Books on the topic 'Alveolar mechanics'

Ventilation can occur only when the respiratory system expands above and then returns to its resting or equilibrium volume. This is just another way of saying that ventilation depends on our ability to breathe. Although breathing requires very little effort and even less thought, it’s nevertheless a fairly complex process. Respiratory Mechanics reviews the interaction between applied and opposing forces during spontaneous and mechanical ventilation. It discusses elastic recoil, viscous forces, compliance, resistance, and the equation of motion and the time constant of the respiratory system. It also describes how and why pleural, alveolar, lung transmural, intra-abdominal, and airway pressure change during spontaneous and mechanical ventilation, and the effect of applied positive end-expiratory pressure (PEEP).

Beside reduction in tidal volume limiting peak airway pressure minimizes the risk for ventilator-associated-lung-injury in patients with acute respiratory distress syndrome. Pressure-controlled, time-cycled ventilation (PCV) enables the physician to keep airway pressures under strict limits by presetting inspiratory and expiratory pressures, and cycle times. PCV results in a square-waved airway pressure and a decelerating inspiratory gas flow holding the alveoli inflated for the preset time. Preset pressures and cycle times, and respiratory system mechanics affect alveolar and intrinsic positive end-expiratory (PEEPi) pressures, tidal volume, total minute, and alveolar ventilation. When compared with flow-controlled, time-cycled (‘volume-controlled’) ventilation, PCV results in reduced peak airway pressures, but higher mean airway. Homogeneity of regional peak alveolar pressure distribution within the lung is improved. However, no consistent data exist, showing PCV to improve patient outcome. During inverse ratio ventilation (IRV) elongation of inspiratory time increases mean airway pressure and enables full lung inflation, whereas shortening expiratory time causes incomplete lung emptying and increased PEEPi. Both mechanisms increase mean alveolar and transpulmonary pressures, and may thereby improve lung recruitment and gas exchange. However, when compared with conventional mechanical ventilation using an increased external PEEP to reach the same magnitude of total PEEP as that produced intrinsically by IRV, IRV has no advantage. Airway pressure release ventilation (APRV) provides a PCV-like squared pressure pattern by time-cycled switches between two continuous positive airway pressure levels, while allowing unrestricted spontaneous breathing in any ventilatory phase. Maintaining spontaneous breathing with APRV is associated with recruitment and improved ventilation of dependent lung areas, improved ventilation-perfusion matching, cardiac output, oxygenation, and oxygen delivery, whereas need for sedation, vasopressors, and inotropic agents and duration of ventilator support decreases.

Positive-end-expiratory pressure (PEEP) is the pressure present in the airway (alveolar pressure) above atmospheric pressure that exists at the end of expiration. The term PEEP is defined in two particular settings. Extrinsic PEEP (applied by ventilator) and intrinsic PEEP (PEEP caused by non-complete exhalation causing progressive air trapping). Applied (extrinsic) PEEP—is usually one of the first ventilator settings chosen when mechanical ventilation (MV) is initiated. Applying PEEP increases alveolar pressure and volume. The increased lung volume increases the surface area by reopening and stabilizing collapsed or unstable alveoli. PEEP therapy can be effective when used in patients with a diffuse lung disease with a decrease in functional residual capacity. Lung protection ventilation is an established strategy of management to reduce and avoid ventilator-induced lung injury and mortality. Levels of PEEP have been traditionally used from 5 to 12 cmH2O; however, higher levels of PEEP have also been proposed and updated in order to keep alveoli open, without the cyclical opening and closing of lung units (atelectrauma). The ideal level of PEEP is that which prevents derecruitment of the majority of alveoli, while causing minimal overdistension; however, it should be individualized and higher PEEP might be used in the more severe end of the spectrum of patients with improved survival. A survival benefit for higher levels of PEEP has not been yet reported for any patient under MV, but a higher PaO2/FiO2 ratio seems to be better in the higher PEEP group.

