Pathophysiology Flashcards

1
Q

Types of pulmonary disease that limit exercise tolerance

A
  1. obstructive diseases (high airway resistance/obstruction)
  2. restrictive diseases (fibrosis-loss of alveoli, non-compliant lung)
  3. chest wall defects (muscle weakness/chest wall deformity)
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2
Q

what is CODP characterized by?

A

by progressive development of airflow limitation, not fully reversible, caused by chronic inflammation of the airways and lung parenchyma

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3
Q

COPD and mortality

A
  • 4th leading cause of death

- only cause of death in USA that continues to climb

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4
Q

what causes COPD

A

long-term exposure to noxious gases and particles

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5
Q

three major mechanisms of COPD

A
  1. Loss of elasticity and alveolar attachments to airways (emphysema)
  2. Narrowing of small airways lumen (inflammation and scarring)
  3. Excessive secretion of mucus that blocks the airways
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6
Q

More of what COPD is characterized by

A
  • High airway resistance (low FEV1%) –> Hyperinflation at end-expiration.
  • Patients have a high functional residual capacity which encroaches on inspiratory capacity
  • Because of hyperinflation inspiratory muscles work more than normal, and are mechanically inefficient.
  • Skeletal muscle deconditioning and/or myopathy
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7
Q

emphysema and barrel chest

A

• Loss of elasticity (increased compliance of the lung) in emphysema leads to hyperinflation of the lungs.
• Hyperinflation leads to increased chest wall diameter (called “barrel-
chest”)

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8
Q

obstructive disease has lower

A

FEV and FEV1%

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9
Q

what is the limiting symptom at rest and exercise of COPD

A
  • Dyspnea = perceived difficulty or distress in breathing

* Shortness of breath

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10
Q

what does poor V/Q matching lead to?

A

increased need for VE (higher VE ) at given work rate to eliminate CO2 and maintain PaO

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11
Q

why is work of breathing increased with COPD

A
  • Due to airflow obstruction (high resistance)

* Due to inefficient breathing mechanics (hyperinflation)

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12
Q

COPD and energy cost of breathing

A
  • low VO2max
  • increased energy of breathing, lactic acidosis at low work rates –> When severe energy cost during exercise can reach 40%!
  • This energy cost “steals” blood away from exercising muscles –> Some COPD pts limited by leg fatigue, not dyspnea, during exercise
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13
Q

what can therapeutic interventions that decrease work of breathing do?

A

increase exercise tolerance

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14
Q

strategies for decreasing dyspnea

A
  • bronchodilation
  • exercise therapy
  • oxygen therapy
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15
Q

bronchodilation for decreasing dyspnea

A
  • Decreases Hyperinflation & Dyspnea

* Increases breathing efficiency

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16
Q

what does oxygen therapy decrease?

A
  • VE
  • Breathing Frequency
  • Dyspnea
  • Hyperinflation
  • Improve Metabolic Status
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17
Q

what is much of the disability in COPD related to?

A

concurrent deconditioning

maybe some evidence for disease related muscle disfunction

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18
Q

evidence for muscle dysfunction in COPD

A
  • low muscle mass and strength, muscle aerobic enzymes and capillarity, and OBLA
  • slow rise in VO2 at exercise onset –> increased O2 deficit and reliance on anaerobic metabolism
  • exercise training improves muscle tolerance and muscle function
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19
Q

Potential abnormalities in muscle structure and function in patients with COPD

A

CS

HADH

20
Q

Mechanisms Underlying Muscle Dysfunction In COPD

A

• Deconditioning
• Malnutrition
• Skeletal muscle myopathy
— Associated with chronic corticosteroid use
— Associated with chronic hypoxia, hypercapnia, and/or inflammatory cytokines
• Low circulating androgens

21
Q

Purposes Of Exercise Training In Persons With Pulmonary Disease

A

Exercise training has NOT been shown to affect the progression or reversal of the actual disease pathology /mechanisms

22
Q

Benefits Of Regular Exercise Training

A
  1. Improve functional capacity for daily activities (work tolerance) via
    improvements in muscle fitness, flexibility, cardiorespiratory endurance
  2. Reduced VE during submaxexercise
  3. Shift OBLA to higher intensity by increasing skeletal muscle aerobic
    capacity
  4. Improved coordination and economy of movement, respiratory muscle endurance, and improved work tolerance by reducing dyspnea severity during submax exercise
23
Q

Selected Evidence Based Clinical Practice Guidelines for Pulmonary Rehabilitation

A
  1. Exercise training of muscles of ambulation recommended as a mandatory component of pulmonary rehabilitation for patients with COPD
  2. Lower-extremity exercise training at higher exercise intensity has greater physiologic benefits than lower intensity training in patient with COPD
  3. Both low-and high-intensity exercise has clinical benefits for patients with COPD
  4. Addition of a strength training to pulmonary rehab increases muscle strength and mass
  5. Supplemental oxygen should be used during rehab exercise training in patients with severe exercise induced hypoxemia
24
Q

A major difference between testing in a patient with cardiac disease and pulmonary disease

A

increased emphasis on measuring pulmonary function before, during and after the testing

