Preoperative Cardiopulmonary Risk Assessment by Cardiopulmonary Exercise Testing

What should be the focus of preoperative evaluation? Traditionally assessment has concentrated on the detection of myocardial ischaemia (MI) and to a lesser extent, congestive cardiac failure (CCF). A comprehensive evaluation should assess objectively the risks of a patient for cardiac and/or respiratory complications in the perioperative period. It must also include recommendations for treatment based on this assessment; in other words the evaluation becomes a tool for triage of the patient to varying levels of postoperative care.

The increased risk of patients with unstable coronary syndromes, decompensated CCF, severe valvular heart disease and symptomatic arrhythmias is well described ^1-3 . Cardiac failure as a cause of postoperative mortality was also highlighted by Goldman ² and CEPOD ⁴ . In the 1960’s the pioneering work of Clowes and Del Guercio ⁵ and the subsequent work of Shoemaker ⁶ , showed that in surgical patients the inability to increase cardiac output postoperatively was associated with increased mortality.

We contend that the major determinant of perioperative mortality is the inability of the heart to increase its output in response to surgical stress. This entity could be termed perioperative cardiac failure (PCF); it may only be apparent postoperatively when oxygen demand is increased. It may occur independently of both CCF and MI though all three may coexist. We contend, therefore, that attention in preoperative evaluation should be focussed on the detection of forward cardiac failure. Cardiac failure, in a forward sense, is frequently occult in the elderly. The problem manifests itself as reduced exercise tolerance; normally elderly patients adjust their level of activity when oxygen demand exceeds supply. The postoperative patient does not have this option.

In two studies that we have published involving over 700 elderly patients we clearly show that mortality risk is associated with PCF. Myocardial ischaemia associated with that failure substantially increases the risk ^7,8 . However in our studies only 35% of patients with cardiac failure additionally had demonstrable myocardial ischaemia. Myocardial ischaemia that is not associated with cardiac failure carries a low postoperative mortality. Myocardial infarction has not caused the death of any patient in our two published series. We have also documented that complications of surgery accounted for only 0.9% mortality overall. In other words, postoperative mortality is a function of preoperative cardiopulmonary failure rather than myocardial ischaemia.

There has been a tendency in studies of perioperative cardiac events over the last decade to assume that a patient has coronary artery disease from the presence of risk factors such as age, diabetes mellitus or smoking ^9,10 . Thus the entry criteria in such studies may well include patients who have risk factors for coronary artery disease but in whom it has not been demonstrated. Determination of perioperative risk according to clinical predictors of cardiopulmonary disease may well miss those patients who are asymptomatic and have no ‘risk factors’. Other studies have grouped all types of surgery together as if the risk is the same regardless of the type of surgery ⁹ . Minor surgery does not carry the same risk as major surgery ⁴ {Tikkanen & Hovi-Viander 1995 ID: 52} . All such studies may be misleading. (TABLE OF CONTENTS)

CLINICAL RISK ASSESSMENT

Age as a single variable for risk assessment is not predictive of the cardiovascular reserve of an individual patient ¹¹ .Although AT diminishes with age, our study of 187 elderly patients showed no significant difference in average AT between age groups from 60 years of age to 85 years of age ⁸ . This was confirmed in a subsequent series involving 548 patients⁷.

It was shown over 15 years ago that the New York Heart Association (NYHA) classification of cardiac failure did not correlate well with aerobic capacity. A study by Lipkin et al ¹² showed a significant difference in maximum oxygen uptake between NYHA functional classes, but there was also considerable overlap. Itoh et al obtained similar results in 1990 ¹³ . Such a classification can obviously not be used for risk assessment of an individual patient. The 1994 Revisions to the NYHA classification include a concept of functional capacity and objective assessment ¹⁴ . Objective assessment is based on measurements such as electrocardiograms, ECG stress tests, echocardiography and radiological imaging. These tests are discussed later but none are suitable as preoperative screening tests. (TABLE OF CONTENTS)

THE ACC/AHA GUIDELINES

These guidelines are published as framework for evaluation of cardiac risk for non-cardiac surgery. ¹⁵

The low risk group is comprised of patients less than 60 years of age with no history of cardiopulmonary disease or non-specific ECG changes, may proceed to surgery with little evaluation.

