Open main menu
Home
Random
Recent changes
Special pages
Community portal
Preferences
About Wikipedia
Disclaimers
Incubator escapee wiki
Search
User menu
Talk
Dark mode
Contributions
Create account
Log in
Editing
T wave
(section)
Warning:
You are not logged in. Your IP address will be publicly visible if you make any edits. If you
log in
or
create an account
, your edits will be attributed to your username, along with other benefits.
Anti-spam check. Do
not
fill this in!
== Abnormalities == Both the abnormalities of the [[ST segment]] and T wave represents the abnormalities of the ventricular repolarization or secondary to abnormalities in ventricular depolarisation.<ref name="Hanna 2011"/> === Inverted T wave === Inverted T wave is considered abnormal if inversion is deeper than 1.0 mm. Inverted T waves found in leads other than the V1 to V4 leads is associated with increased cardiac deaths. Inverted T waves associated with cardiac signs and symptoms ([[chest pain]] and [[cardiac murmur]]) are highly suggestive of [[myocardial ischaemia]].<ref name= "WeiQin 2013"/> Other ECG changes associate with myocardial ischaemia are: [[ST segment]] depression with an upright T wave; ST segment depression with biphasic T wave or inverted T wave with negative [[QRS complex]];<ref name="Hanna 2011"/> T wave symmetrically inverted with a pointed apex, while the ST segment is either bowed upwards or horizontally depressed, or not deviated; and ST segment depression progressing to abnormal T wave during ischaemia free intervals.<ref name= "WeiQin 2013"/> However, ST segment depression is not suggestive of ischaemic location of the heart. ST segment depression in eight or more leads, associated with ST segment elevation in aVR and V1 are associated with left main coronary artery disease or three-vessel disease (blockage of all three major branches of coronary arteries). ST segment depression most prominent from V1 to V3 is suggestive of posterior infarction. Furthermore, tall or wide QRS complex with an upright T wave is further suggestive of the posterior infarction.<ref name="Hanna 2011">{{Cite journal|last=Hanna|first=E.B.|last2=Glancy|first2=D.L.|title=ST-segment depression and T-wave inversion: Classification, differential diagnosis, and caveats|journal=Cleveland Clinic Journal of Medicine|volume=78|issue=6|pages=404β14|doi=10.3949/ccjm.78a.10077|year=2011|pmid=21632912|doi-access=free}}</ref> [[Wellens' syndrome]] is caused by the injury or blockage of the [[left anterior descending artery]], therefore resulting in symmetrical T wave inversions from V2 to V4 with depth more than 5 mm in 75% of the cases. Meanwhile, the remaining 25% of the cases shows biphasic T wave morphology. ST segments remains neutral in this syndrome. Those who were treated without [[angiography]] will develop anterior wall myocardial infarction in a mean period of 9 days.<ref name= "WeiQin 2013"/> An episode of chest pain in Wellens' syndrome is associated with ST elevation or depression and later progressed to T wave abnormality after chest pain subsided. T wave inversion less than 5 mm may still represents myocardial ischaemia, but is less severe than Wellens' syndrome.<ref name="Hanna 2011"/> [[Hypertrophic cardiomyopathy]] is the thickening of the [[left ventricle]], occasionally [[right ventricle]]. It may be associated with left ventricular outflow tract obstruction or may not be associated with it in 75% of the cases. ECG would be abnormal in 75 to 95% of the patients. Characteristic ECG changes would be large [[QRS complex]] associated with giant T wave inversion<ref name= "WeiQin 2013"/> in lateral leads I, aVL, V5, and V6, together with ST segment depression in left ventricular thickening. For right ventricular thickening, T waves are inverted from V2 to V3 leads. ST and T waves changes may not be apparent in hypertrophic cardiomyopathy, but if there is presence of ST and T waves changes indicates severe hypertrophy or ventricular systolic dysfunction.<ref name="Hanna 2011"/> According to Sokolow-Lyon criterion, the height of R wave in V5 or V6 + the height of S wave in V1 more than 35 mm would be suggestive of left ventricular hypertrophy.<ref name= "WeiQin 2013"/> Both right and left [[bundle branch block]]s are associated with similar ST and T wave changes as in hypertrophic cardiomyopathy, but are opposite to the direction of the QRS complex.<ref name="Hanna 2011"/> In [[pulmonary embolism]], T wave can be symmetrically inverted at V2 to V4 leads but [[sinus tachycardia]] is usually the more common finding. T wave inversion is only present in 19% of mild pulmonary embolism, but the T inversion can be present in 85% of the cases in severe pulmonary embolism. Besides, T inversion can also exists in leads III and aVF.