25
Q

General Considerations For Exercise Testing For Persons With Pulmonary Disease

A
  • Pulmonary gas exchange measurements –> static and dynamic lung function tests and respiratory muscle tests
  • ALWAYS includes a measurement of arterial oxygenation: pulse oximetry (SaO2), arterial blood gases (PaO2, PaCO2)
26
Q

Considerations For Exercise Prescription for pulmonary disease

A

•In patients with functional limited by ventilatory variables, prescription of intensity can’t be made based on % age predicted HRmax or HRR –> Monitor S/S dyspnea and breathlessness to adjust individualized exercise prescription

No one optimal strategy

27
Q

FITT Recommendations in COPD - Resistance Training

A
  • F: 2-3 days per wk, non-consecutive days
  • Strength: 60-70% of 1RM for beginners; ≥80% 1 RM for experienced lifters; 2-4 sets, 8-12 reps
  • For endurance, <50% 1RM, 1-2 sets, 15-20 reps
28
Q

FITT Recommendations in COPD - Aerobic Training

A
  • F: 2-3 days per wk, non-consecutive days
  • Strength: 60-70% of 1RM for beginners; ≥80% 1 RM for experienced lifters; 2-4 sets, 8-12 reps
  • For endurance, <50% 1RM, 1-2 sets, 15-20 reps
29
Q

Modified BORG Dyspnea Scale

A

0: nothing
0.5: very, very slight
1: very slight
2: slight
3: moderate
4: somewhat severe
5, 6: severe
7, 8: very severe
9: very, very severe
10: maximal

30
Q

During exercise, oxygen supplementation is indicated if:

A
  • PaO2 < 55mmHg
  • SaO2 < 88%
  • Titrate O2 flow to maintain SaO2 at >=90%
31
Q

Asthma is characterized by:

A

an increased responsiveness of the airways to various stimuli and manifested by a diffuse (functional) narrowing of the airways, that changes in severity either spontaneously or as a result of treatment

32
Q

Underlying pathology of asthma is believed to involve:

A

chronic inflammatory processes

33
Q

What is Exercise-induced Bronchospasm

A

15% or greater postexercise reduction of FEV1 or peak expiratory flow rate (PEFR) from pre-exercise values after standard
submaximal exercise stress

34
Q

what can EIB occur with?

A

chronic asthma as well as in persons with no evidence of asthma at rest

35
Q

what falls with EIB

A

V1%

FEV1/FVC

36
Q

EIB Symptoms/Signs Can Occur During Or Post Exercise

A
  • Wheezing
  • Chest tightness
  • Shortness of breath (dyspnea)
  • Cough
  • Mucus production
  • Need to stop exercising
37
Q

Bronchospasmic Conditions During Exercise

A

• Cold, dry air
• Pollens, dust, air pollution (in individuals with chronic airway hyperresponsiveness)
• The more intense and longer in duration the exercise
(resulting in a larger VE and loss of fluid) the more bronchospasmicthe exercise

38
Q

Why is swimming less bronchospasmic than running or cycling (other than the humid conditions)?

A
  • Interrupted nature of breathing pattern (airflow)
  • Lower ventilation volume
  • Greater catecholamine response b/c of activation of a smaller (upper body) muscle mass to do the same work
39
Q

Potential Causes Of EIB

A
  • Release of “bronchoconstrictor substance” in response to changes in osmolality of the periciliary fluid, from airway fluid loss during conditioning of inspired air (humidification , filtering and warming), mast cell release of histamines, leukotrienes, prostaglandins
  • Result: inflammation, can trigger neurally-mediated constriction, or act directly on smooth muscle
40
Q

airway irritation during exercise –>

A

release of chemical modulators –> smooth muscle constriction, increased mucous –> increased airway resistance –> EIB symptoms- Wheezing, coughing, dyspnea

41
Q

standard test for EIB

A

• Standard test: 6-8 min of exercise (usually treadmill) at 75-85% hrmax
• Under asthmogenic conditions: cold dry air, use of treadmill running, no premedication or caffeine
• 80-90% of asthmatics develop EIB after this test
• Fall in FEV1% or PEFR:
– Mild: 10-24%
– Moderate: 25-39%
– Severe: >40%

42
Q

Avoiding EIB - Refractory Period

A

• About 50% of asthmatics have a refractory period after the first bout of exercise
• Such that a second bout will provoke EIB response that is
~50% of the initial response
– Lasts 1-4 hours
– Value of a warm-up!

43
Q

Avoiding EIB- Pharmacology

A
  • Aerosol beta-2 agonist: at least 15 min prior to exercise
  • also effective in interrupting an EIB in progress (“rescue inhaler”)
  • Cromolyn sodium (mast cell stabilizer)-prior to exercise
  • Inhaled corticosteroids- usually daily use
44
Q

Symptom refractory period

A

sub threshold warmup intense enough to tax system without causing symptoms –> inhaler use immediately following warmup –> 20-30 minute interval for medication delivery to tissues –> symptom free exercise

45
Q

Exercise And Glucose Transport

A

• During exercise and continuing for several hours —there is an insulin-independent, contraction-initiated increase in glucose uptake via translocation of pre-formed GLUT4 transporters to the cell surface

46
Q

most prevalent modifiable risk factor for CV disease

A

sedentary lifestyle