CARDIOVASCULAR BLOCK NAME: NARESHRAJA M. J. NIM: 060100843 SEMESTER: IV TUTORIAL GROUP: A-2 ACILITATOR: !".

LEONARDO SIHOMBING MEDICAL ACULT# UNIVERSITAS SUMATERA UTARA

INDE$ (DAFTAR ISI) Index Preface Discussion points - 1. theme of block - 2. facilitator - 3. data of procedure - 4. trigger - 5. purpose of stud - !. "uestions that arose during discussion - #. ans$ers to "uestions abo%e &. $hat is the embr olog of the heart' (. $hat is the fetal circulation like' ). $hat are the common clinical presentations in a congenital heart disease' D. $hat are the t pes of congenital heart disease' *. $hat is c anosis and $hat are its causes and classifications' +. $hat are the examinations re"uired to detect a congenital heart defect' - ,.)oments -1-.)onclussion .eferences

PRE ACE (PENDAHULUAN) )ardio%ascular is the medical field concerned $ith the diagnosis and treatment of heart and the circulator s stem. It is said that cardio%ascular s stem is the most studied and researched field in medicine. /his is because the number one disease in most de%eloped countr is related to the heart or the circulator s stem. )ardio%ascular disorders are probabl the most common disorders $orld$ide. It is said that most people $ill e%entuall suffer from a h pertension once the began to age. In men0 coronar arter diseases are dominant0 along $ith other heart diseases like m ocardial infarction and heart failure. /his is more prominent in de%eloped countries0 due to their lifest le. *%en in Indonesia and 1ala sia0 cardio%ascular disorders is found in e%er class of societ 0 be it rich or poor0 oung or old0 male or female0 leader or follo$er0 citi2ens or foreigners. /he disorders are %aried from congenital heart defects0 to coronar arter diseases0 heart failures0 rheumatic heart disease0 traumas0 and man other disorders. /herefore it is definitel $ise for us to consider the cardio%ascular s stem as an integral part of medicine and $e should be able to distinguish the normal clinical rele%ance that are usuall associated $ith it.

DISCUSION POINTS (ISI LAPORAN) 1. T%&'& () *+(,- (tema block) Disorders of the cardio%ascular s stem. 2. .,/+/0.0(" (fasilitator) dr. 3eonardo 4ihombing 3. D.0. () 1"(,&!2"& (data elaksa!aa!) Date of tutorial (tanggal tutorial): 1-th 1arch 2--# and 13th 1arch 2--# /rigger (pemicu): 1 /ime (pukul): ,.3- a.m. - 12.-- p.m.5 6.-- a.m. 7 ,.3- a.m. Place (ruangan): &natom Discussion room 18 /utorial &-2 discussion room 4. T"/33&" ( emic") )agil0 a bo aged 3 ears0 $as brought to the cardiolog unit in &dam 1alik 9eneral :ospital0 1edan0 $ith complaints of blueness at the lips and his digits since the age of 3 months that $orsens $hen he cries. :e seems to tire easil and becomes e%en more bluish once he starts $alking or pla ing0 so much till he usuall has to stop and s"uat to rest for a moment before continuing $alking. In the past 1 ear0 he usuall $ill experience acute moments of blueness0 that is accompanied b rapid breathing0 breathlessness0 anxiet 0 and he sometimes suffocate $hile sleeping. /his usuall occurs during the morning $hen he arises0 $hen he cries for a period of time0 or $hen he is pla ing around. /his caused )agil to refuse to pla $ith his friends0 and is more comfortable ;ust sitting around or being carried. <hen the mom $as pregnant in her first trimester0 she usuall experience nausea and %omiting0 till she didn=t eat properl during those times. 4he didn=t experience an other sickness. 4he ne%er had an other trauma or %aginal bleeding0 and ne%er took an other medications0 except those gi%en b the mid$ife.

)agil $as born normal0 at the appropriate month according to the pregnanc 0 $as aided b a mid$ife0 immediatel cried0 and $as not blue0 $ith a $eight of 3--gram and a bod length of 46cm. :e fed on breast milk from birth till the age of 1 ear0 and until this %er point his appetite $as good. :is $eight increase since birth $as normal0 but his de%elopment $as slightl slo$. 4. P2"1(5& () 502!6 (t"#"a! embela#ara!) &. understanding the disorders of the cardio%ascular s stem. (. understanding about tetralog of +allot0 and effect to the human bod . ). differentiating tetralog of +allot from other congenital heart defects. D. understanding the common treatments and management for tetralog of +allot.

