Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

pharm exam 2 > drug therapy for dysrhythmias > Flashcards

drug therapy for dysrhythmias Flashcards

(66 cards)

Start Studying
1
Q

the heart is an

A

electrical pump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

regular intervals with four events

A

stimulation from electrical impulse -> transmission to adjacent tissue -> contraction of atria, then ventricles -> relaxation of atria, then ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

cardiac conduction: automaticity

A

ability of the heart to generate an electrical impulse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

cardiac conduction: conductivity

A

ability of cardiac tissue to transmit electrical impulses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is unique about the cardiac automaticity conduction

A

any part of conduction system can start an impulse, SA node has the fastest rate of automaticity (pacemaker), initiation of impulse dependent on Na and K ion movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

in automaticity, what happens after contraction

A

period of decreased excitability/ cells cannot respond to new stimulus (absolute refractory period)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is unique about the cardiac conductivity conduction

A

impulses originate in the SA node to AV node, impulse then travels predictable route

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

cardiac dysrrhythmias(arrhythmias)

A

abnormalities in cardiac rate or rhythm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

dysrhythmias originate in

A

any part of the conduction system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

dysrhythmias result from

A

electrical impulse formation, conduction or both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

in dysrhythmias, the cardiac automaticity allows

A

cells other than SA node to initiate electrical impulse that reach the highest level in contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

if impulse originates in other than the SA node in dysrhythmias, then it is referred to as

A

ectopic focus or ectopic beat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

result of ectopic beat is

A

hypoxia, ischemia, hypokalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

hypoxia is

A

low O2 in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

ischemia is

A

no blood to the tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

ectopic beats indiciate

A

myocardial irritability; potentially serious cardiac function impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

atrial tachycardia

A

heart rate in the atria are beating faster than normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

atrial flutter

A

narrow QRS; when the atria beats regularly but faster than normal and more often than the ventricles; ratio of 4 to 1; atria could contract 4 times before ventricles: should be 1 to 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

atrial fibrillation

A

when the atria beats irregularly; SA node is firing so fast that the AV node can’t keep up; no P wave because of how fast SA is firing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

ventricular tachycardia

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

ventricular flutter

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

ventricular fibrillation

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

antidysrhythmic nonpharmacologic therapy goal

A

prevent, relieve symptoms, and prolong survival; increase use of nonpharmacologic strategies for dysrhythmia management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

prior goal of pharmacotherapy

A

suppress dysrhythmias resulted in higher mortality rate among patients receiving antidysrhythmic drug therapy than those who were not

