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    Cardiology - Book PDF

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    Postgraduate Pediatric Cardiology By Dr/ Ayman El-Badawy Professor of Pediatrics Cairo University 8 Fifth Edition x Discuss eboeyys obi phoge of pT co 4 porins PHTW 2 BO) 6 monall Corre ony gener Fe Carchoe man ifatder ob. syshare hy? we carl Conte Seas clinpgralty re mbablee consgurl sb thck Meet) a to, clot prblanl 07 sybonte ass. wo Conges cnglon vip of endhcve HTN2 i Caso carclioe richie ra prcla: ple yw Carcle nap hanirlinal ecmb 1 NEBL): elrolegy >wer wp of encwenne HTM? we cop tollonng Gockel Sug 2 ae | x“ cuninb pyrooch > He oh cageshre UE in nfo? enti! enercek. tary for pebo Corclteph v Aen J hyo trolls 9 ee barcle yl bihee pa Spidr ats) Contents Fetal and neonatal ccalat 2. The crt neonate with ean (A Congenta her dae ‘4, Evaluation ofthe infant or child with congenital heart disease. 5. Cade seth 6. infective endocarditis ‘hese of the myocaetan and respiratory distress. 414, Diseases ofthe peripheral vasenlar system. 5 Sytem hypertension 4 145 pote RE, LE vert pump the dane amow! ot blood dniy TH air. Kercb? votudn drt = yc 2-Archytinte 2 Corclromg dlp Hey asod get — _— D250 & cong Cryyindir sient heerh lis ab bar ths rAdingnoshe cvitenier oP infantile corciovaredkt cy ¢ Carchiomysy SE oben xiegvitionnts 6 rebel de obs 2 C2 ende Condibes C comedy elit upd We? 7 begets criteria of soak atrial hint 2 Calta a a a Add brent yararettal= of angls Menbecde hed 2 AS vtoboal: oof 011 F vm old iafonh olenelejud obvions Capel cond sparCordlied snioeinn 7 a gorteg tral Couned of Budlelin oleat ” wnt, ebilelren, Adel dnl > = orearat UT obragmas ond tt 2 - Arterial rsehumte sro kee im real , elhoed 3 : ers ee 29) PEF ARE oT eas [ 4 | \ vad [ges en [mina sae] | ! | 3 SA [overseen yssony punwouey fem sa] ff rweny nr | z | 3 a : 3 as & Mura ees here of sates nee time si sesh 7 Lata] Eee] aster | mii SH PEE Srea| soe ow Tape PGES Bann 7 w Pansies MR TR + VETO = perbenpal hav oe afisyto >, AS oar + catty dnsth >. AR PR 2 Lote chethl . AS -Ts cents PBA. pvpihle » Fainting Easy fatigue / Interrupted feeding. ‘Anginal pain Oliguria (Small pulse volume SS Low blood pressure & Pallor <> Cold extremities Excessive sweating to, Dyspnea atrest or exertion 0. Omthopnea:; dyspnea on lying fat duc to either TTYR (loss of ‘eravity) of elevation of the diaphragm. <0 Paroxysmal noctumal dyspnea. “yj <> Gonigt-> de to pulmonary congestion ¢ Leng pH > Repeated chest infestins=> de op > Homopisis Signs poe 7 lata ine bs rept ovr bot ung isc nary congestion 1 badominal distension — oly a = romiliny > Pain in epigastrium & ighthypochondtium 4. “Swelling im Lie e ‘Signs Tender enlarge liver C> Ascites ‘> Lower lim edema, NB: Symptoms & signs of congestive heart failure in infants Go Feeding difficlliesfess volume, interruption with dyspnea & excessive sweating @o Respiratory dities & whens (PRR, working ala msi Teitactions,eyanosis often mistaken as chest infection Acute cong Mia teibyrie, befyerc, am beagy 7 2+ th sdvchtenbe- vain Sheik Olt bracheotyota be + cpl rhcca apie \ vin sve | Ua peat pain is unsaatariemaifeation a patie pati Paine pa: ain ay be Hower cowl pnd 0 pvr | Sitching ee Panga duet ate eno 2, Sabb pn psa pate ct \( in older children) aE eat duct changss nate acy oF Aap ult in yt. ‘Or Ons SHE yt A cites so al 08 A cal yn ea rss ey FN Ci peck mots ih © Coanaticspall >) ati 2g of cyanosis wine AD Aube ek eevee of onze Fame a ics @r squating > © at Pongal cyanotic her dienes (o> Differential evans real EA, i ype mbes senin css Re Bieter pe ouster ne ete oF _ aration of aot. predicted ConA \Vit-Weak or absent femoral pulsations) > In cases of coartation of aorta n cases of eoaretl _ > Due to Hyperdynamic circulation systole or 44 diastole). © Mead & neck Ma Teed nodding (De Mussel sign) 28 rominent reris(carotd) pulsation °o Saotoie lathe root ofthe neck © Upper limb per Vater amen pulse 277 12 Capillary putsations{oving re Tine) «teu pulse presse (Taal or aso) in nec (Corrigan sian). Lower limb eng sound on femoral arerysyachronos wih cach beat (pistol shot) 0 Pim te systole murmar on fermral i sight pressuse S fpplied (Duroziess sigh). So eangeraton ofthe normal. difesnee in blon! poss Eexangessonuntl ills sign normal 10-20 nnitus —Epistanis-Dizziness Blurring of vision (> Infective endocarditis (© Fever & toxemia + © Development of new: murmur or change in character of already present murmur Yo. Embolie manifestations ‘CNS: hemiplegia -Renal: hematuria spleen: pain -Extcemiies: ischemia > Rheumatic activity: fever or athrtis > Chores “> Syncope (severe AS) <> Sirokes (epi in BE disease). [NB Cardiae manifestations may be pat of ‘ho Congenital malfmation syndvomes (for details se tes) Oe Chromosomal disorders as tsomies 213.1%, tamer” S578 di chat) ©r Symon complexes as CHARGE, VATER, Alagille asplnia syndrome & plyspleniasydrome ‘Leraiogsnicas Rubella, hydantoin& leohol Orr a Apert Holt Oram & Wiliams eralized disorder alfsting heart & other organs Misclardyssphy Se Mcabolic cardomyensthy -» History tacking OF Age of presentation: above 5 years suagestive of rheumatic heart, «lisease while presentation in early infaney & neonatal period is suggestive of congenital heart disease both sexes ae affected equally however rheumatic chorea is ‘more common in females Perinatal history :as