Pulmonary artery catheterization: Interpretation of hemodynamic values and waveforms in adults

INTRODUCTION — The pulmonary artery catheter (PAC; Swan-Ganz or right heart catheter) can be used for a variety of clinical purposes. Interpreting hemodynamic data from PACs is important for the diagnosis and management of a range of conditions including shock and pulmonary artery hypertension (table 1).

The interpretation of hemodynamic values and pressure tracings derived from the PAC is described in this topic. The insertion technique, indications, contraindications, and complications of PACs are discussed separately. (See "Pulmonary artery catheters: Insertion technique in adults" and "Pulmonary artery catheterization: Indications, contraindications, and complications in adults".)

PHYSIOLOGIC MEASUREMENTS — Direct measurements of the following can be obtained from an accurately placed pulmonary artery catheter (PAC):

●Central venous pressure (CVP)

●Right-sided intracardiac pressures (right atrium, right ventricle)

●Pulmonary arterial pressure (PAP)

●Pulmonary artery occlusion pressure (PAOP; pulmonary capillary wedge pressure [PCWP]; pulmonary artery wedge pressure [PAWP])

●Cardiac output (CO)

●Mixed venous oxyhemoglobin saturation (SvO₂)

The PAC can also indirectly measure the following:

●Systemic vascular resistance (SVR = 80 x [mean artery pressure – CVP]/CO)

●Pulmonary vascular resistance (PVR = 80 x [mean PAp – PAOP]/CO)

●Cardiac index (CI = CO/body surface area)

●Stroke volume index (SVI = CI/heart rate)

●Left ventricular stroke work index (LVSWI = [mean systemic artery pressure – PAOP] x SVI x 0.136)

●Right ventricular stroke work index (RVSWI = [mean PAp – CVP] x SVI x 0.136)

●Oxygen delivery (DO₂ = CI x 13.4 x hemoglobin concentration x arterial oxygen saturation)

●Oxygen uptake (VO₂ = CI x 13.4 x hemoglobin concentration x [arterial oxygen saturation – venous oxygen saturation])

●Pulmonary artery pulsatility index (PAPI = [pulmonary artery systolic pressure – pulmonary artery diastolic pressure]/CVP)

●Cardiac power output (CPO = [CO x mean artery pressure]/451)

ENSURING ACCURATE MEASUREMENTS — Certain steps must be performed before a pulmonary artery catheter (PAC) is used to measure hemodynamic variables. These steps include zeroing, referencing, ensuring the catheter is in the correct position, and assessing the dynamic response using the "fast-flush" test.

Zeroing and referencing — The PAC must be appropriately zeroed and referenced to obtain accurate readings [1]. Zeroing and referencing are generally performed with the patient lying in the supine position. Occasionally, in patients who cannot lie flat, zeroing and referencing are performed in the semi-recumbent position at approximately 30 degrees. Importantly, zeroing and referencing should be done prior to placement and repeated when time has elapsed between one set of measurements and another, especially if the patient’s position has been moved. (See "Pulmonary artery catheters: Insertion technique in adults", section on 'Zeroing and referencing'.)

Correct placement — Once the PAC has been zeroed and referenced, it is positioned using either pressure waveform or fluoroscopic guidance. Transesophageal echo has also been used to facilitate placement of the PAC [2]. When the correct position has been confirmed, the arterial waveform and the right atrial pressure waveforms are simultaneously recorded with the pulmonary artery pressure (balloon deflated) or pulmonary artery wedge pressure waveforms (balloon inflated). Detailed discussion of correct PAC placement is provided separately. (See "Pulmonary artery catheters: Insertion technique in adults", section on 'Insertion of the pulmonary artery catheter'.)

The "fast-flush" test — Following catheter placement, the dynamic response of the monitoring system to pressure should be assessed. This can be done at the bedside using the "fast-flush" test, which involves briefly opening and closing the valve in the continuous flush device [3]. The shape of the dynamic response can be interpreted as normal, under damped or over damped (figure 1):

●Normal waveform – This should produce a square wave displacement on the oscilloscope, followed by ringing and a return to baseline.

●Under damped waveform – Underdamping exists if there is excessive ringing following the square wave displacement. Common causes of underdamping include tubing connected with stopcocks, excessive tubing lengths, and patient factors (eg, tachycardia, high output states). These factors should be systematically addressed.

●Over damped waveform – Overdamping exists if there is no ringing following the square wave displacement. The most common cause of overdamping is air bubbles in the tubing, which can be cleared by flushing the system through the stopcock. Additional causes include overly compliant tubing, kinked catheters, blood clot within the tubing, no fluid, or low flush bag pressure, which can generally be eliminated by changing the equipment.

