Clinical Findings

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.

Exercise Findings:

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.

Measurement	Predicted	Measured
Age, yr		40
Sex		Male
Height, cm		180
Weight, kg		72
Hb, g/L	[130-165 g/L]	154
MVV, L/min	127	124
DLCO, ml/mm HG/Min	22.4	29.8

Selected Exercise Data

Measurement	Predicted	Measured
Exercise duration		2:10
Peak workload	199	0
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%)
Breathing Reserve		89.1%
BP (rest, max)		110/70; 110/60
ECG (rest, max)		86; 92 (51%)
Vd/Vt		0.32 – 0.19
VE/VCO2 slope		83.1
O2 pulse		2 – 5 – 2

 

Report:

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). The increase in O2 and CO2 transport are functions of the peripheral circulation, heart pulmonary circulation, blood, lungs and respiratory muscles. Any defect in this interactive system could result in failure of the exercising muscles to take up O2 needed for aerobic regeneration of ATP.   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% confidence limit for normal.   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

Case 1

Clinical Findings

This 22-year-old apprentice was evaluated because of complaints of dyspnoea. He stated that he had been unable to play a full game of rugby for the last 3 years and that he gets out of breath and has to stop after climbing three to four flights of stairs at work. He never smoked. He denied cough, chest pain, oedema, or other symptoms. Physical, X-rays, and laboratory examinations were normal.

Exercise Findings:

The patient performed exercise on a cycle ergometer. He pedalled at 60rpm without added load for 3minutes. The work rate was then increased 20W per minute to his symptom-limited maximum. He stopped exercise because of general fatigue. Resting and exercise ECGs were normal.

Selected Respiratory Function Data – were all within normal limits

Measurement	Predicted	Measured
Age, yr		22
Sex		Male
Height, cm		189
Weight, kg		76
Hb, g/L	[130-165 g/L]	154
VC, L	3.30	4.30
IC, L	2.20	2.80
TLC, L	4.52	5.30
FEV1, L	2.66	3.52
FEV1/VC, %	81	80
MVV, L/min	127	124
DLCO, ml/mm HG/Min	22.4	29.8

 

Selected Exercise Data

Measurement	Predicted	Measured
Exercise duration		13:09
Peak workload	262	254
RER at end		1.22
VO2peak (max) (mL/kg/min)	42.5	46.3 (109%)
VO2 at AT		28.4 (67%)
VE/VCO at AT		25
Maximum VE, L.min	209.0	108.4 (52%)
Breathing Reserve		48%
BP (rest, max)		110/70; 180/60
ECG (rest, max)		82; 194 (98%)
Vd/Vt		0.28 – 0.09
VE/VCO2 slope		26.34
O2 pulse		14 – 18

 

Take some time to ask your questions below or just give us a possible diagnosis for the above case.

panel 3-1

Panel 3-2

Panel 3-3

 

We will discuss these live at 17:00 BST on the 9th of October @CPET_class on Twitter – sign up and join in.

 

This 75-year-old gentleman is normally independent and self caring.  Attended the CPEX to evaluate his fitness for surgery. He underwent a laparoscopic right nephrectomy uneventfully (2013).  His last episode of angina was on a treadmill over four years ago, which was managed with an angiogram and a single stent insertion.  He has had no further symptoms since then.  He is not diabetic and non-hypertensive.  He has a good exercise tolerance and can walk at least half a mile without having to stop.  He has got one flight of stairs at home that he can climb up easily.

Resting ECG revealed Atrial fibrillation

Exercise Findings:

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. Arm blood pressure was measured with a sphygmomanometer. Arterial oxyhemoglobin saturation was measured with a pulse oximeter on the finger. The test was stopped due to severe SOB.

