Severe Hypovolemia Research Articles

Jejunal luminal nitric oxide during severe hypovolemia and sepsis in anesthetized pigs.

Lowered gut blood perfusion and the associated intestinal mucosal barrier dysfunction is considered important in the pathophysiology leading to critical illness. Intestinal mucosal nitric oxide formation has been attributed a key role in the regulation of epithelial permeability and other properties of the intestinal mucosal barrier. This study was performed to delineate intestinal mucosal NO formation during hypovolemia or sepsis, both of which are associated with intestinal hypoperfusion. Seventeen pigs were subjected to 2 h of severe hypovolemia (bleeding induced) or sepsis (systemic infusion of live Escherichia coli) or no treatment (controls). Jejunal mucosal NO production was monitored by a tonometer. Mesenteric blood flow was measured as portal venous blood flow by an ultrasonic transit time flowmeter probe, and oxygen delivery and consumption were calculated from regional blood samples. Intestinal perfusion and oxygen delivery were reduced by the same order of magnitude in both groups. Jejunal mucosal NO production and oxygen consumption decreased markedly in the hypovolemia group but remained stable in the group subjected to septic shock. These data suggest that blood loss inhibits jejunal mucosal NO production as part of a general downregulation of nonvital organs. Sepsis represents a more complex stress condition with activation/maintenance of host defense mechanisms as reflected by maintained jejunal mucosal NO production despite reduced gut blood perfusion.

Pratique et complications de la rachianesthésie en milieu tropical africain

Objective: To evaluate the risk of the practice of spinal anaesthesia (SA) in African tropics. Study design: Prospective study in multiple centres over a two years period. Persons: Twenty-one anaesthesiologists and anaesthetist nurses covering ten African countries. Methods: Two anonymous questionnaires; the first, filled in each anaesthetic problem occurred, to define the type of incident or accident, and its circumstances; the second was designed to define the position occupied, to quantify the global anaesthetic activity, the number of SA, and to value the number of complications or deaths linked to SA. Results: Six anaesthesiologists and one anaesthetist nurse replied to the study, covering six sites in five different countries (Senegal, Chad, Central African Republic, Niger and Madagascar). On the 18,432 anaesthetic acts collected, 2,703 (14.7%) were SA. In the well-equipped centres, general anaesthesia was predominant with a frequency of over 75%. However in the not so well equipped centres or those which supplies were more problematical, SA technique was used with a frequency varying from 48.9 to 68.7%. Forty incidents and accidents were reported (1.5%), five led to the death of the patient (0.2%). Among the seven cardiac arrests (0.3%), four were fatal (0.1%). Eight of the ten accidents and all of the deaths occurred in the least equipped centres. Eight of ten accidents happened during emergency caesarean sections. All cardiac arrests were preceded by a severe hypovolemia. For the four deaths after cardiac arrest, an anaesthetist nurse with isobaric bupivacaine 0.5% carried out SA. Conclusions: This study showed that the practice of SA in African tropics was performing in different practice conditions and people qualification than they were in France. The frequency of cardiac arrests and deaths was respectively five and 20 times more important, in those conditions. The first conclusion that can be drawn from this study is that it is questionable to use SA for emergency Caesarean section under hypovolemic condition. The second is the necessity for specific training on the local anaesthesia for anaesthetist nurses but also training to choose the anaesthesia best adapted to the surgery, the condition of the patient and the means available.

Angiotensin II blockade in existing hypovolemia: effects of candesartan in the porcine splanchnic and renal circulation.

