jae hyoung lee wonkwang health science college [email protected] electro therapy research laboratory...

Jae Hyoung Lee

Wonkwang Health Science College

[email protected]://etgr.wkhc.ac.kr

ElectroTherapyResearch LaboratoryforTissueGrowth &Repair

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SECTION . HVPCS (High Voltage Pulsed Current)

Course Objectives ( 학습목표 )

1. 고전압맥동전류의 특성을 설명한다 . (A) 2. 고전압맥동전류의 생리적 효과를 설명한다 . (A) 3. 고전압맥동전류의 치료 효과를 설명한다 . (A) 4. 고전압맥동전류의 창상치유 기전을 설명한다 .5. 고전압맥동전류의 세균성장 억제 기전을 설명한다 .6. 고전압맥동전류의 부종치유 기전을 설명한다 .7. 고전압맥동전류의 관정가동범위 증가 기전을 설명한다 .8. 고전압맥동전류의 순환증진 기전을 설명한다 .9. 고전압맥동전류의 적응증을 설명한다 . (A) 10. 고전압맥동전류의 금기증을 설명한다 . (A) 11. 고전압맥동전류의 주의사항을 설명한다 . (A) 12. 질환에 따른 고전압맥동전류의 치료조건을 설명한다 . (A)

< 실습 >1. 통증의 고전압맥동전류자극 치료 방법을 익한다 .2. 근경축의 고전압맥동전류자극 치료 방법을 익한다 .3. 창상의 고전압맥동전류자극 치료 방법을 익한다 .4. 부종의 고전압맥동전류자극 치료 방법을 익한다 .5. 관절운동제한의 고전압맥동전류자극 치료 방법을 익한다 .6. 근약화 및 위축의 고전압맥동전류자극 치료 방법을 익한다 .7. 순환장애의 고전압맥동전류자극 치료 방법을 익한다 .

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High Voltage Pulsed Current (HVPCS, 고전압맥동전류 )

Definition An electrical stimulation device with a twin-peak monophasic pulse of

very short duration and a high voltage output and very high peak current.

Wave form : Monophasic twin-peak waveMonophasic twin-peak wavePulse Duration : Very shortVery short (< 100 usec) Voltage : Very highVery high (at least 100 Volts, hundreds V) High Peak Current : Very highVery high (2000 - 2500 mA)Average current : Very lowVery low Constant Voltage Stimulator

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BRIEF HISTORY

1945 Haislip et al (Bell Telephone Laboratories) developed DynaWave neuromuscular stimulator for wound, acute trauma, pain

1966 Young HG reported promote healing in animal wound

1971 Thurman B and Christian E reported tx DM with foot abscess

1974 Lemann P (Electro-Med Health Industries) product high-voltage electro-galvanic stimulator

high-voltage galvanic stimulator (HVGS)

high voltage pulsed current stimulation (HVPCS) serial pulse

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PHYSICS

Wave Form

Monophasic twin-peak wave Rapid rise, slow down 1 pulse has 2 very short phases (Dual peak, 65 ㎲ + 75 ㎲ )

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65 ㎲ 75 ㎲

Characteristics of HVPCCharacteristics of HVPC

Waveform : Monophasic twin-peak wave A. Pulse Duration : 100 ㎲ (Very Short)B. Interpulse Interval : 9900 ㎲ (Very Long) C. Duty Cycle : A + B = 10000 ㎲ (10 ㎳ ) D. Peak Amplitude : 500 V Peak Current : 400 mA (Very High)E. Average Current : 1.5-2 mA (Very Low)

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500 V

A B

C

D E

Pulse Rate (Frequency)• Number of pulses per a second • Range 1 – 140 pps

Pulse Duration • Pulse Duration 1 : Duration of total pulse (100 ㎲ ) Very Short Pulse Duration 2 : Durations of each phases at 50% intensity (28 ㎲ + 17

㎲ )

• Fixed vary 30-200 ㎲

Interpulse Interval• Interpulse Interval : Very Long • Pulse : Interpulse Interval 1 : 99

* less accumulate charge in the tissue• accumulated charge neutralize by homeostasis

• can’t use completely denervated muscle : too short pulse durationtoo short pulse duration ETRLabETRLab

Intensity

• Peak Amplitude : 500 V (Very High) above 100-150 V – High Voltage Stimulator

• Peak Current : 2000-2500 mA (Very High) Zero to Peak x25 then Low Voltage Stimulator High peaks can reach/affect Deeper TissueDeeper Tissue • Average Current : 1.5-2 mA (Very Low) Safe, comfortable

Pulse Charge Amount of electrical energy delivered to the tissue with each phase of each pulse Sufficient pulse charge has beneficial physiological effect Excessive pulse charge may damage tissue, interfere with heart * Do not exceed 10-100 C/phase/cm2 of electrode surface area

