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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)
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ARRYTHMOGENIC ASYNCHRONOUS ACTION CAN LEAD TO 2 BAD THINGS. WHAT ARE THEY?
- REDUCED EF
- MAY INCREASE O2 DEMAND
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THE ELECTROPHYSIOLOGY OF THE NORMAL CARDIAC RHYTHM ARE RELIANT ON 3 THINGS?
- IONIC BASIS OF MEMBRANE ACTIVITY
- ACTIVE CELL MEMBRANE
- RESTING MEM POTENTIAL
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NORMAL FIRING RATE OF THE SA NODE?
60-100
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WHY IS THERE A DELAY FROM THE SA TO AV NODE ELECTRICAL IMPULSE TRANSMISSION?
TO ALLOW TIME FOR ATRIAL FILLING & EMPTYING
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WHAT EFFECT DOES SCLEROSIS AND FIBROSIS HAVE ON THE HEART IN TERMS OF ELECTRICAL IMPULSE PROPOGATION?
THE TISSSUE CHANGES AND LESS ELECTRICAL IMPULSE PROPAGATION.
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REGARDING ACTION POTENTIAL, WHAT IS HAPPENING AT -70mV?
NOTHING, THIS IS RESTING MEM POTENTIAL
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WHICH ION CONDUCTION IS INCREASED AS THE INTRACELLULAR ENVIRONMENT BECOMES LESS NEGATIVE?
SODIUM
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WHAT ION CHANNELS AFFORD THE HEART ITS AUTOMATICITY CHARACTERISTIC?
POTASSIUM LEAK CHANNELS
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THE SODIUM CHANNEL HAS 2 GATES, WHAT ARE THEY?
M AND H GATES
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THE ACTIVATION SODIUM GATE IS KNOWN BY THIS LETTER?
M
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WHAT PHASE OF THE ACTION POTENTIAL IS RESTING MEMBRANE POTENTIAL?
PHASE 4
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WHAT HAPPENS TO THE H GATES WHEN THE INTRACELLULAR ENVIRONMENT BECOMES POSITIVE?
THE CLOSE
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DURING THE PLATEAU OF THE ACTION POTENTIAL, MOST SODIUM CHANNELS ARE IN THIS STATE?
INACTIVATED
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BROADLY, ARRHYTHMICS HAVE 2 BASIC MECHANISMS OF ACTION. WHAT ARE THEY?
- DISTURBANCE OF IMPULSE FORMATION
- DISTURBANCE OF IMPULSE CONDUCTION
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WHAT HAPPENS IF YOU SHORTEN EITHER AP TIME OR DIASTOLIC INTERVAL IN TERMS OF HR?
INCREASED RATE
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WHICH PHASE CORRESPONDS WITH THE DIASTOLIC INTERVAL AND IS THE MOST IMPORTANT?
PHASE 4
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WHICH PHASE CORRESPONDS WITH DEPOLARIZATION?
PHASE 0
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METHODS TO ALTER DIASTOLIC TIME.
- ACTIVE PSNS
- BETA BLOCKER
- THESE REDUCE THE SLOPE OF PHASE 4 (PROLONG TIME) AND DECREASE HR
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SHORTENING OR INCREASING THE PHASE 4 SLOPE OCCURS WITH
- SNS ACTIVATION
- ACIDOSIS
- STRETCH ON THE HEART
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WHAT DOES THE TERM AFTERPOLARIZATION MEAN?
TRIGGERED AUTOMATICITY THAT REQUIRE A NORMAL ACTION POTENTIAL FOR THEIR INITIATION. THEY CAN BE EARLY OR DELAYED.
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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
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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
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HOW DOES PROCAINAMIDE WORK?
IT TAKES THE RMP FURTHER NEGATIVE WHICH MAKES IT HARDER TO REACH THRESHOLD FOR DEPOLARIZATION
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WHAT ARE 2 EFFECTS ON EKG BY PROCAINAMIDE?
- SLOWS UPSTROKE
- PROLONG QRS
- SLOWS CONDUCTION
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DESCRIBE THE TOXIC EFFECTS SEEN WITH PROCAINAMIDE?
- VERY LONG QRS
- SLE LIKE EFFECTS
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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
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NAME 2 DRUGS THAT PROLONG THE ACTION POTENTIAL? WHAT CLASS ARE THEY?
- AMIODARONE & SOTALOL
- CLASS III
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HOW DO CLASS III WORK?
- BLOCK K CHANNELS
- PROLONG REPOLARIZATION
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WHAT CLASS ARE CALCIUM CHANNEL BLOCKERS AND HOW DO THEY WORK?
- CLASS IV
- DEC CONDUCTION TIME AND CONTRACTILITY
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