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

L2 - Physiology of the Heart I Flashcards

(55 cards)

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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?

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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?

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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
How can you measure an AV block?
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
What happens in a third degree heart block?
Atria contract independently of the ventricles Ventricles contract much slower but it keeps you alive Most require pacemakers
27
What are the two ways arrhythmias can be classified?
Origin - Sinus - Atrial - Nodal - Ventricular Heart rate - Bradycardia - Tachycardia
28
Normal sinus rhythm
Originates in sinus node of right atrium After P wave short delay before QRS Rate – 60-80
29
Sinus bradycardia
Same as normal sinus rhythm except the whole thing is slower Rate – 30-40 Occurs during sleep
30
Sinus tachycardia
Same as normal sinus rhythm except the whole thing is faster
31
Atrial tachycardia
Originates in the atria -multiple P waves Atria contract quickly Ventricles contract slightly slower due to delay at AVN node
32
Ventricular tachycardia
Path it is taken through the ventricles is slower - wide complex - Takes longer through heart conduction tissue Ventricles still contracting quickly
33
Ventricular fibrillation
No clear rhythm Wide complex Ventricles in fibrillation Causes cardiac arrest Require defibrillator
34
Atrial fibrillation
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
What are the two types of autonomic control of the heart?
Sympathetic | Parasympathetic
36
What is sympathetic stimulation of the heart?
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
What is parasympathetic stimulation of the heart?
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
How does parasympathetic stimulation of the heart inhibit atrioventricular conduction?
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
How are anti arrhythmic drugs classified?
Vaughan Williams classification
40
Class I anti arrhythmic drugs
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
Class I anti arrhythmic drugs examples
Ia - disopyramide, quinidine, procainamide Ib - lidocaine, mexilitene Ic - flecainide, propafenone
42
Class II anti arrhythmic drugs
Beta adrenceptor antagonists
43
Class II anti arrhythmic drugs examples
Propranolol, nadolol, carvedilol (non-selective) | Bisoprolol, metoprolol (β1-selective)
44
Class III anti arrhythmic drugs
Prolong the action potential
45
Class III anti arrhythmic drugs examples
Amiodarone | Sotalol
46
Class IV anti arrhythmic drugs
Calcium channel blockers | Act on the heart muscle
47
Class IV anti arrhythmic drugs examples
Verapamil | Diltiazem
48
What does Digoxin do?
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
What are digoxin main effects on the heart?
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
What is digoxin used for?
Atrial fibrillation to reduce ventricular rate response - Blocks AV node enough to slow everything down Severe heart failure as positively inotropic
51
What are the issues with digoxin?
Narrow therapeutic range | Can cause nausea, vomiting, diarrhoea, confusion
52
Why does digoxin increase vagal tone?
Vagal nerve decreases the heart rate | This is accentuated by Digoxin
53
What are the issues with class III drugs?
Prolong the QT interval | Can trigger arrythmias -polymorphic ventricular tachycardia
54
What are the adverse effects of amiodarone (class III)?
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
Where does amiodarone spread?
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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