Central Venous Pressure Variation Research Articles

Diagnostic accuracy of the peripheral venous pressure variation induced by an alveolar recruitment maneuver to predict fluid responsiveness during high-risk abdominal surgery

BackgroundIn patients undergoing high-risk surgery, it is recommended to titrate fluid administration using stroke volume or a dynamic variable of fluid responsiveness (FR). However, this strategy usually requires the use of a hemodynamic monitor and/or an arterial catheter. Recently, it has been shown that variations of central venous pressure (ΔCVP) during an alveolar recruitment maneuver (ARM) can predict FR and that there is a correlation between CVP and peripheral venous pressure (PVP). This prospective study tested the hypothesis that variations of PVP (ΔPVP) induced by an ARM could predict FR.MethodsWe studied 60 consecutive patients scheduled for high-risk abdominal surgery, excluding those with preoperative cardiac arrhythmias or right ventricular dysfunction. All patients had a peripheral venous catheter, a central venous catheter and a radial arterial catheter linked to a pulse contour monitoring device. PVP was always measured via an 18-gauge catheter inserted at the antecubital fossa. Then an ARM consisting of a standardized gas insufflation to reach a plateau of 30 cmH2O for 30 s was performed before skin incision. Invasive mean arterial pressure (MAP), pulse pressure, heart rate, CVP, PVP, pulse pressure variation (PPV), and stroke volume index (SVI) were recorded before ARM (T1), at the end of ARM (T2), before volume expansion (T3), and one minute after volume expansion (T4). Receiver-operating curves (ROC) analysis with the corresponding grey zone approach were performed to assess the ability of ∆PVP (index test) to predict FR, defined as an ≥ 10% increase in SVI following the administration of a 4 ml/kg balanced crystalloid solution over 5 min.Results∆PVP during ARM predicted FR with an area under the ROC curve of 0.76 (95%CI, 0.63 to 0.86). The optimal threshold determined by the Youden Index was a ∆PVP value of 5 mmHg (95%CI, 4 to 6) with a sensitivity of 66% (95%CI, 47 to 81) and a specificity of 82% (95%CI, 63 to 94). The AUC’s for predicting FR were not different between ΔPVP, ΔCVP, and PPV.ConclusionDuring high-risk abdominal surgery, ∆PVP induced by an ARM can moderately predict FR. Nevertheless, other hemodynamic variables did not perform better.

Respiratory Variations of Central Venous Pressure as Indices of Pleural Pressure Swings: A Narrative Review

The measurement of pleural (or intrathoracic) pressure is a key element for a proper setting of mechanical ventilator assistance as both under- and over-assistance may cause detrimental effects on both the lungs and the diaphragm. Esophageal pressure (Pes) is the gold standard tool for such measurements; however, it is invasive and seldom used in daily practice, and easier, bedside-available tools that allow for rapid and continuous monitoring are greatly needed. The tidal swing of central venous pressure (CVP) has long been proposed as a surrogate for pleural pressure (Ppl); however, despite the wide availability of central venous catheters, this variable is very often overlooked in critically ill patients. In the present narrative review, the physiological basis for the use of CVP waveforms to estimate Ppl is presented; the findings of previous and recent papers that addressed this topic are systematically reviewed, and the studies are divided into those reporting positive findings (i.e., CVP was found to be a reliable estimate of Pes or Ppl) and those reporting negative findings. Both the strength and pitfalls of this approach are highlighted, and the current knowledge gaps and direction for future research are delineated.

