cardiovascular disease Flashcards
what might you see on an ecg with angina
ST depression
due to sub endocardial ischaemia
what two mechanisms control coronary flow
autoregulation / myogenic
metabolic regulation
what is coronary flow reserve
maximum vasodilation - autoregulated flow
what determines myocardial oxygen consumption
tension contractility HR basal activity mass of tissue
what 4 types of drug are used in angina
B blockers
nitrates
ca channel blockers
Ikf channel inhibitors
what events increase the likelihood of mi
time of day inflammatory activity infection high BP catecholamines (adrenaline)
what preventative drugs would you give someone after a stemi
b blockers
ace inhibitors
statins
what are common complications of stemis
arrhythmia heart failure rupture mitral valve insufficiency VSD mural thrombus and embolism LV dilation recurrent MI
how would you treat a nstemi
antiplatelet
b blockers and nitrates
statin
ace inhibitors
describe age related vascular changes
fibrosis
accumulation of ground substances
fragmentation of elastic lamina
what are the 3 components of atheroma
lipid deposition
inflammation
fibrosis
also: neovascularisation, smooth muscle, macrophages, lymphocytes, collagen
necrotic core: cell debris, cholesterol crystals, foam cells, debris
where are atherosclerotic aneurysms usually found
abdominal aorta, distal to renal arteries
saccular or fusiform, may contain thrombi. often palpable or abdom bruits
where are the origins of dissecting aneurysms found
aortic valve
what is the most common cause of death in a dissecting aneurysm
dissection outward into the peritoneal, pleural or pericardial cavities
what might be the result of a berry aneurysm
sub arachnoid haemorrhage
what is a capillary microaneurysm
small aneurysm of the middle cerebral artery. may lead to intra cerebral haemorrhage
where are syphilitic microaneurysm normally found
thoracic aorta
what is a mycotic aneurysm
wall of artery is weakened often in the brain
what is giant cell arteritis
granulomatous inflammation of arteries, usually temporal, vertebral and opthalmic
what is takaysu arteritis
pulseless disease- (intermittent claudication of UL arteries)
what is polyarteritis nodosa
arteries of abdo organs
fibrinoid necrosis
what is kawasakis disease
very young children
fever , eye and mouth lesions
what are the type of vascular tumours (benign)
angioma haemangioma juvenile capillary cavernous lymphangioma
what are some types of malignant tumours
angiosarcoma
kaposis sarcoma
angioproliferative tumour
what causes dysrhythmia
changes to heart cells
changes in conduction of the impulse
what are the 4 classes of arrhythmias
atrial/ SV
junctional (AVN)
ventricular
tachy/brady cardia
what are the 4 types of arrhythmia event
heart block
ectopic
delayed after depolarisation
circus re entry
what does a delayed after depolarisation cause
atrial or ventricular tachycardias
what usually causes heart block
ischaemia
usually affects AVN, slows or blocks impulses
describe the features of a first degree heart block
conduction is slowed
abnormally long PR interval
every p wave is passed to QRS
normal PR interval is 0.12- 0.2
describe a mobitz 2 heart block
some Ps don’t get through
constant PR interval except when there is missed QRS
describe a wenkebach heart block
progressive lengthening of the PR Interval until a dropped QRS
describe a 3rd degree heart block
complete block
ventricles depolarise at their inherent rate
what are ectopic pacemakers
when other areas of the heart develop pacemaker activity eg due to damage sympathetic activity catecholamines digoxin
ischaemic damage may cause cells to become leaky to Na
catecholamines (B1 rec) increase rate of depolarisation
what is an early after depolarisation
occurs towards the end of phase 2
triggered by increase in Ca permeability
can set off self sustaining depolarisations - tachycardia
long QT
what is a delayed after depolarisation
increase in Ca eg due to cardiac glycosides causes an after depolarisation
can become self perpetuating and trigger an AP
may be due to delayed repolarisation (long qt)
can lead to ventricular dysrhythmia
what is circus reentry
an electrical impulse re enters a region of the heart after its refractory period
comes from an unusual direction and at the wrong time
no extinction by collision due to impulse dying out
may cause paroxysmal tachycardia
what is wolf Parkinson white syndrome
due to an additional electrical connection between the atria and ventricles thereby passing the AVN
causes paroxysmal tachycardia and re entry
delta waves on the ecg
wide qrs
st changes
how might you diagnose a left anterior fascicular hemiblock
left axis deviation
how might you diagnose a left posterior fascicular hemiblock
