lecture 16 - cardiac arrhythmia related to CVD Flashcards
describe the resting membrane potential
the electrical potential across a plasma membrane determined by two main factors
the distribution of ion across the membrane
the selective permeability of the cell membrane
K+ potassium ions are the major determinant of resting membrane potential
the resting membrane is only slightly permeable Na+ (sodium)
what is the absolute refractory period in mycocytes?
250ms
describe the neuro-hormonal influences on parasympathetic
vagal stimulation makes the resting potential more negative and the pacemaker current slower and raise the threshold
describe the neuro-hormal influences on sympathetic system
catecholamines make the resting potential more excited and speeds the pacemaker current and lower the threshold for discharge
what is the definitions and classifications of arrhythmias
tachyarrhythmias > 100bpm
bradyarrhythmias < 60 bpm
supraventricular (originating in the atrium or atrioventricular node) OR ventricular (originating in the ventricle)
narrow complex (describes supraventricualr) OR broad complex (describes ventricular)
persistent OR paroxysmal (intermittent attacks)
heart block
what are the mechanism of arrhythmia ?
Heart rate (tachycardia-) or slower (Brady-) than physiological
site of origin (supraventricualr/ ventricular)
complexes on ECG (narrow/broad)
cardiac rhythm (regular/ irregular)
what must happen for the re entry to occur?
the refractory period must shorten and conduction velocity must decrease
describe the passes of action potential of cardiac cells
phase 0 - rapid depolarisation (inflow of sodium)
phase 1 partial depolarisation (inward Na+ current deactivated , outflow of K+)
phase 2 plateau (slow inward calcium current)
phase 3 depolarisation (calcium current inactivates, K+ outflow)
phase 4 pacemaker potential (slow Na+ inflow, slowing of K+ outflow) ‘audtorhythmicity’
refractory period (phases 1-3)
what is the principal effect of reducing the rate and magnitude of depolarisation by blocking sodium channels?
decrease in conduction velocity
what happens the faster a cell depolarises?
the more rapidly adjacent cells will become depolarised
what does blocking the sodium channels ultimately result in?
reduces the velocity of action potential transmission
what are the function of beta blockers?
inhibit sympathetic driven electrical activity
sympathetic drive increases conduction velocity
increases aberrant pacemaker activity (ectopic beats)
decreases sinus rate
decrease conduction velocity
increase APD and the ERP
what is the primary role of potassium channels in cardiac action? and how do they work?
cell repolarisation
block the potassium channels that are responsible for phase 3 depolarisation.
since the agents do not affect the sodium channel, conduction velocity is not decreased.
prolongation of the action potential duration and refractory period, combined with the maintenance of normal conduction velocity, prevent re-entrant arrhythmias
describe the actions of calcium channel blockers
decreases conduction via the AV node
shorten plateau phase of the Action potential
prolong the action potential duration
prolong the effective refractory period
reduce the contraction force
use in superventricular tachycardia and atrial
not used in ventricular arrhythmias
class IV. agents include verapamil and diltiazem
name miscellaneous antiarrhythmias
adenosine
atropine
digoxin
