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MY REVISION - ALL PHASES > CARDIOVASCULAR > Flashcards

CARDIOVASCULAR Flashcards

1
Q

ATHEROSCLEROSIS
Define atherosclerosis

A

Build up of plaque in the intima of an artery

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2
Q

ATHEROSCLEROSIS
What can an atherosclerotic plaque cause?

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

ATHEROSCLEROSIS
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

ATHEROSCLEROSIS
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

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

A

Peripheral and coronary arteries - circumflex, LAD and RCA

Focal distribution along the length

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6
Q

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

A

Media

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7
Q

ATHEROSCLEROSIS
What is the precursor for atherosclerosis?

A

Fatty streaks

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8
Q

ATHEROSCLEROSIS
What can cause chemoattractant release?

A

Endothelial cell injury

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9
Q

ATHEROSCLEROSIS
What is the function of chemoattractants?

A

Signal leukocytes and produce a concentration gradient

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10
Q

ATHEROSCLEROSIS
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

ATHEROSCLEROSIS
What inflammatory cytokines are found in plaques?

A

IL-1
IL-6
IFN-gamma

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12
Q

ATHEROSLCEROSIS
Describe the process of leukocyte recruitment

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

ATHEROSCLEROSIS
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

ATHEROSCLEROSIS
Describe the 5 steps of progression of atherosclerosis

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

ATHEROSCLEROSIS
At what age do fatty streaks begin to appear?

A

< 10 years old

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16
Q

ATHEROSCLEROSIS
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

ATHEROSCLEROSIS
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

ATHEROSCLEROSIS
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

ATHEROSCLEROSIS
What are fibrous plaques able to do?

A

Impede blood flow and they are prone to rupture

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20
Q

ATHEROSCLEROSIS
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

ATHEROSCLEROSIS
What the primary treatment for atherosclerosis?

A

Percutaneous Coronary Intervention (PCI)

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22
Q

ATHEROSCLEROSIS
What is the major limitation of PCI?

A

Restenosis

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23
Q

ATHEROSCLEROSIS
How can restenosis be avoided following PCI?

A

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

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24
Q

ATHEROSCLEROSIS
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

ATHEROSCLEROSIS
What is the key principle behind pathogenesis of atherosclerosis?

A

It is an inflammatory process

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26
Q

ATHEROSCLEROSIS
Define atherogenesis

A

The development of an atherosclerotic plaque

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27
Q

ECG
What is an electrocardiogram?

A

Representation of electrical events of the cardiac cycle

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28
Q

ECG
What can ECGs identify?

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

ECG
What is depolarisation?

A

Contraction of any muscle associated with electrical changes

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30
Q

ECG
What is the dominant pacemaker of the heart?

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

ECG
What are the pacemakers of the heart?

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

ECG
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

ECG
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

ECG
What does the P wave represent?

A

Atrial depolarisation

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35
Q

ECG
What does the QRS complex represent?

A

Ventricular depolarisation

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36
Q

ECG
What does the T wave represent?

A

Ventricular repolarisation

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37
Q

ECG
What does the PR interval represent?

A

Atrial depolarisation and delay in AV junction

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38
Q

ECG
How long should the PR interval be?

A

120-200 ms

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39
Q

ECG
What might a long PR interval indicate?

A

Heart block

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40
Q

ECG
How long should the QRS complex be?

A

< 110 ms

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41
Q

ECG
What does the ST segment represent?

A

Time between depolarisation and repolarisation of the ventricles (contraction)

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42
Q

ECG
What is the J point?

A

Where the QRS complex becomes the ST segment

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43
Q

ECG
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

ECG
What is the normal axis of the QRS complex?

A

-30° to +90°

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45
Q

ECG
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

ECG
How long should the QT interval be?

A

0.35-0.45s

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47
Q

ECG
Where would you place lead I?

A

From the right arm to the left arm

At 0°

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48
Q

ECG
Where would you place lead II?

A

From the right arm to left leg

At 60°

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49
Q

ECG
Where would you place lead III?

A

From the left arm to left leg

At 120°

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50
Q

ECG
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

ECG
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

ECG
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

ECG
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

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

A

Lead I
aVL
V5
V6

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55
Q

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

A

Lead II
Lead III
aVF

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56
Q

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

A

V1

V2

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57
Q

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

A

V3

V4

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58
Q

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

A

Leads I and II

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59
Q

ECG
In which lead are all waves negative?

A

aVR

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60
Q

ECG
In which leads must the R wave grow?

A

From chest leads V1 to V4

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61
Q

ECG
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

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

A

Leads I, II and V2-V6

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63
Q

ECG
What might tall pointed P waves on an ECG suggest?

A

Right atrial enlargement

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64
Q

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

A

Left atrial enlargement

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65
Q

ECG
Give 3 signs of abnormal T waves

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

ECG
What happens to the QT interval when HR increases?

A

QT interval decreases

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67
Q

ECG
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

ANGINA
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

ANGINA
What is the most common cause of angina?

A

Narrowing of the coronary arteries due to atherosclerosis

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70
Q

ANGINA
Give 5 possible causes of angina

A
  • atheroma/stenosis of coronary arteries
  • valvular disease
  • aortic stenosis
  • arrhythmia
  • anaemia
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71
Q

ANGINA
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

ANGINA
Name 3 types of angina

A
  • Stable angina
  • Unstable angina
  • Prinzmetal’s angina
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73
Q

ANGINA
Name 3 non-modifiable risk factors for angina

A
  1. Increasing age
  2. Family history
  3. Gender - Male
  4. ethnicity - south Asian
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74
Q

ANGINA
Give 5 modifiable risk factors for angina

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

ANGINA
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

ANGINA
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

ANGINA
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

ANGINA
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

ANGINA
Briefly describe the pathophysiology of Prinzmetal’s angina

A

Occurs due to coronary artery spasm

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80
Q

ANGINA
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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81
Q

ANGINA
How would you describe the chest pain in angina?

A

Crushing central chest pain that is heavy and tight - angina pectoris

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82
Q

ANGINA
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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83
Q

ANGINA
Give the clinical presentation 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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84
Q

ANGINA
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. Echocardiography
  3. CT angiography - high NPV and good at excluding disease (gold standard)
  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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85
Q

ANGINA
How can angina be reversed?

A

Resting - reducing myocardial demand

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86
Q

ANGINA
Describe the primary prevention for angina

A
  1. Modify risk factors
  2. Treat underlying causes
  3. Low dose aspirin
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87
Q

ANGINA
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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88
Q

ANGINA
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 (e.g. verapamil)

other medications include statins and aspirin

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89
Q

ANGINA
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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90
Q

ANGINA
Give 3 side effects of beta blockers

A
  1. Bradycardia
  2. Tiredness
  3. Erectile dysfunction
  4. Cold peripheries
  5. nightmares
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91
Q

ANGINA
When might beta blockers be contraindicated?

A

DO NOT GIVE in asthma, heart failure/heart block, hypotension
and bradyarrhythmia

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92
Q

ANGINA
Describe the action of nitrates

A

Venodilators

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

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93
Q

ANGINA
Describe the action of Calcium channel blockers

A

Arterodilators

Reduce BP –> Reduce afterload –> reduced myocardial demand

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94
Q

ANGINA
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 - antiplatelet
  3. Atovostatin - Statin
  4. ACEi - ramipril
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95
Q

ANGINA
How does aspirin work?

A

Antiplatelet

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

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96
Q

ANGINA
What is a caution when prescribing aspirin?

A

Gastric ulceration

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97
Q

ANGINA
How does clopidogrel work?

A

Antiplatelet

P2Y12 inhibitor –> prevents platelet activation

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98
Q

ANGINA
What are statins used for?

A

To reduce the amount of LDL in the blood

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99
Q

ANGINA
What is revascularisation?

A

Used to restore coronary artery and increase blood flow

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100
Q

ANGINA
Name 2 types of revascularisation

A
  1. Percutaneous coronary intervention (PCI)

2. Coronary artery bypass graft (CABG)

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101
Q

ANGINA
Give the pros and cons of PCI

A 
ADVANTAGES 
1. Less invasive 
2. Convenient and acceptable
3. short recovery and repeatable
DISADVANTAGES 
1. High risk of restenosis
2. not good for complex disease
3. risk of stent thrombosis
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102
Q

ANGINA
Give 1 the pros and cons of CABG

A

ADVANTAGES

  1. Good prognosis after surgery
  2. deals with complex disease

DISADVANTAGES

  1. Very invasive
  2. Long recovery time
  3. risk of stroke or bleeding
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103
Q

ANGINA
Name 2 complications of angina

A
  1. Acute coronary syndromes
  2. Congestive cardiac failure
  3. Conduction disease
  4. Arrhythmia
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104
Q

ACS
What are acute coronary syndromes?

A

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

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105
Q

ACS
What is the common cause of ACS?

A

Rupture of an atherosclerotic plaque and subsequent arterial thrombosis

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106
Q

ACS
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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107
Q

ACS
Briefly describe the pathophysiology of ACS

A
  • Rupture/erosion of fibrous cap on plaque leading to platelet aggregation and thrombus formation
  • In unstable angina the plaque has a necrotic centre and ulcerated cap and the thrombus results in partial occlusion
  • In MI the plaque has a necrotic centre and the thrombus results in total occlusion
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108
Q

ACS
Describe type 1 MI

A

Spontaneous MI with ischaemia due to plaque rupture

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109
Q

ACS
Describe type 2 MI

A

MI secondary to ischaemia due to increased O2 demand

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110
Q

ACS
What is troponin a marker for?

A

Cardiac muscle injury

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111
Q

ACS
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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112
Q

ACS
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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113
Q

ACS
Give 4 symptoms of MI

A
  1. Unremitting and usually severe central cardiac chest pain
  2. Pain occurs at rest
  3. Sweating, pale, grey
  4. Breathlessness
  5. Nausea and vomiting
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114
Q

ACS
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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115
Q

ACS
Name 3 possible differential diagnoses of MI

A
  1. Pericarditis
  2. Stable angina
  3. Aortic dissection
  4. GORD
  5. Pneumothorax
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116
Q

ACS
What investigations 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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117
Q

ACS
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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118
Q

ACS
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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119
Q

ACS
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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120
Q

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

A

Normal

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121
Q

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

A

Significantly raised - troponin I and T

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122
Q

ACS
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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123
Q

ACS
Describe the initial management of ACS

A 
MONA
M = morphine
O = oxygen (high flow)
N = nitrate (GTN spray)
A = aspirin 300mg (+clopidogrel 300mg/Ticagrelor 180mg if not high bleeding risk)

1st line = PCI within 12 hours and available

2nd line = thrombolysis (alteplase, streptokinase, retenase)

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124
Q

ACS
What is the treatment of choice for STEMI?

