15. Chapter 18- Gas Exhange and Transport Flashcards
Study diagram Jan 14 slide 12
And Jan 14 Slide 14-15
Okay
What is hypoxia and hypercapnia?
What are the 3 variables the body reps ones to to avoid hypoxia and hypercapnia?
Hypoxia- caused by impaired diffusion from alveoli to blood or impaired blood transport (too little oxygen
Hypercapnia- hypoxia is paired to this (excess CO2)
Body’s has sensors for:
- Oxygen- ATP production
- Carbon dioxide- CNS depressant
- pH- denature gets of protein
Jan 14 S13
Hypoxia can be caused by inadequate amounts of O2 reaching alveoli, what are 2 causes of low alveolar PO2 assuming perfusion remains constant?
What happens if these two reasons aren’t eye cause?
- Inspired air has low O2 content- atmospheric pressure: PO2 at sea level is 160mmHg, in Denver PO2 is 132mmHg
- Alveolar ventilation- if atmospheric PO2 normal and alveolar PO2 is still low, then it must be a ventilation issue
Increase in airway resistance means decrease in lung compliance or CNS issue
If perfusion remains constant and hypoxia is not caused by these two, then the problem usually lies within gas exchange between alveoli and blood
What is diffusion in the lungs?
What are the 4 things that affect the movement of gas between alveoli and capillaries?
Random movement of molecules from high concentration to low concentration (random movement of gas molecules between alveoli and capillaries)
- Concentration gradient (main determinant of diffusion in healthy individuals)
- Surface area
- Barrier permeability (solubility of gas too)
- Diffusion distance
Why must respiratory gases be soluble in liquids?
What are the 3 factors proportional to the movement of gas molecules from air to liquid?
Must be soluble in liquids since alveoli are lined with liquid, the small interstitial space between alveoli and capillaries contains liquid and blood itself is liquid
- Pressure gradient of gas
- Solubility of gas in liquid
- Temp relatively constant
Jan 16 slide 0-1
What is mass flow?
Mass balance?
Fick equation?
Oxygen transport and oxygen consumption by tissues illustrate principle of mass flow and mass balance
Mass flow- movement of X per minute
O2 transport = cardiac output (L blood/min) x O2 concentration (mL O2/L blood)
Mass balance- any substance in the body must remain constant
Arterial O2 transport - Venus O2 transport = Q(O2)
Fick equation- (Cardiac Output x arterial [O2])-(Cardiac output x Venous [O2]) = Q(O2)
Jan 16 Slides 2-3
Where is oxygen in the blood bound?
98% of oxygen in blood is bound to hemoglobin
Less than 2% is dissolved in plasma
Jan 16 Slide 4
What happens as the concentration of free O2 increases?
More oxygen bonds the Hb producing HbO2
Free O2 will be taken up until the plasma and Hb reach equilibrium
Hb + O2 HbO2
Transfer of O2 from alveoli air, to plasma, to red blood cells, to hemoglobin occurs quick
What happens when tissues have low PO2?
Blood travels to them, which draws out O2 from plasma which disrupts equilibrium and causes Hb to release its O2 into the plasma
Jan 18 slide 3-4
What is the difference between the delivery of oxygen per minute for plasma and hemoglobin?
Plasma- 15mL O2/min
Hemoglobin- 1000 mL O2/min
Jan 18 slide 5
How is plasma O2 determined?
3 determinants
Alveolar PO2 which depends on 3 things:
- Composition of inspired air
- Alveolar ventilation rate
- Efficiency of gas exchange
Amount of oxygen in your alveoli is dependant on the amount of air you’re breathing
What does the amount of oxygen bound the Hb depend on? (2 things)
- Plasma O2- determines % saturation of Hb
- Amount of hemoglobin- determines total number of Hb binding sites (calculated from Hb content per RBC x Number of RBCs)
What is the percent saturation of hemoglobin?
How are active muscles affected by this?
The amount of O2 bound to hemoglobin at any given PO2
Active cells can have lower PO2 (active muscles can have PO2 as low as 20mmHg which releases more CO2)
Can be exposed to significant drops in atmospheric oxygen and still get lots of oxygen release from hemoglobin since it stores oxygen
Graph on slide 8 Jan 18
What physical factors alter hemoglobin affinity for O2?
pH effects it (graph slide 9 Jan 18)
Shifts to the right are a decreased ability to hold on to oxygen (seen during maximal exertion, produces excess CO2 and pushes a cell into a aerobic metabolism)
pH or CO2 (PCO2) change!! Bohr effect
Increase CO2, increase release of oxygen or decrease O2 binding
Jan 18 slide 10
Does temperature affect hemoglobins affinity for O2?
Yes
Active muscles produce heat and as blood passed by the warm muscles there will be an increase in oxygen release, change in temp causes slight change in hemoglobin ability to hold on to oxygen (right shift)
Jan 18 slide 11 graph
Does metabolic compound 2,3-DPG affect hemoglobins affinity for O2?
Yes
RBC release ATP which increase 2,3-DPG production which causes a rightward shift
Chronic hypoxia increases 2,3 DPG production
Higher altitudes cause anemia to increase 2,3 dpg production
What type of partial pressure does hemoglobin have to be exposed to to get 100% saturated?
98.5% saturation is max for normal conditions, curve flattens for a long time hard to reach 100
Jan 18 slide 13
What is the importance of removing CO2 from the body?
Elevated PCO2 causes acidosis, low pH leads to interruptions in hydrogen bonds and denaturing of proteins
Abnormally high PCO2 depresses the CNS causing confusion, coma or even death
What is done with CO2 in the body?
