CRAMMER’S GUIDE TO VALVULAR HEART DISEASES

Harrison’s IM 18th ed ren.sama

ETIOLOGY AND PATHOPHYSIOLOGY CLINICAL PHYSICAL EXAM LAB TREATMENT

PATHOLOGY MANIFESTATIONS (MURMUR)

MITRAL Rheumatic fever – N area of mitral orifice 4- Rheumatic carditis – 4th Malar flush with pinched ECG: LAH; Tall peaked P Symptom control: BB,
STENOSIS leading cause or most 6cm2 decade of life and blue facies wave; N QRS complex; nondihydropyridine CCB
(MS) common cause of MS; RAD and RVH if severe or digoxin for rate control
“fish-mouth valve” Hemodynamic hallmark Hemoptysis – rupture of Systemic arterial pressure pulmonary hpn of AF; cardioversion for
of MS: <~2cm of orifice, pulmonary-bronchial N or dec new-onset AF or HF (at
CAREY-COOMBS blood flow from LA to LV venous connection; inc CXR: straightening of least 3 weeks of
MURMUR - short, mid- propelled only by abN inc LAP without markedly inc S1 accentuated and upper L border of cardiac
slightly delayed anticoagulants to
diastolic murmur during of LAVP gradient pulmonary vascular silhouette, prominent therapeutic INR of 2-3, if
ARF resistance; rarely fatal Opening snap (OS) most main pulmonary arteries, urgent then use IV
Mild MS (>1.5cm2) dilation of upper lobe
Thrombus formation and Recurrent pulmonary audible in expiration at or heparin and TEE before
Moderate MS (1-1.5cm2) – medial to apex pulmonary veins, posterior procedure); diuretics for
embolization in calcified emboli – important cause displacement of
valve normal cardiac output of m&m rates; late HF
(CO) Time interval of A2 and OS esophagus by enlarged
Atrial Fibrillation (AF) – VC, TLC, max breathing varies INVERSELY with LA; Kerley B lines in lower Natural history: Warfarin
thrombi more in dilated Severe MS (<1cm2) – subN capacity, O2 uptake/unit severity and mid-lung fields results for AF or PCN for RF
LA CO ventilation – dec from distention of prophylaxis
Duration of murmur
interlobular septae and
Thrombi in LA esp in correlates with severity of Mitral valvotomy: NYHA
lymphatics with edema
enlarged appendages stenosis in preserve CO Class II-IV with isolated MS
when mean LAP
>20mmHg <~1cm2 /m2 by either
Systemic embolization Hepatomegaly, ankle
PMBV (Inoue balloon
(10-20%) esp in >65yo, AF, edema, ascites, pleural
technique) or surgical
dec CO effusion ®
valvotomy (half require
Rumbling sound with BELL reoperation by 10years)
of stet
Successful valvotomy:
MID-DIASTOLIC MURMUR 50% dec in mean mitral
valve gradient and 2x of
mitral valve area

Unless recurrent systemic

embolization or severe
pulmonary hpn (PA
systolic pressure
>50mmHg at rest or
>60mmHg with exercise),
valvotomy is not
recommended for
asymptomatic or with
mild stenosis
Mitral valve replacement
(MVR): with preservation
of chordal attachment to
optimize LV function
recovery

ren.sama
1
MITRAL Affects one or more of the LV afterload dec-> LV
REGURG functional components of decompresses into LA
(MR) mitral valve: leaflets, during ejection-> LV
annulus, chordate dilation with dec LV size
tendineae, papillary during systole->rapid
muscles, and sub decline of LV tension
adjacent myocardium
Initial compensation:
Acute MI: complete LV emptying
POSTEROMEDIAL papillary
muscle more involved Severe nonishemic MR :
(use TTE) regurg vol ≥60mL/beat,
regurgitant fraction (RF)
Other causes: ARF; HOCM ≥50% and effective regurg
(anterior papillary muscle orifice area ≥0.40 cm2
displacement); AV
cushion defect Severe ischemic MR:
effective regurg orifice
“MR begets MR” area of >0.3cm2
Acute severe MR: LAP rise
for any inc in LA
compliance, pulmonary
edema common, murmur
early decrescendo
ending well before S2
Chronic mild-mod : Acute severe: arterial
asymptomatic pressure dec with narrow
PP; signs of pulmonary
Chronic severe: fatigue, congestion is prominent;
exertional dyspnea, S4
orthopnea, palpitation
(signify AF onset) Chronic severe: arterial
pressure N; systolic thrill
palpable at apex; LV
hyperdynamic; S3; apex
displaced laterally; grade
III systolic
HOLOSYSTOLIC at apex
radiates to axillae
Ruptured chordae
tendineae: systolic
murmur “cooing” or “sea
gull” quality
Flail leaflet: musical
quality
ECG: LAH and RAH if Warfarin for AF with target
pulmonary hpn; chronic INR 2-3
severe MR associated
with AF For asymptomatic severe
MR: avoid isometric
CXR: LAH (late); exercise
pulmonary venous
congestion, interstial Surgery: chronic,
edema, Kerley B lines; nonishemic, sever MR with
calcification in lateral symptoms or with LV
view; acute severe MR dysfunction is progressive,
shoes asymmetric with LVEF <60% and/or
pulmonary edema end-systolic dimension
>40mm; recent-onset AF
and pulmonary hpn (PAP
≥50mmHg at rest or
≥60mmHg with exercise)
Percutaneous Mitral Valve
Repair

