Pulse pressure: more than 100 years of changes in stroke volume

Cecconi, Maurizio; Rhodes, Andrew

doi:10.1007/s00134-011-2155-y

Cited by 4 publications

(3 citation statements)

References 25 publications

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“…Although PP can be affected by vascular tone, this rarely has an impact over a short period of time. PP might thus be a potential candidate for bedside monitoring of the SV changes (26).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of radial artery pulse pressure effects on detection of stroke volume changes after volume loading maneuvers in cardiac surgical patients

Hou¹,

Zheng²,

Ma³

et al. 2020

Ann Transl Med

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Background: Fluid responsiveness is defined as an increase in cardiac output (CO) or stroke volume (SV) of >10-15% after fluid challenge (FC). However, CO or SV monitoring is often not available in clinical practice. The aim of this study was to evaluate whether changes in radial artery pulse pressure (rPP) induced by FC or passive leg raising (PLR) correlates with changes in SV in patients after cardiac surgery.Methods: This prospective observational study included 102 patients undergoing cardiac surgery, in which rPP and SV were recorded before and immediately after a PLR test and FC with 250 mL of Gelofusine for 10 min. SV was measured using pulse contour analysis. Patients were divided into responders (≥15% increase in SV after FC) and non-responders. The hemodynamic variables between responders and non-responders were analyzed to assess the ability of rPP to track SV changes.Results: A total of 52% patients were fluid responders in this study. An rPP increase induced by FC was significantly correlated with SV changes after a FC (ΔSV-FC, r=0.62, P<0.01). A fluid-induced increase in rPP (ΔrPP-FC) of >16% detected a fluid-induced increase in SV of >15%, with a sensitivity of 91% and a specificity of 73%. The area under the receiver operating characteristic curve (AUROC) for the fluidinduced changes in rPP identified fluid responsiveness was 0.881 (95% CI: 0.802-0.937). A grey zone of 16-34% included 30% of patients for ΔrPP-FC. The ΔrPP-PLR was weakly correlated with ΔSV-FC (r=0.30, P<0.01). An increase in rPP induced by PLR (ΔrPP-PLR) predicted fluid responsiveness with an AUROC of 0.734 (95% CI: 0.637-0.816). A grey zone of 10-23% included 52% of patients for ΔrPP-PLR.Conclusions: Changes in rPP might be used to detect changes in SV via FC in mechanically ventilated patients after cardiac surgery. In contrast, changes in rPP induced by PLR are unreliable predictors of fluid responsiveness.

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“…Although PP can be affected by vascular tone, this rarely has an impact over a short period of time. PP might thus be a potential candidate for bedside monitoring of the SV changes (26).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of radial artery pulse pressure effects on detection of stroke volume changes after volume loading maneuvers in cardiac surgical patients

Hou¹,

Zheng²,

Ma³

et al. 2020

Ann Transl Med

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“…Excess venous capacity leads to a decrease in venous return during lung inflation and an increase in venous return as the thoracic cage relaxes during expiration. High PPV and SVV are good indicators of inadequate blood volume and thus pre-load responsiveness [8,9] Although there is no net volume deficit following induction the increased capacity of the venous system is the basis for the reduced SV, CO and MAP. For any given inflow to the venous system, the larger venous pathway will result in a delay in the arrival of blood at the heart with a reduction in preload and cardiac output (CO).…”

Section: Evidence For Venous Relaxation and Its Effect On Cardiac Outputmentioning

confidence: 99%

Clarification of the circulatory patho-physiology of anaesthesia – Implications for high-risk surgical patients

