Physiological Monitoring: Static Versus Dynamic Measurements

A central venous pressure describes pressure at a particular time. A passive leg raise examines how flow changes when venous return is temporarily altered. Both provide physiological information, but they answer different questions.

Useful monitoring begins with a defined clinical problem. The measurement must then be reliable, relevant to that problem, and capable of changing the next decision.

5.1 Static Values, Trends, and Dynamic Tests

A static measurement describes the current state of a variable. Examples include arterial pressure, central venous pressure, cardiac output, and a ventricular end-diastolic dimension. These measurements remain static descriptions even when a monitor displays them continuously.

Repeated static measurements form a trend. A falling arterial pressure or rising lactate can identify deterioration. However, the change may result from several simultaneous processes. A trend does not necessarily identify which mechanism caused it.

A dynamic test measures how the circulation or another system responds to a defined change. Passive leg raising deliberately increases cardiac filling for a short time. Mechanical ventilation produces a repeated change in cardiac loading with each breath. Measuring the response can reveal information that a resting value does not provide.

The respiratory system provides another example. During passive constant-flow ventilation, an inspiratory pause changes flow to zero. Comparing peak and plateau pressure then helps separate the pressure needed to overcome resistance from the pressure needed to maintain inflation. The pause adds information that a peak pressure alone cannot provide.

The distinction depends on what the measurement tells us. A continuous display of central venous pressure still reports pressure. It does not show whether more filling will increase stroke volume. A brief, properly measured preload maneuver can answer that response question more directly.

Dynamic measurements are not universally superior. Their value depends on whether the physiological stimulus is appropriate and whether the response can be measured. A test performed outside its valid conditions can be less useful than a carefully interpreted static measurement.

Monitoring should also be distinguished from treatment. A monitor detects or estimates a variable. The clinician interprets that information and chooses an intervention. Benefit depends on the quality of the entire sequence, including the decision to avoid an unnecessary intervention.

5.2 Why a Resting Filling Pressure Cannot Predict Every Response

Cardiac filling pressure does not directly measure preload reserve. A stiff ventricle may develop a high pressure with little added volume. A more compliant ventricle may hold more blood at the same pressure. Pressure outside the heart also contributes to the measured value. The same filling pressure can therefore accompany different chamber volumes and different responses to added preload.

The Frank–Starling relationship describes how ejection changes as preload increases. On its steeper portion, additional filling stretches the myocardium and increases stroke volume. On its flatter portion, further filling produces little additional ejection, although filling pressure may continue to rise. A single pressure identifies neither where the ventricle lies on that relationship nor how much its stroke volume will increase.

Osman and colleagues reviewed 150 volume challenges in 96 patients with sepsis. Baseline central venous pressure and pulmonary artery occlusion pressure poorly predicted an increase in cardiac index after fluid. This study supports the limited predictive value of resting filling pressures in the population examined. It does not imply that these pressures contain no useful information. 1

Central venous pressure still provides useful information. Blood returning from the systemic veins must flow toward the right atrium. A higher right atrial pressure can oppose that return and transmit pressure back toward organs. The waveform and the change during treatment can also help explain the circulation. If pressure rises substantially while flow barely changes, further filling may worsen congestion without producing the intended benefit.

The same principle applies to a ventricular dimension. A small cavity may reflect limited filling, but its size alone does not prove that fluid will improve perfusion. Chamber geometry, contractility, ventricular interaction, and the clinical context remain relevant.

The limitation is therefore specific. A resting value can describe the current state while being a poor predictor of what will happen after a new intervention.

5.3 Measurement Quality Comes Before Interpretation

Every physiological measurement contains uncertainty. A displayed change may reflect a true physiological response, measurement noise, or both.

Accuracy describes how close a measurement is to the true value or an appropriate reference. Precision describes how closely repeated measurements agree with one another. A device can repeatedly report the same wrong value: it is precise but inaccurate. A device can also give readings whose average is close to the reference while individual readings vary widely. That variation can prevent detection of a small physiological change.