Variations of pulse pressure and central venous pressure may predict fluid responsiveness in mechanically ventilated patients during lung recruitment manoeuvre: an ancillary study

BackgroundMaintaining a constant driving pressure during a prolonged sigh breath lung recruitment manoeuvre (LRM) from 20 to 45 cmH20 peak inspiratory pressure in mechanically ventilated patients has been shown to be a functional test to predict fluid responsiveness (FR) when using a linear regression model of hemodynamic parameters, such as central venous pressure (CVP) and pulse pressure (PP). However, two important limitations have been raised, the use of high ventilation pressures and a regression slope calculation that is difficult to apply at bedside. This ancillary study aimed to reanalyse absolute variations of CVP (ΔCVP) and PP (ΔPP) values at lower stages of the LRM, (40, 35, and 30 cm H20 of peak inspiratory pressure) for their ability to predict fluid responsiveness.MethodsRetrospective analysis of a prospective study data set in 18 mechanically ventilated patients, in an intensive care unit. CVP, systemic arterial pressure parameters and stroke volume (SV) were recorded during prolonged LRM followed by a 500 mL crystalloid volume expansion. Patients were considered as fluid responders if SV increased more than 10%. Receiver-operating curves (ROC) analysis with the corresponding grey zone approach were performed.ResultsAreas under the ROC to predict fluid responsiveness for ΔCVP and ΔPP were not different between the successive stepwise increase of inspiratory pressures [0.88 and 0.89 for ΔCVP at 45 and 30 cm H20 (P = 0.89), respectively, and 0.92 and 0.95 for ΔPP at 45 and 30 cm H20, respectively (P = 0.51)]. Using a maximum of 30 cmH2O inspiratory pressure during the LRM, ΔCVP and ΔPP had a threshold value to predict fluid responsiveness of 2 mmHg and 4 mmHg, with sensitivities of 89% and 89% and specificities of 67% and 89%, respectively. Combining ΔPP and ΔCVP decreased the proportion of the patients in the grey zone from 28 to 11% and showed a sensitivity of 88% and a specificity of 83%.ConclusionsA stepwise PEEP elevation recruitment manoeuvre of up to 30 cm H20 may predict fluid responsiveness as well as 45 cm H20. The combination of ΔPP and ΔCVP optimizes the categorization of responder and non-responder patients.

Ventilator-induced central venous pressure variation can predict fluid responsiveness in post-operative cardiac surgery patients.

Ventilator-induced dynamic hemodynamic parameters such as stroke volume variation (SVV) and pulse pressure variation (PPV) have been shown to predict fluid responsiveness in contrast to static hemodynamic parameters such as central venous pressure (CVP). We hypothesized that the ventilator-induced central venous pressure variation (CVPV) could predict fluid responsiveness. Twenty-two elective cardiac surgery patients were studied post-operatively on the intensive care unit during mechanical ventilation with tidal volumes of 6-8 ml/kg without spontaneous breathing efforts or cardiac arrhythmia. Before and after administration of 500mL hydroxyethyl starch, SVV and PPV were measured using pulse contour analysis by modified Modelflow® , while CVP was obtained from a central venous catheter positioned in the superior vena cava. CVPV was calculated as 100 × (CVPmax -CVPmin )/[(CVPmax + CVPmin) /2]. Nineteen patients (86%) were fluid responders defined as an increase in cardiac output of ≥ 15% after fluid administration. CVPV decreased upon fluid loading in responders, but not in non-responders. Baseline CVP values showed no correlation with a change in cardiac output in contrast to baseline SVV (r = 0.60, P = 0.003), PPV (r = 0.58, P = 0.005), and CVPV (r = 0.63, P = 0.002). Baseline values of SVV > 9% and PPV > 8% could predict fluid responsiveness with a sensitivity of 89% and 95%, respectively, both with a specificity of 100%. Baseline CVPV could identify all fluid responders and non-responders correctly at a cut-off value of 12%. There was no difference between the area under the receiver operating characteristic curves of SVV, PPV, and CVPV. The use of ventilator-induced CVPV could predict fluid responsiveness similar to SVV and PPV in post-operative cardiac surgery patients.

