High Intrathoracic Pressure Research Articles

Effects of the Mueller Maneuver on aortic area

Negative intrathoracic pressure, such as occurs in obstructive sleep apnea (OSA), increases the transmural gradient across the aorta. This could predispose to dilation or dissection, particularly when experienced in repetitive fashion over months to years. Studies have observed an association between OSA and thoracic aortic size, both in Marfan subjects [1] and among unselected subjects referred for polysomnography [2]. In addition, one small study found severity of OSA to be greater in patients with dissection vs hypertensive controls [3]. However, it is hard to say that OSA per se contributes to aortic abnormalities because of small sample size and the presence of potential confounders in published work to date [4]. Another study used the Mueller Maneuver (forced inspiration against an occluded airway, MM) as a surrogate for OSA and found that obstructive hypopnea, but not apnea, increased thoracic aortic diameter [5]. It is difficult to explain why hypopnea, but not apnea, would affect aortic diameter. In addition, this study used 2-D echocardiography which may be compromised by off-angle imaging in a straining patient. We therefore used 3-D echocardiography to evaluate changes in aortic area during performance of a sustained MM. This allowed precise alignment of the crop plane perpendicular to the aortic wall, ensuring accurate cross-sectional imaging of the aorta. This study was approved by the Einstein Healthcare Network Institutional Review Board. Twenty-two healthymale subjects≤30 years of agewere enrolled. All subjects gave informed consent before participating. Each was coached in performance of the MMwhile lying supine. A nose clip and mouthpiece were positioned before each maneuver. The mouthpiece was connected to an electronic pressure gauge and incorporated a small air leak to prevent closure of the glottis at the time of inspiratory effort. Mouth pressure was displayed in digital format for the subjects who were instructed to build negative intrathoracic pressure gradually, using the diaphragm, so as to maximize chances of obtaining suitable echocardiographic images. The goal was to achieve and maintain an intrathoracic pressure of −40 mm Hg (−54.4 cm H2O). Imaging was performed with a Philips iE33 system (Philips Medical Systems, Andover, MA) and X5-1 transducer. The “3-D zoom” mode was used, positioning the volume of interest over the left ventricular outflow tract, aortic valve, and ascending aorta. Twenty second loops were recorded, with the MM starting 4–5 s into the recording. Each subject performed 4–5MMs. The resultant 3D datasets were then used to create 2-D slices of the aorta approximately 1 cm above the sinotubular junction. Care was taken to ensure that slices were perpendicular to the aortic wall. Aortic area was measured in diastole when the aorta is relatively motionless. Multiple measurements were made at baseline and during the maneuver, with measurements averaged for each phase. All measurements weremade by a reader blinded to the nature of the study. Paired t-test analysis was used to compare the aortic area at baseline with that during the MM. Among the 22 subjects, ten had images of suitable quality for precise measurements. Of these, 6 maintained a negative inspiratory pressure of at least −30 cm H2O, a minimum value selected to mimic conditions during a naturally occurring apnea. For the group, mean aortic area at baseline was 4.01 ± 0.53 cm rising to 4.47 ± 0.58 cm during the MM (mean difference = 0.46 ± 0.08 cm, p = 0.0017, see Fig. 1). In addition, aortic area was observed to increase to a similar degree in each subject. In this study we observed an increase in aortic area under conditions of high negative intrathoracic pressure (i.e. performance of a MM). Such negative pressure is the defining characteristic of an obstructive apnea. It imposes an afterload burden on the left ventricle and increases the pressure gradient across the aortic wall. While pressure outside the aorta falls, pressure inside remains substantially the same, likely because much of the aorta is extrathoracic. Increased transmural pressure is the likely explanation for the larger aortic area that we observed during the MM. Obstructive sleep apnea is the clinical condition most relevant to this research. Patients with OSA are exposed to recurrent episodes of high negative intrathoracic pressure, up to hundreds of times per night. It is plausible that such repeated barotrauma could predispose to or cause aortic dissection. The chief limitation of this study is its small size. Many subjects could not maintain target negative intrathoracic pressure long enough to acquire useful echocardiographic images. Among those who could, many did not have crisp enough echocardiographic images to allow precise measurements. Thus, only six subjects met all conditions to allow detailed measurement of aortic area during the MM. However,

Importance of alveolar recruitment strategy revisited.