6. 72&50/(85 0%.0 ."(5& !2"/83 !/5,255/(8 ( erta!$aa! $a!% m"!c"l dalam c"ra& e!da at') &. $hat is the embr olog of the heart' (. $hat is the fetal circulation like' ). $hat are the common clinical presentations in a congenital heart disease' D. $hat are the t pes of congenital heart disease' *. $hat is c anosis and $hat are its causes and classifications' +. $hat are the examinations re"uired to detect a congenital heart defect' 9. A85:&"5 0( ;2&50/(85 .*(<& (#a(aba! atas erta!$aa!) A. :%.0 /5 0%& &'*"6(+(36 () 0%& %&."0= /he %ascular s stem appears in the middle of the third $eek0 $hen the embr o is no longer able to satisf its nutrition through diffusion alone. /he progenitor cells lie in the epiblast0 immediatel lateral to the primiti%e streak. +rom there0 the migrate through the streak. )ells destined to form the cranial segments of the heart0 the outflo$ of the tract0 migrate first0 and cells forming more caudal positions. .ight %entricle. 3eft

%entricle and sinus %enosus0 respecti%el migrate in se"uential order. /he cells proceed to$ard the cranium and position themsel%es rostral to the buccopharangeal membrane and the neural folds. :ere the reside in the splannchic la er of the lateral plate mesoderm. &t this time0 late in the presomite dela ing phar ngeal endoderm to form cardiac m oblasts. (lood islands also appear in this mesoderm $here the $ill form blood cells and %essels b the process of %asculogenesis. <ith time0 the islands unite and form a horse-shoe shaped endothelial lined tube surrounded b the m oblasts. /his region is kno$n as the cardiogenic field.1 /he entire cardio%ascular s stem0 originates from the mesodermal germ la er. &ll though initiall paired0 b the 22nd da of de%elopment0 the t$o tubes form a single slightl bend heart tube0 consisting of an inner endocardial tube and a surrounding m ocardial mantle. During the 4th to 6 $eeks0 the heart di%ides into a t pical four chambered structure. 4eptum formation in the heart is part of the endocardial cushion tissue in the atrio%entricular canal and in the conotruncal region. (ecause of the ke location of the tissue0 man cardiac malformations are related to abnormal cushion morphogenesis. 4eptum formation begins $ith the formation of the septum of the atrium. /he septum primum starts of first0 follo$ed b the septum secundum0 and the unilateral opening0 the foramen o%ale persists. /his is follo$ed b the formation in the atrio%entricular canal $here four endocardial cushions surround the atrio%entricular canal. +ormation of the septum in the %entricle follo$s next0 $here the intra%entricular septum consists of a thick muscular part and a thin membranous part. >ext is the formation in the bulbus0 $here the bulbus can be di%ided into the truncus0 the conus and the trabeculated portion of the right %entricle. +inall the %iteline arteries and the %enous s stem are formed.2

B. :%.0 /5 0%& )&0.+ ,/",2+.0/(8 +/-&= ?nderstanding the fetal circulation $ill allo$ us to understand ho$ some forms of congenital heart disease occur. /he fetal circulation allo$s blood to almost totall b pass the lungs0 because a fetus cannot breathe in utero. (lood from the maternal circulation enters the fetal circulation %ia the umbilical %eins. the umbilical %eins is one of %er selected %eins that $ould actuall carr ox genated blood0 a role usuall reser%ed for the arteries because %eins usuall carr deox genated blood. (lood from the umbilical %eins $ill b pass the li%er and enter the inferior %ena ca%a through the ductus %enousus. /his is a useful anatomical ad%antage because the li%er is an organ $hich re"uires a great amount of ox gen. ( almost completel b passing the li%er0 the ox gen saturation is reser%ed for more important %ital organs during the fetal period. (lood from the inferior %ena ca%a $ill then enter the right atrium. +rom the right atrium0 blood is able to enter the left %entricle like normal adult blood flo$0 or to the left atrium %ia the foramen o%ale. /he foramen o%ale is like a hole in bet$een the ostium primum and ostium secundum of the atrial septum. /his $ill allo$ the first b pass of the blood a$a from the lungs0 because the gaseous exchange of ox gen and carbon dioxide is not re"uired $hile in utero. /his role is reser%ed for the maternal placenta. /he b passing of this blood $ill then allo$ a high saturation of ox genated blood to enter the s stemic circulation. (lood that enters the left %entricle $ill ine%itabl be pumped to$ards the heart. (lood from the left %entricle $ill enter the pulmonar trunk0 and from there it is shunted to the aorta %ia the ductus ateriosus. /his shunting is the second %al%e that allo$s much of the blood to b pass the lungs. 3ogic $ill tell us that this is not possible because technicall the blood is suppose to flo$ from the aorta to the pulmonar arter 0 due to the

