7. Arrhythmia Interpretation, Arrhythmia emergencies, and Pacemaker Therapy Flashcards
Arrhythmia Interpretation, Arrhythmia emergencies, and Pacemaker Therapy
Test candidates are expected to have mastered arrhythmia interpretation and have an understanding of ACLS principles, so look these over. An exam question may describe the arrhythmia OR provide an arrhythmia strip for interpretation, but the question will usually be related to pt management.
**For exam questions that include the development of an arrhythmia, pay close attention to the pt’s clinical response to the arrhythmia
** Is the pt stable or unstable? If the clinical description is NOT provided, consider this fact and do NOT assume the pt response!
Conduction Abnormalities: Wolff-Parkinson-White syndrome
WPW is a genetic conduction abnormality in which an abnormal conduction pathway exists that allows a reentrant tachycardia pathway to bypass the normal AV node conduction pathway, resulting in supraventricular tachycardia. WPW is primarily seen in those younger than 30 years old.
Wolff-Parkinson-White syndrome: When in sinus rhythm
the ECG demonstrates a short PR interval and the presence of a delta wave (seen as a slow rise in the initial upstroke of the QRS).
WPW results in ___
SVT when the abnormal pathway takes over, but It may also present as PRE-EXCITED ATRIAL FIBRILLATION (irregular rhythm, rates of 150 beats/minute or greater, and a wide QRS.)
Wolff-Parkinson-White syndrome: Signs and symptoms during SVT include
palpitations, dizziness, chest pain, sob, and syncope
Treatment of Wolff-Parkinson-White syndrome
-Radiofrequency ablation to eliminate the reentrant pathway
-If unstable SVT is present, perform synchronized cardioversion OR administer adenosine
-If pre-excited atrial fibrillation (AF) is present, administer Bblockers, amiodarone, or procainadmide IV.
-Do NOT give adenosine, digoxin, or ca channel blockers for pre-excited AF; these agents may enhance antegrade conduction thru the abnormal pathway by increasing the refractory period in the AV node, RESULTING IN VENTRICULAR FIBRILLATION, VF.
Conduction abnormalities: Prolongation of the QT interval
(causes, treatment) is often addressed on the CCRN exam. QT prolongation may lead to Torsades de pointes.
**Causes of QT prolongation include
-Drugs–amiodarone, quinidine, haloperidol, procainamide.
-Electrolyte problems – hypokalemia, hypocalcemia, hypomagnesemia.
**Treatment for Torsades VT
magnesium
Pacemaker Therapy: Code
A = atria
V = Ventricle
D = dual (both)
Pacemaker Code, paced v sensed
-First initial = chamber paced; this was “invented” first
-Second initial = chamber sensed; this function came
along second
-Third initial = response to sensing; last to be devd
Third initial in pacer code
I = inhibits (pacer detects intrinsic cardiac activity and withholds its pacing stimuli)….demand
D = inhibits AND triggers (pacer detects intrinsic cardiac activity and fires a pacing stimuli in response)
O = none
On the CCRN exam, you may see a Q that asks how a “VVI” or a “DDD” pacer works. If you remember the code, you should be able to figure out the answer.
e.g. Which pacemaker paces both the atria and the ventricles, senses both the atria and the ventricles, and can inhibit and trigger in response to sensing?
DDD