Torr In Group Research Articles

Effects of various concentrations of inhaled oxygen on tissue dysoxia, oxidative stress, and survival in a rat hemorrhagic shock model

Objective To test the hypothesis that a fractional inspired oxygen (F IO 2) of 1.0 compared to 0.4 during hemorrhagic shock (HS) and fluid resuscitation (FR): mitigates tissue dysoxia; however, enhances the oxidative stress; therefore, offsets the benefit on survival. Methods Thirty rats underwent: HS for 75 min, during which 3.0 mL/100 g of blood was withdrawn, followed by FR for 75 min, during which 1.0 mL/100 g of shed blood and 3.0 mL/100 g of crystalloid solution were infused. Ten rats were randomized into one of three F IO 2 (0.21 vs. 0.4 vs. 1.0) groups, and observed for survival until 72 h in each group. Hemodynamics, liver tissue PO 2 (P TO 2), and, plasma antioxidants levels were also monitored. Results Oxygen inhalation increased mean arterial pressure (MAP) and decreased heart rate (HR) during HS and FR. Liver P TO 2 was less than 10 Torr in all groups throughout HS; while it increased to average 26–35 Torr in oxygen groups during FR, it remained at 10 Torr with F IO 2 0.21 ( P < 0.01). MAP, HR, and P TO 2 did not differ significantly between oxygen groups. Plasma antioxidants levels did not differ among the three groups. All rats treated with oxygen, but eight of 10 rats with F IO 2 0.21 survived up to 72 h (NS). Conclusions Supplemental oxygen does not mitigate tissue dysoxia during HS, but does reduce tissue dysoxia without enhancing oxidative stress during subsequent FR. Increased F IO 2 appears to prolong survival. These beneficial effects of supplemental oxygen do not differ between an F IO 2 of 0.4 and 1.0.

Gut mucosal-arterial Pco2 gradient as an indicator of splanchnic perfusion during systemic hypo- and hypercapnia.

By accounting for influences of systemic acid-base disturbances, gut mucosal-arterial Pco2 gradient (Pico2 - Paco2) has been increasingly advocated as a more specific marker of splanchnic perfusion than Pico2 alone. We examined the stability of the Pico2 - Paco2 gradient compared with raw Pico2 measurements during induced systemic hypo- and hypercapnia. A prospective animal study. A university research laboratory. Twenty anesthetized, paralyzed, and mechanically ventilated mongrel dogs. After a baseline period during which Paco2 was maintained near 40 torr, the animals were divided into four groups. Minute ventilation was then altered by adjusting tidal volume, frequency, or both to achieve group Paco2 values of 15, 20, 60, and 80 torr for groups 1 through 4, respectively. Portal blood flow was monitored and maintained near baseline levels by infusion of intravenous fluids. Intestinal Pico2 was measured continuously by using capnometric recirculating gas tonometry. Mean (+/- SE) aggregate baseline Pico2 - Paco2 was 16.9+/-3.3 torr. After 60 mins of hypoventilation, Pico2 - Paco2 decreased to 14.2+/-1.1 and to 13.7+/-2.7 torr in groups 3 and 4, respectively (p = NS, compared with baseline for both). On the other hand, after 60 mins of hyperventilation, Pico2 - Paco2 increased to 37.9+/-3.6 and 28.0+/-6.3 torr in groups 1 and 2, respectively (p < .0001, compared with baseline for both). In this model of maintained portal blood flow, Pico2 - Paco2 remained essentially stable after hypoventilation but increased significantly after inducing hyperventilation. Our findings warrant cautious interpretation of Pico2 - Paco2 as an indicator of splanchnic perfusion during systemic hypocapnia.

Comparison of external jugular and peripheral venous administration of sodium bicarbonate in puppies

We compared the administration of sodium bicarbonate via a catheter inserted in the external jugular and extending to the junction with the subclavian vein (group 1) and a peripheral hindpaw vein (group 2) in puppies. During spontaneous cardiac activity, the increases in pH (0.12 +/- 0.04 in group 1 vs. 0.08 +/- 0.04 in group 2) and PCO2 (11 +/- 2.8 torr in group 1 vs. 6 +/- 3.2 torr in group 2) in blood from the right atrium 10 sec after the injection of bicarbonate differed significantly. However, the increases in pH (0.31 +/- 0.07 in group 1 vs. 0.30 +/- 0.15 in group 2) and PCO2 (86 +/- 33 torr in group 1 vs. 72 +/- 35 torr in group 2) in blood from the right atrium during closed chest CPR were similar in the two groups. We found that the sodium bicarbonate reached the central circulation more rapidly when administered in the external jugular vein as compared to a peripheral site, but this difference was small and did not reach the level of significance during CPR. Our findings do not provide evidence of any advantage to obtaining central venous access (a potentially complicated procedure) in children with cardiac arrest in regard to the delivery of medications to the heart.

