CPET is a diagnostic test that analyzes physiological responses during increasing exercise intensity. It can be used to evaluate causes of exercise limitation and assess functional capacity. There are various CPET protocols that differ in workload increase (incremental, constant, supramaximal). Key parameters measured include VO2 max, anaerobic threshold, ventilatory efficiency, cardiac function, and acid-base balance. Interpretation of these parameters provides insights into cardiorespiratory fitness and identifies abnormalities that may be causing exercise intolerance.
2. • CPET is a diagnostic procedure that
analyzes the responses and cooperation of
the heart, circulation, respiration, and
metabolism during continuously increase
muscular stress.
6. • According to place
a) Field tests (e.g. 6MWT, ISWT).
b) Laboratory tests (treadmill and cycle
ergometry).
• According to applied load
a) Maximal (incremental tests).
b) Sub-maximal (usually constant workload).
c) Supra-maximal.
7. A. Field tests
Advantages:
• Safe Easy Cheap
• Identical movement stereotype
Disadvantages:
- Relatively inaccurate determination of power& measurements.
8. B. Laboratory tests
Advantages:
• Accurate determination of work load.
• Standard laboratory conditions.
Disadvantages:
• Different movement stereotype worsen achievement.
• Less safe Expensive Need exprience
10. Sub-maximal tests
Advantages:
• Safer
• Lower dependence on tested person (more comfortable)
Disadvantages:
• Often based on estimation (presumption) of HR max, etc.
worse accuracy
11.
12. Parameters cycle Treadmill
VO2 max lower Higher
Blood pressure
assessment
Easy -
Work load
measurement
Yes No
ABG collection Yes No
Noise Less Higher
Safty Safer Less Safer
Wt bearing in
obese
Less More
Leg ms training Less More
15. 2. Assessment of functional exercise capacity
– Impairment or disability evaluation
– Selection of patients for cardiac
transplantation
– Prognosis: CF, heart or pulmonary
vascular disease
16. Routine spirometry and DLCO most useful in
evaluating physiologic operability in low-risk patients
In high-risk/borderline patients, CPET may have a
role along with split-lung function studies
Peak VO2 < 50-60% predicted was associated with
higher morbidity and mortality after lung resection
surgery
20. • Acute myocardial
infarction (3–5 days)
• Unstable angina
• Uncontrolled arrhythmias
causing symptoms or
hemodynamic compromis
• Active endocarditis
• Acute myocarditis or
pericarditis
• Symptomatic severe aortic
stenosis
• Uncontrolled heart failure
• Acute pulmonary embolus
or pulmonary infarction
21. • Left main coronary stenosis or its equivalent.
• Moderate stenotic valvular heart disease.
• Severe untreated arterial hypertension at rest
( 200 mm Hg systolic, 120 mm Hg diastolic).
• Tachyarrhythmias or bradyarrhythmias.
• Hypertrophic cardiomyopathy.
• Significant pulmonary hypertension.
• Electrolyte abnormalities.
22.
23. CPET Protocol
Constant work rate
5-10minutes
Incremental
Multistage
Every 2-3 minutes
Progressive incremental
Every one minute
26. Wasserman, et al. Principles of Exercise Testing and Interpretation.
Lea & Febiger, 1987.
1.Approximate VO2 for Unloaded Pedaling:
150+)6x Weight(
2.Estimate VO2 max
Height (cm) - Age(yrs) x 20 (Males(
Height (cm) - Age (yrs) x 14 (Females(
3.Work Rate Increment
VO2 max pred - VO2 Unloaded /100
Example:50 yr old male, 100 kg and 180 cm
1.VO2 unloaded = [150+(6x100) = 750 ml/min
2.VO2 Pred max = [(180-50) x 20 = 2600 ml/min
3.Work = [2600 - 750] / 100 = 18.5 (round to 20(
Selecting the Work Rate
27. For patients with reduced MVV, FEV1, DLCO (<80%
predicted) we reduced expected peak VO2
proportionally
W = [S*BW *(2, 05 + 0.29*I( – 0, 6 * BW –151]
Where W = watt, S = speed, I = inclination,
and BW = body weight.
