Cardiac output obtained by pulse pressure analysis: to calibrate or not to calibrate may not be the only question when used properly

AbstractDynamic parameters of preload have been widely recommended to guide fluid therapy based on the principle of fluid responsiveness and with regard to cardiac output. An equally important aspect is however to also avoid volume-overload. This accounts particularly when capillary leakage is present and volume-overload will promote impairment of microcirculatory blood flow. The aim of this study was to evaluate, whether an impairment of intestinal microcirculation caused by volume-load potentially can be predicted using pulse pressure variation in an experimental model of ischemia/reperfusion injury. The study was designed as a prospective explorative large animal pilot study. The study was performed in 8 anesthetized domestic pigs (German landrace). Ischemia/reperfusion was induced during aortic surgery. 6 h after ischemia/reperfusion-injury measurements were performed during 4 consecutive volume-loading-steps, each consisting of 6 ml kg−1 bodyweight−1. Mean microcirculatory blood flow (mean Flux) of the ileum was measured using direct laser-speckle-contrast-imaging. Receiver operating characteristic analysis was performed to determine the ability of pulse pressure variation to predict a decrease in microcirculation. A reduction of ≥ 10% mean Flux was considered a relevant decrease. After ischemia–reperfusion, volume-loading-steps led to a significant increase of cardiac output as well as mean arterial pressure, while pulse pressure variation and mean Flux were significantly reduced (Pairwise comparison ischemia/reperfusion-injury vs. volume loading step no. 4): cardiac output (l min−1) 1.68 (1.02–2.35) versus 2.84 (2.15–3.53), p = 0.002, mean arterial pressure (mmHg) 29.89 (21.65–38.12) versus 52.34 (43.55–61.14), p < 0.001, pulse pressure variation (%) 24.84 (17.45–32.22) versus 9.59 (1.68–17.49), p = 0.004, mean Flux (p.u.) 414.95 (295.18–534.72) versus 327.21 (206.95–447.48), p = 0.006. Receiver operating characteristic analysis revealed an area under the curve of 0.88 (CI 95% 0.73–1.00; p value < 0.001) for pulse pressure variation for predicting a decrease of microcirculatory blood flow. The results of our study show that pulse pressure variation does have the potential to predict decreases of intestinal microcirculatory blood flow due to volume-load after ischemia/reperfusion-injury. This should encourage further translational research and might help to prevent microcirculatory impairment due to excessive fluid resuscitation and to guide fluid therapy in the future.

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Do changes in pulse pressure variation and inferior vena cava distensibility during passive leg raising and tidal volume challenge detect preload responsiveness in case of low tidal volume ventilation?

Critical Care ◽

10.1186/s13054-021-03515-7 ◽

2021 ◽

Vol 25 (1) ◽

Author(s):

Temistocle Taccheri ◽

Francesco Gavelli ◽

Jean-Louis Teboul ◽

Rui Shi ◽

Xavier Monnet

Keyword(s):

