URGENºE CARDIOVASCULARE LA COPILUL 0-1 AN

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REVISTA ROMN DE PEDIATRIE VOLUMUL LIX, NR. 4, AN 2010 249Adresa de coresponden:Dr. Georgiana Russu, Spitalul Clinic de Urgene pentru Copii Sf. Maria, Str. Vasile Lupu, Nr. 62, IaiURGENE CARDIOVASCULARE LA COPILUL 0-1 ANDr. A.G. Dimitriu1, Dr. Georgiana Russu21Universitatea de Medicin i Farmacie Gr. T. Popa, Iai2Spitalul Clinic de Urgene pentru Copii Sf. Maria, IaiREZUMAT Urgenele cardiovasculare survin adeseori la nou-nscut i sugar cu o inciden i severitate superioar acelora prezente la alte vrste, fi ind datorate n primul rnd anomaliilor cardiace congenitale, dar i unor afeciuni cardiace dobndite. La nou-nscut, malformaiile congenitale de cord cu manifestri de hipoxemie refractar i/sau de insufi cien cardio-circulatorie acut i manifestrile cardiace induse de suferina hipoxic perinatal pot avea un prognostic rezervat, ceea ce implic un diagnostic ct mai precoce i o terapie adecvat prompt. Probleme difi cile de diagnostic i tratament pot aprea i n insufi ciena cardiac congestiv, miocardit, tulburrile de ritm cardiac. Asemenea difi culti n managementul urgenelor cardiace ale primului an de via sunt amplifi cate cnd survin la un sugar la care afectarea cardiac nu era precizat anterior, situaie frecvent ntlnit n practic. Cuvinte cheie: nou-nscut, sugar, urgene cardiace, malformaii congenitale de cord, disritmii neonataleREFERATE GENERALE 3Copiii cu diferite afeciuni cardiovasculare pot fi internai n serviciile de urgen chiar de la natere, din primele zile de via sau i mai trziu n cursul primului an, ca urmare a unei afeciuni diagnosticate n perioada neonatal sau a unei afeciuni cardiace care, dei congenital, nu a fost nc diagnosticat. Primul an de via se caracterizeaz prin incidena i severitatea mult crescut a urgenelor survenite la nivelul diverselor sisteme i organe, comparativ cu alte vrste. Modifi crile hemodinamice care au loc postnatal, cu trecerea la circulaia de tip adult, au durat variabil, n general pn spre vrsta de 3 luni, mai ales n prezena unor anomalii structurale cardiace congenitale i pot favoriza manifestri severe neonatale de tipul detresei neonatale de origine cardiac.Manifestrile clinice de suferin cardiovascular pot fi remarcate chiar de la prima prezentare sau pot surveni ca o complicaie a unei boli diagnosticate anterior (1).DETRESE VITALE NEONATALE DE ETIOLOGIE CARDIAC n momentul naterii i ulterior n primele luni postnatal survin o serie de modifi cri fi ziologice cardiovasculare: dispariia circulaiei placentare; cre-terea debitului sanguin pulmonar prin scderea rezis tenelor vasculare pulmonare (ameliorarea oxi genrii sngelui); nchiderea canalului arterial; ocluzia foramen ovale; maturarea vascular pul-monar. n cazul existenei unor malformaii con-genitale cardi ace (MCC), pot surveni perturbri hemo-dinamice majore cu manifestri clinice dese-ori severe (2).Cardiopatii congenitale cu manifestri A. severe neonatale Hipoxemia refractar izolat. Diagnosticul 1. diferenial include alte cauze de cianoz la aceast vrst (3): hipoventilaie de origine nervos central, boli respiratorii, methemo-globinemie, aport insufi cient de O2, alte cauze: hipoglicemie, policitemie.Sindromul de insufi cien cardiocirculatorie. 2. Diagnosticul diferenial cuprinde: cord in-demn sau malformat (tipul malformaiei) (4), afectare pericardic, prezena i severitatea hipertensiunii arteriale pulmonare (HTAP).Sindromul de hipertensiune arterial pul-B. monar persistent (HTAPP) la nou-nscut Disritmii cardiace severeC. Miocardopatii neonatale de etiologie ische-D. mic, miocarditeREVISTA ROMN DE PEDIATRIE VOLUMUL LIX, NR. 4, AN 2010250Manifestrile clinice care orienteaz diagnosticul ctre o MCC la nou-nscut sau n primele luni de via sunt: difi culti de alimentaie (copilul pri-mete prea lent alimentaia, sau n cantitate insu-fi cient, prezint cianoz i transpiraii i/sau polip-nee n timpul alimentaiei, disfagie, tuse, vrsturi; tahipnee superfi cial constant (inclusiv n somn); stridor; sindrom de detres respiratorie; tahicardie sau bradicardie, alte tulburri de ritm; accese de cianoz sau tent cianotic generalizat; paloare, tegumente umede; extremiti reci, perfuzie cuta-nat diminuat; tulburri de comportament: apatie sau instabilitate.Cardiopatii congenitale cu manifestri se-A. ve re neonatale1. Hipoxemia refractar izolat. Semnul clinic major al acestei entiti este cianoza izolat, fr detres respiratorie sau insufi cien respiratorie, insensibil la testul de hiperoxie. Uneori copilul are stare general aparent foarte bun, iar auscultaia cordului nu deceleaz sufl uri patologice. n general, deteriorarea strii generale survine rapid n absena unei terapii medicale i mai ales chirurgicale pre-coce (4,7). Aspectul radiologic al cordului i circu-laiei pulmonare orienteaz diagnosticul (Tabelul 1).Alte cauze de cianoz la nou-nscut: metabolice (hipoglicemie, hipocalcemie); boala hemolitic a nou-nscutului, neurologice (asfi xia, hemoragia intracranian, meningite), tulburri neuromusculare (boala Werdnig-Hoffman); hipotermie, sepsis, me-the moglobinemie, depresie respiratorie secundar medicaiei materne (narcotice, sulfat de magneziu), obstrucia cilor respiratorii superioare (atrezie coa-nal, stenoz traheal, gu, sindrom Pierre Robin), policitemie, sindrom de hipervscozitate sanguin, oc neonatal, insufi cien cardiac congestiv seve-r; defecte congenitale: hernie diafragmatic, plmn hipoplastic, emfi zem lobar congenital, malformaie chistic adenomatoas pulmonar.Tratament: atrioseptostomie Rashkind (transpo-ziia de vase mari), meninerea deschis a canalului arterial (prin perfuzare de prostaglandin E1 n cardiopatiile ductodependente: atrezie tricuspidian cu sept interventricular intact, atrezie tricuspidian cu defect septal ventricular i atrezie pulmonar. atrezie pulmonar (sau stenoz pulmonar sever) cu sept interventricular intact; sindromul cordului stng hipoplazic (atrezie mitral i atrezie de aort cu ventricul stng virtual) transpoziie de vase mari cu sept in-terventricular intact; cateterism interven-ional-valvuloplastie pulmonar n stenoze pulmonare severe (5).2. Sindromul de insufi cien cardiocirculatorie determin, n general, agravare rapid a strii ge-nerale i chiar evoluie spre deces. Tabloul clinic const n manifestri respiratorii edem pulmonar acut i/sau acidoz: tahipnee postprandial sau per-manent, detres respiratorie important, care de-ter min epuizarea nou-nscutului, hepatomegalie, tahicardie, asurzirea zgomotelor cardiace, zgomot de galop, deseori semne de colaps periferic tent palid cenuie, extremiti reci, cianotice/marmorate, puls periferic tahicardic, fi liform sau neperceptibil, alungirea timpului de recolorare capilar, hipoten-siune arterial, oligoanurie, cianoz (cel mai adesea redus, se amelioreaz prin administrarea de oxi-gen) (7). 