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Intra-abdominal pressure may be decreased non-invasively by continuous negative extra-abdominal pressure (NEXAP).

OBJECTIVE: To investigate the possibility of artificially decreasing intra-abdominal pressure (IAP) by applying continuous negative pressure around the abdomen. MATERIAL AND METHODS: We investigated the effects of negative extra-abdominal pressure (NEXAP) on IAP and central venous pressure (CVP) in 30 patients admitted to our intensive care unit (age 57+/-17 years, BMI 26.1+/-4.0 kg/m2, SAPS II 41.8+/-17.0). Patients with severe hemodynamic instability and/or those admitted following a laparotomy were not studied. Measurements included bladder pressure as an estimate of IAP, CVP, invasive mean arterial pressure (MAP) and heart rate (HR). In five patients extensive hemodynamic measurements were also taken using a Swan-Ganz catheter. Following measurements at baseline (Basal), NEXAP (Life Care - Nev 100, Respironics) was applied on the abdomen, in random order, at a pressure equal to IAP (NEXAP0), 5 cmH(2)O (NEXAP-5) or 10 cmH(2)O (NEXAP-10) more negative than NEXAP0. RESULTS: Basal IAP ranged from 4 to 22 mmHg. NEXAP decreased IAP from 8.7+/-4.3 mmHg to 6+/-4.2 (Basal vs NEXAP0 p<0.001). There was a further decrease of IAP when more negative pressure was applied: 4.3+/-3.2 mmHg, 3.8+/-3.7 mmHg (NEXAP-5 and NEXAP-10 vs NEXAP0, respectively, p<0.001). Similarly, CVP decreased from 9.3+/-3.4 mmHg to 7.5+/-3.8 (Basal vs NEXAP-10, p<0.001). The lower the IAP when NEXAP was applied, the lower the CVP (r2=0.778, p<0.001, multiple linear regression). When measured, cardiac output did not significantly change with NEXAP. CONCLUSIONS: Negative extra-abdominal pressure may be applied in critically ill patients to decrease intra-abdominal pressure non-invasively.

Abdomen↗

Increased intra-abdominal pressure affects respiratory variations in arterial pressure in normovolaemic and hypovolaemic mechanically ventilated healthy pigs.

OBJECTIVE: To evaluate the effect of increased intra-abdominal pressure (IAP) on the systolic and pulse pressure variations induced by positive pressure ventilation in a porcine model. DESIGN AND SETTING: Experimental study in a research laboratory. SUBJECTS: Seven mechanically ventilated and instrumented pigs prone to normovolaemia and hypovolaemia by blood withdrawal. INTERVENTION: Abdominal banding gradually increased IAP in 5-mmHg steps up to 30 mmHg. MEASUREMENTS AND MAIN RESULTS: Variations in systolic pressure, pulse pressure, inferior vena cava flow, and pleural and transmural (LVEDPtm) left-ventricular end-diastolic pressure were recorded at each step. Systolic pressure variations were 6.1+/-3.1%, 8.5+/-3.6% and 16.0+/-5.0% at 0, 10, and 30 mmHg IAP in normovolaemic animals (mean+/-SD; p<0.01 for IAP effect). They were 12.7+/-4.6%, 13.4+/-6.7%, and 23.4+/-6.3% in hypovolaemic animals (p<0.01 vs normovolaemic group) for the same IAP. Fluctuations of the inferior vena cava flow disappeared as the IAP increased. Breath cycle did not induce any variations of LVEDPtm for 0 and 30 mmHg IAP. CONCLUSIONS: In this model, the systolic pressure and pulse pressure variations, and inferior vena cava flow fluctuations were dependent on IAP values which caused changes in pleural pressure swing, and this dependency was more marked during hypovolaemia. The present study suggests that dynamic indices are not exclusively related to volaemia in the presence of increased IAP. However, their fluid responsiveness predictive value could not be ascertained as no fluid challenge was performed.

Abdomen↗

Relationship between colloid osmotic pressure and pulmonary artery wedge pressure in patients with acute cardiorespiratory failure.

