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PHRM 5001 > 11. Anti-arrhythmic Medications > Flashcards

11. Anti-arrhythmic Medications Flashcards

1
Q
  1. What is the definition of automaticity? How do the cells do this? What is this required for?
  2. NO ______ _______ needed.
  3. Describe the automaticity with 2 words.
A
  1. Ability of certain myocardial cells to initiate action potentials –> intercalated discs to allow cell to cell communication required for coordinated muscle contraction
  2. external stimulus
  3. spontaneous and regular
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2
Q
  1. What is an ectopic focus?
  2. What can this do to the heart?
  3. What are 4 possible triggers of an ectopic focus?
  4. Cardiac muscle is highly ________, functioning to regulate _____ _______. What are 3 ways the heart does this?
  5. From the previous question, what does this help to control? (2)
  6. Extrinsic factors can affect ______ _______.
A
  1. Area of electrical activity outside of normal location
  2. Can override the heart’s natural pacemaker (SA node)
  3. Nicotine, Caffeine, Digitalis, and Ischemia
  4. specialized functioning to regulate electrical impulses –> imitates, coordinates, and distributes
  5. BP and C.O.
  6. Intrinsic activity
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3
Q
  1. What does the P wave represent on an ECG?
  2. What does the PR interval represent?
  3. What does the QRS represent?
  4. What does the ST segment represent?
  5. What does the T wave represent?
  6. What does the QT interval represent?
A
  1. depolarization of the atria
  2. delay between atrial ventricular stimulation
  3. depolarization of the ventricles (main pumping action of the heart)
  4. start of ventricular repolarization
  5. repolarization of the ventricles
  6. the time it takes for the ventricles to depolarize and repolarize
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4
Q
  1. What is a supraventricular arrhythmia?

2. What are the 5 possible abnormalities that can be seen on an ECG in this category of arrhythmias?

A
  1. Electrical abnormalities that originate in the SA node, AV node or atrial muscle (originates above the ventricles)
  2. Atrial flutter, Atrial fibrillation, Supraventricular tachycardia, Premature atrial contractions, and Atrial tachycardia
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5
Q
  1. What is a ventricular arrhythmia?
  2. Where specifically in the heart can the electrical abnormalities lie? (4 possible locations)
  3. What are the 4 possible abnormalities that can be seen on an ECG in this category of arrhythmias?
A
  1. Dysfunctions originating below the AV node in the ventricle
  2. Electrical abnormalities in the AV bundle, bundle branches, Purkinje fibres or ventricular muscle
  3. Premature ventricular contractions, Ventricular tachycardia, Ventricular fibrillation, and Torsades de pointes
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6
Q
  1. What is Torsades de Pointes?
  2. What is a cardiac action potential?
  3. 0 is depolarization, what are the other 4 phases that follow in the action potential?
A
  1. Increasing and decreasing in amplitude waveform
  2. 4 phases resulting from differences in ion conductance across cell membranes (usually due to ion movement)
    1. Transient repolarization, 2. Plateau phase of repolarization, 3. Rapid repolarization, and 4. Resting membrane potential
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7
Q
  1. What is the goal of anti-arrhythmic therapy?
  2. What are we concerned with when treating arrhythmias?
  3. What are the 5 signs?
A
  1. To stabilize abnormal heart rhythms
  2. Concerned with signs of instability
  3. Chest pain, ↓ BP, Altered LOC, ↑ WOB/signs of CHF
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8
Q
  1. Cardiac anti-arrhythmic drugs are classified according to what system?
  2. What are the 5 drug classifications within this system?
  3. Class I Na+ channel blockers are ________-________ agents.
  4. What is the MOA?
  5. Effects are exerted on ___-_____ cells. Which 3 are involved?
A
  1. Vaughan-Williams System
  2. Sodium channel blockade, Beta-adrenergic blockade, Potassium channel blockade, Calcium channel blockade, and Other/unknown mechanism
  3. Membrane stabilizing
  4. ↓ slope of phase 0 (depolarization), ↓ amplitude of the action potential
  5. Atrial muscle cells, Ventricular muscle cells, and Conduction tissue
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9
Q
  1. Class Ia Na+ channel blockers pose ______ effects. Class Ib pose ______ effects. Class Ic pose ______ effects.
  2. Class Ia has ______ decrease in slope of phase 0. Class Ib has ______ decrease in slope of phase 0. class Ic has _______ decrease in slope of phase 0.
