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.”

 

 

 

 

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.”

 

 

 

 

36 YOM with Chest Pressure: Reperfusion AIVR

This the case of a 36 year old, black male, at a correctional facility, complaining of chest pressure 8/10 pain scale, for 1 week.

The patient was born with unknown cardiac complications, which led to multiple near death arrhythmias, which is why the patient has an on demand pacemaker/defibrillator in place. He also has a history of Hypertension (HTN), which he takes Lisinopril and Carvedilol for.

EMS was activated by the clinic physician after the inmate presented with chest pressure, no longer able to tolerate it. A 12 lead ECG was obtained approximately 1 1/2 hours prior requesting EMS.

This was their ECG:

aivr-coleman-1

 

This is an Accelerated Idioventricular Rhythm (AIVR) at a rate of approximately 50 beats/min suggestive of reperfusion post Myocardial Infarction. AIVR is one of the most common rhythm post cardiac arrest and reperfusion, following resolution of infarct, commonly seen in the cath lab setting following PCI.

  •  P waves? (the long Lead II strip which may appear to have P waves not correlating to every QRS, i.e. AV Dissociation)
  • Regular rhythm with wide complex QRS > 200 ms (extremely wide and not consistent with a typical Bundle Branch Block)
  • There are Primary changes seen as ST elevation in leads I, aVL and V6 with marked pathological Q waves (a Q wave > 1/3 of the R wave or > .04 s wide) and Hyperacute T waves in the precordial leads, marked in V2-4
  • There is no pacemaker function as the rate is not below the pacemaker’s threshold

(If you do not remember my last post, Primary ST segment changes is due to ischemia or infarction, while Secondary ST changes are due to repolarization abnormalities)

  • Reciprocity in the opposing leads, III and aVR
  • Pathologic Rightward Frontal axis (limb leads), or Right Axis Deviation (RAD)

Note that, the computer interpretation suggests Junctional rhythm or AIVR. As opposed to what many believe, a junctional rhythm should have a narrow complex, since the AV junction is located above the Bundle of His, unless there is a preexisting Bundle Branch Block.

Also notice that although, the QRS complexes may have similarity to a LBBB, these complexes are extremely wide, and there is RAD, also not present during a normal LBBB as these vectors towards the Left Ventricle (LV) are stronger than the Right Ventricle (RV), which is why a LBBB often presents with physiologic and pathologic Left Axis Deviation (LAD).

The physician had administered a total of .8 NTG sublingual prior EMS arrival, and 325 mg ASA.

Baseline vital sings:

BP: 120/90 mmHg
HR: 54 beats/min regular
RR: 16 breaths/min
SpO2: 100 % RA

This is the 12 lead ECG  obtained by EMS upon their arrival and patient contact, approximately 1 hour and 2 minutes after the initial ECG.

LBBB coleman

Now we have a sinus rhythm with a LBBB.

Although there is no Sgarbossa or Dr. Smith’s Modified Sgarbossa criterion met here, there are positive T waves present in Lead II, V4-6. Remember, a normal LBBB has Discordant T waves (the opposite direction of the QRS).

There is no presence of Cabrera’s Sign, which is a notch of the S wave upstroke in V3, which is very specific for prior or acute MI in a LBBB, or Chapman’s Sign, which is a notch in the upslope of the R wave in Lead I, aVL and/or V6, which also support prior or current MI.

 

For more on Sgarbossa’s Criteria, click HERE

For more on Dr. Smith’s Modified Sgarbossa Rule, click HERE

This patient had a prior LBBB confirmed by a previous ECG found in the Emergency Department’s database, which we were not able to obtain, however, it was verified. The only thing that was different from this LBBB was the appropriate T wave discordance present before, which differs here with Inappropriate concordance.

Cardiac Troponin I was .02 ng/mL with all other cardiac enzymes and electrolytes within normal limits. This may be due to normalization of myocardial function, especially after 1 week of the event. The patient was admitted for further observation and we were not able to follow up with the patient.

Conclusion:

AIVR is one of the most common rhythms post reperfusion, and although we can’t fully compare QRS morphology and ST segments from AIVR and LBBB, primary ST-T changes can still be found in both ECG patterns with proper ECG evaluation.

 

45 year old male with “numb hands” – Discussion

Go back to 45 year old male with “numb hands” to read about the presentation, and see the ECGs.

 

The culprit artery?

After arriving at the hospital, the patient bypassed the ED, going directly to the cardiac catheterization lab. The patient was found to have a total occlusion of the proximal RCA, and the cardiologist was able to deploy a stent without problem.

 

Excellent D2B, but …

Despite prompt activation of the 911 system, excellent EMS care, field activation of the cath lab, and an uncomplicated percutaneous coronary intervention, he was left with moderate ventricular dysfunction. The system “did everything right,” but the patient still had significant heart damage – why?

