Pulmonary Artery Catheterization 

Updated: Dec 22, 2017
Author: Bojan Paunovic, MD; Chief Editor: Karlheinz Peter, MD, PhD 

Overview

Background

The flow-directed balloon-tipped pulmonary artery catheter (PAC) (also known as the Swan-Ganz or right heart catheter) was first described in the medical literature in 1970.[1] Initially developed for the management of acute myocardial infarction (AMI), it gained widespread use in the management of a variety of critical illnesses and surgical procedures. This article covers both the clinical and technical aspects of its use.

Settings in Which Use of a PAC Is Appropriate

In 2012, the American College of Cardiology Foundation (ACCF) published guidelines on the appropriate use of diagnostic pulmonary artery catheterization.[2]

Diagnostic

According to the ACCF guidelines, pulmonary artery catheterization is appropriate in the following diagnostic settings[2] :

  • Suspected acute coronary syndrome

  • Suspected coronary artery disease (CAD)

  • On stress testing with imaging, in high-risk findings in patients who are either symptomatic or asymptomatic, or in intermediate-risk findings, discordant findings, or equivocal/uninterpretable findings in patients who are symptomatic

  • On echocardiography, in findings of newly recognized, symptomatic, left ventricular (LV) dysfunction; in symptomatic, new regional wall-motion abnormality of unknown etiology; or in suspected significant ischemic complications related to CAD

  • On computed tomography (CT) angiography, for symptomatic lesions of 50% of greater, left main or non-left main; for symptomatic lesions of 50% or greater in more than one coronary territory; for symptomatic lesions of unclear severity, possibly obstructive (non-left main); and for symptomatic or asymptomatic, possibly obstructive non-left main lesions

Therapeutic

According to the ACCF guidelines, pulmonary artery catheterization is appropriate for aspiration of air emboli.[3]

Settings in Which Use of a PAC Is Inappropriate

According to the 2012 guidelines from the ACCF, pulmonary artery catheterization is inappropriate in the following settings[2] :

  • When CAD is suspected in an asymptomatic patient with low or intermediate global risk for CAD, in the absence of noninvasive stress imaging showing stenosis of 50% or greater; when CAD is suspected in a symptomatic patient with low pretest probability

  • As adjunctive testing in patients undergoing diagnostic coronary angiography, pulmonary artery catheterization is inappropriate in patients who have nonobstructive disease (non–left main) with stenosis of less than 50% in whom there are unexpected angiographic findings or findings of ischemia, or in the absence of noninvasive testing

  • In cases of arrhythmia, pulmonary artery catheterization is inappropriate in patients at low risk for syncope, in patients at low or intermediate risk for new-onset atrial fibrillation or flutter, and in patients with heart block or symptomatic bradyarrhythmia

  • In preoperative coronary evaluation, pulmonary artery catheterization is inappropriate for patients undergoing low-risk surgery, in patients with 4 or more METS (metabolic equivalents of functional capacity), in patients with no risk factors who are to undergo intermediate-risk surgery or vascular surgery, and in patients with 1 or 2 risk factors who are to undergo intermediate-risk surgery

  • Pulmonary artery catheterization is inappropriate in patients with mild or moderate mitral stenosis, mild or moderate mitral regurgitation, mild or moderate aortic stenosis, or mild or moderate aortic regurgitation

  • In patients with chronic native or prosthetic valvular disease who have symptoms related to their valvular disease, pulmonary artery catheterization is inappropriate for the following, provided that the patient's symptoms are concordant with the clinical impression of severity: mild, moderate, or severe mitral stenosis; mild, moderate, or severe mitral regurgitation; mild, moderate, or severe aortic stenosis; and mild or moderate aortic regurgitation

Best Practices

Passage of the PAC is difficult in certain disease states. When right-sided pressures are elevated, the air-filled balloon actually may hinder proper positioning. In such cases, filling the balloon with 1 mL of sterile saline and placing the patient in a more upright position allows gravity to cause the PAC to fall into position. Once the catheter is in position, aspirate the saline and replace it with air to ensure reproducible PCWP tracings. Insertion with a noninflated balloon may also allow passage into the PA. Neither of these techniques is advocated by PAC manufacturers and the techniques have the potential for adverse events. These techniques should only be used in extenuating circumstances and should only be attempted by experienced practitioners under the guidance of fluoroscopy.

The presence of large V waves can make discriminating a PA tracing from a PCWP tracing difficult. Look for subtle signs of waveform differences, such as loss of the dicrotic notch in the PA tracing (see image below).

Pulmonary artery catheter being introduced from pu Pulmonary artery catheter being introduced from pulmonary artery in to wedge position.

Determining the oxygen saturation of a blood sample obtained from the distal lumen while the balloon is inflated also can confirm that the waveform is a true PCWP. After aspirating enough volume (5-7 mL) to clear the blood from the PA distal to the inflated balloon, the oxygen saturation should be similar to that measured by arterial blood gas or pulse oximetry, thus confirming that the catheter is in the correct position to measure PWCP.

Fluoroscopy may be required for proper placement of the PAC in difficult situations.

Potential minimally invasive and noninvasive measures of hemodynamic profile

When pulmonary artery catheterization is not available in patients with a hyperdynamic condition (eg, cirrhotic patients with reduced SVR and increased cardiac output), minimally invasive indicators such as diastolic reflected waveform characteristics may potentially be used to predict high cardiac index and low SVR.[4]  

Transthoracic echocardiography appears to be feasible and accurate for evaluating the hemodynamic profile in patients with decompensated heart failure.[5] As with pulmonary artery catheterization, this imaging modality is also able to measure central venous pressure, pulmonary arterial pressure, pulmonary capillary wedge pressure, pulmonary vascular resistance, stroke volume and cardiac output, and SVR. Transesophageal echocardiography potentially could have similar utlity.[5]

Controversies

Over 1 million PACs are used annually in North America. Given the frequency and duration of their use, it is surprising that only recently were quality randomized clinical trials published. Initially, observational studies from the 1980s and 1990s indicated a greater mortality rate in patients who underwent placement of a PAC than in those who did not. The major criticism of these studies is that the more acutely ill (and therefore at greatest risk of death initially) are more likely to receive a PAC.

