically nocturnal
  3. Ulceration
  4. Gangrene
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197
Q

What can cause acute ischaemia?

A

Embolism/thrombosis

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198
Q

Give 6 symptoms of acute ischaemia

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

Give 2 examples of acute ischaemia

A
  1. Stroke

2. MI

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200
Q

What might you do if you are unable to do a PCI for a STEMI?

A

Thrombolysis

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201
Q

Name a drug that can be used for thrombosis in the treatment of a STEMI

A

Streptokinase

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202
Q

Define cardiomyopathy

A

Group of diseases of the myocardium that affect the mechanical or electrical function of the heart

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203
Q

Name 4 cardiomyopathies

A
  1. Hypertrophic (HCM)
  2. Dilated (DCM)
  3. Arrhythmogenic right/left ventricular (ARVC/ALVC)
  4. Restrictive
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204
Q

Name 4 risk factors for cardiomyopathy

A
  1. FH
  2. High BP
  3. Obesity
  4. Diabetes
  5. Previous MI
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205
Q

What can cause Hypertrophic cardiomyopathy?

A

Sarcomeric gene mutations - Troponin T and B-myosin

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206
Q

What is the usual inheritance pattern for cardiomyopathies?

A

Autosomal dominant (restrictive not familial)

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207
Q

Describe the pathophysiology of Hypertrophic cardiomyopathy

A

Hypertrophic ventricle so impaired diastolic filling resulting in reduced stroke volume and therefore CO
Disarray of cardiac myocytes so conduction is also affected

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208
Q

Give 3 symptoms of HCM

A
  1. Angina
  2. Dyspnoea
  3. Syncope
  4. Palpitations
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209
Q

Give 3 signs of HCM

A
  1. Cardiac arrhythmia
  2. Ejection systolic murmur
  3. Jerky carotid pulse
  4. Double apex beat
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210
Q

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

A
  1. Large QRS complexes

2. Progressive T wave inversion

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211
Q

Briefly describe treatment for HCM

A
  1. BB - atenolol
  2. CCB - Verapamil
  3. Amiodarone - anti-arrhythmic
  4. Anticoagulants
  5. ICD insertion
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212
Q

Describe the pathophysiology of DCM

A

Cytoskeletal gene mutation

Ventricular dilation and dysfunction leading to poor contractility

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213
Q

Name 3 causes of DCM

A
  1. Genetic
  2. Alcohol
  3. Ischaemia
  4. Thyroid disorder
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214
Q

Give 3 symptoms of DCM

A

Presents with symptoms of heart failure

  1. SOB
  2. Fatigue
  3. Oedema
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215
Q

What investigations would you do for someone you suspect has DCM?

A

CXR –> cardiomegaly, pulmonary oedema
ECG –> tachycardia, arrhythmia
ECHO –> dilated ventricles

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216
Q

What is the treatment for DCM?

A

Heart failure and AF treatment

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217
Q

What can cause Arrhythmogenic cardiomyopathy?

A

Desmosome gene mutations

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218
Q

Describe the pathophysiology of ARVC/ALVC

A

Desmosome gene mutation
Cardiac cells not held together properly so myocytes pulled apart and ventricles are replaced with fatty fibrous tissue
Gap junctions are affected too

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219
Q

Give 2 signs of ARVC/ALVC

A
  1. Ventricular tachycardia

2. Syncope

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220
Q

What might an ECG look like from a person with ARVC/ALVC?

A

Epsilon waves

221
Q

What is the treatment for ARVC/ALVC?

A

BB - atenolol - non-life threatening arrhythmias
Amiodarone - symptomatic arrhythmias
ICD - high risk
Occasionally heart transplant

222
Q

What is restrictive cardiomyopathy?

A

Poor dilation of the heart restricts diastole

223
Q

Name 2 causes of restrictive cardiomyopathy

A
  1. Amyloidosis (extra-cellular deposition of an amyloid, a insoluble fibrillar protein)
  2. Sarcoidosis
224
Q

What are channelopathies?

A

Inherited arrhythmias caused by ion channel protein gene mutations
Structurally normal heart but abnormality on an ECG

225
Q

Name 4 channelopathies

A
  1. Long QT syndrome
  2. Short QT syndrome
  3. Brugada
  4. Catecholamine Polymorphic Ventricular Tachycardia (CPVT)
226
Q

What is Brugada?

A

A channelopathy caused by a mutation in sodium channels

227
Q

What might an ECG look like from someone with Brugada?

A

Characteristic ST elevation in chest leads

228
Q

What is the commonest symptom of channelopathies?

A

Recurrent syncope

229
Q

What is familial hypercholesterolaemia?

A

Inherited abnormality of cholesterol metabolism

LDL receptor affected

230
Q

Define heart failure

A

A complex clinical syndrome of signs/symptoms that suggest the efficiency of the heart as a pump is impaired
Heart is unable to deliver blood at a rate that meets the metabolic demands

231
Q

What are the 2 broad categories of heart failure?

A
  1. Systolic failure = ability of heart to pump blood around the body is impaired
  2. Diastolic failure = inability of ventricles to relax and fill fully
232
Q

Give 4 risk factors for heart failure

A
  1. > 65 y/o
  2. African descent
  3. Men
  4. Obesity
  5. Previous MI
233
Q

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

A

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

234
Q

Describe the pathophysiology of heart failure

A

When the heart fails, compensatory mechanisms attempt to maintain CO
As HF progresses, these mechanism are exhausted and become pathophysiological

235
Q

What are the compensatory mechanisms in heart failure?

A
  1. Sympathetic system
  2. RAAS
  3. Natriuretic peptides
  4. Ventricular dilation
  5. Ventricular hypertrophy
236
Q

Explain how the sympathetic system is compensatory in HF and give one disadvantage of sympathetic activation

A

Improves ventricular function by increasing HR and contractility = CO maintained
BUT it also causes arteriolar constriction which increases afterload and so myocardial work

237
Q

Explain how the RAAS system is compensatory in HF and give one disadvantage of RAAS activation

A

Reduced CO leads to reduced renal perfusion, this activates RAAS –> increased fluid retention so increased preload
BUT it also causes arteriolar constriction which increase afterload and so myocardial work

238
Q

Give 3 properties of natriuretic peptides that make them compensatory in HF

A
  1. Diuretic
  2. Hypotensive
  3. Vasodilators
239
Q

Give 5 causes of HF

A
  1. IHD = commonest
  2. Hypertension
  3. Cardiomyopathy
  4. Valvular heart disease
  5. Excessive alcohol
240
Q

What are the 3 cardinal symptoms of HF?

A
  1. SOB
  2. Fatigue
  3. Peripheral oedema
241
Q

Give 3 signs of left HF

A
  1. Pulmonary crackles
  2. S3 and S4 and murmurs
  3. Displaced apex beat
  4. Tachycardia
242
Q

Give 2 signs of right HF

A
  1. Raised JVP

2. Ascites

243
Q

Describe the NYHA classification for HF

A

Class 1 = heart disease present but no limitation = asymptomatic
Class 2 = comfortable arrest but slight limitation on activity = mild HF
Class 3 = marked limitation = moderate HF
Class 4 = SOB at rest, all activity causes discomfort = severe HF

244
Q

What investigations might you do initially do in someone who you suspect has HF?

