Cardiovascular Disease Flashcards

1
Q

what is atherosclerosis?

A

a progressive build up of plaque within the arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is athersclerotic plaque formed from?

A
fatty substances
choleserol
cellular waste
calcium
fibrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is an atherothrombosis?

A

formation of an acute thrombosis superimposed on atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what type of haemodynamic force can cause endothelial damage?

A

hypertension

due to sheer stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how does OXLDL cause vasodilatory impairment?

A

by modifying endothelial response to angiotensin II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

why does a fibrous lesion form over the fatty streak?

A

a protective response to the endothelial damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are 4 major risk factors for cardiovascular disease

A

dyslipiaemia
hypertension
smoking
diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is intermittent claudication a symptom of?

A

peripheral arterial disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

why are many patients with PAD not diagnosed?

A

most are asymptomatic

9/10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the 4 minor risk factors for cardiovascular disease?

A

physical inactivity
alcohol
stress
gender/genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what type of cholesterol do statins reduce?

A

total cholesterol

LDL cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the statin with the greatest efficacy?

A

rosuvastatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

atorvastatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are xanthelasma?

A

xanthomas of the eyelids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

why do tendon xanthomas form?

A

infiltration of tendon by lipid: hypercholesterolaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

where are the most common places for tendon xanthomas?

A

extensor tendons of fingers, patella, elbows

achilles tendon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

why do tuberous xanthomas form?

