Effects of hypervolemia and hypertension on regional cerebral blood flow, intracranial pressure, and brain tissue oxygenation after subarachnoid hemorrhage

OBJECTIVE: Hypertensive, hypervolemic, hemodilution therapy (triple-H therapy) is a generally accepted treatment for cerebral vasospasm after subarachnoid hemorrhage. However, the particular role of the three components of triple-H therapy remains controversial. The aim of the study was to investigate the influence of the three arms of triple-H therapy on regional cerebral blood flow and brain tissue oxygenation. DESIGN: Animal research and clinical intervention study. SETTING: Surgical intensive care unit of a university hospital. SUBJECTS AND PATIENTS: Experiments were carried out in five healthy pigs, followed by a clinical investigation of ten patients with subarachnoid hemorrhage. INTERVENTIONS: First, we investigated the effect of the three components of triple-H therapy under physiologic conditions in an experimental pig model. In the next step we applied the same study protocol to patients following aneurysmal subarachnoid hemorrhage. Mean arterial pressure, intracranial pressure, cerebral perfusion pressure, cardiac output, regional cerebral blood flow, and brain tissue oxygenation were continuously recorded. Intrathoracic blood volume and central venous pressure were measured intermittently. Vasopressors and/or colloids and crystalloids were administered to stepwise establish the three components of triple-H therapy. MEASUREMENTS AND MAIN RESULTS: In the animals, neither induced hypertension nor hypervolemia had an effect on intracranial pressure, brain tissue oxygenation, or regional cerebral blood flow. In the patient population, induction of hypertension (mean arterial pressure 143 +/- 10 mm Hg) resulted in a significant (p < .05) increase of regional cerebral blood flow and brain tissue oxygenation at all observation time points. In contrast, hypervolemia/hemodilution (intrathoracic blood volume index 1123 +/- 152 mL/m) induced only a slight increase of regional cerebral blood flow while brain tissue oxygenation did not improve. Finally, triple-H therapy failed to improve regional cerebral blood flow more than hypertension alone and was characterized by the drawback that the hypervolemia/hemodilution component reversed the effect of induced hypertension on brain tissue oxygenation. CONCLUSIONS: Vasopressor-induced elevation of mean arterial pressure caused a significant increase of regional cerebral blood flow and brain tissue oxygenation in all patients with subarachnoid hemorrhage. Volume expansion resulted in a slight effect on regional cerebral blood flow only but reversed the effect on brain tissue oxygenation. In view of the questionable benefit of hypervolemia on regional cerebral blood flow and the negative consequences on brain tissue oxygenation together with the increased risk of complications, hypervolemic therapy as a part of triple-H therapy should be applied with utmost caution.     

Alterations in regional blood flow during positive end-expiratory pressure ventilation

PEEP improves the gas-exchange abnormalities that accompany adult respiratory distress syndrome (ARDS). However, since PEEP decreases cardiac output, it may also alter regional blood flow and therefore, substrate delivery to specific organs. To test this hypothesis, radiolabeled 15-mu microspheres were used to directly quantify the effects of mechanical ventilation with PEEP on regional blood flow to individual organs in animals. Mechanical ventilation alone produced a -21.2 +/- 3.6% and a -28.1 +/- 5.2% decrease in cardiac output at 30 and 60 min, respectively. The addition of 14 cm H2O PEEP resulted in little further reduction in cardiac output at 30 and 60 min (-28 +/- 2.3% and -36.4 +/- 4.9%, respectively). However, 25 cm H2O PEEP reduced markedly (p less than .01) cardiac output (-59.2 +/- 6.1% at 30 min and -55.1 +/- 4.0% at 60 min). Although blood flows to the kidney and brain were maintained, decreases in cardiac output were invariably accompanied by proportional decreases in blood flow to the heart. Intravascular volume expansion with saline (20 ml/kg) during 14 cm H2O PEEP significantly improved cardiac output (3.23 +/- 0.34 to 4.22 +/- 0.13 L/min; p less than .01) and proportionately increased blood flow to several regional vascular beds, including the heart. These data suggest that PEEP decreases cardiac output to produce reversible alterations in blood flow to a number of regional vascular beds. These PEEP-induced alterations in regional blood flow may have important implications for the development of multiple-organ failure in ARDS patients.     

