Showing papers on "Hypovolemia published in 1993"

Traumatic brain injury, hemorrhagic shock, and fluid resuscitation: effects on intracranial pressure and brain compliance

Abstract: Intracranial hypertension following traumatic brain injury is associated with considerable morbidity and mortality. Hemorrhagic hypovolemia commonly coexists with head injury in this population of patients. Therapy directed at correcting hypovolemic shock includes vigorous volume expansion with crystalloid solutions. It is hypothesized that, following traumatic brain injury, cerebrovascular dysfunction results in rapid loss of brain compliance, resulting in increased sensitivity to cerebrovascular venous pressure. Increased central venous pressure (CVP) occurring with vigorous crystalloid resuscitation may therefore contribute to the loss of brain compliance and the development of intracranial hypertension. The authors tested this hypothesis in miniature swine subjected to traumatic brain injury, hemorrhage, and resuscitation. Elevated CVP following resuscitation from hemorrhage to a high CVP significantly worsened intracranial hypertension in animals with concurrent traumatic brain injury, as compared to animals subjected to traumatic brain injury alone (mean +/- standard error of the mean: 33.0 +/- 2.0 vs. 20.0 +/- 2.0 mm Hg, p < 0.05) or to animals subjected to the combination of traumatic brain injury, hemorrhage, and resuscitation to a low CVP (33.0 +/- 2.0 vs. 24.0 +/- 2.0 mm Hg, p < 0.05). These data support the hypothesis that reduction in brain compliance can occur secondary to elevation of CVP following resuscitation from hemorrhagic shock. This may worsen intracranial hypertension in patients with traumatic brain injury and hemorrhagic shock.

Mild hypovolemic stress alters autonomic modulation of heart rate.

Abstract: In response to changes in central venous volume, changes in vagal efferent cardiac outflow have been demonstrated in animals but not in humans. In this study, frequency domains analysis was used to quantify modulation of heart rate by respiration and blood pressure in normal human adults undergoing mild central hypovolemic stress induced by blood donation and postural change. In supine subjects, blood donation caused no change in mean heart rate, pulse pressure, or in the variance of heart rate or blood pressure. There were small decreases in mean and systolic blood pressure. A significant decrease in vagal modulation of heart rate was seen in the 0.12-0.5-Hz frequency band, as measured by the change in the relation of lung volume to heart rate in this frequency band (-4.49 beats per minute [pbm] per liter [1], p < 0.001). Comparison of supine and tilt positions revealed marked changes in heart rate and blood pressure means and variances consistent with more pronounced decreases in intracardiac filling pressures and unloading of the arterial baroreceptors. A further progressive decrease in the vagal modulation of heart rate by lung volume was observed in the 0.12-0.5-Hz band, with a near-linear response of magnitude of respiratory sinus arrhythmia over a range of estimated central venous volume. Transfer function analysis can detect changes in autonomic response to mild degrees of central hypovolemia, which are insufficient to cause changes in mean heart rate or heart rate variance. This represents evidence for modulation of heart rate control by cardiopulmonary baroreceptors. A near-linear relation between magnitude of respiratory sinus arrhythmia and central venous volume suggests that this may have clinical relevance in patient monitoring.

Neurogenic control of renal function in response to graded nonhypotensive hemorrhage in conscious dogs

Abstract: The reflex control of plasma renin activity (PRA) and urinary sodium excretion (UNaV) was evaluated in 13 dogs instrumented for chronic study and maintained on a normal sodium intake (40 meq/day). Graded blood volume depletion of 14 (BVD1) and 21% (BVD2) of the estimated total blood volume was used to activate renal sympathetic nerve activity (RSNA), and experiments were conducted before and after bilateral renal denervation (DNX). In dogs with innervated kidneys, nonhypotensive BVD1 increased RSNA 40.9 +/- 10.9% (P < 0.05) above control. Blood volume depletion increased PRA from 1.95 +/- 0.52 to 3.5 +/- 0.57 ng.ml-1 x h-1 and decreased UNaV from 58.2 +/- 10.1 to 35.5 +/- 4.3 mu eq/min without changing renal blood flow or glomerular filtration rate. BVD2 failed to further activate RSNA (52.0 +/- 16.7%) but did increase PRA to 4.85 +/- 0.83 ng.ml-1 x h-1 and decreased UNaV to 17.9 +/- 2.7 mu eq/min. Renal DNX (n = 13) abolished both the PRA and antinatriuretic responses to BVD1 and BVD2. Thus volume-invoked reflex activation of RSNA, but not altered renal hemodynamics, mediates, activation of PRA and antinatriuresis. This neurogenic control of renal function may be critical to the rapid regulation of extracellular fluid volume, via alterations in urinary excretion.

