Cardiac Surgery MCQ 1. Which is not true of cardiopulmonary resuscitation (CPR)? . Closed chest massage is as effecti!e as open chest massage. ". #he success rate for out$of$hospital resuscitation may %e as high as &' to '. C. #he most common cause of sudden death is ischemic heart disease. *. Standard chest massage generally pro!ides less than 1+ of normal coronary and cere%ral %lood flo,. ns,er- *SC/SS0- Closed chest massage is not as effecti!e as open$chest massage in normali2ing %lood pressure or perfusion of !ital organs3 and closed chest massage does generally deli!er + to 1+ of normal coronary and cere%ral %lood flo,. #he success rate for out$of$hospital resuscitation has %een as high as &' to ' ,hen communities are prepared to institute CPR early after a cardiac arrest. schemic heart disease is the most common cause of sudden death.
4. Which maneu!er generally is not performed early %efore chest compression in %asic life support outside the hospital? . Call for help. ". 0%tain air,ay. C. 5lectrical cardio!ersion. *. 6entilation. ns,er- C *SC/SS0- "asic life support does in!ol!e calling for help3 o%taining an air,ay3 and %eginning !entilation %efore starting chest compression. 5lectrical cardio!ersion re7uires special e7uipment and trained personnel and thus is part of ad!anced cardiac life support.
&. Which treatment ,ould %e least effecti!e for asystole? . 58ternal pacema9er. ". ntra!enous epinephrine3 1' ml. of 1-1'3'''. C. ntra!enous calcium gluconate3 1' ml. of 1' solution. *. ntra!enous atropine3 '.+ mg. ns,er- C *SC/SS0- Recommended treatment for asystole is administration of atropine. f atropine is unsuccessful epinephrine is gi!en. /ltimately cardiac pacing is necessary if atropine and epinephrine do not esta%lish an ade7uate heart rate. Calcium has no clear role in treating asystole. :. #he most important factor that influences the outcome of penetrating cardiac in;uries is. Comminuted tear of a single cham%er. ". Multiple$cham%er in;uries. C. Coronary artery in;ury. *. #angential in;uries. ns,er- C
*SC/SS0- Multiple studies in the literature confirm that in;uries to the coronary arteries are the most important factor in determining outcome after a penetrating cardiac in;ury. #angential in;uries are the least serious. n;ury to a single cham%er
+. #he most useful incision in the operating room for patients ,ith penetrating cardiac in;ury is. =eft anterior thoracotomy. ". Right anterior thoracotomy. C. "ilateral anterior thoracotomy. *. Median sternotomy. 5. Su%8yphoid. ns,er- * *SC/SS0- #he su%8yphoid incision is useful for determining if there is %lood in the pericardium and if there is an intracardiac in;ury> ho,e!er3 e8posure is e8tremely limited3 and definiti!e repair can rarely %e performed through the incision. =eft (or right) anterior thoracotomy is easily performed3 especially in the emergency room3 and gi!es ade7uate e8posure to certain areas of the heart. o,e!er3 each has significant limitations in e8posure. 5ither may %e e8tended across the thoracotomy into the other side of the chest3 thus producing a %ilateral anterior thoracotomy. 58posure is e8cellent through this incision3 and most in;uries can %e satisfactorily repaired through this approach. Most cardiac operations today are performed through median sternotomy incisions. f the patient is in the operating room3 this incision is easily performed and al,ays pro!ides e8cellent e8posure for all areas of the heart. . n patients ,ho present ,ith a penetrating chest in;ury3 in;ury to the heart is most li9ely ,hen the follo,ing physical sign(s) is@are present. ypotension. ". *istended nec9 !eins. C. *ecreased heart sound. *. ll of the a%o!e. ns,er- * *SC/SS0- ypotension3 increased !enous pressure (distended nec9 !eins)3 and decreased heart sounds ma9e up the classic "ec9As triad associated ,ith cardiac tamponade. f these three findings are present in a person ,ho has a penetrating chest ,ound3 intracardiac in;ury is almost certain and operati!e inter!ention is mandatory. B. Which of the follo,ing ,ould %e an accepta%le method of repair for a neonate ,ith symptomatic isolated coarctation of the aorta? . Resection ,ith end$to$end anastomosis. ". Prosthetic patch aortoplasty. C. Su%cla!ian flap aortoplasty. *. Prosthetic tu%e graft repair. ns,er- C
*SC/SS0- #he most commonly used methods for coarctation repair are resection ,ith anastomosis and su%cla!ian flap aortoplasty. "oth ha!e %een sho,n to pro!ide ade7uate relief of the o%struction ,ith accepta%le rates of restenosis. #he choice of repair depends on the patientAs anatomy and the surgeonAs e8perience. Patch aortoplasty ,as used fre7uently in the past> ho,e!er3 %ecause of concern o!er restenosis and aneurysm formation it is no longer commonly performed. Prosthetic tu%e graft repair is a!oided e8cept in some comple8 cases and some cases of recoarctation.
. Which of the follo,ing constitutes a true !ascular ring? . Pulmonary artery sling. ". *ou%le aortic arch. C. nomalous srcin of right su%cla!ian artery from the descending aorta. *. Cer!ical aortic arch. ns,er- "
*SC/SS0- 0nly the dou%le aortic arch secondary to persistence of the right and left fourth aortic arches forms a true !ascular ring. Pulmonary artery sling may cause symptoms that are due to compression of the trachea3 and an anomalous right su%cla!ian may cause dysphagia3 %ut these anomalies do not constitute complete rings. Cer!ical aortic arch3 ,hich is thought to %e secondary to persistence of the third aortic arch3 is not a complete ring and usually is asymptomatic.
D. Which of the follo,ing may %e physical e8amination findings in a young adult ,ith coarctation of the aorta? . Posterior systolic murmur %et,een the scapulas. ". *iminished femoral pulses. C. 5le!ated %lood pressure in left arm as compared ,ith right arm. *. Peripheral cyanosis. ns,er- "C
*SC/SS0- systolic murmur that radiates posteriorly is characteristic of coarctation of the aorta. Coarctation produces o%struction to aortic flo,3 and thus the femoral pulse has a diminished !olume ,ith delayed upstro9e. ypertension in coarctation is multifactorial3 %ut the most important factors are diminished renal flo, (single clip3 single 9idney$Eold%latt model) and mechanical factors. f the right su%cla!ian artery is anomalous and arises distal to the coarctation3 %lood pressure may %e greater in the left arm than in the right. solated coarctation does not produce cyanosis.
1'. n a premature infant ,ith hyaline mem%rane disease and ina%ility to %e ,eaned from mechanical !entilation3 ,hich of the follo,ing ,ould suggest hemodynamically significant patent ductus arteriosus (P*)? . Continuous murmur. ". yperacti!e precordium ,ith %ounding peripheral pulses. C. Faundice. *. *iminished femoral pulses. ns,er- "
*SC/SS0- P* causes a left$to$right shunt that produces left !entricular !olume o!erload. Physical
findings include e!idence of hyperdynamic circulation ,ith a prominent apical impulse and %ounding peripheral pulses. #he classic murmur of P* is a continuous or mechanical murmur heard o!er the precordium and radiating to the medial third of the cla!icle. *iminished femoral pulses are not seen ,ith isolated P* and ,ould suggest other anomalies. P* may result in hepatomegaly %ut does not cause ;aundice.
11. n an infant ,ith suspected P*3 ,hich of the follo,ing ,ould %e the optimal method of confirming the diagnosis? . Chest film. ". Cardiac catheteri2ation. C. Retrograde aortography !ia an um%ilical artery catheter. *. #,o$dimensional echocardiography ,ith continuous$,a!e and color$flo, *oppler echocardiography. ns,er- *
*SC/SS0- 5chocardiography is the %est method for confirming the diagnosis of a P*. #,o$ dimensional echocardiography can demonstrate P* and e8clude associated anomalies. *oppler echocardiography can demonstrate the shunt3 determine direction of shunting3 and pro!ide an estimate of shunt magnitude. #he chest film is not particularly helpful and may %e normal or sho, cardiomegaly ,ith pulmonary congestion. n general3 cardiac catheteri2ation should %e reser!ed for older patients and those ,ith suspected associated anomalies or pulmonary hypertension.
14. Which of the follo,ing are potential complications of untreated coarctation of the aorta? . 5ndocarditis. ". Pulmonary !ascular disease. C. Cere%ro!ascular accident. *. Congesti!e heart failure. ns,er- C*
*SC/SS0Coarctation the!entricular aorta produces an o%struction to increased %lood flo, and hypertension3 tur%ulent flo,3 and increasedofleft afterload. #here is an incidence of coronary artery disease. Prior to the introduction of effecti!e techni7ues for relief of coarctation3 the most common causes of death ,ere endocarditis3 aortic rupture3 congesti!e heart failure3 and cere%ro!ascular accident. Pulmonary !ascular disease does not occur ,ith isolated coarctation.
1&. #he atrial septal defect (S*) most commonly associated ,ith partial anomalous pulmonary !enous return (PP6R) is. Secundum defect. ". Sinus !enosus defect. C. 0stium primum defect. *. Complete atrio!entricular (6) canal defect. 5. Coronary sinus defect. ns,er- "
*SC/SS0- lthough partial anomalous return of the pulmonary !eins can occur ,ith any of the S*s listed3 it is particularly common ,ith sinus !enosus defects and is considered %y many to %e part of this lesion. #he most common anomaly is drainage of the right superior pulmonary !ein to the lateral aspect of the superior !ena ca!a.
1:. #he direction of an intracardiac shunt at the atrial le!el is controlled %y. #he si2e of the defect ". #he compliance of the right and left !entricles. C. #he systemic o8ygen saturation. *. Right atrial pressure. 5. #he presence or a%sence of an associated !entricular septal defect (6S*). ns,er- "
*SC/SS0- #he direction of an intracardiac shunt is go!erned %y the compliance of the do,nstream cham%ers. Gor an atrial le!el shunt3 the compliance of the right and left !entricles and their a%ility to distend ,ith increased !olume during diastolic filling dictates the direction of the shunt flo,. Since the right !entricle is usually a more compliant
1+. #he S* most commonly associated ,ith mitral insufficiency is. Secundum defect ". Sinus !enosus defect C. 0stium primum defect. *. Coronary sinus defect. ns,er- C
*SC/SS0- 0stium primum defects3 or HpartialI 6 canal defects3 are commonly associated ,ith a HcleftI of the anterior leaflet of the mitral !al!e. *epending on the deformity of the mitral !al!e3 these defects can %e accompanied %y !aria%le degrees of mitral insufficiency. #his cleft of the mitral !al!e needs to %e repaired at the same time that the defect is closed. lthough other types of S*s can %e associated ,ith mitral insufficiency3 this is not as common. When mitral stenosis e8ists ,ith a secundum S* the condition is often referred to as =utem%acherAs syndrome. 1. n electrocardiogram (5CE) in a patient ,ith a systolic e;ection murmur that sho,s an incomplete %undle %ranch %loc9 in the precordial lead is most consistent ,ith. secundum S*. ". sinus !enosus S* ,ith PP6R. C. n ostium primum S*. *. complete 6canal defect. ns,er-
*SC/SS0- Many patients ,ith secundum S*s ha!e an incomplete %undle %ranch %loc9 on their 5CE. #his is in contradistinction to patients ,ith ostium primum defects3 ,ho often ha!e a left a8is de!iation. lthough the 5CE is not pathognomonic of the defect3 the findings are sometimes helpful along ,ith other clinical and diagnostic information to,ard elucidating the nature of the defect.
1B. S*s can all %e closed ,ith a pericardial or prosthetic patch. Which of the follo,ing S*s can also %e safely closed primarily ,ithout the use of a patch? . Secundum S*. ". Sinus !enosus S* ,ith PP6R. C. n ostium primum S*. *. complete 6canal defect. ns,er-
*SC/SS0- Secundum S*s can fre7uently %e closed primarily3 although the use of a prosthetic or pericardial patch is indicated for large defects. #he other types of S*s are more safely closed ,ith a patch.
1. 0%struction to pulmonary !enous return is associated ,ith ,hich of the follo,ing anomalies? . Partial anomalous pulmonary !enous connection (PP6C) to the superior !ena ca!a. ". nfracardiac (#ype ) total anomalous pulmonary !enous connection (#P6C). C. Pulmonary !ein stenosis. *. Cor triatriatum. 5. Supracardiac (#ype ) #P6C. ns,er- "C*5
*SC/SS0- 0%struction to pulmonary !enous return is the most important factor affecting circulatory function ,hen pulmonary !enous anomalies e8ist. #his o%struction is most pre!alent and se!ere in patients ,ith infracardiac #P6C3 %ut it also occurs in as many as +' of patients ,ith supracardiac #P6C and 4' of the patients ,ith intracardiac #P6C sinus. 0%struction tocor pulmonary !enous return is also primary pathophysiologic effectto ofthe %othcoronary pulmonary !ein stenosis and triatriatum. 0%struction3 ho,e!er3 is rare ,ith partial anomalous pulmonary !enous connection3 especially ,ith the common form of PP6C to the superior !ena ca!a.
1D. Postoperati!e complications associated ,ith repair of #P6C include. Complete heart %loc9. ". cute pulmonary hypertensi!e crisis. C. Pleural effusions. *. Pulmonary !enous o%struction. ns,er- "*
*SC/SS0- n the early postoperati!e period after repair of o%structed forms of #P6C3 acute episodes of pulmonary hypertension may de!elop as a response to stress. #o minimi2e this potentially fatal complication3 infants are 9ept anestheti2ed ,ith fentanyl and pancuronium for at least : hours. Residual or recurrent pulmonary !enous o%struction occurs in only + to 1' of patients after #P6C repair3 %ut if identified it re7uires early reoperation. Reoperation is usually successful if the o%struction is at the le!el of the anastomosis. /nfortunately3 in some cases3 the o%struction is in the pulmonary !eins and surgical relief is less successful. lthough complete heart %loc9 and pleural effusions can occur after any cardiac operation3 they rarely occur after #P6C repair.
4'. Which of the follo,ing statements a%out 6S*s is@are correct? . Perimem%ranous lesions are located in the region of the mem%ranous portion of the inter!entricular septum near the anteroseptal commissure of the tricuspid !al!e. ". Muscular 6S*s are holes in the inter!entricular septum that are %ordered %y muscle on three sides and %y the pulmonary and the aortic !al!e annulus superiorly. C. 6S*3 in its isolated form3 is the most commonly recogni2ed congenital heart defect. *. #he conduction %undle runs along the posteroinferior rim of a perimem%ranous 6S*. ns,er- C*
*SC/SS0- Perimem%ranous 6S*s occupy the area of the mem%ranous portion of the inter!entricular septum ad;acent to the anteroseptal commissure of the tricuspid !al!e. 0ften a remnant of the mem%ranous portion of the inter!entricular septum (the mem%ranous flap) is left hanging on the posteroinferior rim of the defect. #he annulus of the tricuspid and aortic !al!es often form a part of the rim of the defect3 %ut in some patients they are separated from the 6S* %y a thin rim of muscle tissue that protects the conduction %undle. Muscular 6S*s ha!e e8clusi!ely muscular rims on all four sides. 6S*s in the outlet septum that e8tend to the annuluses of the aortic and pulmonary !al!es are called dou%ly committed or ;u8ta$arterial defects. solated 6S*s occur at an appro8imate rate of 4 per 1''' li!e %irths and represent &' to :' of all congenital heart malformations at %irth. #he conduction %undle in patients ,ith perimem%ranous 6S*s does run along the posteroinferior rim of the defect on the left !entricular side. Sutures used for repair of a perimem%ranous 6S* should %e placed ,ell a,ay from this area to a!oid the creation of surgically induced complete heart %loc9.
41. Which of the follo,ing statements a%out 6S*s is@are true? . When coarctation of the aorta is associated ,ith 6S*3 it most commonly occurs in infants ,ith large lesions ,ho ha!e to undergo repair %efore age & months. ". n some patients ,ith 6S*3 aortic !al!e incompetence de!elops o!er time and progresses. C. n the /nited States dou%ly committed or ;u8ta$arterial 6S*s are most commonly associated ,ith aortic insufficiency. *. P* is present in appro8imately one fourth of infants ,ith a 6S* and concomitant congesti!e heart failure. ns,er- "*
*SC/SS0- 6S* in com%ination ,ith se!ere coarctation of the aorta occurs in appro8imately 1B of patients. #his com%ination is more common among infants ,ith large 6S*s undergoing operation %efore age & months. ortic !al!e incompetence does de!elop o!er time in some patients ,ith 6S*3 presuma%ly as a result of progressi!e prolapse of the right aortic cusp through the defect. n the /nited States t,o thirds of patients ,ith 6S* and aortic insufficiency ha!e perimem%ranous lesions and one third ha!e a dou%ly committed or ;u8ta$arterial lesion. n Fapan3 ho,e!er3 the re!erse is true- t,o thirds ha!e dou%ly committed or ;u8ta$arterial lesions and one third ha!e perimem%ranous lesions. moderate$ or large$ si2ed P* is associated ,ith 6S* in appro8imately of patients of all ages> ho,e!er3 in infants ,ith 6S* and concomitant congesti!e heart failure3 P* is present in appro8imately 4+.
44. Which of the follo,ing statements a%out 6S* is@are correct? . large 6S* is appro8imately the si2e of the pulmonary !al!e orifice or larger. ". =arge 6S*s associated ,ith high pulmonary %lood flo, result in an enlarged left atrium on chest 8$ ray. C. Patients ,ith small (restricti!e) 6S*s tend to ha!e normal right !entricular and pulmonary arterial pressures ,ith normal pulmonary !ascular resistance and no e!idence of pulmonary !ascular disease. *. pulmonary !ascular resistance greater than 1' to 14 units per s7. m. is considered a contraindication to operation. ns,er- "C*
*SC/SS0- large 6S* is appro8imately the si2e of the aortic !al!e orifice or larger and causes systemic right !entricular systolic pressures. n the a%sence of right !entricular outflo, tract o%struction3 the pulmonary artery systolic pressure ,ill also %e systemic in the presence of a large 6S*. =arge 6S*s associated ,ith a high pulmonary %lood flo, do result in an enlarged left atrium %ecause of increased pulmonary !enous return. When mar9ed enlargement of the left atrium is present in a patient suspected of ha!ing a 6S*3 the presence of coe8isting mitral !al!e regurgitation should also %e considered. Patients ,ith small 6S*s do ha!e normal right !entricular and pulmonary arterial pressures. #here is only a slight ele!ation of pulmonary %lood flo, relati!e to the systemic flo,3 and the pulmonary !ascular resistance is normal ,ithout e!idence of pulmonary !ascular disease. t any age3 the presence of pulmonary !ascular disease so se!ere that the pulmonary !ascular resistance is fi8ed and greater than 1' to 14 units per s7. m. is considered a contraindication to operation.
4&. Which of the follo,ing statements a%out 6S*s is@are correct? . Spontaneous closure of 6S*s occurs in 4+ to +' of patients during childhood. ". #achypnea and failure to thri!e are symptoms fre7uently associated ,ith large 6S*s. C. Patients ,ith normal pulmonary !ascular resistance and left$to$right shunting across the 6S* ha!e 5isenmengerAs comple8. *. Patients ,ith a large 6S* and lo, pulmonary !ascular resistance can present ,ith a middiastolic murmur at the ape8. ns,er- "*
*SC/SS0- Spontaneous and complete closure of 6S*s3 e!en large ones3 has %een estimated to occur in 4+ to +' of patients during childhood. #he pro%a%ility of e!entual spontaneous closure is in!ersely
related to the age at ,hich the patient is o%ser!ed. #achypnea3 poor feeding3 gro,th failure3 recurrent respiratory infections3 e8ercise intolerance3 and se!ere cardiac failure may de!elop in patients ,ith large 6S*s. Patients ,ith 5isenmengerAs comple8 are cyanotic3 polycythemic3 and se!erely limited in their e8ercise tolerance3 o,ing to mar9edly ele!ated pulmonary !ascular resistance associated ,ith a predominantly right$to$left shunt across the 6S*. middiastolic murmur can %e present at the ape8 in patients ,ith a large 6S* associated ,ith lo, pulmonary !ascular resistance. #his indicates high pulmonary %lood flo, ,ith a large flo, across the mitral !al!e into the left !entricle.