maternal complications as gestational diabetes medications ,SLE & substance abuse in cases of congenital heart diseases ° Past history: Recurrent attacks of sore throat & tonsils in Rheumatic heart disease ©> Family history :Consanguinitycongenital heart disease)- Tachemie heart disease ppolyeythemia in congenital eyanotic heart Seoubslyy on oa vieut yo» Barth Eee aged ~ ort signs spa sheet ep = ___ Examination 4~ General examination™ = 7 Observation” = ‘Go Dssubitus & body built-yOrthopnea &asting ©o Conscious level Go. Appearance ->Pallor, cyanosis, malar Dus © ‘Signs oF erica iness RD toxic facies ©o_ Others-» wasting, odd featur ae 8 i , yt charter, vole & equaliiyon both Boer alata) papiodrcytint sin Variable according to age being rapid in nfs & the Tange i 120-140 beatin that may each > 170 betsmin “ring ering & 1 to reach 7090 beatsmin during slesp ‘As the hl row older the average HR | @« ‘Tachyoardia: HR 200 bets inseona 150 seaitnin i infants & 120 beats/min in older ehilden Teadyeardia: HR <90 in neonate &< 60 inthe older. les heam beat asin archytania ‘B.Character: heal, ‘= Wide pulse pressure & bounding pulse denotes AR, PDA Sother causes of hyperdynamic circulation, & Volume: ‘Average & equal on both sides & feitin LL Weak pulsation in the LL may indicate coarctation of (Qo~ Tenpieratire? fever in eases of theumatic activity & Jnfective endocarditis ratory Fate) RD in cases of heart failure. Gro" Blood pressure Big pase pressure & Hills sign AR a > Regiowal examinalion7 rs Mead , (oe Face, > pallor, eyinosis malar ush , + Eyes Dalwonmal upward slanting (Downs) ccema of eye lis & jaundice = Mull) Deyanosis of lips & tongue (Oe Trout Pons « RA contraction: Severe rete wth mint Wa pone ‘inom sess epi sls ora, With bmp ha Hk (cannon wave), ‘ricuspid insufficiency) > fusion ofc and v waves (eneresed verous pressure with prominent v wave! Congestive HF (increase diastolic Pressure in RA and RV in ling heat). ae gant A wore a ae dol ff nodal tockyeurds @ Gannon uve cB, Ces A boat 7 = eperr Mash Mitred Pungorg ent should be on semi sitting position 45%. measuring the degree of congestion by the distance: between congestion & the clavicle (angle of Lewis) + Above 2m is significant (O* Congested neck veins show pulsations with norm! systolic collapse. de ei @e neck veins: constitive pericarditis or pericardial effusion» 5v« => ©+ Nasal neck veins are 2 em above the level of angle of Tews while the patient is semi siting 45 pulsating & showing normal systole collapse AcCarotid arteries) + Inspection > pulsations (Corrigan sign) in AR & other ‘euses of hyperdynamie circulation as PDA thyrotoxicosis, anemia fever © Palpation systolic hil propagated from the base AS Dot propagated AR big pulse volume @o- extremities) De Upper limb ; Clubbing -Cymosis -Edema | “Subeutaneous noduletsheunate fever) "Oster nodes & spincter hemorrhage © Lower timbs: Clubbing -Cyanosis -Edema Dorsalis pedis pub DS Skin) hema marainatum-= 4 12 (Systemic examination © Chest ausclaion 2 t Indicates marked & long stan cardiac enlargement early in ite Se Definition: Owtermost, lowermost area at which heartbeat canbe felt Site: ip to Ayears 4 eft intercostal space just outside MCL. ~ “JAbove 4 years 5 left intercostals space 5 es sons ae b metab ft cpecton sysht aot is FAS confines -M Hid-Diocholee -4 » byob Cre) carly obtth = Sere MS L igen agar -m X 2em & localized to one space -Diflse more than one space (Rt vent enlargement). Character ‘tiyperdynanic (volume overtoa) ~ MI-AR- PDA & ole causes of hyperdynaic creation ‘etleavingor sustained (pressure avert) ‘AS-Systemic hypertension 1 con » HOC S-Slanping Ms ‘Tht: able (ith rani uss oy) + Timing ‘Systolic bulge-oelt ventricle & Systolic retraction right ventrile ®o Oe Shift ie ‘/-Outwatds & downwards > Lt ventricular enlargement © -Outnwards-> Rt ventricular enlargement > ‘-Right sided apex —>Dextrocardia, tension pneumothorax, i Diaphragmatic hernia ations seen & felt at 3" 4 & 5" left intercostals spaces denoting Rt ventricular hypertrophy ‘Systolic thrill is felt in cases of VSD. Denotes Rt ventricular hyperophy Lier or Aorta et intercostal pace) J+ Pulsations seen & felt wth palpable So (diastolic shock) in eases of pulmonary typertenson 177 + Thrill in cases of congenital pulmonary stenosis (2 right intercostal space) * No pulsation + Systolic hil in cases of AS. ‘NB:-Aortic area 2 (A2)93" left intercostal space “Pulmonary & Aortic areas are known asthe base ofthe Heart mediastinal compression | gas) Ul-Pereussion fobsle) > Areas of percussion Find the upper border of liver then space above &percuss from right to left I-Right border Normally no dullness 0/24 «bon Dullness > right arial enlargemen : opemey # w Opening Swap: gt S, TSs pid Hite ve bral 7 Yon ctesdolie nigh pitelud —. propagate! - AB. $3 onbjyon Apex + Getion deh. As, ps epenng of? oe 7 1 ; ib ® R _ll ae cee, etfs oN ee a0 Lip ak Faiz toy iil, . pore (Tang oT : (a mote | eG cashire— pericardial effusion, scultatio "Normal heart sounds $y & Ss additional sounds S) & Sy & opening. snap, Dye to closure of mitt & tricuspid valves 1 Rest heard over mitral & tricuspid area. ‘© Due to closure of aottc & pulmonary ‘© Bes: heard over pulmonary & aortic areas Normally itis splited having 2 components aortic(A} & ppulmionary(P). A component is heard before L component as ‘Aortic valve closes before Pulmonary + Wicening occurs