CPET
Ref: DOI: 10.1002/cphy.c110048
Indications:
- Mechanisms of residual DOE: https://www.atsjournals.org/doi/full/10.1513/AnnalsATS.202004-398FR
2 ways to calc vo2 that correspond to the 2 systems of bulk flow / convective O2 transport: the respiratory system (measuring directly via douglas bag) and the CV system (measure via blood gasses and Fick Equation).
VO2 = VE * (PIO2 - PEO2) = Qt * (CaO2 - CvO2)
CPET measures both
- Grading severity of heart failure (<14L = risk of dying of HF > transplant)
- Lung resection stratification
Adequate
- HR 80%+
- RER > 1.15
- BR < 15%
- Borg > 9
- HCO3 drop of ____
##RER (or equiv at cellular level = RQ)
RER = amount expelled by lungs (measured at mouth or nose). VCO2 / VO2 RQ = metabolism at the cellular level. Proportion of CO2 volume generated to the volume of consumption.
RER estimates RQ.
Over 1.0 implies anaerobic metabolism
Oxygenation
Normally, oxygenation is roughly maintained during exercise. However, A-a Gradient (A-aDO2) increases due to decreased V/Q matching and development of diffusion limitation of oxygen.
V/Q: matching -
The combination of these effects leads to very fit athletes achieving EIAH (Excercise-induced arterial hypoxemia). However, this is near universal at very high altitudes
Why do we have an A-a gradient at all (seems like there would be a lot of selection pressure to maximize inefficiency) => perhaps selection is on exercise physiology, which would be when it matters.
Exertional Hypoxemia in COPD
Dynamic hyperinflation: May have dynamic hyperinflation -> increased deadspace (higher pressures in diseased lung -> less capillary blood flow). -> corrects easily with O2. Also, would push more Q to bases and possibly increase shunting.
Also, if ventilation limitation is present, VO2 might increase more than DO2 => decreased SVo2
Exertional Hypoxemia in ILD / pHTN
Blood flow through lung units is faster => less time for diffusion to occur => may not reach equilibrium
[ ] time course of PO2 in the capillary slide
(The above also explains hypoxemia with altitude, which can occur in normals - Normal people become diffusion limited at high enough)
Pulmonary Vascular pattern = same? Probably reduced effective area for which oxygen diffuses through.
##Ventilatory Thresholds
Determining ET
VCO2 - VO2 plot - spot where the slope increases above 1:1 = AT.
Other ways to check
- VE/VO2 - time plot, where that number starts to go up
- PET O2 starts to increase
Isocapnic buffering - VCO2 increases
Ventilatory Indices
VE / VCO2 - VD/VT should decrease with exercise -> more efficient ventilation (04 -> 0.3). If this doesn't occur (meaning the lungs can't become more efficient), the VD/VT remains high and the VE/VCO2 is high (high in pulmonary vascular disease, ILD, and CHF)
VE / VO2 is less important.
##Cardiac Indices
- Q increases 5-6L for each 1L of O2 consumption
O2 pulse = VO2 / HR = SV * C(a-v)O2
- relatively conserved between AT and max exercise.
- treated as a non-invasive surrogate of stroke volume (assuming you don't have an extraction of O2 problem)
Change in VO2 / for change in WR - roughly 10 in everyone. Decreases in problems with O2 delivery or utilization (most often cardiac disease). Obesity doesn't effect this relationship.
Patterns
1 approach -
- Is study maximal effort? (VO2 plateau, ratings of exertion, RER 1.15+, HR > 80%)
- Is VO2 peak normal or abnormal? (85% or higher)
- Is VO2 at anaerobic threshold normal? (should be ~40%. Identify on VCO2 to VO2 panel at inflection point, or VECO2 panel)
- Is CV response to exercise normal? (Peak HR vs predicted HR, Peak O2 pulse VO2/HR, EKG without signs of ischemia)
- Is ventilatory response to exercise normal (calculate MVV vs Peak Ve - look at UCLA panel 1)
- Is gas exchange normal? (SpO2 drop, VE/VCO2 = efficiency normal?, pattern of EtCO2 (should rise slightly)
