Tissue Oxygenation Parameters Research Articles

Dobutamine in Severe Scorpion Envenomation: Effects on Standard Hemodynamics, Right Ventricular Performance, and Tissue Oxygenation

To document the effects of dobutamine on standard hemodynamics and right ventricular (RV) performance in patients exhibiting pulmonary edema following severe scorpion envenomation, and to characterize the tissue oxygenation profile in patients sustaining scorpion envenomation-related shock. Prospective cohort study. An ICU in a university hospital. Nineteen consecutive patients were admitted to the ICU for severe scorpion envenomation; all 19 patients exhibited hemodynamic pulmonary edema, and 10 patients had peripheral shock. All patients underwent a hemodynamic study with a Swan-Ganz catheter. In 8 of 19 patients, the thermodilution catheter was equipped with a fast-response thermistor. Standard hemodynamic parameters were recorded on admission and following the infusion of dobutamine in all patients at a dosage, from 7 to 20 microg/kg/min, intended to achieve the best hemodynamic and tissue oxygenation compromise. RV ejection fraction (RVEF) and RV volumes were simultaneously recorded in 8 patients, and tissue oxygenation parameters were assessed in the 10 patients with peripheral shock. The clinical signs of tissue hypoperfusion improved, and optimal hemodynamic parameters were achieved at a mean +/- SD dobutamine dosage of 17 +/- 7 microg/kg/min. Dobutamine infusion evoked statistically significant increases in cardiac index, from 2.3 +/- 0.6 to 3.6 +/- 0.7 L/min/m2; stroke volume index, from 18 +/- 5 to 31 +/- 10 mL/m2; and systemic arterial pressure, from 64 +/- 12 to 78 +/- 14 mm Hg. Pulmonary artery occlusion pressure (PAOP) and venous admixture decreased significantly: from 23 +/- 4 to 15 +/- 6 mm Hg and from 29 +/- 7% to 20 +/- 5%, respectively. With respect to RV function, dobutamine infusion significantly increased the RVEF, from 24 +/- 7% to 42 +/- 9%, without significantly changing the RV end-diastolic volume index, reflecting an enhanced RV contractility. In patients with peripheral circulatory failure, the baseline tissue oxygenation profile was consistent with cardiogenic shock, showing increased oxygen extraction as a consequence of a striking depression in oxygen delivery (DO2). After dobutamine infusion, DO2 improved significantly, from 386 +/- 104 to 676 +/- 156 mL/min/m2, with a significant decrease in oxygen extraction, from 34 +/- 8% to 24 +/- 6%. In severe scorpion envenomation, dobutamine infusion improves impaired heart function. The effects involve both left ventricular and RV dysfunction. Impaired tissue oxygenation is also improved.

Utility of clinical parameters of tissue oxygenation in a quantitative model of irreversible hemorrhagic shock.

The aim of this study was to assess the value of parameters of tissue oxygenation in monitoring the progression to irreversibility in a quantitative model of hemorrhagic shock. Rats were bled to a mean arterial pressure of 40 mmHg and were maintained at this level by further blood withdrawal until the compensation endpoint; this point was defined as the time at which the rat was no longer able to maintain its blood pressure at this level and shed blood was required for transfusion. The shock period was maintained until 0%, 20%, 40%, or 50% of the maximum shed blood volume (MBV) had been returned (n = 10 in each group, total n = 40). The animals were then resuscitated with remaining shed blood plus twice MBV as lactated Ringer's solution to MAP > 80 mmHg. Blood gas and serum lactate samples were measured at baseline, compensation endpoint, and at the time of resuscitation, and 24 h survival was recorded. Increasing the severity of shock progressively worsened the acidosis, with increased base deficit and lacticacidemia, and deterioration in central venous oxygen saturation (CvO2). Tissue oxygenation parameters, particularly CvO2, predicted subsequent mortality. Lactate levels only predicted irreversibility in late, severe shock. This quantitative model of hemorrhagic shock showed that tissue oxygenation parameters can be used to monitor the progression from the decompensated phase of hemorrhagic shock to irreversibility. Furthermore, this experimental study suggests that venous indices may be a valuable tool in reflecting the severity of hemorrhagic insult in a setting when arterial blood samples may not be easily available.

