Things that make you go hmmm...

[Paseo Del Norte]

You are called to a rural clinic to transport a "sick" patient to a large centre with subspecialty resources. I will let you guys take it from here.

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[Dwindlin]

You are called to a rural clinic to transport a "sick" patient to a large centre with subspecialty resources. I will let you guys take it from here.

CC?
HPI?

I'll start there. . .

 

[Paseo Del Norte]

You arrive to find a 52 year old male supine on a bed. He appears unkempt and unresponsive. Upon initial assessment, you note that he withdrawals from painful stimuli. He appears to be having Kussmauls respirations at a rate of approximately 32 per minute with occasional snoring type sounds. His pulse is rapid and regular at a rate of 118 at the radial. You do not note any gross indications of trauma.

The clinic NP tells you that the patient is a well known homeless person to the area and is often brought in by acquaintances and treated for acute ethanol intoxication. However, the NP reports that she is concerned about the patient's tachyponea. The HPI appears to be similar to past presentations. Acquaintances found the patient acting "strange" at a homeless camp outside of town and brought the patient to the clinic. Upon presenting to the clinic the patient was found in his current condition.

 

[malkboy]

Vitals?

Altered, so I want a CBG.
HR/BP
SpO2/ETCO2 (supplemental O2?)
Cardiac Rhythm
Temp
Pupils

Any lab work?

 

[Paseo Del Norte]

Current CBG reads 110 mg/dl.

Vital Signs Include:

B/P: 74 by palpation
P: 126 rapid and weak at radial (peripheral) sites, you place him on the monitor and find sinus tachycardia with an occasional, unifocal PVC in lead II.
R: 36 and appearing more shallow with increased snoring and periods of irregularity noted
SpO2: 94% on room air
ETCO2: 45 mmHg via sidestream cannula
Temp: 35.8 Celsius per rectum
Pupils are at 4 mm and sluggish to react bilaterally

You have access to basic labs, what do you want?

What do you think, are any interventions warranted at this time? You can assume the clinic has done nothing for the patient other than obtained history and placed him supine on the bed. There is only a NP available, so you will be making all the assessment and treatment decisions and you can assume you are unable to contact the receiving facilities physician or a physician medical director at this time.

 

[Dwindlin]

Current CBG reads 110 mg/dl.

Vital Signs Include:

B/P: 74 by palpation
P: 126 rapid and weak at radial (peripheral) sites, you place him on the monitor and find sinus tachycardia with an occasional, unifocal PVC in lead II.
R: 36 and appearing more shallow with increased snoring and periods of irregularity noted
SpO2: 94% on room air
ETCO2: 45 mmHg via sidestream cannula
Temp: 35.8 Celsius per rectum
Pupils are at 4 mm and sluggish to react bilaterally

You have access to basic labs, what do you want?

What do you think, are any interventions warranted at this time? You can assume the clinic has done nothing for the patient other than obtained history and placed him supine on the bed. There is only a NP available, so you will be making all the assessment and treatment decisions and you can assume you are unable to contact the receiving facilities physician or a physician medical director at this time.

If there is no gag reflex secure his airway and get some ventilatory support.

ABG? UDS? Ethanol level? BMP?

 

[Paseo Del Norte]

He will not swallow (or cannot swallow) upon command. The patient is no longer reacting to any stimuli. How will you assess for a gag reflex?

UDS is pending.

Blood ethanol testing is not available at this time.

ABG:

pH: 6.78, PaO2: 81 mm Hg, PaCO2: 56 mm Hg, HcO3-: 8 mEq/L.

BMP (significant values):

Glucose: Correlates well with the BGL
Na+: 150 mEq/L
K+: 5.9 mEq/L
Cl-: 110 mEq/L
BUN & Creatinine: Both rather elevated
Ca++: Pending

 

[Apollyon]

His pH is incompatible with life. Brother needs to be stabilized before transfer.

At the same time, it's the law of inverse value; this guy will probably walk out of the hospital intact.

 

[Paseo Del Norte]

His pH is incompatible with life. Brother needs to be stabilized before transfer.

At the same time, it's the law of inverse value; this guy will probably walk out of the hospital intact.

I'm not sure at this point. The person is question is doing rather poorly as far as I know. However, you are right about some people walking like nothing ever happened.

