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Cardiovascular > Cardiovascular Disease > Flashcards

Cardiovascular Disease Flashcards

1
Q

what is atherosclerosis?

A

a progressive build up of plaque within the arteries

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2
Q

what is athersclerotic plaque formed from?

A 
fatty substances
choleserol
cellular waste
calcium
fibrin
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3
Q

what are the 2 main consequences of an artherosclerotic plaque?
(what do these both cause?)

A
  1. bleeding into the plaque
  2. rupture causing clot formation
    (both can result in artery occlusion)
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4
Q

what is an atherothrombosis?

A

formation of an acute thrombosis superimposed on atherosclerosis

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5
Q

what are the stages from normal artery to atherothrombosis?

A
  1. normal artery
  2. fatty streak
  3. fibrous plaque
  4. atherosclerotic plaque
  5. plaque rupture + thrombosis
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6
Q

why does the rupture of a atherosclerotic plaque cause clot formation?

A

platelets adhere to damaged area to try and heal the broken area
(especially since components such as collagen and vWF have been exposed)

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7
Q

why does a fatty streak form on the endothelium of a normal artery?

A
  1. endothelial damage
  2. protective response results in production of cellular adhesion molecules
  3. monocytes and T-cells attach to the sticky surface of endothelial cells
  4. migration into the subendothelial space
  5. macrophages take up oxidised LDL-C
  6. instead of clearing OXLDL, macrophages become lipid-rich foam cells
  7. fatty streak forms
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8
Q

what factors can cause damage to the endothlium?

A
  1. haemodynamic forces
  2. vasoactive substances
  3. cytokines from blood cells
  4. cigarette smoke
  5. atherogenic diet
  6. elevated glucose levels
  7. oxidied LDL-C
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9
Q

what type of haemodynamic force can cause endothelial damage?

A

hypertension

due to sheer stress

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10
Q

what 4 things does OXLDL cause?

A
  1. promotes damage of endothelial cells
  2. promotes inflammatory response
  3. causes vasodilatory impairment
  4. induces prothrombic state (by affecting platelets and coagulation factors)
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11
Q

how does OXLDL cause vasodilatory impairment?

A

by modifying endothelial response to angiotensin II

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12
Q

why does a fibrous lesion form over the fatty streak?

A

a protective response to the endothelial damage

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13
Q

what are 4 major risk factors for cardiovascular disease

A

dyslipiaemia
hypertension
smoking
diabetes

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14
Q

why do CVD risk factors (such as hypertension, dyslipidaemia, diabetes and smoking) cause endothelial cells to decrease production of some compounds and increase production of others? (endothelial dysfunction)

A

by causing oxidative stress in the vessel wall

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15
Q

what is intermittent claudication a symptom of?

A

peripheral arterial disease

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16
Q

why are many patients with PAD not diagnosed?

A

most are asymptomatic

9/10

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17
Q

what are the 4 minor risk factors for cardiovascular disease?

A

physical inactivity
alcohol
stress
gender/genes

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18
Q

what type of cholesterol do statins reduce?

A

total cholesterol

LDL cholesterol

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19
Q

what is the statin with the greatest efficacy?

A

rosuvastatin

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20
Q

which is the statin with the least likelihood of side effects? (myopathy)

A

atorvastatin

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21
Q

what are xanthelasma?

A

xanthomas of the eyelids

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22
Q

why do tendon xanthomas form?

A

infiltration of tendon by lipid: hypercholesterolaemia

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23
Q

where are the most common places for tendon xanthomas?

A

extensor tendons of fingers, patella, elbows

achilles tendon

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24
Q

why do tuberous xanthomas form?

eg elbows

A

lipid deposits

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25
Q

what are the 3 causes of tuberous xanthomas?

A

familial hypertriglyceridemias
acquired hypertriglyceridemias
biliary cirrhosis

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26
Q

what do eruptive xanthomas suggest?

A

abrupt increase in serum triglyceride levels

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27
Q

where are eruptive xanthomas more likely to me?

A

buttocks
posterior thighs
body folds

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28
Q

for patients with diabetes, what is their target blood pressure?

A

below 130/80

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29
Q

what does smoking do to your blood pressure?

A

increases blood pressure

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30
Q

what does smoking do to your HDL?

A

decreases HDL

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31
Q

what are the 5 features of metabolic syndrome?

A 
abdominal obesity
high blood pressure
high triglycerides
low HDL
high fasting glucose
(patients must have 3 of these characteristics)
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32
Q

what does an assign score allow you to measure?

