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    ST Segment and T Waves:: Ischemia, Infarction, Drug & Electrolyte Effects

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    Hibba Nasser
    The document discusses ST segment and T wave changes on electrocardiograms and their clinical significance. It covers: 1) ST segments correspond to the plateau phase of the ventricular action potential and can be modified by factors like resting membrane potential and calcium levels. T waves correspond to the repolarization phase. 2) Ischemia causes ST segment depression or T wave inversion on ECGs. More severe injury leads to ST segment elevation. Infarction results in pathological Q waves. 3) In addition to ischemia, other factors like electrolyte abnormalities, drugs, and diseases can cause non-ischemic ST and T wave changes. Differentiating ischemic from non-ischemic causes is important clinically.

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    ST Segment and T Waves:: Ischemia, Infarction, Drug & Electrolyte Effects

    Uploaded by

    Hibba Nasser
    42 views34 pages
    The document discusses ST segment and T wave changes on electrocardiograms and their clinical significance. It covers: 1) ST segments correspond to the plateau phase of the ventricular action potential and can be modified by factors like resting membrane potential and calcium levels. T waves correspond to the repolarization phase. 2) Ischemia causes ST segment depression or T wave inversion on ECGs. More severe injury leads to ST segment elevation. Infarction results in pathological Q waves. 3) In addition to ischemia, other factors like electrolyte abnormalities, drugs, and diseases can cause non-ischemic ST and T wave changes. Differentiating ischemic from non-ischemic causes is important clinically.

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    ECG 101.5

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    The document discusses ST segment and T wave changes on electrocardiograms and their clinical significance. It covers: 1) ST segments correspond to the plateau phase of the ventricular action potential and can be modified by factors like resting membrane potential and calcium levels. T waves correspond to the repolarization phase. 2) Ischemia causes ST segment depression or T wave inversion on ECGs. More severe injury leads to ST segment elevation. Infarction results in pathological Q waves. 3) In addition to ischemia, other factors like electrolyte abnormalities, drugs, and diseases can cause non-ischemic ST and T wave changes. Differentiating ischemic from non-ischemic causes is important clinically.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    42 views34 pages

    ST Segment and T Waves:: Ischemia, Infarction, Drug & Electrolyte Effects

    Uploaded by

    Hibba Nasser
    The document discusses ST segment and T wave changes on electrocardiograms and their clinical significance. It covers: 1) ST segments correspond to the plateau phase of the ventricular action potential and can be modified by factors like resting membrane potential and calcium levels. T waves correspond to the repolarization phase. 2) Ischemia causes ST segment depression or T wave inversion on ECGs. More severe injury leads to ST segment elevation. Infarction results in pathological Q waves. 3) In addition to ischemia, other factors like electrolyte abnormalities, drugs, and diseases can cause non-ischemic ST and T wave changes. Differentiating ischemic from non-ischemic causes is important clinically.

    Copyright:

    © All Rights Reserved
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    of 34

    "

    ST Segment and T Waves:

    Ischemia, Infarction, Drug & Electrolyte Effects


    "

    "

    ST Segment and T waves


    The ST segment corresponds to the phase 2
    plateau of the ventricular cellular action potential
    It is the 0 potential of the action potential
    Modifiers:

    Resting membrane potential (shifts up or down)


    Extracellular [Ca++] (shortens or prolongs)

    The T wave corresponds to phase 3 of the


    ventricular cellular action potential

    Modifiers:

    Resting membrane potential (indirectly affects


    polarity)
    Extracellular [K+] (shortens or prolongs)

    APs from various areas

    Ion movements all over

    Transmembrane Ion Fluxes During the Action Potential

    0 mV

    -90 mV

    0 mV

    Ischemia, Injury and Infarction


    Ischemia is inadequate blood supply resulting in nutrient
    deprivation as well as incomplete removal of metabolic waste

