Showing papers on "Hypovolemia published in 2008"

Volume assessment in patients with necrotizing pancreatitis: a comparison of intrathoracic blood volume index, central venous pressure, and hematocrit, and their correlation to cardiac index and extravascular lung water index.

Abstract: mL/m 2 ) was decreased. Fifty-one of 96 intrathoracic blood volume index-values were decreased (prevalence of hypovolemia of 53%). No central venous pressure-value was decreased. Fifty three central venous pressure-measurements were elevated despite simultaneous intrathoracic blood volume index levels indicating a normal or decreased preload. Sensitivity, specificity, positive predictive value, and negative predictive value of central venous pressure with regard to volume depletion (intrathoracic blood volume index 40% [female] or hematocrit >44% [male]) was found in 11/51 measurements with decreased intrathoracic blood volume index. Sensitivity, specificity, positive predictive value, and negative predictive value of an increase in hematocrit with regard to volumedepletion according to intrathoracic blood volume index were 22%, 82%, 58%, and 48%. Intrathoracic blood volume index and -intrathoracic blood volume index significantly correlated to cardiac index and -cardiac index (r .566; p< 0.001; r .603; p< 0.001), respectively. Central venous pressure and -central venous pressure did not correlate to cardiac index and -cardiac index, respectively. There was a significant correlation between intrathoracic blood volume index and extravascular lung water index (r .392; p < 0.001), but no correlation between central venous pressure and extravascular lung water index (r .074; p 0.473). Conclusions: Volume depletion according to intrathoracic blood volume index was found in more than half the patients. The predictive values of central venous pressure and hematocrit with regard to volume depletion were low. Intrathoracic blood volume index and its changes significantly correlated to cardiac index and its changes, which was not observed for central venous pressure and -central venous pressure. Therefore, intrathoracic blood volume index appears to be more appropriate for volume management in necrotizing pancreatitis than central venous pressure or hematocrit. (Crit Care Med 2008; 36:000 – 000)

Pathophysiology, diagnosis, and treatment of orthostatic hypotension and vasovagal syncope.

Abstract: Orthostatic hypotension (OH) occurs in 0.5% of individuals and as many as 7-17% of patients in acute care settings. Moreover, OH may be more prevalent in the elderly due to the increased use of vasoactive medications and the concomitant decrease in physiologic function, such as baroreceptor sensitivity. OH may result in the genesis of a presyncopal state or result in syncope. OH is defined as a reduction of systolic blood pressure (SBP) of at least 20 mm Hg or diastolic blood pressure (DBP) of at least 10 mm Hg within 3 minutes of standing. A review of symptoms, and measurement of supine and standing BP with appropriate clinical tests should narrow the differential diagnosis and the cause of OH. The fall in BP seen in OH results from the inability of the autonomic nervous system (ANS) to achieve adequate venous return and appropriate vasoconstriction sufficient to maintain BP. An evaluation of patients with OH should consider hypovolemia, removal of offending medications, primary autonomic disorders, secondary autonomic disorders, and vasovagal syncope, the most common cause of syncope. Although further research is necessary to rectify the disease process responsible for OH, patients suffering from this disorder can effectively be treated with a combination of nonpharmacologic treatment, pharmacologic treatment, and patient education. Agents such as fludrocortisone, midodrine, and selective serotonin reuptake inhibitors have shown promising results. Treatment for recurrent vasovagal syncope includes increased salt and water intake and various drug treatments, most of which are still under investigation.

Noninvasively determined muscle oxygen saturation is an early indicator of central hypovolemia in humans

Abstract: Ten healthy human volunteers were subjected to progressive lower body negative pressure (LBNP) to the onset of cardiovascular collapse to compare the response of noninvasively determined skin and f...

Breathing through an inspiratory threshold device improves stroke volume during central hypovolemia in humans

Abstract: Inspiratory resistance induced by breathing through an impedance threshold device (ITD) reduces intrathoracic pressure and increases stroke volume (SV) in supine normovolemic humans. We hypothesize...