A

risk of developing cardiovascular disease

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33
Q

what is ischaemia?

A

the result of impaired vascular perfusion which deprives the affected tissue of nutrient
(can be reversible)

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34
Q

what is infarction?

A

ischaemic necrosis of a tissue secondary to occlusion/reduction of arterial supply or venous drainage
(irreversible, recovery will depend on tissues regenerative ability)

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35
Q

why can reduced venous drainage cause ischaemia/infarction?

A

venous blood backs up and doesn’t allow oxygenated arterial blood to get to the tissue

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36
Q

what is the difference between a thrombus and a clot?

A
  • thrombus occurs in vasculature, during life

- blood clot is not within vascular space or not in life.

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37
Q

what 2 types of granules to platelets have?

A

alpha granules

dense granules

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38
Q

what type of contents do alpha granules contain?

A

adhesion components eg fibrinogen

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39
Q

what type of contents do dense granules contatin?

A

aggregation components eg ADP

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40
Q

what affects do stasis and turbulence of blood cause?

A
  1. platelets come into contact with endothelium
  2. activated clotting factors are not diluted by the normal rapid flow of blood
  3. inflow of anticoagulant factors is slowed allowing thrombi to persit
  4. activation of endothelial cells is promoted
    (prothrombotic scenario)
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41
Q

what type of situations cause turbulence within blood vessels?

A
  • aneurysms
  • AF
  • blood flowing round and occluding atherosclerotic plaque
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42
Q

what type of situations cause stasis within blood vessels?

A

-impaired venous drainage of lower limbs

non-contractile areas of -myocardium following a myocardial infarction

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43
Q

what are the 2 subsections of abnormal blood flow? (1/3 of virchows triad)

A

stasis

turbulence

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44
Q

list 9 acquired hypercoaguable states?

A 
MI
immobilisation
tissue damage
cancer
prosthetic heart valves
AF
pregnancy
smoking
oral contraceptive use
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45
Q

what 3 genetic abnormalities can cause hypercoaguable states?

A

factor V mutations
defects in anticoagulant pathways (eg AT III deficiency)
defects in fibrinolysis

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46
Q

what type of thrombi show lines of Zahn?

A

arterial thrombi

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47
Q

why do lines of zahn form in an arterial thrombi?

A

alternating pale (platelet and fibrin) and dark (RBC and WBC) bands

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48
Q

what is an emboli?

A

a detached intravascular mass which is carried by the bloodstream to a site distant from point of origin

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49
Q

what are the most common type of emboli?

A

thromboemboli

fragments of a detached thrombus

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50
Q

what are the 7 types of embolism?

A 
thromboembolism
fat embolism
marrow embolism
air embolism
septic embolism
amniotic fluid embolism
tumour embolism
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51
Q

what colour is a lung infarct?

A

red

due to leaking of secondary bronchial blood supply onto infarcts

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52
Q

what colour do arterial infarcts tend to be?

A

white

no secondary blood supply leaking onto area

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53
Q

why might a venous emboli cause an arterial infarct?

A

atrial/ventricular septal defect

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54
Q

when do fat embolisms usually occur?

A

follow major soft tissue trauma or bone fractures

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55
Q

what can gas/air embolisms cause?

A

barotrauma

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56
Q

when do amniotic fluid embolisms occur? and why?

A

post-partum

amniotic fluid and debris enters torn veins after birthing

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57
Q

what is arteriolosclerosis associated with?

A

diabetes and hypertension

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58
Q

what are the main target vessels for atherosclerosis?

A

aorta
coronary arteries
cerebral arteries

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59
Q

what 3 sections make up an atherosclerotic plaque?

A

rasied focal lesion of intima
lipid core of cholesterol and lipoproteins
fibrous cap

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60
Q

what 2 things occur when an atherosclerotic plaque increases in size?

A

luminal diameter decreases

blood flow reduces

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61
Q

how can atherosclerotic plaques lead to aneurysm development?

A

progressively degrade (and therefore weaken) the arterial wall

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62
Q

what are the 3 results of an atherosclerotic plaque?

A

resolution
repair
complication

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63
Q

what does resolution of an atherosclerotic plaque involve?

A

reabsorbtion of the lipids at fatty streak stage

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64
Q

what does repair of an atherosclerotic plaque involve?