    Caused by restriction of supply below the normal amount, or


    increase in demand above what a normal supply can handle
    ECG shows ST segment depression/T wave inversion
    Symmetric T waves are abnormal

    Injury occurs as an extreme of ischemia but still at a stage


    when reversal of ischemia allows full or nearly full recovery

    ECG shows ST segment elevation

    Infarction occurs when ischemia has lasted long enough that


    cell necrosis begins; this is irreversible

    ECG shows pathologic Q waves

    Ischemic ST Segment Changes


    Ischemic ST Segment Changes - physiol
    Partially depolarized cells
    in ischemic zone

    Elevated baseline
    (less negative)

    JMM

    ST Segment level constant

    Ischemic
    ST Segment
    Changes
    Ischemic
    ST Segment
    Changes
    ST segment and T wave abnormalities can suggest ischemia but are not diagnostic;
    examples
    among
    those shown below, downsloping depression is most specific, followed by

    horizontal and then upsloping (non-specific). T wave inversion is likewise non-specific.

    Downsloping
    ST Depression

    Horizontal
    ST Depression

    Upsloping
    ST Depression

    T wave
    Inversion

    Occasionally, T wave abnormalities are present at rest but appear to normalize during
    ischemia; finding a normal ECG in a patient with chest pain can be misleading.

    Baseline

    Ischemia
    T wave normal

    Injury ST
    ST Segment
    Segment Changes
    Changes -ofphysiol
    Injury
    Depressed baseline
    (more negative) ST Segment level constant

    Current flows away from partially


    depolarized ischemic cells to
    normally polarized cells, making
    ischemic zone more negative
    JMM

    Injury-infarct
    ECG Changes
    ST Segment
    of InjuryChanges
    and Infarction
    progression
    Revascularization

    Normal

    Chronic
    Infarction +
    Preservation
    Normal

    Hyperacute
    T waves

    ST elevation

    ST elevation;
    Q wave

    Chronic
    Infarction, no
    Preservation

    Chronic
    Infarction,
    Aneurysm

    Minutes

    Hours

    Days-Years

    Injury-infarct
    Reciprocal
    ST Segment
    Changes
    Changes
    of Injury
    progression
    Injury(ST
    elevation) observed in one region of the heart by one set of ECG leads is often

    reflected in leads viewing the heart from the opposite direction, as the opposite polarity (ST
    depression). This is called reciprocal change and is characteristic of inferior wall injury.

    ST
    STdepression
    depression

    ST
    STelevation
    elevation

    ECG Patterns of Chronic Infarction


    Once myocardial tissue has necrosed and healed
    (replacement by scar), it is electrically transparent
    ECG leads recording over that wall see the opposite
    wall only (Q wave)
    Q waves are generally permanent but can regress in
    some patients
    The site of infarction (wall damaged) can usually be
    inferred from the ECG pattern
    The posterior walls correlate of a Q wave is a tall R
    wave in V1 and V2 (hold up ECG backwards and upside
    down, shine light from behind QR complex of
    infarction magically appears)
    Chronic ST elevation in leads with Q waves suggests a
    left ventricular aneurysm

    Normal ECG
    Normal ECG/Conduction

    Features:
    Narrow/shallow q waves when present (0.04 sec)
    No ST segment shift or T abnormality

    Anterior

    Posterior

    aVR

    aVL

    aVF

    V1

    V2

    V3

    V4

    V5

    V6

    Anterior Infarction

    Ant MI

    Features:
    Q waves in precordial leads
    - anteroseptal MI: Q waves start in V1/V2
    - anteroapical MI: Q waves start in V3/V4
    - anterolateral MI: Q waves start in V4/V5
    Inferior leads minimally affected
    Causes:
    occlusion of left anterior descending coronary artery

    Anterior

    Posterior

    V1

    V2

    Anterior Wall Infarction


    3

    aVR

    aVL

    aVF

    V3

    V4

    V5

    V6

    Inferior Infarction

    Inf MI

    Features:
    Q waves in inferior leads
    precordial leads largely unaffected
    Causes:
    occlusion of right (or circumflex) coronary arteries