Systolic blood pressure and blood volume in preterm infants.

Abstract: Blood volume and systolic blood pressure (SBP) were measured in 43 preterm infants. Mean (SD) blood volume was 83 (19) ml/kg (range 48-119) and SBP 50 (9) mm Hg (range 34-69), showing a significant overall relationship. Blood volume in infants with SBP > 60 mm Hg (110 (6) ml/kg) was significantly higher than in infants with SBP 40-60 mm Hg (78 (16) ml/kg) and in infants with SBP < 40 mm Hg (75 (10) ml/kg). In conclusion, SBP is of limited value in detecting hypovolaemia in very low birthweight infants.

Arterial pulse pressure and vasopressin release in humans during lower body negative pressure.

Abstract: The hypothesis was tested that narrowing of arterial pulse pressure (PP) is a determinant of arginine vasopressin (AVP) release in humans. Six normal males completed a two-step lower body negative pressure (LBNP) protocol of -20 and -50 mmHg, respectively, for 10 min each. None of these subjects experienced presyncopal symptoms. Arterial plasma AVP and plasma renin activity (PRA) (at 2-min intervals) only increased subsequent to a decrease in PP (invasive brachial arterial measurements) and stroke volume (ultrasound Doppler technique, n = 4). Simultaneously, mean arterial pressure did not change. A selective decrease in central venous pressure and left atrial diameter (echocardiography, n = 4) at LBNP of -20 mmHg did not affect AVP or PRA, whereas arterial plasma norepinephrine increased (n = 4). During LBNP, significant (P < 0.05) intraindividual linear correlations were observed between log(AVP) and PP in four of the subjects with r values from -0.75 to -0.99 and between log(PRA) and PP in all six subjects with r values from -0.89 to -0.98. In conclusion, these results are in compliance with the hypothesis that narrowing of PP in humans during central hypovolemia is a determinant of AVP and renin release.

Pharmacologic and clinical considerations in selecting crystalloid, colloidal, and oxygen-carrying resuscitation fluids, Part 1.

Abstract: The pharmacologic properties of crystalloid, colloidal, and oxygen-carrying resuscitation fluids are described, and the findings of clinical trials of these solutions are discussed. Fluid administration is a fundamental part of resuscitation therapy. Crystalloid solutions supply water and sodium to maintain the osmotic gradient between the extravascular and intravascular compartments. Examples are lactated Ringer's injection and 0.9% sodium chloride injection. Colloidal solutions, such as those containing albumin, dextrans, or starches, increase the plasma oncotic pressure and effectively move fluid from the interstitial compartment to the plasma compartment. Oxygen-carrying resuscitation fluids, such as whole blood and artificial hemoglobin solutions, not only increase plasma volume but improve tissue oxygenation. Clinically, colloidal solutions are generally superior to crystalloids in their ability to expand plasma volume. However, colloids may impair coagulation, interfere with organ function, and cause anaphylactoid reactions. Crystalloid solutions represent the least expensive option and are less likely to promote bleeding, but they are more likely to cause edema because larger volumes are needed. Favorable experience with inexpensive hypertonic crystalloids with improved plasma volume expansion properties may favor a return to resuscitation with crystalloid solutions. Oxygen-carrying resuscitation fluids are indicated when the patient has lost more than 25% of the total blood volume. Tailoring therapy to the individual patient and close monitoring are essential to safe and effective fluid resuscitation.

Dynamics of transcapillary fluid transfer and plasma volume during lower body negative pressure.

