Curbside to Bedside

Refusal Heuristic Traps:

How to avoid heuristic traps:

Competency Vs Capacity:

Competency is a global assessment and legal determination made by a judge in court. Capacity is a functional assessment and a clinical determination about a specific decision that can be made by any clinician familiar with a patient’s case.

How does a patient demonstrate capacity?

Dastidar, J., 2011. How Do I Determine If My Patient Has Decision-Making Capacity?. [online] The-hospitalist.org. Available at: [Accessed 23 January 2021].

Karlawish, J., 2021. Uptodate. [online] Uptodate.com. Available at: [Accessed 23 January 2021].

McCammon, I., 2002. [online] Arc.lib.montana.edu. Available at: [Accessed 23 January 2021].

Selde, W., 2015. Know When And How Your Patient Can Legally Refuse Care - JEMS. [online] JEMS. Available at: [Accessed 23 January 2021].

Joined by Peter D. Akpunonu, MD, Haedan Eager and Ben Doty, we discuss their recent paper on "Managing the Effects of Riot Control Agents" and throw in a little trivia - and discuss relevant and practical management principles for patients exposed to incapacitating agents.

Don't you wish someone explained what viral load, viral shedding, and all those other words we use loosely when talking about COVID-19? Well.... our guest on this podcast did, and we think you'll really enjoy getting back to the basics, and then some.

Dr. Ryan Mynatt is a practicing PharmD specializing in infectious disease, and like most academics who know anything about anything, he's responses were a little guarded - which is most appropriate right now.

You can view any of his many publications here.

Oh, he's also on Twitter.

Let us know what you think of the podcast...

In this podcast we discuss a gift box of items regarding treatment considerations for reducing aerosol generating procedures. As with the previous podcast, this is a dynamic situation, and the information is not guaranteed to be accurate. Please share your thoughts and what you are doing at your own department. 

Let's start by saying that I am not an expert. But, specific guidance from the CDC for managing these patients is available, but I feel like the dispersal of this information is critical to front line EMS providers.

For links to important sites and to see images of the BVM and ventilator setup, go to curbtobed.com

In this episode we take a new look at the pathophysiology behind tension pneumothorax and how it presents in the real world population, and discuss why we should pause before inserting the needle in the 2nd intercostal space. 

Hyperkalemia Intro

1. Potassium is primarily an intracellular ion responsible for maintenance of the resting membrane potential for normal cell conduction.
2. Serum measured potassium is typically between 3.5 and 5.0 mEq/L.
3. Serum K greater than 5.0 mEq/L is generally considered the threshold for hyperkalemia.
4. Potassium is mostly excreted via the kidneys, and the "classic" hyperkalemia patient is one who has missed several dialysis appointments complaining of paralysis or diffuse weakness.

Causes of HyperK

1. Most commonly, renal failure. 
2. Transcelluar shift 
   1. DKA
   2. Acidosis 
   3. Other acid-base disturbances
3. Medications 
   1. RAAS or ACE inhibitors

Effects of HyperK 

1. Most drastically affect cardiac myocytes 
   1. Conduction between myocytes is depressed, leading to slower conduction and widened QRS complexes, however, the rate of repolarization is increased. 
      1. Leads to ominous “sine wave” pattern on ECG. 
   2. Arrythmogenic 
   3. May produce classic tall, “peaked” T waves on ECG.
2. Stepwise ECG changes in hyperkalemia:
   1. 5.5-6.5 mEq/L - Peaked T Waves
   2. 6.5-7.5 mEq/L - P waves amplitude becomes smaller and PR intervals prolong
   3. 7.5-8.0 mEq/L - QRS becomes wide
3. ECGs are not always sensitive for hyperkalemia. Patients may have a critical K with no changes on the ECG. 
4. Skeletal muscle tissue is also sensitive to hyperkalemia, and patients may present with weakness or paralysis as a result. 
5. Nondescript symptoms such as muscle cramps, diarrhea, vomiting, nausea, and focal paralysis may also be present - but are also not reliable findings. 

Management 

1. Prioritized by a strategy of:
   1. Stabilization of cardiac cell membranes 
   2. Shifting potassium back into the cells 
   3. Eliminating potassium
2. Calcium (Chloride or gluconate) administered to stabilize cell membranes 
   1. Stabilizing effect is transient and relatively short lived 
   2. Calcium Chloride contains roughly 3 times the amount of elemental calcium as compared to Ca gluconate, but is associated with severe complications if extravasation occurs. 
   3. Effects (narrowing of QRS complex, return of more hemodynamic stability) occurs within minutes 
   4. Calcium Chloride - generally, 1 gram is administered over 3 minutes.
   5. Calcium Gluconate - 1 gram over 2-3 minutes 
   6. Repeat either q5min
3. Albuterol / Beta 2 agonists
   1. These act on beta 2 receptors to assist in moving potassium back into the intracellular space 
   2. Albuterol - 10-20mg (inhalation), with most effect noted in 30 minutes 
4. IV Insulin 
   1. Drives K back into the cells (shift)
   2. Generally administered with dextrose unless the patient’s BGL is below 250mg/dL
   3. 10 units IVP followed by 25G dextrose
   4. Incidence of hypoglycemia is high, and this therapy should be administered cautiously
5. Dialysis 
6. Treating reversible cause
   1. d/c RASS or ACE inhibiting medicaitions 
   2. Volume administration

Transporting a sick DKA patient is challenging. Surprisingly, there's a bit more to it than "just" administering fluid and monitoring an insulin infusion.

