A Whole Litany of Issues

Tigger

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You're dispatched to a residence for a 60 something male with shortness of breath. The patient's wife brings you to a basement living room where you find the patient seated in a recliner, alert, oriented, and mentating appropriately. Patient is on home oxygen at 2lpm. Wife tells you that the patient was recently diagnosed with pulmonary hypertension and has also been struggling with managing his CHF. The patient was admitted last week for pedal edema and ascites, patient was tapped and six liters taken off his abdomen. The patient informs you he is always mildly dyspneic but two hours ago he suddenly became more dyspneic and developed moderate chest tightness while watching TV. You work the patient up and note the following:

No other medical history. His medications include Lasix/KCL, sildenafil, and bactrim. Social history for alcoholism, patient no longer drinks.

Physical exam:
Skin: Pale, warm, dry. Jaundice noted.
HEENT: Atraumatic, pupils equal/round/reactive @4mm, jaundiced sclera.
Chest: Equal rise and fall. Pt appears cachectic. Basilar rales on left, otherwise clear throughout. No cough noted.
Abdomen: Significant distension with ascites.
Pelvis and back without remark.
Extremities: Upper without remark, strong and fast radial pulse. 4+ bilateral pedal edema with skin rupture and weeping. No way you can ascertain a pulse.
Neuro: Not remarkable.

Vitals:
HR 184, BP difficult to obtain but eventually found to be 80/50 manually. 86% on 2lpm. Minor tachypnea noted. EKG attached.

What's next? What else would you like to know?
 

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MonkeyArrow

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Interesting case.

My first priority would be rapid extrication and initiating L&S transport to a an ER that’s hopefully capable of cath and has more than a podunk ICU.

EKG: appears grossly regular narrow complex tachycardia without obvious p-waves. STE in aVR with reciprocal STD in V4-V6 lead me to believe these are likely rate-related changed from global subendocardial ischemia/supply-demand mismatch. However, slight STE in V1-V2 is quite atypical and worrisome for other acute ischemic process. Rightward axis, tall R wave in V1. Would not activate cath lab at this time but a concerning picture.

Obtain peripheral IV x2 if possible, although that sounds like it’s going to be difficult. Defib pads on.

My initial instinct was not to cardiovert him, as I don’t think this is primary SVT. But if he looks like **** and remains hypotensive, I guess you don’t have much of a choice. Would electrically cardiovert knowing in the back of my mind it may not work.

Increase oxygen to NC/NRB as appropriate with low threshold to initiate CPAP/BiPAP, even with lung sounds as presented. Whatever you do, do not intubate this guy in the field. His pulmonary HTN plus current hypoxia (plus likely body habitus) put him at extremely high risk for peri-intubation arrest.

No IV fluids. He’s obviously fluid positive and has some element of RV dysfunction which is going to be exacerbated by fluid and further dilation of the RV, causing a paradoxical drop in BP. Not a candidate for diltiazem for rate control given HF. Could try adenosine, although again not convinced it’s going to work. Amiodarone probably your best bet for rate control if you really want to do something about it, although can cause some hypotension too.

Ddx: PE (ekg findings + clinical picture highly suspicious), Acute-on-chronic CHF exacerbation, SBP vs other cause of septic shock, MI with cardiogenic shock, other occult cause of shock (I.e. GI bleeding from ruptured varices).

Plan: Place on CPAP. IV access, defib pads. Rapid transport.

Edit: Can’t forget to consider COVID. Vax status? Recent hospitalization could place at higher risk for exposure.
 
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Carlos Danger

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Interesting case.

My first priority would be rapid extrication and initiating L&S transport to a an ER that’s hopefully capable of cath and has more than a podunk ICU.

EKG: appears grossly regular narrow complex tachycardia without obvious p-waves. STE in aVR with reciprocal STD in V4-V6 lead me to believe these are likely rate-related changed from global subendocardial ischemia/supply-demand mismatch. However, slight STE in V1-V2 is quite atypical and worrisome for other acute ischemic process. Rightward axis, tall R wave in V1. Would not activate cath lab at this time but a concerning picture.

