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Published: 14 March 2023

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1

Safar, Michel E., Michael F. O'Rourke, and Edward D. Frohlich, eds. Blood Pressure and Arterial Wall Mechanics in Cardiovascular Diseases. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-5198-2.

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2

1952-, Portaluppi Francesco, Smolensky Michael H, and New York Academy of Sciences., eds. Time-dependent structure and control of arterial blood pressure. New York, N.Y: New York Academy of Sciences, 1996.

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3

Cechella, Achutti Aloysio, ed. Controle da hipertensão arterial: Uma proposta de integração ensino-serviço. Rio de Janeiro [i.e. Brasília, Brazil]: Ministério da Saúde, 1993.

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4

Robyn, Barst, ed. Pulmonary arterial hypertension: Diagnosis and evidence-based treatment. Chichester, West Sussex, England: John Wiley & Sons, 2008.

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5

Zandevakili, Roham. Effects of ANG II and its receptor blockers on nasal salt gland secretion and arterial blood pressure in conscious perkin ducks (Anas plalytrhynchos). Ottawa: National Library of Canada, 1998.

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6

Sainz, Jorge G., and Bradley P. Fuhrman. Basic Pediatric Hemodynamic Monitoring. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199918027.003.0005.

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Physiological monitoring using a variety of technological advances supplements, but does not replace, our ability to distinguish normal from abnormal physiology traditionally gleaned from physical examination. Pulse oximetry uses the wavelengths of saturated and unsaturated hemoglobin to estimate arterial oxygenation noninvasively. Similar technology included on vascular catheters provides estimation of central or mixed venous oxygenation and helps assess the adequacy of oxygen delivered to tissues. End-tidal carbon dioxide measurements contribute to the assessment of ventilation. Systemic arterial blood pressure and central venous pressure measurements help evaluate cardiac performance, including the impact of ventilatory support. Intra-abdominal pressure may increase as a result of intraluminal air or fluid, abnormal fluid collections within the peritoneal cavity, or abnormal masses. Increased pressure may impede venous return to the heart and compromise intra-abdominal organ perfusion. Pressure measurement guides related management decisions.
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7

Granger, Joey, and D. Neil Granger. Regulation of Arterial Pressure. Morgan & Claypool Life Science Publishers, 2011.

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8

Epidemiology of Arterial Blood Pressure. Springer, 2011.

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9

Kesteloot, H., and J. V. Joosens. Epidemiology of Arterial Blood Pressure. Springer London, Limited, 2012.

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10

Kesteloot, H., and J. V. Joosens. Epidemiology of Arterial Blood Pressure. Springer Netherlands, 2011.

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11

Arterial Hypertension. Walter de Gruyter, 1996.

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12

Grygoryan, Rafik D. Optimal Circulation: Cells' Contribution to Arterial Pressure. Nova Science Publishers, Incorporated, 2017.

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13

Budwill, Sven *. Advanced computer-based methods for arterial blood pressure monitoring. 1989.

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14

Safar, Michel E., Edward D. Frohlich, and Michael F. O'Rourke. Blood Pressure and Arterial Wall Mechanics in Cardiovascular Diseases. Springer, 2014.

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15

Safar, Michel E., Edward D. Frohlich, and Michael F. O'Rourke. Blood Pressure and Arterial Wall Mechanics in Cardiovascular Diseases. Springer London, Limited, 2014.

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16

Safar, Michel E., Edward D. Frohlich, and Michael F. O'Rourke. Blood Pressure and Arterial Wall Mechanics in Cardiovascular Diseases. Springer, 2016.

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17

Safar, Michel E., Edward D. Frohlich, and Michael F. O'Rourke. Blood Pressure and Arterial Wall Mechanics in Cardiovascular Diseases. Springer, 2014.

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18

Joynt, Gavin M., and Gordon Y. S. Choi. Blood gas analysis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0072.

