Curs 3 EKG IMA, Hipertrofii Modif

8/16/2019 Curs 3 EKG IMA, Hipertrofii Modif

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ELECTROCARDIOGRAMA

ISCHEMIA SI INFARCTUL MIOCARDIC

Asist. Univ. Dr. Mihaela Popescu

Catedra de Cardiologie Spitalul Universitar de

Urgenta Elias


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Ischemie/ Leziune miocardica


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Efectele ischemiei

PA ischemic

PA normal Sistola = ST

Diastola= TPDiastola

PA ischemic

• Depolarizare redusa

• Repolarizare redusa

•

Durata si amplitudine redusa


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CORESPONDENTA ECG - POTENTIAL DEACTIUNE

•Complex QRS = Faza 0 si 1

•Segment ST = Faza 2

•Unda T= Faza 3

•Interval TQ = Faza 4


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Ischemia miocardica

• Ischemia

• Scaderea perfuziei miocardice - reversibila

• Miocit ischemic- repolarizare precoce (+)

• Ischemia subendocardica – unde T negative• Ischemia transmurala – unde T pozitive, ascutite


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Curentul de leziune

• Diferenta de potential intre zonele normale si cele

ischemice: mic curent= curent de leziune

• Flux de ioni de K dinspre zona + spre -

• In sistola (ST) regiunea ischemica este mai negativa-

curent de la normal la ischemic

• In diastola (TP) regiunea ischemica este mai pozitiva-

curent de la ischemic la normal


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Curentul de leziune

ST- curent de la regiunea normala spre cea ischemica

TP – curent de la regiunea ischemica spre cea normala

STTP


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Curent de leziune

Curent sistolic de leziune Curent diastolic de leziune


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Leziune subendocardica



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Leziune transmurala



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Ischemie/ Leziune miocardica

Infarct miocardic• Ischemie persistenta – celulele isi pierd viabilitatea= necroza

• Infarct miocardic:• cu supradenivelare de segment ST (STEMI)

• fara supradenivelare de segment ST (NSTEMI)


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Criterii de diagnostic ECG inSTEMI

• Supradenivelare ST :

• >0.25 mV la barbati sub 40 ani

• >0.20 mV la barbati peste 40 ani• > 0.15 mV la femei in V2-V3, sau > 0.1 mV in orice alta

derivatie

• >0.05mV in V7-V9 (>0.01mV la barbati sub 40 ani)

• avR si subdenivelare ST in 8 sau mai multe derivatii=afectare multivasculara sau de trunchi comun.


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Supradenivelarea de segment ST

R

P

Q

ST

• Apare precoce• Apare in derivatiile directe

• NB: o mica supradenivelare de segment ST

poate fi normala in V1, V2 V3


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ST elevationST segment elevation usually occurs in the early stages of infarction, and may exhibit

quite a dramatic change.ST elevation is often upward and concave, although it can appear convex or horizontal.These changes occur in leads facing the infarction.ST elevation is not unique to MIs and therefore is not confirming evidence. Basicrequirements of ST changes for diagnosis are: elevation of at least 1 mm in two or moreadjoining leads for inferior infarctions (II, III, and aVF), and at least 2 mm in two or more

precordial leads for anterior infarction. You should be aware that ST elevation can beseen in leads V1 and V2 normally. However, if there is also elevation in V3 the cause isunlikely to be physiological


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Unda Q patologica

R

P

Q

T

ST

• Modificare diagnostica in/post infarct

• Durata >0.04 secunde

• Amplitudine de >25% din unda R

Deep Q wave

The only diagnostic changes of acute

myocardial infarction are changes in the QRS

complexes and the development of abnormal Q

waves. However, this may be a late change and

so is not useful for the diagnosis of AMI in the

pre-hospital situation.

Remember that Q waves of more than 0.04

seconds , or 1 little square, are not generally

seen in leads I, II or the precordial leads.


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Modificari ale undei T

R

P

Q

T

ST

•

Negativarea undei T -modificare tardiva• Apare cand segmentul ST incepe sa

revina la normal

T wave inversion

The T wave is the most unstable feature of the ECG

tracing and changes occur very frequently under normal

circumstances, limiting their diagnostic value.

Subtle changes in T waves are often the earliest signs of

myocardial infarction. However, their value is limited for

the reason above, but for approximately 20 to 30% of

patients presenting with MI, a T wave abnormality is the

only ECG sign.