According to recommendation of Wassermann we
had change percent of inclination with fixation of
speed.
28. Calculating speed and
inclination
VO2 running (ml kg-1min-1( = 0.2 (speed m
min-1( + 0.9 (speed m min-1((grade %( + 3.5
(ml kg-1 min-1( (ACSM 2009(.
The grade of the treadmill was set at 1%, and
the speed converted to km h-1.
1 kilometer per hour (km/h( = 16.67 meters
per minute (m/min(
33. • This is the highest attainable oxygen consumption
achieved during an incremental exercise test
• VO2 is defined by the Fick equation:
VO2 = CO* C (a – v)O2
where CO is cardiac output and C (a – v)O2 is the
arterio-venous O2 content difference.
34. ►the response is linear
►slope (DV’O2/change in work rate
(DWR)) approximately 10 mL·min1·W-1
35. Anaerobic threshold (AT or LT)
• Occurs at approximately 40-50% VO2max in
normal individuals.
• Indicates test is at least close to maximal
exercise.
• Not under voluntary control, not affected by
psychological factors
36. • 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”.
38. • The ratio of carbon dioxide output and
oxygen consumption (VCO2/VO2) is called the
respiratory exchange ratio (RER).
• Can be used as a rough index of metabolic
activity, this parameter is ~0.85 on a western
diet as this incorporates fat, protein and
carbohydrate.
39. • RER greater than 1.0 could also be caused by
CO2 derived from lactic acid or by
hyperventilation because of the 20-fold or
more higher tissue solubility of CO2 compared
with O2.
40. • In health, increases in tidal volume are
primarily responsible for increases in
ventilation during low levels of exercise.
• As exercise progresses, both VT and fr
increase until 70 to 80% of peak exercise;
thereafter fr predominates. VT usually
plateaus at 50 to 60% of vital capacity (VC).
41. • In health, the increase in VT is due to both a decrease
in end-expiratory lung volume (EELV) through
encroachment on the expiratory reserve volume but
predominantly to an increase in end-inspiratory lung
volume (EILV).
• In normal subjects, EELV typically decreases with
increasing work rate by as much as 0.5–1.0 L below
functional residual capacity, with a consequent
increase in inspiratory capacity (IC).
42.
43. • the ratio of VE at peak exercise to the estimated maximal
voluntary ventilation (MVV) represents the assessment
of the ventilatory limitation or of the prevailing
ventilatory constraints. Ventilatory limitation is judged
to occur when VE /MVV exceeds 85%.
• In lung diseases, the increase in VE /MVV may reflect
either the reduction in ventilatory capacity (reduction in
MVV), the increase in ventilatory demand (increase in
VE ), or both.
44. Recalling that the anatomic dead space volume is
about 150 in an average-sized subject at rest, with
a tidal volume of 500 ml, VD/ VT would be about
0.30.
The minimal value (which occurs near maximal
exercise) should be less than 0.20 in younger
individuals, less than 0.28 in individuals less than
40 years of age, and 0.30 for those older than 40
years; higher values are seen in many forms of
lung disease.
45. The difference between total Ventilation (VE)
and effective alveolar ventilation (VA) is
wasted or dead space ventilation (Vd)
• A high Vd/Vt indicates wasted or inefficient
ventilation, often indicates pulmonary or
pulmonary vascular disease
Vd/Vt
)Efficiency of gas-exchange)
47. Achievement of age-predicted maximal HR during
exercise is often used as a reflecion of maximal or
near maximal effort and presumably signals the
achievement of VO2max.
The difference between the age maximal HR and the
maximal HR achieved during exercise is referred to
as the HR reserve (HRR). Normally, at maximal
exercise, there is little or no HRR.
