DOCSLIB.ORG

The Pivotal Role of Adrenomedullin in Producing Hyperdynamic Circulation During the Early Stage of Sepsis

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
The Pivotal Role of Adrenomedullin in Producing Hyperdynamic Circulation During the Early Stage of Sepsis PAPER The Pivotal Role of Adrenomedullin in Producing Hyperdynamic Circulation During the Early Stage of Sepsis Ping Wang, MD; Zheng F. Ba; William G. Cioffi, MD; Kirby I. Bland, MD; Irshad H. Chaudry, PhD Background: Initial cardiovascular responses during sep- Results: Cardiac output, stroke volume, and microvas- sis are characterized by hyperdynamic circulation. Al- cular blood flow in the liver, small intestine, kidney, and though studies have shown that a novel potent vasodi- spleen increased, and total peripheral resistance de- latory peptide, adrenomedullin (ADM), is up-regulated creased 0 and 30 minutes after ADM infusion. In addi- under such conditions, it remains unknown whether ADM tion, plasma levels of ADM increased from the preinfu- is responsible for initiating the hyperdynamic response. sion level of 92.7 ± 5.3 to 691.1 ± 28.2 pg/mL 30 minutes after ADM infusion, which was similar to ADM levels ob- Objective: To determine whether increased ADM re- served during early sepsis. Moreover, 5 hours after the lease during early sepsis plays any major role in produc- onset of sepsis, cardiac output, stroke volume, and mi- ing hyperdynamic circulation. crovascular blood flow in various organs increased and total peripheral resistance decreased. Administration of Design, Intervention, and Main Outcome Measure: anti-ADM antibodies, however, prevented the occur- Synthetic rat ADM (8.5 µg/kg of body weight) was infused rence of the hyperdynamic response. intravenously in normal rats for 15 minutes at a constant rate.Cardiacoutput,strokevolume,andmicrovascularblood Conclusions: The results suggest that increased ADM flow in various organs were determined immediately as well production and/or release plays a major role in produc- as 30 minutes after ADM infusion. At 30 minutes after in- ing hyperdynamic responses during early sepsis. Since fusion, plasma ADM level was also measured. In additional our previous studies have shown that vascular respon- groups, rats were subjected to sepsis by cecal ligation and siveness to ADM decreases in late sepsis, maintenance puncture. At 1.5 hours after cecal ligation and puncture, of ADM vascular responsiveness by pharmacological specific anti–rat ADM antibodies were infused, which com- agents during the course of sepsis may prevent transi- pletely neutralized the circulating ADM. Various hemody- tion from the hyperdynamic to the hypodynamic state. namic variables were measured 5 hours after cecal ligation and puncture (ie, the early stage of sepsis). Arch Surg. 1998;133:1298-1304 ESPITE ADVANCES in the leadstoaprogressivedeteriorationofcelland treatmentofsepticpatients, organfunctionsandeventualmortality.Thus, a large number of such pa- it is important to identify the mediator(s) re- tients subsequently die of sponsible for producing hyperdynamic cir- ensuing septic shock and culation during the early stage of sepsis. Dmultiple-organ failure. Septic shock and Adrenomedullin (ADM) is a potent va- multiple-organfailurecontinuetobethemost sodilatory peptide (52–amino acid resi- common causes of death in surgical inten- dues in the human and 50–amino acid resi- sive care units, and the incidence of sepsis dues in the rat) that was first purified in 1993 has increased substantially during the past from human pheochromocytomas.4 The va- 2 decades.1,2 Polymicrobial sepsis is charac- sodilatory effect of ADM is thought to be pri- terized by an initial hyperdynamic phase fol- marily mediated through specific ADM re- lowed by a late hypodynamic phase.2,3 How- ceptors,5 which are functionally coupled to ever, the mechanism responsible for produc- adenylate