Arrythmias And Drugs Flashcards
What is an Arrhythmia/ Dysrhythmia
An abnormal heart rate/ rhythm
Identify 4 causes of tachycardia
Conduction delay-> A re-entry loop
Ectopic pacemaker activity from a damaged area of myocardium
Afterdepolarisations after the action potential (Triggered activity)
Atrial fibrillation/ flutter (Flutter- Regular tachycardia of atria, which also beat more frequently than ventricles)
Identify 2 causes of bradycardia
Conduction block (Problem at AV node or His bundle)
Sinus bradycardia
When are Delayed and Early after-depolarisations more likely to happen
Delayed- High intracellular Ca
Early- If Action Potential is prolonged (Longer QT)
What are the 4 classes of Anti-Arrythmitic drugs
Class 1: Na+ channel blockers
Class 2: B-adrenoceptor antagonists
Class 3: K+ channel blockers
Class 4: Ca2+ channel blockers
How do Na channel blockers work
Why is there little effect in normal tissue
Which tissue do they preferentially work in
Block Na+ channels if in OPEN or INACTIVE state
Little effect in normal cardiac tissue, as it blocks during depolarisation bu dissociates rapidly in time for next AP
Preferentially blocks damaged depolarised tissue (As more channels open)
How do Beta-adrenoceptor antagonists work
How do they affect the slope of pacemaker potential at SA Node
How do they affect conduction at AV Node
Act at Beta-1 adrenoceptors in heart to block sympathetic action
Decreased slope of pacemaker potential
Slowed conduction at AV node
Give 2 reasons Beta-blockers are used after an MI
- Counter increased sympathetic activity (due to MI)
2. Reduce O2 demand, so reduced Myoarcidial Ischaemia
Name 1 Na channel blocker and 2 Beta-adrenoceptor antagonists
Na channe blocker: Lidocaine
B-Adrenoceptor Antagonists: Propranolol, Atenolol (Beta blockers)
How do K+ channel blockers work
Why are they not normally used
Name 1 exception and say when it is used
Prolong action potential, lengthening the Absolute Refractory Period
They prolong the QT interval, so can cause an arrhythmia
Amiodarone, used to treat tachycardia
How do Ca channel blockers work in 4 ways
- Decrease slope of AP at SA node
- Decrease AV Node conduction
- Decreased Inotropy
- Vasodilation
How do Non-dihydropyridine Ca channel blockers differ from dihydropyridine
Non-dihydropyridine: Don’t prevent arrhythmias, but act on vascular smooth ,uncle
How does IV adenosine work in 2 ways
What is it used to treat
What is one con
Acts on A1 receptors at AV node and enhances K+ conductance.
Also, acts on Gi proteins-> Less cAMP-> Reduced ‘Funny current’
Terminating re-entrant Supraventricular Tachycardia
Short half life
What are ACE Inhibitors used to treat
How in 2 ways?
To treat Hypertension and Heart failure
Vasodilation-> Reduced Afterload of heart
Decreased fluid retention-> Reduced Preload of heart as lower blood volume
(Reduced workload of heart)
What is a side effect of using ACE inhibitors to treat Hypertension and Heart Failure
What drugs can be used instead
Dry cough due to Bradykinin buildup
Can use Angiotensin II receptor blockers instead
What 2 things can Diuretics be used to treat
Heart failure and hypertension
What kind of drugs are Cardiac Glycosides and B-adrenoceptor agonists
Name 1 of each
Positive inotropes
Cardiac Glycoside: Digoxin
B agonist: Dobutamine
What can Cardiac Glycosides be used to treat
How do they work primarily in 3 steps
What is the second way they work
Heart failure accompanied by Afib
- Inhibit the Na-K pump, so Intracellular Na+ Increases
- Decreased NCX activity, so Ca2+ builds up SR
- Positive Inotropy
Increasing vagal input to heart, reducing HR
What are 2 used for Beta adrenoceptor agonists
Why are cardiac glycosides not usually used
Treating cardiogenic shock
Treating Acute but reversible heart failure
They make heart contract harder, increasing the workload, so worse in long-run
What is Angina
What drugs can be used to treat this, how do they affect work load/ blood supply to heart
Insufficient supply of O2 to Myocytes, without death of the cells
Reduced workload: Organic nitrates, B antagonists, Ca blockers
Increased blood supply: Ca blockers, Organic nitrates
How do Organic Nitrates work in 3 steps
React with -SH groups in vascular smooth muscle-> NO2- released
NO2- reduced to NO, released from endothelial cells
NO causes vasodilation
Rank the effectiveness of Organic Nitrates on veins, arteries and arterioles
Veins- Most effective
Arteries
Arterioles- Least effective
What is the Primary Action of Organic Nitrates
What is the Secondary Action
Venodilation lowers preload, so heart fills less and contracts less, so less O2 needed
Dilation of coronary arteries= Improved O2 delivery
Name 3 conditions that have increased risk of thrombus formation
Name 2 drug types that can be given to treat
Atrial fibrillation
Acute MI
Valve disease
Anticoagulants
Anti-platelet drugs
