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CDL301 > Physiology of the heart 1 > Flashcards

Physiology of the heart 1 Flashcards

1
Q

How many beats a day?

A

100,000 (70bpm)

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2
Q

Key ions in regulating heart contractions?

A

Na+, K+, Ca2+

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3
Q

Describe phase 0 of the cardiac potential

A

‘Rapid depolarisation’ phase
Na+ influx causes ‘ALL OR NOTHING’ depolarisation if -60mV threshold reached, MP goes from -70mV (due to high Ca2+ and Na+ outside, K+ inside) to positive
Causing a sharp upwards deflection.

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4
Q

Describe phase 1 of the cardiac AP

A

‘Partial repolarisation’ phase
Na+ channels RAPIDLY close
Na+ conductance decreases

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5
Q

Describe phase 2 of the cardiac AP

A

‘plateau’ phase
2 = Ca2+
Ca2+ conductance increases SLOWLY (more into the cell)
Initial fall in outward K+
Both of which helps extend plateau of depolarisation as more +ve inside

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6
Q

Why is extension of the depolarisation in phase 2 important?

A

Doesn’t allow successive heart beats to be fired as can’t fire another AP when still depolarising due to +ve MP
This allow time for ventricles to fill with blood and pump it out - if 100x a second couldn’t do this
I.e. prevents tetany in heart
This is called a refractory period i.e. a limit to how fast the heart can got

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7
Q

Which phase prevents tetany in the heart and why?

A

Phase 2 mostly as Ca2+ conductance increases into cardiomyocytes and K+ decreases, so more +ve intracellular membrane potential i.e. further from threshold

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8
Q

Describe phase 3 in the cardiac AP

A

‘Repolarisation’ phase
Ca2+ channels close - decrease in inwards conductance
K+ channels remain open, increasing K+ outflux
Membrane now -ve again

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9
Q

Describe phase 4 of the cardiac AP

A 
'Pacemaker potential' phase
Gradual depolarisation in diastole
Na+ and Ca2+ increasing INFLUX
K+ OUTWARD conductance decreases
so RP gradually more +ve (in diastole i.e. not contracting) until reaches threshold (-60mV) and fires off another AP.
Found in nodal and conducting tissue.
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10
Q

Which cells have pacemaker activity?

A

SAN, AVN, P fibres

SAN the main one

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11
Q

What can take over if SAN fails?

A

AVN and Purkinje fibres.

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12
Q

A patient has slow and ectopic heart beat. Which cells could be impacted?

A

SAN insult. AVN and P fibres take over but with a slower and ectopic beat.

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13
Q

During phase 4 there is gradual repolarisation

A

FALSE - gradual depolarisation as Na+ and Ca2+ INFLUX increase and K+ OUTFLUX decreases

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14
Q

During phase 3, there is an decrease in Ca2+ outflux.

A

FALSE - Ca2+ channels close that let Ca2+ into cell so decrease in influx.

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15
Q

AVN is the main pacemaker in the heart

A

FALSE - SAN responsible for the 70bpm

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16
Q

Describe how the AP spreads down cardiac conduction tissue

A

SAN fires AP 70bpm
This spreads down atrial walls of myocardium causing them to contract in response to depolarisation
Impulses reach AVN where there is a delay due to slow conduction, allowing full contraction of atria and time for ventricles to fill before contraction
Impulse spreads rapidly down bundle of His and Purkinje fibres to ventricles.

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17
Q

Name 4 unique differences of cardiac conducting tissue

A

1) Pacemaker activity (AVN, SAN and P fibres have but slower)
2) Rapid depolarisation (SAN and AVN dont have this phase 0 due to lack of fast Na+ currents as in nodal tissue APs governed by Ca2+)
3) Long AP and refractory period (in ventricles and P fibres only - important to put a limit on HB)
4) Influx of Ca2+ during plateau
LOOK AT LINES ON GRAPH

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18
Q

Name 2 types of arrhythmia’s

A

Abnormal generation

Abnormal propagation

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19
Q

Increased automaticity of heart cells is an example of abnormal propagation arrhythmia

A

FALSE - increased automaticity = generation error i.e. spontaneous activity causes ectopic beats.

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20
Q

Delayed after depolarisation is an example of abnormal generation arrhythmia

A

TRUE - example of triggered activity abnormal generation arrhythmia caused by e.g. too much Ca2+ from a disease.