90% dintre cazurile de insufi cien car-diac la copii apar n primul an de via, etiologia princi pal fi ind reprezentat de MCC (Tabelul 2).n afara simptomatologiei cardiace, exist di-ferite semne i simptome care orienteaz diag-nosticul la nou-nscutul i sugarul cu insufi cien cardiac (7,8) (Tabelul 3).TABELUL 1. Elemente de orientare n hipoxemia refractar la nou-nscut (1,2,4,7)Aspectul circulaiei pulmonare Aspectul cordului Cardiopatia congenitalVascularizaie pulmonar crescut sau normalCord de volum iniial normal, aspect ovoid, n timp cardiomegalieTMV cu sept inerventricular intactStaz venoas pulmonar Cord mic ntoarcere venoas pulmonar anormal total blocatVascularizaie pulmonar sracCord normal Atrezie pulmonar+DSVCord n sabot Tetralogia FallotCord n sabot Atrezie tricuspid (EKG: axa QRS=-30, suprancrcare VS)Cardiopatii complexe cu atrezie pulmonarCardiomegalie moderat (ICT=0,60-0,65)Atrezie sau stenoz sever pulmonar cu SIV intact (EKG: axaQRS=+60-120, suprancrcare VD, unde P ample)Insufi cien tricuspidianCardiomegalie important (ICT>0,75)Anomalie Ebstein (EKG: QRS mici, bloc ram drept, tulburri de ritm sau conducere)REVISTA ROMN DE PEDIATRIE VOLUMUL LIX, NR. 4, AN 2010 251Tratament: diuretice, inotropice pozitive (digo-xin, dopamin, dobutamin), oxigenoterapie, ven-tila ie asistat n cazurile severe, corecia tulburrilor metabolice care pot agrava asistolia acut (acidoz, hipoglicemie), terapia farmacologic de nchidere a canalului arterial cu unt important (fenilbutazona), obstruciile stngi severe (coarctaia de aort) duc-to dependente (perfuzie cu PGE1), terapie medica-mentoas a tahiaritmiilor, pacemaker pentru bradi-aritmii severe (bloc a.v. grad III congenital), tra ta ment chirurgical sau cardiologie intervenional (8).Cauze particulare de insufi cien cardiac la nou-nscut (n afara MCC) sunt (2): asfi xia la natere, hipoxie, hipoglicemie, hipocalcemie, ane-mie, acidoz, sepsis. Cardiomiopatia postasfi xic este o entitate defi -nit clinic prin hipotensiune arterial, tahicardie, ra luri de staz pulmonar, hepatomegalie, sufl u sistolic de insufi cien mitral sau/i tricuspidian, galop, accentuarea zgomotului II n focarul pulmo-narei. Paraclinic, EKG relev modifi cri ale seg-mentului ST/unde T de tip ischemie, creterea fraciunii MB a CPK, radiologic staz pulmonar i cardiomegalie, i creterea PVC. Ecocardiografi a Doppler deceleaz insufi cien tricuspidian, sc-derea fraciei de scurtare i de ejecie a ventriculului stng, prelungirea intervalelor de timp sistolic, disfuncie diastolic a ventriculului stng. Anomalii metabolice asociate: acidoz metabolic, hipoxemie, hipoglicemie, hipocalcemie, policitemie. Tratament: TABELUL 2. MCC complicate cu insufi cien cardiac n funcie de vrst (adaptat dup 7, 8, 9) Vrsta Malformaia congenital de cordNou-nscut Stenoz aortic, insufi cien pulmonar sau tricuspidian severe, tetralogie Fallot cu absena valvei pulmonare Primele 7 zile de viaStenoz aortic critic, sindromul cordului stng hipoplazic, ntoarcere venoas pulmonar anormal total, trunchi arterial comun2-8 sptmni Tetralogie Fallot noncianotic, canal atrioventricular, coarctaie de aort, canal arterial persistent, defect septal ventricular2-6 luni Anomalie de origine a coronarei stngi, canal arterial persistent, defect septal ventricularTABELUL 3. Elemente de diagnostic n MCC la nou-nscutul i sugarul cu insufi cien cardiacAspectul cordului Alte manifestri orientative MCCCardiomegalie (ICT=0,60-0,70)Sufl u sistolic; ECG HVS; colaps precoce Stenoz aortic valvular medie/severDiferen de puls i TA n favoarea membrelor superioareCoarctaie de aort izolatInsufi cien cardiac precoce i diferen de pulsSindrom de coarctaieECG: deviaie axial stng (-90 -120) Canal atrioventricular completSufl u sistolo-diastolic, puls amplu Canal arterial larg permeabil (prematur)Sufl u sistolic i adesea diastolic, puls amplu, cianoz moderatTrunchi arterial comunSufl uri diverse/fr sufl u Ventricul unicCardiomegalie important (ICT>0,75)Puls carotidian sltre, sufl u continuu (cele cerebrale)Fistule arteriovenoase sistemice (cerebrale, hepatice, periferice, angiom placentar)Infecie septicemic Pericardite purulente (rar serofi brinoase idiopatice sau chilopericard)Semne evocatoare pentru scleroza tuberoas BournevilleTumori-rabdomioameContext familial (diabet), hipoxie la natere Cardiomiopatii (diabetice, metabolice, ischemice)Clinic i ECG FC>220/min Tahicardii heterotopeCord mrime variabil Ecografi e fetal: anasarc fetoplacentar Tahicardie fetal, fl utter atrialClinic i ECG FCREVISTA ROMN DE PEDIATRIE VOLUMUL LIX, NR. 4, AN 2010252pruden prin perfuzie cu dopamin n doze mai mari 15-20 g/kg/minut, doze la care se menine i efectul ei inotrop pozitiv. Meninerea hipotensiunii arteriale se face cu epinefrin 0,05-0,5 g/kg/minut perfuzie intravenoas (4).Un aspect frecvent ntlnit n practica curent este prezentarea la serviciul de urgen a unui sugar cu simptomatologie nespecifi c, fr antecedente cunoscute de cardiopatie. Afeciunile cardiace cu manifestri severe la nou-nscut i sugar i care se adreseaz cel mai frecvent la serviciul de urgene pentru copii pot fi mprite n: boli cardiace con-genitale structurale; aritmiile cardiace; boli cardiace dobndite miocardita. Clasifi carea MCC n funcie de modifi crile fi ziopatologice induse de anomaliile structurale:MCC cu cianoz; MCC cu obstrucie a ejeciei VS sau in su- fi ciena funcional a VS care prezint semne de oc datorit scderii fl uxului de snge sis-te mic; anomalia de origine a coronarei stngi, care poate prezenta infarct miocardic i oc; insufi ciena cardiac congestiv.MCC cianogene Leziunile cele mai frecvente care determin cianoz includ: atrezie pulmonar sau stenoz pul-monar sever, tetralogie Fallot forma cianotic, retur venos pulmonar total aberant, transpoziia de vase mari, atrezia de tricuspid, trunchi arterial comun (2, 