Obtain peripheral IV x2 if possible, although that sounds like it’s going to be difficult. Defib pads on.

My initial instinct was not to cardiovert him, as I don’t think this is primary SVT. But if he looks like **** and remains hypotensive, I guess you don’t have much of a choice. Would electrically cardiovert knowing in the back of my mind it may not work.

Increase oxygen to NC/NRB as appropriate with low threshold to initiate CPAP/BiPAP, even with lung sounds as presented. Whatever you do, do not intubate this guy in the field. His pulmonary HTN plus current hypoxia (plus likely body habitus) put him at extremely high risk for peri-intubation arrest.

No IV fluids. He’s obviously fluid positive and has some element of RV dysfunction which is going to be exacerbated by fluid and further dilation of the RV, causing a paradoxical drop in BP. Not a candidate for diltiazem for rate control given HF. Could try adenosine, although again not convinced it’s going to work. Amiodarone probably your best bet for rate control if you really want to do something about it, although can cause some hypotension too.

Ddx: PE (ekg findings + clinical picture highly suspicious), Acute-on-chronic CHF exacerbation, SBP vs other cause of septic shock, MI with cardiogenic shock, other occult cause of shock (I.e. GI bleeding from ruptured varices).

Plan: Place on CPAP. IV access, defib pads. Rapid transport.

Edit: Can’t forget to consider COVID. Vax status? Recent hospitalization could place at higher risk for exposure.
I generally agree with your overall assessment and plan of care. This is a sick as **** patient who could crump quickly and needs evaluation and management by people much smarter than me as soon as possible. Everything done to this guy should be done slowly and gently. This scenario could just be an exacerbation that he can be easily assisted though with proper management, or it could be his swan song. It is impossible to say for sure, but I would definitely presume the former.

The one point that I disagree with is you on is avoiding intubation at all costs. I mean, as always, I would definitely try to avoid it, but if this guy starts to circle the wagons even a little bit, a gentle intubation with aggressive pre-ox, a whiff of etomidate or ketamine and maybe a little versed (sorry bro, at least you are still alive), perhaps some esmolol, and judicious use of pressors and IVF might be exactly what is needed to get him over the hump. Remember that PPV will likley help a lot with his pulmonary edema. In fact, I would say that ANY further decline at all in his respiratory function is an indication for immediate intubation. If his primary issue is a fatal cardiac or vascular event or the end-stage progression of his overall disease, then nothing you do matters. If his primary issue is acute respiratory failure, then you can potentially fix that. In a patient like this, waiting until you obviously HAVE TO INTUBATE RIGHT NOW!!! means you are so far behind the power curve that you may easily never catch back up. Extreme stress on an already failing heart and failing respiratory system and all that.

And I totally understand that a "gentle intubation" can be hard to achieve in the field within the constraints of protocols, tools, and experience. It would definitely be preferable to have it done by an anesthesia provider or skilled ED doc and all the backup available in the hospital setting. All you can do for the situation you are presented with is the best that you can do with the tools that you have.
 
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MonkeyArrow

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I generally agree with your overall assessment and plan of care. This is a sick as **** patient who could crump quickly and needs evaluation and management by people much smarter than me as soon as possible. Everything done to this guy should be done slowly and gently. This scenario could just be an exacerbation that he can be easily assisted though with proper management, or it could be his swan song. It is impossible to say for sure, but I would definitely presume the former.

The one point that I disagree with is you on is avoiding intubation at all costs. I mean, as always, I would definitely try to avoid it, but if this guy starts to circle the wagons even a little bit, a gentle intubation with aggressive pre-ox, a whiff of etomidate or ketamine and maybe a little versed (sorry bro, at least you are still alive), perhaps some esmolol, and judicious use of pressors and IVF might be exactly what is needed to get him over the hump. Remember that PPV will likley help a lot with his pulmonary edema. In fact, I would say that ANY further decline at all in his respiratory function is an indication for immediate intubation. If his primary issue is a fatal cardiac or vascular event or the end-stage progression of his overall disease, then nothing you do matters. If his primary issue is acute respiratory failure, then you can potentially fix that. In a patient like this, waiting until you obviously HAVE TO INTUBATE RIGHT NOW!!! means you are so far behind the power curve that you may easily never catch back up. Extreme stress on an already failing heart and failing respiratory system and all that.