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21
Q

Name the two type of abnormal propagation arrhythmia’s

A 
Re-entry
Heart Block (AVN blocked so no signals to ventricles)
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22
Q

Name 2 types of abnormal generation arrythmias

A

Triggered e.g. DAD (dad triggers me) - LOOK AT DIAGRAM IN NOTES
Spontaneous (increased automaticity i.e. ectopic beats)

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23
Q

What is the most common type of arrhythmia’s?

A

Re-entry (i.e. abnormal propagation)

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24
Q

Describe each of the arrythmia graphs.

A

Look at diagrams on slides and explanation in notes

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25
Q

The P wave represents ventricular depolarisation

A

FALSE - atrial. P wave = atrial repolarisation = sinus rhythm. Sinus tachycardia is normal duirng exercise.

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26
Q

Sinus tachycardia is normally the sign of a serious illness

A

FALSE - this happens during exercise i.e. P waves will get closer together.

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27
Q

Sinus bradycardia is normally the sign of a serious illness

A

FALSE - normal e.g. sleeping P waves get wider apart

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28
Q

Sinus tachycardia/bradycardia are considered arrythmia’s

A

FALSE - their origin is still SAN (hence Sinus). Atrial tachy/bradycardia = arrythmia’s as AVN origin.

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29
Q

What can cause atrial fibrillation?

A

Atrial thrombus (remember on atrial fibrillation graph theres a pic of CT scan pointing to atrial thrombus)

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30
Q

What’s the difference between atrial and ventricular fibrilation?

A

Atrial occurs in atria so atria can’t contract not ventricles, so defibrilation wont work on atrial.

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31
Q

Ventricular fibrilation is common in older people.

A

FALSE - this is atrial which is more common 1/20 over 65’s have it.

32
Q

What are some outcomes of atrial fibrilation?

A 
Irregular heart beat (V. depol.) due to some beats getting through and some not,
Inefficient output (due to lack of atrial contraction)
Chances of atrial thrombus increase due to lack of atrial contraction which could break off - stroke.
33
Q

What could you treat atrial fibrillation with?

A

Warfarin i.e. anti-coagulants

34
Q

What is a common outcome of ventricular fibrillation?

A

Death due to lack of CO due to lack of V depolarisation (fibrillating instead of contracting). If in first few mins of V fib can shock with defib.

35
Q

What can treat V fib?

A

Defib if in first few mins

36
Q

What can cause V fib?

A

CAD/IHD.

37
Q

Sympathetic stimulation leads to a negative chronotropic effect

A

FALSE - positive i.e. increases force of contraction/HR/CO

38
Q

Positive chronotropic response relates to increased increased heart rate

A

TRUE - brought about by sympathetic NS via B1 adrenergic receptors

39
Q

Which receptors bring about the positive chronotropic response?

A

B1 adrenergic (symp NS).

40
Q

What happens to the slope of the pacemaker potential with sympathetic stimulation

A

Positive chronotropic effect = increase in pacemaker slope as reaches threshold quicker

41
Q

Name 2 effects of the sympathetic NS on the heart

A

Positive chronotropic so increase HR/CO and increases automaticity (bad as increased risk of arrhythmia’s)

42
Q

Why does lots of sympathetic stimulation to the heart increase risks of arrhythmia’s?

A

Increases automaticity.

43
Q

Where does adrenaline get secreted from?

A

adrenal glands

44
Q

Noradrenaline gets secreted from the adrenal glands.

A

FALSE - from sympathetic nerves. Both NE and adrenaline are secreted in sympathetic heart stimulation.

45
Q

Which receptors mediate parasympathetic heart response?

A

Muscarinic Ach receptors in atrial and nodal tissue regulated by vagus nerve (M2)

46
Q

The vagus nerves regulates the sympathetic response.

A

FALSE - para. Acts through Muscarinic Ach R’s

47
Q

When sleeping, the vagus nerve is not dominant

A

FALSE - it is. Para. There is a degree of heart block when you sleep due to increased PR interval prolongation

48
Q

cAMP is involved in parasympathetic response.

A

FALSE - symp. B1 adrenergic receptors act through cAMP.

49
Q

Give an example of a class 1b arrythmia drug

A

Lidocaine (also quinadine, prodainamide)

50
Q

Flecianide is an example of a class 1a arrythmia drug

A

FALSE - 1c (along with propafenone)

51
Q

Which class of anti-arrythmic drugs is disopyramide?

