Friday, December 16, 2011

ECG Interpretation Review #33 (Bundle Branch Block - PACs - Blocked - Aberrant Conduction - RBBB)

Interpret the lead MCL-1 rhythm strip shown in Figure 1.  Can you explain the irregularity?
Figure 1 – Right-sided MCL-1 monitoring lead rhythm strip. 
Can you explain the irregularity? (Figure reproduced from Section 19.0 of ACLS-2013-ePub).
NOTEEnlarge by clicking on FiguresRight-Click to open in a separate window.
INTERPRETATION:  The easiest way to approach interpretation of challenging arrhythmias is to start with what is known.  Save more difficult parts of the tracing until later.  We always look first to see if there is an underlying rhythm.  In Figure 1 – the underlying rhythm is sinus, as determined by beats #1, 3, 5, 7, 9, and 11 which are all preceded by a similar-morphology biphasic P wave with fixed PR interval.  All QRS complexes except for beat #4 are narrow.  Note the interesting bigeminal periodicity of the rhythm – with alternating short-long cycles.  Thus, every-other-QRS complex occurs early.  Every other QRS complex is a PAC (Premature Atrial Contraction = Figure 2).
Figure 2 – Adding arrows facilitates recognition of multiple PACs (See text).  
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ADDITIONAL POINTS ABOUT THIS RHYTHM:
The rhythm in Figure 1 is sinus with multiple PACs.  We highlight a number of additional interesting points about this rhythm:
  • P wave morphology of each PAC in Figure 2 (red arrows) is slightly different in being primarily positive compared to the biphasic P waves of each sinus beat.  This is as it should be since PACs by definition originate from a different site in the atria than the sinus node.
  • Not all PACs in Figure 2 are conducted.  Note that no QRS complex follows the PACs that occur just after beats #2, 6, and 10.  These PACs are “blocked” (nonconducted) – because they arise so early in the cycle as to occur during the ARP (Absolute Refractory Period) when conduction to the ventricles from an impulse arriving early at the AV node is not possible (See ECG Blogs #14 and #15 for Review of this concept).
  • Whether blocked PACs also occur and are hidden within the ST-T wave of beats #4 and 8 cannot be determined with certainty from Figure 2 – but the slight ‘blip’ near the beginning of the ST segment of beat #4 suggests that this may be the case.
  • The widened QRS complex in Figure 2 (beat #4) is not a PVC (Premature Ventricular Contraction).  Instead – it too is a PAC conducted with aberration.  Note that beat #4 is also preceded by a premature P wave (red arrow before beat #4) – which confirms that this beat is an aberrantly conducted PAC.
  • In fact – beats #2, 4, 8 and 10 are all aberrantly conducted PACs!  Normally – QRS morphology of PACs will be virtually identical to QRS morphology of sinus beats.  PACs merely arrive earlier than anticipated at the AV node – but once there, they typically conduct to the ventricles in normal fashion.  It is only when PACs arrive especially early (or when the relative refractory period is for some reason prolonged) that PACs may manifest aberrant conduction.
  • Beats #2, 4, 8 and 10 are all PACs that manifest different degrees of aberrancy.  Of these beats – it is beat #4 that manifests the greatest degree of aberrant conduction (in the form of a complete right bundle branch block pattern).  This makes sense because the coupling interval of the PAC preceding beat #4 (distance between this P wave and beat #3) is shorter than the coupling interval for the other PACs.  The P wave preceding beat #4 therefore arrives earlier at the AV node at a time when it is more likely to encounter the conduction system in a relatively refractory state.  In contrast – the coupling intervals of the P waves following beats #2, 6 and 10 are even shorter.  Physiologically, the P waves following beats #2, 6 and 10 are presumably occurring during the absolute refractory period, which is why these PACs are “blocked”.
  • Beat #6 does not conduct with aberration.  Measurement with calipers shows its coupling interval (from the P preceding beat #6 until beat #5) is slightly longer than the coupling interval preceding premature beats #8 and 10 (ergo slightly more time for recovery and therefore more normal conduction of beat #6).
FINAL THOUGHTS:  The rhythm in Figure 1 is sinus with multiple PACs.  Some of these PACs are blocked, while others are manifest varying degrees of aberrant conduction.  The importance of being comfortable with recognizing blocked PACs and aberrant conduction was highlighted in our Blogs #14 and #15 which illustrate how such PACs may simulate AV block and ventricular tachycardia …
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- See ECG Blogs #14 and #15 for Review on Aberrant Conduction.
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Sunday, November 27, 2011

