nsha 2015 convention, j. coyle, phd, 03/20/2015...

NSHA 2015 Convention, J. Coyle, PhD, Aerodigestive Primer

03/20/2015

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Dysphagia and the respiratory system: Aerodigestive tract primer

James L. Coyle, Ph.D., CCC‐SLP, BCS‐SDepartment of Communication Science and DisordersUniversity of Pittsburgh [[email protected]]

Nevada Speech Language Hearing Association Convention 2015, Las Vegas

Disclosures

• University of Pittsburgh (salary)

• NSHA honorarium

• Continuing education

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Pneumonia, inadequate nutrition,

dehydration

Dysphagia‐aspiration

Pulmonary disease

Digestive diseases

Iatrogenicdisorders

Neurological diseases

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Aging,Frailty


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What are the lungs and how do they work?

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5Public domain

Respiratory System Functions

• Ventilation (air movement)

– Transfer of air into and out of lungs

• Via a pump

• Respiration (gas movement across membranes)

– Trading of atmospheric gas with blood gases

– Trading of blood gases with organ‐produced gases

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Biomechanics of breathing: we need

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+ + =

A PumpLungs attached to pump

An “Easy to inflate” Mechanism

Ventilation

• Ventilation – deconstructed …

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Diaphragm activated

Diaphragm contracts,

stretches lung open, pushes on viscera

Alveolar pulled open, lung volume increases

Atmospheric air rushes into lungs

Diaphragm relaxes

Elasticity of viscera, alveoli

are now unopposed

Compressed viscera, stretched

alveoli, recoil

Alveolar volume

decreases, pressure increases

Intra‐alveolar pressure decreases

(Boyle’s Law)

Alveolar air is “pushed”

out to atmosphere

Ventilation


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Making Ventilation “easy”

• 1. The pump must work

– Innervation, muscles intact

–MESSAGE: DISEASES THAT DISRUPT NEUROMOTOR FUNCTION OR MUSCLE HEALTH PRODUCE VENTILATORY FAILURE

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Diaphragm plus helpers when needed. What nerve innervates diaphragm? From where?

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carina

• 2. Lungs’ connection to chest wall– Partly inflated at all times‐increases compliance

–MESSAGE: DISEASES THAT DISRUPT THIS CONNECTION VENTILATORY FAILURE

Lungs’ connection to the pump

• Lungs, like balloons, tend to deflate

• Partly inflated balloons are easier to inflate

• Lungs are held partly open by connection to chest wall

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16© Conexions

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Rib cage,Diaphragm

Parietalpleura

Visceralpleura

Lung-outersurface

PleuralCavity

P= -5

(P1 V1)

Pleural “spring” is a sealed cavity, with below atmospheric pressure inside.

Biomechanics of Ventilation

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PleuralCavity

P= -15

Rib cage,Diaphragm

Parietalpleura

Visceralpleura

Lung-outersurface

(P1 V1)

B. Pleural cavity volume increases, pressure decreases (rising vacuum force).



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PleuralCavity

Visceralpleura

Lung-outersurface

Rib cage,Diaphragm

Parietalpleura

C. Attached structures (visceral pleura, alveoli) displaced toward source(s).

Volume increases (V2); Pressure becomes subatmospheric (P2), air

rushes into equalize pressures

P= -5


• Healthy pleural connection:

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Parietal pleuraVisceralpleura

rib

• Disruption of pleural membrane:

– Chest expands

– Lung collapses

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Parietal pleuraVisceralpleura

rib rib


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• 3. Compliance of alveoli and chest wall

–Thin alveolar membranes

–Adequate surfactant

–MESSAGE: DISEASES THAT STIFFEN ALVEOLI OR CHEST WALL, OR REDUCE SURFACTANT, PRODUCE VENTILATORY FAILURE

What is pulmonary compliance?

• “Stretchability” property

–Alveoli• Thinness of alveoli

• Partial inflation of alveoli at onset of inspiration

• Reduction in surface tension of alveolar fluid

–Chest wall• Flexibility, elasticity of chest wall

–Muscles, joints, connective tissue

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Factors increasing compliance

–Surfactant, thin membrane

• Thinner balloons are easier to inflate

• Inflation “ease” facilitated by surfactant

• Lowers surface tension of alveolar fluid lining

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Compliance & Elastance

• When alveolar compliance is very low…

– Lungs tough and rubbery

• … workload of breathing increases

– Segments, entire lungs

– Patient effort cannot “pull alveoli open”

• Mechanical ventilation may be necessary

– Tracheostomy if prolonged dependence

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Ventilatory failure

• Damaged respiratory pump– Kyphosis, scoliosis, paralysis, pain

• Damaged chest wall coupling– Atelectasis, pneumothorax (after lung transplant, accidents)

• Alveolar Compliance damaged:– Thickened, damaged alveoli

• Fibrosis, inflammation

– Loss of Surfactant

• ARDS, pneumonitis

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So… ventilation needs:

• An intact pump

• Compliant respiratory membrane and chest wall–Thin respiratory membrane

–Adequate surfactant

• Lungs’ connection to the pump

• What about respiration?