Abstract: Lower body negative pressure (LBNP) is a stimulus frequently used to study reflex circulatory responses in humans. Studies have provided data on LBNP-induced blood pooling; however, the possibility that LBNP also might be associated with an important loss of plasma fluid has attracted little attention. Therefore this problem was analysed in male volunteers exposed to prolonged (10 min) high (70–75 mmHg) LBNP. Data on LBNP-induced blood pooling that were more reliable than in previous literature were also provided. LBNP caused early pooling of more than 870 ml of blood. Rapid filtration of plasma into the exposed tissues occurred throughout LBNP. The cumulative oedema in the legs and buttocks averaged as much as 460 ml, and additional quite large volumes of plasma apparently accumulated in other parts of the lower body. Concomitantly, there was compensatory absorption of extravascular fluid in the upper body. The net decrease in plasma volume (PV) was still large and averaged 491 2 29(SE) ml. Two aspects of the demonstrated process of transcapillary fluid fluxes and PV decline may be emphasized. Firstly, in conjunction with the primary large redistribution of intravascular volume, it certainly implies that LBNP is a potent stimulus as also indicated by a progressive increase in heart rate (HR) and a progressive decline in systolic pressure throughout experimental intervention. In fact, LBNP-induced circulatory stress clearly has bearings on the extreme hypovolaemic situation provided by the pressure-bottle haemorrhage technique used in animals. Secondly, it not only offers an interesting example of the dynamics of PV but appears to have more general validity with regard to states characterized by gravitational shifts of blood (hydrostatic load), like upright exercise and quiet standing.

Occurrence of presyncope in subjects without ventricular innervation.

Abstract: 1. To determine whether activation of the left ventricular C-fibre mechanoreceptors initiates the vasodepressor reflex that often causes syncope, we exposed six orthotopic cardiac transplant patients and six matched, healthy control subjects to progressively increasing lower body negative pressure until the onset of vasodepressor responses. 2. There was no significant difference (P = 0.78) between the central hypovolemia tolerances of the cardiac transplant and the control groups. 3. The decrease in systolic blood pressure before the onset of vasodepressor reflexes was greater in the cardiac transplant group. The cardiac transplant group did not maintain diastolic blood pressure during central hypovolaemia. From baseline to the onset of vasodepression, there were no differences in leg circumference, forearm blood flow and forearm vascular resistance responses between the two groups. 4. We conclude that the left ventricular mechanoreceptors may not be the primary afferent trigger for syncope.

Contribution of vasopressin to blood pressure regulation during hypovolemic hypotension in humans

Abstract: In animals subjected to hemorrhage, plasma arginine vasopressin concentrations increase to levels sufficient to cause vasoconstriction, thus attenuating the hypotensive response. The purpose of this study was to examine the contribution of vasopressin to blood pressure regulation during hypotension in humans. Hypotension was induced in twelve normal subjects by lower body negative pressure (LBNP) before and after intravenous administration of vasopressin V1 receptor antagonist. Before drug administration, LBNP reduced systolic blood pressure from 125 +/- 4 to 78 +/- 12 mmHg (P < 0.01) as vasopressin concentration increased from 2.9 +/- 0.6 to 17 +/- 6 pg/ml (P < 0.05). After administration of the vasopressin antagonist, LBNP reduced systolic blood pressure from 128 +/- 3 to 89 +/- 11 mmHg (P < 0.01). The hypotensive response to LBNP was not potentiated by inhibiting vasopressin's vasoconstrictive effects (P = NS). Thus hypotension causes marked increases in plasma vasopressin concentration. In contrast to findings in animal studies, however, vasopressin does not contribute to the maintenance of blood pressure during hypotension in humans.

Intravascular volume and fluid therapy for severe sepsis.

Abstract: Hypovolemia is one of the principal defects contributing to cardiovascular instability and circulatory failure during septic shock. Fluid infusion is the mainstay of initial resuscitation. Large amounts of fluids may be required and should be titrated to optimal hemodynamic effects while attempting to minimize the development of pulmonary and systemic edema. Hemoglobin and hematocrit should be carefully monitored, with transfusions being used as necessary to maintain adequate levels of systemic oxygen delivery. Crystalloids and colloids are equally effective, although the volume of fluids required with crystalloids is two to four times that of colloids. In older patients, where high filling pressures may be required for optimal hemodynamic effect, colloids may be associated with a lower frequency of pulmonary edema.

