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IPCS 4 > Cardio 1 > Flashcards

Cardio 1 Flashcards

1
Q

What is systole?

A

contraction (pumping)

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2
Q

What is diastole?

A

relaxation

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3
Q

Does systole change with heart rate?

A

no

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4
Q

Does diastole change with heart rate?

A

yes

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5
Q

What are normal heart sounds? (s1/s2/s3/s4)

A

s1 and s2

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6
Q

What heart sounds are heard in heart failure? (s1/s2/s3/s4)

A

s3

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7
Q

What heart sounds are heard in hypertrophied/stiff hearts? (s1/s2/s3/s4)

A

s4

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8
Q

S3 heart sounds are due to __

A

increased ventricular filling/dilation

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9
Q

S4 heart sounds are due to __

A

increased pressure

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10
Q

A ventricular gallop (S3) is correlated with __

A

Ken Tuc KY
early diastole

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11
Q

An atrial gallop (S4) is correlated with __

A

TE Nuh See
Late diastole

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12
Q

Arteries are __ vessels

A

conduit

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13
Q

Arterioles are __ vessels

A

resistance

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14
Q

Capillaries are __ vessels

A

exchange

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15
Q

Venules/Veins are __ vessels

A

capacitance

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16
Q

What are examples of organs that recondition blood?

A

Lungs
Kidneys
Skin

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17
Q

What are examples of organs that are supplied only for metabolic needs?

A

Brain
Heart
Skeletal muscle

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18
Q

Flow only occurs when there is a __

A

pressure difference

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19
Q

Heart need to keep pressure __>__ to maintain flow

A

arteries>veins

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20
Q

What is stroke volume?

A

fraction of blood that is pumped from the left ventricle during ventricular systole

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21
Q

What is stroke volume used for?

A

to calculate ejection fraction

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22
Q

What is left ventricular end diastolic volume (LVEDV)?

A

total amount of volume in the left ventricle at the end of diastole (before it is ejected

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23
Q

What is systemic vascular resistance (SVR)?

A

resistance exerted by the vascular bed impeding blood flow

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24
Q

What is low/narrow pulse pressure usually due to?

A

low stroke volume
(heart failure, trauma/blood loss, aortic stenosis)

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25
Q

What is high/wide pulse pressure usually due to?

A

increase in stroke volume/decrease in SVR
(temporary due to exercise)
(chronic due to anemia, atherosclerosis, aortic regurgitation)

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26
Q

Contraction is triggered by an __

A

action potential

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27
Q

Rate of change of transmembrane voltage IS/IS NOT proportional to the net current across membranes

A

IS

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28
Q

Current is influenced by movement of __

A

ions

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29
Q

What are three ions for cardiac transmembrane potentials?

A

NA, Ca, K

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30
Q

In order for effective pumping, what must be true? (5)

A

not arrhythmic
not stenotic
not regurgitant
not weak
not stiff

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31
Q

B1 receptors are in the __

A

heart

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32
Q

B2 receptors are in the __

A

lungs

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33
Q

M1,35 are excitatory/inhibitory

A

excitatory
increase heart rate/constriction

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34
Q

M2,4 are excitatory/inhibitory

A

inhibitory
decrease heart rate, produces vasodilation

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35
Q

nicotinic receptors are excitatory/inhibitory

A

can be either
several subsets

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36
Q

What does a cardio exam consist of?

A

jugular venous pressure
waveform
blood pressure
arterial pulse
palpitation of the heart
cardiac auscultation

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37
Q

jugular venous pressure (JVP) is an __

A

estimation of volume status

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38
Q

Central venous pressure is estimated by measuring __

A

the vertical distance from the top of the jugular venous pulsation to the sternal inflection point or clavicle

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39
Q

Elevated JVP is suggestive of __

A

right-sided heart failure
constructive pericarditis
pericardial effusion

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40
Q

What is an A wave?

A

right Atrial contraction

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41
Q

What is a C wave?

A

beginning of right ventricular Contraction as the triCuspid Closes, interrupts the x descent

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42
Q

What is the x descent?

A

fall in right atrial pressure (relaXation)

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43
Q

What is a V wave?

A

atrial diastole (Venous filling) and Ventricular Contraction

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44
Q

What is the Y descent?

A

emptYing of atrium into ventricle (ventricular diastole, tricuspid open)

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45
Q

What is the waveform abnormality in atrial fibrillation?

A

no a wave present

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46
Q

What is the waveform abnormality in pulmonary hypertension?

A

large a wave

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47
Q

What is the waveform abnormality in heart block/ventricular arrhythmias?

A

cannon a wave

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48
Q

What is the waveform abnormality in tricuspid regurgitation?

A

large v wave

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49
Q

What is the waveform abnormality in pericardial tamponade/tricuspid stenosis?

A

prolonged or blunted y descent

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50
Q

Too small of a cuff can result in an over/under estimation of BP

A

over

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51
Q

Too large of a cuff can result in an over/under estimation of BP

A

under

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52
Q

Measurement differences >10mmHg in arms may suggest __

A

atherosclerosis
aortic dissection
subclavian artery disease

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53
Q

Large leg-arm differences are seen in __

A

PAD
severe AR

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54
Q

Very low DBP may suggest __

A

severe AR
large AV fistula

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55
Q

Visible left anterior chest heave indicates __

A

enlarge RV

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56
Q

Visible right upper parasternal pulsation indicates __

A

aortic disease

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57
Q

A sternal lift indicates __

A

volume overload

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58
Q

Leftward/downward displacement of apex beat indicates __

A

enlarged LV

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59
Q

What is thrill and what is it from?

A

vibratory sensation felt over skin
due to a murmur

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60
Q

A systolic click indicates __

A

mitral valve prolapse

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61
Q

Friction rub is due to __

A

pericarditis

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62
Q

What is bruit and what is it from?

A

murmur
due to blood flow through vascular abnormality (narrowing)

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63
Q

Class I agents block __ channels, inhibit phase __ of action potential, and __ rate of depolarization WITH/WITHOUT changing the resting potential

A

sodium
0
decrease
without

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64
Q

Class I agents can interact with Na channels via what 3 routes?

A

-external hydrophilic route
-internal hydrophobic-hydrophilic route
-direct membrane spanning route

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65
Q

To cross the membrane and reach the sodium channels, the drugs must be in the __ form

A

neutral (uncharged)

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66
Q

Quinidine has which two rings?

A

quinoline
quinuclidine

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67
Q

Quinidine is BASIC/ACIDIC at physiological pH

A

basic

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68
Q

Quinidine IS/IS NOT protonated at physiological pH.

A

is protonated

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69
Q

Procainamide is a bio-iostere of __. The ester group was replaced with an __. This makes it more resistant to __, less __, and fewer __ effects.

A

procaine
amide
hydrolysis
lipophilic
CNS

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70
Q

The acetylated metabolite of procainamide IS/IS NOT active as an anti arrhythmic.