larger force and pressure exerted b the aorta0 because of the larger left %entricle of the heart. Interestingl enough0 in the during the fetal period0 the right %entricle is slightl larger than the left %entricle0 due to the fact that the right %entricle pla s a more important role in pumping blood to the s stemic circulation. /his $ill cause the pressure and force exerted b the pulmonar arter to be greater than that of the aorta0 allo$ing blood to flo$ from a higher to lo$er pressure gradient. During the fetal period0 the lungs are collapsed0 and the ine%itabilit to expand $ill ensure the lungs exert a much larger pressure to$ard the pulmonar circulation0 the much narro$er pressure different bet$een the lungs and the pulmonar arter ensures more blood is passed through the ductus arteriosus. (lood that enters the aorta $ill the tra%el to the fetal arteries to suppl ox gen to all its tissues. /he blood flo$ then exits the fetal circulation %ia the umbilical arteries0 back into the maternal circulation. It carries $ith it the fetal $aste products.3 C. :%.0 ."& 0%& ,(''(8 ,+/8/,.+ 1"&5&80.0/(85 /8 . ,(83&8/0.+ %&."0 !/5&.5&= )ongenital heart disease usuall manifests during childhood0 but it ma go unnoticed until the person in%ol%ed approaches adult life. )ongenital defects $hich $ere once fatal during childhood0 are able to be treated $ith earl surgical procedures $ith no or minimal s mptoms present later on. /here are se%eral clinical features $hich are usuall present in those $ith congenital heart diseases. /he first is central c anosis and digital clubbing. )entral c anosis occurs $hen digital blood enters the s stemic circulation $ithout passing the lungs0 meaning it undergoes a left to right shunting. /he most common of these is transposition of the great arteries and tetralog of +allot $hich $ill be described later. Prolonged c anosis is then associated $ith digital clubbing. Digital clubbing occur based on tree theories0 h per%ascularisation of the digital %essels0 %asodilation of the %essels0 and h perplasia of the connecti%e tissues.

/he second most common clinical presentations are gro$th retardation and learning difficulties. /hese are most common $ith those $ho experience left to right shunting at the %entricles. & lo$ tissue perfusion of ox genated blood causes the cells to be unable to di%ide itself optimall thus slo$ing gro$th and de%elopment. 4 ncope is also a common clinical presentation. /his usuall causes $hen blood perfusion to the brain is lo$. /his usuall happens $hen there is an obstruction or stenosis at the aortic %al%e or other common left hart defects. .ight to left shunting $ill also cause the ox gen saturation to the brain to be reduced. Pulmonar h pertension is another common clinical presentation in those $ith congenital heart defects. Pulmonar h pertension is usuall caused b increase left atrial pressure. @nce pulmonar h pertension occurs0 ine%itabl 0 the right %entricle $ill begin to undergo h pertroph . @nce right %entricle h pertrophies0 its contraction force increases0 thus causing a right to left shunt if a %entricular septal defect is present. /his is kno$n as the *isenmenger=s s ndrome. *isenmenger=s s ndrome is the main cause of central c anosis in a congenital heart defect.4

