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231 Cards in this Set

  • Front
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Chapter 6 The Basic Beat
Chapter 6 The Basic Beat
normal P wave duration
0.08 to 0.11s
Tp wave represents
repolarization of atria
why cant you see Tp wave normally
blocked by QRS
normal PR segment duration
from beginning of P wave to beginning of QRS; 0.12 to 0.2 s
first neative deflection after P wave
q or Q wave
first positive deflection after P wave
r or R wave
criteria for Q wave significance
greater than or equal to 0.03s or 1/3 of height of R wave
intrinsicoid deflection
measured from beginning of QRS to beginning of negative downslope of R
intrinsicoid deflection represents
time of impulse to travel from purkinje system to surface of epicardium
intrinsicoid deflection is shorter in these leads
right precordials (makes sense because right ventricles are thinner)
ST segment spans from
end of QRS to beginning of T wave
point where QRS ends and ST segment begins
J point
ST elevation in a symptomatic patient
considered MI until proven otherwise
normal QRS duration
0.06 to 0.11s
T wave represents
ventricular repolarization
T wave should be in what direction
same as QRS
repolarization wave of ventricles travels in what way
opposite of the depolarization wave
symmetry of T wave
not expected, first part should rise slowly followed by a fast downstroke
QT intervel represents all events of
ventricular systole
prolonged QT is a harbinger of
arrhythmias (torsades de pointes)
normal QT
variable but usually less than 1/2 of R-R
QTc represents
QT interval corrected for heart rate
formula for QTc
QT+1.75(ventricular rate - 60)
normal, prolonged QTc
normal ~0.41s prolonged > 0.419s
U wave
small flat wave seen after T and before next P wave
U wave may be sign of
hypokalemia
P wave in NSR (normal sinus rhythm) must be positive in
II, III, and aVF
if P wave is inverted in II, III, and aVF there must be an
eptopic pacemaker
last part of ventricle to depolarize
upper posterior part on left
first area of ventricles to depolarize
upper septal area
early part of T wave is
absolute refractory period
late part of T wave is
relative refractory period
Chapter 7 The Rate
Chapter 7 The Rate
Heart Rates by # of big boxes
300, 150, 100, 75, 60, 50,…
additional methods of calculating rate
take number of cycles in a 6 second strip and multiply by 10
regular 12 lead EKG is _____ seconds long
10
Chapter 8 Rhythms

Chapter 8

tachycardia ; bradycardia
>100 or less than 60 BPM
3 irregularly irregular rhythms
atrial ibrilation, WAP, MAT
presense of identical P waves tells you that
they are being generated by the same pacemaker
presense of 3 or more P wave morphologies indicates
WAP or MAT
wide QRS indicates
that the impulse did not travel through normal conduction system but instead through cell-cell contact
sinus arrhythmia is a result of
slowing of rate during exhalation and acceleration of rate during inhalation due to an increase in venous return during inhalation
sinus bradycardia
runs lower than 60bpm ; may be caused by vagal stimulation or beta blockers. Widening of PR and QRS but not beyond normal limits
sinus tachycardia
runs greater than 100bpm, is always secondary to another process (medications, exercise, hypoxia, hypovolemia, acidosis…etc…)
sinus pause / arrest
dropping of beats over a variable time ; no clear cut criteria
sinoatrial block
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
when does a PAC occur
when an eptopic pacemaker cell in atria fires at a rate faster than the SA node
what occurs after a PAC
reset of the SA node
ectopic atrial tachycardia runs at what rate
~100-180
when does atrial tachcardia occur
when an ectopic atrial focus fires more quickly than the underlying sinus rate ; episodes usually not sustained
WAP
wandering atrial pacemaker, runs less than 100BPM, at least 3 different P wave morphologies
how to tell WAP on the EKG
3 different P waves and PR intervals running at less than 100BPM
MAT
same as WAP but >100BPM
atrial rate in atrial flutter
250-350
ventricular rate in atrial flutter
125-175
most common P:QRS interval in flutter
2:01
if you see a ventricular rate of about 150 you should look for
F waves of atrial flutter ; would indicate 2:1 atrial flutter
atrial fibrilation
irregularly irregular, no discernable P waves.
why is ventricular rate irregularly irregular in a fib
not being paced by any one pacemaker,
Premature Junctional Contraction is caused by
beat that originates prematurely in AV node
anterograde P wave
appears before QRS comples (in PJC) with very short PR interval and inversion (II,III,aVF)
retrograde P wave
in PJC this is a P wave that occurs after the premature QRS complex.
