Hemodynamic Monitoring

Hemodynamic Monitoring

Elizabeth J. Bridges

Cardiovascular support of critically ill patients requires noninvasive and invasive monitoring of physiological indicators of cardiovascular function, including factors that affect cardiac performance (preload, afterload, contractility, and heart rate [HR]) and the balance between O2 supply and demand. This chapter reviews technologies for hemodynamic monitoring (arterial blood pressure (BP) monitoring, central venous pressure (CVP)/pulmonary artery (PA) catheterization, and cardiac output (CO) and S[v with bar above]O2 monitoring) and discusses the current recommendations for the effective use of hemodynamic monitoring in optimizing patient outcomes. Newer techniques such as central venous oxygenation saturation (ScvO2) and functional hemodynamic monitoring and new technologies such as transpulmonary indicator dilution (TPID) CO, pulse contour analysis, transesophageal Doppler, partial CO2 rebreathing, and microcirculation and tissue oxygenation monitoring techniques are introduced.



Pressure in blood vessels has three components: dynamic BP (i.e., the BP generated by the heart), hydrostatic pressure (related to fluid density, gravitational acceleration, and height of the column of blood between the heart and the vessels), and static pressure (related to the volume of blood in the vascular system at zero flow).1 The BP is the same at all points along a horizontal level. However, pressure at different vertical levels reflects not only the dynamic pressure but also the hydrostatic pressure.

Referencing, which is performed to correct for the change in hydrostatic pressure in vessels above and below the heart, is accomplished by placing the air-fluid interface (stopcock) of the catheter system at the level of the heart to negate the weight effect of the catheter tubing. All invasive cardiovascular pressure-monitoring systems (PA, CVP, and arterial) are referenced to the heart, not to the catheter tip or the site of insertion.1, 2, 3

The phlebostatic axis and phlebostatic level are the most commonly used reference points for the mid-right atrium (RA) and left atrium (LA) (Fig. 21-1).4,5 As the patient moves from the flat to the backrest elevated position, the phlebostatic level rotates on the axis and remains horizontal (Fig. 21-2). In patients with normal chest wall configuration, the midaxillary line (MAL) is a valid reference level for the RA and the LA; however, use of the MAL in patients with varied chest configuration may result in a pressure difference of up to 6 mm Hg.6

Although the phlebostatic axis is the most commonly cited reference level, other reference levels have been suggested. For CVP measurements Magder suggests using a reference point 5 cm below the angle of the sternum, as this point reflects mid-RA, which remains the same up to a backrest elevation of 60 degrees. Use of this reference, which is also the same reference recommended for the evaluation of jugular venous distention, gives a CVP measurement that is 3 mm Hg lower than a measurement from a system referenced to the phlebostatic axis.7,8 There is no general consensus on which reference is most accurate; however, these studies highlight the importance of using a standardized reference and also interpreting the absolute pressure measurements relative to the different reference levels.

Previous research on the effect of position on hemodynamic pressure measurements has been limited by the use of incorrect reference points. In many of these studies, attainment of accurate PA pressures was not possible because the use of a reference point above or below the LA resulted in the inclusion of hydrostatic pressure component; thus, the measured pressures were underestimated or overestimated.9 For every 1 cm the reference point is above the LA; the measured pressure decreases by 0.73 mm Hg. Conversely, for every 1 cm the reference point is below the LA, the measured pressure increases by 0.73 mm Hg. The position-specific reference points are summarized in Display 21-1. In the lateral position, reference points have been validated for the 30- and 90-degree lateral positions with a 0-degree backrest elevation. Further study of the lateral position with varying degrees of backrest elevation is needed. In studies performed to evaluate the effects of prone position on hemodynamic indices, the MAL or the midanteroposterior diameter of the chest have been used as the reference point.15, 16, 17, 18, 19, 20, 21

Zeroing Versus Referencing

Zeroing is performed by opening the system to air to establish atmospheric pressure as zero, although changes in barometric pressure have minimal effect on measured pressure.22 In addition, zeroing is performed to compensate for offset caused by hydrostatic pressure or offset in the pressure transducer, amplifier, oscilloscope, recorder, or digital delays. The act of simultaneously zeroing and referencing ensures that intracardiac pressures are being measured (Display 21-2).

Infection Control

Catheter-related infection remains the leading cause of nosocomial infections, particularly in critical care and are associated with increased length of hospital stay and resource use.24 In a study of 1,140 central venous and 1,038 arterial catheters, both in situ for an average of 9.5 days, the catheter-related blood stream infection (CR-BSI) incidence was 4.6% and 3.7%, respectively.25 A systematic review of 200 studies found a CR-BSI incidence for nonmedicated central catheters of 2.9/1,000 catheter days (95% cardiac index [CI] = 2.6 to 3.2) and 1.4/1,000 catheter days (95% CI = 0.8 to 2.0) for peripheral arterial lines.26

Evidence-based guidelines exist for the prevention of CR-BSI (Table 21-1).42,43 In 2006, the results of the effect of an evidence-based bundle of the procedures aimed at decreasing CR-BSI was published.44 Use of this bundle, which includes hand washing, using full-barrier precautions during the insertion of central venous catheters, cleaning the skin with chlorhexidine, avoiding the femoral site if possible, and removing unnecessary catheters along with staff education and empowerment and the use of champions, significantly decreased the incidence of CR-BSI from 2.7/1,000 catheter days to 1.4/1,000 catheter days 18 months after the intervention.44,45 Other studies that emphasize the effect of staff education, multifaceted interventions, and performance feedback have also led to a significant decrease in CR-BSI.31,46,47 Despite the risk for CR-BSI from arterial lines there are only limited recommendations for arterial line insertion and care, and consideration should be given to using the Centers for Disease Control and Prevention (CDC) recommendations and procedure bundle for central lines for arterial line maintenance.28,48, 49, 50

Figure 21-1 Magnetic resonance image of a 43-year-old man. White cross marks the phlebostatic axis. (Reproduced from McGee, S. R. [1998]. Physical examination of venous pressure. American Heart Journal, 136[1], 10-18.)

Figure 21-2 The phlebostatic axis and the phlebostatic level. (A) The phlebostatic axis is the intersection of two reference lines: first, an imaginary line from the fourth ICS at the point where it joins the sternum, drawn out to the side of the body; second, a line drawn midway between the anterior and posterior surfaces of the chest. (B) The phlebostatic level is a horizontal line through the phlebostatic axis. The air-fluid interface of the stopcock of the transducer must be level with this axis for accurate measurements. Moving from the flat to erect positions, the patient moves the chest and therefore the reference level; the phlebostatic level stays horizontal through the same reference point. (Adapted from Shinn, J. A., Woods, S. L., Huseby, J. S. [1979]. Effect of intermittent positive pressure ventilation upon pulmonary capillary wedge pressures in acutely ill patients. Heart & Lung, 8, 324.) (C) Two methods for referencing the pressure system to the phlebostatic axis. The system can be referenced by placing the air-fluid interface of either the in-line stopcock or the stopcock on top of the transducer at the phlebostatic level. (From Bridges, E. J., & Woods, S. L. [1993]. Pulmonary artery pressure measurement: State of the art. Heart & Lung, 22, 101.)

Dynamic Response Characteristics

The dynamic response characteristics of the catheter-transducer system reflect the system’s ability to faithfully reproduce a pressure waveform. The dynamic response can be determined by evaluating the system’s damping coefficient and natural (resonant) frequency (Fig. 21-3). The damping coefficient is a measure of how quickly the system dampens and eventually arrests the oscillations. A certain degree of damping is desirable for optimal fidelity and suppression of unwanted high-frequency vibration or noise. The natural frequency (Fn) refers to the frequency at which the system oscillates when shock excited.51 As seen in Figure 21-4, the higher the Fn, the greater the range of acceptable damping. The Fn can be quickly assessed by measuring the horizontal distance between the points of two oscillations (each small box equals 1 mm) and dividing the paper speed (25 mm/s) by this value. For example, if there are two small boxes between oscillations, then the Fn = 25/2 = 12.5 Hz, which is marginally acceptable. Optimizing the Fn has the greatest effect on the reproduction of a waveform. The Fn of the catheter-transducer system decreases over time,52 indicating the need to routinely evaluate the dynamic response characteristics of the system.

