ECG I & II Flashcards
Aberrancy/Aberrant conduction
abnormal pathway of an impulse traveling through the heart’s conduction system
Arrhythmia
disturbance of the normal cardiac rhythm from the abnormal origin, discharge, or conduction of electrical impulses
automaticity
ability of cardiac cell to initiate an impulse on its own
Biphasic
Having an electrical impulse that is shown as deflections above and below the isoelectric line
chronotropy
neural, chemical, or physical factor that influences heart rate; referring to rate or time, such as the rate of cardiac contraction
positive chronotropic agent
increase heart rate
negative chronotropic agent
decrease heart rate
dromotropy
agent the affects the conduction speed of the AV node and subsequently the rate of electrical impulse; referring to the conductivity of a nerve fiber, such as the ability to conduct through the AV node
positive dromotropic agent
increase velocity
negative dromotropic agent
decrease velocity
inotropy
chemicals that influence contractility of the heart
positive inotropic agents
increase contractility
negative inotropic agents
decrease contractility
conductivity
ability of one cardiac cell to transmit and electrical impulse to another cell; the reciprocal of resistivity
depolarization
response of a myocardial cell to an electrical impulse that causes movement of ions across the cell membrane, which triggers myocardial contraction; the process or act of reversing the resting potential in excitable cell membranes when stimulated
deviation
major direction of the overall electrical activity of the heart. It can be normal, leftward (left axis deviation, or LAD), rightward (right axis deviation; RAD) or indeterminate (northwest axis). The QRS is the most important to determine; however, the P wave or T wave axis can also be measured
escape rhythm
a self-generated electrical discharge initiated by, and causing contraction of, the ventricles of the heart; this beat usually follows a long pause in ventricular rhythm and acts to prevent cardiac arrest
excitability
ability of a cardiac cell to respond to an electrical stimulus
infarction
tissue death due to inadequate blood supply to the tissue
intrinsic/inherent
naturally occurring electrical stimulus from within the heart’s conduction system
interval
duration of time that includes one segment and one or more waves
ischemia
local decrease in blood supply
monomorphic
form of ventricular tachycardia in which the QRS complexes have a uniform appearance from beat to beat
multifocal/multiform
type of premature ventricular contractions that have differing QRS configurations as a result of their originating from different irritable site in the ventricle
paroxysmal
episode of an arrhythmia that starts and stops suddenly
polymorphic
type of ventricular tachycardia in which the QRS complexes change from beat to beat
reciprocal leads
leads that take a view of an infarcted area of the heart opposite that taken by indicative leads
pre-excitation
an abnormal heart rhythm in which the ventricles of the heart become depolarized too early, which leads to their partial premature contraction
Threshold
the minimum level to which a membrane potential must be depolarized to initiate an action potential
ST segment
part of the ECG between the QRS complex and the T wave
sympathetic innervation “the gas pedal”
via thoracolumbar spinal nerve (T1-L2)
increase in SA nodal chronotropy (rate), AV nodal dromotropy (speed of AV node conduction) and myocardial intropy (contractility)
parasympathetic innervation “the break pedal”
via vagus nerve
Decreased SA nodal chronotropy and decreased AV nodal dromotropy
Reentry
normally impulse goes from AV to SA node but sometimes it turns around and goes backwards -reactivation of tissue by a returning impulse
accessory pathway
a form of reentry- a delayed or blocked impulse may travel through a different tract (no regulation)
reentry-orthodromic-antidromic
the impulse may travel down the normal pathway and then back up the accessory pathway (orthodromic) or vice versa (antidromic)
causes of reentry
myocardial ischemia
certain medications
hyperkalemia
horizontal plane values
measures time
one small box-0.04 seconds
one large box-0.20 seconds
p wave
atrial depolarization
electrical current generated by the SA node or atrial tissue
duration of p wave
less than 0.12 seconds
PR interval
impulse transmission time from SA node throughout the atria and to the AV node
PR duration
range 0.12 to .20 seconds 3-5 small boxes
QRS complex
depolarization of the ventricular myocardium
QRS duration
less than 0.12 seconds
Q wave
first downward deflection
pathological q wave
can tell if it is pathological if you can drop a little box into it
R wave
first positive upward deflection
more than one positive deflection noted as R’
S wave
first downward deflection after the R wave
ST segment
excited state of the ventricular myocardium
follows QRS
ventricular contractility starts here
j point
landmark for MI to measure elevation or depression
t wave
electrical repolarization of the ventricular myocardium
following the QRS complex
QT interval
represents the return of stimulated ventricular myocardium to a resting state
normal QT
normal if QT interval is less than half distance of R-R interval
U wave
repolarization of the purkinje system
causes of prominent U wave
profound bradycardias
hypokalemia
hypothermia
Define Bachman’s bundle.