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
nonpharmacologic strategy: cardioversion
pads on front of chest and on back(anteriorly & posteriorly) can shock the heart
26
nonpharmacologic strategy: defibrillation
put pads on, check rhythms of the heart (Vtach and Vfib)
27
nonpharmacologic strategy: radiofrequency catheter ablation
procedure dr. uses catheter to send radio frequency energy, makes circular scars around cells around heart
28
pace makers
implantable cardioverter defibrillation; for low HR (30-40), will shock patient if HR goes below 60 to set the pace of the heart
29
antidysrhythmic drug therapy: MOA
reduce automaticity, slow conduction of impulses through the heart, prolong refractory period
30
antidysrhythmic drug therapy: indications for use
conversion of atrial fibrillation or fatter to NSR, maintaining NSR postconversion, suppression of fast or irregular ventricular rate that alters cardiac output, presence of dangerous dysrhythmias that are potentially fatal
31
antiarrhyrthmic agents
sodium channel blockers, beta-adrenergic blockers, potassium channel blockers, calcium channel blockers
32
sodium channel blockers
can cause/ worsen dysrhythmias, block the opening of sodium channels, rarely used
33
sodium channel blockers treat
atrial dysrhythmias, supraventricular tachycardia (bursts of high rapid heart rates)
34
side effects of sodium channel blockers
arrhythmias, bradycardai, hypotension, respiratory depression, dizziness, syncope, drowsiness, fatigue, confusion, anticholinergic
35
nursing concern when using sodium channel blockers
interfere with anticoagulants
36
beta-adrenergic blockers do what
reduce activation of beta receptors = decrease conduction through SA/ AV node = decrease automaticity = slow HR; decreases cardiac excitability, cardiac workload and oxygen consumption
37
beta-adrenergic blockers treat
management of dysrhythmias from excessive SNS stimulation, a-fibrillation, and a-flutter(though to slow ventricular rate), post MI/CHF (thought to prevent v-fib)
38
side effects of beta-adrenergic blockers
bradycardia, AV block, hypotension, dizziness, syncope, bronchospasm, dyspnea, drowsiness, fatigue
39
what rebound side effect will happen with beta-adrenergic blockers if NOT tapered off
hypertension/ tachycardia/ dysrhythmias with abrupt withdrawal
40
nursing concerns when using beta-adrenergic blockers
the use with verapamil (Ca2+ blocker) can increase renal failure and heart block; so check if there are on verapamil before administering
41
examples of beta-adrenergic blockers
propranolol, acebutolol, esmolol
42
potassium
main intracellular ion/ involved with cardiac rhythm (contractility of the myocardium)
43
normal K+ levels
3.5-5.0 mEg/L
44
hypokalemia, s/sx
less than 3.5; ventricular dysrhythmias, muscle weakness/ decreased DTR's, weak peripheral pulses
45
treat hypokalemia
increase dietary K+ rich foods, oral (no more than 20mEg/hr with meals, pills can be spilt), peripheral IV(20-40mEg/L; do not exceed 20/hr; mixed with other solution)(IV not recommended)
46
hyperkalemia, s/sx
greater than 5.0; dysrhythmias, V-fib, HB, cardiac arrest, muscle twitching, numbness in hands feet and mouth
47
hyperkalemia, s/sx
greater than 5.0; dysrhythmias, V-fib, HB, cardiac arrest, muscle twitching, numbness in hands feet and mouth
48
treat hyperkalemia
restrict dietary K+ rich foods, give sodium polystyrene(kayexalate): binds K+ and causes diarrhea, IV administration of insulin with dextrose shifts K+ back into cells
49
potassium channel blockers: inhibits adrenergic stimulation
blocks potassium channels= prolong duration of action potential = slow depolarization = prolong refractory period
50
potassium channel blockers treat
IV for life threatening tachycardia- dysrhythmias (not first line r/t renal failure pulmonary toxicity); PO for recurrent tachycardia, V & A fibrillation and A flutter
51
side effects of potassium channel blockers
Brady cardia. hypotension (weakness, dizziness), worsen or new dysrhythmias, pulmonary toxicity (IV), hepatotoxicity, blurred vision/ photosensitivity
52
contraindications for potassium channel blockers
caution with AV block, shock, hypotension, respiratory depression, renal/hepatic impairment
53
examples of potassium channel blockers
amiodarone, dofetilide (tikosyn), ibutilide, sotalol
54
calcium channel blockers
block calcium ion channels= reduce automaticity in SA node and slow conduction through AV node = slow HR = prolong refractory period
55
calcium channel blockers treat
supraventricular dysrhythmias (at SA & AV nodes), tachycardia; can be emergency medication for A-fub, SVT requiring IV administration
56
side effects of calcium channel blockers
Bradycardia, hypotension(HA, dizziness, lightheaded), flushed skin, MI, hepatotoxicity, peripheral edema
57
contraindications with calcium channel blockers
HB, sick sinus, HF, hypotension, hepatic/renal insufficiency, pregnancy
58
examples of calcium channel blockers
diltiazem, verapamil
59
nursing concerns with calcium channel blockers
avoid grapefruit/ grapefruit juice, monitor with beta blockers and digoxin
60
class I acts on what blocker
sodium channel blocker
61
class II acts on what blocker
beta-adrenergic blocker
62
class III acts on what blockers
potassium channel blocker
63
class IV acts on what blocker
calcium channel blocker
64
unclassified anti arrhythmic
adenosine, digoxin
65
adenosine is used when
emergency medication; used for SVT when a vagal maneuver doesn't work; natural occurring component of all body cells; depressed conduction at AV node = restore NSR in SVT patients; given as a rapid bolus administration r/t rapid metabolism out of the system (if you give slow It won't reach the cardiac tissue)
66
pharmacologic therapy of dysrhythmias
understanding mechanisms of dysrhythmias, requires accurate ID of dysrhythmia, monitoring imperative(observing hemodynamic and ECG effects of dysrhythmia), knowledge of pharmacologic actions of specific medications, therapeutic effects outweigh potential adverse effects

pharm exam 2 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions