BY

• CPET is a diagnostic procedure that

analyzes the responses and cooperation of

the heart, circulation, respiration, and

metabolism during continuously increase

muscular stress.

ObesityPoor effortMusckluscletal diseases

Heart disease - coronary -ValvularAnemia

ObstructionRestrictionChestwall

• 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.

A. Field tests

Advantages:

• Safe Easy Cheap

• Identical movement stereotype

Disadvantages:

- Relatively inaccurate determination of power& measurements.

B. Laboratory tests

Advantages:• Accurate determination of work load.

• Standard laboratory conditions.

Disadvantages:

• Different movement stereotype worsen achievement.

• Less safe Expensive Need exprience

Maximal testsAdvantages:• Direct assessment of maximal capacity

Disadvantages:• Dependence on will and motivation

• Risk factor

Sub-maximal tests

Advantages:• Safer • Lower dependence on tested person (more comfortable)

Disadvantages:• Often based on estimation (presumption) of HR max, etc.

worse accuracy

ParameterscycleTreadmill

VO2 maxlowerHigherBlood pressure

assessmentEasy-

Work load measurement

YesNo

ABG collectionYesNoNoiseLessHigherSaftySaferLess Safer

Wt bearing in obese

LessMore

Leg ms trainingLessMore

1. Diagnostic:

– Unexplained dyspnea

– Exercise limitation

– Documenting exercise-induced hypoxemia,

titrating O2 prescription

– Exercise-induced asthma

2. Assessment of functional exercise capacity

– Impairment or disability evaluation

– Selection of patients for cardiac

transplantation

– Prognosis: CF, heart or pulmonary

vascular disease

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

-pulmonary or cardiac rehabilitation - health maintenance or athletic training

• 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

• 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.

CPET Protocol

Constant work rate5-10 minutes Incremental

Multistage Every 2-3 minutes

Progressive incrementalEvery one minute

Incremental

ConstantB

Exercise portion of test lasts 8-12 minutes .

Ideal Testing Duration

Wasserman, et al. Principles of Exercise Testing and Interpretation. Lea & Febiger, 1987.

1 .Approximate VO2 for Unloaded Pedaling:150(+6 x Weight)

2 .Estimate VO2 maxHeight (cm) - Age(yrs) x 20 (Males)

Height (cm) - Age (yrs) x 14 (Females).3Work 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/min2 .VO2 Pred max = [(180-50) x 20 = 2600

ml/min3 .Work = [2600 - 750] / 100 = 18.5 (round to

20)

Selecting the Work Rate

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.

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)

Indication for termination of CPET

Maximal exercise testing

Measurements Noninvasive Invasive (ABGs) Metabolic gas exchange VO2, VCO2, RER, AT Lactate

Ventilatory BR,VE, VT, RR,VD/VT

Cardiovascular HR, HRR, ECG, BP, O2 pulse,QT

Pulmonary gas exchange SpO2, VE/VCO2, VE/VO2, PETO2,

PETCO2

PaO2, P(A-a)O2

Acid-base pH, PaCO2, HCO3-

SymptomsDyspnea, fatigue, chest pain

• 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.

►the response is linear►slope (DV’O2/change in work rate (DWR)) approximately 10 mL·min1·W-1

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

• 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

• 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.

• 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.

• 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).

• 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).

• 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.

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.

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(

.4 -

.2-

.1-

.3-

Work Rate

Normal

VA/Q mismatch. .

VD/VT

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.

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

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

Normal: HR increases fairly linearly with VO2 until max HR

reached; O2 pulse increases linearly until a plateau occurs.

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.

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.

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.

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).

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).

Ratio of the subject’s minute ventilation

(BTPS) to O2 uptake (STPD).

It is a dimensionless quantity.

This ratio indicates how many liters of air

are being breathed for each liter of O2

uptake.

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.

VE/VO2VE/VO2

VE/VCO250-

0-

ATRC 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

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.

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

100-

80-

60-

40-

20-

PO2

Work Rate

Alvart

Diff

Alv

art

Diff

Alv

art

Diff

)Normal) (Obst) (Restr(

Gas-Exchange: P(A-a)O2

Normal VO2max

ECGABG

O2 pulse at VO2 max

Normal Abnormal

ObeseVD/VT

P(A-a)O2

P(a-ET)CO2

NoNormal

YesBR low

NormalCVD

AbnormalPulmonary disease

Low VO2max Normal LT%

BR

Low normal

Lung disHigh VD/VT, P(A-

a)O2, HRR

RF

<50 ILDs

>50 OAD

ECG

Normal (poor effort or muscle)

Abnormal (myocardial ischaemia)

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