High Intrathoracic Pressure Research Articles

A rare case: negative-pressure pulmonary edema after routine rhinoplasty

Negative-pressure pulmonary edema (NPPE) is a very rare and dangeorus condition that generally occurs after general anesthesia in otorhinolaryngology practices. Post-obstructive pulmonary edema or NPPE caused by an acute pulmonary edema secondary to upper respiratory tract obstruction. Its sudden appearance in the early postoperative period can stress the surgeon and the anesthesiologist. Difficult breathing effort due to upper airway obstruction creates strong changes in intra-thoracic pressure, and high negative intrathoracic pressure increases the permeability of the alveolar capillary membrane, causing significant fluid changes in the pulmonary tissues. Treatment should be evaluated together with anesthesiologist or pulmonologist and the first goal should be to reduce the hypoxia.

Spontaneous Tension Hemothorax in a Patient with Asbestosis.

A 75-year-old man with a history of asbestosis presented to the emergency department with sudden-onset dyspnea and hemoptysis, triggered by coughing. The patient was hemodynamically unstable and in respiratory distress. Computed tomography revealed a massive hemothorax on the left side and compression of the descending thoracic aorta. He underwent emergency surgical exploration after decompression by chest tube insertion. The hemothorax was caused by tears in the pleural adhesions due to asbestosis and induced by coughing. Spontaneous hemothorax is a rare subtype of hemothorax. There have been only a few case reports of spontaneous tension hemothorax. In addition to its typical findings, compression of the thoracic descending aorta was observed in our patient. We hypothesize that severely diminished pulmonary compliance contributed to the extremely high intrathoracic pressure, which led to this unusual finding.

Intra-aortic Balloon Pump May Attenuate Adverse Hemodynamic Effects of Negative Intrathoracic Pressure in Cardiogenic Shock

High negative intrathoracic pressure (NIP), as occurs during obstructive sleep apnea or hiccups, results in adverse hemodynamic consequences, specifically a decrease in left ventricle (LV) performance. These untoward effects can potentially be catastrophic in the case of an already compromised LV in cardiogenic shock. The interplay of intra-aortic balloon pump counter pulsation during abrupt high NIP in cardiogenic shock is described.

Sevoflurane sedation and nephrogenic diabetes insipidus in patients affected with severe acute respiratory syndrome coronavirus 2.

Sevoflurane sedation and nephrogenic diabetes insipidus in patients affected with severe acute respiratory syndrome coronavirus 2.

