Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

60 Cards in this Set

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