 

[JLM]

By definition he meets SIRS criteria. Likely septic which explains the hypotension and metabolic acidosis. The combination of the hypotension and low volume status (from his probable EtOH use) has caused his kidneys to take a hit which has put him in renal failure, explaining the K+ and the BUN, Cr. His body is unable compensate well for his metabolic acidosis because he is a chronic CO2 retainer from his long-term smoking history. So, between the sepsis/acidosis , uremic encephalopathy and hypercapnia this dude is in bad shape.

I would start lots of fluids but be very cautious because his heart may or may not be able to handle the extra fluids due to his other comorbidities. If he starts to look volume overloaded, consider some dopamine (that was the only pressor we carried in our box).

Also, any way you can safely help ventilate this guy to help him blow off some CO2 could be a plus, but that may be tough in the field.

 

[Dwindlin]

He will not swallow (or cannot swallow) upon command. The patient is no longer reacting to any stimuli. How will you assess for a gag reflex?

Meh, it's just my standard response when someone asks me if I think a patient needs their airway secured, honestly I attempt to drop an OPA if they tolerate it they will likely tolerate a tube. If not mask ventilate as best I can (no RSI where I currently work).

Also, any way you can safely help ventilate this guy to help him blow off some CO2 could be a plus, but that may be tough in the field.

With capnography becoming so popular pre-hospital (at least here in the states) ventilating down to a specific EtCO2 is relatively easy.

 

[Paseo Del Norte]

By definition he meets SIRS criteria. Likely septic which explains the hypotension and metabolic acidosis. The combination of the hypotension and low volume status (from his probable EtOH use) has caused his kidneys to take a hit which has put him in renal failure, explaining the K+ and the BUN, Cr. His body is unable compensate well for his metabolic acidosis because he is a chronic CO2 retainer from his long-term smoking history. So, between the sepsis/acidosis , uremic encephalopathy and hypercapnia this dude is in bad shape.

I would start lots of fluids but be very cautious because his heart may or may not be able to handle the extra fluids due to his other comorbidities. If he starts to look volume overloaded, consider some dopamine (that was the only pressor we carried in our box).

Also, any way you can safely help ventilate this guy to help him blow off some CO2 could be a plus, but that may be tough in the field.

Meh, it's just my standard response when someone asks me if I think a patient needs their airway secured, honestly I attempt to drop an OPA if they tolerate it they will likely tolerate a tube. If not mask ventilate as best I can (no RSI where I currently work).



With capnography becoming so popular pre-hospital (at least here in the states) ventilating down to a specific EtCO2 is relatively easy.

My question about gag was because I find many EMT's are taught that flicking the eyelashes/lids is an excellent method for assessing gag reflex. Certainly not aimed at you specifically. I've been taught that assessing for the ability to swallow and manage secretions is a great indicator of ones ability to manage the airway. Eyelash and eye flicking?

Capnography will be interesting here. We initially have a patient with perfusion issues. So, we can currently correlate findings with an ABG; however, with fluid resuscitation and haemodynamic and perhaps metabolism changes, the end tidal CO2 may not correlate unless we can do additional arterial gasses enroute.

So, what about the underlying metabolic acidosis? Can we perhaps do a calculation on the labs to give us a better idea of what may be going on? Think about the two major types of metabolic acidosis we commonly encounter?

 

[Apollyon]

My question about gag was because I find many EMT's are taught that flicking the eyelashes/lids is an excellent method for assessing gag reflex. Certainly not aimed at you specifically. I've been taught that assessing for the ability to swallow and manage secretions is a great indicator of ones ability to manage the airway. Eyelash and eye flicking?

The corneal reflex is CN III, and gag is CN X - the vagus nerve. They're not on the same circuit.

 

[Paseo Del Norte]

The corneal reflex is CN III, and gag is CN X - the vagus nerve. They're not on the same circuit.

Exactly, yet this is standard practice at some schools.

Correct me if I am wrong, but does the corneal reflex not involve CN V and CN VII? In any event, the counter argument is still valid in that we are assessing different pathways.

 

[Apollyon]

Exactly, yet this is standard practice at some schools.

Correct me if I am wrong, but does the corneal reflex not involve CN V and CN VII? In any event, the counter argument is still valid in that we are assessing different pathways.

Haha - you got me! You are absolutely correct! V and VII!

Haha - and here I am, ever the detractor to "paragods"! I've said that the worst I'd seen were those that "don't know what they don't know"...and here I am spewing wrong stuff!