However, since then a number of randomized clinical trials were published.

Sandham et al enrolled nearly 2000 surgical patients (ASA class 3 or 4) aged 60 years or older. The treatment group received a PAC and a guided therapy protocol while the control group received a central venous catheter and therapy based on physician discretion. No difference was noted in the 2 groups in mortality rate (8%), length of stay, or organ dysfunction.[6]

Richard et al randomized almost 700 patients with early shock, ARDS, or both to use of PAC or not. Treatment was left to physician discretion. No significant difference in mortality or morbidity was noted.[7]

Rhodes et al randomized 201 patients and found no difference in 28-day mortality, ICU, or hospital length of stay in patients with or without a PAC. A formal management protocol was not used.[8]

The PACMAN trial enrolled more than 1000 patients to management with or without a PAC. The timing of insertion and management were at the discretion of the treating physician. No difference in hospital mortality (primary outcome) was noted.[9]

The ESCAPE trial enrolled more than 400 patients who were admitted with severe heart failure. Patients were randomized to having therapy guided by clinical assessment and PAC or clinical assessment alone. No difference was noted in overall mortality or hospitalization.[10]

Shah et al published a large meta-analysis that consisted of 13 randomized clinical trials and more than 5000 patients (including the above mentioned trials). Neither an increase in mortality or length of hospital stay nor a significant benefit could be attributed to the use of a PAC.[11]

In 2006, the ARDSNET group looked at the role of the PAC in acute lung injury patients. Patients were randomized to protocolized hemodynamic management with either a PAC or a central venous catheter (CVC). No difference in mortality (primary outcome), ICU length of stay, or lung function was appreciated.[12] As well, economic analysis follow-up confirmed increased cost associated with PAC use.[13]

As well, even in the hallowed ground of PAC use in cardiac surgery patients, Djaiani et al showed that the use of PAC derived data lead to more interventions but no overall clinical benefit.[14]

Two observational, propensity-matched analyses in both trauma and cardiac surgery populations failed to show any benefit for the use of the PAC. In fact, these studies showed increased mortality and morbidity in the PAC use groups.[15, 16]

Unfortunately, a Cochrane Review of 12 studies was only able to support the need for "efficacy studies... to determine optimal management protocols and patient groups who could benefit from management with a PAC."[17] A more recent updated Cochrane Review included the ARDSNET trial but essentially came to similar conclusions.[18]

Data from the Acute Decompensated Heart Failure Syndromes (ATTEND) Registry involving 4842 patients showed appropriate PAC use reduced in-hospital mortality in patients with acute heart failure syndromes, particularly those with lower systolic blood pressure or who received inotropic therapy.[19] In the study, 16.8% patients (n = 813) were managed with PACs, of which 502 were propensity score-matched with 502 control subjects. Patients in the PAC group had lower all-cause mortality than those in the control group.[19]

Overall, the literature does not show a positive effect on patient outcome with PAC use. However, a criticism of the current available research is that patient groups potentially benefit from the use of a PAC but this effect is lost in studies that also include patient groups that gain little or no benefit. Chittock et al published an observational cohort study showing that PAC use was associated with increased mortality in less acutely ill patients but associated with decreased mortality in more acutely ill patients.[20]

As well, the use of a monitoring tool such as the PAC itself is unlikely to show a significant treatment effect. Some criticize the current literature because a number of studies did not use a predefined treatment protocol. The lack of defined specific treatment based on measured PAC-derived variables could contribute more to patient outcome than merely the presence or absence of a PAC.

Contention also exists that PACs do not harm people; people harm people. In other words, operator competence may be the root cause of the mortality difference. Reviews have shown deficiencies in both nursing-dependent information derived from the PAC as well as physician-dependent interpretation and subsequent management.

Nevertheless, the growing evidence of the limitations of PACs may be affecting clinical practice. A time-trend analysis on national estimates of PAC use in the United States from 1993–2004, using data from the Nationwide Inpatient Sample, found a 65% decrease in PAC use during that period; the most prominent decline, by 81%, was in use of PACs for myocardial infarction.[21] Canadian authors also found more than a 50% reduction in PAC use.[22]

The advent of newer noninvasive imaging modalities may also be making inroads into PAC use. For example, noninvasive devices have been developed that measure cardiac output using ultrasound.[23] As well, the measurement of arterial pressure waveforms have shown good correlation when compared to the PAC thermodilution technique.[24]

The increased availability of bedside echocardiography is likely contributing to the decline in PAC use, as was postulated in a recent observational study in patients with acute coronary syndromes.[25]

More recent reviews agree on the importance of a measured approach to PAC use; PACs remain an important tool, but they should be used only in selected patients and only by well-trained physicians.[26, 27, 28, 29, 30]

A concise review by Chatterjee offers some reasonable indications for ongoing PAC use; however, these unfortunately lack empiric evidence at present.[26]

 

Periprocedural Care

Equipment

Pulmonary artery catheter

Typically, a multilumen catheter, 110 cm long, with extra connecting tubes for attachment to the pressure transducer (see image below)

A pulmonary artery catheter is shown here. A pulmonary artery catheter is shown here.

At the tip is the PA lumen, or distal lumen. A 1.5-cc balloon is located just proximal to the tip. Approximately 4 cm proximal to the balloon is the thermistor used to measure temperature changes for calculation of CO.

Two additional lumens usually are present at 19 cm and 30 cm from the tip. Depending on the degree of right heart enlargement and the position of the catheter (ie, distance advanced into the patient), these lumina reside within the right ventricle (RV), right atrium (RA), or the superior vena cava (SVC).

Some catheters are coated with heparin to reduce thrombogenicity and have connections for temporary ventricular pacing. The former is important to remember in case the patient develops heparin-induced thrombocytopenia, because only a small amount of heparin is necessary to sustain this process.

