Printer Friendly

Does the pulmonary artery catheter still have a role in the perioperative period?

Right heart catheterisation was first described by Forsmann, a German urologist in 1929, who cannulated his own right atrium and apparently walked himself to the radiology suite to discover its exact location. After reading his work, Cournand and Richards, two physicians working at Bellevue in New York, applied his technique to cardiopulmonary research which resulted in the trio sharing the Nobel Prize in Physiology in 1956 (1). Much of our fundamental knowledge on cardiac physiology, haemodynamics and gas exchange can be attributed to this early work. However, often there were problems cannulating the pulmonary artery and fluoroscopy was required.

After observing a spinnaker on a sailboat off Santa Monica beach, the idea of a flow-directed catheter was developed by Swan and Ganz in 1970, allowing bedside placement (2). As well as measuring right heart pressures and measuring mixed venous oxygenation, the pulmonary artery catheter (PAC) was modified with a thermistor to allow measurement of cardiac output. Further modifications enabled right atrial and ventricular pacing, with infusion ports to allow administration of drugs. Later modifications allowed continuous cardiac output measurement, right ventricular ejection fraction and right ventricular end-diastolic volume estimations. The device quickly became popular and its use expanded well beyond the initial cardiac patients with acute myocardial infarction (AMI) to other critically ill patients in the intensive care unit (ICU) and operating room (3). The PAC contributed to our current understanding of complications of AMI, pathophysiology of shock states and the pharmacology of vasoactive drugs. This was all well before the ready availability of bedside echocardiography. Significantly, human research and ethics committees and device regulatory authorities such as the Food and Drug Administration in the United States were not yet established. Thus, its use expanded rapidly without ever being subjected to rigorous scrutiny. It seemed intuitive that monitoring a patient's physiology, detecting abnormal variables and then intervening with therapy would improve patient outcome.

However, the PAC is a monitoring device and only provides information. It is not a definitive therapy. The information it provides convincingly leads to a change in management, such as fluids, blood transfusion or vasoactive drugs. Yet it is unclear that these therapies themselves are beneficial in any of the pathological states in which they are utilised. While most us would not administer anaesthesia without a pulse oximeter or capnography, none of the perioperative monitors we use in our daily practice have been shown to convincingly alter outcome and none of the PAC-guided therapies convincingly improve outcome.


Several thousand articles now appear in the literature related to the PAC, yet most of this data is of low quality (6). Many studies have small sample sizes, lack randomisation, have non-standard and unproven therapy, are in inappropriately low risk populations and often have unachievable haemodynamic goals (7). In addition, there is huge variation in the data interpretation by physicians, even amongst experienced cardiac anaesthetists (8). Disturbingly, one-third of critical care physicians are unable to correctly identify pulmonary artery occlusion pressure (PAOP) on a clear trace, or the major components of oxygen transport (9).

In Australia, the risk of major morbidity during cardiac surgery such as stroke, renal failure or pneumonia is in the order of 2 to 4% (10) with an over-all mortality of 3.2% (11). A study of several thousand patients would be required to detect a difference related to PAC monitoring. No study currently achieves these numbers. Only a handful of publications are randomised (5,12-15) and only one of these specifically examines perioperative patients (5). Physicians have been reluctant to randomise critically ill patients in whom they feel the PAC is beneficial (16).


The use of the PAC was embraced enthusiastically during the 1970s and 1980s, with its use steadily increasing in critically ill and perioperative patients. By 1984, 20% of patients with complicated AMI were having a PAC inserted (17) and many centres were inserting the PAC routinely for cardiac surgery. However, over the last decade there has been a 65% decrease in the use of the PAC across medical and surgical ICU patients, and in cardiac and noncardiac surgery (18). Other invasive procedures such as endotracheal intubation and arterial cannulation have remained relatively constant (18). This change seemed to coincide with the publication of several large observational studies and accompanying editorials that questioned the role of the PAC.


Use of the PAC provides haemodynamic data that is used to guide therapy (4). However, several large observational studies in the 1980s suggested the PAC may actually cause harm. In patients with AMI, Gore et al (17) (in 3263 patients) and Zion et al (19) (in 5841 patients) were unable to demonstrate any beneficial effect of the PAC. In fact, the PAC was associated with increased complications, increased length-of-stay and increased mortality. This was accompanied by a provocative editorial titled "Death by pulmonary artery flow directed catheter. Time for a moratorium?", where it was suggested that tens of thousands of patients had died as a result of the PAC and its use could be considered malpractice (20). A further retrospective observational study by Connors et al (21) in 1996 again questioned the safety and efficacy of the PAC. In a multicentre study looking at data from 5735 critically ill patients needing ICU care with predefined disease categories, 38% of patients had insertion of a PAC. Using a propensity score, patients with similar diagnoses and similar severity of illness were matched to estimate the association of a PAC with outcome. The PAC was associated with increased 30- and 180-day mortality and increased costs and resources (21). This was again accompanied by a controversial editorial titled "Is it time to pull the pulmonary artery catheter?" (22). This editorial recommended the immediate commencement of a randomised controlled trial, and if this could not be undertaken, that the Food and Drug Administration should issue a moratorium on its use (22). However, patients who had received a PAC in this study had failed initial therapy, had more cardiac, respiratory and multi-organ failure, were more hypotensive, with lower serum albumin levels and higher severity of illness scores, all of which are associated with an increased mortality, making comparisons difficult.

This controversy continued with consensus statements from the Society of Critical Medicine and also from the American College of Chest Physicians, rejecting calls for a moratorium on the PAC and recommending randomised controlled trials (23,24). This was followed by the Pulmonary Artery Catheter and Clinical Outcomes workshop convened by the Food and Drug Administration and the National Heart Lung Blood Institute (25). They released a consensus statement recommending the development and dissemination of standardised PAC education programs. They also recommended randomised controlled trials, particularly in the areas of PAC use in refractory cardiac failure, low-risk coronary artery bypass grafting, acute respiratory distress syndrome (ARDS) and overwhelming sepsis (25).