Low tidal volume, rather than high tidal volume, ventilation is often used for mechanical ventilation during surgery to avoid lung injury due to alveolar overdistention. Under general anesthesia with a muscle relaxant, there is a risk of compressing the lungs by diaphragmatic displacement, which can be aggravated in patients placed in the supine position. Such a risk becomes even higher during reduced tidal volume ventilation, causing alveolar atelectasis and hypoxemia. Therefore, positive end expiratory pressure (PEEP) is applied to prevent spontaneous closure of alveoli. In this volume, Jung et al. [1] reports on the importance of the alveolar recruitment strategy (ARS). The authors applied ARS before the start of one-lung ventilation (OLV), and compared the oxygenation score between high- and low-tidal volume groups. Repetitive open and closure of collapsed alveoli by positive pressure ventilation could cause damage to the capillary endothelium and alveolar epithelium. Excessive expansion and risk of alveolar injury may even occur during low tidal volume ventilation due to an uneven distribution of ventilated volume to already open alveoli. However, Jung et al. [1] showed that preemptive ARS commonly increases PaO2 without causing hemodynamic instability in groups with or without PEEP during OLV. The improvement in oxygenation was better in the group where ARS was combined with PEEP. Their study design and intriguing results will draw the attention of general readers of the journal. The ARS helps to open collapsed alveoli, which is effectively maintained by PEEP. Therefore, both ARS and PEEP maneuvers are compulsory to improve oxygenation and lung mechanics during general anesthesia [2]. Diverse ARS methods have been reported in recent clinical studies. The recommended ARS is peak inspiratory pressure up to 40 cmH2O at 10 respiratory cycles with 15-20 cmH2O PEEP. Adequate PEEP level following ARS is reportedly 5-20 cmH2O depending on the condition of the patient (i.e., pulmonary function and physical condition) and also the type of operation. The time to apply ARS is typically (1) immediately after intubation before confirming lung sounds, (2) after suctioning, or (3) just before extubation. Functional residual capacity is reduced in 50% of patients after tracheal suctioning, in which case combined ARS and PEEP effectively restores PaO2 [3]. Along with increased PaO2, several reports have indicated that ARS with PEEP during OLV decreases AaDO2, and decreases the alveolar dead space ventilation ratio [4,5,6]. In addition to OLV anesthesia, ARS with appropriate PEEP is required to improve PaO2 in patients with minimal lung injury during other surgeries with a high risk of atelectasis such as laparoscopic surgery [7,8,9], pediatric patients [10], and obese patients [9]. This preemptive ARS effect during low tidal volume OLV has been described previously [11]. Preemptive ARS can also be applied before pneumoperitoneum during laparoscopic surgery [8] with the purpose of improving oxygenation. However, high intrathoracic pressure during ARS may cause hemodynamic instability. Therefore, adjustment of the pressure and application duration should consider a patient's hemodynamic status and the potential risks [5]. In obese patients, higher pressures are required for adequate ARS and PEEP [9]. The risk of hemodynamic derangement by such high pressures can be prevented by intravascular volume replacement [12]. Interestingly, one study reported that applying ARS with PEEP to the donor lung in situ as well as after transplantation lowers the risk of primary graft dysfunction [13]. Several reports have suggested the beneficial effects of ARS with PEEP during general abdominal surgery to reduce post-operational complications [14]. In conclusion, applying ARS and PEEP during surgery or in patients vulnerable to atelectasis is helpful for improving oxygenation and lowering postoperative pulmonary complications. PEEP must be sustained to keep alveoli in their open state and optimize patient oxygenation. In addition, adequate ARS before applying PEEP is essential to maximize the benefits of PEEP.

Case Report: Pneumomediastinum and subcutaneous cervical emphysema: unusual complications of childhood pneumonia

The occurrence of pneumomediastinum and subcutaneous cervical emphysema as complications of childhood pneumonia is very unusual. They results most often from respiratory manoeuvres that produce high intrathoracic pressure. Although they are largely benign, pneumomediastinum can cause compression of major blood vessels in the mediastinum resulting in life threatening complications. Therefore, adequate knowledge of these conditions and their proper management is very important for clinicians. Keywords: Subcutaneous Cervical Emphysema, Pneumomediastinum , Childhood, Pneumonia

Lymphoscintigraphy in plastic bronchitis, A pediatric case report

Plastic bronchitis (PB) is an uncommon, potentially fatal disease, marked by endobronchial cast formation causing variable degrees of respiratory distress. Primary and secondary pulmonary lymphatic abnormalities have been identified among the underlying mechanisms of cast formation. We present a case of PB where lymphoscintigraphy demonstrated the underlying lymphatic defect. A 6-year-old Hispanic male with congenital heart disease (CHD; post-Fontan) presented with recurrent pneumonia, respiratory distress. Bronchoscopy showed inflamed hypervascular mucosa and thick mucus plugs; no casts were seen. Later, PB was diagnosed after the patient expectorated a bronchial cast. Cast analysis showed lymphocytic aggregates with mucin and fibrin. Lymphoscintigraphy revealed abnormal lymphatic collaterals and retrograde trace reflux into the superior mediastinum, a picture consistent with thoracic duct lymph leakage into the tracheobronchial tree. The pathogenesis of PB is not fully understood, especially in patients with CHD. Chyle in bronchial casts suggests abnormal lymphatic flow. Reports of lymph flow abnormalities, especially endobronchial lymph leakage in CHD are limited. Lymphoscintigraphy in our case demonstrated clear evidence of retrograde lymph reflux and leakage into the bronchial tree. The case presented suggests that in some patients following Fontan surgery, high intrathoracic lymphatic pressure and retrograde lymph flow may contribute to recurrent cast formation. Finding the underlying lymphatic abnormality helps in specific case management. Lymphoscintigraphy is a safer and easier method than lymphangiography. Surgical lymphatic-venous shunting may be possible in select cases.

