2.5 Cardbon dioxide transport Flashcards
How is CO2 transported in the blood
3 forms
– 7-10% is dissolved in plasma as PCO2
– 20% of CO2 is bound to the globin part of hemoglobin (carbaminohemoglobin)
– 70% is transported as HCO3– in plasma
explain carbon dioxide pickup at the tissues
CO2 starts in tissue cell
- Tissue cell -> interstitial fluid -> blood plasma (dissolved)
- Tissue cell -> interstitial fluid -> RBC in blood plasma
- in RBC: CO2 + H2O -- carbonic anhydrase —> H2CO3–> HCO3- + H+
- HCO3- can go out RBC into blood plasma and combine wl Cl- causing chloride shift
- ***rush of HCO3– from RBCs is balanced as Cl– moves into RBCs from plasma referred to as chloride shift
- Tissue cell -> interstitial fluid -> RBC in blood plasma
- in RBC: CO2 +Hb –> HbCO2 (carbamino hemoglobin) +
how is CO2 released in the lungs
- CO2 dissolved in plasma -> lungs
- HCO3- in blood plasma -> H2CO3 -> Co2 + H2O –> CO2 diff into lungs
- HCO3- in RBC (same rxn as above) -> diff out RBC, out blood plasma and into lung
- HbCO2 (carbamino hemoglobin -> Co2 + Hb -> into lung
What is a Haldane effect
- lower PO2 and hemoglobin O2 saturation allows more CO2 can be carried by Hb (carbaminohemoglobin)
- Process encourages CO2 exchange at tissues and at lungs
* At tissues, as more CO2 enters blood, more oxygen dissociates from hemoglobin (Bohr effect)
* As HbO2 releases O2, it more readily forms bonds with CO2 to form carbaminohemoglobin
what is teh Carbonic acid (H2CO3)-bicarbonate (HCO3–) buffering system:
- helps resit changes in pH
- if H+ concentration in blood rises, excess H+ is emoved by combining with HCO3– to form H2CO3 -> dissociates into CO2 and H2O
what respiratory systems compensate for acid-base imbalances
- changes in respiratory rate and depth affect blood pH
- slow, shallow breathing causes an increase in CO2 in blood, resulting in drop in pH
- Rapid, deep breathing causes a decrease in CO2 in blood, resulting in rise in pH
what are the neural mechansisms for controlling respiration
- Respiratoryrhythmsareregulatedbyhigher brain centers, chemoreceptors, and other reflexes
- involve neurons in the pons and the reticular formation of medulla
- Pontien respiratory centers: in pons
Medullary respiratory centers: in 2 areas - ventral resp group (VRG) and dorsal resp group (DRG)
what is VRG
Ventral respiratory group (meduallary resp center for control of respiraiton)
- Rhythm-generating and integrative center
- network of neurons in brain stem that extends from spinal cord to pons-medulla junction
- sets eupnea: normal respiratory rate and rhythm (12–15 breaths/minute)
- its inspiratory neurons excite inspiratroy muscles via phrenic (diaphragm) and intercostal nerves (external intercostals)
Expiratory neurons inhibit inspiratory neurons
what is DRG
Dorsal respiratory group (meduallary resp center for control of respiraiton)
- network of neurons located near root of cranial nerve IX
- integrates input from peripheral stretch and chemoreceptors, then sends information to VRG neurons
• Much is not known about this group of neurons
describe the Pontine respiratory centers
* neural mech os respiratory control: in the pons
- Neurons here influence and modify activity of VRG
- Act to smooth out transition between inspiration and expiration and vice versa
- transmit impulses to VRG that modify and fine tune breathing rhythms during vocalization, sleep and exercise
- lesions in this area of brain elad to apneustic breathing, where patient takes prolonged inspirations
how is the respiratory rhythm generated
*origin of breathing not fully understood
- One hypothesis: pacemaker neurons in VRG control intrinsic rhythmicity
- most widely accepted hypothesis: reciprocal inhibition of two sets of interconnected pacemaker neurons in medulla generates rhythm
* Each neuron set controls the other to ensure rhythm
have factors affect respiratory centers
– Chemical factors
– Influence of higher brain centers
– Pulmonary irritant reflexes
– Inflation reflex
describe the chemical factors that infleunce breathing rate and depth
* Most important of all factors affecting depth and rate of inspiration
