bluuebunny/crossref_metadata_2025 huggingface dataset:
Analgesics in critical illness
Authors: Patel Mayur B. , Pandharipande Pratik P.
Published: April 2016

Analgesia is a critical component of intensive care unit (ICU) care. Accordingly, understanding the mechanism, physiological consequences, and assessment of pain is important when caring for the ICU patient. Non-pharmacological approaches should be attempted before supplementing analgesia with pharmacological agents. Pharmacologically-based therapies are divided into regional and systemic therapies. Regional analgesic therapies target specific areas of the body while limiting the systemic effects of intravenous analgesics, but at the risk of invasiveness, local anaesthetic toxicity, and infection of in-dwelling catheters. Systemic analgesic therapy is comprised of two main categories—non-opioids and opioids. Typically, non-opioid analgesics are used as adjunctive therapies and consist of agents such as non-steroidal anti-inflammatory drugs, gabapentinoids, ketamine, or α‎2 agonists. Opioid analgesia in the ICU is commonly infusion-based using fentanyl, hydromorphone, morphine, or recently, remifentanil.
Antidepressants in critical illness
Authors: Beach Scott R. , Stern Theodore A.
Published: April 2016

Selective serotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitors (SNRIs), and atypical antidepressants are considered first-line agents for depression in the intensive care unit (ICU) setting, and are preferred over older antidepressants due to their more benign side effect profile and tolerability. This chapter reviews the literature on the use of antidepressants in the ICU. Common side effects of SSRIs include insomnia and gastrointestinal discomfort, while citalopram may uniquely cause prolongation of the QTc interval. All SSRIs carry a risk for the development of serotonin syndrome following overdose. SNRIs are similar to SSRIs in their side effect profile, although they are more likely to cause hypertension. Mirtazapine is strongly associated with sedation and weight gain. Stimulants may also be used to treat depression in the medically ill, and can be particularly effective in treating apathy, low energy, and loss of appetite. Monotherapy is typically the initial treatment strategy and low doses are generally recommended in the ICU setting. Efficacy may not be apparent for up to 8 weeks. Patients who have been taking an antidepressant prior to their arrival in the ICU should continue on the medication so as to prevent discontinuation syndrome. Delirium may warrant cessation of the antidepressant and potentially dangerous medication interactions also need to be evaluated. At present, there is no evidence to suggest that an antidepressant should be initiated after a significant physical or emotional trauma.
Antiseizure agents in critical illness
Authors: Pollandt Sebastian , Shutter Lori
Published: April 2016

Seizures are a common problem in intensive care units (ICU) and the advent of continuous electroencephalography is demonstrating that the incidence of seizures is still underestimated. Many patients considered encephalopathic from any cause are now found to be in non-convulsive status epilepticus. While the significance of non-convulsive seizures remains unclear, there is little disagreement that these seizures should be treated with antiseizure agents and prevention of any type of seizure is a reasonable therapeutic goal. Many antiseizure agents have been studied in ICU populations and extensive experience exists with drugs such as phenytoin, valproate, or pentobarbital. Since the previous edition of this textbook, several new antiseizure agents have been introduced. Levetiracetam, topiramate, and lacosamide have been established as reasonable pharmacologic options, in particular for treatment of status epilepticus. Patients with seizures in the ICU often present with challenging clinical scenarios, which influence the choice of antiseizure agents. For example, reduced liver or renal function, especially if needing continuous renal replacement therapy or intermittent haemodialysis, has an impact on drug level variability and susceptibility to seizure development. ICU patients will typically require a multitude of pharmacological agents for their specific clinical situation and drug–drug interactions must be considered. Additionally, many medications used in ICUs are associated with seizures, in particular, certain antibiotics. Overall, the development of new drugs and better monitoring methods will undoubtedly improve our ability to control seizures in ICU patients, but currently no treatment has been shown to be universally effective for challenges, such as refractory status epilepticus.
Neuroprotective agents in critical illness
Authors: Perrott Jerrold L. , Reynolds Steven C.
Published: April 2016

The prevention and reduction of secondary injury following primary CNS insult is an important goal in critically-ill patients. Numerous pharmacological therapies have been studied as potential neuroprotective agents with few translating from research to clinical benefit. These are nimodipine and statins in aneurysmal subarachnoid haemorrhage and phenytoin in traumatic brain injury. Additionally, in traumatic brain injury, clinical studies have identified that corticosteroids and albumin colloid resuscitation are associated with increased risk of mortality, and as such should be avoided. Future research into new pharmacological neuroprotective strategies is warranted.
Haemostatic agents in critical illness
Authors: Hunt Beverley J.
Published: April 2016

