Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CVM Exam II > Pharm: Cardiac Arrhythmia > Flashcards

Pharm: Cardiac Arrhythmia Flashcards

1
Q
  • What are the three class IA drugs?
A
  • Quinidine
  • Procainamide
  • Disopyramide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
  • What are two class IB drugs?
A
  • Lidocaine
  • Mexiletine
  • (Phenytoin in sketchy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  • What are 2 class IC drugs?
A
  • Flecainide
  • Propafenone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
  • What are 2 class II drugs?
A
  • Esmolol
  • Propanolol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
  • What are four class III drugs?
A
  • Amiodarone
  • Ibutilide
  • Dofetilide
  • Sotalol

“AIDS”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  • What are 2 class IV drugs?
A
  • Verapamil
  • Diltiazem
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
  • What is happening during the phases of the fast action potential in cardiac muscle?
A
  • Phase 0: voltage-dependent fast Na+ channels open as a result of depolarization; Na+ enters the cells
    down its electrochemical gradient
  • Phase 1: K+ exits cells down its gradient, while fast
    Na+ channels close, resulting in some repolarization
  • Phase 2: plateau phase results from K+ exiting cells
    offset by and Ca2+ entering through slow voltage-
    dependent Ca2+ channels
  • Phase 3: Ca2+ channels close and K+ begins to exit
    more rapidly resulting in repolarization
  • Phase 4: Resting membrane potential is gradually
    restored by Na+/K+ ATPase and the Na+/Ca2+
    exchanger
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  • What is happening during phase 4 of the pacemaker action potential?
A
  • phase 4 is a slow spontaneous depolarization
    • poorly selective ionic influx of Na, K occurs via If and T-Ca2+ channels, respectively.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  • What is happening during phase 0 and 3 of the pacemaker action potential?
A
  • Phase 0 is the upstroke of nodal action potential
    • Ca+2 influx via the relatively slow (L-type**) (long-acting) Ca2+ channels
  • Phase 3 is the repolarization of the nodal action potential
    • inactivation of calcium channels with ^K+ efflux
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  • How does the rate of spontatneous depolarization in phase 4 effect firing rate of nodes?
A
  • decreased slope–> decreased rate of node because it takes more time to reach threshold potential
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  • How does resting potential effect nodal action potential firing rate?
A
  • if potential is less negative, less time needed to reach threshold so the firing rate increases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  • Where is ERP on the action potential?
  • Where is AP on the action potential?
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  • What are the three states of sodium channels in the heart?
    • in which state do the m-gates open?
    • in which state do h-gates close?
A
  • Resting state – the channel is closed but ready
    to generate action potential
  • Activated state – depolarization to the threshold
    opens m-gates greatly increasing sodium
    permeability
  • Inactivated state – h-gates are closed, inward
    sodium flux is inhibited, the channel is not
    available for reactivation – this state is
    responsible for the refractory period
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
  • Class I drugs bind most readily to which states of sodium channels?
A
  • Activated or inactivated
    • very little affinity towards channels in a resting state
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  • What is the order of sodium channel binding affinity in class I drugs?
A
  • CAB
    • C has highest affinity (**slowest to dissociate**)
    • B has lowest affinity (**quickest to dissociate**)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  • Which class I drugs has intermediate dissociation kinetics?
A

