Arrhythmias Flashcards
Right atrial enlargement
large P wave amplitudes
Left atrial enlargement
large P wave durations, notching of P wave often seen due to out-of-sync conduction of right and left atria
2 Main causes of QRS Issues
- excessive generation of electrical potential in a particular direction, 2. more time required for depolarization wave to travel through muscle (ventricular enlargement)
Right ventricular enlargement
large S waves in I, II, aVF
Left ventricular enlargement
not always observed because left ventricle is already larger than right ventricle
Intraventricular conduction defects
impulses aren’t as fast, QRS duration will be longer
Left bundle branch block
wide and positive deflections in I, II, III, aVF, and inverted aVR and aVL, large R waves
Right bundle branch block
right axis deviation usually present, large S waves in I, II, III, aVF
Causes of arrhythmias
- abnormal rhythmicity of the pacemaker
- shift of pacemaker activity
- conduction blocks
- abnormal pathways of impulse transmission
- spontaneous generation of abnormal impulses
Sinus arrhythmia
impulses originate at the SA node at a varying rate, faster then slower, primary cause is respiration
Wandering atrial pacemaker
impulses originate from varying points in atria, P wave changes configuration, originate from various parts of atria, QRS still normal
Sinus arrest
SA node stops firing, escape beat
First degree AV block
not dangerous but will progress, PR interval is very long
Second degree AV block
Mobitz Type I- progressive lengthening of PR interval before dropped beat, block gets thicker, so PR interval length increases
Mobitz Type II- sudden QRS dropped without prior PR lengthening, atrial rate is greater than the ventricular rate (more P waves)
Third degree AV block
QRS rate is greater than the P rate (slower), SA node paces atria, Purkinje fibesr pace ventricular (separate rates), P and T waves are biphasic, ** no relationship between the two rates
Atrial flutter
atria contracting quickly
Atrial fibrillation
no distinct P waves, irregularly spaced QRS complexes, no coordinated direction, AV node drives, no the SA node
Ventricular paroxysmal tachycardia
runs of 3 or more VPCs in sequence
Ventricular bigeminy
normal—->premature—->normal—->premature
Ventricular fibrillation
cardiac output is 0, no QRS waves, decrease in velocity, shortening refractory period, most vulnerable during ventricular repolarization
Supraventricular premature contraction
premature beats, P occurs before T wave
Supraventricular paroxysmal tachycardia
clusters of premature contractions
Ventricular premature contraction
usually no P wave, QRS wide and bizarre, morphology of QRS will vary with each focus