COUGH-INDUCED DIFFUSE BRONCHIAL HEMORRHAGE

SESSION TITLE: Medical Student/Resident Procedures Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Bleeding from the tracheobronchial tree is usually caused by neoplasms, bronchitis, bronchiectasis, mucosal infections, and/or iatrogenic mucosal erosions. We present a rare case of petechial tracheobronchial hemorrhage developing after a severe bout of cough. CASE PRESENTATION: An 81-year-old male with past medical history of Acquired immunodeficiency syndrome (AIDS), combined pulmonary fibrosis and emphysema, pulmonary hypertension, and chronic hypoxemia on supplemental oxygen (3 L/min), presented with gradually worsening dyspnea and non-productive cough over 6 months. Computed tomography (CT) scan of the chest showed a right upper lobe cavitary lesion for which further evaluation with diagnostic flexible fiberoptic bronchoscopy was planned. His home medications included low dose aspirin (81 mg) daily for the primary prevention of cardiovascular disease. He did not have any prior history of hemoptysis or coagulopathy. The patient received aerosolized topical anesthesia with nebulized lidocaine orally prior to bronchoscopy after which he developed a strong coughing fit. Patient was intubated with a laryngeal mask and flexible bronchoscopy was performed under monitored anesthesia care using Propofol. Inspection of the airways incidentally showed numerous mucosal petechiae with oozing of blood in the entire tracheobronchial tree distal to the vocal cords [Figure 1]. Patient was admitted due to worsening hypoxia and hemoptysis post procedure. He had mild hemoptysis for the next two days after which it resolved without any intervention. Broncho alveolar lavage cultures showed Mycobacterium avium intracellulare complex for which he was treated. DISCUSSION: We describe an unusual case of diffuse bronchial hemorrhage that, given the clinical course, developed due to severe coughing fit immediately prior to bronchoscopy. Only a few cases of cough induced diffuse bronchial hemorrhage, also called as the "hemorrhagic bronchial mucosa syndrome", have been previously reported [1-3]. The presence of mucosal petechiae with evidence of bleeding is a characteristic finding and usually improves with conservative management. It has been postulated that high intrathoracic pressures during coughing can increase intravascular pressure resulting in local vessel damage and bleeding [3]. Immunocompromised status due to AIDS, old age, use of aspirin, and pulmonary hypertension may have been additional risk factors predisposing to hemorrhage in this case. CONCLUSIONS: Diffuse bronchial hemorrhage or "hemorrhagic bronchial mucosa syndrome” is a rare complication that can occur during bronchoscopy due to severe coughing and measures to prevent coughing should be considered. Reference #1: Panjwani A. Hemorrhagic bronchial mucosa syndrome. The Egyptian Journal of Internal Medicine. 2015;27(4):151-153. Reference #2: Hira HS. Cough-induced Tracheobronchial Mucosal Bleeding. J Bronchology Interv Pulmonol. 2011;18(1):51-52. Reference #3: Milman N. Diffuse bleeding from the bronchial mucosa on flexible bronchoscopy in lung transplanted patients: 'the hemorrhagic bronchial mucosa syndrome'. Respiration. 2009;77(4):416-419. DISCLOSURES: No relevant relationships by Steven Shaw, source=Web Response No relevant relationships by Abhishek Singla, source=Web Response

THE COMPANY YOU KEEP: A CASE OF REFRACTORY HYPOXEMIC RESPIRATORY FAILURE, THYROID STORM, AND SYSTOLIC HEART FAILURE IN THE POSTPARTUM PERIOD

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: We present a case of acute hypoxemic respiratory failure from flash pulmonary edema in a new mother with Graves’ disease. CASE PRESENTATION: A 36 year old woman, four days postpartum with history of Graves’ disease and pre-eclampsia presented in acute respiratory distress. On admission, she had a systolic BP > 200 mmHg, sinus tachycardia to 150 BPM, bilateral patchy pulmonary infiltrates, and profound hypoxemia requiring intubation. Severe hypoxemia persisted despite paralysis and lung recruitment maneuvers, therefore airway pressure release ventilation (APRV) was used as a rescue strategy. Thyroid studies suggested evidence of thyroid storm (low TSH, high free T3, normal free T4 and a Burch-Wartofsky score of 70). Intravenous esmolol was initiated to achieve peripheral beta blockade but was complicated by PEA arrest. Return of spontaneous circulation was achieved after five minutes of CPR. An echocardiogram showed biventricular failure and ejection fraction of 30%. Hydrocortisone, propylthiouracil, and iodine were initiated for thyroid storm and eventually she was extubated. Repeat echocardiogram revealed recovered ejection fraction of 60%. She was discharged in stable condition on methimazole with close follow-up. DISCUSSION: Therapies invariably consist of both positive and negative effects. The role of an intensivist is to weigh these risks and benefits, make sound judgement, and adapt to unintended consequences. This patient presented in extremis with hypoxemic respiratory failure from flash pulmonary edema. Her history of Graves’ disease combined with laboratory and clinical data pointed strongly to thyroid storm. The best evidence suggests that early treatment of thyroid storm is crucial and mortality rates rise to 75% with delays in therapy. While beta-blockade is considered first line therapy to treat the effects of uncontrolled thyroid hormone, in this case it undoubtedly led to cardiac arrest. Following the successful resuscitation, it was clear that RV dysfunction paired with high intrathoracic pressures generated by APRV mode should be seen as a death knell if paired with beta blockade. Opposing the sympathetic surge and tachycardia required to maintain cardiac output, our patient quickly decompensated, with loss of chronotropy and RV failure leading to cardiac arrest. Rapid removal of the short-acting agent esmolol, along with resuscitative efforts were able to quickly correct the untoward effects and the patient made a full recovery. CONCLUSIONS: This case offers a unique presentation of thyroid storm and highlights the duality of therapies. A high level of suspicion is required for timely diagnosis of thyroid storm and early treatment is critical. Despite this, the benefits of therapy cannot be seen in a vacuum and we must strive to understand the potential negative consequences in our quest to provide exceptional critical care. Reference #1: Chiha M, Samarasinghe S, Kabaker AS. Thyroid Storm: An Updated Review. Journal of Intensive Care Medicine. August 5, 2013. Volume: 30 issue: 3, page(s): 131-140. Reference #2: Karger S, Führer D. Thyroid storm--thyrotoxic crisis: an update. Dtsch Med Wochenschr. 2008;133(10):479-484. doi:10.1055/s-2008-1046737 DISCLOSURES: No relevant relationships by Paul Cooper, source=Web Response No relevant relationships by Dustin Fraidenburg, source=Web Response No relevant relationships by Janae Gonzales, source=Web Response No relevant relationships by Malvika Kaul, source=Web Response No relevant relationships by Shuvani Sanyal, source=Web Response No relevant relationships by Christen Vagts, source=Web Response