A

IS active

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71
Q

Disopyramide is a unique molecule with a chiral carbon directly linked to __

A

a pyridine ring, a phenyl ring, an amide, and an alkyl diisopropyl amine (tertiary amine)

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72
Q

Disopyramide’s tertiary amine is converted into salts such as phosphate to improve __

A

water solubility

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73
Q

Lidocaine is used for __ arrhythmias

A

ventricular

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74
Q

Lidocaine has a __ amine and is weakly BASIC/ACIDIC

A

tertiary
basic

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75
Q

Lidocaine has a RAPID/SLOW onset with administered parenterally

A

rapid

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76
Q

The amide bond of lidocaine is replaced with an ether to make __ more resistant to __

A

Mexiletine
hydrolysis

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77
Q

Mexiletine is weakly BASIC/ACIDIC

A

basic

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78
Q

Mexiletine primarily exits in the __ form in the stomach and in ___ form in the intestine

A

ionized (hydrophilic)
unionized (lipophilic)

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79
Q

Mexiletine undergoes EXTENSIVE/MINIMAL first pass metabolism

A

minimal

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80
Q

Mexiletine is used to slow down rapid __ rates on IV administration

A

ventricular (V-FIB)

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81
Q

Flecainide is a __ derivative and sold as an __ salt

A

bis-trifluoroethoxy benzamide
acetate

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82
Q

Flecainide is used to slow down rapid __ rates on IV administration

A

ventricular (V-FIB)
(after MI)

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83
Q

Propafenone has a __ and is sold as a __

A

chiral center
racemic mixture

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84
Q

The __ isomer of propafenone is mainly responsible for Beta1 blocking properties

A

S-(+)

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85
Q

Propafenone has a __ group and contains a weakly __ secondary amine group

A

phenyloxypropanolamine
basic

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86
Q

Beta2 agonists are used in the treatment of __

A

asthma and COPD

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87
Q

Beta1 antagonists are in the treatment of __

A

cardiovascular disorders

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88
Q

Beta-blockers INCREASE/DECREASE sympathetic stimulation of adrenergic receptors in both peripheral and central nervous system by __

A

decrease
norepinephrine

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89
Q

First generation beta blockers are __

A

nonselective

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90
Q

Second generation beta blockers are __

A

more selective for Beta1

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91
Q

Beta agonists have an __ structure, while beta antagonists have an __ structure

A

arylethanolamine
aryloxypropanolamine

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92
Q

Beta selectivity INCREASES/DECREASES with size of R group

A

increases

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93
Q

What are examples of first generation beta blockers?

A

propranolol
carteolol
nadolol
penbutolol
S-timolol

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94
Q

What are examples of second generation beta blockers?

A

atenolol
metoprolol
acebutolol
betaxolol
bisoprolol

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95
Q

Esmolol has a very SHORT/LONG half life

A

short

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96
Q

What beta blocker has intrinsic sympathomimetic activity?

A

acebutolol

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97
Q

Beta blockers that prevent norepinephrine from binding to the receptor are __

A

antagonists

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98
Q

Beta blockers with intrinsic sympathomimetic activity stimulate the Beta receptors and are __

A

partial agonists

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99
Q

Stimulation of beta receptors by norepinephrine is responsible for increased __ and __

A

heart contraction
heart rate

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100
Q

Propranolol:
has a __ group
LIKELY/NOT LIKELY to pass the BBB

A

hydrocarbon naphthyl
likely

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101
Q

Atenolol:
has a __ group
LIKELY/NOT LIKELY to pass the BBB
a lower dose may be required in patients with __ impairment

A

polar acetamide
not likely
renal

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102
Q

Metoprolol:
is more HYDROPHILIC/LIPOPHILIC
a lower dose may be required in patients with __ impairment

A

lipophilic
hepatic

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103
Q

Class III agents block __ channels
Phase __ of action potential
INCREASE/DECREASE duration of action potential

A

potassium
3
increase

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104
Q

Amiodarone:
a __ derivative
highly HYRDOPHILIC/LIPOPHILIC
weakly BASIC/ACIDIC

A

diionated benzofuran
lipophilic
basic

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105
Q

Dronedarone:
a __ analogue of amiodarone
lack of __ and addition of __ group makes it more hydrophilic
Decreases risk of __
Reduced __ side effects
SHORTENS/LENGTHENS half-life

A

non-iodine containing benzofuran
iodine
methanesulfonyl
neurotoxicity
non-cardiovascular
shortens

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106
Q

Ibutilide:
Structurally similar to __
Contains __ and __ side chains
Has good __ solubility
Sold as a __

A

Sotalol
hydroxybutyl
heptyl
water
racemic mixture
A methanesulfonamide

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107
Q

Dofetilide:
Highly selective ___ blocker compared to amiodarone
POORLY/WELL absorbed

A

potassium channel
well
a bis-methanesulfonamide

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108
Q

What are Class I anti-arrhythmic agents?

A

Na channel blockers

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109
Q

What are Class II anti-arrhythmic agents?

A

beta-adrenergic blockers

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110
Q

What are Class III anti-arrhythmic agents?

A

K channel blockers

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111
Q

What are Class IV anti-arrhythmic agents?

A

Ca channel blockers

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112
Q

What are misc anti-arrhythmic agents?

A

Digoxin
Adenosine

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113
Q

What is the MOA of Class IV anti-arrhythmic agents?

A

inhibit SA nidal firing and decrease AV conduction because Ca involved in depolarization of nodal cells

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114
Q

What medications are Class IV anti-arrhythmic agents?

A

Verapamil
Diltiazem

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115
Q

What is the MOA of Digoxin?

A

Inhibits the Na/K ATPase which in turn serves to increase the calcium concentration inside heart cells
Increases the force of contraction

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116
Q

If adenosine is given IV It causes __

A

transient heart block in the AV node

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117
Q

What is the MOA of adenosine?

A

Binds to A1 receptor in cardiac tissue
inhibits adenylate cyclase, decreased cAMP, increased outward K flux, hyperpolarization

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118
Q

What are the 3 main components of adenosine’s SAR?

A

N at 3 and 7 position required
Ribose required for agonist activity
Substitution at N6 increases affinity for A1

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119
Q

Cardiac glycosides inhibit the __

A

Na/K ATPase pump

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120
Q

Positive intropic agents are used for __

A

heart failure

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121
Q

Negative chronotropic agents are used for __

A

arrhythmia

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122
Q

Cardiac glycosides are found in __ and __

A

plants
poisonous frogs

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123
Q

Glycosides contain both a __ and a __

A

sugar part
non-sugar part

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124
Q

The R group on the steroid ring of the glycoside differs depending on __

A

the origin of the glycoside

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125
Q

Aglycone:
CIS or TRANS fused?
-A/B
-C/D
-B/C
Has a characteristic __ shape

A

-Cis
-Cis
-Trans
U shape

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126
Q

R group at C-17 in aglycone is an __

A

lactone ring

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127
Q

The sugar part of cardiac glycosides are mono or polysaccharides with __ linkages and can be __

A

beta-1,4-glycosidic
acetylated

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128
Q

Lipophilicity of cardiac glycosides depends on __ and __

A

the number of sugar molecules
the number of -OH groups on aglycone

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129
Q

C/D trans fusion leads to __ aglycone

A

inactive

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130
Q

A/B trans leads to __ aglycone

A

decreased activity

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131
Q

What is the sugar attachment point on the cardiac glycoside?

A

C3-OH

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132
Q

The __ is important for receptor binding and __ is very important. (Cardiac glycosides)

A

lactone ring
C=C

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133
Q

If __ or __ are OH the duration of action of the cardiac glycoside is effected.

A

C12
C16

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134
Q

Which drug has a longer half-life: Digoxin or Digitoxin?

