Daniel A. Reuter

Cardiac output monitoring using indicator-dilution techniques: basics, limits, and perspectives.

The ability to monitor cardiac output is one of the important cornerstones of hemodynamic assessment for managing critically ill patients at increased risk for developing cardiac complications, and in particular in patients with preexisting cardiovascular comorbidities. For >30 years, single-bolus thermodilution measurement through a pulmonary artery catheter for assessment of cardiac output has been widely accepted as the “clinical standard” for advanced hemodynamic monitoring. In this article, we review this clinical standard, along with current alternatives also based on the indicator-dilution technique, such as the transcardiopulmonary thermodilution and lithium dilution techniques. In this review, not only the underlying technical principles and the unique features but also the limitations of each application of indicator dilution are outlined.

Assessing cardiac preload or fluid responsiveness? It depends on the question we want to answer.

between these extreme values [4]. Therefore, for physiological reasons, we cannot accurately predict fluid responsiveness simply by assessing cardiac preload. Does it mean that assessing cardiac preload is useless? No, because assessing preload is useful in answering another clinical question: “Does our fluid challenge effectively increase cardiac preload?” The increase in ventricular end-diastolic volumes (i.e. in preload) as a result of fluid therapy depends on the partitioning of the fluid into different cardiovascular compartments organized in series. In this regard, when venous capacitance is increased or ventricular compliance is decreased, fluid infusion will increase intravascular blood volume, but not necessarily cardiac preload [5]. Thus, a patient can be a non-responder to a fluid challenge because preload does not increase or because his heart is operating on the flat portion of the Frank-Starling curve. In the first case, giving more fluid may be useful to increase cardiac preload and hence output significantly, while in the second case only an inotrope may improve cardiac output. Thus, assessment of cardiac preload as well as fluid responsiveness are useful for the clinician, but definitely not to answer the same question. References

The influence of PEEP and tidal volume on central blood volume.

Background and objective: Measurement of central blood volumes (CBV), such as global end‐diastolic volume (GEDV) and right ventricular end‐diastolic volume (RVEDV) are considered appropriate estimates of intravascular volume status. However, to apply those parameters for preload assessment in mechanically ventilated patients, the influence of tidal volume (TV) and positive endexpiratory airway pressure (PEEP) on those parameters must be known. Methods: In 13 mechanically ventilated piglets, the effect of low (10 mL kg−1) and high (20 mL kg−1) TVs on CBV was investigated in absence and presence of PEEP (0 and 15 cmH2O). GEDV, RVEDV, right heart (RHEDV) and left heart end‐diastolic volume (LHEDV) were measured by thermodilution. Blood flow on the descending thoracic aorta measured with an ultrasonic flow‐probe served to determine stroke volume (SV). Measurements were performed during baseline conditions, after volume loading with previously extracted haemodilution blood (20 mL kg−1) and following haemorrhage (30 mL kg−1). Results: Application of PEEP decreased GEDV and SV significantly (P < 0.05). Augmenting TV did not reduce GEDV systematically, but significantly reduced SV (P < 0.05). Changes in ventilator settings only influenced RVEDV following volume loading (P < 0.05). RHEDV and LHEDV decreased following application of PEEP, but only RHEDV decreased after augmenting TV at baseline and following volume loading. Correlation of SV with parameters of CBV was r = 0.487 (P < 0.01) for GEDV, r = 0.553 (P < 0.01) for RVEDV, r = 0.596 (P < 0.01) for RHEDV and r = 0.303 (P < 0.01) for LHEDV. Conclusion: Application of PEEP decreases CBV and SV. Augmenting TV reduces SV but not CBV. There is a moderate correlation between parameters of CBV and cardiac performance.

