HNI 310 - Cardiovascular System BB 2015

7/25/2019 HNI 310 - Cardiovascular System BB 2015

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Cardiovascular Disorders

HNI 310

PathologyKenneth Faulkner, M, !N,

"NP#$C

Department of Undergraduate Studies


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%&'ectives

$y co()letion o* this lecture, students should &e a&le to+

1Descri&e the )rocess o* atherosclerosis

-Di.erentiate sta&le angina, unsta&le angina/NMI, and MI

3Descri&e *actors associated 2ith increased risk o* aneurys(

Descri&e *actors associated 2ith develo)(ent o* D4

5Di.erentiate )eri)heral arterial disease and venous insu6ciency

7Descri&e hy)ertro)hic cardio(yo)athy and descri&e ho2 )athologyin8uences clinical )resentation

9Di.erentiate the sy()to(s o* heart *ailure as they relate to cardiac*unction

:Descri&e di.erence &et2een systolic and diastolic heart *ailure;Di.erentiate rheu(atic heart disease *ro( endocarditis

10Descri&e ho2 di.erent valvular heart diseases )resent

11Di.erentiate cyanotic *ro( non#cyanotic congenital a&nor(alities and)rovide e


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Cardiology &asics

!evie2 cha)ter -1 *or &asic cardiacanato(y , 8o2 o* &lood through theheart, ca)illary e


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4ascular anato(y

3 layersunica inti(a = endothelial cells over connective

tissue

unica (edia = s(ooth (uscle = thicker in arteriesand arterioles

unica adventitia =

collagen and

connective tissue


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4ascular s)eci>cs

Inti(a = controls?rans*er o* (olecules across vessel 2all

Platelet adhesion and clotting

4ascular resistance and &lood 8o2

Hor(one regulation

In8a((atory res)onse@

Ahen distur&ed, inti(a sti(ulates release o* cytokines and other)roducts that induce in8a((ation

4ascular s(ooth (uscle Dilates and constricts in res)onse to signals

Produces collagen, elastin, gro2th *actors and cytokines

!e)airs &lood vessels 2hen da(aged


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er(inology

Ische(ia = reduction in &lood 8o2that doesnBt (eet needs *or o


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"therosclerosis

For(ation o* *atty lesions in inti(al lining o* (ediu( andlarge sied &lood vessels aorta, coronary arteries, arterieso* &rain, etcE

eading cause o* death in the G

!isk *actors+ Gn(odi>a&le

Increasing age

enetic )redis)osition/*a(ily history

Male gender

Modi>a&le High D or lo2 HD

(oking@

HN

DM


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"therosclerosis

hree ty)es o* lesions

1 Fatty streak = early discoloration o* theinti(a due to in>ltration &y

(acro)hages and li)id- Fi&rous athero(atous )laue = *urther

invasion o* the inti(a triggers thein8a((atory )rocess

3 Co()licated lesion = he(orrhage 2ithinthe lesion or ulceration o* the lesionleading to thro(&osis


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Process o* "therosclerosis

1ndothelial in'ury = due to D, HN, s(oking, etc "llo2s entry o* li)ids

Monocytes and )latelets can adhere

Fatty streak &egins to *or(

- In8a((atory cells (igrate into vessel 2all Monocytes enter inti(a and &eco(e (acro)hagesE, release to


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"therosclerosis contE

Fi&rous athero(atous )laue u)er>cial s(ooth (uscle ca) and dense e&rous ca)

Core (ay &e necrotic, calci>ed, and unsta&le


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ta&le "ngina and "cute coronary

syndro(e "CE

Coronary &lood 8o2 regulated &y cardiac o


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Movie ti(e

htt)+//222youtu&eco(/2atchOvgnh*re(Ho
http://www.youtube.com/watch?v=Gg4nhfremHohttp://www.youtube.com/watch?v=Gg4nhfremHohttp://www.youtube.com/watch?v=Gg4nhfremHohttp://www.youtube.com/watch?v=Gg4nhfremHohttp://www.youtube.com/watch?v=Gg4nhfremHohttp://www.youtube.com/watch?v=Gg4nhfremHo


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"cute coronary syndro(econtE

ta&le )laue %&structs &lood 8o2 over ti(e

Gnsta&le )laue Can ru)ture due to he(odyna(ic stress


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Da(age is the result o* conversion to anaero&ic(eta&olis( and loss o* "P ack o* energy to (eet de(ands

Decrease in contractile *orce 2ithin 70 seconds

lycogen is de)leted and (itochondria s2ell

Da(age is irreversi&le a*ter a))ro


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Presentation o* ta&le "ngina and

