Chapter 4: Origin of Biopotentials-2 PDF

Chapter 4: Origin of Biopotientials-2 Generation of the EMG signal The electrical activity which results in the production of the myoelectric signal starts within the Central Nervous system (CNS), when the individual makes a conscious decision to contract the particular muscle...

Chapter 4: Origin of Biopotientials-2 Generation of the EMG signal The electrical activity which results in the production of the myoelectric signal starts within the Central Nervous system (CNS), when the individual makes a conscious decision to contract the particular muscle of interest. The muscular movement starts with an electrical nerve impulse which is delivered via motor neurons. A motor neuron consists of a main cell body, which lies within the spinal cord of the CNS, and an axon which is usually a very long, thin cord-like structure termed the nerve fiber.  The specific type of motor neuron that innervates skeletal muscle is called a somatic motor neuron. The junction between the axon terminal and the muscle fiber is called the motor end plate. Following an electrical impulse being transmitted along the length of the axon and received at the motor end plate, a number of physiological changes occur. When a muscle fiber receives a nerve impulse at the motor end plate, also termed the neuromuscular junction, a number of changes are triggered. Within the fiber itself, and outside its semi-permeable membrane, there are a number of ionized elements, in varying proportions, the most important being sodium, potassium and calcium. Potassium will be more greatly concentrated inside the fiber itself, whereas sodium and calcium will be more greatly concentrated outside the fiber.  This variation in proportions will lead to a tendency for both solutions to diffuse into each other, thereby equalizing the concentrations both within and outside the fiber. However, there are four biological mechanisms which will prevent this: 1) Membrane permeability: the selectively permeable membrane will not allow the sodium ions to travel into the fiber. 2) Membrane polarization: The membrane has a naturally negative charge, repelling other negative charges. 3) Charged ions within the sarcoplasm: Large charged protein ions within the sarcoplasm, or inside the fiber, which are effectively immovable, will attract charged positive ions and repel negative ions. 4) The sodium-potassium pump: This is an active process requiring energy, from Adenosine Tri-Phosphate (ATP), that transports potassium ions and sodium ions in differing proportions across the membrane, effectively helping to create a potential difference across the membrane.  These factors will produce a charged, polarized membrane, which is approximately -70mV inside the fiber with respect to the outside. This potential difference is due only to the distribution of the potassium ions, since the sodium ions cannot pass through the membrane. The exact potential developed by the potassium ions with respect to the different sides of the membrane, called the trans-membrane potential, can be derived from the Nernst equation. Within the motor end plate, there are three distinct structures involved in the instigation of a myoelectric signal: 1) The pre-synaptic terminal; 2) The synaptic cleft, and 3) The post-synaptic membrane.  The pre-synaptic terminal lies at the end of the motor neuron, and contains vesicles which house Acetylcholine, a neurotransmitter. When an action potential is received at the pre-synaptic terminal, calcium gateways within the pre-synaptic terminal are opened and Calcium ions are able to enter into the pre- synaptic terminal. These calcium ions release acetylcholine from vesicles within the pre-synaptic terminal which enter the synaptic cleft. Synaptic cleft is the area between the nerve fiber and the muscle’s post-synaptic membrane within the motor end plate. The acetylcholine binds to receptor within the post-synaptic membrane, opening small channels within the membrane, which specifically allow the passage of (predominantly) sodium ions into the muscle. This rush of positively charged ions effectively depolarizes the membrane, causing an electrical signal to be discharged, which is transmitted along the length of the muscle sarcolemma.  