Respiratory Flashcards

1
Q

functions of the respiratory system

A
  • gas exchange
  • speech
  • warm, humidify and clean air
  • actives hormones (ACE)
  • homeostasis of blood pH
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2
Q

Law of LaPlace

A

magnitude of inward pressure (P) in alveolus = 2 x surface tension (T) / radius of alveolus (r)

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3
Q

role of surfactant molecules

A
  • in alveolus H2O molecules line the bubble and create and inward pressure
  • therefore small alveoli would collapse into bigger ones (law of LaPlace)
  • so surfactant molecules are lipids and proteins that line the alveoli to reduce water tension
  • also reduce water levels
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4
Q

transmural pressure gradient

A

definition: the difference in pressure between two sides of a wall
- when no breathing P in lungs = P in atm (760mmHg)
- intrapleural P is below this due to the alveoli walls getting pulled in by surface tension
- increased V = decreased P
- this stops the lungs from collapsing

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5
Q

dynamic small airway closure

A

pleural sack shuts off small airway in the alveoli

  • during forced exhalation, smooth muscle in airway constricts
  • this causes both the alveoli pressure and the intrapleural pressure to increase
  • air starts rushing out
  • alveolar pressure becomes less due to friction with airway tube
  • when when alveolar pressure = intrapleural pressure airway shuts
  • amount of air left is called the residual volume
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6
Q

what determines lung volumes?

A
  • size
  • gender
  • age
  • build
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7
Q

lung volumes

A

vital capacity, IRV, ERV, TV, RV

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8
Q

early airway closure in asthma

A
  • decreased airway diameter
  • increased airway resistance
  • loss of alveolar pressure faster
  • reach transmural pressure equilibrium quicker
  • airway shut
  • decreased VC, increased RV
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9
Q

early airway closer in emphysema

A
  • destruction of alveolar walls
  • less alveolar surface tension and overall lung recoil
  • increase intrapleural pressure (decreased volume)
  • transmural pressure equilibrium will be smaller
  • decrease VC, increased RV
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10
Q

pulmonary ventilation

A

pulmonary ventilation = tidal vol. (mL/breath) x respiratory rate (breath/min)

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11
Q

alveolar ventilation

A

= (tidal vol - dead space) x respiratory rate

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12
Q

what increases first during exercise, tidal volume or respiratory rate?

A

Tidal volume

  • any increase in tidal volume will increase alveolar ventilation by the same rate
  • increase in respiratory rate will increase alveolar ventilation by a smaller amount due to the dead space
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13
Q

acute asthma attack

A
  • parts of the lungs are totally shut off
  • start to hyperventilate the still open parts of the lungs
  • high diffusion coefficient of CO2
  • increased pH above 7.45
  • PO2 well below normal due to V/Q < 1
  • after several hours respiratory muscles fatigue
  • PCO2 and pH back to normal
  • further decrease in PO2
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14
Q

control of respiration

A
  • factors generating the alternating inspiration/expiration rhythm
  • factors that regulate the magnitude of ventilation to match bodies needs
  • factors the modify respiratory activity to serve other purposes (speech, coughing, holding breath)
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15
Q

medullary respiratory center

A
Rostral ventromedial medulla
- pacemaking
- create pacemaking AP
- breathing rhythm
dorsal respiratory group
- respiration in quite breathing
- fires to contract diaphram
ventral respiratory group 
- when heavy breathing
- insp/exp
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16
Q

Pons respiratory centers

A
  • pneumotaxic center

- apneustic center

17
Q

peripheral chemoreceptors

A
  • carotid bodies (in carotid artery)
  • aortic bodies (in arch)
  • constantly monitoring blood PO2
  • only a lifesaving mechanism
  • hypoxic drive to breath
  • if PO2 < 60mmHg
18
Q

central chemoreceptors

A
  • monitor ECF pH
  • respond to changes in [H+]
  • CO2 can easily cross blood brain barrier and change ECF conc.
19
Q

Some patients with severe lung disease and chronic elevated arterial PCO2 do not show any increase in ventilation. Why?

A
  • long standing CO2 retention
  • leads to prolonged increase in [H+] in ECF
  • after time enough HCO3- may cross the blood brain barrier and buffer excess H+
  • therefore EFC conc. is equalised and at normal levels
  • arterial PCO2 still way higher than normal
  • only breathing of hypoxic drive as peripheral chemoreceptors monitor PO2
20
Q

Oxygen therapy for such patients has to be carefully monitored. Why?

A
  • they rely on life saving mechanisms to breath as PO2 under 60mmHg
  • hypoxic drive to breath
  • O2 therapy increase arterial PO2 above 60mmHg
  • stops peripheral chemoreceptors driving breathing
  • therefore, may stop breathing all together
21
Q

lines of defence against non-CO2 induced [H+]

A

1) chemical buffer system - immediate
2) respiratory compensation - few minutes
3) renal compensation - hours to days
eg: metabolic induced acidosis due to lactic acid (respiratory compensation)

22
Q

cause of increased ventilation during exercise

A
  • joint and muscle receptors
  • body temperature
  • adrenaline
  • cerebra cortex
23
Q

apnea

A
  • person forgets to breath

- can lead to respiratory arrest

24
Q

dysapnea

A
  • person feels like ventilation is inadequate

- claustrophobia