cv top tier Flashcards
which gender is IHD more common in
men
non modifiable risk factors for IHD
family history age smoking ethnicity- SE asia man
what ethnicity is associated with IHD
se asia
what lifestyle factors are associated with IHD
smoking
diet/obesity
excercise/activity
what clinical factors are associated with IHD
Diabetes Hypertension High lipids, high cholesterol Previous history of CHD Kidney disease Premature menopause (i think oestrogen is protective somehow)
psychosocial factors are associated with IHD
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
IHD cause (general)
atherosclerosis
- more resistnace, so flow rate slows
- pressure increased with reduced radius
angina causes
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
causes of MI
IHD/CHD (plague stenosis) Thrombus Embolus Muscle spasm Drug use eg cocaine
excarberating factors of angina
Cold Activity Stress Post prandial (anger/excitement)mi
types of angina
PRINZMETAL (CORONARY SPASM)
MICROVASCULAR
UNSTABLE / CRESCENDO
CUBITIS
prinzmetal’s angina=
-triggers
coronary spasm
- at rest, cold, smoking, cocaine, stress, vasoconstriction, atheroscl
microvascular angina
microartery stenosis
unstable angina
aka crescendo angina
= 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
cubitis angina
when lying down (=recumbent)
MI pathophysiology
ischaemia of heart muscle –> cardiac tissue necrosis/infarction
STEMI vs NSTEMI
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
which area of heart does LAD occlusion infarct
anterior
septal
what area of heart does L circymflex occlusion infarct
posterior
lateral
what area of heart does right coronary artery occlusion infarct
inferior
what blood test reveals MI
why
raised troponin I and T (measure ev 3h)
enzyme that regulates actin/myosin contraction and is a sensitive marker of cardiac muscle injury
unstable agina/MI heart murmur
pansystolic heart murmur
also mitral regurg
is blood pressure high or low with MI/angina
can be either
describe pain of stable angina
weight /tight band
middle of chest
worse when cold/postprandial/ stress/ excercise
may radiate to arm/jaw/neck/teeth/shoulder
relieved with rest/GTN
what other symptoms come with IHD (other than chest pain)
sob, dysponea nausea sweaty, fainty fatigue palpitations distress/anxiety (syncope oedema)
stable angina ECG?
stress ECG = excercise test
imaging for IHD
transthoracic MRI
perfusion MRI
invasive /CT coronary angiography **
CXR
MI management
pain releif
oxygen (if hypoxic)
antiplatelet/anti-coag (clopidogrel, aspirin)
maybe b blocker
what type of drug is clopidogrel
P2Y12 inhibitor
antiplatelet/anticoag (not sure which)
angina medication
nitrates opioid oxygen antiplatelet antihypertensives
how do nitrates work
venodilators
reduce pre load
dilate coronary arteries
pain killer
dual therapy
aspirin + P2Y12i/glycoprotein IIb/IIa/ B block/ACEi/statin
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
stenting technical word
PCI (percutaneous coronary intervention)
or
angioplasty
where does bypass (CABG) connect
artery off aorta to coronary artery
+
vein graft
what is the medical treatment for prinzmetal’s angina
amlopidine (CCB)
coronary spasm
what is tamponade
compression of heart from fluid in pericardial sac
complication of pericarditis
which B block is best for preventing arrythmias post-MI? and why?
propanolol
also blocks sodium channels
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
B blockers side effects
low HR so tired, cold hand/feet, erectile dysfunction
how do CCB work
Dilate arteries (ca channels needed for vasoconstriction) --Reduce afterload so less resistance
how do ACEi work
Vasodilation and less water retention
Lower BP so less resistance
why is mitral regurgitation a complication of MI
myocardial scarring preventing valve closure
what is dressler’s syndrome
a complication of mI
secondary form of pericarditis - injury to heart/pericardium –> fever/ pericarditis/ pain/ effusion
what causes high baseline troponin level
kidney disease chronic heart disease sepsis PE myocarditis pulmonary dissection
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
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
heart failure age distribution
increases with age
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
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)
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
two types of heart failure (other than chronic/acute)
systolic
diastolic
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
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
signs of heart failure (general)
tachy (not specific)
displaced apex beat (specific but insensitive)
signs of R heart failure
Raised jugular venous pressure
Enlarged liver
signs of L heart failure
Wheeze/crackle
Gallop heart rhythm
Murmurs possible
symtpoms of heart failure (general)
- sob (rest/exercise)
- reduction in activity - fatigue, get tired
- weight increase
- dizzy
symptoms of L heart failyre
Oedema in lungs Cough Tachypnoea Sputum wheeze
symptoms of R heart failure
Oedema in legs/ankles
Cold peripheries
what are you looking for with ecg for heart failure
underlying cause
ecg is abnormal
what are you looking for in CXR for heart failure
size of heart
effusioons
alveolar oedema
what are you looking for in echo for heart failure
chamber dimension,
valve disease
wall motion abnormalities
heart failure bloods
BNP = brain natriuretic peptide
secreted in ventricles in response to myocardial stress – levels correspond to severity
diagnositc!!
ANP vs BNP
atrial / brain natruiuretic peptide
anp- released by atria when dysfunctioning
bnp-released by ventricles when dysfunctioning
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
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)
heart failure treatment – nonpharmacological
surgery
- stent
- bypass
- valve repair
- transplant, if young
- pacemaker
lifestyle changes
- diet (avoid large meals)
- exercise
- smoking
- lose weight
acute heart failure treeatment
monitor ecg oxygen pain killers - opiates nitrates loop diuretics (electrolyte sparing)
heart failure complications
arrhythmia renal dysfunction (needs 1/4 of CO) thromboembolism, DVT, PE LBBB, bradycardia hepatic dysfunction neurological /psychological complications
hypertension risk factors
- genetic
- race
- gender (male)
- family history
- smoking
- little exercise/ sedentary
- too much salt
- too much alcohol
- stress
- diabetes
- overweight
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)
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)
signs and symptoms of hypertension
signs -- BP symptoms -- usually none fatigue headaches, migraines
how can you get over white coat syndrome with Hypertension
Do more than one reading – 24 hour ambulatory BP measured (ABPM)- worn at home
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)
coarctation
narrowing (aorta)
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)
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
hypertension complications
Accelerates atherosclerosis Stroke MI Chronic renal disease Cognitive decline Thrombosis etc Premature death Atrial fibrilation
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
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.
single atenolol tablet sees what expected drop in what
BP
8 or 10 mmHg in systolic pressure (top number)
what is and indicator of immediate damage to blood vessels due to hypertension
eyes
how often is a hypertensive patient’s BP checked
3-6months in clinic
MI ECG changes
ST elevation or ST depression (both diagnostic! )
abnormal Q wave
T wave inversion