Measurement	Predicted	Measured
Age, yr		86
Sex		Male
Height, cm		180
Weight, kg		76.2
Hb, g/L	[115 – 155 g/L]	127g/L

Measurement	Predicted	Measured
Exercise duration		5:02
Peak workload	145	51
RER at end		0.88
VO2peak (max) (mL/kg/min)	27.1	8.4 (31%)
VO2 at AT		Not achieved
Maximum VE, L.min	127	17.7
Breathing Reserve	>30%	86.1 %; 109L
BP (rest, max)		115/80mmHg ; 130/70mmHg
ECG (rest, max)	160	130,  178 (123%)
Vd/Vt	0.35 – <0.25	0.34 – 0.22
VE/VCO2 slope		29.4
O2 pulse	15	1 – 4

 

 

Clinical Findings

This 60 yr old female reported to the clinic because she started to experience shortness of breath (SOB), exercise limitation, and easy fatigability starting about 6 months previously. She had two pillow orthopnoea and paroxysmal nocturnal dyspnoea. She did not experience chest pain with activity. An echo was performed and the interpretation reported a 25% ejection fraction. Her current medical therapy include: Furosemide; Ramipril; Bisoprolol; Simvastatin; and furosemide as needed. She was referred to the CPET lab for quantification of her severity of her heart failure. At the time of referral, she was symptomatically improved on therapy, and pretibial oedema was trace.

Resting ECG revealed sinus rhythm and LBBB with rare premature ventricular contractions.

Exercise Findings:

The patient performed exercise on a cycle ergometer. She pedaled at 60rpm without added load for 3 minutes. The work rate was then increased 10W per minute to her symptom-limited maximum. Arm blood pressure was measured with a sphygmomanometer. Arterial oxyhemoglobin saturation was measured with a pulse oximeter on the finger. She stopped the exercise because of leg fatigue.

Selected Respiratory Function Data – were all within normal limits

Measurement	Predicted	Measured
Age, yr		60
Sex		female
Height, cm		161
Weight, kg		47
Hb, g/L	[115 – 155 g/L]	140g/L
VC, L	3.27	3.17
IC, L	2.18	1.98
FEV1, L	2.64	2.17
FEV1/VC, %	81	69
MVV, L/min	97	86
DLCO, ml/mm HG/Min	22.7	17.8

 

 Selected Exercise Data

Measurement	Predicted	Measured
Exercise duration		4:51
Peak workload	105	49
RER at end		1.27
VO2peak (max) (mL/kg/min)		13.2 (42%)
VO2 at AT		9.9  (31%)
VE/VCO at AT	39	49
Maximum VE, L.min	100	42
Breathing Reserve	>30%	57.3 %; 57L
BP (rest, max)		90/60mmHg ; 110/60mmHg
ECG (rest, max)	160	66, 109   (69%)
Vd/Vt	0.35 – <0.25	0.24 – 0.21
VE/VCO2 slope		63
O2 pulse	15	4 – 6

 

 

 

Clinical Findings

This 49 yr old female had been exposed to sandblasting and 25yrs of cigarettes. On questioning,  she admitted to a grinding chest pain, originating in the mid-back and radiating around the left chest into the sub-sternal area. The pain, brought on when walking the dog on cold days and relieved in a few minutes by rest, had not previously been treated or diagnosed. She denied shortness of breath. A physical examination revealed no evidence of peripheral vascular disease, heart murmurs or abnormal heart sounds. The resting 12 lead- ECG was within normal limits.

Exercise Findings

The patient performed exercise on a cycle ergometer. She pedalled at 60rpm without added load for 3 min. The work rate was then increased 10W per minute to his symptom-limited maximum. The patient stopped exercising due to sub-scapular pain and right anterior chest pain. No significant ECG changes. The chest pain resolved within 1 minute of cessation of exercise.