cyclase via G proteins.6 Adreno- ing the transition from the hyperdynamic to From the Center for Surgical the hypodynamic state remains unknown. Research and Department of It is possible that the factor(s) responsible for thetransitionofhemodynamicresponsesdur- This article is also available on our Surgery, Brown University Web site: www.ama-assn.org/surgery. School of Medicine and Rhode ing sepsis is not fully understood and con- Island Hospital, Providence, RI. sequently not prevented, and such factor(s) ARCH SURG/ VOL 133, DEC 1998 1298 ©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 10/01/2021 MATERIALS AND METHODS of incision was bathed with 1% lidocaine hydrochloride to provide analgesia throughout the study period. Sham- operated-on animals underwent the same surgical proce- The experiments described herein were performed in ad- dure except that the cecum was neither ligated nor punc- herence to the National Institutes of Health guidelines for tured. Plasma ADM was neutralized by intravenous the use of experimental animals. This project was ap- administration of specific anti-ADM (rat) antisera (ie, poly- proved by the Institutional Animal Care and Use Commit- clonal antibodies; host: rabbit; Peninsula Laboratories) 1.5 tee of Rhode Island Hospital, Providence. hours after CLP. A total of 0.5 mL of isotonic sodium chlo- ride solution containing 8 µL of undiluted anti-ADM anti- INTRAVENOUS INFUSION sera (according to Peninsula Laboratories information, this OF SYNTHETIC RAT ADM dose of anti-ADM antibodies is adequate to neutralize plasma ADM during early sepsis) was given and various hemody- Male Sprague-Dawley rats (Charles River Laboratory, Wilm- namic measures were determined 5 hours after CLP (n = 5 ington, Mass), weighing 275 to 325 g, were fasted for 16 hours per group). It should be noted that 5 hours after CLP rep- before the experiment but were allowed water ad libitum. resents a typical time point of the early, hyperdynamic stage The animals were anesthetized with methoxyflurane inha- of polymicrobial sepsis.3 Vehicle-treated septic animals re- lation and the left femoral artery was cannulated with poly- ceived 0.5 mL of isotonic sodium chloride solution. ethylene 50 tubing (Becton Dickinson, Sparks, Md) for mea- surement of mean arterial pressure and heart rate or DETERMINATION OF CARDIAC OUTPUT withdrawal of blood samples for ADM assays. The right fem- AND MICROVASCULAR BLOOD FLOW oral vein was cannulated with polyethylene 10 tubing for ADM administration. Subsequent anesthesia was main- Cardiac output (CO) was measured by an indocyanine green tained by intravenous injection of pentobarbital sodium (ap- dilution technique with a 2.4 F fiberoptic catheter and in proximately 30 mg/kg of body weight). After 30 to 60 min- vivo hemoreflectometer, as we described previously.11 The utes of stabilization, synthetic rat ADM 1-50 (Peninsula CO was calculated according to the principle of dye dilu- Laboratories, Belmont, Calif) at a dose of 8.5 µg/kg of body tion. Stroke volume and total peripheral resistance (TPR) weight in 0.5 mL of isotonic sodium chloride solution con- were then calculated. Microvascular blood flow on the sur- taining 0.2% bovine serum albumin or 0.5 mL of vehicle (ie, face of the liver, small intestine, kidney, and spleen was de- isotonic sodium chloride solution with 0.2% bovine serum termined by laser Doppler flowmetry (Laserflo, Model BPM albumin) was infused via the femoral venous catheter dur- 403A; TSI Inc, St Paul, Minn).11 The measured microvas- ing 15 minutes at a constant infusion rate (n = 5 per group). cular blood flow was the microvascular red blood cell flux Various hemodynamic variables were measured immedi- in approximately 1 mm3 on the surface of each organ with ately as well as 30 minutes after the completion of ADM or a unit of milliliters per minute per 100 g of tissue, as indi- vehicle infusion. The mean