Close relationships between progressive respiratory failure, roentgenographic signs of pulmonary opacification and decreases in the difference between colloid osmotic pressure of plasma and the pulmonary artery wedge pressure (colloid-hydrosatic pressure gradient) were demonstrated in 49 critically ill patients with multisystem failure, in patients in shock. The potential importance of this relationship is underscored by the observation that fatal progression of pulmonary edema was related to a critical reduction in the colloid-hydrostatic pressure gradient to levels of less than 0 mm Hg. More often, reduction in colloid osmotic pressure rather than increases in left ventricular filling pressure (pulmonary artery wedge pressure) accounted for the decline in colloid-hydrostatic pressure gradient. Routine measurement of colloid osmotic pressure, preferably in conjunction with pulmonary artery wedge pressure, is likely to improve understanding of the mechanisms of acute pulmonary edema.

Acute Disease↗

Blood pressure in the 'low-pressure system' and cardiac performance in essential hypertension.

Determinations of central venous pressure, cardiac haemodynamics and rapid volume expansion using iso-oncotic dextran were made in 49 men with sustained, uncomplicated essential hypertension and compared with those in 27 normotensive subjects of the same age and sex. In the hypertensives, central venous pressure was significantly increased in basal conditions while the cardiac index was normal and total blood volume was reduced. There was a positive and significant correlation of central venous pressure with age, arterial pressure and pulmonary wedge pressure. After rapid volume expansion, the slope of the curve relating cardiac output to central venous pressure was within the normal range, while the slope of the curve relating blood volume to central venous pressure was significantly reduced. The study provided evidence that in hypertensives: central venous pressure as well as arterial pressure is increased, the elevated central venous pressure is not due to an alteration in the cardiac 'pump function' or to hypervolaemia but rather to a decrease in the compliance of the venous bed or the left ventricle or both, and the strong correlation with age of the venous disturbances is similar to that found for the arterial side of the circulation.

Adult↗

Effect of continuous positive airway pressure on ambulatory blood pressure in patients with obstructive sleep apnoea.

OBJECTIVES: Previous reports on the effects of continuous positive airway pressure (CPAP) therapy for obstructive sleep apnoea (OSA) on blood pressure has shown contradictory results. Accordingly, we have investigated the effects of CPAP on blood pressure and on the potential reversal of the diagnosis of hypertension in patients with OSA evaluated repeatedly by ambulatory blood pressure monitoring. METHODS: We studied 122 patients (104 men and 18 women), 55.1+/-10.5 years of age, with diagnosis of OSA corroborated by overnight polysomnography at the clinic. Among those patients, 83 were treated with CPAP after their first evaluation, while 39 remained without CPAP for the duration of the trial. Blood pressure was measured by ambulatory monitoring at 20-min intervals during the day and at 30-min intervals at night for 48 consecutive hours, at baseline and after 2 and 4 months of intervention. RESULTS: There was a small, but not statistically significant, reduction in ambulatory blood pressure in patients treated with CPAP (0.7 and 1.5 mmHg in 24-h mean of systolic and diastolic blood pressure after 2 months of therapy; 2.0 and 2.3 mmHg after 4 months; P>0.239). The blood pressure reduction was very similar in patients with OSA followed for 4 months without CPAP (1.9 and 2.2 mmHg in 24-h mean of systolic and diastolic blood pressure, respectively; P=0.543). We found a high (77%) prevalence of hypertension among the patients participating in this study, although only 37% were receiving antihypertensive medication at the time of recruitment. The prevalence of hypertension was slightly but not significantly reduced to just 74% after 4 months of treatment with CPAP. CONCLUSIONS: The small reduction in blood pressure for consecutive profiles of ambulatory monitoring can probably be explained by the documented 'ABPM pressor effect' on patients using the ambulatory device for the first time. The high prevalence of hypertension among patients with OSA is not significantly reduced by treatment with CPAP. These results suggest that patients with OSA should always be properly evaluated for diagnosis of hypertension, and provided, if needed, with antihypertensive treatment apart from the recommended CPAP.

Blood Pressure↗

Effects of positive end-expiratory pressure on regional cerebral blood flow, intracranial pressure, and brain tissue oxygenation.

