electricity and the heart Flashcards

1
Q

concentration of calcium in the plasma ( extracellular )

A

2

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2
Q

conc of calcium intracellualryl

A

0

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3
Q

what are the 3 specific needs of the hart

A

Simultaneous , intermittent contraction of all fibres - pump out of ventricles

Prevention of sustained ( tetanic) contraction - fill up to allow second beat

Ability to change rate according to circumstance - ie when you start exercising you can step up the hr - role of calcium

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4
Q

what does a cardiac myocyte AP start at and rise to

A

-85mV and rises to +20mV - little depolarisation then plateau

the graph looks like a quif

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5
Q

in a cardiac myocte action potential in phase 0 what channels allow inflow of ion

A

sodium ions enter through fast sodium channels

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6
Q

in initial repolarisation(1) phase what channels open

A

potassium

sodium close

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7
Q

in phase 2 the plateau occurs why

A

increased calcium ion permeability

decreased potassium ion permeability

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8
Q

in phase 3 of a cardiac myocyte AP what happens

A

calcium channels close and slow potassium channels open so K leave and return the cell membrane potential to resting level

Role of calcium in AP - separate from the role of calcium in the SR involved int eh contraction process
Extended duration of AP ensures total ventricular depolarization

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9
Q

where are the pacemaker cells found

A

The sinoatrial (SA) node or sinus node is the heart’s natural pacemaker. It’s a small mass of specialized cells in the top of the right atrium (upper chamber of the heart). It produces the electrical impulses that cause your heart to beat.

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10
Q

what does a pacemaker cell action potential start at

A

-60mV

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11
Q

which ap has no resting phase

A

pacemaker cell action potential

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12
Q

Starts at -60mV with slower upward trajectory
Sodium inflow is slow and with end calcium inflow
When it hits -40mV hits a higher and quicker depolarization
Repolarization is with potassium otuflow

true or false

A

true

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13
Q

when the sympathetic system affect HR what happens

A

slow sodium channel permeability increases

and the slope of phase 4 so depolarisation becomes stepper so threshold is reached sooner therefore incresing the HR

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14
Q

when the parasympathetic system affects HR what happens

A

increases the resting potassium permeability
trough potential is then lowered and the phase 4 slope becomes flatter so threshold is reached later therefore decreasing the HR

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15
Q

does the AV node slow conduction by 100ms? what does this time allow and prevent

A

allows time for atrial emptying and protects the ventricles from atrial tachyarrhythmias

His-purkinje system → ventricles - depolarize from in to out ( opposite of perfusion)

Myometirum - interconnected webbing so can spread the signal
Branching nature of cardiac muscle alos enables synchronous ventricular contraction

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16
Q

on an ECG describe the polarity of impulses

A

Positive if towards recording electrode

Negative if away from recording electrode

negative to positive is depolarisation

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17
Q

which leads should be the strongest

A

V2
most postive signal
when

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18
Q

the main electrical flow is away from the aVR so produce what kind of signal

A

negative signal

so ECG thing upside down

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19
Q

main electrical impulses are towards what electrode giving a positive signal

A

lead II

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20
Q

the main electrical flow is at 90 degrees t o this lead so signal is largely neutral

