1. Nursing Interpretation of the Electrocardiogram (ECG), Telemetry
By: Teresa Champion
MCC
NURS 2140

2. OBJECTIVES
Describe the configuration of the normal electrocardiogram (ECG).
Identify and calculate heart rate, rhythm, PR interval, QRS complex, and QT interval for normal and abnormal cardiac rhythms.
Discuss the etiology and significant ECG features of the following dysrhythmia classifications: sinus, atrial, junctional, block, ventricular, and asystole.
Interpret the significance of each of the dysrhythmias and formulate nursing responsibilities for each dysrhythmia.
Identify normal rhythms and dysrythmias.
Identify ECG complexes and artifact.
Perform ECG rhythm strips.
Identify correct dysrythmia terminology

3. Cardiac Conduction System
3 Main Parts:
SA node (Sinoatrial node)
AV node (Atrialventricla node)
HIS-Perkinje System

4. VIDEO OF CONDUCTION SYSTEM

5. Anatomy of the Heart - CARDIAC CELLS
Two types of cardiac cells
Myocardial & Pacemaker cells
Automaticity
Excitability
Conductivity
Contractility
Automaticity- ability of pacemaker to generate their own impulses
Excitability – ability of electrical cell to respond to a stimulus
Conductivity – the ability of the cardiac cell to accept and transmit a stimulus
Contractility – the ability of the cardiac cells to shorten and cause the muscle to contract

6. Anatomy of Heart – Cardiac Chemistry Function
Electrolytes Affecting Cardiac Function
Depolarization/Repolarization
Cardiac Output (CO): The amount of blood the
heart pumps out to body in 1 min.
NORMAL: 5 to 8 L
CO= HR x SV (CO can be changed by altering
heart rate, stroke vol. or both)
Stroke Volume = the amount of blood that the
heart ejects in one beat which
depends on activity level, physical
condition, prior heart disease
Electrolytes – positive ion charges are cations (Na++, K+, Ca++, also Mg but not as influential).
K+, Calcium and Mg – intracellular and sodium is extracellular. Negatively charged cells are anions (Cl – Chloride) and provides electroneuttrility in r/t sodium.
Depolarization – contraction . Sodium and potassium move across cell membrane by active transport (ATP pump) or (Na-K pump) Sodium-potassium adenosine triphosphate pump.

7. Cardiac Wave Form on Electrocardiogram (ECG)
P wave
PR interval
QRS complex
J point
ST Segment
T wave
QT Interval
R to R Interval
U wave (not always present)

8. ECG Wave Form

9. ECG Lead Placement in Telemetry
1. The white lead is placed on the right side of the chest. This is usually called the “right arm lead.”
2. The black lead is placed on the left side of the chest. This is called the “left arm lead.”
3. The green lead is placed on the right lower abdomen, it is called the “right leg lead.”
4. The red lead is placed on the right lower abdomen, it is called the “left leg lead.”
5. The brown lead is placed slightly to the right of the midsternum, it is called the “V lead or chest lead.”
 6. The grey lead is

10. Lead Placement ECG Telemetry
White lead
Black Lead
Brown Lead
Green Lead
Red Lead

11. ECG Graph Paper

12. Heart Rate on ECG
Heat Rate
Fastest count R waves in 6 second strip and times by 10.
Count R waves on a full minute strip for accurate HR for irregular rhythms.
Another way is to count the number of small boxes between R waves and divide the total by 1500.

13. Heart Rate on ECG 1 big box (5 small boxes) is equal to a HR of 300
2 big boxes is hr of 150 (300/2)
3 big boxes is hr of 100 (300/3)
4 big boxes is hr of 75 (300/4)
5 big boxes is hr of 60 (300/5)
6 big boxes is hr of 50 (300/6)
7 big boxes is hr of 43 (300/7)
8 big boxes is hr of 38 (300/8)

14. Large box estimate of heart rate works with regular rhythms

15. A dysrhythmia is a disturbance of the rhythm of the heart caused by a problem in the conduction system.
Categorized by site of origin: atria , AV nodal, ventricular
Blocks are interruptions in impulse conduction: 1st, 2nd type 1&2, 3rd or complete heart block

16. P wave
Measures:

17. QRS WAVE
Measures:

18. QT Wave
Measures approx seconds

19. NSR: heart rate is 60-100bpm ST: heart rate 101-180 bpm
Heart rates
NSR: heart rate is bpm
ST: heart rate bpm
SB: heart rate <60 bpm

20. PR interval- 0.12-0.20sec QRS-0.06-0.10sec QT segment 0.36-0.44 sec
Sinus rhythm
PR interval sec
QRS sec
QT segment sec
Heart rate

