STRUCTURAL heart disease and vascular disease Flashcards
what are the cusps of the aortic valve
left coronary cusp
right coronary cusp
non-coronary cusp
what sound does the aortic valve closure produce? and when does that happen?
Closure of the aortic valve during isovolumetric relaxation produces the “S2” heart sound.
what are the three main causes of aortic stenosis
1) calcification and fibrosis (Age)
2) congenital bicuspid valve (because more pressure on each cusp if only 2 instead of 3)
3) rheumatic heart disease
at what ages do calcification and fibrosis occur?
70s- 80s
describe ho calcification and fibrosis of the valves occurs and how it leads to aortic stenosis
repeated mechanical stress (hypertension) results in an atherosclerosis-LIKE fibrosis and calcification of the valve (the body’s way of trying to repair this mech damage done)
this makes the valve less compliant
risk factors for calcification and fibrosis of aortic valve?
Risk factors are therefore similar to those for atherosclerosis:
high bp
smoking
genes?
kidney disease
describe how bicuspid aortic valve occurs and how it leads to aortic stenosis. what age does it present?
Mechanical stress of blood flow across the valve spread across two leaflets instead of the usual three, causing increased endothelial damage to each leaflet
stenosis is caused because:
Ultimately causes calcification and fibrosis
May present earlier in life-
(its basically sam emech as the calcification and fibrosis but happens earlier because of the bicuspid valbe)
risk factors for congenital bicuspid valve?
same as for calcification and fibrosis
what causes rheumatic heart disease?
S. pyogenes infection
when does rheumatic fever occur in the timeline of rheumatic heart disease?
may occur 1-5 weeks after s pyogenes infection
how does rheumatic heart disease lead to aortic stenosis
Antibodies targeting bacterial antigen at that time may cross-react with certain cardiac M- proteins
repeated damage to valvular endothelium results in scarring and fibrosis of aortic valve
fusion of valve leaflets (commissural fusion) occurs
what can aortic stenosis eventually lead to?
heart failure
describe the pathophysiology of aortic stenosis leading to heart failure
1) aortic stenosis reduces the surface area available for blood flow after the valve has opened
2) left ventricle must produce higher pressures to maintain the same force of ejection (stroke work= pressure* stroke volume)
3) heart undergoes conccentric hypertrophy. this compensates for the reduced valvular area for some time
4) eventually the compensation fails leading to heart failure
what is eccentric and conccentric heart failure
conccentric is when the volume of the right ventricle decreases vs eccentric its when it increases
what is preload
its the amount of stretch the heart muscle undergoes while its being filled by blood which determines the strength of the contraction
what does preload depend on?
venous return
what is afterload and what does it depend on
its the pressure in the aorta that the left ventricle has to overcome in order for the semilunar valves to open and blood to be ejected.
so it depends on diastolic bp
symptoms of aortic stenosis
(if that helps which it doesnt really in my case lol- think about symptoms of systolic HF)
-exertional dyspnea
-fatigue
-possible angina
-possible syncope/ presyncope on exertion
signs of aortic stenosis
-ejection systolic murmur over aortic valve
- with crescendo-decrescendo pattern (means the murmur increases in sound intensity and decreases )
- this may radiate to carotid arteries
- possible opening click and diminished S2 sound
what are the 2 first line diagnostic tools you use for all the structural heart diseases
transthoracic echocardiography
and
12-lead ECG
what other investigations can you do for structural heart diseases
CXR
cardiac catheterization
cardiac MRI scan
what can transphoracic echo tell you in aortic stenosis? is it diagnostic?