Quantitative measurement of bleeding following hypertonic saline therapy in 'uncontrolled' hemorrhagic shock.

The effect of small volume hypertonic saline in "uncontrolled" hemorrhagic shock (UCHS) induced by partial resection of the tail was studied in rats. The rats were divided into three groups: in group 1 (n = 15) 10% of the terminal portion of the animal's tail was resected to induce UCHS. In group 2 (n = 14) UCHS was induced as in group 1 and after 5 min 5 ml/kg NaCl 0.9% (NS) was infused intravenously. In group 3 (n = 22) UCHS was induced as in group 1 and after 5 min, 5 ml/kg NaCl 7.5% (HTS) was infused intravenously. Resection of the animal's tail was followed by bleeding of 3.5 +/- 0.3 ml within 5 min, fall in MAP to 63 +/- 4 torr (p less than 0.001) and pulse to 300 +/- 18 per min (p less than 0.05). The amount of bleeding, fall in MAP, and pulse after 5 min were similar in the three groups. Further blood loss after 60 min in group 1 was 3.7 +/- 0.8 ml, in group 2, 2.9 +/- 0.5 ml, and in group 3, 6.5 +/- 0.8 (p less than 0.01). Increased bleeding in group 3 showed two peaks: an early peak of 1.3 +/- 0.2 ml after 15 min (p less than 0.05) and a late peak of 1.2 +/- 0.4 ml at 45 min (p less than 0.05) and 1.7 +/- 0.5 ml at 60 min (p less than 0.01). MAP fell after 60 min to 54 +/- 7 torr in group 1 (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of treatment with fluosol and mannitol during temporary middle cerebral artery occlusion in cats.

Four groups of seven cats each were subjected to 6 hours of temporary middle cerebral artery (MCA) occlusion followed by reperfusion. During the first 30 minutes of the occlusion, Group 1 received 20% Fluosol-DA (FDA) and Group 2 received 20% FDA and mannitol; Group 3 received 20% FDA and mannitol 30 minutes before the occlusion, and Group 4 (control) received an infusion of saline solution during the first 30 minutes of occlusion. All cats breathed 100% oxygen throughout the occlusion and during 2 hours of reperfusion. Blood pressure, PaO2, and pH remained stable for 8 hours. PaO2 increased from an average base line level of 102 +/- 15 (SD) torr to 520 +/- 45 torr in Group 1, 450 +/- 41 torr in Group 2, 480 +/- 28 torr in Group 3, and 396 +/- 151 torr in Group 4 during the administration of 100% oxygen. The average fluorocrit during occlusion was 6% in Groups 1, 2, and 3. The 24-hour mortality rate was 71% in Group 1, 43% in Group 2, 29% in Group 3, and 14% in Group 4; a midline shift and herniation were present after each fatal infarct. The survivors were sacrificed 10 days after the occlusion. There was a trend toward improvement of neurological function at sacrifice in Groups 2 and 3 compared with Groups 1 and 4. The infarct areas on coronal sections were 2.4 times larger in Group 1 (FDA only) than in Group 4 (control) (P less than 0.05). There was no significant difference in infarct size between Group 4 and Group 2 or 3.(ABSTRACT TRUNCATED AT 250 WORDS)

Preparation of the left ventricle for anatomical correction in patients with simple transposition of the great arteries: Surgical guidelines