Computer-controlled positive end-expiratory pressure titration for effective oxygenation without frequent blood gases

We have previously designed a computerized system to automatically deliver PEEP to maintain functional residual capacity (FRC) at a desired value. The purpose of this study was to compare the computerized PEEP titration system with a standard clinical PEEP titration algorithm in the animal adult respiratory distress syndrome (ARDS) model. Thirty mongrel dogs were anesthetized, paralyzed, intubated, and ventilated. An acute pulmonary injury was produced using 0.09 ml/kg of oleic acid. The animals were then given PEEP for 5 h. Arterial and venous blood gases, BP, thermodilution cardiac output, heart rate, body temperature, total respiratory system compliance (Ctr), and end-tidal CO2 were measured every 30 min. FRC was measured using an automated sulfur hexafluoride washout system every 15 min. The animals were allocated randomly to three ten-animal groups. The first group had PEEP titrated using a standard clinical protocol; the remaining two groups had PEEP updated at 15-min intervals under computer control to maintain FRC at 1.4 times the postanesthetized, postparalyzed, preinjury value. The second group received fixed 3-cm H2O PEEP steps. The third group had variable size PEEP steps depending on the output of a proportional, integral, and derivative (PID) controller. PaCO2 was maintained at 35.8 +/- 3.4 (SD) torr. There was a significant difference in PEEP delivered between the three groups (p = .0006) and in FRC (p = .005). There was no significant difference in PaO2 (p = .80) or venous admixture (Qva/Qt) (p = .84) between the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of positive end-expiratory pressure on tissue gas tensions and oxygen transport

To determine whether positive end-expiratory pressure (PEEP) impairs peripheral tissue oxygenation, hemodynamic variables including blood and subcutaneous tissue gas tensions were measured at 0, 5, 10, 15, and 20 cm H2O of PEEP, in 9 patients who were being mechanically ventilated for acute pulmonary failure. Increasing the level of PEEP produced parallel decreases in cardiac output and oxygen delivery (DO2 = cardiac output X arterial oxygen content); however, there were no significant changes in mean arterial blood pressure (MAP), oxygen consumption (VO2), mixed-venous oxygen tension (PvO2), pH, or base excess. Subcutaneous tissue oxygen (PtO2) and carbon dioxide (PtCO2) tensions, which were directly measured in the femoral region by a mass spectrometer, also remained at their baseline levels (zero end-expiratory pressure). We concluded that peripheral tissue oxygenation is not impaired up to the level of 20 cm H2O of PEEP, even though DO2 significantly decreases.     

Effects of hyperbaric treatment in cerebral air embolism on intracranial pressure, brain oxygenation, and brain glucose metabolism in the pig

OBJECTIVE: To evaluate the effects of hyperbaric oxygen treatment after cerebral air embolism on intracranial pressure, brain oxygenation, brain glucose/lactate metabolism, and electroencephalograph. DESIGN: Prospective animal study. SETTING: Hyperbaric chamber. SUBJECTS: Eleven Landrace/Yorkshire pigs. INTERVENTIONS: In 11 anesthetized pigs, intracranial pressure and brain oxygenation were measured with microsensor technology, brain glucose/lactate by microdialysis, and electroencephalograph by conventional methods. After injection of air into the internal carotid artery, animals were treated immediately (at 3 mins; t = 3) or at 60 mins (t = 60) with U.S. Navy Treatment Table 6 for 4.48 hrs. RESULTS: At the end of hyperbaric oxygen treatment, intracranial pressure in the t = 60 group (39 +/- 8 mm Hg) was significantly higher than in the t = 3 group (27 +/- 6 mm Hg), brain oxygenation values for group t = 3 and t = 60 were 66 +/- 14 and 52 +/- 15 mm Hg, respectively (no significant difference from baseline), and there were no pathologic scores in the visually assessed electroencephalograph. However, there was a significant decrease in brain glucose and a significant increase in brain lactate in both groups at the end of the 5-hr study period. CONCLUSIONS: Hyperbaric oxygen treatment initiated at both 3 and 60 mins after embolization decreased the deleterious effects of cerebral air embolism on intracranial pressure and brain metabolism. Therefore, this model appears suitable to test the application of hyperbaric oxygen treatment with a delay >60 mins after embolization, as is often the case in the clinical situation.     

