Cardiopulmonary Exercise
Testing: Some points to ponder
Dr. Mohankumar Thekkinkattil,
MD,ABIM,DSc,DPPR,FCCP,FNCCP,FAARC,FIAB,FISM
Senior Consultant Pulmonologist& HOD,
Institute of Pulmonary Medicine & Research,
Sri Ramakrishna hospital,
Coimbatore 641044
email : tmkdr@yahoo.co.in,tmkdr@sify.com
Objectives
• Review the indications for and applications of
comprehensive cardiopulmonary exercise testing
• Review some aspects of the normal
cardiopulmonary response to maximal exercise
• Review the general approach to interpretation of
CPET
• Some new developements
What is Cardiopulmonary Exercise
Testing (CPET)?
• Measurement of rate of oxygen uptake (VO2),
rate of CO2 production (VCO2), minute
ventilation and other ventilatory parameters
while monitoring 12-lead ECG, BP and O2
saturation during maximal “symptom-limited”
exercise
Rationale for Exercise Testing
• Cardiopulmonary measurements obtained at
rest may not estimate functional capacity
reliably
Clinical Exercise Tests
• 6-min walk test
– Submaximal
• Shuttle walk test
– Incremental, maximal, symptom-limited
• Exercise bronchoprovocation
• Exertional oximetry
• Cardiac stress test
• CPET
Types of Exercise Used for CPET
• Usually use either bicycle ergometer or treadmill
• VO2max with bicycle ergometry usually 5-11%
less than with treadmill (no arm movement, no
weight-bearing)
– Must compare with appropriate normals
• Usual protocols: incremental or ramp
– Increase work rate by 5-25 W/min
– Aim to achieve max exercise in 8-12 minutes
Indications for CPET
• Diagnosis
– Unexplained dyspnea
– Exercise limitation
– Documenting exercise-induced hypoxemia,
titrating O2 prescription
– Exercise-induced asthma
Indications for CPET (cont’d)
• Assessment of functional exercise
capacity
– Impairment or disability evaluation
– Preoperative evaluation
– Selection of patients for cardiac
transplantation
– Prognosis:ILD, CF, heart or pulmonary vascular
disease
Indications for CPET (cont’d)
• Exercise prescription:
– Pulmonary or cardiac rehabilitation
– Health maintenance or athletic training
• Assessing response to therapies
Contraindications to CPET
• Acute ischemic changes on ECG
• Unstable angina
• Uncontrolled CHF
• Uncontrolled dysrhythmia
• Third-degree AV block
• Uncontrolled hypertension (SBP>250, DBP>120)
• Thrombophlebitis or intracardiac thrombi
• Acute myocarditis or pericarditis
• Severe AS
• Acute febrile illness
• O2 saturation < 85% on RA
Kottayam apcc2013
Normal Cardiopulmonary Response to
Exercise
Rest Exercise Increase
VO2, L/min 0.250 3.0-4.5 12-18 x
HR, bpm 70 180 2.5-3 x
SV, ml 70 105-140 1.5-2 x
CO, L/min 5 20-25 4-5 x
Ve, L/min 8 180 20-25 x
Coupling of External Ventilation
and Cellular Metabolism
VO2 = HR x SV x (CaO2 – CvO2)
Sinus node
dysfunction
Drugs
Cardiomyopathies
Valvular heart dz
Conditioning
Genetic factors
PaO2
Hemoglobin
SaO2
Skeletal muscle
dysfunction
Capillary density
Determinants of Peak VO2: the Fick Equation
Anaerobic Threshold
• Estimation of the onset of metabolic acidosis
• Occurs at approximately 40-50% VO2max in
normal individuals
– low (early) AT suggests problems in O2 delivery,
muscle oxidative capacity, or both
• More important is whether it occurs, rather than
at what %VO2max
– indicates test is at least close to maximal exercise
– not under voluntary control, not affected by
psychological factors
Anaerobic Threshold
• Direct measurement requires measuring
lactate levels in blood
– requires frequent blood sampling; impractical
• Noninvasive assessment using gas
exchange parameters
– buffering of lactate by bicarbonate produces
disproportionate increase in VCO2
– “V-slope method”
Anaerobic Threshold: V-Slope Method
Ventilatory Response to Exercise
• Normal resting VE: 5-10 L/min
– Higher suggests anxiety, low suggests either
equipment problems or is of no significance
• Normally, there is adequate ventilatory reserve
during exercise
– MVV = predicted maximum VE
– Peak VE close to or above predicted max VE indicates a
ventilatory limitation
– Early in exercise, increase in VE due to increase in VT;
later mainly from increase in RR
Assessing Gas Exchange
• SpO2 and blood gases
– oxygen desaturation implies wasted pulmonary
circulation or reduced pulmonary vascular bed
– P(A-a)O2: normally increases with exercise
• PaCO2 (or PetCO2) should be close to 40
mmHg before AT
– low values indicate hyperventilation, high
values -- alveolar hypoventilation
Assessing Gas Exchange: Physiologic
Dead Space
• VD/VT= (PaCO2 – PeCO2)/PaCO2
• VD/VTnormally ≈ 0.3, drops to < 0.2 during
exercise
– Tidal volume increases
– Improved V/Q matching
Spirometry
• Always done at baseline; post-test spirometry
may help in identifying exercise induced asthma
• Needed to calculate expected VE max (MVV)
(=40xFEV1)
• Tidal and exercise flow-volume loops may provide
more information on maximal ventilatory capacity
Normal Exercise Tidal Flow-Volume
Loops
AJRCCM 2003; 167:211-277
Exercise Tidal Flow-Volume Loops:
COPD
AJRCCM 2003; 167:211-277
Dynamic hyperinflation (air
trapping) during exercise
resulting in EELV higher than
resting FRC with lack of flow &
volume reserve
shown graphically as lack of
space between exercise tidal
loops & &maximum resting loop
Approach to Interpretation of CPET
• Look at both numerical and graphical data
• Was this a maximal (or near-max) effort?
