Module 3 pt 2

dysfunction of lung tissue or thoracic wall/cavity
not airways - compliance issue
impairment in the ability of the lung or thorax to stretch
lungs: increase in stiffness of tissue
thorax: MS impairments, neuromuscular impairments, tumors
encompasses a large group of diseases/disorders

inhalation
lungs can't expand, volume decrease
pt has to work harder to get air into the lungs

all volumes and capacities decreased
TLC and VC most used to assess
typical restrictive flow loop pattern
flow loop resembles normal but smaller bc restriction

hypoxemia: due t fibrosed and inflammed alveoli, decreased diffusion of gases at alveoli
hypocapnea: hyperventilation, low CO2, short shallow breathing pattern, increase RR
Imaging: fibrosis, granulomas, VQ mismatch

goal -> cause of restrictionnderlying disease
medications, chest tube, surgery

Trauma: rib fractures, surgery, lung contusion
Lung Cancers/tumors
Atelectasis

MSK causes
Connective Tissue Diseases
Neuromuscular Causes
Interstitial Lung Diseases

diaphragmatic paralysis
scoliosis
anklylosing spondylitis
pectus excavatum

rheumatoid arthritis

SCI, ALS, Muscular Dystrophy

large group of restrictive lung disorders that lead to problems w/the diffusion of oxygen into the blood @ alveoli due to fibrosis and scarring of lung tissue + alveoli => gases can't get through
Environmental/Occupation + Pulmonary Fibrosis
difficult to diagnose and often misdiagnosed as asthma, COPD, allergies
actual pathology varies depending on specific disease
-inhalation exposure to toxin => changes over time in lung tissues
-all involve fibrosis + scarring of lung tissue
-others: inflammation, nodules, granulomas, cysts

mechanism not understood
hypothesis: abestos fibers cause alveolitis in resp bronchioles => fibrosis
also causes partial thickening or parietal pleura
-posterior, lateral, and pleural surface of diaphragm
leads to restrictive disease

pneumoconiosis caused by inhalation of dust
due to slow onset and long latency, pts are often in advanced stages before diagnosis => poor prognosis
slow respiratory functional decline
deaths often due to effects of pulm fibrosis (20%) or cancer (39%), risk increase if smoker
ground glass appearance honeycombing, alveoli stretched out

increased work of breathing
dyspnea, effort to expand lungs
lung and thoracic compliance
airway resistance
use of accessory muscles and posture
affects tidal volume
affects RR - tachypnea
disease prog => work of breathing increased
-resp muscle fatigue, overuse, failure
other symptoms related to cause

dimished or absent
inspiratory crackles, bronchial sounds
Cardiovascular:
-right sided HF
-peripheral edema
MSK
-digital clubbing

increased RR
dyspnea, esp on exertion
non productive cough
decreased breath sounds
crackles on inspiration, bases esp
accessory muscle use
digital clubbing
cyanosis
advanced stages => pulm HTN, R sided HF

treatment of any underlying disease
medications w/antifibrotic properties: only 2 w/FDA approval
focus on treating related signs and symptoms: pts often require supp O2 bc decreased SpO2/PaO2
lung transplant

Pulm Impairments:
-impaired ventilationesp
-impaired ventilatory pattern
Pulm Rehab:
-breathing exercises to control dyspnea
-energy conservation/paced breathing
-aerobic + strengthening exercises to maintain func mobility and QOL

idiopathic - Sarcoidosis
medication

early on in disease => alveolitis, inflammation of alveoli
creates granulomas
-small area "clumps" of immune cells, WBC, macrophages, fibroblasts
-may resolve or become fibrotic
leads to restrictive disease