D. :%.0 ."& 0%& 061&5 () ,(83&8/0.+ %&."0 !/5&.5&= )ongenital heart disease can be di%ided into 2 main forms5 ac anotic and c anotic. &c anotic congenital heart diseases are like patent ductus arteriosus0 coarctation of the aorta0 atrial septal defect0 and %entricular septal defect. ) anotic congenital heart diseases are like tetralog of +allot and transposition of the great %essels. Persistent Ductus arteriosus is a condition $here the dutus arteriosus is Apersistent= and fails to close and degenerate normall a fe$ da s after the fetus is born. &s mentioned earlier0 the ductus arteriousus allo$s shunting from the pulmonar arteries to the aorta in the fetal circulation. :o$e%er this shunting is not present in an adult

circulator s stem0 because the duct undergoes %asoconstriction and degeneration to become the arteriousus ligament. /here are usuall no s mptoms for ears0 but d spnoea is usuall the first s mptom present. & continuous machiner murmur is also usuall heard. /he left to right shunting from the aorta to the pulmonar arter $ill cause an increase in pulmonar arter pressure and si2e0 and this ma be detected $ith standard radiograph .5 )oarctation of the aorta is the narro$ing of the aorta0 most commonl in $hich the narro$ ishtmus of the aorta $hich is present during fetal life0 fails to dilate once the fetus is born. /he narro$ isthmus is present ;ust after the origin of the left subcla%ian arter and its function is to ensure a higher blood flo$ due to an increase pressure to the brain during the fetal period. /he common clinical presentation is cardiac failure. :eadaches ma also occur due to h pertension in the cerebral blood flo$. <eakness and cramps ma occur at the legs due to decrease blood flo$ to the lo$er extremities. +emoral pulse is usuall $eak and dela ed in comparison to the radial pulse0 and a s stolic murmur is usuall heard. 1.I is ideal in determining the location of the defect.! &trial septal defect is one of the most common congenital heart disease present. It occurs because of malformation of either the ostium primum0 ostium secundum or fossa o%alis. <hen the defect occurs0 blood is shunted from the left atrium to the right atrium. 4ometimes0 pulmonar h pertension occurs0 along $ith shunt re%ersals. /he common clinical features are d spnoea0 chet infections0 cardiac failures and arrh thmias. /here is also $ide splitting of the second heart sound due to a dela in right %entricular e;ection. &lso present is a s stolic flo$ murmur that can be auscultated o%er the pulmonar trunk. )hest x-ra $ill usuall sho$ enlargement of the pulmonar arteries and the heart itself.6 Bentricular septal defect occurs as a result of incomplete septation of the %entricles. /his can either occur to the membranous or muscular portion. Bentricular septal defects are the most common congenital heart disease that occurs once in about e%er 5-- births. /he common clinical features are shunting from the left to right %entricles. /his occurs because the left %entricle is thicker and therefore exerts more force

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to the blood flo$ compared to the right %entricle. In time0 pulmonar resistance ma increase0 and if this prolongs0 *isenmenger=s s ndrome ma occur. ?suall a murmur is present0 and *)9 scans $ill sho$ bilateral %entricle h pertroph .# /etralog of +allot like its name has four main components $hich include %entricular septal defect0 right %entricular h pertroph 0 pulmonar stenosis and o%erriding aorta. /his combination $ill cause the child to experience c anotic attacks. ) anosis occurs because there is a let to right shunting in this disorder. /he left to right shunting occurs due to the right %entricular h pertroph $hich occurs due to the pulmonar stenosis. /he clinical features include sudden c anotic attacks kno$n as A+allot spells=0 digital clubbing0 and gro$th stunting. @n examination0 a loud e;ection s stole is present and on an x-ra 0 a boot shaped heart is apparent., /ransposition of the great %essels occurs $hen the aorta arises from the right %entricle and the pulmonar trunk arises from the left %entricle. /his causes the ox genated blood to remain in the pulmonar circuit and the deox genated blood to remain in the s stemic circuit. /he main clinical indication is a central c anosis.1E. :%.0 /5 ,6.8(5/5 .8! :%.0 ."& /05 ,.25&5 .8! ,+.55/)/,.0/(85= ) anosis is the bluish discoloration of the skin and mucous membranes resulting from an inade"uate amount of ox gen in the blood. ) anosis is associated $ith heart failure0 ling disease0 the breathing of ox gen deficient atmospheres and asph xia. ) anosis is also seen in blue babies due to congenital heart defects.11 ) anosis is di%ided into central c anosis and peripheral c anosis. )entral c anosis occurs $hen ox gen saturation is reduced or an abnormal deri%ati%e is present. In central c anosis0 the mucous membranes and skin is affected. Peripheral c anosis is due to the slo$ing do$n of the blood flo$ and abnormall great extraction of the ox gen from normall saturated arterial blood. Peripheral c anosis also occurs due to