The high-risk group includes those patients with acute coronary syndromes, decompensated cardiac failure, recent myocardial infarction and supraventricular arrhythmias. They are usually easily identified and will obviously need further assessment and management.

It is in the intermediate group where clinical predictors of cardiopulmonary disease are less reliable or absent that controversy exists as to appropriate preoperative evaluation. This group includes all patients over 60 years of age. A history and clinical examination will often not detect the presence of significant cardiopulmonary pathology. Investigation in this group has focused on the detection of myocardial ischaemia and congestive cardiac failure. Myocardial ischemia is not the only cause of CCF and it is unwise to assume that it is the only cause of PCF. For patients with intermediate clinical predictors of risk, including stable angina pectoris, previous MI, compensated or prior CCF and diabetes mellitus, determination of functional capacity is recommended.

The ACC/AHA guidelines ¹⁵ introduce the concept of ‘surgery-specific risk’. Risk stratification is based on the degree of haemodynamic stress associated with specific procedures. Postoperative haemodynamic stress is recognised as consequent on an increase in oxygen consumption. High risk surgery includes major abdominal and thoracic procedures, particularly in the elderly and specifically major vascular surgery, i.e. prolonged surgery associated with major fluid shifts and/or blood loss. Intermediate risk surgery includes orthopaedic and prostatic surgery and low risk surgery includes peripheral procedures and laparoscopic procedures.

Whilst one may not agree completely with this classification, the recognition of surgery-specific risk represents a major advance in perioperative risk evaluation. We prefer to define surgery specific risk more objectively in terms of expected postoperative oxygen consumption values. The surgery is low risk when the expected postoperative VO₂ is less than 120 ml/min/m²; intermediate risk is equivalent to a VO₂ 120-150 ml/min/m².The average postoperative VO₂ following major intra abdominal surgery including vascular surgery often exceeds 150 ml/M² and this equates to high risk surgery ¹⁶ . This represents about a 40% rise over basal oxygen consumption.

The same guidelines discuss functional capacity as an important determinant of perioperative risk. Functional capacity, they suggest, may be estimated in terms of metabolic equivalents (METS). One MET is defined as the average resting VO₂ for a 70 kg, 40-year-old male and is equal to 3.5 ml/min/kg. These guidelines suggest that patients unable to meet a 4-MET demand are at increased perioperative and long-term risk. The guidelines conclude, “non-cardiac surgery is safe for patients with a moderate or excellent functional capacity (4 METS or greater)”.

The whole concept of an increase in METS is based on the need to increase cardiac output to meet exercise-induced stress. Without CPX an estimation of METS is just that – estimation. What is needed is an accurate and objective measurement of ‘METS’, or to be more precise, functional performance. Cardiopulmonary Exercise (CPX) Testing is designed to quantify functional capacity and is the best and most accurate way to measure cardiac performance. It is acknowledged by Kleber ¹⁷ as the ‘gold standard’ for evaluation of cardiac failure. Further the ACC/AHA Guidelines for Exercise Testing states that data from CPX have proved to be reliable and important in evaluation of patients with heart failure ¹⁸

Our studies suggest that patients unable to meet a 3.0 MET demand are at an increased risk ¹¹ . This equates to a VO₂ of 10.5 ml/min/kg. The entire thrust of this approach is based on cardiac performance under conditions of stress, not rest, and not solely on the presence or absence of MI. Preoperative risk evaluation performed at rest or based solely on evidence of ischaemia, not function, are therefore flawed as a screening test for surgical risk. In our studies MI predicted only 40%-50% of patients at risk ⁷ . The ACC/AHA Guidelines for Exercise Testing ¹⁸ state “One of the strongest and most consistent prognostic markers identified in exercise testing is maximum exercise capacity, which is at least partly influenced by the extent of resting left ventricular dysfunction and the amount of further left ventricular dysfunction induced by exercise”.

