Biopotential changes in the heart are involved in the rhythmicity of heart contractions. The sinoatrial (SA) node is the pacemaker of the heart. It is in the right atrium, which is one of two upper chambers of the heart. (The plural of atrium is “atria.”) The resting potential of the SA node cells is -90 mV. Certain ion channels in the cells of the SA node allow a continuous outflow of K⁺ and inflow of Na⁺ ions, which causes the cell’s intracellular environment to become more positive (i.e., the cells depolarize). When the cells depolarize to their threshold potential at approximately -60 mV, calcium ion channels suddenly open, which allows the sudden influx of Ca²⁺ ions into the cells, further enhancing the depolarization process. An impulse results and spreads quickly throughout the heart’s left and right atria. The impulse spreads so quickly that the atrial myocytes (i.e., heart muscle cells) contract in synchrony. After the atrial contraction, the atria repolarize. Meanwhile, the wave of depolarization spreads downward toward the atrioventricular (AV) node, which is another set of pacemaker cells. The AV node is at the bottom of the right atrium and just above the right ventricle. The AV node acts as a relay point between the atria and ventricles. The resting potential of the AV node cells is -60 mV. Once these cells become depolarized, they relay the signal to the bundle of His (also called the AV bundle; this bundle travels down the ventricular septum and then spreads over both ventricles). Depolarization of the bundle of
His causes the ventricles to contract in synchrony. One heart contraction takes approximately 0.8 seconds.

The brain is made up of billions of neurons. A brain wave represents the collective activity of biopotential changes occurring among the neurons. A neuron has a central portion (i.e., the cell body) and extensions branching from the cell body. A neuron may have one or more short extensions (i.e., dendrites) and a single long extension (i.e., axon) branching from the cell body. Dendrites receive impulses and transmit them through the cell body; an axon carries the impulse away from the cell body. A neuron’s resting potential ranges between -60 and -70 mV; its threshold potential is approximately -55 mV. When a neuron reaches its action potential, an impulse travels down the neuron’s axon to the axon’s terminal. At the terminal, the axon releases neurotransmitters such as serotonin, acetylcholine, and glutamic acid. On exiting the axonal terminal, a neurotransmitter enters a small space between the neuron’s axonal terminal and the dendrite of an adjacent neuron. This space is called the “synaptic cleft.” The average distance between cells in the synaptic cleft is approximately 20 to 30 nm. (A nanometer is one-billionth of a meter.) The neurotransmitter travels across the synaptic cleft and attaches to a receptor on the surface of an adjacent neuron’s dendrites or cell body. Once the neurotransmitter is attached to the receptor, it can depolarize the neuron and cause the neuron to reach its action potential. In this way, electrical impulses are transmitted from neuron to neuron.

A muscle contraction begins when a stimulus triggers an action potential within a neuron that innervates the muscle. The action potential travels down the neuron’s axon toward the axonal terminal. At the terminal, neurotransmitters are released into the neuromuscular junction (i.e., the synapse between the axon of a neuron and a muscle fiber). The neurotransmitter travels across the neuromuscular junction to attach to receptors on the muscle fiber. The resting potential of skeletal muscle is -95 mV, and the threshold potential is -50 mV. Once the neurotransmitter attaches to the receptors on the muscle fiber, Na⁺ ions flood into the muscle fiber. The muscle fiber depolarizes until it reaches its action potential. The action potential quickly spreads to other muscle fibers and results in a muscle contraction.

The outermost layer of the skin (i.e., epidermis) consists of dead cells, which do not have electrical activity. However, two layers beneath the epidermis—the dermis and, below it, the hypodermis—have electrical activity (Fig. 4-2). In polysomnography, the biopotentials of the skin (i.e., dermis and hypodermis) are not measured. However, oil, sweat, and dead skin cells on the surface of the skin can create a barrier between the skin’s surface and an electrode. This electrical barrier is called “resistance.” Resistance can interfere with the recording of EEG, EMG, and ECG signals.