Angiotensin II (AngII) is an important vasoconstrictor during hypovolemia. This study focused on the effects of the AngII receptor blocker candesartan on intestinal, hepatic, and renal hemodynamics during severe hypovolemia when administered in preexisting moderate hypovolemia. It was hypothesized that specific AngII receptor blockade might enhance splanchnic perfusion during hypovolemia. Fasted, anesthetized, ventilated, juvenile pigs were hemorrhaged by 20% of the blood volume for 30 min. Animals were then randomized to receive candesartan (CAND, n = 11) or the vehicle (CTRL, n = 10) prior to further hemorrhage to 40% of the blood volume for 30 min. The shed blood was then retransfused. Systemic and splanchnic hemodynamics were recorded including intestinal mucosal, superficial and parenchymal hepatic, and cortical and medullary renal microcirculation by laser-Doppler flowmetry. Arterial blood gases were analysed. Candesartan-treated animals maintained mesenteric and jejunal mucosal perfusion during 40% hypovolemia compared to CTRL animals, while no differences were observed in the hepatic and renal circulation. Retransfusion restored mesenteric and renal blood flows despite persistent hypotension and reduced cardiac output in both CAND and CTRL animals. Renal medullary and hepatic parenchymal microcirculation failed to recover during retransfusion in both CAND and CTRL animals. Arterial acidosis, hypercarbia, and a negative base excess were observed in CTRL animals following retransfusion whereas those parameters were normalised in CAND animals. Administration of candesartan in moderate hypovolemia ameliorated the reduction and consequences of mesenteric and intestinal, but not hepatic perfusion during severe hypovolemia. No adverse effects were observed in the renal circulation.

Health Care Workers, Predominant Gender Females at High Risk

ABSTRACT“Cluster Outbreaks” of Chronic Fatigue (Immune Dysfunction) Syndrome (CFIDS)/Myalgic Encephalomyelitis (ME) have been well documented in the Healthcare professions. Large bodies of scientific evidence suggest that the endocrine system is very involved. In fact, it may be the most critical piece of the puzzle that needs to be examined in all future research. Although some subtle immunologic changes have been documented in persons with ME/CFIDS, recent studies on the endocrine system suggest that several hormonal abnormalities may account for the myriad of symptoms. Calkins and colleagues at Johns Hopkins have found that most patients have delayed orthostatic hypotension. Streeten and Bell extended these studies finding that most patients studied have severe hypovolemia. Hormones that prevent these conditions in healthy people are controlled by the pituitary and hypothalamus. It is interesting that the symptoms experienced by patients with Pan-Hypothyroidism are virtually identical to CFIDS/ME. Endo...

Albumin and artificial colloids in fluid management: where does the clinical evidence of their utility stand?

Key questions remain unresolved regarding the advantages and limitations of colloids for fluid resuscitation despite extensive investigation. Elucidation of these questions has been slowed, in part, by uncertainty as to the optimal endpoints that should be monitored in assessing patient response to administered fluid. Colloids and crystalloids do not appear to differ notably in their effects on preload recruitable stroke volume or oxygen delivery. Limited evidence nevertheless suggests that colloids might promote greater oxygen consumption than crystalloids. It remains unclear, in any case, to what extent such physiological parameters might be related to clinically relevant outcomes such as morbidity and mortality. Recent randomized controlled trial results indicate that, at least in certain forms of fluid imbalance, albumin is effective in significantly reducing morbidity and mortality. Much further investigation is needed, however, to determine the effects of colloid administration on clinically relevant outcomes in a broad range of critically ill patients. The ability of administered colloids to increase colloid osmotic pressure (COP) constitutes one mechanism by which colloids might reduce interstitial oedema and promote favourable patient outcomes. However, the applicability of this mechanism may be limited, due to the operation of compensatory mechanisms such as increased lymphatic drainage. Attempts to increase COP might also be less useful in states of increased vascular permeability such as acute respiratory distress syndrome, although this issue has by no means been settled by empirical data. Colloids are clearly more efficient than crystalloids in attaining resuscitation endpoints as judged by the need for administration of far smaller fluid volumes. Among the colloids, albumin offers several advantages compared with artificial colloids, including less restrictive dose limitations, lower risk of impaired haemostasis, absence of tissue deposition leading to severe prolonged pruritus, reduced incidence of anaphylactoid reactions, and ease of monitoring to prevent fluid overload. The cost of albumin, nevertheless, limits its usage. Crystalloids currently serve as the first-line fluids in hypovolaemic patients. Colloids can be considered in patients with severe or acute shock or hypovolaemia resulting from sudden plasma loss. Colloids may be combined with crystalloids to obviate administration of large crystalloid volumes. Further clinical trials are needed to define the optimal role for colloids in critically ill patients.

The effect of anti-diuretic hormone on the endolymphatic sac of the inner ear.