Antifibrinolytics can prevent excessive bleeding during surgery and are also used to reduce established bleeding. By blocking the effects of plasmin, they prevent premature clot breakdown and enhance clot stability. The CRASH-2 trial showed that use of tranexamic acid in those with or at high risk of traumatic haemorrhage reduced mortality by 9%. Importantly for a drug that affects haemostasis, there appears to be no increased risk of either arterial or venous thromboembolism. Aprotinin while an excellent agent in reducing bleeding disproves previous assumption that reducing bleeding improves outcome, for the BART study demonstrated an increased mortality compared with tranexamic acid and EACA. It is still used occasionally in very high risk cardiac surgery patients. DDAVP (desmopressin) stimulates platelet function and is of use in patients with uraemia, although needs to be given with an antifibrinolytics, because it does also stimulate fibrinolytic activity. Off-license use of rVIIa is waning, clinical trials have as yet failed to show major benefit. Moreover, there is a high rate of arterial thrombosis after using rVIIA.
Colloids in critical illness
Authors: Webb Andrew
Published: April 2016

Colloid solutions are homogenous mixtures of large molecules suspended in a crystalloid solution. The efficacy of colloids as volume substitutes or expanders, and length of effect are determined by their physicochemical properties. Smaller volumes of colloid than crystalloid are required for resuscitation. The primary use of colloids is in the correction of circulating volume. Rather than using fixed haemodynamic endpoints, fluid can be given in small aliquots with assessment of the dynamic haemodynamic response to each aliquot. The aim of a fluid challenge is to produce a small, but significant (200 mL) and rapid increase in plasma volume with changes in central venous pressure or stroke volume used to judge fluid responsiveness. Colloid fluids give a reliable increase in plasma volume to judge fluid responsiveness.
Crystalloids in critical illness
Authors: Raghunathan Karthik , Shaw Andrew
Published: April 2016

‘Crystalloid’ refers to solutions of crystalline substances that can pass through a semipermeable membrane and are distributed widely in body fluid compartments. The conventional Starling model predicts transvascular exchange based on the net balance of opposing hydrostatic and oncotic forces. Based on this model, colloids might be considered superior resuscitative fluids. However, observations of fluid behaviour during critical illness are not consistent with such predictions. Large randomized controlled studies have consistently found that colloids offer no survival advantage relative to crystalloids in critically-ill patients. A revised Starling model describes a central role for the endothelial glycocalyx in determining fluid disposition. This model supports crystalloid utilization in most critical care settings where the endothelial surface layer is disrupted and lower capillary pressures (hypovolaemia) make volume expansion with crystalloids effective, since transvascular filtration decreases, intravascular retention increases and clearance is significantly reduced. There are important negative consequences of both inadequate and excessive crystalloid resuscitation. Precise dosing may be titrated based on functional measures of preload responsiveness like pulse pressure variation or responses to manoeuvres such as passive leg raising. Crystalloids have variable electrolyte concentrations, volumes of distribution, and, consequently variable effects on plasma pH. Choosing balanced crystalloid solutions for resuscitation may be potentially advantageous versus ‘normal’ (isotonic, 0.9%) saline solutions. When used as the primary fluid for resuscitation, saline solutions may have adverse effects in critically-ill patients secondary to a reduction in the strong ion difference and hyperchloraemic, metabolic acidosis. Significant negative effects on immune and renal function may result as well.
Airway management in cardiopulmonary resuscitation
Authors: Nolan Jerry P. , Soar Jasmeet
Published: April 2016

The most appropriate strategy for managing the airway during cardiopulmonary resuscitation (CPR) depends on the skills of the rescuer. Tracheal intubation is probably the optimal method for securing the airway, but only when undertaken by a highly-skilled individual. In the absence of a skilled intubator, insertion of a supraglottic airway device (SAD) is probably the best way of managing the airway during CPR. Some recent observation studies have suggested worse outcomes for cardiac arrest patients managed with a SAD compared with those receiving tracheal intubation. Such studies are likely to include hidden confounders and prospective randomized controlled trials are awaited. Use of waveform capnography is mandatory whenever tracheal intubation is attempted, but will also provide useful information about the effectiveness of CPR and an early indication of ROSC, even when used with a SAD. Once return of spontaneous circulation has been achieved, the inspired oxygen concentration should be titrated to achieve arterial blood oxygen saturation in the range 94–98%.
Pathophysiology and causes of cardiac arrest
Authors: Morley Peter Thomas
Published: April 2016

