The Value of LP15 Microstream Nasal Capnography

Tonight I reviewed a case with EMS 5 and M 56 at Sta 19.  The patient, an adult female with asthma, was found by the medic crew to be in severe respiratory distress. As the patient was in extremis, multiple therapies were rapidly administered - including oxygen, a duoneb, epinephrine (1:1000) 0.5 mg IM, and decadron 10 mg IV - as the patient was prepared for a priority 1 transport to the ED.  EMS 5 arrived and an end-tidal nasal cannula was placed on the patient.

As the patient was being transferred from the house to the medic unit, one of the providers ran ahead to prepare the CPAP set-up.  During the transfer to the medic unit, the patient appeared to become slightly less agitated - which could be a good thing but is often a very bad thing (i.e. was the patient's becoming so hypercarbic and hypoxic that her mental status was declining?).  Once loaded in the medic unit the crew was faced with the decision of continuing current treatments versus being more aggressive and attempting to assist the patient with a BVM.

It was at this point that the crew noted a nice correlation between steadily declining ETCO2 levels, improving SpO2 levels, and a slowing of the patient's respiratory rate (again, slowing of the respiratory rate could have been a very good thing or a very bad thing).  Based on a synthesis of this graphic and numerical data and clinical reassessment of the patient, the decision was made to continue nebs, oxygen, and hold off on CPAP or more aggressive measures as it appeared the patient was clinically improving.  Her decline in agitation was actually a sign of clinical improvement.  As the hypercarbia and hypoxemia both improved, the patient's tachypnea resolved and her respiratory effort became less labored.

The trend summary above was printed off the LP15 at the end of the call.

This case highlights a few very important items:

1. The value of a case review

There are so many things that can be reviewed in this one call: the severe respiratory distress protocol, the physiology and pharmacology of asthma, the appearance of a capnography tracing in obstructive pulmonary disease states, indications and contraindications for epinephrine and CPAP, the differential diagnosis of an elevated or depressed end-tidal CO2 level, and the list goes on.  Case reviews should never focus on discipline or fault finding - they should focus on education, discussion of best practice, sharing ideas, personal improvement, and system improvement.

2. Examination of trends

We see this theme throughout our practice of prehospital care.  One 12-lead EKG is usually insufficient while caring for and transporting a patient with chest pain.  We often need to examine serial EKGs to detect dynamic changes.  Similarly, trending this patient's ETCO2 levels and correlating this trend with the other vital data points of respiratory rate and SpO2 was highly reassuring to this crew that their therapies were indeed resulting in clinical improvement.  The amount and clarity of the data that can be obtained from the LP15 'Trend Summary' function is awesome.  Providers should get in the habit of looking at trend summaries with their DOs and correlating the hemodynamic and physiologic trends they observe with the patient's clinical status and the treatments rendered.


3. $6 well spent

A microstream end-tidal nasal cannula costs about 10-times that of a regular nasal cannula (6 dollars vs. 60 cents).  Nasal capnography doesn't need to be placed on every patient's face that requires a nasal cannula.  End-tidal CO2 levels (capnometry) and graphic capnography don't need to be monitored for every patient that requires oxygen.  But in the subset of patients with moderate to severe respiratory distress - be it from an asthma or CHF exacerbation, opioid overdose, severe pneumonia, angioedema, or respiratory distress of unclear etiology - there is clearly a role for nasal capnography in monitoring a patient's response to therapy and to aid in guidance of treatment priorities.


4. Gratification

The trend summary here is an essence a report card with an A+ in patient care.  Every once in a while its nice to know that what we do actually works and makes a difference.  In this case, I am confident that the rapid actions of M 56 and EMS 5 prevented this patient from progressing to florid respiratory failure and the need for intubation.

Job well done and thank you for sharing this case with me.

If you have any good or bad experiences or interesting cases with nasal capnography - please share them with me so I can share them with all of our providers as we begin to insert this tool into our arsenal of mobile life saving technology.

