Arrhythmias Flashcards
1
Q
Disturbances in cardiac rhythm
A
- bradycardia
- atrial flutter
- atrial fibrillation
- tachycardia (SV/V)
- ventricular fibr (not contracting normal just fibrillating so co falls to 0 so is emergency
2
Q
c of bradycardia
A
- sinus Brady; d to the exercise nature of the person or sickness like SICK SINUS SYNDROME; SAN node functioning normally , so drives HR b slower rate
- extrinsic factors like beta blockers and calcium blockers , so still in sinus rhythm b too slow
- conduction block, like at the AVN, Bundle of his, this c blockage of conduction between atria and ventricles , or again d to drugs
3
Q
early after depol
A
- hypokalaemia
-lenhgthens AP QT - set off oscillation c ventricular def
-longer AP = more likely to get delayed early afterdepol
and this equates to QT
4
Q
AP equates to for early after-depolarisation
A
qt interval
- longer AP =longer AP (since the graph we are looking at in terms of hypokalaemia is ventricular AP graph, and it takes into account vent depolarisation and repolarisation so hence the q till t)
- this suggest the patient is more likely to get arrhythmia , can be inherited or aquired
5
Q
re-entry mechanism
A
- normally spread of excitation around a piece of area of the heart that doesn’t conduct electricity
- the impulses goes around and meet on the other side where they cancel each other out because the sodium channels have inactivated d to the depolarisation and have reached the refractory period.
- but sometimes more scaring so one pathway of the electrical impulse divisions is blocked, so the other one goes to its place and goes up towards the blocked area and depolarises it and goes around and keeps circling the area of cells c depolarisation of many myocytes in that area in a circuit like manner c tachycardia
6
Q
what do you get further with re entry
A
multiple re-enterant circuits
- multiple c AF
7
Q
WPW
A
- accessory pathway bw atria and v creates a re-entry loop c ventricule to be excited early
8
Q
drugs affecting the rate and rhythm types
A
- block voltage-sensitive sodium channels
- beta adreno antag
- block k
- block ca2+
9
Q
class 1
A
- sodium voltage-senstive sodium channel
- class 1b LIDOCAINE
10
Q
class1b1
A
local anaesthetic lidocaine
- given IV
- ap happens b when na+ channels open it attaches but it works and detaches really quickly so when the next AP occurs it blocks
- it doesnt affect normal tissue, just the damaged the myocardium to prevent the spread of depolarisation to damaged area and this automatic firing only the damaged tissue is affected b it action open or inactive state sodium channels and normal cells aren’t in this state so their AP isn’t affected
11
Q
lidocaine when given?
why’s it a good choice?
A
- given to patients that show pst MI only if shows sign of VT b suggests VF
- not used prophylitically
- old drug
12
Q
class 2
A
beta adrenorecpeotr antagonists
- block synaptic action slow conduction at AVN and SAN
- sp can deal with sinus and supraventiuclar tachycadiara
13
Q
b blockers
A
- supra ventricular T
- down stop b do slow down AVN
- increased CO again
- post MI; b in MI get increases synthetic activity here why they’re pale and sweaty
- also reduced O2 demand
14
Q
block k channels
A
- class 3
- prolong AP
- lengthens absolute refectory period
- b they c more get more
- so noticed anymore
- ami
15
Q
amiodarone
A
- beta block
it blocks other channels Loe ca@+ and beta blockers and b of these other actions still works - B do have proarryhtmic function
-used for WPW
16
Q
class 4
A
- block calcium channels
- 2 tes
- dihydropyridine(on vascular) types and non dihydroppyridine (act on heart )
- Drecued slope of AP at the SAN aP since ca2+ c the upstroke and not the NA+ s this v HR
17
Q
adenosine
A
doesnt have a class
- made physcoligcally in the body but carve administered IV at higher dose prevent SV tach
- a1 receptor ,
- very short half life, stops the heart before letting it work again,
- enhaces the k+ conductance and
18
Q
causes of tachycardia
A
- ectopic pace maker activity ; -damaged area of myocardium d MI becomes depolarised , this spreads around and depolarises neighbouring cells c them to be spontaneously active ,
- latent pacemaker region activated d to ischaemia , dominates over SAN, can occur anywhere in the myocardium
- triggered activity
- reentry roots
- sinus tachycardia d hyperactive thyroid gland c sYM hyperactivity c excess stimulation the SYMP wc tachycardia
19
Q
what’s triggered activity
A
when the heart contracts twice after depolarisation
- there are 2 types ; early after-depolarisation ( occurs with increased intracellular ca2+ b calcium makes it more likely to reach threshold potential and so AP fired
- or EARLY AFTER_DEPO ; occurs with hypokalaemia where there’s oscillations
20
Q
bradycardia c
A
- sinus bradycardia ;
21
Q
sinus bradycardia what is it?
who does it occur in?
what do you see in ECG?
treatment for as and symptomatic ?
A
normal ECG so just get lower P-P interval is longer <70bpm
- get in athletes and genetic and hypokalaemia/hyperkaliemia
-increased vagus tone ; has parasymthaotc effects and c the heart to slow down
-hypothermia
-hypoxia
ASYMPTOMTIC; nothing
-SYMP; atropine wc is a (anticholingeric) , slows down parasympathetic
22
Q
sinus tachycardia
A
- normal patterns
- P-P smaller distance
- c of stress ecg pain/anxiety etc
23
Q
SAN arryhtmias
A
- sinus tachycardia and bradycardia
24
Q
Atrial ARRYTHMIAS
A
- ECG since it bypasses the SAN you see abnormal P wave or absent since P wave are representative of atrial depolarisation
- 100< (just looking at QRS waves since the P wave is absent )
- if one point = FOCAL TACHYCARDIA , many focal points = MULTIFOCAL so in ECG with this you see little ups and down before QRS
- atrial flutters (250-350 bpm) usually d to re-entry mechanism , with ecg you see sawtooth look in the p wave place
- afrib ; due to re-entry occurring in ecg measly line in p wave
- this caused by drugs, or structural abnormalities
- if this
25
Q
what happens with prolonged AVN
A
reduced CO doesn’t give enough time for diastole and also stasis of blood so more likely to clot
26
Q
why is atrial fib less dangerous than ventricular fib
A
- b enough b will fall from atria to ventricles d gravity
27
Q
avn arrythmias types?
A
-AVN block type 1 second degree type 2 second block third degree -2;1 second degree heart block (used to describe the p waves to the qrs
28
Q
ventricular fib ecg look like?
A
- ecg look slike a mess d multifocal points of the ventricle to contract
- c v CO
29
Q
SSS
A
- sick sinus syndrome
- collection of arrhythmia due to the sinus rhythm defects; you can get SAN block, or Sinus arrest or tachycardia or bradycardia tachycardia syndrome where both fast and small