OBJECTIVE: Acute respiratory dysfunction frequently occurs following severe aneurysmal subarachnoid hemorrhage requiring positive end-expiratory pressure (PEEP) ventilation to maintain adequate oxygenation. High PEEP levels, however, may negatively affect cerebral perfusion. The goal of this study was, to examine the influence of various PEEP levels on intracranial pressure, brain tissue oxygen tension, regional cerebral blood flow, and systemic hemodynamic variables. 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 suffering subarachnoid hemorrhage. INTERVENTIONS: Under continuous monitoring of intracranial pressure, brain tissue oxygen tension, regional cerebral blood flow, mean arterial pressure, and cardiac output, PEEP was applied in increments of 5 cm H2O from 5 to 25 cm H2O in the experimental part and from baseline to 20 cm H2O in the clinical part. MEASUREMENTS AND MAIN RESULTS: In animals, high PEEP levels had no adverse effect on intracranial pressure, brain tissue oxygen tension, or regional cerebral blood flow. In patients with severe subarachnoid hemorrhage, stepwise elevation of PEEP resulted in a significant decrease of mean arterial pressure and regional cerebral blood flow. Analyses of covariance revealed that these changes of regional cerebral blood flow depended on mean arterial pressure changes as a result of a disturbed cerebrovascular autoregulation. Consequently, normalization of mean arterial pressure restored regional cerebral blood flow to baseline values. CONCLUSIONS: Application of high PEEP does not impair intracranial pressure or regional cerebral blood flow per se but may indirectly affect cerebral perfusion via its negative effect on macrohemodynamic variables in case of a disturbed cerebrovascular autoregulation. Therefore, following severe subarachnoid hemorrhage, a PEEP-induced decrease of mean arterial pressure should be reversed to maintain cerebral perfusion.

Adult↗

Effect of continuous positive airway pressure on blood pressure : a placebo trial.

This study examined the effect of continuous positive airway pressure (CPAP) treatment on blood pressure in patients with obstructive sleep apnea. Thirty-nine patients with sleep apnea were studied. Ambulatory blood pressure monitoring was obtained before and after patients were randomized to receive either 1 week of CPAP or placebo CPAP (CPAP administered at ineffective pressure). Blood pressure was examined over daytime hours (6 AM to 10 PM) and during nighttime hours (10 PM to 6 AM). Daytime mean arterial blood pressure decreased significantly but equally in both the active treatment group and the placebo treatment group (P=0.001). Nighttime mean arterial pressure levels decreased to a much greater extent over time in the patients who received active CPAP treatment (P=0. 032). CPAP does appear to decrease nighttime blood pressure. However, the decrease in daytime blood pressure may reflect a nonspecific response (ie, placebo), since both the active treatment group and the placebo treatment group developed comparable decreases in blood pressure.

Adult↗

Randomized placebo-controlled trial of continuous positive airway pressure on blood pressure in the sleep apnea-hypopnea syndrome.

Arterial blood pressure rises at apnea termination, and there is increasing evidence that the sleep apnea-hypopnea syndrome (SAHS) is associated with daytime hypertension but no randomized controlled trial evidence of whether SAHS treatment reduces blood pressure exists. We, therefore, conducted a randomized placebo-controlled cross-over study of the effects of 4 wk of continuous positive airway pressure (CPAP) or oral placebo on 24-h blood pressure in 68 patients (55 males, 13 females; median apnea-hypopnea index [AHI], 35) not receiving hypotensive medication. Ambulatory blood pressure was recorded for the last 48 h of each treatment. Epworth Sleepiness Score (ESS) and Functional Outcomes of Sleep Questionnaire (FOSQ) were also recorded. All patients were normotensive. There was a small decrease in 24-h diastolic blood pressure (placebo, 79.2 [SE 0.9] mm Hg; CPAP, 77.8 [SE 1.0] mm Hg; p = 0.04) with the greatest fall occurring between 2:00 A.M. and 9:59 A.M. The observed decrease in 24-h diastolic blood pressure was greater in two a priori groups, CPAP use > or = 3.5 h per night (81.5 [SE 1.2] mm Hg; 79.6 [SE 1.2] mm Hg; p = 0.03) and those with more than twenty 4% desaturations per hour (82.4 [SE 2.1] mm Hg; 77.4 [SE 2.1] mm Hg; p = 0.002). Systolic pressure also fell in the latter group (133.1 [SE 2.8] mm Hg; 129.1 [SE 2.1] mm Hg; p = 0.009). Desaturation frequency was the best predictor of diastolic blood pressure fall with CPAP (r = 0.38; p = 0.002). Both ESS and FOSQ domains improved. Thus, CPAP can reduce blood pressure in patients with SAHS, particularly in those with nocturnal oxygen desaturation, but the decrease is small.