– Subjective assessment of technicians
– Reached predicted HRmax or VO2max
– Ventilatory limitation
– Development of significant metabolic acidosis (bicarb
drop 5mEq or more, R > 1.15)
– O2 sat drop > 5%
Wasserman 9-Panel Plot
Approach to Interpretation of CPET
• Is the exercise capacity normal?
– Peak VO2, max work rate
• Is the cardiovascular response normal?
– HR vs VO2, O2 pulse, anaerobic threshold, VO2 vs work
rate
• Is the ventilatory response normal?
– VE/MVV, max RR, PaCO2
• Is gas exchange normal?
– VD/VT, VE/VCO2, PaO2, P(A-a)O2, SpO2
“Normal” Values
Patterns of Exercise Limitation
• Cardiomyopathy
– Low peak VO2, no HRR, low O2 pulse, early AT,
preserved ventilatory reserve, gas exchange normal (or
mild increase in VD/VT)
• COPD
– Low peak VO2, high HRR, normal or low O2 pulse,
normal or indeterminate AT, low ventilatory reserve,
high VD/VT at rest and less than normal drop with
exercise, oxygenation may be abnormal
Patterns of Exercise Limitation
• Pulmonary vascular disease
– low peak VO2, no HRR, low O2 pulse, early AT, normal ventilatory
reserve, prominent abnormal VD/VT (may be high at rest; little drop
or even increase with exercise), abnormal oxygenation
• Obesity
– low peak VO2/kg, but normal in L/min or normalized to IBW
– VO2 vs work rate shifted up and left (higher O2 cost to perform
external work)
– otherwise normal responses
Patterns of Exercise Limitation
• Deconditioning
– low peak VO2, borderline abnormal cardiovascular
responses, normal ventilatory and gas exchange
parameters
– improves with conditioning
– normal echocardiogram
• Poor effort
– low peak VO2 with no identifiable physiologic
limitation (high HRR, normal/high ventilatory reserve,
normal gas exchange parameters)
“Typical” Response Patterns on CPET
Measurement Heart
Failure
COPD ILD Pulmonary
Vascular
Disease
Obesity Deconditioned
VO2max ↓ ↓ ↓ ↓ ↓ (normal for
IBW)
↓
AT ↓ Normal, ↓ or
indeterminate
Normal or ↓ ↓ Normal Normal or ↓
HRR Usually
none
↑ (normal in
mild disease)
↑ None or
little
None or little None or little
O2 pulse ↓ or ↑ Normal or ↓ Normal or ↓ ↓ Normal ↓
Vent Reserve Normal None or ↓ Normal or ↓ Normal Normal or ↑ Normal
Ve/VCO2 (at
AT)
↑ ↑ ↑ ↑ Normal Normal
Vd/Vt ↑ ↑ ↑ ↑ Normal Normal
P(A-a)O2 Usually
normal
Variable,
often ↑
↑ ↑ May decrease Normal
32
Determinants of VO2max
Atmosphere
Lungs:VE,V/Q, Diffusion
Peripheral circulation: flow,
capillary density, diffusion
Muscle: fiber type, mass, mitochondria, O2
extraction, metabolism
Blood (Hb)
Heart: Qt, SV, HR, BP
Skeletal muscle (pump)
Johnson & Weisman.Clinical exercise testing, 2003
33
LEFT VENTRICULAR DYSFUNCTION
↑VA/Q mismatching ↓Blood (O2) flow
↑VD/VT ↓ pH
↑Ventilatory
requirement
↑ H+La-
↑ CO2
↓ATP
productio
n
Inadequate myocardial
contractility
Dyspnea
EXERCISE
LIMITATION
Dyspnea, fatique
Heart Failure
 Peak VO2 ↓
 O2 pulse ↓
 VE/VCO2 ↑
 HR-VO2 is nonlineer
 VO2/WR ↓
 AT/ VO2 ↓
 Early metabolic
acidosis
 VD/VT-↑
 HRR – N/ ↑
 WR ↓
 BR -N
 VT -↓
 VE –early increase
 PECO2/PETCO2
35
20 Y, M
Dyspnea at rest and
exercise
Nonsmoker
FEV1/FVC= 75 %
FEV1= 70 %
ECHO; EF= 25 %
Heart Failure
36
COPD ± PULMONARY VASCULAR DISEASE
V/Q mismatching Blood flow ↓ Work of breathing
↑
ATP ↓
Lactate ↑
VCO2 ↑
Muscle fatigue ↑
Myopathy
EXERCISE
LIMITATION
VD/VT ↑ PaO2 ↓
pH ↓
Ventilatory recruitment
↑
FEV1 and elastic recoil
↓
Ventilatory capacity
↓
+
COPD
 Peak VO2 ↓
 O2 pulse ↓
 VE/VCO2 –AT ↑
 BR - ↓
 VO2/WR ↓
 AT/ VO2 ↓
 VD/VT-↑
 HRR – N/ ↑
 VT - ↓
 WR ↓
 VE - ↓
 PECO2/PETCO2
38
Normal
COPD
Heart
diseases
W.R.
