Week One Flashcards
automaticity
electrical signals generated by pacemaker cells
pacemaker cells can generate stimulus without outside stimulation
Cardiac Cycle
Electrical (caused by automaticity)
mechanical (muscular) (contraction)
Electrical Activity
depolarization
repolarization
mechanical responses
systole
diastole
depolarization = ______ = contraction
systole
repolarization= ______ = resting or filing phase
diastole
Depolarization begins with?
SA node firing
atrial contraction and atrial kick
SA node beats?
60-100 bpm
AV node beats
40-60 bpm
Ventricles (purkinje fibers) beats?
15-40 bpm
What can the ECG tell us?
orientation of the heart in the chest
conduction disturbances
electrical effects of medication and electrolytes
mass of cardiac muscles
presence of ischemic damage
ELECTRICAL (not mechanical -contraction)
lead 1
records flow from right to left arm
lead 2
Records flow from right arm to left leg
lead 3
records flow from left arm to left leg
augmented limb leads
unipolar center of heart to lead
aVR
from heart to right arm
aVL
heart to left arm
aVF
heart to left foot
lead 2,3, aVF see what part of the heart?
inferior heart
V1 and V2 see?
septal (mid heart)
V3 and V4 see?
anterior heart
1, aVL, V5 and V6 see?
lateral heart
one small ecg square is how many seconds?
0.04 s
how many small squares make up a large square?
5
how many seconds is a large square?
0.20 s
P wave
atrial depolarization (SA node is firing)
normal P wave
round, upright, before every QRS complex, all look the same
QRS complex
ventricular depolarization
Q wave
less than 0.04 s
less than 1/3 the height of the R wave
PR interval
beginning of P wave to beginning of QRS complex
0.12- 0.20 sec (3-5 small blocks)
longer PRI
first degree AV block
shorter PRI
impulse from AV junction
QRS interval
0.06-0.12 s
wide QRS interval means
slowed conduction
ST segment
end of QRS to beginning of T wave
is it elevated or depressed
should be at baseline
T wave
ventricular repolarization
follows QRS complex
bigger than T wave
upright, round, smooth
when is the most vulnerable period of the ECG?
the peak of the T wave
QT interval
beginning of QRS to end of T wave
0.39-0.43s
atrial rate
peak of P to peak of the next P wave
ventricular rate
R-R wave
Normal Sinus Rhythm
regular
6-100 bpm
normal P wave in lead 2
P wave before QRS complex
normal PRI, QRS, and QT intervals
Sinus Tachy
rate: 101- 150 bpm
causes of tachy?
stimulants, exercise, fever, and alteration in fluid status
Symptoms of low CO
change LOC
chest pain
HoTN
SOB (RR distress)
dizziness, syncope
fatigue
restless
Management of STach
find and treat the cause
(pain give pain meds, fever give anti-pyretic)
Sinus Bradycardia
<60 bpm
regular
normal PRI and QRS
Management of SBrady
atropine
pacemaker
Sinus Arrhythmia
irregular RR
rate: 60-100
no real treatment (can live with them)
atrial dysrhythmias
increased automaticity in the atrium (SA node firing)
generally see changes in P wave
PRI normal
QRS normal
Causes of Atrial Dysrhythmias
stress
electrolyte imbalances
hypoxia
atrial injury
digitalis toxicity
hypothermia
hyperthyroidism
alcohol
pericarditis
caffeine
Premature Atrial Contractions
early beats initiated by atrium (SA node firing too early)
P waves and PR interval may vary
P wave may be found on T wave
Atrial Flutter
sawtooth (leads 2, 3, aVF)
RATE: 250-350 bpm
seeing many p waves before QRS (2:1, 4:1, etc)
no true p wave
QRS normal
Management of A Flutter
anticoagulant (blood is just laying in the body so blood thinners are 1st thing to do)
rate control with meds
elective cardio-version
interventional radiology - ablation of irritable site
Atrial Fibrillation
erratic impulse formation in atria
no PRI
P waves do not look the same
irregular ventricular rate
Causes of AFIb
heart disease
ischemia
mitral or tricuspid valve disease
CHF (overstretched chambers)
management of AFib
anticoagulation 4-6 weeks before cardioversion (so clots do not go everywhere in the body after being shocked)
ventricular rate control
emergent synchronized cardioversion if instability and not responsive to meds
CCB, Beta-blockers, digoxin, amiodarone
MAZE procedure
Ventricular Dysrhythmias
in the lower portion of the heart
depolarization occurs (wide QRS complex >0.12s)
the polarity of T wave
no p waves
Causes of Ventricular Dysrhythmias
myocardial ischemia, injury, and infarction
low K+ or Mag
hypoxia
acid-base imbalance (pH is acidic)
Premature Ventricular Contractions (PVCs)
no p wave
compensatory pause
early beat that interrupts the underlying rhythm
QRS > 0.12s
irregular
no PRI
When are PVCs dangerous?
frequently happen
multifocal - look different
two in row
three of more in row
R on T
R on T PVCs can cause what
VTach or VFIb
management of PVCs
find the cause and treat it
anti-dysrhythmic meds
causes of PVCs
drug induces (caffeine, alc, cocaine, sympathomimetic drugs)
hypoxia
cardiac disease, ACS, cardiomyopathy, vent aneurysm
hypokalemia
irritation of ventricle
Supra ventricular Tachycardia (SVT)
above the ventricle
abrupt onset and termination
RATE: 150-250 bpm
regular
note Stachy rate was 101-150, this rate is above 150
normally not tolerated well
ventricular tachycardia
rapid, life-threatening dysrhythmia
three of more PVCs in a row
fast RATE >100 bpm
THERE IS NO CO
wide QRS (>0.12 s)
regular
may or may not have a pulse
HoTN
management of V Tach
pulseless
- defibrillate
-CPR
- epinephrine
pulse
- amiodarone
- sotalol
- lidocaine
- cardioversion
Torsade de Pointes
type of Vtach
smaller to larger looking
Ventricular Fibrillation
chaotic
no P Q, R S, or T waves
no CO
emergent defibrillation
always assess pt for pulse and consciousness
management of VFib
check for pulse
no pulse = shock and CPR for 5 cycles (2 min)
check for pulse again
med: epinephrine
Idioventricular Rhythm (Ventricular Escape Rhythm)
Purkinje Fibers has an escape
RATE: 15-40 bpm
regular
wide QRS (> 0.12s)
no p waves
DO NOT GIVE LIDOCAINE
Asystole
a line
no nothing
no cardiac activity
first check leads
if forreal start CPR
epinephrine every 3-5 min
Pulseless Electrical Activity (PEA)
electrical system of heart works but the muscles do not contract
management: CPR, epine, must treat cause
this is a late sign
First Degree Block
delayed conduction from SA node to AV node
prolonged PRI (>0.20s)
same PRI for each beat
assess cause and treat it
Second Degree Block: Mobitz Type I Wenckebach
progressive lengthening PRI
some P waves without QRS
PP interval regular
RR interval regular
QRS normal
irregular rhythm
Second Degree Type II
more severe block
PR interval is fixed
PP interval is regular
P waves not followed by QRS
Management: transcutaneous (skin) or transvenous (vein) pacing
Third Degree
Complete
atria and ventricles beat independently
P’s not related to QRS
P wave not associated with QRS complex
PP interval regular
RR interval regular
BP is extremely low
Artifact
loose electrodes
broken ECG cables or broken wires
muscle tremor
patient movement
external chest compressions
60 cycle interference