A

stabilisation by fibrosis scarring

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65
Q

what are the general risk factors for DVTs? (8)

A 
age 
obesity
immobilisation (ie hospital, long journeys) 
pregnancy
major surgery
varicose veins
OCP
smoking
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66
Q

what are the medical conditions which have risk factors for DVTs? (9)

A 
cancer
previous DVT
cerebrovascular accident
acute myocardial infarction
congestive heart failure
sepis
nephrotic syndrome
inflammatory bowel disease
vasculitis
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67
Q

what part of virchows triad does sepsis affect?

A

change in blood constituents:

hypercoaguable state

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68
Q

what 4 types of trauma are risk factors to DVTs?

A

multiple trauma
CNS/spinal cord injury
burns
lower extremity fractures

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69
Q

what part of virchows triad do burns affect?

A

change in blood constituents:

hypercoaguable state

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70
Q

what drugs/drug habits can are risk factors to DVTs?

A

intravenous drug abuse
oestrogens (OCP, HRT)
tamoxifen
chemotherapy

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71
Q

what are the symptoms and signs of a DVT?

A 
calf/leg would be:
painful
swelling
redness
hot/inflamed
localised tenderness over certain deep vein
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72
Q

what blood tests do you use as an investigation for a DVT?

A

D-dimer test

(not specific: infection, MI, surgery, liver disease pregnancy

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73
Q

what does a D-dimers test look for? (in order to see the likelihood of a DVT)

A

a fibrin breakdown product

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74
Q

how should you use a D-dimer test when looking for a DVT?

A

rule out test
not a rule in test
(ie low D-dimers- unlikely to be a DVT
high D-dimers- don’t necessarily mean a DVT)

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75
Q

what investigational tests would you use if you suspect a DVT?

A

duplex scan
venous plethysomography
venogram

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76
Q

how do you treat a DVT?

A

anticoagulation with LMWH and warfarin

compression stockings

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77
Q

for the treatment of DVT what stockings should you use?

A

TEDs for 6 weeks

grade 2 compression stockings for up to 5 years to reduce post phlebitic syndrome

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78
Q

what is post-phlebitic syndrome?

A

chronic venous insufficiency when the valves are destroyed and so the vein becomes large and flaccid causing a persistently swollen leg

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79
Q

what is a phlegmasia dolens?

A

A medical emergenct where a DVT causes obstruction of arterial inflow

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80
Q

how do you treat a phlegmasia dolens?

A 
IVC filter
femoral arterial line
tPA intra-arterially
surgical review
decompression
amputation
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81
Q

why do you put in an IVC filter for a patient with phlegmasia dolens?

A

to prevent bits of the clot embolising and causing a PE

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82
Q

what is the difference between wet gangrene and dry gangrene?

A

wet gangrene is due to a venous blockage causing a back flow preventing oxygenation of tissues
dry gangrene is due to an arterial blockage preventing oxygenation of tissues

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83
Q

what are the 4 classifications of an acute PE?

A

minor
major with normal RV function
major with RV dysfunction
massive with shock or syncope

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84
Q

what are the symptoms of a PE?

A 
SOB
collapse
pleuritic chest pain
haemoptysis
sudden death
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85
Q

what are the signs of a PE on general examination?

A

tachypnea, tachycardia hypotenstion, wheeze

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86
Q

what are the signs of a PE on auscultation?

A

wheeze

pleural rub

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87
Q

what are the signs of a PE on CXR?

A

oligemia
pleural effusion
consolidation

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88
Q

what is oligemia?

A

segmental loss of pulmonary vaculature

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89
Q

what are the main investiagtions for a PE?

A 
ABGs
D-Dimers
CXR
V/Q scan
CTPA
echocardiogram
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90
Q

what are the findings of a PE on ECG?

A

sinus tachycardia

S1Q3T3 (rarely)

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91
Q

explain what S1Q3T3 mean on an ECG?

A

large S wave on lead 1
Q wave present on lead 3
inverted T wave present on lead 3

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92
Q

what is the investigation pathway for a PE

A
  1. D-dimer if clinical suspicion is not high
  2. If clinical suspician is high or D-dimers are positive: start fragmin and CXR
  3. if abnormal start warfarin, if normal V/Q scan
  4. if V/Q scan probability is low, discount PE, otherwise do CTPA
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93
Q

why can ventilation-perfusion scan sometimes be a poor discriminator of a PE?

A

if there is background lung disease

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94
Q

when are CT pulmonary angiograms poor in detecting PEs?

A

peripheral lesions

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95
Q

what is the con about CTPA?

A

invasive

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96
Q

what does an echocardiography tell you about a PE?

A

shows right heart strain and pressures

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97
Q

what are the 4 different treatment options in the treatmenf of a PTE?

