Monitoring pulmonary artery wedge pressure in medical patients

Monitoring pulmonary artery wedge pressure in medical patients

Sanjiv Sharma

Pulmonary artery wedge pressure is used in the diagnosis and management of critically ill patients. This measurement provides an accurate assessment of hemodynamic status, cardiac function and venous oxygen saturation. Wedge pressure monitoring has been used in the management of patients with complicated myocardial infarction, refractory heart failure, circulatory shock, pulmonary edema and other critical illnesses. Because measuring the pulmonary artery wedge pressure is an Invasive procedure, the value of the additional data provided by monitoring should be considered carefully before choosing this method. Clinical assessment or noninvasive tests, including chest radiographs and echocardiography, often provide information adequate for planning management. If therapy fails, or if noninvasive data are uncertain, pulmonary artery catheterization is appropriate. Risks and complications may be secondary to either catheter insertion or the continued presence of the catheter.

The concept of pulmonary capillary pressure was identified in the 1950s when techniques to measure the pressure in the distal limb of the pulmonary circuit were developed for use in the cardiac catheterization laboratory. Swan and Ganz developed a practical, bedside means of measuring the pulmonary capillary wedge pressure using a balloon-tipped, flow-directed catheter that could be inserted without fluoroscopic guidance into the pulmonary artery.[1]

The term “pulmonary capillary wedge pressure” refers to the pressure measured when a catheter is “wedged,” or impacted, in a branch of the pulmonary artery and free communication exists between the catheter tip and the pulmonary venous compartment of the lung. The pressure recorded by this right-sided catheter reflects the pulmonary venous pressures transmitted across the pulmonary capillary circuit.

Routine clinical measurement of pulmonary capillary wedge pressure is performed using the flow-directed, balloon-tipped (Swan-Ganz) pulmonary artery catheter. The catheter is inserted through one of the great veins (internal jugular, subclavian, antecubital or femoral) and is advanced into the pulmonary artery segment. During measurement of the pulmonary capillary wedge pressure, the balloon of the catheter is inflated to isolate the distal orifice of the catheter from the upstream arterial pressure. The motionless blood column between the catheter tip and the venous junction serves as a fluid-filled catheter manometer communicating the left heart pressures to a right heart catheter. The pressure sensed by the catheter (pulmonary capillary wedge pressure) equilibrates with the pressure at the venous junction and left atrium.

The pulmonary artery wedge pressure shows a wave form similar to that of the left atrial pressure, but it is dampened and delayed because of transmission through the pulmonary capillary circuit. There are two positive deflections, the A and V waves, reflecting left atrial systole and left atrial filling during left ventricular systole. The A and V waves are followed by the X and Y descents, respectively. The normal range of values is 3 to 15 mm Hg for the A wave, 3 to 12 mm Hg for the V wave and 1 to 10 mm Hg for the mean pulmonary artery wedge pressure. Normal pulmonary veins offer little resistance to flow, so the pulmonary artery end-diastolic pressure accurately approximates the mean pulmonary artery wedge pressure in the absence of pulmonary vascular disease or marked tachycardia.[2]

The pulmonary artery catheter allows the determination of cardiac output by thermodilution techniques. The systemic and pulmonary vascular resistance can be calculated. The mixed venous oxygen saturation can be obtained, and the oxygen delivery and oxygen uptake calculated. Other versions of the pulmonary artery catheter include (1) the paceport pulmonary artery catheter, which has an additional lumen to allow the passage of a pacing wire when cardiac pacing is indicated; (2) the fiber-optic pulmonary artery catheter, which allows continuous measurement of the mixed venous oxygen saturation; (3) the fast response thermistor pulmonary artery catheter that permits determination of the right ventricular ejection fraction and right ventricular volumes,[3] and (4) Doppler and continuous thermodilution pulmonary artery catheters for continuous measurement of the cardiac output.

