Gas Transport and Respiratory Disease Study Guide

Question 1

saturation in terms of hemoglobin

Answer 1

• 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

Question 2

changes in hgb’s shape and resultant changes in its affinity for O2 during unloading/loading

Answer 2

• As O2 binds, Hgb’s affinity for O2 increases – efficient loading
• As O2 is released, Hgb’s affinity for O2 decreases – efficient unloading

Question 3

Safety margin on O2-Hemoglobin Dissociation Curve

Answer 3

at high Po2, Hgb stays almost fully saturated even with a large change in Po2

Question 4

efficiency of O2-Hemoglobin Dissociation Curve

Answer 4

at low Po2, Hgb experiences sharp decreases in saturation with similar changes in Po2

Question 5

cause of right shift in O2-Hemoglobin Dissociation Curve

Answer 5

when Pco2, temperature, or H+ rise

Question 6

cause of left shift in O2-Hemoglobin Dissociation Curve

Answer 6

when Pco2, temperature, or H+ fall

Question 7

How most CO2 is transported in blood

Answer 7

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

Question 8

how bicarbonate ions are formed

Answer 8

• 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

Question 9

Carbonic anhydrase

Answer 9

enzyme found in RBCs that catalyzes reactions to form bicarbonate ions

Question 10

What happens when bicarbonate ions return to the lungs and how do they become the CO2 we exhale?

Answer 10

• 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

Question 11

Bohr effect

Answer 11

o2 unloading from hgb is enhanced by an increased Pco2, enhances o2 delivery where it is most needed (ex – an exercising thigh muscle)

Question 12

Haldane effect

Answer 12

co2 unloading from hgb is enhanced by an increased Po2, enhances co2 delivery for expiration (ex → pulmonary circulation)

Question 13

role of H+ in the bicarbonate buffer system

Answer 13

• 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+

Question 14

Respiratory acidosis

Answer 14

slow, shallow breathing allows co2 to accumulate – carbonic acid forms and pH drops

Question 15

Respiratory alkalosis

Answer 15

rapid, deep breathing depletes co2 – carbonic acid is reduced, and pH rises

Question 16

Hypoxia

Answer 16

inadequate delivery of o2 to the body’s tissues, symptoms include cyanosis when hgb saturation drops below 75%

Question 17

5 types of hypoxia

Answer 17

• 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

Question 18

location of the ventral and dorsal respiratory groups

Answer 18

medulla

Question 19

ventral respiratory group VRG

Answer 19

sets basal respiratory rate (rhythm generating)
- Impulses for inspiration travel along the phrenic and intercostal nerves
- Eupneic respiratory rate of ~12-16 breaths/minute

Question 20

Dorsal respiratory group (DRG)

Answer 20

integrates inputs from chemoreceptors and stretch receptors and communicates them to VRG

Question 21

What determines the depth of ventilation?

Answer 21

intensity of the stimulation to the inspiratory muscles

Question 22

primary driver for changes in respiratory rate

Answer 22

The level of CO2 – a rise in co2 triggers increases in the rate + depth of respiration

Question 22

Why respiratory rate increases during exercise

Answer 22

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

Question 23

Hypernea

Answer 23

increased ventilation in response to metabolic needs

Question 24

Hyperventilation

Answer 24

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

Question 25

hyperventilation in relation to co2 and o2

Answer 25

• 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

Question 26

portions of the higher brain that can temporarily override the medullary control of respiratory rate

Answer 26

• 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

Question 27

Emphysema

Answer 27

permanent enlargement/destruction of the alveoli and pulmonary capillaries, use of accessory muscles, hyperinflation of the lungs

Question 28

Chronic bronchitis

Answer 28

chronic and excessive mucus production, inflamed lower respiratory tract, obstructed airways, impaired ventilation

Question 29

Dyspnea

Answer 29

air hunger, labored breathing (occurs with COPD)

Question 30

COPDs (chronic obstructive pulmonary disease)

Answer 30

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

Question 31

asthma

Answer 31

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

Question 32

branch of the ANS is most active during an asthma attack

Answer 32

Parasympathetic is most active – it causes bronchoconstriction

Question 33

Obstructive sleep apnea(OSA)

Answer 33

collapse of upper airway, musculature of the pharynx relaxes during sleep

Question 34

Central sleep apnea

Answer 34

reduced drive from the brain’s respiratory system
- both apneas are treated by continuous positive airway pressure (CRAP)