"C ta&le angina = )ain associated 2ith e


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Heart *ailure

!eduction in cardiac out)ut due to cardiac a&nor(ality

".ects over 5 (illion "(ericans over the age o* -0

Preload = volu(e o* &lood stretching ventricle at end o* diastole It is the volu(e o* &lood stretching the heart (uscle at the end o* diastole and is nor(ally deter(ined &y the venous

return to the heart During any given cardiac cycle, the (alling the ventricle is )resent at

the end o* diastole Kno2n as the end-diastolic volume, this volume causes an increase in the length of themyocardial muscle bers. Within limits, as end-diastolic volume or preload increases, the stroke volume increases

4enous return

"*terload = resistance the ventricle (ust overco(e to e'ect &lood yste(ic vascular resistance and ventricular 2all tension

he (ain co()onents o* a*terload are the syste(ic )eri)heralE vascular resistance andventricular 2all tension Ahen the syste(ic vascular resistance is elevated, as 2ith

arterial hy)ertension, an increased le*t intraventricular )ressure (ust &e generated to>rst o)en the aortic valve and then (ove &lood out o* the ventricle and into the syste(ic

circulation

Contractility = the contractile *orce o* the ventricle "ctin and (yosin >la(ents shorten


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Heart *ailure contE

ystolic dys*unction Decrease in cardiac contractility+ F Q 0L

Preload increases, ventricle dilates, increased le*tventricular end diastolic 4DE )ressure

Pul(onary hy)ertension leading to )ul(onary ede(aincreased )reload can also lead to one o* the (ost deleterious conseuences o*

systolic ventricular dys*unctionRaccu(ulation o* &lood in the atria and the venoussyste( 2hich e()ties into the atriaE, causing )ul(onary or )eri)heral ede(a

tiology+

I()aired contractility ische(ic heart disease, CM%E 4olu(e overload valve insu6ciencyE

Pressure overload HN, valvular stenosisE


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Heart *ailure contE

Diastolic dys*unction 35#55L o* cases

Diastolic ventricular dys*unction is characteried &y a nor(al e'ection *raction &ut i()aired diastolic ventricular relalling that ulti(ately causes a decrease in )re# load, stroke volu(e, and cardiac out)ut

Higher in 2o(en, and in o&esity, HN, and DM

!elalling is a&nor(al

Increased ventricular )ressures S increased )ul(onary vascular congestion Aith diastolic dys*unction, &lood is una&le to (ove *reely into the le*t ventricle, causing an increase in

intraventricular )ressure at any given volu(e he elevated )ressures are trans*erred backward fromthe left ventricle into the left atrium and pulmonary venous system, causing a decrease in lungcompliance, which increases the work of breathing and evokes symptoms of dyspnea. Cardiac outputis decreased, not because of a reduced ventricular ejection fraction as seen with systolic dysfunction,but because of a decrease in the volume (preload available for ade!uate cardiac output. "nade!uatecardiac output during e#ercise may lead to fatigue of the legs and the accessory muscles ofrespiration.

tiology+ I()aired a&ility o* ventricle to e


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Heart *ailure contE

!ight ventricular dys*unction !ight#sided heart *ailure i()airs the a&ility to (ove deo


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Peri)heral arterial disease

"cute arterial occlusion udden &lockage o* 8o2 through a )eri)heral

artery

tiology (&olus or thro(&us (ost co((on

rau(a can &e a cause

Mani*estations Pain, )allor, )ulselessness, )aralysis, )aresthesia, )olar coldE

"therosclerotic %cclusive disease radual decrease in &lood 8o2 = 50L narro2ing &e*ore onset o*

sy()to(s tiology

"therosclerosis

Mani*estations Claudication = e


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"neurys(s

"&nor(al localied dilation o* &loodvessel

tiology Aeakness in &lood vessel 2all caused &y+

Congenital de*ect

rau(a

In*ection

"therosclerosis

"neurys( gro2s as tension and )ressure continues

Can cause )ressure on surrounding structures or (ay ru)ture

Mani*estations = de)end u)on location and sie May &e asy()to(atic May co()lain o* sta&&ing su&sternal, &ack, and neck )ain

May have dys)nea and cough due to i()inge(ent on trachea

Hoarseness due to )ressure on laryngeal nerve

Di6culty s2allo2ing due to )ressure on eso)hagus


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"ortic dissection

"cute, li*e threatening event He(orrhage into vessel 2all 2ith tearing along the length

o* the vessel = loss o* &lood is usually not signi>cant

Channel (ay o&struct &lood 8o2 to &ranch arteries

"scending aorta (ost a.ected -/3E

tiology

Aeakness o* vessel

HN, connective tissue diseases, surgery increases risk

)ide(iology

Most co((on in (en &et2een 0 and 70 Mani*estations

"&ru)t, e


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Hy)ertro)hiccardio(yo)athy

Gne


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Pericarditis

"ccu(ulation o* 8uid in the)ericardial sac

tiology In8a((ation

In*ection

rau(a

"s 8uid volu(e W in )ericardial sac, )ressure on heart W

Pressures in right side o* heart are lo2er, so(ani*estations ty)ically a))ear as right sided heart *ailure 4enous return V = )reload V

achycardia tries to co()ensate

Prolonged )ressure in )ericardiu( leads to cardiacta()onade Vventricular >lling, V stroke volu(e, V cardiac out)ut


