Increase In Intraventricular Pressure Research Articles

Congenital/Primitive Hydrocephalus: Classification, Clinical Aspects, and Rehabilitation Approach

AbstractHydrocephalus is a heterogeneous disorder of cerebrospinal fluid (CSF) flow that leads to abnormal enlargement of the brain ventricles. The prevalence of infant hydrocephalus is approximately one case per 1,000 births. Hydrocephalus occurs due to an imbalance between the production and the absorption of CSF. The causes of hydrocephalus secondary to CSF overproduction are papilloma of the choroid plexus and rarely diffuse hyperplasia of the villi. All the other hydrocephalus forms are secondary to obstruction to normal CSF reabsorption and are also known as obstructive hydrocephalus. According to the location of obstruction, obstructive hydrocephalus can be defined as communicating, when caused by extraventricular obstruction of the CSF flow or decreased resorption of CSF distal to the fourth ventricle in the cisterns of the base or in the subarachnoid spaces, or as not communicating, in case of intraventricular obstruction to fluid flow. There is a third category, common in preterm infants, called external hydrocephalus which is secondary to delayed development of arachnoid function. Hydrocephalus leads to an increase in intraventricular pressure because of the lack of the mechanism regulating the homeostasis of the CSF flow. Increased intraventricular pressure is responsible for the clinical symptoms in affected child. Clinical presentation varies with age. In the neonatal period, prolonged or frequent apneic or bradycardic events, increasing head circumference, presence of sunsetting eyes or upward gaze palsy, evidence of full or tense anterior/posterior fontanelle, and splayed cranial sutures are signs of increased intracranial pressure. In infants, the most common signs are progressive macrocephaly, irritability, nausea/vomiting, headache, gait changes, and regression of developmental milestones. The extent of brain damage depends on the cause that led to hydrocephalus, the patient's age, and the rapidity of onset. The surgical treatment modalities consist of endoscopic ventriculostomy of the third ventricle and ventriculoperitoneal or ventriculoatrial CSF shunt.

Ventricular septal rupture after blunt chest trauma: a case report

Cardiac injury, including myocardial contusion and valvular damage, is a common complication of blunt chest trauma; however, traumatic ventricular septal rupture is a rare complication. We encountered a rare case of ventricular septal rupture following blunt chest trauma that was successfully repaired by emergency surgery. The mechanism underlying rupture may involve acute compression of the heart between the sternum and the vertebral column when the ventricle is filled, thereby causing a sudden increase in intraventricular pressure and leading to septal rupture. Emergency operation should be considered in cases of large defects and hemodynamic instability.

Dynamic Susceptibility Contrast Perfusion Magnetic Resonance Imaging Demonstrates Reduced Periventricular Cerebral Blood Flow in Dogs with Ventriculomegaly.

The nature of ventriculomegaly in dogs is still a matter of debate. Signs of increased intraventricular pressure and atrophy of the cerebral white matter have been found in dogs with ventriculomegaly, which would imply increased intraventricular pressure and, therefore, a pathological condition, i.e., to some extent. Reduced periventricular blood flow was found in people with high elevated intraventricular pressure. The aim of this study was to compare periventricular brain perfusion in dogs with and without ventriculomegaly using perfusion weighted-magnetic-resonance-imaging to clarify as to whether ventriculomegaly might be associated with an increase in intraventricular pressure. Perfusion was measured in 32 Cavalier King Charles spaniels (CKCS) with ventriculomegaly, 10 CKCSs were examined as a control group. Cerebral blood flow (CBF) was measured using free-hand regions of interest (ROI) in five brain regions: periventricular white matter, caudate nucleus, parietal cortex, hippocampus, and thalamus. CBF was significantly lower in the periventricular white matter of the dogs with ventriculomegaly (p = 0.0029) but not in the other ROIs. Reduction of periventricular CBF might imply increase of intraventricular pressure in ventriculomegaly.

Pediatric Hydrocephalus: Current State of Diagnosis and Treatment.