CATHETER WAVEFORMS AND PRESSURES — Pressure waveforms can be obtained from several locations, including the right atrium, right ventricle, and pulmonary artery.

Right atrium (RA) — In the presence of a competent tricuspid valve, the right atrial (RA) pressure waveform reflects both venous return to the right atrium during ventricular systole and right ventricular end-diastolic pressure. On RA tracings, there is an 80 to 100 ms delay in the detection of mechanical events from their appearance on the electrocardiogram (ECG) due to the length of tubing in the system (figure 2). (See "Examination of the jugular venous pulse".)

Elevated RA pressure — Normal RA pressures range from 0 to 7 mmHg (table 2). Elevations in RA pressure are seen in a number of conditions, including the following:

●Diseases of the right ventricle (eg, right ventricular infarction or cardiomyopathy)

●Pulmonary hypertension

●Pulmonic stenosis

●Left-to-right shunts

●Tricuspid valvular disease

●Cardiac tamponade

●Constrictive pericardial disease

●Restrictive cardiomyopathies

●Left ventricle systolic heart failure

●Hypervolemia

Differentiating among the etiologies depends upon clinical, radiographic, and echocardiographic features as well as additional supportive readings and waveforms measured on pulmonary artery catheter (PAC) (table 3). As examples:

●An elevated RA pressure from pulmonary arterial hypertension is associated with an elevated mean pulmonary arterial pressure ≥25 mmHg whereas the mean pulmonary arterial pressure is normal in patients with pulmonic stenosis or right ventricular infarction.

●An elevated RA pressure from cardiac tamponade and constrictive pericardial disease is classically equal to the right ventricular end-diastolic pressure and pulmonary artery wedge pressure (waveform 1). (See "Differentiating constrictive pericarditis and restrictive cardiomyopathy".)

●Tricuspid regurgitation classically produces tall v waves while tricuspid stenosis causes cannon a waves on the RA waveform (see below).

Abnormal RA waveforms — There are normally three positive components and two negative deflections in the RA waveform (figure 2):

●The a wave reflects contraction in atrial systole, while the x descent reflects the fall in RA pressure following this event.

●The c wave, often small, reflects the closure of the tricuspid valve.

●The v wave represents ventricular systole, as well as passive atrial filling in atrial diastole.

●The y descent reflects the fall in RA pressure following opening of the tricuspid valve and the initiation of passive filling of the right ventricle.

Electrocardiographic (ECG) correlation is required for correct identification of these events. On RA tracings, there is an 80 to 100 ms delay in the detection of mechanical events from their appearance on the ECG due to the length of tubing in the system. Additional discussion of normal RA waveforms is provided separately. (See "Cardiac catheterization techniques: Normal hemodynamics", section on 'Right atrium'.)

Causes of abnormal RA waveforms include the following:

●Tall v waves – Tricuspid regurgitation (TR) classically produces prominent, tall v waves due to blood that is regurgitated into the RA during ventricular systole (waveform 2). When regurgitation is severe, the v wave often obliterates the c wave to become what is termed a c-v or s wave. TR should be easily identified on echocardiography. The echocardiographic and hemodynamic findings of TR are discussed separately. (See "Hemodynamics of valvular disorders as measured by cardiac catheterization", section on 'Tricuspid regurgitation' and "Echocardiographic evaluation of the tricuspid valve", section on 'Tricuspid regurgitation'.)

●Giant/cannon a waves – Conditions associated with atrioventricular dissociation may manifest cannon a waves (or giant a waves) due to the simultaneous contraction of the atrium and ventricle while the tricuspid valve is closed (figure 3). These include:

•Ventricular tachycardia or ventricular pacing

•Complete heart block

•AV nodal tachycardia

•Tricuspid stenosis

In tricuspid stenosis the amplitude of the a wave is also increased in association with a slow descent of the y wave. (See "Hemodynamics of valvular disorders as measured by cardiac catheterization", section on 'Tricuspid stenosis' and "Echocardiographic evaluation of the tricuspid valve", section on 'Tricuspid stenosis'.)

●Loss of a waves – Atrial fibrillation and atrial flutter are associated with lack of organized atrial activity and therefore loss of the normal a wave. In atrial flutter, characteristic saw tooth waves in the RA tracing at a rate of 240 to 340 beats per minute may be seen.

●Loss of y descent – In pericardial tamponade there is an equalization of pressures across the chambers and in this setting after tricuspid opening there is not a rapid outflow from the right atrium into the right ventricle. This corresponds to a loss of the y descent. Notably this finding may be absent in pericardial tamponade in the setting of pulmonary hypertension and right ventricular hypertrophy.

