Article

A robust Fourier-based method to measure pulse pressure variability

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Abstract

Objective To propose a new method to estimate pulse pressure variability (PPV) in the arterial blood pressure waveform. Methods Traditional techniques of calculating PPV using peak finding have a fundamental flaw that prevents them from accurately resolving PPV for small tidal volumes, limiting the use of PPV to only mechanical ventilated patients. The improved method described here addresses this limitation using Fourier analysis of an oscillatory signal that exhibits a time-varying modulation of its amplitude. The analysis reveals a constraint on the spectral representation that must be satisfied for any oscillatory signal that exhibits a time-varying modulation of its amplitude. This intrinsic mathematical structure is taken advantage of in order to improve the robustness of the algorithm. Results The applicability of the method is tested using synthetic data and 100 h of physiologic data collected from patients admitted to Texas Children’s Hospital. Significance and conclusion The proposed method accurately recovers values of PPV at signal-to-noise ratios six times smaller than the traditional method. This is a significant advance for the potential use of PPV to recognize fluid responsiveness during low tidal volume ventilation or spontaneous breathing for which the signal-to-noise ratio is expected to be small.

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... Our team has previously described a new technique for PPV analysis, which relies on Fourier analysis. 22 This method is more precise for calculating PPV and less sensitive to noise (random variations in the data not due to true physiologic changes), remaining robust at signalto-noise ratios 6 times smaller than the traditional method; however, it has not yet been validated in premature infants. ...
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Real-time measurement of stroke volume variation by arterial pulse contour analysis (SVV) is useful in predicting volume responsiveness and monitoring volume therapy in mechanically ventilated patients. This study investigated the influence of the depth of tidal volume (V(t)) on SVV both during the state of fluid responsiveness and after fluid loading in mechanically ventilated patients. Prospective study in a university hospital, adult cardiac surgery intensive care unit. 20 hemodynamically stable patients immediately after cardiac surgery. Stepwise fluid loading using colloids until stroke volume index (SVI) did not increase by more than 10%. Before and after fluid loading V(t) was varied (5, 10, and 15 ml/kg body weight) in random order. Pulse contour SVV was measured before and after volume loading at the respective V(t) values. Thirteen patients responded to fluid loading with an increase in SVI greater than 10%, which confirmed volume responsiveness at baseline measurements. These were included in further analysis. During volume responsiveness SVV at V(t) of 5 ml/kg (7+/-0.7%) and SVV at V(t) of 15 ml/kg (21+/-2.5%) differed significantly from that at V(t) of 10 ml/kg (15+/-2.1%). SVV was correlated significantly with the magnitude of V(t). After volume resuscitation SVV at the respective V(t) was significantly reduced; further, SVV at V(t) of 5 ml/kg(-1) (5.3+/-0.6%) and 15 ml/kg (16.2+/-2.0%) differed significantly from that at V(t) of 10 ml/kg (10.2+/-1.0%). SVV and depth of V(t) were significantly related. In addition to intravascular volume status SVV is affected by the depth of tidal volume under mechanical ventilation. This influence must be regarded when using SVV for functional preload monitoring.
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We designed a new methodology to estimate the pulse pressure variation index (deltaPP) in arterial blood pressure (ABP). The method uses automatic detection algorithms, kernel smoothing, and rank-order filters to continuously estimate deltaPP. The technique can be used to estimate deltaPP from ABP alone, eliminating the need for simultaneously acquiring airway pressure.
