Cardiac Surgery MCQ . #. C. +.
1. Which is not true of cardiopulmonary resuscitation resuscitation (CPR)? Closed Closed chest massag massage e is as e!ecti" e!ecti"e e as open chest chest massage massage.. $he success success rate for out%of%hospital out%of%hospital resuscitation resuscitation may &e as high as ' to *. $he most most common cause cause of sudden sudden death death is ischemi ischemic c heart heart disease. disease. Standard chest chest massage generally generally pro"ides pro"ides less than 1, 1, of normal coronary coronary and cere&ral cere&ral &lood -o. nser/ +0SCSS023/ Closed chest massage is not as e!ecti"e as open%chest massage in normali4ing &lood pressure or perfusion of "ital organs5 and closed chest massage does generally deli"er , to 1, of normal coronary and cere&ral &lood -o. $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. 0schemic heart disease is the most common cause of sudden death.
6. Which maneu"er generally is not performed early &efore chest compression in &asic life support outside the hospital? . Call for help. #. 2&ta 2&tain in air aira ay y. C. 7lectr 7lectrica icall cardio" cardio"ers ersion ion.. +. 8entila entilatio tion. n.ns nser er// C +0SCSS023/ #asic life support does in"ol"e calling for help5 o&taining an airay5 and &eginning "entilation &efore starting chest compression. 7lectrical cardio"ersion re9uires special e9uipment and trained personnel and thus is part of ad"anced cardiac life support. '. Which treatment ould &e least e!ecti"e for asystole? . 7:ternal pacema;er. #. 0ntra"enou 0ntra"enous s epinephr epinephrine5 ine5 1 ml. of 1/15 1/15.. C. 0ntra"enou 0ntra"enous s calcium calcium gluconat gluconate5 e5 1 ml. of 1 1 solution. solution. +. 0ntra"enou 0ntra"enous s atropine atropine55 ., mg.n mg.nser ser// C +0SCSS023/ Recommended treatment for asystole is administration of atropine. 0f atropine is unsuccessful unsuccessful epinephrine is gi"en. ltimately cardiac pacing is necessary if atropine and epinephrine do not esta&lish an ade9uate heart rate. Calcium has no clear role in treating asystole.
. #. C. +.
<. $he most important factor that in-uences the outcome of penetrating cardiac cardiac in=uries is/ Comminute Comminuted d tear tear of a single single cham& cham&er er.. Multip Multiple% le%cha cham&e m&err in=urie in=uries. s. Corona Coronary ry artery artery in=ur in=ury y. $angentia angentiall in=uries. in=uries.ns nser/ er/ C +0SCSS023/ Multiple studies in the literature con>rm that in=uries to the coronary arteries are the most important factor in determining outcome after a penetrating cardiac in=ury. $angential in=uries are the least serious. 0n=ury to a single cham&ere"en if comminutedor to multiple cham&ers is less li;ely to &e fatal than are in=uries that in"ol"e a ma=or coronary artery.
,. $he most useful incision in the operating room for patients ith penetrating cardiac in=ury is/ . @eft @eft anterior anterior thoracotomy thoracotomy. #. Right Right anterio anteriorr thoracot thoracotomy omy.. C. #ilatera #ilaterall anteri anterior or thorac thoracotomy otomy..
+. Media Median n stern sternoto otomy my.. 7. Su&: Su&:yp ypho hoid id. .ns nse err/ + +0SCSS023/ $he su&:yphoid incision is useful for determining determining if there is &lood in the pericardium and if there is an intracardiac in=uryA hoe"er5 e:posure is e:tremely limited5 and de>niti"e repair can rarely &e performed through the incision. @eft (or right) anterior thoracotomy is easily performed5 especially in the emergency room5 and gi"es ade9uate e:posure to certain areas of the heart. Boe"er5 each has signi>cant limitations in e:posure. 7ither may &e e:tended across the thoracotomy into the other side of the chest5 thus producing a &ilateral anterior thoracotomy. 7:posure is e:cellent through this incision5 and most in=uries can &e satisfactorily repaired through this approach. Most cardiac operations today are performed through median sternotomy incisions. 0f the patient is in the operating room5 this incision is easily performed and alays pro"ides e:cellent e:posure for all areas of the heart. *. 0n patients ho present ith a penetrating chest in=ury5 in=ury to the heart is most li;ely hen the folloing physical sign(s) isare present/ . Bypotension. #. +ist +isten ende ded d nec; nec; "eins "eins.. C. +ecre +ecreas ased ed heart heart sound. sound. +. ll of of the a&o" a&o"e. e.ns nse er/ r/ + +0SCSS023/ Bypotension5 increased "enous pressure (distended nec; "eins)5 and decreased heart sounds ma;e up the classic #ec;Ds triad associated ith cardiac tamponade. 0f these three >ndings are present in a person ho has a penetrating chest ound5 intracardiac in=ury is almost certain and operati"e inter"ention is mandatory. E. Which of the folloing ould &e an accepta&le method of repair for a neonate ith symptomatic isolated coarctation of the aorta? . Resection ith end%to%end anastomosis. #. Prosthe Prosthetic tic patch patch aortopla aortoplasty sty.. C. Su&cla"ia Su&cla"ian n -ap -ap aortopl aortoplasty asty.+. Prosthetic tu&e graft repair. nser/ C +0SCSS023/ $he most commonly used methods for coarctation repair are resection ith anastomosis and su&cla"ian -ap aortoplasty. #oth ha"e &een shon to pro"ide ade9uate relief of the o&struction ith accepta&le rates of restenosis. $he choice of repair depends on the patientDs anatomy and the surgeonDs e:perience. Patch aortoplasty as used fre9uently in the pastA hoe"er5 &ecause of concern o"er restenosis and aneurysm formation it is no longer commonly performed. Prosthetic tu&e graft repair is a"oided e:cept in some comple: cases and some cases of recoarctation. F. Which of the folloing constitutes a true "ascular ring? . Pulmonary artery sling. #. +ou& +ou&le le aor aorti tic c arch arch.. C. nomalous origin of right su&cla"ian su&cla"ian artery from the descending descending aorta. aorta. +. Cer"ical Cer"ical aortic aortic arch.n arch.nser ser// #
. #. C. +.
+0SCSS023/ 2nly 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 compression of the trachea5 and an anomalous right su&cla"ian may cause dysphagia5 &ut these anomalies do not constitute complete rings. Cer"ical aortic arch5 hich is thought to &e secondary to persistence of the third aortic arch5 is not a complete ring and usually is asymptomatic. G. Which of the folloing may &e physical e:amination e:amination >ndings in a young adult ith coarctation of the aorta? Posterio Posteriorr systolic systolic murmu murmurr &eteen &eteen the scapulas scapulas.. +imini +iminish shed ed femor femoral al pulse pulses. s. 7le"ated &lood &lood pressure pressure in left arm as compared ith right arm. Periph Peripheral eral cyanosis cyanosis.ns .nser er// #C +0SCSS023/ systolic murmur that radiates posteriorly is characteristic characteristic of coarctation coarctation of the aorta. Coarctation Coarctation produces o&struction to aortic -o5 and thus the femoral pulse has a diminished "olume ith delayed upstro;e. Bypertension in coarctation is multifactorial5 &ut the most important factors are diminished renal -o (single clip5 single ;idney%Hold&latt model) and mechanical
+. Media Median n stern sternoto otomy my.. 7. Su&: Su&:yp ypho hoid id. .ns nse err/ + +0SCSS023/ $he su&:yphoid incision is useful for determining determining if there is &lood in the pericardium and if there is an intracardiac in=uryA hoe"er5 e:posure is e:tremely limited5 and de>niti"e repair can rarely &e performed through the incision. @eft (or right) anterior thoracotomy is easily performed5 especially in the emergency room5 and gi"es ade9uate e:posure to certain areas of the heart. Boe"er5 each has signi>cant limitations in e:posure. 7ither may &e e:tended across the thoracotomy into the other side of the chest5 thus producing a &ilateral anterior thoracotomy. 7:posure is e:cellent through this incision5 and most in=uries can &e satisfactorily repaired through this approach. Most cardiac operations today are performed through median sternotomy incisions. 0f the patient is in the operating room5 this incision is easily performed and alays pro"ides e:cellent e:posure for all areas of the heart. *. 0n patients ho present ith a penetrating chest in=ury5 in=ury to the heart is most li;ely hen the folloing physical sign(s) isare present/ . Bypotension. #. +ist +isten ende ded d nec; nec; "eins "eins.. C. +ecre +ecreas ased ed heart heart sound. sound. +. ll of of the a&o" a&o"e. e.ns nse er/ r/ + +0SCSS023/ Bypotension5 increased "enous pressure (distended nec; "eins)5 and decreased heart sounds ma;e up the classic #ec;Ds triad associated ith cardiac tamponade. 0f these three >ndings are present in a person ho has a penetrating chest ound5 intracardiac in=ury is almost certain and operati"e inter"ention is mandatory. E. Which of the folloing ould &e an accepta&le method of repair for a neonate ith symptomatic isolated coarctation of the aorta? . Resection ith end%to%end anastomosis. #. Prosthe Prosthetic tic patch patch aortopla aortoplasty sty.. C. Su&cla"ia Su&cla"ian n -ap -ap aortopl aortoplasty asty.+. Prosthetic tu&e graft repair. nser/ C +0SCSS023/ $he most commonly used methods for coarctation repair are resection ith anastomosis and su&cla"ian -ap aortoplasty. #oth ha"e &een shon to pro"ide ade9uate relief of the o&struction ith accepta&le rates of restenosis. $he choice of repair depends on the patientDs anatomy and the surgeonDs e:perience. Patch aortoplasty as used fre9uently in the pastA hoe"er5 &ecause of concern o"er restenosis and aneurysm formation it is no longer commonly performed. Prosthetic tu&e graft repair is a"oided e:cept in some comple: cases and some cases of recoarctation. F. Which of the folloing constitutes a true "ascular ring? . Pulmonary artery sling. #. +ou& +ou&le le aor aorti tic c arch arch.. C. nomalous origin of right su&cla"ian su&cla"ian artery from the descending descending aorta. aorta. +. Cer"ical Cer"ical aortic aortic arch.n arch.nser ser// #
. #. C. +.
+0SCSS023/ 2nly 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 compression of the trachea5 and an anomalous right su&cla"ian may cause dysphagia5 &ut these anomalies do not constitute complete rings. Cer"ical aortic arch5 hich is thought to &e secondary to persistence of the third aortic arch5 is not a complete ring and usually is asymptomatic. G. Which of the folloing may &e physical e:amination e:amination >ndings in a young adult ith coarctation of the aorta? Posterio Posteriorr systolic systolic murmu murmurr &eteen &eteen the scapulas scapulas.. +imini +iminish shed ed femor femoral al pulse pulses. s. 7le"ated &lood &lood pressure pressure in left arm as compared ith right arm. Periph Peripheral eral cyanosis cyanosis.ns .nser er// #C +0SCSS023/ systolic murmur that radiates posteriorly is characteristic characteristic of coarctation coarctation of the aorta. Coarctation Coarctation produces o&struction to aortic -o5 and thus the femoral pulse has a diminished "olume ith delayed upstro;e. Bypertension in coarctation is multifactorial5 &ut the most important factors are diminished renal -o (single clip5 single ;idney%Hold&latt model) and mechanical
factors. 0f the right su&cla"ian su&cla"ian artery is anomalous and arises distal to the coarctation5 &lood pressure may &e greater in the left arm than in the right. 0solated coarctation does not produce cyanosis. 1. 0n a premature infant ith hyaline mem&rane disease and ina&ility to &e eaned from mechanical mechanical "entilation5 hich of the folloing ould suggest hemodynamically signi>cant patent ductus arteriosus (P+)? . Continuous murmur. #. Byperacti Byperacti"e "e precord precordium ium ith &ounding &ounding periphe peripheral ral pulses. pulses. C. Iaun Iaund dice ice. +. +iminishe +iminished d femoral femoral pulse pulses.n s.nser ser// # +0SCSS023/ P+ causes a left%to%right shunt that produces left "entricular "olume o"erload. Physical >ndings include e"idence of hyperdynamic 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. 0n an infant ith suspected P+5 hich of the folloing ould &e the optimal method of con>rming the diagnosis? . Chest >lm. #. Cardia Cardiac c cathet catheteri eri4at 4ation ion.. C. Retrograde Retrograde aortography aortography "ia an an um&ilical um&ilical artery artery catheter catheter.. +. $o%dimensional echocardiography echocardiography ith continuous%a"e continuous%a"e and color%-o color%-o +oppler echocardiography echocardiography.. nser/ + +0SCSS023/ 7chocardiography is the &est method for con>rming the diagnosis of a P+. $o% dimensional echocardiography can demonstrate P+ and e:clude associated anomalies. +oppler echocardiography can demonstrate the shunt5 determine direction of shunting5 and pro"ide an estimate of shunt magnitude. $he chest >lm is not particularly helpful and may &e normal or sho cardiomegaly ith pulmonary congestion. 0n general5 cardiac catheteri4ation should &e reser"ed for older patients and those ith suspected associated anomalies or pulmonary hypertension. hypertension. 16. Which of the folloing are potential complications of untreated coarctation coarctation of the aorta? . 7ndo 7ndoca carrditi ditis. s. #. Pulmo Pulmonar nary y "ascula "ascularr diseas disease. e. C. Cere&ro"ascular Cere&ro"ascular accident.+. Congesti"e heart failure. nser/ C+ +0SCSS023/ Coarctation Coarctation of the aorta produces an o&struction to &lood -o and hypertension5 tur&ulent -o5 and increased left "entricular afterload. $here is an increased incidence of coronary artery disease. Prior Prior to the introduction of e!ecti"e techni9ues for relief of coarctation5 the most common causes of death ere endocarditis5 aortic rupture5 congesti"e heart failure5 and cere&ro"ascular accident. Pulmonary "ascular disease does not occur ith isolated coarctation.
#. C. +. 7.
1'. $he atrial septal defect (S+) most commonly associated ith partial anomalous pulmonary "enous return (PP8R) is/ . Secundum defect. Sinus Sinus "enosu "enosus s defect defect.. 2stium 2stium primum primum defect defect.. Complete Complete atrio"en atrio"entric tricular ular (8) (8) canal canal defect. defect. Corona Coronary ry sinus sinus defe defect. ct.ns nse er/ r/ # +0SCSS023/ lthough partial anomalous return return of the pulmonary "eins can occur ith any of the S+s listed5 it is particularly particularly common ith sinus "enosus defects and is considered 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 $he si4e si4e of of the the defe defect ct #. $he complia compliance nce of the the right right and left left "entric "entricles. les.
C. $he systemic systemic o:ygen o:ygen saturati saturation. on. +. Right Right atri atrial al pre press ssur ure. e. 7. $he presence presence or a&sence a&sence of an associated associated "entricular septal defect (8S+). nser/ # +0SCSS023/ $he direction of an intracardiac shunt is go"erned &y the compliance of the donstream cham&ers. Jor an atrial le"el shunt5 the compliance of the right and left "entricles and their a&ility to distend ith increased increased "olume during diastolic >lling dictates the direction of the shunt -o. Since the right "entricle is usually a more compliantand therefore more distensi&le cham&er than the left "entricle5 -o across an S+ occurs from left to right across the open tricuspid "al"e during diastole. diastole. $he si4e of an S+ does not correspond to the degree of shunt as long as the defect is large enough to &e unrestricti"e to -o. large shunt can occur through a relati"ely small defect if the "entricular compliance is fa"ora&le. 1,. $he S+ most commonly associated ith mitral insuKciency is/ . Secu Secund ndum um defe defect ct #. Sinu Sinus s "eno "enosu sus s defe defect ct C. 2stium 2stium primum primum defect.+. defect.+. Coronar Coronary y sinus defect. defect. nser nser// C +0SCSS023/ 2stium primum defects5 or Lpartial 8 canal defects5 are commonly associated ith a Lcleft of the anterior lea-et of t he mitral "al"e. +epending on the deformity of the mitral "al"e5 these defects can &e accompanied &y "aria&le degrees of mitral insuKciency. $his cleft of the mitral "al"e needs to &e repaired repaired at the same time that the defect is closed. lthough other types of S+s can &e associated ith mitral insuKciency5 this is not as common. When mitral stenosis e:ists ith a secundum S+ the condition is often referred to as @utem&acherDs syndrome.
. #. C. +.
1*. n electrocardiogram (7CH) in a patient ith a systolic e=ection murmur that shos an incomplete &undle &ranch &loc; in the precordial lead is most consistent ith/ sec secun undu dum m S+ S+.. sinus sinus "enosus "enosus S+ S+ ith ith PP8R. P8R. n ost ostiu ium m prim primum um S+ S+.. comple complete te 8 8 canal canal defec defect. t. nser/ +0SCSS023/ Many patients ith secundum S+s ha"e an incomplete &undle &ranch &loc; on their 7CH. $his is in contradistinction contradistinction to patients ith ostium primum defects5 ho often ha"e a left a:is de"iation. lthough the 7CH is not pathognomonic of the defect5 the >ndings are sometimes helpful along ith other clinical and diagnostic information toard elucidating the nature of the defect.
1E. S+s can all &e closed ith a pericardial or prosthetic patch. Which of the folloing S+s can also &e safely closed primarily ithout the use of a patch? . Secundum S+. #. Sinus Sinus "enos "enosus us S+ S+ ith ith PP8 PP8R. R. C. n ost ostiu ium m prim primum um S+ S+.. +. complete complete 8 canal canal defect. defect.ns nser/ er/ +0SCSS023/ Secundum S+s can fre9uently &e closed primarily5 although the use of a prosthetic or pericardial patch is indicated for large defects. $he other types of S+s are more safely closed ith a patch.
. #. C. +. 7.