YES its diagnostic: confirms stenosis and can also
evaluate SEVERITY of stenosis
what can a 12-lead ECG tell you for aortic stenosis? is it diagnostic?
reveal LV hypertrophy or ischaemic changes
NO its not diagnostic bc its non specific meaning it doesnt show that these changes were caused by aortic stenosis.
what is the difference between managing non severe artic stenosis and severe/ symptomatic AS?
symptomatic/ severe need to do aortic valve replacement vs non severe only drugs
what is done for non severe AS
RISK FACTOR management
- ACE inhibitors (controlling hypertension reduces afterload)
- statins (lower cholesterol)
when is aortic valve replacement appropriate and what is an alternative? what do you also do in parallel with the procedures?
under65 yrs
transcatheter aortic valve implantation TAVI is an alternative
risk factor management in parallel
what are some factors that make AS severe?
-LV ejection fraction <50%
- abnormal exercise test
- elevated BNP (marker of HF)
What are the two physiological changes that lead to aortic regurgitation
1) aortic root dilation and
2) valve changes
causes of aortic root dilation
marfans syndrome
chest trauma (motor vehicle accidents)
ankylosing spondylitis
idiopathic
causes of valve changes
-infective endocarditis
-chronic rheumatic fever (fibrotic valves do not seal well)
-congenital bicuspid aortic valve
what are the two types of aortic regurgitation
acute and chronic
what happens in acute aortic regurgitation
- sudden valve incompetence
- sudden increase in left ventricule end-diastolic volume
- diastolic blood backlogs to lungs
- pulmonary hypertension causes pulmonary oedema. this causes dyspnoea
= diastolic HF
explain what happens in chronic aortic regurgitation
1) gradual worsening of valve competence so
2) gradual increase in regurgitated volume leading to increase in left ventricle end-diastolic volume
but because this is gradual the heart has time to adapt
3) based on this: storke work = str vol* pressure, since the str volume increased the stroke work has to increase
4) this happens by eccentric hypertrophy
5) now the problem that eventually arises with the eccentric hypertrophy is shown by law of laplace: T= P*R since the R is radius, so has increased with the eccentric hypertrophy meaning the tension (T) also nicreased BEYOND WHAT THE heart is adapted for leading to
6) systolic heart failure
main symptom of acute and chronic AR
DYSPNOEA
signs of chronic AR
Wide pulse pressure (difference between systolic and diastolic BP)
Water hammer pulse* (very bounding on palpation)
Traube’s sign*: like pistol shots when auscultating over femoral artery
SIGNS od acute AR
UNIQUE:
Austin Flint murmur: mid-diastolic rumbling best heard at apex
Cardiogenic shock (tachycardia, > capillary refill time)
Cyanosis (sign of hypoxia due to pulmonary oedema)
+ the same ones as for chronic :
Wide pulse pressure (difference between systolic and diastolic BP)
Water hammer pulse* (very bounding on palpation)
Traube’s sign*: like pistol shots when auscultating over femoral artery
AR investigations
Transthoracic echocardiography
CXR (Cardiomegaly in chronic AR)
Cardiac catheterisation (measure pressures in all chambers)
Cardiac MRI scan (when echo is suboptimal)
acute AR management
1) Inotropes (increase contractility): Adrenaline, dopamine, dobutamine etc.
2) Vasodilators (reduce afterload)
… to stabilize the patient
3) Valve replacement and repair
asymptomatic chronic AR management
Asymptomatic: reassurance with regular echo monitoring or drugs (vasodilators such as calcium channel blockers, ACEI, ARBs)
symptomatic chronic AR management
Symptomatic: Vasodilators and valve replacement and repair
what are the cusps of the mitral valve
2 cusps
anterior coronary cusp
posterior coronary cusp
what sound does the mitral valve closure produce? and when does that happen?
closeure of the mitral valve at end of atrial systole produces S1 heart sound
what is the main cause of mitral stenosis and what is the usual age of onset
rheumatic fever
40-50 yrs
other causes of mitral stenosis (not that important just have a look)
Carcinoid syndrome
Congenital
Rheumatoid Arthritis
Rheumatic Fever
Amyloidosis
Annular Calcification
Whipple Disease
SLE
Serotonergic Drugs
what pathologies can mitral stenosis eventually cause?
pulmonary oedema
systolic heart failure
and atrial fibrilation
describe how mitral stenosis can lead to pulmonary oedema and systolic heart failure
1) mitral stenosis obstructs left ventricular inflow
2) blood backlogs to left atria and to pulmonary veins
3) as pulmonary hypertension worsens it causes pulmonary oedema which can cause dyspnea.
