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Phase 2A revision > CARDIO > Flashcards

CARDIO Flashcards

1
Q

Define atherosclerosis

A

Build up of plaque in the intima of an artery

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2
Q

What can an atherosclerotic plaque cause?

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

what are the risk factors for atherosclerosis?

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

What are the constituents of an atheromatous plaque?

A

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

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5
Q

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

A

Peripheral and coronary arteries - circumflex, LAD and RCA
Focal distribution along the length

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6
Q

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

A

Media

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7
Q

What is the precursor for atherosclerosis?

A

Fatty streaks

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8
Q

What can cause chemoattractant release?

A

Endothelial cell injury

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9
Q

What is the function of chemoattractants?

A

Signal leukocytes and produce a concentration gradient

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10
Q

What is the function of leukocytes?

A

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

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11
Q

What inflammatory cytokines are found in plaques?

A

IL-1
IL-6
IFN-gamma

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12
Q

Describe the process of leukocyte recruitment

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

What types of molecules are present during leukocyte recruitment?

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

Describe the 5 steps of progression of atherosclerosis

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

At what age do fatty streaks begin to appear?

A

< 10 years old

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16
Q

What are the constituents of fatty streaks?

A

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

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17
Q

What are the constituents of intermediate lesions?

A

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

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18
Q

What are the constituents of fibrous plaques?

A

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

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19
Q

What are fibrous plaques able to do?

A

Impede blood flow and they are prone to rupture

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20
Q

Why might a plaque rupture?

A

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

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21
Q

What the primary treatment for atherosclerosis?

A

Percutaneous Coronary Intervention (PCI)

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22
Q

What is the major limitation of PCI?

A

Restenosis

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23
Q

How can restenosis be avoided following PCI?

A

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

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24
Q

What drugs can patients be started on following a PCI?

A

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

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25
Q

What is the key principle behind pathogenesis of atherosclerosis?

A

It is an inflammatory process

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26
Q

Define atherogenesis

A

The development of an atherosclerotic plaque

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27
Q

Define angina

A

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

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28
Q

What is the most common cause of angina?

A

Narrowing of the coronary arteries due to atherosclerosis

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29
Q

Give 5 possible causes of angina

A
  • atheroma/stenosis of coronary arteries
  • valvular disease
  • aortic stenosis
  • arrhythmia
  • anaemia
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30
Q

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

A

Diameter has to fall below 70%

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31
Q

Name 3 types of angina

A
  • Stable angina
  • Unstable angina
  • Prinzmetal’s angina
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32
Q

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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33
Q

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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34
Q

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

A
  1. Anaemia
  2. Hypoxaemia
  3. Polycythaemia
  4. Hypothermia
  5. Hyper/hypovolaemia
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35
Q

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

A
  1. Hypertension
  2. Tachyarrhythmia
  3. Valvular heart disease
  4. Hyperthyroidism
  5. Cold weather
  6. Heavy meals
  7. Emotional stress
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36
Q

Briefly describe the pathophysiology of angina that results from atherosclerosis

A

On exertion there is increase O2 demand
Coronary blood flow is obstructed by an atherosclerotic plaque –> myocardial ischaemia –> angina

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37
Q

Briefly describe the pathophysiology of angina the results from anaemia

A

On exertion there is increased O2 demand
In someone with anaemia there is reduced O2 transport –> myocardial ischaemia –> angina

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38
Q

Briefly describe the pathophysiology of Prinzmetal’s angina

A

Occurs due to coronary artery spasm

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39
Q

Name 3 differential diagnoses for angina

A
  1. Pericarditis/myocarditis
  2. PE
  3. Chest infection
  4. Dissection of aorta
  5. GORD
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40
Q

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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41
Q

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

A
  1. Have central, tight, radiation to arms, jaw and neck
  2. Precipitated by exertion
  3. Relieved by rest or GTN spray
    3/3 = Typical angina
    2/3 = Atypical pain
    1/3 = Non-anginal pain
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42
Q

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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43
Q

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

A
  1. ECG - usually normal, sometimes ST depression, flat or inverted T waves
  2. 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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44
Q

How can angina be reversed?

A

Resting - reducing myocardial demand

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45
Q

Describe the primary prevention for angina

A
  1. Modify risk factors
  2. Treat underlying causes
  3. Low dose aspirin
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46
Q

Describe the secondary prevention of angina

A
  1. Modify risk facotrs
  2. Pharmacological therapies for symptom relief and to reduce the risk of CV events
  3. Interventional therapies (e.g. PCI)
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47
Q

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

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

other medications include statins and aspirin

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48
Q

Describe the action of beta blockers

A

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

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49
Q

Give 3 side effects of beta blockers

A
  1. Bradycardia
  2. Tiredness
  3. Erectile dysfunction
  4. Cold peripheries
  5. nightmares
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50
Q

When might beta blockers be contraindicated?

A

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

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51
Q

Describe the action of nitrates

A

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

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52
Q

Describe the action of Calcium channel blockers

A

Arterodilators
Reduce BP –> Reduce afterload –> reduced myocardial demand

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53
Q

What 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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54
Q

How does aspirin work?

A

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

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55
Q

What is a caution when prescribing aspirin?

A

Gastric ulceration

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56
Q

How does clopidogrel work?

A

Antiplatelet
P2Y12 inhibitor –> prevents platelet activation

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57
Q

What are statins used for?

A

To reduce the amount of LDL in the blood

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58
Q

What is revascularisation?

A

Used to restore coronary artery and increase blood flow

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59
Q

Name 2 types of revascularisation

A
  1. Percutaneous coronary intervention (PCI)
  2. Coronary artery bypass graft (CABG)
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60
Q

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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61
Q

what are 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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62
Q

Name 2 complications of angina

A
  1. Acute coronary syndromes
  2. Congestive cardiac failure
  3. Conduction disease
  4. Arrhythmia
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63
Q

What are acute coronary syndromes?

A

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

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64
Q

What is the common cause of ACS?

A

Rupture of an atherosclerotic plaque and subsequent arterial thrombosis

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65
Q

What are uncommon causes of ACS?