1F. 2&struction to pulmonary "enous return is associated ith hich of the folloing anomalies? Partial Partial anomalous anomalous pulmonary "enous connection connection (PP8C) (PP8C) to the superior superior "ena ca"a. 0nfracardiac 0nfracardiac ($ype ($ype 000) total anomalous pulmonary pulmonary "enous connection connection ($P8C). ($P8C). Pulmo Pulmonar nary y "ein "ein sten stenosi osis. s. Cor Cor tria triatr tria iatu tum. m. Supracar Supracardiac diac ($ype ($ype 0) $P8C. $P8C.ns nser/ er/ #C+7 #C+7 +0SCSS023/ 2&struction 2&struction to pulmonary "enous return return is the most important factor a!ecting circulatory circulatory function hen pulmonary "enous anomalies e:ist. $his o&struction is most pre"alent pre"alent and se"ere in patients ith infracardiac $P8C5 &ut it also occurs in as many as , of patients ith
supracardiac $P8C and 6 of patients ith intracardiac $P8C to the coronary sinus. 2&struction to pulmonary "enous return is also the primary pathophysiologic e!ect of &oth pulmonary "ein stenosis and cor triatriatum. 2&struction5 hoe"er5 is rare ith partial anomalous pulmonary "enous connection5 especially ith the common form of PP8C to the superior "ena ca"a. 1G. Postoperati"e complications associated ith repair of $P8C include/ . Complete heart &loc;. #. cute pulmonary hypertensi"e crisis. C. Pleural e!usions. +. Pulmonary "enous o&struction.nser/ #+ +0SCSS023/ 0n the early postoperati"e period after repair of o&structed forms of $P8C5 acute episodes of pulmonary hypertension may de"elop as a response to stress. $o minimi4e this potentially fatal complication5 infants are ;ept anestheti4ed ith fentanyl and pancuronium for at least ed it re9uires early reoperation. Reoperation is usually successful if the o&struction is at the le"el of the anastomosis. nfortunately5 in some cases5 the o&struction is in the pulmonary "eins and surgical relief is less successful. lthough complete heart &loc; and pleural e!usions can occur after any cardiac operation5 they rarely occur after $P8C repair. 6. Which of the folloing statements a&out 8S+s isare 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 8S+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. 8S+5 in its isolated form5 is the most commonly recogni4ed congenital heart defect. +. $he conduction &undle runs along the posteroinferior rim of a perimem&ranous 8S+. nser/ C+ +0SCSS023/ Perimem&ranous 8S+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. 2ften a remnant of the mem&ranous portion of the inter"entricular septum (the mem&ranous -ap) 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 defect5 &ut in some patients they are separated from the 8S+ &y a thin rim of muscle tissue that protects the conduction &undle. Muscular 8S+s ha"e e:clusi"ely muscular rims on all four sides. 8S+s in the outlet septum that e:tend to the annuluses of the aortic and pulmonary "al"es are called dou&ly committed or =u:ta%arterial defects. 0solated 8S+s occur at an appro:imate rate of 6 per 1 li"e &irths and represent ' to < of all congenital heart malformations at &irth. $he conduction &undle in patients ith perimem&ranous 8S+s does run along the posteroinferior rim of the defect on the left "entricular side. Sutures used for repair of a perimem&ranous 8S+ should &e placed ell aay from this area to a"oid the creation of surgically induced complete heart &loc;. 61. Which of the folloing statements a&out 8S+s isare true? . When coarctation of the aorta is associated ith 8S+5 it most commonly occurs in infants ith large lesions ho ha"e to undergo repair &efore age ' months. #. 0n some patients ith 8S+5 aortic "al"e incompetence de"elops o"er time and progresses. C. 0n the nited States dou&ly committed or =u:ta%arterial 8S+s are most commonly associated ith aortic insuKciency. +. P+ is present in appro:imately one fourth of infants ith a 8S+ and concomitant congesti"e heart failure. nser/ #+ +0SCSS023/ 8S+ in com&ination ith se"ere coarctation of the aorta occurs in appro:imately 1E of patients. $his com&ination is more common among infants ith large 8S+s undergoing operation &efore age ' months. ortic "al"e incompetence does de"elop o"er time in some patients ith 8S+5 presuma&ly as a result of progressi"e prolapse of the right aortic cusp through the defect. 0n the nited States to thirds of patients ith 8S+ and aortic insuKciency ha"e perimem&ranous lesions and one third ha"e a dou&ly committed or =u:ta%arterial lesion. 0n Iapan5 hoe"er5 the re"erse is true/ to thirds ha"e dou&ly committed or =u:ta%arterial lesions and one third ha"e perimem&ranous lesions. moderate% or large%si4ed P+ is associated ith 8S+ in appro:imately * of patients of all agesA hoe"er5 in infants ith 8S+ and concomitant congesti"e heart failure5 P+ is present in appro:imately 6,.
. #. C. +.
66. Which of the folloing statements a&out 8S+ isare correct? large 8S+ is appro:imately the si4e of the pulmonary "al"e ori>ce or larger. @arge 8S+s associated ith high pulmonary &lood -o result in an enlarged left atrium on chest :% ray. Patients ith small (restricti"e) 8S+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 16 units per s9. m. is considered a contraindication to operation. nser/ #C+ +0SCSS023/ large 8S+ is appro:imately the si4e of the aortic "al"e ori>ce or larger and causes systemic right "entricular systolic pressures. 0n the a&sence of right "entricular out-o tract o&struction5 the pulmonary artery systolic pressure ill also &e systemic in the presence of a large 8S+. @arge 8S+s associated ith a high pulmonary &lood -o do result in an enlarged left atrium &ecause of increased pulmonary "enous return. When mar;ed enlargement of the left atrium is present in a patient suspected of ha"ing a 8S+5 the presence of coe:isting mitral "al"e regurgitation should also &e considered. Patients ith small 8S+s do ha"e normal right "entricular and pulmonary arterial pressures. $here is only a slight ele"ation of pulmonary &lood -o relati"e to the systemic -o5 and the pulmonary "ascular resistance is normal ithout e"idence of pulmonary "ascular disease. t any age5 the presence of pulmonary "ascular disease so se"ere that the pulmonary "ascular resistance is >:ed and greater than 1 to 16 units per s9. m. is considered a contraindication to operation. 6'. Which of the folloing statements a&out 8S+s isare correct? . Spontaneous closure of 8S+s occurs in 6, to , of patients during childhood. #. $achypnea and failure to thri"e are symptoms fre9uently associated ith large 8S+s. C. Patients ith normal pulmonary "ascular resistance and left%to%right shunting across the 8S+ ha"e 7isenmengerDs comple:. +. Patients ith a large 8S+ and lo pulmonary "ascular resistance can present ith a middiastolic murmur at the ape:. nser/ #+ +0SCSS023/ Spontaneous and complete closure of 8S+s5 e"en large ones5 has &een estimated to occur in 6, to , of patients during childhood. $he pro&a&ility of e"entual spontaneous closure is in"ersely related to the age at hich the patient is o&ser"ed. $achypnea5 poor feeding5 groth failure5 recurrent respiratory infections5 e:ercise intolerance5 and se"ere cardiac failure may de"elop in patients ith large 8S+s. Patients ith 7isenmengerDs comple: are cyanotic5 polycythemic5 and se"erely limited in their e:ercise tolerance5 oing to mar;edly ele"ated pulmonary "ascular resistance associated ith a predominantly right%to%left shunt across the 8S+. middiastolic murmur can &e present at the ape: in patients ith a large 8S+ associated ith lo pulmonary "ascular resistance. $his indicates high pulmonary &lood -o ith a large -o across the mitral "al"e into the left "entricle.
6<. Which of the folloing isare true of the surgical treatment of 8S+s? . right "entricular approach is employed for the repair of most perimem&ranous 8S+s. #. 0ntracardiac 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 &loc; is a common complication. +. Bospital mortality after repair of 8S+ in infants approaches 6. nser/ # +0SCSS023/ $he right atrial approach is preferred for the repair of most perimem&ranous 8S+s. Prompt intracardiac repair is indicated for infants ith large defects5 large shunts5 and pulmonary hypertension ho present ith intracta&le left "entricular failure5 recurrent pulmonary infections5 se"ere groth failure5 or e"idence of increasing pulmonary "ascular resistance. 0n the modern era5 complete heart &loc; re9uiring a permanent pacema;er is a "ery uncommon complication of surgical closure of a "entricular septal defect. Bospital mortality after closure of a 8S+ currently approaches 4ero. While in earlier years younger age as an incremental ris; factor for hospital death in some surgical e:periences5 this ris; has &een neutrali4ed during the past decade. 6,. $etralogy of Jallot consists of all of the folloing features e:cept/ . S+. #. 8S+.
C. +e:troposition of the aorta. +. Pulmonary stenosis. 7. Right "entricular hypertrophy.nser/ +0SCSS023/ lthough S+ is a fre9uent component of tetralogy of Jallot5 it as not included &y Jallot as part of his classic tetralogy. 2ccasionally5 the inclusion of an S+ prompts use of the term pentalogy of Jallot. $he other four anomalies listed ere all mentioned &y Jallot in his original description of this defect. 6*. Which of the folloing has the greatest impact on the physiology of tetralogy of Jallot? . $he si4e of the S+. #. $he si4e of the 8S+. C. $he degree of pulmonary stenosis.+. $he amount of aortic o"erriding. nser/ C +0SCSS023/ $he 8S+ in tetralogy of Jallot is nonrestricti"e5 and therefore its si4e does not a!ect the degree of shunting that can occur. @i;eise5 an S+5 hich may or may not &e a component of tetralogy of Jallot5 can pro"ide right%to%left shunting at the atrial le"el &ut is not the main contri&utor to the cyanosis of this disease. $he degree of right%to%left shunt across the 8S+ is dictated &y the "aria&le compliance of the donstream cham&ers5 and the increased resistance imposed &y se"ere pulmonary stenosis creates greater amounts of right%to%left shunting and5 therefore5 more intense cyanosis. $he position of the aorta in relation to the 8S+ is not important as long as no su&aortic o&struction e:ists.
#. C. +. 7.
6E. Which of the folloing anomalies is not associated ith tetralogy of Jallot? . &sence of the left pulmonary artery. right aortic arch. retroesophageal su&cla"ian artery. nomalous origin of the left anterior descending coronary artery from the right coronary artery. Primary pulmonary hypertension.nser/ 7 +0SCSS023/ $he >rst four defects listed occasionally are associated ith tetralogy of Jallot. right aortic arch is seen in 6, 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 Jallot unless the patient has had e:cessi"e pulmonary &lood -o from collaterals or systemic%to%pulmonary artery shunts for a long time. 0t is &ecause these patients usually do not ha"e pulmonary hypertension that infant correction ith transannular patches can &e performed ith such great success. 6F. Surgical treatment of a patient ith tetralogy of Jallot can include any of the folloing e:cept/ . Maintenance of ductal patency ith prostaglandins (PH7 1) to pro"ide pulmonary &lood -o hile the &a&y is transferred to an institution e9uipped to pro"ide more de>niti"e therapy. #. #anding of the pulmonary artery in an acyanotic patient ith tetralogy of Jallot to control pulmonary &lood -o 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 8S+ and transannular patching of the right "entricle onto the mainpulmonary artery in a 6%day%old infant. nser/ # +0SCSS023/ Patients ith tetralogy of Jallot ho do not appear cyanotic still ha"e mild arterial hypo:emia &y arterial &lood gas determination. Patients ith tetralogy of Jallot rarely ha"e e:cessi"e pulmonary &lood -o5 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 Jallot5 since the predominant physiologic e!ect of the defect results from too little pulmonary &lood -o to &egin ith. cyanotic patients ith tetralogy of Jallot (Lpin; tets) can usually &e folloed for se"eral months and their defects repaired electi"ely as a >rst%stage procedure (usually &y age * months). ll of the other therapies are appropriate treatment for &a&ies ith tetralogy of Jallot. Prostaglandins maintain patency of the ductus arteriosus5 pro"iding an anatomic systemic%to%pulmonary artery shunt that sustains pulmonary &lood -o 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&ili4ed enough to reach a tertiary care institution and recei"e proper surgical therapy ho might not otherise ha"e sur"i"ed had it not &een for the
a&ility of pulmonary &lood -o to &e maintained through the re"ersal of duct closing. $he choice of palliati"e shunting or total anatomic correction rests largely ith the e:perience and s;ill of the surgical team and is dictated in part &y the anatomy of the pulmonary arteries. 7ither of these options is accepta&le.
#. C. +. 7.
6G. $he predominant determinant of outcome for patients ith pulmonary atresia and an intact "entricular septum re"ol"es around/ . $he si4e of the S+. $he &a&yDs age at presentation. $he si4e of the right "entricular ca"ity and tricuspid "al"e. $he presence of a tricuspidas opposed to a &icuspidpulmonary "al"e. $he le"el of hypo:emia at presentation.nser/ C +0SCSS023/ $he long%term outcome for &a&ies ith pulmonary atresia and intact "entricular septum depends on the a&ility to con"ert the cardiac circulation into a to%"entricle "ersus one% "entricle physiology. Patients ith a good%si4ed right "entricle and tricuspid "al"e can often &e treated ith pulmonary "al"otomy or right "entricular out-o patching alone and can ha"e a fairly accepta&le outcome. Patients ith a small right "entricle that cannot pro"ide ade9uate pumping to the pulmonary &ed and is often associated ith a small tricuspid "al"e annulus may need to &e staged toard a Jontan procedureand5 conse9uently5 a less accepta&le outcome. $he si4e of an S+ is not rele"ant e:cept that in patients ith this syndrome5 the right side of the heart ill decompress across the S+ until antegrade -o can &e esta&lished. $herefore5 an S+ in some part is an essential feature of this lesion. $he degree of arterial hypo:emia5 the nature of the pulmonary "al"e5 and the patientDs age at presentation may all &e factors that relate to clinical management5 &ut they do not imply speci>c conse9uences ith respect to long%term outcome. '. Which of the folloing statements a&out dou&le%outlet right "entricle are true? . 8S+ is usually present. #. 0n the $aussig%#ing type of dou&le%outlet right "entricle5 the 8S+ is usually noncommitted. C. Patients ith dou&le%outlet right "entricle and a su&aortic 8S+ usually ha"e pulmonary stenosis. +. Patients ith dou&le%outlet right "entricle ith a su&pulmonary 8S+ ($aussig%#ingmalformation) tend to mimic patients ith transposition of the great arteries and 8S+ in their presentation and natural history. nser/ C+
. #. C. +.
+0SCSS023/ 8S+ 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 "entricle5 or one or &oth may o"erlie the "entricular septum immediately a&o"e the 8S+. $o categori4e the heart as ha"ing a dou&le%outlet right "entricle5 more than , of each great artery must arise from the right "entricle. 0n the $aussig%#ing type of dou&le%outlet right "entricle5 the 8S+ is related to the pulmonary "al"e annulus and is 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 8S+ 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 Jallot. 0n the a&sence of pulmonary stenosis the presentation5 clinical course5 and natural history of the $aussig%#ing malformation are similar to those of transposition of the great arteries ith 8S+. Cyanosis is present5 usually from &irth5 since streaming directs the desaturated systemic "enous return toard the aorta and the o:ygenated left "entricular &lood toard 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 e:perience symptoms ithin the >rst fe months of life. '1. Which of the folloing statements a&out the surgical repair of dou&le%outlet right "entricle are true? 0n dou&le%outlet right "entricle ith a su&aortic or dou&ly committed 8S+5 a tunnel%type repair connecting a committed 8S+ ith its respecti"e great artery is usually employed. Repair of the $aussig%#ing malformation can &e accomplished using an intra"entricular tunnel techni9ue or &y performing a straight patch closure of the 8S+ com&ined ith an arterial sitch procedure. $he hospital mortality rate is highest hen a su&aortic 8S+ is present. Some hearts ith dou&le%outlet right "entricle and a noncommitted 8S+ must &e repaired using a modi>cation of the Jontan procedure. nser/ #+ +0SCSS023/ When the 8S+ is su&aortic or dou&ly committed5 the tunnel%type repair connects the left "entricle "ia the 8S+ and tunnel to the aorta. $he $aussig%#ing malformation can &e repaired
using an intra"entricular tunnel techni9ue descri&ed &y Naashima. $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 8S+ is connected to the aorta &y an intra"entricular tunnel that runs posterior to the pulmonary artery. $he most common approach for the repair of the $aussig%#ing malformation in"ol"es patch closure of the 8S+ to the pulmonary artery. $his creates transposition of the great arteries ith an intact inter"entricular septum. n arterial sitch procedure then esta&lishes "entriculoarterial concordance. 2f all the types of dou&le%outlet right "entricle the hospital mortality is loest hen a su&aortic or dou&ly committed 8S+ is present. +ou&le%outlet right "entricle is associated ith a noncommitted 8S+ in appro:imately 1 of patients in surgical series. $he repair of this su&set of patients is associated ith a relati"ely high mortality5 as compared ith the results o&tained after repair of other forms of dou&le%outlet right "entricle. t times5 &ecause of the remote location of the 8S+ and &ecause of other compelling anatomic features5 complete repair cannot &e performed. 0n this case5 a modi>cation of the Jontan procedure must &e employed.
. #. C. +. 7.
'6. Management of a patient ith tricuspid atresia ithin the >rst month of life may include/ Creation of a systemic arteryOtoOpulmonary artery shunt. 2&ser"ation. Creation of a &idirectional superior ca"opulmonary anastomosis. Pulmonary artery &anding. Jontan procedure.nser/ #+ +0SCSS023/ 0nitial management of ne&orn infants ith tricuspid atresia is determined &y the anatomic and physiologic factors that a!ect the &alance of pulmonary and systemic &lood -o. 0nfants ith se"erely limited pulmonary &lood -o and arterial o:ygen saturations of less than E should &e sta&ili4ed ith PH7 1 to maintain patency of the ductus arteriosus until a systemic%to% pulmonary artery shunt can &e performed. Patients ith uno&structed pulmonary &lood -o may e:hi&it only mild cyanosis &ut su!er from signi>cant 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 -o may ha"e &alanced deli"ery of &lood to the systemic and the pulmonary circulation. $hese patients can &e carefully folloed until such time as an im&alance de"elops or they &ecome candidates for a &idirectional superior ca"opulmonary (Hlenn) anastomosis or a Jontan procedure. $he normally high pulmonary "ascular resistance present in the >rst month of life precludes the performance of either the Hlenn or the Jontan procedure in the ne&orn.
. #. C. +. 7.
''. Which of the folloing should contraindicate performance of the Jontan procedure? Patient age of 6, years. Se"ere mitral insuKciency. @eft "entricular end%diastolic pressure of 1F mm. Bg. Right pulmonary artery stenosis. Pulmonary "ascular resistance of * Woods units.nser/ C7 +0SCSS023/ Hood "entricular function and lo pulmonary "ascular resistance are essential re9uirements for a successful Jontan procedure. $he Jontan operation should not &e performed hen "entricular e=ection fraction is less than ' or "entricular end%diastolic pressure is greater than 1, mm. Bg. Pulmonary "ascular resistance in e:cess of < Woods units should also &e considered an a&solute contraindication for Jontan correction. ge at the time of Jontan procedure does not appear to &e a ma=or ris; factor5 e:cept &efore age 6 years. lthough patients ho ha"e sur"i"ed into the third or fourth decade are li;ely to ha"e "entricular dysfunction5 a Jontan procedure can &e performed successfully in these older patients if "entricular function and pulmonary "ascular resistance meet the a&o"e criteria. 0n patients ith tricuspid atresia a competent mitral "al"e is important for satisfactory cardiac output after the Jontan procedure. $he presence of se"ere mitral insuKciency5 hoe"er5 should not necessarily contraindicate the procedure. 0n 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 Jontan operation is performed later. +istorted or stenosed pulmonary arteries are common se9uelae of systemic%to%pulmonary artery shunts and may result in unsatisfactorily high pulmonary "ascular resistance. 0n most cases5 these stenoses can &e repaired at the time of Jontan correction or ith a &idirectional superior ca"opulmonary anastomosis.