A dynamic maneuver may produce a small change that lasts only briefly. The monitor must distinguish that response from ordinary variation and display it while it is present. If the monitor averages many earlier and later measurements together, the peak response may appear smaller or arrive on the display after the maneuver has ended.

Suppose measured cardiac output rises from 4.0 to 4.1 L/min during a maneuver. The increase is 0.1 L/min. Express it relative to the starting output:

0.1 ÷ 4.0 × 100 = 2.5%

The displayed output has risen by 2.5%. Next establish whether the device can reliably detect a change this small. If its ordinary variation is similar or larger, the apparent increase may be measurement noise. Extra decimal places do not make a measurement more precise.

Check the signal before using a calculated response. An overly damped arterial system smooths the pulse waveform and tends to underestimate systolic pressure and pulse pressure. A resonant system can exaggerate the pulse. Respiratory pulse-pressure variation is calculated from that waveform, so distortion of the underlying signal can distort the reported variation.

Echocardiographic flow measurements also depend on technique. A change in Doppler alignment changes the measured velocity even if actual flow is unchanged. Moving the sample or choosing beats with different filling intervals can create another apparent response. Keep the view and sampling method consistent, and use appropriate beat averaging.

Before interpreting a dynamic response, establish a stable baseline. Avoid changing a vasopressor, ventilator setting, or sedative at the same time unless the test specifically examines that intervention. Otherwise, the response cannot confidently be assigned to one cause.

5.4 Respiratory Variation in Pulse Pressure and Stroke Volume

During positive-pressure inspiration, intrathoracic pressure rises and can reduce venous return to the right heart. Lung inflation can also increase the load against which the right ventricle ejects. Right ventricular stroke volume may fall during part of the breath. After blood passes through the lungs, that change alters left ventricular filling and stroke volume.

If the ventricles are preload responsive, these cyclic changes in filling can produce a large variation in stroke volume. When arterial properties remain sufficiently stable, pulse pressure varies with the ejected volume as well. Under suitable conditions, that variation predicts whether increasing preload will increase output.

Pulse pressure is systolic pressure minus diastolic pressure. Pulse pressure variation, abbreviated PPV, compares its maximum and minimum values over the respiratory cycle:

Consider illustrative maximum and minimum pulse pressures of 65 and 55 mm Hg. Their difference is 10 mm Hg. Their average is (65 + 55) ÷ 2, or 60 mm Hg. Divide the difference by that average:

10 ÷ 60 × 100 ≈ 16.7%

The pulse pressure varies by about 16.7% according to this formula. Only after calculating it should we decide whether the breathing pattern, rhythm, and measurement conditions allow it to predict fluid responsiveness.

Michard and colleagues studied 40 mechanically ventilated patients with sepsis-related circulatory failure. Respiratory pulse pressure variation predicted the response to volume expansion more reliably than respiratory systolic pressure variation in that study. The result established the clinical promise of heart–lung interactions as a functional test. Its threshold should not be applied independently of the conditions under which it was studied. 2

Spontaneous effort creates pressure changes that may be irregular and opposite in direction to passive inflation. Arrhythmia changes the filling interval from beat to beat. In either case, observed variation may no longer represent a consistent ventilator-induced preload test.

A small tidal volume may produce too small a pressure change to reveal preload dependence. Low respiratory system compliance can also alter how airway pressure reaches the pleural space and pulmonary vessels. A low PPV under these conditions may miss a responsive patient. Chest mechanics and the number of heartbeats within each respiratory cycle also affect the signal.

Right ventricular dysfunction can create a misleadingly high PPV. Inspiration may markedly increase right ventricular afterload and reduce right ventricular ejection. Left ventricular filling then varies because the right ventricle cannot maintain flow through the lungs. Adding volume may further distend that ventricle without correcting its ejection problem. Assess right ventricular function when the clinical findings suggest this explanation.

Stroke volume variation uses the same general principle but depends on the method estimating stroke volume. Both the underlying physiological assumptions and the device’s measurement performance must be considered.

