13. Partially Occluded Artery: Angina and Non-ST Elevation MI

Home » MEDCLIN530 » EKG » 12-Lead EKG Confidence » V. Ischemic Disorders: EKG changes related to ischemia and myocardial infarction » 13. Partially Occluded Artery: Angina and Non-ST Elevation MI
Headshot of Chris Anderson, MD · Clinical Education Director, Pediatrics
Chris Anderson
MD · Clinical Education Director, Pediatrics
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Headshot of Kevin Hodges, Vice Chair, Emergency Medicine
Kevin Hodges
Vice Chair, Emergency Medicine
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Table of Contents
  • Define and identify the following:
    • Normal T wave.
    • Direction of T wave changes in ischemia.
    • Location of ischemia in the myocardium.
  • List two clinical mechanisms of worsening ischemia.
  • List two clinical mechanisms of ameliorating ischemia.
  • Describe the coronary arteries and the structures they supply.
  • Describe the pathophysiology of stable angina.
  • Describe the pathophysiology of the acute coronary syndrome.
  • Name the three rules of the T waves.
  • Describe the inverted T wave patterns for localizing ischemia and infarction.
  • Describe the significance of ST segment depression.

The normal T wave

The T wave is normally the last complex in the cardiac cycle. It represents electrical activity produced during rapid ventricular repolarization. The repolarization process allows the depolarized cardiac cells to reset for the next cardiac cycle, much like a rubber band has to be restretched before it can be released. Repolarization requires a constant supply of oxygen-rich blood flow to supply energy for this process.

Normal T wave direction

The direction of the normal repolarization wave is similar to that of the depolarization wave. We can visualize the direction of the normal T wave axis as pointing inferiorly and to the patient’s left, which is toward the apex of the left ventricle, much as the QRSdoes (Figures 13.1 and 13.2).

Line drawing of body showing the direction of a normal T wave.
Figure 13.1
Segmented circle with horseshoe shape opened left. Arrows point out from horseshoe with normal T wave exiting southeast segments.
Figure 13.2

The T wave in ischemia: Overview

The T wave represents electrical activity produced during the rapid ventricular repolarization. This active process of repolarization requires a constant supply of oxygen to generate energy. If too little oxygenated blood flow is available for the metabolic needs of the tissues, ischemia results. Ischemic areas cannot generate energy to repolarize as readily as nonischemic cells, so the direction of repolarization changes. On the EKG, this appears as a T wave direction pointing away from an area of ischemia. Drug effects and electrolyte abnormalities are also important causes of T wave changes, as is discussed in Chapter 19 (link when ready).

Location of ischemia: The vulnerable subendocardium

The part of the myocardium most distant from the arteries is the subendocardial region. The subendocardium is the farthest away from the arteries, which must penetrate through contracting muscle to deliver the blood to the subendocardial layer. This makes the subendocardial region the most sensitive to ischemic conditions, such as increased demand or decreased supply. Any increase in demand or decrease in supply of blood at the level of the subendocardium can produce ischemia. If the ischemic conditions are severe, not soon relieved, or both, then infarction (cell death) occurs.

Horizontal, 3-layer rectangle. Blood supply enters the subendocardial layer.
Figure 13.5, Subendocardium
Figure 13.6 and 13.7
Clinical mechanisms of Ischemia
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Ischemia occurs when there is an imbalance between the supply of oxygen to the myocardium and the demand for oxygen by the myocardial mitochondria. Any increase in demand or decrease in supply may cause ischemia and, if it continues, can lead to tissue death, which is called infarction. The effects of these precipitating causes are additive. (See Figure 13.7, below)


Oxygen demand is increased by

  1. Tachycardia.
  2. Increased blood pressure.
  3. Increased heart size (harder to squeeze a basketball than a grape).

Oxygen supply is decreased by

  1. Low hemoglobin.
  2. Low pO2.
  3. Fixed atherosclerotic narrowing.
  4. A growing atherosclerotic plaque or clot causing partial obstruction.
  5. Coronary artery spasm.
Clinical mechanisms that can relieve ischemia
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Therapeutic goals in this setting are to either increase the supply, decrease the demand, or both. Any decrease in demand or increase in supply may help relieve ischemia. If the therapeutic intervention is done effectively and quickly, it can prevent the progression to permanent cell death (infarction) of myocardial tissue. If the interventions are not successful, myocardial infarction occurs. (See Figure 13.8, below)


Oxygen demand is decreased by

  1. Decreasing a high heart rate.
  2. Decreasing a high blood pressure.
  3. Decreasing a dilated heart size.

Oxygen supply is increased by

  1. Increasing a low hemoglobin.
  2. Increasing a low pO2.
  3. Dilating or bypassing a fixed lesion.
  4. Decreasing coronary artery spasm, if present.
Figure 13.7
Figure 13.8

Anatomy and pathophysiology of ischemia: Stable angina

The heart normally receives fully oxygenated blood through the right and left coronary arteries. The process of conduction and contraction is energy dependent on a second-to-second basis, and a lack of blood flow can cause problems quickly. Atherosclerotic plaque is the most common underlying cause that creates blockages in these arteries, thereby reducing the supply of oxygen to the ventricle. The obstructive process can occur slowly over years and, at the beginning (Figure 13.9), may not cause any symptoms. As the cross-sectional area of the coronary artery decreases (Figure 13.10), the supply of blood also decreases. This fixed obstruction causes the classic (in men) exertionally provoked, rest-relieved symptoms of stable angina.