The T wave can be lengthened or heightened by coronary

insufficiency.

T wave inversion is a late change in the ECG and tends to

appear as the ST elevation is returning to normal. As the

ST segment returns towards the isoelectric line, the T wavealso decreases in amplitude and eventually inverts.


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Secventa modificarilor aspectuluiECG in infarctul miocardic acut

1 minut dupa debut 1 ora de la debut La cateva ore de la debut

La o zi de la debut Modificari tardive La cateva luni dupa IMA

Q

R

P

Q T

STR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

T

ST

R

P

Q

T


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Note subsol progresie modificari

Sequence of changes in evolving AMI

The ECG changes that occur due to myocardial infarction do not all occur at the same time.There is a progression of changes correlating to the progression of infarction.

Within minutes of the clinical onset of infarction, there are no changes in the QRS

complexes and therefore no definitive evidence of infarction. However, there is ST

elevation providing evidence of myocardial damage.

The next stage is the development of a new pathological Q wave and loss of the r wave.

These changes occur at variable times and so can occur within minutes or can be delayed.

Development of a pathological Q wave is the only proof of infarction.

As the Q wave forms the ST elevation is reduced and after 1 week the ST changes tend to

revert to normal, but the reduction in R wave voltage and the abnormal Q waves usually

persist.

The late change is the inversion of the T wave and in a non-Q wave myocardial infarct,

when there is no pathological Q wave, this T wave change may be the only sign of

infarction.

Months after an MI the T waves may gradually revert to normal, but the abnormal Q waves

and reduced voltage R waves persist.

In terms of diagnosing AMI in time to make thrombolysis a life-saving possibility, the main

change to look for on the ECG is ST segment elevation.


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ARTERELE CORONARE


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ARTERELE CORONARE


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CLASIFICAREA IMA PE BAZA ASPECTULUI ECGCORELAT CU DATELE ANGIOGRAFICE

CATEGORIA LOCALIZAREA OCLUZIEI ECG LA PREZENTARE

1. ADA proximal Proximal de prima perforantaseptala

↑ ST in V1-V6, DI, aVL si blocfascicular sau bloc de ramura

2. ADA mediu Distal de prima perforantaseptala, proximal de mareadiagonala

↑ ST in V1-V6, DI, aVL

3. ADA distal sauartera diagonala

Distal de marea diagonala sauafectarea primei diagonale

↑ ST in V1-V4 sau ↑ ST inV5-V6, DI, aVL

4. IMA inferiormoderat intins

(posterior, lateral, deventricul drept)

ACD proximal sau arteracircumflexa

↑ ST in DII, DIII, aVF sioricare sau toate dintre:

a) V1, V3R, V4R saub) V5-V6 sauc) R>S in V1, V2

5.IMA inferior mic ACD distal sau arteracircumflexa sau ramuri dinartera circumflexa

↑ ST doar in DII, DIII, aVF


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Infarct miocardic anterior

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Artera descendenta anterioara


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Note de subsol IMA anteriorLocation of infarction and its relation to the ECG: anterior infarction

As was discussed in the previous module, the different leads look at different

aspects of the heart, and so infarctions can be located by noting the changes that

occur in different leads. The precordial leads (V1 – 6) each lie over part of the

ventricular myocardium and can therefore give detailed information about this

local area. aVL, I, V5 and V6 all reflect the anterolateral part of the heart and will

therefore often show similar appearances to each other. II, aVF and III record theinferior part of the heart, and so will also show similar appearances to each other.

Using these we can define where the changes will be seen for infarctions in

different locations.

Anterior infarctions usually occur due to occlusion of the left anterior descending

coronary artery resulting in infarction of the anterior wall of the left ventricle and

the intraventricular septum. It may result in pump failure due to loss ofmyocardium, ventricular septal defect, aneurysm or rupture and arrhythmias. ST

elevation in I, aVL, and V2 – 6, with ST depression in II, III and aVF are indicative

of an anterior (front) infarction. Extensive anterior infarctions show changes in V1 –

6 , I, and aVL.