A

PCI within 120 minutes

if not, fibrinolysis - alteplase, streptokinase

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125
Q

ACS
What is the function of P2Y12?

A

It amplifies platelet activation

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126
Q

ACS
Give 2 potential side effect of P2Y12 inhibitors

A
  1. Bleeding
  2. Rash
  3. GI disturbances - ulceration
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127
Q

ACS
Describe the secondary prevention therapy for people after having a STEMI

A
  1. Aspirin - antiplatelet
  2. Clopidogrel - P2Y12 inhibitor
  3. Statins - ATORVASTATIN
  4. Metoprolol - beta blocker
  5. ACE inhibitor - ramipril, lisinopril
  6. Modification of risk factors
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128
Q

ACS
What is involved in antithrombotic therapy?

A 
Dual antiplatelet therapy = aspirin and clopidogrel 
Anticoagulant = heparin
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129
Q

AS
Give 5 potential complications of MI

A
  • sudden death
  • arrhythmias
  • persistent pain
  • heart failure
  • mitral incompetence
  • pericarditis
  • cardiac rupture
  • aneurysm
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130
Q

ACS
what conditions can be caused by a previous MI?

A
  1. Shock
  2. Heart failure
  3. Pericarditis
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131
Q

DVT
What is a DVT?

A

Blood clot within a blood vessel of the lower limb

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132
Q

DVT
What are the clinical features of DVT?

A

may be asymptomatic
pain in calf, often swollen, red, warm
tenderness

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133
Q

DVT
What are the causes of DVT?

A
  • surgery
  • immobility
  • leg fracture
  • oral contraceptive
  • long haul flights
  • malignancy
  • genetic - factor V leiden, antithrombin deficiency, protein c or s deficiency
  • acquired - anti-phospholipid syndrome, lupus
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134
Q

DVT
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
  3. doppler ultrasound
  4. venography
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135
Q

DVT
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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136
Q

DVT
Name the types of DVT

A
  1. Spontaneous

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

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137
Q

DVT
Give 5 risk factors for DVT

A
  • increased age
  • pregnancy, OC
  • trauma, surgery
  • past DVT
  • cancer
  • obesity
  • immobility
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138
Q

DVT
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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139
Q

DVT
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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140
Q

DVT
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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141
Q

DVT
What might be the consequence of a dislodged DVT?

A

Pulmonary embolism

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142
Q

PE
Give 2 symptoms of a PE

A
  1. Breathlessness
  2. Pleuritic chest pain
  3. signs/symptoms of DVT
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143
Q

PE
Give 2 signs of a PE

A
  1. Tachycardia
  2. Tachypnoea
  3. pleural rub
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144
Q

PE
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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145
Q

PE
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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146
Q

PE
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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147
Q

THROMBUS
Define thrombosis

A

Blood coagulation inside a vessel

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148
Q

THROMBUS
How would you describe an arterial thrombus?

A

Platelet rich (a ‘white thrombosis’)

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149
Q

THROMBUS
How would you describe a venous thrombosis?

A

Fibrin rich (a ‘red thrombosis’)

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150
Q

THROMBUS
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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151
Q

THROMBUS
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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152
Q

THROMBUS
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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153
Q

THROMBUS
What are the potential consequences of a venous thrombosis?

A

Deep vein thrombosis

Pulmonary embolism

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154
Q

THROMBUS
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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155
Q

THROMBUS
How does heparin work?

A

Inhibits thrombin and factor Xa

Indirect thrombin inhibitor - binds to antithrombin and increased its activity

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156
Q

THROMBUS
How do you monitor heparin?

A

Activated partial thromboplastin time

Aim ratio: 1.8-2.8

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157
Q

THROMBUS
Why is LMW heparin often used instead of normal heparin?

A

Smaller molecule, less variation in dose and renally excreted

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158
Q

THROMBUS
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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159
Q

THROMBUS
What is warfarin an antagonist of?

A

Vitamin K

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160
Q

THROMBUS
Why is warfarin difficult to use?

A

Lots of interactions
Needs almost constant monitoring
Teratogenic

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161
Q

THROMBUS
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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162
Q

THROMBUS
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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163
Q

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

A

50 ml

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164
Q

PERICARDITIS
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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165
Q

PERICARDITIS
What is the function of the pericardium?

A

Restrains the filling volume of the heart

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166
Q

PERICARDITIS
Describe the aetiology of pericarditis

A
  1. Viral (common) - e.g. enteroviruses, adenoviruses
  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%)
  8. dressler’s syndrome
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167
Q

PERICARDITIS
Define acute pericarditis

A

Acute inflammation of the pericardium with or without effusion

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168
Q

PERICARDITIS
Give 5 symptoms of pericarditis

A
  1. CHEST PAIN - severe, sharp and pleuritic (worse on inspiration/lying flat - relieved by sitting forward)
  2. Dyspnoea
  3. Cough
  4. Hiccups
  5. Skin rash
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169
Q

PERICARDITIS
Describe the chest pain in acute pericarditis

A

Severe, sharp, pleuritic, rapid onset, can radiate to arm (trapezius ridge)

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170
Q

PERICARDITIS
Why might someone with pericarditis have hiccups?

A

Due to irritation to the phrenic nerve

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171
Q

PERICARDITIS
What is the major differential diagnosis of acute pericarditis?

A

Myocardial infarction

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172
Q

PERICARDITIS
Name 3 differential diagnoses for acute pericarditis

A
  1. MI
  2. Angina
  3. Pneumonia
  4. Pleurisy
  5. PE
  6. GORD
  7. pneumothorax
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173
Q

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

A
  1. ECG - diagnostic
  2. CXR
  3. Bloods - FBC, ESR and CRP, Troponin
  4. Echocardiogram - usually normal, rule out silent pericardial effusion
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174
Q

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

A
  1. Saddle shaped ST elevation

2. PR depression

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175
Q

PERICARDITIS
What does a raised troponin in acute pericarditis suggest?

A

Myopericarditis

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176
Q

PERICARDITIS
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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177
Q

PERICARDITIS
What is the treatment for pericarditis?

A
  1. Restrict physical activity until symptoms resolve
  2. NSAID or aspirin
  3. Colchicine - reduces recurrence (SE = nausea and diarrhoea)
  4. Treat the cause
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178
Q

CARDIAC TAMPONADE
What is pericardial effusion?

A

Abnormal accumulation of fluid in the pericardial cavity

It commonly accompanies an episode of acute pericarditis

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179
Q

CARDIAC TAMPONADE
What is a complication of pericardial effusion?

A

Cardiac tamponade

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180
Q

CARDIAC TAMPONADE
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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181
Q

CARDIAC TAMPONADE
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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182
Q

CARDIAC TAMPONADE
What are the signs of Cardiac tamponade?

A

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

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183
Q

CARDIAC TAMPONADE
What is the treatment of cardiac tamponade?

A

Pericardiocentesis (drainage)

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184
Q

CHRONIC PERICARDITIS
What is chronic constrictive pericarditis?

A

Calcification thickens the pericardium and affects cardiac effusion

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185
Q

CHRONIC PERICARDITIS
What is the treatment for chronic constrictive pericarditis?

A

Surgical excision of thickened pericardium

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186
Q

CHRONIC PERICARDITIS
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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187
Q

CHRONIC PERICARDITIS
What is haemopericaridum?

A

Direct bleeding from vasculature through the ventricular wall following MI

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188
Q

MYOCARDITIS
What can cause myocarditis?

A

Viral infection

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189
Q

PVD
Give 5 risk factors for peripheral vascular disease

A 
Smoking
Diabetes
HTN
Sedentary lifestyle
Hyperlipidaemia
History of CAD
Age (>40)
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190
Q

PVD
Give 4 treatments for peripheral vascular disease

A 
Control risk factors:
    - Smoking cessation
    - Regular exercise
    - Weight reduction
    - BP control, DM control
    - Statin 
Antiplatelet therapy:
    - Aspirin/clopidogrel
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191
Q

PVD
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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192
Q

PVD
Give 4 signs of critical ischaemia

A
  1. Rest pain
  2. Classically nocturnal
  3. Ulceration
  4. Gangrene
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193
Q

PVD
What can cause acute ischaemia?

A

Embolism/thrombosis

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194
Q

PVD
Give 6 symptoms of acute ischaemia

A
  1. Pain
  2. Pale
  3. Paralysis
  4. Paraesthesia
  5. Perishing cold
  6. Pulseless
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195
Q

PVD
Give 2 examples of acute ischaemia

A
  1. Stroke

2. MI

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196
Q

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

A

Thrombolysis

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197
Q

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

A

Streptokinase

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198
Q

CARDIOMYOPATHY
Define cardiomyopathy

A

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

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199
Q

CARDIOMYOPATHY
Name 4 cardiomyopathies

A
  1. Hypertrophic (HCM)
  2. Dilated (DCM)
  3. Arrhythmogenic right/left ventricular (ARVC/ALVC)
  4. Restrictive
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200
Q

CARDIOMYOPATHY
Name 4 risk factors for cardiomyopathy

A
  1. FH
  2. High BP
  3. Obesity
  4. Diabetes
  5. Previous MI
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201
Q

CARDIOMYOPATHY
What can cause Hypertrophic cardiomyopathy?

A
  • genetic - autosomal dominant sarcomeric gene mutations - Troponin T and B-myosin
  • 50% = sporadic
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202
Q

CARDIOMYOPATHY
What is the usual inheritance pattern for cardiomyopathies?

A

Autosomal dominant (restrictive is not familial)

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203
Q

CARDIOMYOPATHY
Describe the pathophysiology of Hypertrophic cardiomyopathy

A
  • Gene mutation for the sarcomere protein
  • Impaired diastolic filling
  • Reduced stroke volume
  • Reduced cardiac output
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204
Q

CARDIOMYOPATHY
Give 3 symptoms of Hypertrophic Cardiomyopathy

A
  • Sudden death may be the first symptom
  • Chest pain/angina
  • Dyspnoea
  • Dizziness
  • Palpitations
  • Syncope
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205
Q

CARDIOMYOPATHY
Give 3 signs of hypertrophic cardiomyopathy

A
  • Ejection-systolic murmur
  • Jerky carotid pulse
  • Left ventricular outflow obstruction
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206
Q

CARDIOMYOPATHY
What might an ECG look like from a person with hypertrophic cardiomyopathy?

