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CardioResp Phys HK4550 > Midterm II > Flashcards

Midterm II Flashcards

1
Q

Functional residual capacity

A
  • net work is zero (no inspiratory/expiratory)
  • point at end of normal exhale (not forced exhale)
  • pressure lungs = pressure of ribcage (pressure of ribcage wants to pop open = lungs wanting to collapse)
  • can’t be measured with spirometer
  • increases in COPD vs healthy
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2
Q

Dead space

A
  • air in trachea
  • inhaled but not participating in gas exchange (atmospheric air)
  • body weight in lbs (ideal) = dead space in mls
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3
Q

Non steroidal anti-inflammatory drugs (NSAIDs)

A
  • inhibit COX I and COX II (cyclooxygenase)
  • stomach ulcers issue because COXI involved in muscosal lining of stomach
  • COXII related to inflammation
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4
Q

Neuromuscular transmission failure

A
  • impairment of AP across neuromuscular membrane (diaphragm)
  • not seen in vivo with human/animal models for respiratory failure
  • can only be produced in vitro using supra physiological stimulation rates
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5
Q

High frequency fatigue

A
  • occurs due to some sort of load
  • recovers quickly with rest
  • related to ion imbalance (K+)
  • measured using stimulation frequencies above 50Hz
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6
Q

Z line streaming

A
  • normal muscle zline vertical
  • no longer straight with damage, pulled in one direction
  • evidence of fatigue or injury
  • ultrastructural
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7
Q

Protein Oxidation

A
  • increase in protein oxidation with fatigue/mechanical ventilation
  • when a protein is oxidized, biological function decreases
  • proteasome pathway removes oxidized proteins
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8
Q

2a)
What is the function of CK in a cell?
- 1 mark

A
  • creatine kinase

- transfers “high energy” phosphate from ATP to creatine or phosphocreatine to ADP

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9
Q

2b)
why is ck NOT a good marker for skeletal muscle injury?
- 3 marks

A
  • lacks specificity (found in every cell of the body)
  • lacks sensitivity (low damage = no increase)
  • control range for population is large (40-500 units/L - adults only), making small increase in any one individual (need baseline; individual increase +/- 10 units/L)
  • CK detectable in everyone, better to have a maker that is only detectable when the disease/injury is present
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10
Q

2c)
despite problems, why was it used in clinical study to strongly suggest respiratory muscle in patients with acute exacerbations of asthma?
- 4 marks

A
  • load on respiratory muscles increases as FEV1 decreases
  • increased load = increased muscle damage
  • increased damage = more CK is released from damaged muscle
  • levels of CK reflect degree of load on respiratory muscles
  • with decreases in FEV1, there are increases in CK
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11
Q

FEV1

A
  • forced expiratory volume
  • indicator of airway resistance
  • normal/healthy range 70-80%
  • decrease FEV1 correlated with increase CK (indicating increased muscle injury)
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12
Q

3)
Problem associated with ventilator
- 4 marks

A
  1. atrophy (fast in diaphragm)
    - decrease cross sectional area (CSA) proportional to muscle force
    - CSA proportional to time on ventilator
  2. ultrastructural damage (myofibrils)
    - swollen mitochondria
    - myofibril damage
    - z line streaming
  3. Altered mechanical signals (decreased blood flow, loss of negative intrathoracic pressure)
    - decreased protein synthesis (MHC mRNA - myosin heavy chain **indicator)
    - increased oxidative proteins
    - increased protein degradation (calpain II)
    - increased protease activity (calpain II - ATP independent) + (Ubiquitin-proteasome - ATP dependent)
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13
Q

Oxidation is associated with

A

loss of proteins’ biological function

  • classical assay: formation of aldehydes and ketones
  • proportional to damage
  • oxidative stress caused by mechanical ventilation
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14
Q

Stress increases the production of?

why does this increase CK production?

