structural heart disease Flashcards
what are the basic phases of systole?
systole:
contraction
3 parts
1/3 of total beat
phase2 - isovolumetric contraction:
heart depolarisation, ventricles contract (QRS complex)
mitral valve closes - first heart sound
pressure increases in left ventricle, but volume doesnt change (it is at end diastolic volume)
phase3 - rapid ejection:
pressure in LV continues to rise until it is above that of the aorta
the aortic semilunar valve opens
pressure in LV and aorta continues to rise
volume in LV decreases
phase4 - reduced ejection:
repolarisation gives T wave on ECG
pressure in LV and aorta starts to decrease
the aortic valve closes - gives second heart sound
ventricular muscle relaxes
what are the basic phases of diastole?
diastole:
relaxation
4 parts
2/3 of beat
phase5 - isovolumetric relaxation:
pressure in LV decreases
mitral valve is still closed, so volume in LV stays the same (end systolic volume)
phase6 - rapid passive filling:
pressure in LV is lower than LA, so mitral valve opens
volume in LV starts to increase passively
but pressure in LV remains the same pretty much
phase7 - reduced passive filling:
ventricular volume increases more slowly
phase1 - atrial systole: atria almost full from passive filling they contract to top up volume in them P wave on ECG contributes more to filling during exercise
what is the equation stroke volume?
end diastolic volume - end systolic volume
what are structural heart disease?
covers a number of defects which affect the valves and chambers of the heart and aorta
can be congenital
or develop later in life (eg. due to infection)
congenital - eg. atrial septal defect, ventricular septal defect, coarctation of the aorta, patent foramen ovale, patent ductus arteriosus, tetralogy of fallot
develop later in life - eg. can be due to valvular dysfunctions ( atrial stenosis/regurgitation or muscular (cardiomyopathies))
what is ventricular septal defect?
VSD
congential
hole in wall between ventricles
leads to mixing of oxygenated and deoxygenated blood
presents in children with:
poor weight gain
poor feeding
palpitations
sometimes small enough to close on its own
if too big, requires surgery
what is tetralogy of fallot?
TOF
congenital
involves 4 defects
- Ventricular septal defect
- pulmonary stenosis (pulmonary trunk)
- widening of the aortic valve- so wide it opens into both ventricles (also due to the VSD) and oxygenated and deoxygenated blood mix
- right ventricular hypertrophy
need to undergo many surgeries to correct these defects
what is atrial septal defect?
ASD
congenital
hole in wall between two atria
what is coarctation of the aorta?
congenital
narrowing in wall of descending aorta
ventricle must work much harder to force blood through this narrowing to allow enough blood to be ejected in each stroke
can lead to thickening of the ventricles or heart failure
requires urgent repair
what are valvular defects?
most common:
aortic stenosis (narrowing of aortic valve) aortic regurgitation (incompetence of the aortic valve, leads to backflow)
mitral stenosis (narrowing) mitral regurgitation (incompetence, leading to backflow)
what is the epidemiology of valvular heart disease?
rheumatic heart disease:
biggest cause of problems that can lead to valvular heart disease in developing countries
25-49 Yrs are most commonly effected
higher prevalence in females
calcific aortic valve disease:
highest prevalence above 70 years
equal distribution between men and women
degenerative mitral valve disease:
seen most from 70 onwards
more in females than males
what is the aetiology of aortic stenosis?
most common valvular disease in the US and Europe requiring treatment
second most frequent cause for heart surgery
largely a disease of older people (70+)
preceded by aortic sclerosis (aortic valve thickening without flow limitation)
often suspected by the presence of an early peaking, systolic ejection murmur, and confirmed by Echocardiography
what are risk factors and causes for aortic stenosis?
hypertension LDL levels smoking elevated CRP congenital bicuspid valves (more prone to wear and tear and infections) chronic kidney disease (more prone to infection) radiotherapy older age
causes: most common is rheumatic heart disease (in developing countries) congenital heart disease calcium build up infective endocarditis
what is the pathophysiology of aortic stenosis?