Cross section of artery with increased blockage.
Figure 13.9
A cross-section of artery with partial blockage.
Figure 13.10

Pathophysiology of ischemia: Acute coronary syndrome

The process of atherosclereosis can occur slowly over years. At the beginning (as shown in Figure 13.9), it may not cause any symptoms. This can change in a matter of minutes. An atherosclerotic plaque can unpredictably and acutely rupture and spill its fatty contents (Figure 13.11) into the arterial lumen. This plaque rupture can immediately cause a thrombus to form on top of the partial blockage from the underlying plaque (Figure 13.12) and produce a sudden change in the patient’s symptoms. This is called an acute coronary syndrome.

Regardless of the mechanism causing the obstruction (the one-component large plaque of stable angina or the two-component plaque-with-thrombus of acute coronary syndrome), the area of the ventricle with poor blood supply has less oxygen than it needs. Less oxygen translates immediately into less energy. This interferes with the ischemic area’s ability to repolarize normally, and we see this as a directional change in the T wave. 

Figure 13.11
Cross-section of an artery showing thrombus.
Figure 13.12

The first rule of the T waves

Any process that causes ischemia can eventually result in infarction (cell death) if it is prolonged or severe enough. Ischemia, by interfering with normal repolarization,
changes the direction of the T wave away from the ischemic area. If infarction occurs, the T wave may remain permanently abnormal. This creates a common problem for an EKG reader that can be summed up as The First Rule of the T Waves. It states: On a single EKG-in-hand, neither ST depression nor T wave changes can prove timing or reversibility.


This simply stated rule is probably the least understood principle in all of electrocardiography. If a pattern of T wave inversion or ST depression is NOW present
(see Table 13.1), it makes the presence of significant obstructive coronary disease more likely. It does not distinguish whether the event is new or old. Furthermore, if the finding of T wave inversion or ST depression is found to be new, it still does not determine (on that single EKG!) whether the process is reversible or permanent.

If the T or ST abnormalities are unchanged compared to an old EKG, they represent
an old and irreversible process, a non-ST elevation MI. If the changes are new compared to an old EKG, they represent an acute coronary syndrome—unstable angina or a new non-ST elevation MI. To separate these three possibilities, we need additional information. The old EKG is helpful in deciding whether or not the EKG changes are new. A follow-up EKG is helpful in deciding if the EKG changes are reversible.

Table 13.1

If you understand Table 13.1 and can draw it from memory, then you have a fundamental understanding of how to interpret ischemia or infarction based on T wave changes.

memorize this

Table 13.2 Location of the T wave: Frontal plane patterns

Location of process
(Ischemia or NSTEMI)
Visualize the concept Memorize these patterns
Inferior
T waves point away from inferior wall
II, III, AVF
Lateral
T waves point away from lateral wall
I, AVL
Apical
T waves point away from apex
I, AVF
Nonspecific inferior T wave changes
T waves borderline superior
III, AVF, but not II
Nonspecific lateral T wave changes
T waves borderline rightward
L, but not I
Normal T axis
T waves point toward the apex
If any, only III
Nonspecific septal T wave changes
T wave points borderline away from the septum
V1 only
Septal
T wave points away from septum
V1 and V2
Anterior
T wave points away from the anterior wall
V3 and V4
Lateral
T wave points away from the lateral wall
V5 and V6
Nonspecific lateral T wave changes
T wave points borderline away from the lateral
V6 only
Normal
T wave toward the apex
No T wave inversion

Second rule of the T waves: The ST segment

The ST segment represents electrical activity produced during ventricular repolarization. Normally, the ST segment is at the baseline since only an even exchange of charges is taking place as ions inside and outside the cell change places to be ready for the nextQRS. In severe subendocardial ischemia, the ST segment can become abnormal and point away from regions of subendocardial ischemia. It is a more specific finding of subendocardial ischemia than T wave inversion.

The Second Rule of the T Waves states: On a single EKG, if T wave changes and ST depression are both present, the ST segment depression is more significant. Consider ischemia as a process of overheating the myocardium. Smelling smoke would be comparable to seeing an inverted pattern of T waves. Seeing smoke would compare to the presence of ST segment depression.

ST depression is not only more specific than T wave inversion for an ischemic process, it also carries a worse prognosis. Consider T wave inversion as the cell running out of energy at the very end of the repolarization cycle, while ST depression is a severe lack of enough energy from the very start of repolarization. In addition, downsloping ST segment depression is more specific than horizontal ST segment depression. Both are more specific than upsloping ST segment depression.

Clinical interpretation of abnormal Ts and STs

If you start at the top of table below with an EKG showing T wave inversion or ST segment depression, you can follow the path down to one of three clinical possibilities.

There are three basic clinical question you need to answer first to begin:

  1. Does the patient have chest pain?
  2. Is there an OLD EKG available?
  3. Are the EKG changes new when compared to the old EKG?

If the answer to 1, or 2, or 3 is Yes, then the patient has an Acute Coronary Syndrome, either Unstable (reversible) Angina, or a New NSTEMI.

If the answers to 1, 2, and 3 are all No, then the patient sustained an NSTEMI sometime in the past.

Table 13.3 T wave and ST segment clinical summary

The current EKG shows an abnormal pattern of T wave inversion or ST depression
New compared with old EKG or patient has symptoms
Unchanged compared with old EKG and patient has no symptoms
Follow-up EKG normalizes and biochemical markers negative
Follow-up EKG remains abnormal after 24 hours or biochemical markers positive
Old NSTEMI
Unstable angina
New NSTEMI