“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:

Inf_STEMI_1st

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.

Recap

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.

screenshot696

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:

AAortic_Dissection_ED_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.

Vitals:

  • 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:

ecg720

 

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

ECG720a

 

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?

 

 

 

80 Year Old Male: Fall

A previously well 80-year-old experienced a fall at his home where he lives alone. He was walking from the living room to the kitchen when suddenly he found himself on the ground, which he attributes to tripping on the runner rug in the hallway.

“My son has been telling me to get rid of that thing for years but I don’t like getting the carpet dirty.”

Unfortunately he injured his hip in the process and wasn’t able to get to the phone to call for assistance, spending two days on the floor until the Meals on Wheels volunteer came by. Skin is cool and dry and his mucous membranes are dry. He has severe pain and external rotation of his left hip. You cannot assess shortening because the knee and hip are both flexed, in a position of relative comfort.

Vitals upon your arrival are:

  • Heart rate: 45-65 bpm, irregular
  • Respiratory rate: 14 /min
  • SpO2, room air: 97%
  • NIBP: 179/93 mmHg
  • Temp, oral: 36.3 C (97.3 F)

While you are drawing up an initial dose of morphine your partner captures the following 12-lead.

What does it show? How will this affect your management?

80yo M - Fall

Dont let your bradycardic patient D.I.E.

At the risk of plagiarizing myself, I’d like to revisit a topic that I discussed on my personal blog a couple of years ago. The story goes that I am not very good with mnemonics. For me they are almost never useful in clinical practice, and as the patient gets sicker my chances of properly recalling the applicable mnemonic decreases exponentially.

There is, however, one that I never forget, and it’s the DIE mnemonic for bradycardia. I developed this memory aid based off a talk on bradycardia given by the great Dr. Mel Herbert, where he discusses the above differential but in a different order and with no handy catch-phrase.

[D]rugs
[I]schemia
[E]lectrolytes

When the patient in front of you is sick, these are the three common and reversible causes of bradycardia that you need to recognize in the emergency setting. Yes, there are other causes of bradycardia that should be on your differential, but what makes this list special is that all three have specific emergency treatments and the standard ACLS trio of pacing, atropine, and dopamine does little or nothing to address them.

It’s okay to miss Lev’s disease in the emergency setting because the definitive treatment is contained in the usual ACLS algorithm: pacing. If you don’t recognize that your patient is hyperkalemic, however, then all the atropine and transcutaneous pacing in the world isn’t going to lower her potassium. You don’t even need to have heard of sick sinus syndrome to properly treat it, again with pacing. If you miss ischemia though, and bring the patient to a non-PCI center, then there could be trouble down the line. I don’t think you need the EKG to diagnose hypothermia, but you’d better be considering medication effects in every significantly bradycardic EKG you see. Beta blockers and calcium channel blockers can easily sneak past your differential, while the QT-prolonging effects of other anti-arrhythmics can be magnified by a slow heart rate pose an extra threat of sudden death that must be considered.

If there’s one entity missing from the mnemonic, it’s ‘H’ for hypothyroid or ‘M’ for myxedema coma (let’s just pretend they’re one in the same). Really though, who wants to remember DIME or HIDE when DIE sticks in the mind so well? Use one of the others if you’d like, but I think DIE is just too easy and memorable to make the longer forms worthwhile.

So let’s get into the three major players…

Drugs

It’s fitting that this is the first item in the mnemonic because it is also the culprit I am most likely to overlook. The overdose can be intentional or accidental, and things like decreased renal function can lead to the latter without the patient even taking a single extra pill. I throw around the term “overdose,” but what we’re really talking about is any supratherapeutic levels of drugs or medications the patient may have taken. The culprits I worry about most in the undifferentiated bradycardic patient are calcium channel blockers, beta blockers, and digoxin, but there’s a whole host of medications — lots of anti-arrhythmics — that cause marked bradycardia in excessive doses. Enjoy some examples, and ponder whether you would have considered “overdose” as a possibility when seeing these ECG’s.

Metoprolol and Diltiazem OD

Junctional bradycardia in a patient on both metoprolol and diltiazem. Bradycardia resolved and returned to normal sinus rhythm 24 hrs after discontinuing both medications.

Digoxin toxicity

Junctional bradycardia in a patient with a digoxin level of 4.4 ng/mL (ref 0.8 – 2.0 ng/mL), later treated with digoxin immune fab.

Dig toxicity

Junctional bradycardia in a patient with a digoxin level of 2.9 ng/mL (ref 0.8 – 2.0 ng/mL). The QRS morphology matches his baseline EKG.

TCP in dig toxicity

Transcutaneous pacing was attempted in the prior patient with unrecognized failure to obtain electrical capture at 50mA.

Sinus bradycardia and a prolonged QT-interval in a patient with sotalol overdose, courtesy of Life in the Fast Lane. Click image for source.

Sinus bradycardia and prolonged QT-interval following sotalol overdose, courtesy of Life in the Fast Lane. Click image for source.

 

Ischemia

Despite its relatively high prevalence, ischemia is probably (hopefully?) the least missed of the three topics discussed here. Still it happens, and it’s good to force yourself to at least consider the possibility in any patient with bradycardia. We most commonly discuss ischemia causing bradycardia in the setting of inferior STEMI, especially larger and more obvious infarctions, but it can sometimes present subtly or in unexpected coronary distributions. The often bizarre atrial arrhythmias and various levels of AV-block seen with inferior MI are thought to be due to ischemia of the SA and AV nodes, but the Bezold-Jarisch reflex could also play a role as well. Thankfully, most brady-arrhythmias seen with inferior STEMI’s resolve with reperfusion and time, but those associated with anterior STEMI tend to be more malignant and portend a worse outcome.

