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1

Mäkivirta, Aki. Use of the median filter in haemodynamic monitoring. Espoo: Technical Research Centre of Finland, 1992.

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2

Dillon, A. Haemodynamic profiles and the critically ill patient: A practical guide. Edited by Coombs M. A and Lyon J. Oxford (England): BIOS Scientific Publishers, 1997.

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3

Cold, Georg E., and Niels Juul, eds. Monitoring of Cerebral and Spinal Haemodynamics During Neurosurgery. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-77873-8.

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4

Haemodynamic Monitoring And Manipulation. M&K; Update Ltd, 2009.

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5

(Editor), Jean-Francois Dhainaut, and Didier Payen (Editor), eds. Strategy in Bedside Haemodynamic Monitoring (Update in Intensive Care & Emergency Medicine). Springer-Verlag Berlin and Heidelberg GmbH & Co. K, 1991.

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6

Leach, Dr Richard, and Professor Kevin Moore. Practical procedures and monitoring. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199565979.003.00019.

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Chapter 19 covers practical procedures and monitoring of patients presenting with vascular and haemodynamic, respiratory, gastrointestinal, and other conditions, as well as additional various practical procedures.
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7

HAEMODYNAMIC PROFILES AND THE CRITICALLY ILL PATIENT (Understanding Cardiac Output Studies). Taylor & Francis, 1996.

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8

Bloos, Frank, and Konrad Reinhart. Mixed and central venous oxygen saturation monitoring in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0134.

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Haemodynamic resuscitation should target goals that reflect the tissue oxygen needs of an individual patient. Venous oximetry may be such a tool. Oxygen saturation of blood in the pulmonary artery contains venous blood from the whole body and is referred to as mixed oxygen saturation (SvO2). Measurement of oxygen saturation in blood obtained from a central venous catheter is referred to as central venous oxygen saturation (ScvO2). Both values are not identical since a catheter placed into the superior vena cava only represents venous blood draining the upper body. While it is not possible, in the clinical setting, to predict SvO2 from ScvO2, changes in SvO2 are adequately mirrored by changes in ScvO2. Post-operative patients and patients admitted to intensive care with a low ScvO2 show a higher morbidity and mortality. Early goal-directed therapy (EGDT) combines several haemodynamic goals into a treatment algorithm, including a ScvO2 target. However, recent studies do not support the systematic use of this protocolized approach. A normal value of SvO2 or ScvO2 saturation does not always exclude tissue hypoxia, since it is not possible to identify an inadequate oxygen supply in single organs. A further limitation of this technique is that organ dysfunction can progress, or serum lactate increases, despite normal or even increased venous oximetry values.
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9

Arulkumaran, Nishkantha, and Maurizio Cecconi. Cardiac output assessment in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0136.

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Haemodynamic monitoring facilitates effective resuscitation and the rapid assessment of the response to time-dependent vasoactive and fluid therapyin different shock states. Since the introduction of the pulmonary artery catheter, several minimally and non-invasive CO monitoring devices have been introduced to provide continuous monitoring and a dynamic profile of fluid responsiveness. Several of these monitors provide additional haemodynamic parameters including dynamic indices of preload and volumetric indices. Patient outcome is dependent accurate acquisition and interpretation of data and subsequent management. Whilst data from CO monitors offer valuable information on global hamodynamics, they do not preclude tissue hypoperfusion. Furthermore, there is no ‘ideal’ CO value for an individual patient, and the trend in haemodynamic parameters in response to therapy may be more informative than the absolute values. CO monitoring should be based upon the patient’s needs, the clinical scenario, and the experience of the treating physician.
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10

Sidhu, Kulraj S., Mfonobong Essiet, and Maxime Cannesson. Cardiac and vascular physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0001.

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This chapter discusses key components of cardiovascular physiology applicable to clinical practice in the field of anaesthesiology. From theory development to ground-breaking innovations, the history of cardiac and vascular anatomy, as well as physiology, is presented. Utilizing knowledge of structure and function, parameters created have allowed adequate patient clinical assessment and guided interventions. A review of concepts reveals the impact of multiple physiological variables on a patient’s haemodynamic state and the need for more accurate and efficient measurements. In particular, it is noted that a more reliable index of ventricular contractility is the end-systolic elastance rather than the ejection fraction. Constant direct preload assessment has not yet been achieved but continues to be determined through surrogate variables, and continuous cardiac output monitoring for oxygen delivery, although advancing, has limitations. Considering the effect of compound factors perioperatively, especially heart failure, modifies the goals and interventions of anaesthetists to achieve improved outcomes. Therefore, medical management prior to surgery and complete assessment through history, physical examination, and diagnostic tests are a priority. This chapter also details the expectations following volume expansion to augment haemodynamics during surgery, the concept of functional haemodynamic monitoring, and limitations to the parameters applied in assessing fluid responsiveness. Challenging the accuracy of conventional indices to predict volume status led to the use of goal-directed therapy, reducing morbidity and minimizing length of hospital stay. The mainstay of this chapter is to reinforce the relevance of advances in haemodynamic monitoring and homeostasis optimization by anaesthetists during surgery, using fundamental concepts of cardiovascular physiology.
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11

Vincent, Jean-Louis. Ethical issues in cardiac arrest and acute cardiac care: a European perspective. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0013.

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The respiratory system is key to the management of patients with respiratory, as well as haemodynamic, compromise and should be monitored. The ventilator is more than just a machine that delivers gas; it is a true respiratory system monitoring device, allowing the measurement of airway pressures and intrinsic positive end-expiratory pressure and the plotting of pressure/volume curves. For effective and reliable monitoring, it is necessary to keep in mind the physiology, such as the alveolar gas equation, heart-lung interactions, the equation of movement, etc. Monitoring the respiratory system enables adaptation of not only respiratory management, but also haemodynamic management.
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12

Vincent, Jean-Louis. Ethical issues in cardiac arrest and acute cardiac care: a European perspective. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0013_update_001.

