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OMM Exam 1 Block 4
Lecture 1: LYMPHATICS
Define lymphatic system and lymph node.
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The great integrator of all bodily fluids” “Second circulatory system”
HIS NOTES
a. Mostly passive system
i. relies on arterial pressure, muscle contraction (peripheral pumps),
thoracoabdominal and pelvic diaphragms
ii. system of one-way valves
iii. Some intrinsic contractile activity (7-12/min)
b. We would die within 24 hours from toxin buildup if it stopped functioning
Lymphatic Fluid
a. Ultrafiltrate that leaks out of arterial capillaries into the interstitium and back into
lymphatic vessels
b. Lymph consists of:
i. Lymphocytes (the primary cell of lymph)
ii. Protein and salts
iii. Postprandial water
iv. Soluble fats
v. Clotting factors
vi. Bacteria and smaller viruses
Central Immune Responses
a. Stimulation of B & T cells
b. Ag delivery to lymph nodes or lymph organs
i. Lymphatic drainage of Ag or macrophages containing Ag
ii. *lymph stasis or lymphedema weaken antigenic stimulation (immune
response)
Extracellular Fluid
a. Provides the environment in which cellular exchanges of gases and nutrients take
place.
Inflammation
a. Generalized response of the body to injury or infection.
b. Vasodilatation, increased capillary permeability
Healing Process
a. Inflammatory exudate and mediators removed
i. Fibroblastic activity decreases
b. Lack of lymphatic drainage
i. Increased inflammatory exudate in peripheral tissue
ii. Increased scarring & fibrosis
1. Ex: Chronic inflammatory diseases (RA, etc.)
2. Fibrotic diseases (post op adhesions-abdominal exudate)
Sympathetics Stimulation
a. Increases lymphatic flow
b. * Primary role may be to modify immune response
c.
Define anatomical distribution and drainage of the lymphatic system.
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Anatomy – organized lymphatic tissue
a. Spleen
b. Thymus
c. Tonsils
d. Appendix
e. Visceral Lymphoid tissues
i. GI, pulmonary and liver
f. Lymph Nodes
Fxns
a. Maintaining fluid balance
i. Average of 30 liters of fluid filters out of capillaries every day
ii. 90% of this (27 liters) is resorbed back into capillaries
iii. 10% of this (3 liters) is resorbed by the lymphatic system
iv. Think: removal of protein from extracellular space
b. Purification and cleansing of tissues
c. Defense
i. B-Cell and T-Cell lymphatic systems
d. Nutrition
i. Approximately 50% of all plasma proteins are carried here
ii. Nutrient binding
iii. Fats, cholesterol, chylomicrons
e. Summary
i. Removes fluid, particulates, extravasated proteins from the interstitium.
ii. Maintains osmotic balance between extracellular, intracellular, and
intravascular fluids.
iii. *Virtually all vascularized tissues have lymphatic capillaries that provide
lymph drainage.
Rate of lymph flow (drainage)
a. Severely limits or determines rate of:
i. Blood supply
ii. Delivery of antibodies
iii. Centrally produced mediators
iv. Medication delivery
v. O2 and nutrients necessary to fuel cellular activities
Valve anatomy – lymphatics have more valves
a. Valves
i. One way flow of fluid from extracellular to initial lymphatics
1. Prevents reflux
ii. More valves in lymphatics than veins
b. Smooth muscle begins where valves begin
i. Thickens proximally
ii. Has: tunica intima, media, adventitia
Define horizontal diaphragm. Define and discuss the relationship of the lymphatic system to
horizontal diaphragms.
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He didn’t talk about this. I stole this from an OMM book:
Demonstrate an appropriate general and region-specific examination of the lymphatic system
including lymph nodes and “terminal drainage areas.”
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R Lymphatic and Thoracic duct
a. Histologically like a medium-sized vein, but
b. More smooth mm, More valves
Collecting ducts
a. Largest trunks drain into venous system
b. (Left) Thoracic duct
i. drains into left subclavian vein
ii. drains ¾ of body’s lymph
c. Right lymphatic duct
i. drains into right subclavian vein
ii. drains ¼ (right upper quadrant) of body’s lymph and heart/lungs
Superficial vs deep nodes
a. Superficial (Palpable)
i. Cervical, axillary, supraclavicular, epitrochlear, inguinal
b. Deep (Non-Palpable)
i. Intrathoracic, intra-abdominal, pelvic, deep cervical
Regional Lymphatic Nodes
a. Peripheral Midline Cervico-thoracic junction  Jugular or Subclavian veins.
Important cerv nodes – anterior cervical, post cervical (more viral infxn), occipital (think
scalp wound), postauricular (mastoiditis), preauricular (viral conjunctivitis)
Drainage
a. Superficial drainage  proximal noes at: axilla (UA), inguinal (LE)
b. Deep drainage  popliteal space (good area for obstruction), Sibson’s fascia
(supraclavicular)
i. Synovial fluid is drained by lymphatics
HEART AND LUNGS BELOW – will be a test question
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Pressure gradients
a. Inhalation
i. Lowers intra-lymphatic pressure producing a gradient for influx of fluid
(negative intra-thoracic pressure)
b. Abdomen (resting position)
i. Lymphatics are open
1. Peristalsis
2. Downward movement of diaphragm increases lymphatic flow (positive
intra-abdominal pressure)
Pumping
a. “Intrinsic myogenic pump”
i. Smooth muscle  peristaltic waves
ii. Pacemaker  spontaneous contractions
b. Other ways to improve lymphatic propulsion Production of lymph
i. * any treatment to enhance lymph formation improves lymphatic
drainage.
c. Endotoxin
i. Strong negative effect on lymph pumping activity
ii. Ex: septic shock
What decreases lymphatic flow?
a. Increased venous pressure
b. Congestion in and around the nodes
c. Examples:
i. Popliteal region
ii. Pectoral region
d. Post-nodal (efferent) vessels follow fascial planes
Terminal Drainage Sites used to Dx Regions of Tissue Congestion
a. Supraclavicular Space “Head and Neck” (L supraclavicular node = Virchow’s node…)
b. Posterior Axillary Fold “Arm”
c. Epigastric Area “Abdomen and Chest”
d. Inguinal Area “Lower Extremity”
e. Popliteal Area “Leg”
f. Achilles Tendon “Foot”
Synthesize how to incorporate such examination within the confines of problem-focused examination.
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Pathophysiology
a. Poor fxn
b. Congestion
c. Edema
i. Lymphadenopathy
Two broad categories of OMT lymphatic techniques
a. Remove restrictive barriers
b. Promote/augment flow of lymphatics
Goals of OMT: increase venous and lymphatic return
a. Balance the system to restore function
b. Removing edema
c. Proper fluid dynamics
d. Increased resorption of fluids
e. Increased circulation and respiration
f. Decreased proteins in the interstitium
g. Facilitation from a more beneficial pH balance
h. Maintain proper immune response
Sequencing Tx
a. A thorough lymphatic treatment includes techniques from both categories, starting with
the removal of restrictive impediments to lymphatic flow
b. Release of the central lymphatic system should be accomplished first, followed by
release of the periphery
i. This decreases likelihood of exceeding the system’s innate 7mmHg maximum
increase in capability of handling increased flow
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c. Begin by releasing thoracic inlet, then abdominothoracic diaphragm, and then pelvic
diaphragm
d. Lymphatic treatments should be accompanied by a release of all respiratory restrictions
as well as restrictions of muscles, joints, and the abdomen
Absolute CONTRAINDICATIONS
a. Anuria
b. Necrotizing fasciitis
c. Fx sites
Relative CONTRAINDICATIONS
a. Cancer – no study has shown increased risk of spread
i. Exercise (recommended)-promotes lymphatic flow
ii. Lymphatic Cancer (lymphoma, splenomegaly, etc) - be judicious
b. Infections
i. Ex: mononucleosis with splenomegaly overwhelming bacterial infection (sepsis,
osteomyelitis)
c. Circulatory
i. DVT, hemorrhage
Techniques to remove restrictive barriers and promote/augment flow of lymph
a. Craniocervical junction (occipito-atlantal)
b. Open thoracic inlet (area of greatest restriction)
i. Removes restrictive impediments
c. Rib raising
i. Reduces hypersympathetic activity to the lymphatic vessels and mobilization of
the ribs enhances respiration
d. Doming abdominal diaphragm
i. Improves the ability of this major fibromuscular diaphragm to produce effective
pressure gradients between thoracic and abdominal cavities, therefore
promoting and augmenting lymphatic flow
e. Ischiorectal fossa release (Dome Pelvic Diaphragm)
i. Improves the ability of the pelvic diaphragm to produce effective pressure
gradients between pelvic and thoracic cavities, therefore promoting and
augmenting lymphatic flow
f. Correcting Somatic Dysfunctions in areas of concern
i. Removes restrictive barriers
g. Lymphatic Pump Techniques
i. Promotes and augments lymphatic flow
h. Direct Pressure Techniques
i. Promotes and augments lymphatic flow
Opening thoracic inlet
a. Many neurovascular structures pass through here
b. Know that this is the first area to address with lymphatic techniques
THORACOABDOMENAL DIAPHRAGM
a. Ischiorectal Fossa Release and Dome Pelvic Diaphragm
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i. Distention of the pelvic diaphragm must be in phase with the continual
movements of the thoracic diaphragm and also with the transient changes in
intrapelvic pressure
ii. This aids in free flow of fluids within the vascular and lymphatic channels of the
pelvic region
iii. Curl hand around ischial tuberosity
iv. Lymphatic flow depends on elasticity of the pelvic floor
v. The pelvic floor must compensate for respiratory pressures and the transient
increase of pressure caused from coughing, sneezing, hiccups, pregnancy etc
vi. A rigid pelvic floor leads to dysfunction
Thoracic Lymphatic Pump (once you’ve removed all the impediments)
a. Increases negative intra-thoracic pressure
i. Increases R lymphatic and thoracic duct flow
ii. Stimulates lymph formation in abdomen & thorax
b. Upper or lower thoracic pump. Person takes deep breath, when they bbreath out, I
pump down to try to improve elastic recoil.
c. Improves the ability of this structure to produce effective pressure gradients
d. Cisterna chyli lies directly below the thoracoabdominal diaphragm
e. Doming the thoracoabdominal diaphragm
i. Direct fascial technique
1. Encourage pressure gradients between thoracic and abdominal areas
2. This in turn helps venous and lymphatic return
ii. Myofascial technique
f. Pedal Pumps (feet)
i. Can be done with plantar flexion or dorsiflexion
ii. Moves fluid
iii. Helps pelvic diaphragm move (must release pelvic diaphragm first)
iv. Helps with
1. CHF
2. Pregnancy
3. Hospitalized patients
Rib raising
a. Sympathetic chain lies ant to rib heads; affecting these produces systemic effects
b. Supine
i. Good for hospitalized patients or bedridden
c. Thoracic duct also closely associated with this area
d. Cisterna chyli is a dilatation of the thoracic duct at its inferior pole
i. This drains all of the lower extremities, pelvis and abdomen
e. Focus pressure on erector spinae muscles and transverse processes
f. Can be done seated or supine
Pectoral traction technique
a. Assists in opening the thoracic inlet
b. Encourages venous and lymphatic return through the right lymphatic and thoracic ducts
c. Helps to expand fascial barriers
Lecture 2: Examination of the Chest Wall, Thoracic and Rib Cage
Recall and describe the structural and functional anatomy of the thoracic spine and rib cage.
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T spine General Characteristics
a. Thoracic Cage
i. 12 vertebrae, 12 pairs of ribs, and sternum
ii. Clavicle and scapulae are considered upper extremity
b. Mild kyphotic curvature
i. Can become more acute with age, osteoporosis
1. Leads to biomechanical problems → compensatory adaptations in other
regions of the body and with posture
c. Vertebrae increase in size as you move caudally
i. Corresponding to increased weight bearing
Two anatomic causes for relative immobility of the thoracic spine:
a. intimate connection of the T spine to the rib cage, ribs and sternum, via the
costovertebral articulations.
b. ratio of intervertebral disk height to vertebral body height is small(1:5) which greatly
reduces intersegmental motion.
i. Know diff b/t dermatome, myotome, slcerotome.
Embryology
a. Centrum becomes vertebral body
b. There’s a very detailed slide (12)
Osteology stuff
a. Remember BUM BUL BUM (cervical, thoracic, lumbar orientation of superior facets)
i. Backward upward medial = cervical & lumbar
ii. Backward upward lateral = thoracic
b. Vertebral unit
i. The vertebral unit is given the name of the superior member of the unit.
1. Ex: motion or somatic dysfunction of “T2” means the motion of T2 on
T3.
c. Vertebral size increases as you move caudad from the cervical spine corresponding to
increased weight bearing.
d. T-Spine somatic dysfunction related to rib somatic dysfunction!
i. Treat T-Spine before ribs!
