Left Ventricular Stroke Volume Variation Research Articles

Cardiopulmonary Interactions: Physiologic Basis and Clinical Applications.

The hemodynamic effects of ventilation can be grouped into three concepts: 1) Spontaneous ventilation is exercise; 2) changes in lung volume alter autonomic tone and pulmonary vascular resistance and can compress the heart in the cardiac fossa; and 3) spontaneous inspiratory efforts decrease intrathoracic pressure, increasing venous return and impeding left ventricular ejection, whereas positive-pressure ventilation decreases venous return and unloads left ventricular ejection. Spontaneous inspiratory efforts may induce acute left ventricular failure and cardiogenic pulmonary edema. Reversing the associated negative intrathoracic pressure swings by using noninvasive continuous positive airway pressure rapidly reverses acute cardiogenic pulmonary edema and improves survival. Additionally, in congestive heart failure, states increasing intrathoracic pressure may augment left ventricular ejection and improve cardiac output. Using the obligatory changes in venous return induced by positive pressure breathing, one can quantify the magnitude of associated decreases in venous flow and left ventricular ejection using various parameters, including vena caval diameter changes, left ventricular stroke volume variation, and arterial pulse pressure variation. These parameters vary in proportion to the level of cardiac preload reserve present, thus accurately predicting which critically ill patients will increase their cardiac output in response to fluid infusions and which will not. Common parameters include arterial pulse pressure variation and left ventricular stroke volume variation. This functional hemodynamic monitoring approach reflects a practical clinical application of heart-lung interactions.

Functional haemodynamic monitoring.

Functional haemodynamic monitoring is the assessment of the dynamic interactions of haemodynamic variables in response to a defined perturbation. Fluid responsiveness can be predicted during positive pressure breathing by variations in venous return or left ventricular output using numerous surrogate markers, such as arterial pulse pressure variation (PPV), left ventricular stroke volume variation (SVV), aortic velocity variation, inferior and superior vena cavae diameter changes and pulse oximeter pleth signal variability. Similarly, dynamic changes in cardiac output to a passive leg raising manoeuvre can be used in any patient and measured invasively or noninvasively. However, volume responsiveness, though important, reflects only part of the overall spectrum of functional physiological variables that can be measured to define physiologic state and monitor response to therapy. The ratio of PPV to SVV defines central arterial elastance and can be used to identify those hypotensive patients who will not increase their blood pressure in response to a fluid challenge despite increasing cardiac output. Dynamic tissue O2 saturation (StO2) responses to complete stop flow conditions, as can be created by measuring hand StO2 and occluding flow with a blood pressure cuff, assesses cardiovascular sufficiency and micro-circulatory blood flow distribution. They can be used to identify those ventilator-dependent individuals who will fail a spontaneous breathing trial or trauma patients in need of life-saving interventions. Functional haemodynamic monitoring approaches are increasing in numbers, conditions in which they are useful and resuscitation protocol applications. This is a rapidly evolving field whose pluripotential is just now being realized.

The impact of early goal-directed fluid management on survival in an experimental model of severe acute pancreatitis