Failure of both suction catheter passage and bronchoscopy to diagnose an obstructing tracheal mucus plug

To the Editor, The patient’s spouse gave informed consent for publication of this report. A 55-yr-old male sustained burns in a welding accident extending caudad from shoulder level over 65% of his body surface area. In the intervening two months, he required multiple surgeries, including debridement and skin grafting, a laparotomy for abdominal compartment syndrome, and a tracheostomy. Presenting on this occasion for further skin grafting, he was breathing easily and spontaneously through a size 8 fenestrated Shiley tracheostomy cannula (Covidien, Mansfield, MA, USA) capped with a decannulation plug. In the operating room, the fenestrated inner cannula was exchanged for a non-fenestrated tube. Shortly after this change, the patient indicated some dyspnea. A suction catheter was introduced and moderate amounts of sputum were obtained, after which the patient signalled at least partial relief. Following application of routine monitors, anesthesia was induced using sevoflurane in oxygen through a circle system connected to the tracheostomy tube, supplemented with midazolam 2 mg and propofol 30 mg iv. After induction, it was almost impossible to ventilate the patient’s lungs. We detected a markedly prolonged expiratory phase and made a working diagnosis of severe bronchospasm although minimal rhonchi were present. We administered rocuronium 50 mg iv, increased the inspired sevoflurane concentration to 4%, and administered salbutamol, magnesium sulphate, and small doses (50–100 lg) of intravenous epinephrine. Although the oxygen saturation remained [ 90%, little improvement was achieved in response to these measures. An 18-Fr suction catheter was introduced on at least three further occasions. Each time, a scant amount of sputum was obtained, but no improvement in ventilation resulted. We twice passed a fibreoptic bronchoscope, but saw no obvious impediment to ventilation, and the tracheobronchial tree looked normal. Interestingly, when the tracheostomy tube was disconnected from the circuit for suctioning or bronchoscopy, we observed the patient’s chest gradually fall with loud yet slow gas egress from the tracheostomy cannula, suggesting gas escaping under conditions of high intrathoracic pressure. Following each such thoracic decompression, ventilation was easier for the next two or three positive pressure inspirations. Eventually, an inspiratory:expiratory (i:e) ratio of about 1:10 was observed to allow sufficient time for expiration, such that ventilation was now possible, albeit with ongoing high airway pressures. To rule out a circuit or machine problem, ventilation was assessed with a manual resuscitator, which confirmed that the high airway pressures originated from either the tracheostomy cannula or the patient. A portable chest radiograph showed only bilateral lung hyperinflation. Although substantially hypercarbic (PetCO2 up to 93 mmHg), fortunately, the patient suffered no cardiovascular instability. Ultimately, a change of tracheostomy was planned given the poor response to treatment for bronchospasm, ongoing problems with positive pressure ventilation, evidence of air trapping, and the initial history of dyspnea with tracheostomy manipulation. Repeat bronchoscopy was performed by a different clinician using a videobronchoscope. The visual field was briefly obscured as the videobronchoscope was advanced beyond the distal end of the tracheostomy cannula, after which a clear view of the trachea was observed. At this point, the possibility of cuff herniation was considered. Direct laryngoscopy prior to tracheostomy J. A. Law, MD (&) C. Mariotti, MD T. Mullen, MD Dalhousie University/QEII Health Sciences Centre, Halifax, NS, Canada e-mail: jlaw@dal.ca

Sexual Activity and Cardiovascular Disease

Sexual activity is an important component of patient and partner quality of life for men and women with cardiovascular disease (CVD), including many elderly patients.1 Decreased sexual activity and function are common in patients with CVD and are often interrelated to anxiety and depression.2,3 The intent of this American Heart Association Scientific Statement is to synthesize and summarize data relevant to sexual activity and heart disease in order to provide recommendations and foster physician and other healthcare professional communication with patients about sexual activity. Recommendations in this document are based on published studies, the Princeton Consensus Panel,4,5 the 36th Bethesda Conference,6–10 European Society of Cardiology recommendations on physical activity and sports participation for patients with CVD,11–13 practice guidelines from the American College of Cardiology/American Heart Association14–16 and other organizations,17 and the multidisciplinary expertise of the writing group. The classification of recommendations in this document are based on established ACCF/AHA criteria (Table). View this table: Table. Applying Classification of Recommendation and Level of Evidence Numerous studies have examined the cardiovascular and neuroendocrine response to sexual arousal and intercourse, with most assessing male physiological responses during heterosexual vaginal intercourse.18–24 During foreplay, systolic and diastolic systemic arterial blood pressure and heart rate increase mildly, with more modest increases occurring transiently during sexual arousal. The greatest increases occur during the 10 to 15 seconds of orgasm, with a rapid return to baseline systemic blood pressure and heart rate thereafter. Men and women have similar neuroendocrine, blood pressure, and heart rate responses to sexual activity.24,25 Studies conducted primarily in young married men showed that sexual activity with a person's usual partner is comparable to mild to moderate physical activity in the range of 3 to …

