Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
377 Cards in this Set
- Front
- Back
|
moderate hyperkalemia
|
wide, flat P
wide QRS peaked T http://medinfo.ufl.edu/~ekg/Electrolytes.html |
|
|
severe hyperkalemia
|
no P, QRS widens
|
|
|
moderate hypokalemia
|
flat T
U wave |
|
|
severe hypokalemia
|
prominent U wave
|
|
|
hypercalcemia
|
short QT
|
|
|
hypocalcemia
|
prolonged QT
|
|
|
digitalis effect on ECG (think of the painter)
|
Salvador Dali
T waves depressed or inverted QT interval shortened |
|
|
dig excess (4 types of blocks)
|
SA block
PAT with block AV blocks AV dissociation |
|
|
dig toxicity
ECG finding: effect on atria: effect on junction / ventricles: |
multiple PVCs
irritable foci firing rapidly, afib junctional tac, vtac, vfib |
|
|
ECG effects of quinidine (WWSTUL)
|
wide, notched P
wide QRS ST depression U hump Long QT (Quinidine: WWSTUL) |
|
|
excess quinidine
- or other meds that block K channels - or low serum K |
Torsades de Pointes
|
|
|
myoctes at rest are
|
polarized and
negatively charged |
|
|
depolarizing myocardium is an advancing wave of _____ charge
|
positive
|
|
|
Cell-to-cell depolarization is carried by
|
Na+
|
|
|
depolarization moving toward + electrode
|
upward wave on EKG
|
|
|
wave caused by atrial depolarization
|
P wave
|
|
|
The only conducting path between atria and ventricles
|
AV node
|
|
|
electrically isolates atria and ventricles
|
mitral & tricuspid valves
|
|
|
slow conduction of AV node carried by
|
Ca++ ions
|
|
|
why do the Ca++ ions of the AV node slow the depolarization wave ?
|
to allow blood to enter the ventricles
|
|
|
the pause after the P wave
|
AV conduction (Ca++ channels)
|
|
|
Purkinje Fibers (Name components)
Which Ion do they use ? |
His, RBB, LBB
Na+ (fast conduction) |
|
|
spread out just beneath the endocardium
|
Perkinje fibers
|
|
|
ventricular depolarization direction
|
endocardium to epicardium
|
|
|
"initial" phase of ventricular repolarization
|
ST segment
|
|
|
rapid phase of repolarization
|
T wave
|
|
|
causes repolarization
|
K+ leaving myocytes
|
|
|
phase of contraction from QRS to the end of the T wave
|
systole
|
|
|
QT interval
|
duration of ventricular systole
|
|
|
Syndrome which makes one vulnerable to deadly rapid ventricular rhythms.
|
long QT syndrome
|
|
|
nl QT ?
|
< 1/2 R-R at normal rates
|
|
|
produces myocyte contraction
|
release of Ca++ into myocytes
|
|
|
1 mV
|
10mm (10 squares high)
|
|
|
The 3 cardiac ions
|
Na2+ (conduction except AV [Ca2+])
Ca2+ contraction / depolarization K+ repolarization |
|
|
1 mm horizontally
5 mm horizontally (1 black box) 5 black boxes 6 X 5 black boxes HR in bradycardia ? |
.04s
.2 1s 6s HR / 6s strip X 10 ! |
|
|
positive electrodes
negative electrode |
left arm and leg
right arm |
|
|
< 50% ischemic necrosis of subendocardial wall will cause what finding on EKG ?
|
st - depression
subendocardium - last to be perfused, first necrosed |
|
|
ST elevations + PR depressions
|
acute pericarditis
|
|
|
electrolyte causes of vtac
|
hypokalemia
hypomagnesemia - both caused by loop diuretics |
|
|
broad flat T waves
U waves ST depression PVCs |
hypokalemia
remember HCTZ is a possible cause |
|
|
causes of hypokalemia
|
HCTZ
diarrhea anorexia vomiting Hyperaldosteronism (HCTZ dav H.) |
|
|
left foot positive
both arms connected to a common negative |
AVF (augmented voltage foot)
- augment means "amplified" to reach the voltage magnitude of leads I, II and III |
|
|
combo of leads II and III
|
AVF
|
|
|
right arm positive
left leg, arm negative |
AVR
|
|
|
left arm positive
left leg, right arm to negative terminal |
AVL
|
|
|
AVR, L, F
|
Right arm, Left arm, Left foot positive
|
|
|
leads II & III
|
AVF
|
|
|
leads I & II
|
AVR
|
|
|
leads I & III
|
AVL
|
|
|
the lateral leads
|
I & AVL ("left lateral" is understood)
|
|
|
inferior leads
|
II, AVF, III
|
|
|
chest leads are always
|
positive
- a charge moving towards produces an "up" deflection |
|
|
chest leads project through the:
|
AV node
- the back is negative - AV node is center of a wheel |
|
|
lead projecting directly front to back
|
V2
|
|
|
V1is mostly
V6 is mostly |
negative
positive |
|
|
V1 & V2 are over the
V5 & V6 are over the |
right heart (right ventricle)
left heart (left ventricle) |
|
|
oriented over the intraventricular septum
- what courses through the septum? |
V3 & V4
- the right and left bundle branches |
|
|
parasympathetic system:
sympathetic system: - name neurotransmitter in each |
Ach / cholinergic receptor
NE / adrenergic receptor |
|
|
NE actives which receptors ?