An underdamped system results in falsely high systolic (15 to 30 mm Hg) and low diastolic pressures. An overdamped system loses its characteristic landmarks, and the waveform appears unnaturally smooth with a diminished or absent dicrotic notch. An overdamped system causes falsely low systolic and high diastolic pressure readings. PA catheters have a decreased Fn compared with arterial pressure lines52; thus, taking steps to optimize the system is imperative. The simpler the system (e.g., shorter tubing and fewer stopcocks) the better its ability to reproduce faithfully the pressure waveforms.23,51,53 Use of in-line blood conservation devices decrease the Fn of the system, resulting in an underdamped system.54

Table 21-1 ▪ CR-BSI CONTROL



Skin antisepsis

  • Skin antisepsis with a 2% chlorhexidene preparation is superior to 10% povidone-iodine or 70% alcohol in preventing catheter colonization27

Insertion technique

  • Central venous catheter: maximum sterile technique for insertion (cap, mask, sterile gloves, sterile gown, large sterile drapes)

  • Arterial line (not specifically addressed): technique similar to short-term central venous catheter

Hand hygiene

  • Perform hand hygiene before and after manipulating catheters/catheter site

  • Use of gloves does not obviate the need for good hand washing

Location of insertion site

  • Higher BSI rates associated with internal jugular or femoral vain insertion site compared to subclavian vein insertion site; avoid lower extremity if possible

  • Higher contamination and BSI incidence with femoral artery insertion site compared with radial artery insertion site28, 29, 30

  • Increased BSI with reinsertion over a guidewire at old insertion site

Antimicrobial catheters

  • Antibiotic-impregnated catheters (minocyclin/rifampicin) decrease the risk of CR-BSIs compared with standard catheters and chlorhexidene/silver sulfadiazine catheters31, 32, 33, 34

  • Catheters coated with chlorhexidene/silver sulfadiazine and heparin bonding may decrease the risk of CR-BSI31,40, 41, 42

  • Consider use of antimicrobial catheters if catheter is to remain in place >5 days and current hospital BSI rate exceeds 2%35 or NNIS standards

Catheter sleeve (PA catheter)

  • Use sterile sleeve during PA catheter insertion

Frequency of catheter change

  • Routine catheter replacement is not recommended36

  • Change PA catheters no more frequently than every 7 days37

  • Arterial line (manage similar to short-term central venous catheters)—no specific CDC recommendations for catheters that need to be in place >5 days.

  • Risk for colonization increases wither greater than 4 days in situ;28,29 however, there are no studies suggesting a need for routine catheter replacement for infection control prevention

  • Evaluate daily the patients need for central and arterial catheters


  • Use sterile gauze or sterile, transparent semipermeable membrane dressing

  • Change gauze dressing every 2 days and transparent dressing at least every 7 days, when the dressing becomes, damp, loose, or soiled or for site inspection

Flush solution

  • Do not administer dextrose-containing solutions through the pressure monitoring system

Administration set

  • Continuous-flush device

  • Replace pressure transducers and all tubing and flush solution every 96 hours

Obtaining cultures from central venous and arterial catheters

  • Drawing cultures from only one lumen of a multilumen catheter has a 60% chance of detecting significant colonization. If only one lumen is sampled a negative culture does not necessarily rule out the CVC as a source of infection.38 Colonization of the medial lumen is an independent risk factor for CR-BSI39

  • Cultures obtained through a central venous or arterial catheter have a lower positive predictive value and similar or better negative predictive values compared with peripheral cultures, which indicates that additional cases of bacteremia may be identified from the catheter culture in addition to peripheral cultures40,41

CDC, Centers for Disease Control and Prevention; NNIS, National Nosocomial Infections Surveillance System

Blood Drawing From Arterial and Central Venous Catheters

Arterial blood gases, serum electrolytes, and coagulation studies can be drawn from an arterial line. To avoid contamination of the specimen with saline and/or heparin, two times the deadspace volume (volume from the catheter tip to the aspiration site) or two times the deadspace plus 2 mL (approximately equivalent to six times the deadspace) should be withdrawn for arterial blood gases and electrolytes.56 For coagulation studies (e.g., PT/aPTT), the discard volume should be four to six times the deadspace volume.57,58 If an in-line blood conservation set is used, caution must be exercised to ensure that an adequate discard volume is obtained.59 If heparin is used in the flush solution and the coagulation results are abnormal, consideration should be given to using a venipuncture specimen to confirm the results.

Serum sodium and glucose can be obtained from the infusion port of the PA catheter if the dwell volume plus 2 mL of additional blood is discarded.60 No published research was found regarding measurement of potassium or other electrolytes from PA catheters; however, in a study of central venous lines it was found that a discard volume of 3 mL (corresponding to six times the catheter deadspace) was sufficient after initially flushing the line with 5 mL of saline.61 Coagulation studies (Activated clotting time [ACT]) drawn from heparin-bonded PA catheters,62 and the introducer side-port when the PA catheter is present63 are significantly increased compared with specimens obtained from an arterial catheter although baseline specimens can be obtained from the introducer before placement of the PA catheter.64



Intra-arterial monitoring is indicated when precise and continuous monitoring is required. Examples of clinical conditions warranting direct arterial pressure monitoring include acute hypertensive crises, hypotension, any shock state, frequent drawing of arterial blood samples, monitoring of vasoactive pharmacologic support, and during aggressive respiratory support (e.g., high positive end-expiratory pressures [PEEP]).

Arterial Catheter Placement

Important considerations in site selection for arterial catheters include patient comfort, avoidance of insertion sites at increased risk for infection, and adequate collateral circulation.65 The most common insertion site is the radial artery due to the presence of collateral circulation, which decreases the risk of vascular complications. The radial and ulnar artery/superficial palmar arteries provide a dual blood supply to the hand. Although the Allen test has traditionally been used to evaluate collateral circulation, recommendations in the literature regarding its use are equivocal.66,67 In addition, the implications of a positive Allen test are equivocal. The positive findings may not be consistent with concurrent Doppler ultrasonography evaluation nor does the presence of an abnormal Allen test reliably predict that the patient will develop hand ischemia after radial artery cannulation. Given this limited diagnostic accuracy, newer technologies including digit pressure measurement and plethysmography and Doppler ultrasonography should be considered, particularly for patients who are at increased risk for complications from the catheterization (e.g., peripheral vascular disease or diabetes, previous extremity surgery or trauma, current anticoagulation or vasopressor therapy, and hypotension).68

Figure 21-3 Dynamic response characteristics. (Adapted with permission from Bridges, E. J., & Middleton, R. [1997]. Direct arterial vs. oscillometric monitoring of blood pressure: Stop comparing and pick one [a decision-making algorithm]. Critical Care Nurse, 17[3], 58-72.)

Figure 21-4 Schema of the cardiopulmonary structures demonstrating the relationship between the LA, PA, and pulmonary vasculature, with a correctly positioned PA catheter. RUL PA, right upper lobe PA; RIL, right interlobar PA; RPA, right PA; LPA, left PA; RV, right ventricle; .

The femoral artery is often an alternative to the radial artery. However, there is an increased risk of infection with the femoral site. The brachial artery is used less frequently because it does not have good collateral circulation, which in theory increases the risk for diffuse distal ischemia. The axillary artery is a less common insertion site, with complication rates similar to radial and femoral insertions. The dorsalis pedis artery is another option. Complication rates associated with the dorsalis pedis artery are comparable to radial artery insertion.69 The dorsalis pedis should not be used if the patient has peripheral vascular disease or an absent posterior tibial pulse. In addition, the dorsalis pedis artery pressures are higher than radial pressures, even in the supine position.70

Complications Related to Arterial Catheterization

The most common complication from arterial cannulation is temporary occlusion of the artery (radial 19.7%; femoral 1.5%), although permanent arterial occlusion is rare (0.09% and 0.18%, respectively).65 Given the risk and potentially severe outcomes from arterial occlusion, distal perfusion (skin color, temperature, and capillary refill) should be routinely assessed postinsertion and any time the system is manipulated.68,71 Bleeding is a rare complication for all insertion sites (0.6% to 1.6%), with increased incidence in femoral and axillary lines.65 A summary of risk factors and actions to prevent complications is presented in Table 21-2.