Effect of Obstructive Sleep Apnea on Mitral Valve Tenting

Obstructive apneas produce high negative intrathoracic pressure that imposes an afterload burden on the left ventricle. Such episodes might produce structural changes in the left ventricle over time. Doppler echocardiograms were obtained within 2 months of attended polysomnography. Patients were grouped according to apnea-hypopnea index (AHI): mild/no obstructive sleep apnea (OSA; AHI <15) and moderate/severe OSA (AHI ≥15). Mitral valve tenting height and area, left ventricular (LV) long and short axes, and LV end-diastolic volume were measured in addition to tissue Doppler parameters. Comparisons of measurements at baseline and follow-up between and within groups were obtained; correlations between absolute changes (Δ) in echocardiographic parameters were also performed. After a mean follow-up of 240 days mitral valve tenting height increased significantly (1.17 ± 0.12 to 1.28 ± 0.17 cm, p = 0.001) in moderate/severe OSA as did tenting area (2.30 ± 0.41 to 2.66 ± 0.60 cm(2), p = 0.0002); Δtenting height correlated with ΔLV end-diastolic volume (rho 0.43, p = 0.01) and Δtenting area (rho 0.35, p = 0.04). In patients with mild/no OSA there was no significant change in tenting height; there was a borderline significant increase in tenting area (2.20 ± 0.44 to 2.31 ± 0.43 cm(2), p = 0.05). Septal tissue Doppler early diastolic wave decreased (8.04 ± 2.49 to 7.10 ± 1.83 cm/s, p = 0.005) in subjects with moderate/severe OSA but not in in those with mild/no OSA. In conclusion, in patients with moderate/severe OSA, mitral valve tenting height and tenting area increase significantly over time. This appears to be related, at least in part, to changes in LV geometry.

Year in review 2010: Interstitial lung diseases, acute lung injury, sleep, physiology, imaging, bronchoscopic intervention and lung cancer

Year in review 2010: Interstitial lung diseases, acute lung injury, sleep, physiology, imaging, bronchoscopic intervention and lung cancer

Renal Dysfunction Associated with Intra-abdominal Hypertension and the Abdominal Compartment Syndrome

Once considered mostly a postsurgical condition, intra-abdominal hypertension (IAH) and the abdominal compartment syndrome (ACS) are now thought to increase morbidity and mortality in many patients receiving medical or surgical intensive care. Animal data and human observational studies indicate that oliguria and acute kidney injury are early and frequent consequences of IAH/ACS and can be present at relatively low levels of intra-abdominal pressure (IAP). Among medical patients at particular risk are those with septic shock and severe acute pancreatitis, but the adverse effects of IAH may also be seen in cardiorenal and hepatorenal syndromes. Factors predisposing to IAH/ACS include sepsis, large volume fluid resuscitation, polytransfusion, mechanical ventilation with high intrathoracic pressure, and acidosis, among others. Transduction of bladder pressure is the gold standard for measuring intra-abdominal pressure, and several nonsurgical methods can help reduce IAP. The role of renal replacement therapy for volume management is not well defined but may be beneficial in some cases. IAH/ACS is an important possible cause of acute renal failure in critically ill patients and screening may benefit those at increased risk.

High-frequency oscillatory ventilation and pediatric cardiac surgery: Yes, we can!

In the previous issue of Critical Care, Bojan and colleagues reported their experiences with high-frequency oscillatory ventilation (HFOV) after pediatric cardiac surgery. A total of 120 patients were treated with HFOV on the day of surgery, thus excluding rescue HFOV use. The main finding of the authors was that the duration of mechanical ventilation was significantly shorter in patients in whom HFOV was initiated on the day of surgery. Especially interesting about this work is that the authors used HFOV when there was evidence of pulmonary hypertension or right ventricular (RV) failure in their patients. This is an interesting approach as it is often assumed that high intra-thoracic pressures increase RV afterload and thus may enhance RV dysfunction. The findings of Bojan and colleagues may be explained by the fact that they were able to decrease the pulmonary vascular resistance by finding a proper balance between atelectasis and overdistension of the lung. It can be argued that it is possible to do so by applying positive end-expiratory pressure. But, at the same time, this may coincide with the delivery of high inspiratory pressures (>30 cm H2O). As HFOV is, in fact, a continuous positive airway pressure system, its advantage is that it is possible to maintain sufficient lung volume without large injurious pressure swings. Although the observations by Bojan and colleagues need to be confirmed in a prospective randomized trial, they have provided arguments not to rule out the early use of HFOV in pediatric cardiac surgery patients.

Management of unpredicted postoperative laryngospasm induced pulmonary oedema—A case report

Pulmonary oedema following general anaesthesia or extubation is an uncommon and unpredictable clinical entity. This unusual disease is actually attributed to pulmonary and haemodynamic changes engendered by high negative intra-thoracic pressures during the state of obstructed respiration. We report a case of postoperative pulmonary oedema in a previously healthy 35-year-old female with post-extubation laryngospasm. The patient responded rapidly to conservative management including removal of secretions, re-intubation, oxygen therapy with positive pressure ventilation and administration of diuretics with short term antibiotics. This report emphasizes the importance of rapid identification and proper management of this serious condition.

