T wave

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Normal T wave Tnorm (ECG).svg
Normal T wave

In electrocardiography, the T wave represents the repolarization of the ventricles. The interval from the beginning of the QRS complex to the apex of the T wave is referred to as the absolute refractory period . The last half of the T wave is referred to as the relative refractory period or vulnerable period. The T wave contains more information than the QT interval. The T wave can be described by its symmetry, skewness, slope of ascending and descending limbs, amplitude and subintervals like the Tpeak–Tend interval. [1]

Contents

In most leads, the T wave is positive. This is due to the repolarization of the membrane. During ventricle contraction (QRS complex), the heart depolarizes. Repolarization of the ventricle happens in the opposite direction of depolarization and is negative current, signifying the relaxation of the cardiac muscle of the ventricles. But this negative flow causes a positive T wave; although the cell becomes more negatively charged, the net effect is in the positive direction, and the ECG reports this as a positive spike. [2] However, a negative T wave is normal in lead aVR. Lead V1 generally have a negative T wave. In addition, it is not uncommon to have a negative T wave in lead III, aVL, or aVF. A periodic beat-to-beat variation in the amplitude or shape of the T wave may be termed T wave alternans.

Cardiac physiology

The refractory period of cardiac muscle is distinct from that of skeletal muscle. Nerves that innervate skeletal muscle have an extremely short refractory period after being subjected to an action potential (of the order of 1 ms). This can lead to sustained or tetanic contraction. In the heart, contractions must be spaced to maintain a rhythm. Unlike in muscle, repolarization occurs at a slow rate (100 ms). This prevents the heart from undergoing sustained contractions because it forces the refractory period and cardiac action potential firing to be of the same length of time.

Repolarization depends on the charges of ions and their flow across membranes. In skeletal muscle cells, repolarization is simple. First, sodium ions flow into the cell to depolarize it and cause skeletal muscle contraction. Once the action potential is over, potassium ions flow out of the cell due to increased cell membrane permeability to those ions. This high permeability contributes to the rapid repolarization of the membrane potential. This repolarization occurs quickly enough that another action potential can cause depolarization before the last action potential has dissipated. Cardiac muscle differs in that there are more calcium channels that counteract the potassium channels. While potassium quickly flows out of the cell, calcium slowly flows into the cell. This causes the repolarization to occur more slowly, making the refractory period as long as the action potential, preventing sustained contractions.

The T wave is representative of the repolarization of the membrane. In an EKG reading, the T wave is notable because it must be present before the next depolarization. An absent or strangely shaped T wave may signify disruption in repolarization or another segment of the heartbeat. [3]

Normal T wave

Normally, T waves are upright in all leads, except aVR and V1 leads. Highest amplitude of T wave is found at V2 and V3 leads. The shape of the T wave is usually asymmetrical with a rounded peak. T wave inversions from V2 to V4 leads are frequently found and normal in children. In normal adults, T wave inversions from V2 to V3 are less commonly found but can be normal. [4] The depth of the T wave also becomes progressively shallow from one to the next lead. [5] The height of the T wave should not exceed 5 mm in limb leads and more than 10 mm in precordial leads. [4]

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. [5]

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. [4] 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; [5] 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. [4] 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. [5]

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. [4] 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. [5]

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 [4] 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. [5] 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. [4]

Both right and left bundle branch blocks are associated with similar ST and T wave changes as in hypertrophic cardiomyopathy, but are opposite to the direction of the QRS complex. [5]

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. [5]

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. [5]

Frequency of inverted T-waves

Numbers from Lepeschkin E in [6]

Age (ethnicity)nV1V2V3V4V5V6
Children
1 week – 1 year21092%74%27%20%0.5%0%
1–2 y15496%85%39%10%0.7%0%
2–5 y20298%50%22%7%1%0%
5–8 y9491%25%14%5%1%1%
8–16 y9062%7%2%0%0%0%
Males
12–13 y20946%7%0%0%0%0%
13–14 y26035%4.6%0.8%0%0%0%
16–19 y (whites)5032%0%0%0%0%0%
16–19 y (blacks)31046%7%2.9%1.3%0%0%
20–30 y (whites)28555%0%0%0%0%0%
20–30 y (blacks)29547%0%0%0%0%0%
Females
12–13 y17469%11%1.2%0%0%0%
13–14 y15452%8.4%1.4%0%0%0%
16–19 y (whites)5066%0%0%0%0%0%
16–19 y (blacks)31073%9%1.3%0.6%0%0%
20–30 y (whites)28055%0%0%0%0%0%
20–30 y (blacks)33055%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.

Wellens' Syndrome is a pattern of biphasic T waves in V2–3. It is generally present in patients with ischemic chest pain.