Arterial Pressure Wave

The contour of the arterial pressure wave is illustrated in Figure 21-5. The initial sharp upstroke reflects the pressure increase during the rapid ejection phase of ventricular systole and a slower rise during later systole. The upstroke of the waveform is referred to as the anacrotic limb, which is followed by a brief, peaked, sustained pressure (anacrotic shoulder). At the end of systole, the pressure falls in the aorta and left ventricle (LV) and the downstroke of the pressure wave corresponds to the decrease in aortic pressure during decreased ventricular ejection and the continued flow of blood into the periphery. The downstroke of the wave is interrupted by a sharp notch or incisura, denoting a transient reversal of blood flow just before aortic valve closure. Pressure in the aorta continues to decrease and is reflected on the arterial pressure waveform as a gradual downslope until the next ventricular systole. The interval after the incisura when the aortic pressure continues to decrease is referred to as the diastolic run-off period, and the slope of this period is affected by arterial stiffness and the rate at which the blood flows into the periphery (vascular resistance).79


Risk Factors

Preventive Actions

  • Catheter >20 gauge

  • Catheter in place >3 days

  • Female

  • Low CO/hypotension

  • Peripheral vascular disease

  • Vasopressor agents

  • Anticoagulation (↓ risk)

  • Femoral (↓ risk)

  • Systemic antithrombotics or anticoagulants (↓ risk)

  • Insertion site (femoral or axillary)

  • Insertion site preparation

  • Catheter in place >5-7 days

  • Insertion site

  • Use of heparinized flush solution to maintain patency is equivocal. Consideration should also be given to risk of heparin-induced thrombocytopenia.72, 73, 74, 75, 76, 77

  • Aspirate clot or discontinue line if thrombosis is suspected

  • Perform routine monitoring of distal perfusion (skin color, temperature and capillary refill) and after line manipulation

  • No beneficial effect from repeated flushes

  • No effect from method of blood sampling (waste versus nonwaste)78

  • Catheter length sheaths/arterial lines (↓ risk)

  • Maintain system integrity

  • Monitor waveform for damping (may indicate loose connections) See Table 21-1

The arterial pressure waveform changes its contour when recorded at different sites along the arterial circuit80 (Fig. 21-6). The pulse pressure and the systolic pressure increase, and the ascending limb of the waveform becomes steeper. In addition, the incisura is gradually replaced by a later diastolic wave (dicrotic notch). The change in amplitude and contour of the arterial waveform is primarily caused by peripheral pulse wave reflection.81
Reflection occurs when flow is impeded (i.e., when low-resistance arteries terminate in high-resistance vessels) and the pressure wave is reflected in a retrograde (backward) fashion. This retrograde pressure wave combines with the antegrade (forward) pressure pulse, and the arterial pressure is augmented.

Figure 21-5 Components of the arterial waveform. The upstroke of the arterial waveform, which begins approximately 0.2 second after the onset of the QRS complex indicates the onset of systole. The dicrotic notch reflects closure of the aortic valve and the onset of diastole.

Figure 21-6 Simultaneous recordings of aortic and radial arterial pressure waves. (From Rowell, L. D., Brengelmann, G. L., Blackmon, R. J. et al. [1968]. Disparities between aortic and peripheral pulse pressures induced by upright exercise and vasomotor changes in man. Circulation, 37, 954-964.)

The timing of the return of the reflected pressure wave from the periphery is important because if the reflected wave arrives during systole it increases LV workload.82,83 In young individuals, the reflected waves arrive at the heart after closure of the aortic valves, which beneficially augments the diastolic blood pressure (DBP) and thus coronary perfusion. However, with aging or increased stiffness of the arteries (i.e., hypertension), the retrograde pulse wave arrives back at the heart during systole, which increases the systolic blood pressure (SBP).82,83

Recognition of central aortic systolic pressure augmentation is important in evaluating the effects of various vasodilator agents. Nitroglycerin and nitroprusside substantially decrease aortic pressure without a clinically measurable change in brachial pressure.84,85 This effect, which is the result of the reduction in pulse-wave reflection (Fig. 21-7), may explain why a patient may “look better” after the initiation of vasodilator therapy even though there has been no marked decrease in peripheral BP or preload. Conversely, vasoconstrictive agents (e.g., norepinephrine) increase peripheral pulse pressure and central aortic pressure, with femoral pressure higher than radial pressure.86,87

Figure 21-7 Pressure wave recorded directly in a central and peripheral artery. Nitroglycerine 0.3 mg (SL) on average caused a fall of 11 mm Hg in aortic systolic pressure more than the decrease in the brachial systolic pressure. Note the effect on the reflected (R) wave. (From Kelly, R. P., Gibbs, H. H., O’Rourke, M. F., et al. [1990]. Nitroglycerine has more favourable effects on left ventricular afterload than apparent from measurement of pressure in a peripheral artery. European Heart Journal, 11, 138-144.)

Interpretation of Arterial Pressure Data

The mean arterial pressure (MAP), which represents the average pressure through a cardiac cycle, is affected by the CO and systemic vascular resistance (SVR) as described by the following equation:


Recall of the factors that affect SBP, DBP, and MAPs is important when assessing changes in BP. The SBP is affected by left ventricular stroke volume (SV), peak rate of ejection, and distensibility of the vessel walls. The DBP is primarily affected by arterial peripheral resistance. The pulse pressure, which is the difference between systolic and diastolic pressures, is determined by SV, peak rate of ventricular ejection, and the distensibility of the arterial walls.

On average, more central SBP (aortic, femoral, or brachial) is lower than radial SBP by 7 to 14 mm Hg and central DBP similar to or higher than radial DBP by 1 to 9 mm Hg, while the MAP is unchanged and may be a more consistent value to evaluate and guide therapy.88, 89, 90 The SBP differences change with aging (radial SBP ≈ aortic SBP),91,92 vasoconstriction (radial < brachial and femoral),86,87 vasodilation (femoral ≈ radial; aortic ≤ radial),93,94 and exercise (peripheral SBP may be as much as80 mm Hg higher than central aortic pressure).80 Both peripheral wave reflection and the end-pressure product, which is the result of the conversion of kinetic energy from flowing blood into pressure as the blood strikes the upstream-looking arterial catheter, cause augmentation of the peripheral SBP.95 Regardless of the source or site of BP measurement, a key point is that BP and perfusion are not synonymous, and a higher BP does not necessarily translate to higher perfusion.96

Direct Arterial Versus Cuff Pressure

There is no basis for the practice of comparing the intra-arterial BP with the auscultatory or oscillometric BP to determine if one system should be followed to guide therapy. The direct method is based on pressure, whereas the oscillometric method depends on flow-induced oscillations in the arterial wall. An erroneous assumption is that pressure equals flow. As described by
a derivation of Ohm’s law (pressure = flow × resistance), if resistance remains constant, there is a direct relationship between pressure and flow. However, clinically, resistance is seldom constant. Thus, BP may appear adequate while flow is decreased, or conversely BP may be low although perfusion remains adequate. Algorithms and evidence-based guidelines are available to guide assessment of the physiological and technical factors that affect direct and indirect BP measurements and outline the correct performance and interpretation of these BP measurements.22,23,97,98

In addition to the physical factors that cause the differences in arterial pressure measured in various locations in the body, there are also technical factors that affect measurement accuracy (see Fig. 21-3).23,99,100 In addition, the oscillometric system directly measures the mean pressure and extrapolates the systolic and diastolic pressure based on an algorithm, which may affect the accuracy of the systolic and diastolic pressure measurements.

For direct and oscillometric BP monitoring the correct reference is the heart. If the transducer or the arm is positioned above the heart, there will be a decrease in the measured pressure. Conversely, if the transducer/arm is positioned below the heart, there will be an increase in the measured pressure.101, 102, 103 When the patient is in the sitting position, for oscillometric or auscultated BP measurements, the arm should be supported at the level of the heart (level of the midsternum). If the arm is parallel to the patient or supported on the armrest the SBP and DBP may be 10 mm Hg higher than if the arm is supported horizontally at heart level (level of the midsternum)104, 105, 106, 107, 108, 109 and in patients with hypertension the difference in arm position may cause a 20 mm Hg overestimation of SBP.108 If the patient is in a lateral recumbent position, the noninvasive BP measurements taken from the “up arm” may be 13 to 17 mm Hg lower than those if the patient is in supine position, and BP measurements from the “down arm” are similar to those taken at supine position or inconsistent.110, 111, 112 If the “up arm” is used, the measured pressure can be corrected by measuring the distance from the angle-specific phlebostatic axis (see Display 21-1) and correcting the pressure (1 cm = 0.73 mm Hg or 1 in. = 1.8 mm Hg).

Forearm BP measurements may be necessary in cases in which access to the upper arm is not possible or an appropriate cuff is not available (i.e., the existence of morbid obesity or a conicalshaped arm).113 Two factors need to be considered when comparing the BP from the upper arm and the forearm. First, if the arm is in a dependent position, the hydrostatic pressure increases the BP in the forearm relative to the upper arm. To correct for this hydrostatic effect, the arm should be supported horizontally at heart level. The second factor is that the SBP is normally higher in the periphery (forearm > upper arm), although there is limited research comparing noninvasive upper arm and forearm BP in hemodynamically stable patients.114, 115, 116

A challenge when performing BP measurements in individuals who are morbidly obese is finding an appropriately sized cuff. For every 5 cm increase in arm circumference (starting at 35 cm) use of a standard cuff leads to an overestimation of SBP by 3 to 5 mm Hg and DBP by 1 to 3 mm Hg compared with an appropriately sized large cuff.100 To correctly size the cuff, measure the arm circumference half the distance from the elbow to the wrist. Cuff size should be similar to the guidelines for upper arm circumference.97 The cuff should be centered between the elbow and wrist and the arm should be supported at the level of the heart.