3). De obicei aceti copii sunt diagnosticai la natere sau imediat nainte de externarea din maternitate, dar pot fi externai i nediagnosticai, iar canalul arterial permeabil poate avea un ase-menea debit, nct ofer sufi cient fl ux de snge pentru circulaia pulmonar, permind meninerea unui nivel relativ ridicat de oxigenare pentru circulaia sistemic i astfel mascheaz leziunile, iar hipoxia nu este evident clinic. n cele din urm, atunci cnd canalul arterial se nchide, urmeaz o scdere a fl uxului de snge pulmonar, iar aceti copii devin acut hipoxici. Acest lucru se produce, n general n primele 2 sptmni de via, dar i mai trziu. Cianoza poate fi neobservat la examenul fi zic (copii cu anemie sau tegumente hiperpigmentate). Pulsoximetria este difi cil de efectuat sau rezultatele pot fi modifi cate la un copil agitat sau cu detres, sau la care circulaia periferic este compromis din cauza acidozei. Dac instalarea cianozei nu este surprins la timp, aceasta fi ind un indicator fi del pentru prezena hipoxemiei, copilul poate fi n oc sau se instaleaz insufi cien multiorganic.Pentru cianoza central, testul de hiperoxie este esenial n cadrul diagnosticului diferenial etiologic al cianozei (cauze cardiace sau extracardiace) (8). (Fi O2100% 5-10 minute). Atenie! creterea PaO2 poate induce nchiderea canalului arterial, de aceea este necesar monitorizare clinic i ecocardiogra-fi c, fi ind periculoas n cardiopatiile ductodepen-dente. Radiografi a cardiotoracic poate releva mai multe aspecte: creterea fl uxului pulmonar n trans-poziia marilor vase, retur venos pulmonar anormal parial, trunchi arterial comun; scderea fl uxului pulmonar n atrezia de tricuspid cu sept intact, atrezia arterei pulmonare cu sept intact, tetralogie Fallot, anomalie Ebstein, stenoz pulmonar critic cu sept interventricular intact; staz venoas pul-monar n returul venos pulmonar anormal total, cord stng hipoplazic. Pentru diagnostic este esen-ial efectuarea EKG i ecocardiografi ei. La nou-nscut i la sugarul de vrst mic la care intensifi carea cianozei s-a datorat nchiderii canalului arterial, dup stabilizarea iniial cu per-meabilizarea cilor aeriene i asigurarea respiraiei (uneori prin intubaie), care poate rezolva hipoxia i detresa respiratorie sever, se pune problema redeschiderii canalului arterial-perfuzii cu pros-taglandina E1 (PGE1), concomitent cu terapia o-cului. n acest moment, devine obligatorie solicitarea unui cardiolog pediatru ct mai curnd posibil pentru diagnostic defi nitiv i stabilirea indicaiilor n continuare. Dac situaia pacientului o permite, se impune transferul pacientului ntr-un serviciu cu terapie intensiv cardiologic i posibiliti de in-tervenie chirurgical paleativ sau reparatorie (8).Leziuni cu obstrucia tractului de ejecie al VS i insufi cien ventricularAceste tipuri de MCC constituie alte leziuni ductodependente pentru circulaia sistemic: coarc-taia de aort i stenoza aortic sever. n majoritatea cazurilor cordul stng hipoplazic, de asemenea TABELUL 4. Elemente de difereniere ntre cianoza central (buze, limb, mucoase) i periferic (perioral, mini, picioare = acrocianoza)Periferic (acrocianoz)Elemente de urmrireCentralRoz culoare: mucoase, limb, buze, trunchialbastrReci extremiti calde reciSczut perfuzie periferic normal sczutNormal PaO2, SaO2 sczutDe obicei mai favorabil (sepsis, oc, MCC)prognostic necesit de obicei tratament de urgen (pulmonar, MCC, oc, sepsis)REVISTA ROMN DE PEDIATRIE VOLUMUL LIX, NR. 4, AN 2010 253ductodependent, are o evoluie mult mai rapid, cu agravarea strii generale i oc neonatal, impunnd intervenie chirurgical precoce, n absena creia evoluia este total nefavorabil. nchiderea canalului arterial la aceste leziuni obstructive VS este urmat rapid de hipoperfuzie sistemic, oc i insufi cien cardiac, uneori cu semne nespecifi ce: iritabilitate, letargie, marmorare a tegumentelor care sunt reci, mai ales la extremiti. Recunoterea faptului c instalarea ocului este datorat nchiderii canalului arterial este esenial pentru indicaia de perfuzii cu PGE1. Pacienii cu scderea perfuziei periferice evolueaz rapid spre acidoz metabolic sever i disfuncie organic multipl. n afara administrrii de perfuzii cu PGE1, terapia inotrop, soluia de bicarbonat de sodiu i medicaia de scdere a rezis-tenei vasculare sistemice pot fi utile pn la re-zolvarea chirurgical sau prin cateterism interven-ional (9,10).Anomaliile de origine ale arterelor coronare i infarctul de miocard Infarctul de miocard este excepional la sugar, fi ind cel mai adesea datorat anomaliei coronarei stngi, care are originea n artera pulmonar. Ische-mia miocardic iniial este intermitent, survenind la un efort de tipul alimentaiei sau a plnsului i apare n primele sptmni postnatal (ntre 2 sp-tmni i 6 luni). Simptomatologia nu este spe ci-fi c: episoade recurente de nelinite, iritabilitate, plns nencetat, i dispneea, deseori asociat cu paloare i transpiraii, care survin cel mai adesea n cursul alimentaiei. Creterea consumului de oxigen n miocard prin afeciuni intercurente, de exemplu pulmonare, poate precipita infarctul de miocard la nivelul VS i concomitent insufi ciena cardiac: tahipnee, tahicardie, ritm de galop, cardiomegalie, hepatomegalie, un sufl u de insufi cien mitral, alteori sugarul prezint o respiraie uiertoare gre-it interpretat adesea ca fi ind o broniolit (7,11). Investigaii recomandate: radiografi a tora cic rele-v cardiomegalie cu edem pulmonar interstiial; ECG clasic arat unde Q anormale n DI, AVL, precum i V4-V6, precum i supradenivelarea seg-mentului ST n derivaiile V4 V6, leziuni de infarct antero-lateral; ecocardiografi a confi rm ori-gi nea anormal a unei artere coronare, Dopplerul color arat fl uxul de snge care trece din artera coronar n artera pulmonar, insufi ciena mitral este variabil; mai pot fi observate scderea funciei cardiace, i anomalii de kinetic regionale ale pe-reilor ventriculului stng. Diagnosticul diferenial se face cu cardiomiopatia dilatativ.Cateterismul cardiac are un grad ridicat de risc la aceti pacieni, fi ind necesar doar atunci cnd diagnosticul ecocardiografi c nu este cert. Trata-men tul este chirurgical. Peste 80% dintre sugarii cu aceast anomalie dezvolt simptome de afectare cardiace n copilrie, i aproximativ 65- 85% mor nainte de vrsta de 1 an dac nu se intervine chirurgical. Pacienii diagnosticai dup