Respiratory Physiology Flashcards
What effect does raised CO2 have on cutaneous and cerebral arterioles?
Marked vasodilation in both
What is an average tidal volume? How much of that is dead space vs. ventilated?
500ml
150 dead space in conducting airways
350 available for gas exchange
Describe our two types of pneumocytes in appearance and role.
Type I & II cells line the alveoli
• Type I : flat, large cytoplasmic extensions, primary lining cells
• Type II : granular pneumocytes, thicker and contain numerous lamellar inclusion bodies, secrete surfactant
What are some mechanisms (4) by which our body removes inhaled particles?
- very large particles are filtered out by the NOSE
- mucous from goblet cells catches and propels it by millions of cilia that deposit on the airways are removed by the MUCOUS ELEVATOR
- particles that reach the alveoli are engulfed by MACROPHAGES
- material in the alveoli are then removed from lung via LYMPHATICS
What are the effects of inspiration on
- intrapleural pressure
- intrapulmonary pressure
- venous return
- decreases from falls from -2mmHg to -8mmHg
- decreases to about -3mmHg then air flows into the lung until the intrapulmonary pressure becomes equal to atmospheric
- increase
What is the proportion of carbon dioxide in arterial vs venous blood that is
- dissolved
- bicarbonate
- carbamino
ARTERIAL
- 5%
- 90%
- 5%
VENOUS
- 10%
- 60%
- 30%
What is the Bohr effect?
Bohr effect = the decrease in O2 affinity of Hb when pH of blood falls (because deoxy-Hb binds H+ more actively than oxy-Hb)
What is the Haldane effect?
Haldane effect = deoxygenated Hb has a higher affinity (3.5x) for CO2 than oxyhaemoglobin
(due to the allosteric modulation of CO2-binding sites by the oxygenated haem)
Which factors push our oxygen binding curve to the left, which ones to the right?
LEFT: increased affinity for O2
- increase HbF
- Increased CO
RIGHT: decreased affinity for O2
- decreased pH
- increased CO2
- increased 2,3DPG
- increased temp
Which chemoreceptors (aortic or carotid) respond to fluctuations in pH?
The carotid bodies (but not the aortic bodies) respond to a fall in arterial pH with hyperventilation
What are the 4 factors that determine alveolar pO2 and pCO2?
o The pressure of outside air
o The partial pressures of inspired oxygen and carbon dioxide
o The rate of total body oxygen consumption and carbon dioxide production
o The rates of alveolar ventilation and perfusion
What are the causes of increased a-A gradient with hypoxaemia?
- VQ mismatch
- diffusion defect eg. pulmonary fibrosis
- shunting eg. ASD
- respiratory pump failure (eg. obstructed bronchiole)
What are the causes of increased a-A gradient without hypoxaemia?
- alveolar hypertension
- low FiO2
Of the following, which is diffusion/perfusion limited?
- O2
- NO
- CO
- O2 perfusion limited, reaches equilibrium in 0.3 sec
- NO flow limited, reaches equilibrium in 0.1 sec
- CO diffusion limited, reaches equilibrium at 0.75 sec
When the diaphragm is paralysed, how does it move in inspiration and expiration?
Usually depresses in inspiration as it contracts
When paralysed, moves up due to negative intrathoracic pressure
This is called paradoxical movement
What is the percentage of total resting O2 consumption of quiet breathing?
What about voluntary hyperventilation?
5%
With hyperventilation increases to 30%
What is the breakdown of work done by respiratory muscles?
- 65% stretching elastic tissue sof chest wall and lungs
- 7% moving inelastic tissues eg viscous resistance
- 28% moving air through respiratory passages
Comparing apex to base of lung in the upright position which has greater
- ventilation
- perfusion
- intrapleural pressure
- compliance
- VQ ratio
- alveolar PO2
- ventilation: base (because increase in volume per unit of pressure is higher)
- perfusion: base
- intrapleural pressure: less negative at base
- compliance: base
- V/Q ratio: base
- alveolar PO2: apex
What are the 2 mechanisms used by the pulmonary arterial system to reduce pulmonary vascular resistance?
- recruitment of alternative blood vessels
- distension of blood vessels
Why does pulmonary vascular resistance increase with both high and low volumes?
HIGH VOLUMES
- resistance increases due to stretching and thinning of capillaries
LOW VOLUMES
- extra-alveolar vessels are compressed
During exercise, what happens to
- arterial pCO2
- arterial PO2
- pH
- pCO2 remains steady, may fall with severe exercise due to hyperventilation
- pO2 increases slightly, falls at high work levels
- pH remains nearly constant
What physiological states reduce the ventilatory response to increase in arterial pCO2?
- athletes/divers
- morphine/barbiturates
- increased work of breathing
Why is carbon monoxide poisonous in large amounts?
Reacts with Hb to form carbon monoxyhaemoglobin which cannot take up O2
Total Hb content of blood not changed, but amount that can carry O2 is fucked
Affinity for CO is 210 affinity for O2 and shifts O2 dissociation curve to left
What are the acute changes associated with hyperventilation in
- pCO2
- pO2
- bicarb
- pH
- cardiac output
- ICP
- pCO2 down to 15mmHg
- pO2 120-140 mmHg
- decreased bicarb
- increased pH
- cardiac output increased
- direct vasoconstriction leads to decreased cerebral blood flow and ICP
Basal O2 consumption at rest per minute
Basal O2 production at rest per minute
250ml/min
200ml/minute
Where is the CNS control for
- spontaneous rhythmic breathing
- inspiratory muscles / expiratory muscles
Pre-Bottzinger : medulla
VRG
DRG
(Dorsal and ventral respiratory motor nuclei of vagus in medulla)
What is a J receptor?
Receptor in alveolar walls that, when activated, gives the pulmonary chemoreflex
- apnea followed by rapid breathing, bradycardia, and hypotension (pulmonary chemoreflex)
