ECG Flashcards
Myocytes have 3 properties
automaticity
rhythmicity
conductivity
Automaticity
-able to discharge/depolarize w/o stimulation from a nerve
automatically discharge
Rhythmicity
-depolarization occurs at regular intervals
-cardiac muscle cells can depolarize at regular intervals
SA node- rhythmicity creates sinus rhythm (60-100)
AV
His-purkinje fibers
AV: 40-60 times per min
His: 30-40 times per min
faster/higher discharge rate predominates
autonomic influence >SA>AV>Purk
conductivity
-ability to spread impulses quickly w/o nerve involvement
ECG tracings are…
superficial recordings of electrical events/ ionic events occuring within the myocytes
P wave
atrial depolarization is depicted on ECG as p wave.
impulse spread to L atrium via bachmann bundle
PR interval
when spread of depolarization reaches AV node, slight delay occurs
reads as PR interval
Purkinjes/ bundle branches
-L and R division, L has an A and P division
ventricular depolarization occurs when impulse reaches PFs, carries signal to myocytes .
QRS complex reflects this
greater amp bc of greater muscle mass
T wave
-represents repolarization of ventricles
interval from beginning of QRS complex to apex of t wave = absolute refractory period
most leads- T wave is positive (upward deflection) and reflects repolarization of myocytes
Limb leads
I,II,III (standard limb leads)
aVR,aVL,aVF (augmented)
each leads records from different angle, providing a diff view of same cardiac activity
Chest leads
6, show gradual changes
record in horizontal plane
Single lead assessment
look for:
-heart rhythm or rate
-normal waveforms
-abnormal wavefroms
use lead II!!!
ECG recording
vertical deflections: voltage
horizontal axis- time
1 large square=0.20sec, 5=1 sec
30=6secs
horizontal distance becomes a stopwatch!
determine HR from ECG
count large boxes between two R waves
300/count
lower number R waves= higher BPM and vise versa
can only do this with normal
Assessing cardiac cycle
- eval P wave
- eval PR interval (norm is 0.12-0.20 or 3-5 small boxes)
- eval QRS (look alike?)
- Eval QRS interval (0.06-0.10 or 1.5-2.5 small boxes)
- eval t wave
- eval RR wave interval
- eval HR (6 sec strip, norm 60-100)
- observe pt and eval sxs
First degree AV block
-occurs when impulse initiated in SA node but is delayed on way to AV node
-AV conduction time is prolonged
if R is far from P, you have first degree
2nd degree, Wenckeback
-progressive lengthening of PR interval
longer longer longer drop, that MF in Wenckeback!!
2nd degree AV block Mobitz II
-intermittent non-conducted p waves W/O progressive prolongation of PR interval
P waves constant
RR is exact multiple of preceding RR interval
If some p’s don’t get thru you have Mobitz II!
3rd degree AV block
–NO impulses initiated above the ventricles are conducted to the ventricle
atria fire at own rate
ventricles fire at own rate
If p’s and q’s dont agree, then you have 3rd degree
Tx 1st degree
benign and not treated
2nd degree tx
depends on type
no tx necessary or pacemaker
result of an MI
3rd degree tx
LIFE threatening
MI, degen of conducting system
permanent pacemaker
medical emergency
PAT/PSVT
a sudden recurrence of atrial tachycardia
p waves present but may be merged with t wave
PR less than 0.20
QRS identical but between 0.06-0.10
RR regular and may show start/stop of PAT
PAT/PSVT arryhtmia
-emotional, overexertion, caffeine, nicotine, aspirin, RHD, mitral valve dysfunc, PE
dizziness, weakness, SOB
determine cause and treat accordlingly
atrial flutter
P waves are sawtooth pattern (uniform due to only one ectopic focus)
rapid succession of atrial depolarization, rate of 250-350
A fib
-quiver/twitch of atrial muscle
p waves absent
RR is irregular
QRS between 0.06-0.10
old age, CHF, drugs, stress/pain, RHD, renal failure
not threatening unless HR elevated at rest
lose atrial kick
potential to develop mural thrombi
WPW syndrome
-common
-HB abnorm fast
-preexcitation syndrome
sxs: pounding HB, chest pain, difficult breathing, fainting, SOB, anxiety
cause: congential, or heart defects
tx: cardioversion, propranolol (b blocker)
PVCs
-ectopic focus originates an impulse from somewhere in the ventricles
QRS wide and bizzaew without P wave followed by compensatory pause
heart skips beat
tx depends on cause, frequency, severity, sxs
serious when: paired together, mutlifocal, >6 per min, land on t wave, triplets or more
Vtach
3+ PVCs in a row
twisting of points’
bc rapid firing by a single ventricular focus with increased automaticity
P waves absent
prolonged QT interval
QRS wide and bizzare
100-250
ventricular tachy can be precursor to vent fibrillation
Vtach causes and tx
causes: ischemia, acute infarc, CAD, hypertensive HD, med reaction
tx: cardioversion, defib, meds
MED emergency- mostly unconscious
Vfib
quivering of ventricular muscle = no CO
creates asynchrony
ECG shows irregular up/down in zigzag
MED emergency
causes same as vtach
tx: defib followed by resuscitation, O2, and meds
Hypertrophy
longer QRS
Ischemia
inverted T wave
ST seg depression
ST deg depression at rest in presence of chest pain
-subendocardial infarc
may indicate a pending transmural infarc
ST seg depression in absence of ischemia or angina
may be due to digitalis toxicity
ST seg elevation/depression is diagnostic for
-acute infarc
-also presence of sig Q wave
Leads that demonstrate presence of t wave inversion, ST seg changes, or Q waves identify…
location of ischemia, injury or infarc