vrsta de 1 an dezvolt colaterale pentru circulaia coronarian. La copil, infarctul de miocard, foarte rar, poate surveni n: alte anomalii congenitale ale arterelor coronare, boala Kawasaki, cardiomiopatia hiper-trofi c, postoperator n MCC etc.Cardiomiopatii neonatale de etiologie ischemic (ischemie miocardic tranzitorie)Sunt consecina afectrii cardiace de ctre hi-poxia perinatal. Deseori manifestrile clinice sunt severe n primele zile postnatal, dar sunt posibile manifestri clinice tardive, chiar dup externarea din maternitate. Asfi xia fetal i neonatal determin suferin miocardic, infarct i deces, cardiomiopatie dilatativ aparent idiopatic relevat la sugar. Majoritatea au evoluie spontan favorabil. Clinic, aceti copii prezint cianoz i semne de insufi cien cardiac. EKG relev hipertrofi e atrial i ventri-cular dreapt, subdenivelare ST i inversarea undelor T n precordialele stngi. Radiografi a car-dio toracic deceleaz cardiomegalie cu vascula-rizaie pulmonar normal. Ecocardiografi a vizua-lizeaz insufi cien tricuspidian, dilatarea atriului drept i unt dreapta-stnga prin foramen ovale. Majoritatea cazurilor prezint ameliorare n cteva zile sptmni (1,2). Incompetena miocardic tranzitorieClinic, simptomele sunt manifeste imediat de la natere sau apar n maxim 24 ore: detres respi-ratorie, cianoz, insufi cien cardiocirculatorie cu colaps. EKG deceleaz tulburri difuze de repo-larizare ventricular tip ischemie. Radiologic se observ cardiomegalie, staz interstiial i venoas pulmonar, aspect de edem pulmonar. Ecocar di-ografi a exclude alt cardiopatie congenital sau cardiomiopatie hipokinetic dilatat. Tratament: oxigenoterapie (ventilaie asistat), digoxin, izo-pro terenol, dopamin i dobutamin, diure tice.Evoluia este favorabil n majoritatea cazurilor, dar apar i decese.MiocarditaEtiologia cea mai frecvent la sugari este viral: enterovirusurile, inclusiv Coxsackie tip B, i ade-novirusurile. Debutul este adesea nespecifi c, frecvent REVISTA ROMN DE PEDIATRIE VOLUMUL LIX, NR. 4, AN 2010254n anamnez se deceleaz boli virale infecii ale cilor respiratorii superioare sau gastroenterit. Sugarii pot prezenta iniial simptome nespecifi ce atribuite infeciei virale (letargie, iritabilitate, di-fi culti de alimentaie, paloare), sau pot fi diag-nosticai greit ca broniolit, deshidratare acut sau sepsis. Deseori pot fi prezente simptome de insufi cien cardiac: diaforez sau tahipnee, sau aritmii care nu sunt rare. La nou-nscut, debutul poate fi mai brutal, cu agravarea rapid a strii generale, colaps i chiar moarte subit. Radiologic se constat cardiomegalie, EKG poate arta tahi-cardie sinusal, aritmii, sau microvoltaj QRS. Eco-cardiografi a Doppler vizualizeaz dilatarea ven-triculului stng, disfuncie a contractilitii coronare cu aspect i origine normal, permind diferenierea de anomalia de origine a coronarei stngi (12). Diagnosticul diferenial al etiologiei insufi cienei cardiace ntre miocardita acut, cardiomiopatia dilatat sau leziunile ischemice miocardice se reali-zeaz prin dozarea enzimelor cardiace troponina I i fraciunea MB a fosfocreatinkinazei, dar diag-nosticul de certitudine l stabilete biopsia endo-miocardic.Terapia suportiv respiratorie i cardiac este pe primul plan, intubaia este necesar pentru cei n stare de oc cardiogen. Suportul inotrop i de redu-cere a postsarcinii trebuie iniiat de la nceput dac sunt suportate de pacient. n cazurile deosebit de grave, cnd tratamentul inotrop nu mai este efi cient, ECMO poate contribui la ameliorarea prognosticului. Dozele mari de imunoglobuline intravenos i terapia imunosupresiv, cu rezultate ncurajatoare la aduli nu au aceeai efi cacitate i la copil. TULBURRI DE RITM I DE CONDUCERE SEVERE LA NOU-NSCUT Majoritatea aritmiilor cardiace decelate la nou-nscut i sugar sunt benigne: aritmia sinusal, tahi-cardia i bradicardia sinusal, blocul atrioventricular grad I i grad II tip Mobitz I, extrasistolia atrial, joncional sau ventricular nesistematizat, mono-top i cu o frecven 200 bti/min (180-350/min); interval R-R fi x i regulat; modifi cri minore ale frecvenei cordului la efort (plns, alimentaie, apnee). TPSV poate ap rea sau disprea brusc spontan sau prin tratament, care poate induce trecerea brusc n ritm sinusal, cu scderea brutal a alurii ventriculare la aceea co-respunztoare vrstei sau meninerea la valori ri-dicate ridicate i fi xe (legea totul sau nimic), mai ales n cazul reintrrii. Complexele QRS pot fi : nguste, cel mai frecvent, cu sau fr fenomen T+P, cu sau fr unda P prezent; largi (bloc de ramur preexistent/dependent de frecven/sindrom de pre-excitaie ventricular), cnd se impune diferenierea de tahicardia ventricular. Tratamentul depinde de starea clinic a nou-nscutului sau sugarului (1,2,3 7): instabilitatea hemodinamic impune cardio-versie electric 0,5-2 J/kg; dac sugarul este stabil hemodi namic, se ncearc manevre vagale: pung cu ghea aplicat pe fa. Tratamentul farmacologic const n: adenozin bolus i.v. 0,05 mg/kg, repetat la 1-2 min, 3 administrri, dublnd doza; dac devine in stabil hemodinamic: cardioversie electric 0, 5 2 J/kg (5,6); digoxin intravenos (nu n sindroamele de preexcitaie ventricular); propranolol intrave-nos, sotalol, amiodaron (efecte adverse). Verapami-lul este contraindicat sub vrsta de un an datorit ris cului de colaps cardiovascular. Profi laxia recuren-elor se face cu digoxin (excepie)/propranolol timp de un an. Lipsa de rspuns la antiaritmice impune explorare electrofi ziologic i ablaia prin radiofrec-ven a cii accesorii (13).BRADIARTMII NEONATALE SEVERE La nou-nscut i ulterior la sugar bradiaritmiile pot avea mecanisme de producere diferite: tulburri n formarea impulsului (bradicardia sinusal, pauza sinusal, blocul sinoatrial de ieire, ritmul ectopic lent, sindromul tahicardie-bradicardie-boala nodu-lului sinusal), sau tulburri n conducerea atrioven-tricular-bloc atrio-ventricular (BAV) grad I, II, III.REVISTA ROMN DE PEDIATRIE VOLUMUL LIX, NR. 4, AN 2010 255BAV GRADUL II TIP MOBITZ IIPoate aprea la nou-nscut: cu cord normal; din mam cu LES i poate progresa spre BAV complet; postchirurgie cardiac. Poate fi 2:1, 3:1, 4:1 i poate progresa spre BAV complet, se poate asocia cu tulburri de conducere intraventriculare (QRS largi). Tratament: nou-nscutul neoperat, cu BAV gr.II Mobitz II i QRS fi ne, cu morfologie normal, la care impulsurile sunt blocate