IA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q
  • What does K+ channel blockade do?
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q
  • How is the fast action potential effected by 1A drugs?
    • AP length?
    • Effective refractory period (ERP)?
    • QT interval? Why?
    • QRS?
A
  • AP duration is increased
  • ERP is increased
  • QT interval is increased (Class IA also block potassium channels)***
  • QRS is prolonged (widened)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q
  • What type of cells are preferentially targeted by class IA drugs?
A
  • Ectopic pacemaker cells with faster rhythms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q
  • Which class IA drug has antimuscarinic and ganglionic blocking effects?
    • what can this cause?
A
  • Procainamide
  • can cause hypotension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q
  • What are the indications for procainamide?
    • acute therapy vs quinidine?
    • long term tx?
A
  • PSVT
  • prevent recurrence of VT
  • treat arrhythmias of MI
  • tolerated better than quinidine when given IV as acute therapy
  • long-term treatment poorly tolerated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q
  • What is the active metabolite of procainamide that has class III activity?
    • what patient population can this be worrisome?
A
  • active metabolite N-acetylprocainamide has class III activity, has longer half-life, accumulates in renal dysfunction patients
  • measurements of both parent drug and metabolite are necessary in pharmacokinetic studies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q
  • What are the adverse cardiac effects of procainamide?
A
  • Prolongs QT (K channel blockage) which can lead to TdP, although not as likely to cause torsades as quinidine
  • excessive conduction block
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q
  • What are some extracardiac adverse effects of procainamide?
    • prolonged use can lead to?
A
  • N/V/D, rash, fever, hypotension
  • prolonged use can lead to a positive ANA test drug-induced lupus syndrome, especially in slow acetylators
  • can cause agranulocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q
  • What is the MOA of quinidine?
A
  • open-state blocker of Na+ channels
  • also blocks multiple cardiac K+ channels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q
  • Which class IA drug is a natural alkaloid from cinchona bark that has anticholinergic and alpha-adrenergic blocking effects?
A
  • Quinidine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q
  • What are the effects of quinidine on
    • QRS duration?
    • QT interval?
    • Inotropy?
A
  • 10-20% increase in QRS duration
  • 25% increase in QT interval
  • negative inotrope
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q
  • What are the indications for use of quinidine?
A
  • afib, aflutter (pharmacological conversion) (because Class I are rhythm control drugs)
  • maintenance of sinus rhythm in patients with paroxysmal afib/flutter, or life-threatening ventricular arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q
  • Which drug is associated with decreased hearing, tinnitus, blurred vision, and delirium? What is this called?
A
  • Quinidine
  • Cinchonism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q
  • Which drug with hypersensitivity reactions, thrombocytopenia, and rarely severe hepatotoxic reactions?
A
  • Quinidine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q
  • Which class IA drug is likely to put you in a normal rhythm, but also 2-3x more likely to kill you?
A
  • Qunidine, the prototype class IA drug, which is now seldom used
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q
  • What is the MOA of disopyramide?
    • what effect does it have on peripheral vessels?
A
  • blocks Na channels similar to quinidine
  • is NOT an alpha-adrenergic receptor antagonist like quinidine, instead is a peripheral vasoconstrictor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q
  • How does disopyramide effect
    • QRS?
    • QT?
    • Inotropy?
A
  • prolongs QRS
  • prolongs QT
  • negative inotrope
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q
  • What are the indications for disopyramide?
    • offlabel use?
A
  • used to prevent recurrence of vtach or vfib
  • maintains sinus rhythm in pts with afib/flutter
  • off label use: maintenance of sinuys rhythm in afib patients that have vagally-induced afib or hypertrophic cardiomyopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q
  • Which class IA drug exerts the most anticholinergic side effects?
    • what are these side effects?
A
  • Disopyramide
  • dry mouth, blurred vision, constipation, urine retention, closed-angle glaucoma**
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q
  • Which class IA drug is used to convert supraventricular tachycardias such as WPW when given in IV form
    • how does this work?
A
  • procainamide
  • inhibits conduction in the accessory pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q
  • Which drug is indicated for vagally mediated afib?
A

disopyramide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q
  • What does the action potential look like when a patient is given a class IB drug?
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q
  • What effect do class IB drugs have on sodium and potassium channels?
    • which state of sodium channels do they bind to?
A
  • State-dependent sodium channel blockage
    • binds to inactivated sodium channels
    • preferentially depolarized cells–> ischemic damage causes depolarization of cells due to loss of ATP
  • 1B drugs DO NOT block K+ channels and thus do not (usually) significantly prolong action potential, QT duration.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q
  • What is the MOA of lidocaine?
A
  • blocks both the initiation and conduction of nerve impulses by decreasing the neuronal membrane’s permeability to sodium ions
  • (konorev mentions only inactivated na channels, while wolff says both open and inactivated)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q
  • Which drug is (*used to be*) indicated for the acute IV therapy of ventricular arrhythmias?