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ndocarditis

In*ection o* lining o* heart

tiology Invasion o* heart valves and endocardiu( &y &acteria

$taphylococcus is co((on &acteria *or I4 drug a&users and

heart valve )atients Many others can cause in*ection

$acteria gets into &loodstrea( through )ortal o* entry

ndothelial da(age, altered he(odyna(ics, and&actere(ia lead to thro(&us *or(ation

hro(&us can &e seeded &y &acteria

Continued activation results in develo)(ent and gro2th o**ria&le vegetations

Destruction o* cardiac tissue


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ndocarditis contE

"ortic and Mitral valves (ost a.ected

Continue to release &acteria

Destroy valves, cause )ericarditis, aneurys(, valve)er*oration

Frag(ents (ay *or( e(&oli and travel to &rain, lungs,)eri)hery

)ide(iology I4 drug a&use

Dental )rocedure

Intracardiac devices )rosthetic heart valves, )ace(akers,4"DsE

M4P

Mani*estations Fever, (ur(ur, s)linter he(orrhages

reat(ent = anti&iotics and surgery


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!heu(atic heart disease

Co()lications o* i((une res)onse to grou) "&eta#he(olytic stre)tococcal throat in*ection Develo)(ent o* chronic valvular )ro&le(s

tiology # not clearly understood $elieved to &e autoi((une reaction *ollo2ing creation

o* anti&odies against M )rotein o* grou) " &eta#he(olytic stre)

"nti&odies cross react 2ith sel*#antigens in heart and

'oints (olecular (i(icryE "scho. &odies are *or(ed = necrotic tissue

surrounded &y i((une cells

De*or(ity o* valves occurs


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!heu(atic heart disease

Mani*estations "rthralgia to severe arthritis a.ecting 'oints o*

knees and ankles

Mitral and aortic valves (ost co((onlya.ected = M4 stenosis

4egetations and scarring causing de*or(ities

u&cutaneous nodules over e


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4alvular heart disease

tenosis = narro2ed vascular lu(en

!egurgitation = &ack2ards 8o2

Mitral valve stenosis narro2 (itral valve

tiology = rheu(atic *ever or congenital

a&nor(ality Fi&rous re)lace(ent o* valve resulting in sti.,

*used valves

!esistance W and le*t atriu( dilates, eventually

causing )ul(onary vascular congestion


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4alvular heart diseasecontE

Mitral valve regurgitation 4alve does not close )ro)erly

tiology = rheu(atic heart disease, ru)tured chordaetendinae, ru)tured )a)illary (uscles, 4 dilation

4olu(e overload in " and 4 resulting in )ul(onary vascularcongestion

Mitral valve )rola)se M4PE J8o))y valve

tiology = genetic disorder resulting in enlarged, J8o))yvalves Fi&rotic changes develo) on valves

May or (ay not cause (itral regurgitation

l l h di


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4alvular heart diseasecontE

"ortic stenosis Narro2 aortic valve lu(en

tiology = Most co((only congenital or calci>cation More co((on in (en

Calci>c " is usually slo2 to develo) = 70#90 years old

I()aired 4 out8o2

4 hy)ertro)hies 2ith ti(e to acco((odate *or W resistance

May cause W cardiac 2orkload S angina, synco)e, heart *ailure

"ortic regurgitation Inco()etent "4 allo2ing &ack8o2 *ro( aorta to 4

tiology = rheu(atic *ever, congenital a&nor(alities, aortic dilation Increased )ressure to " and )ul(onary vessels causing congestion

4 enlarges over ti(e

"sy()to(atic at >rst

Develo)s e


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Congenital heart disease

Ma'or changes in heart occur&et2een thand 9th2eek o* gestation De*ects are &elieved to &e co(&ination

o* genetic and environ(ental in8uences 30L can &e attri&uted to (odi>a&le risk

*actors *e&rile illness, alcohol

consu()tion, DM, (edications, etcE Many carry congenital a&nor(alities into

adulthood

C i l h di


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Congenital heart diseasecontE