1. Upper: T1-T4
2. Middle: T5-T9
3. Lower: T10-12
e. Spinal unit
i. Spinal motion: a unit consisting of two vertebrae and associated soft tissues
ii. Vertebrae: anterior body, anterior and posterior ligaments
iii. Vertebral canal with ligamentum flavum, interspinous ligaments, supraspinous
ligaments.
iv. Capsular ligaments for facet articulations also contribute to stability and
limitation of motion
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v. Ligaments with high elastin content can store kinetic energy that can be used to
help restore segment to original position
vi. Intervertebral discs: fibrocartilage annulus fibrosis bound with hyaline cartilage
above and below to each segment, enclosing a gelatinous core, nucleus
pulposus that acts to distribute and redirect stress and store energy.
f. Atypical vertebrae
i. One entire facet on vertebrae 1, 10,11,12
ii. No facet on transverse
iii. process of
iv. vertebrae 11, 12
g. Functional landmarks
i. Suprasternal notch - lies anterior to the vertebral body of T2
ii. Angle of Louis - anterior toT4 at level of second rib anteriorly
1. aortic arch lies superior
2. bifurcation of trachea lies posterior
iii. Xiphoid Process - anterior toT9
iv. Spine of scapula - lies posterior to T3
v. Inferior angle of scapula - lies posterior to T8/T7
Muscles –
a. superficial Layer
i. Trap, lat dorsi, rhomboid maj and minor
b. Intermediate
i. Erector spinae (I L S)
ii. Serratus post superior and inferior
c. Deep
i. Semispinalis thoracis, rotatores longus and brevis, etc
d. Innervation – post curtenous branches…LOOK AT SLIDE.
Recall Fryette’s principles and how they apply to the thoracic region.
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Remember somatic dysfxn = Impaired or altered function of related components of the
somatic system: skeletal, arthrodial and myofascial structures, and related vascular,
lymphatic and neural elements.*
1st Principle
a. When sidebending is attempted from neutral (anatomical) position, rotation of
vertebral bodies follows to the opposite direction.
2nd Principle
a. When sidebending is attempted from non-neutral (hyperflexed or hyperextended)
position, rotation must precede sidebending to the same side.
3rd Principle
a. Motion introduced in one plane limits and modifies motion in the other planes.
Demonstrate both a screening and segmental evaluation of the T-Spine.
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See LAB
Explain and review anterior and posterior landmarks in the thoracic region.
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Thoracic Apertures: Inet vs Outlet
a. The thoracic cavity communicates with the neck and upper limb through the superior
thoracic aperture also known as the (boney) thoracic inlet
i. Trachea, esophagus, major vessels and nerves pass through here
ii. Lymphatic drainage for the whole body drains into the venous system
immediately posterior to the medial end of the clavicle and 1st rib
iii. 6.5 x 11 cm in the adult, sloping antero-inferiorly
iv. Boundaries:
1. posterior by T1 vertebra
2. Laterally by medial margins of 1st ribs and costal cartilages
3. Anteriorly by superior/posterior border of manubrium
v. Anatomical thoracic inlet
1. T1, 1st ribs, sternal manubrium
vi. Functional thoracic inlet
1. T1-4, ribs 1&2, manubrum
b. Thoracic inlet fascia
i. The cervicothoracic (diaphragm) fascia covers the thoracic inlet.
ii. It is the deep fascia of the scalenus muscle group
1. Including variably fibrous bands, this fascia inconsistently includes
muscle fibers from scalenus minimus. This fascial covering of the
superior dome of the lung is also referred to as Sibson’s Fascia (Grey’s
Anatomy).
iii. Sibson’s fascia is the final area of obstruction of the 2 great lymphatic ducts
(Thoracic & R Lymphatic).
c. Thoracic Outlet
i. The thoracic outlet (bony) is often referred to the area bounded by the:
ii. Scapulae
iii. 1st ribs
iv. clavicles.
v.
A compression syndrome can act upon the neurovascular bundle as it
travels from the scalene triangle to the neck.
vi. Subclavian artery
vii. Subclavian vein
viii. Brachial plexus
ix. Thoracic Outlet Syndrome (TOS) common AREAS FOR OBSTRUCTION
1. Ant & Middle Scalenes
2. Costoclavicular
3. Pectoralis minor & upper ribs
Functional Classification
a. CervicoThoracic (CT) Junction: C7 – T3
b. “Typical Thoracics”: T4-T9
c. ThoracoLumbar (TL) Junction: T10-L2
Describe the motion characteristics of the T-Spine.
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Muscles
a. Backward bending (extension)
i. Interspinales thoracis
b. Backward bending (extension) when acting Bilaterally
i. Intertransversari thoracis
ii. Multifidus
iii. Longissimus thoracis
iv. Iliocostalis thoracis
c. Backward bending & Rotation (to opposite side)
i. Semispinalis thoracis
ii. Rotatores thoracis
d. Sidebending (lateral flexion)
i. Longissimus thoracis
ii. Intertransversari thoracis
iii. Iliocostalis thoracis
e. Sidebending and Rotation (to opposite side)
i. Multifidus
f. Flexion- abdominal muscles
Thoracic Motion
a. Motion limited
i. to minimize interference with respiration
ii. to minimize interference with cardiac function
iii. because of ribs
b. The architecture of the posterior segment acts to guide and limit the motion that can
occur between the vertebrae.
c. Orientation of the facets varies through the column
d. Load bearing in the posterior segment can be significant when the spine is
hyperextended, and during forward bending when coupled with rotation
Simple vs Coupled Motion
a. Physiologically normal movements in any of the primary directions induces additional
motion vectors as a consequence of the facet orientation: compound movement:
i. F/E, SB, R.
b. Pure flexion and extension of a vertebral unit is the exception to this = simple
movement or “sagittal plane.”
i. F/E
General Motions – summary
a. Cervicals: C2-7: flexion, extension, sidebending and rotation. (varies thru region)
b. Thoracics: rotation > SB > flexion/extension
c. Lumbars: flexion/extension > SB > rotation
i. So rotation greatest in Cerv and upper thoracics; Flex greatest in cervs, lower
thoracic, lumbars
Thoracics = Think ROTATION
a. Greatest motion: Rotation
i. the orientation of the thoracic superior articular facets (“BUL” backwards/
upward/lateral)
allows them to glide relative to each other with an axis of
rotation near the center of the vertebral body
ii. Limited by multiple ligamentous tensions
b. Next greatest is SIDEBEND
i. articular facets of the articular processes of any two adjacent vertebrae slide
relative to each other
ii. Limited by articular processes on the side of movement, contralateral ligamenta
flava, intertransverse ligaments, RIBS and STERNUM
c. Second least motion – Forward Bend (flex)
i. Interspace between the two vertebrae opens out posteriorly, the nucleus is
displaced posteriorly
ii. Limited by the extensor mm., interspinous ligaments, ligamenta flava, posterior
longitudinal ligament
d. Least – Backbend (extend)
i. Vertebrae approximate posteriorly
ii. Intervertebral disc expands anteriorly as it is compressed posteriorly
iii. Limited by the impact of the articular processes and the spinous processes
(shingle effect)
Describe the rule of 3’s and how this is helpful in identifying a segmental level (ID spinous process)
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T1-T3 - come out LEVEL w/ Trans process
T4-6 – ½ way up to get on corresponding TP
T7-9 – come out laterally and you’re one TP of the one below
T10-12
a. Summary
i. 1-3: SP of each is about the same horizontal plane as the TP of each vertebra
ii. 4-6: SP project slightly downward; the tip of the SP lies in a plane halfway
between that vertebra's TP and the TP of the vertebra below it
iii. 7-9: SP project moderately downward; the tip of the SP is in a plane with the TP
of the vertebra below it
iv. 10-12: have SP that project from a position similar to T9 and rapidly regress until
the orientation of the SP of T12 is similar to that of T1.
Lecture 3: Heart Sounds
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Auscultation Skills
a. Style Points
i. Squeeze earpieces to hear better
ii. Don’t ask about heart disease after you listen (freaks out the patient)
iii. Watch your facial expression
iv. Isolate the sounds - don’t try to hear them all at once
b. Stethoscope parts
i. Earpieces – face forward
ii. Bell – good for hearing low pitched sounds (apply w/ light pressure)
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iii. Diaphragm 0 good for hearing higher pitched sounds (apply w/ firm pressure)
Cardiac Cycle – hemodynamics
i. In diastole, blood flows into the R and L atria and ventricle via vena cava and
pulmonary vein respectively
ii. End diastolic volume – how much the ventricle can hold just before contraction
of the atria begins (measurement of ventricle compliance)
iii. At the start of systole, atria contract to fill the ventricle further (“atrial kick”),
then mitral and tricuspid valves click shut (1st heart sound) when ventricle
pressure becomes greater than atrial pressure
iv. Ventricles contract and push blood to body (left vent to aorta) or lungs (R vent
to pulm artery)
v. When contraction ceases and ventricular pressure is lower than pressure in the
outflow track, the aortic and pulmonic valves close (2nd heart sound)
Relate auscultation to cardiac cycle
i. Know that big cardiac cycle graph Dr. A uses all the time
Terminology
i. Base of heart
ii. Apex of heart
iii. Precordium – ant chest wall overlying heart
iv. Listening posts – 4 sites
v. PMI – point of maximal impulse (where you feel the heart beat through the skin
the most)
Normal Heart Sounds
i. 1st – mitral/tricusp closes
ii. 2nd – pulm and aortic valve closes
1. Erb’s point is the place where S2 is loudest
2. Physiologic splitting of S2
a. With inspiration, pulm artery pressure decreases.
b. Venous return to R heart increases
c. Pulmonary vlave remains opwn longer, resulting in a splot S2
d. Split resolves w/ exhalation
iii. Being systematic
1. Most start at right 2nd intercostal space (aortic listening post), then inch
from R to L (pulmonic post). Then, inch down along the L sternal border
to the 5th intercostal space (tricuspid listening post) then along the 5th
intercostal space to the mid-clavicular line (mitral post)
iv. Note that the interval b/t S1 and S2 is shorter than the interval b/t S2 and the
next S1
Describing heart sounds
i. Rate and rhythm regular
1. Normal heart sounds
2. Too fast = tachycardia
3. Too slow = bradycardia
ii. If irregular
II.
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1. Regularly irregular
2. Irregularly irregular (ie, A Fib)
h. Patient positioning
i. Upright – standing
1. Like sports physical
2. Makes innocent murmurs less audible
ii. Seated – most commonly used
iii. Left lateral decubitus – brings L ventricle close to the cheat wall. Auscultate w/
the bell in this position. At the apex, mitral valve murmers are accentuated
i. Auscultation of the lungs
i. Do ant AND post lung fields (both R and L sides)
ii. Should be standing on the R side of the patient
iii. Auscultate the skin, tell pt to “open your mouth and take deep quiet breaths in
and out”
1. Older pts can get light-headed or hyperventilate w/ repeated deep
breathing so warn them.
iv. Listen w/ diaphragm
v. Start at the apex and alternate side to side in at least 6 sites
vi. Note wheeze, rhonchi, consolidation
1. If you’re uncertain if you hear an abnormality, ask the pt to say “E”
(because in pneumonia, it will sound like “A”)…this is called egophony
Lung Sounds
a. Once you know what normal is, listen for these sounds
i. Wheeze aka sibilant wheeze
1. High pitched, almost musical
2. Inspiration or expiration
3. Usually asthma or chronic bronchitis
4. Treated w/ inhaled Beta 2 agonist
ii. Rhonchi = secretions in large airways or narrowing produced in large airways
produce sonorous sounds (almost like a bubbling), usually heard in expiration;
can clear with coughing
1. Think: right upper lobe pneumonia x-ray
2. Bronchitis or diseases producing secretions may cause
3. In cases where there is consolidation, egophony may be heard
iii. Egophony – think pneumonia
1. See above
iv. Pleural rub
v. Crackles (rales) = crackles produced by air moving thru smaller airways, sounds
like hair rolled between fingers or cellophane crumpled, usually heard in
inspiration
1. CHF, Pulmonary fibrosis, bronchiectasis, chronic bronchitis
vi. Whispered pectoriloqy
vii. Stridor = obstruction of upper airway causes hi-pitched sound
1. Causes
a. Infectious causes: croup and epiglottitis most common
i. If signs of these, DO NOT use tongue depressor, cause
you will trigger gag reflex and cause edema that closes
airwat
b. Foreign bodies
c. Chemical burns, trauma
2. Due to obstruction, kids may adopt “sniffling position” to keep airway
open
3. If present, obtain X-ray to determine if foreign body present
III.