The adjustment of post dialytic dry weight based on non-invasive measurement of extracellular fluid and blood volumes.

Abstract: One of the major problems in the clinical practice of hemodialysis is an incorrect estimation of post dialytic (PD) dry weight. Underestimation of dry weight leads to hypovolemia induced hypotension, and overestimation to hypertension, pulmonary edema, and left ventricular hypertrophy. Because of the insensitivity of clinical variables to estimate dry weight, a more accurate technique is warranted. For this purpose and for the continuous surveillance of changes in blood volume (BV) during hemodialysis, two non-invasive techniques were applied. Based on post dialytically obtained extracellular fluid volume (EFV) values, measured by means of a conductivity method, 30 stable hemodialysis patients were divided into three groups for further analysis: de- (n = 9), normo- (n = 15), and overhydrated (n = 6). Using an on-line optical reflection method, changes in BV were measured continuously during therapy. Mean BV decrease, corrected for UF, differed slightly between the three groups (0 = 1.84 +/- 2.06, N = 3.20 +/- 1.80, D = 4.20 +/- 1.60 %/L). However, eight hypotensive episodes occurred in group D versus none in groups N and O. These hypotensive episodes were characterized by a greater reduction of BV--corrected for ultrafiltration--from the start of treatment until the moment of hypotension (6.96 +/- 2.21 %/L), compared with the 22 non hypotensive controls (2.16 +/- 2.01 %/L, p < 0.001). Based on the PD EFV dry weight of the overhydrated and dehydrated patients was decreased and increased, respectively, by 500 g after each session, until PD EFV was within normal bounds.(ABSTRACT TRUNCATED AT 250 WORDS)

Maternal/fetal dehydration: prolonged effects and responses to oral rehydration

Abstract: Dehydration induces marked alterations in maternal-fetal fluid homeostasis and accompanying fetal endocrine responses. We sought to determine if the increase in fetal plasma arginine vasopressin (AVP) levels during maternal dehydration is mediated by fetal plasma hypovolemia in addition to hyperosmolality and to examine maternal and fetal plasma atrial natriuretic factor (ANF) responses to maternal dehydration and oral rehydration. Seven pregnant ewes (127 +/- 1 day) were water deprived for 72-96 h, and five of these were orally rehydrated. Dehydration induced significant increases in maternal plasma osmolality (pOSM) (300 +/- 2 to 325 +/- 8 mosmol/kg) and AVP (3.0 +/- 0.4 to 18.9 +/- 4.0 pg/ml), and decreases in plasma ANF levels (28.1 +/- 3.1 to 19.7 +/- 3.1 pg/ml). Fetal pOSM (293 +/- 3 to 314 +/- 4 mosmol/kg), AVP (2.5 +/- 0.6 to 8.1 +/- 4.8 pg/ml), and urinary fractional sodium excretion increased significantly, whereas plasma ANF and fetal blood volume did not change. After maternal water access maternal plasma AVP decreased rapidly in comparison to the gradual decrease in maternal pOSM. Fetal plasma AVP levels did not change significantly and fetal pOSM decreased more slowly than maternal pOSM. Fetal plasma ANF increased in association with increased urine flow and glomerular filtration rate after maternal rehydration. These data indicate marked differences in fetal and maternal plasma ANF and AVP responses with dehydration-induced increases in fetal plasma AVP being secondary to plasma hyperosmolality, rather than hypovolemia. Rapid suppression of maternal plasma AVP may contribute to the slower equilibration of fetal pOSM during oral, as compared with intravenous, maternal rehydration.

Is absolute hypovolemia a risk factor for vasovagal response to head-up tilt?

