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).
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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).

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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.

• 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 depression) — 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.

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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- For more information — GO TO:

• See also ECG Blog #26 -
• See Section 11.0 on Lyte Disorders (from ECG-2014-ePub) — Click to download = http://tinyurl.com/ECG-11-Lytes (The part regarding Hypokalemia begins in Section 11.7).

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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.

CLINICAL IMPRESSION:    

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.

CLINICAL APPROACH:

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.

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  - See also ECG Blog #25.

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ECG Blog #25 — Regular SVT and ST Depression

Interpret the 12-lead ECG shown below, obtained from a woman with sensation of “rapid heart beat”.  What is your differential diagnosis?  What diagnostic maneuver might help to determine what the rhythm is?

• Additional Questions: 1) Which leads are most helpful to assess for atrial activity?  2) Do you see atrial activity in all leads on this 12-lead tracing?  3) Do you need to be sure of the rhythm diagnosis before initiating treatment?

Figure 1 – 12-lead ECG from a patient with “rapid heart beat”.  What is your differential diagnosis?  What might you do diagnostically? 

INTERPRETATION:  Our preference is to always obtain a lead II Rhythm Strip whenever a question arises as to rhythm diagnosis.  This is shown in Figure 2.

Figure 2 – Lead II rhythm strip from the patient with tachycardia in Figure 1.  What is your differential diagnosis? 

The rhythm is regular at a ventricular rate that is close to 150/minute (the R-R interval is approximately 2 large boxes in duration — and 300 ÷ 2 = 150/minute).  The QRS complex is narrow (ie, not more than half a large box).  Normal atrial activity is absent, since upright P waves are not seen in lead II.  Instead, there is a suggestion of atrial activity having a negative deflection in lead II (as well as in other inferior leads).  There also appears to be a negative notching in the ST segment in each of the inferior leads.  Could this all represent atrial activity?

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Application of a Diagnostic Maneuver: 

The answer to the question of whether atrial activity is embedded within the 12‑lead tracing is forthcoming from application of a vagal maneuver.  Carotid Sinus Pressure (CSP) is applied at the moment marked by the large arrow in Figure 3. 

• Note shortly after application of CSP — there is reduction in the conduction ratio of impulses passing through the AV Node.  This produces a short pause — during which the typical sawtooth pattern of Atrial Flutter can be readily recognized. 

Figure 3 – Lead II rhythm strip showing the result of CSP, which reveals regular sawtooth flutter waves.

DISCUSSION:  A number of important points are brought out by this case.

• We often do not know definitive diagnosis of the rhythm at the time the patient presents.  This need not hinder our approach to treatment.  First priority in the assessment of any tachycardia is to ensure hemodynamic stability.  Although not explicitly stated in this case (we are not told the patient’s blood pressure) — We may presume the patient is stable because the presenting symptom is “rapid heart beat”.  IF the patient was hemodynamically unstable as a result of the rapid rate (ie, with chest pain, shortness of breath, mental confusion, hypotension) — then regardless of what the rhythm turns out to be, immediate synchronized cardioversion would be indicated.
• Given that this patient is stable — We have time to better assess the rhythm.   Use of a 12‑lead ECG during tachycardia is extremely helpful in this regard.  Next to lead II — lead V1 (which lies in proximity anatomically to the right atrium) is usually the next best lead to look at for atrial activity.  After leads II and V1 — we then direct our attention to all 10 of the remaining leads for clues to atrial activity.  Doing so in Figure 1 — we see suggestion of sawtooth activity in leads II, III, aVF, aVR, and V1 — but no sign of atrial activity in most of the other leads.  The 12‑lead tracing also confirms that the QRS complex is truly narrow in all 12 leads.
• The best description of the tachycardia defined by the rhythm in Figures 1 and 2 is that this represents a regular SVT (SupraVentricular Tachycardia) without sign of normal atrial activity.  This description should prompt consideration of the 3 entities shown in Table 1 as the likely cause of the tachycardia:

Table 1 – List of the 3 most common causes of a regular SVT when normal atrial activity is not seen.

• Practically speaking — 90-to-95% of the regular SVTs that primary care clinicians encounter (in and out of the hospital) will be one of the 3 entities on this list.  Clearly — other causes exist (junctional tachycardia, ectopic atrial rhythms, accessory pathway reentry tachycardias, etc.) — but keeping in mind these 3 entities will simplify and facilitate diagnosis in the majority of cases.
• Heart rate may help in distinguishing between the 3 entities in List #1 — IF the rate exceeds 170/minute in an adult.  This is because it is unusual for a nonexercising adult to be in sinus tachycardia at rates above 170/minute.  Atrial flutter with 2:1 AV conduction is also unlikely when the ventricular rate exceeds 170/minute, since the atrial rate of untreated flutter is rarely faster than 340/minute in adults.  However — when the rate of a regular SVT is approximately 150/minute (as it is in Figures 1,2) — any of the 3 entities in Table 1 may be the cause.
• We suspect the rhythm in Figures 1,2 is not sinus tachycardia, because we do not see an upright P wave in lead II.  Application of a vagal maneuver resolves the issue (Figure 3) — as it brings out flutter waves that had been partially hidden within the QRST complex in Figure 1.
• Although not essential for our initial approach to this patient — knowing definitive diagnosis facilitates treatment.  Use of an AV-Nodal-slowing drug (ie, diltiazem, a beta-blocker) now becomes appropriate at this point. Synchronized cardioversion might ultimately be needed if medical treatment does not convert the rhythm.