- Changing levels of PCO2, PO2, and pH are most important
- levels of these chemicals are sensed by: central chemoreceptors (located throughout brain stem) and peripheral chemoreceptors (foudn in aortic arch and carotid arteries)
describe the infleuince of PCO2 on breathing rate and depth
- Most potent and most closely controlled
- If blood PCO2 levels rise (hypercapnia), CO2 accumulates in brain and joins with water to become carbonic acid
- Carbonic acid dissocaites, releases H+, DEC pH
- increased H+ stimulates central chemoreceptors of brain stem -> synpase with respiratory regualtory centers
- respiratory centers increase depth and rate of breathing -> acts to lower blood Pco2 and pH rises to normal levels
describe the infleuince of PO2 on breathing rate and depth
- Peripheral chemoreceptors in aortic and carotid bodies sense arterial O2 levels
*central chemoreceptors are not sensitive
- Declining PO2 normally has only slight effect on ventilation because of huge O2 reservoir bound to Hb
- Requries substantial drop in arterial PO2 (below 60 mmHg) to stimulate increased ventilation
- When excited, chemoreceptors cause respiratory centers to increase ventilation
summarize the chemical factors taht influence breathing rate and depth
- rising CO2 levels are msot powerful respiratory stimulant
- normally blood PO2 affects breathing ONLY INDIRECTLY by influencing peripheral chemoreceptor sensitivity to changes in PCO2
- when arterial PO2 falls below 60 mmHg, beomes major stimulus for respiration (via peripheral chemoreceptors0
- changes in arterial pH result from CO2 retention or metabolic factors act indirectly thru peripheral chemoreceptors
describe the influence of higher brian centers of breathing rate and depth
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Hypothalamic Controls
-
act thru limbic system to modify rate and depth of resp
- ex: breath holding that occurs in anger or gasping with pain
- Change in body temperature changes rate
-
act thru limbic system to modify rate and depth of resp
-
Cortical Controls
-
direct signals from cerebral motor cortex that bypass medullary controls
- ex: voluntary breath holding at least until brain stem reinstates breathing when blood CO2 becomes critical
- cant old breathe forever, body will override
- ex: voluntary breath holding at least until brain stem reinstates breathing when blood CO2 becomes critical
-
direct signals from cerebral motor cortex that bypass medullary controls
influence of Pulmonary irritant reflexes on Breathing Rate & Depth
- Receptors in bronchioles respond to irritants such as dust, accumulated mucus, or noxious fumes
*Receptors communicate with respiratory centers via vagal nerve afferents
- Promote reflexive constriction of air passages
– Same irritant triggers a cough in trachea or bronchi or a sneeze in nasal cavity
influence ofHering Breuer reflexe on Breathing Rate & Depth
- mechanical strecth receptors in pleurae and airways are sitmualted by lung inflation
- > send inhibitory signals to medullary respiratory centers to end inhalation and allow expiration
- may act as protective response more than as a nromal regualtroy mechanism
*bc of stretch receptors in lungs
what is emphysema
what are the 3 conseqeuences
caused by COPD
Permanent enlargement of alveoli and destruction of alveolar walls result in decreased lung elasticity
3 consequences
- > Accessory muscles (necessary for breathing) leading to exhaustion from using 10–15% more energy to breathe than normal
- > trapped air causes hyperinflation, flattens diaphragm and causes expanded barrel chest (both reduce ventialtion efficiency)
- > damaged pulmonary capillaries: lead to enlarged right ventricle
*Hereditary factors for disease include alpha-1 antitrypsin deficiency
what is chronic bronchitis
consequence of COPD
– Inhaled irritants cause chronic excessive mucus
– Mucosae of lower respiratory passageways become inflamed and fibrosed
– Results in obstructed airways that impair lung ventilation and gas exchange
– Symptoms include frequent pulmonary infections
– Risk factors include smoking and environmental pollutants
