Депрессия st ii avf

by Edward Burns , Last updated November 15, 2017

  • The ST segment is the flat, isoelectric section of the ECG between the end of the S wave (the J point) and the beginning of the T wave.
  • It represents the interval between ventricular depolarization and repolarization.
  • The most important cause of ST segment abnormality (elevation or depression) is myocardial ischaemia or infarction.
  • Causes of ST Segment Elevation

    Morphology of the Elevated ST segment

    Acute STEMI may produce ST elevation with either concave, convex or obliquely straight morphology.

    ST Segment Morphology in Other Conditions

    Patterns of ST Elevation

    Acute ST elevation myocardial infarction (STEMI)

    Causes ST segment elevation and Q-wave formation in contiguous leads, either:

    There is usually reciprocal ST depression in the electrically opposite leads. For example, STE in the high lateral leads I + aVL typically produces reciprocal ST depression in lead III (see example below).

    Follow the links above to find out more about the different STEMI patterns.

    Coronary Vasospasm (Prinzmetal’s angina)

  • This causes a pattern of ST elevation that is very similar to acute STEMI — i.e. localised ST elevation with reciprocal ST depression occurring during episodes of chest pain.
  • However, unlike acute STEMI the ECG changes are transient, reversible with vasodilators and not usually associated with myocardial necrosis.
  • It may be impossible to differentiate these two conditions based on the ECG alone.
  • Acute Pericarditis causes widespread concave (“saddleback”) ST segment elevation with PR segment depression in multiple leads, typically involving I, II, III, aVF, aVL, and V2-6. There is reciprocal ST depression and PR elevation in leads aVR and V1.

    Spodick’s sign was first described by David H. Spodick in 1974 as a downward sloping TP segment with specificity for acute pericarditis.

  • Concave “saddleback” ST elevation in leads I, II, III, aVF, V5-6 with depressed PR segments.
  • There is reciprocal ST depression and PR elevation in aVR.
  • Spodick’s sign is present.
  • Benign Early Repolarization

    Benign Early Repolarization (BER) causes mild ST elevation with tall T-waves mainly in the precordial leads. Is a normal variant commonly seen in young, healthy patients. There is often notching of the J-point — the “fish-hook” pattern. The ST changes may be more prominent at slower heart rates and disappear in the presence of tachycardia.

  • There is slight concave ST elevation in the precordial and inferior leads with notching of the J-point (the “fish-hook” pattern)
  • Left Bundle Branch Block

    In Left bundle branch block (LBBB), the ST segments and T waves show “appropriate discordance” — i.e. they are directed opposite to the main vector of the QRS complex. This produces ST elevation and upright T waves in leads with a negative QRS complex (dominant S wave), while producing ST depression and T wave inversion in leads with a positive QRS complex (dominant R wave).

  • Note the ST elevation in leads with deep S waves — most apparent in V1-3.
  • Also note the ST depression in leads with tall R waves — most apparent in I and aVL.
  • Left Ventricular Hypertrophy

    Left Ventricular Hypertrophy (LVH) causes a similar pattern of repolarization abnormalities as LBBB, with ST elevation in the leads with deep S-waves (usually V1-3) and ST depression/T-wave inversion in the leads with tall R waves (I, aVL, V5-6).

  • Deep S waves with ST elevation in V1-3
  • ST depression and T-wave inversion in the lateral leads V5-6
  • Note in this this case there is also right axis deviation, which is unusual for LVH and may be due to associated left posterior fascicular block.
  • Ventricular Aneurysm

    This is an ECG pattern of Ventricular Aneurysm – residual ST elevation and deep Q waves seen in patients with previous myocardial infarction. It is associated with extensive myocardial damage and paradoxical movement of the left ventricular wall during systole.

  • There is ST elevation with deep Q waves and inverted T waves in V1-3.
  • This pattern suggests the presence of a left ventricular aneurysm due to a prior anteroseptal MI.
  • Brugada Syndrome is an inherited channelopathy (a disease of myocardial sodium channels) that leads to paroxysmal ventricular arrhythmias and sudden cardiac death in young patients. The tell-tale sign on the resting ECG is the “Brugada sign” — ST elevation and partial RBBB in V1-2 with a “coved” morphology.

  • There is ST elevation and partial RBBB in V1-2 with a coved morphology — the “Brugada sign”.
  • Ventricular Paced Rhythm

    Ventricular pacing (with a pacing wire in the right ventricle) causes ST segment abnormalities identical to that seen in LBBB. There is appropriate discordance, with the ST segment and T wave directed opposite to the main vector of the QRS complex.

    Raised Intracranial Pressure

    Raised Intracranial Pressure (ICP) (e.g. due to intracranial haemorrhage, traumatic brain injury) may cause ST elevation or depression that simulates myocardial ischaemia or pericarditis. More commonly, raised ICP is associated with widespread, deep T-wave inversions (“cerebral T waves”).

