Cardiac Surgery MCQ.docx

8/16/2019 Cardiac Surgery MCQ.docx

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Cardiac Surgery MCQ

1. Which is not true of cardiopulmonary resuscitation (CPR)?

. Closed chest massage is as effecti!e as open chest massage.

". #he success rate for out$of$hospital resuscitation may %e as high as &' to '.

C. #he most common cause of sudden death is ischemic heart disease.*. Standard chest massage generally pro!ides less than 1+ of normal coronary and cere%ral %lood flo,.

ns,er- *SC/SS0- Closed chest massage is not as effecti!e as open$chest massage in normali2ing %lood

pressure or perfusion of !ital organs3 and closed chest massage does generally deli!er + to 1+ of

normal coronary and cere%ral %lood flo,. #he success rate for out$of$hospital resuscitation has %een as

high as &' to ' ,hen communities are prepared to institute CPR early after a cardiac arrest. schemic

heart disease is the most common cause of sudden death.

4. Which maneu!er generally is not performed early %efore chest compression in %asic life support

outside the hospital?

. Call for help.

". 0%tain air,ay.

C. 5lectrical cardio!ersion.*. 6entilation.

ns,er- C

*SC/SS0- "asic life support does in!ol!e calling for help3 o%taining an air,ay3 and %eginning

!entilation %efore starting chest compression. 5lectrical cardio!ersion re7uires special e7uipment andtrained personnel and thus is part of ad!anced cardiac life support.

&. Which treatment ,ould %e least effecti!e for asystole?

. 58ternal pacema9er.

". ntra!enous epinephrine3 1' ml. of 1-1'3'''.

C. ntra!enous calcium gluconate3 1' ml. of 1' solution.

*. ntra!enous atropine3 '.+ mg.ns,er- C*SC/SS0- Recommended treatment for asystole is administration of atropine. f atropine is

unsuccessful epinephrine is gi!en. /ltimately cardiac pacing is necessary if atropine and epinephrine do

not esta%lish an ade7uate heart rate. Calcium has no clear role in treating asystole.

:. #he most important factor that influences the outcome of penetrating cardiac in;uries is-

. Comminuted tear of a single cham%er.

". Multiple$cham%er in;uries.

C. Coronary artery in;ury.

*. #angential in;uries.

ns,er- C

*SC/SS0- Multiple studies in the literature confirm that in;uries to the coronary arteries are the mostimportant factor in determining outcome after a penetrating cardiac in;ury. #angential in;uries are the least

serious. n;ury to a single cham%er


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. Which of the follo,ing constitutes a true !ascular ring?

. Pulmonary artery sling.

". *ou%le aortic arch.

C. nomalous origin of right su%cla!ian artery from the descending aorta.

*. Cer!ical aortic arch.ns,er- "

*SC/SS0- 0nly the dou%le aortic arch secondary to persistence of the right and left fourth aortic

arches forms a true !ascular ring. Pulmonary artery sling may cause symptoms that are due to

compression of the trachea3 and an anomalous right su%cla!ian may cause dysphagia3 %ut these anomalies

do not constitute complete rings. Cer!ical aortic arch3 ,hich is thought to %e secondary to persistence of

the third aortic arch3 is not a complete ring and usually is asymptomatic.

D. Which of the follo,ing may %e physical e8amination findings in a young adult ,ith coarctation of the

aorta?. Posterior systolic murmur %et,een the scapulas.

". *iminished femoral pulses.

C. 5le!ated %lood pressure in left arm as compared ,ith right arm.

*. Peripheral cyanosis.ns,er- "C

*SC/SS0- systolic murmur that radiates posteriorly is characteristic of coarctation of the aorta.

Coarctation produces o%struction to aortic flo,3 and thus the femoral pulse has a diminished !olume ,ith

delayed upstro9e. ypertension in coarctation is multifactorial3 %ut the most important factors are

diminished renal flo, (single clip3 single 9idney$Eold%latt model) and mechanical factors. f the right

su%cla!ian artery is anomalous and arises distal to the coarctation3 %lood pressure may %e greater in theleft arm than in the right. solated coarctation does not produce cyanosis.

1'. n a premature infant ,ith hyaline mem%rane disease and ina%ility to %e ,eaned from mechanical

!entilation3 ,hich of the follo,ing ,ould suggest hemodynamically significant patent ductus arteriosus

(P*)?. Continuous murmur.

". yperacti!e precordium ,ith %ounding peripheral pulses.

C. Faundice.

*. *iminished femoral pulses.

ns,er- "

*SC/SS0- P* causes a left$to$right shunt that produces left !entricular !olume o!erload. Physical


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findings include e!idence of hyperdynamic circulation ,ith a prominent apical impulse and %ounding

peripheral pulses. #he classic murmur of P* is a continuous or mechanical murmur heard o!er the

precordium and radiating to the medial third of the cla!icle. *iminished femoral pulses are not seen ,ith

isolated P* and ,ould suggest other anomalies. P* may result in hepatomegaly %ut does not cause

;aundice.

11. n an infant ,ith suspected P*3 ,hich of the follo,ing ,ould %e the optimal method of confirming

the diagnosis?

. Chest film.

". Cardiac catheteri2ation.

C. Retrograde aortography !ia an um%ilical artery catheter.

*. #,o$dimensional echocardiography ,ith continuous$,a!e and color$flo, *oppler echocardiography.

ns,er- *

*SC/SS0- 5chocardiography is the %est method for confirming the diagnosis of a P*. #,o$dimensional echocardiography can demonstrate P* and e8clude associated anomalies. *oppler

echocardiography can demonstrate the shunt3 determine direction of shunting3 and pro!ide an estimate of

shunt magnitude. #he chest film is not particularly helpful and may %e normal or sho, cardiomegaly ,ith

pulmonary congestion. n general3 cardiac catheteri2ation should %e reser!ed for older patients and those,ith suspected associated anomalies or pulmonary hypertension.

14. Which of the follo,ing are potential complications of untreated coarctation of the aorta?

. 5ndocarditis.

". Pulmonary !ascular disease.C. Cere%ro!ascular accident.

*. Congesti!e heart failure.

ns,er- C*

*SC/SS0- Coarctation of the aorta produces an o%struction to %lood flo, and hypertension3tur%ulent flo,3 and increased left !entricular afterload. #here is an increased incidence of coronary artery

disease. Prior to the introduction of effecti!e techni7ues for relief of coarctation3 the most common causes

of death ,ere endocarditis3 aortic rupture3 congesti!e heart failure3 and cere%ro!ascular accident.

Pulmonary !ascular disease does not occur ,ith isolated coarctation.

1&. #he atrial septal defect (S*) most commonly associated ,ith partial anomalous pulmonary !enous

return (PP6R) is-

. Secundum defect.

". Sinus !enosus defect.

C. 0stium primum defect.

*. Complete atrio!entricular (6) canal defect.

5. Coronary sinus defect.

ns,er- "


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*SC/SS0- lthough partial anomalous return of the pulmonary !eins can occur ,ith any of the

S*s listed3 it is particularly common ,ith sinus !enosus defects and is considered %y many to %e part of

this lesion. #he most common anomaly is drainage of the right superior pulmonary !ein to the lateral

aspect of the superior !ena ca!a.

1:. #he direction of an intracardiac shunt at the atrial le!el is controlled %y-

. #he si2e of the defect

". #he compliance of the right and left !entricles.

C. #he systemic o8ygen saturation.

*. Right atrial pressure.

5. #he presence or a%sence of an associated !entricular septal defect (6S*).

ns,er- "

*SC/SS0- #he direction of an intracardiac shunt is go!erned %y the compliance of the do,nstream

cham%ers. Gor an atrial le!el shunt3 the compliance of the right and left !entricles and their a%ility todistend ,ith increased !olume during diastolic filling dictates the direction of the shunt flo,. Since the

right !entricle is usually a more compliant


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*SC/SS0- Many patients ,ith secundum S*s ha!e an incomplete %undle %ranch %loc9 on their

5CE. #his is in contradistinction to patients ,ith ostium primum defects3 ,ho often ha!e a left a8is

de!iation. lthough the 5CE is not pathognomonic of the defect3 the findings are sometimes helpful

along ,ith other clinical and diagnostic information to,ard elucidating the nature of the defect.

1B. S*s can all %e closed ,ith a pericardial or prosthetic patch. Which of the follo,ing S*s can also

%e safely closed primarily ,ithout the use of a patch?

. Secundum S*.

". Sinus !enosus S* ,ith PP6R.

C. n ostium primum S*.

*. complete 6 canal defect.

ns,er-

*SC/SS0- Secundum S*s can fre7uently %e closed primarily3 although the use of a prosthetic or

pericardial patch is indicated for large defects. #he other types of S*s are more safely closed ,ith a patch.

1. 0%struction to pulmonary !enous return is associated ,ith ,hich of the follo,ing anomalies?

. Partial anomalous pulmonary !enous connection (PP6C) to the superior !ena ca!a.

". nfracardiac (#ype ) total anomalous pulmonary !enous connection (#P6C).

C. Pulmonary !ein stenosis.

*. Cor triatriatum.

5. Supracardiac (#ype ) #P6C.

ns,er- "C*5

*SC/SS0- 0%struction to pulmonary !enous return is the most important factor affecting circulatory

function ,hen pulmonary !enous anomalies e8ist. #his o%struction is most pre!alent and se!ere in

patients ,ith infracardiac #P6C3 %ut it also occurs in as many as +' of patients ,ith supracardiac

#P6C and 4' of patients ,ith intracardiac #P6C to the coronary sinus. 0%struction to pulmonary!enous return is also the primary pathophysiologic effect of %oth pulmonary !ein stenosis and cor

triatriatum. 0%struction3 ho,e!er3 is rare ,ith partial anomalous pulmonary !enous connection3 especially

,ith the common form of PP6C to the superior !ena ca!a.

1D. Postoperati!e complications associated ,ith repair of #P6C include-

. Complete heart %loc9.

". cute pulmonary hypertensi!e crisis.

C. Pleural effusions.

*. Pulmonary !enous o%struction.

ns,er- "*


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*SC/SS0- n the early postoperati!e period after repair of o%structed forms of #P6C3 acute

episodes of pulmonary hypertension may de!elop as a response to stress. #o minimi2e this potentially

fatal complication3 infants are 9ept anestheti2ed ,ith fentanyl and pancuronium for at least : hours.