Similar large observational studies in ICU patients by Murdoch et al (26) and Rapoport et al (27) confirmed that insertion of a PAC was strongly associated with mortality, but PAC patients had higher severity of illness scores, more organ failure and more inotropic support. How well data in AMI and ICU patients translates to the perioperative period is unclear. In another large observational series by Polanczyk et al of 4059 patients having major non-cardiac surgery (28), the incidence of matched patients having cardiac events with and without a PAC were compared. However, only 221 of the patients had insertion of a PAC, of which 215 patients were 'matched' with non-PAC patients having the same surgery, based on propensity scoring. Patients with a PAC had longer hospital stays and increased postoperative cardiac failure, but also had higher heart rates, longer surgical times and net positive fluid balance.


In one of the first randomised controlled trials evaluating PAC use, 201 general ICU patients were randomised to care with a PAC or a central venous catheter (CVC) (29). There was no protocolised care and the study was grossly underpowered to detect any differences. It also excluded high-risk surgical patients, because the usual practice in the study's institution was to admit patients early to the ICU and direct therapy towards 'supranormalising' their circulation using a PAC. Not surprisingly, there were no significant differences in 28-day mortality, ICU or hospital stay or organ function. The authors calculated that to detect a 5% reduction in mortality from the use of the PAC, using their baseline mortality of 47%, a study of well over 10,000 patients would be required (29).

In the largest and perhaps most often quoted PAC trial, the Canadian Critical Care Clinical Trials Group published their results of a randomised controlled trial in 1994 high-risk surgical patients (5). Patients were aged 60 and over, American Society of Anesthesiologists (ASA) Class III or IV, having supposedly major surgery, and were randomised to therapy with or without a PAC. Patients randomised to the non-PAC group were allowed to have a CVC which was inserted in 769 of the 997 standard care patients. Patients in the PAC group had catheter placement before surgery. Patients with a PAC had therapy that "was directed to physiological goals and treatment priorities defined by consensus". Essentially, this was goal-directed therapy with supranormal haemodynamic targets that in order of priority, aimed for oxygen delivery of 550 to 600 ml/minute/[m.sup.2], a cardiac index of 3.5 to 4.5 l/minute/[m.sup.2], a mean arterial pressure greater than 70 mmHg, a PAOP greater of 18 mmHg, a heart rate of less than 120 bpm and a haematocrit greater than 27%. 'Suggested' therapy, again in order of priority, included fluid loading, inotropes, vasodilators, vasopressors for hypotension and blood transfusion to maintain a haematocrit above 27%. Patients in the PAC group received more inotropes, more vasodilators, more antihypertensives, more blood transfusion and more colloid. There was no difference in the primary endpoint of in-hospital mortality, with 7.8% vs 7.7% in the PAC versus control group. There were no differences in one-year mortality and no differences in morbidity or hospital stay (5).

However, 87.4% of the patients were ASA III with only 12.6% of the patients being ASA IV. Only 13% of patients were New York Heart Association functional class 3 or 4. Patients having cholecystectomy or fractured neck of femur surgery were eligible. Many of these patients over 60 years of age are only ASA III so insertion of a PAC and ICU admission would be inconsistent with usual practice in Australia and New Zealand.

The supranormal haemodynamic goals that were aimed for in this study have not been well verified independently or in combination. Early data by Shoemaker et al suggested a beneficial effect of supranormal physiological targets in high-risk surgical patients (30). However, this was subsequently questioned and supranormal oxygen delivery may be harmful (31-35). Meta-analyses which were performed on these data are problematic because of significant heterogeneity between populations, different therapeutic goals (e.g. cardiac index vs mixed venous oxygenation) and many small lowquality studies (36). Much of the data still does not support this haemodynamic optimisation, with no clear role in sepsis and multi-organ failure, but perhaps a role in trauma and perioperatively (36). At best it is controversial (37). Rather than supranormal physiological targets, there is some data supporting early goal-directed therapy in patients with severe sepsis (38). Insertion of an arterial line and CVC, optimising central venous pressure (CVP), mean arterial pressure and central venous oxygenation, with fluids, vasoactive drugs and inotropes immediately on arrival to hospital, before microcirculatory dysfunction and refractory tissue hypoxia ensue, reduces mortality and organ dysfunction (38).

In addition, it is unclear whether other interventions are helpful. Perioperative fluid management continues to create controversy with no clear consensus (39,40), but fluid overloading may be harmful (41-43). The requirement for catecholamines such as dobutamine are an independent risk factor for death in patients with heart failure and undergoing cardiac surgery (44,45). Their use in driving supranormal physiological targets is questionable (31). Transfusion triggers have changed dramatically over the past decade with good evidence that most critically ill patients will tolerate a haemoglobin concentration as low as 70 g/l (46). Not only are the haemodynamic goals uncertain, but they are also unachievable. In the preoperative period, oxygen delivery and cardiac index goals were achievable in just 20% of patients, and in the postoperative period in 63% of patients. Other studies have had similar difficulties achieving these goals (31,33). This study also suggested that pulmonary embolism was more common in PAC patients (5). However, only 6% of patients were screened for deep vein thrombosis or pulmonary embolism, and the unblinded nature of a PAC trial makes detection bias possible so this conclusion is questionable.

Importantly, this publication showed that trials based on the use of the PAC are achievable and that contrary to provocative editorials, use of the PAC does not increase mortality when inserted by clinicians with expertise and in centres with experience. PAC-guided therapy increases the number of therapeutic interventions chasing haemodynamic goals that remain elusive despite therapy. Insertion of the PAC into relatively low-risk surgical patients with goal-directed therapy is not beneficial; with no evidence of a treatment benefit, reduction in hospital stay, or mortality.

In a multicentre ICU study from France in patients with sepsis, ARDS or both, 676 patients were randomised to receive a PAC or not (12). However, therapy resulting from the PAC was not subject to protocol and was left to the discretion of each individual physician. How the presence of a PAC alone, without specific therapy, could possibly lead to an improvement in outcome in this group of patients is unclear. In addition, all of the ICUs involved in the study had access to echocardiography, with most patients receiving an echocardiogram to assess left ventricular function, volume status and filling pressure. This study also had issues with slower than expected enrolment of patients, so the steering committee recommended reducing the power of the study and reducing the number of patients required. Recruitment of patients continued to decline until the relevant safety board decided to cease the study for reasons that are unclear. Not surprisingly, there were no significant differences in mortality, ICU stay, renal support, mechanical ventilation or hospital stay (12).