The metal of the electrode and the conductive electrode paste used in electrodes can retain some of the electrical charge recorded from the body. This storage is called “capacitance.” The combination of capacitance and resistance is called “impedance.” Excessive impedance can hinder the recording of a signal received by an electrode and affect the quality of a recording. An impedance meter is an instrument used to measure the impedance formed between an electrode and the surface of the skin. In polysomnography, impedance is measured in kilo-ohms. Properly cleaned skin should ideally have a reading of 5.0 kΩ or less.

The eye is a fluid-filled, globe-shaped organ. A round, clear, convex membrane—the cornea—extends slightly outward from the front of the eye. A circular-colored membrane—the iris—is visible though the cornea and gives a person’s eye its color. The iris opens and contracts in response to light. Light enters the eye though an open circular center (the pupil) in the iris. A transparent biconvex lens situated behind the iris focuses the light onto a membrane, the retina, which lines much of the eye globe (Fig. 4-3).

The process of vision begins in the retina, following the refraction of light through the cornea and lens.
Through chemical reactions triggered by light (i.e., photochemical reaction), visual cells in the retina (e.g., cones, rods) transform light energy into a neurologic impulse that is transmitted from the retina, through the optic nerve, to the visual center of the brain where it is interpreted.

The electrical potential of the retina’s visual cells before undergoing a photochemical reaction (i.e., the retina’s resting potential) is approximately -30 to -40 mV. When a particle of light (i.e., a photon) strikes the rods and cones, ion channels on the surface of these cells change their shape. The shape change prevents positively charged sodium and potassium ions from entering the cells while allowing positively charged calcium ions to exit the cells. These two actions cause the intracellular environment of the rods and cones to become more negatively charged (i.e., hyperpolarized). Hyperpolarization of the rods and cones can approach -80 mV.

Epithelial cells that line the outer surface of the cornea secrete positively charged ions such as sodium (Na⁺) and potassium (K⁺) into the cornea and excrete negatively charged ions out of the cornea. This process creates a potential of approximately +30 to +40 mV across the membrane of the cornea. Because of the positive charge of the cornea and the negative charge of the retina, an electrical potential exists between the front and the back of the eye. This potential is called the “corneoretinal potential.”

An EOG records changes that occur in the corneoretinal potential with eye movement. In polysomnography, two electrodes are used to record an EOG. Both electrodes are placed on the outer canthus (i.e., eye socket ridge), with one electrode placed above the midline of the outer canthus and the other placed below the midline of the outer canthus. (The right electrode is typically placed above the midline and the left electrode is placed below the midline [Fig. 4-4].)

As eyes move in tandem (i.e., conjugate eye movements), one electrode will be closer to the cornea, whereas the other will be closer to the retina. Hence, one electrode will record a positive impulse (recorded as a downward deflection), whereas the other electrode will record a negative impulse (recorded as an upward deflection) as the eyes move around (Fig. 4-5).

Therefore, it is important that one electrode is placed above the midline and the other below the midline on the outer canthus. If both electrodes are placed in the same horizontal plane, vertical eye movements would be recorded as moving conjunctively (i.e., both EOG channels deflect in the same direction, or “in phase”) rather than disjunctively (i.e., both EOG channels deflect in opposite directions, or “out of phase”).

The locus ceruleus (pronounced “LOH-kus suh-ROO-lee-us”), a small blue-tinged area in the back of the brainstem, is involved in rapid eye movement (REM) sleep and in wakefulness (Fig. 4-6). The locus ceruleus contains neurons that release or are activated by norepinephrine, serotonin, and choline (i.e., norepinephrinergic, serotoninergic, and cholinergic neurons, respectively). These neurons fire quickly during wake, begin slow firing with the onset of sleep, continue to slow as sleep deepens, and then nearly stop firing during REM sleep. The locus ceruleus contains
a group of neurons, “REM-off” cells, that inhibit REM sleep (i.e., the action of these cells ends a REM period). The REM-off cells become increasingly active as REM sleep progresses and ultimately hinder the activity of the “REM-on” cells (i.e., these cells induce the onset of a REM period), which are in the pons and basal forebrain.