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

OBJECTIVE: 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. DESIGN: Prospective study. SETTING: University hospital. PATIENTS: 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. INTERVENTIONS: 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. MEASUREMENTS AND MAIN RESULTS: 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. CONCLUSIONS: 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.     

Low systemic vascular resistance state in patients undergoing cardiopulmonary bypass.

OBJECTIVE: To determine the prevalence, hemodynamic characteristics, and risk factors for the low systemic vascular resistance (SVR) state in patients who have undergone cardiopulmonary bypass. DESIGN: Prospective cohort study. SETTING: The intensive care unit of a tertiary care hospital. PATIENTS: Seventy-nine consecutive patients who underwent coronary artery bypass graft, mitral valve, or aortic valve procedures. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Low SVR was defined as an indexed systemic vascular resistance (SVRi) of <1800 dyne x sec/cm5 x m2 at two consecutive times postoperatively. SVRi, cardiac index, mean arterial pressure, temperature, and central venous pressure were recorded before bypass and at 0, 1, 2, 4, 8, and 16 hrs after bypass. We recorded age, gender, urgency of operation, use of angiotensin-converting enzyme inhibitors and calcium channel blockers, ejection fraction, pump time, cross-clamp time, use of antifibrinolytics, type of oxygenator, amrinone use, postoperative biochemical and hematologic values, medication use, fluid balance, intensive care unit admission duration, and hospital admission duration. We assessed the role of diabetes mellitus, current smoking, and systemic hypertension. The incidence of the low-SVR state was 35 of 79 patients during a 3-month period (44%). At 8 hrs postoperatively, the SVRi in low-SVR and non-low-SVR patients was 1594+/-50 (SEM) and 2103+/-56 (SEM) dyne x sec/cm5 x m2, respectively (p < .001). In low-SVR patients, there was an initial and sustained increase in cardiac index and central venous pressure that preceded the decrease in mean arterial pressure. The decrease in mean arterial pressure was maximal at 8 hrs postoperatively. Patients with low SVR were more likely to have longer cross-clamp times, to be male, and to have lower postoperative platelet counts (p < .05 for all). Low-SVR patients were less likely to require dobutamine in the first 4 hrs postoperatively. CONCLUSIONS: Low SVR, a probable manifestation of systemic inflammatory response syndrome, is common in patients after cardiopulmonary bypass. These patients may respond better to a vasopressor to restore vascular tone than to volume loading to further increase cardiac index.     

Inhaled nitric oxide does not improve cardiac or pulmonary function in patients with an exacerbation of chronic obstructive pulmonary disease.

OBJECTIVE: To determine whether inhaled nitric oxide (NO) improves right ventricular function in mechanically ventilated patients with severe chronic obstructive pulmonary disease (COPD). DESIGN: Open, prospective, controlled trial. SETTING: General intensive care unit of a community hospital. PATIENTS: Twelve patients with acute respiratory failure caused by acute exacerbation of COPD requiring mechanical ventilation. INTERVENTIONS: Insertion of a pulmonary artery catheter modified with a rapid response thermistor and a radial arterial catheter. Nitric oxide was then administered to the patient via a T piece placed between the Y piece of the ventilator and the endotracheal tube. MEASUREMENTS AND MAIN RESULTS: Hemodynamic and gasometric variables were recorded before NO inhalation, during administration of inhaled NO (20 ppm, 20 mins), and 20 mins after NO discontinuation. Inhaled NO reduced pulmonary artery pressure from 26 +/- 6 to 22 +/- 5 mm Hg (p = .0004), but arterial oxygenation, cardiac output, and right ventricular ejection fraction remained unmodified (41% +/- 9% vs. 41% +/- 8%; not significant). Calculated pulmonary vascular resistance decreased from 453 +/- 233 to 348 +/- 108 dyne x sec/cm5 x m2 (p = .02), and right ventricular volumes did not change. Subsequently, right ventricular end-systolic pressure/volume ratio decreased from 0.52 +/- 0.22 to 0.44 +/- 0.19 mm Hg/mL/m2 (p = .01). No significant correlation was observed between the changes of pulmonary artery pressure (or pulmonary vascular resistance) and changes of right ventricular ejection fraction. CONCLUSION: Inhalation of NO does not seem to improve either right ventricular function or arterial oxygenation in patients with acute respiratory failure caused by acute exacerbation of COPD.     

Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volume, cardiac performance, or the response to volume infusion in normal subjects

OBJECTIVE: Pulmonary artery occlusion pressure and central venous pressure have been considered to be reliable measures of left and right ventricular preload in patients requiring invasive hemodynamic monitoring. Studies in recent years have questioned the correlation between these estimates of ventricular filling pressures and ventricular end-diastolic volumes/cardiac performance variables in specific patient groups, but clinicians have continued to consider the relationship valid in the broader context. The objective of this study was to assess the relationship between pressure estimates of ventricular preload (pulmonary artery occlusion pressure, central venous pressure) and end-diastolic ventricular volumes/cardiac performance in healthy volunteers. DESIGN: Prospective, nonrandomized, nonblinded interventional study. SETTING: Cardiac catheterization and echocardiography laboratories. SUBJECTS: Normal healthy volunteers (n = 12 group 1, n = 32 group 2). INTERVENTIONS: Pulmonary catheterization and radionuclide cineangiography (group 1) and volumetric echocardiography (group 2) during 3 L of normal saline infusion over 3 hrs. MEASUREMENTS AND MAIN RESULTS: In group 1, the initial pulmonary artery occlusion pressure and central venous pressure did not correlate significantly with initial end-diastolic ventricular volume indexes or cardiac performance (cardiac index and stroke volume index). Changes in pulmonary artery occlusion pressure and central venous pressure following saline infusion also did not correlate with changes in end-diastolic ventricular volume indexes or cardiac performance. In contrast, initial end-diastolic ventricular volume indexes and changes in these ventricular volume indexes in response to 3 L of normal saline loading correlated well with initial stroke volume index and changes in stroke volume index, respectively. The relationship between left ventricular end-diastolic volume index and stroke volume index was confirmed in group 2 subjects using mathematically independent techniques to measure these variables. In addition, initial central venous pressure, right ventricular end-diastolic volume index, pulmonary artery occlusion pressure, and left ventricular end-diastolic volume index failed to correlate significantly with changes in cardiac performance in response to saline infusion in group 1 subjects. CONCLUSIONS: Normal healthy volunteers demonstrate a lack of correlation between initial central venous pressure/pulmonary artery occlusion pressure and both end-diastolic ventricular volume indexes and stroke volume index. Similar results are found with respect to changes in these variables following volume infusion. In contrast, initial end-diastolic ventricular volume indexes and changes in end-diastolic ventricular volume indexes in response to saline loading correlate strongly with initial and postsaline loading changes in cardiac performance as measured by stroke volume index. These data suggest that the lack of correlation of these variables in specific patient groups described in other studies represents a more universal phenomenon that includes normal subjects. Neither central venous pressure nor pulmonary artery occlusion pressure appears to be a useful predictor of ventricular preload with respect to optimizing cardiac performance.     

Hemodynamic effects of intravenous timolol in coronary artery disease.

The hemodynamic effects of intravenous timolol were evaluated in 20 patients with coronary artery disease during diagnostic cardiac catheterization. The threshold dose of 0.25 mg reduced heart rate and cardiac index by 15% (p less than 0.05), left ventricular work index by 21% (p less than 0.05), and left ventricular dp/dt by 16% (p less than 0.05) while increasing left ventricular end-diastolic pressure by 49% (p less than 0.01), mean pulmonary arterial pressure by 17% (p less than 0.01), and systemic vascular resistance by 16% (NS). Larger doses (0.5 mg and 1.0 mg) induced similar responses with a greater effect on systemic vascular resistance (+22%, p less than 0.01, and +31%, p less than 0.001). The mean arterial pressure and stroke volumes were not affected by timolol. Peak effects, occurring at about 10 min after drug injection, did not correlate with plasma levels. The overall hemodynamic effects of timolol were similar to those reported for equipotent doses of propranolol and could be accounted for by the beta-adrenoceptor blocking activity.     

