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respiratory A > hh1606 > Flashcards

hh1606 Flashcards

1
Q

define COPD

A

a disease characterised by airflow obstruction resulting from chronic bronchitis or emphysema

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2
Q

briefly describe clinical features of chronic bronchitis

A

a persistent productive cough for 3 months of the year for 2 consecutive years. - airway disease - insidious onset with morning cough

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3
Q

state the aetiology of chronic bronchitis

A

smoking is primary aetiological factor
recurring bronchial infections
environmental pollution

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4
Q

list secondary effects of chronic bronchitis

A 
V/Q mismatch
increased airway resistance so reduced airflow
airway obstruction
increased WOB
impaired gas exchange
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5
Q

define lung parenchyma

A

the portion of lung involved in gas transfer - alveoli, alveolar duct, capillary bed and respiratory bronchioles

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6
Q

define cor pulmonale

A

widespread hypoxic vasoconstriction within lungs with increased vascular resistance and right ventricular failure

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7
Q

define polycythaemia

A

body’s response to chronic hypoxia, increasing total volume of red blood cells hence increasing blood viscosity with plethoric appearance (red face)

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8
Q

define respiratory failure

A

the inability to maintain the partial pressures in arterial blood of carbon dioxide and oxygen within normal physiological limits where PaO2<8kPa and CO2 >6.7 kPa

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9
Q

define atelectasis

A

the collapse of a lung resulting in reduced gas exchange

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10
Q

what is absorption atelectasis

A

when gases other than oxygen is required to keep the alveolar sacs open e.g. nitrogen

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11
Q

interstitial fibrosis

A

a chronic relentless progressive fibrotic disorder of the lungs of unknown aetiology affecting adults >40years males

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12
Q

what is innervated by the phrenic nerve?

A

C3,4,5 KEEPS THE DIAPHRAGM ALIVE!

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13
Q

what factors generate the pleural pressure gradient?

A

the force acting to inflate the lung within the thorax, is generated by the opposing elastic recoils of the lung and chest wall and the forces generated by respiratory muscles. this tug of war creates pleural pressure gradient.

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14
Q

describe process of quiet inspiration

A

respiratory muscles contract (diaphragm and external intercostals)
increases thoracic lung volume
causing decreased intrapulmonary pressure
airflow into lungs down pressure gradient
airflow stops when intrapulmonary pressure equals atmospheric pressure

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15
Q

describe the process of quiet expiration

A

passive process
inspiratory muscles relax
air flow out of the lungs into atmosphere
thoracic volume decreases
which cause intrapulmonary pressure to increase
lungs recoil
airflows out of lung down pressure gradient until intrapulmonary pressure 0

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16
Q

what happens to pleural pressure in a pneuomothorax

A

becomes positive, colour in x-ray is black

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17
Q

what are the two types of dead space?

A

anatomical and alveolar dead space

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18
Q

if air is missing during v/q it is

A

shunt (alveolar dead space)

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19
Q

in anatomical dead space what are you missing

A

blood

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20
Q

respiratory assessment: what symptoms do you want to know about the pt?

A 
cough
wheeze
sputum
dyspnoea
breathing pattern
exercise tolerance
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21
Q

what do you want to know about the pt’s current symptoms

A

have they changed from the normal

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22
Q

what causes a wheeze?

A

air being pushed through a narrowed airway

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23
Q

what causes chest pain? whats innervated in thorax?

A

the parietal pleura therefore parietal pain

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24
Q

name 3 chest wall deformities

A

scoliosis
kyphosis
sternal - pectus cavinatum
or pectus excivatum

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25
Q

how will a breathless patient change their breathing pattern?

A 
apical breathing pattern
rapid breathing
fixed upper limb 
use of accessory muscle scalenes and scm
pursed lip breathing
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26
Q

name 5 criteria associated with fick’s law

A 
gas solubility
surface area
diffusion gradient
thickness of alveolar membrane
V/Q coupling
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27
Q

what is hypoxic pulmonary vasoconstriction?

