The heart is able to beat independently, devoid of nervous input. This is achieved through special 'pace-maker' cells.
Myocardial contraction is dependent on two cell types:
Conduction through the heart is dependent on pacemaker cells organised into key structures.
Autorhythmic cells do not possess a resting potential, instead they slowly depolarise exhibiting pacemaker potential.
In these cells, the membrane potential slowly drifts until the threshold is reached. This is in contrast to most nerve and skeletal muscle cells, in which membrane potential remains constant unless the cell is stimulated. Through repeated cycles of drifting and firing, these cells rhythmically initiate action potentials.
The action potential of autorhythmic cells is divided into several phases:
'Funny' sodium channels (If) open allowing a slow inward flow of Na+ ions into the cell causing depolarisation. Transient (T-type) calcium channels (IcaT) open at -50mv, bringing the membrane closer to threshold.
Once the threshold is reached, long-lasting (L-type) voltage-gated calcium channels (IcaL) open.
The long-lasting (L-type) calcium channels remain open continuing depolarisation.
Outward potassium channels (Ik) open resulting in repolarisation.
Contractile cells, unlike autorhythmic cells, have a resting potential. They typically require an impulse from another myocardial cell to depolarise.
The action potential of contractile cells is divided into several phases:
Unlike autorhythmic cells, the membrane of contractile cells remains essentially at rest at about -90 mV until excited. Leaky potassium channels (Ik) maintain the cell at resting potential through the outward movement of potassium ions.
Depolarisation occurs in an adjacent cell and the threshold potential is met. Fast voltage-gated sodium channels (INa) open and sodium ions enter the cell rapidly.
The first stage of repolarisation. Potassium ions leave the cell via transient K+ channels (Ikto).
Plateau phase. Inward movement of calcium ions via voltage-gated L-type channels (IcaL) prolongs repolarisation.
Completion of repolarisation. Outward movement of potassium ions (via Ik channels) returns the membrane to its resting potential.
The autonomic nervous system exerts a degree of control over the electrophysiology of the heart; vagal innervation (parasympathetic) tends to dominate sympathetic stimulus.
The vagus nerve supplies the atria, in particular, the SAN and AVN.
Sympathetic fibres supply the atria, SAN, AVN, and ventricles.
An electrocardiogram (ECG) is a recording of the hearts electrical activity.
A 12 lead ECG records from 10 electrodes but offers 12 ‘views’ the heart.
An ECG strip is made up of a baseline with deflections caused by movement of electrical impulses either toward (positive deflection) or away (negative deflection) from electrodes. The deflections that make up a normal ECG are termed waves and are assigned arbitrary letters.
A normal ECG waveform is composed of:
The ECG may be deconstructed into additional key components:
The cardiac axis refers to the net effect of all of the action potentials that are generated.
A normal axis is said to lie between -30° and 90°. If conduction is delayed in one direction or one side exerts greater electrical influence, the axis may be deviated to either the left or right.
Left axis deviation (LAD) may be caused by:
Right axis deviation (RAD) may be caused by:
Isolated left or right bundle branch block has little effect on the axis.
Wigger's diagram illustrates the entirety of the cardiac cycle; it describes the precise relationship between electrical and mechanical activity.
Electrical activity is initiated at the SAN. This sends a wave of excitation across the atria towards the AVN (observed as a p wave on the ECG). This wave of excitation leads to contraction of the atria, which forces blood into the ventricles.
The AVN then continues the wave of excitation throughout the ventricles via the conduction system. This wave of excitation leads to contraction of the ventricles (QRS complex on the ECG). The onset of contraction marks the start of systole.
The ventricles contract leading to the closure of the mitral and tricuspid valves, which generates the first heart sound (S1). As pressure increases the volume within the ventricles stays the same. This is termed isovolumetric contraction. Eventually, the pressure within the ventricles overcomes the pressure within the aortic and pulmonary vessels. This leads to blood being forced out of the ventricles and into the systemic and pulmonary circulation.
As blood leaves the ventricle the volume decreases but the pressure within the aorta (120 mmHg) and pulmonary trunk (30 mmHg) increases. At the end of contraction, the ventricles start to relax. The backflow of blood from the aortic and pulmonary vessels leads to closure of the aortic valve and pulmonary valves, which generates the second heart sound (S2). The rebound of blood off the aortic valve causes the dicrotic notch in the aortic pressure graph.
Initially, the pressure within the ventricles continues to fall without any change in volume. This is termed isovolumetric relaxation. Eventually, pressure within the ventricles falls below that of the atrial pressure and the atrioventricular valves open. This marks the onset of diastole.
The cycle then repeats itself.
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