Lecture 2 Physiology of the Heart I Flashcards
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
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.
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
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
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
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
Which cells exhibit the cardiac action potential in the heart
Contractile cells such as cardiac myocytes
Which cells in the heart exhibit the pacemaker potential
Nodal and conducting tissue such as the AVN SAN Purkinje fibres
What ion movement mediates the rapid depolarisation in the pacemaker potential
Ca2+ influx
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.
Draw and explain the cardiac action potential
See completed diagram below
![](https://s3.amazonaws.com/brainscape-prod/system/cm/233/299/784/a_image_thumb.png?1519820331)
Draw and explain the pacemaker action potential
See completed diagram below
![](https://s3.amazonaws.com/brainscape-prod/system/cm/233/299/785/a_image_thumb.jpg?1519820341)
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
What are the two main mechanisms of arrhythmias
Abnormal impulse generation or abnormal impulse propagation
Give some examples of activity that can cause abnormal impulse generation in arrhythmias
Triggered activity and increase automaticity/ectopics
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
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
What causes triggered activity
Ca2+ overload in the cell
What can be the effects of triggered activity
Triggered activity can lead to ectopic beast ventricular tachycardia and subsequently ventricular fibrillation
What feature of triggered activity is seen on an ECG
The magnitude of after-depolarisations increases with multiple initial depolarisations
What is meant by increased automaticity
Usually a problem with the pacemaker cells whereby the fire impulses spontaneously. This can cause ectopic beats
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
First degree heart block is benign T or F
T
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
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
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
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
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
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
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
What P:QRS ratios are common in patients with Mobitz type 2 second degree heart block
2:1 or 3:1 or higher
Second degree heart block is often referred to as incomplete heart block T or F
T
Third degree heart block referred to as complete heart block is the most severe T or F
T
What happens in third degree heart block two possibilities
Either there are no signals being fired from the SAN or no signals reach the AVN
Why doesn’t third degree heart block result in death
Alternative pacemakers in the ventricles take over and set the rate of contraction
Why in third degree heart block is it common for there to be a mismatch in chamber contraction in the heart
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