21. Atrial arrhythmias Sinus tachycardia Atrial tachycardia
Sinus bradycardia
Premature atrial contraction (PAC)
Supraventricular tachycardia
Atrial fibrillation
Atrial flutter

22. Sinus Tachycardia

23. Atrial Tachycardia

24. Sinus Bradycardia

25. Premature Atrial Contraction (PAC)
Premature depolarization of atrial origin
P wave may be buried in T wave
A pause follows and SA node will start new cycle of sinus beats
Indicates atrial irritability
No risk if occasional
If 6 or more per minute, indicates atrial tachycardia
Treat: digitalis, calcium channel blockers, beta blockers

26. SupraVentricular Tachycardia (SVT)

27. Atrial Fibrillation (Afib)
Atrial rate > 400 bpm with a varying Ventricular rate
Overall rhythm irregular
No P waves, unable to measure PR interval
QRS=normal: Twave undeterminable
Causes: Rheumatic fever, mitral valve stenosis, cad. HTN, MI, hyperthyroidism, COPD, CHF PP. 1091
Concern with A fib is the development of atrial thrombus and loss of atrial kick from ineffective atrial function.
Treatment: Ca channel blockers and anti- arrhythmics to convert, beta blockers to < HR, anticoagulants to prevent embolization.
Synchronized cardioversion

28. Atrial Flutter

29. Atrial fib/flutter

30. Other Atrial Dysrhymias
Wolf Parkingson-White Syndrome (WPW)
Wandering Atrial Pacemaker (WAP)
Sick Sinus Syndrome (SSS)
Wolf-parkingson white – genetic AV conduction disorder, characterised by two different conduction pathways, produces delta waves (p waves) dips just before the R wave.
Wanderind atrial pacemaker – conduction pathways from 3 different sites above the HIS (can include pacemaker site at SA node, AV junction or ectopic atrial sites. Multi-focal p waves.
Sick sinus syndrome – impulse generation disorder, pacemaker disorder, conduction disorders, suseptable to paroxymal or chronic atrial tachycardias. Severe damaged sa node from heart disease. Meds

31. Management of Atrial Dysrhymias
Assess pt response/Monitor Vital Signs
May cause drop in Cardiac Output (CO)
Notify MD (Health Care Practitioner)
Intervention to convert back to NSR
Increase rate – slow rates, Administer drugs (Atropine), Transcutaneous Pacing
Control rate – if fast Ventricular Response
(ie: A-fib, SVT, Aflutter)
Anticoagulate
Cardioversion

32. How to treat SVT
B-blockers ( to decrease conduction thru AV
node:
Calcium channel blockers ( to decrease conduction
thru AV node)
Radio frequency ablation
SVT converted with Adenosine given rapid IV Push stimulates vagal response.

33. Atrial Fibrillation
- - 5 to 6 times more likely to have stroke
- - atrial rate: 300 to 600 times/minute
--prolonged A-Fib may stretch & weaken
heart muscle
- - symptoms: lightheaded, very tired,
SOB, diaphoretic, chest
pain,

34. A Fib electrical cardioversion:
High risk of forming clots & causing stroke
Anticoagulants taken before treatment and 3-4 weeks post treatment
If life-threatening, may need Heparin IV before cardioversion
Best time: recent A fib

35. Ventricular arrythmias
Junctional rhythms
AV blocks
Premature ventricular contraction (PVC)
Ventricular Tachycardia (V-tach)
Ventricular Fibrillation (V-Fib)
Torsade de Pointes (TdP)
Pulseless electrical activity (PEA)
Asystole

36. Junctional Escape Rhythm

37. Accelerated Junctional Rhythm

38. AV Blocks First degree block Second degree block Type I (Wenchebach)
Second degree block Type II (Mobitz II)
Third degree block
Bundle branch block

39. First degree heart block
AV node delays the impulse from the SA node for abnormal length of timeDocument the dysrhythmia
Monitor for progression to slower heart rate or worsening block
If progression noted, monitor pt, notify physician
Causes:
CAD, MI, drugs that act on AV node (digitalis)
Characteristics:
PR interval >0.20 seconds
Not serious but may progress to 2nd degre
Rate is usually WNL
Rhythm is regular
Pwaves are normal in size and shape
The PR interval is prolonged (>0.20 sec) but constant