  • Widespread ST elevation with concave (pericarditis-like) morphology in a patient with severe traumatic brain injury.
  • Less Common Causes of ST segment Elevation

  • Pulmonary embolism and acute cor pulmonale (usually in lead III)
  • Acute aortic dissection (classically causes inferior STEMI due to RCA dissection)
  • Hyperkalaemia
  • Sodium-channel blocking drugs (secondary to QRS widening)
  • J-waves (hypothermia, hypercalcaemia)
  • Following electrical cardioversion
  • Others: Cardiac tumour, myocarditis, pancreas or gallbladder disease
  • Transient ST elevation after DC cardioversion from VF J waves in hypothermia simulating ST elevation

    Causes of ST Depression

  • Myocardial ischaemia / NSTEMI
  • Reciprocal change in STEMI
  • Posterior MI
  • Digoxin effect
  • Hypokalaemia
  • Supraventricular tachycardia
  • Right bundle branch block
  • Right ventricular hypertrophy
  • Left bundle branch block
  • Left ventricular hypertrophy
  • Ventricular paced rhythm
  • Morphology of ST Depression

  • ST depression can be either upsloping, downsloping, or horizontal.
  • Horizontal or downsloping ST depression ? 0.5 mm at the J-point in ? 2 contiguous leads indicates myocardial ischaemia (according to the 2007 Task Force Criteria).
  • Upsloping ST depression in the precordial leads with prominent “De Winter’s” T waves is highly specific for occlusion of the LAD.
  • Reciprocal change has a morphology that resembles “upside down” ST elevation and is seen in leads electrically opposite to the site of infarction.
  • Posterior MI manifests as horizontal ST depression in V1-3 and is associated with upright T waves and tall R waves.
  • ST segment morphology in myocardial ischaemia

    ST segment morphology in posterior MI

    Patterns of ST depression

    Myocardial Ischaemia

    ST depression due to subendocardial ischaemia may be present in a variable number of leads and with variable morphology. It is often most prominent in the left precordial leads V4-6 plus leads I, II and aVL. Widespread ST depression with ST elevation in aVR is seen in left main coronary artery occlusion and severe triple vessel disease.

    NB. ST depression localised to the inferior or high lateral leads is more likely to represent reciprocal change than subendocardial ischaemia. The corresponding ST elevation may be subtle and difficult to see, but should be sought. This concept is discussed further here.

    ST elevation during acute STEMI is associated with simultaneous ST depression in the electrically opposite leads:

  • Inferior STEMI produces reciprocal ST depression in aVL (± lead I).
  • Lateral or anterolateral STEMI produces reciprocal ST depression in III and aVF (± lead II).
  • Reciprocal ST depression in V1-3 occurs with posterior infarction (see below).
  • Reciprocal ST depression in aVL with inferior STEMI Reciprocal ST depression in III and aVF with high lateral STEMI

    Posterior Myocardial Infarction

    Acute posterior STEMI causes ST depression in the anterior leads V1-3, along with dominant R waves (“Q-wave equivalent”) and upright T waves. There is ST elevation in the posterior leads V7-9.

    De Winter’s T waves: a pattern of up-sloping ST depression with symmetrically peaked T waves in the precordial leads is considered to be a STEMI equivalent, and is highly specific for an acute occlusion of the LAD.

    De Winter’s T Waves

    Digoxin Effect: Treatment with digoxin causes downsloping ST depression with a “sagging” morphology, reminiscent of Salvador Dali’s moustache.

    Digoxin reverse tick salvador dali moustache

    Hypokalaemia causes widespread downsloping ST depression with T-wave flattening/inversion, prominent U waves and a prolonged QU interval.

    Right ventricular hypertrophy

    Right ventricular hypertrophy (RVH) causes ST depression and T-wave inversion in the right precordial leads V1-3.

    Right ventricular hypertrophy

    Right Bundle Branch Block

    Right Bundle Branch Block (RBBB) may produce a similar pattern of repolarisation abnormalities to RVH, with ST depression and T wave inversion in V1-3.

    Right bundle branch block

    Supraventricular tachycardia

    Supraventricular tachycardia (e.g. AVNRT) typically causes widespread horizontal ST depression, most prominent in the left precordial leads (V4-6). This rate-related ST depression does not necessarily indicate the presence of myocardial ischaemia, provided that it resolves with treatment.

    AV-nodal re-entry tachycardia

  • Edhouse J, Brady WJ, Morris F. ABC of clinical electrocardiography: Acute myocardial infarction-Part II. BMJ. 2002 Apr 20;324(7343):963-6. Review. PubMed PMID: 11964344; PubMed Central PMCID: PMC1122906. Full text.
  • Smith SW. T/QRS ratio best distinguishes ventricular aneurysm from anterior myocardial infarction. Am J Emerg Med. 2005 May;23(3):279-87. PubMed PMID: 15915398.
  • Brady WJ, Truwit JD. Critical Decisions in Emergency and Acute Care Electrocardiography
  • Chan, TC. ECG in Emergency Medicine and Acute Care
  • Wang, K. Atlas of Electrocardiography
  • ECG A to Z by diagnosis –alphabetical diagnostic approach to the ECG
  • ECG CLINICAL CASES — ECG’s placed in clinical context with a challenging Q&A approach
  • LITFL ECG IMAGE Database — Searchable database of LITFL ECG’s
  • lifeinthefastlane.com

    by Edward Burns , Last updated August 29, 2017

    Clinical Significance

  • Inferior MIs account for 40-50% of all myocardial infarctions.
  • Generally have a more favourable prognosis than anterior myocardial infarction (in-hospital mortality only 2-9%), however certain factors indicate a worse outcome.
  • Up to 40% of patients with an inferior STEMI will have a concomitant right ventricular infarction. These patients may develop severe hypotension in response to nitrates and generally have a worse prognosis.
  • Up to 20% of patients with inferior STEMI will develop significant bradycardia due to second- or third-degree AV block. These patients have an increased in-hospital mortality (>20%).
  • Inferior STEMI may also be associated with posterior infarction, which confers a worse prognosis due to increased area of myocardium at risk.
  • How to recognise an inferior STEMI

  • ST elevation in leads II, III and aVF
  • Progressive development of Q waves in II, III and aVF
  • Reciprocal ST depression in aVL (± lead I)
  • Which Artery Is the Culprit?

    80%) of inferior STEMIs are due to occlusion of the dominant right coronary artery (RCA).