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To evaluate the influence of tidal volume on the capacity of pulse pressure variation (DeltaPP) to predict fluid responsiveness. Prospective interventional study. A 31-bed university hospital medico-surgical ICU. Sixty mechanically ventilated critically ill patients requiring fluid challenge, separated according to their tidal volume. Fluid challenge with either 1,000 ml crystalloids or 500 ml colloids. Complete hemodynamic measurements including DeltaPP were obtained before and after fluid challenge. Tidal volume was lower than 7 ml/kg in 26 patients, between 7-8 ml/kg in 9 patients, and greater than 8 ml/kg in 27 patients. ROC curve analysis was used to evaluate the predictive value of DeltaPP at different tidal volume thresholds, and 8 ml/kg best identified different behaviors. Overall, the cardiac index increased from 2.66 (2.00-3.47) to 3.04 (2.44-3.96) l/min m(2) ( P <0.001). It increased by more than 15% in 33 patients (fluid responders). Pulmonary artery occluded pressure was lower and DeltaPP higher in responders than in non-responders, but fluid responsiveness was better predicted with DeltaPP (ROC curve area 0.76+/-0.06) than with pulmonary artery occluded pressure (0.71+/-0.07) and right atrial (0.56+/-0.08) pressures. Despite similar response to fluid challenge in low (<8 ml/kg) and high tidal volume groups, the percent of correct classification of a 12% DeltaPP was 51% in the low tidal volume group and 88% in the high tidal volume group. DeltaPP is a reliable predictor of fluid responsiveness in mechanically ventilated patients only when tidal volume is at least 8 ml/kg.
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Prediction of fluid responsiveness has become a topic of intense interest. Although measurements of preload, by whatever technique, are still commonly used to guide fluid therapy [1, 2], these fail to estimate the response to fluids in one-half of the patients [3]. Accordingly, many patients may be subjected to the hazards of fluids [4], without benefiting from hemodynamic improvement.
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Frank's Windkessel model described the hemodynamics of the arterial system in terms of resistance and compliance. It explained aortic pressure decay in diastole, but fell short in systole. Therefore characteristic impedance was introduced as a third element of the Windkessel model. Characteristic impedance links the lumped Windkessel to transmission phenomena (e.g., wave travel). Windkessels are used as hydraulic load for isolated hearts and in studies of the entire circulation. Furthermore, they are used to estimate total arterial compliance from pressure and flow; several of these methods are reviewed. Windkessels describe the general features of the input impedance, with physiologically interpretable parameters. Since it is a lumped model it is not suitable for the assessment of spatially distributed phenomena and aspects of wave travel, but it is a simple and fairly accurate approximation of ventricular afterload.
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Objective: Arterial pulse pressure variation (PPV) is widely used for predicting fluid responsiveness and supporting fluid management in the operating room and intensive care unit. Available PPV algorithms have been typically validated for fluid responsiveness during episodes of hemodynamic stability. Yet, little is known about the performance of PPV algorithms during surgery, where fast changes of the blood pressure may affect the robustness of the presented PPV value. This work provides a comprehensive understanding of how various existing algorithmic designs affect the robustness of the presented PPV value during surgery, and proposes additional processing for the pulse pressure signal before calculating PPV. Approach: We recorded arterial blood pressure waveforms from 23 patients undergoing major abdominal surgery. To evaluate the performance, we designed three clinically relevant metrics. Main results and Significance: The results show that all algorithms performed well during episodes of hemodynamic stability. Moreover, it is demonstrated that the proposed processing helps improve the robustness of PPV during the entire course of surgery.
Article
Background: Pulse pressure variation derived from the varied pulse contour method is based on heart-lung interaction during mechanical ventilation. It has been shown that pulse pressure variation is predictive of fluid responsiveness in children undergoing surgical repair of ventricular septal defect. Right ventricle compliance and pulmonary vascular capacitance in children with tetralogy of Fallot are underdeveloped as compared to those in ventricular septal defect. We hypothesized that the difference in the right ventricle-pulmonary circulation in the two groups of children would affect the heart-lung interaction and therefore pulse pressure variation predictivity of fluid responsiveness following cardiac surgery. Methods: Infants undergoing complete repair of ventricular septal defect (n=38, 1.05±0.75 years) and tetralogy of Fallot (n=36, 1.15±0.68 years) clinically presenting with low cardiac output were enrolled. Fluid infusion with 5% albumin or fresh frozen plasma was administered. Pulse pressure variation was recorded using pressure recording analytical method along with cardiac index before and after fluid infusion. Patients were considered as responders to fluid loading when cardiac index increased ≥15%. Receiver operating characteristic curves analysis was used to assess the accuracy and cutoffs of pulse pressure variation to predict fluid responsiveness. Results: The pulse pressure variation values before and after fluid infusion were lower in tetralogy of Fallot children than those in ventricular septal defect children (15.2±4.4% vs 19.3±4.4%, P<.001; 11.6±3.8 vs 15.4±4.3%, P<.001, respectively). In ventricular septal defect children, 27 were responders and 11 nonresponders. Receiver operating characteristic curve area was 0.89 (95% confidence interval, 0.77-1.01) and cutoff value 17.4% with a sensitivity of 0.89 and a specificity of 0.91. In tetralogy of Fallot children, 26 were responders and 10 were nonresponders. Receiver operating characteristic curve area was 0.79 (95% CI, 0.64-0.94) and cutoff value 13.4% with a sensitivity of 0.81 and a specificity of 0.80. Conclusion: Pulse pressure variation is predictive of fluid responsiveness in ventricular septal defect and tetralogy of Fallot patients following cardiac surgery.