Portal blood flow in man during graded positive end-expiratory pressure ventilation

The cardiovascular response to graded PEEP ventilation (5–10 cm H₂O) was studied peroperatively in patients undergoing chllecystectomy (n=8) or hepatic tumour surgery (n=3). Portal blood flow was measured by the continuous thermodilution technique and cardiac output, in a sub-group of the patients, by impedance cardiography. A parallel reduction in cardiac output and portal blood flow was demonstrated in patients undergoing cholecystectomy as the result of the application of PEEP. Thus, ventilation with 5 cm H₂O of PEEP elicited a 17% decrease in cardiac output and a 26% decrease in portal blood flow. During 10 cm H₂O of PEEP cardiac output decreased by 22% and portal blood flow by 32%. However, there were no significant changes in preportal tissue perfusion pressure by the application of PEEP and preportal vascular resistance increased by 22% and 30%, respectively. This indicates that a vasoconstrictor response, elicited by PEEP, in the preportal tissue is the predominating mechanism for the observed decrease in portal blood flow. Systemic oxygen transport decreased by 214 ml/min during PEEP ventilation, but preportal tissue oxygen utilization was not significantly changed due to a concurrent increase (2.9%; p<0.05) in oxygen extraction.     

Hemodynamic relationship between renal venous pressure and blood flow regulation during positive end-expiratory pressure

The hemodynamic relationship between renal venous pressure (RVP) and renal blood flow (RBF) during PEEP was investigated using adult mongrel dogs. When continuous mechanical ventilation (CMV) with 10 cm H2O of PEEP was applied to dogs previously on CMV with zero PEEP, RVP increased from 6.6 to 8.7 mm Hg (p less than .01), and left RBF decreased from 66 to 57 ml/min (p less than .05). RBF recovered by 49% of the difference as soon as PEEP was discontinued when the RVP elevation was maintained at the level observed during 10 cm H2O of PEEP. With 20 cm H2O of PEEP, RVP increased further to 10 mm Hg (p less than .01) and left RBF decreased to 48 ml/min (p less than .05). When the left renal vein was occluded and the RVP was maintained at the level seen during 20 cm H2O of PEEP, left RBF recovered only 50% of the difference from the flow during zero PEEP. We conclude that the reduction in RBF with PEEP application is caused by several factors; however, RVP elevation during CMV with PEEP is influential in decreasing RBF.     

Alterations in regional myocardial blood flows during different levels of positive end-expiratory pressure

A decrease in myocardial blood flow (MBF) has been suggested recently as a contributing factor to the depression of cardiac function during application of PEEP. To test this hypothesis, 7 dogs were anesthetized and their chest wall and pericardium were removed. Hemodynamics, myocardial oxygenation status, and left and right ventricular MBF were measured during controlled ventilation without PEEP (IPPV), with 8 cm H2O of PEEP (CPPV8), 15 cm H2O of PEEP (CPPV15), and 25 cm H2O of PEEP (CPPV25). Compared to IPPV, CPPV8 significantly decreased left ventricular endocardial, epicardial, and septal blood flows. Right ventricular MBF and other measured variables were not affected. Compared to control, CPPV15 decreased left ventricular and septal MBFs in all regions, and right ventricular MBF in the endocardial region. CPPV15 also decreased cardiac index (CI) from 3.94 +/- 0.57 L/min X m2 during control to 2.78 +/- 0.34 L/min X m2 (p less than .05). Compared to IPPV, CPPV25 further decreased MBF in all layers of both ventricles and septum. Compared to CPPV8, there were decreases in left ventricular midwall and septal (left ventricular side and midwall) blood flows during CPPV25. During application of CPPV25, compared to IPPV, mean arterial pressure (MAP) was reduced from 99 +/- 5 to 85 +/- 5 mm Hg, left ventricular stroke work index (LVSWI) decreased from 31.8 +/- 5.4 to 13.8 +/- 2.6 g X m/m2, and CI decreased to 2.13 +/- 0.38 L/min X m2 (p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of hypertonic arginine on cerebral blood flow and intracranial pressure after traumatic brain injury combined with hemorrhagic hypotension