Hemodynamics and oxygen transport dynamics during hepatic resection at different central venous pressures in a pig model

Although low central venous pressure (CVP) has been used to minimize blood loss during hepatectomy, the impact of variations of CVP on the rate of blood loss and on the perfusion of end-organs has not been evaluated. This animal study aimed to evaluate the hemodynamics and oxygen transport changes during hepatic resection at different CVP levels. Forty-eight anesthetized Bama miniature pigs were divided into 8 groups with CVP during hepatic resection controlled at 0 to <1, 1 to <2, 2 to <3, 3 to <4, 4 to <5, 5 to <6, 6 to <7, and 7 to <8 cmH2O. Intergroup comparisons were made for hemodynamic parameters, oxygen transport dynamics, and the rate of blood loss. The rate of blood loss and the hepatic venous pressure during hepatic resection were almost linearly related to the CVP. A significant drop in the mean arterial pressure, cardiac output, and cardiac index occurred between CVP ≥2 and <2 cmH2O. Oxygen delivery (DO2), oxygen consumption (VO2) and oxygen extraction ratio (ERO2) remained relatively constant between CVPs of 2 to <8 cmH2O. There was a significant drop in DO2 when the CVP was <2 cmH2O. There was also a significant drop in VO2 and ExO2 when the CVP was <1 cmH2O. The optimal CVP for hepatic resection is 2 to 3 cmH2O.

Determinants of arterial and central venous blood pressure variation in ventilated critically ill children

Ventilation-induced arterial pressure variation predicts volume responsiveness in adults. Several factors are known to influence the interpretability of these variations. We analysed ventilation-induced variations in critically ill children with reference to ventilatory and circulatory parameters. We prospectively included 20 paediatric patients. Variation of systolic pressure (SPV), pulse pressure (PPV) and central venous pressure (CVP) were assessed during pressure-controlled ventilation with inspiratory pressures (P(insp)) of 20 and 28 cmH(2)O. Blood gases were analysed and echocardiography was performed. SPV, PPV and CVP variation significantly increased with elevated P(insp) (p < 0.001, p = 0.008 and p = 0.003). Baseline CVP and shortening fraction were significant negative predictors of PPV and SPV. This preliminary study identified P(insp) as a determinant of SPV, PPV and CVP variation in children. Further independent determinants of SPV and PPV were baseline CVP and ventricular performance, both of which must be considered when interpreting pressure variations.

Avaliação da responsividade a volume em pacientes sob ventilação espontânea

To assess fluid responsiveness in patients under spontaneous breathing activity ventilation remains a challenge for intensive care physicians. Much of the knowledge on heart-lung interactions and dynamic indexes of fluid responsiveness may not be useful for these patients. Historically, the most frequently used variables to guide fluid responsiveness on this population have been the static preload indexes. However, more recently, dynamic indexes from less invasive devices are being often used, even though their usefulness on spontaneously-breathing subjects remains controversial. The purpose of this article was to review evidences on the assessment of fluid responsiveness in patients under spontaneous ventilation. A search in literature showed poor evidence for use of static variables, such as filling pressures and ventricular end-diastolic volumes. Dynamic indexes, such as pulse pressure variation and other indexes had not been appropriately tested during spontaneous ventilation. Favorable results were found with central venous pressure variation and with transthoracic echocardiography or transesophageal Doppler dynamic indexes, especially when associated to passive lower limb elevation. We conclude that although central venous pressure variation and echocardiography variables could aid bedside clinicians in assessing fluid responsiveness during spontaneous ventilation, more studies on this subject are definitely required.

The effect of airway obstruction on systolic arterial and central venous pressure during sedation in patients undergoing total knee replacement.

Severe respiratory variations of systolic arterial and central venous pressure (CVP) may increase the risk of embolic event in orthopedic patient. As airway obstruction during sedation can cause this respiratory variation, we evaluated the degree of variations of systolic blood (SBP) and CVP during airway obstruction period. Fifteen females who had obstructed airway during total knee replacement (TKR) were included for the study. After regional anesthesia were established, SBP and CVP variations were analyzed according to the three periods; baseline, obstruction, and airway, respectively. Calculated CVP variables were similar to SBP variables as below: DeltaSBP = Expmax (maximal value at expiration) - Inspnadir (minimal value at inspiration), %DeltaSBP = (DeltaSBP/ Exp(max)) x 100. The frequencies of pulsus paradoxus (PP) and negative inspiratory CVP (NIC) were also measured. At obstruction period, DeltaSBP was 21.7 mmHg and 93.3% of patient had PP. Also, DeltaCVP was 19.3 mmHg and 100% of patient showed NIC. %DeltaCVP (140%) was larger than %DeltaSBP (16%). And DeltaCVP was inversely correlated with baseline and obstruction SBP and %DeltaCVP was also inversely correlated with baseline CVP at obstruction period. During airway obstruction in sedated TKR patients, variations of CVP are larger than those of SBP. So we have to monitor CVP continuously as well as SBP so as not to increase the possible risk of respiratory of variation.