A
  1. Coronary vasospasm
  2. Drug abuse
  3. Coronary artery dissection
  4. Thoracic aortic dissection
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66
Q

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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67
Q

Describe type 1 MI

A

Spontaneous MI with ischaemia due to a primary coronary event
e.g. plaque erosion/rupture, fissuring or dissection

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68
Q

Describe type 2 MI

A

MI secondary to ischaemia due to increased O2 demand or
decreased supply such as in coronary spasm, coronary
embolism, anaemia, arrhythmias, hypertension or
hypotension

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69
Q

What is troponin a marker for?

A

Cardiac muscle injury

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70
Q

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

A

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

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71
Q

Give 3 signs of unstable angina

A
  1. Cardiac chest pain at rest
  2. Cardiac chest pain with crescendo pattern
  3. No significant rise in troponin
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72
Q

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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73
Q

Give 3 signs of MI

A
  1. Hypo/hypertension
  2. 3rd/4th heart sound
  3. Signs of congestive heart failure
  4. Ejection systolic murmur
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74
Q

Name 3 possible differential diagnoses of MI

A
  1. Pericarditis
  2. Stable angina
  3. Aortic dissection
  4. GORD
  5. Pneumothorax
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75
Q

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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76
Q

What might the ECG of someone with unstable angina show?

A

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

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77
Q

What might the ECG of someone with NSTEMI show?

A

May be normal or might show T wave inversions and ST depression

Might also be R wave regression, ST elevation and biphasic T wave in lead V3

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78
Q

What might the ECG of someone with STEMI show?

A

ST elevation in the anterolateral leads
After a few hours, T waves inlet and deep, broad, pathological Q waves develop

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79
Q

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

A

Normal

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80
Q

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

A

Significantly raised - troponin I and T

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81
Q

A raised troponin is not specific for ACS. In what other conditions might you see a raised troponin?

A
  1. Gram negative sepsis
  2. PE
  3. Myocarditis
  4. Heart failure
  5. Arrhythmias
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82
Q

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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83
Q

What is the treatment of choice for STEMI?

A

PCI within 120 minutes
if not, fibrinolysis - alteplase, streptokinase

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84
Q

What is the function of P2Y12?

A

It amplifies platelet activation

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85
Q

Give 2 potential side effect of P2Y12 inhibitors

A
  1. Bleeding
  2. Rash
  3. GI disturbances - ulceration
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86
Q

Describe the secondary prevention therapy for people after having a STEMI

A
  1. dual antiplatelet therapy - ASPIRIN and CLOPIDOGREL
  2. Statins - ATORVASTATIN
  3. beta-blocker PROPRANOLOL or CCB (verapamil) if BB are contraindicated
  4. ACE inhibitor - RAMIPRIL
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87
Q

What is involved in antithrombotic therapy?

A

Dual antiplatelet therapy = aspirin and clopidogrel
Anticoagulant = heparin

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88
Q

Give 5 potential complications of MI

A
  • sudden death
  • arrhythmias
  • persistent pain
  • heart failure
  • mitral incompetence
  • pericarditis
  • cardiac rupture
  • aneurysm
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89
Q

what conditions can be caused by a previous MI?

A
  1. Shock
  2. Heart failure
  3. Pericarditis
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90
Q

What is a DVT?

A

Blood clot within a blood vessel of the lower limb

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91
Q

What are the clinical features of DVT?

A

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

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92
Q

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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93
Q

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

A
  1. D-dimer (blood test) - look for fibrin breakdown products –> normal excludes DVT diagnosis (abnormal does NOT confirm)
  2. Ultrasound compression test of proximal veins - if you can’t squash the vein = clot
  3. doppler ultrasound
  4. venography
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94
Q

What is the treatment for DVT?

A
  1. LMW heparin
  2. Oral warfarin or direct acting oral anticoagulant (DOAC)
  3. Compression stockings
  4. Treat the underlying cause (e.g. malignancy or thrombophilia)
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95
Q

Name the types of DVT

A
  1. Spontaneous
  2. Provoked - incidence of recurrence is low if you remove the stimulus
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96
Q

Give 5 risk factors for DVT

A
  • increased age
  • pregnancy, OC
  • trauma, surgery
  • past DVT
  • cancer
  • obesity
  • immobility
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97
Q

How can DVTs and PEs be prevented?

A
  1. Hydration
  2. Early mobilisation
  3. Compression sticking/pumps
  4. Low dose LMW heparin
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98
Q

What is low risk thromboprophylaxis treatment?

A

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

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99
Q

What is high risk thromboprophylaxis?

A

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

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100
Q

What might be the consequence of a dislodged DVT?

A

Pulmonary embolism

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101
Q

what are the clinical features of PE?

A

SYMPTOMS
1. Breathlessness
2. Pleuritic chest pain
3. signs/symptoms of DVT

SIGNS
1. Tachycardia
2. Tachypnoea
3. pleural rub

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102
Q

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

A
  • ECG sinus tachycardia - to exclude cardiac cause
  • Blood gases - to exclude respiratory causes
  • D-dimer - normal excludes diagnosis
  • CTPA spiral with contrast - gaps in dye if PE has occurred
  • Ventilation/perfusion scan (used in pregnancy)
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103
Q

What is the treatment for a PE?

A
  • LMW heparin,
  • oral warfarin for 6 months
  • DOAC - for outpatient with a relatively minor PE
  • Treat cause if possible
  • surgery for massive clot - embolectomy
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104
Q

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

A

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

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105
Q

Define thrombosis

A

Blood coagulation inside a vessel

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106
Q

How would you describe an arterial thrombus?

A

Platelet rich (a ‘white thrombosis’)

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107
Q

How would you describe a venous thrombosis?

A

Fibrin rich (a ‘red thrombosis’)

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108
Q

What are the potential consequences of an arterial thrombosis?

A
  1. Coronary circulation = MI
  2. Cerebral circulation = Stroke
  3. Peripheral circulation = Peripheral vascular disease (e.g. gangrene)
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109
Q

What investigations would you do to diagnose an arterial thrombosis?

A

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

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110
Q

What is the treatment for arterial thrombosis?

A
  1. Aspirin
  2. LMW heparin
  3. Thrombolytic therapy: streptokinase tissue plasminogen factor
  4. Treat risk factors
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111
Q

What are the potential consequences of a venous thrombosis?