Hypertonic saline solutions improve cerebral blood flow (CBF) when used for acute resuscitation from hemorrhagic hypotension accompanying some models of traumatic brain injury (TBI); however, the duration of increased CBF is brief. Because the nitric oxide synthase substrate l-arginine provides prolonged improvement in CBF after TBI, we investigated whether a hypertonic resuscitation fluid containing l-arginine would improve CBF in comparison to hypertonic saline without l-arginine in a model of moderate, paramedian, fluid-percussion TBI followed immediately by hemorrhagic hypotension (mean arterial pressure [MAP] = 60 mm Hg for 45 min). Sprague-Dawley rats were anesthetized with 4.0% isoflurane, intubated and ventilated with 1.5%-2.0% isoflurane in oxygen/air (50:50). After preparation for TBI and measurement of CBF using laser Doppler flowmetry and measurement of intracranial pressure (ICP) using an implanted transducer, rats were subjected to moderate (2.0 atm) TBI, hemorrhaged for 45 min, and randomly assigned to receive an infusion of hypertonic saline (7.5%, 2,400 mOsm total; 6 mL/kg; n = 6) or hypertonic saline with 50, 100, or 300 mg/kg L-arginine (2,400 mOsm; 6 mL/kg; n = 6 in each of the three dose groups) and then monitored for 120 min after the end of infusion. CBF was measured continuously and calculated as a percent of the pre-TBI baseline during the hemorrhage period, after reinfusion of one of the hypertonic arginine solutions, and 30, 60, and 120 min after reinfusion. All four hypertonic solutions initially improved MAP, which, by 120 min after infusion, had decreased nearly to the levels observed during hemorrhage. ICP remained below baseline levels during resuscitation in all groups, although ICP was slightly greater (P = NS) than baseline in the hypertonic saline group. CBF increased similarly in all groups during infusion and then decreased similarly in all groups. At 120 min after infusion, CBF was highest in the group infused with hypertonic saline, but the difference was not significant. We conclude that the improvement of MAP, ICP, and CBF produced by hypertonic saline alone after TBI and hemorrhagic hypotension is not significantly enhanced by the addition of L-arginine at these doses.     

Effects of the neurological wake-up test on clinical examination,intracranial pressure,brain metabolism and brain tissue oxygenation in severely brain-injured patients

Introduction

Daily interruption of sedation (IS) has been implemented in 30 to 40% of intensive care units worldwide and may improve outcome in medical intensive care patients. Little is known about the benefit of IS in acutely brain-injured patients.

Methods

This prospective observational study was performed in a neuroscience intensive care unit in a tertiary-care academic center. Twenty consecutive severely brain-injured patients with multimodal neuromonitoring were analyzed for levels of brain lactate, pyruvate and glucose, intracranial pressure (ICP), cerebral perfusion pressure (CPP) and brain tissue oxygen tension (P_btO₂) during IS trials.

Results

Of the 82 trial days, 54 IS-trials were performed as interruption of sedation and analgesics were not considered safe on 28 days (34%). An increase in the FOUR Score (Full Outline of UnResponsiveness score) was observed in 50% of IS-trials by a median of three (two to four) points. Detection of a new neurologic deficit occurred in one trial (2%), and in one-third of IS-trials the trial had to be stopped due to an ICP-crisis (> 20 mmHg), agitation or systemic desaturation. In IS-trials that had to be aborted, a significant increase in ICP and decrease in P_btO₂ (P < 0.05), including 67% with critical values of P_btO₂ < 20 mmHg, a tendency to brain metabolic distress (P < 0.07) was observed.

Conclusions

Interruption of sedation revealed new relevant clinical information in only one trial and a large number of trials could not be performed or had to be stopped due to safety issues. Weighing pros and cons of IS-trials in patients with acute brain injury seems important as related side effects may overcome the clinical benefit.     