Distribution of Ventilation in Pneumoperitoneum: Comment.

We read with great interest a very informative and well-conducted study by Shono et al. titled “Positive End-expiratory Pressure and Distribution of Ventilation in Pneumoperitoneum Combined with Steep Trendelenburg Position” published in the Journal.1 The study has objectively shown that application of positive end-expiratory pressure (PEEP) of 15 cm H2O resulted in more homogeneous ventilation and favorable pulmonary physiologic effects during robot-assisted laparoscopic prostatectomy, but did not improve postoperative lung function. Whereas that authors have focused on the beneficial pulmonary effects of high PEEP values, the article would benefit readers considerably if the authors could address its potential ill effects on some other organ systems.In this regard we wish to highlight our concern regarding application of high PEEP on intracranial pressure (ICP) in patients given a steep Trendelenberg position. It is known that ICP rises rapidly with pneumoperitoneum and this increase is more pronounced due to the effects of gravity in patients assuming the head-down Trendelenburg position.2,3 Increased intraabdominal pressure displaces the diaphragm cranially, narrowing the inferior vena cava and decreasing venous return which, in turn, increases the ICP.3 The high intrathoracic pressures due to positive pressure ventilation and high intraabdominal pressure due to pneumoperitoneum cause a triple compartment syndrome because of an increase in ICP. In susceptible populations such as patients with head injuries or patients who have undiagnosed intracranial pathology, neurologic deterioration could be a concern. Clinically, even minor adverse effects of raised ICP may present in different ways.4 In a study by Cooke et al., headache and nausea were found to be significantly higher after laparoscopic abdominal surgery, possibly due to raised ICP.4Shono et al. have reported that phenylephrine requirement in the high PEEP group was significantly greater than in the normal PEEP group. For maintenance of cerebral perfusion pressure, a higher mean arterial pressure should have been targeted in view of the raised ICP. The authors have reported a raised arterial carbon dioxide of 49 ± 5 mm Hg which may also have detrimental effect on the ICP. Adjusting the respiratory rate to normalize the end tidal carbon dioxide could have been considered in the study design. In susceptible individuals, surgeries lasting 484 ± 81 min with a persistently high ICP resulting from a high PEEP of 15 cm H2O could result in a greater incidence of complications. These complications should be investigated before we can recommend universal application of a high PEEP in all patients. Prospective authors planning similar studies could consider adding incidence of adverse effects on ICP or intraocular pressure as one of their secondary objectives; otherwise, they could include these concerns as limitations of their study.The authors declare no competing interests.