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The respiratory system is key to the management of patients with respiratory, as well as haemodynamic, compromise and should be monitored. The ventilator is more than just a machine that delivers gas; it is a true respiratory system monitoring device, allowing the measurement of airway pressures and intrinsic positive end-expiratory pressure and the plotting of pressure/volume curves. For effective and reliable monitoring, it is necessary to keep in mind the physiology, such as the alveolar gas equation, heart-lung interactions, the equation of movement, etc. Monitoring the respiratory system enables adaptation of not only respiratory management, but also haemodynamic management.
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13

Vieillard-Baron, Antoine. The respiratory system. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0015.

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The respiratory system is key to the management of patients with respiratory, as well as haemodynamic, compromise and should be monitored. The ventilator is more than just a machine that delivers gas; it is a true respiratory system monitoring device, allowing the measurement of airway pressures and intrinsic positive end-expiratory pressure and the plotting of pressure/volume curves. For effective and reliable monitoring, it is necessary to keep in mind the physiology, such as the alveolar gas equation, heart-lung interactions, the equation of movement, etc. Monitoring the respiratory system enables adaptation of not only respiratory management, but also haemodynamic management.
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14

Kipnis, Eric, and Benoit Vallet. Tissue perfusion monitoring in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0138.

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Resuscitation endpoints have shifted away from restoring normal values of routinely assessed haemodynamic parameters (central venous pressure, mean arterial pressure, cardiac output) towards optimizing parameters that reflect adequate tissue perfusion. Tissue perfusion-based endpoints have changed outcomes, particularly in sepsis. Tissue perfusion can be explored by monitoring the end result of perfusion, namely tissue oxygenation, metabolic markers, and tissue blood flow. Tissue oxygenation can be directly monitored locally through invasive electrodes or non-invasively using light absorbance (pulse oximetry (SpO2) or tissue (StO2)). Global oxygenation may be monitored in blood, either intermittently through blood gas analysis, or continuously with specialized catheters. Central venous saturation (ScvO2) indirectly assesses tissue oxygenation as the net balance between global O2 delivery and uptake, decreasing when delivery does not meet demand. Lactate, a by-product of anaerobic glycolysis, increases when oxygenation is inadequate, and can be measured either globally in blood, or locally in tissues by microdialysis. Likewise, CO2 (a by-product of cellular respiration) and PCO2 can be measured globally in blood or locally in accessible mucosal tissues (sublingual, gastric) by capnography or tonometry. Increasing PCO2 gradients, either tissue-to-arterial or venous-to-arterial, are due to inadequate perfusion. Metabolically, the oxidoreductive status of mitochondria can be assessed locally through NADH fluorescence, which increases in situations of inadequate oxygenation/perfusion. Finally, local tissue blood flow may be measured by laser-Doppler or visualized through intravital microscopic imaging. These perfusion/oxygenation resuscitation endpoints are increasingly used and studied in critical care.
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15

Romagnoli, Stefano, and Giovanni Zagli. Blood pressure monitoring in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0131.

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Two major systems are available for measuring blood pressure (BP)—the indirect cuff method and direct arterial cannulation. In critically-ill patients admitted to the intensive care unit, the invasive blood pressure is the ‘gold standard’ as a tight control of BP values, and its change over time is important for choosing therapies and drugs titration. Since artefacts due to the inappropriate dynamic responses of the fluid-filled monitoring systems may lead to clinically relevant differences between actual and displayed pressure values, before considering the BP value shown as reliable, the critical care giver should carefully evaluate the presence/absence of artefacts (over- or under-damping/resonance). After the arterial pressure waveform quality has been verified, the observation of each component of the arterial wave (systolic upstroke, peak, systolic decline, small pulse of reflected pressure waves, dicrotic notch) may provide a number of useful haemodynamic information. In fact, changes in the arterial pulse contour are due the interaction between the heart beat and the whole vascular properties. Vasoconstriction, vasodilatation, shock states (cardiogenic, hypovolaemic, distributive, obstructive), valve diseases (aortic stenosis, aortic regurgitation), ventricular dysfunction, cardiac tamponade are associated with particular arterial waveform characteristics that may suggest to the physician underlying condition that could be necessary to investigate properly. Finally, the effects of positive-pressure mechanical ventilation on heart–lung interaction, may suggest the existence of an absolute or relative hypovolaemia by means of the so-called dynamic indices of fluid responsiveness.
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16

Dyer, Robert A., Michelle J. Arcache, and Eldrid Langesaeter. The aetiology and management of hypotension during spinal anaesthesia for caesarean delivery. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0023.

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The management of hypotension during spinal anaesthesia for caesarean delivery remains a challenge for anaesthesiologists. Close control of maternal haemodynamics is of great importance for maternal and fetal safety, as well as maternal comfort. Haemodynamic responses to spinal anaesthesia are influenced by aortocaval compression, the baricity and dose of local anaesthetic and opioid employed, the rational use of fluids, and the goal-directed use of vasopressors. The most common response to spinal anaesthesia is hypotension and an increased heart rate, which reflects a decreased systemic vascular resistance and a partial compensatory increase in cardiac output. Phenylephrine is therefore the vasopressor of choice in this scenario. Less commonly, hypotension and bradycardia may occur, possibly due to the activation of cardiac reflexes. This requires anticholinergics and/or ephedrine. The rarest occurrences are persistent refractory hypotension, or high spinal block with respiratory failure. Special considerations include patients with severe pre-eclampsia, in whom spinal anaesthesia is associated with haemodynamic stability, and less hypotension than in the healthy patient. Careful use of neuraxial anaesthesia in specialized centres has an important role to play in the management of patients with cardiac disease, in conjunction with careful monitoring. Prevention is better than cure, but should hypotension occur, rapid intervention is essential, based upon the exact clinical scenario and individual haemodynamic response.
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17

Vieillard-Baron, Antoine. Right ventricular function in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0135.

