1. Arrhythmias:
By Nancy Jenkins

2. The EKG is the electrical activity of the heart.
Electrical precedes mechanical
(Without electricity, we have no pump!!)

3. How is electricity generated
How is electricity generated? By action potentials (view on own) Na, K and Ca very important for this
Na K pump
Calcium channels
Depolarization
Repolarization
YouTube - How the Body Works : A Nerve Impulse
·        ECG waveforms are produced by the movement of charged ions across the semipermeable membranes of myocardial cells.

5. Cardiac Cycle

7. EKG waveforms
P wave associated with atrial depolarization (stimulation)
QRS complex associated with ventricular depolarization (stimulation)
T wave associated with ventricular repolarization (recovery)
Atrial recovery wave hidden under QRS wave
Stimulus causes atria to contract before ventricles
Delay in spread of stimulus to ventricles allows time for ventricles to fill and for atrial kick % CO

8. Yellow is the isoelectric phase. The purple is the "P"wave
Yellow is the isoelectric phase. The purple is the "P"wave. The purple and yellow split is the "PR" interval. The red is the "Q" wave. The light blue is the "R" wave. The light green is the "S" wave. The black is the "ST" segment. The orange is the "T" wave. Yellow again is isoelectric. The dark blue is the "U" wave (seldom seen- hypokalemia).

9. Conduction system- Pacemakers
SA node
AV node 40-60
Bundle of His
Left and Right Bundle Branch
Purkinge Fibers 15-40
Each beat that is generated from the same pacemaker will look identical.
Impulses from other cardiac cells are called ectopic and look different (PVC, PAC)
Primary and secondary pacemakers

10. Pacemakers other than SA node
A pacemaker from another site can lead to dysrhythmias and may be discharged in a number of ways.
o       Secondary pacemakers may originate from the AV node or His-Purkinje system.
o       Secondary pacemakers can originate when they discharge more rapidly than the normal pacemaker of the SA node.
o       Triggered beats (early or late) may come from an ectopic focus (area outside the normal conduction pathway) in the atria, AV node, or ventricles.

11. EKG graph paper Horizontal measures time Vertical measures voltage
Helps us determine rate
Width of complexes- intervals (QRS)
Duration of complexes- intervals (PR and QT)

12. EKG graph paper

13. Intervals-
**PR , QRS , QT

14. Monitoring leads- based on 12 lead EKG
Each lead is either unipolar or bipolar.
Each lead looks at a different area of the heart.
This can be diagnostic in the case of an MI

15. We monitor using 3 leads or 5 leads
RNCEU’s
We monitor using 3 leads or 5 leads
Lead II negative R arm looking to LL positive- upright P waves
and QRS complex and T waves
lead placement:
Depolarization wave moving toward a positive lead will be upright.
Depolarization wave moving toward a negative lead will inverted.
Depolarization wave moving between negative and positive leads will have both upright and inverted components.
*Five lead placement allows viewing all leads within limits of monitor

16. How to place leads
(White is right, grass under clouds, smoke above fire)
**V1 is 4th ICS right of sternum – brown or ground (most important)
Lead II R arm looking to LL positive

17. Leads to monitor in EKG leads
Best for arrhythmias- lead II and MCL(if using 3 leads) or V1 leads- lead II easy to see P waves. MCL or V1 easy to see ventricular rhythms.
If impulse goes toward positive electrode complex is positively deflected or upright
If impulse goes away from positive electrode complex is negatively deflected or goes down form baseline

18. Cardiac cells are either contractile cells influencing the pumping action or pacemaker cells influencing the electrical activity of the heart

19. 4 Characteristics of Cardiac Cells
Automaticity- initiate an impulse
Excitability- respond to stimulus
Conductivity- transmit from cell to cell (if some areas blocked can get re-entering impulses- tachycardia
Contractility- muscle fibers shorten
Refractoriness
Relative
absolute

20. Refractory Period

21. Risk Factors for Arrhythmias
Hypoxia
Structural changes
Electrolyte imbalances
Central nervous system stimulation
Medications
Lifestyle behaviors

22. Steps in Assessment of Rhythms
**Calculate rate
Big block- big blocks in R-R divide into 300
Little block - little blocks in R-R into 1500
Number of R waves in 6 sec times 10
Calculate rhythm-reg or irreg
Measure PR interval, <.20
QRS interval
P to QRS relationship

23. Rate How is the rate controlled? Autonomic Nervous System
Parasympathetic nervous system:when? Vagus nerve
Decreases rate
Slows impulse conduction
Decreases force of contraction
Sympathetic nervous system: when?
Increases rate
Increases force of contraction

