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