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

Abstract

Invasive arterial blood pressure (BP) monitoring is a cornerstone of hemodynamic assessment in critically ill patients. This review explores how the individual components of BP-systolic arterial (SAP), diastolic arterial (DAP), mean arterial (MAP), and pulse pressure (PP)-offer valuable insights into cardiovascular physiology and can be leveraged as real-time therapeutic tools in intensive care settings. A strong emphasis is placed on the technical requirements for accurate BP waveform interpretation and the physiological meaning of each BP component. PP is examined as a surrogate for stroke volume and a dynamic marker of fluid responsiveness, particularly in mechanically ventilated patients. DAP is discussed as a reflection of vasomotor tone, with clinical implications for guiding the initiation of vasopressors. The concept of diastolic shock index (DSI) and the newly proposed VNERi ratio (DAP/[Heart rate × norepinephrine dose]) are introduced as potentially superior markers for assessing vascular tone and vasopressor responsiveness, respectively. These indices may facilitate earlier identification of patients requiring escalation of vasopressor therapy, including the initiation of vasopressin in addition to norepinephrine. The review advocates for a physiology-driven, individualized approach to hemodynamic management, using invasive BP not merely as a safety parameter but as an actionable guide for precision resuscitation.

Keywords: Blood pressure waveform; Diastolic arterial pressure; Mean arterial pressure; Pulse pressure; Pulse pressure variation; Systolic arterial pressure.

Fig. 1

Normal blood pressure curve

Fig. 2

Blood pressure curve and damping artefacts

Fig. 3

Fast flush test: the fast flush test consists of briefly activating the flush device (continuous pressure source of 300 mmHg) to produce a square wave followed by oscillations in the pressure tracing. The test allows assessment of the natural frequency and damping coefficient of the monitoring system. A Underdamped response; B Appropriate response; C Overdamped response

Fig. 4

Pulse wave Amplification between aortic blood pressure and peripheral blood pressure: A In a young subject. B In an old subject

Fig. 5

Physiological phenomenon that transforms discontinuous pulsed blood flow into continuous flow (Windkessel effect)

Fig. 6

Autoregulation curves of organ blood flow based on the presence (red) or absence (blue) of chronic hypertension

Fig. 7

Effect of heart rate on diastolic arterial pressure (DAP). An increase in heart rate reduces the diastolic time and results in higher DAP

Fig. 8

Pulse pression variation (PPV) and Frank-Starling mechanism. Significant increase in stroke volume (SV), which defines preload-responsiveness (blue) is associated with a high PPV. Small increase in SV, which defines preload-unresponsiveness (red), is associated with a low PPV

Fig. 9

A simplified algorithm illustrating how arterial pressure components may assist clinical decision-making in patients with shock. It is important to note that the algorithm does not encompass all possible clinical scenarios; rather, it highlights selected situations where specific components of arterial pressure may be particularly informative. CO: cardiac output; CRT: capillary refill time; CVP: central venous pressure; DAP: diastolic arterial pressure; DSI: diastolic shock index; MAP: mean arterial pressure; MPP: mean perfusion pressure; NE: norepinephrine; PCO₂ gap: difference in carbon dioxide pressure between the central venous blood and the arterial blood; ScvO₂: central venous oxygen saturation; TTE: transthoracic echocardiography