cv top tier Flashcards
1
Q
which gender is IHD more common in
A
men
2
Q
non modifiable risk factors for IHD
A
family history age smoking ethnicity- SE asia man
3
Q
what ethnicity is associated with IHD
A
se asia
4
Q
what lifestyle factors are associated with IHD
A
smoking
diet/obesity
excercise/activity
5
Q
what clinical factors are associated with IHD
A
Diabetes Hypertension High lipids, high cholesterol Previous history of CHD Kidney disease Premature menopause (i think oestrogen is protective somehow)
6
Q
psychosocial factors are associated with IHD
A
Behaviour pattern - type A (modifiable)
–Hostile, impatient, anger, anxiety, determined, competitive
Depression/ Anxiety
- -These cause CHD and CHD causes these :/
- -Could have common antecedents eg deprivation
Work
- -High demand, low control
- -Stress
- -Many hours
Social support
7
Q
IHD cause (general)
A
atherosclerosis
- more resistnace, so flow rate slows
- pressure increased with reduced radius
8
Q
angina causes
A
mismatch of supply and demand
SUPPLY OF HEART
Anaemia
Hypoxia
Atherosclerosis stenosis = main eg aortic stenosis
DEMAND OF HEART
Hypertension
Tachycardia, arrythmia
Vascular heart disease
9
Q
causes of MI
A
IHD/CHD (plague stenosis) Thrombus Embolus Muscle spasm Drug use eg cocaine
10
Q
excarberating factors of angina
A
Cold Activity Stress Post prandial (anger/excitement)mi
11
Q
types of angina
A
PRINZMETAL (CORONARY SPASM)
MICROVASCULAR
UNSTABLE / CRESCENDO
CUBITIS
12
Q
prinzmetal’s angina=
-triggers
A
coronary spasm
- at rest, cold, smoking, cocaine, stress, vasoconstriction, atheroscl
13
Q
microvascular angina
A
microartery stenosis
14
Q
unstable angina
aka crescendo angina
A
= acute coronary syndrome
stenosis is not constant, the atherosclerosis is changing and so thrombus is more likely. Pain changes/worsens. Pain at rest/minimal exertion, more serious
15
Q
cubitis angina
A
when lying down (=recumbent)
16
Q
MI pathophysiology
A
ischaemia of heart muscle –> cardiac tissue necrosis/infarction
17
Q
STEMI vs NSTEMI
A
STEMI- damage to full thickness of wall due to full coronary occlusion
NSTEMI- damage to partial thickness of wall due to partial coronary occusion of ful occlusion of minor coronary artery
18
Q
which area of heart does LAD occlusion infarct
A
anterior
septal
19
Q
what area of heart does L circymflex occlusion infarct
A
posterior
lateral
20
Q
what area of heart does right coronary artery occlusion infarct
A
inferior
21
Q
what blood test reveals MI
why
A
raised troponin I and T (measure ev 3h)
enzyme that regulates actin/myosin contraction and is a sensitive marker of cardiac muscle injury
22
Q
unstable agina/MI heart murmur
A
pansystolic heart murmur
also mitral regurg
23
Q
is blood pressure high or low with MI/angina
A
can be either
24
Q
describe pain of stable angina
A
weight /tight band
middle of chest
worse when cold/postprandial/ stress/ excercise
may radiate to arm/jaw/neck/teeth/shoulder
relieved with rest/GTN
25
what other symptoms come with IHD (other than chest pain)
```
sob, dysponea
nausea
sweaty,
fainty
fatigue
palpitations
distress/anxiety
(syncope
oedema)
```
26
stable angina ECG?
stress ECG = excercise test
27
imaging for IHD
transthoracic MRI
perfusion MRI
invasive /CT coronary angiography **
CXR
28
MI management
pain releif
oxygen (if hypoxic)
antiplatelet/anti-coag (clopidogrel, aspirin)
maybe b blocker
29
what type of drug is clopidogrel
P2Y12 inhibitor
| antiplatelet/anticoag (not sure which)
30
angina medication
```
nitrates
opioid
oxygen
antiplatelet
antihypertensives
```
31
how do nitrates work
venodilators
reduce pre load
dilate coronary arteries
pain killer
32
dual therapy
aspirin + P2Y12i/glycoprotein IIb/IIa/ B block/ACEi/statin
33
angina criteria for stenting
1 - if STEMI elevation is significant
- - >1mm in 2 contingous limb leads
- - >2mm in 2 contiguous precordial (chest) leads
2- new onset LBBB
3 -posterior MI
34
stenting technical word
PCI (percutaneous coronary intervention)
or
angioplasty
35
where does bypass (CABG) connect
artery off aorta to coronary artery
+
vein graft
36
what is the medical treatment for prinzmetal's angina
amlopidine (CCB)
| coronary spasm
37
what is tamponade
compression of heart from fluid in pericardial sac
complication of pericarditis
38
which B block is best for preventing arrythmias post-MI? and why?
