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Therapeutics 3 Kappa Epsilon > Exam 2 - Wendt (Arrhythmia/CHF) > Flashcards

Exam 2 - Wendt (Arrhythmia/CHF) Flashcards

1
Q

_______ cells have automaticity

A

Pacemaker

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2
Q

pacemaker cells have (what ion) dependent spikes

A

Ca2+

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3
Q

Ventricular myocytes have (what ion) dependent spikes

A

Na+

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4
Q

Pacemaker Cells or Ventricular Cells?

have a very fast/immediate/vertical depolarization

A

Ventricular cells

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5
Q

Pacemaker Cells or Ventricular Cells?

have Ca2+ dependent spikes

A

Pacemaker

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6
Q

Pacemaker Cells or Ventricular Cells?

have Na+ dependent spikes

A

Ventricular

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7
Q

Pacemaker Cells or Ventricular Cells?

Have high automaticity

A

pacemakers

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8
Q

Pacemaker Cells or Ventricular Cells?

have low automaticity

A

ventricular

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9
Q

Pacemaker Cells or Ventricular Cells?

are specialized non-contractile cells

A

Pacemaker

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10
Q

Pacemaker Cells or Ventricular Cells?

are contractile cells

A

ventricular

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11
Q

what are the phases of a Pacemaker cells action potential?

A

In order: Phase 4,0,3,4

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12
Q

what is phase 4 in pacemaker cell action potential

A

“funny” current makes diastolic pacemaker current
annnnd
K+ channels/current is activated by vagus

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13
Q

what is phase 0 in pacemaker cell action potential

A

calcium channel carries AP upstroke

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14
Q

what is phase 3 in pacemaker cell action potential

A

repolarizing K+ current

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15
Q

Myocyte action potential phases? (in order)

A

IN ORDER: Phases 4,0,1,2,3,4

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16
Q

what is phase 0 in myocyte cells action potential

A

Na+ channel carries AP upstroke

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17
Q

what is phase 1 in myocyte cells action potential

A

repolarizing K+ current (“transient upward”???)

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18
Q

what is phase 2 in myocyte cells action potential

A

plateau Ca2+ current critical for muscle contraction

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19
Q

what is phase 3 in myocyte cells action potential

A

repolarizing K+ current

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20
Q

what is phase 4 in myocyte cells action potential

A

pacemaker current (very minimal?)

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21
Q

Acetylcholine decrease _____ and ____ currents

A

HCN; Ca2+

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22
Q

ACH activates ______ which causes hyperpolarization

A

GIRK

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23
Q

_____ activates GIRK which causes hyperpolarizaiton

A

ACH

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24
Q

ACH stimulates the G_____ channel

A

G (alpha I)

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25
Q

ACH is a a part of the (sympathetic or parasympathetic) system

A

PARAsympathetic

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26
Q

what does the GIRK channel do when activated?

A

it causes hyperpolarization by kicking K+ out of the cell

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27
Q

how many classes of antiarrhythmic drugs are there (according to Vaughn-Williams-Singh Scale)

A

4

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28
Q

what are the 4 classes of antiarryhthmic drugs

according to Vaughn-Williams-Singh Scale

A

1 - Na+ channel blockers
2- Beta adrenergic antagonists
3- K+ channel blockers aka drugs that prolong refractory period
4 - Ca2+ Channel blockers

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29
Q

If another signal happens when an area is still under its refractory period what happens?

A

nothin’ — if still in refractory period a new beat won’t occur

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30
Q

what are the common arrhythymias

A 
atrial sinus arrhythmia
re-entry arrhythmia
a.fib
wolf-parkinson white
monomorphic ventricular tachycardia
AV nodal re-entrant tachycardia
Premature ventricular complexes
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31
Q

what beta blockers dose wendt mention

A

Esmolol, Acebutolol, Propranolol

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32
Q

Beta Blockers:

slow ______ and _____ currents in SA/AV Node

A

Pacemaker/Ca2+

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33
Q

Beta Blockers:

(increase or decrease) refractoriness of SA/AV node

A

INCREASE

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34
Q

Beta Blockers:

(increase or decrease) P-R interval

A

increase

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35
Q

Beta Blockers:

are good when the arrhythmia involves ______

A

catecholamines…

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36
Q

Ca2+ Channel Blocker Options for arrhytmias?