Ventricular Assist Devices (VADs/LVADs/BiVADs/RVADs)

More and more heart failure patients are being discharged from the hospital with ventricular assist devices (VADs).

VAD centers should notify local EMS agencies when a patient returns home with one of these devices to ensure responders are properly trained to deal with VAD-related emergencies.

Given our proximity to two major VAD centers - the University of Maryland Medical Center and Johns Hopkins - Baltimore County EMS providers will undoubtedly encounter patients with these devices with some frequency.

There is an excellent review article entitled "Prehospital Assessment and Management of Patients with Ventricular-Assist Devices" in the journal Prehospital Emergency Care (PEC 2013;17:223-229).

The Mid-Atlantic Regional Pre-Hospital Mechanical Circulatory Support Task Force 2009 Field Guide contains a FAQ sheet and emergency instructions for each of the devices listed below:

HeartWare HVAD
VentrAssist LVAD
HeartMate II
HeartMate XVE
Thoratec PVAD w/TLC II Driver
Jarvik 2000 FlowMaker

This emergency VAD field guide is available through the University of Maryland Heart Center Mechanical Heart and Lung Support home page found at:

http://www.umm.edu/heart/pdf/mechanical-circulatory-support.pdf

EMS 8 Lt. Barshinger coordinates an online training program to familiarize and educate Baltimore County EMS providers on VADs.  Forward your name and email address to jbarshinger@baltimorecoutnymd.gov to register for this online training.

BCoFD Medical Director Notification Re: July 1, 2013 MIEMSS Protocol Changes (TRAUMA ARREST)

On June 10, 2013 the Baltimore County Fire Department EMS leadership staff convened for its bimonthly meeting.  The EMS staff felt that it was very important to clarify some of the contents contained in the 'Trauma Arrest' protocol update:


o Trauma arrest:
• EMS providers can terminate without medical consult when there are no signs of life and the patient is in asystole
• EMS providers can terminate with medical consult
     • Blunt trauma-- when there are no signs of life and the patient is in a rhythm other than asystole with no ROSC despite 15 minutes of EMS CPR and other appropriate treatment
     • Penetrating trauma-- when there are no signs of life and the patient is in a rhythm other than asystole and there is no ROSC
          o If less than 15 minutes from a trauma center, patient should be transported
          o If greater than 15 minutes from a trauma center, provider should consult for orders to terminate

• With both blunt and penetrating trauma when the patient is in a rhythm other than asystole and there are no obvious signs of death, priority should focus on MINIMAL ON-SCENE TIME and RAPID TRANSPORTATION to the receiving trauma center.
• Unless transport is delayed (i.e. an appropriate aviation request with prolonged MSP trooper ETA, heavily entrapped patient), on-scene time should always be kept to a minimum.  On-scene time goal should be always be less than 10 minutes.  Even after extrication (regardless of time required to extricate the patient), the patient should be transported immediately, without delay, and emergency care provided while enroute to the receiving trauma center.
• Blunt and penetrating trauma patients in cardiac arrest without obvious signs of death should be treated and transported rapidly to a trauma center.  Providers should not remain on-scene to perform CPR or any other resuscitative measures for 15 minutes prior to transportation - the patient should be transported immediately and resuscitated enroute to the trauma center.
• Even if 'great than 15 minutes from a trauma center', transport immediately, and resuscitate enroute. 
• Once treatment and transportation is initiated for patients in traumatic cardiac arrest, treatment should be continued to the receiving hospital and care should be transferred to the receiving facility.  Termination of resuscitative efforts during transport should never occur.
• And a reminder: patients with isolated penetrating trauma do NOT require spinal immobilization - they DO require immediate and rapid transportation to the receiving trauma center.
• And finally: when in doubt, obtain a trauma consult.