A

lead III - so small like one bump in the ECG

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21
Q

what leads are lateral

A

I
aVL
V5
V6

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22
Q

what leads are inferior

A

II
III
AvF

AvR - recriporcla view

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23
Q

what leads are anterior

A

V3,4

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24
Q

count big squares between QRS complex determines what and divide that into 300

A

HR

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25
which segment shouldn't be raised and should be isoelectric with the baseline
ST segment
26
what lead is at 90 degrees to normal axis
Lead III - not good trace unless deviated
27
morphologies - abnormalities of shape can results from
ischemia/infarction Hypertrophy Electrolyte disturbance - potassium changes Metabolic disturbance
28
what problem usually causes Typically produce ST segment (±T wave) changes acutely - not all have these now though - rely on chemical picture and troponin rise - enzymes released when cardiac damage Damaged cells repolarize early, so ST segment is out of step with normal area
ischemia and infarction Full thickness damage → ST elevation Subendocardial damage → ST depression - more dnagerous
29
in a STEMI what does the ECG look like
ST segment Is elevated - Q wave
30
in a NSTEMI - subendocaridal damage
ST segment depression with ± T wave inversion
31
an inferior infarct is indication of what artery occluded
right coronary artery
32
anterograde septal region what artery
Left anterior descending
33
anterograde- apical region what artery
LAD - distal
34
anterograde-lateral what artery occluded
circumflex
35
posterior heart occluded what artery occluded
right coronary
36
inferior MI leads so ST elevation in what leads
II III aVF
37
anterior-septal MI ST elevation in what leads - this is the tombstone
V2,3,4
38
in the tombstone - ST elevation what artery in normally occluded
left anterior descending artery
39
in a Q wave infarct present ( transmural infarct) this acts as an electrical window - the electrode record depolarisation of the opposite wall from inside to out so a negative deflection is detected on the Q wave - true or false
true
40
what are other causes of ST changes
trauma pericarditis hyperkalemia digoxin
41
in hyperkalaemia what does the ECG look like
high , peaked T waves and QRS widening
42
how does hypertrophy present on ECG
negative deflection in V1 and positive deflection in V5 large amplitude of GRS complexes
43
in AF CO decreases by 30% in ventricular fibrillation what happens
no CO
44
In AF what is seen on ECG
no P waves ORS is normal but irregularly irregular align along piece of paper to prove this - no matching up using the scale
45
how do you manage AF
Anti- trhobmotic - warfarin/ dabigatran/rivaroxaban / aspirin Rhythm - cardioversion - synchronised shock ( prevents VF) Rate control - beta blocker, ca antagonist , amiodarone , digoxin Got to deal with another cause if that is what's happening
46
how does digoxin work
- Slows conduction through the AV node (Reduces ventricular rate in AF) - Increase myocardial contractility Sodium potassium pump inhibited , increasing intracellual sodium - ionotrope - increase contwcitlity Sound calcium exchange mechanism now less efficient raising calcium itnrcellualry - stored in SR - increases contwcitlity Force of subsequent contraction enhanced
47
what is seen on ECG of VF
continuous bizarre irregular trace External AED - paramedic, airports etc public places- strategically placed Internal AED - implanted , high risk patients
48
a problem with conduction of the AV node can lead to a heart block of varyign degrees what is a First degree heart block and what is seen on ECG
Av node transmission is delayed Long P-R interval normal QRS
49
second degree heart block
partial transmission through some P waves without associated QRS regular or variable
50
3rd degree. heart block
no transmission through AV node | No link between P waves and QRS and wide QRS
51
What is a bundle branch block
problem with conduction where 1 ventricle depolarise after the other with wide ORS after normal P
52
RBBB what is seen on ECG | MARROW
M pattern in v1 | W pattern in V6
53
LBBB what is seen on ECG | WILLIAM
wide QRS complex with M pattern in V6
54
asystole
Asystole is the most serious form of cardiac arrest and is usually irreversible. Also referred to as cardiac flatline, asystole is the state of total cessation of electrical activity from the heart, which means no tissue contraction from the heart muscle and therefore no blood flow to the rest of the body.
55
how does a ventricular ectopic occur
stimulus arising from ventricles - abnormalities in repolarisation with no p wave and wide and bizarre QRS
56
what is a pacing impulse
Pacemaker that should come from sinoatrial node - sharp artificial stimulus - transferred through to ventricles and cause systolic beat Can be abnormal wide QRS
57
the cardioaccelotry centre in the medulla is the centre for the sympathetic NS what nerve stimulates the heart
sympathetic trunk gnaulino and then cardiac nerve
58
the cardioinhibotry centre is all in the medulla and is part of the parasympathetic NS - dorsal motor nucleus of the vagus nerve - affects what nodes
SA and AV nodes
59
where is the carotid body found
at the bifurcation has chemoreceptors for O2 visceral sensory via 9 and 10 CN
60
where is the carotid sinus found
proximal internal carotid artery has baroreceptors sensitive to blood pressure VA for 9 and 10 CN