A

Digitoxin

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135
Q

Calculate the cardiac output for a 46 year old male with a heart rate of 78 beats per minute and a stroke volume of 70 mL.
a. 5.5 L/min
b. 5,460 L/min
c. 1.1 L/min
d. 897 L/min

A

5.5 L/min

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136
Q

Activation of the sympathetic nervous system would cause:
a. Decrease in heart rate
b. Increase in heart rate
c. Decrease in norepinephrine
d. Increase in acetylcholine

A

Increase in heart rate

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137
Q

During atrial systole, what is occurring?
a. The atria are contracting and allowing blood movement into the lungs and systemic circulation
b. The atria are relaxing and allowing blood to fill within each atria
c. Blood is moving from the atria to the ventricles via the pulmonary and aortic valves
d. Blood is moving from the atria to the ventricles via the tricuspid and mitral valves

A

Blood is moving from the atria to the ventricles via the tricuspid and mitral valves

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138
Q

Which of the following accurately describes phase 0 of the action potential?
a. depolarization due to a rapid influx of Na
b. repolarization due to a rapid efflux of K
c. depolarization due to a rapid efflux of Na
d. repolarization due to a rapid influx of K

A

depolarization due to a rapid influx of Na

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139
Q

Which of the following anchors actin to myosin and allows for contraction of the myofibril?
a. Troponin T
b. Troponin I
c. Troponin A
d. Troponin C

A

Troponin I

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140
Q

Which valve allows blood to move from the left atrium to the left ventricle?
a. mitral valve
b. aortic valve
c. tricuspid valve
d. pulmonary valve

A

mitral valve

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141
Q

Which of the following would cause an increase in blood pressure?
a. decrease in heart rate
b. increase in LVEDV
c. decrease in stroke volume
d. increase in systemic vascular resistance

A

increase in systemic vascular resistance

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142
Q

What is occurring in the heart during S1?
a. Tricuspid and mitral valve closes, ventricular systole
b. Aortic and pulmonic valves open, ventricular diastole
c. Aortic and pulmonic valves close, ventricular systole
d. Tricuspid and mitral valves close, ventricular diastole

A

Tricuspid and mitral valve closes, ventricular systole

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143
Q

Cardiac index corrects the cardiac output based on:
a. heart rate
b. body surface area
c. weight
d. blood pressure

A

body surface area

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144
Q

What purpose does the pericardial fluid within the pericardium serve?
a. Speeds up the action potential to allow for increased conduction
b. The fluid does not have a specific purpose but increases the risk of pericardial effusion
c. Serves as a barrier to protect the heart from trauma
d. Acts as a lubricant to allow the heart to move freely during contraction and relaxation

A

Acts as a lubricant to allow the heart to move freely during contraction and relaxation

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145
Q

What three factors determine O2 delivery to tissues?
a. body surface area
b. ejection fraction
c. weight
d. oxygen saturation
e. hemoglobin
f. cardiac output

A

d. oxygen saturation
e. hemoglobin
f. cardiac output

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146
Q

Which of the following is a normal ejection fraction?
a. 20-25%
b. 90-95%
c. 60-65%
d. 40-45%

A

60-65%

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147
Q

The influx of which cation into the myocardium is most critical in inducing myocardial contraction?
a. Mg
b. K
c. Na
d. Ca

A

Ca

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148
Q

Which of the following is the primary neurotransmitter of the parasympathetic nervous system?
a. vasopressin
b. acetylcholine
c. epinephrine
d. norepinephrine

A

acetylcholine

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149
Q

What vessel supplies blood to the LAD and Circumflex?
a. Diagnol artery
b. Right coronary artery
c. Left main artery
d. Aorta

A

Left main artery

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150
Q

As an antiarrhythmic agent, procainamide has fewer CNS side effects than procaine because:
a. Procainamide has a greater ability to cross cell membranes compared to procaine
b. Procainamide is more susceptible to metabolic hydrolysis than procaine
c. Conversion of the ester to an amide makes the molecule less lipophilic
d. The metabolic hydrolysis of procainamide gives p-aminobenzoic acid

A

Conversion of the ester to an amide makes the molecule less lipophilic

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151
Q

The most basic nitrogen atom in the following molecule is:
a. 3
b. 4
c. 2
d. 1

A

4

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152
Q

Which two of the following statements best describe why Mexiletine can be taken orally whereas Lidocaine is administered IV?
a. Mexiletine has a chiral center but not lidocaine
b. Conversion of the amide function of lidocaine to an ether function in mexiletine makes it metabolically more stable
c. Being more lipophilic mexiletine is almost completely absorbed with a bioavailability of 80-90%
d. Mexiletine is a primary amine whereas lidocaine is a tertiary amine

A

b. Conversion of the amide function of lidocaine to an ether function in mexiletine makes it metabolically more stable
c. Being more lipophilic mexiletine is almost completely absorbed with a bioavailability of 80-90%

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153
Q

The absence of the two iodine atoms and the introduction of a methane sulfonamide group in dronedarone compared to amiodarone result in:
Select ALL that apply.
a. An increase in the ability to cross cell membranes
b. Reduction in the ability to form salts with acids
c. A decrease in the lipophilicity of the molecule
d. A decrease in neurotoxicity

A

c. A decrease in the lipophilicity of the molecule
d. A decrease in neurotoxicity

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154
Q

Which of the following molecules is likely to be the most selective b1 antagonist with shortest duration of action?
a. A
b. B
c. C
d. D
e. E

A

D

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155
Q

What happens in phase 4?

A

resting membran potential

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156
Q

What happens in phase 0?

A

opening of fast Na channels
rapid influx of Na

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157
Q

What happens in phase 1?

A

Opening of transient K channels
K efflux

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158
Q

What happens in phase 2?

A

Plateau is a phase of maintained depolarization
Ca enters the cell by opening L-type Ca channels
K leaves cell by opening transient K channels

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159
Q

What happens in phase 3?

A

opening of K channels
K efflux

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160
Q

Antiarrhythmic drugs suppress arrhythmias by blocking flow through __ or by __

A

specific ion channels
altering autonomic function

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161
Q

Antiarrhythmic drugs can cause __

A

arrhythmias

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162
Q

What medications are Class 1A anti arrhythmic drugs?

A

Disopyramide
Procainamide
Quinidine

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163
Q

What medications are Class 1B anti arrhythmic drugs?

A

Lidocaine
Mexiletine
Phenytoin

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164
Q

What medications are Class 1C anti arrhythmic drugs?

A

Flecainide
Propafenone

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165
Q

Class 1 anti- arrhythmic drugs have no effect in __ cells

A

pacemaker

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166
Q

What is the mechanism of action of class 1 anti arrhythmic agents?

A

Blockage of fast sodium channels
Decrease phase 4 diastolic Na currents
Increase threshold

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167
Q

For blockers, most useful drugs bind readily to RESTING/ACTIVE/INACTIVE channels

A

active or inactive

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168
Q

Dissociation occurs during the RESTING/ACTIVE/INACTIVE stage.

A

resting

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169
Q

Recovery time from Na block is expressed as __

A

Recovery Time Constant (Trec)

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170
Q

If there is a rapid binding/dissociation Trec is SMALL/LARGE

A

small

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171
Q

If there is a slow binding/dissociation Trec is SMALL/LARGE

A

large

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172
Q

Drugs with a SLOW/FAST recovery rate have a greater effect

A

slow

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173
Q

Class 1A anti arrhythmic drugs have a greater affinity for the OPEN/INACTIVE state and have a SLOW/INTERMEDIATE/FAST recovery

A

open
intermediate

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174
Q

Class 1B anti arrhythmic drugs have a greater affinity for the OPEN/INACTIVE state and have a SLOW/INTERMEDIATE/FAST recovery

A

inactive
fast

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175
Q

Class 1C anti arrhythmic drugs have a greater affinity for the OPEN/INACTIVE state and have a SLOW/INTERMEDIATE/FAST recovery

A

open
slow

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176
Q

There are fast and slow acetylators of __

A

prcainamide

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177
Q

What are adverse effects of Disopiramide?

A

Anticholinergic activity
(dry mouth, constipation, urinary retention)

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178
Q

Lidocaine is not effective for __ arrhythmias

A

atrial

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179
Q

Which class 1 subclass is associated with Torsades de pointes?

A

Class 1A

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180
Q

What are some common ADRs for Procainamide?

A

GI problems
hypotension
fatal bone marrow aplasia
lupus syndrome
risk of Torsades

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181
Q

What are some common ADRs for Quinidine?