- what do they do ? |
B1
- increase AV node pacing - increase rate of conduction - increase force of contraction - increase foci irritability - main effect is on artrial & junctional automaticity - minimal effect on ventricular automaticity |
|
|
secreted by adrenal gland
more potent on B1 receptors than NE |
epinephrine
|
|
|
inhibits heart, stimulates gut
|
vagus nerve (ACh)
- opposite effect of NE |
|
|
most cholinergic receptors are in the:
|
atria
|
|
|
vagal stimulation is (parasympathetic or sympathetic ?)
|
parasympathetic
|
|
|
agony of vomiting or painful diarrhea
|
effect of excessive parasympathetic stimulation on GI tract !!
|
|
|
Alpha 1
|
arterial constriction
- adrenergic (NE) - responds more to NE than Epi |
|
|
parasympathetics inhibit directly at receptors and also
|
at the sympathetic ganglia that send fibers to blood vessels
|
|
|
parasympathetic-induced syncope (merciful syncope)
|
severe pain causes bradycardia and hypotension (artial dilation)
(vaso-vagal syncope) |
|
|
convert SVT to sinus rhythm
(2 physical methods) |
- inhibit irritable atrial or AV receptor
- induced gagging or carotid sinus massage |
|
|
diagnose 2:1 AV block or aflutter
|
inhibit AV node (increase refractoriness)
- induced gagging or carotid sinus massage |
|
|
baroreceptors
|
- are not Ach / NE membrane receptors !
|
|
|
standing stimulates pacing but vasonconstion fails causing LV stretch recptors (mechanreceptors) to generate paradoxical parasympathetic response leading to syncope
|
neuro-cardiogenic syncope
- slowed SA pacing + vasodilation - confirm w/ HUT (head-up tilt test) |
|
|
where is SA located ?
|
upper-posterior wall of the RA
|
|
|
sinus bradycardia
|
SA node producing < 1 beat/s
(< 60 beats / min) |
|
|
MC cause of sinus tachycardia ?
|
exercise
sinus tachycardia = HR > 100/min |
|
|
automaticity foci rates:
atria AV junction Ventricles |
atria - 60-80 / min
AV junction - 40-60 / min Ventricles - 20-40 / min |
|
|
which part of the AV node has no automaticity foci ?
|
proximal end of AV node
|
|
|
idio-junctional pace
|
"it's own" juctional pace
idio- Greek - "it's own" |
|
|
when does ventricular pacing emerge ?
|
if all pacemaking centers fail, or,
if there is complete block below the AV node |
|
|
cardiac index
|
CO / BSA or SV*HR / BSA
BSA = body surface area nl = 2.6-4.2 liter/min/sq meter < 1.8 = cardiogenic shock |
|
|
place 0 beside the number of cycles / six second strip
|
bradycardia
|
|
|
inspiration-activated sympathetic stimulation
expiration-activated parasympathetic stimulation |
sinus-arrhythmia
|
|
|
internodal tracts of the right atrium
|
anterior
middle posterior |
|
|
bundle to left atrium
|
Bachmann's bundle
- charge from right to left atrium |
|
|
what produces the P wave ?
does atrial conduction of depolarization record on EKG ? |
depol of atrial myocardium
No. |
|
|
automaticity is concentrated where in the R. atrium ?
|
near the coronary sinus
|
|
|
does purkinje conduction appear on EKG ?
|
No
|
|
|
His bundles transmit to:
Do his branches have automaticity foci ? |
the endocardial surface
No |
|
|
ventricular myocardial depolarization produces:
|
the QRS
|
|
|
Which Purkinje branch has terminal filaments in the septum?
|
The Left Bundle Branch
|
|
|
Which depolarization occurs before the ventricular myocardium ?
|
Left to right depolarization of the intraventricular septum.
|
|
|
QT interval is:
|
ventricular contraction
|
|
|
Purkinje repolarization:
Note: Purkinje fibers finishing repolarizion slightly later than then ventricles. |
U wave (following the T wave)
|
|
|
Name the arrhythmias
|
Irregular rhythms
Escape Premature Beats Tachy-arrhythmias |
|
|
Name the Irregular rhythms
- what usu causes them ? |
Wandering Pacemaker
MAT (Multifocal Atrial Tach) Afib - multiple active automaticity sites |
|
|
automaticity focus with entrance block
|
parasystolic - paces but can't be overdrive-suppressed from above
|
|
|
causes of entrance block:
|
structural pathology
hypoxia |
|
|
when an automaticity focus has entrance block and does not respond to passive depolarization and can't be overdrive-suppressed but still paces at it's inherent rate
|
parasystolic
- unhealthy protection |
|
|
P' wave shape varies
atrial rate < 100 irregular ventricular rhythm |
Wandering Pacemaker
|
|
|
When Wandering Pacemaker rate exceeds 100.