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Respiration

• Blood gas regulation

• No such thing as “respiration for speech”

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Respiration

• Gas exchanged between atmosphere & alveolar air

– External respiration

• Gas exchanged between arterial blood & working tissues

– Internal respiration

• O2 and CO2 concentrations are balanced by the respiratory system

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Atmosphere

Alveolar “air”

High CO2

Low O2

Low CO2

High O2High O2

L

High O2 Low O2

Low CO2 High CO2

R

Workingorgans

Arterial circulation

External Respiration

Internal Respiration

Venous circulation

Lung


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31© Conexions

External Respiration

32© Conexions

Internal Respiration

33© Conexions

O2

O2


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34© Conexions

• Regulation of respiration

• Peripheral, central chemoreceptors

Respiration

• Also needs a thin membrane

–Thinner is more porous (to a point)

• Needs blood in the capillary

–To exchange gas with atmosphere

• Alveolar and capillary gas concentrations need to be different

– For diffusion to take place

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Ventilatory failure

• Inspiration impaired if:– Thickened, damaged alveoli– Loss of Surfactant

– Damaged chest wall coupling

– Damaged respiratory pump

• CO2 retention increased respiratory drive increased respiratory rate fatigue increasing hypercapnia & hypoxemia mechanical ventilation

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Gas exchange (respiratory) failure

• Respiratory membrane obstructed– Airway “clogged” – Insufficient alveolar surface area

• Respiratory membrane too thick for diffusion– Remember ventilatory failure causes

• Afferent bloodflow obstructed– Pulmonary embolism

• Gas exchange impaired CO2 retention in blood respiratory drive/rate increases fatigue…

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Questions ???

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Breathing and Swallowing

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• How are swallowing & respiration orchestrated?

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• Assumptions

– Lungs are partially inflated at rest

• Held partly open by link to chest wall

– Inspiration is active, expiration is passive(at rest)

• Diaphragm contracts inhalation diaphragm stops contracting expiration

– Expiration is active in exercise, certain disease states

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Spirometry

Inspiration Expiration

Resting expiratory level

DeepInspiration

ForcedExpiration

Inspiration

Passive Recoil to REL


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volume

Duration of one swallow(apnea)

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Breathing and swallowing

• Abnormalities

– Stroke: volumes, duration, airflow direction

• Shorter cycle duration at rest*

• Direction of airflow after swallow**–Normals: 96% expiration after swallow

– Stroke: 60% expiration after swallow (p<.01)

*,**Leslie et al., 2002 a,b

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inspiration

expiration

Swallow apnea1.5 – 2.5 seconds

Seconds

Abnormal Breathe‐Swallow Phase

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inspiration

expiration

Swallow apnea1.5 – 2.5 seconds

Seconds

Respiratory Rate = 36/min

Breathing and swallowingAbnormalities: Tachypnea

Abnormalities

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volume

pressurepA

+

_

Duration of one swallow(apnea)

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Aspiration, pneumonia, aspiration pneumonia, other pneumonias

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What are pneumonitis and pneumonia?

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• Pneumo = air [airspaces of lungs = alveoli]

• Bronch… = lower airways [trachea = upper]

• …itis = inflammation of…

• Pneumonitis: inflammation of airspaces

• Bronchitis: inflammation of lower airways

• Tracheitis: …..

