5. Conduction System
Each component of the conductive system has
its own intrinsic rate of self-excitation.
SA node = 60–100 beats per minute
AV node = 40–60 beats per minute
Purkinje system = 15–40 beats per minute
7. Electrocardiographic
Monitoring
Electrocardiogram (ECG) is a graphic record of
the heart’s electrical activity.
Tells you nothing about the heart’s pumping ability,
which you must evaluate by pulse and blood pressure.
The body acts as a giant conductor of electricity.
The heart is its largest generator
Electrodes on the skin can detect the total
electrical activity within the heart.
9. The Electrocardiogram
ECG Leads
Bipolar (Limb)
▪ Einthoven’s Triangle
▪ Leads I, II, III
▪ Provide only one view of the
heart
Augmented (Unipolar)
▪ aVR, aVL, aVF
Precordial
▪ V1 – V6
▪ Measure electrical cardiac activity
on a horizontal axis
▪ Help in viewing the left ventricle
and septum
11. The Electrocardiogram
Routine Monitoring
Routine ECG monitoring generally uses only one lead
Most common monitoring leads are either lead II or the
modified chest lead 1 (MCL1)
Einthoven’s triangle offers a basis for placing the leads
Place the electrodes on the chest wall
Lead placement
12. Single Lead Monitoring
Information from a
single lead shows:
Rate
Regularity
Time to conduct an
impulse
Single lead cannot
show:
Presence of an infarct
Axis deviation or
chamber enlargement
Right-to-left differences
in conduction
Quality or presence of
pumping action
13. The Electrocardiogram
ECG Paper
Speed
A standard speed of
25 mm/sec
Amplitude
and Deflection
Should deflect two
large boxes when 1
mV is present
Calibration
22. The Electrocardiogram
Time Intervals
PR Interval (PRI) or
PQ Interval (PQI)
0.12–0.20 seconds
QRS Interval
0.08–0.12 seconds
ST Segment
QT Interval
0.33–0.42 seconds
23. The Electrocardiogram
Refractory Periods
The all-or-none nature of myocardial depolarization
results in an interval when the heart cannot be
restimulated
Absolute
▪ Cannot accept stimulus
Relative
▪ If stimulus is strong enough, will cause depolarization
24. The Electrocardiogram
ST Segment Changes
The ST segment is usually an isoelectric line
Ischemia causes deflections
Infarctions usually follow this sequence:
Ischemia
ST segment depression or an inverted T wave
Injury
Elevates the ST segment
Necrosis
Significant Q wave presents
25. The Electrocardiogram
Interpretation of Rhythm Strips
Basic Criteria
Always be consistent and analytical
Memorize the rules for each dysrhythmia
Analyze a given rhythm strip according to a specific format
Compare your analysis to the rules for each dysrhythmia
Identify the dysrhythmia by its similarity to established rules
26. The Electrocardiogram
Five-Step Procedure
Analyze the rate
Analyze the rhythm
Analyze the P waves
Analyze the PR interval
Analyze the QRS complex
34. The Electrocardiogram
Analyzing P Waves
Are P waves present?
Are the P waves regular?
Is there one P wave for each QRS complex?
Are the P waves upright or inverted?
Do all the P waves look alike?
Analyzing the PR Interval
Normal PR interval is 0.12–0.20 sec
Analyzing the QRS Complex
Do all the QRS complexes look alike?
What is the QRS duration?
Usually 0.04–0.12 sec
35. Cardiac Rhythms
Normal Sinus Rhythm
Rate
60–100
Rhythm
Regular
P waves
Normal, upright, only before each QRS complex
PR Interval
0.12–0.20 seconds
QRS Complex
Normal, duration of <0.12 seconds
38. Dysrhythmias
Dysrhythmia
Any deviation from the heart’s normal electrical
rhythm
Arrhythmia
The absence of cardiac electrical activity
39. Causes of Dysrhythmias
Myocardial Ischemia, Necrosis, or Infarction
Autonomic Nervous System Imbalance
Distention of the Chambers of the Heart
Blood Gas Abnormalities
Electrolyte Imbalances
40. Causes of Dysrhythmias
Trauma to the Myocardium
Drug Effects and DrugToxicity
Electrocution
Hypothermia
CNS Damage
Idiopathic Events
Normal Occurrences
41. Dysrhythmias
Mechanism of Impulse Formation
Ectopic Foci
Result of enhanced automaticity
Cells other than the pacemaker cells automatically depolarize
PVC’s, PAC’s, and PJC’s
Reentry
Ischemia or another disease process alters two branches of a
conduction pathway
Can result in rapid rhythms such as paroxysmal
supraventricular tachycardia or atrial fibrillation
43. Dysrhythmias
Classification by Site of Origin
Originating in the SA Node
Originating in the Atria
Originating within the AV Junction (AV Blocks)
Originating in the AV Junction
Originating in the Ventricles
Resulting from Disorders of Conduction
45. Dysrhythmias Originating
in the SA Node
NormalQRS
NormalPRI
Upright and normalP Waves
SA node
Pacemaker
Site
RegularRhythm
Less than 60Rate
Sinus Bradycardia
Rules of Interpretation
46. Dysrhythmias Originating
in the SA Node
Sinus Bradycardia
Etiology
Increased parasympathetic (vagal) tone, intrinsic disease of the
SA node, drug effects
May be a normal finding in healthy, well-conditioned persons
Clinical Significance
Decreased cardiac output, hypotension, angina, or CNS
symptoms
In healthy, well-conditioned person, may have no significance
47. Sinus Bradycardia
Treatment
Treat if hypotension or ventricular irritability is
present
Prepare for transcutaneous pacing
Atropine may be considered if delay in pacing
48. NormalQRS
NormalPRI
Upright and normalP Waves
SA node
Pacemaker
Site
RegularRhythm
Greater than 100Rate
Sinus Tachycardia
Rules of Interpretation
Dysrhythmias Originating
in the SA Node
49. Dysrhythmias Originating
in the SA Node
Sinus Tachycardia
Etiology
Results from an increased rate of SA node discharge
Potential causes include exercise, fever, anxiety, hypovolemia,
anemia, pump failure, increased sympathetic tone, hypoxia, or
hypothyroidism
Clinical Significance
Decreased cardiac output for rates >140
Very rapid rates can precipitate ischemia or infarct
Treatment
Treatment is directed at the underlying cause