  • Less commonly (around 18% of the time), the culprit vessel is a dominant left circumflex artery (LCx).
  • Occasionally, inferior STEMI may result from occlusion of a “type III” or “wraparound” left anterior descending artery (LAD). This produces the unusual pattern of concomitant inferior and anterior ST elevation.
  • While both RCA and circumflex occlusion may cause infarction of the inferior wall, the precise area of infarction in each case is slightly different:

  • The RCA territory covers the medial part of the inferior wall, including the inferior septum.
  • The LCx territory covers the lateral part of the inferior wall and the left posterobasal area.
  • This produces subtly different patterns on the ECG:

  • The injury current in RCA occlusion is directed inferiorly and rightward, producing ST elevation in lead III > lead II (as lead III is more rightward facing).
  • The injury current in LCx occlusion is directed inferiorly and leftward, producing ST elevation in the lateral leads I and V5-6.
  • These differences allow for electrocardiographic differentiation between RCA and LCx occlusion.

  • ST elevation in lead III > lead II
  • Presence of reciprocal ST depression in lead I
  • Signs of right ventricular infarction: STE in V1 and V4R
  • Circumflex occlusion is suggested by:

  • ST elevation in lead II = lead III
  • Absence of reciprocal ST depression in lead I
  • Signs of lateral infarction: ST elevation in the lateral leads I and aVL or V5-6
  • (NB. Relative Q-wave depth in leads II and III is not useful in determining the culprit artery. Both RCA and LCx occlusion produce a similar pattern of Q wave changes, often with deeper Q waves seen in lead III)

    Early inferior STEMI:

  • Hyperacute (peaked) T waves in II, III and aVF with relative loss of R wave height.
  • Early ST elevation and Q-wave formation in lead III.
  • Reciprocal ST depression and T wave inversion in aVL.
  • ST elevation in lead III > lead II suggests an RCA occlusion; the subtle ST elevation in V4R would be consistent with this.
  • Note how the ST segment morphology in aVL is an exact mirror image of lead III. This reciprocal change occurs because these two leads are approximately opposite to one another (150 degrees apart).

    The concept of reciprocal change can be further highlighted by taking lead aVL and inverting it… see how the ST morphology now looks identical to lead III.

    (For more about lead aVL and its utility in diagnosing subtle inferior STEMI, check out this post from Dr Smith’s ECG Blog)

  • ST elevation in II, III and aVF.
  • Q-wave formation in III and aVF.
  • Reciprocal ST depression and T wave inversion in aVL
  • ST elevation in lead II = lead III and absent reciprocal change in lead I (isoelectric ST segment) suggest a circumflex artery occlusion
  • Marked ST elevation in II, III and aVF with early Q-wave formation.
  • Reciprocal changes in aVL.
  • ST elevation in lead III > II with reciprocal change present in lead I and ST elevation in V1-2 suggests RCA occlusion with associated RV infarction: This patient should have right-sided leads to confirm this.
  • Hyperacute inferior STEMI:

  • Hyperacute T waves in II, III and aVF.
  • Early ST elevation and loss of R wave height in II, III and aVF.
  • Reciprocal change in aVL and lead I.
  • The concave ST elevation in II, III and aVF may be mistaken for pericarditis.
  • However, the fact that the ST elevation is localised to the inferior leads with reciprocal changes in aVL confirms that this is an inferior STEMI.
  • Massive inferolateral STEMI:

  • Marked ST elevation in II, III and aVF with a “tombstone” morphology.
  • Reciprocal change in aVL.
  • ST elevation is also present in the lateral leads V5-6, indicating an extensive infarct of the inferior and lateral walls.
  • In patients with inferior STEMI, ST elevation of 2mm or more in leads V5 and V6 is predictive of extensive coronary artery disease and a large area of infarction.

    Recent inferolateral STEMI:

  • Well-formed Q waves in III and aVF suggest that this STEMI is not acute.
  • The T waves in III and aVF are beginning to invert.
  • There is still some residual ST elevation in the inferior (II, III, avF) and lateral (V5-6) leads. ST elevation may take 2 weeks to resolve after an acute inferior MI (even longer for an anterior STEMI).
  • NB. If this patient had ongoing chest pain you would still treat them as an acute STEMI!

    Bradycardia and AV Block in Inferior STEMI

  • Ischaemia of the AV node due to impaired blood flow via the AV nodal artery. This artery arises from the RCA 80% of the time, hence its involvement in inferior STEMI due to RCA occlusion.
  • Bezold-Jarisch reflex = increased vagal tone secondary to ischaemia.
  • The conduction block may develop either as a step-wise progression from 1st degree heart block via Wenckebach to complete heart block (in 50% of cases) or as abrupt onset of second or third-degree heart block (in the remaining 50%).

    Patients may also manifest signs of sinus node dysfunction, such as sinus bradycardia, sinus pauses, sinoatrial exit block and sinus arrest. Similarly to AV node dysfunction, this may result from increased vagal tone or ischaemia of the SA node (the SA nodal artery is supplied by the RCA in 60% of people).

    Bradyarrhythmias and AV block in the context of inferior STEMI are usually transient (lasting hours to days), respond well to atropine and do not require permanent pacing.

