01 CVS General and congenital heart disease.ppt

7/23/2019 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



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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



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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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Documents

01 CVS General and congenital heart disease.ppt