A
  1. Large QRS complexes
  2. Progressive T wave inversion
  3. deep Q waves

also do genetic analysis

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207
Q

CARDIOMYOPATHY
Briefly describe treatment for hypertrophic cardiomyopathy

A
  • Amiodarone – anti-arrhythmic
  • Calcium channel blocker – Verapamil
  • Beta-blocker - Atenolol
  • ICD insertion
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208
Q

CARDIOMYOPATHY
Describe the pathophysiology of dilated cardiomyopathy

A
  • autosomal dominant cytoskeleton gene mutation
  • Poorly generated contractile force = progressive dilation of the heart
  • Diffuse interstitial fibrosis
  • Systolic disfunction of the left or both ventricles
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209
Q

CARDIOMYOPATHY
Name 3 causes of dilated cardiomyopathy

A
  1. Genetic
  2. Alcohol
  3. Ischaemia
  4. Thyroid disorder
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210
Q

CARDIOMYOPATHY
Give 3 symptoms of dilated cardiomyopathy

A

Presents with symptoms of heart failure

  1. SOB
  2. Fatigue
  3. dyspnoea
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211
Q

CARDIOMYOPATHY
What investigations would you do for someone you suspect has dilated cardiomyopathy?

A

CXR –> cardiomegaly, pulmonary oedema
ECG –> tachycardia, arrhythmia, T-wave changes
ECHO –> dilated ventricles

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212
Q

CARDIOMYOPATHY
What is the treatment for dilated cardiomyopathy?

A

treat the cause if possible

HF and AF treated in conventional way

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213
Q

CARDIOMYOPATHY
What can cause Arrhythmogenic cardiomyopathy?

A

Desmosome gene mutations - usually autosomal dominant but can be recessive

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214
Q

CARDIOMYOPATHY
Describe the pathophysiology of Arrhythmogenic cardiomyopathy

A
  • Desmosome gene mutation
  • Right ventricle replaced by fat and fibrous tissue
  • Muscle dies and replaced by fat as part of inflammatory process
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215
Q

CARDIOMYOPATHY
Give 2 signs of Arrhythmogenic cardiomyopathy

A
  1. right heart failure
  2. Syncope
  3. conduction issues
  4. arrhythmia
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216
Q

CARDIOMYOPATHY
What might an ECG look like from a person with Arrhythmogenic cardiomyopathy?

A

usually normal
may show T wave inversion
Epsilon waves

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217
Q

CARDIOMYOPATHY
What is the treatment for Arrhythmogenic cardiomyopathy?

A

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

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218
Q

CARDIOMYOPATHY
What is restrictive cardiomyopathy?

A
  • Scar tissue replaces the normal heart muscle and the ventricles become rigid so don’t contract properly
  • rare condition
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219
Q

CARDIOMYOPATHY
Name 2 causes of restrictive cardiomyopathy

A
  1. Amyloidosis (extra-cellular deposition of an amyloid, a insoluble fibrillar protein)
  2. Sarcoidosis
  3. idiopathic
  4. end-myocardial fibrosis
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220
Q

CHANNELOPATHY
What are channelopathies?

A

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

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221
Q

CHANNELOPATHY
Name 4 channelopathies

A
  1. Long QT syndrome
  2. Short QT syndrome
  3. Brugada
  4. Catecholamine Polymorphic Ventricular Tachycardia (CPVT)
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222
Q

CHANNELOPATHY
What is Brugada?

A

A channelopathy caused by a mutation in sodium channels

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223
Q

CHANNELOPATHY
What might an ECG look like from someone with Brugada?

A

Characteristic ST elevation in chest leads

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224
Q

CHANNELOPATHY
What is the commonest symptom of channelopathies?

A

Recurrent syncope

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225
Q

FAMILIAL HYPERCHOLESTEROLAEMIA
What is familial hypercholesterolaemia?

A

Inherited abnormality of cholesterol metabolism

LDL receptor affected

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226
Q

HEART FAILURE
Define heart failure

A

Inability of the heart to deliver blood and thus oxygen at a rate that is commensurate with the requirements of the body

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227
Q

HEART FAILURE
what are the different 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
  3. Acute failure = New onset acute or decompensation of chronic.
  4. Chronic heart failure = Develops/progresses slowly and arterial pressure is well maintained until late
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228
Q

HEART FAILURE
what are the risk factors for heart failure?

A
  1. > 65 y/o
  2. African descent
  3. Men
  4. Obesity
  5. Previous MI
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229
Q

HEART FAILURE
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

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230
Q

HEART FAILURE
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

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231
Q

HEART FAILURE
What are the compensatory mechanisms in heart failure?

A
  1. Sympathetic system
  2. RAAS
  3. Natriuretic peptides
  4. Ventricular dilation
  5. Ventricular hypertrophy
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232
Q

HEART FAILURE
Explain how the sympathetic system is compensatory in heart failure 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

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233
Q

HEART FAILURE
Explain how the RAAS system is compensatory in heart failure 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

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234
Q

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

A
  1. Diuretic
  2. Hypotensive
  3. Vasodilators
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235
Q

HEART FAILURE
What are the 3 cardinal symptoms of heart failure?

A
  1. SOB
  2. Fatigue
  3. Peripheral oedema
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236
Q

HEART FAILURE
what are the clinical signs of left heart failure?

A
  1. Pulmonary crackles
  2. S3 and S4 and murmurs
  3. Displaced apex beat
  4. Tachycardia
  5. fatigue
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237
Q

HEART FAILURE
what are the clinical features of right HF?

A
  1. Raised JVP
  2. Ascites
  3. peripheral oedema
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238
Q

HEART FAILURE
what are the clinical features of heart failure?

A

SOFA PC

  • shortness of breath
  • orthopnea
  • fatigue
  • ankle swelling
  • pulmonary oedema (due to backflow from decreased CO; produced cough with pink frothy sputum)
  • cold peripheries

Raised JVP
End respiratory crackles

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239
Q

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

A
  1. ECG
  2. CXR
  3. BNP - brain natriuretic peptide
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240
Q

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

A 
ABCDE
A - alveolar oedema (bat wing shadowing)
B - Kerley B lines
C - cardiomegaly
D - dilated upper lobes
E - effusions (pleural)
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241
Q

HEART FAILURE
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 - may reveal cause

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242
Q

HEART FAILURE
what is the first line treatment for chronic HF?

A

ACEi -

beta blocker

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243
Q

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

A

Ramipril

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244
Q

HEART FAILURE
Name 3 BB that are used in treatment of HF

A
  1. Propranolol
  2. Bisoprolol
  3. Atenolol
  4. Carvedilol
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245
Q

HEART FAILURE
what is the treatment for acute HF?

A

OMFG

  • oxygen
  • morphine
  • furosemide
  • GTN spray
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246
Q

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

A

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

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247
Q

HEART FAILURE
What is 2nd and 3rd line treatment for HF if 1st line treatment does not work?

A 
2nd = ARB + nitrate
3rd = cardiac resynchronization or digoxin
4th = diuretics (furosemide)
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248
Q

HEART FAILURE
How can chronic HF be prevented?

A 
Stop smoking
Eat more healthy 
Exercise 
Avoid large meals
Vaccinations 
Treat underlying cause - dysarrhythmias or valve disease
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249
Q

HEART FAILURE
What is the treatment for acute HF?

A 
LOON 
Loop diuretic = furosemide
Oxygen 
Opioid = diamorphine 
Nitrates = GTN spray 
and Monitor ECG
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250
Q

HYPERTENSION
What is the clinical diagnosis go hypertension?

A

BP > 140/90 mmHg

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251
Q

HYPERTENSION
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
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252
Q

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

A

5-7 years

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253
Q

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

A

Clinic BP = 140/90

ABPM = 135/85

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254
Q

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

A

Clinic BP = 160/100

ABPM = 150/95

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255
Q

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

A

Systolic BP = >180

Diastolic BP = >110

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256
Q

HYPERTENSION
Name the 2 types of hypertension

A
  1. Essential (primary) hypertension

2. Secondary hypertension

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257
Q

HYPERTENSION
What causes essential hypertension?

A

Unknown cause - multifactorial involving:

  • genetic susceptibility
  • Excessive sympathetic nervous system activity
  • Abnormalities of Na+/K+ membrane transport
  • High salt intake
  • Abnormalities in renin-angiotensin-aldosterone system
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258
Q

HYPERTENSION
Give 5 causes of secondary hypertension

A 
ROPE
R - renal disease
O - obesity
P - pregnancy
E - endocrine (Conn's, Cushing's, pheochromocytoma)

Cortication of the aorta
Drugs - corticosteroids, contraceptive, alcohol
Family history and genetics

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259
Q

HYPERTENSION
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
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260
Q

HYPERTENSION
Name 5 risk factor for hypertension

A

Modifiable:

  • alcohol intake
  • sedentary lifestyle
  • diabetes mellitus
  • sleep apnoea
  • smoking

Non-modifiable:

  • Increasing age
  • family history
  • ethnicity - afro-Caribbean
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261
Q

HYPERTENSION
What is the clinical presentation of hypertension?

A

Usually asymptomatic

Found on screening

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262
Q

HYPERTENSION
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

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263
Q

HYPERTENSION
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
  • urinalysis - protein, albumin:creatine ratio, haematuria
  • blood tests - serum creatinine, eGFR, glucose
  • fundoscopy - retinal haemorrhage, papillodema
  • ECG - left ventricular hypertrophy
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264
Q

HYPERTENSION
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

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265
Q

HYPERTENSION
What are the 2 main types of treatment for hypertension?

A
  1. Lifestyle modifications - reduce salt, loss weight, reduce alcohol
  2. Drug therapy = ACD
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266
Q

HYPERTENSION
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
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267
Q

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

A

Beta blockers - bisoprolol

statins - simvastatin

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268
Q

HYPERTENSION
Will anti-hypertensives make someone feel better?

A

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

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269
Q

HYPERTENSION
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

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270
Q

HYPERTENSION
What is cor pulmonale?

A

Right sided heart failure caused by chronic pulmonary arterial hypertension

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271
Q

HYPERTENSION
Write an equation for BP

A

BP = CO x TPR

272
Q

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

A
  1. RAAS

2. Sympathetic nervous system

273
Q

HYPERTENSION
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
274
Q

HYPERTENSION
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
275
Q

ACEi
In what diseases are ACE inhibitors clinically indicated?

