Gas Transport and Respiratory Disease Flashcards
Molecular O2 is carried in blood in 2 forms
- 1.5% is dissolved in plasma
- 98.5% is loosely bound to the Fe of Hemoglobin (Hgb) in RBCs
How many molecules of O2 can be carried per Hgb
4 molecules of O2
O2 is loaded/unloaded by changes in the shape of Hgb
- As O2 binds, Hgb affinity for O2 increases - efficient loading
- As O2 is released, Hgb affinity for O2 decreases - efficient unloading
a fully saturated Hgb molecule has how many heme groups bound to O2
4 heme groups
a partially saturated Hgb molecule has how many heme groups bound to O2
1-3 heme groups
the rate of loading/unloading is regulated by
pO2, temperature, blood pH, and pCO2
under normal, resting conditions arterial blood Hgb is how saturated
98%
under normal, resting condition venous blood Hgb is how saturated
75%
Venous Reserve
substantial amounts of O2, still available in venous blood
What does the amount of O2 carried by Hgb depends on
pO2
more O2 is present…
more O2 is bound to Hgb
Safety Margin
at a high pO2, Hgb stays almost fully saturated seven with a large change in pO2
Efficiency
at a low pO2, Hgb experiences sharp decreases In saturation with similar changes in pO2
active body cells produce about how much CO2/minute
200mL of CO2/minute
CO2 is transported in blood in 3 forms
- 7-10% dissolved in plasma
- 20% bound to globin of Hemoglobin (carbaminohemoglobin)
- 70% as bicarbonate ions in plasma
carbonic amhydrase
enzyme found in RBCs that catalyzes the reactions
exchange of CO2 slide 6+7
Bohr effect
- O2 unloading from Hgb is enhanced by an increased pCO2
- enhances O2 delivery where it is most needed
ex. an exercising thigh muscle
Haldane effect
- CO2 unloading from Hgb is enhanced by and increased pO2
- enhances CO2 delivery for expiration
ex. pulmonary circulation
bicarbonate buffer system
important for resisting shift in blood pH
- if H+ concentration increases, H+ is removed by forming H2CO3
- if H+ concentration decreases, H2CO3 dissociates into H+
respiratory acidosis
slow, shallow breathing allows CO2 to accumulate – carbonic acid forms, and pH drops
respiratory alkalosis
rapid, deep breathing depletes CO2 - carbonic acid is reduced, and pH rises
hypoxia
inadequate delivery of O2 to the body’s tissues
symptom: cyanosis when Hbg saturation dips below 75%
Anemic hypoxia
too few RBCs or abnormal RBCs
ischemia hypoxia
impaired/blocked blood circulation
histotoxic hypoxia
body cells are unable to use delivered O2
hypoxemic hypoxia
reduced arterial pO2
CO poisoning
CO outcompetes O2 for heme binding sites
Medulla Respiratory centers (2)
- Ventral Respiratory Group (VRG)
- Dorsal Respiratory group (DRG)
Ventral Respiratory Group (VRG)
- impulses for inspiration travel along the phrenic and intercostal nerves
- eupneic respiratory rate of 12-16 breaths/minute
Dorsal Respiratory Greoup (DRG)
- integrates inputs from stretch and chemoreceptors and communications them to the VRG
What determines the depth of ventilation?
the intensity of the stimulation to the inspiratory muscles
chemoreceptors
receptors responding to chemical fluctuations in the blood - the amount of H+, CO2, O2
what increases the rate + depth of respiration
a rise in CO2 triggers
hyperventilation
an increase in the rate + depth of breathing - exceeds the body’s need to remove CO2
- happens involuntarily during stress and anxiety
what happens when we are hyperventilating
- leads to reduced levels of CO2 in the blood and vascular constriction
symptoms of hyperventilation
decreased perfusion, tingling/numbness, dizziness, fainting
hypothalamic controls
strong emotions and pain send signals to the respiratory centers - responses are mediated though the limbic system and the hypothalamus
ex. gasping in shock, breath holding in anger, hyperventilation in excitement
cortical controls
taking conscious control of respiratory rate - direct impulses from the cerebral motor cortex - medullary control are bypassed
ex. voluntary breath holding – the VRG will be automatically reinitiated when CO2 concentrations reach critical levels
exercise
- working muscles consume O2 and produce CO2
- ventilation will increase 10-20 fold
hyperpnea
increased ventilation in response to metabolic needs
high altitude
- in increased altitudes, pO2 is lower
- demands are met despite lower situation of arterial blood
acute mountain sickness
headaches, SOB, nausea, dizziness
Emphysema
permanent enlargement of the alveoli and pulmonary capillaries, use of accessory muscles, hyperinflation of the lungs
chronic bronchitis
chronic and excessive mucus production, inflamed lower respiratory tract, obstructed airways, impaired ventilation
dyspnea
labored breathing
Asthma
- short term or reversible COPD
symptoms: coughing, dyspnea, wheezing and chest tightness
obstructive sleep apnea
collapse of the upper airways, musculature of the pharynx relaxes during sleep
central sleep apnea
reduced drive from the brain’s respiratory centers
