Increase In Total Blood Volume Research Articles

Four-Second Power Cycling Training Increases Maximal Anaerobic Power, Peak Oxygen Consumption, and Total Blood Volume.

High-intensity interval training is an effective tool to improve cardiovascular fitness and maximal anaerobic power. Different methods of high-intensity interval training have been studied but the effects of repeated maximal effort cycling with very short exercise time (i.e., 4 s) and short recovery time (15-30 s) might suit individuals with limited time to exercise. We examined the effects of training at near maximal anaerobic power during cycling (PC) on maximal anaerobic power, peak oxygen consumption (V˙O2peak), and total blood volume in 11 young healthy individuals (age: 21.3 ± 0.5 yr) (six men, five women). Participants trained three times a week for 8 wk performing a PC program consisting of 30 bouts of 4 s at an all-out intensity (i.e., 2 min of exercise per session). The cardiovascular stress progressively increased over the weeks by decreasing the recovery time between sprints (30-24 s to 15 s), and thus, total session time decreased from 17 to <10 min. Power cycling elicited a 13.2% increase in V˙O2peak (Pre: 2.86 ± 0.18 L·min-1, Post: 3.24 ± 0.21 L·min-1; P = 0.003) and a 7.6% increase in total blood volume (Pre: 5139 ± 199 mL, Post: 5529 ± 342 mL; P < 0.05). Concurrently, maximal anaerobic power increased by 17.2% (Pre: 860 ± 53 W, Post: 1,009 ± 71 W; P < 0.001). A PC training program employing 30 bouts of 4 s duration for a total of 2 min of exercise, resulting in a total session time of less than 10 min in the last weeks, is effective for improving total blood volume, V˙O2peak and maximal anaerobic power in young healthy individuals over 8 wk. These observations require reconsideration of the minimal amount of exercise needed to significantly increase both maximal aerobic and anaerobic power.

4‐s Power Cycling Training Increases Maximal Anaerobic Power, Peak Oxygen Consumption and Total Blood Volume

Introduction High-intensity interval training (HIIT) is an effective tool to improve cardiovascular fitness and maximal anaerobic power. Different methods of HIIT have been studied but the effects of repeated maximal effort cycling with very short exercise time (i.e., 4-s) and short recovery time (15-30 s) might suit individuals with limited time to exercise. Purpose We examined the effects of training at near maximal anaerobic power during cycling (PC) on maximal anaerobic power, peak oxygen consumption (VO2peak), and total blood volume in 11 young healthy individuals (age: 21.3±0.5 y) (6 men, 5 women). Methods Participants trained three times a week for eight weeks performing a PC program consisting of 30 bouts of 4-s at an all-out intensity (i.e., 2 minutes of exercise per session). The cardiovascular stress progressively increased over the weeks by decreasing the recovery time between sprints (30 to 24 to 15-s) and thus total session time decreased from 17 to < 10 min. Results PC elicited a 13.2% increase in VO2peak (Pre: 2.86±0.18 L/min, Post: 3.24±0.21 L/min, (p=0.003)) and a 7.6% increase in total blood volume (Pre: 5,139±199 ml, Post: 5,529±342 ml, p<0.05). Concurrently, maximal anaerobic power increased by 17.2% (Pre: 860±53 watts, Post: 1,009±71 watts; p<0.001). Conclusion PC training program employing 30 bouts of 4-s for a total of 2 min of exercise, resulting in a total session time of less than 10 min in the last weeks, is effective for improving total blood volume, VO2peak and maximal anaerobic power in young healthy individuals over 8 weeks. These observations require reconsideration of the minimal amount of exercise needed to significantly increase both maximal aerobic and anaerobic power.

SAT-593 Thyrotoxic Heart Disease: Rare but Serious Manifestation of Congestive Heart Failure