11

%asoconstriction and diminished peripheral blood flo$ such as cold exposure0 shock 0 and peripheral %ascular disease. /here are se%eral causes respecti%el for central and peripheral c anosis. +or central c anosis0 the main causes are decreased ox gen saturation0 anatomic shunts0 and haemaglobin abnormalities. +or peripheral c anosis0 the main causes are reduced cardiac output0 arterial obstruction0 %enous obstruction and redistribution of blood flo$ from the extremities.12 . :%.0 ."& 0%& &>.'/8.0/(85 "&;2/"&! )(" . ,(83&8/0.+ %&."0 !&)&,0= /here are se%eral common examinations $hich are usuall used to detect a congenital heart defect. :o$e%er this examinations are not 1--C accurate as it has a %aried sensiti%it and specifit properties. /he most common is to do a standard radiograph test or better kno$n as an xra . D-ra s help us to see the thorax more clearl and $e are able to determine $hether the thoracic image is normal or abnormal. 1ost congenital heart defects like %entricular septal defect and tetralog of +allot presents $ith a cardiomegal . & cardiomegal is determined b an increase in the cardio thoracic ratio0 $hich has a normal ratio of 35C 5-C. /etralog of +allot also has a special boot-shaped appearance $hich is a strong diagnostic "ualit . @ther abnormalities $hich can be noticed on the x-ra film are more prominent pulmonar %essels0 or h pertroph of the great %essels and man more. /he xra is definitel the most useful tool in detecting a congenital heart defect. /he next most useful tool $ould be an *lectrocardiograph or better kno$s as an *)9. *)9 is able to detect the impulse patterns of the heart. & change in heart structure or impulse conducti%it $ill change the *)9 pattern on the oscilloscope. &n increase in E.4 height $ould usuall mean a h pertroph of the %entricles.

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&uculatation is also an important examination tool in determining a congenital heart defect. /he stethoscope pla s an important role in determining heart murmurs. 1urmurs are the abnormal noises heard in the heart $hich is caused b turbulent blood flo$s. & continuous Amachiner = murmur usuall indicates a persistent ductus arteriousus. +or tetralog of +allot0 an e;ection t pe s stolic murmur is usuall heard ad he left parasternal. 1agnetic .easonance Imaging is also a %er useful tool. 1.I=s are ideal in examining soft tissue damages. /herefore defects to the heart can be clearl reconstructed b 1.I so that a clearer %ie$ of the defect can be seen. /his $ill pre%ent the need and risk of explorator surger . 4eptal defects and persistent ductus arteriousus can be clearl seen on an 1.I image. :o$e%er0 not e%er hospital o$ns an 1.I machine0 and its cost is "uite expensi%e.13 8. C(''&805 ("lasa!) In this case0 )agil came in $ith complaints of bluishness that $orsens $hen he cries0 he is "uick to tired0 he experience breathlessness and sometimes suffocate $hile sleeping. <e kno$ the bluishness of the skin is caused b c anosis. /he first "uestion $ould be $hat t pe of c anosis0 a central or peripheral c anosis' )entral c anosis in%ol%es the mucous membranes and the skin0 $hile peripheral c anosis onl in%ol%es the skin and is usuall present at the extremities. <e notice that )agil=s lips are blue0 so this is a determined that central c anosis occurs. /he second point to discuss is that this bluishness al$a s $orsens $hen he cries0 so ho$ could that be' )entral c anosis occurs $hen the ox gen saturation in the blood is lo$ered compared to normal0 meaning that the suppl of ox gen is inade"uate to meet the bod =s demands. <hen )agil cries0 there is an increase ox gen demand b his bod . /his causes the gap difference bet$een suppl and demand to increase0 thus $orsening the bluishness. /he third s mptom $as that he $as "uick to tired. /iredness or fatigue is based on a fe$ criteria0 firstl is an increase in lactic acid in the bod 0 secondl is the muscle is not in a resting stage et0 and thirdl is because of a lo$ ox gen suppl . In this situation0 the first 2 causes seem "uite unlikel