Knowledge of the relationship between preload, afterload, contractility, and SV is essential for effective hemodynamic monitoring and guiding therapeutic actions that modify these hemodynamic variables. Ventricular function curves demonstrate the interaction between preload, afterload, and contractility and the effects of various disease processes (heart failure [HF], hemorrhage) and therapeutic actions (vasodilator or inotropic drug therapy) on SV and CO (Fig. 21-8). The family of curves varies for each patient but is useful in predicting and evaluating the effects of various therapeutic interventions. The curves are constructed by plotting the PA occlusion pressure (PAOP) (or some measure of end-diastolic volume or preload) on the horizontal axis and the CO, CI, or SV on the vertical axis. A key point is that an increase in SV in response to a fluid bolus (change in preload) cannot be reliably predicted on the basis of the standard preload indices (CVP, PAOP) or volumetric indices (right ventricular [RV] end-diastolic volume, global end-diastolic volume), because the response depends on ventricular function, as indicated by the slope of the ventricular function curve.117 The traditional preload indices remain useful in the differential diagnosis and determining a patient’s risk for pulmonary edema.

Figure 21-8 Family of ventricular function curves representing normal, depressed, and severely depressed function. A change in preload is represented by a move up or down a single curve (Frank-Starling principle). Point A to point B and point B to point A reflect an increase and decrease, respectively, in preload. The response to volume loading is dependent on the position on the ventricular function curve and the shape of the curve. If both ventricles are on the steep portion of the curve the SV will increase in response to volume (responder). In contrast if the heart is on the flat portion of the curve the SV will not increase (nonresponder). A change in afterload results in a shift in the curve that appears similar to that caused by contractility, although the mechanism is different. Point D to E reflects the net effect of a decrease in afterload on a failing heart. This upward and lateral shift is the result of two actions. Point D to C reflects an increase in force of contraction and point C to E a decrease in preload due to increased systolic ejection. A change in contractility is represented by an upward or downward shift of the curve, that is, for any given preload and afterload, the CO is increased or decreased. In a failing heart, an additional effect of decreased contractility is an increase in preload due to decreased systolic ejection; thus, the net effect of a decrease in contractility is to shift the curve down and to the left (Point C to G).


The CVP directly reflects right atrial pressure (RAP) and indirectly reflects the preload of the right ventricle or RV end-diastolic pressure. The CVP is determined by vascular tone, the volume of blood returning to the heart, the pumping ability of the heart, and patient position (supine, standing).

The CVP is measured in the superior vena cava and the RAP is measured from the proximal port of the PA catheter. The CVP and RAP are generally similar as long as there is no vena caval obstruction. Normally, the CVP ranges from 3 to 8 cm H2O or 2 to 6 mm Hg (1 mm Hg = 1.36 cm H2O). In the supine/flat position, a CVP of less than 2 mm Hg may indicate hypovolemia, vasodilation, or increased myocardial contractility. An increased CVP may indicate increased circulatory blood volume, vasoconstriction, or decreased myocardial contractility. An increased CVP is also observed in RV failure, tricuspid insufficiency, positive-pressure breathing, pericardial tamponade, pulmonary embolus, and obstructive pulmonary disease.


The placement of a central venous or RA catheter is indicated to secure venous access, to administer vasoactive drugs and parenteral nutrition, and to monitor right heart preload. Hemodynamic monitoring using a CVP is most often performed when cardiopulmonary function is relatively normal. Monitoring the CVP has regained importance with the recognition of the effect of right heart function on left heart function.7

Effect of Catheter Type and Location on CVP

The CVP may be monitored via a central venous catheter or the distal port of a multilumen catheter.118 One study also suggests that measurements obtained via tunneled catheters are comparable to direct RA pressure measurements.119

In cases where placement of a central venous catheter is not possible, recent studies suggest that the CVP can be indirectly measured from a peripheral venous catheter inserted in the forearm or dorsal hand veins120,121 or from a lower extremity insertion site.122 A key to the use of peripheral venous pressure (PVP) measurements is ensuring that there is continuity between the central and venous systems, which can be assessed by observing for an increase in the PVP with a sustained inspiratory effort (Valsalva) or the occlusion of the arm or leg above the catheter insertion site (Fig. 21-9).122,123 The PVP-CVP difference decreases with increasing CVP,124 which may reflect vascular continuity. No significant pressure differences were found on the basis of catheter size (14 to 20 gauge) and patient position (as long as the system was referenced to the phlebostatic axis)120,122 in patients who were hemodynamically unstable,125 had a decreased ejection fraction (EF), or were receiving vasoactive medications.121 In general, changes in CVP were mirrored by changes in PVP, which suggests that trends in PVP may be useful. However, clinically significant PVP-CVP differences (>2 to 3 mm Hg) may occur; thus, caution must be exercised when interpreting the absolute PVP values.120,121,123, 124, 125, 126, 127, 128

Figure 21-9 Pressure waveforms from simultaneous PVP and CVP measurements demonstrating the effect of manual, circumferential, proximal arm occlusion followed by release. This increase indicates there is continuity between the central and peripheral venous systems. The PVP should not be used if this response is absent. (From Munis, J. R., Bhatia, S., Lozada, L. J. [2001]. Peripheral venous pressure as a hemodynamic variable in neurosurgical patients. Anesthesia & Analgesia, 92, 174[.)

There is limited evidence that suggests that CVP measurements can be obtained through an open-ended peripherally inserted central venous catheter (PICC).129, 130, 131 Measurements from the PICC, overestimate measurements from a central catheter by approximately 1 mm Hg and changes in the PICC CVP are closely related to central line CVP measurements.129,131 Accurate PICC CVP measurements require correct positioning of the PICC tip (at the junction of the vena cava and RA). Passive hydrostatic pressure equilibration across the PICC line takes approximately 60 minutes, but this pressure gradient can be overcome immediately with a pressure line infusing fluid at 3 mL/h.129 The CVP cannot be measured if the system has a valve (e.g., Groshong, PASV, or PowerPICC SOLO). A limitation of the use of peripheral versus central line during resuscitation is that the peripheral catheter cannot be used to obtain central venous oxygen saturation, which is an end-point of resuscitation.132


The CVP is not an accurate indicator of LV function or left heart preload.133 In the presence of normal right heart function, severe deterioration of LV function may not be reflected by a change in
CVP. An increased CVP is usually an indication of later stages of LV failure, although the CVP may remain normal even in the presence of high PA pressures and pulmonary edema.


Complications associated with CVP monitoring include localized infection, arrhythmias, vessel laceration, RV perforation, thrombophlebitis, hematoma formation at the insertion site, and pneumothorax or a malpositioned catheter.134 The most common predictor of complications, particularly pneumothorax, is the number of needle insertions required to access the vein. There is an increased risk of arterial puncture, but fewer malpositioned catheters, with the jugular approach.134 Conversely, there may be a decreased risk of infection with a subclavian versus jugular or femoral insertion.35,135

Measurement Technique

The CVP system is referenced by placing the air-fluid interface of the stopcock at the level of the phlebostatic axis (see + in Fig. 21-1) or at a point 5 cm below the sternal angle. With correct referencing, the hemodynamically stable patient can be positioned up to 45 degrees for CVP measurements.136

An area of confusion when measuring the CVP from a triple lumen catheter is the question of which port to transduce. There are no research-based recommendations regarding port selection. The differences in pressures measured from the various ports are small (<1.5 mm Hg).118 When the distal port is used there is limited effect from fluids administered via the more proximal ports.137 Because of the potential for a clinically significant change in pressure depending on the port transduced, it seems prudent to transduce consistently one port, and if a change in the site of monitoring is necessary, to annotate the change on the flowsheet.

Interpretation of CVP Data

There has been increased use of CVP to guide therapy due to the decreased use of PA catheters and results of a study in patients with acute lung injury, which suggests that outcomes from therapy guided by central venous catheter measurements are similar to those guided by PA pressure measurements.138 Assessment of the dynamic changes in the CVP in response to a fluid bolus or respiration are more sensitive and specific indices of fluid responsiveness than absolute CVP or PAOP values.

