Rise In Venous Pressure Research Articles

Baffle fenestration with subsequent transcatheter closure. Modification of the Fontan operation for patients at increased risk.

Ventricular dysfunction, elevated pulmonary vascular resistance, and residual distal pulmonary artery distortion contribute to early mortality after a Fontan operation; they may be transient or reversible. A baffle fenestration, allowing right-to-left shunting, maintains cardiac output and limits right atrial pressure. A baffle fenestration was surgically created at the time of a modified Fontan repair in 20 consecutive patients. Risk factors included pulmonary artery pressure of 18 mm Hg or more, end-diastolic pressure of 12 mm Hg or more, valvar regurgitation, pulmonary artery distortion, pulmonary vascular resistance of 2 Woods' units or more, ventricular outflow obstruction, and complex anatomy. Nineteen of 20 patients survived. After the operation, mean arterial oxygen saturation was 86%, mean right atrial pressure was 15 mm Hg, and mean duration of pleural effusions was 6 days. Twelve of 19 survivors tolerated early test occlusion and had permanent transcatheter umbrella closure. Four patients failed early test occlusion, with a significant decrease in venous O2 saturation and a rise in central venous pressure, due to ventricular dysfunction, pulmonary artery distortion, or aortopulmonary collaterals. Three of four had successful late closure of the fenestration after correction of these abnormalities.

The effect of intravascular transfusion on umbilical venous pressure in anemic fetuses with and without hydrops

Human fetal umbilical venous pressure was measured during 20 intravascular transfusions performed for treatment of hemolytic anemia. The mean (±1 SEM) gestational age at the time of transfusion was 29.3 ± 1 weeks and the mean beginning hematocrit was 27% ± 2%. The mean volume of infused packed red blood cells (70% hematocrit) was 90.3 ± 7 ml. The mean hematocrit at completion of the procedure was 48% ± 1%. In nonhydropic fetuses umbilical venous pressure rose progressively from 6.7 ± 1 mm Hg at the start of transfusion to 10.9 ± 1 mm Hg at the completion of transfusion ( p n = 2) had elevated umbilical venous pressure values before the initiation of transfusion therapy when compared with the first transfusion of nonhydropic fetuses (12.5 ± 0.5 vs. 5.7 ± 1 mm Hg, p = 0.01). However, the umbilical venous pressure measurements declined into the normal range within 24 hours of the first transfusion; this normalization was too rapid to be explained by the reversal of liver hypertrophy or portal hypertension. There was no demonstrable relationship between the rise in umbilical venous pressure and either the gestational age, the volume transfused, or the rise in hematocrit. This study demonstrated: (1) In terms of the umbilical venous pressure, direct intravenous infusion of the human anemic fetus is well tolerated; (2) the elevated umbilical venous pressure associated with immune hydrops can correct rapidly with red blood cell replacement.

Peripheral venous monitoring with acute blood volume alteration

We investigated the use of a new peripheral hemodynamic monitoring technique, the cuff-occluded rate of rise of peripheral venous pressure (CORRP), in the assessment of volume status in fluid overload. Seven adult mongrel dogs were given a general anesthetic, and monitoring lines were inserted. The animals were then subjected to an incremental volume overload of approximately 13% of estimated initial blood volume at 5-min intervals until a total volume infusion nearly equal to the animal's initial blood volume was reached. Comparison of the various monitoring techniques (e.g., cardiac output, CVP, systemic BP, pulmonary wedge pressure) demonstrated that the peripheral measurement of CORRP had better correlation with known administered volume (r = .96) than any of the other variables. The sensitivity of each of the variables in assessing small amounts of volume overload was also studied. The volume of crystalloid infusion necessary to cause a clinically significant change (defined as greater than 2 SD above the baseline mean) was compared for each of the monitoring variables. CORRP was equivalent to the other variables in sensing early volume overload. In summary, in the anesthetized animal model CORRP appears to be a sensitive, minimally invasive method of assessing volume status in acute volume overload. The efficacy of CORRP in a canine hemorrhagic shock and reperfusion model had previously been demonstrated. This technique could be clinically applicable in situations such as trauma with hemorrhagic shock, intraoperative volume changes, and in the assessment of intravascular volume after resuscitation.

