OzEMedicine - Wiki for Australian Emergency Medicine Doctors

see also:

• cardiology
• basics of the ECG
  • ECG - tall T waves
  • ECG - flat T waves
  • an approach to the ECG with ST elevation
  • ECG Diagnosis of AMI
• the adult patient with chest pain in the ED

• pathologically inverted T waves on an ECG can be very important indicators of significant disease processes

• may represent life threatening Wellen's syndrome indicating critical stenosis of LAD
  • upright T wave then inverted T wave component
  • biphasic in V2-3 often when pain resolves
• technically upright T waves an inverted T with a positive terminal portion and it is the terminal portion that defines whether it is called upright or inverted:
  • hypokalaemia
    • T inversion is first then upright wave
  • pericarditis
    • in stage 2, 40% of patients develop a notched or biphasic positive-negative T wave before full return of the ST segment to the baseline
  • digoxin effect
    • T inversion is first then upright wave usually in a reverse tick pattern with ST depression
  • “Camel's hump T waves”
    • double peaked T waves may indicate a superimposed P wave or a prominent U wave as in hypokalaemia

• normally inverted in aVR
• may be normally inverted in V1, V2, III, aVF
  • HOWEVER, new T inv in III is abnormal
  • NOTE that upright T waves in V1-2 with ST depression and R waves suggest a posterior myocardial infarction (view it upside down to better visualise a STEMI)
• if contiguous leads with dynamic changes, may indicate acute ischaemia, if fixed may represent past AMI, especially in association with pathological Q waves
• many other causes:
  • incorrect lead placement:
    • reversing limb leads can result in abnormal axis and inverted P-QRS-T-waves
    • precordial lead misplacement, with V1-2 placed too high, can also result in TWI - suspect this if biphasic P wave in V2 and it is definite if the P wave is inverted in V2
  • pulmonary embolism
    • may give either:
      • S_I Q_III T_III pattern
      • RVH / strain pattern
      • anterior plus inferior T inv pattern

• Incorrect lead placement
• No bundle (ie LBBB or RBBB)
• Ventricular hypertrophy (LVH or RVH)
• Embolism
• Reciprocal / refractory / reperfused AMI changes
• Sudden death (ARVD)
• Iatrogenic (eg. digoxin)
• Obtunded due to intracranial event - often cause widespread gigantic T inversion +/- ST elevation
• Normal variant

• normal paediatric pattern
  • seen in V1-3
• persistent juvenile pattern - adults
  • may be seen in V1-4 as shallow asymmetric T inv; common in young Afro-Caribbean women; should be a diagnosis of exclusion after considering severe chronic obstructive pulmonary disease, pulmonary embolism, acute myocardial infarction, or pulmonary hypertension, and particularly if there was syncope, arrhythmogenic right ventricular dysplasia.
  • may need further workup if there are any T wave inversions greater than 2mV in two or more contiguous leads
• anterior myocardial ischaemia
• RBBB or RVH / strain
  • along with ST depression, should be discordant with QRS in V1-3
  • if there is superimposed ischaemia, this can produce concordant ST elevation and upright T-waves, or disproportionate ST depression and deeper TWI
• pulmonary embolism
• pulmonary hypertension
• anterior LV aneurysm (may extend to all precordial leads, I and aVL)
• arrhythmogenic right ventricular dysplasia
  • anterior TWI and epsilon waves

• acute neurologic problems such as SAH, raised ICP
  • may cause often strangely shaped deep T inversions across most leads plus prolonged QTc
• stage 3 of pericarditis
• hypertrophic cardiomyopathy (HCM)
  • deep T inversion V1-6
• pulmonary embolism
• hypothyroidism - usually with sinus bradycardia and low QRS voltages
• myocarditis

• inferior myocardial ischaemia

• lead placement issue
  • reversal of the left and right arm electrodes:
    • all of lead I becomes inverted
    • aVL and aVR swap
    • II and III swap
    • aVF is unchanged
• dextrocardia
• hypothermia (with prolonged QTC, bradycardia, precordial J Osborne waves)

• LBBB
• LVH / strain
• myocardial ischaemia
• hypertrophic cardiomyopathy (HCM)
• digoxin:
  • diffuse sagging ST depression with flat or inverted T-waves (reverse tick shape)

• infero-lateral myocardial ischaemia
• hypertrophic cardiomyopathy (HCM)
• biventricular hypertrophy including dilated cardiomyopathy

• RV strain pattern (often with P pulmonale):
  • RVH
  • pulmonary embolism
• juvenile pattern plus an inferior T inv aetiology

• anterior LV aneurysm
• hypertrophic cardiomyopathy (HCM)

• S_I Q_III T_III pattern
  • found in ~17% of patients with PE but is fairly non-specific as it occurs in ~11% of adult non-PE patients
  • other causes include:
    • pneumothorax
    • acute lung disease
    • cor pulmonale
    • acute bronchospasm in severe asthma
    • left posterior fascicular block (LPFB) - also have RAD, rS in I and aVL, qR in II, III, aVF, prolonged R wave peak time in aVF and no evidence of RVH and no other cause of RAD

• NB. aVL is considered a high lateral lead which is fed by diagonal vessels, thus acute blockages that affect the proximal LAD with anterior STEMI in V3, V4, anteroseptal involvement in V1, V2, may also have high lateral involvement in aVL ¹⁾
• may be normal variant
• LV strain - especially if QRS-T angle is > 100degrees and ST is downwardly concave with asymmetry of the T wave
• may represent the reciprocal changes of an inf. STEMI especially if ST depression without concavity occurs
  • sensitivity for inferior STEMI increases from 60% to 77% when criteria includes ≥ 1mm reciprocal ST depression in aVL in addition to ≥ 1mm ST elevation in II, III, aVF
  • >1mm ST depression in aVL has sensitivity of 87% and positive predictive value of 90% for RV involvement with acute inferior MI (check also for ST elevation in V1 +/- V2 and R sided ECG leads)
• may be due to chronic mid LAD lesion
• LAFB - also has LAD (inf QRS is negative, I, aVL QRS are positive), qR in I, aVL, rS in inf, prolonged R wave peak time > 45ms in aVL
• it is considered that isolated T inversion without ST changes does not represent acute ongoing ischaemia because²⁾:
  • patients with stable angina do not develop isolated T inversion on stress testing
  • during acute pain, T inversions never occur without concomitant ST changes

• may be normal variant
• if NEW this is may reflect acute ischaemia
  • lead III is the reciprocal lead of aVL and thus ST depression and T inv in III may represent developing STEMI of a diagonal vessel which will result in ST elevation in aVL ³⁾
• however, it is considered that isolated T inversion without ST changes does not represent acute ongoing ischaemia because⁴⁾:
  • patients with stable angina do not develop isolated T inversion on stress testing
  • during acute pain, T inversions never occur without concomitant ST changes