Visit the FRN Affiliate Blogs!
Logo
  • Home
  • Assessment
  • Current Events
  • EMS 2.0
  • Legal
  • Politics
  • Research
  • Treatment
  • About Me
  • Disclaimer

Holiday Heart Strikes Again – Part 2

Posted by Patrick Lickiss on Dec 6, 2010 in Assessment, General, Treatment | 6 comments

Holiday Heart Strikes Again – Part 2

So I presented a scenario earlier this week and had a few ideas for differential diagnoses.  Click here to read the original post.  Basically it comes down to a patient who eats a huge dinner and while having a few sips of wine (her first of the evening), has a syncopal episode which has not resolved by the time EMS arrives, but which fully resolves en route to the hospital.

DIFFERENTIAL DIAGNOSIS
When looking at possible causes for this syncopal episode a few ideas come to mind:

  • Increased Vagal Tone
  • Dysrhythmia
  • CVA/TIA

After doing some research, a few less obvious causes are possible as well:

  • Holiday Heart Syndrome
  • Nitrate Sensitivity
  • Sulfite Sensitivity

So which could it be?  Let’s look at each cause.

Vagus Nerve Innervation of the Heart via WikiMedia

INCREASED VAGAL TONE
Most responders are likely familiar with the idea of a vasovagal episode.  The vagus nerve (cranial nerve number 10 for those of you keeping track), when stimulated, increases the activity of the parasympathetic nervous system and decreases the activity of the sympathetic nervous system.  What results is a drop in heart rate (due to the increased parasympathetic  activity) and a drop in blood pressure (due to vasodilation from the decreased sympathetic activity).  This combination often results in a syncopal episode and may have accounted for the patient’s bradycardia and low blood pressure.  There are a variety of causes of vasovagal episodes including abdominal straining which would certainly fit with the large meal.  On a personal note, I actually witnessed a friend’s father have a syncope after a large meal.  He had a history of MI and developed increased vagal tone as a result.  Definitely a weird thing to witness.

Increased vagal tone should certainly remain on the list of possible diagnoses for this patient.  Interestingly though, the patient’s vagal symptoms resolve without the cause for the increased vagal tone resolving (i.e. no vomiting or bowel movement).

DYSRHYTHMIA
In the comments of the original post, Christopher suggested the possibility of several dysrhythmias as causes of the patient’s syncopal episode.  Two of these suggestions seemed like they would be worth reviewing:  Stokes-Adams Syndrome and paroxysmal SVT.

Stokes-Adams Syndrome is generally characterized by a sudden onset of syncope lasting for less than a minute, possibly with seizure activity.  Prior to the syncopal episode, the patient presents as profoundly pale.  The interesting thing about Stokes-Adams Syndrome which sets it apart from other types of syncopes is that it is non-positional.  The syncopal episode can occur when seated rather than exclusively when changing position, like you would see when a dehydrated patient stands up quickly.  The syncope episodes are caused by what amounts to a brief cardiac arrest.  Stokes-Adams syncopes are caused by complete heart block (sometimes periodic which explains the short duration of symptoms) and may present with either ventricular fibrillation or asystole.  Sometimes, a slow ventricular rhythm will present.

While the patient’s slow heart rate and sudden syncope (particularly with a history of previous episodes) lends itself to a Stokes-Adams episode, the fact that the patient presents in sinus bradycardia makes it unlikely that this was such a syncope.  A complete heart block would not allow the electrical impulses from the atria continue down the heart and into the ventricles at all.  While Stokes-Adams Syndrome is a condition to be aware of in patients that present with syncope, it does not appear to be the cause here.

On the other end of the dysrhythmia spectrum is paroxysmal SVT.  Just as a review, a supraventricular tachycardia can be any rhythm which originates above the ventricles (i.e. atrial or coming from the SA or AV nodes).  The qualifier of paroxysmal indicates that the SVT is episodic in nature.  These abrupt starts and stops of dysrhythmia can certainly create syncopal episodes.  What, in my mind, rules this out as a potential cause for our patient is the fact that she presents in a bradycardia upon EMS arrival.  It also takes quite a while for her other symptoms to resolve during transport.  If we were looking at a PSVT, it seems reasonable to assume that her symptoms would resolve shortly after the resolution of the dysrhythmia.

CVA/TIA
The last suggestion for this post (and the last of the “obvious” rule outs) is a stroke or TIA.  Stroke is one of those differential diagnoses which is considered “can’t miss” and should be considered for any episode of altered level of consciousness.  While it is certainly possible that the patient is experiencing a stroke which caused her to lose consciousness, it seems unlikely when compared to the remainder of her presentation.  The patient does not present with the “typical” CVA symptoms (Cincinnati Prehospital Stroke Scale findings) and while her bradycardia could be from a significant bleed, her hypotension does not fit that pattern.  Additionally, her vital signs improve over time whereas one would expect them to get progressively worse as the bleed increases.

WHAT’S LEFT?
So we have one probable differential diagnosis (increased vagal tone), but what’s left?  Later this week, we’ll tackle some of the exotic causes of holiday syncope and see if we can’t get to the bottom of this.