REST EXERCISE
VO2
39
62 Y, M
History of 50 pack-years
cigarette smoking
Diagnosis of COPD
FEV1= 0.99L
FEV1/FVC= 60 %
MVV= 44L/min
VE= 42L/min
COPD
Kottayam apcc2013
Ulubay G, Görek A, Savaş S,Öner Eyüboğlu F. Tuberk Toraks,
2005
COPD COPDControl Control
 43 stable patients with COPD and 14 healthy controls
 PFTs and CPET were performed
 Hyperinflation determined at peak exercise, even no findings at
rest
42
COPD ± PULMONARY VASCULAR DISEASE
V/Q mismatching Blood flow ↓ Work of breathing
↑
ATP ↓
Lactate ↑
VCO2 ↑
Muscle fatigue ↑
Myopathy
EXERCISE LIMITATION
VD/VT ↑ PaO2 ↓
pH ↓
Ventilatory recruitment
↑
FEV1 and elastic recoil
↓
Ventilatory capacity
↓
+
PAH
 Peak VO2 ↓
 VE - ↑
 O2 pulse ↓
 VE/VCO2 –AT ↑
 VE/VCO2 ↑
 VD/VT-↑
 AT VO2 ↓
 PETCO2 ↓
 PETO2 ↑
 BR – N
 VT - ↑
 PECO2/PETCO2
 VO2/WR ↓
44
PETCO2 PECO2, PECO2/PETCO2
PECO2/PETCO2 Ratio: 4 Groups
0.40
0.45
0.50
0.55
0.60
0.65
0.70
0.75
0.80
Rest Unloaded AT Peak
Activity
Ratio
Norma
COPD
HF
PAH
PECO2: 4 Groups
15
20
25
30
35
RestUnloaded AT Peak
Activity
PECO2,mmHg Normal
COPD
HF
PAH
PETCO2: 4 Groups
20
25
30
35
40
45
50
RestUnloaded AT Peak
Activity
PETCO2,mmHg
Normal
COPD
HF
PAH
Hansen JE, Ulubay G, Chow BF, Sun XG, Wasserman K. Chest 2007
Secondary to increased VD/VT
N: 25 COPD, N: 25 LVF, N: 25 PVD patients
45
 73Y, F
 Complaint of dyspnea
 1998- diagnosis of CREST syndr
2003- RT plus Tamoxifen for
breast Ca
 Nonsmoker
 2003- ECHO; PAP= 45mmHg
 Cpx= Bilateral crackles
 DLCO= 54 %, DLCO/VA= 58 %
MVV= 66 L/min
 VO2/WR= 5.3
 f=54/min
 Desaturated on test
PHT
46
Left ventricular filling↓
Work of
breathing↑
Cardiac function ↓
Interstıtıal lung dıseases
Parenchymal
destruction /scarring
Capillary
destruction
Hipoxemia
EXERCISE
LIMITATION
Elastic recoil ↑ VD/VT ↑
Ventilatory
recruitment ↑
Pulmonary vascular
resistance ↑
Circulatory
impairment
Increased CO
requirement
Ventilatory impairment
ILD
 Peak VO2 ↓
 O2 pulse ↓
 VE/VCO2 –AT ↑
 VE/VCO2 ↑
 WR ↓
 VO2/WR ↓
 AT/ VO2 ↓
 VD/VT-↑
 R- ↑ (50/min↑)
 HRR –↓ / ↑
 BR - ↓
48
TY 45 F
45 Y, F
HRCT= diffuse bilateral
parenchymal infiltrates
ECG= Normal
 FVC = 61 %
 TLC= 84 %
 FEV1 = 58 %
 FEV1/FVC= 78 %
 MVV = 56 L/min
 DLCO = 18 %
 f = 65/min
VD/VT 0.31 at rest
0.38 peak exercise
49
Obesity
 High O2 cost
 Peak VO2 is normal
 Peak VO2/ body weight is low
 Peak VO2/ height is normal
 Normal VD/VT
 Low PaO2 at rest that normalizes during exercise
50
Obesity
W.R.
Rest Exercise
VO2
Normal
Start exercise
Wasserman K, Hansen JE Principles of Exercise Testing and Interpretation. 2005
 Higher O2 cost than normal at rest and during exercise
51
45 Y, M
Complaints of
exercise limitation
ECG= Normal
 FEV1 = 65 %
 FEV1/FVC= 78 %
 MVV = 140L/min
 PVO2 = 126 %
 ATVO2 = 70 %
Poor effort/ Detraining
 Peak VO2 ↓
 HRR ↑
 AT determination rare
 AT/ VO2 –N
 Peak exercise R< 1.0
 WR ↓
 VO2/WR ↓
 BR – N
 Caotic breathing pattern
53
 37 Y, M
 Complaint of
exercise limitation
 ECG= Normal
 FEV1 = 105 %
 FEV1/FVC= 78 %
 MVV = 170L/min
 PVO2 = 50 %
 ATVO2 =
undetermined
Variable HF COPD PVD Obesity
Peak VO2 ↓ ↓ ↓ N ↓
AT ↓ N/ ↓/ φ ↓ N N/ ↓
HR Variable, N ↓/ N N/ mild↓ N/ mild↓ N/ mild↓
O2
pulse ↓ ↓/ N ↓ N ↓
BR N/ ↓ ↓ N N/ ↑ N
VE/VCO2
N/ ↑ ↓ ↑ N N
VD/VT ↑ ↑ ↑ N N
PaO2 N Variable ↓ N/ ↑ N
SpO2
N Variable N N↓
↓
↓/N
↓/ N
↓
↓
N/↑
↓
↓
ILD
N/ ↑
Detraining
Kottayam apcc2013
• 10 normal subjects
–The major goal of this
study was to relate the
expiratory pressures
during exercise to the
pressures associated with
flow limitation.
The Journal of Clinical Investigation Volume 48 1969
• 20 asthmatics in a stable condition
and aged 32+13 yrs with a FEV1 of
101+ 21% pred.
• Conclusion: In asthmatics with
exercise-induced tidal expiratory
flow limitation, the exercise
capacity is reduced as a result of
dynamic hyperinflation.