Severe acute pancreatitis (SAP) remains a life-threatening disease with classic etiology of systemic inflammatory response and mortality between 30 and 50 %. The aim of the present study is to compare two different treatment strategies of goal-directed hemodynamic management and evaluate their impact on survival, microcirculation, tissue oxygenation, and histopathologic damage in acute pancreatitis in a prospective animal study. Thirty-four domestic pigs were randomly assigned to two different treatment groups. After induction of acute pancreatitis, in group 1 volume administration was guided by central venous pressure (CVP >12 mmHg) and mean arterial pressure (MAP). In group 2, hemodynamic management was guided primarily by left-ventricular stroke volume variation (SVV <10 %), MAP, and cardiac output (CO). Treatment according to randomization was performed for 6 h, and tissue oxygen tension in the pancreas and pancreatic microcirculation were evaluated. Thereafter, animals were observed for 7 days and then sacrificed. Standardized tissue specimens were taken post mortem, and histopathologic scoring was performed. Survival after 7 days was 29.4 % in group 2 versus 11.8 % in group 1 (p < 0.05). Pancreatic oxygen tension (138.0 ± 89.5 mmHg versus 71.1 ± 35.3 mmHg; p < 0.05) and pancreatic microcirculation (1,209.9 ± 630 AU versus 732 ± 315 AU; p < 0.05) were significantly higher in group 2. Significantly less histopathologic damage within the pancreas could be analyzed post mortem in group 2. Goal-directed hemodynamic management guided by stroke volume variation led to improved survival, tissue oxygenation, and microcirculatory perfusion, as well as less histopathologic damage in an animal model of severe acute pancreatitis.

Heart-lung interactions measured by electrical impedance tomography*

The clinical value of stroke volume variations to assess intravascular fluid status in critically ill patients is well known. Electrical impedance tomography is a noninvasive monitoring technology that has been primarily used to assess ventilation. We investigated the potential of electrical impedance tomography to measure left ventricular stroke volume variation as an expression of heart-lung interactions. The objective of this study was thus to determine in a set of different hemodynamic conditions whether stroke volume variation measured by electrical impedance tomography correlates with those derived from an aortic ultrasonic flow probe and arterial pulse contour analysis. Prospective animal study. University animal research laboratory. Domestic pigs, 29-50 kg. A wide range of hemodynamic conditions were induced by mechanical ventilation at different levels of positive end-expiratory pressure (0-15 cm H₂O) and with tidal volumes of 8 and 16 mL/kg of body weight and by hypovolemia due to blood withdrawal with subsequent retransfusion followed by infusions of hydroxyethyl starch. In eight pigs, aortic stroke volume variations measured by electrical impedance tomography were measured and compared to those derived from an aortic ultrasonic flow probe and from arterial pulse contour analysis. Data for four animals were used to develop and train a novel frequency-domain electrical impedance tomography analysis algorithm, while data for the remaining four were used to test the performance of the novel methodology. Correlation of stroke volume variation measured by electrical impedance tomography and that derived from an aortic ultrasonic flow probe was significant (r = 0.69; p < .001), as was the correlation between stroke volume variation measured by electrical impedance tomography and that derived from arterial pulse contour analysis (r = 0.73; p < .001). Correlation of stroke volume variation derived from an aortic ultrasonic flow probe and that derived from arterial pulse contour analysis was significant too (r = 0.82; p < .001). Bland-Altman analysis comparing stroke volume variation measured by electrical impedance tomography and that derived from an aortic ultrasonic flow probe revealed an overall bias of 1.87% and limits of agreement of ± 7.02%; when comparing stroke volume variation measured by electrical impedance tomography and that derived from arterial pulse contour analysis, the overall bias was 0.49% and the limits of agreement were ± 5.85%. Stroke volume variation measured by electrical impedance tomography correlated with both the gold standard of direct aortic blood flow measurements of stroke volume variation and pulse contour analysis, marking an important step toward a completely noninvasive monitoring of heart-lung interactions.

Clinical applicability of functional hemodynamic monitoring.

Recent interest in functional hemodynamic monitoring for the bedside assessment of cardiovascular insufficiency has heightened. Functional hemodynamic monitoring is the assessment of the dynamic interactions of hemodynamic variables in response to a defined perturbation. Accordingly, fluid responsiveness can be predicted in a quantities fashion by measuring as arterial pulse pressure variation and left ventricular stroke volume variation during positive pressure breathing or the change in cardiac output response to a passive leg raising maneuver. However, volume responsiveness, though important, reflects only part of the overall spectrum of functional physiological variables that can be measured to define physiologic state and monitor response to therapy. Dynamic tissue O2 saturation (StO2) responses to complete stop flow conditions, which can be created by measuring hand StO2 and occluding flow with a blood pressure cuff, assesses cardiovascular sufficiency and microcirculatory blood flow distribution. Furthermore, these measures can be made increasingly more sensitive and specific if coupled to other "traditional" measures of organ perfusion, such as blood lactate levels.