A

in areas of lung with poor gas exchange
hypoxia is sensed by baroreceptors in arterioles
the arterioles constrict to reduce wasted perfusion
to areas of low ventilation in an attempt to reduce v/q mismatch. blood flow is redirected to areas of lung with good gas exchange therefore effective

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28
Q

what is poisseuille’s law?

A

flow of gas through an airway is directly proportional to the 4th power of its internal radius

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29
Q

what is type 1 respiratory failure?

A

when oxygen is low and carbon dioxide is normal or low. oxygen is below 8, caused by V/Q mismatch within the lung

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30
Q

what is type 2 respiratory failure?

A

when oxygen is low below 8 and co2 is high above 6kPa. caused by alveolar hypoventilation and failure of the respiratory muscles to generate pressure therefore respiratory pump fails

31
Q

what is the hilum

A

pulmonary arteries, pulmonary veins and lymph nodes

32
Q

why does pursed lips breathing occur?

A

exhaling via pursed lips increases resistance to expiratory airflow, which generates back pressure within airways, to help splint them open during expiration, more open when they breathe out (ppl with floppy airways like emphysema will use pursed lip breathing)

33
Q

whats normal inspiration/expiration ratio?

A

1:2

34
Q

signs of respiratory distress in COPD pt

A 
tachypnoea
pursed lip breathing
prolonged expiration cah obstructive 
active expiration
fixed ULs - use pec minor for insp
use of acc mm scl nd scm
soft tissue recession
35
Q

what happens to static lung volumes with COPD pts?

A 
they are high as gas trap occurs
higher RV,
higher TLC, unaccessed trapped air
higher FRC
reduced diffusing capacity
36
Q

management of COPD

A 
steroids
diuretics
anti-inflammatory drugs
flu vaccine
long term oxygen therapy
lung volume reduction surgery - remove bullae
37
Q

physio management COPD

A

education- smoking cessation, inhaler technique
sputum clearance technique when appropriate
breathlessness management at rest
pulmonary rehab

38
Q

acute type 2 respiratory failure

A

low pao2
high paco2
normal hco3
decreased pH - respiratory alkylosis

39
Q

chronic type 2 respiratory failure

A 
low pao2
high paco2
high hco3 levels
normal pH
eg copd
40
Q

acute on chronic type 2 resp failure

A

low pao2
high paco2
increased hco3 but not enough so resp acidosis
decreased pH
deterioration of kidneys so co2 rised further

41
Q

Why can’t we give people with chronically high co2 levels lots of O2 to breathe?

A

reversed HPVC - increasing V/Q mismatch
Haldane effect
Loss of hypoxic drive

42
Q

factors that affect haemoglobin’s affinity for O2

A 
primarily PO2
DPG (diphosophoglycerate)
temperature
PCO2
pH
43
Q

pulmonary rehabilitation

A

educate patient on ways to breathe
functional exs
prescribe group exs

44
Q

Radial traction

A

The elastic recoil in the alveoli surrounding airways helps to hold them open.

45
Q

define bronchiectasis

A

Chronic dilation and distortion of proximal and medium sized bronchi due to excessive inflammation

46
Q

define cystic fibrosis

A

inherited condition caused by defective chromosome 7 mutating CFTR altering Cl channel, resulting in thick dehydrated intraluminal mucus.

47
Q

aims of breathing retraining

A

• Restore and maintain normal diaphragmatic
breathing pattern
• Re-programme respiratory centre to trigger
inspiration at a higher level of CO2

48
Q

respiratory compliance

A

distensibility of lung elastic tissue, the change in pulmonary volume per unit of pressure change

49
Q

pulmonary surfactant

A

surface acting lipoprotein complex
secreted by type 2 alveolar cells
reduces surface tension, improves alveolar expansion
prevents lung collapsing at end of expiration
increase lung compliance

50
Q

main component of pulmonary surfactant

A

dipalmitoglyphosphatidylcholine

51
Q

what happens if FRC drops to below closing volume?

