Blood Gas Transport + Breathing Control Flashcards

(10 cards)

1
Q

Outline the forms by which O2 and CO2 are carried in blood
(specify their contents in arterial and venous blood)

A

Two types of oxygen transport:
1. physically dissolved in blood (2%)
2. chemically bound to hemoglobin (98%)

Oxygen content:
in arterial blood:
CaO2 = 20 ml O2 / 100 ml blood
in venous blood:
CvO2 = 15 ml O2 / 100 ml blood

Three types of carbon dioxide transport:
1. physically dissolved in blood (7%)
2. physically dissolved as bicarbonate ion, HCO3- (70%)
3. chemically bound to Hb molecule (23%)

Carbon dioxide content:
in arterial blood:
CaCO2 = 48 ml CO2 / 100 ml blood
in venous blood:
CvCO2 = 52 ml CO2 / 100 ml blood

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2
Q

Describe the physioloigcal significance of the oxy-gemoglobin dissociation curve.
(How does the right/left shift of curve relate to the affinity of hemoglobin for oxygen and its ability to load oxygen in lungs and unload it to the tissues)

A

y-axis: % Hb saturation
x-axis: PO2 (mm Hg)

mixed Venous blood
(blood leaving circulatory system)
- 75% Hb saturation and PO2 = 40

blood interfacing with alveoli (arterial blood leaving pulmonary system)
- 98% Hb saturation and PO2 = 100

Plateau region (PO2: 60 - 100)
(“loading oxygen at lungs”)
- safety margin for transport in cases where lung PO2 is low
- increase PO2 above 100 does not improve oxygen saturation

Plateau to steep
(arterial blood reaches tissues –> O2 unbinds from Hb )
- PaO2 falls from 98 to 40 mmHg (PvO2)

Steep region
- small decreases in tissue PO2 result in substantial unbinding from O2 from Hb
- tissue PO2 depends on tissue’s metabolic average (avg = 40 mmHg which is used to indidcated mixed venous blood)

P50
- PO2 required for 50% of Hb to become O2 bound
= 26.6 mmHg in normal human aterial blood (assumes pH = 7.4, PCO2 = 40 mmHg, body temp = 37C)

Shifts in curve
1. left shift
- high affinity of Hb for O2
2. right shift
- low affinity of Hb for O2

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3
Q

Describe the impact of PCO2, pH, temp, 2,3-BPG, anemia, and carbon monoxide on the oxy-hemoglobin dissociation curve
(interpret their physiologic outcome)

A

PCO2
- increased CO2 –> right shift
(ex. exercise produces CO2 resulting in easy unloading of O2 into muscle tissue)

2,3 BPG
- increase [2,3 BPG] –> right shift

Temperature
- increase –> right shfit

pH
- increase in pH –> left shift
(decrease in h+ causes less oxygen to be offloaded –> more oxygen used to make carbaminohemoglobin)

Anemia
- flattens curve (decreases Hb –> decreases O2 carrying capacity and O2 content)
- does NOT change O2 saturation (x-axis)

Carbon monoxide
- increase –> left shift (interferes w/ O2 unloading –> tissue hypoxia)
(CO has higher affinity to Hb than O2 –> competition for binding heme site)

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4
Q

Describe the significance of the enzyme, carbonic anhydrase, in transport of carbon dioxide in blood

A

location:
- resides in blood cells

Function:
- accelerates formation of carbonic acid (H2CO3) from CO2 and water by 1000X

Carbonic acid is part of a series of downstream pathways that creates carbaminohemoglobin (CO2HHb)

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5
Q

Explain how O2 and CO2 influence the transport of each other by hemoglobin (reference the Bohr and Haldane Effects)

A

Haldane Effect:
- CO2 dissociation curve influenced by oxygenation state of Hb
(CO2 transport depends on O2 release from Hb –> so CO2 can bind to Hb)

Molecular basis of Haldane effect
- Hb is better at binding H+ and CO2 than O2
–> forms CO2HHb (carbaminogemoglobin)
- CO2HHb assists blood in loading more CO2 from the tissue (acts as a sink which maintains partial pressure gradient for CO2 diffusion out of tissues into plasma and red blood cells)

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6
Q

Identify key structures responsible for automatic control of breathing rhythm and the sources of input to them

A

Breathing is established in CNS
- initiated by medulla

Medullary Respiratory Groups
1. Dorsal Respiratory Group (DRG)
- inspiratory neurons driving inspiratory muscles
- receive input from peripheral chemo/mechano-receptors

  1. Ventral Respiratory Group (VRG)
    - expiratory neurons driving expiratory muscles
    - active during active expiration

Bulbospinal and spinal nerves
- sends info from medulla to muscles of respiration
1. Phrenic nerves
- (C3,4,5 keep the diaphragm alive
- motor output to diaphragms

  1. Intercostal nerves
    - exit thoracic + lumbar spine
    - motor output to intercostal and abdominal muscles
  2. cranial nerves
    - motor output to upper airway dilator muscles
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7
Q

Specify location of central and periphereal chemoreceptors and describe their impact on ventilation in response to changes in arterial PCO2, PO2 and pH

A
  1. Central chemoreceptors
    Location:
    - few mm below ventral surface of medulla
    Impact:
    - stimulated by small changes in PaCO2 via changes in brain ECFluid
    [H+] levels
    - regulates breathing (low PaCO2 –> decreases ventilation)
  2. Periphereal chemoreceptors
    Location:
    - carotid + Aortic bodies
    Impact:
    - key oxygen sensors
    - ventilatatory response to low PaO2 (below 60 mmHg) = hyperventilation
    - Carotid –> sensory info caried by glossopharyngial (CN IX) afferent nerve fibers
    - Aortic –> sensory info carried by vagal (CN X) afferent nerve fibers
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8
Q

Describe how metabolic acidosis accompanying intense exercise or diabetes impacts ventilation and arterial PO2 and PCO2

A

Metabolic acids stimulate peripheral chemoreceptors

ex. lactic acids produced in skeletal muscle during intense exercise
ex. diabetic ketoacidosis

Increased acid content (acidosis)
–> increased ventilation

Increased basic content (alkalosis)
–> decreased ventilation

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9
Q

Specify the effects of hyperventiliation and hypoventilation on arterial blood gases (PaCO2 and PaO2)

A

Hyperventilation
–> hypocapnia (PaCO2 below resting levels)
–> hyperoxia (PaO2 above resting levels)

Hypoventilation
(opp of hyperventilation)

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10
Q

Describe how congenital hypoventilation syndrome, its treatment and how it informs us about automatic versus the conscious/voluntary control of breathing

A

rare disorder in children

  • breathing adequate when awake
    –> conscious/voluntary ventilation intact
  • breathing inadequate during sleep
    –> inadequate automatic control results in alveolar hypoventilation during sleep
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