“EKG” - electrocardiogram Gail L. Lupica PhD, RN, CNE Nurs 211

“EKG” Take your pulse. What you feel is blood rushing through your radial artery with each systolic contraction. Systole creates that push of blood. Diastole allows the chambers to fill again. That is what’s happening to our heart mechanically. What fuels this machine???

“EKG” Electricity fuels this machine! A spot right above our atrium called the Sinoatrial node has “automaticity”, which means it fires without any other assistance.

“EKG” The SA node fires. The impulse travels through the internodal tracts to the AV node. From there it travels to the bundle of his then down the right and left bundles. The purkinje fibers conduct the impulse rapidly through the muscle until it “depolarizes” The depolarization causes our muscles to contract and that’s what pushes the blood through our arteries.

“EKG” When our patients are in the hospital we not only want to HEAR, and FEEL the heart, we want to SEE how normal the electricity is that’s causing it to pump. We can find that information on an electrocardiogram.

“EKG” We need to use special paper to understand that report completely. That paper looks like this>>>

“EKG” Each teeny tiny box represents .04 seconds. Adding up the teeny tiny boxes across the paper lets you know how long it took for the current to travel. 5 boxes = ?? seconds .04 x 5 = .20 seconds

“EKG”- “normal” Certain pictures or rhythms that we get are considered “normal”. We call these rhythms “normal sinus rhythm” Normal….. Sinus…….. Rhythm (no problems) (from SA node) (pattern)

“EKG” - p wave, qrs complex The p-wave represents atrial depolarization. The electricity started in the SA node, traveled to the AV node. The p wave bump shows you that the atria contracted. (the filling of the ventricles prior to systolic contraction) The distance between the beginning of the p-wave and the beginning of the QRS interval is the P-R interval. The QRS complex represents ventricular depolarization

Components of a normal electrocardiogram Elsevier items and derived items © 2006 by Elsevier Inc. September 18

“EKG” criteria for normal sinus rhythm. To judge what’s normal, you have to understand “normal”. Certain criteria for EKGs meet the criteria for normal sinus rhythm. The distance between the beginning of the p wave to the beginning of the QRS complex needs to be less that .20 seconds, or 5 teeny boxes (= 1 bigger box). Each QRS complex needs to be less than .12 seconds or 3 teeny boxes.

EKG - criteria for normal sinus rhythm. The QRS complexes need to be equal distant apart. Each P wave should be followed by a QRS complex. You should have no more than 10 complexes in a 6 second strip and no LESS than 6. (HR 60-100) The t waves should look upright and round (& stay away from them during defibrillation!!!!!!)

“EKG” Rate determination 15 LARGE boxes is 3 seconds, 30 LARGE boxes is 6 seconds. Count the number of complexes in a 6 sec strip and multiply by 10. Count the number of small boxes between 2 QRS complexes and divide that number into 1500. Ex: 1500/15 = 100bpm Big block method-300, 150, 100, 75…. NOW, Let’s Practice

Rate- 6 second interval x 10 80

Rate: 30 blocks is 6 secs x 10 75

Rate:1500 method: 1500/4 = 75 75

Let’s go onto look at: Sinus bradycardia Sinus tacycardia Atrial fibrillation Atrial flutter Premature ventricular contractions Ventricular tachycardia Ventricular fibrillation Asysytole & HOW TO TREAT THEM!!!

What’s this? Why?

Bradycardia- What’s more important, a patient’s heart rate or the patient signs of perfusion and hemodynamic sufficiency? Absolute bradycardia- HR <60 Relative bradycardia- Pt is showing signs of inadequate CO even with a HR> 60.

Sinus Bradycardia-treat Atropine: The first drug of choice for symptomatic bradycardia. 0.5mg IV push and may repeat up to a total dose of 3mg. anticholinergic drug and increases firing of the SA Node by blocking the action of the vagas nerve on the heart resulting in an increased heart rate.

Sinus Bradycardia-treat Dopamine: Second-line drug for symptomatic bradycardia when atropine is not effective. 2-10 micrograms/kg/min infusion. Epinephrine: equal alternative to dopamine. : 1mg epinephrine is mixed with 500ml of NS or D5W— 2-10 micrograms/min (titrated to effect).