ocazional iar ritmul ventricular de scpare nu este foarte lent va fi monitorizat, existnd riscul evoluiei spre BAV gr. III, care necesit pacemaker implantabil; nou-ns-cutul cu bloc susinut i conducere intraventricular ntrziat (QRS largi) are risc crescut de moarte subit, de aceea necesit pacemaker; nou-nscuii cu BAV gr. II Mobitz II postchirurgie cardiac, cu bloc persistent i ritm ventricular de scpare lent pot benefi cia de pacemaker implantabil. BAV GRADUL III (COMPLET)Debutul afeciunii este aproape ntotdeauna intrauterin (raportat nc din sptmna 17 de gestaie). Etiologie: BAV complet asociat cu defecte structurale cardiace (25-30% din cazuri) (TVM corectat, CAV cu izomerism atrial stng); nou-nscut din mame cu LES (strns legtur ntre nivelul crescut de autoanticorpi materni i prezena BAV complet la nou-nscut), boli infecioase (dif-terie, oreion); cord normal structural tulburare primar a sistemului de conducere. Diagnostic: la ft bradicardia fetal 55/ min; REVISTA ROMN DE PEDIATRIE VOLUMUL LIX, NR. 4, AN 2010256Cardiovascular emergencies in 0-1-year-old childrenA.G. Dimitriu1, Georgiana Russu21Gr. T. Popa University of Medicine and Pharmacy, Iasi, Romania 2St. Mary Children Hospital, Pediatric Clinic I, Iasi, Romania ABSTRACT Cardiovascular emergencies occur in newborn and child more frequent than in other ages, becuase of some congenital cardiac malformations, but also due to other aquired heart conditions. In newborn, congenital cardiac heart defects with refractory hypoxemia and/or acute heart failure and those determined by hypoxic perinatal suffering have a reserved prognosis, which impose an early diagnosis and therapy. Diffi cult problems of diagnosis and treatment can occur also in congestive heart failure, miocarditis, arrhythmias. Such diffi culties in the management of cardiac emergencies in the fi rst year of life are amplifi ed if the heart condition was unknown, as frequently is encountered in the clinical practice.Key words: newborn, infant, cardiac emergencies, congenital heart disease, dysrrhythmiasChildren with various cardiovascular diseases can be admitted in the emergency departments di-rectly from birth, from the fi rst days of life or later during the fi rst year of life, due to a condition diag-nosed in the neonatal period or to a cardiac disease which is congenital but still undiagnosed. The fi rst year of life is characterized by the high incidence and severity of the emergencies of various organs, compared to other ages. The postnatal hemodynamic changes to the adult type circulation last about 3 months, especially when associated with congenital structural defects and can determine severe neonatal problems, like neonatal distress of cardiac origin.Clinical manifestations of cardiovascular suffer-ing can be observed from the fi rst admission or can occur like a complication of a previously diagnosed disease (1). NEONATAL LIFE THREATENING DISTRESS OF CARDIAC ORIGINIn the moment of birth and then during the fi rst months of life there are some physiologic cardio-vascular changes: disappearance of placental circu-lation, increasing pulmonary blood fl ow by de-creasing pulmonary vascular resistance (alleviation of blood oxygenation), occlusion of ductus arterio-sus and foramen ovale, maturation of pulmonary vessels. A congenital heart defect can determine hemodynamic events during these events, with se-vere clinical manifestions (2).Congenital heart defects with severe A. neonatal manifestations Isolated refractory hypoxemia. The differential 1. diagnosis includes other causes of cyanosis at this age (3): hypoventilation of central origin, respiratory disorders, met hemo glo-binemia, abnormal oxygen supply, hypo-glycemia, polycytemia. The syndrome of cardiocirculatory in suf-2. fi ciency. The differential diagnosis in cludes: normal or malformed heart (4), per i cardial disease, pulmonary arterial hyper tension. Persistent pulmonary hypertension in B. newborn Severe cardiac dysrrhythmia C. Neonatal cardiomyopathies of ischemic D. origin, myocarditisThe clinical picture that suggests a congenital heart defect in newborn or in the fi rst months of life are: feeding problems (the child is receiving the milk too slow or cannot eat the entire quantity, has cyanosis or sweating or dyspnea while eating), presents cough, vomiting, constant superfi cial tac-hypnea (during sleep), stridor, respiratory distress syndrome, tachycardia or bradycardia, cyanosis in crisis or generalized, pallor, wet skin, cold extremi-ties, diminished cutaneous perfusion, agitation or instability. Congenital heart defects with severe A. neonatal manifestations1. Isolated refractory hypoxemia. The major clinical sign is the isolated cyanosis, without respi-ratory failure, without response to oxygen adminis-tration. Sometimes the child is apparently well, and the auscultation of the heart is in normal limits, without murmurs. But the degradation occurs rap-idly without medical and/or surgical treatment (4, 7). The x-Ray aspect of the heart and pulmonary circulation suggest the diagnosis (Table 1).REVISTA ROMN DE PEDIATRIE VOLUMUL LIX, NR. 4, AN 2010 257Other causes of cyanosis in newborn: metabolic (hypoglycemia, hypocalcemia), hemolytic disease, neurologic problems (asphyxia, intracranial hem-orrhage, meningitis), neuromuscular disorders (Werdnig-Hoffman disease), hypothermia, sepsis, methemoglobinemia, respiratory distress due to maternal medication (narcotics, magnesium sul-phate), upper airways obstruction (choanal atresia, tracheal stenosis, Pierre Robin syndrome), poly-cytemia, neonatal shock, severe heart failure, con-genital defects (diaphragmatic hernia, hypoplastic lung, congenital lobar emphysema, pulmonary cys-tic adenomatous malformation).Treatment: Rashkind atrioseptostomy (transpo-sition of great vessels with intact ventricular sep-tum), maintenance of ductus arteriosus patency with intravenous prostaglandin E1 (tricuspid atre-sia with intact ventricular septum, tricuspid atresia with ventricular septal defect and pulmonary atre-sia, pulmonary atresia with intact ventricular sep-tum, hypoplastic left heart syndrome); interven-tional catheterism (pulmonary valvuloplasty in severe pulmonary stenosis) (5).2. The syndrome of cardiocirculatory insuffi -ciency determines rapid aggravation and even death of the patient. The clinical picture consists in respi-ratory manifestations acute pulmonary edema and/or acidosis: effort or permanent tachypnea, se-vere respiratory distress leading to exhaustion of the newborn, hepatomegaly, tachycardia, gallop sounds, peripheral hypoperfusion: pallor, cold and cyanotic extremities, weak pulse, increased capil-lary refi ll time, arterial hypotension, oliguria or anuria, cyanosis alleviated by oxygen administra-tion (7). 