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BHRS EP Exam > Cardiac Electrophysiology > Flashcards

Cardiac Electrophysiology Flashcards

(125 cards)

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1
Q

currents that contribute to SAN action potential

A

Calcium

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2
Q

Adrenergic stimulation does what in the SAN?

A

Increases calcium

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3
Q

Cholinergic stimulation does what in the SAN?

A

Decreases calcium by shifting action potential to more negative potential

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4
Q

cholingeric cause of SAN arrest

A

Outward current during Cholinergic stimulation from acetylcholine medicated potassium current and hyper polarisation of SA cells = y excitable cells

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5
Q

Bainbridge Effect (Atrial Reflex)

A

Increased atrial pressure = increased HR

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6
Q

Phase for spontaneous SAN depolarisation

A

Phase 4 using slow calcium channels to trigger action potential

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7
Q

Membrane potential required in SAN cells to trigger spontaneous depolarisation.

A

-40mV

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8
Q

Phase for SAN depolarisation

A

phase 0

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9
Q

Relative depolarisation in SAN is accounted for by what?

A

Small amounts of Kl in phase 3

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10
Q

How many phases are there in the SAN cardiac action potential?

A

3

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11
Q

resting potential in SAN cells

A

no true resting potential but generate regular spontaneous action potentials.

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12
Q

Do fast depolarising NA+ channels occur in SAN cells?

A

no = slower action potentials in SAN

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13
Q

SA curve

A
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14
Q

Channels involved in phase 3 of the SAN cardiac action potential

A

Phase 3 - slow inward Na+ currents and K+ open, outflow of potassium = spontaneous depolarisation
L type Ca++ close.
end of repolarisation cell membrane potential = -60mV

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15
Q

Explain the phases of the SAN cardiac action potential

A

Phase 4 - spontaneous depolarisation at -40mV membrane potential
Phase 0 - depolarisation
Phase 3- repolarisation down to - 60mV

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16
Q

Channels involved in phase 0 of the SAN cardiac action potential

A

L Type Ca++ channels open at end of Phase 4.
If and T type Ca++ close.

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17
Q

Channels involved in phase 4 of the SAN cardiac action potential

A

Phase 4 T type Ca++ opens = influx - further depolarisation of cell to -40mV

L type Ca++ opens - increases Ca influx - further depolarisation down to -30mV
Less K+ out as K+ channels close

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18
Q

Abbreviation for funny Na+ currents in SAN cells

A

If

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19
Q

What state is required for pacemaker cells to be activated?

A

hyperpolarised state - very negative membrane potential

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20
Q

What can happen without very negative membrane potential in a pacemaker cell?

A

remain inactive

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21
Q

Result of inactivated pacemaker cells

A

suppressed pacemaker currents and decreased phase 4 slope

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22
Q

Nodal cells include?

A

SAN
AVN

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23
Q

Non nodal cells include?

A

Purkinje system
atrial and ventricular myocytes.

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24
Q

What kind of action potential do nodal cell display?

