You may have seen this already…funny but sadly all too true (sorry about the language)

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.

Many times throughout the Paramedic Program I have come across a drug that has an unexpected use listed in the profile. Not very often are we given a comprehensive explanation as to why this drug works for this other use and it is left to us to try and figure this out. One example that I have seen recently is the use of Glucagon for beta blocker overdose. Glucagon is a hormone used in diabetic emergencies; its use for beta blocker overdose is actually pretty simple once it is explained.

Glucagon – Profile

Glucagon is a hormone produced by the alpha cells in the pancreas, it is opposed by insulin, a hormone produced by the beta cells in the pancreas. During periods of low blood sugar, for example, between meals, glucagon is secreted into the bloodstream which then begins the process of breaking down glycogen stores in the liver and muscle (glycogenolysis) to increase available blood glucose. After meals and at time of increased blood sugar, insulin is secreted to allow the cells to take up circulating glucose and stimulate the formation of glycogen (glycogenesis). Glucagon is also released during periods of stress to increase available energy during the fight or flight response. Additionally, glucagon possesses an inotropic quality, increasing the contractility of the myocardium thereby increasing stroke volume and cardiac output.

Glucagon – Use in Emergency Medicine

As an emergency drug, glucagon is administered to patients in severe hypoglycemia/insulin shock where IV access is unavailable. The expected response takes around 10 minutes to start and will only work if the patient has adequate glycogen stores available. This will not work for starving patients and alcoholics. The dose is 1mg IM.

Its use for beta blocker and calcium channel blocker overdose relies on its inotropic properties. Being that the beta adrenergic receptors are being blocked, epinephrine cannot exert its inotropic effect on the heart. Glucagon, in high doses (initial dose of 3-5mg IV) may have enough of an inotropic effect to increase cardiac output and blood pressure. For CCB overdoses it works the same way, just this time it the calcium channels that are blocked which also cause reduced contractility.

Glucagon is also used in cases of anaphylactic shock when epinephrine is not working (usually due to beta blocker use). The dose in this case would be 1-2mg IV over 5 minutes.

Hope it’s clear now, worked for me

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….

Components of blood – 45% RBC (hematocrit – 48% men/ 38% women), 54% Plasma, 1% WBC and Platelets

Blood tests:

Hemoglobin (Hgb) usually around 14  (Varies for men and women, adults and children)

Hematocrit is (Hct) usually about three times Hemoglobin levels,

Platelet count usually between 150,000 and 450,000 per uL of blood

CBC – Complete blood count

Diff – Measures percentage of different types of white blood cells (differential hematology blood analyzers)

92% of blood plasma is water, 6-7% Proteins, remainder includes clotting factors, glucose, and electrolytes

Contains 3 Important proteins

Albumins – keep water in blood – low proteins will let water leak out – edema – (seen in poor nutrition, elderly, etc)

Immunoglobulins – immune system response

Fibrinogens – for blood coagulation

 

Red Blood Cells

Most abundant cells in body

Primarily responsible for tissue oxygenation

White Blood Cells

Cells of the immune system, also called leukocytes, 5 types exists. Produced in Bone Marrow. Elevation of WBC count indicative of disease.

Arterial Blood Gas Levels (ABGs)

• Partial pressure of oxygen (PaO2) – 75 – 100 mmHg
• Partial pressure of carbon dioxide (PaCO2) – 35 – 45 mmHg
• A pH of 7.35 – 7.45
• Oxygen saturation (SaO2) – 94 – 100%
• Bicarbonate – (HCO3) – 22 – 26 mEq/L

Note: low HCO3 decreases the effectiveness of many drugs – specifically epinephrine.

I figured I’d write one Mnemonic to help remember all the other acronyms we use. (Not in order but what the heck! – Each one has the full description below) Enjoy!

Mamas Dogs Flips

M – MONA

A- ABC DEF GO

M- MOIST N DAMP

A- AEIOU TIPS

S- SAMPLE

D – DCAP BTLS

O- OPQRST

G- GUT PAINS

S- SIFDO

F – FAST

L- LEAN

I – IPASSO

P- PERRL

S- SLUDGEM

MONA – For ACS – Morphine, Oxygen, Nitrates, Aspirin

ABC DEFG – Airway, Breathing, Circulation, Disabilities, Extremities/Expose, Full set of vitals, GO!