In a multicentre trial in the United Kingdom (PACMan), 1041 mixed ICU patients were randomised to care with or without a PAC (13). Again, there was no protocol for therapy and management was left to the discretion of the treating clinician. In addition, in 47 of the 65 centres in the study, some form of noninvasive cardiac output monitoring was available for the control patients. Almost 10% of patients had a non-fatal complication from insertion of the PAC, with 4% having a local haematoma, 3% having arterial puncture and 3% having an arrhythmia. There were also isolated incidences of pneumothorax, haemothorax and lost guidewires. PAC patients received more fluid and had institution of or changes in their vasoactive drugs, but this change in management in 80% of patients was not clearly beneficial. There were no differences in hospital mortality or ICU stay between groups, and no clear evidence of benefit using a PAC to manage critically ill ICU patients.

In a multicentre trial in North American hospitals, 433 patients with congestive heart failure were randomised to receive therapy guided by a PAC compared to clinical assessment alone (the ESCAPE trial) (14). Treatment goals in the clinical assessment group were resolution of congestion, focusing on the jugular venous pressure, oedema and orthopnoea. Additional treatment goals in the PAC group were a PAOP of 15 mmHg and a CVP of 8 mmHg. There are no supportive references to justify these filling pressure targets. There was no specific protocol for therapy, drugs or drug dosing. Diuretics and vasodilators were primary therapy and use of inotropes was "explicitly discouraged". All patients received intravenous diuretics, fewer than 40% received vasodilators, but 40% still received inotropes despite the 'discouragement'. The trial was stopped before the planned 500 patients were recruited because of data and safety monitoring board concerns with early adverse events and the 'unlikelihood' of showing a significant difference. Therapy in both groups led to a reduction in symptoms, jugular venous pressure, oedema and natriuretic peptides, and there was improved exercise ability and quality of life. However, there were no differences in the primary outcome of days alive out of hospital. There was significant variation of therapy between hospitals. There was echocardiographic evidence of a reduction in severity of mitral regurgitation in PAC patients, but this did not translate into any difference in clinical outcomes (47). There were reductions in CVP, PAOP and increase in cardiac index, but the targeted filling pressures were not achieved. There was a 4.2% incidence of "direct procedural complication". Inpatient therapy for patients with heart failure improved symptoms, but therapy based on clinical assessment resulted in similar outcomes to that with the PAC.

The most recent of the randomised controlled trials evaluating the PAC was the National Heart Lung Blood ARDS Clinical Trials Network that evaluated the PAC versus a CVC to guide fluid management in patients with ARDS (15). One thousand patients with early onset acute lung injury were randomised to receive a PAC or a CVC and haemodynamic management was guided by an "explicit management protocol". Clinical examination, blood pressure and urine output were combined with either PAC data of cardiac index and PAOP, or CVP. Oxygen delivery and mixed venous oxygenation were not used as part of the protocol. Patients were also simultaneously randomised to so-called liberal (high PAOP and CVP) or conservative (low PAOP and CVP) fluid strategies in a two-by-two factorial design (48). These two studies on the same patients were published in separate articles in the same edition of the New England Journal of Medicine. However, it is not clear in either article exactly how many patients in either the CVP or the PAC group had the liberal or the conservative fluid strategy, although 250 patients in each of the four groups was the aim. These unrelated but potentially interacting interventions make interpretation of this data difficult and it is almost certainly underpowered. Reversal of hypotension, oliguria and "ineffective circulation" were the main treatment goals. "Ineffective circulation" is not adequately defined, with cardiac index being measured in the PAC group. Apparently in the CVP group, this relied on assessment of skin colour, temperature and capillary refill (15). Despite assertions of "explicit management", patients in shock were managed at the treating physicians' discretion. Oliguric patients not in shock received fluids if filling pressures were below target range, with only the volume of fluid being controlled and not whether the fluid was crystalloid, albumin or blood. Patients with "ineffective circulation" not in shock were given dobutamine and frusemide if filling pressures were elevated. Patients with elevated filling pressures were given frusemide if normotensive with "adequate circulation". Patients with "adequate circulation", mean arterial pressure >60 mmHg and adequate urine output received fluids or frusemide aiming to return their filling pressures to the target range. Loop diuretics such as frusemide convincingly improve patient symptoms by reducing congestion, weight and increasing urine output, but have never been shown to improve mortality, even in chronic heart failure (49). Over 11,000 patients were eligible for recruitment, but over 10,000 were excluded, with 20% already having a PAC in situ (with a possibility that the sickest patients are excluded), and in a further 16%, the physician declined. There were no significant differences in 60-day mortality, ventilator-free days, ICU duration, fluid balance, renal function or vasoactive drug use between the PAC and CVC groups. It was claimed there were twice as many complications from PAC insertion compared to the CVC, predominantly arrhythmias. However, PAC patients had more observed catheter insertions (sheath, the PAC and then a CVC at day three if haemodynamically stable) than CVC patients, and many patients already had a CVC in situ when enrolled without direct documentation of complications. It appeared the risk of each catheter insertion in the PAC and CVC groups was in fact similar and no deaths occurred as a result of either catheter (15). The relevance of this study to perioperative practice is unclear, but the authors concluded that the PAC was not useful for routine haemodynamic management of patients with ARDS.

In a meta-analysis by Shah et al, including all but the ARDS Network trial, 13 randomised controlled trials were found with over 5000 patients (50). These studies included heterogeneous perioperative patients, critically ill ICU patients with sepsis or ARDS, and patients with heart failure, all of whom had either no or varying haemodynamic goals and treatment strategies. PAC patients had more frequent use of inotropes and intravenous vasodilators, neither of which are of proven benefit in the acute care setting. The PAC neither increased mortality nor conferred any benefit.


Cardiac surgery

The quality of data relating to the PAC in cardiac surgery is particularly poor. Despite dramatic reductions in the routine use of the PAC in cardiac surgery to less than 20% of cases in Europe (51) and less than 10% in Japan (52), some centres in North America and Australia still routinely use the device. Schwann et al in a United States centre, proposes a highly selective use of the PAC, where over 90% of coronary artery graft surgery cases are performed without a PAC (53).

