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CVM Exam II > Pharm: Cardiac Arrhythmia > Flashcards

Pharm: Cardiac Arrhythmia Flashcards

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1
Q
  • What are the three class IA drugs?
A
  • Quinidine
  • Procainamide
  • Disopyramide
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2
Q
  • What are two class IB drugs?
A
  • Lidocaine
  • Mexiletine
  • (Phenytoin in sketchy)
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3
Q
  • What are 2 class IC drugs?
A
  • Flecainide
  • Propafenone
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4
Q
  • What are 2 class II drugs?
A
  • Esmolol
  • Propanolol
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5
Q
  • What are four class III drugs?
A
  • Amiodarone
  • Ibutilide
  • Dofetilide
  • Sotalol

“AIDS”

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6
Q
  • What are 2 class IV drugs?
A
  • Verapamil
  • Diltiazem
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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
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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.
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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
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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
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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
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12
Q
  • Where is ERP on the action potential?
  • Where is AP on the action potential?
A
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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
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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
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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**)
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16
Q
  • Which class I drugs has intermediate dissociation kinetics?
A

IA

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17
Q
  • What does K+ channel blockade do?
A
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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)
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19
Q
  • What type of cells are preferentially targeted by class IA drugs?
A
  • Ectopic pacemaker cells with faster rhythms
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20
Q
  • Which class IA drug has antimuscarinic and ganglionic blocking effects?
    • what can this cause?
A
  • Procainamide
  • can cause hypotension
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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
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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
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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
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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
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25
* What is the MOA of quinidine?
* open-state blocker of Na+ channels * also blocks multiple cardiac K+ channels
26
* Which class IA drug is a natural alkaloid from cinchona bark that has anticholinergic and **alpha-adrenergic _blocking_** effects?
* Quinidine
27
* What are the effects of quinidine on * QRS duration? * QT interval? * Inotropy?
* 10-20% increase in QRS duration * 25% increase in QT interval * negative inotrope
28
* What are the indications for use of quinidine?
* 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
29
* Which drug is associated with decreased hearing, tinnitus, blurred vision, and delirium? What is this called?
* Quinidine * Cinchonism
30
* Which drug with hypersensitivity reactions, thrombocytopenia, and rarely severe hepatotoxic reactions?
* Quinidine
31
* Which class IA drug is likely to put you in a normal rhythm, but also 2-3x more likely to kill you?
* Qunidine, the prototype class IA drug, which is now seldom used
32
* What is the MOA of disopyramide? * what effect does it have on peripheral vessels?
* blocks Na channels similar to quinidine * is NOT an alpha-adrenergic receptor antagonist like quinidine, instead is a peripheral vasoconstrictor
33
* How does disopyramide effect * QRS? * QT? * Inotropy?
* prolongs QRS * prolongs QT * negative inotrope
34
* What are the indications for disopyramide? * offlabel use?
* 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
35
* Which class IA drug exerts the most anticholinergic side effects? * what are these side effects?
* Disopyramide * dry mouth, blurred vision, constipation, urine retention, closed-angle glaucoma\*\*
36
* Which class IA drug is used to convert supraventricular tachycardias such as WPW when given in IV form * how does this work?
* procainamide * inhibits conduction in the accessory pathway
37
* Which drug is indicated for vagally mediated afib?
disopyramide
38
* What does the action potential look like when a patient is given a class IB drug?
39
* What effect do class IB drugs have on sodium and potassium channels? * which state of sodium channels do they bind to?
* 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.
40
* What is the MOA of lidocaine?
* 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)
41
* Which drug is (\*used to be\*) indicated for the acute IV therapy of ventricular arrhythmias? ]
* lidocaine
42
* 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_?
* Lidocaine
43
* Which two class I drugs are likely to cause dizziness, paresthesia, altered consciousness, coma, seizures, etc? (CNS effects)
* Class IB * Lidocaine, Mexiletine
44
* Which class I drug must be given IV due to extensive first-pass metabolism by CYP3A4?
* Lidocaine
45
* Which class IB drug can be given orally?
* mexiletine
46
* which class I drug is indicated for use only to treat_sustained ventricular arrhythmias, but does NOT appear to prolong life?_
* mexiletine
47
* Which CYPs eliminate Mexiletine?
* CYP1A2 * CYP2D6
48
* what is first line therapy for ischemia induced ventricular arrhythmias?
* Amiodarone
49
* Which class IB drug is indicated for use to relieve chronic pain, especially pain _due to diabetic neuropathy and nerve injury?_
* Mexiletine
50
* What does the fast action potential look like due to class IC drugs?
51
* What is the MOA of class IC drugs? * effect on sodium channels? * which state of sodium channel? * kinetics? * effect on QT? QRS?
* 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
* Which _class I drug_ is ideal for use in those with _catecholaminergic polymorphic vtach?_
* flecainide
53
* What are the clinical uses of flecainide?
* 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