(NOTE: although this sounds like diastolic HF its not bc this backlog is NOT caused by too much filling of the left ventricle during diastole, that backlogs to left atrium. its direct overflow of atrium due to the mitral stenosis so not DIASTOLIC)
4) at the same time since LV filling is impaired. This can reduce cardiac output (systolic HF)
what causes atrial fibrillation in mitral stenosis?
left atrial dilation can irritate pacemaker cells which can lead to AF
what are the symptoms of mitral stenosis
exertional dyspnoea (can progress to dyspnoea at rest)
ppulmonary oedema
haemoptysis
orthopnoea (SOB when lying down)
signs of mitral stenosis
mid diastolic murmur
loud p2 (s2= a2 and p2) due to severe pulmonary hypertension
what could you see on an ECG for mitral stenosis?
signs of left atrial enlargement
what could you see on CXR for mitral stenosis?
cardiomegaly
what is the management of severe asymptomatic mitral stenosis
generally no therapy required
possibility of doing ballon valvotomy
management of severe symptomatic mitral stenosis
1) DIURETIC (reducing BP reduces afterload and therefore stroke work)
2) valve replacement and repair with adjunct beta blockers (reduce HR)
top 4 CAUSES of mitral regurgitation
mitral valve prolapse (Marfan’s Syndome causes looser chordae tendinae/ papillary muscle damage post-MI)
rheumatic heart disease
infective endocarditis (cause of acute MR if it causes leaflet rupture)
hypertrophic cardiomyopathy
3 other causes of mitral regurg
autoimmune (SLE, scleroderma)
iatrogenic (surgery)
drugs
what can Mitral regurgitation eventually lead to?
systolic heart failure
describe how MR can lead to systolic HF/ the pathophysiology of MR
1) the regurgitated blood volume flows back into left ventricle form left atria during diastole
2) this increases the left ventricular end diastolic volume
3) so also increases stroke volume : stroke work= stroke vol* pressure
so stroke work has to increase
4)so LV undergoes eccentric hypertrophy to cope with volume overload
5) eventually the compensatory mech fails causing systolic heart failure
MR symptoms
DA FOP
dyspnea
angina
fatigue
orthopnea
palpitations (from atrial fibrilations)
signs of MR
MID-systolic click, followed by murmur (prolapse)
holosystolic murmr
diminished S1 (M+T)->mitral valve does not shut properly
TWO Types of MR
ACUTE AND CHRONIC
acute MR management
emergency surgery
pre op diuretics to reduce afterload and-> stroke work
chronic asymptomatic MR management
if EF> 60% (further from heart failure) ACEi, beta blockers (reduce stroke work- slow HR)
IF EF<60% surgucal replacement and repair
symptomatic CHRONIC MR management
EF >30%: surgical replacement and repair
EF <30%: intra-aortic balloon counterpulsation*
Intra-aortic balloon counterpulsation: therapeutic device that supports systolic heart function.
which physics law explains how eccentric hypertrophy leads to systolic heart failure?
law of laplace stating that
“When the pressure within a cylinder or sphere is held constant, the tension on its walls increases with increasing radius.”
