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60 Cards in this Set
- Front
- Back
transmembrane potential is determined by?
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Na, K, and Ca
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molecular gate status controlled by?
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1) ionic conditions
2) metabolic conditions 3) tranasmembrane voltage |
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conductance is determined by?
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characteristics of ion channel protein
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current flow = ?
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voltage X conductance
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voltage =?
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actual membrane potential - membrane potential at which no current would flow, even with channels open
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cardiac action potential
1) phase 0: depolarization |
1) fast upstroke
2) Na channels open (inflow of Na ions) 3) Quinidine blocks Ns current |
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2) phase 1: rapid repolarization
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1) inactivation of Na channels
2) K channels rapidly open and close 3) early repolarizing K current 4) rapidly inactivated 3) open Ca channels |
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3) phase 2: plateau
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1) Ca chennels left open
2) Ca chnnel blockers act here |
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4) phase 3: final repolarization
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1) Ca channels close
2) K channels open (K move to outside) |
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5) phase 4: slow spontaneous repolarization
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1) all the channels are closed
2) resting potential |
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Na: concentration gradient
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1) 140 mmol/L outside
2) 10 mmol/L inside |
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Na: electrical gradient
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1) 0 mV outside
2) -90 mV inside |
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driving force of Na?
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both electrical and concentration
(tending move Na into the cell) |
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K: concentration gradient
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1) 4 mmol/L outside
2) 140 mmol/L inside |
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concentration gradient tends to drive K?
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out
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electrical gradient tends to?
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hold K in
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some K channels ("inward rectifier") are open in the resting state - however, little K current flows because of?
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the balance between the K [ ] and memb. electrical gradients
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cardiac resting membrane potential is mainly determined by?
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1) extracellular K [ ] and
2) inward rectifier channel state |
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spontaneous depolarization occurs because?
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1) gradual > in depolarizing currents
(increaing memb. permiability to Na or Ca) 2) < in repolarizing K currents (decreasing memb. K permeability) |
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The maximum upstroke slope of phase 0 is proportional to?
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the Na current
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phase 0 slope is related to?
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the conduction velocity
(the more rapid the rate of depolarization the greater the rate of impulse propagation) |
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Phase 2 is the combination of?
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an inward, depolarizing Ca current balanced by an outward, repolarizing K current (delayed rectifier)
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phase 3 is the combination of?
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Ca and K currents
1) > outward (repolarizing) K current 2) < inward (depolarizing) Ca current |
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phase 4 in normal His-Purkinje and ventricular muscle cells is characterized by>
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a balance between
1) outward Na current and 2) inward K current |
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medications for A-fib?
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1) Ca channel blocker (Verapamil, Dilt)
2) beta blocker (Propranolol) 3) Digitalis glycosides |
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Tx/maintenance of normal SR?
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1) Quinidine
2) Procainamide |
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management of PSVT?
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1) vagal maneuver
2) alpha-adrenergic receptor agonist 3) Digoxin 4) drugs that reduce AV transmission |
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the drugs that reduce AV transmission?
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1) Adenosine
2) Verapamil 3) Diltiazem 4) Esmolol 5) DC cardioversion |
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anti-arrythmic drugs may work by?
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1) suppressing initiation site (automaticity/after-depo.)
2) preventing early or delayed afterdepo. 3) disrupting a re-entrant pathway |
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automaticity may be diminished by?
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1) increasing the maximum diastolic memb. potential
2) decreasing the slope of phase 4 depo. 3) increasing AP duration 4) raising the threshold potential |
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1) anatomically determined re-entry (WPW) the arrythmia can be resolved by?
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blocking AP propagation
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2) termination for functional (non-anatomical) reentry circuits?
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to prolong refractoriness
(ex. Na channel blockers) |
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Na cahnnel blockers reduce?
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the percentage of recovered channels
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Na channel blocking antiarrythmic drugs are classified as "use-dependent" because?
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their effectiveness is dependent upon the frequency of channel opening
(they bind to "open" Na channels) |
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Type 1a: Prototype
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1) Quinidine
2) slow the rate of AP rise 3) prolong ventricular effective refractory period |
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Quinidine
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1) type 1a
2) D-isomer of quinine 3) antimalarial 4) antipyretic |
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Quinidine: pharmacokinetics
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1) 80-90% bind to plasma albumin
2) rapid oral absorption 3) No IM 4) limited IV administration |
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IV administration of Quinidine is limited because?
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1) myocardial depression
2) peripheral vasodilation |
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Quinidine is metabolized by?
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1) liver, hydroxylation to inactive metabolites
2) followed by renal excretion 3) careful in pts with impaired renal/hepatic function |
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decreased Quinidine blood levels with?
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1) phenytoin
2) phenobarbital 3) rifampin (P-450 inducers) |
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action of Quinidine?
Quinidine depresses? |
1) ectopic pacemaker activity
2) conduction velocity 3) excitability |
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Quinidine also slows?
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recovery from Na channel blockade in depolarized tissue
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Quinidine (Na channel blocker) also blocks?
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K channels
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Quinidine's effect on the ECG: QT interval lengthening because?
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Quinidine-mediated reduction in repolarizing outward K current
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Na channel blockade results in?
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1) an increased threshold
2) decreased automaticity |
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Quinidine is used for?
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1) A-fib/A-flutter
2) V-tac 3) PVCs 4) SVT from WPW |
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Why do you have to give Digitalis prior to Quinidine administration?
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to prevent paradoxical increase in ventricular response due to Quinidine's vagolytic effect at the AV node
(Digitalis = vagotonic, increase vagal tone at the AV node) |
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cardiovascular side effects of Quinidine (>2 mcg/ml)?
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1) > PR, QRS, QT
2) heart block 3) Quinidine syncope 4) hypotension esp. with IV admi. 5) tachycardia 6) Torsades de pointes (> QT) |
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other adverse effects of Quinidine?
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1) cinchonism
2) N/V, diarrhea 3) Digitalis toxicity 4) enhance the effect of NMB 5) recurrence of skeletal muscle paralysis post-op |
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S/S of cinchonism?
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1) blurred vision
2) decreased hearing acuity 3) GI upset 4) headaches 5) tinnitus |
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Procainamide: class 1a is used for?
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1) SVT
2) Vent. arrythmia 3) suppress PVCs |
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Procainamide is?
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local anesthetic (Procaine) analog
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elimination of Procainamide?
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1) 40-60 % excreted unchanged (renal)
2) Acetylation (hepatic) 3) highly resistant to hydrolysis by plasma esterases |
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cardioactivi metabolite of Procainamide?
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NAPA (N-acetylprocainamide)
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NAPA accumulation lead to?
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Torsades de pointes
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Procainamide: the difference compared to Quinidine?
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1) No vagolytic (antimuscarinic) activity
2) less hypotension (does not block alpha) |
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side effect from long term use of Procainamide?
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reversible lupus erythematosus-like syndrome
(25-50 % occurance) |
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S/S of LE
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1) serositis
2) arthralgia 3) arthritis 4) pluritis 5) pericarditis 6) parenchymal pulmonary disease |
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Disopyramide (Norpace): class 1a
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1) similar to Quinidine
2) greater antimuscarinic effects |
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Class 1a drugs?
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1) Quinidine
2) Procainamide 3) Disopyramide (Norpace) |