Read more and find references at curbtobed.com

In our first official “vodcast”, we discuss pearls and pitfalls of transcutaneous pacing, and how it’s much more difficult than “you either have capture or you don’t”.

“Phantom” complexes are rarely reported on or discussed in Paramedic school, but one monitor manufacturer appreciates how they can make verifying true electrical capture very difficult.

The folks over at ems12lead.com have put a lot of work into providing education and spreading the word around the problem of false capture. 

First, there are two proposed mechanisms of CPR, brilliantly summarized in this paper:

“blood is squeezed from the heart into the arterial and pulmonary circulations, with closure of the mitral and tricuspid valves, preventing retrograde blood flow, and opening of the aortic and pulmonary valves in response to forward blood flow. Air is thought to move freely in and out of the lungs, so that the intrathoracic pressures do not significantly rise and the pulmonary circulation is not adversely affected by chest compressions. With the relaxation of chest compression, the heart fills with blood and air passively returns to the lungs.”

“With each chest compression the intrathoracic pressure rises because of the collapse of the airways; the thoracic pump theory. This theory presumes that the rise in the intrathoracic pressures results in collapse of the pulmonary airways, thereby reducing the movement of air out of the lungs and reducing the size of the intrathoracic structures, but not necessary equally. The collapse of venous structures at the thoracic inlet was postulated to prevent retrograde venous blood flow and with each relaxation of chest compressions, the intrathoracic pressure falls with return of venous blood.”

…In patients with an average chest configuration and those with so‐called “barrel chests,” secondary to emphysema or other causes, the lateral chest roentgenogram often shows a significant distance between the anterior chest‐wall and the heart. In such patients it is nearly inconceivable that sternal compressions of the chest during CPR could result in cardiac compression. Rather, the mechanism of blood flow from chest compressions is probably secondary to the rhythmic alterations of the intrathoracic pressure and releases, for example, the “thoracic pump” theory.

A Meta Analysis from Gates et. al. concluded:

Existing studies do not suggest that mechanical chest compression devices are superior to manual chest compression, when used during resuscitation after out of hospital cardiac arrest.

However, if there’s no difference in survival, and it’s not WORSE than manual CPR, why not use it to cognitively offload tasks? Because, it may be worse.

Gonzales et. al. compared “pit crew” resuscitation with “scripted” mCPR implementation and found:

In this EMS system with a standardized, “pit crew” approach to OHCA that prioritized initial high-quality initial resuscitative efforts and scripted the sequence for initiating mechanical CPR, use of mechanical CPR was associated with decreased ROSC and decreased survival to discharge.

We know based off work by Hwang et. al. who showed that standard CPR (inter-nipple line) often results in compression or narrowing of the LVOT or the aortic root. In this study, the area of maximal compression was over the aorta in 59% of patients!

In another study, anderson et. al. used transthoractic echo to mark the location of the aortic root and the left ventricle of animals, and randomized them to receive CPR at one of the two locations. As you can probably guess, aortic systolic and diastolic pressures as well as ETCO2 were higher in the LV group, and 9 of the LV group (69%) achieved ROSC and survived at least 60 minutes compared to none who received chest compressions over the aortic root. 

All of these studies and more are explained in a wonderful video created by Felipe Teran:

The folks at The Ultrasound Podcast also discuss using TEE to guide hand or device palcement for CPR:

Well, we don’t exactly. However, Qvigstad E et. al. published a study in Resuscitation titled “Clinical pilot study of different hand positions during manual chest compressions monitored with capnography.”

They compared how hand positioning at the inter-nipple line (INL), 2 cm below the INL, 2 cm below and to the left, and 2 cm below and to the right affect ETCO2.

They found that there’s not “one superior hand position”, and that optimal positioning varies:

It doesn’t really, but one argument against mCPR, specifically one based off of the cardiac pump mechanism, is that the device is consistent and doesn’t fatigue, yet this might be it’s downfall. It’s postulated, and demonstrated in the above videos that it may just be consistently compressing the aortic outflow tract, and not the left ventricle. 

Poole et. al discuss this in a paper titled: Mechanical CPR: Who? When? How?

In their paper they discuss how the device is frequently deployed early, even before defibrillating the patient. Others

In clinical practice, published literature reports marked variability in the hands-off time during device deployment, with pauses in excess of 1 minute being reported. In the LINC trial, the median reported chest compression pause associated with device deployment was 36.0 s (IQR 19.5, 45.5)

The authors continue and note that…

subsequent improvement in flow-fraction following device deployment meant that the median flow-fraction over the first 10 minutes of the cardiac arrest was higher in the mechanical CPR arm (mechanical 0.84 (IQR 0.78, 0.91) vs manual 0.79 (IQR 0.70, 0.86), p < 0.001). A similar pattern was observed in the CIRC trial.

So it seems that it takes longer to place the device than most think, but once it’s placed the “flow-fraction” is higher with mCPR. Therefore, the reason outcomes are not better with mCPR compared to manual CPR is that the first few minutes matter the most, and we’re stopping CPR to apply the device during the period in which we’re most likely to obtain ROSC.

• Consider applying your mCPR device later in the arrest, rather than sooner
• When performing manual chest compressions, monitoring ETCO2 can help ensure proper hand positioning
• Perform post event reviews using manufacturer software to measure CPR fraction and pauses associated with mCPR application