Junctional Escape Beat
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
junctional rhythm runs at
40-60bpm
p waves in junctional rhythm
absent (can be antero/retrograde too)
accelerated junctional rhythm
junctional rhyhtm running at a faster rate (60-100) junctional tachycardia is >100
what is a compensatory pause, do you see it in PVC?
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
characteristics of PVC
wide QRS with bizarre appearance followed by a compensatory pause and return to sinus rhythm
cause of PVC
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
P wave in PVC
absent
ventricular escape beat
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)
is the pause of Ventricular escape beat compensatory?
no, pacemaker resets
idioventricular and accellerated idioventricular rhythm
ventricular focus acts as primary pacemaker of heart. Normally runs 20-40bpm but is accellerated if >40bpm
QRS in idioventricular rhyhtm
wide and bizarre
in Vtach, irregular QRS deflections seen at regular intervals are indicative of what
underlying sinus beats (which are detatched from the ventricles)
Vtach runs at
100-200bpm
fusion beat
seen in Vtach, is a hybrid of a sinus beat and the eptopic ventricular beat
capture beat
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.
precordial leads in Vtach show
negative complexes
torade de pointes
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!"
ventricular flutter
rapid V Tach (200-300bpm)
clinical syndrome associated with ventriuclar flutter
wolf-parkinson-white with 1:1 conduction of atrial flutter
Ventricular fibrillation
chaos, death imminent
1st degree heart block
PR >0.2s and regular
Mobitz I (2nd degree) (Wenckebach)
successive lengthening of PR until a beat is dropped, at which point the cycle will reset
Mobitz II (2nd degree)
heart block with grouped normal beats and dropped beats with constant PR interval. Sign of bad things to come ie: complete block
Third degree heart block
complete block of AV node. P-P rate and ventricular rate regular but distinct
Chapter 9 P Wave
Chapter 9 P Wave
P Waves should be positive in these leads
II,III, aVF ; V4-6
P Waves should be negative in
aVR
PAC is followed by what type of pause
non-compensatory
retrograde conduction through atria from an eptopic pacemaker will show up how on EKG
inverted P waves in II,III,aVF
a p wave lasting >0.12s that is notched (>0.04s between humps) is known as a
P-mitrale, finding of severe Left atrial enlargment
where would you see P-mitrale waves in LAE
leads I, II
P mitrale would be seen with which valvular condition
mitral stenosis
why the double hump in P-mitrale
right atria conducts signal quickly, left atria slowly due to enlargement, this causes 2 different depolarization waves that are superimposed on each other
a tall teepee shaped P wave (>2.5mm) in the limb leads is known as and is a sign of
P-pulmonale ; is a sign of right atrial enlargment
P pulmonale waves are most commonly seen in leads
II, III
biphasic P waves are seen in what lead most often, are indicative of what
lead V1, indicative of intraatrial conduction delay (usually because of atrial enlargment)
when the first half of biphasic P wave is taller in V1 than in V6 ______ is more likely
RIGHT atrial enlargment
when the second half of piphasic P wave is wider and deeper than 0.04s ______ is likely
LEFT atrial enlargment
how will biatrial enlargement appear on EKG
signs of both may be seen (ie: P pulmonale and M mitrale, as well as biphasic P wave changes)
Chapter 10 PR Interval
Chapter 10 PR Interval
why does conduction pass slowly through the AV node
to allow time for atria to contract and prime the ventricles with blood
PR depression is considered significant if it is > X mm
0.8mm of depression
significant PR depression is associated with what 2 conditions
1. pericarditis 2. atrial infarction
PR interval includes what events
atrial depolarization, atrial repolarization, AV node stimulation, HIS bundle stimulation, BBB stimulation, purkinje stimulation
normal PR interval
0.12s to 0.2s
signs of pericarditis on EKG (4)
Tachycardia, PR depression, diffuse ST elevation with scooping, notching of S wave
PR should be measured in lead with
widest P wave and widest QRS complex
these pts have shortened PR interval
children, those with sinus tachycardia
these pt have long PR interval
the elderly
PR intervals vary between leads (T/F)
False, even if they appear different the PR interval should be same in all leads.