A
  1. ECG
  2. CXR
  3. Natriuretic peptide levels - raised indicates HF
245
Q

What 4 signs might you see on a CXR taken from someone with HF?

A
  1. Pleural effusion
  2. Bat’s wings
  3. Cardiomegaly
  4. Kerley B lines
  5. Dilated prominent upper lobe vessels
246
Q

You have done an ECG, CXR and blood tests on a patient who you suspect might have HF. These have come back abnormal. What investigation might you do next?

A

An echocardiogram

247
Q

What is first line treatment for HF?

A

Vasodilator therapy = ACEi and BB - via the neurohumoral blockade (RAAS-SNS)

248
Q

Give an example of an ACEi that is commonly used in HF

A

Ramipril

249
Q

Name 3 BB that are used in treatment of HF

A
  1. Propranolol
  2. Bisoprolol
  3. Atenolol
  4. Carvedilol
250
Q

What drugs might you give to someone with HF for symptomatic relief?

A

Diuretics - thiazides (bendroflumethiazide) and loop (furosemide)
Promote Na and water excretion so help with fluid overload

251
Q

What might you give to someone with hypertension if they are ACE inhibitor intolerant?

A

Angiotensin receptor blocker (ARB) - losartan, valsartan, candesartan

252
Q

What is 2nd line treatment for HF?

A

Anticoagulant therapy and aspirin
Calcium channel blocker - amlodipine
Aldosterone antagonist
Digoxin

253
Q

How can chronic HF be prevented?

A 
Stop smoking
Eat more healthy 
Exercise 
Avoid large meals
Vaccinations 
Treat underlying cause - dysarrhythmias or valve disease
254
Q

What is the treatment for acute HF?

A 
LOON 
Loop diuretic = furosemide
Oxygen 
Opioid = diamorphine 
Nitrates = GTN spray 
and Monitor ECG
255
Q

What is the clinical diagnosis go hypertension?

A

BP > 140/90 mmHg

256
Q

Name 4 conditions that hypertension is a major risk factor for

A
  1. Stroke
  2. MI
  3. HF
  4. Chronic renal failure
  5. Cognitive decline
  6. Premature death
257
Q

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

A

5-7 years

258
Q

What are the blood pressure readings for someone to be diagnosed with Stage 1 hypertension?

A

Clinic BP = 140/90

ABPM = 135/85

259
Q

What are the blood pressure readings for someone to be diagnosed with Stage 2 hypertension?

A

Clinic BP = 160/100

ABPM = 150/95

260
Q

What are the blood pressure readings for someone to be diagnosed with severe hypertension?

A

Systolic BP = >180

Diastolic BP = >110

261
Q

Name the 2 types of hypertension

A
  1. Essential (primary) hypertension

2. Secondary hypertension

262
Q

What causes essential hypertension?

A

Unknown cause

263
Q

Give 5 causes of secondary hypertension

A
  1. Renal disease
  2. Genetics and FH
  3. Pregnancy
  4. Endocrine
  5. Cortication of the aorta
  6. Drug therapy - cocaine, OCP, NSAIDs
264
Q

Name 3 endocrine disease that can cause secondary hypertension

A
  1. Conn’s syndrome - hyperaldosteronism
  2. Cushing’s syndrome - excess cortisol –> increase BP
  3. Phaemochromocytoma - adrenal gland tumour, excess catecholamines –> high BP
265
Q

Name 5 risk factor for hypertension

A
  1. Increasing age
  2. FH
  3. Obesity
  4. Sedentary lifestyle
  5. Alcohol intake
  6. High slat intake
  7. Diabetes
266
Q

What is the clinical presentation of hypertension?

A

Usually asymptomatic

Found on screening

267
Q

Why might you examine the eyes of someone with hypertension?

A

Very high BP can cause immediate damage to small vessels –> seen in the eyes –> retinopathy

268
Q

What investigations might you do in someone with hypertension?

A
  1. 24 hour ambulatory blood pressure monitoring –> confirm diagnosis
  2. ECG and Bloods –> identify secondary causes
269
Q

What are the treatment target for the following:

a) People aged <80?
b) People aged >80?

A

a) < 140/90 mmHg

b) < 150/90 mmHg

270
Q

What are the 2 main types of treatment for hypertension?

A
  1. Lifestyle modifications - reduce salt, loss weight, reduce alcohol
  2. Drug therapy = ACD
271
Q

Describe the pharmacological intervention for someone with hypertension

A
  1. ACEi - ramipril (or ARB - candesartan if ACEi contraindicated)
  2. Calcium channel blocker - amlodipine, diltiazem, verapamil
  3. Diuretics - bendroflumethethizaide, furosemide
272
Q

What other pharmacological interventions might you give to someone with hypertension (except ACD)?

A

Beta blockers - bisoprolol

273
Q

Will anti-hypertensives make someone feel better?

A

No, usually treating hypertension doesn’t relive symptoms except headache

274
Q

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

A

1 tablet = 10 mmHg reduction in BP

275
Q

What is cor pulmonale?

A

RV hypertrophy and dilation due to pulmonary hypertension

276
Q

Write an equation for BP

A

BP = CO x TPR

277
Q

Name 2 systems that are targeted pharmacologically in the treatment of hypertension

A
  1. RAAS

2. Synpathetic nervous system

278
Q

Give 4 functions of angiontensin II

A
  1. Potent vasoconstrictor
  2. Activated sympathetic nervous system - increased NAd
  3. Activates aldosterone - Na+ retention
  4. Vascular growth, hyperplasia and hypertrophy
279
Q

Give 3 ways in which the Sympathetic nervous system (NAd) leads to increased BP

A
  1. Noradrenaline is a vasoconstrictor = increase TPR
  2. NAd has positive chronotropic and inotropic effects
  3. It can cause increase renin release
280
Q

In what diseases are ACE inhibitors clinically indicated?

A
  1. Hypertension
  2. Heart failure
  3. Diabetic nephropathy
281
Q

Name 3 ACE inhibitors

A
  1. Ramipril
  2. Enalapril
  3. Perindopril
  4. Trandolapril
  5. Lisinopril
282
Q

Give 4 potential side effects of ACE inhibitors due to reduced angiontensin II formation

A
  1. Hypotension
  2. Hyperkalaemia
  3. Acute renal failure
  4. Teratogenic
283
Q

Give 2 potential side effects of ACE inhibitors due to increased kinin production

A
  1. Cough
  2. Rash
  3. Anaphylactoid reaction
284
Q

Why do ACE inhibitors lead to increased kinin production?

A

ACE also converts bradykinin to inactive peptides

So ACE inhibitors lead to build up of kinin

285
Q

You see a patient who is taking ramipril. They say that since starting the medication they have had a dry and persistent cough. What might have caused this?

