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Cardiovascular > electricity and the heart > Flashcards

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
Q

which segment shouldn’t be raised and should be isoelectric with the baseline

A

ST segment

26
Q

what lead is at 90 degrees to normal axis

A

Lead III - not good trace unless deviated

27
Q

morphologies - abnormalities of shape can results from

A

ischemia/infarction
Hypertrophy
Electrolyte disturbance - potassium changes
Metabolic disturbance

28
Q

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

A

ischemia and infarction

Full thickness damage → ST elevation
Subendocardial damage → ST depression - more dnagerous

29
Q

in a STEMI what does the ECG look like

A

ST segment Is elevated - Q wave

30
Q

in a NSTEMI - subendocaridal damage

A

ST segment depression with ± T wave inversion

31
Q

an inferior infarct is indication of what artery occluded

A

right coronary artery

32
Q

anterograde septal region what artery

A

Left anterior descending

33
Q

anterograde- apical region what artery

A

LAD - distal

34
Q

anterograde-lateral what artery occluded

A

circumflex

35
Q

posterior heart occluded what artery occluded

A

right coronary

36
Q

inferior MI leads so ST elevation in what leads

A

II
III
aVF

37
Q

anterior-septal MI ST elevation in what leads - this is the tombstone

A

V2,3,4

38
Q

in the tombstone - ST elevation what artery in normally occluded

A

left anterior descending artery

39
Q

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

A

true

40
Q

what are other causes of ST changes

A

trauma
pericarditis
hyperkalemia
digoxin

41
Q

in hyperkalaemia what does the ECG look like

A

high , peaked T waves and QRS widening

42
Q

how does hypertrophy present on ECG

A

negative deflection in V1 and positive deflection in V5

large amplitude of GRS complexes

43
Q

in AF CO decreases by 30% in ventricular fibrillation what happens

A

no CO

44
Q

In AF what is seen on ECG

A

no P waves
ORS is normal but irregularly irregular

align along piece of paper to prove this - no matching up using the scale

45
Q

how do you manage AF

A

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
Q

how does digoxin work

A
  • 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
Q

what is seen on ECG of VF

A

continuous bizarre irregular trace

External AED - paramedic, airports etc public places- strategically placed
Internal AED - implanted , high risk patients

48
Q

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

A

Av node transmission is delayed

Long P-R interval
normal QRS

49
Q

second degree heart block

A

partial transmission through
some P waves without associated QRS
regular or variable

50
Q

3rd degree. heart block

A

no transmission through AV node

No link between P waves and QRS and wide QRS

51
Q

What is a bundle branch block

A

problem with conduction where 1 ventricle depolarise after the other
with wide ORS after normal P

52
Q

RBBB what is seen on ECG

MARROW

A

M pattern in v1

W pattern in V6

53
Q

LBBB what is seen on ECG

WILLIAM

A

wide QRS complex with M pattern in V6

54
Q

asystole

A

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
Q

how does a ventricular ectopic occur

A

stimulus arising from ventricles - abnormalities in repolarisation with no p wave and wide and bizarre QRS

56
Q

what is a pacing impulse

A

Pacemaker that should come from sinoatrial node - sharp artificial stimulus - transferred through to ventricles and cause systolic beat
Can be abnormal wide QRS

57
Q

the cardioaccelotry centre in the medulla is the centre for the sympathetic NS what nerve stimulates the heart

A

sympathetic trunk gnaulino and then cardiac nerve

58
Q

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

A

SA and AV nodes

59
Q

where is the carotid body found

A

at the bifurcation

has chemoreceptors for O2
visceral sensory via 9 and 10 CN

60
Q

where is the carotid sinus found

A

proximal internal carotid artery

has baroreceptors sensitive to blood pressure
VA for 9 and 10 CN

Cardiovascular (20 decks)

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