A 76 Year Old Female With Recurrent Syncope, Lightheadedness, Palpitations and Negative Stress Test

Written by Lucas Goss MD, peer reviewed by Meyers, Smith, Bracey

A 76 year old female with a history of arial fibrillation not on anticoagulation, non-obstructive CAD found on coronary CTA 2 years prior, HTN, HLD, recurrent lightheadedness, and syncope status post loop recorder placement, presented for another episode of feeling lightheaded, diaphoretic, and feeling like she “was going to die.” She was discharged just the day prior for her second hospitalization for similar episodes. She was actually at the pharmacy to pick up her medicines the day after discharge when this episode occurred, and pharmacy staff sat her down in a chair while they awaited the ambulance. Her symptoms were mostly gone by the time of arrival.

Vital signs on arrival: BP 143/89, HR 63, RR 18.

During her recent hospitalizations she had a negative CT pulmonary angiogram (CTPA), negative nuclear stress test, normal echo, and her loop recorder did not identify any concerning findings when interrogated. During the first of two prior recent hospitalizations for similar symptoms, her troponin I rose from undetectable to 219 ng/L and trended back down, and the notes seem to attribute this to her blood pressure which was in the 200/110 range. During her second hospitalization (from which she was just discharged yesterday), she had multiple troponins all undetectable, less than 6 ng/L. 

A note on Loop Recorders, thanks to our electrophysiologist: 

They only record if:

1. The HR meets the programmed criteria (eg, pause over 3 seconds, HR<30 bpm, HR>*** etc). It’s unusual to program this “automatic recording trigger as HR of 50 or 40. 

2. The patient triggers recording when they have symptoms. In those scenarios it records a loop of several minutes before and a minute or so after (variable depending on company).

So if the patient did not trigger a recording when she had symptoms, then people usually don’t program automatic recording with HR in 40’s or 50’s otherwise decide memory will be full and there would be a lot of recordings that will be overwritten. 

Smith comment on troponins: the definition of myocardial infarction is 2 of the following:

1. Troponin rise and/or fall with at least one value above the 99th percentile reference range

2. Plus one or more of the following: A. Symptoms of MI; B. ECG evidence of ischemia;  C. Development of pathologic Q waves; D.  Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology; E. • Identification of a coronary thrombus by angiography or autopsy (not for types 2 or 3 MIs).

This patient had 1. and 2A., so she had a myocardial infarction.  

Now one needs to decide which type of Acute MI (usually type 1 or 2).  If type 2 MI, one must find an etiology of supply demand mismatch, or identify coronary dissection or spasm or a few other entities.  Syncope is the result of temporary loss of perfusion to the brain, and there are many etiologies, all of them are bad.  One must find the etiology.  More likely, this is a type 1 MI and the patient needs an angiogram regardless of ECG findings.

Here is her ECG on arrival (symptom free):

Initial ECG#1: (1159) 

ECG from 2 days prior (not "baseline," during prior admission):

Initial interpretation:

Sinus rhythm, normal QRS, no clear signs of ischemia, no signs of hyperkalemia, normal QT.

Meyers note: I read this ECG in real time, compared it to the prior, and did not see any clear signs of ischemia or OMI. In retrospect, I think perhaps the TWI in aVL is slightly more abnormal, and the ST segment and T wave in V3 slightly more "pushed down" than in the ECG from 2 days ago, but it is still not diagnostic to me. 

Case Continued

Labs demonstrated an unremarkable CBC and BMP, however her HS troponin I that was obtained in triage was mildly elevated at 23 ng/L. A repeat was obtained after she was seen by the physician at 1700 and had increased to 138 ng/L. Again, the combination of troponin rise and fall with symptoms is diagnostic of acute MI.

 

ECG #2: (1707)

There is baseline movement and artifact in critical leads such as II, III, aVF, and aVL where there is likely new STE and enlarging T waves in the inferior leads, with slight reciprocal changes in aVL.

The ECG should be immediately repeated to confirm or deny this suspicion, but it seems that it was not repeated at that time. 

Cardiology was consulted for admission and definitive coronary imaging. They accepted the patient, however while she was awaiting a floor bed, she became hypotensive and bradycardic.