Adult↗

Effect of airway pressure on pericardial pressure.

The effect of applied positive airway pressure or PEEP on pericardial pressure was examined in closed-chest, anesthetized dogs with normal lungs and in animals with oleic acid-induced lung injury. Both groups were studied before and after vascular volume loading by dextran infusion. Pericardial pressure was measured using an air-filled flat balloon placed along the lateral left ventricular free wall within the pericardial space. A linear relation between right atrial pressure (RAP) and pericardial pressure (PP) was found (RAP = 3.9 + 0.78 PP, r = 0.76, p less than 0.01) that was independent of acute lung injury but was influenced by the application of PEEP. In the baseline volume condition, pericardial pressure increased linearly with an increase in PEEP to 15 cm H2O. After volume loading, pericardial pressure increased fourfold, but, surprisingly, did not change with applied PEEP. These relations were similar in the two groups despite a reduction in total respiratory system compliance in the oleic acid group. This suggests that transmission of airway pressure to the pericardial surface is independent of the presence of acute lung injury and that changes in pericardial pressure in response to PEEP reflect both the transmission of airway pressure to the pericardial surface and, presumably, PEEP-related changes in cardiac volume and ventricular compliance.

Animals↗

Ventilatory muscle loads and the frequency-tidal volume pattern during inspiratory pressure-assisted (pressure-supported) ventilation.

Pressure support ventilation (PSV) is a new form of mechanical ventilatory support that assists a patient's spontaneous ventilatory effort with a clinician-selected amount of inspiratory pressure. In order to assess the muscle unloading effect and the ventilatory pattern response to increasing levels of this inspiratory pressure assist, we first utilized a computer respiratory system model with variable alveolar ventilation demands and impedances. From this model, we calculated ventilatory muscle loads (expressed either as the work/min or as the pressure time index) during simulated, unassisted breathing and during simulated breathing with levels of inspiratory pressure assist up to that which resulted in a VT of 800 ml and no work being performed by the muscles (defined as PSVmax for the model conditions being studied). The optimal ventilatory pattern (i.e., frequency-tidal volume) under each ventilation and impedance condition was defined as that which resulted in minimal muscle load. Under these model conditions, we found that PSVmax ranged from 5 to 41 cm H2O and that as the level of inspiratory pressure assist was increased from zero to PSVmax, there was a biphasic response of both the ventilatory muscle loading and the ventilatory pattern. Specifically, at low levels of inspiratory pressure assist, the model predicted that the applied pressure would only partially unload the ventilatory muscles. Continued muscle energy expenditure would thus still be required, whereas the ventilatory pattern would change little. Conversely, at higher levels of inspiratory pressure assist, the model predicted that the applied pressure would be sufficient to completely unload the ventilatory muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗

The acute effects of continuous positive airway pressure and oxygen administration on blood pressure during obstructive sleep apnea.