●Rapid y descent – In cardiac conditions that lead to rapid RV filling, an exaggerated y descent can be seen. These include:

•Constrictive pericarditis

•Restrictive cardiomyopathy

•Severe tricuspid regurgitation

Right ventricle — Two pressures are typically measured from the right ventricular (RV) pressure waveform, the peak right ventricular systolic pressure and the right ventricular end-diastolic pressure. These values cannot be measured from an indwelling pulmonary artery catheter; rather, they are measured during catheter insertion using the distal tip of the catheter. (See "Pulmonary artery catheters: Insertion technique in adults", section on 'Transitioning from the SVC or RA to the RV'.)

Normal RV systolic pressure varies from 15 to 25 mmHg and normal RV end-diastolic pressure varies from 3 to 12 mmHg (table 2). As a general rule, elevations in RV pressure are associated with diseases that elevate the pulmonary artery pressure, pulmonic valve disorders, and diseases that primarily affect the right ventricle. Each category differentially elevates the RV pressure in the following manner:

●Pulmonary vascular and pulmonic valve disorders – An elevated RV systolic pressure is seen in pulmonary hypertension and pulmonic stenosis, or pulmonary embolism. Elevations >40 mmHg are unusual but when seen, are typically due to chronic elevations in pulmonary pressures. Pulmonic stenosis is characterized by a systolic pressure gradient between the right ventricle and the pulmonary artery.

●RV disorders – An increase in RV end-diastolic pressure is typically seen in cardiomyopathy, RV ischemia, RV infarction, cardiac constriction, cardiac tamponade, or RV failure secondary to pulmonary hypertension. These pathologies will also cause a mild elevation in RV systolic pressure but generally not as severe as the causes listed above.

On the RV pressure waveform, ventricular systole is represented by a prominent upstroke and downstroke, while ventricular diastole is represented by a more gradual upstroke that consists of an early rapid filling phase (during which approximately 60 percent of filling occurs), a slow filling phase (during which another 25 percent of filling occurs), and an atrial systolic phase (which produces the a wave in the RV tracing). End diastole occurs immediately after the a wave. An illustrative RV pressure waveform is shown in the figure (figure 4). Additional discussion of normal RV waveforms is provided separately. (See "Cardiac catheterization techniques: Normal hemodynamics", section on 'Right ventricle'.)

Pulmonary artery — Normal pulmonary artery (PA) systolic pressures range from 15 to 25 mmHg, while PA diastolic pressures range from 8 to 15 mmHg (table 2). The mean PA pressure (mPAp) is typically 16 mmHg (10 to 22 mmHg). The mean PA pressure can be elevated (eg, mPAp, >22 mmHg) by acute conditions (eg, venous thromboembolism or hypoxemic-induced pulmonary vasoconstriction), by acute-on-chronic conditions (eg, hypoxemic-induced vasoconstriction in a patient with underlying chronic cardiopulmonary disease), or by chronic conditions (eg, pulmonary hypertension [PH]). Many of the etiologies associated with PH will also result in mild elevations of the PA pressure. Causes of PH include (see "Clinical features and diagnosis of pulmonary hypertension of unclear etiology in adults", section on 'Postdiagnostic testing and classification'):

●Pulmonary arterial hypertension (eg, idiopathic, connective tissue disease, congenital heart disease; Group 1)

●PH due to left heart disease (eg, left heart failure, mitral valvular disease; Group 2)

●PH due to chronic lung disease and/or hypoxemia (eg, emphysema, interstitial lung disease; Group 3)

●PH due to chronic pulmonary thromboembolism (Group 4)

●PH due to multifactorial mechanisms (eg, sickle cell disease; Group 5)

The value of PAC findings in distinguishing among the etiologies of PH are discussed in detail separately. (See "Clinical features and diagnosis of pulmonary hypertension of unclear etiology in adults", section on 'Initial diagnostic evaluation (noninvasive testing)' and "Clinical features and diagnosis of pulmonary hypertension of unclear etiology in adults", section on 'Diagnosis'.)

Importantly, many of these conditions may transiently elevate the PA pressure such that the clinician should be aware of any underlying pathologies that may explain an elevated reading. As an example, PA pressure may be elevated acutely by thromboembolism or hypoxemic-induced pulmonary vasoconstriction but may revert back to chronic levels or normal once the acute issue has resolved. Fluctuations in the PA pressure may be seen in irregular heart rhythms (eg, atrial fibrillation) because of variability in the diastolic filling time.

PA systolic pressure, like RV systolic pressure, rarely exceeds 40 to 50 mmHg in acute conditions (eg, pulmonary embolism) whereas severe elevations >50 mmHg are classically due to chronic conditions such as PH.

