valvular heart disease Flashcards
heart sounds
S1: closure of AV valves at start of ventricular systole
S2: closure of semilunar valves at start of ventricular diastole
S3: sound of rapid filling of ventricles during early diastole
S4: sound of late filling from atrial kick in late diastole
Valve opening normally not heard
abnormalities
slide 4-6
esp fixed splitting of S2
myxomas and pericardial knot (S3) may mimic valvular disease
causes of high frequency sound in early diastole
slide 7
more 8,9
how to approach pt with VHD
most important question to ask about valvular condition ??
Correctly diagnosing the affected valve
Estimating severity
Judging its effect on the myocardium
Deciding on antibiotic prophylaxis (not necessary for mitral valve prolapse)
Deciding on timing of surgery or catheter-based intervention
what is the condition’s effect on the cardiac muscle?? esp. LV
5 finger approach
H/P, labs, EKG, XR, cardiac testing (i.e. ECHO)
Aortic Stenosis:
etiology
hx
Etiology
Senile calcific
bicuspid: more turbulent flow, have symptoms younger (think associated with aortipathies (coarctation, etc) if with coarctations and headache, think: berry aneurysm
rheumatic HD (more mitral)
congenital (uni/quad cuspid valves, present early–>respond to valvuplasty)
Paget’s, ESRD
History
long latent period
Angina, Syncope (fixed obstruction and cannot augment CO under conditions of low SVR; ie: meds, vasovagal), CHF
FA: syncope, angina, dyspnea on exertion (SAD)
angina: 50% 5 yr mortality
syncope: 50% 3 yr mortality
CHF: 50% 2 yr mortality
no meds shown to reduce progression of aortic stenosis
aortic stenosis exam:
Harsh, late-peaking SEM (sys. ejection murmur) radiating to the neck, palpable systolic thrill, sustained LV impulse, pulsus parvus et tardus, S2 single (A2 is absent), paradoxical split S2 (A2 closure takes longer), S4 gallop (heard when diastolic dysfunction) Prolongation of LV ejection due to severe outflow obstruction
aortic stenosis EKG?? CXR?? more dx sx?
EKG: LVH, LBBB
CXR
AV calcification, cardiomegaly, LV prominent without dilation
Echo (test of choice): measure doppler gradients,
severe AS if valvular area:
hypertrophic cardiomyopathy
biphasic: old and young
ddx from aortic stenosis
provocative maneuver:
valsalva: gets louder
small LV cavity bc wall is enlarged–>turbulence
make cavity smaller–>lower
dec. venous return into right heart->less blood in LV–>smaller cavity–>louder
softer with squatting: pushing more blood into heart–>larger LV–>less turbulence–>softer murmur
hypertrophic cardiomyopathy
ddx from aortic stenosis
after PVC: same PP in AS
PP gets smaller in hypertrophic myopathy
Brockenbrough phenomenon
Aortic stenosis time course charts
slide 12
long latent period
valve replacement
bioprosthetic (for oldies: last 10-15 yrs) don’t need anticoagulation
mechanical: for younger pts (need anticoagulation)
TAVR
transaortic valve replacement
access from groin
transapical
typically transferal
valve placed on stent and expanded, “crushing” old bad valves, open/closed based on heart pressure gradients
no opening of chest, good for old ppl
aortic stenosis parameters
slide 15
criteria for sx
EF falls below 50
LV outflow tract obstruction
supravalvar AS
congenital, assoc. with William’s syndrome
narrowing above valve
Subvalvular membrane:
subvalvular AS
congenital flap of tissue obstructing valve (before it) and may be a/w coarctation as part of *Shone’s syndrome mitral stenosis due to supravalvular MV membrane, LVOT obstruction, coarctation
needs sx
mean gradient of 40
get measurement from echo
using doppler probe (ECHO) measure velocity and convert velocity into pressure
Bernule formula
if CAD (3 vessel disease) along with AS
might as well replace AS w/ angioplasty
Aortic Regurgitation/insufficiency (Chronic) etiology
Aortic root dilation from HTN (–>dissection, aneurysm), CMN, bicuspid valve, ankylosing spondylitis, syphilis, RA
(secondary: something stretching leaflets open)
(primary: problem with leaflets)
FA: endocarditis, RF
long latent period
can have combo AI/AS
Aortic Regurgitation (Chronic) Hx
Dyspnea, Angina, Fatigue, CHF
Aortic Regurgitation (Chronic) exam
Wide pulse pressure, low diastolic pressure, bounding pulses (quick rising), laterally displaced PMI, long decrescendo diastolic murmur along LSB if valvular or RSB if aortic root etiology, Austin-flint murmur at apex (diastolic MR; MV struck by regurgitant jet–>you will not hear loud S1 or OS which is c/w mitral stenosis), S3 gallop (with dilated ventricle)
Aortic Regurgitation (Chronic) eponyms (FYI?)
