Cardiopulm - Pulm - Restrictive Lung Disease

Front 1

• How is respiratory muscle strength measured?
  
• Endurance?
• What portion of max is typical WOB at rest?

Back 1

• Max inspiratory pressure and max expiratory pressures

• Max voluntary ventilation (MVV) and breathing endurance time (amnt of time pt can sustain sub-max contraction of inspiratory muscles)

• ~5% of max

Front 2

What does effective and efficient inhalation require?

Back 2

• Low resistance to airflow
  
• Compliance of lungs and chest wall
• Adequate diaphragm excursion (physical space and ability to contract)
• Neuromuscular function, strength, & endurance
• No pain
• Adequate exhalation beforehand

Front 3

What does effective and efficient exhalation require?

Back 3

• Low resistance to airflow
• Elasticity of lungs and chest wall
• Adequate expiratory muscle function
• No pain
• Adequate inhalation beforehand

Front 4

What does effective and efficient gas exchange require?

Back 4

• Adequate surface area
  
• Adequate membrane permeability
• Adequate partial pressure differences
• Time
• Adequate HgB levels to carry O₂ in blood

Front 5

• When is somebody considered in respiratory failure?
  
• What are the two types of respiratory failure?
  

Back 5

• When ventilatory pump cannot meet demands at rest, thus there is inadequate oxygenation to maintain tissue viability
• Type I: Primarily hypoxic (PaO₂ < 60 mmHg; >80 is considered normal)
  
• Type II: Primarily hypercapnic (PaCO₂ > 50 mmHg)
  

Front 6

• What is the 1º difficulty in restrictive lung disease?
  
• Why is this an issue?
• What does this mean regarding pressure changes in the body?

Back 6

• Pts have difficulty getting air in
• ↓ lung and chest wall compliance
  
• For a given amount of air to come in, PW-RLD need to generate a much greater negative pressure to drive the air in

Front 7

• How do lung volumes change in PW-RLDs?
  
• What is this a result of?

Back 7

• ↓ volumes and capacities, but expiratory maneuvers and ratios stay the same; TV preservation attempted at sacrifice of ERV/IRV
• ↑ physiologic dead space leading to less ability to tap into reserve volumes

Front 8

• How would WOB change in PW-RLDs?
• How could emaciation result?

Back 8

• WOB would ↑ 2º need to overcome restriction
• ↑ energy expenditure via WOB and difficulty of simultaneous breathing/eating

Front 9

• How would respiratory rate change in PW-RLD?
  
• How would breath sounds present in PW-RLD?
• How would ventilatory index change in PW-RLD?

Back 9

• ↓ inspiratory volume would lead to tachypnea
  
• Less air is flowing through airways, so there'd be decreased breath sounds; Crackles may be heard during inhalation 2º opening of airways
• VI = could approach ~.8 (Ve/MVV) 2º ↓ MVV. .8 is expected at VO₂max

Front 10

• How do pulmonary arteries react to hypoxia without hypercapnia? Why?
  
• What happens to alveoli in RLD? What does this do to V/Q matching?
• How, then, does RLD affect the (R) side of the heart? Why?
  

Back 10

• They vasoconstrict to redirect bloodflow to alveoli with greater ventilation
• Alveoli are hypoxic, leading to V/Q mismatching
• Alveolar hypoxia leads to pulmonary vasoconstriction, which causes the (R) heart to pump harder and (R)-sided failure (cur pulmonale)

Front 11

What are other characteristics of RLD

Back 11

• Dry, non-productive cough
• Dyspnea, initially with exercise
  
• Secretions are not a 1º cause, but may build-up and become 2º cause of illness/re-admission
• ↓ DLCO (air doesn't flow from alveoli into blood well, leading to ↑A-a gradient, ↓ SpO₂)
  

Front 12

• What is hyaline membrane disease aka?
  
• Who develops hyaline membrane disease?
  
• When is surfactant typically produced? When does it become mature, functional surfactant?

Back 12

• Respiratory Distress Syndrome (RDS)
  
• Premature infants with immature surfactant
• 26-28 weeks gestation, matures by 36 weeks

Front 13

• What characterized bronchopulmonary dysplasia?
  
• Who is at greatest risk?

Back 13

• Chronic inflammation and fibrosis
• Babies who are >10 weeks premature, weigh < 2.5#, have breathing problems at birth, or needed long-term breathing support or O₂

Front 14

• What is idiopathic fibrosis?
  
• What effect does the inflammation have?
• What is life expectancy at dx?

Back 14

• Inflammtory process of the lungs with idiopathic, mid-late life onset
  
• Leads to tissue destruction and scarring/fibrotic areas
• 3-5 years

Front 15

• What is pneumonia? What may cause it?
  
• What is pneumothorax?
• Hemothorax?

Back 15

• Infectious process within the lungs caused by bacteria, virus, or fungus
  
• Air in the pleural space
• Blood/bleeding into the pleural space

Front 16

• What is ARDS? What causes it?
  
• What are common causes?
• What are the phases of ARDS?

Back 16

• Adult respiratory distress syndrome, caused by some acute lung insult
  
• Barotraumas or volume trauma from mechanical ventilation
• Acute Phase: Alveolar injury and inflammation leading to ∆ in alveolar permeability
• Sub-acute Phase: Alveolar fibrosis/capillary obliteration
• Resolution: Varying degrees of tissue death/fibrosis

Front 17

• What is pleural effusion?
  
• What is pulmonary edema?
  
• What is pulmonary embolism?
  

Back 17

• Fluid within pleural space
• Fluid build-up within the parenchyma
• Embolic arterial blockage of pulmonary vasculature, usu. the result of DVT