arterial pressure and heart rate cated by the manufacturer. Although this is a reliable tech- were monitored by a blood pressure analyzer (Micro-Med, nique for determining the alterations in organ surface per- Louisville, Ky). The animals were then killed at the end of fusion, the flow unit suggested by the manufacturer should the experiment by an overdose of pentobarbital sodium. be considered as arbitrary rather than absolute units. ANIMAL MODEL OF EARLY SEPSIS DETERMINATION OF PLASMA ADM AND ADMINISTRATION OF ANTI-ADM ANTIBODIES By means of a radioimmunoassay kit specific for rat ADM (Peninsula Laboratories), plasma levels of ADM were as- Polymicrobial sepsis was induced in male Sprague- sayed according to the procedure provided by the manu- Dawley rats (275-325 g) by CLP according to the method facturer. Briefly, 1.5-mL blood samples were collected into of Chaudry et al.10 Briefly, rats were fasted overnight be- a polypropylene tube containing EDTA (1 mg/mL) and apro- fore the induction of sepsis but allowed water ad libitum. tinin (500 kU/mL) at various time points after CLP and The animals were anesthetized with methoxyflurane inha- plasma was separated immediately. The rat ADM assay does lation, and a 2-cm ventral midline incision was made. The not have any cross-reactivity with human ADM, amykin, cecum was then exposed, ligated just distal to the ileoce- or endothelin 1. cal valve to avoid intestinal obstruction, punctured twice with an 18-gauge needle, and returned to the abdominal STATISTICAL ANALYSIS cavity. The abdominal incision was then closed in layers, and the animal received isotonic sodium chloride solu- One-way analysis of variance and Tukey test or Student t tion, 3 mL per 100 g of body weight, subcutaneously im- test were used, and the differences were considered sig- mediately after CLP (ie, fluid resuscitation). The area nificant at P#.05. Results are presented as mean ± SEM. medullin also stimulates Ca2+ mobilization
Load more

Recommended publications
  • Cardiac Dysfunction and Lactic Acidosis During Hyperdynamic and Hypovolemic Shock
    è - \-o(J THESIS FOR TIIE DEGREE OF DOCTOR OF MEDICINE CARDIAC DYSFUNCTION AND LACTIC ACIDOSIS DURING HYPERDYNAMIC AND HYPOVOLEMIC SHOCK DAVID JAMES COOPER DEPARTMENT OF ANAESTIIESIA AND INTENSIVE CARE FACULTY OF MEDICINE UNIVERSITY OF ADELAIDE Submitted: October,1995 Submitted in revised form: November, 1996 2 J TABLE OF CONTENTS Page 5 CH 1(1.1) Abstract (1.2) Signed statement (1.3) Authors contribution to each publication (1.4) Acknowledgments (1.5) Publications arising 9 CH2Introduction (2.1) Shock and lactic acidosis (2.2) Cardiac dysfunction and therapies during lactic acidosis (2.3) Cardiac dysfunction during hyperdynamic shock (2.4) Cardiac dysfunction during hypovolemic shock (2.5) Cardiac dysfunction during ionised hypocalcaemia l7 CH3 Methods (3. 1) Left ventricular function assessment - introduction (3.2) Left ventricular function assessment in an animal model 3.2.I Introduction 3.2.2 Anaesthesia 3.2.3 Instrumentation 3.2.4 Systolic left ventricular contractility 3.2.5 Left ventricular diastolic mechanics 3.2.6 Yentricular function curves 3.2.1 Limitations of the animal model (3.3) Left ventricular function assessment in human volunteers 3.3.7 Left ventricular end-systolic pressure measurement 3.3.2 Left ventricular dimension measurement 3.3.3 Rate corrected velocity of circumferential fibre shortening (v"¡.) 3.3.4. Left ventricular end-systolic meridional wall stress (o"r) 4 33 CH 4 Cardiac dysfunction during lactic acidosis (4.1) Introduction 4.7.1 Case report (4.2) Human studies 4.2.1 Bicarbonate in critically ill patients
    [Show full text]
  • Cardiac Function and Haemodynamics in Alcoholic Cirrhosis and Evects of the Transjugular Intrahepatic Portosystemic Stent Shunt