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Heart Sounds
a. Things to listen for
i. Normal 1 and 2 heart sounds
1. Remember Erb’s point is the location where S2 is loudest
ii. A fib
iii. Physiologic splitting
1. Usually heard at left 2nd intercostal space; split is intermittent w/
respiratory cycle
2. Pathologic splitting of S2
a. Any patho that causes the pulm valves to remain open longer
causes a fixed split
b. R or L Bundle Block – causes fixed splitting by delaying
contraction of the ventricle, w/o other ex. Usually S1 will be
faint
c. Atrial septal defect - fixed splitting due to hole in atria which
shifts blood from L side to right, w/ early midsystolic murmur
d. There is NO resolution of splitting w/ expiration; split remains
fixed
rd
iv. 3 heart sound
1. Occurs immediately after S2
2. L ventricular gallop usually heard best over the apex w/ the bell of the
stethoscope in L lateral decubitus position. Usually SOFTER during
inspiration
3. R ventricular gallop is best heard over the L sternal border and is
LOUDER during inspiration
4. Can be normal in people under 30; older indicates heart failure. Sounds
from stopping ventricular filling due to over-full ventricles
5. Produces a rhythm similar to the cadence of the word “Kentucky” with
the “ky” representing S3
th
v. 4 heart sound
1. Extra heart sound just after atrial contraction and immediately before
S1. Produces a rhythm classically compared to the cadence of the word
“Tennessee” – the first syllable represents S4
vi.
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viii.
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2. Almost always patho. If problem is RIGHT ventricle, the abdominal
sound is best heard at the lower left sternal border, louder w/ exercise
and deep inspiration
3. If the LEFT ventricle is the problem, the sound is best heard at left
lateral decubitus position and will be louder w/ pt holding expiration
Heart Murmur in general
1. Look for timing – when u hear and what immediately precedes it
2. Duration – how long does it last in the cardiac cycle
3. Location – where do you hear it?
4. Radiation – where does it go?
5. Intensity – graded
a. Grade 1 – barely audible, cardiologist can hear
b. Grade 2 – little louder, *if you can hear it, it’s at least Grade 2
c. Grade 3 – clearly audible, no thrill
d. Grade 4 – thrill palpable (a thrill – you can palpate the chest wall
and feel the vibration of the murmur)
e. Grade 5 – audible w/ stethoscope partly off the cheast and thrill
f. Grade 6 – audible w/o stethoscope (ie, metallic aortic ball valve)
6. Pitch – hi or low?
7. Quality – musical? Harsh?
Stenosis murmur - general
1. When the valve becomes stiff or the opening narrow
2. When fluid flows across the narrow opening, flow sound produced is
the murmur (like water rushing by a ‘kink’ in a garden hose)
Aortic stenosis
1. What = Harsh SYSTOLIC crescendo-decrescendo murmur, best heard @
R upper sternal border, 2nd intercostal space
a. Radiation to the carotid aa bilaterally (sound should be
transmitted forward (away) from the heart
2. Etio
a. 50% is age-related calcification of aortic valve
b. 30-40% from congenital bicuspid aortic valves
3. Sx only present w/ severe stenosis (progressive dyspnea on exertion,
syncope, chest pain, heart failure)
4. What to hear: distinct S1, murmur, distinct S2.
5. Graph stuff
a. Narrowing of the aortic valve requires a marked increase in
systolic pressure w/in the L ventricle to drive blood thru the
stenotic valve orifice…
b. when severe, the aortic pulse curve is deformed. Aortic
pressure pulse is narrow, and there’s a slow rise during systole,
w/ notching on the upstroke (anacrotic notch)-this pulse if
called pulsus parvus (small) and pulsus tardus (late)
Mitral stenosis
1. What = a diastolic murmur. Low-pitched diastolic rumble. Best heard
over the L 5th intercostal space at the apex, in the left lateral decubitus
position. May be an opening snap heard, which comes from the forceful
opening of the mitral valve
2. Etio
a. Mostly from diseased valves as a consequence of rheumatic
fever…also bacterial endocarditis
3. Sx = only w/ severe (dyspnea and pulm HTN)
4. What to hear – S1 and S2 are distinct, no sound b/t them. Hear a 3rd
heart sound (opening snap) followed by the rumbling murmur
5. Causes an impediment to blood flow into the L ventricle. As the valve
stiffens, there is more pressure that must build up in the L atrium before
it snaps open
6. As the pressure gradient increases, the amount of time necessary to fill
the ventricle w/ blood increases. If the diastolic filling period is
insufficient, pressure will build up in the L atrium leading to pulm
congestion. Eventually, there will be a L atrial enlargement and possible
A fib.
x. Hypertrophic cardiomyopathy bonus murmur
1. Common cause of sudden cardiac death in athletes.
2. Best heard over the mitral listening post, when there is less volume in
the ventricle
3. Valsalva maneuver increases thoracic pressure and decreases blood
return to the heart, making the murmur louder.
4. Squatting down increases blood return to the heart and makes the
murmur softer.
xi. Aortic regurgitation - a diastolic murmur (aka ‘insufficiency’)
1. Soft, early diastolic decrescendo murmur, best heard at R upper sternal
border, 2nd intercostal space.
2. Caused by leaking of the aortic valve, resulting in blood flow from the
aorta back into the ventricle after ventricular contraction.
3. Sx
a. Dyspnea on exertion, orthopnea, angina, paroxysmal nocturnal
dyspnea
4. What to hear
a. Distinct beginning of the murmur immediately after S@,
gradually diminishes in intensity (decrescendo). Murmur ends
distinctly before the beginning of the next S1
xii. Mitral regurgitation – a systolic murmur
1. High-pitched, blowing, holosystolic murmur best heard at the apex.
2. Radiates to the axilla. Most common form of valvular heart disease
3. If it happens acutely, it may cause dyspnea and CHF; chronic causes are
usually compensated and asymptomatic.
18
4. Note: the tricuspid regurg murmur is similar but is best heard at the L 5th
intercostal space at the sternum
Lecture 4: Cardiac Assess and Tx
I.
II.
III.
IV.
V.
VI.
VII.
19
Systole
a. The time between the S1 and S2 sounds is:
Lub------------Dub
b. The ventricles contracting
c. Blood flowing from the heart to the lungs and body
d. Blood flowing across the Pulmonic and Aortic valves
Diastole
a. The time between S2 and S1 is :
i. The blood is flowing from the atria to the ventricles.
ii. The blood flowing across the bicuspid and tricuspid valves.
iii. The atrial contraction also occurs now.
S1
a. The “lub” in the lub – dub.
b. This sound is primarily because of the closing of the bicuspid and tricuspid valves.
c. Anatomically they are located between the atria and the ventricles
d. They close because the ventricles contract
e. The Pulmonic and Aortic valves are opening and blood is being forced into the arteries
S2
a. S2 is the “dub” in the lub- dub
b. The sounds are because of the closing of the Pulmonic and Aortic valves as the pressure
from the arteries is greater then the pressure in the ventricles.
c. This is the end of systole
What kinds of sounds do you hear?
a. Murmurs-usually indicate turbulence & they range from 1 to 5 in loudness.
b. Does it occur during diastole or systole?
c. Does it crescendo (get progressively louder)?
d. Does it decrescendo (get progressively quieter)?
e. Where do you hear it best? (Neck, Chest, Axilla)
Other sounds
a. Gallops- these are either S3 or S4 sounds.
b. Rubs- pericardial or plural friction rubs and usually indicated either pericarditis or
possible pleurisy ( must be careful to listen to both heart and lung sounds)
c. Rubs- sounds “sandpapery”
d. Clicks- only occur in systole and represent the loud valve closing
e. Diastolic Knock- occurs because of an abrupt arrest of ventricular filling by a noncompliant & constricting pericardium.
f. Continuous Murmurs- indicate a constant shunt flow throughout systole & diastole i.e.
Coarctation, or patent ductus arteriosus.
Now that you hear the sounds, what does it mean?
VIII.
IX.
X.
XI.
XII.
20
a. First Heart Sound
i. Louder than usual - Mitral Stenosis
ii. Variable Atrial Fib./Complete Heart Block
iii. Diminished Mitral or Aortic Regurg.
b. Second Heart Sound
i. Wide split sounds or fixed ( not moving with respiration) may indicate:
1. Atrial Septal Defect
2. RBBB
3. Pulmonic Stenosis
c. Extra heart sounds: S3 and S4
i. Third Heart Sound (S3)  Markedly Diminished Left Ventricular Function
1. (Almost always present with Myocardial Ischemia or early after an AMI)
ii. Fourth Heart Sound (S4) Modestly Diminished Left Ventricular Function
What do you need to hear the sounds?
a. Stethoscope
b. As quite an environment as possible
c. Proper positioning of the patient
d. Stethoscope must touch the skin
e. Patient history
f. Ability to observe the chest, abdomen & neck
Where do you listen?
a. Left Ventricle Area- The apex of the heart is at the 4th or 5th intercostal space (ICS) along
the midclavicular line (MCL).
b. Right Ventricular Area- the 3rd to 5th ICS along the left sternal border (LSB)
c. Pulmonic Area- 2nd ICS along LSB
d. Aortic Area- 2nd ICS along the right sternal border (RSB)
Stethoscope Use
a. The diaphragm of your stethoscope is most useful for picking up high-pitched sounds i.e.
S1, S2, Aortic or Mitral Regurgitation Murmurs or Friction Rubs.
b. The Bell is most useful for picking up low-pitched sounds, S3, S4, or Mitral Stenosis.
TEST QUESTION: CARDIAC RISK FACTORS *FlASH MD
a. Family Hx
b. Lipids
c. Age
d. Smoking
e. HTN
f. Male / postmenopausal female
g. Diabetes
TEST QUESTION: the 6 LEVELS of Heart murmur Intensity
XIII.
XIV.
a.
Bruit = murmur in neck; carotid a. (have to have at least 40% occluded to hear it)
ADC VAN DIML (mnemonic for the “PLAN” of SOAP Note when you have to ADMIT pt to
hospital)
a. Admit
b. Dx
c. Conditions
d. Vitals
e. Allergies
f. Activities
g. Nursing
h. Diet
i. IV fluids
j. Meds
k. Labs and xray
Lecture 5: Osteopathic for Cardiac Disease
Review neurophysiology as it pertains to viscerosomatic and somatovisceral reflexes
I.
II.
21
Sympathetics of heart
a. Pre-ganglionic neurons: T1-6
b. Synapse: Superior, middle, inferior cervical ganglia
c. Post-ganglionic fibers
i. Right - Deep cardiac plexus -> SA node (hypersympathetic -> tachyarrhythmias)
ii. Left - Deep cardiac plexus -> AV node (hypersympathetic -> ectopic foci and v.
fib)
d. Effects
i. Increased force of heart beat
ii. Increased heart rate
iii. Shortened duration of systole
iv. Increased ventricular output and stroke volume
e. Asymmetries in sympathetic tone may play a role in the development of serious
ventricular arrhythmias
f. Increased sympathetic tone increases post MI morbidity (always a BOARDS question)
Parasympathetics of Heart
a. Pre-ganglionic: Vagal nuclei in medulla
III.
IV.
b. Synapse: Parasympathetic ganglia embedded in cardiac plexus
c. Post-ganglion fibers
i. Right Vagus: SA node (hyperactive parasympathetics -> sinus bradyarrhythmias)
ii. Left Vagus: AV node (hyperactive parasympathetics -> AV blocks)
d. Effects
i. Decreased heart rate
ii. Increased duration of diastole
e. Irritation of pulmonary branches of the vagus produce strong inhibitory reflex influence
on the heart
f. Irritation of the larynx, pressure on the carotid body or pressure on the globe of the eye
(oculocardiac reflex) cause slowing of the heart rate from stimulation of visceral
afferents that activate vagal efferents.
g. Oculocardiac reflex can slow heart rate by 5-13 bpm
Vascular Sympathetics
a. T1-L2; Constriction of circular smooth muscle of the tunica media
i. Normal sympathetic tone maintains vessels constricted to 1/2 their maximum
diameter
Vascular Parasympathetics (potential test question)
a. Submaxillary gland vessels - CNVII
b. Parotid gland vessels - CN IX
c. Vessels of the tongue - Lingual nerve
d. Vessels of the penis - Nervus erigens
Review neurophysiology as it pertains to facilitation in the Cardiopulmonary system
I.
II.
