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Hipertrofia

i suprasolicitarea

atrial , ventricular

Unda P complexul atrial, se formeaz n urma excit rii ambelor atrii, suprapunerea excit rii AD i AS Unda P deobicei + durata 0,1 sec. amplituda 2,5 mm ntotdeauna + II, I, aVF, V2 V6 ntotdeauna - aVR Diferit ( + , bifazic, - ) III, aVL, V1 PII>PI>PIII PII, III, aVF < TII, III, aVF Unda P poate fi zim at , dar distan a dintre zim i 0,02 sec.
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n hipertrofia AD
se majoreaz for a electromotorie, creat de AD: - se majoreaz vectorul excit rii AD - se majoreaz durata excit rii AD, n timp ce durata excit rii AS este obi nuit . amplituda I-a (prima) parte a undei P, durata iar a II-a parte a undei P nemodificat . Ca rezultat al sum rii vectorilor AD i AS: - Unda P nalt , ascu it , deseori - simetric - Amplituda > 2,5 mm - Durata nu este modificat , rar 0,11-0,12 sec.

- se vede mai bine n II, III, aVF - tot a a de ascu it, dar - n aVR - axa electric a undei P cu tendin de deviere spre dreapta: PIII >PII >PI - n V1 unda P nalt, ascu it sau bifazic, cu predominarea p r ii pozitive - V2, V3 - unda P nalt, ascu it (cu ct e mai pronun at hipertrofia, cu att mai multe deriva ii manifest P pulmonale ) - PII, III, aVF > TII, III, aVF - semn indirect

- n hipertrofia izolat AD durata undei P, intervalul intersicoid nemodificate - n dilatarea AD - durata undei P intervalul intersicoid AD > 0,04 sec.

n hipertrofia AD - P pulmonale :
maladii pulmonare cronice cord pulmonar stenoza valvei tricuspide hipertensiune pulmonar vicii congenitale cu suprasolicitare de dreapta

Suprasolicitarea AD modific ri EKG-fice caracteristice hipertrofiei AD, survenite dup o situa ie clinic acut :
- pneumonie, - acces astm bron ic - edem pulmonar - IMA - embolia arterelor pulmonare - tahicardii - tireotoxicoz

- deregl ri de conductibilitate i/atrial - afectarea difuz sau de focar al miocardului AD - diafragm jos sau constitu ie astenic

Suprasolicitarea este o situa ie tranzitorie, modific rile dispar treptat, 4 pe m sura normaliz rii st rii acute.

n hipetrofia AS
Se majoreaz for a electromotorie a AS: - se majoreaz vectorul de excitare a AS - se majoreaz durata excit rii AS n acela i timp AD se excit obi nuit. I-a parte a undei P nemodificat a II-a parte a undei P - durata Unda P: - dilatat , durata > 0,10 0,12 sec. - dedublat , biondular - amplituda nu e m rit , sau majorat neesen ial - dac unda P e zim at , distan a dintre zim i > 0,02 sec. - se vede bine n I, II, aVL, V5, V6 - dilatat, dedublat, dar - n aVR - axa electric a undei P deseori e deviat spre stnga sau orizontal : PI >PII >PIII - n V1 unda P - sau + - , cu predominarea - index Macruz > 1,6 (durata undei P/durata segm. PQ) - intervalul intersicoid AS I, aVL, V5, V6 > 0,06 sec. 5

n hipertrofia AS

P mitrale :

- stenoza mitral - vicii aortale - vicii congenitale cu suprasolicitare de stnga - HTA

Suprasolicitarea AS unda P dilatat , dedublat , survine dup o situa ie clinic acut : urgen hipertensiv acces astm cardiac acces edem pulmonar IMA
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Hipertrofia combinat a atriilor


Concomitent se majoreaz vectorii excit rii AD i AS. Hipertrofia AD - n III, aVF P nalt, ascu it Hipertrofia AS - n I, aVL, V5, V6 P dilatat, biondular Hipertrofia combinat a atriilor se manifest cel mai bine n V1: - V1 sau V1, V2 P bifazic: I faz evident + II faz evident Index Macruz = 1,1 - 1,6 Intevalul intersicoid AD > 0,04 sec., AS > 0,06 sec.