Cels produce far more CO2 than plasma is capable of carrying
Only 7% of CO2 carried by venous blood dissolved into plasma
Remaining 93% diffuses into red blood cells
23% binds to hemoglobin HbCO2 (carbaminohemoglobin)
70% is converted to HCO3- (bicarbonate)
Jan 18 slide 16-17
What are the 2 purposes of converting CO2 to HCO3?
How long does CO2 convert to HCO3 (bicarbonate)?
- Provides an additional means of CO2 transport from cells to the lungs
- HCO3 is available to act as a buffer for metabolic acids, stabilization body’s pH
The conversion of CO2 to HCO3 continues until equilibrium is reached
Jan 21 Slide 3
What are the 2 mechanisms used to ensure equilibrium is not reached?
One mechanism removes HCO3- from red blood cells and another mechanism mops up excess H+
Hemoglobin acts as a buffer binds excess H+ ions to prevent large changes in body’s pH and if blood CO2 is too high Hb cannot soak up all the H+ and respiratory acidosis can result
What happens to CO2 when O2 leaves Hb at the tissues?
CO2 binds with free hemoglobin at exposed amino groups (-NH2) which forms carbaminohemoglobin
CO2 binds not only the iron but also free exposed amino groups
Jan 21 Slide 5
Study the diagram of respiratory gas equilibrium on slide 6 Jan 21
Okay
All processes on growth occur until equilibrium is reached
When blood reaches systemic tissues, O2 will be brought in
Study the diagram of CO2 removal in the lungs and compare to the respiratory gas equilibrium diagram on the slide above on slide 7-8 Jan 21
Okay
How is ventilation regulated?
What role to neurons play?
What is the respiratory control centre?
Breathing is rhythmic process that mostly occurs subconsciously similar to beating of the heart
Need neuronal input to go to our muscles to initiate contraction, we dont entirely know the neuronal control of ventilation
Respiratory control centre is found in the medulla of the brain
What do neurons in the pons do?
Integrate sensory information and interact with medullary neurons to influence ventilation
(Send some input into areas in medulla to help coordinate movement. Can help ventilation but not necessary for it)
What is the nucleus tractus solitaris (NTS) and the dorsal respiratory group (DRG)?
NTS- part of medulla that contains the DRG
DRG- mainly controls inspiratory muscles via phrenic nerve and intercostal nerve (QUIET BREATHING)
NTS receives input from peripheral mechanisms and chemoreceptors
SLide 11 Jan 21
What is the pontline respiratory group (PRG)?
What is he ventral respiratory group (VRG)?
PRG- smoothbreathing, receives sensory info from DRG
Provides tonic input to DRG to help medullary networks coordinate a smooth respiratory rhythm (doesn’t create the rhythm)
Slide 12 Jan 21
VRG- pacemaker of the ventilation (pre-botzinger complex)
Controls muscles of active inspiration and expiration, remains quiet otherwise
Outputs that keep upper airways open
Slide 13-14 Jan 21
What are peripheral chemoreceptors?
What is the glomus cell?
Aortic and carotid bodies sense changes in arterial PO2, PCO2, and pH and adjust ventilation accordingly (takes a large drop in PO2 to trigger peripheral chemoreceptors)
Carotid bodies found on carotid sinus
Aortic bodies found on aortic arch
Glomus cell- responsible for sensing the changes in CO2, O2, and pH
Slide 15-16 Jan 21
What are central chemoreceptors?
Where located, what they respond to
Located in the medulla
Provide continuous input to respiratory control centre
Mainly respond to changes in PCO2 (tonically active, always providing some level of input)
Can respond to pH changes in cerebrospinal fluid causes by CO2, but not changes in plasma pH
Slide 18-19 Jan 21
What happens with decreased arterial O2 in terms of inspired PO2, alveolar PO2, arterial PO2, peripheral chemoreceptors, respiratory muscles, and ventilation?
Inspired PO2- goes down Alveolar PO2- goes down Arterial PO2- goes down Peripheral chemoreceptors- firing Respiratory muscles- contractions Ventilation- goes up Return of alveolar and arterial PO2 toward normal
What happens with increased arterial H+ in terms of arterial H+, peripheral chemoreceptors, respiratory muscles, ventilation, Alveolar PCO2, and arterial PCO2?
Production of non-CO2 acid Arterial H+ goes up Peripheral chemoreceptors- firing Respiratory muscles- contractions Ventilation- goes up Alveolar PCO2- goes down Arterial PCO2- goes down Return of arterial H+ toward normal
What happens with increased arterial CO2 in terms of alveolar PCO2, arterial PCO2, Brain extracellular fluid PCO2, Brian extracellular fluid H+, central chemoreceptors, arterial H+, peripheral chemoreceptors, respiratory muscles, and ventilation?
Breathing gas mixture containing CO2 Alveolar PCO2- goes up Arterial PCO2- goes up Brain extracellular fluid PCO2- goes up Brian extracellular fluid H+- goes up Central chemoreceptors- firing Arterial H+- goes up Peripheral chemoreceptors- firing Respiratory muscles- contractions Ventilation- goes up Return of alveolar and arterial PCO2 toward normal
What are irritant receptors in the lungs?
Respond to inhaled particles or noxious gases
Send input to CNS, parasympathetic outputs then respond by causing bronchoconstriction
Leads to rapid shallow breathing and turbulent airflow to deposit irritant in mucosa
Reflexes can initiate coughing or sneezing
What are stretch receptors in the lungs?
Prevent over inflation of lungs (hering-breuer inflation reflex)
How do we have control over breathing?
Higher Brian centres (cerebral cortex) have voluntary control over breathing
Some control over our breathing allows us to over power respiratory centres only to a point though until the chemoreceptors take over (cant hold our breathe forever)
Emotional and pain stimuli can affect breathing
Receptors in muscles anticipate changes and feed forward control respiration before anything actually happens (predicts)