 

ECG#3: (1834) 

 

This repeat ECG demonstrates a junctional escape rhythm with a rate of 36, however no definitive signs of OMI. At this time the patient was ill-appearing, lightheaded, and diaphoretic. Her blood pressure was 80/40. She was given 0.5mg of atropine while pads were being placed and shortly after her junctional rhythm resolved with improvement in her blood pressure and symptoms:

 

ECG#4: (1851)

She is now back in sinus rhythm on repeat ECG. There may be the tiniest hint of STE in lead III, and aVL shows the tiniest bit of reciprocal STD and increase in size of the negative T wave. There is a tiny amount of reciprocal STD in I, and there is a barely-perceptible amount of STD in V2 and V3 compared to prior. These findings are all highly suspicious for inferoposterior OMI.

Interestingly enough, her loop recorder was interrogated again and did not identify this event.

She was admitted to cardiology with plan for non-emergent cath the next day as well as EP evaluation for potential sinus node dysfunction. 

Overnight her troponins rose from 23 to 138 to 390 to 668 to 1,000 to 1,219, then they stopped measuring them at 2am in the morning (we are clearly committed to ignoring them anyway, so why wake us up for them?!).

While awaiting catheterization an EKG was obtained due to worsening symptoms:

 

ECG#5 (Hospital day 2)

This ECG shows sinus bradycardia with signs of inferoposterior reperfusion. Leads III and aVL are diagnostic of acute MI, but, because of the T-wave inversion, it is probably with an open artery (or collateral circulation). There is some STE in inferior leads leading into T waves with terminal inversion, which is reciprocally mirrored in aVL. There are posterior reperfusion T waves in the precordial leads, much taller than on the most recent ECG. 

Another repeat ECG was obtained a few hours later (just prior to catheterization):

ECG#6 (Hospital Day 2)

This ECG is slightly confusing as to the state of the vessel, as there is newly worsened STD maximal in V2-V4, but ongoing terminal T wave inversion in the inferior leads. I would assume that there is ongoing ischemia until proven otherwise.

Smith note: 3 possibilities: 

1. The artery is open but with TIMI-2 flow, enough to perfuse vessels to the inferior wall, but not to the posterior wall.  

2. TIMI-2 flow can be enough to result in T-wave inversion (apparent reperfusion) even though there is ongoing ischemia. 

3. There is collateral flow that is robust enough to result in T-wave inversion in the inferior, but not the posterior, wall.

 

Cardiac catheterization findings:

RCA: 100% stenosis from lesion described as “complex, noncalcified, consistent with atherosclerotic disease as well as a filling defect consistent with thrombus” supplying the inferior and posterior walls, which was successfully stented.

LAD: Mild luminal irregularities

Circumflex: Minor luminal irregularities

 

The patient afterwards underwent dual chamber pacemaker implantation due to sick sinus syndrome, as she continued to revert back into a junctional bradycardia.

 

What was interesting about this case is that she had multiple presentations for similar progressive symptoms, but had both negative stress test as well as echo within 2 weeks of this presentation. Additionally, after her episode of junctional bradycardia her loop recorder was interrogated and did not identify the event.

 

Learning Point #1: Recent Negative Stress Tests Do Not Rule Out ACS

Do not rely on a recent negative stress test to rule out acute coronary syndrome or high risk coronary lesions. A stress test has nothing to do with ACUTE coronary syndrome. A stress test is ostensibly designed to help detect symptomatic, chronic, stable coronary disease, in hopes that a patient's chronic stable exertional symptoms may be attributed to that stable coronary disease. Acute coronary syndrome can arise from small unstable atherosclerotic lesions that can rupture and cause OMI. These lesions may not be picked up on stress testing (because they are not yet ruptured and occluding!), as was the case above.  Several studies have demonstrated concerningly high percentages of patients experiencing acute MI with recent negative stress testing.^{1,2,3, 4} The supposed utility of stress testing is to identify critical, chronic, stenoses causing reduced coronary blood flow which reproduces a patient's stable angina symptoms. Coronary lesions not significant enough to be detected on stress testing can still undergo plaque rupture and thrombosis causing acute MI.

See Chest Pain, "Negative" Stress Tests, POCUS, & ECG Equations -- A Case from Salim Rezaie (R.E.B.E.L. EM)

 

Learning Point #2

Be able to recognize posterior reperfusion T waves as demonstrated here with large tall upright T waves with associated subtle ST depression.