We have measured blood pressure continuously with a digital artery blood pressure monitor in eight patients with severe obstructive sleep apnea (OSA) during 30 min each of wakefulness, OSA, OSA with added oxygen to keep saturation above 96 percent at all times (OSA+O2), and nasal continuous positive airway pressure (CPAP) therapy. Mean blood pressures were not different between wakefulness, OSA, OSA+O2, and CPAP, although the variability in blood pressure was significantly greater during OSA and OSA+O2 than during wakefulness and CPAP. The addition of oxygen did not attenuate the variability in blood pressure. Using multiple linear regression modeling to further dissect out the principal variables determining the postapneic blood pressure rise, we found that only apnea length (r2 = 0.28, p less than 0.0001) and pulse rate changes (r2 = 0.15, p less than 0.0001) remained significantly related to SBPmax, while hypoxemia did not. We found the same trends in the other variables SBPten, DBPmax, and DBPten. Hypoxemia made a small contribution to the size of DBPmax, although this was small by comparison with apnea length. We conclude that CPAP treatment of OSA does not lower mean blood pressure acutely, although it significantly reduces the large oscillations in blood pressure seen in patients with untreated OSA. The rise in blood pressure following each apnea is not primarily due to arterial desaturation but is related to apnea length and may be caused by increased sympathetic activity secondary to arousal.

Blood Pressure↗

Drug-induced changes in ambulatory blood pressure and pulse pressure in patients with or without sustained hypertension.

We retrospectively studied 216 mild to moderate hypertensive patients receiving either an angiotensin converting enzyme inhibitor (ACEI) or a calcium antagonist (CA), as a once-a-day monotherapy; their blood pressure had been measured using both a sphygmomanometer and an ambulatory blood pressure recorder. Numerous discrepancies were found between the two methods of blood pressure measurement with respect to systolic blood pressure (SBP) and diastolic blood pressure (DBP), as well as pulse pressure (PP). Clinic blood pressure measurement did not show any significant differences between the effects of ACEI and those of CA, whereas ambulatory blood pressure measurements (ABPM) showed that in patients with normal ambulatory blood pressure (so-called 'white coat' hypertensive patients), ACEI only (but not CA) significantly lowered SBP, DBP and PP. Accordingly, a threshold of efficacy was sought: it appeared to be lower for ACEI than for CA (120/80 vs 140/85 mmHg). Furthermore, for a given degree of DBP lowering, SBP and PP were more lowered by ACEI than by CA, indicating a greater effect of ACEI on arterial compliance. Likewise, for a given level of mean blood pressure, SBP and PP were lower and DBP slightly higher in patients on ACEI than in those on CA. Our data are consistent with some recent papers, emphasizing a heightened activity of the renin-angiotensin system in 'white coat' hypertensive patients.

Adult↗

A comparison of central venous pressure and common iliac venous pressure in critically ill mechanically ventilated patients.

OBJECTIVE: To investigate the possibility of using common iliac venous pressure (CIVP) as an alternative to superior vena cava pressure (SVCP) in mechanically ventilated, critically ill, adult patients. DESIGN: A randomized, blinded comparison. SETTING: Multidisciplinary intensive care unit at a university teaching hospital. PATIENTS: Twenty mechanically ventilated, critically ill, adult patients. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: All patients had a catheter in situ for measuring the SVCP. A new triple-lumen catheter, with a length ranging from 15 to 20 cm, was placed into the common iliac vein via the femoral route. The SVCP and CIVP were simultaneously measured at hourly intervals for 6 hrs. Positive end-expiratory pressure, mean airway pressure, and intra-abdominal pressure were measured at the same time intervals. For 140 paired measurements of CIVP and SVCP in 20 patients, the mean difference was 0.1 +/- 1.06 (SD) mm Hg (95% confidence interval -0.10 to 0.25); the limits of agreement were -2.04 to 2.20 mm Hg (95% confidence interval -2.34 to 2.50). Mean airway pressure, intra-abdominal pressure, and positive end-expiratory pressure had no measurable effect on the difference between SVCP and CIVP. Serious complications arising from insertion of the catheter through the femoral route were not observed. CONCLUSION: For clinical purposes, CIVP measured by a catheter of 15 to 20 cm placed through the femoral route is interchangeable with SVCP in mechanically ventilated adult patients. This finding provides an alternative route for assessment of central venous pressure when other routes are not appropriate.

Abdomen↗

Sequential variceal pressure measurement by endoscopic needle puncture during maintenance sclerotherapy: the correlation between variceal pressure and variceal rebleeding.