eg elbows

A

lipid deposits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what are the 3 causes of tuberous xanthomas?
familial hypertriglyceridemias acquired hypertriglyceridemias biliary cirrhosis
26
what do eruptive xanthomas suggest?
abrupt increase in serum triglyceride levels
27
where are eruptive xanthomas more likely to me?
buttocks posterior thighs body folds
28
for patients with diabetes, what is their target blood pressure?
below 130/80
29
what does smoking do to your blood pressure?
increases blood pressure
30
what does smoking do to your HDL?
decreases HDL
31
what are the 5 features of metabolic syndrome?
``` abdominal obesity high blood pressure high triglycerides low HDL high fasting glucose (patients must have 3 of these characteristics) ```
32
what does an assign score allow you to measure?
risk of developing cardiovascular disease
33
what is ischaemia?
the result of impaired vascular perfusion which deprives the affected tissue of nutrient (can be reversible)
34
what is infarction?
ischaemic necrosis of a tissue secondary to occlusion/reduction of arterial supply or venous drainage (irreversible, recovery will depend on tissues regenerative ability)
35
why can reduced venous drainage cause ischaemia/infarction?
venous blood backs up and doesn't allow oxygenated arterial blood to get to the tissue
36
what is the difference between a thrombus and a clot?
- thrombus occurs in vasculature, during life | - blood clot is not within vascular space or not in life.
37
what 2 types of granules to platelets have?
alpha granules | dense granules
38
what type of contents do alpha granules contain?
adhesion components eg fibrinogen
39
what type of contents do dense granules contatin?
aggregation components eg ADP
40
what affects do stasis and turbulence of blood cause?
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)
41
what type of situations cause turbulence within blood vessels?
- aneurysms - AF - blood flowing round and occluding atherosclerotic plaque
42
what type of situations cause stasis within blood vessels?
-impaired venous drainage of lower limbs | non-contractile areas of -myocardium following a myocardial infarction
43
what are the 2 subsections of abnormal blood flow? (1/3 of virchows triad)
stasis | turbulence
44
list 9 acquired hypercoaguable states?
``` MI immobilisation tissue damage cancer prosthetic heart valves AF pregnancy smoking oral contraceptive use ```
45
what 3 genetic abnormalities can cause hypercoaguable states?
factor V mutations defects in anticoagulant pathways (eg AT III deficiency) defects in fibrinolysis
46
what type of thrombi show lines of Zahn?
arterial thrombi
47
why do lines of zahn form in an arterial thrombi?
alternating pale (platelet and fibrin) and dark (RBC and WBC) bands
48
what is an emboli?
a detached intravascular mass which is carried by the bloodstream to a site distant from point of origin
49
what are the most common type of emboli?
thromboemboli | fragments of a detached thrombus
50
what are the 7 types of embolism?
``` thromboembolism fat embolism marrow embolism air embolism septic embolism amniotic fluid embolism tumour embolism ```
51
what colour is a lung infarct?
red | due to leaking of secondary bronchial blood supply onto infarcts
52
what colour do arterial infarcts tend to be?
white | no secondary blood supply leaking onto area
53
why might a venous emboli cause an arterial infarct?
atrial/ventricular septal defect
54
when do fat embolisms usually occur?
follow major soft tissue trauma or bone fractures
55
what can gas/air embolisms cause?
barotrauma
56
when do amniotic fluid embolisms occur? and why?
post-partum | amniotic fluid and debris enters torn veins after birthing
57
what is arteriolosclerosis associated with?
diabetes and hypertension
58
what are the main target vessels for atherosclerosis?
aorta coronary arteries cerebral arteries
59
what 3 sections make up an atherosclerotic plaque?
rasied focal lesion of intima lipid core of cholesterol and lipoproteins fibrous cap
60
what 2 things occur when an atherosclerotic plaque increases in size?
luminal diameter decreases | blood flow reduces
61
how can atherosclerotic plaques lead to aneurysm development?
progressively degrade (and therefore weaken) the arterial wall
62
what are the 3 results of an atherosclerotic plaque?
resolution repair complication
63
what does resolution of an atherosclerotic plaque involve?
reabsorbtion of the lipids at fatty streak stage
64
what does repair of an atherosclerotic plaque involve?
stabilisation by fibrosis scarring
65
what are the general risk factors for DVTs? (8)
``` age obesity immobilisation (ie hospital, long journeys) pregnancy major surgery varicose veins OCP smoking ```
66