See Series of Prehospital ECGs Showing Reperfusion

       A woman in her 70s with bradycardia and hypotension

      

 ^{References on evaluating patients in the ED who had a recent negative stress test:}

1. Walker J et al. Coronary disease in Emergency Department Chest Pain Patients with Recent Negative Stress Testing. West J Emerg Med 2010. PMID: 21079714
2. Hoilund-Carlsen PF et al. Usefulness of the Exercise Electrocardiogram in Diagnosing Ischemic or Coronary Heart Disease in Patients with Chest Pain. Am J Cardiol 2005. PMID: 15619400
3. Smith SW et al. Incidence of Myocardial Infarction in Emergency Department Chest Pain Patients with a Recent Negative Stress Imaging Test. Acad Emerg Med 2005.; 12:51 
4. Engineer RS, Lauer MS, Emerman CL. Chest pain after recent stress test: Is there a warranty? Ann Emerg Med [Internet] 2004;44(4, Supplement):S47. Available from: https://www.sciencedirect.com/science/article/pii/S0196064404008765

A Pre-operative ECG on a patient with a hip fracture

An 80-something tripped and sustained a hip fracture.

The patient had no cardiac symptoms, no syncope, no CP or SOB.  He was perfectly fine.

He had a 12-lead ECG in the ED as part of screening:

Interpretation?

You know there is something wrong at least partly because it is on this blog.

But this was looked at in a cursory fashion by a couple very busy emergency physicians and no serious abnormality was noticed.

First note that the QRS complexes are grouped.  Then you can see that there are P-waves which did not conduct (#'s 3 and 8).  There is no PR lengthening prior to the blocked conduction; therefore, it is not Mobitz I (Wenckebach), which would be a benign AV block, but rather Mobitz II.

They did not see that this is 2nd degree AV block Mobitz II.  When I saw it I immediately recognized it, after which it was clear to the providers.

Mobitz II has dropped beats without any prior PR lengthening, and is at risk of progressing to 3rd degree (complete) AV block.  Mobitz II is often below the AV node and therefore often does not respond to atropine.  When the QRS is wide, then it is much more likely to represent blockade below the AV node, and is more likely to be dangerous.

In this case, there is also RBBB with LAFB, which suggests block below the bundle of His.

Clinical Course

Pacer pads were placed on his chest and he was admitted to the ICU with cardiology and EP consultation.

Had he had this rhythm associated with symptoms such as syncope, or associated with acute MI, then he would undergo immediate transvenous pacer placement.

He was kept overnight on telemetry and on the cardiac monitor he was noted to have intermittent bradycardia.  Some of them were during sleep hours, however there was another episode around 10 PM where it is not very clear whether he was asleep or not.  

Of note, the PR interval is normal during the conducted beats.  This is important because it suggests that vagal tone did not have anything to do with the AV block, and suggests a more pernicious etiology.

There was concern that, during hip surgery, he would develop complete AV block.

A temporary pacer was placed.

An EP study to assess need for permanent pacer was undertaken and showed no convincing evidence of Infra-His block.  No permanent pacer was placed.

Learning Point:

Assess the ECG systematically or you will miss something, especially when it is a screening ECG (i. e., the patient does not have cardiac symptoms)!

These are the characteristics of a normal ECG.  

Note that you must assess the rate, rhythm, P-waves, PR interval, and a QRS for every P-wave as part of a systematic approach.

NSR, normal rate

Upright P wave in lead II

Biphasic P wave in V1

PR interval  120 – 200 msec

QRS for every P-wave, same PR interval

QRS less than 110 msec

Normal QRS Axis (-30 to 90 degrees)

Voltage normal

Normal septal Q waves

Normal R-wave progression

Normal ST segments

Normal T-wave size

Normal T wave axis

Normal QT

Normal U-waves

===================================

MY Comment by KEN GRAUER, MD (1/1/2020):

===================================

I like nothing better than a good arrhythmia to start of the new decade! So our THANKS to Dr. Smith for doing just that. I’d add the following thoughts to the excellent discussion by Dr. Smith.

• As per Dr. Smith — perhaps the KEY Learning Point is the need to use a Systematic Approach to ECG Interpretation (and especially to rhythm interpretation). Readers of Dr. Smith’s blog know I constantly emphasize this point (See My Comment in the June 28, 2019 post on Dr. Smith’s blog).
• CLICK HERE — For “My Take” on Systematic 12-Lead interpretation.
• CLICK HERE — For “My Take” on Systematic Rhythm interpretation.