The anti-diuretic hormone vasopressin (AVP) regulates water excretion from the kidney by increasing the water permeability of the collecting duct. AVP binds to V2-receptors and induces the translocation of aquaporin-2 water channels (AQP-2) into the apical plasma membrane of principal cells. By this mechanism AVP controls water reabsorption in the kidney. The effects of AVP on the endolymphatic sac (ES) of the inner ear, which is thought to mediate reabsorption of endolymph, were investigated. Both the V2-receptor and the AQP-2 water channel were found to be expressed in the ES epithelium. In the ES AVP binds to receptors most probably of the V2-subtype. Application of AVP to organotypically cultured ES inhibits membrane turnover in ribosomal-rich cells of the ES epithelia, which is thought to mediate translocation of AQP-2 into the surface membrane. This suggests that AVP has contrasting effects in the inner ear and kidney, which may be physiologically useful for maintaining endolymphatic pressure during severe hypovolemia. Animal experiments show that AVP causes endolymphatic hydrops after systemic application to guinea-pigs, which suggests a causal role for the increased AVP levels found in humans suffering from Ménière's disease.

Asystole Under Hypotensive Epidural Anesthesia

In Response: We thank Dr. Sharrock for his comment regarding our case report. His conclusions that severe hypovolemia existed and that extended monitoring is recommended is in agreement with our explanations [1]. Concerning the vasopressors, we would point out that immediately after the first injection of the local anesthetic, epinephrine 1-4 [micro sign]g/min was given continuously until the cardiac arrest [1]. The additional administration of isoproterenol and boluses of epinephrine was given according to the recommendation of Sharrock and Salvati, who wrote, "if heart rates are less than 55 bpm, one should increase the dose of epinephrine or add isoproterenol." [2]. Thomas Heidegger, MD Georg Kreienbubl, MD Department of Anesthesiology; Kantonsspital St. Gallen, Switzerland

Acute Hypovolemia May Cause Segmental Wall Motion Abnormalities in the Absence of Myocardial Ischemia

New segmental wall motion abnormalities (SWMA) detected by echocardiography are considered sensitive and specific markers of myocardial ischemia.However, we have observed new SWMA during pacing-induced reductions in left ventricular filling, which resolved immediately with cessation of the atrial pacing and simultaneous restoration of filling. Therefore, we designed this study to determine whether acute reduction in filling can induce new SWMA in the absence of ischemia. Institution of cardiopulmonary bypass was used as a clinical model of acute reduction in filling, and a beat-by-beat analysis of left ventricular contraction, filling, blood pressures, and electrocardiogram was performed when the drainage of blood to the cardiopulmonary bypass machine rapidly emptied the heart. Acute reduction in filling induced new SWMA in 4 of 38 study patients. All 4 patients had preexisting abnormalities of left ventricular contraction, but translocation of these preexisting SWMA did not explain the new SWMA, nor did myocardial ischemia. We conclude that acute reduction in left ventricular filling can cause new SWMA in the absence of ischemia. This finding limits the usefulness of new SWMA as a marker of ischemia in the presence of acute reduction in filling, such as that secondary to severe hypovolemia. Implications: This study documented that acute reduction in cardiac filling can be associated with new systolic wall motion abnormalities detected by transesophageal echocardiography in the absence of documented myocardial ischemia. These findings indicate that segmental wall motion may not be a valid marker for ischemia in the setting of acute hypovolemia. (Anesth Analg 1997;85:1252-7)

Effects of severe hemorrhage on plasma ANP and glomerular ANP receptors.