Almost two decades ago in a non-randomised study of 1094 consecutive patients having non-emergent cardiac surgery with either a PAC or a CVC, Tuman et al (54) found no significant differences in any outcome variables. In 39 patients, the CVC was switched to a PAC because of a "clinical need", defined as inadequate perfusion that was unresponsive to volume, pacing and vasoactive drugs (54). They concluded that even high-risk cardiac surgery patients could be managed without routine PAC insertion, reserving PAC insertion for haemodynamically unstable patients.

Ramsey et al (55) retrospectively analysed 13,907 patients having coronary artery bypass grafting, with 58% receiving a PAC. As in most other studies, PAC patients were sicker and higher risk, with higher costs, prolonged hospital stay and increased mortality. Interestingly, this increased mortality was more pronounced in centres where PAC was infrequent, and mortality was not significantly increased in centres where PAC use was more common. It is possible that the PAC is associated with more problems in centres with low volume use of the device. However, the retrospective nature of the analysis, the greater severity of illness in PAC patients, and the possibility that centres inserting fewer PACs also do fewer cardiac surgeries, makes meaningful interpretation of this data difficult.

Polonen et al (56) randomised 403 elective coronary artery bypass graft patients, all of whom received a PAC, to either goal-directed therapy, aiming for a mixed venous saturation of >70% and lactate concentrations less than 2.0 mmol/l, or standard therapy where the PAC was used to measure and optimise filling pressures and cardiac index. Goal-directed patients received more fluids and vasoactive drugs with a reduction in hospital stay, but no difference in major morbidity or mortality.

Resano et al (57) performed a retrospective analysis of low-risk patients having off-pump coronary artery surgery in 2414 patients, where 70% had a PAC and 30% had a CVC. Patients had similar baseline characteristics and there were no significant differences in any outcome, suggesting that CVC placement is sufficient in most off-pump cases.

Djaini et al (58), in 200 patients, evaluated the frequency with which PAC data altered management in low-risk coronary graft surgery, by inserting a PAC into patients but blinding surgeons and anaesthetists to numerical data aside from CVP. PAC data could be revealed in the event of hypotension, acidosis, hypoxaemia, high filling pressures or evidence of myocardial ischaemia. PAC data was used in 23% of patients, with 9% having some alteration in management as a result. The authors concluded that the PAC could be inserted when a "clinical need" arises in the operating room or ICU, rather than used routinely in these low-risk patients.

Unfortunately, there are no large-scale randomised controlled trials in cardiac surgical patients, despite recommendations a decade ago in consensus statements that they be performed (25). Clinical experience and retrospective data would seem to suggest that low-risk cardiac surgery and many high-risk cases can be safely performed without routine insertion of the PAC.

Vascular surgery

Valentine et al (59), in a small trial of 120 patients having aortic surgery, randomised patients to perioperative monitoring with a PAC and preoperative admission to the ICU for "haemodynamic optimisation", compared to intravenous hydration on the ward and no PAC. PAC patients received more fluid and more vasoactive drugs, and there were no differences in ICU, hospital stay, postoperative complications or mortality. Despite this study being grossly underpowered and using controversial goal-directed therapy, the authors concluded that routine PAC use guiding this therapy in major vascular surgery is not beneficial.

In a similarly small study, Bender et al (60) randomised 104 patients having infrarenal vascular surgery to PAC insertion on the morning of surgery or PAC only if "clinically indicated" with insertion of CVC. PAC patients were admitted to the ICU for essentially goal-directed therapy with fluids, dopamine and vasodilators, targeting filling pressures and cardiac index. Only one patient in the CVC group was switched over to the PAC group. PAC patients received more fluid and there were no clear differences in morbidity or mortality. These small underpowered studies are hardly definitive proof of the lack of benefit of the PAC, but along with clinical experience, lend some support to the notion that routine use of the PAC in major vascular surgery is not justified.

Transplant surgery

PAC monitoring during cardiac, lung and liver transplantation is still widespread, despite almost no data to support or refute its use, and despite increasing use of intraoperative echocardiography (61). Rapid infusion of fluid, graft reperfusion, and organ hypothermia can impair the accuracy of thermodilution dependent variables during haemodynamically unstable periods of organ transplantation (62).

Liver transplantation

Liver transplantation without PAC is now well-described with some data suggesting that ventricular arrhythmias as a result of the PAC occur in 37% of patients at insertion or removal, including a 4% incidence of ventricular tachycardia or ventricular fibrillation (62). Transoesophageal echocardiography is increasingly described and may be particularly useful with the rapid diagnosis of thrombus or air embolisation (63). Portopulmonary hypertension affects around 8% of patients with chronic liver disease, and in patients with severe pulmonary hypertension (mean pulmonary artery pressure >50 mmHg) there is a near 100% mortality in the perioperative period during liver transplantation. Even in patients with moderate pulmonary hypertension (mean pulmonary artery pressure between 35 to 50 mmHg), perioperative mortality is 50% (64). Screening for portopulmonary hypertension would normally involve transthoracic echocardiography, which relies on having an adequate jet of tricuspid regurgitation to estimate right ventricular systolic and pulmonary pressures. However, recent publications have questioned the accuracy of this widely accepted technique with both under- and overestimation of pulmonary artery pressures in 50% of patients (65). This potentially could incorrectly exclude patients from transplantation or falsely reassure when mortality may approach 100%, unless some form of right heart catheterisation occurs. In this situation, the PAC may assist in differentiating pulmonary hypertension causes, including high cardiac output and low vascular resistance states, and increased blood volume with high PAOP, which have a better prognosis than patients with elevated pulmonary vascular resistance (66). Preoperative therapy with prostanoids, endothelin antagonists and phosphodiesterase inhibitors may be effective in reducing pulmonary pressures and allow liver transplantation to proceed (67).

Lung transplantation

There is almost no data on the use of the PAC in lung transplantation. Nevertheless, its routine use is still common in centres in North America and Australia. Severe pulmonary hypertension is one of the most common indications for using cardiopulmonary bypass and a PAC is still the most reliable method of measuring beat-to-beat pulmonary artery pressure in the operating room (68). Pulmonary hypertension is associated with primary allograft dysfunction (69). It is not just the absolute level of pulmonary hypertension present, but also the ability of the right ventricle to adapt to the chronically increased afterload. Echocardiography is a complementary technology and patients with coexistent impairment of right ventricular dysfunction have a worse prognosis (70).