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because )agil has not exerted himself in an $a to cause a buildup in lactic acid or his muscles not to be at rest. 4o the most likel problem is that his bod lacks ox gen. /he next problem $as that cagil experience suffocation $hile he sleeps. /his is kno$n as a parox smal nocturnal d spnoea. /he main cause of this is usuall pulmonar oedema0 $hich is caused b a congestion of fluids in the lungs. /his congestion of fluid pre%ents the normal gaseous exchange in his lungs. (ased on this the fe$ main points $e ha%e0 $hich are )agil is a c anotic patient0 he lacks ox gen0 and he is experiencing some sort of pulmonar congestion0 there are man diagnosis $hich are possible. /hese diagnosis are %aried from the cardio%ascular s stem0 to the respirator s stem so to make a definite diagnosis0 $e need more information. (ased on the information $hich $as obtained later0 a ph sical examination0 laborator examination0 thorax x-ra and electrocardiograph $as performed on )agil. In the ph sical examination0 )agil=s heart rate $as at 11- a minute0 his breathing rate $as at 24 a minute and his bod temperature $as at 36-). :is thorax $as as mmetric0 the left being bigger than the right0 the right %entricular acti%it being increased. @n ausculatation there is a normal 41 sound0 a $eakening 42 sound in the pulmonar area and a e;ection t pe s stolic murmur t pe 38! in the 2-3 intercostal area of the left parasternum that radiates to the left cla%icula. Digital clubbing $as also noted. /he laboratorium check sho$ed an increase in haemaglobin le%els and an increase in hametatocrite. &nd the blood gas anal sis shoed h poxia and h poxaemia. /hex-ra film sho$s an enlarged heart0 $ith an apex sifted up$ards to the right and a characteristic boot-shaped appearance. /he *)9 sho$ed a normal sinus rh thm $ith a normal E.4 axis and a h pertroph of the right %entricle and a transitional 2one at B2. &nal 2ing these examinations 1 b 10 $e can firstl notice that )agil=s heart rate and breathing rate $as slightl raised at a basal le%el. <e kno$ that the increase in heart rate and breathing rate is due to a s mpathetic homeostasis feedback to ensure enough ox gen is obtained b the tissues of the bod 0 as based on our earlier diagnosis0 )agil is

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someho$ experiencing a lack of ox gen perfusion in is bod . /his is later pro%en b the blood gas anal sis $hich states that )agil=s blood is under h poxaemia conditions and )agil is experiencing tissue h poxia. It is also noted that there is an increase in :emaglobin and hameatocrite le%els. /his occurs because there is an increase in *r thropoesis. &n increase in *r thropoesis occurs because there is a feedback mechanism that insists on more red blood cells being produce0 because the current amount of red blood cells is not enough to meet the bod =s ox gen demand. <hile examining his thorax0 $e notice the left side is bigger than the right. /his usuall indicates 2 things. /he first is that there is a presence of a tumour and the second is that the heart has undergone h pertroph . <e also noticed that the .ight %entricle=s acti%it has increased. /his $ould usuall indicate a h pertroph of the right %entricle $hich is in line $ith our thought that the heart has h pertrophied. During auscultation0 $e notice that the 41 is normal but the 42 has a $eakened sound in the pulmonar area. /his $ould most probabl mean that there is a problem in the closing of the pulmonar semilunar %al%e. & softer sound $ould usuall indicate either a more Aflaccid= %al%e like those in a regurgitation or that there is a change in the pressure gradient bet$een the pulmonar %essels and the %entricle. /he change $ould mean that the difference in pressure bet$een the pulmonar %essels and the %entricles has reduced. /his $ould usuall occur in 2 $a s0 an increase in right %entricular pressure or a drop in pulmonar pressure. &n increase in right %entricular pressure $ould be inline $ith our thought that a right %entricular h pertroph has occurred. 3ater $e also determined that there are no disorders of the lungs or abdomen during the ph sical examination. 4o far0 all our diagnosis $ould point strongl to some sort of heart disorders. /he clubbing fingers that occur is also usuall a strong indicator for a heart disorder. /his is pro%en b the performing of the *)9 and a chest x-ra . /he *)9 also pro%ed that there $as a h pertroph in the right %entricle0 $hich $as due to an increase

