PPOM 2 Week 9 LEC 78-88 WORK IN PROGRESS

(78) Function of Lymphatic System

maintains fluid balance, clears antigens, and removes inflammatory mediators from tissues; plays central role in both initiation and resolution of inflammation

(78) Antigen Transport of Lymphatic System

Lymph carries antigens from tissues to lymph nodes; Initiates immune response

(78) Drainage of Exudate of Lymphatic System

Increased capillary permeability during inflammation releases proteins into the interstitium; lymphatics remove these proteins; Prevents persistent edema

(78) Resolution Phase of Lymphatic System

Lymphatics drain inflammatory mediators (e.g. cytokines, prostaglandins) to systemic circulation for degradation; Impaired drainage leads to chronic inflammation or fibrosis

(78) Lymphatic Flow

In inflammation, the only means of fluid return once local capillary stasis develops

(78) Lymph dysfunction in Acute Disease

Lymphatic obstruction worsens edema and delays resolution

(78) Lymph dysfunction in Chronic Disease

Persistent lymphatic dysfunction leads to fibrosis and chronic inflammation; Lymph obstruction = prolonged inflammation + fibrosis

(78) Formation of Lymph drainage

Movement of extracellular fluid into initial lymphatics; driven by Tissue motion, arterial pulsation, respiration

(78) Vascular Flow of Lymph drainage

Intrinsic movement of lymph through vessels; driven by Lymphangion contractions (smooth muscle + valves)

(78) Terminal Drainage of Lymph drainage

Entry of lymph into venous system (thoracic duct → subclavian vein). Driven by Respiratory pressure changes (diaphragmatic motion).

(78) _____ occurs against a slight uphill hydrostatic gradient, requiring external mechanical forces (breathing, muscle contraction, pulsation).

Formation of Lymph drainage

(78) Lymphangion

smallest contractile unit of lymphatic vascular flow (smooth muscle + valves); Has intrinsic pacemaker activity, electrically and mechanically coupled. Can be impeded by somatic dysfunction or tissue tension

(78) Common Lymphatic Obstruction Site of Head & Neck

Between mandible & C1 transverse process

(78) Common Lymphatic Obstruction Site of Upper Limb

Costoclavicular space

(78) Common Lymphatic Obstruction Site of Lower Limb

Femoral triangle, diaphragm

(78) Common Lymphatic Obstruction Site of Thorax

Mediastinal fascia

(78) Common Lymphatic Obstruction Site of Abdomen

Intestinal lymphatic congestion

(78) Common Central Lymphatic Obstruction Site

Thoracic inlet; “Bottleneck” for whole-body drainage

(78) Interstitium

Space between capillaries and cells where cellular respiration occurs.

(78) Function of Interstitial Gel Matrix

Medium for molecular exchange, diffusion, and tissue turgor

(78) Function of Extracellular Fluid (ECF)

Continuous with lymph; provides substrate for nutrient and gas exchange

(78) Function of Interstitial Flow

Guides lymphangiogenesis

(78) Fibrosis

Medical condition caused by stagnant interstitial flow leading to reduced lymph drainage

(78) lymph pump

refers to osteopathic manipulative techniques designed to enhance lymph formation and propulsion through rhythmic, compressive, and respiratory movements

(78) OMT Goal of Terminal Drainage

Open thoracic inlet, promote diaphragmatic motion

(78) OMT Goal of Vascular Flow

Release fascial tension along major lymphatic vessels

(78) OMT Goal of Formation (Pump Application)

Enhance local lymph production via rhythmic compression

(78) Contraindications of lymph pump

Acute DVT, localized infection, or untreated malignancy

(79) Thoracic Outlet Syndrome (TOS)

a group of conditions resulting from compression of the neurovascular bundle as it exits the thorax to enter the upper extremity

(79) Inferior Boundary of Thoracic Outlet

First rib

(79) Anterior Boundary of Thoracic Outlet

Clavicle

(79) Posterior Boundary of Thoracic Outlet

Scapula

(79) Medial Boundary of Thoracic Outlet

Cervical vertebrae

(79) Borders of Interscalene (Scalene) Triangle

Anterior scalene (ant), Middle scalene (post), 1st rib (inf)

