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.

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

Andy Rodriguez

First Degree Heart Block

• Not a true block
• Conduction delay at AV node
• All impulses are conducted to ventricles
• PRI will be >0.20 consistently across the strip

Second Degree Heart Block

• Intermittent
• Some get through and some don’t
• pathology can be in AV node or below in Bundle of His
• pathology is often blended with other blocks
• Mobitz Type I (Wenckebach)
• Impulses encounter progressive delays at the AV node until one impulse is blocked completely
• PRI starts getting progressively longer and then dropped QRS
• All conducted QRSs present are tight, <0.12 and preceded by a P wave
• Mobitz Type II
• Can be regular or irregular, depending on conduction ratio
• Usually a Brady rhythm
• More than one P wave for every QRS
• PRI constant on conducted beats can be >0.20
• QRS <0.12
• Conduction Ratios
• 2:1, 3:1, etc. two P waves for every conducted QRS

Third Degree Heart Block (Complete Heart Block)

• All impulses generated by Sinus node are being blocked by AV node
• Separate Sinus and Ventricular Pacemakers –
• Complete disassociation between P waves and QRSs
• Regular
• Rate depends on whether its junctional or ventricular
• P waves, normal and upright, more P waves than QRS
• PRI – no relationship between P waves and QRS , occasional superimposed on QRS
• QRS width depends on whether its junctional or ventricular

Heart blocks are best diagnosed using a 12 Lead EKG Machine. This and other used medical equipment can be found easily online.

Download Excel Version Here

UPDATED 6/15/09

Sinus Blocks, Pauses and Arrest

• In all cases, no P, QRS or T wave present – Impulse is blocked a SA node and Atria are never depolarized.
• Sinus Block – Always a multiple of underlying P-P interval. can be more than one missing complex
• Sinus Pause – Not a multiple of P-P interval. Shorter than three times the P-P
• Sinus Arrest – Same as pause but more than 2 missing complexes (consecutive)