Mechanical ventilation is indicated when the patient’s ability to ventilate the lung and/or effect gas transport across the alveolar capillary interface is compromised to point that harm is imminent. In practice, this means addressing one or more of three fundamental pathophysiological processes—loss of proper ventilatory control, ventilatory muscle demand-capability imbalances, and/or loss of alveolar patency. A fourth general indication involves providing a positive pressure assistance to allow tolerance of an artificial airway in the patient unable to maintain a patent and protected airway. The decision to initiate mechanical ventilation usually involves an integrated assessment that should include mental status, airway protection capabilities, ventilatory muscle load tolerance, spontaneous ventilatory pattern, and signs of organ dysfunction from either acidosis and/or hypoxaemia. Providing mechanical ventilatory assistance can be life-sustaining, but it is associated with significant risk, including ventilator-induced lung injury, infection, and need for sedatives/paralytics, and must be applied only when indications justify the risk.

The acute respiratory distress syndrome (ARDS) is a syndrome of acute respiratory failure characterized by the acute onset of non-cardiogenic pulmonary oedema due to increased lung endothelial and alveolar epithelial permeability. Common predisposing clinical conditions include sepsis, pneumonia, severe traumatic injury, and aspiration of gastric contents. Environmental factors, such as alcohol abuse and cigarette smoke exposure may increase the risk of developing ARDS in those at risk. Pathologically, ARDS is characterized by diffuse alveolar damage with neutrophilic alveolitis, haemorrhage, hyaline membrane formation, and pulmonary oedema. A variety of cellular and molecular mechanisms contribute to the pathophysiology of ARDS, including exuberant inflammation, neutrophil recruitment and activation, oxidant injury, endothelial activation and injury, lung epithelial injury and/or necrosis, and activation of coagulation in the airspace. Mechanical ventilation can exacerbate lung inflammation and injury, particularly if delivered with high tidal volumes and/or pressures. Resolution of ARDS is complex and requires coordinated activation of multiple resolution pathways that include alveolar epithelial repair, clearance of pulmonary oedema through active ion transport, apoptosis, and clearance of intra-alveolar neutrophils, resolution of inflammation and fibrinolysis of fibrin-rich hyaline membranes. In some patients, activation of profibrotic pathways leads to significant lung fibrosis with resultant prolonged respiratory failure and failure of resolution.

In intensive care units practitioners are confronted every day with mechanically-ventilated patients and should be able to sort out from all the data available from modern ventilators to tailored patient ventilatory strategy. Real-time visualization of pressure, flow and tidal volume provide valuable information on the respiratory system, to optimize ventilatory support and avoiding complications associated with mechanical ventilation. Early determination of patient–ventilator asynchrony, air-trapping, and variation in respiratory parameters is important during mechanical ventilation. A correct evaluation of data becomes mandatory to avoid a prolonged need for ventilatory support. During dynamic hyperinflation the lungs do not have time to reach the functional residual capacity at the end of expiration, increasing the work of breathing and promoting patient-ventilator asynchrony. Expiratory capnogram provides qualitative information on the waveform patterns associated with mechanical ventilation and quantitative estimation of expired CO2. The concept of dead space accounts for those lung areas that are ventilated but not perfused. Calculations derived from volumetric capnography are useful indicators of pulmonary embolism. Moreover, alveolar dead space is increased in acute lung injury and its value decreased in case of positive end-expiratory pressure (PEEP)-induced recruitment, whereas PEEP-induced overdistension tends to increment alveolar dead space.

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.

During positive pressure ventilation the lung volume is reduced because of loss of respiratory muscle tone. This promotes airway closure that occurs in dependent lung regions. Gas absorption behind the closed airway results sooner or later in atelectasis depending on the inspired oxygen concentration. The elevated airway and alveolar pressures squeeze blood flow down the lung so that a ventilation/perfusion mismatch ensues with more ventilation going to the upper lung regions and more perfusion going to the lower, dependent lung. Positive pressure ventilation may impede the return of venous blood to the thorax and right heart. This raises venous pressure, causing an increase in systemic capillary pressure with increased capillary leakage and possible oedema formation in peripheral organs. Steps that can be taken to counter the negative effects of mechanical ventilation include an increase in lung volume by recruitment of collapsed lung and an appropriate positive end-expiratory pressure, to keep aerated lung open and to prevent cyclic airway closure. Maintaining normo- or hypervolaemia to make the pulmonary circulation less vulnerable to increased airway and alveolar pressures, and preserving or mimicking spontaneous breaths, in addition to the mechanical breaths, since they may improve matching of ventilation and blood flow, may increase venous return and decrease systemic organ oedema formation (however, risk of respiratory muscle fatigue, and even overexpansion of lung if uncontrolled).

