Conclusion to 80 Year Old Male: Fall

This is the conclusion to 80 Year Old Male: Fall. If you do not remember the particulars, check out the original post and then come back here to find the “answer” and summary.

Case Review

You arrived on scene to meet an 80 year old patient who was found on the floor after suffering what he described as a “trip and fall.” He had severe hip pain and for the most part presented as a straightforward hip fracture, plus or minus some ill effects of being on the ground for 48 hours. Worryingly, however, he could not describe the exact circumstances of how he ended up on the ground.

This should have immediately alerted you that he may have experienced syncope, not a mechanical fall. In fact, even elderly patients who can vividly describe how and why they fell should be screened for possible syncope. Even if it’s not intentional, the brain is good at filling gaps in information to form a cohesive story—especially if the patient doesn’t want to make a big deal about their fall in the first place.

Regardless of your reasoning, an EKG was performed, shown again below and annotated with a ladder diagram.

80yo M - Fall - Laddergram

This ECG shows:

  • Sinus rhythm at 84 bpm (fairly regular, evenly spaced P-waves of normal morphology)
  • Prolonged PR-interval (PR-interval is about 220 ms)
  • Type II AV-block (see below)
  • Effective ventricular rate of 52 bpm
  • Right bundle branch block (QRS is about 140 ms wide; qR wave in V1; tall, narrow R-wave with shallow, wide S-wave in lead I and V6)
  • Left anterior fascicular block (mean QRS axis approx. -45 degrees (left axis deviation), rS waves in III and aVF, tiny initial q-waves in I and aVL)
  • Bifascicular block (RBBB + LAFB)
  • Left atrial abnormality (total P-wave duration of 120 ms (> 110 ms), terminal P-wave deflection in V1 of 80 ms (> 40 ms).

The most important finding here is the type II AV-block, often termed “second degree, type II” or “Mobitz II.” This finding greatly increases our suspicion that the reason the patient ended up on the floor because he experienced syncope secondary to an arrhythmia, not because he tripped.

Type II AV-block is most often associated with disease of the cardiac conduction system below the bundle of His, especially when it is associated with a bundle branch block. In this case, in addition to a simple RBBB, there is also evidence of impaired conduction in the left anterior fascicle, the combination of which is known as a bifascicular block.

There is also a slightly prolonged PR-interval that technically qualifies as first degree AV-block. When this is added to a bifascicular block some folks like to call it a “trifascicular block,” but this author does not use that term unless the PR-interval is markedly elongated. The overall picture is suggestive of extensive conduction system disease, so a bit of PR-prolongation is probably expected and usually seen in this setting. Also, “trifascicular block” is needlessly dramatic.

Assuming no contraindications and a decent chance for recovery from his hip surgery, the ECG suggests this a patient who will need a permanent pacemaker placed.

Prehospital Management

I’ve given this its own section because there was a bit of disagreement in the comments of the original case for how this patient should be managed. Here are my thoughts…

Starting with an easy issue, this patient is not significantly hypothermic. Though most modern oral thermometers aren’t very trustworthy when you get readings of 36.4 C or below, this is good enough for a start on this patient. The fact that a reading was obtained at all suggests this patient is not moderately or severely hypothermia. Definitions vary, but this temperature is not nearly low enough to account for the patient’s arrhythmia. Also, some suggested the presence of Osborn waves, but those are decidedly absent here. I think folks were confused by the RBBB. The only treatment necessary for this patient’s slightly low body temperature is the application of a blanket or two.

Next, the issue of the arrhythmia. Although it was probably related to his fall (likely secondary to syncope), the patient is experiencing no ill effects at the moment. His ventricular rate is reasonable and he has described no other incidents of syncope nor present symptoms. His blood pressure is elevated and his mentation is appropriate. There is no prehospital treatment indicated at this time. In all likelihood he will be admitted for a non-emergent implanted pacemaker in a day or two before hip surgery as long as the situation doesn’t change. Cardiologists don’t get excited about this EKG’s, and there is certainly no role for transcutaneous pacing at this point as the patient is stable and the block not pervasive.

It is likely the patient has experienced some acute kidney injury, if not secondary to rhabdomyolysis then at least secondary to dehydration. An IV with a normal saline bolus at a slow to moderate rate would be indicated. There is no reason to flood the patient with fluids prehospitally; you’re not going to make a huge difference in his kidney injury during a short transport and lab results from the ED will be able to better guide therapy.

Finally, let’s address the most debated point of this case: whether or not to administer opioid analgesics.

Opioids are not contraindicated in AV-block!