Proper attachment of the PAC to the monitoring equipment is essential for accurate measurements.

Transmission of pressures from the body to the display system is accomplished via semirigid, noncompliant tubing filled with fluid, usually isotonic saline with a small amount of heparin. This, in turn, is connected to a fluid-filled pressure transducer.

Often, a constant infusion or "interflow" device is placed into the connecting pressure line. This device does not alter the pressure and provides a small constant infusion of fluid through the catheter to prevent backup of blood. Because the fluid is incompressible and the tubing noncompliant, this system fairly accurately transmits intracardiac pressures to the transducer, causing small amounts of movement in the transducer membrane. Deformation of this membrane generates a proportional electric current that is amplified and transmitted to the monitor.

A guide wire catheter may be useful in patients with large RVs and a lot of tricuspid regurgitation.

Monitoring & Follow-up

Complications associated with PAC use relate to the initial venous access, insertion of the PAC, and maintenance of the catheter in the PA. The incidence of complications varies on the basis of operator skill and patient status. Even with the use of ultrasonography-guided approaches, venous access complications may still occur, including arterial puncture, which may manifest immediately (eg, carotid artery hematoma if inserted via the internal jugular [IJ] route) or insidiously (eg, hemothorax via subclavian route). Also, the risk of pneumothorax relates to the selection of the access route, occurring more often in the subclavian than in the IJ site. However, it is important to note that low IJ approaches also carry this risk. Keep in mind that in ventilated patients, tension pneumothorax can develop rapidly.

Arrhythmias constitute the most common complication associated with PAC insertion. The majority of these are premature ventricular contractions (PVCs) or nonsustained ventricular tachycardia (VT) which resolve either with advancement of the catheter from the RV into the PA, or with prompt withdrawal of the catheter into the RA. Significant VT or ventricular fibrillation requiring treatment occurs in less than 1% of patients, usually those with concurrent cardiac ischemia or electrolyte distubances.

Right bundle-branch block (RBBB) can occur during PAC insertion and is usually transient after positioning the catheter into the PA. However, the presence of a preexisting left bundle-branch block (LBBB) puts the patient at risk for complete heart block should RBBB occur. In these patients, temporary pacing equipment should be kept nearby on standby. The incidence of knotting of the PAC on itself or on intracardiac structures is rare. This risk is potentially increased in patients with dilated cardiac chambers or in situations in which there is a persistent RV tracing despite further advancement (20 cm) of the PAC.

Of the complications associated with maintenance of the PAC, PA rupture is most catastrophic, with a mortality rate of 50%. Fortunately, it is a rare occurrence (< 1%). Patients at risk are those who have pulmonary hypertension, are older than 60 years, or are receiving anticoagulation therapy. The sudden onset of hemoptysis (especially after inflation of the PAC balloon) indicates this possibility. Immediate management includes lateral decubitus positioning (bleeding side down), intubation with a double-lumen endotracheal tube (ETT), and increasing PEEP. Embolization via bronchoscopy or angiography or lobectomy may be necessary if bleeding continues or is massive. A case report describes the use of a vascular plug to tamponade the culprit breach of the pulmonary artery.[31]

PAC-related infection is a fairly common complication. The incidence of positive catheter tip culture result is 45% in some series. Although sterile plastic sleeves have been used to decrease infection risk with PACs, a prospective observational study found positive cultures from the sleeve in some patients; these investigators warn that the sleeve should not be considered a sterile barrier.[32] Fortunately, the risk for clinical sepsis is less than 0.5% per day of catheter use.

The risk for significant catheter colonization increases after 4 days of catheterization.[33] The US Centers for Disease Control and Prevention (CDC) recommends against the routine replacement of PACs to prevent catheter-related infection.[33]

The incidence of pulmonary infarction is low. Unintentional distal migration of the PAC tip is the usual cause. Some evidence indicates that catheter-related thrombi also may be a significant cause. While postmortem studies have shown that rate of endocardial lesions (eg, thrombi, hemorrhage, vegetations) related to PAC use is significant, correlation with clinical events has not been established.

 

Technique

Equipment Setup

Zero reference

Any independent vertical movement of the transducer or the patient will affect the hydrostatic column of this fluid-filled system and thus alter the pressure measurements. At some time before or after PAC insertion, the system must therefore be zeroed to ambient air pressure.

The reference point for this is the midpoint of the left atrium (LA), estimated as the fourth intercostal space in the midaxillary line with the patient in the supine position. With the transducer at this height, the membrane is exposed to atmospheric pressure, and the monitor is then adjusted to zero.

Calibration

Once zeroed, the monitoring system must be calibrated for accuracy. Currently, most monitors perform an automated electronic calibration.

Two methods are used to manually calibrate and check the system, as follows:

  • If the catheter has not been inserted, the distal tip of the PAC is raised to a specified height above the LA. For example, raising the tip 20 cm above the LA should produce a reading of approximately 15 mm Hg if the system is working properly (1 mm Hg equals 1.36 cm H2 O).

  • Alternatively, pressure can be applied externally to the transducer and adjusted to a known level using a mercury or aneroid manometer. The monitor then is adjusted to read this pressure, and the system is calibrated.

Dynamic tuning

Central pressures are dynamic waveforms (ie, they vary from systole to diastole) and thus have a periodic frequency. To monitor these pressures accurately, the system requires an appropriate frequency response. A poorly responsive system produces inaccurate pressure readings, and differentiating waveforms (eg, PA from pulmonary capillary wedge pressure [PCWP]) can become difficult. When signal energy is lost, the pressure waveform is dampened. Common causes of this are air bubbles (which are compressible), long or compliant tubing, vessel wall impingement, intracatheter debris, transducer malfunction, and loose connections in the tubing. A qualitative test of the frequency response is performed by flicking the catheter and observing a brisk high-frequency response in the waveform.