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Under normal conditions, the right ventricle (RV) virtually acts as a passive conduit. In critically-ill patients many situations induce uncoupling between the right ventricle and pulmonary circulation, leading to RV systolic dysfunction, then failure. Mechanical ventilation has a major impact by decreasing RV preload, but also significantly increasing RV afterload. RV function should thus always be interpreted and re-evaluated in the light of respiratory mechanics and ventilator settings. RV systolic function is key to the patient’s haemodynamic profile and must be monitored to achieve optimal haemodynamic management. Echocardiography is the best compromise between clinical effectiveness and invasiveness to monitor RV function. A limitation is its inability to monitor haemodynamics continuously. Acute cor pulmonale is defined by the combination of RV dilatation with paradoxical septal motion during systole. In conclusion, RV function monitoring is strongly recommended in many situations encountered in the intensive care unit, such as ARDS, septic shock, and pulmonary embolism. Many devices are available, but echocardiography constitutes the best compromise between accuracy and invasiveness.
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18

Barthélémy, Romain, Etienne Gayat, and Alexandre Mebazaa. Pathophysiology and clinical assessment of the cardiovascular system (including pulmonary artery catheter). Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0014.

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Haemodynamic instability in acute cardiac care may be related to various mechanisms, including hypovolaemia and heart and/or vascular dysfunction. Although acute heart failure patients are often admitted for dyspnoea, many mechanisms can be involved, including left ventricular diastolic and/or systolic dysfunction and/or right ventricular dysfunction. Many epidemiological studies show that clinical signs at admission, morbidity, and mortality differ between the main scenarios of acute heart failure: left ventricular diastolic dysfunction, left ventricular systolic dysfunction, right ventricular dysfunction, and cardiogenic shock. Although echocardiography often helps to assess the mechanism of cardiac dysfunction, it cannot be considered as a monitoring tool. In some cases (in particular, in cases of refractory shock secondary to both vascular and heart dysfunction or in cases of refractory haemodynamic instability associated with severe hypoxaemia), pulmonary artery catheter can help to assess and monitor cardiovascular status and to evaluate response to treatments. Last, macro- and microvascular dysfunctions are also important determinants of haemodynamic instability.
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19

Orenbuch-Harroch, Efrat, and Charles L. Sprung. Pulmonary artery catheterization in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0133.

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Haemodynamic monitoring is a significant component in the management of critically-ill patients. Flow-directed pulmonary artery catheters (PAC) are a simple and rapid technique for measuring several continuous or intermittent circulatory variables. The PAC is helpful in diagnosis, guidance of therapy, and monitoring therapeutic interventions in various clinical conditions, including myocardial infarction and its complications, non-cardiogenic pulmonary oedema and severely ill patients.The catheter is inserted through a large vein. The PAC is advanced, after ballooninflation with 1.5 mL of air, through the right ventricle across the pulmonary valve and into the pulmonary artery (PA). Finally, the catheter is advanced to the ‘wedge’ position. The pulmonary artery wedge pressure (PAWP) is identified by a decrease in pressure combined with a characteristic change in the waveform. The balloon should then be deflated and the PA tracing should reappear. Direct measurements include central venous pressure, pulmonary artery pressure, and PAWP, which during diastole represents the left ventricular end-diastolic pressure and reflects left ventricular preload. Cardiac output can be measured by thermodilution technique. Other haemodynamic variables can be derived from these measurements. Absolute contraindications are rare. Relative contraindications include coagulopathy and conditions that increase the risk of arrhythmias.
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20

Peake, Sandra L., and Matthew J. Maiden. Management of septic shock in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0298.

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The management of septic shock is a medical emergency. Following prompt recognition, treatment priorities are haemodynamic resuscitation, empirical antimicrobials, urgent control of the source of infection and monitoring the response to therapy. Haemodynamic resuscitation is focused on maintaining an adequate macrocirculation, while also ensuring adequacy of microcirculatory blood flow to the cells. Intravenous fluids and catecholamines have been the mainstay of therapy. However, the amount and type of fluids, choice of vasoactive medications, and the appropriate resuscitation endpoints have been questioned. Greater awareness of the importance of resuscitating the microcirculation and cell function have led to endpoints such as venous O2 saturation and changes in lactate levels becoming resuscitation targets. Urgent definitive treatment of the infection is also crucial. This requires prompt broad-spectrum empirical antimicrobial therapy, draining infected collections and removing infected medical devices. Despite extensive research, no new therapies have improved survival from septic shock.
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21

Lancellotti, Patrizio, and Bernard Cosyns. Heart Valve Disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713623.003.0007.

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Echocardiography plays a major role in the evaluation, monitoring and decision making of patients with valvular heart disease. This chapter examines the aetiologies, haemodynamic measurements, and various consequences in aortic, mitral and pulmonary valve stenosis. It also describes how to assess patients with valvular regurgitation (mitral, aortic and pulmonary), valvular prosthesis and definite or suspected infective endocarditis. For each condition, echocardiographic features of poor prognosis, including complications, embolic risk, and the timing for surgery are discussed. Indications for transoesophageal echocardiography and 3D echocardiography are highlighted, especially when a decision of valve repair is envisioned. The timing echocardiographic monitoring of patients with valvular heart disease is also described.
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22

Paul, Richard, and Susanna Price. Imaging the cardiovascular system in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0143.

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Cardiac imaging in the critically ill can be challenging. Interpretation requires a broad knowledge of cardiovascular pathophysiology, the range of available investigations, and their sensitivity and specificity in diagnosing individual conditions. Applying first principles and interpreting findings in the clinical context are mandatory. Useful non-invasive investigations include simple chest X-ray, thoracic ultrasound, and computed tomography (CT) to detect pulmonary and extrapulmonary pathology, whilst CT coronary angiography can evaluate stent and graft patency, and identify extramural plaques, undiagnosed with conventional angiography. Invasive left heart cardiac catheterization may be indicated in patients with cardiovascular instability and particularly in patients where cardiac surgery has involved manipulation of the coronary arteries, whilst right heart catheterization remains the gold standard for haemodynamic assessment of pulmonary hypertension. Echocardiography has many applications in the ICU, ranging from haemodynamic monitoring to aiding diagnosis of complex pathology and rapid diagnosis in cardiac arrest. Other investigation modalities less frequently used in the critical care population are also discussed within this chapter.
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23

Juul, Niels, Georg E. Cold, M. Rasmussen, A. Tankisi, H. Bundgaard, L. Schlünzen, B. Duch, E. Karatasi, and L. Krogh. Monitoring of Cerebral and Spinal Haemodynamics during Neurosurgery. Springer, 2010.