Residual or recurrent pulmonary !enous o%struction occurs in only + to 1' of patients after #P6Crepair3 %ut if identified it re7uires early reoperation. Reoperation is usually successful if the o%struction is

at the le!el of the anastomosis. /nfortunately3 in some cases3 the o%struction is in the pulmonary !einsand surgical relief is less successful. lthough complete heart %loc9 and pleural effusions can occur after

any cardiac operation3 they rarely occur after #P6C repair.

4'. Which of the follo,ing statements a%out 6S*s is@are correct?

. Perimem%ranous lesions are located in the region of the mem%ranous portion of the inter!entricular

septum near the anteroseptal commissure of the tricuspid !al!e.

". Muscular 6S*s are holes in the inter!entricular septum that are %ordered %y muscle on three sides and

%y the pulmonary and the aortic !al!e annulus superiorly.

C. 6S*3 in its isolated form3 is the most commonly recogni2ed congenital heart defect.*. #he conduction %undle runs along the posteroinferior rim of a perimem%ranous 6S*.

ns,er- C*

*SC/SS0- Perimem%ranous 6S*s occupy the area of the mem%ranous portion of the inter!entricular

septum ad;acent to the anteroseptal commissure of the tricuspid !al!e. 0ften a remnant of the

mem%ranous portion of the inter!entricular septum (the mem%ranous flap) is left hanging on the

posteroinferior rim of the defect. #he annulus of the tricuspid and aortic !al!es often form a part of the

rim of the defect3 %ut in some patients they are separated from the 6S* %y a thin rim of muscle tissue that

protects the conduction %undle. Muscular 6S*s ha!e e8clusi!ely muscular rims on all four sides. 6S*s

in the outlet septum that e8tend to the annuluses of the aortic and pulmonary !al!es are called dou%ly

committed or ;u8ta$arterial defects. solated 6S*s occur at an appro8imate rate of 4 per 1''' li!e %irthsand represent &' to :' of all congenital heart malformations at %irth. #he conduction %undle in

patients ,ith perimem%ranous 6S*s does run along the posteroinferior rim of the defect on the left

!entricular side. Sutures used for repair of a perimem%ranous 6S* should %e placed ,ell a,ay from this

area to a!oid the creation of surgically induced complete heart %loc9.

41. Which of the follo,ing statements a%out 6S*s is@are true?

. When coarctation of the aorta is associated ,ith 6S*3 it most commonly occurs in infants ,ith largelesions ,ho ha!e to undergo repair %efore age & months.

". n some patients ,ith 6S*3 aortic !al!e incompetence de!elops o!er time and progresses.C. n the /nited States dou%ly committed or ;u8ta$arterial 6S*s are most commonly associated ,ith

aortic insufficiency.

*. P* is present in appro8imately one fourth of infants ,ith a 6S* and concomitant congesti!e heart

failure.

ns,er- "*


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*SC/SS0- 6S* in com%ination ,ith se!ere coarctation of the aorta occurs in appro8imately 1B of

patients. #his com%ination is more common among infants ,ith large 6S*s undergoing operation %efore

age & months. ortic !al!e incompetence does de!elop o!er time in some patients ,ith 6S*3 presuma%ly

as a result of progressi!e prolapse of the right aortic cusp through the defect. n the /nited States t,o

thirds of patients ,ith 6S* and aortic insufficiency ha!e perimem%ranous lesions and one third ha!e adou%ly committed or ;u8ta$arterial lesion. n Fapan3 ho,e!er3 the re!erse is true- t,o thirds ha!e dou%ly

committed or ;u8ta$arterial lesions and one third ha!e perimem%ranous lesions. moderate$ or large$si2ed P* is associated ,ith 6S* in appro8imately of patients of all ages> ho,e!er3 in infants ,ith

6S* and concomitant congesti!e heart failure3 P* is present in appro8imately 4+.

44. Which of the follo,ing statements a%out 6S* is@are correct?

. large 6S* is appro8imately the si2e of the pulmonary !al!e orifice or larger.

". =arge 6S*s associated ,ith high pulmonary %lood flo, result in an enlarged left atrium on chest 8$

ray.

C. Patients ,ith small (restricti!e) 6S*s tend to ha!e normal right !entricular and pulmonary arterial

pressures ,ith normal pulmonary !ascular resistance and no e!idence of pulmonary !ascular disease.*. pulmonary !ascular resistance greater than 1' to 14 units per s7. m. is considered a contraindication

to operation.

ns,er- "C*

*SC/SS0- large 6S* is appro8imately the si2e of the aortic !al!e orifice or larger and causes

systemic right !entricular systolic pressures. n the a%sence of right !entricular outflo, tract o%struction3

the pulmonary artery systolic pressure ,ill also %e systemic in the presence of a large 6S*. =arge 6S*s

associated ,ith a high pulmonary %lood flo, do result in an enlarged left atrium %ecause of increased

pulmonary !enous return. When mar9ed enlargement of the left atrium is present in a patient suspected of

ha!ing a 6S*3 the presence of coe8isting mitral !al!e regurgitation should also %e considered. Patients

,ith small 6S*s do ha!e normal right !entricular and pulmonary arterial pressures. #here is only a slightele!ation of pulmonary %lood flo, relati!e to the systemic flo,3 and the pulmonary !ascular resistance is

normal ,ithout e!idence of pulmonary !ascular disease. t any age3 the presence of pulmonary !ascular

disease so se!ere that the pulmonary !ascular resistance is fi8ed and greater than 1' to 14 units per s7. m.

is considered a contraindication to operation.

4&. Which of the follo,ing statements a%out 6S*s is@are correct?

. Spontaneous closure of 6S*s occurs in 4+ to +' of patients during childhood.". #achypnea and failure to thri!e are symptoms fre7uently associated ,ith large 6S*s.

C. Patients ,ith normal pulmonary !ascular resistance and left$to$right shunting across the 6S* ha!e5isenmengerAs comple8.

*. Patients ,ith a large 6S* and lo, pulmonary !ascular resistance can present ,ith a middiastolic

murmur at the ape8.

ns,er- "*

*SC/SS0- Spontaneous and complete closure of 6S*s3 e!en large ones3 has %een estimated to occur

in 4+ to +' of patients during childhood. #he pro%a%ility of e!entual spontaneous closure is in!ersely


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related to the age at ,hich the patient is o%ser!ed. #achypnea3 poor feeding3 gro,th failure3 recurrent

respiratory infections3 e8ercise intolerance3 and se!ere cardiac failure may de!elop in patients ,ith large

6S*s. Patients ,ith 5isenmengerAs comple8 are cyanotic3 polycythemic3 and se!erely limited in their

e8ercise tolerance3 o,ing to mar9edly ele!ated pulmonary !ascular resistance associated ,ith a

predominantly right$to$left shunt across the 6S*. middiastolic murmur can %e present at the ape8 in patients ,ith a large 6S* associated ,ith lo, pulmonary !ascular resistance. #his indicates high

pulmonary %lood flo, ,ith a large flo, across the mitral !al!e into the left !entricle.

4:. Which of the follo,ing is@are true of the surgical treatment of 6S*s?

. right !entricular approach is employed for the repair of most perimem%ranous 6S*s.

". ntracardiac repair is ad!isa%le for patients ,ith intracta%le symptoms and for asymptomatic infants

,ith e!idence of increasing pulmonary !ascular resistance.

C. Complete heart %loc9 is a common complication.

*. ospital mortality after repair of 6S* in infants approaches 4'.

ns,er- "

*SC/SS0- #he right atrial approach is preferred for the repair of most perimem%ranous 6S*s.

Prompt intracardiac repair is indicated for infants ,ith large defects3 large shunts3 and pulmonary

hypertension ,ho present ,ith intracta%le left !entricular failure3 recurrent pulmonary infections3 se!eregro,th failure3 or e!idence of increasing pulmonary !ascular resistance. n the modern era3 complete

heart %loc9 re7uiring a permanent pacema9er is a !ery uncommon complication of surgical closure of a

!entricular septal defect. ospital mortality after closure of a 6S* currently approaches 2ero. While in

earlier years younger age ,as an incremental ris9 factor for hospital death in some surgical e8periences3

this ris9 has %een neutrali2ed during the past decade.

4+. #etralogy of Gallot consists of all of the follo,ing features e8cept-

. S*.

". 6S*.

C. *e8troposition of the aorta.

*. Pulmonary stenosis.5. Right !entricular hypertrophy.

ns,er-

*SC/SS0- lthough S* is a fre7uent component of tetralogy of Gallot3 it ,as not included %y

Gallot as part of his classic tetralogy. 0ccasionally3 the inclusion of an S* prompts use of the term pentalogy of Gallot. #he other four anomalies listed ,ere all mentioned %y Gallot in his original

description of this defect.

4. Which of the follo,ing has the greatest impact on the physiology of tetralogy of Gallot?

. #he si2e of the S*.

". #he si2e of the 6S*.

C. #he degree of pulmonary stenosis.

*. #he amount of aortic o!erriding.

ns,er- C


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*SC/SS0- #he 6S* in tetralogy of Gallot is nonrestricti!e3 and therefore its si2e does not affect the

degree of shunting that can occur. =i9e,ise3 an S*3 ,hich may or may not %e a component of tetralogy

of Gallot3 can pro!ide right$to$left shunting at the atrial le!el %ut is not the main contri%utor to thecyanosis of this disease. #he degree of right$to$left shunt across the 6S* is dictated %y the !aria%le

compliance of the do,nstream cham%ers3 and the increased resistance imposed %y se!ere pulmonarystenosis creates greater amounts of right$to$left shunting and3 therefore3 more intense cyanosis. #he

position of the aorta in relation to the 6S* is not important as long as no su%aortic o%struction e8ists.

4B. Which of the follo,ing anomalies is not associated ,ith tetralogy of Gallot?

. %sence of the left pulmonary artery.

". right aortic arch.

C. retroesophageal su%cla!ian artery.

*. nomalous origin of the left anterior descending coronary artery from the right coronary artery.

5. Primary pulmonary hypertension.ns,er- 5

*SC/SS0- #he first four defects listed occasionally are associated ,ith tetralogy of Gallot. rightaortic arch is seen in 4+ of patients ,ith that lesion. nomalous coronary arteries or a retroesophageal

su%cla!ian artery are found in as many as + to 1' of patients. %sence of a pulmonary artery is

unusual %ut can present in as many as & of patients. Pulmonary hypertension is distinctly unusual ,ith

tetralogy of Gallot unless the patient has had e8cessi!e pulmonary %lood flo, from collaterals or

systemic$to$pulmonary artery shunts for a long time. t is %ecause these patients usually do not ha!e

pulmonary hypertension that infant correction ,ith transannular patches can %e performed ,ith such great

success.

