BHS 116 – Physiology
Notetaker: Jenna Rogers
Date: 10/7/2011, 1st
Page1
Review: Bohr vs Haldane Effect (make sure you know the differences- they are opposites)
Bohr Effect:
-
Changes in PO2 caused by changes in PCO2 and H ion changes
Increased O2 release from hemoglobin by an increase in PCO2 and H ions
Haldane Effect:
-
Changes in PCO2 due to change in oxygen
Increase CO2 and hydrogen at tissues allows release of O2 from hemoglobin
CO2 and H can bind to hemoglobin
Regulation of Respiration
Respiratory center
-
Found in pons and medulla with sub centers (clusters of neuron cell bodies)
main control: phrenic nerve that innervates the diagram
o signals from the respiratory center travel down the spinal cord and synapse on the cell
bodies of the phrenic nerve
o stimulated = diaphragm contraction and inspiration
o inhibited (no signals firing)= diagram relaxes and expiration
Groups of Neurons that control Respiration
Dorsal Respiratory Group (DRG) - normal inspiration
-
located in medullary respiratory center
signals from chemoreceptors that travel along CN IX and X
ONLY inspiratory neurons- control inspiration
o Normal expiration= cease firing of stimulation to the phrenic nerve
expiratory neurons- only stimulated in active respiration
o overload of DRG and ventral respiratory group comes into play
Ventral Respiratory Group- active respiration
-
-
located in medullary respiratory center
both inspiratory and expiratory neurons (majority are inspiratory)
o remain inactive during normal quiet breathing
o activated in active respiration
o don’t need expiratory firing until we hit point where we need extra expiration
Over drive mechanism: only time when expiratory neurons fire:
BHS 116 – Physiology
Notetaker: Jenna Rogers
o
Date: 10/7/2011, 1st
Page2
when there is increased pulmonary ventilation and we are breathing faster and harder,
there is signal spillover from DRG and this stimulates Ventral group neurons causing
inspiration and to a lesser extent expiration
2 Centers in the Respiratory Center
-
-
Pneumotaxic Center- brake on DRG firing to allow relaxation to occur
o In the pons respiratory center
o Modulator of DRG
o Sends signals to DRG that help switch off their firing
o Limit the duration of inspiration- a check and balance system
 Prevents constant breathing in with no relaxation and expiration
o Strong pneumotaxic signals= inspiration doesn’t last very long b/c the DRG neurons are
constantly being inhibited by the pneumotaxic center
 Short inspiratory signals
o Weak pneumotaxic signals= inspiration lasts longer b/c there is no brake
o Role: increase the rate of inspiration by limiting the length of inspiration
Apneustic Center
o In pons
o Inhibits the switching off of the DRG
o Acts against Pneumotaxic
o Encourages prolonged inspirations
o Normal: pneumotaxic is more dominant, inspiration is limited
o Nonfunctional pneumotaxic= prolonged inspirations with short bursts of expiration
(apneusis)
 There are other receptors to trigger expiration
Pre- Botzinger Complex- the SA note of respiration
o
o
Sets the pace for respiratory rhythm
Interacts with DRG
Hering- Breuer Reflex
-
-
Stretch receptors in the muscles of the walls of the bronchi and bronchioles send sensory nerve
signals via the vagus nerve to the DRG
Pulmonary stretch receptors sense and increased volume in the bronchioles
o When apneustic center takes over and there is prolonged inspiration, the smooth
muscles in the bronchi and bronchioles sense a stretch and sends a message to the DRG
to switch off the inspiratory neurons
Internal control in lungs and respiratory tract for expiration to occur when apneustic takes over
BHS 116 – Physiology
Notetaker: Jenna Rogers
Date: 10/7/2011, 1st
Page3
Peripheral Chemoreceptor Systems- control inspiration based on PO2 and PCO2
-
-
-
-
Found in same spots as baroreceptors
Detect changes in the arterial blood PO2
o Not active until P02 drops below 60 mm Hg
Simulate increase in ventilation
o Nerve impulses really increase when PO2 drops below 60 mm Hg
o Increased impulses sent back to respiratory center resulting in increased respiration
Sense H ion concentration- Pathological high acid in the blood
Weakly respond to increased PCO2
Only in emergency situations- in an area when there is a lot less oxygen or if we are climbing a
mountain (atmospheric PO2 drops, alveolar PO2 drops, arteriole PO2 drops)
Effects on alveolar ventilation
o Only a dramatic increase of respiratory rate when we get below a PO2 of 60
o Need more O2 in b/c there is less in the alveoli to exchange with the blood. Need to
increase respiratory rate to bring more O2 in
Hemoglobin dissociation
o PO2 below 60= hemoglobin is giving up O2 at a much faster pace
o Need to increase ventilation to fill up the empty hemoglobin spots with O2
Summary:
o Greatest effect at PO2 below 60
o No peripheral regulation- low PO2 would be inhibitory to the medullary respiratory
center, decreasing ventilation
o With peripheral Regulation- when it does get low, they send signals to increase
ventilation to bring arteriole PO2 back up to normal levels
o Receptors only respond to amount of O2 physically dissolved in blood
