Sunday, August 28, 2011

ECG Interpretation Review #28 (ST-T Wave Changes - Ischemia - RVH - RV "Strain")

Interpret the 12-lead ECG shown below in Figure 1, obtained from a patient who presented with new‑onset dyspnea.  What two clinical diagnoses should come to mind in view of the symmetric T wave inversion seen in leads V1,V2,V3 (arrows)?

Figure 1 – 12-lead ECG obtained from a patient with new-onset dyspnea. 

INTERPRETATION:  The mechanism of the rhythm is sinus, as upright P waves with a fixed PR interval precede each of the QRS complexes in lead II.  The R-R interval varies — defining this as sinus arrhythmia.  The PR, QRS and QT intervals are normal.  There is RAD (Right Axis Deviation) of at least +100 degrees (predominantly negative S wave in lead I ).  P waves are tall, peaked and pointed in lead II (≥2.5 mm tall) — consistent with RAA (Right Atrial Abnormality).

  • QRST Changes:  There are small q waves in the inferior and lateral precordial leads.  R wave progression is normal, with transition occurring between leads V3-to-V4.  T waves are fairly deep and symmetrically inverted in V1,V2,V3 (arrows).

SUMMARY:  Sinus arrhythmia. RAD. RAA. Symmetric T wave inversion consistent with anterior ischemia and/or right ventricular “strain”. 
IMPRESSION:  Clinical correlation is essential to the interpretation of this tracing.  Clearly, symmetric T wave inversion may reflect ischemia from coronary disease.  Determination of whether or not this reflects an acute ECG change would require comparison with one or more prior tracings.  It is important to appreciate that the constellation of findings on this tracing may also suggest RVH (Right Ventricular Hypertrophy) and/or right heart “strain”.


ECG Diagnosis of RVH:  Detection of right ventricular enlargement in adults by ECG criteria is often exceedingly difficult.  This is because the left ventricle is normally so much larger and thicker than the right ventricle in adults — that it masks even moderate increases in right ventricular chamber size.  As a result, many patients with RVH wont be identified — IF assessment for chamber enlargement is limited to obtaining an ECG (an Echo is needed to know for sure).
            The ECG diagnosis of RVH is best thought of as a “detective diagnosis”.  Rarely will any one finding clinch the diagnosis.  Instead — the diagnosis of RVH is most often suspected when one sees a combination of the ECG findings shown in Table 1.  This is especially true when several of these findings occur in a likely clinical setting (ie, COPD, right-sided heart failure, pulmonary hypertension).

Table 1 – List of criteria that taken together suggest RVH 

ECG Diagnosis of Pulmonary Embolism:  The ECG is usually not diagnostic of pulmonary embolism (PE).  That said — there are times when ECG will suggest the diagnosis before V/Q scan or chest CT is done.  Consider PE — IF the clinical setting is “right” (ie, new-onset dyspnea – pleuritic chest pain – predisposing risk factors or previous history of PE/DVT)and – one sees some of the following ECG clues:
  • There is sinus tachycardia (usually seen with large PE, albeit clearly nonspecific for the diagnosis).
  • There are ≥2 signs of acute “right-heart” strain (ie, RAD – RAA – RBBB – tall R in V1 – deep S in V5,V6).
  • There are ST-T wave changes of RV “strain” (ST-T depression in II, III, aVF and/or V1,V2,V3).
  • There is new-onset A Fib (common with PE, but nonspecific).
  • There are nonspecific ST-T wave changes (not diagnostic).

CLINICAL IMPRESSION:  The clinical context for the patient whose initial ECG is shown in Figure 1 is that of “new-onset dyspnea”.  We do not know if the ECG changes seen in Figure 1 are new or old.  Clearly — the anterior symmetric T wave inversion that is seen may reflect ischemia of uncertain duration.  If the RAD and RAA are not new findings — they may reflect longstanding RVH from chronic pulmonary disease.  But IF the RAD, RAA and anterior T wave inversion are all new findings occurring in association with new-onset dyspnea — then acute pulmonary embolus would have to be strongly considered.  PEARL: Anterior T wave inversion may sometimes be an important ECG clue to the possibility of acute pulmonary embolus.

Friday, August 12, 2011

ECG Interpretation Review #27 (ST-T Wave Changes - QT-U Wave - Hypokalemia-Ischemia)

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?

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.

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.

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 (and/or 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.