  • Inferior STEMI with third degree heart block and slow junctional escape rhythm.
  • Inferior STEMI with sinus node dysfunction (either sinus arrest or extreme sinus bradycardia) and a slow junctional escape rhythm.
  • Edhouse J, Brady WJ, Morris F. ABC of clinical electrocardiography: Acute myocardial infarction-Part II. BMJ. 2002; 324: 963-6. [full text]
  • Morris F, Brady WJ. ABC of clinical electrocardiography: Acute myocardial infarction-Part I. BMJ. 2002; 324: 831-4. [full text]
  • Berger PB, Ryan TJ. Inferior myocardial infarction: High-risk subgroups.Circulation. 1990; 81(2): 401-11. [full text]
  • Hampton, JR. The ECG In Practice, 6e
  • Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice: Adult and Pediatric, 6e
  • Wagner, GS. Marriott’s Practical Electrocardiography 12e
  • Mattu, A. ECG’s for the Emergency Physician
  • LITFL Further Reading

  • ECG BASICS — Waves, Intervals, Segments and Clinical Interpretation
  • 100 ECG Quiz — Self-assessment tool for examination practice
  • ECG Reference SITES and BOOKS — the best of the rest
  • ECG and Cardiology Eponymous Syndromes — Cheats guide to eponymous emancipation
  • ECG Exam Template — a framework for answering ECG exam questions.
  • Ed Burns is an Emergency Physician working in Prehospital & Retrieval Medicine in Sydney, Australia. He has a passion for ECG interpretation and medical education. Ed is the force behind the LITFL ECG library | + Edward Burns | @edjamesburns



    • ritme
    • frequentie.
    • hartas.
    • p — q tijd.
    • QRS tijd.
    • eventuele aanwezigheid bundeltakblok.
    • beoordeling QRS complex
    • beoordeling ST segmenten.
    • beoordeling T toppen.
    • Normaal sinusritme: frequentie 60 — 100 sl/min.

      • Sinusbradycardie: ,, 60 — ,,
      • Sinustachycardie: ,, 100 — 170 sl/min.
      • Atriumritme: ,, 50 — 60 sl/min.
      • Snel atriumritme ,, 60 — 100 sl/min.
      • Atriumtachycardie ,, 100 — 240 sl/min.
      • Paroxysmale Atriumtachycardie met blok ( P.A.T. met blok) atriumfrequentie meestal 200sl/min.kamerfrequentie afhankelijk van A.V. geleiding. (digitalisintoxicatie)
      • Atriumflutter: Atriumfrequentie plus of min. 300 s1/min. Kamerfrequentie afhankelijk van de A.V. geleiding dus 2:1 geleiding: kamerfrequentie 135 — 165 s1/min.: 3:1 geleiding kamerfrequentie 90 — 110 s1/min. Ook wisselende A.V. geleiding komt voor.
      • Atriumfibrilleren: Atriumfrequentie 400 — 600 sl/min., irregulair! Kamerfrequentie 150 — 180 sl/min. irregulair.
      • (alleen regulair ritme mogelijk bij een totaal blok op A.V. niveau).
      • Junctionritme frequentie 40- 55 sl/min.
      • Versneld junction ritme frequentie55-100 sl/min.
      • Junction tachycardie frequentie 120-240 sl/min.
      • Ventriculair ritme frequentie 20- 40 sl/min.
      • Versneld Ventriculair ritme: frequentie40-100 sl/min.(a.i.v.r.)
      • Ventriculaire Tachycardie: frequentie 100-260 sl/min.
      • Bidirectionele tachycardie: Tachycardie waarbij opeenvolgende QRS complexen in sommige af leidingen tegen over elkaar staan. Het ritme kan ventriculair en supraventriculair zijn en er is uiting van digitalisintoxicatie.
      • Torsade de pointes: Ventriculaire Tachycardie waarbij het QRS-complex geleidelijk van richting verandert, waardoor de top van het complex als het ware om de iso-elektrische lijn draait.
      • Ventrikelflutter: frequentie + 300 sl/min.
      • Ventrikelfibrilleren: frequentie + 400 sl/min.
      • Geen ritme: asystolie.
      • Geleidingsstoornissen.

      • SSS; (Sick Sinus Syndrome): extreme bradycardie op oudere leeftijd sinusarrest. sino-auriculair blok. boezemfibrilleren met lage kamer frequentie niet veroorzaakt door medicatie. brady- tachycardiesyndroom.
      • 1 ° A.V. Block: verlenging van de P — Q tijd, langer dan 0,21 sec.
      • 2 ° A.V. Block: (mobitz 1 of wenkebach) Verlenging van P — Q tijd, met afname van de toename van de verlenging. "decrement van het increment." Verkorting van RR interval, niet alle slagen worden voortgeleid. Hiervan zijn variaties mogelijk: 3:1, 4:1, 2:1 tweede graads A.V. blok.
      • TOTAAL A.V. Block:Geen enkele slag wordt voort geleid.Normaal ontstaat vlak onder het blok een escaperitme. Er is een A.V. Dissosiatie d.w.z. er is geen samenhang tussen supra-ventriculaire en ventriculaire elektrische aktiviteit. Escaperitme redelijk betrouwbaar.
      • Verkorting van P-Q tijd kan wijzen op W.P.W. syndroom.
      • 2 ° blok op bundeltakniveau: plotselinge uitval, geen verlenging van de P — Q tijd. ( mobitz II )Prognose minder gunstig dan bij Mobitz type I.
      • Totaal blok op bundeltakniveau: geen enkele slag wordt voortgeleid. QRS verbreedt en bizar van vorm. Ongunstig, escaperitme is onbetrouwbaar. Door verlaagde frequentie kans op PVC tot VF. Prognose afhankelijk van oorzaak. Definitieve behandeling: Pacemaker.
      • Stand van de elektrische hartas:

        De normale hartas loopt van + 120 tot — 30 ° zuigelingen en kinderen tot 10 jaar hebben een rechter hartas van 10 — 18 jaar een vertikale hartas.

        Bij mensen van ± 65 jaar en ouder dreigt de stand van de elektrische hartas naar links te gaan.

        Bij een groot Antero/septaal infarct met RBTB en Fasiculus Anticus blok bestaat er een linker asdraai.

        Bij een Fascicuclus posticus blok ontstaat er een rechter asdraai. Ook zonder infarct is het partiлle hemiblok mogelijk; dit uit zich in een linker of rechter asdraai.