5.5 Passive Leg Raising: A Reversible Change in Venous Return

Passive leg raising, or PLR, temporarily redistributes venous blood toward the thorax. It can test the effect of increased cardiac filling without leaving an administered fluid load in the patient.

A commonly used PLR maneuver starts with the patient semirecumbent. The trunk is then lowered to horizontal while the legs are raised. Lowering the trunk helps move blood from abdominal veins toward the thorax, while raising the legs recruits blood from the lower limbs. The resulting increase in cardiac filling is temporary. The position change must be feasible and appropriate for the patient.

Measure stroke volume or cardiac output while the filling increase is present. A late measurement can miss the response. Then return the patient to the starting position. A return of flow toward baseline helps confirm that the change was related to the maneuver rather than a separate change in the patient.

Monnet and colleagues studied 71 mechanically ventilated patients, including patients with spontaneous breathing activity or arrhythmia. PLR-induced changes in aortic blood flow predicted the response to subsequent fluid administration. Changes in pulse pressure were less reliable. This supports measuring flow during the maneuver rather than relying on arterial pressure alone. 3

A rise in flow of approximately 10% has been used in several PLR studies, but a threshold must match the protocol and the measuring method. A borderline response measured imprecisely should not be treated as a definitive result.

The aortic velocity–time integral, or VTI, adds the measured blood velocities over the ejection period. It describes the distance traveled by the sampled blood during one ejection. Multiplying that distance by the outflow tract area estimates stroke volume. If area remains unchanged, the percentage change in VTI estimates the percentage change in stroke volume. This comparison also requires consistent Doppler alignment and sample position.

Cardiac output depends on both stroke volume and heart rate. If heart rate changes during the maneuver, a change in cardiac output cannot automatically be attributed to stroke volume alone.

PLR is less dependent than PPV on a regular rhythm and controlled ventilation. It still requires reliable flow measurements. Pain, coughing, active movement, altered abdominal pressure, or an inadequate position change can make the response difficult to interpret.

5.6 Occlusion Tests and Fluid Challenges

Other dynamic tests create a controlled change in filling or directly measure the response to fluid. Their results depend on how the stimulus is delivered and how the response is measured.

An end-expiratory occlusion briefly holds ventilation at the end of expiration. It prevents the next positive-pressure inflations from repeatedly impeding venous return. More blood can then reach the heart. If the ventricles respond to that additional filling, cardiac output increases.

Monnet and colleagues examined a 15-second end-expiratory occlusion in 34 mechanically ventilated patients with shock. The change in cardiac index predicted the response to subsequent volume expansion. The study used a small response threshold, which makes measurement precision particularly important. The findings cannot be transferred to a device that averages too slowly to capture the change. 4

The patient must be able to tolerate the pause without substantial respiratory effort. A pause interrupted by active breathing is a different physiological stimulus. The result should not be interpreted as though the intended test had been completed.

A fluid challenge tests the response by administering fluid. Specify the amount, infusion duration, flow measurement, and stopping limits beforehand. Measure the response at the planned time. A later blood pressure reading alone cannot show whether the infusion produced an immediate increase in stroke volume.

The response is usually expressed as a relative change from baseline:

The infused sodium and water remain in the body after the challenge, whether or not flow improves. A smaller challenge gives less fluid, but it may produce too small a preload change for the monitor to detect reliably. A larger challenge may produce a clearer signal while raising filling pressures more. Choose the protocol with both measurement quality and the patient’s tolerance in mind.

5.7 Borderline and Conflicting Results

Physiological responses vary gradually. Suppose a method uses a 10% increase as its positive threshold. It will classify increases of 9% and 11% differently, although the measured responses are close. Measurement variation may also move a result from one side of the threshold to the other. A cutoff helps classify results; it does not remove uncertainty near that cutoff.

