Freshmen

I'm more dangerous than a loaded gun, and more insecure than a freshman on the first day of high-school.  I'm a brand new EMT-Cardiac.  I've been cut loose for a few months, and it's been smooth sailing.  I've cracked the drug box more than a few times, but mostly for pain management, occasionally for nitro or Benadryl.  Unlike my paramedic counterparts in other states, my clinical experience is limited to the patients I've treated as an EMT-Basic in the field.  

I haven't been truly pushed since I got my license.  Yet.

I'm working with MedicTrunkMonkey (BrandNewBasicTrunkMonkey at the time) and Sharps-Out-Bobby.  C-Money, another relatively new EMT, has come out for the day to do a ride-along, so I'm happy when we are dispatched for difficulty breathing; maybe she'll get to experience something new.  

We find our way to the house, and are met by the patient's son, who leads us back into a dark room.  Our patient lies on her side in bed, sweat beading on her forehead, taking shallow breaths.  The room reeks of fresh feces; not the week-old stench that permeates nursing homes, but the smell of shit that introduces the patient to the EMT faster than words, saying "Hi, I'm your patient, and although I'm only 50 years old, I'm so sick I just lost control of my bowels."  MTM quickly goes to work setting up a non-rebreather mask to administer oxygen while C$ takes a blood pressure and I interview the patient.  

"Hi, I'm Dan, can you tell me what's going on today?"

"I'm just... tired," the patient tells me.  She says her name is Donna, and that she doesn't have any noteworthy medical problems.

"Are you having trouble breathing?" I ask.

"No, I'm just fatigued," she persists.  MTM tells me her oxygen saturation is low, in the high eighties.  C$ reports a normal blood pressure.  As I listen to her lungs, I see the fire chief in my periphery, collecting information for us and writing it on our clipboard.  Her breath sounds are junky, but not congestive heart failure-bad.  Even in the shadowy bedroom, it's easy to see that this woman is sick.  I reach into the blue bag, producing a plastic bottle.

"Donna, this is some chewable aspirin," I explain.  "It's possible that your heart is causing you some problems, so we want you to take it as a safety measure."  She nods in understanding and I lift the mask off of her face long enough to drop the four orange tablets into her mouth.  The three of us slide her from bed onto the stair chair.  In a flurry, we have her belted in and are on our way out the door.

MTM takes the top of the chair, and I carry the bottom.  Halfway down the front steps, Donna draws in three deep, sharp breaths.  MTM's head and mine snap up instantly.  Neither of us has heard agonal respirations before, but there can be little doubt about what we've just heard.  "DONNA, are you still with us?"

I can't describe my relief when Donna nods and manages an "mhm."

We load her into the ambulance.  We work in concert.  C$ switches the oxygen to the truck's large tank and places the lifepak 12's blood pressure cuff around Donna's arm.  MTM spikes a bag of IV fluids with a drip set.  Sharps-Out-Bobby unlocks the ALS cabinet and breaks the seal on the drug box.  I quickly place the monitor's leads, and print a rhythm strip that shows a normal sinus rhythm (if memory serves me).  I put six more sticker's across Donna's chest before leaning her back in the stretcher and pushing the "12-lead" button.  The printer whirs and I tear the strip off, spreading the printout between my hands.  

Gulp.

The EKG shows a serious STEMI–a blockage has caused a heart attack.  Her heart, starved for oxygen, is struggling to keep squeezing blood through her body with each beat.  "Bobby, let's go,  Rhode Island."  With that, Sharps-Out-Bobby makes his way to the driver's seat and sets the ambulance in motion towards the hospital.

I wrap a tourniquet around Donna's arm then splay out my IV materials on the bench seat.  A catheter, gauze, alcohol preps, Tegaderm, and tape litter the bench.  "I have terrible veins," Donna manages to say before I plunge a 20 gauge catheter into the inside of her elbow, searching for the small spongy spot I had felt moments before.  Nothing.  I weave the needle into flesh, digging for a vein, probing in different directions, changing my angle of attack.  I know the vein is there somewhere, but something is pulling my attention away.  Donna's chest heaves again, as she draws in three more sharp breaths.

"Dude, those are agonal resps..." MTM says. 

I look at Donna.  I look at the monitor.  The yellow lines that trace her heart rhythm look like the furious scribbles of a toddler's drawing.  Her heart has stopped.  

Totally weak.

"MTM, check a pulse, hook up a BVM and start bagging.  C$, start CPR."

"Like... Compressions?" She asks in disbelief.  

"Uh, yeah."  

"Bobby, she's fucking coding!" I call up to the cab.  I probably would have been more tactful if I had known that her son was in the front seat.  Oops.

Bobby has the dispatcher notify the hospital.