24. Rate Calculation
1 lg box= lg boxes =1 sec lg boxes =6sec Therefore there are 300 lg boxes in 1 min.
1 Heartbeat / # of Large Blocks X Large Blocks/1 Minute = ______ Heartbeats/Minute
1 Heartbeat/ # of Small Blocks X 1500 Small Blocks/1 Minute = ________ Heartbeats/Minute

25. Calculating Rate

26. Sinus Rhythm Normal P wave PR interval<.20 QRS.04-.12
T wave for every complex
Rate is regular
Rate >100: Sinus Tachycardia
Causes-anxiety, hypoxia, shock, pain, caffeine, drugs
Treatment-eliminate cause

27. Characteristics for ST include:
Regular rhythm
PR interval less than .20 secs.
QRS .08
Rate greater than 100

28. Sinus Tachycardia Clinical significance
Dizziness and hypotension due to decreased CO
**Increased myocardial oxygen consumption may lead to angina

30. Rate<60: Sinus Bradycardia- relative-symptomatic, absolute-normal
Cause-vagal stimulation, athlete, drugs (Blockers and digoxin), head injuries, MI
Watch for syncope and falls
Treatment- if symptomatic, atropine or pacer

31. Patients with bradycardia may have symptoms such as:
Heart rate less than 60
Dizziness
Hypertension
Confusion

32. Sinus Bradycardia Clinical significance- (dec CO)
Dependent on symptoms
Hypotension
Pale, cool skin
Weakness
Angina
Dizziness or syncope
Confusion or disorientation
Shortness of breath

33. Sinus Arrhythmia (SA) Rate 60-100
Irregular rhythm- increases with inspiration, decreases with expiration
P, QRS,T wave normal
Cause- children, drugs(MS04), MI
Treatment- none

34. Sinus Arrest See pauses
May see ectopic beats(PAC’s PVC’s) do not treat
Cause MI
Treatment
Atropine
Isuprel
Pacemaker

35. Atrial Arrythmias Atria is the pacemaker
Atrial rate contributes 25-30% of cardiac reserve
Serious in patients with MI- WHY?

36. **Medications used to treat the atrial rhythms
Cardizem and Verapamil- calcium channel blockers
Digoxin
Amiodarone or dronedarone- (Multaq)
Corvert- ibutilide
Metropolol and inderal- beta blockers

37. Premature Atrial Contraction (PAC’s)-ectopic
P wave abnormally shaped
PR interval shorter
QRS normal
Cause-age, MI, CHF, stimulants, dig, electrolyte imbalance, stress, fatigue
Treatment- remove stimulants and watch for SVT

39. Paroxysmal Supraventricular Tachycardia (PSVT)
Rate is , regular, p often hidden
Atria is pacemaker (may not see p waves)reentrant phenomenon
Cause-SNS stimulation, MI, CHF,sepsis
Treatment- vagal stimulation, * adenosine, digoxin, verapamil, inderal, cardizem,tikosyn, or cardioversion

41. Paroxysmal Supraventricular Tachycardia (PSVT)
Clinical significance
Prolonged episode and HR >180 bpm may precipitate ↓ CO
Palpitations
Hypotension
Dyspnea
Angina

42. Atrial Flutter Rate of atria is 250-300, vent rate varies
Regular rhythm- single focus in RA
P waves saw tooth, ratio 2:1, 3:1, 4:1
Flutter waves- No PR interval
Cause-diseased heart, dig
Treatment- cardioversion, calcium channel blockers and beta blockers, amiodorone, ablation, coumadin. pradaxa
3:1 flutter

43. Atrial Flutter Clinical significance
High ventricular rates (>100) and loss of the atrial “kick” can decrease CO and precipitate HF, angina
Risk for stroke due to risk of thrombus formation in the atria

44. Atrial Fibrillation-most common
Rate of atria (disorganized rhythm)
Ventricular response irregular (RVR)
No P waves, “garbage baseline”
Cause-#1 arrhythmia in elderly, heart disease- CAD, rheumatic, CHF, alcohol
Complications- dec. CO and thrombi (stroke)
Treatment goals:
Decrease ventricular response (less than 100)
Prevent cerebral embolic events
Convert to SR if possible

45. Treatment
Rate control-start with digoxin, ca channel blockers, beta blockers, multaq- rate control
To convert to SR-amiodorone and ibutilide (corvert), pronestyl, cardioversion (TEE to see if clots before) Coumadin- check PT and INR, ablation and Maze
Prevent embolic events- Coumadin,Pradaxa, ASA if low risk

48. Atrial Fibrillation

49. Atrial Fibrillation Clinical significance
Can result in decrease in CO due to ineffective atrial contractions (loss of atrial kick) and rapid ventricular response
Thrombus formation, pulse deficit, AR>RR
Thrombi may form in the atria as a result of blood stasis
Embolus may develop and travel to the brain, causing a stroke