|
MAT
|
|
|
continuous rapid firing of multiple atrial automaticity foci
|
Afib
|
|
|
No impulse depolarizes the atria completely and a random pulse depolarization reaches the AV node and through it to the ventricles.
|
Afib
|
|
|
rhythm of pts w/ COPD
|
MAT
|
|
|
Associated with digitalis toxicity in pts w/ heart ds.
|
MAT
|
|
|
if you see P or P' waves, it can't be:
|
Afib
|
|
|
P waves not identical and rate does not gradually increase & decrease, this rules out:
|
Sinus Arrhythmia
|
|
|
What rate rules out MAT ?
|
< 100 bpm
|
|
|
rate < 100
P's of different shape |
Wandering Atrial Pacemaker
|
|
|
response of an automaticity focus to a pause in the pacemaking activity
|
escape
|
|
|
When the SA Node ceases pacemaking completely:
When the SA Node misses one pacing cycle: |
Sinus Arrest
Sinus Block |
|
|
What is it called when an atrial focus assumes pacing responsibility in the absence of a Sinus Rhythm.
|
Atrial Escape Rhythm
- look for a change in P-wave shape |
|
|
lone QRSs at 40-60 bpm
|
Junction Escape Rhythm
|
|
|
When atria are polarized from below, producing inverted P' waves with an upright QRS.
|
Junctional Automaticity Focus with Retrograde Atrial Depolarization.
|
|
|
enormous ventricular complexes
|
Ventricular Escape Rhythm
|
|
|
When downward displacement of the pacemaker results in a rhythm so slow the patient loses conscience.
|
Stoke-Adams Syndrome
|
|
|
if a pause is long enough, expect:
|
an escape beat
- remember, the P wave will be different if from another atrial automaticity focus |
|
|
decreased by parasympathetics:
a bust of parasympathetic activity would thus cause: |
SA Node
Atrial Foci Junctional Foci - burst - Ventricular Escape Beat |
|
|
very sensitive to O2
|
ventricular automaticity foci
|
|
|
Premature Atrial Beat (PAB)
|
P' earlier than expected
|
|
|
inverted P' in PAB caused by:
|
irritable focus at bottom of atria
|
|
|
where can a PAB P' hide ?
|
under a tall T-wave
|
|
|
why is the first cycle after a PAB lengthened slightly
|
transient baroreceptor parasympathetic effect on the SA node
|
|
|
what causes aberrant ventricular conduction ?
|
when a PAB depolarizes the ventricles before both the LBB and RBB are repolarized. This slightly widens the QRS.
|
|
|
what causes a non-conducted premature atrial beat ?
|
depolarization arrives at AV node while it is still refractory (early P' with no QRS-T). Pause results b/c SA Node is reset.
|
|
|
PAB coupled to end of nl cycle.
|
Atrial Bigeminy (couplet)
|
|
|
PAB firing after 2 nl cycle.
|
Atrial Trigeminy
|
|
|
Which BB usu takes longer to repolarize ?
|
RBB
|
|
|
Premature Junctional Beat w/ abberant ventricular conduction.
|
Usu due to slower repolarization of RBB. Expect a slightly widened QRS.
|
|
|
Causes of ventricular irritability.
|
Low O2 availablilty.
Low K+ (hypokalemia) |
|
|
Most ventricular tachycardias caused by:
|
coronary insufficieny or infarction
|
|
|
P. 134 make card for causes of irritable ventricular focus.
|
make card
|
|
|
Why are PVCs weaker ?
|
incomplete filling
|
|
|
Why are PVC amplitudes large ?
|
left and right depolarizations aren't balanced
A PVC from a remote ventricular focus gradually spreads out without simultaneous opposition producing unopposed deflections of immense amplitude. |
|
|
In PVC is SA Node depolarized?
Result ? |
No
SA Node is not reset & next beat occurs at expected interval. |
|
|
Sandwiched between beats causing neither pause nor disturbance.
|
Interpolated PVCs.
|
|
|
Compensatory pause.
|
In PVC, the SA Node is not reset, but fires. Depolarized ventricles don't conduct so there is a pause to the next beat from SA Node.
|
|
|
pathological PVCs:
identical PVCs: cause ? |
6 or more / minute
unifocal blood supply to that focus us diminished |
|
|
PVC diff (low O2)
|
decrease blood supply (blocked coronary artery)
drowning pneumothorax PE tracheal obstruction |
|
|
Ventricular automaticity focus that suffers from entrance block but is not irritable.
|
ventricular parasystole
- isn't overdrive suppressed but paces at its inherent rate |
|
|
PVCs that appear to be coupled to a long series of nl cycles.
|
Ventricular Parasytole
|
|
|
ventricular bi, tri & quadrigeminy
|
p 140. PVCs coupled to nl cycles.
|
|
|
3 or more PVCs in succession.
|
VTac
Sustained VTac is > 30s. |
|
|
Cause of multifocal PVCs.
|
severe cardiac hypoxia
|
|
|
Multifocal PVCs lead to:
|
Vfib
|
|
|
mid-systolic click with decrescendo murmur
|
MVP
|
|
|
Barlow Syndrome
- hint - a source of irritable foci |
MVP chordae stretching causes irritable foci.