    Gut 1999;44:743–748 743 Cardiac function and haemodynamics in alcoholic cirrhosis and eVects of the transjugular Gut: first published as 10.1136/gut.44.5.743 on 1 May 1999. Downloaded from intrahepatic portosystemic stent shunt M Huonker, Y O Schumacher, A Ochs, S Sorichter, J Keul, M Rössle Abstract seem to be mainly responsible for the fur- Background—A portosystemic stent ther decrease in systemic vascular resist- shunt may impair cardiac function and ance. TIPS may unmask a coexisting haemodynamics. preclinical cardiomyopathy in patients Aims—To investigate the eVects of a tran- with alcoholic cirrhosis and portal hyper- sjugular intrahepatic portosystemic shunt tension. (TIPS) on cardiac function and pulmo- (Gut 1999;44:743–748) nary and systemic circulation in patients Keywords: alcoholic cirrhosis; portosystemic stent with alcoholic cirrhosis. shunt; cirrhotic cardiomyopathy; ventricular function; Patients/Methods—17 patients with alco- pulmonary circulation; systemic circulation holic cirrhosis and recent variceal bleed- ing were evaluated by echocardiography and catheterisation of the splanchnic and It has been known for more than four decades pulmonary circulation before and after that hepatic cirrhosis is associated with cardio- TIPS. The period of catheter measure- vascular abnormalities. The initial studies per- ment was extended to nine hours in nine of formed in the early 1950s documented the the patients. The portal vein was investi- existence of a hyperdynamic circulation in cir- gated by Doppler ultrasound before and rhosis, manifested by increased cardiac output nine hours after TIPS. and reduced systemic vascular resistance.1 Results—Baseline echocardiography Overt heart failure is generally not a prominent showed the left atrial diameter to be feature of hepatic cirrhosis, because the marked slightly increased and the left ventricular peripheral vasodilation reduces the afterload of volume to be in the upper normal range.
    [Show full text]
  • Regulation of the Cerebral Circulation: Bedside Assessment and Clinical Implications Joseph Donnelly1, Karol P
    Donnelly et al. Critical Care 2016, 18: http://ccforum.com/content/18/6/ REVIEW Open Access Regulation of the cerebral circulation: bedside assessment and clinical implications Joseph Donnelly1, Karol P. Budohoski1, Peter Smielewski1 and Marek Czosnyka1,2* Abstract Regulation of the cerebral circulation relies on the complex interplay between cardiovascular, respiratory, and neural physiology. In health, these physiologic systems act to maintain an adequate cerebral blood flow (CBF) through modulation of hydrodynamic parameters; the resistance of cerebral vessels, and the arterial, intracranial, and venous pressures. In critical illness, however, one or more of these parameters can be compromised, raising the possibility of disturbed CBF regulation and its pathophysiologic sequelae. Rigorous assessment of the cerebral circulation requires not only measuring CBF and its hydrodynamic determinants but also assessing the stability of CBF in response to changes in arterial pressure (cerebral autoregulation), the reactivity of CBF to a vasodilator (carbon dioxide reactivity, for example), and the dynamic regulation of arterial pressure (baroreceptor sensitivity). Ideally, cerebral circulation monitors in critical care should be continuous, physically robust, allow for both regional and global CBF assessment, and be conducive to application at the bedside. Regulation of the cerebral circulation is impaired not only in primary neurologic conditions that affect the vasculature such as subarachnoid haemorrhage and stroke, but also in conditions that affect the regulation of intracranial pressure (such as traumatic brain injury and hydrocephalus) or arterial blood pressure (sepsis or cardiac dysfunction). Importantly, this impairment is often associated with poor patient outcome. At present, assessment of the cerebral circulation is primarily used as a research tool to elucidate pathophysiology or prognosis.