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24

Monitoring Of Cerebral And Spinal Haemodynamics During Neurosurgery. Springer, 2008.

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25

Prout, Jeremy, Tanya Jones, and Daniel Martin. Cardiovascular system. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199609956.003.0001.

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This chapter covers the assessment and investigation of perioperative cardiac risk, the principles of perioperative haemodynamic monitoring and physiological changes in cardiac comorbidity with their relevance to anaesthetic management. Perioperative cardiovascular risk includes assessment of cardiac risk factors, functional capacity and evidence-based guidelines for preassessment. Cardiovascular investigations such as cardiopulmonary exercise testing and scoring systems for cardiac risk are included. Management of the cardiac patient for non-cardiac surgery is detailed. Invasive monitoring with arterial, central venous and pulmonary artery catheters is described. Cardiac output measurement systems including dilution techniques, pulse contour analysis and Doppler are compared. The physiological changes, management and implications for anaesthesia of common cardiac comorbidity including ischaemic heart disease, heart failure, valvular heart disease, pacemakers and pulmonary hypertension are described.
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26

Jörres, Achim, Dietrich Hasper, and Michael Oppert. Fluid overload in acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0229.

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A central objective in the management of acute kidney injury is the restoration and maintenance of adequate systemic and renal perfusion, often requiring the parallel administration of fluids and vasoactive drugs. However, hypovolaemia and fluid overload may both predispose the patient to complications and poor outcomes. Therefore, body weight and daily fluid intake/output should be recorded, patients should continuously be assessed for clinical signs of under- or over-hydration, and adequate monitoring of haemodynamic parameters should be performed. Together these parameters constitute the basis for individualized fluid therapy that needs to be initiated promptly and should be re-evaluated at least on a daily basis.
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27

Marino, Philip, and Laura Price. Diagnosis and management of pulmonary hypertension. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0169.

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The diagnosis of pulmonary hypertension (PH) and associated right ventricular (RV) dysfunction or failure in the setting of critical illness relies on the use of non-invasive tools including echocardiography, and in some cases invasive haemodynamic monitoring. The management for PH and RV failure in the ICU may be challenging, and is dependent on local expertise and drug availability.Systemic vasoactive agents and pulmonary vasodilators play an important role. Patients with pulmonary arterial hypertension, pulmonary embolism or chronic thromboembolic PH should be anticoagulated; those with haemodynamically unstable PE may require thrombolysis.The characteristics of individual agents must be considered and monitored carefully.Few clinical studies or ICU-specific guidelines exist. Surgical options exist for patients with PH and RV failure. This chapter reviews the diagnostic and management strategies of PH and RV failure in the ICU setting.
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28

Wise, Matt, and Paul Frost. Nutritional support in the critically ill. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0334.

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Major injury evokes a constellation of reproducible hormonal, metabolic, and haemodynamic responses which are collectively termed ‘the adaptive stress response’. The purpose of the adaptive stress response is to facilitate tissue repair and restore normal homeostasis. If critical illness is prolonged, the adaptive stress response may become maladaptive, in essence exerting a parasitic effect leaching away structural proteins and impairing host immunity. Primarily therapy should be directed towards the underlying illness, as nutritional support per se will not reverse the stress response and its sequelae. Nonetheless, adequate nutritional support in the early stages of critical illness may attenuate protein catabolism and its adverse effects. This chapter covers nutritional assessment; detection of malnutrition; energy and protein requirements; monitoring the effectiveness of nutritional replacements; nutritional delivery; complications; and refeeding syndrome.
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29

Gill, Harminder S., and Jaswinder S. Gill. Causes, diagnosis, and therapeutic strategy in bradyarrhythmias. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0157.

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Bradyarrhythmias (defined as a heart rate <60 beat/min) occur frequently in the critical care setting. Most are related to underlying disease processes and the multidrug therapies administered. Because of the intense monitoring of these patients, recognition is generally easy. Examination of the ECG will allow diagnosis of the type of bradycardia based on the sinus node, atrioventricular node and the infra-Hissian conducting system. The extent of conduction system disease can be estimated and this has an influence on the prognosis. Bradycardias causing haemodynamic collapse require treatment of underlying causes, resuscitation, and administration of atropine and epinephrine. If there is no response to these then either transcutaneous pacing, or temporary transvenous pacing is necessary. This can be followed by implantation of a permanent pacing system. The outcome of correctly diagnosing and treating a bradyarrhythmia is excellent as long as the causative pathology can be stabilized.
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30

Suri, Ajay, and Jean R. McEwan. Anti-anginal agents in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0037.

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Angina is chest pain resulting from the lack of blood supply to heart muscle most commonly due to obstructive atherosclerotic. Intensive care unit patients are subject to various stresses that will increase the demand on the heart and are in a pro-thrombotic state. Patients in an intensive treatment unit may be sedated and so cardiac ischaemia may be detected by electrocardiogram, haemodynamic monitoring, and echocardiographic imaging of function. These signs may indicate critical coronary perfusion heralding a myocardial infarction and are alleviated by anti-anginal drugs. Beta-blockers and calcium channel blockers are the usual first-line treatments for angina, but may not be ideal in the critically-ill patient. Nitrates reduce blood pressure without typically affecting heart rate. Nicorandil is a similar mechanism of action and tends to be given orally, while ivabridine, an If channel blocker, is a newer anti-anginal, which acts by reducing heart rate, while not affecting blood pressure. Ranolazine is the one of the newest anti-anginal agents and is believed to alter the transcellular late sodium current thereby decreasing sodium entry into ischaemic myocardial cells.
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31

Paul, Richard. Ultrasound-guided vascular access in intensive/acute cardiac care. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0021.