Background: Excess thyroid hormone alters the hemodynamics of the heart and vascular system resulting in a hyper-dynamic circulatory state which can lead to thyrotoxic heart disease. Clinical case: A 48-year-old male presented to the hospital with several days of rapid heart rate and weakness. He denied prior medical history, medication or supplement intake. Pertinent exam revealed a very thin, hoarse gentleman with shallow breathing and obvious hand tremors; heart exam with irregular rate and tachycardia, absent peripheral edema and bibasilar crackles bilaterally. EKG was consistent with atrial fibrillation with rapid ventricular response. Lab work revealed a pro-BNP of 4000 and positive D-dimer. CTA-Thorax was consistent with CHF with cardiomegaly, large pleural effusions, pulmonary edema and an incidental finding of thyromegaly. Echocardiogram revealed global LV hypokinesis with Ejection Fraction of 10-15%. TSH was <0.005, free Thyroxine >8.00, and Triiodothyronine was 27.04. Thyroid ultrasound showed heterogeneous enlarged gland with hypervascularity and no focal nodules. Graves’ Disease was confirmed with thyroid stimulating Immunoglobulin of 507. Methimazole and hydrocortisone were initiated along with Metoprolol and digoxin for rate control. Thyroid hormone has significant impact on cardiac function, structure and the vascular system. In the vasculature, T3 works to decrease systemic vascular resistance via direct vasodilatation. The decrease in SVR activates RAAS resulting in retention of sodium and fluid. Thyroid hormone also stimulates erythropoiesis which results in an increase in blood volume and stroke volume. In the heart, T3 enters the myocyte via specific transport proteins and via transcription-and non-transcription-mediated effects, increases contractility and relaxation of the cells. Given the increased metabolism, low SVR and increase in total blood volume, this creates a high cardiac output state. Untreated high-output state leads to ventricular dilatation, persistent tachycardia and eventual heart failure. Thus, prompt diagnosis and treatment of cardiac dysfunction is key. Of most importance is correction of thyroid dysfunction with either anti-thyroid medication, radioactive iodine ablation or thyroidectomy. This can possibly reverse and “cure” patient’s systolic heart failure. Conclusion: We present a case of thyrotoxicosis -induced cardiomyopathy with left ventricular ejection fraction of 10% secondary to undiagnosed Graves disease and emphasize the importance of thyroid disease as a possible cause of systolic heart failure.

Effect Of Chronic Xenon Supplementation On Hematological Parameters, Cardiorespiratory Fitness, and Athletic Performance

ObjectiveXenon is an inhalational anesthetic with the potential to improve athletic performance and cardiorespiratory fitness via proposed increases in total blood volume. This study aimed to determine the effect of a four‐week xenon supplementation protocol on total blood volume, maximal oxygen uptake (V̇2max) and 3‐kilometre time trial performance in trained individuals.MethodsFourteen subjects (32 ± 12 years; 71% male) were assessed for total blood volume through the carbon monoxide rebreathing method, cardiorespiratory fitness via V̇O2max on a treadmill test, and athletic performance using a 3 km time trial. Following baseline assessments, subjects were matched for sex, age and V̇O2max, and were randomised to 12 sessions of gas inhalation over four weeks (2 minutes of inhalation on 3 days per week); 1) xenon, n = 7 (70% xenon, 21% oxygen, 9% nitrogen) or 2) sham gas, n=7 (7% carbon dioxide, 21% oxygen, 62% nitrogen) dosing. Subjects were blinded to group allocation and all outcomes were re‐assessed following the four‐week dosing period. Within‐group mean differences and 95% confidence intervals for outcomes of interest are presented in Table 1. Differences between the xenon and sham gas group over time were tested using two‐way repeated measures ANOVA and are represented by P values.ResultsXenon and sham groups were equal at baseline for all outcomes of interest (Table 1). Twelve subjects completed the four‐week dosing intervention and are included in the analyses; one subject withdrew after a single xenon dose due to nausea and one subject was withdrawn after one week of xenon inhalation due to adverse symptoms during and after dosing which resembled sleep paralysis. Blinding was equally effective between groups; subjects in the xenon group were 65% certain of group allocation, while subjects in the sham group were 63% certain of group allocation. There were no significant differences between xenon or sham gas groups for changes in total blood volume, V̇O2max, or 3 km time trial performance (Table 1).ConclusionsFour weeks of xenon inhalation did not result in significant changes in total blood volume, cardiorespiratory fitness or athletic performance in comparison to a sham gas. Given the presence of adverse symptoms in approximately 30% (2 out of 7) subjects and a clear absence of physiological and performance benefits, our findings do not support the use of xenon as a performance enhancing substance.Support or Funding InformationThis study was supported in part by funding from the Partnership for Clean Competition Research Collaborative.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Temporal trends in concentrations and total serum burdens of organochlorine compounds from birth until adolescence and the role of breastfeeding

