Download Beachey Ch 18 ECG and Cardiac Arrhythmias

Lecture Notes
Chapter 18
Electrocardiogram and
Cardiac Arrhythmias
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Helpful Hints
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Depolarize = Depolarize = Contracts
Systolic
Afterload
Repolarize = Repolarize = Recover
Diastolic
Preload
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Normal Electrocardiogram (ECG)
EKG
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Electrocardiograph
 Detects micro-voltage changes as the heart
depolarizes and repolarizes
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How? - Leads
ECG “leads” (electrode configurations)
• Plots electrical activity that creates depolarization and
repolarization
• Leads are placed on chest, arms, and legs
• Bipolar standard limb leads
• Unipolar limb and chest leads
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ECG Components
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Waves and complexes
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P wave = atrial depolarization
QRS complex = ventricular depolarization
• 0.08 to 0.10 sec
T wave = ventricular repolarization
Wave height (amplitude) = voltage
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ECG Components
Fig. 18-2
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ConceptQuestion 18-1
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A high amplitude P wave may be associated
with what type of abnormality?
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ECG Components
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Intervals and segments
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PR interval
• From SA node to ventricles
• 0.12 to 0.20 sec
J point
• QRS _______________________________________
ST segment
• Flat, lying on baseline is normal
• Depressed >0.5 mm = ________________________
• Elevated >2 mm =
________________________________
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ECG Components
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Intervals and segments
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QT interval
• ________________________________________
• Usually less than __________ seconds
• The ventricle is in the refractory period
 Refractory Period
____________________________________
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ECG Graph Paper
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Grid
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1 mm (smallest square) vertical = 0.1 mV
1 mm horizontal = 0.04 sec
Heavy 5 mm lines (big square) = 0.20 sec & 0.5
mV
5 large squares = 25 mm (about 1 inch) = 1 sec
25 mm/sec graph speed
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ECG Graph Paper
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Fig. 18-5 11
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ECG Leads
Fig. 18-9
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Hexaxial Reference Figure
Fig. 18-11
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Identifying Common Arrhythmias
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Systematic ECG analysis
Steps
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1: Identify waves and complexes
2: Analyze QRS complexes
3: Analyze P waves
4: Assess AV relationship
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Identifying Common Arrhythmias
Box 18-2
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Normal Sinus Rhythm
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Sinus node initiates each depolarization
Rate: 60 to 100 beats/min
P wave-QRS complex ratio is 1:1
Spacing between QRS is constant
PR interval is <0.16 sec
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Normal Sinus Rhythm
Heart Rate _______
Fig. 18-16
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Abnormal Sinus Rhythms
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Tachycardia
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Sinus tachycardia
• HR >100 beats/min
• Regular and rhythmic
• Causes
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Exercise, fever, anxiety, pain, coffee, smoking, hypoxia
Beta adrenergic drugs
• Treatment: OXYGEN… Then, focus on underlying cause
• Additional Treatment: Vagal Stimulation
• =_____________________________________
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A rapid heart rate
__________________________
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Abnormal Sinus Rhythms
Tachycardia
Heart Rate _______
Fig. 18-17
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Abnormal Sinus Rhythms
Bradycardia
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Bradycardia
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Sinus bradycardia
• HR <60 beats/min
• Regular and rhythmic
• Normal in sleep, physically conditioned individuals
• Carotid sinus syndrome; overly sensitive pressure
receptors (vagal) in the neck… If stimulated = syncope
• SYNCOPE = _________________
• Gagging can also cause bradycardia (Suctioning)
• Symptomatic bradycardia
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hypotension, weakness, sweating, syncope
• Treatment: atropine; pacemaker
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Abnormal Sinus Rhythms
Bradycardia
Heart Rate _______
Fig. 18-18
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Abnormal Sinus Rhythms
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Sinus arrhythmia
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Irregularly generated sinus node impulses
Alternate between fast and slow rates
Irregular spacing between QRS complexes
Follows inspiration & expiration (↑rate insp.; ↓exp.)