Cardiac transplantation

Again, while there is almost no prospective data evaluating the use of PAC in the setting of cardiac transplantation, its routine use is still common in many centres in North America and Australia. In the operating room, right ventricular dysfunction is one of the most common reasons for failing to wean from cardiopulmonary bypass, and is often associated with pulmonary hypertension. Similar to lung transplantation, the PAC and intraoperative echocardiography are complementary technologies, with simultaneous assessment of right ventricular function and pulmonary artery pressures. Inotropes and pulmonary vasodilators such as nitric oxide and prostaglandins may prevent the need for mechanical right ventricular support (71).

Renal transplantation

There is no good prospective data on the use of PAC in renal transplantation. Many centres perform cases with a CVC (72), but there is no good data to support the use of this monitor either. In fact, CVP declines post renal transplantation, even in patients who have positive fluid balances of four litres (73). If the indication for the CVC is to optimise fluid balance, the routine use of the CVC is questionable. Despite no high quality data to support any particular approach, our centre does not insert a PAC or a CVC routinely in any renal transplant patients.


A recent review has evaluated the complications of PAC insertion (74), the incidence of which varies widely. Complications relating to needle insertion include local haematoma (4%)13, arterial puncture (2%), pneumothorax (0.5%) and thoracic duct injury with left subclavian/internal jugular vein cannulation. Catheter-related thrombosis is common, occurring in 1.9% of subclavian catheters, up to 7.9% of internal jugular catheters and 22% of those inserted in the femoral vein. These occur with a PAC or a CVC (74). A small postmortem study showed that 61% of patients with these catheters had mural thrombus in the superior vena cava, right atrium or the pulmonary artery and 11% had evidence of pulmonary infarction (75). Heparin coating has been introduced into some PACs and has reduced the thrombogenicity, but has been associated with an increased incidence of heparin-induced thrombocytopenia (76).

Complications relating to the PAC include cardiac arrhythmia. These are usually transient atrial or ventricular rhythms with no major adverse outcomes and they occur in up to 70% of patients, usually resolving with catheter withdrawal or advancement. Transient right bundle branch block occurs in up to 5% of patients (74). Ventricular tachycardia or ventricular fibrillation occur in less than 1% of patients. Mechanical complications such as injury to the tricuspid valve, subvalvular apparatus, knotting or entanglement in pacemaker wires occur in just under 1% (74). Fortunately, pulmonary artery rupture is rare, with a reported incidence between 0.03 to 0.2%, with haemoptysis being universal, and mortality up to 70% (77). PAC-related bacteraemia or sepsis occurs in 2.3% of insertions with 7.2% of catheter tips culture positive after 72 hours (78).


Recently, the use of perioperative transthoracic echocardiography has been described (79-81). Focused transthoracic echocardiography is non-invasive with no known risks, provides rapid point-of-care assessment of intravascular volume, filling pressures, cardiac function, valvular integrity, pericardial and pleural space, and response to therapy. It can be performed in just a few minutes, and with the exception of mixed venous oxygenation, can provide all of the information a PAC does. Transoesophageal echocardiography is used commonly in cardiac surgery and increasingly in non-cardiac surgery. In fact, echocardiography has been called a "non-invasive Swan Ganz catheter" (82). There is no data comparing monitoring with echocardiography versus a PAC and despite its increasing use, there is no data providing convincing outcome benefits of echocardiography. Like the PAC, transoesophageal echocardiography is not risk-free and it is associated with a 1 in 1000 risk of gastroesophageal injury and a 1 in 5000 risk of death (83).


Widespread use of the PAC was adopted with the apparently intuitive concept that monitoring of haemodynamic variables in perioperative and critically ill patients would be beneficial for patients. In some ways this has been analogous to the widespread use electronic foetal heart rate monitoring technology, which has enhanced our understanding of foetal cardiovascular physiology and response to hypoxaemia, and surely if we knew this, we could improve neonatal and maternal outcomes by intervening. However, interpretation of foetal heart rate patterns is of variable standard in clinical practice and this monitor has clearly been associated with increased instrumental delivery and caesarean section rates, with no obvious improvement in neonatal outcomes (85).

While we can be critical of much of the PAC literature, we have almost no high quality data to support any of the perioperative monitors we use. After all, none of us would provide general anaesthesia without pulse oximetry, yet in a study investigating pulse oximetry in over 20,000 patients, no clear benefit could be established (86).

Despite all of the flaws in the PAC literature, there has thus far been no clear net benefit, nor clear net harm, associated with its use in non-cardiac high risk surgery, critically ill ICU patients with sepsis or ARDS, or patients with heart failure. Relatively healthy patients derive no benefit, nor do patients with irreversible severe organ damage. No PAC trials are linked to a protocol of proven benefit, and information alone, without a proven therapy, is unlikely to improve patient outcomes. We don't know if data obtained by less invasive monitors such as a CVC or echocardiography would alter outcome compared to that obtained with a PAC. The same standards that we use to question the use of the PAC should be applied to all of our haemodynamic monitors and all of our perioperative monitors.

The routine use of the PAC in the operating room, in relatively well patients having cardiac or non-cardiac surgery, and in critically ill ICU patients, cannot easily be justified. In experienced centres, the PAC does not clearly cause net harm. There may be select indications for the PAC, such as complex cardiac surgery and solid organ transplantation. Increasingly, we are able to obtain similar and even enhanced haemodynamic information at the bedside with less invasive alternatives such as echocardiography.


(1.) Shure D. Pulmonary-artery catheters--peace at last? N Engl J Med 2006; 354:2273-2274.

(2.) Swan HJ. The pulmonary artery catheter in anesthesia practice. 1970. Anesthesiology 2005; 103:890-893.

(3.) Chatterjee K. The Swan-Ganz catheters: past, present, and future. A viewpoint. Circulation 2009; 119:147-152.

(4.) Mimoz O, Rauss A, Rekik N, Brun-Buisson C, Lemaire F, Brochard L. Pulmonary artery catheterization in critically ill patients: a prospective analysis of outcome changes associated with catheter-prompted changes in therapy. Crit Care Med 1994; 22:573-579.