Selected Respiratory Function Data – were all within normal limits

Measurement	Predicted	Measured
Age, yr		49
Sex		Female
Height, cm		170
Weight, kg		80
Hb, g/L	[130-165 g/L]	110
VC, L	2.56 – 3.92	3.63
VC, % Predicted		112
PEF, L	300.84 – 477.96	476
FEV1, L	2.06 – 3.31	2.73

 

Selected Exercise Data

Measurement	Predicted	Measured
Exercise duration		7:31
Peak workload	99	80
RER at end		1.31
VO2peak (max) (mL/kg/min)	20.9	14.5 (50%)
VO2 at AT		7.5 (36%)
VE/VCO at AT		34
Maximum VE, L.min	118	38.2 (32%)
Breathing Reserve		67%
BP (rest, max)		110/70; 190/90
ECG (rest, max)		91; 178  (104%)
Vd/Vt		0.19 – 0.15
VE/VCO2 slope		32
O2 pulse		3-4

 

Answer:

Wasserman et al: Chapter 8 refer to the Principles of Interpretation: A flowchart Approach.

Principles of Exercise Testing and Interpretation: including Pathophysiology and Clinical Applications; p. 183.

Referring to flowchart 1 the VO2 is reduced, whereas the anaerobic threshold in normal, which directs us to flowchart 3.

The breathing reserve branch is high and although the ECG is not abnormal, the 9 panel plot directs us the diagnosis of myocardial ischeamia.

Clinical Findings

This 22-year-old shipyard apprentice machinist was evaluated because of complaints of dyspnoea. He stated that he had been unable to play a full game of football (soccer) for the last 3 years and that he gets out of breath and has to stop after climbing three to four flights of stairs on shipboard. He never smoked. He denied cough, chest pain, oedema, or other symptoms. Physical, X-rays, and laboratory examinations were normal.

Exercise Findings:

The patient performed exercise on a cycle ergometer. He pedalled at 60rpm without added load for 3minutes. The work rate was then increased 20W per minute to his symptom-limited maximum. He stopped exercise because of general fatigue. Resting and exercise ECGs were normal.

Selected Respiratory Function Data – were all within normal limits

Measurement	Predicted	Measured
Age, yr		22
Sex		Male
Height, cm		189
Weight, kg		76
Hb, g/L	[130-165 g/L]	154
VC, L	3.30	4.30
IC, L	2.20	2.80
TLC, L	4.52	5.30
FEV1, L	2.66	3.52
FEV1/VC, %	81	80
MVV, L/min	127	124
DLCO, ml/mm HG/Min	22.4	29.8

 

Selected Exercise Data

Measurement	Predicted	Measured
Exercise duration		13:09
Peak workload	262	254
RER at end		1.22
VO2peak (max) (mL/kg/min)	42.5	46.3 (109%)
VO2 at AT		28.4 (67%)
VE/VCO at AT		25
Maximum VE, L.min	209.0	108.4 (52%)
Breathing Reserve		48%
BP (rest, max)		110/70; 180/60
ECG (rest, max)		82; 194  (98%)
Vd/Vt		0.28 – 0.09
VE/VCO2 slope		26.34
O2 pulse		14 – 18

 

 

 Answer:

Is the exercise capacity reduced?

No, when looking at panel 3: VO2 and VCO2 vs work rate.
Assess VO2 max/peak first?
– low, normal, high?

Assess VO2 response
– normal = linear increase with work rate @ 20ml/min/watt

Assess VCO2 response
– increases linearly (y=1<) with VO2 up to lactic acidosis (AT)
– More rapid increase after AT

If it was reduced it could have been any disorder, yet it wasn’t and all was within normal limits.

Wasserman et al: Chapter 8 refer to the Principles of Interpretation: A flowchart Approach.
Principles of Exercise Testing and Interpretation: including Pathophysiology and Clinical Applications; p. 183.

Referring to flowchart 1,

Peak VO2 and the anaerobic threshold are within normal limits.

See Flowchart 2, the ECG and O2 pulse at peak are normal, the patient is NOT obese, the results for this patient are all normal, and his symptoms could be related to a lack of fitness.