Sudden cardiopulmonary arrest (CPA) is still the commonest cause of death globally. CPAs are usually categorized according to where they occur, with out-of-hospital arrests accounting for approximately 75% of CPA deaths and in-hospital the remaining 25%. The arrests are also sub-categorized according to the initial rhythm, with the best outcomes associated with shockable rhythms. Large registries have demonstrated a variable incidence of out-of-hospital CPAs in adults (50–150/100,000 person years), with a range of outcomes (3–16% survival to hospital discharge). The majority of CPAs in adults are due to cardiac causes, but teaching surrounding the management of cardiac arrests now includes an increased focus on the identification and correction of underlying causes, irrespective of the rhythm. While identifying an underlying cause is often challenging, this is probably one of reasons explaining the improved survival seen with in-hospital compared with the out-of-hospital CPA. The incidence of CPAs in children is highest in infants, and decreases with age. The majority of CPAs in children are due to respiratory causes. Cardiac causes in children and young adults include a variety of familial, genetic, and acquired conditions. The pathophysiology of cardiac arrests is also now better understood. A large number of biochemical pathways are activated as a result of the CPA. These result in the post-cardiac arrest syndrome, which affects many systems in the body, but in particular the brain, heart, and kidneys.
Physiology of body fluids
Authors: Delaney Anthony
Published: April 2016

An understanding of the physiology of body fluids is essential when considering appropriate fluid resuscitation and fluid replacement therapy in critically-ill patients. In healthy humans, the body is composed of approximately 60% water, distributed between intracellular and an extracellular compartments. The extracellular compartment is divided into intravascular, interstitial and transcellular compartments. The movement of fluids between the intravascular and interstitial compartments, is classically described as being governed by Starling forces, leading to a small net efflux of fluid from the intravascular to the interstitial compartment. More recent evidence suggests that a model incorporating the effect of the endothelial glycoclayx layer, a web of glycoproteins and proteoglycans that are bound on the luminal side of the vascular endothelium, better explains the observed distribution of fluids. The movement of fluid to and from the intracellular compartment and the interstitial fluid compartment, is governed by the relative osmolarities of the two compartments. Body fluid status is governed by the difference between fluid inputs and outputs; fluid input is regulated by the thirst mechanism, with fluid outputs consisting of gastrointestinal, renal, and insensible losses. The regulation of intracellular fluid status is largely governed by the regulation of the interstitial fluid osmolarity, which is regulated by the secretion of antidiuretic hormone from the posterior pituitary gland. The regulation of extracellular volume status is regulated by a complex neuro-endocrine mechanism, designed to regulate sodium in the extracellular fluid.
Gas exchange assessment in the critically ill
Authors: Wagner Peter D.
Published: April 2016

Chapter 75 laid out the basic principles that govern pulmonary gas exchange, a step necessary for the appropriate application and interpretation of common clinical tests of gas exchange. The present chapter discusses the several common tests and indices used to analyse and quantify gas exchange abnormalities in critically-ill patients. There is special emphasis on inherent limitations of each technique, as well as on ways to minimize technical and experimental errors when the necessary measurements are made. Limitations and errors are considered to be of major clinical importance because, while the measurements and indices themselves are easy to obtain, and have been in routine use for many years, serious errors of interpretation can occur if the limitations and common errors are not appreciated and allowed for. In particular, it is pointed out that factors external to the lungs can dramatically change arterial oxygenation in the critically-ill patient. This means that not all changes in gas exchange reflect changes in lung pathology. It is not uncommon for arterial PO2 to change without change in lung disease severity when external factors such as metabolic rate, cardiac output, and blood temperature change.
Upper airway obstruction in the critically ill
Authors: Cohen Edmond
Published: April 2016

Upper airway obstruction (UAO) from any cause should be considered a life-threatening emergency. In a conscious patient, UAO may present as respiratory distress, stridor, dyspnoea, altered voice, cyanosis, cough, decreased or absent breath sounds, wheezing, the hand-to-the-throat choking sign in the case of a foreign body, facial swelling, and distended neck veins. The cause of UAO should be identified and airway management devices must be immediately available prior to any airway manipulation CT scan, flexible bronchoscopy, and pulmonary function tests should be performed to evaluate the cause and the extent of the obstruction. Obstructive sleep apnoea (OSA) patients are at increased risk of developing UAO. Endotracheal intubation, insertion of a supraglottic device, laser therapy, and endotracheal stents maybe life-saving
Standard intubation in the ICU
Authors: Russo Sebastian G. , Quintel Michael
Published: April 2016