Eur Respir J 2004; 24: 378–384
• 22 years-old female
• Cough, chest tightness and
wheezing
• Diagnosed with EIB with no
response to BD
• Normal flow volume curve at
rest
Sawtooth Pattern
Breathing Kinetics: FVL Analysis
NormalNormal
Breathing Kinetics: FVL Analysis
Flow limitation
Laryngoscope, 109:136-139,1999
• To compare laryngoscopically observed changes
in the larynx during exercise in persons (2) with
exercise-induced laryngomalacia (EIL) with
changes in asymptomatic control subjects (8).
CPET with FV loops and Direct Laryngoscopy
Patient AJ
• 18 year-old athletic female complaining of
dyspnea and wheezing with exertion
• HPI:
– Inspiratory wheezing, epigastric pain and tight
feeling around the shoulders and neck with
exertion
– Symptoms start after a minute or so of
sprinting or 5-10 min. of regular exercise
• Symbicort, Singulair x 1 year with no
improvement
Kottayam apcc2013
Kottayam apcc2013
ENT and speech path consult
Laryngoscopy:
• Thick secretions
• Normal mobility of the true vocal folds
with full abduction and complete
adduction
• The subglottis was clear
• No paradoxical vocal fold when she
attempted to mimic her dyspneic episodes
Kottayam apcc2013
Patient AJ
Kottayam apcc2013
Patient AJ
• Diagnosis: Arytenoid collapse (laryngeal
dysfunction)
• Patient was seen again by ENT and
underwent arytenoidectomy
• Flow volume loop analysis is beneficial in
defining flow limitation and other breathing
abnormalities during exercise
• Continuous video laryngoscopy is a well
tolerated procedure that can assist in
characterizing structural abnormalities of
the upper airway.
SUMMARY
• Cardiopulmonary measurements obtained at rest may
not estimate functional capacity reliably.
• CPET includes the measurement of expired oxygen and
carbon dioxide.
• The Borg scale is a validated instrument for
measurement of perceptual responses.
CPET may assist in pre-op evaluation and risk
stratification, prognostication of life expectancy, and
disability determination.
SUMMARY
• Cycle ergometer permits direct power calculation.
• Peak VO2 is higher on treadmill than cycle ergometer.
• Peak VO2 may be lower than VO2max.
• Absolute contraindications to CPET include unstable
cardiac disease and SpO2 <88% on RA.
• Fall in BPsys >20 mmHg is an indication to terminate
CPET.
• 1 glucose yields 36 ATP in slow twitch fiber, and 2 ATP
+ 2 lactic acid in fast twitch fiber.
• RER= CO2 produced / O2 consumed
SUMMARY
Above the anaerobic threshold, CO2 production exceeds
O2 consumption.
Ventilation will disproportionately increase at lactate
threshold to eliminate excess CO2.
AT may be determined graphically from V slope method
or from ventilatory equivalent for CO2.
Derived from the Fick equation, Oxygen Pulse = VO2 / HR,
and is proportional to stroke volume.
• In pure heart disease, BR is >30% and HRR <15%.
• In pure pulmonary disease, BR is <30% and HRR >15%.
The Bottom Line …
• Important to focus on the reason(s) for testing
– ensures a correct and meaningful interpretation
• Multitude of graphical and numerical results, and
an over-dependence on complicated algorithms
contributes to confusion
– Focus on cardinal measurements and relationships
– No single finding or measurement is diagnostic of any
specific disease entity
– CPET is never ordered, nor should it be interpreted in
isolation
Karlman Wasserman
• Man to whom I am indebted for my training in
CPET
“ The classic”
78
The End!
Questions????
None , the merrier
Are you O.K?

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Kottayam apcc2013

  • 1. Cardiopulmonary Exercise Testing: Some points to ponder Dr. Mohankumar Thekkinkattil, MD,ABIM,DSc,DPPR,FCCP,FNCCP,FAARC,FIAB,FISM Senior Consultant Pulmonologist& HOD, Institute of Pulmonary Medicine & Research, Sri Ramakrishna hospital, Coimbatore 641044 email : tmkdr@yahoo.co.in,tmkdr@sify.com
  • 2. Objectives • Review the indications for and applications of comprehensive cardiopulmonary exercise testing • Review some aspects of the normal cardiopulmonary response to maximal exercise • Review the general approach to interpretation of CPET • Some new developements
  • 3. What is Cardiopulmonary Exercise Testing (CPET)? • Measurement of rate of oxygen uptake (VO2), rate of CO2 production (VCO2), minute ventilation and other ventilatory parameters while monitoring 12-lead ECG, BP and O2 saturation during maximal “symptom-limited” exercise
  • 4. Rationale for Exercise Testing • Cardiopulmonary measurements obtained at rest may not estimate functional capacity reliably
  • 5. Clinical Exercise Tests • 6-min walk test – Submaximal • Shuttle walk test – Incremental, maximal, symptom-limited • Exercise bronchoprovocation • Exertional oximetry • Cardiac stress test • CPET
