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CDL301 Cardiovascular Pharmacology Refesher > Lecture 2 Physiology of the Heart I > Flashcards

Lecture 2 Physiology of the Heart I Flashcards

1
Q

How do cardiovascular drugs intervene with different aspects of physiology

A

Cardiovascular drugs interfere with normal physiology or pathophysiology where abnormal function has occurred as a result of disease

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2
Q

What happens during phase 0 of the cardiac action potential

A

Voltage-gated Na+ channels open and rapid Na+ influx depolarises the me and triggers opening of more Na+ channels creating a positive feedback loop and a rapidly rising membrane potential.

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3
Q

What happens during phase 1 of the cardiac action potential

A

Na+ channels close when the cell depolarises and the membrane potential peaks at around +30mV. At this point there is a deactivation of Na+ influx which results in a partial outward current and a small repolarisation

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4
Q

What happens during phase 2 of the cardiac action potential

A

Ca2+ entering through the now open voltage-gated Ca2+ channels prolongs depolarisation of the membrane potential results in the plateau phase. Plateau falls slightly because of some K+ leakage by most K+ channels remain closed until the end of the plateau. This is extremely important for the timing of the cardiac action potential

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5
Q

What happens during phase 3 of the cardiac action potential

A

Ca2+ channels close and Ca2+ is transported out of the cell. K+ channels open and rapid K+ efflux returns the membrane to its resting potential. This is the repolarisation phase of the cardiac action potential

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6
Q

How does the pacemaker potential differ to the cardiac action potential

A

The pacemaker potential is much shorter than the cardiac action potential due to the absence of a plateau phase. In addition the pacemaker potential has not resting membrane potential but instead is gradually depolarising due to slow Na+ influx

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7
Q

Which cells exhibit the cardiac action potential in the heart

A

Contractile cells such as cardiac myocytes

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8
Q

Which cells in the heart exhibit the pacemaker potential

A

Nodal and conducting tissue such as the AVN SAN Purkinje fibres

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9
Q

What ion movement mediates the rapid depolarisation in the pacemaker potential

A

Ca2+ influx

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10
Q

Explain what currents and ion movements occur in the pacemaker potential

A

In the pacemaker cells there is no resting membrane potential. Instead the membrane potential is gradually depolarising due to cation currents mediated by the funny channels (If). These funny currents bring the membrane potential to threshold where they activated voltage-gated Ca2+ channels. Opening of voltage-gated Ca2+ channels leads to rapid Ca2+ influx which mediates the rapid depolarisation phase of the pacemaker potential. At peak positive potential the Ca2+ channels close and K+ channels open. The fast K+ efflux mediates repolarisation of the pacemaker potential. Once repolarisation occurs the If channels are activated again due to the negative potential and so can mediate the gradual depolarisation once more.

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11
Q

Draw and explain the cardiac action potential

A

See completed diagram below

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12
Q

Draw and explain the pacemaker action potential

A

See completed diagram below

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13
Q

What is meant by atrioventricular delay

A

After the atria contract there is a slight delay before the ventricles do so. This is mediated by the AVN which delays passing the action potential down through the bundle of his to the ventricles. This allows the atria to finish contraction and maximises the amount of blood entering and thus is pumped by the ventricles

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14
Q

What are the two main mechanisms of arrhythmias

A

Abnormal impulse generation or abnormal impulse propagation

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15
Q

Give some examples of activity that can cause abnormal impulse generation in arrhythmias

A

Triggered activity and increase automaticity/ectopics

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16
Q

Give some examples of activity that can cause abnormal impulse propagation in arrhythmias

A

Damage to the heart muscle causing re-entrant activity and heart block

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17
Q

What is meant by triggered activity

A

This is where an action potential fires and after repolarisation there can be further depolarisation that leads to the threshold for further action potential firing

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18
Q

What causes triggered activity

A

Ca2+ overload in the cell

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19
Q

What can be the effects of triggered activity

A

Triggered activity can lead to ectopic beast ventricular tachycardia and subsequently ventricular fibrillation

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20
Q

What feature of triggered activity is seen on an ECG

A

The magnitude of after-depolarisations increases with multiple initial depolarisations

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21
Q

What is meant by increased automaticity

A

Usually a problem with the pacemaker cells whereby the fire impulses spontaneously. This can cause ectopic beats

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22
Q

What is meant by re-entrant activity

A

Re-entrant activity occurs as a result of damage to the cardiac muscle which causes a blockage of anterograde conduction. This results in the impulses travelling in the wrong direction around the heart muscle. Impulses become able to travel in the reverse direction through the region of damaged cardiac muscle. This in turn leads to associated circus movement