T= PxR
SO
1) eccentric hypertrophy
2. increased radius of left ventricle
3. increase wall tension on the heart
4. wall stress exceeds hearts ability to withstand pressure increases
5. systolic HF
dilated cardiomyopathy causes
Idiopathic (most common)
Following heart valve disease (volum overload)
Peripartum cardiomypathy (50% reversible)
Myocarditis (Coxsackievirus B)
Alcohol abuse
Drugs (cocaine, chemotherapy drugs)
dialted cardiomyopathy symtoms
Dyspnea
Angina
Fatigue
dilated CMP signs
Displaced apex beat (cardiomegaly)
S3 additional heart sound
General signs of biventricular heart failure such as enlarged neck veins and leg swelling
age group common for dilated CMP
30-40
INVESTGATIONS for cause identification in dilated CMP
Genetic testing
Viral Serology (myocarditis)
dilated cmp management
treat depending on symptoms
management of someone with heart failure symptoms (dyspnoea, leg oedema) diagosed with dilated CMP
ACE inhibitors and beta blockers reduce stroke work (SW=V*P). If unresponsive you can consider LVAD (left ventricular assist device)
management of someone with arrythmias diagosed with dilated CMP
antiarrhythmics (Amiodarone)
management of someone with high risk of thromboembolic events diagosed with dilated CMP
anticoagulation
what is hypertrophic CMP
Hypertrophy of myocardium, but occurs asymmetrically
More pronounced on the side of the interventricular septum
(INSTEAD OF THE myocardium in the outside side of the ventricles)
causes of hypertrophic CMP
Most commonly autosomal dominant inheritance
Defect in certain sarcomere proteins
what is subendocardial ischaemia (just important for other understanding)
Subendocardial ischemia refers to a condition where there is inadequate blood supply to the innermost layer of the heart muscle, known as the subendocardium. This region is particularly vulnerable to ischemia because it is the farthest from the epicardial coronary arteries, which supply blood to the heart.
pathophysiology of hypertrophic CMP
1) reduced LV volume due to hypertrophic growth impairs LV filling. This puts a limitation on the stroke volume, causing diastolic heart failure.
2) reduced stroke volume means the coronary circulation also gets less blood. ESPECIALLY since hypertrophied heart has an increased myocaridal oxygen demand, the demand outstrips the supply leading to subendocardial ischaemia
3) In situations of high cardiac demand, such as exercise, myocardial ischaemia can cause dangerously fast arrhythmias
symptoms of hypertrophic CMP
Angina
Syncope/Presyncope
signs of hypertrophic CMP
Ejection systolic murmur
Bifid Pulse (double carotid artery pulse): Venturi effect
Arrhythmias
SOME unique investigs for hypertrophic CMP
FBC (anemia exacerbates cardiac ischemia)
- Brain natriuretic peptide (BNP) levels, troponin T levels
hypertrophic CMP management
- Beta-blockers: reduce stroke work by reducing HR
- Alternatively, calcium channel blockers (reduce BP)
If still symptomatic, put in a pacemaker or do surgery to ablate myocardium.
WHAT is restrictive CMP
myocardium stiffens and becomes less compliant but the heart remainssame size
two types of restrictive CMP
infiltrative ( heart muscle is infiltrated or invaded by abnormal substances)
and non infiltrative (intrinsic abnormalities in the heart muscle)
causes of infiltrative restrictive CMP
Amyloidosis (familial forms or as a consequence of ageing)
Sarcoidosis
Haemochromatosis
causes of non infiltrative restrictive CMP
Radiation (produces reactive oxygen species which causes fibrosis)
Carcinoid syndrome
Scleroderma (fibrosis of heart)
Anthracycline (chemotherapy) toxicity
restrictive cmp pathophysiology
1) Myocardium stiffens and becomes less compliant
2) This reduces the ventricular end-diastolic volumes. Therefore there is also a reduced stroke volume and cardiac output. This can lead to diastolic heart failure
Sequelae (consequences after smth. in this case disease)
1) Infiltration/remodelling of the myocardium can disrupt conduction, resulting in arrhythmias
2) Infiltration/remodelling of the myocardium can cause adverse remodelling, which can also cause systolic heart failure
symtpoms of restricitve CMP
HEART FAILURE SYMP
signs of restricitve CMP
Pitting oedema
Ascites
Increased jugular venous pressure (large neck veins)
Decreased pulse volume on palpation (brachial/carotids)
Signs of systemic disease ( coexisting carpal tunnel syndrome increases likelihood of amyloidosis)
restricitve CMP investigations checking for causes
Checking for causes:
FBC
Serology (autoantibodies)
restrictive CMP management
1) Manage symptoms.