Regarding this 12-lead ECG + Rhythm Strip:

• As per Dr. Smith — There is underlying RBBB/LAHB — but there are no acute changes.
• Regarding the rhythm — we look first at the long lead rhythm strip. The underlying rhythm is sinus (ie, upright P wave in lead II) — with slight sinus arrhythmia (slight variation in the R-R interval).
• The QRS complex is wide (as above = RBBB/LAHB).
• The overall R-R interval is fairly regular — but there are 2 pauses on this lead II rhythm strip.
• As per Dr. Smith — the PR interval remains constant for the conducted beats throughout this rhythm strip! PEARL #1 — The KEY to diagnosing Mobitz II, 2nd-Degree AV Block — is that you see consecutively conducted beats, in which the PR interval does not increase. The reason you cannot distinguish with certainty between Mobitz I vs Mobitz II forms of 2nd-Degree AV Block when there is strict 2:1 AV conduction — is that you never get to see 2 conducted beats in a row when there is 2:1 AV block (which means that you can not tell for sure if the PR interval would increase [as in Mobitz I ] IF it had a chance to do so).
• The patient in this case was in his 80s. We have no idea for how long he has lived with bifascicular block + Mobitz II. This AV block could be recent or acute (therefore the rationale for placement of a temporary pacemaker) — but given the subsequent negative EP study — the thought was that permanent pacing was probably not necessary at this point in time (and might never be necessary for this patient in his 80s).
• That said — this potentially serious (life-threatening) form of AV block should not have been overlooked by the initial providers. PEARL #2 — IF emergency providers would begin to routinely carry and use a pair of Calipers — they will doubtlessly surprise themselves by increasing their speed for interpreting complex arrhythmias — and, I bet they will never again miss another case of AV block!
• PEARL #3 — Assuming this 80-something patient maintains his satisfactorily functional lifestyle status — I would recheck a 24-hour Holter monitor on him fairly soon (and perhaps periodically as an outpatient in the future) — to ensure that prolonged bradycardia does not subsequently develop (ie, Despite benign overnight monitoring on telemetry — there still is significant potential risk for subsequent development of prolonged bradycardia).

Additional PEARLS — can be found in my hour-long ECG Video on the Basics of AV Block.

• If you click on SHOW MORE (under the video on the YouTube page) — You’ll find a detailed timed/linked Contents of all in this video.
• CLICK HERE — to go directly to the part (beginning at 30:09) that deals with the 3 types of 2nd-Degree AV Block.

P.S. (1/2/2020): Since there have been some questions regarding atrial activity in this case (P waves are of low amplitude) — I am adding Figure-1, in which I have numbered the beats and labeled P waves.

• Calipers greatly facilitate establishing that P waves are quite regular here (perhaps with slight variation in some P-P interval).
• Calipers also verify that the PR interval is not increasing (ie, this is not Mobitz I ).
• PEARL: The best (easiest) way to tell if the PR interval during a sequence of beats is increasing — is to look at the PR interval just before the pause (ie, the PR interval before beat #2) — and compare this to the PR interval at the end of the pause (ie, the PR interval before beat #3). Do this for each pause in the tracing (ie, Compare the PR interval before beat #6 with the PR interval before beat #7). Note that there is NO difference between any of these PR intervals — thus, the PR interval remains constant throughout, and this is Mobitz II.
• The PR interval is not prolonged. The easiest way to measure the PR interval is to find a P wave on the rhythm strip that begins on a heavy line (BLUE arrow in Figure-1). Note that the QRS complex of beat #2 begins slightly before the next heavy line — which means that the PR interval is definitely not more than 1 large box in duration. This is a normal PR interval (Given the wide range of "normal" PR intervals — my preference is not to call 1st-Degree AV Block until the PR interval is at least 0.22 second in duration).

Figure-1: The ECG in this case (See text).

Chest pain with NonDiagnostic ECG but Diagnostic CT Scan

An elderly woman presented with chest pain that radiated to the back for several hours.

Here is here initial ECG:

There is only a nonspecific flat T-wave in aVL.  It is essentially normal.

The first troponin returned at 0.099 ng/mL (elevated, consistent with Non-Occlusion MI)

Providers were concerned with aortic dissection, so they order a chest aorta CT.