Abstract: To test the hypothesis that hypovolemia is associated with an increased incidence of vasovagal syncope during head-up tilt (HUT) 45 patients with history of syncope or presyncope were studied. Blood volume (radio-iodinated serum albumin) was determined, then subjects underwent a graded HUT (from 15 degrees-60 degrees HUT) with cuff blood pressure and ECG monitoring. All patients were kept on their own medications during evaluation. Thirty patients (12 male, 18 female, mean age 50 +/- 19 [SD] years) had hypovolemia, defined as blood volume < 90% of lab normal for corresponding sex, while 15 patients (7 male, 8 female, mean age 52 +/- 21 years) were normovolemic with blood volume ranging from 91%-110% of sex-matched normal subjects. The normovolemic patients served as controls. During HUT, a vasovagal response was elicited in 5 of the 30 hypovolemics and in 4 of the 15 normovolemic (16.7% and 26.7%, respectively, P = NS). In those who developed vasovagal response, the changes of heart rate and blood pressure during HUT were not significantly different between hypovolemics and normovolemics, neither at the endpoint (vasovagal response) nor immediately before the development of the vasovagal response. In patients with nonvasovagal events, four types of hemodynamic responses to tilt were observed: normal blood pressure response associated with normal heart rate increase, normal blood pressure response in association with accentuated increase in heart rate, orthostatic hypotension with normal acceleration of heart rate, and orthostatic hypotension with accelerated increase in heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Resuscitation of hypovolemia in pigs using near saturated sodium chloride solution in dextran.

Abstract: A 7.5% sodium chloride/6% Dextran solution (HSD) is effective for restoration of cardiovascular function after hemorrhagic shock. In the present experiments, we tested the usefulness and side effects of a 25% NaCl/24% Dextran solution (SSD), compared to HSD and 0.9% NaCl (NS). After 1 hr of baseline observation, 21 anesthetized pigs were submitted to hemorrhagic shock, maintaining a mean arterial pressure of 45 mmHg for 60 min. Continuous intravenous infusion of one of the solutions was then initiated and the infusion rate adjusted to restore and maintain cardiac output at baseline levels for 2 hr. The NS group required 121 +/- 22 ml/kg to achieve full resuscitation, while the HSD and SSD groups required 6.3 +/- 1.3 and 1.7 +/- 0.2 ml/kg, respectively. We conclude that SSD infusions were exceedingly effective at restoring cardiovascular function in volumes equal to only 10% of bled volume, but were associated with transient hemolysis and peripheral vein inflammation.

Temporal patterns of blood volume, hemodynamics, and oxygen transport in pathogenesis and therapy of postoperative adult respiratory distress syndrome.

Abstract: Time relationships of physiologic patterns that are relevant to the pathogenesis of adult respiratory distress syndrome (ARDS) have not been well studied. The purpose of this review is to summarize the temporal relationship of blood volume, hemodynamics, and oxygen transport patterns occurring in postoperative patients before and after ARDS in order to develop a more complete mechanistic evaluation of its pathophysiology and to propose more rational therapeutic strategies. The data indicate that hypovolemia, reduced or uneven blood flow, inadequate delivery of oxygen, and insufficient consumption of oxygen precede the appearance of ARDS and are the primary precipitating physiologic events. This is contrary to conventional thinking which emphasizes capillary leak and fluid overload as the primary problems. The conventional approach also ignores events antecedent to ARDS that produce hypoxia of the lung tissue, result in pulmonary vasoconstriction, and increased pulmonary venous admixture (shunt). Therapy to prevent or rapidly treat these antecedent events has been shown to prevent or attenuate postoperative and posttraumatic ARDS. Various mediators such as interleukin (IL)-1, IL-6, and IL-8 and tumor necrosis factor as measured by plasma concentrations do not precede diagnostic criteria of ARDS, but may accelerate and augment the disorder as it is occurring.

Effect of hypoxemia and hypovolemia on retinal and choroidal blood flow in the newborn piglet.

