L4 Electrical Conducting System of the Heart

Question 1

Define action potential.

Answer 1

An action potential is a transient depolarization of a cell as a result of activity of ion channels.

Question 2

Describe the electrical activity within non-pacemaker cells.

Answer 2

In phase 4, there is resting potential.

There is then a sharp spike in action potential in phase 0 as there is an influx of sodium ions due to a stimulus. This is as sodium voltage gated ion channels are open.

In phase 1 sodium voltage gated ion channels close and potassium voltage gated ion channels open transiently. There is a short, decrease in action potential due to the loss of potassium.

In phase 2, the action potential stabilises as calcium ion channels open transiently and calcium ions enter.

In phase 3, there is a sharp drop in potential due to the loss of potassium. Calcium voltage gated ion channels close and potassium voltage gated ion channels open.

Question 3

How does a heart beat occur?

Answer 3

The contraction of cardiomyocytes is caused by the binding of actin and myosin filaments in the cells. There is a rise in intracellular calcium, which binds to troponin C. This leads to formation of cross-links between myosin filaments and actin filaments. The strength of myocardial contraction depends on the degree of stretch in the muscle fibres prior to contraction. The degree in binding depends on intracellular calcium ion concentration which increases in response to sympathetic stimulation.

Action potential depends on the depolarisation and repolarisation cycle in the sarcolemma. The action potentials are propagated across the sarcolemma and deep into the T-tubules by the activation of voltage-gated sodium channels, following an influx of sodium. This is depolarisation.

Question 4

What is the hierarchy of pacemakers?

Answer 4

The intrinsic frequency of the SAN is higher than the AVN and the Purkinje fibres. Since they operate at a lower frequency, they will not initiate the heart beat. If there is an issue with the SAN. The AVN, with the next highest frequency, will lead. This demonstrates the hierarchy of pacemakers. The primary pacemaker is defined as the tissue with the highest firing frequency.

Question 5

How are pacemaker cells able to show auto-arrhythmic activity?

Answer 5

Cells in the SAN are less polarised than other myocytes, which makes them electrically unstable as there resting potential is close to threshold potential. Between the end of one action potential and the other, there is slow inward sodium and calcium currents reducing outward potassium currents result in gradual depolarisation of the cells in the SAN. They therefore do not have a stable resting potential.

Question 6

Give differences between pacemaker cells and non-pacemaker cells.

Answer 6

The membrane potential in contractile myocardium is stable at -90mV. The membrane potential in auteoarrythmic myocardium is unstable and usually starts at -60mV.

In contractile myocardium depolarisation taht enters via gap junctions causes the potential to reach threshold. In pacemaker cells this is due to net sodium enters through ionotrophic channel reinforced by calcium entry.

The rise phase of action potential is due to sodium entry in contractile myocardium and calcium in pacemaker cells.

The duration of the action potential is 200 ms in contractile myocardium and 150ms in pacemaker cells.

There is a long refractory period in contractile myocardium whereas that is pacemaker cells is not significant.

Question 7

How can different drugs be used to affect cardiac action potential?

Answer 7

Class 1: Na+ channel blockers

Class 2: Beta blockers e.g. propranolol and Metoprolol

Class 3: K+ Channel blockers such as Aminodarone and Sotalol.

Class 4: Ca2+ channel blockers such as Verapamil and Ditiazem

Question 8

What are gap junctions?

Answer 8

• Fascia adherens These are anchor sites of actin and transmit the contractile forces
• Desmosomes, macula adherens These are localised cell-to-cell adhesions (cytoplasmic bridges) randomly arranged on the lateral sides of the sarcolemma. They provide structural support and bind cardiomyocytes together to stop separation during contraction and resist shearing force.

Question 9

What are other types of adherens?

Answer 9

Formed from transmembrane proteins known as connexins which allow action potentials to pass between cardiomyocytes and enable coordinated contraction.

Question 10

How is an electrical impulse conducted through the heart?

Answer 10

1. AP ignited in the SAN proposes to the AV nodes via internal pathways in the atria.
2. The cells in the AVN transmit the AP more slowly and delay the impulse by 100 ms.
3. The impulse spreads down to sth ventricles along the Bundle of His.
4. The AV bundle divides and supplies the left and right bundle branches supplying LV and RV.
5. impulses spread to the contractile cells of the ventricles through an extensive network of Purkinje fibres.

Question 11

How many leads are used in a ECG?

Answer 11

12 with 10 electrodes

Question 12

Where are the leads in an ECG placed?

Answer 12

6 on the Chest and 4 on the arms and legs.