A

GI irritating
Cinchonism
Thrombocytopenia
Risk of Torsades

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182
Q

What are some common ADRs for Lidocaine?

A

CNS effects
Convulsions
Nystagmus

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183
Q

What are some common ADRs for Mexiletine?

A

Very GI irritating
CNS effects

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184
Q

What are some common ADRs for Flecainide?

A

GI problems
Blurred vision

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185
Q

What drugs elevate concentrations of Procainamide?

A

Amiodarone
Cimetidine

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186
Q

Quinidine elevates concentrations of what drugs?

A

Digoxin
Warfarin

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187
Q

Quinidine decreases metabolism of __ into __

A

codeine into morphine

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188
Q

What drug elevates concentrations of quinidine?

A

amiodarone

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189
Q

What drugs decrease lidocaine metabolism?

A

beta blockers
cimetidine

190
Q

Melixetine reduce clearance of what medication?

A

theophylline

191
Q

What increases concentrations of Flecainide?

A

amiodarone

192
Q

Class 1A anti arrhythmic are indicated for __

A

atrial and ventricular arrhythmias

193
Q

Class 1B anti arrhythmic are indicated for __

A

local anesthesia
ventricular arrhythmias

194
Q

Class 1C anti arrhythmic are indicated for __

A

atrial and ventricular arrhythmias

195
Q

Class 1C anti arrhythmic drugs have a high risk of __ in patients with CHF and CAD

A

proarrhythmias

196
Q

What drug specifically inhibits slow Na channels in pacemaker cells?

A

Ivabradine (Corlanor)

197
Q

Ivabradine is FDA approved for and used off label for __ and __

A

CHF (increased ejection fraction)
angina
tachycardia

198
Q

What are adverse effects caused by ivabradine?

A

Bradycardia
risk of increased QT
AV block
vision changes

199
Q

Beta blockers are used to treat __

A

hypertension
ischemic heart disease
heart failure
arrhythmias cause by increased sympathetic tone

200
Q

Which beta blockers are nonselective?

A

nanodol
propranolol
timolol
sotalol

201
Q

Which beta blockers are selective?

A

acebutolol
atenolol
esmolol
metoprolol
pindolol
penbutolol

202
Q

Which beta blockers have vasodilation effects?

A

carvedilol
betaxolol

203
Q

What is the primary effect of beta blockers?

A

in the pacemaker cells:
decreases automaticity in SA node
decrease slope of phase 4
Decrease heart rate
Decrease Na and Ca currents

204
Q

What is a secondary effect of beta blockers?

A

in Cardiomyocytes:
Decrease heart rate
decrease force of contraction
decrease activity of Ca channels

205
Q

What are therapeutic uses for beta blockers?

A

SA node increase automaticity
Supraventricular tachycardia
DADs and EADs
To terminate AV and AV nodal reentry or to prevent such arrhythmias
Controlling ventricular response in AF or Aflutter
Physical or emotional stress induced-arryhtmias
Prophylaxis for post MI arrhythmias
Cocaine induced arrhythmias
Angina, HF, HTN

206
Q

What are non-cardiovascular uses for beta blockers?

A

thyrotoxicosis
anxiety
essential tremors

207
Q

What are common adverse effects of beta blockers?

A

hypotension
bradycardia
dizziness
fatigue
lethargy

208
Q

What are severe ADRs of beta blockers?

A

heart block
Aggravation of heart failure in susceptible individuals
Bronchosonstriction (nonselective)
Can induce DAD and EAD mediated arrhythmias

209
Q

What are drugs that enhance AV nodal inhibition of beta blockers?

A

amidoarone
clonidine
digoxin
diltiazem
dronedarone
verapamil

210
Q

Beta blockers may mask the symptoms of __

A

hypoglycemia

211
Q

What are contraindications for beta blockers?

A

sinus bradycardia
cariogenic shock
second or third degree heart block

212
Q

What are typical class III anti arrhythmic drugs?

A

Dofetilide (Tikosyn)
Ibuteilide (Corvert) (IV)

213
Q

What are drugs that are mainly class II anti arrhythmic but also part of other classes?

A

Amiodarone (Cordarone, Pacerone)
Dronedarone (Multaq)
Sotalol (Betapace)

214
Q

What are common uses of K channel blockers?

A

Atrial fibrillation/flutter
Anatomic reentry
DAD-mediated VT

215
Q

Class II anti arryhtmics delay rectifier ___ in phase __ in __

A

K channels
phase 3
cardiomyocytes

216
Q

K channel blocker have no effect on K channels in phase __ or __ transient K channels

A

phase 4
T1

217
Q

What are effects of K channel blockers?

A

prolonged or increased action potential duration (Increased QT)
Increased refractory period

218
Q

What are adverse effects of K channel blockers?

A

Increased risk of EAD
Increased risk of Tornadoes de pointes

219
Q

What is an oral class III anti arrhythmic?

A

dofetilide

220
Q

What is an IV class III anti arrhythmic?

A

Ibutilide

221
Q

What are common adverse effects of dofetilide?

A

CNS
GI problems
Bradycardia
Torsades

222
Q

What are rare adverse effects of dofetilide?

A

hepatotoxicity
angioedema
AV block

223
Q

What are rare adverse effects of Dofetilide?

A

hepatotoxicity
angioedema
AV block

224
Q

What are common adverse effects of ibutilide?

A

Headache
Nausea
Bradycardia
Torsades

225
Q

What are contraindications of dofetilide?

A

Increased baseline QT
hypersensitivity
Hepatic or renal impairment
Hypokalemia

226
Q

What are contraindications of ibutilide?

A

Increased baseline QT
Hypersensitivity

227
Q

What medications increase Dofetilide effects?

A

loop and thiazide diuretics

228
Q

What medications increase Dofetilide concentrations?

A

Cimetidine
Verapamil
Antifungals

229
Q

Ibutilide may increase concentrations of __

A

lidocaine

230
Q

__ may increase the arrhythmogenic effect of ibutilide

A

propafenone

231
Q

Amiodarone has a SHORT/LONG half-life

A

long
35-110 days

232
Q

What is the mechanism of action of amiodarone?

A

Blocks inactivated Na channels
Blocks K channels
Blocks Ca channels
Blocks beta receptors
Blockas alpha1 receptors

233
Q

What are the effects of amiodarone?

A

Impairs SA nodal function
Modifies automaticity
Decrease AV conduction
Increase refractoriness
Increase APD

234
Q

What is the mechanism of action of sotalol?

A

Blockes adrenergic receptor
Blocks K channels

235
Q

What are the effects of sotalol?

A

Effects of beta blockers
Effects of K channel blockers
Increase action potential duration
Increase refractory period
Decrease adrenergic response
Decrease SA pacemaker rate
Decrease AV conduction rate

236
Q

What are common adverse effects of amiodarone?

A

hypothyroidism
hyperthyroidism
hypotension
CNS
GI disturbances
Eye problems
Blue-gray pigmentation
Bradycardia
Torsades

237
Q

What are effects that happen at toxic rates of amiodarone?

A

pulmonary toxicity
hepatotoxicity

238
Q

What are adverse effects of dronedarone?

A

GI distubrances
Skin rash
Muscle weakness
Torsades
Hepatotoxicity
Renal and lung toxicity

239
Q

What are contraindications of amiodarone?

A

Increased QT interval
iodine hypersensitivity
AV block
Thyroid disease

240
Q

What are contraindications of dronederone?

A

Increased baseline QT
Heart failure

241
Q

What are common adverse effects of sotalol?

A

CNS
bradycardia
dyspnea

242
Q

What are less common adverse effects of sotalol?

A

bronchospasm
hypotension
Torsades

243
Q

What are contraindications of sotalol?

