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EXMD4742 > WK10 - Obstructive Conditions > Flashcards

WK10 - Obstructive Conditions Flashcards

1
Q

How can EP’s address the fear component of respiratory patients? What education tools can we use?

A
  • patho
  • breathlessness Mx
  • benefits of Ex
  • pacing (ADLs/Ex)
  • meds SE
  • lifestyle
  • Ex opportunities
  • action plans
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2
Q

How can EP’s address the fear component of respiratory patients? What exercise tools can we use?

A
  • Ax of functional capacity (co-morbidities implications)
  • spirometry
  • falls risk Ax
  • prescription/programming
  • ADL pacing application
  • Progression/regression
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3
Q

What meds are given to sick respiratory individuals and how does it relate to Fall risk Ax?

A

Corticosteroids!

They weaken the longitudinal tensile strength of bone.

More likely at risk to have fractures

If they cough and have osteoporosis, they cause a systemic change in COPD which increases risk of fractured ribs

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4
Q

What are the 3 main conditions that make up Obstructive Lung Disease?

A
  1. Chronic bronchitis
  2. emphysema
  3. asthma
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5
Q

What 2 diseases make up COPD?

A
  1. chronic bronchitis
  2. Emphysema
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6
Q

Define COPD.

A

Chronic Obstructive Pulmonary Disease

A preventable and treatable disease, characterised by persistent airflow limitation - usually progressive and associatd with chronic inflammatory responses in airways and lung to noxiuos particles and gases.

Exacerbations and comorbidities contribute to overall severity in individual patients

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7
Q

Define emphysema.

A

It is the destruction of alveoli

Reduces amount of oxygen that can be brought into the body.

Reversal of emphysema is unlikely.

Changes with emphysema will not change with exercise capacity improvements.

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8
Q

Define dynamic hyperinflation.

A

When patients are exercising and they continue to trap air on top of trapped air.

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9
Q

Define static hyperinflation.

A

When there is trapped air there at rest.

As emphysema progresses, you will be more likely to have static hyperinflation at rest.

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10
Q

Define chronic inflammation.

A

Able to see inflammation in the walls of the bronchials.

It is inflammation and the production of phlegm.

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11
Q

What are the Sx of COPD?

A
  1. dyspnoea (SOBAR & SOBOE)
  2. wheeze or chest tightness
  3. cough
  4. sputum frequency, volume and perulence
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12
Q

What is the burden of disease statistic for COPD?

A

4th leading cause of death in world
- to be 3rd leading cause in 2020

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13
Q
A
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14
Q

What is the burden of COPD in Australia?

A

5th leading cause of death

  • 2.5% of 40-50y
  • 7% >75y
  • lower socioeconomic = 7.5% more risk
  • acc. for 355k hospital bed days and 15% of preventable hospitalisations
  • health expenditure of COPD hospitalisation = 938mil in 2018
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15
Q

What does the COPD-X Plan stand for?

A

Confirm Dx and Ax severity
Optimise function - EP Role is here
Prevent deterioration
Develop supp. network + self-managed plan
Managed eXacerbations

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16
Q

What are the biomechanics of breathing?

A

Inhale
* chest expands
* diaphragm contracts
* ribcage expands

Exhale
* chest contracts
* lung volume decrease
* diaphragm relaxes

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17
Q

What are the muscles of respiration?

A
  • sternomastoids
  • scalenes
  • inspiratory/expira intercostals
  • diaphragm
  • expiratory abdominalis
  • EXT obliques
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18
Q

What are the accessary muscles of respiration?

A
  1. scalene
  2. traps
  3. pec major
  4. SCM
  5. int intercostals
  6. abs
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19
Q

What are the different types of breathing?

A
  1. Pursed Lip Breathing - CPAP - reduces phrenic nerve activity, commonly used in pts with anxiety
  2. Prolonged expiratory breathing
  3. diaphragmatic breathing
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20
Q

How long do SABA relievers act?

A

Instantaneous - works within 20s

Lasts for 4hrs

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21
Q

What is a SE of large amount of Ventolin?