Introduction: The aims of the present study are to assess the temporal trends of organochlorine compounds (OCs) concentrations and total serum burdens from birth until adolescence and the influence of breastfeeding in these temporal trends. Methods: In 1997 two birth cohort studies were set up in Ribera d'Ebre (N=102) and the island of Menorca (N=482), Spain. Concentrations (ng/mL) of OCs [pentachlorobenzene (PeCB), four isomers of hexachlorocyclohexane (HCH), hexachlorobenzene (HCB), dichlorodiphenyltrichloroethane (4,4′-DDT), dichlorodiphenyldichloroethylene (4,4′-DDE) and seven polychlorobiphenyl congeners (Σ7PCBs)] were measured in cord blood and at the age of 4 and 14years. The total serum burdens (ng) of these compounds were estimated based on the total blood volume (mL) of children at the different ages. We compared median concentrations and total serum burdens of these OCs at the different time-points of follow-up between children of Ribera d'Ebre and Menorca and between breastfed and non-breastfed children. Results: From birth until adolescence concentrations of all OCs drastically reduced. These reductions were mainly derived from the dilution of OCs, associated to an increase in total blood volume of children at the age of 4 and 14years. Despite the reduction in OCs concentrations, the total serum burdens of 4,4′-DDE and Σ7PCBs, were higher in adolescents than at birth. Increases in OCs total serum burden occurred both in breastfed and non-breastfed children, but were significantly higher in the first. Conclusions: Even after decades of banning OCs production and use, current young generations in westernized countries are still bioaccumulating these compounds. Given the potential health effects of OCs, especial attention should be paid in the control of secondary emissions in the environment and in the control of food production and contamination. In countries with endemic malaria it is important to work towards effective alternatives to the use of DDT.

Dilemmas in Human and Rat Pregnancy: Proposed Mechanisms Relating to Arterial Vasodilation

There are several mysteries about the normal physiology of pregnancy (1). Renal sodium and water reabsorption occurs despite an increase in total blood volume. Moreover, the renin-angiotensin-aldosterone system (RAAS) is also stimulated in normal pregnancy, even though an increase in total blood volume normally suppresses the RAAS and increases sodium excretion in the nonpregnant state. Water retention also occurs and leads to hypoosmolality in normal pregnancy, even though total blood volume is expanded. On rare occasions, an extreme polyuria occurs in pregnancy that is unresponsive to arginine vasopressin (AVP). The receptors whereby AVP and oxytocin stimulate the principal cell of the collecting duct, vascular smooth muscle, glomerular mesangial and endometrial cells are in need of clarification. The present study proposes potential mechanisms relating to systemic arterial vasodilation to explain some of the apparent dilemmas of pregnancy.

Haematology of pregnancy

The physiological changes that occur in the blood during pregnancy are largely beneficial to mother and baby, but can sometimes cause problems. • Expansion of RBC mass and tissue proliferation results in increased demand for haematinics, and often nutritional anaemia. • Increase in total blood volume and haemostatic changes help to combat the hazard of haemorrhage at delivery, but pregnancy is thereby a hypercoagulable state and carries risks of various haemostatic disorders (Figure 1), from thromboembolism to disseminated intravascular coagulation (DIC). • Paternal antigens carried by the fetus but not present in the mother may provoke maternal immune responses, and alloimmune anaemia and thrombocytopenia.

Update on ascites and hepatorenal syndrome

Ascites is the most common complication occurring during liver cirrhosis. Even if a significant decrease in renal clearance may be observed in the first step of chronic active liver disease, renal impairment, at times complicated by the typical signs of hepatorenal syndrome, occurs only in patients with ascites, especially when tense and refractory. Experimental and clinical data seem to suggest a primary sodium and water retention in the pathogenesis of ascites, in the presence of an intrahepatic increase of hydrostatic pressure, which, by itself, physiologically occurs during digestion. Abnormal sodium and water handling leads to plasma volume expansion, followed by decreased peripheral vascular resistance and increased cardiac output. This second step is in agreement with the peripheral arterial vasodilation hypothesis, depicted by an increase in total blood volume, but with a decreased effective arterial blood volume. This discrepancy leads to the activation of the sympathetic nervous and renin-angiotensin-aldosterone systems associated with the progressive activation of the renal autacoid systems, especially, that of the arachidonic acid. During advanced cirrhosis, renal impairment becomes more sustained and renal autacoid vasodilating substances are less available, possibly due to a progressive exhaustion of these systems. At the same time ascites becomes refractory inasmuch as it is no longer responsive to diuretic treatment. Various pathogenetic mechanisms leading to refractory ascites are mentioned. Finally, several treatment approaches to overcome the reduced effectiveness of diuretic therapy are cited. Paracentesis, together with simultaneous administration of human albumin or other plasma expanders is the main common approach to treat refractory ascites and to avoid a further decrease in renal failure. Other effective tools are: administration of terlipressin together with albumin, implantation of the Le Veen shunt, surgical porto-systemic shunting or transjugular intrahepatic portosystemic stent-shunt, or orthotopic liver transplantation, according to the conditions of the individual patient.