 All of O2 bound to hemoglobin is not sensed by the chemoreceptors
 Where peripheral chemoreceptors fail:
 Carbon monoxide- dissociates O2 from hemoglobin but
chemoreceptors don’t sense the loss of O2
 Anemia- decreased red cells are not sensed so there is still not much O2
being delivered
Central Chemoreceptors
-
located in the medulla (very close to the DRG)
sensitive to CO2 induced H ion changes in the brain
don’t respond directly to CO2- only respond to H ions
CO2= Trojan horse that brings the H ions across the blood brain barrier (H can’t cross barrier)
o CO2 will bind with water to form carbonic acid which dissociates into bicarbonate and H
o H binds to the central chemoreceptors
o Signal sent to DRG
BHS 116 – Physiology
Notetaker: Jenna Rogers
-
-
Date: 10/7/2011, 1st
Page4
Elevated PCO2= increase in ventilation to blow off CO2
Decrease in PCO2= decrease in ventilation to decrease the amount of CO2 blown off to increase
the amount that stays in the blood
PCO2 is the primary driver of respiration rate until PO2 drops below 60
Why we can’t hold our breath forever
o Central chemoreceptors sense that there is a PCO2 increase in the tissues because we
are not blowing off the CO2 and it sends a signal to force expiration
Desensitize
o Patented short term regulators
o Extended elevated PCO2- they don’t respond as easily anymore
o Ex. Chronic lung disease
 Early disease- central chemo receptors work
 Later- desensitized and cannot respond as efficiently
Pathological high acid in the blood- increase respiration
-
Hydrogen Ions from lactic acid or ketoacidosis (diabetes)
Drive H concentration up and increases acidity of blood
o stimulates the peripheral chemoreceptors to trigger medullary respiratory center to
increase respiration to blow off more CO2
o Indirectly reducing the acidity in the blood by getting rid of CO2
 Amount of H added to the blood from CO2 is adjusted
Acclimatization
-
-
When we climb a mountain and become acclimated to the altered O2 concentration at these
altitudes
Ascend too quickly= mountain sickness
o Low PO2 – atmospheric P is low
o low oxygenated hemoglobin- releasing oxygen more easily at PO2 below 60
o Decrease PCO2 levels
 Peripheral chemoreceptors sense low PO2 and increase ventilation which blows
off more CO2
Slow ascension- allow acclimation- needs TIME (2-3 days)
o No mountain sickness b/c:
o Central chemoreceptors drive respiration normally but then peripheral chemoreceptors
take over at high altitudes. We are giving peripheral chemoreceptors time to kick in
o Erythropoietin production increases- increase # of RBC and increase binding capacity of
blood. Takes a few days
o RBC produce more BPG which stimulates O2 release from the hemoglobin easing the
delivery of O2 to the tissue
BHS 116 – Physiology
Notetaker: Jenna Rogers
Date: 10/7/2011, 1st
Page5
Exercise
-
-
O2 consumption
o Moderate exercise increases O2 consumption and increase ventilation 4-8 fold
o Severe exercise increases ventilation dramatically
 Body needs to adjust ventilation rate to bring in enough oxygen for muscles
Regulation of respiration
o No change in arterial PCO2 pH or PO2- not driving ventilation in exercise
o The major drivers of ventilation during exercise
 Brain transmits impulses to muscles and respiratory center- we know we are
exercising
 Body movements excite joint and muscle proprioceptors which send excitatory
impulses to the respiratory center
 Increased body temperature
 Epinephrine release from adrenal glands
Voluntary control of respiration
-
-
-
Hyperventilate- over breath or deep breaths to bring in more air
o Take in more O2 and blow off more CO2
o Max amount brought in is 6000 ml/min
Hypoventilation- take smaller or no breaths
o PCO2 increases- stimulates central chemoreceptors and override voluntary control to
force expiration
o PO2 decreases
Alter PO2 and PCO2 levels and changes pH
Not mediated through respiratory center
o Contraction and relaxation of diagram signals from the cortex- conscious centers
Other involuntary controls
-
-
Airway irritant receptors- triggers cough
o Sensory nerve endings in epithelium of airway
o Stimulated by irritants and goes directly to DRG to stimulate coughing and sneezing
Lung J Receptors
o J= in the lung in the alveolar wall in close juxtaposition to the pulmonary capillaries
o Stimulated by Increase in BP in lungs
 engorgement of capillaries with blood causes capillaries to touch up against
receptors to trigger them
o Stimulated by edema
 Extra fluid places pressure on the receptors
BHS 116 – Physiology
Notetaker: Jenna Rogers
o
-
-
Gives the feeling of not being able to catch your breath
 Feeling of breathlessness= dyspnea
Brain Edema
o Increase fluid p in brain directly inactivates respiratory center
o Fluid buildup causes pressure in brain and can alter the signals from the DRG to the
diaphragm
Anesthesia- depresses respiratory center
o Why you have to be ventilated
Clicker Question
Peripheral Chemoreceptors most strongly respond to
1.
2.
3.
4.
Date: 10/7/2011, 1st
Page6
Decreased arterial PO2
Decreased arterial PCO2
Increased arterial PO2
Increased arterial PCO2
Ans: Decreased arterial PO2