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4 factors influencing to biological and physiological responses • Pulse duration (pulse width)• Peak current • Pulse rate (frequency) • Pulse charge

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4 Factors Influencing to Biological and Physiological Responses 1. Pulse duration (pulse width)• Degree of chemical effect• Degree of thermal effect• Excitation responses of nerve fiber type• Degree of comfortability• Lowering the Average AmperageMonophasic wave (DC, IDC, Diadynamic current) : 1-300 ms, more thanMonophasic wave (HVPC) : 30-200 ㎲ less chemical & thermal effect, safely use for long duration Comfortability If all fibers are same distance, sufficient peak intensity 400 ㎲ : simultaneously stimulate sensory, motor, pain fiber shorter duration : sensory → motor → pain fiber 20-200 ㎲ : no pain & discomfort

Chronaxie (Li and Bak, 1976)

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1. Pulse duration (pulse width)Chronaxie A-β fiber : 0.02 ms (20 ㎲ ) : Mechanical Stimulation A-δ fiber : 0.45 ms (450 ㎲ ) : Fast (sharp) Pain C fiber : 1.50 ms (1500 ㎲ ) : Slow (dull) PainLi CL and Bak A : Excitability characteristics of the A-δ and C-fibers in a peripheral nerve.Exp Neurol. 50(1):67-79, 1976.

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0

1

2

3

4

5

6

7

8

9

Am

plit

ud

e (

mA

)

0 0.02 0.03 0.2 0.45 1.5 10 100 ms

A-β fiber

A- δ fiber

C fiber

4 Factors Influencing to Biological and Physiological Responses

2. Peak Current• Penetration Depth is proportion to Current Intensity Low peak current – higher resistance, thermal effect, superficial vessel dilation

High peak current – lower resistancelower resistance, no thermal effect, stimulate deeper tissue.

* Developed to produce deeper tissue stimulation without tissue damage

3. Pulse rate (frequency)• Contraction type 1-15 pps : Single contraction 15 pps ↑: Tetanic contraction

• Higher PR induce Muscle fatigue 20-40 pps ↑ On-Off ratio

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Characteristic Interaction of Pulse

• Pulse Rate, Intensity fixation; Pulse Duration ↑ Pulse charge ↑, Average current ↑: feel strong sensation, strong contraction

↑↑: feel Pain

• Pulse Rate, Pulse Duration fixation ; Intensity ↑ Pulse charge ↑, Average current ↑: feel strong sense, strong contraction

↑↑: feel Pain, stimulate deeper tissue

• Pulse Duration, Intensity fixation ; Pulse Rate↑ Pulse charge 0, Average current ↑: feel strong sense, strong contraction

feel less Pain sense

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Physiological and Therapeutic Effects

1. Pain relief • Gate control theory : High Frequency (Conventional TENS) • Endogenous inhibition : Low Frequency (Acupuncture TENS) • Nerve Blocking : Anode (+) decreases nerve irritability by raising th

e nerves resting potential

2. Muscle spasm relief • Muscle fatigue • Disruption of pain-spasm cycle • Contraction – Relaxation

3. Promote inflammation resolve (Wound healing)

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4. Edema absorption endothelial wall permeability of capillary excess plasma proteins to escape into the tissue spaces (exudation ) hydrophilic albumin attracts water → Edema (expansion of tissue space

s)

1) Fluid shift out of area Negative pole : dissolve Blood cell repel Serum protein (albumin) - hydrophilic, negative 2) Absorbs fluid by lymph stimulation • Sensory stimulation – stimulate lymphatic system3) Muscle pumping • Motor stimulation4) Reduced microvascular leakage

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5. Reduced Edema 1) fluid shift out of area Electrorepulsion Negative pole dissolve Blood cell repels blood cells, plasma proteins (albumin - hydrophilic, negative)

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- current source +

Epidermis

Dermis

Blood vessel

_+

Anion

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ⓛ ⓛ

ⓛ

ⓛⓛ

ⓛ ⓛ ⓛ ⓛ ⓛ

ⓛ ⓛ ⓛⓛ

ⓛ ⓛⓛ

ⓛ ⓛ

ⓛ

5. Increase joint mobility • Pain relief • Edema absorption • Increase microcirculation • Mechanical stretching

6. Improve muscular atrophy (Neuromuscular stimulation) • Muscle strengthening • Muscle fiber hypertrophy • Increase enzyme activity • Pain modulation • Isolated muscle contraction • Increase joint mobility • Inhibit spasticity

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7. Increase peripheral circulation • Direct sympathetic activation • Somatic sympathetic reflex • Neuropeptide discharge • Muscle pumping action • Muscle metabolism

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Physiological and Therapeutic Effects