A
  1. anticoagulants
  2. thrombolytic therapy
  3. IVC filter
  4. surgical removal
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98
Q

what is the treatment of choice for a minor PE?

A

anticoagulants

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99
Q

what is the treatment of choice for a major PE without RV dysfunction?

A

anticoagulants

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100
Q

what is the treatment of choice for a major PE with RV dysfunction

A

anticoagulants (and/or)

thrombolysis

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101
Q

what is the treatment of choice for a massive PE with shock or syncope?

A

thrombolysis or surgery

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102
Q

what anticoagulant treatment is given for the treatment of a PE?

A

initially: LMWH/heparin
5 days afterwards: LMWH/heparin
after discharge: warfarin

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103
Q

what are the major pro and major con of an IVC filter?

A

pro: prevent recurrent PE in short term
con: increase risk of recurrent DVT in long term

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104
Q

why are IVC filters not recommened for long term, and if they are needed in the long term why is anticoagulation also needed?

A

because in the long term they increase risk of recurrent DVT

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105
Q

what are the 3 indications for a IVE filter?

A
  1. recurrent PTE despite adequate anticoagulation
  2. PTE when anticoagulation is contraindicated
  3. high risk (eg phlegmasia dolens)
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106
Q

what 4 major reasons might anticoagulants be contraindicated?

A

post op
pre op
severe live disease
pregnancy

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107
Q

what type of surgery is needed for a patient with an acute massive PE with shock/syncope?

A

pulmonary embolectomy

108
Q

what type of elective surgery can be used for patients with chronic thromboembolic pulmonary hypertension?

A

thromboendarterectomy

109
Q

what are the 4 vitamin K dependent clotting factors?

A

II, VII, IX, X

these are the factors that warfarin prevents forming

110
Q

where are the 4 vitamin K dependent clotting factors synthesised?

A

in the liver

111
Q

why is bleeding effects of dabigatran much easier to reverse than warfarin?

A

dabigatran half life is 12-17 hours (compared to warfarins: 40 hours) and so drug cessation is usually sufficient

112
Q

give a reason why a patient might have angina without coronary disease?

A

anaemia

blood supply not supplying enough oxygen for energy

113
Q

what are the main way for testing for angina?

despite angina being a clinical diagnosis

A

exercise training testing
perfusion imaging
CT angiography
angiography

114
Q

what revascularisation techniques can be used for angina patients to releve symptoms?

A

CABG

PCI

115
Q

what are the 4 pros of exercise testing?

A

cheap
non-invasive
reproducible
shows risk stratification (ie positive test at low workload imples poor prognosis)

116
Q

what are the 2 cons of exercise testing?

A
  • poor diagnostic accuracy in certain sub groups (eg less mobile patients)
  • some patients struggle to get a maximal test- submaximal test
117
Q

what are the 3 pros of perfusion imaging?

A
  • non invasive
  • accuracy in sub groups that dont have accuracy in ETT
  • risk strarification
118
Q

what are the 2 cons of perfusion imaging?

A

radiation

false positives/negatives

119
Q

what are the 3 pros of CT angiography?

A

non-invasive
risk stratification
anatomical data

120
Q

what are the 3 cons of CT angiography?

A

radiation
can be less precise when calcium is present
cost

121
Q

what is angiography?

A

a catheter is inserted into artery in wrist or groin and advanced to coronary ostium
contrast agent injected
video recorded X-ray taken in muliple views

122
Q

what are the 4 pros of angiography?

A

gold standard
anatomical information
risk stratification
can follow on with angioplasty if needed

123
Q

what are the 3 const of angiography?

A
  • risk of stroke or death
  • radiation
  • contrast can cause renal dysfunction, rash. nausea
124
Q

what drugs can be used to relieve angina symptoms?

A 
nitrates
B-blockers
calcium antagonists
nicorandil
statin
aspirin
ACE inhibitor
125
Q

what is intermittent claudication?

A

ischaemic pain which develops in the affected limb after variable periods of exercise, pain is relieved by rest

126
Q

what are 2 non-invasive investigations of the lower limb?

A

ABPI (ankle brachial pressure index)

duplex ultrasound scanning

127
Q

what are 3 invasive investigation of the lower limb?

A

MR angiography
CT angiography
catheter angiography

128
Q

how do calculate ABPI?

A

ankle systolic pressure (mmHg)/

brachial systolic pressure (mm Hg)

129
Q

what is does the ABPI value have to be to suggest claudication

A

below 0.9

130
Q

what does an eABPI

(exercise ankle brachial pressure index) show in a normal response?