Article
Objectives: Stroke volume variation and pulse pressure variation do not reliably predict fluid responsiveness during low tidal volume ventilation. We hypothesized that with transient increase in tidal volume from 6 to 8 mL/kg predicted body weight, that is, "tidal volume challenge," the changes in pulse pressure variation and stroke volume variation will predict fluid responsiveness. Design: Prospective, single-arm study. Setting: Medical-surgical ICU in a university hospital. Patients: Adult patients with acute circulatory failure, having continuous cardiac output monitoring, and receiving controlled low tidal volume ventilation. Interventions: The pulse pressure variation, stroke volume variation, and cardiac index were recorded at tidal volume 6 mL/kg predicted body weight and 1 minute after the "tidal volume challenge." The tidal volume was reduced back to 6 mL/kg predicted body weight, and a fluid bolus was given to identify fluid responders (increase in cardiac index > 15%). The end-expiratory occlusion test was performed at tidal volumes 6 and 8 mL/kg predicted body weight and after reducing tidal volume back to 6 mL/kg predicted body weight. Results: Thirty measurements were obtained in 20 patients. The absolute change in pulse pressure variation and stroke volume variation after increasing tidal volume from 6 to 8 mL/kg predicted body weight predicted fluid responsiveness with areas under the receiver operating characteristic curves (with 95% CIs) being 0.99 (0.98-1.00) and 0.97 (0.92-1.00), respectively. The best cutoff values of the absolute change in pulse pressure variation and stroke volume variation after increasing tidal volume from 6 to 8 mL/kg predicted body weight were 3.5% and 2.5%, respectively. The pulse pressure variation, stroke volume variation, central venous pressure, and end-expiratory occlusion test obtained during tidal volume 6 mL/kg predicted body weight did not predict fluid responsiveness. Conclusions: The changes in pulse pressure variation or stroke volume variation obtained by transiently increasing tidal volume (tidal volume challenge) are superior to pulse pressure variation and stroke volume variation in predicting fluid responsiveness during low tidal volume ventilation.
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We evaluated whether pulse pressure variation can predict fluid responsiveness in spontaneously breathing patients. Fifty-nine elective thoracic surgical patients were studied before induction of general anaesthesia. After volume expansion with hydroxyethyl starch 6 ml.kg−1, patients were defined as responders by a ≥ 15% increase in the cardiac index. Haemodynamic variables were measured before and after volume expansion and pulse pressure variations were calculated during tidal breathing and during forced inspiratory breathing. Median (IQR [range]) pulse pressure variation during forced inspiratory breathing was significantly higher in responders (n = 29) than in non-responders (n = 30) before volume expansion (18.2 (IQR 14.7–18.2 [9.3–31.3])% vs 10.1 (IQR 8.3–12.6 [4.8–21.1])%, respectively, p < 0.001). The receiver-operating characteristic curve revealed that pulse pressure variation during forced inspiratory breathing could predict fluid responsiveness (area under the curve 0.910, p < 0.0001). Pulse pressure variation measured during forced inspiratory breathing can be used to guide fluid management in spontaneously breathing patients.