Abstract: The effect of hypoxemia and/or hypovolemia on ocular blood flow was studied in paralyzed and mechanically ventilated newborn piglets with the isotope-labelled microsphere method. Twenty-six piglets were studied in four different groups. One group of piglets (n = 6) was made hypoxemic by breathing 10% O2, a second group (n = 7) and a third group (n = 7) were studied during hypoxemia (10% O2), followed by hypovolemia (bleeding 20 and 30% of estimated blood volume, respectively). A fourth group of piglets (n = 6) was made hypovolemic by bleeding 20% of estimated blood volume. Hypoxemia resulted in a 2- to 3-fold increase in retinal blood flow (RBF), while hypovolemia did not change RBF, not even when preceded by a period of hypoxemia. In the case of choroidal blood flow (ChBF), the increase caused by hypoxemia was only 10-40%. Although ChBF decreased significantly during hypovolemia, no significant correlation between mean arterial blood pressure and ChBF was found. The results indicate that autoregulation is normally seen in RBF, but probably not in ChBF. However, during hypoxemia autoregulation was found neither in RBF nor in ChBF.

Immediate orthostatic hypotension: diagnostic value in acutely ill patients.

Abstract: Hypotension (systolic blood pressure less than 90 mm Hg) was induced immediately in 21 acutely ill normotensive patients when they were raised from a supine to an upright position. Systolic blood pressure declined to 80 mm Hg or lower in all patients and to 65 mm Hg or lower in 10 patients when they assumed an upright posture. Immediate orthostatic hypotension observed in 9 patients suggested hypovolemia, which was promptly corrected by rapid infusion of large volumes of normal saline and/or albumin. Orthostatic hypotension was of diagnostic aid in 16 patients, including 4 with infections (pelvic inflammatory disease, occult septic shock, legionnaires' disease, Rocky Mountain spotted fever), 3 with adrenal insufficiency, 2 with acute myocardial infarction, 1 with hypoglycemia, 2 with severe cardiac valvular obstruction, and 4 with inappropriate drug use (enalapril or trazodone). These findings suggest that immediate orthostatic hypotension in acutely ill patients is a physical sign that might have valuable diagnostic and therapeutic implications.

Endothelial Dysfunction as an Early Critical Event in Ischemia and Shock

Abstract: Splanchnic artery occlusion (SAO) followed by reperfusion (R) of the ischemic splanchnic visceral organs results in precipitous decline in systemic blood pressure, leading to a circulatory shock state [1]. SAO + R shock is a very severe form of shock with a characteristic high mortality rate (i.e., 80%–95%). The pathogenesis of SAO + R shock is complex and involves multiple mechanisms including (a) capillary leakage and hypovolemia, (b) loss of vascular control mechanisms (e.g., tendency towards poor splanchnic perfusion, vasospasm), and (c) depression of myocardial contractility [2]. Recently, neutrophils have been implicated in contributing to SAO + R shock [3, 4]. Neutrophil accumulation in tissues may lead to the release of a variety of humoral mediators of shock including (a) oxygen derived free radicals (e.g., superoxide radical), (b) cytokines (e.g., tumor necrosis factor, TNF), and (c) proteolytic enzymes (e.g., elastase). Additionally neutrophils may accumulate in small blood vessels and physically obstruct blood flow there, thus contributing to the perpetuation of the ischemic state [5]. Similar effects occur during myocardial ischemia and reperfusion (MI + R) [5, 6] except that a lethal form of shock does not develop.

Myocardial and circulatory performance during the ischemic phase of superior mesenteric artery occlusion.

Abstract: OBJECTIVE To investigate myocardial and circulatory parameters during the acute ischemic phase of mesenteric artery occlusion. DESIGN A prospective, randomized, control trial. SUBJECTS Twelve, adult, mongrel dogs. INTERVENTIONS In seven dogs the superior mesenteric artery was occluded with two silk ligatures (experimental group). In five dogs the ligatures were not tied (control group). Measurements were made during 7 hours of occlusion. MAIN OUTCOME MEASURES Myocardial performance and circulatory performance. RESULTS There were significant (p < 0.05) reductions in arterial blood pressure, mean pulmonary artery pressure, diastolic pulmonary artery pressure and cardiac index in dogs exposed to intestinal ischemia compared with the control dogs. No differences were identified in ventricular performance, stroke volume index or peripheral vascular resistance index. CONCLUSIONS Early cardiac and central circulatory changes in massive intestinal ischemia are due to intravascular hypovolemia. Sepsis and myocardial depressant factors were not found to be a cause of death.

