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  1. Absence of all cardiac electrical activity
  2. A total disorganization of atrial electrical activity due to multiple ectopic foci resulting in loss of effective atrial contraction
    Atrial fibrilation
  3. An atrial tachydysrthythimia identified by recurring, regular sawtooth shpaed flutter waves that originate from a single ectopic focus in the right atrium or less commanly, the left atrium
    Atrial Flutter
  4. A defibrillator that has rhythm detection quality capability and the ability to advise the operator to deliver a shock using hands-free defibrillator pads.
    Automatic external defibrillator (AED)
  5. Electronic device used to pace the heart when the normal conduction pathway is damaged.
    Cardiac Pacemaker
  6. One form of AV dissociation in which no impulses from the atria are conducted to the ventricles. The atria are stimulated and contract independently of the ventricles.
    3rd degree AV block (complete heart block)

    • Some medications can cause such as
    • digoxin, B-adrenergic blockers, and calcium channel blockers
  7. A contraction originating from an ectopic focus in the atrium. (ie; a location other than the SA node)The ectopic signal signal originates in the left or right atrium and travels across athe atria by an abnormal pathway, creating a distorted P wave
    premature Atrial Contraction (PAC)
  8. A contraction originating in an ectopic focus in the ventricles. It is the premature occurence of a QRS complex, which is wide and distorted in shape compared with a QRS complex initiated from the normal conduction pathway
    Premature Ventricular contractions (PVC)
  9. A severe derangement of the heart rhythm characterized on ECG by irregular waveforms. of varying shapes and amplitude. Mechanically the ventrical is "quivering"with no effective contraction, and no cardiac output occurs. LETHAL
    Ventricular Fibrillation (VF) or V fib
  10. Occurs when an ectopic focus of foci fire repetivley and the ventricle takes control as the pacemaker. A run of 3 or more PVC's defines this.
    Vetricular tachycardia (VT) V tach

    Omnious sign;life threatening dysrthythmia because of decreased CO and the possibility of V fib
  11. Components of the autonomic nervous system that affect the heart
    Vagus nerve fibers of the parasympathetic nervous system and nerve fibers of teh sympathetic nervous system
  12. Represents time for the passage of the electrical impulse through the atrium casing atrial depolarization(contraction);should be upright
    P wave
  13. Measured from beginning of P wave to beginning of QRS complex;represents time taken for impulse to spread through the atria, AVnode and bundle of His, the bundle branches, and Purkinje fibers, to a point immediately preceding ventricular contraction
    PR interval
  14. Measured from beginning to end of QRS complex;represents time taken for depolorization of both ventricles (systole)
    QRS interval
  15. Measured from the S wave of the QRS complex to the beginning of the T wave;represents the time between ventricular depolarization(diastole);should be isoelectric (flat)
    ST segment
  16. Represents time for ventricular repolarization;should be upright
    T wave
  17. Measured form beginning of QRS complex to end of T wave;represents time taken for entire electrical depolarization and repolarization of the ventricles
    QT interval
  18. Mechanism of action
    Slows sinus rate.Slows conduction time through AV node.Can interrupt reentry pathways through AV nodeCan restore sinus rhythm in PSVT

    Stable, narrow-complex AV nodal or sinus nodal reentry tachycardiasFor unstable reentry SVT while preparations are made for cardioversionUndefined, stable, narrow-complex SVT as a combination therapeutic and diagnostic maneuverStable, wide-complex tachycardias in patients with a recurrence of a known reentry pathway that has been previously definedStable V-tach (first-line medication for ECC2010 guidelines)

    Adult Dosage
    Peripheral IV dose: 6 mg rapid IV push over 1-3 seconds.If no response within 1-2 minutes, administer 12 mg. May repeat 12 mg dose once in 1-2 minutes.Follow each dose immediately with 20-mL normal saline flush.

    Dysrhythmias at time of rhythm conversionUse with caution in patients with emphysema, bronchitis, asthmaDiscontinue in any patient who develops severe respiratory difficulty
  19. Mechanism of action
    Increases heart rate by accelerating SA node discharge rate and blocking vagus nerve Little or no effect on force of contraction May restore cardiac rhythm in asystole or bradycardic pulseless electrical activity (PEA)

    First-line drug for symptomatic narrow-QRS bradycardia Asystole (after epinephrine) Slow PEA (after epinephrine)

    Adult Dosage
    Symptomatic bradycardia 0.5 mg IV push every 3 to 5 min to a total dose of 3.0 mg Asystole/slow Pulseless Electrical Activity ({PEA) IV/IO: 1.0 mg every 3 to 5 minutes to a total dose of 3 mg ET: 2 to 2.5 times IV/IO dose (no longer recommended with ECC2010 guidelines)

    Do not push slowly or in smaller than recommended doses. Small doses (under 0.5 mg) produce modest paradoxical cardiac slowing that may last two min. May worsen ischemia or induce VT or VF. Use with caution in second-degree AV block type II and third-degree AV block with a new wide QRS – may be ineffective or cause paradoxical slowing.

    Special Notes
    Give oxygen before giving atropine. Use with caution in acute MI. Excessive increases in heart rate may further worsen ischemia or increase size of infarction
    Atropine Sulfate
  20. Possesses characteristics of all four classes of antiarrhythmics. Blocks sodium channels (class I action), inhibits sympathetic stimulation (class II action), and blocks potassium channels (class III action) as well as calcium channels (class IV action). Suppresses SA node function Prolongs PR, QRS, and QT intervals Slows conduction at the AV junction
  21. Stimulates alpha, beta-1, and beta-2 receptors Alpha-agonist – constricts arterioles in the skin, mucosa, kidneys, and viscera → increased systemic vascular resistance Beta-1 agonist – increases force of contraction (+ inotropic effect), increases heart rate → increased myocardial workload and oxygen requirements Beta-2 agonist – relaxation of bronchial smooth muscle, dilation of vessels in skeletal muscle; dilation of cerebral, pulmonary, coronary, and hepatic vessels

    Cardiac arrest – (IV bolus) VF, pulseless VT, asystole, pulseless electrical activity (PEA) Symptomatic bradycardia (IV infusion)
  22. Suppresses ventricular ectopy In therapeutic doses, lidocaine does not affect BP, cardiac output, or myocardial contractility.

    Pulseless VT/VF that persists after defibrillation and vasopressor administration
  23. Evidence exists that magnesium: Produces systemic and coronary vasodilation Possesses antiplatelet activity Suppresses automaticity in partially depolarized cells Protects myocytes against calcium overload under conditions of ischemia by inhibiting calcium influx especially at the time of reperfusion

    Polymorphic VT with prolonged QT interval (Torsades de Pointes) For rhythm control of atrial fibrillation ≤48 hours duration
    Magnesium Sulfate
  24. Increases vasoconstriction and arterial tone that results in increased myocardial perfusion

    Cardiac arrest

    Adult Dosage
    IV/IO: One time dose of 40 units IV push

    Tissue necrosis if extravasation occurs

    Special Notes
    May be used in place of first or second dose of epinephrine in cardiac arrest
Card Set:
2011-12-10 21:43:33
Dysrhythmias ekg

Chap 36
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