90% of the cases of heart failure in chil-dren occur in the fi rst year of life and the main cause is a congenital heart defect (Table 2).There are also other signs and symptoms that suggest the diagnosis in the newborn and infant with heart failure (7, 8) (Table 3).Treatment: diuretics, positive inotropic drugs (digoxin, dopamine, dobutamine), oxygen, me-chanical ventilation in severe cases, correction of metabolic inbalance that can aggravate bradycardia (acidosis, hypoglycemia), drug occlusion of patent ductus arteriosus with important shunt (fenilbuta-sone), severe left obstructions (coarctation of the aorta) ductal dependent (prostaglandin E1), drug treatment of tachyarrhythmias, pacemaker for bra-dyarrhythmias. Particular causes of heart failure in newborn (except congenital heart defects) are: birth asphyx-ia, hypoxia, hypoglycemia, hypocalcemia, anemia, acidosis, sepsis (2).Hypoxic cardiomyopathy is an entity manifested by arterial hypotension, tachycardia, rales of pul-monary stasis, hepatomegaly, systolic murmur of mitral and/or tricuspid regurgitation, gallop, and loud second sound in the pulmonary area. ECG re-veals ST changes or T waves of ischemic type, in-creased MB fraction of CPK, x-Ray pulmonary congestion and cardiomegaly, and also increased central venous pressure. Doppler echocardiography shows tricuspid regurgitation, decreased shortening and ejection fraction of the left ventricle, prolonged TABLE 1. Orientation elements for refractory hypoxemia in newborn (1, 2, 4, 7)Pulmonary vessels aspect Heart shape Congenital heart defectIncreased or normal pulmonary vascularizationNormal ovoid heart, then cardiomegalyTransposition of the great arteries with intact ventricular septumPulmonary venous congestion Small heart Total anomalous pulmonary venous return Poor pulmonary circulation Normal heart Pulmonary atresia + ventricular septal defectBoot-shaped heart Tetralogy of FallotBoot-shaped heart Tricuspid atresia (ECG: left axis, left ventricular overload)Complex congenital heart defects with pulmonary atresiaModerate cardiomegaly (cardiothoracic index=0.60 0.65)Pulmonary atresia or severe stenosis with intact ventricular septum (ECG: right axis deviation, right ventricular overload, tall P waves)Severe cardiomegaly (cardiothoracic index>0.75)Ebstein anomaly (ECG: small QRS complexes, right bundle branch block, rhythm or conductance abnormalities)TABLE 2. Congenital heart defects with heart failure (adapted after 7, 8, 9)Age Congenital heart defectNewborn Aortic stenosis, severe pulmonary or tricuspid regurgitation, tetralogy of Fallot with absent pulmonary valveFirst 7 days of lifeCritical aortic stenosis, hypoplastic left heart syndrome, abnormal total pulmonary venous return, truncus arteriosus2-8 weeks Noncyanotic tetralogy of Fallot, atrioventricular septal defect, aortic coarctation, persistent ductus arteriosus, ventricular septal defect2-6 months Anomalous left coronary artery from the pulmonary artery, persistent ductus arteriosus, ventricular septal defect REVISTA ROMN DE PEDIATRIE VOLUMUL LIX, NR. 4, AN 2010258systolic times, diastolic dysfunction of the left ven-tricle. Associated metabolic abnormalities are: met-abolic acidosis, hypoxemia, hypoglycemia, hy-pocalcemia, polycitemia. Treatment. Arterial hypotension is the conse-quence of the direct depressing effect of hypoxia on myocardial contractility associated with the de-creased systemic vascular resistance by decreasing arteriolar tone, so it is not a real hypovolemia, this is why volemic resuscitation will use bolus crystal-loid solutions, monitored by central venous pres-sure because of the risk of heart failure occurrence. Positive inotropic drugs will be given, such as dop-amine 2-4g/kg/min and dobutamine 5-20g/kg/min. Digoxin is contraindicated in the newborn of diabetic mother because of the myocardial hyper-trophy, mostly septal. Systemic vascular resistance will be carefully augmented with high doses of in-travenous dopamine 15-20g/kg/min (4). A frequently encountered situation is the presen-tation at the ER of an infant with nonspecifi c symp-toms, without any known cardiac conditions. The cardiac diseases with severe manifestations in new-born and infant that are most frequently addressing to the ER are: congenital heart defects, cardiac ar-rhythmias, acquired heart disorders myocarditis. Classifi cation of congenital heart defects de-pending on physiopathologic changes induced by the structural anomalies is:Congenital heart defects with cyanosis Congenital heart defects with obstruction of left ventricular ejection tract or functional insuffi ciency of the left ventricle, with signs of shock induced by the decreased systemic blood fl ow Anomalous left coronary artery origin from pulmonary artery, which can present myo-cardial infarction and shock Congestive heart failure Cyanotic congenital heart defects The most encountered lesions with cyanosis in-clude: pulmonary atresia or severe stenosis, tetral-ogy of Fallot, total anomalous venous return, trans-position of the great vessels, tricuspid atresia, truncus arteriosus (2,3). Usually, these children are diagnosed at birth or immediately after discharge, but can be sent home without diagnosis, and the patent ductus arteriosus can has such a fl ow that offer suffi cient blood for the pulmonary circulation, and thus can mask the true lesion and the hypoxia is not clinically evident. Finally, when the ductus closes, the pulmonary blood fl ow decreases and the patient becomes acutely hypoxic. This happens during the fi rst two weeks of life but also later.The cyanosis can be missed in children with anemia or hyperpigmentation of the skin. Blood pres-sure of oxygen is diffi cult to perform or can give er-rors in an agitated child or a child with depression or in which the peripheral circulation