what are the medical conditions which have risk factors for DVTs? (9)
``` cancer previous DVT cerebrovascular accident acute myocardial infarction congestive heart failure sepis nephrotic syndrome inflammatory bowel disease vasculitis ```
67
what part of virchows triad does sepsis affect?
change in blood constituents: | hypercoaguable state
68
what 4 types of trauma are risk factors to DVTs?
multiple trauma CNS/spinal cord injury burns lower extremity fractures
69
what part of virchows triad do burns affect?
change in blood constituents: | hypercoaguable state
70
what drugs/drug habits can are risk factors to DVTs?
intravenous drug abuse oestrogens (OCP, HRT) tamoxifen chemotherapy
71
what are the symptoms and signs of a DVT?
``` calf/leg would be: painful swelling redness hot/inflamed localised tenderness over certain deep vein ```
72
what blood tests do you use as an investigation for a DVT?
D-dimer test | (not specific: infection, MI, surgery, liver disease pregnancy
73
what does a D-dimers test look for? (in order to see the likelihood of a DVT)
a fibrin breakdown product
74
how should you use a D-dimer test when looking for a DVT?
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)
75
what investigational tests would you use if you suspect a DVT?
duplex scan venous plethysomography venogram
76
how do you treat a DVT?
anticoagulation with LMWH and warfarin | compression stockings
77
for the treatment of DVT what stockings should you use?
TEDs for 6 weeks | grade 2 compression stockings for up to 5 years to reduce post phlebitic syndrome
78
what is post-phlebitic syndrome?
chronic venous insufficiency when the valves are destroyed and so the vein becomes large and flaccid causing a persistently swollen leg
79
what is a phlegmasia dolens?
A medical emergenct where a DVT causes obstruction of arterial inflow
80
how do you treat a phlegmasia dolens?
``` IVC filter femoral arterial line tPA intra-arterially surgical review decompression amputation ```
81
why do you put in an IVC filter for a patient with phlegmasia dolens?
to prevent bits of the clot embolising and causing a PE
82
what is the difference between wet gangrene and dry gangrene?
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
83
what are the 4 classifications of an acute PE?
minor major with normal RV function major with RV dysfunction massive with shock or syncope
84
what are the symptoms of a PE?
``` SOB collapse pleuritic chest pain haemoptysis sudden death ```
85
what are the signs of a PE on general examination?
tachypnea, tachycardia hypotenstion, wheeze
86
what are the signs of a PE on auscultation?
wheeze | pleural rub
87
what are the signs of a PE on CXR?
oligemia pleural effusion consolidation
88
what is oligemia?
segmental loss of pulmonary vaculature
89
what are the main investiagtions for a PE?
``` ABGs D-Dimers CXR V/Q scan CTPA echocardiogram ```
90
what are the findings of a PE on ECG?
sinus tachycardia | S1Q3T3 (rarely)
91
explain what S1Q3T3 mean on an ECG?
large S wave on lead 1 Q wave present on lead 3 inverted T wave present on lead 3
92
what is the investigation pathway for a PE
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
93
why can ventilation-perfusion scan sometimes be a poor discriminator of a PE?
if there is background lung disease
94
when are CT pulmonary angiograms poor in detecting PEs?
peripheral lesions
95
what is the con about CTPA?
invasive
96
what does an echocardiography tell you about a PE?
shows right heart strain and pressures
97
what are the 4 different treatment options in the treatmenf of a PTE?
1. anticoagulants 2. thrombolytic therapy 3. IVC filter 4. surgical removal
98
what is the treatment of choice for a minor PE?
anticoagulants
99
what is the treatment of choice for a major PE without RV dysfunction?
anticoagulants
100
what is the treatment of choice for a major PE with RV dysfunction
anticoagulants (and/or) | thrombolysis
101
what is the treatment of choice for a massive PE with shock or syncope?
thrombolysis or surgery
102
what anticoagulant treatment is given for the treatment of a PE?
initially: LMWH/heparin 5 days afterwards: LMWH/heparin after discharge: warfarin
103
what are the major pro and major con of an IVC filter?
pro: prevent recurrent PE in short term con: increase risk of recurrent DVT in long term
104
why are IVC filters not recommened for long term, and if they are needed in the long term why is anticoagulation also needed?
because in the long term they increase risk of recurrent DVT
105
what are the 3 indications for a IVE filter?
1. recurrent PTE despite adequate anticoagulation 2. PTE when anticoagulation is contraindicated 3. high risk (eg phlegmasia dolens)
106
what 4 major reasons might anticoagulants be contraindicated?