1. Zachary Wright, MD* 2. Thomas W. Larrew, MD* 3. Ramin Eskandari, MD, MS* 1. *Department of Neurosurgery, Medical University of South Carolina, Charleston, SC Hydrocephalus is a neurologic condition that requires lifelong vigilance by various health care professionals. Nonsurgical clinicians treating children with hydrocephalus, with or without shunts, often have questions about disease recognition, shunt infection, and shunt malfunction. Imaging modalities such as nonsedated magnetic resonance imaging and nonshunt endoscopic surgery have changed the landscape of the primary pediatric clinician’s interaction with this patient population. This article addresses the practice gap between pediatric outpatient and neurosurgical management of children with hydrocephalus in both the acute and chronic care settings. After completing this article, readers should be able to: 1. Understand basic pathophysiology related to hydrocephalus and available treatments. 2. Recognize presenting signs and symptoms of hydrocephalus. 3. Recognize when neurosurgical consultation is appropriate and manage hydrocephalus until a neurosurgeon is available. Hydrocephalus in the pediatric population is characterized by an initial increase in intraventricular pressure, resulting in pathologic dilation of the cerebral ventricles with an accumulation of cerebrospinal fluid (CSF). Although the pressure may be slight or severe, the balance between CSF production, flow, and absorption is lost in hydrocephalus. This condition is a significant cause of morbidity and mortality within the pediatric population, with a prevalence of approximately 6 in 10,000 live births and a neonatal mortality rate before initial hospital discharge of 13%. (1) The impact of this complex neurologic pathology on society is extremely large. According to nationally representative data sets, every year pediatric hydrocephalus accounts for 38,200 to 39,900 hospital admissions, 391,000 to 433,000 hospital days, and $1.4 to $2.0 billion in total hospital charges in the United States. (2) In the healthy child, CSF is primarily produced in the choroid plexus, …

Magnetic resonance imaging signs of high intraventricular pressure--comparison of findings in dogs with clinically relevant internal hydrocephalus and asymptomatic dogs with ventriculomegaly.

BackgroundMagnetic resonance imaging (MRI) findings of canine brains with enlarged ventricles in asymptomatic dogs were compared to those in dogs with clinically relevant internal hydrocephalus, in order to determine the imaging findings indicative of a relevant increase in intraventricular pressure. Discrimination between clinically relevant hydrocephalus and ventriculomegaly based on MRI findings has not been established yet and is anything but trivial because of the wide variation in ventricular size in different dog breeds and individuals. The MRI scans of the brains of 67 dogs of various breeds, skull conformation and weight were reviewed retrospectively. Based on clinical and imaging findings, the dogs were divided into three groups: a normal group (n = 20), a group with clinically silent ventriculomegaly (n = 25) and a group with severe clinically relevant internal hydrocephalus (n = 22). In addition to the ventricle/brain-index, a number of potential subjective signs of increased intraventricular pressure were recorded and compared between the groups.ResultsThe ventricle/brain-index was significantly higher in dogs with relevant hydrocephalus (p < 0.001) and a threshold value of 0.6 was specified as a discriminator between internal hydrocephalus and ventriculomegaly. Other MR imaging findings associated with clinically relevant hydrocephalus were an elevation of the corpus callosum (p < 0.01), dorsoventral flattening of the interthalamic adhesion (p < 0.0001), periventricular edema (p < 0.0001), dilation of the olfactory recesses (p < 0.0001), thinning of the cortical sulci (p < 0.0001) and/or the subarachnoid space (p < 0.0027) and disruption of the internal capsule adjacent to the caudate nucleus (p < 0.0001).ConclusionA combination of the abovementioned criteria may support a diagnosis of hydrocephalus that requires treatment.Electronic supplementary materialThe online version of this article (doi:10.1186/s12917-015-0479-5) contains supplementary material, which is available to authorized users.

A New Noninvasive Device for Measuring Central Ejection dP/dt Mathematical Foundation of Cardiac dP/dt Measurement Using a Model for a Collapsible Artery

We have developed a novel non-invasive device for the measurement of one of the most sensitive indices of myocardial contractility as represented by the rate of increase of intraventricular pressure (left ventricular dP/dt and arterial dP/dt performance index (dP/dt(ejc)). Up till now, these parameters could be obtained only by invasive catheterization methods. The new technique is based on the concept of applying multiple successive occlusive pressures on the brachial artery from peak systole to diastole using a inflatable cuff and plotting the values against time intervals that leads to the reconstruction of the central aortic pressure noninvasively. The following describes the computer simulator developed for providing a mathematical foundation of the new sensor. At the core of the simulator lies a hemodynamic model of the blood flow on an artery under externally applied pressure. The purpose of the model is to reproduce the experimental results obtained in studies on patients (Gorenberg et al. in Cardiovasc Eng: 305-311, 2004; Gorenberg et al. in Emerg med J 22 (7): 486-489, 2005) and a animal model where ischemia resulted from balloon inflation during coronary catheterization (Gorenberg and Marmor in J Med Eng Technol, 2006) and to describe correlations between the dP/dt(ejc) and other hemodynamic variables. The model has successfully reproduced the trends observed experimentally, providing a solid in-depth understanding of the hemodynamics involved in the new measurement. A high correlation between the dP/dt(ejc) and the rate of pressure rise in the aorta during the ejection phase was observed. dP/dt(ejc) dependence on other hemodynamic parameters was also investigated.

