Matching Of Ventilation Research Articles

Dyspnea during exercise and voluntary hyperpnea in women with obesity

Temporal responses of ratings of perceived breathlessness (RBP) during constant-load and incremental exercise, and during voluntary hyperpnea (EVH) were examined in women with obesity. Following 6 min of constant-load (60W) cycling, 34 women rated RPB≥4 (+DOE) and 22 women rated RPB≤2 (–DOE). Both groups completed an incremental cycling test and an EVH test at 40 and 60L/min; RPB was assessed each minute of incremental cycling and at the end of each EVH trial. RPB increased with ventilation during constant-load (+DOE: R2=0.86; –DOE: R2=0.82) and incremental (+DOE: R2=0.91; –DOE: R2=0.92) exercise, but + DOE had a greater y-intercept than –DOE (60W: -0.16±1.53 vs. -0.73±0.55; incremental: -0.50±1.40 vs. -1.71±0.84). Despite matching ventilation, RPB was greater in + DOE at baseline (0.97±1.14 vs. 0.14±0.28), 40L/min (2.50±1.43 vs. 0.98±0.91), and 60L/min (3.94±2.19 vs. 2.07±1.32) during EVH. These findings show that despite linear associations between RPB and ventilation during exercise and voluntary hyperpnea, breathlessness perception at a given ventilatory demand is heightened in +DOE compared with –DOE.

Prone positioning for ARDS patients-tips for preparation and use during the COVID-19 pandemic.

Many patients with coronavirus disease (COVID-19) will develop acute respiratory distress syndrome (ARDS). Prone positioning is an important non-pharmacologic strategy that should be considered for all invasively ventilated patients with moderate to severe ARDS (including those with COVID-19). Prone positioning offers several physiologic and clinical benefits, including improving hypoxemia, matching ventilation with perfusion, reducing regional hyperinflation, and improving survival. To safely offer prone positioning, appropriate training, simulation, and health system planning should be undertaken. In this review, we offer ten tips, based on the Alberta provincial prone positioning strategy during COVID-19, to safely implement and improve the appropriate use of prone positioning. We provide special considerations for its use during the COVID-19 pandemic or future respiratory pandemics.Supplementary informationThe online version of this article (10.1007/s12630-020-01885-0) contains supplementary material, which is available to authorized users.

Autonomous control of ventilation through closed-loop adaptive respiratory pacing

Mechanical ventilation is the standard treatment when volitional breathing is insufficient, but drawbacks include muscle atrophy, alveolar damage, and reduced mobility. Respiratory pacing is an alternative approach using electrical stimulation-induced diaphragm contraction to ventilate the lung. Oxygenation and acid–base homeostasis are maintained by matching ventilation to metabolic needs; however, current pacing technology requires manual tuning and does not respond to dynamic user-specific metabolic demand, thus requiring re-tuning of stimulation parameters as physiological changes occur. Here, we describe respiratory pacing using a closed-loop adaptive controller that can self-adjust in real-time to meet metabolic needs. The controller uses an adaptive Pattern Generator Pattern Shaper (PG/PS) architecture that autonomously generates a desired ventilatory pattern in response to dynamic changes in arterial CO2 levels and, based on a learning algorithm, modulates stimulation intensity and respiratory cycle duration to evoke this ventilatory pattern. In vivo experiments in rats with respiratory depression and in those with a paralyzed hemidiaphragm confirmed that the controller can adapt and control ventilation to ameliorate hypoventilation and restore normocapnia regardless of the cause of respiratory dysfunction. This novel closed-loop bioelectronic controller advances the state-of-art in respiratory pacing by demonstrating the ability to automatically personalize stimulation patterns and adapt to achieve adequate ventilation.