过度通气对脑血流脑代谢颅内压影响的临床研究

目的　观察过度通气对颅脑手术病人脑血流 (CBF)、脑代谢 (CMR)、颅内压 (ICP)的影响。方法　 2 0例择期行颅脑手术病人 ,行七氟醚麻醉 ,待 1 3MAC时 ,调整呼吸频率 ,使呼气末二氧化碳分压 (PetCO2 )达 30、2 5、2 0mmHg(1kPa =7 5mmHg) ,每阶段稳定 30min。根据颈内静脉球部血、桡动脉血差值计算出CBF、CMRO2 、CMRglu、Clact值的变化。结果　与清醒时通气状态相比 ,在血流动力学维持稳定前提下PetCO2 2 5mmHg时CBF减少 36 %、CMRO2 减少 4 9% ,使CMRglu减少 36 % (P<0 0 5 )。PetCO2 30和 2 0mmHg时CBF比PetCO2 2 5mmHg时增加 2 9% (P <0 0 5 )和减少了 9% (P >0 0 5 )。CMRglu麻醉前与麻醉后相比有显著差异 (P <0 0 5 ) ,但麻醉各时段相比无统计学意义 (P >0 0 5 )。麻醉后不同时段ICP与麻醉前相比有极显著差异 (P <0 0 1) ,PetCO2 2 5和 2 0mmHgICP无明显差异 (P >0 0 5 )。麻醉后颈静脉球部氧饱和度 (SjvO2 )和动脉氧饱和度(PaO2 )与麻醉前相比明显增加 (P <0 0 5 )。麻醉前后SaO2 、pH、Hb、体温 (T)、Clact无明显差异 (P >0 0 5 )。结论　过度换气可降低颅脑手术病人CBF、CMR和ICP ,短时间 (30min)过度换气至PetCO2 2 0mmHg时 ,不仅可以降低ICP ,而且不会引起脑缺氧 ,是过度换气的最低     

Hemodynamic directed CPR improves cerebral perfusion pressure and brain tissue oxygenation

Aim

Advances in cardiopulmonary resuscitation (CPR) have focused on the generation and maintenance of adequate myocardial blood flow to optimize the return of spontaneous circulation and survival. Much of the morbidity associated with cardiac arrest survivors can be attributed to global brain hypoxic ischemic injury. The objective of this study was to compare cerebral physiological variables using a hemodynamic directed resuscitation strategy versus an absolute depth-guided approach in a porcine model of ventricular fibrillation (VF) cardiac arrest.

Methods

Intracranial pressure and brain tissue oxygen tension probes were placed in the frontal cortex prior to induction of VF in 21 female 3-month-old swine. After 7 min of VF, animals were randomized to receive one of three resuscitation strategies: (1) hemodynamic directed care (CPP-20): chest compressions (CCs) with depth titrated to a target systolic blood pressure of 100 mmHg and titration of vasopressors to maintain coronary perfusion pressure (CPP) >20 mmHg; (2) depth 33 mm (D33): target CC depth of 33 mm with standard American Heart Association (AHA) epinephrine dosing; or (3) depth 51 mm (D51): target CC depth of 51 mm with standard AHA epinephrine dosing.

Results

Cerebral perfusion pressures (CerePP) were significantly higher in the CPP-20 group compared to both D33 (p < 0.01) and D51 (p = 0.046), and higher in survivors compared to non-survivors irrespective of treatment group (p < 0.01). Brain tissue oxygen tension was also higher in the CPP-20 group compared to both D33 (p < 0.01) and D51 (p = 0.013), and higher in survivors compared to non-survivors irrespective of treatment group (p < 0.01). Subjects with a CPP >20 mmHg were 2.7 times more likely to have a CerePP >30 mmHg (p < 0.001).

Conclusions

Hemodynamic directed resuscitation strategy targeting coronary perfusion pressure >20 mmHg following VF arrest was associated with higher cerebral perfusion pressures and brain tissue oxygen tensions during CPR.     

Effects of positive end-expiratory pressure on diaphragm function.

Patients admitted to the PACU after surgery may require mechanical ventilation. Knowledge about the anatomy and physiology of the diaphragm and its association with ventilator modes may be helpful in the management of this patient. As the acuity of PACU patients increase, more patients may also be on higher levels of positive end-expiratory pressure (PEEP), requiring PACU nurses to understand the relationship between PEEP and diaphragm function to facilitate weaning. This article provides a review of the mechanical ventilation mode of PEEP and its relationship to diaphragmatic performance. The physiological effects associated with the use of PEEP are also reviewed.     