Simulation of coronary circulation with special regard to the venous bed and coronary sinus occlusion

The vascular beds of the left circumflex and the left anterior descending coronary arteries are modelled by means of coupled differential equations that consider an arterial, a capillary and a venous section. In a stepwise procedure, experimental data from normal coronary perfusion and coronary sinus occlusion are used to assess the model parameters. For venous distensibility, a non-linear form of pressure-volume relationship proved vital to reproduce the characteristics of the rise in venous pressure after the onset of coronary sinus occlusion. Numerical integration was carried out for normal perfusion and for coronary sinus occlusion, yielding time courses of flows, volumes and pressures within large coronary arteries, capillaries and coronary veins. Coronary sinus occlusion reduces total mean flow by 18% and divides intramyocardial flow between the capillaries and the veins into a forward component of 3.03 mls −1 and a backward component of − 1.54 mls −1. This result represents a prediction for a haemodynamic quantity which is therapeutically important but inacessible to measurement. Varying degrees of systolic myocardial squeezing are studied to display the impact of myocardial contractility and vessel collapse on the mean values and phasic components of intra-myocardial flows.

Clinical Diagnosis of Tamponade in Malawi

A consecutive series of 25 Malawian patients with tamponade secondary to tuberculosis were compared to 25 patients with congestive cardiac failure, without pericardial effusion in a retrospective study. More patients with tamponade had an impalpable apex beat (21/1), pulsus paradoxus (13/0), soft heart sounds (13/2), paradoxical rise in jugular venous pressure (6/0), and fewer had a murmur (1/14). All these results are significant (p less than 0.05) by the chi 2 test with Yates' correction. The presence of two or more of these discriminating physical signs has a positive predictive value of 75 per cent, and a negative predictive value of 99.5 per cent for the diagnosis of tamponade. Clinical diagnosis of tamponade by primary health care personnel in Malawi should be possible, and lead to earlier treatment.

Le pantalon antichoc dans la prévention de l'embolie gazeuse

This study aimed to assess the efficiency and safety of military anti-shock trousers (MAST) in preventing venous air embolism in children undergoing neurosurgical procedures in the sitting position. It included 26 children, 7.7 ± 4-year-old and weighing 25.4 ± 10.5 kg. All had the same anaesthetic protocol including premedication with oral lorazepam, induction with thiopentone or propofol with fentanyl and vecuronium, and maintenance with isoflurane and a continuous infusion of fentanyl. In 10 patients, a retrograde central venous catheter was inserted for measurement of pressure in the superior bulb of the internal jugular vein. Haemodynamic measurements were carried out with the patient supine ; with the patient sitting, the MAST not being inflated ; 10 min after inflation of the MAST (40 mmHg in the limbs, 30 mmHg in the abdominal part) ; after starting 10 cmH 2 O positive end expiratory pressure ; and after fluid administration with 5 ml · kg −1 macromolecules (Plasmion®). The criterion for air embolism was a decrease in Petco 2 of more than 5 mmHg over more than 30 s, not preceeded by respiratory or cardiovascular impairment. Inflation of the MAST resulted in a dramatic rise in venous pressure, still reinforced by minor PEEP. Transmission of pressure from the right atrium to the dural sinus was linear, and seemed to be sufficient to prevent occurrence of detectable venous air emboli. No deleterious side-effects were noted. This method would therefore seem to be very efficient, preserving the advantages of the sitting position, and restricting its disadvantages. Unfortunately, the limited availability of different paédiatric sizes of MAST reduces the possible uses of this method.

The drainage of cerebrospinal fluid in hydrocephalic rats.

Cerebrospinal fluid plateau pressures and transverse sinus plateau pressures were measured in response to a series of constant-rate infusions into the CSF in 10-day-old control and hydrocephalic H-Tx rats. In control rats the venous pressure increased with CSF pressure but to a lesser extent and around 60% of the total resistance to absorption was due to the concurrent rise in venous pressure with a hydrostatic gradient maintained between CSF and venous blood. In hydrocephalic rats the same infusion rates resulted in an increase in venous pressure which was the same magnitude as the rise in CSF pressure, resulting in zero hydrostatic gradient from CSF to blood. This suggests that CSF drainage does not take place by this route in hydrocephalic rats and that alternative drainage routes must be operating.