]

A
  • lidocaine
42
Q
  • Which drug is for use in Advanced Cardiac Life Support (ACLS) situations in which amiodarone is not available for hemodynamically stable or monomorphic/polymorphic VT, and for pulseless vfib that is unresponsive to defibrillator, CPR, and vasopressor administration?
A
  • Lidocaine
43
Q
  • Which two class I drugs are likely to cause dizziness, paresthesia, altered consciousness, coma, seizures, etc? (CNS effects)
A
  • Class IB
    • Lidocaine, Mexiletine
44
Q
  • Which class I drug must be given IV due to extensive first-pass metabolism by CYP3A4?
A
  • Lidocaine
45
Q
  • Which class IB drug can be given orally?
A
  • mexiletine
46
Q
  • which class I drug is indicated for use only to treat_sustained ventricular arrhythmias, but does NOT appear to prolong life?_
A
  • mexiletine
47
Q
  • Which CYPs eliminate Mexiletine?
A
  • CYP1A2
  • CYP2D6
48
Q
  • what is first line therapy for ischemia induced ventricular arrhythmias?
A
  • Amiodarone
49
Q
  • Which class IB drug is indicated for use to relieve chronic pain, especially pain due to diabetic neuropathy and nerve injury?
A
  • Mexiletine
50
Q
  • What does the fast action potential look like due to class IC drugs?
A
51
Q
  • What is the MOA of class IC drugs?
    • effect on sodium channels?
    • which state of sodium channel?
      • kinetics?
    • effect on QT? QRS?
A
  • Block sodium channels, slow conduction in cardiac tissue
  • preferentially bind to open (activated) state
  • slow kinetics
  • block some potassium channels
  • do NOT prolong AP or QT interval
  • do prolong QRS interval
52
Q
  • Which class I drug is ideal for use in those with catecholaminergic polymorphic vtach?
A
  • flecainide
53
Q
  • What are the clinical uses of flecainide?
A
  • maintenance of sinus rhythm in patients w/ paroxysmal supraventricular arrhythmias in whom structural heart disease is absent
  • life threatening ventricular arrythmias, such as sustained vtach, in patients who don’t have structural heart disease
54
Q
  • Flecainide can be proarrhythmic, especially in patients who have had which three contraindications?
A
  • patients w/ preexisting vtach
  • patients w/ previous infarction
  • patients w/ ventricular ectopic rhythms
55
Q
  • Which class IC drug has weak beta blocking activity?
A
  • propafenone
56
Q
  • What are the clinical uses of Propafenone?
A
  • used to maintain sinus rhythm in patinets with SVT (including afib)
  • in patients with disabling symptoms and without structural heart disease
  • in sustained ventricular arrhythmias in patients with disabling symptoms and without structural heart disease
57
Q
  • What are some adverse effects of propafenone?
A
  • Exacerbation of ventricular arrhythmias
  • metallic taste
  • constipation
  • exacerbation of asthma (some beta-blockade activity)
58
Q
  • What should you not combine propafenone with?
A
  • do not combine with the CYP2D6 and CYP3A4 inhibitors as the risk of proarrhythmia may be increased
59
Q
  • Overall, what are the indications for use of class IC drugs?
A
  • afib in structurally normal heart
  • svt, including avnrt, avrt, and atrial tachycardia
  • particularly effective at inhibiting reentrant tachycardia using accessory pathways
60
Q
  • good summary of class I drugs
A
61
Q
  • What is the effect of class II drugs on the nodal potential?
A
62
Q
  • How do beta-adrenoceptors work in the heart in the absence of a beta-blocking drug?
    • this was implied in the DSA and I didn’t know it, so found another source.
A
  • coupled to a Gs protein, which activates AC to form cAMP from ATP
  • increase cAMP activates PK-A, which phosphorylates L-type Calcium channels, causing increased calcium entry into the cell
    • increased calcium entry leads to enhanced release of calcium by the sarcoplasmic reticulum. this increases inotropy (contractility) of the heart and also chronotropy.