PULMONARY EDEMA AND HEMOPTYSIS AFTER AN ORTHOPEDIC SURGERY

SESSION TITLE: Wednesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Negative pressure pulmonary edema(NPPE) is an acute respiratory failure usually caused after a strong inspiratory effort generated against an obstructed upper airway[1]. CASE PRESENTATION: A 29-year-old man was admitted to the hospital for an elective open reduction with internal fixation of left bimalleolar ankle fracture. The surgery was uneventful. After extubation, he became hypoxic and started coughing up bloody phlegm without evidence of vomiting. He was afebrile, HR 96, RR 22 and BP 146/96. Chest x-ray showed bilateral alveolar consolidations in the upper and mid zones(Fig1). He was given Lasix 40 mg IV once and was transferred to the ICU. He was hemodynamically stable on high-flow oxygen. Arterial blood gas was showing pH of 7.41, PO2 98, pCO2 46 and HCO3 28.4. There was no evidence of swelling in the posterior pharynx. Lung exam showed good air entry on both sides, bilateral crepitations without wheezes. Laboratory work was unremarkable. Echocardiogram revealed normal ejection fraction, no significant valvular heart disease. He made a strong inspiratory effort after extubation due to upper airway laryngospasm and developed NPPE with alveolar hemorrhage. He was started on steroids. CT chest with contrast showed bilateral ground-glass opacities with alveolar infiltration in parenchymal hemorrhagic pattern(Fig2). He was continued on supportive treatment. Hemoptysis resolved in a day. He was transitioned to nasal cannula. Follow up chest x-ray showed significant improvement in alveolar infiltrates(Fig3). He was discharged home after a 48-h stay in the hospital. DISCUSSION: In adults, the most reported causes of airway obstruction leading to NPPE are in the context of laryngospasm following surgery[2]. The incidence of NPPE is as low as 0.1% of laryngospasm cases [3]. The first case of NPPE was reported and published in 1973 by Capitano and Kirkpatrick. There was a question whether NPPE was a result of high vessel permeability or hydrostatic pressure edema formation[1]. The high negative intrathoracic pressure generated to overcome the upper airway obstruction can reach -140 cm H2O[1]. The hydrostatic pressure in the pulmonary capillaries increases, the rate of interstitial fluid accumulation outgrows the capacity of the lymphatic drainage and fluid floods into the alveoli. Stress fracture can develop in the pulmonary capillaries leading to high permeability edema and blood-tinged secretions. Most cases of NPPE resolve in 24-48h. Diuretics have been used to hasten the resolution of the pulmonary edema. Beta agonist improves the clearance of the fluid by increasing active cation transport. In case of severe obstruction, cricothyroidotomy or tracheostomy can been used. Sedating and paralyzing the patient prevent more laryngospasm or biting of the endotracheal tube. CONCLUSIONS: NPPE is an entity not frequent encountered, but life threatening if not recognized or managed appropriately. Reference #1: M. Bhattacharya, R. H. Kallet, L. B. Ware, and M. A. Matthay, “Negative-Pressure Pulmonary Edema,” Chest, vol. 150, no. 4, pp. 927–933, Oct. 2016. Reference #2: A. Udeshi, S. M. Cantie, and E. Pierre, “Postobstructive pulmonary edema,” J. Crit. Care, vol. 25, no. 3, p. 538.e1-538.e5, 2010. Reference #3: B. Bhaskar and J. F. Fraser, “Negative pressure pulmonary edema revisited: Pathophysiology and review of management,” Saudi J. Anaesth., vol. 5, no. 3, pp. 308–313, 2011. DISCLOSURES: No relevant relationships by Arul Chandran, source=Web Response No relevant relationships by Michele Obeid, source=Web Response

\u201cLow-\u201d versus \u201chigh\u201d-frequency oscillation and right ventricular function in ARDS. A randomized crossover study