BCoFD Medical Director Notification Re: July 1, 2013 MIEMSS Protocol Changes (MEDICAL ARREST)

On June 10, 2013 the Baltimore County Fire Department EMS leadership staff convened for its bimonthly meeting and made the following decision regarding EMS field operations as it pertains to medical cardiac arrest:

• With regard to MEDICAL cardiac arrests, all providers must continue to obtain medical consultation prior to termination of resuscitation - even if there is no ROSC despite 15 minutes of EMS CPR and other appropriate treatments - regardless of the cardiac rhythm.
• This Baltimore County EMS specific directive is contrary to the bolded item highlighted in the new July 1, 2013 MIEMSS protocol update copied below.
• The new July 1, 2013 MIEMSS protocol allows the EMS provider to independently terminate resuscitation without consultation after 15 minutes of EMS CPR and treatment for patients that meet the three criteria of 1. arrest not witnessed by EMS provider; 2. non-shockable rhythm (AED) or manual monitor showing aystole or PEA; and 3. no ROSC despite 15 minutes of EMS CPR.  In Baltimore County we will obtain medical consultation at 15 minutes (or sooner based on the clinical situation) for EVERY medical cardiac arrest where termination is being contemplated - regardless of cardiac rhythm.
• Medical consultation prior to termination of resuscitation will help ensure our providers have rendered all appropriate treatments and that the decision to terminate efforts is completely appropriate.  In addition, medical consultation prior to termination of resuscitation in the presence of family members or bystanders often makes the act of stopping resuscitative efforts more acceptable to those parties as it shows we have done everything possible up to and including consultation with a base station physician.
• Termination of resuscitation during transportation of the patient should rarely and probably never occur.  This can be prevented by resuscitating the medical arrest patient in the place they are found and obtaining medical consultation PRIOR to initiation of transportation.
• Baltimore County EMS providers are reminded that "medical consultation may be obtained at any time for any patient".  When in doubt, consult.

The following is copied from the "2013 revisions, updates, and additions to The Maryland Medical Protocols for EMS Providers":
Termination of Resuscitation
o Exclusions: Arrest secondary to hypothermia/submersion, pregnant patient, patient not reached 18th birthday
o Medical arrest:
• EMS providers can terminate without medical consult when all of the following criteria are met
             • Arrest not witnessed by EMS provider
             • Non-shockable rhythm (AED), or manual monitor with asystole or PEA
             • No ROSC despite 15 minutes of EMS CPR and other appropriate treatment
• EMS providers can terminate with medical consult if no ROSC despite 15 minutes of EMS CPR and other appropriate treatment in the presence of a shockable rhythm or an arrest witnessed by an EMS provider

SpMet

The other day a DO called and advised me that SpMet functionality has been added to the LP15 monitors on the cars.  His question was - what is the clinical significance of SpMet?  And away we go . . .

What is methemoglobin (Met-Hb)?  (I am going to abbreviate hemoglobin as Hb here forward)

Met-Hb: an altered state of Hb in which the FERROUS (Fe 2+) irons of heme are oxidized to the FERRIC (Fe 3+ state).  (The heme portion of the Hb molecule is were oxygen binds).

FERRIC Hb CANNOT bind oxygen.

When there is a lot of FERRIC Hb around, the remaining 'good' FERROUS Hb has a HIGHER affinity for oxygen - that is - the remaining 'good' Hb will not let go of the oxygen it is carrying and oxygen delivery to the tissues is further impaired (if you have studied human physiology, this results in the oxygen dissociation curve shifting to the LEFT).


What is the net effect of Met-Hb formation (increasing Met-Hb levels compared to normal Hb) in the bloodstream?

The patient becomes functionally anemic.  Oxygen delivery to the tissues and organs becomes even more impaired in that the remaining 'normal' Hb won't let go of the oxygen it is carrying.

Do normal healthy individuals produce Met-Hb?

Yes.  We auto-oxidize some of our Hb (from ferrous to ferric form) every day and maintain a steady-state level of about 1% Met-Hb.

What is the disease state know as methemoglobinemia?

There are actually 2 types of methemoglobinemia: CONGENITAL and ACQUIRED.

What is congenital methemoglobinemia?