The absolute CVP may be useful in guiding differential diagnosis. For example, if the PAOP is increased and greater than the CVP, the differential diagnosis should focus on the left heart. If both the PAOP and CVP are increased, the differential diagnosis should include diffuse coronary heart disease or cardiomyopathy, pericardial constriction or tamponade, or over distention of the right heart. If the CVP is increased and greater than the PAOP, consideration should be given to right HF or pulmonary vascular disease.139 In patients with severe HF, CVP ≥ 10 mm Hg had a positive predictive value of 85% for a PAOP ≥ 22 mm Hg and was useful in evaluating 80% of the patients studied.140 Evaluation of left heart function should always include consideration of right heart function. Correct interpretation of the CVP requires knowledge of the patient’s CO. For example, the treatment would be different for a patient with a low CVP and normal CO versus low CO.141

CVP is measured at end-diastole, although consideration must also be given to the effect of the maximal pressure. Useful clinical information can also be obtained by examining the CVP/RAP waveforms. There are five mechanical components (a, c, v waves and x and y descent) of the CVP waveform. A dualchannel strip chart recorder should be used to identify the corresponding venous pressure waves with the electrical events on the ECG (Display 21-3). The mean CVP is determined by bisecting the a, c, and v waves so that there are equal areas above and below the bisection or measured at the leading edge of the c wave (also known as the “z” point). The z point reflects the final pressure in the RA just before the onset of RV systole and the closure of the AV valves; thus, this point represents the RV end-diastolic pressure (preload). Alternatively, if the a and c waves cannot be visualized, draw a straight line through the Q wave or the upstroke of the arterial pressure waveform to identify end-diastole.7 If there are large A and V waves, the CVP measurement should be made at the z point or the base of the a wave if the z point cannot be identified.142 If there is a large A or V wave, the peak A or V wave pressure indicates increased upstream hydrostatic pressures (e.g., hepatic, renal). The CVP tracing may be useful in the diagnosis of wide-complex tachyarrhythmias of unknown origin, tricuspid regurgitation (large V wave that begins with the onset of systole), restriction of RV filling due to ventricular stiffness or volume overload (y descent > 4 mm Hg—these patients are not likely to respond with increased CO if given a fluid bolus),143 pericardial tamponade (loss of x and y descent) (Fig. 21-10), and constrictive pericarditis.



Between 1993 and 2004, the use of PA catheters has decreased 65%,144 with the greatest decrease occurring after the publication of a study of 5,735 patients in 1996, which suggested that PA catheter use may increase morbidity and mortality.145 Since this study, several consensus conferences146, 147, 148 identified patient populations for which PA pressure monitoring may be beneficial or additional outcome studies are needed and that there is a need for standardized education of critical care providers.

In response to the consensus conference recommendations a number studies have been completed. Several studies found no improvement or worsening of patient outcomes from PA catheter guided therapy in general, vascular, or cardiothoracic surgical patients.149, 150, 151, 152, 153 The Pulmonary Artery Catheter in the Management of ICU Patients (PAC-Man) study154 evaluated use of a PA catheter versus transesophageal echocardiography (TEE) monitoring in patients with acute respiratory distress syndrome (ARDS), HF, or multiorgan dysfunction. No specific treatment guidelines or endpoints were used. There was no significant difference between groups in ICU or 28-day mortality; although in the PA catheter group, 80% of the patients had treatment changes made within 2 hours of catheter insertion. The Sepsis Occurrence in Acutely Ill Patients (SOAP) study155 was an observational study that evaluated the association between PA catheter use and outcome. Although the patients with PA catheters had a higher mortality rate, when confounding factors such as acuity, age, organ dysfunction, and comorbidities were controlled for, the use of a PA catheter was not associated with increased 60-day mortality. An interesting aspect of the secondary analysis of the SOAP study
is that there was no significant difference in outcomes between patients managed with a PA catheter or other flow measuring device and those who did not have a flow measuring device, nor was there a difference in outcomes between patients managed with a PA catheter versus another flow measuring device.156 In another study of patients with shock or ARDS there was no difference in 14- or 28-day mortality in patients with a PA catheter compared to those who received standard care without a PA catheter.157 The Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheter Effectiveness (ESCAPE) evaluated the effect in therapy guided by clinical presentation only versus therapy guided by PAC indices in 433 patients with severe, acute, or chronic HF.158 The targets were a resolution of pulmonary congestion and for the PA catheter group a PAOP < 15 mm Hg and an RAP < 8 mm Hg. Results indicated that there was no significant difference between groups in days alive out of the hospital within the first 6 months, 6-month mortality, or the number of days hospitalized. Patients in the PA catheter group did have a significantly higher time-trade-off than those in the control group. One possible explanation for this latter finding is the continued presence of increased PAOP and RAP (hemodynamic congestion) in the absence of clinical congestion.159 There is clinical sequelae associated with hemodynamic congestion, which may have been relieved in the PA catheter group. A limitation of this study was the exclusion of patients with the most advanced HF (e.g., patients with severe renal dysfunction, prior use of inotropes, and the use of mechanical circulatory support devices or mechanical ventilation).160,161

A criticism of these studies is that they did not use a standardized, evidence-based protocol; rather they simply compared the outcomes related to the presence or absence of a PA catheter. In 2006, the ARDSNet Fluids and Catheters Treatment Trial (FACTT) used a standardized protocol to guide fluid therapy (liberal versus conservative),162 and also compared standardized fluid therapy guided by either a PA catheter or CVP.138 Compared with therapy guided by a CVP, there was no increased benefit (or harm) from the PA catheter in terms of 60-day mortality, days in the ICU, or ventilator-free days. However, there were improved outcomes in patients in the conservative fluid therapy versus liberal fluid group, regardless of monitoring method (PA catheter vs. CVP). A retrospective study of 53,312 patients in a trauma database (1,933 with PA catheter), found that after controlling for injury severity, there was a survival benefit associated with the use of a PA catheter for patients who presented with more severe injuries in shock or increased age (61 to 90 years).163

Results of these studies, meta-analyses,164,165 and a consensus conference on the use of hemodynamic monitoring in shock166 indicate that the routine use of a PA catheter is not warranted. However, the PA catheter in a patient with a complex presentation (Table 21-3) and there may be subsets of patients
who may benefit from the use of a PA catheter to guide and evaluate therapy (Display 21-4).

Figure 21-10 Pericardial tamponade in a spontaneously breathing patient. (A) Arterial waveform. Note the electrical alternans, alternating height or duration of the QRS complex, and pulsus paradoxus on the arterial waveform. (B) RAP = 20 mm Hg. (C) PA to PAOP. PAS pressure = 26 mm Hg; PAEDP = 17 mm Hg; PA mean pressure = 19 mm Hg; PAOP = 20 mm Hg. Equalization of the diastolic pressures is the result of circumferential compression of all cardiac chambers.

With the decreased use of PA catheters, one of the challenges for clinicians will be to maintain clinical proficiency in the use of PA catheters and the hemodynamic data obtained (e.g., CO, S[v with bar above]O2). The Pulmonary Artery Catheter Education Program (www.PACEP.org) and the American Thoracic Society Pulmonary Artery Catheter Primer are excellent resources for standardized education.170,171 Consideration should also be given to the creation of a team of nurses who provide care to patients requiring PA catheterization.

Description of the PA Catheter

The PA catheter is a multilumen, polyvinylchloride catheter with a variable external diameter. Many models of PA catheters are available (Fig. 21-11). The thermodilution catheter is 7.5 Fr in diameter and 110 cm long and is marked in 10-cm increments. The balloon is inflated with a maximum of 1.5 mL of air.

Insertion of the PA Catheter

The catheter is inserted percutaneously. Once the RA is reached, the balloon, located on the distal end of the catheter, is inflated and the catheter is “floated” through the RA and RV and out into the PA, where it occludes a branch of the PA. After the characteristic PAOP tracing has been obtained, the balloon is deflated, allowing the catheter to recoil slightly into the PA. The catheter is left in the balloon-down position to prevent pulmonary infarction. The nursing responsibilities during insertion of the PA catheter are summarized in Display 21-5.

PA Waveform Characteristics

As the catheter passes through the heart, three pressure waveforms can be visualized using a PA catheter: RA, PA, and PAOP (Fig. 21-12A).

PA Pressure

PA pressures provide an index of the pressure within the pulmonary vasculature and are affected by compliance of the LV, pulmonary vascular pressure, CO, and the state of the lung tissue. In individuals without preexisting cardiopulmonary disease, PA pressure increases slightly with age (older than 60 years, PA mean ≅ 16 ± 3 mm Hg; younger than 60 years, PA mean ≅ 12 ± 2 mm Hg).172 Similarly, in individuals with hypertension without other cardiac disease there is also an age-related increase in PA pressures (aged less than 45 years, PA mean ≅ 17 ± 5 mm Hg; aged 45 to 64 years, PA mean ≅ 18 ± 6 mm Hg, and aged greater than or equal to 65 years, PA mean ≅ 21 ± 8 mm Hg).173

Three PA pressures are measured: systolic, diastolic, and mean. The PA systolic (PAS) pressure reflects the flow of blood into the PA from the RV. In the absence of elevated pulmonary vascular pressure or RV outflow obstruction, PAS pressure is equal to RV systolic pressure. The PAS is affected by PA compliance and RV ejection. During diastole, the mitral valve is open, and a continuous column of blood from the PA to the LA and LV exists; therefore, the pressure just before contraction (end-diastole) is approximately equal in the PA, LA, and LV. As a result of the diastolic equalization, the PA end-diastolic pressure (PAEDP) is often used as an indirect indicator of PAOP and LV end-diastolic pressure (LVEDP). The difference between the RV end-diastolic pressure and PAEDP (an increase in the diastolic pressure as the catheter passes across the pulmonic valve) is an important characteristic in determining whether the catheter tip is correctly positioned in the PA or has flipped back into the right ventricle (Fig. 21-12A).