A
  1. Hypertension
  2. Heart failure
  3. Diabetic nephropathy
276
Q

ACEi
Name 3 ACE inhibitors

A
  1. Ramipril
  2. Enalapril
  3. Perindopril
  4. Trandolapril
  5. Lisinopril
277
Q

ACEi
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
278
Q

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

A
  1. Cough
  2. Rash
  3. Anaphylactoid reaction
279
Q

ACEi
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

280
Q

ACEi 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

281
Q

ARBs
What are ARBs?

A

Angiotensin II receptor blockers

282
Q

ARBs
At which receptor do ARB’s work?

A

AT-1 receptor - prevent angiotensin II binding

283
Q

ARBs
In what diseases are ARBs clinically indicated?

A
  1. Hypertension
  2. Heart failure
  3. Diabetic nephropathy
284
Q

ARBs
Name 3 ARBs

A
  1. Candesartan
  2. Valsartan
  3. Losartan
285
Q

ARBs
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

286
Q

ARBs
Give 4 potential side effect of ARBs

A
  1. Hypotension
  2. Hyperkalaemia
  3. Renal dysfunction
  4. Rash
    Contraindicated in pregnancy
287
Q

CCBs
In what diseases are calcium channel blockers clinically indicated?

A
  1. Hypertension
  2. IHD
  3. Arrhythmia
288
Q

CCBs
Name 2 calcium channel blockers

A
  1. Amlopipine
  2. Felodipine
  3. Diltiazem
  4. Verapamil
289
Q

CCBs
Name 2 dihydropyridines and briefly explain how they work

A

Class of CCBs
Amlodipine and felodipine
Arterial vasodilators

290
Q

CCBs
Name a calcium channel blocker that acts primarily on the heart

A

Verapamil

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

291
Q

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

A

Diltiazem

292
Q

CCBs
On what channels do CCB work?

A

L type Ca2+ channels

293
Q

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

A
  1. Flushing
  2. Headache
  3. Oedema
  4. Palpitations
294
Q

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

A
  1. Bradycardia
  2. Atrioventricular block
  3. Postural hypotension
295
Q

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

A

Worsening cardiac failure

296
Q

CCBs
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
297
Q

CCBs
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

298
Q

BETA BLOCKERS
In what diseases are beta blockers clinically indicated?

A
  1. IHD
  2. Heart failure
  3. Arrhythmia
  4. Hypertension
299
Q

BETA BLOCKERS
Name 3 beta blockers

A
  1. Bisoprolol (beta 1 elective)
  2. Atenolol
  3. Propranolol (beta 1/2 nonselective)
300
Q

BETA BLOCKERS
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
301
Q

BETA BLOCKERS
Give 3 conditions in which Beta blockers can worsen them

A
  1. Asthma or COPD
  2. PVD
  3. Heart failure
302
Q

DIURETICS
In what diseases are diuretics clinically indicated?

A
  1. Heart failure

2. Hypertension

303
Q

DIURETICS
Name 4 classes of diuretics

A
  1. Thiazides
  2. Loop
  3. Potassium sparing
  4. Aldosterone antagonists
304
Q

DIURETICS
Where in the kidney do thiazide diuretics work?

A

The distal tubule

305
Q

DIURETICS
Name a thiazide

A

Bendroflumethethiazide

306
Q

DIURETICS
Name a loop diuretic

A

Furosemide

Bumetanide

307
Q

DIURETICS
Name a potassium sparing diuretic

A

Spironolactone

Eplerenone

308
Q

DIURETICS
Why are potassium sparing diuretics especially effective?

A

They have anti-aldosterone effects too

309
Q

DIURETICS
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
310
Q

HYPERTENSION
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

311
Q

HYPERTENSION
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

312
Q

HYPERTENSION
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

313
Q

HYPERTENSION
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

314
Q

HYPERTENSION
What is the counter regulatory system to RAAS?

A

Atrial Natriuretic Peptide/BNP (ventricular natriuretic peptide) hormones

315
Q

Where are ANP and BNP produced?

A

The heart

316
Q

What metabolises ANP and BNP?

A

Neprilysin (NEP)

317
Q

What are the functions of ANP and BNP?

A
  1. Increased renal excretion of Na+ and water
  2. Vasodilators
  3. Inhibit aldosterone release
318
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

319
Q

In what diseases are nitrates clinically indicated?

A
  1. IHD

2. Heart failure

320
Q

Name 2 nitrates that are used pharmacologically

A
  1. GTN spray (short acting)

2. Isosorbide mononitrate (long acting)

321
Q

How do nitrates work in the treatment of heart failure?

A

They are venodilators so reduce preload and therefore BP

322
Q

Give 2 potential side effects of nitrates

A
  1. Headache
  2. GTN syncope
  3. Tolerance
323
Q

How do anti-arrhythmic drugs work?

A

Interfere with the action potential of the heart in different phases

324
Q

What classification is used to group anti-arrhythmic drugs?

A

Vaughan Williams classification

325
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)

326
Q

Name three class 2 drugs of the Vaughan Williams classification

A

Class 2 are Beta blockers
Propranolol
Atenolol
Bisoprolol

327
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

328
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

329
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

330
Q

What are the main effect of digoxin?

A
  1. Bradycardia
  2. Reduced atrioventricular conduction
  3. Increased force of contraction (positive inotrope)
331
Q

Give 3 potential side effects of digoxin

A
  1. Nausea
  2. Vomiting
  3. Diarrhoea
  4. Confusion
    Also has a narrow therapeutic range
332
Q

In what disease is digoxin clinically indicated?

A
  1. Atrial fibrillation

2. Severe heart failure

333
Q

What does furosemide block?

A

The Na+/K+/2Cl- transporter

334
Q

Why are beta blockers good in chronic heart failure?

A

They block reflex sympathetic responses which stress the failing heart

335
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
336
Q

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

A

Amlodipine

337
Q

How does amiodarone work?

A

Prolongs action potential by delaying depolarisation

338
Q

Name 4 potential effects of amiodarone

A
  1. QT prolongation
  2. Interstitial lung disease
  3. Hypothyroidism
  4. Abnormal liver enzymes
339
Q

Name a disease that might cause flattening of the P wave

A
  1. Hyperkalaemia

2. Obesity

340
Q

Name a disease that might cause tall P waves

A

Right atrial enlargement

341
Q

Name a disease that might cause broad notched P waves

A

Left atrial enlargement

342
Q

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

A

Inferior aspect

343
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

344
Q

Give 3 effects hyperkalaemia on an ECG

A
  1. Tall tented T waves
  2. Flat P waves
  3. Broad QRS
345
Q

Give 2 effects of hypokalaemia on an ECG

A
  1. Flat T waves
  2. QT prolongation
  3. ST depression
  4. Prominent U waves
346
Q

Give an effect go hypocalcaemia on an ECG

A
  1. QT prolongation
  2. T wave flattening
  3. Narrowed QRS
  4. Prominent U waves
347
Q

Give an effect of hypercalcaemia on an ECG

A
  1. QT shortening
  2. Tall T wave
  3. No P waves
348
Q

What controls the sinus node discharge rate?

A

Autonomic nervous system

349
Q

Define sinus rhythm

A

A P wave precedes each QRS complex

350
Q

Define cardiac arrhythmia

A

Abnormality of cardiac rhythm

351
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
352
Q

Define bradycardia

A

< 60 bpm

353
Q

Define tachycardia

A

> 100 bpm

354
Q

Give 2 causes of bradycardia

A
  1. Conduction tissue fibrosis
  2. Ischaemia
  3. Inflammation/infiltrative disease
  4. Drugs
355
Q

Give 2 broad categories of tachycardia

A
  1. Supraventricular tachycardias

2. Ventricular tachycardias

356
Q

Where do supra-ventricular tachycardia’s arise from?

A

Atria or atrio-ventricular junction

357
Q

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

A

Narrow QRS complexes

358
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)
359
Q

Where do ventricular tachycardia’s arise from?

A

The ventricles

360
Q

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

A

Broad QRS compelxes

361
Q

What is the commonest supra-ventricular tachycardia?

A

AV node re-entry tachycardia (AVNRT)

362
Q

Do you see P waves in AV node re-entry tachycardia (AVNRT)?

A

Loss of P waves

363
Q

what is the clinical presentation of AV node re-entry tachycardia (AVNRT)?

A

Rapid regular palpitations – abrupt onset, sudden termination
Chest pain and breathlessness
Neck pulsations
Polyuria

364
Q

Describe the acute treatment of AV node re-entry tachycardia (AVNRT)

A

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

365
Q

What drugs might you give someone to suppress further episodes of AV node re-entry tachycardia (AVNRT)?

A

Beta blockers, CCB

366
Q

Describe the pathophysiology of atrioventricular reciprocating tachycardia - AVRT (accessory) arrhythmias

A

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

367
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
368
Q

Give an example of an atrioventricular reciprocating tachycardia - AVRT (accessory) arrhythmia

A

Wolff-Parkinson-White Syndrome

369
Q

Give 4 causes of sinus tachycardia

A
  1. Physiological response to exercise
  2. Fever
  3. Anaemia
  4. Heart failure
  5. Hypovolaemia
  6. pain
370
Q

Why do ventricular tachycardia’s arise?

A

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

371
Q

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

A

Crescendo-decrescendo amplitude = torsades de pointes

372
Q

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

A

DC cardioversion

373
Q

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

A

Implantable cardioverter defibrillator (ICD)

374
Q

What is the treatment for stable ventricular tachycardia?

A

IV beta blockers (bisoprolol) and IV amiodarone

375
Q

Define atrial fibrillation

A

Chaotic irregular atrial rhythm at 300-600 bpm

AV node responds intermittently – irregular ventricular rate

376
Q

what is the clinical presentation of atrial fibrillation?

A

can be asymptomatic

  1. SOB
  2. Chest pain
  3. Palpitations
  4. Syncope
  5. fatigue
  6. apical pulse greater than radial pulse
377
Q

what are the causes of atrial fibrillation?