A

increased ABPI during exercise

131
Q

what does an eABPI (exercise ankle brachial pressure index) show in a claudication response?

A

decreased ABPI during exercise

132
Q

how does walking (/exercise programs) improve intermittent claudication?

A

develops collateral circulation

133
Q

for the management of intermittent claudication what exercise training program should be implemented?

A

duration: 1 hr/day to 30mins 3x a weel
for a minimum of 6 months
must be supervised
‘beyond pain’ exercise

134
Q

what drug is used for relivation of intermittent claudication

A

cilostazol

135
Q

what is the name of the disease which causes pain in limbs at rest due to insufficient vascular perfusion?

A

critical limb ischaemia

136
Q

what is the main difference between intermittent claudication and critical limb ischaemia?

A

intermittent claudication is only pain during exercise (pain is relieved by resting(
critical limb ischaemia has pain even during rest

137
Q

why is the pain in critical limb ischaemia worse at night?

A

no gravity to help the blood flow

138
Q

what are 2 major risk factors for a patient with critical limb ischaemia to go on to needing a amputation?

A

smoking

diabetes

139
Q

what would you expect to find on examination of a acute ischaemic leg?

A 
6Ps
Pallor
Perishingly cold
Pulseless
Pain
Paresthesia
Paralysis
140
Q

what are the 10 main risk factors for an aortic aneurysm?

A 
male/ female post-menopaus
family history
age
smoking
PVD
cardiac disease
cerebrovasclar disease
hypercholesterolaemia
diabetes
141
Q

what types of abdominal aortic aneurysms can be symptomatic?

A

both ruptured and non-ruptured

142
Q

what 2 investigations are useful for a suspected asymptomatic abdominal aortic aneurysm?

A

ultrasound scan

CT angiography

143
Q

at what phase must the IV contrast be in during a CT angiography of the abdominal aorta?

A

arterial phase

144
Q

what 1 investigation is useful for a suspected symptomatic abdominal aortic aneurysm?

A

CT angiography

145
Q

what is the difference between elective aneurysm repair and emergency aneurysm repair?

A

elective aneurysm repair is a prophylactic operation to reduce risk of rupture

emergency aneurysm repair is a life saving therapeutic procedure

146
Q

what is endovascular repair of an abdominal aortic aneursym?

A

inserting a graft within the aorta
(via a peripheral artery)
x-ray guided

147
Q

what 2 type of interventions can be used for an elective aneurysm repair?

A 
endovascular repair
open repair (laparotomy)
148
Q

compare an endovascular repair of an abdominal aorta aneurysm to an open repair?

A

elective aorta aneurysm only possible in 25% of patients, less mortality risk, faster recovery but needs ongoing follow up and may need further interventions

open repair is possible in almost everyone, greater mortality risk, slower recovery but noesn’t need ongoing follow up and rarely needs further interventions. known to be effective for life

149
Q

what are the 2 types of venous system?

A

deep veins

superficial veins

150
Q

in the lower limbs what major veins make up the deep system?

A

tibial vein
popliteal vein
femoral vein

151
Q

in the lower limb what major veins make up the superficial system?

A 
saphenous veins (parallel to the deep system) 
perforator veins (link to deep system)
152
Q

what are the 4 major risk factors for varicose veins?

A

age
pregnancy
obesity
prev DVT

153
Q

what are primary varicose veins the result of?

A

incompetent valves (usually in superficial veins)

154
Q

what are secondary varicose veins the result of?

A 
venous obstruction
(causing blood to flow through perforator veins to the superficial veins)
155
Q

what type of varicose veins to DVTs cause?

A

secondary varicose veins

156
Q

how is the appearance of varicose veins effected by standing?

A

more prominent when standing

157
Q

what are the 3 major complications of varicose veins?

A

bleeding and bruising
superficial thrombophlebitis
chronic venous insufficiency

158
Q

what are 3 signs of chronic venous insufficiency on inspection of the leg?

A

haemosiderin deposits
lipodermatoclerosis
ulceration

159
Q

what is thrombophlebitis?

A

inflammation of a vein caused by a blood clot

can be due to chronic venous insufficiencu

160
Q

what are haemosiderin depositis?

A

red cell breakdown and leakage visible on the skin

can be due to chronic venous insufficiency

161
Q

what are the investigations used for suspected chronic venous insufficiency?

A

duplex scan

162
Q

what is the non-interventional management of chronic venous insufficiency?