The main components of the PA tracing are the systolic and diastolic pressures and the dicrotic notch, which represents closure of the pulmonic valve (figure 5). The PA tracing is similar in appearance to the systemic arterial pressure tracing, except that the PA pressures are normally much lower. Detailed discussion of normal PA waveforms is provided separately. (See "Cardiac catheterization techniques: Normal hemodynamics", section on 'Pulmonary artery'.)

Pulmonary artery occlusion pressure (PAOP) — The pulmonary artery occlusion pressure (PAOP; pulmonary capillary wedge pressure [PCWP] or pulmonary artery wedge pressure [PAWP]) estimates the left atrial pressure. It is best measured with the patient in the supine position, at the end of expiration with the tip of the catheter in zone 3 of the lung. Ideally, the value is measured at least three times and the mean is calculated.

The PAOP tracing is obtained by inflating the balloon at the distal tip of the catheter. The balloon obstructs blood flow through a branch of the pulmonary artery. This creates a static column of blood between the catheter tip and the left atrium. Pressure at both ends of the column equilibrates, after which the pressure at the distal end of the catheter is equal to the pressure of the left atrium [4]. Thus, PAOP is a reflection of left atrial pressure. Normal wedge pressures vary from 6 to 15 mmHg, with a mean of 9 mmHg (table 2).

Importantly, the PAOP usually estimates the left ventricular end-diastolic pressure (ie, left ventricular preload) if there is no obstruction to flow between the left atrium and left ventricle and the compliance of the left ventricle is normal. Importantly, it does not directly measure the left ventricular end-diastolic volume, capillary hydrostatic pressure, or transmural pressures [5-10]. Thus, the PAOP may not reliably indicate left ventricular preload when compliance of the left ventricle is abnormal (eg, large myocardial infarction or in cardiac tamponade). (See 'Discordant PAOP and LV end-diastolic pressure' below.)

The technique required to measure an accurate PAOP is discussed separately. (See "Pulmonary artery catheters: Insertion technique in adults", section on 'Identifying the pulmonary occlusion pressure' and "Pulmonary artery catheters: Insertion technique in adults", section on 'Final wedge position'.)

Abnormal PAOP — Any condition that raises left ventricular end diastolic pressure results in an elevated occlusion pressure including the following:

●Left ventricular systolic heart failure

●Left ventricular diastolic heart failure

●Mitral and aortic valve disease

●Hypertrophic cardiomyopathy

●Hypervolemia

●Large right-to-left shunts

●Cardiac tamponade, constrictive and restrictive cardiomyopathies

Conditions that cause a low wedge pressure include:

●Hypovolemia (eg, hemorrhagic shock, severe intravascular volume depletion)

●Pulmonary venoocclusive disease (variably normal or low)

●Obstructive shock due to large pulmonary embolism

Abnormal PAOP waveforms — Physiologically, the PAOP tracing has similar components to the right atrial waveform with three positive and two negative deflections (figure 6):

●The a wave reflects contraction in atrial systole, while the x descent reflects the fall in left atrial pressure that follows.

●The c wave, reflecting the closure of the mitral valve, is often not seen.

●The v wave represents both ventricular systole and passive atrial filling in atrial diastole.

●The y descent reflects the fall in left atrial pressure following opening of the mitral valve and the initiation of passive filling of the left ventricle.

Electrocardiographic (ECG) correlation is required for correct identification of these events. The PAOP waveform is delayed by >120 ms when compared with the ECG waveform due to the time necessary for left atrial pressure to be transmitted through the pulmonary vasculature to the distal tip of the catheter. Additional discussion of normal PAOP waveforms is provided separately. (See "Cardiac catheterization techniques: Normal hemodynamics", section on 'Right atrium'.)

Abnormal PAOP waveforms include:

●Large a waves – Increased amplitude of the a wave in the PAOP tracing can be seen with increased resistance to left ventricular filling of any cause. Potential causes include:

•Mitral stenosis

•Left ventricular systolic dysfunction

•Left ventricular diastolic dysfunction

•Left ventricular volume overload

•Myocardial ischemia or infarction with decreased left ventricular compliance

●Large v waves – Increased amplitude of the v wave in the PAOP tracing may represent mitral regurgitation (MR) (waveform 3). However, an enlarged v wave is not specific for the diagnosis of MR [11]. As an example, an acute increase in volume to the left atrium (eg, an acute ventricular septal defect complicating myocardial infarction) can also increase the amplitude of the v wave. In contrast, the presence of a normal v wave is specific for the absence of moderate to severe MR [11].