4:. Which of the follo,ing is@are true of the surgical treatment of 6S*s? . right !entricular approach is employed for the repair of most perimem%ranous 6S*s. ". ntracardiac repair is ad!isa%le for patients ,ith intracta%le symptoms and for asymptomatic infants ,ith e!idence of increasing pulmonary !ascular resistance. C. Complete heart %loc9 is a common complication. *. ospital mortality after repair of 6S* in infants approaches 4'. ns,er- "
*SC/SS0- #he right atrial approach is preferred for the repair of most perimem%ranous 6S*s. Prompt intracardiac repair is indicated for infants ,ith large defects3 large shunts3 and pulmonary hypertension ,ho present ,ith intracta%le left !entricular failure3 recurrent pulmonary infections3 se!ere gro,th failure3 or e!idence of increasing pulmonary !ascular resistance. n the modern era3 complete heart %loc9 re7uiring a permanent pacema9er is a !ery uncommon complication of surgical closure of a !entricular septal defect. ospital mortality after closure of a 6S* currently approaches 2ero. While in earlier years younger age ,as an incremental ris9 factor for hospital death in some surgical e8periences3 this ris9 has %een neutrali2ed during the past decade.
4+. #etralogy of Gallot consists of all of the follo,ing features e8cept. S*. ". 6S*. C. *e8troposition of the aorta. *. Pulmonary stenosis. 5. Right !entricular hypertrophy. ns,er- *SC/SS0- lthough S* is a fre7uent component of tetralogy of Gallot3 it ,as not included %y Gallot as part of his classic tetralogy. 0ccasionally3 the inclusion of an S* prompts use of the term pentalogy of Gallot. #he other four anomalies listed ,ere all mentioned %y Gallot in his srcinal description of this defect.
4. Which of the follo,ing has the greatest impact on the physiology of tetralogy of Gallot? . #he si2e of the S*. ". #he si2e of the 6S*. C. #he degree of pulmonary stenosis. *. #he amount of aortic o!erriding. ns,er- C
*SC/SS0- #he 6S* in tetralogy of Gallot is nonrestricti!e3 and therefore its si2e does not affect the degree of shunting that can occur. =i9e,ise3 an S*3 ,hich may or may not %e a component of tetralogy of Gallot3 can pro!ide right$to$left shunting at the atrial le!el %ut is not the main contri%utor to the cyanosis of this disease. #he degree of right$to$left shunt across the 6S* is dictated %y the !aria%le compliance of the do,nstream cham%ers3 and the increased resistance imposed %y se!ere pulmonary stenosis creates greater amounts of right$to$left shunting and3 therefore3 more intense cyanosis. #he position of the aorta in relation to the 6S* is not important as long as no su%aortic o%struction e8ists.
4B. Which of the follo,ing anomalies is not associated ,ith tetralogy of Gallot? . %sence of the left pulmonary artery. ". right aortic arch. C. retroesophageal su%cla!ian artery. *. nomalous srcin of the left anterior descending coronary artery from the right coronary artery. 5. Primary pulmonary hypertension. ns,er- 5
*SC/SS0- #he first four defects listed occasionally are associated ,ith tetralogy of Gallot. right aortic arch is seen in 4+ of patients ,ith that lesion. nomalous coronary arteries or a retroesophageal su%cla!ian artery are found in as many as + to 1' of patients. %sence of a pulmonary artery is unusual %ut can present in as many as & of patients. Pulmonary hypertension is distinctly unusual ,ith tetralogy of Gallot unless the patient has had e8cessi!e pulmonary %lood flo, from collaterals or systemic$to$pulmonary artery shunts for a long time. t is %ecause these patients usually do not ha!e pulmonary hypertension that infant correction ,ith transannular patches can %e performed ,ith such great success.
4. Surgical treatment of a patient ,ith tetralogy of Gallot can include any of the follo,ing e8cept. Maintenance of ductal patency ,ith prostaglandins (PE5 1) to pro!ide pulmonary %lood flo, ,hile the %a%y is transferred to an institution e7uipped to pro!ide moretetralogy definiti!eoftherapy. ". "anding of the pulmonary artery in an acyanotic patient ,ith Gallot to control pulmonary %lood flo, and pre!ent the de!elopment of pulmonary hypertension. C. Placement of a su%cla!ian$to$pulmonary artery shunt on the side opposite the aortic arch in a &$day$old infant ,ith se!ere cyanosis. *. Closure of the 6S* and transannular patching of the right !entricle onto the main pulmonary artery in a 4$day$old infant. ns,er- "
*SC/SS0- Patients ,ith tetralogy of Gallot ,ho do not appear cyanotic still ha!e mild arterial hypo8emia %y arterial %lood gas determination. Patients ,ith tetralogy of Gallot rarely ha!e e8cessi!e pulmonary %lood flo,3 and the de!elopment of pulmonary hypertension is not a concern in this population. "anding of the pulmonary artery is ne!er a consideration in patients ,ith tetralogy of Gallot3 since the predominant physiologic effect of the defect results from too little pulmonary %lood flo, to
%egin ,ith. cyanotic patients ,ith tetralogy of Gallot (Hpin9 tetsI) can usually %e follo,ed for se!eral months and their defects repaired electi!ely as a first$stage procedure (usually %y age months). ll of the other therapies are appropriate treatment for %a%ies ,ith tetralogy of Gallot. Prostaglandins maintain patency of the ductus arteriosus3 pro!iding an anatomic systemic$to$pulmonary artery shunt that sustains pulmonary %lood flo, until a more permanent surgical solution can %e pro!ided. #he ad!ent of prostaglandin therapy has ena%led numerous critically ill infants to %ecome sta%ili2ed enough to reach a tertiary care institution and recei!e proper surgical therapy ,ho might not other,ise ha!e sur!i!ed had it not %een for the a%ility of pulmonary %lood flo, to %e maintained through the re!ersal of duct closing. #he choice of palliati!e shunting or total anatomic correction rests largely ,ith the e8perience and s9ill of the surgical team and is dictated in part %y the anatomy of the pulmonary arteries. 5ither of these options is accepta%le.
4D. #he predominant determinant of outcome for patients ,ith pulmonary atresia and an intact !entricular septum re!ol!es around. #he si2e of the S*. ". #he %a%yAs age at presentation. C. #he si2e of the right !entricular ca!ity and tricuspid !al!e. *. #he presence of a tricuspid
&'. Which of the follo,ing statements a%out dou%le$outlet right !entricle are true? . 6S* is usually present. ". n the #aussig$"ing type of dou%le$outlet right !entricle3 the 6S* is usually noncommitted. C. Patients ,ith dou%le$outlet right !entricle and a su%aortic 6S* usually ha!e pulmonary stenosis. *. Patients ,ith dou%le$outlet right !entricle ,ith a su%pulmonary 6S* (#aussig$"ing malformation) tend to mimic patients ,ith transposition of the great arteries and 6S* in their presentation and natural history. ns,er- C*
*SC/SS0- 6S* is usually present in patients ,ith dou%le$outlet right !entricle and is the only outlet from the left !entricle. "oth great arteries may arise totally from the right !entricle3 or one or %oth may o!erlie the !entricular septum immediately a%o!e the 6S*. #o categori2e the heart as ha!ing a dou%le$outlet right !entricle3 more than +' of each great artery must arise from the right !entricle. n the #aussig$"ing type of dou%le$outlet right !entricle3 the 6S* is related to the pulmonary !al!e annulus and is termed a su%pulmonary defect. dditional morphologic characteristics peculiar to this entity ha!e %een descri%ed. Most patients ,ith dou%le$outlet right !entricle and a su%aortic 6S* ha!e concomitant pulmonary stenosis that protects the lungs from pulmonary !ascular disease and also results in a clinical course similar to that of patients ,ith tetralogy of Gallot. n the a%sence of pulmonary stenosis the presentation3 clinical course3 and natural history of the #aussig$"ing malformation are similar to those of transposition of the great arteries ,ith 6S*. Cyanosis is present3 usually from %irth3 since streaming directs the desaturated systemic !enous return to,ard the aorta and the o8ygenated left !entricular %lood to,ard the pulmonary artery. #hese patients tend to de!elop early congesti!e heart failure and can de!elop se!ere pulmonary !ascular disease early in life. #hey usually e8perience symptoms ,ithin the first fe, months of life.
&1. Which of the follo,ing statements a%out the surgical repair of dou%le$outlet right !entricle are true? . n dou%le$outlet right !entricle ,ith a su%aortic or dou%ly committed 6S*3 a tunnel$type repair connecting a committed 6S* ,ith its respecti!e great artery is usually employed. ". Repair of the #aussig$"ing malformation can %e accomplished using an intra!entricular tunnel techni7ue or %y performing a straight patch closure of the 6S* com%ined ,ith an arterial s,itch procedure. C. #he hospital mortality rate is highest ,hen a su%aortic 6S* is present. *. Some hearts ,ith dou%le$outlet right !entricle and a noncommitted 6S* must %e repaired using a modification of the Gontan procedure. ns,er- "*
*SC/SS0- When the 6S* is su%aortic or dou%ly committed3 the tunnel$type repair connects the left !entricle !ia the 6S* and tunnel to the aorta. #he #aussig$"ing malformation can %e repaired using an intra!entricular tunnel techni7ue descri%ed %y Ja,ashima. #his repair can %est %e accomplished ,hen the great arteries are in a more or less side$%y$side relationship ,ith the aorta to the right of the pulmonary artery. #he infundi%ular septum is generously resected and the 6S* is connected to the aorta %y an intra!entricular tunnel thatmalformation runs posteriorin!ol!es to the pulmonary artery. most to common approach for the repair of the #aussig$"ing patch closure of #he the 6S* the pulmonary artery. #his creates transposition of the great arteries ,ith an intact inter!entricular septum. n arterial s,itch procedure then esta%lishes !entriculoarterial concordance. 0f all the types of dou%le$outlet right !entricle the hospital mortality is lo,est ,hen a su%aortic or dou%ly committed 6S* is present. *ou%le$outlet right !entricle is associated ,ith a noncommitted 6S* in appro8imately 1' of patients in surgical series. #he repair of this su%set of patients is associated ,ith a relati!ely high mortality3 as compared ,ith the results o%tained after repair of other forms of dou%le$outlet right !entricle. t times3 %ecause of the remote location of the 6S* and %ecause of other compelling anatomic features3 complete repair cannot %e performed. n this case3 a modification of the Gontan procedure must %e employed.
&4. Management of a patient ,ith tricuspid atresia ,ithin the first month of life may include. Creation of a systemic arteryKtoKpulmonary artery shunt. ". 0%ser!ation. C. Creation of a %idirectional superior ca!opulmonary anastomosis. *. Pulmonary artery %anding. 5. Gontan procedure. ns,er- "*
*SC/SS0- nitial management of ne,%orn infants ,ith tricuspid atresia is determined %y the anatomic and physiologic factors that affect the %alance of pulmonary and systemic %lood flo,. nfants ,ith se!erely limited pulmonary %lood flo, and arterial o8ygen saturations of less than B' should %e sta%ili2ed ,ith PE5 1 to maintain patency of the ductus arteriosus until a systemic$to$pulmonary artery shunt can %e performed. Patients ,ith uno%structed pulmonary %lood flo, may e8hi%it only mild cyanosis %ut suffer from significant congesti!e heart failure. Many of these patients are %est managed %y pulmonary artery %anding to decrease the !olume o!erload on the left !entricle and to pre!ent the early de!elopment of irre!ersi%le pulmonary !ascular disease. Some patients ,ith moderate restriction of pulmonary %lood flo, may ha!e %alanced deli!ery of %lood to the systemic and the pulmonary circulation. #hese patients can %e carefully follo,ed until such time as an im%alance de!elops or they %ecome candidates for a %idirectional superior ca!opulmonary (Elenn) anastomosis or a Gontan procedure. #he normally high pulmonary !ascular resistance present in the first month of life precludes the performance of either the Elenn or the Gontan procedure in the ne,%orn.
&&. Which of the follo,ing should contraindicate performance of the Gontan procedure? . Patient age of 4+ years. ". Se!ere mitral insufficiency. C. =eft !entricular end$diastolic pressure of 1 mm. g. *. Right pulmonary artery stenosis. 5. Pulmonary !ascular resistance of Woods units. ns,er- C5
*SC/SS0- Eood !entricular function and lo, pulmonary !ascular resistance are essential re7uirements for a successful procedure. #he Gontanend$diastolic operation should not %e performed !entricular e;ection fraction isGontan less than &' or !entricular pressure is greater than,hen 1+ mm. g. Pulmonary !ascular resistance in e8cess of : Woods units should also %e considered an a%solute contraindication for Gontan correction. ge at the time of Gontan procedure does not appear to %e a ma;or ris9 factor3 e8cept %efore age 4 years. lthough patients ,ho ha!e sur!i!ed into the third or fourth decade are li9ely to ha!e !entricular dysfunction3 a Gontan procedure can %e performed successfully in these older patients if !entricular function and pulmonary !ascular resistance meet the a%o!e criteria. n patients ,ith tricuspid atresia a competent mitral !al!e is important for satisfactory cardiac output after the Gontan procedure. #he presence of se!ere mitral insufficiency3 ho,e!er3 should not necessarily contraindicate the procedure. n these cases it is recommended that the mitral !al!e %e repaired or replaced in com%ination ,ith the creation of a %idirectional superior ca!opulmonary anastomosis. completion Gontan operation is performed later. *istorted or stenosed pulmonary arteries are common se7uelae of systemic$to$pulmonary artery shunts and may result in unsatisfactorily high pulmonary !ascular resistance. n most cases3 these stenoses can %e repaired at the time of Gontan correction or ,ith a %idirectional superior ca!opulmonary anastomosis.
&:. nitial management of a ne,%orn infant ,ith hypoplastic left heart syndrome should include. ntra!enous administration of PE5 1. ". Supplemental o8ygen. C. Routine intu%ation and mechanical !entilation to achie!e a PC0 4 %et,een &' and &+ mm. g. *. Cardiac catheteri2ation and %alloon atrial septostomy. ns,er-
*SC/SS0- Postnatal sta%ili2ation of infants ,ith hypoplastic left heart syndrome re7uires patency of the ductus arteriosus and %alance of the systemic and the pulmonary circulation. "ecause the ductus is the only path,ay from the right !entricle to the systemic circulation3 duct patency must %e maintained ,ith intra!enous PE5 1. #o minimi2e the ,or9load on the single !entricle and ensure ade7uate deli!ery of o8ygen to the tissues3 an e7ual deli!ery of %lood to %oth the lungs and the %ody is sought. #he normal postnatal decrease in pulmonary !ascular resistance often results in o!erperfusion of the pulmonary circulation and underperfusion of the systemic circulation. Maneu!ers that further decrease pulmonary !ascular resistance3 such as the addition of supplemental o8ygen3 lo,ering the PC0 4 to less than &+ mm. g3 or eliminating any resistance at the atrial septum %y %alloon septostomy only ,orsens the im%alance.
&+. #he performance of a %idirectional superior ca!opulmonary (Elenn) anastomosis as the second stage in the reconstructi!e approach to hypoplastic left heart syndrome. Pro!ides early relief of !olume load on the single right !entricle. ". ncreases peripheral o8ygen saturations to greater than D'. C. Permits concomitant repair of pulmonary artery or aortic arch stenoses. *. mpro!es mortality and mor%idity of su%se7uent Gontan procedure. ns,er- C* *SC/SS0- fter the first$stage reconstructi!e (or,ood) procedure3 the circulation is inherently inefficient %ecause of the o%ligatory recirculation of a portion of %oth saturated and desaturated %lood. Closure of the arterial shunt and creation of a %idirectional Elenn anastomosis eliminates this inefficient recirculation and significantly diminishes the !olume load on the single right !entricle. *istorted and stenosed central pulmonary arteries or aorticn arch o%structions %e repaired at Gontan the same time thehas %idirectional Elenn procedure is performed. almost all seriesshould the mortality of the procedure decreased since the adoption of the three$stage approach for hypoplastic left heart syndrome. "ecause systemic and pulmonary !enous %lood continue to mi8 in the right atrium after a %idirectional Elenn procedure3 cyanosis persists ,ith peripheral o8ygen saturations %et,een B+ and +.
&. Which of the follo,ing statements a%out truncus arteriosus are true? . Most infants sur!i!e ,ithout operations until late childhood. ". Most infants present ,ith cyanosis. C. Most infants present ,ith congesti!e heart failure. *. Repair re7uires a conduit from right !entricle to pulmonary arteries. ns,er- "C*
*SC/SS0- While an occasional child sur!i!es to age & or : years3 ,ithout either palliati!e or totally correcti!e surgical treatment fe, li!e past early infancy. #he lesion is one of e8cessi!e pulmonary %lood flo, %ecause of the srcin of the pulmonary arteries from the truncus arteriosus> physiologically3 the pulmonary arteries arise directly from the aorta. lthough the aortic saturation can ne!er %e 1'' %ecause of some element of %idirectional shunting at the 6S*3 the physiologic manifestations are congesti!e heart failure and e8cessi!e pulmonary %lood flo, rather than cyanosis. #he congesti!e heart failure %ecomes se!ere as pulmonary !ascular resistance drops. f congesti!e heart failure later impro!es spontaneously3 it is %ecause of the de!elopment of pulmonary !ascular disease. Complete repair al,ays re7uires closure of the 6S*3 detachment of the pulmonary arteries from the common trun93 and re$ esta%lishment of an outflo, tract from the right !entricle to the pulmonary artery. #his conduit usually contains a !al!e and can %e either a homograft or a synthetic conduit containing a porcine !al!e.
&B. #runcus arteriosus is a diagnosis ,ith anatomic components including. 6S*. ". %normal srcin of pulmonary arteries. C. Su%aortic stenosis. *. Single !entricular outflo, !al!e. ns,er- "* *SC/SS0- "y definition3 a 6S* is al,ays present immediately %eneath the truncal !al!e. #he pulmonary arteries arise a%normally from the single trun93 ,hich is due to failed partitioning of the em%ryonic conus during the first fe, ,ee9s of fetal de!elopment. n the classification of Collett and 5d,ards3 #ype truncus arteriosus has a single arterial trun9 gi!ing rise to an aorta and a main pulmonary artery> in #ype the right pulmonary arteries arise immediately ad;acent to one another from the dorsal ,all of the truncus> in #ype the right and left pulmonary arteries srcinate from either side of the truncus> and in #ype 6 the pro8imal pulmonary arteries are a%sent and pulmonary %lood flo, is %y ,ay of ma;or aortopulmonary atresia and is no longer considered truncus arteriosus. Su%aortic stenosis cannot occur in this anomaly. #he single !entricular outflo, !al!e is the truncal !al!e. t may contain from t,o to si8 cusps3 %ut most often there are three and3 ne8t most often3 four.