A

Increased baseline QT
heart block
heart failure
bronchial asthma

244
Q

Amiodarone increases the level of which drugs?

A

statins
warfarin
digoxin
quinidine
procainamide
phenytoin
flecainide
cyclosporine

245
Q

What drug decreases amiodarone metabolism?

A

cimetidine

246
Q

What medication decreases amiodarone concentration?

A

rifampicin

247
Q

What medications reduce absorption of sotalol?

A

antacids

248
Q

What medications increase bradycardia effect of sotalol?

A

Ca channel blockers

249
Q

Sotalol in combination with __ increase risk of heart block

A

digoxin

250
Q

What are effects of calcium channel blockers on the heart?

A

Increase vasodilation
decrease contractility
Decrease heart rate
decrease SA conduction
decrease AV conduction

251
Q

What are the major effects on pacemaker cells that calcium channel blockers do?

A

Increase the threshold and slow depolarization
Block Ca channels in later phase 4 and in phase 0 - decrease heart rate
Decrease SA rate
Decrease AV conduction - increase refractory period
Decrease reentrant arrhythmias involving AV node

252
Q

What are common adverse effects of calcium channel blockers?

A

bradycardia
GI irritating
Constipation
Dizziness/lightheadedness
Headache
Hypotension
Peripheral edema

253
Q

What are rare/severe adverse effects of calcium channels blockers?

A

Worsening of heart failure
AV block
Increase hepatic enzymes

254
Q

What are contraindications of calcium channel blockers?

A

Heart failure
Cardiogenic shocl
Second or third degree AV block

255
Q

What are calcium channel blockers used for?

A

reentrant arrhythmias involving AV node
PSVT, Afib, Aflutter
Ventricular rate control

256
Q

What drugs increase the risk of bradycardia if taken with verapamil?

A

amiodarone
beta blcokers

257
Q

What drug increases the effects of verapamil?

A

fluconazole

258
Q

Verapamil increase concentrations of what drugs?

A

statins
digoxin
dofetilide
theophilline
cyclosporine

259
Q

What drugs increase effects of diltiazem?

A

CYP3A4 inhibitors

260
Q

What drugs increase hypotensive effects of diltiazem?

A

sildenafil
azole antifungals
antihypertensive drugs

261
Q

What drugs decrease hypotensive effects of diltiazem?

A

Rifampin
erythromycin

262
Q

If diltiazem is taken with which drugs it can increase risk of bradycardia?

A

amiodarone
beta blockers

263
Q

What is the mechanism of action of adenosine?

A

G protein-coupled adenosine receptors
Activates ACh-sensitive K channels-hyperpolarization
Decrease Ca current

264
Q

What is adensoine used for?

A

PSVT
Inhibition of DADs elicited by sympathetic stimualtion

265
Q

What are adverse effects of adenosine?

A

short lived
flushing
chest tightness
dizziness
syncope
transient SA/AV block
transient asystole

266
Q

What drugs potentiate the effects of adenosine?

A

carbamazepine
dipyridamole

267
Q

What medication diminishes the effects of adenosine?

A

theophylline

268
Q

Digoxin has a LOW/HIGH therapeutic index

A

low

269
Q

Andmistration of __ increases risk of toxicity of dogoxin

A

antibiotics that destroy intestinal microflora

270
Q

What is the site of action for digoxin?

A

Atrium SA and AV nodes for arrhythmias

271
Q

What is the mechanism of action for arrhythmias of digoxin?

A

Increases vagal tone - activation of ACh sensitive K channels in atrium - shortening APD
Decrease Ca currents in AV node - suppresses the AV node

272
Q

What is digoxin used for?

A

terminating re-entrant arrhythmias involving atrium and AV node
Controlling ventricular rate response in afib

273
Q

What are common ADRs of digoxin?

A

GI
Dizziness
headache
blurred or yellow vision

274
Q

What are less common ADRs of digoxin?

A

atrial tachycardia
AV block
ventricular arryhtmias
hyperkalemia

275
Q

What is an antidote for Digoxin toxicity?

A

Digibind

276
Q

What disease states can enhance digoxin toxicity?

A

hypothyroidism
hypokalemia
hypomagnesemia
hypercalcemia

277
Q

What is the potential mechanism of action of magnesium sulfate for arryhtmias?

A

Competes with Ca at ion channel transport site

278
Q

What is Magnesium Sulfate used for?

A

Prevention/treatment of Torsades
Arryhtmias due to digoxin/digitalis toxicity

279
Q

What are adverse effects of magnesium sulfate?

A

hypotension
breathing difficulties

280
Q

You are developing a drug that will affect phase 4 in SA node cells. Which main characteristic should the drug have to produce a specific effect only in these cells?
a. It should inhibit rectifier potassium channels
b. It should inhibit L-type calcium channels
c. It should inhibit T-type potassium channels
d. It should inhibit slow sodium channels

A

It should inhibit slow sodium channels

281
Q

Which drug can cause arrhythmias by affecting K+ channels?
a. Dofetilide
b. Atenolol
c. Flecainide
d. Lidocaine

A

Dofetilide

282
Q

Beta blockers are used to treat arrhythmias because________.
a. They decrease the AV refractory period
b. They increase automaticity
c. They increase AV conduction time
d. They increase phase 4

A

They increase AV conduction time

283
Q

In a patient diagnosed with arrhythmia caused by an AV reentry mechanism, you most likely use ________because it________?
a. Flecainade; blocks sodium channels
b. Verapamil; blocks calcium channels
c. Quinidine; blocks potassium channels
d. Lidocaine; blocks sodium channels

A

Verapamil; blocks calcium channels

284
Q

__________ is used in a patient with a ventricular tachycardia produced by an ectopic focus because it inhibits________ and __________.
a. Procanamide; fast sodium channels; reduces phase 4
b. Adenosine; ACh-sensitive K+ channels; hyperpolarizes cardiomyocytes
c. Propanolol; beta receptors; increases calcium current
d. Phenytoin; slow sodium channels; increases APD

A

Procanamide; fast sodium channels; reduces phase 4

285
Q

Which class I drug has significant cholinergic adverse effects producing dry mouth and constipation?
a. Disopyramide (norpace)
b. Lidocaine (xylocaine)
c. Flecainide (tambocor)
d. Procainamide (procan SR)

A

Disopyramide (norpace)

286
Q

Which drug classes cause both effects: a reduction in the heart contraction force, and a slowing of the AV node conduction?
a. Class I and Class II
b. Class I and Class III
c. Class II and Class III
d. Class II and Class IV
e. Class III and Class IV

A

Class II and Class IV

287
Q

Which of the following electrolyte abnormalities is assocaited with Tosades de Pointes?
Hyperkalemia
Hyponatremia
Hypercalcemia
Hypermagnesemia

A

Hyperkalemia

288
Q

RJ’s rhythm strip shows 5 large boxes between the top of his QRS complexes. What is RJ’s heart rate?
60 beats/min
75 beats/min
90 beats/min
80 beats/min

A

60 beats/min

289
Q

Identify the abnormal aspect of this EKG:
a. Wide QRS complex
b. Prolonged PR interval
c. Delta wave
d. ST segment depression

A

Prolonged PR interval

290
Q

Identify the dysrhythmia that is occuring in this EKG:
a. Atrial fibrillation
b. Ventricular tachycardia
c. Atrial flutter
d. Ventricular fibrillation

A

Atrial fibrillation

291
Q

The rapid influx of sodium in Phase 0 of the action potential correlates to which section of the rhythm strip?
P
S
T
Q