ion that may be responsible for lengthened PR interval
high potassium
3 causes of short PR interval
1. junctional P waves 2. PAC's 3. LGL syndrome 4. Wolff Parkinson White syndrome
Lown-Ganong-Levine syndrome
shortening of PR interval, caused by a bypass tract through the AV node (james fibers)
why are retrograde waves easy to spot on EKG
they are inverted in II,III,aVF
shortened PR, wide QRS, _______ wave, ST-T chanes, and paroxysmal tachycardias are seen in what syndrome
Wolff parkinson white syndrome (delta waves)
shortened PR, wide QRS, delta waves, and ST/T changes without tachycardias is known as
Wolff parkinson white pattern
kent bundle
bypass tract from atria to ventricles that creates an eptopic transmission without the usually AV node delay
delta wave is a result of
fusion of the kent bundle impulse merging with the normal conduction pathway
if delta wave is negative it can be mistaken for
MI, "pseudoinfarct" this is seen in leads III, aVF particularly
most common type of delta wave
A ( QRS upright in precordial leads, can draw a line across to look like an A)
prolonged PR is
longer than 0.2s
how to distinguish WAP and MAT from heart block
in heart block all P's will appear the same
Mobitz 1 is caused by
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
why is Mobitz 2 more dangerous
may be a sign of imminent complete block
3rd degree block is characterized by
regular sinus and ventricular rate that run independently of each other
Chapter 11 The QRS Complex
Chapter 11 The QRS Complex
septum depolarized from _________ to ____________
left to right
main vector of ventricular depolarization
posterior and inferior
final vector of ventricular depolarization
posterior and superior
precordial QRS changes
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)
area on precordial leads where QRS switches from mostly negative to mostly positive
~V3-4
effusion and excess body fat have what effect on QRS voltage
dampen it
how to measure for LVH
measure the deepest S wave in V1/2 and add it to the deepest R in V5/6 ; if >35mm then LVH is present
can you diagnose LVH in presense of a LBBB
no, you cant.
additional criteria for LVH diagnosis
precordial lead >45mm ; R wave in aVL >10mm ; R wave in lead I >11mm ; R wave in aVF >19mm
why use precordial leads to diagnose LVH
they are closer to the heart than the limb leads
why do we look at V1/2 to diagnose RVH
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
typical criteria for diagnosing RVH using V1 and 2
R:S ratio is more than 1
to get true QRS duration, measure the __________ complex in the ECG
widest
any QRS segment > ________s is considered abnormal
0.11s
causes of wide QRS (many)
LBBB, RBBB, PVC, V tach, WPW, IVCD, hyperkalemia, drug effects, idioventricular rhythms and heart block
wide complex tachycardia is assumed __________ until proven otherwise
V Tach
wide complex tachycardias should cause you to suspect ___________kalemia
HYPERkalemia
significant Q wave represents
dead myocardium
septal Q waves are usually found in what leads
I, aVL
why would Q waves vary during respiration
movement of the heart during respiration will also shift the axis
where is it normal to see QS waves
V1
significant Q wave criteria
>0.03s or >1/3 of height of complex
where is the transition zone
where QRS switches from more negative to more positive (is isoelectric)
where does normal transition usually occur
between V3 and V4
counterclockwise rotation means transition occurs
before V3
clockwise rotation means transition occurs
after V4
what is the osborn (J) wave associated with
severe hypothermia
Chapter 12 The Electrical Axis
Chapter 12 The Electrical Axis
to localize the 90 degree quadrant the axis lies in you use what 2 leads
I and aVF
normal axis extends from
-30 to 90 (book) and -20 to 100 (heibel)….choose wisely
steps to isolating the ventricular axis
find the quadrant, isolate the isoelectric lead, isolate the closest lead,isolate the vector
how do you identify the isoelectric lead
has the smallest QRS voltage ; if possible most isoelectric too
how do you form the "T" for isolating the closest lead.
