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Personalised Medicine - Cardiovascular > L2 - Physiology of the Heart I > Flashcards

L2 - Physiology of the Heart I Flashcards

1
Q

What do valves determine?

A

The direction of blood flow

When heart contracts – mitral valves closes so blood goes up the aorta

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2
Q

What is the heart driven by?

A

Its own intrinsic pace maker

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3
Q

What kind of tissue is the heart?

A

Excitable tissue
Voltage gated channels in the membrane
Transmit Na, Ca and K predominantly
Resting membrane potential -70mV

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4
Q

How long does a whole heart beat take?

A

150ms

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5
Q

What are the 4 phases of the cardiac cycle?

A 
Phase 0 - rapid depolarisation 
Phase 1 - partial repolarisation 
Phase 2 - plateau
Phase 3 - repolarisation 
Phase 4 - pacemaker potential
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6
Q

What is phase 0 of the cardiac cycle?

A

Critical membrane potential - 60mV
All or nothing depolarisation
Rapid Na influx

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7
Q

What is phase 1 of the cardiac cycle?

A

If membrane stays depolarised for more than a few ms

Rapid Na influx deactivation

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8
Q

What is phase 2 of the cardiac cycle?

A

Slow inward Ca current
Initial fall in outward K
Heart is refractors –> stops further action potentials occurring too quickly

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9
Q

What is phase 3 of the cardiac cycle?

A

Deactivation of inward Ca current
Increasing outward K current
Cells reset themselves back to baseline

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10
Q

What is phase 4 of the cardiac cycle?

A

Gradual depolarisation in diastole
Found in nodal and conducting tissue
Decreasing outward K
Increasing inward Na and Ca

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11
Q

What 3 things does depolarisation trigger in the heart?

A

Rapid Na influx
Slow Ca influx
Reduced K outflux

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12
Q

Where is the sinoatrial node?

A

Right atrium

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13
Q

What is the role of the SAN?

A

Intrinsic pacemaker
Fires action potential which get transmitted down conduction tissue
Some go across atria

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14
Q

What is the role of the AVN?

A

Delays conduction - by 200ms
If ventricles instantaneously activated after atria – they would contract at same time  inefficient
Fires action potential which gets transmitted down His bundle and Purkinje fibres

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15
Q

Where is pacemaker activity found?

A 
In nodal and conducting tissue 
- AV node
- SA node 
- Purkinje fibres
It is slow depolarisation 
- No fast Na current
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16
Q

What electrical activity is found in Purkinje fibres and ventricles?

A

Long action potential due to plateau –> causes refractory period
This plateau is mediated by Ca

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17
Q

What does each wave in the ECG trace mean?

A

P wave – atrial activity
QRS – rapid ventricular depolarisation
T wave – repolarisation

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18
Q

What two arrhythmias can cause abnormal impulse generation?

A

Triggered activity

Increased automaticity

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19
Q

What is triggered activity?

A

Delayed after-depolarisation

If you narrow timing between stimulations the after polarisation is so big it triggers another action potential

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20
Q

What is increased automaticity?

A

Ectopic activity

Lower level pace maker takes over

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21
Q

What happens if the heart pacemaker breaks down?

A

Other part of the heart with pacemaker potentials can fire to keep you alive

  • Tend to fire at a slower rate
  • E.g. Purkinje fibres

Get abnormal pulse if they do not do this correctly

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22
Q

What two arrhythmias can cause abnormal impulse propagation?

A

Re-entry

Heart block

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23
Q

What is re-rentry?

A

Circular movement of impulses
If impulse has to go around an obstruction - waveforms form normally
As waveforms rushes over heart it leaves behind a trail of refractiveness
- Stops the impulse going backwards
However, if damage to the heart you can get circus movement and re-entrant excitation

24
Q

What is an heart/atrioventricular block?

A

Block between atria and ventricles at the AV node
- AV node normally causes a delay
Disease states can lead to complete blockages
- Can lead to a non-conducting P wave –> transient –> 2nd degree
- If AV node blocked completely –> 3rd degree

25
Q

How can you measure an AV block?

A

Can be measured on an ECG
Gap between P wave and QRS – time delay at the AV node – PR interval
PR interval prolonged in a heart block –> 1st degree

26
Q

What happens in a third degree heart block?

A

Atria contract independently of the ventricles
Ventricles contract much slower but it keeps you alive
Most require pacemakers

27
Q

What are the two ways arrhythmias can be classified?