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 (and/or 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 (in our experience) is not an overly reliable tool for assessing for assessing mild-to-moderate hypokalemia, as both sensitivity and specificity of ECG findings for less-than-severe hypokalemia are relatively low.  That said — the changes that one looks for are sequentially illustrated in Figure 3.
  • Ais a normal ST-T wave.    
  • Bshows flattening of the T wave, which typically is the earliest change.
  • C and DIn association with ST-T wave flattening (and sometimes with slight ST depression) — a U wave develops.  A "pseudo-P-pulmonale" pattern (with P wave peaking) may be seen.     
  • E and FST 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.

As emphasized above — U waves per se are not specific for hypokalemia.  U waves 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.
  • PEARL #1: When the clinical setting is "right" (ie, potentially predisposing to hypokalemia) — by the time U waves become so large that they are bigger than (or almost as big as)  T waves — specificity of the ECG for significant hypokalemia is greatly increased.
  • PEARL #2:  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.
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Thursday, August 4, 2011

ECG Interpretation Review - #26 (Regular SVT - Diffuse ST Depression - List #4)

Interpret the ECG below, obtained from an older woman on multiple drugs who presented to the emergency department.  She was complaining of chest pain, and clinically was in heart failure.  How would you interpret her 12-lead tracing?  Why so much ST segment depression?  Clinically — What would you do?

Figure 1 – 12-lead ECG from a patient with chest pain and heart failure.  What is the rhythm?  Why so much ST depression?

INTERPRETATION:  The rhythm is rapid and regular at a rate of ~180/minute.  The QRS complex is narrow in all 12 leads.  This defines the rhythm as a SupraVentricular Tachycardia (SVT ).  No definite P waves are seen.  It is impossible to know IF the small upright deflection midway between QRS complexes in lead II represents a P wave, T wave, or both.  This leaves us with the differential diagnosis of a regular SVT without definite sign of atrial activity (See below).
  • Otherwise — the rate is too fast for assessment of the QT interval to be meaningful; voltage criteria for LVH are easily satisfied (very deep S in V1 plus tall R in V5 easily exceeding 35 mm); and there is diffuse ST depression that exceeds 2-3 mm in many leads.

The RHYTHM:  As discussed in ECG Review #25 — 3 entities should be considered in the differential diagnosis of a regular SVT when atrial activity is uncertain (Table 1):

Table 1 – List of the most common causes of a regular SVT when there is no definite sign of atrial activity.

In this particular case — the rapid rate (ie, ~180/minute) strongly suggests PSVT (Paroxysmal SupraVentricular Tachycardia) as the diagnosis. 
  • The most common ventricular response with untreated atrial flutter is with 2:1 AV conduction. Because the atrial rate of flutter is most often very close to 300/minute (250-350/minute range) — the ventricular rate will usually be close to 150/minute (most often between 140-160/minute). The substantially more rapid rate seen in Figure 1 makes atrial flutter unlikely.  
  • Similarly — sinus tachycardia in non-exercising adults rarely attains rates in excess of 160-170/minute. By exclusion — PSVT is therefore the likely diagnosis for the regular SVT shown in Figure 1.
Diffuse ST Depression:  Next to the rapid rate — the most remarkable finding in Figure 1 is the deep and diffuse ST segment depression.  Although there are many possible causes of ST depression — we find it helpful to routinely consider the diagnostic entities listed in Table 2:

Table 2 – List of the most common causes of ST segment depression.

It will often not be possible to determine the precise cause(s) of ST depression:
  • In the case presented here — the patient has chest pain, heart failure, and is taking multiple medications. The deep and diffuse ST depression seen in Figure 1 may reflect ischemia (she has chest pain); “strain” (increased voltage; history of heart failure); digitalis effect/electrolyte disturbance (diuretics and possibly also digoxin may be among her multiple drugs); tachycardia (PSVT at 180/minute) — or more likely, some combination of all of these factors.

The first priority in treating this patient is to address her tachycardia.  Clearly — sudden onset of PSVT at 180/minute in an older patient with heart failure may exacerbate her condition.  Chest pain (and ST depression) may result from the associated reduced coronary perfusion or the tachycardia itself.  Both may resolve with conversion to sinus rhythm.  PSVT usually responds promptly to medical treatment (adenosine, diltiazem, a beta-blocker with or without attempted vagal maneuver).  The patient will undoubtedly be admitted to the hospital to optimize treatment for heart failure.  Follow-up ECGs and serum troponin values after conversion to sinus rhythm will hopefully elucidate whether the deep and diffuse ST depression seen in Figure 1 was the result of a transient phenomenon (associated with her PSVT) or a primary cardiac event.

  - See also ECG Blog #25.