Pulmonary Blood Volume Variation Decreases after Myocardial Infarction in Pigs: A Quantitative and Noninvasive MR Imaging Measure of Heart Failure

To prospectively evaluate the usefulness of magnetic resonance (MR) imaging for estimating pulmonary blood volume (PBV) and the variation in PBV throughout the cardiac cycle in experimental heart failure. The animal care committee approved this prospective study. Seven pigs were studied before and after myocardial infarction. PBV measurement was validated in a phantom and calculated as the product of cardiac output determined with velocity-encoded MR imaging and the pulmonary transit time for an intravenous bolus of contrast material to pass through the pulmonary circulation. The difference in arterial and venous pulmonary flow during the cardiac cycle was integrated for calculation of the PBV variation (expressed as percentage of stroke volume). Differences were evaluated with the Wilcoxon test. Calculated and direct phantom measurements of PBV differed by a mean of 4% +/- 3 (standard deviation) (R(2) = 0.97, P < .001). Infarction induced a decrease in left ventricular stroke volume (44 mL +/- 6 vs 27 mL +/- 7; P = .02), ejection fraction (55% +/- 5 vs 41% +/- 4; P = .02), and PBV variation (61% +/- 12 vs 43% +/- 15; P = .04) but not PBV (225 mL +/- 23 vs 211 mL +/- 42; P = .50). The mean pulmonary artery pressure increased after infarction (19 mm Hg +/- 6 vs 27 mm Hg +/- 4; P = .04). Following infarction, the PBV variation but not PBV decreased. PBV variation was the noninvasive measure exhibiting the greatest percentage of change following infarction. MR imaging can be used to assess the variation of the PBV during the cardiac cycle as a marker of heart failure.

Ability of pulse power, esophageal Doppler, and arterial pulse pressure to estimate rapid changes in stroke volume in humans*

Measures of arterial pulse pressure variation and left ventricular stroke volume variation induced by positive-pressure breathing vary in proportion to preload responsiveness. However, the accuracy of commercially available devices to report dynamic left ventricular stroke volume variation has never been validated. We compared the accuracy of measured arterial pulse pressure and estimated left ventricular stroke volume reported from two Food and Drug Administration-approved aortic flow monitoring devices, one using arterial pulse power (LiDCOplus) and the other esophageal Doppler monitor (HemoSonic). We compared estimated left ventricular stroke volume and their changes during a venous occlusion and release maneuver to a calibrated aortic flow probe placed around the aortic root on a beat-to-beat basis in seven anesthetized open-chested cardiac surgery patients. Dynamic changes in arterial pulse pressure closely tracked left ventricular stroke volume changes (mean r .96). Both devices showed good agreement with steady-state apneic left ventricular stroke volume values and moderate agreement with dynamic changes in left ventricular stroke volume (esophageal Doppler monitor -1 +/- 22 mL, and pulse power -7 +/- 12 mL, bias +/- 2 sd). In general, the pulse power signals tended to underestimate left ventricular stroke volume at higher left ventricular stroke volume values. Arterial pulse pressure, as well as, left ventricular stroke volume estimated from esophageal Doppler monitor and pulse power reflects short-term steady-state left ventricular stroke volume values and tract dynamic changes in left ventricular stroke volume moderately well in humans.