High-frequency oscillatory ventilation (HFOV) is a key member of the family of modes called high-frequency ventilation and achieves adequate alveolar ventilation despite using very low tidal volumes, often below the dead space volume, at frequencies significantly above normal physiological values. It has been proposed as a potential protective ventilatory strategy, delivering minimal alveolar tidal stretch, while also providing continuous lung recruitment. HFOV has been successfully used in neonatal and paediatric intensive care units over the last 25 years. Since the late 1990s adults with acute respiratory distress syndrome have been treated using HFOV. In adults, several observational studies have shown improved oxygenation in patients with refractory hypoxaemia when HFOV was used as rescue therapy. Several small older trials had also suggested a mortality benefit with HFOV, but two recent randomized control trials in adults with ARDS have shed new light on this area. These trials not show benefit, and in one of them a suggestion of harm was seen with increased mortality for HFOV compared with protective conventional mechanical ventilation strategies (tidal volume target 6 mL/kg with higher positive end-expiratory pressure). While these findings do not necessarily apply to patients with severe hypoxaemia failing conventional ventilation, they increase uncertainty about the role of HFOV even in these patients.

Moving away from the structure of traditional texts, this chapter follows the journey of oxygen molecules as they move from inspired air to their point of use in mitochondria, with some digressions along the way to cover other relevant aspects of respiratory physiology. The chapter encompasses all the key aspects of respiratory physiology and also highlights physiological alterations that occur under both general and regional anaesthesia, moving the physiological principles discussed into daily anaesthetic practice. The chapter explores relevant anatomy of the airways, lungs, and pleura. The histology and function of the airway lining and alveoli are described, so illustrating the importance of pulmonary defence mechanisms for protecting the internal milieu of the body from this large and fragile interface with the outside world. Key principles and concepts including resistance, compliance, and diffusion are all discussed in their clinical context. Concepts relating to the mechanics of breathing and the control of airway diameter are considered along with lung volumes and their measurement. Both the central and peripheral mechanisms involved in the control of breathing are discussed with particular attention to the impact of anaesthesia. The relationship between ventilation and perfusion and the carriage of oxygen and carbon dioxide are all discussed in detail. The principles behind key respiratory measurements such as dead space, lung volumes, diffusing capacity, and shunt are all described. Overall the chapter provides a comprehensive review of respiratory physiology as well as including additional aspects of variation that occur under anaesthesia.

This chapter describes positive airway pressure (PAP) therapy for sleep disordered breathing. Continuous PAP (CPAP) acts as a mechanical splint on the upper airway and is the treatment of choice for moderate to severe obstructive sleep apnea (OSA). Autotitrating CPAP may be used when the pressure demand for stabilizing the upper airway is quite variable. In other cases, fixed CPAP is sufficient. There is robust evidence that CPAP reduces the symptomatic burden and risk of cardiovascular comorbidity in patients with moderate to severe OSA. Bilevel PAP is indicated for treatment of respiratory diseases characterized by chronic alveolar hypoventilation, which typically deteriorates during sleep. Adaptive servo-ventilation is a mode of bilevel PAP used to treat Cheyne–Stokes respiration with central sleep apnea . It is crucial that caregivers help patients get used to and be compliant with PAP therapy. Education, support, and resolution of adverse effects are mandatory for therapeutic success.

