[Accuracy of pulse contour cardiac index measurements during changes of preload and aortic impedance]. / Arterielle Pulskonturanalyse zur Messung des Herzindex unter Veränderungen der Vorlast und der aortalen Impedanz.

BACKGROUND: Cardiac index obtained by arterial pulse contour analysis (CI(PC)) demonstrated good agreement with arterial or pulmonary arterial thermodilution derived cardiac index (CI(TD), CI(PA)) in cardiac surgical or critically ill patients. However as the accuracy of pulse contour analysis during changes of the aortic impedance is unclear, we compared CI(PC), CI(TD) and CI(PA) during changes of preload and the aortic impedance as occurring during sternotomy. PATIENTS AND METHODS: CI(PC) und CI(TD), were compared in 28 patients, (and CI(PA) in 6 patients) undergoing elective coronary artery bypass grafting, before and after sternotomy. The relative changes DeltaCI(PC) und DeltaCI(PC) were calculated. RESULTS: Sternotomy resulted in a significant increase in CI in 25 out of 28 patients. Regression analysis was performed between CI(PC) and CI(TD) before and after sternotomy (r(2) = 0.87, p<0.0001, r(2) = 0.88, p<0.0001) as well as between CI(PC) and CI(PA), before and after sternotomy (r(2) = 0.85, p<0.0001, r(2) = 0.93, p<0.01) and between DeltaCI(PC) and DeltaCI(TD) (r(2) = 0.72, p<0.0001). Bland Altman-Analysis for determining bias (m) and precision (2SD) between CI(PC) and CI(TD) before and after sternotomy and between DeltaCI(PC) and DeltaCI(TD) resulted in m = -0.03 L/min/m(2), 2SD = -0.34 to 0.28 L/min/m(2), m = -0.06 L/min/m(2), 2SD = -0.45 to 0.33 L/min/m(2) and m = -0.02 L/min/m(2), SD = -0.47 to 0.44 L/min/m(2). CONCLUSION: Pulse contour analysis derived CI(PC) accurately reflects thermodilution derived CI(TD) or CI(PA) during changes of preload and the aortic impedance as occurring during sternotomy.

Assessing fluid responsiveness during open chest conditions.

BACKGROUND: Measurement of ventilation-induced left ventricular stroke volume variations (SVV) or pulse pressure variations (PPV) is useful to optimize preload in patients after cardiac surgery. The aim of this study was to investigate the ability of SVV and PPV measured by arterial pulse contour analysis to assess fluid responsiveness in patients undergoing coronary artery bypass surgery during open-chest conditions. METHODS: We studied 22 patients immediately after midline sternotomy. We determined SVV, PPV, left ventricular end-diastolic area index by transoesophageal echocardiography, global end-diastolic volume index and cardiac index by thermodilution before and after removal of blood 500 ml and after volume substitution with hydroxyethyl starch 6%, 500 ml. RESULTS: Blood removal resulted in a significant increase in SVV from 6.7 (2.2) to 12.7 (3.8)%. PPV increased from 5.2 (2.5) to 11.9 (4.6)% (both P<0.001). Cardiac index decreased from 2.9 (0.6) to 2.3 (0.5) litres min(-1) m(-2) and global end-diastolic volume index decreased from 650 (98) to 565 (98) ml m(-2) (both P<0.025). Left ventricular end-diastolic area index did not change significantly. After fluid loading SVV decreased significantly to 6.8 (2.2)% and PPV decreased to 5.4 (2.1)% (both P<0.001). Concomitantly, cardiac index increased significantly to 3.3 (0.5) litres min(-1) m(-2) (P<0.001) and global end-diastolic volume index increased significantly to 663 (104) ml m(-2) (P<0.005). Left ventricular end-diastolic area index did not change significantly. We found a significant correlation between the increase in cardiac index caused by fluid loading and SVV as well as PPV before fluid loading (SVV, R=0.74, P<0.001; PPV, R=0.61, P<0.005). No correlations were found between values of global end-diastolic volume index or left ventricular end-diastolic area index before fluid loading and the increase in cardiac index. CONCLUSION: Measurement of SVV or PPV allows assessment of fluid responsiveness in hypovolaemic patients under open-chest and open-pericardium conditions. Thus, measuring heart-lung interactions may improve haemodynamic management during surgical procedures requiring mid-line sternotomy.

Effects of mid-line thoracotomy on the interaction between mechanical ventilation and cardiac filling during cardiac surgery.

BACKGROUND: Mid-line thoracotomy is a standard approach for cardiac surgery. However, little is known how this surgical approach affects the interaction between the circulation and mechanical ventilation. We studied how mid-line thoracotomy affects cardiac filling volumes and cardiovascular haemodynamics, particularly variations in stroke volume and pulse pressure caused by mechanical ventilation. METHODS: We studied 19 patients during elective coronary artery bypass surgery. Before and after mid-line thoracotomy, we measured arterial pressure, cardiac index (CI) and global end-diastolic volume index (GEDVI) by thermodilution, left ventricular end-diastolic area index (LVEDAI) by transoesophageal echocardiography and the variations in left ventricular stroke volume and pulse pressure during ventilation by arterial pulse contour analysis. RESULTS: After thoracotomy, CI increased from 2.3 (0.4) to 2.9 (0.6) litre min(-1) m(-2), GEDVI increased from 605 (110) to 640 (94) litre min(-1) m(-2), and LVEDAI increased from 9.2 (3.7) to 11.2 (4.1) cm(2) m(-2). All these changes were significant. In contrast, stroke volume variation (SVV) decreased from 10 (3) to 6 (2)% and pulse pressure variation (PPV) decreased from 11 (3) to 5 (3)%. Before thoracotomy, SVV and PPV significantly correlated with GEDVI (both P<0.01). When the chest was open, similar significant correlations of SVV (P<0.001) and PPV (P<0.01) were found with GEDVI. CONCLUSION: Thoracotomy increases cardiac filling and preload. Further, thoracotomy reduces the effect of mechanical ventilation on left ventricular stroke volume. However, also under open chest conditions, SVV and PPV are preload-dependent.

