1. Rhythm & 12 Lead EKG Review

2. Electrical Cardiac Cells
Automaticity – the ability to spontaneously generate and discharge an electrical impulse
Excitability – the ability of the cell to respond to an electrical impulse
Conductivity – the ability to transmit an electrical impulse from one cell to the next

3. Myocardial Cells
Contractility – the ability of the cell to shorten and lengthen its fibers
Extensibility – the ability of the cell to stretch

4. ECG Paper What do the boxes represent?
How do you measure time & amplitude?
Time is measured horizontally. Amplitude, or voltage, is evaluated by number of boxes cumulatively above/below the baseline. Amplitude, or voltage, is the strength of the current.

5. Components of the Rhythm Strip
ECG Paper
Wave forms
Wave complexes
Wave segments
Wave intervals

6. Wave Forms, Complexes, Segments & Intervals
P wave – atrial depolarization
QRS – Ventricular depolarization
T wave – Ventricular repolarization
Depolarization does not guarantee that a contraction occurred. Contractions must be evaluated by feeling for a pulse and measuring the blood pressure. Depolarization is an electrical response and contractions are a mechanical response.

7. Intervals and Complexes
PR interval – atrial and nodal activity
Includes atrial depolarization & delay in the AV node (PR segment)
QRS complex
Corresponds to the patient’s palpated pulse
Large in size due to reflection of ventricular activity

8. The Electrical Conduction System
AV Node
Bundle of HIS
Left Bundle Branch
SA Node
Right Bundle Branch
Purkinje Fibers
SA node is heart’s dominant pacemaker site with an inherent rate of beats per minute. As you move down the conduction system, the pacemaker site becomes slower and is less reliable.
Inherent rates:
SA node
AV node 40-60
Ventricles 20-40

9. Correlation of ECG Wave Forms

10. Sinus Rhythms Originate in the SA node Inherent rate of 60 – 100
Normal sinus rhythm (NSR)
Sinus bradycardia (SB)
Sinus tachycardia (ST)
Sinus arrhythmia
Inherent rate of 60 – 100
Base all other rhythms on deviations from sinus rhythm

11. Sinus Rhythm

12. Sinus Bradycardia

13. Sinus Tachycardia

14. Sinus Arrhythmia

15. Atrial Rhythms Originate in the atria Atrial fibrillation (A Fib)
Atrial flutter
Wandering pacemaker
Multifocal atrial tachycardia (MAT)
Supraventricular tachycardia (SVT)
PAC’s
Wolff–Parkinson–White syndrome (WPW)

16. A - Fib

17. A - Flutter

18. Multifocal Atrial Tachycardia (MAT) (Rapid Wandering Pacemaker)
MAT rate is >100
Usually due to pulmonary issue
COPD
Hypoxia, acidotic, intoxicated, etc.
Often referred to as SVT by EMS
Recognize it is a tachycardia and QRS is narrow

19. SVT

20. PAC’s

21. Wolff–Parkinson–White - WPW
Caused by an abnormal accessory pathway (bridge) in the conductive tissue
Mainly non-symptomatic with normal heart rates
If rate becomes tachycardic ( ) can be lethal
May be brought on by stress and/or exertion
Delta wave is the slurring at the uptake of the QRS complex.

22. Wolff–Parkinson–White (AKA - Preexcitation Syndrome)

23. AV/Junctional Rhythms
Originate in the AV node
Junctional rhythm rate 40-60
Accelerated junctional rhythm rate
Junctional tachycardia rate over 100
PJC’s
Inherent rate of

24. Junctional Rhythm

25. Accelerated Junctional

26. Ventricular Rhythms Originate in the ventricles / purkinje fibers
Ventricular escape rhythm (idioventricular) rate 20-40
Accelerated idioventricular rate
Ventricular tachycardia (VT) rate over 102
Monomorphic – regular, similar shaped wide QRS complexes
Polymorphic (i.e. Torsades de Pointes) – life threatening if sustained for more than a few seconds due to poor cardiac output from the tachycardia)
Ventricular fibrillation (VF)
Fine & coarse
PVC’s

27. VT (Monomorphic)

28. VT (Polymorphic) Note the “twisting of the points”
This rhythm pattern looks like
ribbon in it’s fluctuations

29. VF

30. PVC’s

31. AV Heart Blocks 1st degree A condition of a rhythm, not a true rhythm
Need to always state underlying rhythm
2nd degree
Type I - Wenckebach
Type II – Classic – dangerous to the patient
Can be variable (periodic) or have a set conduction ratio (ex. 2:1)
3rd degree (Complete) – dangerous to the patient
Second degree Type II and 3rd degree heart blocks are dangerous to the patient because their rates are typically slow. Also, if the block deteriorates, the patient will become increasingly more symptomatic.

