Phys And Pathophys - Antiarrhythmics And Ekg Strip Interpretation Review

Front 1

antiarrhythmic drugs work by

Back 1

blocking ion channels to impact the depolarization or repolarization phases of the nodal and ventricular muscle cells

Front 2

whose classification of antiarrhythmics are we learning

Back 2

Vaughn-Williams - classifications aren't exact - always exceptions - but he does a good job trying to classify them

Front 3

Vaughn-Williams classification is

Back 3

used by ACLS and bases classifications on what channels they impact, what phase of the action potentials, and what side effects they cause

Front 4

Class I drugs are

Back 4

drugs that inhibit sodium channel

Front 5

examples of class I drugs are

Back 5

local anesthetics

Front 6

subdivisions of Class I drugs are

Back 6

IA, IB, and IC

Front 7

subdivisions of Class I drugs are based on

Back 7

speed of onset or speed of binding to the sodium channels

Front 8

class II drugs

Back 8

are beta-adrenergic antagonists (beta blockers). they decrease spontaneous depolarization of phase 4

Front 9

class III drugs work by

Back 9

blocking potassium channels - prolonging depolarization and delaying repolarization

Front 10

class IV drugs are

Back 10

calcium channel blockers that inhibit calcium influx

Front 11

example of miscellaneous drug category

Back 11

adenosine

Front 12

verapamil is what class

Back 12

class IV - calcium channel blocker, but also blocks fast sodium channels

Front 13

RMP of the SA node

Back 13

-60 mv

Front 14

why is the RMP of the SA node so high

Back 14

cell membrane is leaky to sodium and calcium so when -60 mv is reached it doesn't stay there for long and creeps back up to threshold

Front 15

threshold for cardiac conduction tissue is

Back 15

-40 mv

Front 16

why is the rise for depolarization in the nodal action potential not a steep rise?

Back 16

because the fast acting sodium gated channels are already inactivated (around -55mv)

Front 17

phase 0 of the nodal action potential

Back 17

when the interior of the cell becomes positive enough to reach threshold then the slow gated sodium-calcium channels open to cause depolarization

Front 18

what happens in phase 3 of the nodal action potential

Back 18

as the sodium-calcium channels close, the potassium channel opens and potassium leaves the cell to repolarize

Front 19

what happens in phase 4 of the nodal action potential

Back 19

the Na-K pump restores the gradients to baseline

Front 20

automaticity is

Back 20

the ability of the heart to self-depolarize due to leaky sodium calcium channels

Front 21

sodium channel blockers work by

Back 21

decreasing the conduction velocity and decreasing the automaticity by decreasing the permeability of sodium into the cell.

Front 22

a lower level of sodium in the cell as a result of a sodium channel blocker means that

Back 22

the sodium calcium exchanger will kick it up a notch and bring more sodium into the cell and more calcium is kicked out leading to less intracellular calcium and therefore decreased contractility

Front 23

lidocaine is assumed to reduce cardiac contractility because

Back 23

it reduces the intracellular calcium level by blocking the sodium channels which then cause the Na Ca exchanger to kick out Ca in favor of Na

Front 24

the QT interval includes

Back 24

both the depolarization and the repolarization of the ventricles

Front 25

delaying depolarization will affect the QT how

Back 25

will increase the QT interval and will slant the slope of depolarization

Front 26

why is automaticity decreased by sodium channel blockers

Back 26

because it decreases the leakiness of the cell to sodium

Front 27

potassium channel blockers work by

Back 27

inhibiting the opening of the K+ channels in phase 3 of repolarization thereby increasing the duration of the action potential, increasing the refractory period and lengthening the QT interval

Front 28

beta blockers work by

Back 28

affecting the beta receptors on the heart tissue and nodal tissue (predominantly beta 1) and thus blocking these receptors will cause a decreased heart rate and some decrease in contractility

Front 29

a nonselective beta blocker

Back 29

affects both beta 1 and beta 2 receptors

Front 30

beta 2 receptors are

Back 30

found in the lungs and cause bronchodilation

Front 31

a nonspecific or nonselective beta blocker is a problem if

Back 31

in triggers bronchospasm in asthmatics - so always use a specific beta 1 blocker in asthmatics or find another drug entirely

Front 32

labetalol is specific or nonspecific?

Back 32

nonspecific - 7 beta: 1 alpha effect - therefore will reduce heart rate but will also cause some vasodilation

Front 33

beta blockers work on what phase of the action potential

Back 33

phase 4

Front 34

how do beta blockers affect phase 4 of the action potential?

Back 34

i don't know

Front 35

calcium channel blockers

Back 35

inhibit SA and AV node
inhibit cells with abnormal automaticity

Front 36

calcium channel blockers are very good for

Back 36

aberrant rhythms that want to take over - like reentry problems

Front 37

class IA drugs are what

Back 37

sodium channel blockers

Front 38

class IA drugs are used most commonly for

Back 38

conversion of afib, aflutter, and to maintain NSR

Front 39

class IB drugs are used most commonly for

Back 39

ventricular arrhythmias - especially those associated with an MI (but don't use prophylactically)

Front 40

examples of class IA drugs are

Back 40

Quinidine, procainamide, disopyramide (norpace)

Front 41

examples of class IB drugs are

Back 41

lidocaine, mexiletine, phenytoin, tocainide

Front 42

class IC is used for

Back 42

prolonging conduction velocity - afib, aflutter - only if patient has normal heart