Due to secretions, blood, or oedema in the patients’ airways, compromised pulmonary and haemodynamic, as well as limited access to the patients’ head the standard intubation in the ICU is an overall challenging procedure. Planning, preparation, and straight forwarded strategies are therefore mandatory. As a basic measure, sufficient pre-oxygenation should always be performed. Repetitive intubation attempts significantly worsen patients’ outcomes and need to be avoided. As adequate anaesthesia, including full neuromuscular blockade, can facilitate orotracheal intubation, this should be part of the routine. Apnoeic oxygenation during laryngoscopy by oxygen application via a nasal probe seems to be beneficial to prolong time to desaturation. Despite the fact that nowadays orotracheal intubation in the ICU is probably performed using mainly direct laryngoscopy, video laryngoscopes will possibly have increasing value on the ICU. Extraglottic airway devices represent useful tools to ventilate and oxygenate the patients’ lungs in case of an unexpected failed intubation attempt also on the ICU. In order to confirm adequate ventilation, capnography represents the standard of care and has to be a matter of course whenever a patient needs ventilator support on the ICU.
Dyspnoea in the critically ill
Authors: Tarsia Paolo
Published: April 2016

Dyspnoea may be defined as a subjective experience of discomfort associated with breathing. Breathing discomfort arises as a result of complex interactions between signals relayed from the upper airways, the chest wall, the lungs, and the central nervous system. Integration of this information with higher brain centres provides further processing. The final aspects of the sensation of dyspnoea are influenced by contextual, environmental, behavioural, and cognitive factors. At least three qualitatively distinct sensations have been employed to describe discomfort in breathing—air hunger, increased effort of breathing, and chest tightness. Air hunger has been shown to be associated with stimulation of chemoreceptors. Increased effort of breathing may arise in clinical conditions that impair respiratory muscle performance through abnormal mechanical loads or when respiratory muscles are weakened (neuromuscular diseases). Chest tightness is often experienced by asthmatic patients during episodes of acute bronchoconstriction. Measurement of dyspnoea is essential in order to assess it adequately and monitor response to treatment. Dyspnoea assessment may be carried out thorough a number of different scales, questionnaires, or exercise tests. Strategies in controlling dyspnoea should not focus uniquely on decreasing dyspnoea intensity. Patients may profit from interventions that decrease the unpleasantness associated with breathlessness without necessarily affecting the intensity component of the symptom.
Hypercapnia in the critically ill
Authors: Laffey John G. , Kavanagh Brian P.
Published: April 2016

Hypercapnia is a central component of current ‘protective’ ventilator management. Hypercapnia, and the associated acidosis, has potentially important biologic effects on immune responses, injury and repair. Arterial carbon dioxide tension PaCO2 is tightly governed under physiological conditions and small elevations rapidly increase spontaneous minute ventilation. In the mechanically-ventilated patient, elevated PaCO2 usually reflects reduced elimination. This can be because tidal volume or respiratory rate delivered by the ventilator are reduced, or because of the diseased lung per se. Hypercapnia has many effects that are clinically obvious, but research over the last decade reveals important consequences on inflammatory and cellular mechanisms that are not apparent at the bedside.
Cardiovascular interactions in respiratory failure
Authors: Lee Jae Myeong , Pinsky Michael R.
Published: April 2016

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.
Respiratory support with continuous positive airways pressure
Authors: Mojoli Francesco , Braschi Antonio
Published: April 2016

Continuous positive airways pressure (CPAP) is a mechanical ventilation (MV) mode in which the patient breaths spontaneously at a higher than atmospheric pressure. CPAP increases transpulmonary pressure inducing an FRC increase and a WOB decrease in acute restrictive lung pathology, with improvement of gas exchange. The work of breathing (WOB) is also reduced in the resistive component and inspiratory effort can be reduced if the patient experiences airway collapse and flow limitation, where CPAP counteracts the inspiratory threshold load represented by intrinsic PEEP. CPAP has been proven to be useful in many clinical situation and the technique for administration has a pivotal role in clinical efficacy of the technique. It’s crucial to keep the positive pressure as constant as possible and to avoid any technical increase of WOB. These goals can be achieved by continuous or demand flow systems. The modern ventilators work well and have overcome the valve function problem, which made difficult to use CPAP with old-generation machines.
Volume-controlled mechanical ventilation
Authors: Bauman Kristy A. , Hyzy Robert C.
Published: April 2016

The goal of mechanical ventilation is to achieve adequate gas exchange while minimizing haemodynamic compromise and ventilator-associated lung injury. Volume-controlled ventilation can be delivered via several modes, including controlled mechanical ventilation, assist control (AC) and synchronized intermittent mandatory ventilation (SIMV). .In volume-controlled modes, the clinician sets the flow pattern, flow rate, trigger sensitivity, tidal volume, respiratory rate, positive end-expiratory pressure, and fraction of inspired oxygen. Patient ventilator synchrony can be enhanced by setting appropriate trigger sensitivity and inspiratory flow rate. I:E ratio can be adjusted to improve oxygenation, avoid air trapping and enhance patient comfort. There is little data regarding the benefits of one volume-controlled mode over another. In acute respiratory distress syndrome, low tidal volume ventilation in conjunction with plateau pressure limitation should be employed as there is a reduction in mortality with this strategy. This chapter addresses respiratory mechanics, modes and settings, clinical applications, and limitations of volume-controlled ventilation.
Ventilator trauma in the critically ill
Authors: Amato Marcelo , Reske Andreas Wolfgang
Published: April 2016