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Mechanical ventilation causes cyclic changes in the heart's preload and afterload, thereby influencing the circulation. However, our understanding of the exact physiology of this cardiopulmonary interaction is limited. We aimed to thoroughly determine airway pressure distribution, how this is influenced by tidal volume and chest compliance, and its interaction with the circulation in humans during mechanical ventilation. Intervention study. ICU of a university hospital. Twenty mechanically ventilated patients following coronary artery bypass grafting surgery. Patients were monitored during controlled mechanical ventilation at tidal volumes of 4, 6, 8, and 10 mL/kg with normal and decreased chest compliance (by elastic binding of the thorax). Central venous pressure, airway pressure, pericardial pressure, and pleural pressure; pulse pressure variations, systolic pressure variations, and stroke volume variations; and cardiac output were obtained during controlled mechanical ventilation at tidal volume of 4, 6, 8, and 10 mL/kg with normal and decreased chest compliance. With increasing tidal volume (4, 6, 8, and 10 mL/kg), the change in intrathoracic pressures increased linearly with 0.9 ± 0.2, 0.5 ± 0.3, 0.3 ± 0.1, and 0.3 ± 0.1 mm Hg/mL/kg for airway pressure, pleural pressure, pericardial pressure, and central venous pressure, respectively. At 8 mL/kg, a decrease in chest compliance (from 0.12 ± 0.07 to 0.09 ± 0.03 L/cm H2O) resulted in an increase in change in airway pressure, change in pleural pressure, change in pericardial pressure, and change in central venous pressure of 1.1 ± 0.7, 1.1 ± 0.8, 0.7 ± 0.4, and 0.8 ± 0.4 mm Hg, respectively. Furthermore, increased tidal volume and decreased chest compliance decreased stroke volume and increased arterial pressure variations. Transmural pressure of the superior vena cava decreased during inspiration, whereas the transmural pressure of the right atrium did not change. Increased tidal volume and decreased chest wall compliance both increase the change in intrathoracic pressures and the value of the dynamic indices during mechanical ventilation. Additionally, the transmural pressure of the vena cava is decreased, whereas the transmural pressure of the right atrium is not changed.
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Administration of fluid to improve cardiac output is the mainstay of hemodynamic resuscitation. Not all patients respond to fluid therapy, and excessive fluid administration is harmful. Predicting fluid responsiveness can be challenging, particularly in children. Numerous hemodynamic variables have been proposed as predictors of fluid responsiveness. Dynamic variables based on the heart-lung interaction appear to be excellent predictors of fluid responsiveness in adults, but there is no consensus on their usefulness in children. We systematically reviewed the current evidence for predictors of fluid responsiveness in children. A systematic search was performed using PubMed (1947-2013) and EMBASE (1974-2013). Search terms included fluid, volume, response, respond, challenge, bolus, load, predict, and guide. Results were limited to studies involving pediatric subjects (infant, child, and adolescent). Extraction of data was performed independently by 2 authors using predefined data fields, including study quality indicators. Any variable with an area under the receiver operating characteristic curve that was significantly above 0.5 was considered predictive. Twelve studies involving 501 fluid boluses in 438 pediatric patients (age range 1 day to 17.8 years) were included. Twenty-four variables were investigated. The only variable shown in multiple studies to be predictive was respiratory variation in aortic blood flow peak velocity (5 studies). Stroke volume index, stroke distance variation, and change in cardiac index (and stroke volume) induced by passive leg raising were found to be predictive in single studies only. Static variables based on heart rate, systolic arterial blood pressure, preload (central venous pressure, pulmonary artery occlusion pressure), thermodilution (global end diastolic volume index), ultrasound dilution (active circulation volume, central blood volume, total end diastolic volume, total ejection fraction), echocardiography (left ventricular end diastolic area), and Doppler (stroke volume index, corrected flow time) did not predict fluid responsiveness in children. Dynamic variables based on arterial blood pressure (systolic pressure variation, pulse pressure variation and stroke volume variation, difference between maximal or minimal systolic arterial blood pressure and systolic pressure at end-expiratory pause) and plethysmography (pulse oximeter plethysmograph amplitude variation) were also not predictive. There were contradicting results for plethymograph variation index and inferior vena cava diameter variation. Respiratory variation in aortic blood flow peak velocity was the only variable shown to predict fluid responsiveness in children. Static variables did not predict fluid responsiveness in children, which was consistent with evidence in adults. Dynamic variables based on arterial blood pressure did not predict fluid responsiveness in children, but the evidence for dynamic variables based on plethysmography was inconclusive.