Cannesson and colleagues examined PPV in 413 anesthetized, mechanically ventilated patients. They identified an intermediate range in which the response to fluid could not be predicted reliably. The study illustrates the value of recognizing a diagnostic gray zone. Its numerical boundaries describe that study population and should not be assumed to apply to every ICU patient. 5

When a result is borderline, first examine the measurement. A better signal, consistent beat averaging, or a repeated maneuver may clarify whether the response is reproducible. Repeating a test does not help if its physiological assumptions remain invalid.

Conflicting tests require the same approach. A high PPV with a negative PLR may reflect unsuitable PPV conditions, an inadequate PLR, different measurement timing, or a genuine change in the patient between tests. Selecting whichever result supports a preferred treatment does not resolve the discrepancy.

An alternative method should add independent information. Echocardiography can identify ventricular dysfunction or obstruction that changes the interpretation of a flow test. Assessment of perfusion and congestion can establish whether an increase in flow is needed and whether fluid is likely to be tolerated.

Relate uncertainty to the proposed treatment. If further fluid could worsen severe pulmonary edema, a borderline flow prediction gives weak support for that exposure. If circulation is rapidly failing, essential treatment must proceed while the mechanism is assessed. Testing should help choose and reassess treatment without delaying necessary support.

5.8 Responsiveness, Clinical Need, and Tolerance Are Separate

Fluid responsiveness means that cardiac output or stroke volume increases after a defined increase in preload. It does not establish that the patient needs a higher output. It also does not establish that fluid administration will improve an outcome.

A patient can be fluid responsive while maintaining adequate perfusion. Increasing filling in that situation may add volume without addressing an important problem. Responsiveness is therefore a physiological property rather than a treatment indication.

Fluid tolerance describes whether additional fluid can be given without clinically important harm. Additional filling can increase output while also raising ventricular filling pressures. Pressure transmitted to pulmonary veins can worsen lung edema. Pressure transmitted to systemic veins can impair organ drainage. A positive flow response must therefore be interpreted alongside these possible harms.

Conversely, a negative fluid-responsiveness test does not mean that all circulatory treatment should stop. Persistent hypotension or hypoperfusion may require treatment of vascular tone, cardiac dysfunction, arrhythmia, or obstruction. It means that additional preload is less likely to provide the intended increase in output under the conditions tested.

The response itself may also be short-lived. Fluid redistribution, changing vascular tone, and continued losses can alter the effect over time. An immediate rise in output does not guarantee a sustained improvement in organ perfusion.

These distinctions help organize treatment. Establish evidence of a perfusion problem. Assess whether increased filling could improve flow. Assess whether the patient can tolerate the associated pressure and volume changes. Reassess the actual clinical effect after any intervention.

5.9 From Diagnostic Performance to Patient Outcomes

A test can predict a physiological response accurately without necessarily improving patient outcomes. Outcome benefit depends on how clinicians act on the result and on the effects of the treatments selected.

The FRESH trial evaluated a resuscitation strategy incorporating PLR-induced stroke volume changes in patients with sepsis-associated hypotension and shock. In its modified intention-to-treat analysis of 124 patients, the strategy reduced net fluid balance compared with usual care. Some secondary organ-support outcomes also favored the intervention. This was a relatively small, unblinded trial. Its findings support further use and study of an integrated strategy rather than proving a mortality benefit from the maneuver itself. 6

ANDROMEDA-SHOCK-2 tested a broader personalized resuscitation protocol in early septic shock. It combined peripheral perfusion assessment, hemodynamic evaluation, fluid-responsiveness testing, and treatment adjustments. Its main outcome compared death first, then duration of vital support, then hospital stay through day 28. The protocol improved this combined outcome, mainly through shorter vital support. Mortality at 28 days was similar. Because the trial tested several components together, it cannot establish which measurement or maneuver produced the benefit. 7

The distinction between prediction and outcome matters when choosing a monitor. A device should provide information that is sufficiently reliable and timely to change a meaningful decision. More variables do not automatically produce better care.

