Invasive blood pressure waveforms can guide ICU resuscitation decisions

Published in Annals of Intensive Care, the review by Maxime Bertrand, Antoine Goury, Denis Chemla, Jean-Louis Teboul, Olfa Hamzaoui and colleagues makes the case that the individual components of the arterial pressure signal—systolic arterial pressure, diastolic arterial pressure, mean arterial pressure and pulse pressure—each carry distinct physiological meaning and can serve as real-time therapeutic tools rather than passive safety readouts.

The authors stress that none of this interpretation is valid unless the waveform itself is trustworthy. Before reading any value off the monitor, the measurement system must be validated: the transducer should have an adequate frequency response with a natural frequency above 100 Hz, be correctly zeroed, and show no baseline drift. A reliable waveform should show a rapid upstroke, a dicrotic notch confirming proper aortic valve function and the absence of significant aortic regurgitation, and a smooth descending diastolic phase that gradually approaches the diastolic pressure without irregular oscillations. A slow upstroke, the review notes, should first prompt the clinician to rule out recording artifacts that dissipate energy before attributing it to severe cardiocirculatory failure.

Two classic distortions threaten accuracy. Underdamping produces multiple oscillations after the dicrotic notch, overestimating systolic pressure, underestimating diastolic pressure and therefore overestimating pulse pressure. Overdamping flattens the waveform, underestimating systolic pressure and overestimating diastolic pressure. The authors recommend performing the fast-flush test systematically before clinical use: briefly activating the flush device, a continuous 300 mmHg pressure source, produces a square wave followed by oscillations that reveal the system’s natural frequency and damping coefficient. Underdamping can be mitigated with short, rigid, non-compressible tubing, fewer stopcocks, catheter stabilization and adjustable damping devices, while overdamping is usually traced to air bubbles, blood clots or kinked catheters, and may require repositioning the wrist or replacing the catheter or arterial site.

Where the catheter sits also matters. Femoral artery mean arterial pressure was reported to be more often higher than radial measurements in ICU patients, including those with septic shock on high-dose vasopressors, but the average difference of about 3 mmHg has unclear clinical impact, suggesting no immediate need to change current preferences for peripheral cannulation. More fundamentally, peripheral pressures differ from aortic pressures because of pulse wave amplification: as the forward pressure wave travels toward progressively stiffer and narrower vessels, peripheral pulse pressure and systolic pressure rise while diastolic pressure falls slightly, and mean pressure remains largely unchanged. Aging, vasoconstriction, short body size, tachycardia, female sex and traditional cardiovascular risk factors all attenuate this amplification, which is why a peripheral pulse pressure of 40 mmHg may signal a low stroke volume in an elderly patient but is harder to interpret in a younger one.

Mean arterial pressure emerges as the cornerstone of organ perfusion. It depends on cardiac output, systemic vascular resistance and right atrial pressure, and it is the variable around which organ blood flow autoregulates. A recent meta-analysis of 34,829 ICU patients found a significant association between hypotension and mortality, especially pronounced when mean pressure fell below 60 mmHg. In septic shock, a retrospective cohort of 111 patients identified both the time spent below 65 mmHg and the depth of hypotension as independent predictors of 30-day mortality, and a nationwide cohort study reported the lowest risk at roughly 65 mmHg in general ICU patients, about 70 mmHg in sepsis and about 72 mmHg in septic shock. Current guidelines recommend a target of at least 65 mmHg.

For patients with chronic hypertension, the picture is more complicated because the autoregulation curve shifts rightward, so a mean pressure that sits comfortably on the plateau in healthy individuals may lie on the descending slope in a hypertensive patient. A retrospective database analysis found fewer acute kidney injury episodes among septic patients with chronic hypertension whose average admission mean pressure was at least 80 mmHg, although 30-day mortality was lowest in the intermediate 73–80 mmHg group. A randomized trial by Asfar and colleagues comparing targets of 80–85 versus 65–70 mmHg found improved renal function and less renal replacement therapy in patients with chronic hypertension, but no mortality difference. A more recent Japanese trial in patients aged 65 and older, by Endo and colleagues, surprisingly found significantly increased mortality in the higher-target group; the authors note that this trial initiated vasopressin early, at a norepinephrine dose of 0.1 micrograms per kilogram per minute, producing a threefold higher cumulative vasopressin dose plus increased norepinephrine exposure, and that it is impossible to determine whether the harm related to vasopressin, norepinephrine, their combination or other unmeasured factors. An earlier trial in similarly aged patients, in which vasopressin was rarely used, showed no mortality difference between targets. The review concludes that if shock persists despite a mean pressure of 65–70 mmHg, a higher target may be considered, ideally guided by a short vasopressor test of about 30 minutes, an individualized approach applied in the ANDROMEDA-SHOCK trials.