propanolol
also blocks sodium channels
39
how does B blockers work
Slows heart (chron) + reduces force of contraction (inotropic)
- -Less output, less demand (for coronary vessels)
- -Lower HR means better oxygen distribution
40
B blockers side effects
low HR so tired, cold hand/feet, erectile dysfunction
41
how do CCB work
```
Dilate arteries (ca channels needed for vasoconstriction)
--Reduce afterload so less resistance
```
42
how do ACEi work
Vasodilation and less water retention
| Lower BP so less resistance
43
why is mitral regurgitation a complication of MI
myocardial scarring preventing valve closure
44
what is dressler's syndrome
a complication of mI
secondary form of pericarditis - injury to heart/pericardium --> fever/ pericarditis/ pain/ effusion
45
what causes high baseline troponin level
```
kidney disease
chronic heart disease
sepsis
PE
myocarditis
pulmonary dissection
```
46
bypass pros and cons
PROS
revascularization longer than stenting - lower risk of recurrent angina
better for diabetics
```
CONS
risk atherosclerosis + restenosis
invasive- worse for old and young
longer hospitalization
scar
not repeatable - high risk of mortality/morbidity
```
47
PCI pros and cons
```
PROS
less invasive - better for old and young
repeatable
shorter hospitalisation
no scar
```
CONS
high re-stenosis rate- may need repeat
requires dual antiplatelet therapy
48
heart failure age distribution
increases with age
49
risk factors/causes of heart failure, name 5
heart condition
```
1 IHD (angina)
2 pericarditis
3 hypertension
4 cardiomyopathy
5 arrythmias
6 congenital heart problem
7 valve problems
8 pulmonary hypertension
```
not CV related
1 anaemia
2 excess alcohol
50
heart failure pathophysiology
efficiency of heart as a pump is impaired, so unable to deliver blood at a rate equal to the requirements of the metabolising tissues (despite normal/increeased venous return)
51
acute vs chronic heart failure. which is normally associated with venous congestion and which with pulmonary/peripheral oedema
acute- pulmonary/peripheral oedema
chronic- venous congestion
52
two types of heart failure (other than chronic/acute)
systolic
| diastolic
53
systolic heart failure
+ ejection fraction
+ causes
Inability for ventricle to contract normally → decreased contractility → decreased CO
HFREF =reduced ejection fraction (fraction of end-diastolic fraction ejected in systole)
Caused by IHD, MI, cardiomyopathy
54
diastolic heart failure
+ ejection fraction
+ causes
Inability for ventricles to fully relax and fill → decreased stroke volume → decreased CO
HFPEF= preserved ejection fraction
Caused by hypertrophy (less ventricle volume) - as a result of hypertension (more resistance needs more force) and aortic stenosis, which increases afterload and decreases CO
55
signs of heart failure (general)
tachy (not specific)
displaced apex beat (specific but insensitive)
56
signs of R heart failure
Raised jugular venous pressure
| Enlarged liver
57
signs of L heart failure
Wheeze/crackle
Gallop heart rhythm
Murmurs possible
58
symtpoms of heart failure (general)
- sob (rest/exercise)
- reduction in activity - fatigue, get tired
- weight increase
- dizzy
59
symptoms of L heart failyre
```
Oedema in lungs
Cough
Tachypnoea
Sputum
wheeze
```
60
symptoms of R heart failure
Oedema in legs/ankles
| Cold peripheries
61
what are you looking for with ecg for heart failure
underlying cause
| ecg is abnormal
62
what are you looking for in CXR for heart failure
size of heart
effusioons
alveolar oedema
63
what are you looking for in echo for heart failure
chamber dimension,
valve disease
wall motion abnormalities
64
heart failure bloods
BNP = brain natriuretic peptide
secreted in ventricles in response to myocardial stress -- levels correspond to severity
diagnositc!!
