How I Passed the FP-C

Recently I swallowed my pride (and a lot of nervous bile) and took the FP-C. I was fortunate enough to pass my first time around, and I’ve been getting a lot of questions from my peers about it.


  • How did you do?
    Beat it by about 15 points, +- . My understanding is that each test has its own particular % needed to pass, the FP-C site says “usually about 75%”. My test may have been harder, since passing was 70%. I did NOT feel confident walking out of the room, though.
  • How did you study?
    I used the ACE SAT, Back to Basics, CFRN / FPC guide by FlightBridgeED, and Critical Care Transport book from AAOS. Strategy: take one test, looked it up, got my answers, wrote down the things I didn’t know, took the test again, made sure I understood WHY I got something wrong, then went and took the same chapter in the OTHER book).  Rinse/repeat.I also had my CCEMTP, which helped a LOT.
  • Any particularly tricky topics?
    It depends on what you’re used to. Study THEIR airway algorithm and what THEY want for neurology, I ran into some trouble of FPC vs Janus General’s way. Those not used to working with PACs should study them.Understand the relationship between CVP (R-preload), PA (R-afterload), wedge (L-preload), SVR (L-afterload), CO/CI, and different shock states, even if you can’t read PAC waveforms for your life. Understand cyanotic vs acyanotic heart defects in neonates and kids. Understand the reasoning behind prostaglandins, indomethacin, and other neonate meds. Remember what drug gets used for upper GI bleeds. Drill the Parkland and Consensus formulas into your brain, along with the Rule of 9s. Study your oddball overdoses.
  • Was the test difficult?
    Yes—and it damn well should be.
  • Was the test fair?
    This question is implied, but it’s REALLY important. I feel that yes, the test IS fair. Most questions didn’t have much in the way of distractors. It was a lot of questions about how you would treat a particular patient–totally justified.
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The Rumors Of My Death…

Hey everybody! I just wanted to announce that the rumors of my death have been mildly exaggerated. I’ve been pretty busy this past month, and as a result I’ve neglected the podcast a little bit. Things have mostly been positive, including some exciting critical care training, my second wedding anniversary, and some other great things.

With good has also come ill–the anniversary of my father’s death and my personal issues with depression have reared their ugly heads as well, along with a realization that I’ll not be able to go to SMACC this year. But I’m committed to moving forward and bringing you awesome content that you can take to the streets with.

So I wanted to offer you a taste of what we have coming up during the rest of this year:

–A practical discussion of the joys of proximal IV therapy for prehospital providers (tentatively titled Who’s Afraid of the Big Bad EJ?)

–A talk about mental health in EMS, because it’s something we as an industry need to discuss in a way that’s constructive and useful. (No tentative title yet.) The struggle for me here is to discuss this topic without delving into my personal issues.

–In honor of the Transgender Day of Remembrance upcoming on November 20th, we’re going to have an episode about trans* people, their physical and mental health, the prehospital and interfacility clinical implications, and the social aspects of caring for transgender people (tentatively titled How Not to Be A Dick to Trans* People)

–A how-to guide for treating that most common presentation, Alcohol Overimbibement Syndrome, otherwise known as The Care and Feeding of Drunks. Because they’re fine… until they’re really not.

–The ParaIntensivist’s Guide to Vasopressors, coming soon to a podcast near you!

So stick around, folks! There’s great goodies yet to come.

Posted in Blog Entries Tagged with:

PIG-EMS: aDEVILsine – REVERT, Valsalva, and Not Giving Tornados In The Chest

pSVT is a fairly common presentation for tachycardia and a common 911 complaint. I get about 1-2 a year, and I always try the Valsalva maneuver, and it fails most of the time.

But that’s okay! We start a line and bust out… the ADENOSINE!!! Probably the coolest drug in the bag, the one that lets us tell our friends and family “Yeah… I stop hearts for a living, and get them started again.” We feel like badasses, there’s the thrill of watching that transient asystole…

…But what about the patient?

Ain’t Nobody Likes (Getting) Adenosine

Does adenosine WORK? OF COURSE. But patients hate it. “Don’t give me any more of that stuff.” “I feel like I’m going to die.” “I feel like I have a tornado in my chest.” They love not being in SVT anymore… but they hate how they get there.


No Muss! No Fuss! REVERT that SVT!

There’s been a lot floating around in the critical care world about updating the Valsalva technique. Why?