Systolic pressure variation and pulse pressure variation during modifications of arterial pressure

This study was performed to investigate the effect of vasopressor therapy on systolic pressure variation (SPV) and pulse pressure variation (PPV) compared to experimentally measured left ventricular stroke volume variation (SVV). Prospective study in a university laboratory. Twelve anesthetized and mechanically ventilated pigs. Increase in mean arterial pressure (by 100%) using phenylephrine and decrease (by 38%) using adenosine. SPV and PPV were calculated and compared to SVV derived from aortic blood flow measurements. SPV was significantly affected by changes in arterial pressure [4.6% (1.5) vs. 6.3% (2.1), p < 0.05, increased vs. decreased arterial pressure], whereas PPV did not change during modifications of arterial pressure. During baseline conditions and decreased afterload, correlation with SVV was good both for SPV (r =0.892 and r = 0.859, respectively) and for PPV (r = 0.870 and r = 0.871, respectively) (all p < 0.001). Correlation with SVV was only moderate during increased arterial pressure (r = 0.683 for SPV and r = 0.732 for PPV, p < 0.05). For guiding fluid therapy in patients under vasopressor support, PPV seems superior to SPV.

How accurate are different arterial pressure-derived estimates of cardiac output and stroke volume variation measures in critically ill patients?

We compared the cross-correlation between estimates of cardiac output (CO) and left ventricular stroke volume variation (SVV) amongst three commercially available, minimally invasive devices. (LiDCOplus, FloTrac and PiCCO).

Limitations of arterial pulse pressure variation and left ventricular stroke volume variation in estimating cardiac pre‐load during open heart surgery*

In addition to their well-known ability to predict fluid responsiveness, functional pre-load parameters, such as the left ventricular stroke volume variation (SVV) and pulse pressure variation (PPV), have been proposed to allow real-time monitoring of cardiac pre-load. SVV and PPV result from complex heart-lung interactions during mechanical ventilation. It was hypothesized that, under open-chest conditions, when cyclic changes in pleural pressures during positive-pressure ventilation are less pronounced, functional pre-load indicators may be deceptive in the estimation of ventricular pre-load. Forty-five patients undergoing coronary artery bypass grafting participated in this prospective, observational study. PPV and SVV were assessed by pulse contour analysis. The thermodilution technique was used to measure the stroke volume index and global and right ventricular end-diastolic volume index. Trans-oesophageal echocardiography was used to determine the left ventricular end-diastolic area index. All parameters were assessed before and after sternotomy, and, in addition, after weaning from cardiopulmonary bypass before and after chest closure (pericardium left open). Patients were ventilated with constant tidal volumes (8 +/- 2 ml/kg) throughout the study period using pressure control. SVV and PPV decreased after sternotomy and increased after chest closure. However, these changes could not be related to concomitant changes in the ventricular pre-load. The stroke volume index was correlated with SVV and PPV in closed-chest conditions only, whereas volumetric indices reflected cardiac pre-load in both closed- and open-chest conditions. SVV and PPV were correlated with left and right ventricular pre-load in closed-chest-closed-pericardium conditions only (with the best correlation found for the right ventricular end-diastolic volume index). SVV and PPV may be misleading when estimating cardiac pre-load during open heart surgery.

Validation of pulse contour derived stroke volume variation during modifications of cardiac afterload

Left ventricular stroke volume variation (SVV) or its surrogates are useful tools to assess fluid responsiveness in mechanically ventilated patients. So far it is unknown, how changes in cardiac afterload affect SVV. Therefore, this study compared left ventricular SVV derived by pulse contour analysis with SVV measured using an ultrasonic flow probe and investigated the influence of cardiac afterload on left ventricular SVV. In 13 anaesthetized, mechanically ventilated pigs [31(SD 6) kg], we compared cardiac output (CO), stroke volume (SV), and SVV determined by pulse contour analysis and by an ultrasonic aortic flow signal (Bland-Altman analysis). After obtaining baseline measurements, cardiac afterload was increased using phenylephrine and decreased using adenosine (both continuously administered). Measurements were performed with a constant tidal volume (12 ml kg-1) without PEEP. Neither increasing mean arterial pressure (MAP) [from 59 (7) to 116 (19)] nor decreasing MAP [from 63 (7) to 39 (4)] affected CO, SV, and SVV (both methods). Method comparison revealed a bias for SVV of 0.1% [standard error of the mean (SE) 0.8] at baseline, -1.2% (SE 0.8) during decreased and 4.0% (SE 0.7) during increased afterload, the latter being significantly different from the others (P<0.05). Thereby, pulse contour analysis tended to underestimate SVV during decreased afterload and to overestimate SVV during increased afterload. Limits of agreement were approximately 6% for all points of measurement. Left ventricular SVV is not affected by changes in cardiac afterload. There is a good agreement of pulse contour with flow derived SVV. The agreement decreases, if afterload is extensively augmented.