Obesity Cardiomyopathy: Pathophysiology and Evolution of the Clinical Syndrome

Obesity produces an increase in total blood volume and cardiac output because of the high metabolic activity of excessive fat. In moderate to severe cases of obesity, this may lead to left ventricular dilation, increased left ventricular wall stress, compensatory (eccentric) left ventricular hypertrophy, and left ventricular diastolic dysfunction. Left ventricular systolic dysfunction may occur if wall stress remains high because of inadequate hypertrophy. Right ventricular structure and function may be similarly affected by the aforementioned morphologic and hemodynamic alterations and by pulmonary hypertension related to the sleep apnea/ obesity hypoventilation syndrome. The term obesity cardiomyopathy is applied when these cardiac structural and hemodynamic changes result in congestive heart failure. Obesity cardiomyopathy typically occurs in persons with severe and long-standing obesity. The predominant causes of death in those with obesity cardiomyopathy are progressive congestive heart failure and sudden cardiac death.

Effects of increasing blood hemoglobin levels on systemic hemodynamics of acutely anemic cirrhotic patients

Background/Aims: In experimental portal hypertension, blood hemoglobin levels have been shown to influence the hyperdynamic circulatory state. The aim of this study was to assess the hemodynamic effects of increasing hemoglobin concentration in human portal hypertension. Methods: Sixteen cirrhotic patients recovering from a variceal bleeding episode were randomly assigned to receive two units of packed red cells or 500 ml of a protein solution. Systemic and portal hemodynamics, and rheological and hormonal parameters were measured at baseline and after expansion. Results: Both groups were similar with respect to the degree of liver failure, severity of the bleeding episode, activation of the endogenous vasopressor systems, and hemodynamic parameters. The administration of either erythrocytes or a protein solution prompted a similar increase in total blood volume and suppression of vasopressor systems. Both groups of patients experienced similar increases in wedged hepatic venous pressure. Hepatic venous pressure gradient was not significantly modified but tended to increase in erythrocyte-transfused patients. Cardiopulmonary pressures increased, but this increment was significant in the non-blood-transfused patients only. Cardiac output decreased in erythrocyte-transfused patients, while it increased in the group receiving a protein solution. Red blood cell transfusion resulted in an increase in systemic vascular hindrance (resistance/blood viscosity), whereas the administration of a protein solution prompted a decrease in this parameter, thus reflecting true vasoconstriction and vasodilation, respectively. Conclusions: An increase in blood hemoglobin in acutely anemic cirrhotic patients attenuates their hyperdynamic circulation beyond viscosity-dependent changes, an effect which might be counteracted by the effects on portal venous pressure gradient.

FACTORS LIMITING PERFORMANCE IN THE HORSE

1495 The purpose of this seminar is to discuss the contributions of ventilation, gas exchange and its transport, and heat and fluid loss to equine performance. The horse is a large mammal with a high aerobic capacity (VO2max usually > 130 ml/kg.min-1). Contraction of the equine spleen during exercise is associated with increases in hematocrit >60% and a near doubling of the oxygen carrying capacity. This marked increase in total blood volume is associated with major adjustments in blood flow to the muscles of locomotion and ventilation. Horses also undergo marked desaturation of hemoglobin and become hypercapneic during strenuous exercise. Because of their large muscle mass and metabolic capacity, thermoregulartory factors and alterations in fluid and electrolyte balance can also play a major role in limiting the ability of horses to exercise. Due to the relative lack of information that exists regarding the physiologic responses and limitations of elite human athletes to exercise, the horse has proven to be a good model with which to study the physiology of high performance exercise. This symposium should be of considerable scientific interest and educational value to comparative exercise physiologists and students interested in factors that can limit elite athletic performance.

Hemodynamic and hormonal changes during erythropoietin therapy in hemodialysis patients.