• Infection: inflammatory process caused by a pathogen [disease‐producing mircroorganism]

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Pneumonitis: lung inflammation

Inflammation

ChemicalMedications

Irritanttraumatizes lung

Irritants,Allergens

RadiationTherapy

Inhaled or aspirated sources

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Pneumonia: lung infection

Pneumonia (Infection andPneumonitis)

PathogenColonizes lung

Bacterial pathogen

Inhaled or aspirated sources

SystemicSpread

Resolution

Sepsis, Multi‐organ Failure,Shock

Viral pathogen

With or withoutother debris

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Infection causes inflammation: pneumonia = infection + inflammationPathogens and their waste are irritants

Pneumonia

• Most frequent infectious cause of death*

• 40% higher incidence in elderly **

• #2 nosocomial infection (UTI) in hospitals***

• High case fatality rate

– 55% (elderly)

– Leading cause of mortality in children under 5****

Marston, et al., 1997*; National Center for Health Statistics, 2003**; ***Niederman, et al., 2002;****Baine et al., 2001; Almirall, et al., 2000 53

What is Pneumonia?

Capillary – RBC, WBC

O2

O2

O2

O2

O2O2

O2

CO2

CO2

CO2

CO2

O2 enters alveoli, diffuses to blood

CO2 diffuses to alveoli, is exhaled

Pathogen enters alveoli

Pathogen adheres to epithelium,produces waste, reproduces. Wasteproducts are irritants

Inflammation: alveoli become thick,noncompliant.

1. Inoculation, infection

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Capillary – RBC, WBC

O2

O2

O2

O2

O2

O2

O2

CO2

CO2

CO2

CO2

Inflammation traumatizes respiratorymembrane making it excessively permeable.

Red blood cells leak into alveoli.

Volume of debris in alveoli increases

2. Inflammation, RBC leakage

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capillary

O2O2

O2

O2

O2

O2

O2

CO2

CO2

CO2

CO2

Alveoli become more noncompliant

Immunological response, macrophages and other cells accumulate

Volume of debris increases, forming a growing infiltrate (obstructs respiration).

Surface area for respiration shrinks,

Reduced oxygen diffusion to blood (Hypoxemia)

Reduced CO2 diffusion to alveoli(Hypercapnea‐CO2 retention)

3. WBC plasma leakage, respiratory distress

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Clear alveoli

Thickened epithelium

Infiltrates

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capillary

O2

O2

O2

O2

O2

O2

O2

CO2

CO2

CO2

CO2

Infiltrate volume has decreased,RBC eliminated

Inflammation subsiding; compliance improves

Respiratory surface area restoredgas exchange normalizes

WBC eliminated, inflammation ends

Infiltrate clears

4. Resolution

Bacterial debris eliminated

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What is Pneumonia?

• Infectious pneumonitis

– Caused by a pathogen (problem 1)

– Produces inflammation (problem 2)

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What is Pneumonia?

• American Thoracic Society criteria

–New and persistent infiltrate on CXR PLUS ONE OF THE FOLLOWING:

• + pleural or blood culture – same organism as lung

• Radiographic evidence of necrosis or cavitation

• Histopathologic evidence of pneumonia

• Two of the following– Core temp > 38.3C

– Leukocytosis (> 10,000)

– Purulent tracheal secretions 60


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Healthcare Associated Pneumonia

CDC MMWR (1997) Vol. 46, RR‐161

What is aspiration and how do lungs respond to aspiration?

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Aspiration

• Solid or liquid matter

– Not airborne, inhaled pathogen

• Courses by gravity, to its destination

• Crosses plane of true vocal folds

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Aspiration‐destination

• Entrance of liquid or solid matter into the respiratory system, below the vocal folds

– Not airborne

• Aspirated material is gravity dependent

• Airborne is not

R L

RL

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Lung response to aspiration: water

Inside alveolus

Plasma containing water inside capillary

RespiratoryMembrane

Water

H2O

H2O

H2O

H2O

RBC’s

WBC’s

Toward (L) heartFrom (R) heart

Capillary membrane

Alveolar membrane

Effros, et al., 2000 65

Inside alveolus

RespiratoryMembrane

Chemical irritant

Lung response to aspiration: pathogens and particulate matter

RBC’s

WBC’s

Plasma containing water inside capillary

Toward (L) heartFrom (R) heart

H2O H2O plasma H2O

Capillary membrane

Alveolar membrane

infiltrate

Chemical pneumonitis 66


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Aspiration Destinations

Aspiration produces pneumonitis or pneumonia in gravity dependent portions of lung(s).“Dependence” depends on posture when aspiration occurs, density & volume aspirated.

(R) Basilar infiltrates (R) Upper lobe infiltrates

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What is aspiration pneumonia?

• …and what other types of pneumonia are there?

