ACS: NSTEMI and UA

 

Objectives:

• T wave
• normal
• abnormal
• ST elevation/ depression
• Diastolic current of injury
• Systolic current of injury
• Q waves
• normal
• abnormal

T WAVE

The Normal T wave

• Mechanism of a normal T wave
• Because the Purkinje fibers are located subendocardially, depolarization of the myocardium is endocardial to epicardial in direction. A surface electrode overlying the myocardium will record a tall QRS complex. Although the epicardium is the last to be depolarized, it is the earliest to recover because it has the shortest action potential duration when compared to other cells in the myocardium. Because the direction of repolarization is epicardial to endocardial, this causes the T wave to be normally uprigh.
• In general
• Frontal plane: T waves are inverted in aVR, and may be flat/inverted in III,aVL. The usual height is upto 5 mm but can be upto 8 mm
• Horizontal plane: T waves are inverted in V1, V2. The usual height is upto 10 mm but can be upto 12 mm
• FRONTAL PLANE
• In the frontal plane, the axis of the normal T wave is within 45° of the axis of the QRS complex. This is also called the QRS/T angle, which is the angle formed between the axis of the QRS complex and that of the T wave. When this angle is increased, myocardial ischemia should be considered, although this is usually not a specific finding. 
• The tallest T wave in the limb leads is approximately 5 mm but could reach up to 8 mm.
• HORIZONTAL PLANE
• In the horizontal plane, the axis of the normal T wave is within 60° of the axis of the QRS complex. Calculation of the T-wave axis in the horizontal plane is usually not necessary, because the T waves are expected to be upright in most precordial leads other than V1 or V2. If the T waves are inverted in V1, V2, and also in V3, this is abnormal, except in children and young adults.
• Because the precordial leads are closer to the heart than the limb leads, the T waves are taller in the precordial leads, especially V2–V4, and usually measure up to 10 mm but can reach up to 12 mm.

If the axis of the QRS is 60 , the T wave should be within 45 ° (shaded)

to the left or right of the axis of the QRS complex.

Although the T waves are inverted in lead III (arrows), the axis of the T wave is within 45  of the axis of the QRS complex (QRS axis 0 ,T wave axis –5 ), thus the T

wave inversion in lead III is expected. This is not an abnormal finding.

Abnormal T Waves

When coronary blood flow is diminished or when myocardial oxygen demand exceeds blood supply, changes in the T waves are the earliest to occur. Electrocardiographically, changes confined to the T waves indicate myocardial ischemia, which may be subendocardial or transmural. Myocardial ischemia may alter the direction of repolarization depending on the severity of the ischemic process. This will cause changes that are confined to the T waves.

Subendocardial Ischemia 

• EKG finding:  tall and symmetrically peaked  T waves in the area of ischemia
• Mechanism: the direction of depolarization and repolarization is not altered and is similar to that of normal myocardium.
• Differentiating from hyperkalemia
• In subendocardial ischemia, the base is usually broad, and the QT interval is slightly prolonged. Peaking of T waves is confined to the area of ischemia, unlike hyperkalemia, where peaking is generalized
• Peaking of the T wave is nonspecific to MI, other causes are:
• fluoride toxicity, LVH from volume overload as AR, metabolic abnormality, normal variant

Transmural Ischemia

• EKG finding: deep and symmetrically inverted T waves in the area of ischemia
• Mechanism: the direction of the repolarization wave is reversed
• ST segment may or may not be depressed
• T wave inversion is not specific to MI, other causes are:
• HCM, pericarditis, PE, MVP, metabolic conditions, electrolyte abnormalities, drug effects, noncardiac conditions like CVA, craniocerebral abnormalities, peptic ulcer perforation, acute cholecystitis, acute pancreatitis, normal variant.

T Waves. (A) Normal T wave. (B) Peaked T waves from subendocardial ischemia. (C) Classical deep T-wave inversion due to transmural ischemia. (D) Symmetrically but less deeply inverted T wave also due to transmural ischemia. (E) Shallow T-wave inversion (F) Biphasic T wave. (G) Low, flat, or isoelectric

T wave. Although the T-wave configuration of B,C, and D suggests myocardial ischemia, these T-wave abnormalities may also be due to other causes.