4. Surgical treatment of a patient ,ith tetralogy of Gallot can include any of the follo,ing e8cept-

. Maintenance of ductal patency ,ith prostaglandins (PE5 1) to pro!ide pulmonary %lood flo, ,hile

the %a%y is transferred to an institution e7uipped to pro!ide more definiti!e therapy.". "anding of the pulmonary artery in an acyanotic patient ,ith tetralogy of Gallot to control pulmonary

%lood flo, and pre!ent the de!elopment of pulmonary hypertension.

C. Placement of a su%cla!ian$to$pulmonary artery shunt on the side opposite the aortic arch in a &$day$old

infant ,ith se!ere cyanosis.*. Closure of the 6S* and transannular patching of the right !entricle onto the main pulmonary artery in

a 4$day$old infant.ns,er- "

*SC/SS0- Patients ,ith tetralogy of Gallot ,ho do not appear cyanotic still ha!e mild arterial

hypo8emia %y arterial %lood gas determination. Patients ,ith tetralogy of Gallot rarely ha!e e8cessi!e

pulmonary %lood flo,3 and the de!elopment of pulmonary hypertension is not a concern in this

population. "anding of the pulmonary artery is ne!er a consideration in patients ,ith tetralogy of Gallot3

since the predominant physiologic effect of the defect results from too little pulmonary %lood flo, to


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%egin ,ith. cyanotic patients ,ith tetralogy of Gallot (Hpin9 tetsI) can usually %e follo,ed for se!eral

months and their defects repaired electi!ely as a first$stage procedure (usually %y age months). ll of

the other therapies are appropriate treatment for %a%ies ,ith tetralogy of Gallot. Prostaglandins maintain

patency of the ductus arteriosus3 pro!iding an anatomic systemic$to$pulmonary artery shunt that sustains

pulmonary %lood flo, until a more permanent surgical solution can %e pro!ided. #he ad!ent of prostaglandin therapy has ena%led numerous critically ill infants to %ecome sta%ili2ed enough to reach a

tertiary care institution and recei!e proper surgical therapy ,ho might not other,ise ha!e sur!i!ed had itnot %een for the a%ility of pulmonary %lood flo, to %e maintained through the re!ersal of duct closing.

#he choice of palliati!e shunting or total anatomic correction rests largely ,ith the e8perience and s9ill of

the surgical team and is dictated in part %y the anatomy of the pulmonary arteries. 5ither of these options

is accepta%le.

4D. #he predominant determinant of outcome for patients ,ith pulmonary atresia and an intact !entricular

septum re!ol!es around-

. #he si2e of the S*.

". #he %a%yAs age at presentation.C. #he si2e of the right !entricular ca!ity and tricuspid !al!e.

*. #he presence of a tricuspid


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*SC/SS0- 6S* is usually present in patients ,ith dou%le$outlet right !entricle and is the only

outlet from the left !entricle. "oth great arteries may arise totally from the right !entricle3 or one or %oth

may o!erlie the !entricular septum immediately a%o!e the 6S*. #o categori2e the heart as ha!ing a

dou%le$outlet right !entricle3 more than +' of each great artery must arise from the right !entricle. n the

#aussig$"ing type of dou%le$outlet right !entricle3 the 6S* is related to the pulmonary !al!e annulus andis termed a su%pulmonary defect. dditional morphologic characteristics peculiar to this entity ha!e %een

descri%ed. Most patients ,ith dou%le$outlet right !entricle and a su%aortic 6S* ha!e concomitant pulmonary stenosis that protects the lungs from pulmonary !ascular disease and also results in a clinical

course similar to that of patients ,ith tetralogy of Gallot. n the a%sence of pulmonary stenosis the

presentation3 clinical course3 and natural history of the #aussig$"ing malformation are similar to those of

transposition of the great arteries ,ith 6S*. Cyanosis is present3 usually from %irth3 since streaming

directs the desaturated systemic !enous return to,ard the aorta and the o8ygenated left !entricular %lood

to,ard the pulmonary artery. #hese patients tend to de!elop early congesti!e heart failure and can

de!elop se!ere pulmonary !ascular disease early in life. #hey usually e8perience symptoms ,ithin the

first fe, months of life.

&1. Which of the follo,ing statements a%out the surgical repair of dou%le$outlet right !entricle are true?

. n dou%le$outlet right !entricle ,ith a su%aortic or dou%ly committed 6S*3 a tunnel$type repair

connecting a committed 6S* ,ith its respecti!e great artery is usually employed.

". Repair of the #aussig$"ing malformation can %e accomplished using an intra!entricular tunneltechni7ue or %y performing a straight patch closure of the 6S* com%ined ,ith an arterial s,itch

procedure.

C. #he hospital mortality rate is highest ,hen a su%aortic 6S* is present.

*. Some hearts ,ith dou%le$outlet right !entricle and a noncommitted 6S* must %e repaired using a

modification of the Gontan procedure.

ns,er- "*

*SC/SS0- When the 6S* is su%aortic or dou%ly committed3 the tunnel$type repair connects the left

!entricle !ia the 6S* and tunnel to the aorta. #he #aussig$"ing malformation can %e repaired using an

intra!entricular tunnel techni7ue descri%ed %y Ja,ashima. #his repair can %est %e accomplished ,hen the

great arteries are in a more or less side$%y$side relationship ,ith the aorta to the right of the pulmonary

artery. #he infundi%ular septum is generously resected and the 6S* is connected to the aorta %y an

intra!entricular tunnel that runs posterior to the pulmonary artery. #he most common approach for therepair of the #aussig$"ing malformation in!ol!es patch closure of the 6S* to the pulmonary artery. #his

creates transposition of the great arteries ,ith an intact inter!entricular septum. n arterial s,itch

procedure then esta%lishes !entriculoarterial concordance. 0f all the types of dou%le$outlet right !entricle

the hospital mortality is lo,est ,hen a su%aortic or dou%ly committed 6S* is present. *ou%le$outlet right!entricle is associated ,ith a noncommitted 6S* in appro8imately 1' of patients in surgical series. #he

repair of this su%set of patients is associated ,ith a relati!ely high mortality3 as compared ,ith the resultso%tained after repair of other forms of dou%le$outlet right !entricle. t times3 %ecause of the remote

location of the 6S* and %ecause of other compelling anatomic features3 complete repair cannot %e

performed. n this case3 a modification of the Gontan procedure must %e employed.


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&4. Management of a patient ,ith tricuspid atresia ,ithin the first month of life may include-

. Creation of a systemic arteryKtoKpulmonary artery shunt.

". 0%ser!ation.

C. Creation of a %idirectional superior ca!opulmonary anastomosis.

*. Pulmonary artery %anding.5. Gontan procedure.

ns,er- "*

*SC/SS0- nitial management of ne,%orn infants ,ith tricuspid atresia is determined %y the

anatomic and physiologic factors that affect the %alance of pulmonary and systemic %lood flo,. nfants

,ith se!erely limited pulmonary %lood flo, and arterial o8ygen saturations of less than B' should %e

sta%ili2ed ,ith PE5 1 to maintain patency of the ductus arteriosus until a systemic$to$pulmonary artery

shunt can %e performed. Patients ,ith uno%structed pulmonary %lood flo, may e8hi%it only mild cyanosis

%ut suffer from significant congesti!e heart failure. Many of these patients are %est managed %y

pulmonary artery %anding to decrease the !olume o!erload on the left !entricle and to pre!ent the early

de!elopment of irre!ersi%le pulmonary !ascular disease. Some patients ,ith moderate restriction of

pulmonary %lood flo, may ha!e %alanced deli!ery of %lood to the systemic and the pulmonary

circulation. #hese patients can %e carefully follo,ed until such time as an im%alance de!elops or they %ecome candidates for a %idirectional superior ca!opulmonary (Elenn) anastomosis or a Gontan

procedure. #he normally high pulmonary !ascular resistance present in the first month of life precludes

the performance of either the Elenn or the Gontan procedure in the ne,%orn.

&&. Which of the follo,ing should contraindicate performance of the Gontan procedure?

. Patient age of 4+ years.

". Se!ere mitral insufficiency.

C. =eft !entricular end$diastolic pressure of 1 mm. g.

*. Right pulmonary artery stenosis.5. Pulmonary !ascular resistance of Woods units.

ns,er- C5

*SC/SS0- Eood !entricular function and lo, pulmonary !ascular resistance are essential

re7uirements for a successful Gontan procedure. #he Gontan operation should not %e performed ,hen!entricular e;ection fraction is less than &' or !entricular end$diastolic pressure is greater than 1+ mm.

g. Pulmonary !ascular resistance in e8cess of : Woods units should also %e considered an a%solute

contraindication for Gontan correction. ge at the time of Gontan procedure does not appear to %e a ma;or

ris9 factor3 e8cept %efore age 4 years. lthough patients ,ho ha!e sur!i!ed into the third or fourth decadeare li9ely to ha!e !entricular dysfunction3 a Gontan procedure can %e performed successfully in these

older patients if !entricular function and pulmonary !ascular resistance meet the a%o!e criteria. n patients ,ith tricuspid atresia a competent mitral !al!e is important for satisfactory cardiac output after

the Gontan procedure. #he presence of se!ere mitral insufficiency3 ho,e!er3 should not necessarily

contraindicate the procedure. n these cases it is recommended that the mitral !al!e %e repaired or

replaced in com%ination ,ith the creation of a %idirectional superior ca!opulmonary anastomosis.

completion Gontan operation is performed later. *istorted or stenosed pulmonary arteries are common

se7uelae of systemic$to$pulmonary artery shunts and may result in unsatisfactorily high pulmonary

!ascular resistance. n most cases3 these stenoses can %e repaired at the time of Gontan correction or ,ith

a %idirectional superior ca!opulmonary anastomosis.


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&:. nitial management of a ne,%orn infant ,ith hypoplastic left heart syndrome should include-. ntra!enous administration of PE5 1.

". Supplemental o8ygen.C. Routine intu%ation and mechanical !entilation to achie!e a PC0 4 %et,een &' and &+ mm. g.