Benefits of Monitoring

Knowledge of the pulmonary capillary wedge pressure is helpful for several reasons. Routine clinical evaluation of critically ill patients frequently does not provide accurate information for hemodynamic assessment. Hemodynamic parameters are accurately predicted by physicians only 40 to 80 percent of the time using clinical and radiographic assessment.[4-6] Also, studies have shown that clinical prediction of pulmonary capillary wedge pressure is only 30 to 85 percent accurate and that monitoring of the pulmonary capillary wedge pressure results in alteration of therapy 27 to 58 percent of the time.[4-12] Monitoring of the central venous pressure is of limited value in assessing left-sided pressures. Wide disparities exist between the central venous pressure and the pulmonary capillary wedge pressure, both in terms of the absolute magnitude and the direction of change. Also, the central venous pressure does not reflect the probability of pulmonary edema since it does not estimate the pulmonary capillary pressure.

The estimation of pulmonary capillary wedge pressure provides information about two important aspects of cardiopulmonary function. First, the measurement gives an accurate estimate of the pulmonary capillary pressure. The pulmonary capillary pressure is the hydrostatic pressure responsible for the genesis of pulmonary edema. The pulmonary capillary wedge pressure is always high in patients with pulmonary edema of cardiogenic origin and is normal in patients with noncardiogenic pulmonary edema.

Second, the pulmonary capillary wedge pressure gives an accurate estimate of the left-sided filling pressures in the heart. Tn clinical practice, the pulmonary capillary wedge pressure closely approximates the left atrial pressure, which in turn closely approximates the mean left ventricular enddiastolic pressure, an index of left ventricular preload. Since the left ventricular preload is an important determinant of cardiac output, the estimation of pulmonary capillary wedge pressure allows optimization of filling pressures to achieve the maximal cardiac output. Simultaneous measurement of pulmonary capillary wedge pressure and cardiac output allows the physician to construct Starling curves, when clinically relevant, and to determine the optimal pulmonary capillary wedge pressure that is consistent with the maximal cardiac output without causing pulmonary edema.

The pulmonary artery catheter can be used in a treatment strategy designed to maximize oxygen delivery to the tissues in critically ill patients. It has been observed that survivors from critical illnesses have higher values for cardiac index and oxygen delivery than do nonsurvivors and that these values are greater than the physiologic values.[13] It has been suggested that the cardiac index should be maintained above 3.5 L per minute per [m.sup.2] and that oxygen delivery should be greater than 650 mL per minute in critically ill patients in an effort to minimize tissue hypoxia (oxygen debt). This treatment strategy requires use of a pulmonary artery catheter to monitor therapy.

Clinical Applications of Monitoring

The efficacy of pulmonary artery catheterization can be evaluated in several ways.[14] Evidence shows that catheterization has a beneficial effect on diagnosis and treatment because insertion of the catheter often leads to a significant change in therapy after hemodynamic data are made available.[4-6] However, the benefit of pulmonary artery catheterization in terms of altering morbidity and mortality remains controversial.[6,15-17] Although some studies have shown improved outcomes with the use of pulmonary artery catheterization,[6,17] others have shown no benefit in terms of morbidity and mortality.[15,16] These conflicting results have raised some questions about the value of catheterization.[18,19] However, it has been argued that lack of mortality benefit may result from the lack of effective therapeutic modalities for most of the conditions identified by catheterization.[20]

Guidelines for pulmonary artery catheterization have been established in the past five years.[21-24] For all of the indications listed in Table 1, clinical judgment is key to the appropriate use of the procedure. Not all patients with these conditions require pulmonary artery catheterization; many can be managed using noninvasive clinical assessment.[25] If intervention based on results of noninvasive tests has been unsuccessful, and if a specific management decision is being considered, hemodynamic monitoring should be instituted. Hemodynamic monitoring is likely to be most helpful in patients in whom noninvasive assessment is inaccurate or misleading. Once the catheter is placed, the physician is committed to act on the data obtained. Less specific reasons for monitoring, such as the idea that the physician would be better informed or that hemodynamic monitoring is routine in certain clinical settings, are not justifiable.[21]


Indications for Pulmonary Artery Catheterization

Establish a specific diagnosis

Ventricular septal defect versus mitral regurgitation in acute myocardial infarction

Differentiating cardiogenic from noncardiogenic pulmonary edema

Right ventricular infarction (in select cases)

Pulmonary embolism

Aid management of patients with medical illness for whom the availability of hemodynamic information is likely to alter treatment and when clinical estimates are not reliable