Patho)hysiology 3 (a'or (echanis(s

1 hunting o* &lood

- Production o* cyanosis

3 Disru)tion o* )ul(onary &lood 8o2

"&nor(al shunting.Diversion o* &lood *ro( one syste( to another

.Deter(ined &y )resence o* a&nor(al )assage2ay , )ressuredi.erences, and resistance

hunting and Cyanosis.e*t to right shunts usually are acyanotic do not inter*ere 2ith

o


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Cyanosis $luish tint in nail &eds and (ucous (e(&ranes

%ccurs 2hen %-levels *all &elo2 :0L in ca)illaries

hunting o* &lood 2ithout &eing o


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Patent ductus arteriosus Nor(ally closed : hours a*ter &irth due to decrease

in )ul(onary artery resistance, (uscular contraction,increased %-saturation and )rostaglandin decline

$lood shunted *ro( high )ressure on le*t side to lo2)ressure on right side

Mur(ur and 2idened )ulse )ressure are co((on

y)ically not cyanotic

Co()lications include heart *ailure, )ul(onaryvascular disease, aneurys(, thro(&oe(&olis(, andcalci>cation

Corrected &y surgical closure

C it l h t di


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"trial/4entricular se)tal de*ects

Persistent o)ening in se)tu(

"trial+ Incidence 1 in 1000, (ore

*reuently in girls %*ten asy()to(atic

Can develo) to ! shunt

Dilation o* ! heart

Fi


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4entricular+ Incidence -5 in 1000, evendistri&ution in genders y()to(s de)endent u)on sie o* de*ect

May &e asy()to(atic or (ay develo) heart*ailure

Can develo) to ! shunt

achy)nea, dia)horesis, *ailure to thrive

Pul(onary hy)ertension due to increasedvolu(e

Can develo) signi>cant increase in)ul(onary vascular resistance

urgical re)air i* necessary

C it l h t di


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etralogy o* Fallot 5#9L o* all heart de*ects

Four de*ects

1 4entricular se)tal de*ect

-hi*ting o* aorta to the right

3 Pul(onary out8o2 o&struction

!ight ventricular hy)ertro)hy

Deo


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C it l h t di


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rans)osition o* great vessels

"orta arises *ro( right ventricle,)ul(onary artery arises *ro( le*t

ventricle - )er 100,000, (ore co((on in &oys

4entricular se)tal de*ect )resent in 50Lo* )atients allo2s &lood to (i< andallo2s in*ants to survive

Cyanosis is (ost co((on sy()to(

urgical re)air is necessary


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4asculitis

In8a((atory disorders a.ecting vessel 2all

"lso involve endothelial and s(ooth (uscle cells

"ll vessels can &e a.ected

Clinical (ani*estations Fever, (yalgia, (alaise

Causes Direct vascular in'ury

In*ectious agents

"utoi((une disorders

econdary to other diseases

(all vessels = Aegener gra(ulo(atosis

Mediu( sied vessels = )olyarteritis nodosa, Ka2asaki disease

arge vessel = iant cell te()oralE arteritis


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Chronic venous insu6ciency

Failure o* unidirectional 8o2 through venoussyste(

%*ten due to *aulty valves in veins

$lood can 8o2 retrograde

Pooling o* &lood occurs Mani*estations

issue congestion

de(a

!eddened e


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4aricose veins

ortuous, dilated &lood vessels in lo2er

e


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Dee) vein thro(&osis D4E

"ka hro(&o)hle&itis

Presence o* thro(&us and in8a((atory )rocess in vessel

Gsually occur in lo2er e


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Hy)ertensive vasculardisease

$P X 10 ((Hg and D$P X ;0 ((Hg

!isk *actors+

1 enetic )redis)osition- "ge $P increases, D$P decreasesE

3 !ace "*rican/Cari&&ean#"(ericansE

Insulin resistance

5 High salt intake

7 %&esity

9


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Hy)ertensive vascular disease

contE

ssential hy)ertension

levated $P not due to another condition

hought to involve

1 KidneyBs a&ility to regulate sodiu( and 2ater

- y()athetic hy)erreactivity3 !enin#angiotensin#aldosterone syste( dys*unction

Gncontrolled leads to

1 4 hy)ertro)hy

-Heart *ailure

3"therosclerosisKidney disease

5!etino)athy

7troke

H t i l di


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Hy)ertensive vascular disease

contE

econdary hy)ertension Due to another disease )rocess

1 !enal hy)ertension = due to glo(erulone)hritis,acute/chronic renal *ailure, GI, )olycystic kidney disease

Dys*unction o* renin#angiotensin#aldosterone syste(

Decreased 8o2 through kidney results in increase in renin )roduction

- "drenocortical hor(one dys*unction Increased aldosterone due to adrenal hy)er)lasia or e


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HNI 310 - Cardiovascular System BB 2015

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