    [Show full text]
  • The Impact of Arteriovenous Fistula Formation on Central Hemodynamic Pressures in Chronic Renal Failure Patients: a Prospective Study M
    The Impact of Arteriovenous Fistula Formation on Central Hemodynamic Pressures in Chronic Renal Failure Patients: A Prospective Study M. Tessa Savage, PhD, Charles J. Ferro, MD, Antonio Sassano, MSc, and Charles R.V. Tomson, DM ● Background: The presence of an arteriovenous (AV) fistula creates permanently high cardiac output. This may cause an imbalance between available cardiac oxygen supply in response to greater demand and increased arterial stiffness. Methods: Surrogate markers of subendocardial perfusion (subendocardial viability ratio [SEVR]) and arterial stiffness (augmentation index [AIx]) can be measured noninvasively by using pulse wave analysis on the radial pulse to obtain central pressures. We prospectively followed up nine patients with chronic renal failure (CRF) undergoing creation of an AV fistula for vascular access at regular intervals over 6 months. Results: After surgery, blood pressure and heart rate remained unchanged throughout the study period. AIx stayed the same (baseline versus 6 months, 20% ؎ 11% versus 22% ؎ 15%), but there was a decrease in SEVR immediately after surgery (؊9% P < 0.05) that persisted for at least 3 months (؊14% ؎ 7%; P < 0.01). At 6 months, SEVR remained below ;5% ؎ ;baseline values in all but one patient (mean SEVR at baseline, 166% ؎ 22% versus 6 months, 150% ؎ 20%; P < 0.05 ؊9% ؎ 7%). Conclusion: Creation of an AV fistula may directly predispose patients with CRF to a risk for myocardial ischemia caused by an adverse imbalance between subendocardial oxygen supply and increased oxygen demand consequent to a greater cardiac output. © 2002 by the National Kidney Foundation, Inc. INDEX WORDS: Chronic renal failure (CRF); arteriovenous (AV) fistula; pulse wave analysis; augmentation index (AIx); subendocardial viability ratio (SEVR).
    [Show full text]
  • Echocardiography in Pregnant Women Gebelikte Ekokardiyografinin Yeri
    Education E¤itim 169 Echocardiography in pregnant women Gebelikte ekokardiyografinin yeri Nurgül Keser University of Maltepe, Istanbul, Turkey ABSTRACT Beyond evaluating physiologic alterations encountered during pregnancy quantitative pulsed- and continuous Doppler and qualitative co- lor Doppler technology can be used for cardiovascular assessment of the pregnant woman with heart disease or suspected cardiac ab- normality. Echocardiography provides information about disease etiology, leads to accurate and non- invasive assessment of disease se- verity and is a powerful means of monitoring progression. Only with echocardiography it has been clearly demonstrated that during preg- nancy congenital heart disease is the first leading abnormality followed by rheumatic heart disease. Doppler and qualitative color Dopp- ler are useful to illuminate the pathophysiology of the hemodynamic consequences of fixed valve stenosis during pregnancy with respect to the labile nature of gradients resulting from variable loading conditions of pregnancy. Accurate cardiac diagnosis leads to accurate es- timation of prognosis, illuminates the necessity of noninvasive monitoring throughout pregnancy and labor, and leads to determine whet- her surgical or medical intervention should be performed. Need for Fetal echocardiography should also be considered after maternal ec- hocardiography is undertaken. Although there are no strictly defined limits established for the use of Doppler ultrasound in the early preg- nancy there is an unequivocal demand for carefulness
    [Show full text]
  • Wide Pulse Pressure and Quincke's Pulse in High-Output Heart Failure
    Case report BMJ Case Rep: first published as 10.1136/bcr-2021-241654 on 22 July 2021. Downloaded from Wide pulse pressure and Quincke’s pulse in high- output heart failure Katie Lin Berry,1 Peter D Sullivan,2 André Martin Mansoor 2 1School of Medicine, Oregon SUMMARY progressive exertional dyspnoea and weight gain. The Health & Science University, A 74-year -old man with a history of chronic alcohol use patient reported drinking three to four glasses of wine Portland, Oregon, USA 2 presented with progressive exertional dyspnoea and daily for at least 10 years. Physical examination was Department of Medicine, weight gain. On physical examination, he was noted notable for a body mass index of 34.3 kg/m2, blood Oregon Health & Science to have wide pulse pressure, elevated jugular venous pressure of 177/56 mm Hg, dependent pitting periph- University, Portland, Oregon, pressure, and alternating flushing and blanching of eral oedema, jugular venous pressure of 18 cm H O USA 2 the nail beds in concert with the cardiac cycle, known with a normal waveform, unremarkable S1 and S2 Correspondence to as Quincke’s pulse. Transthoracic echocardiography without extra transient sounds or murmurs, and subun- Dr André Martin Mansoor; demonstrated normal biventricular systolic function gual capillary pulsations (Quincke’s pulse) (video 1). mansooan@ ohsu. edu and valvular function, but noted a dilated inferior vena cava. Right heart catheterisation revealed elevated Accepted 1 July 2021 filling pressures, high cardiac output and low systemic INVESTIGATIONS vascular resistance, consistent with high-output heart Laboratory data were notable for haemoglobin of failure.