Acetylcholine is broken down into acetic acid and choline by the enzyme acetyl cholinesterase, which prevents excessive ionic movement through the membrane and limits the time during which a signal may be transmitted (normally around 10 milliseconds). The sodium-potassium pump will help to restore the balance of these ions across the membrane, thereby also restoring its resting potential and preparing it potentially for further activation. The EMG signal is then based on reading the depolarization and repolarization events of these action potentials of a muscle fiber.  Myoelectric control and its advances are based on the identification and understanding of the electrical signals generated during muscle activity termed EMG signals. These signals are generated as a result of the neurological signals that are received by the muscle. Human muscles comprise thousands of tiny muscle fibers.  Motor neurons at the spine are responsible for transmitting the signals from the brain to these muscles via a series of pulses named innervation pulse train(IPT). These IPT‘s causes the corresponding muscle fibers controlled by the neuron to contract and, at the same time, produce a measurable electrical potential, termed Motor Unit action potential(MUAP). This electrical activity can be harvested using either invasively using needle electrodes or at the surface using surface electrodes. EMG signal in the context of upper limb prosthetics are mostly acquired non invasively using surface EMG electrodes(sEMG‘s). These record electrical signals of the underlying muscle fibers termed as Muscle fiber action potentials(MUAP) through the skin.  The signal strength at the skin’s surface will not only be affected by the muscle fibers. Before the signal reaches the skin, it must travel through other layers of tissue, which will all affect the signal size before it reaches the surface. The amount of signal produced within each muscle for different individuals will vary significantly, due to the variations in muscle contraction and signal impedance between the signal source and the electrode interface.  Other factors that will affect signal clarity and magnitude at the skin surface include the following: The composition of the layers of tissue (i.e. the tissue thickness and type) between the electrode and the ‘target’ muscle producing the required myoelectric signal. The alignment of the muscle fibers with respect to the alignment of the electrode. The activities of other muscles within the residual limb when the target muscle is contracted.  The Electrocardiogram (ECG): Heart Anatomy 4 Chambers Right Atrium Right Ventricle Left Atrium Left Ventricle (2.5-3x thicker wall) Artery – carries blood away from the heart Vein - carries blood towards the heart Ventrical contraction  systole Ventrical relaxation (Atrial contraction)  diastole 4 Flow Pathway Superior, inferior vena cava (CO2) Right atrium Tricuspid valve Right ventricle pulmonary valve Pulmonary System Artery Capillaries (CO2-O2 exchange) Vein Left atrium Mitral valve Left ventricle aortic valve 5 Aorta (O2) Conduction system Sinoatrial Node (SA): Impulse generator Internodal Tracks anterior middle posterior Atrioventricular Node (AV) Bundle of His Bundle Branches Purkinje Fibers 6 Sequence of cardiac excitation Sinoatrial Node (SA) Bundle Branches Atrial Muscle (right then left) Pukinje Fibers Atrioventricular Node (AV) Ventricular Muscle Bundle of His 7  Representative electric activity from various regions of the heart. The spatial and temporal superposition of these signals gives the ECG signal 9 Ventricular Cells: Ventricular cells are long, thin, branching and interconnected Each fiber contains many contractile myofibrils Resting at -85mV and depolarizes with a rate of 150V/s Electric systole vs electric diastole (200-300msec) 1 0 Ventricular Activation: Isochronous activation (synchronously excited) Plunge electrodes 1 1 Body-Surface Potentials: ECG is measured at body surface Ventricular activation causes several local current dipoles  net equivalent dipole Thorax  Volume conductor (R and R ) T1 T2 The ECG: The electric activity of the heart is a vector quantity with variable magnitude and orientation Dipole moment vector