The ideal screening test should provide an accurate assessment of myocardial function, detect myocardial ischaemia, and be non-invasive and easily performed in elderly patients, reproducible and cost effective. What are the tests in common use for evaluation of perioperative risk that meet these criteria? (TABLE OF CONTENTS)

PREOPERATIVE SCREENING TESTS

Exercise ECG

Exercise ECG is widely used for the investigation of suspected coronary artery disease. The sensitivity of the test for detecting multi-vessel disease is 81%. In addition it can provide a (very) indirect assessment of functional capacity. Patients who achieve an estimated 7 METS or a heart rate of > 130 beats/min without ischemia are identified as low risk ¹⁹ . In contrast patients who are unable to increase their pulse rate to greater than 100 beats/min are deemed to be at high risk ²⁰ . In two studies of elective surgical patients the negative predictive value was reported at 93% ^21,22 . In such studies, using a treadmill, many patients (30-70% of elderly vascular patients) have non-diagnostic tests due to inability to exercise adequately. Because of this and its poor discrimination of functional capacity, the role of the exercise ECG as a screening test for elderly surgical patients is limited. (TABLE OF CONTENTS)

Radionuclide Ventriculography

This test determines ejection fraction, which is then used as an indicator of ventricular function. It is now accepted that ejection fraction correlates poorly with exercise capacity and peak oxygen uptake. Froelicher showed a poor correlation between ejection fraction and maximal oxygen uptake in patients with coronary artery disease not limited by angina ²³ . In a study by Dunselman et al ²⁴ of NYHA class II and III patients with an ejection fraction of less than 40%, only CPX derived data was able to show differences between groups. The article states further that objective determination of exercise capacity is the only way to select patients for studies on heart failure. Given the inability of RNVG to provide an accurate, reproducible assessment of functional capacity its use as a perioperative screening test is not recommended. (TABLE OF CONTENTS)

Echocardiography

Transthoracic Echocardiography (TTE) is non-invasive and easy to perform. It will not detect myocardial ischaemia but does provide assessment of both systolic and diastolic wall motion. A poor correlation exists between TTE findings and functional capacity; severe ventricular dysfunction on echo may be associated with moderate to good functional capacity. A large cohort study of elective surgical patients performed by the Study of Perioperative Ischaemia Research Group failed to support the use of TTE in the assessment of cardiac risk prior to non-cardiac surgery ²⁵ . More recently Transoesophageal Echocardiography (TOE) has become available but few data regarding the value of preoperative TOE for non-cardiac patients exists. In addition TOE is relatively invasive and frequently requires the administration of a sedative. (TABLE OF CONTENTS)

Dobutamine Stress Echocardiography

Dobutamine Stress Echocardiography (DSE) is designed to detect myocardial ischaemia and has been advocated for patients who are unable to exercise adequately with treadmill testing. No objective measurement of functional capacity can be obtained, though wall motion abnormalities are detected. Its sensitivity and specificity for the detection of myocardial ischaemia is high and as such DSE is a useful adjunct in evaluating coronary artery disease. In addition this test is expensive and the conduct and interpretation is operator dependent ¹⁹ . The use of DSE as a screening test for preoperative evaluation is not recommended. (TABLE OF CONTENTS)

Dipyridamole-thallium scintigraphy

In a study carried out by the Study of Perioperative Ischemia Research group, dipyridamole-thallium scintigraphy has been shown not to be a valid screening test for detection of postoperative cardiac events, even in patients for vascular surgery 26 . Following these results, Single-Photon-Emission Computed Tomography (SPECT) was developed. The combination of this with radionuclide angiography was used as a screening test in 457 patients scheduled for abdominal aortic reconstructive surgery 27 . The authors concluded that dipyridamole-thallium SPECT was not an accurate screening test of cardiac risk for abdominal aortic surgery.(TABLE OF CONTENTS)