Atrial natriuretic peptide (ANP) plays an important role in blood volume and electrolyte homeostasis in normovolemia and in hypervolemic states. The currently available information on the effects of hypovolemia on plasma ANP is contradictory. Moreover, possible regulation of ANP receptors during severe hemorrhagic hypovolemia has not been investigated. This study evaluated the effects of severe hemorrhage on plasma ANP and on the regulation of glomerular ANP receptor subtypes in anesthetized rats. Constant rate bleeding of 50% of total blood volume within 2 h induced a reproducible shock state characterized by marked decreases in blood pressure, heart rate, and hematocrit and an increase in plasma renin activity and aldosterone. Hemorrhaged rats exhibited a gradual significant increase in plasma ANP from 39.3 +/- 2.9 to 114.7 +/- 20.0 pmol/l 1 h after the bleeding (P < 0.001 from the initial value and P < 0.02 from the final value of sham-shock rats). Hemorrhage induced a significant decrease in total glomerular ANP binding sites (172 +/- 25 vs. 363 +/- 39 fmol/mg protein in hemorrhaged and sham-shock rats, respectively, P < 0.05). This decrease was mainly due to a significant decrease in ANPC receptors (132 +/- 22 vs. 312 +/- 40 fmol/mg protein in hemorrhaged and sham-shock rats, respectively, P < 0.05). Hemorrhage did not change glomerular ANPA receptor density. No significant differences in the affinity of the glomerular receptor subtypes for ANP were detected. Our data indicate that plasma ANP increases after prolonged severe hemorrhage. It is suggested that downregulation of renal ANPC receptors leads to reduced clearance of ANP and contributes to elevation of its plasma level after severe hemorrhage.

A mouse model for the renal salt-wasting syndrome pseudohypoaldosteronism.

Aldosterone-dependent epithelial sodium transport in the distal nephron is mediated by the absorption of sodium through the highly selective, amiloride-sensitive epithelial sodium channel (ENaC) made of three homologous subunits (alpha, beta, and gamma). In human, autosomal recessive mutations of alpha, beta, or gammaENaC subunits cause pseudohypoaldosteronism type 1 (PHA-1), a renal salt-wasting syndrome characterized by severe hypovolemia, high plasma aldosterone, hyponatremia, life-threatening hyperkaliemia, and metabolic acidosis. In the mouse, inactivation of alphaENaC results in failure to clear fetal lung liquid at birth and in early neonatal death, preventing the observation of a PHA-1 renal phenotype. Transgenic expression of alphaENaC driven by a cytomegalovirus promoter in alphaENaC(-/-) knockout mice [alphaENaC(-/-)Tg] rescued the perinatal lethal pulmonary phenotype and partially restored Na+ transport in renal, colonic, and pulmonary epithelia. At days 5-9, however, alphaENaC(-/-)Tg mice showed clinical features of severe PHA-1 with metabolic acidosis, urinary salt-wasting, growth retardation, and 50% mortality. Adult alphaENaC(-/-)Tg survivors exhibited a compensated PHA-1 with normal acid/base and electrolyte values but 6-fold elevation of plasma aldosterone compared with wild-type littermate controls. We conclude that partial restoration of ENaC-mediated Na+ absorption in this transgenic mouse results in a mouse model for PHA-1.

Transfusion for respiratory distress in life-threatening childhood malaria.

We have prospectively collected information during resuscitation in 24 children with life-threatening malaria. All had clinical respiratory distress and 16 were severely anemic (hemoglobin < or = 5 g/dL) on admission. Central venous pressure (CVP) measurements were normal (< or = 5 cm of water) prior to treatment but all had a metabolic acidosis. The geometric mean lactate level was significantly higher in children admitted with severe anemia than in those without severe anemia (11.2 mmol/l versus 4.2 mmol/l; P = 0.009). Hypovolemia (a CVP on admission < 0 cm of water) was associated, although not significantly, with a higher admission plasma creatinine concentration (94 mumol/l versus 64 mumol/l; P = 0.06) and probably contributed to the severely reduced creatinine clearances (0-39 ml/min/1.73 ml2) found in 12 of the 13 children in whom this was assessed in the first 24 hr. Treatment resulted in a rapid decrease in blood lactate in 16 of the 13 children in whom this was assessed in the first 24 hr. Treatment resulted in a rapid decrease in blood lactate in 16 of the 20 children transfused, which was most dramatic in severely anemic children, who were rapidly resuscitated. In nonanemic children, early and rapid administration of normal saline usually resulted in both metabolic and clinical improvement. However, in three children, two of whom died, acidosis persisted despite resuscitation. Metabolic acidosis often accounts for respiratory distress in life-threatening childhood malaria. Severe anemia and hypovolemia appear to play major roles in its pathogenesis, are readily treatable, and there appears to be little risk of congestive cardiac failure even with an aggressive approach to fluid replacement.