Oxygen saturation determined from deep muscle, not thenar tissue, is an early indicator of central hypovolemia in humans.

Abstract: Objective:To compare the responses of noninvasively measured tissue oxygen saturation (Sto2) and calculated muscle oxygen tension (Pmo2) to standard hemodynamic variables for early detection of imminent hemodynamic instability during progressive central hypovolemia in humans.Design:Prospective study

Closed-loop control of fluid therapy for treatment of hypovolemia.

Abstract: Closed-loop algorithms and resuscitation systems are being developed to control IV infusion rate during early resuscitation of hypovolemia. Although several different physiologic variables have been suggested as an endpoint to guide fluid therapy, blood pressure remains the most used variable for the initial assessment of hemorrhagic shock and the treatment response to volume loading. Closed-loop algorithms use a controller function to alter infusion rate inversely to blood pressure. Studies in hemorrhaged conscious sheep suggest that: (1) a small reduction in target blood pressure can result in a significant reduction in volume requirement; (2) nonlinear algorithms may reduce the risk of increased internal bleeding during resuscitation; (3) algorithm control functions based on proportional-integral, fuzzy logic, or nonlinear decision tables were found to restore and maintain blood pressure equally well. Proportional-integral and fuzzy logic algorithms reduced mean fluid volume requirements compared with the nonlinear decision table; and (4) several algorithms have been constructed to the specific mechanism of injury and the volume expansion properties of different fluids. Closed-loop systems are undergoing translation from animal to patient studies. Future smart resuscitation systems will benefit from new noninvasive technologies for monitoring blood pressure and the development of computer controlled high flow intravenous pumps.

Is albumin administration in hypoalbuminemic elderly cardiac surgery patients of benefit with regard to inflammation, endothelial activation, and long-term kidney function?

Abstract: BACKGROUND: Because patients with low albumin levels may benefit from human albumin (HA) administration, we studied correction of hypovolemia with HA in hypoalbuminic elderly cardiac surgery patients. METHODS: In a prospective, randomized study, 50 patients aged >80 yr undergoing cardiac surgery using cardiopulmonary bypass with a preoperative serum albumin concentration of 80 yr was without benefit with regard to inflammatory response, endothelial activation, and renal function compared to 6% HES 130/0.4.

Continuous on-line optical absorbance recording of blood volume changes during hemodialysis.

Abstract: 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.

Reactive hyperemia in the human liver

Abstract: We tested whether hepatic blood flow is altered following central hypovolemia caused by simulated orthostatic stress. After 30 min of supine rest, hemodynamic, plasma density, and indocyanine green...

Decreased diameter of the optic nerve sheath associated with CSF hypovolemia.

Abstract: The subarachnoid space around the optic nerve can be detected by fat-saturated T2-weighted MR imaging of the orbit, and dilation of this space reflects increased intracranial pressure. We examined 3 patients with CSF hypovolemia with MR imaging of the orbit and measured the optic nerve sheath diameter before and after treatment. We showed that the subarachnoid space is decreased in patients with CSF hypovolemia and the usefulness of this finding.

Continuous hematocrit monitoring method in an extracorporeal circulation system and its application for automatic control of blood volume during artificial kidney treatment.

Abstract: A two-frequency electrical conductivity method for measuring hematocrit has been developed for use in the continuous monitoring of circulating blood volume during artificial kidney treatment. Using this method, an algorithm for programmed control of blood volume also has been developed. This hematocrit measurement method is based on the beta-dispersion of blood conductivity, and the values measured during hemodialysis are in good agreement with the laboratory hematocrit values obtained by a Coulter counter. Programmed control of blood volume was used 29 times on 11 patients undergoing long-term dialysis. In each case, the blood volume was maintained within 2.5% of the desired level, and stable control was achieved even with disturbances caused by eating, change in body position, and so on. These methods can be used to study the relationship between blood volume and dialysis-induced hypotension during artificial kidney treatment and to achieve adequate ultrafiltration without clinical adverse effects.

Na+/H+ exchange inhibition delays the onset of hypovolemic circulatory shock in pigs.