22
Lymphatic drainage of CV system
a. Primarily from right lymphatic duct
b. Congestion leads to:
c. Arrythmias
d. Atherosclerosis
e. Hypertension
f. Pulmonary edema
g. Ascities
h. Hepatomegaly
i. Peripheral edema
Tx of Somatic Dysfxn
a. Low pressure systems effected in SD: venous, lymphatic
i. Much more susceptible to external factors resulting from dysfunctional
musculoskeletal structures
b. Tx goals
i. Reducing local myofascial tensions that can compress and obstruct peripheral
vessels
ii. Ensuring mechanical efficiency of the thoracoabdominal pump by treating
dysfunction of the rib cage, thoracoabdominal diaphragm, thoracic inlet and
pelvis
iii. Treating thoracic somatic dysfunction to reduce the effects of facilitation and
increased sympathetic tone upon peripheral vasculature and the heart
c. Sympathetic Effects on lympahtics
i. Hypersympathetic tone can cause reductions in lymphatic flow by reducing the
diameter of the thoracic duct and other large lymphatic channels.
d. CI to Lymphatic Tx (is relative)
i. Osseous fractures
ii. Bacterial infections with temperature >102F
iii. Abscess or localized infection
iv. Certain stages of carcinoma
1. There are no absolute contraindications to lymphatic treatment and
some suggest that a case can be made for the delivery of cancerous cells
to the immune system for clearance and destruction rather than
metastasis.
Define Chapman’s reflexes as they pertain to the Cardiopulmonary system
I.
II.
23
Chapman’s points
a. A system of reflex points that present as predictable anterior and posterior fascial tissue
texture abnormalities
b. Initially described as a ganglioform contraction that blocks lymphatic drainage (Charles
Owens, DO first to formally describe them); now, considered a consequence of a v-s
reflex
c. Causes inflammation in tissue distal to blockage
d. Probable concurrent involvement of sympathetic nervous system
e. Reflective of VISCERAL disease or dysfunction
Point characteristics –
a. nodules that are
i. Smooth
ii. Small (approximately 2-3mm diameter)
iii. Firm
iv. Discretely palpable (which may have a feel of surrounding edema).
v. Pain is typically illicited when a lesion is found and is typically: pinpoint,
nonradiating, sharp and fairly distressing.
b. Acute, palpatory characteristics
i. Tender, nonradiating, may be pinpoint
ii. Anterior-may differ depending on location
iii. Posterior-”ganglioform contraction” may be buried in dysfunctional tissue
iv. Pain illicited is much more than would be expected
c. Chronic palpatory characteristics
i. Nontender or less tender
ii. Anterior-generalized increased tension
III.
IV.
V.
iii. Posterior-paraspinal areas (ropiness,stringy)
Use of chapman’s
a. Palpation can aid in determination of presence or absence of visceral dysfunction
b. Reduce adverse sympathetic influence on a particular organ or visceral system
c. Improved function of the disturbed organ usually follows treatment of Chapman point
Cardiac Chapman’s Points
a. Ant TP – bilaterally along 2/3 intercostal space
b. Posterior TP - Bilaterally - 2/3 transverse processes
c. SNS T1-5; PNS vagus
Pulmonary Chapman’s Points
a. Anterior tenderpoints: 2/3/4 intercostal spaces
b. Posterior tenderpoints: 2/3/4 Transverse processes
c. SNS T2-7; PNS vagus
Review the musculoskeletal system as it pertains to Cardiopulmonary health and dysfunction
Define the clinical application and utility of Osteopathic manual treatment in the maintenance of
Cardiopulmonary homeostasis.
I.
24
Physiologic Models of Tx
a. Circulatory-Respiratory
i. Getting nutrients to, removing waste products from
ii. Respiratory mechanics
iii. Junctional areas are key sites
iv. Research = saw response to OMM
b. Viscero-somatic / somato-viscero / somato-somato
i. Facilitated segment
ii. Reflex loop, bi-directional
iii. Wide dynamic range cells
iv. Chapman’s reflex
v. Research = greatest change in rom at T4, of these participants, 75% had
angiogram evidence of CAD
c. Neuro-endocrine-immune
i. Homeostasis vs allostasis
ii. Stressful stimuli may be psychological or physiological
iii. Hypothalamic-thyroid-adrenal-gonadal axis
d. Biomechanical/postural
i. Posture and balance
ii. Motion
iii. Functional anatomy
iv. Tensegrity – tensional integrity (floating compression, is a structural principle
based on the use of isolated components in compression inside a net of
continuous tension, in such a way that the compressed members (usually bars
or struts) do not touch each other and the prestressed tensioned members
(usually cables or tendons) delineate the system spatially.)
e. Bioenergetic
XI.
XII.
25
i. Energy expenditure
ii. Energy conservation
iii. Changes in musculoskeletal system can effect body’s energy requirements.
f. Psycho-somatic
i. Role of limbic system in perception of pain
ii. Depression and musculoskeletal pain
CASES…not much here. Just this slide is important:
TREATMENTS
a. Cervical
i. Condylar decompression
1. Helps open jugular foramen structures to improve parasympathetic
responses to structures innervated by CNX.
2. Other treatment modalities for the manipulation of OA, AA and C2 will
have potential influence over parasympathetic tone via the Vagus nn
3. Directions
a. Patient is supine with physician sitting at the head of the bed
b. Palms of Dr’s hands on the base of the occiput with their 2nd &
3rd fingers supporting the Atlas
c. Gentle anterior pressure on the Atlas allows for the occiput to
relax and float posteriorly
d. Hold for 1-4 minutes
ii. Cervical myofascial stretching
1. To Reduce cervical muscle tension allowing for improved vagal tone
b. Thoracic
i. Thoracic Inlet
1. To Improve lymphatic flow/return in the left and right lymphatic ducts
2. Direct Myofascial release to Thoracic inlet – driving the car
3. Directions
a. Place one hand posterior to the thoracic inlet (transversely) at
the level of the first and second ribs.
b. Place the other hand at the same level on the anterior chest
wall.
c. The area is motion tested for myofascial restrictions. These
motions include a side-to-side movement, a rotational or
twisting movement, a superior or inferior movement, or an
angular movement.
d. The area is treated directly (barrier engagement) or indirectly
(position of fascial ease). Having the patient take three deep
breaths, can facilitate a release.
e. The physician waits for a release and the area is re-evaluated.
f. Modification: Both hands can also be placed on the anterior
thorax. With this position, the thumbs contact the trapezius
muscle and posterior upper two ribs. The fingers lie on the
anterior chest wall spread out.
ii. Thoracic pump
1. Directions
a. Patient Supine
b. Place hands palm down upon the patients anterior chest wall
over the pectoralis major mm
c. Straighten arms and lock elbows
d. Instruct patient to exhale in a relaxed fashion through an open
mouth
e. Lean gently upon the anterior thoracic cage with your hands
and follow the exhalation
f. Toward the end of exhalation, exert a rhythmic pumping action
with you hands by an alternating pressure through your hands
to produce a slight alternating positive and negative
intrathoracic pressure
iii. Thoracoabdominal diaphragm doming
1. Used to relax diaphragm; increase diaphragmatic excursion; potentially
improve lymphatic flow in thorax
2. Directions
a. While patient is supine, the Dr’s hands are placed on both sides
of the costal margin - thumbs towards the xiphoid
b. While the patient is taking slow, deep breaths apply a
compression feeling for asymmetry in motion d/t tension.
c. Once the asymmetry has been identified - treat it by moving
your hands in the direction of ease. Have your patient hold
their breath briefly until a release is felt (INDIRECT)
d. Have patient take a deep breath to reassess motion.
iv. Rib raising
26
1. To Rib raising is employed to enhance rib motion and rib cage
compliance
2. Improved venous and lymphatic return
3. Decrease sympathetic tone (initially this causes an increase in
sympathetic activity followed eventually by a reduction in sympathetic
activity) along the spinal levels treated
c. Pubic Decompression
i. Compression of Pubic Symphysis = pubic bones are forced toward each other at
the pubic symphysis
ii. Characteristic Findings
1. tender over symphysis bilaterally.
2. lack of apparent asymmetry.
3. restriction of motion at pubic ring.
4. ASIS springing affected bilaterally
iii. Note: Pubic shears are usually associated with pubic compression. It’s a good
idea to decompress the pubic bones prior to treating a shear.
iv. Muscle Energy Directions
1. Pt. supine on table, knees and thighs flexed.
2. Feet flat on table 10-12 inches apart.
3. Grasp both knees. “Try to pull your knees apart.” (abductor muscles pull
laterally on innominate compressing the symphysis further to prepare it
to relax.)
4. Repeat.
5. Heel of one hand in knee, posterior distal humerus in other knee.
6. Knees 10 to 12 inches apart. “Try to pull your knees together.”
7. Repeat . (av. 3 times)
d. Pelvic Diaphragm
e. Popliteal Fascia
i. Direct MFR (myofascial release):
1. Technique: supine, direct, MFR
2. Findings: Pain behind the knee or baker’s cyst.
3. Physician: Seated at the side of the table inferior to the patient’s knee,
facing the head of the table.
ii. Directions
1. With the patient’s leg relaxed place your fingertips just above the
popliteal fossa.
2. Fingers of both hands are bent with the fingernails of the two hands
facing each other and thenar eminences about 3” apart to form a
“plow” shape.
3. Press anteriorly just superior to popiliteal fossa.
4. Draw the fingers inferiorly until resistance is felt, then hold until the
release occurs.
f. Interosseous Membrane Release
i. Technique: Supine Direct Ligamentous Articular Release
27
ii. Findings:
1. Posterior and lateral knee pain or unstable ankle with chronic spraining
of the ankle. The latter is a result of an unstable ankle mortise with the
fibula displaced at the knee.
iii. Directions
1. Pt is supine and Physician is seated facing the side of the table at the
level of the affected knee
2. Flex the hip and the knee to 90 deg.
3. Slightly externally rotate the femur
4. With the cephalad arm, bend elbow to 90 deg and prop it on the table
making a pedastal out of your forearm and thumb.
5. With the pad of the thumb push the posterior superior portion of the
fibular head inferiorly toward the pt’s foot.
6. The distal hand inverts and slightly medially rotates the foot.
7. A release occurs when the fibular head moves inferiorly and anteriorly
and slides back into the socket.
iv. Diagnostic Findings
1. Tissue texture changes anywhere between fibula and tibia
2. One or both ends of the fibula restricted
3. Ankle function may be impaired
4. Tenderness at proximal tibiofibular joint, distal tibiofibular joint and/or
ankle
g. Pedal Pump (ie, Dalrymple’s Pump)
i. TO Enhance low-pressure venous and lymphatic return to the heart
1. Reduce passive congestion of the lower extremities, abdominal
contents and lungs
2. Better suited for patients that can’t tolerate thoracic pump
ii. Directions
1. Grasp the patients toes with both hands
2. Abruptly push cephlad, dorsiflexing the patients ankles, and then quickly
return them to the neutral position. This action should send a wave of
motion cephald followed by a rebound wave.
3. As the rebound wave returns to the feet, reapply the dorsiflexion force,
creating an oscillatory pump.
4. The oscillating motion moves the lower extremities in approximation of
the muscular pump. It also moves the abdominal contents
intermittently up against the thoracoabdominal diaphragm, facilitating
alternating positive and negative intraabdominal and intrathoracic
pressure and decongesting the liver and spleen.
IX.
OMT SUMMARY
a. Decrease sympathetic drive by treating T1-6 dysfunction
b. Promote parasympathetic by treating upper cervicals where irritation can inhibit the
vagus
c. Optimize pulmonary function by treating T-spine and rib cage
28
X.
Clinical Application
a. Treat the patient medically
b. Normalize somatic dysfunction to allow for better potential for return to
homeostasis (Host+Disease=Illness)
c. Treat the psychosocial aspects - stress reduction, spiritual aspects, lifestyle changes
Lecture 6: Relative Risk Factors and Prevention of Heart Disease SDL (I’ve bolded
and *** the things he said to know in this summary slide)
***Know how to access various guidelines for screening for coronary heart disease (CHD)***
i.
US Preventive Services Task Force (USPSTF)
I. Decisions about aspirin chemoprevention should reflect overall CHD risk; tools that
incorporate specific information on risk factors provide more accurate risk estimation than
tools based on the number of risks
ii. National Heart, Lung and Blood Institute (NHLBI)
I. For patients with multiple risk factors, 10-year CHD risk should be calculated to allow better
targeting of intensive treatment
II. When filling it out:
 A smoker is anyone who has had any cigs in the past month
 Systolic BP is entered as systolic and diastolic
iii. American Heart Association (AHA)
I. All adults 40 years and older with no history of heart disease should know their absolute risk
of developing CHD and should have global CHD risk calculated every 5 years
II. What is noted on the AHA CAD Risk calculator
 Gender
 Age
 Smoker
 Family history
 Atherosclerosis
 DM
 Elevated BS
 Height
 Weight
 BMI
 Waist circumference
 SBP
 DBP
 Current treatment for BP
 Total cholesterol
 HDL
 Triglycerides
Know the grading of recommendations and the implications to practice
29
Lipids
I.
II.
III.
