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cardio pulmonary hell > respiratory disease > Flashcards

respiratory disease Flashcards

1
Q

low PO2

A

hypoxemia

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2
Q

low O2 in tissues
sciencey word
what does it result from

A
  1. hypoxia

2. results from inadequate oxygen delivery to meet tissue oxidative requirements

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3
Q

causes of hypoxemia
respiratory (4)
other (4)

A

respiratory:
1. reduced inspired O2 tension
2. alveolar hypoventilation (air not moving in and out)
3. impairment of diffusion (ie fibrotic tissue)
4. venous/ perfusion mismatch
others:
1. blood volume loss
2. anemia
3. carbon monoxide
4. hypothermia (lower temp => RBC holding onto O2)

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4
Q

hypercapnia (def [actual #] and cause)

A
  1. increase in PaCO2 >45 torr

2. from inadequate alveolar ventilation in relation to metabolic production of CO2

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5
Q

hypocapnia (def [actual #] and what it causes)

A
  1. low PaCO2 <35 torr

2. increases ventilation

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6
Q

restrictive lung dysfunction (3)
2 basics
1 hallmark of disease*

A
  1. abnormal reduction in pulmonary ventilation, lung expansion is diminished
  2. everything is smaller => less volume of gas moving in and out
  3. hallmark of disease is flow rate stays the same, just the volume decreases
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7
Q

obstruction lung dysfunction (2)

A
  1. diseases of respiratory tract which produce obstruction to airflow
  2. can ultimately affect mechanical function and gas exchange capability
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8
Q

compliance (def)

A
  1. link to P exerted on wall and amt of air lungs can have
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9
Q

pathogenesis of restrictive lung disease (4)

(whats increasing or decreasing)

A
  1. compliance of chest wall and lung decrease => lung is not fully inflated
  2. lung volumes decrease (IRV, tidal volume, and ERV is reduced)
  3. work of breathing increases and we recruit accessory muscles
  4. RR increases because we need to breath more to maintain minute volume (more breaths with less O2)
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10
Q

identifying RLD by spirometry
what measures do we use
what happens to shape
what results do we consider diseased

A
  1. TLC and VC are the two most common measures used to identify RLD
  2. on the spirograph the shape is the same, just smaller
  3. if change of 20% (in either direction) we consider person diseased
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11
Q

clinical manifestations of RLD
signs (6)
symptoms (3)

A

signs:
1. tachypnea
2. hypoxemia
3. decreased breath sounds on auscultation
4. decreased lung volumes
5. decreased diffusing capacity (because of widening of interstitial spaces)
6. cor pulmonale
symptoms:
1. dyspnea (complaint of shortness of breath)
2. cough- dry/ non-productive (*opposite from OLD)
3. emaciation - because breathing causes shortness of breath

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12
Q

cor pulmonale (def and what it can lead to)

A
  1. right side heart failure because pressures got so high

2. can lead to pulmonary hypertension

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13
Q

pathogenesis of OLD (4)
what happens to flow rates? why?
loss of elastic recoil leads to what?
whats increasing or decreasing? (2)

A
  1. altered expiratory flow rate because narrowing => increased airflow resistance
  2. loss of elastic recoil because airways tend to collapse which leads to hyperinflation
  3. increased residual volume
  4. work of breathing increases
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14
Q

4 pathological (physical) changes (in bronchi) resulting from OLD

A
  1. increased mucus prodiction/ impaired secretion
  2. inflammation of mucosal lining of the bronchi and bronchioles
  3. muscosal thickening
  4. spasm of bronchial smooth muscle
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15
Q

why work of breathing is increased with obstructive lung disease (4)

A
  1. respiratory muscles must work harder to overcome increased airway resistance
  2. diaphragm excursion may be limited due to hyperinflation of lungs
  3. alveolar ventilation is reduces because hyperinflated areas cause distortions of perfusion areas
  4. alveolar- capillary membrane surface area may be reduced
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16
Q

clinical manifestations of OLD
signs (5)
symptoms (4)

A

signs:
1. hypoxemia
2. cor pulmonae
3. pulmonary hypertension because of poor bf to certain areas means you dont send blood there
4. increased production of mucous/ impaired clearance
5. polycythemia => viscous blood => increased change of clot
symptoms:
a. chronic cough
b. expectoration of mucus (differs from RLD)*
c. wheezing (asthma)
d. dyspnea on exertion (DOE)