Abstract: Severe blood loss is a major cause of death occurring within hours of traumatic injury. Na+/H+ exchange (NHE-1) activity is an important determinant of the extent of ischemic myocardial injury. The goal of the present study was to test the hypothesis that NHE-1 inhibition delays the onset of hypovolemic circulatory shock, thereby preventing early death due to severe hemorrhage in pigs. Severe hypovolemia was studied in 16 (25.2 kg) anesthetized male pigs in steps of 10-, 20-, 30-, 40-, and 50-mL kg(-1) blood loss, each in 30-min intervals. Shed blood resuscitation was started 30 min after 50 mL kg(-1) blood loss. The experiment was terminated after 3 h of resuscitation. Eight pigs were used as seline control. Eight pigs received 3 mg kg(-1) benzamide, N-(aminoiminomethyl)-4-[4-(2-furanylcarbonyl)-1-piperazinyl]-3-(methylsulfonyl), methanesulfonate (NHE-1 inhibitor) 15 min before hemorrhage. Seven control pigs died at 40- to 50-mL kg(-1) blood loss. One control pig survived initial resuscitation but died soon after. In contrast, all animals treated with NHE-1 inhibitor survived the entire protocol. In control animals, cardiac output and MAP gradually decreased at each step of blood loss with marked increase in heart rate. Cardiovascular decompensation occurred at 40 mL kg(-1) blood loss. Na+/H+ exchange inhibition increased oxygen delivery, attenuated cardiovascular decompensation, delayed the onset of irreversible hypovolemic circulatory shock, and enabled resuscitation to survival. Echocardiography analysis showed that myocardial hypercontracture gradually developed with each step of blood loss in control animals, but this hypercontracture was attenuated in the animals receiving the NHE-1 inhibitor. We conclude that NHE-1 inhibition attenuates ischemic myocardial hypercontracture, cardiovascular decompensation, delays the onset of hypovolemic circulatory shock, and prevents early death in severe hemorrhage.

Fluid and volume monitoring

Abstract: Background: Fluid resuscitation is not only used to prevent acute kidney injury (AKI) but fluid management is also a cornerstone of treatment forpatients with established AKI and renal failure. Ultraffitration removes volume initially from the intravascular compartment inducing a relative degree of hypovolemia. Normal reflex mechanisms attempt to sustain blood pressure constant despite marked changes in blood volume and cardiac output. Thus, compensated shock with a normal blood pressure is a major cause of AKI or exacerbations of AKI during ultrafiltration. Methods: We undertook a systematic review of the literature using MEDLINE, Google Scholar and PubMed searches. We determined a list of key questions and convened a 2-day consensus conference to develop summary statements via a series of alternating breakout and plenary sessions. In these sessions, we identified supporting evidence and generated clinical practice recommendations and/or directions for future research. Results: We defined three aspects of fluid monitoring: i) normal and pathophysiological cardiovascular mechanisms, ii) measures of volume responsiveness and impending cardiovascular collapse during volume removal, and, iii) measured indices of each using non-invasive and minimally invasive continuous and intermittent monitoring techniques. The evidence documents that AKI can occur in the setting of normotensive hypovolemia and that under-resuscitation represents a major cause of both AKI and mortality ion critically ill patients. Traditional measures of intravascular volume and ventricular filling do not predict volume responsiveness whereas dynamic functional hemodynamic markers, such as pulse pressure or stroke volume variation during positive pressure breathing or mean flow changes with passive leg raising are highly predictive of volume responsiveness. Numerous commercially-available devices exist that can acquire these signals. Conclusions: Prospective clinical trials using functional hemodynamic markers in the diagnosis and management of AKI and volume status during ultrafiltration need to be performed. More traditional measure of preload be abandoned as marked of volume responsiveness though still useful to assess overall volume status. © Wichtig Editore, 2008.