Pulmonary Artery Occlusion Pressure

The PAOP is obtained by inflation of the balloon on the distal end of the PA catheter, which allows the catheter to float forward to occlude a segment of the PA. The occluded catheter creates a static column of blood through the pulmonary vasculature (Fig. 21-12B). This static column acts as an extension of the fluid within the catheter system and allows retrograde transmission of left heart pressures to the distal port of the catheter.

There is, in general, a good relationship between the mean PAOP and mean LAP. At end-diastole, pressure equalizes between
the LA and ventricle; thus, the PAOP is used as an indirect measure of LV pressure. The assumption in using pressure as surrogate indicator of volume (preload) is that an increase in pressure indicates an increase in volume, and as described by Starling’s law of the heart, an increase in CO. However, there are several factors that limit the use of pressure as an indicator of volume. First, the relationship between pressure and volume is curvilinear, not linear; thus, an absolute change in pressure (e.g., PAOP) is not associated with an absolute change in volume. Second, any alteration in myocardial compliance may affect the pressure-volume relation and limit the usefulness of the PAOP as an indicator of left heart preload. Absolute PAOP values should be used with caution in any situation that alters myocardial compliance, such as LV dysfunction or myocardial infarction (MI) (particularly involving the posteroinferior surface of the heart).174 Third, the PAOP is affected by changes in pericardial pressure; thus, the PAOP may not accurately reflect transmural pressure. Finally, although the PAOP is useful for differential diagnosis and assessing the risk for pulmonary edema, it does not predict if a patient will respond to a
fluid bolus with an increase in SV.175 Functional hemodynamic indices address this limitation.


Hemodynamic Findings







Additional Findings

Pericardial tamponade

Equalization (within 5 mm Hg) of RAP = PAEDP = PAOP; RAP waveform: prominent x descent with attenuated or absent y descent (d/t decreased ventricular filling); pulsus paradoxus (↓SBP > 10 mm Hg and ↓pulse pressure during inspiration; DBP unchanged); pulsus alternans (Fig. 21-10); absent S3 heart sound; cardiacpressures may be normal if the patient is hypovolemic

Pericardial constriction


RAP waveform: steep x and y descent resulting in an “M”- or “W”-shaped waveform; RAP ≅ PAEDP ≅ PAOP (if no tricuspid or mitral regurgitation); decreased respiratory variation in RAP; Kussmaul’s sign (inspiratory increase in RAP in severe pericardial constriction); pulsus paradoxus (approximately 33% of cases). CO maintained by tachycardia

Massive pulmonary embolism


Increased RA v wave with steep y descent due to tricuspid regurgitation, increased alveolar-arterial oxygen gradient (normal value does not rule out pulmonary embolism), tachypnea, dyspnea, increased pulmonic component of S2, pleuritic chest pain

Mitral regurgitation

If amplitude of V wave 10 mm Hg or more than a wave amplitude, read PAOP at nadir (base) of the x descent (Fig. 21-13C); PAOP > PAEDP (regurgitant v wave)

Left ventricular failure


Pulmonary congestion or edema, S3 or S4, increased a wave height (due to decreased ventricular compliance); increased v wave height due to mitral regurgitation, pulsus alternans. Approximately 50% of patients with HF have mild or no impairment in systolic function

RV infarction





RAP > PAOP or RAP 1 to 5 mm Hg > PAOP, or RAP > 10 mm Hg, RA tracing with prominent x and y descent (M configuration), increased jugular venous pressure, systemic venous congestion, RV gallop, split S2, positive hepatojugular reflux, increased RA a wave, positive Kussmaul’s sign (increased RAP with inspiration), RV S3 or S4

Acute ventral septal defect

Acute hypotension and pulmonary congestion, systolic thrill, holosystolic murmur, acute right HF with increased jugular venous pressure, late PAOP v wave, oxygen step up of >10% RA and PA



Increased SVR (compensatory), decreased S[v with bar above]o2

Septic shock (hyperdynamic)




Systemic hypotension, SBP < 90 mm Hg, metabolic acidosis with compensatory hyperventilation (respiratory alkalosis), decreased vascular resistance (↓SVR) and ↑ S[v with bar above]o2. This profile may be accompanied by distributive shock.

Septic shock (hypodynamic)



Systemic hypotension, SBP < 90 mm Hg, systemic vasoconstriction (increased SVR), decreased S[v with bar above]o2. During the early phase of septic shock, this profile may reflect inadequate fluid resuscitation. This profile also reflects cardiogenic shock.

N, normal; ↓, decreased; ↑, increased.

Figure 21-11 Venous infusion port PA catheter. (Courtesy of Baxter Healthcare Corporation, Edwards Critical Care Division, Santa Ana, California.)

In addition to being an indirect indicator of LVEDP, the PAOP is also an estimate of the capillary pressure (Pcap), which is the most important factor in the development of hydrostatic pulmonary edema. If the alveolar epithelium is intact, an increase in Pcap greater than 18 to 20 mm Hg causes increased fluid flux across the alveolar-capillary membrane and alveolar flooding. For example, in patients with an acute MI, an increase in PAOP to a value greater than 18 mm Hg is associated with the onset of pulmonary congestion, as exemplified in the Forrester subsets.176 In contrast, some patients with chronic HF tolerate a substantially higher PAOP without the development of pulmonary edema.177

Hydrostatic pulmonary edema can be present with a PAOP less than 18 mm Hg under conditions of transient LV dysfunction that have resolved, massive sympathetic discharge that increases Pcap (heroin overdose, intracerebral hemorrhage), and increased pulmonary venous vascular resistance (ARDS).174,178 Other factors that may increase the PAOP to greater than 18 mm Hg without the onset of pulmonary edema include increased pleural pressure, hyperinflation, and active expiration.174

PA Waveform Interpretation

PA waveform interpretation can be simplified by remembering that electrical activity, as indicated by the ECG, precedes mechanical activity (see Display 21-3).179 PA pressure waveforms are useful in the diagnosis of various cardiac abnormalities.

Pulmonary Artery Occlusion Pressure

The PAOP waveform is similar to the LAP waveform but is slightly damped and phase delayed (50 to 70 milliseconds) because of pulmonary vascular transmission (Fig. 21-13A). The PAOP is a mean pressure and is determined by bisecting the a and v waves, so there is an equal area above and below the bisection.

  • Elevated a wave: conditions that increase resistance to LV filling

    • Mitral stenosis

    • LV failure (Fig. 21-13B)

    • Acutely ischemic LV

  • Elevated v wave: conditions that cause increased LA filling during ventricular systole

    • Acute mitral insufficiency (Fig. 21-13C)

    • Ventricular septal defect

    • Aortic regurgitation

The giant V wave in acute mitral regurgitation and ventricular septal defect is caused by augmented LA filling. The height of the v wave is determined by LA loading volume and compliance and LV afterload and the presence or absence of a v wave may vary depending on whether there is acute or chronic mitral regurgitation.180 The height and the presence or absence of a V wave are not indicators of the severity or mitral regurgitation.181 In the presence of a large V wave (V wave 10 mm Hg greater than a wave or the mean PAOP), LVEDP is best correlated (r = 0.89) with the trough or nadir of the x descent182 (Fig. 21-13C). The mean PAOP and peak of the a wave overestimate the LVEDP. The clinical importance of the giant V wave, regardless of cause, is the marked increase in Pcap, with the potential development of pulmonary edema. The ECG is useful in differentiating a bifid PA waveform (V wave apparent in the PA tracing) from a PAOP with a large V wave (Fig. 21-14).

Figure 21-12 (A) Schema of the principle underlying the use of the PAOP as an indicator of LV preload. When the inflated balloon on the catheter obstructs arterial flow, the catheter records the pressure at the junction of the static column of fluid and flowing venous channels (J-point). The J-point occurs in the venous system, approximately 1.5 cm from the LA. The PAOP underestimates Pcap when there is increased resistance in the postcapillary vessels proximal to the J-point (point A). The PAOP overestimates LVEDP if there is obstruction distal to the J-point (point B; e.g., mitral stenosis, left atrial myxoma), whereas the PAOP underestimates the LVEDP in the presence of premature closure of the mitral valve as a result of aortic insufficiency. (B) Characteristic waveforms observed as the PA catheter is “floated” from the RA through the right ventricle and into the PA, where it wedges. Note that the mean RAP is similar to the RVEDP, the RV systolic and PAS pressures are similar, and there is a step-up in pressure as the catheter crosses the pulmonic valve and enters the PA. In a correctly positioned catheter, the PAOP is lower than the mean PA pressure and has a waveform that is relatively similar to the RAP (although slightly delayed relative to the ECG).