A

ACE inhibitors lead to a build up of kinin

One of the side effects of this is a dry and chronic cough

286
Q

What are ARBs?

A

Angiotensin II receptor blockers

287
Q

At which receptor do ARB’s work?

A

AT-1 receptor - prevent angiotensin II binding

288
Q

In what diseases are ARBs clinically indicated?

A
  1. Hypertension
  2. Heart failure
  3. Diabetic nephropathy
289
Q

Name 3 ARBs

A
  1. Candesartan
  2. Valsartan
  3. Losartan
290
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 ARB

e.g. candesartan

291
Q

Give 4 potential side effect of ARBs

A
  1. Hypotension
  2. Hyperkalaemia
  3. Renal dysfunction
  4. Rash
    Contraindicated in pregnancy
292
Q

In what diseases are calcium channel blockers clinically indicated?

A
  1. Hypertension
  2. IHD
  3. Arrhythmia
293
Q

Name 2 calcium channel blockers

A
  1. Amlopipine
  2. Felodipine
  3. Diltiazem
  4. Verapamil
294
Q

Name 2 dihydropyridines and briefly explain how they work

A

Class of CCBs
Amlodipine and felodipine
Arterial vasodilators

295
Q

Name a calcium channel blocker that acts primarily on the heart

A

Verapamil

Negatively chronotropic and inotropic (reduce HR and force of contraction)

296
Q

Name a CCB that acts on the heart and on blood vessels

A

Diltiazem

297
Q

On what channels do CCB work?

A

L type Ca2+ channels

298
Q

Give 3 potential side effects that are due to the vasodilatory ability of CCBs

A
  1. Flushing
  2. Headache
  3. Oedema
  4. Palpitations
299
Q

Give 2 potential side effects that are due to the negatively chronotropic ability of CCBs

A
  1. Bradycardia
  2. Atrioventricular block
  3. Postural hypotension
300
Q

Give a potential side effect that is due to the negatively inotropic ability of CCBs

A

Worsening cardiac failure

301
Q

Give 4 potential side effects of verapamil

A
  1. Worsening of cardiac failure (-ve inotrope)
  2. Bradycardia (-ve chronotrope)
  3. Atrioventricular block (-ve chronotrope)
  4. Constipation
302
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

303
Q

In what diseases are beta blockers clinically indicated?

A
  1. IHD
  2. Heart failure
  3. Arrhythmia
  4. Hypertension
304
Q

Name 3 beta blockers

A
  1. Bisoprolol (beta 1 elective)
  2. Atenolol
  3. Propranolol (beta 1/2 nonselective)
305
Q

Give 5 potential side effects of beta blockers

A
  1. Fatigue
  2. Headache
  3. Sleep disturbances/nightmares
  4. Bradycardia
  5. Hypotension
  6. Cold peripheries
  7. Erectile dysfunction
  8. Bronchospasm
306
Q

Give 3 conditions in which Beta blockers can worsen them

A
  1. Asthma or COPD
  2. PVD
  3. Heart failure
307
Q

In what diseases are diuretics clinically indicated?

A
  1. Heart failure

2. Hypertension

308
Q

Name 4 classes of diuretics

A
  1. Thiazides
  2. Loop
  3. Potassium sparing
  4. Aldosterone antagonists
309
Q

Where in the kidney do thiazide diuretics work?

A

The distal tubule

310
Q

Name a thiazide

A

Bendroflumethethiazide

311
Q

Name a loop diuretic

A

Furosemide

Bumetanide

312
Q

Name a potassium sparing diuretic

A

Spironolactone

Eplerenone

313
Q

Why are potassium sparing diuretics especially effective?

A

They have anti-aldosterone effects too

314
Q

Give 5 potential side effects of diuretics

A
  1. Hypovolaemia
  2. Hypotension
  3. Reduced serum Na+, K+, Mg+, Ca2+
  4. Increased uric acid –> gout
  5. Erectile dysfunciton
  6. Impaired glucose tolerance
315
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

316
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

317
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

318
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

319
Q

What is the counter regulatory system to RAAS?

A

Atrial Natriuretic Peptide/BNP (ventricular natriuretic peptide) hormones

320
Q

Where are ANP and BNP produced?

A

The heart

321
Q

What metabolises ANP and BNP?

A

Neprilysin (NEP)

322
Q

What are the functions of ANP and BNP?

A
  1. Increased renal excretion of Na+ and water
  2. Vasodilators
  3. Inhibit aldosterone release
323
Q

Why can Neprilysin (NEP) inhibitors work for heart failure treatment?

A

NEP metabolises ANP and BNP

NEP inhibitors therefore increase levels of ANP and BNP in the serum

324
Q

In what diseases are nitrates clinically indicated?

A
  1. IHD

2. Heart failure

325
Q

Name 2 nitrates that are used pharmacologically

A
  1. GTN spray (short acting)

2. Isosorbide mononitrate (long acting)

326
Q

How do nitrates work in the treatment of heart failure?

A

They are venodilators so reduce preload and therefore BP

327
Q

Give 2 potential side effects of nitrates

A
  1. Headache
  2. GTN syncope
  3. Tolerance
328
Q

How do anti-arrhythmic drugs work?

A

Interfere with the action potential of the heart in different phases

329
Q

What classification is used to group anti-arrhythmic drugs?

A

Vaughan Williams classification

330
Q

Name two class 1 drugs of the Vaughan Williams classification

A

Class 1 are Na+ channel blockers
1a = disopyramide, quinidine
1b = lidocaine
1c = flecainide (tachycardias)

331
Q

Name three class 2 drugs of the Vaughan Williams classification

A

Class 2 are Beta blockers
Propranolol
Atenolol
Bisoprolol

332
Q

Name a class 3 drug of the Vaughan Williams classification

A

Class 3 rugs prolong the action potential
Amiodarone
Side effects are likely with these

333
Q

Name two class 4 drugs of the Vaughan Williams classification

A

Class 4 drugs are calcium channel blockers (but NOT dihydropyridines as they don’t effect the heart)
Verapamil
Dilitiazem

334
Q

How does digoxin work?

A

Inhibits the Na+/K+ pump therefore making the action potential more positive and ACh is released from parasympathetic nerves

335
Q

What are the main effect of digoxin?

A
  1. Bradycardia
  2. Reduced atrioventricular conduction
  3. Increased force of contraction (positive inotrope)
336
Q

Give 3 potential side effects of digoxin

A
  1. Nausea
  2. Vomiting
  3. Diarrhoea
  4. Confusion
    Also has a narrow therapeutic range
337
Q

In what disease is digoxin clinically indicated?

A
  1. Atrial fibrillation

2. Severe heart failure

338
Q

What does furosemide block?

A

The Na+/K+/2Cl- transporter

339
Q

Why are beta blockers good in chronic heart failure?

A

They block reflex sympathetic responses which stress the failing heart

340
Q

How do beta blockers provide symptom relief in angina?

A
  1. They reduce O2 demand by slowing heart rate (negative chronotrope)
  2. They reduce O2 demand by reducing myocardial contractility (negative inotrope)
  3. They increase O2 distribution by slowing heart rate
341
Q

What drug might you give to someone with angina caused by coronary artery vasospasm?