A

Deep vein thrombosis
Pulmonary embolism

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112
Q

Name 4 causes of a venous thrombosis

A

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

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113
Q

How does heparin work?

A

Inhibits thrombin and factor Xa
Indirect thrombin inhibitor - binds to antithrombin and increased its activity

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114
Q

How do you monitor heparin?

A

Activated partial thromboplastin time
Aim ratio: 1.8-2.8

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115
Q

Why is LMW heparin often used instead of normal heparin?

A

Smaller molecule, less variation in dose and renally excreted

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116
Q

How does warfarin work?

A

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

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117
Q

What is warfarin an antagonist of?

A

Vitamin K

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118
Q

Why is warfarin difficult to use?

A

Lots of interactions
Needs almost constant monitoring
Teratogenic

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119
Q

How is warfarin measured?

A

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

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120
Q

How does Direct Acting Oral Anticoagulant (DOAC) 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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121
Q

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

A

50 ml

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122
Q

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

A

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

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123
Q

What is the function of the pericardium?

A

Restrains the filling volume of the heart

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124
Q

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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125
Q

Define acute pericarditis

A

Acute inflammation of the pericardium with or without effusion

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126
Q

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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127
Q

Describe the chest pain in acute pericarditis

A

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

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128
Q

Why might someone with pericarditis have hiccups?

A

Due to irritation to the phrenic nerve

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129
Q

What is the major differential diagnosis of acute pericarditis?

A

Myocardial infarction

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130
Q

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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131
Q

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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132
Q

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

A
  1. Saddle shaped ST elevation
  2. PR depression
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133
Q

What does a raised troponin in acute pericarditis suggest?

A

Myopericarditis

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134
Q

How can acute pericarditis be clinically diagnosed?

A

Patient has to have at least 2 of the following:
1. Chest pain
2. Friction rub
3. ECG changes
4. Pericardial effusion

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135
Q

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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136
Q

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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137
Q

What is a complication of pericardial effusion?

A

Cardiac tamponade

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138
Q

Why does chronic pericardial effusion rarely cause tamponade?

A

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

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139
Q

Briefly explain the pathophysiology of cardiac tamponade

A

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

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140
Q

What are the signs of Cardiac tamponade?

A

Beck’s triad:
1. low BP but high HR
2. Increased JVP
3. Quiet S1 and S2

  • Pulsus paradoxus = pulses fade on inspiration
  • Kussmaul’s sign = rise in jugular venous pressure with inspiration
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141
Q

What is the treatment of cardiac tamponade?

A

Pericardiocentesis (drainage)

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142
Q

What is chronic constrictive pericarditis?

A

Calcification thickens the pericardium and affects cardiac effusion

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143
Q

What is the treatment for chronic constrictive pericarditis?

A

Surgical excision of thickened pericardium

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144
Q

Name 3 major predictive markers for complications for pericarditis

A
  1. Fever >38 degree
  2. Subacute onset
  3. Large pericardial effusion
  4. Cardiac tamponade
  5. Lack of response to aspirin or NSAIDs after at least 1 week of therapy
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145
Q

What is haemopericaridum?

A

Direct bleeding from vasculature through the ventricular wall following MI

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146
Q

What can cause myocarditis?

A

Viral infection

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147
Q

Give 5 risk factors for peripheral vascular disease

A

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

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148
Q

what are the 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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149
Q

What is critical ischaemia?

A

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

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150
Q

Give 4 signs of critical ischaemia

A
  1. Rest pain
  2. Classically nocturnal
  3. Ulceration
  4. Gangrene
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151
Q

What can cause acute ischaemia?

A

Embolism/thrombosis

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152
Q

Give 6 symptoms of acute ischaemia

A
  1. Pain
  2. Pale
  3. Paralysis
  4. Paraesthesia
  5. Perishing cold
  6. Pulseless
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153
Q

Give 2 examples of acute ischaemia

A
  1. Stroke
  2. MI
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154
Q

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

A

Thrombolysis

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155
Q

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

A

Streptokinase

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156
Q

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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157
Q

Name 2 channelopathies

A
  1. Long QT syndrome
  2. Short QT syndrome
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158
Q

What is the commonest symptom of channelopathies?

A

Recurrent syncope

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159
Q

What is familial hypercholesterolaemia?

A

Inherited abnormality of cholesterol metabolism
LDL receptor affected

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160
Q

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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161
Q

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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162
Q

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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163
Q

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

A

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

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164
Q

Describe the pathophysiology of heart failure

A

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

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165
Q

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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166
Q

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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167
Q

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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168
Q

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

A
  1. Diuretic
  2. Hypotensive
  3. Vasodilators
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169
Q

What are the 3 cardinal symptoms of heart failure?

A
  1. SOB
  2. Fatigue
  3. Peripheral oedema
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170
Q

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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171
Q

what are the clinical features of right HF?

A
  1. Raised JVP
  2. Ascites
  3. peripheral oedema
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172
Q

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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173
Q

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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174
Q

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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175
Q

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

A

An echocardiogram - may reveal cause

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176
Q

what is the management for chronic HF?

A

1st line = ACEi, beta blocker
2nd = ARB + nitrate
3rd = cardiac resynchronization or digoxin
4th = diuretics (furosemide)
5th = aldosterone antagonist (spironolactone)

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177
Q

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

A

Ramipril

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178
Q

Name 3 BB that are used in treatment of HF

A
  1. Propranolol
  2. Bisoprolol
  3. Atenolol
  4. Carvedilol
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179
Q

what is the treatment for acute HF?

A

OMFG
- oxygen
- morphine
- furosemide
- GTN spray

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180
Q

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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181
Q

How can chronic HF be prevented?

A

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

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182
Q

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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183
Q

What is the clinical definition of hypertension?