A

Diltiazem and Verapamil

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37
Q

Ca2+ Channel Blocker:

have a __________ block

A

frequency dependent

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38
Q

Ca2+ Channel Blocker:

(increase or decrease) refractoriness of AV node

A

INCREASE!

not SA node like beta blockers

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39
Q

Ca2+ Channel Blocker:

(increase or decrease) the P-R interval

A

increase

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40
Q

what are the 3 different classes of Na+ Channel blockers (aka Class 1 Na+ Channel blockers)

A

1A; 1B; 1C

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41
Q

what antiarrhythmic drug class is class 1

A

Na+ channel blockers

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42
Q

what antiarrhythmic drug class is class 2

A

beta adrenergic antagonists

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43
Q

what antiarrhythmic drug class is class 3

A

K+ channel blockers (agents that prolong refractory period)

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44
Q

what antiarrhythmic drug class is class 4

A

Ca2+ channel blockers

45
Q

what antiarrhythmic drugs are a part of Class 1A

A

quinidine
procainamide
disopyramide

46
Q

what antiarrhythmic drugs are a part of Class 1B

A

lidocaine
tocainide
Mexilitine
Phenytoin

47
Q

what antiarrhythmic drugs are a part of Class 1C

A

Propafenone
Flecainide
Moricizine

48
Q

what antiarrhythmic drugs are a part of Class 3

A 
(the K+ channel blockers)
Amiodarone
Dronedarone
Sotalol
Ibutilide
49
Q

what antiarrhythmic drugs are a part of Class 5

A 
These are all the misc. Drugs
Digoxin
Magnesium Chloride
Potassium Chloride
Adenosine
50
Q

When beta adrenergic receptors are stimulated cAMP increases which directly increases activity of _____ channels –> increased ______ currents

A

HCN channels; DEPOLARIZING currents

51
Q

When beta adrenergic receptors are stimulated cAMP increases which increases phosphorylation of _______ channels which increases amount of current these channels can pass and allows them to open at more _____ membrane potentials

A

L-type voltage gated Ca2+ channels; negative

52
Q

Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
does pure sodium channel block

A

1B and 1C

53
Q

Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
both widens QRS complex AND prolongs Q-T interval

A

1A

54
Q

Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
can reduce QT interval (but not clinically significant)

A

1B

55
Q

Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
Widens QRS complex

A

1A & 1C

56
Q

Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
will block both the open and inactivated state

A

1B

57
Q

Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
preferentially blocks open state

A

1A & 1C

58
Q

Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
ONLY blocks open state

A

1C

59
Q

Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
has VERY slow dissociation (> 10 secs)

A

1C

60
Q

Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
has rapid dissociation (millisecond)

A

1B

61
Q

Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
has moderate to slow dissociation (seconds)

A

1A

62
Q

QT interval is known as the time from the beginning of _________ to the end of _________

A

beg. of ventricular depolarization; to end of ventricular repolarization

63
Q

what are the 3 mechanisms that can cause arrhythmia

A

enhanced automaticity
triggered activity
re-entry

64
Q

the ____ Node cells exhibit the highest rate of automaticity

A

SA

65
Q

Arrhythmias can be caused by trigger activity — what does trigger activity mean?

A

depolarizations that arise abnormally from a normally generated sinus action potential

66
Q

what does EAD and DAD stand for

A

EAD - early afterdepolarizaiton

DAD - delayed after depolarization

67
Q

what are the different types of trigger activity that cause arrythmias

A

EAD or DAD

68
Q

Triggered Activity - EAD
is caused by ________
Arises from a _________ Vm
Caused by (rapid or slow) HR, or _____kalemia, or ______ syndrome

A

caused by PROLONGED AP
from a DEPOLARIZED
SLOWED HR, HYPOkalemia, or LONG QT syndrome

69
Q 
Triggered Activity - DAD
caused by \_\_\_\_\_\_\_\_
(increase or decrease) NCX current
arises from a \_\_\_\_\_\_ Vm
often seen with: (rapid or slow) HR, MI, \_\_\_\_\_\_\_ stress, or \_\_\_\_\_\_\_ intoxication
A

caused by Ca2+ overload
INCREASE in NCX current
arise from NORMAL Vm
RAPID HR; adrenergic stress, digoxin intoxication

70
Q

what two things make up cardiac output

A

Stroke Volume and HEART RATE

71
Q

what are the consequences of decreased cardiac output

A

Cardiovascular:
Tachycardia, Cardiomelgia, Arrhythmias, Fatigue/exercise intolerance

Respiratory: 
SOB
Pulmonary Edema
Cyanosis
Orthopnea
72
Q

definition of stroke volume

A

amount of blood ejected from da ventricles during contraction

73
Q

______ increase stroke volume

what hemodynamic concept..