Chronic severe MR: LAH

and inc LA compliance
with little inc in LA and
pulmonary venous
pressure for any inc in LA
vol, murmur is holosystolic,
severe fatigue

MITRAL AKA: systolic-click murmur More common in women Posterior leaflet ECG: biphasic/inverted T IE prophylaxis with prior
VALVE syndrome, Barlow’s (15-30yo); most often prolapsed: jet is directed waves and occasional endocarditis
PROLAPSE syndrome, floppy-valve benign; asymptomatic anteriorly and medially supraventricular or PVC
(MVP) syndrome, and billowing and radiates to the base BB to relieve chest pain
mitral leaflet syndrome >50yo often in men are of the heart Echo: systolic and palpitations
severe and requires displacement (in
Other causes: dec type III surgery Anterior leaflet prolapsed: parasternal long axis Severe MR: MV repair
collagen, Marfan’s jet directed radiates to view) of MV leaflets by at (rarely replacement)
syndrome, osteogenesis AD with incomplete axillae or left infrascapular least 2mm into the LA
penetrance Aspirin for transient
imperfect, and Ehlers- region superior to the plane of ischemic attacks and if
Danlos syndrome Arrhythmias: PVC, mitral annulus not effective consider
MOST IMPORTANT
POSTERIOR leaflet more paroxysmal FINIDING: MID-LATE warfarin (esp if AF)
affective and MV annulus supraventricular and SYSTOLIC (nonenjection)
more dilated V.tach, AF -> CLICK
lightheadedness,
palpitations, and syncope “Honking” or “whooping”
sound best at apex
Chest pain often
substernal, prolonged and
not related to exertion