Myocardial infarction complicated by (1) hypotension that is unresponsive to volume challenge; (2) hypotension with congestive heart failure; (3) marked hemodynamic instability requiring inotropic support, vasodilator therapy or intra-aortic balloon counterpulsation, or (4) right ventricular function in selected cases

Cardiogenic pulmonary edema that is unresponsive to usual therapy or associated with hypotension Adult respiratory distress syndrome (ARDS) in the following instances: (1) when it is complicated by fluid overload, left ventricular dysfunction or hypotension; (2) when it is necessary to provide optimal positive end-expiratory pressure and volume therapy in selected cases, and (3) when ARDS is unresponsive to usual therapy

Circulatory shock states that are refractory to initial therapy with fluid loading and vasoactive therapy, or if empiric fluid challenge is likely to be unsafe or complicated by fluid overload, or if patient’s volume or cardiovascular status is unknown Patients with refractory heart failure who require parenteral inotropic and/or vasodilatory therapy

Critically ill patients for whom volume or cardiovascular status is unknown and in whom a diuretic or fluid challenge would be unsafe or likely to yield equivocal results Critically ill patients with one of the following disorders (often in association with cardiac disease):

Gastrointestinal hemorrhage



Renal failure

Drug overdose

Assist in management of patients who have undergone surgery (for detection of cardiac ischemia and failure in patients who are at high risk in the perioperative period and for guiding fluid therapy)

Cardiac surgery

Coronary artery bypass grafting

Valve replacement (multiple, elderly)

Resection of ventricular aneurysm

Severe associated pulmonary disease

Vascular surgery

Dissecting or ruptured aneurysm

Abdominal aortic aneurysm repair

Resection of thoracic aneurysm

Extensive prolonged surgical procedures associated with significant blood loss

Multiple injuries

Severe burns

Management of high-risk obstetric patients

Known cardiac disease

Severe toxemia

Suspected abruptio placentae

Therapeutic indications

Detection and treatment of air emboli in neurosurgical procedures performed in sitting position Atrial and/or ventricular pacing via paceport pulmonary artery catheter


In patients with acute myocardial infarction, the hemodynamic profile can be predicted accurately in a large proportion (80 to 85 percent) of cases using clinical and radiographic assessment.[7] Routine insertion of the pulmonary artery catheter in patients with acute myocardial infarction is unnecessary, and most hemodynamic changes secondary to myocardial infarction can be managed without catheterization.

Pulmonary artery catheterization may be helpful in patients with myocardial infarction who have (1) hypotension that is unresponsive to volume challenge; (2) hypotension with congestive heart failure (CHF); (3) marked hemodynamic instability requiring inotropic support, vasodilator therapy or intra-aortic balloon counterpulsation; (4) mechanical lesions, proven or suspected, such as cardiac tamponade, severe mitral regurgitation or ruptured ventricular septum, and (5) right ventricular infarction, in selected cases.[21]

Once the decision to insert a catheter has been made, the data derived can be used in directing therapy for pump failure. Pump failure in myocardial infarction manifests in two hemodynamic changes: (1) an increase in the pulmonary capillary wedge pressure (pulmonary congestion), and/or (2) a diminution of the cardiac output (hypoperfusion). The cutoff values of pulmonary capillary wedge pressure and cardiac index that distinguish patients with pulmonary congestion and patients with peripheral hypoperfusion are 18 mm Hg and 2.2 L per minute per [m.sup.2], respectively.[7] Patients can be classified into four different subsets, on the basis of pulmonary capillary wedge pressure and cardiac index; each subset defines a different hemodynamic abnormality and requires a different therapeutic approach (Table 2).[7,26]


Patients with pulmonary capillary wedge pressure and a cardiac index in the normal range do not require therapy to improve pump function. In patients with pulmonary congestion and adequate peripheral perfusion, the goal of therapy is to reduce the pulmonary capillary wedge pressure below the level that causes pulmonary congestion but maintain it above the level at which cardiac output begins to fall. The specific aim of therapy is, therefore, to reduce the pulmonary capillary wedge pressure to a range of 15 to 18 mm Hg through use of diuretics and/or peripheral vasodilators.