<ref name="Hanna 2011"/> Inversion of T waves in most of the ECG leads except aVR indicates many causes most commonly myocardial ischaemia and [[intracranial haemorrhage]]. Others include: hypertrophic cardiomyopathy, [[Takotsubo cardiomyopathy]] (stress-induced cardiomyopathy), [[cocaine]] abuse, [[pericarditis]], pulmonary embolism, and advanced or complete atrioventricular block.<ref name="Hanna 2011"/> ==== Frequency of inverted T-waves ==== Numbers from Lepeschkin E in <ref>{{Cite book | last = Antaloczy | first = Z | title = Modern Electrocardiology | publisher = Excerpta Medica | year = 1979 | location = Amsterdam | pages = 401 }}</ref> {| class="wikitable" |- ! ! Age (ethnicity) ! n ! V1 ! V2 ! V3 ! V4 ! V5 ! V6 |- | '''Children''' |- | | 1 week β 1 year | 210 | 92% | 74% | 27% | 20% | 0.5% | 0% |- | | 1β2 y | 154 | 96% | 85% | 39% | 10% | 0.7% | 0% |- | | 2β5 y | 202 | 98% | 50% | 22% | 7% | 1% | 0% |- | | 5β8 y | 94 | 91% | 25% | 14% | 5% | 1% | 1% |- | | 8β16 y | 90 | 62% | 7% | 2% | 0% | 0% | 0% |- | '''Males''' | colspan="8" | |- | | 12β13 y | 209 | 46% | 7% | 0% | 0% | 0% | 0% |- | | 13β14 y | 260 | 35% | 4.6% | 0.8% | 0% | 0% | 0% |- | | 16β19 y (whites) | 50 | 32% | 0% | 0% | 0% | 0% | 0% |- | | 16β19 y (blacks) | 310 | 46% | 7% | 2.9% | 1.3% | 0% | 0% |- | | 20β30 y (whites) | 285 | 55% | 0% | 0% | 0% | 0% | 0% |- | | 20β30 y (blacks) | 295 | 47% | 0% | 0% | 0% | 0% | 0% |- | '''Females''' | colspan="8" | |- | | 12β13 y | 174 | 69% | 11% | 1.2% | 0% | 0% | 0% |- | | 13β14 y | 154 | 52% | 8.4% | 1.4% | 0% | 0% | 0% |- | | 16β19 y (whites) | 50 | 66% | 0% | 0% | 0% | 0% | 0% |- | | 16β19 y (blacks) | 310 | 73% | 9% | 1.3% | 0.6% | 0% | 0% |- | | 20β30 y (whites) | 280 | 55% | 0% | 0% | 0% | 0% | 0% |- | | 20β30 y (blacks) | 330 | 55% | 2.4% | 1% | 0% | 0% | 0% |- |} === Biphasic T wave === As the name suggests, Biphasic T waves move in opposite directions. The two main causes of these waves are myocardial ischemia and hypokalemia. * Ischemic T waves rise and then fall below the cardiac resting membrane potential * Hypokalemic T waves fall and then rise above the cardiac resting membrane potential Wellens' Syndrome is a pattern of biphasic T waves in V2β3. It is generally present in patients with ischemic chest pain. * Type 1: T-waves are symmetrically and deeply inverted * Type 2: T-waves are biphasic with negative terminal deflection and positive initial deflection <ref name="Hanna 2011"/> === Flattened T wave === T wave is considered flat when the wave varies from -1.0 mm to + 1.0 mm in height. [[Hypokalemia]] or [[digitalis]] therapy can cause flattened T wave with a prominent [[U wave]]. As hypokalemia progressively worsens, the T wave becomes more flattened while the U wave becomes more prominent, with progressively deeper ST segment depression. For digitalis toxicity, there will be a sagging QT interval, flattened T wave, and prominent U wave with a shortened QT interval.<ref name="Hanna 2011"/> === Hyperacute T wave === These T waves may be seen in patients displaying [[Prinzmetal's angina|Prinzmetal angina]]. Additionally, patients exhibiting the early stages of [[STEMI]] may display these broad and disproportional waves.<ref>{{Cite journal|last=Verouden|first=N.J.|last2=Koch|first2=K.T.|last3=Peters|first3=R.J.|last4=Henriques|first4=J.P.|last5=Baan|first5=J.|last6=Schaaf|first6=R.J. van der|last7=Vis|first7=M.M.|last8=Tijssen|first8=J.G.|last9=Piek|first9=J.J.|date=2009-10-15|title=Persistent precordial "hyperacute" T-waves signify proximal left anterior descending artery occlusion|url=http://heart.bmj.com/content/95/20/1701|journal=Heart|language=en|volume=95|issue=20|pages=1701β06|doi=10.1136/hrt.2009.174557|issn=1355-6037|pmid=19620137}}</ref> === 'Camel hump' T wave === The name of these T waves suggests the shape it exhibits (double peaks). Since these T wave abnormalities may arise from different events, i.e. hypothermia and severe brain damage, they have been deemed as nonspecific, making them much more difficult to interpret.<ref>{{Cite journal|last=Abbott|first=Joseph A.|last2=Cheitlin|first2=Melvin D.|date=1976-01-26|title=The Nonspecific Camel-Hump Sign|journal=JAMA|volume=235|issue=4|pages=413β14|doi=10.1001/jama.1976.03260300039030|issn=0098-7484}}</ref> ===Peaked T wave=== High blood [[potassium]] levels ([[hyperkalemia]]) can cause "peaked t-waves."<ref>{{cite journal |last1=Hollander-Rodriguez |first1=Joyce C. |last2=Calvert |first2=James F. |title=Hyperkalemia |journal=American Family Physician |date=15 January 2006 |volume=73 |issue=2 |pages=283β290 |pmid=16445274 |url=https://www.aafp.org/link_out?pmid=16445274 }}</ref>
Edit summary
(Briefly describe your changes)
By publishing changes, you agree to the
Terms of Use
, and you irrevocably agree to release your contribution under the
CC BY-SA 4.0 License
and the
GFDL
. You agree that a hyperlink or URL is sufficient attribution under the Creative Commons license.
Cancel
Editing help
(opens in new window)