And I totally understand that a "gentle intubation" can be hard to achieve in the field within the constraints of protocols, tools, and experience. It would definitely be preferable to have it done by an anesthesia provider or skilled ED doc and all the backup available in the hospital setting. All you can do for the situation you are presented with is the best that you can do with the tools that you have.
Agree 100% with you. I think that’s why I hedged with “avoid tubing him in the field”. He maybe needs to be intubated now, almost certainly with further decompensation, tough to say without seeing the patient myself in person. However, I think there are probably very few EMS providers who can achieve a safe gentle intubation in this patient, especially given a single paramedic setup where you have to manage the intubation and hemodynamics all by yourself. That’s the only reason why I said to delay intubating until the ED, but I think we’re on the same page.
 

Aprz

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Did you post this somewhere else? I am pretty sure I saw this 12-lead already and read the outcome. I'm not sure. I *believe* I saw this with someone talking about unsuccessfully converting it with Adenosine, they were talking about how they hadn't been unsuccessful with Adenosine before, and that the patient was successfully electrically cardioverted at the emergency department. I don't know why that's popping up in my mind. I guess maybe that's why I am questioning what I see in lead V3. To me, it looks like there are P-waves in lead V3. I don't see P-waves in any other lead. The "P-waves" I see are almost in the middle of the R-R interval so you could argue possible Bix rule with hidden atrial activity in the the QRS complexes. This is too fast to be 2:1 atrial tachycardia (typically atrial rate is 150-250 bpm, which would have a ventricular rate of 75-125), I don't see any other atrial activity (in lead V1 or inferior leads) to help me further. For his age, it's also somewhat fast for sinus tachycardia (general rule is 220-age), but patient's don't read our textbooks or care much for our numbers, right? LOL. I mean, if it did convert with electrical cardioversion, then it probably wasn't sinus tachycardia. If Adenosine was pushed and it didn't increase the block (for atrial flutter or atrial tachycardia), it probably wasn't those either. At this rate, I don't usually consider ischemia from a clot in the coronary artery, but usually more concerned about rate dependent ischemia. If signs of ischemia persist after treating the rate, then I go down the ACS route. This guy wouldn't be able to get nitroglycerin due to hypotension anyways. If you really wanted to give him aspirin, it probably wouldn't hurt or be a big deal, if you wanted to.

There's honestly a couple of different things you could do and depends on your comfort and what you're allowed to do. I think nobody wouldn't give you a hard time with whatever route you choose, if you chose to be conservative (oxygen, IV, monitor, treat if deteriorate) or aggressive. Either approach you take is risky and probably would depend more on transport time. Short transport, take conservative approach. Long transport, consider the more aggressive approach and strongly consider calling medical direction to bounce ideas off or literally take directions from, haha. To me, I have the impression that his vital signs are not great, but he is awake and talking so he's tolerating. He probably usually has crappy vital signs to be honest. Whether taking the conservative or aggressive approach, I'd bump up his oxygen and start an IV. Even though he is hypotensive, I would probably avoid giving him fluids due to rales, pedal edema, ascites, takes Lasix, and recent history of an abdominal tap. For his blood pressure, if you didn't want to try any cardioversion whatsoever, you could treat it with Levophed without increasing his heart rate. If you don't believe those are P waves, you could go down the "hemodynamically unstable" route with ACLS due chest pain, increased shortness of breath, hypotension, low oxygen saturation while on a nasal cannula. You could try Adenosine for diagnostic (better reveal atrial activity, if any) and hopefully therapeutic purposes (convert the rhythm, if is treatable with Adenosine). Adenosine seems like a more comfortable route.

Just depends on how the patient is presenting to you, your comfort, what your protocols allow, and how far of a transport I think. You probably could get away with most things on this call as long as not negligent.
 

