Hamra Lecture 3- Arrythmias
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| Arrythmia | an abnormality of impulse initiation, impulse conduction or both
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| SA node rate of pacemaking | 60-100 bpm
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| AV junction rate of pacemaking | 40-60 bpm
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| Purkinje fibers | 20-40 bpm
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| Tachycardia | >100 bpm
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| Bradycardia | <60 bpm
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| Abnormal automaticity | Arrythmia associated with non-pacemaker cells that develop automaticity
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| Triggered activity | Oscillations in membrane potential that trigger an action potential
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| Sinus arrythmia | Inspiration causes an acceleration and Expiration causes a deceleration, NORMAL
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| Abnormal automaticity depolarizes tissues by | inactivating fast Sodium channels
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| Can you overdrive suppress abnormal automaticity? | NO
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| Early afterdepolarization can lead to a | Torsades de pointes
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| Delayed afterdepolarization leads to a | ITI- Calcium driven, transient inward current
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| 1st degree block | Consistent prolongation of the PR interval but all impulses get through.
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| Two types of 2nd degree block | Wenckebach (also MobitzI) and Mobitz (also called MobitzII)
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| Wenckeback | Progressive prolongation through the AV node with an eventual dropped beat----prolonged PR interval
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| Mobitz | Dropped beats without prolongation of the PR interval
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| Wenckebach reflects an abnormality in which region? | AV node
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| Mobitz reflects an abnormality in which region? | His bundle and/or bundle branches, usually an anatomical lesion and much worse!
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| 3rd degree block | Complete block through the AV node and another latent pacemaker takes over
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| What can cause an AV block | Increased vagal tone, Calcium channel block, Beta-blocker, Digitalis, Hyperkalemia
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| Re-entry | An arrhythmogenic mechanism in which the impulse does not die out but instead continues to circulate and re-excite tissue
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| Conditions for re-entry to occur | Unidirectional block, Slowed conduction over an alternate pathway, Re-excitation of tissue proximal to the block
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| Re-entry is promoted by things that | Slow conduction velocity, shorten the refractory period or a combination of both
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| Wolf-Parkinson-White syndrome | Patients have an accessory pathway that uses Sodium channels (fast!) instead of the normal Calcium channels (slow) used by the AV node- causes premature excitement and tachycardia
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| Wolf-Parkinson-white EKG | Delta wave, retrograde P waves and wdie QRS intervals
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