HEAVILY CALCIFIED CLOTS IN A PATIENT WITH CHRONIC THROMBOEMBOLIC PULMONARY HYPERTENSION PRESENTING WITH BACTEREMIA

SESSION TITLE: Medical Student/Resident Pulmonary Vascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Antiphospholipid syndrome (APLS) is an autoimmune disorder that can lead to thrombotic disease. Here, we present a challenging case of catastrophic antiphospholipid syndrome with calcified clots, and chronic thromboembolic pulmonary hypertension (CTEPH) presenting with persistent bacteremia. CASE PRESENTATION: A 23-year-old female patient with a history of diabetes mellitus, methamphetamine and intravenous drug use disorder presented to an outside hospital with dry cough, shortness of breath, pleuritic chest pain, chills, and fatigue for 2 weeks. Blood cultures upon admission grew methicillin sensitive staphylococcus aureus (MSSA). Other labs were notable for thrombocytopenia and acute kidney injury. CT scan of chest and abdomen without contrast showed a large clot in her left pulmonary artery, inferior vena cava (IVC) extending into the right atrium (RA) with impressive calcifications (Figure 1). Transesophageal echocardiography showed no vegetations but revealed a large atrial thrombus extending from IVC into a dilated RA, dilated right ventricle, moderate tricuspid regurgitation with calculated right ventricular systolic pressure 55mmHg. Ventilation perfusion (VQ) scan showed a diffuse left lung perfusion defect without matched ventilation defect. She was transferred to our hospital for further care, her work-up revealed positive dilute Russell's viper venom time (dRVVT), cardiolipin antibodies and beta2-glycoprotein antibodies suggesting triple positive antiphospholipid syndrome. She was treated with intravenous heparin, however, developed hemoptysis requiring multiple blood transfusions and intubation, thus bronchial artery embolization was performed. Furthermore, she developed ST elevation myocardial infarction and splenic infarcts which were managed medically with resumption of heparin and antiplatelet therapy. She was eventually discharged on coumadin after completing six weeks of cefazolin and rifampin. DISCUSSION: This case illustrates an unusual presentation and calcification pattern of chronic clot, possibly due to the underlying infection, in a patient with CTEPH secondary to APLS. Mainstay of treatment for CTEPH remains anticoagulation followed by evaluation for pulmonary thromboendarterectomy (PTE) which is the only definite treatment (1). However, patients must tolerate anticoagulation, be clear of any infection and demonstrate adherence to therapy to undergo surgery. Furthermore, coumadin with an INR goal of 2.5 to 3.5 is recommended over direct oral anticoagulants in APLS with thromboembolism (2). CONCLUSIONS: In conclusion, CTEPH is associated with high morbidity and mortality, mainly from right heart failure (3). High level of suspicion is required to diagnose and promptly treat this rare disease with atypical presentation. Reference #1: Fedullo P, Kerr KM, Kim NH, Auger WR. Chronic thromboembolic pulmonary hypertension. Am J Respir Crit Care Med 2011; 183:1605. Reference #2: Pengo V, Denas G, Zoppellaro G, et al. Rivaroxaban vs warfarin in high-risk patients with antiphospholipid syndrome. Blood. 2018;132:1365–71. Reference #3: Hoeper MM, Mayer E, Simonneau G, Rubin LJ. Chronic thromboembolic pulmonary hypertension. Circulation 2006; 113:2011. DISCLOSURES: No relevant relationships by Timothy Fernandes, source=Web Response No relevant relationships by Abdurrahman Husain, source=Web Response No relevant relationships by Alexandra Rose, source=Web Response No relevant relationships by Qais Zawaydeh, source=Web Response

Hypercapnia Attenuates Ventricular Ectopy during Wakefulness in a Young Man with Heart Failure