    • PK-A also phosphorylates other sites on SR that lead to enhanced release of calcium through ryandodine receptors, providing more calcium for binding troponin C–> increases inotropy
    • lastly, PK-A can phosphorylate myosin light chains, which also has positive inotropic effects
63
Q
  • What is the MOA of class II antiarrythmics?
A
  • block sympathetic stimulation of primarily Beta 1 receptors, which decreases cAMP, decreases inward Ca2+ currents, thus suppressing abnormal pacemakers by decreasing the slope of phase 4
64
Q
  • What are the indications for use of propranolol in cardiac arrhythmias?
A
  • Arrythmias associated w/ stress
  • AVNRT, AVRT
  • Afib/flutter
  • Arrythmias associated with myocardial infarcts
65
Q
  • Which class II drug has a half-life of 10 minutes because of hydrolysis by blood esterases?
A
  • esmolol
66
Q
  • How is esmolol given?
  • what is its MOA?
A
  • used as continuous iv infusion, with rapid onset and termination of its action
  • short acting selective beta-1 blocker
67
Q
  • What are four indications for the use of esmolol?
A
  • Supraventricular arrhythmia
  • Arrythmia associated with thyrotoxicosis
  • Myocardial ischemia or acute MI with arrhythmias
  • as an adjunct drug in general anesthesia to control arrhythmias in perioperative period
68
Q
  • There are a plethora of adverse effects of class II drugs; how do they effect the following:
    • cardiac output
    • asthma
    • liver glucose mobilization
    • lipid profile
    • consciousness
    • sexual effect
  • what happens if you lose your bottle of beta blockers and can’t get anymore?
A
  • Reduced cardiact output
  • bronchoconstriction
  • impaired liver glucose mobilization
  • increase VLDL, decrease HDL
  • sedation, depression
  • impotence
  • rapid withdrawal produces rebound hypertension
69
Q
  • What are the (six) contraindcations for use of class IIs?
    • konorev loves this shit
A
  • athma
  • peripheral vascular disease
  • raynauds
  • T1 DM patients on insulin
  • bradyarrythmias and AV conduction abnormalities
  • severe depression of cardiac function
70
Q
  • How do Class III potassium channel blockers effect the fast action potential?
A
71
Q
  • Which class of antiarrythmics bind to channels in the resting state, thus exhibiting reverse use dependence (display their proarrhythmia when HR is slow, raising risk of lethal arrhythmias such as TdP?
A
  • Class III- Potassium channel blockers
72
Q
  • Which potassium channels are opened during the phase 4?
A
  • Inwardly rectifying K+ channels
73
Q
  • What are the effects of class III drugs on:
    • AP
    • QT interval
    • ERP
A
  • Prolong AP
  • Prolong QT
  • Prolong ERP
  • dont change QRS because phase 0 isnt effected
74
Q
  • Which class III drug does not show reverse-use dependence
    • ​aka refractoriness is not increased at slow HRs
A
  • Amiodarone
75
Q
  • Which class III drug blocks inactivated sodium channels and possesses adrenolytic activity? (alpha,beta blocking properties)
A
  • Amiodarone
    • alpha blocking causes peripheral vasodilation, i think
76
Q
  • What are the indications for use of amiodarone?
A
  • oral therapy in patients w/ recurrent vtach or vfib? resistant to other drugs
  • maintaining sinus rhythm in patients w/ afib
77
Q
  • What are four major side effects of amiodarone?
    • what side effect does Amiodarone NOT have that other class III medications do?
A
  • Pulmonary fibrosis
  • hyperthyroidism or hypothyroidism
  • corneal micro-deposits
  • bluish discolaration of the skin
  • ** does not cause torsades**
78
Q
  • If you stop amiodarone, how long are its effects maintained?
    • how long is half life
A
  • half life is around 50 days, but metabolites can be found in tissues 1 year after discontinuation
79
Q
  • How would rifampin (tb drug) effect amiodarone?
  • How would cimetidine effect amiodarone?
A
  • rifampin is a CYP3A4 inducer, so it would decrease the half-life of amiodarone
  • cimetidine in a CYP3A4 inhibitor, so it would increase the half-life of amiodarone