    Anterior

    Posterior

    aVR

    aVL

    aVF

    V1

    V2

    V3

    V4

    V5

    V6

    Infero-Posterior Infarction

    Inf-post MI

    Features:
    Q waves in inferior leads
    tall R waves in right precordial leads (posterior wall)
    Causes:
    occlusion of dominant right (or circumflex) coronary
    artery

    Anterior

    Posterior

    aVR

    aVL

    aVF

    V1

    V2

    V3

    V4

    V5

    V6

    Posterior-Lateral Infarction

    Post-lat MI

    Features:
    Tall R waves in right precordial leads
    Q waves in lateral leads
    Causes:
    occlusion of circumflex (generally) coronary artery

    Anterior

    Posterior

    aVR

    aVL

    aVF

    V1

    V2

    V3

    V4

    V5

    V6

    Anterior Infarction

    Ant + Inf MI

    Features:
    Q waves in precordial leads
    Q waves in inferior leads
    Causes:
    occlusion of left anterior descending artery

    Anterior

    Posterior

    aVR

    aVL

    aVF

    V1

    V2

    V3

    V4

    V5

    V6

    Fragmentation

    MK Das
    Indiana University

    Significance of fQRS in CADPrognosis


    In 998 pts evaluated for CAD (follow up of 56 mths) :
    All cause mortality fQRS vs non fQRS 34% vs 26%
    Cardiac events (MI, death revascularization) 50% vs
    28%

    In pts with Q wave MI fQRS HR of 2.68 (p=0.004)


    for cardiac death and nonfatal mI
    Pietrasik G, Am J Cardiol 2007; 100:583

    In pts with CAD and ICDs implanted for 1


    prevention fQRS predicts appropriate therapy

    Other Types of ST Change


    ST segment changes can be caused by a variety
    of other, non-ischemic abnormalities:
    Extracellular calcium concentration

    Low [Ca++]: lengthens ST segment


    Elevated [Ca++]: shortens ST segment

    ST elevation

    Pericarditis - can mimic injury (actually is a


    myopericarditis), with evolutionary changes
    ST elevation is diffuse, not localized

    Early repolarization - normal variant

    ST depression

    Digitalis effect - scooped ST depression


    Strain pattern of left ventricular hypertrophy

    The greater the magnitude of ST elevation or


    depression, the less likely it is a normal variant

    Non-ischemic
    ST
    Non-Ischemic
    ST Segment Abnormalities
    abnormalities

    Extracellular [Ca++] changes: ST segment length

    Normal

    Low [Ca++]
    Long ST

    High [Ca++]
    Short ST

    Resting membrane potential changes: ST segment level


    <
    <ST
    STelevation
    elevation>
    >

    Normal

    Injury

    (transmural ischemia)

    Pericarditis

    Early
    Repolarization

    <
    <ST
    STdepression
    depression>
    >

    Digitalis
    Effect

    Strain
    HTN

    PericarditisPericarditis
    - ECG with diffuse
    changes
    aVR

    V1

    V4

    aVL

    V2

    V5

    aVF

    V3

    V6

    Cellular
    Recordings

    Pericarditis
    Pericarditis evolution
    Normal
    Acute Pericarditis

    Subepicardial cells have less


    negative resting membrane
    potential, thus more rapid
    repolarization (? due to K+ leak)

    -90

    Surface ECG shows ST in all


    leads (exc. aVR) and a shorter
    QT; larger and earlier atrial
    T wave depressed PR segment

    ECG
    Stage

    ECG

    Description

    Time Course

    ST elevation; short QT Hours-days

    II

    STs return; T inverts

    1-3 days

    III

    T inversion

    2-10 days

    IV

    Return to normal

    7-10 days

    Non-ischemic
    T
    Non-Ischemic
    T Wave Abnormalities
    abnormalities

    A large variety of seemingly unrelated disorders can alter the QT interval and T wave:

