Term
| What is the most serious arrhythmia? What is the most common arrhythmia that can be symptomatic? |
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Definition
*Ventricular Fibrillation
*Atrial Fibrillation |
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Term
| What are the three guidelines for treatment of arrhythmias? |
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Definition
*Can't be corrected by underlying cause
*hemodynamic instability
*Predisposes pt to a more serious arrhythmia |
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Term
| What are structural causes of arrhythmias? |
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Definition
*CAD
*Valvular Disease
*Cardiomyopathies
*Sick Sinus Syndrome
*Prolonged QT Syndromes
*Wolfe Parkinson White |
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Term
| What are transient imbalances that cause arrhythmias? |
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Definition
*Stress
*Electrolyte imbalance or metabolic imbalance
*Hypoxia
*Hypercarbia
*ICD/Pacemaker/EMI
*Surgical Stimulation
*Anesthetic agents (or lack of) |
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Term
| What is the only antiarrhythmic medication that is recommended for prophylactic use in STEMI patients? |
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Definition
| *Class II antiarrhythmics (Beta Blockers) |
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Term
| Why is routine use of class I antiarrhythmics is contraindicated post-MI? |
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Definition
| *Due to increased mortality from both arrhythmic and nonarrhythmic cardiac cases. |
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Term
| What has superceded pharmacologic therapy of sustained post-STEMI arrhythmias? |
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Definition
| *ICDs and Radio frequecy ablation |
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Term
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Definition
*Agents that interfere with the Na+ channel
*Further divided into A,B,& C.
*Example: Lidocaine |
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Term
| What are Class II agents? |
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Definition
*They are anti SNS agents
*Ex: Beta Blockers |
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Term
| What are Class III agents? |
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Definition
*Class III agents affect K+ Efflux
*Amiodarone |
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Term
| What are Class IV agents? |
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Definition
*Agents that affect the AV node
*Ex: Calcium Channel Blockers |
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Term
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Definition
*Agents that work by other unknown mechanisms
*Digoxin and Adenosine |
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Term
| What is the Mneumonic for class I-IV agents? |
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Definition
*SoBe PoCa (SOBE as in south beach or the drink, POCA as in Polka)
*Sodium channel blockers, beta blockers, potassium channel blockers, Calcium channel blockers |
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Term
| Changing what in the action potential changes your heart rate? |
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Definition
| *Changing the slope of phase 4 |
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Term
| What drug was one of the first antiarrhythmics, Class Ib and derived from the Cinchotic plant? |
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Definition
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Term
| What is the dose for Quinidine? Therapeutic level? What is the toxicity called? |
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Definition
*Dose 300-500x 4/day
*Therapeutic level 2-8 ug/mL
*Toxicity: Cinchonism- leads to visual disturbances, confusion. Has the lowest toxicity of any of the anti-arrhythmics. |
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Term
| What is used for ventricular arrhythmias, is effective in suppressing reentry cardiac dysrhythmias such as PVCs and Vtach? |
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Definition
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Term
| What class is Lidocaine and what does it do? |
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Definition
| *Is a Class IB drug that suppresses automaticity and shortens the effective refractory period. |
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Term
| What is the MOA of Lidocaine? |
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Definition
*Delays the rate of spontaneous phase 4 depolarization by preventing or diminishing the gradual decrease in K+ ion permeability
*No significant decrease in BP, contractility or CO |
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Term
| What is the onset of Lidocaine? Peak? Duration? Metabolism? Dose? Infusion? Max dose? Therapeutic Level? |
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Definition
*Onset: 45-90 sec
*Peak: 1-2 min
*Duration: 10-20 min
*Metabolized by liver by oxidative dealkylation to monoethylglycineexylidide
*Dose: 1-1.5mg/kg
*Infusion: 1-4 mg/min
*Max dose: 200-300mg in 1 hour
*Therapeutic level: 2-5mcg/mL |
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Term
| Who is lidocaine contraindicated in? What are the adverse effects with toxicity? |
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Definition
*C/I in patients with amide sensitivity
*Caution with other antidysrhythmics
*Reduced clearance with concomitant use of beta blockers or cimetidine
*Toxicity:
-CV:hypotension and bradycardia (8mcg/mL)
-Pulmonary: Respiratory depression, arrest (>10mcg/mL)
-CNS: Tinnitus, seizures (5-10mcg/mL), CNS depression >10mcg/mL
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Term
| At what plasma level do side effects start to occur with Lidocaine? |
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Definition
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Term
| What drug is used mostly for arrythmia control in MH or treatment of lidocaine/amiodarone resistant ventricular arrythmia, afib or PSVT? |
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Definition
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Term
| What is a Class IA anti-dysrhythmic (membrane stabilizer)? |
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Definition
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Term
| What is the MOA of Procainamide? |
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Definition
*Increases the effective refractory period and reduces impulse conduction velocity in the atria, His-Purkinje fibers and ventricular muscle.
