Term
| WE KNOW THAT ARRHYTHMIAS CAN OCCUR FROM ABNORMAL IMPULSES ANYWHERE IN THE HEART. WHAT KIND OF ARRHYTHMIAS OCCUR IN THE ATRIA OR AV NODE AND THE VENTRICLES? |
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Definition
| ATRIA- A-FIBB/FLUTTER, PSVT, PAT. VENTRICLES VT, V-FIBB, PVCS |
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Term
| CAN PM CELLS INITIATE SPONT. ACTION POTENTIALS? WHERE ARE THEY FOUND AT? |
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Definition
| YES. SA NODE, AV NODE, AND VENTRICULAR CONDUCTING SYSTEM (BUNDLE OF HIS, BUNDLE BRANCHES, AND PURKINJE FIBERS). |
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Term
| WHAT ARE NONPACEMAKER CELLS? |
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Definition
| ATRIAL AND VENTRICULAR MYOCYTES THAT CONTRACT IN RESPONSE TO DEPOLARIZATION. |
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Term
| DESCRIBE THE 3 PHASES OF SA NODE POTENTIAL. |
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Definition
| PHASE 4: SLOW SPONT. DEPLARIZATION CAUSED BY AN INWARD CURRENT OF SODIUM (AND CALCIUM), AND THE CESSATION OF POTASSIUM EFFLUX. PHASE 0 IS RAPID DEPOLARIZATION DUE TO VOLTAGE GATES CALCIUM CHANNELS (CALCIUM INFLUX). PHASE 3 IS CALCIUM CHANNELS CLOSE AND POTASSIUM CHANNELS OPEN IN ORDER TO REPOLARIZE THE CELL (POTASSIUM EFFLUX). |
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Term
| DESCRIBE THE SHAPE BETWEEN THE SA NODE POTENTIAL AND THE VENTRICULAR MYOCYTE POTENTIALS. |
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Definition
| SA NODE LOOKS LIKE A HILL WHEREARS THE VENTRICULAR MYOCYTE POTENTIAL IS LIKE A SQUARE. |
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Term
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Definition
| YES! UNLIKE SA NODE POTENTIALS. THERE IS NO SPONT. DEPOLARIZATION UNDER NML CONDITIONS. |
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Term
| HOW MANY PHASES ARE IN VENTRICULAR ACTION POTENTIAL? |
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Definition
| 5 ALTHOUGH IT IS NUMBERED PHASE 0- PHASE 4. |
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Term
| DESCRIBE PHASE O OF VENTRICULAR MYOCYTE POTENTIAL. |
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Definition
| PHASE 0 IS RAPID DEPOLARIZATION CAUSE BY INCREASE IN SODIUM INFLUX VIA VOLTAGE GATED SODIUM CHANNELS. |
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Term
| DESCRIBE PHASE 1 AND 2 FOR VENTRICULAR MYOCYTE POTENTIALS. |
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Definition
| PHASE 1 IS EARLY REPOLARIZATION FROM INACTIVATION OF SODIUM INFLUX CHANNELS AND ACTIVATION OF POTASSIUM EFFLUX. PHASE 2 IS PLATEAU PHASE D/T CALCIUM INFLUX AND POTASSIUM EFFLUX. |
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Term
| DESCRIBE PHASE 3 AND PHASE 4 OF VENTRICULAR MYOCYTE POTENTIALS. |
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Definition
| PHASE 3 IS LATE REPOLARIZATION FROM INACTIVATION OF CALCIUM CHANNELS AND CONTINUES POTASSIUM EFFLUX. PHASE 4 RMP IS REESTABLISHED BY K CHANNELS. |
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Term
| WHEN IS THE REFRACTORY PERIOD FOR A VENTRICULAR MYOCYTE POTENTIAL? |
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Definition
| FROM PHASE 1 TO END OF PHASE 3. PNS INCREASES THRESHOLD AND INCREASES SLOPE. |
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Term
| ALL ARRHYTHMIAS ARE THE RESULT OF EITHER A DEFECT IN IMPULSE FORMATION _____ OR IMPULSE CONDUCTION _____. |
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Definition
| SA NODE DEFECT, ANYWHERE. |
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Term
| IN RELATION TO SA NODE AS AN IMPULSE FORMATION THE SNS ACTIVATION INCREASES AUTOMATICITY BY DOING WHAT TO THE SLOPE OF PHASE 4. WHAT DOES THE PNS DO TO THE SLOPE.? |
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Definition
| SNS INCREASES THE SLOPE OF PHASE 4 WHILE PNS DECREASES IT R/T DECREASED AUTOMATICITY AND INCREASE IN THRESHOLD. SNS ALSO DECREASES THRESHOLD (ACTION POTENTIALS HAPPENS QUICKER) |
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Term
| CAN ABNORMAL PM CELLS IN THE HEART OVERTAKE THE SA NODAL RATE? |
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Definition
