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231 Cards in this Set
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Chapter 6 The Basic Beat
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Chapter 6 The Basic Beat
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normal P wave duration
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0.08 to 0.11s
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Tp wave represents
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repolarization of atria
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why cant you see Tp wave normally
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blocked by QRS
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normal PR segment duration
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from beginning of P wave to beginning of QRS; 0.12 to 0.2 s
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first neative deflection after P wave
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q or Q wave
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first positive deflection after P wave
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r or R wave
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criteria for Q wave significance
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greater than or equal to 0.03s or 1/3 of height of R wave
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intrinsicoid deflection
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measured from beginning of QRS to beginning of negative downslope of R
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intrinsicoid deflection represents
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time of impulse to travel from purkinje system to surface of epicardium
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intrinsicoid deflection is shorter in these leads
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right precordials (makes sense because right ventricles are thinner)
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ST segment spans from
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end of QRS to beginning of T wave
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point where QRS ends and ST segment begins
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J point
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ST elevation in a symptomatic patient
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considered MI until proven otherwise
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normal QRS duration
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0.06 to 0.11s
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T wave represents
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ventricular repolarization
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T wave should be in what direction
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same as QRS
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repolarization wave of ventricles travels in what way
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opposite of the depolarization wave
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symmetry of T wave
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not expected, first part should rise slowly followed by a fast downstroke
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QT intervel represents all events of
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ventricular systole
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prolonged QT is a harbinger of
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arrhythmias (torsades de pointes)
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normal QT
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variable but usually less than 1/2 of R-R
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QTc represents
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QT interval corrected for heart rate
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formula for QTc
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QT+1.75(ventricular rate - 60)
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normal, prolonged QTc
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normal ~0.41s prolonged > 0.419s
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U wave
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small flat wave seen after T and before next P wave
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U wave may be sign of
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hypokalemia
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P wave in NSR (normal sinus rhythm) must be positive in
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II, III, and aVF
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if P wave is inverted in II, III, and aVF there must be an
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eptopic pacemaker
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last part of ventricle to depolarize
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upper posterior part on left
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first area of ventricles to depolarize
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upper septal area
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early part of T wave is
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absolute refractory period
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late part of T wave is
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relative refractory period
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Chapter 7 The Rate
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Chapter 7 The Rate
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Heart Rates by # of big boxes
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300, 150, 100, 75, 60, 50,…
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additional methods of calculating rate
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take number of cycles in a 6 second strip and multiply by 10
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regular 12 lead EKG is _____ seconds long
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10
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Chapter 8 Rhythms
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Chapter 8 |
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tachycardia ; bradycardia
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>100 or less than 60 BPM
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3 irregularly irregular rhythms
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atrial ibrilation, WAP, MAT
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presense of identical P waves tells you that
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they are being generated by the same pacemaker
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presense of 3 or more P wave morphologies indicates
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WAP or MAT
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wide QRS indicates
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that the impulse did not travel through normal conduction system but instead through cell-cell contact
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sinus arrhythmia is a result of
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slowing of rate during exhalation and acceleration of rate during inhalation due to an increase in venous return during inhalation
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sinus bradycardia
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runs lower than 60bpm ; may be caused by vagal stimulation or beta blockers. Widening of PR and QRS but not beyond normal limits
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sinus tachycardia
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runs greater than 100bpm, is always secondary to another process (medications, exercise, hypoxia, hypovolemia, acidosis…etc…)
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sinus pause / arrest
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dropping of beats over a variable time ; no clear cut criteria
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sinoatrial block
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dropped beat but cycles continue on time and as scheduled (ie: P-P interval remains constant just with a missing beat). There is a nonconducted beat from the normal pacemaker
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when does a PAC occur
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when an eptopic pacemaker cell in atria fires at a rate faster than the SA node
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what occurs after a PAC
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reset of the SA node
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ectopic atrial tachycardia runs at what rate
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~100-180
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when does atrial tachcardia occur
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when an ectopic atrial focus fires more quickly than the underlying sinus rate ; episodes usually not sustained
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WAP
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wandering atrial pacemaker, runs less than 100BPM, at least 3 different P wave morphologies
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how to tell WAP on the EKG
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3 different P waves and PR intervals running at less than 100BPM
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MAT
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same as WAP but >100BPM
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atrial rate in atrial flutter
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250-350
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ventricular rate in atrial flutter
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125-175
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most common P:QRS interval in flutter
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2:01
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if you see a ventricular rate of about 150 you should look for
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F waves of atrial flutter ; would indicate 2:1 atrial flutter
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atrial fibrilation
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irregularly irregular, no discernable P waves.