No clinical significance and do not require
treatment
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Abnormal Sinus Rhythms
Fig. 18-19
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Premature Atrial Contraction (PAC)
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Ectopic focus fires = early atrial contraction
QRS complexes are ____________ but
___________ _____________
Stress, alcohol, tobacco, caffeine, electrolyte
imbalances, sympathetic stimulation
Drugs: sodium & calcium channel inhibitors
may be used: quinidine: verapamil
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Premature Atrial Contraction (PAC)
Fig. 18-20
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Supraventricular Arrhythmias
“Above the Ventricles”
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Atrial flutter
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Single ectopic pacemaker above AV node
Ectopic focus produces F waves (saw-toothed)
• “P waves are now F waves”
AV node normally blocks transmission of many Fwaves
Atrial rate 200-350 bpm and regular; thus QRS
rate is regular, but slower than atrial rate
Symptoms: palpitations, nervousness, anxiety,
possible syncope if inadequate ventricular filling
time
++ blockers; electrical cardioversion
Treatment:
Ca
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Supraventricular Arrhythmias
A-Flutter
Every 4th atrial impulse is transmitted to ventricles,
producing a regular QRS rhythm.
Fig. 18-21
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Supraventricular Arrhythmias
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Atrial fibrillation
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Multiple randomly firing ectopic atrial foci
Atria “quiver” (no pumping) at 300-600 impulses/min;
completely irregular
Loss of atrial kick = reduced ventricular filling→ reduced
stroke volume & CO; occasional peripheral pulse deficit
Fine fibrillatory waves; slightly wavy baseline (no “Ps”)
Slower, irregular ventricular rate
Causes: conditions that ↑ atrial pressure & enlarge atria:
longer depolarization route
May cause hypotension, fainting (syncope)
Pooling of blood in atria: thromboembolism risk:
anticoagulant drugs important preventative treatment
Treatment: Ca++ blockers; electrical cardioversion
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Supraventricular Arrhythmias
A-Fib
Fig. 18-22
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Junctional Arrhythmias
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AV node assumes role of pacemaker
Junctional escape rhythm if SA node fails to fire
Inherent rate of 40 to 60 bpm
QRS normal shape and duration
Retrograde (backward) atrial conduction
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Irritable junctional fibers cause PJC
Junctional tachycardias
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Inverted, hidden, or retrograde P waves (after QRS)
Paroxysmal (PSVT): up to 240/min (caffeine, nicotine,
alcohol, overexertion, electrolyte imbalance, etc.)
Nonparoxysmal (150/min): ↑junctional excitability (drug
toxicity)
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Treatment: vagal
stimulation; IV adenosine; IV Ca++ blocker
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ConceptQuestion 18-4
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Why do chronic congestive heart failure and
high atrial pressures predispose a person to
the development of atrial fibrillation?
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Junctional Arrhythmias
Fig. 18-24
Inverted P waves; slow heart rate
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Junctional Arrhythmias
Junctional Tachycardia
Fig. 18-25
No P waves
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Ventricular Arrhythmias
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Premature ventricular contraction (PVC)
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Ectopic focus/excitability arises from ventricles
QRS not preceded by P wave
Wide (>0.12 sec) and bizarre appearance
Generate T wave of opposite polarity (downward)
Followed by compensatory pause
Frequent PVCs signal life-threatening arrhythmia potential; highly
irritable ventricular muscle fibers
Unifocal vs. multifocal PVCs
Bigeminy
Treatment: antiarrhythmic drug: lidocaine
OXYGEN!
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Ventricular Arrhythmias
Unifocal PVCs
Fig. 18-26
Multifocal PVCs: serious ventricular irritability
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Ventricular Arrhythmias
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Ventricular tachycardia (V-Tach)
 Successive “runs” of PVCs
 Rate of 110-250/min
 Treat as emergency: serious sign of ventricular
irritability
 QRS complexes bizarre and wide
 High potential to progress to ventricular
fibrillation
 Treat with IV lidocaine or amiodarone
 Cardioversion
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Ventricular Tachycardia
Fig. 18-28
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Ventricular Arrhythmias
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Ventricular fibrillation (VF)
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Most lethal arrhythmia = cardiac arrest; CODE BLUE
Ventricles nonfunctional, quivering, no pumping ability
No recognizable waves or complexes
Requires electrical defibrillation—no drug can convert to
normal rhythm
Equivalent to Cardiac Arrest. CPR must be initiated
SHOCKABLE RHYTHM
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Along with a shock, use:
• Epinephrine, Amiodarone, Lidocaine
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Ventricular Fibrillation
Fig. 18-29
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ASYSTOLE
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