50. **AV Conduction Blocks- important to check HR and hold blockers
Arrhythmias of AV Node
**AV Conduction Blocks- important to check HR and hold blockers

51. First Degree AV Block Transmission through AV node delayed
PR interval >.20
QRS normal and regular
Cause-dig toxicity, MI, CAD vagal, and blocker drugs
Treatment- none but watch for further blockage

52. Characteristics of 1st degree block include:
Regular rhythm
Long PR interval
More P’s than QRS’s
Rate less than 100

54. First-Degree AV Block Clinical significance Treatment
Usually asymptomatic
May be a precursor to higher degrees of AV block
Treatment
Check medications
Continue to monitor

55. Second Degree AV Block more P’s than QRS’s
A. Mobitz I (Wenckebach) YouTube - Diagnosis Wenckebach
PR progressively longer then drops QRS (long, longer, longest, drop)
Cause- MI, drug toxicity
Treatment- watch for type II and 3rd degree
B. MobitzII
More P’s but skips QRS in regular pattern 2:1,3:1, 4:1(QRS usually greater than .12-BBB)
Constant PR interval- can be normal or prolonged
Treatment-Pacemaker
Occurs in HIS bundle with bundle branch block

56. Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach)
Clinical significance
Usually a result of myocardial ischemia or infarction
Almost always transient and well tolerated
May be a warning signal of a more serious AV conduction disturbance

58. Second-Degree AV Block, Type 2 (Mobitz II)
Clinical significance
Often progresses to third-degree AV block and is associated with a poor prognosis- pacemaker
Reduced HR often results in decreased CO with subsequent hypotension and myocardial ischemia

60. 3rd Degree AV Block Atria and ventricles beat independently
Atrial rate
Slow ventricular rate 20-40
No PR interval
Wide or normal QRS (depends on where block is)
Cause- severe heart disease, blockers elderly, MI
Complications- dec. CO, ischemia, HF, shock, and syncope
Treatment- atropine, pacemaker

61. Third-Degree AV Heart Block (Complete Heart Block)
Clinical significance
Decreased CO with subsequent ischemia, HF, and shock
Syncope may result from severe bradycardia or even periods of asystole (patient may present with history of fall)

62. 3rd Degree

63. Bundle Branch Blocks Left BBB Right BBB QRS.12 or greater
Rabbit ears- RR’
No change in rhythm

64. Right Bundle Branch Block

67. Junctional Rhythm
AV node is pacemaker- slow rhythm (40-60) but very regular impulse goes to atria from AV node- backward)
P wave patterns
Absent
P wave precedes QRS inverted in II, III, and AVF
P wave hidden in QRS
P wave follows QRS

68. .
                                                                                           

69. Cont. PR interval QRS normal No treatment Absent or hidden
Short <.12
Negative or RP interval
QRS normal
No treatment

71. Ventricular Arrythmias Most serious
Easy to recognize

72. Premature Ventricular Contractions (PVC’s)-ectopic
QRS wide and bizarre
No P waves
T opposite deflection of PVC
Cause- 90% with MI, stimulants, dig, electrolyte imbalance
Treatment- O2, amiodarone, lidocaine, pronestyl,

74. Premature Ventricular Contractions
Clinical significance
In normal heart, usually benign
In heart disease, PVCs may decrease CO and precipitate angina and HF
Patient’s response to PVCs must be monitored
PVCs often do not generate a sufficient ventricular contraction to result in a peripheral pulse
Apical-radial pulse rate should be assessed to determine if pulse deficit exists

75. Premature Ventricular Contractions
Clinical significance
Represents ventricular irritability
May cause HF, angina, and dec CO
May occur
After lysis of a coronary artery clot with thrombolytic therapy in acute MI—reperfusion dysrhythmias
Following plaque reduction after percutaneous coronary intervention

76. PVC’s-unifocal PVC’s multi-focal Multifocal- from more than one foci
Bigeminy- every other beat is a PVC
trigeminy- every third beat is a PVC
Couplet- 2 PVC’s in a row

77. Treat if:
>5 PVC’s a minute
Runs of PVC’s
Multi focal PVC’s
R on T

78. Ventricular Tachycardia (VT)
Ventricular rate , regular or irregular
No P waves
QRS>.12
Can be stable- pulse or unstable –no pulse
Cause- electrolyte imbalance, MI, CAD, dig
Life- threatening, dec. CO, watch for V-fib
Treatment- same as for PVC’s and defibrillate for sustained

79. Ventricular Tachycardia
Clinical significance
Treatment for VT must be rapid
May recur if prophylactic treatment is not initiated
Ventricular fibrillation may develop
Sustained VT: Severe decrease in CO
Hypotension
Pulmonary edema
Decreased cerebral blood flow
Cardiopulmonary arrest