  3. Class Ia ____ duration of AP. Class Ib ____ duration of AP. Class Ic _____ duration of AP.
  4. class Ia ___ absolute refractory period. Class Ib ___ absolute refractory period. Class Ic ___ absolute refractory period.
A
  1. Ia = moderate effects, Ib = weak effects, Ic = strong effects
  2. Ia = moderate, Ib = small, Ic = significant
  3. Ia = increases, Ib = decreases, Ic = increase or decrease (both)
  4. Ia = increase, Ib = decrease, Ic = increase or decrease (both)
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10
Q
  1. With class I Na+ channel blockers, which cells are slower to depolarize? result?
  2. This class of drugs is useful in treating?
  3. What does this class of drugs prevent? What does this help to avoid? (3)
A
  1. surrounding cells –> ↓ conduction velocity therefore, decreasing HR
  2. increased HR caused by re-entry mechanisms.
  3. Prevent leakage of electrical currents back into impulse generating tissue, thereby avoiding:
    re-stimulation, ↓ refractory period, and premature activation
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11
Q
  1. What type of drug is Quinidine?
  2. What is special about this drug?
  3. What are the 4 net effects when taking this drug?
  4. What are the 3 indications/arrhythmias for taking this drug?
A
  1. Class Ia anti-arrhythmic Na+ channel blocker
  2. prototype drug (one of the earliest drugs of its kind)
  3. Slows AV conduction (between atria and ventricles) , Prolongs PR interval, Slows intraventricular conduction –> widens QRS complex, and Lengthens QT interval
  4. SVT, atrial flutter, and atrial fibrillation
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12
Q
  1. What is the contraindication to using Quinidine?
  2. Which patients should we watch out for due to this contraindication?
  3. What is the precaution when taking this drug? When does this effect happen?
  4. What are the 6 adverse effects?
A
  1. Conduction defects –> can severely slow automaticity
  2. CHF patients d/t negative dromotropic effects
  3. Low concentration = anti-vagal effect (↑ HR) –> rebound effect happens when dosing is off
    • Resp depression/distress (Combined with other dugs (loperamide) or allergies)
      • N/V/D
      • Seizures
      • Tinnitus
      • ↓ BP
      • syncope
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13
Q
  1. What is the other drug name for Procainamide?
  2. What type of drug is this?
  3. This drug is a derivative of?
A
  1. Pronestyl
  2. class Ia anti-arrhythmic Na+ channel blocker
  3. local anesthetic procaine
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14
Q
  1. What must be monitored when taking Procainamide? What should this be monitored for?
  2. What 3 arrhythmias can this drug help treat?
  3. What are the 6 adverse effects with this drug?
  4. Large doses of this drug can be associated with which 4 other arrhythmias?
A
  1. active metabolite N-acetyl procainamide for efficacy/toxicity (short therapeutic window)
  2. ventricular tachycardia, atrial fibrillation, and atrial flutter
  3. Leukopenia – WBC’s , Agranulocytosis – WBC’s , Lupus erythematosus-like syndrome, Hypotension, bradycardia, and other arrhythmias
  4. Vfib, Vtach, asystole, and torsades de pointes
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15
Q
  1. What is the other drug name for Lidocaine?
  2. What type of drug is this?
  3. what does this drug specifically cause?