  • 6. Types of Exercise Used for CPET • Usually use either bicycle ergometer or treadmill • VO2max with bicycle ergometry usually 5-11% less than with treadmill (no arm movement, no weight-bearing) – Must compare with appropriate normals • Usual protocols: incremental or ramp – Increase work rate by 5-25 W/min – Aim to achieve max exercise in 8-12 minutes
  • 7. Indications for CPET • Diagnosis – Unexplained dyspnea – Exercise limitation – Documenting exercise-induced hypoxemia, titrating O2 prescription – Exercise-induced asthma
  • 8. Indications for CPET (cont’d) • Assessment of functional exercise capacity – Impairment or disability evaluation – Preoperative evaluation – Selection of patients for cardiac transplantation – Prognosis:ILD, CF, heart or pulmonary vascular disease
  • 9. Indications for CPET (cont’d) • Exercise prescription: – Pulmonary or cardiac rehabilitation – Health maintenance or athletic training • Assessing response to therapies
  • 10. Contraindications to CPET • Acute ischemic changes on ECG • Unstable angina • Uncontrolled CHF • Uncontrolled dysrhythmia • Third-degree AV block • Uncontrolled hypertension (SBP>250, DBP>120) • Thrombophlebitis or intracardiac thrombi • Acute myocarditis or pericarditis • Severe AS • Acute febrile illness • O2 saturation < 85% on RA
  • 12. Normal Cardiopulmonary Response to Exercise Rest Exercise Increase VO2, L/min 0.250 3.0-4.5 12-18 x HR, bpm 70 180 2.5-3 x SV, ml 70 105-140 1.5-2 x CO, L/min 5 20-25 4-5 x Ve, L/min 8 180 20-25 x
  • 13. Coupling of External Ventilation and Cellular Metabolism
  • 14. VO2 = HR x SV x (CaO2 – CvO2) Sinus node dysfunction Drugs Cardiomyopathies Valvular heart dz Conditioning Genetic factors PaO2 Hemoglobin SaO2 Skeletal muscle dysfunction Capillary density Determinants of Peak VO2: the Fick Equation
  • 15. Anaerobic Threshold • Estimation of the onset of metabolic acidosis • Occurs at approximately 40-50% VO2max in normal individuals – low (early) AT suggests problems in O2 delivery, muscle oxidative capacity, or both • More important is whether it occurs, rather than at what %VO2max – indicates test is at least close to maximal exercise – not under voluntary control, not affected by psychological factors
  • 16. Anaerobic Threshold • Direct measurement requires measuring lactate levels in blood – requires frequent blood sampling; impractical • Noninvasive assessment using gas exchange parameters – buffering of lactate by bicarbonate produces disproportionate increase in VCO2 – “V-slope method”
  • 18. Ventilatory Response to Exercise • Normal resting VE: 5-10 L/min – Higher suggests anxiety, low suggests either equipment problems or is of no significance • Normally, there is adequate ventilatory reserve during exercise – MVV = predicted maximum VE – Peak VE close to or above predicted max VE indicates a ventilatory limitation – Early in exercise, increase in VE due to increase in VT; later mainly from increase in RR
  • 19. Assessing Gas Exchange • SpO2 and blood gases – oxygen desaturation implies wasted pulmonary circulation or reduced pulmonary vascular bed – P(A-a)O2: normally increases with exercise • PaCO2 (or PetCO2) should be close to 40 mmHg before AT – low values indicate hyperventilation, high values -- alveolar hypoventilation
  • 20. Assessing Gas Exchange: Physiologic Dead Space • VD/VT= (PaCO2 – PeCO2)/PaCO2 • VD/VTnormally ≈ 0.3, drops to < 0.2 during exercise – Tidal volume increases – Improved V/Q matching
  • 21. Spirometry • Always done at baseline; post-test spirometry may help in identifying exercise induced asthma • Needed to calculate expected VE max (MVV) (=40xFEV1) • Tidal and exercise flow-volume loops may provide more information on maximal ventilatory capacity
  • 22. Normal Exercise Tidal Flow-Volume Loops AJRCCM 2003; 167:211-277
  • 23. Exercise Tidal Flow-Volume Loops: COPD AJRCCM 2003; 167:211-277 Dynamic hyperinflation (air trapping) during exercise resulting in EELV higher than resting FRC with lack of flow & volume reserve shown graphically as lack of space between exercise tidal loops & &maximum resting loop
  • 24. Approach to Interpretation of CPET • Look at both numerical and graphical data • Was this a maximal (or near-max) effort? – Subjective assessment of technicians – Reached predicted HRmax or VO2max – Ventilatory limitation – Development of significant metabolic acidosis (bicarb drop 5mEq or more, R > 1.15) – O2 sat drop > 5%
  • 26. Approach to Interpretation of CPET • Is the exercise capacity normal? – Peak VO2, max work rate • Is the cardiovascular response normal? – HR vs VO2, O2 pulse, anaerobic threshold, VO2 vs work rate • Is the ventilatory response normal? – VE/MVV, max RR, PaCO2 • Is gas exchange normal? – VD/VT, VE/VCO2, PaO2, P(A-a)O2, SpO2