Intramyocardial Oxygen Monitoring in Coronary Artery Bypass Surgery

OBJECTIVE: In coronary artery bypass surgery various parameters have been used to monitor patients clinical status. Direct monitoring of myocardial oxygenation can be performed by measuring intramyocardial partial oxygen tension pressure (p ti O2). This study was performed to determine the perioperative time course of this parameter in correlation to standard monitoring parameters. METHODS: Twenty-three patients underwent standard coronary artery bypass grafting (CABG). A special polarographic microprobes was inserted into the myocardium in the distribution zone of the left anterior descending artery which was one of the target vessels of myocardial revascularization. Intramyocardial p ti O2 was monitored intra- and up to 12 hours postoperatively. Values were correlated to hemodynamic, oxygenation and procedure associated parameters. RESULTS: Myocardial oxygenation during CABG is characterized by a significant decrease of p ti O2 during cross-clamping and a significant increase after removal of the cross-clamp. The postoperative time course of p ti O2 shows a steady increase of p ti O2 in the first 12 postoperative hours investigated. Preoperative ejection fraction as well as cardio-pulmonary bypass time does not seem to have an influence on the postoperative p ti O2 in these patients. Various standard monitoring parameters show complex influence on intramyocardial p ti O2- CONCLUSIONS: Determination of intramyocardial partial oxygen pressure in patients undergoing bypass surgery shows characteristic changes. Changes in p ti O2 as a direct online parameter of myocardial oxygenation occur immediately after procedures that influence myocardial perfusion and therefore, may help to detect potential complications earlier than standard monitoring parameters in cardiac surgery.     

Differentiated and dose-related cardiovascular effects of a dual endothelin receptor antagonist in endotoxin shock

OBJECTIVE: To evaluate the effects of endothelin receptor antagonism on cardiac performance in endotoxin shock. DESIGN: Prospective, experimental study. SETTING: A university-affiliated research institution. SUBJECTS: Domestic anesthetized landrace pigs. INTERVENTIONS: Thirty-seven pigs were anesthetized and subjected to echocardiography, coronary sinus catheterization, and monitoring of central and regional hemodynamics in order to assess cardiac performance. All animals received endotoxin for 5 hrs. Twenty pigs served as endotoxin controls. Tezosentan, a dual endothelin-A and -B receptor antagonist, was administered during established endotoxemic shock. Seven pigs received an infusion of tezosentan of 1 mg x kg(-1) x hr(-1) (tezo1), and an additional ten pigs received a higher dose of 10 mg x kg(-1) x hr(-1) (tezo10). MEASUREMENTS AND MAIN RESULTS: Endotoxemia evoked a state of shock with pulmonary hypertension and metabolic acidosis. A decrease in stroke volume and coronary perfusion pressure as well as an increase in troponin I was also noted. Tezosentan administration resulted in a significant increase in cardiac index, stroke volume index, left ventricular stroke work index, and left ventricular end-diastolic area index. Decreases in systemic and pulmonary vascular resistance indexes were also evident after intervention. This was achieved without changes in heart rate or systemic arterial or pulmonary artery occlusion pressures in tezo, animals compared with controls. In addition, metabolic variables were improved by tezosentan. These effects were sustained only in the tezo, group. In the higher dosage, tezosentan resulted in a deterioration of cardiac performance and 50% mortality rate. The endotoxin-induced increase in troponin I was attenuated in the tezo, group compared with controls. CONCLUSIONS: In this porcine model of volume-resuscitated, endotoxemic shock, endothelin-receptor blockade with tezosentan improved cardiac performance. However, the effect was not sustained with higher doses of tezosentan, possibly due to reduced coronary perfusion pressure. These findings show differentiated, dose-dependent effects by dual endothelin receptor blockade on endotoxin-induced cardiovascular dysfunction.     

Intraoperative contrast echocardiography with intravenous optison does not cause hemodynamic changes during cardiac surgery.

BACKGROUND: The echocardiographic contrast agent Optison may be useful in patients undergoing cardiac surgery. This study investigates its effects on hemodynamics, cardiac performance, and oxygenation in this group of patients. METHODS: Parameters of hemodynamic stability, cardiac performance, and oxygenation were measured in 57 patients by transesophageal echocardiography, electrocardiography, invasive arterial blood pressure and central venous pressure monitoring, capnography, pulsoximetry, and pulmonary artery catheter before and 5 and 10 minutes after an intravenous bolus of 0.3 mL of Optison. RESULTS: No statistically significant differences in ST-segment changes, heart rate, arterial and central venous pressure, peripheral oxygen saturation, cardiac index, left ventricular ejection fraction, and regional wall motion were seen 5 and 10 minutes after injection of Optison compared with baseline parameters. CONCLUSIONS: Optison did not cause clinically important changes in parameters of hemodynamic stability, cardiac performance, and oxygenation in our patients. The intraoperative use of intravenous Optison appears to be safe in patients undergoing cardiac surgery, including in the use of cardiopulmonary bypass.     