&. 0ptimal treatment for the neonate ,ho presents ,ith transposition of the great arteries LS3*3*N and intact !entricular septum includes. PE5 1 infusion to maintain duct patency. ". dministration of intra!enous fluid to increase intra!ascular !olume. C. yper!entilation to decrease pulmonary resistance. *. 08ygen administration to increase arterial o8ygen tension. 5. trial %alloon septostomy to impro!e atrial mi8ing. ns,er- "5
*SC/SS0- "ecause ,ith transposition of the great !essels the systemic and the pulmonary circulations e8ist in parallel rather than in series3 sur!i!al depends on mi8ing %et,een pulmonary and
systemic circulations. nitially infants ,ith transposition and intact atrial septum sur!i!e %ecause of aortopulmonary flo, through P*3 ,hich may %e maintained ,ith prostaglandin infusions. lthough increased pulmonary flo, may cause enlargement of the left atrium and stretching of the foramen o!ale resulting in atrial$le!el mi8ing of o8ygenated and nono8ygenated %lood3 inade7uate mi8ing at the atrial le!el ,ill result in marginal tissue o8ygenation3 ,hich does not impro!e ,ith o8ygen administration. trial %alloon septotomy results in impro!ed admi8ture and o8ygen deli!ery in these patients and should %e performed promptly if peripheral acidemia and se!ere cyanosis are present. Relati!e dehydration may decrease the degree of interatrial shunting and !olume infusion often impro!es hemodynamics in infants. *ecreased pulmonary !ascular resistance may increase pulmonary %lood flo, at the e8pense of systemic %lood flo, and alter the loading conditions of the left !entricle3 ,hich may complicate early arterial repair.
&D. Gactors that preclude the use of a single$stage arterial s,itch reconstruction of de8trotransposition of the great !essels include. ge older than ,ee9s ,ith a left !entricular pressure of less than +' of systemic pressure. ". *ynamic left !entricular outflo, tract o%struction. C. ntramural coronary artery anatomy. *. 6al!ar pulmonic stenosis. 5. Su%pulmonary 6S*. ns,er- * *SC/SS0- Single$stage arterial s,itch procedure for reconstruction of transposition of the great !essels3 ,ith or ,ithout associated 6S* has %ecome the standard of treatment in the ma;ority of cardiac centers. Contraindications to arterial s,itch repair include fi8ed types of left !entricular outflo, tract o%struction3 including !al!ar pulmonic stenosis3 ,hich ,ould render the systemic semilunar !al!e stenotic or incompetent. natomic a%normalities ,ithout stenosis3 such as a %icuspid !al!e3 ho,e!er3 are suita%le for surgical correction. #he location of 6S* does not affect surgical outcome3 and most 6S*s can %e approached ade7uately through the right atrium or the anterior great !essel. Most dynamic forms of left !entricular outflo, tract o%struction are often relie!ed partially or completely %y realignment of the !entricular septum ,ith the hemodynamic changes follo,ing successful arterial s,itch repair. When3 ho,e!er3 the left !entricle has not %een prepared to sustain the pressure load of the systemic circulation %y the decrease in pulmonary !ascular resistance that occurs in the first fe, ,ee9s of life and ,hen the !entricular pressure less than +' ofpulmonary the systemic !entricular pressure3 one$stage repair s,itch is contraindicated3 and is staged repair ,ith %anding and shunt follo,ed %y arterial 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 outflo, tract o%struction. *. Systemic !entricular failure. 5. Progressi!e ele!ation of pulmonary !ascular resistance. ns,er- "*
*SC/SS0- #he atrial repair of transposition of the great arteries
:1. Critical aortic stenosis in the neonate is characteri2ed %y ,hich of the follo,ing? . t is most often due to commissural fusion of a trileaflet !al!e. ". t may %e associated ,ith coarctation of the aorta3 P*3 and mitral stenosis. C. t can %e managed medically until the child is large enough to undergo aortic !al!e replacement. *. Success of !al!otomy is determined %y the ade7uacy of the left !entricle. ns,er- "*
*SC/SS0- Critical aortic stenosis in the neonate most often presents in the first ,ee9 of life ,ith se!ere and progressi!e congesti!e heart failure and may %e associated ,ith coarctation of the aorta3 P*3 and mitral stenosis. #he prognosis is poor unless !al!otomy can %e performed e8peditiously. Medical management cannot sta%ili2e these infants for !al!e replacement at a later age. nfants ,hose left !entricle is too to sustain the systemic circulation unli9ely to sur!i!e aortic !al!e !al!otomy and3 thus3 should %e small managed as patients ,ith hypoplastic leftare heart syndrome. #he aortic in neonatal aortic stenosis is most commonly unicuspid or %icuspid.
:4. Surgical management of aortic !al!e disease in an older child may include. 5nlargement of the aortic annulus. ". ncision of fused commissures. C. nsertion of a porcine !al!e prosthesis. *. #ransfer of the pulmonary !al!e to the aortic position. ns,er- "*
*SC/SS0- #he ma;ority of older children ,ith aortic stenosis and significant trans!al!ular gradients can %e treated successfully %y aortic !al!otomy. #his can %e done percutaneously ,ith %alloon dilatation or surgically ,ith direct !isuali2ation of the aortic !al!e and incision of the fused commissures. ortic !al!e replacement is rarely necessary as a primary procedure %ut may %e re7uired in children ,ho de!elop progressi!e aortic insufficiency after a pre!ious inter!ention. When !al!e replacement is performed it is desira%le to insert the largest prosthesis possi%le3 to allo, for gro,th. 5nlargement of the aortic annulus is commonly performed for this purpose. f a true !al!e prosthesis is employed3 a mechanical !al!e is preferred. *ura%ility of 8enograft !al!es in children is limited o,ing to early calcification and leaflet degeneration. #he pulmonary autograft techni7ue may %e the %est method of aortic !al!e replacement in children. With this operation the patientAs o,n pulmonary !al!e is transferred to the aortic position and a pulmonary allograft is inserted to replace the pulmonary !al!e. lthough the pulmonary autograft may not achie!e the long$term dura%ility of a mechanical !al!e3 the patient does not face the long$term complications of throm%oem%olism and %leeding imposed %y a mechanical !al!e and lifelong anticoagulation.
:&. Which of the follo,ing statements a%out su%!al!ular aortic stenosis are true? . Most patients present in early infancy ,ith se!ere congesti!e heart failure. ". n e;ection clic9 is a specific physical sign of su%aortic stenosis. C. #he su%aortic mem%rane is approached surgically !ia the aorta and aortic !al!e. *. concomitant septal myectomy decreases the incidence of recurrent su%aortic stenosis. ns,er- C*
*SC/SS0- Su%aortic stenosis is rarely encountered in neonates. Most often it is disco!ered in an asymptomatic child during a routine physical e8amination. loud crescendoKdecrescendo systolic murmur ,ithout an e;ection clic9 is usually noted. #he presence of an e;ection clic9 is more consistent ,ith isolated !al!ular aortic stenosis. *iscrete su%aortic stenosis is approached surgically ,ith cardiopulmonary %ypass3 aortic cross$clamping3 and cardioplegic arrest. #he aorta is opened and the aortic !al!e leaflets are retracted3 e8posing the fi%rous mem%rane. #he fi%rous ring is carefully e8cised3 ta9ing care to a!oid in;ury to the anterior leaflet of the mitral !al!e and the penetrating conduction %undle. 0nce the su%aortic mem%rane is e8cised a septal myectomy further opens the left !entricular outflo, tract and diminishes the li9elihood of recurrent su%aortic stenosis.
::. Management of hypertrophic o%structi!e cardiomyopathy may include. Propranolol and !erapamil. ". ortic !al!e replacement. C. *ual$cham%er se7uential pacing. *. Com%ined septal myectomy and mitral !al!e plication. ns,er- C*
*SC/SS0- #he ma;ority of patients ,ith hypertrophic o%structi!e cardiomyopathy are treated medically ,ith %eta$%loc9ers such as propranolol and calcium channel %loc9ers such as !erapamil. Patients ,hose symptoms do not respond to medical therapy are treated surgically ,ith a transaortic septal myectomy. Recent reports indicate that simple plication of the anterior leaflet of the mitral !al!e
performed in addition to the septal myectomy further opens the left !entricular outflo, tract %y eliminating systolic anterior motion of the mitral !al!e. ortic !al!e replacement is not an appropriate treatment for hypertrophic o%structi!e cardiomyopathy. Some patients ,ho are poor surgical candidates may e8perience relief of symptoms and left !entricular outflo, gradients ,ith dual$cham%er permanent pacing. ppropriate pre$e8citation of the !entricular septum can prompt the septum to mo!e a,ay from the left !entricular ,all during systole and open the outflo, tract.
:+. Which of the follo,ing statements a%out supra!al!ular aortic stenosis are true? . Surgical repair is indicated only ,hen the systolic gradient e8ceeds B+ mm. g. ". Simple e8cision of the supra!al!ular mem%rane results in satisfactory relief of the stenosis in most patients. C. #he diffuse form of supra!al!ular aortic stenosis may cause o%struction to %ranches of the aortic arch. *. Reoperation after repair of discrete supra!al!ular aortic stenosis is rare unless a%normalities of the !al!e itself also e8ist. ns,er- C*
*SC/SS0- Supra!al!ular aortic stenosis is a progressi!e disease and should %e repaired surgically if symptoms are present or the systolic gradient e8ceeds +' mm. g. n addition to e8cision of the supra!al!ular mem%rane3 a patch of dacron or pericardium must %e placed across the area of narro,ing and do,n into at least one of the sinuses of 6alsal!a. Reoperation is rare after this procedure unless associated aortic !al!e disease is also present. n the diffuse form of the disease the thic9ening of the aortic ,all commonly results in significant luminal narro,ing of the ascending aorta and its ma;or %ranches.
:. 5ach year the appro8imate num%er of mericans ,ho die from complications of coronary artery disease is. 1''3'''. ". 4+'3'''. C. +''3'''. *. 13'''3'''. 5. 0!er 43'''3'''. ns,er- C *SC/SS0- t is estimated that appro8imately B3'''3''' mericans currently ha!e symptomatic coronary artery disease. 0f these some 13+''3''' e8perience myocardial infarction annually and appro8imately +''3''' die each year from complications.
:B. Which of the follo,ing arteries is most li9ely to %e in!ol!ed ,ith serious atherosclerosis? . #he right coronary artery. ". #he left coronary artery. C. #he anterior descending coronary artery. *. #he circumfle8 coronary artery. ns,er- C
*SC/SS0- n order of fre7uency3 the anterior descending coronary artery is the most commonly in!ol!ed ,ith atherosclerosis3 follo,ed %y the right coronary3 the circumfle83 and the left main coronary artery.
:. Which of the follo,ing statements a%out collaterals in the normal coronary circulation is true? . #here is a rich and 7uite effecti!e collateral circulation in the coronary arterial %ed. ". #he coronary arterial %ed has minimal effecti!e collaterals. C. #he coronary arterial %ed is an a%solute e8ample of anatomic end$arteries. ns,er- "
*SC/SS0- #he collateral circulation to the heart is relati!ely poor. n the human heart there are fe, natural collaterals of sufficient diameter for deli!ery of a significant 7uantity of %lood. Most of the collaterals are appro8imately 4'' mm. or smaller3 and channels of this si2e cannot conduct significant 7uantities of %lood for cardiac re7uirements. #here is no a%solute e8ample of anatomic end$arteries in humans. While the magnitude of arterial collateral circulation !aries considera%ly3 all organs ha!e some collaterals.
:D. f %lood entering the normal arterial circulation of the heart is 1'' saturated ,ith o8ygen3 o8ygen saturation of %lood in the coronary sinus can %e e8pected to %e appro8imately. B+. ". '. C. +'. *. &+. 5. =ess than 4'. ns,er- *
*SC/SS0heartinhas unusually high rate of o8ygen utili2ation consumes appro8imately t,o thirds of the#he o8ygen theanarterial %lood. #he o8ygen saturation of theand %lood in the coronary sinus is usually a%out &' to &+ and !aries ,ith the magnitude of cardiac disease. #he %ody as a ,hole e8tracts appro8imately 4+ of the o8ygen it recei!es3 thus emphasi2ing the great need of the heart for o8ygen at rest as ,ell as at e8ercise.
+'. Coronary %ypass procedures ha!e %een demonstrated to. Reduce the incidence of myocardial infarction. ". Significantly relie!es angina symptoms. C. Statistically impro!e the life span. *. mpro!e the e;ection fraction of the left !entricle in many patients in ,hom it is significantly depressed preoperati!ely. ns,er- "C*
*SC/SS0- n a !ariety of studies3 coronary %ypass procedures ha!e %een demonstrated to reduce the incidence of su%se7uent myocardial infarction as ,ell as to relie!e significantly anginal symptoms. #hey also impro!e the life span of most patients as ,ell as the e;ection fraction of the left !entricle in those in ,hom it ,as depressed preoperati!ely.
+1. #he follo,ing patients are %est treated ,ith coronary artery %ypass grafting (C"E). '$year$old man ,ith class angina3 B+ pro8imal right coronary artery lesion3 and normal !entricular function. ". '$year$old man ,ith unsta%le angina3 three$!essel disease3 and an e;ection fraction of &+. C. '$year$old nondia%etic man ,ith class angina symptoms and focal discrete lesions in the mid$ right coronary artery and mid$left circumfle8 artery. *. '$year$old man ,ith dia%etes3 class 6 angina3 B+ pro8imal left anterior descending and B+ pro8imal right coronary artery o%struction3 and left !entricular e;ection fraction of '. ns,er- "*
*SC/SS0- C"E has %een sho,n to prolong patient sur!i!al compared ,ith medical therapy in those patients ,ith left main occlusi!e disease and those ,ith three$!essel or t,o$!essel disease ,ith pro8imal left anterior descending in!ol!ement in association ,ith class or greater anginal symptoms3 impaired e;ection fraction3 or easily induci%le ischemia ,ith e8ercise. lthough percutaneous transluminal coronary angioplasty (P#C) appears to %e compara%le to C"E in nondia%etic patients3 patients ,ith dia%etes appear to ha!e a significant sur!i!al ad!antage ,hen C"E is used. Similarly3 patients ,ith more e8tensi!e coronary artery disease are %etter treated ,ith C"E than ,ith P#C.
+4. Sternal ,ound infections that spread to the mediastinum are associated ,ith a mortality rate of. '. ". &'. C. 4+. *. =ess than ns,er* 1+. *SC/SS0- lthough the mortality rate follo,ing sternal infections ,ith mediastinitis formerly ,as high3 it is no, greatly reduced. n most series3 mediastinitis is cured in more than D' of patients ,ho are treated aggressi!ely ,ith dO%ridement and placement of muscle flaps or omentum into the mediastinum to speed ,ound healing.
+&. Perioperati!e myocardial infarction occurs follo,ing coronary %ypass procedures in appro8imately. 1+. ". 1'. C. B. *. =ess than +. ns,er- *
*SC/SS0- Gollo,ing impro!ements in myocardial protection and coronary grafting techni7ues3 perioperati!e myocardial infarction no, occurs in less that 4 to : of patients in most series.
+:. Gollo,ing acute myocardial infarction3 !entricular septal defects occur in. 4'. ". 1'. C. 1+ *. 4 or less. ns,er- *
*SC/SS0- Postmortem studies indicate that to 1' of fatal cases of myocardial infarction are due to rupture of the heart. n addition3 infarction of the inter!entricular septum ,ith su%se7uent formation of a !entricular septal defect occurs in 1 to 4 of patients ,ith acute myocardial infarction. #he usual inter!al %et,een the acute infarction and septal rupture<: to 14 days
++. Which of the follo,ing clinical characteristics is@are associated ,ith a higher mortality after emergency C"E for failed P#C? . Multi!essel disease. ". Rescue atherectomy. C. Cardiogenic shoc9 prior to C"E. *. Pre!ious %ypass surgery. 5. ll of the a%o!e. ns,er- C*
+. Which statement(s) a%out operati!e mortality and perioperati!e incidence of myocardial infarction for electi!e C"E () !ersus emergency failed () is@are accurate?infarction is . #he operati!e mortality is higher forC"E %ut follo,ing the incidence of P#C perioperati!e myocardial unchanged %et,een and . ". #he operati!e mortality is unchanged %et,een and %ut the perioperati!e incidence of myocardial infarction is higher in . C. #he operati!e mortality and perioperati!e incidence is higher in than in . *. #he operati!e mortality and perioperati!e incidence of myocardial infarction are no different for and for . ns,er- C
+B. Which of the follo,ing statements a%out patients treated %y placement of an internal mammary artery (M) %ypass graft at primary C"E is@are correct? . #he ris9 for mor%idity and mortality from reoperati!e coronary %ypass grafting is increased. ". =eft !entricular function is %etter preser!ed at the time of reoperation. C. #he ris9 of sternal ,ound complications is greatly increased if the contralateral M is har!ested at the time of reoperation. *. light clamp should %e applied to the M pedicle to limit cardiac ,arming during cardioplegic arrest at the time of reoperation. 5. functional study demonstrating a large portion of myocardium at ris9 should %e o%tained %efore reoperation. ns,er- "*5
*SC/SS0- Patients ,ho ha!e an intact M graft should ha!e se!ere anginal symptoms and a significant portion of myocardium at ris9 %efore reoperati!e coronary %ypass grafting is considered. functional study may %etter define the proportion of myocardium at ris9 for ischemia and infarction. Patients ,ith an intact M graft are less li9ely to re7uire reoperation3 %ut if stenosis distal to the M and disease in other !ein grafts ha!e progressed or if a large portion of myocardium is at ris93 reoperation is recommended. #he presence of an intact M is not a contraindication to reoperation> in fact3 this population of patients ha!e %etter$preser!ed !entricular function and are3 perhaps3 %etter candidates for reoperation. Placement of an M graft at the time of the first operation ,as critically important3 neutrali2ing the ad!erse effects of ele!ated serum cholesterol3 hypertension3 and smo9ing on reoperation$ free sur!i!al. #he ris9 of damaging an intact M graft is & to +. lateral pro;ection of the M at cardiac catheteri2ation ,ill define its course3 particularly in relation to the sternum3 to allo, more careful sternal re$entry. #he M should %e minimally dissected and a light clamp applied during cardioplegic arrest to limit cardiac ,arming and impro!e myocardial protection. #he M may %e detached and recycled if needed. #he use during reoperation of the contralateral M does not increase the ris9 of sternal ,ound complications.
+. Considering the results of coronary reoperation in comparison to primary C"E3 choose the incorrect statement. 0perati!e mor%idity and mortality are increased o!er those for primary C"E. ". Mortality most often stems from cardiac causes after reoperation. C. Sur!i!al ofprimary patientsC"E. after hospital discharge follo,ing coronary reoperation is nearly e7ui!alent to sur!i!al after *. Compared to primary C"E3 return of anginal symptoms is delayed after reoperati!e C"E. 5. Myocardial protection and the ris9 of myocardial infarction in reoperation are complicated %y increased noncoronary collaterals3 patent atherosclerotic saphenous !ein grafts3 and more diffuse coronary atherosclerosis. ns,er- *
*SC/SS0- #he mortality and mor%idity after reoperati!e C"E are appro8imately t,o to three times that of primary C"E. n contrast to primary C"E3 ,here the ma;ority of deaths are a result of failure of other organ systems3 B+ to + of deaths after reoperati!e C"E are due to cardiac causes. #he increased ris9 of reoperation results from more ad!anced nati!e !essel disease3 a longer cross$clamp time3 a longer cross$clamp time per graft3 a longer time to initiate cardiopulmonary %ypass3 and increased %lood loss. #he increased fre7uency of pulmonary complications3 myocardial infarction3 neurologic
in;ury3 and death3 stems from the technical factors of reoperation and the characteristics of the patient population. #echnical factors include difficulty in finding targets secondary to pericardial reaction and more diffusely diseased !essels3 the ris9s of in;uring the heart or great !essels on sternal re$entry3 increased %lood loss and ris9 of re7uiring transfusion3 less a!aila%le conduit for %ypass3 and greater difficulty in pro!iding optimal myocardial protection. Characteristics of this patient population that increase ris9s include ad!anced age and diminished !entricular function. While sur!i!al after reoperation is nearly e7ui!alent to that after primary C"E3 angina symptoms return at t,ice the fre7uency in the first year after operation (:B !ersus 4') then return at a similar annual rate (4 to &).