Case Scenario: Acute Postoperative Negative Pressure Pulmonary Edema

A 25-yr-old man (weight, 68 kg; height, 183 cm) presentedto the surgery center for excision of back and thigh schwan-nomas on the same day. The patient’s medical history wassignificant only for his history of multiple schwannoma re-sections and a history of smoking one pack of cigarettes perweek for the past 5 yr. He denied previous problems withgeneral anesthesia, and his baseline peripheral oxygen satu-ration was 99% on ambient air.Thepatientwaspremedicatedwith2mgmidazolam,andanesthesia was induced with 250 mg fentanyl, 500 mg thio-pental, and 8 mg vecuronium given for facilitation of tra-cheal intubation. He was atraumatically intubated with a7-mm ID endotracheal tube using a no. 3 Macintosh laryn-goscope (Teleflex Medical, Research Triangle Park, NC) onthe first attempt with direct visualization of the vocal cords.The patient was turned prone, bilateral breath sounds werereconfirmed, and schwannoma excisions were performed ontheleftthighandtheleftflank.Atotalof0.5mghydromor-phone was administered for analgesia. The intraoperativecoursewasunremarkable.Thepatientwashemodynamicallystable with minimal blood loss and was easily ventilated andoxygenated. A total of 500 ml lactated Ringer’s solution wasadministeredduringthe65-minsurgicalprocedure.Thepa-

Edema agudo pulmonar por obstrucción de la vía aérea en el periodo postanestésico inmediato

We report a postanesthetic complication that has not been described in the literature. A 22-year-old man (ASA 1) developed acute pulmonary edema on awakening from balanced anesthesia for scheduled sagittal mandibular ramus osteotomy and implantation of a paranasal graft. We discuss the role of airway obstruction, which can generate high intrathoracic negative pressures and lead to acute pulmonary edema. We also review the differential diagnosis of possible causes of acute pulmonary edema during the postanesthetic recovery. The postoperative course in this case was good.

TAKOTSUBO CARDIOMYOPATHY WITH HYPERVASOPRESSINEMIA

To the Editor: An 88-year-old woman presented with shortness of breath and appetite loss. Chest X-ray revealed significant right pleural effusion, and blood examination showed hyponatremia (119 mmol/L). She had no contributory medical history, and electrocardiography (ECG) was normal at admission. Findings on routine laboratory tests were not remarkable except for hyponatremia. The cytological examination of pleural effusion and chest computed tomography demonstrated that pleural metastasis of lung adenocarcinoma caused the effusion. Further blood examinations showed a high serum arginine vasopressin (AVP) concentration (25.0 pg/mL; normal range 0.3–3.5 pg/mL), low serum osmolality (246 mOsm/L), and high urine osmolality (625 mOsm/L). Her thyroid function and adrenal function were normal. Because of these results, she was diagnosed with syndrome of inappropriate secretion of antidiuretic hormone1 caused by high intrathoracic pressure due to marked pleural effusion. On her 14th hospital day, she suddenly complained of chest pain and chest oppression. ECG showed ST-segment elevation in the V3, V4, and V5 leads. She was diagnosed with acute ST-elevation myocardial infarction (STEMI) and transferred to the cardiovascular center. However, before coronary angiography (CAG) could be performed, chest pain and oppression disappeared, and we no longer found ST-segment elevation on ECG. There was no coronary artery atherosclerosis or spasm identified by CAG, and left ventriculography did not detect any abnormality. Blood examination after CAG showed no enzymatic evidence of myocardial necrosis. A diagnosis of Takotsubo cardiomyopathy2 was considered at this point. Follow-up ECG showed T-wave inversion in the V3, V4, and V5 leads on the 19th hospital day. On the 21st hospital day, the pleural effusion was drained and the intrathoracic pressure lowered. Blood examinations on the 30th hospital day showed a decrease in serum AVP concentration (1.5 pg/mL), increased serum osmolality (268 mOsm/L), decreased urine osmolality (339 mOsm/L), and normalization of serum sodium concentration (137 mmol/L). Many previous articles have reported that recurrence of Takotsubo cardiomyopathy is rare,2, 3 and this patient has not complained of chest pain and chest oppression since the initial episode. Takotsubo cardiomyopathy has cardiac symptoms that are difficult to distinguish from acute STEMI and is observed especially in women aged 60 and older.2 The patients diagnosed with Takotsubo cardiomyopathy complain of chest pain and chest oppression. ECG shows ST-segment elevation, and left ventriculography shows wall motion abnormalities, but CAG shows no evidence of obstructive atherosclerosis of the coronary arteries. Takotsubo cardiomyopathy is associated with several clinical events, such as subarachnoid hemorrhage,4 pheochromocytoma,5 Guillain-Barré syndrome,6 and mental stress.7 Although the pathophysiology and the reason for the strong elderly female predominance remain unknown, and accepted criteria for diagnosis have not been established, some hypotheses are suggested: catecholamine-mediated myocardial stunning, catecholamine-induced microcardiac artery spasm, and epicardial coronary artery spasm.2 AVP is a hormone produced in the cells located predominantly in the supraoptic and paraventricular hypothalamic nuclei, the axons of which terminate in the posterior lobe of the pituitary gland, and is well known as a antidiuretic hormone.8 There are three subtypes of receptors for AVP: V1a, V1b, and V2. AVP also functions as a vasoconstrictor and myocardial contractor through V1a receptors, which are located on vascular smooth muscle cells and cardiomyocytes.9 Because AVP causes peripheral vasoconstriction in the skin, skeletal muscles, gastrointestinal organs, fat tissue, renal arterioles, and coronary arteries, it is used as a vasoconstrictor to support blood pressure in refractory septic shock.10 This case showed hypervasopressinemia (20 times as high as normal level) before she was diagnosed with Takotsubo cardiomyopathy. Her blood pressure was always normal (108/66 mmHg), but it went up to 142/82 mmHg when she complained of chest pain. AVP may have been one of the causes of high blood pressure, working as a strong vasoconstrictor. Because of these results, this case can suggest a new hypothesis in the pathophysiology of Takotsubo cardiomyopathy; AVP may have induced microcardiovascular spasm, causing left ventricular wall motion abnormalities “Takotsubo cardiomyopathy.” Although Takotsubo cardiomyopathy is becoming recognized as a common heart disease, especially in elderly women, acceptable criteria for diagnosis are not established, and the pathophysiology remains unknown. More cases and studies are needed to ascertain the pathophysiology and management of this syndrome. We first demonstrated a relation between Takotsubo cardiomyopathy and hypervasopressinemia. Hypervasopressinemia may be an important trigger of reversible left ventricular dysfunction “Takotsubo cardiomyopathy.” Financial Disclosure: Norinaga Urahama's research has no financial and material support. None of the authors have any potential conflicts of interest associated with this study, and no authors have anything to disclose. Author Contribution: Norinaga Urahama participated in the study concept and design and contributed significantly to the treatment of the patient, acquisition of data, and preparation of manuscript. Hideki Nakashima, Hirokazu Kurose, and Tadatsugu Ohno treated the patient and prepared the manuscript. Sponsor's Role: No sponsor.

