Transcript VO2

Cardiopulmonary Stress Testing

Danielle Rowe BS RRT, RPFT Senior Clinical Sales Specialist Carefusion

WHAT IS THE PURPOSE OF CPX TESTING?

 It is an assessment of a subject’s functional (work) capacity under stress.

 We judge this functional capacity by primarily evaluating peak VO2.

 After functional capacity is established, we then are provided with insight on cause of limitations if they exist.

Possible limitations to Exercise

    Ventilation Gas Exchange Circulation (inc. ECG) Metabolism metabolism

O 2 CO 2

Peripheral Gas Exchange Pulmonary Gas Exchange

Indications For Cardiopulmonary Exercise Testing

     Evaluation of exercise tolerance Evaluation of undiagnosed exercise intolerance Evaluation of patients with cardiac disease Evaluation of patients with Respiratory disease Specific Clinical Applications  Preop assessment on certain populations, rehab evaluations, disability, transplantation etc.

From ATS/ACCP

Max or Submax Testing

   For Cardiopulmonary diagnostic purposes, MAXIMAL testing is performed.

We aim to stress the cardio-respiratory system until we identify the factor which limits exercise capacity.

Sub max test are more common in athletics training, rehabilitation etc.

Exercise Protocols

 

Cycle Ergometry

    Ramp, typically increases of 5 -30 W/minute Aim to have exercise portion of testing lasting approx. 10 minutes 1-3 minutes resting data 1-3 minutes unloaded pedaling

Treadmill

  Speed constant and grade increased (Balke Protocol). 2 mph, 0% grade and then the grade is increased 2-3% every minute.

Speed and grade are both increased ( Bruce Protocol). 1.7 mph, 10% grade and then increased by .8 mph and 2% grade every 3 minutes.

Bike vs Treadmill

       VO2 Max Work Rate Meas.

Blood gas collection Noise and artifacts Safety Wt. bearing in obese Leg muscle fatigue

Bike

lower Yes easier less safer less often

Treadmill

higher No harder more less safe?

more less

Bike vs. Treadmill cont.

 

Bike

 All things considered, bike is considered the most appropriate for patients.   This is due to ability to accurately quantify work and the minimizing of test artifacts.

Just remember vigorous encouragement is often needed near peak of exercise test to help overcome and push through leg muscle fatigue.

Treadmill

  VO2 max is often 5-10% higher Most appropriate for athletes and patients in whom abnormalities may occur only with the highest demand ( cardiac ischemia).

5 Watts/min 10 Watts/min 15 Watts/min 20 Watts/min 25 Watts/min 30 Watts/min 40 Watts/min

Selecting the Work Rate

Severe impairment (e.g. patient who is confined to home or walks only short distances) Moderate impairment (e.g. patient who walks one or two city blocks before symptoms) Mild impairment or sedentary older patient Sedentary younger patient Active younger patient physical exercise) (regular sports, Athletic and fit (competitive sports) Extremely fit (highly competitive) Chris Cooper, MD.. Harbor UCLA Medical

Was it a Good Test ?

  How can we tell ?

Most common problem seen is sub-maximal performance.

  Patients are supposed to “suffer” - that is the whole idea of the test - to put them under stress.

Don’t stop when the patient hits Max Predicted Heart Rate - carry on until the patient stops.

Often the best Indicator..

RER

“Although no one RER value defines maximal effort, values greater than 1.15 are more likely to be associated with near maximal or maximal effort.”

From ATS/ACCP Statement

RER (or RQ) = VCO2/VO2

At Baseline, RER < 0.8

   If it isn’t, check for hyperventilation If no hyperventilation, something is wrong Many patients hyperventilate in the baseline state 

At end of test, RER > 1.15

 Indicates maximal exercise effort and therefore a good test

          

Indications for Exercise Termination

Chest pain suggestive of ischemia Ischemic ECG changes Complex ectopy Second or third degree heart block Fall in systolic pressure >20 mmHg from the highest value during the test.