I tear open the defib pads, connect them to the cable, and stick them to Donna's chest.  Defibrillation within the first minute of her heart stopping is her best chance of survival.  I glance down at the 12-lead wires that stretch across her chest.  No one has ever told me if you can defibrillate somebody with the precordial leads on, but I don't want to take any chances.  I rip the leads off before charging the pads to 200 J.  

I have everybody clear the patient, look up and down her body, and hit the shock button on the monitor.  Before C$ can resume compressions, I see that Donna's heart is still quivering.  I noticed that the rhythm, which I assumed to be V-fib, seemed oddly organized.  If I had bothered to print a strip, or if the monitor were still set up to print a six second strip surrounding each shock, I would have recognized that she was actually in a rare rhythm–torsades de pointes.  In the end, the treatment is the same, and we don't carry the one drug that is useful for resolving torsades, but it still would have been satisfying to identify it correctly.

I take out the intubation kit, attach a mac 3 to the handle, grab a 6.5 ET tube, test the balloon, and slide into position to put the tube down Donna's airway.  I maneuver the blade past Donna's teeth, but am surprised when her tongue retracts, snaking away from the cold steel blade invading her mouth–could she really still have a gag reflex?  I suppose it's possible she's been oxygenated well enough to keep one of the more basic reflexes intact.  I grab a nasal airway, lubricate it, and slide it into her nose instead.  

Moving back to the bench, I charge the monitor to 300 joules, and once again call for the patient to be cleared.  MTM holds back the BVM, and C$ sits back in her seat.  Finger on the shock button, I look up and down the patient.  I clear my throat and point to Donna's arm where it rests against C$'s leg.  Grimacing, she flops the arm back on Donna's body.

I push the shock button.  I can tell the rhythm has been converted.  We do compressions a little longer before MTM announces he has a carotid pulse.  I look at the monitor, which shows a rapid atrial fibrillation, and a good blood pressure.  

Again I go to work trying to put in an IV.  We need to give her antiarrhythmic drugs to keep her heart from stopping again.  I feel a vein in her forearm, clean the site, and deftly plunge the catheter into the flesh.  I feel the crisp, satisfying pop of the catheter entering the vein, but when I look down, no blood has filled the flash chamber.  I was sure I was in the vein.  Before I can  think about whether to pull the catheter, or try and run it, MTM draws my attention to the monitor screen.  Her heart has stopped again.  I absentmindedly pull the catheter out, and reach across to charge the defibrillator.  Once again, 300 joules of energy course through Donna's body, restoring her pulse.  

Seconds after the shock is in, I look down at the site where I had tried to start the IV.  Venous blood oozes from the small hole.  I had been in.  Lack of venous pressure probably prevented the flash chamber from filling up.  It's a stupid mistake.

I grab the phone and give a quick report to the waiting team.  "Hi, we're enroute to your facility with a 58-year old female patient, initially alert and oriented and complaining of fatigue.  She had a low room-air sat, congested lung sounds bilaterally, and was pale and diaphoretic.  Her 12-lead showed a large anterior STEMI.  She went into v-fib arrest about 7 minutes ago, we've converted her twice, we're five minutes out."  Hopefully, they'll activate the cath lab team.

I go back to looking for a vein to start an IV in when her heart stops a third time.  Again, we send electricity through her body, arcing her back off of the stretcher.  

"Owwww," Donna says, pulse restored.  "You're hurting me!" She groans, and claws at the mask of the BVM.  When MTM pulls the mask away momentarily, she pulls the nasal airway partially out of her nose.  I take it the rest of the way out.

"Donna," I tell her, "Your heart stopped, we need to help you breathe with this mask."  It's no use.  She rolls her head from side to side to avoid the ambu-bag, and pushes it away from her face.

"Fine," I say to MTM, "Leave the BVM connected to the oxygen and put her on a non-re-breather."  It's more important for her to get high concentration oxygen than positive pressure ventilations if she's breathing adequately.

With that, we pull into the ER parking lot.  When I pull the stretcher out of the truck, I realize just how ridiculous this is going to look: a cardiac arrest patient is being brought into the ER with no tube, no lines, no airway adjunct, not being bagged, no compressions being done.  The only intervention immediately apparent is that we've put her on an oxygen mask.  In fact, as we wheel her into the trauma room to the waiting team of doctors, nurses, aides, respiratory therapists, and med students, I hear somebody let out a disappointed "oh...".

I give my report to the ER team, and make sure the 12-leads and rhythm strips make it into the hands of the cardiologist from the cath lab.  I write my narrative on the run report.  She goes back into cardiac arrest twice, and is converted twice.  We leave.

Was it a cluster-fuck?  Sort of.

Would I do a lot of things differently if I had to do it again today?  Definitely.

Did she survive to hospital discharge?  Yes.  

And that's all that really matters, right?

Let's put this one to rest...