As the name implies, it is a genetic disease - the patient is born with the condition.  In congenital methemoglobinemia the patient can have Met-Hb levels as high as 40% (of total Hb).  Most of these patients, despite having a high SpMet reading will be asymptomatic.  They may have a headache or complain of easy fatigability.  These patients will be chronically cyanotic (bluish discoloration of the skin and mucous membranes).

What is acquired methemoglobinemia?

This is what we are on the look-out for.  It is a rapid increase in Met-Hb levels.  Oxygen binding and oxygen delivery to the tissues is acutely impaired and the patient becomes rapidly cyanotic and symptomatic.  Early symptoms include headache, fatigue, dyspnea, and lethargy.  As Met-Hb levels rise, respiratory depression, decreased LOC, shock, seizures, and death can occur.

What medications or exposures can cause (acute) acquired methemoglobinemia?

• Benzene derivatives: common industrial chemical, also a principal product of combustion of PVC (polyvinyl chloride)
• Chloroquine: a drug used for malaria treatment and prophylaxis
• Dapsone: a drug used to treat PCP pneumonia (which primarily affects patients with HIV/AIDS),
• Local anesthetics (benzocaine, lidocaine): 
• Metoclopramide (Reglan)
• Napthoquinone: found in diesel exhaust particles
• Napthalene: was once the primary ingredient in moth balls
• Nitrites
• Amyl nitrite: component of the Lily Cyanide antidote kit, abused as "poppers"
• Nitroglycerin: an old friend
• Nitric oxide: this is NOT nitrOUS oxide = laughing gas; nitric oxide is used mostly in the ICU setting for patients with severe pulmonary hypertension and ARDS in the setting of right ventricular failure
• Phenacetin: used to be a component of Vicks, used to be sold in pill form as an anti-pyretic, US FDA ordered the drug to be removed from all substances in 1983 due to carcinogenic and kidney damaging properties
• Phenazopyridine: aka Pyridium - a urinary tract analgesic
• Primaquine: a drug used to treat PCP pneumonia and malaria
• Sulfonamides: most medications with contain 'sulfa'

OK.  So that is a long list.  What are some examples of typical clinical scenarios where I might encounter a patient with acute/acquired methemoglobinemia?

Here are a few clinical examples: 

1. You are dispatched to a local urgent care center where a patient has developed acute onset respiratory distress.  The patient presented to the urgent care center 30 minutes ago with complaints of a sore throat and fever.  The patient did not have any respiratory distress.  The doctor discovered an abscess on the right tonsil.  He arranged for the patient to be transported by private ambulance to the University Medical Center for drainage of the abscess by an ENT physician.  Up to this point, the patient was not having any respiratory distress whatsoever.  In the meantime, in an effort to make the patient feel better, he sprayed the back of the oropharynx with Hurricaine Spray.  Within a few minutes the patient developed generalized cyanosis, respiratory distress, and decreased LOC.

2. The mother of a 27-year-old HIV positive patient calls 911 after she finds her son unconscious on the couch in his downstairs apartment.  He was recently started on all of his HIV medications 4 weeks ago after being discharged from a local hospital where he was treated for pneumonia.  He has been on Truvada, Kaletra, zidovudine, dapsone, and azithromycin for only the past 4 weeks.  His skin is cool, he appears pale with some bluish discoloration about his lips and fingers, and he is minimally responsive.  Room air Spo2 is 86%.  SpMet is 14%.  SpCO is 21%.  Upon starting an IV, the paramedic comments that the blood has a 'chocolate' appearance.  Even after the 100% NRB face mask was on the patient's face for 10 minutes, the Spo2 still read 86%.  An engine crew is called to evaluate the elevated SpCO reading and gets no CO readings on their meter.  The mother who lives in the home has no symptoms.

A few caveats about SpMet on the LP15 monitor:

SpMet levels > 20% are associated with clinical symptoms.  However, the SpMet measurement range on the LP15 Masimor Rainbow sensor is only 0-15%.  It is normal to have an SpMet reading of 1-2%.  Anything above 3% with the right clinical scenario, drug exposure, or toxic exposure is abnormal and should heighten your suspicion for methemoglobinemia.  Very sick patients can have as high as 40-70% Met-Hb in their blood - but again - the SpMet probe will only read up to 15%.