Ventilation (V): air reaching alveoli
Perfusion (Q): blood flowing to alveoli to pick up O2 and leave CO2
-need a good match
mismatch -> low blood oxygen levels (hypoxemia) even if pt breathing adequately
as RLD progresses, hypoxemia worsens => breathing harder
Reduced Ventilation in some alveoli
-thickened or stiffened lung tissue or thorax rest. causing atelectasis impairs airflow to certain alveoli, meaning less air reaches some area of the lungs (reduced ventilation)
-despite this, blood flow may still reach alveoli, which leads to poorly oxygenated blood back to heart
Impaired oxygen diffusion
-even in well-ventilated areas, thickened interstitial tissue + damaged alveoli slow down oxygen transfer from alveoli -> blood leading to low oxygen levels in the blood even if perfusion is good
Hypoxic Vasoconstriction Response
-the body attempts to adjust by redirecting blood away from poorly ventilated alveoli
-this response is often incomplete + blood can still flow to areas with poor ventilation => more V/Q mismatch

Pneumothorax
Atelectasis
Pneumonia

collapse of lung due to presence of air in pleural cavity
air enters pleural cavity from ruptured lung or hole in thoracic cavity
lung collapses due to loss of negative intrapleural pressure

aymptomatic if small pneumothorax + no underlying lung disease
If larger or underlying disease:
-acute dyspnea
-pain go away <24hrs even if pneumothorax unresolved
-decreased or absent breath sounds

nothing tbh
mobiity and breathing exercises when surgery done

Iatrogenic
-procedure allows air to enter (biopsy, venous line)
-happens in young skinny men
Traumatic
-air from penetrating wound (ouch!), leaks out
Tension
-enters but can't escape, Bad and life threatening
Increased Thoracic Pressure
-decreases venous return
-decreased cardiac output
-hypotension
-shock
Mediastinal sructures pushed away from affected side

incomplete expansin of lung tissues: collapsed and non aerated
region of lung collapses and lacks aeration at alveoli + bronchioles
condition associated with many thoracic and lung disorders

surfactant deficiency that causes alveolar walls to stick together => alveoli collapse
Causes: smoke inhalation, ARDS, pulm embolism, bypass surgery, pneumonia

compression of lung from space occupying lesion
squeezes air out of lung
Causes: pleural effusion, pleural tumor

most common
obstruction in segmental, lobar, or main bronchus
causes: mucous, foreign body, tumor

volume loss due to poor lung compliance
Cause: pulmonary fibrosis

loss of volume bc hypoventilation
common post op, bedrest, sedatives that limit tidal volume
Causes: surgery, sedation, diaphragm dysfunction

dyspnea
tachypnea
cough
decreased breath sounds
crackles
symptoms related to cause: pain and fever

lung infection in lower resp tract
-affects acinus and gas exchange
causes: bacterial, viral, fungal
around 50k deaths/yr

community acquired
hospital acquired
health-care associated
ventilator associated

Restrictive -> air INTO alveoli
infection in alveoli
large areas of alveli become progressively filled w/fluid and pus
reduces ability of alveoli and surrounding capillaries to perform normal gas exchange

Bacterial
-high fever, chills, dyspnea, tachypnea, productive cough, pleuritic pain
Viral
-moderate fever, dyspnea, tachypnea, non-productive cough, myalgia

Impaired ventilationespiration
Impaired airway clearance
Impaired ventilatory pattern

Increase mobility
-position changes, ambulation, helps with airway clearance
Airway clearance techniques
Breathing techniques
Incentive Spirometry

a state in which there is too much fluid in the pleural space
Over 60 causes:
Heart Failure - elevated venous pressure causes fluid to be pushed into the pleural space
Pneumonia - accumulation of mucous in the alveoli pushes fluid into the pleural space
Malignant neoplasm - tumors in the pulmonary system cause excess fluid to build up in pleural space

Normal: pleural cavity normally has 10-25 mL of pleural fluid that gets reabsorbed by the lymphatic system
-pleural fluid moves from parietal pleural capillaries -> pleural space -> reabsorbed by visceral pleural capillaries to prevent accumulation in pleural space
Abnormal: up to 3L of fluid in pleural cavity
-when this system is interrupted by any cause, the fluids build up in the pleural space + limits the lungs ability to expand, leading to atelectasis

dyspnea
chest pain
cough
fever
tachypnea
other symptoms related to underlying cause
Auscultaion: pleural rub,, decreased breath sounds