A 
Idiopathic 
Hypertension 
Heart failure 
Coronary artery disease 
Valvular heart disease 
Cardiac surgery 
Cardiomyopathy
Rheumatic heart disease
378
Q

Briefly describe the pathophysiology of atrial fibrillation

A

continuous rapid activation of the atria with no organised mechanical action at 300-600bpm

379
Q

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

A
  1. Absent P waves
  2. Irregular and rapid QRS complexes
  3. Fine oscillation of the baseline
    ‘Irregularly irregular’
380
Q

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

A

CHADS2 VAS

381
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

382
Q

Describe the treatment for atrial fibrillation

A
  • cardioversion - LMWH (enoxaparin) and DC shock
  • rate control - BB or CCB
  • rhythm control - BB (bisoprolol), CCB (verapamil), digoxin, anti-arrhythmic (amiodarone)
  • anti-coagulation
383
Q

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

A

BB, CCB and digoxin

384
Q

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

A

Electrical cardioversion or pharmacological cardioversion using flecainide

385
Q

What is the long term treatment for atrial fibrillation?

A

Catheter ablation

386
Q

What is atrial flutter?

A

Fast but organised waves in the atrium

Atrial rate 250-350 bpm

387
Q

Describe the ECG pattern taken from someone with atrial flutter

A
  1. Narrow QRS

2. Saw tooth flutter (F) waves

388
Q

Describe the pathophysiology of atrial flutter

A

the P wave produces a sawtooth pattern with regular conduction to the ventricles
- Wave of contraction around the atria causing the repolarisation of the AV node

389
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

390
Q

What are ventricular ectopics?

A

Extra ventricular contractions –> palpitations/heart missing a beat

391
Q

what are the causes of long QT syndrome?

A
  1. Congenital
  2. hypokalaemia,
  3. hypocalcaemia
  4. Drugs - amiodarone, tricyclic antidepressants
  5. bradycardia
  6. Acute MI
  7. diabetes
392
Q

what is the clinical presentation of long QT syndrome?

A
  1. Palpitations
  2. Syncope
    - may progress to VF
393
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

394
Q

Describe a first degree heart block

A

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

  • PR interval >0.22s
  • asymptomatic
395
Q

Describe a second degree heart block

A

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

396
Q

Describe a Mobitz type 1 second degree heart block

A

PR interval gradually increases until AV node fails and no QRS is seen
PR interval returns to normal and the cycle repeats

397
Q

Describe a Mobitz type 2 second degree heart block

A

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

398
Q

Describe a third degree heart block

A

Atrial activity fails to conduct to the ventricles
P waves and QRS complexes occur independently
ventricular contractions are maintained by spontaneous escape rhythm originating below the block

399
Q

What are the treatments for heart blocks?

A

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

400
Q

what are the causes of heart block?

A 
Athletes
Sick sinus syndrome
IHD – esp MI
Acute myocarditis
Drugs
Congenital 
Aortic valve calcification
Cardiac surgery/trauma
401
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)

402
Q

Explain the pathophysiology of a BBB

A

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

403
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

404
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

405
Q

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

A

DC cardioversion

406
Q

Name 4 valvular heart diseases

A
  1. Aortic stenosis
  2. Mitral regurgitation
  3. Mitral stenosis
  4. Aortic regurgitation
407
Q

Briefly describe aortic stenosis

A

Narrowing of the aortic valve resulting in obstruction to left ventricular stroke volume

408
Q

Name the 3 types of aortic stenosis

A
  1. Surpavalvular
  2. Subvalvular
  3. Valvular = most common
409
Q

What are the causes of aortic stenosis?

A
  • Degeneration and calcification of a normal valve – presenting in the elderly
  • Calcification of a congenital bicuspid valve – presenting in middle age and predominant in males
  • Rheumatic heart disease
410
Q

Describe the pathophysiology of aortic stenosis

A

Obstruction to left ventricular emptying results in left ventricular hypertrophy
Increased myocardial oxygen demand, relative ischaemia of the myocardium and consequent angina and arrhythmias
Left ventricular systolic function typically conserved

411
Q

what are the 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
412
Q

what are the signs of aortic stenosis?

A
  • ejection systolic murmur radiating to carotids and apex - crescendo-decrescendo
  • sustained, heaving apex
  • slow rising pulse
  • narrow pulse pressure
  • soft S2 if severe
413
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 (diagnostic)
    High gradient = severe stenosis
  • CXR - prominence of ascending aorta
  • ECG - depressed ST and T wave inversion
414
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)
415
Q

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

A

Aortic and mitral stenosis are mechanical problems

416
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
417
Q

What is mitral regurgitation?

A

Backflow of blood from the LV to the LA during systole

LV volume overload

418
Q

What can cause mitral regurgitation?

A
  1. Myxomatous degeneration (mitral valve prolapse) - most common cause
  2. Ischaemic mitral valve
  3. Rheumatic heart disease
  4. IE
  5. dilating left ventricle
419
Q

Describe the pathophysiology of mitral regurgitation

A

Circulatory changes depend on speed on onset and severity
Long standing MR produces little increase in left atrial pressure – accommodated by large LV
In acute MR an increased in RA pressure increases pulmonary venous pressure and pulmonary oedema
Left ventricle dilates but more so in chronic MR

420
Q

what are the symptoms of mitral regurgitation?

A

palpitations
exertional dyspnoea
fatigue
weakness

421
Q

Give 3 signs of mitral regurgitation

A
  1. Pan-systolic murmur radiating to left axilla
  2. Soft/absent S1
  3. displaced, thrusting apex
  4. atrial fibrillation
422
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
  4. doppler and colour flow doppler to measure severity
423
Q

What is the management of mitral regurgitation?

A
  • Mild is managed by following patient with echoes every 1-5yrs
  • Beta-blockers - ATENOLOL
  • Calcium channel blockers
  • DIGOXIN
  • Diuretics - FUROSEMIDE
  • ACEIs - RAMIPRIL or HYDRALAZINE
  • Surgical intervention if severe and symptomatic or
    - If ejection fraction <60%
    - New onset AF
424
Q

What is aortic regurgitation?

A

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

425
Q

What causes aortic regurgitation?

A

acute

  • infective endocarditis
  • rheumatic fever
  • aortic dissection

chronic

  • rheumatic disease
  • bicuspid aortic valve
  • aortic endocarditis
426
Q

what is the pathophysiology of aortic regurgitation?

A
  • Chronic regurgitation volume loads the left ventricle and results in hypertrophy and dilation
  • SV increases so increased pulse pressure and myriad of clinical symptoms
  • Contraction of ventricle deteriorates – LV failure
  • Adaptations to the volume load entering the LV do not occur in acute AR and patients present with pulmonary oedema and reduced SV
427
Q

Give 3 symptoms of aortic regurgitation

A
  • palpitations
  • angina
  • dyspnoea
428
Q

Give 3 signs of aortic regurgitation

A
  • early diastolic murmur - decrescendo
  • water hammer pulse
  • wide pulse pressure
  • displaced apex
429
Q

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

A

CXR - cardiomegaly, aortic root enlargement
ECHO - assess severity
ECG - left ventricular hypertrophy
cardiac catheterisation

430
Q

Describe the management for someone with aortic regurgitation

A

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

431
Q

What is mitral stenosis?

A

Obstruction of LV inflow that prevents proper filling during diastole

432
Q

Name 3 causes of mitral stenosis

A
  1. Rheumatic heart disease
  2. IE
  3. Mitral annular calcification - rarer
433
Q

Describe the pathophysiology of mitral stenosis

A

Thickening and immobility of the valve leads to obstruction of blood flow from left atrium to left ventricle
Left atrial pressure increases – left atrium dilation and hypertrophy
Pulmonary venous, arterial and right heart pressure increases

434
Q

what are the symptoms of mitral stenosis?

A
  1. progressive dyspnoea
  2. Haemoptysis (coughing up blood)
  3. palpitations (AF)
  4. chest pain
435
Q

what are the signs of mitral stenosis?

A

rumbling mid-diastolic murmur with opening snap - decrescendo-presystolic crescendo

  1. malar flush
  2. AF
  3. tapping apex beat
  4. low volume pulse
  5. loud snapping S1
436
Q

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

A
  1. ECG - AF, left atrial hypertrophy causes bifid P wave
  2. CXR - large L atrium, pulmonary oedema
  3. Echo - gold standard for diagnosis
437
Q

Describe the management for mitral stenosis

A

If mild treatment is not required
Beta blockers control HR - ATENOLOL and DIGOXIN
Diuretics for fluid overload - FUROSEMIDE
Percutaneous balloon valvotomy to increase size of mitral valve opening
Mitral valve replacement

438
Q

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

A

Mitral stenosis

439
Q

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

A

Mitral regurgitation

440
Q

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

A

Aortic stenosis

441
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

442
Q

What is infective endocarditis?

A

an infection of the endocardium or vascular endothelium of the heart

443
Q

Name 4 types of infective endocarditis

A
  1. Left sided native IE
  2. Left sided prosthetic IE
  3. Right sided IE
  4. Device related IE (pacemaker, defibrillators)
444
Q

Which type of infective endocarditis is more likely to spread systemically?

A

Left sided IE - more likely to cause thrombo-emboli

Right sided IE could spread to the lungs

445
Q

what are the risk factors for infective endocarditis?

A
  • IV drug use
  • poor dental hygiene
  • skin and soft tissue infections
  • dental treatment
  • IV cannula
  • cardiac surgery
  • pacemaker
  • immunocompromised
446
Q

Which bacteria are most likely to cause infective endocarditis?

A
  1. Staphylococcus aureus
  2. Staphlococcus epidermidi (coagulase negative staph)
  3. Streptococcus viridian’s (alpha haemolytic)
447
Q

Give 3 groups of people who are at risk of infective endocarditis

A 
more common in developing countries
males > females
1. Elderly 
2. IV drug users
3. Those would prosthetic valves 
4. Those with rheumatic fever 
5. Young with congenital heart disease
448
Q

Describe the pathophysiology of infective endocarditis

A
  • Usually the consequence of the presence of organisms in the blood and abnormal cardiac endothelium that facilitates adherence and growth
  • A mass of fibrin, platelets and infectious organisms form vegetations along the edges of the valve
  • Virulent organisms destroy the valve, producing regurgitation and worsening heart failure
449
Q

What is the hallmark of infective endocarditis?