A

lung collapses (dynamic compression of small airways and alveoli)

52
Q

describe the clinical relevance of reduced pulmonary surfactant

A

reduced pulmonary surfactant production-> increased surface tension-> decreased lung compliance-> atelectasis-> increased WOB/O2 consumption

53
Q

how is co2 transported

A

10% in plasma, 20% in hb, 70% as bicarbonate

54
Q

consequences of reduced lung volume

A 
decreased frc
decreased lung compliance
increased WOB
increased o2 consumption
airway closure
atelectasis
55
Q

list all respiratory system sensors

A 
central chemoreceptors
peripheral chemoreceptors
juxta-capillary receptors
stretch receptors
irritant receptors
proprioceptors
mechanoreceptors
56
Q

central chemoreceptors

A

located on ventral surface of medulla bilaterally
bathed in cerebral spinal fluid
sensitive to arterial hypercapnia
at BBB, pCO2 = paCO2
feedback responsible for 70% of drive to breathe

57
Q

what is the target saturation range for acutely ill patients who are not at risk of hypercapnic respiratory failure?

A

94-98%

58
Q

target saturation range for acutely ill patient who is at risk of hypercapnic respiratory failure?

A

88-92%

59
Q

where is the apex of the lung located?

A

2.5cm above the medial 1/3 of the clavicle

60
Q

o2 delivery devices

A 
nasal canaliculae (variable)
simple facemask (variable)
reservoir masks (variable)
venturi mask (fixed)
61
Q

benefits of pulmonary rehab

A 
increased exs capacity
reduced dyspnoea
improved health status
increased muscle strength
reduced anxiety and depression
62
Q

explain loss of hypoxic drive if you give too high o2 to chronic hypercapnic pt with copd

A

COPD pt with chronic hypercapnia rely on peripheral chemoreceptors that sense arterial hypoxaemia
if given too high o2 arterial hypoxaemia reversed, hence only remaining drive to breathe reversed

63
Q

explain worsed V/Q mismatch due to reversed hpv

A

COPD pt has areas of lung destruction with poor ventilation leading to hypoxia therefore vq mm
compensatory hypoxic vasoconstriction occurs
if given high o2 good lung tissue reversed
hpv reversed
so perfusion of non ventilating lung causes increased vq mismatch

64
Q

explain haldane effect as a reason not give high o2 to a COPD pt

A

Hb has high affinity for o2
in tissue hb lowers affinity for o2 as o2 low at tissues so unloading dissociation occurs for hb
deox of hb increase co2 affinity
increasing po2 brakes hb off co2 to bind with the o2
co2 dissolves in plasma, unable to be exchanged at lung
thereby raising paco2 decreasing the ph thereby causing respiratory acidosis

65
Q

what are the 6 main symptoms of cardiorespiratory disease

A 
sputum 
haemoptysis
breathlessness (dyspnoea)
chest pain
cough
wheeze
66
Q

what is a wheeze?

A

a whistling or musical sound produced by turbulent airflow through narrowed airways

67
Q

ventilatory pump

A

the ability to sustain spontaneous ventilation depending on the triad of CNS drive, respiratory mm capacity, and load that is imposed upon them

68
Q

emphysema

A

abnormal permanent enlargement of the alveolar septa distal to the terminal bronchioles, accompanied by wall destruction without obvious fibrosis

69
Q

asthma pathophys

A 
narrowing of airway due to: mucosal oedema
constriction bronchial smooth muscle
lumen secretions
thickening of bronchial wall
increased airflow resistance
decreased airflow
breathlessness
70
Q

shape of thorax in copd

A

barrel shaped

71
Q

Pulmonary rehabilitation

A 
• Education
• Breathlessness management – at rest and
on exertion
• Sputum clearance techniques if
appropriate
• Exercise
• Smoking cessation
72
Q

why do we use collateral channel ventilation?

A
  • to re-inflate lung tissue

- remove sputum

73
Q

how does PEP work?

A

The PEP device creates pressure in the lungs and keeps your airways from closing. The air flowing through the PEP device helps move the mucus into the larger airway. for CF.

respiratory A (4 decks)

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