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why is ventricular rate irregularly irregular in a fib
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not being paced by any one pacemaker,
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Premature Junctional Contraction is caused by
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beat that originates prematurely in AV node
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anterograde P wave
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appears before QRS comples (in PJC) with very short PR interval and inversion (II,III,aVF)
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retrograde P wave
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in PJC this is a P wave that occurs after the premature QRS complex.
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Junctional Escape Beat
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if normal SA pacemaker fails to fire, next available (AV) will fire. Distance of escape beat from previous beat is longer than normal P-P
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junctional rhythm runs at
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40-60bpm
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p waves in junctional rhythm
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absent (can be antero/retrograde too)
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accelerated junctional rhythm
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junctional rhyhtm running at a faster rate (60-100) junctional tachycardia is >100
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what is a compensatory pause, do you see it in PVC?
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when a premature beat has a pause that allows the following beat to arrive on schedule. Yes a PVC is followed by a compensatory pause ; a PAC is not
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characteristics of PVC
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wide QRS with bizarre appearance followed by a compensatory pause and return to sinus rhythm
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cause of PVC
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ventricular cell fires early, resulting in that tissue being refractory when the normal impulse arrives. When the impulse following that one arrives, the tissue is no longer refractory and sinus rhythm is restored
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P wave in PVC
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absent
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ventricular escape beat
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normal SA signal and AV signal do not fire, as such the intrinsic beat of the ventricle takes over for a beat. The pacemakers then reset at a new pace (non-compensatory pause)
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is the pause of Ventricular escape beat compensatory?
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no, pacemaker resets
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idioventricular and accellerated idioventricular rhythm
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ventricular focus acts as primary pacemaker of heart. Normally runs 20-40bpm but is accellerated if >40bpm
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QRS in idioventricular rhyhtm
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wide and bizarre
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in Vtach, irregular QRS deflections seen at regular intervals are indicative of what
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underlying sinus beats (which are detatched from the ventricles)
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Vtach runs at
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100-200bpm
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fusion beat
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seen in Vtach, is a hybrid of a sinus beat and the eptopic ventricular beat
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capture beat
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sinus beat that occurs in Vtach, occurs almost by chance, in that the SA impulse passes through at exactly the right time to allow a normal depolarization.
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precordial leads in Vtach show
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negative complexes
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torade de pointes
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occurs with QT prolongation, undulating sinusoidal rhythm that runs ~200-250bpm and can convert back to sinus or Vfib, very dangerous rhythm. "harbinger of death!"
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ventricular flutter
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rapid V Tach (200-300bpm)
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clinical syndrome associated with ventriuclar flutter
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wolf-parkinson-white with 1:1 conduction of atrial flutter
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Ventricular fibrillation
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chaos, death imminent
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1st degree heart block
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PR >0.2s and regular
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Mobitz I (2nd degree) (Wenckebach)
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successive lengthening of PR until a beat is dropped, at which point the cycle will reset
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Mobitz II (2nd degree)
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heart block with grouped normal beats and dropped beats with constant PR interval. Sign of bad things to come ie: complete block
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Third degree heart block
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complete block of AV node. P-P rate and ventricular rate regular but distinct
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Chapter 9 P Wave
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Chapter 9 P Wave
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P Waves should be positive in these leads
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II,III, aVF ; V4-6
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P Waves should be negative in
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aVR
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PAC is followed by what type of pause
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non-compensatory
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retrograde conduction through atria from an eptopic pacemaker will show up how on EKG
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inverted P waves in II,III,aVF
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a p wave lasting >0.12s that is notched (>0.04s between humps) is known as a
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P-mitrale, finding of severe Left atrial enlargment
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where would you see P-mitrale waves in LAE
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leads I, II
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P mitrale would be seen with which valvular condition
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mitral stenosis
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why the double hump in P-mitrale
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right atria conducts signal quickly, left atria slowly due to enlargement, this causes 2 different depolarization waves that are superimposed on each other
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a tall teepee shaped P wave (>2.5mm) in the limb leads is known as and is a sign of
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P-pulmonale ; is a sign of right atrial enlargment
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P pulmonale waves are most commonly seen in leads