is compromised due to the acidosis. If the acidosis is not early detected, as an indicator of hypoxemia, the child can develop shock and/or multiple organs failure. For the central cyanosis, the hyperoxia test is es-sential in the differential diagnosis of cyanosis (8). TABLE 3. Diagnostic fi ndings in the children with congenital heart defectsHeart appearance Other suggestive manifestations Congenital heart defectCardiomegaly (cardiac index=0,60-0,70)Systolic murmur; ECG left ventricle hypertrophy; early colapseMedium/severe aortic valvar stenosisPulse and blood pressure difference between arms and legsIsolated coarctation of the aortaEarly heart failure and pulse difference Coarctation syndromeECG: left axial deviation (-90 -120) Complete atrioventricular septal defectContinuous murmur, high amplitude peripheral pulse Large patent ductus arteriosus (in the premature baby)Systolic and often diastolic murmur, moderate cyanosis Truncus arteriosusVarious murmurs or no murmur Single ventricleSevere cardiomegaly(cardiac index>0,75)High amplitude of carotidian pulse, continuous murmur (the cerebral ones)Systemic arteriovenous fi stula (cerebral, hepatic, peripheral)Sepsis Purulent pericarditisSigns for tuberous sclerosis Tumors rabdomiomasFamilial history (diabetes), birth hypoxia Cardiomyopathies (diabetic, metabolic, ischemic) Clinic and ECG heart rhythm>220 beats/min Heterotopic tachycardiaVariable size of the heartFetal and placental anasarca Fetal tachycardia, atrial fl utterClinical and ECG heart failureREVISTA ROMN DE PEDIATRIE VOLUMUL LIX, NR. 4, AN 2010 259Increased arterial oxygen pressure can induce the closure of ductus arteriosus, this is why the clinical and echocardiographical monitorisation is required (dangerous for the ductus-dependent heart defects). The chest x-Ray can reveal different aspects: in-creased pulmonary blood fl ow in transposition of the great arteries, partial anomalous pulmonary venous return, truncus arteriosus; decreased pulmonary blood fl ow in tricuspid atresia with intact interven-tricular septum, pulmonary artery atresia with intact interventricular septum, tetralogy of Fallot, Ebstein anomaly, critical pulmonary stenosis with intact in-terventricular septum; pulmonary venous stasis in total anomalous pulmonary venous return, hypoplas-tic left ventricle. Electrocardiogram and echocar-diography are main tools for the diagnosis.In newborn and small infant in which the cyano-sis is aggravated by the ductus closure, after per-meabilisation of the respiratory tract and mechani-cal ventilation, if necessary, which can alleviate the hypoxia and severe respiratory depression, prosta-glandin E1 can be administered in order to reopen the ductus parallel to treatment of the shock. At this moment the child must be transferred in an ICU with cardiac surgery clinic (8). Defects with obstruction of the left ventricle and ventricular failure.These types of congenital heart defects repre-sent other ductal dependent lesions for the systemic circulation: coarctation of the aorta and severe aor-tic stenosis. In most of the cases, hypoplastic left heart syndrome has a rapid evolution, with aggra-vation of the general status and neonatal shock, re-quiring early surgery or leading to death. The clo-sure of the ductus in such cases determines systemic hypoperfusion, shock and heart failure, sometimes with nonspecifi c symptoms: irritability, lethargy, cold wet marmorated extremities. The early diagnosis of ductus closure is essential for the treatment with prostaglandin E1. Patients with de-creased peripheral perfusion evolve rapidly to se-vere metabolic acidosis and multiple organ dys-functions. Except prostaglandin E1 perfusions, inotropic drugs, sodium bicarbonate and drugs that decrease systemic vascular resistance can be useful until the surgical treatment (9, 10).Anomalous coronary arteries origin and myocardial infarction. Myocardial infarction is extremely rare in new-born and is determined by the anomalous origin of the left coronary artery from the pulmonary artery. Initially, the myocardial ischemia is intermittent, only during feeding and crying, and occurs usually in the fi rst weeks of life (2 weeks 6 months). The symptoms are not specifi c: irritability, agitation, crying, dyspnea, pallor and sweating during feed-ing. Increased need of oxygen in the myocardium by various diseases, for example pulmonary infec-tions, can precipitate myocardial infarction in the left ventricle and the heart failure: tachypnea, tachycardia, gallop rhythm, cardiomegaly, hepato-megaly, murmur of mitral insuffi ciency, or the in-fant can have whhezing, erronate interpretated as bronchiolitis (7, 11). Chest x-Ray reveales cardio-megaly with interstitial pulmonary edema; ECG shows abnormal Q waves in DI, aVL, V4-V6 and overdenivelation of the ST segment in V4-V6, le-sions of antero-lateral infarction; echocardiography confi rms the abnormal origin of the left coronary artery from the pulmonary artery, variable mitral insuffi ciency, regional dyskinesis of the ventricular walls. The differential diagnosis must be made with dilative cardiomyopathy.Catheterization is very risky in these patients, and the treatment is surgery. Unopperated, 65-80% die before the age of 12 months. Patients diagnosed after 1 year of age have collateral vessels for the coronary circulation. Other causes for myocardial infarction in child: Kawasaki disease, other anoma-lies of the coronary arteries, hypertrophic cardio-myopathy, after heart defects surgery etc.Neonatal cardiomyopathies of ischemic origin (transient myocardial ischemia)These entities are the consequence of the perina-tal hypoxia on the cardiac muscle. Sometimes the clinical picture is severe from the fi rst day of life, but there are also late sever manifestations. Fetal TABLE 4. Elements to differentiate between central and perioheral cyanosisPeripheral (Acrocyanosis) Elements Central cyanosisPink Colour: mucosa, tongue, lips, trunk Blue Cold Extremities Warm coldDecreased Peripheral perfusion Normal decreasedNormal Arterial oxygen saturation Decreased Usually more favorable (shock, sepsis, congenital heart defect)Prognosis Usually requires urgent treatment (pulmonary, congenital heart defect, shock, sepsis)REVISTA ROMN DE PEDIATRIE VOLUMUL