A

Origin

  • Sinus
  • Atrial
  • Nodal
  • Ventricular

Heart rate

  • Bradycardia
  • Tachycardia
28
Q

Normal sinus rhythm

A

Originates in sinus node of right atrium
After P wave short delay before QRS
Rate – 60-80

29
Q

Sinus bradycardia

A

Same as normal sinus rhythm except the whole thing is slower
Rate – 30-40
Occurs during sleep

30
Q

Sinus tachycardia

A

Same as normal sinus rhythm except the whole thing is faster

31
Q

Atrial tachycardia

A

Originates in the atria -multiple P waves
Atria contract quickly
Ventricles contract slightly slower due to delay at AVN node

32
Q

Ventricular tachycardia

A

Path it is taken through the ventricles is slower - wide complex
- Takes longer through heart conduction tissue
Ventricles still contracting quickly

33
Q

Ventricular fibrillation

A

No clear rhythm
Wide complex
Ventricles in fibrillation Causes cardiac arrest
Require defibrillator

34
Q

Atrial fibrillation

A

Atria don’t contract at all
- Just acting as channels to the blood
- Can get blood clots in the atria –> atrial thrombus
Atria fibrillations waves occasionally trigger the AVN and fire off the ventricles
Random ventricular rhythm
Rate – tends to be fast

35
Q

What are the two types of autonomic control of the heart?

A

Sympathetic

Parasympathetic

36
Q

What is sympathetic stimulation of the heart?

A

Increased heart rate –> positive chronotropic (affect on heart rate) effect
Release adrenaline –> β-1 adrenoceptors –> cAMP
Increased slope of pacemaker potential –> fires action potentials quicker
Increases automaticity –> intrinsic ability of heart to fire its own action potentials
Can trigger arrhythmias in people that are susceptible

37
Q

What is parasympathetic stimulation of the heart?

A

Reduces heart rate –> negative chronotropic effect
Release Ach –> Muscarinic (M2) acetylcholine receptors
- M2 mainly in nodal and atrial tissue
Decreased slope of pacemaker potential –> fires action potentials slower
Decreased automaticity
Inhibits atrioventricular conduction

38
Q

How does parasympathetic stimulation of the heart inhibit atrioventricular conduction?

A

Through vagal nerve which acts on the nodal tissue
Inhibits AV node
Nervous system superimposing itself on the hearts normal function
E.g. common in athletes with low heart rates

39
Q

How are anti arrhythmic drugs classified?

A

Vaughan Williams classification

40
Q

Class I anti arrhythmic drugs

A

Sodium channel blockers
If you can influence the depolarisation – can influence tachycardia
Na channels also important for contractility of the heart
Have to be careful not to influence this while stopping the arrythmia

41
Q

Class I anti arrhythmic drugs examples

A

Ia - disopyramide, quinidine, procainamide
Ib - lidocaine, mexilitene
Ic - flecainide, propafenone

42
Q

Class II anti arrhythmic drugs

A

Beta adrenceptor antagonists

43
Q

Class II anti arrhythmic drugs examples

A

Propranolol, nadolol, carvedilol (non-selective)

Bisoprolol, metoprolol (β1-selective)

44
Q

Class III anti arrhythmic drugs

A

Prolong the action potential

45
Q

Class III anti arrhythmic drugs examples

A

Amiodarone

Sotalol

46
Q

Class IV anti arrhythmic drugs

A

Calcium channel blockers

Act on the heart muscle

47
Q

Class IV anti arrhythmic drugs examples

A

Verapamil

Diltiazem

48
Q

What does Digoxin do?

A

Cardiac glycoside
Inhibit Na/K pump
- Works in combination with the Na/Ca pump
If you block Na/K ATP you get an increase in intracellular Ca

49
Q

What are digoxin main effects on the heart?

A

Bradycardia (increased vagal tone)
Slowing of AV node conduction (increased vagal tone)
Increased ectopic activity (due to increased intracellular Ca)
Increased force of contraction (due to increased intracellular Ca)
None of the other drugs increase contraction

50
Q

What is digoxin used for?

A

Atrial fibrillation to reduce ventricular rate response
- Blocks AV node enough to slow everything down
Severe heart failure as positively inotropic

51
Q

What are the issues with digoxin?

A

Narrow therapeutic range

Can cause nausea, vomiting, diarrhoea, confusion

52
Q

Why does digoxin increase vagal tone?

A

Vagal nerve decreases the heart rate

This is accentuated by Digoxin

53
Q

What are the issues with class III drugs?

A

Prolong the QT interval

Can trigger arrythmias -polymorphic ventricular tachycardia

54
Q

What are the adverse effects of amiodarone (class III)?

A

QT prolongation - polymorphic ventricular tachycardia
- Treat one rhythm problem and you cause another rhythm problem
Spreads everywhere in the body
Multiple drug interactions
Large volume of distribution

55
Q

Where does amiodarone spread?

A

Lung - interstitial pneumonitis
Liver - abnormal function
Thyroid - hyperthyroidism / Hypothyroidism
Skin - sun sensitivity, slate grey skin discolouration (only after several years)
Eye - corneal microdeposits and optic neuropathy

Personalised Medicine - Cardiovascular (11 decks)

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