Patients with peripheral hypoperfusion and pulmonary capillary wedge pressure in the normal range require therapy with the goal of improving the cardiac index to a level that is adequate to relieve the signs of hypoperfusion with the least possible increase in oxygen demands of the heart. This goal can be achieved by volume expansion until the pulmonary capillary wedge pressure reaches 15 to 18 mm Hg; beyond this pressure, the cardiac output response to volume expansion is usually limited and inotropic therapy might be used.

The aim of therapy in patients with combined pulmonary congestion and peripheral hypoperfusion is to simultaneously improve the cardiac index and lower the pulmonary capillary wedge pressure. Afterload reduction by means of peripheral vasodilators is particularly suited to achieve this goal. Management of complicated acute myocardial infarction can be assisted by using pulmonary artery catheterization to guide treatment and follow the response to therapy over time.

Pulmonary artery catheterization may be useful in recognizing certain clinical situations that may result in rapid hemodynamic deterioration in a patient with acute myocardial infarction, including right ventricular infarction, severe left ventricular failure, mitral regurgitation and ventricular septal rupture. Although echo Doppler and radioisotope studies can be used to diagnose these conditions, catheterization helps to determine the severity of hemodynamic compromise and assess response to therapy so that appropriate management decisions may be made to optimize hemodynamic improvement.[27]

Clinical subsets developed on the basis of cardiac index and pulmonary capillary wedge pressure have been used to predict mortality after acute myocardial infarction,[7] with progressive increase in mortality occurring as the cardiac index falls and the pulmonary capillary wedge pressure rises (Table 2).

Two large-scale retrospective studies[28,29] have assessed the use of pulmonary artery catheterization in acute myocardial infarction. In one study,[28] approximately 14 percent of all patients with acute myocardial infarction underwent catheterization for CHF, hypotension and shock. The in-hospital mortality rate was higher in patients with CHF and hypotension who underwent catheterization than in patients who did not undergo catheterization. No difference in mortality could be demonstrated for patients with cardiogenic shock. The authors concluded that pulmonary artery catheterization offers no positive therapeutic benefit in a setting of complicated acute myocardial infarction. An accompanying editorial stated that the catheterization contributed to excess mortality and called for a moratorium on its use.[19] However, the study was retrospective, and the method of data analysis may not have adequately adjusted for the fact that the catheter was used in patients with more severe illness.

Another retrospective study[29] of over 5,000 patients who were hospitalized because of acute myocardial infarction reported a higher mortality rate in the 371 patients who underwent catheterization than in patients who did not undergo the procedure. Among patients with cardiogenic shock and persistent hypotension, the mortality rate was essentially the same in patients with a catheter and those without a catheter. A separate analysis of patients with CHF showed that the catheter was used more frequently in patients with more severe illness and that, when severity of CHF was assessed, mortality in patients with mild or moderate CHF did not differ according to whether catheterization was performed. The authors concluded that the use of pulmonary artery catheterization in acute myocardial infarction does not increase in-hospital mortality. The lack of improved survival with the use of pulmonary artery catheterization may partly be caused by the lack of effective therapy to treat many diagnoses defined by the data.[20] Moreover, patient benefit cannot be judged solely on the basis of hard end points such as mortality.[30]

These two studies failed to answer questions about diagnostic, therapeutic and prognostic utility of the technique, specifically whether use of pulmonary artery catheterization helped in the diagnosis of complications of acute myocardial infarction, such as septal rupture, mitral regurgitation, right ventricular infarction or cardiac tamponade; whether pulmonary artery catheterization has better diagnostic value than other noninvasive techniques such as echocardiography; whether catheter data altered major therapeutic decisions, and whether morbidity differed between patients with a catheter and those without a catheter. Answers to these questions will come only from a randomized, controlled trial of the use of pulmonary artery catheterization measuring its therapeutic utility, prognostic usefulness and cost-benefit ratio.