The influence of positive end-expiratory pressure on stroke volume variation and central blood volume during open and closed chest conditions

Intermittent positive pressure ventilation and positive end-expiratory pressure (PEEP) affect cardiac preload. Their effect is dependent on chest wall compliance. This study compares the effects of intermittent positive pressure ventilation and PEEP on stroke volume variation and central blood volume during open and closed chest conditions. Fourteen anesthetized and mechanically ventilated pigs (25-40 kg) were studied. Central blood volume was assessed using global end-diastolic volume and right ventricular end-diastolic volume measured by thermodilution. Further, left and right ventricular stroke volume variations were determined with ultrasonic flow probes placed around the pulmonary artery and ascending aorta, respectively. Measurements were performed during mechanical ventilation without and with PEEP (15 cmH(2)O) in open and closed chest conditions. With the chest closed mean arterial pressure, cardiac output, stroke volume, global end-diastolic volume, and right ventricular end-diastolic volume were significantly lower when compared to open chest conditions. Concomitantly, right ventricular, but not left ventricular stroke volume variation increased significantly. Applying PEEP led to a significant reduction of cardiac output, stroke volume and right ventricular end-diastolic volume, with a concomitant increase in left and right ventricular stroke volume variation both during open and closed chest conditions (all P-values<0.05). We conclude that PEEP increases right and left ventricular stroke volume variation both during open and closed chest conditions. The concomitant reduction of right ventricular end-diastolic volume further indicates that PEEP has a preload reductive effect during open chest conditions, too.

The influence of chest opening and closure on left ventricular stroke volume variation (SVV) and pulse pressure variation (PPV)

The influence of chest opening and closure on left ventricular stroke volume variation (SVV) and pulse pressure variation (PPV)

Prediction of fluid responsiveness in patients during cardiac surgery

Left ventricular stroke volume variation (SVV) has been shown to be a predictor of fluid responsiveness in various subsets of patients. However, the accuracy and reliability of SVV are unproven in patients ventilated with low tidal volumes. Fourteen patients were studied immediately after coronary artery bypass grafting (CABG). All patients were mechanically ventilated in pressure-controlled mode [tidal volume 7.5 (1.2) ml kg(-1)]. In addition to standard haemodynamic monitoring, SVV was assessed by arterial pulse contour analysis. Left ventricular end-diastolic area index (LVEDAI) was determined by transoesophageal echocardiography. A transpulmonary thermodilution technique was used for measurement of cardiac index (CI), stroke volume index (SVI) and intrathoracic blood volume index (ITBI). All variables were assessed before and after a volume shift induced by tilting the patients from the anti-Trendelenburg (30 degrees head up) to the Trendelenburg position (30 degrees head down). After the change in the Trendelenburg position, SVV decreased significantly, while CI, SVI, ITBI, LVEDAI, central venous pressure (CVP) and pulmonary artery occlusion pressure (PAOP) increased significantly. Changes in SVI were significantly correlated to changes in SVV (r=0.70; P<0.0001) and to changes in LVEDAI, ITBI, CVP and PAOP. Only prechallenge values of SVV were predictive of changes in SVI after change from the anti-Trendelenburg to the Trendelenburg position. In patients after CABG surgery who were ventilated with low tidal volumes, SVV enabled prediction of fluid responsiveness and assessment of the haemodynamic effects of volume loading.