(79) Borders of Costoclavicular Space

Clavicle (sup), Subclavius muscle (ant), Anterior scalene (post), 1st rib (inf)

(79) Borders of Subcoracoid (Retropectoralis Minor) Space

Coracoid process (sup), Pectoralis minor (ant), Ribs (post)

(79) Contents Passing Through Interscalene (Scalene) Triangle

Brachial plexus (trunks), Subclavian artery

(79) Contents Passing Through Costoclavicular Space

Brachial plexus, Subclavian artery, Subclavian vein

(79) Contents Passing Through Subcoracoid (Retropectoralis Minor) Space

Brachial plexus, Axillary artery, Axillary vein

(79) Commonly Compressed Structures of Interscalene (Scalene) Triangle

Brachial plexus (most common site of nerve compression)

(79) Commonly Compressed Structures of Costoclavicular Space

Subclavian vein

(79) Commonly Compressed Structures of Subcoracoid (Retropectoralis Minor) Space

Neurovascular bundle (nearly as common as interscalene compression)

(79) Cervical rib

extra rib from C7; rare, can contribute to TOS. Other eponyms include: Cervical rib syndrome, Scalenus anticus syndrome, Costoclavicular space syndrome, First rib syndrome, Paget-von Schroetter syndrome (venous TOS)

(79) Incidence of Thoracic Outlet Syndrome (TOS)

3–80 per 1,000; Female > Male

(79) Age of Thoracic Outlet Syndrome (TOS)

20–50 years

(79) Examples / Causes of Congenital (Structural) TOS

Cervical rib, anomalous fibrous bands

(79) Examples / Causes of Acquired (Traumatic) TOS

Whiplash injury, clavicle fracture

(79) Examples / Causes of Functional TOS

Poor posture, muscle hypertonicity, repetitive strain

(79) % of Cases - Neurogenic TOS

>90%

(79) % of Cases - Venous TOS (Paget–von Schroetter)

10–15%

(79) % of Cases - Arterial TOS

2–5%

(79) Compressed Structure(s) in Neurogenic TOS

Brachial plexus (esp. C8–T1)

(79) Compressed Structure(s) in Venous TOS (Paget–von Schroetter)

Subclavian or axillary vein

(79) Compressed Structure(s) in Arterial TOS

Subclavian or axillary artery

(79) Key Symptoms / Signs of Neurogenic TOS

Paresthesia (98%), neck/trapezius/shoulder pain, muscle weakness or atrophy, occipital headache

(79) Key Symptoms / Signs of Venous TOS (Paget–von Schroetter)

Swelling, cyanosis, heaviness, fatigue, distended veins; may thrombose

(79) Key Symptoms / Signs of Arterial TOS

Pallor, pain, paresthesia, coldness, decreased BP/pulse, possible aneurysm

(79) Typical Triggers of Neurogenic TOS

Overhead activity, prolonged computer use

(79) Typical Triggers of Venous TOS (Paget–von Schroetter)

Repetitive arm motion, heavy lifting

(79) Typical Triggers of Arterial TOS

Often due to cervical rib; not trauma related

(79) Adson’s Test

Provocative Test that assesses subclavian artery compression between scalenes or by a cervical rib

(79) Method of Adson’s Test

Patient extends neck and turns head toward symptomatic side while holding deep inspiration. Examiner palpates radial pulse. Positive test: Decrease/absence of pulse or reproduction of symptoms. Note: False positives/negatives occur—interpret only in context of a thorough history and exam.