48. Predicted HRmax = 220-age
Abnormal HR response may reflect disease of either
the left or right heart
Affected by other factors, including drugs,
anxiety, anemia
Resting HR: high - suggests anxiety or disease, low
- suggests good conditioning or conduction
problems
49. O2 pulse = VO2/HR
ml O2 consumed per beat
taken to reflect stroke volume
assuming PaO2 and C(a-v)O2 respond
normally
O2 pulse < 80% predicted is abnormal
50. Normal: HR increases fairly linearly with VO2 until max HR
reached; O2 pulse increases linearly until a plateau occurs.
51. Blood pressure is related to both cardiac output and
peripheral vascular resistance.
The usual increase in cardiac output with exercise is
thought to result in an increase in systolic blood
pressure.
Also in working muscle, there are local mediators
that cause intense vasodilatation that increases blood
flow to support metabolic demands.
52. In addition, nonworking muscles are vasoconstricted
from reflex increases in sympathetic nerve activity.
The net result is a fall in systemic vascular resistance,
but systolic blood pressure typically rises progressively
with an increase in VO2.
Diastolic blood pressure typically remains constant or
may decline slightly.
53. Po2 of respired gas, determined at the end
of an exhalation.
End tidal O2 normaly at rest 90mmHg or greater and
increases with exercise 10-30 mmHg for exercise
above the anaerobic threshold because of metabolic
acidosis induced hyperventilation and rising R
(respiratory exchange ratio) at maximal exercise.
54. Pco2 of respired gas, determined at the end of
an exhalation.
This is commonly the highest Pco2 measured
during the alveolar phase of the exhalation.
It is expressed in units of millimeters of
mercury (or kilopascals).
55. Normal resting end tidal CO2 ranges between 36 – 44
mmHg, approximating arterial PaCO2.
With exercise end tidal CO2 should increase 3 -8
mmHg from rest to AT and then slightly decline at
maximal exercise secondary to the anaerobically
induced increase in VE (minute ventilation).
56. Ratio of the subject’s minute ventilation
(BTPS) to O2uptake (STPD).
It is a dimensionless quantity.
This ratio indicates how many liters of air
are being breathed for each liter of O2
uptake.
57. Ratio of the subject’s minute ventilation
(BTPS)toCO2 output (STPD).
It is a dimensionless quantity.
This ratio indicates how many liters of air are
being breathed to eliminate 1 liter of CO2.
It is used as a noninvasive estimator of
appropriateness of ventilation.
58. VE/VO2VE/VO2
VE/VCO2
50-
0-
AT
RC AT RC
Normal Obstructive Restrictive/PVD
)Efficiency of ventilation(
Normal values at AT: VE/VO2: 25 (22-27) VE/VCO2: 28 (26-30)
Ventilatory Equivalents
59. ATS/ACCP, 2003 reported that
the ventilatory equivalents for
O2and CO2 are both related to
VD/VT, being higher as VD/VT
increases which the case in
patients with pulmonary diseases.
60. Pulse oximetery provide reasonably accurate
measures of O2 saturation, with errors in the
range of ± 2% - 3% when compared with
direct arterial blood samples.
Measurement of SpO2 allows assessment of
exercise induced desaturation with a fall in
SpO2of >4% considered clinically significant
63. Normal VO2max
ECG
ABG
O2 pulse at VO2 max
Normal Abnormal
Obese
VD/VT
P(A-a)O2
P(a-ET)CO2
No
Normal
Yes
BR low
Normal
CVD
Abnormal
Pulmonary disease
64. Low VO2max
Normal LT%
BR
Low normal
Lung dis
High VD/VT, P(A-
a)O2, HRR
RF
>50ILDs
>50OAD
ECG
Normal (poor effort
or muscle)
Abnormal
(myocardial
ischaemia)
65. Low VO2 max
And LT
BR
low N or H
VD/VT
N Chronic
metabolic acidosis
H Lung disease
VE/VCO2 at LT
N Anaemia, HD, or
PAD H
N (VC) PVD L (VC) LVF