Quinckes pulse, DeMusset’s sign (head bobbing from such strong pulse, uvula can vibrate) duroziez sign, bisferiens
AR (AI)
EKG?
imaging?
ECG: LVH
CXR
Cardiomegaly, boot-shaped heart, LV enlargement
Echo, cath: can see how much blood flowing backwards
AI: timing of sx
Symptoms, EF 55
EDD >75
chronic AI tx
Vasodilator therapy (ACE-Inh/ARB/Nifedipine)
don’t use B-blocker, will prolong diastole??
Remember, in chronic AI, the LV has time to adapt with ?? and ?? with each contraction without increasing LVEDP…eventually, this compensatory mechanism ??
eccentric myocyte hypertrophy
and larger SV
fails
then forward CO will diminish and will have higher LVEDP (back flow) and pulmonary congestion
Aortic Regurgitation (Acute) etiology??
hx?
Etiology
*Endocarditis, *Aortic dissection, ruptured sinus of Valsalva aneurysm
History
Acute pulmonary edema
severe! goes straight back into longs
Aortic Regurgitation (Acute) exam
Short diastolic murmur, faint S1
(brief but severe)
may not hear murmur
Aortic Regurgitation (Acute) EKG? imaging?
ECG: Not helpful
CXR
Normal heart size, pulmonary edema
*ECHO
TEE (look for dissection)
cath (no time)
doppler probe: see diastolic flow
AI acute timing of sx
urgent
causes of AI
slide 23
Mitral Regurgitation (Chronic) etiology
primary (leaflet problem) MVP (mitral valve prolapse), mitral myxomatous disease, rheumatic (more likely MS)
FA: LV dilatation
secondary (pulls annulus open: ischemic (dysfunctional papillary muscles), dilated cardiomyopathy)
Mitral Regurgitation (Chronic) hx
Late-onset of CHF, later R-heart failure
long latent period
C MR: exam
Apical holosystolic murmur radiating to axilla, S3 gallop and wide-split S2
C MR: EKG
LAE, LVH, afib (if LA dilates enough)
LV dysfunction from overloaded state
C MR: imaging
CXR: Cardiomegaly, LV/LA enlargement, pulmonary venous redistribution
Echo, cath
EF should be >65 (supra-normal)
C MR: timing of sx
Symptoms,
EF40
almost never for secondary MR
Mitral Regurgitation (Acute) etiology
hx??
post-MI complication -
papillary muscle rupture in setting of MI
(supplied by RCA: posterior-medial supply)
Endocarditis
Acute pulmonary edema
Mitral Regurgitation (Acute) exam
Decrescendo systolic murmur radiates to neck if posterior leaflet and back if anterior leaflet, loud P2, widely split S2
(may be soft, happens rapidly)
FA: holosystolic, high-pitched “blowing”
Mitral Regurgitation (Acute) EKG
Sinus tachy, AMI changes
Mitral Regurgitation (Acute) imaging
CXR
Pulmonary edema, normal heart size, cardiomegaly, LA, LV enlargement
Echo, cath
Flail leaflet, large v waves
Mitral Regurgitation (Acute) timing of sx
Urgent, can temporize with vasodilators or IABP
put in balloon pump decrease afterload (not if AI)
does not prolong life for secondary MR unless refractory symps or doing sx anyways
“mitral clip”
MVP click changes with maneuvers
Squatting:
The click moves closer to S2 (more blood in R and L heart->more filling–>longer time before click happens–>closer to S2)
Standing:
The click moves closer to S1
(less blood–>valve clicks earlier, closer to S1)
MVP in who
thought to be female, palpitations, anxiety
actually equally men as well: serious progression (also with oldies)
mid-systolic opening click
late systolic crescendo murmur
predispose to inf. endocarditis
etiology: myxomatous degeneration (often 2nd to Marfan/Ehlers-Danlos syndrome), RF, chordae rupture
Mitral Stenosis etiology
RHEUMATIC esp. immigrants
calcific
FA: can result in LA dilatation
Mitral Stenosis hx
Late-onset of CHF, later R-heart failure, a fib, dyspnea (criteria for sx)