'<. 0nitial management of a ne&orn infant ith hypoplastic left heart syndrome should include/ . 0ntra"enous administration of PH7 1. #. Supplemental o:ygen. C. Routine intu&ation and mechanical "entilation to achie"e a PC2 6 &eteen ' and ', mm. Bg. +. Cardiac catheteri4ation and &alloon atrial septostomy. nser/ +0SCSS023/ Postnatal sta&ili4ation of infants ith hypoplastic left heart syndrome re9uires patency of the ductus arteriosus and &alance of the systemic and the pulmonary circulation. #ecause the ductus is the only pathay from the right "entricle to the systemic circulation5 duct patency must &e maintained ith intra"enous PH7 1. $o minimi4e the or;load on the single "entricle and ensure ade9uate deli"ery of o:ygen to the tissues5 an e9ual 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 resistance5 such as the addition of supplemental o:ygen5 loering the PC2 6 to less than ', mm. Bg5 or eliminating any resistance at the atrial septum &y &alloon septostomy only orsens the im&alance. ',. $he performance of a &idirectional superior ca"opulmonary (Hlenn) 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. #. 0ncreases peripheral o:ygen saturations to greater than G. C. Permits concomitant repair of pulmonary artery or aortic arch stenoses. +. 0mpro"es mortality and mor&idity of su&se9uent Jontan procedure.nser/ C+ +0SCSS023/ fter the >rst%stage reconstructi"e (3orood) procedure5 the circulation is inherently ineKcient &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 Hlenn anastomosis eliminates this ineKcient recirculation and signi>cantly 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 Hlenn procedure is performed. 0n almost all series the mortality of the Jontan procedure has decreased since the adoption of the three%stage approach for hypoplastic left heart syndrome. #ecause systemic and pulmonary "enous &lood continue to mi: in the right atrium after a &idirectional Hlenn procedure5 cyanosis persists ith peripheral o:ygen saturations &eteen E, and F,. '*. Which of the folloing 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 re9uires a conduit from right "entricle to pulmonary arteries.nser/ #C+ +0SCSS023/ While an occasional child sur"i"es to age ' or < years5 ithout either palliati"e or totally correcti"e surgical treatment fe li"e past early infancy. $he lesion is one of e:cessi"e pulmonary &lood -o &ecause of the origin of the pulmonary arteries from the truncus arteriosusA physiologically5 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 8S+5 the physiologic manifestations are congesti"e heart failure and e:cessi"e pulmonary &lood -o rather than cyanosis. $he congesti"e heart failure &ecomes se"ere as pulmonary "ascular resistance drops. 0f congesti"e heart failure later impro"es spontaneously5 it is &ecause of the de"elopment of pulmonary "ascular disease. Complete repair alays re9uires closure of the 8S+5 detachment of the pulmonary arteries from the common trun;5 and re%esta&lishment of an out-o 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. 'E. $runcus arteriosus is a diagnosis ith anatomic components including/ . 8S+. #. &normal origin of pulmonary arteries. C. Su&aortic stenosis. +. Single "entricular out-o "al"e.nser/ #+
+0SCSS023/ #y de>nition5 a 8S+ is alays present immediately &eneath the truncal "al"e. $he pulmonary arteries arise a&normally from the single trun;5 hich is due to failed partitioning of the em&ryonic conus during the >rst fe ee;s of fetal de"elopment. 0n the classi>cation of Collett and 7dards5 $ype 0 truncus arteriosus has a single arterial trun; gi"ing rise to an aorta and a main pulmonary arteryA in $ype 00 the right pulmonary arteries arise immediately ad=acent to one another from the dorsal all of the truncusA in $ype 000 the right and left pulmonary arteries originate from either side of the truncusA and in $ype 08 the pro:imal pulmonary arteries are a&sent and pulmonary &lood -o 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 out-o "al"e is the truncal "al"e. 0t may contain from to to si: cusps5 &ut most often there are three and5 ne:t most often5 four.
#. C. +. 7.
'F. 2ptimal treatment for the neonate ho presents ith transposition of the great arteries S5+5+ and intact "entricular septum includes/ . PH7 1 infusion to maintain duct patency. dministration of intra"enous -uid to increase intra"ascular "olume. Byper"entilation to decrease pulmonary resistance. 2:ygen administration to increase arterial o:ygen tension. trial &alloon septostomy to impro"e atrial mi:ing.nser/ #7 +0SCSS023/ #ecause ith transposition of the great "essels the systemic and the pulmonary circulations e:ist in parallel rather than in series5 sur"i"al depends on mi:ing &eteen pulmonary and systemic circulations. 0nitially infants ith transposition and intact atrial septum sur"i"e &ecause of aortopulmonary -o through P+5 hich may &e maintained ith prostaglandin infusions. lthough increased pulmonary -o may cause enlargement of the left atrium and stretching of the foramen o"ale resulting in atrial%le"el mi:ing of o:ygenated and nono:ygenated &lood5 inade9uate mi:ing at the atrial le"el ill result in marginal tissue o:ygenation5 hich does not impro"e ith o:ygen administration. trial &alloon septotomy results in impro"ed admi:ture and o:ygen deli"ery in these patients and should &e performed promptly if peripheral acidemia and se"ere cyanosis are present. Relati"e dehydration may decrease the degree of interatrial shunting and "olume infusion often impro"es hemodynamics in infants. +ecreased pulmonary "ascular resistance may increase pulmonary &lood -o at the e:pense of systemic &lood -o and alter the loading conditions of the left "entricle5 hich may complicate early arterial repair.
. #. C. +. 7.
'G. Jactors that preclude the use of a single%stage arterial sitch reconstruction of de:trotransposition of the great "essels include/ ge older than * ee;s ith a left "entricular pressure of less than , of systemic pressure. +ynamic left "entricular out-o tract o&struction. 0ntramural coronary artery anatomy. 8al"ar pulmonic stenosis. Su&pulmonary 8S+.nser/ + +0SCSS023/ Single%stage arterial sitch procedure for reconstruction of transposition of the great "essels5 ith or ithout associated 8S+ has &ecome the standard of treatment in the ma=ority of cardiac centers. Contraindications to arterial sitch repair include >:ed types of left "entricular out-o tract o&struction5 including "al"ar pulmonic stenosis5 hich ould render the systemic semilunar "al"e stenotic or incompetent. natomic a&normalities ithout stenosis5 such as a &icuspid "al"e5 hoe"er5 are suita&le for surgical correction. $he location of 8S+ does not a!ect surgical outcome5 and most 8S+s can &e approached ade9uately through the right atrium or the anterior great "essel. Most dynamic forms of left "entricular out-o tract o&struction are often relie"ed partially or completely &y realignment of the "entricular septum ith the hemodynamic changes folloing successful arterial sitch repair. When5 hoe"er5 the left "entricle has not &een prepared to sustain the pressure load of the systemic circulation &y the decrease in pulmonary "ascular resistance that occurs in the >rst fe ee;s of life and hen the "entricular pressure is less than , of the systemic "entricular pressure5 one%stage repair is contraindicated5 and staged repair ith pulmonary &anding and shunt folloed &y arterial sitch must &e contemplated.
<. Complications commonly associated ith the atrial (Senning and Mustard) repairs of transposition of the great arteries include/ . trial arrhythmias. #. Systemic or pulmonary "enous o&struction. C. Right "entricular out-o tract o&struction. +. Systemic "entricular failure.
7. Progressi"e ele"ation of pulmonary "ascular resistance.nser/ #+ +0SCSS023/ $he atrial repair of transposition of the great arteriesrerouting systemic and pulmonary "enous &lood at the atrial le"elresults in the right "entricleDs &ecoming the systemic "entricle. $his results in an anatomic right "entricle ith a&normal geometry sustaining the afterload of a more ideally suited left "entricle. @ong%term complications of "entricular dilatation5 8 "al"e regurgitation5 and right "entricular failure ha"e &een reported in as many as 1 of patients many years folloing the atrial operation. $he multiple suture lines in the atrium ha"e &een associated ith a high incidence of late atrial arrhythmias and a lo incidence of sinus rhythm folloing the Mustard and Senning operations. $hese complications do not appear to &e as fre9uent ith the arterial sitch repair. 0n addition5 the complicated interatrial &aes ha"e &een associated ith pulmonary or systemic "enous &ae o&struction. #ecause the right "entricular out-o tract is not addressed during an atrial sitch operation5 right "entricular out-o tract o&struction is not a recogni4ed complication folloing the repair. Right "entricular out-o tract and supra"al"ar pulmonic stenosis5 hoe"er5 ha"e &een reported in patients after the arterial sitch repair5 oing to the reconstruction of the right "entricular out-o tract in that operation. lthough progression of pulmonary arterial o&struction has rarely &een reported folloing early repair ith the atrial or the arterial sitch procedure5 it is an unusual complication if operation is underta;en in infancy. +elayed repair &eyond age * months to 1 year5 hoe"er5 has &een associated ith a higher incidence of progressi"e de"elopment of pulmonary "ascular o&structi"e disease. $he rapidity of the de"elopment of pulmonary "ascular disease is increased &y the coe:istence of a 8S+.
. #. C. +.
<1. Critical aortic stenosis in the neonate is characteri4ed &y hich of the folloing? 0t is most often due to commissural fusion of a trilea-et "al"e. 0t may &e associated ith coarctation of the aorta5 P+5 and mitral stenosis. 0t can &e managed medically until the child is large enough to undergo aortic "al"e replacement. Success of "al"otomy is determined &y the ade9uacy of the left "entricle. nser/ #+ +0SCSS023/ Critical aortic stenosis in the neonate most often presents in the >rst ee; of life ith se"ere and progressi"e congesti"e heart failure and may &e associated ith coarctation of the aorta5 P+5 and mitral stenosis. $he prognosis is poor unless "al"otomy can &e performed e:peditiously. Medical management cannot sta&ili4e these infants for "al"e replacement at a later age. 0nfants hose left "entricle is too small to sustain the systemic circulation are unli;ely to sur"i"e aortic "al"otomy and5 thus5 should &e managed as patients ith hypoplastic left heart syndrome. $he aortic "al"e in neonatal aortic stenosis is most commonly unicuspid or &icuspid.
<6. Surgical management of aortic "al"e disease in an older child may include/ . 7nlargement of the aortic annulus. #. 0ncision of fused commissures. C. 0nsertion of a porcine "al"e prosthesis. +. $ransfer of the pulmonary "al"e to the aortic position.nser/ #+ +0SCSS023/ $he ma=ority of older children ith aortic stenosis and signi>cant trans"al"ular gradients can &e treated successfully &y aortic "al"otomy. $his can &e done percutaneously ith &alloon dilatation or surgically ith direct "isuali4ation 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 re9uired in children ho de"elop progressi"e aortic insuKciency after a pre"ious inter"ention. When "al"e replacement is performed it is desira&le to insert the largest prosthesis possi&le5 to allo for groth. 7nlargement of the aortic annulus is commonly performed for this purpose. 0f a true "al"e prosthesis is employed5 a mechanical "al"e is preferred. +ura&ility of :enograft "al"es in children is limited oing to early calci>cation and lea-et degeneration. $he pulmonary autograft techni9ue may &e the &est method of aortic "al"e replacement in children. With this operation the patientDs on 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"e5 the patient does n ot face the long%term complications of throm&oem&olism and &leeding imposed &y a mechanical "al"e and lifelong anticoagulation. <'. Which of the folloing 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 clic; is a speci>c 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. nser/ C+ +0SCSS023/ Su&aortic stenosis is rarely encountered in neonates. Most often it is disco"ered in an asymptomatic child during a routine physical e:amination. loud crescendoOdecrescendo systolic murmur ithout an e=ection clic; is usually noted. $he presence of an e=ection clic; is more consistent ith isolated "al"ular aortic stenosis. +iscrete su&aortic stenosis is approached surgically ith cardiopulmonary &ypass5 aortic cross%clamping5 and cardioplegic arrest. $he aorta is opened and the aortic "al"e lea-ets are retracted5 e:posing the >&rous mem&rane. $he >&rous ring is carefully e:cised5 ta;ing care to a"oid in=ury to the anterior lea-et of the mitral "al"e and the penetrating conduction &undle. 2nce the su&aortic mem&rane is e:cised a septal myectomy further opens the left "entricular out-o tract and diminishes the li;elihood 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 se9uential pacing. +. Com&ined septal myectomy and mitral "al"e plication.nser/ C+ +0SCSS023/ $he ma=ority of patients ith hypertrophic o&structi"e cardiomyopathy are treated medically ith &eta%&loc;ers such as propranolol and calcium channel &loc;ers 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 lea-et of the mitral "al"e performed in addition to the septal myectomy further opens the left "entricular out-o 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 e:perience relief of symptoms and left "entricular out-o gradients ith dual%cham&er permanent pacing. ppropriate pre%e:citation of the "entricular septum can prompt the septum to mo"e aay from the left "entricular all during systole and open the out-o tract.
. #. C. +.
<,. Which of the folloing statements a&out supra"al"ular aortic stenosis are true? Surgical repair is indicated only hen the systolic gradient e:ceeds E, mm. Bg. Simple e:cision of the supra"al"ular mem&rane results in satisfactory relief of the stenosis in most patients. $he di!use 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 unlessa&normalities of the "al"e itself also e:ist. nser/ C+ +0SCSS023/ Supra"al"ular aortic stenosis is a progressi"e disease and should &e repaired surgically if symptoms are present or the systolic gradient e:ceeds , mm. Bg. 0n addition to e:cision of the supra"al"ular mem&rane5 a patch of dacron or pericardium must &e placed across the area of narroing and don into at least one of the sinuses of 8alsal"a. Reoperation is rare after this procedure unless associated aortic "al"e disease is also present. 0n the di!use form of the disease the thic;ening of the aortic all commonly results in signi>cant luminal narroing of the ascending aorta and its ma=or &ranches.
#. C. +. 7.
<*. 7ach year the appro:imate num&er of mericans ho die from complications of coronary artery disease is/ . 15. 6,5. ,5. 155. 2"er 655. nser/ C +0SCSS023/ 0t is estimated that appro:imately E55 mericans currently ha"e symptomatic coronary artery disease. 2f these some 15,5 e:perience myocardial infarction annually and appro:imately ,5 die each year from complications.
. #. C. +.
cant 9uantity of &lood. Most of the collaterals are appro:imately 6 mm. or smaller5 and channels of this si4e cannot conduct signi>cant 9uantities of &lood for cardiac re9uirements. $here is no a&solute e:ample of anatomic end%arteries in humans. While the magnitude of arterial collateral circulation "aries considera&ly5 all organs ha"e some collaterals.
#. C. +. 7.
,. Coronary &ypass procedures ha"e &een demonstrated to/ . Reduce the incidence of myocardial infarction. #. Signi>cantly relie"es angina symptoms. C. Statistically impro"e the life span. +. 0mpro"e the e=ection fraction of the left "entricle in many patients in hom it is signi>cantly depressed preoperati"ely. nser/ #C+ +0SCSS023/ 0n a "ariety of studies5 coronary &ypass procedures ha"e &een demonstrated to reduce the incidence of su&se9uent myocardial infarction as ell as to relie"e signi>cantly 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. $he folloing patients are &est treated ith coronary artery &ypass grafting (C#H)/ . *%year%old man ith class 00 angina5 E, pro:imal right coronary artery lesion5 and normal "entricular function. #. *%year%old man ith unsta&le angina5 three%"essel disease5 and an e=ection fraction of ',. C. *%year%old nondia&etic man ith class 000 angina symptoms and focal discrete lesions in the mid%right coronary artery and mid%left circum-e: artery. +. *%year%old man ith dia&etes5 class 08 angina5 E, pro:imal left anterior descending and E, pro:imal right coronary artery o&struction5 and left "entricular e=ection fraction of *. nser/ #+
+0SCSS023/ C#H has &een shon to prolong patient sur"i"al compared ith medical therapy in those patients ith left main occlusi"e disease and those ith three%"essel or to%"essel disease ith pro:imal left anterior descending in"ol"ement in association ith class 000 or greater anginal symptoms5 impaired e=ection fraction5 or easily induci&le ischemia ith e:ercise. lthough percutaneous transluminal coronary angioplasty (P$C) appears to &e compara&le to C#H in nondia&etic patients5 patients ith dia&etes appear to ha"e a signi>cant sur"i"al ad"antage hen C#H is used. Similarly5 patients ith more e:tensi"e coronary artery disease are &etter treated ith C#H than ith P$C. ,6. Sternal ound infections that spread to the mediastinum are associated ith a mortality rate of/ . *. #. '. C. 6,. +. @ess than 1,.nser/ + +0SCSS023/ lthough the mortality rate folloing sternal infections ith mediastinitis formerly as high5 it is no greatly reduced. 0n most series5 mediastinitis is cured in more than G of patients ho are treated aggressi"ely ith dT&ridement and placement of muscle -aps or omentum into the mediastinum to speed ound healing. ,'. Perioperati"e myocardial infarction occurs folloing coronary &ypass procedures in appro:imately/ . 1,. #. 1. C. E. +. @ess than ,.nser/ + +0SCSS023/ Jolloing impro"ements in myocardial protection and coronary grafting techni9ues5 perioperati"e myocardial infarction no occurs in less that 6 to < of patients in most series. ,<. Jolloing acute myocardial infarction5 "entricular septal defects occur in/ . 6. #. 1. C. 1, +. 6 or less.nser/ + +0SCSS023/ Postmortem studies indicate that F to 1 of fatal cases of myocardial infarction are due to rupture of the heart. 0n addition5 infarction of t he inter"entricular septum ith su&se9uent formation of a "entricular septal defect occurs in 1 to 6 of patients ith acute myocardial infarction. $he usual inter"al &eteen the acute infarction and septal rupture< to 16 days correlates ith the histologic >nding of ma:imal cardiac muscle degeneration.
#. C. +. 7.
. #. C. +.
,,. Which of the folloing clinical characteristics isare associated ith a higher mortality after emergency C#H for failed P$C? . Multi"essel disease. Rescue atherectomy. Cardiogenic shoc; prior to C#H. Pre"ious &ypass surgery. ll of the a&o"e.nser/ C+ ,*. Which statement(s) a&out operati"e mortality and perioperati"e incidence of myocardial infarction for electi"e C#H (U) "ersus emergency C#H folloing failed P$C (V) isare accurate? $he operati"e mortality is higher for V &ut the incidence of perioperati"e myocardial infarction is unchanged &eteen U and V. $he operati"e mortality is unchanged &eteen U and V &ut the perioperati"e incidence of myocardial infarction is higher in V. $he operati"e mortality and perioperati"e incidence is higher in U than in V. $he operati"e mortality and perioperati"e incidence of myocardial infarction are no di!erent for U and for V. nser/ C
. #. C. +. 7.
,E. Which of the folloing statements a&out patients treated &y placement of an internal mammary artery (0M) &ypass graft at primary C#H isare correct? $he ris; for mor&idity and mortality from reoperati"e coronary &ypass grafting isincreased. @eft "entricular function is &etter preser"ed at the time of reoperation. $he ris; of sternal ound complications is greatly increased if the contralateral 0M is har"ested at the time of reoperation. light clamp should &e applied to the 0M pedicle to limit cardiac arming during cardioplegic arrest at the time of reoperation. functional study demonstrating a large portion of myocardium at ris; should &e o&tained &efore reoperation. nser/ #+7 +0SCSS023/ Patients ho ha"e an intact 0M graft should ha"e se"ere anginal symptoms and a signi>cant portion of myocardium at ris; &efore reoperati"e coronary &ypass grafting is considered. functional study may &etter de>ne the proportion of myocardium at ris; for ischemia and infarction. Patients ith an intact 0M graft are less li;ely to re9uire reoperation5 &ut if stenosis distal to the 0M and disease in other "ein grafts ha"e progressed or if a large portion of myocardium is at ris;5 reoperation is recommended. $he presence of an intact 0M is not a contraindication to reoperationA in fact5 this population of patients ha"e &etter%preser"ed "entricular function and are5 perhaps5 &etter candidates for reoperation. Placement of an 0M graft at the time of the >rst operation as critically important5 neutrali4ing the ad"erse e!ects of ele"ated serum cholesterol5 hypertension5 and smo;ing on reoperation%free sur"i"al. $he ris; of damaging an intact 0M graft is ' to ,. lateral pro=ection of the 0M at cardiac catheteri4ation ill de>ne its course5 particularly in relation to the sternum5 to allo more careful sternal re%entry. $he 0M should &e minimally dissected and a light clamp applied during cardioplegic arrest to limit cardiac arming and impro"e myocardial protection. $he 0M may &e detached and recycled if needed. $he use during reoperation of the contralateral 0M does not increase the ris; of sternal ound complications.
. #. C. +. 7.