*Variable effect on AV conduction, slowing effect on AV node
*Direct myocardial depression level >8mcg/mL |
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Term
| Procainamide: Onset, Peak, Duration, Metabolism, Loading dose, Max dose, maintenance infusion, and therapeutic level |
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Definition
*Onset: Immediate
*Peak Effect: 5-15 min
*Duration- 2.5 OR 5 hours (fast or slow acetylator)
*Metabolism: Undergoes hepatic acetylation to an active metabolite, N-acetyl procainamide (NAPA)
*Load 100mg IV, Q 5 min
*Max dose is 1gm
* Maintenance infusion is 2-6 mcg/min
*Therapeutic level: 4-12 mcg/mL |
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Term
| What are the special considerations with Procainamide? |
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Definition
*Reduce dose in CHF or renal
*Contraindicated in complete heart block, Lupus, and Torsades
*Monitor plasma levels, VS and ECG
-QRS widening of >25% may signify toxicity
*Hypotension may occur with administration
*Caution with digoxin/digoxin toxicity
*Increased serum levels with cimetidine
*Potentiates NDMR and DMR
*Side effects: lupus like syndrome |
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Term
| What is a potent antidysrhythmic with a wide spectrum of activity against refractory SVT and ventricular tachydysrhythmias? |
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Definition
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Term
| What is Amiodarone used in the treatment of? |
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Definition
*Refractory V-fib
*Afib/flutter
*PSVT
*WPW |
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Term
| How does amiodarone act on the body? |
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Definition
*Potent vasodilator
*Acts directly on the myocardium to prolong action potential duration and increase the refractory period
*Weak Na channel antagonism
*Vagolytic and Ca channel blocking effects
*Noncompetitively inhibits alpha and beta receptors |
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Term
| What is the half life of Amiodarone? Onset? Dose? Infusion? |
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Definition
*New addition to VT/VF algorithm (replaced lido) also used in stable tachycardia algorithm
*Extensive protein binding
*Extremely long 1/2 life 40 days
*Onset: IV immediate- PO 2-4 days
*Dose: 150mg load over 10 minutes up to 300mg. Or 300mg over 10 for cardiac arrest
*Infusion 1mg/min for 6 hours, 0.5mg/min for next 18 hours |
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Term
| What are possible side effects with Amiodarone? |
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Definition
*High incidence of side effects 75%
*Caution with Dig and Dilantin d/t extensive protein binding and drug displacement
*Pulmonary toxicity, pulmonary edema, dyspnea, cough ARDS
*Peripheral neuropathy, tremors
*Hepatitis, elevated liver enzymes
*Blurred vision, optic neuropathy, blindness
*Photosensitivity
*Thyroid effects
*Need glass bottle for stability |
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Term
| How do beta blockers work? |
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Definition
| *Beta antagonists bind to Beta receptors and interfere with the ability to catecholamine to provoke Beta responses. |
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Term
| What are Beta Blockers derivatives of? |
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Definition
| *Derivatives of Beta agonist Isoproterenol. Substitutions on the Benzene ring determine whether the drug acts like an agonist or antagonist. |
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Term
| What are the most common uses for Beta Blockade? |
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Definition
*Tx essential HTN
*Angina Management
*Post MI treatment
*Pre-op hyperthyroid management
*Suppression of dysrhythmias
*Prevention of SNS activity |
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Term
| What receptors are blocked with Propranolol (Inderal)? |
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Definition
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Term
| What receptors are blocked by Timolol (Timoptic)? |
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Definition
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Term
| What receptors are blocked by Metoprolol (Lopressor)? |
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Definition
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Term
| What receptors are blocked by Atenolol (Tenormin)? |
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Definition
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Term
| What receptors are blocked by Esmolol (Brevibloc)? |
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Definition
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Term
| What receptors are blocked by Labetolol (Trandate)? |
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Definition
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