A

BP > 140/90 mmHg

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184
Q

Name 4 conditions that hypertension is a major risk factor for

A
  1. Stroke
  2. MI
  3. HF
  4. Chronic renal failure
  5. Cognitive decline
  6. Premature death
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185
Q

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

A

5-7 years

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186
Q

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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187
Q

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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188
Q

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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189
Q

Name the 2 types of hypertension

A
  1. Essential (primary) hypertension
  2. Secondary hypertension
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190
Q

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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191
Q

Give 5 causes of secondary hypertension

A

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

most common = primary hyperaldosteronism - Conn’s syndrome

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192
Q

Name 3 endocrine disease that can cause secondary hypertension

A
  1. Conn’s syndrome - hyperaldosteronism
  2. Cushing’s syndrome - excess cortisol –> increase BP
  3. Phaemochromocytoma - adrenal gland tumour, excess catecholamines –> high BP
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193
Q

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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194
Q

What is the clinical presentation of hypertension?

A

Usually asymptomatic
Found on screening

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195
Q

Why might you examine the eyes of someone with hypertension?

A

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

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196
Q

What investigations might you do in someone with hypertension?

A
  1. 24 hour ambulatory blood pressure monitoring –> confirm diagnosis
  2. ECG and Bloods –> identify secondary causes
  • urinalysis - protein, albumin:creatine ratio, haematuria
  • blood tests - serum creatinine, eGFR, glucose
  • fundoscopy - retinal haemorrhage, papillodema
  • ECG - left ventricular hypertrophy
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197
Q

What is the treatment target for hypertension for the following:
a) People aged <80?
b) People aged >80?

A

a) < 140/90 mmHg
b) < 150/90 mmHg

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198
Q

What are the 2 main types of treatment for hypertension?

A
  1. Lifestyle modifications - reduce salt, loss weight, reduce alcohol
  2. Drug therapy = ACD
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199
Q

Describe the pharmacological intervention for someone with hypertension

A
  1. ACEi - ramipril (or ARB - candesartan if ACEi contraindicated)
  2. Calcium channel blocker - amlodipine, diltiazem, verapamil
  3. Diuretics - bendroflumethethizaide, furosemide
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200
Q

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

A

Beta blockers - bisoprolol
statins - simvastatin

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201
Q

Will anti-hypertensives make someone feel better?

A

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

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202
Q

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

A

1 tablet = 10 mmHg reduction in BP

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203
Q

What is cor pulmonale?

A

Right sided heart failure caused by chronic pulmonary arterial hypertension

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204
Q

Write an equation for BP

A

BP = CO x TPR

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205
Q

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

A
  1. RAAS
  2. Sympathetic nervous system
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206
Q

Give 4 functions of angiontensin II

A
  1. Potent vasoconstrictor
  2. Activated sympathetic nervous system - increased NAd
  3. Activates aldosterone - Na+ retention
  4. Vascular growth, hyperplasia and hypertrophy
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207
Q

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

A
  1. Noradrenaline is a vasoconstrictor = increase TPR
  2. NAd has positive chronotropic and inotropic effects
  3. It can cause increase renin release
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208
Q

In what diseases are ACE inhibitors clinically indicated?

A
  1. Hypertension
  2. Heart failure
  3. Diabetic nephropathy
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209
Q

Name 3 ACE inhibitors

A
  1. Ramipril
  2. Enalapril
  3. Perindopril
  4. Trandolapril
  5. Lisinopril
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210
Q

what are the side effects of ACE inhibitors?

A
  1. Hypotension
  2. Hyperkalaemia
  3. Acute renal failure
  4. Teratogenic
  5. cough - from build up of kinin
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211
Q

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

A

ACE inhibitors lead to a build up of kinin
One of the side effects of this is a dry and chronic cough

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212
Q

What are ARBs?

A

Angiotensin II receptor blockers

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213
Q

At which receptor do ARB’s work?

A

AT-1 receptor - prevent angiotensin II binding

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214
Q

In what diseases are ARBs clinically indicated?

A
  1. Hypertension
  2. Heart failure
  3. Diabetic nephropathy
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215
Q

Name 3 ARBs

A
  1. Candesartan
  2. Valsartan
  3. Losartan
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216
Q

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

A

An ARB
e.g. candesartan

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217
Q

Give 4 potential side effect of ARBs

A
  1. Hypotension
  2. Hyperkalaemia
  3. Renal dysfunction
  4. Rash
    Contraindicated in pregnancy
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218
Q

In what diseases are calcium channel blockers clinically indicated?

A
  1. Hypertension
  2. IHD
  3. Arrhythmia
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219
Q

Name 2 calcium channel blockers

A
  1. Amlopipine
  2. Felodipine
  3. Diltiazem
  4. Verapamil
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220
Q

Name 2 dihydropyridines and briefly explain how they work

A

Class of CCBs
Amlodipine and felodipine
Arterial vasodilators

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221
Q

Name a calcium channel blocker that acts primarily on the heart

A

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

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222
Q

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

A

Diltiazem

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223
Q

On what channels do CCB work?

A

L type Ca2+ channels

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224
Q

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

A
  1. Flushing
  2. Headache
  3. Oedema
  4. Palpitations
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225
Q

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

A
  1. Bradycardia
  2. Atrioventricular block
  3. Postural hypotension
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226
Q

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

A

Worsening cardiac failure

227
Q

Give 4 potential side effects of verapamil

A
  1. Worsening of cardiac failure (-ve inotrope)
  2. Bradycardia (-ve chronotrope)
  3. Atrioventricular block (-ve chronotrope)
  4. Constipation
228
Q

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

229
Q

In what diseases are beta blockers clinically indicated?

A
  1. IHD
  2. Heart failure
  3. Arrhythmia
  4. Hypertension
230
Q

Name 3 beta blockers

A
  1. Bisoprolol (beta 1 elective)
  2. Atenolol
  3. Propranolol (beta 1/2 nonselective)
231
Q

Give 5 potential side effects of beta blockers

A
  1. Fatigue
  2. Headache
  3. Sleep disturbances/nightmares
  4. Bradycardia
  5. Hypotension
  6. Cold peripheries
  7. Erectile dysfunction
  8. Bronchospasm
232
Q

Give 3 conditions in which Beta blockers can worsen them

A
  1. Asthma or COPD
  2. PVD
  3. Heart failure
233
Q

In what diseases are diuretics clinically indicated?

A
  1. Heart failure
  2. Hypertension
234
Q

Name 4 classes of diuretics

A
  1. Thiazides
  2. Loop
  3. Potassium sparing
  4. Aldosterone antagonists
235
Q

Where in the kidney do thiazide diuretics work?