A

Vegetation - lumps of fibrin hanging of heart valves

450
Q

Name 2 sites where vegetation is likely in infective endocarditis

A
  1. Atrial surface of AV valves

2. Ventricular surface of SL valves

451
Q

Give 3 symptoms of infective endocarditis

A 
Fever
Rigors
Night sweats
Malaise
Weight loss
452
Q

Give 4 signs of infective endocarditis

A
  1. Splinter haemorrhages - on nails
  2. Osler’s nodes - on hands
  3. Janeway lesions - on hands
  4. Roth spots - in eyes
  5. embolic skin lesions - skin
  6. petechiae - skin
  7. Heart murmurs

anaemia
splenomegaly
clubbing
valve disease

453
Q

Name the criteria that is used in the diagnosis of infective endocarditis

A

Duke’s criteria

454
Q

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

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

2. Positive echo showing endocardial involvement

455
Q

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

A
  1. Blood cultures - essential
  2. Echo - TTE ot TOE
  3. Bloods - raised ESR and CRP, normochromic normocytic anaemia
  4. ECG - long PR interval, MI
456
Q

what are the pros and cons of a trans-thoarcic echo (TTE)?

A 
Advantages:
1. Safe
2. Non-invasive, no discomfort 
Disadvantage:
1. Poor images
457
Q

what are the pros and cons of a trans-oesophageal echo (TOE)?

A 
Advantage:
1. Excellent images 
Disadvantage:
1. Discomfort 
2. Small risk of perforation or aspiration
458
Q

Describe the treatment for infective endocarditis

A
  1. Antibiotics based on cultures
  2. Treat any complications
  3. Surgery - remove and replace valve
459
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
460
Q

Why is it important to remove large vegetations?

A

To prevent them embolising and causing a stroke, MI etc

461
Q

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

A

They may have previously received antibiotics

462
Q

Name 2 drugs that can prolong the QT interval

A
  1. Sotalol

2 Amiodarone

463
Q

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

A

Block the inactivation gate of the sodium channel

464
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

465
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

466
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
467
Q

what are the different types of shock?

A
  1. Hypovolaemic
  2. Haemorrhagic
  3. Septic
  4. Anaphylactic
  5. Neurogenic
  6. Cardiogenic
468
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
  3. low blood volume
469
Q

What can cause cardiogenic shock?

A

Acute MI
pump failure
cardiac arrest

470
Q

What is septic shock?

A

A systemic inflammatory response associated with an infection (bacterial endotoxins)
it occurs when sepsis is complicated by persistent hypotension that is unresponsive to fluid resuscitation

471
Q

What is anaphylactic shock?

A

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

472
Q

Classification of haemorrhagic 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

slightly anxious

473
Q

Classification of haemorrhagic 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

mildly anxious

474
Q

Classification of haemorrhagic 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

confused

475
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
476
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

477
Q

What are ventricular septal defects?

A

Ventricular septal defect = abnormal connection between the 2 ventricles

478
Q

Would a baby born with ventricular septal defects be 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

479
Q

what is the clinical presentation of ventricular septal defects?

A

Pulmonary hypertension
breathless skinny baby
Increased resp rate,
tachycardia

480
Q

What syndrome might ventricular septal defects lead on to?

A

Eisenmengers syndrome

481
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

482
Q

What are the risks associated with Eisenmengers syndrome?

A
  1. Risk of death
  2. Endocarditis
  3. Stroke
483
Q

What are atrial septal defects?

A

Atrial septal defect = abnormal connection between the two atria
this causes higher pressure in the left atrium (left to right shunt)
women > men - often diagnosed in adulthood

484
Q

Would a baby born with atrial septal defects be cyanotic?

A

NO

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

485
Q

what are the clinical features of an atrial septal defect?

A

Mostly asymptomatic

dyspnoea,
exercise intolerance,
atrial arrhythmias
pulmonary flow murmurs

486
Q

what is the treatment for atrial septal defects?

A

Surgical closure - Percutaneous (key hole)

most close spontaneously

487
Q

What are atrioventricular septal defects?

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

488
Q

What happens to the AV valves in atrioventricular septal defects?

A

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

Usually leaks to a greater or lesser degree

489
Q

Give 2 clinical signs of atrioventricular septal defects

A
  1. Breathlessness
  2. Poor feeding and weight gain
  3. dyspnoea
  4. tachycardia
490
Q

Does an atrioventricular septal defect need surgical repair?

A

Complete AVSD needs repair

Partial can be left alone if no right heart dilation

491
Q

What is patent ductus arteriosus?

A

Patent ductus arteriosus = persistent communication between proximal left pulmonary artery and descending aorta
- causes lung circulation to be overloaded with pulmonary hypertension and right sided cardiac failure

492
Q

what is the clinical presentation of patent ductus arteriosus?

A
  • continuous murmurs
  • bounding pulse
  • large heart
  • breathlessness
  • tachycardia
493
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
stronger perfusion to upper body than lower body causes decreased renal perfusion - leads to systemic hypertension

494
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

495
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

496
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

497
Q

What is pulmonary stenosis?

A

Narrowing of the RV outflow tract

498
Q

How does a patient present with pulmonary stenosis?

A 
Right ventricular failure 
Collapse 
Poor pulmonary blood flow 
right ventricular hypertrophy
Tricuspid regurgitation
499
Q

How is pulmonary stenosis treated?

A

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

500
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
501
Q

Name 3 congenital heart defect that are not cyanotic

A
  1. VSD
  2. ASD
  3. PDA
    Left to right shunt
502
Q

Name a congenital heart defect that is cyanotic

A
  1. Tetralogy of Fallot

Right to left shunt

503
Q

Why does mitral stenosis cause AF?

A

Increased LA pressure

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

504
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

505
Q

Give 3 symptoms of Dressler’s syndrome

A
  1. Fever
  2. Chest pain
  3. Pericardial rub
    Occurs 2-10 weeks after MI
506
Q

Write an equation for mAP

A

mAP = DP + 1/3PP

507
Q

Give the equation for stroke volume

A

SV = EDV - ESV

508
Q

What is a consequence of peripheral arterial occlusion?

A

Gangrene

509
Q

Give 2 diseases that result from stress induced ischaemia

A
  1. Exercise induced angina

2. Intermittent claudication

510
Q

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

A
  1. Critical limb ischaemia

2. Vascular dementia

511
Q

Give an example of infarction

A

Gangrene

512
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

513
Q

What can intermittent claudication lead on to if left untreated?

A

Critical ischaemia

514
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

515
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

516
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

517
Q

Give a symptom of intermittent caludication

A

Muscle cramps

518
Q

Name 2 diseases that are due to moderate ischaemia

A
  1. Angina

2. Intermittent claudication

519
Q

Name a disease that is due to severe ischaemia

A

Critical limb ischaemia

520
Q

Name 3 causes of an aneurysm

A
  1. Atherosclerotic (most common)
  2. Ateriomegaly
  3. Collagen disease - Marfans, vascular Ehlers Danlos
  4. tobacco smoking
521
Q

Name 2 types of aortic aneurysm

A
  1. Abdominal aortic aneurysm (AAA)

2. Thoracic abdominal aneurysm (TAA)

522
Q

What classifies as an Abdominal aortic aneurysm?

A

> 3 cm

Dilation affects all 3 layers of the vascular tunic

523
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

524
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)

525
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

526
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

527
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

528
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

529
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

530
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

531
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

532
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

533
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

534
Q

what are the risk factors for acute coronary syndromes?

A 
age
male
family history
smoking
hypertension
diabetes mellitus
obesity and sedentary lifestyle
535
Q

what is the management for a STEMI?

A
  • PCI within 120 minutes
  • clopidogrel
  • if PCI isn’t available fibrinolysis
  • alteplase
  • ticagrelor and aspirin
536
Q

what is the management for an NSTEMI?

A
  • use grace score to predict 6 month mortality and risk of further cardiac events
  • fondaparinux
  • low risk = ticagrel and aspirin
  • high risk = angiography and PCI
  • prasugrel and aspirin
537
Q

what is the pre-hospital management for MI?

A
  • aspirin
  • GTN spray
  • morphine
538
Q

what is the hospital management for MI?

A
  • IV morphine
  • oxygen
  • beta blocker - atenolol
  • clopidogrel
539
Q

what is the secondary prevention for MIs?

A

statins
aspirin
warfarin
ACEi

540
Q

what is the role of preload in heart failure?

A
  • heart failure causes decreased volume of blood ejected with each heart beat
  • the myocardial fibres stretch and don’t contract as much
541
Q

what is the role of afterload in heart failure?

A
  • increased afterload causes increased EDV
  • this causes decreased SV and decreased CO
  • this is a vicious circle and continues to exacerbates the problem
542
Q

what does the level of brain natriuretic peptide (BNP) tell you?

A
  • levels are directly correlated to ventricular wall stress and the severity of heart failure
  • the levels are increased in those with heart failure
543
Q

what additional investigations should be undertaken for acute heart failure?

A
  • serum troponin

- D-dimer

544
Q

what are the causes of cor pulmonale?

A
  • chronic lung disease
  • pulmonary vascular disorders
  • neuromuscular and skeletal diseases
545
Q

what are the signs of cor pulmonale?

A
  • cyanosis
  • tachycardia
  • raised JVP
  • RV heave
  • pan-systolic murmur due to tricuspid regurgitation
  • hepatomegaly
  • oedema
546
Q

what are the symptoms of cor pulmonale?

A
  • dyspnoea
  • fatigue
  • syncope
547
Q

what investigations should be undertaken for cor pulmonale?

A

arterial blood gas

  • hypoxia
  • sometimes shows hypercapnia
548
Q

what is the management for cor pulmonale?

A
  • treat the underlying cause
  • oxygen
  • diuretics
  • venesection if haematocrit >55
  • heart-lung transplant in young patients
549
Q

what is the epidemiology of hypertension?

A
  • major risk factor for CVD
  • men > women
  • underdiagnosed, undertreated and poorly controlled in the UK
550
Q

what are the complications of atrial fibrillation?

A
  • increased risk of stroke
    • due to static blood in the atria
    • the blood pools and it remains still, causing it to clot and embolise
551
Q

what are the causes of atrial flutter?

A
  • idiopathic
  • CHD
  • hypertension
  • heart failure
  • COPD
  • pericarditis
  • obesity
552
Q

what are the risk factors for atrial flutter?

A
  • atrial fibrillation
553
Q

what is the management for atrial flutter?

A
  • Cardioversion
    - Give a LMWH
    - Shock with defibrillator
  • Catheter ablation – creates a conduction block
  • IV Amiodarone – restore sinus rhythm
554
Q

what are the risk factors for AVNRT?

A 
exertion
emotional stress
coffee
tea
alcohol
555
Q

what is malignant hypertension?