,F. Considering the results of coronary reoperation in comparison to primary C#H5 choose the incorrect statement/ 2perati"e mor&idity and mortality are increased o"er those for primary C#H. Mortality most often stems from cardiac causes after reoperation. Sur"i"al of patients after hospital discharge folloing coronary reoperation is nearly e9ui"alent to sur"i"al after primary C#H. Compared to primary C#H5 return of anginal symptoms is delayed after reoperati"e C#H. Myocardial protection and the ris; of myocardial infarction in reoperation are complicated &y increased noncoronary collaterals5 patent atherosclerotic saphenous "ein grafts5 and more di!use coronary atherosclerosis. nser/ + +0SCSS023/ $he mortality and mor&idity after reoperati"e C#H are appro:imately to to three times that of primary C#H. 0n contrast to primary C#H5 here the ma=ority of deaths are a result of failure of other organ systems5 E, to F, of deaths after reoperati"e C#H are due to cardiac causes. $he increased ris; of reoperation results from more ad"anced nati"e "essel disease5 a longer cross%clamp time5 a longer cross%clamp time per graft5 a longer time to initiate cardiopulmonary &ypass5 and increased &lood loss. $he increased fre9uency of pulmonary complications5 myocardial infarction5 neurologic in=ury5 and death5 stems from the technical factors of reoperation and the characteristics of the patient population. $echnical factors include diKculty in >nding targets secondary to pericardial reaction and more di!usely diseased "essels5 the ris;s of in=uring the heart or great "essels on sternal re%entry5 increased &lood loss and ris; of re9uiring transfusion5 less a"aila&le conduit for &ypass5 and greater diKculty in pro"iding optimal myocardial protection. Characteristics of this patient population that increase ris;s include ad"anced age and diminished "entricular function. While sur"i"al after reoperation is nearly e9ui"alent to that after primary C#H5 angina symptoms return at tice the fre9uency in the >rst year after operation (
,G. Which statements are correct comparisons of gated e9uili&rium and initial%transit radionuclide measurements of left "entricular function? . Hated e9uili&rium techni9ues pro"ide more accurate measurements of e=ection fraction than initial% transit methods. #. @eft "entricular imaging time for a gated e9uili&rium study is at least 1 times that of an initial% transit study. C. #oth techni9ues re9uire the same radiopharmaceuticals.
+. #oth techni9ues re9uire a &olus in=ection.nser/ # +0SCSS023/ #oth techni9ues are e9ually accurate for measuring left "entricular e=ection fraction. $he left "entricular imaging time for gated e9uili&rium studies is at least 1 times that of initial% transit radionuclide angiocardiography. 0nitial%transit techni9ues use data from feer than 1 heart&eats5 hereas e9uili&rium studies re9uire more than 1 heart&eats to ac9uire data ith similar information density. $he initial%transit study can &e performed ith any radioacti"e su&stance5 &ut the gated e9uili&rium techni9ue re9uires a radiopharmaceutical that remains ithin the &lood pool for imaging. $he initial%transit radionuclide study re9uires a &olus in=ection5 &ut an e9uili&rium study can &e ac9uired up to se"eral hours after in=ection and must &e ac9uired hile the tracer is at e9uili&rium. *. $he radionuclide "aria&le that contains the greatest amount of prognostic information in patients ith coronary artery disease is/ . 7:ercise e=ection fraction. #. Change in regional all motion from rest to e:ercise. C. Ma:imal cardiac output during e:ercise.+. Change in heart rate during e:ercise. nser/ +0SCSS023/ $he e:ercise e=ection fraction is the single most important radionuclide "aria&le relating to su&se9uent cardiac death or myocardial infarction5 and this single "aria&le contains F of the prognostic information in the test.
. #. C. +. 7.
*1. Which of the folloing statements a&out left "entricular aneurysm isare correct? 8entricular aneurysms are commonly associated ith systemic arterial em&oli4ation. &sent collateral circulation in an area of myocardium supplied &y an acutely occluded artery fa"ors aneurysm formation. Postero&asal aneurysms are more common than those located in the anteroapical region. neurysm repair can impro"e associated cardiac "al"e dysfunction. Persistent S$ segment ele"ation after acute myocardial infarction suggests aneurysm formation. nser/ #+7 +0SCSS023/ $he mural throm&us fre9uently present on the endocardial surface of an aneurysm is usually adherent and rarely em&oli4es. Collateral circulation5 hen present5 often pre"ents transmural necrosis folloing arterial occlusion. Since the left anterior descending coronary artery is the "essel most commonly occluded in patients ith "entricular aneurysms5 most of the aneurysms are anteroapical. 0mpro"ements in "entricular contour and reduction in "entricular "olume accompany aneurysm repair. lthough persistent ele"ation of S$ segments folloing myocardial infarction is "ery suggesti"e of aneurysm formation5 the diagnosis should &e con>rmed &y more de>niti"e tests.
#. C. +. 7.
*6. Which of the folloing factors doesdo not increase early mortality associated ith repair of left "entricular aneurysm? . Class 08 cardiac status. Si4e of aneurysm. Presence of left main coronary disease. 7mergent operation. @ocation of aneurysm.nser/ #7 +0SCSS023/ Class 08 cardiac status and emergent operation &oth imply e:tensi"e myocardial damage and in most reported series are associated ith increased operati"e mortality. Similarly5 the presence of signi>cant stenosis of the left main coronary artery increases the operati"e mortality of "irtually all cardiac procedures. 2n the other hand5 neither the si4e of the aneurysm nor its location a!ect early operati"e mortality5 despite the fact that posterior aneurysms are technically more diKcult to repair and are much less common.
*'. $he most e!ecti"e medical therapy in ameliorating the symptoms of Naasa;iDs disease and pre"enting the de"elopment of giant coronary artery aneurysms is administration of/ . nti&iotics. #. nti"iral agents. C. spirin.
+. Hamma glo&ulin. 7. Hlucocorticoids.nser/ + +0SCSS023/ Naasa;iDs disease is a multisystemic disorder of un;non cause and is the leading cause of ac9uired heart disease in children in &oth Iapan and the nited States. lthough many clinical aspects of Naasa;iDs disease suggest an infectious agent5 the search for a single agent has &een unsuccessfulA neither anti&acterials nor anti"irals ha"e a role in the therapy of Naasa;iDs disease. $he goal of initial therapy of Naasa;iDs disease is the reduction of in-ammation5 including coronary and myocardial in-ammation. fter the diagnosis of Naasa;iDs disease is secured5 patients are treated ith intra"enous gamma glo&ulin and large doses of aspirin. Hamma glo&ulin5 6 gm. per ;g.5 is administered as a single infusion o"er 16 hours. $reatment ith intra"enous immune glo&ulin has &een shon to decrease the duration of fe"er5 to decrease the pre"alence of cardio"ascular complications5 and to pre"ent the progression to giant coronary aneurysms. Bigh% dose aspirin therapy contri&utes to the resolution of the acute manifestations of Naasa;iDs disease. When Naasa;iDs disease is diagnosed5 children are gi"en a regimen of aspirin5 1 mg. per ;g. per day5 hich is continued until defer"escence. $hereafter5 they are maintained on small doses of aspirin5 ' to , mg. per ;g. per day5 for F ee;s. $he goal of aspirin therapy is amelioration of symptoms and pre"ention of the throm&otic and em&olic complications of Naasa;iDs disease. spirin does not decrease the ris; of the de"elopment of coronary aneurysms. $here is no role for glucocorticoids in the treatment of Naasa;iDs disease.
. #. C. +. 7.
*<. 0ndications for surgical inter"ention in Naasa;iDs disease include hich of the folloing? $he presence of multiple coronary artery aneurysms. Myocardial infarction and se"ere left "entricular dysfunction. $he presence of a , mm. aneurysm in the right coronary artery. Progressi"e stenosis in the left anterior descending coronary artery. 3one of the a&o"e. nser/ + +0SCSS023/ $he indications for surgical treatment of Naasa;iDs disease include/ (1) progressi"ely stenotic coronary lesions demonstrated on coronary arteriography5 ith no distal coronary aneurysms ith stenosisA (6) locali4ed aneurysm ith signi>cant stenosis in the left main coronary arteryA (') signi>cant stenosis in to coronary arteriesA (<) presence of collateral "essels arising from a coronary artery ith a pro:imal aneurysmA (,) progressi"e stenosis in the left anterior descending coronary arteryA 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 folloing statements a&out the pathophysiology of 7&steinDs anomaly isare true? . $he tricuspid "al"e is usually insuKcient. #. $ypically there is a left%to%right shunt across the S+. C. $he redundant anterior lea-et of the tricuspid "al"e may cause o&struction of the right "entricular out-o tract. +. Pulmonary hypertension is a common late complication. 7. Bigh pulmonary "ascular resistance in neonates e:acer&ates tricuspid regurgitation and cyanosis. nser/ C7 +0SCSS023/ 7&steinDs anomaly is characteri4ed &y donard displacement of the tricuspid "al"e into the right "entricular ca"ity. $he anterior lea-et is large and Lsail%li;e5 hile the other to lea-ets are rudimentary. lthough the tricuspid "al"e occasionally may &e stenotic5 it is usually regurgitant. $he tricuspid regurgitation and functional right "entricular out-o tract o&struction caused &y the large anterior lea-et lead to right%to%left shunting across the S+. Systemic "enous hypertension is often present5 &ut pulmonary hypertension almost ne"er occurs ith this malformation. Jinally5 neonates that present ith 7&steinDs anomaly are mar;edly cyanotic5 oing to their high pulmonary "ascular resistance. $his causes a functional pulmonary atresia5 hich increases right%to%left shunting across the S+. **. 0n the surgical treatment of 7&steinDs anomaly5 hich of the folloing isare true? . 0n neonates5 the tricuspid "al"e ori>ce may &e o"ersen and a systemic%pulmonaryshunt created to pro"ide pulmonary &lood -o. #. $echni9ues in repair of the tricuspid "al"e do not utili4e plication of the atriali4ed right "entricle.
C. Closure of the S+ alone is ade9uate repair of the malformation. +. 0f tricuspid "al"e replacement is performed5 the "al"e should &e sutured a&o"e the coronary sinus to a"oid in=ury to the conduction system. 7. Currently5 mechanical prostheses are recommended for tricuspid "al"e replacement &ecause the dura&ility of &ioprosthetic "al"es in the tricuspid position is so poor. nser/ + +0SCSS023/ 0n a recent report on the surgical treatment of 7&steinDs anomaly in neonates5 Starnes descri&ed a techni9ue consisting of o"erseing the tricuspid "al"e5 atrial septectomy5 and placement of a systemic%pulmonary shunt. $hese patients are then later staged to a modi>ed Jontan procedure hen they outgro their shunts. Repair of the S+ alone as performed early in the treatment of 7&steinDs anomaly and as associated ith high mortality rates. 0t is not considered an ade9uate repair. Most techni9ues in tricuspid "al"e repair for 7&steinDs malformation utili4e plication of the atriali4ed right "entricle in addition to e:cision of redundant atrial tissue. 0f tricuspid "al"e replacement is necessary5 current approaches utili4e &ioprosthetic "al"es &ecause of their e:cellent dura&ility in the tricuspid position. Placement of the "al"e ring a&o"e the coronary sinus has &een associated ith a loer rate of postoperati"e heart &loc;.
. #. C. +.
*E. Which of the folloing congenital lesions of the coronary circulation causes a cardiac murmur that is similar to the murmur produced &y a P+? 2rigin of the left coronary artery from the pulmonary artery. 2rigin of the right coronary artery from the pulmonary artery. Coronary artery >stula. Mem&ranous o&struction of the ostium of the left main coronary artery.nser/ C +0SCSS023/ $he ma=or clinical >nding ith a coronary artery >stula is a continuous murmur o"er the site of the a&normal communication. $his murmur may closely resem&le that of P+.
*F. $he congenital coronary lesion most li;ely to cause death in infancy is/ . Coronary artery >stula. #. 2rigin of the left coronary artery from the pulmonary artery. C. 2rigin of the right coronary artery from the pulmonary artery. +. Congenital coronary aneurysm.nser/ # +0SCSS023/ $he prognosis for most patients ith origin of the left coronary artery from the pulmonary artery is poor. 0t has &een estimated that G, of patients ith this anomaly die ithin the >rst year of life unless surgical therapy is underta;en. Patients hose right coronary artery originates from the pulmonary artery are usually asymptomatic. Patients ith coronary >stulas occasionally su!er congesti"e heart failure early. Congenital aneurysms of the coronary arteries are most often asymptomatic until complications occur5 usually later in life.
. #. C. +.
*G. $he congenital coronary lesion associated ith minimal or a&sent clinical manifestations and nearly normal life e:pectancy is/ Congenital origin of &oth coronary arteries from the pulmonary artery. Congenital coronary artery >stula. Mem&ranous o&struction of the ostium of the left main coronary artery. Congenital origin of the right coronary artery from the pulmonary artery. nser/ + +0SCSS023/ 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 G years from unrelated pro&lems.
E. Which of the folloing isare indications for aortic "al"e replacement for aortic stenosis? . Syncope. #. Congesti"e heart failure.
C. ngina. +. $rans"al"ar gradient of ', mm. Bg ithout symptoms.nser/ #C +0SCSS023/ With progressi"e narroing of the aortic "al"e area from the normal ' to < s9. cm. to 1 s9. cm.5 patients &ecome symptomatic. $he classic symptoms produced &y aortic stenosis are syncope5 congesti"e heart failure5 and angina. 2nce symptoms occur5 life e:pectancy is limited to 6 to , years. $herefore5 symptomatic aortic stenosis is an indication for aortic "al"e replacement. $he ris; of death ith asymptomatic aortic stenosis is 9uite lo5 and aortic "al"e replacement is not indicated for asymptomatic patients ith a trans"al"ar gradient less than , mm. Bg. E1. nder hich of the folloing circumstances is medical management logical? . Moderate aortic insuKciency seen on echocardiography ith normal left "entricular end%systolic dimensions. #. Moderate to se"ere aortic insuKciency seen on echocardiography ith cardiomegaly on chest roentgenography. C. Moderate aortic insuKciency seen on echocardiography ith symptoms of congesti"e heart failure. +. Moderate aortic insuKciency ith an end%systolic left "entricular dimension of E mm. as seen on echocardiography. nser/ +0SCSS023/ $he left "entricle is usually a&le to compensate for a long time for the increased "olume load imposed &y aortic insuKciency. $he natural history of asymptomatic aortic stenosis is e:cellentA 1%year sur"i"al for moderate aortic insuKciency managed medically is as high as F, to G,. Medical management typically consists of diuretics and afterload reductionA hoe"er5 once the compensatory mechanisms &egin to fail5 sur"i"al is limited. Balf of patients ith signs or symptoms of congesti"e heart failure die ithin 6 years. $herefore5 e"idence of left "entricular dilation &y echocardiography (left "entricular end%systolic dimension greater than ,, mm.5 cardiomegaly on chest roentgenography) or symptoms of congesti"e heart failure are indications for aortic "al"e replacement. E6. Which of the folloing may &e indications for operation for mitral stenosis? . Systemic em&oli4ation. #. 0nfecti"e endocarditis. C. 2nset of atrial >&rillation. +. Worsening pulmonary hypertension.nser/ #C+ +0SCSS023/ lthough each is only a relati"e indication for operation for mitral stenosis5 systemic em&oli4ation5 infecti"e endocarditis5 onset of atrial >&rillation5 and orsening pulmonary hypertension may each &e an indication for operation for mitral stenosis. Systemic em&oli4ation5 infecti"e endocarditis5 and onset of atrial >&rillation are each complications of mitral stenosis that portend a ris; of further complication ith continued medical therapy. Patients older than < years ith mild class 00 congesti"e heart failure stand to gain symptomatically from operation for signi>cant mitral stenosis and do not run e:cessi"e ris; of multiple reoperati"e procedures. E'. Which of the folloing isare not true? . 2peration impro"es sur"i"al in patients ith se"ere5 symptomatic mitral "al"e disease. #. @eft "entricular dilatation ith class 0 or class 00 heart failure is an indication for operation ith mitral regurgitation. C. $ricuspid regurgitation is most commonly caused &y a&normalities of the lea-ets themsel"es. +. Mitral "al"e replacement re9uires resection of the mitral "al"e lea-ets and chordae. nser/ C+ +0SCSS023/ Relati"e to medical therapy alone5 surgical therapy has &een shon to impro"e sur"i"al in patients ith se"ere5 symptomatic mitral "al"e disease. 0n mitral regurgitation5 left "entricular dilatation is an indication for surgical inter"ention regardless of failure symptoms. $he most common cause of tricuspid regurgitation is tricuspid annular dilatation ithout a&normalities of the lea-ets themsel"es. Mitral "al"e replacement ith preser"ation of &oth lea-ets or at least the posterior lea-et is ell descri&ed and is pro&a&ly ad"isa&le for most patients to preser"e left "entricular function and reduce the pro&a&ility of "entricular%annular separation. E<. Which of the folloing generally are not symptoms of tricuspid "al"e disease? . Pulmonary edema. #. Bepatic failure.
C. nasarca. +. Boarseness.nser/ + +0SCSS023/ Bepatic failure and anasarca are indeed common symptoms of se"ere5 long%standing tricuspid "al"e disease ith increased "enous pressure. Pulmonary edema is a conse9uence of left% sided heart disease and does not result from a tricuspid lesion. Similarly5 hoarseness is most common after mitral "al"e disease ith left atrial enlargement and is rarely due to tricuspid "al"e disease alone.
. #. C. +.
E,. Which of the folloing are relati"e indications for mitral "al"e replacement5 as opposed to mitral "al"e repair? 7:tensi"e lea-et calci>cation. Mitral regurgitation. Chordal rupture of the anterior mitral lea-et. Signi>cant annular dilatation.nser/ +0SCSS023/ 7:tensi"e mitral "al"e calci>cation is a relati"e indication for mitral "al"e replacement. Mitral regurgitation or signi>cant annular dilatation may5 hoe"er5 &e amena&le to mitral "al"e repair. Chordal rupture of the anterior lea-et is generally repara&le using chordal transposition or polytetra-uoroethylene (P$J7) chordae.
. #. C. +.
E*. Which of the folloing are not true? $ricuspid regurgitation due to annular dilatation alone generally does not re9uire "al"e replacement. Mitral "al"e replacement ith either a &ioprosthesis or a mechanical "al"e re9uires arfarin anticoagulation. $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.nser/ # +0SCSS023/ $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 re9uire arfarin anticoagulationA hoe"er5 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 signi>cant incidence of "al"e throm&osis hen a mechanical "al"e is in the tricuspid position. Chronic renal failure is a relati"e indication for tissue "al"es &ecause "al"e calci>cation is rare and &ecause anticoagulation of patients on dialysis carries high ris;s of mor&idity and mortality.
. #. C. +.
. #. C. +.
EE. Which of the folloing are relati"e indications for mechanical5 as opposed to tissue5 "al"e replacement? Patient younger than ' years. Voung female patient ho desires children. n elderly patient. $ricuspid "al"e replacement. nser/ +0SCSS023/ ge younger than ' years is a relati"e indication for mechanical "al"es &ecause of an increased incidence of calci>cation of tissue "al"es in younger persons. young female ho desires children ould &e a relati"e contraindication to mechanical replacement &ecause of the ris; 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 replacement5 oing to the increased incidence of tricuspid "al"e throm&osis ith a mechanical prosthesis. EF. Which of the folloing statements are not true? #ioprosthetic "al"es ha"e a relati"ely high incidence of hemolysis. #ioprosthetic "al"es ha"e a loer incidence of postoperati"e prosthetic "al"e endocarditis. Mechanical "al"es de"elop structural failure after an a"erage of E to 1 years. Mortality attri&uta&le to arfarin therapy approaches , per patient%year.nser/ #C+
+0SCSS023/ #ioprosthetic "al"es ha"e a relati"ely lo incidence of hemolysis. #ioprosthetic and mechanical "al"es do not di!er signi>cantly in the associated incidences of postoperati"e prosthetic "al"e endocarditis. #ioprosthetic "al"es de"elop structural failure after an a"erage of E to 1 years5 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.
