resp Flashcards

1
Q

define hypoxia

A

failure to adequately oxygenate arterial blood

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2
Q

define hypercapnic

A

failure to prevent CO2 retention

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3
Q

causes of hypoxaemia

A
  • reduced inspired oxygen
  • hypoventilation
  • V/Q mismatch
  • R-L shunt
  • diffusion
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4
Q

causes of hypercapnia

A
  • caused by alveolar ventilation (also V/Q mismatch)
  • PaCO2 inversely proportional to alveolar ventilation
  • Ve = Va - Vd

respiratory drive
neuromuscular transmission
load

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5
Q

factors influencing alveolar ventilation and how it causes hypercapnia

A
  • respiratory drive (e.g. depression by drugs)
  • neuromuscular competence (e.g. muscular dystrophy, myasthenia gravis, spinal cord injury)
  • load (gives resistive & elastic work) e.g. obesity, kyphosis-scoliosis
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6
Q

describe COPD

A
  • airflow limitation (not fully reversible)
  • progressive limitation, association w/ abnormal inflammation response to noxious particles/gases
  • often due to cigarettes
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7
Q

features of COPD

A
  • chronic mucus hyper-secretion
  • emphysema
  • small airway inflammation
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8
Q

what is gas exchanged influenced by

A
  • diffusion
  • V/Q mismatch
  • R-L shunt
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9
Q

describe V/Q mismatch

A

is a RATIO between ventilation and perfusion

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10
Q

what is another name given to an area that is ventilated but not perfused

A

dead space

V/Q = 1

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11
Q

shunt

A

whens theres an anatomical abnormality, blood doesn’t come anywhere near the alveolus

= (venous admixture)

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12
Q

in the early stages of COPD why are patients hypoxemic but normocapnic

A

COPD patients have decreased airways, therefore have a V/Q mismatch (shunt). As a result of the mixed venous blood from shunt, theres decreased O2 and increased CO2 levels. Hypercapnia is the major central drive causing hyperventilation. This brings CO2 levels to normal however decreases oxygen levels.

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13
Q

effects of worsening COPD and the dangers

A

overtime they’re unable to undertake compensatory hyperventilation. As a result, theres increased PaCO2 (pH is normalised by renal and other mechanism)

dangers
- high inspired O2 (chemoreceptors in the brain turn off their response to O2 - drive then depends on hypoxemia)
- monitoring O2 saturations only
therefore if you remove that hypoxic drive for ventilation you stop them breathing all together

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14
Q

describe R-L shunt

A
  • venous blood being mixed with arterial blood
  • distinguish from V/Q mismatch by administration of 100% O2
  • in the heart
  • reduced PaO2 in the arteries
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15
Q

what does diffusion depend on

A
  • gas
  • diffusion distance/thickness
  • surface area
  • (Hb)
  • capillary volume
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16
Q

what are causes of abnormal diffusion and what are some examples of pathologies

A

alveolar-capillary block
- diffuse lung disease

loss of diffusing surface
- emphysema

capillary volume / Hb

  • pulmonary hypertension
  • anaemia
17
Q

what initially happens to FEV1 during exercise and why

A
  • initially increases as exercising produces catecholamines and reduce vagal tone. Causing dilation of airways (parasympathetic supply)
  • increases lung function
18
Q

how do you calculate alveoli pressure

A

it is the sum of intrapleural pressure and elastic recoil pressure

Palv = Pel + Pip

19
Q

wheeze in asthma

A

wheeze on expiration

airway narrowing by bronchospasm gives ↑ velocity & ↓P (Bernoulli’s principle) - contributing to dynamic compression → wheeze

20
Q

explain how exercised induced asthma lowers FEV1

A
  • exercise causes drying of airways, this increases the tonicity of fluid lining the airways. Mast cells then degranulate and release broncho-active mediators. Causing airway constriction which lowers FEV1