Ventricular premature beats (VPBs) are common in heart failure (HF). Patients with HF often exhibit oscillations in breathing pattern (or Cheyne‐Stokes Respiration, CSR) that lead to increased VPBs during the hyperpneic phase. In such patients, CO2 inhalation during sleep eliminates CSR and reduces VPB prevalence. Whether this VPB‐lowering effect of CO2 occurs in awake HF patients without CSR remains unexplored. In a young CSR‐free HF patient (26 years; LVEF=20%; BMI=30 kg·m−2) with mild obstructive sleep apnea (AHI=17 events/h) and frequent ectopy, we compared the incidence of VPBs during: 1) resting breathing; 2) volitional hyperventilation; 3) and at standardized intervals (quartiles) during two CO2 rebreathing tests with end‐tidal O2 tension (PETO2) maintained at either 50 mmHg (hypercapnic‐hypoxia) or 150 mmHg (hypercapnic‐hyperoxia). Breath‐by‐breath ventilation, PETO2, and PETCO2 were measured by flowmeter and rapid gas analyzer and ECG and O2 saturation were monitored continuously. At rest (PETCO2=39 mmHg) and during hyperventilation (PETCO2=28 mmHg), VPBs occurred with 15% and 12% of all heart beats, respectively. With hyperoxic CO2 rebreathing (PETO2=148mmHg), as PETCO2 increased from 40, 46, 52, 57 mmHg in the first through fourth quartile, VPB incidence decreased from 11% to 6%, 3%, and 0%, respectively. Hypoxic rebreathing (PETO2=51mmHg) showed a similar trend: VPB incidence fell from 9% at a PETCO2 of 40 mmHg to 0% at 46 mmHg and remained at 0% thereafter. The hypercapnia‐induced reduction in VPB frequency was not dependent on heightened ventilation: VPBs were evident during volitional hyperventilation (12%) but not during the CO2 rebreathing quartiles with matched ventilation (0% for both hypoxia and hyperoxia). Furthermore, blood O2 also did not appear to modulate this response: VPB incidence at rest (15%) was similar to both hypoxic (11%; O2 saturation=86%) and hyperoxic (13%; O2 saturation=99%) CO2 rebreathing quartiles with matched ventilation (~9 L·min−1) and PETCO2 (~39 mmHg). These observations suggest that in HF, acute hypercapnia attenuates ventricular ectopy. The mechanism appears to be unrelated to increased respiratory or sympathetic drive, myocardial stretch accompanying large tidal volumes, or altered O2 availability. How hypercapnia exerts anti‐arrhythmic effects remain uncertain; we hypothesize that CO2 mediated increases in coronary flow may be involved.Support or Funding InformationExperiments were funded by a Project Grant from the Canadian Institutes of Health Research (PJT 159491).

59-Year-Old Woman With Fatigue, Dyspnea, and Lower Extremity Edema

59-Year-Old Woman With Fatigue, Dyspnea, and Lower Extremity Edema

0895 THE EFFECT OF LOOP GAIN ON EFFICACY OF SUPPLEMENTAL OXYGEN FOR TREATMENT OF INFANTS WITH OBSTRUCTIVE SLEEP APNEA (OSA)

Recent work from our group has demonstrated that the use of supplemental oxygen (suppO2) in infants with OSA results in fewer respiratory events and improved oxygenation without adversely affecting alveolar ventilation. However, a common observation in our study was that suppO2 was effective in some, but not all, infants. Based on data for adult patients with OSA, the administration of suppO2 seems most effective in those with a hypersensitive ventilatory control system (i.e. high loop gain). Accordingly, we hypothesized that infants who respond well to suppO2 have a higher measured loop gain than those who respond poorly. We conducted a retrospective analysis of 10 infants with OSA treated with suppO2 from 2007–2013. Subjects underwent a room air, diagnostic sleep study (RA-PSG) followed by a study for suppO2 titration (O2-PSG) on a separate night. The five subjects who best responded to suppO2, defined as those that showed the largest percent reduction in obstructive apnea hypopnea index (O-AHI) and those five with the worst response to suppO2 were identified. Loop gain was estimated from spontaneous breathing using 3 minute windows of sleep containing at least one respiratory event. Square root transformed nasal pressure airflow was used to provide a surrogate of ventilation. A standard model of ventilatory control (gain, time-constant, delay) that best matched ventilation data during periods of unobstructed breathing was used to estimate loop gain at the natural ‘resonant’ frequency (LGn) by a scorer blinded to responder condition. SuppO2 significantly reduced the O-AHI in responders (22.2 ± 10.0 events.hr-1 vs. 2.1 ± 1.0 events.hr-1: p<0.05) whereas it remained unchanged in the non-responders (18.3 ± 14.1 events.hr-1 vs. 20.3 ± 18.1 events.hr-1: p=NS). Compared to non-responders, responders displayed an elevated LGn (0.48 ± 0.07 vs. 0.36 ± 0.06: p<0.05). Our preliminary evidence suggests that infants with OSA who respond to suppO2 therapy have a higher loop gain compared to non-responders. These data suggest that similar to adults with OSA, ventilatory instability is an important mechanism causing OSA in some infants.