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Arterial blood gases allow the assessment of patient oxygenation, ventilation, and acid-base status. Blood gas machines directly measure pH, and the partial pressures of carbon dioxide (PaCO2) and oxygen (PaO2) dissolved in arterial blood. Oxygenation is assessed by measuring PaO2 and arterial blood oxygen saturation (SaO2) in the context of the inspired oxygen and haemoglobin concentration, and the oxyhaemoglobin dissociation curve. Causes of arterial hypoxaemia may often be elucidated by determining the alveolar–arterial oxygen gradient. Ventilation is assessed by measuring the PaCO2 in the context of systemic acid-base balance. A rise in PaCO2 indicates alveolar hypoventilation, while a decrease indicates alveolar hyperventilation. Given the requirement to maintain a normal pH, functioning homeostatic mechanisms result in metabolic acidosis, triggering a compensatory hyperventilation, while metabolic alkalosis triggers a compensatory reduction in ventilation. Similarly, when primary alveolar hypoventilation generates a respiratory acidosis, it results in a compensatory increase in serum bicarbonate that is achieved in part by kidney bicarbonate retention. In the same way, respiratory alkalosis induces kidney bicarbonate loss. Acid-base assessment requires the integration of clinical findings and a systematic interpretation of arterial blood gas parameters. In clinical use, traditional acid-base interpretation rules based on the bicarbonate buffer system or standard base excess estimations and the interpretation of the anion gap, are substantially equivalent to the physicochemical method of Stewart, and are generally easier to use at the bedside. The Stewart method may have advantages in accurately explaining certain physiological and pathological acid base problems.
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19

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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20

Gonzalez-Albarrán, Olga, and Luis M. Ruilope. The kidney and control of blood pressure. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0210.

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The kidneys can be at the root of the development of arterial hypertension or they can participate in the maintenance of hypertension and its sequels. Renal alterations interfering with the regulation of sodium homeostasis or facilitating the generation of vasoconstrictors, particularly angiotensin II, are involved in the dysregulation of arterial blood pressure that underlies the development of arterial hypertension. The biology of angiotensin is described in detail.The kidneys are also the mediator of hypertension in such examples as renal ischaemia and hyperaldosteronism. The role of renal nerves, and renal depressor substances, are also described.Transplantation experiments in animals and observations in human transplantation, as well as some primary gene defects, show the importance of renal mechanisms in hypertension. Once kidneys have been damaged, they often contribute to an increase in arterial pressure. Salt sensitivity is probably a major part of the mechanism, but it is mediated by multiple pathways.
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21

Kjeldsen, Sverre E. Guidelines for the Management of Arterial Hypertension 2003: European Society of Hypertension European Society of Cardiology Guidelines Committee (Special Issue Heart Drug 2004, 1). Not Avail, 2004.

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22

Appleyard, Robert Frank. A new hemodynamic index of proximal arterial function based on the aortic pressure-flow loop. 1986.

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23

Pulmonary Arterial Hypertension: Diagnosis and Evidence - Based Treatment. Wiley & Sons, Incorporated, John, 2009.

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24

Barst, Robyn. Pulmonary Arterial Hypertension: Diagnosis and Evidence-Based Treatment. Wiley & Sons, Limited, John, 2008.

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25

Melo, Luis Gabriel. Chronic regulation of arterial blood pressure by atrial natriuretic peptide: Role of endothelial factors, sympathetic nervous system and renin-angiotensin system. 1998.

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26

Blazeck, Alice Maus. THE EFFECTS ON HEART RATE, HEART RHYTHM, AND ARTERIAL BLOOD PRESSURE OF THREE PROCEDURES USED BY ACUTE MYOCARDIAL INFARCTION PATIENTS TO MOVE TO THE HEAD OF THE BED. 1987.

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27

Whittle, Ian. Raised intracranial pressure, cerebral oedema, and hydrocephalus. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0604.

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The brain is protected by the cranial skeleton. Within the intracranial compartment are also cerebrospinal fluid, CSF, and the blood contained within the brain vessels. These intracranial components are in dynamic equilibrium due to the pulsations of the heart and the respiratory regulated return of venous blood from the brain. Normally the mean arterial blood pressure, systemic venous pressure, and brain volume are regulated to maintain physiological values for intracranial pressure, ICP. There are a range of very common disorders such as stroke, and much less common, such as idiopathic intracranial hypertension, that are associated with major disturbances of intracranial pressure dynamics. In some of these the contribution to pathophysiology is relatively minor whereas in others it may be substantial and be a major contributory factor to morbidity or even death.Intracranial pressure can be disordered because of brain oedema, disturbances in CSF flow, mass lesions, and vascular engorgement of the brain. Each of these may have variable causes and there may be interactions between mechanisms. In this chapter the normal regulation of intracranial pressure is outlined and some common disease states in clinical neurological practice that are characterized by either primary or secondary problems in intracranial pressure dynamics described.
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28

Magder, Sheldon. Central venous pressure monitoring in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0132.