        P — Q interval 0,12 — 0,21 seconde.

        Q — T interval 0,35 — 0,42 seconde.

        QRS interval 0,07 — 0,10 seconde.

        S-T interval 0,24 — 0,32 seconde.

        ECG afleidingen

      • Af l. I, II, III = standaardafleidingen volgens Einthoven.
      • Af l. aVR, AvI en aVf = Versterkte (augmented) afleidingen extremiteiten volgens Goldberger.
      • Af l. V1-V6 = unipolaire precordiale afleidingen volgens Wilson.
      • Lewis-af l. = speciale bipolaire borstafleiding. P top wordt hierdoor meer zichtbaar gemaakt. Plaatsing:R.A. elektrode op 2e intercost. rechts naast sternum, L.A. elektrode op 4e intercostaalruimte rechts registeren op af l. 1.
      • Rechter Ventrikel ECG: standaard afleidingen onveranderd precordiale: VI, V2, V3R, V4R,V5R, V6R . R.V. infarct: V3R en V4R ST elevaties van >1 mm tot 12 — 14 uur na ontstaan infarct zichtbaar.
      • oesophagus elektrode als sonde ingebracht om boezem aktiviteit te registreren.


    • RBTB : Rechterbundeltakblok . Af l. I
    • compleet: Initiele activiteit normaal -af l. V6. QRS complex VI en V2. -af l. V1. VI St depressie en neg. T top -Afl. I en AVL: kleine Q normale R, stompe brede S in V6. Bij A/S infarct geen le R en geen neg. T in V1, maar ST -elevatie. RBTB komt vaak bij jonge mensen voor, heeft op zich geen pathologische betekenis.
    • Incompleet: het enige verschil is dat de duur van het QRS complex langer is dan 0,10 sec. maar korter dan 0,12 sec.
    • LBTB: Linkerbundeltakblok.
    • Compleet: Initiele activatie abnormaal-af l. 1. QRS 0,12 sec. of breder -afl. V6. Brede R -afl. 1 AVL en V6 Geen Q in afl. 1. Meestal geen R in V1, soms wel dan septale vezels vezels intact.Vaak een notch in de R van afl. I . Afleiding 1 diepe S. Afleiding Vl St elevatie bol van vorm, anders dan bij infarct. ST segmenten niet te beoordelen. Onderwandinfarct nog wel vast te stellen d.m.v. Q’s LBTB altijd pathologisch.
    • Incompleet: het enige verschil met compleet is dat de duur van het QRS compleet langer is dan 0,10 sec. maar korter dan 0,12 sec.
    • Een notch in de P top in I en II en/of een bifasische P top in VI, waarbij het negatieve deel van de P-top groter of gelijk is aan 0,04 sec en een diepte heeft van 1 mm of meer kan passen bij linker boezem hypertrofie.

      Als de P toppen in de afleidingen II, III en AVF groter of gelijk zijn aan 2,5 mm en breder of gelijk zijn aan 0,12 sec. dan kan dat wijzen op rechterboezemhypertrofie.

      Een negatieve P top in VI past hier ook bij.

      Normaal: Aanwezig in af l.: I AVL V6 (septumactivatie) Aanwezig in afl.: AVR < 1 mm diep is en een breedte heeft van < O.O4sec. Bij een rechter asdraai is een Q in II, III en AVF normaal.

      Pathologisch: Als hij breder/gelijk is aan 0,03 sec. en groter of gelijk is aan 1/3 deel van de daarop volgende R in af l. I, II, V2 — V6 en AVF. Als hij breder/gelijk is 0,05 sec. en groter/gelijk is aan 1/3 deel van de daarop volgende R in afleiding III. QR patroon in II, V1 — V6.

      Normaal: R toppen zijn klein in afleiding V1 en nemen toe in hoogte tot V4, V5, daarna weer afname in grootte.

      Pathologisch: Abrupte R-top toename, geen geleidelijke toename, maar ineens hoge R toppen (Precordiaal) R-top verlies kan wijzen op infarcing.

      Hoge R top in afleiding V1: Rechter Ventrikel Hypertrofie. RBTB. W.P.W. syndroom. Posterior infarct.

      Normaal: St segment begint op de basislijn, loopt lang zaam omhoog, gaat over in de T-top. 1 — 2 mm ST elevatie in V1 — V2 is normaal.

      Pathologisch: Meer dan 1 mm ST elevatie in af l. I, II, III, AVL, AVF, V3 — V6. Meer dan 2 mm ST elevatie in V1, V2. Meer dan 0,5 mm ST depressie, horizontaal verlopend St segment, of af lopend ST segment in afl. I, II, III, AVL, AVF, V1- V6. Acute infarcering geeft ST elevatie in dat gebied en depressie in het tegenovergestelde gebied.(reciproke Depressie.)

      Normaal: Asymetrisch van vorm, d.w.z. dat het stijgende deel van de T-top langer duurt dan het dalende deel. Positief in I, II, AVL, V3 — V6. T- toppen zijn in de af l. II, III en AVF, vooral afl.III.

      Pathologisch: Vlakke T-top: minder dan 0,5 mm negatief en positief. Negatieve T-top in I, II, V3 — V6 T-top veranderingen in af l. II, III en AVF tegelijk. Neg.T-top III of AVF is niet pathologisch. T-top in AVL beoordelen als de daarop volgende R groter of gelijk is aan 5 mm. (als de R-top kleiner is dan 0,5 mm zijn T-top veranderingen sneller pathologisch. Als T-top in V1 groter is dan dan de T-top in V6 is dat meestal het eerste teken van LVH. T-top veranderingen meer pathologisch dan bij vrouwen. Symmetrische T-toppen, hoge en spitsere T-toppenT top inversie. Nog T top in af 1. I met positief QRS. Als in af 1. I met positief QRS is, dan moet de T top in af l. I groter zijn dan in af l. III.