Ventilator trauma refers to complications of mechanical ventilation, which have an impact on morbidity and mortality. Two major forms of ventilator trauma may be distinguished—an acute form related to rupture of airspaces causing air-leak syndrome and a subacute form causing protracted inflammatory responses. A key feature of mechanically-ventilated lungs is the presence of non-aerated and unstable regions due to atelectasis, oedema, or consolidation. Because of mechanical interdependence, pressures acting in non-uniformly expanded lungs at the boundaries between non-aerated and aerated lung may be a multiple of the apparent transpulmonary pressure. The resulting effects have been reported to precipitate or contribute to ventilator-induced lung injury (VILI). The engineering terms stress and strain were recently proposed for better definition of risk-constellations for VILI. Because the aerated lung volume is positively correlated to compliance, driving-pressure can aid in identifying disproportionate combinations of tidal volumes and compliance.
Inhalation injury in the ICU
Authors: Coppola Silvia , Valenza Franco
Published: April 2016

Inhalation injury represents one of the most serious associated injuries complicating the care of thermally-injured patient. It can result in severe respiratory failure and acute respiratory distress syndrome (ARDS) by three mechanisms—thermal or chemical injury, and impairment of systemic oxygen supply. Thermal injury can cause erythema, ulceration, and progressive, life-threatening oedema, particularly of the upper airways. Chemical injury is due to irritants or cytotoxic compounds, and depends on the material burned, the temperature of the fire, and the amount of oxygen present in the fire environment. It is responsible for irritation, ulceration, and oedema of the mucosal surface, and the initiation of a lung inflammatory reaction when small particles reach the alveoli. Moreover, the increased vascular permeability, and the reduced surfactant production carry a significant risk in the development of pneumonia and ARDS. Bronchospasm and upper airway oedema can occur rapidly, while lower airway oedema can be asymptomatic for up to 24 hours. Lung imaging techniques may not reveal injured areas for the first 24–48 hours. Fibre optic bronchoscopy is considered to be the most direct diagnostic method for the definitive diagnosis of inhalation injury. The patient management includes airways assessment, adequate fluid resuscitation, and mechanical ventilation when required. All victims of smoke inhalation should be always evaluated for cyanide and carbon monoxide poisoning.
Therapeutic strategy in acute or chronic airflow limitation
Authors: Macagno Francesco , Antonelli Massimo
Published: April 2016

The fragility of patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) accounts for their frequent hospitalization and their high intensive care unit risk. Therapy for AECOPD is varied and the need for hospitalization must be always carefully evaluated, considering the risk factors related to the presence of multi-resistant pathogens or the need of invasive procedures. The prolonged use of oxygen therapy requires an accurate monitoring of blood gases and continuous oximetry. Inhalation therapy can be performed using nebulizers, predosed aerosols or powders for inhalation. Corticosteroids for oral and systemic use now play an established role in AECOPD, because bacterial infections account for 50% of exacerbations. Non-invasive ventilation (NIV) must be considered the first option in AECOPD patients and acute respiratory failure if there are no contraindications. The careful monitoring of the patient and the response to NIV are indispensable elements for therapeutic success.
Diagnosis and management of community-acquired pneumonia
Authors: Torres Antoni , Liapikou Adamantia
Published: April 2016

Severe community-acquired pneumonia (SCAP) remains the most common infectious reason for admission to the intensive care unit (ICU), reaching a mortality rate of 30–40%. The microbial pattern of the SCAP has changed with S. pneumoniae still the leading pathogen, but a decrease of atypical pathogens, especially Legionella and an increase of viral and polymicrobial pneumonias. IDSA/ATS issued guidelines on the management of CAP including specific criteria to identify patients for ICU admission with good predictive value. The first selection of antimicrobial therapy should be started early covering all likely pathogens, depending on the presence of the risk factors for Pseudomonas aeruginosa infection. Combination therapy may be useful in patients with non-refractory septic shock and severe sepsis pneumococcal bacteraemia as well. The challenges include the emergence of new pathogens as community-acquired methicillin-resistant Staphylococcus aureus, new influenza virus subtypes and the high prevalence of multidrug resistance, mainly from institutionalizing patients.
Pathophysiology and prevention of sputum retention
Authors: Marini John J. , Formenti Paolo
Published: April 2016