  • 28. Patterns of Exercise Limitation • Cardiomyopathy – Low peak VO2, no HRR, low O2 pulse, early AT, preserved ventilatory reserve, gas exchange normal (or mild increase in VD/VT) • COPD – Low peak VO2, high HRR, normal or low O2 pulse, normal or indeterminate AT, low ventilatory reserve, high VD/VT at rest and less than normal drop with exercise, oxygenation may be abnormal
  • 29. Patterns of Exercise Limitation • Pulmonary vascular disease – low peak VO2, no HRR, low O2 pulse, early AT, normal ventilatory reserve, prominent abnormal VD/VT (may be high at rest; little drop or even increase with exercise), abnormal oxygenation • Obesity – low peak VO2/kg, but normal in L/min or normalized to IBW – VO2 vs work rate shifted up and left (higher O2 cost to perform external work) – otherwise normal responses
  • 30. Patterns of Exercise Limitation • Deconditioning – low peak VO2, borderline abnormal cardiovascular responses, normal ventilatory and gas exchange parameters – improves with conditioning – normal echocardiogram • Poor effort – low peak VO2 with no identifiable physiologic limitation (high HRR, normal/high ventilatory reserve, normal gas exchange parameters)
  • 31. “Typical” Response Patterns on CPET Measurement Heart Failure COPD ILD Pulmonary Vascular Disease Obesity Deconditioned VO2max ↓ ↓ ↓ ↓ ↓ (normal for IBW) ↓ AT ↓ Normal, ↓ or indeterminate Normal or ↓ ↓ Normal Normal or ↓ HRR Usually none ↑ (normal in mild disease) ↑ None or little None or little None or little O2 pulse ↓ or ↑ Normal or ↓ Normal or ↓ ↓ Normal ↓ Vent Reserve Normal None or ↓ Normal or ↓ Normal Normal or ↑ Normal Ve/VCO2 (at AT) ↑ ↑ ↑ ↑ Normal Normal Vd/Vt ↑ ↑ ↑ ↑ Normal Normal P(A-a)O2 Usually normal Variable, often ↑ ↑ ↑ May decrease Normal
  • 32. 32 Determinants of VO2max Atmosphere Lungs:VE,V/Q, Diffusion Peripheral circulation: flow, capillary density, diffusion Muscle: fiber type, mass, mitochondria, O2 extraction, metabolism Blood (Hb) Heart: Qt, SV, HR, BP Skeletal muscle (pump) Johnson & Weisman.Clinical exercise testing, 2003
  • 33. 33 LEFT VENTRICULAR DYSFUNCTION ↑VA/Q mismatching ↓Blood (O2) flow ↑VD/VT ↓ pH ↑Ventilatory requirement ↑ H+La- ↑ CO2 ↓ATP productio n Inadequate myocardial contractility Dyspnea EXERCISE LIMITATION Dyspnea, fatique
  • 34. Heart Failure  Peak VO2 ↓  O2 pulse ↓  VE/VCO2 ↑  HR-VO2 is nonlineer  VO2/WR ↓  AT/ VO2 ↓  Early metabolic acidosis  VD/VT-↑  HRR – N/ ↑  WR ↓  BR -N  VT -↓  VE –early increase  PECO2/PETCO2
  • 35. 35 20 Y, M Dyspnea at rest and exercise Nonsmoker FEV1/FVC= 75 % FEV1= 70 % ECHO; EF= 25 % Heart Failure
  • 36. 36 COPD ± PULMONARY VASCULAR DISEASE V/Q mismatching Blood flow ↓ Work of breathing ↑ ATP ↓ Lactate ↑ VCO2 ↑ Muscle fatigue ↑ Myopathy EXERCISE LIMITATION VD/VT ↑ PaO2 ↓ pH ↓ Ventilatory recruitment ↑ FEV1 and elastic recoil ↓ Ventilatory capacity ↓ +
  • 37. COPD  Peak VO2 ↓  O2 pulse ↓  VE/VCO2 –AT ↑  BR - ↓  VO2/WR ↓  AT/ VO2 ↓  VD/VT-↑  HRR – N/ ↑  VT - ↓  WR ↓  VE - ↓  PECO2/PETCO2
  • 39. 39 62 Y, M History of 50 pack-years cigarette smoking Diagnosis of COPD FEV1= 0.99L FEV1/FVC= 60 % MVV= 44L/min VE= 42L/min COPD
  • 41. Ulubay G, Görek A, Savaş S,Öner Eyüboğlu F. Tuberk Toraks, 2005 COPD COPDControl Control  43 stable patients with COPD and 14 healthy controls  PFTs and CPET were performed  Hyperinflation determined at peak exercise, even no findings at rest
  • 42. 42 COPD ± PULMONARY VASCULAR DISEASE V/Q mismatching Blood flow ↓ Work of breathing ↑ ATP ↓ Lactate ↑ VCO2 ↑ Muscle fatigue ↑ Myopathy EXERCISE LIMITATION VD/VT ↑ PaO2 ↓ pH ↓ Ventilatory recruitment ↑ FEV1 and elastic recoil ↓ Ventilatory capacity ↓ +
  • 43. PAH  Peak VO2 ↓  VE - ↑  O2 pulse ↓  VE/VCO2 –AT ↑  VE/VCO2 ↑  VD/VT-↑  AT VO2 ↓  PETCO2 ↓  PETO2 ↑  BR – N  VT - ↑  PECO2/PETCO2  VO2/WR ↓
  • 44. 44 PETCO2 PECO2, PECO2/PETCO2 PECO2/PETCO2 Ratio: 4 Groups 0.40 0.45 0.50 0.55 0.60 0.65 0.70 0.75 0.80 Rest Unloaded AT Peak Activity Ratio Norma COPD HF PAH PECO2: 4 Groups 15 20 25 30 35 RestUnloaded AT Peak Activity PECO2,mmHg Normal COPD HF PAH PETCO2: 4 Groups 20 25 30 35 40 45 50 RestUnloaded AT Peak Activity PETCO2,mmHg Normal COPD HF PAH Hansen JE, Ulubay G, Chow BF, Sun XG, Wasserman K. Chest 2007 Secondary to increased VD/VT N: 25 COPD, N: 25 LVF, N: 25 PVD patients
  • 45. 45  73Y, F  Complaint of dyspnea  1998- diagnosis of CREST syndr 2003- RT plus Tamoxifen for breast Ca  Nonsmoker  2003- ECHO; PAP= 45mmHg  Cpx= Bilateral crackles  DLCO= 54 %, DLCO/VA= 58 % MVV= 66 L/min  VO2/WR= 5.3  f=54/min  Desaturated on test PHT
  • 46. 46 Left ventricular filling↓ Work of breathing↑ Cardiac function ↓ Interstıtıal lung dıseases Parenchymal destruction /scarring Capillary destruction Hipoxemia EXERCISE LIMITATION Elastic recoil ↑ VD/VT ↑ Ventilatory recruitment ↑ Pulmonary vascular resistance ↑ Circulatory impairment Increased CO requirement Ventilatory impairment