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Central venous pressure (CVP) is at the crucial intersection of the force returning blood to the heart and the force produced by cardiac function, which drives the blood back to the systemic circulation. The normal range of CVP is small so that before using it one must ensure proper measurement, specifically the reference level. A useful approach to hypotension is to first determine if arterial pressure is low because of a decrease in vascular resistance or a decrease in cardiac output. This is done by either measuring cardiac output or making a clinical assessment blood flow. If the cardiac output is decreased, next determine whether this is because of a cardiac pump problem or a return problem. It is at this stage that the CVP is most helpful for these options can be separated by considering the actual CVP or even better, how it changed with the change in cardiac output. A high CVP is indicative of a primary pump problem, and a low CVP and return problem. Understanding the factors that determine CVP magnitude, mechanisms that produce the components of the CVP wave form and changes in CVP with respiratory efforts can also provide useful clinical information. In many patients, CVP can be estimated on physical exam.
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29

Longman, Susan Dawn. Cardiovascular studies with angiotensin converting enzyme inhibitors in the rat: Effects of arterial blood pressure and plasma and tissue angiotensin converting enzyme (ACE) activity of acute and chronic administration of ACE inhibitors in sodium deficient normotensive (NT) rats. Bradford, 1986.

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30

Lee, Richard. Pulse oximetry and capnography in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0073.

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The estimation of arterial oxygen saturation by pulse oximetry and arterial carbon dioxide tension by capnography are vital monitoring techniques in critical care medicine, particularly during intubation, ventilation and transport. Equivalent continuous information is not otherwise available. It is important to understand the principles of measurement and limitations, for safe use and error detection. PETCO2 and oxygen saturation should be regularly checked against PaCO2 and co-oximeter SO2 obtained from the blood gas machine. The PECO2 trace informs endotracheal tube placement, ventilation, and blood flow to the lungs. It is essential their principles of estimation, the information gained and the traps in interpretation are understood.
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31

Voilliot, Damien, Jaroslaw D. Kasprzak, and Eduardo Bossone. Diseases with a main influence on right ventricular function. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0060.

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As an important and independent predictive factor of morbidity and mortality, right ventricular (RV) function should be carefully assessed in patients with chronic obstructive lung disease, lung fibrosis, liver cirrhosis, or obesity. RV assessment requires a complete study of the ‘RV-pulmonary circulation unit’ with estimation of RV preload, RV intrinsic contractility, and RV afterload. Therefore, estimation of pulmonary arterial pressure, pulmonary vascular resistance, and left ventricular systolic and diastolic function should be included in this evaluation, in addition to conventional RV systolic function assessment. Three-dimensional echocardiography has emerged as an interesting tool in RV assessment and exercise echocardiography may be interesting in the risk stratification of patients.
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32

Timperley, Jonathan, and Sandeep Hothi. Hypotension. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0011.

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Hypotension is defined as a systolic arterial blood pressure of less than 90 mm Hg, or a diastolic arterial pressure of less than 60 mm Hg, and may lead to shock, with clinical evidence of inadequate blood supply to critical organs. It can be due to hypovolaemia, cardiac pump failure, or vasodilatation. This chapter describes the clinical approach to patient with hypotension.
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33

Especificaciones técnicas de la OMS para dispositivos automáticos de medición de la presión arterial no invasivos y con brazalete. Organización Panamericana de la Salud, 2020. http://dx.doi.org/10.37774/9789275323052.

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La hipertension es el principal factor de riesgo modificable de algunas enfermedades graves como las enfermedades cardiovasculares (accidentes cerebrovasculares y cardiopatías isquémicas), la preeclampsia y la eclampsia (una causa muy importante de muerte en las embarazadas, así como de retraso del crecimiento fetal y mortinatos) y la enfermedad renal crónica. A nivel mundial, más de mil millones de personas tienen hipertensión, y la prevalencia es mayor en los países de ingresos bajos y medianos. La medición exacta de la presión arterial es esencial para detectar y tratar adecuadamente a las personas con hipertensión, un trastorno que constituye un asesino silencioso que causa pocos síntomas. La falta de acceso a dispositivos de determinación de la presión arterial exactos y asequibles constituye un obstáculo importante para una atención médica adecuada, en particular en los entornos de recursos escasos. La medición manual está siendo reemplazada gradualmente por la medición automatizada debido a los problemas ambientales derivados del mercurio, la falta de calibración y las mediciones incorrectas de los dispositivos aneroides en la práctica clínica, así como por la exactitud uniforme superior que ofrecen los dispositivos automáticos validados. Sin embargo, con frecuencia existe cierta preocupación respecto a la exactitud de los dispositivos automatizados que no se han validado. Este documento actualiza la orientación de la OMS sobre dispositivos de medición de la presión arterial del 2005. También responde a la preocupación existente por la carencia de dispositivos exactos y de buena calidad, especialmente en los países de ingresos bajos y medianos mediante una consulta técnica y examen de expertos. Versión oficial en español de la obra original en inglés: WHO technical specifications for automated non-invasive blood pressure measuring devices with cuff. © World Health Organization, 2020 ISBN 978-92-4-000266-1 (print version)
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34