After insertion, the system can be checked by using the rapid flush test. When flushed, an appropriately responsive system shows an initial horizontal straight line with a high-pressure reading. Once the flushing is terminated, the pressure drops immediately, which is represented by a vertical line that plunges below the baseline. A brief and well-defined oscillation occurs, followed by return of the PA waveform. A dampened system will not overshoot or oscillate, and causes a delay in returning to the PA waveform.

PAC Insertion

The PAC is inserted percutaneously into a major vein (jugular, subclavian, femoral) via an introducer sheath. The actual venous access techniques are not described here, but the following points are important. Preference considerations for cannulation of the great veins are as follows:

  • Right internal jugular vein (RIJ) - Shortest and straightest path to the heart

  • Left subclavian - Does not require the PAC to pass and course at an acute angle to enter the SVC (compared to the right subclavian or left internal jugular [LIJ])

  • Femoral veins - These access points are distant sites, from which passing a PAC into the heart can be difficult, especially if the right-sided cardiac chambers are enlarged. Often, fluoroscopic assistance is necessary. Nevertheless, these sites are compressible and may be preferable if the risk of hemorrhage is high.

As with any catheterization procedure, sterile technique is essential. The total length of a PAC is approximately 150 cm; extra sterile towels around the head, shoulders, and chest ensure that aseptic technique is not compromised.

While the Trendelenburg position is used for venous access (internal jugular [IJ] and subclavian routes), passage of the PAC is easier when the patient subsequently is placed flat or slightly upright.

Before insertion, check the PAC for cracks and kinks. Then, check balloon function (see image below), connect all lumens to stopcocks, and flush them to eliminate air bubbles. Flick the PAC tip to check frequency response. Finally, the PAC is threaded through a sterile sleeve (be sure to check orientation) to ensure sterility of the PAC after insertion and allow some adjustment of position.

The balloon of the catheter should be checked prio The balloon of the catheter should be checked prior to insertion.

The packaging of the PAC causes it to have a preformed curve. This can be used to facilitate passage into the PA. The direction in which the curl is inserted into the introducer depends on which vein is cannulated. For instance, from the head of the bed using the RIJ approach, the curl should be in the direction of the patient's left shoulder (concave-cephalad). Once the PAC is in the RV, a clockwise quarter turn moves the tip anteriorly to allow easier passage into the PA.

After inserting the PAC as far as the 20-cm mark (30-cm mark if the femoral route used), the balloon is inflated with air. Inflation should be slow and controlled (1 mL/s) and should not surpass the recommended volume (usually 1.5 mL). Always inflate the balloon before advancing the PAC, and always deflate the balloon before withdrawing the PAC.

Always use continuous pressure monitoring from the distal lumen. Watch the monitor for changes in the waveform and abnormal cardiac rhythms. From the RIJ approach, the RA is entered at approximately 25 cm, the RV at approximately 30 cm, and the PA at approximately 40 cm; the PCWP can be identified at approximately 45 cm.

If an RV waveform still present approximately 20 cm after the initial RV pattern appears, the catheter may be coiling in the RV. If withdrawal is necessary, always proceed slowly to decrease the risk of knotting the catheter upon itself. If the catheter is knotted, fluoroscopy may be necessary to visualize the catheter and remove the knot. As a last resort, slowly withdraw the PAC to the point where it catches on the introducer tip. From this point, the PAC and introducer can be removed as one unit. Apply prompt pressure for a minimum of 5 minutes. If bleeding persists, suturing the site may be necessary.

Once the PCWP is obtained and the catheter sleeve secured, make sure the PCWP pattern is reproducible before removing the sterile field. Also, determine the volume of air in the balloon required to obtain a PCWP waveform. Volumes less than half the balloon maximum may indicate that the tip is too far distal. Some clinicians advocate that, after establishing that the PA diastolic pressure is equal to the PCWP pressure, further balloon inflations are unnecessary and the PA diastolic pressure should be used as the parameter to assess left ventricular (LV) filling; this relationship may not hold if the clinical situation changes.

Once the procedure is complete, obtain a chest radiograph to check the position of the PAC and to assess for central venous access complications (eg, pneumothorax).

An interesting real-time online video is available to enhance the visualization of the course of the catheter as it passes through the heart.[34, 35, 36]

Measurements

Table 2 below shows the normal range of pressures for the RA, RV, PA, and PCWP.

Other important information provided by a PAC catheter includes the CO, mixed venous oxygen saturation (SaO2), and oxygen saturations in the right heart chambers to assess for the presence of an intracardiac shunt.

Using these measurements, other variables can be derived, including pulmonary or systemic vascular resistance and the difference between arterial and venous oxygen content (see the image and Table 1 below). Obtaining CO and PCWP measurements is the primary reason for inserting most PACs; therefore, understanding how they are obtained and what factors alter their values is of prime importance.

Normal hemodynamic parameters. Normal hemodynamic parameters.

 

Table 1. Calculation of Various Hemodynamic Parameters (Open Table in a new window)

Parameter

Equation

Systemic vascular resistance (SVR)

SVR = (MAP – RAP/CO) × 80

Pulmonary vascular resistance (PVR)

PVR = (PAP – PAOP/CO) × 80

Cardiac output (CO)

CO = VO2 /(CaO2 – CvO2)

Oxygen delivery (DO2)

DO2 = CO × CaO2 × 10

Oxygen consumption (VO2)

VO2 = (CaO2 – CvO2) × CO × 10

Arterial oxygen content (CaO2)

CaO2 = (1.39 × Hb × SaO2) + (0.003 × PaO2)

Venous oxygen content (CvO2)

CvO2 = (1.39 × Hb × SvO2) + (0.003 × PaO2)

Oxygen extraction ratio (O2ER)

O2ER = VO2 /DO2 × 100

Intrapulmonary shunt (Qs/Qt)

Qs/Qt = (PA-aO2) / (Ca­­-vO2) – shunt fraction

Ca­­-vO2 = arteriovenous oxygen content difference; Hb = hemoglobin; MAP = mean arterial pressure; PA-aO2 = alveolar-arterial oxygen tension gradient; PAOP = pulmonary artery occlusion pressure; PaO2 = partial pressure of arterial oxygen; PAP = pulmonary artery pressure; Qs = ratio of shunted blood; Qt = total cardiac output; RAP = right atrial pressure (central venous pressure); SaO2 = arterial oxygen saturation; SvO2 = mixed venous oxygen saturation.