CARDIOPULMONARY EXERCISE TESTING

Cardiopulmonary Exercise (CPX) testing evaluates cardiac and pulmonary responses to exercise induced stress. Cardiac response includes evaluation of ventricular function, circulatory function and evaluation of myocardial ischaemia. It is not possible to evaluate ‘forward cardiac failure’ clinically, other than by inference. As previously discussed the New York Heart Association functional classification of cardiac failure shows little or no correlation to objective measurements of aerobic capacity ^12,13,24 As an alternative objective measurement, Weber and Janicki have classified cardiac failure into five groups on the basis of CPX testing ²⁸(Table 1).(TABLE OF CONTENTS)

We use a CPX test as the preoperative screening test to quantify the extent of cardiac failure; and to determine the presence or absence of myocardial ischaemia as well as its temporal relationship to changes in ventricular function. At the same time we measure respiratory function in terms of obstructive or restrictive disease and any ventilation/perfusion mismatch. No other test or combination of tests is able to derive this information during conditions of exercise. It is non-invasive, simple to perform and costs less than the other tests described above.

The Metabolic Cart

CPX testing involves the use of a Metabolic Cart (Medgraphics Cardi-O2, Medical graphics Corp; St. Paul, MN), a bicycle ergometer (MGC Cardi-O2 Cycle ergometer) and a 12 lead artifact free ECG (Mortara ELI-100XR) (See Picture 1). In physiological terms the metabolic cart measures oxygen consumption (VO₂)and carbon dioxide production (VCO₂) during continuously increasing exercise and simultaneously monitors a twelve lead ECG for detection of myocardial ischaemia and arrhythmias.

The metabolic cart measures VO2 and VCO2 on a breath-by-breath basis. The oxygen concentration in inspired and expired gas is measured by an oxygen analyser with a 90% response time of <90 m.secs; the carbon dioxide concentrations are measured by an infra red analyser with a similar response time. The tidal volume is measured by a pressure differential pneumotachygraph. The tidal volume is multiplied by the respiratory rate to give minute volume and thus VO2 and VCO2 may be calculated on a breath by breath basis and displayed as a ‘per-minute’ calculation.(TABLE OF CONTENTS)

The Physiological Basis of CPX

The relationship between oxygen consumption (VO₂) and oxygen delivery (DO₂) is described by the Fick equation where: -

Oxygen consumption = cardiac output x arteriovenous O₂ difference

VO₂ = Q x C(a-v)_O2

(Remember that oxygen delivery = cardiac output x arterial oxygen content).

Cardiac output has virtually a linear relationship to oxygen consumption during the middle and later stages of exercise because C(a-v)_O2difference remains relatively constant in any individual over a large range of exercise ²⁹ . In fact the C(a-v)_O2is similar in cardiac failure as in health. A patient with heart failure has, therefore, the same mechanisms of exercise limitation as a normal individual i.e.. the limitation in aerobic capacity is due to an inability to increase cardiac output . Cardiac output is also a linear function of heart rate at higher levels of exercise because stroke index is maximally recruited early in exercise ²⁹ . In summary limitation of oxygen consumption is a function of stroke index and pulse rate, under exercise conditions. (TABLE OF CONTENTS)

Conduct of the Test

To conduct the test the patient is seated on the bicycle ergometer breathing via a pressure differential pneumotachygraph and monitored by a 12 lead ECG. (Figure 1)

Figure 1 return to text

A patient seated on the bicycle ergometer breathing via the pneumotachygraph. The gas sampling tube and the pressure lines from the pneumotachygraph mouthpiece are attached to the metabolic cart. A 12-lead ECG is monitored throughout the test, the ECG obtained at rest is printed and can be seen at the left hand side. The screen displays the ECG and gas data in real time.

