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.

Posted with WordPress for BlackBerry.

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.

One last reminder before our finals!

Good luck!

Never forget:
1) SIFO (medical): Scene size up. Initial assessment. Focused Assessment. Ongoing Assessment.
Or
SIFDO (trauma): Scene size up. Initial assessment. Focused Assessment. Detailed assessment. Ongoing Assessment.

2) ABC DEFG (airway, breathing, circulation, disabilities, extremities, full vitals, GO).

3) IPASSO (inspect, palpate, auscultat, stabilize, seal, O2).

4) OPQRSTI (onset, provocations, quality, radiation, severity, time, interventions).

5) SAMPLE (signs/symptoms, allergies, medications, past hx, last intake, events).

6) Pertinent questions regarding call: eg. weight, LMP, PARA, Gravada, drug consumption, Etoh, smoking, etc.

Detailed Exam:* Head to toe assessment *Pay close attention to JVD, Ascites, Pedal Edema.

(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.

Just learned some really fascinating things about shock and volume resuscitation and the importance of crystalloid solutions. I found this lecture by Dr Jeffery Guy while going through the PHTLS class and found it to be a real eye opener (and a great lecture). (More great PHTLS lectures here)

Third Space Resuscitation

Consider the following; in a study a number of dogs were allowed to bleed into Level III shock and then they were all transfused with all their own blood that was lost. They all died shortly thereafter. They tried this again, this time giving them an infusion of an isotonic crystalloid solution before transfusing their blood back and many more of them lived and recovered. What they discovered was that in a state of hypovolemic shock, the body initially compensates by shifting fluid from the interstitial spaces and intracellular fluid into the vascular space to try and maintain plasma volume. Therefore for a favorable outcome,  it is imperative to resuscitate the third spaces as well. This is achieved by infusing hypertonic solutions of which only one third remains in the vascular space with the remaining two thirds moving out into the interstitial and intracellular spaces within an hour. If only blood or colloids were used this third space resuscitation would not happen and the patient would die.

Permissive Hypotension

He speaks about how much is the right amount to infuse in the field, the short answer is just enough to maintain a systolic BP of around 90, or even just enough to maintain a palpable radial pulse. The point of permissive hypotension can be illustrated by filling a balloon with water and making a small hole in it. The more the balloon is squezeed (increased pressure) the faster water will spurt from the “wound” also clots that may have formed can be blown out by higher pressures. Therefore until bleeding can be definitely stopped (i.e. surgery) permissive hypotension will go a long way to enhance patient outcome.

ARDS, Systemic Edema

Another complication of overhydrating shock patients is the development of ARDS and other systemic edema. These situations typically arise days and weeks after the initial trauma and can then cause death. Many organs are susceptible such as the lungs, kidneys, liver and brain. Many protocols therefore speak of switching to a colloid or hypertonic solution once a defined amount of isotonic crystalloids have been infused.

Increased Respiratory Rate in Shock

I always thought that the primary reason for increased respirations in a shock patient was due the patient’s need to hyperoxygenate their remaining blood supply to maintain tissue perfusion. While this may be true, Dr. Guy mentions another reason for the tachypnea. He mentions the “bellows effect” of ventilation whereby the negative pressure created in the chest during inspiration also draws blood up through the vena cava into the heart. He states that this is the reason for tachypnea, to help increase preload and  cardiac output by creating more negative pressure in the thorax.

Normal Saline Vs. Lactated Ringers

PHTLS and many other sources mention that Lactated Ringers is the fluid of choice in hypovolemic shock yet many locales (including NYC and Hudson Valley) generally use normal saline. The reason that LR is the fluid of choice is because prolonged infusion of NS will cause the the patient to become acidotic, impairing many important metabolic functions. The reason given for use of NS is because LR is not compatible with blood products and since the patient will most likely need a transfusion this might be problematic. Dr. Guy mentions that many blood banks use blood that is compatible with LR and also that LR itself is being refined to be more compatible so hopefully many more of us will start using the preferred fluids. (I find this whole thing a bit bizarre, can’t we coordinate with the hospitals and blood banks in order to benefit the patients who need this most?)

Dopamine and other useful Paramedic Drips

My quick and easy way….

400mg in a 250ml bag yields:

• 1600µg per ml
• 26.6µg per gtt (60 gtt set)

So if you need to calculate a drip for a 70kg patient you could do this:

70kg x 5µg (example dose) = 350µg/min . 350/26.6 = 13.15 gtts/min

Works for me…. but some prefer the regular dopamine clock so i have included that below

The clock method

Drug Preparation Rate

Amiodarone (3mg/cc) 150mg in 50cc NS

• 0.5mg/min=10gtts/min

Dopamine (800µg/cc) 200mg in 250cc NS

• 200mcg/min=15gtts/min
• 400mcg/min=30gtts/min
• 600mcg/min=45gtts/min
• 800mcg/min=60gtts/min

Dopamine (1600µg/cc) 400mg in 250cc NS

• 400mcg/min=15gtts/min
• 800mcg/min=30gtts/min
• 1200mcg/min=45gtts/min
• 1600mcg/min=60gtts/min

Epinephrine (4mcg/cc) 1mg in 250cc NS

• 2mcg/min=30gtts/min

Lidocaine (4mg/cc) 1G in 250cc NS

• 1mg/min=15gtts/min
• 2mg/min=30gtts/min
• 3mg/min=45gtts/min
• 4mg/min=60gtts/min

Procainamide (20mg/cc) 1G in a 50cc NS

• 20mg/min=60gtts/min
• 30mg/min=90gtts/min

Procainamide (4mg/cc) 1G in 250cc NS

• 1mg/min=15gtts/min
• 2mg/min=30gtts/min
• 3mg/min=45gtts/min
• 4mg/min=60gtts/min