Sources of error

Incomplete pulmonary artery occlusion — The PAOP is only reflective of left atrial pressure if the inflated catheter balloon is fully occlusive. If the balloon is not fully occlusive, the reading will partially reflect the pulmonary artery pressure and will overestimate the PAOP. This can occur despite confirmation of PAOP occlusion by hemodynamic waveform and fluoroscopy. When accurate PAOP measurement is necessary to diagnose pre- versus post-capillary pulmonary hypertension, the addition of checking an occlusion oxygen saturation can improve accuracy. When the balloon is inflated, an oxygen saturation is measured and if it is >90 percent or within 5 percent of systemic saturation, the PAOP is recorded. If the PAOP saturation is not near systemic saturation, the occlusion should be reattempted [12,13].

Discordant PAOP and LV end-diastolic pressure — There are several situations in which the PAOP and left ventricular end-diastolic pressure (LVEDP) are discordant [14,15]. Examples are listed in the table (table 4) and include the following:

●Decreased left ventricular compliance may cause LVEDP to be transiently higher than the PAOP (due to premature mitral valve closure) [9]. Causes of decreased left ventricular compliance include diastolic dysfunction, positive pressure ventilation, myocardial ischemia or infarction, and cardiac tamponade.

●Severe aortic insufficiency may also cause the LVEDP to be greater than the PAOP, due to premature closure of the mitral valve with regurgitant ventricular filling.

●Pulmonary disease and respiratory failure may cause the PAOP to exceed the LVEDP due to constriction of small veins in hypoxic lung segments.

Lung zone misplacement — The lungs can be divided into three physiologic zones of blood flow. These zones are based upon the alveolar pressure, mean pulmonary artery pressure, and pulmonary capillary pressure (figure 7) [16]. The tip of the catheter should ideally be positioned in zone 3 (ie, below the level of the left atrium), such that PAOP will be overestimated if placed in zone 1 or 2.

●Zone 1 is the least dependent zone. In this zone, the mean alveolar pressure exceeds the mean arterial pressure, which exceeds the mean pulmonary capillary pressure (P_A>P_a>P_c).

●Zone 2 is the middle zone. In this zone, the mean arterial pressure exceeds the mean alveolar pressure, which exceeds the mean pulmonary capillary pressure (P_a>P_A>P_c).

●Zone 3 is the most dependent zone. In this zone, the mean arterial pressure exceeds the mean pulmonary capillary pressure, which exceeds the alveolar pressure (P_a>P_c>P_A).

In general, the PAOP contour has a and v waves in zone 3; these are smoothed out in zones 1 and 2. PA diastolic pressure is greater than PAOP in zone 3, but PAOP is greater than PA diastolic pressure in zones 1 and 2.

Correct placement only occurs in approximately 30 percent of catheter insertions [6]. Indicators that the catheter has been placed into a zone other than zone 3 include an abnormal position on the lateral chest radiograph (rarely performed in the intensive care unit), marked respiratory variation in the PAOP tracing, and an increase in the PAOP due to positive end-expiratory pressure that exceeds 50 percent of the amount of applied positive end-expiratory pressure. (See 'Positive end-expiratory pressure' below.)

Respiratory effects — Regardless of the mode of ventilation, PAOP should be measured at end-expiration to avoid the effects of respiration on PAOP measurements. Intrathoracic pressure (ie, alveolar and pleural pressure) changes with the respiratory cycle; it exerts pressure on the intravascular space within the lung, and consequently, affects PAOP, in a way that is dynamic throughout the respiratory cycle. Thus, during spontaneous breathing, pleural and alveolar pressures (relative to atmospheric pressure) decrease during inspiration and increase during expiration to similarly affect the PAOP. Conversely, during positive pressure ventilation, pleural and alveolar pressure increase during inspiration and decrease during expiration. However, at end-expiration, all intrathoracic pressures are equal to atmospheric pressure which allows the PAOP to be accurately measured regardless of whether the patient is spontaneously breathing or mechanically ventilated.

In the past, many ICU monitors measured PAOP by manually moving a cursor to end-expiration on the peak component of the pressure waveform which introduced error. However, many intensive care and cardiac catheterization units now use electronic pressure monitors that are designed to measure pressure in time intervals of four seconds and to display three different pressures: the systolic (peak), diastolic (trough), and mean pressure. The PAOP pressure can be followed serially on such monitors and measured at end expiration by selecting the systolic (peak) pressure for those breathing spontaneously (with positive intrathoracic pressure at end-expiration) and the diastolic pressure (trough) for those who are receiving positive pressure ventilation (with the intrathoracic positive pressure nadir at end-expiration) (figure 8). This approach avoids false depression or elevation of intravascular pressure measurements due to fluctuations in pressure during respiration.