Goal: prevention of further pulmonary complications
-position changes, breathing exercises/energy conservation, increase mobility
Airway clearance -> not indicated
-atelectasis will remain present until fluid is reabsorbed or removed

increase in the amount of fluid within the lung tissues
fluid moves from pulm capillaries in pulm vascular system to alveoli + lung tissues
Non Cardiogenic: acute respiratory distress syndrome, pulmonary embolism
Cardiogenic (most common): LV failure due to Mit or Aor valve disease, MI, HTN

shortness of breath, esp when lying down (orthopnea)
cough, often producing frothy or pink-tinged sputum
crackles heard on auscultation due to fluid in airways
reduced oxygen saturation

Pulmonary capillary wedge pressure (PCWP) - info on hemodynamics (PA, CVP, CO, SVR, PVR)
-indirect measurement of pressures on the left side of heart using a Swan-Ganz catheter that sits in the pulmonary artery
-used in critically ill individuals to diagnose severity of LV failure, pulm HTN, and provide ongoing monitoring of cardiac function data
-If PCWP >20 mm Hg, puts pts at risk for certain serious conditions

If severe, PT may not be indicated until pt stabilizes
monitor hemodynamics
intervention usually focused on mobiity + breathing exercises to increase aerobic capacity, endurance, and address ventilatory pattern
Airway clearance not indicated bc fluid is in alveoli and interstitial tissues

life threatening, acute complication of venous thrombo embolism
-peripheral clot (venous thromboembolism) dislodges
-travels through venous system to R side Heart and Lungs
-causes blockage in pulm vascular circulation (no blood to lungs)

rapid, unexplained onset of dyspnea
pleuritic chest pain (sharp pain that increases with forceful breathing)
tachypnea
others: hemoptysis, cough, syncope, breath sounds: crackles
Imaging: V/Q scan, xray or CT, pulm angiography
Blood Test: d-dimer (small protein released when clot breaks apart)

Chronic thromboembolic pulmonary HTN: CTEPH
-prolonged obstruction of pulm arteries from thrombi that causes redirection in blood blow, remodeling of pulm vascular bed
-leads to chronic inflammation and fibrosis of pulm tissues + ultimately pulm HTN + R sided HF
Symptoms (Ongoing)
-SOB and DOE
-fatigue
-LE edema
-dizziness
-fainting
-palpitations
Long term consequences:
-worsening dyspnea
-decreased exercise tolerance
-decreased SpO2 w/exertion

1) symptoms - dyspnea, chest pain, syncope, hemoptysis
2) Risk Factors - surgery, immobility, trauma, cancer
3) Clinical Prediction rules - wells criteria for pulm embolism (PE) >4 high risk, geneva score combined w/d-dimer high >11 or simp >5

<50 yo
pulse <100 bpm
SaO2 >94%
no unilateral leg swelling
no hemoptysis
no recent trauma or surgery
no history of VTE
no oral hormonal use
all 8 neg: safe to rule out PE

Primary: anticoagulants
-lower risk of future clots + stop growth of present thrombus
Major concern w/anticoagulants: bleeding in pts w/poor balance who have a high fall risk
-benefits outweigh risk + anticoagulants should be used
Inferior Vena Cava Filter
-only for LE DVT

IVC Filter
-once pt is hemodynamically stable, it is safe to begin mob
-prevents further VTE, negates other effects of bedrest, improves QOL
Once therapeutic level of anticoagulation reached:
-monitor VS
-monitor signs and symptoms of worsening PE
-monitor for evidence of hemodynamic instability: abnormal HR response to exercise, decrease SpO2, hypotension, worsening dyspnea, chest pain

don't mobilize pts at high risk for PE until low risk status in achieved + pt is hemodynamically stable
limiting mobility is critical for pt safety
Once pt is hemodynamically stable, safe to mobilize per low-risk guideline

Lung resection/lobectomy
lung transplant

surgical removal of a lobe, segment, or wedge of lung tissue
Indications: lung cancer (CA)
Other: chronic lung infections, lung abcess, fibrosis, traumatic damage

