FRCA Notes


CPET

The curriculum asks us to understand "...measures of functional capacity [including cardiopulmonary exercise testing]".  In this vein, a CRQ question on CPET appeared in March 2022, with a 60% pass rate. Most marks were dropped on "the sections relating to the CPET variables".

Resources


  • CPET is an objective, dynamic, non-invasive and integrated measure of functional capacity.
  • One can get rather tangled in the minutiae of the nine-panel plot, so the time-poor candidate may wish to learn the three 'key' CPET variables in the table below, and call it quits.
Variable Threshold Value Consequence
Anaerobic threshold ≤11 mlO2/kg/min Increased inpatient post-operative mortality
VO2 peak ≤15 mlO2/kg/min (or ≤60% predicted) Increased post-operative complications
VE/VCO2 ≤32 = normal
>35 = increased risk pulmonary complications
>50 = possible pulmonary HTN
Relates to gas exchange and V/Q matching
Not related to exercise efficiency

Hypothesis

  • The physiological stress of major surgery increases an individual's baseline O2 consumption (VO2)
  • Patients who are less physically fit are more likely to experience adverse perioperative outcomes
  • Therefore patients with insufficient cardiopulmonary capacity to increase O2 delivery perioperatively are more likely to experience organ dysfunction

Uses

  • CPET is used for patients undergoing major surgery from an increasing number of surgical specialties
  • These include:
    • Urological
    • Vascular e.g. elective AAA repair
    • Upper GI e.g. oesophagectomy
    • HPB e.g. liver transplant

  • CPET can help:
    • Inform patients of their individualised risks from surgery, facilitating shared decision making
    • Risk stratify patients, allowing appropriate prehabilitation exercise prescriptions based on in-CPET effort
    • Planning for perioperative management, inc. optimisation of comorbidities, and post-operative care

Process

  • Patient rides an electromagnetically-braked cycle ergometer for approx. 10mins
  • Monitoring
    • Rapid gas analyser (O2, CO2) and pressure-differential pneumotachograph (flowmeter)
    • 12 lead ECG
    • SpO2
    • NIBP
    • Barometer and temperature measurement to ensure standardisation of temperature/pressure
  • Measurements taken at rest, pedalling without resistance, against increasing resistance and during the recovery phase
  • One should remember that CPET is not necessarily a benign intervention, itself carrying a mortality of 2 - 4/100,000 tests

  • There are a host of contraindications to CPET, categorised here in familiar fashion into 'absolute and relative':

Absolute

  • Acute, unstable cardio-respiratory pathology
    • Acute coronary syndrome e.g. MI, unstable angina
    • Arrythmia
    • Severe symptomatic aortic stenosis
    • Aortic dissection
    • Endo- or myo-carditis
    • PE
    • Acute heart failure ± pulmonary oedema
    • Acute respiratory pathology and/or resting saturations <85%

  • Chronic pathology which is uncontrolled
    • Cardiac failure
    • Respiratory disease e.g. asthma
    • Other medical conditions affecting performance e.g. syncope

  • Patient refusal
  • Patient inability to cooperate with the test e.g. due to communication difficulties

Relative

  • Cardiovascular disease not fitting the above criteria, such as:
    • Left main stem disease
    • Moderate valvular stenosis
    • Untreated, severe hypertension
    • HOCM
    • High degree AV nodal block
    • Pulmonary HTN
    • AAA >8cm

  • Advanced pregnancy
  • Electrolyte abnormalities

  • Work rate [Watts]

Gas exchange

  • Oxygen consumption (VO2)
  • Carbon dioxide production (VCO2)
  • Respiratory exchange ratio (RER)
    • I.e. VCO2 divided by VO2
    • A value >1.15 represents maximal effort on a CPET test
    • It is roughly equivalent to the respiratory quotient during steady state conditions

Ventilatory

  • SpO2
  • Minute ventilation (VE)
  • Tidal volume
  • Respiratory rate
  • Ventilatory equivalents of oxygen (VE/VO2)
  • Ventilatory equivalents of carbon dioxide (VE/VCO2)
    • This is a unitless measure
    • Higher numbers imply greater ventilation required for CO2 clearance i.e. inefficient gas exchange or poor V/Q matching
    • High VE/VCO2 does not indicate the cause of the gas exchange inefficiency, which may be due to heart failure, pulmonary fibrosis, fibrotic lung disease etc.
  • Oxygen pulse (VO2/HR)
  • Anaerobic threshold