    [Show full text]
  • Watson's Water Hammer Pulse
    Clinical Signs www.jpgmonline.com Watson’s water hammer pulse Suvarna JC Department of Pediatrics, atson’s water hammer pulse (whp), also known as collapsing pulse, cannonball pulse or Seth GS Medical College W pulsus celer, is used to describe a pulse with a rapid upstroke and descent, characteristically and KEM Hospital, Parel, described in aortic regurgitation.[1] Although the term Corrigan’s pulse has been used at times Mumbai - 400 012, India synonymously with whp, Corrigan’s pulse/sign is largely used to describe the abrupt distension and quick collapse of carotid pulse in aortic regurgitation whereas the term ‘water hammer pulse’ is CCorrespondence:orrespondence: used for the characteristic pulse seen in peripheral arteries like the radial artery. It may be seen in a Suvarna Jyoti C [2] E-mail: [email protected] number of other conditions and with hyperdynamic circulation. History Sir Dominic John Corrigan a British pathologist, in 1833 at a young age of 30, described the visible abrupt distension and collapse of the carotid arteries in patients with aortic insufficiency. However, the similarity of the palpable characteristics of the pulse in aortic insufficiency and that of a 19th century Received : 14-10-07 Victorian ‘water hammer toy’ was pointed out by Thomas Watson in the year 1844. Therefore the [1] Review completed : 01-01-08 eponym, ‘Watson pulse’ substituted ‘Corrigan pulse’. The ‘water hammer toy’ is a hermetically sealed Accepted : 25-02-08 glass tube partly filled with water and exhausted of air. When reversed or shaken, the water being PubMed ID : 18480541 unimpeded by air strikes the sides or ends with the sound and impact of a hammer.[3] The characteristic J Postgrad Med 2008;54:163-5 collapsing carotid pulse seen in aortic regurgitation is still referred to as Corrigan’s sign.[1] Method to Elicit the ‘Water Hammer Pulse’ filling of the radial artery in systole due to an extra large amount of blood pushed by the distended left ventricle into relatively Patient is made to recline.