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II, III
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biphasic P waves are seen in what lead most often, are indicative of what
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lead V1, indicative of intraatrial conduction delay (usually because of atrial enlargment)
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when the first half of biphasic P wave is taller in V1 than in V6 ______ is more likely
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RIGHT atrial enlargment
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when the second half of piphasic P wave is wider and deeper than 0.04s ______ is likely
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LEFT atrial enlargment
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how will biatrial enlargement appear on EKG
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signs of both may be seen (ie: P pulmonale and M mitrale, as well as biphasic P wave changes)
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Chapter 10 PR Interval
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Chapter 10 PR Interval
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why does conduction pass slowly through the AV node
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to allow time for atria to contract and prime the ventricles with blood
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PR depression is considered significant if it is > X mm
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0.8mm of depression
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significant PR depression is associated with what 2 conditions
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1. pericarditis 2. atrial infarction
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PR interval includes what events
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atrial depolarization, atrial repolarization, AV node stimulation, HIS bundle stimulation, BBB stimulation, purkinje stimulation
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normal PR interval
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0.12s to 0.2s
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signs of pericarditis on EKG (4)
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Tachycardia, PR depression, diffuse ST elevation with scooping, notching of S wave
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PR should be measured in lead with
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widest P wave and widest QRS complex
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these pts have shortened PR interval
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children, those with sinus tachycardia
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these pt have long PR interval
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the elderly
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PR intervals vary between leads (T/F)
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False, even if they appear different the PR interval should be same in all leads.
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ion that may be responsible for lengthened PR interval
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high potassium
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3 causes of short PR interval
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1. junctional P waves 2. PAC's 3. LGL syndrome 4. Wolff Parkinson White syndrome
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Lown-Ganong-Levine syndrome
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shortening of PR interval, caused by a bypass tract through the AV node (james fibers)
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why are retrograde waves easy to spot on EKG
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they are inverted in II,III,aVF
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shortened PR, wide QRS, _______ wave, ST-T chanes, and paroxysmal tachycardias are seen in what syndrome
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Wolff parkinson white syndrome (delta waves)
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shortened PR, wide QRS, delta waves, and ST/T changes without tachycardias is known as
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Wolff parkinson white pattern
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kent bundle
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bypass tract from atria to ventricles that creates an eptopic transmission without the usually AV node delay
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delta wave is a result of
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fusion of the kent bundle impulse merging with the normal conduction pathway
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if delta wave is negative it can be mistaken for
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MI, "pseudoinfarct" this is seen in leads III, aVF particularly
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most common type of delta wave
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A ( QRS upright in precordial leads, can draw a line across to look like an A)
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prolonged PR is
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longer than 0.2s
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how to distinguish WAP and MAT from heart block
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in heart block all P's will appear the same
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Mobitz 1 is caused by
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defective AV node that has a long refractory period, next impulse reaches earlier in refractory period and transmitts slower, this continues until a beat is dropped
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why is Mobitz 2 more dangerous
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may be a sign of imminent complete block
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3rd degree block is characterized by
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regular sinus and ventricular rate that run independently of each other
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Chapter 11 The QRS Complex
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Chapter 11 The QRS Complex
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septum depolarized from _________ to ____________
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left to right
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main vector of ventricular depolarization
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posterior and inferior
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final vector of ventricular depolarization
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posterior and superior
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precordial QRS changes
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as the leads move from the front to the side of the heart envision how the deflections caused by the 3 main vectors would change (remember the initial vector is directed anterior and to the right while the second and third vectors are direcred posterior and inferior/superior respectively)
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area on precordial leads where QRS switches from mostly negative to mostly positive
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~V3-4
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effusion and excess body fat have what effect on QRS voltage
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dampen it
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how to measure for LVH
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measure the deepest S wave in V1/2 and add it to the deepest R in V5/6 ; if >35mm then LVH is present
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can you diagnose LVH in presense of a LBBB
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no, you cant.