A

Automaticity = spontaneous depolarisation

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25
How is the behaviour of impusle and rhythm determined?
shape of cardiac action potential
26
How do antiarrhythmic drugs change the behaviour of impulse and rhythm?
changing the shape of the cardiac action potential
27
Excitability of a cells is determined by?
opening and closing of channels changing electrical voltage inside a cell
28
Phase 0 of non nodal cardiac action potential
Rapid depolarisation at 382V/s · Cell = less negative · Ion = NA+ rapidly in
29
Phase 1 of non nodal cardiac action potential
Early repolarisation · Cell = more negative · Ion = Calcium rapidly in (Na+ channel closed)
30
Phase 2 of non nodal cardiac action potential
Plateau phase · Cell = repolarisation interrupted + prolonged refractory period · Ion = slowly - calcium in, potassium out
31
Phase 3 of non nodal cardiac action potential
rapid repolarisation · Cell = more negative · Ions = potassium rapidly out (Ca+ closed)
32
Phase 4 of non nodal cardiac action potential
resting potential · Cell = balanced potential · Ions = sodium out, potassium in
33
Phases within the absolute refractory period of a non nodal cardiac action potential
phase 0,1,2 & early 3
34
Phases within the relative refractory period of a non nodal cardiac action potential
phase 3 & 4
35
Identify 4 types of reversible AV block
·Lyme Carditis disease · Drug toxicity · Vagatonia · Hypoxia
36
Agonists
mimick native body chemicals that bind to cell receptors to restore cellular activity
37
Antagonists
inhibit or block action by occupying cell receptor
38
What do nitrates do?
vasodilation
39
In what setting are nitrates used the most?
manage chest pain
40
Identify a type of nitrate
Nitroglycerine
41
What do inotropes do?
increase calcium and decrease contractility
42
Example of an inotrope
Digitalis
43
What do sympathomimetics do?
mimic sympathetic activity
44
Example of an sympathomimetic
Isoproterenol
45
What do sympatholytics do?
oppose sympathetic activity
46
Example of sympatholytics
Beta blockers
47
What do antiarrhythmics do?
treat symptomatic and life threatening arrhythmias
48
How do antiarrhythmic drugs work?
change shape by changing flow of ions by binding to cells and gates
49
What result does changing the shape of the cardiac action potential achieve/
alters automaticity, conductivity and refractoriness of cardiac tissue.
50
Slow binding drugs
significant block of membrane channels = reduced conduction velocity
51
Fast binding drugs
unbind quickly and have less effect on blocking a channel
52
Class Ia drugs
Quinidine Procainamide Disopyramide
53
Shape of class Ia cardiac action potential
Ia
54
Effect of class Ia drugs on action potential
moderate reduction on phase 0 of slow = increase action potential duration and effective refractory period
55
Effects of quinadine, procainamide and Disoprymide
blocks sodium channels = slows phase 0 Blocks potassium channel = prolongs refractory period
56
Use of Quinadine
Treat AFL, AF, reentrant SVT and VT
57
use of procainamide
Treat AFL, AF, reentrant SVT and VT and AF with rapid conduction down AP
58
Limitations of Disoprymide
negative inotropic potential and strong anticholinergic properties
59
Class Ib drugs
Lidocaine Mexiletine Phenytoin
60
Shape of class Ib cardiac action potential
Ib
61
Effect of class Ib drugs on action potential
small reduction in phase 0 slope = reduced action potential duration and ERP
62
Effects of Lidocaine, mexiletine and phenytoin
slows depolarisation and conduction velocity at fast heart rates and during ischemia, hypokalemia and acidosis
63
Difference in effect of Phenytoin
displays centrally mediated antiadrenergic effect.
64
side effects of lidocaine
suppress automaticity early and late after depolarisations confusion dizziness seizures respiratory arrest
65
Use of Lidocaine and Mexilitine
Treats VT, VF Most common used drug
66
In what cohort is mexilitine not suitable for ?
emergent acute arrhythmia
67
Use of Phenytoin
treat VT caused by digitalis toxicity
68
Class Ic drugs
Flecainide Propafenone Moricizine
69
Class Ic cardiac action potential shape
Ic
70
Effect of Flecanide
slow conduction and conduction velocity due to prolonged binding and unbinding time
71
Use of fleccainide
Treat AT and VT PVCs and NSVT
72
Side effects of fleccainde and propafenone
GI slow binding = slow conduction at low heart rates contraindicated in underlying heart disease Visual disturbances
73
Effect of Propafenone