+D. Which statements are correct comparisons of gated e7uili%rium and initial$transit radionuclide measurements of left !entricular function? . Eated e7uili%rium techni7ues pro!ide more accurate measurements of e;ection fraction than initial$ transit methods. ". =eft !entricular imaging time for a gated e7uili%rium study is at least 1' times that of an initial$transit study. C. "oth techni7ues re7uire the same radiopharmaceuticals. *. "oth techni7ues re7uire a %olus in;ection. ns,er- "
*SC/SS0- "oth techni7ues are e7ually accurate for measuring left !entricular e;ection fraction. #he left !entricular imaging time for gated e7uili%rium studies is at least 1' times that of initial$transit radionuclide angiocardiography. nitial$transit techni7ues use data from fe,er than 1' heart%eats3 ,hereas e7uili%rium studies re7uire more than 1'' heart%eats to ac7uire data ,ith similar information density. #he initial$transit study can %e performed ,ith any radioacti!e su%stance3 %ut the gated e7uili%rium techni7ue re7uires a radiopharmaceutical that remains ,ithin the %lood pool for imaging. #he initial$transit radionuclide study re7uires a %olus in;ection3 %ut an e7uili%rium study can %e ac7uired up to se!eral hours after in;ection and must %e ac7uired ,hile the tracer is at e7uili%rium.
'. #he radionuclide !aria%le that contains the greatest amount of prognostic information in patients ,ith coronary artery disease is. 58ercise e;ection fraction. ". Change in regional ,all motion from rest to e8ercise. C. Ma8imal cardiac output during e8ercise. *. Change in heart rate during e8ercise. ns,er-
*SC/SS0- #he e8ercise e;ection fraction is the single most important radionuclide !aria%le relating to su%se7uent cardiac death or myocardial infarction3 and this single !aria%le contains ' of the prognostic information in the test.
1. Which of the follo,ing statements a%out left !entricular aneurysm is@are correct? . 6entricular aneurysms are commonly associated ,ith systemic arterial em%oli2ation. ". %sent collateral circulation in an area of myocardium supplied %y an acutely occluded artery fa!ors aneurysm formation. C. Postero%asal aneurysms are more common than those located in the anteroapical region. *. neurysm repair can impro!e associated cardiac !al!e dysfunction. 5. Persistent S# segment ele!ation after acute myocardial infarction suggests aneurysm formation. ns,er- "*5
*SC/SS0- #he mural throm%us fre7uently present on the endocardial surface of an aneurysm is usually adherent and rarely em%oli2es. Collateral circulation3 ,hen present3 often pre!ents transmural necrosis follo,ing arterial occlusion. Since the left anterior descending coronary artery is the !essel most commonly occluded in patients ,ith !entricular aneurysms3 most of the aneurysms are anteroapical. mpro!ements in !entricular contour and reduction in !entricular !olume accompany aneurysm repair. lthough persistent ele!ation of S# segments follo,ing myocardial infarction is !ery suggesti!e of aneurysm formation3 the diagnosis should %e confirmed %y more definiti!e tests.
4. Which of the follo,ing factors does@do not increase early mortality associated ,ith repair of left !entricular aneurysm? . Class 6 cardiac status. ". Si2e of aneurysm. C. Presence of left main coronary disease. *. 5mergent operation. 5. =ocation of aneurysm. ns,er- "5
*SC/SS0- Class 6 cardiac status and emergent operation %oth imply e8tensi!e myocardial damage and in most reported series are associated ,ith increased operati!e mortality. Similarly3 the presence of significant stenosis of the left main coronary artery increases the operati!e mortality of !irtually all cardiac procedures. 0n the other hand3 neither the si2e of the aneurysm nor its location affect early operati!e mortality3 despite the fact that posterior aneurysms are technically more difficult to repair and are much less common.
&. #he most effecti!e medical therapy in ameliorating the symptoms of Ja,asa9iAs disease and pre!enting the de!elopment of giant coronary artery aneurysms is administration of. nti%iotics. ". nti!iral agents. C. spirin. *. Eamma glo%ulin. 5. Elucocorticoids. ns,er- *
*SC/SS0- Ja,asa9iAs disease is a multisystemic disorder of un9no,n cause and is the leading cause of ac7uired heart disease in children in %oth Fapan and the /nited States. lthough many clinical aspects of Ja,asa9iAs disease suggest an infectious agent3 the search for a single agent has %een unsuccessful> neither anti%acterials nor anti!irals ha!e a role in the therapy of Ja,asa9iAs disease. #he goal of initial therapy of Ja,asa9iAs disease is the reduction of inflammation3 including coronary and myocardial inflammation. fter the diagnosis of Ja,asa9iAs disease is secured3 patients are treated ,ith intra!enous gamma glo%ulin and large doses of aspirin. Eamma glo%ulin3 4 gm. per 9g.3 is administered as a single infusion o!er 14 hours. #reatment ,ith intra!enous immune glo%ulin has %een sho,n to decrease the duration of fe!er3 to decrease the pre!alence of cardio!ascular complications3 and to pre!ent the progression to giant coronary aneurysms. igh$dose aspirin therapy contri%utes to the resolution of the acute manifestations of Ja,asa9iAs disease. When Ja,asa9iAs disease is diagnosed3 children are gi!en a regimen of aspirin3 1'' mg. per 9g. per day3 ,hich is continued until defer!escence. #hereafter3 they are maintained on small doses of aspirin3 & to + mg. per 9g. per day3 for ,ee9s. #he goal of aspirin therapy is amelioration of symptoms and pre!ention of the throm%otic and em%olic complications of Ja,asa9iAs disease. spirin does not decrease the ris9 of the de!elopment of coronary aneurysms. #here is no role for glucocorticoids in the treatment of Ja,asa9iAs disease.
:. ndications for surgical inter!ention in Ja,asa9iAs disease include ,hich of the follo,ing? . #he presence of multiple coronary artery aneurysms. ". Myocardial infarction and se!ere left !entricular dysfunction. C. #he presence of a + mm. aneurysm in the right coronary artery. *. Progressi!e stenosis in the left anterior descending coronary artery. 5. one of the a%o!e. ns,er- *
*SC/SS0- #he indications for surgical treatment of Ja,asa9iAs disease include- (1) progressi!ely stenotic coronary lesions demonstrated on coronary arteriography3 ,ith no distal coronary aneurysms ,ith stenosis> (4) locali2ed aneurysm ,ith significant stenosis in the left main coronary artery> (&) significant stenosis in t,o coronary arteries> (:) presence of collateral !essels arising from a coronary artery ,ith a pro8imal aneurysm> (+) progressi!e stenosis in the left anterior descending coronary artery> and () presence of a left !entricular aneurysm. d!anced throm%osis of coronary aneurysms causing critical stenoses in multiple coronary arteries is the most common indication for surgical inter!ention.
+. Which of the follo,ing statements a%out the pathophysiology of 5%steinAs anomaly is@are true? . #he tricuspid !al!e is usually insufficient. ". #ypically there is a left$to$right shunt across the S*. C. #he redundant anterior leaflet of the tricuspid !al!e may cause o%struction of the right !entricular outflo, tract. *. Pulmonary hypertension is a common late complication. 5. igh pulmonary !ascular resistance in neonates e8acer%ates tricuspid regurgitation and cyanosis. ns,er- C5
*SC/SS0- 5%steinAs anomaly is characteri2ed %y do,n,ard displacement of the tricuspid !al!e into the right !entricular ca!ity. #he anterior leaflet is large and Hsail$li9e3I ,hile the other t,o leaflets are rudimentary. lthough the tricuspid !al!e occasionally may %e stenotic3 it is usually regurgitant. #he tricuspid regurgitation and functional right !entricular outflo, tract o%struction caused %y the large anterior leaflet lead to right$to$left shunting across the S*. Systemic !enous hypertension is often present3 %ut pulmonary hypertension almost ne!er occurs ,ith this malformation. Ginally3 neonates that present ,ith 5%steinAs anomaly are mar9edly cyanotic3 o,ing to their high pulmonary !ascular resistance. #his causes a functional pulmonary atresia3 ,hich increases right$to$left shunting across the S*.
. n the surgical treatment of 5%steinAs anomaly3 ,hich of the follo,ing is@are true? . n neonates3 the tricuspid !al!e orifice may %e o!erse,n and a systemic$pulmonary shunt created to pro!ide pulmonary %lood flo,. ". #echni7ues in repair of the tricuspid !al!e do not utili2e plication of the atriali2ed right !entricle. C. Closure of the S* alone is ade7uate repair of the malformation. *. f tricuspid !al!e replacement is performed3 the !al!e should %e sutured a%o!e the coronary sinus to a!oid in;ury to the conduction system. 5. Currently3 mechanical prostheses are recommended for tricuspid !al!e replacement %ecause the dura%ility of %ioprosthetic !al!es in the tricuspid position is so poor. ns,er- *
*SC/SS0- n a recent report on the surgical treatment of 5%steinAs anomaly in neonates3 Starnes descri%ed a techni7ue consisting of o!erse,ing the tricuspid !al!e3 atrial septectomy3 and placement of a systemic$pulmonary shunt. #hese patients are then later staged to a modified Gontan procedure ,hen they outgro, their shunts. Repair of the S* alone ,as performed early in the treatment of 5%steinAs anomaly and ,as associated ,ith high mortality rates. t is not considered an ade7uate repair. Most techni7ues in tricuspid !al!e repair for 5%steinAs malformation utili2e plication of the atriali2ed right !entricle in addition to e8cision of redundant atrial tissue. f tricuspid !al!e replacement is necessary3 current approaches utili2e %ioprosthetic !al!es %ecause of their e8cellent dura%ility in the tricuspid position. Placement of the !al!e ring a%o!e the coronary sinus has %een associated ,ith a lo,er rate of postoperati!e heart %loc9.
B. Which of the follo,ing congenital lesions of the coronary circulation causes a cardiac murmur that is similar to the murmur produced %y a P*? . 0rigin of the left coronary artery from the pulmonary artery. ". 0rigin of the right coronary artery from the pulmonary artery. C. Coronary artery fistula. *. Mem%ranous o%struction of the ostium of the left main coronary artery. ns,er- C
*SC/SS0- #he ma;or clinical finding ,ith a coronary artery fistula is a continuous murmur o!er the site of the a%normal communication. #his murmur may closely resem%le that of P*.
. #he congenital coronary lesion most li9ely to cause death in infancy is. Coronary artery fistula. ". 0rigin of the left coronary artery from the pulmonary artery. C. 0rigin of the right coronary artery from the pulmonary artery. *. Congenital coronary aneurysm. ns,er- "
*SC/SS0- #he prognosis for most patients ,ith srcin of the left coronary artery from the pulmonary artery is poor. t has %een estimated that D+ of patients ,ith this anomaly die ,ithin the first year of life unless surgical therapy is underta9en. Patients ,hose right coronary artery srcinates from the pulmonary artery are usually asymptomatic. Patients ,ith coronary fistulas occasionally suffer congesti!e heart failure early. Congenital aneurysms of the coronary arteries are most often asymptomatic until complications occur3 usually later in life.
D. #he congenital coronary lesion associated ,ith minimal or a%sent clinical manifestations and nearly normal life e8pectancy is. Congenital srcin of %oth coronary arteries from the pulmonary artery. ". Congenital coronary artery fistula. C. Mem%ranous o%struction of the ostium of the left main coronary artery. *. Congenital srcin of the right coronary artery from the pulmonary artery. ns,er- *
*SC/SS0- Clinical manifestations of congenital srcin of the right coronary artery from the pulmonary artery are usually minimal or a%sent. #his malformation is thought to ha!e %een associated ,ith death. #he oldest reported patient ,ith this malformation died at age D' years from unrelated pro%lems.
B'. Which of the follo,ing is@are indications for aortic !al!e replacement for aortic stenosis? . Syncope. ". Congesti!e heart failure. C. ngina. *. #rans!al!ar gradient of &+ mm. g ,ithout symptoms. ns,er- "C
*SC/SS0- With progressi!e narro,ing of the aortic !al!e area from the normal & to : s7. cm. to 1 s7. cm.3 patients %ecome symptomatic. #he classic symptoms produced %y aortic stenosis are syncope3 congesti!e heart failure3 and angina. 0nce symptoms occur3 life e8pectancy is limited to 4 to + years. #herefore3 symptomatic aortic stenosis is an indication for aortic !al!e replacement. #he ris9 of death ,ith asymptomatic aortic stenosis is 7uite lo,3 and aortic !al!e replacement is not indicated for asymptomatic patients ,ith a trans!al!ar gradient less than +' mm. g.
B1. /nder ,hich of the follo,ing circumstances is medical management logical? . Moderate aortic insufficiency seen on echocardiography ,ith normal left !entricular end$systolic dimensions. ". Moderate to se!ere aortic insufficiency seen on echocardiography ,ith cardiomegaly on chest roentgenography. C. Moderate aortic insufficiency seen on echocardiography ,ith symptoms of congesti!e heart failure. *. Moderate aortic insufficiency ,ith an end$systolic left !entricular dimension of B' mm. as seen on echocardiography. ns,er- *SC/SS0- #he left !entricle is usually a%le to compensate for a long time for the increased !olume load imposed %y aortic insufficiency. #he natural history of asymptomatic aortic stenosis is e8cellent> 1'$ year sur!i!al for moderate aortic insufficiency managed medically is as high as + to D+. Medical management typically consists of diuretics and afterload reduction> ho,e!er3 once the compensatory mechanisms %egin to fail3 sur!i!al is limited. alf of patients ,ith signs or symptoms of congesti!e heart failure die ,ithin 4 years. #herefore3 e!idence of left !entricular dilation %y echocardiography (left !entricular end$systolic dimension greater than ++ mm.3 cardiomegaly on chest roentgenography) or symptoms of congesti!e heart failure are indications for aortic !al!e replacement.
B4. Which of the follo,ing may %e indications for operation for mitral stenosis? . Systemic em%oli2ation. ". nfecti!e endocarditis. C. 0nset of atrial fi%rillation. *. Worsening pulmonary hypertension. ns,er- "C*
*SC/SS0- lthough each is only a relati!e indication for operation for mitral stenosis3 systemic em%oli2ation3 infecti!e endocarditis3 onset of atrial fi%rillation3 and ,orsening pulmonary hypertension may each %e an indication for operation for mitral stenosis. Systemic em%oli2ation3 infecti!e endocarditis3 and onset of atrial fi%rillation are each complications of mitral stenosis that portend a ris9 of further complication ,ith continued medical therapy. Patients older than :' years ,ith mild class congesti!e heart failure stand to gain symptomatically from operation for significant mitral stenosis and do not run e8cessi!e ris9 of multiple reoperati!e procedures.
B&. Which of the follo,ing is@are not true? . 0peration impro!es sur!i!al in patients ,ith se!ere3 symptomatic mitral !al!e disease. ". =eft !entricular dilatation ,ith class or class heart failure is an indication for operation ,ith mitral regurgitation. C. #ricuspid regurgitation is most commonly caused %y a%normalities of the leaflets themsel!es. *. Mitral !al!e replacement re7uires resection of the mitral !al!e leaflets and chordae. ns,er- C*
*SC/SS0- Relati!e to medical therapy alone3 surgical therapy has %een sho,n to impro!e sur!i!al in patients ,ith se!ere3 symptomatic mitral !al!e disease. n mitral regurgitation3 left !entricular dilatation is an indication for surgical inter!ention regardless of failure symptoms. #he most common cause of tricuspid regurgitation is tricuspid annular dilatation ,ithout a%normalities of the leaflets themsel!es. Mitral !al!e replacement ,ith preser!ation of %oth leaflets or at least the posterior leaflet is ,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.
B:. Which of the follo,ing generally are not symptoms of tricuspid !al!e disease? . Pulmonary edema. ". epatic failure. C. nasarca. *. oarseness. ns,er- *
*SC/SS0- epatic failure and anasarca are indeed common symptoms of se!ere3 long$standing tricuspid !al!e disease ,ith increased !enous pressure. Pulmonary edema is a conse7uence of left$sided heart disease and does not result from a tricuspid lesion. Similarly3 hoarseness is most common after mitral !al!e disease ,ith left atrial enlargement and is rarely due to tricuspid !al!e disease alone.
B+. Which of the follo,ing are relati!e indications for mitral !al!e replacement3 as opposed to mitral !al!e repair? . 58tensi!e leaflet calcification. ". Mitral regurgitation. C. Chordal rupture of the anterior mitral leaflet. *. Significant annular dilatation. ns,er-
*SC/SS058tensi!e mitral !al!e calcification a relati!e indication for mitral !al!e!al!e replacement. Mitral regurgitation or significant annular dilatation is may3 ho,e!er3 %e amena%le to mitral repair. Chordal rupture of the anterior leaflet is generally repara%le using chordal transposition or polytetrafluoroethylene (P#G5) chordae.
B. Which of the follo,ing are not true? . #ricuspid regurgitation due to annular dilatation alone generally does not re7uire !al!e replacement. ". Mitral !al!e replacement ,ith either a %ioprosthesis or a mechanical !al!e re7uires ,arfarin anticoagulation. C. #ricuspid !al!e replacement is generally an indication for using a tissue !al!e. *. Chronic renal failure is a relati!e indication for tissue !al!es. ns,er- "
*SC/SS0- #ricuspid regurgitation due to annular dilatation alone generally can %e treated ,ith tricuspid annuloplasty or ,ith correction of associated mitral !al!e disease. Mitral !al!e replacement ,ith a mechanical !al!e does re7uire ,arfarin anticoagulation> ho,e!er3 mitral !al!e replacement ,ith a %ioprosthesis may %e managed ,ith aspirin alone. #ricuspid !al!e replacement is an indication for using a tissue !al!e %ecause of the significant incidence of !al!e throm%osis ,hen a mechanical !al!e is in the tricuspid position. Chronic renal failure is a relati!e indication for tissue !al!es %ecause !al!e calcification is rare and %ecause anticoagulation of patients on dialysis carries high ris9s of mor%idity and mortality.
BB. Which of the follo,ing are relati!e indications for mechanical3 as opposed to tissue3 !al!e replacement? . Patient younger than &' years. ". oung female patient ,ho desires children. C. n elderly patient. *. #ricuspid !al!e replacement. ns,er-
*SC/SS0- ge younger than &' years is a relati!e indication for mechanical !al!es %ecause of an increased incidence of calcification of tissue !al!es in younger persons. young female ,ho desires children ,ould %e a relati!e contraindication to mechanical replacement %ecause of the ris9 of teratogenesis and hemorrhage during pregnancy secondary to ,arfarin therapy. d!anced age is a relati!e indication for %iologic !al!es to a!oid complications of anticoagulation and %ecause the pro%a%ility of reoperation is lo,. #ricuspid !al!e replacement is a relati!e contraindication to mechanical !al!e replacement3 o,ing to the increased incidence of tricuspid !al!e throm%osis ,ith a mechanical prosthesis.
B. Which of the follo,ing statements are not true? . "ioprosthetic !al!es ha!e a relati!ely high incidence of hemolysis. ". !al!es ha!e a structural lo,er incidence postoperati!e !al!e endocarditis. C. "ioprosthetic Mechanical !al!es de!elop failure of after an a!erage prosthetic of B to 1' years. *. Mortality attri%uta%le to ,arfarin therapy approaches + per patient$year. ns,er- "C*
*SC/SS0- "ioprosthetic !al!es ha!e a relati!ely lo, incidence of hemolysis. "ioprosthetic and mechanical !al!es do not differ significantly in the associated incidences of postoperati!e prosthetic !al!e endocarditis. "ioprosthetic !al!es de!elop structural failure after an a!erage of B to 1' years3 ,hereas mechanical !al!es ha!e a life span of ,ell %eyond 1' years. #he mortality attri%uta%le to ,arfarin therapy approaches 1 per patient$year.
