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1.23.3.10 - Manipulation of the Cardiac Action Potential - Coggle Diagram
1.23.3.10 - Manipulation of the Cardiac Action Potential
pacemaker cells
spontaneous depolarisation
K+ channels close
SA node and others
Influx of Ca2+ speeds final approach to threshold
once threshold reached AP occur
absolute refractory period
particular Na+ channels
Na+ channels spontaneous open once an AP has finished at -65mV
slow Na+ channels
propagation of an action potential
AV next
authrhthmic cells of the bundle of his and purkinje fibres
SA node has the shortest refractory period
if SA node fails or is being ignored there will be changes in the ECG
produces the ECG trace
why treat a dysrhythmia
if cardiac output drops too much = die
degeneration to a fatal rhythm
impact of cardiac output
roles of calcium
calcium is important for actin and myosin cross bridges cross bridges and therefore muscle contraction force
calcium induced calcium release
increased force
heart rate increases
more likely to produce a beat
calcium channels open earlier so reach threshold potential and reset quicker
influx of calcium also leads to release from the sarcoplasmic reticulum
causes of dysrhythmias
toxins
metabolic disease/electrolyte imbalance
drugs
systemic disease
structural cardiac disease
sympathetic tone - increased epinepherine release
ANYTHING THATS AFFECTS/DISRUPTS THE MOVEMENYS OF THE CARDIAC ACTION POTENTIAL THROUGH THE HEART
cardiac action ptoential
calcium
potassium
sodium
stages
phase 0 = sodium
Na+
spike in sodium
membrane potential increases a lot very quicklt
generation of an electrical current
phase 1
calium enters the cell
phase 2
phase 3
K+ leaves the cell
is the muscle cells in the heart contract too quickly the heart cannot fill as quickly and properly, slowing down results in effective output
refractory period is on purpose to slow myocyte contraction down
how to treat dysrhytmias
agonists/antagonists
those acting directly at ion channels - not via a receptor
treat the underlying problem
agonists/antagonists
sympathetically mediated arrythmia - adrenoreceptors
supraventricular tachycardia
beta blockers
propanolol
esmolol
parasympatheticaly mediated arrythmia
acetyl choline mediated
blocks adenylyl cyclase and reduces cAMP
reduces calcium effects
allows potassium efflux - hypopolarisation in phase 3
effects
reduce automaticity
reduces contraction
slow conduction at AV node
muscarinic antagonists - atropine
parasympatholytic
reduces parasympathetic (vagal tone)
increases heart rate by reducing suppression
muscarinic agonists - toxins
muscarine found in mushrooms
bradycardia and hypotension
pilocarpine used in treatment of glaucoma
adenosine - specific receptor
a1 receptor blocks adenylyl cyclase and increases potassium efflux
short acting
treatment for SVT
ion channels
sodium channel blocker
reduces phase 0 depolarisation
lidocaine - sodium channel blocker
treatment for vtack
slows action potential generation
raises depolarisation threshold
sodium channel blockers used extensively as toxins
potassium channel blockers
slow phase 3 of the action potential and therefore increase refractory period and duration of action potential as repolarisation takes longer to occur
ventricular tchycardia
amiodarone,sotalol
calcium channel blockers
verapamil and diltiazem
feline HCM - diltiazem
hypertrophic cardiac myopathy
slow conduction, reduced contraction force and cause coronary vasodilation
SVT
block voltage dependent L-type Ca2+ channels in cardiac muscle and vascular smooth muscle
sodium - when the ventricles are in charge of themselves and not contracting when they are told to
slowing thew heart enough to allow the node to recapture the action potential and take charge again
the exception
digoxin
doesnt affect a receptor or ion channel
inhibits Na/K ATPase
increases intracellular Na+ reducing Na+/Ca2+ exchange
calcium retained within the cell
increases the AV refractory period - slows the heart
increased contraction force
management of supraventricular arrythmias
pharmacokinetics and toxicity
cardiac glycosides have a narrow therapeutic indext
drug-drug and drug-food interactions are important
classification of antidysrhythmic agents
class 2 beta-adrenoreceptor antagonists
class 3 prolong action ptential
class 1 sodium channel blockers
class 4 block voltage-sensitive calcium channels
summary
understanding where a drug works helps inform the correct choice
these drugs are not benign
we can change the action potential at many points
the wrong does (including too low) may produce a dysrhytmia
dont kill it.