Haemodynamic changes during left anterior descending artery exposure in off-pump coronary artery bypass: comparison between use of moist laparotomy pads and deep pericardial traction sutures for heart displacement

Haemodynamic changes occurring during heart displacement, using moist laparotomy pads placed behind the heart (PAD group, n = 26) or deep pericardial traction sutures (DPS group, n = 25) to facilitate exposure of the left anterior descending artery during off-pump coronary artery bypass surgery, were compared. Haemodynamic variables were assessed before and 10 min after displacement of the heart. The central venous pressure, mean pulmonary artery pressure and pulmonary capillary wedge pressure increased in both groups. After heart displacement in the PAD group, the cardiac index, stroke volume index, mixed venous oxygen saturation, right ventricular ejection fraction and left ventricular stroke work index decreased significantly, and the systemic vascular resistance and pulmonary vascular resistance increased significantly; these parameters remained unchanged in the DPS group. It was concluded that displacement of the heart using moist laparotomy pads caused significant haemodynamic derangement compared with that caused by deep pericardial traction sutures.     

Effects of titrated arginine vasopressin on hemodynamic variables and oxygen transport in healthy and endotoxemic sheep

OBJECTIVE: To determine the effects of titrated arginine vasopressin (AVP) alone or in combination with norepinephrine (NE) on hemodynamics and oxygen transport in healthy and endotoxemic sheep. DESIGN: Prospective controlled trial. SETTING: University research laboratory. SUBJECTS: Six adult ewes. INTERVENTIONS: Healthy sheep received AVP as a titrated infusion, initiated with 0.6 units/hr and increased by 0.6 units/hr every 15 mins, either until mean arterial pressure was increased by 20 mm Hg vs. baseline or a maximum of 3.6 units/hr was administered. After 90 mins, AVP infusion was continued with the investigated dosage, and NE (0.2 microg x kg(-1) x min(-1)) was also infused for 90 mins. After a 24-hr period of recovery, endotoxemia was induced and maintained (Salmonella typhosa endotoxin, 10 ng x kg(-1) x min(-1)) in the same sheep for the next 19 hrs. After 16 hrs of endotoxemia, AVP and NE were administered as described previously. MEASUREMENTS AND MAIN RESULTS: Hemodynamics were obtained at baseline, every 15 mins during the titration period, and 60 and 90 mins after additional NE infusion. Variables of oxygen transport were calculated before and after the titration period. In healthy and endotoxemic sheep, AVP reduced heart rate and cardiac index (p <.001) and compromised oxygen delivery (p <.001) and oxygen consumption (healthy sheep, p =.003; endotoxemic sheep, p <.001). Vasopressin infusion did not alter mean pulmonary arterial pressure but increased pulmonary vascular resistance index in both groups (p <.001). Additional infusion of NE further augmented mean arterial pressure and increased cardiac index during endotoxemia (p <.001). This was accompanied by an increase in oxygen delivery and consumption (p <.05 each). CONCLUSIONS: During ovine endotoxemia, AVP decreased cardiac index, compromised oxygen delivery, and increased pulmonary vascular resistance index. These side effects may limit its use as a sole vasopressor during sepsis. Potentially, a simultaneous infusion of AVP and NE could represent a useful therapeutic option.     

Use of a combined right ventricular ejection fraction-oximetry catheter system for coronary bypass surgery.

OBJECTIVE: To evaluate the reproducibility and accuracy of a new pulmonary artery catheter system that provides both right ventricular ejection fraction and continuous venous oxygen saturation monitoring. DESIGN: Criterion standard study. SETTING: University medical center. PATIENTS: A consecutive sample of ten patients undergoing elective coronary artery bypass surgery provided informed consent for the study. Exclusion criteria included emergency surgery or clinically important preoperative tricuspid regurgitation as assessed by echocardiography. None of the patient sample was excluded. MEASUREMENTS: Catheter-derived mixed venous and arterial oximetry data were compared with simultaneous values obtained using conventional laboratory cooximetry methods. Measurements were performed before cardiopulmonary bypass and intermittently up to 48 hrs after cardiopulmonary bypass. The variability of cardiac output and computed right ventricular ejection fraction was also assessed concurrently with the oximetry analysis. RESULTS: A significant correlation was observed for mixed venous oxygen saturation between catheter-derived and laboratory cooximetry data (r2 = .81, p < .01). Similarly, arterial oxygen saturation values obtained from pulse oximetry and laboratory values were significantly related (r2 = .81, p < .01). The coefficient of variation for each set of five repeated measurements for cardiac output was 8%, and for computed right ventricular ejection fraction, it was 16%. CONCLUSIONS: The combined catheter system provides the means to monitor both mixed venous oxygen saturation and right ventricular ejection fraction. These data provide a reliable and detailed assessment of cardiopulmonary function that should prove beneficial in the critical care setting.     