post op pre op severe live disease pregnancy
107
what type of surgery is needed for a patient with an acute massive PE with shock/syncope?
pulmonary embolectomy
108
what type of elective surgery can be used for patients with chronic thromboembolic pulmonary hypertension?
thromboendarterectomy
109
what are the 4 vitamin K dependent clotting factors?
II, VII, IX, X | these are the factors that warfarin prevents forming
110
where are the 4 vitamin K dependent clotting factors synthesised?
in the liver
111
why is bleeding effects of dabigatran much easier to reverse than warfarin?
dabigatran half life is 12-17 hours (compared to warfarins: 40 hours) and so drug cessation is usually sufficient
112
give a reason why a patient might have angina without coronary disease?
anaemia | blood supply not supplying enough oxygen for energy
113
what are the main way for testing for angina? | despite angina being a clinical diagnosis
exercise training testing perfusion imaging CT angiography angiography
114
what revascularisation techniques can be used for angina patients to releve symptoms?
CABG | PCI
115
what are the 4 pros of exercise testing?
cheap non-invasive reproducible shows risk stratification (ie positive test at low workload imples poor prognosis)
116
what are the 2 cons of exercise testing?
- poor diagnostic accuracy in certain sub groups (eg less mobile patients) - some patients struggle to get a maximal test- submaximal test
117
what are the 3 pros of perfusion imaging?
- non invasive - accuracy in sub groups that dont have accuracy in ETT - risk strarification
118
what are the 2 cons of perfusion imaging?
radiation | false positives/negatives
119
what are the 3 pros of CT angiography?
non-invasive risk stratification anatomical data
120
what are the 3 cons of CT angiography?
radiation can be less precise when calcium is present cost
121
what is angiography?
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
what are the 4 pros of angiography?
gold standard anatomical information risk stratification can follow on with angioplasty if needed
123
what are the 3 const of angiography?
- risk of stroke or death - radiation - contrast can cause renal dysfunction, rash. nausea
124
what drugs can be used to relieve angina symptoms?
``` nitrates B-blockers calcium antagonists nicorandil statin aspirin ACE inhibitor ```
125
what is intermittent claudication?
ischaemic pain which develops in the affected limb after variable periods of exercise, pain is relieved by rest
126
what are 2 non-invasive investigations of the lower limb?
ABPI (ankle brachial pressure index) | duplex ultrasound scanning
127
what are 3 invasive investigation of the lower limb?
MR angiography CT angiography catheter angiography
128
how do calculate ABPI?
ankle systolic pressure (mmHg)/ | brachial systolic pressure (mm Hg)
129
what is does the ABPI value have to be to suggest claudication
below 0.9
130
what does an eABPI | (exercise ankle brachial pressure index) show in a normal response?
increased ABPI during exercise
131
what does an eABPI (exercise ankle brachial pressure index) show in a claudication response?
decreased ABPI during exercise
132
how does walking (/exercise programs) improve intermittent claudication?
develops collateral circulation
133
for the management of intermittent claudication what exercise training program should be implemented?
duration: 1 hr/day to 30mins 3x a weel for a minimum of 6 months must be supervised 'beyond pain' exercise
134
what drug is used for relivation of intermittent claudication
cilostazol
135
what is the name of the disease which causes pain in limbs at rest due to insufficient vascular perfusion?
critical limb ischaemia
136
what is the main difference between intermittent claudication and critical limb ischaemia?
intermittent claudication is only pain during exercise (pain is relieved by resting( critical limb ischaemia has pain even during rest
137
why is the pain in critical limb ischaemia worse at night?
no gravity to help the blood flow
138
what are 2 major risk factors for a patient with critical limb ischaemia to go on to needing a amputation?
smoking | diabetes
139
what would you expect to find on examination of a acute ischaemic leg?
``` 6Ps Pallor Perishingly cold Pulseless Pain Paresthesia Paralysis ```
140
what are the 10 main risk factors for an aortic aneurysm?
``` male/ female post-menopaus family history age smoking PVD cardiac disease cerebrovasclar disease hypercholesterolaemia diabetes ```
141
what types of abdominal aortic aneurysms can be symptomatic?
both ruptured and non-ruptured
142
what 2 investigations are useful for a suspected asymptomatic abdominal aortic aneurysm?
ultrasound scan | CT angiography
