I’ve read many opinions over time about which EKG leads we should be monitoring and I’d concluded that my best 3 to monitor are II, aVL & aVF as the 3 that give the best all around picture of what’s going on. I’ve seen many medics that have their lifepak 12 set to monitor II, III and aVF which basically only gives you an inferior wall view, probably not a good thing to work with a blind spot like this. Along comes this article in JEMS and now I think I may have found the elusive perfect lead. Although it’s been around quite a while, its use in the prehospital setting seems to be virtually unheard of. I quote the important stuff below:

A New Lead
The modified lead MCL-1 (originally called CL1) was introduced in 1968 – To run this lead, you keep the limb leads RA and LA in their standard position and place the LL electrode on the V1 position (the fourth intercostal space just at the right sternal border.) Select lead III on the monitor, and you’re now viewing lead MCL-1.

This configuration of leads gives a clear chest for cardioversion and defibrillation, and chest auscultation will also be easy. Lead MCL-1 closely resembles V1, so it offers many diagnostic advantages over lead II:

• MCL-1 is the best lead for differentiating V-tach from SVT with bundle branch blocks.
• You can immediately tell right from left ventricular ectopy.
• In most cases, right and left BBB can be recognized.
• Sometimes, P waves can be seen better.
• See the rest here

I have a Philips MRx 12 Lead monitor and the 3 lead cable has a 5th cable marked V. This allows me to monitor any V lead including v4r if I’m so inclined

GOOD TO KNOW, to say the least!

(RELATIVE) CONTRAINDICATIONS:

• Cardioversion is unlikely to be successful and may be harmful in dysrhythmias due to enhanced automaticity (i.e. digoxin toxicity) because a homogenous depolarization state already exists
• Cardioversion is usually not only ineffective but is associated with a higher incidence of post-shock VT/VF.  Medications are usually more effective than cardioversion to control the rate/convert the rhythm.

I came across this great article focusing on ECG differences seen with pediatric patients. This is quite important to really know as something as simple as a normal PR interval for an adult could signify a AV block in a child.

Electrocardiogram (ECG) interpretation usually is taught in courses that focus on adults. For those who work in pediatrics, identifying appropriate parameters for infants and children is important. This article focuses on the differences between an adult and child’s ECG, differences in common arrhythmias (also called dysrhythmias), and unique treatment approaches to arrhythmias in children.

See complete article here: http://findarticles.com/p/articles/mi_m0FSZ/is_3_27/ai_n18612073/

This chart sums some of it up:

Posted by Unit 122

http://www.wgrz.com/news/local/story.aspx?storyid=79101&catid=37

Very interesting, I had someone this week who was .17, and the cop vehemently disallowed an on scene assessment in favor of rushing the patient to the station to do the breathalyzer so he could nail him on the DWI.

The call was an MVA with a significant MOI involved, and the officer was clearly wrong from a medical standpoint – the front end of the car was obliterated, and a full C-spine was called for. This law makes sense beyond the obvious legal ramifications since it gives medics leverage over any other responding entity who has interests other than patient care in mind. A simple blood draw can ensure that the law-enforcement side of things are covered, and we can then focus on patient care having taken care of the BAC issue.

However, I believe that this would need to be approved by the agency Medical Director, since REMAC protocols only currently indicate blood drawing on standing orders by Cyanide/Smoke Inhalation before Hydroxocobalamin (yes, that was a test question). The GOP states that any other blood drawing would be a discretionary decision made by the agency Medical Director.

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In our protocols we have two beta blockers to choose from depending on the patient’s problem. The two are Metoprolol and Labetalol and they are actually quite different in their actions and therefore, their use.

Metoprolol is a selective beta 1 blocker which will specifically block the effects of epinephrine and norepinephrine on the heart. For our purposes this will blunt their chronotropic and inotropic effects thereby reducing CO and blood pressure. Additionally Metoprolol also has been shown to reduce the incidence of post MI arrhythmias.

Labetalol on the other hand is a non-specific beta blocker and also has alpha 1 blocking effects. This alpha blocking effect would make it specifically useful for lowering a high DIASTOLIC pressure as that number is driven primarily by peripheral vascular resistance.

Our protocols allow for Metoprolol is cases of ACS/MI and allow for either one in cases of hypertensive crisis and CVA with associated hypertension. We also can use nitroglycerin in the latter two but NTG has more of an effect on the veins (preload) than the arteries (afterload). I imagine that the choice would be based on whether its the systolic or diastolic that is really high.