*. Cardiac catheteri2ation and %alloon atrial septostomy.

ns,er-

*SC/SS0- Postnatal sta%ili2ation of infants ,ith hypoplastic left heart syndrome re7uires patency of

the ductus arteriosus and %alance of the systemic and the pulmonary circulation. "ecause the ductus is the

only path,ay from the right !entricle to the systemic circulation3 duct patency must %e maintained ,ith

intra!enous PE5 1. #o minimi2e the ,or9load on the single !entricle and ensure ade7uate deli!ery of

o8ygen to the tissues3 an e7ual deli!ery of %lood to %oth the lungs and the %ody is sought. #he normal

postnatal decrease in pulmonary !ascular resistance often results in o!erperfusion of the pulmonary

circulation and underperfusion of the systemic circulation. Maneu!ers that further decrease pulmonary!ascular resistance3 such as the addition of supplemental o8ygen3 lo,ering the PC0 4 to less than &+ mm.

g3 or eliminating any resistance at the atrial septum %y %alloon septostomy only ,orsens the im%alance.

&+. #he performance of a %idirectional superior ca!opulmonary (Elenn) anastomosis as the second stage

in the reconstructi!e approach to hypoplastic left heart syndrome-

. Pro!ides early relief of !olume load on the single right !entricle.

". ncreases peripheral o8ygen saturations to greater than D'.

C. Permits concomitant repair of pulmonary artery or aortic arch stenoses.

*. mpro!es mortality and mor%idity of su%se7uent Gontan procedure.ns,er- C*

*SC/SS0- fter the first$stage reconstructi!e (or,ood) procedure3 the circulation is inherently

inefficient %ecause of the o%ligatory recirculation of a portion of %oth saturated and desaturated %lood.

Closure of the arterial shunt and creation of a %idirectional Elenn anastomosis eliminates this inefficient

recirculation and significantly diminishes the !olume load on the single right !entricle. *istorted and

stenosed central pulmonary arteries or aortic arch o%structions should %e repaired at the same time the %idirectional Elenn procedure is performed. n almost all series the mortality of the Gontan procedure has

decreased since the adoption of the three$stage approach for hypoplastic left heart syndrome. "ecause

systemic and pulmonary !enous %lood continue to mi8 in the right atrium after a %idirectional Elenn

procedure3 cyanosis persists ,ith peripheral o8ygen saturations %et,een B+ and +.

&. Which of the follo,ing statements a%out truncus arteriosus are true?

. Most infants sur!i!e ,ithout operations until late childhood.

". Most infants present ,ith cyanosis.

C. Most infants present ,ith congesti!e heart failure.

*. Repair re7uires a conduit from right !entricle to pulmonary arteries.

ns,er- "C*


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*SC/SS0- While an occasional child sur!i!es to age & or : years3 ,ithout either palliati!e or totally

correcti!e surgical treatment fe, li!e past early infancy. #he lesion is one of e8cessi!e pulmonary %lood

flo, %ecause of the origin of the pulmonary arteries from the truncus arteriosus> physiologically3 the pulmonary arteries arise directly from the aorta. lthough the aortic saturation can ne!er %e 1''

%ecause of some element of %idirectional shunting at the 6S*3 the physiologic manifestations arecongesti!e heart failure and e8cessi!e pulmonary %lood flo, rather than cyanosis. #he congesti!e heart

failure %ecomes se!ere as pulmonary !ascular resistance drops. f congesti!e heart failure later impro!es

spontaneously3 it is %ecause of the de!elopment of pulmonary !ascular disease. Complete repair al,ays

re7uires closure of the 6S*3 detachment of the pulmonary arteries from the common trun93 and re$

esta%lishment of an outflo, tract from the right !entricle to the pulmonary artery. #his conduit usually

contains a !al!e and can %e either a homograft or a synthetic conduit containing a porcine !al!e.

&B. #runcus arteriosus is a diagnosis ,ith anatomic components including-

. 6S*.". %normal origin of pulmonary arteries.

C. Su%aortic stenosis.

*. Single !entricular outflo, !al!e.

ns,er- "*

*SC/SS0- "y definition3 a 6S* is al,ays present immediately %eneath the truncal !al!e. #he

pulmonary arteries arise a%normally from the single trun93 ,hich is due to failed partitioning of the

em%ryonic conus during the first fe, ,ee9s of fetal de!elopment. n the classification of Collett and

5d,ards3 #ype truncus arteriosus has a single arterial trun9 gi!ing rise to an aorta and a main pulmonary

artery> in #ype the right pulmonary arteries arise immediately ad;acent to one another from the dorsal

,all of the truncus> in #ype the right and left pulmonary arteries originate from either side of thetruncus> and in #ype 6 the pro8imal pulmonary arteries are a%sent and pulmonary %lood flo, is %y ,ay

of ma;or aortopulmonary atresia and is no longer considered truncus arteriosus. Su%aortic stenosis cannot

occur in this anomaly. #he single !entricular outflo, !al!e is the truncal !al!e. t may contain from t,o

to si8 cusps3 %ut most often there are three and3 ne8t most often3 four.

&. 0ptimal treatment for the neonate ,ho presents ,ith transposition of the great arteries LS3*3*N and

intact !entricular septum includes-. PE5 1 infusion to maintain duct patency.

". dministration of intra!enous fluid to increase intra!ascular !olume.C. yper!entilation to decrease pulmonary resistance.

*. 08ygen administration to increase arterial o8ygen tension.

5. trial %alloon septostomy to impro!e atrial mi8ing.

ns,er- "5

*SC/SS0- "ecause ,ith transposition of the great !essels the systemic and the pulmonary

circulations e8ist in parallel rather than in series3 sur!i!al depends on mi8ing %et,een pulmonary and


16/64


17/64

*SC/SS0- #he atrial repair of transposition of the great arteries


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*SC/SS0- #he ma;ority of older children ,ith aortic stenosis and significant trans!al!ular gradients

can %e treated successfully %y aortic !al!otomy. #his can %e done percutaneously ,ith %alloon dilatation

or surgically ,ith direct !isuali2ation of the aortic !al!e and incision of the fused commissures. ortic

!al!e replacement is rarely necessary as a primary procedure %ut may %e re7uired in children ,ho

de!elop progressi!e aortic insufficiency after a pre!ious inter!ention. When !al!e replacement is performed it is desira%le to insert the largest prosthesis possi%le3 to allo, for gro,th. 5nlargement of the

aortic annulus is commonly performed for this purpose. f a true !al!e prosthesis is employed3 amechanical !al!e is preferred. *ura%ility of 8enograft !al!es in children is limited o,ing to early

calcification and leaflet degeneration. #he pulmonary autograft techni7ue may %e the %est method of

aortic !al!e replacement in children. With this operation the patientAs o,n pulmonary !al!e is transferred

to the aortic position and a pulmonary allograft is inserted to replace the pulmonary !al!e. lthough the

pulmonary autograft may not achie!e the long$term dura%ility of a mechanical !al!e3 the patient does not

face the long$term complications of throm%oem%olism and %leeding imposed %y a mechanical !al!e and

lifelong anticoagulation.

:&. Which of the follo,ing statements a%out su%!al!ular aortic stenosis are true?. Most patients present in early infancy ,ith se!ere congesti!e heart failure.

". n e;ection clic9 is a specific physical sign of su%aortic stenosis.

C. #he su%aortic mem%rane is approached surgically !ia the aorta and aortic !al!e.

*. concomitant septal myectomy decreases the incidence of recurrent su%aortic stenosis.ns,er- C*

*SC/SS0- Su%aortic stenosis is rarely encountered in neonates. Most often it is disco!ered in an

asymptomatic child during a routine physical e8amination. loud crescendoKdecrescendo systolic

murmur ,ithout an e;ection clic9 is usually noted. #he presence of an e;ection clic9 is more consistent

,ith isolated !al!ular aortic stenosis. *iscrete su%aortic stenosis is approached surgically ,ith

cardiopulmonary %ypass3 aortic cross$clamping3 and cardioplegic arrest. #he aorta is opened and theaortic !al!e leaflets are retracted3 e8posing the fi%rous mem%rane. #he fi%rous ring is carefully e8cised3

ta9ing care to a!oid in;ury to the anterior leaflet of the mitral !al!e and the penetrating conduction

%undle. 0nce the su%aortic mem%rane is e8cised a septal myectomy further opens the left !entricular

outflo, tract and diminishes the li9elihood of recurrent su%aortic stenosis.

::. Management of hypertrophic o%structi!e cardiomyopathy may include-

. Propranolol and !erapamil.". ortic !al!e replacement.

C. *ual$cham%er se7uential pacing.*. Com%ined septal myectomy and mitral !al!e plication.

ns,er- C*

*SC/SS0- #he ma;ority of patients ,ith hypertrophic o%structi!e cardiomyopathy are treated

medically ,ith %eta$%loc9ers such as propranolol and calcium channel %loc9ers such as !erapamil.

Patients ,hose symptoms do not respond to medical therapy are treated surgically ,ith a transaortic

septal myectomy. Recent reports indicate that simple plication of the anterior leaflet of the mitral !al!e


19/64

performed in addition to the septal myectomy further opens the left !entricular outflo, tract %y

eliminating systolic anterior motion of the mitral !al!e. ortic !al!e replacement is not an appropriate

treatment for hypertrophic o%structi!e cardiomyopathy. Some patients ,ho are poor surgical candidates

may e8perience relief of symptoms and left !entricular outflo, gradients ,ith dual$cham%er permanent

pacing. ppropriate pre$e8citation of the !entricular septum can prompt the septum to mo!e a,ay fromthe left !entricular ,all during systole and open the outflo, tract.

:+. Which of the follo,ing statements a%out supra!al!ular aortic stenosis are true?

. Surgical repair is indicated only ,hen the systolic gradient e8ceeds B+ mm. g.

". Simple e8cision of the supra!al!ular mem%rane results in satisfactory relief of the stenosis in most

patients.

C. #he diffuse form of supra!al!ular aortic stenosis may cause o%struction to %ranches of the aortic arch.

*. Reoperation after repair of discrete supra!al!ular aortic stenosis is rare unless a%normalities of the

!al!e itself also e8ist.

ns,er- C*

*SC/SS0- Supra!al!ular aortic stenosis is a progressi!e disease and should %e repaired surgically if

symptoms are present or the systolic gradient e8ceeds +' mm. g. n addition to e8cision of the

supra!al!ular mem%rane3 a patch of dacron or pericardium must %e placed across the area of narro,ingand do,n into at least one of the sinuses of 6alsal!a. Reoperation is rare after this procedure unless

associated aortic !al!e disease is also present. n the diffuse form of the disease the thic9ening of the

aortic ,all commonly results in significant luminal narro,ing of the ascending aorta and its ma;or

%ranches.