Hipertrofia combinat a atriilor n:


- vicii mitral tricuspidiene, aortal tricuspidiene + suprasolicitare - asocierea maladiilor pulmonare cronice i HTA Suprasolicitarea atriilor n IMA, edem pulmonar, insuficien circulatorie progresiv
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Hipertrofia VS

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Semne diagnostice ale HTF VS


R nalt n V5, V6 > R V4 (RV6 > RV5 > R V4 hipertrofie marcat ) S adnc n V1, V2 Cu ct mai > HTF VS, cu att mai > RV5,V6 , cu att mai adnc SV1,V2 - V5, V6: qR, qRs (rar) q<R q < 0,03 sec - Durata QRS > 0,10 0,11; <0,12 (norma: 0,06-0,10 sec.) - SV5,V6 - lips sau de amplitudine mic - segm. STV5,V6 discordant subdenivelat, curb cu raza n sus - TV5,V6 negativ, asimetric, maxim - la sfr itul undei T V1, V2 rS, QS segm. STV1,V2 sau V1-V3 supradenivelat cu raza n jos TV1,V2 sau TV1-V3 + , TV6 - : sindrom TV1>TV6 zona de tranzi ie deviat spre derivatele drepte

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Axa electric a cordului orizontal sau moderat deviat spre stnga

I, aVL = V5,V6

qR, segm. ST- subdenivelat TI, aVL - , asimetric

III, aVF = V1,V2 rS, QS segm. ST supradenivelat T + , TIII > TI aVR = V1

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Grupul A: 1) Devierea axei electrice n stnga 2) RI > 10 mm 3) S (Q)aVR > 14 mm 4) 5) 6) 7)

Semne cantitative HTF VS

TaVR > 0 (pozitiv), la S (Q) RaVR diagnostic pozitiv: RV5,V6 > 16 mm 2 criterii i mai mult gr. A RaVL > 7 mm TV5,V6 1 mm la RV5,V6 > 10 mm i TV1-V4 > 0 (pozitiv) n lipsa insuf. Coronariene 8) TV1-V6, cnd TV1 > 1,5 mm Grupul B: 1) RI + SIII > 20 mm 2) Subdenivelarea STI > 0,5 mm, la RI > SI 3) TI 1 mm, la diminuarea STI > 0,5 mm, la RI 10 mm 3 criterii i mai mult gr. B 4) TaVL < 1 mm, la diminuarea STaVL > 0,5 mm, la RaVL > 5 mm 5) SV1 > 12 mm 6) SV1 + RV5 sau V6 > 28 mm la persoane > 30 ani > 30 mm la persoane < 30 ani 7) QV4-V6 2,5 mm, la Q 0,03 sec 8) Diminuarea segm. STV5, V6 > 0,5 mm la majorarea STV2-V4 9) R/T V5,V6 > 10, la TV5,V6 > 1 mm 1 criteriu gr. A + 1 criteriu gr. B 10) RII > 18 mm 11) Intervalul intersicoid V5,V6 0,05 sec.
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Criterii Socolov-Lyon voltaj: (49%-sensibilitate, 90%-specificitate)

1) 2) 3) 4)

RI + S III > 25 mm RaVL > 11 mm RV6 > 26 mm RV6 + SV1 > 35 mm

Criterii Cornell voltaj: SV3 + RaVL > 28 mm la b rba i, > 20 mm la femei Produsul Cornell voltaj: (SV3 mm + RaVL mm ) x durata QRSV5V6 milisec > 2440 mmxsec
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A 49 year old woman with a past history of chronic renal insufficiency, congestive heart failure, and hypertension presented to the ED with dyspnea. The examination was remarkable for pulmonary congestion. A 12-lead ECG demonstrated NSR with LVH; the chest radiograph confirmed pulmonary oedema with cardiomegaly. The patient received oxygen, furosemide, topical nitrates, morphine, and aspirin; she slowly improved and was admitted to the hospital. No evidence of myocardial infarction 16 was discovered.