Question 13

What does the p wave represent?

Answer 13

Atrial systole

Question 14

What does the PR segment represent?

Answer 14

Conduction through the AVN and the Bundle of His.

Question 15

What does the QRS complex represent?

Answer 15

Ventricular depolarisation. The repolarisation of the atria is masked as the ECG shows a summation.

Q - Depolarisation of the interventricular septum from left to right
R - Depolarisation of the main mass of the ventricles S - depolarisation of the area of the heart near the base

Question 16

What does the T wave represent?

Answer 16

Ventricular repolarisation.

Question 17

What can an elevated or depressed ST segment indicate?

Answer 17

On a normal ECG, the St segment is isoelectric. It has zero potential. ST wave depression usually indicate myocardial ischaemia. An elevation is characteristic of an actute coronary artery occlusion (ST elevation MI (STEM)) though it may be also caused by pericarditis, an LV aneurysm or a normal variant.

Question 18

What is a U wave?

Answer 18

U wave is a deflection of low amplitude which is sometimes visible after the T wave. It is of uncertain origin but sometimes visible after the T wave. It is of uncertain origin but may be due to repolarisation of the Purkinje fibres. Prominent U waves are associated with hypokalaemia.

Question 19

What is atrial fibrillation?

Answer 19

Atrial fibrillation is the most common sustained cardiac arrhythmia. It occurs when multiple small re-entry circuits travel around the atria producing fibrillary waves are a rate of 300-600/min. These waves are disorganised and fail to trigger atrial depolarisation and function arterial contraction. The slow conduction of the AVB protects against the extremely rapid ventricular rates. On an ECG there is no clear p-wave and irregularly spaced QRS complexes. The ventricles are beating normally due to AV delay. This can lead to thromboembolic stroke. Most patients should therefore be give anticoagulant therapy to reduce the risk.

Question 20

What is atrial flutter?

Answer 20

It is flutter as it is not as disorganised, it is therefore not fibrillation. Due to the AV node delay, the ventricles are fine. It is common with older patients and is associated with increased risk of thromboembolic stroke which indicates the need for anti-coagulants. The flutter waves are larger and more organised than fibrillatory waves. The AVN prevents one-to-one conduction of flutter waves to the ventricles.

Question 21

What is ventricular fibrillation?

Answer 21

The ventricles are disorganised, this is when you get a shock. The ventricles are not pumping blood around properly.
In ventricular fibrillation, you would not be conscious.

Question 22

What is ventricular tachycardia?

Answer 22

If you are pumping too fast you will not have time in diastole for the heart to fill up and so the heart is not pumping any blood. Usually the patients are unconscious.

Question 23

What is 1st degree heart block?

Answer 23

There is a delay - a prolonger PR interval. 1st degree heart block, this causes the PR to increased when there is a problem in conduction. This is not uncommon to see; as you age, there is deterioration of the conducting pathway which an cause this heart block.

If you completely block the pathway, the node will still have the action potential and the atria will contract. The ventricles will still be beating as there are other parts of the conducting system which can take the lead initiating an cation potential. This however will be slower. With a very slow heart rate, syncope can occur.

Question 24

What is 2nd degree heart block?

Answer 24

The presence of second-degree AV block is diagnosed when one or more (but not all) of the atrial impulses fail to conduct to the ventricles due to impaired conduction.

Question 25

What is sinus tachycardia and sinus bradycardia?

Answer 25

Sinus Tachycardia Sinus rhythm of more than 100 bpm - This can be a normal physiological response to exercise, anxiety, pain, and can be a sign of infection, shock or acute respiratory failure.
Sinus Bradycardia Sinus rhythm of less than 60pm - Physiological response during sleep and in trained athletes but can also be caused by SAN disease, drugs, hypothyroidism and hypothermia,. If the SAN discharge falls below 40-50 bpm, the AVN takes over the pacemaker function to generate a nodal bradycardia. These bradycardias are usually asymptomatic but profound bradycardias can produce dizziness or syncope.

Question 26

What are ectopic beats?

Answer 26

Ectopic beat is a disturbance of the cardiac rhythm frequently related to the electrical conduction system of the heart, in which beats arise from fibers or group of fibers outside the region in the heart muscle ordinarily responsible for impulse formation (i.e., the sinoatrial node).

Question 27

What is atrial tachycardia?

Answer 27

Super-ventricular rhythms in which the P wave activity arises from one or more sites in the atrium other than the SAN. The discharge rate is therefore 100-250bpm. This can be indicative of underlying cardiac disease or be caused by digoxin toxicity.