the valvular endocardium is damaged - as the result of abnormal blood flow across the valve (in the case of a bicuspid valve - abnormal) or by an unknown trigger
endocardial injury initiates an inflammatory process - similar to atherosclerosis and ultimately leads to leaflet fibrosis and deposition of calcium on the valve
progressive calcium deposition and fibrosis - limit aortic leaflet mobility and eventually produce stenosis
In aortic valve stenosis,
there is narrowing which prevents the valve from completely opening and facilitating the
flow of blood into systemic circulation through the aorta.
in the case of rheumatic disease - an autoimmune inflammatory reaction is triggered by prior streptococcus infection that targets the valvular endothelium, leading to inflammation and eventually calcification
what is the result of aortic stenosis?
leads to long standing pressure overload -> left ventricular hypertrophy
concentric left ventricular hypertrophy (Sarcomeres are added in parallel to
existing ones). This pathophysiological response is to support a greater contractile force
to open the valve.
ventricle tries to maintain a normal wall stress (pressure increases but it tries to reduce radius. this effects edv capacity) despite the pressure overload produced by stenosis ->
as the stenosis worsens, the adaptive mechanism fails and left ventricular wall stress increases
systolic function declines as wall stress increases
resultant systolic heart failure
what is the history and presentation of aortic stenosis?
presentation:
exertional dyspnoea and fatigue
chest pain
ejection systolic murmur (>3/6 is present with crescendo-decrescendo pattern that peaks mid systole and radiates to the carotid)
history: rheumatic fever high lipoprotein high LDL chronic kidney disease age over 65
what investigations are done for aortic stenosis?
transthoracic echocardiography (can see the structure of the walls and any problems, very helpful) ECG chest X-ray (LVH) cardiac catheterisation cardiac MRI
how is aortic stenosis managed?
usually aortic valve replacement (AVR):
first line in patients who are symptomatic
or in asymptomatic patients with an ejection fraction <50%, or who are undergoing other cardiac surgery
AVR may be considered in asymptomatic patients with rapid progression, an abnormal exercise test, or elevated serum B natriuretic peptide (BNP)
balloon aortic valvuloplasty
antihypertensives
ACE inhibitors
Statins
what is the aetiology of aortic regurgitation?
the diastolic leakage of blood from the aorta back into the left ventricle
occurs due to incompetence of valve leaflets resulting from either intrinsic valve disease or dilation of the aortic root
it is not as common as aortic stenosis or mitral regurgitation
chronic -> culminate into congestive heart failure
acute -> medical emergency, presenting with sudden onset of pulmonary oedema and hypotension or cardiogenic shock
what are the causes of aortic regurgitation?
congenital and acquired: rheumatic heart disease infective endocarditis aortic valve stenosis congenital heart defects congenital bicuspid valves
from aortic root dilation: marfans syndrome connective tissue disease/ collagen vascular disease idiopathic ankylosing spondylitis traumatic
what is the pathophysiology of acute aortic regurgitation?
infective endocarditis can lead to rupture of leaflets or even paravalvular leaks.
Vegetations on the valvular cusps can also cause inadequate closure of leaflets, resulting in leakage of blood.
Chest trauma can cause tear in ascending aorta leading to AR
what is the pathophysiology of chronic aortic regurgitation?
Bicuspid aortic valve
Rheumatic fever -> fibrotic changes causing thickening and retraction of leaflets
what happens as a result of acute aortic regurgitation?
Increase blood volume in LV during systole ->
LV end diastolic pressure increases->
increase in pulmonary venous pressure->
dyspnea and pulmonary oedema->
heart failure->
cardiogenic shock
what happens as a result of chronic aortic regurgitation?
gradually increase in LV volume->
LV enlargement and eccentric hypertrophy
Early stages->
Ejection fraction normal or slightly increase->
after some time, Ejection fraction falls and LV end systolic volume rises
Eventually LV dyspnoea ->
lower coronary perfusion ->
ischemia, necrosis and apoptosis
how does aortic regurgitation present?
Acute AR:
Cardiogenic shock
Tachycardia
Cyanosis
Pulmonary oedem
Chronic AR:
Wide pulse pressure
Pistol shot pulse (Traube sign)