Indeed, though, you are right - different pathways. One don't mean nothin' to the other.

 

[proman]

Testing the corneal (blink) reflex is an integral part of a neurologic exam, as is the pharyngeal (gag) reflex. The corneal reflex seems more readily abolished than the pharyngeal. If I have a comatose patient (which I do, every day, as an anesthesiologist), I want to know what their level of sedation/unconsciousness is before I stick my finger in their mouth. If they still have a corneal reflex the odds of me losing a finger are high. If they have don't have a corneal reflex, then the odds are lower but not zero.

Practically speaking, testing a blink reflex is a very fast and practical way of assessing level of consciousness before proceeding to more invasive probing.

 

[Paseo Del Norte]

Testing the corneal (blink) reflex is an integral part of a neurologic exam, as is the pharyngeal (gag) reflex. The corneal reflex seems more readily abolished than the pharyngeal. If I have a comatose patient (which I do, every day, as an anesthesiologist), I want to know what their level of sedation/unconsciousness is before I stick my finger in their mouth. If they still have a corneal reflex the odds of me losing a finger are high. If they have don't have a corneal reflex, then the odds are lower but not zero.

Practically speaking, testing a blink reflex is a very fast and practical way of assessing level of consciousness before proceeding to more invasive probing.

Agreed, my argument is that some people are taught that a positive corneal reflex equals positive gag reflex as a matter of dogma. I actually had to take some EMT practical exams back in 2006 where it was required to assess corneal reflex and state that there was no gag reflex with a negative corneal reflex. I do not think said exams currently require this. I know national registry does not require such a procedure.

 

[JLM]

This dude has a HUGE anion gap based on his met panel.

I dont remember some of the minutia, but the non-zebras of gap acidosis include:

DKA
Lactate
Toxins
Renal failure

Toxins include ASA and ethylene glycol.
So, home skillet either:
Is septic as **** with pre-renal failure
Or drunk a bunch of antifreeze and has just crystalized his kidneys.

Or something completely different.

The paramedic in me is ashamed to say this, but the anesthesia resident in me has to point out that you are talking about mask-ventilating a non-NPO patient in shock while driving down a country highway, facing backwards. If he is not apneic, I would be looking for other methods.

Back in the day, I would think about an awake nasal tube in this guy. Just be ready for the ragefest when he is no longer as acidotic or hypercapneic.

 

[Paseo Del Norte]

This dude has a HUGE anion gap based on his met panel.

I dont remember some of the minutia, but the non-zebras of gap acidosis include:

DKA
Lactate
Toxins
Renal failure

Toxins include ASA and ethylene glycol.
So, home skillet either:
Is septic as **** with pre-renal failure
Or drunk a bunch of antifreeze and has just crystalized his kidneys.

Or something completely different.

The paramedic in me is ashamed to say this, but the anesthesia resident in me has to point out that you are talking about mask-ventilating a non-NPO patient in shock while driving down a country highway, facing backwards. If he is not apneic, I would be looking for other methods.

Back in the day, I would think about an awake nasal tube in this guy. Just be ready for the ragefest when he is no longer as acidotic or hypercapneic.

Ding, ding, ding we have a winner! Your prize is a personal accolade from Uncle Del Norte himself.

So, upon physical exam you note track marks and he has syringes and a bottle of what appears to be antifreeze in his pile of belongings. Additional history is suddenly available and it appears he is well know to the area for prior suicide ideation and attempts.

Metabolic acidosis with a big anion gap and also an osmolar gap, even though I didn't actually say it. He did fair during transport requiring fluids and pressers along with antidote therapy. He had large amounts of oxalate crystals in his urine upon arrival as well.

Hope you all enjoyed.

 

[fiznat]

Cool case! A little above the scope of your average paramedic I think, but that's what makes it fun.

I could probably google it, but could anyone succinctly explain anion gap, what it means and how it applies to this case?

 

[Paseo Del Norte]

Cool case! A little above the scope of your average paramedic I think, but that's what makes it fun.

I could probably google it, but could anyone succinctly explain anion gap, what it means and how it applies to this case?

Thanks! Obviously, I created the NP clinic scenario and lack of information in order to produce a situation where we had to investigate and identify the problem from scratch so to speak, but I still thought this modification of the original scenario would make a good case.


I thought about talking about the anion gap, but I am somewhat torn. On one hand, I don't want a physician to take it the wrong way and think I am lecturing people who know this well, but I absolutely think the concept is very important for those of us who are not physicians.