The effect of intravascular transfusion on umbilical venous pressure in anemic fetuses with and without hydrops

Human fetal umbilical venous pressure was measured during 20 intravascular transfusions performed for treatment of hemolytic anemia. The mean (+/- 1 SEM) gestational age at the time of transfusion was 29.3 +/- 1 weeks and the mean beginning hematocrit was 27% +/- 2%. The mean volume of infused packed red blood cells (70% hematocrit) was 90.3 +/- 7 ml. The mean hematocrit at completion of the procedure was 48% +/- 1%. In nonhydropic fetuses umbilical venous pressure rose progressively from 6.7 +/- 1 mm Hg at the start of transfusion to 10.9 +/- 1 mm Hg at the completion of transfusion (p less than 0.002). However, most fetuses who began the infusion with a normal umbilical venous pressure ended the transfusion with a normal umbilical venous pressure (less than 10 mm Hg). Fetuses with immune hydrops (n = 2) had elevated umbilical venous pressure values before the initiation of transfusion therapy when compared with the first transfusion of nonhydropic fetuses (12.5 +/- 0.5 vs. 5.7 +/- 1 mm Hg, p = 0.01). However, the umbilical venous pressure measurements declined into the normal range within 24 hours of the first transfusion; this normalization was too rapid to be explained by the reversal of liver hypertrophy or portal hypertension. There was no demonstrable relationship between the rise in umbilical venous pressure and either the gestational age, the volume transfused, or the rise in hematocrit. This study demonstrated: (1) In terms of the umbilical venous pressure, direct intravenous infusion of the human anemic fetus is well tolerated; (2) the elevated umbilical venous pressure associated with immune hydrops can correct rapidly with red blood cell replacement.

Effects of outflow pressure on fetal lymph flow

The purpose of this study was to determine to what extent fetal thoracic duct lymph flow may be reduced by increases in fetal venous pressure. In pregnant sheep the fetal left thoracic lymph duct was catheterized at the base of the neck and this catheter was connected to a jugular-vein catheter so the lymph could spontaneously return to the fetal circulation. At 5 days after catheter implantation in nine unanesthetized fetuses at 133 +/- 1 (SE) days' gestation, lymph flow was measured by disconnecting the lymphatic catheter from that in the jugular vein and varying outflow pressure of the lymphatic catheter independent of venous pressure. Whenever outflow pressure was negative, lymph flow was independent of outflow pressure and averaged 0.66 +/- 0.05 ml/min. When outflow pressure of the left thoracic duct was increased above zero, lymph flow decreased linearly with outflow pressure and flow stopped at an outflow pressure of 11.5 +/- 0.6 mm Hg. At a normal venous pressure of 3 mm Hg, the lymph-flow sensitivity to venous pressure was such that a 1 mm Hg rise in venous pressure reduced lymph flow by 12.7% +/- 1.2%. Thus it appears that fetal lymph flow is very sensitive to outflow pressure and only moderate elevations in venous pressure potentially may lead to fetal edema.

Autonomic modulation of fetal atrial natriuretic factor and urine flow responses to vascular volume expansion

The present study was designed to test the hypothesis that the fetal autonomic nervous system modulates the fetal plasma atrial natriuretic factor and urine flow responses to vascular volume expansion. To do this, isotonic saline solution (2% of estimated body weight) was infused intravascularly over a 10-minute period into autonomically intact or autonomically blocked fetal sheep. The autonomically intact fetuses responded to the infusion with a significant rise in arterial and venous pressures (p < 0.0001), and atrial natriuretic factor increased by 36 ± 8 (SE) pg/ml (p < 0.05). In the autonomically blocked fetuses, the arterial pressure rise was greater (7.5 ± 1.3 vs 2.6 ± 0.7 mm Hg), whereas the venous pressure rise was not different from that seen in the intact fetuses. Atrial natriuretic factor increased by 44 ± 20 pg/ml (p < 0.05) in the blocked fetuses. Urine flow increased by similar amounts in the two groups (maximal increase above control of 0.33 ± 0.11 in the intact and 0.27 ± 0.10 ml/min in the blocked fetuses). Thus autonomic blockade did not significantly alter either the atrial natriuretic factor, urine flow, or venous pressure responses to volume loading in the fetal sheep. Therefore it appears that the autonomic nervous system does not play a major role in modulating atrial natriuretic factor, urine flow, or venous pressure responses to acute vascular volume expansion in the late gestational fetal sheep.