BackgroundRecent, large trials of high-frequency oscillation (HFO) versus conventional ventilation (CV) in acute respiratory distress syndrome (ARDS) reported negative results. This could be explained by an HFO-induced right ventricular (RV) dysfunction/failure due to high intrathoracic pressures and hypercapnia. We hypothesized that HFO strategies aimed at averting/attenuating hypercapnia, such as “low-frequency” (i.e., 4 Hz) HFO and 4-Hz HFO with tracheal-gas insufflation (HFO-TGI), may result in an improved RV function relative to “high-frequency” (i.e., 7 Hz) HFO (which may promote hypercapnia) and similar RV function relative to lung protective CV.MethodsWe studied 17 patients with moderate-to-severe ARDS [PaO2-to-inspiratory O2 fraction ratio (PaO2/FiO2) < 150]. RV function was assessed by transesophageal echocardiography (TEE). Patients received 60 min of CV for TEE-guided, positive end-expiratory pressure (PEEP) “optimization” and subsequent stabilization; 60 min of 4-Hz HFO for “study mean airway pressure (mPaw)” titration to peripheral oxygen saturation ≥ 95%, without worsening RV function as assessed by TEE; 60 min of each tested HFO strategy in random order; and another 60 min of CV using the pre-HFO, TEE-guided PEEP setting. Study measurements (i.e., gas exchange, hemodynamics, and TEE data) were obtained over the last 10 min of pre-HFO CV, of each one of the three tested HFO strategies, and of post-HFO CV.ResultsThe mean “study HFO mPaw” was 8–10 cmH2O higher relative to pre-HFO CV. Seven-Hz HFO versus 4-Hz HFO and 4-Hz HFO-TGI resulted in higher mean ± SD right-to-left ventricular end-diastolic area ratio (RVEDA/LVEDA) (0.64 ± 0.15 versus 0.56 ± 0.14 and 0.52 ± 0.10, respectively, both p < 0.05). Higher diastolic/systolic eccentricity indexes (1.33 ± 0.19/1.42 ± 0.17 versus 1.21 ± 0.10/1.26 ± 0.10 and 1.17 ± 0.11/1.17 ± 0.13, respectively, all p < 0.05). Seven-Hz HFO resulted in 18–28% higher PaCO2 relative to all other ventilatory strategies (all p < 0.05). Four-Hz HFO-TGI versus pre-HFO CV resulted in 15% lower RVEDA/LVEDA, and 7%/10% lower diastolic/systolic eccentricity indexes (all p < 0.05). Mean PaO2/FiO2 improved by 77–80% during HFO strategies versus CV (all p < 0.05). Mean cardiac index varied by ≤ 10% among strategies. Percent changes in PaCO2 among strategies were predictive of concurrent percent changes in measures of RV function (R2 = 0.21–0.43).ConclusionsIn moderate-to-severe ARDS, “short-term” 4-Hz HFO strategies resulted in better RV function versus 7-Hz HFO, partly attributable to improved PaCO2 control, and similar or improved RV function versus CV.Trial registrationThis study was registered 40 days prior to the enrollment of the first patient at ClinicalTrials.gov, ID no. NCT02027129, Principal Investigator Spyros D. Mentzelopoulos, date of registration January 3, 2014.

Cardiopulmonary physiology: why the heart and lungs are inextricably linked.

Because the heart and lungs are confined within the thoracic cavity, understanding their interactions is integral for studying each system. Such interactions include changes in external constraint to the heart, blood volume redistribution (venous return), direct ventricular interaction (DVI), and left ventricular (LV) afterload. During mechanical ventilation, these interactions can be amplified and result in reduced cardiac output. For example, increased intrathoracic pressure associated with mechanical ventilation can increase external constraint and limit ventricular diastolic filling and, therefore, output. Similarly, high intrathoracic pressures can alter blood volume distribution and limit diastolic filling of both ventricles while concomitantly increasing pulmonary vascular resistance, leading to increased DVI, which may further limit LV filling. While LV afterload is generally considered to decrease with increased intrathoracic pressure, the question arises if the reduced LV afterload is primarily a consequence of a reduced LV preload. A thorough understanding of the interaction between the heart and lungs can be complicated but is essential for clinicians and health science students alike. In this teaching review, we have attempted to highlight the present understanding of certain salient aspects of cardiopulmonary physiology and pathophysiology, as well as provide a resource for multidisciplined health science educators and students.