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Infarct inferior


Artera coronara dreapta

sau a circumflexa


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Infarct inferior si de VD



sau a circumflexa


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Infarct postero inferior lateral



sau a circumflexa


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Note subsol IMA inferior

Location of infarction and its relation to the ECG: inferior

infarction

ST elevation in leads II, III and aVF, and often ST depression in I,

aVL, and precordial leads are signs of an inferior (lower)

infarction. Inferior infarctions may occur due to occlusion of the

right circumflex coronary arteries resulting in infarction of the

inferior surface of the left ventricle, although damage can be

made to the right ventricle and interventricular septum. This type

of infarction often results in bradycardia due to damage to the

atrioventricular node.


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Infarct lateral


LAD distal sau a diagonala/ acircumflexa

Location of infarction and its relation to the ECG: lateral infarctionOcclusion of the left circumflex artery may cause lateral infarctions.

Lateral infarctions are diagnosed by ST elevation in leads I and aVL.

Localizarea infarctului


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Localizarea infarctuluiaVR V1 V4

I

II

III

LATERAL

INFERIOR

SEPTAL

ANT

SEPTAL

ANT

LAT

aVL

aVF

V2

V3

V5

V6

Location of infarction: combinations

The previous slides discussed the changes that occur in typical anterior, inferior and lateralinfarctions. However, the area infarcted is not always limited to these areas and infarctions canextend across two regions. For example, an anterior infarction which is also on the lateral side ofthe heart is known as an anterolateral infarction.• ST segment elevation in leads I and aVL represent a lateral infarction• Anteroseptal infarctions show ST segment elevation in leads V1 to V4.

• ST elevation in V4 to V6 is typical of an anterolateral infarction• ST elevation in II, III and aVF is typical of inferior infarction.


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Localizarea infarctului?


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IM inferior


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Localizarea infarctului?


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IM anterior


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For more presentationswww.medicalppt.blogspot.com


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IM anterolateral


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Vectorul ST

Poate indica localizareaocluziei arterei coronare


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Diagnosticul diferential al IMA cusupradenivelare ST

•Angina Prinzmetal

•Pericardita

•Repolarizare precoce

•Sdr. Brugada

•Unda Osborne

•Supradenivelarea “inghetata” -

anevrism


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Anteroseptal

aneurism

Diagnosticul diferential al IMA cusupradenivelare ST

Unda Osborne

Normal Sdr. Brugada


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Asocierea IM cu BRS

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Anterior wall MILeft bundle branch block


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Bundle branch block

Bundle branch block is the pattern produced when either the right bundle or the entire left

bundle fails to conduct an impulse normally. The ventricle on the side of the failed bundle

branch must be depolarised by the spread of a wave of depolarisation through ventricularmuscle from the unaffected side. This is obviously a much slower process and usually the

QRS duration is prolonged to at least 0.12 seconds (for right bundle branch block) and 0.14

seconds (for left bundle branch block).

The ECG pattern of left bundle branch block (LBBB) resembles that of anterior infarction,

but the distinction can readily be made in nearly all cases. Most importantly, in LBBB the

QRS is widened to 140 ms or more. With rare exceptions there is a small narrow r wave (lessthan 0.04 seconds) in V1 to V3 which is not usually seen in anteroseptal infarction. There is

also notching of the QRS best seen in the anterolateral leads, and the T wave goes in the

opposite direction to the QRS in all the precordial leads. This combination of features is

diagnostic. In the rare cases where there may be doubt assume the correct interpretation is

LBBB. This will make up no difference to the administration of a thrombolytic on medical

direction but for the present will be accepted as a contraindication for paramedics acting

autonomously (see later slide).

Right bundle branch block is characterised by QRS of 0.12 seconds or wider, an s wave in

lead I, and a secondary R wave (R’) in V1. As abnormal Q waves do not occur with right

bundle branch block, this remains a useful sign of infarction.


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Asocierea IM cu BRS

•↑ ST > 1mm in derivatii cu QRS pozitiv -5 puncte

•↓ ST > 1 mm in V1-V3 -3 puncte

•↑ ST > 5 mm in derivatii cu QRS negativ – 2 puncte

La un scor cumulativ de 3 puncte – specificitatede peste 90% de a detecta infarctul miocardic acut inprezenta blocului de ramura stang sau a unui ritm de pace-maker.