Infarcted intestinal volvulus detected by prenatal ultrasonography

This article describes a prenatal ultrasonographic finding of an infarcted intestinal volvulus. Ultrasonography showed polyhydramnios, multiple dilated intestinal loops, increased transverse abdominal area, and ascites. After cesarean section due to premature rupture of membranes and fetal distress, derotation of the infarcted volvulus caused postoperative thrombocytopenia, hyperkalemia, and acidosis and a subsequent resection was required. A high output of intestinal juice from the jejunostomy caused severe hypovolemia and electrolyte imbalance with resultant death. Increased transverse abdominal area caused by marked intestinal dilatation, ascites, fetal distress, and hydrops fetalis may suggest an infarcted intestinal volvulus.

Flattened inferior vena cava: A normal finding on unenhanced abdominal computed tomographic scan

Flattening of the infrahepatic inferior vena cava (IVC) on postcontrast computed tomographic (CT) scans has been reported as a sign of severe hypovolemia. The significance of this finding on unenhanced CT scans, however, has not been reported. We retro-spectively studied 60 consecutive outpatient abdominal CT scans in which both unenhanced and postcontrast sequences were performed. Flattening of the infrahepatic IVC on unenhanced CT images was noted in six patients (10%) without evidence of hypovolemia or extrinsic IVC compression. The degree of IVC fullness increased in 43 study patients overall (72%) after contrast administration. We propose several mechanisms for postcontrast IVC distention and conclude that a flattened infrahepatic IVC on unenhanced CT scans does not indicate hypovolemia in the absence of other suggestive clinical or CT findings.

Corpus cavernosum as an emergency vascular access in dogs

We investigated the feasibility of using the corpus cavernosum as an emergency vascular access in dogs with severe hypovolemia. Five male mongrel dogs were brought to hypovolemic shock by withdrawal of blood through an internal jugular venous line. Using the corpus cavernosum as a venous access, normal saline was injected through a 23-gauge needle at the highest possible rate. Cavernosography was performed under fluoroscopy to verify the accurate position of the needle tip. Blood volumes were measured using 125I-labeled human serum albumin. Before the dogs were bled, their mean systolic blood pressure was 121.4 (mean) +/- 5.2 (standard error) mm Hg and their mean blood volume was 1,835.2 +/- 139.7 ml. The mean volume of blood removed from the dogs was 710.0 +/- 67.8 ml. The mean systolic pressure during shock was 40.8 +/- 2.2 mm Hg. After fluid resuscitation, the mean systolic pressure recovered to 114.6 +/- 4.6 mm Hg and their mean blood volume increased to 1,763.2 +/- 112.7 ml. The mean rate of saline infusion into the corpus cavernosum was 50.2 +/- 0.7 ml/min. The results of this study demonstrate the feasibility of using the corpus cavernosum as an alternative route for fluid resuscitation in severely hypovolemic dogs.

Regulation of neurohypophysial hormone secretion in an Australian marsupial

The brushtail possum secretes the typically reptilian mesotocin (MT) and arginine vasopressin (AVP) as its neurohypophysial hormones. In this study we have looked at the regulation of MT and AVP secretion in conscious possums by studying the effects of surgical stress and handling of animals, hypertonic saline infusion, hemorrhage, and angiotensin II (ANG II) infusion on the plasma concentrations of MT and AVP. Surgical insertion of a jugular catheter and handling stress increased MT secretion for 3 days after surgery without affecting plasma AVP concentrations. Hypertonic saline infusion induced a gradual increase in plasma osmolarity and Na+ concentration throughout the infusion, which steadily increased plasma AVP without affecting plasma K+ or hematocrit. The relationship between plasma osmolarity and AVP was exponential. Plasma MT was stimulated only by supraphysiological plasma osmolarities. ANG II increased plasma MT and AVP concentrations equipotently throughout the infusion. Hemorrhage was a relatively specific stimulus for AVP secretion, but MT secretion was highly stimulated during severe hypovolemia. It was concluded that MT and AVP secretion is differentially regulated in the possum.