Hypoglycaemia Modulates The Patterns Of Ventilatory Responses Evoked By Chemoreceptor Stimulation

Hypoglycaemia (HG) evokes a counter‐regulatory response to restore arterial blood glucose levels. Additionally, HG has also been shown to evoke an increase in ventilation whilst maintaining normocapnia suggesting the ventilation remained matched to metabolism. Whilst it has been shown that HG induces an increase in CO2 sensitivity, there is a lack of data on how HG may modulate the pattern of breathing in normoxia as well as during chemoreceptor‐mediated responses. Whole body plethysmography (WBP) allows the measurement of respiratory variables in conscious unanesthetised animals under baseline conditions as well as during hypercpanic or hypoxic challenges.WBP was used to measure the ventilatory responses to air breathing (21% O2), acute hypoxia (10% O2) and hypercapnia (8% CO2) in male Wistar rats that had free access to food, were fasted overnight or were made hypoglycaemic by insulin injection. Blood glucose levels tended to be lower after fasting but not significantly (8±0.8mM vs 6.8±0.5mM), however, insulin injection did induce a significant HG (3.8±0.5mM). HG induced an increase in response to hypercapnia primarily by increasing tidal volume changes. Further, HG induced an increase in expiratory time (Te) that was abolished during hypercapnia but remained present during hypoxia with no changes in inspiratory time (TI). The TI:TE ratio increased in both hypercapnia and hypoxia, however, the magnitude of increase was only dependent on glycaemic state with hypercapnia.HG induces changes in baseline ventilation but also interacts with the response to a hypercapnic stimulus but not a hypoxic stimulus. The dependency on blood glucose levels of the TI:TE increase during hypercapnia may reflect the coordinated neuroendocrine responses seen during the counter‐regulatory response to HG and matching ventilation to an increased metabolic rate.Support or Funding InformationA. Mobley carried out this work in support of his MRes degree

Lung Structure and the Intrinsic Challenges of Gas Exchange.

Structural and functional complexities of the mammalian lung evolved to meet a unique set of challenges, namely, the provision of efficient delivery of inspired air to all lung units within a confined thoracic space, to build a large gas exchange surface associated with minimal barrier thickness and a microvascular network to accommodate the entire right ventricular cardiac output while withstanding cyclic mechanical stresses that increase several folds from rest to exercise. Intricate regulatory mechanisms at every level ensure that the dynamic capacities of ventilation, perfusion, diffusion, and chemical binding to hemoglobin are commensurate with usual metabolic demands and periodic extreme needs for activity and survival. This article reviews the structural design of mammalian and human lung, its functional challenges, limitations, and potential for adaptation. We discuss (i) the evolutionary origin of alveolar lungs and its advantages and compromises, (ii) structural determinants of alveolar gas exchange, including architecture of conducting bronchovascular trees that converge in gas exchange units, (iii) the challenges of matching ventilation, perfusion, and diffusion and tissue-erythrocyte and thoracopulmonary interactions. The notion of erythrocytes as an integral component of the gas exchanger is emphasized. We further discuss the signals, sources, and limits of structural plasticity of the lung in alveolar hypoxia and following a loss of lung units, and the promise and caveats of interventions aimed at augmenting endogenous adaptive responses. Our objective is to understand how individual components are matched at multiple levels to optimize organ function in the face of physiological demands or pathological constraints.

Differences in respiratory muscle activity during cycling and walking do not influence dyspnea perception in obese patients with COPD.

In patients with combined obesity and chronic obstructive pulmonary disease (COPD), dyspnea intensity at matched work rates during weight-supported cycling and weight-bearing walking is similar, despite consistent metabolic differences between test modalities. The present study examined the influence of differences in activity of the diaphragm and abdominal muscles during cycling and walking on intensity and quality of dyspnea at matched ventilation in obese patients with COPD. We compared respiratory muscle activity patterns and dyspnea ratings during incremental cycle and treadmill exercise tests, where work rate was matched, in 12 obese (body mass index 36.6 ± 5.4 kg/m(2); mean ± SD) patients with moderate COPD. We used a multipair electrode-balloon catheter to compare electromyography of the diaphragm and esophageal, gastric, and transdiaphragmatic pressures during the two exercise tests. Ventilation, breathing pattern, operating lung volumes, global respiratory effort, and electrical activation of the diaphragm were similar across exercise modalities for a given work rate. The cycling position was associated with greater neuromuscular efficiency of the diaphragm (P < 0.01), greater diaphragm use (P < 0.01) measured by the ventilatory muscle recruitment index, and less expiratory muscle activity compared (P < 0.01) with treadmill walking. However, intensity and quality of dyspnea were similar between exercise modalities. In obese patients with COPD, altered respiratory muscle activity due to body position differences between cycling and walking did not modulate perceived dyspnea when indirect measures of respiratory neural drive were unchanged.

