Resp1- Resp Phys 4

alveolar perfusion (Q^.); alveolar ventilation (V^._A)

lung compliance, airway resistance, and vascular resistance; ventilated alveoli with no blood supply or blood flowing through unventilated alveoli.

dead space ventilation

right to left shunt- arterial blood does not come into contact with alveolus containing fresh gas

Ventilation/perfusion mismatch

lower; upper

hypoxic vasoconstriction and hypocapnic (state of reduced CO2 in the blood) bronchoconstriction

localized hypoventilation (reduced airflow to alveoli), reducing local P_{A O2}--> causes vasoconstriction of pulmonary arteriole supplying that alveolus, redirecting blood flow towards better-ventilated areas of the lungs

occurs when airways are exposed to gas with lower than normal P_{A CO2} (b/c there is no movement of CO2 from blood to alveoli when no perfusion is occurring)--> leads to local bronchoconstriction to redirect airflow toward better-perfused lung regions

combined with hemoglobin (measured as %oxyHb or %saturation), dissolved in plasma (measured as PO2- ABG)

oxyHb and amount of dissolve O2

oxyhemoglobin (HbO₂- oxidized Fe⁺⁺⁺), deoxyhemoglobin (Hb- reduced Fe⁺⁺)

O₂ + Hb ⇋ HbO₂

fraction of all Hb that is oxyHb; mainly determined by P_{a O2} (b/c the higher the arterial P_O2, the more oxygen there is, the more can be taken up by Hb)

Hb saturation (which depends on P_{a O2}) and [Hb] in blood

amount of O2 carried and O2 saturation

reaction of the first Hb subunit with O2 FACILITATES reaction of the next with O2 [causes altered conformation by freeing up subsequent Hb subunits]

at low P_O2, there is a steep curve (so with small increases in P_O2, there are major increases in %oxyHb); at high P_O2, the curve is plateaued

O2 and Hb rapidly combine/dissociate (need to be able to rapidly release it to the tissues)

further increases in PO2 produce only a small increase in %oxyHb saturation

• very little additional; Hb is 100% saturated at 100mmHg so above this, cannot carry more.
• [HOWEVER, if delivery of air to lungs is impaired by disease, supplemental O2 will considerably increase O2 in blood]

O2 diffusion from alveolus is only governed by O2 dissolved in plasma; O2 bound to Hb DOES NOT contribute to P_{a O2}

Hb is an O2 sink--> O2 diffuses from alveolar air to plasma--> plasma PO2 increases, promoting O2 diffusion into RBCs--> increased RBC P_O2 promotes O2 binding to Hb--> effectively lowering dissolved O2, leading to a decreased P_{a O2}--> that causes an increased gradient for O2 diffusion into plasma

all Hb is saturated.

Tissue P_O2 is lower than systemic PaO2--> O2 diffuses from plasma to interstitial fluid--> IF PO2 increases, which promotes O2 diffusion into cells --> lowers PO2 of IF, promoting diffusion of O2 from plasma--> decrease in plasma PO2--> dissolved O2 diffuses from RBC to plasma--> facilitates dissociation of Hb and O2 [overall consequence is transfer of O2 from Hb to plasma to IF to cells by diffusion]

blood P_CO2, blood [H+], blood temperature, 2,3-DPG

right (Hb decreased affinity for O2- more easily delivered to the tissues)

right(Hb decreased affinity for O2- more easily delivered to the tissues)

right(Hb decreased affinity for O2- more easily delivered to the tissues)

right(Hb decreased affinity for O2- more easily delivered to the tissues)

CO2 and H+ combine with globin and alter the conformation of Hb, decreasing its affinity for O2

increase temp alters conformation of Hb, decreasing affinity for O2

DPG binds reversibly to Hb, reducing its affinity for O2

amount of gas dissolves in a liquid at equilibrium is directly proportional to the partial pressure of the gas with which the liquid is in equilibrium [at equilibrium, partial pressure of gas in liquid and gas phases are identical]

diffuse into liquid [henry's law]

its partial pressure, its solubility in plasma

Higher

both will have identical partial pressure in the liquid but differing concentrations in the liquid [CO2 is way more soluble than O2- if there's the same partial pressure of each, the conc of CO2 will be way higher]

solubility, partial pressure

amount of Hb in blood, carrying capacity of Hb, PO2 in blood, shape of the oxyHb dissociation curve

dissolves O2 and Hb-bound O2; since Hb is 98% saturated at 100mmHg PO2, O2 supplementation will primarily result in an increase in dissolved O2 (which is insignificant int he grand scheme...you're not doing much)

metabolic needs of tissues, heart rate, stroke volume

excess amount of deoxyHb in skin blood vessels (esp. mucous membranes); usually due to an impairment in ventilation (rarely problems with Hb itself).

b/c there is less Hb, so all the Hb that is there is saturated with O2 and therefore red

because CO2 is so much more soluble

small amount carried dissolved in the plasma, most of it is converted to bicarb by erythrocytes, some forms carbamino-Hb

right (decreased Hb affinity for O2-easier to deliver O2 to tissues); there is a need for increased oxygen delivery.

increase; [H+]; lower; respiratory acidosis

decrease; [H+]; increased; respiratory alkalosis

tissue P_O2 falls, increasing the diffusion gradient from blood to tissue and increasing the dissociation of Hb-O2.

hypoxemia is low P_{a O2}, while hypoxia is O2 deficiency at the tissue level; hypoxemia is a cause of hypoxia, but it si not the only cause

hypoxemia, anemia, ischemia, histotoxicity

inability of tissue to utilize O2, even though O2 is being delivered at a normal rate (ex. cyanide poisoning, Vit B deficiency)

low atmospheric or inspired oxygen (fire, improper anesthesia), hypoventilation, impaired diffusion, vascular shunt, V/Q mismatch (most common)

defects i neurologic mechanisms of ventilation, thoracic cage abnormalities, upper airway obstruction

elevated P_{a CO2}

P_{a CO2}; hypoxemia stimulates increased ventilation.

cell death

depressed mental activity (maybe coma), reduced work capacity of muscles

atmospheric hypoxia (high altitude), hypoventilation  due to increased airway resistance, hypoventilation due to pulmonary edema

hypoxia caused by reduced O2 transport by blood or resulting from inadequate tissue O2 utilization

peripheral chemoreceptors stimulate ventilation (at low PaO2), kidneys release erythropoietin in response to hypoxemia, increased DPG synthesis (reduced affinity b/w Hb and O2)

hypoventilation or circulatory deficiency.

reduce atmospheric oxygen, anemia, poisoning of oxidative enzymes (b/c no CO2 even being produced in these circumstances), increased alveolar perfusion distance (CO2 is still diffusible enough to equilibrate)

lethargy/exercise intolerance, increased f or V_T, altered posture, open-mouthed breathing, cyanosis, noisy breathing, excessive nasal secretions, loss of symmetry, cough, sneeze, fever