Arrhythmias and drugs

Question 1

What causes a long QT segment?

Answer 1

long depolarisations

Question 2

What causes tachycardic arrythmias? (4)

Answer 2

• ectopic pacemaker activities (eg from damaged area after MI or latent pace maker activated from ischaemia)
• afterdepolarisations
• atrial flutter/ fibrillation
• re- entry loops (many in atria from dilation and fibrosis cause fibrillaiton, or can get one in AV node, or across to venticles)

Question 3

What causes bradycardic arrhythmias? (2)

Answer 3

• sinus bradycardia (SA node dysfunction due to fibroiss, drugs ect)
• conduction blocks (problems at AV node of bundle of His, drugs can cause these problems)

Question 4

What is a delayed after depolarisation and what increases likelyhood of it occuring?

Answer 4

• a smaller depolarisation of the myocytes 50ms or so after the main one
• more likely if intracellular Ca is high as cell more excitable

Question 5

What is an early- after depolarisation? what increases the likley hood of it ocuring?

Answer 5

Depolarisations of the venticles occuring before the cell has fully repolarised.
They’re more likely to happen if the action potential is prolonged (long QT)
- which can be in hypokalaemia, or lomng QT syndrome (congenital)

Question 6

What are the major concerns with supraventricular and ventricular rythms?

Answer 6

supra= thrombus 
ventricular= high risk of V fib

Question 7

Why is fast tachycardia a problem?

Answer 7

• not enough filling time
• reduced CO
• high o2 demand
• high MI risk

Question 8

why might atrial fibrilliation or atrial flutter occur?

Answer 8

• atria stretch due to vol overload (eg in mitral stenosis)
• fibrosis and damage
• many reentrant loops or ectopic centres

Question 9

What is the difference between atrial flutter and fibrillation?

Answer 9

fibrillation is many foci meaning wavey baseline and irregular rhythm
flutter causes tooth like baseline with regular number of P waves per Q wave

Question 10

Describe the re- entrant mechanism for generating arrhthmias

Answer 10

• excitation spreads normally until it meets something which splits its direction
• normally impulse goes to left or it and right of it and cancels itself out when the two impulses meets behind it
• however if one route is incompletely/ unidirectionally blocked (eg after fibrosis) the impulses will not meet in the middle but travel the whole way round the loop over and over again, creating a centre from which action potentials will be generated from

Question 11

What is AV nodal re- entry?

Answer 11

AV node defect where it gets caught in a re- entry loop where the AV nodes depolarisation causes its own depolarisation again and so this becomes a tachycardic focus. This happens here as it develops a fast and slow pathway.

Question 12

What is ventricular pre excitation?

Answer 12

Where an accessory pathway forms between the atria and the ventricles creating a re- entry loop from the atria all the way across to the ventricles. Wolff- parkinson- white symdrome is an example of this.

Question 13

What are the 4 basic classes of anti- arrhythmic drugs?

Answer 13

1. drugs blocking the voltage sensitive sodium channels
2. antagonists of B- adrenoreceptors
3. drugs blocking K+ channels
4. Drugs blocking ca2+ channels

Question 14

How does lidocaine (voltage dependant Na channel blocker) help reduce risk of V. fib in patients w/ Ventricualr tachycardia following an MI?

Answer 14

• Damaged areas of myocaridum are generally depolarised following MI as its dead, no ATP, Na/K pump stops, Na moves in
• This means they are often centres for tachycardic ectopic beats
• Lidocaine will bind to open Na channels and block them
• so cant act as a center for ectopic beats
• however wont affect heart impulse as it dissociates from Na channel quickly- just after the end of the action potential

Question 15

What drugs should be used to treat supraventricular rhythms and why?

Answer 15

• B adrenoreceptor antagonist (propanolol, atenolol)
  slows conduction to AV node so slow ventricular rate in AF
• Ca channel blockers
  slows conduction to and from AV node and so slows ventricular rate
• adenosine
  enhances K+ conductance so hyperpolarises cells of conducting tissues to help terminate arrhythmias

Question 16

Why do K+ channel blockers tend to be proarrythmic?

Answer 16

• block K+ conductance
• prolong action potential
• in theory should prevent another action potential as longer refreactory period
• but in reality this leads to early after depolarisations

Question 17

Which K+ channel blocker is used post MI to surpress ventricular rhytms and in wolff- parkinsons- white syndrome and why?

Answer 17

• amiodarone
• blocks K+ channels to extend absolute refractory period so cant get re entry loops
• but also has other actions of B1, ca and Na channels which mean it doesnt tend to create early after depolarisations

Question 18

How do cardiac glycosides (such as digoxin) increase cardiac output?

Answer 18

• inhibit Na/K atpase
• Na builds up in cell
• NCX swaps
• Ca into cell
• increased sensitivity of ca channels and machinery to increase force of contraction
• however slows HR as it increases vagal activity

Question 19

When can cardiac glycosides in heart failure and why?

Answer 19

• when Pt have atrial fibrillation
• dont want to give ACE inhibitor ect as would reduce CO too low
• give this to help keep HR low but will keep CO high as increases contractability

Question 20

Why are drugs like B1 agonists not usually used in heart failure?

Answer 20

• it would increase CO short term
• but increases workload of heart so poor prognosis long term
• are used in acute but reversible heart failure for example after surgery

Question 21

What drugs should be used to treat heart failure?

Answer 21

• ACE inhibitors - cause less water reabsorbtion and vasodilates to reduce pre and afterload
• angiotensin2 inhibitors if ACE inhibitors not tolerated
• Beta blockers (low dose, keeps HR low)
• Diuretics (less blood volume, helps reduce the odema)

Question 22

When are organic nitrates used and how to they work?

Answer 22

• treatment of angina
• it is reduced to Nitric oxide in the body (NO)
• this is powerful vasodilator by activating guanylate cyclase which converts GTP to cGMP which activates PKG which decreases intracellular Ca2+
• this helps reduce preload (less work for heart)
• also dilates collateral coronary arteries to help get around plaques

Question 23

Why do nitiric oxides have more of an effect on veins than arteries?

Answer 23

less endogenous NO in veins

Question 24

other than organic nitrates, how is angina treated?

Answer 24

B blockers
Ca channel antagonists
- slow heart rate and vasodilate

Question 25

When are antithrombic drugs needed?

Answer 25

A. fib
acute MI
Mechanical prosthetic heart valves

Question 26

What antithrombic drugs are there? (5) Describe mode of action breifly

Answer 26

• heparin (inhibits thrombin, short term IV)
• fractioned heparin (same but long term, subcutaneous)
• warfarin (oral, inhibits vit K)
• oral thrombin inhibitors (digabatran)
• anti platelet drugs- aspirin- mainly following MI

Question 27

What drug is given following a cardiac arrest?

Answer 27

adrenaline

increase contractability to hope some residual activity will restart heart

Question 28

What is a palpitation? What can cause them?

Answer 28

a noticably strong, rapid or irregular heart beat. 
due to:
- caffine
- stress 
- heighened awareness of normal heart beat (night)
- sinus tachycardia 
- ectopic beats 
- atrial tachycardia (SVT, fibrillation)