(5.) Sandham JD, Hull RD, Brant RF, Knox L, Pineo GF, Doig CJ et al. A randomized, controlled trial of the use of pulmonaryartery catheters in high-risk surgical patients. N Engl J Med 2003; 348:5-14.

(6.) Harvey S, Young D, Brampton W, Cooper AB, Doig G, Sibbald W et al. Pulmonary artery catheters for adult patients in intensive care. Cochrane Database Syst Rev 2006; 3:CD003408.

(7.) Murphy GS, Vender JS. Con: is the pulmonary artery catheter dead? J Cardiothorac Vasc Anesth 2007; 21:147-149.

(8.) Jacka MJ, Cohen MM, To T, Devitt JH, Byrick R. Pulmonary artery occlusion pressure estimation: how confident are anesthesiologists? Crit Care Med 2002; 30:1197-1203.

(9.) Trottier SJ, Taylor RW. Physicians' attitudes toward and knowledge of the pulmonary artery catheter: Society of Critical Care Medicine membership survey. New Horiz 1997; 5:201-206.

(10.) Yap C-H, Zimmet A, Mohajeri M, Yii M. Effect of obesity on early morbidity and mortality following cardiac surgery. Heart Lung Circ 2007; 16:31-36.

(11.) Billah B, Reid CM, Shardey GC, Smith JA. A preoperative risk prediction model for 30-day mortality following cardiac surgery in an Australian cohort. Eur J Cardiothorac Surg 2010; 37:1086-1092.

(12.) Richard C, Warszawski J, Anguel N, Deye N, Combes A, Barnoud D et al. Early use of the pulmonary artery catheter and outcomes in patients with shock and acute respiratory distress syndrome: a randomized controlled trial. JAMA 2003; 290:2713-2720.

(13.) Harvey S, Harrison DA, Singer M, Ashcroft J, Jones CM, Elbourne D et al. Assessment of the clinical effectiveness of pulmonary artery catheters in management of patients in intensive care (PAC-Man): a randomised controlled trial. Lancet 2005; 366:472-477.

(14.) Binanay C, Califf RM, Hasselblad V, O'Connor CM, Shah MR, Sopko G et al. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial. JAMA 2005; 294:1625-1633.

(15.) Wheeler AP, Bernard GR, Thompson BT, Schoenfeld D, Wiedemann HP, deBoisblanc B et al. Pulmonary-artery versus central venous catheter to guide treatment of acute lung injury. N Engl J Med 2006; 354:2213-2224.

(16.) Guyatt G. A randomized control trial of right-heart catheterization in critically ill patients. Ontario Intensive Care Study Group. J Intensive Care Med 1991; 6:91-95.

(17.) Gore JM, Goldberg RJ, Spodick DH, Alpert JS, Dalen JE. A community-wide assessment of the use of pulmonary artery catheters in patients with acute myocardial infarction. Chest 1987; 92:721-727.

(18.) Wiener RS, Welch HG. Trends in the use of the pulmonary artery catheter in the United States, 1993-2004. JAMA 2007; 298:423-429.

(19.) Zion MM, Balkin J, Rosenmann D, Goldbourt U, Reicher-Reiss H, Kaplinsky E et al. Use of pulmonary artery catheters in patients with acute myocardial infarction. Analysis of experience in 5,841 patients in the SPRINT Registry. SPRINT Study Group. Chest 1990; 98:1331-1335.

(20.) Robin ED. Death by pulmonary artery flow-directed catheter. Time for a moratorium? Chest 1987; 92:727-731.

(21.) Connors AF Jr, Speroff T, Dawson NV, Thomas C, Harrell FE Jr, Wagner D et al. The effectiveness of right heart catheterization in the initial care of critically ill patients. SUPPORT Investigators. JAMA 1996; 276:889-897.

(22.) Dalen JE, Bone RC. Is it time to pull the pulmonary artery catheter? JAMA 1996; 276:916-918.

(23.) Pulmonary Artery Catheter Consensus conference: consensus statement. Crit Care Med 1997; 111:261-262.

(24.) Chernow B. Pulmonary artery flotation catheters. A statement by the American College of Chest Physicians and the American Thoracic Society. Chest 1997; 111:261-262.

(25.) Bernard GR, Sopko G, Cerra F, Demling R, Edmunds H, Kaplan S et al. Pulmonary artery catheterization and clinical outcomes: National Heart, Lung, and Blood Institute and Food and Drug Administration Workshop Report. Consensus Statement. JAMA 2000; 283:2568-2572.

(26.) Murdoch SD, Cohen AT, Bellamy MC. Pulmonary artery catheterization and mortality in critically ill patients. Br J Anaesth 2000; 85:611-615.

(27.) Rapoport J, Teres D, Steingrub J, Higgins T, McGee W, Lemeshow S. Patient characteristics and ICU organizational factors that influence frequency of pulmonary artery catheterization. JAMA 2000; 283:2559-2567.

(28.) Polanczyk CA, Rohde LE, Goldman L, Cook EF, Thomas EJ, Marcantonio ER et al. Right heart catheterization and cardiac complications in patients undergoing noncardiac surgery: an observational study. JAMA 2001; 286:309-314.

(29.) Rhodes A, Cusack RJ, Newman PJ, Grounds RMl, Bennett ED. A randomised, controlled trial of the pulmonary artery catheter in critically ill patients. Intensive Care Med 2002; 28:256-264.

(30.) Shoemaker WC, Appel PL, Kram HB, Waxman K, Lee TS. Prospective trial of supranormal values of survivors as therapeutic goals in high-risk surgical patients. Chest 1988; 94:1176-1186.

(31.) Hayes MA, Timmins AC, Yau EH, Palazzo M, Hinds CJ, Watson D. Elevation of systemic oxygen delivery in the treatment of critically ill patients. N Engl J Med 1994; 330:1717-1722.

(32.) Heyland DK, Cook DJ, King D, Kernerman P, Brun-Buisson C. Maximizing oxygen delivery in critically ill patients: a methodologic appraisal of the evidence. Crit Care Med 1996; 24:517-524.

(33.) Gattinoni L, Brazzi L, Pelosi P, Latini R, Tognoni G, Pesenti A et al. A trial of goal-oriented hemodynamic therapy in critically ill patients. SvO2 Collaborative Group. N Engl J Med 1995; 333:1025-1032.