. #. C. +.
EG. Which of the folloing are not generally associated ith mitral stenosis ithout regurgitation? Pulmonary hypertension. Pulmonary edema. @eft "entricular dilatation. n opening snap after the second heart sound.nser/ #+ +0SCSS023/ Pure mitral stenosis ithout regurgitation may &e associated ith pulmonary hypertension5 pulmonary edema5 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 "entricle5 as ith mitral regurgitation.
F. $he most common location of accessory pathays in patients ith the Wol!%Par;inson%White syndrome is the/ . @eft free all. #. Right free all. C. Posterior septum. +. nterior septum.nser/ +0SCSS023/ ll ma=or pu&lished series of the Wol!%Par;inson%White syndrome indicate that the ma=ority of all accessory pathays appear in the left free all space. 0n one series5 appro:imately * of all accessory pathays occur in the left free all space. 0n 7&steinDs anomaly5 pathays are usually located in the posterior septum andor right free all spaces. 0f these patients are e:cluded5 appro:imately E of pathays occur in the left free all space.
. #. C. +.
F1. $he anatomic electrophysiologic &asis of 8 node re%entry tachycardia is dual 8 node conduction pathays. 8 node re%entry tachycardia is most li;ely to occur ith hich of the folloing electrophysiologic a&errations? Pro:imal antegrade &loc; in the slo conduction pathay. Pro:imal retrograde &loc; in the slo conduction pathay. Pro:imal antegrade &loc; in the fast conduction pathay. Pro:imal retrograde &loc; in the fast conduction pathay. nser/ C +0SCSS023/ retrograde conduction &loc; in either the slo or fast pathay ould &e li;ely to pre"ent a re%entrant circuit from de"eloping. pro:imal antegrade &loc; in the slo conduction pathay is e:tremely unusual &ecause of the short refractory period of the slo conduction pathay. $he most common conduction &loc; that occurs in patients ith dual 8 node physiology is a pro:imal antegrade conduction &loc; in the fast pathay &ecause of its longer refractory period. $his antegrade &loc; in the fast conduction pathay allos 8 conduction to occur "ia the slo pathay and to return in retrograde fashion up the fast pathay to esta&lish the re%entrant circuit responsi&le for 8 node re%entry tachycardia.
. #. C. +. 1. 6. '.
F6. Match the four surgical procedures that ha"e &een de"eloped for the treatment of atrial >&rillation ith the ma=or detrimental se9uela(e) of atrial >&rillation that each corrects. Bis &undle a&lation. @eft atrial isolation procedure. Corridor procedure. Ma4e procedure. PatientDs sensation of irregular heart rhythm. Bemodynamic compromise &ecause of loss of 8 synchrony. 0ncreased "ulnera&ility to throm&oem&olism.nser/ %1. #%156. C%1. +1565'
+0SCSS023/ $he surgical procedure most commonly employed for the treatment of atrial >&rillation is catheter a&lation of the Bis &undle. $he 0nternational Catheter &lation Registry re"eals that more than * of patients ho undergo electi"e catheter a&lation of the &undle of Bis do so for the treatment of atrial >&rillation. Bis &undle a&lation is an isolation procedure5 in that it con>nes the atrial >&rillation to the atria and protects the "entricles from the unpleasant sensation of an irregular heart&eat. #ecause the atria continue to >&rillate there is no restoration of 8 synchrony5 and therefore there is no impro"ement in cardiac hemodynamics. Moreo"er5 the continuing >&rillation of the left atrium means that postoperati"ely the patient is still at the same ris; for throm&oem&olism. $hus5 Bis &undle a&lation corrects only one of the three detrimental se9uelae of atrial >&rillation5 namely the arrhythmia pro&lem. $he left atrial isolation procedure con>nes atrial >&rillation to the left atrium5 alloing the sinus node to dri"e the remainder of the heart in a normal sinus rhythm. $hus5 it alle"iates the unpleasant sensation of an irregular heart&eat. 0n addition5 &ecause 8 synchrony is re%esta&lished &eteen the right atrium and right "entricle5 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. 0n the presence of a normal left "entricle the left%sided cardiac output is also normal5 despite the fact that left%sided 8 synchrony is not presentA hoe"er5 &ecause the left atrium is alloed to >&rillate5 the "ulnera&ility to throm&oem&olism remains unchanged postoperati"ely. $he corridor procedure allos the sinus node to dri"e the heart in normal sinus rhythm5 &ut &ecause of the total isolation of the sinoatrial and 8 nodes from the remainder of the atria5 the atria may continue to >&rillate. 7"en if they do not5 in e!ect they are isolated from their respecti"e "entricles so that 8 synchrony is lost on &oth sides of the heart. s a result5 the corridor procedure alle"iates the sensation of arrhythmia &ut does not restore normal hemodynamics5 nor does it decrease "ulnera&ility to throm&oem&olism. $he ma4e procedure a&lates the re%entrant circuits responsi&le for atrial >&rillation and restores the normal sinus rhythm. $hus5 it alle"iates the sensation of arrhythmia5 restores normal hemodynamics5 and alle"iates the "ulnera&ility to throm&oem&olism.
. #. C. +.
F'. ll of the folloing statements a&out nonischemic "entricular tachyarrhythmias are true e:cept/ $hey usually occur in the right "entricle. $hey are usually associated ith a left &undle &ranch &loc; pattern during the tachycardia. $hey are usually more refractory to medical therapy than ischemic "entricular tachyarrhythmias. $hey usually occur as a result of automaticity rather than re%entry.nser/ + +0SCSS023/ 3onischemic "entricular tachyarrhythmias usually occur in the right "entricle5 and as a result the 7CH shos a left &undle &ranch &loc;Otype pattern during "entricular tachycardia. $hese arrhythmias are notoriously refractory to medical therapy and they occur almost e:clusi"ely on a re%entrant &asis.
. #. C. +. 7.
F<. Which of the folloing statements a&out left atrial my:oma are true? $his lesion5 &y site and histology5 is the most common primary cardiac tumor. 0t is &est diagnosed &y cardiac catheteri4ation and angiography. $he symptom comple: can mimic collagen "ascular disease. 0t has an intraca"itary groth pattern. 0t has a multicentric origin in the cham&er all.nser/ C+ +0SCSS023/ 7ighty per cent of primary cardiac tumors are &enign5 and half of these &enign tumors are my:omas. Se"enty%>"e per cent of my:omas arise in the left atrium in the region of the fossa o"alis. 7chocardiography is the techni9ue of choice in the e"aluation of intracardiac tumors5 and >ndings suggesti"e of my:oma occur in G, of patients e:amined. 0n"asi"e procedures5 ith the attendant ris; of tumor em&oli4ation5 are not arranted. 2ing to an autoimmune phenomenon5 left atrial my:omas can present ith systemic constitutional symptoms of fe"er5 malaise5 eight loss5 polymyositis5 and &lood dyscrasias that mimic collagen "ascular disease. 2f surgical signi>cance is the fact that most my:omas rarely e:tend deeper than the endocardium &ut gro as polypoid5 intraca"itary masses. ttachment &y a "ascular stal; thus allos tumor mo&ility5 predisposing to em&oli4ation and interference ith mitral "al"e competence and causing characteristic echocardiographic >ndings.
F,. Which of the folloing statements a&out malignant cardiac tumors are true? . Sarcomas are the most fre9uent primary malignancy. #. Metastatic tumors are usually asymptomatic. C. d=u"ant chemotherapy and irradiation are eKcacious in prolonging sur"i"al.+. 0ntra%atrial e:tension of renal neoplasms is a contraindication for surgical resection.
7. Constricti"e physiology is an indication for operation. nser/ # +0SCSS023/ $enty per cent of primary cardiac tumors are some "ariant of sarcoma. Precise histologic classi>cation is not imperati"e5 as all ha"e a similar clinical picture ith rapid systemic dissemination and aggressi"e local in"asion. 0n contrast5 metastatic tumors cause symptoms in only 1 of patients. nfortunately5 most primary and secondary cardiac malignancies infre9uently respond to systemic chemotherapy or mediastinal irradiation. Surgical treatment is most successful ith renal tumors e:tending into the right atrium. Signi>cant ,%year sur"i"al can &e achie"ed ith concomitant nephrectomy and intra%atrial resection of the tumor throm&us. Relief of tamponade is orthhileA hoe"er5 e:tensi"e decortication pro"ides little help. F*. +isad"antages of temporary pacing through s;in electrodes applied to the anterior chest all include all of the folloing e:cept/ . S;in &urns. #. Painful chest all muscle contractions. C. 8entricular >&rillation. +. 0na&ility to pace.nser/ C +0SCSS023/ 0n 1G,6 oll >rst descri&ed successful pacing through e:ternal metal electrodes applied to the anterior chest all. Clinical e:perience ith this techni9ue has shon t hat it is &oth feasi&le and lifesa"ing for temporary pacingA hoe"er5 disad"antages of the e:ternal pacing techni9ue include s;in &urns hen too little electrode =elly is applied5 painful chest all muscle contractions5 and ina&ility to pace in thic;%chested or emphysematous patients. 8entricular >&rillation induced &y e:ternal temporary cardiac pacing is e:ceedingly rare. FE. 0n adults the most common cause of ac9uired complete heart &loc; is/ . 0schemic heart disease. #. Sclerodegenerati"e disease. C. $raumatic in=ury. +. Cardiomegaly.nser/ # +0SCSS023/ #efore permanent pacema;ers ere a"aila&le5 , of patients ith complete heart &loc; died ithin 1 year. $he most common cause of ac9uired complete heart &loc; in adults is sclerodegenerati"e disease of the cardiac s;eleton and 8 conduction system. 2ther less common causes of complete heart &loc; include ischemic heart disease5 cardiomyopathic processes5 ChagasD disease5 and traumatic in=ury. FF. $he most common indication for permanent pacing is/ . Complete heart &loc;. #. Second%degree 8 &loc;. C. Chronic &ifascicular &loc;. +. Sic; sinus syndrome.nser/ + +0SCSS023/ Patients ith sinus node dysfunction may de"elop a num&er of arrhythmias5 such as inappropriate sinus &radycardia5 chronotropic incompetence5 sinoatrial e:it &loc;5 and sinus arrest. $his group of rhythm disorders typically occurs in older patients ith or ithout underlying heart disease and is collecti"ely ;non as the Lsic; sinus syndrome. 0n addition5 many patients ith sic; sinus syndrome ha"e associated atrial tachyarrhythmias5 particularly atrial >&rillation. $his association of atrial tachyarrhythmias in patients ith the sic; sinus syndrome is called the tachycardia%&radycardia (or tachy%&rady) syndrome. $he most common indication for permanent pacing occurs in patients ith the sic; sinus syndrome. FG. +ecreasing pacema;er electrode tip si4e results in/ . @oer pacing thresholds. #. 0mpro"ed electrogram sensing. C. +ecreased &attery life.+. @ess patient discomfort. nser/ +0SCSS023/ +ecreasing pacema;er electrode tip si4e results in loer pacing thresholds5 &oth at the time of implant and su&se9uently5 &ecause of higher current density. Boe"er5 &etter sensing
function is directly related to electrode area and is ad"ersely a!ected &y small electrode si4e. $herefore5 a compromise &eteen pacing and sensing eKciency is re9uired. $ypical electrode surface areas for pacing are &eteen F and 1 s9. mm. G. t the time of "entricular pacema;er implantation5 lead resistance is determined at a "oltage near that of the pacema;erDs output. $he calculated resistance at , "olts should range from/ . 1 to 1 ohms. #. 16, to 6, ohms. C. ' to F ohms. +. 1 to 1, ohms.nser/ C +0SCSS023/ t the time of pacema;er implantation5 in addition to measuring pulse amplitude ("oltage and current) and pulse idth5 resistance is also determined. s descri&ed &y 2hmDs la5 resistance is calculated &y di"iding "oltage &y current. Resistance calculations are made at a "oltage near that of the pacema;erDs output. $he calculated resistance at , "olts should range from ' to F ohms. n unsatisfactorily lo resistance is unsatisfactory &ecause current is asted and &attery life is shortened. Con"ersely5 e:cessi"ely high resistance (more than F ohms) increases &attery life &ut decreases the current deli"ered to the heart for pacing. G1. "entricular inhi&ited%demand pacema;er using the 0ntersociety Commission for Beart +isease Resources (0CB+) code is designated as/ . +80. #. 880. C. 822.+. 8++. nser/ # +0SCSS023/ "entricular inhi&ited%demand pacema;er using the 0CB+ code is designated as 880. s the 0CB+ code states5 the pacema;er senses intrinsic "entricular acti"ity and is inhi&ited hen this acti"ity e:ceeds the stand&y or escape rate of the pacema;er. When the intrinsic "entricular rate falls &elo the escape rate of the pulse generator5 the pacema;er &egins to function at its programmed rate. G6. 0n rate%modulated pacing5 the pacing rate is determined &y a physiologic parameter other than atrial rate and is measured &y a special sensor in the pacema;er or pacing lead. $he most commonly used physiologic parameter in rate%modulated pacema;ers is/ . Q$ inter"al. #. 8enous &lood temperature. C. Mi:ed "enous o:ygen saturation. +. #ody motion.nser/ + +0SCSS023/ +uring e:ertion5 the re9uired increase in cardiac output is o&tained mostly &y the increase in paced heart rate5 although increased "enous >lling and maintenance of 8 synchrony are also important contri&utors. $he most commonly used physiologic parameters in rate% modulated pacema;ers at the present time are &ody motion and minute "entilation. 2ther parameters that are less commonly used or under e"aluation include Q$ inter"al5 "enous &lood temperature5 mi:ed "enous o:ygen saturation5 contractility5 stro;e "olume5 "enous pB5 and the paced depolari4ation gradient. G'. $he most common pacing mode used in patients ith symptomatic &radycardia and an underlying sinus rhythm is/ . 0. #. +80. C. +++.+. 880. nser/ C +0SCSS023/ Lni"ersal5 or +++5 pacing has &een shon to ha"e many &ene>ts o"er other pacing modalities5 including the a&ility to trac; the intrinsic sinus rate5 pace the atrium and "entricle5 maintain atrio"entricular synchrony5 and a"oid the pacema;er syndrome. Recognition of these
&ene>ts has steadily increased the use of +++ pacema;ers in the last decade5 and at the present time +++ is the most common pacing mode. G<. trans"enous pacema;er generator poc;et should &e placed on the patientDs nondominant side o"er the/ . nteromedial chest all. #. nterolateral chest all. C. 0nferomedial chest all. +. 0nferolateral chest all.nser/ +0SCSS023/ #ipolar impulse generators can &e placed either in the su&cutaneous tissue or &eneath the muscle. Migration of the impulse generator most commonly occurs in infracla"icular pacema;ers poc;ets. Migration tends to follo the cur"ature of the chest all5 and the impulse generator tends to migrate laterally. $his can &e pre"ented &y creating an anteromedial poc;et large enough to contain the impulse generator and lead. 0n suscepti&le persons the impulse generator can &e further secured to the chest all to pre"ent migration.
. #. C. +.
G,. Pacema;er%mediated tachycardia is caused &y/ Pacema;er induction of atrial >&rillation. Sensing of retrograde atrial acti"ation. 0nappropriate "entricular sensing. @ead fracture.nser/ # +0SCSS023/ Pacema;er%mediated tachycardia occurs in the setting of intact "entriculoatrial conduction. $ypically5 premature "entricular contractions may &e conducted retrogradely through the 8 conduction system and cause retrograde acti"ation of the atrium. 0f this retrograde atrial acti"ation occurs after completion of the programmed pacema;er "entriculoatrial refractory period5 the atrial e"ent is sensed &y the +++ pacema;er and e"o;es a paced "entricular e"ent that may cause further 8 conduction. 0f each "entricularly paced e"ent results in atrial acti"ation sensed &y the pacema;er5 pacema;er%mediated tachycardia ill &e generated.
G*. Which cardio"ascular pharmacologic agents are safe to use during routine a&dominal surgery in a E,%year%old oman ith documented hypertension and mild coronary artery disease? . 3ifedipine. #. tenolol. C. Bydrala4ine. +. Captopril.7. Reserpine. nser/ #+ +0SCSS023/ 3ifedipine is tolerated fairly ell &y elderly patients and is safe to use in the perioperati"e period ith close hemodynamic monitoring. tenolol is a safe &eta%&loc;er to use during the perioperati"e period and pro"ides protection from cardiac rhythm distur&ances and re&ound hypertension. Bydrala4ine5 if gi"en ithout a &eta%&loc;er5 often elicits re-e: tachycardia5 hich limits its usefulness. Captopril is a safe agent that does not appear to interfere ith the normal cardio"ascular response to anesthesia5 and a&rupt ithdraal of this agent may result in se"ere hypertension and should &e a"oided. Reserpine is an adrenergic inhi&itor that may depress cardiac output and result in hypotension5 so its use in the perioperati"e setting is limited.
#. C. +. 7.
GE. Which inotropic drugs are safe for use in elderly patients ith mild congesti"e heart failure in the postoperati"e period? . +igitalis compounds. +opamine. mrinone. Melrinone. +o&utamine.nser/ #C+7 +0SCSS023/ +opamine and do&utamine stimulate cardiac &eta%receptors and are "ery useful in pro"iding inotropic support for patients in the postoperati"e period. Melrinone and amrinone are phosphodiesterase inhi&itors that ha"e strong inotropic e!ects hile causing arterial and "enous dilation. Melrinone and amrinone are useful in patients ith lo cardiac output5 especially in the setting of congesti"e heart failure. +igitalis compounds can &e trou&lesome in the postoperati"e period oing to the to:ic e!ects of these agents. Jurthermore5 perioperati"e hypo:ia and hypo;alemia increase myocardial suscepti&ility to digitalis%induced "entricular arrhythmias.
. #. C. +. 7.
GF. Which anticoagulation treatment plan(s) isare appropriate for a E6%year%old man ith a mechanical heart "al"e in place ho ta;es Coumadin (arfarin) and no re9uires electi"e left colon resection? +iscontinuation of Coumadin therapy on the day of the operation. +iscontinuation of Coumadin therapy on the day of the operation ith replacement of clotting factors ith fresh fro4en plasma (JJP) &efore the start of the surgical procedure. +iscontinuation of Coumadin therapy , days &efore operation ith no further anticoagulation therapy &efore surgery. +iscontinuation of Coumadin therapy , days &efore operation ith the institution of intra"enous heparin as the prothrom&in time normali4es. +iscontinuation of Coumadin therapy 6 days &efore operation folloed &y large doses of aspirin. nser/ + +0SCSS023/ Many patients ho re9uire anticoagulation ith Coumadin for underlying cardiac disease need to undergo routine general surgical procedures. $he current recommendations for patients ho ha"e &een on long%term Coumadin therapy is to discontinue Coumadin , days &efore an operati"e procedure. s the patientDs prothrom&in time normali4es intra"enous heparin should &e started. $he patient should &e maintained on a therapeutic dose of heparin ith an acti"ated partial throm&oplastin time (aP$$) of at least * seconds. Beparin should then &e ithheld appro:imately < to * hours &efore the surgical procedure. $he operation is then performed in a Lheparin indo5 here the le"el of anticoagulation can easily &e titrated or totally re"ersed ith protamine if necessary.