      Komt voor bij : Hypokaliemie , Sinusbradycardie , Coronairlijden.

      U-golven zijn het beste zichtbaar in af l. V2 — V4. Inversie van de U-golf tegengesteld aan de T-top is pathologisch

      Q’s of QS patroon, R-top verlies in volgende af leidingen:

      I, AVL Hoog Lateraal.

      I, AVL, VS, V6 Lateraal.

      I, AVL, V3 — V6 Anterolateraal.

      I, AVL, VI — V6 Antero septaal lateraal.

      VI — V4, (I, AVL) Antero septaal.

      V2 — V4 (I, AVL) Anterior.

      II,III, AVF Inferior.

      II, III, AVF V3R, V4R Inferior en rechter ventrikel.

      II, III, AVF, V5, V6,V3R,V4R Inferior rechter Ventrikel en lateraal

      II, II, AVF + Hoge R in VI Infero Postior.

      Hoge R in VI Posterior.

      L.V.H. R in I, II en III groter of gelijk aan 20 mm R in AVL groter of gelijk aan 12 mm. R in V5, V6 groter of gelijk aan 26 mm Intrinsicoide Deflexie: breedt van het stijgende of dalende deel van de R-top. In V6 is dit groter of gelijk aan 0,055 sec. S in VI + R in VS — V6 groter of gelijk aan 35 mm ST depressie in af l. 1, AVL, VS V6 (zonder digitalis gebruik) Neg. T in I, AVL, V5 en V6 (met digitalis gebruik) Linker asdraai.

      R.V.H. R in VI groter of gelijk aan 5 mm. R/S ratio groter of gelijk aan I in VI S is groter dan de R in I. S is groter dan de R in V5.

      Diepe S in afleiding I. ST elevatie in afleiding II. Diepe Q + neg. T in afl. III. Draaiing van de hartas links/rechts Meestal rechts. Vaak sinustachycardie of boezemfibrilleren. Compleet of incompleet RBTB. ST depressie in T-top inversie precordiaal. Toename R/S ratio in VI.

      ST elevaties in vrijwel alle af leidingen. Geen reciproke ST depressies. ST segment is bol van vorm. Daling PTa segment. Verticale stand van de elektrische hartas. Na verloop van dagen wordt het ST segment isoelektrisch en de T-top inverseert. Vaak Supra Ventriculaire ritmestoornissen.

      Smalle spitse T-toppen en/of afwezigheid van T-toppen. Verbreding QRS complex. Ventriculaire ritmestoornissen tot V.F. Verkorte QT tijd.

      Concave depressie van het ST segment. Zwak positieve of negatieve T-toppen. Hoge U-golven die samenvallen met de T-top. Vooral zichtbaar in V2 — V4.

      Verkorting van het ST segment. Verkorting van QT tijd daardoor.

      Verlenging van het ST segment. Toename QT tijd.

      ECG veranderingen passend bij L.V.H.

      Normale spiegel : ST depressie. Komvorming AV geleiding. Vertraging AV geleiding. Kortere QT tijd.

      Toxische spiegel: le tot 3e graads AV blok. P.A.T. met blok. Nodaal tachycardie. PVC tot VF.

      Normale spiegel: ST depressie. vlakkere T-toppen. U-golven.

      Toxische spiegel: Toename qrs breedte. AV geleidingsstoornissen tot 3e gr. AV blok. PVC tot VF.

      Erfelijke aandoening gekenmerkt door verlengde QT tijd daardoor verhoogde kans op ventriculaire ritmestoornissen daardoor kans op mors subita. Syncope vooral bij inspanning. QT tijd varieert van slag tot slag.

      Verlengde QT tijd, doofheid. meestal familair. Verhoogde kans op mors subita door Ventriculaire ritmestoornissen.

      Wolff Parkinson White Syndroom. (Pre-exitatie syndroom)

      Korte PQ tijd Verbinding Boezem — Kamer (Bundel van Kent) Delta golf. Verbreed QRS complex. Kans op Mors Subita bij boezemfibrilleren.

      Lown Ganong Levins Syndroom.(Pre-excitatie syndroom)


      The San Diego Paramedics

      12 Lead E.C.G. Field Diagnosis Made Easy

      Knowledge of the anatomy of the heart, the physiology of the heart, and the electrocardiography of the heart make a paramedic an

      Emergency Cardiac Care Provider.

      A s primary point of care field paramedics, we have been taxed with the new challenge of diagnosing 12 lead cardiographs in the field and making a definitive diagnosis of acute myocardial infarction. This overwhelming task has been at sometimes difficult to manage and to complicate matters, we do not use this skill regularly enough to maintain the skills.

      So, I hope the following information is helpful.

      The 12 lead EKG measures electrical potential

    • All cells membranes in the body are charged.
    • In a polarized state (resting) the membrane carries a net + charge. (results from the difference of intra and extra cellular electrolyte concentrations)
    • Depolarization: The shift in electrolytes which reverses the charge

      Repolarization: Return to the resting state

      Helpful hints and rules to reading the 12 lead.

    • Always be sure to check for an inverted or negative QRS complex in AVR. This will ensure that the lead were correctly connected appropriately and your recordings should be accurate.
    • Analyse and evaluate the right chest leads. V1 & V2 will reveal more than any other two contiguous leads. This is where you check for a Bundle Branch Block, Anterior and Posterior wall infarctions, and «R» wave progression, etc..
    • When checking your axis, always focus on Leads I & AVF. Be sure to check for Bundle Branch Block. Axis vectors are inaccurate in their presence.
    • When checking for signs of infarct, omit AVR. It is of no diagnostic value due to the fact that it misrepresents pathological Q waves and obscures them.
    • Acute Myocardial Infarction cannot be positively identified in the presence of LBBB.