Increased vasoconstriction predisposes to hyperpnea and postural faint

Abstract: Our prior studies indicated that postural fainting relates to splanchnic hypervolemia and thoracic hypovolemia during orthostasis. We hypothesized that thoracic hypovolemia causes excessive sympathetic activation, increased respiratory tidal volume, and fainting involving the pulmonary stretch reflex. We studied 18 patients 13–21 yr old, 11 who fainted within 10 min of upright tilt (fainters) and 7 healthy control subjects. We measured continuous blood pressure and heart rate, respiration by inductance plethysmography, end-tidal carbon dioxide (ETCO2) by capnography, and regional blood flows and blood volumes using impedance plethysmography, and we calculated arterial resistance with patients supine and during 70° upright tilt. Splanchnic resistance decreased until faint in fainters (44 ± 8 to 21 ± 2 mmHg·l−1·min−1) but increased in control subjects (47 ± 5 to 53 ± 4 mmHg·l−1·min−1). Percent change in splanchnic blood volume increased (7.5 ± 1.0 vs. 3.0 ± 11.5%, P < 0.05) after the onset of tilt. Upright tilt initially significantly increased thoracic, pelvic, and leg resistance in fainters, which subsequently decreased until faint. In fainters but not control subjects, normalized tidal volume (1 ± 0.1 to 2.6 ± 0.2, P < 0.05) and normalized minute ventilation increased throughout tilt (1 ± 0.2 to 2.1 ± 0.5, P < 0.05), whereas respiratory rate decreased (19 ± 1 to 15 ± 1 breaths/min, P < 0.05). Maximum tidal volume occurred just before fainting. The increase in minute ventilation was inversely proportionate to the decrease in ETCO2. Our data suggest that excessive splanchnic pooling and thoracic hypovolemia result in increased peripheral resistance and hyperpnea in simple postural faint. Hyperpnea and pulmonary stretch may contribute to the sympathoinhibition that occurs at the time of faint.

Dynamic left ventricular outflow tract obstruction without basal septal hypertrophy, caused by catecholamine therapy and volume depletion

Abstract: Hypertrophic cardiomyopathy (HCM) with hypertrophy of the basal septum is the most common etiology of left ventricular outflow tract (LVOT) obstruction. In this article, we report the case of a patient with a structurally normal heart who developed hemodynamic deterioration due to severe LVOT obstruction following treatment with catecholamines. Hypovolemia accompanied with a hyperdynamic condition, resulting from catecholamine treatment, may cause dynamic LVOT obstruction due to the systolic anterior motion of the mitral valve leaflet. The solution for this is early recognition and correction of aggravating factors such as, withdrawal of catecholamine therapy and volume replacement.

Tako-Tsubo syndrome in an anaesthetised patient undergoing arthroscopic knee surgery.

Abstract: We present a case of stress-induced myocardial stunning, also known as Tako-Tsubo syndrome, in an anaesthetised patient undergoing arthroscopic replacement of the cruciate ligament. The patient's (44 y male, ASA class II) had a history of hypertension with no other known disease. He underwent a femoral nerve block with 20 ml of 0.5% ropivacaine before receiving a balanced general anaesthesia (propofol induction, sevoflurane maintenance, 10 microg/kg sufentanil). Ten min after the beginning of surgery during endoscopic intra-articular manipulation, the patient suffered from bradycardia and hypotension; following the administration of ephedrine and atropine, he developed tachycardia, hypertension and ST segment depression. Subsequently, his systemic blood pressure dropped necessitating inotropic drug support and--later--intraaortic balloon counterpulsation; a TEE revealed no evidence of hypovolemia, anterior and antero-septal hypokinesia with an ejection fraction of 25%. Surgery was finished whilst stabilising the patient haemodynamically. Postoperative cardiac enzymes showed little elevation, an emergency coronary angiogram apical akinesia with typical ballooning and basal hyperkinesias, compatible with Tako-Tsubo syndrome. The patient's postoperative course was uneventful. We theorize that stress caused by sudden surgical pain stimulus (introduction of the endoscope into the articulation), superficial anaesthesia and insufficient analgesia created a stressful event which probably might have caused a catecholamine surge as basis of Tako-Tsubo syndrome.

Bell-shaped relationship between central blood volume and spontaneous baroreflex function.