Cardiac Output ◽

Inferior Vena Cava ◽

Tidal Volume ◽

Pulse Pressure ◽

Pulse Pressure Variation ◽

Inferior Vena ◽

Vena Cava ◽

Pressure Variation ◽

Diagnostic Threshold ◽

Preload Responsiveness

Abstract Background In patients ventilated with tidal volume (Vt) < 8 mL/kg, pulse pressure variation (PPV) and, likely, the variation of distensibility of the inferior vena cava diameter (IVCDV) are unable to detect preload responsiveness. In this condition, passive leg raising (PLR) could be used, but it requires a measurement of cardiac output. The tidal volume (Vt) challenge (PPV changes induced by a 1-min increase in Vt from 6 to 8 mL/kg) is another alternative, but it requires an arterial line. We tested whether, in case of Vt = 6 mL/kg, the effects of PLR could be assessed through changes in PPV (ΔPPVPLR) or in IVCDV (ΔIVCDVPLR) rather than changes in cardiac output, and whether the effects of the Vt challenge could be assessed by changes in IVCDV (ΔIVCDVVt) rather than changes in PPV (ΔPPVVt). Methods In 30 critically ill patients without spontaneous breathing and cardiac arrhythmias, ventilated with Vt = 6 mL/kg, we measured cardiac index (CI) (PiCCO2), IVCDV and PPV before/during a PLR test and before/during a Vt challenge. A PLR-induced increase in CI ≥ 10% defined preload responsiveness. Results At baseline, IVCDV was not different between preload responders (n = 15) and non-responders. Compared to non-responders, PPV and IVCDV decreased more during PLR (by − 38 ± 16% and − 26 ± 28%, respectively) and increased more during the Vt challenge (by 64 ± 42% and 91 ± 72%, respectively) in responders. ∆PPVPLR, expressed either as absolute or as percent relative changes, detected preload responsiveness (area under the receiver operating curve, AUROC: 0.98 ± 0.02 for both). ∆IVCDVPLR detected preload responsiveness only when expressed in absolute changes (AUROC: 0.76 ± 0.10), not in relative changes. ∆PPVVt, expressed as absolute or percent relative changes, detected preload responsiveness (AUROC: 0.98 ± 0.02 and 0.94 ± 0.04, respectively). This was also the case for ∆IVCDVVt, but the diagnostic threshold (1 point or 4%) was below the least significant change of IVCDV (9[3–18]%). Conclusions During mechanical ventilation with Vt = 6 mL/kg, the effects of PLR can be assessed by changes in PPV. If IVCDV is used, it should be expressed in percent and not absolute changes. The effects of the Vt challenge can be assessed on PPV, but not on IVCDV, since the diagnostic threshold is too small compared to the reproducibility of this variable. Trial registration: Agence Nationale de Sécurité du Médicament et des Produits de santé: ID-RCB: 2016-A00893-48.

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SEMI INVASIVE CARDIAC OUTPUT MONITORING IN A CARDIAC PATIENT UNDERGOING TOTAL THYROIDECTOMY USING SMARTPHONE APP CAPSTESIA.

10.36106/ijsr/9114469 ◽

2021 ◽

pp. 4-5

Author(s):

Santosh Kumar Rai ◽

Vishal Vashist ◽

Deepak Bhardwaj ◽

Bhanu Gupta

Keyword(s):

Cardiac Output ◽

Cardiac Index ◽

Real Time ◽

Hemodynamic Monitoring ◽

Pulse Pressure ◽

Pulse Pressure Variation ◽

Output Pulse ◽

Pressure Variation ◽

Smartphone App ◽

Arterial Waveform

Introduction: Advanced hemodynamic monitoring is need of today especially in patients with limited cardiac reserve. With the advent of smartphones & specially designed applications, hemodynamic monitoring becomes quite easy. Materials & Methods: Patient was pre – medicated with Inj. Fentanyl & inj. Glycopyrrolate, induced with Inj. Etomidate & Inj. Vecuronium and maintained with mixture ofIsourane, Nitrous Oxide & Oxygen. An arterial line was secured in Left Radial Artery. We used the CAPSTESIA app to take picture of the arterial waveform using a smartphone. Demographic data of the patient was fed in the app. App used it's pre- fed algorithm to give the real time Cardiac Output, Pulse Pressure variations, Cardiac Index based upon the arterial waveform. Results: Using the application we were able to monitor the cardiac output of the patient in real time using semi- invasive means. It enabled us to regulate the uid management of the patient and avoid any adverse cardiac events (hypotension). With Pulse Pressure variation also available in real time, we were able to restrict use of vasopressors since the Left Ventricle Ejection Fraction of the patient was 35 % on ECHO. Surgery was conducted without any untoward event. Patient was successfully extubated and sent to PACU. Conclusions:Advanced hemodynamic monitoring is time consuming using manual methods. We found the smartphone app CAPSTESIA pretty useful for semi-invasive hemodynamic monitoring of the Cardiac Output, Pulse Pressure variation, Cardiac Index,etc in real time.

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Evaluation of cardiac output variations with the peripheral pulse pressure to mean arterial pressure ratio

Journal of Clinical Monitoring and Computing ◽

10.1007/s10877-018-0210-8 ◽

2018 ◽

Vol 33 (4) ◽

pp. 581-587 ◽

Cited By ~ 1

Author(s):

Audrey Tantot ◽

Anais Caillard ◽

Arthur Le Gall ◽

Joaquim Mateo ◽

Sandrine Millasseau ◽

...

