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

2. “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???

3. “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.

5. “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.

7. “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.

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

10. “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

12. “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)

13. “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

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

17. “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.

18. 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 )
The t waves should look upright and round (& stay away from them during defibrillation!!!!!!)

19. “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 Ex: 1500/15 = 100bpm
Big block method-300, 150, 100, 75….
NOW, Let’s Practice

20. Rate- 6 second interval x 1080

21. Rate: 30 blocks is 6 secs x 10 75

22. Rate:1500 method: 1500/4 = 75 75

25. 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!!!

26. What’s this? Why?

27. 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.

28. 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.

29. 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).

30. 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.

31. What’s this? Why?

32. 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 …..

33. 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.

34. 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.

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

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

38. 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

39. 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

40. 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.)

41. What’s this? Why?

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

44. Atrial fibrillation
Animations
Cardioversion
Diltiazem
Heparin

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

50. 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.

51. What’s this? Why?

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56. 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) Joules to shock.
Then what?
Shock , drug, shock, drug

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

59. 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.

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

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