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Aspiration Pneumonia 15.5%

>Oropharyngeal>Gastric

DAPNon‐DAP

Typical

Pneumonia100%

CAPHospital Acquired Pneumonia

VAPAtypical

Inhaled Pathogen

AspiratedPathogen

Non‐VAP

Inhaled Pathogen

69PEOPLE CAN ASPIRATE ANYWHERE: AP IS NOT SETTING SPECIFIC!


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Aspiration Pneumonias

• 1. DAP (Dysphagia‐related AP)

– Pathogen in solid or liquid matter

– Courses by gravity, to its destination

– Not airborne, inhaled pathogen

– CAN OCCUR ANYWHERE!

• 2. NDAP (Non‐dysphagia related AP)

– Colonized emesis

– gastroesophageal esophagopharyngeal reflux

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Non‐aspiration pneumonias

• Inhaled, airborne pathogen

– Environmental pathogens

– Bacterial, viral

• Hematogenous pathogen

– Septicemia

• Direct inoculation

– Contaminated respiratory circuit/equipment

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CAP, VAP, RSV, Legionella, Hematogenous

Aspiration Pneumonitis(chemical pneumonitis)

• Non‐Infectious‐chemical trauma

– Acute Lung Injury: caustic or particulate aspiration

– Inflammation of alveoli by effects of irritants

• No primary infection

• Inflammatory edema reduces surface area

• Gastric contents

– Sterile, acidic, caustic

– Damage to airways, alveoli72


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ARDS

Ware & Matthay, 2000

Normal acute resolution

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Distinguishing AP, Aspiration Pneumonitis, Other Pneumonias

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Differential Diagnosis

• Pt. has dysphagia‐related Aspiration Pneumonia (DAP) if:– Pt. has pneumonia

– Infiltrates are in gravity dependent segments

– Patient has DYSPHAGIA!

• Pt. has non‐dysphagia related aspiration pneumonia (NDAP) if:– Pt. has pneumonia

– Pt. does not have oropharyngeal dysphagia

– Aspiration is conceivable due to GE reflux, emesis…• Is patient receiving acid suppression therapy?

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• DAP: Dysphagia!

• Dysphagia‐producing disease, symptom onset following oral intake; position during oral intake; esophageal dysmotility

– Dependent for feeding/oral care, oral biofilm

History

76Differential Diagnosis

A new source of AP?

• Aggressive acid suppression may create conditions favoring pathogenesis of pneumonia*

– PPI: twofold increase in pneumonia

• Ambulatory and hospitalized patients

– H2 blockers: increased risk (<2)

• GE reflux and pulmonary fibrosis

77*Marik, 2001; Marik and Zaloga, 2002; Laheij, et al., 2004; Eurich, 2010; Herzig et al., 2009

Other risk factors

• Langmore, et al., 1998. Predictors of aspiration pneumonia: how important is dysphagia? Dysphagia 13: 69‐81.

– 41/189 patients developed pneumonia (22%)

• NH: 44%, Acute care: 19%; Home: 9%

– Dysphagia on VFSS/FEES: 81%

• 58% pneumonia patients aspirate liquids

• 27% aspirated food

• 50% aspirated secretions

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Significant predictorsPneumonia No pneumonia

Dysphagia 81% 47%

Tube feeding at pneumonia dx

27% 9%

Low or no activity 59% 28%

Dependent oral care 34% 10%

Dependent feeding 41% 6%

Brush teeth occasionally or never

40% 12%

# decayed teeth 5.2 2.4

Dry or excess oralsecretions

38% 17%

79But, EACH WAS SIGNIFICANT IN PRESENCE OF OTHER RISK FACTORS

Independent predictors (OR)

All patients

Patients eating orally

Dentate patients

Dentate patients eating orally

Dependent for feeding

‐ 19.98 ns 11.8

Multiple Diagnoses ns ns 4.9 7.3

Now smoking ns 4.1 ns ns

Tube fed before pneumonia

3.0 ‐ ns ‐

Dependent for oral care

2.8 ns ns ns

# decayed teeth ‐ ‐ 1.2 ns

Number of meds ns 1.16 ns ns

Dysphagia/Aspiration

ns ns ns ns

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Increased likelihood of pneumonia, when patient has the risk factor

• Dysphagia/Aspiration– Was not an independent risk factor

– Only significant in presence of other risk factors

– ASPIRATION ALONE IS NOT ENOUGH TO CAUSE PNEUMONIA

• Mitigating other risk factors in dysphagicpatients, lowers pneumonia risk more than efforts to mitigate dysphagia.