Image via Flickr

  • Pingback: Tweets that mention Holiday Heart Strikes Again – Part 2 | 510 Medic -- Topsy.com

  • Pingback: Holiday Heart at 510 Medic – Prehospital 12-Lead ECG

  • VinceD

    Hey, I found your website via Tom Bouthillet’s site, and had a couple of comments to bring to the discussion. I’m far from an expert on the topic, but considering the extended length of the patient’s unresponsive episode (4 min) and slow return to baseline, I’d actually have seizure higher up on my differential than true syncope (which I’ve been taught is shorter in nature and has a rapid return to baseline mental status). I’m not sure how to tie this in with the history of these episodes while eating (coincidence or some mechanism I don’t know), and maybe it was a cardiac syncope and the slow return to baseline was due to the hypoxic or hypercapneic insult of having impaired respirations for so long, but I’m interested in seeing where this topic leads…

    • http://510medic.com Patrick Lickiss

      Thanks for dropping by! I think a seizure is certainly a good rule out to include. Practitioners should definitely have a list of “must not miss” differentials for each call and seizure is a great one for ALOC. While it could always be and absence-type seizure the fact that there were witnesses makes it unlikely in my mind that this is a case of grand-mal or tonic-clonic seizure. But you never know.

      Regarding cardiac syncope and the associated hypoxia and hypercapnea, I think you’re right on. As far as where this goes, I haven’t the foggiest idea! I’m just presenting a scenario to learn from and coming up with differential diagnoses…and I certainly appreciate the help!

  • Chris Freelen

    Quick question regarding TIA/CVA as a lower position in the differential diagnosis:

    What if a brief or initial ischemic episode occurs in the medulla thus effecting the CV Center? Wouldn’t you see atypical stroke presentation (i.e. Signs and symptoms inconsistent with conventional scales)? Wouldn’t the corresponding symptoms present as seemingly cardiac origin. Wouldn’t Brady/hypotension occur as a result in decrease neurologic tone to the sympathetic and parasympathetic affecters that connect with the SA node? Which would decrease rate and cardiac output?

    • http://510medic.com Patrick Lickiss

      Thanks Chris, you bring up a great point. Whenever looking at syncope, cardiac and neurological causes should always be top on the list. I’m admittedly no expert when it comes to locations of CVA but your explanation seems great. Given the resolution of symptoms, I would trend more toward TIA than CVA, but I suppose there is always a possibility of a lucid period before worsening again.

      If presented with this patient in the field, I would struggle with attributing cardiac symptoms to a neurological origin however. Have you seen a patient with cardiovascular symptoms from a CVA in a certain location in the brain? Did your differential diagnosis lead you down that path? If so, what were the particulars that tipped you off? Want to write a guest post about it? :)

      This could certainly turn out to be one of those “rock star” calls where you find a patient with cardiovascular symptoms, attribute them to neurological causes and then look like an amazing diagnostician when you arrive at the hospital and they confirm your suspicions with CT. I love those calls!

    • VinceD

      The problem with looking for stroke/TIA in syncope patients is that in order to lose consciousness, one of two things must go wrong: Either both cerebral hemispheres OR the reticular activating system must be knocked out. The first case is not anatomically possible with a TIA because of the redundancy of our cerebral vasculature (i.e. the Circle of Willis). On the other hand, if they actually do have a posterior circulation stroke/TIA, which could affect the reticular activating system, there will also be other hard signs, such as dysarthria, diploplia, ataxia, and hemiparesis.
      I have to note, however, that would only apply in the face of true syncope, which this may or may not be. If you ever see anyone with cardiac syncope, it’s rare that anyone around them would ever have time to help “assist them to the ground,” like this patient was. They’ll be upright one second and on the floor the next. Also, they will also usually be unresponsive for a shorter period of time than this patient, and return to baseline more quickly. Since the info on this case isn’t too detailed, it’s hard to say just how long she was out for, how quickly she returned to baseline (if she even did), and just what the medics meant when they said her mentation improved. As a result, I wouldn’t say with full confidence that stroke isn’t in the differential, but it certainly isn’t the likely culprit.

      • http://510medic.com Patrick Lickiss

        Very well described, thank you! It occurs to me that many practitioners aren’t very familiar with stroke presentations other than the “classics” as described by the CPSS. This is definitely something I need to research and write a few posts on.

Follow Me

Follow me on FacebookFollow me on TwitterFollow me on LinkedInFollow me on RSSFollow me on E-mail

interventions

facebook fans

what is EMS 2.0?

EMS 2.0

Great reads

  • Ambulance Junkie
  • EMS Garage
  • EMS in the New Decade
  • Everyday EMS Tips
  • First Responders Network
  • Maddog Medic
  • MotorCop
  • NJ Dive Medic
  • Paramedic Pulp Fiction
  • Prehospital 12-lead ECG
  • Red Light Express
  • Rescue Monkey
  • Rogue Medic
  • Setla Films
  • The Happy Medic