. #. C. +. 7.
GG. Which of the folloing treatment plans is appropriate for a *F%year%old patient ith moderate to se"ere congesti"e heart failure folloing a ma=or a&dominal surgical procedure? ggressi"e use of inotropic support ith epinephrine. ggressi"e diuresis ith furosemide and inotropic support ith dopamine. fterload reduction ith nitroprusside and inotropic support ith dopamine. Close perioperati"e monitoring and inotropic support ith melrinone. 0ntra"enous digitalis ith diuresis using furosemide as needed.nser/ C+ +0SCSS023/ $reatment of congesti"e heart failure using epinephrine alone is contraindicated oing to the profound "asoconstricti"e properties of epinephrine5 hich only e:acer&ate the heart failure. +iuresis ith furosemide and inotropic support ith dopamine is accepta&le for patients ith mild congesti"e heart failureA hoe"er5 in the postoperati"e period pharmacologic diuresis can lead to profound hypo"olemia re9uiring continuous in"asi"e hemodynamic monitoring. $he ideal choice for the postoperati"e management of patients ith se"ere congesti"e heart failure is afterload reduction using nitroprusside and inotropic support ith dopamine. $his helps to stimulate the failing heart hile decreasing the afterload pressure against hich the heart must pump. Melrinone is a useful phosphodiesterase inhi&itor5 hich has &een shon to &e useful in the treatment of mild to moderate congesti"e heart failure. +igitalis along ith a diuretic in the postoperati"e period can &e trou&lesome oing to the potential to:icity of digitalis hile the patient has o ngoing -uid and electrolyte shifts.
. #. C. +. 7.
1. Which of the folloing steps isare appropriate for a *,%year%old oman ho de"elops atrial >&rillation ith associated mild hypotension and rapid "entricular response folloing partial gastric resection? Correction of electrolytes and &lood chemistries. 7"aluation for possi&le myocardial infarction. $reatment ith intra"enous lidocaine. ttempt to limit the "entricular response ith digitalis. 0mmediate cardio"ersion.nser/ #+ +0SCSS023/ When a patient de"elops postoperati"e atrial >&rillation folloing an e:tracardiac procedure5 correction of the patientDs &lood chemistries and electrolytes is essential. $he patient must also undergo e"aluation for a possi&le myocardial infarction as the cause of the atrial dysrhythmia. $he >rst rule in treatment is to slo the "entricular response and attempt to limit hemodynamic insta&ility. +igitalis is e!ecti"e in sloing don the "entricular response and thus impro"ing the hemodynamic status of the patient. @idocaine has little use in controlling atrial dysrhythmias &ut is "ery e!ecti"e in decreasing "entricular ectopy. 0mmediate cardio"ersion is rarely indicated for ne%onset atrial >&rillation. 2nly after correction of all underlying meta&olic and
electrolyte defects as ell as an attempt at medical con"ersion and "entricular rate control is cardio"ersion recommended.
#. C. +. 7.
11. $he damaging e!ects of cardiopulmonary &ypass are5 to a large degree5 due to acti"ation of the humoral ampli>cation system. $he humoral ampli>cation system includes hich of the folloing? . $he coagulation cascade. $he >&rinolytic cascade. Complement acti"ation. and C. 5 #5 and C.nser/ 7 +0SCSS023/ Cardiopulmonary &ypass stimulates a hole%&ody in-ammatory response5 and the concentrations of se"eral in-ammatory mediators (e.g.5 complement fraction C,a) ha"e &een associated ith su&system dysfunction folloing cardiopulmonary &ypass. $his in-ammatory response is comple: and has se"eral arms5 including the coagulation5 >&rinolytic5 and complement systems. Simply &loc;ing one pathay is unli;ely to completely pre"ent &ypass%induced in=ury.
16. de9uate -o during cardiopulmonary &ypass is &est indicated &y/ . Systemic &lood pressure of G, mm. Bg. #. rterial P2 6 of 6' mm. Bg. C. Mi:ed "enous hemoglo&in saturation of EF. +. Central "enous pressure of 1 mm. Bg.7. Plasma lactate "alue of * mg. per dl. nser/ C +0SCSS023/ $he purpose of cardiopulmonary &ypass is to pro"ide ade9uate circulation of &lood to sustain aero&ic meta&olism. 2:ygen consumption during &ypass depends on &ypass -o until a critical -o is attained. With higher -os there is no further increase in o:ygen consumption (i.e.5 o:ygen consumption &ecomes -o independent)5 and the mi:ed "enous hemoglo&in saturation increases. mi:ed "enous hemoglo&in saturation of EF indicates that &ypass -o is a&o"e the critical le"el and that -o is ade9uate. $he other "aria&les do not ensure ade9uate &ypass -o.
. #. C. +. 7.
1'. Which of the folloing does not typically occur during the >rst fe minutes of cardiopulmonary &ypass? 0nterstitial -uid increases. #lood -o &ecomes nonpulsatile. Platelet count decreases. Complement is acti"ated. Systemic "ascular resistance falls.nser/ +0SCSS023/ Se"eral e"ents occur during the >rst fe minutes of &ypass. $he tu&ing and o:ygenator surfaces are coated &y serum proteins that in turn acti"ate platelets. $his reduces the platelet count. $he roller pump produces nonpulsatile -o5 hich is di!erent from the usual pulsatile cardiac -o. Serum complement is acti"ated &y e:posure of &lood to the nonphysiologic surfaces of the pump%o:ygenator5 and systemic "ascular resistance falls. 0nterstitial -uid accumulates during &ypassA hoe"er5 this occurs later during &ypass.
1<. Which of the folloing are physiologic &ene>ts of intra%aortic &alloon counterpulsation to the ischemic "entricle? . Preload reduction. #. fterload reduction. C. Coronary &lood -o enhancement. +. +ecreased "entricular end%diastolic pressure.nser/ #C+ +0SCSS023/ 0n general5 preload relates to the "olume of &lood or -uid presented to the left "entricle. lthough all tension does increase ith increased "olume5 Starling properties are called forth for added eKciency. Preload is controlled &y "olume status as ell as capacity of the "enous system. $he e!ects of &alloon counterpulsation on cardiac preload are minimal and secondary to other changes. s the &alloon collapses in the aorta5 the a&sence of the &alloon "olume5 or La&yss5 creates a decrease in "entricular afterload. 0n e!ect this decreases "entricular all tension5 reducing myocardial o:ygen consumption signi>cantly. +uring counterpulsation5 the intra%aortic &alloon in-ates in diastole5 ele"ating coronary perfusion pressure signi>cantly. Ma:imal coronary artery perfusion occurs in this part of the cardiac cycle. $hus5 ischemic "entricles &ene>t especially
from &alloon pumping. $he &alloon pump does not directly decrease the left "entricular end% diastolic pressure. Boe"er5 in "entricles failing from ischemia the com&ination of afterload reduction and impro"ed coronary &lood -o usually augments cardiac function5 producing decreased cardiac >lling pressure or left "entricular end%diastolic pressure.
. #. C. +. 7.
1,. Which of the folloing are the ma=or indications for instituting intra%aortic &alloon pumping? Medically refractory angina. cute papillary muscle rupture. @eft main coronary artery lesion. 8entricular failure after cardiac surgery. P$C failure.nser/ #+7 +0SCSS023/ Medically refractory angina is one of the ma=or indications for implementing the intra% aortic &alloon pump. When intra"enous nitroglycerin &ecomes ine!ecti"e at relie"ing chest pain or results in early hypotension5 the &alloon pump should &e used in preparation for surgical re"asculari4ation or percutaneous angioplasty. #y reducing left "entricular afterload5 the pump reduces regurgitation into the left atrium. $hus5 &alloon counterpulsation is "ery helpful for treating patients ith acute mitral insuKciency secondary to papillary muscle rupture. Patients should undergo "al"e surgical procedures emergently5 as &alloon pump support is only tempori4ing. $he mere presence of a left main coronary lesion is not an indication for use of the &alloon pump. 0n former years such pumps ere inserted prophylactically &efore induction of anesthesia for coronary &ypass surgery. 3eer anesthetic techni9ues ha"e largely o&"iated thisA hoe"er5 in the presence of a left main lesion and medically refractory angina the &alloon pump should &e used. $he &alloon pump is 9uite e!ecti"e in helping to ean patients ho ha"e postcardiotomy left "entricular failure from cardiopulmonary &ypass. $his is one of the ma=or uses of this de"ice. $he 7mory ni"ersity group as the >rst to e:pound on the eKcacy of the &alloon pump in sta&ili4ing patients folloing percutaneous angioplasty failure. With the pump inserted5 most patients can &e transported to the operating room safely5 many &eing sta&le enough to har"est an internal mammary graft instead of ha"ing to defer to the more accessi&le &ut less prefera&le saphenous "ein.
1*. Which of the folloing are the most fre9uent complications of intra%aortic &alloon counterpulsation? . Stro;e. #. @im& ischemia. C. rrhythmias. +. ortic throm&osis.nser/ # +0SCSS023/ Stro;e rarely occurs secondary to intra%aortic &alloon pump use. $he &alloon must &e positioned ell &elo the aortic arch "essels and ne"er pro:imal to the left su&cla"ian artery origin. Stro;es ha"e &een reported from em&oli &eing thron retrograde from the &alloonA hoe"er5 this is "ery rare. @im& ischemia is one of the most fre9uent complications of &alloon pumping. $he com&ination of iliofemoral atherosclerosis and catheter luminal o&struction may impede distal -o. $his may re9uire catheter remo"al to re%esta&lish -o. 0n 6 to 1 of patients5 arterial reconstruction is necessary to repair &alloon%related complications. Smaller catheters ha"e helped pre"ent lim& ischemia. rrhythmias in general are not complications of &alloon pumping. 0n fact5 arrhythmias related to ischemia may &e controlled &y the &alloon pump. ortic throm&osis can occur "ery rarely ith pump use. more fre9uent occurrence is distal em&oli4ation ith lim& ischemia. Patients should &e heparini4ed hile the &alloon catheter is in place. Jolloing cardiac surgery heparini4ation is usually delayed for 16 to 6< hours.
#. C. +. 7.
1E. Permanent arti>cial hearts are &eing de"eloped that are electrically poered. Wireless techni9ues are used to transmit the electrical energy across the &ody all using the principle of/ . 0nfrared sensor. 0nducti"e coupling. $hermionic coupling. Bigh%pressure li9uid chromatography (BP@C). 0nfrared spectroscopy.nser/ # +0SCSS023/ 7lectrical energy can &e transmitted across the &ody all &y tunnelling an electric ireA hoe"er5 e:perience has shon that infection5 starting at the s;in line and &urroing deeper into the &ody5 ill occur o"er time. $his infection can &e delayed5 &ut not stopped5 &y the use of a "elour co"ering on the ire. Wireless electrical energy transmission as >rst used in clinical surgery &y W.W.@. Hlenn in the 1G,s for poering pacema;ers. $he remar;a&le ad"ances in electronics
ha"e facilitated this techni9ueA hoe"er5 the placement of the to coils parallel to one another (ith the s;in &eteen)5 as opposed to interloc;ing as in an industrial transformer5 reduces the eKciency of transmission from appro:imately GG to E.
#. C. +. 7.
1F. $he folloing statements a&out the pneumatic arti>cial heart isare correct/ . 0t can support the circulation for o"er 1 year. 0t may &e complicated &y infection or throm&oem&olism. When further de"eloped5 it ill &e an ideal permanent heart su&stitute. 0t is an ideal L&ridge for transplantation. 0t can &e implanted using techni9ues similar to those used for heart transplantation. nser/ #7 +0SCSS023/ $he pneumatic arti>cial heart as de"eloped as a permanent cardiac su&stitute5 &ut the need for to tu&es to pass through the chest all and the &ul;y poer unit ha"e relegated the pneumatic heart to short%term use as a &ridge to transplantation. $he heart is implanted using similar techni9ues as a heart transplantation. $he presence of foreign surfaces and cre"ices ma;e the de"ice prone to throm&oem&olism and infection. Most surgeons feel that left "entricular support or &i"entricular assist pumps represent a &etter option for those patients ith end%stage congesti"e heart failure ho re9uire use of a &ridge de"ice.
1G. cyanotic infant has echocardiographic e"idence of a uni"entricular heart (8B). $he folloing isare true/ a. &. c. d.
$he most common form of the disorder is a dou&le%inlet right "entricle $o &e classi>ed as a "entricle5 the cham&er must recei"e at least half of an inlet "al"e $his infant is a good candidate for a #laloc;%$aussig shunt 2ptimal correction of 8B di"erts all "ena ca"al &lood -o into the pulmonary arteries (Jontan procedure) e. 0n the a&sence of pulmonic stenosis5 8B usually presents as congesti"e heart failure nser/ &5 c5 d5 e ni"entricular heart is de>ned &y the connection of the atria to only one "entricular cham&er5 usually the left as a dou&le inlet left "entricle. cham&er must recei"e at least half of an inlet "al"e to &e considered a "entricle. $he presentation of 8B depends on the pulmonary &lood -oA if pulmonary stenosis is present there is increased cyanosis and the infant is a candidate for a #laloc;% $aussig shunt. 0n the a&sence of pulmonic stenosis5 pulmonary -o is e:cessi"e and the presentation is congesti"e heart failure. 2ptimal correction of 8B di"erts all "ena ca"al -o into the pulmonary arteries as the Jontan procedure. 11. G%year%old &oy ith hypertension has no palpa&le femoral pulses. Coarctation of the aorta is suspected. $he folloing isare true/ a. &. c. d. e.
$he most common associated a&normality is a &icuspid aortic "al"e Chest radiograph is li;ely to sho ri& notching $he etiology is felt to &e secondary to an in-ammatory aortitis 0n infancy5 coarctation may present ith a pin; upper &ody and cyanotic loer &ody LParado:ical hypertension seen after operati"e repair indicates residual stenosis from incomplete correction nser/ a5 &5 d Coarctation of the aorta occurs =ust distal to the origin of the left su&cla"ian artery and results from contraction of ectopic tissue from the ductus arteriosus. $he most common associated a&normality is a &icuspid aortic "al"e. 7:tensi"e collateral de"elopment in"ol"es the mammary and intercostal arteries producing ri& notching on the chest radiograph. 0n infancy5 -o to the loer &ody is from the ductus arteriosus &efore it closes5 producing di!erential cyanosis. $he Lparado:ical hypertension seen postoperati"ely is thought to relate to sympathetic ner"e stimulation and does not re-ect an incomplete repair. 111.
a. &. c. d. e.
$ransseptal puncture should &e used for de>niti"e diagnosis 0f this is a primary cardiac tumor it is most li;ely to &e malignant 0f this is a my:oma attached to the atrial septum5 the ad=acent septum should &e remo"ed ith it 0n infancy5 the most common cardiac tumor is a rha&domyosarcoma $he most common primary malignant tumor of the heart is angiosarcomanser/ c5 e Primary cardiac tumors commonly arise in the left atrium and can present ith dyspnea5 syncope5 congesti"e failure and systemic em&olism. $ransseptal puncture should not &e used for diagnosis &ecause of the ris; of em&olism. Most primary cardiac tumors are &enign &y a '/1 ratio. $he most common malignant tumor is the angiosarcoma. My:oma is the most common &enign tumor5 &ut it can recur and the ad=acent atrial septum should &e resected ith it. 0n infancy5 the most common cardiac tumor is a rha&domyoma. 116. 6%month%old &oy ho appeared normal at &irth has &ecome cyanotic and is found to ha"e a systolic e=ection murmur o"er the pulmonic area and a &oot%shaped heart on chest radiograph. $he folloing isare true/
a. 7chocardiography alone is suKcient to con>rm the diagnosis of $etralogy of Jallot &. Cyanotic spells may &e appropriately treated &y propranolol c. $he #laloc;%$aussig shunt connects the right "entricle to the pulmonary artery d. 0ncreasing cyanotic spells is the most common indication for operation e. 2perati"e repair of right "entricular out-o o&struction is ne"er e:tended across the pulmonic "al"e since intolera&le pulmonary insuKciency ould result nser/ a5 &5 d 0n this typical scenario for $etralogy of Jallot5 echocardiography can con>rm the diagnosis ith no need for cardiac catheteri4ation. Cyanotic spells are treated &y supplemental o:ygen5 sedation ith morphine and a &eta &loc;er such as propranolol. Jor palliati"e increase in pulmonary &lood -o5 the #laloc;%$aussig shunt is utili4ed connecting the su&cla"ian artery to the pulmonary artery. 0ncreasing cyanosis and cyanotic spells are the most common indication for operati"e repair. $o correct the right "entricular out-o o&struction in $etralogy5 a transannular patch may &e re9uired e:tending into the pulmonary artery. Jortunately the pulmonary "al"ar insuKciency that results is ell tolerated in the a&sence of tricuspid insuKciency or "entricular dysfunction. 11'. 16%year%old &oy is found to ha"e an e=ection systolic murmur o"er the aortic region ith a precordial thrill and normal cardiac si4e on chest radiograph. $he folloing isare true/ a. systolic e=ection clic; ould signify that the stenosis is supra"al"ar &. 0n the a&sence of cardiomegaly5 cardiac catheteri4ation to measure the pressure gradient is necessary c. +e"elopment of syncope ould suggest an intracranial lesion d. 0n "al"ar aortic stenosis a pressure gradient of F mmBg is an indication for operati"e repair regardless of symptoms e. 0n mem&ranous su&"al"ar aortic stenosis a pressure gradient of < mmBg is an indication for operati"e repair nser/ d5 e 0n the patient ith >ndings of aortic stenosis5 a systolic e=ection clic; is e"idence that the o&struction is "al"ular. Cardiac si4e does not pro"ide an indication of the se"erity of the stenosis and is fre9uently normal. $he de"elopment of angina or syncope re-ects inade9uate cardiac output and signi>es late%stage disease. pressure gradient o"er E, mmBg is an indication for operation in "al"ar aortic stenosis e"en if the patient is asymptomatic hile a lesser gradient of ' mmBg or more is considered suKcient for operati"e correction of mem&ranous su&"al"ar stenosis. 11<. Within 6 hours of &irth5 a &a&y girl is o&"iously cyanotic and chest radiograph shos the heart to appear li;e Lan egg on its side. $he folloing isare true/ a. &. is a c.
$he most common cause of cyanosis this early is transposition of the great "essels ($H8) 0f $H8 is present5 echocardiography ill sho that the posterior "essel lea"ing the left "entricle pulmonary artery 0f $H8 is con>rmed &y echocardiography5 cardiac catheteri4ation has little to add
d. $he 7NH is helpful in ma;ing the diagnosis of $H8 since it shos re"ersed dominance of the "entricles e. $o impro"e mi:ing of pulmonary and systemic circulations5 prostaglandin should &eused to increase pulmonary "ascular resistance nser/ a5 & $H8 is the most common cause of cyanosis in the >rst ee; of life5 and this diagnosis can &e con>rmed &y echocardiographic demonstration of a posterior pulmonary artery attached to the left "entricle. Cardiac catheteri4ation is useful to con>rm the anatomy5 detect other lesions5 de>ne the coronary anatomy and impro"e cardiac mi:ing &y &alloon atrial septostomy. $he 7NH is not helpful in the diagnosis of $H8 since it shos only normal right "entricular dominance. Prostaglandin impro"es the mi:ing of the circulation &y opening the ductus arteriosus and reducing pulmonary "ascular resistance. 11,. one%year%old &oy thought to ha"e $etralogy of Jallot is found on cardiac catheteri4ation to ha"e dou&le%outlet right "entricle (+2R8). $he follo isare true/ a. &. c. d. e.