A

The distal tubule

236
Q

Name a thiazide

A

Bendroflumethethiazide

237
Q

Name a loop diuretic

A

Furosemide
Bumetanide

238
Q

Name a potassium sparing diuretic

A

Spironolactone
Eplerenone

239
Q

Why are potassium sparing diuretics especially effective?

A

They have anti-aldosterone effects too

240
Q

Give 5 potential side effects of diuretics

A
  1. Hypovolaemia
  2. Hypotension
  3. Reduced serum Na+, K+, Mg+, Ca2+
  4. Increased uric acid –> gout
  5. Erectile dysfunciton
  6. Impaired glucose tolerance
241
Q

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

A

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

242
Q

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

A

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

243
Q

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

A

You would combine ACE inhibitors or ARB with calcium channel blockers

244
Q

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

A

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

245
Q

What is the counter regulatory system to RAAS?

A

Atrial Natriuretic Peptide/BNP (ventricular natriuretic peptide) hormones

246
Q

Where are ANP and BNP produced?

247
Q

What metabolises ANP and BNP?

A

Neprilysin (NEP)

248
Q

What are the functions of ANP and BNP?

A
  1. Increased renal excretion of Na+ and water
  2. Vasodilators
  3. Inhibit aldosterone release
249
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

250
Q

In what diseases are nitrates clinically indicated?

A
  1. IHD
  2. Heart failure
251
Q

Name 2 nitrates that are used pharmacologically

A
  1. GTN spray (short acting)
  2. Isosorbide mononitrate (long acting)
252
Q

How do nitrates work in the treatment of heart failure?

A

They are venodilators so reduce preload and therefore BP

253
Q

Give 2 potential side effects of nitrates

A
  1. Headache
  2. GTN syncope
  3. Tolerance
254
Q

How do anti-arrhythmic drugs work?

A

Interfere with the action potential of the heart in different phases

255
Q

What classification is used to group anti-arrhythmic drugs?

A

Vaughan Williams classification

256
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)

257
Q

Name three class 2 drugs of the Vaughan Williams classification

A

Class 2 are Beta blockers
Propranolol
Atenolol
Bisoprolol

258
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

259
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

260
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

261
Q

What are the main effect of digoxin?

A
  1. Bradycardia
  2. Reduced atrioventricular conduction
  3. Increased force of contraction (positive inotrope)
262
Q

Give 3 potential side effects of digoxin

A
  1. Nausea
  2. Vomiting
  3. Diarrhoea
  4. Confusion
    Also has a narrow therapeutic range
263
Q

In what disease is digoxin clinically indicated?

A
  1. Atrial fibrillation
  2. Severe heart failure
264
Q

What does furosemide block?

A

The Na+/K+/2Cl- transporter

265
Q

Why are beta blockers good in chronic heart failure?

A

They block reflex sympathetic responses which stress the failing heart

266
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
267
Q

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

A

Amlodipine

268
Q

How does amiodarone work?

A

Prolongs action potential by delaying depolarisation

269
Q

Name 4 potential effects of amiodarone

A
  1. QT prolongation
  2. Interstitial lung disease
  3. Hypothyroidism
  4. Abnormal liver enzymes
270
Q

Name a disease that might cause flattening of the P wave

A
  1. Hyperkalaemia
  2. Obesity
271
Q

Name a disease that might cause tall P waves

A

Right atrial enlargement

272
Q

Name a disease that might cause broad notched P waves

A

Left atrial enlargement

273
Q

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

A

Inferior aspect

274
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

275
Q

Give 3 effects hyperkalaemia on an ECG

A

GO - absent P wave
GO TALL - tall T wave
GO long - prolonged PR
GO wide - wide QRS

276
Q

Give 2 effects of hypokalaemia on an ECG

A
  1. Flat T waves
  2. QT prolongation
  3. ST depression
  4. Prominent U waves
277
Q

Give an effect go hypocalcaemia on an ECG

A
  1. QT prolongation
  2. T wave flattening
  3. Narrowed QRS
  4. Prominent U waves
278
Q

Give an effect of hypercalcaemia on an ECG

A
  1. QT shortening
  2. Tall T wave
  3. No P waves
279
Q

What controls the sinus node discharge rate?

A

Autonomic nervous system

280
Q

Define sinus rhythm

A

A P wave precedes each QRS complex

281
Q

Define cardiac arrhythmia

A

Abnormality of cardiac rhythm

282
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
283
Q

Define bradycardia

284
Q

Define tachycardia

285
Q

Give 2 causes of bradycardia

A
  1. Conduction tissue fibrosis
  2. Ischaemia
  3. Inflammation/infiltrative disease
  4. Drugs
286
Q

Give 2 broad categories of tachycardia

A
  1. Supraventricular tachycardias
  2. Ventricular tachycardias
287
Q

Where do supra-ventricular tachycardia’s arise from?

A

Atria or atrio-ventricular junction

288
Q

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

A

Narrow QRS complexes

289
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)
290
Q

Where do ventricular tachycardia’s arise from?

A

The ventricles

291
Q

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

A

Broad QRS compelxes

292
Q

What is the commonest supra-ventricular tachycardia?

A

AV node re-entry tachycardia (AVNRT)

293
Q

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

A

Loss of P waves

294
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

295
Q

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

A

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

296
Q

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

A

Beta blockers, CCB

297
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

298
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
299
Q

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

A

Wolff-Parkinson-White Syndrome

300
Q

Give 4 causes of sinus tachycardia

A
  1. Physiological response to exercise
  2. Fever
  3. Anaemia
  4. Heart failure
  5. Hypovolaemia
  6. pain
301
Q

Why do ventricular tachycardia’s arise?

A

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

302
Q

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

A

Crescendo-decrescendo amplitude = torsades de pointes

303
Q

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

A

DC cardioversion

304
Q

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

A

Implantable cardioverter defibrillator (ICD)

305
Q

What is the treatment for stable ventricular tachycardia?