Katritsis, Demosthenes G., Bernard J. Gersh, and A. John Camm. Classification and pathophysiology of hypertension. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199685288.003.0431_update_004.

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35

Groeneveld, A. B. J., and Alexandre Lima. Vasodilators in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0035.

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Vasodilators are commonly used in the intensive care unit (ICU) to control arterial blood pressure, unload the left or the right heart, control pulmonary artery pressure, and improve microcirculatory blood flow. Vasodilator refers to drugs acting directly on the smooth muscles of peripheral vessel walls and drugs are usually classified based on their mechanism (acting directly or indirectly) or site of action (arterial or venous vasodilator). Drugs that have a predominant effect on resistance vessels are arterial dilators and drugs that primarily affect venous capacitance vessels are venous dilators. Drugs that interfere with sympathetic nervous system, block renin-angiotensin system, phosphodiesterase inhibitors, and nitrates are some examples of drugs with indirect effect. Vasodilator drugs play a major therapeutic role in hypertensive emergencies, primary and secondary pulmonary hypertension, acute left heart, and circulatory shock. This review discusses the main types of vasodilators drugs commonly used in the ICU.
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36

Wise, Matt, and Simon Barry. Respiratory failure. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0135.

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Respiratory failure is a syndrome characterized by defective gas exchange due to inadequate function of the respiratory system. There is a failure to oxygenate blood (hypoxaemia) and/or eliminate carbon dioxide (hypercapnia). Hypoxaemia is defined as an arterial blood partial pressure of oxygen (PaO2) of <8 kPa, and hypercapnia as an arterial blood partial pressure of carbon dioxide (PaCO2) of >6 kPa. Respiratory failure is divided into two different types, conventionally referred to as type 1 and type 2. The distinction between these two is important because it emphasizes not only different their pathophysiological mechanisms and etiologies, but also different treatments. The preferred terminology and definitions are as follows: oxygenation failure (type I respiratory failure), PaO2 of <8 kPa; ventilation failure (type 2 respiratory failure), PaCO2 >6 kPa. Respiratory failure may be acute (onset over hours to days), or chronic (developing over months to years); alternatively, there may be an acute deterioration of a chronic state.
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37

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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38

Hatfield, Anthea. Monitoring and equipment. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199666041.003.0004.

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Routine monitoring is an essential part of recovery room procedure. Respiration, a vital concern while awakening after anaesthesia, is given specific attention with reference to modern capnography. This chapter also describes additional monitoring in detail: pulse oximetry, blood pressure, central venous pressure, and arterial blood gases are clearly described. A comprehensive description of electrocardiography guides the student through this complicated subject. The monitoring of temperature and warming blankets, with suggestions for purchasing equipment, are included.
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39

Michel, Jean-Baptiste. Biology of vascular wall dilation and rupture. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0016.