•Unda Q in cel putin doua dintre DI, aVL, V5, V6•Regresia undei R din V1 in V4•Incizura pe unda S in V3-V5 –semnul Cabrera

Criteriile Sgarbossa (pt IMA cu BRS)

Criterii pentru detectarea unui IM vechi in prezenta BRS


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Modificari reciproce (in oglinda)Localizare IM Supradenivelare ST Subdenivelare reciproca

de ST

Anterior V1-V6 (progresie lenta a undeiR)

II, III, aVF

Lateral DI, aVL, V5, V6 V1-V3

Inferior II, III, aVF DI, aVL, posibil derivatiileanterioare

Posterior Unde R anormal de inalte inV1- V3

V1-V3


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SUPRAINCARCAREA ATRIALA

HIPERTROFIILEVENTRICULARE


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Supraincarcarea atriala dreapta

•Unda P >2,5mm

•Morfologie: unda ascutita

•In V1, V2, daca unda este bifazica, predomina componenta pozitiva,

initiala

•Axa se verticalizeaza: +75° - +90°

•Titulatura: p pulmonar

•Derivatii preferentiale: DII, DIII, aVF


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Supraincarcarea atriala dreapta

Valvulopatii

• Stenoza tricuspidiana

• Regurgitare tricuspidiana

Hipertensiune pulmonara

• BPOC

• Embolii pulmonare

• Apnee in somn

Boli congenitale

• Stenoza pulmonara

• Tetralogia Fallot

Tranzitor

• Trombembolism pulmonar

• Status astmaticus

Cauze de supraincarcare atriala dreapta

NB: De obicei asociata cu HVD, exceptia stenoza tricuspidiana


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Supraincarcarea atriala stanga

Valvulopatii•Stenoza mitrala

•Regurgitare mitrala

Complianta scazuta a VS

•Hipertensiune arteriala•Cardiomiopatie obstructiva

•Stenoza aortica

•Regurgitare aortica

•Boli infiltrative - amiloidoza


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Dilatare biatriala

• Criterii pentru ambele tipuri de dilatari

• V1: unda larga bifazica• componenta pozitiva > 1,5 mm

• componenta negativa >1 mm, >0.04s• DII:

• Unda > 2.5 mm

• Unda > 0,12 sec


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Hipertrofia ventriculara stanga

• Suprasolicitarea VS – cauze:

• Suprasarcina de volum: IMi, IAo

• Suprasarcina de presiune: HTA, SAo valv./subvalv., CoAo,

CMH

• Suprasolicitarea VS – efect:

• Suprasarcina de volum – dilatare cavitati

• Suprasarcina de presiune – hipertrofie, ingrosare pereti


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HVS


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Criterii de apreciere a HVS

• Indice Sokolow - Lyon: R (V5/V6) + S (V1/V2) > 3.5 mV• (4.5 mV la copil)

• Indicele Cornell: R (aVL) + S (V3) > 2.8 mV (B), 2 mV (F)

•

• Scorul Romhilt - Estes


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Hipertrofia ventriculara dreapta

• Etiologie:• incarcare de volum - DSV, Fallot (sunt stg. - dr.)• incarcare de presiune – HTP primara, HTP secundara

(emfizem, TBC, bronsiectazii bilaterale, fibroze pulm,

SMi) Consecinte:

• balanta vectoriala VD-VS se schimba pana lapredominanta VD, in cazuri extreme de HVD

• inversarea asp. normal pe ECG:R in V1, V2 + S in V5, V6• rotatie orara, catre anterior a VD + rotatie posterioara a

vf. Inimii• prin masa VD asincronism VD-VS


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HVD


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HVD

• 3 patternuri• 1. fara tulburari de conducere intraventriculare drepte

• 2. cu BRD incomplet

•

3. cu BRD complet


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Criterii de apreciere a HVD

• Sokolow Lyon• Unda R in V1 + unda S in V5/ V6>1.1mV

• Alte criterii de apreciere:

•

1) deviatie axiala > 90 grd• 2) R V1 > 7 mm• 3) R/S V1 >1• 4) P pulmonar•

5) S/R V6 >1• 6) aspect de BRD


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Hipertrofie biventriculara

• SV1 + RV5(sau V6) >35 mm (indice Sokolov pozitiv)combinat cu deviere ax frontal QRS la dreapta +90

• SV6 >7 mm (fara BRD)

• probabil cel mai bun semn este combinatia depattern de HVD tipic cu dilatare de

• AS (durata p >=120 ms)• S/R>1 in V5/V6 +dilatare de AS

• SV6 >7 mm + dilatare AS

• ÅQRS >+90 + dilatare de AS (in prezenta de BRD)

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Curs 3 EKG IMA, Hipertrofii Modif