Effects of Different Peep Levels on Mesenteric Leukocyte-Endothelial Interactions in Rats During Mechanical Ventilation

INTRODUCTION:Mechanical ventilation with positive end expiratory pressure (PEEP) improves oxygenation and treats acute pulmonary failure. However, increased intrathoracic pressure may cause regional blood flow alterations that may contribute to mesenteric ischemia and gastrointestinal failure. We investigated the effects of different PEEP levels on mesenteric leukocyte-endothelial interactions.METHODS:Forty-four male Wistar rats were initially anesthetized (Pentobarbital I.P. 50mg/kg) and randomly assigned to one of the following groups: 1) NAIVE (only anesthesia; n=9), 2) PEEP 0 (PEEP of 0 cmH2O, n=13), 3) PEEP 5 (PEEP of 5 cmH2O, n=12), and 4) PEEP 10 (PEEP of 10 cmH2O, n=13). Positive end expiratory pressure groups were tracheostomized and mechanically ventilated with a tidal volume of 10 mL/kg, respiratory rate of 70 rpm, and inspired oxygen fraction of 1. Animals were maintained under isoflurane anesthesia. After two hours, laparotomy was performed, and leukocyte-endothelial interactions were evaluated by intravital microscopy.RESULTS:No significant changes were observed in mean arterial blood pressure among groups during the study. Tracheal peak pressure was smaller in PEEP 5 compared with PEEP 0 and PEEP 10 groups (11, 15, and 16 cmH2O, respectively; p<0.05). After two hours of MV, there were no differences among NAIVE, PEEP 0 and PEEP 5 groups in the number of rollers (118±9,127±14 and 147±26 cells/10minutes, respectively), adherent leukocytes (3±1,3±1 and 4±2 cells/100μm venule length, respectively), and migrated leukocytes (2±1,2±1 and 2±1 cells/5,000μm2, respectively) at the mesentery. However, the PEEP 10 group exhibited an increase in the number of rolling, adherent and migrated leukocytes (188±15 cells / 10 min, 8±1 cells / 100 μm and 12±1 cells / 5,000 μm2, respectively; p<0.05).CONCLUSIONS:High intrathoracic pressure was harmful to mesenteric microcirculation in the experimental model of rats with normal lungs and stable systemic blood pressure, a finding that may have relevance for complications related to mechanical ventilation.

Not All Swelling Is Edema in Eclampsia: A Rare and Life-threatening Potential Complication of Eclamptic Seizures