143
at what phase must the IV contrast be in during a CT angiography of the abdominal aorta?
arterial phase
144
what 1 investigation is useful for a suspected symptomatic abdominal aortic aneurysm?
CT angiography
145
what is the difference between elective aneurysm repair and emergency aneurysm repair?
elective aneurysm repair is a prophylactic operation to reduce risk of rupture emergency aneurysm repair is a life saving therapeutic procedure
146
what is endovascular repair of an abdominal aortic aneursym?
inserting a graft within the aorta (via a peripheral artery) x-ray guided
147
what 2 type of interventions can be used for an elective aneurysm repair?
``` endovascular repair open repair (laparotomy) ```
148
compare an endovascular repair of an abdominal aorta aneurysm to an open repair?
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
what are the 2 types of venous system?
deep veins | superficial veins
150
in the lower limbs what major veins make up the deep system?
tibial vein popliteal vein femoral vein
151
in the lower limb what major veins make up the superficial system?
``` saphenous veins (parallel to the deep system) perforator veins (link to deep system) ```
152
what are the 4 major risk factors for varicose veins?
age pregnancy obesity prev DVT
153
what are primary varicose veins the result of?
incompetent valves (usually in superficial veins)
154
what are secondary varicose veins the result of?
``` venous obstruction (causing blood to flow through perforator veins to the superficial veins) ```
155
what type of varicose veins to DVTs cause?
secondary varicose veins
156
how is the appearance of varicose veins effected by standing?
more prominent when standing
157
what are the 3 major complications of varicose veins?
bleeding and bruising superficial thrombophlebitis chronic venous insufficiency
158
what are 3 signs of chronic venous insufficiency on inspection of the leg?
haemosiderin deposits lipodermatoclerosis ulceration
159
what is thrombophlebitis?
inflammation of a vein caused by a blood clot | can be due to chronic venous insufficiencu
160
what are haemosiderin depositis?
red cell breakdown and leakage visible on the skin | can be due to chronic venous insufficiency
161
what are the investigations used for suspected chronic venous insufficiency?
duplex scan
162
what is the non-interventional management of chronic venous insufficiency?
graduated compression using bandaging (for ulcers) and class II-IV stockings (ulcer prevention/symptomatic relief)
163
when is graduated compression for chronic venous insufficiency contraindicated?
``` low ABPI (intermittent claudication/critical limb ischaemia) ```
164
what is the interventional management of chronic venous insufficiency
``` foam sclerotherapy (duplex guided) endovenous ablation surgical ```
165
what are the complications of chronic venous insufficiency interventions?
``` thrombophlebitis skin staining ulceration wound infection nerve damage recurrence ```
166
what are the 2 revascularisation techniques for coronary heart disease?
CABG | PCI
167
what is the artery usually used for peripheral access for a PCI?
radial artery
168
what is a stroke?
acute onset of focal neurological symptoms and signs due to disruption of blood supply
169
what is the most common type of stroke?
ischaemic
170
what 2 factors contribute to a haemorrhagic stroke?
raised blood pressure | weakened blood vessel wall
171
why might a cerebral artery wall be weakened?
``` structural abnormalities (aneurysm, arteriovenous malformation) inflammation (vasculitis) ```
172
what are the 5 non-modifiable risk factors for a stroke?
``` age family history gender race prev stroke ```
173
what are 10 potentially modifiable risk factors for a stroke?
``` hypertension hyperlipidaemia smoking diabetes AF congestive heart failure alcohol excess obesity physical inactivity poor socioeconomic status ```
174
which blood pressure value (systolic or diastolic?) has the strongest relationship with stroke risk?
systolic
175
what therapy is recommended in all patients who have an ischaemic stroke? (with the intention of controlling hyperlipidaemia)
statin
176
what is the only way of accurately differentiating between an ischaemic and haemorrhagic stroke?
brain imaging
177
what type of brain imaging can be used to differentiate/confirm the type of stroke?
CT +/- angiography MRI with diffusion weighted imaging (DWI) +/- angiography MRI with gradient echo sequences (GRE)
178
what does an MRI with GRE (gradient echo sequences) look for?
looks for old haemosiderin deposits | ie an old bleed
179
how do you differentiate between a cardioembolism (ie cardiac cause for embolism) and an atheroembolism (ie atherosclerosis cause for embolism)?