Gastric Tonometry

Because tissue hypoxia plays a major role in the morbidity and mortality of critically ill patients, achieving adequate tissue oxygenation is considered the main goal in the intensive care unit during initial management of patients with shock, severe sepsis, trauma, and the multiorgan dysfunction syndrome. Unfortunately, systemic parameters of tissue oxygenation are not reliable enough to represent “true” tissue oxygenation status. Methods developed to monitor oxygen tissue metabolism, such as phos-phorus-31 nuclear magnetic resonance, near-infrared spectroscopy, and tissue Po2 electrodes are still far from clinical application. A new approach to this problem is the measurement of gastric intramucosal pH (pHi) with a gastric tonometer. This device consists of a modified nasogastric tube attached to a silicone balloon that is filled with saline. After an equilibration period, saline solution can be sampled and its Pco2 measured in a blood-gas analyzer. Arterial bicarbonate is simultaneously measured. Gastric pHi is then easily calculated using the Henderson-Hasselbalch equation. Its value has been experimentally validated, comparing it with direct electrode tissue pH measurements. A growing body of evidence supports its clinical value at the present time. Several clinical investigations show that pHi is a sensitive and specific prognostic marker. Gastric pHi behavior is able to predict multiorgan dysfunction and mortality in different groups of critically ill patients. Its use to guide resuscitation maneuvers could contribute to mortality reduction. From the few years of basic and clinical research in which this technique has been used, it appears to be a useful tool to assess tissue oxygenation status.

Assessment of left ventricular function in severe scorpion envenomation: combined hemodynamic and echo-Doppler study.

To assess left ventricular function in patients presenting with pulmonary edema following scorpion envenomation. Cohort study. Medical intensive care unit of a teaching hospital. Nine consecutive adult patients stung by Androctonus australis and presenting with pulmonary edema entered the study. Fourteen normal volunteers comprised the control group. Upon admission, all patients had right heart catheterization and, within the first 8 h, a Doppler echocardiographic study. Results of Doppler echocardiographic studies were compared to those of controls. Usual hemodynamic information (heart and vascular pressures, derived data and tissue oxygenation parameters), left ventricular dimensions and indicators of systolic function, and Doppler-derived parameters of left ventricular filling and diastolic function were obtained upon admission. Serial echocardiographic measurements were repeated daily until full clinical recovery (eight patients) or death (one patient). All patients had a hemodynamic profile of acute congestive heart failure (mean PAOP = 24 +/- 2 mmHg; mean SVI = 22 +/- 7 ml/m2; mean CI = 2.5 +/- 0.5 l/min/m2). However, SVR were not increased (mean = 22 +/- 3 U/m2). Left ventricle was hypokinetic in all patients with transient mitral regurgitation present in five patients. Left ventricular systolic function was markedly depressed (FS = 12 +/- 6%; EF = 26 +/- 12%). An associated diastolic dysfunction is suggested by Doppler records of mitral inflow. Left ventricular systolic function evolved toward normalization within 6 +/- 2 days preceded by full clinical recovery. These data suggest that pulmonary edema in scorpion envenomation is of hemodynamic origin and is related to a severe and prominent impairment of left ventricular systolic function.

Hemodynamic and Oxygen Transport Characteristics of Common Ventilatory Modes

We studied hemodynamic and oxygen transport parameters in 12 stable critically ill patients on assist control (ACV), synchronized intermittent mandatory (SIMV), and pressure support (PSV) ventilatory modes. Patients were optimally ventilated on ACV, were awake, and capable of spontaneous breathing. After baseline measurements on ACV, patients were placed on SIMV and PSV for 30 min each and measurements were repeated at the end of each period. The SIMV rate (f) was 75 percent of the rate on ACV. The PSV was set at a level enough to maintain a tidal volume (VT) equal to that on ACV. The FIo2 was kept constant on all three modes. Patients on SIMV and PSV maintained similar minute ventilation as when on ACV but with significantly lower peak and mean inspiratory pressures than on ACV. However, f increased and VT decreased significantly on SIMV. Hemodynamic and oxygen transport parameters were not significantly different among the three groups, although there was a tendency toward higher cardiac index, oxygen transport, and oxygen consumption on SIMV and PSV. We conclude that in stable critically ill patients, SIMV and PSV used according to our study protocol for 30 min can provide adequate ventilation with lower airway pressure and possibly less adverse effects on hemodynamic and tissue oxygenation parameters compared with ACV. Because of a significant decrease in VT and an increase in f seen with SIMV, PSV may be a more desirable mode for ventilatory support.