BD. Which of the follo,ing are not generally associated ,ith mitral stenosis ,ithout regurgitation? . Pulmonary hypertension. ". Pulmonary edema. C. =eft !entricular dilatation. *. n opening snap after the second heart sound. ns,er- "*
*SC/SS0- Pure mitral stenosis ,ithout regurgitation may %e associated ,ith pulmonary hypertension3 pulmonary edema3 and an opening snap after the second heart sound. =eft !entricular dilatation ,ould %e rare in pure mitral stenosis and generally occurs ,ith !olume or pressure o!erload of the left !entricle3 as ,ith mitral regurgitation.
'. #he most common location of accessory path,ays in patients ,ith the Wolff$Par9inson$White syndrome is the. =eft free ,all. ". Right free ,all. C. Posterior septum. *. nterior septum. ns,er- *SC/SS0- ll ma;or pu%lished series of the Wolff$Par9inson$White syndrome indicate that the ma;ority of all accessory path,ays appear in the left free ,all space. n one series3 appro8imately ' of all accessory path,ays occur in the left free ,all space. n 5%steinAs anomaly3 path,ays are usually located in the posterior septum and@or right free ,all spaces. f these patients are e8cluded3 appro8imately B' of path,ays occur in the left free ,all space.
1. #he anatomic electrophysiologic %asis of 6 node re$entry tachycardia is dual 6 node conduction path,ays. 6 node re$entry tachycardia is most li9ely to occur ,ith ,hich of the follo,ing electrophysiologic a%errations? . Pro8imal antegrade %loc9 in the slo, conduction path,ay. ". Pro8imal retrograde %loc9 in the slo, conduction path,ay. C. Pro8imal antegrade %loc9 in the fast conduction path,ay. *. Pro8imal retrograde %loc9 in the fast conduction path,ay. ns,er- C *SC/SS0- retrograde conduction %loc9 in either the slo, or fast path,ay ,ould %e li9ely to pre!ent a re$entrant circuit from de!eloping. pro8imal antegrade %loc9 in the slo, conduction path,ay is e8tremely unusual %ecause of the short refractory period of the slo, conduction path,ay. #he most common conduction %loc9 that occurs in patients ,ith dual 6 node physiology is a pro8imal antegrade conduction %loc9 in the fast path,ay %ecause of its longer refractory period. #his antegrade %loc9 in the fast conduction path,ay allo,s 6 conduction to occur !ia the slo, path,ay and to return in retrograde fashion up the fast path,ay to esta%lish the re$entrant circuit responsi%le for 6 node re$entry tachycardia.
4. Match the four surgical procedures that ha!e %een de!eloped for the treatment of atrial fi%rillation ,ith the ma;or detrimental se7uela(e) of atrial fi%rillation that each corrects. . is %undle a%lation. ". =eft atrial isolation procedure. C. Corridor procedure. *. Ma2e procedure. 1. PatientAs sensation of irregular heart rhythm. 4. emodynamic compromise %ecause of loss of 6 synchrony. &. ncreased !ulnera%ility to throm%oem%olism. ns,er- $1. "$134. C$1. *1343&
*SC/SS0- #he surgical procedure most commonly employed for the treatment of atrial fi%rillation is catheter a%lation of the is %undle. #he nternational Catheter %lation Registry re!eals that more than ' of patients ,ho undergo electi!e catheter a%lation of the %undle of is do so for the treatment of atrial fi%rillation. is %undle a%lation is an isolation procedure3 in that it confines the atrial fi%rillation to the atria and protects the !entricles from the unpleasant sensation of an irregular heart%eat. "ecause the atria continue to fi%rillate there is no restoration of 6 synchrony3 and therefore there is no impro!ement in cardiac hemodynamics. Moreo!er3 the continuing fi%rillation of the left atrium means that postoperati!ely the patient is still at the same ris9 for throm%oem%olism. #hus3 is %undle a%lation corrects only one of the three detrimental se7uelae of atrial fi%rillation3 namely the arrhythmia pro%lem. #he left atrial isolation procedure confines atrial fi%rillation to the left atrium3 allo,ing the sinus node to dri!e the remainder of the heart in a normal sinus rhythm. #hus3 it alle!iates the unpleasant sensation of an irregular heart%eat. n addition3 %ecause 6 synchrony is re$esta%lished %et,een the right atrium and right !entricle3 right$sided cardiac output is restored to normal. #his means that normal cardiac output is deli!ered through the lungs to the left side of the heart. n the presence of a normal left !entricle the left$ sided cardiac output is also normal3 despite the fact that left$sided 6 synchrony is not present> ho,e!er3 %ecause the left atrium is allo,ed to fi%rillate3 the !ulnera%ility to throm%oem%olism remains unchanged postoperati!ely. #he corridor procedure allo,s the sinus node to dri!e the heart in normal sinus rhythm3 %ut %ecause of the total isolation of the sinoatrial and 6 nodes from the remainder of the atria3 the atria may continue to fi%rillate. 5!en if they do not3 in effect they are isolated from their respecti!e !entricles so that 6 synchrony is lost on %oth sides of the heart. s a result3 the corridor procedure alle!iates the sensation of arrhythmia %ut does not restore normal hemodynamics3 nor does it decrease !ulnera%ility to throm%oem%olism. #he ma2e procedure a%lates the re$entrant circuits responsi%le for atrial fi%rillation and restores the normal sinus rhythm. #hus3 it alle!iates the sensation of arrhythmia3 restores normal hemodynamics3 and alle!iates the !ulnera%ility to throm%oem%olism.
&. ll of the follo,ing statements a%out nonischemic !entricular tachyarrhythmias are true e8cept. #hey usually occur in the right !entricle. ". #hey are usually associated ,ith a left %undle %ranch %loc9 pattern during the tachycardia. C. #hey are usually more refractory to medical therapy than ischemic !entricular tachyarrhythmias. *. #hey usually occur as a result of automaticity rather than re$entry. ns,er- *
*SC/SS0- onischemic !entricular tachyarrhythmias usually occur in the right !entricle3 and as a result the 5CE sho,s a left %undle %ranch %loc9Ktype pattern during !entricular tachycardia. #hese
arrhythmias are notoriously refractory to medical therapy and they occur almost e8clusi!ely on a re$ entrant %asis.
:. Which of the follo,ing statements a%out left atrial my8oma are true? . #his lesion3 %y site and histology3 is the most common primary cardiac tumor. ". t is %est diagnosed %y cardiac catheteri2ation and angiography. C. #he symptom comple8 can mimic collagen !ascular disease. *. t has an intraca!itary gro,th pattern. 5. t has a multicentric srcin in the cham%er ,all. ns,er- C*
*SC/SS0- 5ighty per cent of primary cardiac tumors are %enign3 and half of these %enign tumors are my8omas. Se!enty$fi!e per cent of my8omas arise in the left atrium in the region of the fossa o!alis. 5chocardiography is the techni7ue of choice in the e!aluation of intracardiac tumors3 and findings suggesti!e of my8oma occur in D+ of patients e8amined. n!asi!e procedures3 ,ith the attendant ris9 of tumor em%oli2ation3 are not ,arranted. 0,ing to an autoimmune phenomenon3 left atrial my8omas can present ,ith systemic constitutional symptoms of fe!er3 malaise3 ,eight loss3 polymyositis3 and %lood dyscrasias that mimic collagen !ascular disease. 0f surgical significance is the fact that most my8omas rarely e8tend deeper than the endocardium %ut gro, as polypoid3 intraca!itary masses. ttachment %y a !ascular stal9 thus allo,s tumor mo%ility3 predisposing to em%oli2ation and interference ,ith mitral !al!e competence and causing characteristic echocardiographic findings.
+. Which of the follo,ing statements a%out malignant cardiac tumors are true? . Sarcomas are the most fre7uent primary malignancy. ". Metastatic tumors are usually asymptomatic. C. d;u!ant chemotherapy and irradiation are efficacious in prolonging sur!i!al. *. ntra$atrial e8tension of renal neoplasms is a contraindication for surgical resection. 5. Constricti!e physiology is an indication for operation. ns,er- "
*SC/SS0- #,enty per cent of primary cardiac tumors are some !ariant of sarcoma. Precise histologic classification is not imperati!e3 as all ha!e a similar clinical picture ,ith rapid systemic dissemination and aggressi!e local in!asion. n contrast3 metastatic tumors cause symptoms in only 1' of patients. /nfortunately3 most primary and secondary cardiac malignancies infre7uently respond to systemic chemotherapy or mediastinal irradiation. Surgical treatment is most successful ,ith renal tumors e8tending into the right atrium. Significant +$year sur!i!al can %e achie!ed ,ith concomitant nephrectomy and intra$atrial resection of the tumor throm%us. Relief of tamponade is ,orth,hile> ho,e!er3 e8tensi!e decortication pro!ides little help.
. *isad!antages of temporary pacing through s9in electrodes applied to the anterior chest ,all include all of the follo,ing e8cept. S9in %urns. ". Painful chest ,all muscle contractions. C. 6entricular fi%rillation. *. na%ility to pace. ns,er- C
*SC/SS0- n 1D+4 oll first descri%ed successful pacing through e8ternal metal electrodes applied to the anterior chest ,all. Clinical e8perience ,ith this techni7ue has sho,n that it is %oth feasi%le and lifesa!ing for temporary pacing> ho,e!er3 disad!antages of the e8ternal pacing techni7ue include s9in %urns ,hen too little electrode ;elly is applied3 painful chest ,all muscle contractions3 and ina%ility to pace in thic9$chested or emphysematous patients. 6entricular fi%rillation induced %y e8ternal temporary cardiac pacing is e8ceedingly rare.
B. n adults the most common cause of ac7uired complete heart %loc9 is. schemic heart disease. ". Sclerodegenerati!e disease. C. #raumatic in;ury. *. Cardiomegaly. ns,er- "
*SC/SS0- "efore permanent pacema9ers ,ere a!aila%le3 +' of patients ,ith complete heart %loc9 died ,ithin 1 year. #he most common cause of ac7uired complete heart %loc9 in adults is sclerodegenerati!e disease of the cardiac s9eleton and 6 conduction system. 0ther less common causes of complete heart %loc9 include ischemic heart disease3 cardiomyopathic processes3 ChagasA disease3 and traumatic in;ury.
. #he most heart common indication for permanent pacing is. Complete %loc9. ". Second$degree 6 %loc9. C. Chronic %ifascicular %loc9. *. Sic9 sinus syndrome. ns,er- * *SC/SS0- Patients ,ith sinus node dysfunction may de!elop a num%er of arrhythmias3 such as inappropriate sinus %radycardia3 chronotropic incompetence3 sinoatrial e8it %loc93 and sinus arrest. #his group of rhythm disorders typically occurs in older patients ,ith or ,ithout underlying heart disease and is collecti!ely 9no,n as the Hsic9 sinus syndrome.I n addition3 many patients ,ith sic9 sinus syndrome ha!e associated atrial tachyarrhythmias3 particularly atrial fi%rillation. #his association of atrial tachyarrhythmias in patients ,ith the sic9 sinus syndrome is called the tachycardia$%radycardia (or tachy$ %rady) syndrome. #he most common indication for permanent pacing occurs in patients ,ith the sic9 sinus syndrome
D. *ecreasing pacema9er electrode tip si2e results in. =o,er pacing thresholds. ". mpro!ed electrogram sensing. C. *ecreased %attery life. *. =ess patient discomfort. ns,er-
*SC/SS0- *ecreasing pacema9er electrode tip si2e results in lo,er pacing thresholds3 %oth at the time of implant and su%se7uently3 %ecause of higher current density. o,e!er3 %etter sensing function is directly related to electrode area and is ad!ersely affected %y small electrode si2e. #herefore3 a compromise %et,een pacing and sensing efficiency is re7uired. #ypical electrode surface areas for pacing are %et,een and 1' s7. mm.
D'. t the time of !entricular pacema9er implantation3 lead resistance is determined at a !oltage near that of the pacema9erAs output. #he calculated resistance at + !olts should range from. 1' to 1'' ohms. ". 14+ to 4+' ohms. C. &'' to '' ohms. *. 1''' to 1+'' ohms. ns,er- C
*SC/SS0- t the time of pacema9er implantation3 in addition to measuring pulse amplitude (!oltage and current) and pulse ,idth3 resistance is also determined. s descri%ed %y 0hmAs la,3 resistance is calculated %y di!iding !oltage %y current. Resistance calculations are made at a !oltage near that of the pacema9erAs output. #he calculated resistance at + !olts should range from &'' to '' ohms. n unsatisfactorily lo, resistance is unsatisfactory %ecause current is ,asted and %attery life is shortened. Con!ersely3 e8cessi!ely high resistance (more than '' ohms) increases %attery life %ut decreases the current deli!ered to the heart for pacing.
D1. !entricular inhi%ited$demand pacema9er using the ntersociety Commission for eart *isease Resources (C*) code is designated as. *6. ". 66. C. 600. *. 6**. ns,er- "
*SC/SS0- !entricular inhi%ited$demand pacema9er using the C* code is designated as 66. s the C* code states3 the pacema9er senses intrinsic !entricular acti!ity and is inhi%ited ,hen this acti!ity e8ceeds the stand%y or escape rate of the pacema9er. When the intrinsic !entricular rate falls %elo, the escape rate of the pulse generator3 the pacema9er %egins to function at its programmed rate.
D4. n rate$modulated pacing3 the pacing rate is determined %y a physiologic parameter other than atrial rate and is measured %y a special sensor in the pacema9er or pacing lead. #he most commonly used physiologic parameter in rate$modulated pacema9ers is. Q# inter!al. ". 6enous %lood temperature. C. Mi8ed !enous o8ygen saturation. *. "ody motion. ns,er- *
*SC/SS0- *uring e8ertion3 the re7uired increase in cardiac output is o%tained mostly %y the increase in paced heart rate3 although increased !enous filling and maintenance of 6 synchrony are also important contri%utors. #he most commonly used physiologic parameters in rate$modulated pacema9ers at the present time are %ody motion and minute !entilation. 0ther parameters that are less commonly used or under e!aluation include Q# inter!al3 !enous %lood temperature3 mi8ed !enous o8ygen saturation3 contractility3 stro9e !olume3 !enous p3 and the paced depolari2ation gradient.
D&. #he most common pacing mode used in patients ,ith symptomatic %radycardia and an underlying sinus rhythm is. . ". *6. C. ***. *. 66. ns,er- C
*SC/SS0- H/ni!ersal3I or ***3 pacing has %een sho,n to ha!e many %enefits o!er other pacing modalities3 including the a%ility to trac9 the intrinsic sinus rate3 pace the atrium and !entricle3 maintain atrio!entricular synchrony3 and a!oid the pacema9er syndrome. Recognition of these %enefits has steadily increased the use of *** pacema9ers in the last decade3 and at the present time *** is the most common pacing mode.
D:. trans!enous pacema9er generator poc9et should %e placed on the patientAs nondominant side o!er the. nteromedial chest ,all. ". nterolateral chest ,all. C. nferomedial chest ,all. *. nferolateral chest ,all. ns,er-
*SC/SS0- "ipolar impulse generators can %e placed either in the su%cutaneous tissue or %eneath the muscle. Migration of the impulse generator most commonly occurs in infracla!icular pacema9ers poc9ets. Migration tends to follo, the cur!ature of the chest ,all3 and the impulse generator tends to migrate laterally. #his can %e pre!ented %y creating an anteromedial poc9et large enough to contain the
impulse generator and lead. n suscepti%le persons the impulse generator can %e further secured to the chest ,all to pre!ent migration.
D+. Pacema9er$mediated tachycardia is caused %y. Pacema9er induction of atrial fi%rillation. ". Sensing of retrograde atrial acti!ation. C. nappropriate !entricular sensing. *. =ead fracture. ns,er- "
*SC/SS0- Pacema9er$mediated tachycardia occurs in the setting of intact !entriculoatrial conduction. #ypically3 premature !entricular contractions may %e conducted retrogradely through the 6 conduction system and cause retrograde acti!ation of the atrium. f this retrograde atrial acti!ation occurs after completion of the programmed pacema9er !entriculoatrial refractory period3 the atrial e!ent is sensed %y the *** pacema9er and e!o9es a paced !entricular e!ent that may cause further 6 conduction. f each !entricularly paced e!ent results in atrial acti!ation sensed %y the pacema9er3 pacema9er$mediated tachycardia ,ill %e generated.
D. Which cardio!ascular pharmacologic agents are safe to use during routine a%dominal surgery in a B+$ year$old ,oman ,ith documented hypertension and mild coronary artery disease? . ifedipine. ". tenolol. C. ydrala2ine. *. Captopril. 5. Reserpine. ns,er- "* *SC/SS0- ifedipine is tolerated fairly ,ell %y elderly patients and is safe to use in the perioperati!e period ,ith close hemodynamic monitoring. tenolol is a safe %eta$%loc9er to use during the perioperati!e period and pro!ides protection from cardiac rhythm distur%ances and re%ound hypertension. ydrala2ine3 gi!en ,ithout a %eta$%loc9er3 often elicits,ith refle8 ,hich limitsresponse its usefulness. Captopril is aifsafe agent that does not appear to interfere thetachycardia3 normal cardio!ascular to anesthesia3 and a%rupt ,ithdra,al of this agent may result in se!ere hypertension and should %e a!oided. Reserpine is an adrenergic inhi%itor that may depress cardiac output and result in hypotension3 so its use in the perioperati!e setting is limited.
DB. Which inotropic drugs are safe for use in elderly patients ,ith mild congesti!e heart failure in the postoperati!e period? . *igitalis compounds. ". *opamine. C. mrinone. *. Melrinone. 5. *o%utamine. ns,er- "C*5
*SC/SS0- *opamine and do%utamine stimulate cardiac %eta$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 effects ,hile causing arterial and !enous dilation. Melrinone and amrinone are useful in patients ,ith lo, cardiac output3 especially in the setting of congesti!e heart failure. *igitalis compounds can %e trou%lesome in the postoperati!e period o,ing to the to8ic effects of these agents. Gurthermore3 perioperati!e hypo8ia and hypo9alemia increase myocardial suscepti%ility to digitalis$induced !entricular arrhythmias.
D. Which anticoagulation treatment plan(s) is@are appropriate for a B4$year$old man ,ith a mechanical heart !al!e in place ,ho ta9es Coumadin (,arfarin) and no, re7uires electi!e left colon resection? . *iscontinuation of Coumadin therapy on the day of the operation. ". *iscontinuation of Coumadin therapy on the day of the operation ,ith replacement of clotting factors ,ith fresh fro2en plasma (GGP) %efore the start of the surgical procedure. C. *iscontinuation of Coumadin therapy + days %efore operation ,ith no further anticoagulation therapy %efore surgery. *. *iscontinuation of Coumadin therapy + days %efore operation ,ith the institution of intra!enous heparin as the prothrom%in time normali2es. 5. *iscontinuation of Coumadin therapy 4 days %efore operation follo,ed %y large doses of aspirin. ns,er- *
*SC/SS0- Many patients ,ho re7uire anticoagulation ,ith Coumadin for underlying cardiac disease need to undergo routine general surgical procedures. #he current recommendations for patients ,ho ha!e %een on long$term Coumadin therapy is to discontinue Coumadin + days %efore an operati!e procedure. s the patientAs prothrom%in time normali2es 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. eparin should then %e ,ithheld appro8imately : to hours %efore the surgical procedure. #he operation is then performed in a Hheparin ,indo,3I ,here the le!el of anticoagulation can easily %e titrated or totally re!ersed ,ith protamine if necessary.
