Pharmacology
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| Name two calcium channel blockers that slow heart rate and decrease conractility? | Diltiazem
Verapamil
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| What is the drug of choice to decrease oxygen demand? | Beta Blocker
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| How does Ranolazine (non-dihydropyridine)work? | Improves efficiency of oxygen utilization
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| What are three things Ranolazine does not do? | Decrease heart rate or blood pressure and reduce contractility
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| What are the side effects of Ranolazine (non-dihydropyridine)? | Dizziness, headache, constipation, QT prolongation
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| When taking Ranolazine what are some contraindications? | Do not use with antifungals, or grapefruit juice
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| Ranolazine dosage (non-dihydropyridine) | 500 mg BID initially
Can titrate to 1000mg BID
second or third line agent for angina
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| What is drug of choice for acute angina? | Nitroglycerine
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| What are nitrate side effects? | headache, hypotension (causes venous dilation than arterial), nausea/vomiting, dry mouth, **TOLERANCE**
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| True or False, Ranolazine is a 3A4 substrate and grapefruit juice will cause an increase of buildup of this medication? | True
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| After which dose of nitrate do you call 911? | Take first dose and wait 5 minutes, take second dose and wait 5 minutes, if still having CP after 10 minutes, take 3rd dose and call 911
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| What is brand name of Isosorbide mononitrate Extended Release? | Imdur
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| How do you take Imdur? | This is a long acting nitrate, taken once a day in the morning. Runs out after 12-14 hours to give you that nitrate free interval.
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| How do you take Isosorbide dinitrate? | Once in the morning and then in afternoon at least 7 hours apart, do not take evenly spaced to give you the nitrate free period needed.
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| Use nitrates cautiously in patients with? | Glaucoma, severe anemia, hyperthyroidism, hypovolemia, hyperthyroidism
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| What is the shelf life of nitroglycerine? | 6 months, it is sensitive to light and oxygen
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| What is dosage for Isosorbide mononitrate? | 30-120mg once daily
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| What is phase 4 of the cardiac action potential? | The reset phase, where Na-K-ATPase puts cations where they are supposed to be
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| What happens in phase 0? | Na rushes into the cell and becomes very positive.
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| What happens in phase 1 and 2? | Calcium rushes in and Potassium goes out of the cell, plateau phase
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| What happens in phase 3? | Potassium continues to rush out of the cell and produces a hypernegative charge.
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| Mechanism of antiarrhythmics: what phase decreases automaticity? | Phase 4
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| Mechanism of antiarrhythmics: what phase increases the refractory period? | Phase 2 and 3
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| Mechanism of antiarrhythmics: what phase slows conduction velocity? | Phase 0
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| Mechanism of antiarrhythmics: what phase limits reentry? | Phase 1,2,3,and 4
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| What is the resting phase of ion channels? | Closed but ready to go
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| What is the active phase of ion channels? | Open
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| What is the inactive phase of ion channels? | Closed and can't be opened
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| Which medications affect the Na Channel? | Ia. Procainamide, quinidine
Ib. Lidocaine, mexilitine
Ic. Propafenone, flecainide
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| Which medications affect the nodal channel? | Beta blockers (SA and AV node)
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| Which medications affect the K channel? | Amiodarone, sotalol,...
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| Which medications affect the nodal Ca Channel? | Calcium channel blockers
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| Class Ia agents affect which two channels? | Na and K- slow down initial depolarization and lengthen phase 2 and 3 by slowing down K release
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| Class Ib agents have? | Rapid on-off kinetics, have little effect on normal heart rate(work well on tachy arrhytmias in phase 0)
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| Class Ic agents have? | Slow on-off kinetics result in greater effects on phase 0. More pronounced slowing of conduction.
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| Class II and IV Beta and Calcium channel blockers slow which phase? | Phase 4, most specifically at the AV and SA nodes.
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| Which medication effects K to increase refractory period, has beta blocker properties and decreases automaticity, and Na channel blockers to decrease repolarization. | Amiodarone
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| Used for supraventricular and ventricular arrhythmias | Class Ia and Ic
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| Used for ventricular arrythmias | Class Ib
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| Used for supraventricular rate | Class II and IV
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| How do high K levels effect digoxin? | Digoxin won't work as well.
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| How do low K levels effect digoxin? | Digoxin levels can become toxic.
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| What are toxicity signs of digoxin? | Nausea, vomiting, weakness, and altered mental status. May see green halos but not common.
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| Which two drugs can be used with impaired cardiac function for rhythm control? | Amiodarone and Dofetilide
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| When treating atrial fibrillation, which is more important: rate or rhythm control | Rate control
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| What is the half life of amiodarone? | 7 weeks- requires loading dose for sooner steady state.
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| Amiodarone pharmacodynamic drug interactions? | Beta blockers, Ca Channel blockers, digoxin, most other antiarrhythmics, and anything with QT prolongation. Additive effect of bradycardia.
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| Amiodarone pharmacokinetic drug interactions? | Warfarin (increases INR levels), digoxin, cyclosporine, opiates, statins, phenothiazines, triptans, anti-epileptics.
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| Adverse Drug reactions with chronic use of amiodarone | Pulmonary toxicity, pneumonitis, fibrosis, hepatoxicity, optic neuropathy/corneal deposits, hypo/hyperthyroid, peripheral neuropathy paresthesias, ataxia, weakness tremor, photosensitivity, skin discoloration, Stevens-Johnson, blood dyscrasias
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| Important monitoring for amiodarone? | EKG and CXR, electrolytes (esp K and Mg)baseline TSH, LFT and PFTs, Visual exam 6-12 months.
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| Half-life of amiodarone | 7 weeks long
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