Respiratory Flashcards
functions of the respiratory system
- gas exchange
- speech
- warm, humidify and clean air
- actives hormones (ACE)
- homeostasis of blood pH
Law of LaPlace
magnitude of inward pressure (P) in alveolus = 2 x surface tension (T) / radius of alveolus (r)
role of surfactant molecules
- 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
transmural pressure gradient
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
dynamic small airway closure
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
what determines lung volumes?
- size
- gender
- age
- build
lung volumes
vital capacity, IRV, ERV, TV, RV
early airway closure in asthma
- decreased airway diameter
- increased airway resistance
- loss of alveolar pressure faster
- reach transmural pressure equilibrium quicker
- airway shut
- decreased VC, increased RV
early airway closer in emphysema
- 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
pulmonary ventilation
pulmonary ventilation = tidal vol. (mL/breath) x respiratory rate (breath/min)
alveolar ventilation
= (tidal vol - dead space) x respiratory rate
what increases first during exercise, tidal volume or respiratory rate?
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
acute asthma attack
- 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
control of respiration
- 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)
medullary respiratory center
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
Pons respiratory centers
- pneumotaxic center
- apneustic center
peripheral chemoreceptors
- carotid bodies (in carotid artery)
- aortic bodies (in arch)
- constantly monitoring blood PO2
- only a lifesaving mechanism
- hypoxic drive to breath
- if PO2 < 60mmHg
central chemoreceptors
- monitor ECF pH
- respond to changes in [H+]
- CO2 can easily cross blood brain barrier and change ECF conc.
Some patients with severe lung disease and chronic elevated arterial PCO2 do not show any increase in ventilation. Why?
- 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
Oxygen therapy for such patients has to be carefully monitored. Why?
- 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
lines of defence against non-CO2 induced [H+]
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)
cause of increased ventilation during exercise
- joint and muscle receptors
- body temperature
- adrenaline
- cerebra cortex
apnea
- person forgets to breath
- can lead to respiratory arrest
dysapnea
- person feels like ventilation is inadequate
- claustrophobia
