Changes In Central Venous Pressure Research Articles

On the role of the interstitial volume in the response of the rat to blood volume expansion.

Patterns of body fluid distribution and selected cardiovascular and renal responses were studied following vascular expansion in normal rats and in rats with altered interstitial fluid volume produced by dehydration, prehydration or hyperoncotic albumin infusion. In all four groups the patterns of the renal excretory response and the accompanying change in central venous pressure (CVP) were closely parallel and the disturbance in CVP was finally corrected in the presence of a considerable residual vascular expansion. During the diuresis and saluresis following iso-oncotic vascular expansion in prehydrated and dehydrated rats, both groups removed fluid chiefly from the interstitium; this fluid removal was attributable mainly to urinary excretion in prehydrated rats but mainly to redistribution into the cellsin dehydrated rats. In the latter series, preferential renal excretion of sodium over water was observed. Hyperoncotic vascular expansion led to a peak renal excretory response only 70% of that following iso-oncotic expansion. The excreted volume was accounted for by a similar depletion of interstitial fluid after the iso-oncotic load. These findings are consistent with the hypothesis that the renal response to volume expansion regulates some parameter which is more closely related to the mean central venous pressure than to the vascular volume. This regulation was associated with incomplete correction of the vascular expansion and absolute decrease in interstitial fluid volume compared to the initial size of that compartment. This provides support for a functionally important influence of the interstitial volume on venous compliance.

A clinical method for detecting subendocardial ischemia after cardiopulmonary bypass

Subendocardial ischemia with consequent subendocardial necrosis is a frequent cause of death after cardiopulmonary bypass. The problem is caused by an inequity in the oxygen requirements of the subendocardium and the available blood supply. We have developed a means of detecting ischemia early in the postperfusion period. Using an analogue computer, we determine the endocardial viability ratio (EVR). This value may decrease before either systemic or central venous pressure changes. Thus the ratio can reflect early the danger of subendocardial ischemia. Another advantage is that equipment now common in coronary care units can be used to determine the EVR.

Cardiovascular effects of isoflurane in surgical patients.

Cardiovascular responses to isoflurane–nitrous oxide–oxygen anesthesia were studied in 32 older patients undergoing surgical operations. In half of the patients, anesthesia was induced with isoflurane alone, in the remainder, with isoflurane and thiopental All were intubated and mechanically ventilated to maintain normal Paco Stroke volume, heart rate, cardiac output, systemic resistance, systolic, diastolic and mean pressures, and central venous pressure changes were generally similar to those found by other investigators in patients not undergoing surgical operations, except that we observed an increased systemic resistance. A decrease in stroke volume was counterbalanced by increases in pulse rate and systemic resistance, so that the total effect on cardiac output and arterial pressures was negligible. The cardiovascular responses that we found suggest that isoflurane may counteract primary myocardial depression by autonomic mechanisms similar to those seen with diethyl ether anesthesia.

Effective Compliance of the Total Vascular Bed and the Intrathoracic Compartment Derived from Changes in Central Venous Pressure Induced by Volume Changes in Man

In eight male subjects the blood volume was changed (± 10%) by hemorrhage and transfusion. One cycle of blood infusion and withdrawal or hemorrhage and reinfusion was completed within 9 minutes. The effective compliance of the total circulation was calculated from the changes in central venous pressure recorded simultaneously with the changes in blood volume. The effective compliance was 2.3 ml/mm Hg kg -1 body weight. This procedure was repeated while the capacity of the circulatory system was restricted by infusion of norepinephrine (15 µg/min), lower body positive pressure, or both. The compliance values thus obtained were: norepinephrine 1.7 ml/mm Hg kg -1 body weight, lower body positive pressure 1.2 ml/mm Hg kg -1 body weight, and both norepinephrine and lower body positive pressure 0.9 ml/mm Hg kg -1 body weight. The effective compliance of the intrathoracic vascular bed was assumed to be between 1.2 ml/mm Hg kg -1 body weight (lower body positive pressure) and 0.9 ml/mm Hg kg -1 body weight (norepinephrine and lower body positive pressure). These values constitute 55% and 42% of the effective compliance of the total circulation, respectively.