A

“Damaged” proteins

CK aids ATP dependent proteasome pathways
- transfers “high energy” phosphate from ATP to creatine or phosphocreatine to ADP

CrP + ADP –> CK + ATP
- more CK in blood

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15
Q

3 ATP dependent pathways

1 ATP independent proteasome

A

*Ubiquitin-pathway
Sumo
Nedd (can be used in combination)

Calpain II
- targets myofilament proteins

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16
Q

4a)
Skeletal muscle “fatigue” definition
- 2 marks

A
  • loss in capacity for developing force and/or velocity
  • resulting from muscle activity under “load”
  • reversible by rest
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17
Q

4b)
Force (pressure) / Frequency graph
describe how one would be generated in a human subject

A

Y: force (Pdi / Pdi max) % 0-100
X: frequency (Hz) 0-100

control and post fatigue
25-30mins
- low frequency still a gap (damage / injury to muscles, hours-days recovery)
- high frequency (60hz) minimal gap (ion homeostasis K+, fast recovery)

— 2 pressure catheters need to be inserted through the nose into stomach (Pab) and esophagus (Pes) to measure Pdi (Pdi = Pab - Pes)
stimulate phrenic nerve while the airway is occluded

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18
Q

4c)
explain why force frequency curve can’t be used to detect central failure
- 2 marks

A
  • not measuring action potential or nerve stimulation (not measuring brain activity or phrenic nerve)
  • measuring force in diaphragm; central failure could be present and not know it
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19
Q

4d)

what technique is used to detect central failure

A

twitch occlusion

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20
Q

5)
how are both CO2 and O2 perfusion limited when the pressure gradient for CO2 is 1/10th of O2?

  • 3 marks
A

Vgas = A/T x D x (p1 - p2)

D = Sol/ MW^-2

CO2 is approximately 20x more soluble than O2
MW is approximately the same
CO2 greater D (diffusion coefficient)

VCO2 > VO2 despite the pressure

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21
Q

Perfusion limitation

A

P1 = P2

with Vgas = A/T x D x P1-P2

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22
Q

6
reasons why resp. muscle failure techniques aren’t used clinically
- 4 marks

A 
invasive
- patient discomfort
technologically demanding
- equipment and staff
expensive 
time consuming
non-specific
non-sensitive
requires training
need control value
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23
Q

8a)
why does pulmonary blood flow in a capillary depend on its vertical position in the chest relative to the heart
- 4 marks

A

Top: PA > Pa > Pv (closed)
Mid: Pa > PA > Pv (partially closed)
Bot: Pa > Pv > PA (open)

Pa is working against gravity in the upper portions of the lung.

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24
Q

8b)

graph how alveolar hypoxia affects pulmonary blood flow

A

Y: percent blood flow
X: Alveolar PO2

Blood flow decreases with decrease alveolar blood flow below normal levels (PO2 decreases below 100 mmHg)

80% at 100mmHg
gradual increase above
steep decline below

Blood flow shunted from non-ventilated regions to ventilated regions

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25
Q

Shunting blood

mechanisms

A

from non-ventilated to ventilated regions

  • Drop in PO2 causes vasoconstriction
  • when sick, phlegm inhibits ventilation
  1. Nitric Oxide
  2. ET-1
    - methods not well known

mechinisms have no effect with global hypoxia
- COPD patients affect the whole lung

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26
Q

8c)

when is shunting blood useful? when is it counter productive?

A

useful:
local non-ventilatory regions (mucus, atelectasis)

not:
whole lung hypoxia (COPD) - no where to shunt blood

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27
Q

Two factors determining blood flow?

A

Q = P1-P2/R

pressure gradient and resistance

R = 1/r^4

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28
Q

what holds vessels open around alveoli?