The patient breathes at rest for about one minute and one is able to check the baseline values during this time. He is then asked to pedal the bicycle ergometer at about 55-65 revolutions per minute until the doctor asks him to stop.

The first three minutes of exercise are performed at ‘zero’ watts ie. there is no external load on the ergometer and the only work done is overcoming the mass of the legs being moved. With a zero watt bicycle the flywheel is assisted electrically to reduce the load further. This is termed ‘unloaded cycling'. After three minutes the load is increased on the ergometer, in a continuous fashion, toward the maximum predicted work rate for that patient. This is termed a ‘ramp protocol’. If the patient reaches maximum work rate or develops some form of distress or significant ECG change the test is ceased. This is termed a ‘symptom-limited’ test. The test is designed to last about six minutes after the unloaded cycling stage. This figure is calculated from the predicted maximum workload in watts that the subject should achieve based on age and height. (TABLE OF CONTENTS)

Interpretation of the Test

The appearance of a completed test is shown in Figure 2.

Figure 2. return to text

Data collection for completed cardiopulmonary exercise testing. The upper panel shows work rate in watts. The lower panel shows (from top to bottom) heart rate (HR red), minute ventilation (VE green), oxygen consumption (VO₂ pink) and carbon dioxide production (VCO₂ blue). All data plotted with respect to time. Note that values for VCO₂ are initially lower than VO₂ but later approach then exceed those for VO₂ as work rate increases.

The data viewed in this fashion, as a temporal plot, gives very little useable information. Further analysis is necessary in order to derive the information required and this is achieved using mainly bivariate analysis. (TABLE OF CONTENTS)

Anaerobic Threshold

The most important single variables relative to cardiac function are the anaerobic threshold (AT) and the peak VO₂. The latter is difficult to obtain in the elderly and is dependent on patient motivation. The AT is easier to detect and is independent of patient motivation. The AT is the point at which anaerobic metabolism is necessary to supplement the existing aerobic metabolism ie. oxygen supply to the exercising muscles is not adequate. This will result in release of lactate into the circulation and a metabolic acidosis will ensue.

It is possible, therefore, to determine the AT by constant measurement of serum lactate levels. The AT is represented by the VO₂ at the point where the serum lactate starts to rise. Such a method is invasive and cumbersome and has been improved by a method described by Beaver et al³⁰ . At the AT, lactate is being released into the circulation. For each rise in lactate of one m.mol the serum bicarbonate will fall by one m.mol. This causes the metabolic acidosis. In order to compensate for this there will be an increase in the elimination of carbon dioxide. Thus the rate of rise of VCO₂ (DVCO₂) will increase – not because of excessive CO₂ production – but excess CO₂ elimination. If one now plots the VO₂ on the X-axis and the VCO₂ on the Y-axis of a graph the slope will be ‘1’. It will remain at 1 until the point where the rise in DVCO₂ is greater than the rise of DVO₂. At that point the slope will exceed ‘1’; this is the AT and this method of determination is termed the ‘V-slope’ method (Figure 3).

Figure 3 return to text

'V-slope' method for determination of the anaerobic threshold (AT). The plot is bivariate, independent of time. Note the vertical line to the x-axis, the AT is expressed in terms of VO₂

The AT may be confirmed by other means. At the AT there will be a change in the relationship of the minute volume (Ve) to the VO₂ and VCO₂. These relationships are termed the ventilatory equivalents for oxygen and carbon dioxide, the Ve/VO₂ and Ve/VCO₂. They are dimensionless numbers. The nadir for these equivalents occurs at the AT, after that point both of these numbers increase. Thus on a bivariate plot of ventilatory equivalents against VO₂, the point where the Ve/VO₂ rises from its nadir is the AT. These points may also be seen in Figure 3.