Elevated SpMet levels can give you a FALSE HIGH SpCO level.  The LP15 SpCO measurement range is 0-40%.  A CO meter can be used to verify absence of detectable atmospheric CO readings.  Again, you need to use common sense here and look at your environment and the clinical situation.  A patient at an urgent care center in a confined space small examination room surrounded by multiple asymptomatic care givers who is turning blue and did not have respiratory complaints a few minutes ago probably has methemoglobinemia and not CO toxicity.

Elevated SpMet levels can give you FALSE LOW SpO2 level.  It is very common for the SpO2 to sit in the mid 80% range and not change with O2 administration.  The bottom line - give all of these patient's high flow oxygen.

Is there anything we can do to treat suspected methemoglobinemia in the field?

ABCs.  High flow O2 +/- intubation.  IV.  ECG.  SpO2.  SpMet.  FS.  Good history.  Get med list. Consult.  Communicate your suspicion during consultation.  Rapid transport to the ED.
Think about at risk patients and the more common offending drugs: HIV, travel to areas with malaria, industrial chemicals, dapsone, sulfa drugs.
It is important to try to identifying and remove the patient from the offending agent (this is where your history and observation of the scene will be important).
Try to get an updated and accurate list of medications (including over the counter meds) as this will often contain the offending agent.
Rapid transport to the ED (for definitive treatment with administration of methylene blue 1-2 mg/kg IV).

Am I ever going to see this?

In an article from JAMA (April 2013) the overall prevalence of methemoglobinenmia during or after hospital procedures was only 0.035%.  The medical literature is dotted with case reports of methemoglobinemia in every age group with every type of exposure I listed above.  Masimo has the following bold statement on its website:

"Acquired Methemoglobinemia is fairly common and causes morbidity and mortality in both the inpatient and outpatient settings. Acquired methemoglobinemia is often unrecognized and thus untreated."

Dr. Rachel Ash-Bernal
and other researchers at Johns Hopkins Hospital

Acquired methemoglobinemia is probably not as common as Masimo would like you to think it is.  The statement is correct, however, in that you have to have your feelers up for this condition when you respond to a doctor's office, outpatient surgery center, or any health care facility as it is more likely to occur in these settings.

Man v Machine

A few volunteer medic units around Baltimore County have purchased mechanical chest compression devices.  There are two types of mechanical devices available: load-distributing band CPR devices (LDB-CPR) and piston-driven CPR devices (PD-CPR).

Example of LDB-CPR device: AutoPulse (Zoll Medical Corporation)

Example of PD-CPR device: LUCAS (Physio-Control Inc.)   

Manual CPR - the old fashion way - using you hands - is denoted by the abbreviation M-CPR.

Station 500 Chestnut Ridge Volunteer Fire Company has had a LUCAS device in-service aboard Medic 505 for over a year (pictured below).  If Engine 501 first responds to a potential or actual cardiac arrest for a career medic unit - the engine crew grabs the LUCAS device as they roll out the door.  The device rapidly and easily clips onto a small board placed behind the patient's back, has velcro straps to secure the patient's hands, and can be easily loaded with the patient onto a backboard or Reeves stretcher.  Mechanical compressions can be started and stopped with the push of a button.  The device is light-weight and battery powered.  The rechargeable lithium-ion battery can run about 45 minutes.  A spare battery is usually packaged with the device.  When not in use, the LUCAS charges on a shelf in the medic unit.  Specs for this device can be found on Physio Control's website.

Mechanical CPR (LDB-CPR and PD-CPR) devices provide the following benefits:

• More effective and consistent CPR (consistent rate, depth, position)
• Machines do not fatigue
• More consistent compression recoil (upstroke phase of chest compression cycle)
• Defibrillation can be performed without stopping mechanical chest compressions
• Reduce risk of injury to EMS providers during transport to the hospital (i.e. no standing in the back of the medic unit responding priority 1 to the hospital)

High quality CPR is the catch phrase of the year in EMS systems around the US and something that our EMS leadership in Baltimore County is keenly interested in seeing become the standard of care.  