Segmental Hyperperfusion in Lobar Pneumonia Visualized with Respiratory-gated Four-Dimensional Pulmonary Perfusion Positron Emission Tomography–Computed Tomography

A 64-year-oldman underwent a respiratory-gated four-dimensional pulmonary perfusion positron emission tomography (PET)/computed tomography (CT) for preoperative regional lung function quantification. This was performed after intravenous administration of Gamacroaggregated albumin (1–3). At the time of imaging, he had a productive cough, fever, and subsequent clinical diagnosis of bronchopneumonia. Images demonstrated an area of hyperperfusion localized to an area of dense collapse/consolidative change in the lateral segment of the right middle lobe (Figure 1 and supplemental video E1). The abnormality was also clearly apparent on the nonattenuation correction images, excluding an attenuation artifact. Studies have typically documented matched ventilation–perfusion or reverse mismatch phenomenon in pneumonia (4). Although occlusive obstruction of lobar airways is usually accompanied by reflex hypoxic vasoconstriction, the local release of inflammatory mediators with vasodilatory properties with infection results in failure of this mechanism and shunting leading to hypoxia (5). The histopathologic correlate is the red hepatization phase of lobar pneumonia. Tc-macroaggregated albumin single-photon emission computed tomography/CT had also been performed in this patient, but no corresponding perfusion abnormality was found. Although this was performed 72 hours earlier, the CT abnormality was similar; we contend that in addition to the superior imaging characteristics of PET, the absence of respiratory gating and attenuation correction contributed to lack of abnormality on single-photon emission computed tomography. The higher spatial and temporal resolution of PET combined with four-dimensional acquisition (6) provides a major advance in image quality and may improve our understanding of pulmonary physiology in a spectrum of diseases. n

Recent advances in understanding mechanisms regulating breathing during exercise

Recent advances in understanding mechanisms regulating breathing during exercise

Comparison of hyperpolarized 3He and 129Xe MRI for the measurement of absolute ventilated lung volume in rats

MRI using hyperpolarized noble gases, (3)He and (129)Xe, provides noninvasive assessments of lung structure and function. Previous work demonstrated that absolute ventilated lung volumes (aVLV) measured in rats using hyperpolarized (3)He agree well with micro-CT. In this work, aVLV measurements were performed in rats using hyperpolarized (129)Xe MRI and compared with hyperpolarized (3)He measurements of aVLV under matched ventilation conditions. Whole-lung compliance was also determined. Partial volume, apparent diffusion coefficient, and effective transverse relaxation time corrections were applied during postprocessing to reduce bias between methods. Mean apparent diffusion coefficient of the trachea was 0.83 ± 0.09 cm(2)/s and 0.067 ± 0.011 cm(2)/s for (3)He and (129)Xe, respectively. Mean apparent diffusion coefficient of parenchyma was 0.21 ± 0.07 cm(2)/s and 0.027 ± 0.008 cm(2)/s for (3)He and (129)Xe, respectively. Mean transverse relaxation time values were 1.57 ± 0.25 ms and 2.80 ± 0.25 ms for (3)He and (129)Xe, respectively, in a model trachea and 3.18 ± 1.00 ms and 4.88 ± 0.60 ms for (3)He and (129)Xe, respectively, for lung parenchyma. Mean aVLV values were 7.07 ± 0.67 mL and 6.99 ± 1.00 mL at 14 cmH2O and 4.88 ± 0.71 mL and 5.36 ± 0.76 mL at 10 cmH2O obtained with (3)He and (129)Xe, respectively, demonstrating good agreement between (129)Xe and (3)He. (129)Xe offers an important alternative to (3)He for hyperpolarized gas MRI of aVLV in rats.