Effects of positive end-expiratory pressure on brain tissue oxygen pressure of severe traumatic brain injury patients with acute respiratory distress syndrome: A pilot study

PurposeTo verify whether high positive end-expiratory pressure levels can increase brain tissue oxygen pressure, and also their effects on pulse oxygen saturation, intracranial pressure, and cerebral perfusion pressure.Material and MethodsTwenty traumatic brain injury patients with acute respiratory distress syndrome were submitted to positive end-expiratory pressure levels of 5, 10, and 15 cm H₂O progressively. The 3 positive end-expiratory pressure levels were used during 20 minutes for each one, whereas brain tissue oxygen pressure, oxygen saturation, intracranial pressure, and cerebral perfusion pressure were recorded.ResultsBrain tissue oxygen pressure and oxygen saturation increased significantly with increasing positive end-expiratory pressure from 5 to 10 and from 10 to 15 cm H₂O (P = .0001 and P = .0001 respectively). Intracranial pressure and cerebral perfusion pressure did not differ significantly with increasing positive end-expiratory pressure from 5 to 10 and from 10 to 15 cm H₂O (P = .16 and P = .79 respectively).ConclusionsHigh positive end-expiratory pressure levels increased brain tissue oxygen pressure and oxygen saturation, without increase in intracranial pressure or decrease in cerebral perfusion pressure. High positive end-expiratory pressure levels can be used in severe traumatic brain injury patients with acute respiratory distress syndrome as a safe alternative to improve brain oxygenation.     

呼气末正压对急性呼吸窘迫综合征肺复张容积及氧合影响的临床研究

目的　评价呼气末正压 (PEEP)对急性呼吸窘迫综合征 (ARDS)肺复张容积的影响 ,探讨ARDS患者 PEEP的选择方法。方法　以 11例血流动力学稳定、接受机械通气的 ARDS患者为研究对象 ,采用压力容积曲线法分别测定 PEEP为 5、10、15 cm H2 O(1cm H2 O=0 .0 98k Pa)时的肺复张容积 ,观察患者动脉血气、肺机械力学和血流动力学变化。结果　 PEEP分别 5、10和 15 cm H2 O时肺复张容积分别为 (4 0 .2±15 .3) ml、 (12 3.8± 4 3.1) ml和 (178.9± 4 3.5 ) m l,随着 PEEP水平的增加 ,肺复张容积亦明显增加 (P均 <0 .0 5 )。动脉氧合指数也随着 PEEP水平增加而增加 ,且其变化与肺复张容积呈正相关 (r=0 .4 83,P<0 .0 1)。不同 PEEP条件下 ,患者的肺静态顺应性无明显变化 (P>0 .0 5 )。将患者按有无低位转折点 (L IP)分为有 L IP组与无 L IP组 ,两组患者的肺复张容积都随着 PEEP水平的增加而增加 ,其中 PEEP15 cm H2 O时 L IP组患者的肺复张容积大于无 L IP组 (P<0 .0 5 )。结论　 PEEP水平越高 ,肺复张容积越大 ,肺复张容积增加与动脉氧合指数的变化呈正相关     

Impact of positive end-expiratory pressure on cerebral injury patients with hypoxemia

Background

Traumatic brain injury or intracranial hemorrhage patients with acute lung injury/acute respiratory distress syndrome need mechanical ventilation. The use of positive end-expiratory pressure (PEEP) in this situation remains controversial. This study explored the impact of PEEP on intracranial pressure (ICP), cerebral perfusion pressure (CPP), central venous pressure (CVP), and mean arterial pressure (MAP) in cerebral injury patients.

Methods

Nine cerebral injury patients with lung injury who needed mechanical ventilation and met the criteria for ICP monitoring were included in this study. Intraventricular catheters were positioned in 1 of the bilateral ventricles and connected to pressure transducers. Invasive arterial pressure and CVP were monitored continuously. Pressure control ventilation was applied during this clinical trial in a stepwise recruitment maneuver (RM) with 3 cm H₂O intermittent increments and decrements of PEEP.