Article
Continuous noninvasive cardiac output monitoring (NICOM) is a clinically useful tool in the pediatric setting. This study compared the ability of stroke volume variation (SVV) measured by NICOM with that of respiratory variations in the velocity of aortic blood flow (△Vpeak) and central venous pressure (CVP) to predict of fluid responsiveness in mechanically ventilated children after ventricular septal defect repair. The study investigated 26 mechanically ventilated children after the completion of surgery. At 30 min after their arrival in an intensive care unit, a colloid solution of 10 ml/kg was administrated for volume expansion. Hemodynamic variables, including CVP, stroke volume, and △Vpeak in addition to cardiac output and SVV in NICOM were measured before and 10 min after volume expansion. The patients with a stroke volume increase of more than 15 % after volume expansion were defined as responders. The 26 patients in the study consisted of 13 responders and 13 nonresponders. Before volume expansion, △Vpeak and SVV were higher in the responders (both p values <0.001). The areas under the receiver operating characteristic curves of △Vpeak, SVV, and CVP were respectively 0.956 (95 % CI 0.885-1.00), 0.888 (95 % CI 0.764-1.00), and 0.331 (95 % CI 0.123-0.540). This study showed that SVV by NICOM and △Vpeak by echocardiography, but not CVP, reliably predicted fluid responsiveness during mechanical ventilation after ventricular septal defect repair in children.
Article
Commonly used arterial respiratory variation metrics are based on mathematical analysis of arterial waveforms in the time domain. Because the shape of the arterial waveform is dependent on the site at which it is measured we hypothesized that analysis of the arterial waveform in the frequency domain might provide a relatively site-independent means of measuring arterial respiratory variation. Radial and femoral arterial blood pressures were measured in nineteen patients undergoing liver transplantation. Systolic pressure variation (SPV) pulse pressure variation (PPV) area under the curve variation (AUCV) and mean arterial pressure variation (MAPV) at radial and femoral sites were calculated off-line. Two metrics, Spectral Peak Ratio (SPeR) and Spectral Power Ratio (SPoR) based on ratios of the spectral peak and spectral area (power) at the respiratory and cardiac frequencies were calculated at both radial and femoral sites. Variance among radial-femoral differences was compared and correlation coefficients describing the relationship between respiratory variation at the radial and femoral sites were developed. The variance in radial-femoral differences were significantly different (p\0.001). The correlation between radial and femoral estimates of respiratory variation were 0.746,0.658, 0.858, 0.882, 0.941 and 0.925 for SPV, PPV, AUCV, MAPV, SPeR and SPoR, respectively. Assuming a PPV treatment threshold of 12 % (or equivalent) differences in treatment decisions based on radial or femoral estimates would arise in 12, 14, 5.4, 5.7, 4.8 and 5.5 % of minutes for SPV, PPV, AUCV,MAPV, spectral peak ratio and spectral power ratio respectively. As compared to frequency domain-based estimates of respiratory variation, SPV and PPV are relatively dependent on the anatomic site at which they are measured. Spectral peak and power ratios are relatively site-independent means of measuring respiratory variation and may offer a useful alternative to time domain-based techniques.
Article
We evaluated the impact of increasing tidal volume (V (t)), decreased chest wall compliance, and left ventricular (LV) contractility during intermittent positive-pressure ventilation (IPPV) on the relation between pulse pressure (PP) and LV stroke volume (SV(LV)) variation (PPV and SVV, respectively), and intrathoracic blood volume (ITBV) changes. Sixteen pentobarbital-anesthetized thoracotomized mongrel dogs were studied both before and after propranolol-induced acute ventricular failure (AVF) (n = 4), with and without chest and abdominal pneumatic binders to decrease chest wall compliance (n = 6), and during V (t) of 5, 10, 15, and 25 ml/kg (n = 6). SV(LV) and right ventricular stroke volume (SV(RV)) were derived from electromagnetic flow probes around aortic and pulmonary artery roots. Arterial pressure was measured in the aorta using a fluid-filled catheter. Arterial PPV and SVV were calculated over three breaths as (max - min)/[(max + min)/2]. ITBV changes during ventilation were inferred from the beat-to-beat volume differences between SV(RV) and SV(LV). Arterial PP and SV(LV) were tightly correlated during IPPV under all conditions (r (2) = 0.85). Both PPV and SVV increased progressively as V (t) increased and with thoraco-abdominal binding, and tended to decrease during AVF. SV(RV) phasically decreased during inspiration, whereas SV(LV) phasically decreased 2-3 beats later, such that ITBV decreased during inspiration and returned to apneic values during expiration. ITBV decrements increased with increasing V (t) or with thoraco-abdominal binding, and decreased during AVF owing to variations in SV(RV), such that both PPV and SVV tightly correlated with inspiration-associated changes in SV(RV) and ITBV. Arterial PP and SV(LV) are tightly correlated during IPPV and their relation is not altered by selective changes in LV contractility, intrathoracic pressure, or V (t). However, contractility, intrathoracic pressure, and V (t) directly alter the magnitude of PPV and SVV primarily by altering the inspiration-associated decreases in SV(RV) and ITBV.