A 24-yr-old, 65-kg, 152-cm primigravida woman with severe pre-eclampsia and a history of asthma was admitted at 38 weeks’ gestationfor magnesium administration and oxytocin induction of labor. Herlaboratory studies and physical examination were within normal limitsexcept for proteinuria, hypertension, and moderate generalized edemawithout obvious facial edema at admission. Because of her preeclamp-sia, an epidural catheter was easily inserted early before onset of activelabor or pain. Three hours later, the patient had a witnessed tonic–clonic eclamptic seizure, which subsided shortly after administrationof 4 mg intravenous lorazepam and assisted mask ventilation. Becauseof recurring fetal heart rate deceleration, an urgent cesarean deliverywas planned. However, the patient was combatively uncooperativedespite a bilateral T4 anesthetic level achieved epidurally while heroxygen saturation remained 100% and blood pressure was 140/85mmHg. The patient was noted to have a Mallampati class I airway withmoderate generalized edema and mild facial edema. Rapid sequencegeneral anesthesia induction was performed with successful atrau-matic intubation on the first attempt, followed by verification of bilat-eral symmetrical breath sounds. Maintenance of anesthetic consisted ofvolume-controlled mechanical ventilation, 50% oxygen, 50% nitrousoxide, 1–2% sevoflurane, midazolam, and opioid without the need foradditional neuromuscular blocker other than succinylcholine at induc-tion. Intraoperative blood pressure and heart rate were maintainedwithin 20% of preoperative values while oxygen saturation was main-tained at 99–100%, end-tidal carbon dioxide between 30–35 mmHg,and airway pressures less than 25 cm H

Tuba players reproduce a Valsalva maneuver while playing high notes

Playing wind instruments requires expiratory efforts. Blowing low notes on a tuba means a low resistance to expiration while playing high notes requires a strenuous expiratory strain. The resulting high intrathoracic pressure may reproduce a Valsalva maneuver. Ten tuba players were asked to blow medium loud long (15 seconds) notes at three different pitches (low, middle, and high) and to perform Valsalva maneuvers at 10, 40, and 60 mmHg. Blood pressure (BP) was measured continuously with a Finapres monitor. The four classic phases of the Valsalva maneuver were reproduced with the notes. The expiratory effort produced systolic BP and pulse pressure falls reaching about 24 mmHg with the high note or the Valsalva 60. BP and pulse pressure falls were linearly related to stroke volume reductions. Reflex heart rate (HR) changes were inversely related to BP falls, with maximal increases for the high notes (24 beats/minute) and Valsalva 60 (33 beats/minute). High baroreflex sensitivity was associated with a high HR response. Total peripheral resistance was reflexly elevated to counteract cardiac output reductions. During rebreathing, BP overshoots reached 30 mmHg for the high note and 53 mmHg for the Valsalva 60. Altogether, these findings indicate that blowing notes on a tuba reproduces the cardiovascular changes seen with a Valsalva maneuver with the effects of blowing high notes being close to a classic (40 mmHg) Valsalva maneuver. In addition, the baroreflex sensitivity might be a predictor of the ability to surmount the BP intolerance that could occur during wind instrument playing.

Refining Ventilatory Treatment for Acute Lung Injury and Acute Respiratory Distress Syndrome

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) IS the clinical manifestation of inflammatory lung edema originating from a variety of insults. Since its first description 40 years ago, the mainstays of management have been institution of mechanical ventilation to ventilate the incompliant lungs, inspired oxygen for hypoxemia, and when hypoxemia is severe, the addition of positive end-expiratory pressure (PEEP) to increase end-expiration lung volume, which facilitates O2 gas exchange. Early on, physicians recognized that the high intrathoracic pressures of mechanical ventilation caused parenchymal stress or rupture, known as barotrauma. However, it took several years to identify the local injury resulting from intratidal opening and closing of parts of the lung (atelectrauma) and the inflammatory reaction of the lung to nonphysiological stress (biotrauma). Subsequently computed tomographic scanning showed that the lung fraction open to gas exchange in ARDS is small, equivalent in size to that of a young child (baby lung model). This observation provided the anatomical basis for the concept of volutrauma, focused on the excessive strain within the baby lung induced by tidal ventilation. Taken together, these multiple potentially damaging factors are now called ventilatorinduced lung injury (VILI). In the last decade, prevention of VILI through gentle lung treatment, by adjusting either tidal volume or PEEP, has become the major goal of mechanical ventilatory support not just for ARDS but for the broader population of patients with acute lung injury (ALI). With regard to tidal volume, this line of reasoning and research was most conclusively supported by the National Heart, Lung, and Blood Institute ARDS Network trial demonstrating an improvement in survival for patients with ALI or ARDS who were ventilated with low tidal volumes (6 mL/kg of predicted body weight) compared with those ventilated with higher tidal volumes (12 mL/kg of predicted body weight). Although many argued that the tidal volume in the control group might have been higher than existing practice, the tidal volume in the interventional group marked a stark departure from usual care and has resulted in a dramatic change in the approach to tidal volume setting for ALI and ARDS. The optimal PEEP strategy, however, has remained unresolved. Evidence from animal studies suggested that higher PEEP (in the range of 10-15 cm H2O) could prevent VILI. Thus, many clinicians were surprised when the first large randomized clinical trial comparing higher levels of PEEP with lower levels of PEEP in patients with ALI and ARDS, the National Heart, Lung, and Blood Institute’s ARDS Network Assessment of Low Tidal Volume and Elevated EndExpiratory Lung Volume to Obviate Lung Injury (ALVEOLI) study, was stopped for futility. In this issue of the JAMA, 2 new large international randomized trials examining the effects of PEEP on outcome in patients with ALI and ARDS are presented. In the Lung Open Ventilation (LOV) trial, the level of PEEP administered, either lower or higher, was selected according to an oxygenation scale conceptually similar to the one used in the previous ALVEOLI study. In the Expiratory Pressure (Express) trial, PEEP selection was based on a more subtle and refined approach, using bedside assessment of lung mechanics instead of gas exchange. This method identified a minimal distention strategy (lower level of PEEP) and an increased recruitment strategy (higher level of PEEP). Despite the different criteria used for PEEP selection, the PEEP levels tested were similar in the 2 studies. In the LOV study, mean PEEP levels on day 1 were 15.6 cm H2O and 10.1 cm H2O, and the subsequent hospital mortality rates were 36.4% and 40.4%. In the Express study, mean PEEP levels on day 1 were 15.8 cm H2O and 8.4 cm H2O, and the