BACKGROUND/AIMS: The risk factors for esophageal variceal rebleeding are little known. Variceal pressure is one of the major determinants of variceal rupture, but the relationship between variceal pressure and variceal rebleeding during maintenance sclerotherapy has not been determined. This study was undertaken to evaluate the relationship between variceal pressure/gradient change and variceal rebleeding during maintenance sclerotherapy. METHODS: Patients with liver cirrhosis and recent esophageal variceal hemorrhage underwent consecutive variceal pressure measurements by direct puncture of the varices before each elective sclerotherapy. RESULTS: In 46 patients, the initial variceal pressure was no different regardless of age, sex, underlying etiology or hepatic reserve. Variceal pressure was higher in large varices, varices with more severe red wale markings, and varices with slower reduction in size during maintenance sclerotherapy. A larger volume of sclerosant was required to eradicate large varices, varices with more severe red wale markings, and varices with slower reduction in size during maintenance sclerotherapy. There was a positive correlation between initial variceal pressure and total amount of sclerosant (r=0.485, p=0.001). Initial variceal pressure was not related to rebleeding. Variceal pressure increased more in patients with rebleeding from varices per se (n=7) than in those without rebleeding (n= 24). There was no difference in pressure change between patients without rebleeding (n=24) and those with rebleeding from variceal ulcers (n=7). CONCLUSIONS: Large varices, severe red color signs and slow reduction in variceal size were associated with higher initial variceal pressure, and more sclerosant was required to eradicate the varices. An increase in variceal pressure during maintenance sclerotherapy indicates a higher risk of variceal rebleeding, but not of variceal ulcer rebleeding.

Aged↗

Intrathoracic pressure regulator during continuous-chest-compression advanced cardiac resuscitation improves vital organ perfusion pressures in a porcine model of cardiac arrest.

BACKGROUND: A novel device, the intrathoracic pressure regulator (ITPR), combines an inspiratory impedance threshold device (ITD) with a vacuum source for the generation of controlled -10 mm Hg vacuum in the trachea during cardiopulmonary resuscitation (CPR) while allowing positive pressure ventilation. Compared with standard (STD) CPR, ITPR-CPR will enhance venous return, systemic arterial pressure, and vital organ perfusion in both porcine models of ventricular fibrillation and hypovolemic cardiac arrest. METHODS AND RESULTS: In protocol 1, 20 pigs (weight, 30+/-0.5 kg) were randomized to STD-CPR or ITPR-CPR. After 8 minutes of untreated ventricular fibrillation, CPR was performed for 6 minutes at 100 compressions per minute and positive pressure ventilation (100% O2) with a compression-to-ventilation ratio of 15:2. In protocol 2, 6 animals were bled 50% of their blood volume. After 4 minutes of untreated ventricular fibrillation, interventions were performed for 2 minutes with STD-CPR and 2 minutes of ITPR-CPR. This sequence was repeated. In protocol 3, 6 animals after 8 minutes of untreated VF were treated with ITPR-CPR for 15 minutes, and arterial and venous blood gases were collected at baseline and minutes 5, 10, and 15 of CPR. A newer, leak-proof ITPR device was used. Aortic, right atrial, endotracheal pressure, intracranial pressure, and end-tidal CO2 values were measured (mm Hg); common carotid arterial flow also was measured (mL/min). Coronary perfusion pressure (diastolic; aortic minus right atrial pressure) and cerebral perfusion pressure (mean arterial minus mean intracranial pressure) were calculated. Unpaired Student t test and Friedman's repeated-measures ANOVA of ranks were used in protocols 1 and 3. A 2-tailed Wilcoxon signed-rank test was used for analysis in protocol 2. Fischer's exact test was used for survival. Significance was set at P<0.05. Vital organ perfusion pressures and end-tidal CO2 were significantly improved with ITPR-CPR in both protocols. In protocol 1, 1-hour survival was 100% with ITPR-CPR and 10% with STD-CPR (P=0.001). Arterial blood pH was significantly lower and Paco2 was significantly higher with ITPR-CPR in protocol 1. Arterial oxygen saturation was 100% throughout the study in both protocols. Paco2 and Pao2 remained stable, but metabolic acidosis progressed, as expected, throughout the 15 minutes of CPR in protocol 3. CONCLUSIONS: Compared with STD-CPR, use of ITPR-CPR improved hemodynamics and short-term survival rates after cardiac arrest.