Validation of a novel method to determine non-invasively the rate of central aortic pressure changes

Introduction: One of the most sensitive indices of myocardial contractility is represented by the rate of increase of intraventricular pressure during isovolumetric contraction (dP/dt) and (dP/dtejc), which represents the rate of change of pressure during ejection. Today these parameters can be obtained only by invasive catheterization methods. We developed a novel technique that leads to the non-invasive reconstruction of the central aortic pressure. The technique is based on the concept of applying multiple successive occlusive pressures on the brachial artery from peak systole to diastole using an inflatable cuff and plotting the values against time intervals. The hypothesis is that the time intervals required for the aortic pressure wave to overcome a given occlusive brachial pressure applied by a sphyngomanometer on the arm are equal to time needed to reach the same pressure in the central aorta plus the propagation time to the brachial point, which is constant in the same patient throughout the measurements.Methods and results: We tested the hypothesis using an animal experiment. The new non-invasive device was mounted on the left forelimb of the animal. A Millar pressure transducer catheter was inserted to the aorta and the aorta pressure was recorded at time intervals of 1 ms. A second catheter was inserted into the coronary arteries and used to create controlled occlusion of the arteries using a balloon inflated to 10 atm. Measurements were obtained before the intervention was started, and throughout the sequence of repeated occlusions and deflations. At the end of the sequence, IV dobutamine was administered and results were monitored for 10 min while the heart rate and blood pressure were rising. Non-invasive dP/dtejc was reduced typically by 20% in response to balloon inflation. In long occlusion periods, stabilization and sometimes recovery of dP/dtejc is observed. By plotting dP/dtejc measured by the new non-invasive device versus catheter measurements a correlation factor of 0.843 was found.Conclusion: A newly developed method of non-invasive measurement of central dP/dt has been found to correlate to invasive measurements in an animal model.

Aorto–Atrial Fistula: An Important Complication of Aortic Prosthetic Valve Endocarditis

Aorto–Atrial Fistula: An Important Complication of Aortic Prosthetic Valve Endocarditis

Intraventricular Pressure Dynamics in Ventriculocholecystic Shunting: A Telemetric Study

Extracranial cerebrospinal fluid shunting is the current mainstay of therapy for hydrocephalus. The generally preferred extracranial site for cerebrospinal fluid absorption is the peritoneal space; however, the cardiac atrium and the pleura are also commonly used. On occasion other CSF recipient sites, such as the gallbladder, are used secondarily when the more common absorptive spaces are unavailable or unsuitable. The gallbladder, though, exhibits its own pressure dynamics in response to physiological stimuli. The effects of gallbladder contraction on intraventricular pressure (IVP) in the presence of a ventriculocholecystic (VGB) shunt are unknown. We had the opportunity to place a VGB shunt in a 4-year-old child who was coupled to a noninvasive telemonitor. After a period of acclimation, we examined the IVP dynamics of that shunting system both pre- and postprandially. We found that before ingestion of food, the gallbladder provides a CSF recipient site similar to that of the peritoneal space. However, after ingestion of a meal containing fat, we found that IVP rose more than 10 cm water in a stereotypic fashion consistent with postprandial gallbladder contraction. The increase in IVP lasted for several hours reaching a peak at approximately 75 min postprandially. We conclude that the VGB shunt is a viable alternative for extracranial cerebrospinal fluid shunting; however, one must be aware of the peculiar dynamics of this shunt in relation to food ingestion and the potential for unusually high IVPs.

Haemodynamic effects of a sixty minute infusion of dopamine hydrochloride in horses anaesthetised with halothane.