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Tigger

Tigger

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I did post this elsewhere, here’s what I did.
Though his vitals were suboptimal, he was mentating very well. No issues getting an 18 in his AC so I figured we could try some adenosine. To me this looked like pretty cut and dry SVT, though later examination of V3 has me less sure. We start with here, he got 12 and….nothing. Not nothing like it didn’t work but I mean no effect on the patient or EKG. I thought I had pushed it wrong or something but I’ve used it a lot and the other paramedic concurred that the dose was received. So we did 12 again and same thing. I had always learned “treat rate first” and then see if things improved and considering that we hadn’t made any progress, I figured we ought to leave. Stair chaired him up and out and left. In the ambulance he was more hypotensive (presumably from the extrication adventure). Still only moderately tachyoneic, but more hypotensive.
I felt comfortable giving a smaller dose of versed pre cardioversion despite the hypotension, it worked great. Cardioverted at 360 (local protocol is max joules) and he converted immediately to sinus tach at 106. Don’t have that EKG handy, but really not notable for much else aside from right atrial enlargement. Blood pressure and SpO2 improved, capnon was always good and remained so.

Mostly surprised at the lack of any effect of the adenosine.

Patient was found to be septic, had another tap on the ED, and was admitted. No recurrent tachycardia.

I know we kind of teach not to cardiovert septic patients who are likely volume depleted but in this case it seemed to be the right choice.
 

Aprz

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I did post this elsewhere, here’s what I did.
Though his vitals were suboptimal, he was mentating very well. No issues getting an 18 in his AC so I figured we could try some adenosine. To me this looked like pretty cut and dry SVT, though later examination of V3 has me less sure. We start with here, he got 12 and….nothing. Not nothing like it didn’t work but I mean no effect on the patient or EKG. I thought I had pushed it wrong or something but I’ve used it a lot and the other paramedic concurred that the dose was received. So we did 12 again and same thing. I had always learned “treat rate first” and then see if things improved and considering that we hadn’t made any progress, I figured we ought to leave. Stair chaired him up and out and left. In the ambulance he was more hypotensive (presumably from the extrication adventure). Still only moderately tachyoneic, but more hypotensive.
I felt comfortable giving a smaller dose of versed pre cardioversion despite the hypotension, it worked great. Cardioverted at 360 (local protocol is max joules) and he converted immediately to sinus tach at 106. Don’t have that EKG handy, but really not notable for much else aside from right atrial enlargement. Blood pressure and SpO2 improved, capnon was always good and remained so.

Mostly surprised at the lack of any effect of the adenosine.

Patient was found to be septic, had another tap on the ED, and was admitted. No recurrent tachycardia.

I know we kind of teach not to cardiovert septic patients who are likely volume depleted but in this case it seemed to be the right choice.
Nice. I couldn't find it for the life of me, but I recognized the pattern from earlier and had already done all the mental math from earlier. I was like I SAW this ECG somewhere! I kept looking and looking, but couldn't find it. Like I said, you probably could've justified any route and be fine.

Good article on sinus tach vs "SVT" for people that want to refrresh. http://ems12lead.com/2013/04/30/the-trouble-with-sinus-tachycardia/

I've always been under the impression that if you cardiovert sinus tachycardia, the rate will just remain the same. Adenosine it, it'll go down and then slowly back up. I've never witnessed either thing happening. I've been lucky with most of my 12-leads being pretty straight forward or taking the conservative approach due to short transport time.
 
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Tigger

Tigger

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Good article on sinus tach vs "SVT" for people that want to refrresh. http://ems12lead.com/2013/04/30/the-trouble-with-sinus-tachycardia/

I've always been under the impression that if you cardiovert sinus tachycardia, the rate will just remain the same. Adenosine it, it'll go down and then slowly back up. I've never witnessed either thing happening. I've been lucky with most of my 12-leads being pretty straight forward or taking the conservative approach due to short transport time.
I think this is a pretty good article as well. Certainly it’s advisable to hone in on a rate that just doesn’t change, that should be a sign that something is going on conduction wise.
 

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