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34 Cards in this Set
- Front
- Back
- 3rd side (hint)
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describe the conduction velocities
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purkinje
bundle ventricle/atria SA/AV |
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what determines conduction velocities
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size of cells
number of gap junctions rate of rise of AP |
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what are the relative firing rates of SA, AV, purkinje
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SA= 60-100
AV= 56-60 Purkinje= 40-50 |
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what is the maximum SA firing rate
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2x normal, 180-200
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what are causes of sinus tachycardia
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SNS-->fear, pain, exercise, volume depletion, metabolic demand, decreased afterload
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what classifies a tachy as supraventricular
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above the bundle of his (AV or SA)
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how do you treat AVNRT
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vagal manoevers, (PNS innervates the AV node)
adenosine what are the side effects of adenosine? |
sense of impending doom, chest pain (angina like),
aka severe, dont fuck around with this one. only for AVNRT (remember adenosine is what causes angina pain) |
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what is the most common type of SVT
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AVNRT
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what are the requirements for an AVNRT
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two pathways
one with high velocity long refractory one with low velocity short refractory and a premature beat |
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what rhythm is implied by fibrillation
why is afib so dangerous |
irregularly irregular
can cause stasis (just quivering like a bag of worms), embolus |
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what does the speed of the PR interval tell you
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the length of time its taking for transmission from SA through AV node
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Automaticity and tachycardia
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automaticity (increase RMP, increase slope of depolarization, decrease threshold). SNS stimulation.
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automaticity and bradycardia
cause pathology |
automaticity (decrease RMP, decrease slope of depolarization, increase threshold, injury to membrane causing leakage of charge in). Vagus or PNS stimulation.
may result in ectopic beat if things slow too much |
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re entry circuits and tachycardia
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AVNRT (through node and accessory bundle) or AVRT (through accessory bundle that bypasses the node)
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conduction block and bradycardia
causes functional vs fixed where they usually occur possible pathologies |
transient, permanent, unidirectional
caused by ischemia, fibrosis, inflammation, drugs functional= secondary to refractoriness fixed= permanent damage blocks normally happen in the AV purkinje system can result in a third degree heart block |
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afterdepolarizations and tachycardia
early late |
early- phase 2, most Na channels are inactivated but some can be abnormally activated allowing another action potential
usually seen in torsades de pointe (unpredictable number of gates open) late after repolarization is complete: happens when high intracellular calcium, or SNS stimulation high calcium activates the Na/Ca exchanger which causes Na to enter the cell-> depolarizations |
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what are the 3 causes of tachycardia
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re-entry circuit
after hyperpolarization automaticity |
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what are the 2 causes of bradycardia
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automaticity
conduction block |
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where do junctional re-entry tachycardias occur
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AV node
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if tachycardia responds to vagal manoevers what is it most likely
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AV node tachyhcardia
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what do class I antiarrhythmics do
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block Na entry
what are their side effects |
pro arrhythmic (obviously)
*nervous system dysfunction since na channels are required for nerve function. seizures, behaviour changes, tingling and numbness |
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Treatment of bradycardia: when do you treat sinus bradycardia, and how
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symptomatic, pacemaker
when do you treat AV bradycardia |
type II (unpredictable) and third degree: pacemaker
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when would you use cardioversion (what ECG patterns)
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SVT, V tach
(ventricular problem, therefore sync QRS with the ventricular reset) |
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What is the principle behind treating tachycardias for
automaticity re entrant pathways after hyperpolarizations |
automaticity: reduce phase 4 slope
prolong refractory re-entrant pathways prolong refractory, impair impulse propagation triggered activity: suppress or delay after-depolarizations |
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Class I blocker
what it does |
Na channel blockade (phase 0)
IA moderate block, prolong AP IB mild block, short AP IC maximal block , no change in AP example? |
lidocaine
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Class II blocker
what it does |
B blocker
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-olols
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Class III
what it does |
potassium channel blocker phase 3
prolongs AP duration, slower repolarization of pacemaker and myocardial cells |
amiodarone, sotalol (also class 2)
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Class IV
what it does |
Calcium channel blockers
pacemaker depolarization slowed (phase 0) |
verapamil
diltiazam |
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pneumonic for antiarrhythmics
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South
Beach Pol Ca |
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What are the two main effects of digoxin
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positive inotropy
prolong refractory of AV node specifically what do you treat with digoxin |
AVNRT, a fib, a flutter (anything that causes increased APs through
AV node, because this is what is increased in these conditions |
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How does digoxin increase inotropy
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stimulates SERCA to increase the amount of calcium stored in the ER. with each contraction cycle more Ca so more force
clinical application of digoxin? |
heart failure, increased contractility, augment cardiac output
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In the action potential QRS corresponds to.... and the RYRI responds to...
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QRS is phase zero
RYR1 in phase 2 |
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how does digoxin slow conduction
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enhance vagal tone
reduce sympathetic activity |
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pharmacology of atropine
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anticholinergic, suppress vagal stimulation, increase HR
clinical uses? |
bradycardia (symptomatic only)
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