DD. Which of the follo,ing treatment plans is appropriate for a $year$old patient ,ith moderate to se!ere congesti!e heart failure follo,ing 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. C. fterload reduction ,ith nitroprusside and inotropic support ,ith dopamine. *. Close perioperati!e monitoring and inotropic support ,ith melrinone. 5. ntra!enous digitalis ,ith diuresis using furosemide as needed. ns,er- C*
*SC/SS0- #reatment of congesti!e heart failure using epinephrine alone is contraindicated o,ing to the profound !asoconstricti!e properties of epinephrine3 ,hich only e8acer%ate the heart failure. *iuresis ,ith furosemide and inotropic support ,ith dopamine is accepta%le for patients ,ith mild congesti!e
heart failure> ho,e!er3 in the postoperati!e period pharmacologic diuresis can lead to profound hypo!olemia re7uiring 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%itor3 ,hich has %een sho,n 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 o,ing to the potential to8icity of digitalis ,hile the patient has ongoing fluid and electrolyte shifts.
1''. Which of the follo,ing steps is@are appropriate for a +$year$old ,oman ,ho de!elops atrial fi%rillation ,ith associated mild hypotension and rapid !entricular response follo,ing partial gastric resection? . Correction of electrolytes and %lood chemistries. ". 5!aluation for possi%le myocardial infarction. C. #reatment ,ith intra!enous lidocaine. *. ttempt to limit the !entricular response ,ith digitalis. 5. mmediate cardio!ersion. ns,er- "*
*SC/SS0- When a patient de!elops postoperati!e atrial fi%rillation follo,ing an e8tracardiac procedure3 correction of the patientAs %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 first rule in treatment is to slo, the !entricular response and attempt to limit hemodynamic insta%ility. *igitalis is effecti!e in slo,ing do,n the !entricular response and thus impro!ing the hemodynamic status of the patient. =idocaine has little use in controlling atrial dysrhythmias %ut is !ery effecti!e in decreasing !entricular ectopy. mmediate cardio!ersion is rarely indicated for ne,$onset atrial fi%rillation. 0nly after correction of all underlying meta%olic and electrolyte defects as ,ell as an attempt at medical con!ersion and !entricular rate control is cardio!ersion recommended.
1'1. #heamplification damaging effects of cardiopulmonary %ypass are3system to a large degree3 due to of the humoral system. #he humoral amplification includes ,hich of acti!ation the follo,ing? . #he coagulation cascade. ". #he fi%rinolytic cascade. C. Complement acti!ation. *. and C. 5. 3 "3 and C. ns,er- 5
*SC/SS0- Cardiopulmonary %ypass stimulates a ,hole$%ody inflammatory response3 and the concentrations of se!eral inflammatory mediators (e.g.3 complement fraction C+a) ha!e %een associated ,ith su%system dysfunction follo,ing cardiopulmonary %ypass. #his inflammatory response is comple8 and has se!eral arms3 including the coagulation3 fi%rinolytic3 and complement systems. Simply %loc9ing one path,ay is unli9ely to completely pre!ent %ypass$induced in;ury.
1'4. de7uate flo, during cardiopulmonary %ypass is %est indicated %y. Systemic %lood pressure of D'@+' mm. g. ". rterial P0 4 of 4&' mm. g. C. Mi8ed !enous hemoglo%in saturation of B. *. Central !enous pressure of 1 mm. g. 5. Plasma lactate !alue of mg. per dl. ns,er- C
*SC/SS0- #he purpose of cardiopulmonary %ypass is to pro!ide ade7uate circulation of %lood to sustain aero%ic meta%olism. 08ygen consumption during %ypass depends on %ypass flo, until a critical flo, is attained. With higher flo,s there is no further increase in o8ygen consumption (i.e.3 o8ygen consumption %ecomes flo, independent)3 and the mi8ed !enous hemoglo%in saturation increases. mi8ed !enous hemoglo%in saturation of B indicates that %ypass flo, is a%o!e the critical le!el and that flo, is ade7uate. #he other !aria%les do not ensure ade7uate %ypass flo,.
1'&. Which of the follo,ing does not typically occur during the first fe, minutes of cardiopulmonary %ypass? . nterstitial fluid increases. ". "lood flo, %ecomes nonpulsatile. C. Platelet count decreases. *. Complement is acti!ated. 5. Systemic !ascular resistance falls. ns,er-
*SC/SS0- Se!eral e!ents occur during the first fe, minutes of %ypass. #he tu%ing and o8ygenator surfaces are coated %y serum proteins that in turn acti!ate platelets. #his reduces the platelet count. #he roller pump produces nonpulsatile flo,3 ,hich is different from the usual pulsatile cardiac flo,. Serum complement is acti!ated %y e8posure of %lood to the nonphysiologic surfaces of the pump$o8ygenator3 and systemic !ascular resistance falls. nterstitial fluid accumulates during %ypass> ho,e!er3 this occurs later during %ypass.
1':. Which of the follo,ing are physiologic %enefits of intra$aortic %alloon counterpulsation to the ischemic !entricle? . Preload reduction. ". fterload reduction. C. Coronary %lood flo, enhancement. *. *ecreased !entricular end$diastolic pressure. ns,er- "C*
*SC/SS0- n general3 preload relates to the !olume of %lood or fluid presented to the left !entricle. lthough ,all tension does increase ,ith increased !olume3 Starling properties are called forth for added efficiency. Preload is controlled %y !olume status as ,ell as capacity of the !enous system. #he effects of
%alloon counterpulsation on cardiac preload are minimal and secondary to other changes. s the %alloon collapses in the aorta3 the a%sence of the %alloon !olume3 or Ha%yss3I creates a decrease in !entricular afterload. n effect this decreases !entricular ,all tension3 reducing myocardial o8ygen consumption significantly. *uring counterpulsation3 the intra$aortic %alloon inflates in diastole3 ele!ating coronary perfusion pressure significantly. Ma8imal coronary artery perfusion occurs in this part of the cardiac cycle. #hus3 ischemic !entricles %enefit especially from %alloon pumping. #he %alloon pump does not directly decrease the left !entricular end$diastolic pressure. o,e!er3 in !entricles failing from ischemia the com%ination of afterload reduction and impro!ed coronary %lood flo, usually augments cardiac function3 producing decreased cardiac filling pressure or left !entricular end$diastolic pressure.
1'+. Which of the follo,ing are the ma;or indications for instituting intra$aortic %alloon pumping? . Medically refractory angina. ". cute papillary muscle rupture. C. =eft main coronary artery lesion. *. 6entricular failure after cardiac surgery. 5. P#C failure. ns,er- "*5
*SC/SS0- Medically refractory angina is one of the ma;or indications for implementing the intra$ aortic %alloon pump. When intra!enous nitroglycerin %ecomes ineffecti!e at relie!ing chest pain or results in early hypotension3 the %alloon pump should %e used in preparation for surgical re!asculari2ation or percutaneous angioplasty. "y reducing left !entricular afterload3 the pump reduces regurgitation into the left atrium. #hus3 %alloon counterpulsation is !ery helpful for treating patients ,ith acute mitral insufficiency secondary to papillary muscle rupture. Patients should undergo !al!e surgical procedures emergently3 as %alloon pump support is only tempori2ing. #he mere presence of a left main coronary lesion is not an indication for use of the %alloon pump. n former years such pumps ,ere inserted prophylactically %efore induction of anesthesia for coronary %ypass surgery. e,er anesthetic techni7ues ha!e largely o%!iated this> ho,e!er3 in the presence of a left main lesion and medically refractory angina the %alloon pump should %e used. #he %alloon pump is 7uite effecti!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 5mory /ni!ersity group ,as the first to e8pound on the efficacy of the %alloon pump in sta%ili2ing patients follo,ing percutaneous angioplasty failure. With the pump inserted3 most patients can %e transported to theofoperating %eing sta%le to har!estsaphenous an internal!ein. mammary graft instead ha!ing toroom defersafely3 to the many more accessi%le %utenough less prefera%le
1'. Which of the follo,ing are the most fre7uent complications of intra$aortic %alloon counterpulsation? . Stro9e. ". =im% ischemia. C. rrhythmias. *. ortic throm%osis. ns,er- "
*SC/SS0- Stro9e rarely occurs secondary to intra$aortic %alloon pump use. #he %alloon must %e
positioned ,ell %elo, the aortic arch !essels and ne!er pro8imal to the left su%cla!ian artery srcin. Stro9es ha!e %een reported from em%oli %eing thro,n retrograde from the %alloon> ho,e!er3 this is !ery rare. =im% ischemia is one of the most fre7uent complications of %alloon pumping. #he com%ination of iliofemoral atherosclerosis and catheter luminal o%struction may impede distal flo,. #his may re7uire catheter remo!al to re$esta%lish flo,. n 4 to 1' of patients3 arterial reconstruction is necessary to repair %alloon$related complications. Smaller catheters ha!e helped pre!ent lim% ischemia. rrhythmias in general are not complications of %alloon pumping. n fact3 arrhythmias related to ischemia may %e controlled %y the %alloon pump. ortic throm%osis can occur !ery rarely ,ith pump use. more fre7uent occurrence is distal em%oli2ation ,ith lim% ischemia. Patients should %e heparini2ed ,hile the %alloon catheter is in place. Gollo,ing cardiac surgery heparini2ation is usually delayed for 14 to 4: hours.
1'B. Permanent artificial hearts are %eing de!eloped that are electrically po,ered. Wireless techni7ues are used to transmit the electrical energy across the %ody ,all using the principle of. nfrared sensor. ". nducti!e coupling. C. #hermionic coupling. *. igh$pressure li7uid chromatography (P=C). 5. nfrared spectroscopy. ns,er- "
*SC/SS0- 5lectrical energy can %e transmitted across the %ody ,all %y tunnelling an electric ,ire> ho,e!er3 e8perience has sho,n that infection3 starting at the s9in line and %urro,ing deeper into the %ody3 ,ill occur o!er time. #his infection can %e delayed3 %ut not stopped3 %y the use of a !elour co!ering on the ,ire. Wireless electrical energy transmission ,as first used in clinical surgery %y W.W.=. Elenn in the 1D+'s for po,ering pacema9ers. #he remar9a%le ad!ances in electronics ha!e facilitated this techni7ue> ho,e!er3 the placement of the t,o coils parallel to one another (,ith the s9in %et,een)3 as opposed to interloc9ing as in an industrial transformer3 reduces the efficiency of transmission from appro8imately DD to B'.
1'. follo,ing the pneumatic artificial heart is@are correct. t #he can support thestatements circulationa%out for o!er 1 year. ". t may %e complicated %y infection or throm%oem%olism. C. When further de!eloped3 it ,ill %e an ideal permanent heart su%stitute. *. t is an ideal H%ridgeI for transplantation. 5. t can %e implanted using techni7ues similar to those used for heart transplantation. ns,er- "5 *SC/SS0- #he pneumatic artificial heart ,as de!eloped as a permanent cardiac su%stitute3 %ut the need for t,o tu%es to pass through the chest ,all and the %ul9y po,er unit ha!e relegated the pneumatic heart to short$term use as a %ridge to transplantation. #he heart is implanted using similar techni7ues as a heart transplantation. #he presence of foreign surfaces and cre!ices ma9e 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$stage congesti!e heart failure ,ho re7uire use of a %ridge de!ice.
1'D. cyanotic infant has echocardiographic e!idence of a uni!entricular heart (/6). #he follo,ing is@are true-
a. #he most common form of the disorder is a dou%le$inlet right !entricle %. #o %e classified as a !entricle3 the cham%er must recei!e at least half of an inlet !al!e c. #his infant is a good candidate for a "laloc9$#aussig shunt d. 0ptimal correction of /6 di!erts all !ena ca!al %lood flo, into the pulmonary arteries (Gontan procedure) e. n the a%sence of pulmonic stenosis3 /6 usually presents as congesti!e heart failure ns,er- %3 c3 d3 e
/ni!entricular heart is defined %y the connection of the atria to only one !entricular cham%er3 usually the left as a dou%le inlet left !entricle. cham%er must recei!e at least half of an inlet !al!e to %e considered a !entricle. #he presentation of /6 depends on the pulmonary %lood flo,> if pulmonary stenosis is present there is increased cyanosis and the infant is a candidate for a "laloc9$#aussig shunt. n the a%sence of pulmonic stenosis3 pulmonary flo, is e8cessi!e and the presentation is congesti!e heart failure. 0ptimal correction of /6 di!erts all !ena ca!al flo, into the pulmonary arteries as the Gontan procedure.
11'. D$year$old %oy ,ith hypertension has no palpa%le femoral pulses. Coarctation of the aorta is suspected. #he follo,ing is@are true-
a. #he most common associated a%normality is a %icuspid aortic !al!e %. Chest radiograph is li9ely to sho, ri% notching c. #he etiology is felt to %e secondary to an inflammatory aortitis d. n infancy3 coarctation may present ,ith a pin9 upper %ody and cyanotic lo,er %ody e. HParado8ical hypertensionI seen after operati!e repair indicates residual stenosis from incomplete correction ns,er- a3 %3 d
Coarctation of the aorta occurs ;ust distal to the srcin 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. 58tensi!e collateral de!elopment in!ol!es the mammary and intercostal arteries producing ri% notching on the chest radiograph. n infancy3 flo, to the lo,er %ody is from the ductus arteriosus %efore it closes3 producing differential cyanosis. #he Hparado8ical hypertensionI seen postoperati!ely is thought to relate to sympathetic ner!e stimulation and does not reflect an incomplete repair.
111. :$year$old ,oman ,ith episodic syncope has echocardiographic e!idence of a mass in the left atrium. #he follo,ing is@are true statement(s)-
a. #ransseptal puncture should %e used for definiti!e diagnosis %. f this is a primary cardiac tumor it is most li9ely to %e malignant c. f this is a my8oma attached to the atrial septum3 the ad;acent septum should %e remo!ed ,ith it d. n infancy3 the most common cardiac tumor is a rha%domyosarcoma e. #he most common primary malignant tumor of the heart is angiosarcoma ns,er- c3 e
Primary cardiac tumors commonly arise in the left atrium and can present ,ith dyspnea3 syncope3 congesti!e failure and systemic em%olism. #ransseptal puncture should not %e used for diagnosis %ecause of the ris9 of em%olism. Most primary cardiac tumors are %enign %y a &-1 ratio. #he most common malignant tumor is the angiosarcoma. My8oma is the most common %enign tumor3 %ut it can recur and the ad;acent atrial septum should %e resected ,ith it. n infancy3 the most common cardiac tumor is a rha%domyoma.
114. 4$month$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$shaped heart on chest radiograph. #he follo,ing is@are true-
a. 5chocardiography alone is sufficient to confirm the diagnosis of #etralogy of Gallot %. Cyanotic spells may %e appropriately treated %y propranolol c. #he "laloc9$#aussig shunt connects the right !entricle to the pulmonary artery d. ncreasing cyanotic spells is the most common indication for operation e. 0perati!e repair of right !entricular outflo, o%struction is ne!er e8tended across the pulmonic !al!e since intolera%le pulmonary insufficiency ,ould result ns,er- a3 %3 d
n typical scenario for #etralogy of Gallot3 can confirm thesedation diagnosis ,ith no need forthis cardiac catheteri2ation. Cyanotic spells are echocardiography treated %y supplemental o8ygen3 ,ith morphine and a %eta %loc9er such as propranolol. Gor palliati!e increase in pulmonary %lood flo,3 the "laloc9$ #aussig shunt is utili2ed connecting the su%cla!ian artery to the pulmonary artery. ncreasing cyanosis and cyanotic spells are the most common indication for operati!e repair. #o correct the right !entricular outflo, o%struction in #etralogy3 a transannular patch may %e re7uired e8tending into the pulmonary artery. Gortunately the pulmonary !al!ar insufficiency that results is ,ell tolerated in the a%sence of tricuspid insufficiency or !entricular dysfunction.
11&. 14$year$old %oy is found to ha!e an e;ection systolic murmur o!er the aortic region ,ith a precordial thrill and normal cardiac si2e on chest radiograph. #he follo,ing is@are true-
a. systolic e;ection clic9 ,ould signify that the stenosis is supra!al!ar %. n the a%sence of cardiomegaly3 cardiac catheteri2ation to measure the pressure gradient is necessary c. *e!elopment of syncope ,ould suggest an intracranial lesion d. n !al!ar aortic stenosis a pressure gradient of ' mmg is an indication for operati!e repair regardless of symptoms e. n mem%ranous su%!al!ar aortic stenosis a pressure gradient of :' mmg is an indication for operati!e repair ns,er- d3 e
n the patient ,ith findings of aortic stenosis3 a systolic e;ection clic9 is e!idence that the o%struction is !al!ular. Cardiac si2e does not pro!ide an indication of the se!erity of the stenosis and is fre7uently normal. #he de!elopment of angina or syncope reflects inade7uate cardiac output and signifies late$stage disease. pressure gradient o!er B+ mmg is an indication for operation in !al!ar aortic stenosis e!en if the patient is asymptomatic ,hile a lesser gradient of &' mmg or more is considered sufficient for operati!e correction of mem%ranous su%!al!ar stenosis.
11:. Within 4 hours of %irth3 a %a%y girl is o%!iously cyanotic and chest radiograph sho,s the heart to appear li9e Han egg on its side.I #he follo,ing is@are true-
a. #he most common cause of cyanosis this early is transposition of the great !essels (#E6) %. f #E6 is present3 echocardiography ,ill sho, that the posterior !essel lea!ing the left !entricle is a pulmonary artery c. f #E6 is confirmed %y echocardiography3 cardiac catheteri2ation has little to add d. #he 5JE is helpful in ma9ing the diagnosis of #E6 since it sho,s re!ersed dominance of the !entricles e. #o impro!e mi8ing of pulmonary and systemic circulations3 prostaglandin should %e used to increase pulmonary !ascular resistance ns,er- a3 % #E6 is the most common cause of cyanosis in the first ,ee9 of life3 and this diagnosis can %e confirmed %y echocardiographic demonstration of a posterior pulmonary artery attached to the left !entricle. Cardiac catheteri2ation is useful to confirm the anatomy3 detect other lesions3 define the coronary anatomy and impro!e cardiac mi8ing %y %alloon atrial septostomy. #he 5JE is not helpful in the diagnosis of #E6 since it sho,s only normal right !entricular dominance. Prostaglandin impro!es the mi8ing of the circulation %y opening the ductus arteriosus and reducing pulmonary !ascular resistance.
11+. one$year$old %oy thought to ha!e #etralogy of Gallot is found on cardiac catheteri2ation to ha!e dou%le$outlet right !entricle (*0R6). #he follo, is@are true-
a. Spontaneous closure of the 6S* is rare %. =ocation of the 6S* has little effect on the degree of cyanosis c. *ou%le outlet left !entricles do not occur d. Coincidental aortic stenosis ,ith *0R6 is not compati%le ,ith life e. *ou%ly committed 6S* refers to its relationship to the great !essels ns,er- a3 e
n *0R63 the location of the 6S* affects the direction of flo, of o8ygenated %lood and thus determines the degree of cyanosis. Gortunately3 the 6S* rarely closes since that ,ould result in se!ere decompensation or death. *ou%le outlet left !entricles occur %ut are less common than *0R6. num%er of other anomalies are associated ,ith *0R6 including %oth !al!ar and su%!al!ar pulmonary and aortic stenosis. #he 6S* 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 e8amination to ha!e a pulmonic flo, murmur3 fi8ed splitting of P4 and a right !entricular lift. #he follo,ing is@are true-
a. Cardiac catheteri2ation is indicated if the chest film sho,s cardiomegaly %. Radiology report of Hscimitar syndromeI findings on the chest film ,ould indicate need for an arteriogram c. f the catheteri2ation report is Hostium secondum defect3I at least one pulmonary !ein drains anomalously d. Measured pulmonary !ascular resistance of 1: Woods units@m4 ,ith an S* mandates early repair e. n S* ,ith Qp@Qs of 1. can %e o%ser!ed until symptoms occur ns,er- %
#he findings suggest an atrial septal defect (S*) that can %e confirmed %y 4* echocardiography eliminating the need for cardiac catheteri2ation. #he ostium secondum type defect is most commonly found3 %ut it is the sinus !enosus type that is associated ,ith anomalous pulmonary !enous drainage. n the scimitar syndrome3 the anomalous pulmonary !ein can %e seen on a chest radiograph and3 since these are associated ,ith a hypoplastic lung that is supplied %y an anomalous systemic artery from the aorta3 an arteriogram is appropriate. n S* ,ith a significant left$to$right shunt as demonstrated %y a Qp@Qs ratio in e8cess of 1.+ should %e repaired. When the pulmonary !ascular resistance is ele!ated a%o!e 1'K14 Woods units@m4 the patient is not a candidate for repair due to fi8ed pulmonary hypertension.