Hypertension ( >250 mmHg sys; >120 mmHg diastolic) Severe desaturation: SpO2 ≤ 80% when accompanied by symptoms and signs of severe hypoxemia Sudden pallor Loss of confusion Dizziness or faintness Signs of respiratory failure From ATS/ACCP Statement

VO2 Peak/Max

   Maximal Oxygen Uptake (VO2 max)  Represents the highest VO2 that can be reached as evidenced by a failure for VO2 to increase further despite and increase in work rate.

Peak Oxygen Uptake ( VO2 peak)  Represents the highest VO2 reached during the test where a presumed maximal effort was given.

These Terms are often used interchangeably.

Oxygen Consumption

 The amount of oxygen used per minute.

  250 mL/min at rest (3.5 mL/min/kg) 5,000 mL/min at strenuous exercise (>70 mL/min/kg) AGE 20-29 yrs 30-39 yrs 40-49 yrs 50-59 yrs 60-69 yrs Men <25 <23 <20 <18 <16

Low

Women <24 <20 <17 <15 <13

Average

Men 34 - 42 31 – 38 27 – 35 25 – 33 23 – 30 Women 31 - 37 28 - 33 24 -30 21 - 27 18 - 23 Expected Vo2 mL/min/kg values from American Heart Association

Weber- Janicki Classification in heart failure

Severity

None to Mild Mild to Moderate Moderate to Severe Severe Very Severe

Class

D E A B C

Peak Vo2 mL/kg/min

>20 16 – 20 10 – 16 6 -10 <6

Peak VO2 Cont.

 Peak VO2 is often used in the course of treating heart failure and in selecting heart transplant candidates: 

Typically these subjects that test with a peak VO2 <14 ml/min/kg are strongly considered for

transplantation.

 Peak Vo2 is often considered with major surgery especially abdominal surgery in elderly or sick patients.

>20 ml/min/kg good prognosis

<15 ml/min/kg high risk

VO2- Work relationship

VO2/Work slope = Normal is right around 10/ml/min/watt with relatively small range of normal reported in many studies. Typically (8.5- 11) considered normal.

Shallower slope, so a value < 8.5- 8.7 ml/min/watt point to a problem of O2 flow or O2 utilization.

Anaerobic Threshold (AT)

   Lactacte Threshold, Lactic Acid Threshold, Gas Exchange threshold, Ventilatory threshold etc..

The highest level of metabolic acidosis.

oxygen consumption that can be sustained without developing

The point at which anaerobic

metabolism starts to contribute.

AT cont.

Normally occurs at about 50-60% of Vo2 max predicted however there is a wide range of normal reported (35 80%).

40% is the generally accepted lower limit of normal used clinically.

Detecting AT Invasive determination

Arterial Lactate measurements. AT is graphically determined by plotting lactate concentration vs. Vo2.

AT by V-Slope Method

AT by Dual Criteria Method

AT summary

   Athletes can do more activity aerobically so AT is increased.

In diseases ( most cardiovascular) that affect O2 supply to exercising muscles , the AT is often found to be early. This can also occur in more rare conditions with mitochondrial myopathies. In clinical CPX testing you are searching for an early AT. If it is not early, then it really does not matter precisely where it occurred.

Cardiac Parameters

     Heart Rate and HR reserve BP <220/90 O2 pulse ECG HR –VO2 relationship

Heart Rate and HR reserve

  Many formulas exist for predicting max HR.

  220- age 210- (age × 0.65) HR reserve is the difference between the predicted max and the achieved max.  

Normally there is very little to no reserve in normal subjects giving maximal effort.

Often a HRR < 15 beats/min is normal.

HR- VO2 Relationship

200 -

Predicted Maximum Heart Rate

HRR = 0

HR (b/min)

0 0

VO2

| Max Predicted HR/VO2 normal = 3-4 beats/ml/min/kg

O2 pulse

     VO2/HR Amount of O2 uptake per each beat of heart.

Dependent on stroke volume and O2 uptake.

 O2 pulse = SV × C(a-v)O2 O2 pulse normally increases with incremental exercise due to increases in both SV and O2 extraction. When O2 content and C(a-v)O2 are maximal and assumed to be normal ( approx. 15 ml/dl), stroke volume can be estimated:  SV= O2 pulse/15 *100

Ventilatory Parameters

     VE RR Tidal volume Breathing reserve Inspiratory capacity trending ( Ex. FVL)  Capacity, reserve assessment

VE and Breathing reserve

    Measure Spirometry and MVV prior to exercise test. Then decide which to use as predictor of maximal ventilation. Quality of these baseline measurements is key….be careful!