draw a black line across the isoelectric lead and an arrow at 90 degrees from the black line running into the isolated quadrant
how do you go from isolating the isoelectric lead to estimating closer to the true axis
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
causes of right axis deviation (5)
normal for children, RVH, L posterior hemiblock, Dextrocardia, Ectopic beats and rhythms,
causes of LAD (3)
Left anterior hemiblock, ectopic ventricular beats and rhythms, LVH
Chapter 13 Bundle Branch Blocks and Hemiblocks
Chapter 13 Bundle Branch Blocks and Hemiblocks
divisions of the conduction system in the ventricles
left and right bundle branches. Left BB divides into anterior and posterior fasicles
criteria for RBBB
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
why/what leads to you see R'
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).
why the slurred S wave and opposite direction ST wave
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
what is a QR wave, where would you see it
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
criteria for diagnosing LBBB
QRS >0.11s ; Broad monomorphic R in I and V6; broad monomorphic S in V1
some variations seen in LBBB
tall narrow R wave in V1 and notching of R in V6
what is an IVCD, criteria?
intraventricular conduction delay, doesn’t have to be >0.12s ; commonly in III, has features of RBBB and/or LBBB
what can cause IVCD
hyperkalemia is what to focus on here (other causes LVH, peri-infarction, qunindine /flecanide)
can you diagnose LVH in presense of a LBBB
no, you most certianly cannot
left anterior fascicle innervates what
anterior and lateral walls of left ventricle
left posterior fasicle innervates
inferior and posterior walls of left ventricle
main change seen in LAH (left anterior hemiblock)
Left axis deviation (between -30 and -90)
criteria for LAH
-30 to -90 axis ; qR complex or R wave in I ; rS complex in III (possibly II and aVF as well)
shortcut for diagnosing LAH
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
why is axis deviated to left in LAH
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
lead 1 in LAH
positive
lead II in LAH
negative
lead aVF in LAH
negative

why is left posterior fascicile difficult to block

fibers are diffuse and not in a single bundle

what fasicle is more often blocked
left anterior fascile
3 criteria for LPH
axis between 90 and 180, s wave in I, q in III, exclusion of RAE an RVH
stable and unstable bifascicular blocks
RBBB+LAH is stable RBBB+LPH is unstable and will often progress to complete heart block
what do you see in LAH+RBBB bifascicular block
positive lead 1 negative aVF and lead II. RSR' in V1; slurred S in V6
Chapter 14 ST segment and T Waves
CH 14 ST Segment and T Waves
ST depression and inverted T waves are signs of
ischemia
ST elevation is a sign of
infarction
J point is
area where transition between QRS and ST segment occurs
what interval determines baseline
TP segment
concave up ST segment is associated with
early repolarization, pericarditis
concave down ST segment is associated with
strain pattern
flat depressed ST is associated with
subendocardial ischemia
flat elevated ST is associated with
injury pattern
tombstone pattern of ST is associated with
infarction and ventricular aneurysm
Epsilon waves are associated with what population
italian males
tall narrow T waves are common in
hyperkalemia
a pathologic biphasic T wave is positive/negative first
negative
T waves are usually positive where, negative
positive in I,II,V3-6 ; ;; neg in aVR…..this is not the case in BBB
if T wave is more than ________ the height of the R wave then it is abnormal
2/3 the height
RVH with strain pattern
increased R:S ratio in V1 and V2 with a concave down ST segment and a flipped asymmetric T wave
LVH with strain pattern
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
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
1. PR depression 2. diffuse ST elevation 3. scooping and upward concavity of ST 4. notching at end of QRS
what tissue depolarizes first, repolarizes first
endocardium depolarizes first, but the epicardium repolarizes first, this is why T wave is same direction as QRS
in presense of BBB or PVC what is the repolarization pattern
repolarizes in the same order that it depolarized
in a BBB the T wave is always ____________ to the terminal portion of QRS, this is called ___________
opposite direction, discordance
concordance in presense of BBB is a sign of
ischemia
U waves can occur in the presense of
hypokalemia
if U wave occurs opposite of the T wave this is ______ ; could be a sign of
bad, cardiac ischemia until proven otherwise
T wave is _______________ is ischemia ; T wave is ______________ in LVH strain pattern
symmetrical in ischemia ; asymmetrical in strain
Chapter 15 Acute MI
Chapter 15 Acute MI
electrical state of ischemic tissue
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
describe the shape of an infarct, ischemia
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
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 ,
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
anterior wall infarct
LAD
lateral wall infarct
LCX
inferior wall infarct
RCA
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