Variaciones hemodinámicas inducidas por la realización de una curva presión–volumen y una maniobra de reclutamiento alveolar en pacientes con síndrome de distrés respiratorio agudo

The plotting of pressure-volume curves and the performance of alveolar recruitment maneuvers are common practices in the care of patients with adult respiratory distress syndrome (ARDS), even though potentially harmful hemodynamic effects are associated with sustaining a high intrathoracic pressure. Our aim was to analyze hemodynamic and ventilatory changes related to these 2 maneuvers and to assess the short-term effectiveness of recruitment. The patients had ARDS and were being monitored with a catheter connected to a PiCCO system. All measurements were taken in sinus rhythm and with adequate vascular filling. Values recorded during plotting of the quasistatic pressure-volume curve and the recruitment maneuver (sustained airway pressure of 40 cm H2O) were the cardiac index, mean arterial pressure, heart rate, systolic volume index, and oxygen saturation (SpO2). Blood gas measurements were recorded before the maneuvers and 15 minutes afterwards. All parameters decreased significantly in the 14 patients studied. The mean (SD) maximum decreases, from which all patients recovered within 2 minutes, were as follows: cardiac index, 26% (16%); mean arterial pressure, 6% (6%); heart rate, 4% (5%), systolic volume index, 21% (15%); and SpO2, 3% (3%). Significant increases in PaO2 (7% [6%]) and the ratio of PaO2 to the fraction of inspired oxygen were recorded after the recruitment maneuver (P=.016 and P=.014, respectively), but the changes were not clinically significant. The hemodynamic disturbances associated with the alveolar recruitment maneuver based on sustaining a high end-expiratory pressure and the minor improvement in oxygenation achieved as a result suggest that the routine use of that maneuver in ARDS patients is of questionable value.

Recurrent pleural effusion during peritoneal dialysis: answer

Answers1. Leakage of peritoneal dialysis (PD) fluid into thepleural cavity.2. Measurement of the glucose concentration in thepleural effusion.3. Very high intrathoracic pressure during mechanicalventilation for acute respiratory distress syndrome(ARDS) transiently prevented leakage of PD fluid intothe pleural cavity. Reduction of ventilator settingsunmasked the pleuro-peritoneal connection with PDfluid leaking through the incision site.4. To decrease PD dwell volume or temporarily discontinuePD and switch to hemodialysis / hemofiltration.CommentaryHydrothorax - mostly on the right side - is a well-knowncomplication of PD, which is observed in approximately2% of all PD patients [1]. In our patient, the glucoseconcentration in the pleural fluid obtained in the firstpuncture was 24.9 mmol/L (452.7 mg/dL), in the fluiddraining from the insertion site four weeks later this was20.5 mmol/L (372.7 mg/dL). Her blood glucose levels werearound 10 mmol/L (180 mg/dL) during the time of the firstpuncture and around 7 mmol/L (126 mg/dL) on the secondoccasion. Thus, the intrapleural glucose concentrationgreatly exceeded the serum values. This finding can onlybe explained by leakage of PD fluid into the pleural cavity,which ceased transiently during high-pressure ventilation.With these ventilator settings, the intrathoracic pressureexceeded the intraaabdomial pressure thereby preventingperitoneal-pleural shunting.Usually, demonstration of high glucose concentrations inthe pleural fluid is sufficient to confirm a peritoneal-pleuralleak [2]. In ambiguous cases - or if no pleural puncture isdone - peritoneal-pleural shunting can be demonstrated byadding a radioactive tracer to the dialysate [3, 4]. Although2 - 4 times higher than the serum concentrations, theintrapleural glucose concentration was still significantlylower than the glucose concentration in the PD fluid, whichwas 137.5 mmol/L (2475 mg/dL). This reflects incompleteequilibration between the fluid collections in both compart-ments due to inconstant shunting or a small communicationbetween both cavities.Leakage of PD fluid into the pleural cavity has to bedifferentiated from other causes of transudative pleuraleffusionsuchascongestivecardiacfailure,hypoalbuminemia,or fluid overload. In the latter conditions, ultrafiltration ispreserved and can typically be increased by using higherPD fluid glucose concentrations. Pleural effusions from aperitoneal-pleural leak typically do not improve with thisintervention. In this respect the present case is atypical asultrafiltration was preserved and could be increased afterswitch to a higher PD fluid glucose concentration.