Cardiovascular

  • Heart rate
  • Non-invasive blood pressure
  • ECG ST-segment changes

Maximal effort

  • Has the patient demonstrated maximal effort on the test? The answer is 'yes' if they've hit one of the following thresholds:
    • They've achieved >80% predicted maximum work rate (in Watts)
    • They've achieved >80% predicted maximum heart rate
    • They've achieved a RER >1.15

  • The other pertinent question here is: "why did the test stop?"
  • It might have been completed, or the patient may have suffered symptoms (chest pain, leg claudication, MSK pain) or signs (dysrhythmia, ST-segment changes, hypotension) mandating early cessation of the test

VO2 peak

  • VO2 max is the maximum VO2 achievable by an individual performing exercise, but is often not achieved by the elderly, comorbid individuals undergoing CPET
  • VO2 peak is the highest VO2 recorded, and is usually the VO2 at the point when the test is terminated
  • Usually increases linearly in proportion to work
  • A VO2 peak of <15 mlO2.kg-1.min-1 is associated with greater risk of peri-operative complications

VO2 - work relationship

  • VO2 should increase linearly at 10 mlO2/min/W once resistance is added to the ergometer
  • A VO2/W <10 implies anaerobic respiration is required to generate the Watt of energy

Anaerobic threshold

  • The anaerobic threshold is the point at which the oxygen demand of the muscles exceeds the ability of the cardiopulmonary system to supply oxygen
  • Muscle will begin to generate ATP anaerobically, producing lactic acid, which is thus buffered by bicarbonate and extra carbon dioxide is produced
  • It can be found using the 'V-slope' method at the point where VCO2 increases disproportionally to VO2 using lines of best fit
  • Alternatively, it can be found at the point where VE/VO2 increases despite VE/VCO2 remaining constant
  • Mayn't be found in ~10% of tests

  • If the anaerobic threshold is found, the pertinent marker is the VO2 at this point of the test
  • A VO2 of <11 mlO2/kg/min at the anaerobic threshold are at increased risk of perioperative complications

Heart rate response

  • Normally, there is a linear response of HR to increasing exercise intensity
  • Immediately after cessation of exercise there is a rapid decrease in HR
  • This response may be blunted i.e. chronotropic incompetence, which can be due to rate-limiting medications

Oxygen pulse

  • Oxygen pulse = VO2/HR
  • It represents the product of stroke volume and arterial-venous oxygen difference (SV x [CaO2 - CvO2])
  • It is therefore a surrogate marker of stroke volume

  • It should increase at the start of exercise, before slowly plateauing
  • An early flattening off of the trajectory is a strong indicator of cardiac limitation and a sign of ischaemic heart disease

Ventilatory limitations

  • There should be a linear increase in VE up to AT, followed by a disproportionally higher increase in VE (due to extra CO2 production from anaerobic metabolism)
  • In healthy individuals, exercise is never limited by ventilation but in those with obstructive or restrictive lung disease ventilation may be a limiting factor

  • Static spirometry (FEV1 and FVC) is often also performed at the time of CPET
  • Maximum voluntary ventilation (MVV) is also calculated; it is the maximum volume of air that can be inhaled in one minute
    • Roughly equates to FEV1 x 40
    • Normally, VE does not exceed 80% of MVV

  • Saturations should ideally remain >95% throughout the test

ECG changes

  • Cardiac ischaemia may manifest as classic ECG changes during the test, e.g.:
    • 1mm ST depression in two adjacent leads
    • 2mm ST depression in a single lead
    • T-wave inversion
    • New BBB
    • Induced dysrhythmia

  • Excessive post-exercise oxygen consumption is termed oxygen debt
  • It is due to the processes which restores the body to its resting state and adapts the body to the exercise performed

  • It is primarily caused by restoration of:
    • ATP and phosphocreatine stores
    • Myoglobin oxygen stores
    • Muscle and liver glycogen stores
    • Normal intracellular electrolyte values
  • Dissipation of heat and repair/hypertrophy of myofibrils are other contributors