Often MVV may not be the best indicator of capacity as breathing pattern of the 12-15 sec effort is not typically a pattern subject adopts during exercise. FEV1 × 35 or 40 is often used to estimate MVV or capacity.

Things to consider:  Effort and quality of baseline spirometry and MVV. Can I use either?

 It may be better to use actual MVV in cases of upper airway obstruction or neuromuscular weakness.

 Breathing reserve= (MVV-VE max/ MVV)× 100  Normal = 20-30 %. Typically < 15% considered low.

Breathing pattern

   The rise in VE during exercise is associated with an increase in both depth and frequency of breathing.

Tidal Volume - Vt typically increases until it reaches about 50-60% of VC or 70% of IC.

Further increases in VE are accomplished by respiratory rate .

 Typically the rate does not normally exceed around 55 bpm.

Exercise Tidal FVL tracings

Normal

What happens here?

Ventilatory Equivalents

    How many liters of air we need to breath to exchange 1 L of gas.

VEVO2 VECO2 Indicators of efficiency of ventilation.

 Increases in ventilatory equivalents:  Often found in diseases in which pulmonary blood flow is abnormally reduced to ventilated gas exchange units.

Ventilatory Equivalents

(Efficiency of ventilation)

VE/CO2 VE/VO2 40 20 AT RC NORMAL VALUES:

Ref: Wasserman

0 VE/VO2 @ AT: 26.5 (22.1 – 30.9) VE/VCO2 @ AT: 29.1 (24.8 – 33.4)

Arterial Blood Sampling

Sometimes….

Do we need it?

    When the adequacy of pulmonary gas exchange is in question up front. Typically in diseases like ILD, pulmonary vascular disease, COPD with low DLCO etc.

When concern over increased dead space is and issue. You want real VD/VT measurements.

When patients have an abnormal initial CPET maybe showing increased VE/VCO2 but no specific reason. Was it hyperventilation or due to increased VD.

If you do it, do it right! Use and Arterial line. No single samples at peak exercise.

Additional pieces of information when blood gas sampling is done

 Information about ability to exchange oxygen.

   PaO2- normally >80 mmHg and should not decrease with exercise.

P (A-a)O2- should be <35 mmHg at peak.

SaO2

ABG cont..

   VD/VT = (PaCO2 – PECO2)/PaCO2 Fraction of each breath “wasted” on ventilating anatomic and physiologic dead space.

You need PaCO2 to get a true VD/VT. You cannot accurately estimate!

 The estimated VD/VT that is often reported uses end-tidal PCO2 in place of PaCO2 which can be misleading.

  Normally PetCo2 is a little less than PaCO2 at rest but becomes greater than PaCO2 with exercise leading to an overestimation of VD/VT.

With lung disease PetCO2 may remain below PaCO2 even with exercise causing an underestimation of dead space.

VD/VT

   Normal at rest is 30-40%.

Should fall with exercise due to increasing tidal volume.

Typically at peak exercise we should see values less than 28% in subjects < 40 yrs. Values less than 30% normal in subjects >40 yrs.

Putting it all together

      Was it a good test?

Can subject achieve normal VO2 and do normal amount of “work”?

Is there a premature metabolic acidosis?  Low AT Is there a cardiovascular limitation?

Is there a ventilatory (mechanics) limitation?

Does pulmonary gas exchange contribute to exercise limitation?

Obesity

    High O2 cost to perform work.

Peak VO2/kg is low when expressed per kg of actual wt but normal when expressed per kg of ideal wt.

Low PaO2 that often normalizes with exercise.

Failure to develop normal ventilatory compensation for metabolic acidosis.

Cardiovascular disease

      Low VO2 Early AT Reduced maximal O2 pulse Steep HR/VO2 relationship Peak HR variable- may be normal or reduced.

Often increased ventilatory reserve

Ventilatory limitation

      Low VO2 High VD/VT Low breathing reserve High heart rate reserve AT normal or not reached Failure to develop respiratory compensation for metabolic acidosis.

Thank you