3. Promote wound healing

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3 Phase of the Wound Healing 1. Inflammatory Phase : at the moment of injury – 3 (2-5) days 2. Proliferative Phase : 3 (2-5) day to 20 days3. Remodeling Phase : 9 days to 18 (24) months

COURSE OF WOUND HEALINGETRLab

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Inflammatory Phase

Proliferative PhaseRemodeling Phase

Flow Chart of Wound Healing

Trauma Cellular Necrosis

Vasoconstriction

Proliferative Phase

Epithelialization

InflammatoryPhase

Healed Wound

Vasodilation

Clot Formation / Hemostasis

Phagocytosis / Leukocytosis

Neovascularization Begins

Collagen Synthesis / Fibroplasia

Angiogenesis / Granulation

Wound Contraction

Collagen Synthesis - Lysis Balance

Collagen Fiber Reorientation Remodeling Phase

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Table 4. Summary of Biological Effects of ES in Wound Repair Process

1. Inflammatory Phase

• Initiates the wound repair process by its effect on the current of injury • Increases blood flow • Promotes phagocytosis • Enhances tissue oxygenation • Reduces edema perhaps from reduced microvascular leakage • Attracts and stimulates fibroblasts and epithelial cells • Stimulates DNA synthesis • Controls infection • Solubilizes blood products including necrotic tissue

2. Proliferation phase

• Stimulates fibroblasts and protein synthesis • Stimulates DNA synthesis • Increases ATP generation • Improves membrane transport • Produces better collagen matrix organization, • Stimulates wound contraction

3. Epithelialization phase

• Stimulates keratinocytes reproduction and migration • Produces a smoother, thinner scar

BIOLOGICAL EFFECTS OF ESTRETRLab

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Effects of ES in Cellular & Wound Repair Process in Inflammatory Phase

1. Initiates Initiates the wound repair process by its effect on the current of injurycurrent of injury

Disturbs conduction of bioelectricity • Dry skin, Metals (iodide, silver etc) residual, impregnated dressing with vas

eline, use of repeated debriding enzyme, tropic application of antibiotics• Keeping a wound moist with normal saline (0.9% sodium chloride) maintai

ns the optimal bioelectric charge because it is like the electrolytic concentration of wound fluid. Dressings such as amorphous hydrogels and occlusive dressings help promote the body's "current of injury" by keeping the wound moist.


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2. Increased Blood FlowIncreased Blood Flow • increase blood flow in skinflap (Politis, 1989; Reinisch et al, 1974; Im et

al, 1990) increase blood flow in human U/E at Cathode (Hecker et al, 1985) plethy

smography increase blood flow in rat hindlimb at Cathode (Mohr et al, 1987) increase blood flow in dog muscle (Randall et al, 1953)

• angiogenesis in skin flap (Pollack, 1989)

• increase lymphatic flow


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3. Promotes phagocytosis by neutrophil, macrophages

4. Enhances tissue oxygenation increase transcutaneous PO2 (Dodgen et al, 1987) increase transcutaneous PO2 (Gagnier et al, 1988) due to increased cutaneous circulation


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5. Reduced Edema 1) fluid shift out of area Electrorepulsion Negative pole dissolve Blood cell repels blood cells, plasma proteins (albumin - hydrophilic, negative)

2) Absorbs fluid by lymph stimulation3) Muscle pumping4) Reduced microvascular leakage


- current source +

Epidermis

Dermis

Blood vessel

_+

Anion

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ⓛ ⓛ

ⓛ

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ⓛ ⓛ ⓛ ⓛ ⓛ

ⓛ ⓛ ⓛⓛ

ⓛ ⓛⓛ

ⓛ ⓛ

ⓛ

6. Promote attraction and migrationmigration of keratinocytes, fibroblasts, neutrophils, macrophages

* Galvanotaxis of cells


Keratinocyte (+)Keratinocyte (+)

Macrophage (-)Macrophage (-)

Myofibroblast (+)Myofibroblast (+)

Neutrophil (-/+)Neutrophil (-/+)

Mast cell (-)Mast cell (-)

Fibroblast (+)Fibroblast (+)

Positive PolePositive Pole

Negative PoleNegative Pole

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7. Stimulates DNA SynthesisDNA Synthesis

• increase [3H]thymidine, Human fibroblast cell cultures at negative electrode HVPCS with 100 pps at 50 and 75 V (below contraction) for 20 min * greater than 250 V is inhibitory for DNA synthesis (Bourguignon and Bourguignon, 1987)

• increase DNA synthesis chick tendon fibroblasts in primary culture (Guzelsu et al, 1994)

• promotes collagen synthesiscollagen synthesis by fibroblast


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8. Inhibition Bacterial Growth