Positive end-expiratory pressure — Positive end-expiratory pressure (PEEP) prevents alveolar pressure from returning to atmospheric pressure at end-expiration. The effects of PEEP on the PAOP are variable and depend largely upon the compliance of the lung, regardless of whether the PEEP was applied therapeutically (ie, applied or extrinsic PEEP) or the result of incomplete expiration and air trapping (ie, auto-PEEP or intrinsic PEEP).

However, in general, most experts consider the effects of PEEP as being clinically insignificant for the following reasons:

●If the catheter is properly positioned in zone 3, the airway pressure should not be transmitted to the vasculature. Respiratory variation of the PAOP waveform that is greater than respiratory variation of the pulmonary artery pressure waveform suggests that the catheter may not be in zone 3 and, therefore, the PAOP may be unreliable and should be repositioned (figure 8) [17].

●The PAOP is the effective left atrial and ventricular filling pressure (ie, the intravascular pressure necessary to filling the left heart) that theoretically should not be affected by PEEP with a properly positioned catheter tip under zone 3 conditions. (See 'Lung zone misplacement' above.)

If excessive PEEP is a concern, PAOP can be estimated by subtracting one-half of the PEEP level from the PAOP if lung compliance is normal, or one-quarter of the PEEP level if lung compliance is reduced [17]. As an example, for a patient with acute respiratory distress syndrome (decreased lung compliance) who is receiving an applied PEEP of 10 cm H₂O and has a PAOP of 12 mmHg, the recalculated PAOP would be 9.5 mmHg. This small difference indicates that the effects of PEEP on PAOP are usually small and, therefore, unlikely to affect clinical management. (See "Clinical and physiologic complications of mechanical ventilation: Overview", section on 'Falsely elevated hemodynamic measurements'.)

Even though PEEP affects intravascular pressure measurements, it is not advisable to eliminate (ie, turn off) PEEP temporarily while pressure measurements are being made. Doing so may reduce the benefits of PEEP and induce hemodynamic instability due to changes in venous return and the arterial oxygen tension (PaO₂). It also will not accurately reflect the patient's hemodynamic status when PEEP is being used. (See "Positive end-expiratory pressure (PEEP)".)

CALCULATION OF CARDIAC OUTPUT — The pulmonary artery catheter (PAC) measures the cardiac output (CO) via either the indicator thermodilution method or the Fick method. The preferred expression of CO is the cardiac index [CI], which is calculated by dividing the CO by the body surface area. Normal hemodynamic measures for CI are 2.8 to 4.2 L/min/m² (table 2). The causes of a low cardiac output include systolic and diastolic heart failure, but also include severe forms of mitral valve regurgitation, hypovolemia, pulmonary hypertension, and right ventricular failure. Distinguishing these pathologies from one another depends upon presenting clinical and echocardiographic features and well as specific patterns of physiologic variables seen on the PAC (table 5 and table 3).

The cardiac output can be elevated physiologically (eg, exercise, fever, anxiety, pregnancy). In addition, a high cardiac output with or without heart failure can also be seen in a number of conditions, many of which are uncommon (see "Causes and pathophysiology of high-output heart failure"):

●Systemic arteriovenous fistulas

●Hyperthyroidism

●Anemia, including the anemia of chronic kidney disease

●Beriberi (vitamin B1 or thiamine deficiency)

●Dermatologic disorders (eg, psoriasis)

●Renal disease

●Hepatic disease

●Skeletal disorders (eg, Paget disease, multiple myeloma)

●Sepsis

Indicator thermodilution method — The indicator thermodilution principle predicts that, when an indicator substance is added to a stream of flowing blood, the blood flow rate will be inversely proportional to the mean concentration of the indicator at a downstream site. In the case of thermodilution, the indicator is approximately 5 mL of either dextrose or saline that is cooler than blood. It is injected as a bolus through the proximal port of the PAC, where it mixes with blood in the right ventricle. The mixing lowers the temperature of intraventricular blood. As the blood flows past the distal thermistor port located in the tip of the catheter in the pulmonary artery, the thermistor records the temperature change over time and can electronically display a temperature-time curve. The area under this curve is inversely proportional to the flow rate in the pulmonary artery, which is determined by the cardiac output of the left ventricle. This flow rate is considered an estimate of cardiac output, assuming that there is no intracardiac shunt.

The thermodilution method has been well-validated, as compared with the calculation of cardiac output using the Fick method. However, there are several important sources of error of which clinicians should be aware:

●Tricuspid regurgitation leads to an underestimation of CO. This is a consequence of the cold injectate refluxing back into the vena cava, with resultant decreased pulmonary artery cooling (attenuated peak) and delayed appearance of injectate that has moved retrograde into the vena cava and is then recirculated (prolonged washout).