with inspiration due to TTVR to Re atrium =17 Re ventricular ejection ime =>delayed closure of pulmonary valve ab “Wie & tgcspliuing 91 RE ventricular ejection Sime as | insb, PS/RBBB) > Pi pve. 117 {2 Narsow spliting-»Pulmonary hypertension(early closure of P) AS delayed closure of A Paradoxical pling »P before Aas in severd AS FL severe pulmonary hypertension or Pi nota NTE TGA ps. orerAal eva sound : duet rapid ventricular filing in cases of HE & VSD (30 10a) i due to arial contraction incases of HF 7 L “Both are heard at the apex & left lower sternal border ¥ ||__ Gallop thythm-»incases of congestive HF; tachycardia & Ss orSs pane Oe if heart sounds Ss heard with carotid pulsation (bepinning ofthe systole) BD ore 2A ‘+ Mud heart sounds ~>Myocarditis i. ‘© Disiant ft sounds ~rpericardial effusion Ste = Apex (S -Muflled MR 5 -Aecentuated MS f 8 A? Cm, heme ATC veber—s hwy » Shih np (ora ) D Kem bins Oy” re er hay esa) v0 oa HR, TR (wiles yan) PAS PS C mint —» ot J bts Ts (wale —y piel, J ae © Cothim > pos —> mt) + Pulmonary area(S:) -Mutlled >TOF-Severe PS , 7. A -Accentuated ~>Pulmonaty hypertension @®> Murmurs: we should comment on + Site -> maximum intensity ‘+ Timing systolic or diastolic + Intensity —>grading trom 1-6 + Character-> sof-harsh -rumbling + Propagat NB Grading of mur = Gl-sot & not heard in all positions SII» soft but heard in all positions 5II1-—Hlarsb bur no til fel GV Mas with 2 the ele [SG V—Mare harsh with theill, GVI-pHeard without stethoscope Popo murmur Systolic murmurs : cassiied into \* Bjsctionsystolie-> stars shortly afer S; 1? inimensty el reaching its peak & thon 1 in intensity ill end before SAAS &PS) + Pas.sytolic (holosystoic)-»beuins simultaneously with §)& continues though the whole systole (MIR TR & VSD) Xe Latemsate 4, disso mumues * Sol blowing beginning afer S,_ + Rumbng mid diastolic murmur (MS& TS 4. Continuous mans + PDA Mitral area: (Apes 48M eae Sy nud + Site-> maximum intensity atthe apex + Timing -»Pansystolie + Character» son + Propagation-sto the axilla ‘Best heard withthe pationt ying in left lateral potion wit deep expiration using diphrapm of the stethoseore (15 @Mitral tenons 8s aceon + Siler maximum intensity at the apex + Timing —>Mid diastolic -presysttte + Character» rumbling =D Fnvten t anu ner a ee ee - al Sco werel cluriig inter caren t mb or soem = © ejecb rr tysholee mearm + SPL. no thn « syrbhle shod ome pon sat Asymyrtome. © tt shraaheolge 7h on eprmer bo + change & poste» oy eur hem tho — baw He Second Me Abra malor voblt © jrabrertercy muro — voce A PT olan A Somali yp al 1 ry rbete Le How + lis opye abbr fowr weeks. @ SAMS ante — TOD miol H sterral edge - or bratery 4 bola Le tap halernt. arownel ome sel band of 1-7 @ enews Hum 2 at epee blerneSeolge way Dreshol , la Raburn of BL A hued + obs apyas—- on lagicg He AB feelosihe ras ameey Course tarnoeend mirr 7— + Propagation-ynot propagated ‘© Best heard withthe patient lying inthe left lateral positon ‘with deep expiration using the cone of the stethosz0pe + Pulmonary area: (2% left intercostal ) ‘Soft ejection systolic murmur in cases of pulmonsry hypertension + Aortic areas Ay->2" right imercostal space ‘A>>3" left intercostal space. L-Aortic stenosis, Site AL + Timing Ejection systolic = Character» Harsh ‘+ Propagation-ro the apex 8 root of the neck 2 Aortic resurge - + Site» Ay + Timing Early diastolic fn # Character-> Soft fp ‘© Propagation-st0 the apex Loft parasternal area © Pansystolie murmur, harsh & propagated to the apex. > er ogesisticl 0M Symptom 2 Sy ndrpey a— amosgfi) a5 7 4y- FTF ge Koby: tak Safe be ab arching, aetna pe ae lbs cco or _.. Cardiovascular System fi ——} R \()) Fetatand Neonatal Circuation |=) — ‘The feta crsulation “The oxygenated blod fom the pass Sows othe fs ough the bil vena an verge at of 175 mal kg la, with a res about 12 mm, nda PO; about 30-39 rng | 50% ofthis blood pers the liver, whereas the et ($0%) flows through the cts ‘ens nto the inferior ena cava where ines with ess xygeatd blood coming om \ the canal prt of the body te combined blood tas PaO» about 2628 mi then i stor theiht tia RA). ddmefone Ln LF AO. Most of this blood pases acres the framen ovale to thee alm (LA) —» ft vente + ascending acta coronary and ech tes ad arteries t the ups ins (ea id igh PO:=2628rmmH) egg ey y pal hae $e en _Te superior vena caval blood (considerably les onyrated PO: =12-4 mm) ees th RY, savers the tepid ale — igh ventile— plmonary atl trunk ~= A oF this blood flows to the hin vin the pulmonary arteries (as they are vasoconstictes}, 90% g ‘caters the descending acta va the ductus arteriosus (ith PaOs = 1:22 mbt prise the cual part of he body as well asthe placenta ia the two umbiie ateries th he one of veatiaton, make insease in pulmonary Dod flow sce de 0 iaredly reed pulmonary vse resistance a 3 comsqence cf Bath acne (PO> ‘elated de othe diaie eft of oxygen onthe sonar et) and psi (scorched exes of thn) polos vsaiaton. «The pulmonary veo etn ethers the ata —gpoare as A ese is morethen RA presse (insole | Bunions oft des anions is uy empl by 10-bit noma 5) esm nets, When the PO: oF the lod posing tough the Joa reaches abot 30 tne. the cal wal canst nknowwr mei. Du! pore dr ea Hi it] /resintsned by the combined relaxant effects of low ony tens produced prostaglandins, specifically prostaglandin j—) root i Ault icin asus afer clots ft oan ool he ts artes Aad