A

Elastin (spiny)

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29
Q

Respiratory failure

A

(pump failure)

- inability to sustain an expected level of pressure (force) production, sometimes evident as apnea

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30
Q

Ventilatory failure

A

(hypercapnic failure)

alveolar ventilation “insufficient” to achieve adequate “CO2” elimination resulting in hypercapnia

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31
Q

Hypercapnia

A

pCO2 > 50mmHG

  • caused by ventilatory failure
  • insufficient CO2 elimination through alveoli
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32
Q

Central failure

A

decrease in central neural output “despite” adequate or even increased stimuli

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33
Q

Neuromuscular transmission failure

A

impaired transmission of action potential across neuromuscular junction
- not possible in vivo

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34
Q

Problems vs causes

A

Problems

  • respiratory failure
  • ventilatory failure

Causes

  • central failure
  • peripheral muscle fatigue
  • neuromuscular junction failure (not possible in vivo)
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35
Q

Peripheral muscle fatigue

A

impaired output

ex. diaphragm weakens like muscles do during exercise (Rare)

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36
Q 
Blood flow pulmonary circuit
4 relationships (graphs)
A
  1. change with articular or venous pressure
    - Increase pressure / decrease resistance
    - mechanisms: distension and recruitment
  2. height of the lung
    - BF vs height
  3. Lung volume
    - Volume vs vascular resistance
    - Increase resistance above and below FRC
  4. Alveolar PO2
    - Alveolar PO2 vs % blood flow
    - Bf decreases in hypoxic vascular region (<100mmHg)
    - shunting of blood
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37
Q

Main reasons for lack of studies that have clearly identified cause of respiratory failure in patients

A
  • No standard model of respiratory muscle dysfunction
  • Development of respiratory failure poorly characterized
  • Central “failure” or peripheral “fatigue” appear separately or in combination depending on specific situation (no agreement in contributions)
  • lack of “specific” and “sensitive” marker of peripheral muscle fatigue that is clinically useful
38
Q

One method to test for peripheral fatigue

3 problems?

A

Elevated serum creatine levels following acute exacerbations of asthma
- ck levels correlated with severity of airway obstruction (FEV1)

  • not tissue specific
  • not sensitive (+/- 10 units/L)
  • only adults
  • wide baseline of a population (40-500 units/L)
39
Q

biomarker sensitivity vs specificity

A

sensitivity - positive test when disease is present (no false negatives)

specificity - negative when disease is not present (no false positives)

40
Q

Measures of skeletal muscle injury

A

direct
- muscle biopsy (histology)

indirect

  • muscle soreness (DOMS)
  • max pressure / force generation
  • serum markers (CK, myoglobin, LDH, aldolase)
41
Q

different types of creatine kinase

A

CKm - muscle
CKb - brain
CKmit - mitochondria

Combinations:
ADP --> ATP
-CKmm
-CKmb
-CKbb

ATP –> ADP
CKmit

42
Q

Fatigue

A
  1. lost capacity for developing force/velocity of a muscle
  2. result from muscle activity under load
  3. reversible by rest
43
Q

Weakness

A

NOT reversible by rest

  • nerve damage
  • genetic disorder
44
Q

Factors affecting surface area

A

disease*

emphysema (effects of smoking)
atelectasis (collapsed alveoli)
cancer
age (emphysema)
mucus / pulmunary edema
45
Q

collapsed alveoli

A

atelectasis

46
Q

factors affecting pressure gradient

A
  1. altitude
  2. increase Vd (dead space volume)
  3. decrease ventilation
  • non-disease
47
Q

atelectasis

A

collapsed alveoli

  • effects surface area when calculating Vgas
  • surfactan opens alveoli
  • released during lung stretch (deep breathes)
48
Q

srufactan

A

opens alveoli

  • released during lung stretch
  • deep breathes therefor make it easier to breathe
  • surgery (anesthetic) prevents this response
49
Q

factors affecting thickness of alveolar membrane

A
  1. mucus / pulmonary edema

2. fibrosis –> collagen (12 dif types), elastin etc

50
Q

Perfusion limited

A

P1 = P2
diffusion stops

O2
approx. 0.25 sec
CO2
approx .125

51
Q

Perfusion diffusion limitations graph

A

partial pressure / distance (time)

up to .75
perfusion occur .25 for both O2 and CO2
large reserve capacity

52
Q

Extreme athletes Pr / distance graph

A

time less than .2sec

can become “diffusion” limited

53
Q

Abnormal perfusions graphs

A

no problem at rest
become “diffusion limited” with exercise
(exercise shortens time, lowers reserve capacity