●Right-to-left and left-to-right intracardiac shunts can produce falsely elevated cardiac output measurements by the thermodilution technique. Right-to-left intracardiac shunts produce shunting of cold injectate into the left heart, which reduces pulmonary artery cooling, attenuates the peak of the temperature-time curve, and overestimates cardiac output. Left-to-right intracardiac shunts produce increased right heart volumes and dilution of the injectate, which attenuates the height of the temperature-time curve and results in an overestimation of CO.

Continuous thermodilution catheters are available and correlate well with bolus thermodilution methods [18]. Other catheter designs incorporate continuous oximetric monitoring of pulmonary artery oxygen saturation using fiberoptic reflectance spectrophotometry, thereby enabling continuous estimation of CO. This technology has been shown to have acceptable correlation with mixed venous oxygen saturation determined using co-oximetry [19]. However, these catheters are more expensive and did not result in improved patient outcomes in a multicenter observational study of over 3200 patients undergoing cardiac surgery [20].

Fick method — The Fick method of calculating the cardiac output requires oxygen saturation measurement in the pulmonary artery and arterial system, and is shown in the figure (figure 9) (calculator 1):

Oxygen consumption is either measured by exhaled breath analysis or estimated from a nomogram that is based upon age, sex, height, and weight. The arteriovenous oxygen difference requires additional calculations:

The hemoglobin concentration and arterial oxygen saturation are measured, while the mixed venous oxygen saturation is calculated as described in the next section.

DETECTION OF LEFT-TO-RIGHT SHUNTS — Blood sampling from the right atrium (RA), right ventricle (RV), pulmonary artery (PA), superior vena cava (SVC), and inferior vena cava (IVC) is helpful when evaluating a suspected left-to-right intracardiac shunt (eg, from atrial septal defects, ventricular septal defects). Sampling is typically performed during insertion of the catheter under fluoroscopic guidance to ensure that samples are drawn from the proper sites. Detection of an oxygen saturation "step-up" allows confirmation of the shunt and determination of its location [21,22]. A step-up is defined as >10 percent rise in oxygen saturation, when the saturation of blood in the RA, RV, or PA is compared to the calculated mixed venous oxygen saturation (taken from the SVC and IVC).

The mixed venous oxygen saturation is calculated as follows:

●In a patient at rest: [(3 x SVC oxygen saturation) + (IVC oxygen saturation)] / 4 [23].

●In an exercising patient: [(2 x IVC oxygen saturation) + (SVC oxygen saturation)] / 3 [23].

The site of the step-up defines the level of the shunt. The degree of left-to-right shunting can then be quantitated by calculating a ratio of pulmonary flow (Qp) to systemic flow (Qs) (figure 10).

The diagnosis and interpretation of left-to-right shunt measurements are discussed separately. (See "Clinical manifestations and diagnosis of ventricular septal defect in adults", section on 'Cardiac catheterization' and "Clinical manifestations and diagnosis of atrial septal defects in adults" and "Clinical manifestations and diagnosis of atrial septal defects in adults", section on 'Approach to diagnosis and evaluation'.)

SYSTEMIC AND PULMONARY VASCULAR RESISTANCE — Once the cardiac output has been determined, the systemic vascular resistance and pulmonary vascular resistance can be estimated (figure 11) (calculator 2). The estimation is based upon Ohm's Law, which states that the resistance in a circuit is equal to the pressure drop across the circuit divided by flow:

●Systemic vascular resistance is the difference between the mean arterial pressure and the right atrial pressure divided by the cardiac output and then multiplied by 80.

●Pulmonary vascular resistance is the difference between the mean pulmonary artery pressure and the left atrial pressure, divided by the cardiac output, and then multiplied by 80 (calculator 2).

Since the calculations of vascular resistance are based upon direct measurements (ie, pressures) and indirect measurements (ie, cardiac output), each of which has its own intrinsic sources of error, vascular resistance values are the least accurate of all the values obtained from the pulmonary artery catheter. They are also the most sensitive to minor inaccuracies in data acquisition. Nonetheless, systemic vascular resistance (SVR) can provide valuable information when distinguishing the classes of shock from each other (table 5) and pulmonary vascular resistance (PVR) is often useful when determining the prognosis of patients with pulmonary hypertension. (See "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock", section on 'Differential diagnosis' and "Treatment and prognosis of pulmonary arterial hypertension in adults (group 1)".)

SUMMARY AND RECOMMENDATIONS

●Ensuring accurate measurements – Certain steps must be performed before a pulmonary artery catheter (PAC; also called a Swan-Ganz or right heart catheter) is used to measure hemodynamic variables. The steps include zeroing, referencing, ensuring the catheter is in the correct position, and assessing the dynamic response using the "fast-flush" test. (See 'Ensuring accurate measurements' above.)