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Vascular access is an essential requirement for the care of the critically ill cardiac patient, being necessary for drug and fluid delivery and monitoring of a patient’s haemodynamic response to an instigated therapy. The most common vascular access procedures conducted in the acute cardiac care unit are central venous and peripheral venous access, and arterial cannulation. Traditional landmark methods are associated with complication rates, ranging from 18 to 40%, depending on the site of access. The use of ultrasound to guide venous and arterial access has been shown to reduce the incidence of complications, such as inadvertent arterial puncture and pneumothorax formation (venous) and posterior wall puncture (arterial), to reduce the time taken and number of attempts to place a catheter, and to reduce the incidence of complete failure to insert a vascular access device. Since 2002, international consensus groups have published recommendations that two-dimensional ultrasound guidance be the preferred method for elective and emergency internal jugular catheter insertion. This chapter explores the evidence for the use of ultrasound to guide vascular access across multiple sites of insertion and describes the basic equipment and techniques necessary for successful deployment.
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32

Vranckx, Pascal, Wilfried Mullens, and Johan Vijgen. Non-pharmacological therapy of acute heart failure: when drugs alone are not enough. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0053.

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Acute heart failure syndrome has been defined as new-onset or a recurrence of worsening signs and symptoms of heart failure, necessitating urgent or emergency management. The management of acute heart failure syndrome is challenging, given the heterogeneity of the patient population, in terms of the clinical presentation, pathophysiology, prognosis, and therapeutic options. The management of acute heart failure syndrome is a dynamic process, requiring ongoing simultaneous diagnosis (monitoring) and treatment. Pharmacological agents remain the mainstay of therapy for acute heart failure syndrome. However, at all time, during the early diagnostic, aetiologic, and therapeutic work-up, non-pharmacologic therapy may be indicated and should be considered. The management of the complex cardiac patient with acute heart failure syndrome and/or (potential) haemodynamic compromise has become a special dimension for specialized myocardial intervention centres, providing 24 hours per day and 7 days per week state-of-the-art facilities for (primary) percutaneous coronary intervention and cardiac intensive care, including mechanical ventilation, ultrafiltration, with or without dialysis, and short-term percutaneous mechanical circulatory support. Through the understanding of the underlying pathophysiology and approaches into the problems of acute heart failure syndrome, one should be better prepared to understand and treat its many facets.
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33

Goltsov, Alexey, Viktor V. Sidorov, Sergei G. Sokolovski, and Edik Rafailov, eds. Advanced Non-invasive Photonic Methods for Functional Monitoring of Haemodynamics and Vasomotor Regulation in Health and Diseases. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88963-760-7.

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34

Torbicki, Adam, Marcin Kurzyna, and Stavros Konstantinides. Pulmonary embolism. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0066.

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Pulmonary embolism is usually a consequence of deep vein thrombosis, and together the two conditions are known as venous thromboembolism. Non-thromboembolic causes of pulmonary embolism are rare. Pulmonary thromboembolism is a potentially life-threatening disease, if left untreated. This is due to a natural tendency towards early recurrence of pulmonary emboli which may lead to fatal right ventricular failure. In more severe cases, secondary right ventricular failure may result from myocardial ischaemia and injury caused by systemic hypotension and adrenergic overstimulation. Clinical presentation of pulmonary embolism is non-specific and may include dyspnoea, chest pain, haemoptysis, syncope, hypotension, and shock. Patients with suggestive history, symptoms, and signs require an immediate triage which determines further management strategy. Computerized tomographic angiography has become the mainstay of diagnosis. However, depending on the clinical presentation, treatment decisions may also be made based on results from other tests. In particular, in high-risk patients with persistent hypotension or shock, bedside echocardiography may be the only available test to identify patients in need of primary thrombolysis, surgical embolectomy, or percutaneous intervention which will stabilize the systemic cardiac output. For most normotensive patients, anticoagulation is sufficient as initial treatment. However, in the presence of signs of right ventricular dysfunction and myocardial injury monitoring is recommended to allow prompt rescue reperfusion therapy in case of haemodynamic decompensation.
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35

Torbicki, Adam, Marcin Kurzyna, and Stavros Konstantinides. Pulmonary embolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0066_update_001.

Full text
Abstract:
Pulmonary embolism is usually a consequence of deep vein thrombosis, and together the two conditions are known as venous thromboembolism. Non-thromboembolic causes of pulmonary embolism are rare. Pulmonary thromboembolism is a potentially life-threatening disease, if left untreated. This is due to a natural tendency towards early recurrence of pulmonary emboli which may lead to fatal right ventricular failure. In more severe cases, secondary right ventricular failure may result from myocardial ischaemia and injury caused by systemic hypotension and adrenergic overstimulation. Clinical presentation of pulmonary embolism is non-specific and may include dyspnoea, chest pain, haemoptysis, syncope, hypotension, and shock. Patients with suggestive history, symptoms, and signs require an immediate triage which determines further management strategy. Computerized tomographic angiography has become the mainstay of diagnosis. However, depending on the clinical presentation, treatment decisions may also be made based on results from other tests. In particular, in high-risk patients with persistent hypotension or shock, bedside echocardiography may be the only available test to identify patients in need of primary thrombolysis, surgical embolectomy, or percutaneous intervention which will stabilize the systemic cardiac output. For most normotensive patients, anticoagulation is sufficient as initial treatment. However, in the presence of signs of right ventricular dysfunction and myocardial injury monitoring is recommended to allow prompt rescue reperfusion therapy in case of haemodynamic decompensation.
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36

Torbicki, Adam, Marcin Kurzyna, and Stavros Konstantinides. Pulmonary embolism. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0066_update_002.