  • 47. ILD  Peak VO2 ↓  O2 pulse ↓  VE/VCO2 –AT ↑  VE/VCO2 ↑  WR ↓  VO2/WR ↓  AT/ VO2 ↓  VD/VT-↑  R- ↑ (50/min↑)  HRR –↓ / ↑  BR - ↓
  • 48. 48 TY 45 F 45 Y, F HRCT= diffuse bilateral parenchymal infiltrates ECG= Normal  FVC = 61 %  TLC= 84 %  FEV1 = 58 %  FEV1/FVC= 78 %  MVV = 56 L/min  DLCO = 18 %  f = 65/min VD/VT 0.31 at rest 0.38 peak exercise
  • 49. 49 Obesity  High O2 cost  Peak VO2 is normal  Peak VO2/ body weight is low  Peak VO2/ height is normal  Normal VD/VT  Low PaO2 at rest that normalizes during exercise
  • 50. 50 Obesity W.R. Rest Exercise VO2 Normal Start exercise Wasserman K, Hansen JE Principles of Exercise Testing and Interpretation. 2005  Higher O2 cost than normal at rest and during exercise
  • 51. 51 45 Y, M Complaints of exercise limitation ECG= Normal  FEV1 = 65 %  FEV1/FVC= 78 %  MVV = 140L/min  PVO2 = 126 %  ATVO2 = 70 %
  • 52. Poor effort/ Detraining  Peak VO2 ↓  HRR ↑  AT determination rare  AT/ VO2 –N  Peak exercise R< 1.0  WR ↓  VO2/WR ↓  BR – N  Caotic breathing pattern
  • 53. 53  37 Y, M  Complaint of exercise limitation  ECG= Normal  FEV1 = 105 %  FEV1/FVC= 78 %  MVV = 170L/min  PVO2 = 50 %  ATVO2 = undetermined
  • 54. Variable HF COPD PVD Obesity Peak VO2 ↓ ↓ ↓ N ↓ AT ↓ N/ ↓/ φ ↓ N N/ ↓ HR Variable, N ↓/ N N/ mild↓ N/ mild↓ N/ mild↓ O2 pulse ↓ ↓/ N ↓ N ↓ BR N/ ↓ ↓ N N/ ↑ N VE/VCO2 N/ ↑ ↓ ↑ N N VD/VT ↑ ↑ ↑ N N PaO2 N Variable ↓ N/ ↑ N SpO2 N Variable N N↓ ↓ ↓/N ↓/ N ↓ ↓ N/↑ ↓ ↓ ILD N/ ↑ Detraining
  • 56. • 10 normal subjects –The major goal of this study was to relate the expiratory pressures during exercise to the pressures associated with flow limitation. The Journal of Clinical Investigation Volume 48 1969
  • 57. • 20 asthmatics in a stable condition and aged 32+13 yrs with a FEV1 of 101+ 21% pred. • Conclusion: In asthmatics with exercise-induced tidal expiratory flow limitation, the exercise capacity is reduced as a result of dynamic hyperinflation. Eur Respir J 2004; 24: 378–384
  • 58. • 22 years-old female • Cough, chest tightness and wheezing • Diagnosed with EIB with no response to BD • Normal flow volume curve at rest Sawtooth Pattern
  • 59. Breathing Kinetics: FVL Analysis NormalNormal
  • 60. Breathing Kinetics: FVL Analysis Flow limitation
  • 62. • To compare laryngoscopically observed changes in the larynx during exercise in persons (2) with exercise-induced laryngomalacia (EIL) with changes in asymptomatic control subjects (8).
  • 63. CPET with FV loops and Direct Laryngoscopy
  • 64. Patient AJ • 18 year-old athletic female complaining of dyspnea and wheezing with exertion • HPI: – Inspiratory wheezing, epigastric pain and tight feeling around the shoulders and neck with exertion – Symptoms start after a minute or so of sprinting or 5-10 min. of regular exercise • Symbicort, Singulair x 1 year with no improvement
  • 67. ENT and speech path consult Laryngoscopy: • Thick secretions • Normal mobility of the true vocal folds with full abduction and complete adduction • The subglottis was clear • No paradoxical vocal fold when she attempted to mimic her dyspneic episodes
  • 71. Patient AJ • Diagnosis: Arytenoid collapse (laryngeal dysfunction) • Patient was seen again by ENT and underwent arytenoidectomy
  • 72. • Flow volume loop analysis is beneficial in defining flow limitation and other breathing abnormalities during exercise • Continuous video laryngoscopy is a well tolerated procedure that can assist in characterizing structural abnormalities of the upper airway.
  • 73. SUMMARY • Cardiopulmonary measurements obtained at rest may not estimate functional capacity reliably. • CPET includes the measurement of expired oxygen and carbon dioxide. • The Borg scale is a validated instrument for measurement of perceptual responses. CPET may assist in pre-op evaluation and risk stratification, prognostication of life expectancy, and disability determination.
  • 74. SUMMARY • Cycle ergometer permits direct power calculation. • Peak VO2 is higher on treadmill than cycle ergometer. • Peak VO2 may be lower than VO2max. • Absolute contraindications to CPET include unstable cardiac disease and SpO2 <88% on RA. • Fall in BPsys >20 mmHg is an indication to terminate CPET. • 1 glucose yields 36 ATP in slow twitch fiber, and 2 ATP + 2 lactic acid in fast twitch fiber. • RER= CO2 produced / O2 consumed
  • 75. SUMMARY Above the anaerobic threshold, CO2 production exceeds O2 consumption. Ventilation will disproportionately increase at lactate threshold to eliminate excess CO2. AT may be determined graphically from V slope method or from ventilatory equivalent for CO2. Derived from the Fick equation, Oxygen Pulse = VO2 / HR, and is proportional to stroke volume. • In pure heart disease, BR is >30% and HRR <15%. • In pure pulmonary disease, BR is <30% and HRR >15%.