Evaluation of the Boussignac Cardiac arrest device (B-card) during cardiopulmonary resuscitation in an animal model

Aim of the studyThe purpose of this study was to examine continuous oxygen insufflation (COI) in a swine model of cardiac arrest. The primary hypothesis was COI during standard CPR (S-CPR) should result in higher intrathoracic pressure (ITP) during chest compression and lower ITP during decompression versus S-CPR alone. These changes with COI were hypothesized to improve hemodynamics. The second hypothesis was that changes in ITP with S-CPR+COI would result in superior hemodynamics compared with active compression decompression (ACD) + impedance threshold device (ITD) CPR, as this method primarily lowers ITP during chest decompression. MethodsAfter 6min of untreated ventricular fibrillation, S-CPR was initiated in 8 female swine for 4min, then 3min of S-CPR+COI, then 3min of ACD+ITD CPR, then 3min of S-CPR+COI. ITP and hemodynamics were continuously monitored. ResultsDuring S-CPR+COI, ITP was always positive during the CPR compression and decompression phases. ITP compression values with S-CPR+COI versus S-CPR alone were 5.5±3 versus 0.2±2 (p<0.001) and decompression values were 2.8±2 versus −1.3±2 (p<0.001), respectively. With S-CPR+COI versus ACD+ITD the ITP compression values were 5.5±3 versus 1.5±2 (p<0.01) and decompression values were 2.8±2 versus −4.7±3 (p<0.001), respectively. ConclusionCOI during S-CPR created a continuous positive pressure in the airway during both the compression and decompression phase of CPR. At no point in time did COI generate a negative intrathoracic pressures during CPR in this swine model of cardiac arrest.

Hemodynamic effects of lung recruitment maneuvers in acute respiratory distress syndrome

BackgroundClinical trials have, so far, failed to establish clear beneficial outcomes of recruitment maneuvers (RMs) on patient mortality in acute respiratory distress syndrome (ARDS), and the effects of RMs on the cardiovascular system remain poorly understood.MethodsA computational model with highly integrated pulmonary and cardiovascular systems was configured to replicate static and dynamic cardio-pulmonary data from clinical trials. Recruitment maneuvers (RMs) were executed in 23 individual in-silico patients with varying levels of ARDS severity and initial cardiac output. Multiple clinical variables were recorded and analyzed, including arterial oxygenation, cardiac output, peripheral oxygen delivery and alveolar strain.ResultsThe maximal recruitment strategy (MRS) maneuver, which implements gradual increments of positive end expiratory pressure (PEEP) followed by PEEP titration, produced improvements in PF ratio, carbon dioxide elimination and dynamic strain in all 23 in-silico patients considered. Reduced cardiac output in the moderate and mild in silico ARDS patients produced significant drops in oxygen delivery during the RM (average decrease of 423 ml min−1 and 526 ml min−1, respectively). In the in-silico patients with severe ARDS, however, significantly improved gas-exchange led to an average increase of 89 ml min−1 in oxygen delivery during the RM, despite a simultaneous fall in cardiac output of more than 3 l min−1 on average. Post RM increases in oxygen delivery were observed only for the in silico patients with severe ARDS. In patients with high baseline cardiac outputs (>6.5 l min−1), oxygen delivery never fell below 700 ml min−1.ConclusionsOur results support the hypothesis that patients with severe ARDS and significant numbers of alveolar units available for recruitment may benefit more from RMs. Our results also indicate that a higher than normal initial cardiac output may provide protection against the potentially negative effects of high intrathoracic pressures associated with RMs on cardiac function. Results from in silico patients with mild or moderate ARDS suggest that the detrimental effects of RMs on cardiac output can potentially outweigh the positive effects of alveolar recruitment on oxygenation, resulting in overall reductions in tissue oxygen delivery.

Stenting of critical tracheal stenosis with adjuvant cardio-pulmonary bypass.