Pulmonary artery banding in combination with an aortopulmonary shunt was performed on 16 patients with simple transposition of the great arteries to prepare the left ventricle for anatomical correction. Three groups were identified after operation: Group I (four patients) had increased pulmonary blood flow and tight pulmonary artery banding; Group II (four patients) had increased pulmonary blood flow and moderate pulmonary artery banding; Group III (eight patients) had normal pulmonary blood flow and moderate pulmonary artery banding. Postoperative low cardiac output was present in all patients in Group I, whereas mild heart failure was present in two patients in Group II and in two in Group III. There was one hospital death (6%). The follow-up period was 125 patient-months. Left ventricular systolic pressure rose from 63 +/- 11 torr before the operation to 101 +/- 35 torr after the procedure in Group I (p less than 0.05), from 59 +/- 10 to 93 +/- 33 torr in Group II (p less than 0.05), and from 55 +/- 10 to 84 +/- 16 torr in Group III (p less than 0.005). The increase in left ventricular muscle mass was from 44 +/- 2 gm/m2 preoperatively to 108 +/- 12 gm/m2 after operation in Group I (p less than 0.01), from 43 +/- 3 to 93 +/- 8 gm/m2 in Group II (p less than 0.02), and from 46 +/- 3 to 55 +/- 14 gm/m2 in Group III (p = no statistically significant difference). The postoperative change in left ventricular end-diastolic volume was from 100% +/- 17% to 133% +/- 23% of normal in Groups I and II (p less than 0.05) and from 123% +/- 29% to 107% +/- 36% of normal in Group III (p = no statistically significant difference). In preparing the left ventricle for anatomical correction, avoidance of severe pulmonary artery banding decreases the incidence of postoperative myocardial dysfunction, a moderate degree of volume overload and pulmonary artery banding provides the most effective stimulus for ventricular growth, and a small to moderate atrial septal defect is advantageous because it ensures the volume preload necessary for the development of the left ventricle.

Surgical implications

Postoperative cardiac catheterization data of 74 patients with pulmonary insufficiency after tetralogy repair were analyzed. Two groups were identified: Group A, 26 patients with normal right ventricular function (ejection fraction 95% ± 5.5%, end-systolic volume 110% ± 17% of predicted normal) and Group B, 48 patients with right ventricular dysfunction (ejection fraction 80% ± 18% [p < 0.001], and end-systolic volume 218% ± 75% of predicted normal [p < 0.001]). There was no significant difference between the two groups with respect to frequency of previous palliative procedures, age at operative repair, operative techniques, methods of myocardial protection, and follow-up period. Right ventricular dysfunction in Group B was associated with significant distal pulmonary stenosis (right ventricle–pulmonary artery pressure gradient 28 ± 13 torr in Group A versus 55 ± 20 torr in Group B, p < 0.001), moderate pulmonary regurgitation (regurgitant fraction 18% ± 11 % in Group A versus 32% ± 10% in Group B, p < 0.001), and large transannular outflow patch (ratio of patch diameter to descending aorta diameter 1.31 ± 0.16 in Group A versus 2.50 ± 0.28 in Group B, p < 0.001). Pulmonary valve insertion was performed in 42 patients in Group B. Eighteen had subsequent cardiac catheterization. Right ventricular function recovered completely (end-systolic volume 122% ± 24%, and ejection fraction 92% ± 7% of predicted) in five of six patients (83%) who had valve insertion within the first 2 years after tetralogy repair. In contrast, right ventricular function remained abnormal in all 12 patients who had valve insertion later than 2 years after tetralogy repair (p < 0.05). Patients with residual pulmonary stenosis and/or a large transannular outflow patch are at risk for the development of right ventricular dysfunction from pulmonary insufficiency after tetralogy repair. Early correction of these residual lesions and control of pulmonary insufficiency may prevent long-term deterioration in right ventricular function.

Effects of transient intracranial hypertension on lung fluid and protein exchange.