The most important part of the anion gap for me as a provider, is that it can give me a list of problems to consider.

Calculating the anion gap is actually quite easy:

1) You take the major cations and add them up (Sodium + Potassium).
2) Then, you take the major anions and add them up (Chloride and Bicarbonate).
3) Next, you subtract the anion total from the anion total.
4) If the difference falls roughly between 8-16, you have a fairly normal anion gap. The range varies a bit and some people do not include potassium in the calculation.

The basic concept behind this measurement is electroneutrality. In that I mean that the body generally does not like to take on a significant charge, so the positive charge should be about equal to the negative charge. We allow for a range due to measurements and the fact that we normally have some anions floating around that are not measured by basic labs.

In acidotic states, we begin to loose bicarbonate. This loss of bicarbonate is offset by the shifting of chloride to maintain electroneutrality. However, in an anion gap acidosis, an acidic substance breaks down into an acid part and an anion part. The acid part causes the acidosis while the anion part ensures that electroneutrality is maintained. Because of this, chloride will not shift and when you calculate the gap it will appear really large when in fact the gap is simply filled by these phantom (unmeasured) anions.

Several mnemonic exist for memorising common causes of anion gap acidosis. One I have used for years is MUDPILES.

Methanol, Uremia, DKA, propylene glycol, INH, Lactic Acidosis, ethylene glycol, salicylates. Newer mnemonics include problems such as cyanide.


So, when we have an acidic patient, we can look at the anion gap and it may give us a clue or at least remind us to consider certain causes. This can also help us identify certain treatments.

 

[Dwindlin]

Calculating the anion gap is actually quite easy:

1) You take the major cations and add them up (Sodium + Potassium).
2) Then, you take the major anions and add them up (Chloride and Bicarbonate).
3) Next, you subtract the anion total from the anion total.

Hmm. We don't include the K in the anion gap calculation. And we use a cut off of >12 for large gap.

 

[malkboy]

Paseo, I love these posts/cases! Keep them coming.

 

[Paseo Del Norte]

Hmm. We don't include the K in the anion gap calculation. And we use a cut off of >12 for large gap.

There seems to be a fairly wide spread when it comes to the normal range. My current protocols state up to 16, but I have worked at hospitals that state up to 14. So, I would say that the clinical presentation married with the anion gap and it's trend would probably be the best bet.

Paseo, I love these posts/cases! Keep them coming.

Thank you. I will try. School has been kicking my arse, so I have been a little negligent about putting cases up.

 

[Dwindlin]

There seems to be a fairly wide spread when it comes to the normal range. My current protocols state up to 16, but I have worked at hospitals that state up to 14. So, I would say that the clinical presentation married with the anion gap and it's trend would probably be the best bet.

Oh, I was just commenting that I found it interesting that some places include the K in the cations. I figured calculating an anion gap would be fairly standardized.

 

[jbar]

You know it's not Aspirin with that ABG, pt would be dead by that point. By the time you have respiratory failure and have a respiratory acidosis the aspirin has become so intracellular that you are dead.

It's good to have on the differential, but you can eliminate it after the ABG.

 

[Paseo Del Norte]

Oh, I was just commenting that I found it interesting that some places include the K in the cations. I figured calculating an anion gap would be fairly standardized.

I think it probably is pretty standard and I dare say that most people do not use the potassium.

 

[pseudoknot]

You know it's not Aspirin with that ABG, pt would be dead by that point. By the time you have respiratory failure and have a respiratory acidosis the aspirin has become so intracellular that you are dead.

It's good to have on the differential, but you can eliminate it after the ABG.

I had a patient with an aspirin overdose and respiratory acidosis. She was in a coma for a few days but came out of it OK.

 

[group_theory]

In the US, we don't normally include potassium in anion gap calculation. I've been told that in Europe, they do include potassium.

This patient has an anion gap metabolic acidosis (anion gap of 32), a respiratory acidosis (with a bicarb of 8, the expected pCO2 should be 20), and a concurrent metabolic alkalosis (based on the delta-delta, or delta gap)

If you measure the serum osmolality, I'm sure you will also see an osmol gap compare to the calculated serum osmolality.

 

[joeDO2]

Alright, this thread was dying out so I'll throw a new case into the mix....

