This 39-year-old accountant was evaluated because of complaints of severe dyspnoea and extreme fatigue. He stated that he had been unable to climb a flight of stairs for the past 3 months. He used to run marathons and ultra-marathons. He never smoked. He complained of a dry cough, mild chest pain for over 3months after suffering a chest infection.
The patient performed exercise on a cycle ergometer. He pedalled at 60rpm without added load for 3minutes. The work rate was then increased 10W per minute to his symptom-limited maximum. He stopped exercise because of severe SOB and Chest pain. Resting and exercise ECGs were normal.
|Hb, g/L||[130-165 g/L]||154|
|DLCO, ml/mm HG/Min||22.4||29.8|
Selected Exercise Data
|RER at end||1.04|
|VO2peak (max) (mL/kg/min)||35.8||8.6 (24%)|
|VO2 at AT||7.7 (22%)|
|VE/VCO at AT||35|
|Maximum VE, L.min||209.0||108.4 (52%)|
|BP (rest, max)||110/70; 110/60|
|ECG (rest, max)||86; 92 (51%)|
|Vd/Vt||0.32 – 0.19|
|O2 pulse||2 – 5 – 2|
This non-invasive CPET identified a reduced peak VO2 and AT, reflecting reduced O2 transport, and when dysfunction is moderate to severe, an increase in VE/VCO2 (impaired gas exchange efficiency). Because the increase in VE/VCO2 is due to an increased Vd/Vt in proportion to the reduction in exercise tolerance , and is not accompanied by hypoxemia, these findings must reflect decreased perfusion of ventilated lung and not airflow obstruction. CPET with gas exchange measurements is a test especially suited for making the diagnosis and quantifying chronic heart failure secondary to either systolic or diastolic dysfunction.
|Question||Example of disorder||Markers for abnormality||Answer|
|Is exercise capacity reduced?||Any||Peak/max VO2||Yes, the capacity is reduced; this is seen in panel 3.
The basic requirement to sustain muscular exercise is an increase in cellular respiration for regeneration of the adenosine triphosphate (ATP) to fuel the muscular contractions. To support the increase in cellular respiration, O2 and CO2 transport between the cells and the environment must match the rate of cellular respiration (except for transient lags allowed by capacitances in energy stores and the transport system).
This could be due to any disorder.
|Is the metabolic requirement for exercise increased?||Obesity||VO2-WR relationship (panel 3)|| The diagonal work rate plotted on a scale that is one-tenth of the VO2 scale;
therefore, a parallel increase in VO2 to the work rate increase indicates that ∆VO2/∆WR is equal to 10mL/min/W, which is normal.A shallow slope as seen in this case indicates an underutilisation of O2 and anaerobiosis, usually due to a cardio-vascular abnormality.
A significantly reduced peak VO2 and a low AT reflected by a relatively high CO2 output at low work rates.
|Is the exercise limited by impaired O2 flow?||Heart disease – ischemic, myophatic, valvular, congenital
Pulmonary vascular disease
Peripheral arterial disease
Anemia, hypoxemia, elevated COHb, AT
|ECG, AT, VO2/WR, VO2/HR (panels 2,3,5)
VO2/WR, AT, VO2/HR, VE/VCO2 (panels 2,3,5,6)
BP, VO2/WR, VCO2/WR (panels 3,5)
VO2/HR (panels 2,3,5)
|Panel 5 Heart rate normally increases linearly with VO2 to the predicted maximum values for both variables. The heart rate-VO2slope is steeper than normal and often becomes nonlinear
in patients with cardiovascular diseases, including those in which the diseases
affect the pulmonary circulation.
VCO2 increases as a function of VO2 with a slope of approx. 1, of slightly less until the AT is reached. Above that point, VCO2 increases more steeply than VO2 in all of the patients except in the patients with peripheral arterial disease. In this patient, CO2 is presumably trapped in the muscle because of the abnormally low blood flow coming from the ischemic lower limbs.
In the patients with heart failure, the AT is significantly below the 95%
Panel 2 shows the heart rate and O2 pulse plotted against time and work rate. Heart rate normally increases abruptly at the start of unloaded cycling and then increases approx. linearly with work rate to the predicted maximal heart rate.