Sinus Brady-TCP Transcutaneous pacing (TCP)- should be taking place as atropine is being given. If atropine fails, TCP should be initiated. For the patient with signs of poor perfusion, transcutaneous pacing is the treatment of choice.

What’s this? Why?

Sinus Tachycardia- (vs SVT) Dehydration??, hypoxia??, fever??, and sepsis??. …H’s and T’s Administration of OXYGEN and NORMAL SALINE are of primary importance for the treatment of causative factors …..

Sinus Tachycardia- (vs SVT) SVT- Treat the underlying Cause!! (5 Hs and 5 Ts) The H’s:Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hyper-/hypokalemia,Hypoglycemia,Hypothermia. TheT’sinclude:Toxins,Tamponade(cardia),Tension pneumothorax, Thrombosis (coronary and pulmonary), and Trauma.

ST vs SVT- treat With SVT, impulses in the atria fire rapidly and cause interference with the SA node. But in sinus tachycardia, the heart is functioning normally; only the SA node is firing at a higher than normal rate. Also SVTs can originate from several different spots within the atria.

Sinus Tachycardia vs SVT > 120 Stable vs unstable Unstable? Synchronized cardioversion

Synchronized cardioversion vs defibrillation- What’s the difference? ST SVT- treat Synchronized cardioversion vs defibrillation- What’s the difference?

Sinus Tachycardia vs SVT-treat Stable?? Stable (narrow QRS complex) → vagal maneuvers → adenosine (if regular) → beta-blocker/calcium channel blocker → get an expert Stable (wide) → adenosine → consider antiarrhythmic infusion → get an expert

Sinus tachy vs. SVT- adenosine Used when vagal maneuvers fail slows cardiac conduction through the AV node. Interrupts reentry (SVT causing) pathways through the AV node

St-SVT- adenosine 6 mg administered rapidly over 1-3 seconds followed by a 20 ml NS bolus. does not convert out of SVT within 1 to 2 minutes, a second 12 mg dose may be given in similar fashion. Administer adenosine as quickly as possible. side effects -flushing, chest pain/tightness, brief asystole or bradycardia. bolus so that a bolus reaches the heart before it is metabolized. (or else absorbed by red blood cells and endothelial cells and metabolized for natural uses throughout the body.)

What’s this? Why?

Atrial Fibrillation –treat Unstable?- synchronized cardioversion What are you worried about with this dysrhythmia? 1. 2.

Atrial fibrillation Animations Cardioversion Diltiazem Heparin

What’s this? Why?

What’s this? Why?

What’s this? Why?

Ventricular dysrhythmias- PVCs- Amiodarone   Cordarone Antiarrhythmic •Increases the action potential duration Increases the refractory period in the atria, ventricles and AV node

PVCs- Amiodarone- dosing 150 mg IV bolus over10 minutes at 15 mg/min. Maintenance infusion of 1 mg/min for 6 hours, then slowly reducing to 0.5 mg/min over the next 18 hours.

What’s this? Why?

What’s this?

What’s this?

What’s this?

What’s this?

Ventricular Tachycardia-Ventricular fibrillation- treat-defib CPR 2min/5 cycles Biphasic (the electrical current travels from one paddle to the other paddle and then back). 120-200 Joules to shock. Then what? Shock , drug, shock, drug

Ventricular Tachycardia-Ventricular fibrillation- treat-defib Why epi?

Epi Intravenous Push/IO: 1mg epinephrine IV is given every 3-5 minutes. Endotracheal Tube: 2-2.5mg epinephrine is diluted in 10cc NS and given directly into the ET tube.

Amiodarone (Pulseless VT of VF): Initial bolus of 300 mg IV diluted in 20 - 30 ml of NS or D5W. repeat doses of 150 mg IV every 3 - 5 minutes. …1 mg/min infusion for 6 hours, then reduce 0.5 mg/min for the next 18 hours

What’s this?

What’s this?

What’s this?

What’s this?