This showed no dissection but did show the following:

Notice the area of the lateral wall (lower right) that has no contrast enhancement 
(It is dark, where areas of enhancement are light-colored). 
This transmural ischemia, but not necessarily completed infarction (yet).

 A slice at a slightly different level:

Again, an area with absence of contrast enhancement (dark-, not light-colored).

These were read by our fantastic chief of radiology, Gopal Punjabi, who has his own blog on Spectral CT: https://www.ctspectral.com/    https://twitter.com/CtSpectral

Here is the image using Spectral CT:

It is much more obvious with this technique!

See more images of this case at Gopal's Spectral CT Blog:

It's all about confidence

With continued symptoms, an elevated troponin, and no other explanation, this is acute MI with ongoing ischemia until proven otherwise.

The CT scan confirms no other explanation and also confirms that this is acute Transmural ischemia diagnostic of OMI (Occlusion MI).

If the patient were no longer symptomatic, one could conclude that the infarct is completed, and emergent angiogram +/- PCI would not be necessary.

The cardiologists did not want to go to the cath lab.

She had subsequent ECGs:

First at 1.5 hours:

This possibly shows some inferior STD, but probably it is baseline wander.

This one at 5.5 hours:

No significant change

She was admitted on a Nitro drip.

Her troponins went like this:
0.099 ng/mL
1.250
3.712
6.073
8.092
12.170
15.680
21.051
23.159 (this is not a small MI)

Next day echo:

The estimated left ventricular ejection fraction is 60%.

Regional wall motion abnormality-inferolateral

Angiogram:

Culprit for NSTEMI is thrombotic occlusion of small-medium caliber OM1.  It was stented.

===================================

MY Comment by KEN GRAUER, MD (9/27/2019):

===================================

As suggested by the title of this Blog post — confirmation of the diagnosis in this case was made not by ECG — but instead by chest aorta CT! That said — there are some Observations that should be made about the first 2 ECGs in this case.

• For clarity — I’ve put these first 2 tracings together in Figure-1.

Figure-1: The first 2 ECGs in this case (See text).

OBSERVATION #1 — This case describes a high-prevalence situation — because the patient is an elderly woman with new-onset chest pain of several hours’ duration. Once dissecting aneurysm was ruled out by chest aorta CT — the possibility of acute ischemic heart disease becomes paramount.

• Given this History — our scrutiny for detecting ECG abnormalities is heightened. The onus falls on us to prove questionable ECG findings are not acute — rather than the other way around.

OBSERVATION #2 — While not diagnostic — the initial ECG in the ED ( = ECG #1) is not normal (Figure-1). Descriptive Analysis of ECG #1 reveals that the rhythm is sinus @ 80-85/minute — all intervals are normal — small septal q waves are seen in leads V4-6 — and transition (where the R wave becomes taller than the S wave is deep) occurs normally between leads V2-to-V3. Findings to note on ECG #1 include the following:

• There is some baseline artifact. Given that artifactual baseline undulations are largest in leads II, III and aVF — the left leg is most likely the source of this artifact. This artifact was no longer seen in the next 2 tracings. NOTE — While the amount of artifact in ECG #1 is small (ie, not enough to prevent accurate interpretation of this tracing) — knowing how to quickly determine which extremity is the cause of the artifact (due to tremor, a faulty lead connection/inadequate skin contact, etc) is helpful, because this may expedite correction, which may be important when artifact does impede interpretation. (BONUS — The 3 page article by Rowlands and Moore that I’ve posted in Figures-2, 3 and 4 below is the BEST description I’ve seen of how to quickly determine which extremity is the source of the Artifact).
• Returning to ECG #1 — There is probably some type of misplacement of lead V2 (perhaps due to body habitus of this elderly woman — perhaps due to placement of the V2 electrode too high on the chest). It just doesn’t make good physiologic sense for there to be an rSr’ only in lead V2, and not in V1. That said, given nearly identical QRS morphology in all leads for the 3 tracings shown in this case — this technical point does not affect assessment or management in this case.
• The T waves in leads V2 and V3 in ECG #1 look disproportionately tall and peaked compared to R wave amplitude in these respective leads. One reason this abnormal T wave morphology stood out to me — is that the ST segments prior to onset of T wave ascent are relatively flat. Whether this T wave appearance in leads V2 and V3 of ECG #1 is a benign longstanding finding — or — whether it might represent either hyperacute T waves and/or reperfusion changes in this elderly woman with new chest pain of several hours’ duration is (in my opinion) not known from assessment of this single ECG.
• There clearly is voltage for LVH in ECG #1 (ie, R wave amplitude in lead V5 ~25mm — CLICK HERE for Review of Criteria for ECG Diagnosis of LVH). The next bullet tells why recognition of voltage for LVH is relevant in this case.
• What does this patient’s baseline ECG show? Was there LVH with an ST-T wave repolarization abnormality (ie, with LV “strain” ?) on the baseline ECG? IF so — then perhaps the ST segment flattening in V5,V6 with relatively small T wave amplitude in lead V6 represents the combination of baseline LV “strain” (ie, ST-T wave depression) + hyperacute T waves that result in an “intermediate pattern” that might not look acute in the lateral chest leads of ECG #1.