We determined whether a transient increase in intracranial pressure (Pic) increases lung vascular permeability and whether the increase occurs at a Pic threshold. Anesthetized sheep were prepared with lung lymph fistulas. Pic was increased by rapidly injecting 20-45 ml of freshly drawn autologous blood into the cisterna magna from a base line of 4.8 +/- 1.5 Torr to a peak mean value of either 142.0 +/- 17.6 Torr (group I, n = 5) or 70.3 +/- 3.5 Torr (group II, n = 5). Pic decreased to 34.6 +/- 2.2 Torr in group I and to 31.0 +/- 3.2 Torr in group II within 1 h and remained steady at these levels for the study. The Cushing response (i.e., marked systemic hypertension lasting 10-15 min) was elicited only in group I; changes in mean pulmonary arterial (Ppa) and mean pulmonary arterial wedge (Ppw) pressures during the first 15 min were small, pulmonary blood flow (QL) increased, and pulmonary vascular resistance (PVR) decreased only in the first 15 min after the intracisternal injection. In group II, Ppa and QL did not change significantly, but PVR increased after the increase in Pic. Both pulmonary lymph flow (Qlym) and transvascular protein clearance (CL) increased only in sheep with the Cushing response. In group III (n = 8) in which Qlym and CL increased after intracranial hypertension as in group I, the left atrial pressure was raised to increase the pulmonary capillary pressure (Pc) to determine the basis for the increases in Qlym and CL (i.e., whether vascular surface area or permeability increased). The increase in Pc produced a small increase and decrease in lymph-to-plasma protein concentration ratio, indicating that the transient increase in Pic did not increase endothelial permeability to proteins. The increases in Qlym and CL were due to increased pulmonary vascular surface area.

Electrolyte versus Blood Cardioplegia: Randomized Clinical and Myocardial Ultrastructural Study

In 40 consecutive patients undergoing coronary artery bypass, one of two solutions for cardioplegia, each containing 30 mEq/L of K + was used randomly. The groups were comparable except for intramyocardial temperature. With electrolyte solution (Group A), it was 16.5° ± 0.34°C, while with blood from the pump-oxygenator (Group B) it was 20.3° ± 0.41°C ( p < 0.001). After bypass left atrial pressure (LAP) was 11.9 ± 0.67 torr in Group A and 8.1 ± 0.49 torr in Group B ( p < 0.001). CPK-MB was elevated in 45% of Group A patients versus 15% in Group B ( p < 0.05). No patient died. Two myocardial infarctions occurred in Group A and one in Group B. Stereological morphometric electron microscopy was performed on biopsy specimens taken from the left ventricle (1) before perfusion, (2) after cardioplegia, and (3) 30 minutes after reperfusion. Group A showed marked intracellular edema, mitochondrial swelling, pronounced depletion of glycogen stores, and focal myofibrillary disorganization. Group B showed near normal myocardial ultrastructure with increased glycogen stores and minimal mitochondrial swelling. Morphometric analysis revealed a statistically significant increase in the degree of mitochondrial swelling (51%) in Group A compared with Group B after reperfusion ( p < 0.001). Thus, blood K + cardioplegia resulted in better preservation of myocardial ultrastructure, lower ventricular filling pressure, and lesser CPK-MB release compared with this particular electrolyte cardioplegia.

Early PEEP for improvement of prognosis in patients with acute respiratory insufficiency (author's transl)

One hundred twenty-seven artificially ventilated patients with acute respiratory insufficiency (ARI) were investigated. In 61 patients positive endexpiratory pressure (PEEP) was used when ventilation with ZEEP proved to be insufficient for one or more of the following reasons: increasing I-aDO2m PaO3 below 60 Torr at FiO2 greater than or equal to 0.5, deterioration of clinical status (group = secondary PEEP). The time elapse between beginning of artificial ventilation and institution of PEEP was 46 +/- 47 h (median 33 h). In 66 patients PEEP was used from the beginning of artificial ventilation (group II = primary PEEP). The distribution of underlying diseases (severe poisoning, pancreatitis, polytrauma or major surgery, pneumonia, cardiovascular failure, sepsis) as well as the frequency of additional vital function failure (circulatory shock, acute renal failure) were comparable in both groups (p greater than 0.05). At the beginning of artificial ventilation both groups were comparable in respect to respiratory insufficiency. PaO2 was 75 +/- 26 Torr in group I and 70 +/- 29 Torr in group II at comparable levels of FiO2 (p greater than 0.05). PaCO2 was 34.7 +/- 8.2 Torr in group I and 37.4 +/- 10.5 Torr in group II. Significantly more patients in group II received corticosteroids (greater than 1 gr/die). Mortality was 48/61 (79%) in group I and 37/66 (56%) in group II (p less than 0.01). End-inspiratory pressure exceeding 35 cm H2O was necessary in 42/61 patients in group I and 28/66 patients in group II (p less than 0.01) and FiO2 greater than 0.5 was necessary to keep PaO2 above 60 Torr in 39/61 patients in group I and 27/66 patients in group II (p less than 0.01). It is concluded that early institution of PEEP improves the course and outcome of patients with ARI.