Abstract: Spontaneous baroreflex function can be altered by acute changes in central blood volume. Both a reduction in spontaneous baroreflex function at central hypovolemia and augmentation at hypervolemia suggest a dose–effect relationship between central blood volume and spontaneous baroreflex function. However, this relationship has not been quantified over stepwise widespread changes in central blood volume. Twelve individuals underwent central hypovolemia at two levels of lower body negative pressure (LBNP) (− 15 mm Hg, LBNP15; − 30 mm Hg, LBNP30) and hypervolemia with two discrete infusions of normal saline (NS) (15 ml·kg − 1 , NS15; total 30 ml·kg − 1 , NS30). Spontaneous baroreflex function was assessed using transfer function analysis and the sequence method between blood pressure and R–R interval. Both central venous pressure (− 0.6–7.9 mm Hg) and left ventricular end-diastolic volume (72.4–133.1 ml) decreased during LBNP and increased after saline infusion. Both spontaneous baroreflex indices of high-frequency transfer function gain (LBNP30, 17.4 ± 3.2; LBNP15, 22.3 ± 3.8; baseline, 25.6 ± 4.1; NS15, 28.5 ± 4.2 ms·mm Hg − 1 , ANOVA P = 0.001) and of the sequence slope (LBNP30, 14.4 ± 2.2; LBNP15, 17.2 ± 2.5; baseline, 20.5 ± 2.8; NS15, 24.5 ± 3.1 ms·mm Hg − 1 , ANOVA P = 0.001) increased stepwise from hypovolemia of LBNP30 to hypervolemia of NS15. However, these indices were lower at NS30 (high-frequency transfer function gain, 22.0 ± 2.2 ms·mm Hg − 1 , post-hoc P = 0.071; sequence slope, 17.7 ± 1.7 ms·mm Hg − 1 , post-hoc P

Lower capacitance response and capillary fluid absorption in women to defend central blood volume in response to acute hypovolemic circulatory stress.

Abstract: Acute hemorrhage is a leading cause of death in trauma, and women are more susceptible to hypovolemic circulatory stress than men The mechanisms underlying the susceptibility are not clear, however The aim of the present study was to examine the compensatory mechanisms to defend central blood volume during experimental hypovolemia in women and men Twenty-two women (231 +/- 04 yr) and 16 men (232 +/- 05 yr) were included A lower body negative pressure (LBNP) of 11-44 mmHg induced experimental hypovolemic circulatory stress The volumetric technique was used to assess the capacitance response (redistribution of peripheral venous blood to the central circulation) as well as to assess net capillary fluid transfer from tissue to blood in the arm Plasma norepinephrine (NE) and forearm blood flow were measured before and during hypovolemia, and forearm vascular resistance (FVR) was calculated LBNP created comparable hypovolemia in women and men FVR increased less in women during hypovolemic stress, and no association between plasma NE and FVR was seen in women (R(2) = 001, not significant), in contrast to men (R(2) = 059, P < 005) Women demonstrated a good initial capacitance response, but this was not maintained with time, in contrast to men [eg, decreased by 24 +/- 4% (women) vs 4 +/- 5% (men), LBNP of 44 mmHg, P < 001], and net capillary fluid absorption from tissue to blood was lower in women (0086 +/- 0007 vs 0115 +/- 0011 ml100 ml(-1)min(-1), P < 005) In conclusion, women showed impaired vasoconstriction, reduced capacitance response with time, and reduced capillary fluid absorption during acute hypovolemic circulatory stress, indicating less efficiency to defend central blood volume than men

Arterial pulse pressure variation predicting fluid responsiveness in critically ill patients.

Abstract: In critically ill patients, it is important to predict which patients will have their systemic blood flow increased in response to volume expansion to avoid undesired hypovolemia and fluid overloading. Static parameters such as the central venous pressure, the pulmonary arterial occlusion pressure, and the left ventricular end-diastolic dimension cannot accurately discriminate between responders and nonresponders to a fluid challenge. In this regard, respiratory-induced changes in arterial pulse pressure have been demonstrated to accurately predict preload responsiveness in mechanically ventilated patients. Some experimental and clinical studies confirm the usefulness of arterial pulse pressure as a useful tool to guide fluid therapy in critically ill patients.