* Flecainide can be proarrhythmic, especially in patients who have had which three contraindications?
* patients w/ preexisting vtach * patients w/ previous infarction * patients w/ ventricular ectopic rhythms
55
* Which class IC drug has weak beta blocking activity?
* propafenone
56
* What are the clinical uses of Propafenone?
* 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
* What are some adverse effects of propafenone?
* Exacerbation of ventricular arrhythmias * _metallic taste_ * _constipation_ * **exacerbation of asthma** (some beta-blockade activity)
58
* What should you not combine propafenone with?
* do not combine with the CYP2D6 and CYP3A4 inhibitors as the risk of proarrhythmia may be increased
59
* Overall, what are the indications for use of class IC drugs?
* afib in structurally normal heart * svt, including avnrt, avrt, and atrial tachycardia * particularly effective at _inhibiting reentrant tachycardia using accessory pathways_
60
* good summary of class I drugs
61
* What is the effect of class II drugs on the nodal potential?
62
* 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.
* 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
* What is the MOA of class II antiarrythmics?
* 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
* What are the indications for use of propranolol in cardiac arrhythmias?
* Arrythmias associated w/ stress * AVNRT, AVRT * Afib/flutter * Arrythmias associated with myocardial infarcts
65
* Which class II drug has a half-life of 10 minutes because of hydrolysis by blood esterases?
* esmolol
66
* How is esmolol given? * what is its MOA?
* used as continuous iv infusion, with rapid onset and termination of its action * short acting _selective_ beta-1 blocker
67
* What are four indications for the use of esmolol?
* 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
* 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?
* Reduced cardiact output * bronchoconstriction * impaired liver glucose mobilization * increase VLDL, decrease HDL * sedation, depression * impotence * rapid withdrawal produces **rebound hypertension**
69
* What are the (six) contraindcations for use of class IIs? * konorev loves this shit
* athma * peripheral vascular disease * raynauds * T1 DM patients on insulin * bradyarrythmias and AV conduction abnormalities * severe depression of cardiac function
70
* How do Class III potassium channel blockers effect the fast action potential?
71
* 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?_
* Class III- Potassium channel blockers
72
* Which potassium channels are opened during the phase 4?
* Inwardly rectifying K+ channels
73
* What are the effects of class III drugs on: * AP * QT interval * ERP
* Prolong AP * Prolong QT * Prolong ERP * dont change QRS because phase 0 isnt effected
74
* Which class III drug does _not show reverse-use dependence_ * _​aka refractoriness is not increased at slow HRs_
* Amiodarone
75
* Which class III drug blocks inactivated sodium channels and possesses adrenolytic activity? (alpha,beta blocking properties)
* Amiodarone * alpha blocking causes peripheral vasodilation, i think
76
* What are the indications for use of amiodarone?
* **oral therapy** in patients w/ recurrent vtach or vfib? resistant to other drugs * maintaining sinus rhythm in patients w/ afib
77
* What are four major side effects of amiodarone? * what side effect does Amiodarone NOT have that other class III medications do?
* Pulmonary fibrosis * hyperthyroidism or hypothyroidism * corneal micro-deposits * bluish discolaration of the skin * \*\* does not cause torsades\*\*
78
* If you stop amiodarone, how long are its effects maintained? * how long is half life
* half life is around 50 days, but metabolites can be found in tissues 1 year after discontinuation
79
* How would rifampin (tb drug) effect amiodarone? * How would cimetidine effect amiodarone?
* 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
* What should be specifically monitored in patients on amiodarone due to its side effects? * three tests
* 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
* Which class III drug also shows some class II activity? * non-selective beta-blocker
* Sotalol
82
* What are the indications for the use of sotalol?
* life-threatening ventricular tachyarrhythmias * maintenance of sinus rhythm in patients w/ afib
83
* What are some adverse effects of sotalol?
* same as beta blocker--\> depress cardiac function * provokes TdP
84
* 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
* dofetilide
85
* Which class III drug is used for conversion of AF to sinus rhythym and maintenance of sinus rhythm after its been converted?
* dofetilide
86
* Which class III drug must have its dose modified in kidney failure patients based on the Creatinine clearance ?
* dofetilide
87
* Which class III drug is infused intravenously for **acute afib or flutter** for conversion to NSR?
* ibutilide
88
* After converting a patient's acute afib back to NSR with ibutilide, should you let them get up and leave?
* No, must monitor EKG continuously until QTc returns to baseline
89
* 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)
* ibutilide
90
* Which class III drug is indicated for prevention of recurrent afib or vtach due to an old mi?
* sotalol
91
* Which class III drug can be used in CHF patients and why?
* Dofetilide because it is not a negative inotrope due to its pure action on IKr channels
92
* how do class IV drugs effect the nodal action potential?
* note threshold is increased
93
* What is the MOA of class IV drugs? * which state/type of channel? * slope of phase 0 * threshold potential * refractory period in AV node
* 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
* How do class IV drugs effect conduction velocity and PR interval?
* decrease conduction velocity * increase PR interval
95
* What are the clinical indications for verapamil and diltiazem?
* termination of supraventricular tachycardias and prevention of recurrence * ventricular rate control in afib/flutter
96
* What are some cardiac and non cardiac side effects of class IV drugs?
* CHF due to negative inotropy * bradycardia * hypotension * heart block * SA node arrest verapamil can cause constipation\*\*
97
* What are two MOAs of adenosine?
* 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
* What is the name of the GPCR that adenosine binds to?
* A1 adenosine receptor
99
* What are two clinical indications for adenosine?
* rapid IV bolus for the acute termination of **re-entrant SVT**​ * also used to induce controlled hypotension
100
* What drug likely caused this?
* adenosine * produces a transient asytole/AV block
101
* What are some side effects of adenosine?
* 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)

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