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39 Cards in this Set

  • Front
  • Back
Heart Sounds: S3 and S4
S3: rapid filling phase in early/mid diastole
S4: associated with very stiff ventricle; coincides with atrial contraction
Aortic Reguritation
during systole, blood flows out of ventricle into aorta. During disastole, instead of valve staying closed, blood flows back into left ventricle (must pump more blood out to maintatin SV because some comes back in
Mitral Regurge
during systole blood flows into aorta and LA. some blood ejects backwards. That blood refills LV during systole. Franks starling mech. increase LVEDV
Causes of Acute AR
infective endocarditits, Aortic dissection, Trauma
SURGICAL EMERGENCY
problem with valve leaflets
comp vs. demcomp Chronic AR
Compensated: asymptomatic phase with marked LVdilatation, but presssures remain constatnt
Decompsenates: myocardial dysfunction tirggers sympstoms and mortality becomes significan
Stenosis Murmur
occurs when valves are supposed to be open
regurge murmur
occurs when valves are supposed to be closed
Factors affectiving severity of AR
1. size of hole
2. pressure gradient (high BP)
3. duration of diastole (tachy may help)
Treatment of chronic AR
symptoms indicate dysfunction=Surgery
Vasodilators only useful in asymptomatic patients w HTN
Characteristics of Acute AR
Pressure?
Murmur?
volume increase results in an increase ESV and EDP (to time to compensate)
short murmur
Acute MR
organic vs. functional
organic: leaflet, chordae, or pap muscle problem
functional: LV problem --> messed up annulus
Chronic MR compensation
1. LA compensates by dilating and acomodation increase colume with less LAP
2. LV compensates by dilation and hypertrophy resulting in incr. LVEDV with ner normal LVEDP
3. Decomp results in incr. LVEDP and incr. LAP
Volume and pressure overload
AR
just volume overload
MR
compensated MR
EDV incr afterload decr.
PV curve shifts down, decr. ECM, Incr compliance
Decomp MR
Incr ESV and incr LAP and EDP
decr. contractility
Holosystolic Murmur
Chronic MR
C and V waves merge: prominent V Vave
Murmur incr. with clenched fists
incre BV--> S3 sound
symptoms of chronic MR
1. low cardiac output
w. LA dilation stetches myocytes--increase propenisty for arrhythmias (A Fib)
Factors affecting severity of MR
1. size of hole
2.LAP and compliance (resistance to backflow)
3. Systemic Vascular resistance (resist to forward flow)
Regurge
Sypmtoms = Surgery
Fo' Sho'
Are stenotic lessions acute or chronic
Always Chronic, imcompatible w/life
which chambers are affected by:
aortic stenosis
mitral stenosis
aortic stenossis: LV
Mitral: LA

not that similar
Three main causes of aortic stenosis
1. degenerative- old people
2. rheumatic- any age any valve
3. congenital- bicuspid AV

afterload not directly dependent on BP
Peak instantaneous gradient
highest LVP
peak-peak gradient
difference between LV peak P and aortic peak P

no phys significance, diff times
mean gradient
average all through systole
Aortic Stenosis Murmur
during systole (valve supposed to be open)
crescendo-decresendo diamond
short delay afte S1, dwindles befoer S2: ejection systolic murmur
AS Signs
mid systolic murmur
delayed and diminished carotid pulse
stiff ventricle--can be an S4
AS Symptoms and survival rates
Angina: 5 years incre muscle mass and wall stress. EDP compresses coronary ateries and reduces flow

Syncope: 3 years related to exercise CO cant increase

HF 2 years
ECG findings in AS
LVH
increase voltage precordial leads
t waves inverted (abnormal repol)
Treatment of AS
Fix valve : replacement or plasty
med mangage: avoid a fib, avoid exercise, avoid things that dec. pre or afterload, use statins?
mitral stenosis etiology
RHEUMATIC HEART DISEASE
affects LA
What is the problem in mitral stenosis?
diastolic filling
MS murmur
diastolic rumble
can be an opening snap timed with openin of mitral valve; earlier if more severe
MS signs
Loud S1- MV snaps closed
opening snap
mid diastolic rumble
pre-systolic acentuation of murmur
sever: short S2-OS interval, longer mdrumble
MS symptoms
elevated LAP: dyspnea, exercise intolerance
elevated PA pressure-- pulmonary HTN
diminished CO (LV underfilled)
Hemoptysis- incr LAP, incre pvp, bronchiol veins can rupture
Hoarseness- pressure on recurrnet laryngeal nerve by LA or PA
Two mechanisms for elevated PAP in MS
passive pulmonary HTN- increase in LAP, incr pulmonary vp, pulmonary artery p increase

reactive pulmonary HTN: passive increase causes reactive increase; not everyone develops it
ECG findings in MS
LA enlargement RVH (late stages)
V1- p wave deep and wide
right axis deviation, prominent s waves v5 v6
MS treatment
fix stenosis
medical: volume control with diuretics
prevent an increase in HR
prevent clots with anticoag