The fundamental concept of high quality CPR is uninterrupted, proper rate and depth compressions with little to no pause immediately before and after shocks and around pulse/rhythm checks.  Other skills during the course of resuscitation like intubation and IV insertion should ideally be performed without any interruption in the delivery of compressions.

This month in the journal Critical Care Medicine, Westfall et al published a study entitled, "Mechanical Versus Manual Chest Compressions in Out-of-Hospital Cardiac Arrest: A Meta-Analysis".  The study looked at the likelihood of obtaining return of spontaneous circulation (ROSC) in patients treated with manual compressions compared to those treated with mechanical CPR.  A total of 12 studies comprising of 6,538 subjects with 1,824 ROSC events were included in the analysis.

It is important to note that ALL of the four authors of this study either work for, consult for, or have received grants from Zoll (manufacturer of the AutoPulse).

When manual (M-CPR) compressions were compared with BOTH types of mechanical devices (LDB-CPR + PD-CPR devices) there was a significantly increased odds of ROSC when using mechanical CPR devices.  The odds of ROSC were significantly better (in this meta analysis) with LDB-CPR type devices (like the AutoPulse) as compared to the PD-CPR type mechanical devices (like the LUCAS).

There is NO analysis of neurologic outcomes in this study.  Furthermore, the authors conclude that these findings need to be validated in larger randomized controlled clinical trials.

The bottom line - mechanical devices cost money.  The money trees remain elusive.  It would be nice to see these devices on all eight of our DO vehicles.  In this man v machine meta analysis - machine wins.

But we humans can strive to be high quality CPR machines!

We need to focus our efforts on learning and rapidly implementing high quality manual CPR.  Members of Baltimore County's EMS Division recently attended a Resuscitation Academy at the Howard County Fire Rescue Academy jointly sponsored by Seattle Medic One.  This two day conference focused on every aspect of high quality CPR from dispatch directed CPR, to the actual performance of the resuscitation by EMS providers, to data collection, and even touched on caring for the patient's family during and after the arrest.  

Please look for more information on how Baltimore County Fire Department is implementing these high quality CPR initiatives in the next few weeks and months.

  

Win big on the strip

Time sensitive metrics are receiving increasing attention and scrutiny in Baltimore County and EMS jurisdictions throughout the country.  It is expected that we will detect STEMIs immediately, transmit a 12-lead ECG to the hospital within minutes of arrival at the patient's side, and deliver the patient to a cardiac intervention center priority 1 all while getting an IV established and completing a host of other tasks while going down bumpy roads backwards at high rates of speed.  Then there is the 'Golden Hour' of trauma care, the 3.5 hour 'window' for tPA in ischemic stroke, time to first shock for VF/VT arrests, and the list goes on.  There is so much to do and so little time to do it.  But we do.  And we love it.

In the rush to perform all of these tasks and utilize all of the technology floating out of the hospitals into our medic units (12-lead ECGs, video laryngoscopes, EZ IO drills, capnography, etc), we have to remember what is at the center of all of this excitement . . . .  the PATIENT.  

As many of you know, I have an enormously bushy squirrel tail.  I was driving home one night up 83N after a long shift in the ICU.  EMS 1, Engine 17, IV 395, and Medic 475 were dispatched for a medical box aboard an MTA bus in the Timonium area as I approached the Timonium Road exist on 83N.  Unable to resist the urge, I switched to central and called enroute.  EMS 1 beat me to the scene and was already in the bus assessing the patient when I arrived.  What I witnessed next was something I see less and less of these days.  EMS 1 was kneeling over the patient in the center isle of the bus, talking to the patient, and examining the patient.  He was NOT immediately hooking the patient up to the cardiac monitor, placing an Spo2 probe on his finger, or peeling back a shirt sleeve to look for an IV.  He was actually examining the patient - looking, listening, palpating - human contact.