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Arterial pathologies, important causes of death and morbidity in humans, are closely related to modifications in the circulatory system during evolution. With increasing intraluminal pressure and arterial bifurcation density, the arterial wall becomes the target of interactions with blood components and outward convection of plasma solutes and particles, including plasma zymogens and leukocyte proteases. Abdominal aortic aneurysms of atherothrombotic origin are characterized by the presence of an intraluminal thrombus (ILT), a major source of proteases, including plasmin, MMP-9, and elastase. Saccular cerebral aneurysms are characterized by the interaction of haemodynamics and arterial bifurcation defects, of either genetic or congenital origin. They also develop an intrasaccular thrombus, implicated in rupture. Aneurysms of the ascending aorta (TAAs) are not linked to atherothrombotic disease, and do not develop an ILT. The most common denominator of TAAs, whatever their aetiology, is the presence of areas of mucoid degeneration, and increased convection and vSMC-dependent activation of plasma zymogens within the wall, causing extracellular matrix proteolysis. TAA development is also associated with an epigenetic phenomenon of SMAD2 overexpression and nuclear translocation, potentially linked to chronic changes in mechanotransduction. Aortic dissections share common aetiologies and pathology (areas of mucoid degeneration) with TAAs, but differ by the absence of any compensatory epigenetic response. There are main experimental animal models of aneurysms, all characterized by the cessation of aneurysmal progression after interruption of the exogenous stimuli used to induce it. These new pathophysiological approaches to aneurysms in humans pave the way for new diagnostic and therapeutic tools.
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40

Gattinon, Luciano, and Eleonora Carlesso. Acute respiratory failure and acute respiratory distress syndrome. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0064.

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Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.
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41

Gattinon, Luciano, and Eleonora Carlesso. Acute respiratory failure and acute respiratory distress syndrome. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0064_update_001.

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Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.
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42

De Deyne, Cathy, and Jo Dens. Neurological assessment of the acute cardiac care patient. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0016.

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Many techniques are currently available for cerebral physiological monitoring in the intensive cardiac care unit environment. The ultimate goal of cerebral monitoring applied during the acute care of any patient with/or at risk of a neurological insult is the early detection of regional or global hypoxic/ischaemic cerebral insults. In the most ideal situation, cerebral monitoring should enable the detection of any deterioration before irreversible brain damage occurs or should at least enable the preservation of current brain function (such as in comatose patients after cardiac arrest). Most of the information that affects bedside care of patients with acute neurologic disturbances is now derived from clinical examination and from knowledge of the pathophysiological changes in cerebral perfusion, cerebral oxygenation, and cerebral function. Online monitoring of these changes can be realized by many non-invasive techniques, without neglecting clinical examination and basic physiological variables such as invasive arterial blood pressure monitoring or arterial blood gas analysis.
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43

De Deyne, Cathy, Ward Eertmans, and Jo Dens. Neurological assessment of the acute cardiac care patient. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0016_update_001.

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Many techniques are currently available for cerebral physiological monitoring in the intensive cardiac care unit environment. The ultimate goal of cerebral monitoring applied during the acute care of any patient with/or at risk of a neurological insult is the early detection of regional or global hypoxic/ischaemic cerebral insults. In the most ideal situation, cerebral monitoring should enable the detection of any deterioration before irreversible brain damage occurs or should at least enable the preservation of current brain function (such as in comatose patients after cardiac arrest). Most of the information that affects bedside care of patients with acute neurologic disturbances is now derived from clinical examination and from knowledge of the pathophysiological changes in cerebral perfusion, cerebral oxygenation, and cerebral function. Online monitoring of these changes can be realized by many non-invasive techniques, without neglecting clinical examination and basic physiological variables—with possible impact on optimal cerebral perfusion/oxygenation—such as invasive arterial blood pressure monitoring or arterial blood gas analysis.
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44

Kreit, John W. Gas Exchange. Edited by John W. Kreit. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190670085.003.0002.

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Gas Exchange explains how four processes—delivery of oxygen, excretion of carbon dioxide, matching of ventilation and perfusion, and diffusion—allow the respiratory system to maintain normal partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2) in the arterial blood. Partial pressure is important because O2 and CO2 molecules diffuse between alveolar gas and pulmonary capillary blood and between systemic capillary blood and the tissues along their partial pressure gradients, and diffusion continues until the partial pressures are equal. Ventilation is an essential part of gas exchange because it delivers O2, eliminates CO2, and determines ventilation–perfusion ratios. This chapter also explains how and why abnormalities in each of these processes may reduce PaO2, increase PaCO2, or both.
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45

Parikh, Roshni A., and David M. Williams. Clearing the Clogged Microcatheter During Particulate Embolization. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0064.

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This chapter describes the steps in management, applications, challenges, and potential complications when a microcatheter becomes clogged during an embolization. If a microcatheter does become occluded during an embolization, it can be a challenge to clear it without removing the catheter completely, thus losing access to the desired location. If a standard 1-cc syringe is placed and manual pressure is applied to clear the catheter, this can generate pressures up to 100 times the arterial blood pressure, thus risking nontarget embolization from the residual embolic material in the microcatheter. This chapter describes the steps involved in safely clearing an occluded microcatheter with the use of a standard balloon insufflator.
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46

Prout, Jeremy, Tanya Jones, and Daniel Martin. Respiratory system. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199609956.003.0002.

