EKG I - Rhythms Flashcards
arrhythmias - defined
*deviations from normal sinus rhythm
*any disruption in the pattern of electrical signaling that occurs during the cardiac cycle, resulting in a heartbeat that is too fast, too slow, or otherwise irregular
findings of NORMAL SINUS RHYTHM on EKG
*upright P wave (usually in lead II)
*each P wave is followed by a QRS complex at a consistent interval
*normal QRS interval (80-100 msec)
*normal PR interval (120-200 msec)
categories of arrhythmias
- supraventricular arrythmia
- junction escape rhythm
- ventricular arrhythmia
- heart block
supraventricular arrythmias (general)
*arrhythmias originating above the cardiac ventricles (from SA or AV node)
*EKG findings: rapid rate, narrow (normal) QRS complexes
*examples: AF, AFL, SVT
junctional escape rhythms (general)
*bradycardia occurring at the atrioventricular junction (AV node or bundle of His)
*EKG findings: low HR, ABSENT P WAVES, narrow (normal) QRS complexes
ventricular arrhythmias (general)
*occur when the ventricular cardiomyocytes generate action potentials
*EKG findings: rapid rate, WIDE QRS complexes (> 120msec or > 3 small boxes)
*examples: VT, VF
heart block (general)
*corresponds to a failure or slowing of conduction at a point through the AV node, bundle of His, or bundle branches
*EKG findings:
-long PR intervals OR
-dropped QRS complexes OR
-dissociation between atria and ventricles
*examples: 1st, 2nd, or 3rd degree heart block
mechanisms of arrhythmias
- reentry
- increased automaticity
- triggered activity
- decreased automaticity
- conduction block
mechanisms of arrhythmias: reentry
*continuous propagation of an electrical impulse traveling in a circuitous path
*results in reactivation of the original site that generated the electrical impulse, continuing the cycle in a loop and causing tachycardia
*can result from an obstacle in the conducting system that the electrical signal must travel around, such as scar tissue
mechanisms of arrhythmias: increased automaticity
*an increased rate of generating action potentials, by either normal pacemaker tissue or abnormal tissue within the myocardium
*often caused by increased sympathetic activity
mechanisms of arrhythmias: triggered activity
*a normal action potential induces a spontaneous abnormal action potential immediately after it (an “after-depolarization”), causing extra beats
mechanisms of arrhythmias: decreased automaticity
*decreased rate of action potential generation by the SA node, resulting in a low heart rate (bradycardia)
*can be physiologic (sleeping), medication-induced, or pathologic
mechanisms of arrhythmias: conduction block
*occurs when the normal cardiac conduction system is disrupted and the electrical signal is slowed or blocked
*can be incomplete (slow transmission) or complete (no transmission)
premature atrial contractions (PACs)
*characterized by early narrow QRS complexes, always preceded by a P wave
*wide, aberrant P waves with a PR interval > 120 msec (> 3 small boxes)
*can be conduction (followed by ventricular contraction) or non-conducting
*arise from an ectopic focus within the atria, producing an abnormal P wave on ECG
atrial fibrillation (AF)
*characterized by an IRREGULARLY IRREGULAR rate & rhythm with NO DISCRETE P WAVES
*rate of atrial depolarization greatly exceeds rate of ventricular depolarization
*atrium fibrillates (quivers) b/c the atrial depolarizations lead to a lack of true coordinated atrial contractions
*irregularly irregular = R-R interval varies from beat to beat
*no discrete P waves = P waves cannot truly be distinguished; baseline looks wavy and haphazard
atrial flutter (AFL)
*characterized by a rapid succession of identical, consecutive atrial depolarization, causing a “SAWTOOTH” appearance of P waves
*atrium usually beats at rate ~300 bpm
*usually, the R-R intervals are regular
paroxysmal supraventricular tachycardia (PSVT)
*characterized by narrow QRS complexes and fast heart rate (150-250 bpm)
*ABSENT P WAVES
*treat with ADENOSINE
*most often due to a reentrant tract b/w atrium and ventricles, usually in AV node
Wolff-Parkinson-White Syndrome
*characteristic DELTA WAVE with WIDENED QRS COMPLEX and SHORTENED PR INTERVAL
*abnormal fast accessory pathway from atria to ventricles (bundle of Kent) bypasses rate-slowing AV node → ventricles partially depolarize earlier → delta wave + wide QRS + short PR interval
premature ventricular contractions (PVCs)
*characterized by early, WIDE QRS complexes, followed by a compensatory pause
*single abnormal beat with a WIDE QRS complex (> 120 msec or > 3 small boxes) and atypical QRS morphology
*no preceding P wave
*compensatory pause followed the PVC: no more electrical impulses for a period 2x the regular P-P interval
*T wave of the PVC points in the opposite direction of the QRS
*ectopic beat(s) arising from the ventricle instead of the SA node
ventricular tachycardia
*series of 3+ consecutive WIDE QRS complexes (>120 msec or > 3 small boxes) at 100-250 bpm
*can be monomorphic (QRS complexes of the same shape) or polymorphic (QRS complexes of different shapes)
*WIDE QRS complexes with NO PRECEDING P WAVES
*most commonly due to structural heart disease (cardiomyopathy, scarring after MI)
*tx = amiodarone + SHOCK
torsades de pointes
*a polymorphic ventricular tachycardia characterized by irregular waveforms of alternating amplitudes, resembling twisting around a point (shifting sinusoidal waveforms)
*may progress to ventricular fibrillation
*LONG QTc INTERVAL predisposes to torsades
*tx: IV magnesium sulfate
ventricular fibrillation
*disorganized rhythm with no identifiable waves (no discernible pattern)
*P waves and QRS complexes indiscernible
*irregular rate, usually > 300 bpm
*tx: fatal without immediate CPR + defibrillation (SHOCK)