54
Q

Reserve capacity

A

extra time/distance of blood in alveoli after gas exchange

- shortens with exercise in healthy individual

55
Q

Approx. time for blood to travel through alveoli

A

.75sec

perfusion limited .25sec

56
Q

Gas exchange in alveoli at elevation

A

steep curve no longer exists (pressure gradient decreased)

-healthy individual still perfusion limited, take longer to reach

57
Q

circulatory functions of lungs

A
  1. immune
  2. gas exchange
  3. clear blood clots
  4. skin cells
  5. metabolism of vasoactive substances
    a) activation of
    AI –(ACE in lung)–> AII (incr. BP)
b) inactivation of
NE/epi
seratonin
brodykinin
PGs

archidonic acid –> PG (sensitize pain/inflammation control)

  • needs cyclogene (cox 1 and 2)
  • NSAIDS inhibit
58
Q

mean pressure in pulmonary circuit / systemic circuit

A

pulm 15mmHg

syst 100mmHg

59
Q

Flow of pulmonary and systemic circuits

A

BOTH

rest: 6 L/min
exercise: 20 L/min

60
Q

Pressure gradients of pulmonary and systemic circuits

A

systemic

rest: 100-2 – 98mmHg
exercise: 120mmHg

pulmonary

rest: ~10mmHg
exercise: ~16mmHg

61
Q

Resistance of pulmonary and systemic circuits

A

systemic

rest: 16.7
exercise: 6

pulmonary (VERY LOW)

rest: 1,7
exercise: 0.8

mmHg/L/min**

62
Q

To increase flow

A

increase pressure gradient
decrease resistance

two methods

  • recruitment
  • distension (when Pv greater than PA
63
Q

Lung volume / vascular resistance relationship

A

resistance lowest at FRC (95-140 ish)

resistance increases below - capillaries are in series, expansion of capillaries will increase resistance of others

resistance increases above - capillaries stretch from expansion of alveolar space, increasing resistance
- COPD increases work of breathing above FRC

64
Q

Alveolar PO2 / Blood Flow relationship

A

Graudual increase above 100mmHg (above 80%)
steep decline below

below 100mmHg "hypoxic vasoconstriction region"
Local shunting of blood
- from non to ventilated regions
2 mechnisms
- Nitric oxide
- ET-1

NO effect with global hypoxia
- COPD patients

65
Q

COPD can die from what unrelated problem?

A

“right” heart failure (pulmonary side)
too much pressure to deal with increased resistance

2 reasons:

global hypoxia
- No where to shunt blood

increased lung volume
- increases resistance

66
Q

Respiratory failure objective (3)

A
  1. describe the limitation of current models in respiratory failure
    - species, anesthetic, age, health status, gas, type of load (resistive ex. straw, threshold ex. pressure, elastic ex. ballon), size of load, end point
    - NO Consistancy, failure poorly characterized in humans
  2. describe the limitations of current markers of respiratory fatigue
    - CK (40-500units/L, every tissue, adults only)
    - myoglobin, LDH, aldolase
  3. how can central failure and peripheral fatigue be determined in a patient
    - central “twitch occlusion” (failure when twitch at max effort - phrenic nerve)
    very accurate, too long, expensive equipment, few trained people
    - peripheral
    diaphragm fatigue, ultrastructual injury, power spectrum, detection of sarcolemmal damage (procion orange), biomarkers (CK), weaning from mechanical ventilation
    **occur in combination or separate, no agreement
67
Q

clinical studies of muscle fatigue

A
  1. elevated serum CK acute exacerbations of asthma

2. weaning from mechanical ventilation

68
Q

low vs high frequency fatigue

A

high

  • ion homeostasis (K+)
  • buildup in t-tubules, can’t get cells to depolarize
  • quick recovery

low

  • damage/injury to muscle
  • hours to days recovery
69
Q

Diaphragmatic fatigue test

A

measure Pdi and Ephr

60min cardiogenic shock
- Pdi and ePhr go up

140min
- Pdi down, Ephr up

indicates peripheral failure but central not determined

70
Q

Shift in power spectrum

A

average frequency decreases

  1. muscle fatigue
  2. change in ion homeostasis
    - need baseline
    - not all changes from muscle fatigue