3. Elevated a and v waves

  • Cardiac tamponade (Fig. 21-10)

  • Hypervolemia

  • Constrictive pericarditis

  • LV failure (Fig. 21-13B)

  • Mitral stenosis

In mitral stenosis the PAOP is generally similar to LAP (except if PAOP is >25 mm Hg when it may vary as much as 10 mm Hg compared with the LAP180) and the height of the v wave is strongly associated with PA pressure.183 However, because a pressure gradient develops between the LA and LV the PAEDP and PAOP are not accurate indices of LV pressure.180

PA Pressure

The PAS pressure is represented by a steep rise during RV ejection and usually occurs after the QRS complex or near the T wave of the ECG (Display 21-3). The PAEDP is measured 0.08 second after the onset of the QRS,184 and the PA mean pressure is determined by bisecting the end-expiratory waveform, so there is an equal area above and below the bisection. In the presence of LV dysfunction, the presystolic a wave may provide a more consistent index of LVEDP than PAEDP or PAOP; however, the presence of this wave is variable.

Elevated PA pressures occur with:

  • Increased PVR (Fig. 21-15A)

    • Pulmonary hypertension

    • Chronic obstructive pulmonary disease

    • ARDS

    • Hypoxia

    • Pulmonary embolus

  • Increased pulmonary venous pressure

    • LV failure

    • Mitral stenosis

  • Increased pulmonary blood flow

    • Hypervolemia

    • Atrial and ventricular septal defects

  • Mitral insufficiency (Fig. 21-15B)

Use of PA Catheter for HF and Pulmonary Hypertension

Two areas where PA catheter use is recommended are the management of acute decompensated heart failure (ADHF) after initial therapy has failed and the diagnosis and management of pulmonary hypertension. In patients with ADHF, interpreting the hemodynamic data and undertaking appropriate therapy requires
an understanding of the different causes of the HF. For example, in patients with diastolic dysfunction with a normal EF the increased PAOP reflects the primary disease. In contrast, in patients with systolic dysfunction with a decreased EF, the increased PAOP is secondary to a decrease in CO and the subsequent neurohormonal activation.185 Further discussion of the management of HF is presented in Chapter 24.

Figure 21-13 PAOP determination. (A) Normal PAOP tracing. The mean PAOP is read at end-expiration waveform and is determined by bisecting the a and v waves so there is an equal area above and below the bisection. PAOP = 12 mm Hg. (B) Elevated a and v waves. Patient with a history of an inferolateral MI with HF. The increased a and v waves are consistent with LV failure. PAOP = 24 mm Hg. (C) PAOP with elevated V wave in a spontaneously breathing patient who was complaining of chest pain. The PAOP is read at the nadir of the x descent. Note the relation of the v wave to the TP interval of the electrocardiogram. PAOP = 17 mm Hg.

PA catheterization (along with Doppler echocardiography) is part of the diagnosis and management of patients with pulmonary hypertension.186,187 Idiopathic (formerly referred to as primary) pulmonary arterial hypertension is defined as a mean pulmonary artery pressure (PAM) ≥ 25 mm Hg in a setting of a PAOP ≤ 15 mm Hg and a normal or decreased or CO or by a PVR > 3 Wood units (>240 dynes/s/cm−5).188 Secondary pulmonary hypertension is often associated with pulmonary venous hypertension caused by left-sided cardiac disease (e.g., HF, mitral or aortic valvular disease). Pulmonary hypertension is a progressive disorder that may lead to severe RV dysfunction.

PA catheterization is used for the confirmation and differential diagnosis of pulmonary hypertension (idiopathic versus secondary), measurement of cardiac pressures, PVR and vasoreactivity testing. Vasoreactivity testing is performed to determine if a patient will respond favorably to vasodilator therapy (e.g., calcium channel blocker, epoprostenol, inhaled nitric oxide) as indicated by a decrease in PAM greater than 10 mm Hg to a PAM < 40 mm Hg, with an unchanged or increased CO.186 Table 21-4 presents typical hemodynamic profiles for patients with compensated pulmonary hypertension (maintain normal RAP and CO), decompensated pulmonary hypertension (increased RAP and decreased CO) and pulmonary venous hypertension (increased PAOP associated with left heart disease).189 Other conditions associated with pulmonary hypertension include pulmonary stenosis and the three hemodynamic profiles associated with advanced liver disease or portal hypertension.

PA perforation or rupture is often cited as a risk of PA catheterization in patients with pulmonary hypertension. However, the pathophysiological thickening of the vasculature may provide some protection and research indicates that at experienced medical facilities the performance of PA catheterization in these patients is a safe procedure (serious adverse events 1.1%), with the most frequent complications related to central line placement (e.g., hemothorax, pneumothorax).190 One factor that limits the utility of PA catheterization and CO measurement in patients with pulmonary hypertension is severe tricuspid regurgitation, which generally causes an underestimation of the actual CO.191,192 In the case of tricuspid regurgitation or a very low CO, the Fick method can be used to estimate CO.193

Technical Aspects of PA Pressure Monitoring

Numerous research studies have evaluated the technical aspects of PA pressure measurement.14,194 Incorrect techniques may
introduce error into pressure measurements and potentiate therapeutic mismanagement of critically ill patients.

Figure 21-14 PA pressure or PAOP? In the presence of a large V wave, the PAOP tracing may mimic a PA tracing. Comparison of the PA and PAOP relative to the ECG reveals the following: (1) the v wave of the PAOP occurs during the TP interval, whereas the initial systolic upstroke of PA waveform is closely related to the end of the QRS complex; and (2) the PA v wave is a sharp upward deflection on the descending limb of the PA pressure curve, having the same temporal relation as the v wave in the PAOP tracing. PAOP = 30 mm Hg.


Traditionally, PA and PAOP measurements have been obtained with the patient in the flat, supine position; however, this position may be poorly tolerated in patients with increased intracranial pressure or cardiopulmonary dysfunction. Research has shown that in a wide variety of critically ill patients, accurate PA pressures can be obtained in the supine position with legs extended and a backrest elevation up to 60 degrees.195 Measurement of PA pressures in the sitting position (legs dependent) is not recommended.
In the lateral position, PA and PAOP can be obtained in the 30and 90-degree lateral positions, as long as an angle-specific reference is used (Display 21-1). Because some patients respond differently to position change, pressure measurements obtained in the flat, supine position should be compared with those obtained with backrest elevation or lateral position before assuming no difference.

Figure 21-15 PA pressure determination. (A) Elevated PA pressure related to LV failure and ARDS. Patient is on intermittent mandatory ventilation. PAS = 58 mm Hg; PAEDP = 30 mm Hg; PA mean = 38 mm Hg. (B) Patient with vegetation on mitral valve resulting in acute mitral insufficiency. Note the v wave on the downstroke of the PA waveform (bifid waveform). PAS = 68 mm Hg; PAEDP = 32 mm Hg; PAM = 48 mm Hg.


(mm Hg)

(mm Hg)

(mm Hg)

(mm Hg)

(mm Hg)



Compensated PAH








Decompensated PAH








Pulmonary venous hypertension








Pulmonic stenosis








Portal Hypertension

Volume overload








High output








Portopulmonary hypertension








Reproduced from Mathier, M., & Park, M. (2007). Hemodynamic assessment of pulmonary hypertension: Echocardiography and cardiac catheterization, 2007. Retrieved December 28, 2007, from www.medscape.com/viewprogram/8360_pnt.

Hemodynamic measurements (CVP, PA, PAOP, CI, and DO2) can also be obtained in the prone position. Hemodynamic measurements obtained with the patient with acute lung injury or ARDS in the prone position are similar to those obtained in the supine position15, 16, 17, 18, 19; however, patients with normal cardiopulmonary function196,197 may demonstrate a decrease in end-diastolic volume and CI without a change in CVP. The amount of time after proning before the measurements can be obtained has not been defined. Most studies evaluated the changes 60 to 90 minutes after the prone positioning. The shortest stabilization period was 15 minutes in healthy patients undergoing lumbar spine surgery,197 after 20 to 30 minutes in patients with acute lung injury,15,19 and 20 minutes after stabilization of SpO2 (60 to 90 minutes after proning) in patients with ARDS.17 Although abdominal pressure increases slightly in the prone position, there is no effect on the measured cardiac indices.16,20 Areas for future research include evaluation of the measurements in automated proning beds, description of the time to stabilization of hemodynamic indices after proning, and evaluation of the effect of proning on abdominal and cardiac pressures in patients with intraabdominal hypertension or abdominal compartment syndrome.

Pulmonary Effects

Correct function of the PA catheter requires a continuous column of fluid between the catheter tip and the LA. There are three physiologic zones in the lung that depend on the interaction of alveolar, arterial, and venous pressures.198 Alteration in any of these pressures may affect the fluid column between the catheter tip and the LA and alter the accuracy of PA pressure measurements. Because the presence of a Zone-3 vascular bed is crucial for accurate PA pressure measurements, assessment of this factor should be routinely performed (Display 21-1 and Fig. 21-4).