A

markedly raised diastolic BP usually over 120mmHg and progressive renal disease

usually evidence of acute haemorrhage and papilledema

556
Q

what are the consequences of malignant hypertension?

A
  • cardiac failure (LVH)
  • blurred vision (papilledema)
  • haematuria - due to fibrinoid necrosis of glomeruli
  • severe headache and cerebral haemorrhage
557
Q

what is the treatment for recurrent pericarditis?

A
  • The first line treatment is oral NSAIDs e.g. Ibuprofen
  • Colchicine has been proven to be more effective than Aspirin alone
  • In resistant cases, oral corticosteroids e.g. -Prednisolone may be effective, and in some patients, pericardiectomy (removal of part/most of the pericardium) may be appropriate
558
Q

what is the pathophysiology of pericarditis?

A
  • Pericardium becomes acutely inflamed, with pericardial vascularisation and infiltration with polymorphonuclear leukocytes
  • A fibrinous reaction frequently results in exudate and adhesions within the pericardial sac, and a serous or haemorrhagic effusion may develop
559
Q

what is the clinical presentation of pericardial effusion?

A
  • Symptoms of a pericardial effusion commonly reflect the underlying pericarditis
  • Soft & distant heart sounds
  • Apex beat obscured
  • Raised jugular venous pressure
  • Dysponea
560
Q

what investigations are undertaken for angina?

A
  • Diagnosis largely based on clinical history
  • ECG usually normal
    Resting ECG may show ST depression and T wave flattening or inversion during an attack
  • Coronary angiography sometimes used in patients with chest pain where diagnosis of angina is unclear - gold standard for diagnosis
  • Lipid profile - may have high LDL
  • FBC - rule out anaemia
  • HbA1c - exclude DM
561
Q

what are the risk factors of MI?

A

Age, male, history of CVD, FHx
Premature menopause
DM, smoking, hypertension, hyperlipidaemia, obesity, sedentary lifestyle

562
Q

what is the epidemiology of hypertrophic cardiomyopathy?

A
  • autosomal dominant - familial
  • can present at any age
  • most common cause of sudden cardiac death in young people
563
Q

what are the signs of dilated cardiomyopathy?

A
  • heart failure
  • arrhythmia
  • thromboembolism
  • increased JVP
  • sudden death
564
Q

what are the signs of restrictive cardiomyopathy?

A
  • Increased JVP, diastolic collapse, elevated on inspiration
  • Hepatic enlargement
  • Ascites
  • Oedema
  • Third and fourth heart sounds
565
Q

what are the symptoms of restrictive cardiomyopathy?

A

Dyspnoea
Fatigue
Embolic symptoms

566
Q

what are the investigations for restrictive cardiomyopathy?

A

CXR, echo, ECG abnormal but non-specific

Cardiac catheterisation = diagnostic

567
Q

what is the management for restrictive cardiomyopathy?

A
  • no specific treatment

- poor prognosis

568
Q

what is the epidemiology of aortic dissection?

A
  • men>female
  • 40-60yrs
  • 65% occur in ascending aorta
569
Q

what is an aortic dissection?

A

Aortic Dissection is a tear in the intimal layer of the aorta which leads to a collection of blood between the intima and medial layers.

570
Q

what are the risk factors of aortic dissection?

A 
Hypertension- most common risk factor
Trauma
Vasculitis 
Cocaine use
Connective tissue disorders- cause Aortic Dissection in younger adults
571
Q

what are the clinical features of aortic dissection?

A
  • Sudden and severe tearing pain in chest radiating to back
  • Hypotension
  • Asymmetrical blood pressure
  • Syncope
  • Aortic regurgitation, coronary ischaemia, cardiac tamponade
  • Peripheral pulses may be absent
572
Q

what are the investigations of aortic dissection?

A
  • ECG
  • Chest x-ray - widening mediastinum
  • CT scanning- definitive imaging
573
Q

what is the management of aortic dissection?

A

-Maintain hemodynamic stability- fluid resuscitation, inotropes, noradrenaline
-Opioid analgesia for pain control - MORPHINE
-Surgical intervention:
Endovascular stent-graft repair
-Put patient on antihypertensives following surgery and recovery - IV METAPROLOL (beta-blockers) or IV GTN (vasodilators)

574
Q

what is the pathophysiology of peripheral vascular disease?

A

Commonly atherosclerosis leading to claudication of vessels
Other (rarer) causes of claudication:
- aortic coarctation,
- temporal arteritis,
- Buerger’s disease.
End stage PVD= Critical Limb Ischaemia (6 P’s)

575
Q

what is the epidemiology of peripheral vascular disease?

A

Men > women

Usually affects the aorta-iliac and infra-inguinal arteries

576
Q

what is the clinical presentation of peripheral vascular disease?

A
  • Pain in lower limbs on exercise, relieved on rest- intermittent claudication
  • Severe unremitting pain in foot (esp at night- hangs foot out of bed)
  • Leg may be pale, cold, loss of hair, skin changes
577
Q

what are the investigations for peripheral vascular disease?

A

Ankle brachial pressure index (ABPI) - <0.90

Measures ratio of systolic BP at ankle and in arm to provide measure of blood flow at the level of the ankle

578
Q

what is the treatment for critical limb ischaemia?

A

Revascularisation (e.g. stenting, angioplasty, bypassing)

Amputation if unsuitable

579
Q

what is the epidemiology of mitral stenosis?

A
  • men>women

- Prevalence/incidence decreasing due to decrease of rheumatic heart disease

580
Q

what are the risk factors of mitral stenosis?

A
  • history of rheumatic fever

- untreated strep infections

581
Q

what are the risk factors for mitral regurgitation?

A 
female
lower BMI
advancing age
renal dysfunction
prior MI
582
Q

what is the clinical presentation of atrial flutter?

A 
Palpitations
Breathlessness
chest pain 
Dizziness
Syncope
fatigue
583
Q

what are the risk factors for atrial fibrillation?

A 
Over 60 
Diabetes, 
Hypertension
coronary artery disease 
previous MI
structural heart disease
584
Q

what are the causes of RBBB?

A

Pulmonary embolism
IHD
Atrial ventricular septal defect

585
Q

what is the pathophysiology of RBBB?

A

Right bundle doesn’t conduct
Impulse spreads from left ventricle to right
Late activation of RV

586
Q

what is the clinical presentation of RBBB?

A

Asymptomatic

syncope/presyncope

587
Q

what is the treatment for RBBB?

A

Pacemaker
CRT – cardiac resynchronisation therapy
Reduce blood pressure

588
Q

what is the clinical presentation of LBBB?

A

Asymptomatic

syncope/presyncope

589
Q

what is the pathophysiology of LBBB?

A

Left bundle doesn’t conduct
Impulse spreads from right ventricle to left
Late activation of LV

590
Q

what is the treatment for LBBB?

A

Pacemaker
CRT – cardiac resynchronisation therapy
Reduce blood pressure

591
Q

what are the causes of LBBB?

A

IHD

Aortic valve disease

592
Q

what are the investigations for heart block?

A

ECG

593
Q

what is the treatment for heart block?

A 
Cardioversion
   - Give a LMWH
   - Shock with defibrillator 
Catheter ablation – creates a conduction block
IV Amiodarone – restore sinus rhythm
594
Q

what is the presentation of first degree heart block?

A

asymptomatic

595
Q

what is the clinical presentation of Mobitz type 1 second degree heart block?

A

light-headedness
dizziness
syncope

596
Q

what is the clinical presentation of Mobitz type 2 second degree heart block?

A

SOB
postural hypotension
chest pain

597
Q

what is the clinical presentation of third degree heart block?

A

dizziness

blackouts

598
Q

what are the investigations for prolonged QT syndrome?

A

ECG - long QT interval

599
Q

what is the treatment for prolonged QT syndrome?

A
  • Treat underlying cause

- If acquired give IV ISOPRENALINE

600
Q

what is the epidemiology abdominal aortic aneurysm?

A
  • incidence increases with age
  • men > females
  • most commonly occur below renal arteries
601
Q

what are the risk factors for abdominal aortic aneurysm?

A
  • Smoking- MAJOR
  • Family history
  • Connective tissue disorders- Marfan’s, Ehlers-Danlos
  • Age
  • Atherosclerosis
  • Male
602
Q

what is the clinical presentation of an unruptured abdominal aortic aneurysm?

A
  • often asymptomatic
  • causes symptoms if expanding rapidly
  • pain in abdomen, loin or groin
  • pulsatile abdominal swelling
  • bruit on ascultation
603
Q

what is the clinical presentation of a ruptured abdominal aortic aneurysm?

A
  • intermittent/continuous abdominal pain - radiates to back, iliac fossa or groin
  • painful pulsatile mass
  • hypovolaemic shock
  • syncope
  • nausea, vomiting
  • profound anaemia
  • sudden death
604
Q

what are the investigations for abdominal aortic aneurysm?

A
  • Abdominal ultrasound – can assess aorta to degree of 3mm

- CT or MRI angiography scans

605
Q

what is the management for abdominal aortic aneurysm?

A
  • ruptured = urgent repair (do not wait for imaging)
  • symptomatic = repair indicated regardless of diameter
  • asymptomatic AAA = surveillance until high risk of rupture - 5.5cm in men and 5.0cm in women
606
Q

what are the complications of abdominal aortic aneurysm?

A
  • rupture of AAA
  • thromboembolisms
  • fistula formation
607
Q

what can cause septic shock?

A

toxins in blood

608
Q

what can cause anaphylactic shock?

A

severe allergic reaction - release of IgE and histamine

609
Q

what is the pathophysiology of cardiogenic shock?

A

decreased MAP

decreased CO

610
Q

what is the clinical presentation of cardiogenic shock?

A 
tachycardia
tachypnoea
decreased urine output
hypotension
cold peripheries
chest pain
611
Q

what is the treatment for cardiogenic shock?

A

ABCDE

resuscitation

612
Q

what is the pathophysiology of hypovolaemic shock?

A

decreased MAP

decreased CO

613
Q

what is the clinical presentation of hypovolaemic shock?

A

tachypnoea
weak rapid pulse
cyanosis
increased CRT

614
Q

what is the treatment of hypovolaemic shock?

A

ABCDE
resuscitation
fluids
vasodilator - GTN

615
Q

what is the pathophysiology of septic shock?

A

decreased MAP

derangement in physiology

616
Q

what is the clinical presentation of septic shock?