(34.) Velmahos GC, Demetriades D, Shoemaker WC, Chan LS, Tatevossian R, Wo CC et al. Endpoints of resuscitation of critically injured patients: normal or supranormal? A prospective randomized trial. Ann Surg 2000; 232:409-418.

(35.) McKinley BA, Kozar RA, Cocanour CS, Valdivia A, Sailors RM, Ware DN et al. Normal versus supranormal oxygen delivery goals in shock resuscitation: the response is the same. J Trauma 2002; 53:825-732.

(36.) Poeze M, Greve JWM, Ramsay G. Meta-analysis of hemodynamic optimization: relationship to methodological quality. Crit Care 2005; 9:R771-779.

(37.) Drage S, Boyd O. Perioperative goal directed haemodynamic therapy--do it, bin it, or finally investigate it properly? Crit Care 2007; 11:170.

(38.) Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001; 345:1368-1377.

(39.) Vermeulen H, Hofland J, Legemate DA, Ubbink DT. Intravenous fluid restriction after major abdominal surgery: a randomized blinded clinical trial. Trials 2009; 10:50.

(40.) Brandstrup B, Tonnesen H, Beier-Holgersen R, Hjortso E, Ording H, Lindorff-Larsen K et al. Effects of intravenous fluid restriction on postoperative complications: comparison of two perioperative fluid regimens: a randomized assessor-blinded multicenter trial. Ann Surg 2003; 238:641-648.

(41.) Lobo SM, Lobo FR, Polachini CA, Patini DS, Yamamoto AE, de Oliveira NE. Prospective, randomized trial comparing fluids and dobutamine optimization of oxygen delivery in high-risk surgical patients [ISRCTN42445141]. Crit Care 2006; 10:R72.

(42.) Nisanevich V, Felsenstein I, Almogy G, Weissman C, Einav S, Matot I. Effect of intraoperative fluid management on outcome after intraabdominal surgery. Anesthesiology 2005; 103:25-32.

(43.) Lobo DN. Fluid overload and surgical outcome: another piece in the jigsaw. Ann Surg 2009; 249:186-188.

(44.) Fellahi J-L, Parienti J-J, Hanouz J-L, Plaud B, Riou B, Ouattara A. Perioperative use of dobutamine in cardiac sugery and adverse cardiac outcome: propensity-adjusted analyses. Anesthesiology 2008; 108:979-987.

(45.) O'Connor CM, Gattis WA, Uretsky BF, Adams KF Jr, McNulty SE, Grossman SH et al. Continuous intravenous dobutamine is associated with an increased risk of death in patients with advanced heart failure: insights from the Flolan International Randomized Survival Trial (FIRST). Am Heart J 1999; 138:7886.

(46.) Hebert PC, Wells G, Blajchman MA, Marshall J, Martin C, Pagliarello G et al. A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care. Transfusion Requirements in Critical Care Investigators, Canadian Critical Care Trials Group. N Engl J Med 1999; 340:409-417.

(47.) Palardy M, Stevenson LW, Tasissa G, Hamilton MA, Bourge RC, Disalvo TG et al. Reduction in mitral regurgitation during therapy guided by measured filling pressures in the ESCAPE trial. Circ Heart Fail 2009; 2:181-188.

(48.) Wiedemann HP, Wheeler AP, Bernard GR, Thompson BT, Hayden D, deBoisblanc B et al. Comparison of two fluid-management strategies in acute lung injury. N Engl J Med 2006; 354:2564-2575.

(49.) Chiong JR, Cheung RJ. Loop diuretic therapy in heart failure: the need for solid evidence on a fluid issue. Clin Cardiol 2010; 33:345-352.

(50.) Shah MR, Hasselblad V, Stevenson LW, Binanay C, O'Connor CM, Sopko G et al. Impact of the pulmonary artery catheter in critically ill patients: meta-analysis of randomized clinical trials. JAMA 2005; 294:1664-1670.

(51.) Ranucci M. Which cardiac surgical patients can benefit from placement of a pulmonary artery catheter? Crit Care 2006; 10 (Suppl 3):S6.

(52.) Handa F, Kyo Si, Miyao H. [Reduction in the use of pulmonary artery catheter for cardiovascular surgery]. Masui 2003; 52:420-423.

(53.) Schwann TA, Zacharias A, Riordan CJ, Durham SJ, Engoren M, Habib RH. Safe, highly selective use of pulmonary artery catheters in coronary artery bypass grafting: an objective patient selection method. Ann Thorac Surg 2002; 73:1394-1401.

(54.) Tuman KJ, McCarthy RJ, Spiess BD, DaValle M, Hompland SJ, Dabir R et al. Effect of pulmonary artery catheterization on outcome in patients undergoing coronary artery surgery. Anesthesiology 1989; 70:199-206.

(55.) Ramsey SD, Saint S, Sullivan SD, Dey L, Kelley K, Bowdle A. Clinical and economic effects of pulmonary artery catheterization in nonemergent coronary artery bypass graft surgery. J Cardiothorac Vasc Anesth 2000; 14:113-118.

(56.) Polonen P, Ruokonen E, Hippelainen M, Poyhonen M, Takala J. A prospective, randomized study of goal-oriented hemodynamic therapy in cardiac surgical patients. Anesth Analg 2000; 90:1052-1059.

(57.) Resano FG, Kapetanakis EI, Hill PC, Haile E, Corso PJ. Clinical outcomes of low-risk patients undergoing beating-heart surgery with or without pulmonary artery catheterization. J Cardiothorac Vasc Anesth 2006; 20:300-306.

(58.) Djaiani G, Karski J, Yudin M, Hynninen M, Fedorko L, Carroll J et al. Clinical outcomes in patients undergoing elective coronary artery bypass graft surgery with and without utilization of pulmonary artery catheter-generated data. J Cardiothorac Vasc Anesth 2006; 20:307-310.

(59.) Valentine RJ, Duke ML, Inman MH, Grayburn PA, Hagino RT, Kakish HB et al. Effectiveness of pulmonary artery catheters in aortic surgery: a randomized trial. J Vasc Surg 1998; 27:203211.