right axis deviation
what might cause a bradycardia
b blockers diltiazem (Ca channel blocker) hypothyroidism sinus node disease electrolyte abnormalities
you might treat with a pace maker
how do you diagnose a right bundle branch block
widened qrs complex
two r waves
how do you diagnose a left bundle branch block
widening of QRS complex
a notch in the qrs
what is a narrow complex tachycardia
superventricular
atrial/junctional/re-entry
usually no p waves
what is a broad complex tachycardia
usually ventricular
how would you treat an AV node tachycardia eg avnrt or avrt
adenosine
causes transient AV block
how would you treat AF
diltazem, verapamil, b blocker
what is polymorphic ventricular tachycardia also known as
torsade de points
must also have QT prolongation. associated with early after depolarisations
sudden cardiac death after adrenergic setting
what might cause secondary hypertension
renal disease, phaeochromocytoma, cushings, diabetes, coarctation, eclampsia
drugs eg illegal drugs and contraceptive pill
what is stage 1 hypertension
140/90 in the clinic
135/85 ambulatory
what is stage 2 hypertension
160/100
what is severe hypertension
180 syst
or 110 diastolic
may have left axis deviation and inverted t waves on the ecg
albinuria
what can cause an increase in TPR
sympathetic nerve activity
increased vascular reactivity
what are the effects of hypertension on the body
accelerated atherosclerosis and narrowing
retinopathy
renal failure
dilatation
what is stenosis
narrowing of the valve outlet caused by thickening of valve cusps, increased rigidity or scarring
what is valve incompetence
an incomplete seal allowing blood to flow backwards
what are common causes of valve disease
congenital heart disease
cardiomyopathy
acquired - rheumatic fever, MI, age, calcific stenosis, endocarditis
what might result from aortic stenosis
RVH syncope sudden cardiac death dyspnoea angina
what are causes of aortic incompetence
marfan’s
rheumatic fever
infective endocarditis(may causes perforation)
may have calcification of a congenital bicuspid valve
what is the most common cause of mitral incompetence or stenosis
rheumatic fever
leads to pulmonary hypertension and RVH due to back pressure
may cause atrial fibrillation
what is infective endocarditis
infection of the valve with thrombotic vegetations
what are the risk factors for infective endocarditis
valve damage
dental
catheterisation
immunosuppression
what is rheumatic fever
3 weeks post streptococcal infection (usually pharyngitis)
immune mediated
occurs in children
multisystem disease
what might be found in a vegetation
group D strep
gut commensals
skin strep
what are the complications of endocarditis
splinter haemorrhages clubbing emboli renal infarcts pneumonia osler's nodes and janaway lesion
what is acute on chronic heart failure
chronic failure becomes decompensated by an acute event
what is systolic failure
failure to pump blood in systole
reduced ejection fraction
may be caused by reduced contractility volume overload pressure overload (stenosis/hypertension) regurgitation dilated cardiomyopathy severe hypertension increased preload (EDV) dilation and increased tension
what is diastolic failure
failure of the ventricle wall to relax
restrictive, stiff ventricle (cardiomyopathy)
may be caused by scaring or amyloidosis
also may be increased wall thickness( hypertrophy)
or delayed relaxation or increased heart rate
tamponade
normal ejection fraction but impaired filling
what are the causes of heart failure
coronary heart disease hypertension cardiomyopathies drugs toxins endocrine nutritional infiltrative
what is backward heart failure
increased venous pressure
increased heart filling pressures
what is forward failure
reduced tissue perfusion
usually advanced failure
what do cardiac glycosides inhibit
Na/ Ca exchange
what is the NYHA classification of heart failure
1 no limitation
2 slight limitation on physical activity
3 marked limitation
4 unable to carry out physical activity, discomfort at rest
what are the compensatory mechanisms in heart failure
frank starling
sympathetic activity
renin angiotensin
what is the problem with RAAS as compensation for heart failure
increased renin release and angiotensin and aldosterone
vasoconstriction, water reabsorption, increased preload
inflammatory response leading to fibroblast deposition
what is the problem with sympathetic activity as compensation for heart failure
tachycardia, vasoconstriction, decreased tissue perfusion, increases the heart workload
desensitisation of b receptors
what is the problem with the frank starling mechanism in heart failure
pulmonary congestion
increased muscle stretch and O2 consumption