  • Traditional Valsalva success rate is 5-20%
  • REVERT technique gets **43% conversion**!!!!
  • NNT = **3**. That’s HUGELY effective.
  • Free! No cost, no muss, no fuss.
  • ZERO serious adverse events.

How? Have them blow through a straw… then give ’em the Dipsy Doodle!


Okay, But What If That Doesn’t Work?

Look, am I saying NOT to EVER give adenosine? No. But for most patients, I think verapamil and diltiazem are better drugs. Why? No tornadoes. Level I-Class A evidence for their use.

  • Diltiazem: 0.25mg/kg IVB sloooowwwllyyyyy; repeat at 0.35mg/kg
  • Verapamil: 2.5-5mg IVB slooooowwwlyyyyyy; repeat at 5-10mg.
  • Pre-dosing with calcium salts (CaCl) can attenuate hypotension

Beta blockers: Evidence here isn’t as good, but they are a viable option.

Yes, they do risk hypotension (verapamil more than diltiazem). Give them slowwwwwlllyyyyyy. Like, over 2 minutes slowly. Or do them as a drip. Monitor BP continually. Be careful.

If You HAVE to Give Adenosine….

  • Ask about caffeine intake before you give the drug. Caffeine attenuates adenosine. (Ironic, considering how many SVTs are caffeine-related!) If a lot of intake, consider Ca++ Channel Blocker (CCB) or increasing the dose.


A FlowChart, Then?


  • SBP <= 90 OR looks shocky?
    • IV
    • Anaesthetise (etomidate, propofol, fentanyl, midazolam, ….)
    • SYNC!!!!!
    • Cardiovert @ 100J, 120J, 150J, 200J
  • SBP > 90?
    • REVERT (have pt blow through a syringe HARD, then lay flat & raise legs)
      • Success? ==> Observe, transport/monitor
      • Failed?
        • IV
        • Can tolerate adenosine with LITTLE TO NO caffeine on board?
          • Yes ==> Give adenosine
              • “You may feel like you’re going to die.”
              • Explain that it slows your heart way down, “you may feel as if you’re going to die, but the feeling will pass quickly”.
            • Give adenosine 6mg, RAPID flush
              • Reveals underlying a-fib/flutter? GO TO CCB
              • No fib/flutter? Repeat adenosine @ 12mg, consider threepeat @ 12mg, RAPID flush
          • Hesitant / Refuses adenosine?
            • No contraindication to CCB?
              • *Give calcium gluconate 1g IVB slooooowwwllyyy > 3 mins (Optional)
              • (OR give CaCl 90mg IVB slooooowwwwly > 3 mins (optional) )
              • Diltiazem: 0.25mg/kg IVB sloooowwwllyyyyy > 2 mins; repeat at 0.35mg/kg
              • Verapamil: 2.5-5mg IVB slooooowwwlyyyyyy > 2 mins; repeat at 5-10mg.
            • Contraindication to CCB?
              • Beta Blocker (labetalol, ….) at appropriate dose



Posted in Uncategorized Tagged with: , ,

PIG-EMS: Synthetic Cannabinoids — A Report From the K2 Triangle

Disclaimer: The contents of this episode are from PERSONAL EXPERIENCE. K2 and synthetic cannabinoids are new enough that there’s not enough published research, and the nature of the drugs makes them extremely variable. This is current as of October 2015, and is my experience only. Got it? Good.

Imagine if you will a hospital, in the center of a triangle. At each point, you’ll find a shelter, a place for undomiciled men fallen on hard times to lay down their heads. On the surface, all is well. But a wave of darkness has overtaken each point on the triangle, separate and unique, a plague of unconsciousness and psychosis, all connected to what is supposedly the same drug.

You’ve entered… The K2 Zone.

*cue Twilight Zone music*

Synthetic Cannabinoids? That’s Basically Pot, Right?


These drugs target the same receptors, true. But they’re very different on a molecular level. They’re designed to hit them HARD.

  • A typical joint of marijuana only hafs a few mg of THC
  • A typical joint of K2 may have gram-levels of ???
  • Formulas constantly change; no two products are exactly the same
What does it look like? How do people get it?

It’s sold over-the-counter in smoke shops, head shops, gas stations, etc. It’s packaged as potpourri, or incense. It’s all labeled “not for human consumption.” It’s cheap, it’s “legal” (dubiously; not actually legal in State of Janus), it’s readily available. It has names like K2 and Spice and AK-47.

