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:

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.

(Hat tip Medic 122)

An explanation I found….

Because the aortic valve is tight/stenosed, it restricts the amount of blood being ejected from the ventricle. With nitro (and most other drugs that effect peripheral resistance) the peripheral vessels will dilate. A normal ventricle would be able to ‘relax’ a bit because peripheral resistance is lowered and the heart’s work-load is lessened. However, in aortic stenosis, the afterload (pressure the heart beats against) isnt being dictated by peripheral resistance, but rather the stenosed valve. This stenosed valve is unaffected by nitro (or any other drug) and so the hearts work-load (and amount of ejected blood) stays the same…regardless of nitro/drugs/less peripheral resistance. Giving this patient nitro/drugs can become a big problem because if you dilate out the vessels, and the the restriced cardiac output does not change, you drop your ability to perfuse even more…(you take a hose and turn it on to ‘perfuse’…but when you suddenly dilate/widen the hose while keeping the water supply constant, your pressure will drop…as well as your ability to perfuse…)

This is why people become syncopal and (with pre-existing coronary disease) will experience angina…

Can anyone tell me what this EKG is? Vfib in lead II and NSR in lead III? Checked all leads and no patient movement.

Patient was an 87 y/o female nursing home patient, unresponsive in respiratory failure secondary to pneumonia.

Great article here: http://ems12lead.blogspot.com/2008/11/transcutaneous-pacing-tcp-problem-of_15.html

Some highlights from the end:

Here are some clinical pearls to get you through the procedure.
• The most common cause of failure with transcutaneous pacing (TCP) is poor pad placement combined with insufficient milliamperes! Remember, the pacer goes up to 200 mA! If you lose your nerve at between 70-90 mA, there’s a good chance you’re not going to achieve capture. Consider anterior/posterior pad placement to "sandwich" the left ventricle between the pads and reduce transthoracic resistance.
• Look for a tall, broad T wave that is the telltale sign of true electrical capture.
• Perform, but do not rely solely on a manual pulse check. Consider using an instrument like an SpO2 monitor, doppler, or bedside 2D echo (for inhospital patients) to verify mechanical capture.
• Run a continuous rhythm strip that shows the transition from "false" capture to true electrical capture. Be able to document the exact milliamperes that capture is gained, and capture is lost. (Note: one of the "quirks" of the human heart is that once you gain capture it is harder to lose. In other words, you might achieve capture at 120 mA, but then you might have to dial it back down to 80 mA to lose it again). Many protocols state that you should add 10 mA as a "safety margin" once capture is achieved. In my experience this is unnecessary for the reason stated.
• Finally, you can consider placing the pacer in "non-demand" mode and examine the absolute refractory periods of the underlying rhythm and the (presumed to be) paced rhythm. If the paced rhythm and the underlying rhythm are marching through each others’ absolute refractory periods, you don’t have true electrical capture.

During a recent shift on the ICU I found the nurses relying on the HR displayed on the lifepak 12 to document capture at a rate of 72. Meanwhile, the patient’s palpable radial pulse was 36 and the Spo2 captured a heart rate of 32! This was not effective pacing at all! The mA was set at 40mA and they refused to increase it because the patient was AxOx3 and it caused her pain. I don’t know if she made it through the night at that rate or maybe they finally sedated her and increased the mA to achieve mechanical capture. I tried explaining the difference between electrical capture and mechanical capture and which is more important but she seemed pretty adamant that if she had electrical capture it was fine. The patient was in 3rd degree AVB as well.

Some great new blog posts over at EMS 12 Lead

• Discordant ST-Segment Elevation in LBBB or Paced Rhythm
• The Six Step Method for 12-Lead ECG Interpretation
• "New" LBBB – What’s the big deal?
• Identifying AMI in the presence of LBBB

Relates well the the Tim Phalen lecture we had on 12 Lead EKGs.

Good Stuff….

Been a while since we did cardiology so I wanted to do a quick review on the normal deflections you should expect to find in each lead of an EKG

Limb Leads

Lead I – Looks across top of heart with positive electrode at left arm – so QRS complexes are upright but not that tall

Lead II – Follows normal electrical axis of heart, top right to bottom left . All complexes should be upright and tall.

Lead III – Looks from top left towards bottom left – at this angle P waves may be inverted but QRS should be upright (more than in lead I)

Lead aVR – Positive on right arm, so everything negatively deflected

Lead aVL – Positive on left arm – similar to Lead I but this lead looks down AND to the right so QRS are upright but very small

Lead aVF – Positive at left leg, looking at bottom of heart. Electricity is coming right at this lead so QRS should be upright and prominent.

 

Chest Leads

Leads V1-V6 – R wave starts very small and S wave is prominent. As the leads progress the R wave is more prominent and S wave is gone in V6. This is known as R wave progression.

  P Wave

P wave should be upright in Leads I and II as well as V3-V6

P wave always inverted in aVR

P wave usually upright in aVF and V3 but occasionally biphasic or flat

P wave is variable in leads III,  aVL, V1 and V2 (upright, inverted, biphasic)

Inverted P wave in II, III and aVF and upight in aVR is diagnostic for a Junctional or low ectopic atrial rythm.

Most people say that your best view of the P wave is in Lead II – others say V1. The truth is that every patient is different, find the best one on your patients EKG and study that one well.

 

See this page for some quick review and this page

According to the AHA, Nitrates should not be given both to someone with a systolic of less than 90 OR 30 or more points below their normal baseline!! (Also severe bradycardia <50BPM or Tachycardia >100BPM) This obviously makes sense, as someone with a normal BP of 160 needs close to that 160 to maintain adequate tissue perfusion. A BP of 130 will not cut it for him as he will be in a state of relative hypovolemia.

Also, with regard to O2, according to study published in the 70s high flow o2 may actually be detrimental to a patient experiencing an uncomplicated MI (i.e. no CHF, COPD, etc). This is because o2 is known to have vasocontrictive effects and as such by increasing afterload (increased peripheral vasoconstriction) you are reducing the cardiac output for a patient that really needs whatever he can get. The AHA it seems, advocates high concentration o2 only when the patient has an spo2 of less than 90% – Also see this study published in 2009 – relevant quote below.

Oxygen
Supplemental oxygen is given because of the theoretical benefit of maximizing oxygen delivery in a patient with an ischemic condition. This was first recommended for myocardial infarction over 100 years ago. However, there have been several studies dating back to the 1950s demonstrating concerning harmful effects. Specifically, they have shown that when supplemental oxygen is given to non-hypoxic patients, it produces increased systemic vascular resistance and decreases cardiac output. In hypoxic patients, the data have varied between no effect to improvement. Our current practice is based on the first randomized controlled clinical trial done on the effects of oxygen therapy for MI patients. It showed a reduction in MI-associated enzyme elevation, but these results did not achieve statistical significance (p=0.08). Given the small numbers involved in this study (n=151), it may have been underpowered to detect an actual clinical and/or statistical effect (type II error), but the results are not sufficient enough to support the routine administration of oxygen to all MI patients. In line with this evidence, the ACC/AHA’s STEMI guidelines  only recommend supplemental oxygen for hypoxic patients. It is worth noting that all but one of these studies were done before the advent of the pharmacologic agents, fibrinolytics, or PCI. In conclusion, the evidence is thin, and this highlights the need to re-consider the risks and benefits of oxygen therapy in both hypoxic and non-hypoxic patients, in the context of modern medical management of STEMI.

Comments welcome!