A

1a (Na+ channel blocker)

52
Q

Describe class 2 of anti-arrythmic drugs and give 2 examples

A

Class 2 = beta blockers (beta adrenergic antagonists)
Non-selective - propanolol
Selective - bisoprolol

53
Q

What type of drugs are class II anti-arrythmics?

A

Beta-adrenergic antagonists. (beta-blockers but better to say this).

54
Q

What do class III anti-arrhythmics do?

A

Prolong the cardiac AP, so refractory period also (which is why they’re anti-arrhythmic)

55
Q

Give an example of a class III anti-arrhythmic drug

A

Amiodarone

56
Q

Give an example of a class IV anti-arrhythmic drug

A

Verapamil

57
Q

Class IV drugs act to block adrenergic beta receptors

A

FALSE - this is class II. Class IV are Ca2+ channel blockers

58
Q

Which class of anti-arrhythmic drug is digoxin?

A

TRICK QU - doesn’t fit into any. It belongs to cardiac glycosides (contain sugar group).

59
Q

How does digoxin work?

A

Inhibits the Na+/K+ pump Which interacts directly with Na+/Ca2+ pump
If Na+/K+ pump inhibited, gradient of Na+ inside to outside cell is reduced
Na+/Ca2+ pump therefore reduced activity of extruding Ca2+ from cell
Increased intracellular Ca2+
1) Force of contraction increase (positive ionotropic)
2) Therefore ectopic activity increased (bad)

Increases vagal tone (para NS) to work on nodal tissue, so 3) bradycardia and 4) slower AVN conduction
Decreases heart rate (negatively chronotropic)

60
Q

Why is digoxin seen as better in some cases of arrhythmia’s?

This might be wrong!!!

A

It doesn’t suppress HR like other’s, increases it slightly (positive ionotropic) due to increase Ca2+ (and thus ectopic activity) THIS MIGHT BE WRONG !!!!!

61
Q

Why is digoxin sometimes more dangerous in some cases of arrhythmia’s?

A

Increases Ca2+ which increases ectopic activity i.e. pro-arrhythmic - fine line between treating arrhythmia’s and triggering.

62
Q

Why does digoxin often come with adverse effects?

A

Narrow therapeutic window

63
Q

What are common digoxin side effects?

A

Nausea, vomiting, confusion (easy to think gastroentitis but if taking digoxin probs digoxin toxicity).

64
Q

What condition could the side effects of digoxin often be confused with?

A

Gastroentitis

65
Q

Why is digoxin useful in treating atrial fibrillation?

A

Reduces ventricular response to atrial fibrillation as AVN delay encouraged so impulses to ventricles reduced (in atrial fibrillation there are increased ventricular firing)

66
Q

Digoxin is often used in heart failure

A

TRICK QU - only in severe HF as positively ionotropic (increases force of contraction or contractility)

67
Q

What syndrome can anti-arrthmics cause?

A

QT prlongation. Especially amiodarone.

68
Q

Why may Na+ channel blockers be seen as superior in some cases of arrhythmia?

A

Use dependance. They only bind to Na+ channels in the inactive state i.e. when they are being used more so will only affect part of the heart affected by arrhythmia (tachycardia as Na+). They do not bind to closed/open state.

69
Q

What is a problem is class III anti-arrhythmics?

A

QT prolongation. Their mechanism of action is to extend the cardiac AP, so extend repolarisation as well which can extend QT interval and can cause ventricular polymorphic tachycardia (V tac with variable amplitude). E.g. amiodarone

70
Q

Name 2 disadvantages of amiodarone

A

QT prolongation so polymorphic V tachy.
Large volume of distribution so takes 3 months to build up in system and 3 months to leave after stopping treatment. This means it affects a lot of tissues - liver, thyroid, eyes etc.

71
Q

What drug would be advised against taking amiodarone with?

A

Warfarin because amiodarone has a large volume of distribution so it displaces warfarin i.e. leading to coagulation

72
Q

Why would amiodarone affect the thyroid?

A

Because it has an iodine rich structure which generates free iodine which influences iodine metabolism due to large V of distribution so can cause hypo or hyperthyroidism - need to treat this on top.

73
Q

A patient is breathless who is taking amiodarone. Why?

A

Interstitial pneumonia (inflammatory condition of the lungs)

74
Q

A patient has a slate grey colour. What may be wrong with him?

A

Chronic use of amiodarone.

75
Q

What effect may amiodarone have on the eyes?

A

Corneal micro-deposits, blueish halo, optic neuropathy, damage to optic nerve.

CDL301 (3 decks)

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