Potential of hybrid V/P SPECT-low-dose CT in lung diagnostics

<h3>Summary</h3> Ventilation/perfusion single photon emission computed tomography (V/P SPECT), is the scintigraphic technique of choice for the diagnosis of pulmonary embolism (PE) and other conditions that affect lung function. In the study of ventilation, hydrophobic radioaerosol Technegas shows advantages over radiolabelled liquid aerosols because of its more even distribution and better peripheral penetration; this is very important in patients with COPD. Macro-aggregated human albumin is the imaging agent for perfusion scintigraphy. V/P SPECT is recommended as a one-day protocol and the whole study is conducted in 20 minutes under a gamma camera. An optimal combination of nuclide activities for ventilation and perfusion, general purpose collimators and a 64×64 imaging matrix yields an adequate sensitivity and ensures that radiation doses are kept very low. It is important that the patient remains in an unchanged supine position to allow reconstructed images of matching ventilation and perfusion slices in all projections as well as in rotating volume images. Probabilistic interpretation applied earlier for planar technique is replaced by a holistic interpretation strategy. This has resulted in a decrease in the number of nondiagnostic findings to less than 3%. To reduce costs and radiation exposure, pre-imaging assessment of clinical probability is recommended. PE is diagnosed when there is more than one subsegment showing a ventilation/perfusion mismatch conforming to an anatomic vascular lung unit. Apart from PE, other pathologies should be identified and reported, <i>e.g</i>. COPD, heart failure and pneumonia. Comparison of V/P SPECT with multidetector CT (MDCT) showed higher sensitivity for V/P SPECT, similar specificity and a similar number of nondiagnostic findings. The advantage of V/P SPECT is a 25-times lower absorbed radiation dose to the female breast and its applicability to all patients. The advantage of MDCT is its wider availability. Hybrid SPECT/CT imaging is a novel technique primarily developed to improve sensitivity and specificity of oncological diseases and it is not recommended as the primary tool for PE diagnosis in all patients with suspected PE. The application of SPECT/CT may be relevant in the case of COPD patients where small tumours may be identified as part of the diagnosis; in addition, it may help in the classification of COPD degree. <h3>Aims</h3> To increase awareness of the importance of optimal V/P SPECT and familiarity with the procedure. To explain the value of the new holistic, as opposed to probabilistic, interpretation in the diagnosis of PE. To show how the quantification of ventilation/perfusion defects can be used to define patient-specific treatments. To understand the role of V/P SPECT scintigraphy in other cardiopulmonary diseases, in addition to PE. To outline the pros and cons of angio-CT and V/P SPECT in the diagnosis of PE. To introduce the role of V/P SPECT and low-dose CT hybrid system in patients with suspected PE.

Recherche d’embolie pulmonaire : expérience nancéenne de la TEMP-TDM

The new recommendations from the EANM advocate the acquisition of SPECT images for the detection of acute pulmonary embolism. The increasing availability of hybrid cameras allows an easy combination with CT scan acquisition. Unenhanced CT scan is easy to perform and may provide: the diagnosis of pulmonary embolism, even when ventilation scan is not available, and an alternative diagnosis in case of matched ventilation and perfusion defects. Thus, CT scan associated with SPECT is becoming a reliable diagnostic tool for the diagnosis of pulmonary embolism. CT scan settings allow to deliver a low additional radiation burden to the patient.