  4. What can this drug be used to treat?
A
  1. Xylocaine
  2. Class Ib anti-arrhythmic Na+ channel blocker
  3. depression of automaticity
  4. ventricular arrhythmias (Vfib/Vtach) during surgery or after an MI
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16
Q
  1. What is needed in order for lidocaine to maintain NSR?
  2. What are the 2 ways this drug can be given to a patient?
  3. What are the 3 precautions when using this drug?
  4. What are the 5 adverse effects?
A
  1. continuous infusion needed
  2. IV (loading dose 50-100mg) and ETT (dose must be doubled)
  3. hepatic failure, CHF, and certain heart blocks
  4. CNS toxicity –> Drowsiness, Agitation, Seizures, Coma, and Hypotension
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17
Q
  1. What type of drug is Flecainide?
  2. What is this drug used to treat specifically?
  3. What 3 arrhythmias can this drug also be used to treat?
  4. What can this drug cause in some patients?
A
  1. Class Ic anti-arrhythmic Na+ channel blocker (strong)
  2. refractory ventricular arrhythmias
  3. SVT, atrial flutter, and atrial fibrillation
  4. May cause ventricular arrhythmias in some patients (limited usefulness)
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18
Q
  1. What does long term prophylaxis of taking Flecainide pose a risk of? Especially which patients?
  2. When should this drug be taken?
  3. This drug can be used for which type of cases/patients?
A
  1. ↑ morbidity and mortality –> especially CAD patients
  2. when have a structurally normal heart
  3. refractory cases
19
Q
  1. What type of treatment approach should be used with Flecainide? What does this mean in regards to when this medication should be taken?
  2. 94% efficacy rate in converting which arrhythmia into NSR?
  3. What is difficult to treat when using this drug? How is this difficulty treated if it happens? (5)
A
  1. “pill-in-pocket” approach –> taken at the onset of palpitations
  2. atrial fibrillation
  3. toxicity –> Admission to ICU, Activated charcoal administration, Electrolyte replacement, Aggressive use of IV fluids & NaHCO3, and +/- IV fat emulsion
20
Q
  1. The toxicity of Flecainide can be refractory to which 2 classes of drugs?
  2. Following question 1, if the toxicity is refractory, how can we help treat this?
  3. B1 adrenergic receptors are located t/o the heart, found in which 3 areas of the heart?
A
  1. antiarrhythmics and vasopressors
  2. VA-ECMO
  3. Nodal tissue (SA and AV nodes), Conducting tissue, and Atrial and ventricular myocytes
21
Q
  1. Sympathetic stimulation of b1-adrenergic receptors causes what 4 effects?
  2. Blockade of cardiac b1-recpeptors causes which 4 effects?
  3. Non-specific class II b-blockers cause blockade at which 2 receptors? What are 2 examples of this class?
  4. Cardioselective class II b-blockers cause blockade at which receptor(s)? What are 3 examples of this class?
A
  1. Activation of adenylyl cyclase, ↑ cAMP levels, Activation of kinase –>↑ Ca2+ influx,release of stored Ca2+, and Binding of Ca2+ to troponin –> cell contraction
  2. Suppression of SA node automaticity (not fire as often), ↓ force of contraction , ↓ conduction velocity, and ↓ aberrant pacemaker activity
  3. b1 and b2 receptors –> Nadolol and Propranolol
  4. b1 receptors –> Metoprolol, Atenolol, and Esmolol
22
Q
  1. What are the indications for class II b-blockers? (2)
  2. What are the 3 precautions to this class of drugs?
  3. What are 2 adverse effects?
A
  1. Tachyarrhythmia caused by ↑ sympathetic activity, and Baroreceptor-mediated reflex tachycardia
  2. heart failure, bradycardia, and asthma
  3. bronchospasm, and reflex arteriolar vasoconstriction
23
Q
  1. Class III K+ channel blockers delay what phase of the action potential? How does this manifest on an ECG?
  2. What are the 4 net results when taking this class of channel blockers?
  3. What is the other drug name for Amiodarone?
A
  1. Phase 3 repolarization –> manifests as prolonged QT interval
  2. Prolong AP duration, Prolong absolute refractory period, ↓ excitability of cardiac tissue, and Suppress re-entry mechanism
  3. Cordarone
24
Q
  1. Amiodarone is a very _________ drug. Which channel blocker class of actions does this drug portray?
  2. What type of drug is this?
  3. This drug is mainly used for the treatment of which 3 arrhythmias?
  4. What are the 3 MOA’s of this drug?
A
  1. versatile –> class I-IV actions
  2. class III K+ channel blocker
  3. Afib, Vfib and Vtachycardia
  4. ↑ duration of AP, ↓ phase 3 slope, and ↓ conduction velocity
25
Q
  1. What are the 2 precautions to using Amiodarone?
  2. What are 3 adverse effects?
  3. What is the other drug name for Sotalol?
  4. What type of drug is this?
A
  1. caustic (must be diluted before injected in peripheral sites), and increases iodine content causing thyroid problems