A

Amlodipine

342
Q

How does amiodarone work?

A

Prolongs action potential by delaying depolarisation

343
Q

Name 4 potential effects of amiodarone

A
  1. QT prolongation
  2. Interstitial lung disease
  3. Hypothyroidism
  4. Abnormal liver enzymes
344
Q

Name a disease that might cause flattening of the P wave

A
  1. Hyperkalaemia

2. Obesity

345
Q

Name a disease that might cause tall P waves

A

Right atrial enlargement

346
Q

Name a disease that might cause broad notched P waves

A

Left atrial enlargement

347
Q

What aspect of the heart is represented by leads II, III and aVF?

A

Inferior aspect

348
Q

What might ST elevation in leads II, II and aVF suggest?

A

RCA blockage

Leads represent inferior aspect of heart, RCA supplies inferior aspect

349
Q

Give 3 effects hyperkalaemia on an ECG

A
  1. Tall tented T waves
  2. Flat P waves
  3. Broad QRS
350
Q

Give 2 effects of hypokalaemia on an ECG

A
  1. Flat T waves
  2. QT prolongation
  3. ST depression
  4. Prominent U waves
351
Q

Give an effect go hypocalcaemia on an ECG

A
  1. QT prolongation
  2. T wave flattening
  3. Narrowed QRS
  4. Prominent U waves
352
Q

Give an effect of hypercalcaemia on an ECG

A
  1. QT shortening
  2. Tall T wave
  3. No P waves
353
Q

What controls the sinus node discharge rate?

A

Autonomic nervous system

354
Q

Define sinus rhythm

A

A P wave precedes each QRS complex

355
Q

Define cardiac arrhythmia

A

Abnormality of cardiac rhythm

356
Q

Give 3 potential consequences of arrhythmia

A
  1. Sudden death
  2. Syncope
  3. Heart failure
  4. Chest pain
  5. Palpitations
    May also be asymptomatic
357
Q

Define bradycardia

A

< 60 bpm

358
Q

Define tachycardia

A

> 100 bpm

359
Q

Give 2 causes of bradycardia

A
  1. Conduction tissue fibrosis
  2. Ischaemia
  3. Inflammation/infiltrative disease
  4. Drugs
360
Q

Give 2 broad categories of tachycardia

A
  1. Supraventricular tachycardias

2. Ventricular tachycardias

361
Q

Where do supra-ventricular tachycardia’s arise from?

A

Atria or atrio-ventricular junction

362
Q

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

A

Narrow QRS complexes

363
Q

Name 3 types of supraventricular tachycardia

A
  1. Atrial fibrillation
  2. Atrial flutter
  3. AV node re-entry tachycardia
  4. AV re-entry tachycardia (accessory pathway)
364
Q

Where do ventricular tachycardia’s arise from?

A

The ventricles

365
Q

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

A

Broad QRS compelxes

366
Q

What is the commonest supra-ventricular tachycardia?

A

AV node re-entry tachycardia (AVNRT)

367
Q

Do you see P waves in AVNRT?

A

Loss of P waves

368
Q

Give 4 symptoms of AVNRT

A
  1. Sudden onset/offset palpitations
  2. Neck pulsation
  3. Chest pain
  4. SOB
369
Q

Describe the acute treatment of AVNRT

A

Vagal manoeuvre, catheter ablation and adenosine (block AVN to terminate the SVT)

370
Q

What drugs might you give someone to suppress further episodes of AVNRT?

A

Beta blockers, CCB

371
Q

Describe the pathophysiology of AVRT (accessory) arrhythmias

A

Congenital muscle strands connect atria and ventricles = accessory pathway
Result in pre-excitaiton of ventricles

372
Q

Describe 3 characteristics of an ECG from someone with accessory pathway arrhythmia

A
  1. Delta wave
  2. Short PR interval
  3. Slurred QRS complex
373
Q

Give an example of an AVRT (accessory) arrhythmia

A

Wolff-Parkinson-White Syndrome

374
Q

Give 4 causes of sinus tachycardia

A
  1. Physiological response to exercise
  2. Fever
  3. Anaemia
  4. Heart failure
  5. Hypovolaemia
375
Q

Why do ventricular tachycardia’s arise?

A

Extra circuits in ventricles or abnormal muscle depolarisation
Can come from previous MI or cardiomyopathy

376
Q

What ECG changes might you see with someone with ventricular tachycardia?

A

Crescendo-decrescendo amplitude = torsades de pointes

377
Q

What is the treatment for ventricular tachycardia in an urgent situation?

A

DC cardioversion

378
Q

What is long term treatment for ventricular tachycardia in high risk patients

A

Implantable cardioverter defibrillator (ICD)

379
Q

What is the treatment for stable ventricular tachycardia?

A

IV beta blockers and IV amiodarone

380
Q

Define atrial fibrillation

A

Chaotic irregular atrial rhythm at 300-600 bpm

381
Q

Give 4 symptoms of atrial fibrillation

A
  1. SOB
  2. Chest pain
  3. Palpitations
  4. Syncope
382
Q

Name 3 causes of atrial fibrillation

A
  1. Idiopathic
  2. Hypertension
  3. IHD
  4. Mitral valve stenosis
  5. PE
  6. HF
383
Q

Briefly describe the pathophysiology of atrial fibrillation

A

Chaotic irregular atrial rhythm –> AV response = irregular ventricular rhythm

384
Q

Describe 2 characterics of an ECG taken from someone with atrial fibrillation

A
  1. Absent P aves
  2. Irregular QRS complexes
  3. Fine oscillation of the baseline
    Irregularly irregular
385
Q

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

A

CHADS2 VAS

386
Q

What does the CHADS2 VASc score take into account

A 
CCF
HTN
Age (>75) = 2 points
DM
Stroke (previous) = 2 points
Vascular disease
Age 65-74 
Sex (female)

Score >1 = anticoagulation

387
Q

Describe the treatment for atrial fibrillation

A
  1. Treat underlying cause
  2. Rate control - BB, CCB and digoxin
  3. Rhythm control 0 electrical cardioversion or pharmacological cardioversion using flecainide
  4. Felcainide can be taken on a PRN basis in people with infrequent systemic paroxysms of AF
  5. Long term - catheter ablation and a pacemaker
388
Q

What might you give someone to help with rate control in atrial fibrillation?

A

BB, CCB and digoxin

389
Q

What might you give someone to help restore sinus rhythm in atrial fibrillation?

A

Electrical cardioversion or pharmacological cardioversion using flecainide

390
Q

What is the long term treatment for atrial fibrillation?

A

Catheter ablation

391
Q

What is atrial flutter?

A

Fast but organised waves in the atrium

Atrial rate 250-350 bpm

392
Q

Describe the ECG pattern taken from someone with atrial flutter

A
  1. Narrow QRS

2. Saw tooth flutter waves

393
Q

Describe the pathophysiology of atrial flutter

A

Re-entry mechanism - blockage of normal circuit

Another pathway forms, takes different course and re-enters the circuit –> tachycardia

394
Q

What are ectopic beats?

