Session 7 Flashcards
Two specific causes of arrythmias?
Issue with arrythmias?
Note:look at cardio summary sheet for cardiac myocyte AP diagram and may need to look at drug revision sheet
Disturbances in Pacemaker impulse formation
Disturbances in Contraction impulse conduction
Rate/timing of contraction insufficient for desirable cardiac output to be maintained
What do class 1 drugs do?
What does this do?
Block V gated NA channels, so NA stops moving out of the cells in cardiac myocytes.
Slowed conduction in tissues, doesn’t really effect action potential duration
Class 2 drugs action?
Effects?
B blockers which stop v gated Ca influx
Diminishes phase 4 depolarisation automaticity as prolonged AP due to reduced Ca influx.
REDUCES CONDUCTION VELOCITY as phase 0 less steep in Sa node as reduced slope increases the refractory period so Sa node conduction slowed.
Class 3 drugs action?
Effect? Problem?
Use of refractory period?
Block k channels thus blocks k from leaving cell
Action potential duration increased due to longer effective refractory period. Can lead to early after depolarisations.
Another AP can’t happen preventing tetany
Class 4 drugs action?
Effect?
Calcium channel blockers decreasing inward Ca currents
Decrease in phase 4 spontaneous depolarisation due to the AP plateau effect of depolarisation
Effect of b agonist on automaticity?
Muscarinic agonists/adenosine?
Increases as increases initial NA influx by HCN channels so threshold is reached more quickly.
Reduce automaticity as shallower slope
Causes of arrythmogenesis?
Automatic rhythms-ectopic/enhanced AP from SA node
Triggered rhythms-early after depols/delayed after depol from increased cytosolic Ca (digoxin toxicity)
Conduction block-layups but recise
Reentry-circus movement/Reentry
Describe an abnormal anatomic conduction in the heart
Bundle of Kent, leads to preexcitation thus Wolf Parkinson White syndrome. Episodes of rapid heart rate.
Action of drugs required if random generation of AP?
What in case of abnormal conduction?
Decreases phase 4 slope or raise the threshold
Reduce conduction velocity in phase 0 or increase the effective refractory period so heart won’t be excited too soon after.
3 main methods of antiathrymatic drugs?
Learn all the drugs written on a piece of card
Reduce conduction velocity
Suppress abnormal automaticity
Change duration or effective refractory period
A fib can cause?
Differentiate between venous/arterial thrombosis?
DVT and PE
Venous-from stasis of blood, high RBC/fibrin count, low content of platelets
Arterial-low fibrin and high platelet, from plaque rupture following atherosclerosis,
Describe why a healthy endothelium produces/releases prostacyclin?
What happens when endothelium is damaged?
PGl2 binds to platelet receptors increasing Camp in platelets, lowers Ca preventing platelet aggregation so platelets don’t adhere as much as fewer platelet aggregators signals so receptors GPIIb/IIIa are stabilized.
Platelets are activated and adhere to damaged endothelium releasing signalling molecules (thromboxane/ADP/serotonin) which bring more activated platelets and fibrinogen forming a platelet plug via GPIIb/IIIa receptors. Calcium is increased and camp lowered in platelets. Cascade and amplification from platelet to platelet.
If thrombosis are white?
Treat?
If red?
High platelet count
Anti platelet and fibrinolytic drugs
Venous, Treat with paraenteral anticoagulants (heparin), oral anticoagulants (warfarin).
Action of cyclo-oxygenase inhibitor and role?
What does aspirin not completely inhibit platelets?
What does aspirin do at higher doses?
Side effects of aspirin?
Why does aspirin inhibition only last platelet life (7-10days)?
Aspirin, inhibits COX-1 mediated production of thromboxane A2 from arachidonic acid, without this powerful platelet aggregater.
Given at low doses 75mg
Inhibits prostacyclin
Increased bleeding time (haemorrhaged stroke, GI bleeding from peptic ulcer), hypersensitivity, Reye’s syndrome (liver/brain swelling as blocks ox phos)
COX-1 polymorphism resulting in lack of efficacy.
Initial coaxing dose of aspirin in acute coronary syndrome?
Acute ischaemia stroke?
3oo mg
300mg daily twice a week