A

IV beta blockers (bisoprolol) and IV amiodarone

306
Q

Define atrial fibrillation

A

Chaotic irregular atrial rhythm at 300-600 bpm

AV node responds intermittently – irregular ventricular rate

307
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

308
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

309
Q

Briefly describe the pathophysiology of atrial fibrillation

A

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

310
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’
311
Q

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

A

CHA2D2 VAS

312
Q

What does the CHA2DS2 VASc score take into account

A

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

Score >1 = anticoagulation

313
Q

Describe the treatment for atrial fibrillation

A
  • cardioversion - LMWH (enoxaparin) and DC shock
  • rate control - 1st line = beta blocker, 2nd line = CCB
  • rhythm control - BB (bisoprolol), CCB (verapamil), digoxin, anti-arrhythmic (amiodarone)
  • anti-coagulation
314
Q

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

A

BB, CCB and digoxin

315
Q

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

A

Electrical cardioversion or pharmacological cardioversion using flecainide

316
Q

What is the long term treatment for atrial fibrillation?

A

Catheter ablation

317
Q

What is atrial flutter?

A

Fast but organised waves in the atrium
Atrial rate 250-350 bpm

318
Q

Describe the ECG pattern taken from someone with atrial flutter

A
  1. Narrow QRS
  2. Saw tooth flutter (F) waves
319
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

320
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

321
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
322
Q

what is the clinical presentation of long QT syndrome?

A
  1. Palpitations
  2. Syncope
    - may progress to VF
323
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
324
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

325
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

326
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

327
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

328
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

329
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

330
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

331
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)

332
Q

Explain the pathophysiology of a BBB

A

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

333
Q

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

A

WiLLiaM
slurred S wave in V1 (resembles W)
R wave in V6 (resembles M)

wide QRS with notched top in V6

334
Q

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

A

MaRRoW
R wave in V1 (resembles M)
slurred S wave in V6 (resembles W)

wide QRS
RSR pattern in V1

335
Q

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

A

DC cardioversion

336
Q

Name 4 valvular heart diseases

A
  1. Aortic stenosis
  2. Mitral regurgitation
  3. Mitral stenosis
  4. Aortic regurgitation
337
Q

Briefly describe aortic stenosis

A

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

338
Q

Name the 3 types of aortic stenosis

A
  1. Surpavalvular
  2. Subvalvular
  3. Valvular = most common
339
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
340
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

341
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

342
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
343
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
344
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)
345
Q

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

A

Aortic and mitral stenosis are mechanical problems

346
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
347
Q

What is mitral regurgitation?

A

Backflow of blood from the LV to the LA during systole
LV volume overload

348
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
349
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 LA pressure increases pulmonary venous pressure and pulmonary oedema
Left ventricle dilates but more so in chronic MR

350
Q

what are the symptoms of mitral regurgitation?

A

palpitations
exertional dyspnoea
fatigue
weakness

351
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
352
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
353
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
354
Q

What is aortic regurgitation?

A

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

355
Q

What causes aortic regurgitation?

A

acute
- infective endocarditis
- rheumatic fever
- aortic dissection

chronic
- rheumatic disease
- bicuspid aortic valve
- aortic endocarditis

356
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
357
Q

Give 3 symptoms of aortic regurgitation

A
  • palpitations
  • angina
  • dyspnoea
358
Q

Give 3 signs of aortic regurgitation

A
  • early diastolic murmur - decrescendo
  • water hammer (collapsing) pulse
  • wide pulse pressure
  • displaced apex
359
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

360
Q

Describe the management for someone with aortic regurgitation

A

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

361
Q

What is mitral stenosis?

A

Obstruction of LV inflow that prevents proper filling during diastole

362
Q

Name 3 causes of mitral stenosis

A
  1. Rheumatic heart disease
  2. IE
  3. Mitral annular calcification - rarer
363
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

364
Q

what are the symptoms of mitral stenosis?

A
  1. progressive dyspnoea
  2. Haemoptysis (coughing up blood)
  3. palpitations (AF)
  4. chest pain
365
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
366
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
367
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

368
Q

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

A

Mitral stenosis

369
Q

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

A

Mitral regurgitation

370
Q

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

A

Aortic stenosis

371
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

372
Q

What is infective endocarditis?

A

an infection of the endocardium or vascular endothelium of the heart

373
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)
374
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)

375
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
376
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)
377
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

378
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
379
Q

What is the hallmark of infective endocarditis?

A

Vegetation - lumps of fibrin hanging of heart valves

380
Q

Name 2 sites where vegetation is likely in infective endocarditis

A
  1. Atrial surface of AV valves
  2. Ventricular surface of SL valves
381
Q

Give 3 symptoms of infective endocarditis

A

Fever
Rigors
Night sweats
Malaise
Weight loss

382
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

383
Q

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

A

Duke’s criteria

384
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
385
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
386
Q

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

A

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

387
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

388
Q

Describe the treatment for infective endocarditis

A
  1. Antibiotics based on cultures
  2. Treat any complications
  3. Surgery - remove and replace valve
389
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
390
Q

Why is it important to remove large vegetations?

A

To prevent them embolising and causing a stroke, MI etc

391
Q

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

A

They may have previously received antibiotics

392
Q

Name 2 drugs that can prolong the QT interval

A
  1. Sotalol
    2 Amiodarone
393
Q

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

A

Block the inactivation gate of the sodium channel

394
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

395
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
396
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

397
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

398
Q

What are the risks associated with Eisenmengers syndrome?

A
  1. Risk of death
  2. Endocarditis
  3. Stroke
399
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

400
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

401
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

402
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

403
Q

What is pulmonary stenosis?

A

Narrowing of the RV outflow tract

404
Q

How does a patient present with pulmonary stenosis?

A

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

405
Q

How is pulmonary stenosis treated?

A

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

406
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
407
Q

Name 3 congenital heart defect that are not cyanotic

A
  1. VSD
  2. ASD
  3. PDA
    Left to right shunt
408
Q

Name a congenital heart defect that is cyanotic

A
  1. Tetralogy of Fallot
    Right to left shunt
409
Q

Why does mitral stenosis cause AF?

A

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

410
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

411
Q

Give 3 symptoms of Dressler’s syndrome

A
  1. Fever
  2. Chest pain
  3. Pericardial rub
    Occurs 2-10 weeks after MI
412
Q

Write an equation for mAP

A

mAP = DP + 1/3PP

413
Q

Give the equation for stroke volume

A

SV = EDV - ESV

414
Q

What is a consequence of peripheral arterial occlusion?