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23
Q

First degree heart block is benign T or F

A

T

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24
Q

What is seen in patients with first degree heart block

A

Increase in the PR interval due to electrical signals taking longer to get some the atria to the ventricles

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25
Q

First degree heart block is commonly seen in a certain group of people why is this

A

It is often seen in athletes where the high levels of training has caused changes at the level of the heart

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26
Q

What is often seen in patients with second degree heart block

A

Normal P wave corresponding to atrial depolarisation but the occasional absence of ventricular depolarisation and a missing QRS complex

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27
Q

What causes the features seen on the ECGs of patients with second degree heart block

A

The SAN node impulses reach the AVN but some of these impulses fail to generate ventricular depolarisation

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28
Q

What are the subtypes of second degree heart block and how do they differ

A

Mobitz type 1 is where patients have an increased PR interval and occasional failure to generate QRS complexes. Mobitz type 2 occurs where there is more frequent absence of the QRS complex and is much more serious

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29
Q

Which type of second degree heart block is also seen in some athletes and what is the name of this condition

A

Mobitz type 1 second degree heart block is often seen and is referred to as Wenckebach heart block

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30
Q

What is significant about the ratio of P waves to QRS complexes in patients with heart block

A

The higher the ratio of P:QRS the more severe the heart block

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31
Q

What P:QRS ratios are common in patients with Mobitz type 2 second degree heart block

A

2:1 or 3:1 or higher

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32
Q

Second degree heart block is often referred to as incomplete heart block T or F

A

T

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33
Q

Third degree heart block referred to as complete heart block is the most severe T or F

A

T

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34
Q

What happens in third degree heart block two possibilities

A

Either there are no signals being fired from the SAN or no signals reach the AVN

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35
Q

Why doesn’t third degree heart block result in death

A

Alternative pacemakers in the ventricles take over and set the rate of contraction

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36
Q

Why in third degree heart block is it common for there to be a mismatch in chamber contraction in the heart

A

The rate of beating in the ventricles due to the alternative pacemakers at a lower rate than the SAN. This causes incidents where the atria will be contracting against closed AV valves due to the existing presence of blood in the ventricles

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37
Q

In third degree heart block it is often seen that there is no consistent PR interval T or F

A

T

38
Q

In third degree heart block what is the relationship between the P wave and the QRS complex

A

There is no relationship between the P wave and the QRS complex as different pacemakers are driving the activity of the atria and the ventricles

39
Q

How can the origins of arrhythmias differ

A

Arrhythmias can be sinus (from the SAN) atrial nodal (from the AVN) or ventricular in origin

40
Q

What does the following ECG show?

A

1st degree heart block

41
Q

What does the following ECG show?

A

Increased automaticity/ectopic beats

42
Q

What does the following ECG show?

A

Atrial fibrillation

43
Q

What does the following ECG show?

A

Triggered activity

44
Q

What does the following ECG show?

A

Sinus tachycardia

45
Q

What does the following ECG show?

A

Normal sinus rhythm

46
Q

What does the following ECG show?

A

Sinus bradycardia

47
Q

What does the following ECG show?

A

Atrial tachycardia

48
Q

What does the following ECG show?

A

2nd degree heart block

49
Q

What does the following ECG show?

A

Ventricular tachycardia

50
Q

What does the following ECG show?

A

Polymorphic ventricular tachcardia

51
Q

What does the following ECG show?

A

3rd degree heart block

52
Q

What does the following ECG show?

A

Ventricular fibrillation

53
Q

What are the two different effects of arrhythmia on heart rate

A

Tachycardia or bradycardia

54
Q

What signifies atrial tachycardia

A

Multiple P waves signifying multiple atrial depolarisations

55
Q

What signifies a ventricular rhythm

A

Wide complexes

56
Q

Ventricular tachycardia is often fatal T or F

A

T

57
Q

What is seen in the ECG of patients with atrial fibrillation

A

No true P waves as the atria aren’t contracting

58
Q

Atrial fibrillation patients will have an normal heart rhythm T or F

A

F – they will have an irregular heart rhythm due to an irregular ventricular response and fibrillation waves

59
Q

What is the major risk with atrial fibrillation

A

Because the atria are fibrillating it’s possible that a thrombus can form in the atrium. This can break off into the circulation and cause stroke

60
Q

What drugs are often given to patients in atrial fibrillation

A

Anti-coagulant drugs to prevent thrombus formation and possible strokes

61
Q

Ventricular fibrillation is extremely fata T or F

A

T

62
Q

How is ventricular fibrillation often treated

A

With electrical cardioversion (defibrillation)

63
Q

What is the effect of sympathetic nervous system regulation of the pacemaker potential

A

Sympathetic nervous system stimulation of the pacemaker cells increases the slope of the prepotential phase of the pacemaker potential. This means that these cells reach action potential threshold quicker thus speeding up heart rate (positive chronotropic effects)