:. 5ach year the appro8imate num%er of mericans ,ho die from complications of coronary artery

disease is-

. 1''3'''.

". 4+'3'''.

C. +''3'''.

*. 13'''3'''.5. 0!er 43'''3'''.

ns,er- C

*SC/SS0- t is estimated that appro8imately B3'''3''' mericans currently ha!e symptomatic

coronary artery disease. 0f these some 13+''3''' e8perience myocardial infarction annually andappro8imately +''3''' die each year from complications.

:B. Which of the follo,ing arteries is most li9ely to %e in!ol!ed ,ith serious atherosclerosis?

. #he right coronary artery.

". #he left coronary artery.

C. #he anterior descending coronary artery.

*. #he circumfle8 coronary artery.

ns,er- C


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*SC/SS0- n order of fre7uency3 the anterior descending coronary artery is the most commonly

in!ol!ed ,ith atherosclerosis3 follo,ed %y the right coronary3 the circumfle83 and the left main coronary

artery.

:. Which of the follo,ing statements a%out collaterals in the normal coronary circulation is true?

. #here is a rich and 7uite effecti!e collateral circulation in the coronary arterial %ed.

". #he coronary arterial %ed has minimal effecti!e collaterals.

C. #he coronary arterial %ed is an a%solute e8ample of anatomic end$arteries.

ns,er- "

*SC/SS0- #he collateral circulation to the heart is relati!ely poor. n the human heart there are fe,

natural collaterals of sufficient diameter for deli!ery of a significant 7uantity of %lood. Most of the

collaterals are appro8imately 4'' mm. or smaller3 and channels of this si2e cannot conduct significant7uantities of %lood for cardiac re7uirements. #here is no a%solute e8ample of anatomic end$arteries in

humans. While the magnitude of arterial collateral circulation !aries considera%ly3 all organs ha!e some

collaterals.

:D. f %lood entering the normal arterial circulation of the heart is 1'' saturated ,ith o8ygen3 o8ygen

saturation of %lood in the coronary sinus can %e e8pected to %e appro8imately-

. B+.

". '.

C. +'.*. &+.

5. =ess than 4'.

ns,er- *

*SC/SS0- #he heart has an unusually high rate of o8ygen utili2ation and consumes appro8imatelyt,o thirds of the o8ygen in the arterial %lood. #he o8ygen saturation of the %lood in the coronary sinus is

usually a%out &' to &+ and !aries ,ith the magnitude of cardiac disease. #he %ody as a ,hole e8tracts

appro8imately 4+ of the o8ygen it recei!es3 thus emphasi2ing the great need of the heart for o8ygen at

rest as ,ell as at e8ercise.

+'. Coronary %ypass procedures ha!e %een demonstrated to-

. Reduce the incidence of myocardial infarction.

". Significantly relie!es angina symptoms.

C. Statistically impro!e the life span.

*. mpro!e the e;ection fraction of the left !entricle in many patients in ,hom it is significantly

depressed preoperati!ely.

ns,er- "C*


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*SC/SS0- n a !ariety of studies3 coronary %ypass procedures ha!e %een demonstrated to reduce the

incidence of su%se7uent myocardial infarction as ,ell as to relie!e significantly anginal symptoms. #hey

also impro!e the life span of most patients as ,ell as the e;ection fraction of the left !entricle in those in,hom it ,as depressed preoperati!ely.

+1. #he follo,ing patients are %est treated ,ith coronary artery %ypass grafting (C"E)-

. '$year$old man ,ith class angina3 B+ pro8imal right coronary artery lesion3 and normal

!entricular function.

". '$year$old man ,ith unsta%le angina3 three$!essel disease3 and an e;ection fraction of &+.

C. '$year$old nondia%etic man ,ith class angina symptoms and focal discrete lesions in the mid$

right coronary artery and mid$left circumfle8 artery.

*. '$year$old man ,ith dia%etes3 class 6 angina3 B+ pro8imal left anterior descending and B+

pro8imal right coronary artery o%struction3 and left !entricular e;ection fraction of '.

ns,er- "*

*SC/SS0- C"E has %een sho,n to prolong patient sur!i!al compared ,ith medical therapy in

those patients ,ith left main occlusi!e disease and those ,ith three$!essel or t,o$!essel disease ,ith pro8imal left anterior descending in!ol!ement in association ,ith class or greater anginal symptoms3

impaired e;ection fraction3 or easily induci%le ischemia ,ith e8ercise. lthough percutaneous

transluminal coronary angioplasty (P#C) appears to %e compara%le to C"E in nondia%etic patients3

patients ,ith dia%etes appear to ha!e a significant sur!i!al ad!antage ,hen C"E is used. Similarly3

patients ,ith more e8tensi!e coronary artery disease are %etter treated ,ith C"E than ,ith P#C.

+4. Sternal ,ound infections that spread to the mediastinum are associated ,ith a mortality rate of-

. '.

". &'.

C. 4+.

*. =ess than 1+.ns,er- *

*SC/SS0- lthough the mortality rate follo,ing sternal infections ,ith mediastinitis formerly ,as

high3 it is no, greatly reduced. n most series3 mediastinitis is cured in more than D' of patients ,ho are

treated aggressi!ely ,ith dO%ridement and placement of muscle flaps or omentum into the mediastinum tospeed ,ound healing.

+&. Perioperati!e myocardial infarction occurs follo,ing coronary %ypass procedures in appro8imately-

. 1+.

". 1'.

C. B.

*. =ess than +.

ns,er- *


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*SC/SS0- Gollo,ing impro!ements in myocardial protection and coronary grafting techni7ues3

perioperati!e myocardial infarction no, occurs in less that 4 to : of patients in most series.

+:. Gollo,ing acute myocardial infarction3 !entricular septal defects occur in-

. 4'.

". 1'.

C. 1+

*. 4 or less.

ns,er- *

*SC/SS0- Postmortem studies indicate that to 1' of fatal cases of myocardial infarction are

due to rupture of the heart. n addition3 infarction of the inter!entricular septum ,ith su%se7uent

formation of a !entricular septal defect occurs in 1 to 4 of patients ,ith acute myocardial infarction.#he usual inter!al %et,een the acute infarction and septal rupture


23/64

+B. Which of the follo,ing statements a%out patients treated %y placement of an internal mammary artery

(M) %ypass graft at primary C"E is@are correct?

. #he ris9 for mor%idity and mortality from reoperati!e coronary %ypass grafting is increased.

". =eft !entricular function is %etter preser!ed at the time of reoperation.

C. #he ris9 of sternal ,ound complications is greatly increased if the contralateral M is har!ested at thetime of reoperation.

*. light clamp should %e applied to the M pedicle to limit cardiac ,arming during cardioplegic arrestat the time of reoperation.

5. functional study demonstrating a large portion of myocardium at ris9 should %e o%tained %efore

reoperation.

ns,er- "*5

*SC/SS0- Patients ,ho ha!e an intact M graft should ha!e se!ere anginal symptoms and a

significant portion of myocardium at ris9 %efore reoperati!e coronary %ypass grafting is considered.

functional study may %etter define the proportion of myocardium at ris9 for ischemia and infarction.

Patients ,ith an intact M graft are less li9ely to re7uire reoperation3 %ut if stenosis distal to the M

and disease in other !ein grafts ha!e progressed or if a large portion of myocardium is at ris93 reoperation

is recommended. #he presence of an intact M is not a contraindication to reoperation> in fact3 this population of patients ha!e %etter$preser!ed !entricular function and are3 perhaps3 %etter candidates for

reoperation. Placement of an M graft at the time of the first operation ,as critically important3

neutrali2ing the ad!erse effects of ele!ated serum cholesterol3 hypertension3 and smo9ing on reoperation$

free sur!i!al. #he ris9 of damaging an intact M graft is & to +. lateral pro;ection of the M atcardiac catheteri2ation ,ill define its course3 particularly in relation to the sternum3 to allo, more careful

sternal re$entry. #he M should %e minimally dissected and a light clamp applied during cardioplegic

arrest to limit cardiac ,arming and impro!e myocardial protection. #he M may %e detached and

recycled if needed. #he use during reoperation of the contralateral M does not increase the ris9 of

sternal ,ound complications.

+. Considering the results of coronary reoperation in comparison to primary C"E3 choose the incorrect

statement-

. 0perati!e mor%idity and mortality are increased o!er those for primary C"E.

". Mortality most often stems from cardiac causes after reoperation.

C. Sur!i!al of patients after hospital discharge follo,ing coronary reoperation is nearly e7ui!alent tosur!i!al after primary C"E.

*. Compared to primary C"E3 return of anginal symptoms is delayed after reoperati!e C"E.

5. Myocardial protection and the ris9 of myocardial infarction in reoperation are complicated %y

increased noncoronary collaterals3 patent atherosclerotic saphenous !ein grafts3 and more diffuse coronaryatherosclerosis.

ns,er- *

*SC/SS0- #he mortality and mor%idity after reoperati!e C"E are appro8imately t,o to three

times that of primary C"E. n contrast to primary C"E3 ,here the ma;ority of deaths are a result of

failure of other organ systems3 B+ to + of deaths after reoperati!e C"E are due to cardiac causes.

#he increased ris9 of reoperation results from more ad!anced nati!e !essel disease3 a longer cross$clamp

time3 a longer cross$clamp time per graft3 a longer time to initiate cardiopulmonary %ypass3 and increased

%lood loss. #he increased fre7uency of pulmonary complications3 myocardial infarction3 neurologic


24/64

in;ury3 and death3 stems from the technical factors of reoperation and the characteristics of the patient

population. #echnical factors include difficulty in finding targets secondary to pericardial reaction and

more diffusely diseased !essels3 the ris9s of in;uring the heart or great !essels on sternal re$entry3

increased %lood loss and ris9 of re7uiring transfusion3 less a!aila%le conduit for %ypass3 and greater

difficulty in pro!iding optimal myocardial protection. Characteristics of this patient population thatincrease ris9s include ad!anced age and diminished !entricular function. While sur!i!al after reoperation

is nearly e7ui!alent to that after primary C"E3 angina symptoms return at t,ice the fre7uency in thefirst year after operation (:B !ersus 4') then return at a similar annual rate (4 to &).

+D. Which statements are correct comparisons of gated e7uili%rium and initial$transit radionuclide

measurements of left !entricular function?

. Eated e7uili%rium techni7ues pro!ide more accurate measurements of e;ection fraction than initial$

transit methods.