Assessment of volume responsiveness in mechanically ventilated patients

Monitoring and management of intravascular volume status is of crucial importance in critically ill patients. Hypovolemia, induced by hemorrhage or pathologic fluid shifts in the presence of systemic inflammation, is frequently the cause for hemodynamic instability and hypotension. This deficit of central blood volume leads to a reduction in biventricular cardiac preload. With respect to the Frank-Starling mechanism, this causes an alteration in left ventricular stroke volume. If this reduction in stroke volume cannot be compensated by an increase in heart rate, this finally results in a decline of cardiac output. In this clinical situation fluid loading is the treatment of choice. However, insufficient peripheral vascular resistance and thus reduced cardiac afterload as well as impaired myocardial contractility also have to be taken in account to be causative for hypotension. Potential hazards of fluid loading specifically in the latter situation include pulmonary edema, worsening of pulmonary gas exchange and myocardial failure. Thus, prediction of fluid responsiveness, i.e. the prediction of the hemodynamic response to fluid loading is of utmost importance in critically ill patients. Several conventional parameters of systemic hemodynamic monitoring such as the cardiac filling pressures CVP and PAOP, the estimation of the left ventricular end-diastolic area (LVEDA) by echocardiography and measurement of central blood volumes as the right-ventricular end-diastolic volume (RVEDV) or the global end-diastolic volume (GEDV) by thermodilution are frequently used for preload monitoring. Further, functional preload parameters such as the left ventricular stroke volume variation (SW), describing the specific interactions of the heart and the lungs under mechanical ventilation, have been recently proposed to be useful for predicting fluid responsiveness. Thus, it is the aim of the present article to analyze these different concepts of hemodynamic monitoring regarding their usefulness and clinical applicability to predict fluid responsiveness at the bedside.

Usefulness of left ventricular stroke volume variation to assess fluid responsiveness in patients with reduced cardiac function.

Stroke volume variation as measured by the analysis of the arterial pressure waveform enables prediction of volume responsiveness in ventilated patients with normal cardiac function. The aim of this study was to investigate the ability of monitoring stroke volume variation to predict volume responsiveness and to assess changes in preload in patients with reduced left ventricular function after cardiac surgery. Prospective study. University hospital. Fifteen mechanically ventilated patients with a left ventricular ejection fraction <0.35 (study group) and 15 patients with an ejection fraction >0.50 (control group) after coronary artery bypass grafting following admission to the intensive care unit. Volume loading with 10 mL of hetastarch 6% times body mass index. If stroke volume index increased >5%, successive volume loading was performed until no further increase in stroke volume index was reached. Stroke volume variation, central venous pressure, pulmonary artery occlusion pressure (PAOP), and left ventricular end-diastolic area index (LVEDAI) were measured at baseline and immediately after each volume loading step. In both groups, stroke volume variation at baseline correlated significantly with changes in stroke volume index caused by volume loading (p <.01). Further, changes in stroke volume variation as a result of volume loading correlated significantly with the concomitant changes in stroke volume index in both groups (p <.01). Using receiver operating characteristic analysis, in the study group areas under the curve for stroke volume variation, PAOP, central venous pressure, and LVEDAI did not differ significantly. In the control group, the area under the curve for stroke volume variation was statistically larger than for PAOP, central venous pressure, and LVEDAI. Continuous and real-time monitoring of stroke volume variation by pulse contour analysis can predict volume responsiveness and allows real-time assessment of the hemodynamic effect of volume expansion in patients with reduced left ventricular function after cardiac surgery.

Influence of tidal volume on left ventricular stroke volume variation measured by pulse contour analysis in mechanically ventilated patients

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.

Dependence of ventricular distensibility on filling of the opposite ventricle.

Dependence of ventricular distensibility on filling of the opposite ventricle.