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additional criteria for LVH diagnosis
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precordial lead >45mm ; R wave in aVL >10mm ; R wave in lead I >11mm ; R wave in aVF >19mm
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why use precordial leads to diagnose LVH
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they are closer to the heart than the limb leads
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why do we look at V1/2 to diagnose RVH
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these leads are anterior and on the right of the heart. The strong vector produced by an RVH is directed this way. These leads will have a predominantly positive QRS with RVH
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typical criteria for diagnosing RVH using V1 and 2
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R:S ratio is more than 1
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to get true QRS duration, measure the __________ complex in the ECG
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widest
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any QRS segment > ________s is considered abnormal
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0.11s
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causes of wide QRS (many)
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LBBB, RBBB, PVC, V tach, WPW, IVCD, hyperkalemia, drug effects, idioventricular rhythms and heart block
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wide complex tachycardia is assumed __________ until proven otherwise
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V Tach
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wide complex tachycardias should cause you to suspect ___________kalemia
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HYPERkalemia
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significant Q wave represents
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dead myocardium
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septal Q waves are usually found in what leads
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I, aVL
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why would Q waves vary during respiration
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movement of the heart during respiration will also shift the axis
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where is it normal to see QS waves
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V1
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significant Q wave criteria
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>0.03s or >1/3 of height of complex
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where is the transition zone
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where QRS switches from more negative to more positive (is isoelectric)
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where does normal transition usually occur
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between V3 and V4
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counterclockwise rotation means transition occurs
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before V3
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clockwise rotation means transition occurs
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after V4
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what is the osborn (J) wave associated with
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severe hypothermia
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Chapter 12 The Electrical Axis
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Chapter 12 The Electrical Axis
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to localize the 90 degree quadrant the axis lies in you use what 2 leads
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I and aVF
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normal axis extends from
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-30 to 90 (book) and -20 to 100 (heibel)….choose wisely
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steps to isolating the ventricular axis
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find the quadrant, isolate the isoelectric lead, isolate the closest lead,isolate the vector
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how do you identify the isoelectric lead
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has the smallest QRS voltage ; if possible most isoelectric too
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how do you form the "T" for isolating the closest lead.
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draw a black line across the isoelectric lead and an arrow at 90 degrees from the black line running into the isolated quadrant
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how do you go from isolating the isoelectric lead to estimating closer to the true axis
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see if the isoelectric lead has positive or negative complexes. If it is more positive then add 10 degrees to the vector, if it is more than 2x as positive, add 20 degrees. The same applies to negative but you would subtract instead of adding
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causes of right axis deviation (5)
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normal for children, RVH, L posterior hemiblock, Dextrocardia, Ectopic beats and rhythms,
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causes of LAD (3)
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Left anterior hemiblock, ectopic ventricular beats and rhythms, LVH
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Chapter 13 Bundle Branch Blocks and Hemiblocks
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Chapter 13 Bundle Branch Blocks and Hemiblocks
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divisions of the conduction system in the ventricles
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left and right bundle branches. Left BB divides into anterior and posterior fasicles
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criteria for RBBB
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1. QRS >0.11 ; 2. RSR' pattern in V1 with R' > R ; 3. slurred S wave in I and V6 ; 4. ST wave in opposite direction as QRS
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why/what leads to you see R'
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there is a new slowed vector created by the late depolarization of the right ventricle. This shows as a second positive deflection on the right precordial leads (V1,2).
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why the slurred S wave and opposite direction ST wave
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same as above, this time however we are looking at the left ventricular leads I and V6. The slow right ventricular depolarization traveling away from these leads causes the slurred S wave
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what is a QR wave, where would you see it
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when an EKG shows changes of a septal MI and a RBBB there will be a QR or "floppy eared bunny" The ear that is flopping down is the significant Q wave and the R' is still upright
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criteria for diagnosing LBBB
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QRS >0.11s ; Broad monomorphic R in I and V6; broad monomorphic S in V1
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some variations seen in LBBB
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tall narrow R wave in V1 and notching of R in V6
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what is an IVCD, criteria?