BOTTOM LINE: In my opinion, at the point that we saw ECG #1 in this case about this elderly woman with new chest pain of several hours’ duration — it would be impossible to rule out acute changes on the basis of this single initial ECG.

• Finding a prior ECG on this patient could be invaluable! Otherwise — more information will be needed (ie, serial ECGs, troponin, Echo, etc.) before we'll be able to tell if the findings I describe above might be acute ...

OBSERVATION #3 — Compared to ECG #1 — the 2nd ECG (obtained 1.5 hours later) in this case ( = ECG #2) — does show a change that should be noted and which may be relevant (Figure-1).

• Isn’t T wave amplitude in both leads V2 and V3 of ECG #2 proportionately taller than it was in ECG #1, compared to R wave amplitude in these respective leads? That is — the T wave in lead V2 of ECG #2 measures 5 mm tall, whereas it was only 3 mm tall in ECG #1. In lead V3 — the T wave in ECG #2 is clearly taller than the R wave in this lead — whereas in ECG #1 — the T wave in lead V3 was clearly not as tall as the R wave in this lead. BOTTOM LINE: From comparison of ECG #1 with ECG #2 — I do not know how to rule out the possibility that T waves in leads V2 and V3 have become more hyperacute in ECG #2.

CONCLUSION of this Case: The 3rd ECG (done at 5.5 hours) did not show significant change compared to ECG #2 — so at this point, it had become apparent that this patient’s serial ECGs were not acutely evolving. And, as noted in detail by Dr. Smith — serial troponins had become markedly positive — the chest aorta CT showed regional contrast enhancement abnormality — and, Echo the next day confirmed regional wall abnormality. Therefore — the ECG findings I point out above were not needed in this case for diagnosis. That said, in the interest of optimizing ECG interpretation ability:

• Please take another look at the tracings in Figure-1 if you did not initially note the findings I described above. While it turned out in this case that serial ECGs did not evolve — this could not have been known from assessment of only those first 2 ECGs!
• Keep in mind that finding a prior ECG on your patient can sometimes prove invaluable! I wish a prior ECG on this patient was available! IF a prior ECG had been available — it is possible that recognition of an acute cardiac event could have been accomplished much earlier (ie, as early as the moment ECG #1 was recorded)!
• As should be apparent from the unique clinical correlations routinely provided on Dr. Smith’s ECG Blog — the BEST way to continue honing your ECG interpretation skills — is to GO BACK and review tracings in each case after the definitive diagnosis is revealed. In this particular case, the most important teaching point to me — is to appreciate that we can not be certain the ECG findings I describe above for ECG #1 are not acute on the basis of this single initial ECG. It was not until time had passed and the 3rd ECG recorded at 5.5 hours was obtained, that lack of serial ECG evolution became evident ...

Our THANKS to Dr. Smith for this illustrative case!

BONUS — The 3 Figures below reproduce the article by Rowlands and Moore for determining the source of artifact when a single limb lead is responsible. 

• Knowing which extremity is at fault is helpful for expediting correction (ie, from a faulty lead connection/inadequate skin contact, etc.).

Figure-2: Page 475 from Rowlands — Determining the extremity responsible for Artifact (See text).

Figure-3: Page 476 from Rowlands — Determining the extremity responsible for Artifact (See text).

Figure-4: Page 477 from Rowlands — Determining the extremity responsible for Artifact (See text).