Effects of Rapid Paracentesis

Eight paracenteses were performed on patients with ovarian carcinomatosis, with the rapid removal of 2,400 to 11,000 ml of ascitic fluid. There were no important changes in central venous pressure, blood pressure, pulse rate, hematocrit value, or serum electrolytes during the procedures or the ensuing 48 hours. Serum protein concentration fell to approximately two thirds of the base line level in each patient.

Effects of rapid paracentesis. Cardiovascular dynamics and body fluid composition

Eight paracenteses were performed on patients with ovarian carcinomatosis, with the rapid removal of 2,400 to 11,000 ml of ascitic fluid. There were no important changes in central venous pressure, blood pressure, pulse rate, hematocrit value, or serum electrolytes during the procedures or the ensuing 48 hours. Serum protein concentration fell to approximately two thirds of the base line level in each patient.

Splanchnic vasoconstriction in hyperthermic man--role of falling blood pressure.

Results of a study in which six supine resting subjects, wearing water-perfused suits, had body skin temperature controlled at 35 C for 30 min (control period), then rapidly increased to 40.5 C for 43 to 50 min (heating period) in a two-part experiment. In the first part of the experiment arterial mean pressure (MP) in three men was increased back to, or above control levels at the 30 to 35th min of heating by total occlusion of both legs for 8 to 10 min. Splanchnic blood flow (SBF), which had fallen from 1.4 to 0.9 L/min at occlusion, rose only 0.05 L/min during occlusion. Splanchnic vascular resistance (SVR) rose throughout heating and occlusion. In the second part of the experiment (three men) SBF fell despite a spontaneous rise in MP and aortic pulse pressure prior to leg occlusion. Cardiac output (CO) was measured just before, during and after occlusion. Occlusion raised MP 10 to 15 mm Hg and reduced CO only slightly. It is concluded that falling MP or aortic pulse pressure are not major causes of the splanchnic vasoconstriction in response to heating man.

Total systemic vascular compliance measured as incremental volume-pressure ratio.

We developed a method to measure the compliance, defined as ΔVΔP, of the total systemic vascular bed (C t ) without stopping systemic flow. In 10 open-chest dogs, venous return (and cardiac output) was maintained at a constant level by inserting a perfusion pump (with no reservoir) between the caval veins and the right atrium. About 5% of the estimated total blood volume was withdrawn from the dog within 45 seconds. Resultant changes in central venous pressure were measured 10, 30, 60, 120, and 180 seconds after the volume change. The bled volume was then reinfused to repeat similar venous pressure measurements for another 180 seconds. The measurements were repeated after slightly increasing the blood volume or sectioning the vagi. The mean value of C t measured 10 seconds after hemorrhage or reinfusion was 1.96 ± 0.10 ( SE ) ml/mm Hg/kg body weight before vagotomy. Paired t -tests indicated no significant difference between measurements of bleeding and reinfusion, measurements with different initial venous pressures or blood volume, or measurements before and after vagotomy. However, C t increased with time during the 2-minute period by about 25% of the initial 10-second value ( P <0.001) and remained constant thereafter.

Haemodynamic responses to sustained hand-grip in patients with hypertension.

Abstract. The haemodynamic responses to sustained handgrip were studied in 15 hypertensive patients. The response pattern was found to be similar to that in normotensive subjects, and was characterized by marked increase in systolic, diastolic and mean arterial pressure, moderate increase in heart rate and cardiac output, and no change in central venous pressure, stroke volume or total peripheral resistance. Mean arterial blood pressure was found to be higher in our patients than it is in normotensive subjects during static muscular contraction, and higher than it is in hypertensive subjects during dynamic exercise.