A

Tachycardia

If patient is tachy, important to ask when last Ventolin puff was performed

Minimise dose before the session - once resting values are taken, then it is advised to take a puff

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22
Q

What is the difference between MDI puffer and MDI plus spacer?

A

Puffer alone - content is dispersed to mouth, throat, lungs and stomach - <10% goes into lungs

Puffer w spacer - allows content to solely go the lungs - 40% deposition

Take 4 puffs to equal 1 puff w spacer

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23
Q

What are some lifestyle modifications?

A
  • diet
  • weight management (esp. for wt loss)
  • smoking cessation
  • falls
  • Daily PA lvls

Consider Scope of Practice!!

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24
Q

Why is vaping just as dangerous as smoking?

A
  • Nicotine is absorbed in the mouth and goes straight into bloodstream faster than if smoked a ciggy
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25
Q

What to know and talk about smoking?

A
  • nicotine contained in tobacco causes dependence
  • addiction now seen as chronic relapsing disease
  • needs med Tx
  • not just a “bad habit”
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26
Q

How to talk about smoking cessation?

A
  • should be known in every clinician

Does not need to be…
- long
- complicated
- confronting

Online/F2F training available

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27
Q

What are the limitations of pulse oximeters?

A

Cannot distinguish difference between O2 and CO2 molecules in blood

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28
Q

What are the 5 A’s

A

Ask
Assess
Advise
Assist
Arrange follow-up

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29
Q

What to “ask” regarding smoking?

A
  • smoking status on initial Ax
  • check again during review
  • Ax readiness to quit
  • if not interested - no point in telling facts about smoking cessation
  • still advise them to quit

2 Q’s to ask if they are ready to quit.
1. When waking, how quickly do you want to smoke?
2. How many ciggies do you smoke a day

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30
Q

How to Ax a smoker?

A
  • daily smoking (no. and type)
  • med Hx (psychiatric)
  • quitting Hx
  • family Hx
  • environmental context - triggers of smoking
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31
Q

What are some smoking considerations?

A
  • gender (women slower nicotine stabilisers)
  • ethnicity (faster/slower metabolisers)
  • co-morbidities (esp. MH and pregnancy)
  • concomitant meds (caffeine, alcohol, insulin, antipsychotics)
  • expired CO (deep vs shallow inhalations)
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32
Q

What are some nicotine withdrawal Sx?

A
  • cravings
  • depressed mood
  • insomnia
  • irritabiltiy
  • frustration/anger
  • anxiety
  • restlessness
  • difficulty in concentrating
  • increased appetite or weight gain (within 24h of smoking cessation)
33
Q

What is the Pack Year Equation?

A

(No. ciggies/day divided by 20) * no. of yrs smoked

34
Q

What is the Alpha-1 Antitrypsan Deficiency?

A

AAT protein produced in liver - brought to lungs to help regenerate lungs to use cilia to move irritant out of lungs.

AAT protein deficiency increases risk of COPD
* inherited; 2/1000 have AAT
* occurs in varying degrees
* AAT thought to protect against macrophage damage
* walls of bronchial tubes/alveoli both damaged = severe disease

35
Q

Where else in the body does AAT affect?

A

Skin - necrotising panniculitis, psoriasis, urticaria

Liver - cirrhosis, neonatal hep

Kidneys - proliferative golumerulonephritis, IgA nephropathy

Intestines - IBD

Lungs - COPD, bronchiectasis, asthma

Vascular - ANCA +ve vasculitis, ab/intracranial aneurysm, arterial fibromuscular dysplasia

36
Q

What is part of the EP Ax in relation to respiratory concerns?

A

PMHx
* exacerbations, triggers, hospitalisation, smoking Hx

Spirometry
* small/large airways, reversibility with BDs, ratios

Condition Classification
* COPD stage (mild-severe), asthma (controlled vs uncontrolled), restrictive process

Med adh.
* relievers, preventers, anticholinergics, rescue, O2

Comorbidities
* osteoporosis, CVD risk, surgeries, obesity, arthritis, HTN, PHTN/PAH, RHF, OSA

37
Q

What are some objective measures performed by EP’s?

