ISCHEMIA SI INFARCTUL MIOCARDICAsist. Univ. Dr. Mihaela PopescuCatedra de Cardiologie Spitalul Universitar de Urgenta Elias

PA ischemicPA normalSistola = STDiastola= TPDiastolaPA ischemic Depolarizare redusaRepolarizare redusaDurata si amplitudine redusa

IschemiaScaderea perfuziei miocardice - reversibilaMiocit ischemic- repolarizare precoce (+)Ischemia subendocardica unde T negativeIschemia transmurala unde T pozitive, ascutite

Diferenta de potential intre zonele normale si cele ischemice: mic curent= curent de leziuneFlux de ioni de K dinspre zona mai pozitiva spre cea mai negativaIn sistola (ST) regiunea ischemica este mai negativa- curent de la normal la ischemicIn diastola (TP) regiunea ischemica este mai pozitiva- curent de la ischemic la normal

ST- curent de la regiunea normala spre cea ischemicaTP curent de la regiunea ischemica spre cea normalaSTTP

Curent sistolic de leziuneCurent diastolic de leziune

Curent sistolic de leziuneCurent diastolic de leziune

Curent sistolic de leziuneCurent diastolic de leziune

Infarct miocardicIschemie persistenta celulele isi pierd viabilitatea= necrozaInfarct miocardic: cu supradenivelare de segment ST (STEMI)fara supradenivelare de segment ST (NSTEMI)

CATEGORIALOCALIZAREA OCLUZIEIECG LA PREZENTARE1. ADA proximalProximal de prima perforanta septala ST in V1-V6, DI, aVL si bloc fascicular sau bloc de ramura2. ADA mediuDistal de prima perforanta septala, proximal de marea diagonala ST in V1-V6, DI, aVL 3. ADA distal sau artera diagonalaDistal 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:V1, V3R, V4R sauV5-V6 sauR>S in V1, V25.IMA inferior micACD distal sau artera circumflexa sau ramuri din artera circumflexa ST doar in DII, DIII, aVF

Artera descendenta anterioara

Artera coronara dreapta

sau a circumflexa

Artera coronara dreapta

sau a circumflexa

Artera coronara dreapta

sau a circumflexa

LAD distal sau a diagonala/ a circumflexa

Poate indica localizarea ocluziei arterei coronare

Apare precoceApare in derivatiile directe

NB: o mica supradenivelare de segment ST poate fi normala in V1, V2 V3

Modificare diagnostica in infarctDurata >0.04 secundeAmplitudine de >25% din unda R

Negativarea undei T -modificare tardivaApare cand segmentul ST incepe sa revina la normal

1 minut dupa debut1 ora de la debutLa cateva ore de la debutLa o zi de la debutModificari tardiveLa cateva luni dupa IMAQRPQTSTRPQSTPQTSTRPSTPQTSTRPQT

Angina PrinzmetalPericarditaRepolarizare precoceSdr. BrugadaUnda OsborneSupradenivelarea inghetata - anevrism

Unda OsborneNormalSdr. Brugada

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 pace-maker. Unda Q in cel putin doua dintre DI, aVL, V5, V6Regresia undei R din V1 in V4Incizura pe unda S in V3-V5 semnul CabreraCriteriile Sgarbossa (pt IMA cu BRS)Criterii pentru detectarea unui IM vechi in prezenta BRS

Localizare IMSupradenivelare STSubdenivelare reciproca de STAnteriorV1-V6 (progresie lenta a undei R)II, III, aVFLateralDI, aVL, V5, V6V1-V3InferiorII, III, aVFDI, aVL, posibil derivatiile anterioarePosteriorUnde R anormal de inalte in V1- V3V1-V3

Unda P >2,5mmMorfologie: unda ascutitaIn V1, V2, daca unda este bifazica, predomina componenta pozitiva, initialaAxa se verticalizeaza: +75 - +90Titulatura: p pulmonarDerivatii preferentiale: DII, DIII, aVF

Cauze de supraincarcare atriala dreapta

NB: De obicei asociata cu HVD, exceptia stenoza tricuspidiana

Unda P > 0.11 sMorfologie: unda bifidaIn V1, V2 predomina componenta negativaAxa se orizontalizeazaTitulatura: p mitralDerivatii preferentiale: DI, aVL, V5, V6

Criterii pentru ambele tipuri de dilatariV1: unda larga bifazicacomponenta pozitiva > 1,5 mmcomponenta negativa >1 mm, >0.04sDII:Unda > 2.5 mmUnda > 0,12 sec

Suprasolicitarea VS cauze:Suprasarcina de volum: IMi, IAoSuprasarcina de presiune: HTA, SAo valv./subvalv., CoAo, CMHSuprasolicitarea VS efect:Suprasarcina de volum dilatare cavitatiSuprasarcina de presiune hipertrofie, ingrosare pereti

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

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 HVDinversarea asp. normal pe ECG:R in V1, V2 + S in V5, V6rotatie orara, catre anterior a VD + rotatie posterioara a vf. Inimiiprin masa VD asincronism VD-VS

3 patternuri1. fara tulburari de conducere intraventriculare drepte 2. cu BRD incomplet3. cu BRD complet

Sokolow LyonUnda R in V1 + unda S in V5/ V6>1.1mV

Alte criterii de apreciere:1) deviatie axiala > 90 grd2) R V1 > 7 mm3) R/S V1 >14) P pulmonar5) S/R V6 >16) aspect de BRD

SV1 + RV5(sau V6) >35 mm (indice Sokolov pozitiv) combinat cu deviere ax frontal QRS la dreapta +90SV6 >7 mm (fara BRD)probabil cel mai bun semn este combinatia de pattern de HVD tipic cu dilatare deAS (durata p >=120 ms)S/R>1 in V5/V6 +dilatare deASSV6 >7 mm + dilatare ASQRS >+90 + dilatare deAS (in prezenta de BRD)

*Location of infarction and its relation to the ECG: anterior infarctionAs 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 V16 , I, and aVL.Location of infarction and its relation to the ECG: inferior infarctionST 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. Location of infarction and its relation to the ECG: inferior infarctionST 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. Location of infarction and its relation to the ECG: inferior infarctionST 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. 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.Location of infarction: combinationsThe 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.

Sequence of changes in evolving AMIThe 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.

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. 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.

Deep Q waveThe 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.

T wave inversionThe 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. Sequence of changes in evolving AMIThe 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.

Bundle branch blockBundle 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.Sequence of changes in evolving AMIThe 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.

Sequence of changes in evolving AMIThe 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.