or cardiac vector Heart electric potential appears on body surface Different pairs of electrodes give different ΔV Limbs are normally used to measure ECG Lead = pair of electrodes 12 ECG signal: Individual waves PQRSTU and their duration Intervals: P-R, QRS, Q-T, and S-T Segments: P-R, S-T 17 1 8 ECG signal: P  atrial depolarization QRS  ventricular depolarization. atrial repolarization is masked T  ventricular repolarization U  slow repolarization of ventricular papillary muscles P-R  conduction delay in the AV node S-T  plateau region in the ventricular potential 1 9 Normal and Abnormal Cardiac Rhythms: 70 beats/min Bradycardia: ↓heart beat rate  sleep Tachycardia: ↑heart beat rate  emotion, exercise, fever Abnormal conditions in the conduction system: Parts other than the SA node become the pacemaker: SA node depression Bundle of His is interrupted Atrial or ventricular tissue discharge at rate faster than SA node 2 1 List of Abnormal Cardiac Rhythms: 1) Third degree heart block: Bundle of His is completely interrupted  atria beat at normal rate but ventricles beat at their own slow rate (idioventricular rhythm, 30-45 bpm) 2 2 List of Abnormal Cardiac Rhythms: 1) Third degree heart block: Bundle of His is completely interrupted  atria beat at normal rate but ventricles beat at their own slow rate (idioventricular rhythm, 30-45 bpm) Patients with third-degree AV block typically experience a lower overall measured heart rate (as low as 28 beats per minute during sleep), low blood pressure, and poor circulation. In some cases, exercising may be difficult, as the heart cannot react quickly enough to sudden changes in demand or sustain the higher heart rates required for sustained activity. 2 3 List of Abnormal Cardiac Rhythms: 2) First degree heart block: partial His interruption. All atrial pulses reach ventricles but P-R is prolonged 3) Second degree heart block: Not all atrial pulses reach ventricles. 2:1 block, 3:1 block 2 4 List of Abnormal Cardiac Rhythms: 4) Wenckebach phenomenon (a disease of the AV node): P- R is prolonged until a beat (R) is dropped. P:R ratio determines the block P-R Wenckebach Period 5) One branch of the bundle of His is interrupted  AP reaches one ventricle normally and then reach the other ventricle through musculature 2 5 Arrhythmias: Sometimes a portion of the myocardium become irritable  independent discharge  ectopic (abnormal) focus 1) Discharge once  premature ventricular contraction PVC  extra systole 2 6 Arrhythmias: Example 4.4: PVC: (1) arrive early (Rt-1–Rt < 0.8 Rt-2–Rt-1) (2) the following beat occurs at the normal time (Rt-1–Rt + Rt–Rt+1 = 2 Rt-2–Rt-1) (3) QRS is wider (Wt > 1.3 Wt-1) ThH ThL t-2 t-1 t t+1 Rt-2–Rt-1 Rt-1–Rt Rt–Rt+1 2 7 Arrhythmias: Example 4.4: PVC: (1) arrive early (Rt-1–Rt < 0.8 Rt-2–Rt-1) (2) the following beat occurs at the normal time (Rt-1–Rt + Rt–Rt+1 = 2 Rt-2–Rt-1) (3) QRS is wider (Wt > 1.3 Wt-1) ECG ThL S(t) W(t) BPF ThH R(t) R-R(t) Arrhythmias: 2) Repetitive discharge at regular rate > SA node rate a)Paroxysmal tachycardia: all QRS no P waves b)Atrial flutter: rapid, perfectly regular flapping 200-300 bpm 200/70 = 2.86 1. A sudden outburst of emotion or action: a paroxysm of laughter. 2. a. A sudden attack, recurrence, or intensification of a disease. 28 b. A spasm or fit; a convulsion. 2 9 Arrhythmias: 3) Irregularly discharging focus (or foci): a) Atrial fibrillation b) Ventricular fibrillation 3 0 Arrhythmias: Ischemia Another cause for rhythm disturbances is ischemia (deficiency in blood supply)  depressed conductivity  electrophysiological changes  ECG arrhythmias 3 1 Arrhythmias: Ischemia In late ischemia, we have: Low resting potential Low voltage increase rate Low AP amplitude and duration The slope of plateau increases Intracellular AP  changes exracellular field potential  changes current dipoles  changes ventricular ECG: QRS, S-T, and T Ischemia causes electrolytic changes: [Na+]↑ [K+]↓ inside  indicate Na-K pump depression  resting potential ↓  action potential amplitude ↓ B C Premature Ventricular A Normal Rat ECG ECG from ischemia Beat (fusion beat) D Premature ventricular E Bigeminy F Salvos Beat G Non-sustained Ventricular H Sustained Ventricular I Ventricular Fibrillation Tachycardia Tachycardia