At the AT the minute ventilation increases in order to increase elimination of CO₂ to correct the metabolic acidosis. This is not associated with an increase in DVO₂ thus if the minute volume increases and DVO₂ remains the same then the end tidal oxygen concentration will rise. This may also be seen in Figure 4.

Figure 4 return to text

Bivariate graph showing ventilatory equivalents as confirmatory means for anaerobic threshold (AT) determination. The main panel shows plots for end tidal oxygen tension (PETO₂ red), ventilatory equivalent for carbon dioxide (V_E/VCO₂ green) and the 'V-slope' (blue). Note the increase in ventilatory equivalents and end tidal oxygen which occur after the AT. The grey/black lines are the 'best fit' lines for the 'V-slope', their intersection is the AT. These lines are generated by the software of the metabolic cart and show a slope of '1' for the VO₂/VCO₂ relationship below AT, with a slope above '1' after the AT; important data at the AT and the maximum VO₂ are displayed in the panel at lower right.

If the DVCO₂ rises and DVO₂ remains the same then the respiratory exchange ratio (RER) will increase. Some authorities use this point where the RER exceeds 1 as representative of the AT. This method will clearly overestimate the true AT as determined by ‘V-slope’.

The ‘V-slope’ method is the most reliable and reproducible for determination of AT. The other three points are confirmatory only. Sometimes, however, where the AT is difficult to obtain the use of all four methods of identification may be useful.(TABLE OF CONTENTS)

Other physiological variables

Stroke index may also be evaluated by CPX testing. As stated before C(a-v)02 is maximised early in exercise and any further increase in oxygen consumption must be achieved by increase in cardiac output. The latter is a function of stroke index and pulse rate. Stroke index is also fully recruited early in exercise thus cardiac output becomes linearly related to pulse rate. The increase in VO₂ on a bicycle ergometer is linear at 10 ml/min/watt for aerobic exercise; it is thus possible to relate the increase in VO₂ to the pulse rate. There is a defined normal relationship between these two parameters. If the relationship between pulse rate and VO₂ is above normal this is interpreted as a reduction in stroke index. This signifies poor contractility. Beta-adrenergic blocking agents may interfere with this interpretation by reducing the pulse rate response during exercise.

This concept may be carried further. If the stroke index remains constant the HR/VO₂ relationship should be linear. If the stroke index decreases for any reason during exercise, this relationship is lost, and there will be an increase in the slope of HR/VO₂. Myocardial ischaemia reduces ventricular compliance and stroke index; this will result in a rise in the HR/VO₂ slope. Figure 5 shows a normal HR/VO₂ response. Other causes of reduction in stroke index include exercise-induced asthma severe enough to increase pulmonary vascular resistance resulting in inadequate filling of the left heart.

Figure 5 return to text

Heart rate/VO₂ response graph. This relationship gives an indication of stroke index. The grey/black dashed 'line of identity' runs from a heart rate of 70 at resting VO₂ to the predicted maxima for heart rate and VO₂. The 'I' bars indicate submaximal predicted ranges for heart rate with respect to VO₂ (mean +/- 4SEM)

As a further extension of this concept, primary pulmonary artery hypertension may also be suspected from CPX testing. This condition results in a poor left ventricular function resulting in a low AT. Left heart filling will be compromised due to flow resistance. This may worsen at moderate to high exercise rates producing a change in slope of the graph as described above. If the increase in pulmonary artery resistance has been brought about by long standing pulmonary disease this will result in a poor ventilatory equivalent for oxygen. Thus a patient with a triad of; 1) a low AT, 2) an elevated HR/VO₂ slope, and 3) a significantly elevated Ve/VO₂, almost certainly has pulmonary artery hypertension. This should be confirmed and further evaluated preoperatively by a pulmonary artery catheter.