Table 2. Circulatory Pressures (Open Table in a new window)

Circulatory Pressures, mm Hg

 

Systolic

Diastolic

Mean

AO

120

80

100

LV

120

8

-

LA*

7

10

4

PA

15

7

12

RV

15

2

-

RA*

4

4

0

PCW*

7

10

4

*

A wave

V wave

 

Wave Form Analysis

Wave form analysis in healthy states

Cardiac pressures

Right- and left-sided heart pressure waveforms share many physiologic similarities, but, in the healthy individual, the waves are of different magnitudes.

Right-sided pressures

The central venous pressure (CVP) and right atrial pressure (RAP) are nearly equal to the diastolic RV pressure in the absence of heart or lung disease (see image below).

Central venous pressure (CVP) measured in superior Central venous pressure (CVP) measured in superior vena cava (SVC) is identical to right atrial pressure (RAP).

The mean CVP and RAP normally range from 0-5 mm Hg, and vary as intrathoracic pressure changes with respiration (see image below).

Respiratory variation is easily identified on the Respiratory variation is easily identified on the right atrial waveform.

RA contraction creates pressure changes, which are influenced strongly by the patient's volume status. Atrial contraction produces an increase in pressure called the A wave. The C wave is a small convexity noted on the initial descent of the A wave and is thought to be secondary to closure of the tricuspid valve. The initial descent after the A wave is called the X descent. This decline in RAP is secondary to RA relaxation and downward movement of the tricuspid valve. Following this is the V wave, which is somewhat smaller than the A wave, and reflects RA filling during ventricular systole. The Y descent occurs after the V wave and represents rapid filling of the RV after opening of the tricuspid valve (see image below).

Various waveforms of central venous pressure (CVP) Various waveforms of central venous pressure (CVP) monitoring are shown here.

CVP is most commonly elevated in the setting of biventricular heart failure. Other causes of RAP elevation are tricuspid regurgitation or stenosis, pulmonary hypertension, volume overload, constrictive pericarditis, and cardiac tamponade. Large, so-called cannon A waves occur when the RA contracts against a closed tricuspid valve. Cannon A waves are detected in certain cardiac rhythm disturbances, including junctional rhythms and ventricular tachycardia, and in some patients with ventricular pacemakers. Large V waves may occur in the presence of tricuspid regurgitation, with their magnitude affected by the size and compliance of the RA.

Pulmonary arterial pressure

In the pulmonary artery pressure (Ppa) tracing, an initial positive upstroke secondary to RV systole occurs, and a dicrotic notch is formed on the downstroke when the pulmonary valve closes. A normal PA systolic pressure ranges from 20 to 30 mm Hg and is equal to the RV systolic pressure. Ppa is elevated in some high-flow states (eg, hypervolemia), left ventricular failure, and high-resistance states (eg, pulmonary hypertension, mitral valve disease) (see image below).

Pulmonary arterial pressure (Ppa) waveform. Pulmonary arterial pressure (Ppa) waveform.

Pulmonary artery occlusion pressure (wedge pressure)

Understanding the theory and required assumptions behind PCWP measurement and conditions that alter it are essential for proper use of this often misunderstood measurement. When the PAC tip is positioned properly and the balloon is inflated, the PAP tracing disappears. This occurs because inflation of the balloon causes distal migration (approximately 2 cm) of the tip into a smaller branch of the PA, where it occludes blood flow. The resulting nonpulsatile pressure tracing is called the PCWP (or pulmonary artery occlusion pressure [Ppao]) (see image below).

Pulmonary artery wedge pressure (PAWP) waveform ca Pulmonary artery wedge pressure (PAWP) waveform can be distinguished easily from the pulmonary arterial waveform in most clinical scenarios.

Under the proper circumstances, this pressure reflects the mean left atrial pressure (LAP) (see image below).

Pulmonary artery wedge pressure (PAWP) reflects le Pulmonary artery wedge pressure (PAWP) reflects left atrial pressure (LAP).

The assumption is that a static column is created between the PAC tip and the LA. This assumption is correct only if the tip is in the proper lung zone and no vascular obstruction, such as pulmonary vein stenosis, occurs downstream. When the PAC catheter balloon is inflated, the balloon stops antegrade blood flow and allows an uninterrupted column of blood to exist between the catheter tip and the LA (see images below).

Inflated balloon obstructs arterial flow and refle Inflated balloon obstructs arterial flow and reflects pressures at J point. Redrawn from Principles of Critical Care by Jesse B. Hall, Gregory A. Schmidt, Lawrence D. H. Wood, 2000, McGraw-Hill, Inc.
Having an inflated balloon in a proximal vessel is Having an inflated balloon in a proximal vessel is better because a vessel branch is likely to reflect left atrial pressure (LAP) accurately. Redrawn from Principles of Critical Care by Jesse B. Hall, Gregory A. Schmidt, Lawrence D. H. Wood, 2000, McGraw-Hill, Inc.

The PCWP waveform reflects events in the LA. The A, C, and V waves have origins similar to those that appear in the RAP waveform (see image below).

Right or left atrial pressure waveform. Right or left atrial pressure waveform.

The waveforms can be discerned by using simultaneous ECG monitoring (see image below).

Timing of the pulmonary artery waveforms in relati Timing of the pulmonary artery waveforms in relation to electrocardiographic monitoring is shown here. An A wave follows the QRS wave on ECG, whereas V wave follows the T wave on ECG.