MVP - mitral valve prolapse |
|
|
6-17% of females
1.5% of males |
MVP - dizzy spells after age 20
|
|
|
PVC on the peak of T wave
|
R on T phenomena
|
|
|
PAT
Flutter Fib |
150-250 bpm (4 blocks)
250-350 bpm 350-450 bpm |
|
|
Arises suddenly from an irritable automaticity focus.
|
Paroxysmal (sudden) Tachycardia
|
|
|
make higher level foci irritable
make lower (ventricular) foci irritable |
epi
hypoxia or low K |
|
|
PAT P' wave are different from
|
P wave of SA node origin.
|
|
|
PAT with block.
- rapid, spiked P' waves - 2:1 ration of P':QRS cause ? |
digitalis excess or toxicity
|
|
|
irritates an atrial focus while inhibiting the AV node
|
digitalis (look for low K+)
|
|
|
AVNRT
- theoretical origin ? |
AV node reentry tachycardia
- origin thought to be dense automaticy foci around the coronary sinus |
|
|
area loaded with automaticity foci is near the:
tx in AVNRT ? |
coronary sinus
- catheter ablation |
|
|
Supraventricular Tachycardia is either __ or __.
|
Supraventricular Atrial Tachycardia.
Supraventricular Junctional Tachycardia - tx of both is the same |
|
|
Paroxysmal VTac (or just VTac)
|
irritable ventricular focus pacing at 150-250 bpm
|
|
|
A run of VTac is really just a bunch of:
|
PVCs
|
|
|
P waves are ___ in Vtac.
|
hidden
|
|
|
AV dissociation
|
SA Node continues to pace the atria in Vtac. An occasional depolarization conducts to the ventricles and makes a little spike. (capture beat)
|
|
|
fusion beat
|
blending on EKG of a nl QRS with a PVC-like complex.
|
|
|
confirms dx of VTac because they could not occur during SVT.
|
fusion or capture beats
- excellent - P.155 |
|
|
Rapid SVT with aberrant conduction can mimic VT. How ?
|
Widened QRS due to slower repolarization of RBB.
|
|
|
Distinguish "wide QRS complex SVT with aberrant conduction" from VTac.
|
Pt w/ CAD or infarction uncommon vs common
QRS <.14s / >.14s AV dissociation w/ captures or fusions rare / common Extreme RAD rare / common |
|
|
Think VT:
|
AV dissociation (capture or fusion)
Extreme RAD (-90 to -180) |
|
|
QRS usu < .14 sec
|
SVT with aberrant ventricular conduction.
|
|
|
QRS usu > .14 sec
|
VTac
|
|
|
Torsades diff
|
hypokalemia
K+ channel blockers Long QT syndrome (congenital) |
|
|
2 competitive irritable foci in different ventricular areas cause:
|
Torsades de Pointes
|
|
|
Torsades rate ?
|
250 - 350 bpm (no effective pumping at this rate)
|
|
|
saw tooth
|
atrial flutter (250-350 bpm)
|
|
|
how many beats reach ventricles in aflutter (remember the long refractory period of the AV node)
|
one of two or three
|
|
|
ID atrial flutter
|
invert tracing
vagal maneuver |
|
|
how does vagal maneuver help dx aflutter ?
|
increased AV node refractoriness reveals more flutter waves
|
|
|
V Flutter is what rate ?
Usually leads to what ? |
250-350 bpm
Deadly Vfib - b/c there is no time for filling. Coronary arteries get no blood and neither does the myocardium and hypoxic foci take off wildly trying to compensate. |
|
|
V Flutter pattern ?
vs Torsades ? |
smooth sine wave
Torsades gets smaller and larger |
|
|
R/O ventricular tachycardia
|
narrow, normal looking QRSs
|
|
|
R/O junctional focus.
|
No inverted P' waves.
|
|
|
Name 2 conditions that result when:
- all foci suffer from entrance block and are parasystolic - cannot be overdrive suppressed and pace at their own rate |
Afib & Vfib
|
|
|
many parasystolic atrial foci with entrance block (which can't be overdrive-suppressed) firing rapidly
|
Afib
- foci near AV node drive conduction causing a very irregular rhythm |
|
|
think a rain-showing striking a pool
|
Afib
|
|
|
What usu initiates Afib ?
|
Parasystolic foci in the pulmonary vein ostia of the left atrium.
|
|
|
What dictates HR in Afib ?
|
AV node refractoriness.