65
ANP vs BNP
atrial / brain natruiuretic peptide
anp- released by atria when dysfunctioning
bnp-released by ventricles when dysfunctioning
66
NYHAclassification =
how many classes. what are each
new york heart association classification
class1 : no limitation, asymptoamtic. excercise= no symptoms
2- slight limitation: comfortable at rest. Normal exercise = symptoms
3- marked limitation: comfortable at rest. Gentle exercise = symptoms
4- inability to carry out any physical activity without discomfort
67
heart failure treatment
| pharmacological
better to block RAAS and symp nervoud system on heart than to make the LV do more:
- ACE i
- ARB
- B blockers
- aldosterone antagonists (sprinoloactone)
- Nitrates
- digoxin -- slows heart, increases force
- loop diuretics- electrolyte sparing (blood pressure and preload decrease so congestion decreases)
68
heart failure treatment -- nonpharmacological
surgery
- stent
- bypass
- valve repair
- transplant, if young
- pacemaker
lifestyle changes
- diet (avoid large meals)
- exercise
- smoking
- lose weight
69
acute heart failure treeatment
```
monitor ecg
oxygen
pain killers - opiates
nitrates
loop diuretics (electrolyte sparing)
```
70
heart failure complications
```
arrhythmia
renal dysfunction (needs 1/4 of CO)
thromboembolism, DVT, PE
LBBB, bradycardia
hepatic dysfunction
neurological /psychological complications
```
71
hypertension risk factors
- genetic
- race
- gender (male)
- family history
- smoking
- little exercise/ sedentary
- too much salt
- too much alcohol
- stress
- diabetes
- overweight
72
hypertension causes
may be due to ‘white coat’- higher BP with doctors than home
Primary
- Genetic susceptibility
- Excessive sympathetic nervous system activity
- Na/K transport abnormalities
- High salt intake
- RAAS system abnormalities
secondary hypertension
- kidney issues
- Coarctation of the aorta (narrowing)
- Endocrine (cushings, conns, hyperparathyroidism, thyroid problems, pheochromocytoma)
- medication including depression -venlafaxine, oral contraceptive, NSAIDs aspirin, blocked nose medication
- Alcohol , amphetamine, ecstasy, cocaine
suspect secondary when patient is young, resistant to antihypertensive medication, or symptoms of an underlying cause (kidneys, adrenals)
73
pathophysiology of hypertension
```
Higher pressure in blood vessels due to
Increased CO (HR and stroke vol)
Increased peripheral resistance
Vasoconstriction
Stenosis
Increased fluid volume (RAAS, kidneys)
```
74
signs and symptoms of hypertension
```
signs -- BP
symptoms --
usually none
fatigue
headaches, migraines
```
75
how can you get over white coat syndrome with Hypertension
Do more than one reading -- 24 hour ambulatory BP measured (ABPM)- worn at home
76
investigations into hypertension
BP in clinic
ABPM at home
bloods = ANP increase
look for end organ damage (as a result)
- eyes are an indicator of vessel damage : fundoscopy/ ophthalmoscopy for hemorrhage / papilloedema
- bloods : serum creatinine, eGFR, glucose
- ECG/echo : ventricular hypertrophy
- urinalysis: albumin:creatinine ratio, haematuria
rule out secondary hypertension (medication, kidney, endocrine, coarctation of aorta)
77
coarctation
narrowing (aorta)
78
hypertension management
regular BP check (3-6month)
medication
first line = ACEi/ ARB if caucasian / <55
if not that person, first line is CCB (old or A-C)
then add the other (so if A-C, now take CCB and ARB OR ACEi.. ).... then all 3 .... then ....
```
also :
diuretics
statins
B blockers
A blocker (doxazosin)
lifestyle (diet - reduce alc/salt, high fruit/veg, weight loss, exercise, stop smoking)
```
79
who to treat for hypertension
```
Treat stage one (systolic 140-160mmHg) if ‘at risk’
diabetes,
qrisk2 over 20%,
renal disease,
CV disease eg previous MI,
organ damage due to BP
```
Treat stage two (160+) always
think this may be wrong based on prev exam q - they seem to treat stage one when those conditinos arent mentioned
80
hypertension complications
```
Accelerates atherosclerosis
Stroke
MI
Chronic renal disease
Cognitive decline
Thrombosis etc
Premature death
Atrial fibrilation
```
81
should A-C patient be put on ramipril
no.
ramipril is ACEi
they already have repressed RAS system due to salt sensitivity and low renin
so ACE i will be less effective as opposed to those with high RAS system
82
keen adrenal/ adrenal tumour. how does this relate to heart issues
too much aldosterone
this causes calcium retention and K+ excretion
so low K+
hypokalemia -- ST segment sagging, T wave depression, and U wave elevation.
83
single atenolol tablet sees what expected drop in what
BP
8 or 10 mmHg in systolic pressure (top number)
84
what is and indicator of immediate damage to blood vessels due to hypertension
eyes
85
how often is a hypertensive patient's BP checked
3-6months in clinic
86
MI ECG changes
ST elevation or ST depression (both diagnostic! )
abnormal Q wave
T wave inversion