The 3 lung zones of West

The lung can be divided into 3 vertical zones with varying pressure changes (see image below).[37]

Physiologic lung zones. For pulmonary capillary we Physiologic lung zones. For pulmonary capillary wedge pressure (PCWP) to be reliable, the catheter tip must lie in zone 3. Pulmonary artery pressure (Ppa) is greater than pulmonary venous pressure (Ppv), which is greater than alveolar pressure (Palv) at end-expiration. In zones 1 and 2, Ppw reflects Palv if Palv is greater than Ppv. Redrawn from Principles of Critical Care by Jesse B. Hall, Gregory A. Schmidt, Lawrence D. H. Wood, 2000, McGraw-Hill, Inc.

In zone 1 (apex), alveolar pressure (Palv) exceeds both mean Ppa and pulmonary venous pressures (Ppv). Flow depends on Palv. In zone 2 (central), Ppa is greater than Palv, which is greater than Ppv, and flow depends on a balance between Ppa and Palv. Because capillary collapse is present, neither zone 1 nor zone 2 allows a direct connection with the LA. In zone 3 (lung bases), Palv is less than Ppa and Ppv. Flow is not interrupted, and a direct column of blood extends to the LA.

Fortunately, the actual practice of placing the tip in zone 3 to ensure more accurate measurements of LAP is not complicated. In the supine patient, most of the lung is considered zone 3. Blood flow to this area is increased, making balloon flotation easier. In critically ill patients who require positive end expiratory pressure (PEEP) levels greater than 10 cm H2 O, the zone 3 area can be reduced.

To assess proper location, a supine chest radiograph showing the tip below the level of the LA is sufficient, although occasionally a lateral chest radiograph is required. If the tip position remains questionable, blood can be aspirated from the distal port during balloon inflation.

Preload (left ventricular end-diastolic pressure)

PCWP is a reflection of LAP, which, in the absence of mitral valve disease, is an indication of LV diastolic pressure. Often, the inference is made that PCWP reflects left ventricular end-diastolic volume (LVEDV) or end-diastolic pressure (LVEDP). Numerous conditions in critically ill patients preclude this assumption.

PCWP is the measurement by which changes in lung water (pulmonary capillary hydrostatic pressure [PCHP]) can be assessed. This concept holds true only if the resistance of the pulmonary venous system is assumed to be zero. In fact, the small pulmonary veins and capillaries account for approximately 40% of the total pulmonary vascular resistance. This value may be even higher in critically ill patients in whom pulmonary venoconstriction is common secondary to conditions such as hypoxemia and acute respiratory distress syndrome (ARDS). PCHP is always greater than PCWP. PCWP can be used to estimate the contribution of PCHP to lung edema if evidence of chronically elevated Ppv, permeability, pleural pressure, and osmotic pressure are considered.

Effect of respiration

The final critical concept in PCWP interpretation is the effect of the respiratory cycle on PCWP measurements. The timing of PCWP measurement is critical because intrathoracic pressures can vary widely with inspiration and expiration and are transmitted to the pulmonary vasculature. During spontaneous inspiration, the intrathoracic pressures decrease (more negative); during expiration, intrathoracic pressures increase (more positive). Positive pressure ventilation (eg, in an intubated patient) reverses this situation. To minimize the effect of the respiratory cycle on intrathoracic pressures, measurements are obtained at end-expiration, when intrathoracic pressure is closest to zero.

In patients with severe respiratory distress, end-expiration can be difficult to determine. In these situations, sedation, or even paralysis, may be necessary to remove the transmission of respiratory efforts to the pressure tracings.

Positive end-expiratory pressure

PEEP (intrinsic or extrinsic) also transmits pressure to the vascular space. Lung compliance is the main determinant of the amount of pressure transmission. For example, in disease states (eg, ARDS) associated with low compliance (ie, stiff lungs), pressure transmission is minimal. Debate exists over how to correct PCWP in the presence of PEEP. Although previously advocated, temporary discontinuation of PEEP may have adverse effects, such as cardiovascular collapse or hypoxemia, that are difficult to reverse.

For PEEP greater than 10 cm H2 O, the following general rule can be applied: Corrected PCWP equals measured PCWP minus one half the quotient of PEEP divided by 1.36. If available, an intraesophageal balloon can be used. Esophageal pressure equals pleural pressure, so corrected PCWP equals measured PCWP minus esophageal pressure.

Wave form analysis in pathologic states

Shock has been defined as inadequate perfusion to meet the metabolic demands of body tissues. The most common forms of shock are hypovolemic, cardiogenic, septic, and obstructive. PACs are used frequently in the management of various forms of shock, as described in this section (see image below).

Hemodynamic parameters in different pathologic sta Hemodynamic parameters in different pathologic states.

Hypovolemic shock

Hypovolemic shock is due to a reduction in circulating blood volume resulting from either hemorrhage or fluid depletion. Preload is markedly decreased, leading to inadequate ventricular filling. The patient with hypovolemic shock manifests hypotension and tachycardia. Systemic, venous, and intracardiac pressures are abnormally low. The overall PAC pressure tracing has a damped appearance.

Cardiogenic shock

Cardiogenic shock is the result of severe depression in cardiac performance. Cardiogenic shock is characterized by systolic blood pressure less than 80 mm Hg, cardiac index less than 1.8 L/min/m2, and PCWP greater than 18 mm Hg. This form of shock can occur from a direct insult to the myocardium (eg, large AMI, severe cardiomyopathy) or from a mechanical problem that overwhelms the functional capacity of the myocardium (eg, acute severe mitral regurgitation, acute ventricular septal defect).

Common causes of acute mitral regurgitation in critical care units are ruptured papillary muscles secondary to AMI, myocardial ischemia leading to papillary muscle dysfunction, bacterial endocarditis, ruptured chordae, and trauma. Other causes are rheumatic fever and myxomatous degeneration of the mitral valve. With acute mitral regurgitation, large volumes of blood regurgitate into a poorly compliant LA, raising Ppv and causing pulmonary edema.

Large V waves usually are observed in the PCWP pressure tracing (see images below).