Animals↗

The relation between pelvic pressure and bladder pressure during pelvic perfusion with standardized flow rates.

The aim of this study was to elucidate the relation between pelvic pressure and bladder pressure during pelvic perfusion with standardized flow rates. Anaesthetized Danish Landrace Breed pigs (n = 5) weighing 35-40 kg were studied. Transparenchymally two 6-F catheters were placed in both renal pelves for pressure measurement and perfusion. Transurethrally two catheters were placed in the bladder for pressure measurements and for urine collection and infusion. Bladder filling was done with a constant infusion rate of 45 ml/min during perfusion of both pelves with saline consecutively with the flow rates: 0, 2, 4, 6 and 8 ml/min during continuous measurement of bladder and bilateral pelvic pressure. The baseline diuresis varied from 0.4-1.0 ml/min. Without pelvic perfusion a negative pressure gradient between pelvis and bladder was seen demonstrating the importance of ureteral peristalsis. Pelvic perfusion with 2 ml/min showed that pelvic and bladder pressure were equal demonstrating weakening of ureteral peristalsis. During perfusion with higher flow rates pelvic pressure was higher than bladder pressure, showing that the positive gradient was important for urine transport. In conclusion ureteral peristalsis is important at low flow rates during increasing bladder pressure. At higher flow rates peristalsis weakens and the pressure gradient is the determining factor.

Animals↗

Intracranial pressure monitoring: modeling cerebrovascular pressure transmission.

OBJECTIVES: To examine changes in cerebrovascular pressure transmission derived from arterial blood pressure (ABP) and intracranial pressure (ICP) recordings by autoregressive moving average modeling technique. METHODS: Digitized ICP and ABP recordings were obtained from patients with brain injury. Two groups were defined: Group A with 4 patients who demonstrated plateau waves, and Group B with 4 intracranial hypertensive, hypoperfused patients. For each 16.5 s interval, mean values of ICP, ABP, cerebral perfusion pressure (CPP), and corresponding highest modal frequency (HMF) of cerebrovascular pressure transmission were computed. RESULTS: Mean values of CPP and HMF of 56.2 mmHg and 2.0 Hz for Group A were significantly higher (p < 0.005) than corresponding mean values of 31.9 mmHg and 0.744 Hz for Group B. The mean value of the slope of the regression line between HMF and CPP for group A of -0.034 Hz/mmHg was significantly different (p < 0.025) than the mean value of 0.0077 Hz/mmHg for Group B. Computations of HMF, pressure reactivity, and correlation pressure reactivity index on continuous pressure recordings are illustrated. CONCLUSIONS: Values of HMF of cerebrovascular pressure transmission are inversely related to CPP when pressure regulation is thought to be intact, and directly related when regulation is likely lost.

Algorithms↗

[The influence of vasodilatators on intraocular pressure and blood pressure (author's transl)].

The influence of different vasodilatators on blood pressure and intraocular pressure has been tested in animal experiments. For that purpose substances with alphasympathicolytic effect (Hydergin, Trental) have been tested as well as substances which are of direct influence on the muscles. In all cases a decrease of the blood pressure was noticed. Furthermore in most of the cases an increase of the intraocular pressure could be seen. This is due to a direct dilatation of ocular vessels. The effects were short-lived and reversible. We tried to find an explanation for the variations of intraocular pressure during the decrease of blood pressure. The low transmural pressure (PTM) and the corresponding low starting point of the muscle tonus seemed to be responsible for this phenomenon. Without doubt the starting point of the blood pressure, the dose, and the cardiac ability for compensation are of great influence in the development of the curve. Only a sufficiently high blood pressure is able to dilate the ocular vessels, so that one has to draw therapeutic conclusions from the constellation blood pressure/intraocular pressure before deciding on treatment.

Animals↗