Download ANPS 020 Black 03-30

ANPS020
March 30, 2012
GAS TRANSPORT (cont’d)
Carbon monoxide
-CO from burning fuels
--binds strongly to hemoglobin
--takes place of O2
--can result in carbon monoxide poisoning
To get rid of CO, you need a huge partial pressure of O2 to get of sites
GAS TRANSPORT
Environmental Factors Affecting Hemoglobin
PO2 of blood
Blood pH
Temperature
Metabolic activity within RBCs
GAS TRANSPORT
The oxygen Hemoglobin Saturation Curve
-is standardized for normal blood (pH 7.4, 37 degrees centigrade)
When pH drops or temperature rises
-more oxygen is released
-curve shifts to right
When pH rises or temperature drops
--less oxygen is released
--curve shifts to left
GAS TRANSPORT
The Bohr Effect: increased o2 release from hemoglobin in presence of CO2 (or pH decrease)
Is the effect of Ph on hemoglobin-saturation curve
Caused by CO2
-CO2 diffuses into RBC
-an enzyme called carbonic anhydrase, catalyzes reaction with water
-produces carbonic acid
Carbonic acid
-dissociates into hydrogen ion (H+) and bicarbonate ion
-hydrogen ions diffuse out of RBC, lowering pH
Slide 239: Bohr Effect Formula
---need to know
GAS TRANSPORT: BPG
2,3 biphosphoglycerate (BPG)
-RBCs generate ATP by glycolysis
--forming lactic acid and BPG
-BPG directly affects O2 biding and release
--more BPG, more oxygen released
BPG levels
--BPG levels rise—causes O2 release
GAS TRANSPORT
Fetal and adult hemoglobin
-the structure of fetal hemoglobin
--differs for that of adult Hb
At the same PO2
-fetal Hb binds more O2 than adult Hb
-which allows fetus to take O2 form maternal blood
GAS TRANSPORT
Carbon Dioxide Transport (CO2)
-is generated as a by-product of aerobic metabolism (cellular respiration)
CO2 in the bloodstream
-may be: (different ways for body to carry around CO2)
1. Converted to carbonic acid
2. Bound to protein portion of hemoglobin (Not heme groups)
3. Dissolved in plasma
CO2 TRANSPORT
CO2 in the Bloodstream
70% in transported as carbonic acid
-which dissociates into H+ and bicarbonate
23% is bound to amino groups of globular proteins in Hb molecule
--forming carbaminohemoglobin
7% is transported as CO2 dissolved in plasma
CO2 TRANSPORT
Bicarbonate Ions
-Move into plasma by an exchange mechanism (the chloride shift) that takes in Cl- ions without using
ATP
CONTROL OF RESPIRATION
To control respiration 00 what cells should you actually control
-skeletal muscles
These cells control respiratory minute volume
-nerves
Is this control voluntary and involuntary
-both
CONTROL OF RESPRIATION
How does one know when control is needed? Where do signals originate?
-thinking above, used 5 senses
-chemoreceptors
-Baroreceptors
-others
LOCAL CONTROL OF RESPIRATION
Peripheral and alveolar capillaries maintain balance during gas diffusion by
–changes in depth and rate and respiration
-changes in blood flow and oxygen delivery
This requires excellent coordination between the respiratory and cardiovascular systems
Ventilation – perfusion Coupling
LOCAL CONTROLS: RESPIRATORY AND CARDIOVASCULAR
Scenario: cells in interstitium are very active soo
-O2 is being used PO2 goes down)
-CO2 is being produced (PCO2 go up)
remember: O2 is good and CO2 is band so
-you want to bring in O2 and remove CO2
To bring in a gas, you open up the tube in which it flows, dilate that tube (relaxing muscles)
To slow (Restrict) flow of a gas, you constrict the tube in which is a flow (constricting muscles)
LOCAL CONTROLS: RESPIRATORY AND CARDIOVASCULAR
Scenario: cells in interstitium care very active (muscle cells), so ..