Respiratory systolic variation test in acutely impaired cardiac function for predicting volume responsiveness in pigs

BACKGROUND Predicting the response of cardiac output (CO) to volume administration remains difficult, in particular in patients with acutely compromised cardiac function, where, even small amounts of i.v. fluids can lead to volume overload. We compared the ability to predict volume responsiveness of different functional haemodynamic parameters, such as pulse pressure variation (PPV), stroke volume variation (SVV), the static preload parameter right atrial pressure (RAP), and global end-diastolic volume (GEDV) with the recently proposed respiratory systolic variation test (RSVT) in acutely impaired cardiac function. METHODS In 13 mechanically ventilated pigs, cardiac function was acutely reduced by continuous application of verapamil to reach a decrease in peak change of left ventricular pressure over time (dP/dt) of 50%. After withdrawal of 20 ml kg(-1) BW blood to establish hypovolaemia, four volume loading steps of 7 ml kg(-1) BW using the shed blood and 6% hydroxyethylstarch 130/0.4 were performed. Volume responsiveness was considered as positive, if CO increased more than 10%. RESULTS Receiver operating characteristic curve analysis revealed an area under the curve (AUC) of 0.88 for the RSVT, 0.84 for PPV, 0.82 for SVV, 0.78 for RAP, and 0.77 for GEDV. CONCLUSIONS Functional parameters of cardiac preload, including the RSVT, allow prediction of fluid responsiveness in an experimental model of acutely impaired cardiac function.

The influence of cardiac preload and positive end-expiratory pressure on the pre-ejection period

The pre-ejection period (PEP) has recently been described as a potential parameter for monitoring cardiac preload. This study further investigated the influence of changes in intravascular volume status and the application of positive end-expiratory pressure (PEEP) on the pre-ejection period. In ten pigs, ECG, arterial pressure and stroke volume derived from an aortic flowprobe were registered. Global end-diastolic volume (GEDV) was measured by transcardiopulmonary thermodilution. Total blood volume (TBV) and intrathoracic blood volume (ITBV) were measured by the dye-dilution technique. Measurements were performed during normovolaemic conditions, after volume loading with haemodilution blood (20 ml kg(-1)) and following haemorrhage (30 ml kg(-1)) without PEEP and with PEEP (15 cm H(2)O) applied. Volume loading increased GEDV, ITBV, TBV and SV, whereas PEP remained constant. However, the changes were not significant (P > 0.05). Subsequent haemorrhage significantly decreased GEDV (from 436 to 308 ml), ITBV (from 729 to 452 ml), TBV (from 2,131 to 1,488 ml) (all P-values <0.05), and SV (from 20.7 ml to 14.3 ml, P < 0.001). However, PEP did not change significantly (from 73 to 82 ms, P > 0.05). No correlation between the changes in PEP and changes in any other variable was observed. It is concluded that PEP is not sensitive to the changes in intravascular volume status.

The ryanodine contracture test may help diagnose susceptiblity to malignant hyperthermia

PurposeThe ryanodine contracture test (RCT) using the plant alkaloid ryanodine as the triggering agent has been proposed to reduce equivocal results of thein vitro caffeine-halothane-contracture test (IVCT), which is the accepted and standardized procedure to diagnose malignant hyperthermia (MH). However, the response of skeletal muscle of non-MH affected patients (controls) to ryanodine has not yet been characterized.MethodsSkeletal muscle biopsies were studied in 33 controls and in six patients with a history of fulminant MH. Following the IVCT, the RCT was performed in all specimens using ryanodine 1 μM. Onset time of contracture and time to reach a contracture level of 10 mN above lowest resting tension and above predrug tension were calculated.ResultsWith the standard IVCT, all controls were labelled MH non-susceptible; all clinically diagnosed MH patients were labelled MH susceptible. With ryanodine, control muscle differed from MH susceptible muscle regarding onset time of contracture (26 vs 3.8 min,P < 0.05) and time to reach a contracture of 10 mN (49 vs 12.5 min, P < 0.05; all median). Tissue viability and patient’s age significantly influenced contracture times.ConclusionsDespite the highly specific binding of ryanodine at the myocytic sarcoplasmic reticulum, the wide range of contracture times of the controls points toward heterogeneity of ryanodine receptors within physiologic limits. This may also be caused in part by tissue viability and the patients’ age. The ryanodine contracture test performed in addition to the IVCT may add clarity into diagnosing a patient as MH-susceptible or not.RésuméObjectifLe test decontracture à la ryanodine (TCR), qui utilise un alcaloïde de la ryania comme agent déclencheur, a été proposé pour réduire les résultats équivoques du test de contracture in vitro à la caféinehalothane (TIVC), lequel est accepté et normalisé pour le diagnostic de l’hyperthermie maligne (HM). Cependant, la réaction des muscles squelettiques des patients non affectés d’HM (témoins) à la ryanodine n’a pas encore été définie.MéthodeDes biopsies de muscles squelettiques ont été étudiées chez 33 témoins et six patients présentant des antécédents d’HM fulminante. À la suite du TIVC, le TCR a été réalisé pour tous les prélévements en utilisant 1 μM de ryanodine. Ont été calculés : le délai d’installation de la contracture et le temps nécessaire pour atteindre un niveau de 10 mN audessus de la plus faible tension de repos et audessus de la tension de prémédication.RésultatsPour le TIVC standard, les témoins ont été étiquetés comme non susceptibles d’HM et les patients ayant un diagnostic d’HM, comme susceptibles d’HM. Pour le test à la ryanodine, les muscles témoins différaient des muscles susceptibles d’HM, quant au délai d’installation de la contracture (26 vs 3,8 min, P < 0,05) et au temps nécessaire pour obtenir une contracture de 10 mN (49 vs 12,5 min, P < 0,05 ; médiane). La viabilité tissulaire et l’âge des patients ont eu une influence significative sur les temps de contracture.ConclusionMalgré une importante fixation de la ryanodine au réticulum sarcoplasmique myocytaire, la grande variation des temps de contracture des témoins indique une hétérogénéité des récepteurs de ryanodine qui se situe à l’intérieur des limites physiologiques. Cette situation peut dépendre aussi, en partie, de la viabilité tissulaire et de l’âge du patient. Le test de contracture à la ryanodine, ajouté au TIVC, peut aider à poser le diagnostic de susceptibilité ou non à l’HM.