". =eft !entricular imaging time for a gated e7uili%rium study is at least 1' times that of an initial$transit

study.

C. "oth techni7ues re7uire the same radiopharmaceuticals.*. "oth techni7ues re7uire a %olus in;ection.

ns,er- "

*SC/SS0- "oth techni7ues are e7ually accurate for measuring left !entricular e;ection fraction. #he

left !entricular imaging time for gated e7uili%rium studies is at least 1' times that of initial$transit

radionuclide angiocardiography. nitial$transit techni7ues use data from fe,er than 1' heart%eats3 ,hereas

e7uili%rium studies re7uire more than 1'' heart%eats to ac7uire data ,ith similar information density. #he

initial$transit study can %e performed ,ith any radioacti!e su%stance3 %ut the gated e7uili%rium techni7ue

re7uires a radiopharmaceutical that remains ,ithin the %lood pool for imaging. #he initial$transit

radionuclide study re7uires a %olus in;ection3 %ut an e7uili%rium study can %e ac7uired up to se!eral hours

after in;ection and must %e ac7uired ,hile the tracer is at e7uili%rium.

'. #he radionuclide !aria%le that contains the greatest amount of prognostic information in patients ,ith

coronary artery disease is-. 58ercise e;ection fraction.

". Change in regional ,all motion from rest to e8ercise.

C. Ma8imal cardiac output during e8ercise.

*. Change in heart rate during e8ercise.ns,er-

*SC/SS0- #he e8ercise e;ection fraction is the single most important radionuclide !aria%le relating

to su%se7uent cardiac death or myocardial infarction3 and this single !aria%le contains ' of the

prognostic information in the test.


25/64

1. Which of the follo,ing statements a%out left !entricular aneurysm is@are correct?

. 6entricular aneurysms are commonly associated ,ith systemic arterial em%oli2ation.

". %sent collateral circulation in an area of myocardium supplied %y an acutely occluded artery fa!ors

aneurysm formation.

C. Postero%asal aneurysms are more common than those located in the anteroapical region.*. neurysm repair can impro!e associated cardiac !al!e dysfunction.

5. Persistent S# segment ele!ation after acute myocardial infarction suggests aneurysm formation.ns,er- "*5

*SC/SS0- #he mural throm%us fre7uently present on the endocardial surface of an aneurysm is

usually adherent and rarely em%oli2es. Collateral circulation3 ,hen present3 often pre!ents transmural

necrosis follo,ing arterial occlusion. Since the left anterior descending coronary artery is the !essel most

commonly occluded in patients ,ith !entricular aneurysms3 most of the aneurysms are anteroapical.

mpro!ements in !entricular contour and reduction in !entricular !olume accompany aneurysm repair.

lthough persistent ele!ation of S# segments follo,ing myocardial infarction is !ery suggesti!e of

aneurysm formation3 the diagnosis should %e confirmed %y more definiti!e tests.

4. Which of the follo,ing factors does@do not increase early mortality associated ,ith repair of left

!entricular aneurysm?. Class 6 cardiac status.

". Si2e of aneurysm.

C. Presence of left main coronary disease.

*. 5mergent operation.

5. =ocation of aneurysm.

ns,er- "5

*SC/SS0- Class 6 cardiac status and emergent operation %oth imply e8tensi!e myocardial damage

and in most reported series are associated ,ith increased operati!e mortality. Similarly3 the presence of

significant stenosis of the left main coronary artery increases the operati!e mortality of !irtually all

cardiac procedures. 0n the other hand3 neither the si2e of the aneurysm nor its location affect early

operati!e mortality3 despite the fact that posterior aneurysms are technically more difficult to repair and

are much less common.

&. #he most effecti!e medical therapy in ameliorating the symptoms of Ja,asa9iAs disease and

pre!enting the de!elopment of giant coronary artery aneurysms is administration of-. nti%iotics.

". nti!iral agents.

C. spirin.

*. Eamma glo%ulin.

5. Elucocorticoids.

ns,er- *


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*SC/SS0- Ja,asa9iAs disease is a multisystemic disorder of un9no,n cause and is the leading cause

of ac7uired heart disease in children in %oth Fapan and the /nited States. lthough many clinical aspects

of Ja,asa9iAs disease suggest an infectious agent3 the search for a single agent has %een unsuccessful>

neither anti%acterials nor anti!irals ha!e a role in the therapy of Ja,asa9iAs disease. #he goal of initial

therapy of Ja,asa9iAs disease is the reduction of inflammation3 including coronary and myocardialinflammation. fter the diagnosis of Ja,asa9iAs disease is secured3 patients are treated ,ith intra!enous

gamma glo%ulin and large doses of aspirin. Eamma glo%ulin3 4 gm. per 9g.3 is administered as a singleinfusion o!er 14 hours. #reatment ,ith intra!enous immune glo%ulin has %een sho,n to decrease the

duration of fe!er3 to decrease the pre!alence of cardio!ascular complications3 and to pre!ent the

progression to giant coronary aneurysms. igh$dose aspirin therapy contri%utes to the resolution of the

acute manifestations of Ja,asa9iAs disease. When Ja,asa9iAs disease is diagnosed3 children are gi!en a

regimen of aspirin3 1'' mg. per 9g. per day3 ,hich is continued until defer!escence. #hereafter3 they are

maintained on small doses of aspirin3 & to + mg. per 9g. per day3 for ,ee9s. #he goal of aspirin therapy

is amelioration of symptoms and pre!ention of the throm%otic and em%olic complications of Ja,asa9iAs

disease. spirin does not decrease the ris9 of the de!elopment of coronary aneurysms. #here is no role for

glucocorticoids in the treatment of Ja,asa9iAs disease.

:. ndications for surgical inter!ention in Ja,asa9iAs disease include ,hich of the follo,ing?

. #he presence of multiple coronary artery aneurysms.

". Myocardial infarction and se!ere left !entricular dysfunction.C. #he presence of a + mm. aneurysm in the right coronary artery.

*. Progressi!e stenosis in the left anterior descending coronary artery.

5. one of the a%o!e.

ns,er- *

*SC/SS0- #he indications for surgical treatment of Ja,asa9iAs disease include- (1) progressi!ely

stenotic coronary lesions demonstrated on coronary arteriography3 ,ith no distal coronary aneurysms ,ithstenosis> (4) locali2ed aneurysm ,ith significant stenosis in the left main coronary artery> (&) significant

stenosis in t,o coronary arteries> (:) presence of collateral !essels arising from a coronary artery ,ith a

pro8imal aneurysm> (+) progressi!e stenosis in the left anterior descending coronary artery> and ()

presence of a left !entricular aneurysm. d!anced throm%osis of coronary aneurysms causing critical

stenoses in multiple coronary arteries is the most common indication for surgical inter!ention.

+. Which of the follo,ing statements a%out the pathophysiology of 5%steinAs anomaly is@are true?. #he tricuspid !al!e is usually insufficient.

". #ypically there is a left$to$right shunt across the S*.C. #he redundant anterior leaflet of the tricuspid !al!e may cause o%struction of the right !entricular

outflo, tract.

*. Pulmonary hypertension is a common late complication.

5. igh pulmonary !ascular resistance in neonates e8acer%ates tricuspid regurgitation and cyanosis.

ns,er- C5


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*SC/SS0- 5%steinAs anomaly is characteri2ed %y do,n,ard displacement of the tricuspid !al!e into

the right !entricular ca!ity. #he anterior leaflet is large and Hsail$li9e3I ,hile the other t,o leaflets are

rudimentary. lthough the tricuspid !al!e occasionally may %e stenotic3 it is usually regurgitant. #he

tricuspid regurgitation and functional right !entricular outflo, tract o%struction caused %y the large

anterior leaflet lead to right$to$left shunting across the S*. Systemic !enous hypertension is often present3 %ut pulmonary hypertension almost ne!er occurs ,ith this malformation. Ginally3 neonates that

present ,ith 5%steinAs anomaly are mar9edly cyanotic3 o,ing to their high pulmonary !ascular resistance.#his causes a functional pulmonary atresia3 ,hich increases right$to$left shunting across the S*.

. n the surgical treatment of 5%steinAs anomaly3 ,hich of the follo,ing is@are true?

. n neonates3 the tricuspid !al!e orifice may %e o!erse,n and a systemic$pulmonary shunt created to

pro!ide pulmonary %lood flo,.

". #echni7ues in repair of the tricuspid !al!e do not utili2e plication of the atriali2ed right !entricle.

C. Closure of the S* alone is ade7uate repair of the malformation.

*. f tricuspid !al!e replacement is performed3 the !al!e should %e sutured a%o!e the coronary sinus to

a!oid in;ury to the conduction system.5. Currently3 mechanical prostheses are recommended for tricuspid !al!e replacement %ecause the

dura%ility of %ioprosthetic !al!es in the tricuspid position is so poor.

ns,er- *

*SC/SS0- n a recent report on the surgical treatment of 5%steinAs anomaly in neonates3 Starnes

descri%ed a techni7ue consisting of o!erse,ing the tricuspid !al!e3 atrial septectomy3 and placement of a

systemic$pulmonary shunt. #hese patients are then later staged to a modified Gontan procedure ,hen they

outgro, their shunts. Repair of the S* alone ,as performed early in the treatment of 5%steinAs anomaly

and ,as associated ,ith high mortality rates. t is not considered an ade7uate repair. Most techni7ues in

tricuspid !al!e repair for 5%steinAs malformation utili2e plication of the atriali2ed right !entricle in

addition to e8cision of redundant atrial tissue. f tricuspid !al!e replacement is necessary3 currentapproaches utili2e %ioprosthetic !al!es %ecause of their e8cellent dura%ility in the tricuspid position.

Placement of the !al!e ring a%o!e the coronary sinus has %een associated ,ith a lo,er rate of

postoperati!e heart %loc9.

B. Which of the follo,ing congenital lesions of the coronary circulation causes a cardiac murmur that is

similar to the murmur produced %y a P*?

. 0rigin of the left coronary artery from the pulmonary artery.". 0rigin of the right coronary artery from the pulmonary artery.

C. Coronary artery fistula.*. Mem%ranous o%struction of the ostium of the left main coronary artery.

ns,er- C

*SC/SS0- #he ma;or clinical finding ,ith a coronary artery fistula is a continuous murmur o!er the

site of the a%normal communication. #his murmur may closely resem%le that of P*.


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. #he congenital coronary lesion most li9ely to cause death in infancy is-

. Coronary artery fistula.