endogenously al awl! 4 WE Q> fecbyarehyHmiy > _L2a torent eopemess » 7 Cordive wa sses 2 omunye of rrbactalle HE 2 Cy ohal qooin > poolig Lo pol aT (mew clsifrealion ) prt vwoneus HTH s er a LZ mye lorcat hy C3 rele mye pally Fron grils yrapel ot a) — Myo tarchat brebwmts 9 Chol oloon A~ hetere Cote ZZ Casas DID Aboud 56 murmur 1% Ind HM Goiie— Ce toraky Covel portal rn cbaitetros! A Asymplonalie ble rnns mr~ wre rnp Hi 1 clad hrawol votre! C4 oe ehdd ) ON perk Faboy © LPS WIC) A WT 9 0 poodionsly mrernod chill (obng vis he Orton ge of UT te wppodk _ a Carcbue omen Fat of sys fem dir alas LED D of Recurrent &yp cope a cbayat pproh te Ai 8 enti : zy corclite rm agng Ste valonre Mercola or'ed: SE CA sudolumn clued ‘The Critically Ill Neonate with Cyanos l Respiratory Distress (Causes (ee table: Drea) dagnosis of cyanguis in the mentor; in Poste ‘Nenitoony) 1 eae dees) a: Congenital heart a et sion ight veneer outflow fr pulmonary vaseulr obsinction, Complex anatomic defects, unasocited wih pulmonary steno cas distur of monary and yt veno et inthe hea ‘Heart fate: wil eat pulmona edema end panos, _& Persistence ofthe fetal circulation (PFC) syndrome: See later. 2. Centrakn@rvaus system diseases) Intracranial hemonage accounts for rcs cases dug administration + CNS depression egal shallow breathing ese alveoli veniation lw PaO nse: LL ch SLBA sea3e aot ‘A Uppersirway obstruction, -° s 4 yale mene disease alesis, and preumosia. -infant wt breathing patern: 4 CNS discases: Weahor regular respiration, 2+ Candia and pulmonary diseases: Vigorous or labored respiration with taehypnes. DcConvutsions aud. general depression (weak sucking reflex): I strongly suggests CNS some, QA siguiicamt tes our; 1 sugges cae case of eyass (bower, severe be sce ith en) Beggin tt rns o 00 ony wo eae ft and esting th PaO tension. Normalization of Pa it indicates CNS dzone. nereaving PaO; (bat not fo sora: Hints pulmonary disease, oF PaO Windctes congenial het eae, ofc > Xe! Plenary discs (memo leit) and puimonay vcr smarking may be densa. ‘ECHO nigra (wines can dt congenital ea df. ‘hemsotropharei ison te! sine tal) ofthe Hb vara As eran US choll tpsat F 2 Av cutped oO! Bley 1880, ASO, Poa +A, TOFS HS, AS —> Sat a BTR RLU TA yy VHS, TALS, Dory we beng Q-T (LATS) 5. be layed spoloizdy, o tndut med k cle “to peoionga bent of vont oct protertoal = predlpsss be onsale perntes yah fiohe + omy beads bo palpation, Partoo'y , Sa rielen clea vont. fib eilalion (WED Bey Le asserted « syudaed, goatbiet = Deng related Poem; ttt fay beorghethate (amie laren, setala WS + Crsapride —. halo porole - * aelenen + kbocons gol + Types: evs Me Serve, Lange. Hielson 8 (Go. of of ones) adress e LOT 2 (25% of alas) LRT 39 Winders Tawil 2) _ = Remant—arerd B 2 MD fore of OTS ister & rapmostee critwrd :. (Hpprome beelitprore). — jLiphasre ce Jong AED + Torte ch pombe GP) « abrroraad T-v0m% @ 2 bry Godin Cdeak wis GP) FU @ tt 2. blocks (rachel) 2. KE Spats 3 Md hanr 1 Grwtal cymprhetomy | Congenital Heart Diseases (CHD) | fi G Imekdences 015% % of fll tra livebis “ 2 in peematre infin” - © | Wenirieatar septal defect v = r, ~ / © | tia septal eect (secundum) wy / fated res | ont Aenea owes hemeonipel Trion whe tress eee | Heme ate eels aS . Merman tater Soros see y ‘Hypoplastic right ventricle ic mn a : a vy 13 So (2008) netic predisposition and TP M4 gene 2 SRR Maro Noman sy) eprsens BBD al ewes - ‘4 cup win soi romosonat anomalies rresenis (Mot al cases of CHD, CHD with | eee fh : | | | | | | | 7 T teisomy 18 DY Thom 210% | ches 0100 o . | TOF, dbs RY, rede, pono i nd interrupted sorte are) ave deletions of segment of now the i So CATCH 2 dy aces yl Hinked to mutations in 10) fn cot Freie . fe aie: linked to mutations in dystrophin q a . <——_perible ary long Q-sort) Unked to Q tere po So aml, =o (rae) . fay -s120j0 12 © gent + el coronas TEKS ger Lats ev eSeerL bang Melen 5: = ne = 0077. ofeoPmiss Lats FOr ob at apenk ays abou 6 emb-tch far @ Komanouree 1 synd “dO one cleo l-mess = fie G OEE bad Leenyed corte vahe da CHD Is tu mesh commer sheuclarah ee perm va childlweh MW joo chil # vse 1/500 oe HLS loco “ thee Tint > oo ho a eyenats 15 Fable vg Ridetad He a tab ea = Fgh xe Me prolapse - ei didll-s Viv /uopon © al cus parach vrais In Decry as soy erke st ceoger lh pyubyeliee prtilarditr 2 syraloele ps 2 poutactial «ff | [a Pabeeld > sopmuek. ps Phy nite 80, ASn, co po aleohol. -4 Ase vay = valerie A> Cox oy HLHSSPAA we HTM th Neonale 55 nchealon hospi taliqa ltd Clo.) to avoid. encphals pally or Revel faslors | Yr —> Ws0,4m,ppn Crnvdmre oA Lf nme Sis. WB I Moonen 5 p Shar Similirs typve fy TAR TOF Eg itn 5 prriabl ders > “ps astrenbeas von Tum pre Irnddey bey Hh palm wn Ber Pane ie & bgpeotelritm onpatew arate! tripadits in Down Be bow hair be rm Ferrer erent apr) vad (0 | BANS. (aciosicgio-senabral | TOF. VSO 7 “apecten) CCH +4 | BHD Cconseia Fomyaptana | Miclanas Syndromes sociated with Congenital Heart Disease 3 21(Down syndrome) Endocarileuthion defet, VSD, ASD. Trlsomy 2 (ca eye syndrome) mPa Miseslnens, ot! aonslous pulmonary vena Ya VSD, ASD, PDA, couctsion of sta, bewpid pulmonary ave Om F Ceotan ds VWSD, ASD, POA, coatalion of avi Fpl tot pulmonary ale = "Fiaay Doce a7 PDA,ASD —} PDANSD, Tripoiy ‘VSD, ASD PDA (Turse drome) jew arc vlelgpieiion aT aa lacie ra valve proages tie tdi selene eon dp "VSD, POA, sor enol Deletion 9p Misalaneos ton 5p (eda chat | VSD, PDA, ASD yadrome - Deletion og "VED TOR, contend sons? = Delton 1, VSD Deiton It i association (colobom, ‘rer oesia. chown, ‘retaniton, genital andar ‘rams vs. ‘VSD, ASD, PDA, TOF, enc cation det ‘Siodaton—(encba ‘na macheocsophageal, radia ‘it ihthyesfons erodes, Lis defect yy iia: sae Toc Trer ei ong conse ve pees 1 Lasplena syndrome 4 “Te poor Hood ret, detec, single vere sngle novela val Reva ‘neers ploy Boe ow. a8 nttion of infer vern nv, pata anomalous pinoy eons rtm, estos, sige yeni common ‘ow espoon of eat stteanomate plonay vets |” hprertyen & Hopet > ea #Hi as a velo lovelic ute Risk Factor of CHO » bthum— Fe 2. warkhrn —> pS, RDA ith see a 5 ple 1 YS™POR 4 phinftori—> ps, Ass @AROA ~ 19E (Rabel, ),PDM,prighal ps &- TABI» Hoot, TEA Bem Stl cues a- PKU Ter n [swale ® supra v- aol: (Mere anil Sopmroqreite— bso \iy periph pos - - slghl cock bape plaster & hgper Col ett = Serrall fee th (corp chypud mwutl hagpe Pe fo res o cock bart jrarby chalk. * prloliya of Contra Top + Abeent j+ Sterna «peri Carcliy oe \) cMaphagmy hurt Cecteyrc) + merenad buoy! (ref) G fo + AO disorot I = Eker s.Domes eons S = Reonamssurect ecpAv —nene lordine bg 5) pbkensturerfunn—s POA eos pulonty sei, VSD t VSD, ASD, PDA, gration ofr rea anos” PDA ‘VSD_POR. PDA, concaton oom Pulmonary hypertension, pone aaa YD, {isbn age i crdiomoatly, VSD, comarca nana Destro -ASDSD monic soos ASDy TEE al eushion defect Cont ‘VSD tothe fro era er coe Made ype tplan a7 He Tan Ao FR riper monic oni at dc seo TOF Faby oT A Are pe = bt} Orom' = TAR. foment! GED, de bak ophira Lnbolificl \. O24 L CHO hed mere Ham ome Grbiae amcmaby— enon cqpevoe anomaly @elriwoy TK onmjoety rs divgnettl onhrbly , on ty Edbse posbrabes B® misbofiolfch fs rysaired bq srngl etage pretabuts © Cath 15 nok rybsteg mal wr” : B® poutine 4 chasgloer ab 18 ur anleralal diopneces (sort bivms-nly) ee we aS -~ pA we Nhe nal Ayyi?? : : = inpaiced pit Parcln > Hips ; = cleluper! Cnah, prolerged labour high dan oger= —» duck cletors perasl teil HT ober mictoras omy Corel? ¢ seem ” SHIN AKIN = pl HOW ~ P95, tbo endo condi = Heo, DEM pert nen . = af + ABDI Ts} crf = WMD /eHS / icchemdi- om gru cer Tfirembest ME He < + Lindo / rebel bonalelegy Mp Peml hier fej - Syndrmn + art hy Yronie, + valvidn Leon = ECG Abnermbitis < — wie Ordial Fibres Qramelna, arejlodasr? ‘Sstbeect®) one ean oy i: soot oro ne oa Toa a een te ae emo = © deta ence ene 29, 198.5192 aca owt / oe \ Marlon i fiver le abe Gol 150, met bok Papal pmo por, ie 50,50, F08 PAS, 0 FOR, ‘econo Simao AS poets ‘Seniesa fi, ae 5D. 80,FOA Vb ‘ante Seneca, G jebry vs Gene ( aCab~ wo Blac \ Coe is en ERD za aspen = Baie song 2] rer be a oe ssl dena Apap gent | Taian BRR So Pai EN ch [1 Parents who have had child wth CHD should know: eMac 29 467, 1. The recrence atin the presence of genetic factor high, 2. The recurrence rate in case of multifactorial inheritance i low (2.6%) for following the bi ofa child with CHD peenaney” lying? 3. The ecurenee mate 20.30% for a third child when? siblings ee have CHD, red 9 sare ex patient has courcation of 8 rectrences may include coettion, AS, sorte When acting the mosher uring the 1 ¥ mo of pregnmey (2 | scent ements san Ps () (4: Nana me han pico nt ues, thalidomide, hiv, Afar, [vitamin derivatives. and aimetboties. Aspe”? [a | ay Higher ncidence of PDA : Seth able 7 a ofthe reining case of unknown tise. Ce oteniok, metalation pica efsian pulmonary fetes «| ies itd aes TEA —| Pred res mee * [Sten inseothemsions si Pecans Ga SiktealasaiiGowagy-WeHE ony atheros ers with seri), cangenal vt blo | = EE [Pula hypesesion, myocar Aisa ecient “fesse arn lek | Geena ater asa nd von, aaa Taner Any Vali WH] rug ode isney. gar fallure, won CT er 6 | Jaye ol | : car cll rmanifoalaens f 5yflin' al j WW. encea & | Vs 48580 ! ows ate oy - ott, win, CDH, Sono 1 ME YH, pHACE _réet 2 FA oni. difaton CM - 68D Wee - fk ve Le a Aaloyile = Rumah: ARE, AE ~ Goonsbic ane ‘Siem Dea ‘ire Copan 1 jews "some dese [Bor PR Cardomez hear a aS | trompe dine) CSET fi + [Gamine detieney a) —| He lr carfonyonay + [ihe diene rca = © [Honostiris Corsa Le [Aton roles, valli das 9 | More Ur yarome 2 sehoeaymrome {fences eS aleiieation of in Caleinasis of coronary arte, sort [iar sje [Abc sot mia ty, AR OE a] pg ae lia ve rin ‘ eae inde waa TH . ri neompeinc J 4 ihe rea da Ano D vvopatny (AOD , ee — Tea fle > FD [Canc heron i cexsonaly atin a ei Pulmonic eos, pheocvoneevne,Suralon af mai Episode hypertension, postal ypeeison Hemongiors,peiciomoeyomas Tachycaa anhythnis,hert le ype ‘Besdyenria parca efsion,eardionyaihy,wvaRaae “ree. . 