EMG —–> Power spectrum
(fast fornia transformation FFT)

71
Q

Ultrastructual injury

A

biopsy

z-line streaming
swollen mitochondria
posse of muscle

risk of death from biopsy
2 day process
shows only one area of diaphragm

72
Q

Detection of sarcolemmal damge

A

procion orange stains damaged cells

  • healthy has existing damaged cells
  • need baseline
73
Q

Diaphragm life expectancy

A

only 3 days

  • high turnover
  • looking for ways for diaphragm to stimulate the diaphragm to regenerate itself
74
Q

COPD before and after 2010

A

pre
- not reversible
- treatment limited success reserving lung function
post
- not “fully” reversible
- airflow limitation progressive and associated with abnormal inflammatory response of the lung to noxious particles or gas

75
Q

COPD def

A

chronic (repeated exposure) of inflammation
chronic decrease in flow

heterogeneous disorder of emphysema and/or chronic bronchitis

76
Q

pathogenesis of COPD

A

noxious agent (tobacco smoke, pollutants, occupational agent)

  • -> inflamation (chronic exposure)
  • -> COPD

other factors:

  • genetics (alpha1-antitrypsin deficiency)
  • respiratory infection as a child, or chronic pneumonia
  • age
77
Q

Chronic bronchitis

A

excess mucus production (3 months of year for 2 successive years) sufficient to cause expectoration of septum

  • partially blocked lumen
  • thickening of airway wall
78
Q

Emphysema

A

anatomic alteration of lung characterized by enlargement of the air spaces distal to the terminal bronchioles with destruction of alveolar walls

  • determined only by biopsy
  • 2% chance of death

loss of radial traction

79
Q

Chronic bronchitis and emphysema similarities

A

treated the same way - no benefit distinguishing between the two

80
Q

Exercise intolerance caused by 2? how to distinguish?

A

heart failure or COPD

- FEV1, decrease with COPD

81
Q

Partially blocked lumen

A

chronic bronchitis

  • mucus in airspace
  • increase resistance = decrease flow
82
Q

Thickening of airway wall

A

chronic bronchitis

  • mucus gland hypertrophy
  • mucus buildup suffocates cell of bronchial wall
  • decrease # of cilia
83
Q

Loss of radial traction

A

emphysema

  • air trapping
  • elastin lost, nothing to hold airways open
  • reduced radial traction
  • SA decrease –> # capillaries decrease
84
Q

Diagnosing COPD

A

irreversible progressive airflow limitation

FEV1.0

normal - 80% FVC in 1 sec (~4L)
COPD - 60% FVC in 1 sec (~2.5L)

85
Q

FVC

A

Forced Vital Capacity

  • termination of vital capacity with the maximum force used
  • approx 5% less than VC
86
Q

FEV1.0

A

Forced expiratory capacity

% volume of air expired in 1sec with maximal force of the FVC

  • decrease indicates COPD
87
Q

Angiotensin II

A

vasoactive substance activated by the lung which has 50x vasocontrictive affect of angiotensin I

  • ACE (angiotensin converting enzyme)
88
Q

3 mechanisms of airway obstruction

A
  1. partially blocked lumen
  2. thickening of airway wall
    (chronic bronchitis)
  3. loss of radial traction
    (emphysema)
89
Q

hyperplasia

A

increase number of mucus cells (thickening of airway wall)

90
Q

reid index

A

size of cluster of mucus glands with respect to airway wall

  • healthy < 0.4
  • COPD > 0.4

CardioResp Phys HK4550 (5 decks)

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