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59 Cards in this Set
- Front
- Back
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Digoxin
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Na/K ATPase blocker
Positive inotropic effect Negative chronotropic effect |
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Dig therapy
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Sinus node- DecreasedRate
Atrial muscle- Decreased Refractory period Atrioventricular node-Decreased Conduction velocity, increased refractory period Purkinje system, ventricular muscle-Slight decrease refractory period Electrocardiogram-Increased PR interval, decreased QT interval |
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Pharmacokinetics of dig
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75% good oral bioavailability, T 1/2 40 hrs., greater than 40% metabolized
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ADR of dig
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N/V/D, anorexia, visual distrubances, headache, confusion, hallucinations
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Dig toxicity
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VT, VF, hypokalemia, hyperkalemia, hypercalcemia, AV block, PVC
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Treatment of dig toxicity
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K+ salts, antiarrythmics, dig immune fab
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drug interactions with dig
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diuretics, quinidine
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Beta adrenergic drugs
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Dopamine and dobutamine
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Dobutamine mechanism
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Stimulate beta 1 adrenergic receptors and increase cardiac contractility, enhance intracellular calcium in myocytes
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Phosphodiesterase inhibitor
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Inamrinone
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Inamrinone mechanism
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Inhibits degredation of cAMP increasing myocardial contractility
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Inamrinone use and ADR
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use: acute heart failure
ADR: liver and bone marrow toxicity and arrythmias |
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Drugs used in CHF
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Diuretics, aldosterone receptor antagonists, ACE inhibitors, angiotensin receptor blockers, beta blockers, cardiac glycosides, vasodilators, beta agonists, bypyradines,
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forward heart failure
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systolic failure, ventricle unable to pump effectively, so reduced CO
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backward heart failure
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CHF, diastolic failure, ventricles cannot fill adequately so back flow of fluid causing pulmonary congestion
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Excitability def and formula
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measure of strength of stimulus needed to form action potential
Excitability= (Resting potential - Threshold potential)^(-1) |
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Conductivity and times of conductance of different cardiac tissues
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Rate of movement of a stimulus from one cell or tissue to the next.
Atria 1 m/s A/V node 0.1 m/s His/perkinje 1-2 m/s Ventricle 0.4 m/s |
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Refractoriness
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inability to stimulate an action potential
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Effective refractory period
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another stimulus at this time will not generate another action potential
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relative refractory period
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a larger than normal stimulus at this time may produce another action potential
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Reentry
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A loop which allows electricity to flow back into cell and repeatedly depolarize cells and can lead to tachyarrythmias.
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Escape beats
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at a conduction block ectopic pacemakers take over pacemaker function
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by pass tracts
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pathway that avoids AV conduction. mechansim that Wolff-Parkinson-White disease uses. can lead to reentry problems
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verapamil
diltiazem (CARDIZEM) |
calcium channel blockers
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Amiodarone
Bretylium Sotolol |
K+ channel blockers
Prolong repolarization |
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Metoprolol
Esmolol Propranolol |
Beta blockers
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Quinidine
Procainamide Disopyramide |
Moderate Na+ channel blockers
Class Ia Prolong repolarization |
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Lidocaine
Tocainide Mexiletine Phenytoin |
Class Ib
Shorten repolarization Mild Na+ blockade |
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Flecainide
Propafenone |
Class 1C
No repolarization change Marked block of Na |
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class 1a antiarrythmics effects
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prolong QRS
prolong QT prolong ventricle repolarization decrease automaticity anticholinergic effects |
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class 1a toxicity
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VTach
Fainting |
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indications for class 1a drugs
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SVT
AFib/flutter ventricle arrythmias |
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quinidine info
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derived from quinine
antimalarial causes gi disturbances Vtach interacts with dig, diuretics, |
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procainamide info
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can cause lupu like symptoms
undergoes N-acetylation |
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class 1b effects
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shorten QT
decrease ventricular automaticity |
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ADR class 1b antiarrythmics
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dizziness, psychosis, CNS depression, tremor, convulsions
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class 1b indications
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post MI, ventricular arrythmias
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lidocaine info
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extensive first pass metabolism, no PO, T1/2 2 hrs, IV loading/maintainance dosing,
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mexiletine
tocainide |
orally active analogs of lidocaine
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class 1c antiarrythmic effect
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widening QRS and PR interval, minimal QT
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1c toxicity
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aggravate an AV block, V-tach
increased mortality with encainide and flocainide |
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1c indications
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WPW syndrome, re-entry problems, ventricular arrythimas
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class 1c drugs
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flecainide
propafenone moricizine |
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class 2 anti arrythmic beta blocker effects
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decrease rate of firing, decrease automaticity, decrease HR, increase PR, decrease cardiac work and oxygen consumption, reduce reinfarction
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class 2 beta blocker examples
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esmolol and propranolol
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K channel blockers class III mechanism
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increase effective refractory period, decrease reentry
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K channel blocker examples
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Amidorone, Sotolol, Bretylium
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Amiodarone effects
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Prolong resting potential and action potential duration
No significant Na channel blockade Increased PR, QRS, QT intervals Vasodilation |
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Amiodarone ADR
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microdeposits in cornea
pulmonary fibrosis peripheral neuropathy abnormal liver function thyroid dysfunction photosensitivity |
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class IV, Ca channel blockers
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increase refractory period of AV node, decrease conduction velocity at AV node
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verapamil mechanism
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reduce contractility,
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treatments of angina
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nitrates, beta blockers, Ca channel antagonist
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steal effect
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blood is shunted away from ischemic region of heart towards a region which is well perfused due to less resistance
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drugs to decrease preload during angina
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nitrates/nitrites
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drugs to decrease afterload in angina
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Ca channel blockers
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mechanism of nitroglycerine
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NO activates guanyly cyclate to activate cGMP which dephosphorylates the myosin light chain to promote vasodilation
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Ca channel blocker mechanism in angina
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decrease myocardial contractility to reduce O2 consumption
decreased vascular resistance relief of coronary artery spasm |
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beta adrenergic blockers mechanism in angina
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decreased contractility and rate to reduce O2 demands
lower HR increases diastolic perfusion times which reduces ischemic damage often used as a prophylactic |
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ADR of beta blockers in angina
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increase in EDV and increase in ejection time increase myocardial demand
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