". 0rigin of the left coronary artery from the pulmonary artery.C. 0rigin of the right coronary artery from the pulmonary artery.

*. Congenital coronary aneurysm.ns,er- "

*SC/SS0- #he prognosis for most patients ,ith origin of the left coronary artery from the pulmonary

artery is poor. t has %een estimated that D+ of patients ,ith this anomaly die ,ithin the first year of life

unless surgical therapy is underta9en. Patients ,hose right coronary artery originates from the pulmonary

artery are usually asymptomatic. Patients ,ith coronary fistulas occasionally suffer congesti!e heart

failure early. Congenital aneurysms of the coronary arteries are most often asymptomatic until

complications occur3 usually later in life.

D. #he congenital coronary lesion associated ,ith minimal or a%sent clinical manifestations and nearly

normal life e8pectancy is-

. Congenital origin of %oth coronary arteries from the pulmonary artery.". Congenital coronary artery fistula.

C. Mem%ranous o%struction of the ostium of the left main coronary artery.

*. Congenital origin of the right coronary artery from the pulmonary artery.

ns,er- *

*SC/SS0- Clinical manifestations of congenital origin of the right coronary artery from the

pulmonary artery are usually minimal or a%sent. #his malformation is thought to ha!e %een associated,ith death. #he oldest reported patient ,ith this malformation died at age D' years from unrelated

pro%lems.

B'. Which of the follo,ing is@are indications for aortic !al!e replacement for aortic stenosis?

. Syncope.

". Congesti!e heart failure.

C. ngina.*. #rans!al!ar gradient of &+ mm. g ,ithout symptoms.

ns,er- "C

*SC/SS0- With progressi!e narro,ing of the aortic !al!e area from the normal & to : s7. cm. to 1

s7. cm.3 patients %ecome symptomatic. #he classic symptoms produced %y aortic stenosis are syncope3

congesti!e heart failure3 and angina. 0nce symptoms occur3 life e8pectancy is limited to 4 to + years.

#herefore3 symptomatic aortic stenosis is an indication for aortic !al!e replacement. #he ris9 of death

,ith asymptomatic aortic stenosis is 7uite lo,3 and aortic !al!e replacement is not indicated for

asymptomatic patients ,ith a trans!al!ar gradient less than +' mm. g.


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B1. /nder ,hich of the follo,ing circumstances is medical management logical?

. Moderate aortic insufficiency seen on echocardiography ,ith normal left !entricular end$systolic

dimensions.

". Moderate to se!ere aortic insufficiency seen on echocardiography ,ith cardiomegaly on chest

roentgenography.C. Moderate aortic insufficiency seen on echocardiography ,ith symptoms of congesti!e heart failure.

*. Moderate aortic insufficiency ,ith an end$systolic left !entricular dimension of B' mm. as seen onechocardiography.

ns,er-

*SC/SS0- #he left !entricle is usually a%le to compensate for a long time for the increased !olume

load imposed %y aortic insufficiency. #he natural history of asymptomatic aortic stenosis is e8cellent> 1'$

year sur!i!al for moderate aortic insufficiency managed medically is as high as + to D+. Medical

management typically consists of diuretics and afterload reduction> ho,e!er3 once the compensatory

mechanisms %egin to fail3 sur!i!al is limited. alf of patients ,ith signs or symptoms of congesti!e heart

failure die ,ithin 4 years. #herefore3 e!idence of left !entricular dilation %y echocardiography (left

!entricular end$systolic dimension greater than ++ mm.3 cardiomegaly on chest roentgenography) or

symptoms of congesti!e heart failure are indications for aortic !al!e replacement.

B4. Which of the follo,ing may %e indications for operation for mitral stenosis?

. Systemic em%oli2ation.

". nfecti!e endocarditis.

C. 0nset of atrial fi%rillation.

*. Worsening pulmonary hypertension.

ns,er- "C*

*SC/SS0- lthough each is only a relati!e indication for operation for mitral stenosis3 systemic

em%oli2ation3 infecti!e endocarditis3 onset of atrial fi%rillation3 and ,orsening pulmonary hypertension

may each %e an indication for operation for mitral stenosis. Systemic em%oli2ation3 infecti!e endocarditis3

and onset of atrial fi%rillation are each complications of mitral stenosis that portend a ris9 of further

complication ,ith continued medical therapy. Patients older than :' years ,ith mild class congesti!e

heart failure stand to gain symptomatically from operation for significant mitral stenosis and do not rune8cessi!e ris9 of multiple reoperati!e procedures.

B&. Which of the follo,ing is@are not true?. 0peration impro!es sur!i!al in patients ,ith se!ere3 symptomatic mitral !al!e disease.

". =eft !entricular dilatation ,ith class or class heart failure is an indication for operation ,ith mitral

regurgitation.

C. #ricuspid regurgitation is most commonly caused %y a%normalities of the leaflets themsel!es.

*. Mitral !al!e replacement re7uires resection of the mitral !al!e leaflets and chordae.

ns,er- C*


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*SC/SS0- Relati!e to medical therapy alone3 surgical therapy has %een sho,n to impro!e sur!i!al in

patients ,ith se!ere3 symptomatic mitral !al!e disease. n mitral regurgitation3 left !entricular dilatation is

an indication for surgical inter!ention regardless of failure symptoms. #he most common cause of

tricuspid regurgitation is tricuspid annular dilatation ,ithout a%normalities of the leaflets themsel!es.

Mitral !al!e replacement ,ith preser!ation of %oth leaflets or at least the posterior leaflet is ,elldescri%ed and is pro%a%ly ad!isa%le for most patients to preser!e left !entricular function and reduce the

pro%a%ility of !entricular$annular separation.

B:. Which of the follo,ing generally are not symptoms of tricuspid !al!e disease?

. Pulmonary edema.

". epatic failure.

C. nasarca.

*. oarseness.

ns,er- *

*SC/SS0- epatic failure and anasarca are indeed common symptoms of se!ere3 long$standing

tricuspid !al!e disease ,ith increased !enous pressure. Pulmonary edema is a conse7uence of left$sided

heart disease and does not result from a tricuspid lesion. Similarly3 hoarseness is most common after

mitral !al!e disease ,ith left atrial enlargement and is rarely due to tricuspid !al!e disease alone.

B+. Which of the follo,ing are relati!e indications for mitral !al!e replacement3 as opposed to mitral

!al!e repair?

. 58tensi!e leaflet calcification.

". Mitral regurgitation.C. Chordal rupture of the anterior mitral leaflet.

*. Significant annular dilatation.

ns,er-

*SC/SS0- 58tensi!e mitral !al!e calcification is a relati!e indication for mitral !al!e replacement.Mitral regurgitation or significant annular dilatation may3 ho,e!er3 %e amena%le to mitral !al!e repair.

Chordal rupture of the anterior leaflet is generally repara%le using chordal transposition or

polytetrafluoroethylene (P#G5) chordae.

B. Which of the follo,ing are not true?

. #ricuspid regurgitation due to annular dilatation alone generally does not re7uire !al!e replacement.

". Mitral !al!e replacement ,ith either a %ioprosthesis or a mechanical !al!e re7uires ,arfarin

anticoagulation.

C. #ricuspid !al!e replacement is generally an indication for using a tissue !al!e.

*. Chronic renal failure is a relati!e indication for tissue !al!es.

ns,er- "


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*SC/SS0- #ricuspid regurgitation due to annular dilatation alone generally can %e treated ,ith

tricuspid annuloplasty or ,ith correction of associated mitral !al!e disease. Mitral !al!e replacement ,ith

a mechanical !al!e does re7uire ,arfarin anticoagulation> ho,e!er3 mitral !al!e replacement ,ith a %ioprosthesis may %e managed ,ith aspirin alone. #ricuspid !al!e replacement is an indication for using a

tissue !al!e %ecause of the significant incidence of !al!e throm%osis ,hen a mechanical !al!e is in thetricuspid position. Chronic renal failure is a relati!e indication for tissue !al!es %ecause !al!e

calcification is rare and %ecause anticoagulation of patients on dialysis carries high ris9s of mor%idity and

mortality.

BB. Which of the follo,ing are relati!e indications for mechanical3 as opposed to tissue3 !al!e

replacement?

. Patient younger than &' years.

". oung female patient ,ho desires children.

C. n elderly patient.*. #ricuspid !al!e replacement.

ns,er-

*SC/SS0- ge younger than &' years is a relati!e indication for mechanical !al!es %ecause of an

increased incidence of calcification of tissue !al!es in younger persons. young female ,ho desires

children ,ould %e a relati!e contraindication to mechanical replacement %ecause of the ris9 of

teratogenesis and hemorrhage during pregnancy secondary to ,arfarin therapy. d!anced age is a relati!e

indication for %iologic !al!es to a!oid complications of anticoagulation and %ecause the pro%a%ility of

reoperation is lo,. #ricuspid !al!e replacement is a relati!e contraindication to mechanical !al!e

replacement3 o,ing to the increased incidence of tricuspid !al!e throm%osis ,ith a mechanical prosthesis.

B. Which of the follo,ing statements are not true?

. "ioprosthetic !al!es ha!e a relati!ely high incidence of hemolysis.

". "ioprosthetic !al!es ha!e a lo,er incidence of postoperati!e prosthetic !al!e endocarditis.C. Mechanical !al!es de!elop structural failure after an a!erage of B to 1' years.

*. Mortality attri%uta%le to ,arfarin therapy approaches + per patient$year.

ns,er- "C*

*SC/SS0- "ioprosthetic !al!es ha!e a relati!ely lo, incidence of hemolysis. "ioprosthetic andmechanical !al!es do not differ significantly in the associated incidences of postoperati!e prosthetic !al!e

endocarditis. "ioprosthetic !al!es de!elop structural failure after an a!erage of B to 1' years3 ,hereas

mechanical !al!es ha!e a life span of ,ell %eyond 1' years. #he mortality attri%uta%le to ,arfarin therapy

approaches 1 per patient$year.


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BD. Which of the follo,ing are not generally associated ,ith mitral stenosis ,ithout regurgitation?

. Pulmonary hypertension.

". Pulmonary edema.

C. =eft !entricular dilatation.

*. n opening snap after the second heart sound.ns,er- "*

*SC/SS0- Pure mitral stenosis ,ithout regurgitation may %e associated ,ith pulmonary

hypertension3 pulmonary edema3 and an opening snap after the second heart sound. =eft !entricular

dilatation ,ould %e rare in pure mitral stenosis and generally occurs ,ith !olume or pressure o!erload of

the left !entricle3 as ,ith mitral regurgitation.