Para-myth #472: Giving Albuterol to someone in congestive heart failure (CHF) will cause an increase in pulmonary edema

"The Rhode Island protocols are terrible," my partner tells our patient, a nurse.

"Why?" I ask, "I think the BLS protocols are great."

In Rhode Island, EMT-Bs have a wide scope of practice that allows them to deal with a number of situations without the need for ALS.

"Well, for example, Albuterol is in the CHF protocols.  Albuterol will kill someone in CHF.  When I showed that to my medic instructor in Massachusetts, he just laughed."

I roll my eyes.  "I've had this debate before," I tell him.  "Why do you think that Albuterol kills people in CHF?"

"The wheezing you hear in CHF is from compensatory bronchoconstriction.  It's the body's defense mechanism, and it prevents edema from filling up the lungs.  Albuterol opens up the airway and increases the negative pressure in the lungs that draws in each breath, and also helps draw fluid into the alveoli."

It's a new one.  In the past I've been told that albuterol opens up the upper airways, directly creating more space for fluid to fill the lungs, or that albuterol is bad because it allows fluid to return to circulation before the fluid overload problem has been resolved.  Either way, I've been laughed at for suggesting that albuterol might not really be that bad, and yet I've never been given a satisfactory mechanism through which it kills all the victims of the terrible Rhode Island congestive heart failure protocol.  

The first thing I did was look up the contraindications to albuterol through epocrates on my iphone.  This is what I found:

While neither pulmonary edema nor CHF is listed as a contraindication or caution to albuterol administration, many common CHF comorbidities–ischemic heart disease, hypertension, arrhythmia, diabetes, and old age- are.  Nonetheless, I point this out to my partner:

"If albuterol were really so terrible for CHFers, don't you think CHF or pulmonary edema would be listed as a contraindication in the drug insert?"  I ask him.

"I don't go by drug inserts," he tells me.  I wonder what he does go by.

Well, after some debate, and being told that I've forgotten my anatomy and physiology, I'm still not satisfied, so when I go home I surf over to pubmed to see what I can find.  I type in "albuterol" and "congestive heart failure" and am happy to see the first result: 

Maak A, Tabas J, and McClintock D.  Should Acute Treatment with Inhaled Beta Agonists be Withheld from Patients with Dyspnea Who May Have Heart Failure? Journal of Emergency Medicine.  2008 (published online before print)

This paper is a meta-analysis of 24 different studies on the effects of beta-agonists, including albuterol, in patients with heart failure.  Here are some interesting points:

• Many patients with chronic heart failure who do not have COPD as a comorbidity still have an airway obstruction problem–"cardiac asthma"– that results from CHF directly.  When bronchial vessels become congested, edema of the airway wall occurs, much as pulmonary edema occurs when pulmonary vessels become backed up.  The plasma that causes the edema also brings with it paracrine cell-signaling molecules that are bronchoconstrictors, and further cause upper airway swelling.  

• We know that albuterol decreases bronchial edema, but in animal and human trials, it has also been shown to increase fluid clearance from the alveoli themselves.  In one sheep study, nebulized salmeterol, another beta-2 agonist, decreased pulmonary edema by 60%.  

• 20 human studies demonstrated a 13-51% reduction in systemic vascular resistance after administration of beta-2 agonists in heart failure patients.

• While the beta-1 effects of albuterol might be concerning when treating a patient in heart failure or with a suspected MI, one study showed that 31 patients suffering from MI and cardiogenic shock improved hemodynamically when administered albuterol, and none developed worsening ischemia.  Two other studies found similar results in patients with left sided failure. In other words, the benefit derived from decreasing cardiac workload indirectly by decreasing respiratory effort outweighs any increase in workload caused by increased heart rate or contractile force.

• Chronically administered inhaled beta-2 agonists have been associated with increases in mortality, incidence of dysrhythmias, and hospitalization for CHF in heart failure patients.  Despite the trend, the causal link is unestablished.  

• The authors were unconcerned with the possibility of pulmonary edema when acutely administering beta-2 agonists to CHF patients.  They were more concerned with the possibility of dysrhythmia secondary to beta-2 agonists' induction of hypokalemia, or low potassium.  However, no link was found between inhaled beta-2 agonist use and an increase in incidence of dysrhythmia in heart failure patients.

I'm not saying that my next CHF patient is going to see me walk into the room with an albuterol bullet in hand; they won't.  But, if after a nitro or two and some Lasix, I hear wheezes in the upper fields, I certainly won't worry about albuterol causing a biblical-lung-flood.  And if I'm debating the cause of a patient's dyspnea, it's good to know that albuterol may help, even if left ventricular failure is to blame.  

I was going to print out a copy of this paper to show to my partner, but then I remembered what he told me– "I can get a study to say anything."  Good thing he's got all those anecdotes and that in-depth understanding of A&P to rely on.