A

graduated compression using bandaging (for ulcers) and class II-IV stockings (ulcer prevention/symptomatic relief)

163
Q

when is graduated compression for chronic venous insufficiency contraindicated?

A 
low ABPI
(intermittent claudication/critical limb ischaemia)
164
Q

what is the interventional management of chronic venous insufficiency

A 
foam sclerotherapy (duplex guided)
endovenous ablation
surgical
165
Q

what are the complications of chronic venous insufficiency interventions?

A 
thrombophlebitis
skin staining
ulceration
wound infection
nerve damage
recurrence
166
Q

what are the 2 revascularisation techniques for coronary heart disease?

A

CABG

PCI

167
Q

what is the artery usually used for peripheral access for a PCI?

A

radial artery

168
Q

what is a stroke?

A

acute onset of focal neurological symptoms and signs due to disruption of blood supply

169
Q

what is the most common type of stroke?

A

ischaemic

170
Q

what 2 factors contribute to a haemorrhagic stroke?

A

raised blood pressure

weakened blood vessel wall

171
Q

why might a cerebral artery wall be weakened?

A 
structural abnormalities (aneurysm, arteriovenous malformation)
inflammation (vasculitis)
172
Q

what are the 5 non-modifiable risk factors for a stroke?

A 
age
family history
gender
race
prev stroke
173
Q

what are 10 potentially modifiable risk factors for a stroke?

A 
hypertension
hyperlipidaemia
smoking
diabetes
AF
congestive heart failure
alcohol excess
obesity
physical inactivity
poor socioeconomic status
174
Q

which blood pressure value (systolic or diastolic?) has the strongest relationship with stroke risk?

A

systolic

175
Q

what therapy is recommended in all patients who have an ischaemic stroke? (with the intention of controlling hyperlipidaemia)

A

statin

176
Q

what is the only way of accurately differentiating between an ischaemic and haemorrhagic stroke?

A

brain imaging

177
Q

what type of brain imaging can be used to differentiate/confirm the type of stroke?

A

CT +/- angiography
MRI with diffusion weighted imaging (DWI) +/- angiography
MRI with gradient echo sequences (GRE)

178
Q

what does an MRI with GRE (gradient echo sequences) look for?

A

looks for old haemosiderin deposits

ie an old bleed

179
Q

how do you differentiate between a cardioembolism (ie cardiac cause for embolism) and an atheroembolism (ie atherosclerosis cause for embolism)?

A

atheroembolism:
infarcts present in the same side as teh affected carotid artery

cardioembolism: infarcts present in more than one arterial territory- bilateral

180
Q

what are transient ischaemic attackes?

A

focal neurological symptoms that resolve within 24 hours

181
Q

what is the medical management post ischaemic stroke?

A

aspirin 300mg
statins
(if in AF- anticoagulation)
antihypertensives

182
Q

what is the medical management for an ischaemic acute stroke?

A

thrombolysis
aspirin 300mg
(if prev aspirin-associated dyspepsia also give PPI)

183
Q

what is the post-ischaemic stroke surgical management?

A

carotid endartectomy

184
Q

what type of atheromatous plaque causes chronic stable angina?

A

fixed atheromatous plaque

185
Q

how would you describe the ischaemia that occurs in chronic stable angina?

A

demand led ischamia

186
Q

why can eating a large meal cause angina to occur?

A

because cardiac work load increases

187
Q

what 3 conditions does the phrase ‘acute coronary syndromes’ cover?

A

unstable angina
NSTEMI
STEMI

188
Q

what are acute coronary syndromes caused by?

A

atherosclerotic plaque rupture/fissure and thrombosis occluding the coronary arteries

189
Q

how would you describe the ischaemia that occurs in acute coronary syndromes?

A

supply led ischaemia

190
Q

how do MI’s lead to cardiac failure?

A

infarctions causes chunks of myocardium to die, resulting in poorly-contracting scar tissue. heart loses efficiency.

191
Q

what type of chest pain occurs in MIs?

A

severe crushing central chest pain

192
Q

in an MI, where does the pain radiate?

A

jaws and arms

especially the left

193
Q

how can an MI be differentiated to angina?

A

angina only lasts max 15 minutes, MI is prolonged
angina is relieved by GTN, MI is not
angina occurs on exertion, MI occurs at rest

194
Q

what symptoms are often associated with an MI?

A

sweating, nausea, vomitting

195
Q

what are the main changes in an acute STEMI?