Monitoring of hypovolemia

Abstract: Hypovolemia, the inadequacy of the intravascular blood volume, still remains a diagnostic challenge for the anesthesiologist and critical care physician. Conventional hemodynamic parameters, such as blood pressure, heart rate, and even central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP), have been shown repeatedly to be insensitive and misleading in the assessment of effective blood volume. Therefore, newer monitoring methods are constantly being introduced. This review will re-examine the current role of conventional and new parameters in the diagnostic challenge of hypovolemia detection.

Managing low cardiac output states: maintaining volume after cardiac surgery.

Abstract: Low cardiac output after cardiac surgery may be caused by hypovolemia, myocardial depression, vasoconstriction, and dysrhythmias Postoperative hypovolemia occurs because of blood volume loss and decreased diastolic filling Diuresis, intravascular fluid shift into the interstitium, hormonal influences, and bleeding deplete blood volume Diastolic filling may be compromised by positive end-expiratory pressure, vasodilation, dysrhythmias, and venous return obstruction The primary indicator of intravascular volume is ventricular preload, which may be measured indirectly with central venous pressure, left atrial pressure, or pulmonary capillary wedge pressure Recognition of hypovolemia is aided through the use of cardiac pressure trend monitoring and evaluation of noninvasive indicators of hypovolemia Nursing goals, in response to hypovolemia, are to increase the circulating volume, optimize oxygen delivery, stabilize hemodynamics, improve tissue perfusion, and prevent shock

Cardiac Function During Hypovolemia

Abstract: Shock is defined by an impaired tissue perfusion which causes malfunction of vital organs. An inadequate cardiac output and/or maldistribution of blood flow can induce shock providing that vital organs are underperfused. An inappropriate cardiac output may result from an inadequate filling of the heart and/or an impairment of pump function. Restrictive changes of the heart walls or obstruction within the cardiac chambers may jeopardize cardiac filling, but the most common cause of heart failure in shock is a reduction of venous return due to absolute or relative hypovolemia. Changes in autonomic function which occur with hypovolemia limit many of the detrimental effects of reduced cardiac output. If the hypovolemia is severe or persists over a long period of time, the compensatory changes of cardiac function may deteriorate to progressive cardiac failure. Cardiac output is determined by four physiologic parameters: preload (end-diastolic fiber length), afterload (ventricular wall tension during ejection), contractility, and heart rate (Weems and Downey 1992; Guyton 1991). The changes in the cardiac factors induced by lack of intravascular volume and the associated systemic response of the organism are primarily dependent on the amount of volume loss (Table 1).

Spinal anesthesia: practical applications.

Abstract: The recent widespread popularity of spinal anesthesia can be traced to two events. One is the appreciation that, when used for operations below the level of the umbilicus, anesthetically induced physiologic trespass is less with spinal than with general anesthesia. The other is the recognition that modest hypotension with peripheral vasodilation, that may be seen with spinal anesthesia or intravenous infusion of nitroprusside, is, unlike hypotension associated with hypovolemia, unaccompanied by physiologically significant changes in peripheral distribution of cardiac output or changes in the balance between tissue oxygen supply and demand in the myocardium or elsewhere. Spinal anesthesia also has special advantages specific to urinary tract surgery in the geriatric patient.

The effects of an intravenous nicardipine injection on baroreflex control of heart rate in man.

Abstract: The effects of nicardipine injection on baroreflex control of heart rate were investigated by both pressor and depressor tests in 17 adult patients. Baroreflex sensitivity was attenuated after nicardipine injection by the pressor test using phenylephrine, whereas it was not changed by the depressor test using nitroglycerine. No resetting of the baroreflex occurred after nicardipine injection. By the pressor test, the plasma norepinephrine level was decreased, indicating that parasympathetic activity increased, and by the depressor test, the plasma norepinephrine concentration was increased, indicating that sympathetic activity increased. These results suggest that it is safe to use nicardipine clinically even when reduction in blood pressure for hypovolemia or unclamping the main artery is expected, and it is disadvantageous to administer the drug when an increase in blood pressure due to crossclamping of the main artery is forecasted.