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  - See also ECG Blogs #23 and #24 -
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ECG Interpretation Review - #24 (Wide Tachycardia - WCT - VT vs SVT vs Flutter)

The lead II rhythm strip shown below was obtained from a patient admitted to the Emergency Department. Interpret the rhythm. How certain are you of your answer?  What would you do?

• Scenario #1:  The patient is unresponsive with a BP = 60 palpable.
• Scenario #2:  The patient is alert and asymptomatic.  BP = 120/80 mmHg.

Figure 1 – Lead II rhythm strip showing tachycardia. What to do?

INTERPRETATION:  The rhythm is fast and fairly (but not completely) regular. The QRS looks to be wide (ie, more than half a large box) and there are no definite P waves.  Thus, this appears to be a WCT (Wide Complex Tachycardia) of uncertain etiology.  As to the question of What To Do? — the answer depends on the clinical scenario. 

• IF the patient is unstable (Scenario #1) — immediately cardiovert.  Regardless of whether the rhythm is VT or SVT with bundle branch block or aberrant conduction — hemodynamic instability is an indication for immediate cardioversion.  
• On the other hand — IF the patient is stable (Scenario #2) — then by definition, you have at least some time to contemplate treatment (while you work to determine the rhythm). We would obtain more history (previous episodes of WCT?) — look for prior tracings on the patient (either on telemetry or from the patient’s chart) — and get a 12‑lead ECG during tachycardia (Figure 2). 

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The 12-lead ECG during tachycardia is shown below (Figure 2):

Figure 2 – 12-lead ECG obtained during tachycardia. Does this help with your answer?  

12-Lead Analysis:  The rhythm is rapid and looks to be regular (albeit with occasional minor variation in the R-R interval).  The rate is ~150/minute (the R-R is ~2 large boxes in duration).

• The QRS is wide (clearly more than half a large box in leads II,III,V3,V4).  That said — overall QRS morphology looks to be supraventricular (in the form of LAHB with LVH and “strain”).
• “Normal atrial activity” is absent in Figure 2 (RED arrow showing no upright P in lead II). 
  

Beyond-the-Core:  One wonders if the RED arrow and negative deflections before the QRS in the inferior leads might represent some form of atrial activity … (Figure 3):

Figure 3 – Short vertical lines have been added to Figure 2 highlighting what might represent underlying atrial activity (See Figure 4).

IMPRESSION (What to do?): This case illustrates the importance of the clinical situation in the approach to this patient.  Whereas immediate cardioversion would be indicated if the rhythm in Figure 1 was associated with hemodynamic instability — additional diagnostic assessment would be appropriate IF the patient is stable (Scenario #2).  Clearly — sometimes “ya just gotta be there” to know which approach is best for an individual patient.  Our Hunch (based on Figures 1,2,3) — is that the rhythm is supraventricular.

• Slight QRS widening (~0.1-0.2 msec) may be seen with both LVH (it takes longer to get through a thicker ventricle) and with LAHB (conduction is delayed through the left hemifascicle).  Thus — QRS widening (as seen in Figure 2) may occur IF there is both LVH and LAHB. 

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To PROVE Our Hunch:

• Find a prior ECG on this patient.  See IF QRS morphology in the past (during sinus rhythm) is the same as on the Figure 2 12-lead obtained during tachycardia (which shows LAHB; LVH with strain). 
• Get more History (prior episodes of WCT that look like Figure 2? ) 
• Consider a vagal maneuver or “chemical Valsalva” (ie, administration of IV adenosine, which may produce similar effect as carotid massage). 
• Treatment will clearly be more effective IF we can be sure of the diagnosis — BUT — IF at any time during the process the patient becomes unstable — Be ready to immediately cardiovert! 
  

Chemical Valsalva in the form of an IV bolus of adenosine was attempted.  The result is shown below (Figure 4).

Figure 4 – Result of “chemical Valsalva”. What does this prove?

Result of “Chemical Valsalva”:  Administration of IV adenosine results in reduced AV conduction with slowing of the ventricular response (RED arrow).  This reveals underlying flutter activity at an atrial rate of ~300/minute (sawtooth flutter waves occurring approximately each large box).  

• Retrospective review of the 12-lead ECG during tachycardia suggests that the negative deflections previously noted in the inferior leads (and to a lesser extent in lead aVR) were in fact flutter waves (short vertical RED lines in Figure 3).
  

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KEY Points in this Case:

The 2 scenarios proposed in this case illustrate how to clinically work though assessment and management of a patient with WCT of uncertain etiology.

• Always presume VT until proven otherwise.  Immediate cardioversion is indicated if the patient is unstable.  BUT — IF the patient is stable, there is at least some time to work through the diagnosis.
• Treatment will be much more effective (and you as clinician will be more confident) — IF you are able to determine what the WCT actually is.  In this case — Knowing that the rhythm in Figure 1 is atrial flutter with 2:1 AV conduction and QRS widening from LVH/LAHB allows us to treat the patient with IV diltiazem (bolus and drip) — whereas diltiazem would be contraindicated if the rhythm was an ischemic form of VT.
• BOTTOM Line: You will not always know the etiology of a tachycardia at the time you first encounter the patient.  No matter — as you can still proceed with an appropriate clinical approach as outlined above.  

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  - See also ECG Blog #23 - 

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