(LV is protected?? eventually doesn’t fill, low CO)
Mitral Stenosis exam
Diastolic rumble at apex, short S2-OS (opening snap) interval, loud P2, RV heave
The longer the murmur and the shorter the time from S2-OS-more severe* , high pressure
(if no longer hear OS: no longer pliable, end stage)
Anything that increases the gradient will increase the murmur intensity
(diff to hear)
increase HR–>higher the diastolic gradient -(should be zero), louder the murmur
MS EKG
LAE, afib
MS imaging
CXR
Pulmonary vein congestion, LAE, huge LA, compression of esophagus and recurrent laryngeal nerve (hoarse voice)
Echo, cath
MS timing of sx
depends on MVA, pressure gradient
tx with balloon valvatomy; need favorable valves
-know if meet criteria via ECHO
if primary MR: try to repair valve
MS: can’t repair, have to replace
Tricuspid Regurgitation etiology
could be rheumatic (would have MR, AR before)
*functional from RV failure (TR secondary to pulmonary HTN)
**Ebstein’s anomaly: congenital displacement of ant. tricuspid leaflet–>atrialization of RV–>sev. TR (assoc. with WPW, ASD)
- *carcinoid tumor against liver–>release of vasoactive substances; serotonin–>glistening appearance “smoldering” of tricuspid valve
- may have pulmonic valve involvement but lung filters out
FA: RV dilitation, endocarditis
Tricuspid Regurgitation hx
R-sided CHF predominates
TR exam
Holosystolic murmur at LLSB, louder with inspiration (Carvallo’s sign), prominent cv waves and rapid y descent
TR EKG
nothing?
TR: imaging
ECHO
TR tx
Tx underlying condition,
-sx if carcinoid or Ebsteins
annuloplasty can be considered
normal JVD
JVP estimation
8 cm H2O
should be same as LVEDP
ACVXY for JVP
see chart
A: atrial contraction (end of ventr. diastole: A-wave (S4)
C: closure of TV in early ventricular systole raises pressure in RA (FA: RV contraction)
X: atrial relaXation (descent)
V: ventricular systole nearly over (RA filling occurs and pressure rise in RA) big V wave if backwards flow (TR, MR)
Y: opening of TV (FA: RA emptying into RV, descent)
2 types TR
Secondary (Functional)
Left-sided CHF, MS, MR, primary pulmonary disease, L to R shunt, pulmonic valve stenosis, PA stentosis
Primary
Carcinoid, due to pacemaker, endocarditis, rheumatic fever, marantic, drug-induced, Ebsteins
Tricuspid stenosis (rare)
Rheumatic, carcinoid (once metastatic carcinoid to liver, the neuroendocrine tumor releases serotonin and other vasoactive substances which directly affect R-sided valves and these substances are usually cleared by lungs so L-sided vlave typically not affected)
Prolonged y descent, prominent a wave
Diastolic murmur, LLSB; increases with inspiration
Pulmonic stenosis
Noonan’s, TOF, congenital rubella, acquired form carcinoid
Valvular, subvalvular, supravalvular
Indication for balloon valvuloplasty
Symptoms: > 30 mmHg peak
Asymptomatic: > 40 mmHg peak
Pulmonic regurgitation
Secondary to TOF(tetralogy of fallot) tx of RVOT obstruction
Carcinoid; endocarditis
Graham Steell murmur:
High-pitched blowing murmur louder with inspiration (not in isolation)
Drug-induced valve disease
Ergot alkaloids (for migraines) Fen-fen Pergolide MDMA (ecstasy) IVDA (endocarditis)
cannon a waves in
heart block atria contract (have p wave) but valves can't open-->pressure transmitted backwards
VSD (FA) murmur
holosystolic, harsh-sounding
loudest @ tricuspid area
PDA (FA) murmur
continuous machine-like murmur
loudest at S2, best heard @ left infraclavicular area
often due to congenital rubella or prematurity