A

ST elevation
T wave inversion
Q waves

196
Q

when do signs of ST elevation occur in an acute STEMI?

A

first few hours

197
Q

when do Q wave formation and T wave inversion occur in an acute STEMI?

A

first day

198
Q

what is the usual evidence of an old STEMI?

A

Q waves present,
+/- inverted T waves
(ST no longer as elevated)

199
Q

how much must ST segment be raised by for an STEMI?

A

1mm+ ST elevation in 2 adjacent limb leads
or
2mm+ ST elevation in at lesat 2 contingous precordial leads
or
new onset bundle branch block

200
Q

what leads have ST elevation in an inferior STEMI?

A

II, III, aVF

201
Q

what leads have ST elevation in an anteroseptal STEMI?

A

V1-V4

202
Q

what leads have ST elevation in a lateral STEMI?

A

1, aVL, V5, V6

203
Q

what leads show ischaemic changes that correlate with a STEMI?

A

leads which look at the opposite location of the heart to the infarction

204
Q

what are 2 diagnostic markers of an MI?

A

TnT (troponin T)

CK (creatinine kinase)

205
Q

which is more specific for cardiac muscle damage- troponin or creatinine kinase?

A

troponin

creatinine kinase also peaks in skeletal muscle and brain

206
Q

what is the treatment of an acute MI?

A 
MONA+C
morphine (diamorphine) + anti-emetic
oxygen (if hypoxic)
nitrate (GTN)
aspirin (antiplatelet)
clopidogrel (antiplatelet)
207
Q

in the treatment of an acute MI how is the diamorphine and the anti-emetic administered?

A

IV

208
Q

what are the doses of aspirin and clopdiogrel in the treatment of an acute MI?

A

aspirin 300mg

clopidogrel 300mg

209
Q

when would you not give GTN in the treatment of an acute MI?

A

if blood pressure is below 90mmHg

210
Q

if PCI (angioplasty) is not available within 90 minutes what is the alternative treatment for an acute MI?

A

thrombolysis

211
Q

in patients who have had an STEMI, what aspirin and clopidogrel therapy should be continued?

A

long-term aspirin

clopigorel for up to 4 weeks

212
Q

what are the 2 indicatations for reperfusion therapy? (PCI or thrombolysis)

A
  1. chest pain suggestive of acute MI (>20mins)
  2. ECT changes (acute ST elevation or new left bundle branch block)

[only if no contraindications]

213
Q

why does thrombolysis need to be administered early?

A

as time increases the clot becomes organised and hard and so cannot be broken down by anti-thrombolytics

214
Q

what percentage of patients does thrombolysis not work in?

A

50%

215
Q

how long must the ambulance drive be over for prehospital thrombolytics to be given instead of PCI?

A

40mins

216
Q

what happens to the 50% of patients where thrombolysis doesnt work? (but is used because the ambulance drive is over 40 minutes)

A

rescue angioplasty

217
Q

what are the 4 categories of complications of an acute MI?

A

death
arrhythmic complications
structural complications
functional complications

218
Q

what structural complications can occur due to an acute MI?

A 
cardiac rupture (untreatable)
ventricular septal defect
valve defects
mural thrombus +/-sysemic emboli
LV aneurysm formation
inflammation
acute pericarditis
dresslers syndrome
219
Q

what dunctional complications can occur due to an acute MI?

A

acute ventricular failure
chronic cardiac failure
cardiogenic shock

220
Q

usually when a valve defect occurs as a structural complication of an MI, what sign is heard on precordial auscultation?

A

new heart murmur

221
Q

after the acute MI, what intervention should occur once patient is stable?

A

coronary angiography

222
Q

what are the 4 phases of cardiac rehabilitation?

A

phase 1: in patient
phase 2: early post discharge period
phase 3: structured exercise programme (hospital based)
phase 4: long term maintenance of physical activity and lifestyle change (community based)

223
Q

what is dresslers syndrome?

A

secondary pericarditis which occur after damage to the heart (eg few weeks post MI) and causes fever and pleuritic pain

224
Q

what is ischaemic heart disease (a type of congestive cardiac failure) the result of?

A

MIs

225
Q

what is cor pulmonale?

A

hypertrophy and failure of the right ventricle due to resistance in the pulmonary circulation (pulmonary hypertension)

226
Q

what are the 4 main symptoms of left heart failure?

A

dyspnoea on exertion/rest
orthopnoea
paroxysmal nocturnal dyspnoea
pink frothy sputum

227
Q

what are the 4 clinical signs of LVF?