A

Non sustained beats arising from ectopic regions of atria or ventricles
Very common, generally benign arrhythmias caused by premature discharge

395
Q

What are ventricular ectopics?

A

Extra ventricular contractions –> palpitations/heart missing a beat

396
Q

Give 3 causes of long QT syndrome

A
  1. Congenital
  2. Electrolyte disturbances - hypokalaemia, hypocalcaemia
  3. Drugs
397
Q

Give 2 signs of long QT syndrome

A
  1. Palpitations

2. Syncope

398
Q

Where can heart blocks occur?

A
  1. Block in either AVN or bundle of His = AV block

2. Block lower in conduction system = Bundle Branch Block

399
Q

Describe a first degree AV block

A

Fixed prolongation of the PR interval due to delayed conduction to the ventricles

400
Q

Describe a second degree AV block

A

There are more P waves to QRS complexes because some atrial impulses fail to reach the ventricles

401
Q

Describe a Mobitz type 1 second degree AV block

A

PR interval gradually increases until AV node fails and no QRS is seen

402
Q

Describe a Mobitz type 2 second degree AV block

A

Sudden unpredictable loss of AV conduction and so loss of QRS
PR interval is constant but every nth QRS is missing

403
Q

Describe a third degree AV block

A

Atrial activity fails to conduct to the ventricles

P waves and QRS complexes occur independently

404
Q

What are the treatments for AV heart blocks?

A

1st = asymptomatic, watch and wait –> atropine
Mobitz 1 = no pacemaker
Mobitz 2 = pacemaker
3rd = permanent pacemaker

405
Q

Give 4 causes of heart block

A
  1. Coronary artery disease
  2. Cardiomyopathy
  3. Fibrosis
  4. Previous MI
406
Q

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

A

Right bundle branch block (RBBB) and Left bundle branch block (LBBB)

407
Q

Explain the pathophysiology of a BBB

A

Lack of simultaneous ventricular contractions
LBBB = R before L
RBBB = L before R

408
Q

What changes would you see on an ECG from someone with a LBBB?

A

A ‘W’ Shape would be seen in QRS complex of Lead V1
‘M’ shape seen in V6
WiLLiaM

409
Q

What changes would you see on an ECG from someone with a RBBB?

A

A ‘M’ Shape would be seen in QRS complex of Lead V1
‘W’ shape seen in V6
MaRRoW

410
Q

Cardiac arrhythmias: what is the treatment of choice in a patient who is hemodynamically unstable due to the underlying rhythm?

A

DC cardioversion

411
Q

Name 4 valvular heart diseases

A
  1. Aortic stenosis
  2. Mitral regurgitation
  3. Mitral stenosis
  4. Aortic regurgitation
412
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

413
Q

Name the 3 types of aortic stenosis

A
  1. Surpavalvular
  2. Subvalvular
  3. Valvular = most common
414
Q

What are the causes of aortic stenosis?

A
  1. Congenital bicuspid valve

2. Acquired –> age related degenerative calcification and rheumatic heart disease

415
Q

Describe the pathophysiology of aortic stenosis

A

Aortic orifice is restricted by calcific deposits
Pressure gradient develops between LV and aorta
LV function initially maintained due to compensatory hypertrophy
Mechanism become exhausted = LV failure

416
Q

Give 3 symptoms of aortic stenosis

A

Occur when valve area is 1/4 of normal (normal - 3-4 cm2)

  1. Exertional syncope
  2. Angina
  3. Exertional dyspnoea
417
Q

Give 3 signs of aortic stenosis

A
  1. Slow rising carotid pulse (pulsus tradus) and decreased pulse amplitude (pulsus parvus)
  2. Soft or absent heart sounds
  3. Ejection systolic murmur - crescendo-decrescendo character
418
Q

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

A

Echocardiography - assess LV size and function and doppler derived gradient and valve area
High gradient = severe stenosis

419
Q

Describe the management for someone with aortic stenosis

A
  1. Ensure good dental hygiene
  2. Consider IE prophylaxis
  3. Aortic valve replacement or Transcatheter aortic valve replacement (TAVI)
420
Q

Why does medical intervention have a limited role in aortic and mitral stenosis treatment?

A

Aortic and mitral stenosis are mechanical problems

421
Q

Who should be offered an aortic valve replacement?

A
  1. Symptomatic patient with AS
  2. Any patient with decreasing ejection fraction
  3. Any patient undergoing CABG with moderate/severe AS
422
Q

What is mitral regurgitation?

A

Backflow of blood from the LV to the LA during systole

LV volume overload

423
Q

What can cause mitral regurgitation?

A
  1. Myxomatous degeneration (mitral valve prolapse)
  2. Ischaemic mitral valve
  3. Rheumatic heart disease
  4. IE
424
Q

Describe the pathophysiology of mitral regurgitation

A

LV volume overload
Compensatory mechanism = LA enlargement, LVH and increase contractility
Progressive LV volume overload –> dilation and progressive HF

425
Q

Give 2 symptoms of mitral regurgitation

A
  1. Dyspnoea on exertion
  2. HF
  3. Fatigue and lethargy
426
Q

Give 3 signs of mitral regurgitation

A
  1. Pan-systolic murmur
  2. Soft 1st heart sound
  3. 3rd heart sound
    In chronic MR, intensity of murmur correlates with severity
427
Q

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

A
  1. ECG
  2. CXR
  3. Echo - estimates LA/LV size and function
428
Q

What is the management of mitral regurgitation?

A 
Rate control for AF - BB, CCB, digoxin
ACEi = vasodilator 
Anticoagulation for AF 
Diuretics for fluid overload 
IE prophylaxis 
If symptomatic = surgery
429
Q

What is aortic regurgitation?

A

Leakage of blood into LV from aorta duding diastole due to ineffective coaptation of aortic cusps

430
Q

What causes aortic regurgitation?

A
  1. Bicuspid aortic valve
  2. Rheumatic fever
  3. IE
431
Q

Describe the pathophysiology of aortic regurgitation

A

Pressure and volume overload
Compensatory mechanism = LV dilation, LVH
Progressive dilation –> HF

432
Q

Give 3 symptoms of aortic regurgitation

A
  1. Dyspnoea on exertion
  2. Orthopnoea
  3. Palpitations
  4. Paroxysmal nocturnal dyspnea
433
Q

Give 3 signs of aortic regurgitation

A
  1. Diastolic blowing murmur
  2. Wide pulse pressure
  3. Systolic ejection murmur
434
Q

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

A

CXR - cardiomegaly, aortic root enlargement

ECHO - LV size and function and aortic root evaluation

435
Q

Describe the management for someone with aortic regurgitation

A

IE prophylaxis
ACEi = vasodilators
Regular echos - motion progression
Surgery if symptomatic

436
Q

What is mitral stenosis?