Article
: A systematic review of the literature to determine the ability of dynamic changes in arterial waveform-derived variables to predict fluid responsiveness and compare these with static indices of fluid responsiveness. The assessment of a patient's intravascular volume is one of the most difficult tasks in critical care medicine. Conventional static hemodynamic variables have proven unreliable as predictors of volume responsiveness. Dynamic changes in systolic pressure, pulse pressure, and stroke volume in patients undergoing mechanical ventilation have emerged as useful techniques to assess volume responsiveness. : MEDLINE, EMBASE, Cochrane Register of Controlled Trials and citation review of relevant primary and review articles. : Clinical studies that evaluated the association between stroke volume variation, pulse pressure variation, and/or stroke volume variation and the change in stroke volume/cardiac index after a fluid or positive end-expiratory pressure challenge. : Data were abstracted on study design, study size, study setting, patient population, and the correlation coefficient and/or receiver operating characteristic between the baseline systolic pressure variation, stroke volume variation, and/or pulse pressure variation and the change in stroke index/cardiac index after a fluid challenge. When reported, the receiver operating characteristic of the central venous pressure, global end-diastolic volume index, and left ventricular end-diastolic area index were also recorded. Meta-analytic techniques were used to summarize the data. Twenty-nine studies (which enrolled 685 patients) met our inclusion criteria. Overall, 56% of patients responded to a fluid challenge. The pooled correlation coefficients between the baseline pulse pressure variation, stroke volume variation, systolic pressure variation, and the change in stroke/cardiac index were 0.78, 0.72, and 0.72, respectively. The area under the receiver operating characteristic curves were 0.94, 0.84, and 0.86, respectively, compared with 0.55 for the central venous pressure, 0.56 for the global end-diastolic volume index, and 0.64 for the left ventricular end-diastolic area index. The mean threshold values were 12.5 +/- 1.6% for the pulse pressure variation and 11.6 +/- 1.9% for the stroke volume variation. The sensitivity, specificity, and diagnostic odds ratio were 0.89, 0.88, and 59.86 for the pulse pressure variation and 0.82, 0.86, and 27.34 for the stroke volume variation, respectively. : Dynamic changes of arterial waveform-derived variables during mechanical ventilation are highly accurate in predicting volume responsiveness in critically ill patients with an accuracy greater than that of traditional static indices of volume responsiveness. This technique, however, is limited to patients who receive controlled ventilation and who are not breathing spontaneously.
Article
Heart-lung interactions are used to evaluate fluid responsiveness in mechanically ventilated patients, but these indices may be influenced by ventilatory conditions. The authors evaluated the impact of respiratory rate (RR) on indices of fluid responsiveness in mechanically ventilated patients, hypothesizing that pulse pressure variation and respiratory variation in aortic flow would decrease at high RRs. In 17 hypovolemic patients, thermodilution cardiac output and indices of fluid responsiveness were measured at a low RR (14-16 breaths/min) and at the highest RR (30 or 40 breaths/min) achievable without altering tidal volume or inspiratory/expiratory ratio. An increase in RR was accompanied by a decrease in pulse pressure variation from 21% (18-31%) to 4% (0-6%) (P < 0.01) and in respiratory variation in aortic flow from 23% (18-28%) to 6% (5-8%) (P < 0.01), whereas respiratory variations in superior vena cava diameter (caval index) were unaltered, i.e., from 38% (27-43%) to 32% (22-39%), P = not significant. Cardiac index was not affected by the changes in RR but did increase after fluids. Pulse pressure variation became negligible when the ratio between heart rate and RR decreased below 3.6. Respiratory variations in stroke volume and its derivates are affected by RR, but caval index was unaffected. This suggests that right and left indices of ventricular preload variation are dissociated. At high RRs, the ability to predict the response to fluids of stroke volume variations and its derivate may be limited, whereas caval index can still be used.