  2. Photosensitivity, Thyroid disorders, and Hepatoxicity
  3. Betapace
  4. Class III K+ channel blocker
26
Q
  1. What does Sotalol do to the action potential?
  2. This drug also exhibits which drug class of activity?
  3. Used to stabilize which 4 arrhythmias?
  4. This drug should be used with caution when treating which population of patients?
A
  1. prolongs it
  2. class II
  3. Afib, A flutter, Vfib, and Vtachycardia
  4. patients with history of asthma
27
Q
  1. What is the MOA of class IV Ca+ channel blockers? Where are these effects exerted in the body?
  2. What is essential in nodal cells that is required for an AP to occur?
  3. What 2 Ca+ drugs are used as antiarrhythmics?
A
  1. Inhibit Ca2+ influx through trans-membrane channels –> vascular smooth muscle and cardiac muscle cells
  2. Ca2+ influx essential to nodal depolarization and have an action potential
  3. Verapamil and Diltiazem
28
Q
  1. Blockade of the calcium channels results in which 4 net effects?
  2. This class of drugs is used to prevent? What can this class of drugs be used to control?
  3. What is the other drug name for Verapamil?
A
  1. ↓ HR, ↓ force of contraction, ↓ conduction velocity, and Prolongation of repolarization
  2. SVT’s, can be used to control ventricular rate in Afib (partially effective at AV node)
  3. Isoptin
29
Q
  1. What type of drug is Verapamil?
  2. This drug is a _____ of class ____ agents.
  3. What are the 3 net effects of this drug?
  4. Which drug exhibits the same MOA as Verapamil?
A
  1. class IV Ca+ channel blocker
  2. prototype of class IV agents
  3. Suppresses firing of SA node, Prolongs AV refractory period, and Slows AV conduction velocity
  4. Diltiazem
30
Q
  1. What are 2 contraindications to using Verapamil?
  2. What 2 drugs are good alternatives to b-blockers for asthmatics?
  3. MOA of class V antiarrhythmics? What are the two drugs of interest in this class?
A
  1. preexisting bradycardia and CHF
  2. Verapamil or Diltiazem
  3. miscellaneous drugs that work by unknown or other mechanisms –> digoxin and adenosine
31
Q
  1. What is the other drug name for Adenosine?
  2. What type of drug is this?
  3. This drug is an endogenous _______.
  4. Exhibits negative _________ effects causing?
A
  1. Adenocard
  2. class V antiarrhythmic drug
  3. nucleoside
  4. dromotropic effects slowing conduction through AV node
32
Q
  1. Adenosine has ____/________ hemodynamic effects.
  2. Used to restore NSR in patients with?
  3. This drug has an ultra short half life, of how long?
  4. How should this drug be administered for best results?
  5. What can help to speed the delivery?
A
  1. minimal/transient
  2. PSVT
  3. 12 seconds
  4. through a central line for rapid arrival to site of action
  5. saline flush
33
Q
  1. What is the dose of Adenosine that is required to cause asystole and convert the heart to NSR?
  2. What are the 6 adverse effects of Adenosine?
  3. What is the other drug name for Digoxin?
A
  1. 6-12mg dose
  2. Prolonged bradycardia, Palpitations, Hypotension, Dyspnea, Hyperventilation, and a Cough
  3. Lanoxin
34
Q
  1. What type of drug is Digoxin?
  2. What 2 properties does this drug exhibit? What does this cause?
  3. What are the 3 net effects when taking this drug?
  4. What 3 arrhythmias can this drug be used to treat?
A
  1. Class V antiarrhythmic drug
  2. AV blocking and vagotonic properties –> irritability of vagus nerve reducing HR
  3. Negative dromotropic effect, Prolongs refractory period of AV node, and ↓ conduction through SA and AV nodes
  4. Afib, A flutter, and paroxysmal atrial tachycardia
35
Q
  1. What are 2 contraindications to using Digoxin?
  2. What is a precaution when using this drug?
  3. What are the 2 adverse effects?
  4. This medication is really good for patients with?
A
  1. ventricular arrhythmias and known hypersensitivity
  2. Used with caution in patients with electrolyte disturbances (↓ K+ and Ca2+)
  3. may cause arrhythmias and bradycardia secondary to improvements in force of contraction