A

contractility

74
Q

what are the axis on a FrankSterling Relationship

A

Y-axis: Stroke Volume

X-axis: PreLoad (aka left ventricular diastolic volume)

75
Q

Preload is also known as ……

A

LV (left ventricular) End diastolic volume

76
Q

Afterload and ____ are inversely related

A

SV (stroke volume)

77
Q

Frank-Starling Relationship

a failing heart can’t compensate and increase _____ when _____ increases

A

can’t increase SV when preload increases

78
Q

what are the axis in a force tension graph

A

Y-axis: Stroke Volume

X-axis: Afterload

79
Q

what are the two types of CHF

A

Systolic Failure

or Diastolic Failure

80
Q

Types of CHF:
Systolic Failure has….
deficit in _______
and a ______ heart

A

deficit in CONTRACTION

THIN/DILATED heart

81
Q

Types of CHF:
Diastolic Failure has….
deficit in _______
_______ walls that cannot relax

A

deficit in FILLING

STIFF/THICK that cannot relax

82
Q

what are the 3 types of cardiac remodeling (due to CHF is why we talked about them)

A

Cardiac Dilation
Pathological Hypertrophy
Physiological Hypertrophy

83
Q

CHF - Cardiac Remodeling:

which one does NOT have fibrosis

A

Physiological hypertrophy

84
Q

CHF - Cardiac Remodeling:

which one has thinning walls

A

cardiac dilation

85
Q

CHF - Cardiac Remodeling:

what can cause pathological hypertrophy

A

Chronic HTN

Aortic valve stenosis

86
Q

CHF - Cardiac Remodeling:

what can cause physiological hypertrophy

A

Chronic Exercise

Pregnancy

87
Q

CHF - Cardiac Remodeling:

what can cause cardiac dilation

A

MI or other insults (like HF)

88
Q

Renin/Angiotensin System:

______ makes angiotensinogen

A

Liver

89
Q

Renin/Angiotensin System:

_____ makes Renin

A

kidney

90
Q

Renin/Angiotensin System:

______ makes ACE

A

Lungs

91
Q

Renin/Angiotensin System:

Angiotensin II causes _____ and _____ secretion

A

Aldosterone/ADH

92
Q

Renin/Angiotensin System:
overall leads to
increased ________ and increase _______ and increased __________

A

water retention; blood volume; sympathetic activity

93
Q

2 Main CHF Tx Strategies

A

Manipulate Hemodynamics

Inhibit compensation

94
Q

CHF Tx Strategies
Manipulate Hemodynamics and Inhibit Compensation -
which one improves mortality

A

inhibiting compensation

95
Q

CHF Drugs

what drugs are used to manipulate hemodynamics

A

vasodilators (organic nitrates, hydralazine)
diuretics
angiotensin inhibitors
inotropic agents (digoxin, PDE3 inhibitors, Bera-adrenergic agonists)

96
Q

what are the 3 classes of inotropic agents used in CHF and are they used for chronic or for acute therapy only?

A

Cardiac glycosides - chronic

PDE (phosphodiesterase) inhibitors - acute only

Beta adrenergic agonists - acute only

97
Q

what drugs are known as PDE inhibitors and used in CHF as inotropic agents

A

milrinone and inamrinone

98
Q

what drugs are known as Beta adrenergic agonists and used in CHF as inotropic agents

A

dopamine; dobutamine

99
Q

how does Na+/K+ ATPase blockade cause higher contractility

A

when the ATPase is inhibited it creates more Na+ inside - the NCX channel then compensates and kicks out Na+ and brings in Ca2+ which causes more contraction/greater contraction

100
Q

what drug is a cardiac glycoside

A

digoxin

101
Q

what are some common digoxin toxicities

A

psychiatric - delirium/fatigue/malaise/confusion
G.I - anorexia, N/V, abdominal pain
Respiratory - increased response to hypoxia
C.V - pro-arrhythmic (atrial tachy, AV block)

102
Q

what drugs are Vasopressin receptor antagonists

A

tolvaptan

conivaptan

103
Q

Tolvaptan or Conivaptan:

which one is V2 selective

A

Conivaptan

104
Q

Tolvaptan or Conivaptan:

which one is V1A/V2 receptors

A

Tolvaptan

105
Q

Vasopressin Receptor Antagonists are used for treating ________ in HF and ______

A

hyponatremia; SIADH

106
Q

ADEs of Vasopressin Receptor Antagonists

A

hypotension

osmotic demyelination

107
Q

why is neprilysin inhibition helpful in CHF

A

under normal circumstances, neprilysin breaks down natriuretic peptides. but natriuretic peptides cause VSMC relaxation

108
Q

what drug is a neprilysin inhibitor

A

Sacubitril

109
Q

Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
has mixed block for Na+ and K+

A

1A

Therapeutics 3 Kappa Epsilon (20 decks)

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