198 research outputs found

    The physiology of ventilation

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    The diffusion of gases brings the partial pressures of O2 and CO2 in blood and alveolar gas to an equilibrium at the pulmonary blood-gas barrier. Alveolar PCO2 (PACO2) dependson the balance between the amount of CO2 being added by pulmonary blood and the amount being eliminated by alveolar ventilation (V\u2d9 A). In steady-state conditions, CO2 output equals CO2 elimination, but during nonsteadystate conditions, phase issues and impaired tissue CO2 clearance make CO2 output less predictable. Lung heterogeneity creates regional differences in CO2 concentration, and sequential emptying raises the alveolar plateau and steepens the expired CO2 slope in expiratory capnograms. Lung areas that are ventilated but not perfused form part of the dead space. Alveolar dead space is potentially large in pulmonary embolism, COPD, and all forms of ARDS. When PEEP recruits collapsed lung units, resulting in improved oxygenation, alveolar dead space may decrease; however, when PEEP induces overdistention, alveolar dead space tends to increase. Measuring physiologic dead space and alveolar ejection volume at admission or examining the trend during mechanical ventilation might provide useful information on outcomes of critically ill patients with ARDS

    Effect of external PEEP in patients under controlled mechanical ventilation with an auto-PEEP of 5 cmH2O or higher.

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    In some patients with auto-positive end-expiratory pressure (auto-PEEP), application of PEEP lower than auto-PEEP maintains a constant total PEEP, therefore reducing the inspiratory threshold load without detrimental cardiovascular or respiratory effects. We refer to these patients as complete PEEP-absorbers. Conversely, adverse effects of PEEP application could occur in patients with auto-PEEP when the total PEEP rises as a consequence. From a pathophysiological perspective, all subjects with flow limitation are expected to be complete PEEP-absorbers, whereas PEEP should increase total PEEP in all other patients. This study aimed to empirically assess the extent to which flow limitation alone explains a complete PEEP-absorber behavior (i.e., absence of further hyperinflation with PEEP), and to identify other factors associated with it.One hundred patients with auto-PEEP of at least 5 cmH2O at zero end-expiratory pressure (ZEEP) during controlled mechanical ventilation were enrolled. Total PEEP (i.e., end-expiratory plateau pressure) was measured both at ZEEP and after applied PEEP equal to 80 % of auto-PEEP measured at ZEEP. All measurements were repeated three times, and the average value was used for analysis.Forty-seven percent of the patients suffered from chronic pulmonary disease and 52 % from acute pulmonary disease; 61 % showed flow limitation at ZEEP, assessed by manual compression of the abdomen. The mean total PEEP was 7 ± 2 cmH2O at ZEEP and 9 ± 2 cmH2O after the application of PEEP (p < 0.001). Thirty-three percent of the patients were complete PEEP-absorbers. Multiple logistic regression was used to predict the behavior of complete PEEP-absorber. The best model included a respiratory rate lower than 20 breaths/min and the presence of flow limitation. The predictive ability of the model was excellent, with an overoptimism-corrected area under the receiver operating characteristics curve of 0.89 (95 % CI 0.80-0.97).Expiratory flow limitation was associated with both high and complete PEEP-absorber behavior, but setting a relatively high respiratory rate on the ventilator can prevent from observing complete PEEP-absorption. Therefore, the effect of PEEP application in patients with auto-PEEP can be accurately predicted at the bedside by measuring the respiratory rate and observing the flow-volume loop during manual compression of the abdomen

    Pressure-flow breath representation eases asynchrony identification in mechanically ventilated patients

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    Breathing asynchronies are mismatches between the requests of mechanically ventilated subjects and the support provided by mechanical ventilators. The most widespread technique in identifying these pathological conditions is the visual analysis of the intra-tracheal pressure and flow time-trends. This work considers a recently introduced pressure-flow representation technique and investigates whether it can help nurses in the early detection of anomalies that can represent asynchronies. Twenty subjects—ten Intensive Care Unit (ICU) nurses and ten persons inexperienced in medical practice—were asked to find asynchronies in 200 breaths pre-labeled by three experts. The new representation increases significantly the detection capability of the subjects—average sensitivity soared from 0.622 to 0.905—while decreasing the classification time—from 1107.0 to 567.1 s on average—at the price of a not statistically significant rise in the number of wrong identifications—specificity average descended from 0.589 to 0.52. Moreover, the differences in experience between the nurse group and the inexperienced group do not affect the sensitivity, specificity, or classification times. The pressure-flow diagram significantly increases sensitivity and decreases the response time of early asynchrony detection performed by nurses. Moreover, the data suggest that operator experience does not affect the identification results. This outcome leads us to believe that, in emergency contexts with a shortage of nurses, intensive care nurses can be supplemented, for the sole identification of possible respiratory asynchronies, by inexperienced staff

