atrial stenosis Flashcards
(25 cards)
most common causes of AS
congenital bicuspid valve - in young people
calcific degeneration - most common
when are symptoms apparent in AS
when it becomes severe
all causes of AS
congenital aortic stenosis
congenital bicuspid
rheumatoid heart disease
degenerative calcific degeneration
most common cause of AS in 30-50s
congenital bicuspid
most common cause of AS in 60+ yrs
calcific
AS symptoms
- fatigue
- SOB
- angina
- orthostatic syncope or syncope upon exersion
- swelling, opnoea, paroxysamal nocturnal dysponea
AS signs
- narrow pulse pressure <25
- slow rising / weak pulse
- ejection systolic murmur exaggerated on right side of sternum border at 2nd intercostal space
- quiet S2
as investigation
- echocardiogram - can also assess if its severe
- assess LV function
- ECG bc aortic valve sits near AV node
- cardiopulmonary exersize test
- stress echo + ecg
why is a CPET useful?
in comorbidities - assess weather heart or lungs which is causing the worsening of exersize
what does the endocardiagram measure?
valve area
speed of flow
pressure gradient
AS management
SAVR / CABG
TAVR
no medicine
what are the types of valve which can be used during surgical valve replacement?
mechanical - 10-20 years - lifelong warfarin
tissue - 5-10 years - no warfarin
risks of SAVR and TAVR
- stroke
- heart block
murmur for AS
ejection systolic murmur
harsh
diamond
how is diastolic dysfunction caused in AS
LV hypertrophy
risk factors
Smoking
Age
CKD
Hypertension
Family history
Diabetes
Hyperlipidaemia
after a metallic heart valve replacement what should be given and for how long?
lifelong warfarin (vitamin K antagonist)
what heart sound suggests severe AS and why?
soft S2 - shows immobalisation of valve
aortic sclerosis findings
ejection systolic murmur - no radiation to carotids and normal S2, pulse and volume
whats the loud S4 about?
LV hypertrophy
echo findings that suggest severe AS
velocity - more than 4
gradient - 40
valve area - less than 1
how does LV damage come about with AS?
- because less blood is being pushed into the ventricle - the LV needs to contract harder to push blood through
- it, therefore, adapts compensatory mechanisms such as cardiac hypertrophy to beat more forcefully
- however the hypertrophy - dysfunctional diastole
- this also means it has a higher oxygen requirment so needs more blood from the coronary artery
- eventually these fail and blood is backed up - through pulm vein
- leads to reduced cardiac load which causes bodily mechanisms to kick into place
- RAAS increase and hypoperfusion of organs
rheumatic heart disease
post-streptococcal infection
S4 why?
-prominent S4 seen in LV hypertrophy