11B. 4$month$old infant has 5JE e!idence of myocardial ischemia and echocardiography suggests anomalous srcin of the left coronary artery from the pulmonary artery. #he follo,ing is@are true-
a. schemia is due to perfusion of the myocardium ,ith inade7uately o8ygenated %lood %. Selecti!e coronary angiography should not %e attempted %ecause of the ris9 of myocardial infarction c. Conser!ati!e treatment is preferred to allo, the coronary artery to gro, to a si2e that ,ill allo, %ypass construction d. f the infant deteriorates3 ligation of the coronary at its srcin is a !ia%le option e. #he se!erity of the a%normality insures that it ,ill al,ays %e detected in the first year of life ns,er- d
nomalous srcin of the left coronary artery from the pulmonary artery results in re!erse flo, in the coronary into the lo,$pressure system as a steal from the coronary circulation. f collaterals from the right coronary de!elop to allo, ade7uate myocardial perfusion3 the disorder is fre7uently not diagnosed until later in life ,hen a murmur is heard. Selecti!e coronary arteriography is appropriate to define the anatomy and operati!e repair is underta9en promptly. =igation of the anomalous coronary can %e lifesa!ing %ut lea!es the child dependent on a single !essel and coronary %ypass is preferred.
11. 4$month$old %oy is found to %e in congesti!e heart failure manifested %y tachypnea3 tachycardia and diaphoresis ,ith poor ,eight gain. #he physical findings suggest a !entricular septal defect (6S*). Management should include-
a. Pulmonary artery %anding %. /rgent closure if a 6S* is found on echocardiography c. Medical treatment only ,ith digitalis and diuretics d. f a 6S* is found3 repair is unli9ely to %e possi%le %ecause of ele!ated pulmonary !ascular resistance e. f a restricti!e 6S* is found3 spontaneous closure is a possi%ility and operati!e repair should %e delayed ns,er- c3 e
=arge 6S*s present at K ,ee9s of age ,hen the normally ele!ated pulmonary !ascular resistance falls3 allo,ing an increase in the left$to$right shunt. Since roughly half of all 6S*s undergo spontaneous closure3 particularly ,ith restricti!e defects3 the initial management is medical. #he diagnosis is confirmed %y echocardiography and cardiac catheteri2ation. d!anced pulmonary !ascular changes do not occur usually until 4 years of age and %anding is only rarely indicated for palliation for multiple comple8 muscular 6S*s.
11D. 1$year$old girl ,ith dyspnea and poor feeding is found to %e in congesti!e heart failure. 5chocardiography sho,s an atrio$!entricular septal defect (6S*). #he follo,ing is@are true-
a. #he second heart sound ,ill sho, fi8ed splitting %. *espite diagnostic echocardiography3 cardiac catheteri2ation is indicated to assess pulmonary artery resistance c. Pulmonary artery %anding is indicated to limit pulmonary flo, and allo, the child to gro, d. 6S* is classified according to the morphology of the anterior leaflet of the common $6 !al!e e. 0perati!e repair is %est performed after 4 years of age ns,er- a3 %3 d
6S* is a defect of endocardial cushion de!elopment ,hich produces morphologic a%normalities of %oth 6 !al!es and %oth atrial and !entricular septa. t is usually classified according to the morphology of the anterior leaflet of the 6 !al!e. #he pulmonary !ascular resistance remains ele!ated in infancy delaying diagnosis and producing fi8ed splitting of the second heart sound. Cardiac catheteri2ation is indicated to assess pulmonary !ascular resistance3 %ut pulmonary artery %anding is no longer performed to protect the pulmonary %ed. nstead3 operati!e repair is made3 prefera%ly %efore the age of months.
14'. #he child in the pre!ious 7uestion undergoes cardiac catheteri2ation confirming a 6S* ,ith Qp@Qs ratio of 4.' and right !entricular systolic pressure half of systemic pressure. #he follo,ing is@are true-
a. f aortic insufficiency is detected3 the defect is li9ely to %e su%pulmonic in location %. Ginding aortic stenosis in addition to the 6S* ,ould %e highly unli9ely c. #he cath data indicate a restricti!e type of 6S* d. f pulmonary !ascular resistance falls ,ith tola2oline administration3 it is safe to close the 6S* e. 0perati!e closure of 6S*s is possi%le ,ithout !entriculotomy ns,er- a3 c3 d3 e #he finding of aortic insufficiency in a patient ,ith 6S* suggests prolapse of the aortic !al!e due to a su%pulmonic or supracristal defect. ssociated aortic stenosis3 mitral stenosis and coarctation are common ,ith 6S*s. #he finding of a moderate left$to$right shunt and a right !entricular pressure ,ell %elo, systemic indicates a restricti!e 6S*. f ele!ated !ascular is found3 the a%ility to respondle!els to a !asodilator li9e tola2oline indicates thatpulmonary the resistance is notresistance fi8ed and operati!e repair is possi%le. 0perati!e repair of 6S*s is fre7uently possi%le !ia atriotomy or through the pulmonary artery. 141. premature infant in respiratory distress is found to ha!e a continuous HmachineryI murmur o!er the precordium. #he follo,ing is@are truea. #he most li9ely diagnosis is coarctation of the aorta %. f large pulmonary arteries are noted3 a patent ductus is li9ely c. #o discriminate %et,een a and %3 prostaglandin administration can %e used ,hich ,ill constrict the patent ductus arteriosus d. f a ductus if found3 operati!e repair should %e delayed until the respiratory symptoms impro!e to reduce mortality rates e. ormal ductus closure depends on increased o8ygen saturation in the pulmonary artery ns,er- %3 e
continuous HmachineryI murmur is characteristic of patent ductus arteriosus typically seen in the premature infant. ormal closure of the ductus is prompted %y a fall in pulmonary !ascular resistance that increases the left$to right shunt and o8ygen le!els from the aorta. ndomethacin can cause ductus closure %y cycloo8ygenase inhi%ition ,hich decreases endogenous prostaglandins. Prostaglandin infusion ,ould 9eep the ductus open. 0perati!e closure can %e done safely in e!en the smallest neonates and usually promptly relie!es the respiratory distress.
144. neonate in congesti!e heart failure has echocardiographic e!idence of a single truncal !essel from ,hich the pulmonary arteries arise3 a 6S* and truncal !al!ar stenosis. #he follo,ing is@are true-
a. atural history of this anomaly allo,s only 4' one$year sur!i!al %. #he most li9ely configuration of the truncal !al!e is %icuspid c. =ocation of the pulmonary arteries minimi2es the ris9 of pulmonary !ascular o%structi!e disease (5isenmengers) d. Repair of the lesion re7uires an e8tracardiac conduit e. 0ptimal timing of operati!e repair is at K14 months ns,er- a3 d
#he defect descri%ed is truncus arteriosus ,hich carries an ' one year mortality rate uncorrected. #he truncal !al!e is most commonly tricuspid (+) or 7uadricuspid (4+)> least li9ely %icuspid (D). #he large left$to$right shunt ma9es these patients particularly li9ely to de!elop pulmonary !ascular o%struction (5isenmengerTs syndrome). 0perati!e repair re7uires detachment of the pulmonary arteries ,hich are reconnected to the right !entricle %y an e8tracardiac conduit3 and the optimal timing for repair is ,ithin the first months of life.
14&. neonate in respiratory distress has echocardiographic e!idence of hypoplastic left heart syndrome (=S). #he follo,ing is@are true-
a. nitial management should include prostaglandin infusion %. 6entilatory ad;ustment should maintain PaC04 at appro8imately :' mmg c. Sur!i!al depends on sustained patency of the ductus arteriosus d. Cardiac transplantation for =S re7uires inclusion of the donor aortic arch e. Reconstruction for =S con!erts the pulmonary artery into the main outlet for a functional single !entricle (or,ood) ns,er- a3 %3 c3 d3 e
#he neonate ,ith =S has a se!erely underde!eloped left !entricular and aortic arch and is dependent on patency of the ductus ,hich is facilitated %y prostaglandin infusion. 6entilator ad;ustment to reduce supplemental o8ygen and maintain PC04 of :' mmg a!oids e8cessi!e pulmonary flo,. #he options for treatment include cardiac transplantation ,hich re7uires a donor aortic arch and reconstruction %y the
or,ood procedure ,hich con!erts the pulmonary artery into the main outlet for a functional single !entricle.
14:. +4$year$old man ,ith 9no,n aortic stenosis de!elops angina pectoris and has a single episode of syncope. #he follo,ing is@are true-
a. 0nset of angina indicates concomitant coronary artery disease independent of !al!ular lesion %. Percutaneous aortic %alloon !al!uloplasty should %e considered since it has generally fa!ora%le results c. Patient is not an operati!e candidate since heart failure has not occurred d. measured trans!al!ular pressure gradiant U +' mmg ,ould %e an operati!e indication ns,er- d
#he !entricular hypertrophy ,hich accompanies aortic stenosis increases o8ygen demand ,hile mechanical forces increase resistance to perfusion3 resulting in ischemia. 0nly one half of these patients ,ith angina ha!e coronary artery disease. Percutaneous %alloon !al!uloplasty of the aortic !al!e has high complication and recurrence rates. ny such patient ,ith symptoms has an indication for operations as ,ould the patient ,ith a trans!al!ular gradiant U +' mmg.
14+. #he patient in the pre!ious 7uestion ,ith progresses to profound heart failure re7uiring medical management. #he follo,ing is@are true-
a. Perperal !asdilators are contraindicated %. #he inta$aortic %alloon pump can %e used to impro!e cardiac output c. Gurosemide and nitroglycerin ,ould %e appropriate d. 6al!e replacement is necessary ns,er- c3 d
Peripheral !asodilators are 9ey to the treatment of fa!oring peripheral %lood flo,. #he intraaortic pump is contraindicated diastolic ,orsens aortic regurgitation. "oth furosemide and nitroglycerin ,ould %ecause %e of !alue to treataugmentation the failure3 %ut the most effecti!e treatment re7uires replacement of the !al!e.
14. :4$year$old ,oman has noted progressi!e e8ercise intolerance and fatiga%ility. 58amination discloses an opening snap in the mitral area suggesti!e of mitral stenosis. #he follo,ing is@are true-
a. Critical mitral stenosis is defined as an orifice area reduced to 4 cm4 %. With a fi8ed mitral orifice3 the change from sinus rhythm to atrial fi%rillation has little effect on cardiac output c. Mural throm%i and throm%oem%olism are directly related to the presence of atrial fi%rillation d. *epressed cardiac output is usually due to depressed myocardial contractility ns,er- c
ormal adults ha!e a :K cm4 mitral orifice and reduction to 4 cm4 is mild stenosis ,hile reduction to 1 cm4 is considered critical mitral stenosis. 5!en ,ith a fi8ed orifice3 the onset of atrial fi%rillation reduces cardiac output %y 4'. Mural throm%i and throm%oem%olism are directly related to the presence of atrial fi%rillation. Mitral stenosis spares !entricular function3 and the loss of cardiac output is from decreased preload.
14B. Concerning !al!ular heart disease3 the follo,ing is@are true-
a. Mitral stenosis is the most common lesion %. 0f all cardiac !al!es3 the aortic is the most anterior c. Stenosis is the most common lesion of the aortic !al!e d. Rheumatic heart disease is the most common cause of !al!e dysfunction ns,er- c3 d
ortic !al!ular stenosis is the most common type of !al!ular lesion follo,ed %y mitral stenosis. natomically3 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.
14. :B$year$old male ,ith fatigue and cardiac failure has a high$pitched3 decrescendo diastolic murmur along the left sternal %order and an apical diastolci rum%le. is %lood pressure is 1:@:+ mmg. #he follo,ing is@are true-
a. Chest radiograph ,ill sho, cor %o!inum %. #he apical murmur is due to the Ealla!ardin phenomenon c. carotid shudder ,ould %e e8pected d. %dominal e8am ,ill sho, a pulsatile li!er ns,era
#his patient ,ith aortic insufficiency has a !olume loading strain on the heart ,hich produces cor %o!inum as dramatic enlargement. #he apical murmur produced %y tur%ulence ,ith mitral for,ard flo, mimics mitral stenosis and is called an ustin$Elint murmur. carotid shudder occurs ,ith aortic stenosis and a pulsatile li!er is typical of tricuspid insufficiency.
14D. Concerning the adaptation to cardiac !al!ular dysfunction3 the follo,ing is@are true-
a. Se!ere heart failure is more li9ely from acute than chronic !al!ular dysfunction %. 6al!ular dysfunction produces %oth !olume and pressure afterload stress on the heart c. 5arly cardiac dilation from !al!e dysfunction shifts the Gran9$Starling cur!e to depress cardiac output d. #he =aPlace la, predicts that ,all stress decreases ,ith increasing !entricular radius ns,er- a3 %
6al!ular dysfunction produces %oth !olume and pressure o!erload representing afterload stress on the heart. lthough cardiac reser!es allo, for gradual adaptation to chronic !al!ular dysfunction3 acute dysfunction is less ,ell tolerated and more li9ely to result in se!ere heart failure. #he increase in diastolic filling ,hich initially dilates the heart3 shifts the Gran9$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 thic9ness.
1&'. &1$year$old male drug a%user presents ,ith fe!er3 chills and multiple %ilateral lung a%scesses. Right heart endocarditis is suspected. #he follo,ing is@are true-
a. #he organisms most li9ely responsi%le are gram$negati!e and fungal %. #he pulmonic !al!e is most li9ely to %e affected c. negati!e echocardiogram is useful to e8clude the diagnosis d. 6al!e replacement is necessary if the nati!e !al!e is e8cised to treat infection ns,er- a
#he typical endocarditis in a drug$a%user in!ol!es fungal and gram$negati!e organisms ,hich infect the tricuspid rather than the pulmonic !al!e. n echocardiogram is useful to confirm the presence of !egetations %ut it may o!erloo9 smaller ones so it cannot %e used to e8clude the diagnosis. lthough !al!e replacement is usually prefera%le3 the infected tricuspid !al!e can %e e8cised ,ithout prosthetic replacement.
1&1. n the initial management of the patient in the pre!ious 7uestion ,ith suspected acute M3 the follo,ing is@are true-
a. 08ygen and lidocaine should %e administered prophylactically %. f chest pain persists3 6 nitroglycerin should %e used to limit infarct si2e c. Ca$channel %loc9ers are also of !alue to limit infarct si2e d. Morphine 6 can %e used %ut has no therapeutic effect ns,er- %
nitial treatment during an early e!ol!ing M should include o8ygen3 %ut lidocaine should %e used only if arrhythmias occur. itroglycerin 6 is of !alue to limit infarct si2e %ut not Ca$channel %loc9ers ,hich
ha!e no such %enefit. "y decreasing pain and an8iety3 morphine 6 has a significant therapeutic effect in decreasing myocardial o8ygen demand.
1&4. Concerning the physiology of the coronary circulation3 the follo,ing is@are true-
a. /nder circumstances of increased o8ygen demand %y the myocardium3 04 e8traction from arterial %lood can increase %. Coronary flo, is ma8imal during systole c. denosine is the most important meta%olic regulator of coronary %lood flo, d. Sympathetic ner!e stimulation constricts coronary arteries despite the need for increased cardiac output ns,er- c3 d
Since myocardium ma8imally e8tracts 04 from %lood at rest3 increased demand re7uires increased deli!ery. Systolic pressures compress intramyocardial !essels3 so ma8imal coronary flo, is during diastole. denosine3 a %rea9do,n product of #P3 is a !asodilator and the most important meta%olic regulator of coronary %lood flo,. lthough sympathetic ner!es produce coronary !asoconstriction3 the autoregulatory !asodilatory responses to increased myocardial demand o!er,helm that effect.
1&&. #rue statement(s) concerning cardiac !ascular anatomy include the follo,ing-
a. n 'K+ of cases the posterior descending coronary artery (P*) arises from the circumfle8 coronary artery %. #he P* gi!es off the 6 nodal artery c. #he great cardiac !ein ascends along the right coronary artery to empty into the coronary sinus d. #he%esian !eins drain from only left and right !entricles ns,er- %
n 'K+ of cases the circumfle8 coronary artery ends ,ith %ranches to the left !entricle ,hile the P* srcinates from the right coronary in 'K+ of cases. #he P* gi!es off the 6 nodal artery and its occlusion can result in heart %loc9. #he great cardiac !ein ascends along the left anterior descending coronary artery and the #he%esian !eins drain all : cham%ers.
1&:. n the medical management of coronary artery disease3 the follo,ing is@are truea. itroglycerin primarily dilates coronary arterioles %. %$%loc9ing agents act to reduce myocardial 04 demand c. Ca$channel %loc9ing agents reduce !entricular contractility d. Ca$channel agents should not %e used if there is an element of coronary !asospastic disease ns,er- %3
itroglycerin primarily dilates !enous capacitance !essels3 %ut at higher doses can produce coronary and systemic arterial dilation. %$adrenergic %loc9ing agents reduce myocardial 04 demand %y decreasing heart rate and contractility. Ca$channel %loc9ing agents reduce !entricular contractility3 produce !asodilation and may protect myocytes. #hey are particularly effecti!e for coronary !asospastic disease.
1&+. B$year$old man ,ith documented acute M progresses in 4: hours to cardiogenic shoc9. #he follo,ing is@are true-
a. #he mortality rate for cardiogenic shoc9 after acute M is increased more than 1' fold in comparison to no shoc9 %. ge3 e;ection fraction3 M si2e and pre!ious M ser!e as predictors of cardiogenic shoc9 c. cute loss of more than 4' of myocardium fre7uently results in cardiogenic shoc9 and death d. 5mergency re!asculari2ation is contraindicated for the M patient in cardiogenic shoc9 ns,er- a3 %
Cardiogenic shoc9 is unusual after acute M %ut increases the mortality rate from : to +. ll of the ris9 factors descri%ed plus a history of dia%etes mellitus can predict cardiogenic shoc9. #he !olume of myocardium lost acutely that is associated ,ith shoc9 is :'. Recent studies suggest that emergency coronary %ypass can %e used ,ithin 1 hours of shoc9 to reduce the mortality rate to B.
1&. +4$year$old man ,ith chest pain and tachycardia has 5CE e!idence of an acute M. #he follo,ing is@are true-
a. #hrom%olytic therapy should %e considered immediately since the %enefit is greater the earlier it is gi!en %. 0f the drugs a!aila%le3 recom%inant tP produces %etter results than SJ or PSC although it is more e8pensi!e c. therapy re7uires catheteri2ation for intracoronary administration d. #hrom%olytic ddition of heparin and antiplatelet drugs produces no incremental %enefit ns,er- a
#hrom%olytic therapy for acute M is of significant !alue in reducing mortality ,ith %enefit related to early administration. lthough rtP can produce higher coronary patency rates3 the results of treatment are no %etter than ,ith SJ or PSC. #hrom%olytic drugs ,ere initially gi!en intracoronary %ut can %e used effecti!ely ,hen gi!en systemically 6. #here is an added %enefit from heparin and antiplatelet drugs to pre!ent rethrom%osis.