    Acute esophageal necrosis following cardiac arrest: A rare and lethal syndrome with diagnostic challenges

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    Introduction and clinical relevance: Acute esophageal necrosis (AEN) is a condition characterized by the necrosis of the distal portion of the esophageal mucosa. Risk factors predisposing to this condition are associated to compromised vascular perfusion (e.g. diabetes mellitus, chronic kidney disease, advanced age, and hypertension, shock states). Complications of AEN can be severe including UGI stricture, perforation and overall increased mortality. The true incidence of AEN remains uncertain due to potential subclincal presentations and early resolution. Case presentation: The case outlined involves a 66-years-old obese male with history of alcoholism and lymph-edema of the left leg who presented to the emergency department with hematemesis, haemodynamic instability and impaired consciousness. Shortly after initial assessment, the patient went into cardiac arrest with pulse-less electrical activity (PEA). Return of spontaneous circulation (ROSC) was achieved following instigation of ALS protocol, fluid resuscitation and the administration of a total of 5 mg of adrenaline. Following stabilization, a CT scan was performed which reported a moderately enlarged esophagus with a thickened wall, liquid hypodense material within the esophagus and stomach, and liver cirrhosis. The emergent esophagogastroduodenoscopy (EGDS) revealed extensive mucosal findings indicative of diffuse necrosis with initial scarring, which was later diagnosed as AEN. The patient unfortunately deceased in ICU after developing progression of the AEN, post-cardiac arrest syndrome and liver failure. Clinical discussion: The presented case highlights several crucial clinical issues and management problems related to AEN. To diagnose AEN, EGDS is still the gold-standard since it allows direct inspection of the esophageal mucosal layer. The management of AEN necessitates a multidisciplinary approach that includes aggressive resuscitation, treatment of underlying comorbidities, and supportive care (e.g. proton pump inhibitors). The mortality rate for AEN remains high despite improvements in diagnosis and treatment highlighting the need to recognize this condition early and intervene promptly in the patients affected. Moreover, long-term sequelae like stricture formation of the esophagus and impaired esophageal motility may contribute to morbidity requiring continuos monitoring. Therefore, to optimize outcomes while reducing complications among affected patients, prompt identification associated with appropriate medical measures are essential. More research needs to be done aiming to better understand the pathophysiology of AEN thereby identifying strategies for its prevention or cure. Conclusions: AEN is a rare syndrome characterized by upper gastrointestinal bleeding and hypoxic damage of the esophageal mucosa, often associated with ischemia, gastric outlet obstruction, and compromised protective barriers. Treatment involves aggressive resuscitation, proton pump inhibitors, and monitoring for infection or perforation. However, despite intensive efforts, the mortality rate for AEN remains high at 32 %

    Prediction of successful defibrillation in human victims of out-of-hospital cardiac arrest: a retrospective electrocardiographic analysis

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    In the present study we sought to examine the efficacy of an electrocardiographic parameter, 'amplitude spectrum area' (AMSA), to predict the likelihood that any one electrical shock would restore a perfusing rhythm during cardiopulmonary resuscitation in human victims of out-of-hospital cardiac arrest. AMSA analysis is not invalidated by artefacts produced by chest compression and thus it can be performed during CPR, avoiding detrimental interruptions of chest compression and ventilation. We hypothesised that a threshold value of AMSA could be identified as an indicator of successful defibrillation in human victims of cardiac arrest. Analysis was performed on a database of electrocardiographic records, representing lead 2 equivalent recordings from automated external defibrillators including 210 defibrillation attempts from 90 victims of out-of-hospital cardiac arrest. A 4.1 second interval of ventricular fibrillation or ventricular tachycardia, recorded immediately preceding the delivery of the shock, was analysed using the AMSA algorithm. AMSA represents a numerical value based on the sum of the magnitude of the weighted frequency spectrum between two and 48 Hz. AMSA values were significantly greater in successful defibrillation (restoration of a perfusing rhythm), compared to unsuccessful defibrillation (P < 0.0001). An AMSA value of 12 mV-Hz was able to predict the success of each defibrillation attempt with a sensitivity of 0.91 and a specificity of 0.97. In conclusion, AMSA analysis represents a clinically applicable method, which provides a real-time prediction of the success of defibrillation attempts. AMSA may minimise the delivery of futile and detrimental electrical shocks, reducing thereby post-resuscitation myocardial injury

