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ELECTROCARDIOGRAMA

ISCHEMIA SI INFARCTUL MIOCARDIC

Asist. Univ. Dr. Mihaela Popescu


Catedra de Cardiologie Spitalul Universitar de
Urgenta Elias

Ischemie/ Leziune miocardica

Efectele ischemiei
PA ischemic
Depolarizare redusa
Repolarizare redusa
Durata si amplitudine redusa

PA ischemic

PA normal
Sistola = ST
Diastola

Diastola= TP

CORESPONDENTA ECG - POTENTIAL DE


ACTIUNE

Complex QRS = Faza 0 si 1


Segment ST = Faza 2

Unda T= Faza 3
Interval TQ = Faza 4

Ischemia miocardica
Ischemia

Scaderea perfuziei miocardice - reversibila


Miocit ischemic- repolarizare precoce (+)
Ischemia subendocardica unde T negative
Ischemia transmurala unde T pozitive, ascutite

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 negativacurent de la normal la ischemic

In diastola (TP) regiunea ischemica este mai pozitivacurent de la ischemic la normal

Curentul de leziune
ST- curent de la regiunea normala spre cea ischemica
TP curent de la regiunea ischemica spre cea normala

ST

TP

Curent de leziune

Curent sistolic de leziune

Curent diastolic de leziune

Leziune subendocardica

Curent sistolic de leziune

Curent diastolic de leziune

Leziune transmurala

Curent sistolic de leziune

Curent diastolic de leziune

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)

Supra/sub denivelare ST

Criterii de diagnostic ECG in


STEMI
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.

Supradenivelarea de segment ST

ST
P

Apare precoce

Apare in derivatiile directe

NB: o mica supradenivelare de segment ST


poate fi normala in V1, V2 V3

ST elevation
ST 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. Basic
requirements of ST changes for diagnosis are: elevation of at least 1 mm in two or more
adjoining 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 be
seen in leads V1 and V2 normally. However, if there is also elevation in V3 the cause is
unlikely to be physiological

Unda Q patologica

Modificare diagnostica in/post infarct

Durata >0.04 secunde

Amplitudine de >25% din unda R

ST
P

T
Q

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.

Modificari ale undei T

Negativarea undei T -modificare tardiva

Apare cand segmentul ST incepe sa


revina la normal

R
ST

T
Q

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 wave
also decreases in amplitude and eventually inverts.

Secventa modificarilor aspectului


ECG in infarctul miocardic acut
R

ST

ST

P
Q S

P
T

1 minut dupa debut

1 ora de la debut

La cateva ore de la debut

R
ST

ST

P
T

La o zi de la debut

P
T

Modificari tardive

La cateva luni dupa IMA

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.

ARTERELE CORONARE

ARTERELE CORONARE

CLASIFICAREA IMA PE BAZA ASPECTULUI ECG


CORELAT CU DATELE ANGIOGRAFICE
CATEGORIA

LOCALIZAREA OCLUZIEI

ECG LA PREZENTARE

1. ADA proximal

Proximal de prima perforanta


septala

ST in V1-V6, DI, aVL si bloc


fascicular sau bloc de ramura

2. ADA mediu

Distal de prima perforanta


septala, proximal de marea
diagonala

ST in V1-V6, DI, aVL

3. ADA distal sau


artera diagonala

Distal de marea diagonala sau


afectarea primei diagonale

ST in V1-V4 sau ST in
V5-V6, DI, aVL

4. IMA inferior
moderat intins
(posterior, lateral, de
ventricul drept)

ACD proximal sau artera


circumflexa

ST in DII, DIII, aVF si


oricare sau toate dintre:
a) V1, V3R, V4R sau
b) V5-V6 sau
c) R>S in V1, V2

5.IMA inferior mic

ACD distal sau artera


circumflexa sau ramuri din
artera circumflexa

ST doar in DII, DIII, aVF

Infarct miocardic anterior


I II III

Artera descendenta anterioara

aVR aVL aVF

V1 V2 V3

V4 V5 V6

Note de subsol IMA anterior


Location 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 (V16) 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 the
inferior 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 of
myocardium, ventricular septal defect, aneurysm or rupture and arrhythmias. ST
elevation in I, aVL, and V26, 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.