Pre op
-pt and family education
-cardiovascular endurance training
-msk strength training
-breathing exercises
Post op 12-24 hrs:
Cardiopulm assessment
-assess need for airway clearance
-assess breathing pattern
-assess ventilation/ respiration
Functional Assessment
-positioning + splinting for mobility
MSK Assessment
Early Mobility!

surgical removal of one or both lungs due to disease
Indications:
-end stage pulm diseases (COPD, CF)
-waiting list for transplants: eligibility criteria + complete eval from transplant team
-primary concern: rejection, remain on meds to prevent

pre op:
prevent further decline in function
prep pt and family for post op rehab
Post Op: outpatient
self monitoring VS during activity
signs of rejection - decreased SpO2 + ex tolerance
Ex testing: 6MWT
Cardiovascular endurance training: aerobic conditions
MSK Strength training - large skeletal muscles + WB ex
Breathing exercise

respiratory system unable to maintain adequate gas exchange/ resp

Low PaO2 <60 mmHG
Low - normal PaCO2 <45-50 mmHg
Primary Problem: poor oxygenation of blood
-O2 avail but can't get through alveolar wall (respiration)

pneumonia
PE
pulmonary edema
Fibrosis
ARDS

characterized by severe pulmonary edema that is not cardiogenic
Initial "injury" damages alveolar - capillary membrane + fluid floods alveoli
widespread inflammation of pulm tissues
results in hypoxemia

exudative
proliferative
fibrotic

fluid
pulmonary edema, hemorrhage, fibrous membrane forms on alveoli

hours
influx of neutrophils + other inflammatory cells
increased inflammatory + tissue damage

days
lung tissue replaced by fibrotic tissue
restrictive pulm disease

Direct Lung Injury
Indirect Injury

blunt chest trauma (MVA)
pulm contusion
pneumonia
aspiration (gastric contents in trachea)
inhalation injury (smoke)

sepsis (blood infection)
major trauma
pancreatitis
hypovolemia (blood loss, dehydration)
burns (inflammatory process)

mortality rate 40-60%
some recover fully, others have some permanent damage
-DOE, hypoxemia, rapid/shallow breathing, increased use of accessory muscles of inspiration
-survivors normally have restrictive breathing pattern for 12 mos

severe shortness of breath and hypoxemia
labored and very rapid breathing
pink, frothy sputum
low blood pressure
confusion and extreme tiredness

pH - alkalosis (hyperventilation
decreased PaO2
PaCO2 may be normal or decreased

mismatch - areas that are perfused are not ventilated due to fluid, inflammation of alveoli

diminished breath sounds
crackles and wheezes
tachypnea

tachycardia
arrhythmia

lungs are unable to remove CO2 from the blood
PaO2 <60 mm Hg
PaCO2 >50 mmHg
Primary problem: ventilatory pump failure - resp muscles, nerves, chest, wall mechanics (no thorax expansion)
hypoventilation: not enough O2 in alveoli to cross
Result of failure of resp muscles + chest wall mechanics
-COPD
-neuromuscular diseases
-MSK diseases (scoliosis)
-Central resp depression (head,trauma,meds)

dyspnea
headache (increased CO2)
confusion
drowsiness
cyanosis
tachycardia
tachypnea

low pH - acidemia
elevated PaCO2 >45
decreased PaO2 - hypoxemia

mismatch may be present but is not a primary factor in RF

tachycardia
arrhythmias

diminshed breath sounds
crackles and wheezes
tachypnea

intubation and mechanical ventilation
extracorporeal membranous oxygenation (ECMO) - oxygenated outside the body
-gives lungs chance to heal, 1-4 wks
Medications
-supplemental O2
-antibiotics to control/prevent infection
-bronchodilators to manage underlying condition (COPD, CF)

non invasive mechanical ventilation (NIV)
CPAP and BiPAP
Invasive mechanical ventilation