Wolff

Green

2014

International Journal of Surgery

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The paper examines the effects of anaesthesia on circulatory physiology and their implications regarding improvement in perioperative anaesthetic management. Changes to current anaesthetic practice, recommended recently, such as the use of flow monitoring in high risk patients, are already beginning to have an impact in reducing complications but not mortality [1]. Better understanding of the patho-physiology should help improve management even further. Analysis of selected individual clinical trials has been used to illustrate particular areas of patho-physiology and how changes in practice have improved outcome. There is physiological support for the importance of achieving an appropriate rate of oxygen delivery (DO2), particularly following induction of anaesthesia. It is suggested that ensuring adequate DO2 during anaesthesia will avoid development of oxygen debt and hence obviate the need to induce a high, compensatory, DO2 in the post-operative period. In contrast to the usual assumptions underlying strategies requiring a global increase in blood flow [1] by a stroke volume near maximization strategy, blood flow control actually resides entirely at the tissues not at the heart. This is important as the starting point for understanding failed circulatory control as indicated by 'volume dependency'. Local adjustments in blood flow at each individual organ - auto-regulation - normally ensure the appropriate local rate of oxygen supply, i.e. local DO2. Inadequate blood volume leads to impairment of the regulation of blood flow, particularly in the individual tissues with least capable auto-regulatory capability. As demonstrated by many studies, inadequate blood flow first occurs in the gut, brain and kidney. The inadequate blood volume which occurs with induction of anaesthesia is not due to blood volume loss, but probably results from redistribution due to veno-dilation. The increase in venous capacity renders the existing blood volume inadequate to maintain venous return and pre-load. Blood volume shifted to the veins will, necessarily, also reduce the arterial volume. As a result stroke volume and cardiac output fall below normal with little or no change in peripheral resistance. The resulting pre-load dependency is often successfully treated with colloid infusion and, in some studies, 'inotropic' agents, particularly in the immediate post-operative phase. Treatment during the earliest stage of anaesthesia can avoid the build up of oxygen debt and may be supplemented by drugs which maintain or restore venous tone, such as phenylephrine; an alternative to volume expansion. Interpretation of circulatory patho-physiology during anaesthesia confirms the need to sustain appropriate oxygen delivery. It also supports reduction or even elimination of supplementary crystalloid maintenance infusion, supposedly to replace the "mythical" third space loss. As a rational evidence base for future research it should allow for further improvements in anaesthetic management.

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“…Thus, Ohm's law predicts that the mean arterial pressure and cardiac output are mathematically related; on the other hand, the pulse pressure reflects the pulsatile component of blood pressure [2]. The Vigileo™/FloTrec™ technology is based on the direct proportionality of pulse pressure and stroke volume [3,4,5]. As a consequence, the pressure ejection fraction can be viewed as a parameter containing pressure and flow.…”

mentioning

confidence: 99%

Ejection fractions and pressure–heart rate product to evaluate cardiac efficiency

Kunig¹,

Tassani-Prell

Engelmann

2013

Med Klin Intensivmed Notfmed

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Continuous, real-time diagnosis using blood pressure and heart rate (Volume) ejection fractions, defined as the ratio of difference of ventricular volumes prior to and after ejection of blood measures to the ventricular volume prior to ejection, measure the efficiency with which the heart pumps. The American Heart Association recognizes it as a quality indicator in the management of heart failure patients [1]. Universal use of (volume) ejection fraction as a diagnostic tool is limited by the lack of continuous measurements. As the heart must satisfy instant demand, ejection fraction should be measured continuously, in real time, and preferably noninvasively. These conditions can be met, if (pressure) ejection fractions are derived from blood pressure data.The numerator of the pressure ejection fraction is represented by the pulse pressure. Clinical experience shows that pulse pressure provides information concerning blood flow. In case of an equal arterial mean pressure of 65 mmHg, the peripheral tissue of the extremities will be cold in low pulse pressure of 75/60 mmHg compared with warm skin in higher pulse pressure of 105/50 mmHg, for example.The pulse wave analysis technology, applied in PiCCO™ and Vigileo-™/ FloTrec™, draws flow information from arterial blood pressure. Thus, Ohm's law predicts that the mean arterial pressure and cardiac output are mathematically related; on the other hand, the pulse pressure reflects the pulsatile component of blood pressure [2]. The Vigileo™/FloTrec™ technology is based on the direct proportionality of pulse pressure and stroke volume [3,4,5]. As a consequence, the pressure ejection fraction can be viewed as a parameter containing pressure and flow.Another important parameter is the pressure-heart rate product [6], which is given by the product of systolic pressure and heart rate. The product has been found to be indicative of myocardial oxygen consumption. It can also be measured continuously and non-invasively; thus, it reflects instant status.The objective of this investigation is to determine whether ejection fractions derived as the ratio of the difference of arterial systolic pressure and arterial diastolic pressure to arterial systolic pressure, pressure-heart rate product, and/or combinations thereof yield useful diagnostic results, which may be obtained noninvasively, continuously, and in real time. A further objective is to demonstrate the possible use of ejection fractions and the pressure-heart rate product to monitor patient safety. Materials and methods (Volume) ejection fraction, EF(V) is defined aswhere EDV is the end-diastolic volume and ESV is the end-systolic volume. In analogy to the definition of EF(V), a (pressure) ejection fraction, EF(P), can be defined as

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Pulse pressure: more than 100 years of changes in stroke volume

Cited by 4 publications

References 25 publications

Evaluation of radial artery pulse pressure effects on detection of stroke volume changes after volume loading maneuvers in cardiac surgical patients

Evaluation of radial artery pulse pressure effects on detection of stroke volume changes after volume loading maneuvers in cardiac surgical patients

Clarification of the circulatory patho-physiology of anaesthesia – Implications for high-risk surgical patients

Ejection fractions and pressure–heart rate product to evaluate cardiac efficiency

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