    • It is prudent to suspect it per the patients presentation: however, serum enzyme tests among other things are needed to make the diagnosis.

    • As a rule, standard criteria for diagnosing AMI dictates that ST elevation of 1 mm. or more in the presence of pathological Q waves in 2 or more contiguous leads is sufficient.
    • Einthoven’s Triangle represents the leads that we all use with our monitors on a regular basis:

    • Lead I: The positive lead is above the left breast or on the left arm and the negative lead is on the right arm.

    Records the difference of potential between the Left arm and Right arm.

    Records the difference of potential between the left leg and the right arm.

    Records the difference of potential between the left leg and the right arm.

    The hexaxial view

    Leads I, II & III & AVR, AVL, and AVF.

  • I: Left Chest
  • II: Left Upper Quadrant
  • III: Right Upper Quadrant
  • AVR: Right lateral arm
  • AVL: Left lateral arm
  • AVF: Right lateral lower leg
  • The four limb leads go on the four extremities as follows: The upper extremities need placement of the electrodes on the area of the lateral humoral aspect of the arms. The lower extremities need placement of the electrodes on the lateral lower legs near the lateral mallelous.
  • Lead aVR faces the heart from the right shoulder and is oriented to the cavity of the heart.
  • Lead aVL faces the heart from the left shoulder and is oriented to the Left Ventricle.
  • Lead aVF face the heart from the left hip and is oriented to the inferior surface of the Left Ventricle.
  • Six Precordial Electrode Placement:

    The precordial views make up a cross section view of the heart in a transverse horizontal plane projecting a view across the AV Node.

    Einthoven’s Triangle and the four limb leads make up the «HEXAXIAL VIEW!» This view is a vertical/frontal-posterior — ventral/dorsal plane making a star with 6 points intersecting through the heart in a flat frontal plane across the patients chest.

    So, adding this up: lead I, II and III, lead AVR, AVL, AVF, and the 6 precordial leads equals 12 leads. RIGHT.

    ( 4 on the limbs and 6 on the chest )

    The cardiac monitor uses the four Limb Leads to make up Lead I, II, III & AVR, AVL, AVF; six views.

    The following situation constitutes activation of the cardiac response team at the hospital by reporting the field diagnosis of AMI!

  • Category one: AMI that clearly meets the criteria. Example: 1 mm or more of ST elevation in the inferior leads (II, III, AVF) with reciprocal changes in the lateral leads (I, AVL, V5, V6) Reciprocal changes not necessary to make the diagnosis.
  • Category two: The following will result in your reporting the specific findings of concern that may or may not result in the Cardiac Response team. Example: 1 mm of ST elevation in the anterior leads. (V1-V4) Example: Injury/Infarct pattern in the presence of LBBB with cardiogenic clinical presentation.
  • The following situation will result in the 12 Lead ECG being reported as «normal». No subsequent activation of the cardiac response team.

  • Category Three: No patterns of ischemia or infarction.
  • Other Signals to use as a diagnostic tool:

  • Tachycardia: (heart rate above 100) indicates damage to the left Ventricle and an «anterior» or «lateral» infarct. The Left Circumflex and or Left Descending Coronary Artery is occluded.

    Visable elevation in the CHEST LEADS: V-3, 4, 5, & 6.

    Systematic Infarct Recognition Approach

    • Assure that aVR is primarily negative.
    • Rule out a :eft Bundle Branch Block (LBBB) in V1 and or V2. Verify in V6.
    • Check all leads for patterns of ischemia, injury, infarction and reciprocal changes.
    • AMI diagnosis criteria: 1mm. or more of ST elevation in 2 or more contiguous leads.

      Anterior wall requires 2mm. or more of ST elevation (V1-V4)

      Diagrams below indicate which part the heart is being affected and what lead would show the changes.

      12 lead rapid assessment

      • Verify aVR is negative
      • Assess rate and rhythm
      • Axis determination — Leads I and aVF
      • Conduction abnormalities: LBBB — seen in V1

      Drugs or Electrolytes

      Early repolarization

    • Ischemia, Injury, Infarct signs: T-wave inversions ST segment elevation Significant Q waves
    • Acute MI pattern:Anterior: ST elevation in V1, V2, V3, V4 ST depression in II, III, aVF Inferior: ST elevation in II, III, aVF ST depression in V1, V2, V3, or I, aVL Lateral: ST elevation in I, aVL, V5, V6 ST depression in II, II, aVF Septal wall: ST elevation in I, aVL, V1, V2

      Posterior: tall and wide R waves and ST depression in V1, V2

      Right Ventricular: ST elevations in V4R, V5R, V6R (5 additional right chest wall electrodes placed on the chest in the same positions as the precordial leads)

    • Clinical presentation
    • Treatment plan
    • If you can comprehend which way the current is expected to flow in The HEXAXIAL VIEW and The PRECORDIAL VIEW of the heart, then you can diagnose which area is effected if it is an abnormal flow.

      12 lead rapid interpretation

      Making the accurate Field Diagnosis:

    • There are elevations ( 1 mm )in two contiguous (connecting) leads:

    Leads adjacent to each other.

  • There is at least one lead with reciprocal changes..
  • If the Q wave is more than 1/3 the size of the R wave.
  • Table below shows what the ECG would look like in the Vector where the heart is being affected. All other areas would look normal, without elevation or depression. unless there is an «old MI.» In that case, the prior damage would show up as a depressed segment.