Baroreceptor-mediated suppression of osmotically stimulated vasopressin in normal humans.

Increases in central venous pressure and arterial pressure have been reported to have variable effects on normal arginine vasopressin (AVP) levels in healthy humans. To test the hypothesis that baroreceptor suppression of AVP secretion might be more likely if AVP were subjected to a prior osmotic stimulus, we investigated the response of plasma AVP to increased central venous pressure and mean arterial pressure after hypertonic saline in six normal volunteers. Plasma AVP, serum osmolality, heart rate, central venous pressure, mean arterial pressure, and pulse pressure were assessed before and after a 0.06 ml.kg-1.min-1-infusion of 5% saline give over 90 min and then after 10 min of 30 degrees head-down tilt and 10 min of head-down tilt plus lower-body positive pressure. Hypertonic saline increased plasma AVP. After head-down tilt, which did not change heart rate, pulse pressure, or mean arterial pressure but did increase central venous pressure, plasma AVP fell. Heart rate, pulse pressure, and central venous pressure were unchanged from head-down tilt values during lower-body positive pressure, whereas mean arterial pressure increased. Plasma AVP during lower-body positive pressure was not different from that during tilt. Osmolality increased during the saline infusion but was stable throughout the remainder of the study. These data therefore suggest that an osmotically stimulated plasma AVP level can be suppressed by baroreflex activation. Either the low-pressure cardiopulmonary receptors (subjected to a rise in central venous pressure during head-down tilt) or the sinoaortic baroreceptors (subjected to hydrostatic effects during head-down tilt) could have been responsible for the suppression of AVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Cardiovascular Responses to Internal Carotid Artery Occlusion During Carotid Endarterectomy and to the Restoration of Internal Carotid Flow

Heart rate, central venous pressure, radial artery pressure and electrocardiograph were recorded in 14 patients undergoing carotid endarterectomy under general anaesthesia supplemented with fentanyl and halothane and muscle relaxation as required. Induction of anaesthesia was followed by a significant reduction in systolic arterial pressure and a rise in central venous pressure (CVP). Thereafter CVP did not vary significantly and heart rate did not change significantly at any stage. After internal carotid artery occlusion, mean systolic pressure at one minute, 143 (SD 17) mmHg, and three minutes, 160 (SD 27) mmHg, were both significantly higher than prior to occlusion, 132 (SD 17) mmHg (P less than 0.01 and P less than 0.002 respectively). Similar significant changes occurred in diastolic pressure after carotid occlusion (P less than 0.02 and P less than 0.002 respectively). The restoration of flow through the internal carotid artery in patients operated on without a shunt was associated with a significant reduction in mean systolic pressure. The mean systolic pressure at one minute, 145 (SD 20) mmHg, and three minutes, 135 (SD 19) mmHg, were both significantly lower than that before restoration of flow, 159 (SD 17) mmHg (P less than 0.02 and P less than 0.05 respectively). Changes in mean diastolic pressure in this group at these times, while in the same direction, were not significant. The observed hypertensive response to carotid occlusion may assist in preserving cerebral perfusion while the internal carotid artery is occluded, but may be hazardous for patients with ischaemic heart disease.

Hemodynamic responses to atrial natriuretic factor in nephrectomized rabbits: attenuation of the circulatory consequences of acute volume expansion.

We investigated the hemodynamic responses to three doses of atrial natriuretic factor [human atrial natriuretic factor-(99-126)] (ANF) in nephrectomized rabbits anesthetized with ketamine and acepromazine. The influence of the different doses of the peptide on the hemodynamic consequences produced by acute volume expansion (0.9% NaCl, 1.4 ml/kg/min for 60 minutes) was also studied. All three dosages of ANF (0.001, 0.01, and 0.2 micrograms/kg/min for 20 minutes) significantly reduced blood pressure. With the lowest dose, the hypotensive effect was associated with reduction in systemic vascular resistance and no significant change in heart rate, stroke volume, central venous pressure, and hematocrit. In contrast, the intermediate and high doses, which resulted in markedly higher plasma levels, caused a significant decrease in heart rate, central venous pressure, and stroke volume; a slight rise in hematocrit; and no change in systemic vascular resistance. Volume expansion produced by saline infusion in an additional group of nephrectomized rabbits increased central venous pressure and decreased hematocrit. When ANF infusion was associated to volume expansion, each dosage of ANF was able to reduce the rise in central venous pressure, while only the higher dosage attenuated the progressive fall in hematocrit caused by volume expansion. Plasma volume, measured at the end of volume expansion was lower in the group treated with the highest dose of ANF than in the control animals (28.2 +/- 9 vs. 35.1 +/- 3 ml/kg, p less than 0.05). We conclude that 1) ANF induces significant hemodynamic effects independently from its renal action.(ABSTRACT TRUNCATED AT 250 WORDS)