ren.sama
2
AORTIC ¼ in chronic valvular
STENOSIS heart disease
(AS)
80% with symptoms are
male
Causes: degenerative
calcification and most
commonly in bicuspid
aortic valve (BAV) 53%,
chronic (tri-) leaflet
deterioration or previous
rheumatic inflammation
(commissural fusion)
Most have systemic
hypertension
Death with severe AS is
most common in 7th or 8th
decade
Calcific AS is a progressive
disease with annual
reduction of valve 0.1cm2
and annual inc in peak jet
velocity 0.3 m and mean
valve gradient 7mmHg
BAV – MOST COMMON ONCE SYMPTOMS Rhythm is regular until late ECG: ST-segment severe AS: no strenuous
CONGENICAL VALVE OCCURS VALVE depression and T-wave activity or competitive
DEFECT; more in males; REPLACEMENT IS Thrill or anacortic inversion (LV strain) sports; avoid dehydration;
AD with incomplete INDICATED “shudder” over carotid tx hpn or CAD (BB or
predominance; X-linked (more common in the L) Echo: LVH; eccentric ACEI); statins for
component as in Turner’s 3 CARDINAL SYMPTOMS: closure of aortic valve is prevention of CAD
EXERTIONAL DYSPNEA LV impulse displaced characteristic of
syndrome; coarctation or laterally; palpable S4 in L
medial degeneration with (due to inc PCWP caused congenital bicuspid valve Surgery (within 3-4mo)
by inc LV diastolic lateral recumbent; systolic indicated in: severe AS
ascending aortic thrill at base of the heart Severe AS <1cm2;
aneurysm pressure secondary to who are symptomatic, LV
dec LV compliance and to R of sternum leaning moderate AS 1-1.5cm2; EF <50%, BAV and
LV outflow obstruction-> impaired relaxation); forward or in suprasternal mild AS 1.2-2cm2 aneurysm or expanding
pressure gradient bet LV ANGINAL PECTORIS notch aortic root (max
CXR: hypertrophy without
and aorta-> LV dilates (imbalance of myocardial Paradoxical splitting of S2; dilation-> rounding of dimension of >4.5cm or
and dec stroke vol oxygen demand and dec S3 and S4; rough and cardiac apex in front and annual inc in size of
O2 availability); and rasping in character slight backward >0.5cm/yr) even if
LV contraction is SYNCOPE (dec in arterial asymptomatic
maintained by presence loudest in the base (2nd displacement in lateral
pressure due to RICS) view; dilated proximal
of concentric LVH-> LV vasodilation in exercising Relatively indicated in:
systolic function dec and ascending aorta along very severe AS <0.6cm2
muscles and inadequate MOST COMMON CAUSE upper R heart border;
abN diastolic fx progress vasoconstriction in non OF MID-SYSTOLIC and sever LVH >15mm
and irreversible absence of calcification thick
exercising muscles in the MURMUR IN ADULT suggest that severe AS is
myocardial fibrosis face of fixed CO or not present! CABG surgery and AVR:
develops GALLAVARDIN EFFECT –
sudden fall of CO by asymptomatic mod or
murmur high pitched at Aortic sclerosis: jet
Severe obstruction to LV arrhythmia) severe AS
apex, confused with MR velocity <2.5m (peal
outflow: mean systolic LATE: marked fatigue,
gradient >40mmHg with N PARVUS ET TARDUS – small gradient <25mmHg) Homograft AVR reserved
weakness, peripheral for pt with aortic valve
CO or effective aortic delayed upstroke Catheterization:
cyanosis, cachexia; endocarditis
orifice area <~1cm2 (or orthopnea, PND, multivalvular disease,
~<0.6cm2/m2 BSA) pulmonary edema; young asymptomatic with ROSS PROCEDURE:
SUBENDOCARDIUM – esp severe pulmonary hpn noncalcific congenital AS, replace aortic valve with
vulnerable to ischemia leading to RV failure and and pt with suspective LV autologous pulmonic
systemic venous hpn, outflow obstruction at sub valve and implant
hepatomegaly, AF and TR or supravalvular level homograft in native
pulmonic position
Percutaneous Balloon
Aortic Valvuloplasty:
children and young adults
with congenital and
noncalcific AS
ren.sama
3
AORTIC See table 237-1 page Inc total stroke vol
REGURG 1930 ejected by LV
(AR)
EARLY SIGN OF LV
DYSFUNCTION IS DEC EF
MAJOR HEMODYNAMIC
COMPENSATION: inc in LV
end-diastolic vol (INC
PRELOAD)
Severe AR: vol
regurg=effective forward
stroke vol
Chronic AR: both preload
and afterload is inc
Acute severe: LV
compliance is N or dec
and LV diastolic pressure
rise rapidly >40mmHg;
premature closure of MV
Chronic severe: effective
forward CO is N or dec at
rest and fails to rise during
exercise
¾ of pure or predominant Chronic severe: jarring of
AR are men entire body and bobbing
motion of head with each
women predominated if systole; abrupt distention
associated with and collapse of large
rheumatic mitral valve arteries
Acute severe: LAP rise Typically for chronic AR:
rapidly with LA and PA high-pitched, blowing,
wedge pressure markedly decrescendo, DIASTOLIC,
elevated; shock develops best in 3rd ICS along LSB
rapidly
AUSTIN FLINT MURMUR –
Chronic severe: long low-pitched rumbling mid-
latency; asymptomatic
late grade1-2 diastolic
for 10-15yrs; early murmur, due to
complaint palpitations
displacement of anterior
lying down; EXERTIONAL leaflet by AR stream, (-)
DYSPNEA FIRST SYMPTOM OS and response to
OF DIMINISHED CARDIAC vasodilators
RESERVE; followed by
orthopnea, PND, and CORRIGAN’S PULSE –
excessive diaphoresis; water-hammer pulse,
anginal pain wide PP
QUINCKE’S PULSATIONS –
capillary pulsations, an
alternate flushing and
paling or skin at the root
of nail while pressure is
applied to the tip of the
nail (chronic severe AR)
TRAUBE’S SIGN – booming
“pistol-shot” sound over
femoral arteries
DUROZIEZ’S SIGN – to-and-
fro murmur audible if
femoral artery is lightly
compressed by stet
Chronic severe AR: LV
heaving displaced
laterally and inferiorly;
systolic thrill in the
suprastenal notch and
transmitted upward to
carotids; diastolic thrill in
LSB
4
ECG: LVH; ST depression
and T-wave inversion; LAD
or QRS prolongation
Echo: rapid high-
frequency diastolic
fluttering of the anterior
mitral leaflets produced
by the impact of regurg
jet – characteristic finding
CXR: apex is displaced
downward and L in frontal
projection
Acute AR: IV diuretics and
vasodilators; urgent
operations; AVOID BB;
surgery is tx of choice esp
within 24H of diagnosis
Chronic AR: diuretics;
vasodilators (first choice
of antihypertensive
agents); SBP goad
<140mmHg; control
arrhythmias; syphilitic
aortitis needs PCN;
optimal time for surgery
after LV dysfunction but
before severe symptoms
SURGERY:
2 points to consider: (1) pt
with chronic severe AR
usually don’t become
symptomatic until after
the development of
myocardial dysfunction
(2) when delayed too
long (>1yr from onset of
s/s) surgery don’t often
restore normal LV function
AVR: for severe
symptomatic AR
irrespective of LV
function; if asymptomatic
but with progressive LV
dysfunction (LVEF <50%,
LV ESD >55mm or end-
systolic vol >55ml/m2, LV
diastolic dimension
>75mm
Follow-up for severe AR
without indications for
surgery: echo every 3-
12mon
ren.sama
TRICUSPID Generally rheumatic; Diastolic pressure gradient
STENOSIS more common in women; bet RA and RV – defines
(TS) doesn’t occur as isolated TS
lesion; associated with MS
Mean diastolic pressure
gradient 4mmHg is
sufficient to elevate mean
RAP = systemic venous
congestion
CO at rest is depressed
and fails during exercise;
a wave tall and y descent
is prolonged
MS precedes TS, initially
pulmonary congestion
Severe TS: little dyspnea,
hepatomegaly, ascites,
ad edema; fatigue
secondary to low CO
Jugular veins distended;
hepatic congestion
(jaundice, cirrhosis, serious
malnutrition anasarca);
prominent presystolic
pulsations of enlarged
liver
MID-DIASTOLIC, best at
LLSB and xiphoid and inc
in inspiration; prolonged y
descent
ECG: tall peaked P waves Intensive salt restriction;
bed rest; diuretics during
CXR: prominent RA and pre-op
SVC without enlargement
of PA Surgery at the time of
mitral valvotomy or MVR
Echo: tricuspids are with mod to severe TS
thickened and domes in
who have mean diastolic
diastole pressure gradient
~4mmHg and tricuspid
orifice <1.5-2cm2
TVR preferably
bioprosthetic valve

