ECG Interpretation Review #30 (Bundle Branch Block - RBBB - LAHB - LPHB - PACs - Aberrant Conduction)

Interpret the 12-lead ECG shown below in Figure 1, obtained from a 72-year-old woman as a “baseline tracing”. 

• What type of “block” and what kind of “early” findings do you see? 
• Is there evidence of recent infarction?
• Clinically – What would you do?

NOTE: Parts of our answer to this very interesting tracing are advanced.  That said – I think there are lessons to be learned for all levels of interpreters.  Are you up for the challenge?

Figure 1 – 12-lead ECG obtained as a “baseline” from a 72-year-old woman. What type of "block" do you see. What to do?

INTERPRETATION:  The underlying rhythm for the 12-lead ECG shown in Figure 1 is sinus, as confirmed by the upright P waves with fixed PR interval for the 2^nd and 4^th beats in lead II.  There is variability in the overall ventricular response, in part due to sinus arrhythmia and in part due to the 3 PACs (Premature Atrial Contractions) that are seen on the tracing.  Lack of a lead II rhythm strip makes it more difficult to identify these rhythm characteristics.  We’ve therefore labeled the 14 beats in this tracing (Figure 2).

Figure 2 – 12-lead ECG from Figure 1 with each beat and key findings labeled. 

Note the following in Figure 2:

• The 3rd beat (seen in simultaneously recorded leads I,II,III ) is a PAC.  The premature P wave is well seen notching the preceding T wave in leads II,III (small red arrow in lead III ) – but not seen in the small amplitude QRST complex of lead I.  This emphasizes one benefit of assessing rhythms in more than a single lead – which is that some leads are better than others for identifying certain findings.
• Beats #7 and #11 are also PACs (Note small red arrows highlighting the premature P wave in leads aVF and V1,V2,V3).  We would need a longer rhythm strip to determine if the pattern seen here (every 4th beat being a PAC) continues – in which case the rhythm would be atrial “quadrigeminy”.
• There is slight (subtle) alteration in QRS morphology of these PACs.  That is – the q wave of beat #3 in lead III is not as deep as it is for the 3 normally-conducted beats in this lead. The same holds true for the QRS of prematurely conducted beat #7 in lead aVF.  We suspect this same phenomenon (slight alteration in QRS morphology) also occurs for beat #11 – although it is difficult to tell because beat #11 occurs just before the lead change …  This interesting advanced concept is known as aberrant conduction – which sometimes is seen when a PAC occurs early enough in the cycle to fall within the relative refractory period (See ECG Blog #15).

Now that we’ve interpreted the rhythm for Figures 1,2 – it is time to proceed with the rest of our Systematic Approach.  We’ll avoid the QRST complexes for beats #3, 7 & 10 in our assessment – because of the above noted alteration in morphology resulting from aberrant conduction of these PACs:

• The QRS complex is wide (more than half a large box or ~0.11 second in lead V1).  QRS morphology in the 3 key leads (I,V1,V6) is consistent with complete RBBB = Right Bundle Branch Block (See ECG Blog #3).  Thus (as shown within the RED-BLACK rectangles in leads I,V1,V6 of Figure 2) – there is an rsR’ in lead V1, and wide, terminal S waves in leads I and V6 that satisfy criteria for RBBB. 
• There is also LPHB (Left Posterior HemiBlock), making the conduction disturbance in Figure 2 a bifascicular block (RBBB plus LPHB).  Because the posterior hemifascicle of the left bundle branch receives a dual blood supply and is much thicker than the anterior hemifascicle – LPHB is far less common than LAHB.  The diagnosis is made by the finding of a disproportionately deep S wave in lead I (Figure 3) in a patient with underlying RBBB.  Note that leads II and III show the opposite QRS pattern as lead I with LPHB (small q with tall R in leads II,III – vs small r with deep S in lead I ).  The occurrence of bifascicular block with LPHB is often associated with more extensive underlying cardiac disease – and the inferior and lateral precordial Q waves seen on this tracing may be indicative of prior infarction in these areas. 
• There is no chamber enlargement in Figure 2.

Figure 3 – Schematic drawing of bifascicular blocks. 

— LEFT – RBBB/LAHB, recognized by the net negative QRS deflection in lead II. This is by far the most common form of bifascicular block. 

— RIGHT – RBBB/LPHB, recognized by the very deep straight component to the S wave in lead I with tall qR complex in lead II. 

The final part to our Systematic Approach to interpretation of the ECG shown in Figure 2 relates to assessment of Q-R-S-T Changes:

• As noted above – there are small inferior and lateral precordial q waves of uncertain significance.
• Transition is early (with the tall R wave in lead V1 due to the RBBB).
• There are typical secondary ST-T wave changes of RBBB – with ST-T waves in the 3 key leads (I,V1,V6) being opposite the last QRS deflection in these leads as is expected with BBB (Secondary ST-T wave changes were explained in ECG Blog #3).
• Perhaps the most interesting part of this tracing lies with assessment of ST-T wave morphology for beat #8 in lead V3 and beat #12 in lead V4 (within the RED ovals).  The ST segment is coved for both of these beats, with suggestion of ischemic-looking T wave inversion.  However, there is resolution of these ST-T wave abnormalities in the beats that immediately follow (beats #9 and 13, within the BLUE ovals).  At times – the normally-conducted beat following a PAC or PVC may show ST-T wave changes that are not seen on other sinus-conducted beats on the tracing.  Whether such changes reflect underlying ischemia or not is uncertain.  Thus, there is no evidence of acute ischemia or injury on this tracing with PACs and bifascicular block.