1) Disruption of homeostasis 2) Inhibit intracelullar activity irreversible disrupt the cell membrane transport and enzymatic activity Negative pole of LIDC, HVPC Evidences Escherichia coli, Staphylococcus aureus, Pseudononas aeruginosa in vitr

o [Rowley, 1972] Pseudomonas aeruginosa, in vivo [Rowley, 1974] Staphylococcus aureus, in vivo [Barranco et al., 1974]Pseudononas aeruginosa in pressure ulcer [Karba et al., 1990]


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9. Debridement

Negative pole Negative pole • solubilize clotted blood (necrotic tissue is made up of combined blood ele

ments)• promotes rapid absorption of hemorrhagic material, usually within 48 hour

s. (Sussman)

Positive pole Positive pole • coagulate leukocytes and forming of thrombosis in the small vessels

Gentzkow This may explain a clinical observation that hematoma or hemorrhaging at t

he wound margin or on granulation tissue are dissolved and reabsorbed following application of HVPC with the negative pole. Hemorrhagic material goes on to necrosis if not dissolved and reabsorbed quickly


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Effects of ES in Cellular & Wound Repair Process in Proliferative Phase

1. Changes the electrical properties of cell membranes• lateral redistribution of membrane proteins (ion channels and receptors)

(Brown and Loew, 1994)

• changes in intracellular Ca++ concentration ([Ca++]i regulates biological processes including

signal transduction cascades cytoskeletal reorganization cell orientation and migration cell differentiation and proliferation (Bourguignon and Bourguignon, 1987; Cho et al, 1994; Kim et al, 1998).


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Effects of ES in Cellular & Wound Repair Process in Proliferative Phase

1. Changes the electrical properties of cell membranes• lateral redistribution of membrane proteins (ion channels and receptors) • changes in intracellular Ca++ concentration ([Ca++]i • accelerate the cellular metabolism by alteration of the electrical micro-env

ironment

Exogenous electricity stimulates voltage gated ion channel at cell membrane open voltage gated Na+ channel at cell membrane

open voltage-gated Ca++ channels in fibroblast cells (Biedebach, 1989)

Stimulated fibroblasts and keratinocytes by changes in Ca++ flux (Wood et al, 1993)


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Figure 1. Proposed Pathways for Ca 2+ Release and Capacitive Ca 2+ Influx in Keratinocytes.

Raised extracellular Ca2+ is proposed to bind to a Ca2+ receptor (CaR), located in the plasma membrane and the Golgi, producing the second messenger inositol-1,4,5-trisphosphate (IP3). IP3 causes Ca2+ release from the endoplasmic reticulum (ER) and possibly also the Golgi (denoted with?) by binding to IP3 receptors (IP3R). Emptying of ER Ca2+ stores activates ICRAC,either by a direct interaction between the ER and p

lasma membrane or by the action of an as yetunidentified diffusible substance on the ICRAC (denoted by ?).

Intracellular Ca2+ release and Ca2+ influx through the ICRAC raise cytoplasmic (cyt) free Ca2+. This Ca2+ sig

nal is amplified by Ca2+ entry through the INSC, which is activated either by Ca2+ flux through the ICRAC (de

noted by ?) or directly by raised cytoplasmic Ca2+.


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2. Stimulates Fibroblast and Protein synthesis Electrical stimulation activated Fibroblast - increased Protein synthesis (Collagen Synth

esis) Human fibroblast cell cultures HVPCS with 100 pps at 50 and 75 V for 20 min • increase [3H]proline at negative electrode * greater than 250 V is inhibitory for Collagen synthesis (Bourguignon and Bourguigno

n, 1987)

* Collagen deposit in dermal wound by HVPCS (Lee, 2002) Cultured tendon Fibroblast (Gum et al, 1997) Liver Fibroblast (Guler et al, 1996) Dermal wound (Canseven and Atalay, 1996; Alvarez et al, 1983)


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Fibroblast

• Protean cell, can do everything

• Form : flatten and long shape with irregular process

• Nucleus : oval shape, nucleolus

• Cytoplasm : mitochondria, Golgi body, endoplasmic reticulum, centriole, fatlet etc

• Synthesis ECM of dermis (collagen, elastin, proteoglycan, fibronectin, lamine etc)

• collagen 70-85%


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Effects of ES in Wound Repair Process in Proliferative Phase

3. Stimulate certain Growth Factors activity stimulated to secrete TGF-beta 1 (Todd et al, 2001) induces the level of TGF-beta 1 mRNA in osteoblastic cells (Zhuang et al,

1997) increase receptor site for TGF-beta 1 (Falanga et al, 1987)

4. Stimulates DNA Synthesis

5. Increases ATP generation ATP resynthesis (Biedebach, 1989)


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jae hyoung lee wonkwang health science college [email protected] electro therapy research laboratory...

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