RAISED VENOUS PRESSURE: A DIRECT CAUSE OF RENAL SODIUM RETENTION IN OEDEMA?

Contemporary theories of oedema formation are often based on the idea that "effective" blood volume is reduced, and that sodium retention and oedema are a result of the kidney responding, as in haemorrhage, to a perception by receptors in the circulation that blood volume is inadequate. This idea has enhanced understanding of the pathophysiology of such conditions as cardiac failure and cirrhosis, but has obscured the fact that blood volume is almost always increased in oedematous states. Evidence is presented that an increase in renal venous pressure can cause sodium retention by a direct action on the kidney: a rise in venous pressure could thereby initiate a vicious circle by causing sodium retention, expansion of plasma volume, and further increase in venous pressure. This sequence of events may be crucial in the pathophysiology of cor pulmonale, and an exacerbating factor in other oedematous states.

中耳腔内圧の変動要因に関する研究

The author investigated the effect of changing posture and blood flow on the middle ear pressure of humans. First, a sudden change of posture, from sitting to the head down position was induced in 38 normal persons (65 ears) in normal and hyper and hypobaric environments. Then blood flow was changed by SGB or excercise. The SGB procedure was applied to 3 normal persons and 3 patients with sudden deafness, and 9 normal persons were tested during exercise. PO2 in the middle ear was measured simultaneously with the measurement of the middle ear pressure. The change of pressure was estimated by tympanometry, and the PO2 value was measured by a sensor introduced into the middle ear via the Eustachian tube.At both normal and abnormal atmospheric pressures, the middle ear pressure increased when the posture was changed from the sitting to the head down position. Pressure change caused by posture change was 2.4 times greater in a relatively hypobaric than in a relatively hyperbaric environment. When blood flow was raised by SGB or excercise, PO2 in the middle ear increased, but the pressure decreased.It was concluded that middle ear pressure is increased by a rise of venous pressure and also by adiminution of middle ear volume caused by temporary swelling of mucous membranes. Middle ear pressure changes due to variations of blood flow may also be related to changes in gas metabolism, especially the production and influence of CO2.

EVIDENCE FOR INVOLVEMENT OF HYPOCAPNIA AND HYPOPERFUSION IN AETIOLOGY OF NEUROLOGICAL DEFICIT AFTER CARDIOPULMONARY BYPASS

Arterial and jugular bulb pressures and blood gas tensions were recorded for later analysis in 65 patients having coronary artery graft surgery. In the first 35 (group A) routine peroperative monitoring was used; and in the next 30 (group B), similar in age and other characteristics, special measures were adopted to maintain normocapnia (PaCO 2 35-45 mm Hg) by continuous monitoring during surgery. On the third postoperative day clinical neurological deficits were observed in 46% of group A and 27% of group B, and psychometric deficits in 71% and 40%, respectively. On analysis of the records, more than half of group A proved to have been hypocapnic immediately before onset of cardiopulmonary bypass, and those with postoperative deficits differed from the others in this group in having had greater changes in PaCO 2 after onset of bypass and lower cerebral perfusion pressures in the first 10 minutes of bypass, usually because of a rise in cerebral venous pressure.

Seventy years of the Bainbridge reflex.