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intraventricular conduction delay, doesn’t have to be >0.12s ; commonly in III, has features of RBBB and/or LBBB
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what can cause IVCD
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hyperkalemia is what to focus on here (other causes LVH, peri-infarction, qunindine /flecanide)
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can you diagnose LVH in presense of a LBBB
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no, you most certianly cannot
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left anterior fascicle innervates what
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anterior and lateral walls of left ventricle
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left posterior fasicle innervates
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inferior and posterior walls of left ventricle
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main change seen in LAH (left anterior hemiblock)
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Left axis deviation (between -30 and -90)
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criteria for LAH
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-30 to -90 axis ; qR complex or R wave in I ; rS complex in III (possibly II and aVF as well)
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shortcut for diagnosing LAH
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use quadrant identification for lead I, II, and aVF. Lead I will be positive, and lead II and AVF will be negative. The resultant axis will be somewhere between -30 and -90
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why is axis deviated to left in LAH
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since the anterior/lateral walls are not stimulated by the normal conducting pathway they are instead depolarized by the inferior and posterior section which creates a vector superior and to the left
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lead 1 in LAH
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positive
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lead II in LAH
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negative
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lead aVF in LAH
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negative
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why is left posterior fascicile difficult to block |
fibers are diffuse and not in a single bundle |
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what fasicle is more often blocked
|
left anterior fascile
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3 criteria for LPH
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axis between 90 and 180, s wave in I, q in III, exclusion of RAE an RVH
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stable and unstable bifascicular blocks
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RBBB+LAH is stable RBBB+LPH is unstable and will often progress to complete heart block
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what do you see in LAH+RBBB bifascicular block
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positive lead 1 negative aVF and lead II. RSR' in V1; slurred S in V6
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Chapter 14 ST segment and T Waves
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CH 14 ST Segment and T Waves
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ST depression and inverted T waves are signs of
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ischemia
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ST elevation is a sign of
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infarction
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J point is
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area where transition between QRS and ST segment occurs
|
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what interval determines baseline
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TP segment
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concave up ST segment is associated with
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early repolarization, pericarditis
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concave down ST segment is associated with
|
strain pattern
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flat depressed ST is associated with
|
subendocardial ischemia
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flat elevated ST is associated with
|
injury pattern
|
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tombstone pattern of ST is associated with
|
infarction and ventricular aneurysm
|
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Epsilon waves are associated with what population
|
italian males
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tall narrow T waves are common in
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hyperkalemia
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a pathologic biphasic T wave is positive/negative first
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negative
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T waves are usually positive where, negative
|
positive in I,II,V3-6 ; ;; neg in aVR…..this is not the case in BBB
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if T wave is more than ________ the height of the R wave then it is abnormal
|
2/3 the height
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RVH with strain pattern
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increased R:S ratio in V1 and V2 with a concave down ST segment and a flipped asymmetric T wave
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LVH with strain pattern
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in V4-6 you see ST depression with downward concavity and a flipped asymmetric T wave ; in V1-3 you see a concave up ST elevation with an upright asymmetric T wave
|
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in LVH with strain the strain pattern is greatest ___________________________
|
in the lead with tallest and deepest QRS pattern
|
|
when differentiating LVH strain from ischemia a sharp J point is more indicitave of
|
ischemia/infarction
|
|
additional factor to help determine LVH strain from ischemia
|
the condition of the patient
|
|
criteria for PR changes in pericarditis
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1. PR depression 2. diffuse ST elevation 3. scooping and upward concavity of ST 4. notching at end of QRS
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what tissue depolarizes first, repolarizes first
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endocardium depolarizes first, but the epicardium repolarizes first, this is why T wave is same direction as QRS
|
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in presense of BBB or PVC what is the repolarization pattern
|
repolarizes in the same order that it depolarized
|
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in a BBB the T wave is always ____________ to the terminal portion of QRS, this is called ___________
|
opposite direction, discordance
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concordance in presense of BBB is a sign of
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ischemia
|
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U waves can occur in the presense of
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hypokalemia
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if U wave occurs opposite of the T wave this is ______ ; could be a sign of
|
bad, cardiac ischemia until proven otherwise
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T wave is _______________ is ischemia ; T wave is ______________ in LVH strain pattern
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symmetrical in ischemia ; asymmetrical in strain
|
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Chapter 15 Acute MI
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Chapter 15 Acute MI
|
|
electrical state of ischemic tissue
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ischemic tissue is more negative, causes ST depression and inverted T wave
|
|
electrical state of injured tissue
|
does not repolarize completely, ST elevation, T remains inverted
|
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describe the shape of an infarct, ischemia
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they are both wedge shaped, however in ischemia the fattest side is near the pericardium and in infarct the fattest side is near the endocardium
|
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decribe the electrical changes (on an ion level) that occur in cardiac ischemia
|
decrease in ATP leads to less activity of NA/K/ATPase, leads to increased extracellular K and an injury current ,
|
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why significant Q waves
|
if tissue is dead all electrical activity will move away from it. In the lead that is over this tissue there will be a negative deflection that shows this, this is the Q wave
|
|
non Q MI is usually
|
subendocardial
|
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anterior wall infarct
|
LAD
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lateral wall infarct
|
LCX
|
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inferior wall infarct
|
RCA
|
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what is a reciprocal change in an MI
|
leads opposite of the damaged area will show opposite changes : ie ST depresison as opposed to elevation
|