The O2 pulse, the product of stroke volume and arteriovenous O2 difference, normally increases but with a gradual decreasing rate of rise to the predicted normal value.
However, O2 pulse fails to increase normally in patients with CAD in whom myocardial ischemia reduces stroke volume and therefore exercise capacity. The O2 pulse also fails to increase normally in heart failure.
Panel 6 VE/VO2 and VE/VCO2 are plotted against time and work rate, and when Vd/Vt and PaCO2 are normal, VE/VO2 decreases and reaches a nadir at the AT with a value approx. less 28, and VE/VCO2 decreases to a nadir between the AT and ventilator compensation point with a value approx. less than 32. The nadir values of VE/VO2 and VE/VCO2 are normal for patients with CAD, but increased for patients with chronic heart failure, disease associated with an increase in Vd/Vt. The more severe the disease or the lower the PaCO2, the higher the values of VE/VO2 and VE/VCO2.
|Is exercise limited by reduced ventilatory capacity?||Lung, chest wall||BR, ventilatory response (panels 1,7,9)||Panel 1 VE is plotted as a function of time and work rate, VE normally increases linearly with work rate and time in normal subjects up to the point where ventilator compensation for the developing lactic acidosis starts. The slope of VE vs increasing work rate and time remains relatively linear in patients whose ventilation is relatively restricted, such as in obesity.Panel 7 Tidal volume (Vt) is plotted as a function of VE. Tidal volume normally increases, preferentially, more than breathing frequency during low – and moderate intensity exercise to account for the early increase in VE in normal subjects. Above the AT, breathing frequency is the primary variable accounting for the increase in VE. At peak exercise, there is normally a breathing reserve of greater than 10 to 15L/min, calculated as the difference between the maximal voluntary ventilation (MVV) and peak exercise VE. The tidal volume may increase to the inspiratory capacity, but not above it.
Panel 9 PETO2 and PETCO2 and, when available PaO2 and PaCO2 – are plotted against time and work rate. Similarly, oxyhemoglobin saturation values determined by pulse oximetry are plotted, if arterial blood gas measurements are unavailable. Normally, PETO2 and PETCO2 track their arterial blood counterparts, with PaCO2 higher than PETCO2 at rest, but PETCO2 becoming approx. 4mmHg higher than PaCO2 during exercise. PETCO2 increases with exercise to the AT to a value slightly above 40 mmHg at sea-level altitudes when the pulmonary circulation is normal, such as shown in the cases of the patients with CAD. PETO2 shows a reciprocal decrease to the AT.
In severe heart failure, PETCO2 is reduced because blood flow is slow relative to ventilation in regional lung units. At rest and low work rates, PETCCO2 might be quite variable in LV failure because of the periodic breathing that these patients commonly develop.
|Is there an abnormal degree of V/Q mismatching?||Lung disease, pulmonary vascular disease, heart failure||P(A-a)O2, P(a-ET)CO2, Vd/Vt, VE/VCO2 @ AT (panels 4,6,9)||Yes.|
|Is there a defect in muscle utilization of O2 or substract?||Muscle glycolytic or mitochondrial enzyme defect||AT, R, VCO2, HR vs VO2, lactate, lactate/pyruvate ratio (panels 3,5,8)||R as a function of time at rest, before the start of exercise,
during increasing work rate exercise. After the start of exercise,
there is usually a slight dip in R, followed by an increase to a
value <1.0, as muscle respiration contributes to a greater degree to total body R.
R then still steeper bicarbonate starts buffering lactic acid,
with degree of steepening depending on the rate of lactic acid production
and the ventilator compensation for the metabolic acidosis.
During the immediate recovery period, R normally increases because
repayment of the O2 debt is rapid, while CO2 elimination remains high.
The R is of particular importance at rest (R>1.0). Also, R is useful in identifying
those patients who are greatly cardiovascular limited.
These patients commonly reveal a decreasing rather than an increasing R at
the start of recovery.
|Is exercise limited by a behavioural problem?||Psychogenic dyspnea, hysteria||Breathing pattern (panels 7-9)||No|
|Is work output reduced because of poor effort?||Poor effort with secondary gain||Increased HRR, increased BR, peak R<1.0, normal AT, P(A-a)O2, P(a-ET)CO2 (panel 2,5,7,8)||No|