ECG Interpretation Review #32 (Bundle Branch Block - Rate Related - Aberrant Conduction - LBBB)

Interpret the rhythm strip shown in Figure 1.  The widened beats on the tracing are not ventricular.  What else might they be?
Figure 1 – Right-sided MCL-1 monitoring lead rhythm strip. 
Why might beats #4-thru-7 be wide? (Figure reproduced from Section 19.0 of ACLS-2013-ePub).  
NOTEEnlarge by clicking on FiguresRight-Click to open in a separate window.
INTERPRETATION:  The rhythm strip in Figure 1 shows the rhythm to be irregularly irregular in this right‑sided MCL-1 monitoring lead.  No P waves are seen – so that the underlying rhythm is atrial fibrillation.  Fine undulations in the baseline represent “fib waves”.  The interesting part of the rhythm strip is intermittent widening of the QRS complex.  
  • Although at first glance one might be tempted to interpret the run of widened beats (beats #4-thru-7) as AIVR (Accelerated IdioVentricular Rhythm) — subsequent rhythm strips proved this not to be the case.  AIVR is often an “escape rhythm” that arises when the patient’s underlying rhythm slows.  AIVR is typically (although not always) a regular rhythm.  In contrast to this – the widened beats in Figure 1 do not manifest the delayed timing of escape beats, nor is the run (beats #4-thru-7) regular.  
An alternative explanation for the QRS widening seen in Figure 1 is rate-related BBB (Bundle Branch Block).  We make the following points:
  • It is admittedly difficult to be certain of the diagnosis of rate-related BBB from inspection of the single rhythm strip shown in Figure 1.  That said, the important point is to be aware of this entity – since it helps to explain why the run of widened beats in Figure 1 is not AIVR or NSVT (NonSustained Ventricular Tachycardia). 
  • In support of the premise that the widened run in Figure 1 represents rate-related BBB – QRS morphology of these widened beats 1 is consistent with the predominantly negative QS or rS complex expected in right-sided lead V1 when LBBB (left bundle branch block) is present. 
  • Rather than two competing rhythms – the overall irregular irregularity of the rhythm suggests that all beats seen represent atrial fibrillation.  Rate-related BBB characteristically begins when heart rate speeds up.  In atrial fibrillation – it is typically seen following a longer R‑R interval, since the relative refractory period of the next beat is dependent on the length of the preceding R‑R interval. 
  • Close inspection of Figure 1 reveals that beat #3 is slightly widened.  This beat follows a longer R‑R interval (the R‑R between beats #1-to-2).  Thus, beat #3 actually represents the onset of LBBB-conduction in this tracing (albeit with a less complete form of LBBB given its lesser degree of QRS widening). 
  • The run of rate-related LBBB conduction continues until beat #8 when the rate of atrial fibrillation slows. 
  • Beat #11 at the end of the tracing represents a final widened beat that manifests LBBB‑conduction as a result of its short coupling interval with beat #10. 
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FINAL THOUGHTS:  Subsequent rhythm strips on this patient proved beyond doubt that LBBB conduction consistently occurred during periods of more rapid atrial fibrillation – and consistently resolved soon after the rate slowed down.  Of interest (and further complicating diagnostic recognition of this important but uncommon phenomenon) is the fact that: i) the rate of onset of BBB conduction is often not the same as the rate where normal conduction resumes (ie, rate-related BBB may begin when heart rate exceeds 90 or 100/minute – but normal conduction may not resume until heart rate goes back down to 80/minute or less); and ii) AIVR is not always a precisely regular rhythm (making it more difficult to determine when irregular widened beats represent AIVR vs atrial fibrillation with rate-related BBB conduction).
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  - See also ECG Blogs #14 and #15.
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Wednesday, November 23, 2011