Article
Both tidal volume and effective blood volume may affect the variation in the arterial pressure waveform during mechanical ventilation. The systolic pressure variation (SPV), which is the difference between the maximal and minimal systolic pressure values following one positive pressure breath was analyzed in 10 anesthetized and ventilated dogs, during ventilation with tidal volumes of 15 and 25 ml/kg. The dogs were studied during normovolemia, hypovolemia (after bleeding of 30% of estimated blood volume) and hypervolemia (after retransfusion of shed blood with additional 50 ml/kg of plasma expander). The SPV reflected hemodynamic changes and was maximal during hypovolemia and minimal during hypervolemia. Unlike all other hemodynamic parameters it was also affected by the tidal volume and significantly increased at higher tidal volumes during each volume state. We conclude that the SPV and its components are useful parameters in evaluating the intravascular volume state. They also reflect the magnitude of the tidal volume employed.
Article
In 13 patients on respiratory support we combined two-dimensional echocardiography with hemodynamic monitoring to determine the mechanism of cyclic changes in arterial pulse, defined as an inspiratory rise in radial artery pulse pressure. Beat-to-beat evaluation of cardiac performance was obtained during the following three distinct consecutive phases of the controlled respiratory cycle: exhalation (phase I), preinspiratory pause (phase II), and lung inflation (phase III). Airway pressure, left ventricular filling pressure (i.e., pulmonary capillary wedge minus esophageal pressure), and pulmonary artery and radial artery pressures were simultaneously recorded during mechanical ventilation along with beat-to-beat two-dimensional echocardiographic left ventricular end-systolic and end-diastolic dimensions. From a reference value for pulmonary artery and radial artery pulse contour obtained during a brief period of imposed apnea, beat-to-beat measurements of left and right ventricular stroke output were also performed during the controlled respiratory cycle with the pulse contour method. Cyclic changes in arterial pulse appeared to result directly from a transitory increase in left ventricular stroke output during lung inflation (41.4 ± 14.6 ml/m2), whereas right ventricular stroke output exhibited a steep fall (31.7 ± 12.4 ml/m2) at this time. An opposite variation was also observed during exhalation, during which a fall in left ventricular stroke output (31.9 ± 11.2 ml/m2) was accompanied by a rise in right ventricular stroke output (38.6 ± 11.9 ml/m2). Both stroke outputs reached an identical level during preinspiratory pause (37.4 ± 14.1 ml/m2 for left ventricle and 39.1 ± 13.8 ml/m2 for right ventricle). Such an inspiratory increase in left ventricular stroke output during lung inflation was no doubt largely due to a transient improvement in left ventricular preload and this is supported by our finding of a concomitant increase in left ventricular filling pressure and end-diastolic dimensions during the inspiratory phase.
Article
In 14 anesthetized mongrel dogs, we studied the factors that influenced aortic systolic pressure (PaO) and peak aortic systolic flow (Qao) during positive-pressure inflations at three respiratory rates: 8, 14, and 24 breaths/min. At all three respiratory rates, pulmonary arterial flow fell by 15% of the preinspiratory value by end inhalation. Qao also fell at all three respiratory rates, reaching a nadir close to end exhalation (EE). Qao fell less (7% of the base line) at the fast respiratory rate than at the medium and slow respiratory rates (15% of the base line). Pao rose more during the early part of inflation at the medium and fast rates (5 +/- 0.9 Torr) than at the slow rate (3 +/- 0.7 Torr); then Pao fell to a nadir near EE at the slow (-5.6 +/- 1.6 Torr) and at the medium (-2.3 +/- 1 Torr) respiratory rates. At the fast rate it fell to a value not different from control (0.1 +/- 0.5 Torr). The ratio of peak arterial pressure to peak arterial flow increased throughout inflation reaching a peak at EE. A model was developed that predicted the major qualitative features of the changes in Qao seen in these studies. Changes in Pao resulted from the interaction between decreases in Qao and transmitted increases in pleural pressure, and are modified by changes in systemic impedance.
