01 CVS General and congenital heart disease.ppt
Transcript of 01 CVS General and congenital heart disease.ppt
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Pathology andPathophysiology:
CardiovascularPathology
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Overview of heart
disease
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Overview of heart disease
Fetal heart fully functional by 8 weeks
Heart disease responsible for 40 deaths in
!"
#$0% deaths per annu&
'$0% are (pre&ature) *+#$yrs,
-.00 billion cost re /sche&ic heart disease peryr
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C" disease: 1hat can gowrong2
Pu&p failure
Obstruction to 3ow egurgitation
"hunts
Conduction defects
Heart rupture
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Heart failure :CHF
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Heart failure :CHF
5nd stage of several disorders
Progressive usually
67ects $ &illion people in !"
. &illion hospitaliations
900% deaths
-.8 billion cost to health service
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CHF types
"ystolic Heart unable to pu&p blood into
circulation
5g &uscle da&aged
iastolic *elderly; diabetics; wo&en, Heart unable to regurgitation
alve abnor&alities
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CHF types
?ow output *+ ($ ?) per &in,
"ystolic
iastolic
High output *@ ($?) per &in,
6ne&ia Hyper&etabolic states
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CHF types
6cute
"udden loss of &uscle
"udden loss of valve function
Chronic
Aradual develop&ent of disorder
Co&&onest type
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CHF &echanics
Backward failure
/nto venous syste&
/ncreased enddiastolic volu&e andpressure
/ncreased venous pressure
Forward failure
/nade=uate nutrition>ODygen to tissues
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CHF : atte&pts toco&pensate .E
Frank "tarling &echanis&
?onger
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CHF : atte&pts toco&pensate 'E
Geurohu&oral co&pensation
Nor-epinephrine ++ heart rateIyocytes &ore contractile
Blood pressure increased
Renin Angiotensin bloodvolu&e
Atrial Natriuretic peptide 2 "odiu& out blood volu&e lowered
elaDes s&ooth &uscle BP lowered
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Blood pressure
BP CO J P
Blood pressure
Cardiac output Peripheral resistanceE
CHF tt t t
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CHF : atte&pts toco&pensate 9E
Pressure overload *eg hypertension, Parallel hypertrophy *concentric,
Gew sarco&eres parallel to eDisting ones
1all thickening
olu&e overload *eg regurgitation,
Gew sarco&eres in se=uence
1all &ay not thicken *heart weightincrease,
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Proble&s with hypertrophy
Iore *thicker,
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"u&&ary
"tarling
Hu&oral
5pinephrineenin L angiotensin
6GF
Iuscle hypertrophy
6ltered gene eDpression
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?eft sided heart failure
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?eft sided heart failure :5tiology
/H 6rteries
Hypertension Iuscle *secondary,
alve disease *obstruction or
regurg,
Pri&ary &yocardial disease
*Cardio&yopathies,
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?eft sided heart failure :e7ects
Output decreased *Forward,
yspnea L increasing
Orthopnea *recu&bent,
/ncreased venous return fro& legs
iaphrag& i&pinges on lungs
Pul&onary congestion *Backward,
Pressure increase
educed oDygenation22
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?eft sided heart failure :signs
Cardio&egaly *blood in cha&bers, Iitral regurgitation *valve ring
distended,
Khird heart sound *"9,
Pul&onary rales *3uid in alveoli,
Kachycardia *co&pensatory,
6trial
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e s e ear a ure :conse=uences elsewhere in
body ecreased perfusion of tissues
eninangiotensin syste& activated
Ga and 3uid retention
Pul&onary ede&aHypertension
Prerenal aote&ia due to decreasedperfusion
CG" sy&pto&s if severe reduction inperfusion
(HypoDic encephalopathy)
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ight L sided heart failure
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ight L sided heart failure :etiology
"econdary to leftsided failure
"econdary to lung disease *corpul&onale,
6lso
"hunts in congenital heart disease*overload,
alve disease
*Pul&onary stenosis; Kricuspid/nco&petence,
i h id d h f il
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ight L sided heart failure :clinical
"yste&ic venous congestion
Few pul&onary sy&pto&s if only sidea7ected
?iver L congested and enlarged *Gut&eg,
%idney L ditto prerenal aote&ia etc
Peritoneu&> pleural e7usions
CG" L HypoDic signs
6nkles L ede&atous
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Biventricular failure
Fre=uent end stage of heart failure
"y&pto&s and signs as before but
6?"O
Cyanosis6cidosis
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Congenital Heart disease
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Congenital Heart disease
(Present at birth)
'0 L 90 of all birth defects
8 > .000 live births
@ in pre&aturity and still births
80% per year in !"