  • ST elevation without abnormal Q wave
  • Usually associated with occlusion of the left anterior Descending branch of the left coronary artery (LCA)
  • ST elevation with/without abnormal Q wave
  • May be a component of a mutiple-site infarction
  • Usually associated with obstruction of the left circumflex artery
  • Usally associated with right coronary artery (RCA) occlusion
    • Usually accompanies inferior MI due to proximal occlusion of the RCA
    • Best diagnosed by 1 — 2 mm ST elevation in lead V4R
    • An important cause of hypotension in inferior MI recognized by jugular venous distension with clear lung fields
    • Aggressive therapy is indicated, including: reperfusion, adequate IV fluids for right heart filling, and pacing to maintain A-V synchrony if necessary
    • Tall, broad (>0.04 sec) R wave and ST depression in V1 and V2 (reciprocal changes)
    • Frequently associated with inferior MI
    • Usually associated with obstruction of RCA and or left circumflex coronary artery
    • If the Q wave ( the first downward «negative» deflected wave ) is more than 1/3 the size of the R wave ( the first upward deflected «positive» wave ) it is pathological and indicative of an A.M.I.

      Bundle Branch Block In Bundle Branch Block, the firing of the Ventricles does not occur simultaneously as it should (It occurs in series instead of parallel). Conduction reaches a block in one of the branches (in the cardiac septum) and refers it to the opposing branch to be conducted completely. It is then when conduction jumps the Intra-Ventricular Septum to ultimately conduct to the remaining blocked Bundle Branch. It is because of this that you see two different distinctly separate QRS complexes over-lapping one another. Hence, the «Rabbit Ear» and «RSR pattern.» Remember, the QRS complex will always be at least .12 in width and posses abnormal morphology. ALWAYS CHECK RIGHT AND LEFT CHEST LEADS FOR BUNDLE BRANCH BLOCK (V-1, V-2, & V-5, V-6) Infarction associated with a

      Left Bundle Branch Block

      A LBBB may result from an acute myocardial infarction (AMI), but field paramedics cannot diagnose AMI in the presence of LBBB. The presence of LBBB negates meaning ful interpretation of other EKG criteria

      A LBBB pattern prior to the onset of clinical findings of AMI with marked reduction in voltage of the QRS complex may offer clues to the diagnosis of an infarction.

      LBBB obscures the pattern of AMI since the initial QRS vector is abnormally directed in a LBBB pattern. It will obscure the infarction vector and abnormal Q waves will not appear. The most diagnostic feature of AMI is the abnormal direction of the initial 0.04 sec of the QRS vector (ie; the abnormal Q wave).

    • LBBB is usually associated with an Inferior wall AMI when an AMI is diagnosed.
    • LBBB is usually associated with hypertensive ischemia or primary myocardial disease.
    • Diagnosing the Bundle Branch Block:

      The last 0.04 seconds of deflection on the QRS complex is used to determine the direction of the block.

      Certain easily identifiable ECG changes that are observed in the presence of cardiogenic chest pain, reveal some strong presumptive evidence toward the positive diagnosis of AMI. This pattern of changes is referred to as the «evolution of Myocardial Infarction.»

      It is often suggested that the first observable evolutionary change is the ischemia we associate with T-wave inversion or ST segment depression. Then, onto what is referred as the hyperacute phase. In the hyperacute phase of the MI, (usually the first few minutes) the T-wave may simply increase in height, and/or the ST segment becomes elevated. The finale phase is the acute phase. In the acute phase, (usually the first hour or more) the ST segment elevation is accompanied by the development of a pathological Q wave. This Q-wave confirms the diagnosis of MI.

      This evolution is not precise, however. Often times the T-wave may invert in the presence of ST segment elevation during the end of the hyperacute phase. In any event. the most critical observation should be the recognition of ST elevation in 2 or contiguous leads. This is most important to paramedic in the pre-hospital phase because the development of the Q-wave may take hours and could easily be missed in the field.

      Eventually, the ST segment will return to its baseline and the T-wave resumes its normal position, leaving only the Q-wave as evidence that an infarction has occurred. Recent research and studies have produced 95% accuracy in field diagnosis by paramedics. Perhaps some reasons would include other indications for ST changes. They would include simple angina, drug effects, and electrolyte imbalance.

      Use Lead I, II, and aVF to diagnose Axis Deviation

      • Vector: A quantity of electrical force that has a known magnitude and direction.
      • Axis: A hypothetical line which joins the poles of a lead which measure electrical force.
      • Mean Cardiac Vector: The average of all the instantaneous vectors. ( AKA mean electrical axis ).
      • For pre-hospital purposes, the axis is either «normal» or «not normal.»

      • Normal Deviation: The QRS deflection is upright or positive in I and either aVF or Lead II. A normal axis means the QRS axis falls between 30 and 90 degrees in the chest. The heart is lying in an angle between these parameters.
      • Right Axis Deviation: The QRS is downward or negatively deflected in I and positive in aVF or Lead II. The heart is lying in an angle lower the 30 degrees in the chest.

      As stated above. the electrical current should flow to the positive lead. If it does not flow in a positive direction, the heart is pointing toward the upper right or the left. So, if the QRS is negative in aVF, the heart is pointing more to the left than normal; hence, Left Axis Deviation. If the QRS is negative in Lead I, the heart is pointing more to the right than normal; hence, Right Axis Deviation.

      This is very complicated and difficult to explain in this forum. If you need info on AXIS deviation or 12 lead diagnosis, please send E-Mail and information will be provided by E-Mail or conventional postage.

    • Eric Yeargain, Paramedic
    • San Diego Paramedic Association field handbook.
    • Palomar College, San Marcos, CA. Paramedic Program
    • More information and educational Software from these companies:

      Click here to send E-Mail to The San Diego Medic Association.

      To contact Eric Yeargain send him E-Mail here.


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