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, T wave becomes more flatten while U wave becomes more prominent, with progressively deeper ST segment depression. For digitalis toxicity, there will be sagging QT interval, flattened T wave, and prominent U wave with a shortened QT interval. [5]

Hyperacute T wave

These T waves may be seen in patients displaying Prinzmetal angina. Additionally, patients exhibiting the early stages of STEMI may display these broad and disproportional waves. [7]

'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. [8]

Peaked T wave

High blood potassium levels (hyperkalemia) can cause "peaked t-waves." [9]

See also

Related Research Articles

<span class="mw-page-title-main">Electrocardiography</span> Examination of the hearts electrical activity

Electrocardiography is the process of producing an electrocardiogram, a recording of the heart's electrical activity through repeated cardiac cycles. It is an electrogram of the heart which is a graph of voltage versus time of the electrical activity of the heart using electrodes placed on the skin. These electrodes detect the small electrical changes that are a consequence of cardiac muscle depolarization followed by repolarization during each cardiac cycle (heartbeat). Changes in the normal ECG pattern occur in numerous cardiac abnormalities, including:

<span class="mw-page-title-main">Ventricular fibrillation</span> Rapid quivering of the ventricles of the heart

Ventricular fibrillation is an abnormal heart rhythm in which the ventricles of the heart quiver. It is due to disorganized electrical activity. Ventricular fibrillation results in cardiac arrest with loss of consciousness and no pulse. This is followed by sudden cardiac death in the absence of treatment. Ventricular fibrillation is initially found in about 10% of people with cardiac arrest.

<span class="mw-page-title-main">Premature ventricular contraction</span> Skipped beat with ventricular origin

A premature ventricular contraction (PVC) is a common event where the heartbeat is initiated by Purkinje fibers in the ventricles rather than by the sinoatrial node. PVCs may cause no symptoms or may be perceived as a "skipped beat" or felt as palpitations in the chest. PVCs do not usually pose any danger.

<span class="mw-page-title-main">Cardiac conduction system</span> Aspect of heart function

The cardiac conduction system transmits the signals generated by the sinoatrial node – the heart's pacemaker, to cause the heart muscle to contract, and pump blood through the body's circulatory system. The pacemaking signal travels through the right atrium to the atrioventricular node, along the bundle of His, and through the bundle branches to Purkinje fibers in the walls of the ventricles. The Purkinje fibers transmit the signals more rapidly to stimulate contraction of the ventricles.

<span class="mw-page-title-main">Torsades de pointes</span> Type of abnormal heart rhythm

Torsades de pointes, torsade de pointes or torsades des pointes is a specific type of abnormal heart rhythm that can lead to sudden cardiac death. It is a polymorphic ventricular tachycardia that exhibits distinct characteristics on the electrocardiogram (ECG). It was described by French physician François Dessertenne in 1966. Prolongation of the QT interval can increase a person's risk of developing this abnormal heart rhythm, occurring in between 1% and 10% of patients who receive QT-prolonging antiarrhythmic drugs.

<span class="mw-page-title-main">Ventricular tachycardia</span> Medical condition of the heart

Ventricular tachycardia is a cardiovascular disorder in which fast heart rate occurs in the ventricles of the heart. Although a few seconds of VT may not result in permanent problems, longer periods are dangerous; and multiple episodes over a short period of time are referred to as an electrical storm. Short periods may occur without symptoms, or present with lightheadedness, palpitations, shortness of breath, chest pain, and decreased level of consciousness. Ventricular tachycardia may lead to coma and persistent vegetative state due to lack of blood and oxygen to the brain. Ventricular tachycardia may result in ventricular fibrillation (VF) and turn into cardiac arrest. This conversion of the VT into VF is called the degeneration of the VT. It is found initially in about 7% of people in cardiac arrest.

<span class="mw-page-title-main">Sinus rhythm</span> Cardiac rhythm

A sinus rhythm is any cardiac rhythm in which depolarisation of the cardiac muscle begins at the sinus node. It is necessary, but not sufficient, for normal electrical activity within the heart. On the electrocardiogram (ECG), a sinus rhythm is characterised by the presence of P waves that are normal in morphology.

<span class="mw-page-title-main">Bundle branch block</span> Medical condition

A bundle branch block is a partial or complete interruption in the flow of electrical impulses in either of the bundle branches of the heart's electrical system.

<span class="mw-page-title-main">QRS complex</span> Represents ventricular depolarization, which results in ventricular contraction

The QRS complex is the combination of three of the graphical deflections seen on a typical electrocardiogram. It is usually the central and most visually obvious part of the tracing. It corresponds to the depolarization of the right and left ventricles of the heart and contraction of the large ventricular muscles.

<span class="mw-page-title-main">Right bundle branch block</span> Heart block in the right ventricle

A right bundle branch block (RBBB) is a heart block in the right bundle branch of the electrical conduction system.

<span class="mw-page-title-main">Left bundle branch block</span> Medical condition

Left bundle branch block (LBBB) is a conduction abnormality in the heart that can be seen on an electrocardiogram (ECG). In this condition, activation of the left ventricle of the heart is delayed, which causes the left ventricle to contract later than the right ventricle.