Monitoring also creates work and potential harm. Invasive access can cause complications, and misleading signals can trigger unnecessary treatment. The appropriate level of monitoring depends on the severity of illness, the unresolved physiological problem, and whether the additional information is likely to alter management.

5.10 Applying Static and Dynamic Information at the Bedside

Consider an illustrative patient with septic shock and persistent peripheral hypoperfusion. Central venous pressure is 14 mm Hg. The arterial monitor reports a PPV of 18%. The patient is making spontaneous respiratory efforts and has atrial fibrillation.

The PPV is numerically high, but two major conditions for its standard interpretation are absent. Irregular beat-to-beat filling and variable respiratory effort can produce variation that does not represent the intended ventilator-induced test. The result should not be used alone to predict a response to fluid.

The central venous pressure adds different information. It identifies a measured downstream pressure, but it does not prove either fluid responsiveness or unresponsiveness. The reference level, intrathoracic pressure, waveform, and evidence of congestion need assessment.

If positioning is appropriate, perform a PLR with a sufficiently rapid and reproducible flow measurement. Suppose cardiac output increases from 4.0 to 4.6 L/min. The heart is pumping an additional 0.6 L each minute. Relative to the starting output:

0.6 ÷ 4.0 × 100 = 15%

Cardiac output has increased by 15%. When the starting position is restored, it returns toward 4.0 L/min. Heart rate and vasoactive treatment remain comparable throughout the maneuver.

The temporary increase and subsequent return toward baseline support a preload-related flow response. Next apply the threshold validated for the measurement method. Then decide whether the persistent perfusion problem needs more flow and whether retained fluid could worsen lung edema or systemic venous congestion. A positive maneuver answers the response question; it does not answer all three questions.

If a fluid intervention is selected, its purpose is to produce a useful flow increase that improves perfusion. Both that response and signs of poor tolerance should be monitored. If filling pressure rises without the intended gain in flow, further loading requires reconsideration.

The static pressure and the maneuver provide complementary information. Central venous pressure describes pressure at the right atrium and helps assess the consequences of further filling. PLR tests whether a temporary increase in filling produces more flow. Combining them with perfusion and congestion findings makes the next treatment decision more informed.

References

1. Osman D, Ridel C, Ray P, et al. Cardiac filling pressures are not appropriate to predict hemodynamic response to volume challenge. Critical Care Medicine. 2007;35(1):64–68. doi:10.1097/01.CCM.0000249851.94101.4F.

2. Michard F, Boussat S, Chemla D, et al. Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure. American Journal of Respiratory and Critical Care Medicine. 2000;162(1):134–138. doi:10.1164/ajrccm.162.1.9903035.

3. Monnet X, Rienzo M, Osman D, et al. Passive leg raising predicts fluid responsiveness in the critically ill. Critical Care Medicine. 2006;34(5):1402–1407. doi:10.1097/01.CCM.0000215453.11735.06.

4. Monnet X, Osman D, Ridel C, Lamia B, Richard C, Teboul JL. Predicting volume responsiveness by using the end-expiratory occlusion in mechanically ventilated intensive care unit patients. Critical Care Medicine. 2009;37(3):951–956. doi:10.1097/CCM.0b013e3181968fe1.

5. Cannesson M, Le Manach Y, Hofer CK, et al. Assessing the diagnostic accuracy of pulse pressure variations for the prediction of fluid responsiveness: a “gray zone” approach. Anesthesiology. 2011;115(2):231–241. doi:10.1097/ALN.0b013e318225b80a.

6. Douglas IS, Alapat PM, Corl KA, et al. Fluid response evaluation in sepsis hypotension and shock: a randomized clinical trial. Chest. 2020;158(4):1431–1445. doi:10.1016/j.chest.2020.04.025.

7. The ANDROMEDA-SHOCK-2 Investigators. Personalized hemodynamic resuscitation targeting capillary refill time in early septic shock: the ANDROMEDA-SHOCK-2 randomized clinical trial. JAMA. 2025;334(22):1988–1999. doi:10.1001/jama.2025.20402.