As the relationship between VO₂ and work rate is normally 10 ml/min/watt ²⁹ then a graph of VO₂ vs. watts should confirm such a slope if the patient has normal aerobic response to exercise. This is useful when interpreting difficult tests and is a useful confirmation that the aerobic capacity is normal. (TABLE OF CONTENTS)

Respiratory Evaluation

During exercise there is a continuing increase in minute volume. This may be achieved by an increase in tidal volume, respiratory rate or a mixture of both. The computer is able to display on a continuous basis, flow volume loops, capnograhy and oxygrams. This allows accurate diagnosis of restrictive and obstructive lung disease without the artifact normally associated with resting spirometry. The Ve/VO₂ alluded to previously is able to quantify ventilation/perfusion imbalance. If this variable is abnormally high it implies that the work of breathing for any given VO₂ will be elevated and that there is a V/Q mismatch. (TABLE OF CONTENTS)

Myocardial Ischaemia

The temporal relationship between the onset of myocardial ischaemia and the anaerobic threshold is important. We have shown that exercise ischaemia may be broadly grouped into two subsets ³¹ . The first subset comprises patients in whom MI develops early in exercise and is associated with a low AT. The average AT in this subset was 10.4 ml/min/kg (SD 1.74) – Weber & Janicki Class C (Table 1). The second subset comprises patients in whom the ischaemia develops at or above the AT. The average AT in this subset was 13.9 ml/min/kg (SD 2.28) – Weber & Janicki Class B . In our studies the latter subset of MI did not appear to be a major risk factor and was not evident postoperatively. Conceptually this would suggest that the increase in oxygen consumption postoperatively did not exceed a critical level i.e.. over the surgical AT, and thus MI was not manifest.

Grading Of Perioperative Risk

As discussed above the ACC/AHA guidelines accept that there are two components to perioperative risk assessment. The first relates to the patient and the second to the proposed surgery. We have published a classification system that includes both parameters ³¹ (Table 2). An alphanumeric system is used to describe the extent of cardiac failure based on the Weber & Janicki classification (A-D); the surgery specific risk in terms of VO2 (1-3) and modifiers of risk including MI (I) or arrhythmias (A) and pulmonary function (P). The latter data is taken from the CPX study, not the history or clinical risk factors. Thus a B3I classification describes a patient with mild cardiac failure (B), significant myocardial ischaemia (I) scheduled for major surgery (3). (TABLE OF CONTENTS)

Triage Based On CPX

Patients who are classified as high surgery specific risk are admitted electively to ICU preoperatively regardless of AT. This group comprises surgery involving large fluid shifts or prolonged operating time (abdominal aneurysm surgery, Whipple’s procedure etc.) Patients who are classified as Weber & Janicki class C or D scheduled for major abdominal or thoracic surgery are also admitted to ICU. They are invasively monitored and oxygen derived parameters are optimised. Renal function is measured by creatinine clearance and pulmonary function assessed by measurement of intrapulmonary shunt. This provides our anaesthetists and intensivists with comprehensive baseline physiological data, reduces anaesthetic induction time and guarantees a bed postoperatively in ICU.

Patients for major abdominal or thoracic surgery who have significant ischaemia or pulmonary dysfunction are admitted to HDU postoperatively for ECG and respiratory monitoring, even if they are class A or B.

All other patients are managed on the ward regardless of the surgery or history of clinical risk factors. We have demonstrated that patients who have neither cardiac failure nor MI do not need to be in a special care area postoperatively. (TABLE OF CONTENTS)

SUMMARY

CPX testing is a totally non-invasive test that is quick, cheap easy to perform and requires no special preparation. It has clear advantages over any other preoperative test by defining operative risk and allowing logical triage according to objective risk assessment. It is able to objectively evaluate the extent of any cardiac failure and/or myocardial ischaemia, provides insight into stroke index, the presence of pulmonary artery hypertension and defines obstructive and restrictive lung disease and ventilation perfusion inequality better than conventional preoperative respiratory function tests. No other test is able to offer such a comprehensive preoperative risk evaluation for an operative patient. (TABLE OF CONTENTS)

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