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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ECG Interpretation Review #23 (Wide Tachycardia - WCT - VT vs SVT)

Is the rhythm below in Figure 1 sinus tachycardia? It was obtained from a hemodynamically stable man (BP=120/80 mmHg) with new-onset palpitations.

Figure 1 – Lead II rhythm strip from a patient with palpitations. BP = 120/80. Is this sinus tachycardia?

INTERPRETATION:  The lead II rhythm strip shows a regular tachycardia at about 150/minute. Although the red arrow suggests sinus tachycardia – We are uncertain about QRS width, and therefore do not know how to proceed …

• The “good news” – is that the patient is stable (BP=120/80). This means that there is time to confirm the diagnosis before beginning treatment.
• The “less good” news – is that we do not yet know what the rhythm is …

The first steps (given that this patient is hemodynamically stable) – are to: i) obtain more history (History of underlying heart disease? of tachyarrhythmias such as documented SVT or VT? ) – and ii) obtain a 12-lead ECG during the tachycardia (being ready to cardiovert the patient if he at any time decompensates).

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

Figure 2 – 12-lead ECG during tachycardia. Does this provide the answer?

The 12-lead ECG obtained during tachycardia clearly reveals that the QRS complex is wide!

• The small upright deflection in lead II (red arrow) is not a P wave after all.  Instead – the vertical red time lines show this deflection to be the initial part of the QRS complex! 
• All other leads show the QRS to be very wide (>0.16 second).
• The rate is about 150/minute.  The rhythm is regular. No P waves. 

IMPRESSION: This is a regular WCT (Wide Complex Tachycardia) with no sign of atrial activity. As emphasized in our KEY List below (Table 1) – always presume VT until proven otherwise! Statistically – the odds that a regular WCT without definite atrial activity is VT are at least 80%.  This goes up to over 90% if the patient also has underlying heart disease.

Table 1 – Common Causes of a Regular WCT without P waves.  

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KEY Points in the Assessment of this Regular WCT:

• VT  is by far the most common cause of a WCT when there is either no atrial activity or uncertain atrial activity. Although possible that a WCT may be due to supraventricular tachycardia with either preexisting bundle branch block or aberrant conduction – Always presume VT until proven otherwise. Treat accordingly.
• Not all patients in VT immediately decompensate. Some may remain hemodynamically stable despite ongoing VT for hours, or even days …
• Obtaining  a 12-lead tracing during tachycardia may be invaluable for honing in on the etiology of a tachycardia.  In this case, there are a number of clues that overwhelmingly suggest VT as the diagnosis.  These include: i) marked QRS widening in all other leads; ii) bizarre QRS axis during the tachycardia (extreme left axis deviation); iii) bizarre QRS morphology (not resembling any form of organized bundle branch block); iv) markedly negative QRS complex in left-sided lead V6 (which virtually always has more than a tiny r wave of positive activity); v) delayed R-to-S-nadir (VT very likely when there is an RS complex in any precordial lead with an interval from onset of the R until deepest point of the S >0.10 sec. - as it is in V5 and V6); and vi) concordance of the QRS in precordial leads (all precordial lead QRS complexes are predominantly negative). BOTTOM Line: “12 leads are better than one” – and - a WCT without definite P waves should always be presumed to be VT until proven otherwise (regardless of whether or not the patient is hemodynamically stable).

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- See Sections 08.0, 09.0 in our ACLS-2013-ePub -
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ECG Interpretation Review #22 (AV Block - What Type?)

The lead II rhythm strip below was obtained from a patient on telemetry. Is there AV block?  If so - what type?

Figure 1 - What type of AV block do you suspect? (Reproduced from ACLS-2013-ePub).
- Note - Enlarge by clicking on Figures - Right-Click to open in a separate window.

INTERPRETATION: The rhythm is irregular. The QRS complex is narrow, indicating a supraventricular mechanism. P waves of similar morphology are present - but they do not all seem to be conducting. This suggests that some form of AV block may be present. The most striking finding on this tracing is the presence of group beating (alternating short-long cycles). Recognition of "group beating" should make one suspect that a type of Wenckebach conduction may be present.  Looking closer:

• As noted - P waves of similar morphology are seen in this lead II rhythm strip.  However, the P-P interval varies.  This suggests that the underlying rhythm is sinus arrhythmia.
• Beats are being dropped (ie, one would definitely expect the P waves following beats #2 and #4 to conduct). Complete (3rd degree) AV block is unlikely because the ventricular response is so variable). Thus, this tracing most probably represents a type of 2nd degree AV block (See ECG Blog Review #20). The narrow QRS and the presence of group beating suggest Mobitz I as the prime suspect.
• The KEY lies with analysis of beats #1, #3, and #5.  On close inspection, it can be seen that QRS morphology of each of these beats differs slightly from that of beats #2, #4, and #6 (the latter 3 beats having a shorter R wave and slightly deeper S wave). The PR interval preceding beat #5 is definitely too short to conduct. This implies that this beat (and probably also the other two beats like it [beats #1 and #3]) are junctional escape beats. Supporting this contention is the fact that the R-R interval of the two escape beats that are seen on this tracing (the R-R interval between beats #2-3 and #4-5) is the same, and corresponds to a junctional escape rate of 38 beats/minute. Subsequent rhythm strips on this patient confirmed our suspicion that the arrhythmia was indeed 2nd degree AV block, Mobitz type I (AV Wenckebach).

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COMMENT: This tracing is an excellent example of how in addition to group beating, recognition of subtle differences in QRS morphology between junctional and sinus conducted beats may also provide a major clue to diagnosis.

• FINAL POINT: It is important to appreciate that the emergence of escape beats in this tracing is appropriate - and that without them the ventricular response would be even slower.  However, their presence makes definitive diagnosis of the conduction disturbance a difficult task from this tracing alone.

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  - See also ECG Blogs #19, 20, 21 - and Section 20.0 in our ACLS-2013-ePub - 
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