Aspiration pneumonitis during the perioperative period is a serious complication and involves passage of sterile gastric contents into the airway resulting in alveolar damage. The mechanism of aspiration pneumonitis is characterized by a significant inflammatory reaction. The risk of aspiration is highest during anesthesia induction, but it is also present during emergence and extubation. The risk factors include delayed gastric emptying (gastritis, pain, pregnancy, obesity, elevated intracranial pressure), emergency surgery, upper abdominal surgery, and difficulty securing the airway. Anesthesiologists should focus on prevention of pulmonary aspiration with consideration of the patient’s NPO status and risk factors when planning anesthesia induction and emergence. If aspiration of gastric contents occurs, the patient may exhibit a variety of symptoms, with severity based on the volume and pH of the aspirate. Subsequently, patients with observed or suspected aspiration need supportive treatment that varies depending on the severity of symptoms.

Intramural pressures within a tube or circuit determine the rate and direction of flow, whereas the transmural pressure of an elastic structure determines its volume. In Chapter 1, we applied these principles when talking about the pressure needed to overcome viscous forces and elastic recoil during ventilation. In this chapter, we use them to explain changes in blood flow between two portions of the circulatory system and changes in the volume and size of the heart chambers. Cardio–Pulmonary Interactions provides an overview of essential cardiovascular physiology as well as an in-depth discussion of how and why changes in pleural, alveolar, lung transmural, and intra-abdominal pressure during spontaneous and mechanical ventilation can alter right and left ventricular preload, afterload, and stroke volume, cardiac output, and blood pressure. The chapter also reviews the beneficial and detrimental effects of positive end-expiratory pressure (PEEP) on cardiovascular function.

Out of 15–30 × 10–3 moles/day of protons derived from the hydration of CO2 only 40–60 × 10–9 moles/day remain unbounded in the plasma. If the CO2 production exceeds the excretion, the CO2 content in plasma and tissue rises (respiratory acidosis) until a new equilibrium is reached. In fact, doubling the PCO2 may compensate the halving of alveolar ventilation with unchanged excretion of the CO2 metabolically produced. Body reacts to respiratory acidosis increasing the secretion of chloride associated with ammonium. The process leads to an increase of bicarbonate in the plasma with an associated increase of pH. All the steps described may be altered in critically-ill patients due to hyper-metabolism, decreased excretion, decreased content of buffering proteins and impaired kidney response. Several options are available for therapy, from mechanical ventilation to artificial lung, up to lung transplant, depending on the severity of clinical conditions and their possible reversibility.

The airway lining fluid is a biphasic layer covering the respiratory tract epithelium. It has antimicrobial and immunomodulatory properties, and it is formed by a gel-phase (mucus), and a low-viscosity inner layer (sol-phase) that provides lubrication for ciliary beating. Mucus is continuously cleared from the airways through the ciliated epithelium and via the two-phase gas–liquid flow mechanism (i.e. coughing). Mucus production in healthy subjects is approximately 10–100 mL/day. Whereas, mucociliary clearance rates range between 4 and 20 mm/min. Critically-ill, mechanically-ventilated patients often retain mucus. Several chest physiotherapy techniques are applied to promote mucus clearance in these patients. The role of chest physiotherapy in mechanically-ventilated patients is debated, due to the lack of evidence from well-designed clinical trials. Retained mucus is aspirated through tracheobronchial suctioning. Closed suctioning is beneficial in patients with severe lung failure and at risk of alveolar collapse upon ventilator disconnection.

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.

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.

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.