Assessing volume responsiveness during open chest conditions in cardiac surgery patients: 113

Department of Anaesthesiology and Department of Cardiac Surgery, University of Munich, Munich, Germany Introduction: Assessment of heart–lung interactions under positive pressure ventilation by measurement of left ventricular stroke volume variations (SVV) is useful to optimize preload in patients following cardiac surgery [1]. The aim of the present study was to investigate the ability of SVV measured by arterial pulse contour analysis to detect volume responsiveness in patients undergoing coronary artery bypass grafting under open thorax conditions. Method: With approval of the ethics committee and written informed consent we studied 22 patients immediately following sternotomy. SVV, central venous pressure (CVP), left ventricular end-diastolic area index (LVEDAI) by transoesophageal echocardiography, global end-diastolic area index (GEDVI) and cardiac index (CI) by thermodilution were measured after removal of 500 mL blood and after subsequent volume substitution with 500 mL hydroxyethyl starch 6%. The saved blood was retransfused after termination of cardiopulmonary bypass. Isovolaemic haemodilution is performed in our service routinely to minimize the need of autologous blood transfusions. Results: All data are expressed as mean SD. One way ANOVA for repeated measurements with Bonferroni adjustment and Pearson product moment correlations were performed. Blood removal led to a significant increase of SVV from 6.7 2.2% to 12.7 3.8%. CI (from 2.9 0.6 to 2.3 0.5 L min 1m 2) and GEDVI (from 650 98 to 565 98 mL m 2) decreased (all P 0.025). LVEDAI and CVP did not change significantly. After volume loading SVV decreased significantly to 6.8 2.2%. Concomitantly, CI (to 3.3 0.5 L min 1 m 2), GEDVI (to 663 104 mL m 2), and CVP (to 3 4 mmHg) increased significantly (all P 0.025), whereas the increase in LVEDAI (to 11.3 4.8 cm2 m 2) was not significant. We found a significant correlation between the increase in CI caused by volume loading ( CI) and SVV before volume loading (R 0.80; P 0.001). Modest correlations were found between CI and GEDVI (R 0.44; P 0.05) and LVEDAI (R 0.52; P 0.05) before volume loading, whereas no correlation was found for CVP. Discussion: These findings demonstrate that changes in CI caused by volume loading can be predicted by measurement of SVV under open thorax conditions. Thus, assessing heart lung interactions may improve hemodynamic management during surgical procedures requiring thoracotomy. Reference: 1 Reuter DA, Felbinger TW, Schmidt C, et al. Stroke volume variations for assessment of cardiac responsiveness to volume loading in mechanically ventilated patients after cardiac surgery. Intensive Care Med 2002; 28: 392–398.