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42 Cards in this Set

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SA Node
*located rt atrium at the junction of the SVC & rt atrium
*intinsic rate: 60-100 x/min
*pm of the heart
How are impulses spread from the SA node through the atrial chambers?
Internodal tracts
AV node
*floor of the rt atrium near the junction of interatrial and interventricular septa
*slows conduction=atrial kick, packing (30% of ventricular filling); protects ventricle from fast arrythmias
Bundle of His
*inferior portion of the AV node
*passes thru the IV septum
AV junction
*PM cells generate impulses 40-60 x/min
Bundle branches
*traverse the IV septum to the left and right ventricle
Purkinje network
*arises from the terminal branches of the bundle braches
*conduct impulses to mechanical cells of the myocardium
*PM cells umpulse at rate 40 x/min
depolarization
Mvmt of sodium and calcium to the inside of the cell
repolarizaiton
Occurs wehn the electrical celss return to their resting state
A positive deflection occurs
when an impulse moves toward the + electrode
When an impulse moves away from the + electrode...
a - deflecitons will be recorded
Lead II
the + electrode is placed over the 4th-5th ICS/MCL(apex)
depolarization of atrial cells
p wave
PR segment
the time the impulse takes to pass thru the AV junction, isoelectric
PR interval
time required for the impulse to depolarize the atria, travel thru AV node and B of H to the ventricles.
Measured at the beginning of the P to the beginning of the QRS complex.
NORMAL:
0.12 sec to 0.20 sec.
*depolarization of the ventricular cells
QRS complex
QRS width
*amt of time impulse to traverse the r/l ventricles
*NORMAL: 0.10 sec or less
ST segment
*represents the beginning of ventricular repolarization (phase 1 and 2)
*isoelectric
T wave
*represents last 2 phases of ventricular repolarizaiton
*upright, round deflection
measures how long it takes the ventricle to depolarize and repolarize
QT interval
QT interval
*varies with gender, age and HR
*beginning og QRS to end of the T wave
3 steps to ID basic rhythm
1) ID the PM site
if p waves, measure PRI
< 0.12 sec = SA node/atria
> 0.12 sec = AV junction
2) look for evidence of conduction delay/HB
PRI > 0.20 sec
QRS > 0.10 sec
P waves w/o QRS complexes
atrial rate>ventricular rate
3) ID PM of any premature beats
atria, av junction or ventricles
Asystole
Origin: NO electrical act'y
Conduction: N/A
Features: flat, baeline
Hemodynamic effect: NO cardiac output
Tx: CPR, epi, intubate. Check 2nd lead (r/o v-fib).
ventricular fibrillation
Origin:
Conduction: PM is several sites in the ventricle
Features: chaotic, wavy, undulating baeline
Hemodynamic effect: NO cardiac output
Tx: defibrillation, epi, lidocaine, CPR
NSR
Origin: SA node, depolarizing 60-100 x/min
Conduction: conducted thru atria, AV junction, ventricles. PRI 0.12-0.20sec, QRS 0.10 or less.
Features: atrial rate = 60-100/min; PRI 0.12 sec or greater
Hemodynamic effect: NAE
Tx: n/a
sinus tachycardia
Origin:SA node
Conduction: thru AV junction and ventricles nml/abnml
Features: atrial rate 101-150/min; PRI 0.12 sec or >
Hemodynamic effect: de/increased CO (individualized)
Tx: usually secondary to stimulation of SNS, direct tx toward specific cause (fear, pain, anxiety, shock, infection)
sinus bradycardia
Origin: SA node
Conduction: thru AV node nml/abnml.
Features: atrial rate < 60/min; PRI 0.12 sec or >
Hemodynamic effect: in/decrease CO, may be protective post-MI
Tx: increase rate w/atropine and pacing if symptomatic
sinus block
Origin: SA NODE
Conduction: abnl thru the SA node, the SA node fires but the impulse to the atria is blocked = pause.
Features: complete absence of P wave, QRS complex and T wave creating a pause in the rhythm
Hemodynamic effect: varies w/frequency
Tx: if symptomatic, atropine/pacing
sinus arrythmia
Origin: SA node, normal variation seen w/respiratory cycle
Conduction: may be nml/abnml
Features: P-P irregular; difference b/t shortest and longest P-P interval is 0.12 sec or GREATER
Hemodynamic effect: n/a
Tx: n/a
1st degree block
Origin: SA node, abnormality seen in NSR, SB, ST
Conduction: abnormal thru the AV junction (usually the AV node), every impulse is conducted to the ventricles but conduction takes longer
Features: every P wave is followed by QRS; PRI > 0.20 sec
Hemodynamic effect: n/a
Tx: observe for progression
2nd degree block
Type I or Wenkebach
Origin: SA node, occurs w/ NSR, SB, ST
Conduction: impulse is conducted abnormally thru AV junciton, usually at the node, progressive delay in conduction until an impulse is not generated to the ventricles. PRI lenghtens. The impulse generated to the ventricles is usually normal
Features: P-P regular; R-R IRREGULAR; PRI lenghtens until a P wave appears w/o QRS complex; QRS width is 0.10 sec or less
Hemodynamic effect: effect is dependent on ventricular rate
Tx: if v. rate is too slow to maintain an adequate CO then atropine and/or pacing
2nd degree
Type II
Origin: SA node, occurs w/NSR, SB, ST
Conduction: conduciton delay is below the AV node, usually produces a WIDE QRS.