$0 clinically signi
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+++
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Pathogenesis
9 L 8 weeks of intrauterine develop&ent
M0 unknown etiology
ubella
Keratogens Iaternal diabetes
Aenetic abnor&alities *6 usually,
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Broad classi
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Conse=uences to heart
Cha&ber dilatation > hypertrophy
High pressure
Iuscle hypoplasia *prenatal,
Or atrophy *post natal,
?ow pressure
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?eft to right shunts
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?eft to right shunts
6"
"
P6
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? shunts
(ed) blood (Blue) blood
Blood going into aorta is red body
GO cyanosis
High pressure Hypertrophy
?ater : 3ow reversal KH5GCyanosis
Eisenmenger complex
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Fora&en ovale
/n fetus : patency necessary to allowblood to 3ow fro& 6 ?6
Blood canNt 3ow through the fetalpul&onary circulation which is collapsed
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LA
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LA
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Patent fora&en ovale
Fora&en ovale is closed by
"eptu& pri&u& *lower,
Khen "eptu& secundu& *upper,
80 Fora&en ovale (sealed) by ?6pressure
'0 transient ? 3ow possible
/f 6 pressure @ ?6 *alsalva,
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6"
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LA
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6" Clinical
6sy&pto&atic until adulthood
? L shunts initially
Clinically tolerated if s&all *+.c&,
Pul Hypertension later if large
ParadoDical e&bolis&2
"urgical repair
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LA
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"
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"
M0 are in Ie&branous portion of septu&
*!pper part,
Iost close spontaneously during childhood
/n adults " ++ 6" clinically
#0 L 80 are associated with other cardiacabnor&alities
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" Clinical
6sy&pto&atic if very s&all
?arger lesions Pul&onaryhypertension
"hunt reversal > Cyanosis
5isen&enger co&pleD
et lesions
5ndocardial da&age L nidus for
infection
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P6
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uctus arteriosus
Blood fro& ? pul&onary artery aortaduring intrauterine life
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uctus arteriosus
Blood fro& ? pul&onary artery aortaduring intrauterine life
Closes in
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P6 : clinical # of congenital heart defects
*M0 are isolated defects,
HypoDia associated
Iachinery &ur&er
Pressure proble&s 5isen&enger
5ndocarditis
PA5 D *B!K not if 2,
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Arterial pressure
In Pul circulation
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ight to ?eft shunts
i h ? f h
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ight to ?eft shunts
5arly cyanosis (blue babies)
Ketralogy of FallotKransposition of great vessels
Kruncus arteriosus
ight to ?eft shunts :
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ight to ?eft shunts :Clinical
Cyanosis
Clubbing *hypertrophicosteoarthropathy,
Polycythe&ia
ParadoDical e&bolis&
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Ketralogy of Fallot
Ketralogy of Fallot
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Ketralogy of Fallot "
out3ow obstruction *subpul&onic,
Overriding 6orta
hypertrophy
6nterosuperior displace&ent
of infundibular septu&
6bnor&al septu& for&ation
6orta pul&onary trunk
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P th l
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Pathology
(Boot shaped hypertrophy
? and ?6 nor&al sie wall
" lies in &e&branous septu&
6ortic valve is over the "
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Pathology
Pul out3ow tract is narrowed
Pul&onic valve &ay be stenotic
Iay also have P6 or 6"
Iay be bene
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Ketralogy of Fallot out3ow obstruction
*subpul&onic,
hypertrophy "
Overriding 6orta
K t l f F ll t Cli i l
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Ketralogy of Fallot : Clinical
epends on severity of out3owobstruction
Iay not be detected till adult life in
&ild cases
Co&&only L cyanosis at birth
1orsens as child grows
Obstruction re&ains at sa&e sie
Ketralogy of Fallot :
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gyOther conse=uences
Polycythe&ia
Hyperviscosity
Clubbing
5ndocarditis
5&bolis&
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Kransposition of great
arteries
Kransposition of great
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p garteries
Only viable if co&&unication eDists"yste&ic > Pul&onary circulations
" in 90 cases *other also,
*arterial pressure, ?
Cyanosis "urgical repair usually necessary
"urvival to adulthood
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Transposition of Great Vessels
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Transposition of Great Vessels
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Kruncus 6rteriosus
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Persistent
Truncus
Arteriosus
VSD
K 6 t i
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Kruncus 6rteriosus
Both ventricles e&pty
into co&&on tuncus
Cyanosis early
Pul&onary hypertension
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Obstructive lesions
Obstructive lesions :
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Coarctation of 6orta
Iales ': . Fe&ales
*cf Kurners syndro&e,
/nfantile for& : ProDi&al to P6
6dult for& : Beside liga&entu&
arteriosu&
$0 have other cardiac abnor&ality
Obstructive lesions :
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/nfantile type
uctus open
"upplies blood to body*eoDygenated,
ilated pul&onary trunk
Hypertrophied
/nfantile type
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/nfantile type
?ower body cyanosis Poor prognosis without treat&ent
Obstructive lesions :
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6dult type
6ortic arch and vessels dilated
? Hypertrophied
6dult type
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6dult type
6sy&pto&atic : "ystolic &ur&ers
High BP in upper body
/ntercostal and internal &a&&arydilation
ib notching
?ow BP lower body *enin 6ngiotensin2,
1eak pulses in legs; cold; claudicationE
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