While very large doses—like those used in cardiac anesthesia—may be associated with sinus bradycardia (through a couple of different mechanisms), and there is a possibility of AV-block with toxic doses, the normal doses used for acute pain in the emergency setting will not affect this patient’s heart block significantly. Though there could be some minor slowing of the sinus rate due to reduction of the patient’s sympathetic response to pain; morphine, hydromorphone, or fentanyl will NOT worsen AV-block.

That said, this is an elderly patient with dehydration and decreased renal function; I would suggest titrating his dose of opioid up slowly. He’s going to be susceptible to the direct histamine release characteristic of the class (namely hypotension), though the effects seen with fentanyl and hydromorphone are low compared to morphine. Still, his vasculature is relatively depleted so any vasodilation is more likely to result in significant hypotension than we would see in an otherwise healthy patient—even if the effects are supposed to be “minimal.”


In this case the patient received IV hydromorphone for his pain, was admitted for pacemaker placement the next day, and received his new hip soon after that. He experienced no lingering complications from his stay except for slightly decreased renal function and was discharged to rehab in good condition.


“Bad heartburn” – Conclusion


In “Bad Heartburn” – 82 y.o. female without chest pain, the paramedic had obtained an ECG on an elderly woman who only complained of mild “heartburn.” An initial ECG was obtained:

STE in II, III, aVF, STD in aVL and V2-V4. Also, the T wave is fully inverted in V2 and V3.

ECG interpretation :

The degree of ST elevation is significantly higher in lead II than lead II, which usually supports an RCA occlusion. Furthermore, there is mild ST depression in lead I, also typical for RCA occlusion. There is apparent sinus arrest, with a junctional escape rhythm, which suggests that the SA nodal artery (usually a branch off the RV) is involved.

The ST depression and T wave inversion in V2 and V3 suggest an acute posterior infarct.

Grauer's "mirror test" suggests acute posterion MI.

Grauer’s “mirror test” suggests acute posterion MI.

The “classic” pattern of high R waves and upright T waves is actually not representative of acute occlusion – for more on this, read this discussion on old versus “new” teaching on recognizing posterior MIs. We do not see ST elevation in aVR or V1 that would suggest a concomitant RV infarct, however.

Patient Course:

Although the protocols did not require a computerized interpretation to verify a STEMI, the absence of “typical” ischemic symptoms made a prehospital cath lab activation modestly more difficult to justify. Since the computer interpretation algorithms may miss a STEMI up to half of the time, the medic obtained a second tracing less than a minute later:


Ah, that makes more sense…

The ED was contacted while EMS was still on scene, and medical direction quickly agreed with alerting the cath lab, despite the atypical symptoms. As noted before, ASA was given, but NTG was withheld. Ten minutes later, during transport, the medic shot a repeat ECG with V4R.


No STE in V4R, which suggests against an RV infarct.

The patient stayed in the ED for 10 minutes while the cath team was assembling, and a repeat ECG was obtained.

screenshot743Angiography results:

A complete occlusion of a LEFT-dominant circumflex was found during PCI, and was successfully stented. A transvenous pacer was placed, but was used only for a brief period. The patient recovered well.

Some discussion points:

1. You will miss STEMIs in the elderly unless you do them on practically everyone.

A study conducted in an ED found that, in patients over the age of 79, you should get an ECG on any patient with chest pain, dyspnea, altered mental status, upper extremity pain, weakness, syncope, nausea/vomiting, or abdominal pain. And even then they missed a bunch of STEMIs!


2. The computer interpretation can be falsely negative.

In a recent study using Lifepak-12 monitors, the computer only diagnosed a STEMI in 58% of the cases, while another study found that the computer got 69% of the STEMIs. Despite the high quality of the first tracing (no artifact or baseline wander), the computer missed an ECG pattern that most medic students would recognize after their first day of cardiology class!

3. Nitroglycerin probably would have been fine, but it likely isn’t worth the bother.

Aspirin therapy, fibrinolysis, and percutaneous coronary angiography have all been demonstrated to reduce mortality. Nitroglycerin, despite an appealing rationale, has not been shown save lives. Reduction of discomfort should be a goal of EMS, of course, but there isn’t much evidence that nitro does much more than that.

Okay, but what if a medic elected to give a tab or 2 of NTG to this patient – would this be harmful? Despite the standard teaching that RV MI must be ruled out before giving nitro to a patient with an inferior MI, the current data is reassuring.

I go over this in more depth in my post “Nitroglycerin – Old and New: Pt 2“, but the boiled-down version is:

 The Bottom Line

Although computers are pretty good at playing chess, they aren’t always right about STEMI diagnosis. Be very suspicious of atypical symptoms, and grab an ECG. And whether or not you give NTG, this patient needs emergent reperfusion!

