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BIPN 100 > lecture 13: electrocardiography > Flashcards

lecture 13: electrocardiography Flashcards

1
Q

electrocardiogram (ECG or EKG)

A

extracellular recording that reflects the electrical activity of cardiac contractile cells
pacemaker cells are too small and too few to pick up on a signal for ECG
recorded from limb or frontal lead and chest leads

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2
Q

bipolar frontal leads

A

I —-> + LA , - RA
II —–> + LL, - RA
III——-> + LL , - LA

imaginary lines between two electrodes
get mV measurement from - electrode, subtract from + electrode

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3
Q

monopolar augmented frontal leads

A

amplifying the voltage
make a tiny signal look bigger
easiest way to see if something is wrong with your heart (noninvasive/easy)
3 + leads
AVR —–> + electrode on R arm
AVL —-> + electrode on L arm
AVF —–> + electrode on L leg
compare what is picking up with + electrode and take the difference from the other two

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4
Q

axial reference system

A

heart in center
AVR @ -150
AVL @ -30
AVF @ -90
lead I @ 0
lead II @ 60
lead III @ 120

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5
Q

chest leads

A

+ monopolar
only one + electrode
compare/subtract by all others and what theyre picking up
V1 - V6
different view of the electrical activity of the heart

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6
Q

ICS

A

intercostal space

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7
Q

MCL

A

midclavicular line

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8
Q

mean electrical vector

A

averages of all electrical vectors
angle tells you which cells are depolarizing and which direction the signal is moving in
length tells the number of cells which are depolarizing at that time

  1. moving towards + electrode = positive deflection (highest + voltage)
  2. moving away from + electrode = negative deflection (highest - voltage)
  3. moving perpendicular to lead = no change in electrical activity, baseline (0 voltage)
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9
Q

comparison between AP and ECG

A

AP in single myocardial cell —> have to do intracellular recording to measure electrical activity, would have to poke one specific cell to measure
ECG —-> sum of multiple APs taking place in many heart muscle cells

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10
Q

AV blocks

A

arrhythmias
conduction through AV nodal cells is affected
1st degree, 2nd degree, and 3rd degree

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11
Q

1st degree AV block

A

every P wave —> QRS (or just ventricular depolarization)
prolonger PR interval (>0.2 seconds)
signal still being able to move through AV node to atria/ventricles BUT taking longer than it should
person may not have any symptoms (monitor)

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12
Q

2nd degree AV block

A

intermittent conduction through the AV node
no QRS complex after some P waves
show the ratio (duration between P wave and 2nd P wave peak, seconds/beat)
ex: (60 s/m) / P to P interval
ex: atrial rate is 100 bpm and ventricular rate is 50 bpm -> 2:1
treatment: place a pacemaker

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13
Q

3rd degree AV block

A

no conduction through the AV node
signal is stuck
atria depolarizing and contracting way faster than ventricles
P waves (regular depolarization rate of pacemaker/SA nodal cells) and QRS (following depolarization rate of bundle of His) are independent
affects proper filling of blood in ventricles
cant have normal amount ejected from ventricles to rest of body
affects cardiac output
treatment: place a pacemaker

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14
Q

sinus rhythm

A

every P wave has QRS complex follow
normal: 60-100 bpm
calculate by using RR interval and using HR equation
SA node as pacemaker and driving rhythm

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15
Q

sinus tachycardia

A

fast
heart rate is >100 bpm

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16
Q

sinus bradycardia

A

slow
heart rate is <60 bpm

17
Q

fibrillation

A

cells or groups of cells fire individually
no coordination of chamber contraction/depolarization

18
Q

atrial fibrillation

A

atria not contracting effectively
ventricular filling is affected, not allowing to happen properly/cant finish
increase of blood clots (lead to stroke, heart attacks, pulmonary embolism)
SA node loses control of depolarization of cardiac contractile cells in atria, not as pacemaker
quivering
uncoordinated depolarization, contraction of ventricles
treatment: anticoagulants and medications to stop fibrillations, medications to slow ventricular rate

19
Q

ventricular fibrillation

A

ventricles not contracting/depolarizing effectively
CO and BP affected
life threatening
treatment: CPR, defibrillator

20
Q

ex: vectorcardiogram/QRS loop for Lead I

A
  1. Lead I at horizontal
  2. AVF as perpendicular to Lead I
  3. determine which side of perpendicular is (+) and (-) —> R is +, L is -
  4. from origin, move in direction of loop (clockwise)
  5. every time perpendicular is crosses, go back to baseline
    can determine size, direction, sign
21
Q