  4. concurrent heart failure
36
Q
  1. Many patients experiencing cardiac arrhythmias will also experience?
  2. As circulation takes precedence over airway and breathing, it is essential to manage what? To maintain what?
  3. Catecholamines can be administered to? Resulting in an increase in? (2)
  4. What are the 5 catecholamine vasopressors?
A
  1. hypotension
  2. essential to manage shock to maintain perfusion to vital organs (heart, brain especially)
  3. elicit vasoconstriction of vascular smooth muscle –> increase in SVR and BP
  4. Norepinephrine, Epinephrine, Dopamine, Phenylephrine, and Vasopressin
37
Q
  1. What is the other drug name for Epinephrine? Norepinephrine?
  2. What type of neurotransmitters are these drugs? Secreted by the?
  3. Where do these neurotransmitters travel to? What do they elicit?
  4. How do we titrate these drugs as infusions?
A
  1. epi = Adrenalin and norepi = levophed
  2. Endogenous secreted by adrenal medulla
  3. Travel to sympathetic nerve endings to elicit excitatory response
  4. Titrate to effect
38
Q
  1. Epi and Norepi stimulate which receptors? Located where?
  2. Which receptors are more profound in the vasculature? Therefore, what is the net effect?
  3. What are the 7 adverse effects of taking norepi or epi?
  4. What is extravasation?
A
  1. alpha receptors on vessels and beta receptors in the vasculature
  2. a-receptors> b-receptors in the vasculature therefore, net effect is vasoconstriction
  3. tachycardias, arrhythmias, HTN, ↑ myocardial oxygen consumption, ↑ blood glucose, renal failure, and extravasation of drug may cause tissue necrosis
  4. IV dislodged and gets into tissue, drug into tissue level acts on capillaries within the tissue = vasoconstriction (not enough O2/nutrients to the area)
39
Q
  1. What is the other drug name for Dopamine?
  2. This drug is a precursor to?
  3. What dose is needed to treat septic shock?
  4. This drug causes an increased risk of tachyarrhythmias, why? therefore which drug should be used first to treat shock?
A
  1. Intropin
  2. Norepinephrine
  3. High dose of 15-20 mcg/kg/min (dose dependent)
  4. Due to Dopamine having an increased affinity for b1 receptors therefore, Norepinephrine should be used as initial therapy
40
Q
  1. What is Dopamine used to treat?
  2. What are the 8 adverse effects?
  3. What is the other drug name for Phenylephrine
  4. What type of drug is this? What does this induce?
A
  1. Hypotension
  2. tachycardia, ↑ afterload and myocardial O2consumption, arrhythmias, ↓ peripheral perfusion, ↓ blood glucose, renal failure (doses > 20 mcg/kg/min), fixed, dilated pupils, and extravasation of drug will cause tissue necrosis
  3. Neo-Synephrine
  4. Pure alpha agonist inducing vasoconstriction in vascular beds
41
Q
  1. What does Phenylephrine help to increase? (3)
  2. How is the drug often given? why? dose?
  3. What can infusions of this drug lead to? why?
  4. What are the 8 adverse effects of this drug?
A
  1. SBP, DBP, and SVR
  2. often bolused for transient increase in BP (100mcg/ml increments)
  3. reflex bradycardia d/t unopposed alpha stimulation
  4. bradycardia, arrhythmias, ↑ myocardial oxygen consumption;avoid in patients with left ventricular dysfunction, peripheral or mesenteric ischemia, renal failure, headache, restlessness or excitability, and extravasation of drug will cause tissue necrosis and ulceration
42
Q
  1. What is the other drug name for Vasopressin?
  2. What two effects does this drug exert?
  3. Vasopressin mimics what naturally occurring hormone in our bodies? how?
  4. What levels are decreased in patients with septic shock? Therefore, this drug is useful as __________ therapy.
A
  1. Pitressin
  2. pressor and water-retentive effects
  3. ADH –> Stimulation of vasopressin receptors in the collecting ducts of the kidneys contribute to water conservation
  4. decreased vasopressin levels, therefore this drug is useful in combination therapy
43
Q
  1. How should Vasopressin be administered?
  2. Why does this drug have limited titration ability?
  3. What should an infusion be started at? What can the drug be titrated to?
  4. What are the 9 adverse effects of this drug?
A
  1. via a central line
  2. because drug runs at fixed doses
  3. 1.8-2.4 U/hr, titrated to 1.2 U/hr
  4. GI ischemia, coronary ischemia, fluid retention, sweating, tremor, N/V/D, bradycardia, arrhythmias, and
    ↓ cardiac output

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