    [Show full text]
  • Pulmonary Hypertension Post Liver-Kidney Transplant
    CONTRIBUTION Pulmonary Hypertension Post Liver-Kidney Transplant HAFIZ IMRAN, MD; MATTHEW JANKOWICH, MD; GAURAV CHOUDHARY, MD 23 26 EN ABSTRACT pulmonary pressures on echocardiogram 9 months after Porto-pulmonary hypertension has been recently rec- simultaneous liver-kidney transplants. The patient received ognized in patients post-liver transplantation with or deceased donor simultaneous liver-kidney transplants for without pre-transplant hepatopulmonary syndrome. We liver cirrhosis (secondary to chronic hepatitis C infection present a unique case of pulmonary hypertension in a and alcohol use) and end-stage renal disease (secondary to 65-year-old patient after simultaneous liver-kidney trans- diabetic nephropathy). The patient’s medical history was sig- plantation for cirrhosis secondary to chronic hepatitis C nificant for systemic hypertension, diabetes mellitus with infection and alcohol use disorder and end-stage renal diabetic nephropathy and neuropathy and permanent atrial disease secondary to diabetic nephropathy. He presented fibrillation. The patient had quit drinking and smoking 8 to pulmonary hypertension clinic with progressive short- years ago after 50-pack years and had denied any illicit sub- ness of breath and elevated right-sided pulmonary pres- stance use since then. His pre-transplant course was compli- sures on echocardiogram. He did not have pre-transplant cated by portal hypertension, ascites and variceal bleeding hepatopulmonary syndrome and his post-transplant liver requiring band ligation and hepatocellular carcinoma treated and kidney functions were normal. His right heart cath- with radiofrequency ablation. His pre-transplant echocar- eterization showed normal capillary wedge pressure, diogram showed normal left ventricular systolic function elevated mean pulmonary artery pressure and high pul- (Ejection Fraction- 65–70%) with severe left atrial dilata- monary vascular resistance with normal cardiac index.
    [Show full text]
  • Maternal Left Ventricular Mass and Diastolic Function During Pregnancy Kametas Et Al
    Ultrasound Obstet Gynecol 2001; 18: 460–466 BlackwellMaternal Science Ltd left ventricular mass and diastolic function during pregnancy N. A. KAMETAS, F. McAULIFFE, J. HANCOCK*, J. CHAMBERS† and K. H. NICOLAIDES Harris Birthright Research Centre for Fetal Medicine and *Cardiac Department, King’s College Hospital and †Cardiothoracic Centre, Guy’s and St Thomas’s Hospitals, London, UK KEYWORDS: Echocardiography, Left ventricular diastolic function, Left ventricular mass, Pregnancy, Transmitral velocities symptomatic phase of the disease and a subsequent depletion ABSTRACT of the intravascular space coinciding with the onset of the Objective To evaluate changes in left ventricular mass and clinical syndrome2–4. Furthermore, there is evidence that diastolic function during normal pregnancy. pregnancies complicated by intrauterine growth restriction are associated with impaired expansion of the maternal Methods This was a cross-sectional study of 125 pregnant intravascular space and a lack of increase in cardiac output women at 9–42 weeks of gestation and 19 non-pregnant female from 4 to 5 weeks of gestation5. It is thus evident that the controls. Two-dimensional and M-mode echocardiography study of maternal cardiovascular adaptation during pregnancy of the maternal left ventricle and left atrium was performed. provides an insight into the interaction between maternal and Results During pregnancy left ventricular mass increased by fetal homeostasis and may prove a useful screening tool for 52%. There was an increase in left ventricular end-diastolic pregnancy complications. and end-systolic diameters (12% and 20%, respectively), left Although impairment of diastolic function of the left ventricular posterior wall diameter during diastole and systole ventricle (LV) precedes systolic dysfunction in the evolution 6,7 (22% and 13%, respectively) and left intraventricular septum of most cardiac diseases there is a scarcity of reports on during diastole and systole (15% and 19%, respectively).