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Summary‐pneumonia

• Knowledge of normal and abnormal respiratory function is essential

– Not just swallowing function…

• There are many clues pointing to, or away from, a diagnosis of DAP

• This is important background knowledge for the SLP

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• Things to remember

– Aspiration can occur without dysphagia

– Aspiration is one potential source of pneumonia pathogens

– All respiratory illnesses are NOT dysphagia related

– ALL PNEUMONIAS ARE NOT ASPIRATION RELATED

– Patient appearance with pneumonia is NOT baseline

• History, course, physical signs are our data!!!

Summary‐pneumonia

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Common Respiratory Diseases in adults

• Types/categories

• The respiratory conditions seen in the elderly

– Are they suspicious for a dysphagia etiology?

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ACUTE OBSTRUCTIVE PATHOLOGICAL

CHRONIC RESTRICTIVE IATROGENIC

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Duration of condition, Recurrence

Mechanism of pulmonary effects

1. Acute: rapid onset2. Chronic: longstanding, recurrent , progressive

1. Obstructive: blocks atmospheric air from respiratory membrane2. Restrictive: restricts amount of air that can be inhaled

Source of condition

1. Pathological: caused by disease2. Iatrogenic: caused by treatment of another disease

Respiratory Diseases

• Obstructive Diseases

– Inspired air is obstructed from the respiratory membrane

• Obstructed gas exchange

• Respiratory pump works

• Restrictive Diseases

– Airflow or volume is mechanically restricted

• Gas exchange is intact

• Patient cannot inhale sufficient volume

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• Chronic respiratory conditions

– COPD (obstructive)

– Congestive Heart Failure (obstructive and restrictive)

– Pulmonary Fibrosis (restrictive)

– Asthma (obstructive and restrictive)

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• Acute respiratory conditions

– Pneumonia (obstructive and restrictive)

– Pneumothorax (restrictive)

• Atelectasis (restrictive)

– ARDS (obstructive and restrictive)

• Other acute pneumonitis (usually both)

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Respiratory Disease‐obstructive

Obstructive diseases air is “obstructed” from contact with respiratory membrane

Reduced oxygen supply

Reduced waste elimination Acidosis

Increased respiratory rate Overlap with swallow

obstruction

Alveolarmembranedestroyed

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Respiratory Disease‐Restrictive

Restrictive Diseases Limit amount of air that can be inhaled

Mechanical

Pain, paralysis, fibrosis

Poor compliance

restriction

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• COPD– Chronic bronchitis: chronic mucus…obstruction

– Emphysema: Alveoli and capillary destruction

– Resistance to blood flow into lungs• Can cause heart failure

– Increased rate, decreased cough effort

– Reduced mucociliary clearance

• Diffuse aspiration bronchiolitis– chronic aspiration of particulate matter

Respiratory Diseases

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Chronic Obstructive Pulmonary Disease

• Respiratory membrane surface area is obstructed– Chronic bronchitis

Respiratory membrane surface area is destroyed emphysema

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CHF

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(R) ventricle

(L) ventricle

Respiration

O2

CO2Pulm Artery

Aorta

CO2 O2

Vena cavae

Pulm. V.

(c) James L. Coyle 94

(R) ventricle

(L) ventricle

CHF

Hypertension/occlusion

Hypertension/occlusion

High Pressure

Pulmonary EdemaObstructs resp. membrane

Peripheral Edema

(c) James L. Coyle 95

Pulmonary edema

• Leakage of circulatory fluid into alveoli

– Most common cause = congestive heart failure

– Pulmonary hypertension “pushes” fluid out of capillaries

Pulmonary hypertension96


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CHF and Pulmonary Edema

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AsthmaA. Allergic/reactive bronchial smooth muscle spasm (obstructive)

narrow airway, increased resistance, reduced flow (restrictive)

B. Asthmatic bronchitis Mucus production

Obstructive & restrictive components

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Mechanically restrictive

• Disable complete expansion of thoracic cavity

– Kyphosis

• Abnormally flexed thoracic spine, compressed thorax

– Pulmonary fibrosis

• Tough, leathery segments tether adjacent segments

– Paralysis

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Kyphosis

03/20/2015 100

Mechanically Restrictive

• Pulmonary Fibrosis

– Fibrosis: toughening

– Idiopathic: from an unknown cause/etiology

Idiopathic PF

Tobin et al., 1998

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Pneumothorax

• Perforation of pleural membrane

– Destroys intrapleural vacuum that holds lung open

Subatmospheric pressure

Pleural cavity

Atmospheric pressure102


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Mechanically Restrictive

Pneumothorax Perforation caused by empyema/

abscess Chronic aspiration

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Atelectasis Areas of collapsed alveoli