Hypotension in preterm infants.

Abstract: PURPOSE Hypotension is a frequent occurrence in sick preterm neonates. It is important to appropriately recognise and treat hypotension in preterm infants due to the possible association with short and long term adverse outcomes. SEARCH STRATEGY An extensive search for relevant articles was carried out on PubMed, Embase and Cochrane database of systematic reviews. Cross references were hand searched. CONCLUSIONS The pathophysiology hypotension in preterm infants is multifactorial. Hypovolemia plays only a minor role in the absence of overt fluid losses. Cardiac dysfunction seems to be a factor in some neonates. Assessment of hypotension should be based on an overall clinical condition. Overzealous fluid administration seems to be associated with adverse outcomes and should be avoided in the absence of obvious fluid losses. Inotropes should be used if fluid boluses fail to correct hypotension. Dopamine is the most effective inotrope. Dobutamine can be used as add on therapy or as first line if cardiac dysfunction is an obvious cause. Evidence points to hypocortisolism in at least some hypotensive infants. Steroids have been used successfully in inotrope-resistant hypotension in some infants. Steroids should be used judiciously since there have been concerns about adverse neurological outcome in preterm infants who received steroids in the neonatal period.

Fluid Therapy in Vomiting and Diarrhea

Abstract: Fluid therapy in the patient with vomiting and diarrhea is essential to correct hypovolemia, dehydration, acid-base imbalance, and serum electrolyte abnormalities. Prediction of acid-base or electrolyte disturbances is difficult; therefore, point of care testing is beneficial to optimize therapy. This article focuses on the pathophysiology and treatment of hypovolemia, dehydration, electrolyte disturbances, and acid-base derangements resulting from and associated with vomiting and diarrhea.

Tissue hemoglobin monitoring of progressive central hypovolemia in humans using broadband diffuse optical spectroscopy

Abstract: We demonstrate noninvasive near-infrared diffuse optical spectroscopy (DOS) measurements of tissue hemoglobin contents that can track progressive reductions in central blood volume in human volunteers. Measurements of mean arterial blood pressure (MAP), heart rate (HR), stroke volume (SV), and cardiac output (Q) are obtained in ten healthy human subjects during baseline supine rest and exposure to progressive reductions of central blood volume produced by application of lower body negative pressure (LBNP). Simultaneous quantitative noninvasive measurements of tissue oxyhemoglobin (OHb), deoxyhemoglobin (RHb), total hemoglobin concentration (THb), and tissue hemoglobin oxygen saturation (S(t)O(2)) are performed throughout LBNP application using broadband DOS. As progressively increasing amounts of LBNP are applied, HR increases, and MAP, SV, and Q decrease (p<0.001). OHb, S(t)O(2), and THb decrease (p<0.001) in correlation with progressive increases in LBNP, while tissue RHb remained relatively constant (p=0.378). The average fractional changes from baseline values in DOS OHb (fOHb) correlate closely with independently measured changes in SV (r(2)=0.95) and Q (r(2)=0.98) during LBNP. Quantitative noninvasive broadband DOS measurements of tissue hemoglobin parameters of peripheral perfusion are capable of detecting progressive reductions in central blood volume, and appear to be sensitive markers of early hypoperfusion associated with hemorrhage as simulated by LBNP.

Drug-induced renal failure in the ICU.

Abstract: Drug-induced renal failure is a frequent complication in the setting of ICU. Generally spoken pathomechanisms leading to drug-induced renal failure can be divided into hemodynamic effects, epithelial toxicity or crystalline nephropathy. The risk of drug-induced renal failure is increased by any form of hypovolemia (i.e. true hypovolemia or reduced effective circulating volume), older age, pre-existent renal impairment, and concomitant application of two or more nephrotoxins. This article reviews drugs most frequently responsible for renal failure in the ICU and discusses preventive measures.