So I'm as guilty as the rest of you.  When a patient gets rushed into my ICU from the general medical or surgical floor crashing and burning, I grab my glidescope and ultrasound and get suited up to insert lines and tubes all while the nurses attach the patient to an array of bedside monitors.  The exam often gets squeezed between necessary procedures and a detailed examination often gets pushed back until well after the patient has been stabilized.  Sometimes priorities like the need to establish an airway get in the way - but more often than not - the ABCs are OK and we can actually leave the monitor and pulse oximeter alone for a minute, talk to the patient, examine the patient, and use the oldest tool in EMS - our hands.

Bottom line - technology is great. It saves lives, it makes our job more interesting, and often gives us important information to guide care and to aid with making clinical decisions.   But we need to pause, put our hands back on our patients and get back to fundamentals - we need to revisit the lost art of the physical examination.  I'm not even going to get into the kumbaya side of the reassurance and compassion of a human touch - I will leave that training to you and your DO (or not). 

I recently conducted a case review in the Western Battalion that I would like to share with all of our providers.  A medic unit was dispatched in the early afternoon for reports of a 67-year-old woman with trouble breathing.  The crew arrived to find the women seated upright, in mild distress, with complaints of recent vomiting and feeling dizzy.  The patient also reported having syncope a few days prior - the cause of which was not known.  The patient denied chest pain, shortness of breath, and abdominal pain.  The GCS was 15.  Initial VS were BP 98/70, HR 110/min, RR 22/min, Spo2 96% on room air.  Finger stick glucose was 223 mg/dL.  The care plan read like so many of our emeds reports do: "O2, IV LR, monitor".  No medications were listed on the emeds report and a brief medical history including "gastric reflux, lupus, chronic fatigue, and syncope" were listed.  The patient was bolused 500 cc LR enroute to the hospital.  The crew reported that enroute to the hospital the patient felt better, skin color improved, and the patient became more alert.

Here is the 12-lead ECG that was obtained:

How do you think this ECG was interpreted?  How did you interpret it?  If you're not sure what the rhythm is - is there anything else you can do to aid in interpretation?  How might simple physical examination skills aid in making the diagnosis?

The patient was transported priority 2 to the ER and transferred to hospital staff without incident.  Review of the emeds report and ECG by the DO a few days after the incident resulted in this case being brought to my attention for review with the provider.

Where did this seasoned ALS provider go wrong?  Aside from the "O2, IV, monitor" and LR bolus - should anything else have been done for this patient?  

How could a basic EMT with only their hands have saved this ALS provider and helped clinch the diagnosis?

I look forward to your comments and will post the conclusion to this case shortly.

CONCLUSIONS:

1. Quick glance at this 12-lead ECG might lead the provider to think they are looking at a normal sinus rhythm with low voltage and an occasional PVC.  The P-waves do indeed march out at a rate of about 90/min.  However, none of these P-waves are followed by QRS complexes.  The QRS complexes that do appear do not communicate with the P-waves.  Thus, this is complete (3rd degree) heart block.

2. Usually a 12-lead ECG will give you much more information than a simple rhythm strip.  However, in this case, a longer rhythm strip would have probably made it easier for the provider to see the QRS complexes marching out independent of the P-waves.  Simply looking at a continuous lead display (i.e. lead II) on the LP15 is less ideal than printing out a 10-15 second strip.

3. Never underestimate the importance of the basics.  Always take your patient's pulse manually.  As some of you astutely pointed out - actually palpating the patient's pulse should have clinched the diagnosis of complete heart block (as only the profoundly bradycardic ventricular beats should have generated a palpable radial pulse).  It is unlikely but remotely possible that the regularly occuring atrial activity might have generated a faint carotid pulsation.

4. Pacing/debrillation pads should have been applied to the patient's chest so that transcutaneous pacing could be initiated immediately had the patient become hemodynamically unstable.

5. While atropine often does not work in complete heart block, 2013 protocols state that it may be considered after medical consultation for Mobitz type II AV block or 3rd degree (complete) AV block.