A

Q

292
Q

Which of the following best describes the path of electricity within the heart?
SA node, AV node, Bundle of His, Purkinje fibers
Purkinje fibers, Bundle of His, AV node, SA node
Bundle of His, SA node, Purkinje fibers, AV node
AV node, Purkinje Fibers, SA node, Bundle of His

A

SA node, AV node, Bundle of His, Purkinje fibers

293
Q

The characteristic of an EKG that can lead to torsades de pointe is:
a. Widened QRS complex
b. Prolonged QT interval
c. ST segment elevation
d. Prolonged PR interval

A

Prolonged QT interval

294
Q

Calculate the heart rate of this rhythm on the EKG strip.
a. Less than 60 BPM
b. Within 60-80 BPM
c. Within 80-100 BPM
d. Over 100 BPM

A

Within 60-80 BPM

295
Q

Which of the following electrolytes is not directly involved with action potential electrophysiology?
Sodium
Potassium
Calcium
Bicarbonate

A

Bicarbonate

296
Q

Which of the following leads are formed by voltage triangles, otherwise known as Einthoven’s triange?
Leads I, II, III
Leads V1, V2, V3
Leads aVR, aVL, aFV
Leads V1, aVR, V3

A

Leads I, II, III

297
Q

Atrium action potential has a more narrow phase __ and more gradual phase __

A

phase 2
phase 3

298
Q

What happens during the p wave?

A

atria contraction

299
Q

What happens during the QRS complex?

A

ventricle contraction

300
Q

What happens during the t wave?

A

ventricular repolarization

301
Q

Absolute refractory period is when there is __ to any stimulus, and is in phase(s) __

A

no reaction from cells
phases 1 and 2

302
Q

Effect refractory period is when there is __ to any stimulus and is in phase(s) __

A

a lock, weak response
phase 3

303
Q

Relative refractory period is when __ and happens in phase(s) __

A

large stimulus may propogate a response, but slower than normal
phase 4

304
Q

How many positive electrodes are used for an EKG?

A

one

305
Q

The EKG tracing is based on the sensing of the __

A

positive electrode

306
Q

An electrical wavefront approaching a positive electrode causes a __

A

positive deflection

307
Q

An electrical wavefront moving away from a positive electrode creates a __

A

negative deflection

308
Q

An electrical wavefront moving perpendicular to a positive electrode causes an __

A

isoelectric deflection

309
Q

A 12 lead EKG includes:

A

I, II, III, aVF, aVL, and aVR

310
Q

An average PR interval is __ or __ small squares

A

0.12-0.2 seconds
<5

311
Q

An average QRS interval is __ or __ small squares

A

0.008-0.1 seconds
<2.5

312
Q

An average QTc interval is __ for males or __ for females

A

<0.46 seconds
<0.47 seconds

313
Q

An average ST interval is __ or __ small squares

A

0.08-0.12 seconds
<3

314
Q

If Q wave is >1 small box or amplitude is 1/3 of the QRS indication of __

A

past MI

315
Q

Increased PR interval may indicate __

A

1st degree AV block

316
Q

Prolonged QTc (>0.48s) puts patients at risk of __

A

Torsades

317
Q

Elevation or depression of ST segment may indicate __

A

an acute MI

318
Q

QT has to be corrected for heart rate using __

A

Bazett’s formula

319
Q

What information can be obtained from the EKG?

A

rate
rhythm
axis
hypertrophy
infarction

320
Q

What structure normally starts electric conduction in the heart?

A

SA node

321
Q

What is the most accurate way to determine rate on an EKG?

A

60/(# of small boxes x 0.04)

322
Q

What are the steps to determining rhythm on an EKG?

A

Is there a p wave in front of every QRS complex?
Is there a QRS complex after each p wave?
Is the rhythm regular?
Is the heart rate 60-100bpm?
Is the PR interval prolonged or QRS complex wide?
Is there a delta wave?

323
Q

What is enhanced automaticity?

A

non-pacemaker myocardial tissue fires on its own instead of waiting to be stimulated by a neighboring cell

324
Q

What are causes of enhanced automaticity?

A

Ischemia
Electrolyte imbalances
Acidemia
Medications

325
Q

What is the proposed underlying mechanism of triggered activity causing dysrhythmias?

A

spontaneous depolarization during phases 2-4 of the action potential
leads to sustained triggering of action potentials

326
Q

What is EAD?

A

early afterdepolarization
during phase 2/3
factors that prolong the QTc or increase intracellular Na

327
Q

What is DAD?

A

delayed afterdepolarization
during phase 3/4
factors that increase intracellular Ca

328
Q

What are the 3 conduction requirements for re-entry to occur?

A

At least two pathways for impulse conduction
One area with unidirectional block in one pathway
Slowed conduction in the other pathway

329
Q

Accessory pathways are __ dependent

A

NA

330
Q

What is a conduction block?

A

occurs when conduction tissue is unexcitable
Cannot communicate the impulse to the next area
can be permanent or transient?

331
Q

What are causes of conduction block?

A

ischemia
trauma
scarring
fibrosis
medications

332
Q

Describe Sinus tachycardia

A

regular rhythm
rate >100 bpm
always has an underlying cause
Most common: overactivation of SNS
Infection/fever, exercise, pain, stress

333
Q

Describe Sinus Bradycardia

A

regular rhythm
rate <60 bpm
Due to decreased SNS or increased PNS activity
Common causes: hypothyroidism, hypertension, medications, vagal nerve stimulation

334
Q

Describe Premature Ventricular Contractions

A

Single abnormal beat earlier than expected
originates in the ventricle
QRS is wider, taller, and early
Cause: electrolyte abnormalities, exercise, ischemia, heart failure

335
Q

Describe Ventricular Tachycardia

A

originates in the ventricles, wide complex
Don’t see p wave
>140-260 bpm
Requires at least 3 beats Sustained >30s or requires intervention, Nonsustained <30 seconds
Monomorphic or polymorphic
Common causes are CAD and heart fialure

336
Q

Describe Torsades de Pointes

A

type of polymorphic VT, but with changes in direction of the complex
If not treated, can lead to vfib quickly
Cause: prolonged QTc, drugs, hypokalemia

337
Q

Describe Ventricular Fibrillation

A

chaotic electrical discharge that does not effectively depolarize ventricles
Wide QRS complex, usually >300 bpm
Fatal if not rapidly terminated
Causes: AMI, HF, hypokalemia

338
Q

Describe Asystole

A

total absence of electrical activity
heart is unable to generate a single QRS complex
Myocardium is functionally dead

339
Q

Describe PEA

A

no pulse, but some electrical activity
heart is unable to generate a single QRS complex
Myocardium is functionally dead

340
Q

Describe Premature Atrial Contractions

A

premature ectopic beat
still a visible P wave before the PAC
Causes: increased SNS, decreased PNS, stimulants, alcohol

341
Q

Describe Atrial Fibrillation

A

no organized atrial contraction or normal P waves
Atria beating at 400-600 bpm
Normal contracting ventricles but beating fast >100-200 bpm
Causes: advanced age, valvular heart disease, HF, COPD

342
Q

Describe Atrial Flutter

A

presence of flutter waves with atrial rate of 200-300 bpm
rhythm is regular
sawtooth appearance
Cause: HF, valvular heart disease, COPD

343
Q

Describe Supraventricular Tachycardia

A

regular rhythm
rate 160-260 bom
P wave looks different than normal
Cause: increased SNS activation

344
Q

Describe Wolff Parkinson White Syndrome

A

type of SVT
preexcitation syndrome
accessary pathway leading to tachyarrhythmia
congenital heart defect
delta wave

345
Q

Describe 1st degree AV block

A

abnormally long delay in transmission of the atrial impulse through the AV node
prolonged PR interval
Causes: medications, sick sinus syndrome

346
Q

Describe 2nd degree AV block Mobitz Type I

A

Wenckebach
progressive prolonging of PR interval
Suddent QRS drop
Cause: disease of AV node (medications, inferior MI)

347
Q

Describe 2nd degree AV block Mobitz Type II

A

PR intervals are consistent, sudden drop of QRS complex
Due to disease of the His bundle or Purkinje fibers
Cause: anteroseptal MI, HF, sarcoidosis

348
Q

Describe 3rd degree AV block

A

No association between P wave and QRS complex due to AV dissociation
Two pacemakers, one in atria and one In ventricles
Length of PR intervals may vary, no pattern
Cause: advanced age, infarction, medications

349
Q

Which of the following cannot be detected from the ECG?
a. heart rate
b. an abnormal heart rhythm
c. prior MI
d. ejection fraction

A

ejection fraction

350
Q

A patient presents to ED with a pulse of 30 bpm. You overhear the ED physician reading the ECG and they state there is no association between the P wave and the QRS complex. What kind of arrhythmia is this?