The ace-inhibitor enalapril improves duodenal mucosal bicarbonate secretion and PD during severe hypovolemia in the pig

The ace-inhibitor enalapril improves duodenal mucosal bicarbonate secretion and PD during severe hypovolemia in the pig

Systematic Transesophageal Echocardiography for Detection of Mediastinal Lesions in Patients with Multiple Injuries

A prospective study assessing the interest in and the results of systematic transesophageal echocardiography (TEE) examination in nonselected intubated multiple injury patients was carried out from January 1992 through June 1993. Seventy patients were included and divided into two groups according to the results of admission screening, including clinical examination, EKG, CK-MB and chest radiograph. Group 1 (60 patients) had abnormalities on initial screening, while group 2 (10 patients) had no symptom of thoracic or mediastinal injury. TEE was performed within 48 hours following admission and its results were compared with those of the initial screening. TEE usefulness was evaluated on a score grade from 0 (no interest) to 4 (outstanding interest). Myocardial contusion was suspected in 25 patients. TEE invalidated 18 suspected and found 5 unsuspected myocardial contusions. Pericardial effusion was suspected in only one case, while TEE documented 13 additional cases. A mediastinal enlargement was seen in 13 patients, but TEE invalidated aortic lesions in all these cases and made an unsuspected diagnosis of aortic tears. Eight cases of severe hypovolemia and seven cases of left ventricle dysfunction were detected by TEE. The score of interest showed that TEE allowed new interesting diagnoses in 70% of group I patients and in 33% of group II patients. TEE is of utmost importance in multiple injury patients, with or without any evidence of thoracic or mediastinal injury, providing a safe and rapid examination of the mediastinal structures and an evaluation of the hemodynamic status.

Ultrasonographically guided subclavian vein catheterization in critical care obstetrics and gynecologic oncology

Invasive hemodynamic monitoring has become an integral part of intensive care management. Whereas the pulmonary artery catheter is the mainstay for determination of the hemodynamic profile and differentiation between cardiogenic and noncardiogenic forms of pulmonary edema, immediate central venous access in itself is of importance in rapid volume replacement in cases complicated by severe hypovolemia. Central venous catheters are also the preferred route of administration of total parenteral nutrition to patients with cancer. We present our experience with real-time ultrasonographic guidance during subclavian vein catheterization in critical care obstetrics and gynecologic oncology.

Continuous On‐Line Optical Absorbance Recording of Blood Volume Changes during Hemodialysis

Conventional techniques that measure blood volume changes during hemodialysis are invasive, hard to reproduce, and provide only intermittent evaluations. To overcome these drawbacks, we have developed an optoelectronic instrument that estimates intradialytic blood volume percentage changes by the optical absorbance of blood. This device is based on the absorption of light transmitted through blood, which is directly related to the hemoglobin concentration. A personal computer interfaced to the device provides a continuous on-line graphic display of the hemoglobin levels and the percentage changes in blood volume. The noninvasive measurement of dialysis blood volume changes by an optical method may be helpful in detecting the appearance of severe hypovolemia that can be dangerous in critically ill patients.

The cerebral hemodynamics of normotensive hypovolemia during lower-body negative pressure.

Although severe hypovolemia can lead to hypotension and neurological decline, many patients with neurosurgical disorders experience a significant hypovolemia while autonomic compensatory mechanisms maintain a normal blood pressure. To assess the effects of normotensive hypovolemia upon cerebral hemodynamics, transcranial Doppler ultrasound monitoring of 13 healthy volunteers was performed during graded lower-body negative pressure of up to -50 mm Hg, an accepted laboratory model for reproducing the physiological effects of hypovolemia. Middle cerebral artery flow velocity declined by 16% +/- 4% (mean +/- standard error of the mean) and the ratio between transcranial Doppler ultrasound pulsatility and systemic pulsatility rose 22% +/- 8%, suggesting cerebral small-vessel vasoconstriction in response to the sympathetic activation unmasked by lower-body negative pressure. This vasoconstriction may interfere with the autoregulatory response to a sudden fall in blood pressure, and may explain the common observation of neurological deficit during hypovolemia even with a normal blood pressure.