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89 Cards in this Set
- Front
- Back
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Two major physiologic mechanisms that cause ectopic cardiac dysrhythmias
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1. Reentry
2. Automaticity |
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Factors associated with cardiac dysrhythmias are:
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1. Arterial hypoxia
2. Electrolyte and acid-base abnormalities 3. Myocardial ischemia 4. Altered sympathetic nervous system activity 5. Bradycardia 6. Administration of certain drugs |
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Phase 0
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Voltage dependent sodium channel opens and rapid sodium influx depolarizes cell
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Phase 1
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Rapid phase of repolarization caused by inactivation of sodium influx and activation of a transient outward potassium current
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Phase 2
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Plateau phases characterized by low membrane conductance and activation of a slow inward calcium current
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Phase 3
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Repolarization to resting potential results from outward K+ current
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Phase 4
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outward K+ current is deactivated and an inward Na+ current reduces transmembrane potential
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Class I
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Sodium Channel Blockers
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Class II
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Beta Blockers
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Class III
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Prolong Repolarization
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Class IV
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Calcium Channel Blockers
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MOA of CCB
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increase action potential threshold of calcium channels
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CLass I Drugs MOA
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slow conduction velocity
prolongs refractory period decreases rate of phase 0 repolarization |
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Two main ways Class I drugs work
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decrease automaticity
prolongs refractory period depress conduction in bypass tracts |
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Class IA MOA
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depress phase o depolarization, prolong the action potential duration, and slow conduction velocity
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Class IB drugs MOA
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shorten the action potential duration and have little effect on phase O depolarization
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Class IC MOA
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Markedly depress phase O depolarization, minimally affect the action potential duration and profoundly slow conduction velocity
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IA examples
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Quinidine
Procainamide (pronestyl) Disopyramide (norpace) |
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IB examples
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Lidocaine (xylocaine)
Mexiletine (mexitil) Tocainide (tonocard) Phenytoin (dilantin) |
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IC examples
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Flecainide (tambocar)
Propafenone (rythmol) |
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Class II examples
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Propranolol (Inderal)
Esmolol (kerlone) |
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Class III examples
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Amiodarone
Ibutilide (corvert) |
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Class IV examples
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Verapamil
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Unclassified Drugs Examples
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Moricized (ethmozine)
Digoxin (lanoxin) Adenosine (adenocard) Sotaol (betapace) |
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Important consideration for Procainamide
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decrease dose for renal impairment
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Procainamide IA use
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tachyarrythmias
AFib |
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Procainamide IA MOA
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Prolong QRS and cause ST-T changes
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Procainamide IA Dose (prior to control of dysrythmia)
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100mg q 5 min until cardiac dysrhythmia is controlled or the total dose reaches about 15mg/kg
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Procainamide IA Dose (after control of dysrythmia)
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Once the cardiac dysrhythmia is controlled infusion of 2-6mg/min
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Lidocaine IB MOA
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Decreases the rate of phase 4 Depolarization
by diminishing K ion permeability |
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Lidocaine IB use
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Ventricular dysrhythmias
Suppress reentry PVC, V—TACH |
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Lidocaine IBDose
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IV 2mg/kg, 1-4mg/min infusion
IM 4-5mg/kg absorption 15 min |
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Important note about Lidocaine IB metabolites
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Metabolites may poses cardiac antidysrhythmic activity
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Lidocaine IB Metabolism
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liver
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plasma concentration at which lidocaine causes seizures
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5-10ug/ml
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Lidocaine IB plasma concentration < 5ug/ml causes
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Devoid of effects on the ECG or CV when plasma concentration < 5ug/ml.