“Bad heartburn” – 82 y.o. female without chest pain.

This case is courtesy of paramedic Jason Cameron, who works for Stratford EMS in Connecticut.

The ALS unit had been dispatched for an older female with “chest pain.” Upon arrival, however, the 80 y.o. patient denied any pain or pressure, and only endorsed some mild “heartburn,” localized to the epigastrium, non-radiating, and rated it at a 2/10. It had started about 30 minutes prior, and had not been relieved by Maalox. Her husband had called 911. The patient denied all other symptoms, and specifically denied any jaw, arm, or back discomfort, and denied any dyspnea or sweating.

Her medical history was significant only for mild hypertension and elevated cholesterol. She took a statin and an ACE inhibitor

Vital signs

  • HR – 40
  • BP – 118/72
  • RR – 18
  • SaO2 – 98% RA

The physical exam was unremarkable.

The paramedic obtained an ECG:


Aspirin was given, but nitroglycerin was withheld. An IV was established, but the patient did not became hypotensive.

Suggested Discussion Points:

  • Do you believe that this patient requires PCI for acute coronary occlusion?
  • If so, what was the likely site of the occlusion?
  • Are there any other management concerns, given this ECG pattern?
  • Should you routinely obtain ECGs in patients who complain of GI symptoms, but who deny any chest pain, pressure, or discomfort?
  • Lastly, although the local protocols do not require that the computer interpretation display ***MEETS ST ELEVATION MI CRITERIA *** in order to activate the cath lab, they limit activation to patients with “active chest pain and/or dyspnea.” In that context, how should the paramedic have proceeded?

I will have follow up posted within 48 hours!

Conclusion: 38 Year Old Male – Chest Pain and Leg Paralysis.


In the post yesterday , the paramedic crew was evaluating a 38 y.o. male who had sudden, severe chest pain, as well as leg numbness and paralysis, and whose vital signs showed a mild bradycardia and pronounced hypertension.


The ECG obtained by EMS appears to be junctional, with an unclear contribution from the SA node. More concerning, however, is the ST segment elevation in V2-V5, with modest ST depression in aVF and perhaps in III. This would usually define an anterior wall acute coronary occlusion (i.e. STEMI). However, the depth of the S wave in V2 and V3, combined with the high R wave in V5 and V6, strongly suggest that left ventricular hypertrophy (LVH) is complicating interpretation of the ECG.

Clinical Course

At the time, the ED did not activate the cardiac catheterization lab based on paramedic interpretation of a STEMI. However, the emergency physician met the EMS crew as they were backing in, and immediately called for cath lab activation from the parking lot.

Given the “off-hours” presentation, the patient was evaluated in the ED while the cath lab team was assembling. The patient received multiple doses of morphine for the unremitting pain, and in fact was administered over 60 mg of morphine over the next hour, with no hypoxia or lethargy. The ED physician asked for a repeat ECG, assuming that it would demonstrate evolution of an ongoing and large MI. This ECG was obtained about 20 minutes after the EMS ECG:


Although there were minor changes in R wave height, the ST morphology in the anterior leads had not changed significantly. In fact, the mild ST depression in the inferior leads seemed to have resolved.

Although acute coronary occlusions sometimes spontaneously reperfuse, the patient’s continuing pain did not suggest clinical resolution. A bedside echo demonstrated aortic root dilation, and a CT angiogram of the aorta was performed. This image from the scan is transverse, with the chest up, at the level of about the 3rd intercostal space:

screenshot702It shows a massively dilated aorta, with a clear dissection flap (shown between the 2 red arrows above). It extended from the aortic root down to the iliac bifurcation, looking pretty much exactly like the “Stanford A” in the figure below.

The cath lab team was cancelled, and the cardiothoracic surgeon immediately began planning for surgery.

The patient received maximal medical therapy before the OR was ready. In addition to the liberal use of opioids, labetalol was delivered in escalating amounts until the maximum dose was reached. As this was being given, a nitroprusside drip was being prepared, and was was started after the beta-blockers had been initiated. The goal in aortic dissection is to drop the SBP as low as possible, as fast as possible. In our patient’s case, a SBP of 140 was the lowest pressure obtained before he left for surgery.

Was the ECG “typical” for aortic dissection?

Yes and no.
Yes, since the ECG criteria for LVH suggested severe, chronic hypertension, which is a well-established risk factor for dissection.
No, since there are no such typical ECG signs to look for.  In a 2010 article (which is free, so go download it), Japanese researchers found that, on the one hand, most people with dissection have either chronic or acute ECG changes – only 27% are normal.