Spontaneous gasping generates cardiac output during cardiac arrest

OBJECTIVES: To measure stroke volumes coincident with spontaneous gasping during untreated ventricular fibrillation and to evaluate the effects of gasping. DESIGN: Prospective study in laboratory animals. SETTING: University-affiliated research institute. SUBJECTS: Male Yorkshire-X domestic pigs. INTERVENTIONS: Pigs were anesthetized (ketamine, 20 mg/kg intramuscularly and sodium pentobarbital, 30 mg/kg intravenously), intubated, and mechanically ventilated. Ventricular fibrillation was electrically induced and untreated for 7 mins. The right femoral artery and vein were cannulated. A 5.5/7.5-MHz biplanar transesophageal echocardiography transducer was advanced into the esophagus. MEASUREMENTS AND MAIN RESULTS: Stroke volumes were measured as the product of the transaortic blood flow velocity and transesophageal echocardiographic measurements of valve area. In addition, left ventricular volumes were echocardiographically estimated at peak inspiration and at peak expiration of each gasp by transesophageal methods. The stroke volume produced by gasping averaged 23 +/- 6 mL, which represented approximately 60% of a precardiac arrest stroke volume (38 +/- 8 mL, p <.001). Increases in end-tidal carbon dioxide tension coincident with each gasp were consistent with comparable increases in pulmonary blood flow and therefore stroke volumes. Both were associated with increases in aortic pressure from 20 +/- 3 to 33 +/- 8 mm Hg (p <.001) and coronary perfusion pressure from 4 +/- 3 to 13 +/- 7 mm Hg (p <.001). CONCLUSIONS: Our studies confirm that preterminal gasping during ventricular fibrillation increases both ventilation and forward blood flow.     

Pulmonary vascular resistance index during coronary artery bypass surgery with aprotinin

Low pulmonary vascular resistance index (PVRI) reflects favorable redundant pulmonary circulation following coronary artery bypass grafting with cardiopulmonary bypass surgery (CPB). This randomized study investigated whether aprotinin given in different modalities impacts PVRI after coronary artery bypass grafting. A total of 40 patients undergoing coronary artery bypass grafting were randomized to four groups according to aprotinin dose: (1) high dose, (2) early low dose, (3) late low dose, and (4) without aprotinin. Oxygenation index, pulmonary shunt, alveolar-arterial oxygen gradient and PVRI were determined. PVRI was calculated as the transpulmonary pressure gradient divided by cardiac index multiplied by 80. The results showed that PVRI remained relative low in all patients provided aprotinin regardless of treatment dosage; PVRI increased at 4?h after restarting ventilation after CPB in patients without aprotinin as compared with aprotinin (266?±?137, 266?±?115, 244?±?86 vs. 386?±?121, dynes-s-cm^?5, respectively, p?=?.047). Elevated postoperative PVRI was predictive for patients without aprotinin (AUC 0.668; SE 0.40; p?相似文献   

Haemodynamic effects of dopamine in septic shock

The Haemodynamic response to dopamine infusion has been assessed in 30 patients in septic shock with myocardial dysfunction. Dopamine infusion resulted in a haemodynamic improvement as indicated by significant increases in cardiac output of 38.4% (p>.001), stroke volume 18.7% (p<.001), and mean arterial pressure of 33% (p<.001). Despite the inotropic effect, left ventricular filling pressure did not change in 20 cases and increased in 10 cases. Mean peripheral resistance remained unchanged with a scatter of individual responses depending upon factors such as dopamine dose and initial vascular resistance.Dopamine increased intrapulmonary shunting by 48% (p<.001), insignificantly decreased PaO₂, increased mixed venous oxygen saturation by 16% (p<.02) and decreased pulmonary vascular resistance by 15% (p<.02).Both isoprenaline and dopamine improve stroke volume by an inotropic action, with an increase in venous return in the case of the latter and a reduction in afterload in the former.It is cocluded that the usefulness of dopamine in septic shock may be limited in patients with previous myocardial disease because of the risk of increasing preload and in hypoxaemic patients because of the risk of increasing intrapulmonary shunting.A preliminary report of this work was presented at the Fifth Annual Society of Critical Care Medicine meeting, Pittsburgh, PA, USA, May 1976     

Comparison between selective and nonselective nitric oxide synthase inhibition and phenylephrine in normal and endotoxic swine