<span class="mw-page-title-main">U wave</span>

The U wave is a wave on an electrocardiogram (ECG). It comes after the T wave of ventricular repolarization and may not always be observed as a result of its small size. 'U' waves are thought to represent repolarization of the Purkinje fibers. However, the exact source of the U wave remains unclear. The most common theories for the origin are:

<span class="mw-page-title-main">Right axis deviation</span> Medical condition

The electrical axis of the heart is the net direction in which the wave of depolarization travels. It is measured using an electrocardiogram (ECG). Normally, this begins at the sinoatrial node ; from here the wave of depolarisation travels down to the apex of the heart. The hexaxial reference system can be used to visualise the directions in which the depolarisation wave may travel.

<span class="mw-page-title-main">Wellens' syndrome</span> Medical condition

Wellens' syndrome is an electrocardiographic manifestation of critical proximal left anterior descending (LAD) coronary artery stenosis in people with unstable angina. Originally thought of as two separate types, A and B, it is now considered an evolving wave form, initially of biphasic T wave inversions and later becoming symmetrical, often deep, T wave inversions in the anterior precordial leads.

<span class="mw-page-title-main">Vectorcardiography</span>

Vectorcardiography (VCG) is a method of recording the magnitude and direction of the electrical forces that are generated by the heart by means of a continuous series of vectors that form curving lines around a central point.

<span class="mw-page-title-main">ST elevation</span> Elevation of the ST segment on an electrocardiogram

ST elevation refers to a finding on an electrocardiogram wherein the trace in the ST segment is abnormally high above the baseline.

<span class="mw-page-title-main">ST depression</span> Depression of the ST segment on an electrocardiogram

ST depression refers to a finding on an electrocardiogram, wherein the trace in the ST segment is abnormally low below the baseline.

<span class="mw-page-title-main">P wave (electrocardiography)</span> Represents atrial depolarization, which results in atrial contraction

The P wave on the ECG represents atrial depolarization, which results in atrial contraction, or atrial systole.

Cardiac physiology or heart function is the study of healthy, unimpaired function of the heart: involving blood flow; myocardium structure; the electrical conduction system of the heart; the cardiac cycle and cardiac output and how these interact and depend on one another.

<span class="mw-page-title-main">Electrocardiography in myocardial infarction</span>

Electrocardiography in suspected myocardial infarction has the main purpose of detecting ischemia or acute coronary injury in emergency department populations coming for symptoms of myocardial infarction (MI). Also, it can distinguish clinically different types of myocardial infarction.

References

  1. ↑ Haarmark C, Graff C, Andersen MP, et al. (2010). "Reference values of electrocardiogram repolarization variables in a healthy population". Journal of Electrocardiology . 43 (1): 31–39. doi:10.1016/j.jelectrocard.2009.08.001. PMID   19740481.
  2. ↑ "Physiology: Cardiovascular".
  3. ↑ Raff, Hershel; T., Strang, Kevin; Vander, Arthur J. (2015-11-03). Human physiology: the mechanisms of body function. ISBN   978-1259294099. OCLC   914339346.{{cite book}}: CS1 maint: multiple names: authors list (link)
  4. 1 2 3 4 5 6 7 Wei Qin, Lin; Swee, Guan Teo; Kian Keong, Poh (2013). "Electrocardiographic T wave abnormalities" (PDF). Singapore Medical Journal. 54 (11): 606–610. doi: 10.11622/smedj.2013218 . Retrieved 18 April 2018.
  5. 1 2 3 4 5 6 7 8 9 10 11 Hanna, E.B.; Glancy, D.L. (2011). "ST-segment depression and T-wave inversion: Classification, differential diagnosis, and caveats". Cleveland Clinic Journal of Medicine. 78 (6): 404–14. doi: 10.3949/ccjm.78a.10077 . PMID   21632912.
  6. ↑ Antaloczy, Z (1979). Modern Electrocardiology. Amsterdam: Excerpta Medica. p. 401.
  7. ↑ Verouden, N.J.; Koch, K.T.; Peters, R.J.; Henriques, J.P.; Baan, J.; Schaaf, R.J. van der; Vis, M.M.; Tijssen, J.G.; Piek, J.J. (2009-10-15). "Persistent precordial "hyperacute" T-waves signify proximal left anterior descending artery occlusion". Heart. 95 (20): 1701–06. doi:10.1136/hrt.2009.174557. ISSN   1355-6037. PMID   19620137.
  8. ↑ Abbott, Joseph A.; Cheitlin, Melvin D. (1976-01-26). "The Nonspecific Camel-Hump Sign". JAMA. 235 (4): 413–14. doi:10.1001/jama.1976.03260300039030. ISSN   0098-7484.
  9. ↑ Hollander-Rodriguez, Joyce C.; Calvert, James F. (15 January 2006). "Hyperkalemia". American Family Physician. 73 (2): 283–290. PMID   16445274.
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