Respiratory 8 Flashcards
What happens when O2 leaves Hb at the tissues
CO2 binds with free Hb at exposed amino groups (-NH2)
Forms carbaminohemoglobin
What happens to O2 on Hb when CO2 very high
Can cause o2 release and CO2 will bind
When CO2 bound to Hb or converted to bicarbonate what happens to partial pressure
Does not contribute to partial pressure so gradient continues
CO2 removal at the lungs
- Plasma CO2 to alveoli
- Cytosol co2 to plasma
What happens to CO2 and Hb during CO2 removal
CO2 unbinds from Hb and diffuses out of RBC
What happens to CO2 and HCO3 during CO2 removal in lungs
CO2 levels in RBC drop and equilibrium of CO2 and HCO3 is disturbed causing reverse reaction
- Hb releases H+ and joins HCO3 to become CA
- CA converts to H20 + CO2
What happens when HCO3 drops in plasma during CO2 removal
Cl-/HCO3- exchanger reverses
When O2 moves out of the alveoli how much stays in plasma and how much moves in RBC
<2% in plasma
>98% joins Hb in RBC
How much of CO2 that is picked up from cells diffuses in plasma and how much in RBC
7% co2 in plasma
93% in RBC
Breathing
Rhythmic process that occurs subconsciously
- mix of voluntary and involuntary
What happens during subconscious breathing
Involuntary contraction and relaxation of inspiratory muscles
What can skeletal muscles not do when controlling ventilation
Cannot contract spontaneously
What causes skeletal muscle contraction of the muscles that control ventilation
- spontaneously firing networks of pacemaker neurons in the brainstem (medulla)
What is the network of pacemaker neurons influenced by
Sensory and chemoreceptors, and higher brain centres
What is neural control of ventilation considered
Blackbox
Where are the respiratory neurons that control inspiratory and expiratory muscles
Medulla
What do the neurons in the pons do to control respiration
Integrate sensory info and interact with medullary neurons to influence ventilation
Where does rhythmic pattern of breathing arise from
Neural network with spontaneously discharging neurons
What is ventilation continuously modulated by
Various chemoreceptors (primarily) and mechanoreceptor linked reflexes and higher brain centres (hypothalamus, cerebral cortex, limbic system)
What are the 3 bundles of neurons in the medulla control breathing
- Dorsal respiratory group
- Pontine respiratory group
- Ventral respiratory group
What contains the DRG
Nucleus tractus solitaris (NTS)
What does the DRG control during quiet breathing
Inspiratory muscles via phrenic nerve and intercostal nerve to influence inspiration
Where does the NTS receive input
The peripheral mechano and chemoreceptors
Where does pontine respiratory group (PRG) receive info from
Receives sensory info from DRG
What does the PRG do
Provides tonic input to DRG to help the medullary networks coordinate a smooth respiratory rhythm
- does to create rhythm
What is PRG not necessary for
Not necessary for ventilation to occur but helps smooth it out
What are the areas of the ventral respiratory group
Pre-botzinger complex
Outputs to control muscles
Outputs that keep upper airways open
Pre-botzinger complex
Contain pacemaker neurons that may initiate respiration
What do the outputs to control muscles do
Control muscles of active inspiration and expiration, remain quiet otherwise
What do outputs that keep upper airways open sometimes do
Sometimes outputs slow down to munch while asleep (sleep apnea, snoring)
What causes the activity of inspiratory neurons to increase steadily
Positive feedback mechanism
What causes feedback loop to be shut off
End of inspiration
- abruptly shuts off and expiration takes place
How does positive feedback loop work
Believed to be initiated by pacemaker
- recruits more neurons “ramping” recruiting more outputs to inspiratory muscles
What do levels of CO2, O2, pH within blood influence
Ventilation
Where are peripheral chemoreceptors
Aortic arch and carotid bodies
What do peripheral chemoreceptors do
Sense changes in arterial PO2, PCO2, and pH and adjust ventilation accordingly
What region of carotid bodies sense changes in levels of O2, H+ and CO2
Type 1 (glomus) cell
What do afferent neurons of carotid bodies do
Synapse with glomus cells and provide input back to medulla
How do glomus cells respond to low PO2
- ATP sensitive ATP channels close
- Cell depolarizes
- Voltage gated Ca channels open
- Ca enters
- Exocytosis of neurotransmitters signals AP
- Signal to medulla increase ventilation
What type of drop in PO2 does it take to trigger peripheral chemoreceptors
Large drop
What can peripheral chemoreceptors respond to
- pO2 in plasma
- increases in H+
- increases in CO2
Where are central chemoreceptors located and what do they do
Medulla
- provide continuous input to respiratory control center
- respond mainly to changes in PCO2
If PCO2 increases what happens to ventilation
Increase
If PCO2 decreases what happens to ventilation
Decreases
Where can central chemoreceptors respond to changes in CO2
PH changes in cerebrospinal fluid causes by CO2 but not in plasma pH
(H+ cannot cross blood brain barrier)
What do neurons in the region of central chemoreceptors contain
H+ sensitive channels (ASIC)
What do the H+ sensitive channels do
Become activated and transmit APs to respiratory control center
What happens with decreased arterial o2 when it is peripheral chemoreceptor mediated
Peripheral chemoreceptors fire, reflex via medullary respiratory neurons, respiratory muscle contract, increase ventilation, return of alveolar and arterial O2 to normal
What happens when increased arterial H+ independent of CO2 increase
Peripheral chemoreceptor mediated
Increase peripheral chemoreceptors firing, reflex via medullary respiratory neurons, respiratory muscle contract, increase ventilation, decrease arterial and alveolar PCO2, return of H+ to normal
What is is arterial CO2 mediated by
Central chemoreceptors (70%)
Peripheral chemoreceptors (30%)
What are irritant receptors
In lungs and respond to inhaled particles of noxious gases
What do the irritant receptors do
Send sensory input into CNS, then parasympathetic outputs cause bronchoconstriction
What does the bronchoconstriction caused by irritant receptors cause
Rapid shallow breathing and turbulent airflow to deposit irritant in mucosa
- reflexes can initiate coughing or sneezing
What do stretch receptors in lungs prevent
Over inflation of the lungs “hering-Breuer inflation reflex”
- terminated inspiration in very active inspiration
What causes the feedforward component to the exercise ventilatory response
Proprioceptors in muscles and joints
- arterial PCO2 or PO2 have not changed
Why does the feedforward response begin at onset of exercise
Initiates change in ventilation in anticipation that O2, CO2, and H+ levels will change
How much can minute ventilation increase during exercise
20-fold
Why is there large increase in minute ventilation during exercise
Compensates for O2 requirements because O2 demands remain constant until max exercise
What is limiting factor during moderate to strenuous exercise
CV system is limiting factor not ventilation