Retention of airway mucus is one of the major problem that confronts post-operative and critically-ill patients, as well as the caregivers that address it. Retained secretions increase the work of breathing and promote hypoxaemia, atelectasis, and pneumonia. The airway-intubated patient is at particular risk of retaining mucus, as the presence of the tube interrupts normal flow of airway secretions toward the larynx by the mucociliary escalator and coughing effectiveness is degraded by a glottis that is stented open and cannot close effectively. Clearance of mucus is aided by using sufficient gas stream and total body hydration to reduce sputum viscosity and lubricate secretion plugs. Airway suctioning, a routine, but inherently traumatic experience for the patient, may clear the central airway, but leave peripheral airways unrelieved of their secretion burden. Prone positioning appears to confer an advantage regarding secretion drainage and clearance. Physiotherapy techniques may be useful in re-establishing and maintaining airway patency.
Management of pneumothorax and bronchial fistulae
Authors: Abouzgheib Wissam , Nahra Raquel
Published: April 2016

The management of pneumothorax is dependent on size and associated symptoms. A conservative approach is preferred in small and asymptomatic ones. While a large pneumothorax warrants chest tube drainage, small bore could be as effective as large chest tubes and should be used first. The use of bedside ultrasound plays a major role in the acute management of pneumothorax and has an excellent negative predictive value. In some instances, there may be an associated air leak, caused by a broncho- or alveolopleural fistula, which can be managed by chest tube drainage, with or without suction, depending on the severity and extent of lung collapse. With a large air leak, wall suction is needed to keep the lung inflated. In small, intermittent air leaks, suction should be avoided to promote healing of the fistula. With the availability of one-way valves, management of these fistulae became easier, allowing blockage of the airway causing the air leak, and promoting healing and early chest tube removal.
Normal physiology of the cardiovascular system
Authors: Montgomery Hugh , Astin Rónan
Published: April 2016

Preload modulates contractile performance, and is determined by end-diastolic volume (EDV) and ventricular compliance. Compliance falls with increasing preload, muscle stiffness or ventricular hypertrophy, making central venous pressure (CVP) a poor surrogate for EDV. Responsiveness to fluid loading can be identified by seeking a change in stroke volume (SV) with changes in cardiac loading. Afterload, the force to be overcome before cardiac muscle can shorten to eject blood, rises with transmural pressure and end-diastolic radius, and inversely with wall thickness. Afterload, being the tension across the ventricular wall, is influenced by pleural pressure. Reductions in afterload increase SV for any cardiac work, as do reductions in vascular resistance. Resistance is modified by changes in arteriolar cross-sectional area. A rise in resistance increases blood pressure and microvascular flow velocity. Increased resistance may reduce CO if cardiac work cannot be augmented sufficiently. Flow autoregulationis the ability of vascular beds to maintain constant flow across varied pressures by adjusting local resistance.
ECG monitoring in the ICU
Authors: Gandhi Sanjay , Lewis William R.
Published: April 2016

Electrocardiographic (ECG) monitoring is routinely used in hospitals for patients with a wide range of cardiac and non-cardiac diagnoses. Besides simple monitoring of heart rate and detection of life-threatening arrhythmias, the goals of ECG monitoring include detection of myocardial ischaemia, diagnosis of complex arrhythmia, and identification of a prolonged QT interval. The ECG remains a cornerstone in diagnosis and management of patients with coronary ischaemia. Over the past decade, there has been an increase in the number and complexity of electrophysiological interventions, including complex ablations, biventricular pacing, and insertion of implantable defibrillators. ECG monitoring in these patients can serve both a protective and diagnostic purpose. They detect life-threatening arrhythmias and double up as in-patient Holter monitors. Unfortunately, there are no randomized controlled trials of in-hospital cardiac monitoring—expert opinions based on clinical experience and published research in the field of electrocardiography form the basis of current guidelines.
Cardiac output assessment in the ICU
Authors: Arulkumaran Nishkantha , Cecconi Maurizio
Published: April 2016

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.
Oxygen transport in the critically ill
Authors: Jakob Stephan M. , Takala Jukka
Published: April 2016

Adequate oxygen delivery is crucial for organ survival. The main determinants of oxygen delivery are cardiac output, haemoglobin concentration, and arterial oxygen saturation. The adequacy of oxygen delivery also depends on oxygen consumption, which may vary widely. Mixed venous oxygen saturation reflects the amount of oxygen not extracted by the tissues, and therefore provides useful information on the relationship between oxygen delivery and oxygen needs. If not in balance, tissue hypoxia may ensue and arterial lactate concentration increases. This occurs at higher oxygen delivery rates in acute compared with chronic diseases where metabolic adaptions often occur. Arterial and mixed venous oxygen saturation are related to each other. The influence of mixed venous saturation on arterial saturation increases with an increasing intrapulmonary shunt. This chapter discusses interactions between the components of oxygen transport and how they can be evaluated. Various methods for measuring tissue oxygenation and oxygen consumption are also presented, together with their limitations.
Doppler echocardiography in the ICU
Authors: Maizel Julien , Slama Michel
Published: April 2016