(60.) Bender JS, Smith-Meek MA, Jones CE. Routine pulmonary artery catheterization does not reduce morbidity and mortality of elective vascular surgery: results of a prospective, randomized trial. Ann Surg 1997; 226:229-236.

(61.) Della RG, Brondani A, Costa MG. Intraoperative hemodynamic monitoring during organ transplantation: what is new? Curr Opin Organ Transplant 2009; 14:291-296.

(62.) Ozier Y, Klinck JR. Anesthetic management of hepatic transplantation. Curr Opin Anaesthesiol 2008; 21:391-400.

(63.) Burtenshaw AJ, Isaac JL. The role of trans-oesophageal echocardiography for perioperative cardiovascular monitoring during orthotopic liver transplantation. Liver Transpl 2006; 12:1577-1583.

(64.) Krowka MJ, Plevak DJ, Findlay JY, Rosen CB, Wiesner RH, Krom RA. Pulmonary hemodynamics and perioperative cardiopulmonary-related mortality in patients with portopulmonary hypertension undergoing liver transplantation. Liver Transpl 2000; 6:443-450.

(65.) Fisher MR, Forfia PR, Chamera E, Housten-Harris T, Champion HC, Girgis RE et al. Accuracy of Doppler echocardiography in the hemodynamic assessment of pulmonary hypertension. Am J Respir Crit Care Med 2009; 179:615-621.

(66.) Swanson KL, Krowka MJ. Screen for portopulmonary hypertension, especially in liver transplant candidates. Cleve Clin J Med 2008; 75:121-122, 125-130, 133 pasim.

(67.) Ramsay M. Portopulmonary hypertension and right heart failure in patients with cirrhosis. Curr Opin Anaesthesiol 2010; 23:145-150.

(68.) McRae KM. Pulmonary transplantation. Curr Opin Anaesthesiol 2000; 13:53-59.

(69.) Fang A, Studer S, Kawut SM, Ahya VN, Lee J, Wille K et al. Elevated pulmonary artery pressure is a risk factor for primary graft dysfunction following lung transplantation for idiopathic pumonary fibrosis. Chest 2010; (Epub ahead of print).

(70.) Ghio S, Klersy C, Magrini G, D'Armini AM, Scelsi L, Raineri C et al. Prognostic relevance of the echocardiographic assessment of right ventricular function in patients with idiopathic pulmonary arterial hypertension. Int J Cardiol 2010; 140:272-278.

(71.) Ramakrishna H, Jaroszewski DE, Arabia FA. Adult cardiac transplantation: a review of perioperative management Part-I. Ann Card Anaesth 2009; 12:71-78.

(72.) SarinKapoor H, Kaur R, Kaur H. Anaesthesia for renal transplant surgery. Acta Anaesthesiol Scand 2007; 51:1354-1367.

(73.) Ferris RL, Kittur DS, Wilasrusmee C, Shah G, Krause E, Ratner L. Early hemodynamic changes after renal transplantation: determinants of low central venous pressure in the recipients and correlation with acute renal dysfunction. Med Sci Monit 2003; 9:CR61-66.

(74.) Evans DC, Doraiswamy VA, Prosciak MP, Silviera M, Seamon MJ, Rodriguez FV et al. Complications associated with pulmonary artery catheters: a comprehensive clinical review. Scand J Surg 2009; 98:199-208.

(75.) Lange HW, Galliani CA, Edwards JE. Local complications associated with indwelling Swan-Ganz catheters: autopsy study of 36 cases. Am J Cardiol 1983; 52:1108-1111.

(76.) Laster JL, Nichols WK, Silver D. Thrombocytopenia associated with heparin-coated catheters in patients with heparinassociated antiplatelet antibodies. Arch Intern Med 1989; 149:2285-2287.

(77.) Kearney TJ, Shabot MM. Pulmonary artery rupture associated with the Swan-Ganz catheter. Chest 1995; 108:1349-1352.

(78.) Damen J, Bolton D. A prospective analysis of 1,400 pulmonary artery catheterizations in patients undergoing cardiac surgery. Acta Anaesthesiol Scand 1986; 30:386-392.

(79.) Cowie BS. Focused transthoracic echocardiography in the perioperative period. Anaesth Intensive Care 2010; 38:823-836.

(80.) Cowie B. Focused cardiovascular ultrasound performed by anesthesiologists in the perioperative period: feasible and alters patient management. J Cardiothorac Vasc Anesth 2009; 23:450-456.

(81.) Canty DJ, Royse CF. Audit of anaesthetist-performed echocardiography on perioperative management decisions for non cardiac surgery. Br J Anaesth 2009; 103:352-358.

(82.) Oh JK. Echocardiography as a noninvasive Swan-Ganz catheter. Circulation 2005; 111:3192-3194.

(83.) Piercy M, McNicol L, Dinh DT, Story DA, Smith JA. Major complications related to the use of transesophageal echocardiography in cardiac surgery. J Cardiothorac Vasc Anesth 2009; 23:62-65.

(84.) Schober P, Loer SA, Schwarte LA. Perioperative hemodynamic monitoring with transesophageal Doppler technology. Anesth Analg 2009; 109:340-353.

(85.) Steer PJ. Has electronic fetal heart rate monitoring made a difference. Semin Fetal Neonatal Med 2008; 13:2-7.

(86.) Young D, Griffiths J. Clinical trials of monitoring in anaesthesia, critical care and acute ward care: a review. Br J Anaesth 2006; 97:39-45.


Department of Anaesthesia, St Vincent's Hospital, Melbourne, Victoria, Aust ralia

* M.B., B.S., F.A.N.Z.C.A., Staff Anaesthetist.

Address for correspondence: Dr B. Cowie, Department of Anaesthesia, St Vincent's Hospital, Melbourne, 45 Victoria Parade, Fitzroy, Vic. 3065. Email:

Accepted for publication on January 13, 2011.
COPYRIGHT 2011 Australian Society of Anaesthetists
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2011 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author:Cowie, B.S.
Publication:Anaesthesia and Intensive Care
Article Type:Report
Geographic Code:8AUST
Date:May 1, 2011
Previous Article:Retraction of articles with misleading information.
Next Article:Erythropoietin as a novel brain and kidney protective agent.

Terms of use | Copyright © 2017 Farlex, Inc. | Feedback | For webmasters