80
Q
  • What should be specifically monitored in patients on amiodarone due to its side effects?
    • three tests
A
  • LFTs due to hepatotoxicity
  • PFTs due to pulmonary fibrosis side effect
  • TFTs due to amiodarone being 40% iodine by weight which can cause both hypo or hyper thyroidism
81
Q
  • Which class III drug also shows some class II activity?
    • non-selective beta-blocker
A
  • Sotalol
82
Q
  • What are the indications for the use of sotalol?
A
  • life-threatening ventricular tachyarrhythmias
  • maintenance of sinus rhythm in patients w/ afib
83
Q
  • What are some adverse effects of sotalol?
A
  • same as beta blocker–> depress cardiac function
  • provokes TdP
84
Q
  • Which class III drug specifically blocks the rapid component of the delayed rectifier potassium current, thus its effect is more pronounced at lower HRs?
    • _​_delayed rectifier potassium channel is IKr
A
  • dofetilide
85
Q
  • Which class III drug is used for conversion of AF to sinus rhythym and maintenance of sinus rhythm after its been converted?
A
  • dofetilide
86
Q
  • Which class III drug must have its dose modified in kidney failure patients based on the Creatinine clearance ?
A
  • dofetilide
87
Q
  • Which class III drug is infused intravenously for acute afib or flutter for conversion to NSR?
A
  • ibutilide
88
Q
  • After converting a patient’s acute afib back to NSR with ibutilide, should you let them get up and leave?
A
  • No, must monitor EKG continuously until QTc returns to baseline
89
Q
  • Which class III drug is indicated for arrhythmias that are acute, or have short duration?
    • also used for converting cardiac surgery induced afib, and in WPW syndrome (accessory pathway arrhythmias)
A
  • ibutilide
90
Q
  • Which class III drug is indicated for prevention of recurrent afib or vtach due to an old mi?
A
  • sotalol
91
Q
  • Which class III drug can be used in CHF patients and why?
A
  • Dofetilide because it is not a negative inotrope due to its pure action on IKr channels
92
Q
  • how do class IV drugs effect the nodal action potential?
A
  • note threshold is increased
93
Q
  • What is the MOA of class IV drugs?
    • which state/type of channel?
    • slope of phase 0
    • threshold potential
    • refractory period in AV node
A
  • Block both activated and inactivated L-type calcium channels
  • decrease slope of phase 0
  • increase L-type calcium channel threshold potential
  • prolong refractory period in AV node
94
Q
  • How do class IV drugs effect conduction velocity and PR interval?
A
  • decrease conduction velocity
  • increase PR interval
95
Q
  • What are the clinical indications for verapamil and diltiazem?
A
  • termination of supraventricular tachycardias and prevention of recurrence
  • ventricular rate control in afib/flutter
96
Q
  • What are some cardiac and non cardiac side effects of class IV drugs?
A
  • CHF due to negative inotropy
  • bradycardia
  • hypotension
  • heart block
  • SA node arrest

verapamil can cause constipation**

97
Q
  • What are two MOAs of adenosine?
A
  • Activates potassium curent and inhibits Calcium and funny currents, causing marked hyperpolarization and suppression of action potentials in slow cells
  • inhibits av conduction and increases nodal refractory period
98
Q
  • What is the name of the GPCR that adenosine binds to?
A
  • A1 adenosine receptor
99
Q
  • What are two clinical indications for adenosine?
A
  • rapid IV bolus for the acute termination of re-entrant SVT​
  • also used to induce controlled hypotension
100
Q
  • What drug likely caused this?
A
  • adenosine
    • produces a transient asytole/AV block
101
Q
  • What are some side effects of adenosine?
A
  • Chest fullness, burning sensation
  • AV block
  • Rarely triggers bronchospasm due to A1/A2B adenosine receptors causing bronchoconstriction
  • hypotension
  • impending doom, cutaneous flush (sketchy)

CVM Exam II (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions