Cloned from: EKG study guide



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What is an ECG
an indirect measurement of the electrical activity within the heart
Chief complaint suggestive of ECG
chest pain, exert ional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, pedal edema, fainting, palpations, nausea and indigestion in high risk pts
Past medical hx suggestive of ECG
hx of heart disease, hx of cardiac surgery
physical exam suggestive of ECG
unexplained tachycardia at rest, hypotension,
SA Node
normally is pacemaker, has greatest automaticity, causes depolarization
AV Node
normally acts as back up pacemaker (40-60 bpm)
Atrioventricular Junction
AV Node and bundle of His (.05 second delay)
electrical conduction of the ventricles
from bundle of his in AV junction to bundle branches (30-40 bpm) to purkinje network (30-40 bpm)
Systole
ventrical contraction
Diastole
ventrical relax
atrial kick
contraction of the atria (at latter end of systole) just before ventrical contraction-aids in ventrical filling and accounts for 10-20% of CO in healthy person
AV Node delay
.05 seconds, delay before passing into bundle of his, allows for complete filling of ventricals before contraction (also protects vents from fast rates)
automaticity
cells that have the ability to generate electrical activity spontaneously
pacemaker cells
cells w/high degree of automaticity that provide electrical power to heart
myocardial cells
contract in response to elec stimuli and pump blood
ectopic impulse
impulse originating outside the SA Node
SA Node is stimulated by the sympathetic nervous system, what kinds of things can increase SA Node rate
(fight or flight) stress, anxiety, exercise, medication. CHF, hyperthyroidism
what can slow the SA node rate (or stop it)
vagal stimulation (parasympathetic), also drugs, disease etc
coronary arteries
supply 02 and nutrients to heart, arise from descending aorta and branches to coronary vessels
Infarctions
blockage of one or more coronary vessels leading to regionalized tissue ischemia and tissue death
MI and ischemia cause what
dysrrhythmias and
Hypoxia and ischemia of myocardium causes
how can sympathetic stimulus cause ischemia
>workload w/o concurrent blood flow (blocked coronary arteries)
what electrolyte imbalance cause dysrrhythmias
potassium, magnesium and calcium are most common
poor cardiac output and HR
to slow causes
causes of dysrrhythmias
hypoxia, ischemia, sympathetic stimulation, drugs, electrolyte imbalance
acetycholine
neurotransmitter of the parasympathetic NS, aka cholinergic,
norepinephrine
neurotransmitter of the sympathetic NS, aka adrenergic, >HR, >contractility
alpha and beta adrenergic receptor sites
alpha are in blood vessels through out body and B receptor are in heart and lung only
receptor site mnemonic ABCD
alpha constrict-beta dilate
heart receptor
alpha and B1
lung receptor
B2
blood vessel receptor
alpha and B2
4 major characteristics of cardiac cells
automaticity, excitability/irritability, conductivity, contractility/rhythmical
action potential
electrical charge passing through cell and propagating to other cells (all in one fashion)
polarized
resting state
depolarization
muscle contraction(loss of negative charge)
re-polarization
return to resting state (negative charge returns)
Pwave
(.10 seconds) depolarization of the atria, impulse spreads across atria and triggers atrial contractions
QRS complex
impulse spreads to ventricals, triggers ventrical contraction, (depolarization)
T-Wave
ventricals returning to resting state
PRI
PR interval, .12-.20, measures time from onset of atrial contraction to onset of vent contraction, aka time for elec impulse to spread through and AV node (3-5 small squares)
short PRI indicates
progression of elec impulse is outside normal path
long PRI indicates
delay in conduction or AV block
normal QRS
<.12
wide QRS indicates
originates in ventricular if supraventricular it has deviated from normal course
narrow QRS
normal, supraventricular
ST Segment
begins at end of QRS and ends at beginning of Twave, normally flat
elevated or depressed ST segment
possible MI
U-wave
follows Twave, may be seen or unseen, final phase of ventrical re-polarization
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