Keyword(s):

Cardiac Output ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Pulse Pressure ◽

Pressure Ratio ◽

Peripheral Pulse

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Postoperative Vasodilatory Shock

Cardiothoracic Critical Care ◽

10.1093/med/9780190082482.003.0035 ◽

2020 ◽

pp. 333-342

Author(s):

Fiona Roberts ◽

Alan Gaffney

Keyword(s):

Septic Shock ◽

Cardiac Output ◽

Fluid Resuscitation ◽

Antimicrobial Therapy ◽

Pulse Pressure ◽

Vasodilatory Shock ◽

First Line ◽

Treatment Interventions ◽

Common Cause ◽

Early Fluid

This chapter discusses vasodilatory shock. The hallmark of vasodilatory shock is hypotension with normal or increased cardiac output. The hyperdynamic circulatory state of vasodilatory shock results in a tachycardia and an increased pulse pressure. Radiological and biochemical investigations can assist with determining the diagnosis of shock. The causes of vasodilatory shock are diverse; they include sepsis, surgical insult, anaphylaxis, and others such as trauma, burns, and pancreatitis. However, sepsis is by far the most common cause of vasodilatory shock. The pathophysiology of vasodilatory shock is also complex and multifactorial. Although still not fully understood, it is widely accepted that it includes activation of several intrinsic vasodilatory pathways and a vascular hyporesponsiveness to vasopressors. Early fluid resuscitation and appropriate antimicrobial therapy are the most crucial treatment interventions in septic shock. Meanwhile, noradrenaline is the first-line vasopressor of choice in septic shock.

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THE CARDIAC OUTPUT AND CAROTID AND TIBIAL BLOOD PRESSURE OF THE TURKEY

Canadian Journal of Biochemistry and Physiology ◽

10.1139/o63-262 ◽

1963 ◽

Vol 41 (11) ◽

pp. 2337-2341 ◽

Cited By ~ 9

Author(s):

Elwood W. Speckmann ◽

Robert K. Ringer

Keyword(s):

Body Weight ◽

Cardiac Output ◽

Pulse Pressure ◽

Mature Male ◽

Systemic Resistance ◽

Hemodynamic Parameters ◽

Radioactive Phosphorus ◽

Arterial Blood ◽

Tibial Arteries ◽

The Mean

The cardiac output of untreated mature male Broad Breasted Bronze (BBB) turkeys was determined by an isotope dilution technique using radioactive phosphorus (P32). A Geiger–Mueller tube was connected to a rate meter which in turn was connected to a moving graph to continuously record the indicator concentration, thus obtaining the initial dilution curve. Posterior tibial and common carotid arterial blood pressures were measured directly and were recorded simultaneously with the cardiac output determinations by means of two strain gauges connected to a recording polygraph.From the cardiovascular measurements systemic resistance was calculated. The mean cardiac output of the mature male BBB turkey was 231 ml per kg body weight0.734 per minute. The mean carotid hemodynamic parameters were: systolic BP, 302 mm Hg; diastolic BP, 204 mm Hg; and pulse pressure, 98 mm Hg. Heart rate was 149 beats per minute. The mean tibial hemodynamic parameters were; systolic BP, 286 mm Hg; diastolic BP, 200 mm Hg; and pulse pressure, 85 mm Hg. The mean systemic resistance units were 0.17 and 0.16 for carotid and tibial arteries respectively on a bird basis and 1.13 and 1.08 respectively per kg body weight0.734.

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Central Venous Pulse Pressure Analysis Using an R-Synchronized Pressure Measurement System

Journal of Clinical Monitoring and Computing ◽

10.1007/s10877-006-9035-y ◽

2006 ◽

Vol 20 (6) ◽

pp. 385-389 ◽

Cited By ~ 2

Author(s):

Yoshihisa Fujita ◽

Daisuke Hayashi ◽

Shinya Wada ◽

Naoki Yoshioka ◽

Takeshi Yasukawa ◽

...

Keyword(s):

Measurement System ◽

Pulse Pressure ◽

Pressure Measurement ◽

Central Venous ◽

Venous Pulse ◽

Pressure Measurement System ◽

Pressure Analysis

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The influence of different surgical procedures on hypertension after repair of coarctation

Cardiology in the Young ◽

10.1017/s1047951105001332 ◽

2005 ◽

Vol 15 (5) ◽

pp. 477-480 ◽

Cited By ~ 11

Author(s):

Ugo Giordano ◽

Salvatore Giannico ◽

Attilio Turchetta ◽

Fatma Hammad ◽

Flaminia Calzolari ◽

...

