Lecture 7 - Cardiac Action Potentials; Drugs and the CVS Flashcards
how is the cardiac resting membrane potential generated?
cell membrane mostly permeable to K
K move out taking positive charge with them
what is the cardiac resting membrane potential?
around -90mV
how is heart rate increased?
sns on san
noradrenaline (alpha 2 receptor) makes the pacemaker potential steeper
how is heart rate decreased?
pns on san
acetylcholine (m3 receptor) makes the pacemaker potential shallower
what is the role of baroreceptors?
role in controlling heart rate
stretch sensitive
pass information to medulla to cause pns innervation of san
slows heart rate
what are cardiovascular drugs used to treat?
arrhythmias heart failure angina hypertension risk of thrombus formation
what do cardiovascular drugs alter?
rate and rhythm of heart
force of myocardial contraction
peripheral resistance and blood flow
blood volume
what are causes of arrhythmias?
ectopic pacemaker activity
after depolarisation
reentry loop
what is ectopic pacemaker activity?
damaged area of myocardium becomes depolarised and spontaneously active
latent pacemaker activated due to ischaemia
dominates over san
what are after depolarisations?
abnormal depolarisations after the ap
maybe caused by high intracellular Ca
longer ap
longer qt
what is the reentry loop?
conduction delay
normal spread of excitation disrupted due to damaged area
incomplete conduction damage
what are the four classes of anti arrhythmic drugs?
- drugs that block voltage gated Na channels
- antagonists of beta-adrenoceptors
- drugs that block K channels
- drugs that block Ca channels
describe class 1 anti arrhythmic drugs
eg lidocaine blocks open or inactive channels dissociates rapidly in time for next ap prevents firing of ap too close together after depolarisations cant cause another ap
describe class 2 anti arrhythmic drugs
eg propanolol, atenolol
block sympathetic action by acting on beta 1 receptors
decreases slope of pacemaker potential
inhibits adenyl cyclase decreasing inotropy
after an am increases sns activity and reduces O2 demand of mycardium
describe class 3 anti arrhythmic drugs
prolong ap by blocking K channels which repolarise
arp is lengthened
can also be pro arrhythmic