Flashcards in Na+ channel blockers and Beta blockers Deck (26):
Na+/K+/ATPase pump inhibitor
positive inotrope --> increased intracellular Ca2+ (reduced NCX activity) --> increased contractility and SV
negative chronotrope --> prolongation of AP in SA node = decreased HR
**toxic side effects, not first line
Class I Na+ channels blockers alter effective refractory period based on________.
non-specific K+ channel blockage
moderate Na+ channel blockade
increased effective refractory period
weak Na+ blockade
decreased effective refractory period
strong Na+ blockade
no net effect on effective refractory period
-inhibit sympathetic activation of cardiac automaticity
-used to prevent and treat supraventricular arrhythmias
Beta blockers effect on AV node conduction:
What would this look like on EKG?
Decreased AV node conduction
Increased PR interval
Beta blockers effect on AV node refractory period:
Beta blockers effect on ventricular conduction and repolarization:
little to none
Beta blocker with some Class I activity
-AE: bronchospasm, bradycardia, fatigue
-better for pts with asthma
Short acting B-blocker
-used intraoperatively and in acute arrhythmias
-prolongs action potential (delays slow outward K+ current)
Cardiac effects: slows AP, slows conduction, prolongs QRS, prolongs APD via non-specific K+ blockade
Extracardiac effects: ganglion blocking --> reduces peripheral vascular resistance can cause hypotension
Tox: excessive AP prolongation, long QT, TORSADES de POINTES arrhythmia and syncope, excessive slowing of conduction
-long term can cause lupus like syndrome
PK: metabolite (NAPA) has class III activity associated w/ TORSADES
-hepatic metabolism of NAPA and renal excretion
-NAPA has longer half-life than procainamide
-plasma protein binding 15-20%
Used in: atrial and ventricular arrhythmias
-2nd or 3rd line for sustained ventricular arrhythmias associated with acute MI
Cardiac effects: slows upstroke of AP, long QRS, long APD (non-specific K+ blockade), ANTIMUSCARINIC effects
Extracardiac effects: GI, cinchonism (HA, dizziness, tinnitus) at toxic conc.
Tox: long QT, TORSADES
PK: GI absorption, hepatic metabolism, renal excretion
Used in: rarely used d/t side effects and availability of less toxic drugs
Cardiac Effects: slow upstroke of AP, slow conduction, long QRS, long APD (via non-specific K+ blockade), antimuscarinic
Extracardiac effects: Atropin-like activity --> urinary retention, dry mouth, blurred vision, constipation
Toxicity: same as Quinidine. may precipitate HF de novo or in preexisting depression of LV function. Not first line in USA or in pts with HF.
PK: NO loading dose --> de novo HF.
-Hepatic metabolism, renal excretion.
-protein binding 50-60%
Used in: ONLY ventricular arrythmias in USA.
Cardiac effects: selective depression of conduction in depolarized cells. Little effects on EKG in NSR.
Extracardiac effects: not much?, pretty well tolerated
Tox: one of the least toxic class I's, neurologic: paresthesias, tremor, nausea of central origin, lightheadedness, hearing disturbances, slurred speech, and convulsions. These occur most commonly in elderly or otherwise vulnerable patients or when a bolus of the drug is given too rapidly
PK: extensive first pass hepatic metabolism --> only 3% of oral admin gets to plasma...... must give parenterally. Half-life 1-2 hours.
Used in: first line for V-tach and preventing V-fib AFTER cardioversion in acute ischemia
****prophylactic use may increase total mortality
Cardiac effects: orally active congener of lidocaine
Extracardiac effects: good efficacy in relieving chronic pain --> esp d/t diabetic neuropathy and nerve injury (off-label)
Tox: predominantly neurologic, including tremor, blurred vision, and lethargy
PK: elimination half-life is 8–20 hours and permits administration two or three times per day
Uses: Ventricular arrhythmias, chronic pain (off label)
Cardiac effects: selective depression of conduction of depolarized cells (not much change on EKG in NSR)
Lidocaine analog withOUT sig first pass metabolism
***not sold in USA
Cardiac effects: slows upstroke of AP, slows conduction. Potent Na+ and K+ blocker--SLOW unblocking kinetics. Does NOT prolong AP or QT.
Tox: severe exacerbation of arrhythmia in patients with preexisting ventricular tachyarrhythmias, previous myocardial infarction and ventricular ectopy
PK: half-life of approximately 20 hours. Elimination is both by hepatic metabolism and by the kidney
Uses: PVCs, supraventricular arrhythmias
Cardiac effects: slows upstroke of AP, slows conduction. Weak Beta-blocker. No effect on AP duration.
Tox: metallic taste and constipation
PK: metabolized in the liver, with an average half-life of 5–7 hours
Uses: supraventricular arrhythmias
Cardiac effects: Potent Na+ channel blocker, no prologation of AP.
used to treat ventricular arrhythmias
***not sold in USA
Cardiac effects: non-selective beta antagonist. decreases heart rate, myocardial contractility, blood pressure, and myocardial oxygen demand
Tox: a lot; see Katzung's
PK: Extensive first-pass effect, hepatically metabolized. Oral: ~25%; oral bioavailability may be increased in Down syndrome children; protein-rich foods increase bioavailability of immediate release formulations by ~50%
Uses: mostly HTN, also migraine prophylaxis
Cardiac effects: β1, β2 antagonist, with intrinsic sympathomimetic (partial agonist) effect
-Lower BP • modestly lower HR
Uses: Hypertension • arrhythmias • migraine • may avoid worsening of bradycardia
PK: Oral •
Toxicity: Fatigue • vivid dreams • cold hands
Cardiac effects: Blockade of β1 > β2. Very brief cardiac β blockade
Uses: Rapid control of BP and arrhythmias, thyrotoxicosis, and myocardial ischemia intraoperatively
PK: Parenteral only • half-life ∼10 min •
Toxicity: Bradycardia • hypotension