Article
To examine determinants of right ventricular function throughout the ventilatory cycle under volume-controlled mechanical ventilation with various positive end-expiratory pressure (PEEP) stages. Prospective observational animal pilot study. Animal research laboratory at a university hospital. Eight healthy swine under volume- controlled mechanical ventilation. Flow probes were implanted in eight swine in order to continuously measure blood flow in the pulmonary artery and inferior vena cava. After a recovery phase of 14 days, the swine were subjected to various PEEP stages (0, 5, 10 cm H2O) during volume-controlled positive pressure ventilation. Continuous flow measurement took place in the pulmonary artery and inferior vena cava. Data on standard hemodynamic parameters were additionally acquired. Respiration-phase-specific analysis of right ventricular cardiac output and of additional hemodynamic function parameters followed, after calculation of mean values throughout five respiration cycles. PEEP at 5 cm H2O led to significant decreases in inferior vena cava flow (4.1%), and in right ventricular cardiac output (5.2%); the respective decreases at PEEP 10 cm H2O were 13.9% and 18.3%. In the inspiration phase at PEEP 10 cm H2O, results revealed an overproportionally pronounced decrease in comparison with the expiration phase in inferior vena cava flow (-24.6% vs. -10%) and right ventricular cardiac output (-35% vs. -13.5%). This phenomenon is presumably caused by a PEEP-related increase in mean airway pressure by the amount of 10.7 cm H2O in inspiration. Increases in PEEP during volume-controlled mechanical ventilation leads to respiration-phase-specific reduction of right ventricular cardiac output, with a significantly pronounced decrease during the inspiration phase. This decrease in cardiac output should be taken into particular consideration for patients with already critically reduced cardiac output.
Article
Positive-pressure ventilation (PPV) may affect left ventricular (LV) performance by altering both LV diastolic compliance and pericardial pressure (Ppc). We measured the effect of PPV on LV intraluminal pressure, Ppc, LV volume, and LV cross-sectional area in 17 acute anesthetized dogs. To account for changes in lung volume independent of changes in Ppc and differences in contractility, measures were made during both open- and closed-chest conditions, during closed chest with and without chest wall binding, and after propranolol-induced acute ventricular failure (AVF). Apneic end-systolic pressure-volume relations (ESPVR) were generated by inferior vena caval occlusions. With the open chest, PPV had no effects. With the chest closed, PPV inspiration decreased LV end-diastolic volume (EDV) along its diastolic compliance curve and decreased end-systolic volume (ESV) such that the end-systolic pressure-volume domain was shifted to a point left of the LV ESPVR, even when referenced to Ppc. The decrease in EDV was greater in control than in AVF conditions, whereas the shift of the ESV to the left of the ESPVR was greater with AVF than in control conditions. We conclude that the hemodynamic effects of PPV inspiration are due primarily to changes in intrathoracic pressure and that the inspiration-induced decreases of LV EDV reflect direct effects of intrathoracic pressure on LV filling. The decreases in LV ESV exceed the amount explained solely by a reduction in LV ejection pressure.
Article
Mechanical ventilation induces cyclic changes in vena cava blood flow, pulmonary artery blood flow, and aortic blood flow. At the bedside, respiratory changes in aortic blood flow are reflected by "swings" in blood pressure whose magnitude is highly dependent on volume status. During the past few years, many studies have demonstrated that arterial pressure variation is neither an indicator of blood volume nor a marker of cardiac preload but a predictor of fluid responsiveness. That is, these studies have demonstrated the value of this physical sign in answering one of the most common clinical questions, Can we use fluid to improve hemodynamics?, while static indicators of cardiac preload (cardiac filling pressures but also cardiac dimensions) are frequently unable to correctly answer this crucial question. The reliable analysis of respiratory changes in arterial pressure is possible in most patients undergoing surgery and in critically ill patients who are sedated and mechanically ventilated with conventional tidal volumes.