|
|
|
numerous parasystolic ventricular foci pacing rapidly and which cannot be overdrive suppressed
|
Vfib
- each tiny amt of ventricle depolarized causes a twitch |
|
|
totally erratic and with no identifiable waves
|
Vfib
|
|
|
no electrical activity on EKG:
when the heart is too weak to respond mechanically to electrical activity (no pulse): |
asystole
pulseless electrical activity (PEA) |
|
|
illusion of shortened PR & elongated QRS
|
Wolf-Parkinson-White syndrome
|
|
|
Bundle of Kent aberrant conduction causes:
|
WPW
|
|
|
Bundle of Kent associated problems:
|
rapid conduction of SVT
self-contained automaticity foci re-entry "circus" |
|
|
AV Node bypassed by extension of the Anterior Internodal Tract (James Bundle) - eliminates AV Node filtering and can allow conduction of SVTs)
|
Lown-Ganong-Levine (LGL) syndrome
|
|
|
No PR delay with P waves adjacent to QRS.
|
LGL (James Bundle of Anterior Internodal Tract)
|
|
|
Name the Blocks (BASH)
|
Bundle Branch
AV node Sinus Node Hemi Block |
|
|
unhealthy SA Node fails to pace for a cycle
- there will be no P wave |
Sinus Block
|
|
|
P waves before and after are identical
|
Sinus Block
|
|
|
Sinus Bradycardia without the normal escapes
|
SSS Sick Sinus Syndrome
|
|
|
Appear to have SSS b/c of parasympathetic activity at rest
|
Marathon runners and the like
- pseudo Sick Sinus Syndrome |
|
|
SSS w/ intermittent SVT
|
Bradycardia-Tachycardia syndrome
|
|
|
lengthened delay between atrial & ventricular depolarization
|
first-degree AV block
|
|
|
PR > 1 large square (.2 sec)
|
first degree AV block
|
|
|
Some P waves conducted, some blocked.
|
second degree AV block
|
|
|
second degree blocks of the AV Node
|
Wenckebach
|
|
|
successive blocking until the P wave is totally blocked always in the same ratio. The PR interval lengthens.
|
Wenckebach
|
|
|
Second degree Purkinje (HIS or BB) blocks.
|
Mobitz
|
|
|
Nl P-QRS-T preceded by a series of paced P waves that fail to conduct, with consistent ratio.
|
Mobitz
|
|
|
caused by parasympathetic excess or drugs that mimic or induce parasympathetic response
|
Wenckebach
|
|
|
"2:1 AV block"
|
Mobitz
|
|
|
Punctual P waves but never a premature P'
|
Mobitz
|
|
|
PR lengthened, QRS nl
PR nl, QRS widened |
Wenckebach
Mobitz |
|
|
AV Node is rich in parasympathetics.
Vagal maneuvers thus increase the number of cycles in: |
Wenckebach
|
|
|
Vagal manuevers eliminate the block producing 1:1 conduction or have no effect.
|
Mobitz
|
|
|
totally variable in third degree block
decreased in WPW & LGL |
PR
|
|
|
complete block between atria and ventricle
- automaticity focus from below escapes to pace ventricles |
third-degree block
|
|
|
pacing resulting from complete block in the upper AV node
|
Junctional Pacing
|
|
|
complete block of entire AV Node or below results in:
|
Ventricular Pacing
|
|
|
Type of block occurring in AV dissociation, which is when a Regular P is sometimes superimposed over an independent junctional or ventricular rate.
|
third-degree block
|
|
|
Normal-appearing QRSs (usu)
Wide QRSs. |
Junctional Rhythm
Ventricular Rhythm |
|
|
Block below AV junction. Expected rate ?
(it's below the the junction so it can't be a junctional escape beat !) |
20 - 40 bpm from a ventricular pacing focus
|
|
|
AV Node obliteration or block below AV junction.
- Causes what kind of pacing ? |
Ventricular (not Junctional) Pacing
|
|
|
Bradycardia with wide ventricular complexes is usually what kind of block ?
|
3rd degree block.
- But be sure there is no atrial activity. |
|
|
What can produce same EKG appearance as 3rd degree block ?
|
hyperkalemia
|
|
|
Conduction creeps around the blocked BB and is picked up by the BB distally.
|
BBB
|
|
|
Two QRSs out of phase caused by:
|
BBB
|
|
|
QRS width in BBB ?
|
.12 s (3 small squares or greater)
and R + R' pattern (2 QRSs) best noted on limb leads |
|
|
looks like Vtac
|
SVT with BBB
(rapid, wide QRS complexes) |
|
|
refractory period is from what point to what point on the ECG ?
|
Ventricular depolarization up to the middle of the T wave
|
|
|
refractory periods aren't identical
|
BBs
|
|
|
SVT can produce rate-dependent BBB. How ?
|
The BBs don't have identical refractory times.
|
|
|
R, R' in V1, V2
|
RBBB
|
|
|
Can display a RBBB or LBBB pattern sometimes.
|
PVCs. P.196. Makes sense.
|
|
|
RR' in QRS of nl duration occurs in:
|
incomplete BBB
|
|
|
Block of one BB with intermittent block of the other - a continuous BBB pattern with occasional dropped QRS's (P is present).
|
Intermittent Mobitz (second deg)
- this actually forms a complete (3rd degree) heart block |
|
|
mimics intermittent Mobitz
|
punctual P (no QRS) - 2deg block W vs M.
premature P' (no QRS) - non-conducted PAB missed P-QRS-T - SA block |
|
|
AV block
BBB |
PR > 5 blocks
QRS > 3 blocks |
|
|
Block of a LBB fascicle.
|
Hemiblock
|
|
|
the general direction of simultaneous ventricular depolarization:
- can't determine in BBB b/c ventricles don't depolarize simultaneously |
Mean QRS
|
|
|
can be dx in presence of BBB
can't be dx in presence of BBB |
atrial hypertrophy
ventricular hypertrophy |
|
|
Where is the tail of QRS vector ?