●Catheter waveforms and pressure – A PAC can obtain pressure waveforms from several locations, including the following:

•Right atrium – Normal right atrial (RA) pressures range from 0 to 7 mmHg (table 2). Elevated RA pressures can be caused by several conditions including diseases of the right ventricle, pulmonary hypertension, pulmonic stenosis, left-to-right shunts, tricuspid valvular disease, cardiac tamponade, constrictive and restrictive cardiomyopathies, left ventricle systolic heart failure, and hypervolemia. Differentiating among the etiologies depends upon clinical, radiographic, and echocardiographic features as well as additional supportive readings or waveforms measured on PAC (table 3). (See 'Right atrium (RA)' above.)

•Right ventricle – Normal right ventricular (RV) systolic pressure ranges from 15 to 25 mmHg and normal RV end-diastolic pressure ranges from 3 to 12 mmHg (table 2). As a general rule, elevations in RV pressure are associated with diseases that elevate the pulmonary artery pressure, pulmonic valve disorders, and diseases that primarily affect the right ventricle. Severe elevations in RV pressure are generally associated with chronic conditions (eg, idiopathic pulmonary arterial hypertension) while acute conditions rarely raise the RV systolic pressure above 40 mmHg (eg, acute pulmonary embolism). (See 'Right ventricle' above.)

•Pulmonary artery – Normal pulmonary artery (PA) systolic pressures range from 15 to 25 mmHg, while PA diastolic pressures range from 8 to 15 mmHg; the mean PA pressure (mPAp) is typically 16 mmHg (10 to 22 mmHg) (table 2). The mean PA pressure can be elevated (eg, mPAp, >22 mmHg) by acute conditions (eg, venous thromboembolism or hypoxemic-induced pulmonary vasoconstriction) or acute-on-chronic conditions (eg, hypoxemic-induced vasoconstriction in a patient with underlying chronic cardiopulmonary disease). Additionally, chronic conditions including idiopathic pulmonary hypertension and pulmonary hypertension [PH] due to left heart disease, chronic lung disease, chronic thromboembolism, and other miscellaneous causes can elevate the PA pressure; when the mPAp is ≥20 mmHg, this is known as pulmonary arterial hypertension. (See 'Pulmonary artery' above and "Clinical features and diagnosis of pulmonary hypertension of unclear etiology in adults" and "Clinical features and diagnosis of pulmonary hypertension of unclear etiology in adults", section on 'Postdiagnostic testing and classification'.)

•Pulmonary artery occlusion pressure – The PAC can measure the pulmonary artery occlusion pressure (PAOP; pulmonary capillary wedge pressure [PCWP]; pulmonary artery occlusion pressure). PAOP is best measured with the patient in the supine position, at the end of expiration with the tip of the catheter in zone 3 of the lung (ie, region of lung below left atrium). Any condition that raises left ventricular end-diastolic pressure results in an elevated wedge pressure including left ventricular systolic heart failure, left ventricular diastolic heart failure, mitral and aortic valve disease, hypertrophic cardiomyopathy; hypervolemia, right-to-left shunts, cardiac tamponade, and constrictive and restrictive cardiomyopathies. (See 'Catheter waveforms and pressures' above and 'Pulmonary artery occlusion pressure (PAOP)' above.)

●Cardiac output – The PAC measures the cardiac output (CO) via either the indicator thermodilution method or the Fick method. The preferred expression of CO is the cardiac index [CI], which is calculated by dividing the CO by the body surface area. Normal hemodynamic measures for CI are 2.8 to 4.2 L/min/m² (table 2). The causes of a low cardiac output include systolic and diastolic heart failure, but also include severe forms of mitral valve regurgitation, hypovolemia, pulmonary hypertension, and right ventricular failure. Distinguishing these pathologies from one another depends upon presenting clinical and echocardiographic features and well as specific patterns of physiologic variables seen on the PAC (table 5 and table 3). (See 'Calculation of cardiac output' above.)

●Shunt detection – Detection of an oxygen saturation "step-up" on PAC allows confirmation of a suspected left-to-right shunt and determination of its location by measuring oxygen saturation from the RA, RV, PA, superior vena cava (SVC) and inferior vena cava (IVC). A step-up is defined as >10 percent rise in oxygen saturation, when the saturation of blood in the RA, RV, or PA is compared to the calculated mixed venous oxygen saturation (taken from the SVC and IVC). (See 'Detection of left-to-right shunts' above and "Clinical manifestations and diagnosis of atrial septal defects in adults", section on 'Approach to diagnosis and evaluation'.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Frank Silvestry, MD, who contributed to earlier versions of this topic review.