SUMMARIZING THOUGHTS:  This interesting 12-lead ECG obtained on an apparently asymptomatic 72-year-old woman shows underling sinus arrhythmia with PACs (some of which conduct with aberration). There is RBBB/LPHB (bifascicular block) — but no evidence of acute ST-T wave change (albeit with some alteration in ST-T wave morphology in the beat following PACs). This case provides an excellent illustration of the uncommonly encountered form of bifascicular block with LPHB — and — serves as a reminder of the importance of carefully scrutinizing QRS morphology of PACs, and ST-T wave morphology of the beat that follows the PAC.

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  - See also ECG Blog #3 (on BBB) - and Blog #15 (on aberrant conduction) - 
 - Please check out our ECG Video on the Basics of BBB (www.bbbecg.com).

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ECG Interpretation Review #29 (Infarction- Hemiblock- Normal Q Waves)

Interpret the ECG shown below in Figure 1, obtained from a 50-year-old man with a history of longstanding hypertension.  Is there is evidence of prior infarction?

Figure 1 – 12-lead ECG from a patient with longstanding hypertension.
Is there evidence of prior infarction?

INTERPRETATION: There is normal sinus rhythm at 60/minute.  Intervals are normal.  There is significant LAD (left axis deviation) sufficient to qualify as LAHB (left anterior hemiblock) — since the QRS complex in lead II is predominantly negative (which places the QRS axis at more negative than minus 30 degrees).  There is no evidence of chamber enlargement.  The remarkable findings on this tracing lie with assessment of Q-R-S-T morphology.  They include:

• a deep Q wave (QS complex) in lead III.
• a subtle r’ in lead V1 with some concave upward J-point ST segment elevation in V1,V2.
• early transition between V1-to-V2 (with a surprisingly tall R wave already by lead V2).
• persistence of S waves throughout the precordial leads.

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IMPRESSION:  The significance of the above findings that we note in our descriptive analysis is uncertain.  Isolated Q waves (even when deep) are often found in leads III and/or aVF without necessarily implying that there has been prior inferior infarction (See below).  

• Unless there are Q waves in each of the 3 inferior leads (II, III, and aVF) — we tend to interpret this finding as a “Q wave in lead III of uncertain significance”.  A terminal r’ in lead V1, and persistence of S waves across the precordial leads are findings that are often associated with pulmonary disease — but the rest of this tracing is not suggestive of this.  
• Slight J-point ST elevation with upward concavity in a few isolated anterior leads, but in the absence of other evidence of acute infarction — is usually a benign finding.  
• The most eye-catching finding on this tracing is the abrupt early transition caused by the unexpectedly tall R wave in lead V2. Possible reasons for this finding include posterior infarction, cardiomyopathy, abnormal body habitus, anatomic chest wall abnormality and/or lead misplacement.  
• Clinical correlation (and comparison with a prior tracing) is essential to determine which of these possibilities may be operative.

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Leads with Normal Q Waves/T Wave Inversion:  Five leads (III,aVR,aVL,aVF,V1) may normally display moderate-to-large Q waves and/or T wave inversion in otherwise healthy adults. Thinking of a “reverse Z” (à la Zorro) may help recall which leads these are (Figure 2).

Figure 2 – Leads that may normally display large Q waves or T inversion. 

We emphasize the following additional points regarding variants in Q and T wave morphology:

• Small and narrow normal septal q waves will often be seen in one or more lateral leads (I,aVL,V4,V5,V6) in asymptomatic individuals without heart disease.
• In general we can ignore lead aVR (a Q and/or T inversion in aVR is not indicative of MI/ischemia).
• Isolated T wave inversion (or an isolated Q wave) in lead III, aVF or aVL (as in Figure 2) — is most likely not to reflect ischemia IF the QRS is also negative in these leads.     But IF ischemia or infarction is present — then lead II (in addition to III and aVF) should also show a Q wave and/or T wave inversion.
• In adults — Lead V1 typically shows a QS or rS complex and T wave inversion. The QS may normally persist until V2 (but there should normally be at least some r wave by V3).  
• In children — all bets are off! (children often manifest a Juvenile T wave variant in which there may normally be T wave inversion in leads V1-thru-V3,V4).

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ADDENDUM (December 22, 2017):

• BOTTOM Line: It is difficult to know from this single tracing whether the isolated QS complex in lead III is a marker of a prior, silent inferior infarction — or, whether it is an incidental finding of no consequence. 
• If it does reflect prior inferior infarction — then the abrupt transition by lead V2 (with a markedly positive QRS complex in this lead) might reflect prior associated posterior involvement. At times, the presence of LAHB may mask prior inferior infarction (and vice versa) — since there is some opposition of forces in these 2 clinical conditions. Therefore, the ECG picture seen here could also reflect both LAHB and prior infero-postero infarction. 
• What can be said — is that there do not appear to be any acute changes on this ECG. At the least — a more detailed history on this patient is indicated, asking about any potential symptoms that might signal a prior event. Whether further evaluation beyond that is indicated would depend on clinical correlation ...

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”. 

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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”.

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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 won’t 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).

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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.

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).

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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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