'. #he most common location of accessory path,ays in patients ,ith the Wolff$Par9inson$White

syndrome is the-

. =eft free ,all.". Right free ,all.

C. Posterior septum.

*. nterior septum.

ns,er-

*SC/SS0- ll ma;or pu%lished series of the Wolff$Par9inson$White syndrome indicate that the

ma;ority of all accessory path,ays appear in the left free ,all space. n one series3 appro8imately ' of

all accessory path,ays occur in the left free ,all space. n 5%steinAs anomaly3 path,ays are usually

located in the posterior septum and@or right free ,all spaces. f these patients are e8cluded3 appro8imately

B' of path,ays occur in the left free ,all space.

1. #he anatomic electrophysiologic %asis of 6 node re$entry tachycardia is dual 6 node conduction

path,ays. 6 node re$entry tachycardia is most li9ely to occur ,ith ,hich of the follo,ing

electrophysiologic a%errations?. Pro8imal antegrade %loc9 in the slo, conduction path,ay.

". Pro8imal retrograde %loc9 in the slo, conduction path,ay.

C. Pro8imal antegrade %loc9 in the fast conduction path,ay.

*. Pro8imal retrograde %loc9 in the fast conduction path,ay.ns,er- C

*SC/SS0- retrograde conduction %loc9 in either the slo, or fast path,ay ,ould %e li9ely to

pre!ent a re$entrant circuit from de!eloping. pro8imal antegrade %loc9 in the slo, conduction path,ay

is e8tremely unusual %ecause of the short refractory period of the slo, conduction path,ay. #he most

common conduction %loc9 that occurs in patients ,ith dual 6 node physiology is a pro8imal antegrade

conduction %loc9 in the fast path,ay %ecause of its longer refractory period. #his antegrade %loc9 in the

fast conduction path,ay allo,s 6 conduction to occur !ia the slo, path,ay and to return in retrograde

fashion up the fast path,ay to esta%lish the re$entrant circuit responsi%le for 6 node re$entry

tachycardia.


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4. Match the four surgical procedures that ha!e %een de!eloped for the treatment of atrial fi%rillation

,ith the ma;or detrimental se7uela(e) of atrial fi%rillation that each corrects.

. is %undle a%lation.

". =eft atrial isolation procedure.

C. Corridor procedure.*. Ma2e procedure.

1. PatientAs sensation of irregular heart rhythm.4. emodynamic compromise %ecause of loss of 6 synchrony.

&. ncreased !ulnera%ility to throm%oem%olism.

ns,er- $1. "$134. C$1. *1343&

*SC/SS0- #he surgical procedure most commonly employed for the treatment of atrial fi%rillation is

catheter a%lation of the is %undle. #he nternational Catheter %lation Registry re!eals that more than

' of patients ,ho undergo electi!e catheter a%lation of the %undle of is do so for the treatment of

atrial fi%rillation. is %undle a%lation is an isolation procedure3 in that it confines the atrial fi%rillation to

the atria and protects the !entricles from the unpleasant sensation of an irregular heart%eat. "ecause the

atria continue to fi%rillate there is no restoration of 6 synchrony3 and therefore there is no impro!ement

in cardiac hemodynamics. Moreo!er3 the continuing fi%rillation of the left atrium means that postoperati!ely the patient is still at the same ris9 for throm%oem%olism. #hus3 is %undle a%lation

corrects only one of the three detrimental se7uelae of atrial fi%rillation3 namely the arrhythmia pro%lem.

#he left atrial isolation procedure confines atrial fi%rillation to the left atrium3 allo,ing the sinus node to

dri!e the remainder of the heart in a normal sinus rhythm. #hus3 it alle!iates the unpleasant sensation ofan irregular heart%eat. n addition3 %ecause 6 synchrony is re$esta%lished %et,een the right atrium and

right !entricle3 right$sided cardiac output is restored to normal. #his means that normal cardiac output is

deli!ered through the lungs to the left side of the heart. n the presence of a normal left !entricle the left$

sided cardiac output is also normal3 despite the fact that left$sided 6 synchrony is not present> ho,e!er3

%ecause the left atrium is allo,ed to fi%rillate3 the !ulnera%ility to throm%oem%olism remains unchanged

postoperati!ely.

#he corridor procedure allo,s the sinus node to dri!e the heart in normal sinus rhythm3 %ut %ecause of the

total isolation of the sinoatrial and 6 nodes from the remainder of the atria3 the atria may continue tofi%rillate. 5!en if they do not3 in effect they are isolated from their respecti!e !entricles so that 6

synchrony is lost on %oth sides of the heart. s a result3 the corridor procedure alle!iates the sensation of

arrhythmia %ut does not restore normal hemodynamics3 nor does it decrease !ulnera%ility to

throm%oem%olism. #he ma2e procedure a%lates the re$entrant circuits responsi%le for atrial fi%rillation

and restores the normal sinus rhythm. #hus3 it alle!iates the sensation of arrhythmia3 restores normal

hemodynamics3 and alle!iates the !ulnera%ility to throm%oem%olism.

&. ll of the follo,ing statements a%out nonischemic !entricular tachyarrhythmias are true e8cept-

. #hey usually occur in the right !entricle.". #hey are usually associated ,ith a left %undle %ranch %loc9 pattern during the tachycardia.

C. #hey are usually more refractory to medical therapy than ischemic !entricular tachyarrhythmias.

*. #hey usually occur as a result of automaticity rather than re$entry.

ns,er- *

*SC/SS0- onischemic !entricular tachyarrhythmias usually occur in the right !entricle3 and as a

result the 5CE sho,s a left %undle %ranch %loc9Ktype pattern during !entricular tachycardia. #hese


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arrhythmias are notoriously refractory to medical therapy and they occur almost e8clusi!ely on a re$

entrant %asis.

:. Which of the follo,ing statements a%out left atrial my8oma are true?. #his lesion3 %y site and histology3 is the most common primary cardiac tumor.

". t is %est diagnosed %y cardiac catheteri2ation and angiography.

C. #he symptom comple8 can mimic collagen !ascular disease.

*. t has an intraca!itary gro,th pattern.

5. t has a multicentric origin in the cham%er ,all.

ns,er- C*

*SC/SS0- 5ighty per cent of primary cardiac tumors are %enign3 and half of these %enign tumors are

my8omas. Se!enty$fi!e per cent of my8omas arise in the left atrium in the region of the fossa o!alis.

5chocardiography is the techni7ue of choice in the e!aluation of intracardiac tumors3 and findings

suggesti!e of my8oma occur in D+ of patients e8amined. n!asi!e procedures3 ,ith the attendant ris9 oftumor em%oli2ation3 are not ,arranted. 0,ing to an autoimmune phenomenon3 left atrial my8omas can

present ,ith systemic constitutional symptoms of fe!er3 malaise3 ,eight loss3 polymyositis3 and %lood

dyscrasias that mimic collagen !ascular disease. 0f surgical significance is the fact that most my8omas

rarely e8tend deeper than the endocardium %ut gro, as polypoid3 intraca!itary masses. ttachment %y a!ascular stal9 thus allo,s tumor mo%ility3 predisposing to em%oli2ation and interference ,ith mitral !al!e

competence and causing characteristic echocardiographic findings.

+. Which of the follo,ing statements a%out malignant cardiac tumors are true?

. Sarcomas are the most fre7uent primary malignancy.". Metastatic tumors are usually asymptomatic.

C. d;u!ant chemotherapy and irradiation are efficacious in prolonging sur!i!al.

*. ntra$atrial e8tension of renal neoplasms is a contraindication for surgical resection.

5. Constricti!e physiology is an indication for operation.

ns,er- "

*SC/SS0- #,enty per cent of primary cardiac tumors are some !ariant of sarcoma. Precise

histologic classification is not imperati!e3 as all ha!e a similar clinical picture ,ith rapid systemic

dissemination and aggressi!e local in!asion. n contrast3 metastatic tumors cause symptoms in only 1'of patients. /nfortunately3 most primary and secondary cardiac malignancies infre7uently respond to

systemic chemotherapy or mediastinal irradiation. Surgical treatment is most successful ,ith renal tumorse8tending into the right atrium. Significant +$year sur!i!al can %e achie!ed ,ith concomitant

nephrectomy and intra$atrial resection of the tumor throm%us. Relief of tamponade is ,orth,hile>

ho,e!er3 e8tensi!e decortication pro!ides little help.


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D. *ecreasing pacema9er electrode tip si2e results in-

. =o,er pacing thresholds.

". mpro!ed electrogram sensing.

C. *ecreased %attery life.

*. =ess patient discomfort.ns,er-

*SC/SS0- *ecreasing pacema9er electrode tip si2e results in lo,er pacing thresholds3 %oth at the

time of implant and su%se7uently3 %ecause of higher current density. o,e!er3 %etter sensing function is

directly related to electrode area and is ad!ersely affected %y small electrode si2e. #herefore3 a

compromise %et,een pacing and sensing efficiency is re7uired. #ypical electrode surface areas for pacing

are %et,een and 1' s7. mm.

D'. t the time of !entricular pacema9er implantation3 lead resistance is determined at a !oltage near that

of the pacema9erAs output. #he calculated resistance at + !olts should range from-. 1' to 1'' ohms.

". 14+ to 4+' ohms.

C. &'' to '' ohms.

*. 1''' to 1+'' ohms.ns,er- C

*SC/SS0- t the time of pacema9er implantation3 in addition to measuring pulse amplitude (!oltage

and current) and pulse ,idth3 resistance is also determined. s descri%ed %y 0hmAs la,3 resistance is

calculated %y di!iding !oltage %y current. Resistance calculations are made at a !oltage near that of the

pacema9erAs output. #he calculated resistance at + !olts should range from &'' to '' ohms. n

unsatisfactorily lo, resistance is unsatisfactory %ecause current is ,asted and %attery life is shortened.Con!ersely3 e8cessi!ely high resistance (more than '' ohms) increases %attery life %ut decreases the

current deli!ered to the heart for pacing.

D1. !entricular inhi%ited$demand pacema9er using the ntersociety Commission for eart *isease

Resources (C*) code is designated as-

. *6.

". 66.C. 600.

*. 6**.ns,er- "

*SC/SS0- !entricular inhi%ited$demand pacema9er using the C* code is designated as 66. s

the C* code states3 the pacema9er senses intrinsic !

Cardiac Surgery MCQ.docx

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