To better understand the mechanism of recombinant human erythropoietin (rhEPO)-induced increase in BP, hemodynamic parameters, body fluid volumes, and the hormones implicated in BP regulation were studied in 32 anemic hemodialysis patients before and after 3 to 4 mo of rhEPO therapy. Hemoglobin levels increased from 83 +/- 1.5 to 119 +/- 2.3 g/L (P < 0.01) after rhEPO therapy (25 to 43 U/kg) administered subcutaneously three times weekly. Mean 24-h systolic and diastolic ambulatory BP were significantly increased by 14 +/- 3 and 10 +/- 2 mmHg, respectively (P < 0.01 for both groups). Systemic vascular resistance consistently increased by 28 +/- 5% (P < 0.01), whereas cardiac output was decreased by 6 +/- 3% (P < 0.05). Red blood cell mass increased by 510 +/- 35 ml (P < 0.01), whereas plasma volume decreased by 420 +/- 66 ml (P < 0.01), which resulted in a nonsignificant increase in total blood volume. Extracellular fluid volume and exchangeable sodium were decreased by 873 +/- 255 ml (P < 0.01) and 125 mmol (P < 0.01), respectively. There was a positive correlation between the changes in exchangeable sodium and in systolic BP (r = 0.41, P < 0.05). Furthermore, a greater increase in 24-h systolic BP was observed in patients in whom exchangeable sodium increased or remained unchanged (n = 10) compared with patients (n = 22) with decreased exchangeable sodium (20 +/- 4 mmHg versus 8 +/- 2 mmHg, respectively, P < 0.01). Plasma catecholamines, plasma renin concentration, plasma atrial natriuretic peptide, and plasma endothelin-1 did not significantly change with rhEPO treatment, whereas plasma aldosterone increased significantly (P < 0.01). Although volume-independent mechanisms may contribute to rhEPO-induced BP increase, the results presented here suggest the importance of optimally reducing extracellular fluid volume to prevent, at least in part, the development of hypertension often observed with improved uremic anemia in these patients.

Interleukin-6-Assoeiated Anemia: Determination of the Underlying Mechanism

Recombinant human interleukin-6 (rhIL-6) is a pluripotent cytokine with proinflammatory, antitumor, and growth factor effects. Clinical investigations of rhIL-6 either alone as immunotherapy or as a colony-stimulating factor in conjunction with chemotherapy have shown a dose-dependent, rapid onset, and largely reversible decrease in venous hematocrit levels. In an effort to determine the mechanism for the rhIL-6-associated anemia, we measured red blood cell volume serially in patients receiving rhIL-6 at either 30 micrograms/kg/day as a 120-hour continuous intravenous infusion (renal cell carcinoma) or 100 micrograms/kg/d intravenously over 1 hour for 5 days (melanoma) as part of two separate phase II trials. Radioisotope dilution assays with 51Cr-labeled autologous red blood cells and hemolysis screens were performed on day 1 before the initiation of therapy and on day 5 shortly before the end of therapy. In the 6 patients studied, the mean decrease in hemoglobin concentration was 1.9 +/- 0.94 g/dL. The mean decrease in the hematocrit level was 6% +/- 2% and the mean increase in total blood volume was 731 +/- 337 mL. These changes were explained by a mean decrease in red blood mass of 106 +/- 109 mL and a mean increase in plasma volume of 743 +/- 289 mL. The decrease in red blood cell mass was largely explained by phlebotomy during the hospitalization, but was not statistically significant (paired t-test, P = .06). All other changes were statistically significant (P < .05). Simple regression analysis indicated that the decrease in hematocrit level and increase in plasma volume were related (y = -1.78 - .0066X; R = -.74). Measurements of lactate dehydrogenase, bilirubin, haptoglobin, and reticulocyte counts and serial stool hemoccults did not indicate hemolysis or blood loss. We conclude that the anemia caused by IL-6 is caused by an increase in plasma volume.

Erythropoiesis in pregnancy.