Keyword(s):

Blood Pressure ◽

Cardiac Output ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Systolic Blood Pressure ◽

Diastolic Blood Pressure ◽

Pulse Pressure ◽

Ambulatory Monitoring ◽

Peak Exercise ◽

End To End

We measured resting and exercise haemodynamics, as well as 24-hour ambulatory blood pressure, so as to study the influence on development of hypertension in children after repair of coarctation by either construction of a subclavian flap or end-to-end anastamosis. The patients in both groups were studied a mean time of 13 years after surgery. Thus, we divided 43 children who had undergone surgical repair of coarctation, and who were not on antihypertensive therapy, into a group of 22 patients who had undergone subclavian flap repair, with a mean age of 14 plus or minus 2.6 years, and another group of 21 patients undergoing end-to-end anastomosis, with a mean age of 13.5 plus or minus 3.9 years. We examined blood pressure at rest and during exercise, along with the measurement of cardiac output using impedance cardiography, and during 24-hour ambulatory monitoring. We recorded systolic and diastolic blood pressures, pulse pressure, cardiac output and total peripheral vascular resistance at rest and at peak exercise. During ambulatory monitoring, we measured mean pressures over 24 hours, in daytime and nighttime, 24-hour pulse pressure, and 24-hour mean arterial pressure. Student's t test was used to judge significance, accepting this when p was less than 0.05. The group repaired using the subclavian flap showed significantly disadvantageous differences for diastolic blood pressure at rest, systolic blood pressure at peak exercise and for 24-hour systolic and diastolic blood pressure, 24-hour mean arterial pressure, and daytime and nighttime systolic blood pressure during ambulatory monitoring. Our findings suggest that, after repair using the subclavian flap in comparison to end-to-end anastomosis, patients show a higher incidence of late hypertension, both during exercise and ambulatory monitoring. The data indicate different residual aortic stiffnesses, these being lower after end-to-end anastomosis, which may be due to the greater resection of the abnormal aortic tissue when coarctation is repaired using the latter technique.

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Cardiac output by Modelflow® method from intra-arterial and fingertip pulse pressure profiles

Clinical Science ◽

10.1042/cs20030303 ◽

2004 ◽

Vol 106 (4) ◽

pp. 365-369 ◽

Cited By ~ 55

Author(s):

Marcel AZABJI KENFACK ◽

Federic LADOR ◽

Marc LICKER ◽

Christian MOIA ◽

Enrico TAM ◽

...

Keyword(s):

Cardiac Output ◽

Steady State ◽

Radial Artery ◽

Pulse Pressure ◽

Pressure Head ◽

Mean Values ◽

Pressure Profiles ◽

Contralateral Hand ◽

Left Radial Artery ◽

Q Values

Modelflow®, when applied to non-invasive fingertip pulse pressure recordings, is a poor predictor of cardiac output (Q, litre·min-1). The use of constants established from the aortic elastic characteristics, which differ from those of finger arteries, may introduce signal distortions, leading to errors in computing Q. We therefore hypothesized that peripheral recording of pulse pressure profiles undermines the measurement of Q with Modelflow®, so we compared Modelflow® beat-by-beat Q values obtained simultaneously non-invasively from the finger and invasively from the radial artery at rest and during exercise. Seven subjects (age, 24.0±2.9 years; weight, 81.2±12.6 kg) rested, then exercised at 50 and 100 W, carrying a catheter with a pressure head in the left radial artery and the photoplethysmographic cuff of a finger pressure device on the third and fourth fingers of the contralateral hand. Pulse pressure from both devices was recorded simultaneously and stored on a PC for subsequent Q computation. The mean values of systolic, diastolic and mean arterial pressure at rest and exercise steady state were significantly (P<0.05) lower from the finger than the intra-arterial catheter. The corresponding mean steady-state Q obtained from the finger (Qporta) was significantly (P<0.05) higher than that computed from the intra-arterial recordings (Qpia). The line relating beat-by-beat Qporta and Qpia was y=1.55x-3.02 (r2=0.640). The bias was 1.44 litre·min-1 and the precision was 2.84 litre·min-1. The slope of this line was significantly higher than 1, implying a systematic overestimate of Q by Qporta with respect to Qpia. Consistent with the tested hypothesis, these results demonstrate that pulse pressure profiles from the finger provide inaccurate absolute Q values with respect to the radial artery, and therefore cannot be used without correction with a calibration factor calculated previously by measuring Q with an independent method.

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