ECG CONSULT

In addition to my 1-2/month ECG Blogs that I'll continue to post on this site - I've just started ECG CONSULT (= a new service that I've added to my web site).  Here you'll find tracings and answers to ECG-related questions that have been submitted to me.  Click HERE for the link to this site.  Send tracings (and your permission for me to post them on-line) to me at ekgpress@mac.com.  Hope this site is of use to you - Ken Grauer, MD

Friday, October 28, 2011

ECG Interpretation Review #31 (A Fib – RBBB – LBBB – IVCD – LAD – Infarct with BBB/Conduction Defects)

The ECG shown below was obtained from a 63 year old man with chest pain.  How would you interpret his tracing and accompanying lead II rhythm strip?  What is there to worry about?
Figure 1 – 12-lead ECG and lead II rhythm strip from a man with chest pain. 
NOTEEnlarge by clicking on Figures 
Right-Click to open in a separate window.
INTERPRETATION:  There is a lot to be concerned with on this tracing.  The rhythm is irregularly irregular at an average rate of more than 100/minute.  Although there are fine undulations in the baseline, no definite P waves are seen in the lead II rhythm strip at the bottom of the tracing.  Thus, the rhythm is atrial fibrillation with a fairly rapid ventricular response.
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REGARDING QRS MORPHOLOGY:
The QRS complex is clearly wide.  QRS morphology in leads V1 and V6 is consistent with a bifascicular block pattern of RBBB (Right Bundle Branch Block) with LAHB (Left Anterior HemiBlock).  However, the monophasic R wave in lead I is not consistent with RBBB, but rather with a LBBB (Left Bundle Branch Block) pattern.  Description of QRS morphology in this tracing might therefore better be classified as IVCD with LAD (IntraVentricular Conduction Delay with Left Axis Deviation)
  • NOTE: The basics of assessing ECGs for the presence of RBBB, LBBB, and IVCD were covered in ECG Blogs #3, #11 and #13. We review this entire subject in our ECG Video on the Basics of BBB.
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PUTTING IT TOGETHER:
In view of this patient’s presentation (ie, chest pain) – the most important finding on this tracing is the subtle appearance of Q waves with slight but definite ST segment coving and elevation in leads V1 and V2.  T wave inversion in these two leads is an expected accompaniment of RBBB – but the ST segment elevation is not.  At times, a QR rather than RSR’ complex may be seen in lead V1 with RBBB – but a Q wave will usually not be seen in both leads V1 and V2 with RBBB unless there has been infarction.
  • Detection of acute myocardial infarction is always more challenging in the presence of a conduction defect.  This is especially true with LBBB, since infarction Q waves are rarely written, and ST-T wave changes will often be masked by the underlying LBBB.  Recognition of acute ischemia or infarction is still challenging in the presence of RBBB, but the findings seen in leads V1 and V2 of this tracing in the setting of new-onset chest pain should suggest the possibility that acute infarction may be occurring.  
Clinical correlation and comparison with a prior tracing on this patient would help clarify if the findings in leads V1 and V2 are new or old.
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– See also ECG Blog Reviews #3, #11, #13 – and our ECG Video on Basics of BBB
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Monday, October 3, 2011

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? 
NOTEEnlarge by clicking on Figures 
Right-Click to open in a separate window.
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 2nd and 4th 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. 
NOTEEnlarge by clicking on Figures 
Right-Click to open in a separate window.
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. 
NOTEEnlarge by clicking on Figures 
Right-Click to open in a separate window. (Reproduced from ECG-2014-ePub)
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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Tuesday, September 6, 2011

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?
– NOTE – Enlarge by clicking on Figures 

– Right-Click to open in a separate window.
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. 
(Figure reproduced from ECG-2014-ePub). 
NOTEEnlarge by clicking on Figures 
Right-Click to open in a separate window.
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 childrenall 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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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. (Figure reproduced from ECG-2014-ePub). – NOTEEnlarge by clicking on Figures – Right-Click to open in a separate window.
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 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 (Figure reproduced from ECG-2014-ePub).
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.
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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? (Figure reproduced from ECG-2014-ePub). – NOTEEnlarge 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.
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-2014-ePub).
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-2014-ePub).
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).
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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 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.
  • 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 depresssion) — 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. (Figure reproduced from ECG-2014-ePub).
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.
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- For more information  GO TO:
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