    Haemodynamics and oxygenation improvement induced by high frequency percussive ventilation in a patient with hypoxia following cardiac surgery: a case report

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    <p>Abstract</p> <p>Introduction</p> <p>High frequency percussive ventilation is a ventilatory technique that delivers small bursts of high flow respiratory gas into the lungs at high rates. It is classified as a pneumatically powered, pressure-regulated, time-cycled, high-frequency flow interrupter modality of ventilation. High frequency percussive ventilation improves the arterial partial pressure of oxygen with the same positive end expiratory pressure and fractional inspiratory oxygen level as conventional ventilation using a minor mean airway pressure in an open circuit. It reduces the barotraumatic events in a hypoxic patient who has low lung-compliance. To the best of our knowledge, there have been no papers published about this ventilation modality in patients with severe hypoxaemia after cardiac surgery.</p> <p>Case presentation</p> <p>A 75-year-old Caucasian man with an ejection fraction of 27 percent, developed a lung infection with severe hypoxaemia [partial pressure of oxygen/fractional inspiratory oxygen of 90] ten days after cardiac surgery. Conventional ventilation did not improve the gas exchange. He was treated with high frequency percussive ventilation for 12 hours with a low conventional respiratory rate (five per minute). His cardiac output and systemic and pulmonary pressures were monitored.</p> <p>Compared to conventional ventilation, high frequency percussive ventilation gives an improvement of the partial pressure of oxygen from 90 to 190 mmHg with the same fractional inspiratory oxygen and positive end expiratory pressure level. His right ventricular stroke work index was lowered from 19 to seven g-m/m<sup>2</sup>/beat; his pulmonary vascular resistance index from 267 to 190 dynes•seconds/cm<sup>5</sup>/m<sup>2</sup>; left ventricular stroke work index from 28 to 16 gm-m/m<sup>2</sup>/beat; and his pulmonary arterial wedge pressure was lowered from 32 to 24 mmHg with a lower mean airway pressure compared to conventional ventilation. His cardiac index (2.7 L/min/m<sup>2</sup>) and ejection fraction (27 percent) did not change.</p> <p>Conclusion</p> <p>Although the high frequency percussive ventilation was started ten days after the conventional ventilation, it still improved the gas exchange. The reduction of right ventricular stroke work index, left ventricular stroke work index, pulmonary vascular resistance index and pulmonary arterial wedge pressure is directly related to the lower respiratory mean airway pressure and the consequent afterload reduction.</p

    Reactivation of Herpes Simplex Virus Type 1 (HSV-1) Detected on Bronchoalveolar Lavage Fluid (BALF) Samples in Critically Ill COVID-19 Patients Undergoing Invasive Mechanical Ventilation: Preliminary Results from Two Italian Centers

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    Reactivation of herpes simplex virus type 1 (HSV-1) has been described in critically ill patients with coronavirus disease 2019 (COVID-19) pneumonia. In the present two-center retrospective experience, we primarily aimed to assess the cumulative risk of HSV-1 reactivation detected on bronchoalveolar fluid (BALF) samples in invasively ventilated COVID-19 patients with worsening respiratory function. The secondary objectives were the identification of predictors for HSV-1 reactivation and the assessment of its possible prognostic impact. Overall, 41 patients met the study inclusion criteria, and 12/41 patients developed HSV-1 reactivation (29%). No independent predictors of HSV-1 reactivation were identified in the present study. No association was found between HSV-1 reactivation and mortality. Eleven out of 12 patients with HSV-1 reactivation received antiviral therapy with intravenous acyclovir. In conclusion, HSV-1 reactivation is frequently detected in intubated patients with COVID-19. An antiviral treatment in COVID-19 patients with HSV-1 reactivation and worsening respiratory function might be considered
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