Results

A total of 28 RMs were completed in 9 patients. Mean values of MAP, CVP, ICP, and CPP 5 minutes after RMs showed no significant differences compared with baseline (P > 0.05). Correlation analysis of all the mean values of MAP, CVP, ICP, and CPP showed significant correlation between MAP and CPP, PEEP and CVP, PEEP and ICP, and PEEP and CPP with all P values less than 0.05.

Conclusion

The impact of PEEP on blood pressure, ICP, and CPP varies greatly in cerebral injury patients. Mean arterial pressure and ICP monitoring is of benefit when using PEEP in cerebral injury patients with hypoxemia.     

Bronchial blood flow reduction with positive end-expiratory pressure after acute lung injury in sheep

Smoke inhalation increases bronchial blood flow (Qbr) and produces edema of the airway system. This study investigates whether the increased Qbr seen 24 h after inhalation injury can be affected by mechanical ventilation with PEEP (5, 10, 15 cm H2O). Sheep (n = 8) previously prepared with cardiopulmonary catheters and ultrasonic transit time flow probes mounted around their bronchial arteries were insufflated with four sets of 12 breaths each of cotton smoke. Different levels of PEEP were added to the mechanical ventilation 24 h after injury; each PEEP level was applied for 45 min. There were significant increases in Qbr and lung lymph flow (QL) associated with a marked decrease in bronchial vascular resistance (BVR) 24 h after injury. However, no change was observed in mean arterial pressure (MAP) or cardiac index (CI). There was a substantial reduction in PaO2/FIO2 (P/F), which indicated a deterioration in arterial oxygenation. The application of varying levels of PEEP decreased Qbr (p less than .05) while BVR increased (p less than .05), but QL and P/F did not. CI and MAP were recorded. After removal of PEEP, none of the cardiopulmonary variables were significantly different from their postsmoke control values. These findings suggest that mechanical ventilation with PEEP markedly decreases the smoke-induced hyperemia edema frequently seen after inhalation injury without any significant alterations in MAP or CI.     

Effect of positive end-expiratory pressure on intra-abdominal pressure

Massive elevation of intra-abdominal pressure (IAP) causes renal, cardiovascular, and respiratory dysfunction. Positive end-expiratory pressure (PEEP) markedly increases the detrimental effect of IAP on the cardiovascular system. The purpose of this study was to determine the effect of PEEP on IAP. In 15 patients requiring mechanical ventilation, IAP was measured, after 15-minute equilibration intervals, at PEEP levels of 0, 5, 10, and 15 cm H2O. Parametric analysis with multiple paired t tests and nonparametric analysis with Spearman's rho and Kendall's tau tests were used to determine correlation between PEEP and IAP. All patients were male. The mean age was 39 years (range, 18-77). Ten patients had just had laparotomy. No correlation was found between PEEP and IAP. We conclude that PEEP of 15 cm H2O or less has no effect on IAP, and we discuss the clinical implications.     

Effects of positive end-expiratory pressure on gas exchange and expiratory flow limitation in adult respiratory distress syndrome