A convenient technique of rapid detection and correction of misplaced central venous catheter

A 71 year old male patient was treated conservatively for subarachnoid haemorrhage with septic shock. The subclavian vein cannulation was done after starting mechanical ventilation and a pressure transducer was attached but the absence of typical waveforms led to doubt of correct placement of the catheter. An internal jugular vein (IJV) occlusion test showed flattened trace and central venous pressure (CVP) rise of 5 mmHg indicating misplacement of the catheter into the IJV, later confirmed by chest radiography. The central venous catheter (CVC) was withdrawn under image intensifier guidance and reinserted after applying pressure over the ipsilateral IJV. The position of the CVC was rechecked by connecting a pressure transducer. This time after IJV occlusion, the CVP trace was good and there was no change in waveforms and CVP reading.DOI: 10.3329/pulse.v3i1.6553Pulse Vol.3(1) July 2009 p31-32

Vasopressin Effect on Portal and Systemic Hemodynamics

Parumbilical (portal) vein, arterial, and central venous pressures were monitored continuously during sham and vasopressin injection (Pitressin) infusion in ten adult patients in the intact, unanesthetized state. Five of these patients at rest (group A) had portal pressures greater than, and five (group B) lower than, 30 cm H₂O. Twenty clinical units of vasopressin injection infused intravenously over 20 minutes caused an average fall in portal pressures of 19.8% (group A) and 25% (group B), abrupt arterial pressure elevations with bradycardia, and no changes in central venous pressure (CVP). Side portal flow diminished an average of 21%, and variable elevations of lactate levels in portal blood were observed. Valsalva maneuvers caused 46 to 64 cm H₂O increases in portal pressure, unaffected by administration of the drug. In none of the patients in group A did vasopressin succeed in lowering portal pressure below 30 cm H₂O.

The significance of central venous pressure and cardiac output measurements in shock.

Summary The central venous pressure changes which occur in shock syndromes vary with the aetiology and other factors. Two methods of measuring CVP have given different results, and their advantages and disadvantages are discussed, together with an appraisal of the diagnostic and therapeutic value of such measurements. The CVP changes produced by transfusion are related to changes in cardiac output and the value of the latter as a guide to treatment is discussed. The relationship of these measurements to clinical signs is emphasized.

Effect of blood volume, mean circulatory pressure, and stress relaxation on cardiac output.

Effect of blood volume, mean circulatory pressure, and stress relaxation on cardiac output.

Role of the vagus nerve in the control of the concentration of angiotensin II in the circulation.

HAEMORRHAGE causes an increase of the concentration of renin1–4 and of angiotensin5–8 in blood; when the blood volume of anaesthetized dogs is reduced this rise in concentration of renin4 and of angiotensin7 can be prevented by local anaesthesia of the renal nerves, which suggests that it is brought about by reflex activation of the nerves. The changes of angiotensin concentration correlate not with changes of arterial pressure but with changes of central venous pressure7. Changes of central venous pressure are usually accompanied by changes of pressure in the atria and the pulmonary circulation; these areas are plentifully supplied by vagal afferent fibres and so it seemed possible that the vagus nerve might form the afferent limb of the reflex. We have therefore studied the effect on the generation of angiotensin of interrupting conduction in the vagus nerve.

AN INDIRECT METHOD FOR ESTIMATING TISSUE PRESSURE WITH SPECIAL REFERENCE TO TISSUE PRESSURE IN MUSCLE DURING EXERCISE.