Features: P-P reg; R-R irreg or reg; PRI constant/< 0.20 sec; EVERY P WAVE DOES NOT HAVE A QRS COMPLEX; QRS WIDTH > 0.20 SEC
Hemodynamic effect: determined by the ventricular rate
Tx: pacing, observe for progression to CHB
2nd degree
w/ 2:1 conduction pattern
Origin: SA node, occurs w/ a sinus rhythm
Conduction: exists when EVERY OTHER sinus impulse is blocked and not conduted to the ventricles. VENTRICULAR RATE IS 1/2 ATRIAL RATE.
Features: P-P reg, R-R reg, PRI constant, v rate is 1/2 a rate, EVERY OTHER P WAVE IS FOLLOWED BY QRS COMPLEX
Hemodynamic effect: determined by the ventricular rate
Tx: based on the location of the block and the actual ventricular rate. pacing and/or drugs may be necessary to maintain adequate CO
determine location of 2nd block w/2:1 conduciton
2nd degree, Mobitz I
(block in AV node)
PRI > 0.20 sec
QRS width 0.10 sec or less

2nd degree, mobitz II
(block in ventricles)
PRI 0.20 sec or less
QRS width > 0.10 sec
3rd degree block
Origin: TWO SEPARATE RHYTHMS, one SA and AV junction or ventricles
Conduction: NO CONDUCITON THRU THE AV JUNCTION OR THE BB
Features: P-P reg, R-R reg, PRI varies
Hemodynamic effect: CO is decreased
Tx: pacing
atrial tachycardia
Origin: atrial
Conduction: if conduction normal, p wave then QRS w/ 1:1 conduction and PRI > 0.12sec.
if abnormal thru AV junction, some impulses will be blocked. This prevents rapid ventricluar rates = atrial tachycardia w/block
Features: ATRIAL RATE 151-250/min; PRI 0.12 sec if 1:1; P-P reg; R-R reg/irreg; QRS width normal
Hemodynamic effect: usually decreased
Tx: is directed at controlling the number of impulses delivered to the ventricles. ADENOSINE, PROPANOLOL, METOPROLOL, DIGITALIS.
ATRIAL FLUTTER
Origin: ATRIA
Conduction: ABNORMAL thru atria and AV junction
Features: atrial rate 251-400/min; saw toothed baseline; P-P regular; R-R reg/irregular
Hemodynamic effect: decreases CO
Tx: control v rate or convert. ADENOSINE, PROPANOLOL, METOPROLOL, DIGITALIS.
ATRIAL FIBRILLATION
Origin: ATRIA
Conduction: RAPID ATRIAL DEPOLARIZATION, AV JUNCTION IS BOMBARDED W/IRREG IMPULSES, RANDOMLY CONDUCTS SOME IMPULSES TO VENTRICLES
Features: P WAVES NOT IDENTIFIABLE; R-R IRREGULAR
Hemodynamic effect: MAY DECREASE CO, DEPENDING ON V RATE
Tx: CONTROL V RATE OR CONVERT. PROPANOLOL, METOPROLOL, DIGITALIS.
JUNCITONAL RHYTHM
origin:
conduction: AV JUNCTION
features: PRI<0.12 SEC -> A THEN V 2) V -> A THEN RETROGRADE P WAVE USUALLY FOUND IN ST SEGMENT 3) A AND V ARE DEPOLARIZED AT THE SAME TIME. ALL 3, THE ATRIA IS IMPULSE IS REC'D BY THE ATRAI IN RETROGRADE FASHION.
QRS <0.10
VENTRICULAR RATE IS 40-60/MIN
hemodynamic effect: MAY DECREASE CO B/C LOWER V RATE
tx: RESTORE SA NODE AS THE PRIMARY PM, OR INCREASE RATE TO INCREASE CO
ACCELERATED JUNCTIONAL
ORIGIN: AV JUNCTION
CONDUCTION:IMPULSE IS CONUCTIED RETROGRADE TO ATRIA AND ANTEGRADE TO VENTRICLES. THE RELATIONSHIP OF THE P WAVE AND QRS COMPLEX ARE DETERMINES BY THE ACTIVATION OF THE ATRIA AND VENTRICLES.
FEATURES: RATE 61-100/MIN; QRS NORMAL 0.10SEC OR LESS
HEMODYNAMIC EFFECT: CO USUALLY NOT EFFECTED
TX:N/A UNLESS CO IS INADEQUATE
JUNCITONAL TACHYCARDIA
ORIGIN:
CONDUCTION: AV JUNCTION
FEATURES: VENTRICULAR RATE IS > 100/MIN
HEMODYNAMIC EFFECT: CO USUALLY WILL DECREASE B/C FAST RATE AND INAPPROPRIATE ATRIAL CX/PACKING.
TX:PROCAINAMIDE, DIGITALIS, BETA BLOCKERS ARE USED WHEN THE CO IS AFFECTED SECONDARY TO FASTER RATE.
JUNCTIONAL ESCAPE BEAT
ORIGIN: AV JUNCITON
CONDUCTION: SAMES AS JUNCTIONAL RHYTHM
FEATURES: LATE QRS THAT FOLLOWS A PAUSE IN THE RHYTHM, P WAVE VARIES, QRS 0.10 SEC OR >.
HEMODYNAMIC EFFECT: IMPROVE CO
TX: N/A