30
Total cholesterol - Total cholesterol is the sum of all the cholesterol in your blood. The
higher your total cholesterol, the greater your risk for heart disease. Here are the total
values that matter to you:
a. Less than 200 mg/dL 'Desirable' level that puts you at lower risk for heart disease. A
cholesterol level of 200 mg/dL or greater increases your risk.
b. 200 to 239 mg/dL 'Borderline-high.'
c. 240 mg/dL and above 'High' blood cholesterol. A person with this level has more than
twice the risk of heart disease compared to someone whose cholesterol is below 200
mg/dL.
HDL cholesterol - High density lipoproteins (HDL) is the 'good' cholesterol. HDL carry
cholesterol in the blood from other parts of the body back to the liver, which leads to its
removal from the body. So HDL help keep cholesterol from building up in the walls of the
arteries.
a. Here are the HDL-Cholesterol Levels that matter to you:
i. Less than 40 mg/dL A major risk factor for heart disease
ii. 40 to 59 mg/dL The higher your HDL, the better
iii. 60 mg/dL and above An HDL of 60 mg/dL and above is considered protective
against heart disease.
***USPSTF Recommendations for lipids***
a. Screen men age 35 and older (grade A)
b. Screen men age 20-35 if at increased risk for CHD (grade B)
c. Screen women age 45 and older if at increased risk (grade A)
d. Screen women age 20-45 if at increased risk for CHD (grade B)
e. No recommendation to screen men 20-35 or women age 20-45 if not at increased risk
(grade C)
f. Insufficient evidence to screen under age 20 (grade I)
i. Defining “Increased risk”: DM, previous CHD, non coronary atherosclerosis
(AAA,PAD,CAS), fam hx of CAD in males before age 50 or female before age
60, tobacco use, hypertension, obesity (BMI > or = 30)
IV.
V.
Risk
a. Randomized trials show decreased risk with lower cholesterol levels
b. There may also be an independent risk reduction from statins
c. Risk increased with:
i. elevated LDL
ii. total cholesterol
iii. low HDL
iv. Increased ratio of total to HDL cholesterol level
v. Hypertriglyceridemia
vi. Increased non-HDL cholesterol
vii. Increased Lipoprotein(a)
viii. Increased apolipoprotein B(LDL) and decreased apolipoprotein A-1 (HDL)
ix. Small dense LDL
x. Apolipoprotein E genotypes
***CHD and recommended LDL Levels***
a. CHD or CHD Risk Equivalents or 10-year risk >20%
i. <100 mg/dl
b. 2 + risk factors and 10-year risk < 20%
i. <130 mg/dl
c. 0-1 risk factor
i. <160 mg/dl
ASA Use for CHD Prevention
I.
II.
III.
IV.
V.
ASA for men age 45-79 when risk reduction for MI outweighs GI risk (grade A); women age
55-79 when risk reduction of ischemic strokes outweighs GI risk (grade A)
Over age 80 insufficient evidence for or against use for cardiovascular prevention(grade I)
Against use in women < 55 for stroke prevention or male < 45 for prevention of MI (grade
D)
Estimated number of MI’s prevented varies with 10 year CHD risk
Estimated harms of ASA vary with age so both should be considered
***Major Risk Factors for Coronary Heart Disease***
I.
31
Increasing age
II.
III.
IV.
V.
VI.
VII.
VIII.
IX.
X.
32
a. 80% of people who die from CHD > 65yo
b. Women more likely to die than men at older ages from MI
Gender – men > risk than women even after menopause
Heredity – includes race, Family History counts
a. Significant independent risk factor particularly for younger individuals
b. Physicians health study (22,000 patients for 13 years) and Womens’ health Study
(40,000 for 6 years)
i. Paternal MI before age 60 was associated with increased risk
ii. Any maternal history associated with elevated risk
c. Framingham offspring study
i. Increased risk of cardiovascular events if premature CAD was found in males
(father) prior to age 55 and females(mother) prior to age 65
ii. Increased risk if siblings affected also
Tobacco
a. 2-3x > than non smokers
b. Second hand smoke also increases risk
Cholesterol – risk increases with > cholesterol
Hypertension – increase hearts workload causing the heart to become stiff and thick
Physical inactivity – regular moderate to vigorous physical activity helps prevent heart and
blood vessel disease
Obesity – increased risk especially midline
a. Framingham offspring study; adjusting for risk factors increased BMI associated with
increased risk of CHD, and CVD.
b. Metabolic syndrome – abdominal obesity, hypertension, diabetes, and
hyperlipidemia; increased risk for CAD
c. Recent studies suggest that there is increased risk from hypertriglyceridemia ( > 200)
and waist (> 90 cm) regardless of other risk factors predict risk; previous studies show
waist to height ratio and waist as risk; regardless of BMI
d. ***Waist-to-height ratio***
i. Significant predictor of cardiovascular and all cause mortality
ii. Waist-to-Height Ratio is the calculated by dividing a person’s waist
measurement by their height. Waist is measured at the narrowest point of
one’s midsection between their bottom rib and the top of their hipbone. This
is usually one inch above the navel.
iii. As a rule of thumb, 50% is considered the general healthy cutoff.
DM – risk equivalent for CAD/CHD
a. Copenhagen heart study showed increased risk of MI or stroke was 2-3x, and death 2x
(independent of other CHD risk factors)
b. Interheart study showed DM responsible for 10% risk
c. 2002 NCEP designated DM a CAD risk equivalent
d. Higher blood glucose levels correlate with increased cardiovascular risk for diabetics and
nondiabetics
e. 1% increase in HgbA1c associated with pooled relative risk of CHD and stroke of 1.18
Chronic Kidney Disease is a CHD risk equivalent
XI.
XII.
33
Lifestyle
a. Exercise – regular exercise has protective effect against CHD and all cause mortality
i. Interheart study showed lack of regular exercise had 12% increased risk of first
MI
ii. Women's Health Initiative study showed 30% reduction in vascular events with
regular exercise
b. Cigarette smoking
i. Increase risk 6X in women and 3x in men (smoking > 20/day)
ii. Interheart study showed 20% PAR for first MI
iii. Benefits of quitting no matter how long or how much smoked
c. Diet
i. Consumption of fruit and vegetables is inversely related to risk of CHD
ii. Interheart study- lack of daily consumption of fruit and vegetables has PAR of
14%.
d. Alcohol use
i. Relative risk reduction in both men and women who are moderate drinkers
ii. Interheart study showed PAR of 7% for non drinkers
iii. Reduced risk from elevation of HDL and antioxidant, antithrombotic, and
antiinflammatory effects
e. Psychosocial factors
i. increased stress , increased risk but may be due to coping factors
(smoking,overeating, increased alcohol)
ii. strong association between depression and CAD
f. Estrogen deficiency
i. CHD increases in women after menopause
ii. Women’s Health Initiative and HERS trial showed no cardioprotective effect for
estrogen-progestin replacement and may have been harmful.
Possible Risk Factors
a. Physiological?
i. LVH
ii. ECG
iii. Homocyteine levels
iv. Endothelial progenitor cells
v. Asymmetrical dimethylarginine ADMA – Hyperuricemia
vi. Arterial intima-media thickness IMT
vii. Arterial stiffness
viii. Collagen vascular disease
ix. Aortic arch/abdominal aorta calcification
x. Coronary artery calcification
xi. Phosphate
b. Inflammation markers
i. Erythrocyte Sedimentation Rate (ESR)
ii. Leukocyte enzyme myeloperoxidase
iii. Plasma interleukin-6
iv. Lipoprotein-associated phospholipase A2 (platelet activating factor
acteylhydrolase)
v. Intercellular adhesion molecule 1 (sICAM1) and p-selectin
vi. Infection
c. Coagulation Factors
i. Plasma fibrinogen levels
ii. Fibrin d-dimer
iii. Thrombomodulin
iv. Hemophilia
d. Other
i. Air pollution
ii. Iron overload – may be increased risk; increased in HH
iii. Antioxidants – may reduce the risk.
iv. Socioeconomic factors – combination of factors
v. Mercury increased risk?
vi. Obstructive sleep Apnea increased risk for CAD, arrhythmias, hypertension
vii. Genetics – locus 9p21.3 genome wide study; Iceland study showed 5lipoxygenase activating protein(FLAP) 2x risk of MI and CVA
viii. Inhaled anticholinergic agents – increased risk
Prevention Summary
I.
II.
III.
IV.
V.
VI.
VII.
Stop smoking
Reduce alcohol use
Blood Pressure normal
Blood Sugar under control
Physical exercise
Normal BMI / waist circumference
Mediterranean diet – dark colored fruits and vegetables, whole grains, lean meats, avoid
excess sugars, avoid trans fats, hydrogenated fats, and saturated
Lecture 7: Nutrition SDL
Identify lifestyle risk factors for hypertension and heart disease.
I.
34
HTN Background
a. Etiology
i. Combination of genetics and lifestyle/environmental factors
ii. Vascular inflammation?
iii. Endocrine disorder
b. Pathophysiology
i. Heart failure
ii. Stroke
iii. End-stage renal disease
iv. Peripheral vascular disease
II.
35
v. Retinopathy
c. RISK FACTORS for HTN
i. DIETARY
1. Dietary factors
a. Excessive sodium consumption (> 2400 mg/day)
b. Excessive alcohol consumption
i. > 1 drink/day for women, 2 drinks/day for men
c. Low potassium consumption (< 2400 mg/day)
d. Low calcium consumption (< 1000 mg/day)
i. May be related to source: milk proteins may function to
inhibit angiotensin-converting enzyme (ACE)
e. “Maybes”
i. low magnesium consumption
1. Inhibitor of vascular smooth-muscle contraction
ii. “low” antioxidant/phytochemical consumption
1. ↓ inflammatory response
iii. high total fat, saturated fat
1. PUFA, omega-3 fatty acids may be protective
due to effects on inflammatory response
Atherosclerosis
a. Etiology
i. Combination of genetics and lifestyle/environmental factors
ii. Plaque accumulation in arteries
iii. LDL cholesterol, calcium, fibrin
iv. Ischemia in affected tissue
b. Risk factors for precipitating endothelial dysfunction
i. Inflammation (cytokines)
ii. Dyslipidemia (↑ LDL, ↓ HDL, ↑ TG)
iii. Cigarette smoking
iv. Diabetes
v. Obesity
vi. Hypertension
vii. Diet ↑ saturated fat, trans fatty acids, cholesterol
c. Pathophys
i. Ischemic stroke
ii. Transient ischemic attack
iii. Angina pectoris
iv. Myocardial infarction
v. Critical limb ischemia, gangrene, necrosis
vi. Dyslipidemia (serum lipids that ↑ risk)
1. ↑ LDL
a. Different cutoffs depending on risk category
i. 100 mg/dl, 130 mg/dl, 160 mg/dl
2. ↑ TG (↑ in VLDL, chylomicrons)
III.
36
3. ↓ HDL
4. Primary target for intervention = LDL
d. Focus on LDLs
i. Saturated fat, cholesterol, trans fatty acids
1. ↓ activity of LDL receptors in liver; less cleared from plasma
2. ↑ cholesterol synthesis in liver
ii. Obesity
1. ↑ VLDL → ↑ LDL
iii. Oxidation of LDL
1. ↑ macrophages
2. Stimulates autoantibodies
3. ↑ LDL uptake by endothelium
4. ↑ vascular tone/ coagulability
e. Focus on TG
i. Independent risk for atherosclerosis
ii. Levels inversely related to HDL
iii. Hypertriglyceridemia common in obesity
1. Especially metabolic syndrome and central obesity
iv. Tissue inflammation ↑ TG
v. Dietary factors (↑ TG)
1. Low-fat, high refined carbohydrates
2. Alcohol
f. Focus on HDL
i. Factors that ↓HDL:
1. Obesity
2. Inflammation
3. Inactivity
4. Cigarette smoking
5. Elevated TG
6. Factors that ↑ HDL
7. Exercise
8. Moderate alcohol consumption
9. Estrogen
10. Loss of body fat
Metabolic Syndrome
a. Have any 3 of these = Dx of Metabolic Syndrome
i. Abdominal obesity
1. Waist circumference
a. > 40 inches (102 cm) for men
b. > 35 inches (88 cm) for women
ii. Triglycerides
1. ≥ 150 mg/dl or drug therapy to lower TG
iii. HDL cholesterol
1. < 40 mg/dl men
IV.
2. < 50 mg/dl women
3. drug therapy for low HDL
iv. Blood pressure
1. ≥ 130 mm Hg systolic or ≥ 85 mm Hg diastolic
2. History of hypertension with drug therapy for hypertension
v. Fasting glucose
1. ≥ 100 mg/dl or drug therapy to lower blood glucose
Overall risks for obesity
a. ↑ LDLC, ↓ HDLC
b. ↑ TG
c. ↑ BG
d. ↑ BP
e. ↑ CHD, CHF, stroke
f. ↑ arrhythmias
Describe appropriate medical nutrition therapy to decrease blood pressure. Identify components of
the DASH diet for lowering blood pressure.