A

Obstruction of LV inflow that prevents proper filling during diastole

437
Q

Name 3 causes of mitral stenosis

A
  1. Rheumatic heart disease
  2. IE
  3. Mitral annular calcification
438
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
439
Q

Give 3 symptoms of mitral stenosis

A
  1. Dyspnoea
  2. Haemoptysis
  3. RHF symptoms
440
Q

Give 3 signs of mitral stenosis

A
  1. ‘a’ wave in jugular venous pulsations
  2. Signs of RHF
  3. Pink patches on cheeks due to vasoconstriction
  4. Low pitched systolic murmur
  5. Loud opening S1 snap
  6. Diastolic murmur
441
Q

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

A
  1. ECG
  2. CXR
  3. Echo - gold standard for diagnosis
442
Q

Describe the management for mitral stenosis

A 
If in AF rate control - BB, CCB 
Anticoagulation if AF 
Diuretics for fluid overload
Percutaneous mitral balloon valvotomy 
Mitral vale replacement 
IE prophylaxis
443
Q

In what type of valvular heart disease would you hear a mid-diastolic murmur and a 1st heart sound snap?

A

Mitral stenosis

444
Q

In what type of valvular heart disease would you hear a pan systolic murmur?

A

Mitral regurgitation

445
Q

In what type of valvular heart disease would you hear an ejection systolic murmur?

A

Aortic stenosis

446
Q

In what type of valvular heart disease would you see a wide pulse pressure and hear an early diastolic blowing murmur and systolic ejection murmur?

A

Aortic regurgitation

447
Q

What is infective endocarditis?

A

Infection of heart valve/s or other endocardial lined structure within the heart

448
Q

Name 4 types of IE

A
  1. Left sided native IE
  2. Left sided prosthetic IE
  3. Right sided IE
  4. Device related IE (pacemaker, defibrillators)
449
Q

Which type of IE is more likely to spread systemically?

A

Left sided IE - more likely to cause thrombo-emboli

Right sided IE could spread to the lungs

450
Q

Give 2 risk factors for IE

A
  1. Having a regurgitant o prosthetic valve
  2. If infectious material is introduced into blood stream (drugs) or during surgery
  3. Poor dental hygiene and dental treatment
451
Q

Which bacteria are most likely to cause IE?

A
  1. Staphylococcus aureus
  2. Staphlococcus epidermidi (coagulase negative staph)
  3. Streptococcus viridian’s (alpha haemolytic)
452
Q

Give 3 groups of people who are at risk of IE

A
  1. Elderly
  2. IV drug users
  3. Those would prosthetic valves
  4. Those with rheumatic fever
  5. Young with congenital heart disease
453
Q

Describe the pathophysiology of IE

A

Microbial adherence (infection) –> vegetation on valve –> cardiac valve distortion –> cardiac failure and septic problems

454
Q

What is the hallmark of IE?

A

Vegetation - lumps of fibrin hanging of heart valves

455
Q

Name 2 sites where vegetation is likely in IE

A
  1. Atrial surface of AV valves

2. Ventricular surface of SL valves

456
Q

Give 3 symptoms of IE

A
  1. Signs of systemic infections - fever, sweats etc
  2. Embolism - stroke, PE, MI
  3. Valve dysfunction - HF, arrhythmia
457
Q

Give 4 signs of IE

A
  1. Splinter haemorrhages
  2. Osler’s nodes
  3. Janeway lesions
  4. Roth spots
  5. Heart murmurs
458
Q

Name the criteria that I used in the diagnosis of IE

A

Duke’s criteria

459
Q

Give the 2 major points in the Duke’s criteria that if presence can confirm a diagnosis of IE

A
  1. Positive blood culture with typical IE micro-organism

2. Positive echo showing endocardial involvement

460
Q

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

A
  1. Blood cultures - essential
  2. Echo - TTE ot TOE
  3. Bloods - raised ESR and CRP
  4. ECG
461
Q

Give 2 advantages and 1 disadvantage of a trans-thoarcic echo (TTE)

A 
Advantages:
1. Safe
2. Non-invasive, no discomfort 
Disadvantage:
1. Poor images
462
Q

Give 1 advantage and 2 disadvantages of a trans-oesophageal echo (TOE)

A 
Advantage:
1. Excellent images 
Disadvantage:
1. Discomfort 
2. Small risk of perforation or aspiration
463
Q

Describe the treatment for IE

A
  1. Antibiotics based on cultures
  2. Treat any complications
  3. Surgery - remove and replace valve
464
Q

Give 4 indications for surgery in IE

A
  1. Antibiotics not working
  2. Complications
  3. To remove infected devices
  4. To replace valve after infection cured
  5. To remove large vegetations before they embolism
465
Q

Why is it important to remove large vegetations?

A

To prevent them embolising and causing a stroke, MI etc

466
Q

Why might blood cultures be negative in a person with IE?

A

They may have previously received antibiotics

467
Q

Name 2 drugs that can prolong the QT interval

A
  1. Sotalol

2 Amiodarone

468
Q

Give 5 potential side effects of drugs that prolong the QT interval

A
  1. Pro-arrhythmic effects
  2. Interstitial pneumonitis
  3. Abnormal liver function
  4. Hyper/hyopthyroidism
  5. Sun sensitivity
  6. Grey skin discolourations
  7. Corneal micro-deposits
  8. Optic neuroapthy
469
Q

How do sodium channel blockers work in the treatment of ventricular tachycardia?

A

Block the inactivation gate of the sodium channel

470
Q

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

A

It can also block sodium channels

471
Q

Define shock

A

Acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in generalised hypoxia and/or an inability of the cells to utilise oxygen

472
Q

Give 6 symptoms/signs of shock

A
  1. Pale
  2. Sweaty
  3. Cold
  4. Pulse is weak and rapid
  5. Reduced urine output
  6. Confusion
  7. Weakness/collapse
  8. Low BP
473
Q

Name 5 types of shock

A
  1. Hypovolaemic
  2. Haemorrhagic
  3. Septic
  4. Anaphylactic
  5. Neurogenic
  6. Cardiogenic
474
Q

What can cause hypovolaemic shock?

A
  1. Loss of blood = acute GI bleeding, trauma, post-op, splenic rupture
  2. Loss of fluid = dehydration, burns, vomiting , pancreatitis
475
Q

What can cause cariogenic shock?

A
  1. Cardiac tamponade
  2. PE
  3. Acute MI
  4. Fluid overload
  5. Myocarditis
476
Q

What is septic shock?

A

A systemic inflammatory response associated with an infection (bacterial endotoxins)

477
Q

What is anaphylactic shock?

A

An intense allergic reaction associated with massive histamine release = haemodyanmic collapse
Patient may be breathless, wheezy and have a rash

478
Q

What is the treatment for anaphylactic shock?

A

Adrenaline and supportive therapy - O2 delivery, fluid replacement

479
Q

What is the treatment for shock?

A

ABC

480
Q

Classification of shock: describe the vital signs in class 1 e.g. blood loss, pulse, blood pressure, pulse pressure, respiratory rate and urine output.