A
  • previous/current Ex/ ADL hx
  • postural/msk screening
    –> general msk
    –> for pulmonary: thoracic kyphosis, barrel chest, scap positioning, over active traps, scalenes and SCM, breathing biomechanics, upp/low lobe breathing
  • baseline observations and anthro
    –> tachy, pre-existing CVD, obesity)

Ex testing - dependant on disease severity

38
Q

What are some 6MWT respiratory considerations?

A
  • complete 2 w 30/60s rest fro Rx and minimise learning effect
  • record: BP, SpO2, HR, BORG, leg fatigue, TTR (to resting values)
  • meds noted and used before testing
  • O2 used pre/post test and noted what level

Contraindications:
* unstable angina/MI within past 1/12
* HR >80% age predicted max., BP >200/100
* Caution if SpO2 <92% both Room air and Domiciliary O2

Termination:
* chest pain, intolerable dyspnoea, leg cramps, staggering, diaphoresis, pale/ashen appearance

NB: <88% STOP & REST - encourage to continue one O2 increases

39
Q

What are the equations of the 6MWT predictive values for respiratory conditions (COPD)?

A

Male
= 867-(5.71age)+(1.03height)

Female
= 525-(2.86aeg)+(2.71height)-(6.22*BMI)

Percentage = (distance walked/predicted distance)*100

40
Q

How to use 6MWT outcome measure?

A
  • evaluate effectiveness of PRP Ex training component
    *trace natural Hx of change in Ex capacity over time
  • min. important difference = 30m (95% confidence limits 25-33m)
41
Q

How to confirm Dx of COPD?

A

Spirometry!
Demonstrates airflow limitation which is not fully reversible through spirometry.

Asthma demonstrates airflow limitation is reversible. Restrictive condition will have normal FEV1 but decreased FVC but a normal elevated ratio.

Clinical Dx for COPD:
FEV1%Pred <80% Post BD

42
Q

Define FEV1, FVC and FEV1/FVC.

A

FEV1 = Forced expiratory volume in 1st one sec

FVC = forced vital capacity - total lung capacity >6s

FEV1/FVC = ratio of amount blown in 1st sec / total lung capacity

43
Q

What to see on spirometry results to indicate whether it is COPD or asthma?

A

Reversibility is seen by…
Baseline FEV1 >1.7L

12% change and 200mL improvement in FEV1 after BD

44
Q

Based on respiratory function tests, define what the 4 stages are.

A

Stage I = mild, FEV1 >80% of predicted

Stage II = mod, FEV1 50-80%

Stage III = severe, FEV1 20-50%

Stage IV = very severe, FEV1 30% of predicted

45
Q

What additional tests can asisst in Dx?

A
  • chest x-ray and CT scan
  • single breath diffusing capacity
  • arterial blood gases/pulse oximetry (esp. during Ex)
46
Q

Lung volume changes with respiratory disease. T or F?

A

T!

If it is an obstructive - lung volume is signficantly higher.

If it is restricted typically sits between 50-100% - static hyperinflation

47
Q

Ex intolerance is the hallmark feature of chronic lung diseases. T or F?

A

True

48
Q

Explain the relationship between CV and MSK impairments.

A

As COPD increases - start to see decrease in PA = deconditioning
* CV deconditioning
* peripheral muscle deconditioning, wasting, weakness
* increase accum. of lactic acid at low work rates
* increase WOB = increase in ventilatory demand and sense of dyspnoea
* reduced pulmonary vascular conductance = increase risk of PHTN 2ndary development
*RV systolic dysfunction = increase risk fo RHF

49
Q

define PHTN

A

Pulmonary HTN

Increase resistance to get blood into lungs

As disease progress there is more pressure on RV = increase pressure on pulmonary arteries.

50
Q

What are ventilatory impairments?

A

Increased airway resistance esp. in obstructive conditions

Obstruction compromises mainly expiration

Slowly progress (bronchitis/emphysema) or acute/intermittent (asthma/ACOS) or have both

Biomechanical factors related to hyperinflation occurs with expiratory airflow obstruction
- increase WOB
- hyperinflation places inspiratory muscles at mechanical disadvantage
- increase dead space = inappropriate high ratio of physio. dead space and tidal volume (VD/VT) = wasted ventilation.