Sinus brady, inferior STEMI

Marked sinus bradycardia in a patient with obvious inferior STEMI.

Sinus brady, subtle inferior STEMI

Sinus bradycardia in a patient with somewhat subtle infero-posterior STEMI.

Complete heart block, inferior STEMI

Complete heart block in a patient with an extensive infero-posterior STEMI and cardiogenic shock. The patient experienced PEA arrest and expired shortly after this ECG was acquired.

AV-dissociation, inferior STEMI

AV-dissociation (probably CHB) in a patient with a large inferior STEMI.

Atrial bradycardia, global MI

Uncertain and irregular atrial bradycardia in a patient who presented with vague epigastric discomfort and hypotension. Echo showed near-global LV dysfunction, troponin-I (ref < 0.04 ng/mL) peaked at almost 100 ng/mL!

 

Electrolytes

In terms of overall numbers, I believe that electrolyte disturbances are certainly the most missed cause of bradycardia. It’s unusual to miss ischemia significant enough to cause bradycardia, and drug toxicity is a fairly uncommon presentation, but electrolyte abnormalities are an everyday event in most emergency departments.

When we talk about electrolytes and brady-arrhythmias, we mean potassium. And, by far, the most common bradycardia-producing electrolyte abnormality is hyperkalemia. While calcium can affect your ST/T-waves, it is typically not a direct cause of bradycardia. Despite it’s huge role in cardiac action potentials, serum sodium levels actually have little effect on the surface ECG (though sodium channel blockers do…). Similarly, though magnesium plays a role in some arrhythmias, there are no direct EKG signs of hyper/hypo magnesemia. It’s an even less exciting story for the rest of the electrolytes.

While emergency care providers know to look for peaked T-waves and wide QRS rhythms, it is constantly sobering just how subtle the signs of hyperkalemia can present on the EKG. Below are just a handful of the subtle hyperkalemia cases I’ve encountered. Importantly, hypokalemia can also present with bradycardia in rare cases, but it is much more often associated with a normal or tachycardic rate. Still, it’s worth keeping in mind.

Hyperkalemia K+ 6.5

Severe sinus bradycardia in a patient with a serum K+ level of 6.5 mEq/L (ref 3.6 – 5.1 mEq/L).

Hyperkalemia K+ 6.6

Junctional bradycardia in a patient with a K+ of 6.6 mEq/L (ref 3.6 – 5.1 mEq/L).

Hyperkalemia K+ 6.7

Complete heart block in a patient with a K+ of 6.7 mEq/L (ref 3.6 – 5.1 mEq/L).

Hyperkalemia K+ 6.9

Sinus brady with slight QRS widening (compared to baseline) in a patient with a K+ of 6.9 mEq/L (ref 3.6 – 5.1 mEq/L).

Hyperkalemia K+ 7.2

Junctional bradycardia (with artifact) in a patient with a K+ of 7.2 mEq/L (ref 3.6 – 5.1 mEq/L).

Hyperkalemia K+ 7.7

Junctional bradycardia in a patient with a K+ of 7.7 mEq/L (ref 3.6 – 5.1 mEq/L). Note that exceedingly normal appearance of the T-waves without even a hint of peaking despite the very high potassium level.

Hyperkalemia K+ 8.1

Wide complex bradycardia of uncertain origin (RBBB+LAFB morphology) and “sharp” but small T-waves from a patient with a K+ of 8.1 mEq/L (ref 3.6 – 5.1 mEq/L).

Hyperkalemia K+ 8.7

Irregular, fairly-narrow-complex bradycardia with small but only slightly pointed T-waves. Amazingly, this subtle EKG was from a patient with a K+ of 8.7 mEq/L (ref 3.6 – 5.1 mEq/L)!

Hypokalemia K+ 2.0

Severe sinus bradycardia in a patient with a K+ of 2.0 mEq/L (ref 3.6 – 5.1 mEq/L) and an Mg++ of 2.2 mEq/L (ref 1.7 – 2.2 mg/dL). While hypokalemia typically presents with a normal or tachycardic rate, on rare occasions severe hypokalemia can present with marked bradycardia.

 

Final Notes

I’d like to make it a final point to always remember that the sick bradycardic patient is free to combine any two (or even all three!) of the above inciting factors. Just because you think you’ve identified hyperkalemia doesn’t mean the patient hasn’t also reached supratherapeutic digoxin levels with renal failure as the root of both issues.

Digoxin toxicity 4.1 Hyperkamleia K+ 6.9

Junctional bradycardia with “scooped” ST-degments and peaked T-waves in a patient with a digoxin level of 4.1 ng/mL (ref 0.8 – 2.0 ng/mL) and a K+ of 6.9 mEq/L (ref 3.6 – 5.1 mEq/L).

Digoxin toxicity 2.6 Hyperkamleia K+ 7.1

Junctional bradycardia with “scooped” ST-segments and slightly peaked T-waves in a patient with a digoxin level of 2.6 ng/mL (ref 0.8 – 2.0ng/mL) and a K+ of 7.1 mEq/L (ref 3.6 – 5.1 mEq/L).

 

With that I wish you the best, and remember, “Don’t let your bradycardic patient D.I.E.”