Spontaneous Versus Mechanical Ventilation

During spontaneous ventilation, the alveolar pressure decreases during inspiration and increases during expiration. Conversely, during positive-pressure ventilation, intrathoracic pressure increases during inspiration and decreases during expiration. The changes in intrathoracic pressure are transmitted to the cardiovascular structures in the thorax and are reflected by corresponding changes in CVP and PA pressures. Because the pressure of interest is the distending pressure of the cardiac chamber (transmural pressure), it is important to correct for changes in pleural pressure. At end-expiration, when no airflow occurs, pleural pressure is closest to atmospheric pressure and provides the most accurate measurement of transmural pressure. If a patient has any condition that increases end-expiratory intrathoracic pressure (PEEP, auto-PEEP, active expiration, or increased abdominal pressure) or pericardial fluid the end-expiratory intracardiac pressure measurements will overestimate true transmural pressure.

In patients with respiratory variation in the PA waveform tracing, the digital readings are unreliable because of the unselective nature of electrical averaging.199,200 In addition, the “stop cursor” method (freezing the monitor screen) is less reliable than the graphic method.200 The analysis of graphic recordings to identify the end-expiratory phase remains the recommended method for interpreting PA waveforms.201 The validation of accurate pressure measurements in the medical record is imperative as electronic records may “pull” data from the digital readings, and these data may be less accurate than those obtained using the stop cursor or analog approach. The addition of an airway pressure tracing may further improve the accuracy of the measurements.202 Display 21-1 reviews guidelines for recording PA pressure measurements.

Other ventilatory patterns may require modification of the methods to interpret the PAOP. Active expiration, which should be suspected when there is a respiratory-induced fluctuation in the PAOP greater than 10 to 15 mm Hg, may cause an overestimation of the PAOP by as much as 10 mm Hg. With active expiration, the PAOP should be read at the midpoint between the expiratory peak and the end-inspiratory nadir (Fig. 21-16).203 Another possible method to correct for active expiration is to subtract the expiratory change in bladder pressure from the CVP.204 Inverse ratio ventilation, which decreases end-expiratory time and increases end-expiratory lung volume, may cause an overestimation of the PAOP. In this case, the use of the airway pressure waveform may help identify the end-expiratory phase and consideration should be given to correcting for PEEP or auto-PEEP. With airway pressure release ventilation, the PAOP should be measured at the end of the positive pressure plateau, which can be observed on the ventilator and is the point immediately before the release of airway pressure and the initiation of inspiration.205

Figure 21-16 (Top) PAOP tracings showing the end expiratory, end inspiratory (nadir) and the midpoint values in a patient with marked respiratory variation. (Bottom) PAOP in same patient post muscle relaxation with paralytic. (Reprinted with permission from Hoyt, J. D., Leatherman, J. W. [1997]. Interpretation of the pulmonary artery occlusion pressure in mechanically ventilated patients with large respiratory excursion in intrathoracic pressure. Intensive Care Medicine, 23[11], 1126.)

Manipulation/Removal of PA Catheter

To safely manipulate or discontinue the catheter, critical care nurses must have knowledge of the correct technique for catheter insertion, be able to interpret waveforms (normal and abnormal) to confirm catheter position, to have knowledge of the appropriate action required should an abnormal waveform occur, and be able to troubleshoot the catheter system206 (Table 21-5). Potential complications during repositioning include PA rupture, cardiac perforation or tamponade, thrombus formation, sepsis or catheter-related infection, and cardiac arrhythmias.

Factors that contribute to PA rupture include balloon hyperinflation, peripheral location of the catheter tip, and hypothermia. Steps to avoid these risks are to slowly inflate the balloon to volume (1.25 to 1.5 mL of air, never fluids), at which time the pressure tracing should change from a PA to a PAOP waveform, and to limit inflation time to less than 15 seconds. If an overwedge is observed, stop immediately. To avoid distal migration of the catheter, the PA tracing should be continuously monitored and the chest radiograph should be assessed to determine if the tip of the catheter is correctly positioned within 5 cm of the mediastinum.

During PA catheter removal (Display 21-6), additional risks include air embolism, arrhythmias, and myocardial or valvular damage. Risk factors for air embolization include a decreased intravascular pressure (hypovolemia, tachycardia), negative intrathoracic pressure (tachypnea, upright position, catheter removal during deep inspiration), an incompetent diaphragm on the introducer, and right to left intracardiac shunt. To minimize the risk of an air embolism, the patient should be placed in a supine/flat position and the catheter removed during breath holding at the end of a deep inspiration or positive pressure ventilation (to increase CVP). After removal of the catheter, the introducer should be sealed with a sterile obturator or a male cap. The incidence of cardiac arrhythmias during catheter removal ranges from 5% to 19%, with a small percentage of arrhythmias considered life threatening.207 Patients at increased risk for arrhythmias are those with electrolyte imbalances myocardial ischemia or infarction, CI < 2.5 L/min/m2 or prolonged manipulation time. The use of a steady, continuous withdrawal of the catheter may decrease the incidence of arrhythmias. Myocardial or valvular damage can occur because of kinking or knotting of the catheter around cardiac structures or failure to deflate the balloon before withdrawal of the catheter. Caution should be taken if the patient has another cardiac catheter (i.e., transvenous pacemaker) or excessive catheter length (dilated heart).


Clinical Problem


Possible Causes


Overdamped pressure tracing

Falsely low systolic readings

Air bubbles in the pressure tubing or transducer

Flush all air from system (including microbubbles).

Falsely increased diastolic readings

Remove excess stopcocks

More than three stopcocks between catheter and transducer

Tighten all connections

Flush tubing of all blood (if unable to clear, change transducer-tubing set-up)

Loose connections

Collection of blood in tubing or in and around transducer

Maintain pressure in infusion bag at 300 mm Hg

Aspirate blood from catheter if clot suspected (do not flush)

Catheter kinked internally or at insertion site

If PA catheter kinked, notify MD to reposition

Catheter wedged against vessel wall

If fibrin occluding catheter, catheter may need to be replaced

Excessive tubing length (>4 ft)

Clot or fibrin deposition on catheter tip

Use noncompliant/wide-bore tubing

Underdamped pressure tracing

Overestimation of systolic pressure

Air bubbles in tubing, stopcocks, or transducer

Remove all air bubbles from system

Underestimation of diastolic pressure

Limit tubing to 4 ft maximum

Excessive tubing length (>4 ft)

Remove unnecessary stopcocks

Excess number of stopcocks

If all attempts to resolve unsuccessful, consider the addition of an in-line damping device

Catheter whip (fling) or artifact

Overestimation of systolic pressure

Location of distal tip of PA catheter near pulmonic valve

Assess dynamic response characteristics (troubleshoot system)

Underestimation of diastolic pressure

Hyperdynamic heart

Notify MD or qualified RN to reposition PA catheter

Difficult interpretation of waveform

Looping of PA catheter in RV

External disruption of PA catheter system

If fling fails to resolve, use mean pressure

Absence of PA occlusion tracing

Potential for air embolism or blood leaking from balloon port

Balloon rupture

If balloon is inflated without return of air into syringe on passive deflation, assess for signs of air embolism (if present, place in Trendelenburg in left lateral decubitus position, treat symptoms, notify MD)

Improper positioning of PA catheter

If stable, label balloon port “DO NOT WEDGE.”

Notify MD of need to replace catheter

If balloon is inflated to 1.5 mL, without change in waveform from PA to PA wedge pattern, notify MD or qualified RN of need to reposition catheter

Once catheter is repositioned, assess the amount of air required for wedge (ideal volume 1.25-1.5 mL)

Migration of the PA catheter into the RV

Presence of RV arrhythmias

Accidental or spontaneous withdrawal of catheter into the RV

Inflate the balloon fully to engulf the tip of the catheter and reduce ectopy

Decreased diastolic pressure (equal to RAP)

Notify MD or, if approved for RN, reposition catheter into PA

If compromised by arrhythmias, ensure balloon is deflated and withdraw catheter into RA (15-20 cm marking on PA catheter and RAP waveform observed from distal port)


Overwedging (eccentric balloon inflation or inflation in a small vessel) is potential risk for PA perforation and rupture

Catheter migration

Slowly inflate balloon while constantly observing the waveform

Balloon position in small pulmonary vessel

If overwedge pattern observed, immediately stop inflation and allow balloon to deflate passively

Notify MD or, if approved for RN, reposition catheter

Spontaneous wedge

Potential for loss of blood supply to branch of pulmonary vessel and risk of PA infarction

Catheter migration (patient movement, warming up of catheter after placement)

Turn patient to side opposite catheter placement.

Have patient straighten arm or turn head to dislodge catheter

Have patient gently cough

Notify MD or RN, reposition catheter

Modified from Gardner, P. E. (1993). Pulmonary artery pressure monitoring. AACN Clinical Issues in Critical Care Nursing, 4, 98-119.

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Jan 10, 2021 | Posted by in NURSING | Comments Off on Hemodynamic Monitoring
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