AbstractTissue pressure is one of the determinants of capillary filtration and appears to be a major limiting factor of filtration exchange during muscular exercise. Since direct measurement of tissue pressure through a needle was considered impossible, an indirect method was developed to record tissue pressure in skeletal muscle during rest and exercise. This method is based on the fact that veins are normally collapsible and that the pressure inside patent veins can never be less than the extramural pressure i. e. tissue pressure. When the tissue pressure exceeds the central venous pressure, the pressure in the local veins is dictated by, and becomes a measure of the tissue pressure. Instead of measuring this pressure the changes in volume of the muscle were recorded plethysmographical‐ly and the pressure below which changes of central venous pressure did not influence volume was noted. This pressure was regarded as corresponding to the minimum tissue pressure. The maximum tissue pressure was obtained from distensibility curves for the veins. The accuracy of the method is about 2 cm H2O. During rest the tissue pressure was only little above zero and rose during exercise in relation to the amount of filtrate accumulated in the muscle.

The cerebrospinal fluid pressure response to certain acute vascular changes.

A perfused cat preparation is described which permits controlled and independent alterations of certain major vascular variables. The effects of such alterations upon the cerebrospinal fluid pressure are examined. The information obtained together with that derived from experiments on non-perfused animals is used to explain the cerebrospinal fluid pressure response to temporary obstruction of a vena cava. An increase in a caval pressure produces a sustained rise of cerebrospinal fluid pressure which resists lowering, and the rise of the latter pressure accompanying an increase in cardiac input is due mainly to the increase of central venous pressures. A decrease of cardiac input produces first a fall followed by a rise of cerebrospinal fluid pressure. When the input is restored the pressure rises steeply, ex­ceeding the resting level. None of these effects is due to changes in central venous pressures. In the non-perfused animal a caval obstruction produces a rise of distal caval pressure and a fall of cardiac input and the result of these two opposing influences is usually an increase of cerebrospinal fluid pressure. The rise of caval pressure raises the cerebrospinal fluid pressure by increasing the regional intracraniovertebral venous sinus pressure. On releasing an obstructed inferior vena cava a supernormal rise of cerebrospinal fluid pressure is observed, as after restoration of a reduced cardiac input. This response is dependent upon a mechanism restricted to the cranial end of the neuraxis and appears to be caused by a brief increase of cerebral blood flow. On releasing an obstructed superior vena cava a supernormal rise of cerebrospinal fluid pressure is not seen.

Changes in central venous pressure after moderate hemorrhage and transfusion in man.

Changes in central venous pressure were recorded continuously before, during and for 40 to 50 minutes after hemorrhage and transfusion in the amounts of 6.5 cc. per Kg. and 8.1 cc. per Kg. The pressures obtained 15 to 20 minutes after onset of blood volume changes were independent of the rate of hemorrhage or transfusion. In the average subject of 70 Kg., Δ P /ΔV for zero time was 0.7 cm. of water pressure change per 100 cc. volume change. Recovery from hemorrhage was imperceptible during the one hour observation period, but recovery from transfusion was slightly faster.

The continuous recording of central venous pressure changes from an arm vein.

With the subject in the right lateral decubitus position, changes of central venous pressure can be recorded accurately and conveniently from a vein in the antecubital fossa of the dependent arm. Theoretically the hydrostatic, pressure transforms the venous bed between the heart and the site of puncture into uninterrupted wide channels with relatively low distensibility. Simultaneous recordings of pressure by the method described and by catheterization of the central veins showed that induced changes of central venous pressure were identically recorded from both sites. The mean pressure gradient between the peripheral and central veins was 35 mm. of water.

Mean Circulatory Filling Pressure Measured Immediately After Cessation of Heart Pumping

Mean Circulatory Filling Pressure Measured Immediately After Cessation of Heart Pumping

A technic of vascular catheterization with small plastic catheters; its utilization to measure the arterial pulse wave velocity in man.

A method of vascular catheterization is presented in which small polyvinyl catheters are introduced into peripheral vessels through 18 to 21 gage needles and then advanced into the central vascular bed. This technic has been utilized in the study of hemodynamic events occurring in the central arterial vessels in man. The results obtained from 31 arterial catheterizations done in 21 subjects are reported. Utilizing this technic, it has been impossible to catheterize the pulmonary artery in man. However, the method has proved useful in the study of right atrial and central venous pressure changes.