Where does it usu point ? What causes depolarization ? |
AV node
Down and to the left. Advancing wave of Na+ ions. |
|
|
horizontal heart
vertical heart |
obese people
tall, thin people |
|
|
QRS points toward:
QRS points away from: |
hypertrophy
necrosis |
|
|
Nl QRS axis.
|
0 - 90 degrees
|
|
|
inferior limb leads
lateral limb leads |
+ II, III, AVF
+ I, AVL |
|
|
if QRS in lead 1 is mainly negative, QRS vector points:
if QRS in lead 1 is mainly positive, QRS vector points: |
right
left |
|
|
Negative QRS in lead I is:
|
right axis deviation
|
|
|
Best place to detect right axis deviation ?
|
Lead I
|
|
|
If mean QRS is down, AVF is:
|
upright.
|
|
|
If QRS is negative in AVF, QRS points:
|
up
|
|
|
Normal Axis.
|
QRS up in I and AVF.
|
|
|
Anytime the QRS is negative in lead I there is:
|
RAD
|
|
|
Positive in I, neg in AVF.
|
LAD
|
|
|
Can calculate the vector for the initial or terminal __ if you like.
|
.04s
|
|
|
perpendicular depolarization
|
isoelectric QRS (the "same" voltage)
|
|
|
Axis location (remember the short cut ?) Think of the isoelectric lead.
|
90 degrees from most isoelectric limb lead.
|
|
|
Lead I negative
AVF positive QRS isoelectric in II |
RAD + 150 degrees
|
|
|
P wave vector generally points:
|
down toward II, III, AVF (inf leads)
& left toward (I, AVL) - P is usu upright in these leads. |
|
|
inverted P' in II, III, AVF (inf) or
in I, AVL (lateral) |
from low atrial focus or retrograde atrial depolarization moving up the AV node
|
|
|
usu negative in inferior and lateral leads
|
PVCs
|
|
|
emanate from peripheral focus in a ventricular wall
|
PVC
|
|
|
"upward" PVC originate from:
|
a septal focus and appear nl
|
|
|
deviation
rotation |
frontal plane
horizontal plane |
|
|
V2 location
|
4ICS
|
|
|
QRS in V2 is mostly ___ b/c it points into the negative half of the sphere.
|
negative
|
|
|
Most useful to determine anterior & posterior infarction.
|
V2
|
|
|
chest lead transitional zone (negative to positive)
|
V3 & V4
|
|
|
rotation toward V1, V2
rotation toward V5, V6 (toward hypertrophy, away from infarction) |
rightward rotation
leftward rotation |
|
|
directly over atria
- best source of info regarding atrial enlargement (dilation or hypertrophy) |
V1
|
|
|
diphasic P in V1
peaked P in V1 |
V1 P in left atrial enlargement
V1 P in right atrial enlargement |
|
|
deflections above & below baseline are called:
|
diphasic
|
|
|
initial component of P in V1 is larger in:
must be > mm ? |
right atrial enlargement
2.5 mm |
|
|
a cause of left atrial enlargement:
MC cause of atrial enlargement ? |
stenosed mitral valve
systemic hypertension |
|
|
Large R in V1 (as opposed to the usually mostly negative V1)
|
RVH
- S in V1 smaller than R in V1 |
|
|
R smaller as V1 - V6.
|
RVH
|
|
|
Right Axis deviation in frontal plane and rightward rotation in the horizontal plane.
|
RVH
|
|
|
Large S in V1 & large R in V5.
|
LVH (SV1 RV5) > 35 mm
- big vector away from V1 and toward V5 |
|
|
T wave inversion with asymmetry (a type of hypertrophy)
- use V5, V6 since they are over the left ventricle. |
LVH
|
|
|
ST becomes depressed & humped.
ECG findings for RV & LV. Cause of this phenomenon> |
Strain pattern in LVH.
RV strain noted in V1, LV strain noted in V5. HTN |
|
|
provides most info regarding hypertrophy of heart chambers.