Hypovolemia and sepsis are the most common causes of noncardiogenic shock. Most patients with noncardiogenic shock can be managed by empiric therapy with fluid loading, followed by vasoactive drug treatment if fluid challenge alone is not effective. However, if the patient continues to have hypotension that is refractory to this empiric therapy, if fluid challenge is likely to be unsafe or complicated by the risk of fluid overload, or if the volume or cardiovascular status is uncertain, a pulmonary artery catheter may be inserted to help define hemodynamics and guide therapy.[21]

Once the pulmonary artery catheter is in place, data obtained can be used to differentiate the various types of shock and direct therapy (Table 3). In patients with hypovolemic shock, volume replacement guided by pulmonary capillary wedge pressure monitoring may be continued to avoid fluid overload and subsequent pulmonary edema. Patients in the “warm phase” of septic shock who have low blood pressure in the face of high cardiac output and low pulmonary capillary wedge pressure can benefit from volume expansion. Caution is appropriate since all patients with sepsis are at a risk of high permeability pulmonary edema, or adult respiratory distress syndrome (ARDS).


Some patients with shock may have oliguria, despite a high cardiac output. They may benefit from low-dose dopamine (Dopastat, Intropin) to enhance renal blood flow. A “mixed” picture may emerge in patients with septic shock who begin to manifest cardiac dysfunction. This is recognized as a decrease in the cardiac index. Such patients may benefit from inotropic therapy with dopamine, dobutamine (Dobutrex) or both.[25] In one study[6] of patients in shock who did not respond to standard therapy, the placement of a pulmonary artery catheter and determination of hemodynamic data prompted a change in therapy in 63 percent of cases, which led to a decrease in mortality.

A newly emerged concept is that the common denominator in the shock syndromes is a reduction in the amount of oxygen consumed by the tissues.[31] It has been suggested that treatment should be aimed toward decreasing tissue hypoxia by achieving supranormal cardiac output and oxygen delivery. The pulmonary artery catheter allows the physician to titrate therapy using fluids and drugs toward this goal and also allows determination of oxygen delivery and oxygen consumption. Some studies have shown that this treatment strategy improves survival in patients with shock.[32,33]


Some patients with cardiomyopathy develop transient episodes of increased ventricular dysfunction presenting as severe heart failure refractory to usual previous therapy. The hemodynamic findings include low cardiac output, high pulmonary capillary wedge pressure, elevated systemic vascular resistance and low mixed venous saturation. These episodes may require treatment with short-term inotropic support (dopamine, dobutamine or both), and vasodilators (nitroprusside, nitroglycerin) to optimize preload and afterload in order to improve the cardiac output and decrease pulmonary congestion. The pulmonary artery catheter should be used in patients with refractory heart failure that necessitates parenteral inotropic or vasodilator therapy.


In some cases, it may be difficult to differentiate cardiogenic from noncardiogenic pulmonary edema using clinical and radiographic assessment. Pulmonary artery catheterization may be needed to make this differentiation; pulmonary capillary wedge pressure is high (exceeds 25 mm Hg) in cardiogenic pulmonary edema and is normal or low in ARDS. Since echocardiography also provides a reliable means of making this distinction, pulmonary artery catheterization is not usually indicated unless echocardiography results are uncertain.

Although not all patients with ARDS require catheterization, this technique may be useful in several ways. First, pulmonary edema in ARDS is caused by a leaky alveolar-capillary membrane. This predisposes to development of an exponential increase in lung edema if the pulmonary capillary wedge pressure rises to a high level because of an unrecognized fluid overload or coexistent left ventricular dysfunction. In such situations, pulmonary capillary wedge pressure should be reduced promptly to normal or low-normal range while an adequate cardiac output is maintained.[23] These goals may be difficult to achieve without monitoring of the pulmonary capillary wedge pressure and cardiac output.

Second, positive end-expiratory pressure used to improve oxygenation in ARDS depresses cardiac output. Positive end-expiratory pressure therapy may need to be adjusted to a level that achieves improved arterial oxygenation without causing a decrease in the net oxygen transport to the tissues. This may be achieved by monitoring the mixed venous oxygen saturation and cardiac index with a pulmonary artery catheter.