| YES IF THE SA NODAL FIRING IS SLOW OR IMPAIRED, AN ESCAPE BEAT MAY BE INITIATED BY ANOTHER PM CELL. ECTOPIC BEATS OCCUR AT A FASTER RATE THAN THE SA NODE, AND CAN OCCUR EVEN IF THE SA NODE IS FIRING NORMALLY. EX. PAC, PVC |
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Term
| WHAT ARE AFTER-DEPOLARIZATIONS? |
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Definition
| THEY OCCUR WHEN A NORMAL ACTION POTENTIAL CAUSES THE FORMATION OF ABNORMAL IMPULSES. |
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Term
| WHAT ARE THE 2 AFTER DEPOLARIZATIONS? DESCRIBE THEM. WHICH 1 IS MORE DANGEROUS. |
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Definition
| THERE IS EARLY AFTER-DEPOLARIZATION AND LATE AFTER-DEPOLARIZATION. EARLY AFTER-DEPOLARIZATION = CELL NEVER FULLY REPOLARIZED; MORE DANGEROUS. LATE AFTER-DEPOLARIZATIONS = CELL HAS FULLY REPOLARIZED; LESS DANGEROUS. |
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Term
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Definition
| WHEN AN IMPULSE STIMULATES THE SAME CARDIAC TISSUE REPEATEDLY. LIKE WPW |
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Term
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Definition
| OCCURS WHEN A UNIDERECTIONAL BLOCK IS PRESENT IN A BIFURCATING CONDUCTION PATHWAY, AND RETROGRADE CONDUCTION OCCURS. |
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Term
| WHEN DOES CONDUCTION BLOCKS EXIST? DESCTRIBE THEM. |
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Definition
| WHEN TISSUE IS INEXCITABLE (ISCHEMIA, SCARRING OR REFRACTORY). CONDUCTION SLOWS UNTIL IT REACHES THE INEXCITABLE TISSUE, THEN STOPS. |
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Term
| WHEN A CONDUCTION BLOCK IS PRESENT HOW DOES THE AREA PAST ISCHEMIA GET CONDUCTION? |
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Definition
| RETROGRADE CONDUCTION IS ABLE TO MAINTAIN VELOCITY AND "JUMP" OVER THE ISCHEMIC AREA. |
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Term
| WHAT IS THE MOST COMMON MECHANISM FOR PSVT? |
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Definition
| AV NODAL REENTRY. THE REENTRY CIRCUIT IS ENTIRELY WITHIN THE AV NODE. |
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Term
| AVNRT IS MOST COMMON WITH WHAT? |
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Definition
| AV NODAL RE-ENTRY TACHYCARDIA IS MOST COMMON WITH SVT. |
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Term
| FOR THE BUNDLE OF KENT WHAT DOES IT BYPASS, WITH IS THE FIRST LINE DRUG, AND WHAT IS THE LONG TERM TREATMENT? |
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Definition
| BYPASSES AV-NODE. FIRST LINE DRUG IS AMIODARONE. LONG TERM TREATMENT IS ABLATION. |
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Term
| BLOCKAGE OF WHAT 2 CHANNELS CAN SUPPRESS OR PREVENT ABNORMAL IMPULSES FORMATION OR CONDUCTION ABNORMALITIES BY ALTERING THE THRESHOLD POTENTIAL? |
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Definition
| SODIUM AND CALCIUM CHANNELS. |
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Term
| BLOCKAGE OF WHAT CHANNELS CAN PROLONG REPOLARIZATION AND REFRACTORY PERIOD OF TISSUE? |
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Definition
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Term
| WHAT KIND OF DRUG CLASSIFICATION CAN DECREASE AUTOMATICITY AND CONDUCTION VELOCITY? |
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Definition
| SYMPATHOLYTICS (B-BLOCKERS) |
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Term
| WHAT DRUGS WORK ON CLASS 1? |
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Definition
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Term
| WHAT DRUGS WORK ON CLASS 2? |
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Definition
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Term
| WHAT DRUGS WORK ON CLASS 3? |
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Definition
| POTASSIUM CHANNEL BLOCKERS |
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Term
| WHAT DRUGS WORK ON CLASS 4? |
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Definition
| CALCIUM CHANNEL BLOCKERS. |
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