The capacity of echocardiography to non-invasively identify the major causes of circulatory failure has made it increasingly popular in the intensive care unit (ICU) setting. Assessing cardiac performance in shocked patients is a key point in therapeutic support decision-making. Analysing left and right ventricular function and morphology should be mandatory in the training curriculum of ICU physicians. Haemodynamic evaluation relies on several parameters examining left ventricular systolic and diastolic function, left ventricular filling pressure, fluid responsiveness, and right ventricular function. To correctly interpret the echocardiographic findings and adapt patient management appropriately, physicians must be aware of the limits of these parameters.
Pathophysiology of coronary syndromes
Authors: Bell Robert M.
Published: April 2016

The pathophysiology of acute coronary syndromes is characterized by an acute mismatch of blood supply to the myocardium to meet the prevailing metabolic need. By far the commonest aetiology of myocardial ischaemia is coronary artery disease . An inflammatory process that evolves over the period of many decades, coronary artery disease is characterized by the deposition of cholesterol and cholesterol laden macrophages within the intima of the vessel wall. This process can be accelerated by a number of cardiovascular risk factors (smoking, hypertension, hyperlipidaemia, hypercholesterolaemia, diabetes), which can culminate in the formation of the unstable plaque responsible for the emergent presentation of ST-elevation myocardial infarction. This chapter reviews the prolonged inflammatory process responsible for atheroma formation, along with rarer, non-atheroma-related causes of acute coronary syndromes.
Therapeutic strategy in tachyarrhythmias
Authors: Walkey Allan J. , Magnani Jared
Published: April 2016

The therapeutic approach to tachyarrhythmias in the critically-ill patient involves rapid diagnosis and haemodynamic assessment. Patients who become haemodynamically unstable due to tachyarrhythmia warrant direct current cardioversion. Effects of direct current cardioversion during critical illness are often transient unless the underlying arrhythmia precipitant is eliminated and longer-acting rate- or rhythm-controlling medications are instituted. Atrial fibrillation often responds favourably to a rate-control strategy and treatment of the underlying precipitants. After initial clinical stabilization, clinical management involves elimination of potential arrhythmogenic triggers and administration of appropriate rate or rhythm control medications. Assessment of the QT interval in patients with polymorphic ventricular tachycardia is important in determining the underlying aetiology and treatment strategy. This chapter presents an evidence-based review of the therapeutic approach to tachyarrhythmias.
Pathophysiology and causes of severe hypertension
Authors: Levy Jerrold H. , Faraoni David
Published: April 2016

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.
Management of acute non-cardiogenic pulmonary oedema
Authors: Tanaka Sébastien , Duranteau Jacques
Published: April 2016

Severe capillary leak is an important factor in the pathogenesis of organ dysfunction following inflammatory syndromes such as sepsis-induced acute lung injury and acute respiratory distress syndrome (ARDS). Various interventions, such as a conservative fluid strategy, albumin, and diuretics are designed to maintain an adequate intravascular colloid osmotic pressure, reduce capillary leak and reduce extravascular water. Of these, only a conservative, rather than liberal fluid strategy is currently recommended. Preclinical studies in ARDS and sepsis suggest that preventing microvascular leak may represent a viable therapeutic approach to prevent or ameliorate organ dysfunction. The challenge is to now go further with carefully designed clinical trials.
Pathophysiology and causes of pericardial tamponade
Authors: Schairer John R. , Keteyian Steven J.
Published: April 2016

Pericardial disease leading to pericardial effusion (PEF) is a common clinical disorder. The most common causes are viral infections, metastatic cancer, renal disease, and bleeding disorders. PEF that accumulates slowly can become quite large before haemodynamic embarrassment occurs, while PEF that accumulates rapidly from trauma or aortic dissection can be small,yet cause haemodynamic embarrassment. As the PEF increases in size, the pressure in the pericardial space increases, leading to a decrease in atrial and ventricular chamber sizes, and limiting filling of the chambers. Ultimately, cardiac output is decreased,resulting in cardiac tamponade. When the limits of the pericardial stretch are reached, the volume in the pericardial sac becomes fixed. Any additional increase of PEF results in decreased cardiac size and any change in chamber size with respiration results in a paradoxical change in size of the other chambers. Tamponade is divided into three phases based on changes in pericardial and arterial pressure and cardiac output. Doppler echocardiography is the cornerstone of the diagnosis, follow-up, and management of PEF. It provides information about the presence, size, and location of the PEF, its impact on right ventricle, right atrium, and inferior vena cava size, and assesses tamponade physiology. Comorbid conditions may modify the signs of tamponade and need to be considered during the clinical assessment. Tamponade is not an all-or-nothing diagnosis, but instead should be viewed along a continuum of progressively worsening haemodynamics.
Management of pericardial tamponade
Authors: Biswas Santanu , Frank John J.
Published: April 2016