However, these chronic and acute ECG findings, as shown in the table, are all over the map. For example, the most common acute ECG change is ST depression, which is quite non-specific. The ECG will not be the key to diagnosing a dissection in  the field.

 When to suspect dissection

Of course, aortic dissection is far less common than ACS or STEMI, so most of the time the patient won’t have it. However, a few clinical elements can suggest it, as illustrated in this case, although I withheld a number of them in the presentation. Our patient had abrupt, severe pain that was actually described as “ripping.” Furthermore, he had a neurologic deficit (paralysis) as well as a pulse deficit (unable to doppler a pulse in his left foot).  A recent retrospective study validates our impression that this patient had high risk features for aortic dissection

Take-home Points

  • LVH can mimic STEMI, and sometimes fool the computer.
  • Obtain serial ECGs if the first is atypical or equivocal for ACS. Lack of dynamic evolution suggests an alternative diagnosis.
  • Aggressive efforts at treating hypertension should likely be delayed until after evaluation in the ED.
  • Aggressive pain control, however, is an essential component of prehospital treatment of suspected aortic dissection.

38 Year Old Male – Chest Pain and Leg Paralysis.

You are called for severe chest pain.

The patient is a 38 year old male who describes the abrupt onset of a severe pain in his chest about 30 minutes before his wife called EMS. While sweat streams off his face, he tells you that he has never felt pain this intense. He isn’t sure if it’s pleuritic, and he endorses some shortness of breath. The pain radiates to his shoulders, back, and epigastrium. Despite the severity of the pain, he is actually far more worried that his left lower extremity is numb, and that he can’t move it – he repeatedly tells you in a loud voice that “Something’s wrong with my leg! What’s wrong with my leg?”

With the assistance of his wife, you find that he takes HCTZ and lisinopril for HTN, but he doesn’t smoke or use recreational drugs. In fact, he’s a coach for a high school cross-country running team, and looks like he’s in pretty good shape.

Vitals signs are

  • HR: 50
  • RR: 30
  • BP: 230/140
  • SaO2: 99%

Besides profound diaphoresis, the exam is unrevealing. An ECG is obtained:

screenshot696You give him aspirin 325 mg, and 3 sprays of nitroglycerin, with neither a change in his symptoms nor in his vitals. In fact, 10 mg of morphine IV (max per your protocol) doesn’t improve the discomfort, and he is still yelling about both the chest pain and his leg. Your partner mutters to you “I’m starting to think this is mostly anxiety…”

It is almost 2300 hours. You have three choices of destination hospital:

  1. A “stand-alone” ED that is capable of delivering tPA for STEMI within 30 minutes. It’s just around the corner.
  2. A small community hospital ED that just started performing primary PCI, but they’ll have to call a team in from home. Despite that delay, they will activate based on a prehospital report, and their door-to-balloon times have been excellent. They are 20 minutes away.
  3. A level 1 academic hospital that is 35 minutes away. They don’t activate the cath lab based on EMS interpretation, since they usually “want to see it for ourselves.”


57 Year Old Male–Chest Discomfort


It is a bright Sunday morning when you and your partner are dispatched for an “adult male-chest pain”.

You arrive at a well kept residence, noting a ladder and paint cans as you enter.

You find your patient, a 57 year old male, sitting on the sofa in mild distress.

“I was doing some painting, and about 20 minutes ago I felt some pressure here (points to central chest just left of sternum), and my arm started hurting too (rubs left bicep area).”

He rates the discomfort at 7/10. He also says he became very sweaty and nauseous at the time of onset. Oh, and just for good measure, he tells you he had some trouble breathing as well. He denies being nauseous at the moment, and his skin is warm and moist. PD had given him O2 via NRB, and he says his breathing is “better”.

He has not taken anything for this episode. In fact, the reason he called so fast:

“I just saw a show on TV where a guy had a heart attack and waited too long to call 911. I figured I better call fast.”

Pt hx is significant only for hypertension and hypercholesterolemia. He denies ever experiencing this before. He takes Toprol, and has no allergies.


  • Pulse: 74 regular
  • BP: 180/104
  • RR: 20, mild distress
  • Spo2: 97% on O2
  • Skin: warm and moist


Your patient is a heavy set gentleman, and you acquire the first 12 Lead ECG:



Here is a second 12 Lead ECG taken several minutes later:



Destination options:

  • Community Hospital: 20 minutes by ground
  • PCI center:  50 minutes by ground


What is interpretation of the 12 Lead ECGs?

Are there any changes between #1 and #2?

How do you want to treat your patient, and where do you want to take him?