Tall V waves presented here on pulmonary arterial Tall V waves presented here on pulmonary arterial and wedge pressure waveforms are characteristic of severe mitral regurgitation.
Large V waves in a case of mitral regurgitation. Large V waves in a case of mitral regurgitation.
Simultaneous recording of ECG helps identify V wav Simultaneous recording of ECG helps identify V waves in mitral valve regurgitation; V waves correspond to T waves on ECG.

The PA waveform appears falsely elevated because of the large V wave reflected back from the LA through the compliant pulmonary vasculature. The Y descent is quite rapid as the overdistended LA quickly empties. Care must be exercised to distinguish a large V wave from a systolic PA waveform. Failure to recognize a large V wave may cause the PAC to be advanced further in an attempt to record a PCWP pressure, increasing the risk of perforation.

In chronic mitral regurgitation, an equivalent volume of blood may regurgitate, but this volume is better tolerated by a markedly dilated LA. Compared with acute mitral regurgitation, LA pressure may be less and large V waves may be absent.

Septic shock

Septic shock is the most common cause of death in intensive care units in the United States. Septic shock is an example of distributive shock, a form of shock characterized by profound peripheral vasodilation. Although the CO may be normal or even elevated in this type of shock, organ and tissue perfusion are inadequate. Other types of distributive shock include anaphylaxis, neurogenic shock, and adrenal insufficiency. Swan-Ganz catheter measurements frequently demonstrate low filling pressures.

Extracardiac obstructive shock

Pericardial tamponade is an example of this form of shock. Cardiac tamponade results from abnormal rapid fluid accumulation in the pericardial sac. The increased pericardial pressure impairs ventricular diastolic filling, decreasing preload, stroke volume, and CO. This may occur secondary to viral infections, malignancy, trauma, or myocardial rupture. As little as 50 mL of fluid accumulation can begin to impair cardiac filling during systole, leading to a severe reduction in CO. Ventricular filling is impaired throughout all of diastole, thereby causing equalization of all diastolic pressures.

The RAP approximates the RV diastolic pressure, which approximates the PA diastolic pressure, and also approximates PCWP (see image below).

Hemodynamic monitoring can confirm the diagnosis o Hemodynamic monitoring can confirm the diagnosis of pericardial tamponade. Equalization of diastolic pressures on the left and right sides of the heart, elevated right atrial pressure, and Kussmaul sign (ie, increase in right atrial pressure with inspiration) are noted.

The RA waveform shows a minimal X and small and/or absent Y descent, and the mean RAP is elevated. Ppa loses its usual respiratory variation. In pericardial tamponade, the systemic arterial pressure shows evidence of pulsus paradoxus (see image below). Other causes of extracardiac shock include massive PE and tension pneumothorax.

In cardiac tamponade, systemic arterial pressure ( In cardiac tamponade, systemic arterial pressure (Pa) reflects pulsus paradoxus. Right atrial pressure (RAP) is elevated. Pulmonary artery (PA) diastolic pressure equals mean right atrial (RA), right ventricular (RV) diastolic, and wedge pressures.

Hemodynamics of other cardiac abnormalities

Constrictive pericarditis

Thickening of the pericardial sac creates an indolent process that may lead to constrictive pericarditis. This can occur in patients with rheumatic diseases, tuberculosis, metastatic cancer, or prior chest radiation or open-heart surgery. Idiopathic cases also occur. Early diastolic filling is normal until limited by the rigid pericardial shell. Once this occurs, ventricular filling is stopped abruptly, creating a plateau in the RV pressure, which is typical of constrictive pericarditis. This is called the "dip and plateau" pattern or square root sign; the RAP waveform has a characteristic configuration suggestive of an M or W. A and V waves are accentuated with rapid X and Y descents, in contrast to pericardial tamponade, above. PCWP may be as high as 20-25 mm Hg, and usually appears similar to the RA waveform. Pulsus paradoxus is present much less commonly with constrictive pericarditis than with pericardial tamponade (see images below).

Simultaneous recordings of pulmonary capillary wed Simultaneous recordings of pulmonary capillary wedge pressure and left ventricular pressure waveforms in a patient with constrictive pericarditis. Note the equalization of diastolic pressures and "square root sign" or "dip and plateau sign" of the left ventricular waveforms, which are confirmatory of the diagnosis of constrictive pericarditis.
Right atrial pressure waveform of a patient with c Right atrial pressure waveform of a patient with constrictive pericarditis. Please note rapid X and Y descents, and elevated A and V waves. This gives an impression of the letter "M" or "W" and is confirmatory of the diagnosis of constrictive pericarditis.

Mitral stenosis

In severe mitral stenosis, LAP, and thus PAWP, is elevated. Pulmonary hypertension also develops as the severity of the valve lesion progresses. This leads to increase in RV systolic pressure and in the RA A wave. RV diastolic pressure may increase if RV failure or important tricuspid regurgitation develops. Atrial fibrillation is a common complication in mitral stenosis and results in loss of A waves in both the RA and PCWP pressure tracings.

Aortic stenosis

Aortic stenosis can be supravalvular, valvular, or subvalvular in origin. The RA, RV, and PA waveforms usually are normal unless congestive heart failure is present. PCWP may show large A waves in severe cases because of poor LV compliance.

Aortic regurgitation

The hemodynamic abnormalities are different in acute and chronic aortic regurgitation. Acute regurgitation is observed most often in bacterial endocarditis, chest trauma, ascending aortic dissection, and degeneration of valve leaflets. The hemodynamics in acute aortic regurgitation include modestly elevated RAP and elevated RV systolic and diastolic pressures. PA systolic and diastolic pressures also are elevated, as is PCWP. A widened and elevated systemic arterial pressure without a dicrotic notch is sometimes observed. Acute and chronic aortic regurgitation often present with contrasting manifestations; a wide pulse pressure usually is not observed in acute regurgitation.