 

Faster STEMI treatment, but no change in mortality?

A recent study in the New England Journal of Medicine describes this question on a larger scale. The authors of  “Door-to-Balloon Time and Mortality among Patients Undergoing Primary PCI” found that, although D2B times for STEMI have decreased significantly over the past few years, the mortality for STEMI hasn’t changed.

The researchers looked at 515 hospitals across the country, using a Medicare database. Over a period of 4 years, the percent of STEMI patients who received PCI within 90 minutes of hospital arrival increased from 60% to 83%. Unfortunately, mortality rates in those STEMI patients did not change. Even when they looked only at the high-risk sub-groups (> 75 years-old, anterior infarct, or cardiogenic shock), they failed to find any improvement.

screenshot651

So why have we (EMS, EM, and cardiology) been able to improve the process so much, but not the outcomes, at least in term of mortality in this population? Clearly, this is a multifaceted issue, with no single explanation. For example, the adjunctive medical care of these patients has improved in many ways over the years, which might “hide” the benefit of the shorter D2B. Also, cardiologists may be bringing more patients with unmeasured comorbid conditions for emergent cath, which would also serve to understate the benefits of the faster process.

However, some suggest that part of the problem has to do with how long many of these patients wait to call EMS, if they call at all. As the D2B interval shrinks, the time from symptom onset to first medical contact (FMC) takes on a greater significance. A decrease of 10 minutes in the D2B time won’t help much if the time to FMC exceeds, say, 3 hours! But that didn’t seem to be the problem with Tim’s patient, right?

 

Why the 90 minute “on-scene” time?

In the case of our patient, EMS was called fairly soon after the symptoms started. However, you can see that the 2 ECGs are separated by about 90 minutes. Why?

Because he declined transport the first time EMS arrived. Although EMS and the patient’s girlfriend did all they could to convince him to go to the hospital, he refused to go. After EMS left his symptoms did not improve, and indeed worsened. EMS was called back, with the same paramedic responding, and the patient was willing to be transported at that point.

In the hospital, his first troponin was 6 times normal, suggesting that his infarct had been going on for several hours, leading to significant myocardial loss, leading to the moderate heart failure he left the hospital with.

 

Any signs on the first ECG?

So, was there anything on that first ECG? I think it’s very difficult to say, but there are certainly no obvious features which would warrant cath lab activation. Indeed, the relative “normalness” of this ECG could have worked against the patient. What I mean by this is …

 

One last thought

Frankly, this ECG only makes it more surprising that ECG #2 was ever obtained.

Consider the context: A young-ish opioid addict, with a history of “anxiety,” who is clearly hyperventilating, and has a chest pain that is reproduced on palpation. Some paramedics, upon being called back to a patient who had just refused transport, would not bother to acquire a second ECG. It speaks volumes about this medic’s clinical sense, and their professionalism, that they immediately obtained ECG #2 without delay, and acted on it.

45 year old male with “numb hands”

This case illustrates both how good modern EMS can be at expediting emergency cardiac care, but also the challenges that still confront us. Yes, there is a “twist,” but only a small one.

Note: I never saw this patient, but the ECGs and outcome were brought to my attention by a colleague, Dr K. Thrace, who moonlights at a number of EDs in the region.  Paramedic Tim Y. also generously shared his recollections of the patient.

The Case

EMS was called for a 45 year-old man with chest pain. The patient was initially reluctant to talk with the paramedic, Tim, since “my girlfriend called for you guys, not me.” He was eventually persuaded to discuss his symptoms, however, and stated that he had been out shoveling snow when the chest discomfort started He rated it at a 5/10, and also described “numbness” in both of his hands, saying he couldn’t move them, but denied nausea or sweating.

  • PMHx: Anxiety, opioid abuse
  • Meds: Methadone
  • Shx: Smoker

Vital Signs:

  • P-70
  • BP-120/90
  • RR-30
  • SaO2-99% RA

Physical Exam:

  • Gen: Anxious, unable to sit still. Hyperventilating.
  • Skin: pink/warm/dry
  • Pulm: Clear lungs
  • Cardiac: No JVD, RRR
  • Chest: Tenderness over the precordium

An ECG was obtained:

D2B_pt_delay#1

The symptoms persisted, and and the chest pain worsened to a 10/10. A second ECG was obtained:

D2B_pt_delay#2

Upon seeing this ECG, the paramedic immediately notified the a local PCI center that the cath lab should be activated. There were no extrication issues, and the drive to the hospital took only 9 minutes. Because of the early activation, the D2B time was only 37 minutes.

Questions

  • First, what is the likely culprit artery?
  • Second, are there any early signs of MI on the first ECG?
  • Lastly, even though “time is muscle,” the very short D2B time probably did not improve his outcome. Why?