|
V1
- p.258 |
|
|
progression of infarction (IIN)
|
ischemia
injury necrosis |
|
|
causes inverted T waves which inverted and symmetrical, vs strain, which is asymmetrical
|
ischemia
|
|
|
transient T wave inversion
|
angina
|
|
|
Wellen's syndrome
ECG finding: vascular cause: |
- marked T inversion in V2, V3
- stenosis of anterior descending - visualize a T dropped inverted into a well with V2 & V3 written on its sides. |
|
|
any T inversion in V2 - V6 is:
|
pathological
|
|
|
acute injury
- earliest consistent sign of infarction to appear on EKG |
ST elevation
|
|
|
angina w/o exertion with transient ST elevation in absence of infarction
|
Prinzmetal's angina
|
|
|
STEMI w/o Q
|
non-Q wave infarction
- small infarction signaling a coming larger infarction |
|
|
persistent ST elevation
|
pericarditis
aneurysm |
|
|
RBBB + ST elevation in V1-V3
|
Brugada Syndrome
|
|
|
sudden cardiac arrest without heart disease
Mech: |
Brugada syndrome
familial syndrome of dysfunctional Na2+ channels - vfib - must have ICD implant |
|
|
responsible for 1/2 of sudden deaths in young persons w/o heart ds
|
Brugada syndrome
|
|
|
flat or concave elevated T or
ST & T segment elevated |
Pericarditis
|
|
|
ST depression causes:
|
subendocardial infarct (a non-Q wave infarction)
positive stress test digitalis |
|
|
just beneath the endocardial lining and not transmural
|
subendocardial (non-Q wave) infarct
|
|
|
necrosis
|
Q wave
|
|
|
if there is any positive wave, the following down part must be a _ wave, and there is no Q
|
S (the upward preceding wave is thus an R wave)
|
|
|
non-pathological tiny q's produced by:
must be < _ |
left bundle branch fibers at mid-septum
.04s |
|
|
at least .04s or 1/3 QRS amplitude
|
significant Q wave
|
|
|
Like an upside down II. Q waves are thus unreliable.
|
AVR
|
|
|
always record leads with:
|
Q waves
ST elevation or depression inverted T waves |
|
|
detects no "toward" vectors, only away vectors, thus the (-) Q wave.
|
electrode nearest the infarct
|
|
|
Q in V1-V4
Q in I and AVL Q in II, III, AVF |
anterior infarct
lateral infarct inferior infarct |
|
|
isolated Qs in V1, V2
isolated Qs in V3, V4 insignificant Qs usu seen in: |
septal infarct
antero-lateral infarct V5-V6 |
|
|
1/3 of inferior infarcts include parts of the:
|
right ventricle
|
|
|
Posterior Left Ventricle Infarction Appearance on EKG?
- remember - Qs appear in leads closest to infarct |
Large R in V1 (the opposite of the Q in V1 which would appear in an Anterior Infarction) + ST depression (not elevation)
|
|
|
2 causes of large R in V1
|
Posterior Infarction
RVH |
|
|
ST depression on right chest leads think:
(expect also large RV1 & RV2) |
acute posterior infarction
|
|
|
Reversed Transillumination or Mirror Test is to detect:
EKG finding: |
acute posterior infarction
- Q waves & ST elevation in V1, V2 |
|
|
V1 & V2:
anterior infarction findings: posterior infarction findings: |
ST elevation & Q waves
ST depression & R waves |
|
|
Why can't we see an LV Q wave in LBBB ?
|
Because the RV depolarizes first and the LV Q wave is hidden.
|
|
|
Q wave in LBBB could only mean:
|
septal infarct
|
|
|
large R in V1, V2
maybe Q in V6 mirror test |
Posterior Infarct
|
|
|
Q in I, AVL
|
Lateral Infarct
|
|
|
Q in V1, V2, V3 or V4
|
Anterior Infarct
|
|
|
Q in II, III, AVF
|
Inferior Infarct
|
|
|
ECG findings when Isolated areas of ischemia are present: (2)
|
T wave inversion
ST elevation without Qs |
|
|
branches of left coronary artery
|
circumflex branch
anterior descending branch |
|
|
right coronary artery (RCA) serves the:
|
right ventricle
|
|
|
occlusion of circumflex artery:
|
lateral infarction
|
|
|
anterior descending artery occlusion causes:
|
anterior infarction
|
|
|
circumflex artery occlusion causes:
|
lateral LV infarction
|
|
|
occlusion of RCA or one of its branches causes:
|
posterior infarction
|
|
|
provides blood to SA node, AV nodes and His bundle
|
RCA
|
|
|
what do posterior infarction and arrhythmia have in common ?
|
RCA
|
|
|
inferior (II, III, AVF) infarct is either __ or __ depending on which is dominant.
MC dominant: |
RCA, LCA
RCA |
|
|
block of anterior or posterior LBB
|
hemiblock
|
|
|
RCA & LCA both have a variable twig to the:
|
posterior division of the LBB
|
|
|
Cause of RBBB + Anterior LBB hemiblock
|
total occlusion of anterior descending artery
|
|
|
Left Axis Deviation
Normal or slightly widened QRS Q1S3 |
Anterior Hemiblock
|
|
|
Left Axis Deviation Diff: (AHHIP)
|
anterior hemiblock (must have previous EKG to prove)
horizontal heart hypertrophy Inferior infarction Pre-existing |
|
|
% who develop hemi-block after anterior infarction (anterior descending artery)
|
50%
|
|
|
late, up-left unopposed depolarization of the LV
|
anterior hemiblock of LBB
|
|
|
ECG findings in anterior infarction with axis change from nl to -60 (LAD) - suspect anterior hemiblock:
|
Q1S3
|
|
|
Mean QRS is nl or shows minimal right axis deviation in:
|
RBBB
|
|
|
RBBB + LAD =
|
Anterior Hemiblock
|
|
|
RAD due to unopposed forces to the right
slightly widened QRS S1Q3 |
Posterior Hemiblock
|
|
|
In presence of a lateral MI, dx of Posterior Hemiblock is:
Why ? |
equivocal
they both cause RAD |
|
|
chronic RAD is probably due to:
|
slender body (vertical heart)
RVH pulmonary ds |
|
|
AV block is usu in:
Can also be caused by: |
AV node or His bundle.
