Emergency Medicine and Firefighting

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There is quite a lot to be said about the medications we use for patients with arrhythmias. It’s easy to get lost as to what drugs do what and how, but thankfully there was a kind enough person by the name of Vaughan Williams, who actually broke them down into separate classes. Each class effects separate parts of the cardiac cycle, ultimately changing the electrical current of the heart.

Cardiac Action Potential

Before looking at the medications, we have to understand the cardiac cycle and how it actually works.

Source: x

The above chart presents the four phases of an action potential in a ventricular myocardial cell and how the electrolytes are used to cause the depolarization and repolarization of myocardial cells.

Phase 0  begins with a slight influx of sodium until it passes the potential threshold. Once past the threshold, more sodium channels will open and flood the cell, causing it the depolarize.

Phase 1 is an efflux of potassium from the cell, causing the cell to reach 0mV.

Phase 2 happens at this point. This is when calcium influx happens, prolonging the repolarization period. This period also goes by the name of an absolute refractory period for the cell, since it cannot depolarize during this time.

Phase 3 Calcium channels close again and potassium continues to efflux from the myocardial cell until the internal cell voltage returns to -90mV. Majority of potassium channels then close and the heart enters phase 4, which potassium is allowed to continue to leak into from the cell.

This process happens anywhere from 60 to 100 times per MINUTE!

Vaughan Williams Classifications

The major purpose of the medications in this class effect they way the cardiac action potential works in the cells of the heart. The drugs usually help to slow down specific phase to the heart and allow the heart to fix itself a bit.

Class I - Sodium Channel Blockers

These medications are designed to disrupt phase 0, causing a prolongation of it. There are 3 subcategories (a,b,c) that are broken down into moderate, weak, and strong.

This article won’t go into great depths, but the major goal of the class is to prolong the QRS complex and prolong or shorten QTi.

Medications include:

Lidocaine

Verapamil

Procainamide

Propafenone

Class II - Beta Blockers (-olol or -alol)

Quite commonly used out of hospital for patients with hypertension, beta blockers are actually a common antidysrhythmic. The basic pharmacology is: by blocking the beta-1 receptor sites, it prevents stimulation of the cardiac muscle to beat faster. The increase of sympathetic tone will decrease the rate the heart will beat.

Medications include:

Propranolol

Metoprolol

Carvedilol

Class III - Potassium Channel Blockers

Similar to the Class Ia medications, potassium channel blockers are used to prolong APD, which can cause a prolongation of ERP. This class of medication is commonly known to treat different ventricular dysrhythmias (Vtach or Vfib). The most common medication for this class is Amiodarone and deserves a post of its own.

It’s most common use is during CPR, when the patient is in pulses Vtach or Vfib rhythm and is then followed by a drip with ROSC is achieved. An important note to make about Amiodarone is it can take 16 weeks to leave the system.

Medications include:

Amiodarone

Sotalol 

Ibutilide

Class IV - Calcium Channel Blockers

Commonly uses for Afib with RVR and PSVT, a calcium channel blocker will prolong phase 2 of the action potion in the cell. The goal is to slow the conduction through the atrioventricular (AV) node, slowing the ventricular tachycardia that is occurring. By prolonging the ERP in the AV node, the heart is able to regulate the rate better.

Calcium channel blockers are commonly prescribed by physicians to assist in the care of such arrhythmias. One side effect of these drugs is it may drop the patient’s BP, so ensure you have an SBP >100 or a MAP >65, prior to administering the medication

Class V - Others

This is the mix bag class. These drugs do not truly fit in any category but are still highly important to mention anyways. Two of these medications are Adenosine and Digoxin.

Adenosine prevents the re-entry of a signal in a sinus rhythm, preventing SVT. A warning though is for patients that have WPW syndrome may cause an increase in heart rate instead, so make sure you’re reading the rhythm correctly.

Digoxin effects vagal tone and is seen less as an emergency drug and more as a maintenance drug for chronic heart issues. A major issue with this drug is it holds a very narrow therapeutic index. Toxicity is quite possible if given too much.

Summary

Each class works in its own way on the action potential in the cardiac conduction system. How they affect the heart greatly determines when and how the medication should be used in different medical scenarios. The point of this article is to help a bit with the pharmacodynamics involved with the medications and to hint at the situations a person in the medical field would use them?

Remember to check out my facebook page. Feel free to send suggestions for possible article ideas, it might pop up some time. Always remember that medicine is an art, just as much as a science.

Handoffs occur in trauma care all the time. EMS hands the patient off to the trauma team. ED physicians hand off to each other at end of shift. They also hand off patients to the inpatient trauma service. Residents on the trauma service hand off to other residents at the end of their call shift. Attending surgeons hand off to each other as they change service or a call night ends. The same process also occurs with many of the other disciplines involved in patient care as well.

Every one of these handoffs is a potential problem. Our business is incredibly complicated, and given that dozens of details on dozens of patients need to be passed on, the opportunity for error is always present. And the fact that resident work hours are becoming more and more limited increases the need for handoffs and the number of potential errors.

Today, I’ll look at information transfer at the first handoff point, EMS to trauma team. Some literature has suggested that there are 16 specific prehospital data points that affect patient outcome and must be included in the EMS report. How good are we at making sure this happens?

An observational study was carried out at a US Level I trauma center with video recording capabilities in the resuscitation room. Video was reviewed to document the “transmission” part of the EMS report. Trauma chart documentation was also reviewed to see if the “reception” half of the process by the trauma team occurred as well.

Here are the factoids:

A total of 96 handoffs were reviewed over a one year period

The maximum number of data elements in the study was 1536 (96 patients x 16 data elements)

The total number “transmitted” was 473, but only 329 of those were “received.”

This is not quite as bad as it seems, since 483 points were judged as not applicable by the reviewers. However, this left 580 that were applicable but were not mentioned by EMS.

Of the 16 key elements, the median number transmitted was 5, with a range of 1-9.

This sounds bad. However, the EMS professionals and the physicians have somewhat different objectives. EMS desperately wants to share what they know about the scene and the patient. The trauma team wants to start the evaluation process using their own eyes and hands. What to do?

Bottom line: EMS to trauma team handoffs are a problem for many hospitals. EMS has a lot of valuable information, and the trauma team wants to keep the patient alive. They are both immersed in their own world, working to do what they think is best for the patient. Unfortunately, they could do better if the just worked together a bit more.

Tomorrow I’ll share a solution to the EMS-trauma team handoff problem.

Reference: Information loss in emergency medical services handover of trauma patients. Prehosp Emerg Care 13:280-285, 2009.

Formation of Clubbing

Respiration Rate and Blood pH