You are called to a rehabilitation facility for a patient with a change in mental status..... good luck

 

[joeDO2]

Alright, this thread was dying out so I'll throw a new case into the mix....

You are called to a rehabilitation facility for a patient with a change in mental status..... good luck

I suppose I should give a bit more info....

You arrive to find a male patient in his 70's minimally responsive to pain....

 

[DoC352]

I suppose I should give a bit more info....

You arrive to find a male patient in his 70's minimally responsive to pain....

obviously support ABCs as needed
O2, finger stick, check for PERRL, pupil size, 4 lead.

 

[JLM]

I'll bite

Vitals?
Glucose?
Pupils?
Does he smell like booze, a GI bleed, or a UTI?
Can you find his meds?

 

[Paseo Del Norte]

I suppose I should give a bit more info....

You arrive to find a male patient in his 70's minimally responsive to pain....

Any safety issues? Move to the airway and assess, position with a jaw thrust if trauma is suspected, otherwise a head tilt and chin lift. Consider placing an adjunct and supplemental oxygen.

Perform a rapid survey and identify any obvious life threats and listen to lungs along with a mental status exam (posturing, pupils, and so on). Obtain a baseline set of vitals along with a BGL as already stated. Place the patient on the monitor and get a history and the chart if possible.

 

[joeDO2]

I'll bite

Vitals?
Glucose?
Pupils?
Does he smell like booze, a GI bleed, or a UTI?
Can you find his meds?

sorry for the delay....

initial vitals- BP 86/40, HR 160 (irregular wide complex rhythm on 4-lead), glucose 60mg/dL, pupils equal and reactive at 3mm. no significant odors noted. partial med list obtained = coumadin, ASA, antihypertensives, statins

 

[joeDO2]

Any safety issues? Move to the airway and assess, position with a jaw thrust if trauma is suspected, otherwise a head tilt and chin lift. Consider placing an adjunct and supplemental oxygen.

Perform a rapid survey and identify any obvious life threats and listen to lungs along with a mental status exam (posturing, pupils, and so on). Obtain a baseline set of vitals along with a BGL as already stated. Place the patient on the monitor and get a history and the chart if possible.

no safety issues. airway is patent and the patient is breathing at 12 per minute with slight irregularity. there are signs of adequate perfusion (good skin color, temp, condition) oxygen is applied via non-rebreather mask.

lungs are clear bilaterally. no obvious signs of trauma on rapid exam. a pacemaker is noted in the left chest wall.

Hx: patient is in the facility for rehabilitation following a pacemaker placement. there is a history of afib and periods of symptomatic bradycardia. the patient was last seen normal 1-2 hours prior to your arrival, where he was fully oriented and conversational. patient will groan to painful stimuli

 

[DoC352]

sorry for the delay....

initial vitals- BP 86/40, HR 160 (irregular wide complex rhythm on 4-lead), glucose 60mg/dL, pupils equal and reactive at 3mm. no significant odors noted. partial med list obtained = coumadin, ASA, antihypertensives, statins

ACLS and local protocol says immediate synchronized cardioversion at 100 joules... Might consider Cardizem for the irregular rhythm but with the wide complex as medic you would probably need to consult medical control.

 

[DoC352]

ACLS and local protocol says immediate synchronized cardioversion at 100 joules... Might consider Cardizem for the irregular rhythm but with the wide complex as medic you would probably need to consult medical control.

to correct myself: ACLS (2010) actually calls for defibrillation for patients presenting with irregular wide complex tachycardias.

Again though, I'm worried about the afib. With the guy in the condition he's in, throwing a clot might be an improvement, but I don't know if I want to risk it without medical control.

 

[JLM]

O2 sats & lung exam
Are all of the QRS complexes wide? Do they look the same? Do any have pacer spikes?
Is there any digoxin on the MAR?
How does the pacemaker site look?
Did he get his rate-control meds?

 

[Dwindlin]

to correct myself: ACLS (2010) actually calls for defibrillation for patients presenting with irregular wide complex tachycardias.

Again though, I'm worried about the afib. With the guy in the condition he's in, throwing a clot might be an improvement, but I don't know if I want to risk it without medical control.

You mean cardiovert right? You don't ever (to the best of my knowledge) straight up defib. someone with a pulse.

 

[DoC352]

You mean cardiovert right? You don't ever (to the best of my knowledge) straight up defib. someone with a pulse.