Cardiac tamponade is an emergency, and definitive therapy is fluid removal by pericardiocentesis. In certain conditions, fluid removal is still the optimal choice, but a conservative approach using haemodialysis may be employed. Factors that influence the management strategy include evaluating the cause, providing haemodynamic support, and choosing the technique. Fluid resuscitation to maintain venous pressure and circulation may be beneficial up to a point, after which, tamponade may be aggravated. While inotropes have theoretical benefit, studies involving humans are few. Fluid removal strategies are broadly grouped into percutaneous and surgical methods. In most cases, the percutaneous approach is favoured. However, surgery is typically the first choice in blunt trauma or in proximal aortic dissection. While the safety of percutaneous methods is well established, imaging guidance is needed to avoid common complications associated with a blind technique. The proper management strategy should also minimize effusion recurrence, common methods to do so include placement of a drainage catheter, infusion of a sclerosing agent, and a balloon pericardiotomy procedure. Surgical methods for removal of pericardial fluid include the creation pericardial window, insertion of a pericardioperitoneal shunt, and pericardiectomy. The creation of a pericardial window and pericardioperitoneal shunt are safe, but pericardiectomy is associated with increased morbidity. After fluid removal has been completed, the patient should be placed in a unit that is both familiar with the signs of tamponade and has the capacity to quickly treat a significant effusion if it recurs.
Pathophysiology and causes of pulmonary hypertension
Authors: Price Laura , Wort S. John
Published: April 2016

Pulmonary hypertension (PH) in the setting of critical illness may reflect the acute syndrome itself (such as acute massive pulmonary embolism or acute lung injury), and/or pre-existing ‘chronic’ causes of PH. To compound this, iatrogenic factors may also contribute to PH including the effects of positive pressure ventilation and certain vasoactive drugs. The presence of PH, especially when complicated by resulting right ventricular (RV) dysfunction and failure, is a poor prognostic feature in all settings. This chapter reviews the pathophysiology of acute PH in critical illness, and pre-existing chronic causes of PH, including acute decompensation in patients with pre-existing pulmonary arterial hypertension.
Diagnosis and management of pulmonary hypertension
Authors: Marino Philip , Price Laura
Published: April 2016

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.
Hepatic function in the critically ill
Authors: Kortgen Andreas , Bauer Michael
Published: April 2016

The liver with its parenchymal and non-parenchymal cells plays a key role in the organism with manifold functions of metabolism, synthesis, detoxification, excretion, and host response. This requires a portfolio of different tests to obtain an overview of hepatic function. In the critically ill hepatic dysfunction is common and potentially leading to extrahepatic organ dysfunctions culminating in multi-organ failure. Conventional laboratory measures are used to evaluate hepatocellular damage, cholestasis, or synthesis. They provide valuable (differential) diagnostic data and can yield prognostic information in chronic liver diseases, especially when used in scoring systems such as the ‘model for end-stage liver disease’. However, they have short-comings in the critically ill in assessing rapid changes in hepatic function and liver blood flow. In contrast, dynamic quantitative liver function tests measure current liver function with respect to the ability to eliminate and/or metabolize a specific substance. In addition, they are dependent on sinusoidal blood flow. Liver function tests have prognostic significance in the critically ill and may be used to guide therapy.
Pathophysiology and causes of upper gastrointestinal haemorrhage
Authors: Pirani Tasneem , Rahman Tony
Published: April 2016

Specific causes for upper gastrointestinal haemorrhage (UGIH) can often be ascertained through accurate history and examination. Causes can be thought of anatomically, as certain pathophysiological processes have a predilection for specific areas of the upper gastrointestinal tract, while other processes are diffuse. Specific treatment modalities exist for certain causes and therefore accurate assessment aids the tailoring of therapy. Peptic ulcer disease (PUD) is the most common cause of UGIH and Helicobacter pylori testing is recommended for all patients diagnosed with PUD. Understanding the risk factors associated with UGIH enables the physician to adopt preventative strategies such as gastric protection for high-risk patients on non-steroidal anti-inflammatory agents.