A

tachycardia
fine crepitations
pleural effusion
3rd heart sound

228
Q

what is gallop rhythm?

A

third heart sound + tachycardia

229
Q

what are the 4 signs of LVF on a CXR?

A

cardiomegaly
bats wing shadowing
kerbey B lines
interstitial fluid

230
Q

what is the main symptoms of right heart failure?

A

oedema

231
Q

what are the 4 clinical signs of RVF?

A

oedema (ankle/sacral
JVP elevated
hepatomegaly
ascites

232
Q

what are the sings of RVF on CXR?

A

none

233
Q

what 3 causes of CCF dont use standard CCF treatment, and instead treating the underlying problem is enough?

A

cor pulmonale: diuretics and oxygen
valvular disease: surgery
fast AF: digoxin or shock

234
Q

what 6 drugs are standard medical treatment options for congestive cardiac failure?

A 
diuretics
ACE inhibitors
beta blockers
spironolactone
(digoxin
nitrates)
235
Q

when is spironolactone used in congestive cardiac failure?

A

in severe cases only

236
Q

what 3 interventions can be used for congestive cardiac failure?

A

implantable cardiac defibrillators
cardiac resynchronisation therapy
tranplantation

237
Q

what type of diuretic is used in congestive cardiac failure?

A

loop diuretics

thiazide diruretics occasionally used in mild CCF

238
Q

what is spironolactone?

A

an aldosterone receptor antagonist

239
Q

what are the 3 possible side effects of spironolactone?

A

hyperkalaemia
renal dysfunction
gynaecomastia

240
Q

what is cardiac resynchronisation therapy?

A

3 pacemakers inserted to force LV and RV to contract together

241
Q

what type of patients need cardiac resynchronisation therapy?

A

prolonged QRS

242
Q

what is digoxins main use?

A

AF

can sometimes be used for CCF

243
Q

what are the 4 steps of management of a patient with acute LVF?

A
  1. sit up
  2. oxygen (caution in COPD)
  3. IV durosemide
  4. IV diamorphine (not in COPD)
244
Q

what cardiovascular drug should be used with caution in patients with COPD?

A

B-blockers

245
Q

what CVD are diuretics used in?

A

CCF

hypertension

246
Q

what CVD are B blockers used in?

A

angina
hypertension
CCF

247
Q

what CVD are ACE inhibitors used in?

A

CCF

hypertension

248
Q

what CVD are calcium antagonists used in?

A

hypertension
angina
arrhythmias

249
Q

what CVF are nitrates used in?

A

angina

CCF

250
Q

what are the 2 main markers of deterioration of a patient?

A

hypoxia

hypotension

251
Q

what type of rhythm does the patient in cardiac arrest need to have for a defibrillator to work?

A

shockable rhythm

252
Q

what are shockable rhythms that a patient might have if in cardiac arrest?

A

VF

pulseless VT

253
Q

what are non-shockable rhythms that a patient might have if in cardiac arrest?

A

asystole

pulseless electrical activity (PEA)

254
Q

what are the 8 reversible causes of cardiac arrest?

A 
hypoxia
hypovolaemia
hypothermia
hyper/hypo glycaemia
toxin
thrombus
tension pneumothorax
tamponade
255
Q

during the assessment of an unconscious patient how long should you look, listen and feel for breathing?

A

10s

256
Q

what is the rate of chest compressions during CPR?

A

100-120compressions per minute

257
Q

what is the depth of chest compressions during CPR?

A

5-6cm

258
Q

what is marfans syndrome?

A

a genetic condition that affects the connective tissue in the body

259
Q

what are the main 3 side effects of beta blockers?

A

impotence
shortness of breath
cold peripheries

260
Q

what is the main side effect of ACE I?

A

persistent dry cough

261
Q

what is the side effect caues by both digoxin and spironolactone?

A

gynaecomastia

262
Q

what are the 3 main side effects of amiodarone?

A

hyper/hypothyroidism
corneal microdeposits
lung/liver fibrosis

263
Q

what is the main GI side effect of verapamil?

A

constipation

264
Q

what are the 3 main side effects of nifedipine? (calcium channel blocker)

A

flushing
headache
ankle oedema

265
Q

what is the main side effect of thiazide diuretics?

A

gout

266
Q

what is the main side effect of minoxidil?

vasodilator for hypertension

A

increased hair growth

267
Q

what is the main side effect of hydralazine?

vasodilator for hypertension

A

drug induced-SLE

Cardiovascular (12 decks)

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