51
Q

What are some abnormalities in gas exchange?

A

Anatomical and physio. changes in lung structure undermine gas exchange
- destruction of alveolar-capillary membrane in emphysema
- ventilation - perfusion (V/Q) inequality (particularly in COPD)

52
Q

What are some respiratory adaptations to Ex training?

A
  • no change in lung volume or diffusion capacity
  • increased stroke volume 2ndary to volume overload hypertrophy
  • increased oxidative capacity
  • increase capillary density
53
Q

Compare the % of total O2 used for breathing between a healthy and COPD person.

A

Healthy
Sitting = 4%
Ex = 10-15%

COPD
Sitting = 15%
Ex = 35-40%

54
Q

Define dyspnoea.

A
  • feeling breathless - subjective to nature
  • frightening sensation - anxiety & depression compounded
  • reuslting from summation of neurological inputs from pulmonary, chemo, mechan -receptors in chest wall and peripheries
  • can be disproportionate to ventilatory limitations
55
Q

How to manage transient exertional desaturation?

A
  • those that use long-term O2 therapy (LTOT) should use supplemental O2 when Ex
  • challenge is managing those that use arterial O2 Sat at rest - do not meet requirements to be presribed LTOT, but demonstrates severe transient exertional desaturation
  • Lvl of desaturation tolerated by clinicians delivering pulmonary rehab program is arbitrary - differs greatly
  • some offer supplemental O2
  • some attempt to min. desaturation by implementing an interval or intermittment training program.
56
Q

How to manage exertional breathlessness?

A
  • BD
  • Rx positions
  • manage anxiety
  • breathing strategies - relaxed/prolonged expiration breathing
  • pace the session
  • establish breathing pattern that matches exertion
57
Q

What is VE?

A

Minute ventilation

58
Q

What is Fb?

A

Breathing frequency

59
Q

what is VT?

A

tidal volume

60
Q

What is VD?

A

dead space ventilation

61
Q

What is VA?

A

Alveolar ventilation

62
Q

What is the normal pulmonary function response to Ex?

A

increase VE = increase Fb * VT –> increase VD and VA

63
Q

What are the effects of changes in breathing patterns?

A

increase Fb = increase VD and VA (less effective)

Increase VT = increase VA (more effective)

64
Q

What is expected in Ex in normal healthy people?

A

Pulmonary function is not a limiting factor
- adequate ventilation and gas exchange
- normal SpO2 (~100%) at max Ex intensities

At max Ex: VE = <65% MVV
- >35% breathing reserve

Normal ventilation/perfusion rate

65
Q

What is the pulmonary response to Ex in pulmonary disease?

A

increase VE = sig. increase Fb * VT = sig. increase VD and VA

Primary function is limiting factor
- at peak Ex VE = MVV (compromised)
- increased VA & gas = decrease SpO2
- increased WOB
- compromised ventilation/perfusion in some pts

66
Q

What are the Ex training impacts?

A
  • impaired lung mechanics
  • inefficient pulmonary gas exchange
  • pulmonary vascular insufficiency
  • abnormal skeletal muscle metabolism
67
Q

What are specific breathing limtations during Ex for COPD pts?

A

Obstructive lung disease: increase airflow obstruction

air trapping (increase FRC) - dynamic hyperinflation

IC** = VT (by sig. increase Fb

68
Q

What are some key factors in Ex training in respiratory patients?

A
  • doesn’t improve pulmonary patho
  • increase oxidative capacity of skeletal muscle (increase Vo2peak)
  • increase fitness = increase function
  • Ex training = increase function w/o sig. measurable gains in Vo2 due to improving…
  • confidence, mobility, anxiety, breathing mechanics, adpative strategies, muscle recruitment efficiency
  • difference between “functional status” and “Ex capacity”
69
Q

What are some Ex options for Pulmonary patients?

A
  • pulmonary rehab (gold standard)
  • home based individualised Ex programs
  • linking w communiyt based Ex professionals
  • community Ex groups
70
Q

What are the recommended FITT-PRO for pulmonary patients?