Severe and critical central airway obstruction causing impaired ventilation and/or oxygenation can impose tremendous challenges on the interventional pulmonologist. Near total airway obstruction can rapidly evolve into potentially fatal complete airway occlusion during bronchoscopic airway manipulation under moderate sedation; as well as during the induction of the general anesthesia. Although there are currently interventional pulmonary procedures available to tackle the critical airway obstruction in extreme situations, cardio-pulmonary bypass should be considered prior to the intervention to maintain the adequate gas exchange during the procedure. Orotracheal intubation with mechanical ventilation in this situation can be fatal itself if the obstructing airway lesion functions as a “one way valve” allowing air to follow distally during inspiration but impeding expiratory flow leading to gas trapping, high intrathoracic pressure, tension pneumothorax, and ultimately a cardiac arrest.

Evaluation of Gastroesophageal Reflux in Anesthetized Dogs with Brachycephalic Syndrome.

Brachycephalic airway syndrome may predispose to gastroesophageal reflux (GER) because of the high negative intrathoracic pressures required to overcome conformational partial upper airway obstruction. To investigate this, 20 dogs presenting for elective correction of brachycephalic airway syndrome (cases) and 20 non-brachycephalic dogs (controls) undergoing other elective surgeries were prospectively enrolled. Dogs underwent a standardized anesthetic protocol, and esophageal pH was monitored. Signalment, body weight, historical gastrointestinal and respiratory disease, complete blood count, serum biochemical values, radiographic findings, and anesthetic and surgical time were compared between cases and controls, and dogs that did and did not have basic (pH > 7.5), acidic (pH < 4), or any GER. Controls had higher mean esophageal pH (6.3) compared to cases (5.6, P = .019), but there was no difference in % with GER (cases 60%, controls 40%, P = .34). When all dogs were evaluated, dogs with GER had increased creatinine (P = .01), % positive for esophageal fluid on radiographs (P = .05), and body weight (P = .04) compared to those without GER. GER was common in both cases and controls, and cases had lower esophageal pH; however, greater numbers are required to determine if a true difference exists in % GER.

Evidence Is Important: Safety Considerations for Emergency Catheter Cricothyroidotomy.

Evidence Is Important: Safety Considerations for Emergency Catheter Cricothyroidotomy.

Acute Postoperative Negative Pressure Pulmonary Edema as Complication of Acute Airway Obstruction: Case Report

Acute postoperative negative pressure pulmonary edema (NPPE) is a respiratory complication due to acute airway obstruction (UAO) that occurs shortly after extubation of patients who underwent general anesthesia (incidence 0.05 to 0.1% ). Usually, this complication develops in healthy young patients, capable of generating high negative intrathoracic pressures(NIP), which is the catalyst in the pathophysiological cascade of acute pulmonary edema.Commonly presents as acute respiratory distress that requires immediate intervention. We report a case of postoperative NPPE occurred immediately after tracheal extubation in an adult patient, who underwent a minor elective orthopedic surgery under general anesthesia(GA). After extubation, UAO due to laryngospasm was observed and the patient started desaturating rapidely. Application of positive pressure via face mask ventilation (FiO2 100%) was unsuccessful in providing effective ventilation so we decided to reintubate the patient. Soon after reintubation, there were bilateral pulmonary rales and pink frothy secretion inside the tracheal tube, compatible with NPPE. Treatment was rapidly instituted with diuretic, corticosteroid and ventilator support with added PEEP. Pulmonary edema resolved completely near after 8 hours later without any complications in the intensive care unit.

Prevalence of systemic air-embolism after prolonged cardiopulmonary resuscitation in newborns: A pilot study