4 Fhancromosyona Types, jacana! chen, myocar cughynn , eildit on ‘cd ded eneara Haa Or. POL Highoupa beat fare, cadionyoqmthy, omyomty, pulmonary 1. ess (Ean | Cra roth, pana Iyperin Basar i i se een an ina aden e_—_——_——————} Pulnone sei raed al : ovens stl (lang. Rar maces ere) neva saat Patent dct aot ecie sles, aR 7 e008 lee loI/e a “eps Groceries! ef, |< Eeopagea Foreign by } Esotgra spasm |. Chotecysts| + Suanhmgmatic abscess / Perheatts Fit ogh-Cunts symdroms) let ee jemi Seen cere paneer eee ee ea ce es ee cae eee ees hyperventilation yes Veo BO cca ALO ~ |i conker ae comrsion reste pth conton Cstlemanciegee (ph ode neoplasm 2008) - chs usully bengin contr chtod por en pobolwe apvovp it unlikby tebe Corire - £4 cney Lend to chook miStirg 6 clecnerinel other G © A8Socrull & (sy neqoos ql tale \ B He porepur -srranne ke Q rvgl -eccerctng te sagytived pe bo 14 fowl bo Cored legeat ( camploneld >. Reatsaran O— Ce + Pa Pe U, iwi, tyntapie, Pe atlas Gp Yad teochehs orm -nabie (sbhog Fp « dareling (o00 or min) ~ Rectalorg (neck VE Wg) Wh) bit op Tie ine Str Be emp hr S)\ | spied: DHS?) yas 1 Cai discase, Kawasaki disease, hypercholesterolemia «© “Asthma, recent espzatary illness + Aaoimmune ease A 4. Sickle ell disease «Other ehonic diseases (Surgical history’) 3 previous chest or abdominal surgery | “Cardiomyopathy «<7 sen cardi death vy _Aaythmia ~Dystipidemia |, Premature coronary artery disease ‘Genel aiseases) Marfan syndrome & Tumer syndrome \Y “Ehles-Danlos syndrome, type 1V Chest wall abnormalities (peetus exeavatum or cainatum) sealiosis Signs of trauma, healed surgical sears Reproducible chest wll tenderness on palpation Caraiae stant heart sounds, bnormally loud second heat sound ‘y _ Murmur), systole lick (1), gallop (1/) 1 Upper extremity (ight arm) hypertension (greater than 20 mm Hg difference berween or Electrophysiological Study , elo we siutcon assent of te fe nwa Nw, gas exshange, ap el sts] ee eee ey thn rds aay oti Icep, when abnormalities /of ena respaty control, muscular ior [es sf q ‘Colnwcry eomplonons fom gastoesonhape! reflux are suspected (pH probe suis J )Atubsnmognny ow cniterel he bs waa et for abrasive sep sone u ‘ehypoventialion during seep. - Boat 0 [smaaenssira Death Syndrome | guy. 5y— ‘th laelainaed of infant mortality inthe USA gion ease of postiennata infant morality (1 mo-t yr of age)” 5 Dai : = gue death ofan 7 anythin is(Sneecte ty” (HER ant Unexplained by a thorSugh postmortem) @ EES 0 nucleus are identified by neurotrinsminrstuies in fomea x poe SIDS wt ng amen Tua = : ha ai ine nin =a eae or abivon weet marly ye aT dcvsytryptami a me i SHTT) 1 incobox 2 naan 5) Remangd dng ote ae 22) FEtOnE cmettog cna omeben Toll Senlcnst f feukin I ing ‘Male gender U { Falectcluse Raceletiniciy (eg, AfticanAmeria and ng 2,6, ccsin, roi) Naive American) ' s -«| Grow ae fC hiss pena Gro Nobreat feeding nce a {mit ss No gaiferumay) HB sa nd ovr econ ~| Peet nN En Single marial stats tae (and side) steep position Shr ner eeancy neva Rest be) nt (i ston) {} fotraaerine hypoxia E | Inadequate immunization Cte ion 3] Saree peta) | =] Sosa soe, soh tens (Este sharin with parca or other chilren Tema sesovereting - C3 Caan scon wo ese Eoin _| - Ne <<) slesp position is he cast common leasing cause of SIDS 011) [= Destin of 50% or more in rates of SIDS can atributed largely to reductions in placing - ‘nants prog for sleep and increases in placing them supine. A Slospiag pfs has consis Aen shown to Inrease these of SIDS. Side sleeping, g althougi/is much safer chan the prone position, sidesleepig infants are twice as likely to cig SIDS compaved with init sleping spine, isAl contsindiceions of supine postion include micrognathia, macraglssia, and por eustesopagal fly or eo a my Anomoly 2 unsatenbrerd vai te child abous~ a cinten Wenal cv fhec= tern on url pes REMUS KCN KCNOI, KCN ‘Seeman charm! gene SENSA Feng OT rare 3 Baca i ace cannon gad one) SG lone yc) eae Sie homecbox ts HON «era ng aeons REN Entei comeing ese SCE x Reinier aby ° Tiptine ening HOY) =o le Bo itn ohana 3 AHED festa eitoy contd ‘hte gee orca ecptor reget eb Moteur) (Iter SIC protons ssciated wih prone seeping 5 - tees 14 2 Na nab arnt tor VEGA aint “Tmo neers aaa oman CER monn praise tei UCR eae mea nce Yak ‘rere orang mca le sd CYT gene socte it mate Sten a wth nnd Soc its was inant) a % Short QTS (SQTS) is more recently recognized as another cause of liesreatening H ~ arthythmia or sudden death, otten during resto lep. +r Impaired central respiratory regulation is an important biologie abnormality in SIDS and {enetc polymorphisms have been iden in SIDS infants that aft both rotons and adrenergic neurons, = Monamine oxidase A has observed a high association e SIDS | | # c Environmental Risk Factors Genetic Risk Factors ‘So bing and | a_i fon | Prone oF ide [© Comtement or ‘ytokine polymorphism Hehe po Sng [Emery production Figure 2 asain of peta iatrsins betwee ropreenatne ‘vont an gente ret forenddn wespoaed esl ne {SUD0 tn sen ant dent scree ta A5=ansnaisneneayoea: Sica st pee, ot 4S OS BLES. Dilferenal Diagnais of Sudden Unexpected Death in tnfanc;_S Causal [Pima Digest Cilenighcet rae Ce Ditton rr nial dings, SIDS] 35.4094 1 nial Hades, SIDS | TaD or inetonal ise S| “hiumatis cid abuse i Uainietonl ayy aa TF iininal Fadings, SIDS] ZT or inetiona uecation Hae SS gan beats a peas Espa neon, | SIDS—————— Two saToeton Calo absence of | explinable : faareat avops SIDS = idan an dsth syndeee won 5 pereenage ofall sudden unexpected infant dents explained at auapry As percentage of natural causes of sudden unexpected infin deaths explained at autopsy u rigvenous' malformation, Wbdual hemaiama, Bie fia a Wheeler | te a oe “omalous corsiwry artery, Eanfiomivenatli, werhythmins (prolonged Q-T) SL ead ‘paca Apiration daryasrachead | T° ia gece in seeming omer [oid ar oti ‘deci Fpoonen ate? “a Steen = a comets ye pr es) eae ll ai “ [S16 EV a ATV oy FABLE 7. Differential Diagnose of 4 Sndden fant Death ne Siship—_ a [Recunet wonder nim dh done Seta é Cong cl pan soma di Tah ad congenial hee block ulnar hyper See the previous table infanticide, Manchausen syodrome By proxy coy 8 SIDS can not be prevented in individual