When central venous pressure is elevated, mean pressure alone becomes an unreliable surrogate for perfusion. The review emphasizes mean perfusion pressure, the difference between mean arterial and central venous pressure, and cites evidence that this difference, but not mean pressure alone, independently predicts acute kidney injury progression, with a critical threshold of 60 mmHg. When venous congestion compromises perfusion pressure, the primary goal should be to reduce central venous pressure; raising mean pressure is a secondary, not yet validated strategy. The authors also note that in abdominal compartment syndrome, elevated intra-abdominal pressure can reduce kidney perfusion pressure even when mean arterial pressure appears preserved.

Diastolic pressure, the review argues, is the most underappreciated component: it is a marker of vasomotor tone, closely related to peripheral resistance, and it can guide the decision to start norepinephrine. It must be interpreted in light of heart rate, since tachycardia shortens diastole and raises diastolic pressure even when tone is normal—a diastolic pressure of 50 mmHg at a heart rate of 90 beats per minute implies higher tone than the same value at 150 beats per minute. Arterial stiffening also lowers diastolic pressure with age, but never to the very low values seen in vasodilatory shock. Diastolic pressure is also the upstream pressure for left coronary perfusion during diastole, so persistently low values raise the risk of myocardial ischemia, particularly with prior coronary disease. In a retrospective study of 77,328 septic patients, thresholds of 48 mmHg overall and 44 mmHg in septic shock were identified, below which the likelihood of acute kidney injury, myocardial damage and mortality rose significantly. Building on this, the diastolic shock index—the ratio of heart rate to diastolic pressure—was proposed as a more robust marker of vascular tone; higher values were strongly associated with increased mortality, its performance was comparable to the SOFA score and lactate, and early norepinephrine initiation appeared to benefit patients with elevated values.

The review also highlights a newly proposed index of vasomotor tone responsiveness to norepinephrine, defined as diastolic pressure divided by the product of heart rate and norepinephrine dose. In a post-hoc analysis of the ANDROMEDA-SHOCK database, this index showed the strongest association with in-hospital mortality compared with diastolic pressure alone, diastolic pressure divided by heart rate, and mean pressure divided by norepinephrine dose, emerging as the most significant covariate in a multivariate model. The relationship with mortality was inverted J-shaped, with a nadir at 6.7 below which mortality increased. The authors suggest that when the index indicates poor responsiveness, adding a vasopressor with a different mechanism, such as vasopressin, may be physiologically sounder than escalating catecholamine doses, though further studies are needed before such decisions can be guided by the index.

Finally, pulse pressure variation during mechanical ventilation offers a dynamic test of fluid responsiveness, reflecting cyclic respiratory changes in stroke volume when both ventricles operate on the ascending portion of the Frank-Starling curve. Its three main limitations are cardiac arrhythmias, tidal volumes below 8 milliliters per kilogram, and spontaneous breathing activity. For low-tidal-volume patients, a tidal volume challenge—measuring the change in pulse pressure variation during a one-minute increase from 6 to 8 milliliters per kilogram, with a difference above 3.5 percent indicating fluid responsiveness—has performed well, including in the prone position, as has measuring the reduction in pulse pressure variation during passive leg raising, which requires no cardiac output monitor. Together, the review argues, these waveform-derived indices support a physiology-driven, individualized approach to resuscitation, transforming the arterial line from a passive safety parameter into an actionable guide for precision hemodynamic management.

Subject of Research: Use of invasive arterial blood pressure components as physiological monitoring and therapeutic guidance tools in critically ill patients

Article Title: Applied physiology at the bedside: using invasive blood pressure as a true monitoring tool

Article References: Bertrand, M., Goury, A., Chemla, D., Teboul, J.-L., & Hamzaoui, O. (2025). Applied physiology at the bedside: using invasive blood pressure as a true monitoring tool. Annals of Intensive Care, 15(1), Article 192. https://doi.org/10.1186/s13613-025-01608-y

Image Credits: AI Generated

DOI: 10.1186/s13613-025-01608-y

Keywords: invasive blood pressure, hemodynamic monitoring, intensive care, septic shock, mean arterial pressure, pulse pressure variation, vasopressors, fluid responsiveness, arterial stiffness, diastolic shock index, norepinephrine, waveform artifacts