MOIST N DAMP – For CHF –

Morphine
Oxygen
Intubation
Sit-up
Twelve lead
Nitrates
Dangle legs
Ativan (lorazepam)
Monitor Q 3-5
Pulmonary Congestion (CPAP)

AEIOU TIPS – AMS/Seizures

Alcohol

Epilepsy

Infection

Overdose

Uremia

Trauma

Insulin

Psychosis

Poison

Stroke

SAMPLE – Signs/Symptoms, Allergies, Medications, Past History, Last oral intake, Events leading up

DCAP BTLS – Deformities Contusions Abrasions Punctures/Penetrations Burns Tenderness Lacerations Swelling

OPQRST – Onset, Provokes/Palliates, Quality, Radiation, Severity, Time

GUT PAINS – (For Abdominal Pain)

G- Gallbladder, Gas, Gastritis,Gynecological
U- Ulcer
T- Trauma such as ruptured spleen, etc.
P- Pancreatitis, PID, Pregnancy (ectopic), Perforated Ulcer
A- Aortic Aneurysm, Appendicitis, Abdominal Angina
I-  Intestinal Obstruction, Infection, Ischemia of the bowel
N- Neoplasm
S- Spasm of the esophagus, Splenic rupture

SIFDO (Order of exam) Scene Size Up, Identify life threats, Focused Exam, Detailed Exam, Ongoing Assessment

FAST – Neuro assessment for Stroke/CVA – Facial paralysis, Arm weakness, Speech difficulties, Time to act

LEAN – Meds that can given down the ET tube. Lidocaine, Epi, Atropine, Narcan

IPASSO – Inspect, Palpate, Auscultate, Stabilize, Seal, Oxygen

PERRL – Pupils Equal Round Reactive to Light

SLUDGEM – Organophosphate exposure, Salivation, Lacrimation, Urination, Defecation, Gastric Upset, Emesis, Miosis

Ok, so i cheated.. I used this anagram creator to come up with the word; you can plug in these letters and choose from 1000 other variations. (saiosafdmmsplg)

This pharmacology booklet was handed out the other night, it is very useful and comprehensive. This was originally prepared for the St Vincent’s class and any references to protocols refer to NYC REMAC (as of 2006).

Sample page:

_________

También encontré un gran recurso si usted está buscando para comprar en línea de equipos médicos. Ellos llevan las máquinas de EKG, máquinas de ultrasonido, así como desfibriladores

By Miguel

"This is why people fail exams and/or lose their certifications"

Rule #1: BLS before ALS.

Rule #2: Treat your patient not the monitor.

Rule #3: An ‘excellent’ EMT = a ‘good’ medic.

Rule #4: Protocols are guidelines, not set in stone.

Rule #5: Refrain from getting tunnel vision.

Never forget:

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

2) IPASSO (inspect, palpate, auscultate, stabilize, seal, O2).

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

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

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

* Head to toe assessment *

** approximately 40 questions before you begin ALS, unless the call is obvious **

Rookie Mistakes:

#1 Uses monitor for everything.

#2 Every call becomes ALS.

#3 Every chest pain is cardiac.

#4 Every patient gets an IV.

** don’t go by what the EMT’s tell you **

***Become a Clinician***

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

NYC 911 System – Sat night 21:00 – 09:00

I had two "good" calls on Sat night

16 y/o female, pedestrian struck by a cab. Unconscious with agonal respirations. Paddles applied shows sinus tach at 174 but no palpable carotid or radial (PEA?). CPR performed for approx two minutes and faint pulses felt. We arrived same time as BLS, we were on scene for under 5 and had her in Belleview in about 12 minutes from going on scene. Attempted to intubate but unable due to blood and vomit (preceptor). Our brief exam revealed a flail chest (could I have done that with cpr?), distended abdomen, bruising to tib/fibs and ankles. I was asked to bag the patient in the ER so I got to observe them put in two chest tubes as well as the rest of the trauma team workup. (Got to watch an abdominal ultrasound with a Sonosite Titan) She was off to OR within 20 minutes of our arrival. Checked back later and her biggest problem seems to be an ICP of 35 and a probable Diffuse Axonal Injury. Not good, even if she makes it…

2nd call dispatched at 02:50 for an unconscious lying by his car. Talk while enroute was of a probable intox or OD. Arrive on scene at parking garage and told that vehicle was seen driving in at around 02:00 and he was found lying next to the open drivers door of his still running vehicle at around 02:40.

As we ran up the ramp we could see an elderly male lying on the floor looking everything like an arrest, as we got closer though we could hear loud snoring respirations. Assessment reveals HR 48 regular, respirations of 24, GCS 3, Pupils fixed and dilated, no obvious trauma. Loaded him into bus and worked out the differentials. Dilated pupils and Tachypnea – Not an opiate OD, Glucose at 79 so not likely that either. BP at 220+ with fixed and dilated pupils – likely a massive CVA. (We did not have time to do a 12 lead EKG)

I asked if I could intubate, I was told that I have one try. He was breathing so everything was moving and I didn’t get a good visual but tried to aim for where I thought it was but I didn’t push it far enough in. I wanted a second shot but we were at the hospital and he didn’t let me (I consoled myself later when I saw the resident take 10 minutes and a bougie to get it done)

At Belleview again they worked up a stroke code and Dr Chung literally forced us to stick around for the results of the CT. He spent quite some time with us going over the pedestrian struck patient’s CT and then again when the results of the second CT came back. Massive intracranial bleed – ventricles entirely filled with blood – also not good for this guy. If any of you meet this Dr just hang on to him, he really treated us like part of the team and explained and showed everything.

Other than that we had 1 Anxiety, 1 A fib (who vomited all over me) and 1 severe chest pain (probable gall stone per ED staff) Wind chills under 0 degrees F all night.

Good stuff