Full text
Abstract:
Pulmonary embolism is usually a consequence of deep vein thrombosis, and together the two conditions are known as venous thromboembolism. Non-thromboembolic causes of pulmonary embolism are rare. Pulmonary thromboembolism is a potentially life-threatening disease, if left untreated. This is due to a natural tendency towards early recurrence of pulmonary emboli which may lead to fatal right ventricular failure. In more severe cases, secondary right ventricular failure may result from myocardial ischaemia and injury caused by systemic hypotension and adrenergic overstimulation. Clinical presentation of pulmonary embolism is non-specific and may include dyspnoea, chest pain, haemoptysis, syncope, hypotension, and shock. Patients with suggestive history, symptoms, and signs require an immediate triage which determines further management strategy. Computerized tomographic angiography has become the mainstay of diagnosis. However, depending on the clinical presentation, treatment decisions may also be made based on results from other tests. In particular, in high-risk patients with persistent hypotension or shock, bedside echocardiography may be the only available test to identify patients in need of primary thrombolysis, surgical embolectomy, or percutaneous intervention which will stabilize the systemic cardiac output. For most normotensive patients, anticoagulation is sufficient as initial treatment. However, in the presence of signs of right ventricular dysfunction and myocardial injury monitoring is recommended to allow prompt rescue reperfusion therapy in case of haemodynamic decompensation.
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37

Torbicki, Adam, Marcin Kurzyna, and Stavros Konstantinides. Pulmonary embolism. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0066_update_003.

Full text
Abstract:
Pulmonary embolism is usually a consequence of deep vein thrombosis, and together the two conditions are known as venous thromboembolism. Non-thromboembolic causes of pulmonary embolism are rare. Pulmonary thromboembolism is a potentially life-threatening disease, if left untreated. This is due to a natural tendency towards early recurrence of pulmonary emboli which may lead to fatal right ventricular failure. In more severe cases, secondary right ventricular failure may result from myocardial ischaemia and injury caused by systemic hypotension and adrenergic overstimulation. Clinical presentation of pulmonary embolism is non-specific and may include dyspnoea, chest pain, haemoptysis, syncope, hypotension, and shock. Patients with suggestive history, symptoms, and signs require an immediate triage which determines further management strategy. Computerized tomographic angiography has become the mainstay of diagnosis. However, depending on the clinical presentation, treatment decisions may also be made based on results from other tests. In particular, in high-risk patients with persistent hypotension or shock, bedside echocardiography may be the only available test to identify patients in need of primary thrombolysis, surgical embolectomy, or percutaneous intervention which will stabilize the systemic cardiac output. For most normotensive patients, anticoagulation is sufficient as initial treatment. However, in the presence of signs of right ventricular dysfunction and myocardial injury monitoring is recommended to allow prompt rescue reperfusion therapy in case of haemodynamic decompensation.
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38

Ebm, Claudia, and Andrew Rhodes. Post-operative fluid and circulatory management in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0363.

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Fluid and circulatory management is an integral part of the peri-operative care of critically-ill patients. Precisely estimating the volumetric needs of post-operative patients remains difficult. While the majority of patients tolerate intra-operative fluid loss easily, patients with reduced physiological reserve present more of a challenge. Targeting specific physiological goals and optimizing haemodynamics with fluids and inotropes, means outcomes of these patients can be improved. This approach is often referred as goal-directed therapy (GDT). ‘Individualized goal-directed therapy’ can vary in timing, monitoring techniques, and endpoints used. The emergence of minimal invasive devises has allowed us to integrate cardiac output monitoring as a safe and reliable tool in the routine care of high risk patients. This dynamic assessment of haemodynamics provides a reliable technique to assess volume responsiveness and guide fluids to optimize cardiac output and oxygen delivery.
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39

Debaveye, Yves, and Greet Van den Berghe. Pathophysiology and management of pituitary disorders in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0262.

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The pituitary gland plays a predominant role in the endocrine system. Consequently, patients with pituitary diseases or after pituitary surgery present unique challenges to the intensivist. Failure of the anterior pituitary gland to secrete one or more pituitary hormones results in a clinical syndrome known as hypopituitarism. While hypopituitarism is mostly encountered in patients in whom the diagnosis has already been made, acute exacerbation of an undiagnosed insufficiency may occasionally occur. Acute decompensated patients with suspected hypopituitarism should be admitted to an intensive care unit for haemodynamic stabilization, replacement of missing hormones, and identification and treatment of the causative stressor. Prompt administration of hydrocortisone is the single most important acute medical intervention in hypopituitaric patients. Failure of the posterior pituitary to secrete antidiuretic hormone results in diabetes insipidus (DI). DI is characterized by excess volumes of severely diluted urine, which can lead to hyperosmolality and hypernatraemia as many critically-ill patients do not have free access to oral fluids due to obtundation or sedation. Management of DI includes the correction of free water deficit and the reduction of polyuria with desmopressin. The post-operative care following pituitary surgery focuses on vigilant observation for neurosurgical complications (visual loss, meningitis, and cerebrospinal fluid leakage) and monitoring of neuroendocrinological perturbations (hypopituitarism and disorders of water balance, such as DI and SIADH). SIADH presents with hyponatremia, hypo-osmolality, and inappropriately concentrated urine in a setting of euvolaemia and can be managed in most cases by fluid restriction. Potential disruption of the pituitary-adrenal function is covered with peri-operative glucocorticoids.
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40

Peacock, Linzi, and Rachel Hignett. Acquired heart disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0041.

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Heart disease in pregnancy is a leading cause of maternal death worldwide. In the United Kingdom and United States, heart disease in pregnancy is the commonest cause of maternal death. In Europe, over 1% of maternal deaths are attributable to structural heart disease. In addition, heart disease in pregnancy is a significant cause of severe maternal and fetal morbidity. Whilst the vast majority of women with heart disease in pregnancy have underlying congenital heart disease, most maternal deaths are due to acquired heart disease (AHD). As the risk factors for AHD become ever more prevalent, the expectation is that disease burden from AHD in pregnancy will also increase. Women with AHD benefit from preconception or early assessment in pregnancy by a multidisciplinary team including obstetricians, cardiologists, and obstetric anaesthetists. Risk assessment using the modified World Health Organization classification of cardiac disease in pregnancy will inform frequency of review in pregnancy. A detailed plan for delivery should be agreed in the third trimester. Where possible, a vaginal delivery is advised: caesarean delivery is reserved for women with obstetric indications or with specific severe underlying cardiac conditions. Slow incremental epidural analgesia is usually recommended to reduce the cardiorespiratory work of labour and an assisted second-stage delivery will limit exertion due to pushing. Neuraxial anaesthesia for operative delivery is becoming a more familiar approach and techniques such as low-dose spinal component combined spinal–epidural or slow incremental epidural top-up maximize haemodynamic stability. Invasive monitoring is often beneficial. Post-delivery care is safely delivered in a high dependency or intensive therapy setting. This chapter looks at the general principles of management of women with AHD, and then examines in detail ischaemic heart disease, arrhythmias, cardiac transplantation, aortic pathology and aortic dissection, cardiomyopathy, valvular heart disease, and infective endocarditis.
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41

Gevaert, Sofie A., Eric Hoste, and John A. Kellum. Acute kidney injury. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0068.