There is a dramatic increase in total blood volume during healthy pregnancy. The disproportionate expansion in plasma volume (50%) and red cell mass (18-25% depending on iron status) results in a decrease in haemoglobin concentration maximal at 32 weeks gestation. This should not fall below 11 g/dl at any time during pregnancy. Deficiency of essential haematinics arising from increased requirements and inadequate intake may have far reaching effects on mother, fetus and neonate which bear no relationship to the impaired oxygen carrying capacity of the reduced cell mass. Pathological anaemia of pregnancy is due to over 90% of cases to iron deficiency associated with depleted stores and deficient intake. The single largest demand for iron arises from the increased red cell mass under the influence of erythropoietin. Tissue enzyme malfunction occurs even in the very first stages of iron deficiency before significant anaemia develops. Increased blood loss at delivery and preterm birth are observed associated complications. Off-spring of iron deficient mothers have decreased iron stores and may develop anaemia in the first year of life. Studies have shown behavioural abnormalities in children with iron deficiency and poor performance in the Bayley Mental Developmental Index. The poor performance in mental and motor development can be improved to the level of iron-sufficient infants by treatment with ferrous sulphate. Folate deficiency often accompanies iron deficiency as they are both associated with a poor diet. The haematological effects of folate deficiency are usually masked by iron deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Nitrates in congestive heart failure.

Nitrates are commonly used in the therapy of congestive heart failure (CHF). They exert beneficial hemodynamic effects by decreasing left ventricular filling pressure and systemic vascular resistance while modestly improving cardiac output. The improvement in left ventricular function caused by nitrates is the result of combined reduction in outflow resistance and mitral regurgitation, while decreased pericardial constraint and subendocardial ischemia may also contribute to the process. With continuous nitrate administration, complete arterial tolerance develops, while venous tolerance appears to be only partial. The major mechanism of tolerance is loss of vascular smooth muscle sensitivity to nitrates. An increase in total blood volume occurring during the first few hours of an acute administration may partly contribute to tolerance. The importance of reflex neurohumoral activation is controversial; although it may contribute to tolerance in CHF, its role does not appear to be major. Chronic continuous nitrate therapy in CHF improves submaximal and maximal exercise tolerance. In combination therapy with hydralazine, isosorbide dinitrate reduces mortality, although to a lesser extent than the angiotensin converting enzyme inhibitor enalapril. Intravenous or sublingual nitrates are first-line agents in the therapy of acute pulmonary edema. In severe CHF, refractory to standard medical therapy, a short course of intravenous nitroglycerin, with or without inotropic agents, can help break the vicious spiral of CHF. Because tolerance occurs without nitrate-free intervals and until an optimal schedule of administration is determined, it makes good sense to include a nightly nitrate-free interval when prescribing nitrates for CHF in order to maintain maximal benefit during the hours of activity.

Serum immunoreactive erythropoietin and red blood cell mass during pregnancy in conscious rats

Serum erythropoietin concentration increases during human pregnancy and presumably accounts for expansion of red blood cell mass. The mechanism(s) underlying gestational changes of serum erythropoietin are unknown. Moreover, if erythropoietin synthesis increases, then the organ(s) questions about erythropoietin in pregnancy, we first set out to establish an animal model. Chronically instrumented, conscious unrestrained rats were studied. 51Cr-labeled red blood cells and radioimmunoassay were used to assess red blood cell mass and serum erythropoietin, respectively. Except for a lower hematocrit (P < 0.05 vs. virgin rats) and a slightly higher plasma volume (P value not significant) for gravid rats on gestational day 6, all other variables measured in early pregnancy rats were comparable to those measured in virgin control animals. Significant increases in total blood volume, plasma volume, and red blood cell mass were observed by gestational day 13 (midpregnancy) when compared with virgin control rats. These changes were even more pronounced on gestational day 20. Serum immunoreactive erythropoietin was also significantly increased at both of these stages of pregnancy. We conclude that the gravid rat is a reliable animal model of human gestation in which to further investigate erythropoietin in pregnancy.

Transesophageal echocardiography: a useful monitor for the anesthetic management of cesarean section in a woman with dilated cardiomyopathy

Both peripartum cardiomyopathy (PPCM) and idiopathic dilated cardiomyopathy (IDCM) should be considered in pregnant patients presenting with symptoms of congestive heart failure.’ Cardiovascular changes associated with pregnancy, such as an increase in total blood volume and cardiac output, peak early in the third trimester and, for a second time, during labor and immediately after delivery.* These changes progressively stress cardiac reserve and may contribute to overt compromise of pump performance in patients with preexisting heart disease. Therefore patients suffering from IDCM, as was our patient, usually present with signs of acute cardiac decompensation before or during the third trimester of pregnancy.3 In contrast, patients with PPCM present with signs of cardiac failure in the last month of pregnancy or, in the majority of cases, during the 6 months after childbirth.4-6 We report the case of a woman who developed congestive heart failure early in the third trimester of pregnancy. We present our experience with twodimensional transesophageal echocardiography (TEE) used as a monitor of cardiac function and intravascular volume status during operative delivery. These findings are supplemented by echocardiographic data acquired during the initial clinical assessment and a follow-up 3 months after delivery. The patient was a 28year-old gravida 4 para 2, 153 cm, 65 kg woman who presented at 28 weeks gestation with orthopnea, shortness of breath and dyspnea on exertion. She had received no antenatal care because, as a refugee from Albania, she was

Pathophysiology of ascites formation in cirrhosis of the liver.