Why K2? Why not “real pot”?
  • Experiment!
  • Cheaper ($5 for 3 “doses”)
  • Easier to find
  • “Legal” (not really, but EXTREMELY low on PD’s priority list)
  • Euphoria
  • Doesn’t show up on urine / toxicology tests
Who Uses This Crap, Anyway?
  • Students (HS especially)
  • Military (remember, drug tests)
  • Psych facility patients
  • Homeless/undomiciled people
    • Large proportion of homeless population have mental health, substance dependence problems

Janus Regional (not Janus General) happens to be in a bad neighborhood. There are 3 local shelters that generally form a triangle around the hospital. K2 has invaded each of these shelters like a disease. These guys hang out outside, they smoke up, they….

…behave very differently based on which shelter they come from.

Wait, huh?

A Passed-Out Piggy. Courtesy of

A Passed-Out Piggy. Courtesy of and Himalayan Misadventures.


Synthetic cannabinoids are designer drugs, and they’re constantly changing to stay ahead of legislation. Different locations may sell different products. So why is each shelter different? Because the retailer(s) supplying each shelter are different.

Point A: Complete cardiovascular collapse. These patients will present with:

  • Tremors
  • Seizures
    • Benzos can cause them to CRASH REALLY HARD (resp/cardiac crash)
  • Unconsciousness OR unconsciousness with transient psychosis
    • Take NPAs like champs
  • Pupils are sluggish/unreactive, dilated or constricted
  • Tachypnea (40) OR bradypnea (4)
  • Hypoxemia (80s or less)
  • Tachycardic (~130, sinus tach) OR bradycardic (40s)
  • Initially normotensive; 10 minutes later they’re VERY hypotensive (MAP ~50)
    • Vasodilatory? Cardiogenic? Neurogenic? NO ONE KNOWS. Pressors?
    • Can require fluids > 2 L to maintain MAP 65
    • Pressors?
  • Can be extremely hypoglycemic (“LO” even in non-diabetics)
  • One particular patient with severe cardiac issues has been intubated by 2+ of our medics

Point B: Ragers against EVERYTHING — Think PCP

  • Psychosis +- violence
  • Require physical restraint (LEO! Big blue lions!)
    • Cuffs vs soft restraint
    • I always prefer one-up-one-down for arm restraint
  • Require chemical restraint (benzos safe in this population)
  • Hyperthermic (excited delirium)
  • Tachycardic / tachypneic
  • Usually don’t require fluid challenges
  • Not dissimilar to PCP presentations

Point C: Baby Bear?

  • AMS (usually not unconscious)
  • “High” / detached affect
  • Normo/hypertensive
  • May be tachycardic OR bradycardic
    • Anecdotally respond well to atropine
  • Not much supportive care required


Trenchside Tips-N-Tricks
    • Violence
    • Off-gassing!!! Burnt/acrid smell? Open windows, turn on vents, limit your exposure
      • N/V, H/A, dizziness, …? (Anecdotal)
      • N-95s not likely to work (gas, not particulate)
  • BIG IVs
    • Don’t wait for them to fall off the cliff!
    • Distal brachial IVs are AMAZING in this group
    • Seriously consider B/L 16ga
    • Start fluids BEFORE their BP drops
  • NPAs Are Your Friends
    • Don’t forget the lube (even if they don’t need it, you’ll feel more humane)
  • I’m not a fan of oxygen… but if they look tachy/bradypneic, give some O’s
  • Restraining them? Right arm up, Left arm down
    • Maintains brachial access (L)
    • “Junkie special” (R) – vein in the posterior forearm “in the seam” between flexor carpi ulnaris and extensor carpi ulnaris muscle
  • Be SUPER cautious with benzos in the absence of excited delirium
    • If you need benzos, be prepared to resuscitate & intubate
Posted in EMS Tagged with: , ,


See Part 1 for pathophysiology

Things What Known Be Worky

–First and Foremost, treat the underlying condition.

–ALL these patients need to be on THE BREATHY MACHINES: vents. Anything else will kill them. This is by definition a ventilator disease. (You MAY  be able to get away with CPAP / BiPAP, maybe?)

–Low tidal volumes (4-6 mL/kg IBW) with high RRs to maintain minute volume (oxygen delivered per minute). These patients are really prone to overinflation injuries because their lungs become stiff with that fibrosis, so low TV is really important.

–PEEP is your friend! He wants to come to the party! Sure, he can be rowdy and break your furniture, but let him come! He’s here to stay. Why? He stents open some of those shut-off alveoli. BUT, a PEEP too low can actually derecruit the alveoli you’re recruiting on your inspiration, and if you recruit and then derecruit, it’s actually HARDER to open the airway.