1&B. Gollo,ing repair of an a%dominal aortic aneurysm3 a $year$old man de!elops se!ere chest pain3 diaphoresis3 %radycardia and hypotension. #he follo,ing is@are true-
a. #he electrocardiogram is most li9ely to sho, a prominent Q in lead & if this is an M %. f Q ,a!e is present3 the infarct is su%endocardial rather than transmural c. Creatine 9inase measurement alone is diagnostic of M d. Since %radycardia rarely occurs ,ith M3 another diagnosis should %e considered ns,er- a Pain is the most common complaint in patients ,ith myocardial infarction although 4'K4+ are asymptomatic. nferior Ms in!ol!ing the right coronary fre7uently ha!e parasympathetic acti!ity ,ith %radycardia3 hypotension and a prominent Q ,a!e in lead &. #he presence of a Q ,a!e indicates a transmural M ,hich can %e confirmed %y measurement of the specific isoen2yme for cardiac tissue (CJ$ M") since creatine 9inase can %e ele!ated non$specifically after stro9e or operation.
1&. B'$year$old ,oman ,ith intracta%le angina pectoris undergoes cardiac catheteri2ation for possi%le mechanical inter!ention. She prefers P#C to open correction. #he follo,ing is@are true-
a. long symmetric lesion in the left main coronary artery ,ould %e appropriate for P#C %. Multiple o%structi!e lesions in the same artery ,ould %e a contraindication to P#C c. focal lesion in the left anterior descending coronary artery ,here the !essel is 1 mm in diameter ,ould allo, P#C d. Successful P#C for a simple lesion carries a recurrent stenosis ris9 of less than 1' ns,er- %
#he ideal lesion for P#C is focal symmetric stenosis in an epicardial !essel. o,e!er3 it is relati!ely contraindicated for significant disease in the left main coronary3 for multiple o%structi!e lesions in the same artery3 and for !essels less than 4 mm in diameter. Restenosis rates of 4' to :' occur ,ithin the first :K months after successful dilation for simple lesions.
1&D. B$year$old patient ,ho is a candidate for C"E is concerned a%out the ris9s@%enefits of the procedure. #he follo,ing is@are true-
a. 0perati!e mortality in patients U B' years is more than dou%le that of younger patients %. f the patient is a ,oman3 the ris9 is higher than it ,ould %e for a man c. pre!ious C"E procedure increases the comple8ity and complication rate3 %ut does not alter mortality rate d. Results are %etter if there is ischemic cardiomyopathy than if there is hi%ernating myocardium ns,er- a3 %
0perati!e mortality for patients U B' years ,as in the CSS study as compared to & in younger patients. Gor reasons not entirely clear3 the ris9 of C"E is higher in ,omen than in men. Reoperati!e procedures carry a higher operati!e mortality due to technical difficulties3 more ad!anced disease3 and less complete re!asculari2ation. Congesti!e heart failure is a ma;or determinant of poor surgical outcome3 %ut the results are %etter ,hen there is !ia%le myocardium (hi%ernating) than ,hen there is irre!ersi%le ischemic cardiomyopathy.
1:'. Gour days after a transmural M3 a B:$year$old man de!elops hypotension and congesti!e heart failure. #he follo,ing is@are true-
a. n intra$aortic %alloon pump should %e used and cardiac catheteri2ation performed %. f the infarct ,as posterior3 this is most li9ely due to a !entricular septal defect c. Pulmonary ,edge pressure tracing of prominent 6 ,a!es ,ithout an 04 step$up suggests papillary muscle rupture d. 0perati!e repair of a post M 6S* should %e delayed to allo, strengthening of the myocardium to hold sutures ns,er- a3 c
"oth !entricular septal defect (6S*) and ruptured papillary muscle occur from &K+ days post$M and should %e managed %y intra$aortic %alloon pump3 decreasing afterload and cardiac catheteri2ation for diagnosis. 6S* is most li9ely in an elderly hypertensi!e female ,ho has sustained an anterior transmural M> posterior Ms typically lead to papillary muscle rupture ,hich is diagnosed %y prominent 6 ,a!es on pulmonary ,edge pressure tracing. Sur!i!al rate for %oth of these complications is impro!ed %y early rather than late repair.
1:1. +4$year$old ,oman ,ith chest pain is considered for coronary arteriography on the %asis of her ris9 factors. #he follo,ing is@are true statement(s)-
a. ll patients ,ith typical anginal symptoms should ha!e coronary arteriography %. typical patients ,ith %orderline positi!e stress tests should ha!e arteriography c. Patients ,ho re7uire !al!e procedures do not re7uire arteriography d. Patients in refractory heart failure a,aiting cardiac transplantation should ha!e coronary arteriography ns,er- %
Patients ,ith typical angina and 5CE changes should ha!e angiography only if they are refractory to medical management and@or a candidate for re!asculari2ation. Patients ,ith atypical signs and symptoms should ha!e angiography to confirm or e8clude the diagnosis. Patients ,ith !al!e disease and ris9 of coronary artery disease should ha!e angiography %ut patients a,aiting cardiac transplantation are not candidates for re!asculari2ation and do not re7uire coronary angiography.
1:4. #he patient in the pre!ious 7uestion is found to ha!e disease unsuita%le for P#C. Concerning operati!e re!asculari2ation (C"E) the follo,ing is@are true-
a. C"E is more effecti!e than medical treatment for relie!ing angina and impro!ing physical ,or9 capacity %. n C"E for unsta%le angina3 there is no difference in late outcome %et,een sta%le and unsta%le cohorts c. Gor C"E3 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 difference in the early mortality rate ns,er- a3 %3 c Randomi2ed studies sho, that C"E is more effecti!e than medical therapy for relie!ing angina3 impro!ing physical ,or9 capacity and impro!ing o!erall 7uality of life. When C"E is used for unsta%le angina3 the initial complication and mortality rates are higher than for sta%le angina3 %ut the late outcomes are similar. /se of arterial grafts for C"E has increased ,ith the left internal mammary artery used most commonly> ,hen at least one mammary artery is used3 the early mortality rate is impro!ed.
1:&. n the ,or9up of a :+$year$old man ,ith suspected coronary artery disease3 the follo,ing is@are true-
a. #hyroid tests are included to rule out hyperthyroidism %. #ypically positi!e stress 5CE ,ould sho, ele!ated S# segments c. *ipyridamole is a useful ad;unct to thallium scanning as it increases coronary perfusion pressure d. Persisting defects on thallium scan indicate re!ersi%le myocardial ischemia ns,er- a
*iagnostic studies for coronary artery disease should detect ris9 factors such as dia%etes mellitus3 hyperlipidemia and hyperthyroidism. #he stress 5CE typically sho,s do,n,ard sloping S# segment depression. *ipyridamole is a coronary artery !asodilator that reduces systemic and coronary perfusion pressures. #he persisting thallium scan defect reflects irre!ersi%ly scarred myocardium.
1::. Gollo,ing successful throm%olytic treatment of the patient in the pre!ious 7uestion3 he de!elops recurrent chest pain in 4: hours. #he follo,ing is@are true-
a. Rethrom%osis is most li9ely and throm%olytic therapy alone should %e repeated %. #he pro%lem could ha!e %een pre!ented %y early electi!e catheteri2ation and P#C c. Patient has an indication for catheteri2ation and P#C if single !essel disease is found d. Gindings of multi!essel disease at catheteri2ation ,ould indicate need for operati!e %ypasses e. f operati!e %ypass is deemed necessary3 there should %e a &'$day delay to allo, myocardial healing ns,er- c3 d
fter throm%olytic therapy for acute M3 angina recurs in &'K&+ and is an indication for cardiac catheteri2ation and mechanical inter!ention to pre!ent infarct e8tension. Prophylactic catheteri2ation3
ho,e!er3 has not %een found to pro!ide %enefit. f the findings at catheteri2ation sho, limited disease treata%le %y P#C3 then it should %e performed. "ut if multi!essel disease or unfa!ora%le anatomy is found3 operati!e %ypass should %e carried out early since results are %est ,ithin &' days of the M.
1:+. +D$year$old male has undergone successful C"E ,ith : grafts constructed %ut remains in lo, cardiac output (V 4=@min@m4) postoperati!ely. #he follo,ing is@are truea. n inotropic drug should %e used initially to increase cardiac output %. f lo, cardiac output persists despite optimal physiological and pharmacological support3 a %alloon pump ("P) should %e inserted c. *ecreased cardiac filling pressures suggest the possi%ility of cardiac tamponade d. When "P is used3 the %alloon is inflated during diastole ns,er- %3 d
nitial efforts to impro!e cardiac output should include correction of poor o8ygenation or acidosis and optimi2ation of rhythm3 preload and afterload %efore an inotropic agent is used. f lo, cardiac output persists despite physiological and pharmacological support3 an "P should %e inserted. t impro!es coronary artery perfusion %y counterpulsation during diastole. Cardiac tamponade is heralded %y increased cardiac filling pressures3 narro,ed pulse pressure and pulsus parado8us.
1:. :4$year$old asymptomatic attorney undergoes a routine e8ercise test ,hich is reported positi!e for myocardial ischemia. #he follo,ing is@are true-
a. #his is a rare e!ent since less than + of patients ,ith coronary artery disease (C*) are asymptomatic ,ith e8ercise %. Such a patient could progress to heart failure from ischemic cardiomyopathy c. #ypical angina pectoris is promptly relie!ed %y rest or rela8ation d. *yspnea onde8ertion can represent an angina e7ui!alent ns,er%3 c3
s many as 4+ of C* patients found %y e8ercise 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 rela8ation. schemic reductions in !entricular contractility and compliance can produce dyspnea on e8ertion as an angina e7ui!alent.
1:B. +4$year$old man de!elops postoperati!e supra!entricular tachycardia to a rate of 1'@min. and hypotension. #he follo,ing is@are true-
a. Since a heart rate of 1'@min should %e tolerated at his age3 the hypotension must ha!e another cause %. !agal maneu!er that %rea9s the tachycardia suggests atrial flutter as the etiology c. trial o!erdri!e pacing should %e tried for paro8ysmal atrial tachycardia (P#) d. 6erapamil 6 should %e used for rate control e. Cardio!ersion is preferred for patients on digo8in ns,er- c3 d
tachyarrhythmia o!er 1+' %eats@min can produce hypotension and myocardial ischemia and demands urgent therapy. 6agal maneu!ers may %rea9 P# %ut are not usually effecti!e for atrial flutter or fi%rillation. trial o!erdri!e pacing should %e attempted for P# or atrial flutter. 6erapamil is the most effecti!e approach to rate control for supra!entricular arrhythmias3 %ut cardio!ersion of patients on digo8in should %e underta9en cautiously since they are prone to !entricular tachycardia.
1:. BB$year$old man ,ith a healed transmural myocardial infarction has a medically refractory !entricular arrhythmia. #he follo,ing is@are truea. *irect current catheter endocardial a%lation has a high li9elihood of success. %. f the arrhythmia is induci%le at 5P study3 there is an indication for operati!e inter!ention. c. recent M ,ould %e a contraindication to operation d. 6entricular failure ,ould %e a contraindication to operation e. Monomorphic !entricular tachycardia is least amena%le to surgical resection. ns,er- %3 c3 d
fter catheter a%lation3 only 4+ of patients remain free of !entricular arrhythmia off of drug therapy. f the arrhythmia is induci%le at 5P study and the patient is an accepta%le ris93 ,ith a myocardial scar he has an indication for operation. "oth recent M and !entricular failure are contraindications to operation. Monomorphic !entricular tachycardia is the arrhythmia most amena%le to surgical resection.
1:D. $year$old man suffers sudden cardiac death (SC*) %ut is resuscitated and %rought to the hospital for e!aluation and treatment. #he follo,ing is@are true-
a. #he most li9ely cause of SC* is !entricular arrhythmia %. #here is &'K:' chance of recurrent SC* in one year c. 5mpiric antiarrhythmic drug therapy impro!es sur!i!al d. n induci%le !entricular tachyarrhythmia at 5P study carries a fa!ora%le prognosis e. f a !entricular aneurysm is found ,ith arrhythmia3 aneurysm resection is ade7uate treatment ns,er- a3 %
6entricular arrhythmias cause B+ of SC*3 ,hile 4+ are due to acute M. #here is a &'K:' chance of recurrent SC* in one year. n induci%le !entricular tachyarrhythmia carries a poor prognosis ,ith V +' fi!e year sur!i!al from SC* unless it can %e a%olished. 5mpiric antiarrhythmic drug therapy does not impro!e sur!i!al. neurysmectomy alone is not ade7uate therapy for arrhythmias associated ,ith aneurysms since the arrhythmia usually srcinates in ad;acent mechanically stressed myocardium.
1+'. #he follo,ing is@are true concerning the anatomy of the conduction system-
a. #here is no special conduction path from the sinoatrial (S) to the atrio!entricular (6) node %. #he %lood supply to the 6 node is from the anterior descending coronary artery c. #he only normal muscular connection %et,een atria and !entricles is the %undle of is d. #he aortomitral continuity is the only area ,here supra!entricular accessory path,ays cannot occur e. #he sinus node artery arises from the right or circumfle8 coronary artery ns,er- a3 c3 d3 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 circumfle8 coronary artery. #here is no special conduction path %et,een S and 6 nodes. #he %undle of is is the only normal atrio!entricular muscle connection %ut a%normal path,ays can occur any,here e8cept the area 9no,n as the aortomitral continuity. #he %lood supply to the 6 node is from the posterior descending coronary artery.
1+1. #he follo,ing is@are true concerning the physiology of arrhythmias-
a. physical or electrical stimulus causes sodium fast channels and calcium slo, channels to open %. *uring the effecti!e refractory period3 only the slo, calcium channels are closed c. repolari2ation follo,s potassium egress from the cell d. Rapid 58tracellular hypo9alemia increases sodium channel si2e increasing automaticity e. Catecholamines increase out,ard potassium flo, from myocytes ns,er- a3 c3 d
Physical or electrical stimuli cause sodium fast channels and calcium slo, channels to open. *uring the effecti!e refractory period3 %oth slo, calcium channels and fast sodium channels are closed and the myocardium cannot %e e8cited. #hen potassium channels reopen3 allo,ing potassium out3 and rapid repolari2ation occurs. 58tracellular hypo9alemia increases transmem%rane potassium gradient and sodium channel si2e increasing automaticity. Catecholamines decrease out,ard potassium flo, from myocytes enhancing automaticity.
1+4. B4$year$old man has had se!eral episodes of !entricular tachycardia and is a candidate for electrophysiological (5P) study. #he follo,ing is@are true-
a. #he goal of the 5P study is either sustained or non$sustained !entricular tachycardia %. Patients ,ith less than + repetiti!e comple8es in response to stimulation are considered noninduci%le c. n induced reentry from !entricular stimulation is not necessarily pathological d. Microreentry arrhythmias are typical after myocardial infarction e. Macroreentry arrhythmias are typical of myocardial ischemia ns,er- a3 %
Gor arrhythmias of !entricular srcin3 the 5P study goal is either sustained or nonsustained !entricular tachycardia. Patients ,ith less than fi!e repetiti!e comple8es in response to stimulation are considered noninduci%le. 6entricular reentry does not occur in normal myocardium3 so all reentrant arrhythmias are pathological. Macroreentry arrhythmias are typical after myocardial infarction3 ,hile microreentry arrhythmias are typical of myocardial ischemia.
1+&. 4D$year$old male ,ith supra!entricular tachyarrhythmias is suspected to ha!e Wolff$Par9inson$ White (WPW) syndrome. #he follo,ing is@are true-
a. 5lectrophysiologic studies (5PS) ,ill re7uire catheters in or at the right atrium3 is %undle3 right !entricle and coronary sinus %. Pacing for 5PS uses stimuli t,ice the diastolic threshold c. #he anomalous conducting %undle (Jent) is found in the right free ,all if the coronary sinus catheter records the earliest atrial acti!ity during reciprocating tachycardia d. f the atrial catheter records the earliest acti!ity during tachycardia3 the %undle of Jent is located in the left free ,all e. f neither left or right %undle$%ranch %loc9 prolong the 6 inter!al3 the anomalous %undle is in the septum ns,er- %3 e
Gor supra!entricular arrhythmias3 5PS re7uires catheters placed in the right atrium and !entricle3 coronary sinus and is %undle. programma%le stimulator is used for stimuli that are t,ice the diastolic threshold and 4 msec in duration. When the coronary sinus catheter records the earliest acti!ity during reciprocating tachycardia3 the %undle of Jent is in the left free ,all ,hile it is in the right free ,all if the earliest acti!ity is in the atrial catheter. When neither left or right %undle$%ranch %loc9 prolong the 6 inter!al3 the %undle is in the septum.
1+:. 4$year$old ,oman ,hose arrhythmia is noninduci%le at 5P study has depressed =6 function ,ithout aneurysm. #he follo,ing is@are true-
a. f her arrhythmia is !entricular tachycardia3 she is not a candidate for an utomatic mplanta%le Cardiac *efi%rillator (C*) since it only recogni2es fi%rillation %. f an C* is appropriate3 it offers a +' impro!ement in mortality compared to drug therapy c. Poor !entricular function is a contraindication to C* implantation d. C* should not %e used for patients a,aiting cardiac transplantation e. C* can pro!ide antitachycardia pacing as ,ell as defi%rillation ns,er- %3 e
#he C* is capa%le of recogni2ing !entricular tachycardia as ,ell as fi%rillation and can pro!ide antitachycardia pacing3 lo, or high$energy defi%rillation or some com%ination. t offers a +' impro!ement in mortality ,ith D+ freedom from SC* at + years after implantation. either poor !entricular function nor pending transplantation are contraindications to C* implantation.
1++. 4B$year$old surgery resident has had multiple episodes of supra!entricular tachycardia (S6#) and on 5P study is felt to ha!e WPW syndrome. #he follo,ing is@are truea. #he pathophysiology of WPW is a single %undle of Jent %. *angerous !entricular responses in WPW are due to the shorter refractory period of the accessory path,ay c. dentification of the accessory path,ay of WPW is an indication for its interruption d. ppro8imately half of the patients ,ho ha!e successful di!ision of accessory path,ays demonstrate 6 %loc9 postop e. "oth radiofre7uency catheter and surgical a%lation offer e8cellent results ,ith lo, mor%idity ns,er- %3 d3 e
#he pathophysiology of WPW is the Jent %undle of ,hich 1'K4' are multiple rather than single. #he shorter refractory periods permit rapid path,ays and dangerous !entricular responses %ut to atrial flutter or fi%rillation. n '.4+ of the population3 accessory of WPW can %e identified3 in the a%sence of a history of S6#3 they ha!e a normal life e8pectancy. ppro8imately half the patients ,ho ha!e successful di!ision of accessory path,ays demonstrate 6 %loc9 postop. "oth radiofre7uency catheter and surgical a%lation offer e8cellent results ,ith lo, mor%idity and the catheter techni7ue is less costly.
1+. n the pharmacological management of cardiac arrhythmias3 the follo,ing is@are true-
a. Mem%rane$sta%ili2ing local anesthetics (Class 1) act !ia sodium channel %loc9age %. Class 1 drugs also shorten the refractory period c. %$%loc9ing drugs (Class 4) %loc9 the sympathetic ner!ous system %ut not circulating catecholamines d. "retylium and other Class & drugs inhi%it potassium influ8 into cells e. Calcium channel %loc9ers (Class :) directly affect the S and 6 nodes ns,er- a3 d3 e Class 1 drugs are local anesthetics that act !ia sodium channel %loc9ade3 and lengthen the refractory period. Class 4 %$%loc9ing drugs inhi%it %oth the sympathetic ner!ous system and circulating catecholamines. Class & drugs inhi%it potassium influ8 into cells and Class : drugs affect slo, channel$ dependent pacema9er tissue (S and 6 nodes).