Spontaneous closure of the 8S+ is rare @ocation of the 8S+ has little e!ect on the degree of cyanosis +ou&le outlet left "entricles do not occur Coincidental aortic stenosis ith +2R8 is not compati&le ith life +ou&ly committed 8S+ refers to its relationship to the great "esselsnser/ a5 e 0n +2R85 the location of the 8S+ a!ects the direction of -o of o:ygenated &lood and thus determines the degree of cyanosis. Jortunately5 the 8S+ rarely closes since that ould result in se"ere decompensation or death. +ou&le outlet left "entricles occur &ut are less common than +2R8. num&er of other anomalies are associated ith +2R8 including &oth "al"ar and su&"al"ar pulmonary and aortic stenosis. $he 8S+ may &e directed to either or &oth great "essels (dou&ly committed) or remote from them (noncommitted). 11*. ,%year%old girl is found on routine e:amination to ha"e a pulmonic -o murmur5 >:ed splitting of P6 and a right "entricular lift. $he folloing isare true/
a. Cardiac catheteri4ation is indicated if the chest >lm shos cardiomegaly &. Radiology report of Lscimitar syndrome >ndings on the chest >lm ould indicateneed for an arteriogram c. 0f the catheteri4ation report is Lostium secondum defect5 at least one pulmonary"ein drains anomalously d. Measured pulmonary "ascular resistance of 1< Woods unitsm6 ith an S+ mandates early repair e. n S+ ith QpQs of 1.F can &e o&ser"ed until symptoms occurnser/ & $he >ndings suggest an atrial septal defect (S+) that can &e con>rmed &y 6+ echocardiography eliminating the need for cardiac catheteri4ation. $he ostium secondum type defect is most commonly found5 &ut it is the sinus "enosus type that is associated ith anomalous pulmonary "enous drainage. 0n the scimitar syndrome5 the anomalous pulmonary "ein can &e seen on a chest radiograph and5 since these are associated ith a hypoplastic lung that is supplied &y an anomalous systemic artery from the aorta5 an arteriogram is appropriate. n S+ ith a signi>cant left%to%right shunt as demonstrated &y a QpQs ratio in e:cess of 1., should &e repaired. When the pulmonary "ascular resistance is ele"ated a&o"e 1O16 Woods unitsm6 the patient is not a candidate for repair due to >:ed pulmonary hypertension. 11E. 6%month%old infant has 7NH e"idence of myocardial ischemia and echocardiography suggests anomalous origin of the left coronary artery from the pulmonary artery. $he folloing isare true/ a. 0schemia is due to perfusion of the myocardium ith inade9uately o:ygenated &lood &. Selecti"e coronary angiography should not &e attempted &ecause of the ris; of myocardial infarction c. Conser"ati"e treatment is preferred to allo the coronary artery to gro to a si4e that ill allo &ypass construction d. 0f the infant deteriorates5 ligation of the coronary at its origin is a "ia&le option e. $he se"erity of the a&normality insures that it ill alays &e detected in the >rst year of life nser/ d
nomalous origin of the left coronary artery from the pulmonary artery results in re"erse -o in the coronary into the lo%pressure system as a steal from the coronary circulation. 0f collaterals from the right coronary de"elop to allo ade9uate myocardial perfusion5 the disorder is fre9uently not diagnosed until later in life hen a murmur is heard. Selecti"e coronary arteriography is appropriate to de>ne the anatomy and operati"e repair is underta;en promptly. @igation of the anomalous coronary can &e lifesa"ing &ut lea"es the child dependent on a single "essel and coronary &ypass is preferred. 11F. 6%month%old &oy is found to &e in congesti"e heart failure manifested &y tachypnea5 tachycardia and diaphoresis ith poor eight gain. $he physical >ndings suggest a "entricular septal defect (8S+). Management should include/ a. &. c. d.
Pulmonary artery &anding rgent closure if a 8S+ is found on echocardiography Medical treatment only ith digitalis and diuretics 0f a 8S+ is found5 repair is unli;ely to &e possi&le &ecause of ele"ated pulmonary "ascular resistance e. 0f a restricti"e 8S+ is found5 spontaneous closure is a possi&ility and operati"erepair should &e delayed nser/ c5 e @arge 8S+s present at *OF ee;s of age hen the normally ele"ated pulmonary "ascular resistance falls5 alloing an increase in the left%to%right shunt. Since roughly half of all 8S+s undergo spontaneous closure5 particularly ith restricti"e defects5 the initial management is medical. $he diagnosis is con>rmed &y echocardiography and cardiac catheteri4ation. d"anced pulmonary "ascular changes do not occur usually until 6 years of age and &anding is only rarely indicated for palliation for multiple comple: muscular 8S+s. 11G. 1%year%old girl ith dyspnea and poor feeding is found to &e in congesti"e heart failure. 7chocardiography shos an atrio%"entricular septal defect (8S+). $he folloing isare true/ a. $he second heart sound ill sho >:ed splitting &. +espite diagnostic echocardiography5 cardiac catheteri4ation is indicated to assess pulmonary artery resistance c. Pulmonary artery &anding is indicated to limit pulmonary -o and allo the childto gro d. 8S+ is classi>ed according to the morphology of the anterior lea-et of the common %8 "al"e e. 2perati"e repair is &est performed after 6 years of agenser/ a5 &5 d 8S+ is a defect of endocardial cushion de"elopment hich produces morphologic a&normalities of &oth 8 "al"es and &oth atrial and "entricular septa. 0t is usually classi>ed according to the morphology of the anterior lea-et of the 8 "al"e. $he pulmonary "ascular resistance remains ele"ated in infancy delaying diagnosis and producing >:ed splitting of the second heart sound. Cardiac catheteri4ation is indicated to assess pulmonary "ascular resistance5 &ut pulmonary artery &anding is no longer performed to protect the pulmonary &ed. 0nstead5 operati"e repair is made5 prefera&ly &efore the age of * months.
a. &. c. d. e.
16. $he child in the pre"ious 9uestion undergoes cardiac catheteri4ation con>rming a 8S+ ith QpQs ratio of 6. and right "entricular systolic pressure half of systemic pressure. $he folloing isare true/ 0f aortic insuKciency is detected5 the defect is li;ely to &e su&pulmonic in location Jinding aortic stenosis in addition to the 8S+ ould &e highly unli;ely $he cath data indicate a restricti"e type of 8S+ 0f pulmonary "ascular resistance falls ith tola4oline administration5 it is safeto close the 8S+ 2perati"e closure of 8S+s is possi&le ithout "entriculotomynser/ a5 c5 d5 e $he >nding of aortic insuKciency in a patient ith 8S+ suggests prolapse of the aortic "al"e due to a su&pulmonic or supracristal defect. ssociated aortic stenosis5 mitral stenosis and coarctation are common ith 8S+s. $he >nding of a moderate left%to%right shunt and a right "entricular pressure ell &elo systemic le"els indicates a restricti"e 8S+. 0f ele"ated pulmonary "ascular resistance is found5 the a&ility to respond to a "asodilator li;e tola4oline indicates that the resistance is not >:ed and operati"e repair is possi&le. 2perati"e repair of 8S+s is fre9uently possi&le "ia atriotomy or through the pulmonary artery.
161. premature infant in respiratory distress is found to ha"e a continuous Lmachinery murmur o"er the precordium. $he folloing isare true/ a. $he most li;ely diagnosis is coarctation of the aorta &. 0f large pulmonary arteries are noted5 a patent ductus is li;ely c. $o discriminate &eteen a and &5 prostaglandin administration can &e used hich ill constrict the patent ductus arteriosus d. 0f a ductus if found5 operati"e repair should &e delayed until the respiratory symptoms impro"e to reduce mortality rates e. 3ormal ductus closure depends on increased o:ygen saturation in the pulmonary artery nser/ &5 e continuous Lmachinery murmur is characteristic of patent ductus arteriosus typically seen in the premature infant. 3ormal closure of the ductus is prompted &y a fall in pulmonary "ascular resistance that increases the left%to right shunt and o:ygen le"els from the aorta. 0ndomethacin can cause ductus closure &y cycloo:ygenase inhi&ition hich decreases endogenous prostaglandins. Prostaglandin infusion ould ;eep the ductus open. 2perati"e closure can &e done safely in e"en the smallest neonates and usually promptly relie"es the respiratory distress. 166. neonate in congesti"e heart failure has echocardiographic e"idence of a single truncal "essel from hich the pulmonary arteries arise5 a 8S+ and truncal "al"ar stenosis. $he folloing isare true/ a. 3atural history of this anomaly allos only 6 one%year sur"i"al &. $he most li;ely con>guration of the truncal "al"e is &icuspid c. @ocation of the pulmonary arteries minimi4es the ris; of pulmonary "ascular o&structi"e disease (7isenmengers) d. Repair of the lesion re9uires an e:tracardiac conduit e. 2ptimal timing of operati"e repair is at *O16 monthsnser/ a5 d $he defect descri&ed is truncus arteriosus hich carries an F one year mortality rate uncorrected. $he truncal "al"e is most commonly tricuspid (*,) or 9uadricuspid (6,)A least li;ely &icuspid (G). $he large left%to%right shunt ma;es these patients particularly li;ely to de"elop pulmonary "ascular o&struction (7isenmengerXs syndrome). 2perati"e repair re9uires detachment of the pulmonary arteries hich are reconnected to the right "entricle &y an e:tracardiac conduit5 and the optimal timing for repair is ithin the >rst * months of life.
a. &. c. d. e.
16'. neonate in respiratory distress has echocardiographic e"idence of hypoplastic left heart syndrome (B@BS). $he folloing isare true/ 0nitial management should include prostaglandin infusion 8entilatory ad=ustment should maintain PaC26 at appro:imately < mmBg Sur"i"al depends on sustained patency of the ductus arteriosus Cardiac transplantation for B@BS re9uires inclusion of the donor aortic arch Reconstruction for B@BS con"erts the pulmonary artery into the main outlet for a functional single "entricle (3orood) nser/ a5 &5 c5 d5 e $he neonate ith B@BS has a se"erely underde"eloped left "entricular and aortic arch and is dependent on patency of the ductus hich is facilitated &y prostaglandin infusion. 8entilator ad=ustment to reduce supplemental o:ygen and maintain PC26 of < mmBg a"oids e:cessi"e pulmonary -o. $he options for treatment include cardiac transplantation hich re9uires a donor aortic arch and reconstruction &y the 3orood procedure hich con"erts the pulmonary artery into the main outlet for a functional single "entricle. 16<. ,6%year%old man ith ;non aortic stenosis de"elops angina pectoris and has a single episode of syncope. $he folloing isare true/
a. 2nset of angina indicates concomitant coronary artery disease independent of "al"ular lesion &. Percutaneous aortic &alloon "al"uloplasty should &e considered since it has generally fa"ora&le results c. Patient is not an operati"e candidate since heart failure has not occurred
d. measured trans"al"ular pressure gradiant Y , mmBg ould &e an operati"e indication nser/ d $he "entricular hypertrophy hich accompanies aortic stenosis increases o:ygen demand hile mechanical forces increase resistance to perfusion5 resulting in ischemia. 2nly one half of these patients ith angina ha"e coronary artery disease. Percutaneous &alloon "al"uloplasty of the aortic "al"e has high complication and recurrence rates. ny such patient ith symptoms has an indication for operations as ould the patient ith a trans"al"ular gradiant Y , mmBg. 16,. $he patient in the pre"ious 9uestion ith 0 progresses to profound heart failure re9uiring medical management. $he folloing isare true/ a. &. c. d.
Perperal "asdilators are contraindicated $he inta%aortic &alloon pump can &e used to impro"e cardiac output Jurosemide and nitroglycerin ould &e appropriate 8al"e replacement is necessarynser/ c5 d Peripheral "asodilators are ;ey to the treatment of 0 fa"oring peripheral &lood -o. $he intraaortic pump is contraindicated &ecause diastolic augmentation orsens aortic regurgitation. #oth furosemide and nitroglycerin ould &e of "alue to treat the failure5 &ut the most e!ecti"e treatment re9uires replacement of the "al"e. 16*. <6%year%old oman has noted progressi"e e:ercise intolerance and fatiga&ility. 7:amination discloses an opening snap in the mitral area suggesti"e of mitral stenosis. $he folloing isare true/
a. Critical mitral stenosis is de>ned as an ori>ce area reduced to 6 cm6 &. With a >:ed mitral ori>ce5 the change from sinus rhythm to atrial >&rillation has little e!ect on cardiac output c. Mural throm&i and throm&oem&olism are directly related to the presence of atrial >&rillation d. +epressed cardiac output is usually due to depressed myocardial contractilitynser/ c 3ormal adults ha"e a ce and reduction to 6 cm6 is mild stenosis hile reduction to 1 cm6 is considered critical mitral stenosis. 7"en ith a >:ed ori>ce5 the onset of atrial >&rillation reduces cardiac output &y 6. Mural throm&i and throm&oem&olism are directly related to the presence of atrial >&rillation. Mitral stenosis spares "entricular function5 and the loss of cardiac output is from decreased preload. 16E. Concerning "al"ular heart disease5 the folloing isare true/ a. &. c. d.
Mitral stenosis is the most common lesion 2f all cardiac "al"es5 the aortic is the most anterior Stenosis is the most common lesion of the aortic "al"e Rheumatic heart disease is the most common cause of "al"e dysfunctionnser/ c5 d ortic "al"ular stenosis is the most common type of "al"ular lesion folloed &y mitral stenosis. natomically5 the pulmonic "al"e is the most anterior of the cardiac "al"es. Rheumatic heart disease is the most common cause of "al"e dysfunction and the most common cause of multi"al"ular disease. 16F.
a. &. c. d.
Chest radiograph ill sho cor &o"inum $he apical murmur is due to the Halla"ardin phenomenon carotid shudder ould &e e:pected &dominal e:am ill sho a pulsatile li"ernser/ a $his patient ith aortic insuKciency has a "olume loading strain on the heart hich produces cor &o"inum as dramatic enlargement. $he apical murmur produced &y tur&ulence ith mitral forard
-o mimics mitral stenosis and is called an ustin%Hlint murmur. carotid shudder occurs ith aortic stenosis and a pulsatile li"er is typical of tricuspid insuKciency. 16G. Concerning the adaptation to cardiac "al"ular dysfunction5 the folloing isare true/ a. Se"ere heart failure is more li;ely from acute than chronic "al"ular dysfunction &. 8al"ular dysfunction produces &oth "olume and pressure afterload stress on the heart c. 7arly cardiac dilation from "al"e dysfunction shifts the Jran;%Starling cur"e to depress cardiac output d. $he @aPlace la predicts that all stress decreases ith increasing "entricular radius nser/ a5 & 8al"ular dysfunction produces &oth "olume and pressure o"erload representing afterload stress on the heart. lthough cardiac reser"es allo for gradual adaptation to chronic "al"ular dysfunction5 acute dysfunction is less ell tolerated and more li;ely to result in se"ere heart failure. $he increase in diastolic >lling hich initially dilates the heart5 shifts the Jran;%Starling cur"e to impro"e e=ection and cardiac output. $he @aPlace la predicts that all stress increases ith increasing "entricular radius &ut is in"ersely related to all thic;ness. 1'. '1%year%old male drug a&user presents ith fe"er5 chills and multiple &ilateral lung a&scesses. Right heart endocarditis is suspected. $he folloing isare true/ a. &. c. d.
$he organisms most li;ely responsi&le are gram%negati"e and fungal $he pulmonic "al"e is most li;ely to &e a!ected negati"e echocardiogram is useful to e:clude the diagnosis 8al"e replacement is necessary if the nati"e "al"e is e:cised to treat infectionnser/ a $he typical endocarditis in a drug%a&user in"ol"es fungal and gram%negati"e organisms hich infect the tricuspid rather than the pulmonic "al"e. n echocardiogram is useful to con>rm the presence of "egetations &ut it may o"erloo; smaller ones so it cannot &e used to e:clude the diagnosis. lthough "al"e replacement is usually prefera&le5 the infected tricuspid "al"e can &e e:cised ithout prosthetic replacement. 1'1. 0n the initial management of the patient in the pre"ious 9uestion ith suspected acute M05 the folloing isare true/
a. &. c. d.
2:ygen and lidocaine should &e administered prophylactically 0f chest pain persists5 08 nitroglycerin should &e used to limit infarct si4e Ca%channel &loc;ers are also of "alue to limit infarct si4e Morphine 08 can &e used &ut has no therapeutic e!ectnser/ & 0nitial treatment during an early e"ol"ing M0 should include o:ygen5 &ut lidocaine should &e used only if arrhythmias occur. 3itroglycerin 08 is of "alue to limit infarct si4e &ut not Ca%channel &loc;ers hich ha"e no such &ene>t. #y decreasing pain and an:iety5 morphine 08 has a signi>cant therapeutic e!ect in decreasing myocardial o:ygen demand. 1'6. Concerning the physiology of the coronary circulation5 the folloing isare true/
a. nder circumstances of increased o:ygen demand &y the myocardium5 26 e:traction from arterial &lood can increase &. Coronary -o is ma:imal during systole c. denosine is the most important meta&olic regulator of coronary &lood -o d. Sympathetic ner"e stimulation constricts coronary arteries despite the need for increased cardiac output nser/ c5 d Since myocardium ma:imally e:tracts 26 from &lood at rest5 increased demand re9uires increased deli"ery. Systolic pressures compress intramyocardial "essels5 so ma:imal coronary -o is during diastole. denosine5 a &rea;don product of $P5 is a "asodilator and the most important meta&olic regulator of coronary &lood -o. lthough sympathetic ner"es produce coronary "asoconstriction5 the autoregulatory "asodilatory responses to increased myocardial demand o"erhelm that e!ect.
1''. $rue statement(s) concerning cardiac "ascular anatomy include the folloing/ a. 0n FOF, of cases the posterior descending coronary artery (P+) arises from the circum-e: coronary artery &. $he P+ gi"es o! the 8 nodal artery c. $he great cardiac "ein ascends along the right coronary artery to empty into the coronary sinus d. $he&esian "eins drain from only left and right "entriclesnser/ & 0n FOF, of cases the circum-e: coronary artery ends ith &ranches to the left "entricle hile the P+ originates from the right coronary in FOF, of cases. $he P+ gi"es o! the 8 nodal artery and its occlusion can result in heart &loc;. $he great cardiac "ein ascends along the left anterior descending coronary artery and the $he&esian "eins drain all < cham&ers.
a. &. c. d.
