Interpret the ECG below, obtained from a patient with a history of alcohol abuse and atypical chest pain. Is there ischemia? — an electrolyte disturbance?
|Figure 1 – 12-lead ECG obtained from a patient with atypical chest pain and a history of alcohol abuse. What might the ST-T wave changes be due to? (Figure reproduced from ECG 2011 Pocket Brain – pg 57A). – NOTE – Enlarge by clicking on Figures – Right-Click to open in a separate window.|
INTERPRETATION: There is sinus arrhythmia. The PR and QRS intervals are normal. However — the QT interval is long (clearly more than half the R‑R interval). The axis is normal (about +65°). There may be LAA (left atrial abnormality) given the fairly deep negative component to the P wave in lead V1 — but otherwise no sign of chamber enlargement.
- QRST Changes: There is a Q wave in aVL, and a QS in V1,V2. Transition is slightly delayed. The most remarkable finding is diffuse ST-T wave flattening/depression with in addition symmetric T inversion in leads V4,V5,V6. The QT interval is markedly prolonged, and there are U waves in multiple leads (best seen in V3, as shown by the RED arrow in Figure 2 below).
|Figure 2 – Blowup of leads V2,V3 from Figure 1. U waves are best seen in lead V3 (red arrow). It is impossible to tell if there is QT or Q-“U” prolongation. (Figure reproduced from the ECG Web Brain).|
CLINICAL IMPRESSION: The diffuse ST-T wave changes seen in Figure 1 may be due to any of the common causes of ST depression. To facilitate recall — these common causes are listed in Table 1 and include ischemia; “strain” from LVH; electrolyte disturbance (hypokalemia; hypomagnesemia); digoxin effect; and/or tachycardia (See also ECG Blog #26). Given the history of chest pain — one has to consider ischemia that may be acute (difficult to know IF the T wave inversion in Figure 1 is a new finding without availability of a prior ECG for comparison).
|Table 1 – List of the most common causes of ST segment depression. (Figure reproduced from ECG 2011 Pocket Brain – pg 47).|
The markedly long QT (or “Q‑U”) interval in Figure 1 should suggest one or more of the common causes of QT prolongation. To facilitate recall — these common causes are listed in Table 2 and include “Drugs – Lytes – and CNS catastrophes” (See also ECG Blog #4). The ECG signs and history of alcohol abuse in this case should place hypokalemia/hypomagnesemia high on your list. Electrolyte disturbance is further supported as a contributing factor to the ST-T wave changes in this case by the finding of U waves in multiple leads.
|Table 2 – List of the common causes of QT prolongation. (Figure reproduced from ECG 2011 Pocket Brain – pg 29).|
CLINICAL CORRELATION / USE of the “Lists”: Clinical correlation is needed to determine the likely cause(s) of ST-T wave abnormalities in Figure 1. At the least — We suspect ischemia and hypokalemia/hypomagnesemia. Serum electrolytes, serial troponins and follow-up ECGs/comparison with prior tracings should be revealing, although at times it may not be possible to precisely determine each contributing factor …
- The ECG in this Blog post provides an excellent example of how we use our “Lists” to assist with ECG interpretation. We intentionally limit both the number and length of each of our 6 “Lists” to facilitate recall. On recognizing a particular ECG finding (such as QT prolongation or ST depression) — recall of the entities on the relevant list help us to expediently hone in on the differential diagnosis (See Tables 1 and 2 above — plus Table 1 in Blog #23 and Table 1 in Blog #26).
ECG CHANGES of HYPOKALEMIA: We conclude this ECG post by brief review of the ECG changes of Hypokalemia. In contrast to hyperkalemia — the ECG is not a reliable tool for assessing for assessing hypokalemia, as both sensitivity and specificity of ECG findings are low. That said — the changes that one looks for are sequentially illustrated in Figure 3.
- A — is a normal ST-T wave.
- B — shows flattening of the T wave, which typically is the earliest change.
- C and D — In association with ST-T wave flattening (and sometimes with slight ST depresssion) — a U wave develops. A "pseudo-P-pulmonale" pattern (with P wave peaking) may be seen.
- E and F — ST depression is more noticeable and the U wave increases in amplitude (arrow) — until ultimately the U wave overtakes the T wave. At this point, distinguishing between T wave and U wave may be almost impossible (ie, there may be “Q-U" rather than “Q-T” prolongation — as in F).
|Figure 3 – Sequential development of ST-T wave changes of hypokalemia. Note increasing U wave amplitude. (Figure reproduced from ECG 2011 Pocket Brain – pg 57).|
As emphasized above — U waves are not specific for hypokalemia. They may also be found in patients with LVH and/or bradycardia, or occasionally as a normal variant. However, the setting and ECG findings in this case (given the history of alcohol use with diffuse ST-T wave flattening and relatively large amplitude U waves in multiple leads) strongly suggests the possibility of electrolyte disturbance.
- Final PEARL: Hypomagnesemia produces virtually identical ECG changes as hypokalemia. Low body magnesium is often encountered in association with other electrolyte abnormalities (ie, low sodium, potassium, calcium or phosphorus); acute MI; cardiac arrest; digoxin/diuretic use; alcohol use and abuse; renal impairment.
- See also ECG Blog #26 -