infants because it isnot possible 1 “curently to prospectively identify future SIDS victims or effectively intervene | obstructed breaths, central apnes, bradycardia, oF oxygen desaturation occurring part ‘of the terminal event could be reliably detected sufficiently early, they are anecnable to intervention, 2 GP hfe Prerealnney Le a ‘sali The ifn shuld bei coe fr see and ‘he thermostat se at a comfortable temperature ‘. Deis ave oman say Pens “protet” abe sharing infant, oF reduce - the risk of ebeathng re not recommended, - | Actos should have some ‘ime inthe prone position (tummy tine) whie awake and r ] 1 should netamoke dain "Pregnancy and infants should not be exposed to on-hand smoke, national Bask to Seep campaign should comin and be expanded to emphasize ‘he multiple characteristics \ ‘eeu onthe groups who continuc to have higher res of SIDS @ Gus f moval joolgrs ae oh Khinils 3. Apo bypranatiort cr 4 RA = HS Sampo tes briad —m pore? ee | dieron. ape seni x Gusey of Inge beegu—? Thy tyre "= APS/ESD, — - Down = parrre - Reb ra SY = Bech with — widlonen B - ® Ciba car (oh 1) = Box of childen have glue cor (Bere mucous flurd 14 midll 201), Argo oflr~ mid - jrimrs the! 03-9) seareing Mppmnlst oor middle env dt, vrerclin en = Ty pom ane Sumit ond nek Mo of Aloe input « @clft br. wf boo bBbuths « ghieklars sl wards & pate 0.59 4 asses a onanly ve lll a 260 otf fbr @ ch ot The omat ee Auge oh cmobrclve bani end speck ole } an + dolene jolreberg rmporer Sy hs Te babe Cgrom mil 15). . reaming 1S rob hero fol. Dz» ArynplomeBe Carolee qnurmu~2 Eres «bint Aprth te CHO? ae <7 epee been Classification of CHD A) Congenital Cyanotic HD (20%) ‘Causes (Individual lesions) ‘Congenital janodie HD Congenital seyanotic HD “Others [Ses pRaan | A) RVIL A) RVEL /* Fallot tetralogy 'TGat / DOFV = TGA with PS. | + Tarver | 2+ DORY with PS | BLES: ‘= PSiwith VSD © | 4 * Palmonary-atresia-with VSD. © py B) LV 1B) LVH, RVH or both * Tricuspid atresia * ‘Single ventricle Daf * Pulmonary atresia © Truneus arteriosus AP” © RA Falargement ©) Bisenmenger syndrome * Ebstein anomaly Onset of Cyanosis | AariabI oases) TGA fo’ 0) [+ Fallotteralogy * Ebstein anomaly, TAPYR = TGA with PS. * Single ventiele HLHs @®£6°* | « DORV with PS: Truncus arteriosus “Tricuspid atresia | + ps witn VSD. | |dPulmonary atresia * Pulmonary atresia with VSD ‘A) History * Recurrent chest infection | + + Squatting ; 4 esa t d | B) Ex + Precordim © Investigation = cxR = ECG Die CEO teeter | ressereees eet PUD DF silen pMweiee paste opr deere: of LS ob flaeat 7 + sealer = oo RE Longe toes Re o Nein ee WIRY EIT 00 5. 5y SMR HERS be = Rhy tln omaha for | arhy tania) <4 gra PRange

    + Hypoplasi elt heart syndrome Dash oute it venie wat PS <7 Tanposton of great anes (FAD) S16 with “Total anomalous pulmonary Ss Pimonary aires with VSD{extreme Fay ream CTALVI. Pulmonary stenosis with VSD see 1 Ecenmnngins TAME Deh ‘FLA ventvcular enlargement HL scotrcula enlargement o bath 1 Pulmonary atresia = *Trunus arterosise” Tricuspid atresia (>. «Single ventricle luge Rt ateiuin weiige abalone * Shen anomaly , r | / fics " dott Peso cme ey unpre TeLaION leven per (sme Tit Y 7 t peer yt seO» aeemet yh aiseqdig ° < sf by Pry Xe re BC Up pape m+ 10 per) wo buipuadep), s¥O ase4dlg bomoys peo] 40 . buy to5 SEE fer fgge vious! sroiz go sud funongeg ber * YL FU! [ome sny po oy py uns oys ww sopoipurdsad ners howe PPT G29 jo ybue rues =~ SRP SIO upyyp(piean an © peep hue yo 2paij22 art spiemeg pyebedad voypzuejodad:a/ny * a HOTT 7 on pojebodard $1 TAPZTEOF TERIA ayy YOyN prewey Uol~roure jessvab ayy 61 4 * m8 | jowoypoyp jo uoyeuniere fq prumery * | 20 HP vareer ebm’ ~ beyper ke oonia ‘need AE vera te fSL 2 eal Ber 8) wide QRS AL Prolergde.ete tea ASL hand Porat 4 A Sire weave a | asysfol f= | 4 > _eonses of swturted Trove | A Sau aA SAT ayy b tschumin 2. aT Ve sehamtar a. Lv 3 Shroin aterm ye parieneltsy | 2 AAPMUS elfeck ae ett = 5+ Se emde davcliak tae & ABER (v2) £0CB Cv .6) Pa Sh aluvehcn Fo ch atal’s pla a ~ Be Hormel 14 awe ganna | MT ge { 2- tsehroniy Digitales eFPt 1 ebesity re eebhgsiona Be as ae iflnss peycacdal inf a wftbibel) ~~ See yne | = So Paupeol 2 sngubel T | Arn aactral “5 — + Lew, Small QRS ewson (W522) 2d apm Nerntal C17 fetes m ifent S <7, Gielevation — or Hyperacube'y + Dla in unt leads sae pede or + Samm inched ads” Sibyl eat , 1 Goved 3 2g nce Seolving phases" “Tilawe became Biphasic then ‘Seeply inverted Bnd’ a © whale: st eee ene persist re Overlap injury abage B) Myocardhal Necross Stage. Gey bobo eos ne Fata f merry ee Jif preselal onf 2 Dep @ +.Qs F Suctesive jad’ or epth-> b fllaaingR | more | — BlaaiogR Latol ME | = Wider than ‘non twotched. above chonp M0" Ab i normal IP preseal sa VP, 1% alones snp edatmy "7. F avi esata; a Imereti if present TG, . =< Ime width 2 ME oer at ermal if presead o'any other lead 1» fale: Pain Usually persist, Somehimes decrease), ty sappeat = Poor progression of t ware in anterior leads ace QS | doar [zimm sah | sma in fer progression tm anl. Leads J Localization oP Teansmural (Q) We * fobertor MI: above changes preseal in leads um , aVg— xa ns IS Aker Mi: above changes resent bats vy —_*2 6 ‘2: Antroseptal —V3.V4; Shrich shtervor fe: Low Vateral . Clinical Classification of ‘Congenital Heart Diseases 1.) Cyanotic lesions with decreased pulmonary blood flow ¢bS2 and tung igen in X-ray) ~ These kesions mus inl both an ostton to pulmonary lod fw (tthe eid TaN or fr ulnome av aa yy Which ee es shun rom right ean ene the systemic circulation (va PFO, ASD, of VSD). ‘Common sions inthis op inlode _Tetnlogy of Fallot (OR) Pulmonary asa with VSD is cassie aan extreme fom of TOF. © Pulmonary atresia wth intact ventricular septum. [& PFO, e pA 1A gy 8 «Tees atesia with PRO, oF VSD, oF PDA. (ety 5 «Double outright ventricle Ter v 5 2 /H Le Single ventricle with pulmonary stenosis. 