1'<. 0n the medical management of coronary artery disease5 the folloing isare true/ 3itroglycerin primarily dilates coronary arterioles &%&loc;ing agents act to reduce myocardial 26 demand Ca%channel &loc;ing agents reduce "entricular contractility Ca%channel agents should not &e used if there is an element of coronary "asospastic disease nser/ &5 c 3itroglycerin primarily dilates "enous capacitance "essels5 &ut at higher doses can produce coronary and systemic arterial dilation. &%adrenergic &loc;ing agents reduce myocardial 26 demand &y decreasing heart rate and contractility. Ca%channel &loc;ing agents reduce "entricular contractility5 produce "asodilation and may protect myocytes. $hey are particularly e!ecti"e for coronary "asospastic disease. 1',. *E%year%old man ith documented acute M0 progresses in 6< hours to cardiogenic shoc;. $he folloing isare true/ a. $he mortality rate for cardiogenic shoc; after acute M0 is increased more than 1fold in comparison to no shoc; &. ge5 e=ection fraction5 M0 si4e and pre"ious M0 ser"e as predictors of cardiogenic shoc; c. cute loss of more than 6 of myocardium fre9uently results in cardiogenic shoc;and death d. 7mergency re"asculari4ation is contraindicated for the M0 patient in cardiogenic shoc; nser/ a5 & Cardiogenic shoc; is unusual after acute M0 &ut increases the mortality rate from < to *,. ll of the ris; factors descri&ed plus a history of dia&etes mellitus can predict cardiogenic shoc;. $he "olume of myocardium lost acutely that is associated ith shoc; is <. Recent studies suggest that emergency coronary &ypass can &e used ithin 1F hours of shoc; to reduce the mortality rate to E. 1'*. ,6%year%old man ith chest pain and tachycardia has 7CH e"idence of an acute M0. $he folloing isare true/
a. $hrom&olytic therapy should &e considered immediately since the &ene>t is greater the earlier it is gi"en &. 2f the drugs a"aila&le5 recom&inant tP produces &etter results than SN or PSC although it is more e:pensi"e c. $hrom&olytic therapy re9uires catheteri4ation for intracoronary administration d. ddition of heparin and antiplatelet drugs produces no incremental &ene>tnser/ a $hrom&olytic therapy for acute M0 is of signi>cant "alue in reducing mortality ith &ene>t related to early administration. lthough rtP can produce higher coronary patency rates5 the results of treatment are no &etter than ith SN or PSC. $hrom&olytic drugs ere initially gi"en intracoronary &ut can &e used e!ecti"ely hen gi"en systemically 08. $here is an added &ene>t from heparin and antiplatelet drugs to pre"ent rethrom&osis. 1'E. Jolloing repair of an a&dominal aortic aneurysm5 a **%year%old man de"elops se"ere chest pain5 diaphoresis5 &radycardia and hypotension. $he folloing isare true/
a. &. c. d.
$he electrocardiogram is most li;ely to sho a prominent Q in lead ' if this is an M0 0f Q a"e is present5 the infarct is su&endocardial rather than transmural Creatine ;inase measurement alone is diagnostic of M0 Since &radycardia rarely occurs ith M05 another diagnosis should &e considerednser/ a Pain is the most common complaint in patients ith myocardial infarction although 6O6, are asymptomatic. 0nferior M0s in"ol"ing the right coronary fre9uently ha"e parasympathetic acti"ity ith &radycardia5 hypotension and a prominent Q a"e in lead '. $he presence of a Q a"e indicates a transmural M0 hich can &e con>rmed &y measurement of the speci>c isoen4yme for cardiac tissue (CN%M#) since creatine ;inase can &e ele"ated non%speci>cally after stro;e or operation. 1'F. E%year%old oman ith intracta&le angina pectoris undergoes cardiac catheteri4ation for possi&le mechanical inter"ention. She prefers P$C to open correction. $he folloing isare true/
a. long symmetric lesion in the left main coronary artery ould &e appropriate for P$C &. Multiple o&structi"e lesions in the same artery ould &e a contraindication to P$C c. focal lesion in the left anterior descending coronary artery here the "essel is 1 mm in diameter ould allo P$C d. Successful P$C for a simple lesion carries a recurrent stenosis ris; of less than 1 nser/ & $he ideal lesion for P$C is focal symmetric stenosis in an epicardial "essel. Boe"er5 it is relati"ely contraindicated for signi>cant disease in the left main coronary5 for multiple o&structi"e lesions in the same artery5 and for "essels less than 6 mm in diameter. Restenosis rates of 6 to < occur ithin the >rst ts of the procedure. $he folloing isare true/ a. 2perati"e mortality in patients Y E years is more than dou&le that of younger patients &. 0f the patient is a oman5 the ris; is higher than it ould &e for a man c. pre"ious C#H procedure increases the comple:ity and complication rate5 &ut does not alter mortality rate d. Results are &etter if there is ischemic cardiomyopathy than if there is hi&ernating myocardium nser/ a5 & 2perati"e mortality for patients Y E years as F in the CSS study as compared to ' in younger patients. Jor reasons not entirely clear5 the ris; of C#H is higher in omen than in men. Reoperati"e procedures carry a higher operati"e mortality due to technical diKculties5 more ad"anced disease5 and less complete re"asculari4ation. Congesti"e heart failure is a ma=or determinant of poor surgical outcome5 &ut the results are &etter hen there is "ia&le myocardium (hi&ernating) than hen there is irre"ersi&le ischemic cardiomyopathy. 1<. Jour days after a transmural M05 a E<%year%old man de"elops hypotension and congesti"e heart failure. $he folloing isare true/ a. n intra%aortic &alloon pump should &e used and cardiac catheteri4ation performed &. 0f the infarct as posterior5 this is most li;ely due to a "entricular septal defect c. Pulmonary edge pressure tracing of prominent 8 a"es ithout an 26 step%up suggests papillary muscle rupture d. 2perati"e repair of a post M0 8S+ should &e delayed to allo strengthening of themyocardium to hold sutures nser/ a5 c #oth "entricular septal defect (8S+) and ruptured papillary muscle occur from 'O, days post%M0 and should &e managed &y intra%aortic &alloon pump5 decreasing afterload and cardiac catheteri4ation for diagnosis. 8S+ is most li;ely in an elderly hypertensi"e female ho has sustained an anterior transmural M0A posterior M0s typically lead to papillary muscle rupture hich is diagnosed &y
prominent 8 a"es on pulmonary edge pressure tracing. Sur"i"al rate for &oth of these complications is impro"ed &y early rather than late repair. 1<1. ,6%year%old oman ith chest pain is considered for coronary arteriography on the &asis of her ris; factors. $he folloing isare true statement(s)/ a. &. c. d.
ll patients ith typical anginal symptoms should ha"e coronary arteriography typical patients ith &orderline positi"e stress tests should ha"e arteriography Patients ho re9uire "al"e procedures do not re9uire arteriography Patients in refractory heart failure aaiting cardiac transplantation should ha"ecoronary arteriography nser/ & Patients ith typical angina and 7CH changes should ha"e angiography only if they are refractory to medical management andor a candidate for re"asculari4ation. Patients ith atypical signs and symptoms should ha"e angiography to con>rm or e:clude the diagnosis. Patients ith "al"e disease and ris; of coronary artery disease should ha"e angiography &ut patients aaiting cardiac transplantation are not candidates for re"asculari4ation and do not re9uire coronary angiography. 1<6. $he patient in the pre"ious 9uestion is found to ha"e disease unsuita&le for P$C. Concerning operati"e re"asculari4ation (C#H) the folloing isare true/
a. C#H is more e!ecti"e than medical treatment for relie"ing angina and impro"ing physical or; capacity &. 0n C#H for unsta&le angina5 there is no di!erence in late outcome &eteen sta&le and unsta&le cohorts c. Jor C#H5 the most common arterial graft is the left internal mammary artery d. @ong term patency is impro"ed hen arterial grafts are used &ut there is no di!erence in the early mortality rate nser/ a5 &5 c Randomi4ed studies sho that C#H is more e!ecti"e than medical therapy for relie"ing angina5 impro"ing physical or; capacity and impro"ing o"erall 9uality of life. When C#H is used for unsta&le angina5 the initial complication and mortality rates are higher than for sta&le angina5 &ut the late outcomes are similar. se of arterial grafts for C#H has increased ith the left internal mammary artery used most commonlyA hen at least one mammary artery is used5 the early mortality rate is impro"ed. 1<'. 0n the or;up of a <,%year%old man ith suspected coronary artery disease5 the folloing isare true/ a. &. c. d.
$hyroid tests are included to rule out hyperthyroidism $ypically positi"e stress 7CH ould sho ele"ated S$ segments +ipyridamole is a useful ad=unct to thallium scanning as it increases coronary perfusion pressure Persisting defects on thallium scan indicate re"ersi&le myocardial ischemianser/ a +iagnostic studies for coronary artery disease should detect ris; factors such as dia&etes mellitus5 hyperlipidemia and hyperthyroidism. $he stress 7CH typically shos donard sloping S$ segment depression. +ipyridamole is a coronary artery "asodilator that reduces systemic and coronary perfusion pressures. $he persisting thallium scan defect re-ects irre"ersi&ly scarred myocardium. 1<<. Jolloing successful throm&olytic treatment of the patient in the pre"ious 9uestion5 he de"elops recurrent chest pain in 6< hours. $he folloing isare true/
a. &. c. d. e.
Rethrom&osis is most li;ely and throm&olytic therapy alone should &e repeated $he pro&lem could ha"e &een pre"ented &y early electi"e catheteri4ation and P$C Patient has an indication for catheteri4ation and P$C if single "essel disease is found Jindings of multi"essel disease at catheteri4ation ould indicate need for operati"e &ypasses 0f operati"e &ypass is deemed necessary5 there should &e a '%day delay to allo myocardial healing nser/ c5 d
fter throm&olytic therapy for acute M05 angina recurs in 'O', and is an indication for cardiac catheteri4ation and mechanical inter"ention to pre"ent infarct e:tension. Prophylactic catheteri4ation5 hoe"er5 has not &een found to pro"ide &ene>t. 0f the >ndings at catheteri4ation sho limited disease treata&le &y P$C5 then it should &e performed. #ut if multi"essel disease or unfa"ora&le anatomy is found5 operati"e &ypass should &e carried out early since results are &est ithin ' days of the M0. 1<,. ,G%year%old male has undergone successful C#H ith < grafts constructed &ut remains in lo cardiac output (Z 6@minm6) postoperati"ely. $he folloing isare true/ a. n inotropic drug should &e used initially to increase cardiac output &. 0f lo cardiac output persists despite optimal physiological and pharmacological support5 a &alloon pump (0#P) should &e inserted c. +ecreased cardiac >lling pressures suggest the possi&ility of cardiac tamponade d. When 0#P is used5 the &alloon is in-ated during diastolenser/ &5 d 0nitial e!orts to impro"e cardiac output should include correction of poor o:ygenation or acidosis and optimi4ation of rhythm5 preload and afterload &efore an inotropic agent is used. 0f lo cardiac output persists despite physiological and pharmacological support5 an 0#P should &e inserted. 0t impro"es coronary artery perfusion &y counterpulsation during diastole. Cardiac tamponade is heralded &y increased cardiac >lling pressures5 narroed pulse pressure and pulsus parado:us. 1<*. <6%year%old asymptomatic attorney undergoes a routine e:ercise test hich is reported positi"e for myocardial ischemia. $he folloing isare true/ a. $his is a rare e"ent since less than , of patients ith coronary artery disease (C+) are asymptomatic ith e:ercise &. Such a patient could progress to heart failure from ischemic cardiomyopathy c. $ypical angina pectoris is promptly relie"ed &y rest or rela:ation d. +yspnea on e:ertion can represent an angina e9ui"alentnser/ &5 c5 d s many as 6, of C+ patients found &y e:ercise testing are asymptomatic. Progressi"e coronary o&struction in these patients can produce heart failure from ischemic cardiomyopathy. $ypical angina is relie"ed promptly &y rest or rela:ation. 0schemic reductions in "entricular contractility and compliance can produce dyspnea on e:ertion as an angina e9ui"alent. 1&rillation. trial o"erdri"e pacing should &e attempted for P$ or atrial -utter. 8erapamil is the most e!ecti"e approach to rate control for supra"entricular arrhythmias5 &ut cardio"ersion of patients on digo:in should &e underta;en cautiously since they are prone to "entricular tachycardia. 1
+irect current catheter endocardial a&lation has a high li;elihood of success. 0f the arrhythmia is induci&le at 7P study5 there is an indication for operati"e inter"ention. recent M0 ould &e a contraindication to operation 8entricular failure ould &e a contraindication to operation Monomorphic "entricular tachycardia is least amena&le to surgical resection.nser/ &5 c5 d
fter catheter a&lation5 only 6, of patients remain free of "entricular arrhythmia o! of drug therapy. 0f the arrhythmia is induci&le at 7P study and the patient is an accepta&le ris;5 ith a myocardial scar he has an indication for operation. #oth recent M0 and "entricular failure are contraindications to operation. Monomorphic "entricular tachycardia is the arrhythmia most amena&le to surgical resection. 1
$he most li;ely cause of SC+ is "entricular arrhythmia $here is 'O< chance of recurrent SC+ in one year 7mpiric antiarrhythmic drug therapy impro"es sur"i"al n induci&le "entricular tachyarrhythmia at 7P study carries a fa"ora&le prognosis 0f a "entricular aneurysm is found ith arrhythmia5 aneurysm resection is ade9uate treatment nser/ a5 & 8entricular arrhythmias cause E, of SC+5 hile 6, are due to acute M0. $here is a 'O< chance of recurrent SC+ in one year. n induci&le "entricular tachyarrhythmia carries a poor prognosis ith Z , >"e year sur"i"al from SC+ unless it can &e a&olished. 7mpiric antiarrhythmic drug therapy does not impro"e sur"i"al. neurysmectomy alone is not ade9uate therapy for arrhythmias associated ith aneurysms since the arrhythmia usually originates in ad=acent mechanically stressed myocardium. 1,. $he folloing isare true concerning the anatomy of the conduction system/
a. $here is no special conduction path from the sinoatrial (S) to the atrio"entricular (8) node &. $he &lood supply to the 8 node is from the anterior descending coronary artery c. $he only normal muscular connection &eteen atria and "entricles is the &undle of Bis d. $he aortomitral continuity is the only area here supra"entricular accessory pathays cannot occur e. $he sinus node artery arises from the right or circum-e: coronary arterynser/ a5 c5 d5 e $he S node is located at the =unction of the superior "ena ca"a and the right atrial appendage and recei"es its &lood supply from the right or circum-e: coronary artery. $here is no special conduction path &eteen S and 8 nodes. $he &undle of Bis is the only normal atrio"entricular muscle connection &ut a&normal pathays can occur anyhere e:cept the area ;non as the aortomitral continuity. $he &lood supply to the 8 node is from the posterior descending coronary artery. 1,1. $he folloing isare true concerning the physiology of arrhythmias/ a. &. c. d. e.
physical or electrical stimulus causes sodium fast channels and calcium slo channels to open +uring the e!ecti"e refractory period5 only the slo calcium channels are closed Rapid repolari4ation follos potassium egress from the cell 7:tracellular hypo;alemia increases sodium channel si4e increasing automaticity Catecholamines increase outard potassium -o from myocytesnser/ a5 c5 d Physical or electrical stimuli cause sodium fast channels and calcium slo channels to open. +uring the e!ecti"e refractory period5 &oth slo calcium channels and fast sodium channels are closed and the myocardium cannot &e e:cited. $hen potassium channels reopen5 alloing potassium out5 and rapid repolari4ation occurs. 7:tracellular hypo;alemia increases transmem&rane potassium gradient and sodium channel si4e increasing automaticity. Catecholamines decrease outard potassium -o from myocytes enhancing automaticity. 1,6. E6%year%old man has had se"eral episodes of "entricular tachycardia and is a candidate for electrophysiological (7P) study. $he folloing isare true/
a. $he goal of the 7P study is either sustained or non%sustained "entricular tachycardia &. Patients ith less than , repetiti"e comple:es in response to stimulation are considered noninduci&le c. n induced reentry from "entricular stimulation is not necessarily pathological
d. Microreentry arrhythmias are typical after myocardial infarction e. Macroreentry arrhythmias are typical of myocardial ischemianser/ a5 & Jor arrhythmias of "entricular origin5 the 7P study goal is either sustained or nonsustained "entricular tachycardia. Patients ith less than >"e repetiti"e comple:es in response to stimulation are considered noninduci&le. 8entricular reentry does not occur in normal myocardium5 so all reentrant arrhythmias are pathological. Macroreentry arrhythmias are typical after myocardial infarction5 hile microreentry arrhythmias are typical of myocardial ischemia. 1,'. 6G%year%old male ith supra"entricular tachyarrhythmias is suspected to ha"e Wol!% Par;inson%White (WPW) syndrome. $he folloing isare true/ a. 7lectrophysiologic studies (7PS) ill re9uire catheters in or at the right atrium5 Bis &undle5 right "entricle and coronary sinus &. Pacing for 7PS uses stimuli tice the diastolic threshold c. $he anomalous conducting &undle (Nent) is found in the right free all if the coronary sinus catheter records the earliest atrial acti"ity during reciprocating tachycardia d. 0f the atrial catheter records the earliest acti"ity during tachycardia5 the &undle of Nent is located in the left free all e. 0f neither left or right &undle%&ranch &loc; prolong the 8 inter"al5 the anomalous &undle is in the septum nser/ &5 e Jor supra"entricular arrhythmias5 7PS re9uires catheters placed in the right atrium and "entricle5 coronary sinus and Bis &undle. programma&le stimulator is used for stimuli that are tice the diastolic threshold and 6 msec in duration. When the coronary sinus catheter records the earliest acti"ity during reciprocating tachycardia5 the &undle of Nent is in the left free all hile it is in the right free all if the earliest acti"ity is in the atrial catheter. When neither left or right &undle% &ranch &loc; prolong the 8 inter"al5 the &undle is in the septum. 1,<. *6%year%old oman hose arrhythmia is noninduci&le at 7P study has depressed @8 function ithout aneurysm. $he folloing isare true/ a. 0f her arrhythmia is "entricular tachycardia5 she is not a candidate for an utomatic 0mplanta&le Cardiac +e>&rillator (0C+) since it only recogni4es >&rillation &. 0f an 0C+ is appropriate5 it o!ers a , impro"ement in mortality compared to drug therapy c. Poor "entricular function is a contraindication to 0C+ implantation d. 0C+ should not &e used for patients aaiting cardiac transplantation e. 0C+ can pro"ide antitachycardia pacing as ell as de>&rillationnser/ &5 e $he 0C+ is capa&le of recogni4ing "entricular tachycardia as ell as >&rillation and can pro"ide antitachycardia pacing5 lo or high%energy de>&rillation or some com&ination. 0t o!ers a , impro"ement in mortality ith G, freedom from SC+ at , years after implantation. 3either poor "entricular function nor pending transplantation are contraindications to 0C+ implantation. 1,,. 6E%year%old surgery resident has had multiple episodes of supra"entricular tachycardia (S8$) and on 7P study is felt to ha"e WPW syndrome. $he folloing isare true/ a. $he pathophysiology of WPW is a single &undle of Nent &. +angerous "entricular responses in WPW are due to the shorter refractory period of the accessory pathay c. 0denti>cation of the accessory pathay of WPW is an indication for its interruption d. ppro:imately half of the patients ho ha"e successful di"ision of accessory pathays demonstrate 8 &loc; postop e. #oth radiofre9uency catheter and surgical a&lation o!er e:cellent results ith lo mor&idity nser/ &5 d5 e $he pathophysiology of WPW is the Nent &undle of hich 1O6 are multiple rather than single. $he shorter refractory periods permit rapid and dangerous "entricular responses to atrial -utter or >&rillation. 0n .6, of the population5 accessory pathays of WPW can &e identi>ed5 &ut in the a&sence of a history of S8$5 they ha"e a normal life e:pectancy. ppro:imately half the patients ho ha"e successful di"ision of accessory pathays demonstrate 8 &loc; postop. #oth radiofre9uency catheter and surgical a&lation o!er e:cellent results ith lo mor&idity and the catheter techni9ue is less costly.