I.
II.
37
For HTN
a. Weight loss if overweight
b. Limit alcohol
c. Physical activity (30 minutes moderate/vigorous most days)
d. Sodium restriction (1 teaspoon salt = 2300 mg Na+) (< 1500 mg/day)
e. DASH Diet
i. Successful in prevention and treating hypertension
ii. Combines dietary recommendations :Sodium, potassium, calcium, magnesium,
fat/type of fat
iii. More effective than addressing individual components
iv. Possible synergistic effects
v.
For Atherosclerosis
a. Overall goals:
i. ↓ LDL, maintain or ↑ HDL, maintain or ↓ TG
ii. Therapeutic Lifestyle Change Dietary Pattern
1. Adult Treatment Panel III, National Cholesterol Education Program,
2002
iii. DASH diet principles also appropriate
1. Usually more restrictive than TLC
iv. Referral for nutrition counseling appropriate
1. Individualize according to current lifestyle habits
b. Med Nutrition Therapy
i. Energy
1. Maintain desirable weight (wt. loss if necessary)
ii. Physical activity
1. At least moderate daily activity (~ 200 kcals minimum)
iii. Carbohydrate
1. 50-60% of calories
2. Focus on fruits, vegetables, whole grains, legumes
iv. Fiber
1. 25-30 grams/day
2. 6-10 grams soluble
v. Total fat
1. 25-35% of calories
vi. Saturated fat
1. < 7% of calories
vii. Trans fat
1. < 1% of calories
viii. Polyunsaturated fat
1. ≤ 10% of calories
ix. Monounsaturated fat
1. ≤ 20% of calories
x. Protein
1. ~ 15% of calories
xi. Substitute soy protein ↓ dietary fat and provide other protective nutrients: 1-2
ounces/day Cholesterol
1. < 200 mg/day recommended
xii. Fish oil supplements
1. 1-3 grams/day
2. ↓ TG; possible anti-inflammatory, anti-coagulative effects
xiii. Plant stanols/sterols
1. 2-3 grams per day
2. ↓ intestinal cholesterol absorption
xiv.
38
Describe appropriate lifestyle modifications to reduce risk of cardiovascular disease. Steps in
Therapeutic LCs
I.
II.
39
2006 Goals for CVD risk reduction
a. Consume overall healthy diet
b. Aim for healthy body weight
c. Aim for recommended levels of LDL, HDL & TG
d. Aim for normal BP
e. Aim for normal BG levels fasting (<100)
f. Be physically active
g. Avoid tobacco (use and exposure)
Clinical Practice Recommendations
a. A1c <6% (AACE <6.5)
b. Fasting Glycemic control:
i. Glucose 90-130mg/dl
ii. 2 hour postprandial glucose <180mg/dl
c. Blood pressure:
i. <130/80mmHg
d. Lipids:
III.
IV.
V.
VI.
40
i. LDL <100mg/dl (<70 w/CAD)
ii. TG <150mg/dl
iii. HDL >40mg/dl
iv. BMI 18.5 - <25
AHA Pediatric dietary strategies for individuals >2years of age: Recommendations to All
Patients and Families
a. Balance dietary calories with physical activity to maintain normal growth
b. Engage in 60 min of moderate to vigorous play or physical activity daily
c. Eat vegetables and fruits daily and limit juice intake
d. Use vegetable oils and soft margarines low in saturated and trans fatty acids instead of
butter or most other animal fats in the diet.
e. Eat whole-grain breads and cereals rather than refined-grain products.
f. Reduce the intake of sugar-sweetened beverages and foods.
g. Use nonfat (skim) or low-fat milk and dairy products daily
h. Eat more fish, especially oil fish, broiled or baked.
i. Reduce salt intake, including salt from processed foods.
Portion Control
a. Know caloric needs
b. Know caloric contents
c. Track weight, activity and intake
d. Prepare and eat smaller amounts
e. Eat on smaller plates
f. Read labels for portion size and portions per container
g. Use measuring tools for accuracy
h.
Increase Vegetables
a. Low calorie
b. Moderate-high fiber
c. Moderate-high water content
d. Reduce energy density of overall diet
e. Nutrient dense
i. phytonutrients
ii. vitamins, minerals
Proven Benefits of Diets Rich in Vegetables and Fruits from studies/clinical trials
VII.
i. ↓BP
ii. ↓stroke
iii. ↓CRP
iv. Improve lipids
v. ↓obesity risk
Limit intake of sat fat, trans fatty acids, cholesterol
a. <7% Saturated Fat (meats, dairy, tropical oils)
b. <1% Trans Fat (partially hydrogenated fats)
c. <200 mg Cholesterol (eggs, meats, dairy)
d. 25 – 35% Total Fat (% represents % of total caloric intake)
Describe appropriate medical nutrition therapy to achieve desirable blood lipid levels.
I.
II.
III.
IV.
V.
41
Dietary Fat
a. Why 25-35% of calories from fat?
i. Low fat diet ↑ TG
ii. Low fat diet ↓ HDL along with LDL
b. Recommendations balance effects of dietary fat
i. Higher fat, focus on MUFA
ii. Keeps TG low, HDL high
Fats to choose
a. Olive oil, safflower oil,
b. Canola oil, peanut oil
c. Nuts, natural nut butters
d. Avocado
e. Oily fish
f. Flax seed meal
i. *Replacing 80 calories of carb w/80 cal from mono or poly fats↓ heart
disease risk by 30-40%
Fats to Avoid
a. Trans fats: shortening, solid/regular margarine, partially hydrogenated fat, commercially
fried foods
Very low-fat diets have shown potential for plaque regression
a. Almost no animal products
b. Focus on low-fat grains, legumes, fruits, vegetables, nonfat dairy foods
c. Total fat < 10%
d. Saturated fat < 3%
e. Cholesterol < 5mg/day
Choose Whole Grains and Fiber-Rich Foods
a. Slows absorption of carbohydrate
b. ↑Insulin sensitivity
c. Promotes satiety
d. Slows gastric emptying
e. ↓LDLC (soluble/viscous)
f. ↓TG
VI.
VII.
VIII.
IX.
X.
42
g. ↓CRP
h. ↓BP
Fiber Reccomendations
a. 20-30 gm total dietary fiber/day (ATP III); 14 gm/1000 kcal (Inst. of Med.)
i. Average intake for most Americans is 10-15 gm
b. Minimum 5-10 gm soluble fiber/day (ATP III)
c. Increase bran-rich whole grains (insoluble fiber)
d. Include oatmeal, dried beans, pectin-rich fruits, soluble fiber-rich supplements
(Benefiber, FiberSure)
Decrease Added Sugar (from beverages and foods)
a. To lower caloric intake
b. To promote nutritional adequacy
c. Average intake = 20-25 tsp. sugar/day
d. Sweet beverages = excess calories & weight gain (avoid juice, sports drinks, etc…)
e. “No sugar added” does not mean no carbs or no calories!
Eat more fish (~1gm EPA and DHA/day)
a. ↓ risk of arrhythmias & fatal MI’s
b. ↓ TG (2-4 gm EPA & DHA/day)
c. ↓ platelet aggregation & blood clotting
d. ↓ BP
e. ↓inflammation
f. Omega 3’s
i. 3 oz salmon = 1.8 gm (from EPA & DHA)
ii. All fish and shellfish contains some EPA & DHA (fatty fish richest)
iii. Flax, walnuts, soy and canola supply alpha-linolenic acid (converts to EPA/DHA
but benefits for CVD not established)*
Eat less sodium
a. Prevents HTN in non-hypertensive persons
b. Dose related response
c. Rec. upper limit 1500mg/day
d. Achievable limit is ~2300 mg/day (AHA)
e. Average intake for Americans
i. 4000 – 6000 mg/day
1. 77% from processed foods
2. 12% occurs naturally
3. 6% added at the table
4. 5% added while cooking
Easy Recommendations That “Sum It Up” (Mediterranean-Style)
a. Control amounts
b. Eat whole grains/higher fiber
c. More vegetables/fresh fruits
d. Nonfat milk & dairy foods only
e. Moderate lean meats & poultry
f. Fish very often
g.
h.
i.
j.
k.
Legumes, nuts & seeds regularly (daily)
Limit sweets; avoid sweet beverages
Avoid saturated & trans fats
Alcohol only in moderation
Regular physical activity
Lecture 8: Preventive Med SDL (has a required reading, apparently)
I.
II.
43
ASA Use in MEN recommendations
a. use of aspirin for men ages 45 to 79 years when the potential benefit of a reduction in
myocardial infarction outweighs the potential harm of an increase in gastrointestinal
hemorrhage.
Grade: A recommendation.
b. current evidence is insufficient to assess the balance of benefits and harms of the use of
aspirin for cardiovascular disease prevention in men and women age 80+
Grade: I statement.
ASA and CV Risk (see link http://www.medscape.com/viewarticle/780923 )
a. GI Risk Estimations reading
III.
GI Risk Estimations
IV.
For GI risk estimations we used data reported by Hernandez-Diaz and
Garcia-Rodriguez[24] as a baseline for the construction of tables and
algorithms. This study characterised LDA users in terms of major GI risk
factors and provided incidence rates as well as excess risk of upper GI
complications linked to LDA based on the General Practice Research
Database (UK) and systematic reviews of the literature. Based on their
results, we assumed an incidence rate for overall baseline upper GI
bleeding of 1 per 1000 person-years. We then constructed absolute
incidence rates within each risk subgroup based on pooled estimates
reported from meta-analysis of others and our own studies. The risk of
upper GI bleeding associated with LDA has been reported among a range
of RRs between 1.5 and 3.0 in many studies. Here, we have followed the
assumption provided by Hernandez-Diaz and Garcia-Rodriguez[24] that the
pooled relative risk of upper GI bleeding was 2.0 for LDA, considered as
doses ≤325 mg/day. Major risk factors for the development of upper GI
bleeding are: age, male gender, history of peptic ulcer and concomitant
use of NSAIDs, anticoagulants, or clopidogrel.[2] Table 1summarises the
relative risk and 95% CI estimates and the main bibliographic sources
supporting the reported estimates.
V.
VI.
Age was considered a risk factor with variables estimated depending on
the age range. The incidence increases exponentially after the age of 50
up to a relative risk of 9.2 for patients aged 80 or older. The risk and
incidence rates among men and women are different, with men having a
twofold increase compared with women in all age groups. Together with
older age, ulcer history is the primary risk factor, with a higher risk among
patients with a history of bleeding ulcer. History of dyspepsia was also
considered a risk factor within this group because several studies found
this variable to be associated with an increased risk of upper GI
bleeding;[2] it is probably a subclinical marker of peptic ulcer in investigated
individuals, especially in areas with substantial H. pylori infection rates.
NSAID use is another important risk factor among patients who use
aspirin; NSAIDs cause a fourfold increase in the risk of upper GI bleeding.
In patients with a history of peptic ulcer disease, the absolute risk is higher
but the relative risk lower, as described widely elsewhere.[24]
There is wide consensus that antiplatelet and/or anticoagulant agents
increase the risk of upper GI bleeding. We have assumed, as did others, [6,
24, 25] that LDA doubles the risk of upper GI bleeding in each of the risk
groups described above. Hernandez and Garcia Rodriguez[24] validated
most of these assumptions in control groups of NSAID outcome trials.
Other drugs that are widely used in CV treatments are clopidogrel and
warfarin. Based on recent data, clopidogrel use has been reported to have
a risk profile similar to aspirin for upper GI bleeding, whereas warfarin in
general produces a higher risk.[10] Combinations of these compounds
further increase the risk, which may be additive (e.g. clopidogrel plus
aspirin) or greater (aspirin plus warfarin).
a. Table 1
44
VII.
VIII.
IX.
45
A Calculator exists to evaluate GI vs CV risk with ASA
AAA Recommendations (longstanding)
a. one-time screening for abdominal aortic aneurysm (AAA) by ultrasonography in men
ages 65 to 75 years who have ever smoked.
Grade: B Recommendation
b. no recommendation for or against screening for AAA in men ages 65 to 75 years who
have never smoked.
Grade: C Recommendation
c. recommends against routine screening for AAA in women.
Grade: D Recommendation.