LIX, NR. 4, AN 2010260and neonatal asphyxia determine myocardial suf-fering, infarction and death or dilated cardiomyo-pathy without obvious etiology, discovered during infancy. Most of them have spontaneous favorable evolution. The patients present with cyanosis and signs of heart failure. ECG reveals right heart hy-pertrophy, underwaved ST segment and inverted T wave in the left leads. Chest x-Ray shows cardio-megaly with normal pulmonary vessels. Echocar-diography reveals tricuspid insuffi ciency, dilated right atrium and right-left shunt by patent foramen ovale. Most of the cases improve in a few days-weeks (1, 2). Transient myocardial incompetenceClinically, the symptoms are clinically apparent immediately from birth or in the fi rst 24 hours: re-spiratory failure, cyanosis, heart failure and circu-latory insuffi ciency. ECG reveals diffuse ventricu-lar repolarization disturbancies of ischemic type. Chest x-Ray shows cardiomegaly, venous stasis or pulmonary edema. Echocardiography excludes an-other congenital heart defect or dilated hypokinetic cardiomyopathy. Treatment: oxygen, isoproterenol, digitalis, dopamine, dobutamine, diuretics. The prognosis is good, but death can occur.Myocarditis The most encountered etiology is viral: entero-viruses (including Coxsackie B) and adenoviruses. The onset is usually nonspecifi c, anamnesis reveals viral diseases respiratory or digestive infections. Infants present initially with the symptoms of the viral infection (lethargy, irritability, feeding diffi -culties, palor) or can be misdiagnosed as bronchi-olitis, acute dehydration or sepsis. Sometimes pa-tients can have clinical picture of heart failure: diaphoresis, tachypnea, arrhythmia. The newborn can present sudden onset, with collapse and sudden death. Chest x-Ray reveals cardiomegaly, and ECG shows sinus tachycardia, arrhythmias or small QRS waves. Doppler echocardiography discovers left ventricular dilation, disturbed contractility, normal aspect and origin of the coronary vessels, allowing the differetio-al diagnosis with ALPACA syndrome (12). The differential diagnosis for the etiology of heart failure is performed by myocardial enzymes troponin I and MB fraction of creatinkinase, but the positive diagnosis is established by endomyocardial biopsy. The supportive respiratory and cardiac therapy is the fi rst step, the patients in cardiogenic shock require intubation. The inotropic support and after-load reduction must be instituted from the begin-ning. In the very severe cases, when the inotropic treatment is no longer effi cient, ECMO can allevi-ate the prognosis. High doses of intravenous im-munoglobulines and immunosupresive therapy have encouraging results in adults, but the effi cien-cy is not the same in children. SEVERE CARDIAC DYSRRHYTHMIAS IN NEONATE Most of the cardiac arrhythmias in newborn and infant are benign: sinus arrhythmia, sinus tachycar-dia and bradycardia, 1st and 2nd degree atrioven-tricular block, atrial, jonctional or ventricular extra-systoles, 200 beats/minute (180-350/min); fi xed R-R interval; minor variation of heart rate during crying, feeding, apnea; sudden onset and ending of the crisis spontaneous or with treatment, which can induce suddenly the sinus rhythm, with decreasing of the heart rate to normal values according to age or maintenance at high and fi x rates (the all or nothing law), especially if the case of reentrance mechanism. The QRS complexes can be: thin, most frequently, with or without T+P phenomenon, with or without P wave; wide complexes (preexistent bundle branch/rate-dependent/ventricular preexci-tation syndrome), when the differential diagnoses with ventricular tachycardia is required. The treat-ment depends on the clinical status of the newborn or infant (1,2,3,7): hemodynamic instability re-quires electric cardioversion 0,5-2 J/kg; if the in-fant is unstable, the vagal maneuvers can be effi -cient (ice bag on the face). The medical treatment is: adenosine bolus i.v. 0,05mg/kg repeated at 1-2 minutes, 3 doses, with double dose; if the child be-comes unstable: electric cardioversion0,5-2 J/kg REVISTA ROMN DE PEDIATRIE VOLUMUL LIX, NR. 4, AN 2010 261(5, 6); intravenous digoxin (not in the ventricular preexcitation syndrome); intravenous propranolol, sotalol, amiodarone (side effects). Verapamil is contraindicated under the age of 1 year because of the risk of cardiovascular collapse. Recurrences prophylaxis is made with digoxin or propranolol for 1 year. Lack of response to antiarrhythmics re-quires electrophysiologic studies and radiofrequen-cy ablation of the accessory pathway (13). Severe neonatal bradycardias can have different pathophysiologic mechanisms: troubles in the im-pulse formation (sinus bradycardia, sinus pause, sinoatrial block, slow ectopic rhythm, tachycardia-bradycardia syndrome, sick sinus syndrome), or troubles in the atrioventricular conduction system (1st, 2nd or 3rd degree atrioventricular block).2nd degree atrioventricular block Mobitz II: can occur in newborn with normal heart, in newborn from a mother with systemic lupus erhytematous and can progress to complete atrioventricular block, or after heart surgery. It can be 2:1, 3:1, 4:1 and can progress to complete atrioventricular block, can as-sociate intraventricular conduction abnormalities (wide QRS waves). Treatment:the newborn with normal QRS complexes in which the impulses are occasionally blocked and the escape ventricular rhythm is not very slow will be carefully monitorised, because there is the risk of evolution to complete block, requiring implantable pace-maker; the newborn with sustained block and delayed intraventricular conduction (wide QRS complexes) has a high risk of sudden death and requires pace-maker; the newborn with persistent block after cardiac surgery and slow escape ventricular rhythm must receive implantable pace-makerComplete atrioventricular block (3rd degree): the onset is almost always intrauterine (from the 17th week of gestation) and can be determined by other congenital heart defects (25-30% cases), mothers with systemic lupus erythematous, infec-tions, or can occur on a normal heart, as a primary conduction disturbance. The diagnosis in the fetus is established by the fetal rhythm 55/minute and requires treatment for heart fail-ure;