QRS loop

A

part of vectorcardiography
1. early —> depolarization of the septum
upwards and towards the right
not many cells
2. middle —-> depolarization of ventricular walls
downward and towards the left
many cells
3. late —> end of the depolarization of the R ventricle
upward and towards the right
not many cells

22
Q

vector

A

part of vectorcardiography
1. length: number of cells going through an electrical event
short with septal cells
2. angle: which cells are depolarizing
orientation moving up —> septal cells depolarizing

23
Q

vectorcardiography

A

how ECGs are built
calculate all mean electrical vectors
look at them on an axis

24
Q

mean electrical vector 2

A

bulk of cardiac contractile cells depolarizing
long because lots of cells present
facing L. ventricle due to more muscle mass there

25
Q

mean electrical vector 3

A

Purkinje fibers causing depolarizing of deep cells in myocardium
fewer cells

26
Q

RR interval

A

time between contractions
HR(bpm): 60 (s/m) / RR (s/beat)
determine HR

27
Q

PR interval

A

atrial depolarization and AV node conduction
depolarization of cardiac contractile cells of atria (P wave) usually doesnt change in duration too much
(0.12-0.2 sec)

  1. longer than 0.2 seconds —-> conduction through AV node is taking longer than it should, problem with AV node/nodal cells, could affect contraction of ventricles
  2. shorter than 0.12 seconds —-> signal bypassing AV node, unsynchronized depolarization of heart and contraction, cardiac output of blood pushed from ventricles is affected in unit time, affects how much oxygen gets to tissues

not ‘PQ’ because sometimes you dont have Q wave depending on lead used
gives indication of health of conduction system or conduction through AV node

28
Q

QT interval

A

ventricular depolarization and repolarization
affected by HR, can correct it
~0.4 seconds
needs to be treated ASAP if its too long, heart can go into defibrillation, can indicated congenital disease or pathology
one of the main things looked at in ECG

29
Q

electrocardiogram

A

measure duration of all wave segments and intervals in cardiac cycle
measure amplitude in mV of all waves
detect pathologies

30
Q

P wave

A

atrial depolarization of cardiac contractile cells in R and L atria (<0.1 second)
occurs before atrial contraction

31
Q

QRS complex

A

ventricular depolarization of cardiac contractile cells of ventricles (<0.12 seconds)
happens right before ventricular contraction
move very fast through His
dont always get all waves on ECG
1. Q wave: - wave before any + wave
2. R wave: + wave (most common)
3. - wave following a + wave
masks repolarization of atrial contractile cells (Tp wave)

32
Q

Tp wave

A

atrial repolarization
usually masked/covered by QRS complex

33
Q

T wave

A

ventricular repolarization (0.16 seconds)
takes longer than depolarization because no bundle of His to travel through

34
Q

PR segment

A

signal in AV node, no electrical change
contraction of atrial contractile cells
conduction through AV node and AV bundle

35
Q

ST segment

A

all ventricular contractile cells are in phase 2 (Ca plateau)
depolarized
mechanical event of contraction
no electrical change

36
Q

electrical events of the cardiac cycle

A
  1. AP moving through cardiac contractile cells of atria through gap junctions
    —–positive deflection at P wave
    —–SA nodal cells spontaneously depolarizing
    —–atrial depolarization
  2. PQ or PR segment, atria contracts
    —–signal stuck in AV node delay, isoelectric, no change in electrical activity
    —–Ca to be released due to mechanical contraction
  3. Q wave
    —–signal travels from AV node to bundle of His (quickly) to apex of heart
    —-negative deflection, depolarization of septal cells that stiffen
    —–cause depolarization of cardiac contractile cells of ventricle
    —–septal depolarization
  4. R wave
    ——more muscle mass on L ventricle than R ventricle
    ——large deflection, facing + electrode of Lead II
    ——ventricular depolarization
  5. S wave
    —–negative deflection, going up and vector facing - electrode away from + electrode of Lead II
    ——depolarization traveling through Purkinje fibers that go deep in muscle
  6. ST segment
    —–all cardiac contractile cells in L and R ventricle depolarize, now on Ca plateau
    ——Ca in through LTCC, VG K channels open
    ——-no electrical change mechanical event to pump blood into circulatory system
    ——-ventricles contract
  7. T wave
    —–repolarization of ventricles from bottom to top
    —–positive deflection
  8. end (baseline, rest)
37
Q

AV node delay

A

cells way smaller than bundle of His
accumulate lots of Ca in cells to bring bundle of His cells to threshold/depolarize and carry signal

38
Q

intraventricular septum

A

muscular ridge that completely divides L and R ventricles
depolarize at Q wave of cardiac cycle
stiffen when contracted

39
Q

Ca release into cytosol

A

need electrical event/MAP before mechanical event
for contraction to happen

BIPN 100 (8 decks)

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