DRAFT of NEW 2014 RECS for AAA
a. The U.S. Preventive Services Task Force (USPSTF) recommends one-time screening for
abdominal aortic aneurysm (AAA) by ultrasonography in men ages 65 to 75 years who
have ever smoked.
b. This is a B recommendation.
c. The USPSTF recommends that clinicians selectively offer screening for AAA in men ages
65 to 75 years who have never smoked rather than routinely screening all men in this
group. Existing evidence indicates that the net benefit of screening all men ages 65 to 75
years who have never smoked is small. In determining whether this service is
appropriate in individual cases, patients and clinicians should consider the balance of
benefits and harms on the basis of evidence relevant to the patient's medical history,
family history, other risk factors, and personal values. This is a C recommendation.
X.
XI.
XII.
46
d. The USPSTF concludes that the current evidence is insufficient to assess the balance of
benefits and harms of screening for AAA in women ages 65 to 75 years who have ever
smoked. This is an I statement.
e. The USPSTF recommends against routine screening for AAA in women who have never
smoked.
f. This is a D recommendation.
i. These recommendations apply to asymptomatic adults age 50 years and older.
g. Screening in Men Ages 65 to 75 Years Who Have Never Smoked
h. Despite the demonstrated benefits of screening for AAA in men overall, the much lower
prevalence of disease in male never-smokers than in male ever-smokers suggests that
clinicians should consider the patient's risk factors as well as the potential for causing
harm when making the decision whether to screen, instead of routinely offering
screening to all men who have never smoked.
i. Important risk factors that increase risk for developing an AAA include : older age and
a first-degree relative with AAA; other risk factors include a history of other vascular
aneurysms, coronary artery disease, cerebrovascular disease, atherosclerosis,
hypercholesterolemia, obesity, and hypertension. African American race, Hispanic
ethnicity, and diabetes are associated with reduced risk for developing an AAA
AAA required reading – read Intro and Discussion sections only
a. Consider why screening is not recommended for women, for those with family history
or other high risk groups – do you agree?
b. Why just men – hint single risk factor validation
Vitamin, Mineral, Multivitamin supplements for Primary Prevention of CV Disease and
Cancer Recs
a. The USPSTF concludes that the current evidence is insufficient to assess the balance of
benefits and harms of the use of multivitamins for the prevention of cardiovascular
disease or cancer.
Grade: I statement.
b. The USPSTF concludes that the current evidence is insufficient to assess the balance of
benefits and harms of the use of single- or paired-nutrient supplements (except βcarotene and vitamin E) for the prevention of cardiovascular disease or cancer.
Grade: I statement.
c. The USPSTF recommends against the use of β-carotene or vitamin E supplements for
the prevention of cardiovascular disease or cancer.
Grade: D recommendation.
d. Required reading: Discussion: effectiveness of preventive medication
CAD Screening w/ EKG
a. recommends against screening with resting or exercise electrocardiography (ECG) for
the prediction of coronary heart disease (CHD) events in asymptomatic adults at low
risk for CHD events.
Grade: D Recommendation.
b. current evidence is insufficient to assess the balance of benefits and harms of
screening with resting or exercise ECG for the prediction of CHD events in
III.
asymptomatic adults at intermediate or high risk for CHD events.
Grade: I Statement
c. Factors assoc w/ higher risk for CHD
i. older age, male sex, high blood pressure, smoking, abnormal lipid levels,
diabetes, obesity, and sedentary lifestyle
ii. there are online calculators
iii. Risk and people
1. Persons with a 10-year risk >20% are considered to be high-risk,
2. those with a 10-year risk <10% are considered to be low-risk,
3. those in the 10%–20% range are considered to be intermediate-risk.
d. Required reading: Rationale section
INFO FROM CASES in REQUIRED READING on ASA and CHD
Diabetic
DIABETIC: Low-dose aspirin use for prevention might be considered for those with diabetes at
intermediate CVD risk (patients with 10-year CVD risk of 5–10%) until further research is
available. (ACCF/AHA Class IIb, Level of Evidence: C) (ADA Level of Evidence: E).
The estimated number of GI events INDUCED by ASA is LOWER than the number of estimated
CV events prevented.
For this type of patient, the 10 year Cardiovascular Risk is
The estimated basal incidence of upper GI complication events in 10 years in a cohort of 1000 patients is
7.4 %
10
Continue...
Estimations and Recommendations
For this type of patient, the 10 year Cardiovascular Risk is
The estimated basal incidence of upper GI complication events in 10 years in a cohort of 1000 patients is
7.4 %
10
This person can be considered as a:
DIABETIC: Low-dose aspirin use for prevention might be considered for those with diabetes at intermediate CVD risk
(patients with 10-year CVD risk of 5–10%) until further research is available. (ACCF/AHA Class IIb, Level of Evidence: C)
(ADA Level of Evidence: E).
Estimations and Treatments
ASA
If ASA treatment is added:
The estimated number of CV events PREVENTED in 10 years in a cohort of 1000 patients will be
11
The estimated number of upper GI complication events INDUCED by ASA in 10 years in a cohort of 1000 patients will be
10
The estimated number of upper GI complication events (Basal + ASA induced) in 10 years in a cohort of 1000 patients will be
20
Proton Pump Inhibitor (PPI)
47
The estimated number of GI events INDUCED by ASA is LOWER than the number of estimated CV events prevented.
If PPI treatment is added, the estimated minimum number of upper GI complication events PREVENTED in 10 years in a cohort of 1000 patients will be
SMOKER
Low Risk CV case: ASA treatment is NOT RECOMMENDED.
The estimated number of GI events INDUCED by ASA is LOWER than the number of
estimated CV events prevented.
For this type of patient, the 10 year Cardiovascular Risk is
8.2 %
The estimated basal incidence of upper GI complication events in 10 years in a cohort of 1000 patients is
10
This person can be considered as a:
Low Risk CV case: ASA treatment is NOT RECOMMENDED.
Estimations and Treatments
ASA
If ASA treatment is added:
The estimated number of CV events PREVENTED in 10 years in a cohort of 1000 patients will be
12
The estimated number of upper GI complication events INDUCED by ASA in 10 years in a cohort of 1000 patients will be
10
The estimated number of upper GI complication events (Basal + ASA induced) in 10 years in a cohort of 1000 patients will
be
20
Proton Pump Inhibitor (PPI)
The estimated number of GI events INDUCED by ASA is LOWER than the number of estimated
CV events prevented.
If PPI treatment is added, the estimated minimum number of upper GI complication events PREVENTED in 10 years in
a cohort of 1000 patients will be
SMOKER AND DIABETIC
Estimations and Recommendations
For this type of patient, the 10 year Cardiovascular Risk is
The estimated basal incidence of upper GI complication events in 10 years in a cohort of 1000 patients is
12.2 %
10
This person can be considered as a:
DIABETIC: Low-dose aspirin use for prevention is reasonable for adults with diabetes and no
previous history of vascular disease who are at increased CVD risk (10 year risk of CVD
events over 10%). (ACCF/AHA Class IIa, Level of Evidence: B) (ADA Level of Evidence: C).
48
Estimations and Treatments
ASA
If ASA treatment is added:
The estimated number of CV events PREVENTED in 10 years in a cohort of 1000 patients will be
18
The estimated number of upper GI complication events INDUCED by ASA in 10 years in a cohort of 1000 patients will be
10
The estimated number of upper GI complication events (Basal + ASA induced) in 10 years in a cohort of 1000 patients will
be
20
Proton Pump Inhibitor (PPI)
The estimated number of GI events INDUCED by ASA is LOWER than the number of estimated
CV events prevented.
If PPI treatment is added, the estimated minimum number of upper GI complication events PREVENTED in 10 years in
a cohort of 1000 patients will be
Intermediate Risk CV case: ASA treatment is NOT RECOMMENDED.
The estimated number of GI events INDUCED by ASA is equal or greater than the number of
estimated CV events prevented: PPI treatment is RECOMMENDED
Estimations and Recommendations
For this type of patient, the 10 year Cardiovascular Risk is
The estimated basal incidence of upper GI complication events in 10 years in a cohort of 1000 patients is
12.4 %
24
This person can be considered as a:
Intermediate Risk CV case: ASA treatment is NOT RECOMMENDED.
Estimations and Treatments
ASA
If ASA treatment is added:
The estimated number of CV events PREVENTED in 10 years in a cohort of 1000 patients will be
19
The estimated number of upper GI complication events INDUCED by ASA in 10 years in a cohort of 1000 patients will be
24
The estimated number of upper GI complication events (Basal + ASA induced) in 10 years in a cohort of 1000 patients will
be
48
Proton Pump Inhibitor (PPI)
The estimated number of GI events INDUCED by ASA is equal or greater than the number of
estimated CV events prevented: PPI treatment is RECOMMENDED
If PPI treatment is added, the estimated minimum number of upper GI complication events PREVENTED in 10 years in
a cohort of 1000 patients will be
49
DIABETIC
DIABETIC: Low-dose aspirin use for prevention is reasonable for adults with diabetes and
no previous history of vascular disease who are at increased CVD risk (10 year risk of CVD
events over 10%). (ACCF/AHA Class IIa, Level of Evidence: B) (ADA Level of Evidence: C).
The estimated number of GI events INDUCED by ASA is LOWER than the number of
estimated CV events prevented.
Continue...
Estimations and Recommendations
For this type of patient, the 10 year Cardiovascular Risk is
The estimated basal incidence of upper GI complication events in 10 years in a cohort of 1000 patients is
18.3 %
24
This person can be considered as a:
DIABETIC: Low-dose aspirin use for prevention is reasonable for adults with diabetes and no previous history of vascular
disease who are at increased CVD risk (10 year risk of CVD events over 10%). (ACCF/AHA Class IIa, Level of Evidence: B)
(ADA Level of Evidence: C).
Estimations and Treatments
ASA
If ASA treatment is added:
The estimated number of CV events PREVENTED in 10 years in a cohort of 1000 patients will be
27
The estimated number of upper GI complication events INDUCED by ASA in 10 years in a cohort of 1000 patients will be
24
The estimated number of upper GI complication events (Basal + ASA induced) in 10 years in a cohort of 1000 patients will be
48
Proton Pump Inhibitor (PPI)
The estimated number of GI events INDUCED by ASA is LOWER than the number of estimated CV events prevented.
If PPI treatment is added, the estimated minimum number of upper GI complication events PREVENTED in 10 years in a cohort of 1000 patients will be
SMOKER
Intermediate Risk CV case: ASA treatment is NOT RECOMMENDED.
50
29
The estimated number of GI events INDUCED by ASA is LOWER than the number of
estimated CV events prevented.
Continue...
Estimations and Recommendations
For this type of patient, the 10 year Cardiovascular Risk is
20 %
The estimated basal incidence of upper GI complication events in 10 years in a cohort of 1000 patients is
24
This person can be considered as a:
Intermediate Risk CV case: ASA treatment is NOT RECOMMENDED.
Estimations and Treatments
ASA
If ASA treatment is added:
The estimated number of CV events PREVENTED in 10 years in a cohort of 1000 patients will be
30
The estimated number of upper GI complication events INDUCED by ASA in 10 years in a cohort of 1000 patients will be
24
The estimated number of upper GI complication events (Basal + ASA induced) in 10 years in a cohort of 1000 patients will be
48
Proton Pump Inhibitor (PPI)
The estimated number of GI events INDUCED by ASA is LOWER than the number of estimated CV events prevented.
If PPI treatment is added, the estimated minimum number of upper GI complication events PREVENTED in 10 years in a cohort of 1000 patients will be
SMOKER and DIABETIC
Estimations and Recommendations
For this type of patient, the 10 year Cardiovascular Risk is
The estimated basal incidence of upper GI complication events in 10 years in a cohort of 1000 patients is
28.9 %
24
This person can be considered as a:
DIABETIC: Low-dose aspirin use for prevention is reasonable for adults with diabetes and no
previous history of vascular disease who are at increased CVD risk (10 year risk of CVD
events over 10%). (ACCF/AHA Class IIa, Level of Evidence: B) (ADA Level of Evidence: C).
Estimations and Treatments
ASA
If ASA treatment is added:
51
The estimated number of CV events PREVENTED in 10 years in a cohort of 1000 patients will be
58
The estimated number of upper GI complication events INDUCED by ASA in 10 years in a cohort of 1000 patients will be
24
The estimated number of upper GI complication events (Basal + ASA induced) in 10 years in a cohort of 1000 patients will
be
48
Proton Pump Inhibitor (PPI)
The estimated number of GI events INDUCED by ASA is LOWER than the number of estimated
CV events prevented.
If PPI treatment is added, the estimated minimum number of upper GI complication events PREVENTED in 10 years in
a cohort of 1000 patients will be
Lecture 9: Rib OMM
Review and describe the structural and functional anatomy of the rib cage. Recognize the anatomic
differences between true vs. false ribs as well as typical vs. atypical ribs.
I.
II.
III.
IV.