OBJECTIVE: To compare the cardiopulmonary and peripheral circulatory effects of the nonselective nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) to the more selective inducible NOS inhibitor S-methylisothiourea (SMT) and to phenylephrine (PE) in endotoxic and normal swine. DESIGN: Prospective, randomized, unblinded study. SETTING: Research laboratory of academic medical center. SUBJECTS: Nonanesthetized, sedated, mechanically ventilated, minimally invasive swine model. INTERVENTIONS: Animals received either lipopolysaccharide (LPS, LPS groups) or equivalent volume of saline (normal groups). LPS animals were further randomized into four groups when mean arterial pressure (MAP) had dropped to <60 mm Hg: the LPS/saline group received saline only; the other groups received either L-NAME, SMT, or PE. These were titrated to elevate MAP by 20-25 mm Hg, and animals were followed for another 3 hrs. Pulmonary artery occlusion pressure was maintained at one to two times baseline with the infusion of saline. Normal groups received the same agents 1 hr after baseline measurements, and drugs were titrated to achieve similar increases in MAP. We measured gastric-arterial PCO2 gradient by tonometry as an index of gastric mucosal perfusion. Left ventricular volumes were determined echocardiographically; right ventricular volumes were determined by a pulmonary arterial catheter equipped with a rapid thermistor. Plasma nitrite/nitrate (NOx) concentrations were measured hourly. MEASUREMENTS AND MAIN RESULTS: In the LPS groups, all agents elevated MAP and systemic vascular resistance similarly. By hr 4, cardiac output had decreased in all groups, but the decrease with L-NAME (35% +/- 16%) occurred earlier (at hr 3) and was larger than the decrease with SMT at hrs 3 and 5 and larger than the decrease with saline at hrs 3 to 5. L-NAME resulted in a larger increase in mean pulmonary arterial pressure (MPAP) when compared with saline (130% +/- 44% vs. 61% +/- 25%; p < .001) and SMT groups (130% vs. 97% +/- 80%; p < .007). Only L-NAME had detrimental effects on right ventricular function as indicated by an increase in right ventricular end-systolic volume (54 +/- 10 to 87 +/-6 mL; p < .05) and right ventricular end-diastolic volume (90 +/-11 to 128 +/- 18 mL; p < .05). SMT decreased both left ventricular end-systolic volume (10.4 +/- 2 to 7.7 +/- 4 mL; p < .05) and left ventricular end-diastolic volume (18.5 +/- 3 to 14.2 +/- 5 mL; p < .05), indicating improved left ventricular function, whereas L-NAME did not affect left ventricular volumes. Both SMT and PE corrected LPS-induced gastric mucosal acidosis, but L-NAME did not. We did not detect changes in plasma NOx concentrations in any of LPS groups. In the normal groups, all agents increased MAP without changes in plasma NOx concentrations. L-NAME caused a larger decrease in cardiac output, but the increase in MPAP was higher with SMT. Both NOS inhibitors led to left ventricular dilation, but PE did not. Only L-NAME caused right ventricular dilation. There were no changes in gastric-arterial PCO2 gradient. CONCLUSIONS: In LPS animals, we failed to detect changes in plasma NOx concentrations. Furthermore, for similar increases in MAP, SMT improved gastric mucosal acidosis, had less adverse effects on right ventricular function and MPAP, and may have improved left ventricular function. However, apart from its bene-ficial effects on left ventricular function, SMT was not superior to PE. The results from normal animals indicate that both NOS inhibitors have adverse effects on cardiac function beyond those attributed to increased MAP.     

Hemodynamic effects of different lung-protective ventilation strategies in closed-chest pigs with normal lungs

OBJECTIVE: The benefits of lung-protective ventilation strategies used for acute respiratory distress syndrome in subjects with normal lungs are uncertain. The purpose of this study was to investigate the hemodynamic effects of conventional lung-protective ventilation (CLPV) and high-frequency oscillatory ventilation (HFOV) in a normal lung animal model. DESIGN: Prospective laboratory investigation. SETTING: Animal laboratory in a university medical center. SUBJECTS: Seven landrace pigs (mean weight 41 kg). INTERVENTIONS: Pigs were ventilated at random conventionally with positive end-expiratory pressure 2-3 cm H2O and tidal volume 10-12 mL/kg (control), with CLPV (positive end-expiratory pressure 10 cm H2O, tidal volume 6 mL/kg), or with HFOV. Hemodynamics were analyzed after insertion of biventricular conductance catheters and a pulmonary artery catheter. MEASUREMENTS AND MAIN RESULTS: The protective strategies led to higher mean airway pressures and severe hypercapnia with acidosis, which was only significant with CLPV. Compared with control, oxygenation was worse with CLPV and HFOV. With HFOV and CLPV, mean arterial pressure, cardiac output, and stroke volume decreased significantly; pulmonary arterial elastance increased. The slope of the end-diastolic pressure volume relationship for the left and right ventricle remained unchanged (preserved ventricular function), whereas the intercept increased with both protective strategies (augmented intrathoracic pressure); left and right end-diastolic volumes decreased significantly. CONCLUSIONS: In the absence of a fluid resuscitation strategy, CLPV and HFOV caused decreased mean arterial pressure, cardiac output, and stroke volume and worsened oxygenation in this normal lung animal model. This resulted primarily from a biventricular decrease in preload.     

