High-frequency oscillation and tracheal gas insufflation in patients with severe acute respiratory distress syndrome and traumatic brain injury: an interventional physiological study

In acute respiratory distress syndrome (ARDS), combined high-frequency oscillation (HFO) and tracheal gas insufflation (TGI) improves gas exchange compared with conventional mechanical ventilation (CMV). We evaluated the effect of HFO-TGI on PaO2/fractional inspired O2 (FiO2) and PaCO2, systemic hemodynamics, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) in patients with traumatic brain injury (TBI) and concurrent severe ARDS

The effect of high frequency oscillatory ventilation combined with tracheal gas insufflation on extravascular lung water in patients with acute respiratory distress syndrome: a randomized, crossover, physiological study.

Purpose: High frequency oscillation combined with tracheal gas insufflation (HFO-TGI) improves oxygenation in patients with Acute Respiratory Distress Syndrome (ARDS). There is limited physiologic data regarding the effects of HFO-TGI on hemodynamics and pulmonary edema during ARDS. The aim of this study was to investigate the effect of HFO-TGI on extravascular lung water (EVLW). Materials and Methods: We conducted a prospective, randomized, crossover study. Consecutive eligible patients with ARDS received sessions of conventional mechanical ventilation (CMV) with recruitment maneuvers (RMs), followed by HFO-TGI with RMs, or vice versa. Each ventilatory technique was administered for 8 hours. The order of administration was randomly assigned. Arterial/central venous blood gas analysis and measurement of hemodynamic parameters and EVLW were performed at baseline and after each 8-hour period using the single-indicator thermodilution technique. Results: Twelve patients received 32 sessions. PaO2/FiO2 and respiratory system compliance were higher (p<0.001 for both), while EVLW indexed to predicted body weight (EVLWI) and oxygenation index were lower (p=0.021 and 0.029, respectively) in HFO-TGI compared with CMV. There was a significant correlation between PaO2/FiO2 improvement and EVLWI drop during HFO-TGI (Rs=-0.452, p= 0.009). Conclusions: HFO-TGI improves gas exchange and lung mechanics in ARDS, and potentially attenuates EVLW accumulation

Advances in the Clinical Management of Cardiac Arrest

Cardiac arrest constitutes an extremely life-threatening condition that inevitably and promptly results in death if left untreated. Cardiac arrest outcomes still remain very poor, especially when the presenting cardiac rhythm is nonshockable. Important, recent, clinical research has focused on the quality of cardiopulmonary resuscitation (CPR), the mechanical augmentation of the circulation during CPR, CPR drugs, and therapeutic hypothermia. Chest compression depth of at least 51 mm increases the probability of neurologically favorable survival. Despite initially promising results, a large effectiveness study failed to confirm the efficacy of the mechanical augmentation of the circulation. Epinephrine has finally been shown to slightly improve functional outcome after out-of-hospital cardiac arrest, especially when given early. In a recent, in-hospital study of 268 patients, the addition of vasopressin and methylprednisolone during CPR and the administration of hydrocortisone in postresuscitation shock improved functional outcome after vasopressor-requiring cardiac arrest; however, corticosteroid efficacy still needs to be separately confirmed in a large, international trial. Lastly, preliminary human data may support the conduct of high quality trials evaluating the efficacy of beta adrenergic antagonists in shockable cardiac arrest. The purpose of this paper is to review these potentially important advances in the management of cardiac arrest.

Current Pharmacological Advances in the Treatment of Cardiac Arrest

Cardiac arrest requires immediate treatment, in order to prevent patient death. Cardiac arrest outcomes still remain very poor, especially when the patient requires vasopressor treatment. Vasopressors have been advocated, in order to increase the coronary and cerebral perfusion pressure during cardiopulmonary resuscitation (CPR). Recent data suggest an epinephrine-related benefit with respect to short- and long-term outcomes, only when epinephrine is administered within the first 10 min of collapse. Also, increasing the epinephrine dosing interval from 3-5 to 6-10 min during CPR may be associated with improved long-term outcomes. In the in-hospital setting, the combination of vasopressin, epinephrine, and corticosteroid supplementation during and after CPR (in the presence of postresuscitation shock) may be superior to epinephrine alone during CPR. The use of new formulations of amiodarone, potentially devoid of serious hypotensive effects, may contribute to increased rates of sustained return of spontaneous circulation in patients with ventricular fibrillation / pulseless ventricular tachycardia cardiac arrest. Encouraging preliminary results have been reported on the use of beta blockers in patients with shockable cardiac arrest. Other potentially promising pharmacological interventions include the use of cariporide, nitrates (and particularly inhaled nitric oxide), noble gases, levosimendan, and erythropoietin. The purpose of the current paper is to review the clinical and laboratory evidence that support new and potentially useful pharmacological interventions during CPR

“Low-” versus “high”-frequency oscillation and right ventricular function in ARDS. A randomized crossover study

Abstract Background Recent, 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. Methods We 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. Results The 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 (R 2 = 0.21–0.43). Conclusions In 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 registration This 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