415
Q

Give 2 diseases that result from stress induced ischaemia

A
  1. Exercise induced angina
  2. Intermittent claudication
416
Q

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

A
  1. Critical limb ischaemia
  2. Vascular dementia
417
Q

Give an example of infarction

418
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

419
Q

What can intermittent claudication lead on to if left untreated?

A

Critical ischaemia

420
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

421
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

422
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

423
Q

Give a symptom of intermittent caludication

A

Muscle cramps

424
Q

Name 2 diseases that are due to moderate ischaemia

A
  1. Angina
  2. Intermittent claudication
425
Q

Name a disease that is due to severe ischaemia

A

Critical limb ischaemia

426
Q

Name 3 causes of an aneurysm

A
  1. Atherosclerotic (most common)
  2. Ateriomegaly
  3. Collagen disease - Marfans, vascular Ehlers Danlos
  4. tobacco smoking
427
Q

Name 2 types of aortic aneurysm

A
  1. Abdominal aortic aneurysm (AAA)
  2. Thoracic abdominal aneurysm (TAA)
428
Q

What classifies as an Abdominal aortic aneurysm?

A

> 3 cm
Dilation affects all 3 layers of the vascular tunic

429
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

430
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)

431
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

432
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

433
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

434
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

435
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

436
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

437
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

438
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

439
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

440
Q

what are the risk factors for acute coronary syndromes?

A

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

441
Q

what is the management for a STEMI?

A
  • PCI within 120 minutes
  • clopidogrel
  • if PCI isn’t available fibrinolysis
  • alteplase
  • ticagrelor and aspirin
442
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
443
Q

what is the pre-hospital management for MI?

A
  • aspirin
  • GTN spray
  • morphine
444
Q

what is the hospital management for MI?

A
  • IV morphine
  • oxygen
  • beta blocker - atenolol
  • clopidogrel
445
Q

what is the secondary prevention for MIs?

A

statins
aspirin
warfarin
ACEi

446
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
447
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
448
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
449
Q

what additional investigations should be undertaken for acute heart failure?

A
  • serum troponin
  • D-dimer
450
Q

what are the causes of cor pulmonale?

A
  • chronic lung disease
  • pulmonary vascular disorders
  • neuromuscular and skeletal diseases
451
Q

what are the signs of cor pulmonale?

A
  • cyanosis
  • tachycardia
  • raised JVP
  • RV heave
  • pan-systolic murmur due to tricuspid regurgitation
  • hepatomegaly
  • oedema
452
Q

what are the symptoms of cor pulmonale?

A
  • dyspnoea
  • fatigue
  • syncope
453
Q

what investigations should be undertaken for cor pulmonale?

A

arterial blood gas
- hypoxia
- sometimes shows hypercapnia

454
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
455
Q

what is the epidemiology of hypertension?

A
  • major risk factor for CVD
  • men > women
  • underdiagnosed, undertreated and poorly controlled in the UK
456
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
457
Q

what are the causes of atrial flutter?

A
  • idiopathic
  • CHD
  • hypertension
  • heart failure
  • COPD
  • pericarditis
  • obesity
458
Q

what are the risk factors for atrial flutter?

A
  • atrial fibrillation
459
Q

what is the management for atrial flutter?

A
  • Cardioversion
    - Give a LMWH
    - Shock with defibrillator
  • Catheter ablation = definitive treatment – creates a conduction block
  • IV Amiodarone – restore sinus rhythm
460
Q

what are the risk factors for AVNRT?

A

exertion
emotional stress
coffee
tea
alcohol

461
Q

what is malignant hypertension?

A

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

usually evidence of acute haemorrhage and papilledema

462
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
463
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
464
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
465
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
466
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
467
Q

what are the risk factors of MI?

A

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

468
Q

what is the epidemiology of aortic dissection?

A
  • men>female
  • 40-60yrs
  • 65% occur in ascending aorta
469
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.

470
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

471
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

472
Q

what are the investigations of aortic dissection?

A

-ECG/cardiac enzymes - rule out MI
-Chest x-ray - widening mediastinum
-CT scanning- definitive imaging
- echo - TTE/TOE

  • gold standard = CT angiography
473
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)

474
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)

475
Q

what is the epidemiology of peripheral vascular disease?

A

Men > women
Usually affects the aorta-iliac and infra-inguinal arteries

476
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
477
Q

what are the investigations for peripheral vascular disease?

A

1st line = ankle brachial pressure index (ABPI), duplex ultrasound

< 0.3 = critical ischaemia

478
Q

what is the treatment for critical limb ischaemia?

A

Revascularisation (e.g. stenting, angioplasty, bypassing)
Amputation if unsuitable

479
Q

what is the epidemiology of mitral stenosis?

A
  • men>women
  • Prevalence/incidence decreasing due to decrease of rheumatic heart disease
480
Q

what are the risk factors of mitral stenosis?

A
  • history of rheumatic fever
  • untreated strep infections
481
Q

what are the risk factors for mitral regurgitation?

A

female
lower BMI
advancing age
renal dysfunction
prior MI

482
Q

what is the clinical presentation of atrial flutter?

A

Palpitations
Breathlessness
chest pain
Dizziness
Syncope
fatigue

483
Q

what are the risk factors for atrial fibrillation?

A

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

484
Q

what are the causes of RBBB?

A

Pulmonary embolism
IHD
Atrial ventricular septal defect

485
Q

what is the pathophysiology of RBBB?

A

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

486
Q

what is the clinical presentation of RBBB?

A

Asymptomatic
syncope/presyncope

487
Q

what is the treatment for RBBB?

A

Pacemaker
CRT – cardiac resynchronisation therapy
Reduce blood pressure

488
Q

what is the clinical presentation of LBBB?

A

Asymptomatic
syncope/presyncope

489
Q

what is the pathophysiology of LBBB?

A

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

490
Q

what is the treatment for LBBB?

A

Pacemaker
CRT – cardiac resynchronisation therapy
Reduce blood pressure

491
Q

what are the causes of LBBB?