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Acute kidney injury is a serious condition, occurring in up to two-thirds of intensive care unit patients, and 8.8-55% of patients with acute cardiac conditions. Renal replacement therapy is used in about 5-10% of intensive care unit patients. The term cardiorenal syndrome refers to combined heart and kidney failure; three types of acute cardiorenal syndrome have been described: acute cardiorenal syndrome or cardiorenal syndrome type 1, acute renocardiac syndrome or cardiorenal syndrome type 3, and acute cardiorenal syndrome type 5 (cardiac and renal injury secondary to a third entity such as sepsis). Acute kidney injury replaced the previously used term ‘acute renal failure’ and comprises the entire spectrum of the disease, from small changes in function to the requirement of renal replacement therapy. Not only failure, but also minor and less severe decreases, in kidney function are of clinical significance both in the short and long-term. The most recent definition for acute kidney injury is proposed by the Kidney Disease: Improving Global Outcomes clinical practice guidelines workgroup. This definition is a modification of the RIFLE and AKIN definitions and staging criteria, and it stages patients according to changes in the urine output and serum creatinine (see Tables 68.1 and 68.2). Acute kidney injury is a heterogeneous syndrome with different and multiple aetiologies, often with several insults occurring in the same individual. The underlying processes include nephrotoxicity, and neurohormonal, haemodynamic, autoimmune, and inflammatory abnormalities. The most frequent cause for acute kidney injury in intensive cardiac care patients are low cardiac output with an impaired kidney perfusion (cardiogenic shock) and/or a marked increase in venous pressure (acute decompensated heart failure). Predictors for acute kidney injury in these patients include: baseline renal dysfunction, diabetes, anaemia, and hypertension, as well as the administration of high doses of diuretics. In the intensive cardiac care unit, attention must be paid to the prevention of acute kidney injury: monitoring of high-risk patients, prompt resuscitation, maintenance of an adequate mean arterial pressure, cardiac output, and intravascular volume (avoidance of both fluid overload and hypovolaemia), as well as the avoidance or protection against nephrotoxic agents. The treatment of acute kidney injury focuses on the treatment of the underlying aetiology, supportive care, and avoiding further injury from nephrotoxic agents. More specific therapies have not yet demonstrated efficacy. Renal replacement therapy is indicated in life-threatening changes in fluid, electrolyte, and acid-base balance, but there are also arguments for more early initiation.
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42

Gevaert, Sofie A., Eric Hoste, and John A. Kellum. Acute kidney injury. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0068_update_001.

Full text
Abstract:
Acute kidney injury is a serious condition, occurring in up to two-thirds of intensive care unit patients, and 8.8-55% of patients with acute cardiac conditions. Renal replacement therapy is used in about 5-10% of intensive care unit patients. The term cardiorenal syndrome refers to combined heart and kidney failure; three types of acute cardiorenal syndrome have been described: acute cardiorenal syndrome or cardiorenal syndrome type 1, acute renocardiac syndrome or cardiorenal syndrome type 3, and acute cardiorenal syndrome type 5 (cardiac and renal injury secondary to a third entity such as sepsis). Acute kidney injury replaced the previously used term ‘acute renal failure’ and comprises the entire spectrum of the disease, from small changes in function to the requirement of renal replacement therapy. Not only failure, but also minor and less severe decreases, in kidney function are of clinical significance both in the short and long-term. The most recent definition for acute kidney injury is proposed by the Kidney Disease: Improving Global Outcomes clinical practice guidelines workgroup. This definition is a modification of the RIFLE and AKIN definitions and staging criteria, and it stages patients according to changes in the urine output and serum creatinine (see Tables 68.1 and 68.2). Acute kidney injury is a heterogeneous syndrome with different and multiple aetiologies, often with several insults occurring in the same individual. The underlying processes include nephrotoxicity, and neurohormonal, haemodynamic, autoimmune, and inflammatory abnormalities. The most frequent cause for acute kidney injury in intensive cardiac care patients are low cardiac output with an impaired kidney perfusion (cardiogenic shock) and/or a marked increase in venous pressure (acute decompensated heart failure). Predictors for acute kidney injury in these patients include: baseline renal dysfunction, diabetes, anaemia, and hypertension, as well as the administration of high doses of diuretics. In the intensive cardiac care unit, attention must be paid to the prevention of acute kidney injury: monitoring of high-risk patients, prompt resuscitation, maintenance of an adequate mean arterial pressure, cardiac output, and intravascular volume (avoidance of both fluid overload and hypovolaemia), as well as the avoidance or protection against nephrotoxic agents. The treatment of acute kidney injury focuses on the treatment of the underlying aetiology, supportive care, and avoiding further injury from nephrotoxic agents. More specific therapies have not yet demonstrated efficacy. Renal replacement therapy is indicated in life-threatening changes in fluid, electrolyte, and acid-base balance, but there are also arguments for more early initiation.
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43

Ramsay, Michael A. E. Anaesthesia for transplant surgery. Edited by Philip M. Hopkins. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0067.