Ventilator-induced respiratory muscle weakness

The most common reason to institute mechanical ventilation is to decrease patient distress resulting from an increase in work of breathing (1). In this situation, the ventilator is functioning as an additional set of muscles, and so decreases the load placed on the patient’s own respiratory muscles. The second major indication for mechanical ventilation is to improve oxygenation, as, for example, in patients with the acute respiratory distress syndrome (ARDS) (1). A ventilator improves oxygenation by increasing tidal volume and end-expiratory lung volume, and by better matching of ventilation and perfusion within the lung parenchyma (2). While the oxygen-enhancing action of the ventilator is not directed at the respiratory muscles per se, patients with impaired oxygenation are commonly treated with antibiotics (3), corticosteroids (4), sedatives (5) and neuromuscular agents (6), all of which can weaken respiratory muscles. Every patient who survives an episode of acute respiratory failure faces a major challenge at the point of ventilator discontinuation. The main reason that patients fail weaning attempts is because their work of breathing is high consequent to abnormal lung mechanics (increased resistance, decreased compliance) and their respiratory muscles are unable to cope with the increased load (7). From the above account, it is evident that performance of the respiratory muscles is a dominant consideration at the points when mechanical ventilation is first instituted and when it is being withdrawn. A major concern of critical care physicians is the growing awareness that mechanical ventilation can harm the lung. From the earliest days of intensive care, it has been recognized that use of high airway pressure can rupture the lung parenchyma, causing a pneumothorax. In 1974, Webb and Tierney demonstrated that mechanical ventilation can cause hemorrhagic and edematous lesions independent of barotrauma (8). This seminal observation was extended by other animal experiments and the alveolar injury has been shown to result from the use of high tidal volumes; the injury has been named volutrauma or ventilator-induced lung injury (9). Studies in animals were followed by studies in patients, which culminated in randomized controlled trials that have shown that use of high tidal volume leads to increased mortality in patients with ARDS. Just as mechanical ventilation can damage the lung parenchyma, investigators have postulated that the ventilator can damage the respiratory muscles (10). The fear is that mechanical ventilation lowers demands on a patient’s respiratory muscles to such an extent that they become inactive, resulting in injury and atrophy at a structural level. In contrast to research on ventilator-induced lung injury, scientific understanding of ventilator-induced respiratory muscle injury has not reached the stage where it is possible to undertake meaningful randomized controlled trials and thus it is not possible to render concrete recommendations for patient management. Nevertheless, the accruing biological and pathophysiological research on the effect of mechanical ventilation on the respiratory muscles is leading many experts to change their approach to ventilator management.

Pathophysiology of Neonatal Respiratory Distress Syndrome

Neonatal respiratory distress syndrome (RDS) remains one of the major causes of neonatal mortality and morbidity despite advances in perinatal care. The initial management of infants with RDS has almost become 'too routine' with little thought about the pathophysiological processes that lead to the disease and how the clinician can use the existing therapeutic interventions to optimize care. The transition from fetus to infant involves many complex adaptations at birth; the most important is the function of the lungs as a gas exchange organ. Preterm surfactant-deficient infants are less well equipped to deal with this transition. Optimum gas exchange is achieved through matching of ventilation and perfusion. In RDS, ventilation may be affected by homogeneity of the airways with atelectasis and over distension, as hyaline membranes block small airways. In turn this contributes to the inflammation that becomes bronchopulmonary dysplasia. Exogenous surfactant given early, particularly with positive end-expiratory pressure and, where necessary, gentle ventilation, would seem to be the optimum way to prevent atelectasis. How this can be achieved in neonates after surfactant therapy is explored through a review of the normal physiology of the newborn lung and how this is affected by RDS. The therapeutic interventions of resuscitation, exogenous surfactant, ventilation and inhaled nitric oxide are discussed in relation to their effects and what are currently the optimum ways to use these. It is hoped that with a better understanding of the normal physiology in the newborn lung, and the effects of both disease and interventions on that physiology, the practising clinician will have a greater appreciation of management of preterm infants with, or at risk of, RDS.

Démarche diagnostique et thérapeutique devant une hypoxémie

Since it may induce tissue hypoxia, arterial hypoxemia has fatal consequences on the organism. Evidence of hypoxemia by arterial blood gases, depending on its severity, may require emergency management in an intensive care unit. In any case, the screening for the cause is mandatory prior to any treatment initiation, but this must not delay the oxygen therapy. Alveolar hypoventilation, inadequate distribution and matching of ventilation and perfusion, true shunt and impaired diffusion across the alveolar capillary membrane are the main responsible mechanisms of hypoxemia. In most cases, clinical history, physical examination, and non invasive laboratory tests constitute sufficient basis for etiological diagnosis. In accordance with the recommendations, the therapeutic management associates etiological treatment and oxygen therapy.

Chapter 15 Matching of Ventilation and Perfusion in the Lung

Chapter 15 Matching of Ventilation and Perfusion in the Lung

Making sense of oxygen sensing.

Making sense of oxygen sensing.