Goal: assist with ventilatory needs short term
CPAP and BiPAP
-first line support for pts w/acute resp failure without need for intubation
-provided w/mask or high flow nasal prongs instead of ETT
-helpful in COPD, CHF, CF, sleep apnea, neuromuscular diseases + others withou intubation
-can also be used for weaning off invasive mechanical ventilators/ETT

delivered via mask of high flow nasal prongs instead of ETT
maintains continous positive pressure similar to positive end exp pressure (PEEP) on a ventilator, but pt breathing spontaneously
prevents airway collapse, maintains alveolar ventilation by providing pressure during exhalation

delivered via mask or high flow nasal prongs instead of ETT
provide a higher positive pressure during inspiration + lower positive pressure during expiration
helps maintain airway + alveolar function by providing support during inspiration + expiration

headaches
skin irritation
stomach bloating
nasal congestion
claustrophobia
anxiety

for acute respiratory failure
a machine (ventilator) must often do the work of breathing
requries use of endotracheal or tracheostomy tube
in some chronic conditions, ventilation required indefinitely
endotracheal - mouth, tracheostomy - throat, can't speak

FiO2
PEEP
RR
Respiratory Volumes

maximal support: ventilator does most/all the work
minimal support: pt breathes spontaneously; assisted by ventilator as needed

percentage of O2 in atmosphere air (21%)
adjusted to maintain or restore PaO2
FiO2 <50% to avoid O2 toxicity
FiO2 temporarily increased to 100% during suctioning, position changes

slight positive pressure maintained by ventilator at end of expiration
Typically around 5cm H2O: as high as 20 cm H2O in severe cases
Keeps small airways open at end of expiration to prevent alveolar collapse
Distributes air throughout alveoli to prevent or reverse atelectasis
Maintains V/Q matching

12-16 b/min
Tidal Volume: adjusted for each patient
Inspiratory flow rate: usually >6 L/min
Inspiratory/expiratory (I:E) ratio: normally 1:2 but can be adjusted depending on pt needs

assist control ventilation: volume or pressure control
pressure support ventilation
synchronized intermittent mandatory ventilation control: volume or pressure control (ppl who can't breathe on their own)

the ventilator can be set (triggered) to deliver a breath as the patient tries to breathe
sensitivity of the machine is adjusted so that the patient must exert a certain effort to initiate a breath
pressure triggering or flow by triggering (volume)

breath is initiated if the machine
senses a negative airway pressure greater than trigger sensitivity
generated by pt trying to initate a breath

flow of gas in/out of the ventilator circuit is monitored
ventilator breath delivered when return flow<delivered flow, indicating pt is trying to take a breath

ventilator set to a specific respiratory rate
volume control: delivers a specific Vt or
Pressure control: set pressure and time
additional ventilator breaths given if triggered by patient, can breathe "around" set RR

patient is required to initiate every breath
pt generates RR, TV, duration of inspiration, inspiratory flow rate
ventilator provides pressure support to overcome the increased work of breathing imposed by the disease process, the ETT, the inspiratory values ...

ventilator provides mandatory breaths according to preset pressure/volume
if pt tries to breathe as ventilator is about to administer a breath -> ventilator synchronizes mandatory breath w/pt's voluntary effort ot achieve a specific pressure or volume

requires intubation via mouth ETT, incision in trachea (tracheostomy)
can irritate, damage trachea + larynx
impair cough
-decrease humidity of inspired air -> dry out airway
-decrease mucociliary function
-cause respiratory muscle weakness, fatigue
-cause tracheal collapse upon removal
-cause "ventilator induced lung injury" VILI

mechanical ventilation causes diffuse alveolar damage + inflammation similar to ARDS
4 possible causes that can lead to ARDS
-ventilator pressure too high -> alveolar rupture (barotrauma)
-volume too high (volutrauma)
-repetetive opening/closing of alveoli (atelectrauma)
-cytokines released due to mechanical injury (biotrauma): prevention - keep ventilator pressure + volume settings lower than pt needs, better to have moderate increased Pco2 than damage alveoli

