Gas Transport and Respiratory Disease Study Guide Flashcards
saturation in terms of hemoglobin
- Fully saturated hemoglobin molecule: has all 4 heme groups bound to O2
- Partially saturated hemoglobin molecule: has 1-3 heme groups bound to O2
- Arterial blood saturation: under normal, resting conditions, Hgb is 98% saturated
- Venous blood saturation: under normal, resting conditions, Hgb is 75% saturated
changes in hgb’s shape and resultant changes in its affinity for O2 during unloading/loading
- As O2 binds, Hgb’s affinity for O2 increases – efficient loading
- As O2 is released, Hgb’s affinity for O2 decreases – efficient unloading
Safety margin on O2-Hemoglobin Dissociation Curve
at high Po2, Hgb stays almost fully saturated even with a large change in Po2
efficiency of O2-Hemoglobin Dissociation Curve
at low Po2, Hgb experiences sharp decreases in saturation with similar changes in Po2
cause of right shift in O2-Hemoglobin Dissociation Curve
when Pco2, temperature, or H+ rise
cause of left shift in O2-Hemoglobin Dissociation Curve
when Pco2, temperature, or H+ fall
How most CO2 is transported in blood
as bicarbonate ions in plasma
- 7-10% is dissolved in plasma
- 20% is bound to globin of hemoglobin (as HbCO2 or carbaminohemoglobin)
- 70% as bicarbonate ions (HCO3-) in plasma
how bicarbonate ions are formed
- inside RBCs, Co2 combines with water to form carbonic acid: co2+h2o → h2co3
- Carbonic acid is unstable and dissociates into hydrogen and bicarbonate ions: h2co3→ h+ and hco3
Carbonic anhydrase
enzyme found in RBCs that catalyzes reactions to form bicarbonate ions
What happens when bicarbonate ions return to the lungs and how do they become the CO2 we exhale?
- The hco3- moves back into the RBCs and Cl- moves out
- Hco3 will bind with h+ to form h2co3
- H2co3 is split by carbonic anhydrase into co2 and h2o
- Co2 is diffused from the blood into the alveoli and expelled
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 an increased Po2, enhances co2 delivery for expiration (ex → pulmonary circulation)
role of H+ in the bicarbonate buffer system
- Bicarbonate buffer system: important for resisting shifts in blood pH
- H+ concentration increase: h+ is removed by forming h2co3
- H+ concentration decrease: 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, symptoms include cyanosis when hgb saturation drops below 75%
5 types of hypoxia
- Anemic hypoxia: too few RBCs or abnormal RBCs
- Ischemic 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
location of the ventral and dorsal respiratory groups
medulla
ventral respiratory group VRG
sets basal respiratory rate (rhythm generating)
- Impulses for inspiration travel along the phrenic and intercostal nerves
- Eupneic respiratory rate of ~12-16 breaths/minute
Dorsal respiratory group (DRG)
integrates inputs from chemoreceptors and stretch receptors and communicates them to VRG
What determines the depth of ventilation?
intensity of the stimulation to the inspiratory muscles
primary driver for changes in respiratory rate
The level of CO2 – a rise in co2 triggers increases in the rate + depth of respiration
Why respiratory rate increases during exercise
Working muscles consume O2 and produce CO2, causing your body to want to produce more O2. the rise in co2 causes chemoreceptors to pick up on it and send signals and ultimately increase heart rate
Hypernea
increased ventilation in response to metabolic needs
Hyperventilation
an increase in the rate + depth of breathing – exceeds the body’s needs to remove co2 – NOT an action to meet the body’s needs
hyperventilation in relation to co2 and o2
- often happens involuntarily during times of stress and anxiety
- Leads to reduced levels of co2 in the blood and vascular constriction
- Symptoms: decreased perfusion, tingling/numbness, dizziness, fainting
portions of the higher brain that can temporarily override the medullary control of respiratory rate
- Cortical controls: taking conscious control of respiratory rate – direct impulses from the cerebral motor cortex – medullary controls are bypassed
Ex: voluntary breath holding – the VRG will be automatically initiated when co2 concentrations reach critical levels - hypothalamic controls: strong emotions and pain sends signals to the respiratory cetners – responses are mediated through the limbic system and the hypothalamus
Ex: gasping in shock, breath holding in anger, hyperventilation in excitement
- hypothalamic controls: strong emotions and pain sends signals to the respiratory cetners – responses are mediated through the limbic system and the hypothalamus
Emphysema
permanent enlargement/destruction 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
air hunger, labored breathing (occurs with COPD)
COPDs (chronic obstructive pulmonary disease)
emphysema and chronic bronchitis
- 80% of people with a COPD (chronic obstructive pulmonary disease) have a smoking history
- Coughing + frequent pulmonary infections
- Development of respiratory failure – hypoventilation, respiratory acidosis, hypoxemia
- Treatments: bronchodilators, corticosteroids, supplemental O2
asthma
Short term reversible COPD, affects about 1/10 americans (children > adults), symptoms: coughing, dyspnea, wheezing, and chest tightness. Active inflammation of airways proceeds bronchospasms. - Airways are inflamed by immune response, thickened with inflammatory exudate. Common triggers: suits, mites, dogs, fungi. Treatments: bronchodilators, corticosteroids
branch of the ANS is most active during an asthma attack
Parasympathetic is most active – it causes bronchoconstriction
Obstructive sleep apnea(OSA)
collapse of upper airway, musculature of the pharynx relaxes during sleep
Central sleep apnea
reduced drive from the brain’s respiratory system
- both apneas are treated by continuous positive airway pressure (CRAP)