–BUT: high PEEP Increases pulmonary shunting in PFOs! Be. Careful. Also, high pressures can cause pneumothorax and hypotension due to increased intrathoracic pressure (reduces venous return).

ARDSNet stepwise vent settings! Source:

ARDSNet stepwise vent settings! Source:

–Paralytics: Improved P:F, decreased mortality. More to the point this allows us to override their ventilations entirely, increases vent compliance, reduces bucking.

–Fluids? Fluids BAD! Treat sepsis aggressively in the first 48 hours, but 48 hours is the tipping point with ARDS. Be restrictive! Be strict! Because of capillary leakage, excess fluid is going to wind up in the lungs! Reduced fluid doesn’t have a proven mortality benefit BUT increased number of ventilator-free days during admission.

–Pressors >> Fluids! If their BP drops, give pressors. If they need transfusions, give transfusions.

–ECMO. Yep, put ‘em on V/V ECMO and your problems are more or less over though not completely. Reduced mortality is a wonderful thing. You’re not going to take them off the vent completely, but you are buying the lungs time to heal and recuperate and hopefully to let that inflammation start to subside before you wean them back onto the vent.


Things What Maybe Might Work Ish And/Or Hurt?

–Proning: LIE EM ON THEIR FACE! This actually recruits large portions of the lungs that are normally dependent (eg filled with fluid). Data is unclear; no mortality benefit evident; improves P:F ratios; use as a rescue tool for severe ARDS and worsening failure. Last-ditch effort.

–SYSTEMIC vasodilators — Prostaglandins, sildenafils – DECREASE oxygenation and INCREASE MORTALITY, maybe, depending on who you read.

–INHALED vasodilators…. say, INO? Interesting stuff. Might improve oxygenation just a smidge, but doesn’t lower Pulm. Artery pressures the way you’d think it would. In other words? No really good data yet on INO.

–Systemic Corticosteroids: Who knows?? Mixed data, no mortality benefit. Maybe that has to do with mixed causes.

–High-Flow Oscillatory Vents? Resp rates 300-900/min? Useful? WHO KNOWS?! Data isn’t clear! Lastest study from Britain says NO mortality benefit.

–Liquid Ventilation / Partial Liquid Ventilation: Still in early phases of work. The idea is to fill the lungs with an oxygenating fluid, perfluorocarbons (PFCs) , just like in The Abyss. That should, theoretically, cause better ventilation in dependent areas of the lungs, give better oxygenation across the capillaries, etc. Research is ongoing. So far no big trials, some results in porcine models.

–Continuous External Negative Pressure Ventilation (CENPV) – tank ventilators, AKA the modern man’s Iron Lung. NEGATIVE pressures -33 on inspiration to -15 cmH2O at exhalation (basically, it’s counterPEEP, or NEEP). Needs a lot of research but has some serious benefits in reduced airway, transpulmonary, and intraabdominal pressures. Also case reports of this type of tx being done with CENPV with a traditional vent on the outside providing pressure support. That sounds counterintuitive to me, but I’m just a PIG!


Posted in Intensive & Critical Care Tagged with: , ,


Acute Respiratory Distress Syndrome = non-cardiogenic pulmonary edema

Syndrome — one disease, many causes;

–Secondary disease! It’s always ARDS secondary to another diagnosis. It’s a complication, not a primary illness, but the treatment of ARDS is actually separate from the treatment of the underlying disease.

–Disease of inflammation, and prone to happen in high-inflammation states:

  • Trauma (not just pulmonary trauma!) Early onset in trauma (< 48 hrs) is usually capillary leakage; late onset (> 48 hrs) is usually PNA or MODS/MOF.
  • Sepsis
  • Pneumonia
  • Smoke inhalation
  • Shock of any kind
  • Aspiration
  • Surgery
  • Narcotics use

Often a byproduct of bad vent settings! High tidal volumes during vent can cause injury ==> ARDS.

–SEVERE dyspnea REQUIRING intubation  — ARF ==> ALI ==> ARDS

Diagnostics: Requires ABGs (maybe not, but this is gonna be a long admission anyway). Hypoxemia; “Ground glass” / diffuse patchy infiltrates on CXR; PaO2 / FiO2 (.21 to 1.0) < 200. **

Courtesy of UMIN. Source:

Differentiation With P:F Ratios: Acute Respiratory Failure (>300) ==> ALI (200-300) ==> ARDS (<200) ; PETAL is the new ARDSNet trying to get a focus on prevention of ARDS and “catch it in the act” in ALI.