Subendocardial Ischemia. Peaking of the T waves is confined to V1 to V4, consistent with subendocardial ischemia involving the anterior wall. Note also that the T waves are taller in V1 than in V6 and are biphasic in leads II, III, and aVF. Peaking of the T waves mark the area of ischemia and can occur as the initial manifestation of acute coronary syndrome before the onset of ST segment elevation.

Hyperkalemia. Peaking of the T waves from hyperkalemia (serum potassium   6.6 mEq/L). In subendocardial ischemia, the abnormally peaked T waves are localized to the ischemic area. In hyperkalemia, peaking of the T waves is generalized (arrows).

Transmural Myocardial Ischemia. The Twave changes shown are typical of transmural ischemia. Ischemic T waves are deeply inverted, usually measuring  >2 mm, and resemble the tip of an arrowhead as shown in V3 to V6.

(A) The T Wave Normal myocardium.Depolarization starts from endocardium to epicardium since the Purkinje fibers are located subendocardially. Repolarization is reversed and is epicardial to endocardial, thus the T wave and QRS complex are both upright. (B) Subendocardial Ischemia. The shaded portion represents the area of ischemia. The direction of depolarization and repolarization is similar to normal myocardium.After the repolarization wave reaches the ischemic area, the repolarization wave is delayed causing the T wave to be tall and symmetrical. (C) Transmural Ischemia. The direction of repolarization is reversed that of normal and is endocardial to epicardial resulting in deeply and symmetrically inverted T waves.

Difference bw ischemia, injury and infarction

Classically, there are three phases after a coronary artery occlusion:

• Ischemia: Reduction of myocardial oxygen for less than 20 minutes. The damage is reversible. In the electrocardiogram, ischemia produces changes in T wave.
• Injury: Persistence of oxygen deficiency (more than 20 min). Damage is still reversible. Injury is characterized by ST-segment abnormalities.
• Infarction: Persistence of oxygen deficiency for more than two hours. Damage is irreversible. Infarction is characterized by pathological Q waves on the electrocardiogram.

ST ELEVATION/DEPRESSION

There are 2 theories that explain ST segment elevation/ depression. There is no real explanation, but theories. Keep the following points in mind:

• Direction of systolic current of injury is towards the injured myocardium
• Direction of diastolic current of injury is directed away from the injured myocardium
• Systolic current of injury causes direct ST elevation/ depression
• Diastolic current of injury causes apparent ST elevation/depression through effect on TQ segment depression/elevation

Diastolic current of injury: Apparent ST segment elevation/depression from TQ segment depression/elevation 

• The resting potential of injured myocardial cells is less negative compared with normal cells. 
• This difference in potential occurs during phase 4, which corresponds to the TQ segment in the ECG. Because the injured cells have a less negative resting potential, they will have a more negative (less positive) extracellular charge relative to normal myocardium. This difference in potential between normal and injured myocardium will create an electrical gradient during diastole. Because the injured cells are in a state of partial depolarization, a diastolic current of injury is directed away from the injured subendocardium.
•  Diastolic current of injury video on Youtube

• Transmural or subepicardial injury:
• TQ segment shifts downward, away from the surface electrode overlying the area of injury. 
• During systole, all myocardial cells are discharged, erasing the potential difference between injured cells and normal cells. This will cause the ECG to compensate and return the ST segment to its previous baseline before the injury, resulting in apparent ST elevation. 

• Subendocardial injury: 
• TQ segment shifts upward, toward the surface electrode overlying the ischemic area. 
• During systole, all myocardial cells are discharged simultaneously, erasing the diastolic gradient between injured cells and normal cells. This will cause the ECG to compensate and return the ST segment to its previous baseline before the injury, resulting in apparent ST segment depression.

Diastolic Current of Injury causing apparent ST elevation: The yellow shaded areas in the upper and lower diagrams represent electrical diastole showing a change in resting potential from –90 to –60 mV after myocardial injury. Because the resting potential of injured cells is less negative, the cells are relatively in a state of partial depolarization. Thus, the extracellular membrane of the injured cells is more negative (less positive) compared with that of the normal myocardium, causing a diastolic current of injury directed away from the injured myocardium. This diastolic current of injury causes the TQ segment to be displaced downward away from the overlying electrode. When all cells are discharged during systole, the potential gradient between injured and normal cells is diminished, shifting the electrocardiogram baseline to its original position, resulting in apparent ST elevation.