A

IHD
Aortic valve disease

492
Q

what are the investigations for heart block?

493
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

494
Q

what is the presentation of first degree heart block?

A

asymptomatic

495
Q

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

A

light-headedness
dizziness
syncope

496
Q

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

A

SOB
postural hypotension
chest pain

497
Q

what is the clinical presentation of third degree heart block?

A

dizziness
blackouts

498
Q

what is the epidemiology abdominal aortic aneurysm?

A
  • incidence increases with age
  • men > females
  • most commonly occur below renal arteries
499
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
500
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
501
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
502
Q

what are the investigations for abdominal aortic aneurysm?

A
  • Abdominal ultrasound – can assess aorta to degree of 3mm
  • CT or MRI angiography scans
503
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
504
Q

what are the complications of abdominal aortic aneurysm?

A
  • rupture of AAA
  • thromboembolisms
  • fistula formation
505
Q

what antibiotics are used for endocarditis?

A

staph = vancomycin
if MRSA add rifampicin

other bacteria = benzylpenicillin and gentamycin

506
Q

how can endocarditis be prevented?

A
  • good oral health
  • no IV drug use
  • educate surgery patients on symptoms
507
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

508
Q

what are the investigations of tetralogy of fallot?

A

CXR shows boot shaped heart
Echocardiogram

509
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
510
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
511
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
512
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
513
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
514
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

515
Q

what are the causes of AVRT?

A

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

516
Q

what is the clinical presentation of AVRT?

A

Palpitations
Severe dizziness
Dyspnoea
Syncope

517
Q

what are the investigations for AVRT?

A

ECG - pre excitation
- short PR interval
- delta waves (wide QRS complex that begins slurred)

518
Q

what is the treatment for AVRT?

A

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

519
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
520
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

521
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
522
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
523
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

524
Q

what is the management for coarctation of the aorta?

A

surgery, balloon dilation and stenting

525
Q

what is the epidemiology of coarctation of the aorta?

A

men > women
associated with turner’s syndrome, patent ductus arteriosus

526
Q

what are the causes of left sided heart failure?

A

Coronary artery disease
Myocardial infection
Cardiomyopathy
Congenital heart defects
Valvular heart disease
Arrhythmias

527
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

528
Q

what are the causes of systolic heart failure?

A

Ischaemic heart disease
Myocardial infection
Cardiomyopathy

529
Q

what are the causes of diastolic heart failure?

A

aortic stenosis
chronic hypertension

530
Q

what is congestive heart failure?

A

both sided heart failure

531
Q

what murmur is heard with mitral stenosis?

A

rumbling mid-diastolic murmur with opening snap

532
Q

what murmur is heard with mitral regurgitation?

A

pan systolic murmur radiating to the left axilla

533
Q

what murmur is heard with aortic stenosis?

A

ejection systolic murmur radiating to carotids and apex

534
Q

what murmur is heard with aortic regurgitation?

A

early diastolic murmur (best heard on expiration with patient sat forwards)
heard loudest at left sternal edge

535
Q

ECG changes in which regions indicates a lateral MI?

A

lead I
aVL
V5
V6

536
Q

ECG changes in which regions indicates an inferior MI?

A

lead II
lead III
aVF

537
Q

ECG changes in which regions indicates a septal MI?

538
Q

ECG changes in which regions indicates an anterior MI?

539
Q

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

A

lateral = circumflex

540
Q

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

A

inferior = RCA

541
Q

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

A

anterior = LAD

542
Q

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

A

anterior - V3, V4
septal - V1, V2

543
Q

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

A

inferior - leads II, III, aVF

544
Q

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

A

lateral - lead I, aVL, V5, V6

545
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

546
Q

what pharmacological treatments can be used for mitral stenosis?

A
  • beta blockers - atenolol
  • digoxin
  • diuretics - furosemide
547
Q

what pharmacological treatments can be used for mitral regurgitation?

A

Vasodilation
- ACEi - ramipril
- hydralazine - smooth muscle relaxer

HR control
- B blockers - atenolol
- CCB
- digoxin

fluid overload
- loop diuretic - furosemide

AF/atrial flutter
- anticoagulation

548
Q

which tool is used to estimate the risk of bleeding in patients on anticoagulation?

549
Q

which tool is used to estimate the risk of developing a heart attack or stroke in the next 10 years?

550
Q

what is the management for SVT?

A

1st line = valsalva manoeuvre
2nd = carotid sinus massage
3rd = cardioversion with adenosine
4th = DC cardioversion with defibrillator

551
Q

what is the mechanism of action for adenosine?

A
  • causes transient AV node heart block
  • very short half life of 8-10 seconds
  • feeling of impending doom
552
Q

what are the 2 different types of aortic dissection?

A

type A = ascending aorta
type B = descending aorta

553
Q

what is the treatment for type A aortic dissection?

A

medical emergency - urgent surgical repair

554
Q

what is the treatment for type B aortic dissection?

A

conservative management to reduce HR and BP
- IV beta blockers / CCBs
- bed rest
- consider TEVAR surgery

555
Q

which abnormal heart rhythm are people with long QT syndrome at risk of developing?

A

torsades de pointes

556
Q

which congenital heart defects are common in people with trisomy 21 (downs syndrome)?

A

VSD - 30% (heard as a pansystolic murmur)
ASD - 10%
tetralogy of fallot - 5%
PDA - 5%

557
Q

what type of murmur is heard in a ventricular septal defect?

A

pansystolic

558
Q

which microorganism causes rheumatic fever?

A

group A streptococcus - s.pyogenes

559
Q

what is the mechanism of action for apixaban?

A

DOAC - inhibits factor Xa

560
Q

what is hypertrophic cardiomyopathy?

A

genetic disorder characterised by left ventricular hypertrophy -> causes diastolic ventricular malfunction

561
Q

what is the pathophysiology of hypertrophic cardiomyopathy?

A

thickened septum below aortic valve causes outflow tract obstruction -> causes left ventricular hypertrophy

562
Q

what is the most common cause of secondary hypertension?

A

primary hyperaldosteronism - Conn’s syndrome

563
Q

What are the side effects of colchicine?

A

Diarrhoea and nausea

Phase 2A revision (38 decks)

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