17
Q 
pulmonary fibrosis
 disease
 etiology
 clinical manifestations (3)
 PFTs- 4 decreased measures 
 what happens to flow rates 
 what happens to diffusing capacity? 
 does anything increase?
A
  1. restrictive: inflammatory process involving all components of alveolar wall that progress to gross distortion of lung architecture
  2. etiology- unknown , maybe viral genetic or autoimmune
  3. clinical manifestations
    a. dyspnea
    b. repetitive non-productive cough (restrictive)
    c. weight loss/ anorexia
  4. PFTs
    a. decreased TLC, VC, FRC and RV
    b. normal or slightly decreased flow rates
    c. diffusing capacity is decreased
    d. as disease progresses the Vt decreases and RR increases
18
Q

pulmonary fibrosis
breath sounds
CV findings
treatment

A

(restrictive disease)

  1. breath sounds: dry rales and decreased breath sounds
  2. CV findings: pulmonary hypertension (from R sided heart failure)
  3. treatment- steroids, O2 and supportive measures
19
Q 
asthma
 disease
 etiology
 pathophysiology
 clinical manifestations (3)
 treatment
A

obsructive

  1. disease of airways characterized by increased responsiveness of tracheobronchial tree to a variety of stimuli
  2. triggered by allergens, because airways are dynamic
  3. pathophysiology: most allergens are airborne, initially they must be abundant but once sensitization has occurred, only minute quantities are necessary to provoke bronchospasm
  4. clinical manifestations:
    a. wheezing* on expiration
    b. during attack- acute respiratory distress = chest is hyperinflated
    c. forced expiratory vol in 1 second (FET)= are reduced during attack
  5. treatment: relieve bronchspasm with drugs
20
Q 
Bronchiectasis
 disease
 etiology (3 disease processes)
 clinical manifestations (3)
 PFTs - 2 decreased, 1 increased
A

obstructive

  1. permanent abnormal dilation and distortion of one or more bronchi that is caused by destruction of elastic and muscular components of bronchial walls (occurs in cystic fibrosis)
  2. etiology: pertussis, obstruction, cystic fibrosis
  3. clinical manifestations
    a. cough
    b. recurrent infections and hemoptysis
    c. mucopurulent sputum and fetid breath
  4. PFTs; reduced FVC, FEV1,
    e. increased RV
21
Q

bronchiectasis
breath sounds (3)
CV findings (3)
treatment

A

obstructive
breath sounds: bronchial breath sounds, rales, rhonchi with mucus retentions
CV findings:
a. bronchial artery enlargement
b. l-> r shunts
c. pulmonary hypertension (from cor pulmonale)
treatment: alleviate symptoms of disease and control infection

22
Q 
emphysema
 disease
 pathophysiology
 clinical manifestations (2)
 PFTs 1 decrease, 3 increases
 breath sounds
A

obstructive

  1. alveolar or parenchyma disease- abnormal and permanent enlargement of air spaces => loss of recoil, elastic collapse and chronic airway obstuction
  2. pathophysiology; degradation of elastin from smoking cigarettes and resultant chronic inflammation
  3. clinical manifestations:
    a. dyspnea
    b. rosy skin tones (common from CO2 retention)
  4. PFTs- decreased FEV
    d. increased - FRC, RV, and TLC\
  5. breath sounds- distant because recoil not good
23
Q

effects of SCI on pulmonary pathophysiology
paradoxical breathing begins at what level of injury?
what happens to compliance over time? why?

A
  1. paradoxical breathing if injury C5 or lower and you lose abs and supporting muscles
  2. over time compliance is decreased due to shallow breathing and atelectasis w/i lung
24
Q 
effects of ankylosing spondylitis
 disease
 pathophysiology
 PFTs 2 decreases, 2 increases
 breath sounds
 symptoms (3)
A
  1. chronic inflammatory disease of spine => immobility
  2. pathophysiology- decreased compliance of chest wall
  3. PFTs
    a. VC and IC are decreased
    b. RV and FRC are increased
  4. breath sounds are generally normal
  5. symptopms: DOE, productive cough, hemoptysis (cough up blood because inflammation and lesions => bleeding)
25
Q

chronic bronchitis (2)
what it is
where it starts, where it goes
breath sounds

A
  1. hypersecretion of mucus sufficient to produce productive cough on most days
  2. begins in larger airways and progresses to smaller as it gets worse- the degree which small aiways are involved is the determining factor in disability* (because this is where gas exchange occurs)
  3. breath sounds are associated with rales (crackles)
26
Q

brain injury affects on respiration

A
  1. if they have physical impairments (loss of movements) this affects breathing
27
Q

chronic liver conditions affect on respiration

A

enlarged liver (or fluid in abdomen) leads to lungs on fully expanding = restrictive disease side effects (lung volumes decreased)

28
Q 
SCI
PFTs
 3 decreases, 1 increases
 what happens to flow rates?
 what happens if abs are knocked out
A
  1. TLV, VC, IC are decreased
  2. flow rates decreased
  3. RV increased
  4. ERV is eliminated if not active expiration

cardio pulmonary hell (7 decks)

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