The discovery of the Bainbridge reflex 70 years ago, of a tachycardic response to a rise in central venous pressure, stimulated a lot of interest in this and other cardiovascular reflexes. The mechanoreceptors that elicit the reflex are located at the junction of the right atrium and caval veins or at the junctions of the pulmonary veins and the left atrium. The Bainbridge reflex is controversial, however, because its existence cannot always be demonstrated. Intravenous infusions, which usually elicit a reflex tachycardia, sometimes cause a bradycardic response. This paper reviews the history of the studies associated with the reflex. Results are reported, which demonstrate that the chronotropic response to i.v. infusions depends upon the resulting change in aortic diameter; bradycardia is evoked by infusions leading to a rise in aortic baroreceptor activity through increases in aortic diameter, volume or pressure; tachycardia follows whenever the infusion fails to trigger the baroreflex. The importance of the Bainbridge reflex as a counterbalance to the baroreceptor reflex is discussed.

Hepatic venous resistance site in the dog: localization and validation of intrahepatic pressure measurements.

Intrahepatic pressure (9.4 +/- 0.3 mmHg; 1 mmHg = 133.32 Pa), measured proximal to a hepatic venous resistance site, was insignificantly different from portal venous pressure (9.6 +/- 0.4 mmHg). This lobar venous pressure is not wedged hepatic venous pressure as it is measured from side holes in a catheter with a sealed tip. Validation of the lobar venous pressure measurement was done in a variety of ways and using different sizes and configurations of catheters. The site of hepatic venous resistance in the dog is localized to a narrow sphincterlike region about 0.5 cm in length and within 1-2 cm (usually within 1 cm) of the junction of the vena cava and hepatic veins. Sinusoidal and portal venous resistance appears insignificant in the basal state and large increases in liver blood volume (histamine infusion or passive vena caval occlusion) or large decreases in liver blood volume (passive vascular occlusion) do not alter the insignificant pressure gradient between portal and lobar venous pressures. Norepinephrine infusion (1.25 microgram X kg-1 X min-1 intraportal) and hepatic sympathetic nerve stimulation (10 Hz) led to a significantly greater rise in portal venous pressure than in lobar venous pressure, indicating some presinusoidal (and (or) sinusoidal) constriction and this indicates that lobar venous pressure cannot be assumed under all conditions to accurately reflect portal pressure. However, most of the rise in portal venous pressure induced by intraportal infusion of norepinephrine or nerve stimulation and virtually all of the pressure rise induced by histamine could be attributed to the postsinusoidal resistance site.(ABSTRACT TRUNCATED AT 250 WORDS)

Retrograde infusion of blood into a pulmonary vein promotes natriuresis in anaesthetized dogs.

Retrograde infusion of blood into a pulmonary vein raised the pressure by 0.5-1 kPa in the cannulated vein. There were no changes in heart rate, arterial blood pressure, left atrial pressure, right atrial pressure or the pressure in the other pulmonary veins. The rise in pulmonary venous pressure was associated with an increase in urinary sodium concentration and excretion. However, there was no change in urine volume. The natriuresis was abolished by cooling the vagi to 9 degrees C. It is argued that receptors up-stream in the pulmonary veins themselves may be involved in the increase in sodium excretion that follows a rise in left atrial pressure.

Lung lymph flow during volume infusions.

We investigated the effect of intravenous isotonic crystalloid solution infusion on lung lymph flow. Tracheobronchial lung lymph vessels were cannulated in 13 anesthetized dogs. The lymph flow rate was measured 1) with the lymph flowing against atmospheric pressure (QL), and 2) with the pressure at the outflow end of the lymph cannula equal to systemic venous pressure (QLV). QL and QLV were measured alternately in each lymph vessel. In one group of nine dogs, the base-line QL and QLV were 18 +/- 9 and 13 +/- 6 (SD) microliter/min, respectively (P less than 0.05). QL increased by 4.8 +/- 1.4-fold, and QLV increased by 3.5 +/- 2.1-fold during a 4-h infusion of 25 ml X kg-1 X h-1 of Ringer solution. QLV was significantly less than QL at all times. The increases in lymph flow were caused primarily by a reduction in the effective resistance of the lymph vessels with little rise in the pressure driving lymph from the lungs. Because QLV flowed against systemic venous pressure, the increase in QLV was blunted by a 3.1 +/- 2.3 cmH2O rise in venous pressure during the infusions. In the remaining four dogs, we infused Ringer solution rapidly in order to raise venous pressure to greater than 15 cmH2O. This caused QL to increase by 25 +/- 7-fold; however, QLV decreased to zero. We conclude that elevations in venous pressure which occur during volume infusions oppose lung lymph flow and lead to accumulation of excess fluid in the lungs.