Diastolic Current of Injury causing apparent ST elevation: When there is subendocardial injury, the ST segment is depressed because the baseline is shifted upward away from the injured subendocardium toward the direction of the recording electrode.

Systolic current of injury: ST segment elevation/ depression

• When the myocardial cells are injured, the resting potential of injured cells is less negative compared with normal cells (because damaged cells become leaky). A less negative resting potential will diminish the height, amplitude, and duration of the action potential. 
• This difference in the action potential between normal cells and injured cells creates a current of injury during electrical systole (phases 1–3 or ST segment and T wave in the ECG) that is directed toward the injured myocardium. 
• Transmural or subepicardial injury: the injury current is directed subepicardially resulting in elevation of the ST segment in the recording ECG electrodes that overlie the area of injury (figure below). 
• Subendocardial injury: the current of injury is directed subendocardially, away from the recording electrodes, resulting in depression of the ST segment

Systolic Current of Injury. The upper row represents transmembrane action potentials before and after myocardial injury, and the lower row the corresponding electrocardiogram (ECG). A change in resting potential from –90 to approximately –60 mV will occur when cells are injured. A less negative resting potential causes the amplitude and duration of the action potential to diminish when compared to normal cells. This difference in potential creates a current of injury during electrical systole (corresponding to phases 1–3 of the action potential equivalent to the ST segment and T wave in the ECG) between normal and injured myocardium. This current flows from the normal myocardium toward the injured myocardium. Thus, if the injury is subepicardial or transmural, the current of injury is directed toward the overlying electrode resulting in ST elevation. (0 to 4 represent the different phases of the action potential.)

Q WAVE

Normal Q Waves

• Normal Q waves represent activation of the ventricular septum in a left to right direction. These Q waves are often called septal Q waves. Septal Q waves are normally recorded in leads located at the left side of the ventricular septum including V5, V6, and leads I and aVL.
• The size of the normal Q wave is variable and depends on the thickness of the ventricular septum. In normal individuals, the Q waves are usually narrow measuring <0.03 seconds (roughly 1 small square) in duration and are <25% of the height of the R wave. 
• Q waves in lead III may be wide and deep but are not necessarily pathologic even when it exceeds 0.03 seconds in duration.

Abnormal Q Waves

• Although Q waves are the usual sequelae of ST elevation MI, not all patients with ST elevation MI will develop Q waves. Additionally, some patients with non-ST elevation MI may develop Q waves. Progression of ST elevation MI to a Q wave MI may be prevented if reperfusion is timely and successful.
• The development of Q waves during ST elevation MI may take a few hours to several days, depending on collateral flow. When collaterals are absent or are inadequate, Q waves may develop very early, within a few hours after symptom onset and may be present when the initial ECG is recorded. 
• Similar to ST elevation, pathologic Q wave serves as a useful marker in identifying the infarct related coronary artery, even after the ST-T abnormalities have resolved. Pathologic Q waves may be recorded unexpectedly in a rountine EKG and may be the only marker that a previous MI had occured.
• Some Q waves, however, are not permanent. Contraction of the scar tissue may occur during the healing process and may cause the Q waves to become narrower and may even disappear.
• Differential diagnosis of abnormal Q waves:
• Idiopathic hypertrophic subaortic stenosis (excessive thickness of the ventricular septum)
• preexcitation
• LBBB
• ectopic ventricular rhythms
• Abnormal Q waves criteria
• In leads I, II, aVL, aVF, V4, V5, or V6: a pathologic Q wave should measure ≥0.03 seconds in duration. The abnormal Q wave must be present in any two contiguous leads and should be ≥1 mm deep. (some texts mention ≥2 mm)
• In V2, and V3: any Q wave is pathologic regardless of size or duration.
• QRS confounders such as LBBB, LVH, and WPW syndrome should not be present.

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