A

complete heart block

351
Q

What arrhythmia is fatal if not treated immediately?

A

ventricular fibrillation

352
Q

Name the arrhythmia.

A

Sinus tachycarida

353
Q

Name the arrhythmia.

A

Sinus bradycardia

354
Q

Name the arrhythmia.

A

Premature Ventricular Contractions

355
Q

Name the arrhythmia.

A

Ventricular tachycardia

356
Q

Name the arrhythmia.

A

Torsades de Pointes

357
Q

Name the arrhythmia.

A

Ventricular Fibrillation

358
Q

Name the arrhythmia.

A

Top Asystole
Bottom PEA

359
Q

Name the arrhythmia.

A

Premature Atrial COntractions

360
Q

Name the arrhythmia.

A

Atrial Fibrillation

361
Q

Name the arrhythmia.

A

Atrial Flutter

362
Q

Name the arrhythmia.

A

Supraventricular Tachycardias

363
Q

Name the arrhythmia.

A

Wolff Parkinson White Syndrome

364
Q

Name the arrhythmia.

A

1st degree AV block

365
Q

Name the arrhythmia.

A

2nd degree AV block Mobitz Type I
Wenckebach

366
Q

Name the arrhythmia.

A

2nd degree AV block Mobitz Type II

367
Q

Name the arrhythmia.

A

3rd degree AV block

368
Q

What is the acronym for antiarrhythmic drugs?

A

South - Class 1 Na Channel Blockers
Beach - Class 2 Beta Blockers
Pol - Class 3 Potassium blockers
ka - Class 4 calcium channel blockers

369
Q

What is the mechanism of each class of antiarrhythmic drugs?

A

Class 1: phase 0 (odd)
Class 2: phase 4 (opposite)
Class 3: phase 3 (=)
Class 4: phase 2 (opposite)

370
Q

What is the acronym for class I AADs?

A

Double Quarter Pounder
(1A: Disopyramide, Quinidine, Procainamide)
Lettuce Mayo
(1B: Lidocaine, Mexiletine)
Fries Please
(1C: Flecainide, Propafenone)

371
Q

Which class 1 subtype has the strongest Na blockade?

A

Class 1c

372
Q

Which class 1 subtype has the weakest Na blockade?

A

Class 1b

373
Q

Which class 1 subtype has moderate Na blockade ability?

A

Class 1a

374
Q

What is the acronym for class 3 AADs?

A

DAD IS
(Dronedarone, Amiodarone, Dofetilide, Ibutilide, Sotalol))

375
Q

Which of the following best describes the primary ion channel inhibited by sotalol, the corresponding action potential phase affected, and its effects on the ECG?
a. Na, phase 4 causing prolongation of QTc
b. Na, phase 1 causing widening of the QRS
c. K, phase 2 causing a widening of the QRS
d. K, phase 3 causing a prolongation of the QTc

A

d. K, phase 3 causing a prolongation of the QTc

376
Q

What are examples of atrial arrhythmias?

A

PACs
SVT
WPWS
Afib
Aflutter

377
Q

What is pharmacological therapy for PAC?

A

typically do not require medication
if symptomatic or clinically indicated can do low dose metoprolol

378
Q

What is nonpharm treatment for atrial arrhythmias?

A

minimize alcohol intake
avoid smoking
minimize caffeine intake
stress

379
Q

What are symptoms of SVT?

A

palpatations
dizziness
syncope
weakness
polyuria

380
Q

Chronic oral anticoagulation IS/IS NOT recommended for SVT

A

IS NOT

381
Q

If patients present acutely with symptoms or rapid ventricular rate with SVT can medicate with __

A

Vagal maneuvers
IV adenosine
IV beta blocker
IV non-DHP CCB
IV amiodarone

382
Q

If recurrent/refractory symptoms of SVT can do oral maintenance therapy with __

A

beta blockers
non-DHP CCB
catheter ablation

383
Q

What is the Valsalva maneuver?

A

lay patient supine
blow through syringe or obstructed straw for 10-15 seconds

384
Q

What is the diving reflex?

A

Take multiple deep breaths
hold breath
then immersing face in a basin of water

385
Q

What is bearing down?

A

bearing down as if making a bowel movement

386
Q

What is a carotid sinus massage?

A

should be done by a provider
applying pressure with fingertips to carotid sinus areas on face

387
Q

Adenosine administration is useful if patients do not respond to __

A

vagal maneuvers

388
Q

Can adenosine be repeated?

A

yes

389
Q

What is the half-life of adenosine?

A

10 seconds

390
Q

What are contraindications of adenosine therapy?

A

heart transplant
SVT with an accessory pathway

391
Q

What are types of catheter ablations?

A

radiofrequency ablations
cryofrequency ablations
AV node ablation
epicardial ablation
maze ablation

392
Q

What are the treatment options for WPWS?

A

IV procainamide
IV ibutilide
Direct current cardioversion
Catheter ablation preferred if patients are symptomatic and known accessory pathway

393
Q

What medications are contraindicated in WPWS?

A

IV amiodarone
adenosine
digoxin
non-DHP CCBs
lidocaine
use caution with beta blockers

394
Q

Once WPWS accessory pathway has been eliminated do the CI agents still need to be avoided?

A

no

395
Q

Stop bolus IV Procainamide if __

A

QRS widens >50% original width
hypotension occurs
or max was given

396
Q

IV procainamide should be reduced by __ in renal/hepatic impairments

A

50%

397
Q

IV procainamide is contraindicated in patients with __

A

recent MI (6 days - 2 years)

398
Q

Discontinue IV ibutilide as soon as __

A

arrhytmia terminates
VT occurs
prolongation of QTc

399
Q

Can IV ibutilide be repeated?

A

yes

400
Q

When is IV ibutilide contrainidicated?

A

chronic AF
electrolyte imbalance
requires continuous ECG monitoring
ejection fraction <40% (HF)

401
Q

What are risk factors for AFib?

A

CAD
heart failure
older age
diabetes mellitus
obesity
obstructive sleep apnea
cardiothoracic surgery
hyperthyroidism
alcohol use

402
Q

What is the most common arrhythmia in clinical practice?

A

atrial fibrillation

403
Q

What are signs/symptoms of AFib?

A

fatigue
palpitations
shortness of breath
syncope
angina

404
Q

Afib poses an increased risk of __

A

SSE
heart failure
dementia
hospitalization
mortality

405
Q

In a patient with Afib and LV dysfunction or HFrEF with medications should be used for rate control?

A

Beta blockers +/- digoxin
amiodarone

406
Q

In a patient with afib without LV dysfunction or HFrEF which medications should be used for rate control?

A

beta blockers or non-dhp CCB
amiodarone

407
Q

Which beta blocker are given IV push?

A

Metoprolol
propranolol

408
Q

Which beta blockers are given by infusion?