To describe the haemodynamic effects of a 60 min infusion of dopamine 4 microg/kg bwt/min during halothane anaesthesia, 7 mature Thoroughbred horses were studied. The infusion began 1 h after induction of anaesthesia by romifidine (100 microg/kg) and ketamine (2.2 mg/kg bwt). Throughout the period of dopamine infusion and for 30 min after its discontinuation, the horses were ventilated by intermittent positive pressure to maintain PaCO2 between 4.6-5.4 KPa. Inspired halothane concentration was adjusted to maintain an end tidal halothane concentration of 0.9%. Haemodynamic variables were measured using intracardiac strain gauge transducers sited in the left and right ventricle, aorta, and pulmonary artery. Left ventricular pressure was differentiated to obtain maximal rate of increase of intraventricular pressure (LVdp/dtmax). Transoesophageal Doppler echocardiography was performed to measure maximum aortic blood flow velocity (vmax) and acceleration (dv/dtmax), left ventricular velocity time integral (vTI) and cardiac output (CO), and left ventricular pre-ejection period (PEP) and ejection time (ET). Measurements were made during the 60 min infusion, and for 30 min after the infusion was discontinued. Infusion of dopamine 4 microg/kg/min significantly decreased mean aortic pressure, while left and right ventricular end-diastolic pressure and mean pulmonary artery pressure remained unchanged. There was a small, but significant, increase in heart rate during dopamine infusion. Maximum acceleration of aortic blood flow, CO and vTI were also significantly increased by dopamine infusion. Maximal rate of increase of intraventricular pressure (LVdp/dtmax) was significantly decreased 10 min after commencing infusion, but then returned to baseline for the remainder of the study. Left ventricular pre-ejection period (PEP) decreased during dopamine infusion whilst ejection time (ET) significantly increased. All measured variables except LVET had returned to baseline values within 30 min of discontinuing the infusion. This study demonstrated beneficial effects of dopamine infusion upon left ventricular systolic function. However, the therapeutic value of the drug is likely to be limited in clinical anaesthesia due to the simultaneous falls in arterial blood pressure which accompany its administration.

Protection of ischemic myocardium by inhibition of contracture in isolated rat heart.

Protection of the ischemic myocardium by pretreatment with a high dose of 2,3-butanedione monoxime (BDM) is attributed to the enhancement of glycolytic ATP production rather than to the inhibition of contracture during mild ischemia. Our objective was to investigate whether the inhibition of contracture would protect the arrested heart during prolonged ischemia. Isolated perfused rat hearts were subjected to 30 min of low-flow ischemia followed by reperfusion. Ischemic hearts were treated with BDM (5 mmol/l) after beating stopped. BDM ameliorated the increase in intraventricular pressure after ischemia without significant changes in ATP levels and with a decreased accumulation of lactate. BDM treatment accelerated the recovery of function and high-energy phosphates with reduced myocardial Ca2+ overload. The results of this study suggested that inhibition of contracture can protect the heart from ischemia-reperfusion injury.

Effect of intraventricular hemorrhage on pulmonary function in newborn piglets.

Intracranial hemorrhage in the premature infant is often associated with respiratory failure and need for mechanical ventilation. We therefore addressed the question of possible interactions with and pulmonary consequences of intraventricular hemorrhage. Newborn piglets were studied during intraventricular hemorrhage simulated by intraventricular blood infusion. Infusion volume amounted to 8% of estimated brain weight. Respiratory rate, minute ventilation, lung resistance and dynamic lung compliance, as well as arterial blood gases, arterial and intraventricular pressures were measured. The piglets were mechanically ventilated with a low basal rate of 20 breaths per minute throughout the study. All piglets experienced significant rise in intraventricular pressure and respiratory failure during the study. Respiratory failure was mainly a result of a reduction in respiratory frequency and minute ventilation until apnea. However, a rise in lung resistance was also noted while lung compliance did not change. We conclude that increased need for mechanical ventilation during intracranial hemorrhage is primarilty a consequence of hypoventilation. The increase seen in lung resistance could also suggest that intraventricular hemorrhage causes an element of bronchiolar constriction. Furthermore, these effects are not only a result of the increase in intraventricular pressure, but specific effects of blood components within the central nervous system must be considered.

The relationship between cerebral metabolic rate of oxygen and cerebral blood flow in the acute phase of head injury.

In 20 comatose patients (Glasgow coma scale less than or equal to 6 at admission) with severe head injury, the cerebral metabolic rate of oxygen (CMRO2) was calculated as the product of the hemispheric cerebral blood flow (CBF) and the arterio-venous oxygen content difference (AVDO2). The hemispheric CBF was calculated by the intracarotid 133xenon washout method by stochastic analysis as the average of 16 regions, and the measurements were performed within 3 weeks after the acute trauma. Generally no significant correlation (P less than 0.05) between CMRO2 and CBF was found, either in the total number of paired observations, in studies of hyperaemia defined as CBF greater than or equal to 30 ml 100 g-1 min-1; or in studies with reduced flow (CBF less than 30 ml 100 g-1 min-1). However, in about 50% of patients subjected to repeated studies within days, CBF was positively correlated to CMRO2, and this correlation was observed independently of the CBF value. Hyperaemia was associated with a significant decrease in AVDO2, a significant increase in both absolute and relative CO2 reactivity, and a significant increase in ventricular fluid pH; but not to an increase in intraventricular pressure, mean arterial blood pressure or significant changes in ventricular fluid lactate or lactate/pyruvate ratio.