A 
tachycardia
diarrhoea and vomiting
decreased urine output
decreased O2
hypotension
617
Q

what is the treatment for septic shock

A

broad spectrum IV antibiotics
fluids
O2

618
Q

what is the pathophysiology of anaphylactic shock?

A

histamine release
vasodilation
hypoxia

619
Q

what is the clinical presentation of anaphylactic shock?

A 
Signs of profound vasodilation 
Warm peripheries 
Low BP and tachycardia 
Bronchospasm 
Pulmonary oedema
620
Q

what is the treatment for anaphylactic shock?

A

resuscitation

adrenaline

621
Q

what antibiotics are used for endocarditis?

A

staph = vancomycin
if MRSA add rifampicin

other bacteria = benzylpenicillin and gentamycin

622
Q

how can endocarditis be prevented?

A
  • good oral health
  • no IV drug use
  • educate surgery patients on symptoms
623
Q

what is rheumatic fever?

A

systemic infection common in developing countries from a Lancefield group A B-haemolytic streptococci

An antibody from the cell wall cross-reacts with valve tissue which can cause permanent damage to the heart valves

624
Q

what are the symptoms of rheumatic fever?

A 
Fever 
Arthritis – painful, tender joints
Chest pain
SOB
Fatigue
Chorea – jerky movements
625
Q

what are the signs of rheumatic fever?

A 
Tachycardia
Murmur – dependant on the valve
Pericardial rub 
Erythema marginatum – red rash with raised edges and clear centre on trunk, thighs or arms
Prolonged PR interval
626
Q

what are the investigations for rheumatic fever?

A
  • Jones criteria - Recent strep infection and 2 major or 1 major and 2 minor criteria

Major criteria:

  • Carditis - tachycardia, murmurs, pericardial rub, cardiomegaly
  • Arthritis - polyarthritis, usually larger joints
  • Erythema marginatum - red rash with raised edges and clear centre
  • Sydenham’s chorea - unilateral/bilateral involuntary semi-purposeful movements

Minor criteria:

  • Fever
  • Raised ESR/CRP
  • Arthralgia - as long as no arthritis
  • Prolonged PR interval
  • Previous rheumatic fever
627
Q

what is the management for rheumatic fever?

A
  • bed rest until CRP is normal for 2 weeks
  • BENZYLPENICILLIN IV, then PHENOXYMETHYLPENICILLIN for 10 days
  • Analgesia - ASPIRIN
  • HALOPERIDOL / DIAZEPAM for chorea
628
Q

what is the clinical presentation of tetralogy of fallot?

A 
central cyanosis
low birthweight and growth
dyspnoea on exertion
delayed puberty
systolic ejection murmur
629
Q

what are the investigations of tetralogy of fallot?

A

CXR shows boot shaped heart

Echocardiogram

630
Q

what is the management of tetralogy of fallot?

A
  • Full surgical treatment during first 2 years of life due to the progressive cardiac debility and cerebral thrombosis risk
  • Often get pulmonary valve regurgitation in adulthood and require another surgery
631
Q

what are the signs of pericardial effusion?

A
  • Muffled heart sounds - effusion obscures apex beat, and heart sounds are soft
  • Kussmaul’s sign – elevated jugular pressure that rises with inspiration
  • Fall in BP of more that 10mmHg on inspiration (result of increased venous return to right side of heart)
  • Bronchial breathing at left base
632
Q

what are the investigations for pericardial effusion?

A
  • Chest x ray shows large globular heart
  • ECG - low voltage QRS complexes with sinus tachycardia
  • Echocardiography is diagnostic - echo-free space around heart
633
Q

what is the management for pericardial effusion?

A
  • Most effusions resolve naturally
  • Underlying cause should be sought and treated
  • If effusion recurs despite treatment of underlying cause, excision of pericardial segment allows fluid to be absorbed
  • Pericardiocentesis - Diagnostic or therapeutic
634
Q

what are the investigations for cardiac tamponade?

A
  • CXR – large globular heart
  • Beck’s triad – falling BP, rising jugular venous pressure, muffled heart sounds
  • ECG – low voltage QRS complexes with sinus tachycardia
  • Echocardiography is diagnostic – echo-free space around heart
635
Q

what is cardiac tamponade?

A

Cardiac tamponade occurs when a large amount of pericardial fluid restricts diastolic ventricular filling and causes marked reduction in cardiac output

636
Q

what are the causes of AVRT?

A 
Congenital
Hypokalaemia 
Hypocalcaemia 
Drugs: amiodarone, tricyclic antidepressants
Bradycardia
Acute MI
Diabetes
637
Q

what is the clinical presentation of AVRT?

A

Palpitations
Severe dizziness
Dyspnoea
Syncope

638
Q

what are the investigations for AVRT?

A

ECG - pre excitation

  • short PR interval
  • delta waves (wide QRS complex that begins slurred)
639
Q

what is the treatment for AVRT?

A 
Vagal manoeuvre
     Breath holding 
     Carotid massage
     Valsalva manoeuvre
IV adenosine
Surgery – catheter ablation of pathway
640
Q

what is the pathophysiology of AVNRT?

A
  • 2 pathways in AVN in this pathway
    • 1 has short refractory period and slow conduction
    • 1 has longer effective refractory period and fast conduction
  • In sinus rhythm the atrial impulse usually conducts through fast pathways
  • If impulse occurs early when the fast pathway is still refractory the slow pathway takes over
  • Once the fast pathway is out of refractory the same impulse can travel back up the fast pathway
  • By this time the slow pathway is out of refractory and the signal can go back down the slow pathway
    This sets up a re-entry loop – heart rate of 100-250bpm
    Atria contract quickly in one cycle then slow in the next
641
Q

what are the investigations for AVNRT?

A

Sometimes ECG QRS complexes will show BBB
P wave not visible or seen immediately before (normal) or after QRS complex due to simultaneous atrial and ventricular activation

642
Q

what is the epidemiology of AVNRT?

A
  • women > men
  • sudden onset but some risk factors
  • can stop spontaneously or continue to indefinitely until medical intervention
643
Q

what is the clinical presentation of coarctation of the aorta?

A
  • right arm hypertension
  • bruits over scapulae and back
  • Murmur
  • headaches and
  • nosebleeds
  • hypertension in upper limbs
  • discrepancy in bp in upper and lower body
644
Q

what are the investigations for coarctation of the aorta?

A

CXR - dilated aorta indented at the site of the coarctation
ECG - left ventricular hypertrophy
CT - can accurately demonstrate coarctation and quantify flow

645
Q

what is the management for coarctation of the aorta?

A

surgery, balloon dilation and stenting

646
Q

what is the epidemiology of coarctation of the aorta?

A

men > women

associated with turner’s syndrome, patent ductus arteriosus

647
Q

what are the investigations for patent ductus arteriosus?

A
  • CXR - large shunt of aorta and pulmonary arterial system may be prominent
  • ECG - may demonstrate left atrial abnormality and left ventricular hypertrophy
  • echocardiogram - may show dilated left atrium and left ventricle
648
Q

what is the treatment for patent ductus arteriosus?

A

Closed surgically or percutaneously

- INDOMETACIN -(prostaglandin inhibitor) can be given to stimulate duct closure

649
Q

what are the investigations for a ventricular septal defect?

A

CXR shows big heart, murmur

Echocardiogram - High pressure in left ventricle – left to right shunt

650
Q

what is the treatment for ventricular septal defects?

A 
If small no intervention, otherwise treat with surgery 
If moderately sized
     - FUROSEMIDE
     - ACE inhibitor - RAMIPRIL
     - DIGOXIN
651
Q

what are the investigations for atrial septal defects?

A

CXR show large heart and pulmonary arteries
ECG – RBBB
echocardiogram

652
Q

what is the clinical presentation of ventricular ectopic?

A

Uncomfortable if frequent
Irregular pulse
Usually asymptomatic but may feel faint/dizzy

653
Q

what are the investigations for ventricular ectopic?

A

ECG – widened QRS >0.12s

654
Q

what is the management for ventricular ectopic?

A

Beta blockers if symptomatic

655
Q

what are the risk factors for ventricular ectopic?

A

MI

656
Q

what are the causes of left sided heart failure?

A 
Coronary artery disease
Myocardial infection
Cardiomyopathy
Congenital heart defects
Valvular heart disease
Arrhythmias
657
Q

what are the causes of right sided heart failure?

A 
Right ventricular infarct 
Pulmonary hypertension
Pulmonary embolism 
COPD
Progression of left sided heart failure
Cor Pulmonale
658
Q

what are the causes of systolic heart failure?

A

Ischaemic heart disease
Myocardial infection
Cardiomyopathy

659
Q

what are the causes of diastolic heart failure?

A

aortic stenosis

chronic hypertension

660
Q

what is congestive heart failure?

A

both sided heart failure

661
Q

what murmur is heard with mitral stenosis?

A

rumbling mid-diastolic murmur with opening snap

662
Q

what murmur is heard with mitral regurgitation?

A

pan systolic murmur radiating to the left axilla

663
Q

what murmur is heard with aortic stenosis?

A

ejection systolic murmur radiating to carotids and apex

664
Q

what murmur is heard with aortic regurgitation?

A

early diastolic murmur (best heard on expiration with patient sat forwards)

665
Q

ECG changes in which regions indicates a lateral MI?

A

lead I
aVL
V5
V6

666
Q

ECG changes in which regions indicates an inferior MI?

A

lead II
lead III
aVF

667
Q

ECG changes in which regions indicates a septal MI?

A

V1

V2

668
Q

ECG changes in which regions indicates an anterior MI?

A

V3

V4

669
Q

ECG changes in lateral regions are caused by which artery in an MI?

A

lateral = circumflex

670
Q

ECG changes in inferior regions are caused by which artery in an MI?

A

inferior = RCA

671
Q

ECG changes in anterior regions are caused by which artery in an MI?

A

anterior = LAD

672
Q

A blockage in the LAD will cause ECG changes in which regions?

A

anterior - V3, V4

septal - V1, V2

673
Q

A blockage in the RCA will cause ECG changes in which regions?

A

inferior - leads II, III, aVF

674
Q

A blockage in the circumflex artery will cause ECG changes in which regions?

A

lateral - lead I, aVL, V5, V6

675
Q

what is the secondary prevention of ACS?

A

ACE inhibitor
Beta-blocker
Dual antiplatelet - clopidogrel and aspirin 75mg for minimum 12 months
Statin
Lifestyle advice - exercise, diet, smoking, alcohol

MY REVISION - ALL PHASES (26 decks)

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