52
Fxn of ribs and sternum
a. Respiration
b. Protection of vital organs
c. Pump for venous and lymphatic return
d. Support structure for the upper extremities
Sternum Embryology
a. The sternum develops independently in somatic mesoderm in the ventral body wall
b. Two sternal bands are formed on either side of the midline and later fuse to form
cartilaginous models of the manubrium, sternebrae, and xiphoid process (xyphoid fusion
at age 40 ish)
c. The middle embryonic germ layer, lying between the ectoderm and the endoderm, from
which connective tissue, muscle, bone, and the urogenital and circulatory systems
develop.
Ribs are derived from sclerotermal region
a. sclerotome is part of a somite, a structure in vertebrate embryonic development.
Sclerotomes eventually differentiate into the vertebrae and most of the skull.
Sternum Anatomy
a. Manubrium
b. Sternal Notch
c. Anterior to T2
d. Angle of Louis
e. Articulation of second rib
f. Synchondrosis
g. Anterior to T4
h. Gladiolus (Body)
29
V.
VI.
VII.
i. Xiphoid Process
j. Joint is anterior to T9
Rib nomenclature
a. True ribs: 1-7
i. Attach directly to the sternum via costochondral cartilage
b. False ribs: 8-10
i. Attach via a synchondroses to the costochondral cartilage of rib 7
c. Floating: 11-12
i. Do not attach to the sternum at all
ii. Typical ribs (3-9) will have all of the following anatomical landmarks
1. Tubercle- articulates with corresponding transverse process
2. Head- articulates with corresponding and immediately superior
vertebrae via demifacets
3. Neck- between tubercle and head
4. Angle- beginning of anterior curve, 5-6 cm lateral to head
5. Shaft- AKA the body, contains costal grove inferiorly
d. Atypical Ribs
i. Rib 1 - articulates only with T1, has no angle and no costal groove
ii. Rib 2 – atypical because of large tuberosity on shaft for serratus anterior and
lack of costal groove
iii. Rib 10 – atypical because articulates with corresponding vertebrae only
iv. Ribs 11,12 – articulates only with corresponding vertebrae and lack of tubercles
(articulation laterally with the vertebrae)
Rib Articulations
a. Rib 1
i. Synchondrosis (non-synovial)
b. Ribs 2-7
i. Synovial articulations
c. Posterior Rib articulations
i. Three articulations
1. Costotransverse joint
2. Superior costovertebral joint (inferior costal facet)
3. Inferior costovertebral joint (superior costal facet)
The Rule of 3’s - approximates the positions of the thoracic spinous processes in regard to
the transverse processes
a. T1-3  equal
b. T4-6  ½ level up
c. T7-9  1 level up
i. Reverses each level
from T10-12
Identify the motion characteristics predominant in each rib group atypical and typical ribs (i.e.
describe pump handle, bucket handle, and caliper motions). Explain the role of the diaphragm in
breathing mechanics and its relationship to the spine.
53
I.
II.
III.
54
Muscles of Inspiration (reathing takes up to 50% of your caloric expendature every day.
Good function of these muscles, rib and vertebral mechanics is vital to the efficiency of your
respiration)
a. Principal
i. Intercostalis int and ext
ii. Diaphragm
1. Central tendon makes up most of the horizontal aspect of the muscle
2. Actual muscular portion of diaphragm is oriented vertically
3. Efficient contraction relies on using the abdominal viscera as a fulcrum
and the verticality of the muscle in relation to the chest wall as a lever
Major accessory muscles activated w/ inhalation
a. Sternocleidomastoid muscles- Attaches to clavicle & sternum from the base of the
occiput/mastoid
b. Anterior and posterior serratus
i. Serratus ANT
1. Origin: outer aspects of upper 8 to 10 ribs
2. Inserts: anterior surface of vertebral (medial border of scapula
3. Action draws scapula forward & laterally; rotates scapula in raising arm
ii. Serratus POST
c. Scalenes - Attaches from the cervical spine to the first two ribs
i. calenus anterior
ii. Origin: transverse process of 3rd to 6th cervical vertebrae
iii. Inserts scalene tubercle of 1st rib
iv. Raises ist rib bends neck forward and rotates to opposite side
v. Scalenus Medius
vi. Origin: TP of ist 6 cevical vertebra;
vii. Inserts upper surface of 1st rib
viii. Raises 1st rib bends neck to same side
ix. Scalenus Posterior
x. Oriigin: transverse process of 4th to 6th rib
xi. Inserts: outer aspect of 2nd rib
xii. Raises 1st & 2nd rib bends neck to same side.
xiii. Scalenus Minimus
xiv. Origine tp 7th cerv vertebrae
xv. Inserts 1st rib & Pleura
xvi. Tenses dome of the pleura
d. External intercostals
e. Levatores Costarum
Muscles that aid in
a. Active breathing
i. Intercostalis int.
1. External lower border of one rib to upper border of rib below
a. Draws ribs together
2. Internal lower border of rib; costal cartilage inserts
IV.
V.
VI.
VII.
55
a. Upper border of rib and costal cartilage below
b. Draws ribs together
3. Intimi
a. Internal surface of superior border of rib
b. Inserts internal surface of inferior border of rib above
c. Draws ribs together.
ii. Rectus abdominis
1. Origin: crest & symphysis of pubis
2. Inserts:xiphoid process; 5th to 7th costal cartilages
3. Action: tenses abdominal wall, flexes vertebral column; draws thorax
downward
iii. Obliques, int. & ext.
iv. Transversus abdominis
b. Quiet Breathing
i. Results from passive recoil of the lungs
c. Latissimus dorsi
i. Origin: Sp of Vertebrae T7 to S3, thoracolumbar fascia, iliac crest, lower four ribs
inferior angle of scapula
ii. Inserts: floor of intertubercular of humerus in bicipital groove
iii. Adducts, extends, rotates arms medially.
RIBS and MUSCLES: MECHANICAL PUMP FLUID MODEL
a. Pressure gradient between the thoracic and abdominal cavities allow lymphatic and
venous fluids to flow from the body to the upper thoracic area.
b. Contraction of muscles and pulsation of arteries also helps to propel lymphatic fluids
c. The diaphragm has been shown to play an important role in lymphatic absorption from
the peritoneal cavity
d. Diaphragmatic contraction increases relative negative pressure of thoracic cage and
increases relative positive pressure in abdomen.
Costal Lymphatics
a. Parasternal (internal thoracic) lymph nodes
b. Intercostal lymph nodes
c. Diaphragmatic lymph nodes
Costal Nerves
a. Intercostal nerves
i. Lie on inferior portion of rib in the costal groove
ii. Derived from the sympathetic chain ganglia via white and grey rami
communicantes
iii. Provide innervation to thoracic and abdominal walls (1 and 2 send fibers to
upper extremities, subcostal sends fibers to gluteals)
b. Sympathetic chain ganglia lay just anterior to the rib heads bilaterally
Ribs Motions
a. Pump-Handle motion
i. Primarily ribs 1-5
ii. Ribs move anterior and superior with inhalation
iii.
iv.
v.
vi.
vii.
VIII.
Motion predominantly in sagittal plane
Best palpated at mid-clavicular line
Axis of motion is costovertebral-costotransverse line
Motion felt best furthest from the axis, anterior in this case
Motion = As Inspiration occurs:
1. Anterior aspect moves cephalad (superiorly)
2. Posterior rib head moves caudad (inferiorly)
3. Expiration: Opposite of inspiration!
b. Bucket-Handle motion
i. Primarily ribs 6-10
ii. Ribs move laterally and increase transverse diameter with inhalation
iii. Motion predominantly in coronal plane
iv. Best palpated at mid-axillary line
v. Axis of motion is a costovertebral-costosternal line
vi. Motion
1. rib shaft is the handle of the bucket
2. Rib shaft lifts during inhalation, falls with exhalation
3. Increases the transverse diameter of rib cage
4. (best palpated FURTHEST FROM THE AXIS – Lateral rib cage)
c. Caliper motion
i. Primarily ribs 11,12
ii. Ribs externally rotate with inhalation
iii. Motion predominantly in transverse plane
iv. Best palpated 3-5 cm lateral to transverse processes
v. Axis of motion is vertical line
vi. tend to separate as 11 is pulled superior by latisimus dorsi and 12 is pulled
inferiorly by quadratus lumborum
Rib Groups and Motion
a. “Typical” Ribs:
i. Ribs 3-9 display both transverse axis (pump handle) and AP axis (bucket handle)
motion
ii. Upper 1/3 ribs- predominant pump handle type mechanics around a transverse
axis
iii. Middle 1/3 ribs- mix of pump and bucket handle mechanics
iv. Lower 1/3 ribs- predominant bucket handle mechanics around an AP axis
b. “Atypical” Ribs
i. Ribs 1,2, 10-12
Recognize and explain the types of rib somatic dysfunction and how to screen and diagnose.
I.
56
Rib Somatic Dysfxn defined
a. Impaired or altered function of related components of the somatic system (body
framework): skeletal, arthrodial, and myofascial structures, and related vascular,
lymphatic, and neural elements.
II.
III.
b. Identified through palpation to determine the presence of tissue texture changes,
asymmetry, restricted motion (barrier) and tenderness
Specific Dysfxns
a. Specific Structural Dysfunctions
i. Superior subluxations (first rib)
ii. A/P subluxations
b. Respiratory Dysfunctions
i. Inhalation SD Pump handle (exhalation restriction)
ii. Inhalation SD Bucket handle (exhalation restriction)
iii. Inhalation SD Caliper (exhalation restriction)
iv. Exhalation SD Pump handle (inhalation restriction)
v. Exhalation SD Bucket handle (inhalation restriction)
vi. Exhalation SD Caliper (inhalation restriction)
Goals in Rib Tx
a. Improve Rib Motion
i. Improved rib motion modulates sympathetic function
ii. Improved rib motion allows for improved respiration and improves
diaphragmatic function
iii. Improved rib motion increases intrathoracic pressure during respiration, which
increases lymphatic and venous return to the heart
b. Decrease Pain
c. Improve spinal mechanics
Identify the “key rib” to be treated in inhalation and exhalation somatic dysfunction.
a. When treating an inhalation somatic dysfunction (“stuck up in inhalation”)
i. Treat the lowest rib of the group of ribs that is restricted
b. When treating an exhalation somatic dysfunction (“stuck down in exhalation”)
i. Treat the highest rib of the group of ribs that is restricted
c. His mnemonic: “people who are stuck UP (inhalation) need to be brought down. People
who are depressed (exhale), need to be pulled up by the bootstraps.”
Review treatment techniques for ribs: indirect and direct (ME).
I.
II.
57
General Tx Principles for Ribs
a. First unclog the sink!!!(address the Thoracic inlet/CT junction)
b. Treat thoracic spine (especially Non-neutral Type 2 SD)
c. Warm up the soft tissues
d. Inhalation somatic dysfunction (stuck up need to be brought to knees/down a
notch/humbled) – tx the lowest rib
e. Exhalation somatic dysfunction (stuck down pull up by your bootstraps) tx the highest
rib with dysfunction
f. Recheck and if not improved with tx focus to identify the key rib or tx the other side
(Inhalation on R may be Exhalation on L)
Inhal/Exhalation
III.
IV.
58
a. When treating an inhalation somatic dysfunction (“stuck up in inhalation”)
i. Treat the lowest rib of the group of ribs that is restricted
b. When treating an exhalation somatic dysfunction (“stuck down in exhalation”)
i. Treat the highest rib of the group of ribs that is restricted
Differential Dx of Thoracic Pain
a. Non-traumatic
i. Infection (pnuemonia/bronchitis, effusion/empyema, TB, herpes zoster)
ii. Pleurisy or Costochondritis (inflammation)
iii. Pneumothorax spontaneous
iv. Tumor (Pulm CA, LN CA, distant metastasis, sarcoidosis)
v. Asthma/COPD (bronchospasm with inflammation)
vi. Pulmonary embolus
vii. Cardiac (ie MI, pericarditis, CHF, aneurysm)
viii. Esophageal (ie GERD, Esophagitis, etc)
ix. Viscerosomatic (Gallbladder, Pancreas, etc)
b. Traumatic
i. Fracture
ii. Pneumothorax (esp tension)
iii. Costochondritis
iv. Somatic Dysfunction
v. Pulmonary contusion
vi. Effusion (cardiac tamponade, hemothorax)
The MOPSE Trial – basically there aren’t enough of these trials, and even when they are
conducted, there aren’t enough participants. The end.
a. Pneumonia treatment osteopathically by all levels of residents/students/OMM
attendings in hospitalized patients who received standard antibiotics. Length of stay,
time of IV antibiotics reduced by tx osteopathically
b. Treatment protocol
c. Thoracic inlet, OA decompression, Soft tissue to cervical spine (phrenic nerve), rib
raising, diaphragm redoming, pectoral traction/thoracic pump, specific rib or thoracic SD
if identified