    Normal

    Hyperkalemia
    (Peaked T)

    Hypokalemia
    (Long QT)

    Quinidine
    (Long QT)

    Congenital
    Long QT

    Cerebral Ts
    (CNS damage)

    The QT interval ordinarily shortens with increasing heart rate; several correction
    factors have been developed over the years, the most commonly-used being the
    Bazett formula:
    QTc =

    QTmeasured
    (R-R)

    Hyperkalemia

    Hyperkalemia
    Note peaked T waves, absence of ST segment
    Young woman with renal failure, K+ = 8.4 mEq/L

    Hyperkalemia

    Hyperkalemia
    Young woman with renal failure, K+ = 8.4 mEq/L

    Hyperkalemia

    Rxd Hyperkalemia
    Young woman with renal failure; post-dialysis K+ = 4.4 mEq/L

    Long QT-Related Polymorphic VT

    LQT - PMVT - (Tung)

    ST Segment/T Waves: Drug Effects


    Most drug effects impinge on the T wave

    Many antiarrhythmic drugs block IKr (repolarizing


    current), prolonging the QT interval

    This can result in early afterdepolarization-related


    polymorphic VT

    A long [growing] list of other drugs also block I Kr


    and produce long QT and polymorphic VT

    Antibiotics, antihistamines, chemotherapeutics


    Some alter metabolism of otherwise safe drugs

    Some drugs act on extracellular ion


    concentrations and indirectly affect the ECG:
    Citrate (blood transfusion) can chelate Ca++
    ACE inhibitors, heparin, etc. can increase K +

    Drug Effects on the ECG


    Drugs can exert important influences on the
    ECG in a variety of ways:

    Altering rate (beta blockers/agonists, calcium


    channel blockers)
    Prolonging PR interval (beta/calcium blockers)
    Prolonging QRS duration (type 1A, 1C
    antiarrhythmic drugs; amiodarone; tricyclics)
    Altering ST segment (digitalis, tricyclic
    antidepressants, phenothiazines)
    Prolonging QT interval (type 1A, 1C
    antiarrhythmic drugs; amiodarone; tricyclics)

    Drug Effects

    Drug effects

    A sampling of the wide variety of drug effects on the ECG is shown below:

    Normal

    Prolonged
    PR interval
    (metoprolol)

    Prolonged
    QRS duration
    (procainamide)

    ST Segment
    depression
    (digitalis)

    Prolonged
    QT interval
    (erythromycin)

    All
    kinds
    of ST-T
    ST-T
    Changes:
    Potpourri
    changes

    Normal

    Normal

    ST segment
    ST
    depression
    depression
    (ischemia)
    (ischemia)

    Hyperkalemia
    Peaked T Hypokalemia
    Long QT
    ( potassium) ( potassium)

    T wave
    T wave
    inversion
    inversion

    Hyperacute
    Hyperacute
    T wave
    T wave
    (injury)
    (ischemia)

    ST
    STsegment
    elevation
    elevation
    (ischemia)
    (injury)

    Hypocalcemia
    Hypercalcemia
    Drug
    Short QT
    Long QT
    Longeffect
    QT
    ( calcium)
    ( calcium)
    (Quinidine)

    ST
    STsegment
    elevation
    elevation
    (pericarditis)
    (pericarditis)

    Prominent
    U wave

    ST Segments and T waves - Summary


    ST segment and T waves changes have many and
    diverse causes:
    Ischemia and injury
    Pericarditis
    Electrolyte abnormalities
    Drug effects

    Careful analysis of the ECG often - but not always yields the correct diagnosis and thus proper therapy
    Wrong diagnosis can lead to catastrophic mistakes
    Thrombolytic therapy for hemorrhagic pericarditis
    Procainamide for drug-related polymorphic VT

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