TRICUSPID Secondary to marked Clinical features from Neck veins distended; Prominent RV pulsations ECG: RVH Isolated TR without PA
REGURG dilation of tricuspid systemic venous prominent v waves and over L parasternal and hpn are well tolerated
(TR) annulus from RVH due to congestion and dec CO rapid y descents; marked blowing HOLOSYSTOLIC at Severe TR: hepatic vein
PA hpn hepatomegaly; ascites; LLSB systolic flow reversal; CO Tx L CHF dec severity of
pleural effusion; edema; dec and RAP pulse has no functional TR
Seen in late HF due to systolic pulsations of liver; CARVALLO’S SIGN – inc in x descent during early
rheumatic or congenital murmur intensity with systole but prominent c-v Correct mitral valve
and (+) hepatojugular disease
heart disease with sever reflex inspiration wave with rapid y
PA hpn (PA systolic descent
pressure >55mmHg);
ischemic and idiopathic CXR: RAH and RVH
dilated cardiomyopathies

PULMONIC Most common acquired Pulmonary GRAHAM STEELL MURMUR Percutaneous pulmonic
VALVE abnormality affecting the stenosis/regurg: carcinoid - decrescendo, early-mid valve replacement with
REGURG pulmonic valve is syndrome diastolic blowing murmur severe PR after TOF or
regurgitation secondary that begins after P2, best pulmonic valve
to dilation of pulmonic Repair of TOF -> at 2nd LICS and radiates stenosis/atresia repair
valve ring as pulmonary regurg along LSB
consequence of severe
PA hpn

Note: for any questions, comments, and typos please refer to the book :D

For more explanation about murmurs pls read chapter e13 & 227 and valve replacement and repair page 1949 v(^_^)v

ren.sama
5