64
Q

What are the mediators of the sympathetic nervous systems effects of heart rate

A

Noradrenaline acting on the β1 adrenoceptors which acts to increase cAMP levels

65
Q

What is the downside of sympathetic nervous system stimulation of the heart

A

It increases automaticity which could then lead to arrhythmia

66
Q

What is the effect of parasympathetic nervous system regulation of the pacemaker potential

A

Parasympathetic nervous system stimulation of the pacemaker cells decreases the slope of the prepotential phase of the pacemaker potential. This means that these cells reach action potential threshold slower thus slowing down heart rate (negative chronotropic effects)

67
Q

What are the mediators of the parasympathetic nervous systems effects of heart rate

A

Vagus nerve releasing acetylcholine which acts on the M2 receptors in nodal and atrial tissue

68
Q

What is the downside of parasympathetic nervous system stimulation of the heart

A

It decreases automaticity inhibits atrioventricular conduction and increases the PR interval

69
Q

What are the class I anti-arrhythmic drugs

A

Na+ channel blockers

70
Q

What are the class II anti-arrhythmic drugs

A

Β-adrenoceptor antagonists

71
Q

What are the class III anti-arrhythmic drugs

A

Action potential prolonging agents

72
Q

What are the class IV anti-arrhythmic drugs

A

Ca2+ channel blockers

73
Q

Most class I anti-arrhythmic drugs are use-dependent blockers what is meant by this

A

They preferentially bind to open or refractory channels/active channels. This means that they actually block the channels causing tachycardia without a total inhibition of heart rate

74
Q

How are class I anti-arrhythmic drugs sub-classified

A

There are subclassified depending on their effects on the duration of the cardiac action potential. Class 1A increased the duration class 1B slightly decrease the duration and class 1C have no effect on the duration of the cardiac action potential

75
Q

Give an example of a class 1A anti-arrhythmic drug

A

Disopyramide quinidine procainamide

76
Q

Give an example of a class 1B anti-arrhythmic drug

A

Lidocaine mexiletine

77
Q

Give an example of a class 1C anti-arrhythmic drug

A

Flecainide propafenone

78
Q

What is the downside to using class 1 anti-arrhythmic drugs

A

Because the electrical activity of the heart is intrinsically linked to the contractility of the heart these drugs impair heart function

79
Q

What are the subclasses of class II anti-arrhythmic drugs

A

Non-selective or β1 selective antagonists

80
Q

Give an example of a non-selective β blocker

A

Propranolol atenolol nadolol carvedilol

81
Q

Give an example of a β1 selective blocker

A

Bisoprolol metoprolol

82
Q

Class III anti-arrhythmic drugs supress arrhythmias and increase the duration of the cardiac action potential. Give an example of this type of drug

A

Amiodarone sotalol

83
Q

Give an example of a Class IV anti-arrhythmic drug

A

Verapamil diltiazem

84
Q

Digoxin is a non-classical anti-arrhythmic drug. Describe its how it acts

A

Digoxin inhibits the Na+/K+ATPase which leads to an increase in intracellular Na+. This Increase in intracellular Na+ leads to the reversal of the action of the Na+/Ca2+ exchanger which now brings Ca2+ into the cell. This increases intracellular Ca2+ increasing cardiac contractility. In addition digoxin also slows down heart rate through its effects on Na+ directly hence causing bradycardia

85
Q

What are the downside to digoxin use

A

Digoxin has a narrow therapeutic window and causes a number of side effects such as nausea vomiting diarrhoea and confusion

86
Q

What kind of compound is digoxin

A

Cardiac glycoside

87
Q

Where is digoxin often used

A

Most commonly used in atrial fibrillation to reduce ventricular rate of response Its also used in severe heart failure due to its positive inotropic effect

88
Q

What is QT prolongation what causes it and what are the effects

A

QT prolongation is where the interval from the start of the QRS complex to the end of the T wave is increased. Anti-arrhythmic drugs can sometimes lead to a prolongation of the QT interval which can lead to polymorphic ventricular tachycardia

89
Q

Which two anti-arrhythmic drugs often cause polymorphic ventricular tachycardia

A

Amiodarone and sotalol

90
Q

Why does amiodarone have so many side effects

A

It has a large volume of distribution meaning it becomes distrusted throughout the body

91
Q

What are some of the side effects of amiodarone use

A

QT prolongation polymorphic ventricular tachycardia interstitial pneumonitis abnormal liver function hyperthyroidism/hypothyroidism sun sensitivity slate grey skin discolouration corneal microdeposits optic neuropathy

CDL301 Cardiovascular Pharmacology Refesher (17 decks)

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