Dead space – Flashcards

the volume of the conducting airways in which no gas exchange takes place that part of the inspired volume which is expired unchanged at the beginning of expiration, or "the volume of gas exhaled before CO2 reaches the alveolar plateau - according to Fowler (1948)" (Nunn - now the commonly used definition) also termed series dead space

that part of the inspired gas which passes through the anatomical dead space and enters alveoli, but does not take part in gaseous exchange also termed parallel dead space results from failure of adequate perfusion of the alveoli to which gas is distributed

V/Q > 0.8 (snowman has reduce perfusion)

total dead space anatomical + alveolar

volume of fresh gas entering alveoli and effective in arterialising mixed venous blood VA =VT-VDAnat VA does not = alveolar volume

Fowler's method Bohr's method by conservation of mass

single breath analysis using an indicator gas - N2 ,CO2 , O2 , He - marks the transition between dead space and alveolar gas following inspiration of 100% O2 → plot of VEXP vs. %[N2] → wash-in phase

in patients with non-uniform distribution of ventilation, ie. regions of the lung with different time constants, a slow "wash-in" is seen and the method is inaccurate

Expired N2 vs tIme

then plot the Expired N2 vs expired volume

basis: VD doesn't contribute to expired CO2 using the conservation of mass principle

1891 (bunny) When mean FECO2 measured from a Douglas bag Fe = Fraction expired CO2, and Fa = Alveolar fraction of CO2. - Substitute FACO2 with End-tidal CO2 conc - You get VD as Anatomical dead space - Substitute FACO2 with "Ideal" alveloar CO2 conc - You get VD as Physiological dead space - When mean FECO2 substituted by ETCO2 conc and "Ideal" alveolar CO2 conc as FACO2 - You get VD as Alveolar dead space

originally used to estimate FACO2 using estimates of VDAnat from autopsy cast specimens not used to estimate VDAnat until the constancy of alveolar air was established by Haldane and Priestly (1905) - FACO2 is estimated from ETCO2 - mean FECO2 from a Douglas bag

air tight; one way valve

1. body size ↑ VDAnat ~ 2.2 ml/kg (noon) 2. Age ↑ VDAnat with age (?VD/VT) 3. Lung volume;↑ VDAnat ~ 20 ml/l above FRC 4. Posture: - ↓ VDAnat with supine posture - supine 101ml; sitting 147ml (Fowler) 5. Respiratory flow pattern: ↓ VDAnat using Fowler technique with low VT due to the mixing affect of the heart beat below the carina, and the cone advance of laminar flow, seen at low flow velocities 6. Hypoxia: reduce Vd, due to bronchoconstrtion 7. Drugs / Anes: increase dead space; due to bronchodilation 8. Lung disease (emphysema increase anatomical dead space; exicision of lung reduce dead space) 9. Endotracheal intubation; reduce anatomical dead space by 50% (but there is addition volume of the circuit) 10. Position of Jaw and neck; increase with Jaw protrusion in non -intubated people

1. - increase with age 2. - reduce Pul artery pressure, increase zone 1 and increase alveolar dead space 3. - Posture; upright and lateral position increase zone 1 (therotical) 4. - IPPV; increae alveolar dead space due to exaggeration of hydrostatic perfusion gradient; also decreases total pulmonary blood flow; IPPV with short inspiration (t < 0.5 s) applied wave-form → ↑ VDAlv due to maldistribution of ventilation; IPPV & lateral posture → gross V/Q mismatch 5. Tidal volume; VDAlv increases but the ratio remains constant 6. Oxygen: hyperoxic vasodilatation→ increase dead space alv hypoxic vasoconstriction; decrease dead space alv 7. anesthetic gas; increase alveolar dead space don't know why; increase subcarinal dead space 70 ml 8. Lung disease; ARDS microemboli and ventilaion of non vascular air space

estimated from the arterial - end tidal PCO2 difference gas from non-perfused alveoli will contain some CO2, since these receive mixed alveolar gas from anatomical dead space prior to fresh gas gas from poorly perfused alveoli will contain more CO2 than from non-perfused alveoli but the PCO2 will be less than the mixed alveolar PCO2 as represented by the arterial PaCO2 hence the end-tidal alveolar gas will have a lower PCO2 than the PaCO2

this may be estimated from a modification of the Bohr equation to calculate VDAlv/VA - here the equation becomes (PaCO2 - PE'CO2) / PaCO2 where PE'CO2 is the end-tidal CO2

0ml so physiological = anatomical dead space = 150ml

that part of the tidal volume which does not participate in gas exchange and is ineffective in arterialising mixed venous blood, because either, - it doesn't reach the alveoli - VDAnat - it reaches alveoli with no capillary flow, or - it reaches alveoli with inadequate flow - VDAlv