blocks sodium channels and increase in refractory periods
74
Effect of Ic drugs
pronounced reduction in phase 0 Decreases conductivity no effect on action potential duration or ERP.
76
Use of Morcizine
treats atrial and ventricular arrhythmias
79
Effects of Class II drugs
decreases slope of phase 4 block sympathetic activity - reduced HR and conduction
80
81
Effect of Carvediolol, Metroprolol and Atenolol
reduces catecholamines, decreased SAN automaticity, slow AVN conduction and prolonged refractory periods
83
Use of IC drugs
Terminate or prevent AVNRT, SAN reentry, macro-reentrant tachycardia, Slow ventricular response in AT, AFL or AF
85
Use of amiodarone and sotalol
Treats AT and VT
86
Disadvantage of sotalol
less effective than amiodarone May prolong QT interval
87
Disadvantages of Sotalol
bradyarrhythmias negative inotropy exacerabtion of asthma may cause torsades
88
89
Use of Ibutilide and Dofetilide
Treat AF and AFL
90
Effect of Ibutilide
slow inward Na+ activatior = delayed repolarisation inhibits Na+ inactivation = increased ERP
91
Effect of Dofetilide
very selective potassium channel blocker
92
Side effects of Ibutilide and Dofetilide
can cause life threatening ventricular arrhythmias
93
Class IV drugs
Verapamil Diltiazem
94
Effects of Class IV drugs
decreases sympathetic vascular resistance and prolong phase 2
95
Effects of verapamil and diltiazem
Blocks calcium channels in SAN and AVN depolarisation = increased refractoriness, depressed automaticity and slow conduction
96
Use of verapamil and diltiazem
SVT, AT, multifocal Atrial reentry, AVNRT, macroreentrant VT, exercise induced/idiopathic VT
97
Class V drugs
adenosine, digoxin, magnesium sulfate
98
Effects of Digoxin
Decreases heart rate and reduces conduction velocity through AVN
99
Use of Digoxin
Treat AF/AFL
100
Effects of adenosine
decreases phase 4 slope in pacemaker action potential = decrease spontaneity Reduces conduction velocity in AVN = AVB
101
Side effects of Digoxin
plasma >2.0ng/ml = digitalis toxicity manifested as arrhythmias
102
Results of Digoxin effects seen in AFFIRM trial
significantly increased all cause mortality in patients in AF
103
Use of Adenosine
Rapid treatment of SVTs in which AVN is part of the circuit
104
Limitations of Adenosine
very short half-life <10s
105
Effects of magnesium sulfate
hypomagnesemia inhibts ion transportation = cellular depolarisation
106
Use of magnesium sulfate
Treat VT, VF, PVCs, SVT, AT, Flutter and AF and arrhythmias related to digitalis toxicity
107
Class I drugs affect what ion channels
sodium channel blockers decreased depolarisation
108
Class II affect what ion channels
beta blocking agents - decreased sympathetic tone SAN and AVB
109
Class III affect what ion channels
Potassium channel blockers - increase action potential duration
110
Class IV affect what ion channels
Calcium channel blockers - affects SA and AVN
111
Class V affect what ion channels
Digitalis agents - affects SAN and AVN
112
Which current is responsible for maintaining stable resting membrane in atrial and ventricular cells?
Ikl
113
Which antiarrhythmic does not prolong the QT interval but may shorten it?
Lidocaine weak sodium channel blocker so no effect of potassium channels used in repolarisation (QT interval)
114
Which drug may promote AF?
Adenosine
115
Drugs that have potassium and sodium channel effects can cause what?
Torsades from QT prolongation
116
Resting membrane potential in AVN
40 to 70 mV.
117
Identify medical therapy that might be appropriate to initiate in PAF
digoxin diltiazem metroprolol work on AVN for ventricular rate control
118
What effect does procainamide have in AF?
restores SR but also enhances AVN conduction Have appropriate rate control before administering
119
Identify reasons to implant a PPM in a patient with congenital CHB
declining exercise junctional instability or wide complex QRS escape rhythm progressive cardiomyopathy with declining ventricular performance QT prolongation
120
Drugs for HF treatement
Amiodarone Dofetilide
121
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123
124
125
126
Advantage of class Ic drugs
Shown to significantly reduce SCD
129
Effects of class III drugs
delay repolarisation = increase action duration and ERP
131
Effects of amiodarone
Blocks potassium channel and prolongs action potentials
132
Limitations of amiodarone
may take weeks to take effect Non competitive beta blocker effect, may block CA++ channels
133

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