OBJECTIVE: To assess the effects of different positive end-expiratory pressure (PEEP) levels (0, 5, 10, and 15 cm H2O) on tidal expiratory flow limitation (FL), regional intrinsic positive end-expiratory pressure (PEEPi) inhomogeneity, alveolar recruited volume (Vrec), respiratory mechanics, and arterial blood gases in mechanically ventilated patients with acute respiratory distress syndrome (ARDS). DESIGN: Prospective clinical study. SETTING: Multidisciplinary intensive care unit of a university hospital. PATIENTS: Thirteen sedated, mechanically ventilated patients during the first 2 days of ARDS. INTERVENTIONS: Detection of tidal FL and evaluation of total dynamic PEEP (PEEPt,dyn), total static PEEP (PEEPt,st), respiratory mechanics, and Vrec from pressure, flow, and volume traces provided by the ventilator. The average (+/-sd) tidal volume was 7.1 +/- 1.5 mL/kg, the total cycle duration was 2.9 +/- 0.45 secs, and the duty cycle was 0.35 +/- 0.05. MEASUREMENTS: Tidal FL was assessed using the negative expiratory pressure technique. Regional PEEPi inhomogeneity was assessed as the ratio of PEEPt,dyn to PEEPt,st (PEEPi inequality index), and Vrec was quantified as the difference in lung volume at the same airway pressure between quasi-static inflation volume-pressure curves on zero end-expiratory pressure (ZEEP) and PEEP. RESULTS: On ZEEP, seven patients exhibited FL amounting to 31 +/- 8% of tidal volume. They had higher PEEPt,st and PEEPi,st ( p<.001) and lower PEEPi inequality index ( p<.001) than the six nonflow-limited (NFL) patients. Two FL patients became NFL with PEEP of 5 cm H2O and five with PEEP of 10 cm H2O. In both groups, PaO2 increased progressively with PEEP. In the FL group, there was a significant correlation of PaO2 to PEEPi inequality index ( p=.002). For a given PEEP, Vrec was greater in NFL than FL patients, and a significant correlation of Pao to Vrec ( p<.001) was found only in the NFL group. CONCLUSIONS: We conclude that on ZEEP, tidal FL is common in ARDS patients and is associated with greater regional PEEPi inhomogeneity than in NFL patients. With PEEP of 10 cm H2O, flow limitation with concurrent cyclic dynamic airway compression and re-expansion and the risk of "low lung volume injury" were absent in all patients. In FL patients, PEEP induced a significant increase in PaO2, mainly because of the reduction of regional PEEPi inequality, whereas in the NFL group, arterial oxygenation was improved satisfactorily because of alveolar recruitment.     

Pharmacologic reduction of mean arterial pressure does not adversely affect regional cerebral blood flow and intracranial pressure in experimental intracerebral hemorrhage.

OBJECTIVE: To determine the effect of mean arterial pressure (MAP) reduction on regional cerebral blood flow and intracranial pressure (ICP) in intracerebral hemorrhage. We tested the hypothesis that there is ischemia in the perihematoma region after intracerebral hemorrhage, which can be exacerbated by a pharmacologic reduction of MAP. DESIGN: Prospective, controlled, laboratory trial. SETTING: Animal research laboratory. SUBJECTS: Eighteen mongrel dogs, weighing 15 to 25 kg. INTERVENTIONS: We introduced intracerebral hemorrhage in 12 anesthetized dogs by autologous blood injection under arterial pressure in the deep white matter adjacent to the left caudate region. We measured serial regional cerebral blood flow using radiolabeled microspheres in animals with two different volumes of injected blood (2.8 mL [Group A, n = 6] and 4.4 mL [Group B, n = 6]) and compared them with control animals (n = 6). Intravenous labetalol was administered 90 mins after administration of hematoma, while maintaining cerebral perfusion pressure >65 mm Hg. Regional cerebral blood flow measurements were repeated 10 and 30 mins after labetalol administration. MAP and ICP were monitored continuously using intra-arterial and cisterna magna catheters, respectively. MEASUREMENTS AND MAIN RESULTS: Compared with control animals, significant elevation in ICP was observed in Groups A and B and elevation in MAP was observed in Group B at 45 mins after injection of blood. These hemodynamic alterations were not accompanied by any significant differences in regional cerebral blood flow in any group. Administration of labetalol resulted in a decrease in MAP (mm Hg+/-SEM) in Groups A (119.0+/-9.2 to 103.0+/-9.1) and B (124.5+/-7.4 to 100.5+/-4.8) and controls (103.5+/-4.3 to 85.0+/-8.0). No differences were observed in regional cerebral blood flow after MAP reduction in both Groups A and B compared with controls in regions around or distant to the hematoma. There were no changes in ICP in Groups A and B both at 10 and 30 mins after reduction in MAP compared with pretreatment values. CONCLUSIONS: In our model, pharmacologic reduction of MAP within the normal autoregulatory limits of cerebral perfusion pressure, 90 mins after onset, had no adverse effect on ICP and regional cerebral blood flow in regions around or distant to the hematoma. These results support the controlled use of antihypertensive treatment in intracerebral hemorrhage in the initial time period.