atheroembolism: infarcts present in the same side as teh affected carotid artery cardioembolism: infarcts present in more than one arterial territory- bilateral
180
what are transient ischaemic attackes?
focal neurological symptoms that resolve within 24 hours
181
what is the medical management post ischaemic stroke?
aspirin 300mg statins (if in AF- anticoagulation) antihypertensives
182
what is the medical management for an ischaemic acute stroke?
thrombolysis aspirin 300mg (if prev aspirin-associated dyspepsia also give PPI)
183
what is the post-ischaemic stroke surgical management?
carotid endartectomy
184
what type of atheromatous plaque causes chronic stable angina?
fixed atheromatous plaque
185
how would you describe the ischaemia that occurs in chronic stable angina?
demand led ischamia
186
why can eating a large meal cause angina to occur?
because cardiac work load increases
187
what 3 conditions does the phrase 'acute coronary syndromes' cover?
unstable angina NSTEMI STEMI
188
what are acute coronary syndromes caused by?
atherosclerotic plaque rupture/fissure and thrombosis occluding the coronary arteries
189
how would you describe the ischaemia that occurs in acute coronary syndromes?
supply led ischaemia
190
how do MI's lead to cardiac failure?
infarctions causes chunks of myocardium to die, resulting in poorly-contracting scar tissue. heart loses efficiency.
191
what type of chest pain occurs in MIs?
severe crushing central chest pain
192
in an MI, where does the pain radiate?
jaws and arms | especially the left
193
how can an MI be differentiated to angina?
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
what symptoms are often associated with an MI?
sweating, nausea, vomitting
195
what are the main changes in an acute STEMI?
ST elevation T wave inversion Q waves
196
when do signs of ST elevation occur in an acute STEMI?
first few hours
197
when do Q wave formation and T wave inversion occur in an acute STEMI?
first day
198
what is the usual evidence of an old STEMI?
Q waves present, +/- inverted T waves (ST no longer as elevated)
199
how much must ST segment be raised by for an STEMI?
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
what leads have ST elevation in an inferior STEMI?
II, III, aVF
201
what leads have ST elevation in an anteroseptal STEMI?
V1-V4
202
what leads have ST elevation in a lateral STEMI?
1, aVL, V5, V6
203
what leads show ischaemic changes that correlate with a STEMI?
leads which look at the opposite location of the heart to the infarction
204
what are 2 diagnostic markers of an MI?
TnT (troponin T) | CK (creatinine kinase)
205
which is more specific for cardiac muscle damage- troponin or creatinine kinase?
troponin | creatinine kinase also peaks in skeletal muscle and brain
206
what is the treatment of an acute MI?
``` MONA+C morphine (diamorphine) + anti-emetic oxygen (if hypoxic) nitrate (GTN) aspirin (antiplatelet) clopidogrel (antiplatelet) ```
207
in the treatment of an acute MI how is the diamorphine and the anti-emetic administered?
IV
208
what are the doses of aspirin and clopdiogrel in the treatment of an acute MI?
aspirin 300mg | clopidogrel 300mg
209
when would you not give GTN in the treatment of an acute MI?
if blood pressure is below 90mmHg
210
if PCI (angioplasty) is not available within 90 minutes what is the alternative treatment for an acute MI?
thrombolysis
211
in patients who have had an STEMI, what aspirin and clopidogrel therapy should be continued?
long-term aspirin | clopigorel for up to 4 weeks
212
what are the 2 indicatations for reperfusion therapy? (PCI or thrombolysis)
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
why does thrombolysis need to be administered early?
as time increases the clot becomes organised and hard and so cannot be broken down by anti-thrombolytics
214
what percentage of patients does thrombolysis not work in?
50%
215
how long must the ambulance drive be over for prehospital thrombolytics to be given instead of PCI?
40mins
216
what happens to the 50% of patients where thrombolysis doesnt work? (but is used because the ambulance drive is over 40 minutes)
rescue angioplasty
217
what are the 4 categories of complications of an acute MI?
death arrhythmic complications structural complications functional complications
218
what structural complications can occur due to an acute MI?
``` cardiac rupture (untreatable) ventricular septal defect valve defects mural thrombus +/-sysemic emboli LV aneurysm formation inflammation acute pericarditis dresslers syndrome ```
219
what dunctional complications can occur due to an acute MI?
acute ventricular failure chronic cardiac failure cardiogenic shock
220
usually when a valve defect occurs as a structural complication of an MI, what sign is heard on precordial auscultation?