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The provision of anaesthesia for organ transplantation requires a team of specialist anaesthetists who are available 24 hours a day. The cold and warm ischaemia times may have very deleterious effects on the graft. The team must have a basic understanding of the immune system and the strategies of immunosuppression therapy. The preoperative assessment of the patient requires an understanding of the cause and effects of the compromised organ that is to be replaced. The procedure in many instances will result in a reperfusion syndrome when the graft is revascularized and also an ischaemia–reperfusion injury. The understanding of these entities is essential as is the preparation and protocols to treat or ameliorate the effects of these syndromes if they occur. The preparation for many organ transplants includes invasive monitoring of haemodynamics, cardiac function, pulmonary function, and acid–base balance. Access for massive transfusion therapy and coagulation assessment is essential for many transplant procedures. The maintenance of body temperature and fluid balance may be challenging. The protection and monitoring of the function of major organs such as the brain, heart, lungs, and kidneys is essential but the homeostasis of endocrine function and electrolytes is also important. The provision of excellent anaesthesia is a key component of a successful transplant programme. A small team of highly trained professionals with extensive training and experience in transplant anaesthesia provide the best results.
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44

Lameire, Norbert, Raymond Vanholder, and Wim Van Biesen. Clinical approach to the patient with acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0222_update_001.

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The prognosis of acute kidney injury (AKI) depends on early diagnosis and therapy. A multitude of causes are classified according to their origin as prerenal, intrinsic (intrarenal), and post-renal.Prerenal AKI means a loss of renal function despite intact nephrons, for example, because of volume depletion and/or hypotension.There is a broad spectrum of intrinsic causes of AKI including acute tubular necrosis (ATN), interstitial nephritis, glomerulonephritis, and vasculitis. Evaluation includes careful review of the patient’s history, physical examination, urinalysis, selected urine chemistries, imaging of the urinary tree, and eventual kidney biopsy. The history should focus on the tempo of loss of function (if known), associated systemic diseases, and symptoms related to the urinary tract (especially those that suggest obstruction). In addition, a review of the medications looking for potentially nephrotoxic drugs is essential. The physical examination is directed towards the identification of findings of a systemic disease and a detailed assessment of the patient’s haemodynamic status. This latter goal may require invasive monitoring, especially in the oliguric patient with conflicting clinical findings, where the physical examination has limited accuracy.Excluding urinary tract obstruction is necessary in all cases and may be established easily by renal ultrasound.Distinction between the two most common causes of AKI (prerenal AKI and ATN) is sometimes difficult, especially because the clinical examination is often misleading in the setting of mild volume depletion or overload. Urinary chemistries, like calculation of the fractional excretion of sodium (FENa), may be used to help in this distinction. In contrast to FENa, the fractional excretion of urea has the advantage of being rather independent of diuretic therapy. Response to fluid repletion is still regarded as the gold standard in the differentiation between prerenal and intrinsic AKI. Return of renal function to baseline or resuming of diuresis within 24 to 72 hours is considered to indicate ‘transient, mostly prerenal AKI’, whereas persistent renal failure usually indicates intrinsic disease. Transient AKI may, however, also occur in short-lived ATN. Furthermore, rapid fluid application is contraindicated in a substantial number of patients, such as those with congestive heart failure.‘Muddy brown’ casts and/or tubular epithelial cell casts in the urine sediment are typically seen in patients with ATN. Their presence is an important tool in the distinction between ATN and prerenal AKI, which is characterized by a normal sediment, or by occasional hyaline casts. There is a possible role for new serum and/or urinary biomarkers in the diagnosis and prognosis of the patient with AKI, including the differential diagnosis between pre-renal AKI and ATN. Further studies are needed before their routine determination can be recommended.When a diagnosis cannot be made with reasonable certainty through this evaluation, renal biopsy should be considered; when intrarenal causes such as crescentic glomerulonephritis or vasculitis are suspected, immediate biopsy to avoid delay in the initiation of therapy is mandatory.
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45

Waje-Andreassen, Ulrike, and Nicola Logallo. Vascular imaging: Ultrasound. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0009.

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After computed tomography and computed tomography angiography or magnetic resonance imaging and magnetic resonance angiography at admission, ultrasound is the most important diagnostic tool to confirm angiographic findings and to closely follow-up patients until the clinical situation has stabilized. Thrombolysis and interventional therapy have given transcranial ultrasound a very important role in bedside monitoring of occlusions, collaterals, cerebral haemodynamics, and vasoreactivity. Detection of flow changes in sickle cell disease, circulating emboli, and right-to-left shunts may guide treatment decisions. Sonothrombolysis and targeted drug delivery are today’s research projects for acute treatment by ultrasound. Extracranial cerebrovascular ultrasound is an ‘all-round’ diagnostic tool modifying angiographic results, showing minor arterial wall disease, plaques, and plaque instability. Microembolic signals during scanning may contribute to finding the cause of stroke. In stroke prevention, ultrasound delivers the possibility for staging of arteries and improving targeted intervention. Ultrasound images may also serve as educational tools for patients to underline the need for continuous medical treatment and lifestyle changes, and may improve compliance.
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46

Lancellotti, Patrizio, and Bernard Cosyns, eds. The EACVI Echo Handbook. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713623.001.0001.

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Echocardiography has become the most requested imaging modalities. It is the first line imaging in the diagnostic work-up and monitoring of most cardiac diseases. Echocardiography is harmless and combines low-cost high technology with easy accessibility. The advent of the new modalities such as harmonic imaging, tissue Doppler imaging, speckle tracking, real time 3-dimensional imaging, ad contrast cavity enhancement have also contributed to expand the role of echocardiography. It provides rapid quantitative information about cardiac structure and function, valvular motion, vascular system and haemodynamics at bedside. This imaging technique is considered an extension of the physical examination. Proper technical skills and knowledge are required for the optimal application of echocardiography. Disease-focused and succinct, the present handbook covers the information needed to perform and interpret echocardiogramsaccurately, including how to set up the echomachine to optimize an examination and how to perform echocardiographic disease assessment, and the clinical indicators, procedures, and contraindications. Sections include assessment of the left ventricular systolic dysfunction and diastolic function, discussion on ischaemic heart disease, heart valve disease, cardiomyopathies, pericardial disease, congenital heart disease, and many other aspects of echocardiology. Many talented people have contributed to the present handbook, which represents the pocket echocardiography book flagship of the European Association of Cardiovascular Imaging. This book is intended principally as a clinical guide to the broad field of echocardiography at a glance.
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