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in . $a%e height and also the transitional 2one being at B20 $hich in normal conditions $ould be in bet$een B3 and B4. /he x-ra film $ould then confirm our earlier thoughts b sho$ing an enlarged heart $ith an increase in the cardio thoracic ratio. <e also noted a characteristic boot shaped heart $hich is a diagnosis for tetrallog of +allot. ?. C(8,+25/(8 ()esim "la!) @ur conclusion $ould be that )agil has a congenital heart disease kno$ as tetralog of +allot. /his is pro%en because of the characteristic boot shaped appearance found on the D-ra film0 the diagnosis of right %entricular h pertroph 0 c anosis $hich could ha%e occurred because of a %entricular septal defect0 and d spnoea on exertion $hich are all clinical findings of that particular defect.

1!

RE ERENCES 1. 4adler0 /. <.0 )hapter 12F )ardio%ascular s stem0 4adler0 /. <.0 3angman=s 1edical Dictionar 1-th edition0 ?nited 4tates of &merica0 3ipincott <illiams G <ilkins0 2--!5 15, 2. 4adler /. <.0 )hapter 12F )ardio%ascular s stem0 4adler /. <.0 3angman=s 1edical Dictionar 1-th edition0 ?nited 4tates of &merica0 3ipincott <illiams G <ilkins0 2--!5 1,2-1,3 3. (loomfield0 P.0 (radbur 0 &.0 9rubb >. ..0 >e$b 0 D. *.0 )hapter 1#F )ardio%ascular disease0 (oon0 >.&.0 )olledge0 >. ..0 <alker0 (. ..0 Da%idson=s Principles G Practice of 1edicine 2-th *dition0 ?nited 4tates of &merica0 *lse%ier 3imited0 2--!5 !33-!34

4. (loomfield0 P.0 (radbur 0 &.0 9rubb >. ..0 >e$b 0 D. *.0 )hapter 1#F )ardio%ascular disease0 (oon0 >.&.0 )olledge0 >. ..0 <alker0 (. ..0 Da%idson=s Principles G Practice of 1edicine 2-th *dition0 ?nited 4tates of &merica0 *lse%ier 3imited0 2--!5 !35-!3!

5. (loomfield0 P.0 (radbur 0 &.0 9rubb >. ..0 >e$b 0 D. *.0 )hapter 1#F )ardio%ascular disease0 (oon0 >.&.0 )olledge0 >. ..0 <alker0 (. ..0 Da%idson=s Principles G Practice of 1edicine 2-th *dition0 ?nited 4tates of &merica0 *lse%ier 3imited0 2--!5 !3!

!. (loomfield0 P.0 (radbur 0 &.0 9rubb >. ..0 >e$b 0 D. *.0 )hapter 1#F )ardio%ascular disease0 (oon0 >.&.0 )olledge0 >. ..0 <alker0 (. ..0 Da%idson=s Principles G Practice of 1edicine 2-th *dition0 ?nited 4tates of &merica0 *lse%ier 3imited0 2--!5 !36

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6. (loomfield0 P.0 (radbur 0 &.0 9rubb >. ..0 >e$b 0 D. *.0 )hapter 1#F )ardio%ascular disease0 (oon0 >.&.0 )olledge0 >. ..0 <alker0 (. ..0 Da%idson=s Principles G Practice of 1edicine 2-th *dition0 ?nited 4tates of &merica0 *lse%ier 3imited0 2--!5 !36-!3#

#. (loomfield0 P.0 (radbur 0 &.0 9rubb >. ..0 >e$b 0 D. *.0 )hapter 1#F )ardio%ascular disease0 (oon0 >.&.0 )olledge0 >. ..0 <alker0 (. ..0 Da%idson=s Principles G Practice of 1edicine 2-th *dition0 ?nited 4tates of &merica0 *lse%ier 3imited0 2--!5 !3#

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