40. Second degree heart block type 1 (Mobitz I or Wenchebach)
Pwaves are normal in size and shape;
Some pwaves are not followed by QRS
PR interval: lengthens with each cycle until it appears without QRS Complex
then the cycle starts over
QRS is usually narrow
RISK: often a temporary block after MI
May progress to complete(3rd degree)block
TREATMENT: freq. none needed
slow vent rate:
ATROPINE will increase AV conduction
EPINEPHRINE To increase rate of SA node
AV node delays progression of SA node impulse for longer than normal
Some of the SA impulses never reach ventricles
P waves regular
Progressive lengthening of PR interval until one P wave is not conducted
CAUSE: ischemia or injury to AV node

42. Second degree heart block type 2 (Mobitz II)
Ventricular rate is usually slow
Rhythm is irregular
Pwaves are normal in size and shape (more pwaves than QRS)
PR interval is within normal limits
QRS is usually wide
RISK: unpredictable & may suddenly advance to complete hrt block
Especially common after inferior infarction
A DANGEROUS WARNING DYSRHYTHMIA
TREATMENT: if vent rate slow, atropine or epinephrine
may need temporary pacer
Determine width of QRS
WATCH for widening QRS complex
*width of QRS indicates location in the conduction system of the block
the wider the complex, the lower in the bundle branch system the block will be.
IF QRS WIDENS, NOTIFY PHYSICIAN IMMEDIATELY.
Prepare for insertion of pacer
Assess vitalsAtrial rate 60 to 100
More P waves than QRS complexes
Ventricular response 2:1 or 3:1
No change in PR intervals of conducted P waves
CAUSES: disease of AV node, AV junctional tissue, or His-Purkinje system, inferior MI

43. 3rd degree heart block or complete heart block
More atrial waves than ventricular
No conduction of atrial impulses
Atrial/ventricles beat independently
RISKS: bradycardia which produces
a decrease in CO leading to hypotension & myocardial ischemia
TREATMENT; pacer
NURSING INTERVENTION; monitor , hemodynamics , prepare for pacer
Ventricular rate is regular but there is no correlation between p-waves and QRS
P waves are normal in size and shape
No true PR interval

44. Premature ventricular conduction (PVC)
uniform=go the same direction
multifocal= go in different direction
R on T=when the pvc fall on the preceding twave
couplet= 2 pvcs together
bigeminy= pvc every other beat
trigeminy=pvc every third beat

45. PVC
Unifocal
Multifocal

46. PVC: ventricular origin
Complex is wide followed by compensatory pause
An irritable focus in ventricle initiates a contraction before normally expected beat.
Acute MI most common cause
QRS is wide and bizarre
Risks: increasing myocardial irritability, leading to increased freq. of PVCs
Can occur as bigeminy (every other beat)
or short runs

47. Ventricular tachycardia
Monomorphic: beats are same size and shape
Polymorphic: different size and shape

48. Torsades de pointe This is a polymorphic VT
Usually electrical imbalance in r/t NA+ or K+

50. V-tach
Advanced irritability of ventricles due to ASHD, CHF, acute MI electrolyte imbalance. Hypoxia, acidosis, occasionally drugs
RISKS: low to no Cardiac output
Nursing Interventions: monitor, if pt unconscious, immediately defibrillate

51. Torsade de pointes Will see prolonged QT interval when in sinus rhythm
Will see prominent U wave
If lasts >10 seconds pt will progress to unconsciousness, life threatening with ineffective cardiac output
TREATMENT: IV magnesium

52. Ventricular Fibrillation (Course)
Rate can not be determined because of no identifiable waves
Rapid chaotic rhythm with no pattern
No p waves
No PR interval
No QRS

53. Ventricular Fibrillation (Fine)

54. Vtach/Vfib Both can be life threatening VT= V HR 100-250 bpm
Causes: AMI, CAD, hypokalemia, dig toxic
S/S: palpitations, dizzy, angina, <LOC
Treatment: assess for pulse, if none, defibrillate
VF=Rate undeterminable Cause: same
Treatment: CPR, Defibrillate

55. V-fib May occur after MI Extensive ventricular irritability
Very little or no cardiac output (No Pulse)
Death within 4 to 8 minutes
TREATMENT: immediate defibrillation
immediate defibrillation at 200 J (100J)
if unsuccessful, repeat at 300 J (150J)
If unsuccessful, repeat at 360 J (200J)
CPR
If do not know type of defibrillator start at 200J

56. Asystole

57. Pulsless Electrical Activity (PEA)

58. Asystole and PEA CPR Oxygen
Epinephrine 1 mg IV/IO (repeat 3-5 minutes)
May give Vasopressin 40U IV/IO to replace
1st or 2nd dose of epinephrine
Consider Atropine 1 mg IV/IO Repeat every 3 to 5 min (up to 3 doses)

59. Paced beat Pacer spike should fall before the P wave unless a dual
Chamber pacemaker; if it does not there could be a problem

60. ARTIFACT