Other hemodynamic measurements made by the pulmonary artery catheter

Cardiac output

CO can be determined via the PAC by several methods. It can be determined by using the Fick principle, which is a variation of the law of conservation and states that consumption of a substance must equal the product of blood flow to the organ and the difference between the arterial and venous concentrations of the substance. In this circumstance, the substance is oxygen, and CO is determined by the following formula:

CO equals oxygen consumption per minute (VO2) divided by arterial oxygen content (CaO2) minus mixed venous oxygen content (CvO2)

CO is determined by using systemic arterial and PA blood samples, and by measuring or estimating VO2. The Fick method is most accurate when the CO is low and the arterial-venous oxygen difference is high. Unfortunately, in critically ill patients, establishing a steady-state and estimating or measuring VO2 is difficult; thus, the reliability of this technique is poor.

The indicator-dilution technique is more accurate and reproducible. A known amount of dye (indocyanine green) is injected into the PA. Arterial blood is withdrawn from the aorta as the dye circulates, and a concentration-versus-time curve is derived. The first-pass curve is used to determine CO, which is calculated by dividing the initial mass of the injectate by the average concentration. This value then is corrected (60 s/time of the curve) to obtain CO. This procedure requires considerable blood sampling and is time consuming, because recirculation of the dye complicates the calculation.

Many PACs also allow CO to be measured by using a variation of the indicator-dilution method known as the thermodilution method. This method is more efficient because the injectate does not recirculate to a significant degree and no blood sampling is necessary. A saline bolus of known volume (5-10 mL) and temperature (usually ≤25ºC) is injected through the proximal (RA) lumen. The thermistor at the end of the PAC monitors the change in blood temperature, and a temperature-versus-time curve is generated (see image below).

Principle of cardiac output measurement. Principle of cardiac output measurement.

The change in temperature as warm venous blood dilutes the injectate is inversely proportional to the derived CO. The Stewart-Hamilton formula shows this relationship: CO equals the volume of injectate multiplied by blood temperature minus injectate temperature multiplied by computation constants, and divided by change of blood temperature as a function of time (area under the curve).

Understanding this formula allows discernment of artifact errors that can lead to underestimation or overestimation. Loss of injectate or inadvertent administration of a volume lower than required results in a low-amplitude temperature-versus-time curve that produces a falsely elevated CO value. Causes of this are system leak, right-to-left intracardiac shunts, inappropriately rapid injection, and a poorly positioned PAC. Conversely, too much injectate or too slow an injection leads to a falsely low CO reading. Temperature errors can occur when continuous infusions are used. Thrombus or vessel wall impingement can alter the thermistor function.

Physiologic causes for CO measurement discrepancies include tricuspid and pulmonary regurgitation, which may produce recirculation peaks and thus increase the area under the curve, resulting in a falsely low CO estimate. Arrhythmias alter steadiness of PA flow and may cause difficulty in obtaining a consistent CO.

CO alterations occur during the respiratory cycle and are accentuated by respiratory distress and positive pressure ventilation. Proper timing of the injection to the same phase of respiration (preferably end-expiration) provides more consistent measurements. Averaging the values of 3 injections is recommended to minimize sampling errors.

While CO is one of the most important measurements that the PAC provides, the absolute value should be normalized for the size of the patient. To account for this, the cardiac index (CI), which equals CO divided by body surface area [BSA], is calculated. The physician should keep in mind that, as independent variables, CO and CI are of limited use for assessing tissue perfusion because these must be interpreted along with other clinical data.

 

Questions & Answers

Overview

What is pulmonary artery catheterization (PAC)?

According to ACCF guidelines, what are the appropriate uses for pulmonary artery catheterization (PAC)?

According to ACCF guidelines, when is use of pulmonary artery catheterization (PAC) inappropriate?

What are alternatives to pulmonary artery catheterization (PAC)?

What are best practices for pulmonary artery catheterization (PAC) when right-sided pressures are elevated?

What is the efficacy of pulmonary artery catheterization (PAC)?

What are the controversies about the use of pulmonary artery catheterization (PAC)?

Periprocedural Care

What equipment is used to perform pulmonary artery catheterization (PAC)?

What are the possible complications of pulmonary artery catheterization (PAC)?

Technique

How is the pulmonary artery catheterization (PAC) system zeroed to ambient air pressure?

How is the pulmonary artery catheterization (PAC) system manually calibrated?

How is the pulmonary artery catheterization (PAC) system dynamically tuned?

How is pulmonary artery catheterization (PAC) performed?

How are hemodynamic parameters calculated during pulmonary artery catheterization (PAC)?

What is the role of cardiac pressures in pulmonary artery catheterization (PAC)?

What is the role of pulmonary arterial pressure in pulmonary artery catheterization (PAC)?

What is the role of pulmonary artery occlusion pressure in pulmonary artery catheterization (PAC)?

What are the vertical lung zones relevant to pulmonary artery catheterization (PAC)?

What is the role of left ventricular end-diastolic volume (LVEDV) in pulmonary artery catheterization (PAC)?

What is the role of respiratory cycle in pulmonary artery catheterization (PAC)?

What is the role of positive-end expiratory pressure (PEEP) in pulmonary artery catheterization (PAC)?

What is the wave form analysis in the different pathologic states of pulmonary artery catheterization (PAC)?

What is the clinical presentation of hypovolemic shock in pulmonary artery catheterization (PAC)?

What is the clinical presentation of cardiogenic shock in pulmonary artery catheterization (PAC)?

What is the clinical presentation of septic shock in pulmonary artery catheterization (PAC)?

What is the clinical presentation of extracardiac obstructive shock in pulmonary artery catheterization (PAC)?

What is the clinical presentation of constrictive pericarditis in pulmonary artery catheterization (PAC)?

What is the clinical presentation of mitral stenosis in pulmonary artery catheterization (PAC)?

What is the clinical presentation of aortic stenosis in pulmonary artery catheterization (PAC)?

What is the clinical presentation of aortic regurgitation in pulmonary artery catheterization (PAC)?

What is the clinical presentation of cardiac output in pulmonary artery catheterization (PAC)?