    [Show full text]
  • Acute Liver Failure
    Acute Liver Failure A. W. HOLT Department of Critical Care Medicine, Flinders Medical Centre, Adelaide, SOUTH AUSTRALIA ABSTRACT Objective: To consider the classification and to present an approach to the diagnosis and management of complications associated with acute liver failure. Data sources: A review of studies reported from 1966 to 1998 and identified through a MEDLINE search on treatment of acute liver failure. Summary of review: Acute liver failure can be subdivided into hyperacute, (encephalopathy within 7 days of onset of jaundice) acute (8-28 days from jaundice to encephalopathy) and subacute (29 to 72 days from jaundice to encephalopathy) forms. Management of all forms involves largely supportive care until hepatocyte regeneration and recovery occurs (predominantly in the hyperacute group), or bridging supportive therapy until orthotopic liver transplantation can be performed. New therapies such as bioartificial liver support devices and ex-vivo liver perfusion offer exciting possibilities for this bridging therapy. While orthotopic liver transplantation remains the definitive treatment for many patients with acute liver failure, N- acetyl-cystine (150 mg/kg over 15 minutes followed by 12.5 mg/kg/hour) and PGE1 (10 – 40 µg/hour) are reported to have an additional role and are being used increasingly in the management of all forms of acute liver failure. Conclusions: Acute liver failure is the end stage of many acute viral and drug induced hepatic diseases. Management is largely supportive until hepatic repair or transplantation can be performed. Recently, additional hepatic protective, regenerative and supportive therapies have been successfully used. (Critical Care and Resuscitation 1999; 1: 25-38) Key words: Acute liver failure, hepato-renal syndrome, hepatic encephalopathy, cerebral oedema, liver assist device, orthotropic liver transplantation Classification King’s group, the French do not recognise the Two different classifications of acute liver failure ‘hyperacute’group.
    [Show full text]
  • Cardiovascular Effects of Mechanical Ventilation
    Cardiovascular Effects of Mechanical Ventilation G. J. DUKE Intensive Care Department, The Northern Hospital, Epping, VICTORIA ABSTRACT Objective: To review the cardiovascular effects of spontaneous breathing and mechanical ventilation in healthy and pathological states. Data sources: A review of articles published in peer-reviewed journals from 1966 to 1998 and identified through a MEDLINE search on cardiopulmonary interaction. Summary of review: Respiration has a hydraulic influence upon cardiovascular function. Pulmonary and cardiac pathology alter this interaction. Spontaneous inspiration increases right ventricular (RV) preload and left ventricular (LV) afterload. Mechanical ventilation with positive pressure (MV) reduces LV preload and afterload. The influence of MV upon the cardiovascular system (CVS), particularly in critically ill patients, depends upon the mode of ventilation and the pre-existing cardiac and respiratory status. The influence of these factors is reviewed. Consideration of these parameters will enable the clinician to predict the likely effect of MV and develop strategies to minimise adverse events. Conclusions: Mechanical ventilation has an adverse effect upon the CVS in healthy subjects and in patients with pulmonary pathology, particularly in the presence of preload-dependent LV dysfunction or afterload-induced RV dysfunction. Mechanical ventilation may benefit cardiac function in patients with respiratory failure and afterload-dependent or exercise-induced LV dysfunction. (Critical Care and Resuscitation 1999;
    [Show full text]
  • Pulse 1 Pulse
    Pulse 1 Pulse In medicine, a person's pulse is the arterial palpation of a heartbeat.[1] It can be felt in any place that allows for an artery to be compressed against a bone, such as at the neck (carotid artery), at the wrist (radial artery), behind the knee (popliteal artery), on the inside of the elbow (brachial artery), and near the ankle joint (posterior tibial artery). The pulse rate can also be measured by measuring the heart beat directly (auscultation), usually using a stethoscope. Physiology The pulse is a decidedly low tech/high yield and antiquated term still useful at the bedside in an age of computational analysis of cardiac performance. Claudius Galen (129AD?) was perhaps the first physiologist to describe the pulse. The pulse is an expedient tactile method of determination of systolic blood pressure to a trained observer. Diastolic blood pressure is non-palpable and unobservable, occurring between heartbeats. Pressure waves generated by cardiac systole move the artery walls, which are pliable and compliant. These properties form enough to create a palpable pressure wave. The heart rate can be (much) higher than the pulse rate depending upon the cause or etiology. In this case, the heart rate is determined by auscultation of the heart apex, in which case it is not the pulse. The pulse deficit (difference between heart beats and pulsations at the periphery) is determined by simultaneous palpation at the radial artery and auscultation at the heart apex. Pulse velocity, pulse deficits and much more physiologic data is readily and simplistically visualized by the use of one or more arterial catheters connected to a transducer and oscilloscope.
    [Show full text]