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Lidocaine IB effect on QRS and SNS
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Does not alter the duration of the QRS and the sympathetic nervous system is not changed
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Lidocaine IB seizure threshold decreases with:
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arterial hypoxia, hyperkalemia, acidosis
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Dilantin IB use
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Ventricular dysrhythmias associated with digitalis toxicity, torsade de pointes
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Dilantin IB Dose
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100mg (1.5mg/kg) every 5 min
10-15mg/kg(max 1000mg) |
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Dilantin IB base fluid
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NS
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Dilantin IB ideal blood level
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blood level 10-18 ug/ml
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Dilantin IB effect on SA node
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depressed
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Dilantin IB effect on QT
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Shortens
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Dilantin IB effect on QRS, ST-T waves
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No effect
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Dilantin IB Metabolism
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Liver – hydroxylated and then conjugated with glucuronic acid and excreted in the urine
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Dilantin IB 1/2 Life
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24 hrs
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Dilantin IB CNS s/e
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CNS cerebellar
ataxia nystagmus vertigo slurred speech sedation mental confusion (seen with blood levels >18ug/ml) |
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serum level of Dilantin IB when mental confusion is seen
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>18ug/ml
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Dilantin IB s/e
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Hyperglycemia
leukopenia nausea megaloblasic anemia |
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Principle s/e effect of Lidocaine IB
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CNS/seizures
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dose at which s/e of procainamide IA occurs
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15mg/kg
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Lidocaine IB MOA
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decreases phase 4 depolarization
blocks K+ and Na channels |
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Dilantin IB via IVP causes
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asystole
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Only clinical use of Dilantin
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Digoxin toxicity
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Amiodarone III uses
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-Given preop to decrease incidence of post-op A-fib after cardiac surgery
-Suppress tachydysrhythmias associated with WPW -Decreases mortality after MI |
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Amiodarone III MOA
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Depresses conduction in the AV node and the accessory bypass tracts
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Amiodarone III Intravenous Dose
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IV 5mg/kg over min
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Amiodarone III PO Dose
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PO maintenance 200-400mg
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Amiodarone III Therapeutic blood levels
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1.0-3.5 ug/ml
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Amiodarone III 1/2 time
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29 days
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Amiodarone III metabolism dependent on
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renal excretion
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Amiodarone III s/e
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pulmonary edema
pulmonary alveolitis ARDS prolonged QT bradycardia resistant to atropine hypotension AV block catecholamine resistance Corneal microdeposits neuro toxicity peripheral neuropathy tremors headache |
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Amiodrane + Halothane/Lidocaine
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Lidocaine and halothane could accentuate the effects of the SA node—sinus arrest
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Amiodarone III and Digoxin
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causes Digoxin toxicity
Displaces digoxin from protein binding sites and can increase its plasma concentration as much as 70% |
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Amiodarone III increases drug levels of
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digoxin, quinidine, procainimide, and phenytoin
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Amiodarone III + Warfarin
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Increases Warfarin effects
depress vitamin K-dependent clotting factors which can increase the anticoagulant effects of warfarin |
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Amiodarone III effects on thyroid
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can cause hypo or hyper- thyroidism , may need thyroidectomy
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Digoxin Use
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Atrial tachydysrythmias, cardiac failure
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Digoxin MOA
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Positive inotrope-drug induced inhibition of the NA-K ATPase ion transport system,
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Digoxin effect on SV
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increase
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Digoxin effect on LVEDP
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decrease
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Digoxin Chronotropy and Dromotropy
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Negative
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Digoxin automaticity
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Decreases resting membrane potential and thus increases automaticity
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Digoxin effects on t wave
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diminished ampitude or inversion of T waves
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Digoxin effects on PR
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prolonged
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Digoxin effects on QT
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shortened
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Digoxin effects on ST
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depression
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states that increase the risk of digoxin toxicity
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Hypercalcemia, hypomagnesemia and impaired renal function
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Treatment for Hyperkalemia and specific results
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Hyperventilation can decrease serum K 0.5meq/liter for every decrease 10-mmhg in Paco2
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Digoxin toxic level
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>3ng/ml toxic
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early signs of digoxin toxicity
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Anorexia, nausea, vomiting, pain stimulating trigeminal neuralgia
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Avoid digoxin in pts with this disease
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WPW
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Digoxin interaction quinidine
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increases effect of digoxin
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Digoxin interaction Sux
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succinylcholine theoretically, have an additive effect but, clinically this is not supported,
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Digoxin interaction Calcium
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calcium may precipitate cardiac dysrhythmias
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Drug of choice for A-tach
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Digoxin (but takes a long time to work)
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vasodilator good for angina
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amiodarone
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Potassium imbalance that causes digoxin toxicity
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HYPOkalemia
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