  • 76. The Bottom Line … • Important to focus on the reason(s) for testing – ensures a correct and meaningful interpretation • Multitude of graphical and numerical results, and an over-dependence on complicated algorithms contributes to confusion – Focus on cardinal measurements and relationships – No single finding or measurement is diagnostic of any specific disease entity – CPET is never ordered, nor should it be interpreted in isolation
  • 77. Karlman Wasserman • Man to whom I am indebted for my training in CPET “ The classic”
  • 78. 78 The End! Questions???? None , the merrier Are you O.K?

Editor's Notes

  • #5: Measuring dyspnea at rest, fev1, ef inadequately predicts. Two teams well matched on paper, 2 patients with same
  • #7: Advantages of bike: no balance problems, allows accurate measurements of external work output (watts, resistance) not available on the treadmill, cheaper/less space needed, easier to measure BP and ABGs. Advantages of treadmill: more natural exercise, often more comfortable for patients. Start by estimating clinically the patient&apos;s exercise capacity -- if low use lower increments. Begin with 2 min at rest with mouthpiece and then 2 min free wheeling or walking at lowest speed, then increase the power output by appropriate increments until exhaustion.
  • #8: Diagnostic evaluation of otherwise unexplained exertional dyspnea or exercise intolerance. Resting measurements of respiratory or cardiac function cannot accurately predict exercise performance. Clinical applications – specific indications Assessment of functional capacity: disability evaluation, preoperative evaluation, selection for cardiac transplantation, prognostic evaluation Diagnostic: unexplained dyspnea or exercise limitation, picking up early (occult) disease, documenting exercise-induced hypoxemia Assessment of response to treatment Exercise prescription: pulmonary or cardiac rehabilitation, athletic training.
  • #9: May be helpful when patients’ symptoms do not match resting PFTs/echo Preop evaluation for lung cancer resection surgeries – may have a role in evaluation of borderline patients. Prognostic utility esp in CHF and CF
  • #10: More clinically meaningful endpoint than resting PFTs in evaluation of new therapies
  • #13: With maximal exercise, O2 consumption can increase up to 18 times, HR 2 to 3-fold, SV by 2x, CO by 5x, minute ventilation 20-25x, and muscle O2 utilization 2-3x. VO2, VCO2, Ve, and HR increase linearly with increasing external work rate (expressed in watts), with metabolic work accomplished by aerobic mechanisms, until at some point increasing proportions of work are done by anaerobic mechanisms and an “anaerobic threshold” is said to be reached. After this point, VCO2 and Ve increase disproportionately to VO2.
  • #15: Summarizes the determinants of O2 delivery at rest and with exercise Normally CO increases linearly with workload or VO2. This is accomplished initially by increases in stroke volume primarily, later mainly by increases in HR.
  • #16: Normally most of the metabolic work of muscles during exercise is done aerobically, but there will be some workload above which a given person exceeds capacity to do work aerobically and further workloads lead to lactic acidosis due to anaerobic metabolism. This threshold is called AT (LT), thought to correspond to the appearance of increased lactate in the blood. Can be used to indicate level of fitness, to monitor the effects of physical training, and to help in diagnosis of exercise limitation. Thought to reflect hypoxia of the exercising muscles.
  • #18: VCO2 plotted against VO2 and intersection of the 2 regression lines is taken to be the anaerobic threshold.
  • #19: Once Vt reaches 50-60% of VC it starts to plateau; further increases in Ve are due to increases in RR. total Ve = effective or alveolar ventilation + dead space ventilation normally, below the anaerobic threshold, Ve increases linearly with VO2 finding a ventilatory limitation is always abnormal Ventilatory slope = Ve/VO2, measured between 25-50% of VO2max (before - variable, after- increases disproportionately past AT); normal = 25-30 high implies wasted ventilation or anxiety -- use Vd/Vt to help differentiate
  • #20: Oxygen saturation easily monitored noninvasively by pulse oximetry O2 sat: need to see change &gt;4% to consider significant
  • #21: PeCO2 = mixed expired CO2, the average CO2 concentration of expired gases Measure of “efficiency” of lung for CO2 elimination (closer PeCO2 is to PaCO2 the more efficient the system) Improved perfusion of upper lung zones during exercise with increased CO and PAP, leading to reduction in high V/Q areas, or reduced dead space ventilation.
  • #23: Compares curves for young and old adults achieving roughly same peak VO2. Normally there is flow and volume reserve at rest and throughout exercise. EELV goes below resting FRC during exercise. With aging, there is some flow limitation – initially mainly encroach on inspiratory reserve volume with minimal inspiratory reserve as exercise progresses, as well as some expiratory flow reserve. Little reserve to either flow or volume at peak exercise.
  • #24: With COPD there is dynamic hyperinflation during exercise (air trapping) resulting in EELV higher than resting FRC, with lack of flow and volume reserve – shown graphically as lack of space between exercise tidal loops and maximal resting loop.
  • #29: Normal limitation to maximal exercise thought to be due to cardiovascular factors With reduced VO2max (i.e. &lt; 80% predicted), limitation may be due to one or more of the above categories. Deconditioning often a component of limitation with other factors, e.g., COPD patients with associated peripheral muscle abnormalities and deconditioning; improves with exercise training -- part of why rehabilitation may help
  • #30: If VO2max is reduced and HRR is low but there is ventilatory reserve, a cardiovascular limitation to exercise is suspected If there is no VR and there is HRR, a ventilatory limitation can be suspected. May have both in a given patient. With peripheral limitation to exercise, will have low VO2max with preserved HRR and VR. Examples include severe deconditioning, neuromuscular problems, myopathies.
  • #52: PVO2 ve AT ulaşımı normal, BR reserve düşük ancak VD/VT normal, PETCO2 normal; Sonuç: obezite
  • #54: Oksijen tüketimi normal, AT’ye ulaşmadan test sonlandırılmış, HRR normal, maksimum kalp hızı 112/183 (hızlanmadan durmuş), irregüler solunum paterni ve buna bağlı olarak irregüler gaz değişimi var.