ANTI-BAD RHYTHMIA.txt

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Author:
kgerber
ID:
197977
Filename:
ANTI-BAD RHYTHMIA.txt
Updated:
2013-02-04 20:39:43
Tags:
anti arrhythmia
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Description:
Anti Arrhythmia
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  1. NAME NEGATIVE EFFECTS OF ARRHYTHMIAS.
    • INC MYOCARDIAL O2 DEMAND
    • DEC DIASTOLE
    • DEC PERFUSION OF HEART
    • INC OR DEC HR (MAY LEAD TO END ORGAN ISCHEMIA)
  2. ARRYTHMOGENIC ASYNCHRONOUS ACTION CAN LEAD TO 2 BAD THINGS. WHAT ARE THEY?
    • REDUCED EF
    • MAY INCREASE O2 DEMAND
  3. THE ELECTROPHYSIOLOGY OF THE NORMAL CARDIAC RHYTHM ARE RELIANT ON 3 THINGS?
    • IONIC BASIS OF MEMBRANE ACTIVITY
    • ACTIVE CELL MEMBRANE
    • RESTING MEM POTENTIAL
  4. NORMAL FIRING RATE OF THE SA NODE?
    60-100
  5. WHY IS THERE A DELAY FROM THE SA TO AV NODE ELECTRICAL IMPULSE TRANSMISSION?
    TO ALLOW TIME FOR ATRIAL FILLING & EMPTYING
  6. WHAT EFFECT DOES SCLEROSIS AND FIBROSIS HAVE ON THE HEART IN TERMS OF ELECTRICAL IMPULSE PROPOGATION?
    THE TISSSUE CHANGES AND LESS ELECTRICAL IMPULSE PROPAGATION.
  7. REGARDING ACTION POTENTIAL, WHAT IS HAPPENING AT -70mV?
    NOTHING, THIS IS RESTING MEM POTENTIAL
  8. WHICH ION CONDUCTION IS INCREASED AS THE INTRACELLULAR ENVIRONMENT BECOMES LESS NEGATIVE?
    SODIUM
  9. WHAT ION CHANNELS AFFORD THE HEART ITS AUTOMATICITY CHARACTERISTIC?
    POTASSIUM LEAK CHANNELS
  10. THE SODIUM CHANNEL HAS 2 GATES, WHAT ARE THEY?
    M AND H GATES
  11. THE ACTIVATION SODIUM GATE IS KNOWN BY THIS LETTER?
    M
  12. WHAT PHASE OF THE ACTION POTENTIAL IS RESTING MEMBRANE POTENTIAL?
    PHASE 4
  13. WHAT HAPPENS TO THE H GATES WHEN THE INTRACELLULAR ENVIRONMENT BECOMES POSITIVE?
    THE CLOSE
  14. DURING THE PLATEAU OF THE ACTION POTENTIAL, MOST SODIUM CHANNELS ARE IN THIS STATE?
    INACTIVATED
  15. BROADLY, ARRHYTHMICS HAVE 2 BASIC MECHANISMS OF ACTION. WHAT ARE THEY?
    • DISTURBANCE OF IMPULSE FORMATION
    • DISTURBANCE OF IMPULSE CONDUCTION
  16. WHAT HAPPENS IF YOU SHORTEN EITHER AP TIME OR DIASTOLIC INTERVAL IN TERMS OF HR?
    INCREASED RATE
  17. WHICH PHASE CORRESPONDS WITH THE DIASTOLIC INTERVAL AND IS THE MOST IMPORTANT?
    PHASE 4
  18. WHICH PHASE CORRESPONDS WITH DEPOLARIZATION?
    PHASE 0
  19. METHODS TO ALTER DIASTOLIC TIME.
    • ACTIVE PSNS
    • BETA BLOCKER
    • THESE REDUCE THE SLOPE OF PHASE 4 (PROLONG TIME) AND DECREASE HR
  20. SHORTENING OR INCREASING THE PHASE 4 SLOPE OCCURS WITH
    • SNS ACTIVATION
    • ACIDOSIS
    • STRETCH ON THE HEART
  21. WHAT DOES THE TERM AFTERPOLARIZATION MEAN?
    TRIGGERED AUTOMATICITY THAT REQUIRE A NORMAL ACTION POTENTIAL FOR THEIR INITIATION. THEY CAN BE EARLY OR DELAYED.
  22. 4 BASIC PHARMACOLOGIC MECHANISMS OF ACTION FOR THE ANTIARRYTHMICS.
    • SODIUM CHANNEL BLOCKERS
    • SYMPATHETIC BLOCKERS OF AUTONOMIC EFFECTS IN THE HEART
    • PROLONG THE REFRACTORY PERIOD
    • CALCIUM CHANNEL BLOCKERS
  23. HOW MANY CLASSES ARE THERE OF ANTYARRYTHMICS?
    • 4 CLASSES
    • CLASS I: SODIUM CHANNEL BLOCKERS
    • CLASS II: SYMPATHOLYTIC BLOCKERS
    • CLASS III: PROLONG THE APD
    • CLASS IV: CALCIUM CHANNEL BLOCKERS
  24. HOW DOES PROCAINAMIDE WORK?
    IT TAKES THE RMP FURTHER NEGATIVE WHICH MAKES IT HARDER TO REACH THRESHOLD FOR DEPOLARIZATION
  25. WHAT ARE 2 EFFECTS ON EKG BY PROCAINAMIDE?
    • SLOWS UPSTROKE
    • PROLONG QRS
    • SLOWS CONDUCTION
  26. DESCRIBE THE TOXIC EFFECTS SEEN WITH PROCAINAMIDE?
    • VERY LONG QRS
    • SLE LIKE EFFECTS
  27. HOW DO BETA BLOCKERS WORK? WHAT CLASS ARE THEY?
    • REDUCE PHASE 4 SPONTANEOUS CONDUCTION AND REDUCE NE AT BETA 1. THIS REDUCES RATE AND SLOWS CONDUCTION
    • CLASS II
  28. NAME 2 DRUGS THAT PROLONG THE ACTION POTENTIAL? WHAT CLASS ARE THEY?
    • AMIODARONE & SOTALOL
    • CLASS III
  29. HOW DO CLASS III WORK?
    • BLOCK K CHANNELS
    • PROLONG REPOLARIZATION
  30. WHAT CLASS ARE CALCIUM CHANNEL BLOCKERS AND HOW DO THEY WORK?
    • CLASS IV
    • DEC CONDUCTION TIME AND CONTRACTILITY

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