  1. Exudative (leaking)
    • Capillary damage – capillary leakage
    • Diffuse endothelial injury due to micro / macro thrombi formation. Can lead to defects in peripheral pulmonary vasculature.
      • Can cause pulmonary HTN, RV dilation, & therefore cor pulmonale
    • Atelectasis (alveolar collapse)
  2. Proliferative (fibroproliferative; stiff lung, “shock lung”) – This is the most dangerous phase in terms of ventilation, because the lung tissues are developing fibrotic scar tissue. Also prone to PNA, sepsis, MODS/MOF at this stage. Typically lasts 3-10 weeks.
  3. Fibrotic stage / repair and recovery stage. In terms of mortality, this is the “out of the woods” phase. Inflammation starts to resolve. Extubation becomes possible. Recovery and improvement can last as long as 6 months.


  • MODS/MOF – Hypoxemia is bad for organs, and these patients often will have poor systemic oxygenation. That leads to organ failure in various systems depending on the individual’s base health and what the inciting disease is that prompted development of ARDS.
  • Pulmonary HTN & Cor Pulmonale – vascular damage causes blood backup in the PA, which in turn causes RV dilation and “D”ing of the septal wall – the intraventricular septum buckles into the left ventricle during contraction. Of the Cor Pulmonale patients, it gets worse—25% have a PFO with right-to-left shunting, causing deoxygenated blood to enter systemic circulation. That PFO is exacerbated by high PEEP, which is too bad, because that’s one of the main treatments for ARDS.

Next Time, On PIG-ICC, ARDS PART TWO! Treatment, vent management, and what doesn’t work (but should).

Posted in Pathophysiology Tagged with: , ,

What the Hell is a ParaIntensivist, Anyway?

Hi there! Welcome to the ParaIntensivist Podcast. This episode is here to lay down some ground rules.

Maybe you’ve Googled. Maybe you’ve searched. Maybe you’ve asked your friends. Scratched your butt a little. You know, researched. Couldn’t figure out what a paraintensivist is? I know why not.

Paraintensivist is a word that I made up. Got it? Good. Okay. Great.

So let’s define that term, shall we?

Para-: Kind of.
Intensivist: ICU doctor.

A paraintensivist is someone who operates in the world of intensive or critical care medicine, but is not a physician (or mid-level provider). That still leaves a lot of people out there–ICU nurses, flight nurses, respiratory therapists, EMTs, ICU techs, and, like me, critical care paramedics.

And that term is something you can own. I stake no claim to the Paraintensivist nomenclature. Much like the term resuscitationist, it’s yours to own. It doesn’t come with one title or one certification. It’s not exclusive to nurses, or to medics or RTs. So walk into a party and hold your head high, and when people ask you what you do, tell them you care for the sickest patients on the planet. Tell them you’re a paraintensivist. Be proud. Own it.

Sure, there are a million podcasts out there for ER and ICU docs. I can name a dozen great ones, like EmCrit, and Taming the SRU, and ERCast, and PEM-ED, and RAGE, and Life in the Fast Lane. Holy cow, you guys. There’s so much great stuff out there!

But not all of it is geared towards us, the grunts, the people actually getting our mitts dirty and get it done. So this podcast is for us, the how-tos, the tips-n-tricks. It’s also aimed at people who want to be us when they grow up, like EMTs who dream of flying, or CNAs who work part-time while they’re in school.

So this podcast is gonna have 4 different subsections to it, mostly because I like pigs. Ready? We’re going to have:

  • The ParaIntensivist’s Guide to Pathophysiology (PIG-PP)
  • The ParaIntensivist’s Guide to Intensive & Critical Care (PIG-icc, like what happens when a pig throws up).
  • The ParaIntensivist’s Guide to EMS (PIG-ems)
  • The ParaIntensivist’s Guide to Pediatrics (PIG-peds)

This blog is gonna be COVERED in piglets. No, I’m not sorry.

And the cool part? The cool part is that you got in on the ground floor! That means that the comments you leave here and now will shape this podcast going forward! You get to help pick the content, the topics, the format, everything! It’s all open to feedback and I’m excited to hear what you have to say!

So drop it all in the comments, people. Are you excited? Anxious? Love pigs? (Love bacon?) What do you want from this podcast going forward? What topics are you itching to learn more about and haven’t yet?

Posted in Blog Entries