A
  1. 15% blood loss
  2. Pulse < 100 bpm
  3. Blood pressure - normal
  4. Pulse pressure - normal
  5. Respiratory rate: 14 - 20
  6. Urine output > 30ml/h
481
Q

Classification of shock: describe the vital signs in class 2 e.g. blood loss, pulse, blood pressure, pulse pressure, respiratory rate and urine output.

A
  1. 15-30% blood loss
  2. Pulse > 100 bpm
  3. Blood pressure - normal
  4. Pulse pressure - decreased
  5. Respiratory rate: 20 - 30
  6. Urine output: 20 - 30ml/h
482
Q

Classification of shock: describe the vital signs in class 3 e.g. blood loss, pulse, blood pressure, pulse pressure, respiratory rate and urine output.

A
  1. 30-40% blood loss
  2. Pulse > 120 bpm
  3. Blood pressure - decreased
  4. Pulse pressure - decreased
  5. Respiratory rate: 30 - 40
  6. Urine output: 5 - 15ml/h
483
Q

What are the 4 main features of tetralogy of fallot?

A
  1. Ventricular septal defect
  2. Over-riding aorta
  3. RV hypertrophy
  4. Pulmonary stenosis
484
Q

Would a baby born with tetralogy of fallot be cyanotic?

A

YES
RV pressure higher than LV
Blood passes from RV to LV so patients are blue = cyanosis

485
Q

What is VSD?

A

Ventricular septal defect = abnormal connection between the 2 ventricles

486
Q

Would a baby born with VSD cyanotic?

A

NO
High pressure in LV than RV so blood shunted from left to right
Increased amount of blood going to the lungs
Not cyanotic

487
Q

Give 4 clinical sins of a large VSD

A
  1. High pulmonary signs of a large VSD
  2. Breathless, poor feeding, failure to thrive
  3. Increased respiratory rate
  4. Tachycardia
  5. Requires surgical repair
488
Q

Give 2 clinical signs of a small VSD

A

Asymptomatic
No intervention needed
Loud systolic murmur

489
Q

What syndrome might VSD lead on to?

A

Eisenmengers syndrome

490
Q

Briefly decscribe the pathophysiology if Eisenmengers syndrome

A

High pressure pulmonary blood flow damages pulmonary vasculature –> increase in resistance to blood flow (pulmonary hypertension) –> RV pressure increase –> shunt direction reverses (RV to LV) = cynanosis

491
Q

What are the risks associated with Eisenmengers syndrome?

A
  1. Risk of death
  2. Endocarditis
  3. Stroke
492
Q

What is ASD?

A

Atrial septal defect = abnormal connection between the two atria

493
Q

Would a baby born with ASD be cyanotic?

A

NO

Higher pressure in the LA than the RA and so blood is shunted from the left to right

494
Q

Give 5 clinical signs of a large ASD

A
  1. Significant increased flow through right heart and lungs = pulmonary flow murmur
  2. Right heart dilation
  3. Enlarged pulmonary arteries
  4. SOB on exertion
  5. Increased chest infections
495
Q

Give 3 signs of a small ASD

A

Asymptomatic
No right heart dilation
Increases with age but left alone

496
Q

How are ASDs closed?

A

Surgically

Percutaneous (key hole)

497
Q

What is AVSD?

A

Atrio-ventricular septal defects
Basically a hole in the very centre of the heart
Involves the ventricular septum, atrial septum and the mitral and tricuspid valves
Can be complete or partial

498
Q

What happens to the AV valves in AVSD?

A

Instead of 2 separate AV valves there is 1 big malformed one

Usually leaks to a greater or lesser degree

499
Q

Give 2 clinical signs of AVSD

A
  1. Breathlessness

2. Poor feeding and weight gain

500
Q

Does a AVSD need surgical repair?

A

Complete AVSD needs repair

Partial can be left alone if no right heart dilation

501
Q

What is PDA?

A

Patent ductus arteriosus = persistent communication between proximal left pulmonary artery and descending aorta

502
Q

Give 4 clinical signs of PDA

A
  1. Torrential flow from aorta to pulmonary arteries can lead to hypertension and RHF
  2. Breathless
  3. Poor feeding, failure to thrive
  4. Risk of endocarditis
503
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

504
Q

What happens with severe coarctation of the aorta?

A

Complete or almost complete obstruction to aortic flow
Collapse with heart failure
Needs urgent repair

505
Q

How does mild coarctation of the aorta present?

A

Presents with hypertension
Incidental murmur
Should be repaired to try to prevent problems in the long term

506
Q

What long term problems can occur due to coarctation of the aorta?

A

Hypertension - early CAD, early stroke, subarachnoid haemorrhage
Re-coarctation requiring repeat intervention
Aneurysm formation at the site of repair

507
Q

What is pulmonary stenosis?

A

Narrowing of the RV outflow tract

508
Q

How does a patient present with pulmonary stenosis?

A 
Right ventricular failure 
Collapse 
Poor pulmonary blood flow 
RVH 
Tricuspid regurgitation
509
Q

How is pulmonary stenosis treated?

A

Ballon valvuloplasty
Open valvotomy
Open trans-annular patch
Shunt (to bypass blockage)

510
Q

What are 3 problems with a bicuspid aortic valve?

A
  1. Degenerate quicker than normal valves
  2. Become regurgitant earlier than normal valves
  3. Associated with coarctation and dilation of ascending aorta
511
Q

Name 3 congenital heart defect that are not cyanotic

A
  1. VSD
  2. ASD
  3. PDA
    Left to right shunt
512
Q

Name a congenital heart defect that is cyanotic

A
  1. Tetralogy of Fallot

Right to left shunt

513
Q

Why does mitral stenosis cause AF?

A

Increased LA pressure

Stretches myocytes in the atria and irritates pacemaker cells –> AF

514
Q

Why does mitral stenosis lead to a raised JVP?

A

Pulmonary congestion –> pulmonary hypertension causing a raised JVP

515
Q

What is Dressler’s syndrome?

A

Myocardial injury stimulates formation of autoantibodies against the heart
Cardiac tamponade may occur
Dressler’s is a secondary form of pericarditis

516
Q

Give 3 symptoms of Dressler’s syndrome

A
  1. Fever
  2. Chest pain
  3. Pericardial rub
    Occurs 2-10 weeks after MI
517
Q

Write an equation for mAP

A

mAP = DP + 1/3PP

518
Q

Give the equation for stroke volume

A

SV = EDV - ESV

519
Q

What is a consequence of peripheral arterial occlusion?

A

Gangrene

520
Q

Give 2 diseases that result from stress induced ischaemia

A
  1. Exercise induced angina

2. Intermittent claudication

521
Q

Give 2 disease that result from ischaemia due to structural/functional breakdown

A
  1. Critical limb ischaemia

2. Vascular dementia

522
Q

Give a sign infarction

A

Gangrene

523
Q

Name the classification system for Peripheral vascular disease (PVD)

A

Fontaine classification

524
Q

What is intermittent claudication?

A

A symptom describing muscle pain that is caused by moderate ischaemia
Intermittent claudication occurs when exercising (stress induced) and is relieved with rest

525
Q

What can intermittent claudication lead on to if left untreated?

