4BBY1060 Electrical and Mechanical events of the cardiac cycle PDF

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KCL notes, my own personal need to know version...

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4BBY1060 Electrical and Mechanical events of the cardiac cycle The hierarchy of pacemakers on the mammalian heart: Primary pacemaker of the heart is the Sino-atrial node, which is a bunch of specialised muscle cells that are capable of spontaneously generate action potentials. Those action potentials can then spread through the muscle of the right atrium towards the atrioventricular node. There is a pause at the AVN and then the excitation spread down this specialised conducting tissue bundle of his, which divides into two separate bundles (left and right bundle branches) and then comes down to the apex of the heart and spread into the Purkinje fibres. All of these structures have an unstable resting membrane potential:

The SAN dictates the rate at which the action potentials are being fired off.

There are a hierarchy of pacemakers, the fastest one with the fastest intrinsic rate is the SAN. Intrinsic heart rate is defined as the rate at which the heart beats when all cardiac neural and hormonal inputs are removed. SAN -> AVN -> Bundle of his -> Purkinje fibres Whilst their rate may be different, they are all capable of having their own rate.

Similarly, if these structures go wrong themselves as they are capable of spontaneously generate action potentials, they can start imposing rates when they shouldn’t, causing arrythmia (spontaneous beats where they shouldn’t be).

The SA node action potential: -

Its resting membrane potential is unstable In the SAN there is depolarisation in-between beats called the diastolic depolarisation.

The SA node cell does not have a steady resting potential but, instead, undergoes a slow depolarization (Diastolic depolarisation). This gradual depolarization is known as a pacemaker potential (funny current); it brings the membrane potential to threshold, at which point an action potential then occurs. Three ion channel mechanisms contribute to the pacemaker potential: 1. The first is a progressive reduction in K+ permeability. The voltage-gated K+ channels that opened during the repolarisation phase of the previous action potential gradually close due to the membrane’s return to negative potential. 2. Pacemaker cells have a unique set of channels that, unlike most voltage-gated ion channels, these opens when the membrane potential is at negative values. These nonspecific cation channels conduct an inward, depolarising, Na+ current. These channels are known as the If-type channels (hyperpolarisation-activated cyclic nucleotide-gated channels). 3. The third pacemaker channel is a type of Ca2+ channel that opens only briefly but contributes inward Ca2+ current and an important final depolarizing boost to the pacemaker potential. These channels are called T-type Ca2+ channels (T = transient).

Once the pacemaker mechanisms have brought a nodal cell to threshold, an action potential occurs. The depolarizing phase is caused not by Na+ but rather by Ca2+ influx through Ltype Ca2+ channels. These Ca2+ currents depolarize the membrane more slowly than voltage-gated Na+ channels, and one result is that action potentials propagate more slowly along nodal-cell membranes than in other cardiac cells. This explains the slow transmission of cardiac excitation through the AV node. As in cardiac muscle cells, the long-lasting L-type Ca2+ channels prolong the nodal action potential, but eventually they close and K+ channels open and the membrane is repolarized. The return to negative potentials activates the pacemaker mechanisms once again, and the cycle repeats. Therefore, the pacemaker potential provides the SA node with automaticity, the capacity for spontaneous, rhythmic self-excitation.

Note: - Conduction form SA to AV nodes is via the atria muscle and is slow - Conduction through the AV node is slow – causing the AV pause. i. This allows ventricular filling to occur before passing on the electrical impulse ii. It also prevents transmission of high rates from atria - After passing the AV node, the conduction through the ventricular conduction system (bundle of his and the purkinje fibres) is really fast i. This allows the apex to contract before the base

The ECG: The dipole is formed because cells are depolarising and resting, so there is a difference of charge across the cells. It goes from minus to plus (remember electrode detects charge on the outside of the cell). If the excitation is going towards the positive end, a positive deflection is seen on the ECG. P Q

Atrial depolarisation Depolarisation of the septum (towards the atria)

R

Depolarization of the ventricles (towards the apex)

S

Depolarisation of the ventricles (towards atria)

T

Repolarisation of the ventricles (towards endocardium)

PQ interval – shows atrial conduction and AV node delay. QRS duration – ventricular conduction velocity ST segment – the ventricle has depolarised, but it has yet to repolarise. It shows the heterogeneity of ventricular polarisation. QT interval - shows the ventricular action potential duration from depolarisation to repolarisation of the VENTRICLES.

The contractile cycle:

4 valves: - Aortic valve - Pulmonary valve - Tricuspid valve - Bicuspid valve (mitral valve) Healthy valves have very little resistance, so a small pressure gradient across them is sufficient for them to open. The cardiac cycle: 1. Left atrial pressure is higher than left ventricle pressure at this point, which causes the mitral valve to open and the blood flow into the left ventricle. 2. Left atrium contract increasing the volume of blood in the left ventricle.

3. During the first part of systole, the ventricles are contracting but all the valves in the heart are closed so blood is not ejected. 4. This is because the pressure at this point is not enough to open the aortic valves. This period is termed isovolumetric ventricular contraction because the ventricular volume is constant. 5. Once the increasing pressure in the ventricles exceeds that in the aorta and pulmonary trunk, the aortic valves open and the ventricular ejection period of systole occurs. 6. Blood is forced into the aorta as the contracting ventricular muscle fibres shorten. The volume of blood ejected from each ventricle during systole is called the stroke volume (SV).

7. End-systolic pressure falls. 8. Left ventricle pressure falls below the aortic pressure, therefore, the aortic valve shuts. At this time the mitral valve also closes. 9. Period of isovolumic ventricular relaxation occur because all valves are closed. Therefore, the volume inside the LV is constant. 10. Left ventricular pressure falls below atrial pressure and mitral valve opens again and the ventricles begins to fill. Cycle repeats....