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Info from 'Respiratory Care Anatomy and Physiology' 5th edition
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overall VA/Qc ratio
important for maintaining gas exchange
resting VA ~4 L/min
resting Qc ~5 L/min
VA/Qc ratio ~0.8
V/Q as determinant of PAO2
ratio affects PAO2 and PACO2
normal PAO2 = 100 torr
normal PACO2 = 40 torr
conditions when V/Q is high
↑PAO2 and ↓PACO2
causes: pulmonary emboli, obstructed pulmonary artery or arterioles, extrinsic pressure on pulmonary vessels, ↓Q
conditions when V/Q is low
↓PAO2 and ↑PACO2
causes: obstructive/restrictive lung disorders, hypoventilation
alveolar O2-CO2 diagram
absolute shunt (V/Q = 0)
perfusion without ventilation
relative shunt (V/Q > 0 but < 1)
absolute dead space (V/Q = ∞)
ventilation without perfusion
relative dead space (V/Q < ∞ but > 1)
regional PACO2 and PAO2 in lungs
hypoventilation → ↑PACO2 → ↑PAO2
V/Q distribution in normal lung
blood flow and ventilation larger at bases, less at apices
base to apex: ↓blood flow > ↓ventilation
apex usually over-ventilated
apex to base: PAO2 ↓ by 40 mmHg and PACO2 ↑ by 15 mmHg
normal gas exchange
room air: PA-aO2 ~7-14 mmHg
100% O2: PA-aO2 ~50-100 mmHg
shunting disease: ↓V/Q and ↑PA-aO2
why PA-aO2 increases when FiO2 increases
Hb saturated to capacity when PO2 is 100-663 mmHg
mechanisms of hypoxemia
hypoventilation
↑PCO2 with ↓PO2
causes: muscle paralysis/weakness, drug-induced respiratory center depression
absolute shunt
R-to-L shunting (venous admixture)
anatomical
intrapulmonary
doesn’t respond well to O2 therapy
V/Q mismatch (V/Q > 0, < 1 [relative shunt])
most common cause, responds well to O2 therapy
variable effect of V/Q imbalances on gas exchange
normal O2 consumption + normal CO2 production + hypoventilation = ↑PaCO2 + ↓PaO2
V/Q mismatch and shunt → normal or ↓ PaCO2 within limits
medullary response to ↑PaCO2 → hyperventilation
↑VE lowers PCO2 without ↑PO2
equilibrium curve shapes different for O2 and CO2
effect of increased V/Q on PaO2 and PaCO2
hyperventilation as cause of VD
ventilation increases out of proportion to blood flow
↓pulmonary blood flow as cause of VD
shock, embolism, overdistended alveoli
blood flow diminished/absent in ventilated alveoli
physical compensatory responses to dead space and shunt
shunt (↓PaO2)
local hypoxic pulmonary vasoconstriction
blood flow diverted to well-ventilated alveoli
poorly-ventilated units have less blood flow
less hypoxemic effect on arterial blood
dead space (↓PaCO2)
local alveolar duct constriction
↑Raw and hypoventilation match V/Q better
indicators of shunt
PA-aO2
most common index of O2 transfer efficiency
↑A-a gradient: ↑shunting
Pa-AO2
more stable than A-a gradient when FiO2 changes
normal ratio: 0.80-0.95
used to predict FiO2 needed to achieve desired PaO2
PaO2/FiO2 (oxygenation ratio)
normal: 380-475 mmHg
poor indicator
affected by changes in PaCO2
PA-aO2, PaO2/PAO2, PaO2/FiO2 are sensitive to pulmonary factors, don’t take CvO2 into account
shunt equations
QTQS=CcO2−CvO2CcO2−CaO2
CcO2=(PAO2⋅0.003)+(Hb⋅1.34⋅ScO2)
(Qs = shunted cardiac output, QT = total cardiac output, [CcO2 − CaO2] = O2 lost from Q mixing, [CcO2 − CvO2] = total O2 uptake)
shunt estimation formulas
[(A−a)⋅0.003]+5(A−a)⋅0.003
3.5+(CcO2−CaO2)CcO2−CaO2
significance of shunt
shunt fraction % | clinical significance |
<10% | normal lungs |
10-19% | seldom requires significant ventilatory support |
20-29% | significant abnormality; requires PEEP/CPAP |
≥30% | severe disease; life-threatening; mechanical ventilation with PEEP |