A

Critical ischaemia

526
Q

Intermittent claudication: is O2 supply normal or low at rest and when you begin exercise?

A

Normal

Intermittent claudication is stress induced so at rest and when you begin exercise O2 supply is able to meet demand

527
Q

Intermittent claudication: is O2 supply normal or low when you do moderate/hard exercise?

A

Low

O2 supply is unable to meet demand –> anaerobic respiration –> lactic acid

528
Q

Intermittent claudication: is O2 supply normal or low after a short rest?

A

Low
It takes longer to recover as you’re getting rid of the lactic acid
After a long rest = normal

529
Q

Give a symptom of intermittent caludication

A

Muscle cramps

530
Q

Name 2 diseases that are due to moderate ischaemia

A
  1. Angina

2. Intermittent claudication

531
Q

Name a disease that is due to severe ischaemia

A

Critical limb ischaemia

532
Q

Name 3 causes of an aneurysm

A
  1. Atherosclerotic (most common)
  2. Ateriomegaly
  3. Collagen disease - Marfans, vascular Ehlers Danlos
533
Q

How do you treat peripheral vascular disease?

A 
Risk factor modification 
 - Stop smoking 
 - lower cholesterol 
 - control BP, diabetes
 - Aspirin = antiplatelets 
Revascularisation for critical ischaemia 
 - Stent
 - Bypass 
 Open aneurysm repair
Amputation is very severe
534
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

535
Q

Name 2 types of aortic aneurysm

A
  1. Abdominal aortic aneurysm (AAA)

2. Thoracic abdominal aneurysm (TAA)

536
Q

What classifies as an Abdominal aortic aneurysm?

A

> 3 cm

Dilation affects all 3 layers of the vascular tunic

537
Q

Describe the pathophysiology of a thoracic abdominal aneurysm

A

Aorta loses distensibility so that a rise in BP can excess arterial wall strength and many trigger dissection or rupture

538
Q

Describe the pathophysiology of an aortic dissection

A

Tear in intimal lining of aorta –> column of blood under pressure enters aortic wall forming haematoma –> separates intima from adventitia –> false lumen
False lumen extends –> intimal tears

539
Q

Mr newton, a 64-year-old male attends a GP complaining that this week he’s started experiencing some chest pain when he’s out birdwatching. It’s in the centre of his chest and eases off if he sits down for a few minutes. Which of the following would you expect to see on a stress ECG?
a. Saddle shaped ST with PR depression
b. Tall tented T waves and pathological Q waves
c. ST elevation
d. ST depression
e. Absent P waves
What are the others ECG traces for?

A

= ANGINA so…
d. ST depression = Angina

a. Saddle shaped ST with PR depression = Pericarditis
b. Tall tented T waves and pathological Q waves = Hyperkalaemia
c. ST elevation = STEMI
d. ST depression = Angina
e. Absent P waves = AF (irregularly irregular)

540
Q

She has acute pericarditis pain; how does she describe the pain?

a. Sitting –> standing
b. When leaning forward alleviated by lying down
c. When lying down alleviated by leaning forward
d. On inspiration
e. On exertion

A

c. When lying down alleviated by leaning forward

541
Q

Mitral regurgitation, what murmur do you hear?
a. Early diastolic murmur
b. Early systolic click murmur
c. Ejection systolic crescendo-decrescendo murmur
d. End diastolic murmur
e. Pansystolic murmur
What are the others murmurs of?

A

e. Pansystolic murmur = occurs throughout duration of systole = Mitral regurgitation

a. Early diastolic murmur = Mitral stenosis
b. Early systolic click murmur = Mitral valve replacement (click = replacement as metal)
c. Ejection systolic crescendo-decrescendo murmur = Aortic stenosis
d. End diastolic murmur
e. Pansystolic murmur = occurs throughout duration of systole = Mitral regurgitation

542
Q 
Trystan, a 54-year old Caucasian gentleman, attends his annual diabetes check with the nurse practitioner. His BP is 143/82. He’s currently on metformin and simvastatin but reckons three’s a charm and wants another pill. Which is the appropriate anti-hypertensive to give him?
a. Amlodipine 
b. Bendroflumethiazide 
c. Candesartan 
d. Diltiazem 
e. Isomorbide mononitrate (GTN spray) 
What type of drugs are the others?
A

c. Candesartan = ACEi/ARB first line for younger than 55 non afro-Caribbean’s patients with

a. Amlodipine = CCB
b. Bendroflumethiazide = thiazide like diuretic
c. Candesartan = ACEi/ARB first line for younger than 55 non afro-Caribbean’s patients with hypertension

543
Q

What is the mechanism of action of Heparin?
a. Increases cGMP and reduces intracellular Ca2+ concentration
b. Inhibits COX reducing production of thromboxane A2
c. Inhibits production of vitamin K dependent clotting factors
d. Inhibits thrombin and factor Xa
e. Induces vagal nerve stimulation
What are drugs are the other mechanisms of actions?

A

d. Inhibits thrombin and factor Xa = Heparin

a. Increases cGMP and reduces intracellular Ca2+ concentration = CCB
b. Inhibits COX reducing production of thromboxane A2 = NSAIDs (Ibuprofen, Aspirin)
c. Inhibits production of vitamin K dependent clotting factors = Warfarin
d. Inhibits thrombin and factor Xa = Heparin

544
Q

Infective endocarditis, which would you not see on the patient’s hands?

a. Roth spots
b. Janeaway lesion
c. Oslar nodes
d. Splinter haemorrhages
e. Clubbing

A

a. Roth spots

Seen in the eye, not on the hands

545
Q

Ellie’s boyfriend commented that she had fat calves. Over the past 2 days she has noticed her left calf has become swollen and red compared to the right. You have conducted a wells score which gives a score less than 4. This is a medium risk. What test would you request too further investigate this case?

a. Full blood count
b. CRP
c. D-dimer
d. Tropomyosin I
e. Anti-phospholipid antibody

A

c. D-dimer

546
Q

What is the definition of BP?

a. CO x Total vascular resistance
b. HR x SV
c. Diastolic + pulse pressure
d. End diastolic volume – end systolic volume

A

a. CO x Total vascular resistance

547
Q 
What is the diagnostic test for heart failure?
a. Troponin I 
b. ANP 
c. BNP 
d. CK-MB 
e. FBC
When do the others increase?
A

c. BNP = increased in ventricular dysfunction

a. Troponin I = MI
b. ANP = produced in problem with atrium
c. BNP = increased in ventricular dysfunction
d. CK-MB = MI, increases when there is damage to the heart

548
Q

A 43-year-old male is started on an ACE inhibitor as part of his management for angina. He presents to your clinic complaining of a cough which he thinks he’s has since his last visit with you. The GP changes the ACEi for an ARB. Which substance is responsible for the cough?

a. ACH
b. Bradykinin
c. Histamine
d. IgE
e. Prostaglandin

A

b. Bradykinin

PHASE 2A (16 decks)

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