Early postoperative 30 degrees lateral positioning after coronary artery surgery: influence on cardiac output

Aims and objectives. We investigated whether: (i) Early postoperative lateral position after coronary artery bypass surgery may have a negative influence on the cardiac output and (ii) Whether turning procedures cause practical problems. Background. Directly following surgery, coronary artery bypass patients are not receiving routine turning every two hours to prevent pressure ulcers, because a negative influence on hemodynamic parameters is assumed. Design. Clinical trial. Methods. Fifty‐five coronary artery bypass patients were randomly assigned to four intervention regimens and underwent a two‐hour period of 30° lateral position. Fourteen patients in supine position served as a reference group. We hypothesized that 30° lateral position does not cause a relevant change in the cardiac output. Results. Turning the patients did not have any significant influence on the cardiac index, not even in the patients in a poor hemodynamic condition. The cardiac index in 30° lateral position and supine position two to eight hours postoperatively after coronary artery bypass surgery is statistically bioequivalent. No clinically relevant deviations from preset ‘safe’ values for mean arterial pressure, right atrial pressure, pulmonary artery wedge pressure and pulmonary arterial pressure were observed, which would require ending the lateral position. There were no practical problems hindering the turning regimen, not even in the patients with an intra‐aortic balloon pump. Conclusions. Early postoperative turning of coronary artery bypass surgery patients in lateral position is an easy and feasible procedure that does not influence the cardiac index not even in patients receiving antihypertensive or inotropic/vasopressor therapy. Further research is needed to find out whether our findings are also valid in other patient groups and other position conditions. Relevance to clinical practice. If there are no strict contra‐indications, lateral position has to be considered to prevent complications of continuous supine position within two hours after coronary artery bypass surgery patients have been admitted to the intensive care unit.     

Arterial pH and carbon dioxide tension as indicators of tissue perfusion during cardiac arrest in a canine model.

BACKGROUND AND METHODS: Previous studies have shown that Paco2 and end-tidal CO2 reflect coronary artery perfusion pressures during cardiac arrest. We investigated the relationship of coronary artery perfusion pressure to central arterial pH and Paco2 values during resuscitation from cardiac arrest in a canine model. Twenty-four mongrel dogs were block randomized to three different resuscitation groups after induction of ventricular fibrillation and cardiac arrest: a) standard cardiopulmonary resuscitation (CPR) and advanced life support (n = 8); b) cardiopulmonary bypass (n = 8); or c) open-chest CPR (n = 8). Central arterial blood gases and perfusion pressures were monitored during cardiac arrest and during resuscitation. RESULTS: Prearrest blood gases and hemodynamic values were similar between groups. Sixteen dogs from all three groups were successfully resuscitated. Survivors had significantly higher coronary artery perfusion pressure (p = .03), Paco2 (p = .015), and lower pH (p = .01) values than nonsurvivors. There was no correlation of pH and Paco2 during mechanical external CPR. However, after institution of the different resuscitation techniques, pH and Paco2 each showed a statistically significant correlation (r2 = .50 and .33, respectively) with coronary artery perfusion pressure. CONCLUSIONS: Central arterial pH and Paco2 monitoring during cardiac arrest may reflect the adequacy of tissue perfusion during resuscitation and may predict resuscitation outcome from ventricular fibrillation.     