Tissue oxygenation during liver transplantation.

a) To assess perioperative changes in tissue oxygenation parameters during liver transplantation; b) to evaluate the need for venovenous bypass as hemodynamic support; and c) to assess the efficacy of mixed venous oxygen saturation monitoring and the importance of lactate determinations in the management of patients following liver transplantation. Prospective case series. Liver transplant unit in a university hospital. A total of 68 consecutive patients undergoing liver transplantation. The entire population was analyzed before and after transplantation, dividing the patients into two groups, based on whether their initial cardiac index was higher (n = 37) or lower (n = 31) than 4.5 L/min/m2. Hemodynamic measurements and blood gas analyses were made before incision, before vascular clamping (including hepatic artery, portal vein and inferior vena cava), during the anhepatic phase, and at 5, 30, 60, and 120 mins following unclamping. Oxygen transport and oxygen consumption values were calculated. Serum lactate concentrations were measured by enzymatic technique. Mixed venous oxygen saturation was correlated with oxygen transport (Do2) in the whole population in which an abnormal oxygen consumption (Vo2)-Do2-dependent relationship occurred from the beginning of operation until 30 mins following unclamping. The comparison between hyperdynamic patients (initial cardiac index greater than 4.5 L/min/m2) with impaired tissue oxygenation and normodynamic patients showed that mixed venous oxygen saturation failed to correlate with Do2 when the cardiac index was greater than 4.5 L/min/m2 and that the Vo2-Do2 dependency was only noted in these patients. The serum lactate concentrations were similar in both groups. The Vo2-Do2-dependent relationship and mixed venous oxygen saturation-Do2 correlation noted in the 68 studied patients suggest the need for venovenous bypass and the reliability of mixed venous oxygen saturation monitoring in all patients scheduled for liver transplantation. However, a sharper comparison between hyperdynamic and normodynamic patients demonstrated the lack of efficacy of mixed venous oxygen saturation monitoring in predicting adequate tissue oxygenation in the first group and the mandatory need for venous shunting to limit tissue hypoxia which occurred despite its use only in these patients. Lactic acidosis appeared similarly in both groups and could not be linked to tissue hypoxia.

Visceral and Peripheral Tissue Perfusion after Cardiac Surgery

Visceral and peripheral tissue perfusion and oxygenation were studied in ten patients in the early phase after coronary artery bypass grafting. Visceral perfusion was assessed indirectly, by determining gastric intramucosal pH. As parameters of peripheral tissue perfusion and oxygenation, subcutaneous tissue PO2 (PscO2), transcutaneous PO2 (PtcO2). PtcO2 index (PtcO2/PaO2), laser-Doppler skin red-cell flux (RCF) and fingertip temperature (Tft) were recorded in the upper extremity. Central haemodynamics, rectal temperature and blood gases were also measured. The inspired oxygen concentration was maintained at 30 v/v%. Gastric intramucosal pH declined progressively during the first 3 hours in the intensive care unit, reached its minimum at 5 hours and thereafter slowly increased. The peripheral vascular bed was shut down on admission to the ICU, as indicated by low values of PscO2, PtcO2, PtCO2 index, RCF and Tft. These parameters began to rise after the next 2-4 hours and peaked by the end of the 8-hour study period, indicating complete opening of the peripheral vascular bed.

Polycythemia in Chronic Obstructive Pulmonary Disease: A Study of Serum and Urine Erythropoietin and Medullary Erythroid Progenitors

In order to investigate the mechanism of polycythemia in chronic obstructive pulmonary disease (COPD), serum and urinary levels of erythropoietin and medullary erythroid progenitors were studied in 21 patients; nine were nonpolycythemic (hematocrit, 39 +/- 4 percent; red blood cell [RBC] mass, 28 +/- 5 ml/kg; forced expiratory volume in one second [FEV1], 0.6 +/- 0.1 L), and 12 patients were polycythemic (hematocrit, 52 +/- 7 percent; RBC mass, 46 +/- 7 ml/kg; FEV1, 0.9 +/- 0.3 L). Hypoxia was severe in both groups, with mean arterial oxygen pressure of 47 mm Hg. The following parameters of tissue oxygenation were not significantly different between the two groups: arterial and mixed-venous oxygen saturations; cardiac output; oxygen utilization coefficient; 2, 3-diphosphoglycerate, and carboxyhemoglobin level. The level of erythropoietin was measured by bioassay in vitro. The level was increased in the serum of 85 percent (18) and in the urine of 38 percent (8) of the patients. There was no significant difference between the nonpolycythemic and polycythemic groups. Without exogenous erythropoietin, none of the subjects showed spontaneous colonies of erythroid progenitors. The addition of one unit of erythropoietin induced a similar normal proliferation of erythroid progenitors in both groups. The absence of adaptative polycythemia in the nonpolycythemic group with severe hypoxia was seemingly related neither to a quantitative deficit of erythropoietin nor to a lack of sensitivity of erythroid progenitors to its action.