RBBB + Ant & Post LBBB |
|
|
nl to RAD related to:
nl to LAD related to: |
Posterior Hemiblock
Anterior Hemiblock |
|
|
bifascicular block
|
RBBB + Ant or Post LBBB
|
|
|
intermittent wide QRS or
intermittent change of QRS axis (usu QRS flips up or down) |
intermittent block of 1 fascicle
|
|
|
Causes of intermittent Mobitz:
|
RBBB + A Hemi + Inter Post Hemi
RBBB + P Hemi + Inter Ant Hemi A + P Hemi (LBBB) + Int. RBBB |
|
|
Trifascicular blocks are dx only when one or more of the blocks are
|
intermittent
|
|
|
Bilateral BB dx made only if one of the blocks is
|
intermittent
|
|
|
every cycle has a punctual P and never a premature P' in:
|
intermittent Mobitz
|
|
|
3 important syndromes
|
Brugada (RBBB + STe in V1-V3)
Wellens (Ti in V2-V3) ant desc coronary artery stenosis Long QT (QT > 1/2 coron. cycle) |
|
|
low voltage + RAD
mech? |
COPD
heart works against resistance. the hypertrophy causes RAD |
|
|
low voltage full diff:
|
COPD
hypothyroidism chronic constrictive pericarditis |
|
|
COPD - expectations ? (LMR)
- COPD think "LAMER" |
Low voltage
MAT RAD |
|
|
S1 (large S in I)
ST depression in II large Q in III with T wave inversion |
PE (acute cor pulmonale)
|
|
|
another important sign of PE
|
T wave inversion in V1-V4
RBBB (RR' in right chest leads) |
|
|
incomplete RBBB:
|
RR' with QRS of nl width
|
|
|
peaked T think:
(depolarization takes longer) |
hyperkalemia
|
|
|
first T wave flattens then as the situation worsens it inverts and a U wave is formed
|
hypokalemia
|
|
|
irritates vent automaticity foci
initiates Torsades can evoke vTac increases digitalis toxicity |
hypokalemia
|
|
|
from beginning or QRS complex to the end of the T wave
- should be < 1/2 cycle length |
QT interval
|
|
|
what drug effect causes the lowest portion of ST to be depressed below baseline ? Think Salvador Dali.
|
Digitalis effect
|
|
|
- unique, gradual downward curve of the ST segment
- no demonstrable S wave |
digitalis effect
|
|
|
- AV node conduction slowed
- inhibits AV node receptiveness to multiple stimuli |
digitalis
|
|
|
earliest sign of dig excess:
|
PABs
(atrial automaticity foci are very effective digitalis sensors) |
|
|
digitalis toxicity
|
atrial & junctional tachyarrythmias
PVCs ventricular bigeminy, trigeminy vTac, Vfib |
|
|
retards depolarization and repolarization in atrial & ventricular myocardium
|
quinidine
|
|
|
sign of delayed repolarization
|
U wave
|
|
|
pacemaker position if QRS shows LBBB w/ nl axis.
|
mid-inflow tract of RV
|
|
|
pacemaker position if QRS shows
LBBB w/ RAD |
just below pulmonic valves
|
|
|
pacemaker position if QRS shows
LBBB w/ LAD |
apex of right ventricle (ideal)
|
|
|
implantable cardioverter defibriallator
|
ICD
|
|
|
automated external defibrillator
|
AED
|
|
|
2 EKGs
|
native & donor hearts
- see freaky QRS on p. 328 |
|
|
atomic numbers:
Na Ca K |
11
20 19 |
|
|
early repolarization (slight ST elevation in V5, V6) + rightward rotation
|
nl finding in young, athletic males
|
|
|
Low voltage QRS DDX: (EEH)
|
electrical alternans (pericardial effusion)
emphysema hypothyroidism |
|
|
Definition of an incomplete BBB
|
QRS < .12
|
|
|
What is "early repolarization".
|
A normal variant of ST elevation in healthy young persons.
|
|
|
Masquerading RBBB
|
Small LBBB in I in the setting of large RBBB in V1
|
|
|
terminal conduction delay
complete conduction delay |
RBBB
LBBB |
|
|
At a rate of of 175 could the dx be "sinus tachycardia" - No. Then what ?
|
Paroxysmal SVT
|
|
|
Slurred S's in I, AVL, V6
- hint- it's a type of BBB |
Another definition of RBBB.
|
|
|
What is an ST-T change ?
|
non-specific repolarization abnormalities
|