new heart murmur
221
after the acute MI, what intervention should occur once patient is stable?
coronary angiography
222
what are the 4 phases of cardiac rehabilitation?
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
what is dresslers syndrome?
secondary pericarditis which occur after damage to the heart (eg few weeks post MI) and causes fever and pleuritic pain
224
what is ischaemic heart disease (a type of congestive cardiac failure) the result of?
MIs
225
what is cor pulmonale?
hypertrophy and failure of the right ventricle due to resistance in the pulmonary circulation (pulmonary hypertension)
226
what are the 4 main symptoms of left heart failure?
dyspnoea on exertion/rest orthopnoea paroxysmal nocturnal dyspnoea pink frothy sputum
227
what are the 4 clinical signs of LVF?
tachycardia fine crepitations pleural effusion 3rd heart sound
228
what is gallop rhythm?
third heart sound + tachycardia
229
what are the 4 signs of LVF on a CXR?
cardiomegaly bats wing shadowing kerbey B lines interstitial fluid
230
what is the main symptoms of right heart failure?
oedema
231
what are the 4 clinical signs of RVF?
oedema (ankle/sacral JVP elevated hepatomegaly ascites
232
what are the sings of RVF on CXR?
none
233
what 3 causes of CCF dont use standard CCF treatment, and instead treating the underlying problem is enough?
cor pulmonale: diuretics and oxygen valvular disease: surgery fast AF: digoxin or shock
234
what 6 drugs are standard medical treatment options for congestive cardiac failure?
``` diuretics ACE inhibitors beta blockers spironolactone (digoxin nitrates) ```
235
when is spironolactone used in congestive cardiac failure?
in severe cases only
236
what 3 interventions can be used for congestive cardiac failure?
implantable cardiac defibrillators cardiac resynchronisation therapy tranplantation
237
what type of diuretic is used in congestive cardiac failure?
loop diuretics | thiazide diruretics occasionally used in mild CCF
238
what is spironolactone?
an aldosterone receptor antagonist
239
what are the 3 possible side effects of spironolactone?
hyperkalaemia renal dysfunction gynaecomastia
240
what is cardiac resynchronisation therapy?
3 pacemakers inserted to force LV and RV to contract together
241
what type of patients need cardiac resynchronisation therapy?
prolonged QRS
242
what is digoxins main use?
AF | can sometimes be used for CCF
243
what are the 4 steps of management of a patient with acute LVF?
1. sit up 2. oxygen (caution in COPD) 3. IV durosemide 4. IV diamorphine (not in COPD)
244
what cardiovascular drug should be used with caution in patients with COPD?
B-blockers
245
what CVD are diuretics used in?
CCF | hypertension
246
what CVD are B blockers used in?
angina hypertension CCF
247
what CVD are ACE inhibitors used in?
CCF | hypertension
248
what CVD are calcium antagonists used in?
hypertension angina arrhythmias
249
what CVF are nitrates used in?
angina | CCF
250
what are the 2 main markers of deterioration of a patient?
hypoxia | hypotension
251
what type of rhythm does the patient in cardiac arrest need to have for a defibrillator to work?
shockable rhythm
252
what are shockable rhythms that a patient might have if in cardiac arrest?
VF | pulseless VT
253
what are non-shockable rhythms that a patient might have if in cardiac arrest?
asystole | pulseless electrical activity (PEA)
254
what are the 8 reversible causes of cardiac arrest?
``` hypoxia hypovolaemia hypothermia hyper/hypo glycaemia toxin thrombus tension pneumothorax tamponade ```
255
during the assessment of an unconscious patient how long should you look, listen and feel for breathing?
10s
256
what is the rate of chest compressions during CPR?
100-120compressions per minute
257
what is the depth of chest compressions during CPR?
5-6cm
258
what is marfans syndrome?
a genetic condition that affects the connective tissue in the body
259
what are the main 3 side effects of beta blockers?
impotence shortness of breath cold peripheries
260
what is the main side effect of ACE I?
persistent dry cough
261
what is the side effect caues by both digoxin and spironolactone?
gynaecomastia
262
what are the 3 main side effects of amiodarone?
hyper/hypothyroidism corneal microdeposits lung/liver fibrosis
263
what is the main GI side effect of verapamil?
constipation
264
what are the 3 main side effects of nifedipine? (calcium channel blocker)
flushing headache ankle oedema
265
what is the main side effect of thiazide diuretics?
gout
266
what is the main side effect of minoxidil? | vasodilator for hypertension
increased hair growth
267
what is the main side effect of hydralazine? | vasodilator for hypertension
drug induced-SLE