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This chapter includes a summary of respiratory physiology, respiratory mechanics (pressure-volume relationships and compliance, airway resistance and the work of breathing) and the pulmonary circulation (pulmonary vascular resistance, shunt and lung zones). Measurement of respiratory flow, lung volumes and diffusion capacity is summarized, as well as measurement and interpretation of arterial blood gases. The physics behind capnography and pulse oximetry are explained with abnormalities related to clinical contexts. The common clinical scenarios of respiratory failure and asthma are discussed with initial management and resuscitation.
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47

Rascher, Wolfgang. Treatment of hypertension in children. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0219_update_001.

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Management of hypertension is dependent on the underlying cause and the magnitude of the blood pressure abnormality. Healthy behavioural changes are the primary management tool for treating primary hypertension in adolescents and other cardiovascular risk factors and obesity. In children and adolescents with renal hypertension, high blood pressure requires pharmacological treatment. There is randomized controlled trial evidence to support a blood pressure target for those with proteinuria of not higher than the 50th centile for age. The use of angiotensin-converting enzyme inhibitors is safe in patients with proteinuria, and assumed to be equally beneficial. For those without proteinuria, less stringent targets may be acceptable. Often a combination of two or three drugs is required to lower arterial blood pressure to the target blood pressures. In children and adolescents at or near end-stage renal failure, fluid removal by dialysis may be necessary to control hypertension.
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Rascher, Wolfgang. The hypertensive child. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0218_update_001.

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Arterial hypertension is a well-recognized manifestation of various forms of renal disease both in adults and children. In the paediatric age group, standards for normal blood pressure are different from adults and have now been satisfactorily defined as have standards for measuring blood pressure. The epidemic of overweight and obesity in youth is increasing the prevalence of hypertension among children and adolescents. Measurement of blood pressure requires a technique specific for different age groups of the paediatric population, is more complex and requires particular expertise. Reference values in children requires adaptation to the age and size of the child and interpretation must be related to normative values specific for age, sex, and height. Evaluation for causes of secondary hypertension and for end-organ damage is basically similar in children as in adults. This chapter discusses measuring blood pressure, blood pressure standards, definition, classification, clinical presentation, and diagnostic approach to hypertension in children.
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Lee, Jae Myeong, and Michael R. Pinsky. Cardiovascular interactions in respiratory failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0087.

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Acute respiratory failure not only impairs gas exchange, but also stresses cardiovascular reserve by increasing the need for increased cardiac output (CO) to sustain O2 delivery in the face of hypoxaemia, increased O2 demand by the increased work of breathing and inefficient gas exchange, and increased right ventricular afterload due to lung collapse via hypoxic pulmonary vasoconstriction. Mechanical ventilation, though often reversing these processes by lung recruitment and improved arterial oxygenation, may also decrease CO by increasing right atrial pressure by either increasing intrathoracic pressure or lung over-distention by excess positive end-expiratory pressure or inadequate expiratory time causing acute cor pulmonale. Finally, spontaneous negative swings in intrathoracic pressure also increase venous return and impede left ventricular ejection thus increasing intrathoracic blood volume and often precipitating or worsening hydrostatic pulmonary oedema. Positive-pressure breathing has the opposite effects.
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Levy, Jerrold H., and David Faraoni. Pathophysiology and causes of severe hypertension. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0162.

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Hypertension affects multiple groups of patients characterized by different clinical presentations and a spectrum of potential causes. The pathophysiology is complex and multifactorial. Although most patients are labelled ‘essential hypertension’, multiple mechanisms are involved in blood pressure regulation. Factors that influence blood pressure homeostasis include endothelial function, the renin-angiotensin system, and the sympathetic nervous system. In elderly patients, hypertension is common as the vascular system and arterial stiffness also contribute. Other important factors include inflammatory processes as part of systemic diseases, including atherosclerosis,which may contribute to renal and vascular injury. Hypertension is also associated with metabolic disturbances including dyslipidaemia that manifests in obese patients who also have insulin resistance. These different pathways all represent potential targets for treatment, but also increase the challenge of multimodal pathophysiology.
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