Any public debate about air pollution starts with the premise that air pollution cannot be good for you, so we should have less of it. However, it is much more difficult to determine how much is dangerous, and even more difficult to decide how much we are willing to pay for improvements in measured air pollution. Recent UK estimates suggest that fine particulate pollution causes about 6500 deaths per year, although it is not clear how many years of life are lost as a result. Some deaths may just be brought forward by a few days or weeks, while others may be truly premature. Globally, household pollution from cooking fuels may cause up to two million premature deaths per year in the developing world. The hazards of black smoke air pollution have been known since antiquity. The first descriptions of deaths caused by air pollution are those recorded after the eruption of Vesuvius in ad 79. In modern times, the infamous smogs of the early twentieth century in Belgium and London were clearly shown to trigger deaths in people with chronic bronchitis and heart disease. In mechanistic terms, black smoke and sulphur dioxide generated from industrial processes and domestic coal burning cause airway inflammation, exacerbation of chronic bronchitis, and consequent heart failure. Epidemiological analysis has confirmed that the deaths included both those who were likely to have died soon anyway and those who might well have survived for months or years if the pollution event had not occurred. Clean air legislation has dramatically reduced the levels of these traditional pollutants in the West, although these pollutants are still important in China, and smoke from solid cooking fuel continues to take a heavy toll amongst women in less developed parts of the world. New forms of air pollution have emerged, principally due to the increase in motor vehicle traffic since the 1950s. The combination of fine particulates and ground-level ozone causes ‘summer smogs’ which intensify over cities during summer periods of high barometric pressure. In Los Angeles and Mexico City, ozone concentrations commonly reach levels which are associated with adverse respiratory effects in normal and asthmatic subjects. Ozone directly affects the airways, causing reduced inspiratory capacity. This effect is more marked in patients with asthma and is clinically important, since epidemiological studies have found linear associations between ozone concentrations and admission rates for asthma and related respiratory diseases. Ozone induces an acute neutrophilic inflammatory response in both human and animal airways, together with release of chemokines (e.g. interleukin 8 and growth-related oncogene-alpha). Nitrogen oxides have less direct effect on human airways, but they increase the response to allergen challenge in patients with atopic asthma. Nitrogen oxide exposure also increases the risk of becoming ill after exposure to influenza. Alveolar macrophages are less able to inactivate influenza viruses and this leads to an increased probability of infection after experimental exposure to influenza. In the last two decades, major concerns have been raised about the effects of fine particulates. An association between fine particulate levels and cardiovascular and respiratory mortality and morbidity was first reported in 1993 and has since been confirmed in several other countries. Globally, about 90% of airborne particles are formed naturally, from sea spray, dust storms, volcanoes, and burning grass and forests. Human activity accounts for about 10% of aerosols (in terms of mass). This comes from transport, power stations, and various industrial processes. Diesel exhaust is the principal source of fine particulate pollution in Europe, while sea spray is the principal source in California, and agricultural activity is a major contributor in inland areas of the US. Dust storms are important sources in the Sahara, the Middle East, and parts of China. The mechanism of adverse health effects remains unclear but, unlike the case for ozone and nitrogen oxides, there is no safe threshold for the health effects of particulates. Since the 1990s, tax measures aimed at reducing greenhouse gas emissions have led to a rapid rise in the proportion of new cars with diesel engines. In the UK, this rose from 4% in 1990 to one-third of new cars in 2004 while, in France, over half of new vehicles have diesel engines. Diesel exhaust particles may increase the risk of sensitization to airborne allergens and cause airways inflammation both in vitro and in vivo. Extensive epidemiological work has confirmed that there is an association between increased exposure to environmental fine particulates and death from cardiovascular causes. Various mechanisms have been proposed: cardiac rhythm disturbance seems the most likely at present. It has also been proposed that high numbers of ultrafine particles may cause alveolar inflammation which then exacerbates preexisting cardiac and pulmonary disease. In support of this hypothesis, the metal content of ultrafine particles induces oxidative stress when alveolar macrophages are exposed to particles in vitro. While this is a plausible mechanism, in epidemiological studies it is difficult to separate the effects of ultrafine particles from those of other traffic-related pollutants.

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are characterized by rapidly developing hypoxaemic respiratory failure and bilateral pulmonary infiltrates on chest X-ray. ALI/ARDS are a relatively frequent diagnosis in protracted-stay patients in the intensive care unit. The pathology is a non-specific response to a wide variety of insults. Impaired gas exchange, ventilation-perfusion mismatch, and reduced compliance ensue. Mechanical ventilation is the mainstay of management, along with treatment of the underlying cause. Mortality remains very high at around 40%. The condition is challenging to treat. Injury to the lungs, indistinguishable from that of ARDS, has been attributed to the use of excessive tidal volumes, pressures, and repeated opening and collapsing of alveoli. Lung-protective strategies aim to minimize the effects of ventilator-induced lung injury. Use of low tidal volume ventilation has been shown to improve mortality. Emerging ventilatory therapies include high-frequency oscillatory ventilation and extracorporeal membrane oxygenation.