Lecture 2 Physiology of the Heart I Flashcards Preview

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

Flashcards in Lecture 2 Physiology of the Heart I Deck (91)
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1

How do cardiovascular drugs intervene with different aspects of physiology

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

2

What happens during phase 0 of the cardiac action potential

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.

3

What happens during phase 1 of the cardiac action potential

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

4

What happens during phase 2 of the cardiac action potential

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

5

What happens during phase 3 of the cardiac action potential

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

6

How does the pacemaker potential differ to the cardiac action potential

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

7

Which cells exhibit the cardiac action potential in the heart

Contractile cells such as cardiac myocytes

8

Which cells in the heart exhibit the pacemaker potential

Nodal and conducting tissue such as the AVN SAN Purkinje fibres

9

What ion movement mediates the rapid depolarisation in the pacemaker potential

Ca2+ influx

10

Explain what currents and ion movements occur in the pacemaker potential

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.

11

Draw and explain the cardiac action potential

See completed diagram below

12

Draw and explain the pacemaker action potential

See completed diagram below

13

What is meant by atrioventricular delay

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

14

What are the two main mechanisms of arrhythmias

Abnormal impulse generation or abnormal impulse propagation

15

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

Triggered activity and increase automaticity/ectopics

16

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

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

17

What is meant by triggered activity

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

18

What causes triggered activity

Ca2+ overload in the cell

19

What can be the effects of triggered activity

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

20

What feature of triggered activity is seen on an ECG

The magnitude of after-depolarisations increases with multiple initial depolarisations

21

What is meant by increased automaticity

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

22

What is meant by re-entrant activity

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

23

First degree heart block is benign T or F

T

24

What is seen in patients with first degree heart block

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

25

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

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

26

What is often seen in patients with second degree heart block

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

27

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

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

28

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

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

29

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

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

30

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

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