A

F = 2/7 in PR setting + 2-3/7 independent wtihin 1-2/52
I (initial) = ~80% 6MWT METs: (2.7METS*0.8)=2.2METs); RPE/RPD = 3-4/10
T=40-60min session
T = treadmill, flat ground walking, windjammer, bike, step ups
P= titrate to Sx; ongoing throughout program (time then intensity); use Ex test info (i.e. peak HR = Ex training ceiling HR and Sx eliciting HR/RPE level), daily responses, program and pt goals to guide.

71
Q

What is part of the re-Ax for pulmonary patients?

A

*6MWT, strength tests, SPPB/balance
* evaluate program effectiveness - outcome values
* modify training prescription as approrpiate (Goal: progress >3METs)
* any inclusions ot meet pt goal?

Re-test every 8-12wks or 6-8wk for pulmonary rehab program

72
Q

What are some Ex training considerations for COPD?

A
  • pursed lip breathing
  • allow adequate rests between modes
  • supplemental O2 (SpO2 >88%)
  • optimise med management
  • improved disease self-managed skills
  • low lbl pats: consider short duration repeated bouts w rest
  • consider interval training
73
Q

What are some contra-indications for respiratory patients?

A
  • observations: BP, HR, SpO2 pre/post Ex
  • BP >200/100; SPo2 >85% for rom air and domciliary (88-92% concerned)
  • HR >120bpm dependent on SABA intake- shoulde decrease at rest. If not then NO Ex due to EIB and hyperinflation risk
  • Sx compare with patient normal
    –> nay increased dyspnoea (SOBOE, SOBAR), wheeze, persistent cough, phlegm thickness/colour change, chest tightness, fever, appetite loss
74
Q

What are medication contraindications to Ex?

A

Prednison/oral corticosteroids >25mg due to systemic effects w large doses and long-term effects - catabolic effects on skeletal muscles & long bone integrity

No adh. to preventers >1/7 esp if respiratory Sx present

Nil reliever meds or spacer on person in Ex session

Utilising/following Action Plan iwth rescue meds prescribed in COPD action

75
Q

What is the recommendation for endurance/aerobic training?

A

F = 3-5/7
- 2-3days in PR + 2-3 days independently

I = individualised based on Ex test

RPE: 3-5/10 or 12-14, RPD 4-6
Initial intensity >60^ max. work rate
target training zone: 60-80% peak VO2 (METs)

Time: 20-60mins/session - intervals considered if cannot tolerate continuous
PR 8-12wks –> lifelong

Type: mulitple types
walking as primary & cycling/similar modality type + upper extremity Ex

Progression: titrate to Sx
RPE 3-5/10, RPD3-4/10 or <5
Use Ex test, target intensity, goals, ceiling HR, Ex HR, RPE, RPD and Sx to guide

76
Q

What is the resistance training recommendation for pulmonary patients?

A

F = 2-3 non-consec. days/wk

I=60-70% 1RM or workload allowing 10-15max
- alt. approach, use perception ratings (0-10pt scale)
- mod intensity = 5-6
- high intensity = 7-8

T= >1S 8-12R for upto 8-10Ex with 2-3mins rest between S

Type=target large UB/LB muscle groups
- graded in application, safe to use, motivation, appeals to pt, can be completed in long-term/ FUNCTIONAL!

Progression: increase resistance, R, S and decrease rest intervals

77
Q

What are the Ex benefits of COPD patients?

A
  • facilitates ADLs
  • CV reconditioning
  • improved ventilatory efficiency
  • improved lactate and vent. thresholds
  • desensitised to dyspnoea and fear of exertion
  • increased muscle strength/endurance
  • improvements in flexibility/balance
  • improved body composition
  • enhanced body image
78
Q

How is interval training performed in individuals with COPD?

A
  • experience early actic acidosis due to impaired O2 delivery to peripheral muscle
  • combined skeletal muscle dysfunction - vent. can become severely taxed
  • blood lactate concentrations shown to lower during interal trianing relative to continuous training - reducing breathing stimulus
  • systematic reviews support interval training

NOTE! Potential risk w higher intensities of Ex training

79
Q
A

EXMD4742 (9 decks)

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