Blood pressure modulation by central venous pressure and respiration. Buffering effects of the heart rate reflexes.

Despite constant fluctuations in cardiac preload caused by the effects of respiration and changes in posture on venous return to the heart, arterial blood pressure remains remarkably constant. The effects of instantaneous lung volume (ILV) and variations of central venous pressure (CVP) on blood pressure (BP) were studied by use of frequency domain techniques to quantify the contribution of heart rate (HR) reflexes to attenuation of the effects of changes in right ventricular preload on arterial pressure. Random independent variation of ILV, then CVP (obtained using lower-body negative pressure), was performed in eight humans in the supine position. HR, ILV, CVP, and systolic (SBP) and diastolic (DBP) BPs were recorded during control periods and after complete blockade obtained by use of 0.04 mg/kg atropine and 0.2 mg/kg propranolol. A frequency-domain analysis was performed on pairwise relations by the cross-spectral technique. During autonomic blockade, fluctuations in CVP were induced up to 0.14 Hz but caused corresponding changes in arterial pressure only up to 0.08 Hz (P < .02), indicating a mechanical damping effect of the heart and pulmonary vasculature. Fluctuations of BP were also delayed from CVP by 1.55 to 2.10 seconds. At frequencies < 0.1 Hz, relations of CVP to all indices of BP increased with blockade (CVP-SBP, 0.9 +/- 0.5 versus 2.7 +/- 0.8 mm Hg/mm Hg, P < .01; CVP-DBP, 1.3 +/- 0.4 versus 4.3 +/- 1.4 mm Hg/mm Hg, P < .01; CVP-pulse pressure [PP], 1.0 +/- 0.3 versus 1.9 +/- 0.8 mm Hg/mm Hg, P < .05). Higher-frequency fluctuations of arterial BP were a relatively pure manifestation of respiratory activity. At frequencies from 0.15 to 0.35 Hz, the relation of ILV to SBP was unchanged with blockade, whereas relations of ILV to DBP and PP decreased (ILV-DBP, 6.1 +/- 3.5 versus 3.3 +/- 2.2 mm Hg/L, P < .02; ILV-PP, 7.0 +/- 4.3 versus 2.7 +/- 2.2 mm Hg/L, P < .01). An associated change in phase of these relations suggested that neurally mediated changes in HR may offset mechanical effects caused by respiration. Both slow changes of BP (< 0.08 Hz) induced by variations of CVP and more rapid changes induced by ILV are actively buffered by heart rate reflexes. During blockade, the mechanical properties of interposed cardiopulmonary structures limit CVP-induced fluctuations of BP. These findings have implications for BP regulation in pathological conditions associated with impairment of HR control.

Effect of central venous pressure on arterial baroreflex control of heart rate

There is considerable evidence that the level of afferent cardiopulmonary receptor activity modulates sinus node responses to arterial baroreflex stimulation in experimental animals. We tested the hypothesis that this reflex interaction occurs also in man by measuring sinus node responses to arterial baroreceptor stimulation with phenylephrine injection or neck suction, before and during changes of central venous pressure provoked by lower body negative pressure or leg and lower trunk elevation. Variations of central venous pressure between 1.1 and 9.0 mmHg did not influence arterial baroreflex mediated bradycardia. Baroreflex sinus node responses were augmented by intravenous propranolol, but the level of responses after propranolol was comparable during the control state, lower body negative pressure, and leg and trunk elevation. Sinus node responses to very brief baroreceptor stimuli applied during the transitions of central venous pressure also were comparable in the three states. We conclude that physiological variations of central venous pressure do not influence sinus node responses to arterial baroreceptor stimulation in man.