Third, some patients with ARDS develop hypotension as a result of hypovolemia, sepsis, cardiac dysfunction or high positive end-expiratory pressure. Management of hypotension in these patients often requires close monitoring of the pulmonary capillary wedge pressure, cardiac index and oxygen transport. Fourth, pulmonary artery catheterization may be indicated when pulmonary function does not improve despite 24 to 48 hours of appropriate therapy and adequate circulatory and ventilatory management.[23]


Cardiac tamponade is diagnosed by echocardiography, which also aids in assessing the adequacy of pericardial drainage. Pulmonary artery catheterization is not routinely indicated. If a catheter is already in place for other reasons, it may aid in early detection of tamponade and documenting the efficacy of drainage. Pulmonary artery catheterization has been used to exclude or recognize left ventricular dysfunction in ventilated patients with COPD who are having difficulty with weaning.[23] In cases of pulmonary embolism with obstructive shock, catheterization is useful in making the diagnosis, assessing the severity and guiding hemodynamic therapy. However, pulmonary artery catheterization should not delay pulmonary angiography. In the absence of shock, echocardiography is usually sufficient to monitor the effects of thrombolytic and vasoactive therapy on right ventricular function.[23]

Patients with multiple critical illnesses, such as gastrointestinal hemorrhage, renal failure, sepsis, pancreatitis, drug overdose and other conditions, especially in the setting of concomitant cardiac disease, may require pulmonary artery catheterization to guide therapy when knowledge of the intravascular pressures is likely to alter treatment and clinical estimates of hemodynamics are not reliable.[21] Certainly, in addition to hemodynamic parameters, other clinical indices of their overall status (such as daily weight, intake and output, urine flow, pH and base deficit, and mental status) must also be carefully monitored to gauge the severity of the illness and plan management.

Complications and Limitations

Complications associated with catheter insertion include inadvertent vascular puncture, pneumothorax, air embolism, surgical trauma and arrhythmias. Premature ventricular complexes are especially common but usually self-limited. Sustained ventricular tachycardia and ventricular fibrillation have been reported in up to 2 percent of cases.[3] Right bundle branch block may develop temporarily as a result of transient trauma by the balloon tip during passage through the right heart. In patients with old left bundle branch block, routine placement of a temporary transvenous pacemaker before pulmonary artery catheterization is not indicated because the risk of causing complete heart block is low.[34] Right or left bundle branch block is no longer considered a contraindication to pulmonary artery catheterization.

Complications related to the presence of the catheter inside the pulmonary artery include infections, thromboembolism and rupture of the pulmonary artery. Although colonization of the catheter occurs more frequently, catheter-related sepsis has been reported to occur in up to 4.6 percent of patients.[35] Asymptomatic thrombotic vegetations have been reported in the right atrium, and in tricuspid and pulmonary valves. Pulmonary infarction may occur as a result of persistent wedging of the catheter. One of the most devastating complications is rupture of a pulmonary artery, leading to fatal pulmonary hemorrhage. While uncommon, this is more likely in the setting of advanced age, pulmonary hypertension, cardiopulmonary bypass, overinflation of the balloon or persistent wedging of the catheter. Fortunately, death resulting from pulmonary artery catheterization is rare. Table 4 lists the contraindications to pulmonary artery catheterization.


Relative Contraindications

to Pulmonary Artery Catheterization

Lack of experienced personnel

Lack of suitable monitoring equipment

Presence of a recently inserted transvenous


Tricuspid or pulmonic valvular stenosis

Prosthetic valve in tricuspid or pulmonary position

Frequent ventricular arrhythmias uncontrolled by

antiarrhythmic drugs

Infection at proposed vascular site

Severe vascular disease at proposed vascular site

Severe coagulopathy or thrombocytopenia

The Authors SANJIV SHARMA, M.D. is a fellow in cardiology at Loma Linda University Medical Center, Los Angeles. Dr. Sharma completed a residency at the Boston University Affiliated Hospitals. Dr. Sharma earned a medical degree from the All India Institute of Medical Sciences, New Delhi.

KIM A. EAGLE, M.D. is an associate professor of internal medicine and co-director of the Heart Care Program at the University of Michigan Medical Center, Ann Arbor. Dr. Eagle earned a medical degree from Tufts University, Boston, and completed a residency in internal medicine at Yale-New Haven Hospital. Dr. Eagle has completed research and clinical fellowships in cardiology at Harvard Medical School, Boston.

Address correspondence to Kim A. Eagle, M.D., Division of Cardiology, University of Michigan Medical Center, 1500 E. Medical Center Drive, Ann Arbor, M148109-0366.

COPYRIGHT 1996 American Academy of Family Physicians

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