Infarct inferior
I II III

Artera coronara dreapta


sau a circumflexa

aVR aVL aVF

V1 V2 V3

V4 V5 V6

Infarct inferior si de VD
I II III

Artera coronara dreapta


sau a circumflexa

aVR aVL aVF

V1 V2 V3

V4 V5 V6

Infarct postero inferior lateral


I II III

Artera coronara dreapta


sau a circumflexa

aVR aVL aVF

V1 V2 V3

V4 V5 V6

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.

Infarct lateral
I II III

aVR aVL aVF

V1 V2 V3

LAD distal sau a diagonala/ a


circumflexa
Location of infarction and its relation to the ECG: lateral infarction
Occlusion of the left circumflex artery may cause lateral infarctions.
Lateral infarctions are diagnosed by ST elevation in leads I and aVL.

V4 V5 V6

Localizarea infarctului
I

aVR

aVL

V2

V3
III

INFERIOR

V4

SEPTAL

LATERAL
II

V1

ANT
SEPTAL

V5

V6

ANT
LAT

aVF

Location of infarction: combinations


The previous slides discussed the changes that occur in typical anterior, inferior and lateral
infarctions. However, the area infarcted is not always limited to these areas and infarctions can
extend across two regions. For example, an anterior infarction which is also on the lateral side of
the 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.

Localizarea infarctului?

IM inferior

Localizarea infarctului?

IM anterior

For more presentations


www.medicalppt.blogspot.com

IM anterolateral

Vectorul ST
Poate indica localizarea
ocluziei arterei coronare

Diagnosticul diferential al IMA cu


supradenivelare ST
Angina Prinzmetal
Pericardita
Repolarizare precoce
Sdr. Brugada

Unda Osborne
Supradenivelarea inghetata anevrism

Diagnosticul diferential al IMA cu


supradenivelare ST
Anteroseptal
aneurism
Unda Osborne

Normal

Sdr. Brugada

Asocierea IM cu BRS
Anterior wall MI
I II III

aVR aVL aVF

Left bundle branch block


V1 V2 V3

V4 V5 V6

I II III

aVR aVL aVF

V1 V2 V3

V4 V5 V6

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 ventricular
muscle 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 (less
than 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.

Asocierea IM cu BRS
Criteriile Sgarbossa (pt IMA 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 specificitate
de peste 90% de a detecta infarctul miocardic acut in
prezenta blocului de ramura stang sau a unui ritm de pacemaker.

Criterii pentru detectarea unui IM vechi in prezenta BRS


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

Modificari reciproce (in oglinda)


Localizare IM

Supradenivelare ST

Subdenivelare reciproca
de ST

Anterior

V1-V6 (progresie lenta a undei II, III, aVF


R)

Lateral

DI, aVL, V5, V6

V1-V3

Inferior

II, III, aVF

DI, aVL, posibil derivatiile


anterioare

Posterior

Unde R anormal de inalte in


V1- V3

V1-V3

SUPRAINCARCAREA ATRIALA
HIPERTROFIILE
VENTRICULARE

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

Supraincarcarea atriala dreapta


Cauze de supraincarcare 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

NB: De obicei asociata cu HVD, exceptia stenoza tricuspidiana

Supraincarcarea atriala stanga


Unda P > 0.11 s
Morfologie: unda bifida
In V1, V2 predomina componenta negativa
Axa se orizontalizeaza

Titulatura: p mitral
Derivatii preferentiale: DI, aVL, V5, V6

Supraincarcarea atriala stanga


Valvulopatii

Stenoza mitrala
Regurgitare mitrala
Complianta scazuta a VS

Hipertensiune arteriala
Cardiomiopatie obstructiva
Stenoza aortica
Regurgitare aortica
Boli infiltrative - amiloidoza

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

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

HVS

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

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 la
predominanta 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

HVD

HVD
3 patternuri
1. fara tulburari de conducere intraventriculare drepte
2. cu BRD incomplet
3. cu BRD complet

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

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 de
pattern 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
QRS >+90 + dilatare de AS (in prezenta de BRD)