Lecture 2

Question 1

cardiac action potential - phase 0

Answer 1

Rapid depolarisation
all or nothing
Rapid Na+ influx

Question 2

cardiac action potential - phase 1

Answer 2

Partial depolarisation

Rapid Na influx deactivated

Question 3

cardiac action potential - phase 2

Answer 3

Platau
slow inward Ca current
initial fall in outward K
heart contracts

Question 4

cardiac action potential - phase 3

Answer 4

Repolarisation
deactivation of inward Ca current
increasing outward K current
ready for another activation

Question 5

cardiac action potential - phase 4

Answer 5

Pacemaker potential 
Gradual depolarisation in diastole (relaxation)
Found in nodal and conducting tissue 
increasing inward Na/Ca
Decreasing outward K

Question 6

Function of the AV node

Answer 6

conduction tissue to the ventricles
causes delay - so atria dont contract at same time as ventricles
instant activation of ventricles following this

Question 7

Features of nodal tissue

Answer 7

drives pacemaker

no rapid depolarisation - no fast Na current, fast Ca current instead`

Question 8

Features of abnormal impulse propagation

Answer 8

o Re entry – trail of refractoriness – circus movement – go back to cells
o Heart block – AV block – block at AV node – 200milliseconds – PR interval
o 2nd degree – transient –
o 3rd degree – complete block – atria contract independently – ventricles rely on backup pacemaker

Question 9

Features of abnormal impulse generation

Answer 9

triggered activity - delayed after depolarisation

increased automaticity - ectopic activity

Question 10

Tachycardia

Answer 10

faster heart rate

Question 11

Bradycardia

Answer 11

Slowed heart rate

Question 12

Atrial tachycardia

Answer 12

faster heart rate - due to atria
multiple p waves
atria contract too quickly
ventricles dont contract at same speed due to AV

Question 13

Ventricular tachycardia

Answer 13

Ventricles contract quicker
slower passage through the ventricles
wide complex ventricular rhythm

Question 14

atrial fibrillation

Answer 14

• Atria act as passive channels for blood flow
• Not contracting
• Irregular chaotic
• Just P waves
• Heart rate fast
• Can get atrial thrombus – anticoagulants

Question 15

ventricular fibrillation

Answer 15

cardiac arrest 
no defined rhythm or outfit 
wide complex
irregular ventricular response 
use defibrilator to trigger heart back to normal rhythm

Question 16

Sympathetic stimulation of heart

Answer 16

o Increased heart rate (positive chronotropic effect – affects heart rate)
o β-1 adrenoceptors (cAMP)
o Increased slope of pacemaker potential
o Increases automaticity – intrinsic capacity of the heart to fire off APs

Question 17

Parasympathetic stimulation of heart

Answer 17

o	Reduces heart rate
o	Muscarinic (M2) acetylcholine receptors
o	M2 mainly in nodal and atrial tissue
o	Decreased slope of pacemaker potential
o	Decreased automaticity
o	Inhibits atrioventricular conduction

Question 18

what are the 4 classes of Vaughan Williams classification

Answer 18

• Class I: Sodium channel blockers
o Ia - disopyramide, quinidine, procainamide
o Ib - lidocaine, mexilitene
o Ic - flecainide, propafenone
• Class II: Beta adrenceptor antagonists –
o propranolol, nadolol, carvedilol (non-selective)
o bisoprolol, metoprolol (β1-selective)
• Class III: Prolong the action potential
o amiodarone, sotalol
• Class IV: Calcium channel blockers
o verapamil, diltiazem

Question 19

What are the features of digoxin

Answer 19

• Cardiac glycoside
• Inhibit Na/K pump
• Can get increased intracellular Ca
• Main effects are on the heart:
o Bradycardia (increased vagal tone)
o Slowing of atrioventricular conduction (increased vagal tone)
o Increased ectopic activity
o Increased force of contraction (by increased intracellular Ca) – important
• Narrow therapeutic range
o Nausea, vomiting, diarrhoea, confusion
• Used in atrial fibrillation (AF) to reduce ventricular rate response
• Use in severe heart failure as positively inotropic

Question 20

what are the adverse affects

Answer 20

• Has iodine in – thyroid
• Causes QT prolongation and Polymorphic ventricular tachycardia
• Goes everywhere in the body:
o Interstitial pneumonitis – lungs
o Abnormal liver function
o Hyperthyroidism / Hypothyroidism – iodine metabolism – overactive or underactive
o Sun sensitivity
o Slate grey skin discolouration
o Corneal microdeposits
o Optic neuropathy – v serious
• Multiple drug interactions
o Esp coagulants – warfarin – patient becomes over anti-coagulated
• Very large volume of distribution
o If u stop it will stay in system for 3 months