(81) (82) Arrhythmia (also Dysrhythmia)

Any disturbance in the normal rate, rhythm, or conduction sequence of the heart; lack of normal rhythm

(81) Conduction Pathway through Heart

SA node → atria → AV node → His bundle → bundle branches → Purkinje fibers → ventricular myocytes

(81) Mechanism of Bradyarrhythmia

Conduction block or reduced automaticity (e.g. Sinus bradycardia, AV block)

(81) Mechanism of Tachyarrhythmia

Increased automaticity, triggered activity, or reentry (e.g.  Atrial fibrillation, ventricular tachycardia)

(81) Location of Supraventricular Arrhythmia

At or above His bundle

(81) Location of Ventricular Arrhythmia

Below His bundle

(81) QRS Width of Supraventricular Arrhythmia

Narrow QRS

(81) QRS Width of Ventricular Arrhythmia

Wide QRS

(81) Core Mechanisms of Arrhythmias

Abnormal Impulse Initiation (Altered or abnormal automaticity, Triggered activity (EADs, DADs)), Abnormal Impulse Conduction (Conduction block, Reentry); “self-starting” problem.

(81) Automaticity

Spontaneous depolarization during phase 4 of the action potential that leads to impulse generation

(81) Altered normal automaticity

SA node fires too fast (sinus tachycardia) or too slow (sinus bradycardia)

(81) (82) Abnormal Automaticity

Spontaneous, inappropriate depolarization by pacemaker cells (e.g., SA or AV node) due to injury, hypoxia, or ischemia

(81) Afterdepolarizations

secondary depolarizations during or after repolarization of an action potential

(81) Mechanism of Early Afterdepolarization (EAD)

Reopening of L-type Ca²⁺ channels

(81) Mechanism of Delayed Afterdepolarization (DAD)

Ca²⁺ overload → ↑ Na⁺/Ca²⁺ exchange current

(81) Timing of Early Afterdepolarization (EAD)

During late phase 2 or early phase 3

(81) Timing of Delayed Afterdepolarization (DAD)

During phase 4

(81) Associated Conditions with Early Afterdepolarization (EAD)

Long QT, hypokalemia, bradycardia

(81) Associated Conditions with Delayed Afterdepolarization (DAD)

Digitalis toxicity, reperfusion injury, CPVT

(81) _____ occurs at slow heart rates and can initiate tachyarrhythmias if threshold potential is reached.

Early Afterdepolarization (EAD)

(81) _____ occurs at fast heart rates and can initiate tachyarrhythmias if threshold potential is reached.

Delayed Afterdepolarization (DAD)

(81) Reentry

Occurs when an electrical impulse re-excites tissue that has recovered excitability, leading to a self-perpetuating loop

(81) Wavelength (WL) Formula

Conduction Velocity (CV) × Effective Refractory Period (ERP)

(81) A _____ WL (short circuit) leads to a increased risk of reentry.

decreased

(81) A decreased WL (short circuit) leads to a _____ risk of reentry.

increased

(81) A _____ WL (longer circuit) leads to a decreased risk of reentry.

increased

(81) A increased WL (longer circuit) leads to a _____ risk of reentry.

decreased

(81) Anatomic Reentry

Occurs around fixed obstacles (e.g., scar). Includes Atrial flutter

(81) Functional Reentry

No fixed pathway; relies on regional differences in refractoriness. Includes Ventricular fibrillation

(81) Anti-tachycardia pacing or defibrillation can terminate reentry by:

exciting the entire excitable gap simultaneously, breaking the loop

(81) Electrolyte disturbances Effect on Arrhythmogenesis

Prolong AP duration → EAD/DAD

(81) Ischemia/Hypoxia Effect on Arrhythmogenesis

Promotes abnormal automaticity and reentry

(81) Drugs Effect on Arrhythmogenesis

Cause DADs or prolong QT

(81) Autonomic tone Effect on Arrhythmogenesis

Alters automaticity and conduction velocity

(81) Structural remodeling Effect on Arrhythmogenesis

Creates reentry substrate

(81) Inflammation/Injury Effect on Arrhythmogenesis

Membrane depolarization leading to ectopic firing

(81) Examples of Electrolyte disturbances Affecting Arrhythmia Formation

Hypokalemia, hypomagnesemia, hypercalcemia

(81) Examples of Ischemia/Hypoxia Affecting Arrhythmia Formation

Myocardial infarction