Hypovolemic shock and cardiac contractility: assessment by end-systolic pressure-volume relations.

The end-systolic pressure-volume relation (ESPVR) is accepted as a load-independent measure of cardiac contractility. Potential curvilinearity of the ESPVR, dependency on coronary perfusion pressure (CPP) and sensitivity to the type of loading intervention might limit its use in hemorrhagic shock. This study compared ESPVRs obtained by caval and aortic occlusion under physiological loading conditions at baseline with those obtained during hemorrhagic shock (mean arterial pressure 45 mmHg). The left ventricular (LV) pressure (tip manometer) and volume (conductance catheter) were measured in ten anesthetized pigs. ESPVRs were fitted to linear and quadratic models. Within end-systolic pressure (Pes) ranges obtained under baseline conditions, ESPVR displayed only minimal curvilinearity (second-order coefficient a < 0.007) and could be accurately described by a linear model. However, nonlinearity of ESPVRs obtained over wider load ranges is suggested by negative volume axis intercepts of the linear model. Steeper ESPVR with aortic than with caval occlusion (2.28 +/- 0.22 vs 3.41 +/- 0.51 mmHg/ml, ns) could not be proven owing to the large interindividual variance of ESPVR slopes with both loading interventions. During shock the Pes range obtained by caval occlusion decreased to very low levels (from 49 +/- 2 to 34 +/- 1 mmHg), ESPVR did not adequately fit either of the two models (mean R < 0.66), and critical reduction of CPP induced negative ESPVR slope in four of ten experiments. In contrast, aortic occlusion at shock resulted in linear ESPVR (R = 0.927 +/- 0.029), Pes ranges (92 +/- 3 to 58 +/- 4 mmHg) comparable to the ones obtained by caval occlusion at control (113 +/- 5 to 73 +/- 6 mmHg), and steeper ESPVR than at control (3.41 +/- 0.51 to 7.38 +/- 1.0 mmHg/ml, P < 0.05). Interpretation of the increased ESPVR slope obtained with aortic occlusion as due to increased contractility in shock is, however, complicated by different Pes ranges. It is concluded that within Pes ranges obtained with caval or aortic occlusion in situ the ESPVR can be adequately fitted to a linear model. For assessment of the inotropic response to shock the ESPVR is of limited value because (1) caval occlusion is not suitable to generate ESPVR during shock, and (2) Pes ranges obtained with identical loading interventions differ greatly between baseline and shock and, therefore, apparent ESPVR changes are influenced by the potential nonlinearity of the ESPVR. Combining caval occlusion at baseline with aortic occlusion at shock would result in comparable Pes ranges. Interpretation of results is, however, complicated by diverging effects of the different loading interventions on the shape and slope of the ESPVR.

Hypertonic saline dextran does not increase cardiac contractile function during small volume resuscitation from hemorrhagic shock in anesthetized pigs.

Small volumes of hypertonic saline dextran (10% of shed blood volume [SBV] restore cardiac output (CO) and increase arterial pressure in hemorrhagic shock. Besides rapid expansion of plasma volume, a positive inotropic effect has been proposed as an additional mechanism for the immediate onset of the cardiovascular response. This study compares the effects of 7.2% saline/10% dextran 60 (HSDex, n = 8) and normal saline (NS; n = 6) on central hemodynamics and cardiac contractility assessed by end-systolic elastance (Ees; conductance technique) and segmental preload recruitable stroke work (sPRSW; sonomicrometry). In anesthetized open chest pigs (28 +/- 1 kg, mean +/- SEM) shock was induced by blood withdrawal (40% of blood volume) to maintain mean arterial pressure (MAP) at 45 mm Hg for 75 min. Resuscitation was started by bolus infusion (2 min) of either HSDex (10% of SBV) or the identical sodium load of NS (80% of SBV); 30 min later both groups received 6% dextran (10% of SBV). Hemorrhagic shock reduced CO (-45%) and left ventricular end-diastolic volume (Ved; -70%) while Ees increased (NS:2.2 +/- 0.4 to 7.5 +/- 1.8 mm Hg/mL, P < 0.05; HSDex: 1.9 +/- 0.2 to 9.1 +/- 2.6 mm Hg/mL, P = 0.085). Within 5 min after infusion of either solution CO returned to baseline values and MAP (NS +55%, HSDex +64%) and Ved (+100%) increased. Neither HSDex nor NS increased Ees above shock levels (NS, 8.7 +/- 4.9 mm Hg/mL; HSDex, 7.3 +/- 2.6 mm Hg/mL) and no group differences occurred in other measurements of contractility (dP/dt40,sPRSW). Plasma osmolality increased to 328 +/- 3 mOsmol/kg with HSDex.(ABSTRACT TRUNCATED AT 250 WORDS)