O2 is being used (PO2 foes down)( in tissues
CO2 is being produced (PCO2 go up in tissues)
PO2 ratio (95 mm blood vs. 40 mm interstitium) gets steeper so more goes to inerstitium
PCO2 ratio changes (45 mm interstitium vs. 40 mm blood) so more CO2 goes to blood and increased
CO2 causes smooth muscle relaxation in systemic BVs = vasodilation , blood flow increases CO2 leaves
and more )2 enters via blood
LOCAL CONTROLS VENTILATION PERFUSION COUPLING
Blood flow toward alveolar capillaries directed toward lung lobules where PO2 levels relatively high
(CO2 levels are low)
-alveolar capillaries constrict when PO2 is low
-blood is directed to areas to pick up O2
Smooth muscles cells in walls of bronchioles are sensitive to PCO2
-increases PCO2 causes bronchiodilation
-air flow directed toward lobules where PCO2 is high and CO2 is decreased (CO2 is bad)
-these lobules contain CO2 obtained from blood
CNS CONTROL OF RESPIRATION
Voluntary centers – thinking about it
-in cerebral cortex affect
--respiratory centers of pons and medulla oblongata
--motor neurons that control respiratory muscles
Involuntary Centers – brain stem (not thinking about it)
-Regulate respiratory muscles
-in response to sensory information
-resulting in changes in respiration patterns
CONTROL OF RESPIRATION
Five sensory modifiers of respiratory center activities
Chemoreceptors: are sensitive to PCO2 PO2 of pH of blood or cerebrospinal fluid
Baroreceptors in aortic or carotid sinuses are sensitive to changes in blood pressure
Stretch receptors respond to changes in lung volume
Irritating physical or chemical stimuli in nasal cavity, larynx, or bronchial tree –SNEEZING AND
COUGHING
Other sensations: including pain, changes in body temperature, abnormal visceral sensations
CONTROL OF RESPIRATION
Chemoreceptors Stimulation
Responses to changes in blood pH of P02
In carotid or aortic bodies (in carotid and aorta blood vessels)
Leads to increased depth and rate and respiration
Is subject to adaption
-decreased sensitivity due to chronic stimulation
Receptors Monitoring CSF by chemoreceptors
On ventrolateral surface of medulla oblongata
Respond to increase PCO2 results in decrease in Ph of CSF
Chemoreceptors increase rate and depth of breathing
Causes more air to move in and alveolar CO2concentrations decrease
BARORECEPTOR
Carotid and aortic baroreceptor stimulation
-affects blood pressure and respiratory centers
When blood pressure falls
-respiration increases
When blood pressure increase
-respiration decreases
THE RESPIRATORY CENTERS – brain stem
-Three pairs of nuclei formation of medulla oblongata and pons
Respiratory Rhythmicity Centers of the Medulla Oblongata
-Set the pace of respiration
-can be divided into two groups
--dorsal respiratory group (DRG)
--ventral respiratory group (VRG)
CONTROL OF RESPIRATION
Doral respiratory group
-Inspiratory center
-Functions in quiet and forced breathing
Ventral Respiratory Group
-Inspiratory and expiratory center
-Functions only in forces breathing
RESPIRATORY RHYTMICITY CENTERS
Quiet breathing
-activity in the DRG
--stimulates inspiratory muscles
DRG neurons becomes inactive
--allowing passive exhalation
Forced Breathing
-increased activity in DRG
--stimulates VRG
--which activates accessory inspiratory muscles
After inhalation
-expiratory center neurons stimulate active exhalation
The Apneustic and Pneumotaxic Centers of the Pons
-Paired nuclei that adjust output of respiratory rhythmicity centers
--regulating respiratory rate and depth of respiration
Apneutsitc Center
-Provides continuous stimulation to its DRG center
Pneumotaxic Centers
-inhibit the apneustic centers
-promote passive or active exhalation
Respiratory Centers of Reflex controls
-interactions between VRG and DRG
--establish basic pace and depth of respiration
The pneumotaxic center
-modifies the pace
CONTROL OF RESPIRATION
SIDS
Disrupts normal respiratory reflex pattern
May result from connection problems between pacemaker complex and respiratory centers
1. LOCAL CONTROLS
2. CNS CONTROLS