32. Atrioventricular (AV) Blocks
Delay or interruption in impulse conduction in AV node, bundle of His, or His/Purkinje system
Classified according to degree of block and site of block
PR interval is key in determining type of AV block
Width of QRS determines site of block

33. AV Blocks cont. Clinical significance dependent on:
Degree or severity of the block
Rate of the escape pacemaker site
Ventricular pacemaker site will be a slower heart rate than a junctional site
Patient’s response to that ventricular rate
Evaluate level of consciousness / responsiveness & blood pressure
Assume a patient presenting in Mobitz II or 3rd degree heart block to have an AMI until proven otherwise

34. 1st Degree Block

35. 2nd Degree Type I

36. 2nd Degree Type II (constant)
P Wave PR Interval QRS Characteristics
Uniform Narrow & Uniform Missing QRS after every other P wave
(2:1 conduction)
Note: Ratio can be 3:1, 4:1, etc. The higher the ratio, the “sicker” the heart. (Ratio is P:QRS)

37. 2nd Degree Type II (periodic)
P Wave PR Interval QRS Characteristics
Uniform Narrow & Uniform Missing QRS after some P waves

38. 3rd Degree (Complete)

39. How Can I Tell What Block It Is?

40. Helpful Tips for AV Blocks
Second degree Type I
Think Type “I” drops “one”
Wenckebach “winks” when it drops one
Second degree Type II
Think 2:1 (knowing it can have variable block like 3:1, etc.)
Third degree - complete
Think completely no relationship between atria and ventricles

41. Implanted Pacemaker Most set on demand
When the heart rate falls below a preset rate, the heart “demands” the pacemaker to take over 41

42. Paced Rhythm - 100% Capture

43. Where do those chest stickers go?
Make sure to “feel” for intercostal space – don’t just use your eyes!

44. ……and the FEMALES Not all nipple lines are created equal
Measure intercostal spaces to be accurate in electrode placement
All 12 leads measured from same electrode placement

45. Lead Placement in the Female
Avoid placing electrodes on top of breast tissue
Use the back of the hand to displace breast tissue out of the way to place electrode
Avoids perception of “groping”
Can ask the patient to move left breast out of way.

46. Myocardial Insult Ischemia Injury Infarct lack of oxygenation
ST depression or T wave inversion
permanent damage avoidable
Injury
prolonged ischemia
ST elevation
Infarct
death of myocardial tissue; damage permanent; may have Q wave
TIME IS MUSCLE! Need to get the patient to the most appropriate care prior to the infarct to save as much myocardium as possible.
Ischemia is an imbalance of metabolic needs of the myocardial demand and the amount of oxygenated blood provided. Ischemia can result from can increased demand for myocardial oxygen, reduced myocardial oxygen supply, or both.
Angina is not a disease but a symptom of myocardial ischemia.

47. Evolution of AMI A - pre-infarct (normal)
B - Tall T wave (first few minutes of infarct)
C - Tall T wave and ST elevation (injury)
D - Elevated ST (injury), inverted T wave (ischemia), Q wave (tissue death)
E - Inverted T wave (ischemia), Q wave (tissue death)
F - Q wave (permanent marking)

48. Sinus w/ 1st degree Block
No symptoms are due to the first degree heart block; symptoms would be related to the underlying rhythm

49. 2nd Degree Type 1 – Wenckebach
PR getting longer and finally 1 QRS drops; patient generally asymptomatic; can be normal rhythm for some patients

50. 2nd Degree Type II (2:1 conduction)
Patient’s symptoms will be dependent on the heart rate – the slower the heart rate the more symptomatic the patient will be.
2nd Degree Type II (2:1 conduction)
Should be preparing the TCP for this patient

51. 3rd degree heart block (complete)
with narrow QRS
Symptoms usually based on overall heart rate – the slower the heart rate the more symptomatic the patient. Prepare the TCP.

52. NSR to Torsade des Pointes
If torsades is long lasting, patient may become unresponsive and arrest. Prepare for defibrillation followed immediately with CPR

53. Intermittent 2nd Degree Type II
(Long PR intervals; periodic dropped beat)
Consider need to apply TCP and then turn on if patient symptomatic

54. Why would this patient have symptoms of a stroke?
Atrial fibrillation puts patient at risk from clots in the atria breaking loose and lodging in a vessel in the brain
Rhythm irregularly irregular
Patient most likely on Coumadin and digoxin

55. Ventricular Tachycardia
What 2 questions should you ask for all tachycardias?
Is the patient stable or unstable?
If stable, then you have time to determine if the QRS is narrow or wide
What’s this strip?

56. Paroxysmal Supraventricular Tachycardia (PSVT) into sinus rhythm
Evidence of abrupt stopping of the SVT

57. Sinus Arrhythmia
Common in the pediatric patient and influenced by respirations. Treatment is not indicated

58. Sinus with unifocal PVC’s in trigeminy
Often PVC’s go away after administration of oxygen

59. Multifocal Atrial Tachycardia (MAT)
Rapid Wandering Pacemaker
Identification can be SVT and treatment would be based on patient symptoms
Focus on the P wave irregularity, not necessarily the name of the rhythm. Can be referred to as a rapid wandering pacemaker. 59

60. 12 – Lead Time! Same as Lead II strips
Identify ST elevation and try to give anatomical locations
May not be able to view grid lines but should be able to pick up ST elevation when present
Remember to be watchful for typical complications based on location of infarct and blocked coronary vessel

61. ST elevation in V2 – V5 (Anterior wall)

62. No ST elevation but peaked T waves (Hyperkalemia)