Heart failure: ACE inhibitors, ARBs, diuretics, aldosterone inhibitors (spironolactone)
Arrhythmias: antiarrhythmics
Immunosuppression: Steroids
Pacemaker or Heart Transplant if all else fails
2) Treat underlying disease (Hereditary Haemochromatosis and venesection)
what is infective endocarditis, where does it most commonly happen and why?
Infection of the endocardium, typically the heart valves as they are the location of turbulent blood flow.
describe pathophysiology of infective endocard
1) Turbulent blood flow around valves damages endothelial lining
2) Non-bacterial thrombi form at locations of damage
Physiological Process but can happen more frequently if there is valvulopathy.
3) If patients acquire bacteraemia, bacteria can attach to thrombi and form a vegetation (adhesins)
4) This can cause valuvolpathies, e.g. aortic regurgitation, and rapid-onset heart failure and cardiogenic shock
most common heart valves affected in infective endocarditis in averga person and IV drug users
Most commonly left-sided heart valves (aortic>mitral) du eto higher pressures
Tricuspid valve most common in IV drug users as bacteraemia most likely comes from venous system
causes of infective endocarditis, in averge person and IV drug user
1) Streptococcus Viridans most common (e.g. dental procedures). Causes milder valve damage.
2) Staphylococcus aureus: most common in IV drug users. Causes more severe valve damage.
signs of infective endocarditis
what are 5 congenital heart diseases
ventricular septal defect
these two are mebryonic reminants:
atrial septal defect
ductus arteriosus
tetralogy of falot
aortic coarctation
what does ventricular septal defect cause
Causes hypoxia and cyanosis as oxygenated and deoxygenated blood mixes.
tetralogy of falot state the 4 pathologies
PROVe
pulmonary stenosis
right ventricular hypertrophy
aortic wall widening (Which is sitting right on top of:)
ventricular septal defect
example of an atrial septal defect and explainwhat it is
An example is a patent (open) foramen ovale.
It is a fetal cardiac shunt, allowing blood to pass from the right atrium directly to the left atrium. The fetus receives oxygen from placenta so does not need to oxygenate lungs. Right atrial (deoxygenated) blood passes directly into the left atrium rather than passing through the pulmonary arteries to the lungs first.
how common is patent foramen ovale
25% of people have it
what can patent foramen ovale cause
It can cause paradoxical embolism (DVT clot can enter arterial circulation and cause a stroke.
what is aortic coarctation and who commonly gets it
Aortic Coarctation is the severe narrowing of the aortic lumen.
It is more common in patients with Turner’s Syndrome.
consequences of aortic coarctation
It can cause different BP measurements in the left and right arm depending on the location of the coarctation.
what is patent ductus arteriosus
The ductus arteriosusis usually a connection between the aorta and pulmonary artery. In the embryo, it allows blood in the pulmonary artery to flow into the aorta, bypassing the pulmonary circulation (no need to perfuse lungs as oxygen is supplied by mother).
After birth, the ductus arteriosus usually obliterates to form the ligamentum arteriosum. If it the ductus remains open, this is patent ductus arteriosus.
name of criteria used for infective endocarditis infection
duke criteria
what duke criteria combo is needed for diagnosis of infective endocard?
There are major and minor criteria
2 major OR 1 major + 3 minor OR 5 minor are required to make the diagnosis
what are the major duke criteria
Positive blood cultures (usually at least 2 separate positive cultures >12h apart)
Evidence of endicardial involvement (abscess, new valvular regurgitation, metallic valve dehiscence)
what are the minor duke criteria
Fever
Predisposing cardiac conditions (e.g. mitral valve prolapse, bicuspid aortic valves)
Vascular phenomena
Immunological phenomena (Osler’s nodes, Roth spots, Janeway lesions, glomerulonephritis)
Microbiological and echocardiograohic evidence not fulfilling a major criterion