Cerebrospinal fluid and plasma vasopressin during short-time induced intracranial hypertension.

The response of plasma and ventricular cerebrospinal fluid vasopressin concentration to short-time induced intracranial hypertension was studied in 8 patients with hydrocephalus, defined as ventricular enlargement on computerized tomography. In connection with measurement of conductance to cerebrospinal fluid outflow, the concentration of vasopressin in plasma and cerebrospinal fluid was measured during perfusion at a low (less than 10 mmHg) and at a high (greater than 20 mmHg) intraventricular pressure level. Mean plasma vasopressin concentration was increased from 2.4 +/- 0.4 pg/ml (SEM) during perfusion at the low pressure level to 4.2 +/- 0.8 pg/ml (p less than 0.01) at the high pressure level. The cerebrospinal fluid concentrations of vasopressin at the low and high intraventricular pressure were 1.2 +/- 0.1 pg/ml and 1.7 +/- 0.2 pg/ml (p less than 0.05), respectively. However, only half of the patients responded to the increase in intraventricular pressure with an increase in cerebrospinal fluid vasopressin concentration exceeding 50%. The results of the present study suggest that an increase in the intracranial pressure might be a stimulus for vasopressin release in both the blood and the cerebrospinal fluid.

Left ventricular cavity obliteration: hemodynamic behavior of the postextrasystolic beat

Thirteen patients with angiographic left ventricular cavity obliteration are analyzed. No transvalvular or subvalvular gradients were present except in two cases with a mild gradient after amyl nitrite inhalation. The commonest clinical features were chest pain (60%) and dyspnea (23%). Electrocardio-graphically proved left ventricular hypertrophy (70%) was prominent. The echocardiograms showed asymmetric septal hypertrophy (40%), symmetric hypertrophy (20%), systolic anterior motion of the anterior leaflet of the mitral valve (60%), and mitral valve prolapse (20%). In all the patients changes in systolic intraventricular pressure in the post-extrasystolic beat were evaluated and a decrease in intraventricular pressure was found in every case. In the four cases with extrasystoles recorded in the aorta a similar decrease of aortic pressure was found. This behavior is completely different in the hypertrophic cardiomyopathy with obstruction to the left ventricular outflow tract, where there is an increase in intraventricular pressure and a decrease in aortic pressure in the postextrasystolic beat. Left ventricular cavity obliteration is an angiographic phenomenon which is common in hypercontractile states, being an usual finding in hypertrophic cardiomyopathy. In cases without obstruction to the left ventricular outflow tract, the decrease in aortic pressure is caused by a different mechanism than the one involved in cases with obstruction. In cases without obstruction, the decrease in post-extrasystolic aortic pressure corresponds to a decrease in intraventricular pressure, whereas in subaortic stenosis there is an increase both of intraventricular pressure and gradient with the subsequent decrease in aortic pressure.

The electroencephalogram in cases of tumors of the posterior fossa and third ventricle

This report is based on a study of the electroencephalograms of 66 patients with tumors of the posterior fossa, 12 patients with tumors of the third ventricle, and 9 patients with obstructive hydrocephalus. The principal abnormality seen consisted of rhythmic, bilaterally synchronous slow waves. Less often, irregular, arrhythmic waves were seen. With the exception of tumors of the cerebellopontine angle, the incidence of abnormal records was approximately equal regardless of the nature or site of the pathologic process. There was no correlation between the site of the electroencephalographic abnormalities and the anatomic site of the lesion. The rhythmical abnormalities tent to be increased with hyperventilation and to be inhibited by opening of the eyes. In contrast, the arrhythmic abnormalities are only rarely affected by these procedures. Increased pressure within the third and lateral ventricles appears to be of major importance in the production of abnormality in the electroencephalogram. An acute increase in intraventricular pressure appears to produce an abnormality more often than a slow increase. Abnormality is more likely to be seen in young patients than in old patients.

To the pathology of the thoracic toad

The author sees the thoracic attack as a consequence of left ventricular weakness, which is the first stage of insufficiency. In such weakness, a sudden increase in resistance in the peripheral circulation or a sudden increase in blood flow to the heart, moments that increase the work of the latter, can cause an increase in the residual blood in the left ventricle, its distension and an increase in intraventricular pressure.