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a.
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(2)
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1. Bipolar (i.e., detect a change in electric potential between two points) and
detect an electrical potential change in frontal plane.
Lead I- between right arm and left arm electrodes,- left arm being positive.
Lead II is between right arm and left leg electrodes, left
leg being positive.
Lead III is between left arm and left leg electrodes, left
leg again being positive.
A diagrammatic representation of these three leadstermed Einthoven's triangle (shown in blue below), after
Dutch doctor who first described the relationship. Central
source of electrical potential in triangle is heart.
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*Refer to p. 847 Table 36-2- Values may vary slightly with different sources-use text
book for test purposes
a. P wave: atrial depolarization and contraction= p , upright (0.060.12)
b. PR interval-time for sinus impulse to travel from SA node to AV node
and into bundle branches (beginning of P wave to beginning of QRS
complex) (0.12 - 0.20 seconds
c. QRS Complex-ventricular depolarization and contraction; transmission
of impulse through ventricular conduction system *(0.04 0.12)
seconds
d. ST segment-beginning of ventricular repolarization; end of QRS
complex to beginning of T wave; isoelectric; *Recall significance of
elevated ST segment with MI (0.12)
e. T wave- ventricular repolarization; smooth and round, < 10 mm tall;
same direction as QRS complex; abnormalities due to myocardial
injury or ischemia, electrolyte imbalances. *Danger area if shock on
T wave!
f. QT interval- total time ventricular depolarization and repolarization;
beginning of QRS complex to end of T wave; prolonged QT: prolonged
relative refractory period = greater risk for dysrhythmias; shortened
QT: due to medications or electrolyte imbalance; *measure QT interval
prior to admin. some meds (0.34 0.43 seconds)
g. U wave- repolarization of terminal Purkinje fibers; same direction as T
wave; seen with hypokalemia (contact healthcare provider!)
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5. Normal Sinus Rhythm- sinus node fires 60-100 bpm; follows normal
conduction pattern
a. Normal P wave
b. PR interval<.20
c. QRS.06-.12
d. T wave for every complex
e. Rate is regular 60-100
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Evaluation of Dysrhythmias- *p. 848, 753 Tab 32-7 for description, care
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2.
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6.
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3. Sinus Arrhythmia
a. Description: normal conduction, however irregular rhythm- rate 60100, increases with inspiration, decreases with expiration; P, QRS,T
wave normal
b. Clinical association/causes- normal in children, drug effect as (MS04),
MI
c. Treatment- none
Supraventricular dysrhythmias (atrial arrythmias) Can be serious: atria
contributes 25-30% cardiac output (atrial kick); especially in patients with MIalready decreased cardiac reserve. *ectopic pacemaker overrides the SA node; may
develop as escape rhythm if SA node fails- paroxysmal (occur in bursts- abrupt
onset and end) *Pacemaker- no longer SA node-atria becomes pacemaker.
Frequently used meds to treat atrial dysrhymias- *diltiazem (Cardizem)
calcium channel blocker (Class IV), digoxin (Lanoxin) inhibits sodium-potassium
ATPase, dec. AV conduction speed), amiodarone (Cardarone) Class III potassium
channel blocker), dofetilide (Tikosin) potassium channel blocker), verapamil *Calan)
calcium channel blockers * Know these
4. Premature Atrial Contraction
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6. Atrial Flutter
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8. Junctional Dysrhythmias
a. Description: *AV node- pacemaker; SA node failed to fire or impulse
blocked at AV node; rate- 40-60 BPM, can have junctional tachycardia
or 60-140 BPM; P wave patterns vary, may be absent or precede QRS
inverted in II, III and AVF, or hidden in QRS or follow QRS); PR
interval is absent or hidden <.10; QRS normal at 0.06-0.10 sec
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c. Clinical Significance
1) Usually asymptomatic
2) May be precursor to higher degrees of AV block
d. Treatment
1) Check medications * If on digitalis or beta blockers, hold
meds
2) Continue to monitor
10. Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach)
a. Description: *Gradual lengthening PR interval, due to prolonged
AV conduction timeLong, longer, longest, drop, then you
have a Wenkeback!; PR progressively longer until drops QRS; PR
interval variable
1) Atrial impulse nonconducted; QRS complex blocked (missing)
2) Block usually at AV node, but can occur in His-Purkinje
system
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Digitalis toxicity
Clinical Significance; *Progress to third-degree AV block;
associated with a poor prognosis; reduced HR result in dec. CO with
hypotension and myocardial ischemia
Treatment: If symptomatic (e.g., hypotension, angina) before
permanent pacemaker, use temporary transvenous or transcutaneous
pacemaker; May try atropine (likely not to be effective) , Isuprel
(why these drugs? ); long term-*Permanent pacemaker
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Pulseless Electrical Activity -Electrical activity can be observed on the ECG, but
there is no mechanical activity of the ventricles and the patient has no pulse;
Treatment- CPR followed by intubation and IV epinephrine; Atropine is used if the
ventricular rate is slow; directed toward correction of the underlying cause
Sudden Cardiac Death (SCD)- Death from a cardiac cause; majority of SCDs due
to ventricular dysrhythmias (ventricular tachycardia, ventricular fibrillation)
Prodysrhythmia - Antidysrhythmic drugs may cause life-threatening dysrhythmias
esp. Digoxin and class IA, IC, and III antidysrhythmia drugs; first several days of
drug therapy most vulnerable period for developing prodysrhythmias. *ideally be
monitored in hospital.
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Transcutaneous pacing
2) Permanent pacemaker: implanted totally within body: Singlechamber pacing (atria or ventricles stimulated) or dualchamber pacing (both are stimulated)
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