A

esmolol

409
Q

Non-DHP CCBs are given by IV PUSH/INFUSION

A

push

410
Q

Which non-dhp CCB is preferred in patients with labile/low BP?

A

diltiazem

411
Q

Dosing of Digoxin varies based on patient’s

A

weight
renal function
age
medications
heart failure diagnosis

412
Q

Reduce loading dose of digoxin by 50% if __

A

renal dysfunction
elderly
drug interactions (amidoarone, dronedarone, verapamil)

413
Q

What are signs of toxicity of digoxin?

A

bidirectional VT
blurred vision
heart block

414
Q

Digoxin is a good option for a patient with afib and __

A

acute decompensated HF

415
Q

What steady state should be chosen for digoxin dose calculation?

A

1

416
Q

What CL NR should be used for non-heart failure or for only mild symptoms in digoxin calculations?

A

40 mL/min

417
Q

What Cl NR should be used for severe heart failure in digoxin calculations?

A

20 mL/min

418
Q

What is the Afib trough goal for digoxin?

A

0.8-2 ng/mL

419
Q

What is the heart failure trough goal for digoxin?

A

0.5-0.9 ng/mL

420
Q

Higher risk of death in trough levels of >__ of digoxin

A

1.2 ng/mL

421
Q

If loading dose of digoxin is given, check level ___ after loading dose

A

12-24 hours

422
Q

If no loading dose of digoxin is given, obtain trough __ after therapy

A

3-5 days

423
Q

If changing maintenance dose of digoxin check trough in __

A

5-7 days

424
Q

If renal function, check digoxin trough in __

A

15-20 days

425
Q

1 vial of digoxin immune fab (Digifab) will bind __ digoxin

A

500mcg

426
Q

In acute digoxin overdose, if dose is unknown, give __

A

10 vials
may repeat with another 10 vials

427
Q

In acute digoxin overdose, if vial is known give __

A

number of vials = total body load (0.8*mg digoxin ingested) x2

428
Q

In chronic digoxin toxicity, and serum concentration is unknown give __

A

6 vials

429
Q

In chronic digoxin toxicity, and serum concentration is known, give __

A

number of vials = (serum conc (ng/mL) x body weight (kg) / 100

430
Q

After giving Digifab, monitor __ hourly for 4-6 hours and then daily

A

potassium

431
Q

Should you check digoxin level after giving digifab? why or why not?

A

no
bound in the blood, will be falsely high

432
Q

Can amiodarone be used in heart failure?

A

yes

433
Q

For rhythm control of afib first line therapy is __

A

cardio version

434
Q

For afib rhythm control no HFrEF which medications can be used?

A

amiodarone
dofetilide
flecainide
ibutilide
propfenone
procainamide

435
Q

For afib rhythm control with HFrEF with medications can be used?

A

amiodarone
dofetilide

436
Q

What should be done before doing cardioversion?

A

anticoagulation
ensure no clot

437
Q

Amiodarone has a higher dose for afib for RATE/RHYTHM control

A

rate

438
Q

What FDA requirements are there for dofetilide?

A

hospitalization for first 3 days (5 doses)
baseline QTc and 2-3 hours after every dose
If >500 Etc discontinue

439
Q

Monitor __ every 3 months on dofetilide

A

SCr
K
Mg
QTc

440
Q

What medications CANNOT be taken with dofetilide?

A

hydrochlorothiazide
prochlorperazine
trimethoprim
verapamil

441
Q

What medications can be taken as needed for afib?

A

flecainide
propafenone

442
Q

Risk of __ with class 1C antiarrhythmics

A

1:1 AV node conduction

443
Q

What medicatoin should be given with flecainide or propafenone bc of 1:1 AV node conduction?

A

beta blocker or non-dhp CCB

444
Q

For afib maintenance therapy with CAD which medications can be used?

A

dofetilide
dronedarone
sotalol
amiodarone

445
Q

For afib maintenance therapy with HF which medications can be used?

A

amiodarone
dofetilide

446
Q

For afib maintenance therapy without structural heart disease (CAD/HF) which medications can be used?

A

dofetilide
dronedarone
flecainide
propafenone
sotalol
amiodarone

447
Q

Dronedarone is contraindicated in patients with __

A

heart failure

448
Q

Sotalol is contraindicated in CrCl <__, __ HF, EF </=__, or baseline QTc >__

A

CrCL <40
acute decomponsated HF
EF </=30%
baseline QTc >450

449
Q

What drugs should have continuous ECG monitoring for 3 days upon initiation/dose adjustments?

A

Dofetilide
Sotalol

450
Q

Flecainide or Propafenone? Renal dose adjustment

A

Flecainide

451
Q

Flecainide or Propafenone? Hepatic dose adjustment

A

Propafenone

452
Q

When is rate control preferred for Afib?

A

prefers rate control
older
longer history of AF
fewer symptoms

453
Q

When is rhythm control preferred for Afib?

A

prefers rhythm control
younger (<60yo)
shorter history of AF
more symptoms

454
Q

Most clots in patients with afib originate in the __

A

left atrial appendage

455
Q

Nonvalvular AF excludes patients with __ or __

A

moderate/severe mitral stenosis
mechanical heart valves

456
Q

Patients with VALVULAR/NON-VALVULAR Afib should be anticoagulated regardless of score

A

valvular

457
Q

Patients with valvular afib SHOULD/SHOULD NOT be put on a DOAC

A

should not

458
Q

What are the components of a CHA2DS-VASc Score?

A

(Congestive) heart failure
Hypertension
Age >/=75
Diabetes mellitus
Prior Stroke, TIA, or VTE
Vascular disease (prior MI, PAD, aortic plaque)
Age 65-74
Sex category (female)

459
Q

A CHA2DS2-VASc score of __ or higher indicated high risk of thrombosis

A

2

460
Q

DOACs are indicated in a CHA2DS2-VASc score of __ in men and __ in women

A

2
3

461
Q

Is aspirin recommended for afib?

A

no

462
Q

What are the components of a HAS-BLED score?

A

Hypertension SBP>160
Abnormal renal or hepatic function
History of stroke
History of Bleeding
Labile INRs
Older adults >65
Drugs or alcohol excess

463
Q

What HAS-Bled score warrants more frequent monitoring?

A

3

464
Q

What is considered abnormal renal function for HAS-BLED score?

A

chronic dialysis
renal transplant
SCr 2.26 or greater

465
Q

What is considered abnormal liver function for HAS-BLED score?

A

chronic hepatic disease
bilirubin >2x UNL
Phos >3x UNL

466
Q

Apixaban should be decreased to 2.5mg BID if what is true?

A

2/3 of the following:
80yo+
SCr 1.5+
60kg or less

467
Q

A 75 YOM presents to the ED with palpatations, dizziness, and lightheadedness. PMH: moderate mitral valve stenosis. Has Afib. BP 110/72 HR 140. What is the most appropriate treatment?

A

Diltiazem

468
Q

A 68YOF presents with AF. After her HR is controlled with metoprolol, she is asymptomatic. PMH: HTN, T2DM, osteoarthritis, and depression. Meds: metoprolol, lisinopril, tylenol, metformin, citalopram. HR 82 BP 130/88 SCr 0.8 CrCl 60 normal hepatic function. CHA2DS2-VASc and HAS-BLED scores?

A

4
1

469
Q

What are types of ventricular arrhythmias?

A

PVC
vtach
vfib
torsades
asystole/PEA

470
Q

If patient presents with PVC, is asymptomatic, but has CAD, what should be considered?

A

beta blockers

471
Q

If patients presents with symptomatic PVC what should be considered?

A

beta blockers
non-DHP CCBs

472
Q
A

IPCS 4 (5 decks)

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