Front 43

what class of drugs should not be used for patients post MI

Back 43

class IC (unless you want to kill them)

Front 44

class II drugs are

Back 44

beta blockers

Front 45

class III drugs cause

Back 45

prolonged action potential

Front 46

class III drugs are used to treat

Back 46

both atrial and ventricular arrhythmias (but can also cause arrhythmias)

Front 47

examples of class IC drugs are

Back 47

Flecainide, propafenone, moricizine

Front 48

examples of class III drugs are

Back 48

amiodarone, sotalol (betapace), bretylium, ibutilide (covert)

Front 49

the proarrythmic effects of class III drugs are due to their

Back 49

prolonging the QT

Front 50

why do we not use as many class III drugs anymore

Back 50

more use of the electrical pacemakers

Front 51

why don't we use bretylium any more

Back 51

because it came from the bark of a rainforest tree that doesn't exist anymore

Front 52

class IV drugs are

Back 52

specific calcium channel blockers that have an antiarrythmic effect

Front 53

examples of class IV drugs

Back 53

verapamil, cardizem

Front 54

why are some calcium channel blockers not a class IV

Back 54

they don't affect heart tissue - only smooth muscle receptors

Front 55

all antiarrhythmic drugs work best when

Back 55

EF is high

Front 56

antiarrhythmic drugs are more likely to cause arrhythmias when

Back 56

EF is low

Front 57

which classes of drugs are negative inotropes

Back 57

Ia, Ic, II, IV (and possibly lidocaine)

Front 58

what to consider before using an antiarrhymic

Back 58

risk vs benefit
will it alleviate symptoms?
will it prolong survival?
is there another cause that could be treated to fix the arrhythmias? (intrinsic vs extrinsic cause)

Front 59

treat arrhythmias in the OR only if

Back 59

continue despite removal of event
hemodynamic compromise
predisposes to a more serious arrhythmia

Front 60

hypoxemia can produce what arrhythmias

Back 60

PAC's or PVC's

Front 61

do you take your prescribed antiarrhymic drug on the day of surgery?

Back 61

yes

Front 62

when do you see bradycardia in surgery

Back 62

with inflation of the belly - will often self correct - as will most OR arrhythmias

Front 63

common cause of a prolonged PR is

Back 63

a conduction delay in the AV node (as long as p wave looks normal meaning that the atria are contracting ok)

Front 64

1st degree AV block is defined as

Back 64

a long PR interval (>.20)

Front 65

2nd degree type I or a Mobitz type I is defined by

Back 65

increasing PR interval and dropped ventricular beats (sometimes don't even have a p wave on the dropped beats)

Front 66

what do you set pacers at

Back 66

about 20% higher than initial capture

Front 67

if you turn down or off your volatile remember

Back 67

to give versed so they don't remember

Front 68

mobitz type II or 2nd degree type II is

Back 68

a consistent PR interval with some dropped beats

Front 69

mobitz type II may degenerate to

Back 69

3rd degree or complete heart block

Front 70

3rd degree heart block is defined as

Back 70

no coordination between p waves and q waves but they march out consistently between themselves

Front 71

if pressure drops with irregular rhythm

Back 71

try to fix the rhythm first - if fixed and still a problem then address preload, afterload, and contractility

Front 72

a mobitz type II can have

Back 72

up to 4 p's for every q wave but more often is 2:1 or less

Front 73

treatment for 3rd degree heart block

Back 73

pacer - if not available try atropine

Front 74

atropine works by

Back 74

blocking the parasympathetic stimulation of the vagus nerve allowing for more epi from the sympathetic system to bind to the muscarinic receptors to speed up the heart

Front 75

muscarinic receptors are found predominantly in the

Back 75

AV node

Front 76

sinus arrhythmia is

Back 76

found a lot in kids and young people and isn't usually a concern at all

Front 77

treat a fib with

Back 77

esmolol

Front 78

treat a flutter with

Back 78

cardizem (1st choice), digoxin (2nd choice)

Front 79

afib with rapid response can cause

Back 79

CHF in older paitents

Front 80

new onset a flutter can cause

Back 80

a clot to be flicked and cause a stroke

Front 81

torsades de pointes looks like

Back 81

a twisted party streamer

Front 82

torsades de pointes is often caused by

Back 82

prolonged QT intervals

Front 83

what classes of drugs will cause a prolonged QT interval?

Back 83

K+ and Na+ channel blockers (Class III and Class IA)

Front 84

a danger associated with a long QT is

Back 84

the R on T phenomenon

Front 85

describe the action potential in torsades de point

Back 85

slanted depolarization to peak and extended repolarization

Front 86

hyperkalemia will show on the EKG as

Back 86

a peaked T wave

Front 87

SVT is defined as

Back 87

rate over 160 or so (usually can't see the p waves anymore)

Front 88

RVR is differentiated from SVT by

Back 88

the width of the QRS
(a wide QRS is ventricular response, a thin QRS in SVT)

Front 89

treat SVT with

Back 89

Adenosine to slow it down and see what it really is

Front 90

dosing of adenosine is

Back 90

6 mg, 12 mg, 12 mg then done (push it fast)

Front 91

vtach or vfib treatment

Back 91

look at what's going on - make sure it's not bovie - check waveform on sat monitor to make sure it is real - check for pulse, give adenosine or lidocaine and then start ACLS if necessary