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ECG of patient with left ventricular hypertrophy according to the Sokolow-Lyon criteria

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Another example of extreme left ventricular hypertrophy in a patient with severe aortic valve stenosis.
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Twelve-lead ECG showing left and right ventricular hypertrophy (by voltage criteria), biatrial enlargement (biphasic P waves with high amplitude and duration), and anterior strain pattern (right ventricular strain)
Manchanda, A. et al. Circulation 2009;119:e1-e3 22

Hipertrofia VD
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Hipertrofia VD
3 variante HTF VD: 1. HTF pronun at VD 2. depolarizarea ntrziat VD 3. HTF moderat VD

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Semne diagnostice HTF VD


R nalt V1,V2 QRS nu este l rgit S adnc V5,V6 Cu ct > RV1, >SV5V6, mai pronun at HTF VD V1,V2: 1) Tip I qR sau R Tip II rsRI, rSRI, rRI Tip III RS, Rs, rS (R=S, R>S, R<S) 2) segm. STV1V2 discordant subdenivelat, curb cu raza n sus unda T - , asimetric intervalul intersicoid VD > 0,3 sec. V5,V6 : 1) Tip I rS, SV5V6 > rV5V6 RS, RV6 = SV6 Tip II Rs, RV5V6 > SV5V6 Tip III qRS sau qRs RV5V6 diminuarea amplitudei 2) segm. STV5V6 la izolinie sau moderat supradenivelat cu raza n jos unda T + Zona de tranzi ie se deplaseaz n derivatele stngi (V5,V6)
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Se mai distinge tipul S de HTF VD: R V1-V6 S pronun at V1-V6 Axa electric SI SII SIII (deplasare n posterior) emfizem pulmonar n HTF VD axa electric : vertical deviere spre dreapta SI SII SIII III, aVF, = V1,V2, cu dominarea R I, aVL = V5,V6, cu dominarea S aVR R tardiv (> 4 mm) QR sau rSRI RaVR > Q (S)aVR
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Semne cantitative HTF VD


1) 2) 3) 4) 5) 6) 7) RV1 > 7 mm SV1V2 2 mm SV5 7 mm RV5V6 < 5 mm RV1 + SV5 sau RV1 + SV6 > 10,5 mm RaVR > 4 mm TV1 n lipsa insuficien ei subdenivelare STV1V2 coronariene RV1 > 5 mm
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In V1 the QRS are positive with tall R waves. This is because increased right ventricular muscle mass causes the net ventricular depolarization current to move towards this right chest lead. R wavesthat are taller than S waves are deep in V1 are highly suggestive of RVH. The S waves are unusually deep in V6 and may be even deeper than the R wave is tall.

Right axis deviation due to the overpowering current generated by a hypertrophied right ventricle. Ventricular repolarization changes manifest as downward sloping of the ST segment and T wave inversion, the so called ventricular strain pattern, may or may not be present in the right chest leads. (See V1 in above ECG.) P wave > 2.5 mm tall in lead II, III, aVF or biphasic P wave in V1 suggesting the presence of right atrial enlargement. (Right atrial abnormality results from the right atrium having to pump blood into a thick-wall noncompliant hypertrophied right ventricle.)
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In this case of severe pulmonary hypertension, RVH is recognized by the prominent anterior forces (tall R waves in V1-2), right axis deviation (+110 degrees), and "P pulmonale" (i.e., right atrial enlargement). RAE is best seen in the frontal plane leads; the P waves in lead II are >2.5mm in amplitude.
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A standard 12 leads ECG showing sinus rhythm with rate of 94/minute. There is Right Ventricular Hypertrophy (RVH) by the voltage criteria.
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Right ventricular hypertrophy and right atrial enlargement.


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Patients presenting with RAE demonstrate an ECG pattern in which the P wave duration is unaffected, but its shape is peaked and its amplitude is increased to greater than 2.5 mm in leads II, III, aVF (arrows below) and sometimes V1. With extreme enlargement of the right atrium, the P wave may demonstrate terminal negativity in lead V1, resembling LAE. Right atrial enlargement is commonly associated with congenital heart disease, tricuspid valve disease, pulmonary hypertension and diffuse lung disease. Furthermore, patients presenting with RAE often demonstrate ECG changes associated with right ventricular hypertrophy as well. 36

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