That's what I thought at first, but looking at the ACLS protocol it clearly says irregular wide complex tachys with a pulse are cardioverted at "defibrillation dose (NOT synchronized)"

http://1.bp.blogspot.com/_8Z869lPmoNo/TMVWRZWYlFI/AAAAAAAAA9Y/FM7bGo62X2g/s1600/Adult+Tachycardia+with+a+pulse+-+2010+ACLS+algorithm.jpeg

 

[joeDO2]

O2 sats & lung exam
Are all of the QRS complexes wide? Do they look the same? Do any have pacer spikes?
Is there any digoxin on the MAR?
How does the pacemaker site look?
Did he get his rate-control meds?

spo2 94%, lungs are clear. all of the QRS complexes are wide and the rhythm appears to be widening as the call progresses. there are no pacer spikes noted. the pacemaker site is freshly bandaged- no discharge noted or other signs of infection. there is no digoxin on the med list. the patient is not on rate control medications due to a history of symptomatic bradycardia (the reason for the pacemaker placement in the first place)

at this point IV access is attempted and failed. the rhythm widens and becomes a regular, monomorphic, wide complex rhythm at 160bpm.

 

[joeDO2]

to correct myself: ACLS (2010) actually calls for defibrillation for patients presenting with irregular wide complex tachycardias.

Again though, I'm worried about the afib. With the guy in the condition he's in, throwing a clot might be an improvement, but I don't know if I want to risk it without medical control.

remember that the patient is anticoagulated. this significantly lessens the risk of thromboembolism secondary to cardioversion

 

[joeDO2]

That's what I thought at first, but looking at the ACLS protocol it clearly says irregular wide complex tachys with a pulse are cardioverted at "defibrillation dose (NOT synchronized)"

http://1.bp.blogspot.com/_8Z869lPmoNo/TMVWRZWYlFI/AAAAAAAAA9Y/FM7bGo62X2g/s1600/Adult+Tachycardia+with+a+pulse+-+2010+ACLS+algorithm.jpeg

you bring up an interesting point. I'm curious as to what others have to say on this subject. in this case, the patient has a hx of afib, so the likely initial rhythm is atrial fibrillation with aberrancy.

with the change in rhythm, how would you proceed now? what is on your differential diagnosis? do you think the glucose level of 60 is significant? what else would you be considering at this point?

 

[mlw47]

So what does the 12 lead show? And is there an old one for comparison?

Given the history of recent pacemaker placement, it's most likely that he either has 1) tracking of a rapid atrial rate, or 2) a pacemaker mediated tachycardia (PMT) conducting up then causing a discharge with a positive feedback loop. Of course, there are others on the differential, but those are the most common.

If the 12 lead shows capture with retrograde p waves, you could argue to just attempting a diagnostic and therapeutic maneuver of putting a magnet over the pacemaker. If it breaks the tachycardia, voila, it's PMT, and his new pacemaker might have had a too short post-ventricular atrial refractory period. If it's not PMT, then try rate control and investigate other etiologies.

 

[mlw47]

spo2 94%, lungs are clear. all of the QRS complexes are wide and the rhythm appears to be widening as the call progresses. there are no pacer spikes noted. the pacemaker site is freshly bandaged- no discharge noted or other signs of infection. there is no digoxin on the med list. the patient is not on rate control medications due to a history of symptomatic bradycardia (the reason for the pacemaker placement in the first place)

at this point IV access is attempted and failed. the rhythm widens and becomes a regular, monomorphic, wide complex rhythm at 160bpm.

Oh, didn't see this.

If the pacemaker is out of the question then don't worry about it. His QRS is widening and he's in VTach, it's time to start throwing ACLS drugs at him.

1) Start at least one IO.
2) Magnessium
3) CaGluconate
4) NaCl bolus
5) Prepare for a crash landing.
6) Consider cardioversion/defib.



Some might raise the question of whether he's in VTach or in an SVT with abberancy. The point is moot. 1) There are weak tools to help distinguish the two. 2) His history via meds and known cardiac history, and his age, put him in high risk for VTach instead of SVT w/ abberancy in this instance. 3) If in doubt, treat like VTach.

 

[joeDO2]

looks like this case died out a bit in the forums. to wrap things up here, the pt received an IO (not able to obtain access by other means). 1 cardioversion produced a return of sinus rhythm and pt being normotensive. unknown at the time, there was a hx of fall at the facility and a large subdural bleed was found on CT.