Enoximone in contrast to dobutamine improves hepatosplanchnic function in fluid-optimized septic shock patients

OBJECTIVE: To investigate the impact of dobutamine and enoximone on hepatosplanchnic perfusion and function in fluid-optimized septic patients. DESIGN: Prospective, randomized, double-blinded interventional study. SETTING: Intensive care unit of a university hospital. PATIENTS: Forty-eight septic shock patients were examined within 12 hrs after onset of septic shock. Patients were conventionally resuscitated, achieving an optimal pulmonary artery occlusion pressure at which the left ventricular stroke work was on the maximal plateau. Liver blood flow was estimated by venous suprahepatic catheterization using the continuous indocyanine green infusion technique. Microsomal liver function was assessed by the plasma appearance of monoethylglycinexylidide, and release of hepatic tumor necrosis factor-alpha (TNF-alpha) was measured to estimate the severity of hepatic ischemia-reperfusion syndrome. INTERVENTIONS: Patients were randomly treated with dobutamine or enoximone. Within the first 10 hrs after baseline measurements, the dosage was increased until no further increase in the left ventricular stroke work index occurred. Then, positive inotropes were kept constant throughout the study. MEASUREMENTS AND MAIN RESULTS: Measurements were performed at baseline and after 12 and 48 hrs after baseline measurements. Cardiac index, systemic oxygen delivery, systemic oxygen consumption, and liver blood flow increased significantly in both groups during treatment (p <.01) without a significant difference between groups. Fractional liver blood flow (liver blood flow/cardiac index) did not change in the enoximone group and showed a significant but only minor (median, 10%) decrease in the dobutamine group (p <.05 after 12 hrs and p <.01 after 48 hrs vs. baseline). After 12 hrs of enoximone treatment, monoethylglycinexylidide kinetics and hepatosplanchnic oxygen consumption demonstrated a significant increase (p <.05). The release of hepatic TNF-alpha after 12 hrs of dobutamine treatment was twice as high (p <.05) as during enoximone. CONCLUSION: The increase in hepatosplanchnic oxygen consumption, together with an increased lignocaine metabolism and decreased release of hepatic TNF-alpha, indicates improved hepatosplanchnic function and antiinflammatory properties after 12 hrs of enoximone treatment. Therefore, if the inflammatory response should be attenuated in high-risk patients, administration of enoximone in fluid-optimized septic shock patients may be favorable compared with dobutamine.     

Prospective trial of high-frequency oscillation in adults with acute respiratory distress syndrome.

OBJECTIVE: To evaluate the safety and efficacy of high-frequency oscillatory ventilation (HFOV) in adult patients with the acute respiratory distress syndrome (ARDS) and oxygenation failure. DESIGN: Prospective, clinical study. SETTING: Intensive care and burn units of two university teaching hospitals. PATIENTS: Twenty-four adults (10 females, 14 males, aged 48.5 +/- 15.2 yrs, Acute Physiology and Chronic Health Evaluation II score 21.5 +/- 6.9) with ARDS (lung injury score 3.4 +/- 0.6, Pao2/Fio2 98.8 +/- 39.0 mm Hg, and oxygenation index 32.5 +/- 19.6) who met one of the following criteria: Pao2 < or =65 mm Hg with Fio2 > or =0.6, or plateau pressure > or =35 cm H2O. INTERVENTIONS: HFOV was initiated in patients with ARDS after varying periods of conventional ventilation (CV). Mean airway pressure (Paw) was initially set 5 cm H2O greater than Paw during CV, and was subsequently titrated to maintain oxygen saturation between 88% and 93% and Fio2 < or =0.60. MEASUREMENTS AND MAIN RESULTS: Fio2, Paw, pressure amplitude of oscillation, frequency, blood pressure, heart rate, and arterial blood gases were monitored during the transition from CV to HFOV, and every 8 hrs thereafter for 72 hrs. In 16 patients who had pulmonary artery catheters in place, cardiac hemodynamics were recorded at the same time intervals. Throughout the HFOV trial, Paw was significantly higher than that applied during CV. Within 8 hrs of HFOV application, and for the duration of the trial, Fio2 and Paco2 were lower, and Pao2/Fio2 was higher than baseline values during CV. Significant changes in hemodynamic variables following HFOV initiation included an increase in pulmonary artery occlusion pressure (at 8 and 40 hrs) and central venous pressure (at 16 and 40 hrs), and a reduction in cardiac output throughout the course of the study. There were no significant changes in systemic or pulmonary pressure associated with initiation and maintenance of HFOV. Complications occurring during HFOV included pneumothorax in two patients and desiccation of secretions in one patient. Survival at 30 days was 33%, with survivors having been mechanically ventilated for fewer days before institution of HFOV compared with nonsurvivors (1.6 +/- 1.2 vs. 7.8 +/- 5.8 days; p =.001). CONCLUSIONS: These findings suggest that HFOV has beneficial effects on oxygenation and ventilation, and may be a safe and effective rescue therapy for patients with severe oxygenation failure. In addition, early institution of HFOV may be advantageous.