BackgroundChest compressions (CC) during cardiopulmonary resuscitation (CPR) are the cornerstone of adult CPR protocols and are meant to restore circulation and improve outcome. Although adverse effects such as air-embolisms have been reported, these are rare and considered to be outweighed by beneficial effect. In newborns, however, the lung tissue is more fragile. Thus, the high intra-thoracic pressures resulting from CC may make the newborns more vulnerable for air-embolisms. ObjectivesWe studied the postmortem prevalence of air-embolism in neonates that have received CPR. MethodsProspective cohort analysis of newborns receiving CC during CPR. CPR was performed by trained staff according to ILCOR guidelines, in a tertiary hospital. Air-embolisms were sought after using CT/MRI and autopsy. ResultsDuring a 61/2 year period (2007–2014), n=56 newborns received CC. Newborns were resuscitated following severe perinatal hypoxia, or due to complications during NICU treatment. In n=14 (25.0%) circulation could not be restored (mean CPR duration: 32.7±15.2min). Post-mortem CT/MRI was performed in n=9, of whom n=8 (88.9%) had air-embolisms. Autopsy was performed in n=9. The air-embolisms could not be retraced on autopsy except for n=1 patient.In patients with CPR resulting in restored circulation (n=42), no CT or MRI was performed for comparison due to radiation and/or hemodynamic instability. Cerebral ultrasound could not identify or exclude air-embolisms in this subgroup. ConclusionsPost-mortem CT after prolonged resuscitation showed a high prevalence of intravascular air-embolism. Autopsy was not suited to detect air-embolism. The clinical importance of air-embolisms on the lethal outcome needs further research.

Effects of the Mueller Maneuver on Functional Mitral Regurgitation and Implications for Obstructive Sleep Apnea

Obstructive sleep apnea is prevalent and adversely affects cardiovascular health. However, little is known of the acute effects of an obstructive apnea on cardiovascular physiology. We hypothesized that pre-existing functional mitral regurgitation (MR) would worsen during performance of a Mueller maneuver (MM) used to simulate an obstructive apnea; 15 subjects with an ejection fraction ≤35% and pre-existing functional MR were studied with Doppler echocardiography. The radius of the proximal flow convergence was used as a measure of mitral regurgitant flow. Measurements were made at baseline, during the MM, and post-MM. Areas of all 4 chambers were also measured at these time points, both in systole and diastole. Mean flow convergence radius for the group decreased significantly during the transition from the late-MM to post-MM (0.65 → 0.57mm, p= 0.001), implying increased MR during the MM. In addition, in 3 subjects, duration of MR increased during the MM. Right atrial (RA) areas, both systolic and diastolic, increased during the maneuver, whereas RA fractional area change decreased, indicating reduced RA emptying. Left ventricular emptying decreased early in the maneuver, probably because of the increased afterload burden, and then recovered. In conclusion, high negative intrathoracic pressure produces changes that, repeated hundreds of times per night in patients with obstructive sleep apnea, have the potential to worsen heart failure and predispose affected subjects to atrial fibrillation.

Deleterious Effects of Increased Intra-Abdominal Pressure on Kidney Function

Elevated intra-abdominal pressure (IAP) occurs in many clinical settings, including sepsis, severe acute pancreatitis, acute decompensated heart failure, hepatorenal syndrome, resuscitation with large volume, mechanical ventilation with high intrathoracic pressure, major burns, and acidosis. Although increased IAP affects several vital organs, the kidney is very susceptible to the adverse effects of elevated IAP. Kidney dysfunction is among the earliest physiological consequences of increased IAP. In the last two decades, laparoscopic surgery is rapidly replacing the open approach in many areas of surgery. Although it is superior at many aspects, laparoscopic surgery involves elevation of IAP, due to abdominal insufflation with carbonic dioxide (pneumoperitoneum). The latter has been shown to cause several deleterious effects where the most recognized one is impairment of kidney function as expressed by oliguria and reduced glomerular filtration rate (GFR) and renal blood flow (RBF). Despite much research in this field, the systemic physiologic consequences of elevated IAP of various etiologies and the mechanisms underlying its adverse effects on kidney excretory function and renal hemodynamics are not fully understood. The current review summarizes the reported adverse renal effects of increased IAP in edematous clinical settings and during laparoscopic surgery. In addition, it provides new insights into potential mechanisms underlying this phenomenon and therapeutic approaches to encounter renal complications of elevated IAP.

Understanding negative pressure pulmonary edema.

Understanding negative pressure pulmonary edema.