81. Nursing Assessment Apical rate and rhythm Apical/radial deficit
Blood pressure
Skin
Urine output
Signs of decreased
cardiac output

82. VT- Torsades de Pointes- polymorphic VT (Magnesium)
French for twisting of the points

83. Ventricular Fibrillation
Garbage baseline-quivering
No P’s
No QRS’s
No CO
Cause-MI, CAD, CMP, shock, K+, hypoxia, acidosis, and drugs
Treatment- code situation, ACLS, CPR, **defibrillate- if available no delay

86. Complications of Arrhythmias
Hypotension
Tissue ischemia
Thrombi- low dose heparin, ASA, or coumadin, pradaxa
Heart failure
Shock
Death

87. Diagnostic Tests Telemetry- 5 lead( lead II and V1) 12 lead EKG
Holter monitor- pt. keeps a diary
Event monitoring- pt. records only when having the event
Exercise stress test
Electrophysiology studies- induce arrhythmias under controlled situation

88. Nursing Diagnoses Decreased cardiac output Decreased tissue perfusion
Activity intolerance
Anxiety and Fear
Knowledge deficit

89. Goals

90. Antiarrhythmics
Remembering that of all anti-arrhythmics "some block potassium channels" can help you:
Class I "Some" = S = Sodium
Class II "Block" = B =Beta blockers
Class III "Potassium" = Potassium channel blockers
Class IV "Channels" = C =Calcium channel blockers

91. Comfort Measures
Rest O2
Relieve fear and anxiety- valium

92. Invasive procedures Defibrillation
Emergency- start at 200 watt/sec, go to 400
Safety precautions
AED’s
Synchronized Cardioversion- for vent. or SVT
Can be planned- if stable
Get permit
Start at 50 watt/sec
Awake, give O2 and sedation
Have to synchronize with rhythm

93. cardioversion

94. Implanted Cardiac Defibrillator (ICD)
Senses rate and width of QRS
Goes off 3 times, then have to be reset
Combined with pacemaker- overdrive pacing or back up pacing

96. Medications –Table 36-9 p.832 Classified by effect on action potential
Class I- fast Na blocking agents-ventricular
Quinidine, Pronestyl, Norpace,Lidocaine, Rhythmol
Class II-beta blockers (esmolol, atenolol, inderal) atrial- SVT,Afib,flutter
Class III- K blocking (amiodorone, tikosyn, sotalol, corvert) both atrial and ventricular
Class IV- Ca, channel blockers (verapamil cardizem)SVT,Afib,flutter
Other- adenosine, dig, atropine, magnesium

97. Pacemaker Permanent- battery under skin
Temporary- battery outside body
Types
Transvenous
Epicardial- bypass surgery
Transcutaneous- emergency
Modes
Asynchronous- at preset time without fail
Synchronous or demand- when HR goes below set rate
Review classifications-

98. Pacemaker Classification

100. Pacemakers
Fig
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

102. Pacemaker Problems:
Failure to sense
Failure to capture

103. Ablation Done in special cardiac procedures lab
Use a laser to burn abnormal pathway
# cardioversion

104. 3 ECG Changes Associated with Acute Coronary Syndrome (ACS)
Ischemia
ST segment depression and/or T wave inversion
ST segment depression is significant if it is at least 1 mm (one small box) below the isoelectric line

105. ECG Changes Associated with Acute Coronary Syndrome (ACS)
Injury/Infarction- ST elevation
ST segment elevation is significant if >1 mm above the isoelectric line
If treatment is prompt and effective, may avoid infarction
If serum cardiac markers are present, an ST-segment-elevation myocardial infarction (STEMI) has occurred (code stemi)

106. ECG Changes Associated with Acute Coronary Syndrome (ACS)
Infarction/Necrosis- Q wave
Note: physiologic Q wave is the first negative deflection following the P wave
Small and narrow (<0.04 second in duration)
Pathologic Q wave is deep and >0.03 second in duration

107. ECG Changes Associated with Acute Coronary Syndrome (ACS) FYI only
Fig A
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

108. ECG Changes Associated with Acute Coronary Syndrome (ACS)
Fig B
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

109. ECG Changes Associated with Acute Coronary Syndrome (ACS)
Fig
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

110. Syncope Brief lapse in consciousness CausesVasovagal
Cardiac dysrhythmias
Other- hypoglycemia, seizure, hypertrophic cardiomyopathy
1-year mortality rate as high as 30% for syncope from cardiovascular cause

112. Quizzes Discussion Questions
Casestudies 2-6

113. Video acting out rhythms
YouTube - cardiac arrhythmias

114. Practice-
Rhythm Practice
ACLS