5 eaten anomaly “RAVE Total anomalous pulmonary venous etm with obsrction, 7 2, Cyanotic lesions with increased pulmonary blood flow (182 and increased pulmonary vascular markings in X-ray) 1 this eroupoffesions, thee ix 8 struction o pulmonary Mood flow Cyanass is caused ty eter abnormal veneararteril conection 0 by ttl mixing of systemic venous tod plonary venous lod within the ert Caron sons inthis roped «Transposition ofthe grt aneries (TGA). 2 True ateroms. $Y Single vente Hypoplasic lft heat syndrome (cb a + singer syrome. ‘Tora anomalous pulmonary venous tum without obstruction, u - obach chypevdn Elierons CAE fe ite shat) phe vso 2. pA eno bra 4- Derv a ps s TGA Aa Tvs 2- HLS g- TANS qe Ter lunch obypenchahlre = ph er ek veo - TA. Ddervt ps, - TOR 7 pays. 74 Dev. ve oukps HL HS etashhined ren | qApue - TA @ Kestel : cre8 «TA | erhrad suithh «TER 1 cv pe 2 PCE: ps 2 pa ITA» Dorvars reacts -TGAE TS LL.T6A . LEA Meus ~ TApVC ar all antl (DeeV © PSs TAT, SWS urn je BE cht os abhot pog ee 1- pA VSO 2- Dow 2 PS TGA E ps yrs HSV @ aX paiwo 1 6) phtotuo Ve , \\ Dew if \ Ebr © Theauaomieds fede 0-3 “er arn cerew itr tag yeny “|. Ld 2. Mild right vertieular hypertrophy. erbvehelar” RE S 3. VSD. ere ane ih Spal oer. . Aer? com mm yen Dump nthe presence of cbstcton wo RV cow, The lod is peril shunted acs the VSD ino isan on ~ [ie inoncybldfow i spent by bench enlta cea fae splot collaea ers APEAS) oy BDAC ~Acjntc oink” Fallot somal: Wie oon o RY otfow is ld nd hari bane! shut aot VSD. The pale ay nae way uote sts rs of hae Wag pce of he ah Gh lon) and te obs is freee rman ot at ‘sshmodto the notes “Chey ceca ing nen pero i cstion eee ar cleo dun ere) = roe ®: ic Rare a osc af ine ding the (ear, may ei the neo pid win Hee ate carat, poems wees lapse pte ce! by sang (2a nn rn a cay ftigabity, svetng, and Is eed rte oor gen i hypo, eo "pedo to Itiction ofa sed capil ino en hea (Antes in mony vs eau hp nd neat in onraton oft peed mice of nantun rm lod enc ee Sol for exeaon he plan a (Adm inten lian ey cae vers st ages ta ene ny prepa te ype ae +The yan is fe he nrg ra ‘episode of vigorous cry nosis increases, dywonea, MBtlessness, ing respiration, in hypoxia Ue Toc mg en tin, (Rn Tepe ea oui sw set Ey ott nd sen iy te The ple sre lowe bY Beit Seren nny (edced pleas * a Asal ole akin appeor 0 bed TT } WAis Rao) LADY AO sto) AP eff LL ur 7. oe \ a — } | Drugs + Herphine (o2mp lly dare) = Fndal (o-F- -AwgityiQ) = prestia (0-0&- ot mic lty{un ) “iS « Tabpe he + patpat 3 Ais elbades 519 ty [torphite p tong 466 4 Area blo gases Hypoxia hyperapi, nd metabolic acidosis B © Management of hspsrsyantic spell A No consti cates Bouter = BeMteemen te fon sam nee est sion gang A Seton (opine SC, no moe han 02. 5. Sodium bicarbonate: TV conection of metab acidosis + rapid vesovery of pel once the ias retuned t9normal, B Bete-rensrzic blocker (propranolol 0.L-02-amgé-kg-IV) to relieve the spasm of ‘nfm, b obit ‘A, Drs tat increise the systemic vascular resistance as IV ghenepvine improve RV outlow, decrease the Rt4o-t shunt and his improve the symptoms (Selatan of tigers ai tes} tecomes parent by 121 of ee GiGRovil and developieNt? Mey maybe delayed in severe unre case. Delayed _ puberty occu in unoperated survivors. Hear HE fo sun lini presetaton of TOF. tft with mid deprees ‘FR outflow obstrston may intl present wit HP caused by a vesicular level Lo. Rishon. Pause: Normal © Venous and arterial presse: Noma, sy cuekal bly Left ator het: Kmay ale ferns Hover, te et is wnay noma ini, 1. Apia pulses topping (RV hypertrophy) and there isa sbstenaTRV impulse. > =) 7” 4. Asso til may be felt log the ef steal border (RY culow at ©.§|: Norma, Sz: Single (ue to closure of etic valve and the pulmonic epenet st) The murmur Ejection or ansstote murmieistining, loud in intensity, as in charter, !aximum tensity at lef 3° and 4 spaces (urtlence of blood over RY outiow tac). ‘comes less prominent or disappears when severe obstruction (ve se, Infeqenty selops) = berth L DIC = osdhat ~ Aape aalionvo—~ bronclospatm A ype g'y lini Guutges of 2A eve @ ME ae Ihe port howiblok 4- pul. embols So Se we verre } sy6F | Oreyil : ibm | ae f é | = kr vink | 29-4] Ce pecs arailemira s/t) DN pata | 25 > ar » A. atsence of ranch puimonary ary: Mos fen thee, tule supe: Tay spears ofthe pulmonary vse fle on the wo sie Osco of the Temhng pulmonary anery ding suger sly compromise aay ried pulmonary blood ow (Ac As ne of he otras maformatos he TOF can be sine wih CATCH 72 (oe bef). CATCH 22 ier pens with nial fue o be DSDerge sme the Sigrnas eostol syene (rma ee ple) DOHENY Typical configurasion (onus canine size, narrow base, concavity of the left border ofthe heart at res acai! by pulmonary artery rounded pial shadow with \\ 5) some levaion ofthe cardiac apex (RY hypsntapy (boot shoe Sh the cor: Largs aches to teh (neal of Ie) in 20% of ases. This cn be

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