Restrictive Pulmonary Disease

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Pleural effusion

• Fluid filling parts of pleural cavity

• Preventing lung expansion during inspiration

• Gravity dependent “bag of water”

Pleural cavity105


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CHF (transudative), Inflammatory (exudative)

Restrictive Pulmonary Disease

Pleural Effusion

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Iatrogenic causes of respiratory conditions

• Iatrogenic condition: a disease cause by treatment of another disease

– Sedation (restrictive)

• CNS depression

– Disruption of pleural linkage (restrictive)

• Cardiothoracic surgery

– Phrenic nerve injury (restrictive)

• Cardiothoracic surgery

– Vagal injury (obstructive: vocal fold paralysis)107

The effects of Aging

• An unavoidable risk factor..

– That is NOT a disease

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Homeostasis

• Maintenance of a constant, stable condition

–Organ systems maintain homeostatic equity

• Baseline

– Few resources used to maintain homeostasis

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Aging effects

• Homeostenosis

– the characteristic, progressive constriction of homeostatic reserve that occurs with aging in every organ system.

–With aging, physiologic reserves are increasingly used to maintain homeostasis

• Fewer reserves left for meeting new challenges

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Homeostenosis

Available reserve for WHEN WE NEED IT

Amount of reserve used to maintain homeostasis

111

Young Old


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Homeostenosis

Age

Available reserve for WHEN WE NEED IT

Amount of reserve used to maintain homeostasis

112

Young Old

Disease

More reserve for emergency Less reserve for emergency

RESERVE DEPLETED

Prevalence of Dysphagia

0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

<45 years 45‐64 65‐74 >75 all

Percentage of All Admissions With Dysphagia

Altman et al., 2010, (raw data from National Hospital Discharge Summary, 2004–2005)113

• Patients over 75 had double risk of dysphagia associated with hospitalization

• Patients with dysphagia had 40% longer LOS than patients without dysphagia

• Patients with dysphagia undergoing rehabilitation had a 13‐fold increase in mortality than those without dysphagia

114

Aging and Dysphagia


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Aging and pulmonary function

115Cronin & Kenny, 2008Palliative Medicine, Saunders.

Young vs. old:loss of reserve

Aging of respiration

• Chest wall

– Reduced muscle mass

– Altered spinal configuration (kyphosis)

– Less compliant

• Lungs have less elasticity AND…

• Chest wall stiffens

– Respiratory muscles lose mass and strength

– Affecting work of inspiration and expiration

• 70 year old: 2x work of 20 year old

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• Declining number of alveoli

– Alveolar surface area is 25% less at age 70 compared to age 20

• Gas diffusion capacity diminishes

• Reduced central ventilatory drive

– Older adults respond up to 50% less to oxygen deprivation, CO2 retention.

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• Diminished esophageal motility

• Immune system degradation

– Masks signs of common illness like pneumonia

• Blunted febrile response

• Reduced sputum production

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Aging and respiration

• Decreased tidal volume increased rate

• Breathlessness: detecting changes in respiration

– Has there been a change in activity level?

• Reduced activity may be a dyspnea compensation

– Perception of :fatigue: changes with age

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Age predicts lung capacity

20 y/o female, 60” tall

80 y/o female, 60” tall

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Aging and disease

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The elderly lungs have been exposed

• Today’s aged have highest exposure to

– Cigarette smoking

– Particulate air pollution

• So, some of the information on the aging lung may reflect this cohort’s exposure and not aging

– Evidence: FEV1 and FVC population norms have risen in subsequent cohorts

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Lung function

• Impaired lung function may cognitive decline

• Diminished expiratory air flow

– Impaired cough airway protection

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Respiratory problems affect swallowing, what is to be done about

them?

• Reversal of swallow‐breathing discoordination

• Consider added fatigue of “eating and drinking”

– Increase respiratory rate even more?

– Mitigating rate increases with supplemental O2

• …because we can’t pull off more CO2.

124

Summary

• Ventilation and pulmonary physiology are essential knowledge for the SLP

• Pulmonary disease affects swallow/breathing coordination

• Pulmonary disease can cause, or be caused by, dysphagia

– Mainly characterized by disruption of swallow‐respiratory coordination

125

Questions• Thank you

126

[email protected]

nsha 2015 convention, j. coyle, phd, 03/20/2015...

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