-position pt correctly: supine if ventilated
-pt must have oxygen: increase FiO2 to 100% for a min prior to suctioning
-use sterile field if open suctioning system: gloves, catheter
-vacuum suction: <200 mmHg (adults), <120 mmHg (peds)
-use inline suction system to avoid removing patient from ventilator + manually ventilate during suctioning only if necessary using Ambu bag
-insert catheter into tube slowly until resistance is met then pull catheter back slightly
-turn on suction + gently pull catheter out
Suction: shallow - 15 sec max, deep - only if shallow ineffective
maintain O2 Sat at 90%, give additional O2 if necessary

check ventilator settings
check ventilator tubing + connections
-know length of tubing, wires, etc
-make sure you have oxygen + enough tubing
know mode
know alarm settings
-continual monitoring of hemodynamics during activity
ETT or TT is secured
Bring support + wheelchair
-rest periods, quickly return to bed as necessary

mechanical system that temporarily takes over the work of heart/lungs
-oxygenates blood and removes CO2 outside the body allowing lungs + heart to rest and heal
Indications:
severe ARDS w/low O2 despite max ventilator support
cardiac arrest or severe HF where heart cannot pump effectively
bridge to transplant: pts waiting for heart or lung transplant
post cardiac surgery complications when hear needs additional support to recover

Veno venous (VV)
Veno arterial (VA)

only supports lungs
blood drawn from a large vein, passed through ECMO machine to recieve oxygen + returned to a vein, by passing the lungs
commonly used for severe respiratory failue (ARDS) when heart is still functioning + well

supports heart and lungs
blood is drawn from a vein, oxygenated, then pumped back into an artery, bypassing heart + lungs
typically used in pts with cardiac failure + respiratory failure

acute brain dysfunction or altered mental status that can not otherwise be explained
Essential Features:
-acute onset + fluctuating course
-inattention or distraction
-disorganized thinking or altered level of consciousness

disturbance in attention + awareness
acute change, fluctuates throughout the day
disturbance in cognition

60-80% of mechanical ventilation, pts develop delirium
40-60% non vent
predictor of mortality at 6mos
-longer post ICU stay
-for each day a pt is delirious, 10% increase of death
higher probability of developing dementia

neurocognitive squelae following critical illness
-common, may be permanent
-associated w/impaired ADLs/QOL + inability to return to work
Evidence from 10 cohorts -> 25-78% survivors experience neurocog. impairments
-in pts with ARDS, prevalence 78% at d/c, 46% at 1 yr, 25% at 6 years

acute onset/prodromal phase
fluctuation
psychomotor disturbance
disturbance of consciousness
disruption of sleep/wakefulness
emotional disturbance
disorders of thought, language, memory, attention
perceptual disturbances

Hyperactive, Mixed, Hypoactive

restless/agitated
aggressive/hyper-reactive
autonomic arousal
15-47% of cases

lethargic/drowsy
apathetic/inactive
quiet/confused
often escapes diagnosis
often mistaken for depression
19-71% of cases

assess safety
establish physiological stability
address modifiable risk factors
optimize communication
support routines
enocurage self care
optimize environment
mobilize

monotherapy -> neuroleptics
high potency w/low anticholinergic activity
low dose
haloperidol or risperidone
taper as soon as possible
start low + go slow

acute confusional state, extremely common among hospitalized adults and is strongly associated with poor short-term + long-term outcomes
risk can be assessed according to the presence of predisposing (baseline) and precipitating (acute) factors
the first step in delirium management is accurate diagnosis: use of a validated instrument (CAM) recommended
after diagnosis, evaluate for reversible causes
manage behavioral disturbances w/nonpharcologic approaches first
proactive, multifactorial interventions have been shown to reduce incidence, severity + duration of delirium

new or worsened physical, cognitive, or mental health status arising after critical illness + persisting beyond acute care hospitalization
Includes:
ICU AW, cog or brain dysfunction, mental health problems
up to 50% of pts w/PICS may not be able to return to occupation

clinically important symptoms in 1/5 at 1yr
worse HR, QOL
higher prevalence in pts who had:
-comorbid psychopathology
-received bezodiazepines
-had early memories of frightening ICU experiences

enhances cardiovascular function
enhances endothelial function
decreases chronic inflammation
preserves msk + neuromsk integrity
decreases depression + improves cognition