Current concepts of the pathophysiology of ascites formation in cirrhosis of the liver have become more complex. Traditionally, the initiating event of renal sodium and water retention in cirrhosis was considered to be ascites formation ("underfilling" hypothesis) or primary renal dysfunction ("overflow" hypothesis). Changes in systemic, splanchnic and renal hemodynamics, as well as of volume regulating hormones observed in cirrhosis are compatible with a decrease in effective blood volume as suggested by the "underfilling" hypothesis. These changes, however, have been shown to precede ascites formation. This observation, together with the demonstration of an increase in total blood volume in cirrhosis prompted the "overflow" hypothesis. However, many studies are incompatible with this concept and, in addition, the agent causing primary renal sodium retention in cirrhosis still remains to be defined. The recently proposed "vasodilation" hypothesis reconciles the most salient features of both theories, proposing peripheral arterial vasodilation as the initiating event of decreased effective blood volume and renal sodium retention. Further studies are needed to elucidate the temporal relationship and more precisely define the character of hemodynamic, humoral and renal changes in cirrhosis of the liver.

The effects of rapid infusions of saline and mannitol on cerebral blood volume and intracranial pressure in dogs.

The role of osmotic brain dehydration in the early reduction of intracranial pressure (ICP) following mannitol administration has recently been questioned and a decrease in cerebral blood volume (CBV) proposed as the mechanism of action. To evaluate this hypothesis, relative CBV changes before and after mannitol infusion were determined by collimated gamma counting across the biparietal diameter of the exposed skull in six dogs. Red blood cells were labelled with chromium-51. Cerebral blood volume (CBV), total blood volume (TBV), ICP, mean arterial pressure (MAP), central venous pressure (CVP), haematocrit and osmolality were serially measured after infusions of 10 ml X kg-1 of normal saline (control study) and of 20 per cent mannitol (mannitol study). The solutions were administered over a two-minute period; a 30-minute equilibration period intervened between the saline and mannitol infusions. We demonstrated that the mannitol infusion was associated with significant increases in relative CBV (25 per cent), ICP (7 mmHg), CVP (11 cm H2O), and TBV (50 per cent). MAP declined significantly (14 per cent) after mannitol infusion. The administration of saline, although associated with an increase in TBV (18 per cent), was not associated with any significant change in CBV, ICP, MAP or CVP. The increase in relative CBV persisted for 15 minutes after mannitol infusion, while the ICP returned to control within five minutes and continued to decrease. This study supports the fact that after rapid mannitol infusion, ICP begins to decrease only once the dehydrating effect has counteracted the increase in brain bulk caused by the increase in cerebral blood volume.

The blood volume in pheochromocytoma patients before and during treatment with phenoxybenzamine.

Total blood volume (TBV), red cell volume (RCV) and plasma volume (PV) were determined in 15 pheochromocytoma patients (9 males and 6 females) prior to and during preoperative treatment with phenoxybenzamine. Seventeen healthy male volunteers served as controls. Untreated male patients did not differ from the controls with respect to TBV, RCV or PV. In the total group of pheochromocytoma patients, phenoxybenzamine, in a dose of 145.6 +/- 45.2 (SD) mg/day over 14.3 +/- 5.7 (SD) days, induced significant increases in TBV (+9.4%) and PV (+14.5%), whereas RCV remained unchanged. During phenoxybenzamine, the mean PV in male patients significantly exceeded the control mean. We conclude that pheochromocytoma patients adapt their TBV to excessive catecholamine production and that they rarely present with profound hypovolemia. Moderate but higher doses of phenoxybenzamine than previously recommended induced marked increases in TBV secondary to PV expansion. Phenoxybenzamine counteracts the development of hypovolemia most effectively, thereby constituting one of several important measures for successful surgical management of pheochromocytoma patients.