The anterior tract that divides and extends into the LA.
Where is the triangle of Koch located?
In the floor of the right atrium superior to the septal leaflet of the tricuspid valve.
What is the only pathway to the ventricles called (in a normal person)?
Triangle of Koch
Why is the AV node delayed?
- to allow for atrial contraction (increase preload and subsequent contraction due to Frank-Starling mechanism)
- protects the ventricles from inappropriate high atrial rates (ie atrial fibrillation and flutter)
Is the refractory period longer for the SA or the AV node?
The AV node refractory period is longer.
Why is Ca++ important for electrical conduction in the heart?
Calcium is the major ion responsible for the action potential.
Define automaticity
Self-excitation
(accomplished by P cells which are located in the SA node, atrial tissue, AV node, and ventricular tissue —they have different rates bc different refractory periods)
What maintains the negative resting potential?
The sodium-potassium ATPase pump
How does the ATPase pump reset the membrane to pre-depolarizing electrolyte levels?
It exchanges 3 Na+ ions OUT of the cell for
2 K+ ions INTO the cell
Using the sodium-potassium ATPase pump is an active process. What does it require?
Magnesium and ATP(energy)
Which phase of the action potential plot corresponds with the resting membrane potential?
Phase 4
Describe phase 4 of the action potential
resting membrane potential (-80 to -90mV)
negativity maintained by the sodium/potassium pump
sodium out/potassium in
(corresponds with the baseline between the T and P wave)
Where happens during phase 0 of the action potential?
Rapid depolarization of the cell (stimulus applied)
Sodium rushes out of the cell making it less negative
(Potassium leaks out of the cell)
In what phase do the drugs lidocaine and procainamide work?
Phase 0
Describe phase 1 of the action potential.
(Brief rapid initiation of repolarization)
(closure of the sodium channels)
Chloride ions enter the cell (makes it more negative)
Describe Phase 2 of the action potential.
“Plateau” phase
Slowing of repolarization
Calcium enters the cell, leading to contraction of the muscle in a sustained, slower manner
Which class of antiarrhythmics work at phase 2 of the action potential?
Class IV antiarrhythmics (calcium channel blockers)
Verapamil, Diltiazem
Describe Phase 3 of the action potential.
Sudden acceleration in the rate of repolarization.
Potassium movement into the cell causes this rapid return in intracellular negativity
Sodium-potassium pump operates at this phase
What class of antiarrhythmics work in phase 3?
Class III
Amiodarone, sotalol (by prolonging the return to a resting potential)
Bachman’s bundle
anterior tract divided and extends into L atrium (near intra-atrial pathways)
intra-atrial pathway
conduct impulse through atria from SA–> AV
triangle of koch
septal leaflet of the tricuspid valve (below AV node)
major ion responsible for AP
Ca
orthodromic
AV node cycling
antidromic
down AV node then backup through accessary pathway
conduction velocity
necessary for synchronized myocardial contraction
funny channels (If)
unstable membrane potential (-60mV) gradually drifts toward threshold due to opening of ___
what ion do funny channels (If) permeable to?
K+ and Na+
absolute refractory period
cell can’t depolarized again, no matter how strong the impulse
AP: phase 0- mid-phase3
ECG: QRS-to peak of T wave
