pathologically inverted T waves on an ECG can be very important indicators of significant disease processes
Biphasic T waves
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:
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
Inverted T waves
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:
SI QIII TIII pattern
RVH / strain pattern
anterior plus inferior T inv pattern
useful mnemonic:
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
anterior leads only (V1-3)
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
most leads have T inversion
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
diffuse sagging ST depression with flat or inverted T-waves (reverse tick shape)
inferior and lateral leads
infero-lateral myocardial ischaemia
hypertrophic cardiomyopathy (HCM)
biventricular hypertrophy including dilated cardiomyopathy
inferior and anterior leads including V3
RV strain pattern (often with P pulmonale):
RVH
pulmonary embolism
juvenile pattern plus an inferior T inv aetiology
lateral and anterior leads including V3-4
anterior LV aneurysm
hypertrophic cardiomyopathy (HCM)
S1 Q3 T3 pattern
SI QIII TIII 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
isolated aVL inversion
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
isolated III inversion
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